DIARRHOEA 

• passage of faecal material with increased water content

  •   Disruption of normal balance between fluid/electrolyte secretion and absorption

  •   Adult horses – almost exclusively due to disorders of the large intestine (LI -

    normally reabsorbs approx. 100L/day), although may be a secondary response

    to another disease process (e.g. endotoxaemia, liver disease)

  •   Acute diarrhoea may result in significant water and electrolyte losses and acid-

    base disturbances (normal adult horse produces approximately 11-13kg faeces/day; some acute colitis cases produce >90L (kg) diarrhoea) 

• Mechanisms of diarrhoea 

• Malabsorption 

• decrease in functional absorptive surface area (decreased fluid

  absorption and retention) 

•   Increased secretion 

• increased solute and water secretion by inflamed colon

  (inflammatory mediators / bacterial enterotoxins / protein loss [decreased

  vascular oncotic pressure]) 

• Abnormal motility (decreased transit time) 

• poorly understood in horses (e.g.

  stress / excitement) 

• Osmotic overload:  

• e.g. carbohydrate overload / magnesium sulphate

  administration 

• Increased hydraulic pressure from blood to intestinal lumen 

•  e.g. congestive

  cardiac failure, inflammatory bowel disease 

•   Potential causes of acute diarrhoea 

• Infectious causes

  •   Salmonella typhimurium (see notes in appendix: Salmonellosis)

  •   Clostridium difficile (see notes in appendix Clostridium difficile colitis)

  •   Clostridium perfringens (see notes in appendix: Clostridium perfringens

    colitis)

•   Parasitic

   Cyathostomiasis(see notes in appendix: Cyathostomiasis)

•   Toxic

   NSAIDs (see notes in appendix: NSAID toxicity)

•   Miscellaneous

   Antibiotic associated (see notes in appendix: Antibiotic associated colitis)  Carbohydrate overload (see notes in appendix: Carbohydrate overload) 

• Potential causes of chronic diarrhoea 

• (often difficult to obtain a definitive diagnosis)

 Chronic inflammatory conditions
 Chronic salmonellosis (see notes in appendix: Salmonellosis)
 Chronic cyathostomiasis (see notes in appendix: Cyathostomiasis)
 Lawsonia intracellularis (see notes in appendix: Proliferative enteropathy)  Sand (see notes in appendix: Sand enteropathy)
 NSAID toxicity (see notes in appendix: NSAID toxicity)

0. General diagnostic approach to acute diarrhoea 

History

clinical exam

clinical pathology

evaluation of faeces

diagnostic imaging 

Dietary changes? / Adequate anthelmintic program? / More than one animal affected? / Sand exposure? / Medications (e.g. antibiotics, NSAIDs)? / Concurrent diseases? / Known toxin exposures (e.g. monsenin containing feeds, mycotoxin contaminated feeds)? / Associated weight loss? 

Important findings include: Ventral oedema (protein loss), Fever (infectious

causes), Dehydration (Skin turgor, CRT, Gum moisture), Endotoxaemia (Injected mucous membranes, Prolonged CRT, Tachycardia, Poor pulse pressure), Abdominal distension, Auscultation findings, Signs of laminitis (lameness, digital pulses) 

• Rarely identifies a cause

•   Important parameters include: PCV (elevated with dehydration), WBCC

  (leucopaenia especially if neutropaenic with a left shift and toxic changes in WBCs is suggestive of endotoxaemia [may also have thrombocytopaenia and coagulopathies]), Serum protein concentration (consider protein loss [usually albumin] in face of dehydration – therefore may have erroneously near normal protein concentration initially - compare with clinical signs of dehydration and PCV – may have associated hyperglobulinaemia [inflammation], therefore check albumin/globulin ratios, Acid base status (acute colitis case frequently have a metabolic acidosis), Electrolyte abnormalities (hyponatraemia, hypochloraemia, hypokalaemia, Serum BUN (may have pre-renal azotaemia) 

•   Evaluation of faece for acute diarrhea  

Gross appearance, haemorrhage, odour, sand, nematode larvae, helminth

eggs (may be negative even in the face of a massive larval burden), leucocytes and epithelial cells (indicative of severity), bacterial culture (multiple [usually 5] sequential samples; aerobic and anaerobic, toxin analysis (e.g. C. difficile ELISA), faecal PCR (Salmonella / Lawsonia) 

Diagnostic imaging: acute diarrhoea 

Limited use / Mural gas shadows in necrotising enterocolitis (foals) / Right

dorsal colon mural thickening in right dorsal colitis (NSAID toxicity). 

Dietary changes?, Adequate anthelmintic program?, More than one animal affected?, Exposure to sand?, Medications (e.g. antibiotics, NSAIDs)?, Concurrent diseases?, Known toxin exposures (e.g. monensin containing feeds, mycotoxin contaminated feeds)?, Associated weight loss? 

• Often mildly dehydrated and with moderate weight loss. Evidence of

  toxaemia? 

