INTESTINAL OBSTRUCTION
 |
| OBSTRUCTION AND ADYNAMIC ILEUS OF SMALL INTESTINE |
Small intestinal obstruction occurs when the normal propulsion of luminal contents is hindered by either mechanical obstruction or abnormal intestinal motility. The obstruction may be partial or complete and can occur at any level of the small bowel.
The majority of mechanical intestinal obstructions result
from adhesive bands or incarceration of a loop of small bowel in an internal
hernia caused by previous surgery. Intestinal obstruction can arise in the
absence of previous surgery in cases of intussusception, abdominal hernia,
volvulus, or congenital malrotation. Strictures related to tumors, Crohn
disease, prior intestinal ischemia, or irradiation are common luminal causes of
obstruction, whereas peritoneal inflammation seen in tuberculosis peritonitis
and peritoneal carcinomatosis can lead to adhesive bands causing obstruction.
Impaction by foreign bodies such as gallstones, enteroliths, or parasites can
also cause mechanical obstruction. Irrespective of the cause, obstruction of
the small intestine causes distention of the segment proximal to the block-age
while the distal bowel decompresses. Early in the course, intestinal
contractility increases to propel luminal contents past the obstructed point.
This explains the diarrhea seen early in partial or complete obstruction. Later
in the course, the intestine becomes fatigued and dilates, with rapid
accumulation of gas and fluid. The gas is mainly swallowed air in addition to
gas produced from bacterial fermentation as gastric, intestinal, and biliary
secretions are added to the luminal contents. With progression of the
obstruction, the distended proximal intestine loses its absorptive function,
causing sequestration of electrolyte-rich fluid (sodium, chloride, potassium)
and further influx of fluid and electrolytes. The emesis that invariably ensues
leads to loss of electrolyte-rich fluid and metabolic alkalosis, aggravating
the hypovolemia, which can progress to renal insufficiency and circulatory
collapse. In cases with severe bowel distention; in closed loop obstruction,
where a loop of bowel is occluded at two points by an internal hernia; or in
cases where there is torsion of bowel, the excessive stretching of the bowel
wall can impair venous return and interfere with normal perfusion. Unless
treated, this can progress to ischemia, necrosis, and frank perforation.
Abdominal pain, vomiting, and distention are the hallmarks of acute intestinal
obstruction. The onset of these symptoms varies depending on the cause of the
obstruction, the location (proximal versus distal), and the degree of
obstruction (partial versus complete). Proximal obstruction tends to cause early
and severe vomiting, whereas more distal locations present with abdominal
distention and failure to pass flatus or feces. The pain is typically located
in the periumbilical area and is “colicky” in nature, with cramping episodes
occurring at certain intervals. The progression to a more constant pain and
focal localiza- tion may be an indication of complications with peritoneal
irritation, ischemia, and gangrene. The physical examination should include
assessment for dehydration and for clues to the cause of the obstruction.
Abdominal inspection will assess the degree of distention and identify surgical
scars or abdominal wall hernias. Examination of the groin is key in these cases
because an incarcerated indirect inguinal hernia can easily be missed without
close attention. Abdominal auscultation may reveal a high-pitched “tinkling”
sound typically found in acute obstruction; as the bowel progressively
distends, the sounds become muffled and eventually disappear. Bowel distention
results in tympany upon percussion, but areas with fluid-filled bowel can be
dull to percussion. In early obstruction, the abdomen may be soft with minimal
tenderness; therefore, the presence of significant tenderness and rigidity
indicates the setting of peritonitis and compromised bowel.
Laboratory studies can assess the presence and degree of
fluid and electrolyte abnormalities. Leukocytosis and acidosis may indicate
complications. There are no reliable laboratory markers for ischemia, but an
elevated serum lactate level can be a sensitive marker for the presence of
hypoperfusion; it is not a specific marker, however. Plain abdominal
radiography is the first-line imaging modality for suspected intestinal
obstruction. The presence of fluid-and gas-filled loops of small intestine and
a paucity of gas in the colon is pathognomonic for small bowel obstruction.
Abdominal CT scanning can identify the specific site of obstruction and often
determine the cause.
The initial management includes volume resuscitation and
correction of metabolic derangements. Conservative management of the
obstruction with nasogastric suction may be successful in patients with partial
obstruction, but these patients should be monitored closely. Patients with
signs of complicated bowel obstruction with evidence of ischemia, necrosis, or
perforation require prompt surgical exploration.
 |
| COMPUTED TOMOGRAPHY OF SMALL INTESTINE OBSTRUCTION |
Paralytic or adynamic ileus refers to the bowel distention and obstipation
caused by the nonmechanical factors that disrupt the normal coordinated
propulsive motor activity of the gastrointestinal tract. It is commonly seen
following abdominal or nonabdominal surgery. A wide variety of conditions,
including peritoneal or retroperitoneal inflammation caused by blood,
chemicals, or intestinal juices, can lead to paralytic ileus, however. Certain
infections, such as pneumonia and sepsis, and use of drugs such as opiates and
anticholinergics are also frequent causes of ileus.
Patients present with symptoms similar to those of
mechanical obstruction, but there are certain distinct differences. Abdominal
distention, without the colicky abdominal pain, is usually present. Nausea and vomiting
may or not be present, and patients may continue to pass flatus and even have
diarrhea. Plain abdominal radiographs typically reveal a distended small and
large bowel with no transition point. The diagnosis can further be confirmed
with orally enhanced CT scanning.
The management of ileus is mainly supportive, with intravenous hydration and bowel rest. Underlying conditions such as electrolyte imbalance and sepsis should be sought and treated. Offending drugs should be discontinued, and opiate use should be minimized. If vomiting persists, nasogastric decompression should be initiated. Pharmacologic agents that stimulate gut motility, such as the sympatholytic guanethidine or the parasympathomimetic neostigmine, have been used to treat ileus but have mostly been ineffective. Erythromycin, which stimulates motilin receptors, and dexloxiglu-mide, which is a cholesystokinin-1 stimulator, have been evaluated but did not appear to alter intestinal ileus.
