Sandbox:Aditya

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.
• 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 .
• 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
  • 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.
• 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
• 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.

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:

• 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.

A directed history may also alert to consider unusual causes.

• 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===

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.

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.

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.
• 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%.
• 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:

• 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.
• 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.
• 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:

• 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.

• 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.

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.

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.
• 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

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.

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.
  • Varices are large, tortuous veins and protrude into the lumen, rupturing.
  • Helicobacter pylori disrupts the mucosal barrier and causes inflammation of the mucosa of the stomach and duodenum.
  • 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.
  • NSAIDs inhibit cyclooxygenase, leading to impaired mucosal defenses by decreasing mucosal prostaglandin synthesis.
  • 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.

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		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 Epithelial regeneration.
Esophagitis	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			Basal cell hyperplasia Elongation of the lamina propria papillae Mixed intraepithelial inflammation Neutrophils, eosinophils, and lymphocytes Squamous cell degeneration.
Barrett Esophagus			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		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		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		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		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.

Initial Laboratory Studies

• The hematocrit level is used to identify the degree of blood loss and suggests the acuity or chronicity of blood loss.
• 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.
• 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.
• 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

Patient’s hemodynamic stability

Stable with low volume bleeding

Unstable with large volume bleeding

Repeat endoscopy

Surgery exploration and partial gastrectomy

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:

• 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.

