Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

VIII. Disturbances of Gastrointestinal Function
437
of the neonatal enteric infection is complex, often involving
nutritional or environmental factors as well as infectious
agents, such as enteropathogenic strains of E. coli , the
transmissible gastroenteritis virus (TGE), rotaviruses, and
other bacterial and viral pathogens. The severe clinical signs
and frequently fatal outcome of acute diarrheal disease are
often directly related to dehydration and to associated H
and electrolyte disturbances ( Dalton et al., 1965 ; Fisher and
McEwan, 1967a ; Tennant et al., 1972, 1978 ).
In acute diarrhea with large-volume, watery stools, the
fecal fluid originates primarily from the small intestine. The
electrolyte composition of the stool in such cases is similar
to that of the fluid found normally in the lumen of the small
intestine, which in turn is similar to that of an ultrafiltrate of
the plasma. The rapid dehydration that accompanies acute
enteritis in the newborn soon produces hemoconcentration
and leads to hypovolemic shock. These cases are characterized
by metabolic acidosis ( Dalton et al., 1965 ) caused by
(1) decreased excretion of H resulting from decreased renal
perfusion and (2) increased production of organic acids,
the result of which is observed characteristically in young,
severely dehydrated animals. Hyperkalemia in such cases is
the result of increased movement of cellular K into the extracellular
fluid and to decreased renal excretion. Cardiac irregularities
caused by hyperkalemia can be demonstrated with the
electrocardiogram, and cardiac arrest related to hyperkalemia
is a direct cause of death in calves with acute diarrhea ( Fisher,
1965 ; Fisher and McEwan, 1967b ). Marked hypoglycemia
also has been observed occasionally before death in calves
with acute enteric infections. Hypoglycemia is believed to be
due to decreased gluconeogenesis and increased anaerobic
glycolysis, the result of hypovolemic shock ( Tennant et al.,
1968 ). The sequence of metabolic changes that occur during
acute neonatal diarrhea is summarized in Figure 14-10 .
In chronic forms of diarrheal disease, excessive fecal
losses of electrolyte and fluid are compensated in part
by renal conservation mechanisms and in part by ingestion.
If water is consumed without adequate ingestion of
electrolytes, hyponatremia and hypokalemia may develop
(Patterson et al., 1968 ). In such cases, the osmolality of the
plasma is significantly decreased and hypotonic dehydration
occurs. In longer-standing cases of chronic diarrhea, the
plasma K concentration may become dangerously low. It is
imperative, in this case, that intravenous fluids contain sufficient
K to prevent further reduction in concentration and to
avoid additional cardiac irregularities or cardiac arrest.
E . Malabsorption
Decreased absorption of nutrients may occur either as a
result of defective intraluminal digestion (maldigestion)
associated with pancreatic insufficiency (juvenile pancreatic
atrophy, chronic pancreatitis) or because of defects in mucosal
transport (malabsorption). Intestinal malabsorption is
(mEq/liter)
HCO 3
30 7.4 pH
20
10
7.2
7.0
HCO 3
Ca 2
Ca 2 Mg2 HPO2
4
HPO2
4
8 5 12
Ca 2
Mg2
(mEq/liter) 4 6
0 0 0
Glucose
(mg/100 ml)
BUN
100
HPO 4
2
Glucose
BUN
PCV Plasma protein
(%) (gm/100 ml)
50 10
PCV
40
30
Blood pH
50
0
5
Profuse diarrhea
Protein
Coma
0 12 24 36 48
Age in hours
HCO 3
associated with several types of intestinal disease including
chronic inflammatory diseases (lymphocytic-plasmacytic
enteropathy, eosinophilic enteritis), granulomatous diseases
(Johne’s disease, intestinal parasitism), and lymphoma. The
cardinal clinical signs of malabsorption include persistent
or recurrent diarrhea, steatorrhea, and weight loss. In the
horse, small intestinal malabsorption such as that associated
with granulomatous enteritis may be associated with weight
loss, but diarrhea may not be present because of the compensatory
capacity of the uninvolved cecum and colon.
The initial reports of primary or idiopathic intestinal
malabsorption in dogs ( Kaneko et al., 1965 ; Vernon, 1962 )
were compared to nontropical sprue (adult celiac disease,
gluten-induced enteropathy) of humans, but association with
gluten sensitivity was not demonstrated. Wheat-sensitive
enteropathy has been described in the Irish setter breed ( Batt
et al., 1984 ). Most of the dogs were seen between 7 months
to 2 years of age and had poor weight gain, weight loss,
inappetence, or hyperphagia. Diarrhea was not a consistent
observation. The most consistent morphological abnormality
in peroral jejunal biopsies was partial villus atrophy.
pH
Protein
PCV
60 72
FIGURE 14-10 Metabolic alterations during the course of fatal enteric
infection in a neonatal calf. From Tennant et al. (1972 ).