Evidence of chronic inflammation (decreased PCV and erythrocyte count), elevated WBCC, elevated fibrinogen, peritoneal fluid analysis (cytology, protein concentration), electrolyte concentration (often normal), serum protein (often slight hypoalbuminaemia; hyperglobulinaemia), liver derived enzymes and bile acids (primary liver disease) 

• Nematode larvae, helminth eggs (may be negative even in the face of a

  massive larval burden), bacterial culture (multiple [up to 15] sequential

  samples; eerobic and anaerobic, faecal PCR (Salmonella, Lawsonia) 

0. glucose/xylose absorption occurs in small intestine – therefore use when suspect small (weight loss) as well as large intestinal involvement (diarrhoea) 

• Rectal (less reflective of colonic cytology)
   Caecal/colon (requires laparotomy; however permits abdominal exploration)

•   Response to therapy: (see below) 

• Fluid / electrolyte / protein replacement:

  - Control of colonic inflammation and reduction in fluid secretion

  - 

  • Control of endotoxaemia
    

    - 

    • Promotion of mucosal repair

      • Control of pain

        • Antibiotics

          • Anticoagulation

            • Re-establishment of normal flora

              Nutrition

              Specific therapies 

             

           

         

       

   

• Fluid / electrolyte / protein replacement: acute diarrhea  

• Fluid / electrolyte / protein replacement:

  •   Orally (most acute diarrhoea cases will not voluntarily drink - can administer

    via indwelling nasogastric tube if no small intestinal ileus; 4-8L every 20-

    30min)

  •   Intravenous fluids (preferred in most cases):

    •   Isotonic sodium chloride or Lactated Ringers: Volume and rate depends on degree of fluid and electrolyte losses; Monitor PCV, serum protein conc., electrolytes, venous blood gases, BUN, creatinine; Approximately 50-100L/day; May add potassium chloride at rate up to 0.5-1.0mEq/kg/hr)

    •   Hypertonic NaCl: If severe hyponatraemia; Contraindicated if severely dehydrated and should always be followed by administration of isotonic solutions

    •   Colloids (Plasma, Synthetic colloids (dextrans, starches, polymerised Hb: Protein losses may result in interstitial oedema formation (organ dysfunction); Drop in oncotic pressure may worsen with crystalloid fluid administration (haemodilution); Colloids - more effective and longer duration of plasma volume expansion – (Plasma (6-8L/day, Hetastarch (5-10ml/kg of 6% solution increases colloidal oncotic pressure for up to 24h); N.B. When using synthetic colloids – plasma protein may be poor indicator of plasma oncotic pressure 

Control of colonic inflammation and reduction in fluid secretion for acute diarrhea 

Control of colonic inflammation and reduction in fluid secretion
 Prostaglandins likely play a large role in infectious diarrhoea (Salmonella,

Clostridia); COX inhibitors (NSAIDs) – antisecretory effects; however PGE2 and PGI2 are critical for mucosal repair – therefore NSAID use is controversial; Other anti-inflammatory/antisecretory drugs - Metronidazole (oral), Bismuth subsalicylate (3-4L every 4 to 6h) 

• Control of endotoxaemia
   Low dose NSAIDs (0.25mg/kg flunixin meglumiine every 6 to 8h) 

• Promotion of mucosal repair

 Sucralfate (20mg/kg orally every 6h; efficacy in large intestine -

questionable); Misoprostol (synthetic PGE analogue; 2 [image]g/kg orally 3 to 4 times daily – especially for treatement of NSAID toxicity – side effects!!); Psyllium mucilloid (5 tablespoons once to twice daily added to diet; increases production of SCFAs = energy source for enterocytes, stimulate salt and fluid absorption, hasten epithelial maturation) 

•   Control of pain for acute diarrhea  

• Mild to severe pain associated with: gas/fluid distension

•   Options: NSAIDs (Care re. mucosal healing - COX-2 inhibitors may be useful

  analgesics; Best to avoid NSAID use at high doses if possible; Alpha-2 agonists – temporary relief; Butorphanol (0.1mg/kg i.m every 6h or as continuous i.v. infusion 13.2 [image]/kg/hr); Lidocaine (loading dose 1.3mg/kg i.v. [slow over 5 mins] – followed by 3mg/kg/h continuous infusion) 

• Antibiotics for acute diarrhea treatment  

 Broad spectrum antibiotics may be indicated in neutropaenic horses -

increased risk of septicaemia either from primary bacterial cause (Salmonella, Clostridia) or GI bacteria breaching a compromised mucosal barrier; CHO overload - Antibiotics indicated; Salmonellosis - Antibiotic use is controversial (Specifically targeting salmonella may be indicated in cases with septicaemic form of salmonellosis); Clostridiosis - If antibiotics administered since the onset of diarrhoea – should stop ASAP and initiate specific treatment with metrodidazole (15-25mg/kg orally every 8h); Proliferative enteropathy (Lawsonia intracellulare) - Susceptible to variety of antibiotics – lipid soluble antibiotics preferable (intracellular organism) 

• Anticoagulation for acute diarrhea  

• Hypercoagulability – complication of colitis associated endotoxaemia

•   Heparin (20-80 IU/kg s/c or i.v. every 6 to 12 h); Low dose aspirin treatment

  (15mg/kg orally every 24-48h) – inhibition of platelet function 

• Re-establishment of normal flora for acute diarrhea  

Probiotics - Little work to support efficacy in the horse; Prophylactic use in

face of Salmonella outbreak; Therapeutic use in Clostridial or antibiotic associated diarrhoea; Sour milk (1L/100kg; advocated in C. perfringens type A infection; Caecal transfaunation (see appendix) - Very valuable procedure, Aids repopulation of intestinal bacterial and protozoal microflora. 

