HEMATEMESIS & MELENA

June 30, 2005

Glen E. Hastings MD

I Definitions:
o Hematemesis is the vomitus of bright red blood or “coffee-ground” material 1 .
o Melena is black, tarry stool which is foul smelling1 because of the presence of partially digested
blood products. Melena implies that the blood has been in the GI tract for at least 14 hours, &
that usually indicates an upper GI source, but melena may also occur with bleeding from the
small bowel or the right colon. Table 1: UGI Causes of Hematemesis & Melena
II Introduction: Sources %
Hematemesis &/or melena are caused by acute bleeding Duodenal Ulcerations 24.3%
Gastric Erosions 23.4%
from the upper GI tract or the mouth or pharynx. Profuse Gastric Ulcers 21.3%
hematemesis is a very common hospital emergency that Gastric or esophageal varices 10.3%
still caries an 8%- 14% hospital mortality 2 . Among adults, Mallory-Weiss tears 7.2%
hemorrhage from gastric or duodenal ulceration & Erosive Esophagitis 6.3%
Erosive Duodenitis 5.8%
esophageal varices are the most frequent causes. Other Neoplasms 2.9%
common causes & their relative frequency is shown in Stomal Ulcers 1.8%
3
Table 1. In children mucosal lesions and variceal Esophgeal Ulceration 1.7%
hemorrhage (commonly secondary to extra hepatic portal Miscellaneous 6.8%
venous obstruction) are common & in intensive care settings, ventilator management, infections and
drugs predominate as causes for stress ulceration 4 .
III Medical History & Physical Examination:
In no other situation is the medical history more important than in an acute GI bleed. Not only does
the history usually point to the diagnosis, more importantly it determines prognosis because patients
rarely die from exsanguinations, but more frequently from co-morbid conditions or complications. The
most important items of the physical examination are the vital signs, pulse, blood pressure,
respiratory rate & body temperature. The examining physician needs to obtain these measurements
personally or to verify their accuracy as well as to evaluate the patient for postural changes in pulse
or BP indicative of blood volume depletion. It takes at least 24 hours for a brisk GI bleed to be fully
reflected by decreased hematocrit & hemoglobin levels.
Differential Diagnosis of the Bleeding Source:
o Duodenal Ulcer & Erosive Duodenitis 5 :
General Considerations: 10% of UGI bleeding episodes caused by duodenal ulcer (DU) present
without prior symptoms. 70% stop spontaneously. Continuous infusion of a proton pump
inhibitor (PPI) keeping the gastric pH between 6 & 7 or infusion with octreotide or somatostatin
reduces rebleeding risk about 53%.
Symptoms & Signs: The pain of DU is characteristically burning in quality & epigastric in location
occurring about 2 hours after meals & relieved by antacids & two thirds of DU patients are
awakened at night by this symptom between 12 & 3AM. Others describe the pain as gnawing or
ill-defined and aching or “like a hunger pain”.
Physical examination usually demonstrates epigastric point tenderness, although this finding
does not distinguish between DU gastric ulcer (GU) or non-ulcer dyspepsia (NUD).
Diagnostic Testing: Upper endoscopy is the diagnostic modality of choice as it not only provides
an avenue for diagnosis but also provides information determining the likelihood of rebleeding as
well as an avenue for direct therapeutic intervention. Electrocoagulation or epinephrine injection
of an endoscopically visible blood vessel in the ulcer bed reduces the risk of recurrent bleeding
from 33% to less than 10%. Patients with a clean be ulcer with no visible vessel enjoy a
rebleeding rate approaching 0%, so once stabilized they can be discharged to outpatient care.
Both the rapid urease test & tissue biopsy of the ulcer bed are ≈ 95% sensitive & 95% specific for
H pylori. Serum gastrin levels >200pg/mL suggests Zollinger Ellison (ZE) syndrome.
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Prognosis: About ⅓ of patients rebleed with 2 years, so long term maintenance deals with the
causes of peptic ulceration, which are 3 in number: NSAIDS, H pylori & excessive gastric acid
(≈0.5% to 1% have Zollinger-Ellison syndrome)
Long Term Management: 90% of bleeding duodenal ulcers are H pylori related, so H pylori
eradication is the hallmark of long term medical management. No matter what the
pharmaceutical reps tell you, the most effective H pylori therapy as well as the cheapest is the
combination of a PPI, Pepto-Bismol, tetracycline & metronidazole QID for 2 weeks.
About 20% of peptic ulcers are NSAID related. NSAID use should be discontinued if at all
possible, because 15 to 30% of NSAID users develop ulcers. When this is impossible either a
PPI or misoprostol 200μg QID provide effective prophylaxis. The question of whether or not to
use a COX-2 NSAID must be evaluated alongside the increased risk of CAD associated with
these agents. PPIs are far & away the best agents for suppressing gastric acid production.
Surgery is reserved for refractory or persistently recurrent situations & is unusual today.
Complications & Comorbidities: Post-bulbar DU, multiple DUs or recurrent or refractory disease
suggests the possibility of ZE syndrome & is evaluated by testing for basal gastric acid secretion
>15mMol/hour, serum gastrin >1000pg/mL of elevated serum gastrin >200pg/mL within 2 minutes
