Idiopathic acute haemorrhagic diarrhoea syndrome (AHDS) in dogs is described as acute onset haemorrhagic diarrhoea, often after vomiting. They have an increased haematocrit level (in half the dogs reported it was above the reference range) and a stress leukogram with neutrophilic left shift. There has been a seasonality reported (more common in winter) and often in young adult small breed dogs (Mortimer et al. 2015). Previously it was known as haemorrhagic gastroenteritis, though the histopathological changes have been shown to be in the intestines, not in the stomach (Unterer et al. 2014).
We are still unaware of the causative agent and, therefore, a diagnosis is made by excluding other cases of acute diarrhoea, for example canine parvovirus, salmonellosis, Campylobacter infection, NSAID use. Clostridium species have been identified in dogs with AHDS, though only small numbers were identified and there are other studies which have not identified Clostridial involvement. Clostridial perfringens enterotoxin and clostridial difficile toxin A/B have also been examined and shown not to be associated with AHDS (Busch et al. 2014). This has been postulated to different populations of dogs that have been examined, and even that clostridial overgrowth might be after the initial injury. Viral infection has also been postulated as an independent cause, such as circovirus (Anderson 2017), or even with concurrent clostridial overgrowth. More work needs to be undertaken to understand the causative agent(s) and it appears that the aetiology is far more complex than Koch’s postulates.
We are beginning to understand a little more about the influence of the microbiome in the gastrointestinal tract and how that can assist with immune response amongst in addition to assisting with nutritional support. It is apparent that AHDS leads to a dysbiosis and this itself might lead to viral or bacterial organisms influencing the course of the disease. This is the area where novel therapies could be found.
As we do not know the causative agent(s) of AHDS, diagnosis, as mentioned earlier, is by excluding other diseases. Though in a similar way to ruling out all other cause of dysuria for FLUTD cats, often only common conditions are eliminated. Examining a blood smear might assist with the differential diagnosis, as well as parvovirus detection tests (where appropriate). Abdominal imaging might have some utility for the peracute presentation of vomiting if a differential diagnosis is gastrointestinal foreign body. Abdominal radiographs should be performed if that is a concern. Recent literature has argued that a complete abdominal ultrasound in patients presenting with only diarrhoea has no utility in the majority of cases, this did not include the use of patient-side ultrasound in the ICU (Mapletoft et al. 2018).
Treatment has included fluid therapy, antiemetics, antacids, gastrointestinal diets, antibiotics, and analgesia. Fluid therapy should always be tailored to the individual and restoration of the profound fluid losses needs to be corrected. Despite many of these patients having a higher than normal haematocrit it is not uncommon in the sicker individuals with AHDS to require blood transfusion therapy. Isotonic (replacement) crystalloid fluids are the preferred fluid to use and to tailor to the individual. Care must be taken to reassess the patient regularly to make sure that the fluid balance is appropriate.
Antiemetics are utilised in patients that continue to vomit, or are nauseous (e.g., maropitant, ondansetron). Antacids are also often used (ranitidine, famotidine, omeprazole).
Nutrition is important to address, and enteral feeding is the preferred route. More information on nutrition can be found in notes on enteral feeding.
Antibiotics have been reported not to change the outcome of AHDS and for the most cases of AHDS antibiotics are not required, however, often the majority of veterinarians would prescribe them. It is difficult to know which patients might require antibiotics, though those patients with a neutrophilic left shift are unlikely to have any benefit, and in neutropenic patients it might be prudent.
Although there are groups working on identifying the causative agent for these cases, it is a complex problem. In the meanwhile, improving effective therapies for the sicker patients would be beneficial to the patients that do not seem to improve with traditional supportive therapy. Clinically the patients that take longer to improve continue to have haemorrhagic diarrhoea, despite all interventions. A treatment strategy might be to re-establish the microbiome either with lactobacillus cultures, or faecal transplantation. The former has only shown to be beneficial in some small animal patients who have diarrhoea (oncology patients inflammatory bowel disease), though it appears to anecdotally only be effective when the patients remain on the therapy. There has been a recent case report on the use or oral faecal microbiota transplantation for Clostridium difficile associated diarrhoea in a dog (Sugita et al. 2019) and last year in puppies with parvovirus, showing a faster resolution of diarrhoea. It seems prudent that we should examine this therapy in dogs with AHDS.
References
1. Busch K, Suchodolski JS, Kühner KA, Minamoto Y, Steiner JM, Mueller RS, et al. Clostridium perfringens enterotoxin and Clostridium difficile toxin A/B do not play a role in acute haemorrhagic diarrhoea syndrome in dogs. Vet Rec. 2014;176(10):253.
2. Anderson A, Hartmann K, Leutenegger CM, Proksch AL, Mueller RS, Unterer S. Role of canine circovirus in dogs with acute haemorrhagic diarrhoea. Vet Rec. 2017;180(22):542–542.
3. Mapletoft EK, Allenspach K, Lamb CR. How useful is abdominal ultrasonography in dogs with diarrhoea? J Small Anim Pract. 2018;59(1):32–37.
4. Mortier F, Strohmeyer K, Hartmann K, Unterer S. Acute haemorrhagic diarrhoea syndrome in dogs: 108 cases. Vet Rec. 2015;176(27):627.
5. Sugita K, Yanuma N, Ohno H, Takahashi K, Kawano K, Morita H, et al. Oral faecal microbiota transplantation for the treatment of Clostridium difficile-associated diarrhoea in a dog: a case report. BMC Vet Res. 2019;15(1):11.
6. Pereira GQ, Gomes LA, Santos IS, Alfieri AF, Weese JS, Costa MC. Fecal microbiota transplantation in puppies with canine parvovirus infection. J Vet Intern Med. 2018;32(2):707–711.
7. Unterer S, Busch K, Leipig M, Hermanns W, Wolf G, Straubinger RK, 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.