Melena
Bradford P. Smith
Melena (dark, tarry feces) is caused by blood in the lumen of the stomach or proximal intestinal tract, resulting in black (digested) blood appearing in the feces (Boxes 7.9 and 7.10).
Usually blood is a result of a bleeding ulcer in the stomach or abomasum but may also result from ingestion, oral or pharyngeal bleeding, or coughing up blood that is then swallowed. In ruminants the presence of dark red feces from an intussusception is the main differential to be considered. Blood must stay in the intestinal tract for hours before the hemoglobin is altered and turns black. Small amounts of hemoglobin can be detected by using one of the tests for occult blood. In general, fairly large volumes of blood (1 to 2 L) are required to produce a positive fecal occult blood test in the horse (Carlson G, personal communication, 1990). A 24- to 48-hour time period is necessary for orally administered blood to reach the rectum in the horse. In ruminants, smaller volumes of blood are necessary to produce a positive fecal occult test, and a faster transit time is expected (Carlson G, personal communication, 1990).In approaching a diagnosis, rule out pulmonary, oral, or pharyngeal bleeding. Bleeding of gastrointestinal origin can be determined to be caused by mucosal disease or full-thickness bowel disease (such as an intussusception or neoplasia) by examining peritoneal fluid for abnormalities. Abnormalities in peritoneal fluid are usually present in the case of serosal
■ BOX 7.9
Causes of Melena in Horses
Common Causes
Gastric or duodenal ulcer
Gastric squamous cell carcinoma
Coughing up and swallowing blood
Less Common Causes
Phenylbutazone toxicity (nonsteroidal antiinflammatory drugs
[NSAIDs])
Purpura hemorrhagica
Gastroenteritis with bleeding
Warfarin toxicity or other coagulation disorder Colonic hematomas
Disseminated intravascular coagulation with mucosal hemorrhage Anterior or proximal enteritis (duodenitis or proximal jejunitis) Arsenic toxicity
Hepatic failure with hemolysis
NSAID toxicity
Uncommon Causes
Lupus erythematosus
Factor VIII deficiency, hemophilia A
Histoplasmosis Hemangiosarcoma
Snake bite
■ BOX 7.10
Causes of Melena in Ruminants
Common Causes
Abomasal ulcer
Intussusception
Less Common Causes
Lung abscess with ruptured blood vessel Oak toxicity
Coccidiosis
Gastroenteritis with bleeding Arsenic toxicity
Ingestion of blood after parturition
Intestinal parasites
Toxicity from nonsteroidal antiinflammatory drugs Abomasal torsion or volvulus
Hemorrhagic bowel syndrome
Uncommon Causes
Duodenal ulcers
Hemophilia A, factor VIII deficiency
Bacillary hemoglobinuria
Sulfur toxicity
Warfarin poisoning or other coagulation disorder Snake bite
Bovine viral diarrhea
Malignant catarrhal fever
Winter dysentery
Narthecium asiaticum maxim poisoning (exotic)
involvement. Bleeding abomasal ulcers are probably the leading cause of melena in ruminants.
They can be silent except for the dark feces and weakness if severe anemia develops. In older horses, gastric squamous cell carcinoma is a frequent cause of gastric hemorrhage. Significant bleeding is much less common in foals and calves with gastric ulcers, and melena is rare in foals and calves with gastric ulcers.Consideration should be given to whether or not the melena is the result of clotting abnormalities associated with such diseases as DIC or warfarin poisoning. In cattle with colic and dark red-to-black feces, intussusception should be considered likely.
When severe anemia develops, there is evidence of blood loss because the decrease in PCV and RBCs is accompanied by a decrease in plasma proteins. Nonspecific therapy for melena consists principally of blood transfusions in life-threatening cases. Sudden, massive gastric or abomasal bleeding may result in anemia and collapse before melena has appeared.
In the foal, gastric ulcers may be treated with histamine-2 (H2) blockers such as ranitidine or cimetidine, or with hydrogen pump blockers. The H2 blockers are probably less effective in ruminants. Their benefit in ruminants with abomasal ulcers is not well understood at present. Drugs such as the hydrogen pump blocker omeprazole are useful and potent gastric pH effectors. Therapy with protectants such as sucralfate (which coats the ulcer) is a viable and clinically useful therapy in the horse. In ruminants, orally administered protectants and antacids are so diluted by the time they reach the abomasum that they are probably of limited benefit.