Introduction
Acute diarrhoea is second only to pruritic dogs in numbers of sick dogs presented to veterinarians. There is however a large difference in the pathophysiology and the consequences of a "run of the mill acute diarrhoea" and an Acute Critical Care Gastroenteritis
Acute Small Intestinal Diarrhoea
Caused by diet change, over eating, ingestion of a preformed toxin, garbage disease, dietary indiscretion and infectious triggers. Abrupt onset and has a short clinical course that ranges from transient and self-limiting to fulminating.
Typical treatment of acute diarrhoea
Usually needs only supportive and symptomatic therapy, since most animals that die from [non critical care] diarrhoea do so not as a result of the inciting cause but from the loss of electrolytes and water, with subsequent dehydration, acidosis and shock.
The Mucosal lining of the SI
The intestinal epithelial cells carry out a multitude of functions:
Villus crypts function primarily to secrete fluid into the bowel.
After division in the crypts, the cells migrate up the villus reaching the tip in 3-5 days. During migration, the cells mature and change their primary function from secretion to surface digestion and absorption.
Villus tip carries out the final stages of protein and carbohydrate digestion together with absorption of nutrients, salts and water. The villus tip gives an increase of absorptive surface area of over 30 times.
Rapid cell turnover is the major reason why most acute diseases of the small intestine are self-limiting. Normal mucosal integrity and function are usually restored in 2-3 days, provided the inciting cause is eliminated and the initial insult is not sufficiently severe to damage the crypts.
Non-specific, symptomatic treatment of acute diarrhoea
Treatment may not always be indicated as many animals improve spontaneously in a day or two without treatment.
All cases require a minimum date base consisting of a history, clinical exam, faecal float, urinalysis and a blood smear examination.
General treatment measures include:
Dietary restriction (12-18 hours - but no longer in puppies), maintenance of fluid and electrolyte levels and acid-base homeostasis.
Small, bland meals frequently [when resume feeding], then gradually convert to regular commercial food once the diarrhoea resolves.
Deworming - empirical deforming in all cases
Antibacterials:
Antibiotics have long been part of standard treatment of acute diarrhoea; yet there is little evidence for bacterial infection as a major cause of diarrhoea in small animals. Antimicrobial agents can cause rapid changes in normal intestinal flora which are protective of the host, inhibiting colonisation by resistant organisms. The disruption of bacterial flora exposes the host to more pathogenic processes and may prolong the return of normal intestinal function.
Antibiotics are only indicated when extensive damage to the intestinal mucosal barrier occurs. Haemorrhagic Diarrhoea, fever and sever toxic left shift are examples where antibiotics are indicated.
Severe Acute Diarrhoea [e.g. critical care cases]
Parvo virus colonises fast dividing cell lines and through it's replication process's, destroys them. The typical parvo puppy thus loses the bone marrow and the lining of the GIT. So you are left with an immuno-compromised dog with probable septicaemia!!
Therapeutic Goal(s):
Rehydration
Treat /Prevent sepsis
Correct potassium and glucose levels
Normalise blood pressure
Stop vomiting
Pain control
Enteral nutrition
Our Current Treatment Protocol for Canine Parvo Virus
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Acute general Treatment
At Admission |
Place IV catheter, administer IV penicillin/cephalosporin [repeat TID], plus quinolones in small breed puppies.
Test - Ht / TSP/glucose
Replacement fluid with 20 meq. KCL(1 vial) + 20 ml 50% dextrose |
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1st 2 hours |
Work out the sum of re-hydration + Maintenance for 1st 12 hours
Give ¼ to ½ of amount over first 2 hours to correct intra-vascular volume and blood pressure (warm fluids to body temp).
Colloids can be used at 5-20ml/kg over 1-4 hours if in severe shock or if albumin low. |
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After 1st 2 h |
Give rest of fluid over next 10 hours.
