Colic Flashcards
Clinical signs of colic (varied presentation)
Quiet
Laying down more
Inappetant
Flank watching
Pawing
Bruxism/lip curling
Rolling
Causing themselves injury
What is colic?
Presentation of abdominal pain, not a specific disease entity
What can colic be associated with?
- Gastrointestinal tract
- Peritoneal cavity
- Reproductive tract
- Renal disease - relatively uncommon
- Hepatic disease
- ‘False colic’
○ E.g. laminitis
And many more
How much is colic surgery likely to cost?
£500-700 but often much higher and have often already spent a lot by this point.
Specific cause of colic that old, overweight geldings are at higher risk of
Pedunculated lipoma
Specific cause of colic that box rested horses which usually graze 24/7 are at higher risk of
Pelvic flexure impaction
Which type of heart murmur is common in horses with colic?
Flow murmurs - reassess for presence when the horse is well
Chemical restraint for colic assessment
⍺2 agonists – xylazine first choice
Analgesia
Wait to administer drugs until after you’ve made a clinical assessment
BUT give drugs before doing anything else if that’s what you need to do to make it safe
Which analgesia would you use for colic patients?
NSAIDs
Do not be afraid of using flunixin
Why would you pick xylazine as chemical restraint in colic cases
Shortest acting and as ⍺2 agonists can have detrimental effects on blood pressure you don’t want that for too long
Diagnostic techniques used in colic
Nasogastric intubation *
Rectal palpation *
Abdominocentesis
Haematology and biochemistry
Ultrasonography
Why would you pass a nasogastric tube in a colic patient?
Need to pass one if you think the horse is severe
Diagnostic test
○ Most important if a small intestinal obstruction
Analgesic
Life saving
○ Gastric rupture is fatal – do not travel a colic case for referral without having passed a nasogastric tube
Nasogastric intubation technique
Restraint
○ Nose twitch
○ Sedation
Stand to one side - NOT in front
Pass tube up ventral meatus to nasopharynx
○ ‘ventral and central’
Flex chin towards chest
○ Encourages swallowing and helps to avoid passing tube into trachea
Pass into proximal oesophagus then check location
Should get negative pressure if in the right place
How can you tell if a nasogastric tube is placed correctly?
Negative pressure (you can’t breathe down the tube)
Visualise it passing down the oesophagus
May get a gurgle of gas
What is an abnormal volume of reflux after passing a nasogastric tube?
> 2 litres of reflux considered abnormal*
○ Net fluid – deduct any you added
Use buckets so that you can measure, don’t just throw it on the floor
What is the active ingredient in Buscopan?
Hyoscine
What does buscopan do?
Spasmolytic and anticholinergic
May allow increased safety in rectal palpation
Acts within a few minutes
Abdominocentesis in colic cases
Serosanguineous appearance sensitive indicator of devitalised intestine -> surgical lesion
Compare lactate concentration to blood lactate, >16mmol/l associated with non-survival
Normal/low protein transudate (abdominocentesis)
Colourless/pale yellow
Clear
<5000 nucleated cells/uL
<2.5 g/dL protein conc by refractometry
Transudative effusion (high protein) (abdominocentesis)
Courless/pale yellow
Clear to slightly hazy
1500-10,000 nucleated cell count/uL
2.5-3.5 g/dL protein conc.
Exudative effusion (abdominocentesis)
Variable
Turbid/hazy
> 10,000 nucleated cell count/uL
> 3.0 g/dL protein concentration
Haemoatology and biochemistry in colic cases
Serum lactate from peripheral tissues - correlated with survival
PCV/TP can show whether it needs fluids, does it need surgery etc.
GGT often increased
Glucose often increased
Pre-renal azotaemia
Hyperlipaemia (donkeys and inappetant horses)
FLASH ultrasound scanning
Better for SI pathology
- gastric distension
- distended small intestine
- ventrum
- Gastrosplenic window
- Nephrosplenic window
- Left middle third
- Duodenal window
- RIght middle third
- Cranial ventral thorax
Red flags that would make you think about referral in colic cases
Refractory to analgesia
Distended small intestine
> 2L reflux
Systemically sick (HR, MM etc.)
