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==Epidemiology==
==Causes==
[[Image:Cortisol-2D-skeletal.png|thumb|[[Cortisol]]]][[Image:Aldosterone-2D-skeletal.png|thumb|[[Aldosterone]]]]
===Common causes===
===Incidence===
*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.<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>
*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 .<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>
*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 <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>
** 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.<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
 
==Risk factors==
*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>
*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.
{| 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


United States
* Bleeding from the bile duct due to
The prevalence of Addison disease is 40-60 cases per 1 million population.
** Liver biopsy
===Mortality/Morbidity===
** Trauma
** Arteriovenous malformations
** Liver tumors
|}


Morbidity and mortality associated with Addison disease usually are due to failure or delay in making the diagnosis or a failure to institute adequate glucocorticoid and mineralocorticoid replacement. [6]
===Associated Conditions===
If not treated promptly, acute addisonian crisis may result in death. This may be provoked either de novo, such as by adrenal hemorrhage, or in the setting of an acute event superimposed on chronic or inadequately treated adrenocortical insufficiency.
*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>
With slow-onset chronic Addison disease, significant low-level, nonspecific, but debilitating, symptomatology may occur.
Even after diagnosis and treatment, the risk of death is more than 2-fold higher in patients with Addison disease. Cardiovascular, malignant, and infectious diseases are responsible for the higher mortality rate. [7]
White and Arlt examined the prevalence of and risk factors for adrenal crisis in patients with Addison disease, utilizing a survey of Addison patients in the United Kingdom, Canada, Australia, and New Zealand. The authors' results indicated that approximately 8% of patients diagnosed with Addison disease require annual hospital treatment for adrenal crisis. In addition, the investigators concluded that exposure to gastric infection is the most important risk factor for adrenal crisis in the presence of Addison disease; diabetes and/or asthma [8] concomitant with Addison disease also increase the risk, according to White and Arlt. [9]
A study by Chantzichristos et al indicated that in patients with type 1 or 2 diabetes, those who also have Addison disease have a higher mortality rate than do those with diabetes alone. Over a median follow-up period of 5.9 years, the mortality rate for diabetes patients with Addison disease was 28%, compared with 10% for those without Addison disease. The increase in the estimated relative overall mortality risk was 3.89 for the Addison disease patients compared with the other group. Although cardiovascular deaths accounted for the highest mortality rate in both groups, the death rate from diabetes complications, infectious diseases, and unknown causes was greater in the patients with Addison disease than in those with diabetes alone. [10]
===Race===
Addison disease is not associated with a racial predilection.
===Sex===
Idiopathic autoimmune Addison disease tends to be more common in females and children.
===Age===
The most common age at presentation in adults is 30-50 years, but the disease could present earlier in patients with any of the polyglandular autoimmune syndromes, congenital adrenal hyperplasia (CAH), or if onset is due to a disorder of long-chain fatty acid metabolism.


==Historical perspective==
==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:<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>
*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.<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>
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.


==Classification==
===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>
Adrenal insufficiency disorders may be classified into acute and chronic forms, depending on the timing of presentation and duration and into primary and secondary, depending on the etiology of adrenal insufficiency.
===Based on the duration of symptoms===
'''Acute adrenal insufficiency'''
*Adrenal crisis
'''Chronic adrenal insufficiency'''
*Chronic primary adrenal insufficiency
*Chronic secondary adrenal insufficiency
===Based on etiology===
'''Primary adrenal insufficiency(Addisons disease)'''
*Anatomic destruction of the adrenal gland
*Infection (TB)
*Congenital adrenal hyperplasia
'''Secondary adrenal insufficiency'''
*Hypothalamic-pituitary axis suppression
==Pathology==
Cortisol is normally produced by the adrenal glands, which are located just above the kidneys. It belongs to a class of hormones called glucocorticoids, which affect almost every organ and tissue in the body. Scientists think that cortisol possibly has hundreds of effects in the body. Cortisol's most important job is to help the body respond to stress. Among its other vital tasks, cortisol;


Helps maintain blood pressure and cardiovascular function
==Primary Prevention==
Helps slow the immune system's inflammatory response
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.
Helps balance the effects of insulin in breaking down sugar for energy
===Patients with stress ulcers===
Helps regulate the metabolism of proteins, carbohydrates, and fats
*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>
Helps maintain proper arousal and sense of well-being
===Patients on NSAID, aspirin, or antiplatelet therapy===
Because cortisol is so vital to health, the amount of cortisol produced by the adrenals is precisely balanced. Like many other hormones, cortisol is regulated by the brain's hypothalamus and the pituitary gland, a bean-sized organ at the base of the brain. First, the hypothalamus sends "releasing hormones" to the pituitary gland. The pituitary responds by secreting hormones that regulate growth, thyroid function, adrenal function, and sex hormones such as estrogen and testosterone. One of the pituitary's main functions is to secrete ACTH (adrenocorticotropin), a hormone that stimulates the adrenal glands. When the adrenals receive the pituitary's signal in the form of ACTH, they respond by producing cortisol. Completing the cycle, cortisol then signals the pituitary to lower secretion of ACTH.
*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.


Aldosterone
==Secondary Prevention==
Aldosterone belongs to a class of hormones called mineralocorticoids, also produced by the adrenal glands. It helps maintain blood pressure and water and salt balance in the body by helping the kidney retain sodium and excrete potassium. When aldosterone production falls too low, the kidneys are not able to regulate salt and water balance, causing blood volume and blood pressure to drop.
Effective measures for the secondary prevention of UGIB include discouraging the use of NSAIDS in all patients with a history of UGIB.
===Symptoms===
===Seondary Prevention===
Characteristics of the disease are:
*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>


===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"
!Type of presentation
! colspan="4" |The Glasgow Blatchford Score (GBS)
!Harmone deficiency
|-
!Common symptoms
! colspan="3" |'''Admission risk markers'''
!Less common symptoms
!'''Score'''
|-
| colspan="2" rowspan="4" |'''Blood urea nitrogen level (mg/dl)'''
|  ≥ 18.2 to < 22.4
|2
|-
|  ≥ 22.4 to < 28
|3
|-
|≥ 28 to < 70
|4
|-
|  ≥ 70
|6
|-
| rowspan="5" |'''Hemoglobin level (g/dl)'''
| rowspan="3" |'''Men'''
|   ≥ 12 to < 13
|1
|-
|  ≥ 10 to < 12
|3
|-
|< 10
|6
|-
|-
|Acute adrenal insufficiency
| rowspan="2" |'''Women'''
|Mainly cortisol
|   ≥ 10 to < 12
|
|1
* Sudden penetrating pain in the lower back, abdomen, or legs
|-
* Severe [[vomiting]] and [[diarrhea]]
| < 10
* [[Dehydration]]
|6
* Low blood pressure - [[dizziness]] and [[fainting]]
|-
* [[Loss of consciousness]]
| colspan="2" rowspan="3" |'''Systolic blood pressure (mmHg)'''
|In acute adrenal hemorrhage,
|   ≥ 100 to < 109
* Deteriorates with sudden collapse,
|1
* Abdominal or flank pain,
|-
* Nausea with or without hyperpyrexia.
| ≥ 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
|-
|-
| rowspan="2" |Chronic adrenal insufficiency
|Heart failure
|Primary: Both glucocorticoid, mineralocorticoid
|2
| rowspan="2" |
* Hyperpigmentation (prominent on the sun-exposed areas of the skin, extensor surfaces, knuckles, elbows, knees)
* Progressive weakness, fatigue, poor appetite, and weight loss.
* Nausea, vomiting, and occasional diarrhea.
* [[Myalgia|Muscle pains]]
* [[Arthralgia|Joint pains]]
 
| rowspan="2" |
|-
|-
|Secondary: Glucorticoid
| colspan="4" |
Scores of 0-2 -Low-risk group<br>
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.<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>
*The score is based upon
**Age
**Presence of shock
**Comorbidity diagnosis
**Endoscopic ulcer characteristics
**Stigmata of recent hemorrhage.
{| class="wikitable"
{| class="wikitable"
!Symptoms
! colspan="4" |The Rockall score
!Pathophysiology
|-
!
! colspan="3" |Markers
!
!Score
|-
| colspan="2" rowspan="3" |'''Age'''
|<60
|0
|-
|60 - 79
|1
|-
|≥ 80
|2
|-
| rowspan="5" |'''Shock stage'''
| rowspan="3" |Blood pressure
|>120
|0
|-
|100-119
|1
|-
|<100
|2
|-
|-
|Hyperpigmentation
| rowspan="2" |Heart rate
|Stimulant effect of excess ACTH on the melanocytes to produce melanin
|>100
|
|0
|
|-
|-
|Dizziness with orthostasis
|<100
|
|1
* Volume depletion, loss of the mineralocorticoid effect of aldosterone,
 
* Loss of the permissive effect of cortisol in enhancing the vasopressor effect of the catecholamines.
|
|
|-
|-
|Myalgias and flaccid muscle paralysis
| colspan="2" rowspan="3" |'''Comorbidity'''
|Hyperkalemia
|No major comorbidity
|
|0
|
|-
|-
|Amenorrhea
|Cardiac failure
|Combined effect of weight loss and chronic ill health or secondary to premature autoimmune ovarian failure
Ischemic heart disease
|
|
|}
==History==
A detailed and thorough history from the patient is necessary. Specific areas of focus when obtaining a history from the patient of addison's disease include:
*Recent changes in diet: Patients with Addison disease often crave salty foods and are often anorexic.
*Periods regularity: Oligomenorrhea or amenorrhea are features of Addison disease
*Any signs of postural hypotension
*Any recent changes in weight
*History of tuberculosis ? or any exposure to anyone who has been diagnosed with tuberculosis.
*History of any cancer?
*History of other autoimmune disease, such as Graves disease, Hashimoto thyroiditis, hypoparathyroidism, vitiligo , pernicious anemia, or diabetes mellitus
*Family history of Addison's disease or any other adrenal disorder?


==Laboratory==
Any major comorbidity
Evaluating a patient with suspected adrenal insufficiency is a three-step process: establishing the diagnosis, differentiating between primary and secondary adrenal insufficiencies, and looking for the cause of adrenal insufficiency.
|2
{{familytree/start}}
|-
{{familytree | | | | | | | | | A01 | | | | | |A01=8 am cortisol}}
|Renal failure
{{familytree | | | | | | | | | |!| | | | | | | | }}
Liver failure
{{familytree | | |,|-|-|-|-|-|-|+|-|-|-|-|-|-|.| }}
{{familytree | | B01 | | | | | B02 | | | | | B03 |B01=>15Ug/dL|B02=3-15Ug/dL|B03=<3Ug/dL}}
{{familytree | | |!| | | | | | |!| | | | | | |!| }}
{{familytree | | I01 | | | | | |!| | | | | | I02 | I01=Adrenal insufficiency is <br>ruled out|I02=Measure ACTH}}
{{familytree | | | | | | | | | C01 | | | | | | |C01= 30 min cortisol during<br>
cosyntropin stimulation test }}
{{familytree | | | | | | | | | |!| | | | | | | | }}
{{familytree | | | | | |,|-|-|-|^|-|-|-|-|.| | | }}
{{familytree | | | | | D01 | | | | | | | D02 | | |D01=>18Ug/dL|D02=<18Ug/dL}}
{{familytree | | | | | |!| | | | | | | | |!| | | }}
{{familytree | | | | | J01 | | | | | | | |!| | |J01=Adrenal insufficiency is ruled out }}
{{familytree | | | | | | | | | | | | | | E01 | | |E01=Adrenal insufficiency confirmed}}
{{familytree | | | | | | | | | | | | | | |!| | | }}
{{familytree | | | | | | | | | | | | | | F01 | | |F01=Measure ACTH}}
{{familytree | | | | | | | | | |,|-|-|-|-|^|-|-|-|-|.|}}
{{familytree | | | | | | | | | G01 | | | | | | | | | G02 |G01=Low/normal|G02=Elevated}}
{{familytree | | | | | | | | | |!| | | | | | | | | |!|}}
{{familytree | | | | | | | | | H01 | | | | | | | | | H02 |H01=Secondary<br> Adrenal insufficiency|H02=Primary<br> Adrenal insufficiency}}


{{familytree/end}}
Disseminated malignancy
|3
|-
| colspan="2" rowspan="3" |'''Diagnosis'''
|Mallory-Weiss tear, no lesion identified and no SRH
|0
|-
|All other diagnosis
|1
|-
|Malignancy of upper GI tract
|2
|-
| colspan="2" rowspan="2" |'''Major SRH'''
|None or dark spot only
|0
|-
|Blood in upper GI tract, adherent clot,<br> visible or spurting vessel
|2
|-
| 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.
|}


==Medical therapy==
==Complications==
==Adrenal crisis===
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>
===Supportive Therapy===
*End-organ damage
*IV access should be established immediately with an infusion of isotonic sodium chloride solution should be begun to restore volume deficit and correct hypotension.
** Cardiac ischemia
===Mecial Management===
** Renal failure
*Preferred regimen (1): Dexamethasone sodium phosphate 4 mg iv q24h
** Ischemic hepatitis
*Preferred regimen (2): Hydrocortisone sodium succinate 50-100 mg iv q8h
** Anoxic brain injury
*Note: Infusion may be initiated with 100 mg of hydrocortisone as an IV bolus with saline and infuse over 24 h to avoid needing to renew the infusion every 8-10 hours.
*Iron-deficiency anemia