of injecting 2U secretin/kG IV. 60% of the gastronomas causing ZE syndrome are malignant.
50% are located in the duodenium, 20% in the pancreas & another 10% in the local area.
o Gastric Ulcer (GU) presents in an older age group (peaking in the 6th decade) is unlikely to be
relieved by food & frequently occurs during meals. The pain is usually epigastric & may be
described as burning or aching & much more likely to be accompanied by bloating, anorexia,
nausea or vomiting. GU is much less likely related to H pylori & more likely related to NSAIDS &
baseline gastric acid is usually normal or decreased. Gastric ulcers that are not located in the
prepyloric area & the lesser curvature of the stomach are suspicious for gastric malignancy.
Diagnostic testing & management are as in DU.
o Hemorrhagic Erosive Gastritis:
Alcoholic Gastritis typically occurs in binge alcoholics (rarely in chronic continuous alcoholism)
after several weeks of heavy binging, frequently with little food intake. Antral gastritis supervenes
causing epigastric burning, cramping or aching pain, nausea & vomiting. This usually terminates
the drinking binge & the patient frequently arrives at the emergency room sober with a serum
ethanol level of zero. The pivitol diagnostic test is upper endoscopy. The degree of hemorrhage
is usually minimal unless the patient has an alcohol related coagulopathy. The treatment of the
bleeding is medical management with PPI therapy, but the most serious task is to look for & to
exclude more life threatening emergencies such as incipient delirium tremens, alcoholic
ketoacidosis or incipient hepatic coma induced by breakdown of blood in the GI tract in a patient
with borderline liver function, or acute pancreatitis.
NSAID Induced Antral Gastritis also may present with hematemesis. The diagnosis is made
endoscopically. The bleeding is usually minor & the treatment similar to NSAID induced ulcers.
H pylori also produces an antral gastritis which is treated similar to H pylori ulcers. MALT
lymphomas of the stomach as well as gastric carcinomas are associated with H pylori. It is
uncertain whether eradication of H pylori reduces their incidence.
“Stress Ulceration” with UGI bleeding is a life threatening emergency in the ICU setting that
occurs in severely ill patients (often requiring ventilator management). The most effective
prophylaxis to prevent stress related GI bleeding is a continuously infused PPI. Sucralfate is less
effective than the PPIs but has the advantage of not suppressing gastric acid production. Some
pulmonologists believe gastric acid suppression to be an important contributor to bacterial
overgrowth in the stomach leading to late-onset ventilator associated pneumonia (a major cause
of ventilator-associated mortality). Those pulmonologists prefer sucralfate prophylaxis. Both
reduce bleeding, neither reduce overall mortality.
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o Esophageal Varices1,6 :
General Considerations: When advanced cirrhosis of the liver increases venous pressures within
the portal system beyond 12cm/H2O, the result is venous engorgement & owing to the absence
of valves within the portal venous system, venous varicosities that may bleed unpredictably.
Variceal bleeding usually presents with massive painless hematemesis without apparent
precipitating factors in a patient with advanced liver disease. Variceal bleeding is always a
medical emergency & should be managed in an ICU setting.
Clinical Evaluation & Emergency Management: begins with careful assessment of the circulating
blood volume status & careful measurement of blood loss. A postural drop > 15mm/Hg in blood
pressure coupled with tachycardia or bradycardia are important signs of blood volume depletion &
an indication for emergency transfusion regardless of the hematocrit or hemoglobin. Physical
examination will usually reveal other evidence of portal hypertension such as ascites or peripheral
edema as well as evidence of impaired hepatocellular function such as “spider nevi”, “paper dollar
teleangectasia” or erythematous palms (caused by accumulation of estrogens usually detoxified
in the liver) or hepatic encephalopathy caused by the accumulation of nitrogenous products. INR,
aPTT & platelet count should be obtained & parenteral vitamin K & clotting factors should be
replaced as needed. Fresh frozen plasma is the emergency source of vitamin K dependent
coagulation factors during an acute bleeding episode & platelet packs are indicated if
thrombocytopenia (<20,000) is a contributing factor. Cryoprecipitate has no role in this setting.
Octreotide (50μg bolus followed by 50μg/hour IV drip) has replaced vasopressin as the agent of
choice to help control acute bleeding. Esophageal tamponade using a Sengstaken-Blakemore or
Minnesota tube is rarely used today because of high complication rates. When used, prior
endotracheal intubation is recommended because of the high incidence of aspiration pneumonia.
Diagnosis & Interventional Management is best done endoscopically. Variceal banding is
superior to sclerotherapy in mortality & morbidity for eradication of bleeding varices. Those in
whom bleeding persists or recurs may require a transjugular intrahepatic portosystemic shunt
(TIPS) procedure, which reduces variceal pressures more effectively & thereby decreases
bleeding more effectively than endoscopic therapy. The trade-off is that TIPS is more likely to
