5. Diagnostics, therapy, and prevention of forestomach/abomasum diseases

What are non-infectious diseases of the forestomach?

1. Simple indigestion

2. Acute and chronic ruminal acidosis

3. Ruminal alkalosis

4. Bloat

5. Hoflund syndrome

6. Traumatic reticuloperitonitis

7. Ruminal drinking

8. Ruminal parakeratosis

What are non-infectious diseases of the abomasum?

1. Abomasal displacement (left and right)

2. Volvulus

3. Impaction

4. Ulcers

What is simple indigestion in ruminants?

A minor disturbance in gastrointestinal function, most common in cattle, rarely in sheep and goats

What causes simple indigestion?

Abrupt changes in diet quality/quantity, dietary factors affecting intraruminal environment, stress, antibiotics

What is the pathogenesis of simple indigestion?

Changes in ruminal pH from rapid fermentation of carbohydrates or hypomotility leading to putrefaction

What are clinical signs of simple indigestion?

Anorexia, drop in milk production, decreased defecation (silage); soft, watery, foul-smelling faeces (grain)

How is simple indigestion diagnosed?

History, ruminal fluid examination (pH change, fewer protozoa, prolonged methylene blue reduction time)

How is simple indigestion treated?

Supportive care: saline via stomach tube, good-quality feed, ruminal fluid transfer, acetic acid

What causes acute ruminal acidosis?

Excessive intake of highly fermentable carbohydrates (decrease acetic acid, increase propionic acid) causing pH decrease

What is the pathogenesis of acute ruminal acidosis?

Decreased pH → Lactobacillus overgrowth → lactic acid build-up (+increased VFA and decreased salivation) → ruminal stasis → water influx → hypovolaemia, circulatory shock, metabolic acidosis → shock → death

What are clinical signs of acute ruminal acidosis?

Dehydration, anuria, diarrhoea, recumbency, anorexia, hypothermia, tachycardia, ruminal stasis, tetraparesis

How is acute ruminal acidosis diagnosed?

Milky grey ruminal fluid, acidic odour, pH <5, elevated blood lactate and phosphate, hypocalcaemia

How is acute ruminal acidosis treated?

Ruminal lavage, sodium bicarbonate, electrolytes, antacids, correct acidosis and dehydration

What is chronic ruminal acidosis?

Periods of low ruminal pH (5.2-5.6) due to high fermentable carbohydrate intake and low fibre

What is the cause of chronic ruminal acidosis?

Ingestion of diets high in rapidly fermentable carbohydrates and/or deficient in physically active fibre.

What are consequences of chronic ruminal acidosis?

1. Parakeratosis: increased thickness and cornification of ruminal epithelium that reduces absorption.

2. Rumenitis and liver abscesses: ulceration is caused by endotoxins of bacteria. Ulcers allow bacteria to access to portal circulation and reach the liver, forming abscesses. 

3. Low-fat milk syndrome: the shift in VFA initiates insulin secretion that inhibits lipolysis. 

4. Cerebrocortical necrosis: acidosis leads to thiamine deficiency Without thiamine there will be oedema and haemorrhages in the brain, as well as lysis of cortex.

5. Laminitis: LPS produce histamine, cause vasodilation and increase blood pressure so more blood is accumulated in the hooves.

6. Bone demineralization: ions are released from bone, causing osteoporosis + milk fever

   1. Clinical signs: Reduced feed intake, decreased milk production, reduced fat, poor body condition, and unexplained diarrhoea. High rates of culling or unexplained deaths may be noted in the herd.

How is chronic ruminal acidosis diagnosed and prevented?

Diagnosis: ruminal pH measurement;

Prevention: proper diet, slow adaptation to high-grain diets, dietary buffers

What causes acute ruminal alkalosis?

Ingestion of large quantities of urea

What is the pathogenesis of acute ruminal alkalosis?

Urea converts to ammonia, raising pH, with rapid ammonia absorption leading to toxicity (brain, liver)

What are signs of acute ruminal alkalosis?

Ruminal motility disorders, severe pain, incoordination, bloat, paralysis, death

How is acute ruminal alkalosis diagnosed?

Rumen fluid (pH >7, content dark grey and putrid)

How is acute ruminal alkalosis treated?

Rumen lavage, IV saline, acetic acid orally, oral VFAs

How is acute ruminal alkalosis prevented?