The infusion method maintains plasma cortisol levels more adequately at steady stress levels, especially in the small percentage of patients who are rapid metabolizers and who may have low plasma cortisol levels between the IV boluses.
==Classification==
Clinical improvement, especially blood pressure response, should be evident within 4-6 hours of hydrocortisone infusion. Otherwise, the diagnosis of adrenal insufficiency would be questionable.
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>
After 2-3 days, the stress hydrocortisone dose should be reduced to 100-150 mg, infused over a 24-hour period, irrespective of the patient's clinical status. This is to avoid stress gastrointestinal bleeding.
:*'''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>
As the patient improves and as the clinical situation allows, the hydrocortisone infusion can be gradually tapered over the next 4-5 days to daily replacement doses of approximately 3 mg/h (72-75 mg over 24 h) and eventually to daily oral replacement doses, when oral intake is possible.
:*'''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).
As long as the patient is receiving 100 mg or more of hydrocortisone in 24 hours, no mineralocorticoid replacement is necessary. The mineralocorticoid activity of hydrocortisone in this dosage is sufficient.
:*'''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.
Thereafter, as the hydrocortisone dose is weaned further, mineralocorticoid replacement should be instituted in doses equivalent to the daily adrenal gland aldosterone output of 0.05-0.20 mg every 24 hours. The usual mineralocorticoid used for this purpose is 9-alpha-fludrocortisone, usually in doses of 0.05-0.10 mg per day or every other day.
Patients may need to be advised to increase salt intake in hot weather.


hese drugs are used for replacement therapy in Addison disease and secondary adrenocortical insufficiency. [3, 4]
==Epidemiology and Demographics==
Prednisone (Deltasone, Sterapred, Orasone)
===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>


View full drug information
===Gender===
Used for glucocorticoid hormone replacement. Longer acting than hydrocortisone, with a biologic half-life of 18-36 h.
Males are more commonly affected by UGIB than females. The males to female ratio is approximately 2 to 1.
Fludrocortisone (Florinef)


View full drug information
Synthetic adrenocortical steroid with very potent mineralocorticoid activity. For use in Addison disease and states of aldosterone deficiency.
Hydrocortisone sodium succinate or phosphate (Cortef, Hydrocortone)
View full drug information
Drug of choice for steroid replacement in acute adrenal crisis and for daily maintenance in patients with Addison disease or secondary adrenocortical insufficiency. Has both glucocorticoid and mineralocorticoid properties. Biologic half-life is 8-12 h. Easiest way to set up infusion is to have pharmacy mix 100 mg of hydrocortisone in 100 mL of 0.9 saline.
==Surgery==
Parenteral steroid coverage should be used in times of major stress, trauma, or surgery and during any major procedure.
During surgical procedures, 100 mg of hydrocortisone should be given, preferably by the IM route, prior to the start of a continuous IV infusion. The IM dose of hydrocortisone assures steroid coverage in case of problems with the IV access.
When continuous IV infusion is not practical, an intermittent IV bolus injection every 6-8 hours may be used.
After the procedure, the hydrocortisone may be rapidly tapered within 24-36 hours to the usual replacement doses, or as gradually as the clinical situation dictates.
Mineralocorticoid replacement usually can be withheld until the patient resumes daily replacement steroids.
Addison’s disease (also known as primary adrenal insufficiency or hypoadrenalism) is a rare disorder of the adrenal glands. It affects the production of two essential hormones called cortisol and aldosterone.
==PCOS==
==Pathophysiology==
==Pathophysiology==
*Hyperinsulinemia is noted in 50% to 70% of PCOS patients. It is defined as impaired action of insulin on glucose transport and antilipolysis in adipocytes in the presence of normal insulin binding.
===Blood supply of Foregut===
*Hyperinsulinemia causes or exacerbates hyperandrogenemia. Increased insulin levels at the ovarian level lead to increased androgen production from the ovarian thecal cells.
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>
*Also, by suppressing hepatic production of sex hormone binding globulin (SHBG), insulin increases unbound levels of testosterone.
{| class="wikitable"
*At the level of the granulosa cell, insulin amplifies the response of granulosa cells to LH. Thus, these cells undergo abnormal differentiation and premature arrest of follicular growth, and thus anovulation.
! colspan="2" |Foregut
*Elevated androgen levels also lead to decreased levels of SHBG. Greater unbound androgen levels are likely to produce a greater clinical response, such as hirsutism and acne.
!Blood supply
*Most patients with PCOS show evidence of clinical hyperandrogenism.
|-
*In such cases, measurement of free testosterone should be considered, although most direct assays for free testosterone have limited value for evaluating the hyperandrogenic woman. The methods recommended at the consensus meeting to determine free testosterone are by equilibrium dialysis, by calculation of free testosterone from measurement of SHBG and total testosterone, or by ammonium sulfate precipitation. DHEAS may be measured, because a small percentage of patients with PCOS have isolated elevations in this hormone.
| rowspan="3" |'''<u>Esophagus</u>'''
*Another key feature of PCOS is altered gonadotropin dynamics. Several studies have shown higher LH pulse and amplitude in women with PCOS. 
|
*Although a higher LH level drives the ovarian theca cells to produce more androgens, insufficient follicle-stimulating hormone (FSH) may be the more immediate cause of anovulation.
Upper esophageal sphincter<br>
*In most women with PCOS, LH levels are elevated or the LH/FSH ratio is high; however, the mean LH pulse amplitude is attenuated in obese women with PCOS. Thus, the LH value or LH/FSH ratio is not helpful in establishing this diagnosis in such patients.
Cervical esophagus 
 
| Inferior thyroid artery 
===Historical Perspective===
|-
PCOS was first described in 1935 by American gynecologists Irving F. Stein, Sr. and Michael L. Leventhal, from whom its original name of Stein–Leventhal syndrome is taken. The earliest published description of PCOS was in 1721 in Italy. Cyst-related changes to the ovaries were described in 1844.
|Thoracic esophagus
*In 1721, a description symptoms resembling PCOS was published in Italy
|Aortic esophageal arteries or branches of the bronchial arteries 
*In 1844, Cyst-related changes to the ovaries were first described.
|-
*In 1935, Irving F. Stein, Sr. and Michael L. Leventhal, American gynecologists, described PCOS for the first time.
|
===Pathophysiology===
Distal esophagus<br>
*The pathophysiology of PCOS is not well understood. There are several organ systems involved in the pathogenesis of PCOS like ovary, adrenal, hypothalamus, pituitary, or insulin-sensitive tissues. It is possible that there are subsets of women with PCOS wherein each of these proposed mechanisms serves as the primary defect.
Lower esophageal sphincter
*Insulin resistance leads to compensatory insulin hypersecretion by the pancreas in order to maintain normoglycemia.
|Left gastric artery and left phrenic artery 
*The resulting hyperinsulinemia promotes ovarian androgen output and may also promote adrenal androgen output.
|-
*High insulin levels also suppress hepatic production of sex hormone binding globulin (SHBG), which exacerbates hyperandrogenemia by increasing the proportion of free circulating androgens.
| rowspan="3" |'''<u>Stomach</u>'''
*Another factor that promotes ovarian androgen output is the fact that women with PCOS are exposed long term to high levels of LH.
|Lesser curvature
*This LH excess seems to be a result of an increased frequency of gonadotropin releasing hormone pulses from the hypothalamus.  
|Right and left gastric arteries
*The abnormal hormonal milieu also probably contributes to incomplete follicular development which results in polycystic ovarian morphology.
|-
 
|Greater curvature
 
|Right and left gastroepiploic arteries
{{familytree/start |summary=Sample 1}}
|-
{{familytree | | | B01 | | | | | | | | | | |B02| | |B01=↑ 5α-reductase<br>reductivity|B02=↓ Hβ-HSD1<br>activity }}
|Gastric fundus
{{familytree | | | |`|-|-|-|-|-|v|-|-|-|-|-|'| | | | }}
|Short gastric arteries
{{familytree | | | | | | | | | B01 | | | | | |B01=↑ Cortisol<br>metabolism}}
|-
{{familytree | | | | | | | | | |!| | | | | |}}
| rowspan="2" |'''<u>Duodenum</u>'''
{{familytree | | | | | | | | | B01 | | | | | |B01=↑ ACTH}}
|First and second parts
{{familytree | | | | | |,|-|-|-|^|-|-|-|-|.| | | }}
|
{{familytree | | | | | B01 | | | | | | | B02 |B01=↑ Adrenal <br>androgens|B02=Normal serum<br>cortisol}}
Gastroduodenal artery (GDA) and<br>
{{familytree | | | | | |!| | | | | | | | | |}}
Superior pancreaticoduodenal artery
{{familytree | | | | | B01 | | | | | | | | | |B01=PCOS}}
|-
{{familytree/end}}
|Third and fourth parts
 
|Inferior pancreaticoduodenal artery
==Risk Factors==
|}
Common risk factors in the development of polycystic ovary syndrome are
[[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]]
*Hyperinsulinemia secondary to insulin resistance; associated with type 2 diabetes mellitus<ref name="pmid28642705">{{cite journal |vauthors=Sortino MA, Salomone S, Carruba MO, Drago F |title=Polycystic Ovary Syndrome: Insights into the Therapeutic Approach with Inositols |journal=Front Pharmacol |volume=8 |issue= |pages=341 |year=2017 |pmid=28642705 |pmc=5463048 |doi=10.3389/fphar.2017.00341 |url=}}</ref>
===Mucosal barrier===
*Obesity
*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>
*Family history of PCOS among first-degree relatives
*This mucosal barrier consists of three protective components which include:
 
**Layer of epithelial cell lining.
==Associated Conditions==
**Layer of mucus, secreted by surface epithelial cells and foveolar cells.  
Common conditions associated with PCOS are
**Layer of bicarbonate ions, secreted by the surface epithelial cells.
*Type 2 diabetes
[[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]]
*Endometrial hyperplasia and cancer
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>
*Infertility
*Hypertension
*Gestational diabetes
*Preeclampsia
*Hirsutism
*Acne
==History==
Obtaining the history is the most important aspect of making a diagnosis of PCOS. It provides insight into the cause, precipitating factors and associated comorbid conditions.
*Menstrual abnormalities
*Infertility
*Signs of virilization on physical examination
*Family history of PCOS among first-degree relatives
 
==Symptoms==
The most common symptoms of PCOS include
*Amenorrhea or oligomenorrhea
*Abnormal uterine bleeding
*Androgenization, including hirsutism (often slowly progressive), acne, oily skin (common)
*Polycystic ovaries, with or without ovarian enlargement
*Insulin resistance
*Endometrial hyperplasia
==Laboratory Findings==
Measurement of the plasma levels of several hormones is helpful in supporting the diagnosis of PCOS and especially in excluding other disorders. Determining the LH/FSH ratio of 3:1 is virtually diagnostic of PCOS; however, a normal ratio does not exclude the diagnosis, as LH levels fluctuate widely throughout the course of a day. Other androgens are measured to screen for other virilizing adrenal tumors. Fasting blood glucose is measured to look for diabetes; screening for lipid abnormalities is also employed. Testosterone is  measured to exclude a virilizing tumor. Prolactin is measured to exclude a prolactinoma. Thyroid-stimulating hormone (TSH) is measured to rule out hypothyroidism
{| class="wikitable"
{| class="wikitable"
! colspan="2" |Harmone
! colspan="2" |Defense mechanisms of gastric mucosal barrier
!Normal value
!PCOS Laboratory Findings
|-
|-
| colspan="2" |LH/FSH ratio
|Mucus layer
|<3;1
|Forms a protective gel-like coating over the entire gastric mucosal surface
|A ratio >3:1 is indicative of PCOS
|-
|-
| colspan="2" |Testosterone
|Epithelial layer
|Free: 100 to 200 pg/dL
|Epithelial cell layer are bound by tight junctions that repel fluids
|-
|Bicarbonate ions
|Neutralize acids
|}


Total: 20 to 80 ng/dL
===Pathogenesis===
|An elevated free testosterone level (200-400 pg/dL) is suggestive of PCOS,
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
|-
|-
| colspan="2" |Prolactin
|Peptic ulcer disease
|3.8 to 23.2 μg/L
|50%
|A level >300 μg/L is virtually diagnostic of prolactinoma.
|-
|-
| colspan="2" |TSH
|Variceal bleeding
|0.4 to 4.2 mIU/L
|20%
|Levels are normal in patients with PCOS
|-
|-
| rowspan="5" |Androgens
|Esophagitis, gastritis, and duodenitis
|Sex hormone–binding globulin
|10-15%
|1.5 to 2.0 μg/mL
|Decreased
|-
|-
|Androstenedione
|Mallory-Weiss tear
|75 to 205 ng/dL
|15%
|Increased
|-
|-
|Estrone:
|Malignancy
|1.5 to 25.0 pg/mL
|3-5%
|Increased
|-
|-
|Dehydroepiandrosterone sulfate
|Arteriovenous malformation
|50 to 450 μg/dL
|<3%
|Increased but are <800 μg/dL
|-
|-
|17-Hydroxyprogesterone (follicular phase)
|Gastric antral vascular ectasia
|15 to 70 ng/dL
|<1%
|Normal
|-
|-
| colspan="2" |Fasting blood glucose
|Dieulafoy lesion
|<110 mg/dL
|<1%
|>126mg/dL Indicates DM
|}
|}
==Ultrasound findings==
===Pathogenesis===
Typical  ultrasound findings in patients with PCOS include
*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>
*Two- to 5-fold ovarian enlargement
**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>
*Thickened stroma (tunica albuginea)
**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>
*Thecal hyperplasia with an increase in stromal content
**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>
*Multiple (12+) subcapsular follicles ranging from 2 to 9 mm in diameter ('pearl necklace' appearance)
**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>
*Hyperplastic endometrium despite low estrogen production (due to high estrone production from the increased circulating androgens and lack of opposition by progesterone)
**During stress, there is acid hypersecretion; therefore, the breakdown of mucosal defenses leads to injury of the mucosa and subsequent bleeding.
==Epidemiology and demographics==
**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>
===Prevalence===
{{familytree/start}}
*Approximately 5% to 10% of women of reproductive age are affected
{{familytree | | | | | | | | | | A01 | | | | | |A01=NSAIDS}}
*Prevalence among first-degree relatives of patients with PCOS is 25% to 50%, suggesting a strong inheritance of the syndrome; there is evidence for possible X-linked dominant transmission
{{familytree | | | | | | | | | | |!| | | | | | | | }}
 
{{familytree | | | | | | | | | | A01 | | | | | |A01=Inhibits cycloxygenase pathway}}
===Demographics===
{{familytree | | | | | | | | | | |!| | | | | | | | }}
===Age===
{{familytree | | | | | |,|-|-|-|-|^|-|-|-|-|-|.| | | }}
*PCOS can appear anytime from menarche until menopause but generally is seen around menarche and is diagnosed then or in early adulthood
{{familytree | | | | | B01 | | | | | | | | | B02 |B01=COX-1|B02=COX-2}}
==Differentiating PCOS from other diseases==
{{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"
{| class="wikitable"
!Disease
! colspan="2" |
!Differentiating Features
!Gross Pathology
!Microscopic Pathology
|-
|-
|Pregnancy
| 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
|
|
* Pregnancy always should be excluded in a patient with a history of amenorrhea
*Defects in the esophageal squamous mucosa.
 