precipitate hepatic encephalopathy, the shunt tends to restenose after a year or two & although
variceal bleeding is reduced it doesn’t change mortality. Distal (splenorenal) shunting is reserved
for more compensated milder cases.
Long Term Management: Nonselective β-blocker therapy with propanolol or nadolol in dosages
reducing the hepatic porto-venous gradient (HPVG) to < 12cm/H2O, or to reduce pulse rate ≈25%
reduces bleeding rates 40 to 50% & improves mortality, when combined with variceal banding.
o Portal Hypertensive Gastropathy is associated with variceal bleeding as it is a congestive
gastropathy caused by increased portal pressures in cirrhotic patients. The endoscopic
appearance is a friable engorged gastric mucosa & its treatment is β-blockade as with
esophageal varices. PPIs, H2 antagonists & sucralfate are ineffective & have no role in this
setting.
o Mallory-Weiss Tears1: also occur in the setting of alcoholic gastritis as well as other conditions
featuring violent retching or coughing. Hemorrhage, which may quite profuse occurs immediately
from a tear at or nearby the squamocolumnar border & resolves spontaneously in 80 to 90% of
cases. Rebleeding occurs in less than 5%. Persistent or recurrent bleeding may respond to
vasopressin or octreotide infusion & has also been managed by arterial embolization. Surgical
oversewing is rarely required.
o Erosive Esophagitis 7 : is characterized endoscopically as inflamed, friable mucosa with linear
ulcers that are usually superficial & exudates. Most patients will have several years’ history of
heartburn, reflux of sour caustic material into the oropharynx, hoarseness & sometimes nocturnal
asthma or repeated episodes of aspiration pneumonia (in severe cases) prior to the occurrence of
hematemesis or (more frequently) dysphagia. The bleeding is usually not severe & tends to
resolve spontaneously. Erosive gastritis, over time however tends to stimulate the development
of metaplastic columnar endothelial changes in the distal esophagus (Barrett’s esophagitis).
Barrett’s esophagitis increases the risk of esophageal cancer by 30 to 125 times that of the
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general population. The rate of cancer development is about 0.5%/year so intensive treatment
with PPI therapy is indicated along with periodic surveillance endoscopy. When high grade
dysplasia is found the treatment of choice is surgical esophagectomy of the involved mucosal
segment.
o Malignancies:
o Unusual Causes of Hematemesis or Melena:
Hemorrhage from the small bowel causes melena or hematochezia & will be discussed in the
outline by that title. Other unusual causes of UGI bleeding include teleangectsias such as in
hereditary Osler-Weber-Rendu syndrome, gastric antral ectasia (“watermelon stomach”) or a
superficial mucosal Dieulafoy vessel, bleeding from gastric prolapse secondary to violent
retching, ruptured aortic aneurism or bleeding from the pancreatic or bile ducts.
Common Comorbidities & Complications:
Because alcoholism is an increasing pandemic in the developed & developing world & is ubiquitous
among most of the patients seen on any medical school hospital service, the potentially lethal
comorbidities of alcoholism should always be considered & excluded by appropriate testing or clinical
observation.
o Alcoholic Ketoacidosis 8,9 occurs among binge drinking alcoholics when antral gastritis causes
abdominal pain nausea & vomiting & termination of the drinking binge. By the time of arrival at
the ER the patient may be sober with an ethanol level of zero. Hyperglycemia is usually not
present or not impressive & the dipstick Acetest for ketones may not be impressive because it
detects only acetoacetic acid & the vast majority of the acidosis is because of β-hydroxybutyrate.
Its presence is detected by a low serum bicarbonate & a markedly elevated anion gap. The
problem is severe metabolic acidosis secondary to depleted liver glycogen stores, low serum
insulin levels, elevated glucagon levels & starvation ketosis. Vomiting will likely have produced a
concomitant metabolic hypokalemic alkalosis. The most serious danger is that, as the
ketoacidosis improves & the pH returns toward normal, the resulting intracellular influx of
potassium may be so abrupt & profound as to result in a lethal cardiac dysrythmia. Concomitant
seizures or delirium tremens may produce a respiratory alkalosis while pneumonia, GI bleeding,
thiamin deficiency or pancreatitis may produce lactic acidosis. Treatment is with saline & glucose
resuscitation, aggressive potassium, glucose and thiamin replacement. Insulin is not required
unless the patient is diabetic. Magnesium or calcium supplementations are sometimes required
o Hepatic Encephalopathy5: Gastrointestinal hemorrhage is the most common event precipitating
hepatic encephalopathy in previously stable cirrhotic patients. Its onset is heralded by a subtle
loss of the ability of the patient to follow a linear train of conversation which progresses to frank
confusion & mood lability, then to slurred speech & “sundowning”, followed by astarixis, lethargy
& characteristic triphasic EEG waves, then to coma & death. It is useful to grade the level of
hepatic encephalopathy as a guide to monitoring therapy & assessing prognosis. The grades of
hepatic coma are shown in Table 2:
Table 2: Stages of Hepatic Coma:

