Acute diarrhoea

Question 1

What are the 4 broad types of acute diarrhoea?

Answer 1

• osmotic
  ◦ maldigestion (eg EPI, damage to the brush border)
  ◦ malabsorption (eg mucosal damage, villus atrophy, infiltrative disease such as lymphoma)
• secretory
  ◦ toxin
  ◦ infection related
• inflammatory (altered permeability)
  ◦ inflammatory bowel disease (eg adverse food reaction, idiopathic chronic enteropathy)
• motility disorder

Question 2

What are the causes of acute diarrhoea?

Answer 2

• Diet – acute gastroenteritis
• Change, allergy, intolerance, scavenging
• Food poisoning – suggests infectious agent
• Toxins – usually through dietary indiscretion
• Drugs – antimicrobials, chemotherapy etc
• Infections – viral, bacterial, parasitic
• Inflammatory disease – CE, Pancreatitis
• Metabolic disease – hypoadrenocorticism
• Anatomic disease – intussusception/FB
• Neoplasia – peracute lymphoma, paraneoplasia
• Anomalous - Stress/anxiety – usually mixed/large bowel

Question 3

How is parvovirus spread? What dogs are mostly affected?What clinical signs are associated? How is it diagnosed?

Answer 3

Virus stable in environment for years
Faecal-oral – 3-6 days incubation
Generally see in young puppies with low maternal immunity (pre-vaccination), older unvaccinated dogs (breed predisposition – black and tan?)

Infects rapidly dividing cells - Gut crypts, bone marrow, lymphoid tissue, (myocytes and CNS in some neonates)

• Vomiting
• Haemorrhagic diarrhoea – profuse and foetid, mucosal sloughing
• Rapid dehydration
• Panleucopaenia
• Depressed, anorexic, pyrexic
• Loss of mucosal barrier – septicaemia/endotoxaemia and shock/DIC
• Ileus
• Diagnosis
  ◦ Signalment and clinical signs strongly supportive
  ◦ Faecal analysis – EM for virus, Ag tests (SNAP) or PCR
  ‣ Care with positive results after MLV vaccination (SNAP ok….)
  ‣ Severe necrosis of GIT can lead to false negative Ag tests
  ◦ Haematology and biochemistry – consequences of disease
  ‣ Panleucopenia – consequence of viral replication
  ‣ Azotaemia, acid-base disturbance, electrolyte disturbances, liver enzymes abnormal, possibly low total protein
  ◦ Clotting times may be prolonged if severe systemic consequences present

Question 4

Why would you radiograph a parvovirus abdomen?

Answer 4

Helps to determine between major ddx - FB or intussusception

Question 5

How is a CPV case managed?

Answer 5

Fluid therapy
LRS – be aggressive, maintain electrolytes via supplementation – requires monitoring of blood pressure, and regular assessment of weight
Acid-base status assessment – can be severe imbalance
Colloid/plasma/whole blood

Antibiotics
Broad spectrum due to GI translocation of bacteria - Clav-amox, +/- quinolone –care with age of patient, gram negative coverage is difficult in young animals

Anti-emetics
important as marked nausea – metoclopramide, maropitant and ondansetron/dolasetron

Pro-motility medication
Metoclopramide – enteritis reduces GI motility, major consequences

**Antacid drugs and ulcer coating medication **
severe gastritis can develop along with reflux oesophagitis and strictures

Question 6

What is the aetiology of Acute haemorrhagic diarrhoea syndrome (AHDS)? What are the clinical signs? How is it diagnosed? How is it treated?

Answer 6

Aetiology may be type I intestinal hypersensitivity reaction or the result of Clostridium perfringens enterotoxin production
Small breed dogs usually

Vomiting +/- blood
Foetid diarrhoea – inc protein loss – brown water
Depression, anorexia – very poorly
Haemoconcentration –
* fluid shift into GIT means severe hypovolaemia before clinical dehydration is apparent
* PCV high
* TP not so high as GI loss
* No leucopenia (c.f. parvo)

Treatment
Fluid therapy – must be aggressive as with CPV
Colloid/plasma/whole blood
Depends on degree of haemorrhage and complications
**Antimicrobial ** –
Potential for clostridial infection and sepsis
Four quadrant cover only if signs consistent with sepsis – G+, G-, aerobes and anaerobes
Clav-amox, metronidazole, fluoroquinolone

Question 7

What clinical signs are associated with a Campylobacter infection? How is it diagnosed? How is it treated?

Answer 7

• Commensal in dogs therefore potential long-term zoonosis
• Clinical disease in young, immunocompromised animals or those with additional infectious agents (giardia, parvo etc)
• Acute enterocolitis (NOT CHRONIC LOW-GRADE DIARRHOEA)
  ◦ d+ +/- blood/mucus
  ◦ Vomiting
  ◦ Straining – large intestinal “type” d+
  ◦ Fever, abdominal pain
  ◦ Can become enteroinvasive due to host stress (IFN and noradrenaline mediated)
• Diagnosis
  ◦ Faecal stain/culture
  ‣ Fragile therefore best isolated from fresh faeces
  ‣ slender motile seagull-shaped bacteria
  ‣ Standard culture may be misleading as speciation is not performed,
  ◦ PCR
• Treat underlying disease if present – e.g. CE/IBD
• Treatment most frequently with 4-fluoroquinolones (can use erythromycin, can lead to vomiting)

Question 8

What are the 3 main outcomes of the initial clinical approach when ivestigating diarrhoea?

Answer 8

• Not worried - Manage consequences of diarrhoea
• Not sure – screen and support
• Worried – investigate and (likely) more intensive suppor