Introduction

Acute hemorrhagic diarrhea syndrome (AHDS) is a new name proposed to describe the syndrome known for decades as hemorrhagic gastroenteritis (HGE). The new name defines the disease better since studies out of Germany have demonstrated that affected dogs do not display any gastric inflammation. The syndrome can affect dogs of all breeds and all ages, although middle-aged dogs of small and toy breeds seem to be predisposed.

Etiology

The etiology of AHDS is not known, although abundant Clostridium perfringens were shown to be present in the duodenum of affected dogs. Other hypotheses about the etiology include dietary or microbial toxins and severe dietary indiscretion. It is unclear if clostridial proliferation is a cause or a consequence of the disease. Clostridium perfringens enterotoxins and C. difficile toxins A/B do not appear to be involved in the pathogenesis. However, a newly discovered pore-forming cytotoxic toxin (netF) produced by type A C. perfringens has been co-localized with severe necrotic intestinal lesions in affected dogs. In addition, acute enteritis strongly impacts the intestinal microbiota, particularly with respect to species diversity, and causes acute dysbiosis.

Clinical Presentation

Most affected dogs are small-breed and middle-aged. A large German study reports a predisposition in Yorkshire terriers, miniature pinscher, miniature schnauzer, and Maltese, and a mean age of 5 years. Dogs with AHDS are typically presented with acute-onset bloody diarrhea, possibly with vomiting and anorexia. They are usually very dehydrated and in various stages of hypovolemic and/or distributive shock. Lethargy and abdominal pain are also common.

Diagnostic Approach

Dogs with AHDS typically have a high PCV (often above 65%) and a normal or low serum concentration of total solids (or total proteins, albumin, or globulins). White blood cell counts may be normal, high or low depending on the severity of disease. Mild thrombocytopenia is common. Other serum biochemistry changes may include prerenal azotemia, increased liver enzymes, hypoglycemia, and electrolyte abnormalities. Metabolic acidosis is often present. Abdominal radiographs are usually of limited diagnostic utility and show an enteritis pattern with fluid and gas-filled small intestinal loops.

Differential Diagnoses

All steps should be taken to rule out diseases with similar clinical presentation (hemorrhagic diarrhea and vomiting) that may come into consideration based on the dog’s signalment, environment, history and physical exam. These include parvovirus infection, bacterial infections (Salmonella, Campylobacter, Clostridium perfringens, Clostridium difficile), severe parasitic infestations, dietary indiscretion, toxicosis (e.g., mushrooms, vitamin K antagonist rodenticides, etc.), intestinal volvulus or intussusception, acute necrotizing pancreatitis, acute liver disease, hypoadrenocorticism, sepsis, and immune-mediated thrombocytopenia.

Management

Management consists of aggressive fluid therapy. Intravenous boluses of isotonic crystalloid solutions (10–20 mL/kg) should be used to treat hypovolemic shock. Perfusion and cardiovascular status should be reassessed every 15 minutes, and further boluses administered as required until normal blood pressure is restored. Fluid deficits should be replaced over a 6–12-h period with crystalloid solutions, adding the maintenance requirements and estimated ongoing losses due to continuing diarrhea. In severe cases with distributive shock that do not respond to fluid boluses, vasopressors should be used. Electrolyte deficits such as hypokalemia should also be corrected. Other symptomatic treatment modalities include antiemetic drugs such as maropitant 1 mg/kg IV or SC, and possibly gastric antacids if the gastric mucosa is compromised due to hypoperfusion (e.g., pantoprazole 1 mg/kg q 12 h IV, omeprazole 1 mg/kg q 12 h PO, as a less efficacious 2nd choice famotidine 1 mg/kg IV q 12 h). The PCV generally normalizes in response to aggressive fluid therapy, and the serum protein concentration usually drops to levels indicative of hypoproteinemia with both low serum albumin and globulin concentrations.

Use of antibiotics is not recommended in most cases. A recent study showed that cases of mild to moderate severity do not appear to benefit from antimicrobial treatment when endpoints such as time to resolution of diarrhea and length of hospital stay are compared between dogs given amoxicillin and clavulanic acid and those receiving placebo. Broad-spectrum antibiotics should be administered intravenously only to severe cases with existing or impending sepsis and those showing mucosal sloughing.

Dogs with HGE/AHDS should be fasted for a maximum of 12–24 h and then offered small quantities of easily digestible food frequently (boiled chicken and rice, adequate commercial prescription diets) in order to support the intestinal mucosal barrier.

Probiotics have the potential to be helpful in the long-term treatment of AHDS. They may modulate intestinal immune function, promote epithelial cell homeostasis, exert neuromodulatory effects, block the effects of pathogenic bacteria, and have nutritional benefits. Probiotics designed for use in dogs and cats, such as those manufactured by reputable pharmaceutical or pet food companies, are preferred, as over-the-counter products have been shown not to be as reliable. Some products contain one bacterial strain while others consist of multiple strains. They have been shown to shorten the duration of acute diarrhea in shelter cats and decrease the time to first normal feces in dogs with acute enteritis. Probiotics should be administered for 2–4 weeks to animals with acute enteritis. It may be preferable to delay the initiation of probiotic treatment in dogs with bloody diarrhea and compromised intestinal mucosal barrier until the hemorrhagic diarrhea has resolved.

Prognosis

The prognosis of AHDS is good when dogs are presented early in the course of the disease, and aggressive supportive treatment can be initiated promptly. Most dogs can be discharged after a median hospital stay of 3 days (range 1–7 days). Serious complications may include DIC, sepsis, and aspiration pneumonia in vomiting animals. AHDS may be fatal if the emergent needs of the patient are addressed too late.

References

1.  Busch K, Suchodolski JS, Kuhner KA, et al. Clostridium perfringens enterotoxin and Clostridium difficile toxin A/B do not play a role in acute haemorrhagic diarrhea syndrome in dogs. Vet Rec. 2015;176(10):253.

2.  Mortier F, Strohmeyer K, Hartmann K, et al. Acute haemorrhagic diarrhoea syndrome in dogs: 108 cases. Vet Rec. 2015. doi: 10.1136/vr.103090

3.  Unterer S, Strohmeyer K, Kruse BD, et al. Treatment of aseptic dogs with hemorrhagic gastroenteritis with amoxicillin/clavulanic acid: a prospective blinded study. J Vet Intern Med. 2011;25(5):973–979. (Open access)

4.  Unterer S, Busch K, Leipig M, et al. Endoscopically visualized lesions, histologic findings, and bacterial invasion in the gastrointestinal mucosa of dogs with acute hemorrhagic diarrhea syndrome. J Vet Intern Med. 2014;28(1):52–58. (Open access)

5.  Leipig-Rudolph M, Busch K, Prescott JF, et al. Intestinal lesions in dogs with acute hemorrhagic diarrhea syndrome associated with netF-positive Clostridium perfringens type A. J Vet Diag Invest. 2018. Early view https://journals.sagepub.com/doi/10.1177/1040638718766983