Nutrition for acute diarrhea 

Pelleted diet (at least 30% dietary fibre; frequent meals); Restrict long stem

roughage (reduce mechanical load on colon); Increase caloric intake (many cases are severely catabolic; add 1 cup corn oil to pelleted feed every 12 to 24h) 

Specific therapies for treatment for acute diarrhea  

• Cyathostomiasis: Larvicidal anthelmintics (Fenbendazole [7.5-10mg/kg orally

  every 24h for 5days] followed by ivermectin on day 6 [200 [image]g/kg orally]; Moxidectin (400 [image]g/kg orally); Dexamethasone

   May be efficacious in refractory cases when used in conjunction with larvicidal anthelmintics

   Pre-treatment (prior to anthelmintics) may be indicated in suspected cases of heavy infestation

  
  

  CHO overload:

• •   Exclusion of grains form diet

  •   Mineral oil/magnesium sulphate – clearance of CHO from LI before

    fermentation

  •   Charcoal administration – decreases absorption of endotoxin

  •   May require large amounts of bicarbonate containing solutions i.v. 

0. General treatment approach to undifferentiated chronic diarrhoea 

0. Change diet:

    Hay and alfalfa (good source of easily digestible protein - helps hypoproteinaemia).

•   Stop NSAID and antibiotic therapy if this could be possible cause

•   Caecal transfaunation or probiotics

•   Larvicidal dose anthelmintics (+ corticosteroids if suspect cyathostomiasis)

   May need to wait for several weeks to determine whether this is effective

•   Corticosteroids

  •   Last resort

  •   May improve inflammatory enteritis

  •   Since may have malabsorption best to give injectable dexamethasone

    therapy (20-30mg/horse daily) for first week, then 1.1 mg/kg prednisolone

    every other day orally. Taper dose off over at least a 2 week period

  •   May need intermittent or long-term low dose therapy. NOT a high success

    rate. 

Definition: clinical signs consistent with abdominal (usually gastrointestinal pain)

pain

•   (N.B. be aware of “false colics” – origin of pain form non-GI structures [refer to

  notes in appendix: Peritonitis, Cholangiohepatitis, Pleuritis])

•   Symptom - not a diagnosis

•   Commonly encountered problem in equine practice. 

• Mild colic 

• Stretching of abdomen, Looking at flanks, Teeth grinding, Yawning 

• Moderate colic: 

• Pacing the box, Pawing the ground, Kicking at belly, Crouched

  stance, Grunting, Frequent getting up and down, Prolonged periods in lateral

  recumbency 

• Severe colic:  

• Includes many of the above signs in addition to generalised

  sweating, rolling and self-inflicted trauma 

0. Clinical evaluation of the colic patient 

• Systematic and thorough

•   Often difficult to establish a precise cause

•   Main objective: can the condition can be treated medically or does it require

  surgery

•   Important to recognise clinical findings that indicate the need for surgery early 

• General information:colic 

• Age: e.g. young horses – intussusceptions; old horses - pedunculated lipomas; neonates -

  meconium impactions

•   Breed: e.g. large breeds - large colon displacements

•   Sex: e.g. recently foaled mares - colonic torsions; stallions - inguinal herniation

•   Insurance: is the horse insured (medical/mortality)? – colic surgery may cost as much as

  £5,000 

• History: colic 

When were the clinical symptoms first noticed?; How rapidly have the symptoms

progressed?; Feed/water intake: what, when, how much?; Faeces/urine output: volume, consistency?; Repeated episodes of colic? (tumour, abscess, enterolith, intussusception); Weight loss?; Worming program?; At grass (pasture): grass sickness, intestinal parasitism, tympanic colics (lush spring grass), rarely get primary impactions; Recent changes in diet?; Stages of work: (horses in work that are given time off commonly get mild impactions); Bedding: horses that eat their bedding may get impactions; Season: incidence of grass sickness peaks in spring/summer; in the winter season there is often an increased frequency of primary impactions. 

Clinical Examination:colic 

• Degree / nature of pain:

  •   Intermittent, continuous, increasing or decreasing?

  •   Visceral pain (unrelenting): most common: Increased peristalsis (spasm); Distension;

    Ischaemia; Stretching of mesentery.

  •   Parietal pain (agony): less common: Inflammation of the parietal peritoneum; tend to be

    immobile, “boarding” of the abdomen, resent external abdominal compression.

•   Abdominal distension:

 Indicates large colon and or caecal distension in the adult horse this 

Rectal temperature:

  Increase - anterior enteritis, colitis, peritonitis and intestinal abscessation  Decrease (coupled with a rapid, weak pulse) - indicates shock (grave prognosis).

