Production medicine

Goals of a clinical investigation of an individual sick cow

To identify which organ system(s) are affected, generate differential diagnoses and progress from a tentative to a definitive diagnosis using ancillary tests

Pathophysiology of ketosis

1. Development of NEB + hypoglycaemia

2. Adipose tissue breakdown - release of NEFAs

3. NEFAs enter the bloodstream and are taken up by the liver

4. Liver’s capacity to metabolise NEFAs is exceeded

5. Incomplete oxidation leads to the production of ketone bodies

Risk factors for ketosis

• Late pregnancy/ early lactation

• Overconditioned cows/ cows that have been overfed pre-calving

• Cows that are underfed

• Cows with a secondary/ underlying issue that reduces appetite

Goals of ketosis treatment

1. Correct hypoglycaemia

2. Reduce ketone production

3. Restore energy balance

Oral propylene glycol for ketosis

250-300mL daily for up to 5 days

Converted to glucose via gluconeogenesis and provides an ongoing energy supply

Vitamin B12 injections for ketosis

1.25-2.5 mg/ cow/ day for 3-5 days

Often used in combination with propylene glycol - helps stimulate gluconeogenesis

Nervous ketosis treatment

IV 300-500mL of 50% dextrose

Short-lived reversal of hypoglycaemia, requires repeat dosing every 6-12 hours

Liver abscessation aetiology

Caused by anaerobic bacterium (Fusobacterium necrophorum) that proliferate during reticuloruminitis

Bacteria migrate to the liver via the portal vein, causing infection

Can also occur secondary to TRP

Liver abscessation risk factors

High concentrate diets

SARA/ acute RA

Traumatic reticulitis

Liver abscessation clinical signs

Asymptomatic - clinical signs usually arise from pressure on other structures

Fever, anorexia, weight loss and reduced milk production

Can lead to CVC thrombosis - cough, dyspnoea, pulmonary haemorrhage

Liver abscessation diagnosis

Usually seen post-mortem

Can do ultrasound of liver

Liver abscessation treatment

When recognised, can do antibiotics ± surgical drainage

• Once causing clinical signs, prognosis is guarded

Liver abscessation gross pathology

Single/ multifocal encapsulated abscesses containing thick, greenish-yellow pus

Fatty liver syndrome aetiology

Metabolic disorder caused by severe NEB and lipolysis, causing triglyceride accumulation in the liver

Accumulated fat impairs gluconeogenesis and reduces glucose production needed for milk and energy

Fatty liver syndrome risk factors

Late pregnancy/ early lactation

Reduced DMI

Overconditioned cows

Fatty liver syndrome clinical signs

Decreased appetite, decreased milk yield, weight loss

Ketosis signs

Often occurs concurrently with other disease

Fatty liver syndrome diagnosis

Usually diagnosed after death

Liver biopsy is the only accurate way to tell

Can use low glucose and high ketone concentration as an indicator

Fatty liver syndrome treatment

Primarily supportive

Correct energy balance + treat ketosis

Fatty liver syndrome gross pathology

Enlarged, swollen liver with rounded edges and a distinct yellow-ish colour

Vagal indigestion aetiology

Caused by injury, inflammation or damage anywhere along the vagus nerve that leads to forestomach or abomasal dysfunction

Can have an acute or delayed onset

Ruminal distension either due to a physical or functional outflow obstruction

Vagal indigestion risk factors

TRP

Chronic inflammation

Intra-abdominal adhesions/ abscesses

Vagal indigestion clinical signs

Decreased appetite, decreased milk production

Abdominal distension that may be constant or intermittent but tends to be progressive

Can have bradycardia

Abnormal rumen motility

Vagal indigestion diagnosis

History

Clinical exam - key is papple abdominal distension and abnormal rumen motility

Vagal indigestion treatment

Treat primary cause

If there is a bad prognosis, euthanasia

Vagal indigestion gross pathology

Papple bloat shape - left dorsal and right ventral distension

Simple indigestion aetiology

Mild, temporary disturbance of rumen function due to a sudden change in ruminal pH from dietary factors

May involve abnormal rumen contractions without an obstruction

Simple indigestion risk factors

Sudden dietary changes

Overfeeding of grains/ silage

Poor quality feed

Simple indigestion clinical signs

Decreased appetite, decreased rumen motility

Mild abdominal distension, firm or doughy rumen

Simple indigestion diagnosis

History of recent dietary change

Clinical signs

Simple indigestion treatment

Cessation of abnormal diet and feeding of a typical diet

Warm water/ saline orally followed by kneading the rumen vigourously may restore rumen function

Acute ruminal tympany aetiology

Rapid, life-threatening accumulation of fermentation gases in the rumen

Frothy bloat is where a stable foam traps gas inside the rumen - results from exposure to succulent legumes and clovers

Free-gas bloat is where there is a motility failure or obstruction and can be due to a variety of factors

Acute ruminal tympany risk factors

Sudden availability/ overingestion of highly-digestible, high protein green forages