Lack of response to treatment
Serosanguinous peritoneal fluid
Heart rate >60 beats/min ? (if other signs etc)
Spasmodic/gas colic
Most common
Not well defined
No physical abnormalities, except maybe distended intestines
Responds to basic treatment (analgesia and buscopan)
Signs of spasmodic/gas colic
Increased borborygmi, systemically well, may have loose faeces (e.g. lush grass with be bright green loose droppings)
Risk factors for spasmodic/gas colic
Change in diet
Tapeworm
Other changes in management, poor dentition etc.
Pelvic flexure impaction
Prone to developing impactions due being a tight ‘bend’ in the colon, and due to the broader, sacculated ventral colon narrowing at this bend to become narrower dorsal colon
Primary impacted ingesta (pelvic flexure impaction)
E.g. diet change, box rest, reduced water intake etc.
Secondary impacted ingesta (pelvic flexure impactions)
E.g. colon displacements, altered motility for example due to grass sickness/equine dysautonomia
Risk factors for pelvic felxure impaction
Less turnout (box rest, weather etc.)
Diet change
Poor dentition
Clinical signs of pelvic flexure impaction
Mild to moderate pain
Reduced faecal output
Diagnosis of pelvic flexure impaction
Ractal palpation
- firm mass in pelvic flexure
- ventral midline/left of midline
- variation in size/consistency
- can be very large
- consitency can be very firm, or softer and indentable
Treatment of pelvic flexure impaction
Enteral fluid therapy is superior to IVFT
§ Isotonic solution superior to liquid paraffin
§ Magnesium sulphate (irritates gut lining into secreting fluid itself)
Use meaningful volumes
§ 1L/100Kg bodyweight
§ Every 2-4 hours unless contraindicated
Sometimes leave tube indwelling if in the hospital
Withhold feed
Risk factors for caecal impaction
Orthopaedic surgery, ocular disease (NSAID use – correlation isn’t necessarily causation! - seen in very painful horses rather than horses)
Dentition
Tapeworm
Decreased turnout
Two types of caecal impaction
Type I: dry ingesta
Type II: underlying motility disorder, more fluid consistency
Clinical signs of caecal impaction
Reduced faecal output
Although will continue to pass faeces, so often this early warning sign is missed
Often deceptively mild colic
Often have a normal heart rate
Sometimes very subtle until point of rupture - life threatening
Diagnosis of caecal impaction
Rectal palpation (4-5 o’clock)
Treatment of Type I caecal impaction
Enteral fluid therapy, surgery if not improving (more quickly than for pelvic flexure impaction)
Withhold feed
Treatment of type II caecal impaction
Surgical?
More likely to rupture
Prokinetics?
Withold food
Primary Gastric impactions
Feed that swells in stomach
Secondary gastric impaction
Motility disorders
Liver disease
Small colon impactions
Poor quality hay, lack of exercise, parasite burden, reduced water intake,salmonella
Relatively rare
Sand enteropathy
Regional – sandy soil
Diarrhoea/weight loss, or acute colic - due to how abrasive it is
Diagnosis of sand enteropathy
Auscultation: specific, not sensitive (may sound like waves on a beach)
Sand sedimentation (faecal) test: not sensitive/specific. Do it because its free but don’t rely on it
Radiography - gold standard
Treatment of sand enteropathy
Magnesium sulphate and psyllium found to be superior to either alone
If very severe sometimes do require surgery - difficult! Colon very heavy, sand is abrasive and causes injury to the colon epithelium -> very sick
Minimise sand ingestion
Large colon displacements
Mild to moderate colic, may wax and wane
Proposed causes:
- Large concentrate meals
fermentation -> gas distension -> migration of large colon
- Altered motility
Right dorsal displacement of the large colon (RDD)
Cranial displacement of pelvic flexure towards diaphragm
Colon moves cranially - either medially or laterally to the caecum
Diagnosis of right dorsal displacement of the large colon (RDD)
Rectal
§ Gas distended colon
§ Tight taenial bands
§ Abnormal location (may be coursing laterally) or absence in normal location
Ultrasound
§ ‘turtle sign’: visualisation of colonic mesenteric vessels against right body wall
§ Mural oedema
Often have increased GGT concentration
Treatment of right dorsal displacement of the large colon (RDD)
64% reported to respond to medical treatment
Withhold feed
Fluid therapy (enterally/IV/both)
Exercise
Can progress into a colon torsion which is always critical and needs surgery
Left dorsal displacement of the large colon (LDD)
Pelvic flexure moves dorsally into the nephrosplenic space
Diagnosis of Left dorsal displacement of the large colon (LDD)
Rectal - colon in nephrosplenic space
US - large colon obscures left kindey
Treatment of Left dorsal displacement of the large colon (LDD)
76% reported to respond to medical treatment
Lunging
Phenylephrine and lunging
§ Sympathomimetic – splenic contraction
§ Contraindicated if > 15 yrs, increased risk of haemorrhage (general vessel compliance issue?)