Stage Symptoms Neurological Changes EEG

I. Impaired attention/cognition,
Tremor, apraxia, poor Triphasic wave activity (5 cps).
Psychiatric/personality changes,
handwriting.
"Sundowning".

II. Gross mental confusion, Drowsiness Astarixis, dysarthria, ataxia &

Amnesia, Speech disorders, hypoactive reflexes Triphasic wave activity (5 cps).
Inappropriate behavior.

III. Somnolent but arousable, Astarixis, hyperactive reflexes, Grossly abnormal EEG with theta &
Disoriented; bizarre. rigidity. 5 cps triphasic waves

IV. Comatose Decerebration Delta waves

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Acute alcohol intoxication, delirium tremens, sepsis, head injury or subdural hematoma or
Wernicke-Korsakoff syndrome may all mimic hepatic coma, particularly inn its earlier stages.
There is no single diagnostic test for hepatic encephalopathy, but an elevated serum ammonia
level is helpful in patient with stigmata of advanced liver disease, a prolonged INR, an obvious
precipitating event (like a GI bleed), progressive neurological findings as described above,
characteristic EEG findings & the exclusion of other diagnostic possibilities.
Treatment is with bowel evacuation of blood & other nitrogenous products, treatment of the
precipitating event & good supportive care. The Child-Pugh staging classification shown in Table
3 is useful for estimating long term prognosis 10 :
Table 3: Child-Pugh Classification of the Stages of Cirrhosis
Assessment Category Assessment Score
1 Point 2 Points 3 Points
Stage of Encephalopathy None Stage 1-2 Stage 3-4
Ascites None Mild Moderate
Total Bilirubin (mg/dL) ≤2.0 mg/dL 2.1-2.9 mg/dL ≥3.0 mg/dL
Exception: Primary Biliary Cirrhosis ≤4.0 mg/dL 4.1-9.9mg/dL ≥10.0mg/dL
Serum Albumin (mg/dL) <3.5mg/dL 2.8-3.5mg/dL < 2.8mg/dL
Prothrombin Time Ratio (International Normalized Ratio) < 1.4 1.4-2.0 > 2.0
Scoring:
Class A (Well Compensated) 5-6 Points. Class B (Mildly Decompensated): 7-9 Points. Class C (Decompensated) 10-15 Points.
A series of 402 Spanish cirrhotic patients were reported in 2002 after being followed for an
average of 73 months following a first episode of GI bleeding. Only about 40% of Class C
patients survived 6 weeks. The median survival of Class B patients was about 40 months & the
median survival of Class A patients was just short of 100 months9.
o Alcohol Withdrawal, Seizures & Delirium Tremens 11 :
In 90% of cases, alcohol withdrawal is limited to mental confusion, anxiety, tremulousness,
anorexia, mood lability visual tactile or auditory hallucinations and agitation which peak at 24-36
hours & gradually subside. Seizures may occur within 8-24 hours of the last drink & generally
peak at about 24 hours. About 1% of cases worsen, autonomic instability occurs and about 72-96
hours after the last drink full-blown delirium tremens supervenes. In DT’s the patient becomes
globally disoriented, autonomic instability manifests itself as fever > 101o, tachycardia
>120/minute, diaphoresis, disruption of the sleep/wake cycle and severe agitation. The duration
is variable, averaging 2-5 days. Expected mortality is about 10%.
Benzodiazepines are the treatment of choice. The advantage of longer acting benzodiazepines is
that they are more effective at preventing seizures & produce better symptom control, since their
blood levels do not fluctuate as much as shorter acting agents. Their disadvantage is a longer
period of sedation in the event of overdose. The shorter acting agents are also safer in patients
with liver failure. In patients without evidence of liver failure long acting agents are preferable.
The initial dose is established at presentation and decreased by 20% each day thereafter. Some
programs administer the drugs on a fixed schedule (such as 50mg chlordiazepoxide or 20mg
diazepam every 6 hours). Others tailor the dose to the severity of the withdrawal symptoms &
signs.
o Wernicke-Korsakoff Syndrome10:
Wernicke’s syndrome is a neurological emergency calling for immediate administration of
parenteral thiamin. It is a disease of acute onset consisting of a triad of: Cranial Nerve VI palsy
(weakness of lateral gaze) accompanied by nystagmus, diplopia, and strabismus, ataxia of gait &
stance & global confusion and apathy. As the delirium clears, it may be replaced by an often
permanent defect in retentive memory and learning, frequently accompanied by confabulation,
Korsakoff’s syndrome in which the sensorium is not clouded. Wernicke-Korsakoff Syndrome is
