A nurse is monitoring a client receiving total parenteral nutrition (TPN). Which of the following complications should the nurse prioritize?

Choice A reason: Frequent bowel movements are not typical in peritonitis. Inflammation of the peritoneal cavity causes ileus, reducing bowel motility and leading to constipation or obstipation. Peristalsis slows due to irritation, and the body diverts energy to combat infection, making diarrhea unlikely unless another condition, like gastroenteritis, is present, which is not indicated here.

Choice B reason: A rigid abdomen is a classic sign of peritonitis due to peritoneal inflammation causing muscle guarding and rigidity. The peritoneal irritation from infection or chemical irritants (e.g., bile, gastric contents) triggers involuntary abdominal wall contraction to protect inflamed tissues, resulting in a board-like abdomen, often with severe pain.

Choice C reason: Decreased urinary output occurs in peritonitis due to systemic inflammation and potential hypovolemia from fluid shifts into the peritoneal cavity (third-spacing). The kidneys receive reduced perfusion, activating the renin-angiotensin-aldosterone system, leading to oliguria. This reflects the body’s attempt to conserve fluid in response to systemic stress and inflammation.

Choice D reason: Inability to pass stools is expected in peritonitis due to paralytic ileus, where intestinal motility ceases from inflammation. Peritoneal irritation disrupts normal peristalsis, causing bowel obstruction symptoms like constipation or obstipation. This results from the body’s inflammatory response inhibiting gastrointestinal function, leading to stool retention.

Choice E reason: Hyperactive bowel sounds are not typical in peritonitis. The condition causes paralytic ileus, reducing or absent bowel sounds due to decreased peristalsis from peritoneal inflammation. Hyperactive sounds may occur in early mechanical obstruction but not in peritonitis, where inflammation halts bowel motility, leading to hypoactive or absent sounds.

Choice A reason: Methylprednisolone, a corticosteroid, reduces inflammation in anaphylaxis by inhibiting immune responses. However, its onset is slow, taking hours to act, making it unsuitable as the first-line treatment for acute anaphylactic shock. It is used as an adjunct to stabilize symptoms after epinephrine addresses immediate life-threatening bronchoconstriction and hypotension.

Choice B reason: Epinephrine is the first-line treatment for anaphylactic shock. It acts rapidly via alpha- and beta-adrenergic receptors to reverse bronchoconstriction, vasodilation, and hypotension. It constricts blood vessels, increases cardiac output, and relaxes airway smooth muscles, alleviating life-threatening symptoms like airway obstruction and shock, making it critical for immediate administration.

Choice C reason: Dobutamine, a beta-agonist, enhances cardiac contractility and is used in cardiogenic shock. It does not address the histamine-mediated vasodilation, bronchoconstriction, or angioedema in anaphylaxis. Its use could worsen hypotension by increasing cardiac demand without correcting the underlying immune-mediated mechanisms, making it inappropriate for this emergency.

Choice D reason: Furosemide, a diuretic, treats fluid overload in conditions like heart failure. In anaphylactic shock, it would exacerbate hypotension by reducing intravascular volume, worsening tissue perfusion. Anaphylaxis involves histamine-induced vascular leak, not fluid overload, so furosemide is contraindicated and would not address the acute airway or cardiovascular symptoms.