Kenneth Hoover, age 71, is admitted to your orthopedic unit with telemetry after a posterior lumbar decompression fusion done under general anesthesia. His initial postoperative course is stable and uncomplicated.
History and assessment hints
On postop day 4, you note the patient’s abdomen is distended, and he complains of a poor appetite and nausea. Knowing abdominal distention isn’t normal after spinal surgery, you notify the physician. Further assessment and an abdominal flat plate X-ray lead to a diagnosis of postoperative paralytic ileus. The physician orders supportive management and I.V. fluids, and places the patient on nothing-by-mouth status. A nasogastric (NG) tube is inserted for decompression. The physician orders I.V. acetaminophen and morphine for pain management.
Over the next few hours, Mr. Hoover develops severe abdominal pain, nausea, and vomiting. Suspecting his ileus is worsening, you inform the physician of these new symptoms and start more intensive monitoring.
Two hours later, you observe that Mr. Hoover’s urine output has fallen abruptly to about 5 mL/hour. Also, he is febrile and continues to complain of abdominal pain; assessment reveals a rigid, boardlike abdomen with quiet bowel sounds. Within a few minutes, he develops significant hypotension and tachycardia. Concerned he might have a bowel obstruction with intestinal perforation or ischemia, you call the rapid response team.
On the scene
When the team arrives, they begin volume resuscitation and pain control and prepare the patient for additional diagnostic tests. Because Mr. Hoover is volume depleted (from fluid losses into the bowel wall and intraluminal fluid absorption), team members administer isotonic crystalloids at a rate of 1,000 mL/hour.
Laboratory tests show significant elevations in his white blood cell count and lactate level. A computed tomography scan of the abdomen reveals free intraperitoneal air and a probable colonic perforation. These findings suggest perforation resulting from bowel obstruction rather than intestinal ischemia. The patient requires emergency surgery to control the source of sepsis.
The surgeon finds a grossly distended large bowel, along with a bowel perforation, ischemia, and necrosis (from distention caused by compressing mesenteric vessels). The surgeon resects the bowel and performs a temporary colostomy.
After surgery, Mr. Hoover is admitted to the intensive care unit (ICU). He receives aggressive fluid resuscitation and undergoes hemodynamic monitoring. The ICU nurse encourages him to cough, deep breathe, and use an incentive spirometer, and begins mobilization on postop day 2. On postop day 4, Mr. Hoover is transferred to the intermediate-care unit, where he receives education on how to care for his new ostomy. On postop day 7, he is transferred to the general surgery unit, where his NG tube is discontinued and his diet is advanced as tolerated. On day 10, he is discharged home.
Education and follow-up
Mr. Hoover’s colonic perforation resulted from Ogilvie syndrome—acute colonic pseudo-obstruction (ACPO) of the large bowel without a mechanical occlusive process. ACPO may follow surgery, spinal trauma, and many other medical and surgical conditions. Experts believe its pathogenesis may relate to autonomic nervous system innervation of the colon and its effect on motor function. The condition suppresses colonic motility and causes massive colonic dilation. Mortality can run as high as 40% when ischemia and perforation occur.
ACPO calls for supportive management with bowel rest and fluids. If these measures prove ineffective, the physician may order colonoscopic decompression or I.V. neostigmine (2 to 2.5 mg over 3 minutes to enhance muscle tone) to relieve the obstruction. However, Mr. Hoover wasn’t a candidate for this more conservative management because of his colonic perforation.
Note: All names are fictitious.
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Eleanor Fitzpatrick is a clinical nurse specialist at Thomas Jefferson University Hospital in Philadelphia, Pennsylvania.