38. bovine forestomach conditions (some overlap with surgical lectures)

acute rumen acidosis pathophysiology

• highly fermentable, carb-rich feedstuff rapidly broken down into lactic acid (D & L isomers) within the rumen

  • Streptococcus bovis responsible for excessive production of lactic acid

• no enzymatic mechanism for metabolism of D lactic acid → within a few hours, severe D lactic acidosis develops

• rumen pH ↓

  • once pH 4.5-5.0, most normal rumen microorganisms die (Strep bovis persists)

  • complete rumen stasis occurs

  • chemical/acid rumenitis → damages rumen mucosa

• initially may demonstrate free gas rumen bloat, but within hrs, develop large, highly fluid-filled “splashy” rumen

• excessive lactic acid acts as osmotically active solute, pulling fluid out of vascular & interstitial spaces into rumen lumen → cow dehydrates into her own rumen

• systematically → severe dehydration & life-threatening acidemia

  • predominant cause of acidemia is metabolic acidosis due to excessive lactic acid production & absorption, poor peripheral perfusion, and endotoxemia

acute rumen acidosis — clinical signs

• completely off feed, dehydrated (sunken eyes, protracted skin tent), tachycardic, and tachypneic

• dairy cows → precipitous drop in milk production

• large, fluid filled rumen

• initially, cattle will pass scant watery feces, but profuse diarrhea may develop over next several hours

• untreated cattle become recumbent, comatose, and die

acute rumen acidosis — diagnosis

• often, history of recent feed change or inadvertent access to inciting feedstuff

• rumenocentesis or obtaining rumen fluid via orogastric tube can provide sample for pH testing

  • beware falsely high rumen pH if examining mild-moderate case 12-24 hrs after ingestion occurred or if obtaining sample by orogastric tube → salivary buffering

severe acute rumen acidosis treatment

rumen pH <5, HR >100 bpm, >5% dehydration

• rumenotomy — evacuate rumen as well as possible & perform repeated high volume lavage of all remaining contents

• administer laxatives, antacids, rumen transfaunates, fresh hay (into rumen), parenteral calcium, and IV fluids supplemented with sodium bicarb if blood pH <7.15

note: these cases do poorly even with aggressive therapy

acute rumen acidosis treatment #2 (slightly less severely affected individuals)

• pass a large bore stomach tube (Kingman tube) and attempt to siphon out and/or lavage as much of the rumen contents as possible — repeated flushes with 10-20 galls should be attempted

• administer laxatives, antacids, rumen transfaunates, and parenteral calcium

• high volume IV fluids should be given if possible

• never allow these cattle to have ad libitum access to water — will overdrink to the point of rumen atony

mild acute rumen acidosis treatment

HR <100 bpm, slight to absent dehydration, rumen pH 5.0-5.5

• treat with oral antacids, laxatives, and parenteral calcium

acute rumen acidosis adjunct therapies

• anti-endotoxic doses of flunixin meglumine (give IV)

• oral thiabendazole

  • reduce chances of mycotic rumenitis

• oral penicillin

  • reduce numbers of Streptococcus bovis in rumen

• ± 1-2 lbs of activated charcoal as adsorbent / gut protectant

sequelae to acute rumen acidosis

• bacterial rumenitits

  • abscessation of the rumen wall, usually with anaerobes such as Fusobacterium necrophorum

    • usually clinically silent unless embolic spread via portal circulation occurs

• hepatic abscessation and caudal vena caval thrombosis syndrome

• mycotic rumenitis and potential disseminated fungal disease with multiple organ involvement (liver, lungs, brain) — FATAL

chronic rumen acidosis

• more common than acute in dairy cattle; more common in component-fed herds than TMR-fed

• frequently a herd problem that is hard to diagnosis due to non-specificity of signs

  • ↓ than anticipated production & ↑ prevalence of common post-parturient diseases

• less severe, recurrent, and transient episodes of acidosis

• sequelae are less common but can occur and should alert you to a problem with herd nutrition

• significant predisposing cause of many common foot problems in dairy cattle

  • association between chronic/subclinical rumen acidosis & laminitis

rumen bloat definition

• obvious abdominal distention causing the left side of the abdomen to be distended both dorsally & ventrally

• in severe cases, right ventral abdominal quadrant will also be distended

causes of acute free gas bloat (adults)

• acute ingestion of highly fermentable carb-rich feedstuffs such as cracked corn & wheat (acute rumen acidosis)

• metabolic diseases (hypocalcemia)

• obstructive diseases (choke, papillomata at cardia, enlarged tracheobronchial lymph nodes)

• inflammatory conditions of the vagus (vagal indigestion)

cause of acute frothy bloat (adults)

• ingestion of lush leguminous pastures, especially alfalfa

• “froth” = stable foam produced by rapid fermentation of large amount of plant material rich in soluble protein & specific chloroplast membrane fragments, to which the cow was inadequately acclimated

causes of chronic rumen bloat (adults)

in adults, most are associated with lesions of the vagus nerve (vagal indigestion) and are frothy, or a mixture of free gas & frothy

acute free gas bloat in calves

• occasionally develops in calves pre-weaning on milk replacer or cow’s milk, usually within a few minutes of feeding

