Acute hemorrhagic diarrhea syndrome in dogs is characterized by both acute vomiting and diarrhea. The diagnosis is based on clinical signs and a PCV >60%. Prompt IV fluid therapy is the main treatment. Parenteral antibiotics may also be helpful, especially if there is sepsis or neutropenia.
Acute hemorrhagic diarrhea syndrome (AHDS) in dogs is characterized by acute vomiting and hemorrhagic diarrhea, often accompanied by hemoconcentration. Young (median age 5 years), small and toy breed dogs (Yorkshire Terrier, Miniature Pinscher, Miniature Schnauzer, Miniature Poodle, Maltese) are overrepresented.
Etiology and Pathophysiology of Acute Hemorrhagic Diarrhea Syndrome
The precise etiology and pathogenesis are unclear. Acute hemorrhagic diarrhea syndrome may be the result of infection with or hypersensitivity to Clostridium perfringens. Clostridium spp have been identified by bacterial culture or immunohistopathology in small-intestinal biopsies from dogs with AHDS, suggesting an association with clostridial overgrowth. Leakage of fluid, plasma proteins, and RBCs into the intestinal lumen occurs secondary to increased intestinal permeability.
Clinical Findings of Acute Hemorrhagic Diarrhea Syndrome
An acute onset of profuse hemorrhagic diarrhea (often said to resemble raspberry jam) in a small or toy breed dog is characteristic of AHDS. 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. AHDS is not considered contagious.
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 to a change in name from hemorrhagic gastroenteritis to AHDS.
Diagnosis of Acute Hemorrhagic Diarrhea Syndrome
Acute onset of hemorrhagic diarrhea
Severe hemoconcentration (PCV >60%)
Diagnosis of acute hemorrhagic diarrhea syndrome is typically based on signalment and acute onset of clinical signs with hemoconcentration (PCV >60%) and normal to slightly decreased total plasma protein concentration. Abnormalities on CBC are usually limited to hemoconcentration and neutrophilic leukocytosis. If neutropenia is present, sepsis and/or parvovirus enteritis may be a concern.
The 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.
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)
coagulopathy (eg, rodenticide toxicosis, thrombocytopenia, thrombocytopathia, etc)
severe GI ulceration
neoplasia
GI perforation of any etiology
Treatment and Prognosis of Acute Hemorrhagic Diarrhea Syndrome
Prompt IV fluid therapy titrated against the PCV
Parenteral antibiotics may be needed
Prompt 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 at 10–50 mg/kg, IV, every 6–8 hours; or metronidazole at 10–44 mg/kg, IV, every 12 hours) may be considered, but it is uncertain if this is needed in all cases.
In a prospective study of dogs with AHDS 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 AHDS are due to primary bacterial infection or that the bacteria involved may not be susceptible to amoxicillin-clavulanic acid.
Additional antibiotic coverage for gram-negative bacteria (eg, enrofloxacin at 5–20 mg/kg, IV, every 24 hours) is indicated in animals with sepsis or neutropenia.
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%). Additional supportive care, including antiemetic therapy and dietary management, are as described for and .
Prognosis is good with appropriate treatment. However, serious complications, including marked hypoproteinemia, DIC, sepsis, hypovolemic shock, and death, can occur.
Key Points
Dogs with acute hemorrhagic diarrhea syndrome present with acute vomiting and acute hemorrhagic diarrhea.
Diagnosis is based on clinical presentation and evidence of hemoconcentration (PCV >60%).
The primary treatment is prompt IV fluid therapy.
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