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==Typhus fever==
==Causes==
*Typhus refers to a group of zoonotic diseases caused by bacteria that are spread to humans by fleas, lice, and chiggers.  
===Common causes===
*Typhus fevers include scrub typhus, murine typhus, and epidemic typhus.
*Peptic ulcer disease
*The most common symptoms are fever, headaches, and sometimes rash.
**Responsible for around 33%-50% of upper GI bleeding
==Historical perspective==
**Peptic ulcer disease is most commonly due to H.pylori or nonsteroidal anti-inflammatory drugs (NSAIDs).
*In 1083, Typhus was first identified as a disease in Spain.
**Upper GI bleeding is the most common complication of peptic ulcer disease  and may be the initial presentation.<ref name="pmid28798512">{{cite journal |vauthors=Drini M |title=Peptic ulcer disease and non-steroidal anti-inflammatory drugs |journal=Aust Prescr |volume=40 |issue=3 |pages=91–93 |year=2017 |pmid=28798512 |pmc=5478398 |doi=10.18773/austprescr.2017.037 |url=}}</ref>
*In 1489, during the Spanish siege of Moorish Granada, the first reliable description of the disease was made.
*Esophageal varices
*In 1546, Fracastoro extensively described the disease and distinguished it from plague in his book Contagione.
** Responsible for around 14% of upper GI bleeding
*In 1676, Von Zavorziz wrote a book on  typhus called The Infection of Military Camps.
** These dilated veins within the esophagus are usually secondary to portal hypertension from cirrhosis.
*In 1739, Huxham stated typhus and typhoid as two different entities, later in the same year Boissier de Sauvages confirmed this and called it exanthematic typhus.
** Massive variceal hemorrhage is responsible for acute life-threatening upper GI bleeding which is an medical emergency .<ref name="pmid14959953">{{cite journal |vauthors=Pilotto A, Franceschi M, Leandro G, Paris F, Niro V, Longo MG, D'Ambrosio LP, Andriulli A, Di Mario F |title=The risk of upper gastrointestinal bleeding in elderly users of aspirin and other non-steroidal anti-inflammatory drugs: the role of gastroprotective drugs |journal=Aging Clin Exp Res |volume=15 |issue=6 |pages=494–9 |year=2003 |pmid=14959953 |doi= |url=}}</ref><ref name="pmid23356751">{{cite journal |vauthors=Hreinsson JP, Kalaitzakis E, Gudmundsson S, Björnsson ES |title=Upper gastrointestinal bleeding: incidence, etiology and outcomes in a population-based setting |journal=Scand. J. Gastroenterol. |volume=48 |issue=4 |pages=439–47 |year=2013 |pmid=23356751 |pmc=3613943 |doi=10.3109/00365521.2012.763174 |url=}}</ref>
*In 1829, Louis, French clinician clearly differentiated Typhus Fever from Typhoid Fever.
*Mallory-Weiss syndrome :
*In 1836, Gerhard(United States) clearly distinguished the two diseases from each other based on pathologic findings.
**Responsible for around 5% of upper GI bleeding
*In 1909, Charles Nicolle for the first time described the role of lice bite in transmission of typhus. In 1928, he was awarded the Nobel Prize for his discovery.
**A longitudinal mucosal laceration in the distal esophagus and/or proximal stomach that usually results from forceful retching
*In 1916, Weil and Felix reported the isolation of a Proteus that was agglutinated by the sera of patients with typhus, which was the basis for the first serological test for the disease.
 
*In 1916, DaRocha-Lima isolated and identified Rickettsia prowazeki.
===Less common causes===
*In 1926, Maxcy described the various forms of typhus.
*Neoplasms
*In 1938, Starzyk demonstrated  that patients are infected by the feces and not the bite of the louse.
** gastric cancer
*In 1922, Wolbach described the human histopathology of R prowazekii infection.<ref name="pmid4997497">{{cite journal |vauthors=Woodward TE |title=Typhus verdict in American history |journal=Trans. Am. Clin. Climatol. Assoc. |volume=82 |issue= |pages=1–8 |year=1971 |pmid=4997497 |pmc=2441062 |doi= |url=}}</ref>
** esophageal tumors
*In 1938, Cox was successful in growing cell cultures of R prowazekii in embryonated eggs.<ref name="Cox1938">{{cite journal|last1=Cox|first1=Herald R.|title=Use of Yolk Sac of Developing Chick Embryo as Medium for Growing Rickettsiae of Rocky Mountain Spotted Fever and Typhus Groups|journal=Public Health Reports (1896-1970)|volume=53|issue=51|year=1938|pages=2241|issn=00946214|doi=10.2307/4582741}}</ref>
*Esophagitis (complications due to erosive or necrotizing infectious esophagitis )
*In 1940, Cox and Bell prepared an Epidemic Typhus vaccine based upon the use of tissue culture.
*Gastric erosions/gastropathy <ref name="pmid20871188">{{cite journal |vauthors=Kaviani MJ, Pirastehfar M, Azari A, Saberifiroozi M |title=Etiology and outcome of patients with upper gastrointestinal bleeding: a study from South of Iran |journal=Saudi J Gastroenterol |volume=16 |issue=4 |pages=253–9 |year=2010 |pmid=20871188 |pmc=2995092 |doi=10.4103/1319-3767.70608 |url=}}</ref>
*In 1943–1944, during World war II DDT (a pesticide) was employed to control lice and typhus.
** Acute erosive gastritis caused by drugs, radiation, infection, or direct trauma.
*In 1998, Andersson et al, sequenced the entire genome after much study of the fundamental mechanisms of R prowazekii's intracellular life and its effects on host cells.<ref name="pmid9823893">{{cite journal |vauthors=Andersson SG, Zomorodipour A, Andersson JO, Sicheritz-Pontén T, Alsmark UC, Podowski RM, Näslund AK, Eriksson AS, Winkler HH, Kurland CG |title=The genome sequence of Rickettsia prowazekii and the origin of mitochondria |journal=Nature |volume=396 |issue=6707 |pages=133–40 |year=1998 |pmid=9823893 |doi=10.1038/24094 |url=}}</ref>
** Reactive gastropathy may be due to bile reflux, particularly after partial gastrectomy.
** Portal hypertensive gastropathy, which results in increased friability of gastric mucosa in patients with cirrhosis.<ref name="pmid4078920">{{cite journal |vauthors=Davidson AT |title=Upper gastrointestinal bleeding: causes and treatment |journal=J Natl Med Assoc |volume=77 |issue=11 |pages=944–5 |year=1985 |pmid=4078920 |pmc=2571206 |doi= |url=}}</ref><ref name="pmid18346679">{{cite journal |vauthors=van Leerdam ME |title=Epidemiology of acute upper gastrointestinal bleeding |journal=Best Pract Res Clin Gastroenterol |volume=22 |issue=2 |pages=209–24 |year=2008 |pmid=18346679 |doi=10.1016/j.bpg.2007.10.011 |url=}}</ref>
*Dieulafoy lesions
**Dilated aberrant submucosal vessels that erode the overlying epithelium in the absence of an ulcer
*Gastric varices
*Gastric antral vascular ectasia
**Dilated gastric vessels of unknown etiology that cause chronic UGIB and iron-deficiency anemia
 
===Rare causes===
*Bleeding from the hepatobiliary tract
**Most commonly secondary to a liver or biliary tract injury, from trauma or following procedures or surgery.
**Diagnosed by endoscopic retrograde cholangiopancreatography (ERCP) and treated with arteriography
*Aortoenteric fistulas,
**Most commonly involves the lower duodenum.
**Common causes include aortic aneurysms or prosthetic vascular grafts, syphilis and tuberculosis
**Presents with frank UGIB along with a pulsatile mass and abdominal pain radiating to the back.
**Diagnosed by endoscopy.
*Crohn disease involving the upper gastrointestinal tract
*Metastatic malignancy involving the upper gastrointestinal tract, such as melanoma or renal cell carcinoma
*Hemosuccus pancreaticus
**Pancreatic inflammation or cancer may result in bleeding into the pancreatic duct, which connects to the duodenum


==Pathophysiology==
==Risk factors==
Typhus fever is a zoonotic disease, Humans could be infected by bites from ticks, lice, inhalation of the bacteria, and direct contact of bacteria with skin wounds or mucous membranes. Following transmission, white blood cells phagocyte the pathogen and transports it via hematologic or lymphatic route to different organs, specially to those of the reticuloendothelial system. The pathophysiology of typhus fever can be described in the following steps.
*Advancing age<ref name="pmid21341933">{{cite journal |vauthors=Morales Uribe CH, Sierra Sierra S, Hernández Hernández AM, Arango Durango AF, López GA |title=Upper gastrointestinal bleeding: risk factors for mortality in two urban centres in Latin America |journal=Rev Esp Enferm Dig |volume=103 |issue=1 |pages=20–4 |year=2011 |pmid=21341933 |doi= |url=}}</ref><ref name="pmid19744387">{{cite journal |vauthors=Rodríguez-Hernández H, Rodríguez-Morán M, González JL, Jáquez-Quintana JO, Rodríguez-Acosta ED, Sosa-Tinoco E, Guerrero-Romero F |title=[Risk factors associated with upper gastrointestinal bleeding and with mortality] |language=Spanish; Castilian |journal=Rev Med Inst Mex Seguro Soc |volume=47 |issue=2 |pages=179–84 |year=2009 |pmid=19744387 |doi= |url=}}</ref><ref name="pmid24108375">{{cite journal |vauthors=Corzo Maldonado MA, Guzmán Rojas P, Bravo Paredes EA, Gallegos López RC, Huerta Mercado-Tenorio J, Surco Ochoa Y, Prochazka Zárate R, Piscoya Rivera A, Pinto Valdivia J, De los Ríos Senmache R |title=[Risk factors associated to mortality by upper GI bleeding in patients from a public hospital. A case control study] |language=Spanish; Castilian |journal=Rev Gastroenterol Peru |volume=33 |issue=3 |pages=223–9 |year=2013 |pmid=24108375 |doi= |url=}}</ref><ref name="pmid5192276">{{cite journal |vauthors=Soldatov IB, Tokman AS, Esipovich IaN |title=[On the forms of dissemination of advanced experience of otorhinolaryngologists in dispensary work] |language=Russian |journal=Zdravookhr Ross Fed |volume=11 |issue=4 |pages=19–21 |year=1967 |pmid=5192276 |doi= |url=}}</ref>
===Transmission===
*Previous history of gastrointestinal bleed
*Rickettsial pathogens are harboured by parasites such as fleas, lice, mites, and ticks.  
*Chronic kidney disease
*Organisms are transmitted by the bites from these parasites or by the inoculation of infectious fluids or feces from the parasites into the skin.  
*Underlying cardiovascular disease
*Cirrhosis and portal hypertension
*Presence of H.pylori
*NSAID or aspirin use in patients with a history of ulcer disease
** Those on dual antiplatelet therapy; those on anticoagulant therapy; or those with two or more of the following risk factors
*** Age 60 years or older
*** Glucocorticoid use
*** Dyspepsia
*** Gastroesophageal reflux disease
* Critical illness
** Nosocomial stress ulcers due the to the use of mechanical ventilation for more than 48 hours, and coagulopathy
** Other risk factors for nosocomial stress ulcerations in critically ill patients include a history of gastrointestinal ulceration or bleeding within the past year; or two or more of the following risk factors: presence of sepsis, ICU admission lasting longer than 1 week, occult gastrointestinal bleeding lasting 6 days or longer, and administration of more than 250 mg of hydrocortisone or equivalent glucocorticoid therapy
*Rare conditions associated with gastric acid hypersecretion, such as Zollinger-Ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy.
{| class="wikitable"
! colspan="2" |Causes of Acute Upper GI bleeding
|-
|Esophagus
|
* Esophagitis
* Mallory–Weiss tear
* Esophageal varices
* Esophageal ulcers
* Esophageal cancer
|-
|Gastric
|
* Gastric ulcer
* Gastric cancer
* Gastritis
* Gastric varices
* Portal hypertensive gastropathy
* Gastric antral vascular ectasia
* Dielafuoy lesions
|-
|Duodenal
|
* Duodenal ulcer
* Vascular malformations, including aorto-enteric
* Fistulae


{|
* Bleeding from the bile duct due to
class="wikitable"
** Liver biopsy
!Disease
** Trauma
!Etiological agent
** Arteriovenous malformations
!Vector
** Liver tumors
|-
|Epidemic typhus 
|''Rickettsia prowazekii''
|Human body louse
|-
|Murine typhus
|''Rickettsia typhi''
|Infected fleas 
|-
|Scrub typhus
|''Orientia tsutsugamushi'' 
|Larval mites 
|}
|}


===Dissemination===
===Associated Conditions===
*Scratching a louse-bite site allows the rickettsia-laden excrement to be inoculated into the bite wound.  
*Heyde syndrome, aortic valve stenosis with associated gastrointestinal bleeding thought to be due to acquired reduction of von Willebrand factor.<ref name="pmid26124230">{{cite journal |vauthors=Hudzik B, Wilczek K, Gasior M |title=Heyde syndrome: gastrointestinal bleeding and aortic stenosis |journal=CMAJ |volume=188 |issue=2 |pages=135–8 |year=2016 |pmid=26124230 |pmc=4732965 |doi=10.1503/cmaj.150194 |url=}}</ref>
*Following transmission, rickettsia are ingested by [[macrophages]] and [[Polymorphonuclear cells|polymorphonuclea]]<nowiki/>r cells. On ingestion, they replicate intracellularly inside the lysed cells and disseminate systemically.
 
===Incubation===
==History==
Incubation period of Typhus fever varies from one to two weeks.
Obtaining the history is the most important aspect of making a diagnosis of upper GI bleed. It provides insight into the cause, precipitating factors and associated comorbid conditions and also helps in determining the severity of the bleed as well as in identifying the potential source of bleed:<ref name="pmid25400991">{{cite journal |vauthors=Kim BS, Li BT, Engel A, Samra JS, Clarke S, Norton ID, Li AE |title=Diagnosis of gastrointestinal bleeding: A practical guide for clinicians |journal=World J Gastrointest Pathophysiol |volume=5 |issue=4 |pages=467–78 |year=2014 |pmid=25400991 |pmc=4231512 |doi=10.4291/wjgp.v5.i4.467 |url=}}</ref><ref name="pmid23547576">{{cite journal |vauthors=Bull-Henry K, Al-Kawas FH |title=Evaluation of occult gastrointestinal bleeding |journal=Am Fam Physician |volume=87 |issue=6 |pages=430–6 |year=2013 |pmid=23547576 |doi= |url=}}</ref>
===Pathogenesis===
*A history of epigastric pain, dyspepsia, or prior peptic ulcer may suggest the diagnosis of peptic ulcer disease.  
*On transmission, Rickettsia is actively phagocytosed by the endothelial cells of the small venous, arterial, and capillary vessels.
*A history of documented prior upper GI bleeding is important because approximately 60% of upper GI bleeders are rebleeding from the same site.  
*It is followed by systemic hematogenous spread resulting in multiple localizing vasculitis. The major pathology is caused by vasculitis and its complications.
*Prior use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) is important because these patients have an increased risk of gastric ulcer and a fourfold risk of significant GI bleeding compared with other patients.
*This process of inflammatory response (aggregation of leukocytes, macrophages, and platelets) along with occlusion of small blood vessels results in formation of nodules.
*A history of alcoholism increases the likelihood of cirrhosis and consequently of bleeding from esophageal varices or congestive gastropathy but alcoholics also frequently have peptic ulcers or gastritis.
*Occlusion of supplying blood vessels also causes gangrene of the distal portions of the extremities, nose, ear lobes, and genitalia.
*Cigarette smokers have a significantly higher rate of the recurrent duodenal ulcer as compared with nonsmokers and a history of cigarette smoking should be elicited.
*This vasculitic process also results destruction of the endothelial cells and leakage of the blood leading to volume depletion and subsequently leading to decreased tissue perfusion and, possibly, organ failure.
*Vomiting, coughing, or retching before bleeding is suggestive of a Mallory-Weiss tear.<ref name="pmid28839832">{{cite journal |vauthors=Jafar W, Jafar AJN, Sharma A |title=Upper gastrointestinal haemorrhage: an update |journal=Frontline Gastroenterol |volume=7 |issue=1 |pages=32–40 |year=2016 |pmid=28839832 |pmc=5369541 |doi=10.1136/flgastro-2014-100492 |url=}}</ref>
*Endothelial damage lead to activation of clotting system
A directed history may also alert to consider unusual causes.<ref name="pmid17942452">{{cite journal |vauthors=Palmer K |title=Acute upper gastrointestinal haemorrhage |journal=Br. Med. Bull. |volume=83 |issue= |pages=307–24 |year=2007 |pmid=17942452 |doi=10.1093/bmb/ldm023 |url=}}</ref>
*A history of pancreatitis suggests possible hemorrhage from a pancreatic pseudocyst. Erosion of a pancreatic pseudocyst into the duodenum or stomach may cause massive hematemesis, and the patient may present in shock.
*Patients with prior abdominal aortic aneurysm repair may present with severe GI hemorrhage from an aortoenteric. This fistula often presents with a herald bleed followed within 4 to 96 hours by massive bleeding.
*A personal or family history of recurrent epistaxis may suggest the diagnosis of Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia), and a careful examination for skin telangiectasias should be performed.
*Patients with renal failure frequently have GI bleeding. This bleeding is often due to peptic ulcer disease or angiodysplasia. This bleeding may be severe because of clotting dysfunction associated with renal disease.
 
===Symptoms===<ref name="pmid11100986">{{cite journal |vauthors=Lau JY, Chung S |title=Management of upper gastrointestinal haemorrhage |journal=J. Gastroenterol. Hepatol. |volume=15 Suppl |issue= |pages=G8–12 |year=2000 |pmid=11100986 |doi= |url=}}</ref><ref name="pmid26417980">{{cite journal |vauthors=Gralnek IM, Dumonceau JM, Kuipers EJ, Lanas A, Sanders DS, Kurien M, Rotondano G, Hucl T, Dinis-Ribeiro M, Marmo R, Racz I, Arezzo A, Hoffmann RT, Lesur G, de Franchis R, Aabakken L, Veitch A, Radaelli F, Salgueiro P, Cardoso R, Maia L, Zullo A, Cipolletta L, Hassan C |title=Diagnosis and management of nonvariceal upper gastrointestinal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) Guideline |journal=Endoscopy |volume=47 |issue=10 |pages=a1–46 |year=2015 |pmid=26417980 |doi=10.1055/s-0034-1393172 |url=}}</ref>


==Natural history==
==Primary Prevention==
Without treatment, fever may last 2 weeks, followed by a prolonged recovery time and a significantly greater chance of developing complications. Delay in treatment may result in advanced disease, including neurologic manifestations such as confusion, seizures, or coma, and widespread vasculitis (damage to the endothelial cells that line blood vessels).  
Effective measures for the primary prevention of upper GI bleeding include administration of PPI in patients with an increased risk due to critical illness or use of NSAIDs or aspirin. In patients with cirrhosis and suspected portal hypertension, who found to have esophageal varices patients are given prophylactic treatment with a nonselective β-blocker or undergo endoscopic variceal ligation (EVL) with surveillance endoscopy.
===Complications===
===Patients with stress ulcers===
*Hearing loss
*The American Society of Health-System Pharmacists developed clinical practice guidelines that recommend prophylaxis with a PPI or with a histamine-2 receptor antagonist (H2RA) for ICU patients at high risk for UGIB.<ref name="pmid23997925">{{cite journal |vauthors=Brooks J, Warburton R, Beales IL |title=Prevention of upper gastrointestinal haemorrhage: current controversies and clinical guidance |journal=Ther Adv Chronic Dis |volume=4 |issue=5 |pages=206–22 |year=2013 |pmid=23997925 |pmc=3752180 |doi=10.1177/2040622313492188 |url=}}</ref><ref name="pmid25685721">{{cite journal |vauthors=Yasuda H, Matsuo Y, Sato Y, Ozawa S, Ishigooka S, Yamashita M, Yamamoto H, Itoh F |title=Treatment and prevention of gastrointestinal bleeding in patients receiving antiplatelet therapy |journal=World J Crit Care Med |volume=4 |issue=1 |pages=40–6 |year=2015 |pmid=25685721 |pmc=4326762 |doi=10.5492/wjccm.v4.i1.40 |url=}}</ref><ref name="pmid19633792">{{cite journal |vauthors=Biecker E, Heller J, Schmitz V, Lammert F, Sauerbruch T |title=Diagnosis and management of upper gastrointestinal bleeding |journal=Dtsch Arztebl Int |volume=105 |issue=5 |pages=85–94 |year=2008 |pmid=19633792 |pmc=2701242 |doi=10.3238/arztebl.2008.0085 |url=}}</ref>
*Myocarditis
===Patients on NSAID, aspirin, or antiplatelet therapy===
*Vasculitis
*Joint gastroenterology and cardiology society practice guidelines recommend gastroprotective therapy with a PPI for patients considered to be at increased risk of bleeding from chronic NSAID and aspirin therapy.
*Aseptic meningitis
===Patients with cirrhosis and varices===
===Prognosis===
*EGD is used to screen for the presence of varices in patients with cirrhosis complicated by portal hypertension.
Prognosis depends on age and immunization status of the individual. With prompt, appropriate treatment, most individuals recover completely.The fatality rate for epidemic typhus varies from 1% to 20%.
*In patients with cirrhosis who do not have varices, no prophylaxis is indicated.
*In patients with cirrhosis and varices that have not bled, prophylactic treatment with nonselective β-blockers, such as nadolol or propranolol, may decrease portal blood flow and thus decrease the risk of variceal bleed.
*In patients with cirrhosis who have medium or large varices that have not bled, EVL is an alternative prophylactic treatment.
*EVL is repeated every several weeks until obliteration of varices is seen.
*Surveillance EGD should then be performed 1 to 3 months after obliteration and then every 6 to 12 months to check for variceal recurrence.


==History==
==Secondary Prevention==
*History of travel to endemic areas
Effective measures for the secondary prevention of UGIB include discouraging the use of NSAIDS in all patients with a history of UGIB.
*History of tick bite
===Seondary Prevention===
*NSAID use in all patients with a history of UGIB should be discouraged.<ref name="pmid22142030">{{cite journal |vauthors=Chan FK |title=Anti-platelet therapy and managing ulcer risk |journal=J. Gastroenterol. Hepatol. |volume=27 |issue=2 |pages=195–9 |year=2012 |pmid=22142030 |doi=10.1111/j.1440-1746.2011.07029.x |url=}}</ref>


==Symptoms==
===UGIB from peptic ulcer disease===
*Avoid NSAIDs.
*For patients who are at high risk for rebleeding (elderly patients; those taking anticoagulant and antiplatelet medications), indefinite use of a PPI may be recommended.<ref name="Garcia-TsaoSanyal2007">{{cite journal|last1=Garcia-Tsao|first1=Guadalupe|last2=Sanyal|first2=Arun J.|last3=Grace|first3=Norman D.|last4=Carey|first4=William D.|title=Prevention and Management of Gastroesophageal Varices and Variceal Hemorrhage in Cirrhosis|journal=The American Journal of Gastroenterology|volume=102|issue=9|year=2007|pages=2086–2102|issn=0002-9270|doi=10.1111/j.1572-0241.2007.01481.x}}</ref>
*H pylori status should be determined, and patients should be treated if positive.
*Eradication is confirmed with stool sample or repeat endoscopy with biopsy.
===UGIB from varices===
*A combination of nonselective β-blockers plus EVL is the best option for secondary prophylaxis of UGIB from varices.
*The nonselective β-blocker should be titrated up as tolerated.
*Variceal banding should be repeated every 2 to 3 weeks until the varices are obliterated.
**EGD must be performed 1 to 3 months after initial obliteration then every 6 to 12 months to check for variceal recurrence.
==Prognosis==
*Prognosis is generally good with appropriate treatment, and the 1-year mortality rate of patients with nonvariceal UGIB is approximately 10%.<ref name="pmid23251344">{{cite journal |vauthors=Roberts SE, Button LA, Williams JG |title=Prognosis following upper gastrointestinal bleeding |journal=PLoS ONE |volume=7 |issue=12 |pages=e49507 |year=2012 |pmid=23251344 |pmc=3520969 |doi=10.1371/journal.pone.0049507 |url=}}</ref><ref name="pmid7908623">{{cite journal |vauthors=Katschinski B, Logan R, Davies J, Faulkner G, Pearson J, Langman M |title=Prognostic factors in upper gastrointestinal bleeding |journal=Dig. Dis. Sci. |volume=39 |issue=4 |pages=706–12 |year=1994 |pmid=7908623 |doi= |url=}}</ref><ref name="pmid26430191">{{cite journal |vauthors=Kurien M, Lobo AJ |title=Acute upper gastrointestinal bleeding |journal=Clin Med (Lond) |volume=15 |issue=5 |pages=481–5 |year=2015 |pmid=26430191 |doi=10.7861/clinmedicine.15-5-481 |url=}}</ref><ref name="pmid24267496">{{cite journal |vauthors=Feinman M, Haut ER |title=Upper gastrointestinal bleeding |journal=Surg. Clin. North Am. |volume=94 |issue=1 |pages=43–53 |year=2014 |pmid=24267496 |doi=10.1016/j.suc.2013.10.004 |url=}}</ref>
*In UGIB, the prognosis doesn't depend on the severity of bleeding but depends upon patients age and comorbid conditions.
*The majority of patients with UGIB will stop bleeding spontaneously.
*A clean ulcer base has less than a 3% chance of rebleeding; therefore, these lesions are not usually treated or scoped again.
*In otherwise stable patients, patients with a clean ulcer base has less than a 3% chance of rebleeding and are good candidates for early discharge.
*Treatment includes management of underlying liver disease and prevention of complications of cirrhosis.
*Despite advances in gastric acid suppression as well as improved endoscopic diagnostic and therapeutic techniques, the mortality rate from UGIB has remained stable.
===Scoring systems===
Two scoring systems identify those at risk for adverse outcomes from UGIB:<ref name="pmid28286843">{{cite journal |vauthors=Ebrahimi Bakhtavar H, Morteza Bagi HR, Rahmani F, Shahsavari Nia K, Ettehadi A |title=Clinical Scoring Systems in Predicting the Outcome of Acute Upper Gastrointestinal Bleeding; a Narrative Review |journal=Emerg (Tehran) |volume=5 |issue=1 |pages=e36 |year=2017 |pmid=28286843 |pmc=5325906 |doi= |url=}}</ref>
*The Glasgow Blatchford Score (GBS)
*The Rockall score
===The Glasgow Blatchford Score (GBS)===
*The Glasgow Blatchford Score (GBS) helps in identifying low-risk patients with UGIB who can be managed safely as outpatients without an urgent endoscopy.<ref name="pmid11073021">{{cite journal |vauthors=Blatchford O, Murray WR, Blatchford M |title=A risk score to predict need for treatment for upper-gastrointestinal haemorrhage |journal=Lancet |volume=356 |issue=9238 |pages=1318–21 |year=2000 |pmid=11073021 |doi=10.1016/S0140-6736(00)02816-6 |url=}}</ref><ref name="pmid22719181">{{cite journal |vauthors=Stanley AJ |title=Update on risk scoring systems for patients with upper gastrointestinal haemorrhage |journal=World J. Gastroenterol. |volume=18 |issue=22 |pages=2739–44 |year=2012 |pmid=22719181 |pmc=3374976 |doi=10.3748/wjg.v18.i22.2739 |url=}}</ref>
*GBS parameters include
**Blood urea nitrogen level
**Hematocrit level
**Heart rate
**Systolic blood pressure
**Presence of syncope or melena, as well as presence of comorbid heart and liver disease.
*GBS is the more effective system for predicting the need for transfusion in patients with UGIB.
{| class="wikitable"
{| class="wikitable"
!Typhus fever
! colspan="4" |The Glasgow Blatchford Score (GBS)
!Rash
|-
! colspan="3" |'''Admission risk markers'''
!'''Score'''
|-
| colspan="2" rowspan="4" |'''Blood urea nitrogen level (mg/dl)'''
|  ≥ 18.2 to < 22.4
|2
|-
|  ≥ 22.4 to < 28
|3
|-
|-
|Scrub typhus
|≥ 28 to < 70
|About 25–50% of scrub typhus patients develop a rash. The rash is usually macular or maculopapular. Typically, it will begin on the abdomen of an infected individual and then spread to the extremities. Petechiae are uncommon
|4
|-
|-
|Murine Typhus
|  ≥ 70
|The rash typically occurs at the end of the first week of the illness and lasts 1–4 days. It generally starts as a maculopapular eruption on the trunk and spreads peripherally, sparing the palms of the hands and soles of the feet. Rash may vary among individuals, or may be absent altogether and should not be relied upon for diagnosis.
|6
|-
|-
|Epidemic Typhus
| rowspan="5" |'''Hemoglobin level (g/dl)'''
|The rash usually begins a couple of days after the onset of symptoms. It typically begins as a maculopapular eruption on the trunk of the body and spreads to the extremities, usually sparing the palms of hands and soles of feet. When the disease is severe, petechiae may develop. The rash may be variable among individuals and stage of infection, or may be absent altogether and should not be relied upon for diagnosis
| rowspan="3" |'''Men'''
|   ≥ 12 to < 13
|1
|-
|  ≥ 10 to < 12
|3
|-
|< 10
|6
|-
| rowspan="2" |'''Women'''
|   ≥ 10 to < 12
|1
|-
| < 10
|6
|-
| colspan="2" rowspan="3" |'''Systolic blood pressure (mmHg)'''
|   ≥ 100 to < 109
|1
|-
| ≥ 90 to < 99
|2
|-
|  < 90
|3
|-
| colspan="2" rowspan="5" |'''Other markers'''
|Pulse rate ≥ 100 beats/min
|1
|-
|Presentation with melena
|1
|-
|Presentation with syncope
|2
|-
|Hepatic disease
|2
|-
|Heart failure
|2
|-
| colspan="4" |
Scores of 0-2 -Low-risk group<br>
Score of >6- High risk group
|}
|}
About 25–50% of scrub typhus patients develop a rash. The rash is usually macular or maculopapular. Typically, it will begin on the abdomen of an infected individual and then spread to the extremities. Petechiae are uncommon.
Murine Typhus
The rash typically occurs at the end of the first week of the illness and lasts 1–4 days. It generally starts as a maculopapular eruption on the trunk and spreads peripherally, sparing the palms of the hands and soles of the feet. Rash may vary among individuals, or may be absent altogether and should not be relied upon for diagnosis.
Epidemic Typhus
The rash usually begins a couple of days after the onset of symptoms. It typically begins as a maculopapular eruption on the trunk of the body and spreads to the extremities, usually sparing the palms of hands and soles of feet. When the disease is severe, petechiae may develop. The rash may be variable among individuals and stage of infection, or may be absent altogether and should not be relied upon for diagnosis.
'''Most common symptoms'''
*Fever
*Headache
*Malaise
*Maculopapular, vesicular, or petechial rash
*Eschar
*Nausea and vomiting.
'''Less common symptoms'''
*Abdominal pain
*Cough
*Prostration
*Confusion
*Photophobia
*Diarrhea


==Lab diagnosis==
===The Rockall score===
*Laboratory studies are not particularly helpful in confirming a diagnosis of typhus.  
*The complete Rockall score identifies those patients with evidence of acute UGIB on endoscopy who are at low risk for further bleeding or death.<ref name="pmid">{{cite journal |vauthors=Monteiro S, Gonçalves TC, Magalhães J, Cotter J |title=Upper gastrointestinal bleeding risk scores: Who, when and why? |journal=World J Gastrointest Pathophysiol |volume=7 |issue=1 |pages=86–96 |year=2016 |pmid= |pmc=4753192 |doi=10.4291/wjgp.v7.i1.86 |url=}}</ref><ref name="pmid18346681">{{cite journal |vauthors=Atkinson RJ, Hurlstone DP |title=Usefulness of prognostic indices in upper gastrointestinal bleeding |journal=Best Pract Res Clin Gastroenterol |volume=22 |issue=2 |pages=233–42 |year=2008 |pmid=18346681 |doi=10.1016/j.bpg.2007.11.004 |url=}}</ref>
*They assess the degree of severity of the illness and in help in excluding other diseases.
*The score is based upon
*The diagnosis of typhus is clinically suggested when the appropriate historical elements are elicited from a patient who presents with the characteristic symptoms and signs.
**Age
*Antibiotic therapy should begin promptly when the diagnosis is suspected; thereafter, appropriate laboratory studies can be serially performed as needed.
**Presence of shock
*Diagnosis may be confirmed using laboratory tests; however, more than one week may pass before patients mount a demonstrable immune response that can be measured serologically.
**Comorbidity diagnosis
*Typhus is a vasculitic process, any organ may be affected, and multiorgan system dysfunction or failure may occur if the illness is not diagnosed and treated in the early stages.  
**Endoscopic ulcer characteristics
*Renal - Azotemia/proteinuria
**Stigmata of recent hemorrhage.
*Hematologic
{| class="wikitable"
*Leukopenia (common in the early stages of disease)
! colspan="4" |The Rockall score
*WBC count normal/mildly elevated later
|-
*Thrombocytopenia
! colspan="3" |Markers
*Hepatic - Mild transaminase elevations
!Score
*Metabolic - Hypoalbuminemia/electrolyte abnormalities (particularly hyponatremia)
|-
*Indirect immunofluorescence assay (IFA) or enzyme immunoassay (EIA) testing can be used to evaluate for a rise in the immunoglobulin M (IgM) antibody titer, which indicates an acute primary disease.
| colspan="2" rowspan="3" |'''Age'''
*Brill-Zinsser disease can be confirmed in a patient with a history of primary epidemic typhus who has recurrent symptoms and signs of typhus and a rise in the immunoglobulin G (IgG) antibody titer, which indicates a secondary immune response.
|<60
*IFA and EIA tests can be used to confirm a diagnosis of typhus, but they do not identify the various rickettsial species.
|0
*Polymerase chain reaction (PCR) amplification of rickettsial DNA of serum or skin biopsy specimens can be used for diagnosing typhus. [9]
|-
*The complement fixation (CF) test is a serological test that can be used to demonstrate which specific rickettsial organism is causing disease by detection of specific antibodies.
|60 - 79
===Histologic Findings===
|1
*Rickettsia may be observed in tissue sections using Giemsa or Gimenez staining techniques.
|-
|≥ 80
|2
|-
| rowspan="5" |'''Shock stage'''
| rowspan="3" |Blood pressure
|>120
|0
|-
|100-119
|1
|-
|<100
|2
|-
| rowspan="2" |Heart rate
|>100
|0
|-
|<100
|1
|-
| colspan="2" rowspan="3" |'''Comorbidity'''
|No major comorbidity
|0
|-
|Cardiac failure
Ischemic heart disease


==Xray chest==
Any major comorbidity
*No imaging studies are specifically indicated to aid in diagnosing typhus.
|2
*Imaging studies are indicated only on a case-by-case basis to evaluate potential complications or as needed.
*Chest radiography may be a complementary tool to evaluate the clinical course of scrub typhus.
*Chest radiographic examinations should be obtained during the first week after the onset of illness.
==Differential==
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
|+
! style="background: #4479BA; width: 120px;" | {{fontcolor|#FFF|Disease}}
! style="background: #4479BA; width: 550px;" | {{fontcolor|#FFF|Findings}}
|-
|-
| style="padding: 5px 5px; background: #DCDCDC;" | '''[[Ebola]]'''
|Renal failure
| style="padding: 5px 5px; background: #F5F5F5;" | Presents with [[fever]], [[chills]] [[vomiting]], [[diarrhea]], generalized [[pain]] or [[malaise]], and sometimes [[Internal bleeding|internal]] and external [[bleeding]], that follow an [[incubation period]] of 2-21 days.
Liver failure
 
