EMS - Dem Medicine

Question 1

Caecum Anatomy

• Location
• Length & transit time
• Openings
• Smooth muscle features

Answer 1

• Lies on RIGHT abdo wall (b/w ileum and R colon)
• ~1m long, transit time 5h
• SI → caecum via ileocaecal orifice → colon via caecocolic orifice
• 4 bands of smooth m. (taeniae = longitudinal) forming pouches (haustrae)

Question 2

Caecum Motility

• Location and role of pacemaker
• Role of segmentation vs. progressive contractions
• Inhibiting and stimulating drugs

Answer 2

• Pacemaker in ventral caecal wall, 10-15cm from apec and generates neural impulses
• Segmentation contractions mix ingesta (toward apex) vs. progressive contractions that produce mass movements forcing caecal contents into colon (emptying). No retrograde flow.
• Inhibited by alpha2 agonists (Xylazine, Detomidine) & opioids
• Stimulated by parasympathomimetics (Neostigmine, Bethanechol, Erythromycin)

Question 3

3 functions of caecum

Answer 3

1. Water resorption (70% water from ileum)
2. Electrolyte resorption (Na, Cl)
3. Initiates microbial digestion of complex carbs = major site of VFA production

Question 4

Caecal Impaction

• Incidence & cause
• Risk factors
• Clinical signs
• Diagnosis
• Medical treatment
• Surgical treatment
• Prognosis

Answer 4

• Most common caecal disease - accounts for 5% of GIT impactions, and up to 43% of fatalities, caused by dehydrated faecal material accumulating at caecal base
• RF = hospitalisation / Sx (esp. musculoskeletal & ophto cases), poor dentition, poor quality hay / water access, parasites (Anoplocephala perfoliata)
• CS = very mild and intermittent colic → commonly missed, can suddenly rupture → death! Need to monitor faecal prod^<u>n</u> in hospital Pt’s! May rupture w/o significant pain.
• Dx = rectal palpation → tight ventral caecal band palpable on RIGHT abdomen
• Medical Tx = analgesia, NGT if reflux, soften digesta, withhold feed, address RF
  
  • Success up to 90% if <24h duration and respond w/in 24h
• Surgical Tx = typhlectomy, caecocolostomy, jejunocolostomy, ileocolostomy
  
  • Good Px if no systemic deterioration
• Px = dependent on early Dz recognition & Tx. Recurrence possible..

Question 5

Caecal Tympany

• Primary vs. secondary causes
• Clinical signs
• Rectal palpation findings
• Clinical pathology
• Diagnosis
• Treatment

Answer 5

= gaseous distension of the colon

• Primary dt rapid gas production (lush pasture, high grain) or reduced caecal motility vs. Secondary dt outflow obstruction (i.e. colon displacement)
• CS = R flank abdo distension, intermittent severe pain, increased HR & RR, decrease borborygmi, PING on R dorsal flank
• Rectal findings = caecal distension, palpable R ventral taenia (R dorsal to L ventral)
• CP = non-specific; stress leukogram reflects primary Dz
• Dx = risk factors, clinical exam & rectal palpation
• Tx = analgesia (Xylazine), gastric decompression (Sx - commonly needed), FT +/- NGT, laxatives, withhold feed, trocarisation if severe (salvage procedure ONLY - high risk)

Question 6

Caecal Perforation

• Primary vs. Secondary disease
• Common site of rupture
• Risk factors
• Outcomes

Answer 6

• Primary = broodmares after parturition (w/o evidence of outflow obstruction) vs. Secondary = caecal outflow obstruction (most common)
• Rupture at caecal base most common (empty ventral colon, ingesta filled caecum)
• RF = hospitalisation, Tx for other Dz, caecal impaction

→ Sudden death (FATAL)

Question 7

Caecal Intussusception

• Incidence and pathogenesis
• Risk factors
• 3 syndromes
• Clinical signs
• Clinical pathology
• Rectal exam findings
• Treatment
• Prognosis