High concentrate diets, reduced rumen motility

Acute ruminal tympany clinical signs

Rapid, obvious left-sided abdominal distension in both dorsal and ventral quadrants

Dyspnoea due to pressure on diaphragm

Large gas ‘ping’ on the left upper abdomen

Acute ruminal tympany diagnosis

Clinical signs

Free-gas bloat confirmed by immediate gas release with stomach tube

Acute ruminal tympany treatment

Relief of ruminal distension - usually with stomach tube

Correction of primary cause

Frothy bloat - adminster surfactants, consider emergency rumenotomy for severe distension

Acute ruminal tympany gross pathology

Severe ruminal distension

PM: line of demarcation in the oesophagus due to thoracic pressure blocking blood flow

Rumen atony aetiology

Secondary condition characterised by a lack of tone or complete absence of contraction in the rumen

Primary - direct digestive disturbances

Secondary - rumen motility is inhibited by systemic causes

Rumen atony risk factors

Rapid diet changes

Excessive consumption of fermentable carbohydrates

Rumen atony clinical signs

Absent or reduced rumen motility

Anorexia

Clinical signs more related to what is causing the atony

Rumen atony diagnosis

Auscultation of left paralumbar fossa - no or very few contraction sounds

Rumen atony treatment

Treat underlying cause

Rumen compaction aetiology

Rumen becomes overloaded with and physically obstructed by indigestible material

Can lead to atony, severe discomfort and death

Omasal impaction aetiology

A disorder caused by a physical blockage in the omasum, most commonly due to the accumulation of dry, dense feed

Rumen/ omasal compaction risk factors

Low-quality roughage

Dehydration and water scarcity

Foreign materials

Rumen/ omasal compaction clinical signs

Firm left distension

Reduced appetite

Rumen hypomotility

Scant faeces

Rumen compaction diagnosis

Clinical signs

Palpation per rectum/ ballotment of a distended, doughy rumen

Omasal impaction diagnosis

Clinical signs

Hard, enlarged mass palpable behind the liver in the right flank

Papple shaped distension

Rumen/ omasal compaction treatment

Massive oral administration of lubricants

Fluids if dehydration

Remove obstruction via rumenotomy in severe cases

Traumatic reticuloperitonitis aetiology

Hardware disease - a common, often fatal, condition where ingested metal objects (nails, wire) puncture the reticulum wall, causing localised or diffuse inflammation

Traumatic reticuloperitonitis risk factors

Feeding off ground

Stall feeding

Late pregnancy - weight of uterus can apply pressure on the rumen/ reticulum, causing perforation

Traumatic reticuloperitonitis clinical signs

Influenced by the anatomic region of perforation

Sudden and dramatic anorexia and cessation of milk production

Fever

Abducted elbows, anxious expression, arched stance

Traumatic reticuloperitonitis diagnosis

Withers pinch test (reluctant to ventroflex)

Physical exam

Lab tests if not obvious

Traumatic reticuloperitonitis treatment

Rumen magnet (if rumen motility is present)

Systemic antibiotics

Stall rest

Fluids if dehydrated

Traumatic reticuloperitonitis gross pathology

Fibrinous peritonitis

Abscesses where the object has penetrated (e.g. diaphragm, liver, spleen)

LDA aetiology

Displacement of a gas-filled abomasum to the left side, between the rumen and the body wall

Occurs due to reduced abomasal motility, which causes gas accumulation - buoyancy - displacement

RDA/ RTA aetiology

Displacement of the abomasum (usually filled with gas) up to the right abdominal wall

Much more serious than LDA as it can progress to RTA, causing vascular compromise, severe abdominal pain and shock

LDA/ RDA risk factors

First 6w of lactation

Metabolic diseases causing GI stasis

NEB/ decreased DMI

LDA clinical signs

Decreased appetite, decreased milk production

Left side ping

Small bulge behind last rib in left paralumbar fossa

Faeces softer and reduced

RDA/ RTA clinical signs

Decreased appetite, decreased milk production

Right-sided ping

Right sided abdominal distension

RTA - marked CS, dehydration, intense pain, tachycardia

LDA diagnosis

High pitched ‘ping’/ ‘tinkles’ on the left side between the 9th to 13th ribs in the middle to upper third of the abdomen

RDA/ RTA diagnosis

High pitched ‘ping’/ ‘tinkles’ between the 10th and 13th ribs on the right side

LDA treatment

Surgical correction - right flank abomasopexy most effective

Rolling (but high relapse rate)

RDA treatment

SURGERY - right flank abomasopexy (caution with incision)

Abomasal ulcers aetiology

Ulceration of the abomasal mucosa due to an imbalance between protective and damaging factors

Occurs in high-producing dairy cows and can result from superficial erosions to severe, perforating ulcers that cause fatal peritonitis

Abomasal ulcers risk factors

Intensive management

High acidic, high-energy, finely ground diets consisting of concentrates and silage