Disseminated malignancy
|3
|-
|-
| style="padding: 5px 5px; background: #DCDCDC;" | '''[[Typhoid fever]]'''
| colspan="2" rowspan="3" |'''Diagnosis'''
| style="padding: 5px 5px; background: #F5F5F5;" | Presents with [[fever]], [[headache]], [[rash]], gastrointestinal symptoms, with [[lymphadenopathy]], relative [[bradycardia]], [[cough]] and [[leucopenia]] and sometimes [[sore throat]]. [[Blood]] and [[stool culture]] can confirm the presence of the causative bacteria.
|Mallory-Weiss tear, no lesion identified and no SRH
|0
|-
|-
| style="padding: 5px 5px; background: #DCDCDC;" |'''[[Malaria]]'''
|All other diagnosis
| style="padding: 5px 5px; background: #F5F5F5;" |Presents with acute [[fever]], [[headache]] and sometimes [[diarrhea]] (children). A [[blood smear]]s must be examined for malaria parasites. The presence of [[parasites]] does not exclude a concurrent viral infection. An [[antimalarial]] should be prescribed as an [[empiric therapy]].
|1
|-
|-
| style="padding: 5px 5px; background: #DCDCDC;" | '''[[Lassa fever]]'''
|Malignancy of upper GI tract
| style="padding: 5px 5px; background: #F5F5F5;" |Disease onset is usually gradual, with [[fever]], [[sore throat]], [[cough]], [[pharyngitis]], and [[facial edema]] in the later stages. [[Inflammation]] and exudation of the [[pharynx]] and [[conjunctiva]] are common.
|2
|-
|-
| style="padding: 5px 5px; background: #DCDCDC;" | '''[[Yellow fever]] and other [[Flaviviridae]] '''
| colspan="2" rowspan="2" |'''Major SRH'''
| style="padding: 5px 5px; background: #F5F5F5;" | Present with [[hemorrhage|hemorrhagic]] complications. [[Epidemiological]] investigation may reveal a pattern of disease [[transmission]] by an insect vector. Virus isolation and serological investigation serves to distinguish these [[viruses]]. Confirmed history of previous [[yellow fever]] [[vaccination]] will rule out [[yellow fever]].
|None or dark spot only
|0
|-
|-
| style="padding: 5px 5px; background: #DCDCDC;" | '''[[Shigellosis]] & other bacterial enteric infections'''
|Blood in upper GI tract, adherent clot,<br> visible or spurting vessel
| style="padding: 5px 5px; background: #F5F5F5;" | Presents with [[diarrhea]], possibly [[Dysentery|bloody]], accompanied by [[fever]], [[nausea]], and sometimes [[toxemia]], [[vomiting]], [[cramps]], and [[tenesmus]]. [[Stool]]s contain [[blood]] and mucous in a typical case. A search for possible sites of bacterial infection, together with cultures and [[blood smear]]s, should be made. Presence of [[leucocytosis]] distinguishes bacterial infections from [[viral infections]].
|2
|-
| style="padding: 5px 5px; background: #DCDCDC;" | '''Others'''
| style="padding: 5px 5px; background: #F5F5F5;" |[[Leptospirosis]], [[viral hepatitis]], [[rheumatic fever]], and [[mononucleosis]] can produce [[signs]] and [[symptoms]] that may be confused with [[Ebola]] in the early stages of [[infection]].
|-
|-
| colspan="4" |GI: Gastrointestinal, SRH: Signs of recent hemorrhage.
Range of score is 0-11.
Score of ≤ 3 predicts low mortality risk, while ≥ 8 is a predictor of high mortality risk.
|}
|}
==Complications==
Complications of UGIB include:<ref name="pmid22233622">{{cite journal |vauthors=Sonnenberg A |title=Complications following gastrointestinal bleeding and their impact on outcome and death |journal=Eur J Gastroenterol Hepatol |volume=24 |issue=4 |pages=388–92 |year=2012 |pmid=22233622 |doi=10.1097/MEG.0b013e328350589e |url=}}</ref>
*End-organ damage
** Cardiac ischemia
** Renal failure
** Ischemic hepatitis
** Anoxic brain injury
*Iron-deficiency anemia
==Classification==
According to The American Gastroenterological Association, upper GI bleeding can be classified based on the rate of blood loss into overt(acute), occult or obscure(chronic) forms.<ref name="pmid12208839">{{cite journal |vauthors= |title=Non-variceal upper gastrointestinal haemorrhage: guidelines |journal=Gut |volume=51 Suppl 4 |issue= |pages=iv1–6 |year=2002 |pmid=12208839 |pmc=1867732 |doi= |url=}}</ref><ref name="pmid23547576">{{cite journal |vauthors=Bull-Henry K, Al-Kawas FH |title=Evaluation of occult gastrointestinal bleeding |journal=Am Fam Physician |volume=87 |issue=6 |pages=430–6 |year=2013 |pmid=23547576 |doi= |url=}}</ref><ref name="pmid17983811">{{cite journal |vauthors=Raju GS, Gerson L, Das A, Lewis B |title=American Gastroenterological Association (AGA) Institute medical position statement on obscure gastrointestinal bleeding |journal=Gastroenterology |volume=133 |issue=5 |pages=1694–6 |year=2007 |pmid=17983811 |doi=10.1053/j.gastro.2007.06.008 |url=}}</ref><ref name="pmid10387941">{{cite journal |vauthors=Rockey DC |title=Occult gastrointestinal bleeding |journal=N. Engl. J. Med. |volume=341 |issue=1 |pages=38–46 |year=1999 |pmid=10387941 |doi=10.1056/NEJM199907013410107 |url=}}</ref>
:*'''Overt GI bleeding''':- Overt GI bleeding is defined as acute bleeding which is visible and can present in the form of hematemesis, “coffee-ground” emesis, melena, or hematochezia.<br>
:*'''Occult or chronic GI bleeding''':- Occult GI bleeding  is defined as a microscopic hemorrhage which can present as Hemoccult-positive stools with or without iron deficiency anemia. It is the initial presentation in patients with no evidence of visible blood loos and is positive on fecal occult blood test(FOBT).
:*'''Obscure GI bleeding''':- Obscure GI bleeding is defined as recurrent bleeding in which a source is not identified after upper endoscopy and colonoscopy. It can be either overt or occult.
==Epidemiology and Demographics==
===Incidence===
The incidence of acute UGIB is approximately 50 to 100 per 100,000 individuals worldwide.<ref name="pmid22468077">{{cite journal |vauthors=El-Tawil AM |title=Trends on gastrointestinal bleeding and mortality: where are we standing? |journal=World J. Gastroenterol. |volume=18 |issue=11 |pages=1154–8 |year=2012 |pmid=22468077 |pmc=3309903 |doi=10.3748/wjg.v18.i11.1154 |url=}}</ref><ref name="pmid18346679">{{cite journal |vauthors=van Leerdam ME |title=Epidemiology of acute upper gastrointestinal bleeding |journal=Best Pract Res Clin Gastroenterol |volume=22 |issue=2 |pages=209–24 |year=2008 |pmid=18346679 |doi=10.1016/j.bpg.2007.10.011 |url=}}</ref>
===Gender===
Males are more commonly affected by UGIB than females. The males to female ratio is approximately 2 to 1.
==Pathophysiology==
===Blood supply of Foregut===
The digestive system is supplied by the celiac artery. The celiac artery is the first major branch from the abdominal aorta, and is the only major artery that nourishes the digestive organs.<ref name="pmid18730308">{{cite journal |vauthors=Feldman SE |title=Blood supply to stomach |journal=Calif Med |volume=112 |issue=4 |pages=55 |year=1970 |pmid=18730308 |pmc=1501289 |doi= |url=}}</ref><ref name="pmid26140727">{{cite journal |vauthors=Granger DN, Holm L, Kvietys P |title=The Gastrointestinal Circulation: Physiology and Pathophysiology |journal=Compr Physiol |volume=5 |issue=3 |pages=1541–83 |year=2015 |pmid=26140727 |doi=10.1002/cphy.c150007 |url=}}</ref><ref name="pmid11355897">{{cite journal |vauthors=Geboes K, Geboes KP, Maleux G |title=Vascular anatomy of the gastrointestinal tract |journal=Best Pract Res Clin Gastroenterol |volume=15 |issue=1 |pages=1–14 |year=2001 |pmid=11355897 |doi=10.1053/bega.2000.0152 |url=}}</ref><ref name="pmid986621">{{cite journal |vauthors=Varga F, Csáky TZ |title=Changes in the blood supply of the gastrointestinal tract in rats with age |journal=Pflugers Arch. |volume=364 |issue=2 |pages=129–33 |year=1976 |pmid=986621 |doi= |url=}}</ref><ref name="pmid4599528">{{cite journal |vauthors=Matuchansky C, Bernier JJ |title=[Prostaglandins and the digestive tract] |language=French |journal=Biol Gastroenterol (Paris) |volume=6 |issue=3 |pages=251–68 |year=1973 |pmid=4599528 |doi= |url=}}</ref><ref name="pmid4372738">{{cite journal |vauthors=Radbil' OS |title=[Prostaglandins and the digestive system organs] |language=Russian |journal=Ter. Arkh. |volume=46 |issue=4 |pages=6–14 |year=1974 |pmid=4372738 |doi= |url=}}</ref><ref name="pmid6990725">{{cite journal |vauthors=Robert A |title=Prostaglandins and digestive diseases |journal=Adv Prostaglandin Thromboxane Res |volume=8 |issue= |pages=1533–41 |year=1980 |pmid=6990725 |doi= |url=}}</ref>
{| class="wikitable"
{| class="wikitable"
!Diseases
! colspan="2" |Foregut
! colspan="5" |Clinical features
!Blood supply
! colspan="2" |Diagnosis
|-
|-
| rowspan="3" |'''<u>Esophagus</u>'''
|
|
|Fever
Upper esophageal sphincter<br>
|Rash
Cervical esophagus 
|Diarrhea
| Inferior thyroid artery 
|Cough
|-
|Specific
|Thoracic esophagus
|Aortic esophageal arteries or branches of the bronchial arteries 
|-
|
|
Distal esophagus<br>
Lower esophageal sphincter
|Left gastric artery and left phrenic artery 
|-
| rowspan="3" |'''<u>Stomach</u>'''
|Lesser curvature
|Right and left gastric arteries
|-
|Greater curvature
|Right and left gastroepiploic arteries
|-
|Gastric fundus
|Short gastric arteries
|-
| rowspan="2" |'''<u>Duodenum</u>'''
|First and second parts
|
|
Gastroduodenal artery (GDA) and<br>
Superior pancreaticoduodenal artery
|-
|Third and fourth parts
|Inferior pancreaticoduodenal artery
|}
[[Image:Stomach blood supply.svg.png|frame|center|Blood supply of stomach<br> Source: By Mikael Häggström.https://commons.wikimedia.org/w/index.php?curid=3416062]]
===Mucosal barrier===
*The gastric mucosa is protected from the acidic environment by mucus, bicarbonate, prostaglandins, and blood flow.<ref name="pmid6846549">{{cite journal |vauthors=Hills BA, Butler BD, Lichtenberger LM |title=Gastric mucosal barrier: hydrophobic lining to the lumen of the stomach |journal=Am. J. Physiol. |volume=244 |issue=5 |pages=G561–8 |year=1983 |pmid=6846549 |doi= |url=}}</ref><ref name="pmid2657286">{{cite journal |vauthors=Clamp JR, Ene D |title=The gastric mucosal barrier |journal=Methods Find Exp Clin Pharmacol |volume=11 Suppl 1 |issue= |pages=19–25 |year=1989 |pmid=2657286 |doi= |url=}}</ref><ref name="pmid10677782">{{cite journal |vauthors=Werther JL |title=The gastric mucosal barrier |journal=Mt. Sinai J. Med. |volume=67 |issue=1 |pages=41–53 |year=2000 |pmid=10677782 |doi= |url=}}</ref>
*This mucosal barrier consists of three protective components which include:
**Layer of epithelial cell lining.
**Layer of mucus, secreted by surface epithelial cells and foveolar cells.
**Layer of bicarbonate ions, secreted by the surface epithelial cells.
[[Image: Stomach mucosal layer labeled.svg.png|center|frame|Diagram of alkaline Mucous layer in stomach with mucosal defense mechanisms<br> '''Source''': By M•Komorniczak (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons]]
The following table demonstrates the defense mechanisms of gastric mucosal barrier<ref name="pmid3072665">{{cite journal |vauthors=Forssell H |title=Gastric mucosal defence mechanisms: a brief review |journal=Scand. J. Gastroenterol. Suppl. |volume=155 |issue= |pages=23–8 |year=1988 |pmid=3072665 |doi= |url=}}</ref>
{| class="wikitable"
! colspan="2" |Defense mechanisms of gastric mucosal barrier
|-
|Mucus layer
|Forms a protective gel-like coating over the entire gastric mucosal surface
|-
|Epithelial layer
|Epithelial cell layer are bound by tight junctions that repel fluids
|-
|-
|Ebola
|Bicarbonate ions
|
|Neutralize acids
|}
 
===Pathogenesis===
The main inciting event in the pathogeneis of upper GI bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to ligament of Treitz, it is defined as upper GI bleeding.<ref name="pmid18346679">{{cite journal |vauthors=van Leerdam ME |title=Epidemiology of acute upper gastrointestinal bleeding |journal=Best Pract Res Clin Gastroenterol |volume=22 |issue=2 |pages=209–24 |year=2008 |pmid=18346679 |doi=10.1016/j.bpg.2007.10.011 |url=}}</ref><ref name="pmid15173790">{{cite journal |vauthors=Boonpongmanee S, Fleischer DE, Pezzullo JC, Collier K, Mayoral W, Al-Kawas F, Chutkan R, Lewis JH, Tio TL, Benjamin SB |title=The frequency of peptic ulcer as a cause of upper-GI bleeding is exaggerated |journal=Gastrointest. Endosc. |volume=59 |issue=7 |pages=788–94 |year=2004 |pmid=15173790 |doi= |url=}}</ref>
{| class="wikitable"
!Etiology
!Frequency of occurance
|-
|Peptic ulcer disease
|50%
|-
|Variceal bleeding
|20%
|-
|Esophagitis, gastritis, and duodenitis
|10-15%
|-
|Mallory-Weiss tear
|15%
|-
|Malignancy
|3-5%
|-
|Arteriovenous malformation
|<3%
|-
|Gastric antral vascular ectasia
|<1%
|-
|Dieulafoy lesion
|<1%
|}
===Pathogenesis===
*Regardless of etiology, if the balance of gastric acid secretion and mucosal defenses is disrupted, acid interacts with the epithelium to cause damage.<ref name="pmid6499">{{cite journal |vauthors=Gartner AH |title=Aspirin-induced gastritis and gastrointestinal bleeding |journal=J Am Dent Assoc |volume=93 |issue=1 |pages=111–7 |year=1976 |pmid=6499 |doi= |url=}}</ref><ref name="pmid23555156">{{cite journal |vauthors=Iwamoto J, Saito Y, Honda A, Matsuzaki Y |title=Clinical features of gastroduodenal injury associated with long-term low-dose aspirin therapy |journal=World J. Gastroenterol. |volume=19 |issue=11 |pages=1673–82 |year=2013 |pmid=23555156 |pmc=3607744 |doi=10.3748/wjg.v19.i11.1673 |url=}}</ref><ref name="pmid8898449">{{cite journal |vauthors=Hawkey CJ |title=Non-steroidal anti-inflammatory drug gastropathy: causes and treatment |journal=Scand. J. Gastroenterol. Suppl. |volume=220 |issue= |pages=124–7 |year=1996 |pmid=8898449 |doi= |url=}}</ref>
**Varices are large, tortuous veins and protrude into the lumen, rupturing.<ref name="pmid26467538">{{cite journal |vauthors=Quan S, Yang H, Tanyingoh D, Villeneuve PJ, Stieb DM, Johnson M, Hilsden R, Madsen K, van Zanten SV, Novak K, Lang E, Ghosh S, Kaplan GG |title=Upper gastrointestinal bleeding due to peptic ulcer disease is not associated with air pollution: a case-crossover study |journal=BMC Gastroenterol |volume=15 |issue= |pages=131 |year=2015 |pmid=26467538 |pmc=4604641 |doi=10.1186/s12876-015-0363-6 |url=}}</ref>
**Helicobacter pylori disrupts the mucosal barrier and causes inflammation of the mucosa of the stomach and duodenum.<ref name="Quan2002">{{cite journal|last1=Quan|first1=C|title=Management of peptic ulcer disease not related to Helicobacter pylori or NSAIDs|journal=The American Journal of Gastroenterology|volume=97|issue=12|year=2002|pages=2950–2961|issn=00029270|doi=10.1016/S0002-9270(02)05485-0}}</ref><ref name="MalfertheinerChan2009">{{cite journal|last1=Malfertheiner|first1=Peter|last2=Chan|first2=Francis KL|last3=McColl|first3=Kenneth EL|title=Peptic ulcer disease|journal=The Lancet|volume=374|issue=9699|year=2009|pages=1449–1461|issn=01406736|doi=10.1016/S0140-6736(09)60938-7}}</ref>
**As the ulcer progresses beyond the mucosa to the submucosa the inflammation causes weakening and necrosis of arterial walls, leading to pseudoaneurysm formation followed by rupture and hemorrhage.<ref name="pmid25516672">{{cite journal |vauthors=Quan S, Frolkis A, Milne K, Molodecky N, Yang H, Dixon E, Ball CG, Myers RP, Ghosh S, Hilsden R, van Zanten SV, Kaplan GG |title=Upper-gastrointestinal bleeding secondary to peptic ulcer disease: incidence and outcomes |journal=World J. Gastroenterol. |volume=20 |issue=46 |pages=17568–77 |year=2014 |pmid=25516672 |pmc=4265619 |doi=10.3748/wjg.v20.i46.17568 |url=}}</ref>
**NSAIDs inhibit cyclooxygenase, leading to impaired mucosal defenses by decreasing mucosal prostaglandin synthesis.<ref name="pmid26870237">{{cite journal |vauthors=Xi B, Jia JJ, Lin BY, Geng L, Zheng SS |title=Peptic ulcers accompanied with gastrointestinal bleeding, pylorus obstruction and cholangitis secondary to choledochoduodenal fistula: A case report |journal=Oncol Lett |volume=11 |issue=1 |pages=481–483 |year=2016 |pmid=26870237 |pmc=4727103 |doi=10.3892/ol.2015.3908 |url=}}</ref>
**During stress, there is acid hypersecretion; therefore, the breakdown of mucosal defenses leads to injury of the mucosa and subsequent bleeding.
**Mucosal defects along with dilated and tortuous vessels in dieulafoy lesion put them at risk for rupture because of necrosis of the arterial wall from exposure to gastric acid.<ref name="pmid313784">{{cite journal |vauthors=Stern AI, Korman MG, Hunt PS, Hansky J, Hillman HS, Schmidt GT |title=The Mallory-Weiss lesion as a cause of upper gastrointestinal bleeding |journal=Aust N Z J Surg |volume=49 |issue=1 |pages=13–8 |year=1979 |pmid=313784 |doi= |url=}}</ref><ref name="pmid8307643">{{cite journal |vauthors=Katz PO, Salas L |title=Less frequent causes of upper gastrointestinal bleeding |journal=Gastroenterol. Clin. North Am. |volume=22 |issue=4 |pages=875–89 |year=1993 |pmid=8307643 |doi= |url=}}</ref><ref name="pmid17633871">{{cite journal |vauthors=Sabljak P, Velicković D, Stojakov D, Bjelović M, Ebrahimi K, Spica B, Sljukić V, Pesko P |title=[Less frequent causes of upper gastrointestinal bleeding] |journal=Acta Chir Iugosl |volume=54 |issue=1 |pages=119–23 |year=2007 |pmid=17633871 |doi= |url=}}</ref><ref name="pmid11727185">{{cite journal |vauthors=Depolo A, Dobrila-Dintinjana R, Uravi M, Grbas H, Rubini M |title=[Upper gastrointestinal bleeding - Review of our ten years results] |language=German |journal=Zentralbl Chir |volume=126 |issue=10 |pages=772–6 |year=2001 |pmid=11727185 |doi=10.1055/s-2001-18265 |url=}}</ref>
{{familytree/start}}
{{familytree | | | | | | | | | | A01 | | | | | |A01=NSAIDS}}
{{familytree | | | | | | | | | | |!| | | | | | | | }}
{{familytree | | | | | | | | | | A01 | | | | | |A01=Inhibits cycloxygenase pathway}}
{{familytree | | | | | | | | | | |!| | | | | | | | }}
{{familytree | | | | | |,|-|-|-|-|^|-|-|-|-|-|.| | | }}
{{familytree | | | | | B01 | | | | | | | | | B02 |B01=COX-1|B02=COX-2}}
{{familytree | | | | | |!| | | | | | | | | | |!| | | }}
{{familytree | |,|-|-|-|+|-|-|-|.| | | |,|-|-|^|-|-|-|.| }}
{{familytree | C01 | | C02 | | C03 | | C04 | | | | | C05 | |C01=Reduced<br>mucosal blood flow|C02=Reduced<br> mucosal and<br> bicarbonate secreation|C03=Impaired<br>platelet aggregation|C04=Reduced<br>angiogenesis|C05=Increased<br>leucocyte adherence|}}
{{familytree | |!| | | |!| | | |!| | | |!| | | | | | |!| | | }}
{{familytree | |`|-|-|-|^|-|-|-|+|-|-|-|^|-|-|-|-|-|-|'| | | }}
{{familytree | | | | | | | | | |!| | | | | | | | | | | | | | }}
{{familytree | | | | | | | | | E01 | | | | | | | | | | | | |E01=Impaired defence<br>Impaired healing}}
{{familytree | | | | | | | | | |!| | | | | | | | | | | | | | }}
{{familytree | | | | | | | | | F01 | | | | | | | | | | | | |F01=Mucosal Injury}}
{{familytree/end}}
 
===Gross and Microscopic Pathology===
{| class="wikitable"
! colspan="2" |
!Gross Pathology
!Microscopic Pathology
|-
| colspan="2" |Varices
|Large and tortuous veins that protrude into the lumen
|Varices may be difficult to demonstrate in surgical specimens
|-
| colspan="2" |Mallory-Weiss Tear<ref name="pmid1465928">{{cite journal |vauthors=Renoult E, Biava MF, Aimone-Gastin I, Aouragh F, Hestin D, Kures L, Kessler M |title=Evolution and significance of Toxoplasma gondii antibody titers in kidney transplant recipients |journal=Transplant. Proc. |volume=24 |issue=6 |pages=2754–5 |year=1992 |pmid=1465928 |doi= |url=}}</ref>
|Isolated or multiple cleft like mucosal defects
|
|
*Defects in the esophageal squamous mucosa.
*Cells of acute inflammation.
*Multiple ruptured blood vessels in the lamina propria or submucosa.
*Prior lacerations may show various degrees of healing
**Granulation tissue
**Fibrosis<ref name="pmid1465928">{{cite journal |vauthors=Renoult E, Biava MF, Aimone-Gastin I, Aouragh F, Hestin D, Kures L, Kessler M |title=Evolution and significance of Toxoplasma gondii antibody titers in kidney transplant recipients |journal=Transplant. Proc. |volume=24 |issue=6 |pages=2754–5 |year=1992 |pmid=1465928 |doi= |url=}}</ref>
**Epithelial regeneration.
|-
| rowspan="5" |Esophagitis<ref name="pmid24868280">{{cite journal |vauthors=Rosołowski M, Kierzkiewicz M |title=Etiology, diagnosis and treatment of infectious esophagitis |journal=Prz Gastroenterol |volume=8 |issue=6 |pages=333–7 |year=2013 |pmid=24868280 |pmc=4027832 |doi=10.5114/pg.2013.39914 |url=}}</ref>
|Herpes esophagitis
|
|
* Shallow ulcers
* Sharp and raised edges
* Normal intervening erythematous mucosa
|Ground glass inclusion bodies
|-
|Cytomegalovirus esophagitis
|
|
* Superficial ulcers
* Well-circumscribed
* CMV infects mesenchymal cells in the lamina propria and submucosa
|Intranuclear inclusions
|-
|Fungal esophagitis
|
|
* Erythematous
* Hyperemic
* Friable
* Discrete and raised white plaque
|Neutrophils within the squamous epithelium
|-
|Pill esophagitis
|
|
* Discrete ulcers
|Not specific and include
* Necrosis
* Prominent eosinophilic infiltrate
* Spongiosis
|-
|Toxic esophagitis
|
|
* Mucosal erythema,
* Edema
* Hemorrhage
* Necrosis
|'''<u>Acid injury</u>'''
* Coagulative necrosis
* Eschar
'''<u>Alkaline injury</u>'''
* Liquefactive necrosis
* Acute inflammation
* Abundant granulation tissue
|-
|-
|Typhoid fever
| colspan="2" |Gastroesophageal
|
Reflux Disease<ref name="pmid28943113">{{cite journal |vauthors=Pandit S, Boktor M, Alexander JS, Becker F, Morris J |title=Gastroesophageal reflux disease: A clinical overview for primary care physicians |journal=Pathophysiology |volume= |issue= |pages= |year=2017 |pmid=28943113 |doi=10.1016/j.pathophys.2017.09.001 |url=}}</ref>
|
|
|
|
* Basal cell hyperplasia
* Elongation of the lamina propria papillae
* Mixed intraepithelial inflammation
* Neutrophils, eosinophils, and lymphocytes
* Squamous cell degeneration.
|-
| colspan="2" |Barrett Esophagus<ref name="pmid28501084">{{cite journal |vauthors=Rajendra S, Sharma P |title=Barrett Esophagus and Intramucosal Esophageal Adenocarcinoma |journal=Hematol. Oncol. Clin. North Am. |volume=31 |issue=3 |pages=409–426 |year=2017 |pmid=28501084 |doi=10.1016/j.hoc.2017.01.003 |url=}}</ref>
|
|
|Columnar metaplasia
* Mucinous columnar cells
* Goblet cells, and enterocyte-like cells, among others.
* Cells of  acute inflammation
|-
| colspan="2" |Acute Gastritis
|Mucosal hyperemia associated with
* Bleeding
* Erosions
* Ulcers
|
|
* Dilation and congestion of mucosal capillaries, edema, and hemorrhage in the lamina propria.
* Ischemic-type changes such as
** Degenerated and necrotic epithelium
** Fibrinoid necrosis
** Adherent fibrinopurulent debris
|-
| colspan="2" |Gastric Ulcers<ref name="pmid28798512">{{cite journal |vauthors=Drini M |title=Peptic ulcer disease and non-steroidal anti-inflammatory drugs |journal=Aust Prescr |volume=40 |issue=3 |pages=91–93 |year=2017 |pmid=28798512 |pmc=5478398 |doi=10.18773/austprescr.2017.037 |url=}}</ref>
|
|
* Solitary, typically less than 2 cm in diameter, and have sharply defined borders.
* The ulcer edges are usually flat, and the base of the ulcer usually appears smooth.
* The presence of a radiating pattern of rugal folds is characteristic of peptic ulcers
|
|
* Fibrinopurulent debris
* Necrosis
* Granulation tissue
|-
|-
|Malaria
| colspan="2" |Portal Hypertensive Gastropathy<ref name="pmid26564121">{{cite journal |vauthors=Garg H, Gupta S, Anand AC, Broor SL |title=Portal hypertensive gastropathy and gastric antral vascular ectasia |journal=Indian J Gastroenterol |volume=34 |issue=5 |pages=351–8 |year=2015 |pmid=26564121 |doi=10.1007/s12664-015-0605-0 |url=}}</ref>
|
|
|
|
|
|
* Mosaic pattern of congestion
* Most commonly involves the fundus
|
|
* Dilation, tortuosity, and thickening of small submucosal arteries and veins.
* Mucosal capillaries may also show congestion, dilation, and proliferation.
|-
| colspan="2" |Gastric Antral Vascular Ectasia<ref name="pmid26564121">{{cite journal |vauthors=Garg H, Gupta S, Anand AC, Broor SL |title=Portal hypertensive gastropathy and gastric antral vascular ectasia |journal=Indian J Gastroenterol |volume=34 |issue=5 |pages=351–8 |year=2015 |pmid=26564121 |doi=10.1007/s12664-015-0605-0 |url=}}</ref>
|Linear pattern of mucosal congestion in the antrum termed “watermelon stomach
|'''<u>Antral biopsies</u>''' show
* Congestion
* Dilated mucosal capillaries
* Vascular microthrombi
The mucosa also shows
* Foveolar hyperplasia
* Fibromuscular hyperplasia
* Edema and regenerative changes
|-
| colspan="2" |Reactive (Chemical) Gastropathy
|'''<u>Stomach</u>'''
* Edema
* Surface erosions
* Polypoid changes, and friability
|The mucosa shows
* Congestion
* Edema
* Fibromuscular hyperplasia
* Foveolar hyperplasia
|-
| colspan="2" |Peptic Disease
|Wide range of findings
* From normal/slightly edematous mucosa to increased friability, erosions, and ulcers
|
|
* Increased plasma cells
* Neutrophilic infiltrate
* Reactive epithelial changes, including villous blunting.
* The surface epithelium usually shows mucous cell (pseudopyloric) metaplasia
|-
|-
|Lassa fever
| colspan="2" |Ischemia
|
|Hypoperfused ulcers
|
|'''<u>Acute ischemia</u>'''
|
* Mucosal edema
|
* Congestion
|
* Superficial necrosis
|
* Coagulative necrosis
|
'''<u>Chronic ischemia</u>'''
* Fibrosis
* Strictures
|-
|-
|'''[[Yellow fever]] and'''
| colspan="2" |Structural Abnormalities of Blood Vessels<ref name="pmid11355900">{{cite journal |vauthors=Gordon FH, Watkinson A, Hodgson H |title=Vascular malformations of the gastrointestinal tract |journal=Best Pract Res Clin Gastroenterol |volume=15 |issue=1 |pages=41–58 |year=2001 |pmid=11355900 |doi=10.1053/bega.2000.0155 |url=}}</ref>
'''other [[Flaviviridae]] '''
|Large-caliber artery within the submucosa
|
|Dilated venules and arteriole in direct communication with each other
|
|
|
|
|
|
|-
|-
|'''[[Shigellosis]] &'''
| colspan="2" |Inflammatory Bowel Disease
'''other bacterial enteric infections'''
|
|
|
|
|
|
|
|
|Lymphoplasmacytic infiltrate with numerous neutrophils
|}
|}


==Labs==
==Diagnosis==
Serologic assays are the most frequently used methods for confirming cases of scrub typhus. The indirect immunofluorescence assay (IFA) is generally considered the reference standard, but is usually not available in developing countries where this disease is endemic. Other serological tests include ELISA and indirect immunuoperoxidase (IIP) assays. Weil-Felix OX-K agglutination assays may be used in some international settings but lack sensitivity and specificity and are not generally used in the United States. These assays can detect either IgG or IgM antibodies. Diagnosis is typically confirmed by documenting a four-fold rise in antibody titer between acute and convalescent samples. Acute specimens are taken during the first week of illness and convalescent samples are taken 2–4 weeks later. IgG antibodies are considered more accurate than IgM, but detectable levels of IgG antibody generally do not appear until 7–10 days after the onset of illness.
In patients with acute Upper GI bleeding who are unstable rapid assessment and resuscitation should be initiated even before diagnostic evaluation. Once hemodynamic stability is achieved, a proper clinical history, physical examination, and initial laboratory findings are crucial not only in determining the likely sources of bleeding but also in directing the appropriate intervention. The hematocrit level is measured soon after the onset of bleeding, but will not accurately reflect the amount of blood loss. Equilibration between the intravascular and extravascular spaces is not complete until 24 to 72 hours after bleeding has occurred. Low mean corpuscular volume, low iron and ferritin levels, and high transferrin and total iron-binding capacity (TIBC) confirm iron deficiency. Blood urea nitrogen (BUN) level may be elevated out of proportion to any increase in the creatinine level in patients with UGIB, secondary to the breakdown of blood proteins to urea by intestinal bacteria. Platelet count and coagulation studies should be checked, especially in patients with known or suspected coagulopathy. Nasogastric lavage should be performed if the presence or source of bleeding is unknown. Upper gastrointestinal endoscopy is the primary diagnostic tool, performed for both diagnosis and treatment of active bleeding. The American Society of Gastrointestinal Endoscopy guidelines recommend that upper endoscopy be performed within 24 hours of presentation in all patients with UGIB. Angiography and tagged erythrocyte scan are rarely needed, but may be used to diagnose (and embolize) active UGIB, particularly in patients who cannot tolerate EGD. Also, upper gastrointestinal tract radiographic studies using barium are generally not advised, as they may obscure visualization during EGD.<ref name="pmid20083829">{{cite journal |vauthors=Barkun AN, Bardou M, Kuipers EJ, Sung J, Hunt RH, Martel M, Sinclair P |title=International consensus recommendations on the management of patients with nonvariceal upper gastrointestinal bleeding |journal=Ann. Intern. Med. |volume=152 |issue=2 |pages=101–13 |year=2010 |pmid=20083829 |doi=10.7326/0003-4819-152-2-201001190-00009 |url=}}</ref><ref name="pmid10836189">{{cite journal |vauthors=Hussain H, Lapin S, Cappell MS |title=Clinical scoring systems for determining the prognosis of gastrointestinal bleeding |journal=Gastroenterol. Clin. North Am. |volume=29 |issue=2 |pages=445–64 |year=2000 |pmid=10836189 |doi= |url=}}</ref><ref name="pmid19091393">{{cite journal |vauthors=Stanley AJ, Ashley D, Dalton HR, Mowat C, Gaya DR, Thompson E, Warshow U, Groome M, Cahill A, Benson G, Blatchford O, Murray W |title=Outpatient management of patients with low-risk upper-gastrointestinal haemorrhage: multicentre validation and prospective evaluation |journal=Lancet |volume=373 |issue=9657 |pages=42–7 |year=2009 |pmid=19091393 |doi=10.1016/S0140-6736(08)61769-9 |url=}}</ref><ref name="pmid8609747">{{cite journal |vauthors=Rockall TA, Logan RF, Devlin HB, Northfield TC |title=Selection of patients for early discharge or outpatient care after acute upper gastrointestinal haemorrhage. National Audit of Acute Upper Gastrointestinal Haemorrhage |journal=Lancet |volume=347 |issue=9009 |pages=1138–40 |year=1996 |pmid=8609747 |doi= |url=}}</ref>
==Initial Laboratory Studies==
*The hematocrit level is used to identify the degree of blood loss and suggests the acuity or chronicity of blood loss.<ref name="pmid17983811">{{cite journal |vauthors=Raju GS, Gerson L, Das A, Lewis B |title=American Gastroenterological Association (AGA) Institute medical position statement on obscure gastrointestinal bleeding |journal=Gastroenterology |volume=133 |issue=5 |pages=1694–6 |year=2007 |pmid=17983811 |doi=10.1053/j.gastro.2007.06.008 |url=}}</ref><ref name="pmid23547576">{{cite journal |vauthors=Bull-Henry K, Al-Kawas FH |title=Evaluation of occult gastrointestinal bleeding |journal=Am Fam Physician |volume=87 |issue=6 |pages=430–6 |year=2013 |pmid=23547576 |doi= |url=}}</ref>
*Serial complete blood count (CBC) tests are important for monitoring the presence of ongoing blood loss.
*Initial CBC may not fully reflect the actual degree of acute blood loss.
*Qualitatively, on peripheral blood smear prepared with Wright-Giemsa stain, normal erythrocytes should be smaller than the nucleus of a normal lymphocyte, and the central clear area should not be overly prominent.
*In iron-deficiency anemia associated with chronic blood loss, erythrocytes are smaller (microcytic) and appear lighter (hypochromic) than normal cells.
*Mild to moderate thrombocytopenia (>30 × 103/µL) does not usually result in spontaneous bleeding, although patients with a pre-existing lesion may bleed in the presence of even mild thrombocytopenia.
*Platelet count may rise in response to significant gastrointestinal bleeding and may fall with multiple blood transfusions.
*Low ferritin level is the most specific test for iron-deficiency anemia. This finding together with a low iron and high TIBC levels are helpful in diagnosing iron-deficiency anemia, a common complication of ongoing or significant UGIB.
*BUN level may be elevated out of proportion to any increase in the creatinine level in patients with UGIB, secondary to breakdown of blood proteins to urea by intestinal bacteria.
*In patients with esophageal varices, acquired coagulopathies are common due to cirrhosis.


Because antibody titers may persist in some individuals for years after the original exposure, only demonstration of recent changes in titers between paired specimens can be considered reliable confirmation of an acute scrub typhus infection. The most rapid and specific diagnostic assays for scrub typhus rely on molecular methods like polymerase chain reaction (PCR), which can detect DNA in a whole blood, eschar swab, or tissue sample. Immunostaining procedures can also be performed on formalin-fixed tissue samples. Since scrub typhus is not common in the United States, confirmatory tests are not typically available at state and local health departments; nonetheless, IFA, culture, and PCR assays can all be performed at the CDC through submission from state health departments.
==Naso-Gastric Lavage==
===Murine typhus===
*Nasogastric lavage is only indicated when the diagnosis of UGIB doubtful.<ref name="pmid22032314">{{cite journal |vauthors=Pallin DJ, Saltzman JR |title=Is nasogastric tube lavage in patients with acute upper GI bleeding indicated or antiquated? |journal=Gastrointest. Endosc. |volume=74 |issue=5 |pages=981–4 |year=2011 |pmid=22032314 |doi=10.1016/j.gie.2011.07.007 |url=}}</ref><ref name="pmid6978482">{{cite journal |vauthors=Marshall JB |title=Management of acute upper gastrointestinal bleeding |journal=Postgrad Med |volume=71 |issue=5 |pages=149–54, 157–8 |year=1982 |pmid=6978482 |doi= |url=}}</ref>
Rickettsia typhi can be detected via indirect immunofluorescence antibody (IFA) assay, immunohistochemistry (IHC), polymerase chain reaction (PCR) assays using blood, plasma, or tissue samples, or culture isolation. PCR is most sensitive on samples taken during the first week of illness, but prior to the start of doxycycline.
*It is rarely used now
*Nasogastric lavage also helps in documenting active or recent UGIB and the need for urgent endoscopy.
*Occasionally used to empty gastric contents in preparation for endoscopy.
===Complicatiions===
Complications of the procedure include:
*Bleeding from trauma during tube passage in patients with coagulopathy is a possible complication.
*Other rare complications include
**Pharyngeal and esophageal perforation
**Cardiac arrest
**Ethmoid sinus fracture with brain trauma
**Bronchial intubation.
===Interpretation===
*Evidence of old (brown colored or 'coffee grounds') or fresh blood documents presence of UGIB.  
*Evidence of bilious material rules out bleeding distal to the pylorus.
*Any other appearances of GI contents are non-diagnostic.
*There is no evidence that performing a nasogastric lavage to clear clots or otherwise manage bleeding improves clinical outcome.
===Contraindications===
*Avoid gastric lavage in patients with suspected perforated abdominal viscus.