Adequate dietary mixing of urea or slow introduction.

What is acute ruminal tympany (bloat)?

Overdistension of the rumeno-reticulum with fermentation gases

What are the types of bloat?

Primary (foam bloat), secondary (free-gas bloat)

What causes primary acute ruminal tympany?

Dietary factors like lush leguminous pastures or high cereal grain diets

What is the pathogenesis of primary acute ruminal tympany?

Legumes contain pectic substances → pectin → polygalacturonic acid and pectic acid, which cause jellification of the rumen content → increase the rumen fluid viscosity → inhibition of eructation.

What causes secondary acute ruminal tympany?

Oesophageal obstruction, failure of oesophageal groove function, nerve damage, or muscular motility disorders

What are consequences of acute ruminal tympany?

Increased ruminal, intra-abdominal, and intraluminal pressure causing circulatory and respiratory compromise

What are clinical signs of acute ruminal tympany?

Left abdominal distension, dyspnoea, hypersalivation, distress, rapid death within 3–4 hours

How is acute ruminal tympany diagnosed?

Clinical signs, clinical examination- free gas produces a higher pitched ping on percussion than frothy bloat. The distention of the rumen can be detected on rectal examination. Examination of oesophageal patency, urinalysis, CRT, blood analysis (pH, urea, calcium)

What are differential diagnoses for acute ruminal tympany?

Abomasal displacement, hoflund syndrome, caecum dilation, uterine hydrops, subcutaneous emphysema

How is acute ruminal tympany treated?

Relieve pressure (trocarisation, oesophageal passage), antifoaming agents, metabolic support

What are examples of antifoaming agents to treat float?

Vegetable oils (e.g., peanut, corn, soybean) and mineral oils (paraffins)

What are causes of chronic tympany?

Hoflund, listeria, tetanus, botulism, foreign body, reticular or liver abscess, abomasal volvulus, diaphragmatic hernia, omasum impaction, lymphosarcoma

How is chronic tympany diagnosed?

History, clinical exam, sonography, explorative laparotomy, laparoscopy

What is the treatment for chronic tympany?

Depends on aetiology DO NOT RISK ruminitis - rather slow and perfect treatment

What is ruminal drinking?

Failure of the reticular groove reflex causing milk to enter the rumen, leading to ruminal acidosis

What is the pathogenesis of ruminal drinking?

Calves on milk feeding have sensitive reflex for glowing oesophageal tube to prevent milk entering rumen

When weak reflex, or force feeding, can enter rumen → anaerobic bacteria, putrid bacteria, suboptimal gases formed

What are clinical signs of ruminal drinking?

Abdominal distension, inappetence, depression, poor growth, recurrent tympany, clay-like faeces

How is ruminal drinking diagnosed?

Characterised by metallic percussion/splashing sound. Stomach tube= stinky grey fluid

How is ruminal drinking treated?

Rumen lavage, correcting the cause, adjusting diet to eliminate milk if reflex is weak

What is Hoflund syndrome (vagus indigestion)?

Functional or mechanical disturbance causing ruminoreticular distension and impaired GI transit

What are causes of Hoflund syndrome?

1. Reticuloperitonitis

2. Foreign bodies

3. Abscesses

4. Bronchopneumonia

5. Pyloric stenosis

What are signs of Hoflund syndrome?

L-shaped abdomen, decreased appetite, progressive apathy, bradycardia, ruminal contractions

How is Hoflund syndrome diagnosed?

1. Clinical examination: clinical signs, rectal exam (dilation of ventral ruminal sac), sonography,

2. Blood analysis: protein, leucocytes, BHB, AST, GGT, pH, BE, urea

3. Urinalysis: paradoxical aciduria

What are differential diagnoses of Hoflund syndrome?

1. Abomasal displacement

2. Primary tympany: no rumen movement and TACHYCARDIA (Hoflund - rumen contraction, BRADYCARDIA)

How is Hoflund syndrome treated?

Based on cause: paraffin oil, rumenotomy (reticuloperitonitis), abomasal correction (DA), rehydration, antibiotics, and supportive care

What is traumatic reticuloperitonitis (hardware disease)?

Perforation of the reticulum by ingested metallic objects causing local or diffuse peritonitis

What are contributing factors to traumatic peritonitis?

