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Equine michaelmas 23 > Colic > Flashcards

Colic Flashcards

1
Q

Clinical signs of colic (varied presentation)

A

Quiet
Laying down more
Inappetant
Flank watching
Pawing
Bruxism/lip curling
Rolling
Causing themselves injury

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2
Q

What is colic?

A

Presentation of abdominal pain

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3
Q

What can colic be associated with?

A
  • Gastrointestinal tract
  • Peritoneal cavity
  • Reproductive tract
  • Renal disease - relatively uncommon in horses
  • Hepatic disease
  • ‘False colic’
    ○ E.g. laminitis
    And many more
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4
Q

Chemical restraint for colic assessment

A

⍺2 agonists – xylazine first choice
§ Shortest acting
§ detrimental effects on blood pressure
§ Good for the sedation to have worn off before you leave

Analgesia
§ Painful fractious animals
§ NSAIDs first choice
§ Do not be afraid of using flunixin

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

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5
Q

Nasogastric intubation technique

A

Restraint
○ Nose twitch
○ Sedation

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

More than 2 litres considered abnormal

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5
Q

Diagnostic tools for colic

A

Nasogastric intubation *
Rectal palpation *

Abdominocentesis
Haematology and biochemistry
Ultrasonography

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6
Q

Abdominocentesis

A

Serosanguineous appearance sensitive indicator of devitalised intestine -> surgical lesion

Compare lactate concentration to blood lactate, >16mmol/l associated with non-survival

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7
Q

Normal/low protein transudate (abdominocentesis)

A

Colourless/pale yellow

Clear

<5000 nucleated cells/uL

<2.5 g/dL protein conc by refractometry

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8
Q

Transudative effusion (high protein) (abdominocentesis)

A

Courless/pale yellow

Clear to slightly hazy

1500-10,000 nucleated cell count/uL

2.5-3.5 g/dL protein conc.

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9
Q

Exudative effusion (abdominocentesis)

A

Variable

Turbid/hazy

> 10,000 nucleated cell count/uL

> 3.0 g/dL protein concentration

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10
Q

Haemoatology and biochemistry

A

Serum lactate from peripheral tissues - correlated with survival
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)

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11
Q

FLASH ultrasound scanning

A

Better for SI pathology
- gastric distension
- distended small intestine

  1. ventrum
  2. Gastrosplenic window
  3. Nephrosplenic window
  4. Left middle third
  5. Duodenal window
  6. RIght middle third
  7. Cranial ventral thorax
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12
Q

Spasmodic/gas colic

A

Most common

Not well defined

No physical abnormalities, except maybe distended intestines

responds to basic treatment (analgesia and buscopan)

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13
Q

Signs of spasmodic/gas colic

A

Increased borborygmi, systemically well, may have loose faeces (e.g. lush grass with be bright green loose droppings)

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14
Q

Pelvic flexure impaction

A

pelvic flexure is 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

Impacted ingesta
○ Primary
§ E.g. diet change, box rest, reduced water intake, etc
○ Secondary
§ E.g. colon displacements, altered motility for example due to grass sickness/equine dysautonomia

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15
Q

Risk factors for pelvic felxure impaction

A

Less turnout (box rest, weather etc.)
Diet change
Poor dentition

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16
Q

Clinical signs of pelvic flexure impaction

A

Mild to moderate pain
Reduced faecal output

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17
Q

Diagnosis of pelvic flexure impaction

A

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

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18
Q

Treatment of pelvic flexure impaction

A

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
§ Rule of thumb: 1L/100Kg bodyweight
§ Every 2-4 hours unless contraindicated

Sometimes leave tube indwelling if in the hospital

Withhold feed

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19
Q

Risk factors for caecal impaction

A

Orthopaedic surgery, ocular disease (NSAID use – correlation isn’t necessarily causation! - seen in very painful horses rather than horses

Dentition

Tapeworm

Decreased turnout

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20
Q

Two types of caecal impaction

A

Type I: dry ingesta
Type II: underlying motility disorder, more fluid consistency

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21
Q

Clinical signs of caecal impaction

A

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

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22
Q

Diagnosis of caecal impaction

A

Rectal palpation (4-5 o’clock)

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23
Q

Treatment of caecal impaction

A

Type I: enteral fluid therapy, surgery if not improving (more quickly than for pelvic flexure impaction)

Type II: surgical? More likely to rupture

Prokinetics?

There isn’t a consensus!

