Hemorrhagic Gastroenteritis in Small Animals

The precise etiology and pathogenesis are unclear, but suspicion that HGE is the result of infection with or hypersensitivity to Clostridium perfringens seems reasonable. Clostridium spp has been identified by bacterial culture or immunohistopathology in small-intestinal biopsies from dogs with HGE, suggesting an association with clostridial overgrowth. Acute intestinal mucosal hemorrhagic necrosis and neutrophilic inflammation are the predominant histologic lesions, with the most severe lesions occurring in the large intestine. Histologic mucosal lesions are not generally identified in the stomach, leading some to suggest "acute hemorrhagic diarrhea syndrome" may be a more appropriate descriptor. Leakage of fluid, plasma proteins, and RBCs into the intestinal lumen occur secondary to increased intestinal permeability.

An acute onset of profuse hemorrhagic diarrhea (often said to resemble raspberry jam) in a small or toy breed dog is characteristic of HGE. Vomiting, anorexia, lethargy, and abdominal pain are common. Vomiting may precede the onset of bloody diarrhea. Marked, peracute fluid loss can result in hypovolemic shock before clinically recognizable dehydration. Other historical findings (eg, dietary indiscretion, vaccination status, etc) are unremarkable. HGE is not considered contagious.

The diagnosis is typically based on signalment and acute onset of clinical signs with hemoconcentration (PCV 55%) and normal to slightly decreased total plasma protein concentration. Selective culture for fecal pathogens (eg, Clostridium spp, Salmonella spp, Yersinia spp, Clostridium spp, Campylobacter spp, enterotoxigenic Escherichia coli, etc) and evaluation for Clostridium spp enterotoxin by fecal ELISA can be considered. Abnormalities on CBC are usually limited to hemoconcentration and neutrophilic leukocytosis. If neutropenia is present, sepsis and/or parvovirus enteritis may be a concern. Serum biochemical profile may be unremarkable or show mild panhypoproteinemia, hypoglycemia (sepsis, decreased intake with limited hepatic glycogen stores), and electrolyte abnormalities consistent with GI loss and decreased intake (ie, hypokalemia, hyponatremia, hypochloremia). There have been anecdotal reports of mildly prolonged (<10%) coagulation times (activated clotting time, prothrombin time, partial thromboplastin time), potentially attributable to inflammation or interference due to hemoconcentration. If coagulation times are moderately or markedly prolonged, coagulopathy or disseminated intravascular coagulation (DIC) should be investigated. Basal serum cortisol concentration should be normal to increased and is an appropriate screening test for hypoadrenocorticism. Radiographic and ultrasound abnormalities should be limited to diffuse ileus and fluid-filled loops of bowel. Differential diagnoses include bacterial, viral (eg, parvovirus, coronavirus), and parasitic (eg, Trichuris vulpis, Ancylostoma spp, Uncinaria spp) gastroenteritis; systemic disturbances with secondary GI involvement (eg, hypoadrenocorticism, pancreatitis, renal failure, hepatic disease, etc); coagulopathy (eg, rodenticide toxicosis, thrombocytopenia, thrombocytopathia, etc); severe GI ulceration; neoplasia; and GI perforation of any etiology.

Aggressive IV fluid therapy is the mainstay of treatment. The rate of isotonic fluid administration is based on patient perfusion, degree of dehydration, and ongoing losses. Dogs markedly hypoproteinemic or in shock may benefit from synthetic or natural colloid (stored or fresh frozen plasma) therapy. Parenteral antibiotics effective against Clostridium spp (eg, ampicillin 22 mg/kg, IV, tid-qid, or metronidazole 7.5 mg/kg, IV, bid) and to decrease the potential for sepsis secondary to intestinal bacterial translocation are indicated. Additional antibiotic coverage for gram-negative bacteria (eg, enrofloxacin 5–10 mg/kg/day, IV) is indicated in animals with sepsis or neutropenia. In a prospective study of dogs with HGE and no clinical indices of sepsis, treatment with amoxicillin-clavulanic acid did not affect mortality rate, duration of hospitalization, or severity of clinical signs. This might suggest not all cases of HGE are due to primary bacterial infection or that the bacteria involved may not be susceptible to amoxicillin-clavulanic acid. Depending on serum potassium concentration, maintenance fluids should be supplemented with potassium chloride at 20–40 mEq/L to prevent development of hypokalemia. Hypoglycemic dogs require dextrose supplementation (2.5%–5%) of maintenance IV fluids. Additional supportive care, including antiemetic therapy and dietary management, are as described above (see Canine Parvovirus and see Acute Gastritis). Rehydration with a balanced oral electrolyte solution (an initial volume of 7% dehydration [to be replaced over 12 hr] should be offered every 4 hr, along with volumes to account for maintenance fluid requirements and ongoing losses) may be appropriate for dogs with mild dehydration and mild clinical signs.

Prognosis is good with appropriate treatment. However, serious complications, including marked hypoproteinemia, DIC, sepsis, hypovolemic shock, and death, can occur.