1. Late pregnancy: gravid uterus press on rumen and reticulum

2. Calving: sudden increase in abdominal pressure

3. Tenesmus: proctitis, vaginitis, cystitis, obstipation

What are clinical signs of acute localised reticuloperitonitis?

Anorexia, sudden milk drop, arched back, elbow abduction, pain on ventral abdomen, tachycardia

What are signs of diffuse reticuloperitonitis?

(most dangerous): fever, severe tachycardia/pnoe, no milk, complete GIT stasis, strong pain signs (grunts), hard tension of abdominal wall, reluctance to move, scant manure, lift abdomen (sensitive to pressure), short CRT

How is traumatic reticuloperitonitis diagnosed?

1. Clinical exam: clinical signs, test for foreign bodies (back grip, box sounds, pain percussion)

2. Laboratory examination

   1. Blood analysis: increased WBC, increased protein, increased BHB, high pH (alkalosis due to restricted feed intake) 

   2. Abdominal puncate (10cm right of navel): increased exudate (normal: nothing) 

   3. Urine: pH (alkalic, paradoxic aciduria), high protein (nb always high during alkaline urine) 

   4. GAT (glutaraldehyde test): tell length of inflammatory process. 5000 leu

How is traumatic reticuloperitonitis treated?

Non-surgical: magnet, antibiotics; Surgical: rumenotomy

How is traumatic reticuloperitonitis prevented?

Use of magnets in feed or cattle, electromagnetic plates for machinery

What allows the abomasum to be displaced in cows?

Its loose suspension by the greater omentum and lesser omentum

Which cows are most commonly affected by abomasal displacement?

Female dairy cows between 4-7 years old, especially in the first month post-parturition

What are key contributing factors to abomasal displacement?

1. Abomasal hypomotility

2. High concentrates and low fibre in TMR

3. Hypocalcaemia

4. Hypokalemia

5. Lipo-mobilisation/ketosis

6. Concurrent diseases like mastitis and metritis

7. Heredity

What is the metabolic pathway leading to abomasal displacement from high concentrates in TMR?

High NEFA → high VFA → metabolic acidosis → decreased circulating calcium, fermentation in the abomasum, and gas production

What does hypocalcaemia cause in relation to abomasal displacement?

Partial atony of the abomasum, preventing gas removal and causing displacement, especially to the left side

What is the role of hypokalemia in abomasal displacement?

It decreases abomasal motility and emptying

How does heredity affect the risk of abomasal displacement?

High milk production genes in deep-bodied cows are associated with a higher risk

What happens during left abomasal displacement (LDA)?

The abomasum moves below and to the left of the rumen due to gas and digesta accumulation, resulting in gaseous distension and inhibition of motility

What are common metabolic findings in left abomasal displacement?

Mild metabolic alkalosis with hypochloremia and hypokalemia

What is the primary danger in right abomasal displacement (RDA)?

Acute and life-threatening volvulus with ischemia and haemorrhagic strangulating obstruction → melena

What metabolic condition develops in right abomasal displacement?

Hypochloremic, hypokalemic metabolic alkalosis, possibly progressing to metabolic acidosis

What are clinical signs of abomasal displacement?

Anorexia, decreased milk production, reduced watery faeces, lifted tail, arched back, dehydration, and enophthalmos

What diagnostic tools are used for abomasal displacement?

Clinical signs, auscultation for metallic or splashing sounds, liver percussion, puncture fluid analysis, sonography, rectal examination, and pH measurement

What laboratory findings are indicative of abomasal displacement?

Ketonuria, metabolic alkalosis, and paradoxical aciduria

What are the common methods for treating displaced abomasum?

1. Rolling (LDA only)

2. Laparotomic omentopexy right (LDA + RDA)

3. Percutaneus abomasopexy (LDA) - toggle or blind stitch

4. Laparoscopy (Christiansen method) (LDA)

What is the treatment for left abomasal displacement using rolling?

Casting the cow on her right side and rolling through a 180° arc

What is laparotomic omentopexy?

A surgical procedure where the abomasum is decompressed, repositioned, and secured using omentopexy through the right paralumbar fossa

What is the Christiansen method of abomasopexy?

A laparoscopic procedure using a spieker to place toggle pins and tie them externally to stabilize the abomasum

What is the cause of abomasal volvulus?