•  Abdominal auscultation: colic  

• Auscultate for several minutes in each of 4 sites (right/left/dorsal/ventral)

•   Note site and nature of the sounds heard (haustral [short duration; 2-4 per minute] and

  peristaltic [longer duration; once every 2-4 minutes], caecal filling, caecal emptying)

•   Increased gut sounds may be heard with spasmodic or tympanitic colics.

•   Decreased gut sounds usually heard with most other types of colic, grass sickness and

  various metabolic/systemic disorders (hypocalcaemia, anorexia, pain, peritonitis).

•   Generally (not always), the quieter the abdomen the more serious the problem

  (endotoxaemia)

•   Percussing the abdomen will often elicit a “ping” over tympanitic areas (especially over a

  gas distended caecum) 

• increased pulses with laminitis; sequel to severe endotoxaemia 

• Temperature of distal extremities: assessment of peripheral perfusion

•   Muscle tremors:

 Slight tremors are common with colic; Grass sickness horses usually show characteristic fine fasciculations of triceps and flanks.

•   Faeces:

  •   Early in the course of colic some horses will continue to pass normal faeces (e.g.

    spasmodic colics, gastric colics, impactions of the colon)

  •   Very little or no faeces is passed with more severe conditions (e.g. ischaemic conditions)

    or grass sickness

  •   Check faeces for consistency, blood, worms, sand and mucous (indicate that transit time

    has been prolonged) 

• Rectal examination: for colic  

• Probably the single most important part of the clinical examination of a horse with colic

•   Only the caudal 1/3 of the abdominal cavity is palpable (foals and small ponies too small to permit examination)

•   Adequate restraint - necessary to ensure the safety of the personnel and horse

•   Procedure – (see appendix)

•   It is not possible to palpate small intestinal loops in a normal horse. The jejunum has a

  long mesenteric attachment and moves away from the hand. Palpation of distended loops of small intestine is one indication in which referral should be considered.

  • It may be necessary to perform rectal examinations at hourly or two hourly intervals if the case is seen close to the onset of colic, as it may take some time for changes to become palpable

  •   Specific abnormal rectal findings:

    •   Impaction of the pelvic flexure (PFI): Very common / often easily diagnosed on rectal

      examination; Feels like doughy mass - can be indented by gentle manual pressure; Gut wall around the impaction is smooth; When severely impacted - often palpable within the pelvis

    •   Secondary impaction of the pelvic flexure occurs in some conditions with colonic stasis (e.g. subacute grass sickness): Absorption of fluid from the colon; Remaining ingesta feels extremely firm; Characteristic corrugated contour (c.f. primary impaction)

    •   Small intestinal distension: May be palpable in grass sickness, enteritis, strangulating obstructions, small intestinal (ileal) impactions, intussusceptions and non-strangulating infarctions; Number of loops palpable depends on the nature, the duration and the location of the lesion; In severe cases involving the more distal jejunum or ileum - multiple loops are palpable within the abdomen and may extend back to the pelvic cavity; Loops are recognised by their diameter (often 5 to 10 cm) and lack of taenial bands

    •   Caecal intussusception: Caecocaecal intussusception (invagination of the caecal apex) may be palpated as a mass within the caecum; Ileocaecal intussusception may be detected as a painful, oedematous mass within the caecal base – likely to also result in small intestinal distension (obstruction to caecal filling)

    •   Large intestinal gaseous distension: Occurs in a number of conditions including: Primary flatulent colic, Transverse or small colon obstruction (e.g. enteroliths or pedunculated lipomas), Large colon displacements, Large colon torsions; Degree of distension varies but the abnormal viscus may be palpable at the pelvic inlet or within the pelvis

    •   Nephrosplenic entrapment of large colon (left dorsal displacement of the large colon): Occurs when the left large colon migrates dorsally between the spleen and the body wall and ultimately hooks over the nephrosplenic ligament; Colon may be palpated in left / dorsal abdominal quadrant running in a dorsoventral direction; May palpate colon overlying the nephrosplenic ligament; In some cases - secondary impaction or gaseous distension of the left colon is present which hinders diagnosis by rectal examination

    •   Intra-abdominal abscess formation or neoplasia: May be palpable per rectum if situated in a suitable position; Can range in size from golf ball-sized to football-sized; May be one or more large abscesses or tumours or there may be discernible increases in the lymphoid tissue (palpable particularly in the mesocolon) 

   

0. Ultrasonographic examination:colic  

Extremely useful tool – complements rectal examination Identification of lesion – more likely consequences of lesion
FLASH approach (Fast Localised Abdominal Sonography of Horses)

 

Left side – small intestinal distension, duodenum, caecal wall
Right side – small intestinal distension, caudal gastric margin, nephrosplenic space
Ventral – increased fluid accumulation and colon wall 

• Indications: Diagnosis of gastric distension with gas or liquid (gastric reflux) - Since

  gastric reflux is not normally spontaneous, it is always necessary to pass a stomach tube (on every colic case) to determine if excessive fluid/gas is present (>2L net reflux considered abnormal); Relief of gastric distension (before gastric rupture occurs); Administration of therapeutic agents directly into the stomach (via funnel or pump)