caused by profound thiamin deficiency & may be inadvertently precipitated by the administration
of intravenous or oral glucose, which accelerates the use of thiamin. To prevent this eventuality
all patients treated with parenteral as well as oral thiamin administered before or simultaneously
with any IV fluids containing glucose or fructose. Parenteral therapy is especially important in the
malnourished. Oral therapy should be continued for several weeks. Korsakoff’s syndrome is
permanent & irreversible but potentially preventable.
 Hematemesis: Page 6 of 7

o Acute Alcoholism: Occasionally, acutely intoxicated patients become combative during

treatment for UGI bleeding & are sedated with parenteral benzodiazepines, sometimes at doses
sufficient to produce profound respiratory depression, once behavioral controls established. It is
sometimes difficult to empathize with such patients but it is nonetheless essential to continuously
monitor the O2 saturation & respiratory status of during the first few hours. A greater number of
anesthetic deaths may well occur on the way to x-ray or to the endoscopy suite than in the OR.
o Acute Pancreatitis: Many causes of GI bleeding regularly produce mild elevations of serum
amylase. In order to be considered indicative of acute pancreatitis the level must be at least 3X
the upper limit of normal at the lab doing the test. Even then serum amylase has only a 68%
sensitivity & 75% specificity for pancreatitis. Serum lipase is a much better test with a sensitivity
of 95% & a specificity of 95%. CT without contrast characteristically shows pancreatic
parenchymal & peripancreatic edema & sometimes fluid collections & is virtually 100% accurate
for the diagnosis. When pancreatitis coexists it is imparitive that Ranson’s or the Glascow criteria
be determined (see Table 3). When 3 or more of Ranson’s criteria are present, a mortality in
excess of 15% is predicted indicating the need for prophylactic antibiotic therapy & evaluation
after the 3rd day after onset, for pancreatic necrosis using “rapid bolus” CT technique.
Table 3: Prognostic Criteria for Acute Pancreatitis
Ranson’s Criteria Modified Glasgow Criteria
Non-gallstone Pancreatitis Gallstone Pancreatitis
• Age >55
On Admission: On Admission: • WBC > 15,000
• Age > 55 • Age > 70 • Blood glucose> 180 mg/dL
• WBC > 16,000 • WBC > 18.5 K • BUN > 45 (after rehydration)
• Blood glucose>200 mg/dL • Blood glucose> 180 mg/dL • pO2 < 60 mm Hg
• Serum LDH > 350 IU/L • LDH > 400 U/dL • Ca < 8 mg/dL
• AST (SGOT) > 250 IU/L • AST >250 U/dL • Albumin < 3.4 gm/dL
Within 48 hours: Within 48 Hours: • LHD > 600 IU
• Hematocrit decrease > • Hematocrit decrease > • AST or ALT > 200 IU
10% 10%
• BUN increase > 5 mg/dL • BUN increase > 2 mg/dl Interpretation:
• Serum calcium < 8 mg/dL • Serum Calcium < 8 mg/dl 3 or more at any time during the first
• Arterial pO2 < 60 mm Hg • Base deficit > 5 mmol/L 48 hours indicates severe
• Base deficit > 4 • Fluid deficit > 4 liters pancreatitis.
• Fluid deficit > 6L
Interpretation:
mild attack: < 0-2 sign (<1% mortality)
moderate attack: 3-4 signs (16% mortality)
severe attack: 5 or more signs (>40% mortality)
Similar to alcoholism, tobacco habituation, obesity & their attendant risks for atherosclerotic,
hypertensive & pulmonary comorbidities need always be considered & excluded in UGI bleeding:
o Acute Myocardial Infarction: Coexisting chest pain, new onset dyspnea or (in patients > age
65) a new neurological event or symptom, require exclusion of acute myocardial infarction by
serial EKGs & troponin. ST segment elevation in 2 contiguous EKG leads is 45% sensitive &
95% specific for AMI 12 . A baseline EKG is required for all adult patients with GI bleeding.
o Respiratory Failure: can occur either because of coexistent community acquired pneumonia,
Nosocomial pneumonia, aspiration pneumonia or depression of the respiratory drive. The latter
has already been discussed. The diagnosis of aspiration or Nosocomial pneumonia is usually
straight forward unless the resident fails to look for it. Aspiration pneumonia evolves in 3 phases:
The first, acute aspiration is managed sometimes supplemented with tracheobronchial lavage.
The second phase, which occurs within a few hours shows x-ray shadowing caused by the tissue
irritant effects of gastric contents. The bacterial phase only occurs about ⅓ of the time & not until
3 days later. It is only in this last phase that an antibiotic (i.e. clindamycin) is indicated.
 Hematemesis: Page 7 of 7

