SA GI Medicine 3 - Approaching Acute GI Disease

Question 1

Define…
1. Gastritis.
2. Enteritis.
3. Gastroenteritis.
4. Colitis.

Answer 1

Inflammation of…
1. Stomach.
2. Small intestine.
3. Stomach and small intestine.
4. Large intestine.

Question 2

Define…
1. Emesis.
2. Haematemesis.
3. Emetic.
4. Anti-emetic.
5. Haematochezia.

Answer 2

1. Vomiting.
2. Vomiting bloods.
3. Substance that stimulates vomiting.
4. Substance that inhibits vomiting.
5. Fresh blood in/on faeces/diarrhoea.

Question 3

Define…
1. Melaena.
2. Diarrhoea.
3. Tenesmus.
4. Dyschezia.

Answer 3

1. Faecal passage of digested blood.
2. Increased faecal water content.
3. Straining to pass faeces.
4. Difficulty passing faeces.

Question 4

1. Define acute in terms of diarrhoea.
2. What may present before diarrhoea presents?
3. How long would the condition need to have been occurring before being classed as chronic.

Answer 4

1. Sudden onset - <1 week, definitely <3 weeks.
2. Vomiting.
3. > 3 weeks.

Question 5

1. What factors of signalment need to be considered when approaching v+/d+ cases?
2. What should be asked about when taking a Hx in v+/d+ cases?

Answer 5

1. Age, breed, neuter status.
2. Meds incl. anthelmintics.
   Vac Hx.
   Diet indescretion/toxins - scavenger?
   Recent contacts.
   Any other clinical signs?
   Characterise the vomit - colour, blood?, food?, bile?, consistency, froth?, thickness?, texture?
   Characterise the diarrhoea - colour, consistency, blood?, content?, thickness?

Question 6

Clinical signs in v+/d+ cases?

Answer 6

Vomiting.
Diarrhoea.
Variable appetite.
Flatus, borborygmi, bloating, eructation (gas production).
Haematemesis.
Melaena / fresh blood in faeces.
Weight loss (more notable in chronic v+/d+).

Question 7

1. Stages of vomiting.
2. Features of v+.

Answer 7

1. Prodromal.
   Retching.
   Expulsion.
   Relaxation.
2. Active, abdo effect, brainstem involved.
   Clinical sign, not Dx.
   Expulsion of gastric and upper intestinal content.
   May be due to GI or extra-GI disease.

Question 8

Diarrhoea localisation.

Answer 8

Small intestinal - large vol., norm. freq., no urgency, +/- other signs of SI disease - malabsorption, weight loss (assess clinically or w/ lab testing), inappetence vs. polyphagia, coprophagia or pica, gas production.

Large intestinal - small vol., increased freq., w/ urgency, w/ straining (tenesmus), w/ difficulty (dyschezia), +/- blood (haematochezia), +/- mucus.

Can see mixed patterns

Question 9

PE of acute GI patient.

Answer 9

Consider PPE/barrier nursing.
Hydration and fluid status:
- dehydrated? hypovolaemic?
Assess pain - and localise.
- on palp and behavioural.
Palpable abnormalities on abdo palp?
Evidence of systemic disease.
Rectal exam - FBs?, assess material on glove.

Question 10

Differential diagnoses for the acute GI patient.

Answer 10

Scavenging and ingesting food, substances or objects that they are not supposed to, causing obstructions, GI upset and irritation, toxicity.
Obstructions primarily cause vomiting.
Stomach/SI disease may cause v+ and/or d+.
Large intestinal disease usually causes d+.
- alternatively causes constipation.
Primary:
- masses, inflammation (focal vs acute, infectious vs sterile), dietary intolerances, GI ulceration, FBs, torsion, intussusception, stricture, tumour, toxins/drugs direct on GIT.
Secondary:
- pancreatic disease, renal disease, hepatic disease, endocrinopathy, pyo, peritonitis, systemic inflammation, neoplasia, motion sickness, vestibular disease, drugs.
Rule out extra-GI disease before Dx tests for primary GI disease.
- UNLESS – Hx/exam directs is towards primary GI disease.
–> known FB ingestion.
–> palpable GI mass lesion.
–> Haematemesis/melaena.
–> Young puppy/kitten w/ worms in d+.

Question 11

Clinical signs of acute pancreatitis.

Answer 11

Vomiting.
Diarrhoea (less common).
Inappetence.
Abdominal pain.
- prayer position (not specific).
Pyrexia - sterile inflammatory response.
Jaundice?
- extra-hepatic bile duct obstruction (EHBDO).

Question 12

Presentation of acute pancreatitis vs chronic pancreatitis.

Answer 12

Acute:
- sudden onset.
- pancreatic inflammation of variable.
- potentially fully reversible.
Chronic:
- Waxing/waning, insidious – may be persistently symptomatic or have intermittent episodes.
- progressive – inflammatory/fibrosis cycles.
- At end stage, can result in:
– exocrine pancreatic insufficiency.
– DM.

Question 13

Pancreatitis triggers.