Serologic tests (typically using IFA) are the most common means of confirming murine typhus and can be used to detect either IgG or IgM antibodies. Diagnosis is usually confirmed by demonstrating a four-fold rise in antibody titer between acute and convalescent samples. Acute specimens are taken during the first week of illness and convalescent samples are taken 2–4 weeks later. IgG antibodies are considered more accurate than IgM. Detectable levels of IgG antibody generally do not appear until 7–10 days after the onset of illness.
==Upper GI Endoscopy==
*Upper GI Endoscopy is considered investigation of choice for diagnosing and assessing the source of UGIB.<ref name="pmid12510452">{{cite journal |vauthors=Cappell MS, Friedel D |title=The role of esophagogastroduodenoscopy in the diagnosis and management of upper gastrointestinal disorders |journal=Med. Clin. North Am. |volume=86 |issue=6 |pages=1165–216 |year=2002 |pmid=12510452 |doi= |url=}}</ref><ref name="pmid23245297">{{cite journal |vauthors=Jaskolka JD, Binkhamis S, Prabhudesai V, Chawla TP |title=Acute gastrointestinal hemorrhage: radiologic diagnosis and management |journal=Can Assoc Radiol J |volume=64 |issue=2 |pages=90–100 |year=2013 |pmid=23245297 |doi=10.1016/j.carj.2012.08.001 |url=}}</ref><ref name="pmid12145792">{{cite journal |vauthors=Jensen DM, Kovacs TO, Jutabha R, Machicado GA, Gralnek IM, Savides TJ, Smith J, Jensen ME, Alofaituli G, Gornbein J |title=Randomized trial of medical or endoscopic therapy to prevent recurrent ulcer hemorrhage in patients with adherent clots |journal=Gastroenterology |volume=123 |issue=2 |pages=407–13 |year=2002 |pmid=12145792 |doi= |url=}}</ref>
*The American Society of Gastrointestinal Endoscopy guidelines recommend that upper gastrointestinal endoscopy be performed within 24 hours of presentation in all patients with UGIB
===Indications===
*Active UGIB
*Used for biopsy lesions for tissue diagnosis and to treat currently bleeding lesions.
===Complications===
Complications include
*Aspiration
*Esophageal perforation
*Cardiopulmonary complications secondary to anesthesia
*Increased bleeding while attempting therapeutic intervention


Because antibody titers may persist in some individuals for years after the original exposure, only demonstration of recent changes in titers between paired specimens can be considered reliable serological confirmation of an acute murine typhus infection. R. typhi antigens frequently cross-react with those of R. prowazekii and R. felis, and less often with R. rickettsii. When possible, species-specific assays for R. typhi, R. prowazekii, R. felis, and R. rickettsii should be run in parallel. IHC can be used to detect infection with typhus group Rickettsia (including R. prowazekii and R. typhi) in formalin-fixed tissue samples. PCR of whole blood or tissue can distinguish between infection with R. typhi and R. prowazekii although the sensitivity of these assays varies considerably based on the sample type, timing of sample collection, and the severity of disease.
===Epidimic===
Rickettsia prowazekii can be detected via indirect immunofluorescence antibody (IFA) assay, immunohistochemistry (IHC), polymerase chain reaction (PCR) assay of blood, plasma, or tissue samples, or culture isolation. Serologic tests are the most common means of confirmation and can be used to detect either IgG or IgM antibodies. Diagnosis is typically confirmed by documenting a four-fold rise in antibody titer between acute and convalescent samples. Acute specimens are taken during the first week of illness and convalescent samples are taken 2–4 weeks later. Detectable levels of IgG or IgM antibodies generally do not appear until 7–10 days after the onset of illness.


Because IgG antibody titers may persist in some individuals for years after the original exposure, only demonstration of recent changes in titers between paired specimens can be considered reliable serological confirmation of an acute epidemic typhus infection. R. prowazekii antigens may cross react with those of R. typhi, and occasionally with R. rickettsii. When possible, species-specific serological assays for R. prowazekii, R. typhi, and R. rickettsii should be run in parallel. Persons with Brill-Zinsser disease generally show a rise in IgG but not IgM antibodies to R. prowazekii. IHC can be used to detect infection with typhus group Rickettsia (including R. prowazekii and R. typhi) in formalin-fixed tissue samples. PCR of whole blood or tissue can distinguish between infection with R. typhi and R. prowazekii although the sensitivity of these assays vary considerably based on the sample type, timing of sample collection, and the severity of disease. Since epidemic typhus is not common in the United States, testing is not typically available at state and local health departments. IFA, culture, and PCR can all be performed at the CDC, through submission from state health departments.
{{Family tree/start}}
==Epidemiology and Demographics==
{{Family tree | | | | | | A01 | | | |A01= If upper GI Endoscopy<br>undiagnostic<ref name="pmid12208839">{{cite journal |vauthors= |title=Non-variceal upper gastrointestinal haemorrhage: guidelines |journal=Gut |volume=51 Suppl 4 |issue= |pages=iv1–6 |year=2002 |pmid=12208839 |pmc=1867732 |doi= |url=}}</ref>}}
All age groups are at risk for rickettsial infections during travel to endemic areas. Both short and long-term travelers are at risk for infection. Transmission is increased during outdoor activities in the spring and summer months when ticks and fleas are most active. However, infection can occur throughout the year. Because of the 5- to 14-day incubation period for most rickettsial diseases, tourists may not necessarily experience symptoms during their trip, and onset may coincide with their return home or develop within a week after returning. Although the most commonly diagnosed rickettsial diseases in travelers are usually in the spotted fever or typhus groups, travelers may acquire a wide range of rickettsioses, including emerging and newly recognized species.
{{Family tree | | | | | | |!| | | | | }}
Tickborne spotted fever rickettsioses are the most frequently reported travel-associated rickettsial infections. Game hunting and traveling to southern Africa from November through April are risk factors for African tick-bite fever, and this consistently remains the most commonly reported rickettsial infection acquired during travel. Mediterranean spotted fever infections are less commonly reported but occur over an even larger region, including (but not limited to) much of Europe, Africa, India, and the Middle East. Rocky Mountain spotted fever (also known as Brazilian spotted fever, as well as other local names) is reported throughout much of the Western Hemisphere, including Canada, the United States, Mexico, and various countries in Central and South America. Contact with dogs (in both rural and urban settings) and outdoor activities such as hiking, hunting, fishing, and camping increase the risk of infection.
{{Family tree | | | | | | B01 | | | |B01= Patient’s hemodynamic stability}}
 
{{Family tree | | | | | | |!| | | | | }}
Scrub typhus, which is transmitted by mites encountered in high grass and brush, is endemic in northern Japan, Southeast Asia, the western Pacific Islands, eastern Australia, China, maritime areas and several parts of south-central Russia, India, and Sri Lanka. More than 1 million cases occur annually. Most travel-acquired cases of scrub typhus occur during visits to rural areas in endemic countries for activities such as camping, hiking, or rafting, but urban cases have also been described.
{{Family tree | | | |,|-|-|^|-|-|.| | }}
 
{{Family tree | | | C01 | | | | C02 |C01= Stable<br>with low volume bleeding| C02= Unstable<br>with large volume bleeding}}
R. typhi and R. felis, which are transmitted by fleas, are widely distributed, especially throughout the tropics and subtropics and in port cities and coastal regions with rodents. Humans exposed to flea-infested cats, dogs, and peridomestic animals while traveling in endemic regions, or who enter or sleep in areas infested with rodents, are at most risk for fleaborne rickettsioses. Murine typhus has been reported among travelers returning from Asia, Africa, and the Mediterranean Basin and has also been reported from Hawaii, California, and Texas in the United States.
{{Family tree | | | |!| | | | | |!| | |}}
 
{{Family tree | | | D01 | | | | D02 | |D01=Repeat endoscopy|D02=Surgery<br>exploration and partial gastrectomy<ref name="pmid11997827">{{cite journal |vauthors=Zmora O, Dinnewitzer AJ, Pikarsky AJ, Efron JE, Weiss EG, Nogueras JJ, Wexner SD |title=Intraoperative endoscopy in laparoscopic colectomy |journal=Surg Endosc |volume=16 |issue=5 |pages=808–11 |year=2002 |pmid=11997827 |doi=10.1007/s00464-001-8226-3 |url=}}</ref> }}
R. akari, the causative agent of rickettsialpox, is transmitted by house-mouse mites, and circulates in mainly urban centers in Ukraine, South Africa, Korea, the Balkan states, and the United States. Outbreaks of rickettsialpox most often occur after contact with infected rodents and their mites, especially during natural die-offs or exterminations of infected rodents that cause the mites to seek out new hosts, including humans. The agent may spill over and occasionally be found in other wild rodent populations.
{{Family tree/end}}
 
Epidemic typhus is rarely reported among tourists but can occur in communities and refugee populations where body lice are prevalent. Outbreaks often occur during the colder months when infested clothing is not laundered. Travelers at most risk for epidemic typhus include those who may work with or visit areas with large homeless populations, impoverished areas, refugee camps, and regions that have recently experienced war or natural disasters. Active foci of epidemic typhus are known in the Andes regions of South America and some parts of Africa (including but not limited to Burundi, Ethiopia, and Rwanda). Louseborne epidemic typhus does not regularly occur in the United States, but a zoonotic reservoir occurs in the southern flying squirrel, and sporadic sylvatic epidemic typhus cases are reported. Tick-associated reservoirs of R. prowazekii have been described in Ethiopia, Mexico, and Brazil, but documented human cases are rare.


Ehrlichiosis and anaplasmosis are tickborne infections most commonly reported in the United States. A variety of species are implicated in infection, but E. chaffeensis and A. phagocytophilum are most common. Infections with various Ehrlichia and Anaplasma spp. have also been reported in Europe, Asia, and South America. Neoehrlichia mikurensis is a tickborne pathogen that occurs in Europe and Asia. Sennetsu fever, caused by Neorickettsia sennetsu, occurs in Japan, Malaysia, and possibly other parts of Asia. This disease can be contracted from eating raw infected fish.
==Other Diagnostic studies==
 
In cases where the source of bleeding is unidentified after upper endoscopy, the utilization of subsequent diagnostic modalities depends upon the hemodynamic stability of the patient. Other diagnostic studies include:<ref name="pmid6604219">{{cite journal |vauthors=Steer ML, Silen W |title=Diagnostic procedures in gastrointestinal hemorrhage |journal=N. Engl. J. Med. |volume=309 |issue=11 |pages=646–50 |year=1983 |pmid=6604219 |doi=10.1056/NEJM198309153091106 |url=}}</ref><ref name="pmid3094466">{{cite journal |vauthors=Browder W, Cerise EJ, Litwin MS |title=Impact of emergency angiography in massive lower gastrointestinal bleeding |journal=Ann. Surg. |volume=204 |issue=5 |pages=530–6 |year=1986 |pmid=3094466 |pmc=1251335 |doi= |url=}}</ref><ref name="pmid2334015">{{cite journal |vauthors=Hunter JM, Pezim ME |title=Limited value of technetium 99m-labeled red cell scintigraphy in localization of lower gastrointestinal bleeding |journal=Am. J. Surg. |volume=159 |issue=5 |pages=504–6 |year=1990 |pmid=2334015 |doi= |url=}}</ref>
==Physical examination==
*CT angiography
===Vitals===
*Catheter angiography
*Fever
*Radionuclide imaging
*Relative bradycardia with the fever.
*Tachypnea and cough
 
===Skin===
*Rash
The macular, maculopapular, or petechial rash initially occurs on the trunk and axilla and spreads to involve the rest of the body except for the face, palms, and soles.
Rash may be petechial in patients with epidemic or murine typhus.
*Eschar
This is found in the scrub form of typhus and is essential in confirming a clinical diagnosis. It occurs in up to 60% of cases.
Eschar occurs at the site of the arthropod bite. It starts as a painless papule, and the lesion becomes indurated and enlarged. The center of the lesion becomes necrotic and develops into a black scab.
Other features
===Lymph nodes===
Regional lymphadenopathy
Lymph nodes are often tender and enlarged.
Generalized lymphadenopathy
===Abdomnen===
*Hepatomegaly
*Splenomegaly
===HEENT===
Conjunctival suffusion occurs in scrub typhus.
==Medical therapy==
==Medical Therapy==
===Pharmacotherapy===
===Typhus, louse-borne===
* '''Louse born typhus, Rickettsia prowazekii''' (epidemic typhus, sylvatic typhus and  Brill–Zinsser typhus''' <ref name="pmid23253320">{{cite journal| author=Botelho-Nevers E, Socolovschi C, Raoult D, Parola P| title=Treatment of Rickettsia spp. infections: a review. | journal=Expert Rev Anti Infect Ther | year= 2012 | volume= 10 | issue= 12 | pages= 1425-37 | pmid=23253320 | doi=10.1586/eri.12.139 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23253320  }} </ref>
:* Pathogen-directed antimicrobial therapy
::* In adults
:::* Preferred regimen (1): [[Doxycycline]] 200 mg PO for 5 days or 2-3 days after defervescence
:::* Preferred regimen (2): [[Doxycycline]] 100-200 mg PO single dose in outbreak situation
:::* Alternative regimen: [[Chloramphenicol]] 60 to 75 mg/kg/day PO in four divided doses
::* In children
:::* Preferred regimen (1): [[Doxycycline]] 100-200 mg PO single dose
::* In pregnant women
:::* Preferred regimen: [[Doxycycline]] 100-200 mg PO single dose
 
===Typhus, murine===
* '''Murine typhus,Rickettsia typhi''' (flea-borne infection) <ref name="pmid23253320">{{cite journal| author=Botelho-Nevers E, Socolovschi C, Raoult D, Parola P| title=Treatment of Rickettsia spp. infections: a review. | journal=Expert Rev Anti Infect Ther | year= 2012 | volume= 10 | issue= 12 | pages= 1425-37 | pmid=23253320 | doi=10.1586/eri.12.139 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23253320  }} </ref>
:* Pathogen-directed antimicrobial therapy
::*  1. '''Adults'''
:::* Preferred regimen : [[Doxycycline]] 100 mg PO bid continued for 3 days after the symptoms have resolved, [[Doxycycline]] 100-200 mg, PO single dose
:::* Alternative regimen (1): [[Oxacillin]] 2-12 g/24 hr  IV q4-6h IV (maximum dose: 12 g/24)
:::* Alternative regimen (2): [[Chloramphenicol]] 60 to 75 mg/kg/day PO in qid
::*  2. '''Children'''
:::* Preferred regimen: [[Doxycycline]] 100-200 mg, PO for 3-7 days
:::* Alternative regimen: [[Chloramphenicol]] 50-75 mg/kg/24 hr IV/PO q 6-8 hr
::*  3. '''Pregnant women'''
:::* Preferred regimen: [[Doxycycline]] 100-200 mg, PO single dose ( late trimester)
:::* Alternative regimen (1): [[Erythromycin]] Base: 333 mg PO tid or estolate/stearate/ base: 250-500 mg PO qid
:::* Alternative regimen (2): [[Chloramphenicol]] 50 mg/kg/24 hr IV/PO  q6h (maximum dose: 4 g/24 hr) (early trimester: first and second trimesters)
===Typhus, scrub===
* '''Scrub typhus,  Orientia tsutsugamushi''' (previously called Rickettsia tsutsugamushi- mite-borne infectious disease) <ref name="pmid12137646">{{cite journal| author=Panpanich R, Garner P| title=Antibiotics for treating scrub typhus. | journal=Cochrane Database Syst Rev | year= 2002 | volume=  | issue= 3 | pages= CD002150 | pmid=12137646 | doi=10.1002/14651858.CD002150 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12137646  }} </ref>
:* Pathogen-directed antimicrobial therapy
::* Preferred regimen (1): [[Doxycycline]] 100 mg PO/IV q12h for 3 days
::* Preferred regimen (2): [[Chloramphenicol]] 500 mg PO/IV q6h
::* Alternative regimen: [[Azithromycin]] 500 mg PO day 1 followed by 250 mg for 4 days
==Prevention==
==Primary Prevention==
 
Avoid areas where you might encounter rat fleas or lice. Good sanitation and public health measures reduce the rat population. Measures to get rid of lice when an infection has been found include:
* Bathing
* Boiling clothes or avoiding infested clothing for at least 5 days (lice will die without feeding on blood)
* Using insecticides (10% DDT, 1% malathion, or 1% permethrin)
 
===Vaccine===
The first major step in the development of the [[vaccine]] was [[Charles Nicolle]]'s 1909 discovery that [[lice]] were the [[Vector (biology)|vectors]] for epidemic typhus.  This made it possible to isolate the bacteria causing the disease and develop a vaccine; he was awarded the 1928 [[Nobel Prize in Physiology or Medicine]] for this work.  Nicolle attempted a vaccine but was not successful in making one that worked on a large enough scale.<ref>Gross, Ludwik (1996) [http://www.pnas.org/cgi/reprint/93/20/10539.pdf ''How Charles Nicolle of the Pasteur Institute discovered that epidemic typhus is transmitted by lice: reminiscences from my years at the Pasteur Institute in Paris''] Proc. Natl. Acad. Sci. Vol. 93, pp. 10539-10540.</ref> 
 
[[Henrique da Rocha Lima]] in 1916 then proved that the bacteria ''Rickettsia prowazekii'' was the agent responsible for typhus; he named bacteria after H. T. Ricketts and [[Stanislaus von Prowazek]], two zoologists who died investigating a typhus epidemic in a prison camp in 1915. Once these crucial facts were recognized, Rudolf Weigl in 1930 was able to fashion a practical and effective vaccine production method by grinding up the guts of infected lice that had been drinking blood. It was, however, very dangerous to produce, and carried a high likelihood of infection to those who were working on it.
 
A safer mass-production-ready method using egg yolks was developed by [[H. R. Cox|Herald R. Cox]] in 1938.<ref name =Mazal1>[http://www.mazal.org/archive/nmt/01/NMT01-T508.htm ''Nuernberg Military Tribunal, Volume I''] pp. 508-511</ref>  This vaccine was used heavily by 1943.
 
==Colonic abscess==
A colonic abscess develops as a complication of diverticulitis. A colonic abscess is a localized collection of pus within the wall of the colon that may cause swelling and destroy tissue. If the abscess is small and remains within the wall of the colon, it may clear up with antibiotics alone. If the abscess is large > 5cms, or unresponsive to medical treatment, it must be drained using a catheter facilitated by sonography or x-ray.
===Causes===
Colon abscess is a rare entity and arises as a compliecation of diseases such as IBD, colorectal cancer, diverticulosis or diverticulitis. Natural gut flora which includes [[Gram-negative bacteria|gram negative]] and [[anaerobic bacteria]] play a major role in the development of colonic abscess.<ref name="pmid20034345">{{cite journal| author=Solomkin JS, Mazuski JE, Bradley JS, Rodvold KA, Goldstein EJ, Baron EJ et al.| title=Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. | journal=Clin Infect Dis | year= 2010 | volume= 50 | issue= 2 | pages= 133-64 | pmid=20034345 | doi=10.1086/649554 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20034345  }} </ref>
 
====Most common causes====
* [[Enterococcus]] 
* [[Escherichia coli]]
* [[Staphylococcus aureus]]
* [[Bacteroides fragilis]]
* [[Clostridium perfringens]]
 
====Less common causes====
* [[Klebsiella pneumoniae]] 
* [[Pseudomonas aeruginosa]]
* [[Proteus]]
 
===Pathophysiology===
*The primary process is thought to be an erosion of the diverticular wall by increased intraluminal pressure or inspissated food particles.
*Inflammation and focal necrosis ensue, resulting in the abscess formation.
====Gross Pathology====
*The serosal surface of the [[colon]] looks pale with rough edges and yellowish [[exudate]] along with [[hyperemia]]
 
====Microscopic findings====
*A focally [[necrotic]] debris is seen in the [[Mucosa|mucosal]] wall.
*[[Intravascular|Intravascular fibrin]] is seen in medium-sized [[blood vessels]].
*Clusters of [[neutrophils]] are seen on the [[Serosa|serosal]] aspect.
 
===Risk factors===
Risk factors in the development of colonic abscess include same as that of diverticular diseases of the colon, such as advanced age, chronic constipation, connective tissue diseases (such as Marfan syndrome or Ehlers-Danlos syndrome), low dietary fiber intake, high intake of fat and red meat, and obesity.
===Screening===
Screening for colonic abscess is not recommended in the general population.
===Epidemiology and Demographics===
====Prevalance====
*The prevalence of diverticulosis is age-dependent.
*The prevalence increases from fewer than 20% at age 40 to approximately 60% by age 60.<ref name="pmid1109818">{{cite journal |vauthors=Painter NS, Burkitt DP |title=Diverticular disease of the colon, a 20th century problem |journal=Clin Gastroenterol |volume=4 |issue=1 |pages=3–21 |year=1975 |pmid=1109818 |doi= |url=}}</ref><ref name="pmid">{{cite journal |vauthors=Peery AF, Barrett PR, Park D, Rogers AJ, Galanko JA, Martin CF, Sandler RS |title=A high-fiber diet does not protect against asymptomatic diverticulosis |journal=Gastroenterology |volume=142 |issue=2 |pages=266–72.e1 |year=2012 |pmid= |doi=10.1053/j.gastro.2011.10.035 |url=}}</ref>
====Incidence====
*Incidence rates among age groups 18 to 44 is 0.151 to 0.251 per 1000 population.
*Incidence rates among age groups  45 to 64 years of age is 0.659 to 0.777 per 1000 population.
 
====Gender====
*At young age (<50 years), males are more commonly affected with diverticulosis than females.
*At older age, women are more frequently affected with diverticulosis than males.<ref name="pmid17299613">{{cite journal |vauthors=Warner E, Crighton EJ, Moineddin R, Mamdani M, Upshur R |title=Fourteen-year study of hospital admissions for diverticular disease in Ontario |journal=Can. J. Gastroenterol. |volume=21 |issue=2 |pages=97–9 |year=2007 |pmid=17299613 |pmc=2657668 |doi= |url=}}</ref>
====Race====
*There is a slight racial predilection to the development of diverticulosis.
*Caucasian individuals are at higher risk of developing diverticulosis compared with Asian and non-African Black individuals.<ref name="pmid21448352">{{cite journal |vauthors=Golder M, Ster IC, Babu P, Sharma A, Bayat M, Farah A |title=Demographic determinants of risk, colon distribution and density scores of diverticular disease |journal=World J. Gastroenterol. |volume=17 |issue=8 |pages=1009–17 |year=2011 |pmid=21448352 |pmc=3057143 |doi=10.3748/wjg.v17.i8.1009 |url=}}</ref>
===Natural history===
If left untreated colonic abscess will rupture through the wall, and this may eventually lead to death if peritonitis develops.
 
===Complications===
*Peritonitis
*Septicemia
*Hemorrhage
*Death
===Prognosis===
*Majority of the patients with colonic abscess recover quickly with drain and IV antibiotics, but complications can occur if treatment is delayed or if peritonitis occurs.[3][4]
*It usually takes between 10 and 28 days to recover completely.
*Typical abscess responds quickly to antibiotics and percutaneous drain and resolves spontaneously.
===History and symptoms===
The most common symptom of colonic abscess is left lower quadrant abdominal pain along with fever and chills. The most common sign is tenderness around the left side of the lower abdomen. Nausea, vomiting, chills, cramping, diarrhea and constipation may occur as well. The severity of symptoms depends on the extent of the infection.
===Differentiating Colonic abscess from other diseases===
{| class="wikitable"
{| class="wikitable"
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;"|Diseases
!
! colspan="5" align="center" style="background:#4479BA; color: #FFFFFF;"|Clinical features
!CT angiography
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;"|Diagnosis
!Catheter angiography
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;"|Associated findings
!Radionuclide imaging
|-
|-
! colspan="4" align="center" style="background:#4479BA; color: #FFFFFF;"|Symptoms
|Bleeding at rates
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;"|Signs
detection
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;"|Laboratory fingdings
|At least 0.5 mL/min
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;"|Radiological findings
|0.5 to 1.5 mL/min
|0.1 mL/min
|-
|-
|style="background:#4479BA; color: #FFFFFF|'''Fever'''
|Indications
|style="background:#4479BA; color: #FFFFFF|'''Abdominal pain'''
|style="background:#4479BA; color: #FFFFFF|'''Nausea'''
'''vomiting'''
|style="background:#4479BA; color: #FFFFFF|'''Diarrhea'''
|-
|style="background:#4479BA; color: #FFFFFF|'''Crohn's disease'''
| '''+'''
|
|
LLQ continuous localized [[pain]]
* Hemodynamically stable
| '''+'''
* Endoscopy undiagnostic
|
|
Bloody
* Endoscopy not feasible due to severe bleeding with hemodynamic instability
 
* Persistent or recurrent GI bleeding
* Non-diagnostic upper endoscopy
|
|
Fullness or a discrete [[mass]] in the LLQ of the [[abdomen]]
|-
|Advantages
|
|
[ASCA]) are found  in [[Crohn disease]]
* Minimally invasive 
 
* Demonstrate neoplasms or vascular malformations
 
* Can provide evidence of recent bleeding
|
|
Transmural [[ulcerations]] are seen on colonoscopy
* Diagnostic and therapeutic
* Allows for infusion of vasoconstrictive drugs and/or embolization.
* Does not require bowel preparation. 
|
|
* H/O [[weight loss]],
* Most sensitive imaging modality for GI bleeding
* Extra [[intestinal]] manifestaions
* More commonly utilized for investigation of patients with obscure, intermittent bleeding
* [[Endoscopic]] [[biopsy]]  for diagnosis
|-
|-
|style="background:#4479BA; color: #FFFFFF|'''Gastroenteritis'''
|Disadvantages
(Bacterial and viral)
| '''+'''
|
|
Diffuse crampy intermittent [[abdominal pain]]
* Lacks therapeutic capability
| '''+'''
* Risk of contrast induced nephropathy in patients with renal impairment and contrast allergy
|
|
Bloody or watery
* Access-site hematoma or pseudoaneurysm
* Arterial dissection
* Spasm, bowel ischemia
* Contrast-induced nephropathy or allergic reaction
|
* Poor anatomic localization of the bleeding site
* Unable to diagnose the pathological cause of GI bleeding
|}
 
==Differentiating UGIB==
Blood that originates from the oro-pharynx, if swallowed, can present as melena, leading to a false concern of a gastrointestinal source. Examination of nasal area and mouth will help to identify source of bleeding.<ref name="pmid27653583">{{cite journal |vauthors=Graham DY |title=Upper Gastrointestinal Bleeding Due to a Peptic Ulcer |journal=N. Engl. J. Med. |volume=375 |issue=12 |pages=1197–8 |year=2016 |pmid=27653583 |doi=10.1056/NEJMc1609017#SA2 |url=}}</ref><ref name="pmid25214975">{{cite journal |vauthors=Chen ZJ, Freeman ML |title=Management of upper gastrointestinal bleeding emergencies: evidence-based medicine and practical considerations |journal=World J Emerg Med |volume=2 |issue=1 |pages=5–12 |year=2011 |pmid=25214975 |pmc=4129733 |doi= |url=}}</ref><ref name="pmid10566713">{{cite journal |vauthors=Kaufman DW, Kelly JP, Wiholm BE, Laszlo A, Sheehan JE, Koff RS, Shapiro S |title=The risk of acute major upper gastrointestinal bleeding among users of aspirin and ibuprofen at various levels of alcohol consumption |journal=Am. J. Gastroenterol. |volume=94 |issue=11 |pages=3189–96 |year=1999 |pmid=10566713 |doi=10.1111/j.1572-0241.1999.01517.x |url=}}</ref><ref name="pmid16015555">{{cite journal |vauthors=Lee EW, Laberge JM |title=Differential diagnosis of gastrointestinal bleeding |journal=Tech Vasc Interv Radiol |volume=7 |issue=3 |pages=112–22 |year=2004 |pmid=16015555 |doi= |url=}}</ref><ref name="pmid12872092">{{cite journal |vauthors=Lee YT, Walmsley RS, Leong RW, Sung JJ |title=Dieulafoy's lesion |journal=Gastrointest. Endosc. |volume=58 |issue=2 |pages=236–43 |year=2003 |pmid=12872092 |doi=10.1067/mge.2003.328 |url=}}</ref><ref name="pmid11796865">{{cite journal |vauthors=Ghosh S, Watts D, Kinnear M |title=Management of gastrointestinal haemorrhage |journal=Postgrad Med J |volume=78 |issue=915 |pages=4–14 |year=2002 |pmid=11796865 |pmc=1742226 |doi= |url=}}</ref><ref name="pmid9382039">{{cite journal |vauthors=Chalasani N, Clark WS, Wilcox CM |title=Blood urea nitrogen to creatinine concentration in gastrointestinal bleeding: a reappraisal |journal=Am. J. Gastroenterol. |volume=92 |issue=10 |pages=1796–9 |year=1997 |pmid=9382039 |doi= |url=}}</ref>
{| class="wikitable"
!
!History
!Physical Examination
!Laboratory Results
|-
|Peptic ulcer disease
|
|
[[Rebound tenderness]], [[rash]]
* Dyspepsia
* Early satiety
* NSAID use
* Previous ulcer disease
|
|
* Fecal [[leukocytes]]
* Hematemesis
* [[Stool culture]]
* Possible hematochezia, melena
* [[Stool]] [[toxin]] assay
* Hemodynamic instability
|No specific findings
** Tachycardia
** Hypotension
|
|
* H/O [[food poisoning]], travel 
* Decreased hemoglobin
* Increased BUN/creatinine
* Increased WBC's
* Helicobacter pylori positive
|-
|-
|style="background:#4479BA; color: #FFFFFF|'''Primary peritonitis'''
|Mallory-Weiss tear
| '''+'''
|
|
Abrupt diffuse abdominal pain
* Vomiting/retching
| '''+'''
* Weakness
* Dizziness
|
|
Bloody/watery
* Hematemesis
* Possible hematochezia, melena
* Hemodynamic instability
** Tachycardia
** Hypotension
|
|
[[Abdominal distension]], rebound tenderness
* Decreased hemoglobin
* Increased creatinine
* Increased WBCs
|-
|Stress gastritis
|
|
[[Peritoneal fluid]] shows >500/microliter count and >25% polymorphonuclear [[leukocytosis]].
* History of head injury, severe burns, trauma
* Mechanical intubation
* Chronic steroid use
* Coagulopathy
|
|
* X-ray [[abdomen]] identifies free air under the [[diaphragm]]
* Hematemesis (coffee grounds more common)
* CT demonstrates [[abscess]] or [[fluid]] in [[abdomen]]
 
* Melena
|
|
* History of advanced [[cirrhosis]] or [[nephrosis]]
* Decreased hemoglobin
* Peritoneal fluid analysis confirms the diagnosis
* Increased WBCs
|-
|-
|style="background:#4479BA; color: #FFFFFF|'''Pelvic inflammatory disease'''
|Dieulafoy lesion
| '''+'''
|
* Dyspepsia
* Weakness
* Dizziness, syncope,
* May have no prior history before bleed.
|
|
Bilateral lower quadrant pain
* Hematemesis (bright red)
| '''+'''
* Hematochezia or melena
| '''-'''
* Hemodynamic instability
|
|
* [[Purulent]] discharge from cervical os.
* Decreased hemoglobin
* Cervical motion tenderness
* Decreased hematocrit
* Increased WBCs
|-
|Gastro-esophageal
varices
|
|
*Abundant white blood cells ([[White blood cell (WBC) count|WBCs]]) on saline microscopy of [[vaginal]] secretions
* Alcohol/tobacco use,
*Laboratory evidence of cervical infection with ''[[N gonorrhoeae]]'' or ''[[Chlamydia trachomatis|C trachomatis]]''(via culture or DNA probe)
* Weakness, dizziness, syncope
|
|
Transvaginal ultrasonographic scanning or magnetic resonance imaging (MRI) shows thickened fluid-filled tubes with or without free pelvic fluid or [[tubo-ovarian abscess]] (TOA). 
* Stigmata of chronic liver disease
* Hematemesis, hematochezia or melena
* Hemodynamic instability
|
|
[[Laparoscopy]] helps in confirmation of the diagnosis
* Decreased hemoglobin
 
* Decreased hematocrit
 
* Electrolyte abnormalities
 
* Increased bilirubin/liver enzymes
|-
|-
|style="background:#4479BA; color: #FFFFFF|'''Ruptured ectopic pregnancy'''
|Gastric cancer
| '''+'''
|
* Alcohol/tobacco use
* Often asymptomatic
|
|
Diffuse abdominal pain
* Hematemesis,
| '''+'''
* Melena,
| '''-'''
* Lymphadenopathy
** Palpable supraclavicular or anterior axillary lymph node
** Palpable firm stomach
|
|
* Unilateral or bilateral abdominal  tenderness
* Decreased hemoglobin
* [[Abdominal]] rigidity, guarding
* Electrolyte abnormalities
* On pelvic examination, the [[uterus]] may be slightly enlarged and soft, and cervical motion tenderness
* May have elevated CEA or CA 19-9
|-
|Hemobilia
|
|
[[HCG|BHCG]] [[hormone]] level is high in serum and in urine
* Recent trauma
* Bliary tree instrumentation
* Gallstones
|
|
Ultrasound reveals presence of mass in [[fallopian tubes]].
* RUQ abdominal pain
* Jaundice
* Hematemesis, melena
|
|
* Triad of [[amenorrhea]], [[abdominal pain]] and [[vaginal bleeding]]
* Decreased hemoglobin,
* SIgns of [[hypotension]]
* Transvaginal ultrasound with [[BHCG]] levels are the gold standard for diagnosis
|}


==Laboratory findings==
* Increased bilirubin
Hematologic parameters suggestive of [[infection]] like, [[leukocytosis]], [[anemia]], [[Thrombosis|abnormal platelet counts]], and [[Abnormal liver function test|abnormal liver function]] frequently are present in patients with colonic abscess, although patients who are debilitated or elderly often fail to mount reactive [[leukocytosis]] or [[Fever|fever]]. [[Blood cultures]] indicating persistent polymicrobial [[bacteremia]] strongly implicate the presence of an abscess.
==CT Abdomen==


*Colonic and paracolic inflammation in the presence of underlying diverticula (diverticula are identified on CT scans as outpouchings of the colonic wall).
* Increased WBCs
*Symmetric thickening of the colonic of approximately 4-5 mm is common.
|-
* Enhancement of the colonic wall is commonly noted. This usually has inner and outer high-attenuation layers, with a thick middle layer of low attenuation.
|Aortoduodenal
* Free diverticular perforation results in the extravasation of air and fluid into the pelvis and peritoneal cavity.
fistula
* Air in the bladder in the presence of a nearby segment of diverticulitis is suggestive of a colovesical fistula.
|
* Abdominal pain
* Back pain
* History of AAA repair
* May be asymptomatic
|
* Hematemesis or melena (herald bleed)


==Medical therapy==
* Pulsatile abdominal mass
[[Antibiotics]] should be started immediately once the diagnosis of abscess is made. Preoperative antibiotics have been associated with lower rates of [[wound]] and [[Intra-abdominal infection|intra-abdominal infections]].<ref name="pmid20034345">{{cite journal| author=Solomkin JS, Mazuski JE, Bradley JS, Rodvold KA, Goldstein EJ, Baron EJ et al.| title=Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. | journal=Clin Infect Dis | year= 2010 | volume= 50 | issue= 2 | pages= 133-64 | pmid=20034345 | doi=10.1086/649554 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20034345  }} </ref> <ref name="SartelliViale2013">{{cite journal|last1=Sartelli|first1=Massimo|last2=Viale|first2=Pierluigi|last3=Catena|first3=Fausto|last4=Ansaloni|first4=Luca|last5=Moore|first5=Ernest|last6=Malangoni|first6=Mark|last7=Moore|first7=Frederick A|last8=Velmahos|first8=George|last9=Coimbra|first9=Raul|last10=Ivatury|first10=Rao|last11=Peitzman|first11=Andrew|last12=Koike|first12=Kaoru|last13=Leppaniemi|first13=Ari|last14=Biffl|first14=Walter|last15=Burlew|first15=Clay Cothren|last16=Balogh|first16=Zsolt J|last17=Boffard|first17=Ken|last18=Bendinelli|first18=Cino|last19=Gupta|first19=Sanjay|last20=Kluger|first20=Yoram|last21=Agresta|first21=Ferdinando|last22=Di Saverio|first22=Salomone|last23=Wani|first23=Imtiaz|last24=Escalona|first24=Alex|last25=Ordonez|first25=Carlos|last26=Fraga|first26=Gustavo P|last27=Junior|first27=Gerson Alves Pereira|last28=Bala|first28=Miklosh|last29=Cui|first29=Yunfeng|last30=Marwah|first30=Sanjay|last31=Sakakushev|first31=Boris|last32=Kong|first32=Victor|last33=Naidoo|first33=Noel|last34=Ahmed|first34=Adamu|last35=Abbas|first35=Ashraf|last36=Guercioni|first36=Gianluca|last37=Vettoretto|first37=Nereo|last38=Díaz-Nieto|first38=Rafael|last39=Gerych|first39=Ihor|last40=Tranà|first40=Cristian|last41=Faro|first41=Mario Paulo|last42=Yuan|first42=Kuo-Ching|last43=Kok|first43=Kenneth Yuh Yen|last44=Mefire|first44=Alain Chichom|last45=Lee|first45=Jae Gil|last46=Hong|first46=Suk-Kyung|last47=Ghnnam|first47=Wagih|last48=Siribumrungwong|first48=Boonying|last49=Sato|first49=Norio|last50=Murata|first50=Kiyoshi|last51=Irahara|first51=Takayuki|last52=Coccolini|first52=Federico|last53=Lohse|first53=Helmut A Segovia|last54=Verni|first54=Alfredo|last55=Shoko|first55=Tomohisa|title=2013 WSES guidelines for management of intra-abdominal infections|journal=World Journal of Emergency Surgery|volume=8|issue=1|year=2013|pages=3|issn=1749-7922|doi=10.1186/1749-7922-8-3}}</ref>
|
:*'''1 Emperic therapy:'''
* Decreased hemoglobin
::*'''1.1 Single agent:'''
* Increased WBCs
:::*Preferred regimen (1): [[Imipenem-Cilastatin]] 500 mg IV q6h {{or}} 1 g q8h
|}
:::*Preferred regimen (2): [[Meropenem]] 1 g IV q8h
:::*Preferred regimen (3): [[Doripenem]] 500 mg IV q8h
:::*Preferred regimen (4): [[Piperacillin-tazobactam]] 3.375 g IV q6h


