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

VIII. Disturbances of Gastrointestinal Function
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VIII . DISTURBANCES OF
GASTROINTESTINAL FUNCTION
A . Vomition
Vomiting is a coordinated reflex act that results in rapid,
forceful expulsion of gastric contents through the mouth.
The reflex may be initiated by local gastric irritation
caused by a variety of toxic irritants, infectious agents,
foreign bodies, gastric tumors, obstructions of the pyloric
canal or the small intestine, or by drugs such as apomorphine
or other toxic substances that act centrally on the
“ vomiting center ” of the medulla.
Severe vomiting produces loss of large quantities of water
and of H and C1 ions. These losses cause dehydration,
metabolic alkalosis with increased plasma HCO 3
, and hypochloremia.
Chronic vomiting may also be associated with
the loss of significant tissue K and with hypokalemia. The
K deficit is caused primarily by increased urinary excretion
resulting from alkalosis ( Leaf and Santos, 1961 ). Gastric
secretions contain significant quantities of K , and losses in
the vomitus also contribute to the K deficiency. K deficiency,
which develops initially because of the alkalosis,
perpetuates the alkalotic state by interfering with the ability
of the kidney to conserve H (Brazeau et al.,1956 ; Darrow,
1964 ). Both K and the hypovolemia caused by dehydration
may result in renal tubular damage and in renal failure.
Vomiting occurs frequently in the dog, cat, and pig but is
an unusual sign in the horse, which has anatomical restrictions
of the esophagus that interfere with expulsion of gastric
contents. In cattle, sheep, and goats, the physiological process
of rumination utilizes neuromuscular mechanisms similar
to those involved in vomiting. Uncontrolled expulsion
of ruminal contents is an uncommon sign, most frequently
occurring after ingestion of toxic materials or associated
with traumatic reticulitis and resulting “ vagal indigestion. ”
The contents of the abomasum are not expelled directly
even when the pyloric canal is obstructed. Pyloric outflow
obstruction does occur in cattle, which is similar metabolically
to that observed in nonruminants. This obstruction
may be observed in right-sided displacement of the abomasum
with or without torsion, occasionally with left-sided
displacement of the abomasum, in cows with functional
pyloric obstruction as a result of reticuloperitonitis and
from “ vagal indigestion. ” When the pylorus is obstructed,
abomasal contents are retained, causing distension of the
abomasum, which in turn stimulates further secretion and
retention. Retained abomasal contents may be regurgitated
into the large reservoir of the rumen and sequestered there
from other fluid compartments of the body. The net result is
loss of H and Cl ions and development of metabolic alkalosis,
hypochloremia, and hypokalemia. This metabolic syndrome
often is associated with fluid distension of the rumen
related to pyloric outflow obstruction. Similar distension of
the rumen in the absence of hypochloremic, hypokalemic
metabolic alkalosis suggests more proximal obstruction of
rumen outflow, namely the omasum.
Brachycephalic , middle-aged, small breed dogs (e.g.,
Shih Tzus) seem predisposed to hypertrophy of the pyloric
mucosa or muscularis ( Simpson, 2005 ); this syndrome, as
well as other causes of pyloric outflow obstruction, can
result in vomiting, metabolic alkalemia, and paradoxic
aciduria. Chronic hypertrophic gastritis, which resembles
Menetrier’s disease in humans, has been demonstrated in
the dog ( Happe and van der Gagg, 1977 ; Kippins, 1978 ;
van der Gagg et al., 1976 ; Van Kruiningen, 1977 ). Van
Kruiningen’s series of cases were basenjis that had concomitant
lymphocytic-plasmocytic enteritis. The primary
disease, however, has been observed in other breeds
without intestinal lesions. Signs of illness usually involve
chronic vomiting, weight loss, and occasionally diarrhea.
Hypoalbuminemia occurs in most cases. In humans, hyperchlorhydria
or achlorhydria can occur. The morphological
changes in the stomach wall (hypertrophic rugae) and
some of the clinical features help to differentiate this disease
from gastric neoplasia.
Functional gastrinomas have been rarely diagnosed in
the dog and have been compared to the Zollinger-Ellison
syndrome in humans ( English et al., 1988 ; Straus et al.,
1977 ; van der Gagg and Happe, 1978 ) . Clinical disease is
associated with hypergastrinemia, hyperchlorhydria, hypertrophic
gastritis, peptic esophagitis, and duodenal ulcers.
A more recent overview by Simpson (2000) revealed a
wide variety of breeds with a mean age of 9 years; no sex
bias was identified. The diagnostic workup usually centered
around the problems of vomiting, weight loss and
anorexia, and the pursuit of localizing findings of melena,
hematemesis, and abdominal pain. Some of these dogs
had signs associated with gastrointestinal preformation/
peritonitis. Surgical treatment or medical management, to
include omeprazole, famotidine, sucralfate, or octreotide,
is indicated. Because metastasis is frequently present, the
prognosis for recovery is poor.
B . Gastric Dilatation-Volvulus
Gastric dilatation-volvulus (GDV) is an acute gastrointestinal
disorder associated with high mortality ( Leib and
Blass, 1984 ; Morgan, 1982 ). It typically occurs in large
deep-chested dogs but has been reported in smaller dogs,
the cat, and other species. Gastric dilatation precedes
development of volvulus and is the result of the accumulation
of gas and fluid in the stomach as a result either of
mechanical or functional disturbances in pyloric outflow.
As the stomach distends and rotates about the distal esophagus,
displacement and occlusion of the pylorus and duodenum
occur. Necrosis and perforation of the stomach wall
and peritonitis are common causes of death.
Distension and displacement of the stomach cause
obstruction of the caudal vena cava and portal vein resulting