*Cells of acute inflammation.
* Features include amenorrhea or oligomenorrhea, abnormal uterine bleeding, nausea/vomiting, cravings, weight gain (although not in the early stages and not if vomiting), polyuria, abdominal cramps and constipation, fatigue, dizziness/lightheadedness, and increased pigmentation (moles, nipples)
*Multiple ruptured blood vessels in the lamina propria or submucosa.
 
*Prior lacerations may show various degrees of healing
* Uterine enlargement is detectable on abdominal examination at approximately 14 weeks of gestation
**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>
* Ectopic pregnancy may cause oligomenorrhea, amenorrhea, or abnormal uterine bleeding with abdominal pain and sometimes subtle or absent physical symptoms and signs of pregnancy
**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
|-
|-
|Hypothalamic amenorrhea
|Toxic esophagitis
|
|
* Diagnosis of exclusion
* Mucosal erythema,
* Seen in athletes, people on crash diets, patients with significant systemic illness, and those experiencing undue stress or anxiety
* Edema
* Predisposing features are as follows weight loss, particularly if features of anorexia nervosa are present or the BMI is <19 kg/m2
* Hemorrhage
* Recent administration of depot medroxyprogesterone, which may suppress ovarian activity for 6 months to a year
* Necrosis
* Use of dopamine agonists (eg, antidepressants) and major tranquilizers
|'''<u>Acid injury</u>'''
* Hyperthyroidism
* Coagulative necrosis
* In patients with weight loss related to anorexia nervosa, fine hair growth (lanugo) may occur all over the body, but it differs from hirsutism in its fineness and wide distribution
* Eschar
'''<u>Alkaline injury</u>'''
* Liquefactive necrosis
* Acute inflammation
* Abundant granulation tissue
|-
|-
|Primary amenorrhea
| 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>
|
|
* Causes include reproductive system abnormalities, chromosomal abnormalities, or delayed puberty
|
* If secondary sexual characteristics are present, an anatomic abnormality (eg, imperforate hymen, which is rare) should be considered
* Basal cell hyperplasia
* If secondary sexual characteristics are absent, a chromosomal abnormality (eg, Turner syndrome ) or delayed puberty should be considered
* Elongation of the lamina propria papillae
* Mixed intraepithelial inflammation
* Neutrophils, eosinophils, and lymphocytes
* Squamous cell degeneration.
|-
|-
|Cushing syndrome
| 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>
|
|
* Cushing syndrome is due to excessive glucocorticoid secretion from the adrenal glands, either primarily or secondary to stimulation from pituitary or ectopic hormones; can also be caused by exogenous steroid use
|Columnar metaplasia
 
* Mucinous columnar cells
* Features include hypertension, weight gain (central distribution), acne, and abdominal striae Patients have low plasma sodium levels and elevated plasma cortisol levels on dexamethasone suppression testing
* Goblet cells, and enterocyte-like cells, among others.
* Cells of  acute inflammation
|-
|-
|Hyperprolactinemia
| colspan="2" |Acute Gastritis
|Mucosal hyperemia associated with
* Bleeding
* Erosions
* Ulcers
|
|
* Mild hyperprolactinemia may occur as part of PCOS-related hormonal dysfunction
* Dilation and congestion of mucosal capillaries, edema, and hemorrhage in the lamina propria.
 
* Ischemic-type changes such as
* Other causes include stress, lactation, and use of dopamine antagonists
** Degenerated and necrotic epithelium
* A prolactinoma of the pituitary gland is an uncommon cause and should be suspected if prolactin levels are very high (>200 ng/mL)
** Fibrinoid necrosis
* Physical examination findings are usually normal
** Adherent fibrinopurulent debris
* As in patients with PCOS, hyperprolactinemia may be associated with mild galactorrhea and oligomenorrhea or amenorrhea; however, galactorrhea also can occur with nipple stimulation and/or stress when prolactin levels are within normal ranges
* A large prolactinoma may cause headaches and visual field disturbance due to pressure on the optic chiasm, classically a gradually increasing bitemporal hemianopsia
|-
|-
|Ovarian or adrenal tumor
| 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
|
|
* Benign ovarian tumors and ovarian cancer are rarely causes of excessive androgen secretion; adrenocortical tumors also can increase the production of sex hormones
* Fibrinopurulent debris
* Abdominal swelling or mass, abdominal pain due to fluid leakage or torsion, dyspareunia, abdominal ascites, and features of metastatic disease may be present
* Necrosis
* Features of androgenization include hirsutism, weight gain, oligomenorrhea or amenorrhea, acne, clitoral hypertrophy, deepening of the voice, and high serum androgen (eg, testosterone, other androgens) levels
* Granulation tissue
* In patients with an androgen-secreting tumor, serum testosterone is not suppressed by dexamethasone
|-
|-
|Congenital adrenal hyperplasia
| 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
|
|
* Congenital adrenal hyperplasia is a rare genetic condition resulting from 21-hydroxylase deficiency
* Dilation, tortuosity, and thickening of small submucosal arteries and veins.
* The late-onset form presents at or around menarche Patients have features of androgenization and subfertility
* Mucosal capillaries may also show congestion, dilation, and proliferation.
* Affects approximately 1% of hirsute patients More common in Ashkenazi Jews (19%), inhabitants of the former Yugoslavia (12%), and Italians (6%)
* Associated with high levels of 17-hydroxyprogesterone
* A short adrenocorticotropic hormone stimulation test with measurement of serum17-hydroxyprogesterone confirms the diagnosis Assays of a variety of androgenic hormones help define other rare adrenal enzyme deficiencies, which present similarly to 21-hydroxylase deficiency
|-
|-
|Anabolic steroid abuse
| 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
|
|
* Anabolic steroids are synthetic hormones that imitate the actions of testosterone by increasing muscle bulk and strength
* Increased plasma cells
* Should be considered if the patient is a serious sportswoman or bodybuilder
* Neutrophilic infiltrate
* Features include virilization (including acne and hirsutism), often increased muscle bulk in male pattern, oligomenorrhea or amenorrhea, clitoromegaly, gastritis, hepatic enlargement, alopecia, and aggression
* Reactive epithelial changes, including villous blunting.
* Altered liver function test results are seen
* The surface epithelium usually shows mucous cell (pseudopyloric) metaplasia
|-
|-
|Hirsutism
| colspan="2" |Ischemia
|Hypoperfused ulcers
|'''<u>Acute ischemia</u>'''
* Mucosal edema
* Congestion
* Superficial necrosis
* Coagulative necrosis
'''<u>Chronic ischemia</u>'''
* Fibrosis
* Strictures
|-
| 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>
|Large-caliber artery within the submucosa
|Dilated venules and arteriole in direct communication with each other
|-
| colspan="2" |Inflammatory Bowel Disease
|
|
* Hirsutism is excessive facial and body hair, usually coarse and in a male pattern of distribution
|Lymphoplasmacytic infiltrate with numerous neutrophils
* Approximately 10% of women report unwanted facial hair
* There is often a family history and typically some Mediterranean or Middle Eastern ancestry
* May also result from use of certain medications, both androgens, and others including danazol, glucocorticoids, cyclosporine, and phenytoin
* Menstrual history is normal
* When the cause is genetic, the excessive hair, especially on the face (upper lip), is present throughout adulthood, and there is no virilization
* When secondary to medications, the excessive hair is of new onset, and other features of virilization, such as acne and deepened voice, may be present
|}
|}
==Complications==
*Endometrial hyperplasia
*Endometrial cancer
*Type 2 diabetes and its microvascular and macrovascular complications
==Prognosis==
*The prognosis for fertility is very good with treatment. With careful follow-up, ovarian hyperstimulation, multiple pregnancy, and endometrial hyperplasia can be avoided
*Patients should be counseled regarding the long-term risk of diabetes, hypertension, and endometrial hyperplasia, including the importance of maintaining a BMI <25 kg/m2and control of type 2 diabetes.
==Diagnostic Criteria==
Two definitions are commonly used:
*In 1990 a consensus workshop sponsored by the [[NIH]]/[[NICHD]] suggested that a patient has PCOS if she has
**Signs of [[androgen]] excess (clinical or biochemical)
**[[Oligoovulation]]
**Other entities are excluded  that would cause polycystic ovaries.
*In 2003 a consensus workshop sponsored by [[ESHRE]]/[[ASRM]] in Rotterdam indicated PCOS to be present if 2 out of 3 criteria are met: <ref name="pmid14711538">{{cite journal |vauthors= |title=Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome |journal=Fertil. Steril. |volume=81 |issue=1 |pages=19–25 |year=2004 |pmid=14711538 |doi= |url=}}</ref>
**[[Oligoovulation]] and/or [[anovulation]]
**Excess androgen activity
**Polycystic ovaries (by [[gynecologic ultrasound]]), and other causes of PCOS are excluded.
The Rotterdam definition is wider, including many more patients, notably patients without androgen excess, whereas in the NIH/NICHD definition androgen excess is a prerequisite. Critics maintain that findings obtained from the study of patients with androgen excess cannot necessarily be extrapolated to patients without androgen excess.


==Surgery==
==Diagnosis==
Surgery is not considered first-line therapy for PCOS and it does not affect insulin resistance or obesity
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>
===Indication===
==Initial Laboratory Studies==
Surgery is indicated in the treatment of PCOS only in patients desiring fertility in whom at least 1 year of conservative therapy has failed
*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.


===Surgial options===
==Naso-Gastric Lavage==
'''Ovarian drilling'''
*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>
*Laparoscopic surgery that uses a laser or electrosurgical needle to puncture a number of small follicles visible on the surface of the ovary, which are presumably the source of hormone production
*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.<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===
*Bleeding and/or infection
Complications include
*Postoperative adhesions
*Aspiration
==Medical Therapy==
*Esophageal perforation
The first step in the management of PCOS is weight loss if the patient is obese, and treatment of type 2 diabetes, if present, with metformin. In significantly overweight patients, weight loss alone usually effects a cure and should always be vigorously attempted. Diet and exercise are recommended in all women with PCOS. The next step is initiation of treatment to break the self-perpetuating anovulatory cycling, either by stimulating ovulation or suppressing androgenic and ovarian activity. The selection of treatment depends on whether pregnancy is desired. All antiandrogen treatments will take at least 3 months to affect hirsutism.
*Cardiopulmonary complications secondary to anesthesia
The goals of treatment are:
*Increased bleeding while attempting therapeutic intervention
*Exclude androgen-secreting tumors, endometrial tumors, and endometrial hyperplasia
*Reduce ovarian androgen secretion and/or antagonist activity at target tissues
*Interrupt the self-sustaining abnormal hormonal cycle
*Normalize the endometrium
*Restore fertility by correcting anovulation, if desired
*Reduce insulin resistance
==Medical Management==
===If fertility is not desired===
*Preferred regimen (1): Combined oral contraceptive pills one tablet of formulations containing 30 to 35 μg estrogen orally daily for 21 days, then nothing for 7 days
*Preferred regimen (2): Progesterone-only contraceptive pills (eg, norethindrone , norgestrel ) are the treatment of choice if combined oral contraceptive pills are contraindicated
*Alternative regimen(1): Medroxyprogesterone may be used, although it is not approved by the U.S. Food and Drug Administration (FDA) for this indication
*Alternative regimen(2): Glucocorticoids (eg, hydrocortisone , cortisone , dexamethasone ) may be used to suppress adrenal androgen production, although they are not approved by the FDA for this indication
*Alternative regimen(3): Spironolactone and flutamide are androgen receptor antagonists that may be added to the oral contraceptive pill, but they are not approved by the FDA for this indication; flutamide is not usually recommended because of its unproven efficacy and associated risk of hepatic impairment


===If fertility is desired===
 
*Preferred regimen (1): Clomiphene, alone or in combination with glucocorticoids, is the first-choice treatment
{{Family tree/start}}
*Preferred regimen (2): Follicle-stimulating hormone may be administered in conjunction with timed human chorionic gonadotropin for ovulation induction
{{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>}}
*Preferred regimen (3): Metformin
{{Family tree | | | | | | |!| | | | | }}
==Primary Prevention==
{{Family tree | | | | | | B01 | | | |B01= Patient’s hemodynamic stability}}
There is no established method for prevention of PCOS
{{Family tree | | | | | | |!| | | | | }}
==Secondary Prevention==
{{Family tree | | | |,|-|-|^|-|-|.| | }}
Secondary preventive measures for PCOS include
{{Family tree | | | C01 | | | | C02 |C01= Stable<br>with low volume bleeding| C02= Unstable<br>with large volume bleeding}}
*Weight loss and metformin may prevent diabetes and atherosclerosis.
{{Family tree | | | |!| | | | | |!| | |}}
*Lifestyle modification, including increased physical activity and healthy diet resulting in weight loss, is also likely to prevent diabetes in PCOS.
{{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> }}
{{Family tree/end}}
 
==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>
*CT angiography
*Catheter angiography
*Radionuclide imaging
{| class="wikitable"
{| class="wikitable"
! rowspan="2" |Disease
!
! rowspan="2" |Headache
!CT angiography
! rowspan="2" |Symptoms
!Catheter angiography
! colspan="2" |Diagnosis
!Radionuclide imaging
|-
|-
!CT/MRI
|Bleeding at rates
!Other Investigation Findings
detection
|At least 0.5 mL/min
|0.5 to 1.5 mL/min
|0.1 mL/min
|-
|-
|[[Subarachnoid hemorrhage]]
|Indications
|
|
* Hemodynamically stable
* Endoscopy undiagnostic
|
|
* [[Headache|Severe headache]] (as a worst headache of the life)
* Endoscopy not feasible due to severe bleeding with hemodynamic instability
* [[Double vision]]
 