Answer 13

Idiopathic - majority.
Hyperlipaemia:
- dietary indiscretion – common.
- obesity.
- hyperlipidaemia – increased blood viscosity so O2 to pancreas decreased.
Mini schnauzers.
Blunt abdominal trauma:
- RTA/high rise.
- Surgical handling.
Hypoperfusion - hypovolaemia etc.
Drug-related: - KBr, phenobarbitone, azathioprine, L-asparaginase, glucocorticoids.
– lipaemia.
Immune-mediated - cocker spaniel?

Question 14

Local and systemic effects of pancreatitis.

Answer 14

Pancreatitis: autodigestion of varying severity.
- mild intestinal inflammation to severe haemorrhage.
Local enzyme release:
- localised pancreatitis.
- fat necrosis.
Systemic enzyme effects:
- acute kidney injury.
- cardiac arrhythmias.
- effusions.
- shock, sirs, DIC, death.

Question 15

Bacteria enterocolitis.

Answer 15

E. coli, Clostridium perfringens, Campylobacter spp., and salmonella spp. can all be isolated from healthy dogs faeces.
Zoonoses and reverse zoonoses.
Biggest challenge is knowing significance/proving causality.
ONLY look for them if you think they are causing the problem.
- Risk factors – raw fed, young, unsanitary/crowded environment.
- Immunocompromised owners? BUT, may induce resistance or a carrier status.

Question 16

Bacteria enterocolitis clinical signs.

Answer 16

Haemorrhagic v+ and/or d+.
Pyrexia.
Sepsis.
+/- abdo pain.
Enterotoxaemia possible.
Consider faecal culture in these cases:
- remember evaluate for parvo.
- may also need to do PCR testing to speciate +/- ELISA for toxins (difficult to interpret?).

Question 17

Acute haemorrhagic diarrhoea syndrome (AHDS).

Answer 17

Previously called haemorrhagic gastroenteritis.
Acute haemorrhagic diarrhoea and marked haemoconcentration (fluid loss) (+/- v+).
Increasing evidence for C. perfringens in pathogenesis.
- NetF toxin leads to pore formation in enterocytes.
- Fluid and leakage into intestines leading to d+.

Question 18

AHDS signalment and presentation.

Answer 18

Small breeds of any age.
- mini schnauzer ++.
Acute onset haemorrhagic v+/d+.
Bloody gelatinous d+ - strawberry jam.
Abdo pain.
Obtundation.
Extreme fluid losses into gut lumen:
- hypovolaemic shock rapidly.
- marked haemoconcentration.

Question 19

AHDS Dx.

Answer 19

Consistent w/ clinical signs.
Marked elevation in PCV (often >60%).
- WITHOUT commensurate increase in proteins.
Exclude other causes w/ similar presentations:
- acute dietary indiscretion/intoxication.
- acute pancreatitis.
- hypoadrenocorticism.
- parvo.
- other bacterial enteritides.
- intussusception (esp. if young).

Question 20

Canine parvo.

Answer 20

Major cause of HGE.
Faeco-oral spread - v. effective.
- large quantities shed in d+.
- low infective dose.
- resistant virus – remains infective for up to 1yr.
Inactivated by formalin and hypochlorite disinfectants.
Part of CORE canine vacs - for prevention!

Question 21

Canine parvo signalment.

Answer 21

Inadequately protected puppy.
- immunity gap, not vac, no ab’s from mother.
- typically 3-6m old.
- concurrent infections may exacerbate e.g. Coronavirus, campylobacter spp.
Unvaccinated adult (less common).
Black and tan breeds susceptible:
- Dobermans.
- Rottweilers.

Question 22

Canine parvo clinical signs.

Answer 22

Haemorrhagic d+:
- anorexia.
- depression.
- abdo pain.
- considerable fluid defects.
+/- v+.
Neutropenia - on bloods.

Question 23

Feline Parvo.

Answer 23

Feline panleukopenia/Feline infectious enteritis.
Core vac (modified live) cats.
Closely related to canine parvovirus.
- Same clinical syndrome.
Natural infection or live vac of queen during pregnancy - can lead to cerebellar hypoplasia in kittens, hypermetric ataxia and intention tremors.

Question 24

Tritrichomonas foetus.

Answer 24

Asymptomatic - chronic recurrent large intestinal d+.
- +/- peri-anal oedema.
- +/- faecal incontinence.
Kittens and young cats.
<12-18 months old.
Maturity leads to an effective immune response.

Question 25

Consequences of acute GI disease.

Answer 25

Dehydration - may lead to pre-renal azotaemia.
Acid-base disturbance:
- loss of water/electrolytes.
- loss of acid from stomach or loss of bicarbonate from duodenum.
- fed or fasted state affects acid loss.
- pattern depends on whether pylorus obstructed or non-obstructed.
Aspiration pneumonia:
- esp. if sedated / neuromuscular disease / upper airway incompetency.

Question 26

1. What typically happens acid base wise in v+ and what results (patent pylorus)?
2. What typically happens acid base wise in v+ and what results (pyloric obstruction)?

Answer 26

1. Loss of hydrochloric acid and potassium from the stomach and loss of bicarbonate from the duodenum resulting in metabolic acidosis and hypokalaemia.
2. Loss of hydrochloric acid and potassium from the stomach but no loss of bicarbonate from the duodenum resulting in metabolic alkalosis and hypokalaemia.