•   Conditions that result in gastric dilation/reflux include: Acute grass sickness; Ileus (functional S.I. obstruction); Small intestinal strangulating obstruction; Proximal jejunitis (anterior enteritis); Some cases of large intestinal obstruction (especially nephrosplenic entrapment)

•   Technique for passage: (see appendix)

   

• Should be considered in most cases of colic unless confident they are simple medical

  colics

•   Technique: (see appendix)

•   Interpretation:

  •   Initial response of the peritoneum to inflammation or ischaemia is an increase in protein and fibrinogen levels (in the peritoneal fluid).
     Fibrinogen > 0.1 g/1 is suggestive of an acute inflammatory response or

    haemoabdomen

  •   With progressive insult - leukocyte counts (WBC) increase

    •   Acute ischaemia is characterised by a neutrophilia and increased erythrocytes (latter) due to diapedesis

    •   Acute inflammatory responses such as abscessation or bacterial peritonitis may increase neutrophil counts without increasing red blood cell numbers

    •   Chronic inflammatory conditions show increases in both neutrophils and mononuclear cells

  •   N.B. peritoneal fluid may remain normal in horses with devitalised bowel if inflammatory debris is trapped, as occurs in epiploic entrapment and intussusceptions

  •   Gross Appearance: Normal fluid - straw colour. Some turbidity or swirling of fluid when shaken, contains some small particulate material. Normally does not coagulate; Turbid fluid - indicated by inability to read newspaper when viewed through fluid - due to increased protein or cell count; Purulent fluid - seen in peritonitis (common definition of peritonitis >10 x109 cells/1); Serosanguinous fluid - indicative of infarction (ischaemia) in which there is leakage of Hb and RBCs from the intestine. Can be dark red in colour with severe bowl devitalisation. Is an indication for surgery / euthanasia; Fresh blood - two possible causes: Haemoperitoneum from intra-abdominal haemorrhage (uniform red (blood) coloration and microscopy may shows RBCs ingested by macrophages); Iatrogenic haemorrhage from inadvertent puncture of a blood vessel or spleen (is much more common) - Since the bleeding is fresh, blood is not uniformly mixed with peritoneal fluid (see streaking) and sample often clots soon after collection into tube that does not contain EDTA (plain tube); Digesta - attempts must be made to differentiate iatrogenic intestinal puncture from a ruptured viscus. If a viscus is ruptured, clinical signs of shock and endotoxaemia will be evident

  •   Laboratory Assessment Of Peritoneal Fluid: Total protein: normal - <25g/l (although most horses will be <l5 g/l); Cell count: normal - <5xl09cells/l; Cytology: degenerate neutrophils may indicate a toxic process (e.g. viscus rupture, bacterial peritonitis); neoplastic cells are occasionally recognised, but most abdominal neoplasms do not shed free cells into the peritoneal cavity; Eosinophilic peritonitis - rarely reported, and presumed to be due to parasite migration; Bacteriology: aerobic and anaerobic culture if bacterial peritonitis is suspected; Gram stained smear - more rapid indication 

0. Blood / faecal analyses: colic  

0. Total protein / PCV (easily done, helps to assess hydration status); Creatinine; Acid/base balance (may be of value prognostically); Serum electrolytes (Na, K, Cl); Plasma fibrinogen:  with inflammation, takes 48-72 hours for blood levels to rise; Faecal occult blood assay: many false +ve and –ve; Faecal egg count: may be useful for parasitic colics 

0. Suggested indications for surgery / euthanasia of colics 

• Severe, continuous pain showing no or only short duration improvement with

  analgesia

•   Pulse >60; progressively rising and weakening

•   Progressive cardiovascular collapse: PCV >55; injected or cyanotic mms despite

  fluids

•   Rectal findings positive for acute abdominal disease (see rectal exam section)

•   Progressive reduction in the intestinal motility (ileus) or continual gastric reflux

  • Increasing abdominal distension

  •   Serosanguineous peritoneal fluid with  protein (>2.5g/1) and WBC's

    (>10X109/l).

    •   N.B. Important not to consider one criteria in isolation – look at the “whole picture”

    •   If none of the above seven criteria are present, treat medically, but reassess at short intervals (every 2-3 hours) so that any subsequent development of indications for surgical therapy can be detected early and treated appropriately. 

   

0. When referring colics to a referral centre 

• Refer early: Give an advance warning to the referral centre if possible.

•   Decompress the stomach (just prior to departure): If there is ongoing gastric

  reflux it may be necessary to place an indwelling nasogastric tube and tape it to

  the head collar

•   Analgesia: may be necessary for travel. Only give the minimum amount

  required to keep the horse comfortable (avoid masking clinical signs of

  pain/endotoxaemia – may complicate future assessment)

•   Stabilise the patient prior to referral:

   If hypovolaemic - start IV fluids via jugular catheter while awaiting transportation (hypertonic saline works well in the absence of adequate volumes of fluid and time)

   Probably best not to delay a critical case, but must be stable enough to survive the journey

•   Put a rug on the horse and apply leg bandages

•   Send with the horse or Fax a referral letter with detailed history and treatments

  given.
   Provide the owners with good directions to the referral centre. 