* [[Nausea]] and [[vomiting]]
* Persistent or recurrent GI bleeding
* Symptoms of [[meningeal irritation]]
* Non-diagnostic upper endoscopy
* Sudden [[Loss of consciousness|decreased level of consciousness]]
* Rapid progression of symptoms
|
|
* [[Computed tomography|CT]] shows hyperattenuating material filling the subarachnoid space.
|
LP will show:
* Elevated opening pressure
* Elevated [[Red blood cell|red blood cell (RBC)]]
* [[Xanthochromic|Xanthochromia]]
|-
|-
|[[Meningitis]]
|Advantages
|
|
* Minimally invasive 
* Demonstrate neoplasms or vascular malformations
* Can provide evidence of recent bleeding
|
|
* [[Headache]]  
* Diagnostic and therapeutic
* [[Neck stiffness]]
* Allows for infusion of vasoconstrictive drugs and/or embolization.
* [[Fever]]
* Does not require bowel preparation. 
* [[Photophobia]] 
* [[Phonophobia]] 
* [[Irritability]], [[altered mental status]] (in small children)
|
|
* [[CT]] scan of the head may be performed before [[Lumbar puncture|LP]] to determine the risk of [[herniation]].
* Most sensitive imaging modality for GI bleeding
|
* More commonly utilized for investigation of patients with obscure, intermittent bleeding
* Diagnosis is based on clinical presentation in combination with [[CSF]] analysis.
* For more information on [[CSF]] analysis in meningitis please [[Meningitis#Diagnosis|click here.]]
|-
|-
|[[Intracranial mass]]
|Disadvantages
|
|
* Lacks therapeutic capability
* Risk of contrast induced nephropathy in patients with renal impairment and contrast allergy
|
|
* [[Headache]]
* Access-site hematoma or pseudoaneurysm
* [[Nausea]]
* Arterial dissection
* [[Vomiting]]
* Spasm, bowel ischemia
* [[Change in mental status]]
* Contrast-induced nephropathy or allergic reaction
* [[Seizures]]
* Focal symptoms of brain damage
* Associated co-morbid conditions like [[tuberculosis]], etc
|
|
* Poor anatomic localization of the bleeding site
* Unable to diagnose the pathological cause of GI bleeding
|}


* Imaging tests determine the location of [[intracranial mass]] lesion(s) and help in guiding [[therapy]].
==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
|
* Dyspepsia
* Early satiety
* NSAID use
* Previous ulcer disease
|
* Hematemesis
* Possible hematochezia, melena
* Hemodynamic instability
** Tachycardia
** Hypotension
|
|
* [[Biopsy]] of the lesion is needed to identify the nature of the lesion such as:
* Decreased hemoglobin
** [[Tumor]]
* Increased BUN/creatinine
** [[Abscess]]
* Increased WBC's
* Helicobacter pylori positive
|-
|-
|[[Cerebral hemorrhage]]
|Mallory-Weiss tear
|
|
* Vomiting/retching
* Weakness
* Dizziness
|
|
* [[Headache]]
* Hematemesis
* Vomiting
* Possible hematochezia, melena
* Depressed level of [[consciousness]] from [[increased intracranial pressure]] (ICP)  
* Hemodynamic instability
* Progression of focal neurological deficits over periods of hours
** Tachycardia
** Hypotension
|
|
* [[CT]] is very sensitive for identifying acute [[hemorrhage]] which appears as hyperattenuating clot.
* Decreased hemoglobin
* Gradient echo and T2 susceptibility-weighted [[MRI]] are as sensitive as [[CT]] for detection of acute hemorrhage and are more sensitive for identification of prior hemorrhage.
* Increased creatinine
* Increased WBCs
|-
|Stress gastritis
|
|
* [[PT]]/ [[INR]] and [[aPTT]] should be checked to rule out [[coagulopathy]].
* History of head injury, severe burns, trauma
* Mechanical intubation
* Chronic steroid use
* Coagulopathy
|
* Hematemesis (coffee grounds more common)


* Melena
|
* Decreased hemoglobin
* Increased WBCs
|-
|-
|[[Cerebral]] [[Infarction]]
|Dieulafoy lesion
|
|
* Dyspepsia
* Weakness
* Dizziness, syncope,
* May have no prior history before bleed.
|
|
* The [[symptoms]] of an [[ischemic stroke]] vary widely depending on the site and blood supply of the area involved.
* Hematemesis (bright red)
* For more information on [[symptoms]] of [[ischemic stroke]] based on area involved please [[Ischemic stroke#Diagnosis#History and symptoms|click here]].
* Hematochezia or melena
* Hemodynamic instability
|
|
* CT may show hypo-attenuation and swelling of involved area.
* Decreased hemoglobin
|
* Decreased hematocrit
* [[Carotid]] [[doppler]] may be done to check for patency of [[carotid arteries]] and blood supply to the [[brain]].
* Increased WBCs
* Cerebral [[angiogram]] is an [[Invasive (medical)|invasive]] test and detect [[abnormalities]] of the [[blood vessels]], including narrowing, blockage, or [[malformations]] (such as [[Aneurysm|aneurysms]] or [[arterio-venous malformations]]). 
|-
|-
|[[Intracranial venous thrombosis]]
|Gastro-esophageal
varices
|
|
* Alcohol/tobacco use,
* Weakness, dizziness, syncope
|
|
* [[Headache]]: It is a common presentation (present in 90% of cases) ([[thunderclap headache]]).<sup>[[Cerebral venous sinus thrombosis history and symptoms#cite note-Stam2005-1|[1]]]</sup> 
* Stigmata of chronic liver disease
* Inability to move one or more limbs.
* Hematemesis, hematochezia or melena
* Weakness on one side of the face.
* Hemodynamic instability
* [[Seizure|Seizures]]
* [[Coma|Depressed level of consciousness]] and otherwise unexplained changes in [[mental status]] <sup>[[Cerebral venous sinus thrombosis history and symptoms#cite note-4|[4]]]</sup>
|
|
* The classic finding of sinus thrombosis on unenhanced [[CT]] images is a hyperattenuating thrombus in the occluded sinus.
* Decreased hemoglobin


* [[CT]] and [[MRI]] may identify [[Cerebral edema]] and venous [[infarction]] may be apparent.
* Decreased hematocrit
|
 
* CT [[venography]] detects the [[thrombus]], [[computed tomography]] with [[radiocontrast]] in the venous phase (CT venography or CTV) has a detection rate that in some regards exceeds that of [[MRI]].
* Electrolyte abnormalities


* [[Cerebral angiography]] may demonstrate smaller clots, and obstructed veins may give the "corkscrew appearance".
* Increased bilirubin/liver enzymes
|-
|-
|[[Migraine]]
|Gastric cancer
|
|
|
* [[Headache]] which is often one-sided and pulsating) lasts between several hours to three days.
* Alcohol/tobacco use
* Other [[symptoms]] include gastrointestinal upsets, such as [[nausea and vomiting]], and a heightened sensitivity to bright lights ([[photophobia]]) and noise ([[phonophobia]]). Approximately one third of people who experience [[migraine]] get a preceding [[Aura (symptom)|aura]].<sup>[[Migraine overview#cite note-4|[4]]]</sup> 
* Often asymptomatic
|
|
* [[CT]] and [[MRI]] may be needed to rule out other suspected possible causes of [[headache]].
* Hematemesis,
 
* Melena,
* Lymphadenopathy
** Palpable supraclavicular or anterior axillary lymph node
** Palpable firm stomach
|
|
*[[Migraine]] is a clinical [[diagnosis]].
* Decreased hemoglobin
*Laboratory tests can be ordered to rule out any suspected coexistent metabolic problems or to determine the baseline status of the patient before initiation of [[migraine]] therapy.
* Electrolyte abnormalities
* May have elevated CEA or CA 19-9
|-
|-
|[[Head injury]]
|Hemobilia
|
|
* Recent trauma
* Bliary tree instrumentation
* Gallstones
|
|
* [[Headache]]
* RUQ abdominal pain
* [[Confusion]]
* Jaundice
* [[Drowsiness]]
* Hematemesis, melena
* Personality change
* [[Seizure|Seizures]]
* [[Nausea]] and [[vomiting]]
* [[Headache|Loss of consciousness]]
* [[lucid interval]]
|
|
* [[CT]] scan demonstrates [[hemorrhage]] as hyperattenuating clot following head injury.
* Decreased hemoglobin,
* [[MRI]] is more sensitive, is done in patients with symptoms unexplained and a neagtive [[Computed tomography|CT]] scan.
 
|
* Increased bilirubin
* The [[Glasgow Coma Scale]] is a tool for measuring degree of unconsciousness and is thus a useful tool for determining severity of injury.
 
* Increased WBCs
|-
|-
|[[Lymphocytic hypophysitis]]
|Aortoduodenal
fistula
|
|
|
* Abdominal pain
Seen in late pregnancy or the [[postpartum]] period with the following symptoms:
* Back pain
* [[Hypopituitarism]]
* History of AAA repair
* Mass lesion effect such as [[headache]] , [[Visual field defect|visual field defects]]
* May be asymptomatic
|
|
* [[CT]] & [[MRI]] typically reveal features of a pituitary mass.
* 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.<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
|-
|-
|[[Radiation injury]]
|
|
|
*Age >60yr
* [[Headache]]
*Transfusion required.
* Impairment of [[mental function]]
*Initial Sys BP < 100.
** [[Personality change due to another medical condition|personality change]]
*Red blood in NG lavage.
** Impairment of memory
*History of cirrhosis or ascites on examination.
** [[Confusion]]
** [[Learning difficulties]].
* Focal [[neurological]] abnormalities
* [[Raised ICP].
|
[[CT]] & [[MRI]] will show:
* Focal [[radiation]] [[necrosis]]
* Diffuse [[white matter]] injury
* Contrast-enhancing mass surrounded by [[edema]] and mass effect
|[[PET scan]]
* [[Radiation]] [[necrosis]] is hypo metabolic and will have decreased uptake of [[fluorodeoxyglucose]].
 
|}
|}
*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


==Medical Therapy==
* Resuscitate with 1:1:1 of packed red blood cells (PRBCs) to fresh frozen plasma (FFP) to platelets.
===Pharmacotherapy===
Consider massive transfusion protocol
Medical treatment of PCOS is tailored to the patient's goals. Broadly, these may be considered under three categories:
* Restoration of fertility
* Treatment of hirsutism or acne
* Restoration of regular menstruation, and prevention of endometrial hyperplasia and endometrial cancer


In each of these areas, there is considerable debate as to the optimal treatment.  One of the major reasons for this is the lack of large scale clinical trials comparing different treatments.  Smaller trials tend to be less reliable, and hence may produce conflicting results.
Resuscitate to a target hemoglobin of 7 mg/dL.


General interventions that help to reduce weight or insulin resistance can be beneficial for all these aims, because they address what is believed to be the underlying cause of the syndrome.  Where PCOS is associated with overweight or obesity, successful weight loss is probably the most effective method of restoring normal ovulation/menstruation, but many women find it very difficult to achieve and sustain significant weight loss. [[Low-carbohydrate diet]]s and sustained regular exercise may help, and some experts recommend a [[Glycemic index|low-GI]] diet in which a significant part of the total carbohydrates are obtained from fruit, vegetables and wholegrain sources.
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


Many women find [http://www.ivf.com/pcostreat.html insulin-lowering medications] such as [[metformin]] hydrochloride (Glucophage®), [[pioglitazone]] hydrochloride (Actos®), and [[rosiglitazone]] maleate (Avandia®) helpful, and ovulation may resume when they use these agents. Many women report that [[metformin]] use is associated with upset stomach, diarrhea, and weight-loss. Such side effects usually resolve within 2&ndash;3 weeks.  Starting with a lower dosage and gradually increasing the dosage over 2&ndash;3 weeks and taking the medication toward the end of a meal may reduce side effects. It may take up to six months to see results, but when combined with exercise and a [[Glycemic index|low glycemic index diet]] up to 85% will improve menstrual cycle regularity and ovulation.
{{Family tree/start}}
====Treatment of Infertility====
{{Family tree | | | | | A01 | | | |A01=Acute GI bleeding}}
*[[Clomiphene citrate]] and [[metformin]] are the principal treatments used to help infertility. <ref>{{cite journal |author=Legro RS, Barnhart HX, Schlaff WD |title=Clomiphene, Metformin, or Both for Infertility in the Polycystic Ovary Syndrome|journal=N Engl J Med|volume=356 |issue=6 |pages=551-566 |year=2007 |pmid=17287476 |doi=}}</ref>
{{Family tree | | | | | |!| | | | | }}
*In a random trial, 626 women were randomized to three groups: metformin alone, clomiphene alone, or both.  The live birth rates after 6 months were 7.2% (metformin), 22.5% (clomiphene), and 26.8% (both). 
{{Family tree | | | | | B01 | | | |B01= Initial evaluation and resuscitation}}
*The major complication of clomiphene was multiple pregnancies, affecting 0%, 6% and 3.1% of women respectively.
{{Family tree | | | | | |!| | | | | }}
*However, many specialists continue to recommend metformin which has, separately, been shown to increase ovulation rates <ref>{{cite web | title = Efficacy of metformin for ovulation induction in polycystic ovary syndrome | url = http://www.endocrine-abstracts.org/ea/0003/ea0003p228.htm | publisher = Endocrine Abstracts}}</ref> and reduce miscarriage rates.<ref>{{cite web | title = Diabetes Drug Helps Prevent Miscarriage | url = http://www.webmd.com/infertility-and-reproduction/news/20020301/diabetes-drug-helps-prevent-miscarriage | publisher = WebMD }}</ref>.  Metformin may be a rational choice in women in whom significant insulin resistance is diagnosed or suspected, as clomiphene works through a different mechanism and does not affect insulin resistance.
{{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}}


Diet adjustments and weight loss also increase rates of pregnancy. The most drastic increase in ovulation rate occurs with a combination of diet modification, weight loss, and treatment with metformin and clomiphene citrate<ref>{{cite web | title = Do insulin-sensitizing drugs increase ovulation rates for women with PCOS? | url = http://findarticles.com/p/articles/mi_m0689/is_2_54/ai_n10299300 | publisher = Find Articles }}</ref>.  It is currently unknown if diet change and weight loss alone have an effect on live birth rates comparable to those reported with clomiphene and metformin.
===Pharmacotherapy===
 
Though the use of [[basal body temperature]] or BBT charts is sometimes advised to predict ovulation, clinical trials have not supported a useful role.
 