	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.
• 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 Abnormal LFT Ultrasound shows biliary dilatation/stents/tumor Biliary drainage (ERCP) + IV antibiotics Acute cholecystitis RUQ + − + + − − − − − − − Hypoactive Hyperbilirubinemia Leukocytosis Ultrasound shows: Gallstone Inflammation Murphy’s sign Acute pancreatitis Epigastric + − + ± − − + − ± − − N Increased amylase / lipase 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 ↑ Alkaline phosphatase ↑ serum bilirubin ↑ gamma-glutamyl transpeptidase ↑ CA 19-9  MDCT with  PET/CT MRI Skin manifestations may include: Bullous pemphigoid Cicatricial pemphigoid Migratory superficial thrombophlebitis (classic Trousseau's syndrome) Pancreatic panniculitis 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 Increased liver enzymes Increased IgM, IgG4 Anti-neutrophil cytoplasmic antibody (p-ANCA) Anti-nuclear antibody (ANA) Anti-smooth muscle antibody (Anti-Sm) Anti-endothelial antibody Anti-cardiolipin antibody 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 Leukocytosis Ultrasound shows gallstone Fatty food intolerance Gastric causes Peptic ulcer disease Diffuse ± − + − − − + Gastric ulcer- melena and hematemesis Duodenal ulcer- melena and hematochezia Positive if perforated Positive if perforated Positive if perforated N Ascitic fluid LDH > serum LDH Glucose < 50mg/dl Total protein > 1g/dl Air under diaphragm in upright CXR Upper GI endoscopy for diagnosis 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 H.pylori infection diagnostic tests Endoscopy H.pylori gastritis guideline recommendation Gastroesophageal reflux disease Epigastric − − ± − − − − − − − − N N Gastric emptying studies Esophageal manometry Endoscopy for alarm signs Gastric outlet obstruction Epigastric − − ± − − − + − − − − Hyperactive Complete blood count Basic metabolic panel Abdominal x-ray- air fluid level Barium upper GI studies- narrowed pylorus Succussion splash Gastroparesis Epigastric − − + − − − + − ± − − Hyperactive/hypoactive Hemoglobin Fasting plasma glucose Serum total protein, albumin, thyrotropin (TSH), and an antinuclear antibody (ANA) titer HbA1c 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 Air under diaphragm in upright CXR Hamman's sign Dumping syndrome Lower and then diffuse − − + − − + + − + − − Hyperactive Glucose challenge test Hydrogen breath test Upper GI series Gastric emptying study 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 Leukocytosis Ct scan Ultrasound Positive Rovsing sign Positive Obturator sign Positive Iliopsoas sign Acute diverticulitis LLQ + ± + − + ± − + Positive in perforated diverticulitis + + Hypoactive Leukocytosis CT scan Ultrasound History of constipation Inflammatory bowel disease Diffuse ± − − ± − + + + − − − Normal or hyperactive Anti-neutrophil cytoplasmic antibody (P-ANCA) in Ulcerative colitis Anti saccharomyces cerevisiae antibodies (ASCA) in Crohn's disease String sign on abdominal x-ray in Crohn's disease Extra intestinal findings: Uveitis Arthritis Irritable bowel syndrome Diffuse − − − − ± ± + − − − − N Normal Normal Symptomatic treatment High dietary fiber Osmotic laxatives Antispasmodic drugs Whipple's disease Diffuse ± − − ± − + + − ± − − N Thrombocytopenia Hypoalbuminemia Small intestinal biopsy for Tropheryma whipplei Endoscopy is used to confirm diagnosis. Images used to find complications Chest and joint x-ray CT MRI Echocardiography Extra intestinal findings: Uveitis Endocarditis Encephalitis Dementia Hepatosplenomegaly Arthritis Ascites 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 Anemia Leukocytosis especially in patients with Clostridium difficile infection Hypoalbuminemia Metabolic alkalosis associated with a poor prognosis Metabolic acidosis secondary to ischemic colitis 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 Fat soluble vitamin deficiency Hypoalbuminemia Fecal stool test Barium studies: Dilation and edema of mucosal folds Steatorrhea- 10-40 g/day (Normal=5 g/day) Celiac disease Diffuse − − − − − + + − − − − Hyperactive IgA endomysial antibody IgA tissue transglutaminase antibody Anti-gliadin antibody Small bowel biopsy US: Bull’s eye or target pattern Pseudokidney sign Gluten allergy Infective colitis Diffuse + − ± − − + − + Positive in fulminant colitis ± ± Hyperactive Stool culture and studies Shiga toxin in bloody diarrhea PCR 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 CBC Blood cultures Abnormal liver function tests US CT Hepatocellular carcinoma/Metastasis RUQ + − − + − − + − − − − Normal Hyperactive if obstruction present High levels of AFP in serum Abnormal liver function tests US CT Liver biopsy Other symptoms: Splenomegaly Variceal bleeding Ascites Spider nevi Asterixis 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 Elevated 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 levels, decreased serum albumin level. Findings on CT scan suggestive of Budd-Chiari syndrome include: Early enhancement of the caudate lobe and central liver around the inferior vena cava 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 In the chronic phase, there is caudate lobe enlargement and atrophy of the peripheral liver in affected areas Ascitic fluid examination shows: Total protein more than 2.5 g per deciliter White blood cells are usually less than 500/μL. 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 Hypoalbuminemia Prolonged PT Abnormal LFTs Hyponatremia Thrombocytopenia US Nodular, shrunken liver Ascites 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 Hematuria Ultrasound CT scan Colicky abdominal pain Dysuria Hollow Viscous Obstruction Small bowel obstruction Diffuse + − + − + − + − + + ± Hyperactive then absent Leukocytosis with left shift indicates complications 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 Leukocytosis CT scan and abdominal X ray U shaped sigmoid colon "Whirl sign" Biliary colic RUQ − − + + − − − − − − − N ↑ bilirubin and alkaline phosphatase 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 Leukocytosis and lactic acidosis Amylase levels D-dimer CT angiography SMA or SMV thrombosis Also known as abdominal angina that worsens with eating Acute ischemic colitis Diffuse + ± + − − + + + + + + Hyperactive then absent Leukocytosis 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 Fibrinogen D-dimer Focused Assessment with Sonography in Trauma (FAST)  Unstable hemodynamics Intra-abdominal or retroperitoneal hemorrhage Diffuse ± − ± − − − − + + − − N ↓ Hb ↓ Hct CT scan History of trauma 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 ↑ ESR ↑ CRP Ultrasound Sudden onset & severe pain Acute salpingitis RLQ / LLQ + ± − − − − − − − ± ± N Leukocytosis Pelvic ultrasound Vaginal discharge Cyst rupture RLQ / LLQ − − + − − − − − + ± ± N ↑ ESR ↑ CRP Ultrasound Pregnancy Ruptured ectopic pregnancy RLQ / LLQ − − + − − − − − + + + N Positive pregnancy test Ultrasound History of Missed period Vaginal bleeding Extra-abdominal causes Pulmonary disorders Pleural empyema RUQ/Epigastric + ± − − − − + − − − − N Thoracentesis Chest X-ray Pleural opacity Localization of effusion Physical examination Crackles Egophony Increased tactile fremitus Pulmonary embolism RUQ/LUQ ± − − − − − − − ± − − N ABGs D-dimer CXR V/Q scan Spiral CT pulmonary angiogram 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 Cardiac enzymes ECG Echocardiogram Wall motion abnormality Wall rupture Septal rupture Chest pain, tightness, diaphoresis Complications: Arrythmias Mitral regurgitation Ventricular wall rupture Septal rupture

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.
Appendicitis	Pain localized to the right iliac fossa, vomiting, abdominal ultrasound sensitivity for diagnosis of acute appendicitis is 75% to 90%.
Rupturedovarian cyst	Usually spontaneous, can follow history of trauma, mild chronic lower abdominal discomfort may suddenly intensify, ultrasound is diagnostic.
Ovarian cyst torsion	Presents with acute severe unilateral lower quadrant abdominal pain, nausea and vomiting, tender adnexal mass palpated in 90%, ultrasound is diagnostic.
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.
Endometriosis	Presents with cyclic pain that is exacerbated by onset of menses, dyspareunia. laparoscopic exploration is diagnostic.
Acute cystitis	Presents with features of increased urinary frequency, urgency, dysuria, and suprapubic pain.

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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References

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