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Colic in horses (Pathophysiological mechanisms (Obstruction (Impactions…
Colic in horses
Pathophysiological mechanisms
Abnormal bowel movements
Hypermotility, ileus, spasmodic colic etc.
Inflammation
Colitis, enteritis, peritonitis. No other causes of colic will primarily produce pyrexia. If no pyrexia, then look for other markers of inflammation (SAA, abdominal U/S findings, abdominocentesis)
Bowel stretching/distension
Impactions
Obstruction
Impactions (typically at pelvic, sternal and diaphragmatic flexures or terminal ileum/between large and small colon).
Parasites (P. equorum in foals < 6 mths, cyathostomins, S. vulgaris)
Impaired bowel perfusion
Congestion (impaired venous return), ischaemia (impaired perfusion following congestion). Typically entrapped/strangulating lesions.
Tension on support structures
Adhesions, tension on mesocolon.
Dietary changes
Intense/prolonged exercise
Diagnostic approach
History
Duration/nature of onset, behaviour, diet, faecal/urine output, previous diarrhoea/laminitis, vaccination/worming status, sand/dirt access, crib biting/windsucking behaviour, current medications, state of other horses
Physical exam
Pain assessment
Immediate cessation of pain MOST important (NSAIDs, alpha-2s, opioids). Assess evidence of trauma, reluctance to walk, kicking/rolling intensity, response to initial analgesia.
Vitals
Signs of hypovolaemia (HR > 60, cool extremities, delayed CRT, poor peripheral pulse), HR > 60-80 associated with decreased survival.
Temp (normal 37-38.6): pyrexia indicates an inflammatory process (no other cause of colic associated with pyrexia). Often normal/subnormal in surgical cases.
RR (normal 10-24 BPM): tachypnoea due to pain, abdominal distension or potentially metabolic acidosis secondary to hypoperfusion.
Gut sounds
DO NOT OVER INTERPRET. Gut sounds are most useful for monitoring disease progression.
Hydration status
8-10%: skin tent remains for 6-10 seconds; prolonged CRT (2-4 secs); dry mucous membranes; sunken eyes; possible signs of shock (irregular heartbeat, weak pulse, poor jugular filling)
NGT
Nature of fluid may indicate cause (large volumes with more severe processes).
Increased pH with small intestinal pathology.
Orange/red fowl odour with proximal enteritis (difficult to distinguish from intestinal accident). Horses with proximal enteritis tend to be dull/obtunded following NGT decompression.
Rectal exam
Intra-rectal lignocaine + 0.9% NaCl
Organ distension/displacement, and note type of distension (surgery indicated by distended small intestine/large colon, severe impaction or foreign body.
Abdominal ultrasound
Assess thickness of intestinal wall, nature of intestinal contents, intestinal motility and presence of peritoneal fluid (+/- fibrinous flecks)
Abdominocentesis
Typically only valuable in early stages of severe colic or if you think it will alter outcome
Normal peritoneal fluid: straw-coloured, TP < 25 g/L, < 3000 cells/μl, lactate < 1 mmol/L, some neutrophils
Abnormal colour/turbidity indicates referral. NCCs and TP less indicative of medical/surgical lesions.
Band neuts/toxic change indicates peritonitis.
Transudate (increased hydrostatic pressure): TP < 25 g/L, NCC < 1.5 x 10^9/L
Modified transudate (increased hydrostatic pressure, inflammation, organ torsion): clear/serosanguinous to turbid, TP > 25 g/L, NCC < 5 x 10^9/L
Exudate (inflammation): cloudy, turbid to flocculent, TP > 25 g/L, NCC > 5 x 10^9/L
Lactate > 3mmol/L indicates ischaemia
Faecal testing
Assess for strongyle eggs and sedimentation of sand in a glove
Haematology/biochemistry
Typically performed last as it provides the least information. Assess for haemoconcentration, multi-organ dysfunction, APPs, and serum [lactate] (normally < 0.7 mmol/L).
Typical changes are haemoconcentration, +/- inflammatory/stress leukon, azotaemia, hyperlactataemia, hypoproteinaemia, hypokalaemia, hypochloraemia, hyponatraemia, metabolic acidosis (increased AG and decreased HCO3).