For patients who do not respond to clomiphene, metformin, other insulin-sensitizing agents, diet and lifestyle modification, there are options available including [[assisted reproductive technology]] procedures such as controlled ovarian hyperstimulation and [[in vitro fertilisation]].  Ovarian stimulation has an associated risk of ovarian hyperstimulation in women with PCOS &mdash; a dangerous condition with morbidity and rare mortality.  Thus recent developments have allowed the oocytes present in the multiple follicles to extracted in natural, unstimulated cycles and then matured ''in vitro'', prior to IVF.  This technique is known as IVM (in-vitro-maturation)
 
Though surgery is usually the treatment option of last resort, the polycystic ovaries can be treated with surgical procedures such as
* laparoscopy electrocauterization or laser cauterization
* ovarian wedge resection (rarely done now because it is more invasive and has a 30% risk of adhesions, sometimes very severe, which can impair fertility) was an older therapy
* ovarian drilling
 
====Treatment of Hirsutism and Acne====
[[Cyproterone acetate]] is an anti-[[androgen]], which blocks the action of male hormones that are believed to contribute to acne and the growth of unwanted facial and body hair.  Cyproterone acetate is also contained in the contraceptive pill Dianette®.  [[Spironolactone]] also has some benefits, again through anti-androgen activity, and metformin can also help.  [[Eflornithine]] is a drug which is applied to the skin in cream form (Vaniqa®), and acts directly on the hair follicles to inhibit hair growth.  It is usually applied to the face.
 
Although all of these agents have shown some efficacy in clinical trials, the average reduction in hair growth is generally in the region of 25%, which may not be enough to eliminate the social embarrassment of hirsutism, or the inconvenience of plucking/shaving.  Individuals may vary in their response to different therapies, and it is usually worth trying other drug treatments if one does not work, but drug treatments do not work well for all individuals.  Alternatives include electrolysis and various forms of laser therapy.
 
====Treatment of Menstrual Irregularity and Prevention of Endometrial Hyperplasia/Cancer====
* If fertility is not the primary aim, then menstruation can usually be regulated with a contraceptive pill.
* Most brands of contraceptive pill result in a withdrawal bleed every 28 days.
* Dianette® (a contraceptive pill containing [[cyproterone acetate]]) is also beneficial for hirsutism and is therefore often prescribed in PCOS.
* If a regular menstrual cycle is not desired, then a standard contraceptive pill is not appropriate.
* Women who are having irregular menses do not necessarily require any therapy; most experts consider that if a menstrual bleed occurs at least every three months, then the endometrium (womb lining) is being shed sufficiently often to prevent an increased risk of endometrial abnormalities or cancer.
* If menstruation occurs less often or not at all, some form of progestogen replacement is recommended.  Some women prefer a uterine progestogen implant such as the [[intrauterine system|Mirena®]] coil, which provides simultaneous contraception and endometrial protection for years, though often with unpredictable minor bleeding.
*  An alternative is oral progestogen taken at intervals (e.g. every three months) to induce a predictable menstrual bleed.
==Approach to hyperandrogenism==
{{familytree/start |summary=Sample 1}}
{{familytree | | | | | | | | A01 |A01='''Signs of hyperandrogenism'''<br> hirsutism, alopecia,<br>masculine appearance, acne}}
{{familytree | | | | | | | | |!| | | | }}
{{familytree | | | | |,|-|-|-|^|-|-|-|-|.| | | }}
{{familytree | | | B01 | | | | | | | | B02 | | |B01=History of Drug use|B02=Presence of oligomenorrhea }}
{{familytree | | | |!| | | | | | | | | |!| }}
{{familytree | | | C01 | | | | | | | | |!| |C01=Stop using the drug<br> PCOS ruled out}}
{{familytree | | | | | | | | | | | | | |!| }}
{{familytree | | | | | | | | | | | | | D03 |D03=Perform an ultrsound of pelvis}}
{{familytree | | | | | | | | | | | | | |!| }}
{{familytree | | | | | | | |,|-|-|-|-|-|^|-|-|-|.| }}
{{familytree | | | | | | | E02 | | | | | | | | E03 |E02=Normal morphology of ovaries|E03=Cystic morphology of ovaries}}
{{familytree | | | | | | | |!| | | | | | | | | |!| | }}
{{familytree | | | | | | | F01 | | | | | | | | F02 |F01=PCOS is ruled out<br> Look for adrenal tumors, ovarian tumors|F02=Measure testosterone levels}}
{{familytree | | | | | | | |!| | | | | | | | | |!| | }}
{{familytree | | | | | | | N01 | | | | | | | | |!| | N01=*17-hydroxyprogesterone/DHEAs elevated = CAH,adrenal tumors<br>*Cortisol elevated = Cushings syndrome, cortisol resistance<br> Prolactin,TSH,IGF1 abnormal = hyperprolactinoma, thyroid dysfunction acromegaly}}
{{familytree | | | | | | | | | | | | | | | | | |!| | }}
{{familytree | | | | | | | | | | | |,|-|-|-|-|-|^|-|-|-|-|-|.| }}
{{familytree | | | | | | | | | | | |!| | | | | | | | | | | |!| }}
{{familytree | | | | | | | | | | | G01 | | | | | | | | | | G02|G01=Normal|G02=Elevated }}
{{familytree | | | | | | | | | | | |!| | | | | | | | | | | |!| }}
{{familytree | | | | | | | | | | | O01 | | | | | | | | | | O02|O01=Risk factors of hirutism<br>present?|O02=PCOS}}
{{familytree | | | | | | | | | | | |!| | | | | | | | | | | }}
{{familytree | | | | | | | |,|-|-|-|^|-|-|-|.| | | | | | | }}
{{familytree | | | | | | | |!| | | | | | | |!| | | | | | | }}
{{familytree | | | | | | | P02 | | | | | | P01 | | | | | | |P01=Yes|P02=No }}
{{familytree | | | | | | | |!| | | | | | | |!| | | | | | | }}
{{familytree | | | | | | | Q01 | | | | | | Q02 | | | | | | Q01=PCOS ruled out|Q02=Hirutism present?}}
{{familytree | | | | | | | | | | | | | | | |!| | | | | | | | | | | |}}
{{familytree | | | | | | | | | | | | | | | |!| | | | | | | | | | | |}}
{{familytree | | | | | | | | | | | |,|-|-|-|^|-|-|-|.| | | | | | | | | | | }}
{{familytree | | | | | | | | | | | |!| | | | | | | |!| | | | | | | | | }}
{{familytree | | | | | | | | | | | I01 | | | | | | I02 | | | | | | | |I01=Mild hirutism|I02=Severe Hirutism}}
{{familytree | | | | | | | | | | | |!| | | | | | | |!| | | | | | | | | }}
{{familytree | | | | | | | | | | | |!| | | | | | | J01 | | | | | | | |J01=PCOS }}
{{familytree | | | | | | | | | | | |!| | | | | | | | | | | | | | | | | }}
{{familytree | | | | | | | | | | | K01 | | | | | | | | | | | | | | | |K01=Trial of OCP }}
{{familytree | | | | | | | | | | | |!| | | | | | | | | | | | | | | | | }}
{{familytree | | | | | | |,|-|-|-|-|^|-|-|-|-|.| | | | | | | | | | | | }}
{{familytree | | | | | | |!| | | | | | | | | |!| | | | | | | | | | | | }}
{{familytree | | | | | | L01 | | | | | | | | L02 | | | | | | | | | | |L01=Positive response|L02=Negative <br> worsening of symptoms }}
{{familytree | | | | | | |!| | | | | | | | | |!| | | | | | | | | | | | }}
{{familytree | | | | | | M01 | | | | | | | | M02 | |M01=Idiopathic hirutism|M02=PCOS }}
{{familytree/end}}
==Schistosomiasis==
===Historical Perspective===
*In 1847, Japanese Doctor Y. Fujii described  “Katayama fever” as a manifestation of acute schistosomiasis.
*1851, Dr.Theodore Billharz, working in Egypt, identified the worms responsible for Schistosomiasis.
*1904, S. japonicum was identified in a housecat.
*1915, the snail was identified as an intermediate host for Schistosomiasis.
 
=== Classification ===
{| class="wikitable"
{| class="wikitable"
!Organ involved
! colspan="4" |Correlation between physical signs and
!Species
the severity of upper gastrointestinal bleeding
!Geographical distribution
|-
! rowspan="2" |Physical signs
! colspan="3" |Bleeding severity
|-
|-
| rowspan="4" |Intestinal schistosomiasis
!Mild
|Schistosoma mansoni
!Moderate
|Africa, the Middle East, the Caribbean, Brazil, Venezuela and Suriname
!Severe
|-
|-
|Schistosoma japonicum
|Blood loss
|China, Indonesia, the Philippines
|<1L
|1-2L
|>2L
|-
|-
|Schistosoma mekongi
|Systolic blood pressure
|Several districts of Cambodia and the Lao People’s Democratic Republic
|<120
|100-119
|<99
|-
|-
|Schistosoma guineensis
|Orthostasis
 
|'''-'''
S. intercalatum
|'''-'''
|Rain forest areas of central Africa
|'''+'''
|-
|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
|-
|-
|Urogenital schistosomiasis
|Sensorium
|Schistoma haematobium
|Alert
|Africa, the Middle East, Corsica (France)
|Anxious
|Confused/Drowsy
|}
|}
===Pathophysiology===
*Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with humans being the definitive host.
*The life cycles of all five human schistosomes are broadly similar
====Snail cycle====
*Parasite eggs are released into the environment from infected individuals, hatching on contact with fresh water to release the free-swimming [[miracidium]].
*Miracidia infect fresh-water snails by penetrating the snail's foot. 
*After infection, the miracidium transforms into a primary (mother) sporocyst.
*Germ cells within the primary sporocyst will then begin dividing to produce secondary (daughter) sporocysts, which migrate to the snail's hepatopancreas.
*Once at the hepatopancreas, germ cells within the secondary sporocyst begin to divide producing thousands of new parasites, known as cercariae, which are the larvae capable of infecting mammals.
*Cercariae emerge daily from the snail host in a [[circadian]] rhythm, dependent on ambient temperature and light.
*Young cercariae are highly motile, alternating between vigorous upward movement and sinking to maintain their position in the water.
*Cercarial activity is particularly stimulated by water turbulence, by shadows and by chemicals found on human skin.
====Human cycle====
*Penetration of the human skin occurs after the cercaria have attached to and explored the skin.
*The parasite secretes enzymes that break down the skin's protein to enable penetration of the cercarial head through the skin. 
*As the cercaria penetrates the skin it transforms into a migrating schistosomulum stage. 
*The newly transformed schistosomulum may remain in the skin for 2 days before locating a post-capillary [[venule]]. The schistosomulum travels from the skin to the lungs where it undergoes further developmental changes necessary for subsequent migration to the liver.
*Eight to ten days after penetration of the skin, the parasite migrates to the [[liver sinusoid]]s.
*''S. japonicum'' migrates more quickly than S. mansoni, and usually reaches the liver within 8 days of penetration.
*Juvenile ''S. mansoni'' and ''S. japonicum'' worms develop an oral sucker after arriving at the liver. During this period that the parasite begins to feed on red blood cells. 
*The nearly-mature worms pair, with the longer female worm residing in the gynaecophoric channel of the male.


*Adult worms are about 10 mm long.  Worm pairs of S. mansoni and S. japonicum relocate to the [[mesenteric]] or rectal veins.
==Physical examination==
*''S. haematobium'' schistosomula ultimately migrate from the liver to the perivesical venous plexus of the bladder, ureters, and kidneys through the hemorrhoidal plexus. 
Common physical exam findings include:
*Parasites reach maturity in six to eight weeks, at which time they begin to produce eggs.
===Vitals===
*Adult ''S. mansoni'' pairs residing in the mesenteric vessels may produce up to 300 eggs per day during their reproductive lives. 
*Hypotension
*''S. japonicum'' may produce up to 3000 eggs per day.  Many of the eggs pass through the walls of the blood vessels, and through the intestinal wall, to be passed out of the body in faeces. 
*Tachycardia
*''S. haematobium'' eggs pass through the ureteral or bladder wall and into the urine.  Only mature eggs are capable of crossing into the digestive tract, possibly through the release of [[proteolytic]] enzymes, but also as a function of host immune response, which fosters local tissue ulceration.
*Thready pulse
*Up to half the eggs released by the worm pairs become trapped in the mesenteric veins, or will be washed back into the liver, where they will become lodged.
*Hypoxia
*Worm pairs can live in the body for an average of four and a half years but may persist up to 20 years. 
===Abdomen===
*Trapped eggs mature normally, secreting [[antigens]] that elicit a vigorous [[immune]] response.
*+Bowel sounds
*The eggs themselves do not damage the body rather it is the cellular infiltration resultant from the immune response that causes the pathology classically associated with schistosomiasis.
*Abdominal tenderness
 
*Hepatomegaly
===Pathogenesis===
*Splenomegaly
====Transmission====
*Caput medusa
Infection can occur by penetration of the human skin by cercaria or following the handling of contaminated soil or through the consumption of contaminated water or food sources (eg, unwashed garden vegetables).
*Spider angiomata
 