• tends to be associated with recent antibiotic administration & inadequate dietary fiber

chronic bloat in calves

• can occur post-weaning, usually in calves on total pelleted rations, with inadequate dietary fiber

• can also be seen in post-weaned calves with a history of chronic bronchopneumonia

  • enlarged tracheobronchia LN → compression of esophagus

  • adhesions → vagal neuropathy

• “rumenal drinkers” — older calves that are still receiving milk (veal calves); associated with failure of esophageal groove closure

diagnosing bloat

• usually visually obvious from external appearance, but should always confirm diagnosis via compete PE + rectal exam & passage of stomach tube

• passage of stomach tube allows distinction between free gas bloat & frothy bloat and is instantaneously diagnostic for obstructive lesions

  • free gas bloat will be relieved by passage of a stomach tube; frothy bloat will not

bloat treatment

• frothy bloat — should include administration of surface tension acting substances such as vegetable oil or poloxalene (therabloat)

• attend to primary disease diagnostically, prognostically, and therapeutically

• temporary rumen fistulas — chronic free gas bloat, especially in calves; enteral feeding of valuable cattle

what is the most common cause of colic in adult dairy cattle? when does it commonly occur?

• simple indigestion

• can occur at any stage of lactation, but most cases seem to occur in the first few weeks post-calving

• usually just 1 individual is affected, but occasionally outbreaks may occur coincident with feed changes, or consumption of spoiled feedstuffs

clinical signs of simple indigestion

• non-specific — anorexia, reduced production, cold extremities, rumen hypomotility (hypocalcemia)

• colic of variable severity

• tachycardia — consistent with degree of colic

• mild rumenal tympany and right-sided abdominal distention

• rectal examination — no loops of palpable small bowel

treatment of simple indigestion

• parenteral calcium borogluconate

• oral laxatives — magnesium salts frequently used

  • prepare owner for inevitable diarrhea over next few days

• analgesics — single IV injection of flunixin meglumine can be used for pain relief in very colicky individuals

  • do not use repeatedly

where do foreign objects tend to penetrate the reticular wall?

typically right medial wall

• ventral vagal nerve branches run through this region!

classic presentation of traumatic reticuloperitonitis

• acute perforation associated with sudden, precipitous drop in milk yield & appetite

• may have fever (103-105F°), tachycardia, tachypnea, and signs of cranial abdominal pain due to localized peritonitis

• scant feces, mild rumenal tympany, and severe rumenal hypomotility

• (rare — severe acute diffuse peritonitis, cattle may be moribund)

traumatic reticuloperitonitis — clinical signs (partial / intermittent perforation; after acute perforation)

more subtle, vague signs; challenging to diagnose

• partial anorexia

• moderate rumen hypomotility

• mild to moderate reduction in milk yield

• normal temp, pulse, and resp. rates

• less obvious signs of abdominal pain & resentment to palpation or withers pinch may be seen

traumatic reticuloperitonitis — clinical signs of thoracic perforation

• may present acutely with septic pericarditis

  • “washing machine” sounds on cardiac auscultation while the pericardial effusion is still effusive

  • with fibrin deposition & fibrous maturation of pericardial adhesions, heart may just sound muffled

• eventually signs of right-sided CHF will develop

• occasionally, results in acute septic pneumonia

traumatic reticuloperitonitis diagnosis

• usually clinical diagnosis based on history and PE

• enquire whether cow has received a magnet

• cranial abdominal radiography usually diagnostic

• (abdominocentesis reveals peritonitis, not the cause)

traumatic reticuloperitonitis treatment

• most cases treated medically

  • systemic antibiotics, magnet, stall rest

• adjunct therapies include calcium and oral laxatives / rumen stimulants

• surgery (valuable cattle

  • left paralumbar fossa exploratory & rumenotomy, either at time of initial visit, or after lack of response to conservative medical therapy

traumatic reticuloperitonitis sequelae

• septic pericarditis / pleuritis

• reticular abscess formation

  • usually located in right medial wall and visible as fluid/gas interface on radiographs

• vagus indigestion

what are the most common causes of vagal indigestion?

• traumatic reticuloperitonitis = most common cause due to proximity of vagus nerve to right medial wall of reticulum (also seen in association with reticular abscesses)

• right-sided abomasal volvulus

  • may develop several days to a few weeks following surgical correction

other causes of vagal indigestion

• other causes of cranial abdominal peritonitis — abomasal ulcer perforation

• hepatic abscesses

• abomasal lymphosarcoma / impaction

• idiopathic vagal indigestion of late pregnancy (transient, rare)

• in association with cervical vagal n. injury — esophageal / pharyngeal trauma

• in association with thoracic vagal nerve injury — chronic bronchopneumonia (most cases in calves)

clinical signs of vagal indigestion

• gradual abdominal distention and development of “papple” shape

• some chronic cases demonstrate bradycardia

• rectal palpation reveals “L” or “V” shape to the rumen

• other signs may be found consistent with inciting cause

vagal indigestion treatment

• medical treatment with fluids, cathartics / laxatives often tried but rarely works

• surgical exploration (valuable cattle)

generally poor prognosis

forestomach neoplasia

• papillomas / fibropapillomas of distal esophagus, rumen, and reticulum quite common in young cattle

  • usually clinically silent, unless they cause obstruction and bloat

• treatment is via surgical excision at rumenotomy