::*'''1.2 Combination:'''
==Management==
:::*Preferred regimen (1): [[Cefepime]] 2 g  q8–12 h {{and}} [[Metronidazole]] 500 mg IV q8–12 h or 1500 mg q24h
The management of GI bleeding includes
:::*Preferred regimen (2): [[Ceftazidime]] 2 g q8h {{and}} [[Metronidazole]] 500 mg IV q8–12 h or 1500 mg q24h
*'''Initial resuscitation and pharmacotherapy'''
:::*Preferred regimen (3): [[Ciprofloxacin]] 400 mg q12h {{and}} [[Metronidazole]] 500 mg IV q8–12 h or 1500 mg q24h
*'''Risk stratification'''
:::*Preferred regimen (4): [[Levofloxacin]]  750 mg q24h {{and}} [[Metronidazole]] 500 mg IV q8–12 h or 1500 mg q24h
*'''Surgery'''
:::*Note: Antimicrobial therapy of established infection should be limited to 4–7 days, unless it is difficult to achieve adequate source control. Longer durations of therapy have not been associated with improved outcome.
**Pre-endoscopy management
***Initial management of antithrombotic agents (anticoagulants and antiplatelet agents)
***Pharmacological therapy
***Role of gastric lavage and prophylactic endotracheal intubation
***Timing of endoscopy
**Endoscopic management
***Endoscopic diagnosis
***Endoscopic therapy
*Management following endoscopy/endoscopic hemostasis
===Initial resuscitation===
*The initial steps in the management of a patient with UGIB is to assess the severity of bleeding, and then institute fluid and blood resuscitation as needed.<ref name="pmid15703679">{{cite journal |vauthors=Wassef W |title=Upper gastrointestinal bleeding |journal=Curr. Opin. Gastroenterol. |volume=20 |issue=6 |pages=538–45 |year=2004 |pmid=15703679 |doi= |url=}}</ref><ref name="pmid19006607">{{cite journal |vauthors=Kovacs TO |title=Management of upper gastrointestinal bleeding |journal=Curr Gastroenterol Rep |volume=10 |issue=6 |pages=535–42 |year=2008 |pmid=19006607 |doi= |url=}}</ref><ref name="pmid26417980">{{cite journal |vauthors=Gralnek IM, Dumonceau JM, Kuipers EJ, Lanas A, Sanders DS, Kurien M, Rotondano G, Hucl T, Dinis-Ribeiro M, Marmo R, Racz I, Arezzo A, Hoffmann RT, Lesur G, de Franchis R, Aabakken L, Veitch A, Radaelli F, Salgueiro P, Cardoso R, Maia L, Zullo A, Cipolletta L, Hassan C |title=Diagnosis and management of nonvariceal upper gastrointestinal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) Guideline |journal=Endoscopy |volume=47 |issue=10 |pages=a1–46 |year=2015 |pmid=26417980 |doi=10.1055/s-0034-1393172 |url=}}</ref>
*Any patient with hemodynamic instability or who is actively bleeding should be admitted to the ICU for monitoring and resuscitation
*The patient’s hemodynamic status is of great importance in determining the degree of severity and triage status.
{| class="wikitable"
!
Criteria for
Admission of patient
|-
|
*Age >60yr
*Transfusion required.
*Initial Sys BP < 100.
*Red blood in NG lavage.
*History of cirrhosis or ascites on examination.
|}
*The rate of fluid resuscitation is proportional to the severity of bleeding with the goal of restoring and maintaining the patient’s blood pressure.
*Two large caliber (16-gauge or larger) peripheral catheters or a central venous line should be inserted in patients who are hemodynamically unstable. *Supportive care includes administration of supplemental oxygen and monitoring of urine output.
*Patients with severe bleeding will need to be transfused; the indications for transfusion in patients with less severe bleeding should be based on the patient’s age and presence of comorbid conditions.
*The target hematocrit value varies according to age and clinical conditions.
**In the elderly patient, the target hematocrit is 30%.
**In younger, healthy patients, the target hematocrit is 25%.
**In patients with portal hypertension, the target hematocrit should not be above 27% or 28%, so as not to raise portal venous pressure.
*Fresh frozen plasma, platelets, or both should be given to patients with coagulopathy who are actively bleeding and to those who have received more than 10 units of packed erythrocytes
{| class="wikitable"
! colspan="4" |WORKUP AND INITIAL TREATMENT
Initial Resuscitation
|-
| colspan="4" |Basic ABC
* Airway Breathing, Circulation
|-
| colspan="4" |Ensure patent and protected airway
* Intubate if needed
* Consider mechanical ventilation
2 large-bore, peripheral intravenous lines
* Can consider large-bore central venous catheter or intraosseous line if rapid transfuser will be needed


==Surgery==
* Resuscitate with 1:1:1 of packed red blood cells (PRBCs) to fresh frozen plasma (FFP) to platelets.
Percutaneous drainage can be performed under ultrasound or CT guidance, using either the Seldinger or trocar technique. Ultrasound is limited if the abscess is small, obscured by other structures, or if precise placement is required because of nearby vessels or organs. In these cases, CT is the optimal imaging modality. When an abscess is deep in the pelvis, depending on the specific location of the fluid collection, access may be obtained via transgluteal, transvaginal, or transrectal approaches. If the fluid collection is sterile, a transgluteal approach is preferred because it allows for sterile technique. Depending on the location of abscess, patient is placed in prone or supine position on the CT table. Localization scan using CT allows in selecting a safe window of access into the collection. A coaxial micropuncture introducer set is advanced into the abscess under CT guidance. An Amplatz guidewire is advanced through the sheath and coiled within the abscess. After serial dilatation of the tract with a dilator, an pigtail drain is advanced over the guidewire and deployed.
Consider massive transfusion protocol
{{#ev:youtube|f5KvsjHaOnI}}
==Prevention==
Dietary fiber and a vegetarian diet may reduce the incidence of symptomatic diverticular disease by decreasing intestinal [[inflammation]] and altering the intestinal microbiota.<ref name="pmid7942584">{{cite journal |vauthors=Aldoori WH, Giovannucci EL, Rimm EB, Wing AL, Trichopoulos DV, Willett WC |title=A prospective study of diet and the risk of symptomatic diverticular disease in men |journal=Am. J. Clin. Nutr. |volume=60 |issue=5 |pages=757–64 |year=1994 |pmid=7942584 |doi= |url=}}</ref>.
Vigorous physical activity appears to reduce the risk of [[diverticulitis]] and diverticular bleeding.<ref name="pmid7883230">{{cite journal |vauthors=Aldoori WH, Giovannucci EL, Rimm EB, Ascherio A, Stampfer MJ, Colditz GA, Wing AL, Trichopoulos DV, Willett WC |title=Prospective study of physical activity and the risk of symptomatic diverticular disease in men |journal=Gut |volume=36 |issue=2 |pages=276–82 |year=1995 |pmid=7883230 |pmc=1382417 |doi= |url=}}</ref>.
==Acute kidney injury in cancer patients==
===Types of Acute Kidney Injury in Patients with Hematologic Cancers===
====Cancer-related injury====
*Tumor infiltration of the kidneys
*Obstructive nephropathy related to retroperitoneal lymphadenopathy
*Lysozymuria (CMML or AML) with direct tubular injury
*Hemophagocytic lymphohistiocytosis with acute interstitial disease
*Vascular occlusion associated with DIC and hyperleukocytosis (rare)
*Hypercalcemia with hemodynamic acute kidney injury and acute nephrocalcinosis
*Glomerular diseases (minimal change disease, focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis, membranous
nephropathy, amyloidosis, immuno-tactoid glomerulonephritis, fibrillary glomerulonephritis, crescentic glomerulonephritis)
====Therapy-related injury====
*Nephrotoxicity (including thrombotic microangiopathy, acute tubular injury, tubulointerstitial nephritis, and glomerular disease)
*Tumor lysis syndrome with acute uric acid nephropathy (may occur spontaneously)
*Intratubular obstruction from medications (e.g., methotrexate)
====Other types of injuries====
*Volume depletion
*Sepsis and septic shock
*Nephrotoxicity of radiocontrast agents
*Nephrotoxicity of common medications, such as NSAIDs, ACE inhibitors,
*ARBs, and antibiotics
===Cancers and association===
*MM
*RCC
*
==Types of Haemophilus influenzae Infections==
H. influenzae, including Hib, can cause many different kinds of infections. These infections can range from mild ear infections to severe diseases, like bloodstream infections. When the bacteria invade parts of the body that are normally free from germs, like spinal fluid or blood, this is known as "invasive disease." Invasive disease is usually severe and can sometimes result in death.<br>
The most common types of invasive disease caused by H. influenzae are:
*Pneumonia
*Bacteremia
*Meningitis (infection of the covering of the brain and spinal cord)
*Epiglottitis (swelling of the windpipe that can cause breathing trouble)
*Cellulitis (skin infection)
*Infectious arthritis (inflammation of the joint)
H. influenzae can also be a common cause of ear infections in children and bronchitis in adults.


==Causes==
Resuscitate to a target hemoglobin of 7 mg/dL.
*Haemophilus influenzae disease is caused by the bacterium Haemophilus influenzae.
*There are six identifiable types of H. influenzae (a through f) and other non-identifiable types (called nontypeable). The one that people are most familiar with is H. influenzae type b, or Hib.
*These bacteria live in the nose and throat, and usually cause no harm. However, the bacteria can sometimes move to other parts of the body and cause infection. Some of these infections are considered “invasive” and can be very serious and sometimes even deadly.


==Incubation period==
Consider Sengstaken-Blakemore tube for control of immediately life-threatening upper GI bleeding
The incubation period (time between exposure and first symptoms) of H. influenzae disease is not certain, but could be as short as a few days.
|}
.
*The National Institute for Health and Care Excellence (NICE) guidline on blood product management in upper GI bleeding:
 
:*Platelets should only be given if the patient is actively bleeding or hemodynamically unstable and has a platelet count of <50×109/L.
==Natural history==
:*Fresh frozen plasma should be given if the fibrinogen level is <1 g/L or the prothrombin time (PT) or activated partial thromboplastin time is >1.5 times normal.
*Between 3% to 6% of Hib cases in children are fatal; up to 20% of patients who survive Hib meningitis have permanent hearing loss or other long-term neurological sequelae.
:*Prothrombin complex should be provided to those on warfarin and actively bleeding.
*Patients ≥65 years of age with invasive H. influenzae disease (Hib, non-b, and nontypeable) have higher case-fatality ratios than children and young adults.
:*Recombinant factor VIIa should only be used when all of the above measures have failed.
==Epidemiology==
===Endoscopic intervention===
===Incidence===
*In UGIB, diagnostic and therapeutic endoscopy may be performed simultaneously.  
*Before vaccine became available in 1988, the annual attack rate of invasive Hib disease was estimated at 64-129 cases per 100,000 children younger than 5 years.  
*Therapeutic upper gastrointestinal endoscopy should be performed in all patients with suspected UGIB to evaluate and possibly treat the source of bleeding.  
*The estimated annual incidence of Hib infection is 0.04 cases per 100,000 general population.
*The urgency of endoscopy depends on the anticipated source of bleeding, rapidity of blood loss, and hemodynamic stability of the patient.
*The estimated annual incidence of non-Hib infection is 0.36 cases per 100,000 general population.
*Endoscopic intervention should be undertaken within 24 hours, as early intervention is associated with reduced transfusion needs and a decreased length of stay in high-risk patients with nonvariceal bleeding.
===Gender===
====Endoscopic procedures====
*Hib disease has no sexual predilection
*The most common procedures used to manage bleeding caused by peptic ulcer disease are injection, coagulation (thermal, electric, and argon plasma), and hemostatic clips.
===Age===
*The most common procedures used to manage esophageal varices are sclerotherapy and variceal band ligation
*Hib infections are rare in patients older than 6 years.
*There is evidence supporting the use of two different endoscopic procedures, rather than a single procedure to better control bleeding and decrease the incidence of rebleeding
*Hib infections are most common in children aged 6 months to 6 years.
*Other successful methods for controlling bleeding are available when endoscopy fails:
==Risk factors==
**Balloon tamponade and TIPS are temporizing measures for patients with actively bleeding esophageal varices who cannot be managed endoscopically.
*Unimmunized children younger than 4 years of age, as well as household contacts and daycare classmates of a person with Hib disease are at increased risk of Hib disease.  
**Emergency surgery for bleeding peptic ulcers that cannot be managed endoscopically involves oversewing of the ulcer to ligate the bleeding artery plus truncal vagotomy to decrease acid secretion and pyloroplasty to improve gastric drainage.
*Close contacts of patients with non-b or nontypeable H. influenzae has not been identified.
=====Endoscopic band ligation (EBL)=====
*Patients with sickle cell disease, asplenia, HIV, and certain immunoglobulin and complement component deficiencies, as well as recipients of hematopoietic stem cell transplant and chemotherapy or radiation therapy for malignant neoplasms are at increased risk for invasive H. influenzae disease.  
*EBL involves the placement of elastic circular ring ligatures around the varices to cause strangulation, while the patient is under sedation and analgesia. *Bands are typically delivered at the gastroesophageal junction first, then proximally; six to ten bands may be delivered with a single intubation.
*Immigrants
*The primary drawback of EBL is that during active bleeding, operator visibility is limited by the device holding the bands prior to their delivery. *Endotracheal intubation is prudent in patients with active bleeding to reduce the risk of aspiration pneumonia.  
==Complications==
*Systemic antibiotics should be considered in patients with ascites to reduce the risk of bacterial infection
*Complications depend on the type of invasive infection caused the bacteria.
*Follow-up endoscopies are recommended at various intervals depending on the size/appearance of varices and severity of liver disease.
*Meningitis can result in hearing loss.
*Typically, visits every 2 to 4 weeks until obliteration. An interval of 1 to 3 months is recommended for initial surveillance of recurrence of varices, then every 6 to 12 months
*Bacteremia (blood infection) can result in loss of limb(s).
*Endoscopic therapy can halt bleeding in 80% to 90% of patients
*Invasive H. influenzae infections can sometimes result in death. Even with antibiotic treatment, about 3 to 6 out of every 100 children with meningitis caused by Hib die from the disease.
*EBL is equivalent to EIS in establishing initial control of bleeding, but EBL is challenging in the actively bleeding patient
*When H. influenzae cause a non-invasive infection, like bronchitis or an ear infection, complications are rare and typically not severe. If appropriate, antibiotics can be given to prevent complications
*EBL is widely favored over EIS for primary prevention due to similar or superior efficacy with fewer complications
==Medical therapy==
====Endoscopic injection sclerotherapy (EIS)====
A number of medical treatments are utilized with the goal of putting and keeping the disease in [[remission (medicine)|remission]].  These include [[mesalazine|5-aminosalicylic acid]] (5-ASA) formulations (Pentasa capsules, Asacol tablets, Lialda tablets, Rowasa retention enemas), [[prednisone|steroid]] medications, immunomodulators (such as [[azathioprine]], [[mercaptopurine]] (6-MP), and [[methotrexate]]), and newer [[biological therapy for inflammatory bowel disease|biological]] medications, such as [[infliximab]] (Remicade) and [[adalimumab]] (Humira).<ref name=Podolsky>{{Cite journal|last=Podolsky|first= Daniel K.|title=Inflammatory bowel disease|journal=New England Journal of Medicine|month=August|year=2002|volume=346|issue=6|pages=417-29
*Comprises endoscopic delivery of a sclerosant, such as ethanol, morrhuate sodium, polidocanol, or sodium tetradecyl sulfate, while patient is under sedation and analgesia.
|url=http://content.nejm.org/cgi/content/extract/347/6/417|accessdate=2006-07-02|id=PMID 12167685}}</ref>Also in January 2008 the U.S. Food and Drug Administration approved a new biological medication known as [[natalizumab]] (Tysabri) for both induction of remission and maintenance of remission in moderate and severe Crohn's Disease.
*Injections may be intravariceal or be delivered into the esophageal wall near the varices.
Treatment is only needed for people exhibiting symptoms. The therapeutic approach to Crohn's disease is sequential: to treat [[acute (medical)|acute]] disease and then to maintain [[remission]]. Treatment initially involves the use of medications to treat any infection and to reduce inflammation. This usually involves the use of aminosalicylate anti-inflammatory drugs and corticosteroids, and may include antibiotics. 
*Bucrylate is an adhesive that has been used successfully.  
 
*Typical injection volume is 1 to 2 mL per injection, for a total volume of 10 to 15 mL. Interval between injections varies according to patient tolerance and response, and complications
Once remission is induced, the goal of treatment becomes maintaining remission and avoiding flares. Because of side-effects, the prolonged use of corticosteroids must be avoided. Although some people are able to maintain remission with aminosalicylates alone, many require immunosuppressive drugs.
*After an initial injection to control bleeding, there is usually a follow-up injection 2 to 3 days later, followed by weekly or biweekly procedures until complete obliteration of the varices is achieved, which usually takes five or six sessions
On 14 January 2008 the U.S. Food and Drug Administration approved [[natalizumab]] (Tysabri) for both induction of remission and maintenance of remission in Crohns. Natalizumab is humanized monoclonal antibody (MAb), and the first alpha-4 antagonist in a new class of agents called selective adhesion-molecule (SAM) inhibitors. Alpha-4 integrin is required for [[leukocyte]]s to adhere to the walls of blood vessels and migrate into the gut; natalizumab prevents leukocytes from doing that. Natalizumab was previously approved for [[multiple sclerosis]]. However, because it suppresses the [[immune system]], natalizumab has been linked to a very rare adverse effect that is usually fatal if undetected. Leukocytes also protect the body from viruses, and 2 patients on natalizumab, who were also receiving other immuno-suppressive drugs ([[Interferon beta-1a|Avonex]] and Immuran), died of a rare brain infection, [[progressive multifocal leukoencephalopathy]]. Because of this danger, patients must be in a special monitoring program, and natalizumab is given as a mono-therapy.<ref name="FDA-Tysbari">{{cite press release|title=FDA Approves Tysabri to Treat Moderate-to-Severe Crohn's Disease|publisher=U.S. Food and Drug Administration|date=2008-01-14|url=http://www.fda.gov/bbs/topics/NEWS/2008/NEW01775.html|accessdate=2008-01-16
}}</ref> As of late December 2007, more than 21,000 MS patients were receiving natalizumab mono-therapy without a single incidence of PML occurring.<ref>.http://www.elan.com/News/full.asp?ID=1091942</ref>
 
[[Surgery]] may be required for complications such as obstructions, fistulas and/or abscesses, or if the disease does not respond to drugs within a reasonable time. For patients with an obstruction due to a stricture, two options for treatment are strictureplasty and resection of that portion of bowel.  According to a retrospective review at the Cleveland Clinic, there is no [[statistical significance]] between strictureplasty alone versus strictureplasty and resection specifically in cases of duodenal involvement. In these cases, re-operation rates were 31% and 27%, respectively, indicating that strictureplasty is a safe and effective treatment for selected patients with duodenal involvement.<ref name="pmid8918424">{{cite journal | author = Ozuner G, Fazio VW, Lavery IC, Milsom JW, Strong SA | title = Reoperative rates for Crohn's disease following strictureplasty. Long-term analysis | journal = Dis. Colon Rectum | volume = 39 | issue = 11 | pages = 1199-203 | year = 1996 | pmid = 8918424 | doi = }}</ref>
 
Recent studies using [[Helminthic therapy]] or [[hookworm]]s to treat Crohn's Disease and other (non-viral) auto-immune diseases seem to yield promising results.<ref>British Medical Journal [http://gut.bmj.com/cgi/content/full/55/1/136 A proof of concept study establishing Necator americanus in Crohn’s patients and reservoir donors]</ref><ref name="Daily Mail">Daily Mail. [http://www.dailymail.co.uk/pages/live/articles/technology/technology.html?in_article_id=481875&in_page_id=1965  The bloodsucking worm that fights allergies from inside your tummy] 14-09-2007.</ref><ref>[http://www.kuro5hin.org/story/2006/4/30/91945/8971 How to cure your asthma or hayfever using hookworm - a practical guide]. 01-05-2006.</ref>
 
==Pathophysiology of Sepsis==
*Sepsis is defined as a collection of physiologic responses by the immune system in response to an infectious agent.
*The clinical course of sepsis depends on the type and resistance of the infectious organism, the site and size of the infecting insult, and the genetically determined or acquired properties of the host's immune system.
*The pathogenesis of sepsis can be discussed as follows
 
===Immune system activation===
*The immune system is activated by pathogen entry which is facilitated by contamination of tissue either by surgery or infection, foreign body insertion (catheters) and in an immunocompromised state.
*Products of activation include
**Bacterial cell wall products such as lipopolysaccharide
**Binding to host receptors, including Toll-like receptors (TLRs).
*Toll-like receptors are found in leukocytes and macrophages, and endothelial cells.
*These have specificity for different bacterial, fungal, or viral products.
*TLRs are associated with a predisposition to shock with gram-negative organisms.
*Activation of the innate immune system results in a complex series of cellular and humoral responses.
 
===Immune repsonse===
*Immune response includes the release of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha and interleukins 1 and 6 along with reactive oxygen species, nitric oxide (NO), proteases, and pore-forming molecules, which bring about activation of immune cells and bacterial killing.
*Nitrous oxide is responsible for vasodilatation and increased capillary permeability and has been implicated in sepsis-induced mitochondrial dysfunction.
*The complement system also gets activated which mediates activation of leukocytes, attracting them to the site of infection (phagocytes, cytotoxic T lymphocytes),
*Complement system also helps as a mediator for antigen-presenting cells and B lymphocytes
*This response by complement system helps the B lymphocyte to produce memory cells in case of future infection and is responsible for the increased production and chemotaxis of more T helper cells.
 
===The endothelium and coagulation system===
*The vascular endothelium plays a major role in the host's defense to an invading organism, but also in the development of sepsis.  
*Activated endothelium not only allows the adhesion and migration of stimulated immune cells but becomes porous to large molecules such as proteins, resulting in the tissue edema.
*Alterations in the coagulation systems include an increase in procoagulant factors, such as plasminogen activator inhibitor type I and tissue factor, and reduced circulating levels of natural anticoagulants, including antithrombin III and activated protein C (APC), which also carry anti-inflammatory and modulatory roles.
===Inflammation and organ dysfunction===
*Through vasodilatation (causing reduced systemic vascular resistance) and increased capillary permeability (causing extravasation of plasma), sepsis results in relative and absolute reductions in circulating volume.
*A number of factors combine to produce multiple organ dysfunctions.
*Relative and absolute hypovolemia are compounded by reduced left ventricular contractility to produce hypotension.
*Initially, through an increased heart rate, cardiac output increases to compensate and maintain perfusion pressures, but as this compensatory mechanism becomes exhausted, hypoperfusion and shock may result.
*Impaired tissue oxygen delivery is exacerbated by pericapillary edema.
*It makes oxygen to diffuse a greater distance to reach target cells.
*There is a reduction of capillary diameter due to mural edema and the procoagulant state results in capillary microthrombus formation.
===Additional contributing factors===
*Disordered blood flow through capillary beds, resulting from a combination of shunting of blood through collateral channels and an increase in blood viscosity secondary to loss of red cell flexibility.
*As a result, organs become hypoxic, even with increase blood flow.
*These abnormalities leads to lactic acidosis, cellular dysfunction, and multiorgan failure.
*Cellular energy levels fall as metabolic activity begins to exceed production.
*However, cell death appears to be uncommon in sepsis, implying that cells shut down as part of the systemic response.
*This could explain why relatively few histologic changes are found at autopsy, and the eventual rapid resolution of severe symptoms, such as complete anuria and hypotension, once the systemic inflammation resolves.
==H influenza infection==
===Overview===
H.influenzae is a type of bacteria that can cause infections in people of all ages ranging from mild, such as an ear infection, to severe, such as a bloodstream infection.
===Causes===
*Haemophilus influenza disease is caused by the bacterium Haemophilus influenza.
*There are six identifiable types of H.influenza (a through f) and other non-identifiable types (called nontypeable).
*The most common type of H.influeza  that is most familiar is H. influenza type b, or Hib.
*These bacteria are a normal commensal of throat and nose. However, the bacteria can sometimes move to other parts of the body and cause infection.
*Some of these infections are considered “invasive” and can be very serious.
 
===Classification===
H. influenzae, including Hib, can cause many different kinds of infections. These infections can range from mild ear infections to severe diseases, like bloodstream infections. When the bacteria invade parts of the body that are normally free from germs, like spinal fluid or blood, this is known as "invasive disease." Invasive disease is usually severe and can sometimes result in death.<br>
The most common types of invasive disease caused by H.influenza are:
*Pneumonia
*Bacteremia
*Meningitis (infection of the covering of the brain and spinal cord)
*Epiglottitis (swelling of the windpipe that can cause breathing trouble)
*Cellulitis (skin infection)
*Infectious arthritis (inflammation of the joint)
The most common types of Non-invasive disease caused by H.influenza are:
*Otitis media
*Conjuctivitis


{{Family tree/start}}
{{Family tree/start}}
{{Family tree | | | | | | | | | | | | | | | | | | | | | | | A01 | | | | | | | | | | | | |A01= '''[[H influenza infection]]'''}}
{{Family tree | | | | | A01 | | | |A01=Acute GI bleeding}}
{{Family tree | | | | | | | | | | |,|-|-|-|-|-|-|-|-|-|-|-|-|^|-|-|-|-|-|-|-|-|-|-|-|-|-|.| | }}
{{Family tree | | | | | |!| | | | | }}
{{Family tree | | | | | | | | | | C01 | | | | | | | | | | | | | | | | | | | | | | | | | C02 |C01= Infection due to capsulated [[H influenza]]| C02= Infection due to non-capsulated [[H influenza]]}}
{{Family tree | | | | | B01 | | | |B01= Initial evaluation and resuscitation}}
{{Family tree | | |,|-|-|-|v|-|-|-|^|-|-|-|v|-|-|-|v|-|-|-|v|-|-|-|.| | | | | |,|-|-|-|-|^|-|-|-|-|.|}}
{{Family tree | | | | | |!| | | | | }}
{{Family tree | | D01 | | D02 | | | | | | D03 | | D04 | | D05 | | D06 | | | | D07 | | | | | | | | D08 |D01= [[Meningitis]] |D02=[[Cellulitis]]|D03=[[Epiglottitis]] |D04= [[Pneumonia]]|D05=[[Pericarditis]]|D06=[[Septic arthritis]]|D07=[[otitis media]]|D08=[[Conjunctivitis]]}}
{{Family tree | | | | | C01 | | | |C01=Uppe GI endoscopy}}
{{Family tree | | | | | |!| | | | | }}
{{Family tree | | |,|-|-|^|-|-|.| | }}
{{Family tree | | C01 | | | | C02 |C01= Source found| C02= Undiagnostic}}
{{Family tree | | |!| | | | | |!| | |}}
{{Family tree | | D01 | | | | |!| |D01=Specific Treatment|}}
{{Family tree | | | | | | | | |!| | |}}
{{Family tree | | | | | |,|-|-|^|-|-|-|-|.| |}}
{{Family tree | | | | | E01 | | | | | | E02 |E01=Unstable|E02=Stable|}}
{{Family tree | | | | | |!| | | | | | | |!| | |}}
{{Family tree | | | | | F01 | | | | | | F02 | |F01=Urgent CT|F02=Repeat Endoscopy/Angiograpghy}}
{{Family tree | | | | | |!| | | | | | | |!| | |}}
{{Family tree | | | | | G01 | | |,|-|-|-|+|-|-|-|v|-|-|-|.| |G01=No source identified|}}
{{Family tree | | | | | |!| | | I01 | | I02 | | I03 | | I04 |I01=Angioembolization|I02=Endoscopic intervention|I03=TIPS|I04=Surgery|}}
{{Family tree | | | | | H01 | | | | | | |!| | | | | |H01=Surgery<br>(Laprotomy)}}
{{Family tree | | | | | | | | | | | | | |!| | | | | |}}
{{Family tree | | | | | |,|-|-|-|v|-|-|-|+|-|-|-|v|-|-|-|.| }}
{{Family tree | | | | | J01 | | J02 | | J03 | | J04 | | J05 |J01=Sclerotherapy|J02=Banding|J03=Injection|J04=Thermocoagulation|J05=Clips|}}
{{Family tree/end}}
{{Family tree/end}}


==Pathophysiology==
===Pharmacotherapy===
===Transmission===
{| class="wikitable"
*Transmission is by direct contact or by inhalation of respiratory tract droplets.
! colspan="4" |Correlation between physical signs and
*Neonates can acquire the infection by aspiration of amniotic fluid or contact with genital tract secretions containing the bacteria.
the severity of upper gastrointestinal bleeding
===Incubation period===
|-
The incubation period (time between exposure and first symptoms) of H. influenzae disease is not certain, but could be as short as a few days.
! rowspan="2" |Physical signs
===Seeding===
! colspan="3" |Bleeding severity
*A larger bacterial load or the presence of a concomitant viral infection can potentiate the infection.
|-
*The colonizing bacteria invade the mucosa and enter the bloodstream.
!Mild
*The spread of bacteria by direct extension to the eustachian tubes causes otitis media.
!Moderate
*Spread to the sinuses leads to sinusitis.
!Severe
*Spread down the respiratory tract results in bronchitis and pneumonia.
|-
*Eustachian tube dysfunction, antecedent viral upper respiratory tract infection (URTI), foreign bodies, and mucosal irritants, including smoking, can promote infection.
|Blood loss
*In patients with underlying chronic obstructive pulmonary disease (COPD) or cystic fibrosis (CF), NTHi frequently colonizes the lower respiratory tract and can exacerbate the disease.
|<1L
===Pathogenesis===
|1-2L
*The capsule of H influenza plays a key role in the pathogenesis of the all the capsulated H influenza infections.
|>2L
*The antiphagocytic nature of the Hib capsule makes it resistant to natural host phagocytic defense mechanisms and facilitating bacterial proliferation.
|-
*After proliferation, the bacterial load disseminates to various sites, including meninges, subcutaneous tissue, joints, pleura, pericardiam, and lungs triggering an inflammatory response and subsequently activating the complement system.
|Systolic blood pressure
*Capsulated H influenza can penetrate the normal epithelium and are therefore responsible for invasive infections.
|<120
*Non-capsulated are non-invasive but can still induce the inflammatory response similar to that of capsulated organisms
|100-119
*The Hib conjugate vaccine induces protection by inducing antibodies against the PRP capsule.
|<99
*The Hib conjugate vaccine does not provide protection against Non-typable H influenza strains. Since the widespread use of the Hib conjugate vaccine,  Non-typable H influenza strains has become more of a pathogen
|-
==Toxoplasmosis==
|Orthostasis
==== Transmission ====
|'''-'''
|'''-'''
|'''+'''
|-
|Tachycardia
|<100
|101-120
|>140
|-
|Skin
|Warm, well perfused
|Diaphoretic
|Cool–cold, clammy
|-
|Urine output(ml/hour)
|>25
|10-25
|Negligible
|-
|Respiratory rate
|14-20
|20-30
|>35
|-
|Sensorium
|Alert
|Anxious
|Confused/Drowsy
|}


Transmission may occur through:
==Physical examination==
* Ingestion of raw or partly cooked meat, especially pork, lamb, or venison containing Toxoplasma cysts. Infection prevalence in countries where undercooked meat is traditionally eaten, such as France, has been related to this transmission method. Oocysts may also be ingested during hand-to-mouth contact after handling undercooked meat, or from using knives, utensils, or cutting boards contaminated by raw meat.<ref name=CDC>{{cite web
Common physical exam findings include:
 
===Vitals===
| url=http://www.dpd.cdc.gov/DPDx/HTML/Toxoplasmosis.htm
*Hypotension
| title=Toxoplasmosis
*Tachycardia
| publisher=Centers of Disease Control and Prevention
*Thready pulse
| date=2004-11-22 }}</ref>
*Hypoxia
 
===Abdomen===
* Ingestion of contaminated cat faeces. This can occur through hand-to-mouth contact following gardening, cleaning a cat's litter box, contact with children's sandpits, or touching anything that has come into contact with cat faeces.
*+Bowel sounds
* Drinking water contaminated with Toxoplasma.
*Abdominal tenderness
* Transplacental infection [[Uterus|in utero]].
*Hepatomegaly
* Receiving an infected [[organ transplant]] or [[blood transfusion]], although this is extremely rare.<ref name=CDC />
*Splenomegaly
* Accidental inoculation of tachyzoites
*Caput medusa
 
*Spider angiomata
====[[Transplacental]] Transmission====
===Skin===
 
*Palmar erythema
*infection in [[1st trimester]] - incidence of transplacental infection is low (15%) but disease in neonate is most severe.
*Cold clammy extremities
*Infection in [[3rd trimester]] - incidence of transplacental infection is high (65%) but infant is usually asymptomatic at birth.
===Neurological examination===
 
*Altered sensations
The cyst form of the parasite is extremely hardy, capable of surviving exposure to freezing down to −12 degrees Celsius, moderate temperatures and chemical disinfectants such as bleach, and can survive in the environment for over a year. It is, however, susceptible to high temperatures&mdash;above 66 degrees Celsius, and is thus killed by thorough cooking, and would be killed by 24 hours in a typical domestic freezer.<ref>[http://www.ncagr.com/vet/ToxoplasmosisTxt.htm]</ref>
*Poor mentation
 
*Drowsiness
Cats excrete the [[pathogen]] in their faeces for a number of weeks after contracting the disease, generally by eating an infected rodent. Even then, cat faeces are not generally contagious for the first day or two after excretion, after which the cyst 'ripens' and becomes potentially pathogenic. Studies have shown that only about 2% of cats are shedding oocysts at any one time, and that oocyst shedding does not recur even after repeated exposure to the parasite.  Although the pathogen has been detected on the fur of cats, it has not been found in an infectious form, and direct infection from handling cats is generally believed to be very rare.
===Rectal examination===
===Pathophysiology===
*Occult blood
====Life cycle of Toxoplasma gondii====
*Gross blood
*T gondii has 2 distinct life cycles.
**Bright red blood per rectum
*The sexual cycle occurs only in cats, the definitive host.
**Melena
*The asexual cycle occurs in other mammals (including humans) and various strains of birds.
**Burgundy stools
*It consists of 2 forms: tachyzoites (the rapidly dividing form observed in the acute phase of infection) and bradyzoites (the slowly growing form observed in tissue cysts).
**Blood coating stools versus within stools
*A cat becomes infected with T gondii by eating contaminated raw meat, wild birds, or mice.
**Bloody diarrhea
*The organism’s sexual cycle then begins in the cat’s gastrointestinal (GI) tract. Macrogametocytes and microgametocytes develop from ingested bradyzoites and fuse to form zygotes.
==Surgery==
*The zygotes then become encapsulated within a rigid wall and are shed as oocysts.
*The zygote sporulates and divides to form sporozoites within the oocyst.
*Sporozoites become infectious 24 hours or more after the cat sheds the oocyst via feces.
*During a primary infection, the cat can excrete millions of oocysts daily for 1-3 weeks.
*The oocysts are very strong and may remain infectious for more than one year in warm humid environments.
*T gondii oocysts, tachyzoites, and bradyzoites can cause infection in humans.
====Transmission====
*Infection can occur by ingestion of oocysts following the handling of contaminated soil or cat litter or through the consumption of contaminated water or food sources (eg, unwashed garden vegetables).
*Transmission of tachyzoites to the fetus can occur via the placenta following primary maternal infection.
*Rarely, infection by tachyzoites occurs from ingestion of unpasteurized milk or by direct entry into the bloodstream through a blood transfusion or laboratory accident.
*Transmission can also occur via ingestion of tissue cysts (bradyzoites) in undercooked or uncooked meat or through transplantation of an organ that contains tissue cysts. (Slaughterhouse workers and butchers may be at increased risk of infection.)
====Seeding====
*T gondii oocysts are ingested in material contaminated by feces from infected cats.
*When T gondii is ingested, bradyzoites are released from cysts or sporozoites are released from oocysts, and the organisms enter gastrointestinal cells. *Host cell receptors consisting of laminin, lectin, and SAG1 are involved in T gondii tachyzoite attachment and penetration.
*Tachyzoites multiply, rupture cells, and infect contiguous cells.
*The ability of T gondii to actively penetrate host cells results in formation of a parasitophorous vacuole that is derived from the plasma membrane, which is entirely distinct from a normal phagocytic or endocytic compartment.
*Following apical attachment, the parasite rapidly enters the host cell in a process that is significantly faster than phagocytosis.
*The vacuole is formed primarily by invagination of the host cell plasma membrane, which is pulled over the parasite through the concerted action of the actin-myosin cytoskeleton of the parasite.
*During invasion, the host cell is essentially passive and no change is detected in membrane ruffling, the actin cytoskeleton, or phosphorylation of host cell proteins.
====Dissemination====
*They are transported via the lymphatics and are disseminated hematogenously throughout the tissues.
====Immune response====
*Tachyzoites proliferate, producing necrotic foci surrounded by a cellular reaction.
*Upon the development of a normal immune response, tachyzoites disappear from tissues.
*In immunodeficient individuals and in some apparently immunologically healthy patients, the acute infection progresses, resulting in potentially lethal consequences such as pneumonitis, myocarditis, and necrotizing encephalitis.
====Changes in T-lymphocyte levels====
*Alterations in subpopulations of T lymphocytes are profound and prolonged during acute acquired T gondii infection.
*These have been correlated with disease syndromes but not with disease outcome.
*Some patients with prolonged fever and malaise have lymphocytosis, increased suppressor T-cell counts, and a decreased helper-to-suppressor T-cell ratio.
*In some patients with lymphadenopathy, helper-cell counts are diminished for more than 6 months after infection onset.
*Ratios of T-cell subpopulations may also be abnormal in asymptomatic patients.
*Some patients with disseminated toxoplasmosis have a very marked reduction in T cells and a marked depression in the ratio of helper to suppressor T lymphocytes.
*Depletion of inducer T lymphocytes in patients with AIDS may contribute to the severe manifestations of toxoplasmosis observed in these patients.
 
