Overview of Digestive Tract Obstructions
Any organic or functional condition that primarily or indirectly impedes the normal propulsion of luminal contents from the esophagus to the anus could be considered a partial or complete obstruction. In the newborn, a variety of congenital anomalies (esophageal, intestinal, anal atresias, colonic malrotation, volvulus of the midgut, meconium ileus, aganglionic megacolon) resulting in obstruction are illustrated here. Other causes of mechanical interference of intestinal function in early infancy include incarceration in an internal or external (inguinal) hernia, congenital peritoneal bands, intestinal duplications, volvulus due to mesenteric cysts, and annular pancreas, though the latter may not become clinically manifested until the patient is an adult or an aged adult.
Esophageal
diseases that interfere with the normal passage of fluids and solids are
illustrated in the upper-most row of the drawing. Esophageal strictures can be
iatrogenic from endoscopic procedures, irradiation, medications, or surgery;
vascular; neoplastic; or, most commonly, gastroesophageal reflux. Congenital or
acquired webs and rings, particularly Schatzki rings, are common, easily
treatable causes of esophageal obstruction. Fundoplications performed to treat
reflux and repair an esophageal hernia will, by design, reduce the size of the
lumen at the gastroesophageal junction and hence produce a functional
stricture. Creating a surgical narrowing that is snug but not excessively tight
(so that it causes a functional or mechanical obstruction) is the essence of a
successful surgical intervention. Extraluminal pressure on the esophagus by a
tumor mass, goiter, aberrant or enlarged arteries, or visceral abnormalities in
the neck or mediastinum will lead to the same results.
Functional
or mechanical impairment of gastric emptying is common. Gastroparesis implies a
functional delay, but this diagnosis should only be made when intrinsic and
extrinsic causes of mechanical obstruction, metabolic causes, and
medication-related causes have been excluded. Gastroparesis is commonly seen in
patients with hypothyroidism, amyloidosis, or connective tissue disease;
following surgery; and as a complication of diabetes. Gastroparesis can be
difficult to distinguish clinically from partial gastric obstruction because
both present with early satiety, nausea, vomiting, bloating, distention, and,
if prolonged, weight loss. Habitual intake of excessive indigestible material
that accumulates in the stomach—such as hair (trichobezoar), fruit or vegetable
fibers (phytobezoar), undissolved medications (pharmacobezoar), and even
plastic materials—can result in chronic partial gastric obstruction. Initially
these materials may persist as accumulations of loose semisolids, but with
time, they will be compressed by gastric contractions into a solid ball that
can add to the impaired emptying. Intrinsic benign mechanical occlusion occurs
most commonly from antral, prepyloric, or pyloric peptic ulcer. Surgery, irradiation,
ingestion of caustic substances, and benign neoplasms such
as large epithelial polyps, leiomyomas, or gastrointestinal stromal tumors
commonly also lead to partial gastric obstructions. Intrinsic or extrinsic
malignant neoplasms are all too common mechanical causes of gastric outlet
obstruction.
Obstruction
of the duodenum is most commonly due to peptic ulcer disease. As with other
severe complications of peptic ulcer, peptic strictures should raise concern
for the presence of a gastrinoma (Zollinger-Ellison syndrome).
Extraluminal compression may occur, as in superior mesenteric artery
syndrome, in which local extension of a carcinoma of the head of the
pancreas, colon, or upper pole of the left kidney puts pressure on or invades
other structures. Other extrinsic neoplastic causes of duodenal obstruction
include lymphadenopathy in the small bowel mesentery or extension of cancer
into the transverse mesocolon.
Small
intestinal obstruction typically leads to periumbilical pain, bloating, and,
eventually, vomiting of feculent liquids. Of the wide variety of conditions
that can lead to obstruction of the small intestine, the
most common in adults are adhesions following previous surgery. In children and
adults, the presence of an incarcerated loop of small bowel in a hernia should
be considered as a potential cause that will require urgent surgical attention
before ischemic injury ensues. Hernias are described, based on their location,
as inguinal, femoral, diaphragmatic, paraesophageal, incisional, umbilical,
ventral, or internal, including spigelian hernia. Incarceration of a hernia
resulting from entrapment of a loop of small intestine in a congenital, traumatic,
or surgical ring is a surgical emergency. The small intestine can also be
obstructed by large intra-luminal objects, including ingested foreign bodies,
bezoars, or a large biliary calculus, or as a consequence of an accumulation of
parasitic worms. Mechanical obstruction of the small intestine may also be
produced by intussusception, which will be found to be secondary to a mucosal
lesion in a frequency that increases with the patient’s age. Varying degrees of
small bowel obstruction may be the result of
segmental fibrotic stricture formation in patients with Crohn disease, most commonly
in the ileum and jejunum. Small bowel loops may become stenotic as the result
of healing following localized infarction sustained in hernial incarceration or
mesenteric vascular occlusion. Primary neoplasms of the small intestine, while
rare, should always be considered in the differential diagnosis and include
carcinomas, neuroendocrine tumors, gastrointestinal stromal tumors,
leiomyosarcomas, and lymphomas. Finally, iatrogenic intestinal obstruction may occur
on occasion, including anastomotic stenosis, torsion or angulation, or
antiperistaltic anastomosis of intestinal loops, or as the result of other
faulty surgical techniques. Common extrinsic causes of intestinal obstruction
other than postoperative adhesions include congenital peritoneal bands,
metastatic tumor implants, Meckel diverticulum, and adhesive peritonitis (tuberculosis,
Mycobacterium avium intracellulare, or other foreign body granulomas).
Nonmechanical
impairment of intestinal motor function has been descriptively termed reflex,
adynamic, or paralytic ileus. The continued use of this term is
unfortunate. Although it is used widely to describe functional intestinal
motility, it almost never is restricted to the ileum alone and, in fact, is
often used indiscriminately when both the small bowel and large bowel are
dysfunctional. The term ileus should not be used to describe impaired
motility isolated to the colon. The patient typically presents with failure to
pass flatus, abdominal distention, a “silent abdomen,” and the radiographic
findings of dilatation of the small and/or large intestine with accumulation of
fecal material, fluids, and excess gas.
Ileus
can be a complication of various conditions that can lead to delayed intestinal
transit, including metabolic disorders, metastatic neoplasms, vascular or
inflammatory disorders, and infectious mesenteritis. Other causes include
central nervous system lesions, spinal disorders, postoperative complications,
or complications following pancreatitis,
peritonitis, penetrating or blunt trauma, or extensive rib fractures. Other
clinical conditions in which ileus has been said to occur as a “reflex”
phenomenon include renal or biliary colic, pneumonia, torsion infarction of an
ovarian cyst, coronary thrombosis, and retro-peritoneal hemorrhage (incident to
fracture of the spine or pelvis, a dissecting aortic aneurysm, urinary
extravasation, or rupture of the kidney). Causes of constipation are described
elsewhere.
So-called paralytic or adynamic ileus occurs commonly in the setting of purulent peritonitis (due to a perforated appendix, perforated hollow viscus, pelvic inflammatory disease, leakage or dehiscence of an intestinal suture line, wound evisceration, and other problems). Ileus may follow the intraperitoneal extravasation of gastric or duodenal contents (perforated peptic ulcer), pancreatic juice (acute hemorrhagic pancreatitis), bile (perforated gallbladder, bile leakage from the liver or bile ducts), and blood (postoperative hemorrhage, rupture of the liver or spleen, ectopic gestation, or “chocolate” cyst of the ovary).