===Skin===
====Dissemination====
*Palmar erythema
Cercaria gets transformed into migrating schistosomulum stage in the skin. Then migrating schistosomulum are transported via the blood stream to respective organ system.
*Cold clammy extremities
====Incubation period====
===Neurological examination===
The incubation period for acute schistosomiasis is usually 14-84 days. However, many people are asymptomatic and have subclinical disease during both acute and chronic stages of schistosomiasis.
*Altered sensations
====Infective stages====
*Poor mentation
*Cercaria are the infective stage of schistosomiasis to humans
*Drowsiness
====Diagnostic stages====
===Rectal examination===
*Miracidium are diagnostic for schistosomiasis.
*Occult blood
====Pathogenesis====
*Gross blood
*The pathogenesis of acute human schistosomiasis is mainly related to egg deposition and liberation of [[antigens]] of adult worms and eggs.
**Bright red blood per rectum
*A strong inflammatory response characterized by high levels of pro-inflammatory cytokines, such as interleukins 1 and 6 and tumor necrosis factor-α, and by circulating immune complexes participates in the pathogenesis of the acute phase of the disease.
**Melena
====Immune response====
**Burgundy stools
*Both the early and late manifestations of schistosomiasis are immunologically mediated.
**Blood coating stools versus within stools
*The major pathology of infection occurs with chronic schistosomiasis in which retention of eggs in the host tissues is associated with chronic granulomatous injury.
**Bloody diarrhea
*Eggs may be trapped at sites of deposition (urinary bladder, ureters, intestine) or be carried by the bloodstream to other organs, most commonly the liver and less often the lungs and central nervous system.
==Surgery==
*The host response to these eggs involves local as well as systemic manifestations.
*The cell-mediated immune response leads to granulomas composed of lymphocytes, macrophages, and eosinophils that surround the trapped eggs and add significantly to the degree of tissue destruction.
*Granuloma formation in the bladder wall and at the ureterovesical junction results in the major disease manifestations of schistosomiasis haematobia (hematuria, dysuria, and obstructive uropathy).
*Intestinal as well as hepatic granulomas underlie the pathologic sequelae of the other schistosome infections( ulcerations and fibrosis of intestinal wall, hepatosplenomegaly, and portal hypertension) due to pre-sinusoidal obstruction of blood flow.
*In terms of systemic disease, antischistosome inflammation increases circulating levels of proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6, associated with elevated levels of C-reactive protein.
*These responses are associated with hepcidin-mediated inhibition of iron uptake and use, leading to anemia of chronic inflammation.
*Schistosomiasis-related undernutrition may be the result of similar pathways of chronic inflammation.
*Acquired partial protective immunity against schistosomiasis has been demonstrated in some animal species and may occur in humans.
===Associated conditions===
*Recurrent Salmonella infections can occur in patients with schistosomiasis. Salmonella bacteria live in symbiosis within the parasite's integument, allowing them to evade eradication by many antibiotics.
*Chloramphenicol-sensitive Salmonella entericaserotype Typhi has been shown to be refractory to chloramphenicol therapy in patients coinfected with Schistosoma.
*Patients coinfected with hepatitis C virus and Schistosoma have increased progression of liver fibrosis compared to patients with hepatitis C alone.
*Urogenital schistosomiasis is a co-factor in the spread and progression of human immunodeficiency virus (HIV) infection and other sexually transmitted infections, especially in women, and also is associated with female infertility.
 
===Microscopic Findings===
*Adult worms are about 10 mm long
 
{{#ev:youtube|X0eQxiwecIA}}
 
===Associated conditions===
*Recurrent Salmonella infections can occur in patients with schistosomiasis. Salmonella bacteria live in symbiosis within the parasite's integument, allowing them to evade eradication by many antibiotics.
*Chloramphenicol-sensitive Salmonella entericaserotype Typhi has been shown to be refractory to chloramphenicol therapy in patients coinfected with Schistosoma.
*Patients coinfected with hepatitis C virus and Schistosoma have increased progression of liver fibrosis compared to patients with hepatitis C alone.
*Urogenital schistosomiasis is a co-factor in the spread and progression of human immunodeficiency virus (HIV) infection and other sexually transmitted infections, especially in women, and also is associated with female infertility.
 
==Differentiating schistosomiasis from other diseases==
Schistosomiasis must be differentiated from other tapeworms that cause abdominal pain, fever,chills, cough, and muscle aches such as [[diphyllobothriasis]], [[taeniasis]], [[hymenolepiasis]]. The table below summarizes the findings that differentiate schistosomiasis from other conditions that may cause abdominal pain, fever,chills, cough, and muscle aches.
{| class="wikitable"
{| class="wikitable"
! colspan="2" |Surgical options for upper GI bleeding
|-
|-
! style="background:#4479BA; color: #FFFFFF;" |Infections
!Disease Process
! style="background:#4479BA; color: #FFFFFF;" |Common causative threadworms
!Surgical Options
! style="background:#4479BA; color: #FFFFFF;" |Suggestive findings
! style="background:#4479BA; color: #FFFFFF;" |Diagnostic approach
! style="background:#4479BA; color: #FFFFFF;" |Treatment
|-
|-
| style="background:#DCDCDC;" align="center" | [[Schistosomiasis]]
| rowspan="5" |Peptic ulcer disease
|
|Oversew
* [[Schistosoma japonicum|''Schistosoma japonicum'']]
|-
* [[Schistosoma mansoni|''Schistosoma mansoni'']]
|3-point ligation of gastroduodenal artery
* [[Schistosoma haematobium|''Schistosoma haematobium'']]
|-
|
|Vagotomy and pyloroplasty
*[[Abdominal pain]]
|-
*[[Cough]]
|Vagotomy and antrectomy
*[[Diarrhea]]
|-
*[[Fever]]
|Highly selective vagotomy
*[[Fatigue]]
|-
|
|Mallory-Weiss tear
*[[Stool examination]] for the eggs
|Oversew
*[[Ultrasound]] of [[liver]]
|-
|
| rowspan="2" |Dieulafoy lesion
* [[Praziquantel]]
|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
|-
|-
| style="background:#DCDCDC;" align="center" |[[Diphyllobothriasis]]
|Extra-anatomic bypass
|
|}
* ''[[Diphyllobothrium|Diphyllobothrium latum]]''
===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


===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>
'''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.<br>
'''Indications'''<br>
*For bleeding varices that are refractory to banding or sclerosant injection.<br>
'''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"
|-
|
|
*[[Epigastric pain]]
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
*[[Diarrhea]]
! colspan="3" rowspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" |Classification of pain in the abdomen based on etiology
*[[Fatigue]]
! rowspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" |Disease
*[[Nausea]]
| colspan="13" rowspan="1" style="background:#4479BA; color: #FFFFFF;" align="center" |'''Clinical manifestations'''
*[[Vomiting]]
! colspan="2" rowspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" |Diagnosis
*[[Numbness]]
! rowspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" |Comments
*[[Tingling]]
|-
| 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]]


|
* [[Osmotic]] [[laxatives]]
*[[Stool examination]] for the eggs and adults
* [[Antispasmodic]] drugs
*[[PCR]]
|-
|
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Whipple's disease]]
* [[Praziquantel]]
| 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
|-
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Toxic megacolon]]
| 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" |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)


| style="background:#DCDCDC;" align="center" |[[Taeniasis]]
* Insignificant dilation of ileal bowel loops (diameter >18 mm) with increased intraluminal gas and fluid
|
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Taenia solium|''Taenia solium'']]
|-
* [[Taenia saginata|''Taenia saginata'']]
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Tropical sprue]]
 
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diffuse
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
*[[Nausea]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
*[[Vomiting]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
*[[Epigastric pain]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
*[[Stool examination]] for the eggs and [[Proglottid|proglottids]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
*[[Computed tomography|Brain CT scan]] or Biopsy (for cysticercosis)
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* [[Praziquantel]]
| 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
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Budd-Chiari syndrome|Budd-Chiari syndrome]]
| 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" | Positive in liver failure leading to varices
| 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" |
*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"
|-
|-
| style="background:#DCDCDC;" align="center" | [[Hymenolepiasis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Findings on [[CT scan]] suggestive of Budd-Chiari syndrome include:
||
*Early enhancement of the [[caudate lobe]] and [[central liver]] around the [[Inferior vena cavae|inferior vena cava]]
* [[Hymenolepis infection causes|''Hymenolepis nana'']]
*Delayed enhancement of the peripheral [[liver]] with accompanying central low density (flip-flop appearance)
|
*Peripheral zones of the [[liver]] show reversed [[portal]] [[venous]] [[blood flow]]
*[[Nausea]]
*In the [[chronic]] phase, there is [[caudate lobe]] enlargement and [[atrophy]] of the [[Liver|peripheral liver]] in affected areas
*[[Vomiting]]
*[[Abdominal pain]]
*[[Dizziness]]
|
*[[Stool examination]] for the eggs and [[Proglottid|proglottids]]
|
* [[Praziquantel]]
|}
|}
===History===
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Ascitic tap|Ascitic fluid examination]] shows:
===Symptoms===
*[[Total protein]] more than 2.5 g per deciliter
Clinical manifestations of schistosomiasis are divided into schistosome dermatitis, acute schistosomiasis (Katayama fever), and chronic schistosomiasis.
*[[White blood cells]] are usually less than 500/μL.
====Common symptoms====
|-
====Acute schistosomiasis(Katayama fever)====
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Hemochromatosis]]
*Acute schistosomiasis occurs 20 to 50 days after primary exposure.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RUQ
*Malaise, diarrhea, weight loss, cough, dyspnea, chest pain, restrictive respiratory insufficiency, and pericarditis are important symptoms of acute schistosomiasis.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
*Mild disease resolves on its own, as the infection progress into an asymptomatic phase, which is often misinterpreted for an effective antibiotic therapy.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
*The clinical syndrome (i.e., fever, chills, liver and spleen enlargement, and marked eosinophilia) originally described for S. japonicum infection is increasingly being diagnosed in Brazil in individuals with S. mansoni infection with similar presentation.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
*Acute disease is not observed in individuals living in endemic areas of schistosomiasis because of the down-modulation of the immune response by antigens or idiotypes transferred from mother to child.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
====Chronic schistosomiasis====
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
*In chronic schistosomiasis, abdominal pain, irregular bowel movements, and blood in the stool are the main symptoms of intestinal involvement.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
*Colonic polyposis may occur.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
**Hepatosplenic involvement is the most important cause of morbidity with S. mansoni and S. japonicum infection.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | Positive in cirrhotic patients
**Patients may remain asymptomatic until the manifestation of hepatic fibrosis and portal hypertension develops.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
**Hepatic fibrosis is caused by a granulomatous reaction to Schistosoma eggs that have been carried to the liver.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
*Hematemesis from bleeding esophageal or gastric varices may occur.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
**In such cases, anemia and decreasing levels of serum albumin are observed. Some patients have severe hepatosplenic disease with decompensated liver disease. Jaundice, ascites, and liver failure are then observed.
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N
*Concomitant infection by Salmonella species, and less extensively by other gram-negative bacteria, with S. mansoni or S. haematobium leads to a picture of prolonged fever, hepatosplenomegaly, and mild leukocytosis with eosinophilia.
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*Glomerulonephritis, infantilism, and hypersplenism are other complications associated with hepatosplenic schistosomiasis.
* >60% TS
*The detection of pulmonary hypertension is increasing with the use of more advanced diagnostic technology.
* >240 μg/L SF
**Pulmonary hypertension, which used to be exclusively linked to the hepatosplenic form of the disease, has been documented in patients without liver fibrosis. 
* Raised LFT <br>Hyperglycemia
*In hospitalized adult patients with S. japonicum infection, cerebral schistosomiasis occurs in 1.7 to 4.3%. 
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
**It may occur as early as 6 weeks after infection, and the most common sign is focal jacksonian epilepsy.
* Ultrasound shows evidence of cirrhosis
**Signs and symptoms of generalized encephalitis may occasionally be found. In S. mansoni infection, neurologic involvement is rare and mainly characterized by transverse myelitis, which occurs mainly in patients without liver fibrosis and hepatosplenomegaly.
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Extra intestinal findings:
===Less common symptoms===
* Hyperpigmentation
====Schistosome dermatitis====
* Diabetes mellitus
*Schistosome dermatitis, or swimmer's itch, is an uncommon manifestation seen mainly when avian cercariae penetrate the skin and are destroyed.
* Arthralgia
*Schistosome dermatitis is a sensitization phenomenon occurring in previously exposed persons.
* Impotence in males
*The cercariae evoke an acute inflammatory response with edema, early infiltration of neutrophils and lymphocytes, and later invasion of eosinophils.
* Cardiomyopathy
*A pruritic papular rash occurs within 24 hours after the penetration of cercariae and reaches maximal intensity in 2 to 3 days.
* Atherosclerosis
{| class="wikitable"
* Hypopituitarism
!
* Hypothyroidism
!Symtoms
* 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
|-
|-
|Acute schistosomiasis
! rowspan="4" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Gynaecological Causes
(Katayama fever)
! 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
* Fever
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RLQ / LLQ
* Malaise
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* Arthralgia/myalgia
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* Dry cough, wheezing
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<nowiki>+</nowiki>
* Abdominal discomfort
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
* Diarrhea
| 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
|-
|-
| rowspan="5" |Chronic schistosomiasis
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Salpingitis|Acute salpingitis]]
|Schistosomal nephropathy present with varying degrees of fatigue and asthenia
| 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]]
|-
|-
|Intestinal schistosomiasis may develop episodic intestinal bleeding and tenesmus.
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |Cyst rupture
*Patients infected with S japonicumcan develop upper abdominal pain unrelated to meals, gastric bleeding, and pyloric obstruction due to eosinophilic inflammation and fibrosis.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |RLQ / LLQ
*Patients infected with S mansonican develop inflammation with symptoms that resemble those of Crohn disease or ulcerative colitis.
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | −
Hepatosplenic schistosomiasis may present with cataclysmic esophageal variceal hemorrhage.
| 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" |
|-
|-
|Urinary schistosomiasis presents with  hematuria and dysuria
! style="padding: 5px 5px; background: #DCDCDC;" align="center" |Pregnancy
Urogenital schistosomiasis present with genital pain, pelvic pain, coital bleeding, and dyspareunia.
| 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
|-
|-
|Neuro-schistosomiasis may present with seizures, transverse myelitis or symptoms similar to those of cauda equina syndrome (eg, low back pain, lower extremity weakness, bowel and bladder symptoms) due to inflammation at the nerve roots
! rowspan="4" style="background:#4479BA; color: #FFFFFF;" align="center" |Extra-abdominal causes
! rowspan="3" style="padding: 5px 5px; background: #DCDCDC;" align="center" |Pulmonary disorders
| colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Pleural empyema]]
| 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" |<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


