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The Challenge of Assessing and Diagnosing Acute Abdomen in Tetraplegics: A Case Study

Mowrey, Kelly

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Author Information

Questions or comments about this article may be directed to Kelly Mowrey, MS RN ANP‐C CNRN, at kmowrey@sdpapc.org. She is a nurse practitioner at South Denver Pulmonary Associates in Englewood, CO.

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Abstract

The assessment and diagnosis of an acute abdomen in a spinal cord‐injured patient presents a significant challenge to even the most experienced practitioners because of the muted or altered presentations secondary to paralysis. Because the patient with spinal cord injury is at increased risk for peptic or duodenal ulcers and a number of other gastrointestinal emergencies, clinicians need to maintain a high index of suspicion for acute abdomen when working with this population.

Assessing and diagnosing an acute abdomen in patients with spinal cord injury (SCI) presents a considerable challenge. Because of SCI's devastating effects on every organ system, including the gastrointestinal (GI) system, patients are often asymptomatic or have mild or atypical symptoms (Rajan & Nemchausky, 2001). Furthermore, nearly all patients with SCI are plagued with gastroparesis, paralytic ileus, constipation, and colitis that can mimic the signs and symptoms of acute abdomen (Steins, Fajardo, & Korsten, 2003).

In neurologically intact patients, abdominal pain or distress is the most common presenting symptom of an acute abdomen. However, because the GI system is controlled by the central nervous system (CNS), the peripheral nervous system (PNS), and more specifically by the enteric nervous system (ENS), patients with SCI at T12 and above will likely have altered presentations of acute abdominal processes. The degree of pain perception in patients with SCI is highly variable and unpredictable depending on the level and completeness of injury. Overall, it is important to remember when working with this population that the normal presentation of acute abdomen may be altered or muted (Rajan & Nemchausky, 2001). This case study describes the presentation, assessment, diagnosis, and management of a young male tetraplegic who experienced a perforated duodenal ulcer.

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Case Presentation

MP was a 20‐year‐old, C4 ventilator‐dependent tetraplegic hospitalized for acute rehabilitation after a diving accident. Past medical history was unremarkable. MP's hospital course was complicated by severe neuropathic pain in the neck and left shoulder, nococeptive pain at his tracheostomy site secondary to an erosion wound, asymptomatic vertebral artery injury requiring anticoagulation with aspirin, fevers secondary to urinary tract infection, Clostridium Difficile colitis, and pneumonia. He had frequent complaints of nausea attributed to gastroparesis, which is common in SCI, and colitis as a side effect of antibiotics.

MP's prescribed medications included the following

* oral vancomycin for colitis

* fluconazole for oral thrush

* famotidine for stress‐ulcer prophylaxis

* enteric‐coated aspirin to prevent stroke after vertebral artery injury

* lovenox to prevent deep vein thrombosis (DVT)

* fentanyl patch, hydrocodone/acetaminophen, hydromorphone, acetaminophen, and gabapentin for pain

* trazodone for insomnia,

* midodrine for orthostatic hypotension

* lorazepam for anxiety

* ondansetron for nausea, and

* maintenance intravenous fluids for hydration.

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Day 1

MP's routine day included rehabilitation, being mobilized out of bed to a wheelchair, and attending therapies. His vital signs were stable (98.2 °F, heart rate 76 beats/minute, respirations 14/minute via ventilator, blood pressure 111/50 mm Hg) and his exam was benign except for hypoactive bowel sounds and rhonchi. His only complaints were left shoulder pain and anxiety. His complete blood count and basic chemistry were relatively normal except for a low hematocrit and hemoglobin (10.8 g/dL and 32.5%), BUN of 4 mg/dl, and creatinine of 0.7 mg/dl. A test of liver enzymes revealed bilirubin total 0.4 mg/dl, AST 31 U/L, ALT 101 U/L (twice the upper limit of normal; etiology unknown), and ALKP 213 U/L.