Answer 7

• Uncommon - can be caeco-caecal OR caeco-colic, caused by altered motility
• RF = tapeworm infestation
• 3 syndromes = acute (55%) - cause severe pain, need immediate Sx; sub-acute (3-8d, 30%); and chronic (6-180d, 13%)
• CS = similar to other caecal Dz, abdominocentesis normal but → serosanguinous w/ Dz progression
• CP = normal → dehydration & metabolic acidosis
• Rectal findings = normal if caeco-caecal, mass or malposition if caeco-colic; thickened caecal wall on U/S (“double donut”)
• Tx = Sx (manual reduction of intussusception +/- typhlectomy +/- anastomosis)
• Px = good if remove all diseased portions of caecum; can get chronic wt loss as sequelae

Question 8

Other caecal diseases

Answer 8

Rare - mimic signs of other caecal Dz → torsion, volvulus, infarction (foals <1yo dt Strongylus vulgaris), tumour / abscess (>20yo)

Question 9

2 Stages of Reperfusion Injury of GIT

• Cause and parts affected
• Part 1 - Ischaemia
• Part 2 - Reperfusion

Answer 9

• All parts of GIT - damage to tissue when blood supply returns after period of ischaemia
• Part 1 - Ischaemia
  
  • Decrease in blood supply to tissue / organ dt construction / obstruction of blood vessels (need O₂ but has risk of oxidative damage)
  • Membrane ion pump function altered when no O₂ present → entry of Ca, Na, H₂O into cell → mitochondrial dysfunction → cell membrane failure → cell necrosis
  • ROS production → pro-inflammatory cytokine production → increased tissue vulnerability to further reperfusion injury
• Part 2 - Reperfusion
  
  • Leukocyte chemotaxis & activation → release ROS → damage cell membranes → increased vascular permeability, oedema, thrombosis, cell death
  • Production of pro-inflammatory mediators → altered vascular homeostasis, leukocyte function, cytokine release
  • Intracellular Ca overload → cell dysfunction & smooth m. contraction

Question 10

Implications of Reperfusion Injury (of GIT)

• Which organs affected first?
• Small intestinal and large intestinal effects
• Consequences
• Prognosis
• Recovery
• Treatment

Answer 10

Reperfusion injury → MOD → MOFS → Death.

• Myocardium and pulmonary parenchyma = first organs that circulating toxins & inflamm. products reach
  
  • “Gut is the motor of MOFS” = vicious cycle of inflamm. mediator release
• SI implications = fluid sequestered in subepithelial space, epithelium loosens from BM → sloughing of sheets of cells → villi denuded of epithelium to crypt level (within 3h) → complete necrosis of mucosal epithelium extending to crypt base (within 4-5h)
  
  • → Ileus & Loss of Absorption Function +/- Increased Secretion
• LI implications = necrosis of clumps of surface epithelium, cells loosen from BM and neighbouring cells → sloughing of small clusters of surface epithelium (rather than sheets of cells as in SI)
  
  • → Ileus & Loss of Absorption Function +/- Increased Secretion
• Consequences = mucosal epithelial injury disrupts mucosal barrier leading to migration of luminal bacteria and endotoxin into circulation → endotoxaemia; sequestration of large volumes of fluid → hypovolaemia, hypotension, impaired perfusion
• Px = dependent on degree and duration of ischaemia. Despite Sx correction & medical Tx & supportive care - peri-op mortality is high
• Recovery = if horse survive initial period of mucosal necrosis & sloughing and there are still viable enterocytes, mucosa can regenerate. Defects covered within 12-24h.
• Tx = prevent formation of ROS, stop cytokine prod^<u>n</u>, prevent endothelial cell damage, stop neutrophil chemotaxis, treat inflammation in tissues.
  
  • Flunixin meglumine (NSAID) 0.25-1.1mg/kg IV q8-12h
  • Lignocaine (analgesia, anti-inflamm., membrane stabilisation) 1.3mg/kg loading as slow bolus followed by 0.05mg/kg/min CRI