Stress

Young, rapidly growing calves

Abomasal ulcers clinical signs

If mild: decreased appetite and decreased milk production

If bleeding: melena, anaemia, fever

If perforated: acute abdominal pain, fever, dehydration, septic shock, death

Abomasal ulcers diagnosis

Physical signs

Can use ultrasound examination/ abdominal paracentesis to find localised peritonitis

Abomasal ulcers treatment

Hold animal off silage/ concentrates for 5-14 days

Stall/ box rest

Antibiotics for 7-14 days

Peritonitis will often require IV fluids

Abomasal impaction aetiology

Accumulation of dry, firm ingesta in the abomasum

Secondary sometimes due to pyloric outflow disturbances

Abomasal impaction risk factors

Dehydration/ reduced water intake

Poor-quality roughage

Late pregnancy/ early lactation

Abomasal impaction clinical signs

Progressive abdominal distension

Intermittent appetite

Reduced manure production

Loose/ watery faeces

Abomasal impaction diagnosis

History

Palpation of abomasum on rectal exam

Confirmation through exploratory laparotomy

Abomasal impaction treatment

Massive oral administration of lubricants

Laxatives

Fluid if dehydrated

Haemorrhagic jejunitis aetiology

An acute, highly fatal, sporadic disease

Sudden intraluminal haemorrhage and formation of blood clots within the small intestine, causing physical obstruction

Haemorrhagic jejunitis risk factors

First 4 months of lactation

High producing dairy cows

SARA

Haemorrhagic jejunitis clinical signs

Peracute onset

Increased HR and RR

Abdominal pain

Decreased temperature

Melena/ haematochezia

Haemorrhagic jejunitis diagnosis

Clinical signs - particularly melena/ haematochezia

Auscultation of fluid in right ventral quadrant

‘Pings’ in lower RHS

Haemorrhagic jejunitis treatment

Often poor prognosis - often death with several hours to 1-2 days

Surgery - manipulation of intestine to break down clots, enterotomy to remove clots

Haemorrhagic jejunitis gross pathology

Affected segments show purple or red discolouration of the intestinal wall with some discolouration

Acute intestinal obstruction aetiology

Occurs when there is a mechanical blockage of intestinal contents, causing an accumulation of fluid and gas proximal to the obstruction

Causes abdominal distension and severe pain

Can be due to LOTS of factors

Acute intestinal obstruction risk factors

Foreign bodies

High-concentrate rations

Rapid changes in diet or anything that alters intestinal motility

Acute intestinal obstruction clinical signs

Acute onset of anorexia and GI stasis

Abdominal distension, colic

Absence of faeces

Acute intestinal obstruction treatment

Clinical signs

Rectal palpation/ ultrasound of distended loops of bowel

Acute intestinal obstruction treatment

Right-sided exploratory laparotomy to identify the anatomic malposition and then correct it

Paralytic ileus aetiology

A functional, non-mechanical obstruction caused by failure of normal motility

Often occurs secondary to systemic disease or inflammation

Paralytic ileus risk factors

Peritonitis

Hypocalcaemia

Systemic illness

Post-surgical states

Paralytic ileus clinical signs

Reduced or absent gut sounds

Abdominal distension

Decreased faeces

Anorexia

Abdominal pain

Paralytic ileus diagnosis

Reduced or no intestinal motility on auscultation

History of underlying disease

No evidence of mechanical obstruction

Paralytic ileus treatment

Treat underlying cause

Fluid therapy if dehydrated

Intussusception aetiology

Telescoping of one segment of intestine into an adjacent segment

Causes luminal obstruction and vascular compromise

If left untreated, the ischaemia may cause necrosis of segments of intestine

Intussusception risk factors

Anything that alters intestinal motility

Could be the result of irregular peristaltic movements related to enteritis, intestinal parasitism, dietary disorders and mural masses

Intussusception clinical signs

Sudden abdominal pain

Anorexia

Minimal to absent faeces

Colic

Can progress to shock in severe cases

Intussusception diagnosis

Clinical signs

Combination with any other factors that may cause irregular peristalsis

Intussusception treatment

Surgery - usually a right flank laparotomy to reduce or resect the affected portion

Caecal dilation aetiology

Accumulation of gas and/or fluid within the caecum, causing distension and impairing outflow

The apex of the caecum typically rises within the abdomen

Volvulus/ torsion of the caecum aetiology

Distension of the caecum can lead to a rotation, which tends to occur in a clockwise direction

This leads to obstruction and compression of the blood vessels

Caecal dilation/ torsion risk factors

Early lactation

High concentrate/ low fibre diets

Reduced feed intake

Caecal dilation clinical signs

Inappetence

Reduced manure production

Mild to moderate abdominal distension

Right sided ping

Sometimes dehydration

Caecal dilation diagnosis

‘Ping’ in the right paralumbar fossa 1-3 rib spaces cranial to the fossa

Rectal palpation of the dilated caecum

Caecal dilation treatment

If otherwise normal - laxative ruminotorics, transfaunation and rehydration