IV Requisite Laboratory Evaluation:

o When bleeding is brisk especially if signs of hemodynamic instability are present t is wise to type
4 to 6 units of packed red blood cells “stat”.
o Upper endoscopy is the immediately preferred diagnostic & therapeutic modality.
o EKG, comprehensive metabolic profile (CMP), CBC with platelet count & differential, O2
saturation, INR & aPTT are always indicated to screen for serious comorbidities as well as
specifically additional laboratory work indicated by the initial workup or preexisting conditions.
V Bibliography:
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2
Meier R, Wettstein AR. Treatment of acute nonvariceal upper gastrointestinal hemorrhage. Digestion. 1999;60 Suppl 2:47-52.
3 th
Elta, GH, Approach to the patient with gross gastrointestinal hemorrhage. Ch 33 in Textbook of Gastroenterology 4 Edition.
Editor: Yamada T. Lippincott, Williams & Wilkins Philadelphia PA 2002; pages 696-723.
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Arora NK, Ganguly S, Mathur P, Ahuja A, Patwari A. Upper gastrointestinal bleeding: etiology and management. Indian J
Pediatr. 2002;69(2):155-68.
5
Valle JD. Peptic Ulcer Disease & Related Disorders. Ch. 274 in Harrison’s Principles of Internal Medicine 16thEdition. Eds:
Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 pages 1746-62.
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Chung RT, Podolsky DK. Cirrhosis & Its Complications. Ch. 289 in Harrison’s Principles of Internal Medicine 16thEdition. Eds:
Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 pages 1858-69.
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Goyal RK. Diseases of the Esophagus. Ch. 273 in Harrison’s Principles of Internal Medicine 16thEdition. Editors: Kasper DL,
Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 pages 1739-46.
8
Wrenn KD, Slovis CM, Minion .GE, Rutkowski R: The syndrome of alcoholic ketoacidosis. Amer J Med 1991;91:119-28.
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Fulop M: Alcoholic ketoacidosis. Endocrinol Metab Clin North Am. 1993;22:209-19.
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del Olmo JA, Peña A, Serra MA, et al. Predictors of morbidity and mortality after the first episode of upper gastrointestinal
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11 th
Mayo-Smith MF, Chapter 2: Management of Alcohol Intoxication and Withdrawal in Schuckit MA Drug and Alcohol Abuse 4
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12
1999 Update: ACC/AHA Guidelines for the management of patients with acute myocardial infarction: A report of the ACC/AHA
task force on practice guidelines. J Am Coll Cardiol 1999;34:890-911.