Hemorrhagic gastroenteritis (HGE) is a clinically recognized but poorly described syndrome of dogs characterized by acute hemorrhagic diarrhea and marked hemoconcentration. Small and toy breed dogs appear overrepresented. No sex or age predilections have been identified.
Etiology and Pathophysiology
The etiology is unknown, but an intestinal hypersensitivity to or a consequence of Clostridium perfringens infection and ente-rotoxin production is suspected. Hypersensitivity to other bacterial, dietary, or parasitic antigens cannot be excluded. Leakage of fluid, plasma proteins, and RBC 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. 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, 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, thrombo-cytopathia, etc); severe GI ulceration; neoplasia; and GI perforation of any etiology.
Treatment and Prognosis
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 that are 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) and to decrease the potential for sepsis secondary to intestinal bacterial translocation are indicated. 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 (seecanine parvovirus, see Canine Parvovirus, and acute gastritis, see Acute Gastritis).
Prognosis is good with appropriate treatment. However, serious complications, including marked hypoproteinemia, DIC, sepsis, hypovolemic shock, and death, can occur.
Last full review/revision March 2012 by Kelly D. Mitchell, DVM, DVSc, DACVIM (SAIM)