0. Medical treatment of colic 

• Important to interpret all clinical findings before making a treatment decision.

•   Always think carefully before you administer drugs to a colic case

  •   Drugs useful in one type of colic may be contraindicated in another

  •   Be careful not to blindly treat and thus mask the clinical signs of a colic case that

    needs to be referred for surgery or euthanased

•   Avoid large volumes of fluids / liquid paraffin orally if intestinal motility reduced

•   Listed below are many of the drugs that you are likely to encounter in practice.

  While you should be familiar with all of these, only a few are commonly indicated. 

0.  Analgesics: colic  

NSAIDs: Act peripherally by inhibiting prostaglandin production; Do not

depress gut motility; Some have potent anti-endotoxin properties; Excess usage - side effects include: gastrointestinal ulceration, renal papillary necrosis and blood dyscrasias. Options:

•   Phenylbutazone (Equipalazone injection: 200mg/ml, slow i.v.): suitable choice as the first line of treatment in most types of colic; Duration of action depends on severity of pain, but may last for 12 hours or longer with low-grade pain; Less likely than flunixin to mask the clinical signs of endotoxaemia; Causes severe irritation if injected perivascularly

•   Flunixin meglumine (Finadyne injection: 50mg/ml, slow i.v.): Duration of analgesia depends on the severity of the pain but may be >12 hours; Especially effective in reducing the effects of endotoxins on cardiovascular parameters (may mask the clinical signs of endotoxaemia thus prolonging the decision for referral/surgery); Use only after a thorough evaluation

•   Ketoprofen (Ketofen injection: 100mg/ml): Effects very comparable to those of flunixin meglumine

  Opioids: Very potent analgesics; Temporarily prolong gut transit time (reduce audible gut sounds); Cause respiratory and cardiovascular depression; Do not mask the clinical signs of endotoxaemia
   Options:

  •   Butorphanol (Torbugesic (R) injection: 10 mg/ml): Most commonly used opioid in first opinion practice; Duration of action of 3-4 hours; Good analgesic, but provides minimal sedation; May decrease gut motility; Often used in conjunction with other alpha-2 agonists to provide better analgesia

  •   Morphine (morphine injectable 30/60 mg/ml) : Schedule II controlled substance; Much less commonly used in first opinion practice; “Gold standard” for providing visceral analgesia; Often used following premedication with an alpha-2 agonist (wait 5 minutes); Duration of action varies with dosage and degree of discomfort 

   

0. Sedatives: colic  

alpha-2 agonists: Provide good sedation along with varying degrees of

visceral analgesia; Side effects include reduced gut motility, ataxia and bradycardia; Often used in combination with an opioid
 Options:

•   Romifidine (Sedivet injection: 10mg/ml): Most commonly used alpha-2 agonist in practice; mild/moderate visceral analgesia of 30-40 minute duration; Causes the least amount of ataxia (when compared to others)

•   Xylazine (AnaSed injection: 100mg/ml): potent visceral analgesia, with a short duration of action (20-30 minutes); Not as commonly used as romifidine, causes some degree of ataxia

•   Detomidine (Domosedan injection: 10mg/ml): Very potent visceral analgesic (especially when combined with an opioid) and sedative; Longest duration of action (60+ minutes); May result in the greatest degree of ataxia 

0. Spasmolytic drugs: colic  

0. Buscopan compositum: contains metamizole (NSAID) and butylscopolamine (spasmolytic); Commonly used first line of treatment 

0. Laxatives:colic  

Best used in conjunction with fluid therapy when treating impactions;

Important to ensure good intestinal motility before administration; In a 500 kg horse the total volume administered into the stomach should not exceed 4-5 litres per treatment. Options:

•   Isotonic fluid: Superior to liquid paraffin in softening large intestinal impactions. Requirements for frequent administration (2hourly to 4hourly) and therefore may require hospitalization. Always check for reflux before administration (4-6 litres to adult horse).

•   Liquid paraffin: Care should be taken when administering this substance as it can cause fatal lipoid pneumonia if aspirated into the lungs; Common initial treatment of choice for treating simple impactions; Dose: 2-6 litres/adult horse sid/bid. Foals: 20 ml for meconium impactions

•   Dioctyl sodium sulfosuccinate (Dioctyl): Anionic wetting agent with lubricant properties; Do not administer with liquid paraffin as systemic absorption of the liquid paraffin may occur; Overdosage may cause diarrhoea and colic; Give fluid therapy before Dioctyl if horse dehydrated; Dose: 10-25 mg/kg in 4-8 1itres of water via stomach tube (120-240 ml of the 5% solution). Best to give no more than two doses, 48 hours apart

•   Oral magnesium sulphate: Cathartic laxative and acts as an osmotic agent to draw water into the intestine; Can be irritating to the intestinal mucosa; Ensure the horse is adequately hydrated before use; Can be toxic at high doses; Dose: 0.5-1.0 g/kg in 4-8 litres of water via a stomach tube 