Complication of RDA. Rotation of the abomasum on its mesenteric axis, leading to circulatory impairment, ischemia, and necrosis

What are clinical signs of abomasal volvulus?

Severe anorexia, marked milk production reduction, toxaemia, dehydration, recumbency, and death

How is abomasal volvulus diagnosed?

Characteristic "ping" on auscultation and percussion, excluding other causes of left- or right-side pings

How is abomasal volvulus treated?

Volvulus is corrected surgically using right paralumbar fossa omentopexy when economically feasible.

What are the causes of abomasal ulcers?

Unknown, can be due to viral diseases, prolonged inappetence, lymphosarcoma, abomasal disorders, other disorders.

What is the pathogenesis of abomasal ulcers?

Erosion of the abomasal wall due to gastric juice action at damaged areas, causing acute haemorrhage, distension, and metabolic imbalances

What are the classifications of abomasal ulcers?

• Type I: erosion without haemorrhage;

• Type II: haemorrhagic;

• Type III: perforated with acute localised peritonitis;

• Type IV: perforated with acute diffuse peritonitis;

• Type V: perforated within the omental bursa

What are clinical signs of abomasal ulcers?

Asymptomatic cases, mild abdominal pain, bruxism, anorexia, tachycardia, and intermittent melena

How are abomasal ulcers diagnosed?

Physical examination and excluding other causes of peritonitis.

What is the treatment for abomasal ulcers?

Encouraging eating to buffer gastric acid, broad-spectrum antimicrobials, and antacids

How is traumatic reticuloperitonitis treated for low-income farmers?

By using a magnet and antibiotics

What is the key diagnostic difference between Hoflund syndrome and primary tympany?

Hoflund syndrome is associated with bradycardia, while primary tympany causes tachycardia

What is the surgical correction of left and right abomasal displacement?

Right laparotomic omentopexy

What is the most recent type of abomasopexy invented?

Christiansen laparoscopic abomasopexy.

What is the difference in changes of shape in Hoflund vs. tympany?

Tympany is distended left side of abdomen, right if very acute

Hoflund is L-shaped

How is hardwire disease diagnosed and treated?

• Dx: Grip back, increased TP and WBC, abdominal punctuation

• Treatment: rumenotomy and magnet

Which abomasal displacement is more severe, LDA or RDA?

RDA is more severe but LDA is more common

What is a secondary cause of ruminal tympany?

Obstruction and therefore not able to regurgitate, e.g. apple

How is Hoflund syndrome treated?

Soften reticular content w/ paraffin oil, rumenotomy, correction of abomasal displacement, supportive

How is an LDA diagnosed?

Percussion and auscultation, splashing sound.

What is worse: ruminal tympany or Hoflund syndrome, and what's the difference?

Ruminal tympany (acute and life-threatening). RT: no rumen contraction, tachycardia. HS: rumen contraction, bradycardia.

What is a common preventive measure for hardware disease?

Administering a magnet to cows over 1 year old (usually 14-16 months at first AI)

Which abomasal displacement causes melena in faeces (dark/black faeces)?

Right abomasal displacement due to volvulus.

How is the Christiansen method carried out?

• Percutaneous/laparoscopic abomasopexy standing procedure. This procedure requires a special instrument named a spieker to push the toggle ends through the ventral abdomen from a standing left flank approach.

• Two 10 cm x 10-cm squares are shaved and prepared for the introduction of the laparoscope and instruments.

• The laparoscope is introduced just behind the last rib and ventrally to the transverse process of the lumbar vertebras.

• Room air is allowed to enter the abdomen.

• The instrument portal is located at the 11th or 12th intercostal space at the same level or slightly ventral compared with the laparoscope portal.

• A long trocar and its cannula are introduced through the instrument portal into the abomasum.

• The trocar is removed, and the toggle pin is introduced within the abomasum.

• The abomasum is deflated, and the toggle ends are kept outside the abdomen.

• They are passed through the push rod within the spieker. This unit is then introduced in the abdomen through the instrument portal and directed in the cranial right paramedian part of the abdomen.

• The tip of the spieker is felt or seen before pushing the rods through the abdominal wall.

• Finally, the toggle ends are tied over a roll of gauze until the markers are visualized (5 cm from the pin) 

  
  

What is the most dangerous type of rumen acidosis?

Acute.