===Retinochoroiditis===
*Retinochoroiditis usually results from reactivation of congenital infection, although cases have been recorded that were part of acute infection.
*There are 5 hypotheses related to the inflammatory process of ocular toxoplasmosis, as follows
**Infection and inflammatory response after spontaneous cyst rupture
**Parasitic toxic mediators released from T gondii
**Lytic effect of inflammatory mediators
**Delayed-type hypersensitivity reaction to antigens of T gondii
**Cell-mediated immunity against retinal antigens
*When the organism reaches the eye through the bloodstream, depending on the host's immune status, a clinical or subclinical focus of infection begins in the retina.
*As the host's immune system responds and the tachyzoites convert themselves into bradyzoites, the cyst forms.
*The cyst is extremely resistant to the host's defenses, and a chronic, latent infection ensues.
*If a subclinical infection is present, no funduscopic changes are observed.
*The cyst remains in the normal-appearing retina. Whenever the host's immune function declines for any reason, the cyst wall may rupture, releasing organisms into the retina, and the inflammatory process restarts.
*If an active clinical lesion is present, healing occurs as a retinochoroidal scar.
*The cyst often remains inactive within or adjacent to the scar.
==Strongyloidiasis==
Strongyloidiasis is a disease caused by a nematode, or a roundworm, in the genus Strongyloides. Though there are over 40 species within this genus that can infect birds, reptiles, amphibians, livestock and other primates, Strongyloides stercoralis is the primary species that accounts for human disease. The larvae are small; the longest reach about 1.5mm in length -- the size of a mustard seed or a large grain of sand.
===Classification===
'''Acute strongyloidiasis'''<br>
'''Chronic strongyloidiasis'''<br>
'''Hyperinfection syndrome and disseminated strongyloidiasis'''
 
===Pathogenesis===
Strongyloides is classified as a soil-transmitted helminth. This means that the primary mode of infection is through contact with soil that is contaminated with free-living larvae. When the larvae come in contact with skin, they are able to penetrate it and migrate through the body, eventually finding their way to the small intestine where they burrow and lay their eggs. Unlike other soil-transmitted helminths such as hookworm and whipworm whose eggs do not hatch until they are in the environment, the eggs of Strongyloides hatch into larvae in the intestine. Most of these larvae will be excreted in the stool, but some of the larvae may molt and immediately re-infect the host either by burrowing into the intestinal wall, or by penetrating the perianal skin. This characteristic of Strongyloides is termed auto-infection. The significance of auto-infection is that unless treated for Strongyloides, persons may remain infected throughout their lifetime.
====Transmission====
*Contact with soil and auto-infection, there have been rare cases of person-to-person transmission in:
*Organ transplantation
*Institutions for the development nfeclly disabled
*Long-term care facilities
*Daycare centers
====Incubation period====
Most people do not know when their exposure occurred. For those who do, a local rash can occur immediately. The cough usually occurs several days later. Abdominal symptoms typically occur approximately 2 weeks later, and larvae can be found in the stool about 3 to 4 weeks later.
====Life cycle====
*The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host.
*Two types of cycles exist:
'''Free-living cycle''':
*The rhabditiform larvae passed in the stool  can either become infective filariform larvae (direct development) or free living adult males and females 
*These adult forms mate and produce eggs from which rhabditiform larvae hatch, eventually become infective filariform larvae.
*The filariform larvae penetrate the human host skin to initiate the parasitic cycle.
'''Parasitic cycle:'''
*Filariform larvae in contaminated soil penetrate the human skin and by various, often random routes, migrate into the small intestine.
*Historically it was believed that the larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed.
*However, there is also evidence that larvae can migrate directly to the intestine via connective tissues.
*In the small intestine they molt twice and become adult female worms.
*The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs which yield rhabditiform larvae.
*The rhabditiform larvae can either be passed in the stool or can cause autoinfection.
*In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body.
*To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria philippinensis infections.
*In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunosuppressed individuals.
[[Image:Strongyloides LifeCycle.gif|center|Life cycle of Strongyloides stercoralis]]
 
===Signs and Symptoms===
The majority of people infected with Strongyloides are without symptoms.The symptomatic spectrum of Strongyloides ranges from subclinical in acute and chronic infection to severe and fatal in hyperinfection syndrome and disseminated strongyloidiasis, which have case-fatality rates that approach 90%. In either case, patients’ symptoms are a result of the parasite’s larval form migrating through various organs of the body. Those who do develop symptoms tend to have non-specific, or generalized complaints. Some people develop abdominal pain, bloating, heartburn, intermittent episodes of diarrhea and constipation, a dry cough, and rashes. Rarely people will develop arthritis, kidney problems, and heart conditions.
Strongyloidiasis can be severe and life-threatening in persons who:
*People who use oral or intravenous steroids -- such as those with asthma or chronic obstructive pulmonary disease (COPD) exacerbations, lupus, gout, or in persons using steroids for immunosuppression or symptomatic relief
*HTLV-1 infection
*Have hematologic malignancies such as leukemia or lymphoma
*Transplant recipients.
===Acute strongyloidiasis===
*The initial sign of acute strongyloidiasis, if noticed at all, is a localized pruritic, erythematous rash at the site of skin penetration.
*Patients may then develop tracheal irritation and a dry cough as the larvae migrate from the lungs up through the trachea.
*After the larvae are swallowed into the gastrointestinal tract, patients may experience diarrhea, constipation, abdominal pain, and anorexia.
===Chronic strongyloidiasis===
*Chronic strongyloidiasis is generally asymptomatic, but in patients with clinical disease gastrointestinal and cutaneous manifestations are the most common. *Of the gastrointestinal complaints, epigastric pain, postprandial fullness, heartburn, and brief episodes of intermittent diarrhea and constipation are the most frequent.
*Less commonly, patients may present with fecal occult blood, or massive colonic and gastric hemorrhage.
*Presentations resembling inflammatory bowel disease, specifically ulcerative colitis, are rare. Also rare, but documented, are endoscopic exams revealing pathology similar to pseudopolyposis.
*Cutaneous symptoms include chronic urticaria and the pathognomonic larva currens- a recurrent serpiginous maculopapular or urticarial rash along the buttocks, perineum, and thighs due to repeated auto-infection.
*It has been described as advancing as rapidly as 10cm/hr.
*Rarely, patients with chronic strongyloidiasis have complained of arthritis, cardiac arrhythmias, and signs and symptoms consistent with chronic malabsorption, duodenal obstruction, nephrotic syndrome, and recurrent asthma.
*Up to 75% of people with chronic strongyloidiasis have mild peripheral eosinophilia or elevated IgE levels.
 
===Hyperinfection syndrome and disseminated strongyloidiasis===
*Hyperinfection syndrome and disseminated strongyloidiasis are most frequently associated with subclinical infection in patients receiving high-dose corticosteroids for the treatment of asthma or chronic obstructive pulmonary disease (COPD) exacerbations.
*Subsequent impaired host immunity leads to accelerated autoinfection and an overwhelming number of migrating larvae.
*Whereas in chronic strongyloidiasis and in hyperinfection syndrome the larvae are limited to the GI tract and the lungs, in disseminated strongyloidiasis the larvae invade numerous organs.
*Left untreated, the mortality rates of hyperinfection syndrome and disseminated strongyloidiasis can approach 90%.
The following are signs and symptoms that can be seen with hyperinfection syndrome and disseminated strongyloidiasis:
 
'''Gastrointestinal manifestations'''
*Abdominal pain, nausea, vomiting, diarrhea, ileus, bowel edema, intestinal obstruction, mucosal ulceration, massive hemorrhage, and subsequent peritonitis or bacterial sepsis
'''Pulmonary manifestations and findings'''
*Cough, wheezing, dyspnea, hoarseness, pneumonitis, hemoptysis, respiratory failure, diffuse interstitial infiltrates or consolidation on chest radiographs
'''Neurologic findings'''
*Aseptic or gram-negative meningitis
*Larvae have been reported in the CSF, meningeal vessels, dura, epidural, subdural, and subarachnoid spaces
'''Systemic signs and symptoms'''
*Peripheral edema and ascites secondary to hypoalbuminemia from protein losing enteropathy
*Recurrent gram negative bacteremia/sepsis from larvae carrying bacteria that penetrate mucosal walls
*Syndrome of inappropriate secretion of anti-diuretic hormone (SIADH)
*Peripheral eosinophilia is frequently absent
'''Cutaneous manifestations'''
*Recurrent maculopapular or urticarial rash most commonly found along the buttocks, perineum, and thighs due to repeated auto-infection, but can be found anywhere on the skin
*Larva currens - pathognomonic serpiginous or urticarial rash that advances as rapidly as 10cm/hr.
===Laboratory findings===
*The gold standard for the diagnosis of Strongyloides is serial stool examination.
*However, traditional stool examinations are insensitive and require up to seven stool exams to reach a sensitivity of 100%.
*Specialized stool exams include Baermann concentration, Horadi-Mori filter paper culture, quantitative acetate concentration technique, and nutrient agar plate cultures.
*Duodenal aspirate is more sensitive than stool examination, and duodenal biopsy may reveal parasites in the gastric crypts, in the duodenal glands, or eosinophilic infiltration in the lamina propria.
*Frequently, larvae can be seen by a simple wet-mount in fluid from a bronchoalveolar lavage (BAL).
*Many of the serologic tests that are available are quite sensitive, but cross-react with other filarial parasites, schistosomes, and Ascaris lumbricoides, decreasing the specificity of the tests.
*Furthermore, it can be difficult to distinguish between active cases and historical cases as traditional antibodies can persist for some time.
* More sensitive and specific serologic tests using recombinant antigens have been, and are being developed, and are available at specific laboratories.
*An additional advantage to these serologic tests is that there is typically a significant drop in titer by 6 months after parasite eradication, which may make it possible to use these tests as a "test of cure."raph
===Epidimeology and Demographics===
====Geographic distrubution====
*Strongyloides is known to exist on all continents except for Antarctica, but it is most common in the tropics, subtropics, and in warm temperate regions.
==== Incidence and Prevalance====
*The global prevalence of Strongyloides is unknown, but experts estimate that there are between 30–100 million infected persons worldwide.
*In the United States, a series of small studies in select populations have shown that between 600-1000 per 100,000 persons sampled were infected.
*Studies in immigrant populations have shown a much higher percentage of infected persons ranging from 460-1000 per 100.000 persons.
===Risk Factors===
*Strongyloides is found more frequently in the socioeconomically disadvantaged, in institutionalized populations, and in rural areas. It is often associated with agricultural activities.
*The most common way of becoming infected with Strongyloides is by contacting soil that is contaminated with Strongyloides larvae. Therefore, activities that increase contact with the soil increase the risk of becoming infected, such as:
**Walking with bare feet
**Contact with human waste or sewage
**Occupations that increase contact with contaminated soil such as farming and coal mining.
**Association with Strongyloides and infection with Human T-Cell Lymphotropic Virus-1 (HTLV-1).
===differentiating strongyloidosis ===
{| class="wikitable"
{| class="wikitable"
! colspan="7" |Differentiating Ascaris lumbricoides infection from other Nematode infections<ref name="Principles and Practice">Durand, Marlene (2015). "Chapter 288:Intestinal Nematodes (Roundworms)". Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases Updated Edition, Eighth Edition. Elsevier. pp. 3199–3207. ISBN 978-1-4557-4801-3.</ref><ref name="Murray and Nadel's Textbook of Respiratory Medicine">{{cite book |last1=Kim |first1=Kami |last2=Weiss |first2=Louis |last3=Tanowitz |first3=Herbert |title=Murray and Nadel's Textbook of Respiratory Medicine Sixth Edition |publisher=Elsevier |date=2016 |pages=682-698 |chapter=Chapter 39:Parasitic Infections |isbn=978-1-4557-3383-5}}</ref>
! colspan="2" |Surgical options for upper GI bleeding
|-
|-
|Nematode
!Disease Process
|Transmission
!Surgical Options
|Direct Person-Person Transmission
|Duration of Infection
|Pulmonary Manifestation
|Location of Adult worm(s)
|Treatment
|-
|-
|[[Ascaris lumbricoides]]
| rowspan="5" |Peptic ulcer disease
|Ingestion of infective ova
|Oversew
|No
|-
|1-2 years
|3-point ligation of gastroduodenal artery
|
|-
* [[Löffler's syndrome]] (usually about 9-12 days after exposure to ova)
|Vagotomy and pyloroplasty
* [[Cough]]
|-
* Substernal discomfort
|Vagotomy and antrectomy
* [[Crackles]]
|-
* [[Wheezing]]
|Highly selective vagotomy
* Transient opacities
|-
|Free in the lumen of the small bowel
|Mallory-Weiss tear
(primarily jejunum)
|Oversew
|
|-
* [[Albendazole]]
| rowspan="2" |Dieulafoy lesion
|Oversew
|-
|Wedge resection
|-
| rowspan="3" |Varices
|Portacaval shunt
|-
|Mesocaval shunt
|-
|Distal splenorenal shunt
|-
| rowspan="3" |Gastric cancer
|Distal gastrectomy
|-
|Total gastrectomy
|-
|D2 lymphadenectomy
|-
| rowspan="4" |Hemobilia
|Selective ligation
|-
|Resection of aneurysm
|-
|Nonselective ligation
|-
|Liver resection
|-
| rowspan="3" |Aortoduodenal fistula
|Angiography and stent (if hemodynamically stable)
|-
|Open repair
|-
|Extra-anatomic bypass
|}
===TIPS===
TIPS is a complex nonsurgical shunt which involves insertion of an expandable metal stent that bridges the hepatic vein and an intrahepatic branch of the portal vein. TIPS can halt bleeding in almost all patients, including those with bleeding refractory to other therapies.<br>
'''Indications'''
*For treatment of bleeding varices that are refractory to banding or sclerosant injection.
*For treatment of refractory variceal bleeding as a bridge to liver transplantation.
'''Procedure'''
*TIPS involves the percutaneous puncture of the right internal jugular vein and insertion of a vascular sheath into the inferior vena cava and the hepatic vein.
*A needle is inserted through the sheath, into the liver parenchyma, and then into the portal vein.
*Aspiration of blood and injection of contrast media ensure accurate placement.
*An angioplasty balloon catheter is used to dilate the tract between the hepatic and portal veins, and a stent is then placed across the tract.
*Portal venography is used to confirm the placement
*Patients should be monitored closely for bleeding for 12 to 24 hours
'''Complications'''
*Hepatic encephalopathy
*Hemolytic anemia
*Intra-abdominal bleeding during stent placement


* [[Mebendazole]]
===Balloon tamponade===
 
Balloon tamponade is only used as a temporary measure in patients who fail to respond to pharmacologic and endoscopic intervention. Balloon tamponade stabilizes patients until more definitive treatment can be instituted (TIPS or liver transplantation).<br>
* [[Pyrantel pamoate]]
'''Procedure'''
 
*Balloon tamponade involves the passage of a specialized nasogastric tube, fitted with an inflatable balloon.
* [[Ivermectin]]
*When the balloon is inflated, direct pressure staunches bleeding by compressing the varices.
 
*Controls active bleeding in 80% to 90% of patients although rebleeding after balloon deflation is common.<br>
* [[Levamisole]]
'''Indications'''<br>
 
*For bleeding varices that are refractory to banding or sclerosant injection.<br>
* [[Piperazine]]
'''Complications'''<br>
*Rebleeding upon balloon deflation
*Esophageal rupture
===Emergency laparotomy===
Emergency laparotomy is performed as a last resort for complications such as bleeding and perforation. Emergency laparotomy involving open exploration of the abdomen, oversewing of the ulcer (to ligate the bleeding artery), plus truncal vagotomy (to decrease acid secretion) and pyloroplasty (for improved gastric drainage).<br>
'''Indications'''
*Treatment of bleeding ulcer that cannot be managed with endoscopy
*Treatment of patients who cannot tolerate endoscopy
'''Complications'''
*Risks of major surgery and general anesthesia
{| align="center"
|-
|-
|[[Trichuris trichiura]]
(whipworm)
|Ingestion of infective [[ova]]
|No
|1-3 years
|No pulmonary migration, therefore, no pulmonary manifestation
|Anchored in the superficial mucosa of cecum and colon
|
|
* [[Albendazole]]
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
! colspan="3" rowspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" |Classification of pain in the abdomen based on etiology
! rowspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
| colspan="13" rowspan="1" style="background:#4479BA; color: #FFFFFF;" align="center" |'''Clinical manifestations'''
! colspan="2" rowspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" |Diagnosis
! rowspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
| colspan="9" rowspan="1" style="background:#4479BA; color: #FFFFFF;" align="center" |'''Symptoms'''
! colspan="4" rowspan="1" style="background:#4479BA; color: #FFFFFF;" align="center" | Signs
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! colspan="1" rowspan="1" style="background:#4479BA; color: #FFFFFF;" align="center" | Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! colspan="1" rowspan="1" style="background:#4479BA; color: #FFFFFF;" align="center" | Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! colspan="1" rowspan="1" style="background:#4479BA; color: #FFFFFF;" align="center" | Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
|-
! rowspan="55" style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal causes
! rowspan="40" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Inflammatory causes
! rowspan="10" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Pancreato-biliary disorders
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Acute suppurative cholangitis
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[RUQ]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*Abnormal [[LFT]]
*WBC >10,000
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound shows [[biliary]] dilatation/stents/tumor
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Septic shock occurs with features of [[SIRS]]
|-
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" | [[Cholangitis|Acute cholangitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | [[RUQ]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Abnormal [[LFT]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound shows [[biliary]] dilatation/stents/tumor
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Biliary drainage ([[Endoscopic retrograde cholangiopancreatography|ERCP]]) + IV antibiotics
|-
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" | [[Acute cholecystitis|Acute cholecystitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | [[RUQ]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Hyperbilirubinemia]]
* [[Leukocytosis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Ultrasound shows:
* Gallstone
* Inflammation
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Murphy's sign|Murphy’s sign]]
|-
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |  [[Acute pancreatitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | [[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Increased [[amylase]] / [[lipase]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound shows evidence of [[inflammation]]
* CT scan shows severity of pancreatitis
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Pain radiation to back
|-
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Chronic pancreatitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Increased [[amylase]] / [[lipase]]
* Increased stool fat content
* Pancreatic function test
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |CT scan
* Calcification
* Pseudocyst
* Dilation of main pancreatic duct
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Predisposes to pancreatic cancer
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Pancreatic carcinoma]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ↑ [[Alkaline phosphatase]]
* ↑ [[Bilirubin|serum bilirubin]]
* ↑ [[gamma-glutamyl transpeptidase]]
* ↑ [[CA 19-9]] 
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Computed tomography|MDCT]] with   [[Positron emission tomography|PET]]/[[Computed tomography|CT]]
* MRI
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
[[Skin]] manifestations may include:
* [[Bullous pemphigoid]]
* [[Mucous membrane pemphigoid|Cicatricial pemphigoid]]
* [[Thrombophlebitis|Migratory superficial thrombophlebitis]] (classic [[Trousseau's syndrome]])
* [[Panniculitis|Pancreatic panniculitis]]
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! style="background:#4479BA; color: #FFFFFF;" align="center" |Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! style="background:#4479BA; color: #FFFFFF;" align="center" |Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! style="background:#4479BA; color: #FFFFFF;" align="center" |Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
! style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Primary biliary cirrhosis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[RUQ]]/[[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Increased AMA level, abnormal [[LFTs]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ERCP
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Pruritis
|-
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Primary sclerosing cholangitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[RUQ]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Increased liver enzymes
* Increased [[IgM]], [[IgG]]4
* [[Anti-neutrophil cytoplasmic antibody]] ([[p-ANCA]])
* [[Anti-nuclear antibody]] ([[ANA]])
* [[Anti-smooth muscle antibody]] (Anti-Sm)
* Anti-endothelial antibody
* Anti-cardiolipin antibody
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |ERCP and MRCP shows
* Multiple segmental [[strictures]]
* Mural irregularities
* [[Biliary]] dilatation and diverticula
* Distortion of biliary tree
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* The risk of [[cholangiocarcinoma]] in patients with primary sclerosing cholangitis is 400 times higher than the risk in the general population.
|-
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Cholelithiasis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[RUQ]]/[[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Normal to hyperactive for dislodged stone
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Leukocytosis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound shows [[gallstone]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Fatty food intolerance
|-
! colspan="1" rowspan="8" style="padding: 5px 5px; background: #DCDCDC;" align="center" | Gastric causes
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" | [[Peptic Ulcer Disease|Peptic ulcer disease]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | <nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | <nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |
* Gastric ulcer- [[melena]] and [[hematemesis]]
* Duodenal ulcer- [[melena]] and [[hematochezia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive if perforated
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive if perforated
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive if perforated
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ascitic fluid
** [[LDH]] > serum [[LDH]]
** Glucose < 50mg/dl
** Total protein > 1g/dl
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Air under [[diaphragm]] in upright [[CXR]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Upper GI [[endoscopy]] for diagnosis
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! style="background:#4479BA; color: #FFFFFF;" align="center" |Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! style="background:#4479BA; color: #FFFFFF;" align="center" |Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! style="background:#4479BA; color: #FFFFFF;" align="center" |Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
! style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Gastritis|Gastritis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | <nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in chronic gastritis
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[H.pylori infection diagnostic tests]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Endoscopy]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[H.pylori gastritis guideline recommendation]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Gastroesophageal reflux disease|Gastroesophageal reflux disease]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Gastric emptying studies
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Esophageal]] [[manometry]]
* [[Endoscopy]] for alarm signs
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Gastric outlet obstruction|Gastric outlet obstruction]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | <nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hyperactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Complete blood count]]
* [[Basic metabolic panel]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Abdominal x-ray]]- air fluid level
* Barium [[Upper GI series|upper GI studies]]- narrowed pylorus
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Succussion splash
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Gastroparesis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Hyperactive/hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*[[Hemoglobin]]
*Fasting plasma glucose
*Serum total protein, albumin, [[thyrotropin]] ([[Thyroid-stimulating hormone|TSH]]), and an [[antinuclear antibody]] (ANA) titer
*[[HbA1c]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*Scintigraphic gastric emptying
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*Succussion splash
*Single photon emission computed tomography (SPECT)
*Full thickness gastric and small intestinal biopsy
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Gastrointestinal perforation]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>-</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hyperactive/hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* WBC> 10,000
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Air under [[diaphragm]] in upright [[CXR]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Hamman's sign]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Dumping syndrome]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Lower and then diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hyperactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Glucose challenge test
* [[Hydrogen Breath Test|Hydrogen breath test]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Upper gastrointestinal series|Upper GI series]]
* Gastric emptying study
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Postgastrectomy
|-
! rowspan="13" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Intestinal causes
! style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! style="background:#4479BA; color: #FFFFFF;" align="center" |Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! style="background:#4479BA; color: #FFFFFF;" align="center" |Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! style="background:#4479BA; color: #FFFFFF;" align="center" |Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
! style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Acute appendicitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Starts in [[epigastrium]], migrates to RLQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in pyogenic appendicitis
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in perforated appendicitis
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Leukocytosis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ct scan
* Ultrasound
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Positive Rovsing sign
* Positive Obturator sign
* Positive Iliopsoas sign
|-
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Diverticulitis|Acute diverticulitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |LLQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |−
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in perforated diverticulitis
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Leukocytosis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* CT scan 
* Ultrasound
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* History of [[constipation]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Inflammatory bowel disease]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Normal or hyperactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Anti-neutrophil cytoplasmic antibody]] ([[P-ANCA]]) in [[Ulcerative colitis]]
* [[Anti saccharomyces cerevisiae antibodies]] (ASCA) in [[Crohn's disease]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[String sign]] on [[abdominal x-ray]] in [[Crohn's disease]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
Extra intestinal findings:
* [[Uveitis]]
* [[Arthritis]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Irritable bowel syndrome]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Symptomatic treatment
* High [[dietary fiber]]


* [[Mebendazole]]
* [[Osmotic]] [[laxatives]]
* [[Antispasmodic]] drugs
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Whipple's disease]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Thrombocytopenia]]
* [[Hypoalbuminemia]]
* [[Small intestinal]] [[biopsy]] for [[Tropheryma whipplei]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Whipple's disease other diagnostic studies|Endoscopy]] is used to confirm diagnosis.
Images used to find complications
*[[Whipple's disease x ray|Chest and joint x-ray]]
*[[Whipple's disease CT|CT]]
*[[Whipple's disease MRI|MRI]]
*[[Whipple's disease ultrasound|Echocardiography]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Extra intestinal findings:
* [[Uveitis]]
* [[Endocarditis]]
* [[Encephalitis]]
* [[Dementia]]
* [[Hepatosplenomegaly]]
* [[Arthritis]]
* [[Ascites]]
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! style="background:#4479BA; color: #FFFFFF;" align="center" |Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! style="background:#4479BA; color: #FFFFFF;" align="center" |Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! style="background:#4479BA; color: #FFFFFF;" align="center" |Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
! style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
|-
|[[Hookworm]] ([[Necator americanus]] and [[Ancylostoma duodenale]])
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Toxic megacolon]]
|Skin penetration by filariform larvae
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
|No
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* 3-5 years (Necator)
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* 1 year (Ancylostoma)
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* [[Löffler's syndrome]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
* Transient opacities
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
|Attached to the mucosa of mid-upper portion of the [[small bowel]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
* [[Albendazole]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Anemia]]
*[[Leukocytosis]] especially in patients with [[Clostridium difficile infection|''Clostridium difficile'' infection]]
*[[Hypoalbuminemia]]
*[[Metabolic alkalosis]] associated with a poor [[prognosis]]
*[[Metabolic acidosis]] secondary to [[ischemic colitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |CT and [[Ultrasound]] shows:
*Loss of colonic haustration
*Hypoechoic and thickened bowel walls with irregular internal margins in the [[sigmoid]] and descending colon
*Prominent dilation of the transverse colon (>6 cm)


* [[Mebendazole]]
* Insignificant dilation of ileal bowel loops (diameter >18 mm) with increased intraluminal gas and fluid
 
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Levamisole]]
|-
 
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Tropical sprue]]
* [[Pyrantel pamoate]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Fat soluble vitamin deficiency
* [[Hypoalbuminemia]]
* Fecal stool test
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Barium studies:
* Dilation and edema of mucosal folds
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Steatorrhea]]- 10-40 g/day (Normal=5 g/day)
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Celiac disease]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hyperactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[IgA]] endomysial antibody
* [[IgA]] [[tissue transglutaminase]] antibody
* [[Anti-gliadin antibodies|Anti-gliadin antibody]]
* Small bowel biopsy
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |US:
* Bull’s eye or target pattern
* Pseudokidney sign
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Gluten allergy
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Infective colitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in fulminant colitis
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hyperactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Stool culture]] and studies
* Shiga toxin in bloody diarrhea
* [[PCR]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |CT scan
* Bowel wall thickening
* Edema
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! style="background:#4479BA; color: #FFFFFF;" align="center" |Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! style="background:#4479BA; color: #FFFFFF;" align="center" |Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! style="background:#4479BA; color: #FFFFFF;" align="center" |Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
! style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Colon carcinoma]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse/ RLQ/LLQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Normal or hyperactive if obstruction present
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* CBC
* Carcinoembryonic antigen (CEA)
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Colonoscopy
* Flexible sigmoidoscopy
* Barium enema
* CT colonography 
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* PILLCAM 2: A colon capsule for CRC screening may be used in patients with an incomplete colonoscopy who lacks obstruction
|-
! rowspan="8" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Hepatic causes
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Hepatitis|Viral hepatitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[RUQ]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in Hep A and E
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in fulminant hepatitis
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in acute
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Abnormal LFTs
* Viral serology
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* US
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Hep A and E have fecal-oral route of transmission
* Hep B and C transmits via blood transfusion and sexual contact.
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Liver abscess]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RUQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Normal or hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* CBC
* Blood cultures
* Abnormal [[Liver function test|liver function tests]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* US
* CT
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Hepatocellular carcinoma]]/[[Metastasis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RUQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Normal
* Hyperactive if obstruction present
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* High levels of [[Alpha-fetoprotein|AFP]] in serum
* Abnormal [[Liver function test|liver function tests]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* US
* CT
* Liver biopsy
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
Other symptoms:
* [[Splenomegaly]]
* [[Variceal bleeding]]
* [[Ascites]]
* [[Spider nevi]]
* [[Asterixis]]
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! style="background:#4479BA; color: #FFFFFF;" align="center" |Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! style="background:#4479BA; color: #FFFFFF;" align="center" |Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! style="background:#4479BA; color: #FFFFFF;" align="center" |Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
! style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
|-
|[[Strongyloides stercoralis]]
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Budd-Chiari syndrome|Budd-Chiari syndrome]]
|Filariform larvae penetrates skin or bowel mucosa
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[RUQ]]
|Yes
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
|Lifetime of the host
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* [[Löffler's syndrome]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
* Chronic [[cough]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* [[Pneumonia]] or [[sepsis]] in hyperinfection
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
|Embedded in the mucosa of the [[duodenum]], [[jejunum]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in liver failure leading to varices
* [[Ivermectin]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* [[Albendazole]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* [[Thiabendazole]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*Elevated [[Aspartate aminotransferase|serum aspartate aminotransferase]] and [[alanine aminotransferase]] levels may be more than five times the upper limit of the normal range.
*Elevated serum [[alkaline phosphatase]] and [[Bilirubin|bilirubin levels]], decreased [[Albumin|serum albumin level]].
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
|-
|-
|[[Enterobius vermicularis]] ([[pinworm]])
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Findings on [[CT scan]] suggestive of Budd-Chiari syndrome include:
|Ingestion of infective [[ova]]
*Early enhancement of the [[caudate lobe]] and [[central liver]] around the [[Inferior vena cavae|inferior vena cava]]
|Yes
*Delayed enhancement of the peripheral [[liver]] with accompanying central low density (flip-flop appearance)
|1 month
*Peripheral zones of the [[liver]] show reversed [[portal]] [[venous]] [[blood flow]]
|Extraintestinal migration is very rare<ref name="pmid21879805">{{cite journal| author=Serpytis M, Seinin D| title=Fatal case of ectopic enterobiasis: Enterobius vermicularis in the kidneys. | journal=Scand J Urol Nephrol | year= 2012 | volume= 46 | issue= 1 | pages= 70-2 | pmid=21879805 | doi=10.3109/00365599.2011.609834 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21879805  }} </ref>
*In the [[chronic]] phase, there is [[caudate lobe]] enlargement and [[atrophy]] of the [[Liver|peripheral liver]] in affected areas
|Free in the lumen of [[cecum]], [[appendix]], adjacent [[colon]]
|
* [[Albendazole]]
* [[Mebendazole]]
* [[Pyrantel pamoate]]
* [[Ivermectin]]
* [[Levamisole]]
* [[Piperazine]]
|}
|}
===Historical Perspective===
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Ascitic tap|Ascitic fluid examination]] shows:
*In 1876, Louis Alexis Normand, a French physician discovered strongyloides for the first time.
*[[Total protein]] more than 2.5 g per deciliter
*Later in the same year, Professor Arthur Réné Jean Baptiste Bavay at the French Conseil Supérieur de Santé, gave a detailed description of the worm.
*[[White blood cells]] are usually less than 500/μL.
*In 1883, Karl Georg Friedrich Rudolf Leuckart German parasitologist discovered the alternation of generations involving parasitic and free-living phases. *The discovery that infection occurred through the skin was made by a Belgian physician, Paul Van Durme, whose studies were based on the work of Looss.
|-
*In 1940, detailed studies on disseminated infections of strongyloides in immunosuppressed patients were described.
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Hemochromatosis]]
==Sepsis Differential==
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RUQ
{| align="center"
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in cirrhotic patients
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* >60% TS
* >240 μg/L SF
* Raised LFT <br>Hyperglycemia
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound shows evidence of cirrhosis
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Extra intestinal findings:
* Hyperpigmentation
* Diabetes mellitus
* Arthralgia
* Impotence in males
* Cardiomyopathy
* Atherosclerosis
* Hypopituitarism
* Hypothyroidism
* Extrahepatic cancer
* Prone to specific infections
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Cirrhosis|Cirrhosis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[RUQ]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Hypoalbuminemia]]
* Prolonged PT
* Abnormal LFTs
* [[Hyponatremia]]
* [[Thrombocytopenia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |US
* Nodular, shrunken liver
* [[Ascites]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Stigmata of liver disease
* Cruveilhier- Baumgarten murmur
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! style="background:#4479BA; color: #FFFFFF;" align="center" |Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! style="background:#4479BA; color: #FFFFFF;" align="center" |Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! style="background:#4479BA; color: #FFFFFF;" align="center" |Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
! style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
! rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" | Peritoneal causes
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Spontaneous bacterial peritonitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in cirrhotic patients
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ascitic fluid [[PMN]]>250 cells/mm<small>³</small>
* Culture: Positive for single organism
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound for evaluation of liver cirrhosis
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
|-
! colspan="2" rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Renal causes
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |Pyelonephritis
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Unilateral
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Urinalysis
* Urine culture
* Blood culture
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* CT
* MRI
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*CVA tenderness
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Renal colic]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Flank pain]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Hematuria]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound
* CT scan
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Colicky [[abdominal pain]]
* [[Dysuria]]
|-
! colspan="2" rowspan="4" style="padding: 5px 5px; background: #DCDCDC;" align="center" | Hollow Viscous Obstruction
| colspan="1" rowspan="1" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Small bowel obstruction]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hyperactive then absent
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Leukocytosis]] with left shift indicates complications
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Abdominal X-ray|Abdominal X ray]]
* Dilated loops of bowel with air fluid levels
* Gasless abdomen
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* "Target sign"– , indicative of intussusception
* Venous cut-off sign" –  suggests thrombosis
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Volvulus]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in perforated cases
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hyperactive then absent
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Leukocytosis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |CT scan and [[Abdominal x-ray|abdominal X ray]]
* U shaped sigmoid colon
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* "Whirl sign"
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Biliary colic]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RUQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ↑ [[bilirubin]] and [[alkaline phosphatase]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! style="background:#4479BA; color: #FFFFFF;" align="center" |Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! style="background:#4479BA; color: #FFFFFF;" align="center" |Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! style="background:#4479BA; color: #FFFFFF;" align="center" |Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
! style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
! rowspan="5" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Vascular Disorders
! rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Ischemic causes
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Mesenteric ischemia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Periumbilical
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Positive if bowel becomes gangrenous
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive if bowel becomes gangrenous
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive if bowel becomes gangrenous
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hyperactive to absent
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Leukocytosis]] and [[lactic acidosis]]
* [[Amylase]] levels
* [[D-dimer]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |CT angiography
* SMA or SMV thrombosis
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Also known as abdominal angina  that worsens with eating
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Ischemic colitis|Acute ischemic colitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hyperactive then absent
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Leukocytosis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Abdominal x-ray]]
* Distension and pneumatosis
CT scan
* Double halo appearance, thumbprinting
* Thickening of bowel
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* May lead to shock
|-
! rowspan="3" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Hemorrhagic causes
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Ruptured abdominal aortic aneurysm]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Fibrinogen]]
* [[D-dimer]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Focused Assessment with Sonography in Trauma (FAST) 
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Unstable hemodynamics
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |Intra-abdominal or [[retroperitoneal hemorrhage]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Diffuse
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ↓ Hb
* ↓ Hct
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* CT scan
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* History of [[trauma]]
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" |Abdominal Pain
! style="background:#4479BA; color: #FFFFFF;" align="center" |Fever
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rigors and chills
! style="background:#4479BA; color: #FFFFFF;" align="center" |Nausea or vomiting
! style="background:#4479BA; color: #FFFFFF;" align="center" |Jaundice
! style="background:#4479BA; color: #FFFFFF;" align="center" |Constipation
! style="background:#4479BA; color: #FFFFFF;" align="center" |Diarrhea
! style="background:#4479BA; color: #FFFFFF;" align="center" |Weight loss
! style="background:#4479BA; color: #FFFFFF;" align="center" |GI bleeding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Hypo-
tension
! style="background:#4479BA; color: #FFFFFF;" align="center" |Guarding
! style="background:#4479BA; color: #FFFFFF;" align="center" |Rebound Tenderness
! style="background:#4479BA; color: #FFFFFF;" align="center" |Bowel sounds
! style="background:#4479BA; color: #FFFFFF;" align="center" |Lab Findings
! style="background:#4479BA; color: #FFFFFF;" align="center" |Imaging
! style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
|-
! rowspan="4" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Gynaecological Causes
! rowspan="3" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Tubal causes
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |Torsion of the cyst/ovary
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RLQ / LLQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ↑ [[ESR]] 
* ↑ [[CRP]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Sudden onset & severe pain
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Salpingitis|Acute salpingitis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RLQ / LLQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Leukocytosis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Pelvic ultrasound]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Vaginal discharge]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |Cyst rupture
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RLQ / LLQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ↑ [[ESR]] 
* ↑ [[CRP]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
|-
! style="padding: 5px 5px; background: #DCDCDC;" align="center" |Pregnancy
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |Ruptured [[ectopic pregnancy]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RLQ / LLQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Positive [[pregnancy test]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ultrasound
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |History of
* Missed period
* Vaginal bleeding
|-
|-
|
! rowspan="4" style="background:#4479BA; color: #FFFFFF;" align="center" |Extra-abdominal causes
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
! rowspan="3" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Pulmonary disorders
!style="background:#4479BA; color: #FFFFFF;" |Disease
| colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Pleural empyema]]
!style="background:#4479BA; color: #FFFFFF;" |Symptoms and signs
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[RUQ]]/[[Epigastric]]
!style="background:#4479BA; color: #FFFFFF;" |Labs
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
!style="background:#4479BA; color: #FFFFFF;" |Other findings
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Thoracentesis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Chest X-ray]]
* Pleural opacity
 
