Abdominal Diseases

“Abdominal Catastrophe”

• Clinical signs

• 4 Mechanisms/causes (+ DDx)

Clinical Signs: Colic with distended abdomen and usually SHOCK

Mechanisms/Causes:

1. Torsions

   1. RDA with torsion

   2. Caecal dilation and torsion

   3. Mesenteric torsion

   4. Ileus

2. Blockages

   1. Intussusception

   2. Haemorrhagic bowel disease

   3. Phytobezoar

   4. Constricting bands (tears in ligaments at parturition/congenital which trap intestine)

   5. Tears in omentum → Herniation

3. Toxic

   1. Rumen acidosis

   2. Septic mastitis → 2˚ ileus

4. Other

   1. Bloat

   2. Diffuse peritonitis

   3. Perforating abomasal ulcer

Abdominal diseases NOT characterised by shock

• Forestomach (5)

• Abomasum (3)

• Other (3)

Forestomach

1. Rumen acidosis

2. Traumatic reticuloperitonitis

3. Vagal atony

4. Actinobacillus of rumen/reticulum

5. Simple indigestion

Abomasum (esp. system grade 4 with high grain)

1. LDA or RDA without torsion

2. Impaction

3. Ulceration

Other

1. Caecal dilation

2. Chronic peritonitis

3. Non-gastrointestinal (eg. urinary tract)

5 Steps of abdominal disease diagnosis

1. History

   • Often associated with sudden drop in milk production due to visceral pain → Activation of sympathetic nervous system → Inhibit milk letdown

2. Distance examination

3. Physical examination

4. Rectal palpation

5. Additional tests

Good history and PE → Diagnosis made in up to 90% of cases (+ve: Save money for farmer)

9 Features to assess on distance examination for abdominal disease

1. Mentation (alert vs. depressed)

   • Interaction with environment

2. Behaviour (eating, chewing cud, urinating, defaecating)

   • Caution: Some sick animal still eat in new environments (eating = Stress response)

   • Chewing cud = GOOD sign

3. Posture (down, hunched)

4. Signs of colic (abdominal discomfort) = More subtle in cattle

   • Obvious colic with rolling and repeated recumbency is UNUSUAL

   • DDx:

     1. Adult = Mesenteric torsion

     2. Calf = Abomasal bloat

5. Gait (may appear slightly lame or subtly looking at flank)

6. BCS

7. Body symmetry and abdominal distension

8. Observe other cows in herd

9. Faeces present? Consistency, contents, contamination of hindlimbs

   • Large volumes of faeces = No obstruction → Immediate surgical intervention unlikely required

     • Some conditions resolve on transport

   • Mucus ONLY = Obstruction and no passage of digesta → Surgical management

   • Diarrhoea = LDA/RDA

   • Blood = Abomasal ulcer, haemorrhagic bowel disease (blackberry jam)

   • Large undigested fibre particles (>2cm length) = Hardware disease

DDx: Body symmetry/abdominal distension

1. Normal

2. Free gas bloat (2˚ bloat)

3. Froth bloat (1˚ bloat)

4. Vagal indigestion aka. “papple”

5. Paralytic ileus, intestinal obstruction

6. Pneumoperitoneum

7. RDA

8. Abomasal impaction (sand, food particles etc.)

11 Features to assess on left/right abdominal examination (+ signs indicating abdominal disease)

1. Rumen: Contraction, eructation, rumen fill, layers

2. Left paralumbar fossa

3. Percussion (“ping”) along line between olecranon and tuber coxae

   • Left AND right side

4. Ballottement: Splashing sounds

5. HR: ≥120/min → BAD

6. RR: Tachypnoea

7. Wither’s pinch test → Cranial abdominal pain

8. Hydration status → Severe dehydration is a concerning sign

   • Do not lose fluid, but usually sequestered in large organs

9. Percussion of liver: Absent → RDA (abomasum between liver and abdominal wall)

10. Spontaneous gut sounds: Hyper-/hypomotility

11. Percussion of ventral abdominal wall with hammer and spoon: Hollow sound → Fibrin adhesions/abomasal ulcers

List 5 requirements of a “ping” on percussion

1. Gas distended organ

2. Gas/fluid interface (will NOT ping if fibre present in rumen)

3. Gas under pressure

4. Gas distended organ against body wall

5. Precussor AND stethoscope over gas distended organ → Determine extent of gas distension

   • Changing pitch in same spot indicates residual contractility of intestine

DDx for “pings”