Intravenous fluids:colic 

Often essential in cases of severe dehydration or endotoxic shock;

Administration in the field - often quite difficult; Very effective in softening

intestinal impactions



Options:

•   Polyionic fluid (Isolec): Commercially available polyionic fluid containing Na, K,

  Ca, Cl, HCO3 precursor (lactate); Available in 3 or 5 litre bags; Most practical /

  cost effective form of iv fluid therapy for horses

•   Isotonic glucose saline: Can be used to replace the second 50% of a deficit, and

  for maintenance requirements

•   8.4% sodium bicarbonate: Use with care; Best to use only if you can assess

  acid-base balance accurately; Best to rehydrate with a polyionic solution first - the improved circulation will often correct the acid base deficits without the need for bicarbonate

•   Hypertonic (7.2%) saline: 2 litres/500 Kg of hypertonic saline to temporarily improve circulating volume in cases of ensuing shock; Acts by osmotically drawing interstitial fluid into intravascular space; Interstitial deficit that is created must then be corrected by subsequent and immediate IV infusion of large volumes (e.g. 20-40 litres) of isotonic fluid. 

0. General management of simple colics 

0. (For those horses that have no indications for surgery or aggressive medical treatment after having been thoroughly evaluated)

•   Administer analgesics according to diagnosis (see above section).

•   House in a warm, loose box with deep inedible bedding (shavings/paper). If

  necessary, put on a muzzle to prevent them from eating. Remove all objects on which the horse could injure itself if it were to become painful and begin to thrash about.

•   Remove all feed for several hours (even up to 12 hours) and make sure the horse passes several piles of normal faeces prior to reintroduction of feed.

•   Provide free access to water.

•   Have the owner hand walk the horse 10-15 minutes every 2-3 hours (encourages

  them to watch the horse closely) on 3 or 4 occasions.

•   Reassess regularly to ensure suitable improvement occurs. If you’re unhappy with

  the way things are progressing, it may be necessary to reassess every 2-3 hours.

   

0. Icterus 

yellow colouration of the sclera and mucous membranes resulting from increased tissue and serum bilirubin

•   Usually indicative of:

  •   Decreased excretion of bilirubin with liver or biliary tract disease (regurgitation icterus)

  •   Increased production of bilirubin with haemolytic anaemia (haemolytic/prehepatic icterus; see separate notes on haemolytic anaemia)

  •   Impaired hepatic uptake or conjugation of bilirubin with liver disease (retention/hepatic icterus)

•   Accumulation of conjugated bilirubin results in more pronounced jaundice than uncongugated bilirubin; therefore most pronounced jaundice seen with hepatic or biliary obstructive disease

•   Icterus more likely with acute liver disease compared with chronic liver disease (production and elimination of bilirubin may be equal)

•   Fasting/anorexia in the horse can result in an increase in uncongugated bilirubin (horse may have subtle icterus) 

0. Laboratory examination to determine cause of icterus: 

• Relative amounts of conjugated and unconjugated bilirubin: Less useful in

  the horse with liver disease c.f. other species; Increases in conjugated: >25% total bilirubin – strongly indicative of hepatocellular disease; >30% total bilirubin – strongly indicative of cholestasis

•   Liver-derived enzymes (to determine if associated with liver damage): Hepatocyte-derived - GLDH (liver-specific; peak 1-2 days (half life 12-24h); AST (non liver-specific); Biliary tract-derived - GGT (liver-specific; very sensitive and specific esp for chronic disease); AP (non liver-specific)

•   Bile acids (to determine if associated with liver failure): 95% restricted to enterohepatic circulation; Increase in serum levels indicates loss of approx >70% hepatic function ie failure; Values < 20umol rule out liver failure fairly reliably; Values >20umol consistent with hepatic failure; Values >40 poor prognosis; May have mild increase with fasting

•   PCV and RBC count (to determine if associated with haemolysis)

•    uncongugated bilirubin and normal PCV+liver enzymes – anorexia?

•    uncongugated (+/- conjugated) bilirubin and  PCV – haemolysis?

•    uncongugated + conjugated bilirubin and  liver enzymes+bile acids – liver

  disease! 

0.  Differential diagnosis of equine liver disease 

• Ragwort toxicity: (see notes in appendix: Ragwort toxicity)

•   Undifferentiated hepatic failure (see notes in appendix: Chronic liver disease of

  undetermined cause)

•   Haemachromatosis: (see notes in appendix: Haemachromatosis)

•   Echinococcosis (see notes in appendix: Echinococcosis)

•   Liver abscesses

•   Aflotoxicosis (see notes in appendix: Aflotoxicosis)

•   Hepatic neoplasia: (see notes in appendix: Hepatic neoplasia)

•   Cholangiohepatitis (see notes in appendix: Cholangiohepatitis)

•   Leptospirosis

•   Liver fluke (see notes in appendix: Liver fluke)

  Obstructive cholelithiasis (see notes in appendix: Cholangiohepatitis)  Portocaval shunts
   Tyzzer's disease - see foal notes
   Hyperlipaemia (see notes in appendix: Hyperlipaemia)