* Localization of effusion
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Physical examination
* Crackles
* [[Egophony]]
* Increased [[tactile fremitus]]
|-
|-
|align="center" style="background:#DCDCDC;"|Heat stroke
| colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Pulmonary embolism]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RUQ/LUQ
* CNS dysfunction ([[disorientation]], [[headache]], irrational behavior, irritability, emotional instability, [[Confusion|confusion,]] [[coma]], or [[seizure]])
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
* [[Hypotension]] and [[tachycardia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* [[Hyperventilation]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* [[Weakness]], [[nausea and vomiting]], profuse sweating, [[dehydration]].
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Electrolyte disturbances, increased [[Creatine kinase|CK]], [[Aspartate transaminase|AST]], and [[Alanine transaminase|ALT]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Relevant history of excessive exercise and lack of water access
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ABGs
* D-dimer
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* CXR
* V/Q scan
* Spiral [[CT pulmonary angiogram]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Dyspnea
* Tachycardia
* Pleuretic chest pain
|-
|-
| align="center" style="background:#DCDCDC;" |[[Sepsis]]
| colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Pneumonia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RUQ/LUQ
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Normal or hypoactive
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ABGs
* Leukocytosis
* Pancytopenia
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Altered mental status ([[confusion]], altered consciousness, [[coma]], or [[seizure]])
*CXR
* Respiratory rate ≥22/minute
*CT chest
* Systolic blood pressure ≤100 mmHg
*Bronchoscopy
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Thrombocytopenia]], [[leukocytosis]], [[leukopenia]], elevated [[Creatinine|Cr]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Shortness of breath
* Cough
|-
|-
| align="center" style="background:#DCDCDC;" |[[Malignant hyperthermia]]
! style="padding: 5px 5px; background: #DCDCDC;" align="center" |Cardiovascular disorders
| colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Myocardial Infarction]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Epigastric]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | ±
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in cardiogenic shock
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Cardiac enzymes]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[ECG]]
[[Echocardiogram]]  
* Wall motion abnormality
* Wall rupture
* Septal rupture
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Masseter muscle|Masseter]] [[muscle rigidity]] (early)
* Chest pain, tightness, diaphoresis
* Generalized muscle rigidity
Complications:
* [[Sinus tachycardia]]
* [[Arrythmias]]
* [[Arrhythmias|Arrhythmia]]
* [[Mitral regurgitation]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Hypercarbia]] (PaCO2) >65 mmHg, [[hyperkalemia]]
* Ventricular wall rupture
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |History of receiving anaesthetic agent
* Septal rupture
|-
|}
|}
</small></small>
{|
|-
| [[Image:Right_upper_quadrant.PNG|link=Right upper quadrant abdominal pain resident survival guide]]||[[Image:Epigastric_quadrant_pain.PNG|link=Epigastric pain resident survival guide]]||[[Image:Left_upper_quadrant.PNG|link=Left upper quadrant abdominal pain resident survival guide]]
|-
| [[Image:Right_flank_quadrant.PNG|link=Right flank pain resident survival guide]]||[[Image:Umbilical_pain.PNG|link=Umbilical region pain resident survival guide]]||[[Image:Left_flank_quadrant.PNG|link=Left flank quadrant abdominal pain resident survival guide]]
|-
| [[Image:Right_lower_quadrant.PNG|link=Right lower quadrant abdominal pain resident survival guide]]||[[Image:Hypogastric.PNG|link=Hypogastric pain resident survival guide]]||[[Image:Left_lower_quadrant.PNG|link=Left lower quadrant abdominal pain resident survival guide]]
|}
 
The following is a list of diseases that present with acute onset severe lower abdominal pain:
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
|+
! style="background: #4479BA; width: 180px;" | {{fontcolor|#000|Disease}}
! style="background: #4479BA; width: 650px;" | {{fontcolor|#000|Findings}}
|-
| style="padding: 7px 7px; background: #DCDCDC;" | '''[[Ectopic pregnancy]]'''
| style="padding: 7px 7px; background: #F5F5F5;" | History of missed menses, positive [[pregnancy test]], [[ultrasound]] reveals an empty [[uterus]] and may show a mass in the [[fallopian tubes]].<ref name="pmid27720100">{{cite journal |vauthors=Morin L, Cargill YM, Glanc P |title=Ultrasound Evaluation of First Trimester Complications of Pregnancy |journal=J Obstet Gynaecol Can |volume=38 |issue=10 |pages=982–988 |year=2016 |pmid=27720100 |doi=10.1016/j.jogc.2016.06.001 |url=}}</ref>
|-
| style="padding: 7px 7px; background: #DCDCDC;" |'''[[Appendicitis]]'''
| style="padding: 7px 7px; background: #F5F5F5;" |Pain localized to the [[right iliac fossa]], [[vomiting]], [[Ultrasound|abdominal ultrasound]] [[Sensitivity (tests)|sensitivity]] for diagnosis of [[acute appendicitis]] is 75% to 90%.<ref name="pmid8259423">{{cite journal |vauthors=Balthazar EJ, Birnbaum BA, Yee J, Megibow AJ, Roshkow J, Gray C |title=Acute appendicitis: CT and US correlation in 100 patients |journal=Radiology |volume=190 |issue=1 |pages=31–5 |year=1994 |pmid=8259423 |doi=10.1148/radiology.190.1.8259423 |url=}}</ref>
|-
| style="padding: 7px 7px; background: #DCDCDC;" | '''Ruptured[[ ovarian cyst]]'''
| style="padding: 7px 7px; background: #F5F5F5;" |Usually spontaneous, can follow history of trauma, mild chronic lower abdominal discomfort may suddenly intensify, [[ultrasound]] is diagnostic.<ref name="pmid19299205">{{cite journal |vauthors=Bottomley C, Bourne T |title=Diagnosis and management of ovarian cyst accidents |journal=Best Pract Res Clin Obstet Gynaecol |volume=23 |issue=5 |pages=711–24 |year=2009 |pmid=19299205 |doi=10.1016/j.bpobgyn.2009.02.001 |url=}}</ref>
|-
| style="padding: 7px 7px; background: #DCDCDC;" | '''[[Ovarian cyst ]]torsion'''
| style="padding: 7px 7px; background: #F5F5F5;" |Presents with acute severe unilateral [[Lower abdominal pain|lower quadrant abdominal pain]], [[nausea and vomiting]], tender adnexal mass palpated in 90%, [[ultrasound]] is diagnostic.<ref name="pmid26760839">{{cite journal |vauthors=Bhavsar AK, Gelner EJ, Shorma T |title=Common Questions About the Evaluation of Acute Pelvic Pain |journal=Am Fam Physician |volume=93 |issue=1 |pages=41–8 |year=2016 |pmid=26760839 |doi= |url=}}</ref>
|-
| style="padding: 7px 7px; background: #DCDCDC;" | '''Hemorrhagic [[ovarian cyst]]'''
| style="padding: 7px 7px; background: #F5F5F5;" |Presents with [[Abdominal pain|localized abdominal pain]], [[nausea and vomiting]]. [[Hypovolemic shock]] may be present, [[abdominal tenderness]] and guarding are physical exam findings, [[ultrasound]] is diagnostic.<ref name="pmid26760839">{{cite journal |vauthors=Bhavsar AK, Gelner EJ, Shorma T |title=Common Questions About the Evaluation of Acute Pelvic Pain |journal=Am Fam Physician |volume=93 |issue=1 |pages=41–8 |year=2016 |pmid=26760839 |doi= |url=}}</ref>
|-
|-
|align="center" style="background:#DCDCDC;"|[[Neuroleptic malignant syndrome]]
| style="padding: 7px 7px; background: #DCDCDC;" | '''[[Endometriosis]]'''
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |
| style="padding: 7px 7px; background: #F5F5F5;" |Presents with cyclic pain that is exacerbated by onset of menses, [[dyspareunia]]. [[Laparoscopy|laparoscopic]] exploration is diagnostic.<ref name="pmid26760839">{{cite journal |vauthors=Bhavsar AK, Gelner EJ, Shorma T |title=Common Questions About the Evaluation of Acute Pelvic Pain |journal=Am Fam Physician |volume=93 |issue=1 |pages=41–8 |year=2016 |pmid=26760839 |doi= |url=}}</ref>
* Change in mental status
* [[Muscle rigidity]]
* Autonomic instability (labile [[BP]], [[tachypnea]], profuse sweating)
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Electrolyte disturbances, increased [[Creatine kinase|CK]], [[Lactate dehydrogenase|LDH]], [[ALP]], [[Aspartate transaminase|AST]], and [[Alanine transaminase|ALT]], [[leukocytosis]], [[myoglobinuria]].
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Relevant history of recent use of anti-psychotics
|-
|-
|align="center" style="background:#DCDCDC;"|[[Serotonin syndrome]]
| style="padding: 7px 7px; background: #DCDCDC;" | '''[[Acute cystitis]]'''
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |
| style="padding: 7px 7px; background: #F5F5F5;" |Presents with features of increased urinary [[frequency]], [[urgency]], [[dysuria]], and suprapubic pain.<ref>{{Cite journal
* Mental status changes ([[anxiety]], agitated [[delirium]], [[restlessness]], and [[disorientation]])
<nowiki> </nowiki><nowiki>|</nowiki> author = [[W. E. Stamm]]
* Autonomic instability ([[diaphoresis]], [[tachycardia]],, [[hypertension]], [[vomiting]], and diarrhea)
| title = Etiology and management of the acute urethral syndrome
* Neuromuscular hyperactivity ([[tremor]], [[myoclonus]], [[hyperreflexia]], and bilateral [[Babinski sign]])
| journal = [[Sexually transmitted diseases]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Elevated [[Creatine kinase|CK]], [[Lactate dehydrogenase|LDH]], [[Alkaline phosphatase|ALP]], [[Aspartate transaminase|AST]], and [[Alanine transaminase|ALT]]
| volume = 8
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |History of recent use of [[Selective serotonin reuptake inhibitor|SSRIs]], [[Serotonin-norepinephrine reuptake inhibitor|SNRIs]] , or [[Monoamine oxidase inhibitor|MAOIs]].
| issue = 3
| pages = 235–238
| year = 1981
| month = July-September
| pmid = 7292216
</ref><ref>{{Cite journal
<nowiki> </nowiki><nowiki>|</nowiki> author = [[W. E. Stamm]], [[K. F. Wagner]], [[R. Amsel]], [[E. R. Alexander]], [[M. Turck]], [[G. W. Counts]] & [[K. K. Holmes]]
| title = Causes of the acute urethral syndrome in women
| journal = [[The New England journal of medicine]]
| volume = 303
| issue = 8
| pages = 409–415
| year = 1980
| month = August
| doi = 10.1056/NEJM198008213030801
| pmid = 6993946</ref>
|}
|}
==Fibromyalgia==
===Historical perspective===
*In 1800s, the first case study of fibromyalgia was reported. It was known by other names such as muscular rheumatism and fibrosita.
*In 1904, Sir William Gowers coined the term “fibrositis”.
*In 1906, later the term Fibromyalgia was coined.
*In 1981, Dr. Muhammad B. Yunus published the "first controlled study of the clinical characteristics" of the fibromyalgia syndrome, for which he is considered "the father of our modern view of fibromyalgia."<ref name=Winfield>John B. Winfield (2007), "Fibromyalgia and Related Central Sensitivity Syndromes: Twenty-five Years of Progress", ''Seminars in Arthritis and Rheumatism'' '''36''' (6): 335-338.</ref><ref name=sciencedaily>[http://www.sciencedaily.com/releases/2007/06/070625095756.htm Further Legitimization Of Fibromyalgia As A True Medical Condition], ''[[Science Daily]]'', June 25, 2007.</ref>
*In 1986, [[serotonergic]] and norepinephric [[drug]]s were proved to be effective for fibromyalgia.<ref name=Inanici>F. Fatma Inanici and Muhammad B. Yunus (2004), "History of fibromyalgia: Past to present", '''8''' (5): 369-378.</ref>
*In 1987, American Medical Association recognized fibromyalgia as an illness and a cause of disability.
*In 1984, he proposed the important concept that the fibromyalgia syndrome and other similar conditions are interconnected.
*In 1990, the ACR published criteria for fibromyalgia and developed [[Neurohormone|neurohormonal]] mechanisms with central [[sensitization]].


===Classification===
DSM 5 divides fibromyalgia into four groups based on the differences in psychological and autonomic nervous system profiles among affected individuals
*Extreme sensitivity to pain but no associated psychiatric conditions
*Fibromyalgia and comorbid, pain-related depression
*Depression with concomitant fibromyalgia syndrome
*Fibromyalgia due to somatization
===Risk Factors===
The possible risk factors  for fibromyalgia include:
*Sex. Women are twice as likely to have fibromyalgia as men
*Stressful or traumatic events, such as car accidents, post-traumatic stress disorder (PTSD)
*Repetitive injuries. Injury from repetitive stress on a joint, such as frequent knee bending
*Illness (such as viral infections)
*Family history
*Obesity
===Differential===
It is a clinical diagnosis and all other conditions that present with muscular pain and stiffness all over the body such as polymyalgia rheumatica, myofascial pain syndrome (MPS), chronic fatigue syndrome, myositis, malingering
===Epidemiology and Demographics===
====Incidence and Prevalance====
*The Prevalence of Fibromyalgia in the United States was reported to range from 500-5000 per 100,000 persons.
====Gender====
*Females are more commonly affected than males.
====Age====
20-50 year age group is more commonly affected
====Race====
Fibromyalgia has no racial predilication.
===Natural History===
If left untreated, chronic pain could cause permanent changes in how the body perceives pain.
===Complications===
Complications that can develop as a result of Fibromyalgia are
*Marked functional impairment
*Depression
*Anxiety
*Insomnia
*Obesity
*Allodynia
===Prognosis===
Fibromyalgia is a long-term disorder. Various factors play a key role in the outcomes<br>
'''Factors associated with poor outcomes'''
*Female gender
*Low socioeconomic status
*Being unemployed
Even with appropriate treatment, symptoms of fibromyalgia improve other times, the pain may get worse and continue for months or years.
==Diagnosis==
==Diagnosis==
The most widely accepted set of diagnostic criteria for fibromyalgia was elaborated in 2010 by the Multicenter Criteria Committee of the the American College of Rheumatology.
*The presence of renal tubular acidosis (RTA) should be considered in any patient with an otherwise unexplained normal anion gap (hyperchloremic) metabolic acidosis.
===Criteria===
*The first step in the diagnosis of a patient with a reduced serum bicarbonate and elevated chloride concentration is to confirm that metabolic acidosis is present by measuring the blood pH.
A patient satisfies diagnostic criteria for fibromyalgia if the following 3 conditions are met:
*The next steps in the diagnosis of possible RTA in patients who have a normal anion gap metabolic acidosis are measurement of the urine pH and estimation of urinary ammonium excretion.  
*1) Widespread pain index (WPI) > 7 and symptom severity (SS) scale score >5 or WPI 3–6 and SS scale score >9.
===Urine PH===
*2) Symptoms have been present at a similar level for at least 3 months.
*Patients with normal renal function and normal renal acidification mechanisms who develop metabolic acidosis usually have a urine pH of 5.3 or less.  
*3) The patient does not have a disorder that would otherwise explain the pain.
*In most cases of distal RTA, the urine pH is persistently 5.5 or higher, reflecting the primary defect in distal acidification, and a urine pH below 5.5 generally excludes distal (but not proximal) RTA.  
===Ascertainment===
*However, the urine pH can be reduced below 5.5 in occasional patients (2 of 17 in one study) with distal RTA.  
1) WPI: note the number areas in which the patient has had pain over the last week. In how many areas has the patient had pain?
*In contrast to the persistently elevated urine pH in distal RTA, the urine pH is variable in proximal RTA, a disorder characterized by diminished proximal bicarbonate reabsorption.  
*Score will be between 0 and 19.
*The urine pH will be inappropriately elevated if patients with proximal RTA are treated with alkali, increasing the serum bicarbonate concentration enough to produce a filtered bicarbonate load that exceeds the reduced proximal reabsorptive capacity; this most commonly occurs when alkali is given for the diagnosis or treatment of this disorder.  
*Shoulder girdle, left Hip (buttock, trochanter), left Jaw, left Upper back, Shoulder girdle, right Hip (buttock, trochanter), right Jaw, right Lower back, Upper arm, left Upper leg, left Chest Neck, Upper arm, right Upper leg, right Abdomen, Lower arm, left Lower leg, left, Lower arm, right Lower leg, right
*In patients presenting with a normal anion gap metabolic acidosis, two scenarios can produce a misleading elevation in the urine pH that incorrectly suggests the presence of RTA:
2) SS scale score:
**Urinary tract infections with urea-splitting organisms may increase the urine pH because urea is converted to ammonia and bicarbonate.  
*Fatigue
***Thus, assessment of the urine pH should include a urinalysis and, if indicated, a urine culture.
*Waking unrefreshed
**Severe volume depletion (which indirectly and reversibly limits hydrogen ion secretion by reducing distal sodium delivery) can impair urine acidification.  
*Cognitive symptoms
***Thus, reliable interpretation of an inappropriately high urine pH requires that the urine sodium concentration be greater than 25 meq/L.
For the each of the 3 symptoms above, indicate the level of severity over the past week using the following scale:
===Urine ammonium excretion===
*0 = no problem
*Urine ammonium excretion is reduced in distal RTA Thus, either direct measurement or indirect estimation of the urine ammonium concentration can be helpful in establishing the correct diagnosis.
*1 = slight or mild problems, generally mild or intermittent
*Urinary NH4 excretion cannot be directly measured in most clinical laboratories. However, an indirect estimate can be obtained by measurement of the urine anion gap and/or the urine osmolal gap.  
*2 = moderate, considerable problems, often present and/or at a moderate level
*Estimation of NH4 excretion is not useful in patients with proximal RTA.
*3 = severe: pervasive, continuous, life-disturbing problems
Considering somatic symptoms in general, indicate whether the patient has:
*0 = no symptoms
*1 = few symptoms
*2 = moderate number of symptoms
*3 = Severe symptoms
The SS scale score is the sum of the severity of the 3 symptoms (fatigue, waking unrefreshed, cognitive symptoms) plus the
extent (severity) of somatic symptoms in general. The final score is between 0 and 12.
==History and symtpoms==
The defining symptoms of fibromyalgia are chronic, widespread pain and tenderness to light touch. Other symptoms include
*Severe fatigue
*Allodynia
*Tingling of the skin
*Achiness in the muscle tissues
*Prolonged muscle spasms
*Muscle weakness
*Sleep disturbances
*Cognitive dysfunction
==Laboratory findings==
Fibromyalgia is a diagnosed clinically by careful history and examination. Blood and urine tests are usually normal. However, tests may be done to rule out other conditions that may have similar symptoms.
==Medical therapy==
===Single agent therapy===
*Preferred regimen (1): Amitriptyline 10-70 mg orally once daily at bedtime
*Preferred regimen (2): Cyclobenzaprine 5-30 mg orally once daily at bedtime
*Preferred regimen (3): Duloxetine : 30-60 mg orally once daily
*Preferred regimen (4): Milnacipran 12.5 mg orally once daily initially, followed by 12.5 mg twice daily for 2 days, followed by 25 mg twice daily for 4 days, then 50-100 mg twice daily thereafter
*Preferred regimen (5): Pregabalin 75-225 mg orally twice daily, maximum 450 mg/day
===Combination Thereapy===
*Preferred regimen (1): Amitriptyline 10-70 mg orally once daily at bedtime '''(OR)'''
*Preferred regimen (2): Cyclobenzaprine 5-30 mg orally once daily at bedtime
'''AND'''
*Preferred regimen (3): Duloxetine 30-60 mg orally once daily; higher doses have been used, consult specialist for guidance '''(OR)'''
*Preferred regimen (4): Milnacipran 12.5 mg orally once daily initially, followed by 12.5 mg twice daily for 2 days, followed by 25 mg twice daily for 4 days, then 50-100 mg twice daily thereafter
'''AND'''
*Preferred regimen (5): Pregabalin 75-225 mg orally twice daily, maximum 450 mg/day '''(OR)'''
*Preferred regimen (6): Gabapentin 300 mg orally once daily on first day, followed by 300 mg twice daily on second day, followed by 300 mg three times daily on third day, then titrate dose according to response up to 1800-2400 mg/day given in 3 divided doses
==Pathophysiology==
The cause of fibromyalgia is unknown. In fact it is not be due to a singular factor at all, but r due to a multiplicity of causes. Fibromyalgia can, but most often does not, start as a result of some [[Physical trauma|trauma]] such as a traffic accident, major surgery, or disease. Some evidence shows that [[Lyme Disease]] may be a trigger of fibromyalgia symptoms.<ref>{{cite web | url = http://www.immunesupport.com/library/showarticle.cfm/ID/3579 | title = Late and Chronic Lyme Disease: Symptom Overlap with Chronic Fatigue Syndrome & Fibromyalgia}}</ref> Another study suggests that more than one clinical entity may be involved, ranging from a mild, idiopathic [[inflammation|inflammatory]] process to [[clinical depression]]<ref>http://www.springerlink.com/content/1271314042w8405g/  Mueller W, et al.  The classification of fibromyalgia syndrome.  Rheumatol Int. 2007 Jul 25</ref> 
 
=== Genetics ===
By using self-reported "Chronic Widespread Pain" (CWP) as a surrogate marker for fibromyalgia, the [http://www.meb.ki.se/twinreg/index_en.html Swedish Twin Registry] found that a modest genetic contribution may exist:<ref name="PMID16646040">{{cite journal |author=Kato K, Sullivan P, Evengård B, Pedersen N |title=Importance of genetic influences on chronic widespread pain |journal=Arthritis Rheum. |volume=54 |issue=5 |pages=1682-6 |year=2006 | doi=10.1002/art.21798 |pmid=16646040}}</ref><ref name="PMID16908799">{{cite journal |author=Kato K, Sullivan P, Evengård B, Pedersen N |title=Chronic widespread pain and its comorbidities: a population-based study |journal=Arch. Intern. Med. |volume=166 |issue=15 |pages=1649-54 |year=2006 | url=http://archinte.ama-assn.org/cgi/content/full/166/15/1649 |pmid=16908799}}</ref>
* [[Monozygotic twins]] with CWP have a 15% chance that their twin sibling has CWP
* Dizygotic [[twins]] with CWP have a 7% chance that their twin sibling has CWP
 
=== Stress ===
Studies have shown that [[Stress (medicine)|stress]] is a significant precipitating factor in the development of fibromyalgia,<ref>{{cite journal | author = Anderberg UM, Marteinsdottir I, Theorell T, von Knorring L | title=The impact of life events in female patients with fibromyalgia and in female healthy controls. | journal=Eur Psychiatry | month=Aug| year=2000 | pages=33-41 | volume=15 | issue=5 | id=PMID 10954873 }}</ref> and that [[PTSD]] is linked with fibromyalgia.<ref>{{cite journal | author= Amital D, Fostick L, Polliack ML, Segev S, Zohar J, Rubinow A, Amital H | title=Posttraumatic stress disorder, tenderness, and fibromyalgia syndrome: are they different entities? | journal=J Psychosom Res | month=Nov | year=2006 | pages=663-9 | volume=61 | issue=5 | id=PMID 17084145}}</ref><ref>{{cite journal | author= Raphael KG, Janal MN, Nayak S | title=Comorbidity of fibromyalgia and posttraumatic stress disorder symptoms in a community sample of women. | journal=Pain Med. | month=Mar| year=2004 | pages=33-41 | volume=5 | issue=1 | id=PMID 14996235}}</ref> The Amital study found that 49% of PTSD patients fulfilled the criteria for FMS, compared with none of the controls.
 
A non-mainstream hypothesis that fibromyalgia may be a [[psychosomatic illness]] has been described by John E. Sarno's "[[tension myositis syndrome]]". He believes many cases of [[chronic pain]] result from changes in the body caused by the mind's subconscious strategy of distracting painful or dangerous emotions. Education, attitude change, (and in some cases, psychotherapy) are treatments proposed to stop the brain from using that strategy.<ref>{{cite book |last=Sarno|first=Dr. John E,|authorlink=John E. Sarno|title=The Mindbody Prescription: Healing the Body, Healing the Pain |year=1998 |isbn=0-446-67515-6 |pages=76-78}}</ref><ref>{{cite book |last=Sarno|first=Dr. John E. et al,| title=The Divided Mind: The Epidemic of Mindbody Disorders |year=2006 |isbn=0-06-085178-3 |pages=21-22,235-237,294-298}}</ref> Robert G. Schwartz, MD has proposed an alternative view where in mind-body connections may play an important role in chronic disease (not just fibromyalgia). Through his program strategies to align incentives are offered.
 
===Dopamine abnormality===
*[[Dopamine]] is a [[catecholamine]] [[neurotransmitter]]  known for its role in the pathology of [[schizophrenia]], [[Parkinson's disease]] and [[addiction]].
*Fibromyalgia has been commonly referred to as a "stress-related disorder" due to its frequent onset and worsening of symptoms in the context of stressful events.<ref>[http://www.ncbi.nlm.nih.gov/pubmed/16174484?ordinalpos=18&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum The role of life stress in fibromyalgia. [Curr Rheumatol Rep. 2005&#93; - PubMed Result<!-- Bot generated title -->]</ref><ref>[http://www.ncbi.nlm.nih.gov/pubmed/12849719?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Chronic widespread pain and fibromyalgia: what we ...[Best Pract Res Clin Rheumatol. 2003&#93; - PubMed Result<!-- Bot generated title -->]</ref>
*It was therefore proposed that fibromyalgia may represent a condition characterized by low levels of central dopamine  that likely results from a combination of genetic factors and exposure to environmental stressors, including psychosocial distress, physical trauma, systemic viral infections or inflammatory disorders (e.g. [[rheumatoid arthritis]], systemic [[lupus erythematosus]]).<ref>[http://www.ncbi.nlm.nih.gov/pubmed/14975515?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Stress and dopamine: implications for the pathophy...[Med Hypotheses. 2004&#93; - PubMed Result<!-- Bot generated title -->]</ref>
*This conclusion was based on three key observations:  (1) fibromyalgia is associated with stress; (2) chronic exposure to stress results in a disruption of dopamine-related neurotransmission and (3) dopamine plays a critical role in modulating pain perception and central [[analgesia]] in such areas as the [[basal ganglia]];including the [[nucleus accumbens]], [[insular cortex]], [[anterior cingulate cortex]] [[thalamus]], [[periaqueductal gray]], and [[spinal cord]]<ref>[http://www.ncbi.nlm.nih.gov/pubmed/6314870?ordinalpos=113&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Dopamine-containing neurons in the spinal cord: an...[Ann Neurol. 1983&#93; - PubMed Result<!-- Bot generated title -->]</ref> <ref>[http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15975975 Direct inhibition of substantia gelatinosa neurones in the rat spinal cord by activation of dopamine D2-like receptors<!-- Bot generated title -->]</ref><ref>[http://www.ncbi.nlm.nih.gov/pubmed/9355111?ordinalpos=27&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum The effects of stress on central dopaminergic neur...[Neurochem Res. 1997&#93; - PubMed Result<!-- Bot generated title -->]</ref><ref>[http://www.ncbi.nlm.nih.gov/pubmed/7715939?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum The role of the basal ganglia in nociception and p...[Pain. 1995&#93; - PubMed Result<!-- Bot generated title -->]</ref> <ref>[http://www.ncbi.nlm.nih.gov/pubmed/10597883?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum The role of dopamine in the nucleus accumbens in a...[Life Sci. 1999&#93; - PubMed Result<!-- Bot generated title -->]</ref><ref>[http://www.jneurosci.org/cgi/content/full/19/10/4169 Dopamine Reuptake Inhibition in the Rostral Agranular Insular Cortex Produces Antinociception - Burkey et al. 19 (10): 4169 - Journal of Neuroscience<!-- Bot generated title -->]</ref> <ref>[http://www.ncbi.nlm.nih.gov/pubmed/15327817?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Dopamine and NMDA systems modulate long-term nocic...[Pain. 2004&#93; - PubMed Result<!-- Bot generated title -->]</ref><ref>[http://www.ncbi.nlm.nih.gov/pubmed/1611515?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Neurophysiological, pharmacological and behavioral...[Brain Res. 1992&#93; - PubMed Result<!-- Bot generated title -->]</ref><ref>[http://www.ncbi.nlm.nih.gov/pubmed/15275769?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Opiate anti-nociception is attenuated following le...[Pain. 2004&#93; - PubMed Result<!-- Bot generated title -->]</ref>
*As is the case with several of the neurotransmitters, there is evidence for a role of dopamine in [[restless leg syndrome]], which is a common co-morbid condition in patients with fibromyalgia. <ref>[http://www.bmj.com/cgi/content/full/312/7042/1339 Restless legs syndrome and leg cramps in fibromyalgia syndrome: a controlled study - Yunus and Aldag 312 (7042): 1339 - BMJ<!-- Bot generated title -->]</ref><ref>[http://www.ncbi.nlm.nih.gov/pubmed/16816393?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Support for dopaminergic hypoactivity in restless ...[Brain. 2006&#93; - PubMed Result<!-- Bot generated title -->]</ref>
*Patients with restless legs syndrome have also been demonstrated to have [[hyperalgesia]] to static mechanical stimulation.<ref>[http://brain.oxfordjournals.org/cgi/content/full/127/4/773 Static mechanical hyperalgesia without dynamic tactile allodynia in patients with restless legs syndrome - Stiasny-Kolster et al. 127 (4): 773 - Brain<!-- Bot generated title -->]</ref>
 
===Serotonin===
[[Serotonin]] is a [[neurotransmitter]] that is known to play a role in regulating sleep patterns, mood, feelings of well-being, concentration and descending inhibition of pain. Accordingly, it has been hypothesized that the [[pathophysiology]] underlying the symptoms of fibromyalgia may be a dysregulation of serotonin metabolism, which may explain (in part) many of the symptoms associated with the disorder.  This [[hypothesis]] is derived in part by the observation of decreased serotonin metabolites in patient [[plasma]] <ref>[http://www.ncbi.nlm.nih.gov/pubmed/1313504?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Platelet 3H-imipramine uptake receptor density and...[J Rheumatol. 1992&#93; - PubMed Result<!-- Bot generated title -->]</ref> and [[cerebrospinal fluid]].<ref>[http://www.ncbi.nlm.nih.gov/pubmed/1374252?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Cerebrospinal fluid biogenic amine metabolites in ...[Arthritis Rheum. 1992&#93; - PubMed Result<!-- Bot generated title -->]</ref>  However, [[selective serotonin reuptake inhibitors]] (SSRIs) have met with limited success in alleviating the symptoms of the disorder, while drugs with activity as mixed [[serotonin-norepinephrine reuptake inhibitor]]s (SNRIs) have been more successful<ref>[http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16762044 Biology and therapy of fibromyalgia. New therapies in fibromyalgia<!-- Bot generated title -->]</ref>.  Accordingly, [[duloxetine]] ([[Cymbalta]]), a SNRI originally used to treat depression and painful [[diabetic neuropathy]], has been demonstrated by controlled trials to relieve symptoms of some patients.  Eli Lilly and Company, the manufacturer of duloxetine has submitted a supplementary new drug application (sNDA) to the [[FDA]] for approval of it use in the treatment of FM. The relevance of dysregulated serotonin metabolism to the pathophysiology is a matter of debate.<ref>[http://www.ncbi.nlm.nih.gov/pubmed/17693607?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Serum serotonin levels are not useful in diagnosin...[Ann Rheum Dis. 2007&#93; - PubMed Result<!-- Bot generated title -->]</ref>  Ironically, one of the more effective types of medication for the treatment of the disorder (i.e. serotonin [[5-HT3 antagonist]]s) actually block some of the effects of serotonin.<ref>[http://www.ncbi.nlm.nih.gov/pubmed/12122920?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Current experience with 5-HT3 receptor antagonists...[Rheum Dis Clin North Am. 2002&#93; - PubMed Result<!-- Bot generated title -->]</ref>
 
===Sleep disturbance===
[[Electroencephalography]] studies have shown that people with fibromyalgia lack [[slow-wave sleep]] and circumstances that interfere with stage four sleep (pain, depression, serotonin deficiency, certain medications or [[anxiety]]) may cause or worsen the condition. According to the sleep disturbance hypothesis, an event such as a trauma or illness causes sleep disturbance and possibly initial chronic pain that may initiate the disorder.  The hypothesis supposes that stage 4 sleep is critical to the function of the [[nervous system]], as it is during that stage that certain neurochemical processes in the body 'reset'. In particular, pain causes the release of the [[neuropeptide]] [[substance P]] in the [[spinal cord]] which has the effect of amplifying pain and causing nerves near the initiating ones to become more sensitive to pain. Under normal circumstances, areas around a wound to become more sensitive to pain but if pain becomes chronic and body-wide this process can run out of control. The sleep disturbance hypothesis holds that deep sleep is critical to reset the substance P mechanism and prevent this out-of-control effect.
 
The sleep disturbance/substance P hypothesis could explain "tender points" that are characteristic of fibromyalgia but which are otherwise enigmatic, since their positions don't correspond to any particular set of nerve junctions or other obvious body structures. The hypothesis proposes that these locations are more sensitive because the sensory nerves that serve them are positioned in the spinal cord to be most strongly affected by substance P. This hypothesis could also explain some of more general neurological features of fibromyalgia, since substance P is active in many other areas of the nervous system.  The sleep disturbance hypothesis could also provide a possible connection between fibromyalgia, [[chronic fatigue syndrome]] (CFS) and [[post-polio syndrome]] through damage to the ascending reticular activating system of the [[reticular formation]]. This area of the brain, in addition to apparently controlling the sensation of fatigue, is known to control sleep behaviors and is also believed to produce some neuropeptides, and thus injury or imbalance in this area could cause both CFS and sleep-related fibromyalgia.
 
Critics of the hypothesis argue that it does not explain slow-onset fibromyalgia, fibromyalgia present without tender points, or patients without heightened pain symptoms, and a number of the non-pain symptoms present in the disorder.


