This information is provided by Provet for educational purposes only.

You should seek the advice of your veterinarian if your pet is ill as only he or she can correctly advise on the diagnosis and recommend the treatment that is most appropriate for your pet.

Note for Pet Owners:

  • If your dog shows signs of blood in vomit or faeces seek veterinary attentions as soon as possible. Any delay could risk your pet's life .

Topics on this Page:

Haemorrhagic gastroenteritis (HGE) is an extremely acute disease characterised by life-threatening haemorrhage into the gastrointestinal tract.

The cause of HGE is unknown. There is no evidence for the underlying cause to be an infection, due to dietary factors or a toxin. The most likely cause seems to be an abnormal immune response.

A similar syndrome of acute intestinal haemorrhage (often colonic) has been reported to occur in association with pancreatitis, the administration of corticosteroids and trauma to the central nervous system.

Breed Occurrence
HGE can affect all breeds and ages, but it is more common in toy and miniature breeds of dog particularly
Miniature Schnauzers, Dachshunds, Toy and Miniature Poodles and also in Pekingese. HE is rare in large breed dogs.

HE starts as sudden onset vomiting and diarrhoea with blood in both the vomit (called
haematemesis and in the diarrhoea (see dysentery) described as looking like raspberry jam. Some dogs are already in shock because of blood loss into the lumen of the bowel when they are presented to a veterinary practice. Swollen fluid-filled intestines can sometimes be palpated in the abdomen. This disease can result in rapid death due to shock even if treatment is commenced immediately signs are noticed.

Disseminated intravascular coagulopathy can develop in advanced cases, also leading to death.

The disease most often affects young dogs between 2-4 years of age.

HGE needs to be differentiated from canine parvovirus infection. Vaccination history is helpful with this.

On routine haematology the packed cell volume is often very high , 60-75% in most patients, reflecting fluid loss.


  • Nothing by mouth for 2-3 days.
  • Intravenous fluid replacement - lactated Ringers solution with 5% dextrose at 45-90 ml/hr for 1 hour (replacement ) and then a maintenance dose given at 5-15 ml/hour to satisfy the animals individual requirement of 50ml/kg body weight/day.
  • Antibiotics - To minimise secondary bacterial invasion (especially anaerobes) through a damaged intestinal wall. Penicillin, trimethoprim sulpha drugs, amoxycillin or ampicillin are preferred drugs. However, fluoroquinolones and clindamycin are also useful. Gentamycin (which is potentially nephrotoxic) should be avoided because these animals may have prerenal failure due to shock.
  • Corticosteroids - to treat shock
  • If disseminated intravascular coagulation is present the patient should be treated with heparin.
  • Dietary management in the post-acute phase. - the damaged mucosa can regenerate within 24 hours and returns to fully normal function within 3 days, so feeding of a highly digestible, bland, hypoallergenic diet can be started after 2-3 days after the acute symptoms have subsided. 
  • Total parenteral nutrition may be useful in these cases where such facilities are available to delay the return to oral feeding until the mucosa has fully recovered.

Post-recovery complications
Occasionally cases are reported to develop sensitivity to foods fed during the recovery phase. This may be due to leakage of protein through the damaged intestine wall resulting in an immune response to the food proteins.


Updated October 2013