The distension on the left is more diffuse and located in the middle to dorsal region of the flank (“apple” shaped), whereas the distension on the right is in the ventral flank (“pear” shaped) resulting in papple shaped abdomen due to asymmetric bilateral distension in type II, III and IV vagal indigestion
(Hussain et al., 2017). The case was diagnosed as type II vagal indigestion as the rectal examination could reveal the L-shaped rumen due to gradual expansion of fluid filled ventral sac resulting in bilateral distension occupying the right ventral quadrant of the abdomen. In type II vagal indigestion associated with failure of rumen outflow, cases may have fluid distension only on the left, but most commonly they are distended bilaterally
(Derek Foster, 2017). Functional failure in this case could be associated with most commonly peritonitis or inflammations and adhesions around the reticulum, resulting in achalasia of the reticulo-omasal orifice, omasal transport failure (OTF) and thereby type II vagal indigestion
(Dore et al., 2007), as this could be supported by the haemato-biochemical changes like leukocytosis, neutrophilia, and hyperglobulinemia and absence of mechanical obstruction was confirmed by the radiological examination. In this case, normal architecture of omasum was observed as
Braun et al., (2007) also reported normal sonographic appearance of the omasum in cows with paralytic ileus.
Absence of type I vagal indigestion was recognized by the unilateral distension only on the left side which is almost always due to enlargement of the rumen, due to failure of eructation associated with an inability to clear the cardia of fluid, failure of the cardia to open, or esophageal obstruction
(Derek Foster, 2017). In this case, absence of the type III vagus indigestion due to failure of abomasal outflow was indicated by the normal serum chloride level as animals with a type III vagal indigestion will have a severe hypochloremic metabolic alkalosis due to internal vomiting of chloride abomasum into rumen, not entering into duodenum for absorption
(Derek Foster, 2017). Further, abomasocentesis and ultrasonogram of abomasum indicated absence of impaction and hypomotility (Fig 3). Absence of type IV vagus indigestion associated with failure of pyloric outflow in late pregnancy indigestion (LPI) was indicated by the response to the therapy with normal appetite, defecation and normal contour of the abdomen bilaterally before parturition.
This study concurred with that of
Braun (2009),
Khalphallah et al., (2016), Saravanan et al., (2019) and
Dos Santos et al., (2021) who by transrectal palpation observed anorexia, depression, arched back, dilated intestinal loops, empty rectum, scant/tarry/mucous coated foul smelling feces in ileus and other gastrointestinal disorders.
Muino et al., (2021) observed moderate abdominal distension in lower right abdomen, fluids sounds by auscultation in right side of the abdomen in bovine paralytic ileus.
In this case, the incidence of paralytic ileus in late pregnancy could be attributed to the deficiency of calcium and potassium, as hypocalcemia
(Callan et al., 2017), hypokalemia
(Constable et al., 2017) and hypochloremia
(Elhanafy et al., 2013) are reported to be the risk factors for functional ileus and gastro-intestinal reflux in cattle. Vagal indigestion and ileus resulted in no changes in the acid-base balance. Ileo-gastric reflex could also lead to inhibition of gastric motility when the ileum is distended
(Constable et al., 2017). In this case, toxemic signs like congested mucosa and enlarged prescapular lymph node, leukocytosis, neutrophilia and hyperglobulinemia levels indicated the presence of systemic inflammation which could also result in paralytic ileus
(Derek Foster 2017). In this case, chronic vagal indigestion could also lead to functional ileus as prolonged illness could turn in a cranial disorder into a caudal functional disorder due to intestinal ileus
(Hussain et al., 2017). Previously,
Yogeshpriya et al., (2011) reported paralytic ileus associated with enteritis due to amphistomosis in a cross bred cow, however with normal serum sodium and potassium values.
The case was treated with parentral administration of streptopenicillin @ 5 gm to combat the inflammatory process/peritonitis (Hussain,
et al., 2014), IM, 5% dextrose normal saline@10ml/kg bwt, Ringer’s lactate@ 10 ml /kgbwt as a source of electrolytes, pheniramine maleate @ 0.5 mg /kg bwt, as an antihistaminic, metoclopromide @0.2 mg/kg bwt as cholinergic drug, B-complex (Tribivet®) and oral administration of oral potassium chloride solution (POTKLOR®) @ 0.4 gm/kg bwt
(Constable et al., 2014) at12 hrs interval rumenotorics (Blusacc®) with lactobacillus yeast. The cow showed gradual reduction in the abdominal distension on both sides on day 3 post treatment and returned to normal appetite, abdominal contour, and colour and consistency of the dung on day 5 post treatment (Fig 5). The cow gave rise to normal parturition for a healthy calf (Fig 6) after 30 days of treatment.