===Human growth hormone===
==References==
An alternate hypothesis suggests that stress-induced problems in the [[hypothalamus]] may lead to reduced sleep and reduced production of [[human growth hormone]] (HGH) during [[slow-wave sleep]]. People with fibromyalgia tend to produce inadequate levels of HGH. Most patients with FM with low IGF-I levels failed to secrete HGH after stimulation with clonidine and l-dopa.
{{Reflist|2}}
{{Gastroenterology}}


This view is supported by the fact that those hormones under the direct or indirect control of HGH, including [[IGF-1]], [[cortisol]], [[leptin]] and [[neuropeptide Y]] are abnormal in people with fibromyalgia,<ref>{{cite journal | last = Anderberg  | first = UM | coauthors = Liu Z, Berglund L, Nyberg F | pmid = 10700334 | title = Elevated plasma levels of neuropeptide Y in female fibromyalgia patients. | journal = European Journal of Pain | volume = 3 | issue = 1 | year = 1999 | pages = 19-30}}</ref>  In addition, treatment with exogenous HGH or growth hormone secretagogue reduces fibromyalgia related pain and restores slow wave sleep<ref> {{ cite journal | last = Jones  | first = KD | coauthors = Deodhar P, Lorentzen A, Bennett RM, Deodhar AA | title = Growth hormone perturbations in fibromyalgia: a review. | journal = Seminars in Arthritis and Rheumatism | year =  2007 | volume  = 36 | issue = 6 | pages = 357-79 | pmid = 17224178 }}</ref><ref>{{cite journal | last = Shuer | first = ML | title = Fibromyalgia: symptom constellation and potential therapeutic options | journal = Endocrine | volume = 22 | issue = 1 | pages = 67-76 | pmid = 14610300 }}</ref><ref>{{cite journal | last = Yuen | first = KC | coauthors =  Bennett RM, Hryciw CA, Cook MB, Rhoads SA, Cook DM | journal = Growth hormone & IGF research | title = Is further evaluation for growth hormone (GH) deficiency necessary in fibromyalgia patients with low serum insulin-like growth factor (IGF)-I levels? | volume = 17 | issue = 1  | year = 2007 | pages = 82-8 | pmid = 17289417 }}</ref><ref>{{cite journal | last = Bennett  | first = RM | coauthors =  Cook DM, Clark SR, Burckhardt CS, Campbell SM. | pmid = 9228141  | title = Hypothalamic-pituitary-insulin-like growth factor-I axis dysfunction in patients with fibromyalgia | | Journal of Rheumatology | volume = 24 | issue = 7 | pages = 1384-9 }}</ref> though there is disagreement about the proposition.<ref>{{cite journal | last = McCall-Hosenfeld | first = JS | coauthors = Goldenberg DL, Hurwitz S, Adler GK. | title = Growth hormone and insulin-like growth factor-1 concentrations in women with fibromyalgia | journal = Journal of Rheumatology | volume = 30 | issues = 4 | pages = 809-14 | pmid = 12672204 }}</ref>
[[Category:Emergency medicine]]
[[Category:Gastroenterology]]
[[Category:Gynecology]]
[[Category:Medicine]]


===Deposition disease===
[[Category:Surgery]]
The 'deposition hypothesis of fibromyaglia' poses that fibromyalgia is due to intracellular [[phosphate]] and [[calcium]] accumulations that eventually reaches levels sufficient to impede the [[Adenosine triphosphate|ATP]] process, possibly caused by a [[kidney]] defect or missing [[enzyme]] that prevents the removal of excess phosphates from the blood stream. Accordingly, proponents of this hypothesis suggest that fibromyalgia may be an inherited disorder, and that phosphate build-up in cells is gradual but can be accelerated by trauma or illness. Calcium is required for the excess phosphate to enter the cells. The additional phosphate slows down the ATP process; however the excess calcium prods the cell to continue producing ATP.


The phosphate build-up hypothesis explains many of the symptoms present in fibromyalgiaand proposes an underlying cause. The guaifenesin treatment, based on this hypothesis, has received mixed reviews, with some practitioners claiming many near-universal successes and others reporting no success. Of note, guaifenesin is also a central acting [[muscle relaxant]] used in veterinary anaesthesia<ref>[http://www.ncbi.nlm.nih.gov/pubmed/2282545?ordinalpos=13&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Intravenous anesthesia. [Vet Clin North Am Equine Pract. 1990&#93; - PubMed Result<!-- Bot generated title -->]</ref> that is structurally related to [[methocarbamol]], a property that might explain its utility in some fibromyalgia patients.  A controlled trial of guaifenesin  for the treatment of fibromyalgia demonstrated no evidence for efficacy of this medication. However, this study has been criticized by the chief proponent of the deposition hypothesis for not limiting salicylic acid exposure in patients, and for studying the effectiveness of only guaifenesin, not the entire treatment method.<ref>{{cite journal | url = http://www.fibromyalgiatreatment.com/Research_Oregon.htm | title = A Response To The Oregon Study's Implication | accessdate = 2007-06-23 | first = R. Paul | last = St. Amand | journal = Clinical Bulletin of Myofascial Therapy | volume = 2 | issue = 4 | year = 1997 }}</ref> As of 2005, further studies to test the protocol's effectiveness are in the planning stages, with funding for independent studies largely collected from groups which advocate the hypothesis.  It should be noted that ''nothing'' in the scientific literature supports the proposition that fibromyalgia patients have excessive levels of phosphate in their tissues.
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{{WikiDoc Sources}}
<references />


===Other hypotheses===
==References==
Other hypotheses have been proposed related to various [[toxin]]s from the patient's environment, [[virus|viral]] causes such as the [[Epstein-Barr Virus]], [[growth hormone]] deficiencies possibly related to an underlying (maybe autoimmune) disease affecting the hypothalamus gland, an aberrant immune response to [[intestinal bacteria]],<ref name="ClinExpDermatol2004-KendallSN">{{cite journal | author=Kendall SN | title=Remission of rosacea induced by reduction of gut transit time. | journal=Clin Exp dermatol. | month=May | year=2004 | pages=297-9 | volume=29 | issue=3 | pmid=15115515}}</ref><ref name="AnnRheumDis2004-PimentalM">{{cite journal | author=Pimental M, Wallace D, Hallegua D et .al | title=A link between irritable bowel syndrome and fibromyalgia may be related to findings on lactulose breath testing. | journal=Ann Rheum Dis. | month=April | year=2004 | pages=450-2 | volume=63 | issue=4 |pmid=15020342}}</ref> [[neurotransmitter]] disruptions in the [[central nervous system]], and erosion of the protective chemical coating around sensory nerves. A 2001 study suggested an increase in fibromyalgia among women with extracapsular silicone gel leakage, compared to women whose implants were not broken or leaking outside the capsule.<ref name="Brown2001">{{cite journal | author=Brown SL, Pennello G, Berg WA, Soo MS, Middleton MS | title=Silicone gel breast implant rupture, extracapsular silicone, and health status in a population of women | journal=J Rheumatol | year=2001 | pages=996-1003 | volume=28 | issue=5 | pmid=11361228}}</ref><ref>{{cite web |title=Study of Silicone Gel Breast Implant Rupture, Extracapsular Silicone, and Health Status in a Population of Women |url=http://www.fda.gov/cdrh/breastimplants/extracapstudy.html |date=May 29, 2001 |publisher=FDA}}</ref> This association has not repeated in a number of related studies,<ref name=Lipworth>{{cite journal | author=Lipworth L, Tarone RE, McLaughlin JK.| title=Breast implants and fibromyalgia: a review of the epidemiological evidence.| journal=Ann Plast Surg. | year=2004 | pages=284-7| volume=52 | issue=3 |pmid=15156983}}</ref> and the US-FDA concluded "the weight of the epidemiological evidence published in the literature does not support an association between fibromyalgia and breast implants."<ref>{{cite web |title=FDA Breast Implant Consumer Handbook 2004 |url=http://www.fda.gov/cdrh/breastimplants/handbook2004/diseases.html#1 |date=June 8, 2004 |publisher=FDA}}</ref> Due to the multi-systemic nature of illnesses such as fibromyalgia and [[chronic fatigue syndrome]] (CFS/ME), an emerging branch of medical science called [[psychoneuroimmunology]] (PNI) is looking into how the various hypotheses fit together.
{{Reflist|2}}
{{Gastroenterology}}


Another hypothesis on the cause of symptoms in fibromyalgia states that patients suffer from [[vasomotor]] dysregulation causing improper [[Blood vessel|vascular]]flow and [[hypoperfusion]] (decreased blood flow to a given tissue or organ).<ref name="pmid17376601">{{cite journal |author=Katz DL, Greene L, Ali A, Faridi Z |title=The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation |journal=Med Hypotheses. |volume=(Epub ahead of print) |issue= |pages= |year=2007 |month=19 Mar |pmid=17376601 |doi=10.1016/j.mehy.2005.10.037}}</ref>
[[Category:Emergency medicine]]
[[Category:Gastroenterology]]
[[Category:Gynecology]]
[[Category:Medicine]]


===Always a comorbid disease?===
[[Category:Surgery]]
Cutting across several of the above hypotheses is the proposition that fibromyalgia is almost always a [[comorbidity|comorbid]] disorder, occurring in combination with some other disorder that likely served to "trigger" the fibromyalgia in the first place. Two possible triggers are [[gluten sensitivity]] and/or irritable bowel. Irritable bowel is found at high frequency in fibromyalgia,<ref name="pmid16042909">{{cite journal | author = Frissora CL, Koch KL | title = Symptom overlap and comorbidity of irritable bowel syndrome with other conditions | journal = Current gastroenterology reports | volume = 7 | issue = 4 | pages = 264-71 | year = 2005 | pmid = 16042909 | doi = }}</ref> and a large coeliac
support group survey of adult celiacs revealed that 7% had fibromyalgia and also has a co-occurrence with chronic fatique.<ref name="pmid12741468">{{cite journal | author = Zipser RD, Patel S, Yahya KZ, Baisch DW, Monarch E | title = Presentations of adult celiac disease in a nationwide patient support group | journal = Dig. Dis. Sci. | volume = 48 | issue = 4 | pages = 761-4 | year = 2003 | pmid = 12741468 | doi = }}</ref>


According to this hypothesis, some other disorder (or trauma) occurs first, and fibromyalgia follows as a result.  In some cases, the original disorder abates on its own or is separately treated and cured, but the fibromyalgia remains. This is especially apparent when fibromyalgia seems triggered by major surgery.  In other cases the two disorders coexist. Since it can be extremely complex to treat the source of fibromyalgia, and since it is most probably a multifactoral disorder that is different from one afflicted patient to the next, the concept of [http://wehelpwhathurts.homestead.com/diseasemanagement.html Reducing Total Load] has been proposed. In this instance the total number of things that does not allow a patient to get well is treated, one at a time, taking into consideration the unique conditions of that individual patient.
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===Controversies===
{{WikiDoc Sources}}
The validity of fibromyalgia as a unique clinical entity is a matter of some contention among researchers in the field.  For example, it has been proposed that the pathophysiology responsible for the symptoms that are collectively classified as representing "fibromyalgia" is poorly understood, thereby suggesting that the fibromyalgia [[phenotype]] which is the difference between an individual’s heredity and what that heredity produces, may result from several different disease processes that have global hyperalgesia - an increased sensitivity to pain - and allodynia in common, <ref>http://www.springerlink.com/content/1271314042w8405g/  Mueller W, et al.  The classification of fibromyalgia syndrome.  Rheumatol Int. 2007 Jul 25</ref><ref>The association or otherwise of the functional somatic syndromes.Psychosom Med. 2007 Dec;69(9):855-9. Review. PMID: 180400</ref><ref>Comorbidity of fibromyalgia and psychiatric disorders.Curr Pain Headache Rep. 2007 Oct;11(5):333-8. Review. PMID: 17894922</ref>  an observation that has led to the proposition that current diagnostic criteria are insufficient to differentiate patient groups from each other.<ref>An integrated model of group psychotherapy for patients with fibromyalgia.Int J Group Psychother. 2007 Oct;57(4):451-74</ref>  Alternatively, there is evidence for the existence of differing pathophysiological - which is the study of the disturbance of normal mechanical, physical, and biochemical functions of the body - within the greater fibromyalgia construct<ref>[http://www.ncbi.nlm.nih.gov/pubmed/17084146?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Psychophysiological responses in patients with fib...[J Psychosom Res. 2006&#93; - PubMed Result<!-- Bot generated title -->]</ref><ref>[http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16356200 Heterogeneity of psychophysiological stress responses in fibromyalgia syndrome patients<!-- Bot generated title -->]</ref>, which may be interpreted to represent evidence for the existence of biologically distinct "sub-types" of the disorder akin to conditions such as [[epilepsy]], [[schizophrenia]] and [[major depressive disorder]].  In a January 14, 2008 article in the New York Times, the controversy of the reality of the disease and its proposed cures are discussed, while citing that the [[American College of Rheumatology]], the [[Food and Drug Administration]] and insurers recognize fibromyalgia as a diagnosable disease. Drug companies are aggressively pursuing fibromyalgia treatments, seeing the potential for a major new market.
<references />


==References==
==References==
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{{reflist|2}}

Latest revision as of 06:41, 28 July 2020

Causes

Common causes

  • Peptic ulcer disease
    • Responsible for around 33%-50% of upper GI bleeding
    • Peptic ulcer disease is most commonly due to H.pylori or nonsteroidal anti-inflammatory drugs (NSAIDs).
    • Upper GI bleeding is the most common complication of peptic ulcer disease and may be the initial presentation.[1]
  • Esophageal varices
    • Responsible for around 14% of upper GI bleeding
    • These dilated veins within the esophagus are usually secondary to portal hypertension from cirrhosis.
    • Massive variceal hemorrhage is responsible for acute life-threatening upper GI bleeding which is an medical emergency .[2][3]
  • Mallory-Weiss syndrome :
    • Responsible for around 5% of upper GI bleeding
    • A longitudinal mucosal laceration in the distal esophagus and/or proximal stomach that usually results from forceful retching

Less common causes

  • Neoplasms
    • gastric cancer
    • esophageal tumors
  • Esophagitis (complications due to erosive or necrotizing infectious esophagitis )
  • Gastric erosions/gastropathy [4]
    • Acute erosive gastritis caused by drugs, radiation, infection, or direct trauma.
    • Reactive gastropathy may be due to bile reflux, particularly after partial gastrectomy.
    • Portal hypertensive gastropathy, which results in increased friability of gastric mucosa in patients with cirrhosis.[5][6]
  • Dieulafoy lesions
    • Dilated aberrant submucosal vessels that erode the overlying epithelium in the absence of an ulcer
  • Gastric varices
  • Gastric antral vascular ectasia
    • Dilated gastric vessels of unknown etiology that cause chronic UGIB and iron-deficiency anemia

Rare causes

  • Bleeding from the hepatobiliary tract
    • Most commonly secondary to a liver or biliary tract injury, from trauma or following procedures or surgery.
    • Diagnosed by endoscopic retrograde cholangiopancreatography (ERCP) and treated with arteriography
  • Aortoenteric fistulas,
    • Most commonly involves the lower duodenum.
    • Common causes include aortic aneurysms or prosthetic vascular grafts, syphilis and tuberculosis
    • Presents with frank UGIB along with a pulsatile mass and abdominal pain radiating to the back.
    • Diagnosed by endoscopy.
  • Crohn disease involving the upper gastrointestinal tract
  • Metastatic malignancy involving the upper gastrointestinal tract, such as melanoma or renal cell carcinoma
  • Hemosuccus pancreaticus
    • Pancreatic inflammation or cancer may result in bleeding into the pancreatic duct, which connects to the duodenum

Risk factors

  • Advancing age[7][8][9][10]
  • Previous history of gastrointestinal bleed
  • Chronic kidney disease
  • Underlying cardiovascular disease
  • Cirrhosis and portal hypertension
  • Presence of H.pylori
  • NSAID or aspirin use in patients with a history of ulcer disease
    • Those on dual antiplatelet therapy; those on anticoagulant therapy; or those with two or more of the following risk factors
      • Age 60 years or older
      • Glucocorticoid use
      • Dyspepsia
      • Gastroesophageal reflux disease
  • Critical illness
    • Nosocomial stress ulcers due the to the use of mechanical ventilation for more than 48 hours, and coagulopathy
    • Other risk factors for nosocomial stress ulcerations in critically ill patients include a history of gastrointestinal ulceration or bleeding within the past year; or two or more of the following risk factors: presence of sepsis, ICU admission lasting longer than 1 week, occult gastrointestinal bleeding lasting 6 days or longer, and administration of more than 250 mg of hydrocortisone or equivalent glucocorticoid therapy
  • Rare conditions associated with gastric acid hypersecretion, such as Zollinger-Ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy.
Causes of Acute Upper GI bleeding
Esophagus
  • Esophagitis
  • Mallory–Weiss tear
  • Esophageal varices
  • Esophageal ulcers
  • Esophageal cancer
Gastric
  • Gastric ulcer
  • Gastric cancer
  • Gastritis
  • Gastric varices
  • Portal hypertensive gastropathy
  • Gastric antral vascular ectasia
  • Dielafuoy lesions
Duodenal
  • Duodenal ulcer
  • Vascular malformations, including aorto-enteric
  • Fistulae
  • Bleeding from the bile duct due to
    • Liver biopsy
    • Trauma
    • Arteriovenous malformations
    • Liver tumors

Associated Conditions

  • Heyde syndrome, aortic valve stenosis with associated gastrointestinal bleeding thought to be due to acquired reduction of von Willebrand factor.[11]

History

Obtaining the history is the most important aspect of making a diagnosis of upper GI bleed. It provides insight into the cause, precipitating factors and associated comorbid conditions and also helps in determining the severity of the bleed as well as in identifying the potential source of bleed:[12][13]

  • A history of epigastric pain, dyspepsia, or prior peptic ulcer may suggest the diagnosis of peptic ulcer disease.
  • A history of documented prior upper GI bleeding is important because approximately 60% of upper GI bleeders are rebleeding from the same site.
  • Prior use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) is important because these patients have an increased risk of gastric ulcer and a fourfold risk of significant GI bleeding compared with other patients.
  • A history of alcoholism increases the likelihood of cirrhosis and consequently of bleeding from esophageal varices or congestive gastropathy but alcoholics also frequently have peptic ulcers or gastritis.
  • Cigarette smokers have a significantly higher rate of the recurrent duodenal ulcer as compared with nonsmokers and a history of cigarette smoking should be elicited.
  • Vomiting, coughing, or retching before bleeding is suggestive of a Mallory-Weiss tear.[14]

A directed history may also alert to consider unusual causes.[15]

  • A history of pancreatitis suggests possible hemorrhage from a pancreatic pseudocyst. Erosion of a pancreatic pseudocyst into the duodenum or stomach may cause massive hematemesis, and the patient may present in shock.
  • Patients with prior abdominal aortic aneurysm repair may present with severe GI hemorrhage from an aortoenteric. This fistula often presents with a herald bleed followed within 4 to 96 hours by massive bleeding.
  • A personal or family history of recurrent epistaxis may suggest the diagnosis of Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia), and a careful examination for skin telangiectasias should be performed.
  • Patients with renal failure frequently have GI bleeding. This bleeding is often due to peptic ulcer disease or angiodysplasia. This bleeding may be severe because of clotting dysfunction associated with renal disease.

===Symptoms===[16][17]

Primary Prevention

Effective measures for the primary prevention of upper GI bleeding include administration of PPI in patients with an increased risk due to critical illness or use of NSAIDs or aspirin. In patients with cirrhosis and suspected portal hypertension, who found to have esophageal varices patients are given prophylactic treatment with a nonselective β-blocker or undergo endoscopic variceal ligation (EVL) with surveillance endoscopy.

Patients with stress ulcers

  • The American Society of Health-System Pharmacists developed clinical practice guidelines that recommend prophylaxis with a PPI or with a histamine-2 receptor antagonist (H2RA) for ICU patients at high risk for UGIB.[18][19][20]

Patients on NSAID, aspirin, or antiplatelet therapy

  • Joint gastroenterology and cardiology society practice guidelines recommend gastroprotective therapy with a PPI for patients considered to be at increased risk of bleeding from chronic NSAID and aspirin therapy.

Patients with cirrhosis and varices

  • EGD is used to screen for the presence of varices in patients with cirrhosis complicated by portal hypertension.
  • In patients with cirrhosis who do not have varices, no prophylaxis is indicated.
  • In patients with cirrhosis and varices that have not bled, prophylactic treatment with nonselective β-blockers, such as nadolol or propranolol, may decrease portal blood flow and thus decrease the risk of variceal bleed.
  • In patients with cirrhosis who have medium or large varices that have not bled, EVL is an alternative prophylactic treatment.
  • EVL is repeated every several weeks until obliteration of varices is seen.
  • Surveillance EGD should then be performed 1 to 3 months after obliteration and then every 6 to 12 months to check for variceal recurrence.

Secondary Prevention

Effective measures for the secondary prevention of UGIB include discouraging the use of NSAIDS in all patients with a history of UGIB.

Seondary Prevention

  • NSAID use in all patients with a history of UGIB should be discouraged.[21]

UGIB from peptic ulcer disease

  • Avoid NSAIDs.
  • For patients who are at high risk for rebleeding (elderly patients; those taking anticoagulant and antiplatelet medications), indefinite use of a PPI may be recommended.[22]
  • H pylori status should be determined, and patients should be treated if positive.
  • Eradication is confirmed with stool sample or repeat endoscopy with biopsy.

UGIB from varices

  • A combination of nonselective β-blockers plus EVL is the best option for secondary prophylaxis of UGIB from varices.
  • The nonselective β-blocker should be titrated up as tolerated.
  • Variceal banding should be repeated every 2 to 3 weeks until the varices are obliterated.
    • EGD must be performed 1 to 3 months after initial obliteration then every 6 to 12 months to check for variceal recurrence.

Prognosis

  • Prognosis is generally good with appropriate treatment, and the 1-year mortality rate of patients with nonvariceal UGIB is approximately 10%.[23][24][25][26]
  • In UGIB, the prognosis doesn't depend on the severity of bleeding but depends upon patients age and comorbid conditions.
  • The majority of patients with UGIB will stop bleeding spontaneously.
  • A clean ulcer base has less than a 3% chance of rebleeding; therefore, these lesions are not usually treated or scoped again.
  • In otherwise stable patients, patients with a clean ulcer base has less than a 3% chance of rebleeding and are good candidates for early discharge.
  • Treatment includes management of underlying liver disease and prevention of complications of cirrhosis.
  • Despite advances in gastric acid suppression as well as improved endoscopic diagnostic and therapeutic techniques, the mortality rate from UGIB has remained stable.

Scoring systems

Two scoring systems identify those at risk for adverse outcomes from UGIB:[27]

  • The Glasgow Blatchford Score (GBS)
  • The Rockall score

The Glasgow Blatchford Score (GBS)

  • The Glasgow Blatchford Score (GBS) helps in identifying low-risk patients with UGIB who can be managed safely as outpatients without an urgent endoscopy.[28][29]
  • GBS parameters include
    • Blood urea nitrogen level
    • Hematocrit level
    • Heart rate
    • Systolic blood pressure
    • Presence of syncope or melena, as well as presence of comorbid heart and liver disease.
  • GBS is the more effective system for predicting the need for transfusion in patients with UGIB.
The Glasgow Blatchford Score (GBS)
Admission risk markers Score
Blood urea nitrogen level (mg/dl)   ≥ 18.2 to < 22.4 2
  ≥ 22.4 to < 28 3
≥ 28 to < 70 4
  ≥ 70 6
Hemoglobin level (g/dl) Men    ≥ 12 to < 13 1
  ≥ 10 to < 12 3
< 10 6
Women    ≥ 10 to < 12 1
 < 10 6
Systolic blood pressure (mmHg)    ≥ 100 to < 109 1
 ≥ 90 to < 99 2
  < 90 3
Other markers Pulse rate ≥ 100 beats/min 1
Presentation with melena 1
Presentation with syncope 2
Hepatic disease 2
Heart failure 2

Scores of 0-2 -Low-risk group
Score of >6- High risk group

The Rockall score

  • The complete Rockall score identifies those patients with evidence of acute UGIB on endoscopy who are at low risk for further bleeding or death.[30][31]
  • The score is based upon
    • Age
    • Presence of shock
    • Comorbidity diagnosis
    • Endoscopic ulcer characteristics
    • Stigmata of recent hemorrhage.
The Rockall score
Markers Score
Age <60 0
60 - 79 1
≥ 80 2
Shock stage Blood pressure >120 0
100-119 1
<100 2
Heart rate >100 0
<100 1
Comorbidity No major comorbidity 0
Cardiac failure

Ischemic heart disease

Any major comorbidity

2
Renal failure

Liver failure

Disseminated malignancy

3
Diagnosis Mallory-Weiss tear, no lesion identified and no SRH 0
All other diagnosis 1
Malignancy of upper GI tract 2
Major SRH None or dark spot only 0
Blood in upper GI tract, adherent clot,
visible or spurting vessel 		2
GI: Gastrointestinal, SRH: Signs of recent hemorrhage.

Range of score is 0-11.

Score of ≤ 3 predicts low mortality risk, while ≥ 8 is a predictor of high mortality risk.

Complications

Complications of UGIB include:[32]

  • End-organ damage
    • Cardiac ischemia
    • Renal failure
    • Ischemic hepatitis
    • Anoxic brain injury
  • Iron-deficiency anemia

Classification

According to The American Gastroenterological Association, upper GI bleeding can be classified based on the rate of blood loss into overt(acute), occult or obscure(chronic) forms.[33][13][34][35]

  • Overt GI bleeding:- Overt GI bleeding is defined as acute bleeding which is visible and can present in the form of hematemesis, “coffee-ground” emesis, melena, or hematochezia.
  • Occult or chronic GI bleeding:- Occult GI bleeding is defined as a microscopic hemorrhage which can present as Hemoccult-positive stools with or without iron deficiency anemia. It is the initial presentation in patients with no evidence of visible blood loos and is positive on fecal occult blood test(FOBT).
  • Obscure GI bleeding:- Obscure GI bleeding is defined as recurrent bleeding in which a source is not identified after upper endoscopy and colonoscopy. It can be either overt or occult.

Epidemiology and Demographics

Incidence

The incidence of acute UGIB is approximately 50 to 100 per 100,000 individuals worldwide.[36][6]

Gender

Males are more commonly affected by UGIB than females. The males to female ratio is approximately 2 to 1.

Pathophysiology

Blood supply of Foregut

The digestive system is supplied by the celiac artery. The celiac artery is the first major branch from the abdominal aorta, and is the only major artery that nourishes the digestive organs.[37][38][39][40][41][42][43]

Foregut Blood supply
Esophagus

Upper esophageal sphincter
Cervical esophagus 

 Inferior thyroid artery 
Thoracic esophagus Aortic esophageal arteries or branches of the bronchial arteries 

Distal esophagus
Lower esophageal sphincter

Left gastric artery and left phrenic artery 
Stomach Lesser curvature Right and left gastric arteries
Greater curvature Right and left gastroepiploic arteries
Gastric fundus Short gastric arteries
Duodenum First and second parts

Gastroduodenal artery (GDA) and
Superior pancreaticoduodenal artery

Third and fourth parts Inferior pancreaticoduodenal artery
Blood supply of stomach
Source: By Mikael Häggström.https://commons.wikimedia.org/w/index.php?curid=3416062

Mucosal barrier

  • The gastric mucosa is protected from the acidic environment by mucus, bicarbonate, prostaglandins, and blood flow.[44][45][46]
  • This mucosal barrier consists of three protective components which include:
    • Layer of epithelial cell lining.
    • Layer of mucus, secreted by surface epithelial cells and foveolar cells.
    • Layer of bicarbonate ions, secreted by the surface epithelial cells.
Diagram of alkaline Mucous layer in stomach with mucosal defense mechanisms
Source: By M•Komorniczak (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons

The following table demonstrates the defense mechanisms of gastric mucosal barrier[47]

Defense mechanisms of gastric mucosal barrier
Mucus layer Forms a protective gel-like coating over the entire gastric mucosal surface
Epithelial layer Epithelial cell layer are bound by tight junctions that repel fluids
Bicarbonate ions Neutralize acids

Pathogenesis

The main inciting event in the pathogeneis of upper GI bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to ligament of Treitz, it is defined as upper GI bleeding.[6][48]

Etiology Frequency of occurance
Peptic ulcer disease 50%
Variceal bleeding 20%
Esophagitis, gastritis, and duodenitis 10-15%
Mallory-Weiss tear 15%
Malignancy 3-5%
Arteriovenous malformation <3%
Gastric antral vascular ectasia <1%
Dieulafoy lesion <1%

Pathogenesis

  • Regardless of etiology, if the balance of gastric acid secretion and mucosal defenses is disrupted, acid interacts with the epithelium to cause damage.[49][50][51]
    • Varices are large, tortuous veins and protrude into the lumen, rupturing.[52]
    • Helicobacter pylori disrupts the mucosal barrier and causes inflammation of the mucosa of the stomach and duodenum.[53][54]
    • As the ulcer progresses beyond the mucosa to the submucosa the inflammation causes weakening and necrosis of arterial walls, leading to pseudoaneurysm formation followed by rupture and hemorrhage.[55]
    • NSAIDs inhibit cyclooxygenase, leading to impaired mucosal defenses by decreasing mucosal prostaglandin synthesis.[56]
    • During stress, there is acid hypersecretion; therefore, the breakdown of mucosal defenses leads to injury of the mucosa and subsequent bleeding.
    • Mucosal defects along with dilated and tortuous vessels in dieulafoy lesion put them at risk for rupture because of necrosis of the arterial wall from exposure to gastric acid.[57][58][59][60]
 
 
 
 
 
 
 
 
 
NSAIDS
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Inhibits cycloxygenase pathway
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
COX-1
 
 
 
 
 
 
 
 
COX-2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Reduced
mucosal blood flow
 
Reduced
mucosal and
bicarbonate secreation
 
Impaired
platelet aggregation
 
Reduced
angiogenesis
 
 
 
 
Increased
leucocyte adherence
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Impaired defence
Impaired healing
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Mucosal Injury
 
 
 
 
 
 
 
 
 
 
 
 

Gross and Microscopic Pathology

Gross Pathology Microscopic Pathology
Varices Large and tortuous veins that protrude into the lumen Varices may be difficult to demonstrate in surgical specimens
Mallory-Weiss Tear[61] Isolated or multiple cleft like mucosal defects
  • Defects in the esophageal squamous mucosa.
  • Cells of acute inflammation.
  • Multiple ruptured blood vessels in the lamina propria or submucosa.
  • Prior lacerations may show various degrees of healing
    • Granulation tissue
    • Fibrosis[61]
    • Epithelial regeneration.
Esophagitis[62] Herpes esophagitis
  • Shallow ulcers
  • Sharp and raised edges
  • Normal intervening erythematous mucosa
 Ground glass inclusion bodies
Cytomegalovirus esophagitis
  • Superficial ulcers
  • Well-circumscribed
  • CMV infects mesenchymal cells in the lamina propria and submucosa
 Intranuclear inclusions
Fungal esophagitis
  • Erythematous
  • Hyperemic
  • Friable
  • Discrete and raised white plaque
 Neutrophils within the squamous epithelium
Pill esophagitis
  • Discrete ulcers
 Not specific and include
  • Necrosis
  • Prominent eosinophilic infiltrate
  • Spongiosis
Toxic esophagitis
  • Mucosal erythema,
  • Edema
  • Hemorrhage
  • Necrosis
 Acid injury
  • Coagulative necrosis
  • Eschar

Alkaline injury

  • Liquefactive necrosis
  • Acute inflammation
  • Abundant granulation tissue
Gastroesophageal

Reflux Disease[63]

  • Basal cell hyperplasia
  • Elongation of the lamina propria papillae
  • Mixed intraepithelial inflammation
  • Neutrophils, eosinophils, and lymphocytes
  • Squamous cell degeneration.
Barrett Esophagus[64] Columnar metaplasia
  • Mucinous columnar cells
  • Goblet cells, and enterocyte-like cells, among others.
  • Cells of acute inflammation
Acute Gastritis Mucosal hyperemia associated with
  • Bleeding
  • Erosions
  • Ulcers
  • Dilation and congestion of mucosal capillaries, edema, and hemorrhage in the lamina propria.
  • Ischemic-type changes such as
    • Degenerated and necrotic epithelium
    • Fibrinoid necrosis
    • Adherent fibrinopurulent debris
Gastric Ulcers[1]
  • Solitary, typically less than 2 cm in diameter, and have sharply defined borders.
  • The ulcer edges are usually flat, and the base of the ulcer usually appears smooth.
  • The presence of a radiating pattern of rugal folds is characteristic of peptic ulcers
  • Fibrinopurulent debris
  • Necrosis
  • Granulation tissue
Portal Hypertensive Gastropathy[65]
  • Mosaic pattern of congestion
  • Most commonly involves the fundus
  • Dilation, tortuosity, and thickening of small submucosal arteries and veins.
  • Mucosal capillaries may also show congestion, dilation, and proliferation.
Gastric Antral Vascular Ectasia[65] Linear pattern of mucosal congestion in the antrum termed “watermelon stomach Antral biopsies show
  • Congestion
  • Dilated mucosal capillaries
  • Vascular microthrombi

The mucosa also shows

  • Foveolar hyperplasia
  • Fibromuscular hyperplasia
  • Edema and regenerative changes
Reactive (Chemical) Gastropathy Stomach
  • Edema
  • Surface erosions
  • Polypoid changes, and friability
 The mucosa shows
  • Congestion
  • Edema
  • Fibromuscular hyperplasia
  • Foveolar hyperplasia
Peptic Disease Wide range of findings
  • From normal/slightly edematous mucosa to increased friability, erosions, and ulcers
  • Increased plasma cells
  • Neutrophilic infiltrate
  • Reactive epithelial changes, including villous blunting.
  • The surface epithelium usually shows mucous cell (pseudopyloric) metaplasia
Ischemia Hypoperfused ulcers Acute ischemia
  • Mucosal edema
  • Congestion
  • Superficial necrosis
  • Coagulative necrosis

Chronic ischemia

  • Fibrosis
  • Strictures
Structural Abnormalities of Blood Vessels[66] Large-caliber artery within the submucosa Dilated venules and arteriole in direct communication with each other
Inflammatory Bowel Disease Lymphoplasmacytic infiltrate with numerous neutrophils

Diagnosis

In patients with acute Upper GI bleeding who are unstable rapid assessment and resuscitation should be initiated even before diagnostic evaluation. Once hemodynamic stability is achieved, a proper clinical history, physical examination, and initial laboratory findings are crucial not only in determining the likely sources of bleeding but also in directing the appropriate intervention. The hematocrit level is measured soon after the onset of bleeding, but will not accurately reflect the amount of blood loss. Equilibration between the intravascular and extravascular spaces is not complete until 24 to 72 hours after bleeding has occurred. Low mean corpuscular volume, low iron and ferritin levels, and high transferrin and total iron-binding capacity (TIBC) confirm iron deficiency. Blood urea nitrogen (BUN) level may be elevated out of proportion to any increase in the creatinine level in patients with UGIB, secondary to the breakdown of blood proteins to urea by intestinal bacteria. Platelet count and coagulation studies should be checked, especially in patients with known or suspected coagulopathy. Nasogastric lavage should be performed if the presence or source of bleeding is unknown. Upper gastrointestinal endoscopy is the primary diagnostic tool, performed for both diagnosis and treatment of active bleeding. The American Society of Gastrointestinal Endoscopy guidelines recommend that upper endoscopy be performed within 24 hours of presentation in all patients with UGIB. Angiography and tagged erythrocyte scan are rarely needed, but may be used to diagnose (and embolize) active UGIB, particularly in patients who cannot tolerate EGD. Also, upper gastrointestinal tract radiographic studies using barium are generally not advised, as they may obscure visualization during EGD.[67][68][69][70]

Initial Laboratory Studies

  • The hematocrit level is used to identify the degree of blood loss and suggests the acuity or chronicity of blood loss.[34][13]
  • Serial complete blood count (CBC) tests are important for monitoring the presence of ongoing blood loss.
  • Initial CBC may not fully reflect the actual degree of acute blood loss.
  • Qualitatively, on peripheral blood smear prepared with Wright-Giemsa stain, normal erythrocytes should be smaller than the nucleus of a normal lymphocyte, and the central clear area should not be overly prominent.
  • In iron-deficiency anemia associated with chronic blood loss, erythrocytes are smaller (microcytic) and appear lighter (hypochromic) than normal cells.
  • Mild to moderate thrombocytopenia (>30 × 103/µL) does not usually result in spontaneous bleeding, although patients with a pre-existing lesion may bleed in the presence of even mild thrombocytopenia.
  • Platelet count may rise in response to significant gastrointestinal bleeding and may fall with multiple blood transfusions.
  • Low ferritin level is the most specific test for iron-deficiency anemia. This finding together with a low iron and high TIBC levels are helpful in diagnosing iron-deficiency anemia, a common complication of ongoing or significant UGIB.
  • BUN level may be elevated out of proportion to any increase in the creatinine level in patients with UGIB, secondary to breakdown of blood proteins to urea by intestinal bacteria.
  • In patients with esophageal varices, acquired coagulopathies are common due to cirrhosis.

Naso-Gastric Lavage

  • Nasogastric lavage is only indicated when the diagnosis of UGIB doubtful.[71][72]
  • It is rarely used now
  • Nasogastric lavage also helps in documenting active or recent UGIB and the need for urgent endoscopy.
  • Occasionally used to empty gastric contents in preparation for endoscopy.

Complicatiions

Complications of the procedure include:

  • Bleeding from trauma during tube passage in patients with coagulopathy is a possible complication.
  • Other rare complications include
    • Pharyngeal and esophageal perforation
    • Cardiac arrest
    • Ethmoid sinus fracture with brain trauma
    • Bronchial intubation.

Interpretation

  • Evidence of old (brown colored or 'coffee grounds') or fresh blood documents presence of UGIB.
  • Evidence of bilious material rules out bleeding distal to the pylorus.
  • Any other appearances of GI contents are non-diagnostic.
  • There is no evidence that performing a nasogastric lavage to clear clots or otherwise manage bleeding improves clinical outcome.