• Left-sided ping (4)

• Right-sided ping (5)

Left-Sided Ping

1. LDA (metallic)

2. Rumen gas cap (ABNORMAL as no fibre in rumen → Gas-fluid interface)

3. Physometra = Gas in uterus

4. Pneumoperitoneum

Right-Sided Ping

1. RDA ± torsion

2. Caecal dilation/volvulus

3. Spiral colon/small intestinal gas (ileus, intussusception, haemorrhagic bowel syndrome)

4. Physometra

5. Pneumoperitoneum

List 6 further diagnostic tests to perform for suspected abdominal disease

1. Rumen fluid analysis via rumenocentesis or stomach tube→ pH, protozoa, rumen Cl-

2. Ultrasound (rectal probe)

3. Radiography

4. Haematology

5. Serum biochemistry: Na, K, Cl, Ca, P, Mg, HCO3, TP

6. Abdominocentesis

3 Abdominal diseases which can be diagnosed on U/S

1. Peritonitis = Fibrin looks like moving seaweed

2. Free abdominal fluid (uroperitoneum or ascites): Place probe along right caudoventral abdomen

3. Intestinal ileus/obstruction

   1. Hypoechoic lumen (fluid-filled)

   2. Lack of gut motility

   3. Diameter of intestinal loops >4.cm → Surgery (normal < 3.5cm)

Abomaso-ruminal reflux

• 2 Causes

• Electrolyte features

• Pathogenesis

Causes:

1. Abomasal outflow obstruction (eg. LDA or RDA)

2. Proximal intestinal obstruction

Electrolytes:

1. Hypokalaemia

2. Hypochloraemia (>30mEq/L = Abomasal reflux)

3. Metabolic alkalosis

Opposite results (acidosis and hyperkalaemia) = Decompensation and poor prognosis

Pathogenesis:

• Normal: Cl- from abomasal lumen exchanged for HCO3- in blood → Cl- enters circulation and HCO3- enters abomasum to buffer H+

• Obstructed abomasal outflow: Cl- cannot be absorbed into blood (hypochloraemia) and HCO3- remains in blood (alkalosis)

3 Aetiologies of left OR right displaced abomasum

Multifactorial

1. Anatomy = Deep-bodied and lack of fixation of the abomasum in the abdominal cavity

   • Signalment: Holstein-Friesians (genetics and deep-bodied)

2. Mechanical = Reduced feed intake peripartum AND reduced forage:concentrate ratio (lactation rotation) → Lower rumen fill

   • Normal: Rumen prevents abomasal flipping/displacement

3. Metabolic → Abomasal atony

   • Signalment: FAT cows

     • Produce VFAs and ketones → Reduced abomasal motility

   • Concurrent Diseases: Cause reduced smooth muscle contraction

     1. Hypocalcaemia

     2. Metritis, mastitis, RFMs → Septicaemia and toxaemia

Are displaced abomasums caused by space left after calving?

NO!

1. LDA are NOT seen immediately post-calving

   • Timing: First 4 - 5 weeks post-calving

2. Calves positioned on RIGHT side of abdomen → Would expect more RDA as consequence (no calf as blocker)

Left Displaced Abomasum

• Mechanism

• 6 Clinical signs

• 2 Methods of diagnosis

Mechanism:

1. Anatomy, mechanical and metabolic factors cause abomasum to shift to the LEFT of midline

2. Abomasum distends with gas to occupy space between left body wall and rumen

3. Partial obstruction of pyloric outflow

Clinical Signs:

1. Sudden drop in milk production

2. Anorexia

3. Bright(ish) and no fever

4. Mild constipation OR diarrhoea

5. Concurrent illness

6. Distended left paralumbar fossa (no dorsal triangle)

Diagnosis: History and PE →

1. Metallic ping between the 9 - 12th ribs on the LEFT

   • Differentiate abomasal ping from rumen ping caused by anorexia) with DOUBLE auscultation:

     1. Blow air into rumen via orogastric tube → Listen for bubbling sounds over the left paralumbar fossa from the rumen

        • No bubbles = Abomasal ping

     2. Listen for rumen contraction over site of pig

        • No rumen contractions = Abomasal ping (abomasum between abdominal wall and rumen)