Granulomatous inflammation in the CNS can result in conus medullaris syndrome or schistosomal cerebritis (most commonly caused by S. japonicum)
* Localization of effusion
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Physical examination
* Crackles
* [[Egophony]]
* Increased [[tactile fremitus]]
|-
| colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Pulmonary embolism]]
| 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" | −
| 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" |
* 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
|-
| 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" |
*CXR
*CT chest
*Bronchoscopy
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Shortness of breath
* Cough
|-
|-
|Pulmonary schistosomiasis experience dyspnea on exertion, fatigue, and hemoptysis.
! 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" |
* Chest pain, tightness, diaphoresis
Complications:
* [[Arrythmias]]
* [[Mitral regurgitation]]
* Ventricular wall rupture
* Septal rupture
|-
|-
|Schistosome dermatitis
|}
( swimmer's itch)
|}
|Uncommon manifestation.
</small></small>
A pruritic papular rash occurs within 24 hours after the penetration of cercariae and reaches maximal intensity in 2 to 3 days.
{|
|-
| [[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]]
|}
|}


===Risk factors===
The following is a list of diseases that present with acute onset severe lower abdominal pain:
The most potent risk factor in the development of schistosomiasis is skin exposure to contaminated fresh water (wading, swimming, washing, or working in fresh water that is infested with cercariae). Other risk factors include travel to endemic areas.
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
===Screening===
|+
Screening is recommended only to guide mass public health treatment programs to targeted villages in endemic areas. Routine screening of travelers is not recommended.
! style="background: #4479BA; width: 180px;" | {{fontcolor|#000|Disease}}
===Epidemiology===
! style="background: #4479BA; width: 650px;" | {{fontcolor|#000|Findings}}
====Incidence and prevalence====
|-
*More than 600 million persons are exposed to Schistosoma parasites, 200 million persons are infected, and 20 million symptomatic cases of schistosomiasis are reported worldwide
| style="padding: 7px 7px; background: #DCDCDC;" | '''[[Ectopic pregnancy]]'''
===Demographics===
| 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>
====Race====
|-
*There is no racial predilection to schistosomiasis.
| style="padding: 7px 7px; background: #DCDCDC;" |'''[[Appendicitis]]'''
===Gender===
| 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>
*Schistosomiasis affects men and women equally.
|-
====Geographic Distrubution====
| style="padding: 7px 7px; background: #DCDCDC;" | '''Ruptured[[ ovarian cyst]]'''
*Schistosoma species are endemic in many areas of Africa, South America, the Caribbean, Southeast Asia, and the Middle East.
| 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>
===Natural History===
|-
If left untreated, most of the patients with schistosomiasis may progress to develop ulceration or cancer of the bladder, liver or kidney failure.
| style="padding: 7px 7px; background: #DCDCDC;" | '''[[Ovarian cyst ]]torsion'''
===Complications===
| 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>
Common complications of schistosomiasis include:
|-
*Hematuria
| style="padding: 7px 7px; background: #DCDCDC;" | '''Hemorrhagic [[ovarian cyst]]'''
*Malnutrition and growth retardation
| 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>
*Anemia of chronic disease
|-
*Cervicitis
| style="padding: 7px 7px; background: #DCDCDC;" | '''[[Endometriosis]]'''
*Iron-deficiency anemia
| 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>
*Splenomegaly
|-
*Intestinal polyps
| style="padding: 7px 7px; background: #DCDCDC;" | '''[[Acute cystitis]]'''
*Hydronephrosis
| style="padding: 7px 7px; background: #F5F5F5;" |Presents with features of increased urinary [[frequency]], [[urgency]], [[dysuria]], and suprapubic pain.<ref>{{Cite journal
*Glomerulonephritis
<nowiki> </nowiki><nowiki>|</nowiki> author = [[W. E. Stamm]]
*Recurrent Salmonella bacteremia
| title = Etiology and management of the acute urethral syndrome
*Bladder polyps
| journal = [[Sexually transmitted diseases]]
*Bladder cancer
| volume = 8
*Infertility (male, female)
| issue = 3
*Ectopic pregnancy
| pages = 235–238
*Portal hypertension
| year = 1981
*Esophageal varices
| month = July-September
*Ascites
| pmid = 7292216
*Intestinal obstruction
</ref><ref>{{Cite journal
*Obstructive uropathy
<nowiki> </nowiki><nowiki>|</nowiki> author = [[W. E. Stamm]], [[K. F. Wagner]], [[R. Amsel]], [[E. R. Alexander]], [[M. Turck]], [[G. W. Counts]] & [[K. K. Holmes]]
*Renal failure
| title = Causes of the acute urethral syndrome in women
*Generalized seizures
| journal = [[The New England journal of medicine]]
*Spinal cord compression
| volume = 303
*Cor pulmonale
| issue = 8
===Prognosis===
| pages = 409–415
*Depending on the extent of the disease progression at the time of diagnosis, the prognosis of schistosomiasis may vary. However, the prognosis is generally regarded as good with treatment.
| year = 1980
*The 1-year mortality rate of patients with schistosomiasis ranges approximately 0.1-11% depending upon underlying complications.
| month = August
*If symptoms of schistosomiasis persisting after 2 rounds of praziquantel treatment, more urine or stool samples should be taken and tested for viable parasite eggs, and re-treatment must be given if persistent infection is detected.
  | doi = 10.1056/NEJM198008213030801
===Physical Examination===
  | pmid = 6993946</ref>
Common physical examination findings of schistosomiasis include generalized lymphadenopathy, hepatosplenomegaly, rash, fever, right upper quadrant tenderness, urticaria, bloody stool.
|}
====Appearance of the Patient====
Patients withg schistosomiasis usually appear tired.
====Vital Signs====
*High-grade / low-grade fever.
*Tachycardia with a regular pulse.
*Tachypnea
*High blood pressure
====Skin====
*Pallor
*Urticaria
*Purpuric rash
====Neck====
*Cervical lymphadenopathy
*Jugular venous distension in cases of cor pulmanale.
====Lungs====
*Normal vesicular breathe sounds.
*Ocassional Wheezeing
====Heart====
*Normal S1, S2
*Signs of right hear failure in cases cor-pulmonale
====Abdomen====
*Right upper quadrant tenderness
*Abdominal distention
*Hepatosplenomegaly
*Distended abdominal veins
*Ascites
====Genitourinary====
*Genital ulcers
*Hypertrophic lesions or nodular lesions of the cervix, vulva, or vagina
*Vesicovaginal fistula.
*Uterine enlargement
*Pelvic pain
*Dysuria
====Neuromuscular====
*Joint tenderness
====Extremities====
*Clubbing
 
===Laboratory Findings===
Visualization of schistosoma eggs in stool, urine, and crushed biopsy tissues is diagnostic of schistosomiasis. Laboratory findings consistent with the diagnosis of schistosomiasis include detection of circulating antibodies to schistosomes and schistosomal antigen in serum. Diagnostic tests for schistosomiasis include the following:
*Microscopic examination of stool
*Urine testing for schistosome eggs
*Serologic testing
*Schistosomal antigen testing (urine or serum)
*Microscopic examination of tissue
*PCR to detect schistosomal DNA
====Microscopic examination of stool====
*The classic and most commonly used method for identification of schistosome eggs in stool is a modified Kato-Katz thick smear.
*Testing should be done on formed stool, as schistosomiasis typically does not cause diarrhea.
*Several areas of a stool specimen should be evaluated independently, as eggs are not deposited uniformly throughout. In addition, eggs are not deposited uniformly throughout the day, and, thus, three different stool specimens should be evaluated.
*One to 99 eggs/g is suggestive of mild infection, 100 to 299 eggs/g indicate moderate infection, and more than 300 eggs/g are indicative of high-intensity infection.
*Kato Katz smears are not sufficiently sensitive for detection of low-intensity infections. Other techniques may be superior but often are unavailable or more difficult to use.
{{#ev:youtube|WpcZejHa_jM}}
[[Image:Schistosoma japonicum (3) histopathology.JPG|thumb|center|''S. japonicum'' eggs in hepatic portal tract.]]
 
====Other Methods====
'''Formalin-ethyl acetate sedimentation'''
*In formalin-ethyl acetate sedimentation 2 to 5 g of stool is mixed, strained, diluted with normal saline solution.
*It is then centrifuged.
*The sediment is collected and treated with formalin-ethyl acetate and subsequently used for slide preparation
*A single formalin-ethyl acetate sedimentation test is not as sensitive for detection of low-intensity infection as multiple Kato-Katz smears
 
====Urine testing for schistosome eggs====
*The classic method used for identification of S.haematobium eggs is filter concentration of a urine sample collected over 4 hours (ending around noon) into a jug with formalin preservative
*10 mL of urine is filtered through a 12-μm pore membrane that traps the eggs, and the membrane surface then is examined under a microscope.
*Standard microscopic urinalysis will not identify low-intensity Schistosoma infections.
*Each separate microscopic urinalysis has a sensitivity of 55% to 62% for detection of low-intensity infection; therefore, at least three different urine samples need to be evaluated to achieve diagnostic accuracy.
====Schistosomal antigen testing (urine or serum)====
*Urine sample is taken for measurement of circulating cathodic antigen released by schistosomes or serum sample for measurement of both circulating cathodic and anodic antigen.
*Identifies active infection rather than past infection
*May not be sufficiently sensitive for detection of low-intensity infection
====Serologic testing====
*Serologic testing help in detection of schistosoma-specific antibodies in serum. These tests include:
**Enzyme-linked immunosorbent assay
**Indirect hemagglutination assay
**Indirect immunofluorescent antibody testing
*More useful for evaluating recent travelers than immigrants, as it is not possible to distinguish between active infection and past infection.
*Due to the long life of schistosomes, positive test results cannot be discounted simply because exposure was historically distant.
*Sensitivity is highest when the assay is targeted to the suspected species (S.mansoni, S.japonicum, or S.haematobium)
 
====Microscopic examination of tissue====
*A biopsy specimen is obtained from the rectum during anoscopy, genital tissues, or the urinary bladder wall during cystoscopy and then crushed and examined under a microscope
*S.mansoni and S.japonicum eggs can be identified in crushed random rectal biopsy specimens.
*S.haematobium eggs can be identified in crushed biopsy specimens from genital tissues or the urinary bladder wall
*Sensitivity of microscopic analysis of six crushed rectal biopsies is similar to that of two Kato-Katz thick smears.
*Liver biopsy is notoriously insensitive for diagnosis of schistosomiasis; a negative liver biopsy result does not exclude infection
*Standard sectioned intestinal biopsies are not sufficiently sensitive for diagnosis of intestinal schistosomiasis
====PCR to detect schistosomal DNA====
*Gene amplification technique used to detect schistosomal DNA.
====Other laboratory tests====
Other diagnostic tests that are helpful in diagnosis of schistosomiasis include
*Urinalysis, including dipstick testing and microscopic analysis for leukocytes, erythrocytes, and casts.
**If obstruction is causing a urinary tract infection, leukocyte esterase or nitrites may be present
**Erythrocytes are seen in the urine of patients with glomerulonephritis.
**Urinary casts, which are aggregates of protein, blood cells, tubular epithelial cell constituents, or all three, develop secondary to urinary stasis in renal tubules and significant proteinuria.
*Measurement of blood urea nitrogen (BUN) and serum creatinine to test renal function.
*Liver function tests.
**AST and ALT levels usually remain normal, even in patients with hepatosplenic disease
**Albumin levels may be low due to malnutrition or nephrotic forms of schistosomiasis
*Complete blood count (CBC).
**Anemia may be seen in patients with chronic blood loss due to intestinal or urinary schistosomiasis and in those with glomerular disease.
**Eosinophilia may be prominent early in the disease course but may be minimal in patients with longstanding disease.
=====MAIN====
Eggs can be present in the stool in infections with all ''Schistosoma'' species. The examination can be performed on a simple smear (1 to 2 mg of fecal material).  Since eggs may be passed intermittently or in small amounts, their detection will be enhanced by repeated examinations and/or concentration procedures (such as the formalin-ethyl acetate technique).  In addition, for field surveys and investigational purposes, the egg output can be quantified by using the [[Kato-Katz technique]] (20 to 50 mg of fecal material) or the Ritchie technique.


Eggs can be found in the urine in infections with (recommended time for collection: between noon and 3 PM) S. japonicum' and with S. intercalatum. Detection will be enhanced by [[centrifugation]] and examination of the sediment.  Quantification is possible by using filtration through a [[nucleopore]] membrane of a standard volume of urine followed by egg counts on the membrane. Investigation of ''S. haematobium'' should also include a pelvic x-ray as bladder wall calcificaition is highly characteristic of chronic infection.
==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.


Recently a field evaluation of a novel handheld microscope was undertaken in Uganda for the diagnosis of intestinal schistosomiasis by a team led by Dr. Russell Stothard who heads the Schistosomiasis Control Iniative at the Natural History Museum, London. His report abstract may be found here: [http://looksmall.com/news.asp]
==References==
{{Reflist|2}}
{{Gastroenterology}}


===Electrocardiogram===
[[Category:Emergency medicine]]
There are no ECG findings associated with schistosomiasis.
[[Category:Gastroenterology]]
===Chest X-ray===
[[Category:Gynecology]]
There are no x-ray findings associated with schistosomiasis. However, chest radiographs can demonstrate patchy infiltrates in acute schistosomiasis. Chest radiographs can also demonstrate signs of increased vascular and interstitial marking and mild lymphadenopathy in cases presence of pulmonary hypertension and cor-pulmonale.
[[Category:Medicine]]
*Abdominal X-ray in urinary schistosomiasis may demonstrate bladder and ureteral calcifications("fetal head" calcification)
===CT scan===
There are no CT scan findings associated with schistosomiasis. However, a CT scan may be helpful in the diagnosis of complications of schistosomiasis, which includes CNS disease or in the detection of periportal fibrosis.
*CT scan of the brain in CNS schistosomiasis may demonstrate nodular and ring-enhancing lesions with surrounding edema.
*CT scan of the liver in hepatosplenic schistosomiasis may demonstrate calcified capsules.
*CT scan of the lung in pulmonary schistosomiasis may demonstrate interstitial fibrosis.