Withhold feed

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24
Q

Gastric impactions

A

Primary
- Feed that swells in stomach

Secondary
- Motility disorders
- Liver disease

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25
Q

Small colon impactions

A

Poor quality hay, lack of exercise, parasite burden, reduced water intake,salmonella

Relatively rare

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26
Q

Sand enteropathy

A

Regional – sandy soil

Diarrhoea/weight loss, or acute colic - due to how abrasive it is

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27
Q

Diagnosis of sand enteropathy

A

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

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28
Q

Treatment of sand enteropathy

A

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

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29
Q

Large colon displacements

A

Mild to moderate colic, may wax and wane

Proposed causes:
- Large concentrate meals
fermentation -> gas distension -> migration of large colon
- Altered motility

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30
Q

Right dorsal displacement of the large colon (RDD)

A

Cranial displacement of pelvic flexure towards diaphragm

Colon moves cranially - either medially or laterally to the caecum

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31
Q

Diagnosis of right dorsal displacement of the large colon (RDD)

A

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

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32
Q

Treatment of right dorsal displacement of the large colon (RDD)

A

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

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33
Q

Left dorsal displacement of the large colon (LDD)

A

Pelvic flexure moves dorsally into the nephrosplenic space

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34
Q

Diagnosis of Left dorsal displacement of the large colon (LDD)

A

Rectal - colon in nephrosplenic space

US - large colon obscures left kindey

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35
Q

Treatment of Left dorsal displacement of the large colon (LDD)

A

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

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36
Q

Equine grass sickness (EGS, equine dysautonomia)

A

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

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37
Q

Risk factors for Equine grass sickness (EGS, equine dysautonomia)

A

○ 2-7yrs old
○ Recent movement
○ Recent anthelmintics
○ Particular pasture
○ Disturbed pasture
○ Mechanical poo picking
○ Cool, dry weather, frost

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38
Q

Three presentations of Equine grass sickness (EGS, equine dysautonomia)

A

Acute
- Fatal (<48hrs)
- Definitively they will die

Subacute
- Fatal (<7 days)

Chronic
- Some survive
- Reports vary, approx. 40-50% fatality rate

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39
Q

Clinical signs of acute Equine grass sickness (EGS, equine dysautonomia)

A

Sometimes colic
Tachycardia (80-120bpm)
Innapetance
Patchy/generalised sweating
Muscle fasciculations
Normal to distended abdominal stance

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40
Q

Clinical signs of subacute Equine grass sickness (EGS, equine dysautonomia)

A

Sometimes colic
HR 60-80bpm
Dyspahgia
Mild rhinitis sicca
Patchy/generalised sweating
Muscle fasciculations
Normal to distended abdomen
May progress to narrow-based stance

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41
Q

Clinical signs of chronic Equine grass sickness (EGS, equine dysautonomia)

A

Usually no colic
HR: 45-60bpm
Patchy sweating
Muscle fasciculations
Tcuked up
Narrow based stance

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42
Q

Diagnosis of Equine grass sickness (EGS, equine dysautonomia)

A

Ileal biopsies

Phenylephrine eye drops
- reverse ptosis, poor sensitivity and sensitivity

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43
Q

Treatment of chronic Equine grass sickness (EGS, equine dysautonomia)

A

Select appropriate cases to treat
- Ability to swallow?
- Degree of colic?

Treatment
- Nutritional support
- Monitor hydration status
- Analgesia
- Treat secondary problems

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44
Q

Prognosis of chronic Equine grass sickness (EGS, equine dysautonomia)

A

Very, very difficult if they cannot swallow

Stop if continuous weight loss, no recovery of appetite

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45
Q

Post operative ileus

A

Common post surgery

Nasogastic reflux, distended SI, discomfort, tachycardia

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46
Q

Pathophysiology of post-operative ileus

A

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

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47
Q

Management of post-operative ileus

A

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

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48
Q

Treatment of post-operative ileus

A

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)

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49
Q

Peritonitis

A

Commonly idiopathic
Usually secondary

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50
Q

Reported causes of peritonitis in adult horses

A

Iatrogenic
Septic
Traumatic
Parasitic
Miscellaneous

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51
Q

Reported causes of peritonitis in foals

A

Meconium impaction
Ascarid impaction
Enteritis
Ulcer
Perforation
Intussusception
Ruptured bladder
Urachal abscess
Septicaemia
Abscess
Neoplasia

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52
Q

Clinical signs of peritonitis

A

Colic (50%)
Pyrexia of unknown origin (>80%)
Lethargy (80%)
Anorexia (68%)
Uveitis