Test Ht + TSP + K + Glucose
Warm patient on heating pad at this point [NB - not before as may dilate peripheral vasculature]
[Spike drip with more glucose if needed. [50ml 50% =2.5% / 100ml 50% = 5%]
Plasma can be administered as an immunotherapy and for oncotic pressure. Indicated if plasma albumin <15.
Blood transfusion or Oxyglobin is indicated if puppy worsening with Ht <15-20. |
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Approx. 2-3 hrs |
Metoclopramide IV or IM or as a constant rate infusion (CRI) to treat ileus and/or vomiting.
Pain control - Buprenorphine [TID/QID]
Start Cimetidine/Ranitidine IV for GI ulceration and reflux oesophagitis
Ulsanic 1ml/3kg TID if dogs vomiting a lot (for reflux oesophagitis)
Amikacin IV if blood pressure improved or quinolones if concerned re nephrotoxicity
(Test blood pressure or check for urine in bladder and CRT<2 sec's) |
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Approx. 4 - 5 hrs. |
Start to feed (aim for at least 1/3 of requirements over next 24 hours).
Feed through vomiting
Work out requirements with formula - [(bwx30) +70] x illness factor (1.25 - 1.5)
See below for added control of vomiting and diet. |
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Approx. 12 hrs. |
Re-assess hydration [weight patient daily]: continue rehydration or change to 1 ½ to 2x maintenance fluid rate. |
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IV - intravenous, IM - intra-muscular TID - 8 Hourly, Ht - Haematocrit, TSP - Total serum protein, KCL - Potassium chloride, K -Potassium, CRT - capillary refill time. |
Monitoring
The following should be monitored at admission, after 2 hours of fluids and then on a daily basis [or 2-3x/day] in patients that are still ill:
Body weight
Blood glucose
Haematocrit and TSP (Microhaematocrit tube and refractometer)
Serum potassium - check around time of admission and up to 2-3x daily after that - even if you are not suspicious of hypokalaemia.
Use paediatric sampling tubes or take very small quantities of blood.
Fluid Therapy
Rehydration - Body mass x 10 x % dehydration = volume in ml.
Ongoing losses - Estimated at 10 - 20 ml/kg/24 Hrs if still vomiting/diarrhoea
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Potassium supplementation |
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Serum Potassium mEq/l of patient |
Supplementation potassium (per 1000ml)
replacement fluid
(mmol KCL = meq K+) |
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3.5 - 5.5 (N) |
20 mEq K (1 vial KCL 15 % = 20mmol) |
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3.0 - 3.4 |
30 mEq K |
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2.5 - 2.9 |
40 mEq K |
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2.0 - 2.4 |
60 mEq K |
Chronic Treatment
Repeat blood, plasma, colloid or Oxyglobin transfusions as often as needed.
To control vomiting [ensure no intussusception]
Step 1 - CRI metoclopramide
Step 2 - Add Ondansetron 2-3 x/day
Step 3 - Add Prochlorpemazine suppositories
Diet/Nutrition
The previous "NIL PER OS" is not followed anymore
Start to feed once rehydration is underway (+/- 4-12 hours after admission?)
(We try to never starve a puppy for longer than 12 hours)
Aim for a minimum of 1/3 of nutritional requirements over next 24 hours
If vomiting a lot, miss out 1-2 hours, cut back on quantity but do not starve!
Feed high protein, high calorie foods
It is the authors opinion that small volume is far more important that ultra low fat content
Deworming
Fenbendazole [PO] course for 3-5 days [even if vomiting].
Ivermectin [S/C]
Drug Interactions
Flunixin meglumine is nephrotoxic and should be avoided in shocked patients
Quinolones used for 5-8 days should be safe and not cause cartilage problems
Ivermectin deworming not advised in debilitated patients
Recommended Reading
1. Mohr AJ et al: Effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and outcome in dogs with severe parvoviral enteritis, Journal of Veterinary internal medicine 2003;17:791-798.