   Cushing's disease – see separate notes on Cushings disease 

Clinical signs of liver disease 

• Develop only when >60-70% hepatocytes destroyed; Despite a long history of

  exposure to hepatotoxins, signs of hepatic failure may appear suddenly; Often history of gradual weight loss, decreased appetite and recurrent bouts of photosensitization before hepatic failure develops; Once hepatic failure develops, the prognosis is usually hopeless, with most cases dying in a few weeks; None of clinical signs are pathognomonic for liver disease

•   Most signs are non specific: Depression, anorexia, weight loss, mild to severe abdominal pain (hepatomegaly and/or gastric impaction)

•   Some signs are more suggestive:

 Icterus (also seen with anorexia!!); photosensitisation (care to differentiate

from simple sunburn) - cutaneous accumulation of phylloerythrin (derivative of chlorophyll) produced by gastrointestinal microflora and normally removed by the liver following absorption into portal circulation - compromised removal with liver failure - exposure of phylloerythrin to UV radiation results in free radical formation and cell membrane damage - erythema on unpigmented hairless areas - progressing to painful exfoliative dermatitis with sloughing; severe pruritus; hepatic encephalopathy (HE) - increased NH3 and other false neurotransmitters resulting in dull vacant expression, yawning, ataxia, tremors, circling, head pressing, aggression; coagulopathy; petechiae; bilateral laryngeal paralysis - inspiratory dyspnoea and stridor at rest 

Laboratory diagnosis of liver disease

Difficult to diagnoses purely on clinical grounds alone, therefore heavy reliance

on laboratory disease confirmation - Liver enzymes (see details above), bile acids (see details above), bilirubin (see details above), ammonia (not very useful - increased due to failure of liver to convert NH3 to urea - only in acute severe or end stage chronic disease - blood ammonia levels - increased only in some cases of hepatic encephalopathy; glucose (non-specific - most affected horses are hyperglycaemic, but occasionally severely affected horses may be hypoglycaemic); coagulation indices (often reduced); plasma proteins (contrary to popular opinion hypoproteinaemia and hypoalbuminaemia - rare in horses; most are hyperproteinaemic); urinalysis (may get bilirubinuria despite most being conjugated (water soluble); peritoneal fluid analysis (rarely gives useful information but helpful at ruling out other diseases) 

Other ancillary diagnostic techniques for liver disease  

• Ultrasonography (may identify severe fibrosis, space occupying lesions,

  distended bile ducts, alterations in liver size, choleliths)

•   Liver biopsy (very useful since most diseases are diffuse - can provide definitive

  aetiological diagnosis in many cases and good prognostic information - ultrasound guided biopsy – preferable - theoretically should assess coagulation before taking biopsy and supplement with 1-2 L platelet-rich plasma prior to procedure, but rarely practical - Infection and haemorrhage real but rare complications); For procedure (see appendix) 

Treatment of equine liver disease 

•   Largely supportive until adequate liver function returns or regeneration occurs

•   Acute failure best prognosis

•   Chronic liver disease with extensive fibrosis - hopeless prognosis

•   Treatment of horses with hepatic encephalopathy - rarely warranted 

• Remove form source of hepatotoxins (if applicable and identifiable)

•   Dietary management: High carbohydrate diet (ideally in the form of simple

  sugars); Should be given frequently (ideally 6x daily); Supply higher than maintenance energy requirements (Increased demands of tissue repair, 2.5% bw/day [normal M = 1.5% bw]); Low protein - Minimise production of dietary amines which could execerbate HE and avoid alfalfa and legumes (high protein content)

  So what does this diet mean in practice? - If photosensitisation is not a major problem - grazing should be encouraged; Alternatively: 2 parts soaked beet pulp and one part of maize in molasses, fibre - in the form of fresh cut grass or grass nuts, vitamins (B vitamins - brewers yeast supplement, Vitamins A and C - from fresh grass)

•   Antibiotics: Only indicated when suppurative cholangitis or abscessation suspected; Suitable empirical choices prior to obtaining sensitivity - penicillin- gentamicin or parenteral potentiated sulphonamides

•   Tracheostomy: May be required if bilateral laryngeal paralysis

•   Corticosteroids: No evidence to indicate inhibit development of liver fibrosis;

  May be contraindicated - increase metabolic load on liver (metabolised by liver and stimulate gluconeogenesis and protein catabolism); May be indicated in cases of chronic non-suppurative cholangiohepatitis

•   Specific treatment of hepatic encephalopathy

 Sedation (low dose alpha-2 agonists): Only if horse is uncontrollable and

poses a danger to handlers (Care - most sedatives are liver metabolised and can exacerbate HE); Correction of metabolic, fluid and electrolyte abnormalities; Reduction in GIT production/absorption of potential neurotoxins (laxative [liquid paraffin] and oral neomycin or metronidazole - Reduce number of anaerobes and gram-negative urea splitting organisms (major producers of gut derived neutrotoxins); Lactulose - Reduces intestinal neurotransmitter production and absorption