2. Biochemistry = Hypochloraemia, hypokalaemia, hypocalcaemia

List 3 methods of LDA treatment (+ success rates)

1. Conservative (non-surgical): Rolling OR bumpy ride

   • 20% success rate

2. Open Surgery: Standing right flank omentopexy

   • 90% success rate

3. Blind Surgery: Cast and percutaneous toggling (Grymer/Sterner toggle suture)

   • 80 - 90% success rate

Describe the method of rolling to treat an LDA

1. Gently cast cow into RIGHT lateral

2. Auscultate and ping the LDA to determine location

3. Rock into dorsal then LEFT lateral to help evacuate gas

OR prolonged LEFT lateral recumbency (eg. tilt table for claw trimming) BUT care with radial nerve

Describe the method of right flank omentopexy for LDA treatment

1. Right flank laparotomy

2. Systematic exploration of abdominal cavity

3. Reached over rumen and deflate abomasum with needle with flutter valve attached to a long tube

4. Reposition abomasum

5. Omentopexy = Tack omentum to ventral abdominal wall to prevent future abomasal displacement

   1. Pull omentum through incision until pylorus can just be seen

   2. Place mattress sutures through peritoneum, omentum and muscle

   3. Place continuous sutures on inner layers of muscle incorporating the omentum

Grymer/Sterner toggle suture

• Advantage

• Kit

+ve: Introduced as improvement on the blind stitch method → Uses litmus paper to test pH of fluid to be certain abomasum is being sutured

Kit:

1. Trocar/canula

2. Nylon handle

3. Suture push rod

4. Suture

Describe the method of grymer/Sterner percutaneous toggle suture for LDA treatment

1. Cast cow onto right side using Reuff’s method → Roll onto back (0.1mg/kg xylazine IV)

2. Tie front and rear legs if required

3. Insert 10 - 15cm behind xyphoid and 5 - 8cm to the right of midline

4. Use pressure to push abomasum into right position

5. Push trocar through wall avoiding milk vein and other vital structures

6. Draw off fluid and check pH is 2 - 4

7. Remove nylon handle and introduce toggle

8. Push toggle clear of trocar/cannula with the push rod

9. Pull to ensure toggle is clear of trocar (not too tightly)

10. Remove trocar/cannula and clamp nylon with needle holder

11. Place 2nd toggle 5 - 7cm anterior of 1st toggle

12. Before removing 2nd trocar, remove as much free gas as possible from abomasum

13. Place surgeon’s knot tied with hands (clamps still remain on)

14. Leave a hand width’s distance between knot and body wall

15. Consider placing a toggle button to distribute pressure (MANY knots to secure in place)

Right Displaced Abomasum

• Mechanism

• 4 Clinical signs

Mechanism:

1. Rumen acts as barrier to prevent LDA, but anatomical, mechanical and metabolic factors cause gas distension and atony of the abomasum

2. Allows abomasum to float up on the right side

3. Torsion = Dorsal displacement of the greater curvature

4. → Counterclockwise (180 - 360˚) torsion as the pylorus moves cranially via the abdominal wall side (2nd flip)

5. → Complete inflow AND outflow obstruction

6. Vagus nerve compromised within twist

Clinical Signs: More acute and serious than LDA

1. Severe dehydration

2. ± Diarrhoea

3. more fluid sounds than LDA

4. Severe illness when torsion develops (shock)

→ Emergency surgery required ASAP

Describe treatment and prognosis for RDA

Treatment: EMERGENCY → Euthanasia OR right flank omentopexy

1. Right flank paracostal approach

2. Correct displacement by pushing greater curvature cranioventrally → Push pylorus caudally

   • → Bubbling (toilet-flushing) sound when gas evacuates from pylorus (good sign)

3. Decompress (may need to remove fluids too with stomach tube purse-string suture)

4. Check viability of abomasum

5. Anchor with omentopexy

Prognosis: Good(ish) success rate if caught early BUT vagal indigestion may occur after severe RDA despite a successful surgery

Caecal Dilation ± Torsion

• Seasonality

• Clinical signs

• Risk factor

Seasonality: More variable than LDA/RDA

Clinical Signs: As for RDA

• Fluid sounds more caudodorsal than RDA (ventral to short ribs on RIGHT side)

• French load palpated on rectal exam projecting into pelvis = Distal end of caecum OR curve of flipped caecum