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53
Q

Diagnostic tests for peritonitis

A

Often haematology/biochemistry first due to presentation

Peritoneal fluid analysis

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54
Q

Diagnosis of peritonitis

A

Abdominocentesis
- Gross appearance
□ Turbid, abnormal colour
- TNCC – increased
- Total protein – increased
- Culture
□ Often negative even in cases of septic peritonitis
- Lactate, pH, glucose – see previous lecture

Ultrasonography, rectal palpation, gastroscopy, parasite investigation…

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55
Q

Treatment of peritonitis

A

Broad spectrum antimicrobials pending culture
§ Penicillin, gentamicin, metronidazole (hospital)
§ Doxycycline more feasible for non-hospitalised cases as long as oral medication possible
§ NOT TMPS

Analgesia/anti-inflammatories

Supportive treatment
§ Fluid therapy, nutritional support, laminitis prophylaxis

Lavage may be required

May require surgical exploration if non-responsive/recurrent

Monitor response to treatment with serial abdominocentesis/haematology and biochemistry

56
Q

Analgesia for colic

A

NSAIDs
- Flunixin
- Phenylbutazone
- Ketoprofen
- Others

Opioids
- Reduce motility

Other
- Lidocaine

57
Q

Laminitis prophylaxis

A

Ice feet if you think they are prone to septic laminitis
- Continuously
- 10°C for 72h
- Different systems

58
Q

Indications for colic surgery

A

Unremitting, severe pain, despite analgesia

Large volume of naso-gastric reflux

Combination of:
- certain rectal findings
- signs of severe CV compromise/toxaemia
- peritoneal tap (high WBC count, serosanguinous, presence of RBC, high peritoneal lactate)

59
Q

Prognosis after collic surgery

A

Generally good

LI>SI>caecum

Non-strangulating>srtangulating

60
Q

Non-strangulating lesions

A

Pain less acute, often reponds to analgesia

CV compromise less severe, slowly progressing

Usually doesn’t need surgery but if complete obstruction of SI then it will

61
Q

Strangulating lesion

A

Typically severe pain, may reduce once section is completely dead

CV compromise severe and rapidly deteriorating

Always requires surgery (or euthanasia)

62
Q

How is colic surgery performed?

A

General anaesthesia

Dorsal recumbency

Ventral midline (maybe lateral if LDD)

Sew prepuce shut if gelding

63
Q

Pre-op prep for colic surgery

A

Clip while standing and sedated if poss

If hypovolaemic: hypertonic saline

If diluted SI loops: induce with stomach tube in place

If severe colic sedate heavily, flash US scan

64
Q

Areas of the GI tract that can be exteriorised in surgery

A

Jejunum
Distal caecum
Left ventral colon
Left dorsal colon
Small colon

65
Q

Gastric lesions

A

VERY uncommon to have a surgical gastric lesion
Normal sized stomach not surgically accessible in adult
Can palpate it deep in cranial abdomen

66
Q

Gastric impactions

A

Rare
* Primary motility problem
* Unsuitable feeding

DX: Difficult to diagnose ultrasound – detect stomach much more caudally than normal

Tx: medical first lavage (sedated, via naso gastric tube) Occasionally - evacuation at surgery

67
Q

Pyloric/duodenal stenosis

A

FOALS

Rare

<4mo : congenital?
Older foals: secondary to gastro-duodenal ulceration syndromes

Surgery rarely indicated - difficult due to poor exposure

68
Q

Strangulated small intestine

A

Jejunum ORAL to strangulated portion becomes distended because it is obstructed -> ileus

As it progresses orally -> stomach fills with fluid

If left -> eventually stomach ruptures which is fatal

69
Q

SI surgery

A

Ileus often a post-op problem

Start lidocaine infusion intra-operatively (expensive)

Gentle handling

Keep lubricated with fluids

Decompression - empty contents into caecum to promote motility

70
Q

Stomach

A

Surgically inaccessible unless very distended

Gastric impactions are the only surgical lesion – often managed medically first

High risk of abdominal contamination when emptying at surgery.

Pyloric stenosis foals – very rare.