The evening shift assessment was unremarkable except for a low‐grade fever and hypoactive bowel sounds. MP's vital signs were 99.5 °F, heart rate 108 beats/minute, respirations 13/minute via ventilator, blood pressure 84/50 mm Hg (a normal blood pressure in a tetraplegic), and he had a moderate sized bowel movement. At 11:30 pm, he complained of nausea and was medicated with ondansetron. At this time his vital signs were 100.1 °F, heart rate 115 beats/minute, respirations 14/minute via ventilator, blood pressure 94/49 mm Hg. The exam remained unremarkable except for hypoactive bowel sounds. At 5 am, MP complained of nausea and was medicated again with ondansetron. However, at 5:30 am, the patient's temperature climbed to 102.2 °F. His physician was notified, resulting in an order for pan‐culturing of urine, sputum, and blood. Cooling measures were instituted by the nursing staff.

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Day 2

At 8 am the patient complained of “feeling sick” and the dayshift nurse noted a firm abdomen without tenderness and hypoactive bowel sounds, and notified the physician; MP's vital signs were 99.2 °F, heart rate 112 beats/minute, respirations 14/minute via ventilator, blood pressure 83/57 mm Hg. MP was in no acute distress lying supine in bed. The physician noted oliguria along with a silent abdomen that was slightly distended. An abdominal X ray (kidney, ureters, bladder), labs (ionized calcium, comprehensive metabolic panel, complete blood count, sedimentation rate, urine analysis), additional intravenous fluid, and NPO status were ordered.

The lab results revealed a marked leukocytosis of 36,000 K/mm3 with 16% bands, sodium 131 mEq/L, potassium of 6 mEq/L, BUN 18 mg/dl, creatinine 0.7 ng/dl, bilirubin total 1.1 mg/dl, AST 66 U/L, ALT 235 U/L, ALKP 334 U/L. Abdominal X rays showed free intraperitoneal air consistent with a perforated viscus. MP was taken immediately to the operating room, where the perforation was closed laparoscopically. The diagnosis was a perforated duodenal ulcer secondary to aspirin or NSAID use leading to peritonitis.

The presentation of acute abdomen in this patient demonstrates the difficulty of assessing and diagnosing acute abdominal processes in SCI patients. There were no warning signs or symptoms of peptic ulcer until he had already perforated, at which time he presented with only muted signs and symptoms. There was no complaint of abdominal pain at any time.

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Background

Most peptic ulcer perforations are due to duodenal ulcers and most commonly result from H. Pylori infections, the physiologic stress of being critically ill (stress ulcers), and aspirin or NSAID use (Rajan & Nemchausky, 2001). Ulcers caused by the use of aspirin or NSAIDs involve the inhibition of gastric mucosal prostaglandin synthesis and a direct erosive effect on the mucosal lining. About 15% of longterm aspirin and NSAID users demonstrate ulcers (Goroll & Mulley, 2000). Risk factors for aspirin or NSAID‐induced ulceration include advanced age, comorbid diseases, smoking, concomitant use of corticosteroids and anticoagulation drugs, ethanol use, prior peptic ulcer disease, and high‐dose aspirin or NSAID use (Cryer, 2001).

The spinal cord‐injured patient is at increased risk for ulcers due to the frequent use of NSAIDs for pain, corticosteroids used in acute SCI treatment protocols, anticoagulants used to prevent DVTs, and aspirin used in the treatment of vertebral artery injuries and hypovolemic shock in the hyperacute phase of the injury (Barton & Vaziri, 2003). MP had all of these risk factors. Efforts to prevent ulcers in high‐risk populations include the administration of high‐dose histamine 2‐receptor antagonists (famotidine 40 mg twice a day; Cryer, 2001) and preferably, proton‐pump inhibitors or synthetic prostaglandins (misoprostol; Graham et al., 2002).