Risk: High VFAs in circulation

Describe treatment of caecal dilation ± torsion

1. Right flank approach but more caudal than RDA

2. Exteriorise caecum (care as necrotic)

3. Stab end of caecum and drain, using left hand inside to massage contents out

4. Invert and oversew caecum (± amputation of distal caecum if necrotic)

5. Return caecum to abdomen and hope it sorts itself out

Rumen acidosis:

• Prevalence

• Severity

• Aetiology

Prevalence: Common and important disease (esp. South Island)

Severity: Mild inappetence/vague clinical signs → Severe/life-threatening

Aetiology: Excessive soluble/readily fermentable CHO in diet OR poor quality, sour feeds which animal has not had time to adapt to

• Poor transition is KEY

Describe the normal mechanism of CHO metabolism in ruminants

1. Cow ingests non-structural CHO (eg. cellulose) which enters the rumen for microbial fermentation

2. Microbes produce volatile fatty acids (VFAs): Acetate, propionate and butyrate which are kept within a certain ratio

3. VFAs absorbed through rumen wall to enter the Kreb’s cycle for energy

   • Acetate (~60 - 70%) = Major energy source and used for fat synthesis (eg. milk fat in mammary gland)

   • Propionate (~15 - 25%) = Major precursor for glucose production in liver via gloconeogenesis

   • Butyrate (~10 - 15%) = Converted to ketones in rumen epithelium as source of energy

List 7 causes of rumen acidosis

1. Poor transition onto crops (eg. fodder/sugar beet) = Fodder beet farmer management disorder

2. General issue with feedlots (TMRs with highly soluble CHO to maximise growth)

3. Malfunction of automatic feeders

4. Mischievous/greedy cows which escape and get into grain

5. Improper mixing of TMR → Allows cattle to preferentially eat highly soluble CHO

6. Very lush pasture

7. Other cheap food sources: Grain, fruit, potatoes, turnips, brewer’s grain, fodder/sugar beet, cookie waste

Describe the pathogenesis of rumen acidosis (ACRA)

Downward spiral

1. Readily fermentable CHO broken down by bacteria within 2 - 6hr → D/L-lactate

2. D-lactic acidosis decreases rumen pH allowing lactic acid-producing bacteria to increase (Strep. bovis and Lactobacillus)

3. Rumen pH ≤ 4.5 as more lactic acid is produced (wrong type of VFA eg. more butyrate and less acetate)

4. Rumen microbes die (pH < 5) → Rumen stasis and increased intraruminal osmolarity

5. Only Strep. bovis survives and produces more lactic acid → Local and systemic metabolic acidosis

6. Acid and increased osmolarity (unabsorbed nutrients) draws water into rumen via osmosis → Dehydration (fluid sequestration)

7. Irritation of rumen mucosa and reduced rumen epithelial blood flow → Rumenitis and no absorption of nutrients from the rumen wall

8. Plasma transudation into rumen

9. Endotoxin and bacteria escape into portal circulation

7 Clinical signs of rumen acidosis (ACRA)

1. Distended rumen and abdomen

2. Reduced/absent rumen motility

3. Recumbent/staggering/drunk (hypocalcaemia and D-lactic acidosis)

4. Non-specific signs of pain: Depression, inactivity, dehydration, weak, anorexia, teeth grinding

5. Soft to foetid diarrhoea ± undigested grains

6. Hypovolaemic shock (low temperature and increased HR)

7. ± Acute death (within 2 - 3d after rumenitis event)

4 Methods of acidosis (ACRA) diagnosis

History #1 →

1. Rumen fluid pH < 5 and no motile protozoa with lots of G+ bacteria

2. Biochemistry = Increased PCV, metabolic acidosis and hyperlactaemia

3. Acidic urine

4. PM exam = Severe inflammation with rumen mucosal sloughing

List 3 goals or rumen acidosis (ACRA) treatment

1. Correct ruminal and systemic acidosis → Prevent further production of lactic acid

2. Restore fluid and electrolyte losses → Maintain circulating blood volume

3. Restore forestomach and intestinal motility

5 Treatments for rumen acidosis (ACRA)

1. Prevent further access to CHO → Offer good hay and exercise animal where possible

2. Triage if outbreak in herd

   • Cull if unlikely to survive

   • 80 - 90% of cows during acidosis outbreak recover WITHOUT treatment as they stop eating in time (disease causes anorexia)