Sx = pyloromyotomy or bypass of affected area

71
Q

Anatomy of small intestine

A

Duodenum: 1m, attached to transverse colon (duodenocolic fold), unable to be exteriorized

Jejunum: 20-25 m, mesentery lengthens as go distal; most exteriorizable

Ileum: 1m, thicker walled (muscle) distinctive antimesenteric band (ileocecal fold) that attaches to dorsal band of cecum; distal ileum and cecum cannot be exteriorized

72
Q

SI resection and anastomosis

A

Resection of affected segment and ligation of vessels supplying it

3 techniques of small intestinal anastomosis:

End to end SI anastomosis
– usually jejuno-jejunal.
- Best for post-operative function.

Side to side SI anastomosis
– not commonly utilised in horses

Jejuno-caecal anastomosis
– peformed if the resection involves the ileum

73
Q

Common non-strangulating SI conditions

A

Impaction
Inflammation/anterior enteritis
Adhesions
Neoplasia

74
Q

Common strangulating SI conditions

A

Pedunculated lipoma
Entrapment (epiploic foramen, gastrosplenic ligament, mesenteric rent)
Volvulus (foals, yearlings)
Intussusception
Inguinal hernia
Diaphragmatic hernia

75
Q

Simple obstruction (impaction)

A

Commonly ileum or jejunum

Mild/moderate colic

Risk factors: fine stem hay, switch from grass to hay, tapeworm, ascarids etc.

Diagnose with NGI, rectal, abdominocentesis

76
Q

Functional obstructions

A

Anterior enteritis

Eosinophilic enteritis

Grass sickness

Ileus

Adhesions

Neoplasia

77
Q

Anterior enteritis

A

Inflammatory condition, proximal SI only

Aetiol: unknown ?clostridial?

Better treated medically but sometimes is mis-diagnosed as a surgical colic

Marked fluid distention of SI, thickened and red wall but no ‘impaction’

Tx = decompress SI-> caecum

Prog = 50-70% survival

78
Q

Eosinophilic enteritis

A

small red lesions along SI, often ileum—usually diagnosed at surgery

79
Q

Ileus

A

Due to previous surgery; idiopathic, after frost

80
Q

Adhesions

A

Due to previous colic surgery

81
Q

Neoplasia

A

Rare

lymphosarcoma most common

Also adenocarcinoma etc.

82
Q

General approach to strangulating lesion

A

Identify cause of strangulation

Reduce (disentangle) strangulation

Assess gut viability once reduced

Decompress, resect, and anastomose if gut non-viable

Prognosis depends on length of gut involved- 60-85% survival

83
Q

Lipoma

A

Benign smooth walled tumour

Grow from mesentery

Often grow on long stalks which entrap loops of SI

84
Q

Signalment for lipoma

A

Older horses, usually >14

ponies, arabs, QH

Can be in obese or poor conditioned horses

85
Q

Clinical signs of lipoma

A

may start as non-strangulating but then progress to venous +/- arterial occlusion.

Colic is often severe and palpate distended SI on rectal + dx on u/s.

Progressing CV compromise over time.

NG reflux as/when fluid backs up to the stomach

86
Q

Surgery for lipoma

A

Resection of entrapped gut often required + suitable anastomosis

87
Q

Epiploic foramen entrapment

A

Small intestine entraps in potential space – almost always strangulating lesion

88
Q

Epiploic foramen borders

A

Caudate liver lobe
Portal vein
Gastropancreatic fold

89
Q

Risk factors for epiploic foramen entrapment

A

Cribbers (68% of horses with this condition are cribbers), stabled horses, males, TB

90
Q

Clinical signs of epiploic foramen entrapment

A

Signs of SI strangulating disease

91
Q

Surgery for epiploic foramen entrapment

A

Resection often required and suitable anastomosis

92
Q

SI entrapment

A

Can get trapped almost anywhere

Naturally occuring locations
- epiploic foramen
- inguinal ring (hernia, post-castration)
- umbilicus (hernia)

Through rents (tears) in structures
- mesenteric rent
- gastrosplenic rent
- diaphragmatic hernia

ETC.