Rolling under anaesthesia with phenylephrine superior
Equine grass sickness (EGS, equine dysautonomia)
Enteric and autonomic neuronal degeneration
○ Variation in severity/extent of neuronal damage
○ Different sub-categories of EGS (acute, subacute, chronic)
Functional obstruction - may also develop impactions secondary to this
Pathogenesis unknown
GI absorption and haematogenous spread of a putative neurotoxin
Strongly associated with grazing
Risk factors for Equine grass sickness (EGS, equine dysautonomia)
○ 2-7yrs old
○ Recent movement
○ Recent anthelmintics
○ Particular pasture
○ Disturbed pasture
○ Mechanical poo picking
○ Cool, dry weather, frost
Three presentations of Equine grass sickness (EGS, equine dysautonomia)
Acute
- Fatal (<48hrs)
- Definitively they will die
Subacute
- Fatal (<7 days)
Chronic
- Some survive
- Reports vary, approx. 40-50% fatality rate
Clinical signs of acute Equine grass sickness (EGS, equine dysautonomia)
Sometimes colic
Tachycardia (80-120bpm)
Innapetance
Patchy/generalised sweating
Muscle fasciculations
Normal to distended abdominal stance
Clinical signs of subacute Equine grass sickness (EGS, equine dysautonomia)
Sometimes colic
HR 60-80bpm
Dyspahgia
Mild rhinitis sicca
Patchy/generalised sweating
Muscle fasciculations
Normal to distended abdomen
May progress to narrow-based stance
Clinical signs of chronic Equine grass sickness (EGS, equine dysautonomia)
Usually no colic
HR: 45-60bpm
Patchy sweating
Muscle fasciculations
Tucked up
Narrow based stance
Diagnosis of Equine grass sickness (EGS, equine dysautonomia)
Ileal biopsies
Phenylephrine eye drops
- reverse ptosis, poor sensitivity and specificity
Treatment of chronic Equine grass sickness (EGS, equine dysautonomia)
Select appropriate cases to treat
- Ability to swallow?
- Degree of colic?
Treatment
- Nutritional support
- Monitor hydration status
- Analgesia
- Treat secondary problems
Prognosis of chronic Equine grass sickness (EGS, equine dysautonomia)
Very, very difficult if they cannot swallow
Stop if continuous weight loss, no recovery of appetite
Post operative ileus
Common post surgery
Nasogastic reflux, (distended SI, discomfort, tachycardia)
Pathophysiology of post-operative ileus
Neurogenic phase - sympathetic stimulation of GI tract after moving the abdominal contents during surgery
Inflammatory phase - due to touching the GI tract, good surgical technique is key
Management of post-operative ileus
Nasogastric intubation
Early feeding - stimulate GI tract
NSAIDs
- May affect healing of anastomosis
- Deleterious effects on mucosal healing
- Analgesic
- Beneficial effects WRT systemic inflammation
- Consensus between specialists is to use flunixin – but we actually have little data, may move towards using cox 2 selective drugs
Treatment of post-operative ileus
Restrictive fluid therapy?
§ Don’t overload them
§ Monitor electrolyte status
Prokinetics
§ Lidocaine, Probably more useful as an anti-inflammatory, Beneficial to give alongside flunixin
§ Metoclopramide - works better on proximal GI tract, so better to use with something else like lidocaine
(Erythromycin, neostigmine (better for LI disease)