3. Rumen lavage (liquid content eg. grain) OR rumenotomy (solid content eg. fodder beet) when severe

   • Ideally with transfaunation to replace rumen microflora

   • ONLY treatment that addresses issues (other treatments are symptomatic management)

4. IV sodium bicarbonate (5L of 5% Na₂HCO₃ for 450kg) (wobbly cow)

5. SC/IV calcium borogluconate (wobbly cow)

6. Additional therapy: NSAIDs, antibiotics (severe rumenitis), antihistamine (prevent laminitis), thiamine (prevent PEM), fluid therapy

   • Care with fluid therapy as it may be sequestered into the highly osmotic rumen

Indication of intraruminal alkalinising agents (eg. MgO)

Do NOT give!

Rumen has no absorptive capacity for alkaliniser AND will exert increased osmotic effect

4 Sequelae of rumen acidosis (ACRA)

1. Abortion 10 - 14d later

2. Laminitis

3. Fungal rumenitis

4. Caudal vena cava syndrome

   1. Liver abscess → Lung abscess

   2. Pulmonary embolic aneurysm

   3. Fatal epistaxis

Subacute rumen acidosis (SARA)

• Cause

• 4 Clinical signs

Cause: HERD problem due to incorrect feeding (eg. fibre:CHO imbalance from lush pasture)

Clinical Signs:

1. Inappetence

2. Poor rumen function (empty and reduced motility)

3. Soft faeces

4. Low milk fat syndrome due to altered ratio of VFAs

   • Reduced acetate required for milk fat production

Mesenteric torsion

• Clinical signs

• Treatment

• Prognosis

Clinical Signs: Classic signs of colic with rapid deterioration

Treatment: Right flank laparotomy → ID twist in mesentery and reposition intestines

Prognosis: Poor, but can get lucky

Intussusception

• 4 Clinical signs

• Pathogenesis

• Signalment

• Method of diagnosis

Clinical Signs:

1. Colic may disappear after 12hr

   • ± Saw-horse stance

   • ± High HR → Drop

   • ± Groaning and collapse

2. Shock, dehydration and metabolic acidosis

3. Distended bowel on rectal examination (± fist-shaped mobile mass to right if lucky)

4. ± Ping over right paralumbar fossa

Pathogenesis: Orad segment of intestine slides into adjacent aborad intestine → Partial to complete obstruction

Signalment: Young animals (motility disorders = enteritis)

• Older animals → Intra- or extramural masses

Diagnosis: ± Exploratory laparotomy

Treatment and prognosis of intussusception

Treatment:

1. Standing right flank approach

2. ID intussusception

3. Inject local into mesentery

4. Exteriorise intussusception and use clamps to resect devitalised bowel

5. Side-to-side anastomosis (superior than end-to-end)

6. Close defect in mesentery

7. Wash bowel with sterile saline

8. Close abdomen

Prognosis: Success if faeces passed in 24 - 48hr (BUT guarded prognosis)

Haemorrhagic Bowel Syndrome

• Aetiology

• Pathogenesis

• 8 Clinical signs

• Diagnosis

• 2 Treatments

• Prognosis

Aetiology: Acute and highly fatal enterotoxaemic disorder caused by

1. Clostridium perfringens type A

2. Aspergillus fumigatus mycotoxin

Pathogenesis: Haemorrhaging bowel → Large blood clot obstructs intestinal lumen

Clinical Signs:

1. Depressed, inappetence, dehydration

2. Decreased rumen motility

3. Sudden/severe drop in milk production

4. Succussible fluid with ballottement of right abdomen AND right-sided abdominal ping

5. Reduced to scant faecal production

6. Colic

7. Melaena and clotted blood in faeces (blackberry jam) → SCANT

8. Tachycardia

Diagnosis: U/S or exploratory laparotomy

Treatment:

1. Surgery = Laparotomy to find obstruction and break down clot

• Do NOT open bowel → Generalised fibrinous peritonitis

2. Lignocaine CRI = Pro-kinetic and analgesia for 1 - 3d until faeces passed

   • Loading dose 1.3mg/kg → CRI @ 0.05mg/kg/min

Prognosis: 60% survival with surgery (100% mortality without treatment)

Aetiology of traumatic reticuloperitonitis (TRP)

aka. Hardware disease

• Cattle are prey species with no defence mechanisms → Rapid grazing with tongue to gulp down feed without chewing (non-selective eaters)