93
Q

Gastro-splenic ligament entrapment/mesenteric rent

A

Rent in the ligament or mesentery

Causes:
congenital/trauma/Stretched due to another lesion/post partum mare/previous sx

Can be difficult to close the defect at surgery

94
Q

Volvulus of SI

A

acute severe colic with rapidly deteriorating CV signs (foals or yearlings usually)

95
Q

Diaphragmatic hernia

A

abdominal contents in thoracic cavity

rare

usually after trauma

96
Q

Intussusception

A

Obstruction or strangulated (depends on length of SI that is involved – longer segment -> more likely strangulating lesion)

Many locations possible - Ileocecal most common, jejuno-jejunal, jejuno-ileal etc

Mainly a disease of foals, weanlings-3 yo

Can be acute or chronic

97
Q

Aetiology of intussusception

A

Segmental motility differences due to enteritis, ascarids or tapeworms, abrupt diet change

98
Q

Clinical signs of enteritis

A

if chronic/partial obstruction, sometimes just weight loss/unthrifty

But often acute colic episode esp if strangulated

99
Q

Treatment of intussusception

A

Surgery: reduction +/- resection and anastomosis or incomplete bypass with ileocecostomy

100
Q

Thrombo-embolic colic

A

Strongylus vulgaris larval migration -> vascular infarction

Rarer now

Mesenteric vascular thrombi -> thickened, devitalised section of SI

101
Q

Inguinal hernias in stallions

A

Usually acquired after breeding or strenuous exercise (jumping)

Usually strangulates quite quickly because inguiinal ring is quite small/tight

Testicle becomes cold and firm, may not feel strangulated intestine externally and need rectal of internal inguinal ring/US

102
Q

Inguinal hernia in foals

A

Usually congenital, reducible and larger amounts of bowel

Most spontaneously resolve over first 3-4 months of life – tell owner to manually reduce daily

Only become emergency if non reducible, assoc with colic or large increase in size

103
Q

Diagnosis of inguinal hernia

A

easy if palpate testicle and u/s probe on testicle/inguinal area,

plus rectal exam in adults: feel distended SI entering inguinal ring

104
Q

Treatment of inguinal hernia in foals

A

no surgery required unless >5-6 months and no resolution or become strangulated

105
Q

Treatment of inguinal hernia in stallions

A

Surgery
- Can manually reduce in adult by massage if acute and no major CV compromise (i.e. quick referral).
- Unilateral (hemicastration) castration recommended as testicle can become non functional due to vascular compromise
- +/- closure of internal inguinal ring – easier done laparoscopically at later date

106
Q

Anatomy of caecum

A

Water resorption (mostly cecum) and microbial digestion/fermentation

1.25 m, 30 L.

Right side; extends down to xyphoid, Base is dorsal, body, apex is ventral

Attached dorsally to body wall/kidney

Ileocecal fold - attaches to ileum.

Caecocolic fold - attaches to RVC (lateral band)

Ileum empties into cecum via ileocecal orifice

Only apex and part of body are exteriorisable

107
Q

Large colon anatomy

A

Caecum -> RVC -> LVC -> LDC -> RDC -> transverse colon -> small colon

Water resorption (mostly cecum) and microbial digestion/fermentation

3.5 m, 50-60L

Short mesenteric attachment between dorsal and ventral colons ONLY—no attachment to body wall.

Ventral colon well sacculated, dorsal colon less sacculated

Transverse colon: continuation of RDC aborally and joins to small colon; attached to body wall and also duodenum via duodenocolic ligament

108
Q

Small colon anatomy

A

Fecal ball formation
3.5 m
Caudodorsal within abdomen; palpable rectally

109
Q

Caecal impaction

A

Primary impaction or secondary to motility disorder.

Most common in hospitalized patients due to pain/stall rest/not moving/change in diet.

Watch hospitalized horses for faecal output and rectal if reduced – may not show overt signs of colic.

110
Q

Caecal impaction treatment

A

Tx medically first.

Surgery may be required if any deterioration of clinical signs or increasing distension on rectal

Surgical procedure: typhlotomy and empty out contents – occasionally require caecal bypass because condition often recurs.

111
Q

Caecal intussusception

A

Caeco-caecal or caeco-colic.

Tx = reduce and may require resection if gut is compromised.

Caeco-caecal:
- Starts at apex (occasionally at base)
- Chronic/intermittent pain
- No complete obstruction until-> obstruct caecocolic area = simple obstruction

Caeco-colic:
- Caecum -> into RVC
- Caecocolic artery obstructed - > strangulating lesion
- Need to do a caecal bypass
- Difficult surgery with lots of contamination

112
Q

Common large and small colon conditions

A

Gas colic
Impaction
Displacement
Torsion
Enterolith/faecolith
Colitis
Small colon impactions

113
Q

Anatomy of large colon

A

Ventral = large, sacculated
Dorsal = smaller, smoother surface
Pelvic flexure on the left side (narrowest)

114
Q

Evacuation of colon contents

A

For most surgical procedures on large intestine

Improves post-op motility

For relief of colon impaction/distension
- eases manipulation of colon
- allows re-positioning
- improves post operative motility