Field therapy
Fluid therapy
Enteral requires functioning GIT. Contraindicated if reflux > 2 L. Lack of reflux doesn't mean they are indicated. Typically 6-8 L electrolytes delivered via NGT.
IV used either in combo with enteral or if non-functional GIT. Usually polyionic, isotonic crystalloids (Hartmann's, Normosol-R) used for resuscitation. Can give 9-18 L (20-40 mL/kg)bolus over 1-2 hrs, or 10-20 mL/kg/hr CRI (approx. 1 L/hr maintenance + deficit + ongoing losses).
Resuscitative fluids (Hartmann's, Normosol-R) are low in K and have no Ca. Generally not spiked with K.
Maintenance fluids should be lower in Na and higher in K (generally spiked with KCl). 0.9% NaCl is acidifying and is only indicated with uroperitoneum/renal failure.
Analgesia
NSAIDs (flunixin) generally a good first choice (horses will break through if severe), but it is long-acting (12 hrs).
Xylazine is shorter acting (30 mins) but provides poorer analgesia
Butorphanol often used in combination with alpha-2s (e.g. xylazine + butorphanol). Primary role is for sedation/completion of diagnostics.
Faecal softeners/laxatives
Potentially useful with impactions. Examples include psyllium husk, tympanyl (a surfactant) and paraffin oil (don't use the latter two together).
Prokinetics
Not common in the field. Lignocaine is the most common agent (routinely given as a CRI post-operatively) to combat ileus.
Trocharisation
Uncommon, but typically used to relieve caecal distension
Preparation for transport to hospital
Rug & bandage limbs/potentially foot cryotherapy (dig a hole, fill with ice and water)
Provide detailed treatment report to hospital
Decompress stomach and leave NGT in if necessary
Analgesia
Assessing clinical severity
Pain: refractory pain (analgesia breakthrough) indicates severe colic.
Peritoneal fluid: serosanguinous with bowel infarction, high [lactate] with strangulation, digesta confirms bowel rupture.
Rectal findings (sedate with butorphanol + xylazine with fractious horses): Distended viscera/small intestine palpation indicates severe colic.
Passage of NGT: large volumes of reflux indicates severe colic.
Pulse & perfusion: slow CRT + bounding pulse indicates distributive shock, along with injected MMs.
Major prognostic indicators
Pain
CVS compromise (perfusion parameters)
Presence of endotoxaemia
Persistently high serum [lactate]
Large intestinal lesions have better prognosis than small intestinal lesions (due to post-surgical outcome)
Indications for referral
Severe abdominal pain/distension
Tachycardia (HR > 60) and signs of hypovolaemia
Absent gut sounds
Abnormal rectal findings
Gastric reflux > 4 L
Surgical management
Anaesthesia
Lower pre-med doses in toxaemic patients (xylazine preferred)
Emphasis on fluid replacement during surgery
Dopamine/dobutamine (inotropes) used often to manage hypotension
Surgical approach
Ventral midline coeliotomy
GIT decompression
Ensure gentle handling/constant lubrication of viscera
Much more small intestine (up to 8m) can be resected than large intestine
Post-operative care
Ileus, shock, diarrhoea and laminitis are major post-op complications
IV fluids (Hartmann's, may require KCl, MgSO4 and dextrose supplementation)
Antibiosis contraindicated unless peritonitis (if so, use pen + gent + metro)
Prokinetics (lignocaine CRI) to combat ileus
Low-dose flunixin (analgesia, anti-endotoxic effect, laminitis prevention)
All cases of post-op diarrhoea should be isolated
Continuing NGT decompression
Sequelae
Endotoxaemia
Congested MMs, delayed CRT, tachycardia.
Particularly an issue with large intestinal lesions due to high Gram(-) load.
May lead to laminitis, SIRS-MODS
At least 20 L (approx. half the deficit in a moderately dehydrated horse) of balanced electrolytes (Hartmanns, Normosol-R) are required for fluids to be beneficial.
Laminitis
Principally due to SIRS (ischaemic and neutrophil-mediated damage to lamellae). Only effective prevention is distal limb cryotherapy.
Clinical signs
Pawing, flanking, kicking abdomen, rolling, bruxism, flehman, inappetence, sweating, recumbency.