  • → Cattle will pick up metal without knowing

• Hide in bushes later to ruminate away from predators

• Metal only causes issues when in reticulum due to strong biphasic contractions which normally sort ingesta and presents for rumination (reticulum impales itself onto nail)

  • No effect when in rumen as organ is massive and will simply contract around it

7 Clinical signs of traumatic reticuloperitonitis (TRP)

Acute, subacute and chronic syndromes

• Usually INDIVIDUAL cows (may be outbreaks with lots of metal eg. construction at the farm)

1. Sudden drop in milk yield

2. Anorexia and off-colour

3. Elevated TPR

4. Pain

   • Teeth-grinding, grunting on eructation

   • Hunched posture, abducted elbows or sawhorse stance

   • Positive Wither’s pinch test (x2), William’s test or bar test

5. ± Large particles in faeces (sorting function of reticulum is impaired)

6. Severe = Generalised peritonitis → No negative pressure in abdomen

   • No paralumbar fossa

   • Tense abdominal wall

   • Rough peritoneum on rectal exam

   • Free fluid in abdomen

7. ± Clinical signs of pericarditis or pleuritis (20%)

List 5 DDx for traumatic reticulopericarditis

DDx for cranial abdominal/caudal thoracic pain

1. Liver abscesses

2. Abomasal ulcers

3. Acute intestinal obstruction

4. Diaphragmatic hernia

5. Omasal impaction

5 Caudal thoracic structures and 7 cranial abdominal structures that may cause positive Wither’s pinch test

Caudal Thoracic Structures:

1. Heart

2. Pleura

3. Pericardium

4. Oesophagus

5. Caudal lung lobes

Cranial Abdominal Structures:

1. Reticulum

2. Diaphragm

3. Liver

4. Abomasum

5. Omasum

6. Kidney

7. Small intestine

3 Methods of diagnosis of traumatic reticuloperitonitis

History, PE and signs of cranial abdominal pain →

1. U/S over left cranioventral abdomen (near olecranon) to assess reticulum for normal biphasic contraction

   • Lack of reticular contractions does NOT confirm hardware disease, but presence CAN rule OUT

2. Radiography (high power) to ID metallic foreign bodies

3. Biochemistry = Increased WBC, TP and fibrinogen

   • Fibrinogen sequestered within minutes to save the cow’s life (wall off disease to localised peritonitis → survivable)

     • -ve: Location of fibrin may reduce function of other organs (eg. vagal indigestion)

2 Treatment options for traumatic reticuloperitonitis

1. Conservative management 1st

   1. Oral magnet within plastic cage → Prevents further penetration of metallic foreign body

      • Can check success of magnet with radiographs

   2. NSAIDs

   3. ± Fluid therapy

2. → Left flank rumenotomy to remove foreign body

   1. Left flank approach: Small incision as close to the last rib as possible (± rib resection if arm too short to reach reticulum)

   2. Use anchoring sutures (continuous sutures around serosa/muscularis of rumen → Submucosa/mucosa) OR device to anchor rumen wall to abdominal wall to prevent rumen fluid leaking into abdominal cavity → Contamination

   3. Use fingers to explore reticulum (honey combed)

   4. Check oesophageal groove and reticulo-omasal opening → Should contract)

   5. Remove foreign body ± fibre if necessary

   6. Close rumen in TWO layers with continuous Cushing/Lembert

6 Sequelae of traumatic reticuloperitonitis

Depends on direction of foreign body migration

1. Cranial → Lung abscessation and pleurisy

   • Outbreak of caudal lobe pneumonia/pleurisy/thoracic abscess in ADULT cows → TRP should be considered a major DDx

2. Cranial/lateral → Localised peritonitis

3. Cranial → Traumatic pericarditis and cardiac puncture

4. Generalised peritonitis = Poor prognosis

5. Medial → Liver abscess

6. Medial → Vagal indigestion

Traumatic reticuloperitonitis → Pericarditis

• Pathogenesis

• 3 Additional clinical signs

• PM findings

• Prognosis

• Treatment

• Prevention

Pathogenesis:

1. ~20% of TRP cases have foreign bodies puncture through the reticulum into the pericardium

2. Infection with Trueperella pyogenes

3. Effusion and fibrinous inflammation

4. RCHF

Clinical Signs:

1. Jugular cording/distension and elevated pulse

2. Brisket oedema

3. Abnormal sounds (eg. muffled heart sounds, murmur, splashing)

Prognosis: Grave

Treatment: Euthanasia

Prevention:

1. Rumen magnet

2. Environmental management

Aetiology and 6 example causes of vagal indigestion

Aetiology: Vagal nerve dysfunction → Disruption of ingesta transportation from rumen to omasum

Causes: ANYTHING affecting the vagus nerve

1. Local abscess

2. Post-pneumonia → Swelling of the mediastinal lymph nodes

   • Common in weaner calves

   • Bovine leukosis

3. Prolonged RDA (vagal nerve runs through abomasal twist)

4. Reticulo-omasal (oesophageal) adhesions

5. Infection/neoplasia of the reticulo-omasal (oesophageal) groove

6. Sequelae of TRP

10 Clinical signs of vagal indigestion

CHRONIC DISEASE

1. Chronic and non-specific signs: Anorexia, reduced production, loss of BCS, lethargy, rough coat

2. Papple (10-to-4) shape of abdomen due to rumen overload

   • Apple on left and pear on right due to distension of the right ventral rumen sac too

   • Free gas bloat with NO oesophageal obstruction (check by passing tube)

3. Increased frequency but decreased intensity of rumen contractions (inefficient contractions)

4. Bradycardia (<60bpm) due to hypokalaemia caused by anorexia

5. ± Absent rumen layers and rare rumen ping

   • Iceberg effect = Fibre content form ball creating areas of gas-fluid interface

6. Palpable ventral rumen sack on rectal exam

7. Flaccid reticulo-omasal opening on laparotomy

8. NOT painful

9. Normal temperature and RR

10. Scant, sticky faeces with long fibres (not chewing cud)

Prognosis and 2 treatments of vagal indigestion

Prognosis: Guarded to poor (nerve damage)

Treatment:

1. Treat 1˚ cause if known (eg. bronchopneumonia in calves)

2. Rumenotomy to empty rumen, permanent rumen fistula or red devil trocar (similar to bloat treatment) = Symptomatic treatment

   • Aim: Address stretching of rumen to allow normal contractions to occur

6 Advantages and 3 disadvantages of standing surgery with paralumbar approach in cattle

Advantages: Cattle are stoic

1. Similar regardless of indication (eg. C-section and LDA)

2. Most practitioners are familiar with this approach

3. Do not need to cast cow → Fewer staff required

4. Easier closure of abdominal wall (vs. recumbent approaches)

5. Less risk for cow AND staff (vs. casting and recumbency)

   • Risks of Recumbency:

     1. Muscle/nerve damage

     2. Bloat/regurgitation

     3. Risk of sedation

     4. Risk of casting cow/getting kicked

6. No need to starve cow → Better for emergency interventions

Disadvantages:

1. Require minimum facilities (head bail, race with good flank access)

2. Cow can move around more

3. Risk of cow going down during surgery → Contamination

5 Steps of decision-making in abdominal surgery

1. Pick cases carefully to maximise chances of success (full PE essential to assess risk and concurrent disorders)

   • Give accurate prognosis

2. Get help

3. Location (head bail or other facilities)

4. Honest opinion of success rate to farmer

5. Honest opinion of likely cost to farmer

Clinical signs of surgical abdominal diseases

• Acute < 3hr

• Subacute 3 - 6hr

• Chronic (>6hr)

Acute (<3hr): Colic

1. Kicking at abdomen and stretching out legs

2. Paddling in recumbency

3. Frequent lying down and getting up

Subacute (3 - 6hr):

1. Restless

2. Lethargy

3. Anorexia

Chronic (>6hr):

1. Recumbent

2. Depressed

3. Abdominal distension

7 Indications for surgery

1. Very high HR (>100 in cow and >120 in calf) that does not drop with removal of stressors

2. Severe colic (kicking abdomen and severe discomfort)

3. Full abdomen and very dehydrated

4. Not enough faeces and mucus in rectum

5. Palpable loops of distended intestines on rectal exam

6. Severely distended intestinal loops on U/S

7. No diagnosis after full clinical exam ± additional tests → Exploratory laparotomy

Indication of right vs. left flank approach for abdominal surgery

Right = Better access to most of the abdominal viscera (liver, abomasum, caecum, small intestine)

• More dorsal incision to prevent spontaneous prolapse of viscera through incision