115
Q

Pelvic flexure enterotomy

A

To decompress colon

Pass water up dorsal and then ventral colons

Colon evacuated bit by bit

Sterile saline used to wash colon surface

Closed in two layers

116
Q

Displacements

A

Non strangulating – but get secondary distention with gas -> can get CV compromise over time

117
Q

Right dorsal displacement

A

Displaces cranial then clockwise or counter clockwise

118
Q

Left dorsal displacement (nephrosplenic entrapment)

A

Entrapment of the colon between the spleen and the kidney causes total or partial obstruction

119
Q

Pelvic flexure retroflexion

A

Flips 180 degrees

120
Q

Surgical procedures for displacement

A

Correction of displacement

LDD: Phenylephrine may assist with correction by shrinking spleen in surgery

Standing or anesthetized

Can recur - if the second surgery consider colopexy (for RDD) or closure of nephrosplenic space (LDD)

Good prognosis >80% survival

121
Q

Torsion/volvulus

A

Strangulating Lesion - true emergency - one of most painful, emergent and devastating GI problems in horse

Success depends on rapid referral and surgical intervention

Can start as a displacement that becomes torsion

122
Q

Risk factors for torsion/volvulus

A

Large horses,
post foaling broodmares,
spring (lush pasture),
recent diet change

123
Q

Diagnosis of torsion/volvulus

A

Rectal: gas, tension/bands.

US: position, thickening/edema, dilated colonic vessels

124
Q

Treatment of torsion/volvulus

A

Most require surgery and quickly

270-720 degree torsions described – more rotation -> more severe pain and CV compromise

Surgical Options (depending on colonic viability):
- Reduce the torsion then evacuate the colon contents and re-evaluate bowel
- May require resection (if devitalized) or even euthanasia

125
Q

Colon volvulus/torsion

A

Gut wall is compromised (purple, thickened)

Haemorrhage into colon interior

Treatment: surgical correction

126
Q

Colon resection (partial)

A

If torsed at caeco-colic juntion there will be some compromised tissue left in situ -> post op complications

127
Q

Enterolith/faecolith

A

Not common in UK

Common sites: RDC, transverse colon, small colon

Presdisposed in arabs, or on alfalfa hay

128
Q

Clinical signs of enterolith/faecolith

A

Intermittent mild/moderate colic

129
Q

Diagnosis of enterolith/faecolith

A

Often diagnosed at surgery
Rectal: +/- large colon distension

130
Q

Treatment of enterolith/faecolith

A

Surgical intervention required
Enterotomy and removal of stone

131
Q

Small colon impaction

A

Non-strangulating

Medical treatment first

Surgery recommended with increasing pain
- enema performed intra op and manual massage
- may need small colon enterotomy

Increased shedding of salmonella therefore isolation necessary

132
Q

Small colon strangulating lesion

A

Less common
Same etiology as small intestine
- Pedunculated lipoma
- mesenteric rent
- volvulus

133
Q

Complications after colic surgery

A

Recurrent episodes of colic

Post operative SI ileus

Incisional infection

Adhesions

134
Q

Recurrent episodes of colic after surgery

A

common – particularly in first year after surgery.

Severity varies.

135
Q

Post operative SI ileus

A

Approximately 10-20% cases (upwards of 30% with SI lesion)

Associated with 38-40% post op deaths in horses treated for colic

Aetiology: Inflammation, surgical manipulation, endotoxemia, distension of gut (pre-operatively or post-operatively)

136
Q

Incisional infection

A

10-40% prevalence after colic surgery—higher if >1 surgery

Pyrexia, pain at incision site, sudden increase in oedema

Remove sutures/staples over site of drainage, bacterial culture & sensitivity

Wipe incision twice daily with saline and gently milk out any drainage fluid if present +/- lavage

17.8 x more likely to develop incisional hernia if infection

137
Q

Incisional hernia

A

Can occur upto 2-3 months post op

138
Q

Adhesions

A

Foals more predisposed than adults

Occur frequently after surgery, mostly for strangulating lesions

May cause colic or may never cause a problem - Can cause low grade recurrent colic

Usually diagnosed at repeat celiotomy

Prevent:
Minimize trauma/good technique, keep intestines moist, reduce inflammation post op (NSAIDs, Lidocaine), CMC (carboxymethycellulose—lubricating), heparin (inhibits thrombin mediated conversion of fibrinogen to fibrin)

Equine michaelmas 23 (17 decks)

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