===Ultrasound===
[[Category:Surgery]]
====Abdominal ultrasound====
* Multiple echogenic areas, each with central echolucency are characteristic of classic periportal fibrosis.
====Urogenital ultrasonography====
*Urogenital ultrasonography may demonstrate scarring patterns of bladder characteristic of urogenital schistosomiasis.
*Urogenital ultrasonography is more sensitive than intravenous pyelography and plain radiography for detection of urinary tract pathologies.


===MRI===
{{WikiDoc Help Menu}}
There are no MRI findings associated with schistosomiasis.
{{WikiDoc Sources}}
===Primary Prevention===
<references />
*The most important preventive measure is education regarding the risk associated with contact with fresh water in endemic areas reduces parasite acquisition.
*Avoid swimming or wading in freshwater.
*Although schistosomiasis is not transmitted by swallowing contaminated water, if mouth or lips come in contact with water containing the parasites, infection can occur.
*Water used for bathing should be brought to a rolling boil for 1 minute to kill any cercariae, and then cooled before bathing to avoid scalding.
*Water held in a storage tank for at least 1 - 2 days should be safe for bathing.
*Vigorous towel drying after an accidental, very brief water exposure may help to prevent the Schistosoma parasite from penetrating the skin. However, do not rely on vigorous towel drying alone to prevent schistosomiasis.
*Repeated doses of [[artesunate]] or [[artemether]] (6 mg/kg every 1 or 2 weeks) appear to provide chemoprophylactic protection against infection with ''S.japonicum'' after episodic exposure.
===Medical therapy===
The mainstay of treatment for schistosomiasis is pharmacotherapy. Praziquantel is the drug of choice in treating schistosomiasis. Corticosteroids should be administered in addition to praziquantel in patients with symptoms due to neuro-schistosomiasis and patients with severe Katayama fever. The goals of treatment of schistosomiasis are to eradicate the helminth and correct any sequelae of infection.
===Antimicrobial Regimen===
:*'''1. Schistosoma mansoni, S. haematobium, S. intercalatum'''<ref name="pmid24698483">{{cite journal| author=Colley DG, Bustinduy AL, Secor WE, King CH| title=Human schistosomiasis. | journal=Lancet | year= 2014 | volume= 383 | issue= 9936 | pages= 2253-64 | pmid=24698483 | doi=10.1016/S0140-6736(13)61949-2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24698483  }} </ref>
::*Preferred regimen: [[Praziquantel]] 40 mg/kg per day PO in qd or bid for one day
::*Alternative regimen (1): [[Oxamniquine]] 20 mg/kg PO single dose<ref>National Center for Biotechnology Information. PubChem Compound Database; CID=4612, https://pubchem.ncbi.nlm.nih.gov/compound/4612 (accessed July 16, 2015).</ref><ref>BINA, J. C.  and  PRATA, A.. Tratamento da esquistossomose com oxamniquine (xarope) em crianças. Rev. Soc. Bras. Med. Trop.[online]. 1975, vol.9, n.4 [cited  2015-07-16], pp. 175-178 . Available from: <http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0037-86821975000400002&lng=en&nrm=iso>. ISSN 0037-8682.  http://dx.doi.org/10.1590/S0037-86821975000400002.</ref>
::*Alternative regimen (2): [[Artemisinin]] no dose is established yet<ref name="pmid24698483">{{cite journal| author=Colley DG, Bustinduy AL, Secor WE, King CH| title=Human schistosomiasis. | journal=Lancet | year= 2014 | volume= 383 | issue= 9936 | pages= 2253-64 | pmid=24698483 | doi=10.1016/S0140-6736(13)61949-2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24698483  }} </ref>
::*Alternative regimen (3): [[Mefloquine]] 250 mg PO single dose
::*Note: There is no benefit in associating the alternative therapies to Praziquantel.
::*Note: Praziquantel is not effective against larval/egg stages of the disease.<ref name="pmid24445340">{{cite journal| author=Paramythiotou E, Frantzeskaki F, Flevari A, Armaganidis A, Dimopoulos G| title=Invasive fungal infections in the ICU: how to approach, how to treat. | journal=Molecules | year= 2014 | volume= 19 | issue= 1 | pages= 1085-119 | pmid=24445340 | doi=10.3390/molecules19011085 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24445340  }} </ref>


:*'''2. S. japonicum, S. mekongi'''<ref name="pmid24698483">{{cite journal| author=Colley DG, Bustinduy AL, Secor WE, King CH| title=Human schistosomiasis. | journal=Lancet | year= 2014 | volume= 383 | issue= 9936 | pages= 2253-64 | pmid=24698483 | doi=10.1016/S0140-6736(13)61949-2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24698483  }} </ref>
==References==
::*Preferred regimen: [[Praziquantel]] 60 mg/kg per day PO bid for one day
{{Reflist|2}}
::*Alternative regimen (1): [[Artemisinin]] no dose is established yet
{{Gastroenterology}}
::*Alternative regimen (2): [[Mefloquine]] 250 mg PO single dose
::*Note: There is no benefit in associating the alternative therapies to Praziquantel.


:*'''3. Katayama Fever'''
[[Category:Emergency medicine]]
::*Preferred regimen: Prednisone 20-40 mg/day PO for 5 days, {{then}} Praziquantel<ref name="pmid20222897">{{cite journal| author=Jauréguiberry S, Paris L, Caumes E| title=Acute schistosomiasis, a diagnostic and therapeutic challenge. | journal=Clin Microbiol Infect | year= 2010 | volume= 16 | issue= 3 | pages= 225-31 | pmid=20222897 | doi=10.1111/j.1469-0691.2009.03131.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20222897  }} </ref>
[[Category:Gastroenterology]]
::*Note: Praziquantel should be used after 4-6 weeks of exposure, because it cannot kill the larvae stages of the Schistosoma. Praziquantel should be used after acute schistosomiasis syndrome symptoms have resolved always together with corticosteroids, only when ova are detected in stool or urine samples.<ref name="pmid19292640">{{cite journal| author=Jauréguiberry S, Paris L, Caumes E| title=Difficulties in the diagnosis and treatment of acute schistosomiasis. | journal=Clin Infect Dis | year= 2009 | volume= 48 | issue= 8 | pages= 1163-4; author reply 1164-5 | pmid=19292640 | doi=10.1086/597497 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19292640  }} </ref>
[[Category:Gynecology]]
[[Category:Medicine]]


====Praziquantel====
[[Category:Surgery]]
*Praziquantel is first-line therapy for infection with all five Schistosoma species (S.japonicum, S.mansoni, S.intercalatum, S.mekongi, and S.haematobium).
*Praziquantel is also used as part of mass chemotherapy campaigns in endemic areas to decrease individual worm burden so as to reduce community transmission.
*Inexpensive
*Not effective against immature schistosomes (schistosomules)
*Not useful for treatment of cercarial dermatitis (ie, cutaneous schistosomiasis or swimmer's itch) caused by transient, self-limited infection withAustrobilharziaspecies
*Very well tolerated; adverse effects are usually mild and transient and do not require treatment.
*Women who are breastfeeding should not breastfeed on the day of treatment
*Rifampin significantly reduces the bioavailability of praziquantel and, thus, should be discontinued 4 weeks before treatment
*Schistosome eggs may take weeks to pass out of the intestinal and bladder wall; therefore, egg passage continues for approximately a month after treatment
====Corticosteroids====
*Corticosteroids are indicated as an adjunctive treatment (in addition to praziquantel) in patients with symptoms due to:
**Neuro-schistosomiasis (transverse myelitis, seizures, or other symptoms of increased intracranial pressure)
**Patients presenting with severe Katayama fever
*Corticosteroids help to alleviate acute allergic reactions and mass effects caused by excessive granulomatous inflammation in the CNS.
====Artemisinin compounds====
*Artemisinin compounds are employed in the eradication of migrating schistosome larvae in recently infected patients.
*Artemether also may provide chemoprophylactic protection against S.mansoniandS haematobium.
==Medical therapy==
The mainstay of treatment for Addison's disease is pharmacotherapy which is replacement of deficient hormones. Medical management of Addison's disease can be discussed under two categories
*Acute management ( Addison's crisis)
*Chronic management 
===Acute management ===
The main stay of treatment includes glucocorticosteroids and supportive therapy
====Goals====
*Normalization of blood pressure and volume status
*Supplementation of adequate glucocorticoids plus mineralocorticoid.
====Supportive therapy====
*Maintain airway, breathing, and circulation, and refer immediately to tertiary care center for intravenous corticosteroids.
*If the patient has pre filled syringes (emergency kit) and presents with Addisonian crisis while far from a hospital, an intramuscular injection should be given and the patient transferred to the nearest emergency room for intravenous normal saline and intravenous hydrocortisone.
*Normal saline 0.9% or 5% dextrose in normal saline should be administered to correct hypotension and dehydration.
*It is usually necessary to administer 1 L rapidly and a further 2 to 4 L over the first 24 hours, to correct hypotension.
*Careful monitoring of BP, fluid status, and serum sodium and potassium levels should be maintained.


===Pharmocotherapy===
{{WikiDoc Help Menu}}
*Dexamethasone should be given to patients with suspected Addisonian crisis prior to any laboratory measurements.
{{WikiDoc Sources}}
*Intravenous hydrocortisone is used to treat Addisonian crisis following dexamethasone.
<references />
*In addition, fludrocortisone is needed for mineralocorticoid replacement.
====Adult====
:*Preferred regimen (1): Dexamethasone IV 2-8 mg/dose q12h followed by a Oral 0.5 mg  maintenance dose.
:*Preferred regimen (1): Hydrocortisone 100 mg bolus immediately; followed by either 100 mg q8h '''(or)''' 300 mg q24 by continuous infusion for 2 to 3 days; then 100 to 150 mg q24h and taper to 75 mg/d before switching to oral maintenance dose
:**Note: Maintenance dose 10 mg in the morning, 5 mg around noon, and 5 mg in the afternoon '''(or)''' 10 to 15 mg in the morning and 5 to 10 mg in the afternoon.
====Pediatric====
:Preferred regimen (1): Hydrocortisone 1 to 2 mg/kg/dose bolus immediately; followed by 25 to 150 mg/d, given in divided doses every 6 to 8 hours (in infants and young children)or150 to 250 mg/d given in divided doses every 6 to 8 hours (in older children).
===Chronic management===
The main stay of treatment includes glucocorticosteroids and mineralocorticoids.
====Goals====
*Adequate daily supplementation of glucocorticoid and mineralocorticoid to mimic normal physiology. This should aim to maintain normal blood pressure, blood glucose, and fluid volume, and instill a sense of well-being in the patient
*Advise patients on medication for minor illness (febrile illness or emesis) to double or triple their usual dose of glucocorticoid. In case of severe illness, they should inject themselves with a large dose of glucocorticoid and seek immediate medical attention
*If patients are monitored to normalize ACTH level, they are almost invariably overtreated with glucocorticoid resulting in iatrogenic Cushing syndrome. Monitoring is primarily based on clinical features
*Ensure that patients are aware that they must be vigilant in maintaining their therapeutic regimen
====Precautions====
*All patients with known Addison disease should have an emergency plan in place for corticosteroid supplementation (oral or intramuscular), to be implemented if significant illness occurs
*Immediate action is needed for the signs of Addisonian crisis in a known Addison disease patient
*If the patient has pre filled syringes (emergency kit) and presents with Addisonian crisis while far from a hospital, an intramuscular injection should be given and the patient transferred to the nearest emergency room for intravenous normal saline and intravenous hydrocortisone.
*In an undiagnosed patient who requires immediate corticosteroid treatment, dexamethasone may be given as it does not interfere with ACTH stimulation testing.
====Pharmacotherapy====
'''Glucocorticosteroid'''
:*Preferred regimen (1): cortisone 10 to 37.5 mg q12h orally given in 2 divided doses with two-thirds of the total dose given in the morning (around 8 a.m.) and one third in the afternoon (noon to 4 p.m.) or
:*Preferred regimen (2): hydrocortisone : 15-30 mg/day orally given in 2 divided doses with two-thirds of the total dose given in the morning (around 8 a.m.) and one third in the afternoon (noon to 4 p.m.) or
:*Preferred regimen (3): dexamethasone : 0.25 to 0.75 mg orally once daily
:*Preferred regimen (4): prednisone : 2.5 to 5 mg orally once daily
'''Mineralocorticosteroid''''
:*Preferred regimen (1): fludrocortisone : 0.1 to 0.2 mg orally once daily
mild-to-moderate stress:
:*Alternative regimen (1): cortisone  50-100 mg/day orally given in 2 divided doses with two-thirds of the total dose given in the morning (around 8 a.m.) and one third in the afternoon (noon to 4 p.m.) for 3 days
:*Alternative regimen (2): hydrocortisone 30-90 mg/day orally given in 2 divided doses with two-thirds of the total dose given in the morning (around 8 a.m.) and one third in the afternoon (noon to 4 p.m.) for 3 days
:*Alternative regimen (3): dexamethasone 0.50 to 2.25 mg orally once daily for 3 days
:*Alternative regimen (4): prednisone  5-15 mg orally once daily for 3 days
'''Severe stress'''
:*Alternative regimen (5): hydrocortisone sodium succinate 100 mg intravenously every 6-8 hours
===Women with decreased libido===
====Androgen replacement====
*The ovaries and the adrenals are the main source of androgens in women.
*The adrenals produce dehydroepiandrosterone (DHEA) and its sulfate, which are converted peripherally to androstenedione and testosterone.
*Women with complaints of decreased libido or sexual well-being may be treated with DHEA replacement.
*DHEA should be discontinued periodically to assess these symptoms.
:*Preferred regimen (1): DHEA 50 mg orally once daily
==Differentiation==


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

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  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.
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  94. ↑ {{Cite journal | 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

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