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Major Nursing Issues and Interventions

The perforation of an ulcer can be a life‐threatening emergency requiring early detection and, often, immediate surgical intervention. When an ulcer perforates, gastric contents empty into the peritoneal cavity, resulting in chemical or bacterial peritonitis that potentially leads to septicemia and hypovolemic shock. Mortality rates under these circumstances are estimated at 20%‐40% (Azer, 2006).

In neurologically intact patients, a sudden, sharp, severe pain spreads over the entire abdomen, which then becomes tender, hard, and rigid (Hawks, 1997). The bowel becomes silent as peristalsis stops and paralytic ileus develops (Kinney, Dunbar, Brooks‐Brunn, & Vitello‐Cicciu, 1998). Other signs and symptoms resulting from peritoneal irritation include guarding, rebound pain, referred pain (to the shoulders), abdominal distention, nausea, vomiting, diarrhea, decreased or absent bowel sounds, lack of flatus, fever, and leukocytosis (Kinney et al., 1998). Hiccups are also a late symptom in perforated ulcers (Azer, 2006).

Some of the signs and symptoms common in patients with SCI experiencing an acute abdominal process include anorexia, fever, persistent ileus, sweating, pallor, palpitations, tachycardia, hypotension, nausea, vomiting, increased spasticity, and infrequently, pain. Assessment findings may include distention and hypo/hyperactive bowel sounds (Steins et al., 2003; Rajan & Nemchausky, 2001).

The differential diagnosis includes perforated appendicitis, gastritis, colitis, ischemic colitis, inflammatory bowel disease, cholecystitis, and pancreatitis, amongst others (Azer, 2006). In the spinal cordinjured patient the differential diagnosis must also include myocardial infarction, intestinal obstruction, fecal impaction, dissecting aortic aneurysm, urinary tract infection, and gastroparesis.

Lab tests that can aid in determining the correct diagnosis include a complete blood count (leukocytosis), amylase, lipase, liver enzymes, and basic chemistry (primarily to rule out other diagnoses). Diagnostic imaging tests that are of the most value include computed tomography (CT) and ultrasound, although an abdominal plain film is often the first diagnostic test ordered (Rajan & Nemchausky, 2001). A finding of free air trapped subdiaphragmatically or an air‐fluid level confirms the diagnosis (Kinney et al., 1998).

The most common treatment is emergent surgery, where the surgeon will evacuate the spilled gastric contents, cleanse the peritoneal cavity by flushing it out with normal saline and potentially antibiotics (Azer, 2006), and patch the perforation with a small piece of omentum (Hawks, 1997). However, if the perforation is sealed and the patient is free of any signs and symptoms of peritonitis, a nonoperative approach may be considered (Azer).

Preoperative nursing interventions include frequent monitoring of vital signs; establishing intravenous access for fluids; dispensing pain medications, antibiotics, blood, and electrolytes as ordered; inserting a nasogastric tube for suction, to prevent further spillage of gastric contents into the peritoneum; maintaining NPO status; placing a urinary catheter, and preparing for emergency surgery (Azer, 2006). Postoperatively, patients require continued close monitoring of their intravascular volume by central venous pressure and urinary output monitoring. Intravenous fluids, antibiotics, pain medications, and nasogastric suctioning are also continued. Bowel rest is required so total parenteral nutrition is administered until peristalsis returns. Potential postoperative complications include subphrenic abcess, hemorrhage, duodenal or gastric fistula, atelectasis, pneumonia (Hawks, 1997), wound infection, sepsis, and renal failure (Azer).

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Outcomes

Overall, positive outcomes are improved with early diagnosis and treatment. Factors that place individuals at increased risk of complications include advanced age, malnutrition, and underlying disease (Azer, 2006).

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Days 3‐7

MP recovered in the ICU and returned to the acute rehabilitation unit on day 7. He was treated with antibiotics, high‐dose proton‐pump inhibitors, bowel rest, nasogastric suction, and total parenteral nutrition. He continued to suffer from severe neuropathic pain in his neck and shoulders, which required polypharmacy but resulted in only moderate relief. Multi‐modal treatments were initiated to combat MP's severe depression.