Contraindications

  • Avoid gastric lavage in patients with suspected perforated abdominal viscus.

Upper GI Endoscopy

  • Upper GI Endoscopy is considered investigation of choice for diagnosing and assessing the source of UGIB.[73][74][75]
  • The American Society of Gastrointestinal Endoscopy guidelines recommend that upper gastrointestinal endoscopy be performed within 24 hours of presentation in all patients with UGIB

Indications

  • Active UGIB
  • Used for biopsy lesions for tissue diagnosis and to treat currently bleeding lesions.

Complications

Complications include

  • Aspiration
  • Esophageal perforation
  • Cardiopulmonary complications secondary to anesthesia
  • Increased bleeding while attempting therapeutic intervention


 
 
 
 
 
If upper GI Endoscopy
undiagnostic[33]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Patient’s hemodynamic stability
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stable
with low volume bleeding
 
 
 
Unstable
with large volume bleeding
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Repeat endoscopy
 
 
 
Surgery
exploration and partial gastrectomy[76]
 

Other Diagnostic studies

In cases where the source of bleeding is unidentified after upper endoscopy, the utilization of subsequent diagnostic modalities depends upon the hemodynamic stability of the patient. Other diagnostic studies include:[77][78][79]

  • CT angiography
  • Catheter angiography
  • Radionuclide imaging
CT angiography Catheter angiography Radionuclide imaging
Bleeding at rates

detection

At least 0.5 mL/min 0.5 to 1.5 mL/min 0.1 mL/min
Indications
  • Hemodynamically stable
  • Endoscopy undiagnostic
  • Endoscopy not feasible due to severe bleeding with hemodynamic instability
  • Persistent or recurrent GI bleeding
  • Non-diagnostic upper endoscopy
Advantages
  • Minimally invasive 
  • Demonstrate neoplasms or vascular malformations
  • Can provide evidence of recent bleeding
  • Diagnostic and therapeutic
  • Allows for infusion of vasoconstrictive drugs and/or embolization.
  • Does not require bowel preparation. 
  • Most sensitive imaging modality for GI bleeding
  • More commonly utilized for investigation of patients with obscure, intermittent bleeding
Disadvantages
  • Lacks therapeutic capability
  • Risk of contrast induced nephropathy in patients with renal impairment and contrast allergy
  • Access-site hematoma or pseudoaneurysm
  • Arterial dissection
  • Spasm, bowel ischemia
  • Contrast-induced nephropathy or allergic reaction
  • Poor anatomic localization of the bleeding site
  • Unable to diagnose the pathological cause of GI bleeding

Differentiating UGIB

Blood that originates from the oro-pharynx, if swallowed, can present as melena, leading to a false concern of a gastrointestinal source. Examination of nasal area and mouth will help to identify source of bleeding.[80][81][82][83][84][85][86]

History Physical Examination Laboratory Results
Peptic ulcer disease
  • Dyspepsia
  • Early satiety
  • NSAID use
  • Previous ulcer disease
  • Hematemesis
  • Possible hematochezia, melena
  • Hemodynamic instability
    • Tachycardia
    • Hypotension
  • Decreased hemoglobin
  • Increased BUN/creatinine
  • Increased WBC's
  • Helicobacter pylori positive
Mallory-Weiss tear
  • Vomiting/retching
  • Weakness
  • Dizziness
  • Hematemesis
  • Possible hematochezia, melena
  • Hemodynamic instability
    • Tachycardia
    • Hypotension
  • Decreased hemoglobin
  • Increased creatinine
  • Increased WBCs
Stress gastritis
  • History of head injury, severe burns, trauma
  • Mechanical intubation
  • Chronic steroid use
  • Coagulopathy
  • Hematemesis (coffee grounds more common)
  • Melena
  • Decreased hemoglobin
  • Increased WBCs
Dieulafoy lesion
  • Dyspepsia
  • Weakness
  • Dizziness, syncope,
  • May have no prior history before bleed.
  • Hematemesis (bright red)
  • Hematochezia or melena
  • Hemodynamic instability
  • Decreased hemoglobin
  • Decreased hematocrit
  • Increased WBCs
Gastro-esophageal

varices

  • Alcohol/tobacco use,
  • Weakness, dizziness, syncope
  • Stigmata of chronic liver disease
  • Hematemesis, hematochezia or melena
  • Hemodynamic instability
  • Decreased hemoglobin
  • Decreased hematocrit
  • Electrolyte abnormalities
  • Increased bilirubin/liver enzymes
Gastric cancer
  • Alcohol/tobacco use
  • Often asymptomatic
  • Hematemesis,
  • Melena,
  • Lymphadenopathy
    • Palpable supraclavicular or anterior axillary lymph node
    • Palpable firm stomach
  • Decreased hemoglobin
  • Electrolyte abnormalities
  • May have elevated CEA or CA 19-9
Hemobilia
  • Recent trauma
  • Bliary tree instrumentation
  • Gallstones
  • RUQ abdominal pain
  • Jaundice
  • Hematemesis, melena
  • Decreased hemoglobin,
  • Increased bilirubin
  • Increased WBCs
Aortoduodenal

fistula

  • Abdominal pain
  • Back pain
  • History of AAA repair
  • May be asymptomatic
  • Hematemesis or melena (herald bleed)
  • Pulsatile abdominal mass
  • Decreased hemoglobin
  • Increased WBCs

Management

The management of GI bleeding includes

  • Initial resuscitation and pharmacotherapy
  • Risk stratification
  • Surgery
    • Pre-endoscopy management
      • Initial management of antithrombotic agents (anticoagulants and antiplatelet agents)
      • Pharmacological therapy
      • Role of gastric lavage and prophylactic endotracheal intubation
      • Timing of endoscopy
    • Endoscopic management
      • Endoscopic diagnosis
      • Endoscopic therapy
  • Management following endoscopy/endoscopic hemostasis

Initial resuscitation

  • The initial steps in the management of a patient with UGIB is to assess the severity of bleeding, and then institute fluid and blood resuscitation as needed.[87][88][17]
  • Any patient with hemodynamic instability or who is actively bleeding should be admitted to the ICU for monitoring and resuscitation
  • The patient’s hemodynamic status is of great importance in determining the degree of severity and triage status.

Criteria for Admission of patient

  • Age >60yr
  • Transfusion required.
  • Initial Sys BP < 100.
  • Red blood in NG lavage.
  • History of cirrhosis or ascites on examination.
  • The rate of fluid resuscitation is proportional to the severity of bleeding with the goal of restoring and maintaining the patient’s blood pressure.
  • Two large caliber (16-gauge or larger) peripheral catheters or a central venous line should be inserted in patients who are hemodynamically unstable. *Supportive care includes administration of supplemental oxygen and monitoring of urine output.
  • Patients with severe bleeding will need to be transfused; the indications for transfusion in patients with less severe bleeding should be based on the patient’s age and presence of comorbid conditions.
  • The target hematocrit value varies according to age and clinical conditions.
    • In the elderly patient, the target hematocrit is 30%.
    • In younger, healthy patients, the target hematocrit is 25%.
    • In patients with portal hypertension, the target hematocrit should not be above 27% or 28%, so as not to raise portal venous pressure.
  • Fresh frozen plasma, platelets, or both should be given to patients with coagulopathy who are actively bleeding and to those who have received more than 10 units of packed erythrocytes
WORKUP AND INITIAL TREATMENT

Initial Resuscitation

Basic ABC
  • Airway Breathing, Circulation
Ensure patent and protected airway
  • Intubate if needed
  • Consider mechanical ventilation

2 large-bore, peripheral intravenous lines

  • Can consider large-bore central venous catheter or intraosseous line if rapid transfuser will be needed
  • Resuscitate with 1:1:1 of packed red blood cells (PRBCs) to fresh frozen plasma (FFP) to platelets.

Consider massive transfusion protocol

Resuscitate to a target hemoglobin of 7 mg/dL.

Consider Sengstaken-Blakemore tube for control of immediately life-threatening upper GI bleeding

  • The National Institute for Health and Care Excellence (NICE) guidline on blood product management in upper GI bleeding:
  • Platelets should only be given if the patient is actively bleeding or hemodynamically unstable and has a platelet count of <50×109/L.
  • Fresh frozen plasma should be given if the fibrinogen level is <1 g/L or the prothrombin time (PT) or activated partial thromboplastin time is >1.5 times normal.
  • Prothrombin complex should be provided to those on warfarin and actively bleeding.
  • Recombinant factor VIIa should only be used when all of the above measures have failed.

Endoscopic intervention

  • In UGIB, diagnostic and therapeutic endoscopy may be performed simultaneously.
  • Therapeutic upper gastrointestinal endoscopy should be performed in all patients with suspected UGIB to evaluate and possibly treat the source of bleeding.
  • The urgency of endoscopy depends on the anticipated source of bleeding, rapidity of blood loss, and hemodynamic stability of the patient.
  • Endoscopic intervention should be undertaken within 24 hours, as early intervention is associated with reduced transfusion needs and a decreased length of stay in high-risk patients with nonvariceal bleeding.

Endoscopic procedures

  • The most common procedures used to manage bleeding caused by peptic ulcer disease are injection, coagulation (thermal, electric, and argon plasma), and hemostatic clips.
  • The most common procedures used to manage esophageal varices are sclerotherapy and variceal band ligation
  • There is evidence supporting the use of two different endoscopic procedures, rather than a single procedure to better control bleeding and decrease the incidence of rebleeding
  • Other successful methods for controlling bleeding are available when endoscopy fails:
    • Balloon tamponade and TIPS are temporizing measures for patients with actively bleeding esophageal varices who cannot be managed endoscopically.
    • Emergency surgery for bleeding peptic ulcers that cannot be managed endoscopically involves oversewing of the ulcer to ligate the bleeding artery plus truncal vagotomy to decrease acid secretion and pyloroplasty to improve gastric drainage.
Endoscopic band ligation (EBL)
  • EBL involves the placement of elastic circular ring ligatures around the varices to cause strangulation, while the patient is under sedation and analgesia. *Bands are typically delivered at the gastroesophageal junction first, then proximally; six to ten bands may be delivered with a single intubation.
  • The primary drawback of EBL is that during active bleeding, operator visibility is limited by the device holding the bands prior to their delivery. *Endotracheal intubation is prudent in patients with active bleeding to reduce the risk of aspiration pneumonia.
  • Systemic antibiotics should be considered in patients with ascites to reduce the risk of bacterial infection
  • Follow-up endoscopies are recommended at various intervals depending on the size/appearance of varices and severity of liver disease.
  • Typically, visits every 2 to 4 weeks until obliteration. An interval of 1 to 3 months is recommended for initial surveillance of recurrence of varices, then every 6 to 12 months
  • Endoscopic therapy can halt bleeding in 80% to 90% of patients
  • EBL is equivalent to EIS in establishing initial control of bleeding, but EBL is challenging in the actively bleeding patient
  • EBL is widely favored over EIS for primary prevention due to similar or superior efficacy with fewer complications

Endoscopic injection sclerotherapy (EIS)

  • Comprises endoscopic delivery of a sclerosant, such as ethanol, morrhuate sodium, polidocanol, or sodium tetradecyl sulfate, while patient is under sedation and analgesia.
  • Injections may be intravariceal or be delivered into the esophageal wall near the varices.
  • Bucrylate is an adhesive that has been used successfully.
  • Typical injection volume is 1 to 2 mL per injection, for a total volume of 10 to 15 mL. Interval between injections varies according to patient tolerance and response, and complications
  • After an initial injection to control bleeding, there is usually a follow-up injection 2 to 3 days later, followed by weekly or biweekly procedures until complete obliteration of the varices is achieved, which usually takes five or six sessions
 
 
 
 
Acute GI bleeding
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Initial evaluation and resuscitation
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Uppe GI endoscopy
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Source found
 
 
 
Undiagnostic
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Specific Treatment
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Unstable
 
 
 
 
 
Stable
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Urgent CT
 
 
 
 
 
Repeat Endoscopy/Angiograpghy
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
No source identified
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Angioembolization
 
Endoscopic intervention
 
TIPS
 
Surgery
 
 
 
 
Surgery
(Laprotomy)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Sclerotherapy
 
Banding
 
Injection
 
Thermocoagulation
 
Clips

Pharmacotherapy

Correlation between physical signs and

the severity of upper gastrointestinal bleeding

Physical signs Bleeding severity
Mild Moderate Severe
Blood loss <1L 1-2L >2L
Systolic blood pressure <120 100-119 <99
Orthostasis - - +
Tachycardia <100 101-120 >140
Skin Warm, well perfused Diaphoretic Cool–cold, clammy
Urine output(ml/hour) >25 10-25 Negligible
Respiratory rate 14-20 20-30 >35
Sensorium Alert Anxious Confused/Drowsy

Physical examination

Common physical exam findings include:

Vitals

  • Hypotension
  • Tachycardia
  • Thready pulse
  • Hypoxia

Abdomen

  • +Bowel sounds
  • Abdominal tenderness
  • Hepatomegaly
  • Splenomegaly
  • Caput medusa
  • Spider angiomata

Skin

  • Palmar erythema
  • Cold clammy extremities

Neurological examination

  • Altered sensations
  • Poor mentation
  • Drowsiness

Rectal examination

  • Occult blood
  • Gross blood
    • Bright red blood per rectum
    • Melena
    • Burgundy stools
    • Blood coating stools versus within stools
    • Bloody diarrhea

Surgery

Surgical options for upper GI bleeding
Disease Process Surgical Options
Peptic ulcer disease Oversew
3-point ligation of gastroduodenal artery
Vagotomy and pyloroplasty
Vagotomy and antrectomy
Highly selective vagotomy
Mallory-Weiss tear Oversew
Dieulafoy lesion Oversew
Wedge resection
Varices Portacaval shunt
Mesocaval shunt
Distal splenorenal shunt
Gastric cancer Distal gastrectomy
Total gastrectomy
D2 lymphadenectomy
Hemobilia Selective ligation
Resection of aneurysm
Nonselective ligation
Liver resection
Aortoduodenal fistula Angiography and stent (if hemodynamically stable)
Open repair
Extra-anatomic bypass

TIPS

TIPS is a complex nonsurgical shunt which involves insertion of an expandable metal stent that bridges the hepatic vein and an intrahepatic branch of the portal vein. TIPS can halt bleeding in almost all patients, including those with bleeding refractory to other therapies.
Indications

  • For treatment of bleeding varices that are refractory to banding or sclerosant injection.
  • For treatment of refractory variceal bleeding as a bridge to liver transplantation.

Procedure

  • TIPS involves the percutaneous puncture of the right internal jugular vein and insertion of a vascular sheath into the inferior vena cava and the hepatic vein.
  • A needle is inserted through the sheath, into the liver parenchyma, and then into the portal vein.
  • Aspiration of blood and injection of contrast media ensure accurate placement.
  • An angioplasty balloon catheter is used to dilate the tract between the hepatic and portal veins, and a stent is then placed across the tract.
  • Portal venography is used to confirm the placement
  • Patients should be monitored closely for bleeding for 12 to 24 hours

Complications

  • Hepatic encephalopathy
  • Hemolytic anemia
  • Intra-abdominal bleeding during stent placement

Balloon tamponade

Balloon tamponade is only used as a temporary measure in patients who fail to respond to pharmacologic and endoscopic intervention. Balloon tamponade stabilizes patients until more definitive treatment can be instituted (TIPS or liver transplantation).
Procedure

  • Balloon tamponade involves the passage of a specialized nasogastric tube, fitted with an inflatable balloon.
  • When the balloon is inflated, direct pressure staunches bleeding by compressing the varices.
  • Controls active bleeding in 80% to 90% of patients although rebleeding after balloon deflation is common.

Indications

  • For bleeding varices that are refractory to banding or sclerosant injection.

Complications

  • Rebleeding upon balloon deflation
  • Esophageal rupture

Emergency laparotomy

Emergency laparotomy is performed as a last resort for complications such as bleeding and perforation. Emergency laparotomy involving open exploration of the abdomen, oversewing of the ulcer (to ligate the bleeding artery), plus truncal vagotomy (to decrease acid secretion) and pyloroplasty (for improved gastric drainage).
Indications

  • Treatment of bleeding ulcer that cannot be managed with endoscopy
  • Treatment of patients who cannot tolerate endoscopy

Complications

  • Risks of major surgery and general anesthesia
Classification of pain in the abdomen based on etiology Disease Clinical manifestations Diagnosis Comments
Symptoms Signs
Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging
Abdominal causes Inflammatory causes Pancreato-biliary disorders Acute suppurative cholangitis RUQ + + + + − − − − + + + N
  • Abnormal LFT
  • WBC >10,000
  • Ultrasound shows biliary dilatation/stents/tumor
  • Septic shock occurs with features of SIRS
Acute cholangitis RUQ + − − + − − − − − − − N
  • Ultrasound shows biliary dilatation/stents/tumor
  • Biliary drainage (ERCP) + IV antibiotics
Acute cholecystitis RUQ + − + + − − − − − − − Hypoactive Ultrasound shows:
  • Gallstone
  • Inflammation
Acute pancreatitis Epigastric + − + ± − − + − ± − − N
  • Ultrasound shows evidence of inflammation
  • CT scan shows severity of pancreatitis
  • Pain radiation to back
Chronic pancreatitis Epigastric − − ± ± − + + − − − − N
  • Increased amylase / lipase
  • Increased stool fat content
  • Pancreatic function test
 CT scan
  • Calcification
  • Pseudocyst
  • Dilation of main pancreatic duct
  • Predisposes to pancreatic cancer
Pancreatic carcinoma Epigastric − − + + − + + − − − − N

Skin manifestations may include:

Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Primary biliary cirrhosis RUQ/Epigastric − − − + − − − − − − − N
  • Increased AMA level, abnormal LFTs
  • ERCP
  • Pruritis
Primary sclerosing cholangitis RUQ + − − + − − − − − − − N ERCP and MRCP shows
  • Multiple segmental strictures
  • Mural irregularities
  • Biliary dilatation and diverticula
  • Distortion of biliary tree
  • The risk of cholangiocarcinoma in patients with primary sclerosing cholangitis is 400 times higher than the risk in the general population.
Cholelithiasis RUQ/Epigastric ± − ± ± − − − − − − − Normal to hyperactive for dislodged stone
  • Fatty food intolerance
Gastric causes Peptic ulcer disease Diffuse ± − + − − − + Positive if perforated Positive if perforated Positive if perforated N
  • Ascitic fluid
    • LDH > serum LDH
    • Glucose < 50mg/dl
    • Total protein > 1g/dl
Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Gastritis Epigastric ± − + − − − Positive in chronic gastritis + − − − N
Gastroesophageal reflux disease Epigastric − − ± − − − − − − − − N N
  • Gastric emptying studies
Gastric outlet obstruction Epigastric − − ± − − − + − − − − Hyperactive
  • Succussion splash
Gastroparesis Epigastric − − + − − − + − ± − − Hyperactive/hypoactive
  • Scintigraphic gastric emptying
  • Succussion splash
  • Single photon emission computed tomography (SPECT)
  • Full thickness gastric and small intestinal biopsy
Gastrointestinal perforation Diffuse + ± - ± − − − + + + ± Hyperactive/hypoactive
  • WBC> 10,000
Dumping syndrome Lower and then diffuse − − + − − + + − + − − Hyperactive
  • Postgastrectomy
Intestinal causes Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Acute appendicitis Starts in epigastrium, migrates to RLQ + Positive in pyogenic appendicitis + − − ± − − Positive in perforated appendicitis + + Hypoactive
  • Ct scan
  • Ultrasound
  • Positive Rovsing sign
  • Positive Obturator sign
  • Positive Iliopsoas sign
Acute diverticulitis LLQ + ± + − + ± − + Positive in perforated diverticulitis + + Hypoactive
  • CT scan
  • Ultrasound
Inflammatory bowel disease Diffuse ± − − ± − + + + − − − Normal or hyperactive

Extra intestinal findings:

Irritable bowel syndrome Diffuse − − − − ± ± + − − − − N Normal Normal Symptomatic treatment
Whipple's disease Diffuse ± − − ± − + + − ± − − N Endoscopy is used to confirm diagnosis.

Images used to find complications

Extra intestinal findings:
Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Toxic megacolon Diffuse + − − − − + − − + ± + Hypoactive CT and Ultrasound shows:
  • Loss of colonic haustration
  • Hypoechoic and thickened bowel walls with irregular internal margins in the sigmoid and descending colon
  • Prominent dilation of the transverse colon (>6 cm)
  • Insignificant dilation of ileal bowel loops (diameter >18 mm) with increased intraluminal gas and fluid
Tropical sprue Diffuse + − − − − + + − − − − N Barium studies:
  • Dilation and edema of mucosal folds
Celiac disease Diffuse − − − − − + + − − − − Hyperactive US:
  • Bull’s eye or target pattern
  • Pseudokidney sign
  • Gluten allergy
Infective colitis Diffuse + − ± − − + − + Positive in fulminant colitis ± ± Hyperactive CT scan
  • Bowel wall thickening
  • Edema
Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Colon carcinoma Diffuse/ RLQ/LLQ − − − − ± ± + + ± − −
  • Normal or hyperactive if obstruction present
  • CBC
  • Carcinoembryonic antigen (CEA)
  • Colonoscopy
  • Flexible sigmoidoscopy
  • Barium enema
  • CT colonography 
  • PILLCAM 2: A colon capsule for CRC screening may be used in patients with an incomplete colonoscopy who lacks obstruction
Hepatic causes Viral hepatitis RUQ + − + + − Positive in Hep A and E + − Positive in fulminant hepatitis Positive in acute + N
  • Abnormal LFTs
  • Viral serology
  • US
  • Hep A and E have fecal-oral route of transmission
  • Hep B and C transmits via blood transfusion and sexual contact.
Liver abscess RUQ + + + + − ± + − + + ± Normal or hypoactive
  • US
  • CT
Hepatocellular carcinoma/Metastasis RUQ + − − + − − + − − − −
  • Normal
  • Hyperactive if obstruction present
  • US
  • CT
  • Liver biopsy

Other symptoms:

Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Budd-Chiari syndrome RUQ ± − − ± − − − Positive in liver failure leading to varices − − − N
Findings on CT scan suggestive of Budd-Chiari syndrome include:
Ascitic fluid examination shows:
Hemochromatosis RUQ − − − − − − − Positive in cirrhotic patients − − − N
  • >60% TS
  • >240 μg/L SF
  • Raised LFT
    Hyperglycemia
  • Ultrasound shows evidence of cirrhosis
 Extra intestinal findings:
  • Hyperpigmentation
  • Diabetes mellitus
  • Arthralgia
  • Impotence in males
  • Cardiomyopathy
  • Atherosclerosis
  • Hypopituitarism
  • Hypothyroidism
  • Extrahepatic cancer
  • Prone to specific infections
Cirrhosis RUQ − − − + − − + + + − − N US
  • Stigmata of liver disease
  • Cruveilhier- Baumgarten murmur
Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Peritoneal causes Spontaneous bacterial peritonitis Diffuse + − − Positive in cirrhotic patients − + − − ± + + Hypoactive
  • Ascitic fluid PMN>250 cells/mm³
  • Culture: Positive for single organism
  • Ultrasound for evaluation of liver cirrhosis
Renal causes Pyelonephritis Unilateral + ± + − − − − − + − − Hypoactive
  • Urinalysis
  • Urine culture
  • Blood culture
  • CT
  • MRI
  • CVA tenderness
Renal colic Flank pain − − + − − − − − − − − N
  • Ultrasound
  • CT scan
Hollow Viscous Obstruction Small bowel obstruction Diffuse + − + − + − + − + + ± Hyperactive then absent Abdominal X ray
  • Dilated loops of bowel with air fluid levels
  • Gasless abdomen
  • "Target sign"– , indicative of intussusception
  • Venous cut-off sign" – suggests thrombosis
Volvulus Diffuse - − + − + − − − Positive in perforated cases + + Hyperactive then absent CT scan and abdominal X ray
  • U shaped sigmoid colon
  • "Whirl sign"
Biliary colic RUQ − − + + − − − − − − − N
  • Ultrasound
Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Vascular Disorders Ischemic causes Mesenteric ischemia Periumbilical Positive if bowel becomes gangrenous − + − − + + + Positive if bowel becomes gangrenous Positive if bowel becomes gangrenous − Hyperactive to absent CT angiography
  • SMA or SMV thrombosis
  • Also known as abdominal angina that worsens with eating
Acute ischemic colitis Diffuse + ± + − − + + + + + + Hyperactive then absent Abdominal x-ray
  • Distension and pneumatosis

CT scan

  • Double halo appearance, thumbprinting
  • Thickening of bowel
  • May lead to shock
Hemorrhagic causes Ruptured abdominal aortic aneurysm Diffuse ± − + − − − + + + − − N
  • Focused Assessment with Sonography in Trauma (FAST) 
  • Unstable hemodynamics
Intra-abdominal or retroperitoneal hemorrhage Diffuse ± − ± − − − − + + − − N
  • ↓ Hb
  • ↓ Hct
  • CT scan
Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Gynaecological Causes Tubal causes Torsion of the cyst/ovary RLQ / LLQ − − + − − − − − − ± ± N
  • Ultrasound
  • Sudden onset & severe pain
Acute salpingitis RLQ / LLQ + ± − − − − − − − ± ± N
Cyst rupture RLQ / LLQ − − + − − − − − + ± ± N
  • Ultrasound
Pregnancy Ruptured ectopic pregnancy RLQ / LLQ − − + − − − − − + + + N
  • Ultrasound
 History of
  • Missed period
  • Vaginal bleeding
Extra-abdominal causes Pulmonary disorders Pleural empyema RUQ/Epigastric + ± − − − − + − − − − N Chest X-ray
  • Pleural opacity
  • Localization of effusion
 Physical examination
Pulmonary embolism RUQ/LUQ ± − − − − − − − ± − − N
  • ABGs
  • D-dimer
  • Dyspnea
  • Tachycardia
  • Pleuretic chest pain
Pneumonia RUQ/LUQ + + + − − ± − − + − − Normal or hypoactive
  • ABGs
  • Leukocytosis
  • Pancytopenia
  • CXR
  • CT chest
  • Bronchoscopy
  • Shortness of breath
  • Cough
Cardiovascular disorders Myocardial Infarction Epigastric ± − + − − − − − Positive in cardiogenic shock − − N ECG

Echocardiogram

  • Wall motion abnormality
  • Wall rupture
  • Septal rupture
  • Chest pain, tightness, diaphoresis

Complications:

The following is a list of diseases that present with acute onset severe lower abdominal pain:

Disease Findings
Ectopic pregnancy History of missed menses, positive pregnancy test, ultrasound reveals an empty uterus and may show a mass in the fallopian tubes.[89]
Appendicitis Pain localized to the right iliac fossa, vomiting, abdominal ultrasound sensitivity for diagnosis of acute appendicitis is 75% to 90%.[90]
Rupturedovarian cyst Usually spontaneous, can follow history of trauma, mild chronic lower abdominal discomfort may suddenly intensify, ultrasound is diagnostic.[91]
Ovarian cyst torsion Presents with acute severe unilateral lower quadrant abdominal pain, nausea and vomiting, tender adnexal mass palpated in 90%, ultrasound is diagnostic.[92]
Hemorrhagic ovarian cyst Presents with localized abdominal pain, nausea and vomiting. Hypovolemic shock may be present, abdominal tenderness and guarding are physical exam findings, ultrasound is diagnostic.[92]
Endometriosis Presents with cyclic pain that is exacerbated by onset of menses, dyspareunia. laparoscopic exploration is diagnostic.[92]
Acute cystitis Presents with features of increased urinary frequency, urgency, dysuria, and suprapubic pain.[93][94]

Diagnosis

  • The presence of renal tubular acidosis (RTA) should be considered in any patient with an otherwise unexplained normal anion gap (hyperchloremic) metabolic acidosis.
  • The first step in the diagnosis of a patient with a reduced serum bicarbonate and elevated chloride concentration is to confirm that metabolic acidosis is present by measuring the blood pH.
  • The next steps in the diagnosis of possible RTA in patients who have a normal anion gap metabolic acidosis are measurement of the urine pH and estimation of urinary ammonium excretion.

Urine PH

  • Patients with normal renal function and normal renal acidification mechanisms who develop metabolic acidosis usually have a urine pH of 5.3 or less.
  • In most cases of distal RTA, the urine pH is persistently 5.5 or higher, reflecting the primary defect in distal acidification, and a urine pH below 5.5 generally excludes distal (but not proximal) RTA.
  • However, the urine pH can be reduced below 5.5 in occasional patients (2 of 17 in one study) with distal RTA.
  • In contrast to the persistently elevated urine pH in distal RTA, the urine pH is variable in proximal RTA, a disorder characterized by diminished proximal bicarbonate reabsorption.
  • The urine pH will be inappropriately elevated if patients with proximal RTA are treated with alkali, increasing the serum bicarbonate concentration enough to produce a filtered bicarbonate load that exceeds the reduced proximal reabsorptive capacity; this most commonly occurs when alkali is given for the diagnosis or treatment of this disorder.
  • In patients presenting with a normal anion gap metabolic acidosis, two scenarios can produce a misleading elevation in the urine pH that incorrectly suggests the presence of RTA:
    • Urinary tract infections with urea-splitting organisms may increase the urine pH because urea is converted to ammonia and bicarbonate.
      • Thus, assessment of the urine pH should include a urinalysis and, if indicated, a urine culture.
    • Severe volume depletion (which indirectly and reversibly limits hydrogen ion secretion by reducing distal sodium delivery) can impair urine acidification.
      • Thus, reliable interpretation of an inappropriately high urine pH requires that the urine sodium concentration be greater than 25 meq/L.

Urine ammonium excretion

  • Urine ammonium excretion is reduced in distal RTA Thus, either direct measurement or indirect estimation of the urine ammonium concentration can be helpful in establishing the correct diagnosis.
  • Urinary NH4 excretion cannot be directly measured in most clinical laboratories. However, an indirect estimate can be obtained by measurement of the urine anion gap and/or the urine osmolal gap.
  • Estimation of NH4 excretion is not useful in patients with proximal RTA.

References

  1. ↑ 1.0 1.1 Drini M (2017). "Peptic ulcer disease and non-steroidal anti-inflammatory drugs". Aust Prescr. 40 (3): 91–93. doi:10.18773/austprescr.2017.037. PMC 5478398. PMID 28798512.
  2. ↑ Pilotto A, Franceschi M, Leandro G, Paris F, Niro V, Longo MG, D'Ambrosio LP, Andriulli A, Di Mario F (2003). "The risk of upper gastrointestinal bleeding in elderly users of aspirin and other non-steroidal anti-inflammatory drugs: the role of gastroprotective drugs". Aging Clin Exp Res. 15 (6): 494–9. PMID 14959953.
  3. ↑ Hreinsson JP, Kalaitzakis E, Gudmundsson S, Björnsson ES (2013). "Upper gastrointestinal bleeding: incidence, etiology and outcomes in a population-based setting". Scand. J. Gastroenterol. 48 (4): 439–47. doi:10.3109/00365521.2012.763174. PMC 3613943. PMID 23356751.
  4. ↑ Kaviani MJ, Pirastehfar M, Azari A, Saberifiroozi M (2010). "Etiology and outcome of patients with upper gastrointestinal bleeding: a study from South of Iran". Saudi J Gastroenterol. 16 (4): 253–9. doi:10.4103/1319-3767.70608. PMC 2995092. PMID 20871188.
  5. ↑ Davidson AT (1985). "Upper gastrointestinal bleeding: causes and treatment". J Natl Med Assoc. 77 (11): 944–5. PMC 2571206. PMID 4078920.
  6. ↑ 6.0 6.1 6.2 van Leerdam ME (2008). "Epidemiology of acute upper gastrointestinal bleeding". Best Pract Res Clin Gastroenterol. 22 (2): 209–24. doi:10.1016/j.bpg.2007.10.011. PMID 18346679.
  7. ↑ Morales Uribe CH, Sierra Sierra S, Hernández Hernández AM, Arango Durango AF, López GA (2011). "Upper gastrointestinal bleeding: risk factors for mortality in two urban centres in Latin America". Rev Esp Enferm Dig. 103 (1): 20–4. PMID 21341933.
  8. ↑ Rodríguez-Hernández H, Rodríguez-Morán M, González JL, Jáquez-Quintana JO, Rodríguez-Acosta ED, Sosa-Tinoco E, Guerrero-Romero F (2009). "[Risk factors associated with upper gastrointestinal bleeding and with mortality]". Rev Med Inst Mex Seguro Soc (in Spanish; Castilian). 47 (2): 179–84. PMID 19744387.
  9. ↑ Corzo Maldonado MA, Guzmán Rojas P, Bravo Paredes EA, Gallegos López RC, Huerta Mercado-Tenorio J, Surco Ochoa Y, Prochazka Zárate R, Piscoya Rivera A, Pinto Valdivia J, De los Ríos Senmache R (2013). "[Risk factors associated to mortality by upper GI bleeding in patients from a public hospital. A case control study]". Rev Gastroenterol Peru (in Spanish; Castilian). 33 (3): 223–9. PMID 24108375.
  10. ↑ Soldatov IB, Tokman AS, Esipovich I (1967). "[On the forms of dissemination of advanced experience of otorhinolaryngologists in dispensary work]". Zdravookhr Ross Fed (in Russian). 11 (4): 19–21. PMID 5192276. Vancouver style error: initials (help)
  11. ↑ Hudzik B, Wilczek K, Gasior M (2016). "Heyde syndrome: gastrointestinal bleeding and aortic stenosis". CMAJ. 188 (2): 135–8. doi:10.1503/cmaj.150194. PMC 4732965. PMID 26124230.
  12. ↑ Kim BS, Li BT, Engel A, Samra JS, Clarke S, Norton ID, Li AE (2014). "Diagnosis of gastrointestinal bleeding: A practical guide for clinicians". World J Gastrointest Pathophysiol. 5 (4): 467–78. doi:10.4291/wjgp.v5.i4.467. PMC 4231512. PMID 25400991.
  13. ↑ 13.0 13.1 13.2 Bull-Henry K, Al-Kawas FH (2013). "Evaluation of occult gastrointestinal bleeding". Am Fam Physician. 87 (6): 430–6. PMID 23547576.
  14. ↑ Jafar W, Jafar A, Sharma A (2016). "Upper gastrointestinal haemorrhage: an update". Frontline Gastroenterol. 7 (1): 32–40. doi:10.1136/flgastro-2014-100492. PMC 5369541. PMID 28839832. Vancouver style error: initials (help)
  15. ↑ Palmer K (2007). "Acute upper gastrointestinal haemorrhage". Br. Med. Bull. 83: 307–24. doi:10.1093/bmb/ldm023. PMID 17942452.
  16. ↑ Lau JY, Chung S (2000). "Management of upper gastrointestinal haemorrhage". J. Gastroenterol. Hepatol. 15 Suppl: G8–12. PMID 11100986.
  17. ↑ 17.0 17.1 Gralnek IM, Dumonceau JM, Kuipers EJ, Lanas A, Sanders DS, Kurien M, Rotondano G, Hucl T, Dinis-Ribeiro M, Marmo R, Racz I, Arezzo A, Hoffmann RT, Lesur G, de Franchis R, Aabakken L, Veitch A, Radaelli F, Salgueiro P, Cardoso R, Maia L, Zullo A, Cipolletta L, Hassan C (2015). "Diagnosis and management of nonvariceal upper gastrointestinal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) Guideline". Endoscopy. 47 (10): a1–46. doi:10.1055/s-0034-1393172. PMID 26417980.
  18. ↑ Brooks J, Warburton R, Beales IL (2013). "Prevention of upper gastrointestinal haemorrhage: current controversies and clinical guidance". Ther Adv Chronic Dis. 4 (5): 206–22. doi:10.1177/2040622313492188. PMC 3752180. PMID 23997925.
  19. ↑ Yasuda H, Matsuo Y, Sato Y, Ozawa S, Ishigooka S, Yamashita M, Yamamoto H, Itoh F (2015). "Treatment and prevention of gastrointestinal bleeding in patients receiving antiplatelet therapy". World J Crit Care Med. 4 (1): 40–6. doi:10.5492/wjccm.v4.i1.40. PMC 4326762. PMID 25685721.
  20. ↑ Biecker E, Heller J, Schmitz V, Lammert F, Sauerbruch T (2008). "Diagnosis and management of upper gastrointestinal bleeding". Dtsch Arztebl Int. 105 (5): 85–94. doi:10.3238/arztebl.2008.0085. PMC 2701242. PMID 19633792.
  21. ↑ Chan FK (2012). "Anti-platelet therapy and managing ulcer risk". J. Gastroenterol. Hepatol. 27 (2): 195–9. doi:10.1111/j.1440-1746.2011.07029.x. PMID 22142030.
  22. ↑ Garcia-Tsao, Guadalupe; Sanyal, Arun J.; Grace, Norman D.; Carey, William D. (2007). "Prevention and Management of Gastroesophageal Varices and Variceal Hemorrhage in Cirrhosis". The American Journal of Gastroenterology. 102 (9): 2086–2102. doi:10.1111/j.1572-0241.2007.01481.x. ISSN 0002-9270.
  23. ↑ Roberts SE, Button LA, Williams JG (2012). "Prognosis following upper gastrointestinal bleeding". PLoS ONE. 7 (12): e49507. doi:10.1371/journal.pone.0049507. PMC 3520969. PMID 23251344.
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