• Indicated with exploratory laparotomy, LDA/RDA, caecal dilation, mesenteric torsion, intussusception

Left = Access to rumen, spleen, uterus and ovaries

4 Types of anaesthesia for abdominal surgery

• Method

• Advantages

• Disadvantages

• OR indications

1. Line Infiltration

   • Method: Local anaesthetic under skin (into muscles) directly over area of incision

   • +ve: Easy

   • -ve: NOT accurate

     • May not be deep enough to block the peritoneum OR risk of perforation through abdominal wall

2. Inverted L-Block

   • Method: Block nerves CRANIAL to incision

   • +ve:

     1. No oedematous tissue to incise

     2. Less risk of slow wound healing (local away from incision)

   • -ve: NOT accurate

3. Proximal/Distal Paravertebral Anaesthesia = T13 - L2

   • Method:

     • Proximal = Block more proximal to where spinal nerves exit spinal canal

     • Distal = Block dorsal and ventral to transverse processes where spinal nerve exits spinal canal

   • +ve: Lower risk for peritonitis/adhesions and contamination → Superior post-op survival

   • -ve: More skill and anatomical knowledge required

4. General Anaesthesia = CALVES (avoid in cows)

   • Indications:

     1. Regional anaesthesia cannot be used

     2. Maximum relaxation required

     3. Long surgery duration anticipated

     4. Maximum asepsis needed (eg. umbilical surgery in calves or fracture repairs)

Describe the process of opening the abdominal wall (skin → muscle → peritoneum)

SKIN

• Location: 4 - 5 fingers below transverse processes and 4 - 5 fingers caudal to last rib

  • Too high → Retroperitoneal

  • Too low → Viscera prolapses through incision

• Size: Depends on indications (must be able to pass at least arm)

  • Skin cut = LONGEST

• Method: Hold scalpel FLAT with index finger OR thumb over tip to protect cow from scalpel

MUSCLE

• Layers:

  1. External abdominal oblique muscle = Thickest

  2. Internal abdominal oblique muscle

  3. Transverse abdominal muscle = Thinnest

• Methods:

  1. Sharp approach = Cut straight through muscle layers

     • +ve: Easy and straight line to suture

     • -ve: More bleeding, trauma and higher risk of injury to internal structures

  2. Grid approach = Stretch muscle fibres in direction they run with fingers/blunt dissection

     • +ve: Little bleeding, good healing, minimal trauma and protection of internal organs

     • -ve: Harder to suture and NOT suitable for C-section/larger manipulations

PERITONEUM

1. Form tent with clamps/forceps

2. Make small incision with scissors OR scalpel

3. Listen to air rush into abdomen (rule out pneumoperitoneum)

4. Standing animal: Wait a few seconds to allow internal organs to fall away from abdominal wall

5. Extend cut under finger protection

Describe the process of closing the abdominal wall

• Layers

• Pattern

• Suture material

• Needle type

3 - 4 layers

FIRST LAYER = Apposition of peritoneum and transverse fascia/muscle (peritoneum too fragile alone)

• Pattern: Simple continuous AND tight → Most important layer to prevent wound emphysema

  • Begin suture line at ventral commissure and tie dorsally →

    1. Less pressure on knot

    2. Easier to make final knot

    3. No spillage of guts ventrally during suturing

• Suture: Monofilament absorbable

• Needle: Round bodied

SECOND LAYER = Apposition of external and internal abdominal oblique muscles (separately OR together)

• Pattern: Simple continuous OR cruciate

• Suture: Braided absorbable → More tensile strength and less concern for abrasion

• Needle: Round bodied

THIRD LAYER = Apposition of skin

• Pattern: Ford interlocking, cruciate or interrupted horizontal mattress (ideal for midline surgery)

  • Pull sutures tight as less concern for skin necrosis

• Suture: Monofilament nylon OR supramid

• Needle: Cutting edge, semi-curved

3 After-care treatments for abdominal surgery

1. ± Antibiotics

   • Routine intra-abdominal medication NOT necessary (no evidence of therapeutic/prophylactic antibiotic levels achieved)

     • IF required: penicillin 20,000 IU/kg for 3 - 5d #1 prophylactic choice (unless dirty/contaminated)

2. NSAIDs for 3 - 5d

3. Supportive environment (shelter, water, high quality forage)

4. 20L oral fluids

5. Propylene glycol drench for 5d ± dextrose IV