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Days 8‐30

The patient's recurrent nausea and vomiting led to a diagnosis of pancreatitis and recurrent paralytic ileus. However, hospital staff were able to discontinue total parenteral nutrition and enteral feeding via the nasogastric tube was initiated. But MP was unable to tolerate weaning from the ventilator and was minimally involved in rehabilitation therapies as a result of severe depression and neuropathic pain.

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Days 31‐90

Finally recovered from pancreatitis and ileus, the nasogastric tube was removed and MP was able to wean off the ventilator. Unfortunately, chronic neuropathic pain continued to limit his ability to fully participate in rehabilitation.

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Six Months Later

After a prolonged stay secondary to his perforated ulcer, MP was discharged to his home. He plans to return to college as soon as possible. Other than a continued battle with anorexia, MP has suffered no adverse effects from the perforation.

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Summary

Nurses who work with SCI patients, whether in the ICU, medical or surgical unit, or rehabilitation unit, need to be aware of the altered or muted presentation of acute abdomen in this population. While the routine abdominal assessment of these patients does not differ from that of a neurologically intact patient, the scope of differential diagnoses must be more broad and inclusive. Acute abdominal emergencies including gastrointestinal bleeding, appendicitis, pancreatitis, cholecystitis, obstruction, tumor, dissecting aneurysm, and others need to be considered in the differential diagnosis of any patient with spinal cord injury presenting with disturbances in gastrointestinal function, especially if anticoagulated or on aspirin or NSAID therapy (Rajan & Nemchausky, 2001). Often, the most important step in the diagnosis is just remembering the possibility that acute abdomen might exist (Steins et al., 2003).

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References

Azer, S. (2006). Intestinal perforation. Retrieved May 14, 2006, from www.emedicine.com

Barton, C. H. & Vaziri, N. D. (2003). Renal insufficiency in patients with spinal cord injury. In V. W. Lin (Ed.), Spinal cord medicine (pp. 263-298). New York: Demos.

Cryer, B. (2001). Non-steroidal anti-inflammatory drug gastrointestinal toxicity. Current Opinion in Gastroenterology, 17(6), 503-512.

Graham, D. Agrawal, N., Campbell, D., Haber, M., Collis, C., Lukasik, N., et al. (2002). Ulcer prevention in long-term users of nonsteroidal anti-inflammatory drugs: Results of a double-blind, randomized, multicenter, active- and placebo-controlled study of misoprostol vs lansoprazole. Archives of Internal Medicine, 162(2), 169-175.

Goroll, A. & Mulley, A. (2000). Gastrointestinal problems. In Primary care medicine (pp. 434-447). Philadelphia: Lippincott, Williams & Wilkins.

Hawks, J. (1997). Gastrointestinal disorders. In J. Black & E. Matassarin-Jacobs (Eds.), Medicalsurgical nursing (pp. 1748-1786). Philadelphia: WB Saunders.

Kinney, M., Dunbar, S., Brooks-Brunn, J., Vitello-Cicciu, J. (1998). AACN: Clinical reference for critical care nursing. (4th ed.) St. Louis: Mosby.

Rajan, R. K. & Nemchausky, B. A (2001). Gastrointestinal emergencies in patients with spinal cord injury. In I. M. Eltorai & I. M. Schmitt (Eds.), Emergencies in chronic spinal cord injury patients (pp. 47-65). Jackson Heights, NY: Eastern Paralyzed Veterans Association.

Steins, S. A., Fajardo, N. R., & Korsten, M. A. (2003). The gastrointestinal system after spinal cord injury. In V. W. Lin (Ed.), Spinal cord medicine (pp. 321-348). New York: Demos.

© 2007 American Association of Neuroscience Nurses

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