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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.
All steps should be taken to rule out diseases with similar clinical presentation (hemorrhagic diarrhea and vomiting) that may come in 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 consists in 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. Electrolytes 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 1mg/kg q12h IV, omeprazole 1 mg/kg q12h PO, as a less efficacious 2nd choice famotidine 1 mg/kg IV q12h). 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 max. 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 multiple strains. They have been shown to shorten the duration of acute diarrhea in shelter cats and in 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.
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.
· Busch K, Suchodolski JS, Kuhner KA et al.: Clostridium perfringens entero- toxin and Clostridium difficile toxin A/B do not play a role in acute haemor- rhagic diarrhea syndrome in dogs. Vet Rec 2015 March 176 (10): 253
· Mortier F, Strohmeyer K, Hartmann K et al. Acute haemorrhagic diarrhoea syndrome in dogs: 108 cases. Vet Record 2015, doi: 10.1136/vr.103090
· 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 Sep-Oct; 25(5):973- 9. (Open access)
· Unterer S, Busch K, Leipig M, et al.: Endoscopically visualized lesions, histologic findings, and bacterial invasion in the gastrointestinal mu- cosa of dogs with acute hemorrhagic diarrhea syndrome. J Vet Intern Med. 2014 Jan-Feb; 28(1):52-8. (Open access)
· Leipig-Rudolph M, Busch K, Prescott JF et al. Intestinal lesions in dogs with acute hemorrhagic diarrhea syndrome associated with netF-positive Clos- tridium perfringens type A. J Vet Diag Invest 2018. Early view http://journals.
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