A 30-year-old at 32 weeks gestation reports severe headache and blurred vision. What complication should the nurse suspect?

Hyperemesis gravidarum is a pathological state of intractable vomiting resulting in ketonuria, dehydration, and significant electrolyte depletion. The clinical management aims to restore hemodynamic stability and suppress the overactive emetic reflex. Interventions focus on maintaining metabolic homeostasis and preventing Wernicke’s encephalopathy through thiamine and fluid replacement.

A. Antiemetics: Pharmacological management using pyridoxine, doxylamine, or ondansetron is necessary to interrupt the vomiting cycle. These medications act on the chemoreceptor trigger zone or vestibular system to reduce nausea. Effective suppression of emesis allows for the gradual reintroduction of oral nutrition and hydration.

B. Fluid restriction: Restricting fluids is contraindicated and dangerous for a client already suffering from intravascular dehydration. Adequate hydration is the cornerstone of therapy to prevent renal failure and maintain uteroplacental perfusion. Restricting intake would exacerbate tachycardia and orthostatic hypotension.

C. Avoid triggers: Identifying and eliminating environmental stimuli like strong odors, flickering lights, or specific textures reduces sensory input to the emetic center. Behavioral modification is a non-pharmacological necessity to prevent recurrent episodes of nausea. This helps stabilize the gastric mucosa and CNS.

D. IV fluids: Intravenous rehydration with isotonic crystalloids is the priority intervention for clients unable to tolerate oral intake. This corrects volume deficits and replenishes depleted electrolytes like potassium and chloride. It is essential for reversing metabolic alkalosis caused by loss of gastric acid.

E. Small frequent meals: Once vomiting is controlled, consuming low-fat, high-carbohydrate snacks every 2 to 3 hours prevents an empty stomach. Maintaining stable blood glucose levels minimizes gastric contractions and acid irritation. This dietary strategy supports weight gain and fetal development.

Opioid-induced respiratory depression is a life-threatening complication characterized by a decreased respiratory rate and impaired gas exchange. Opioids act on the mu-receptors in the brainstem, reducing the responsiveness to carbon dioxide levels. Immediate reversal is necessary to prevent respiratory arrest and hypoxic brain injury.

A. Increase opioid use: Administering more opioids would further suppress the respiratory center in the medulla, leading to total apnea and death. This is the opposite of the required intervention. The goal is to discontinue or reverse the sedative effects of the medication.

B. Reassess in 1 hour: A respiratory rate of 8 breaths per minute is a clinical emergency that requires immediate intervention. Waiting one hour would likely lead to severe hypercapnia, acidosis, and cardiopulmonary collapse. Frequent, minute-by-minute monitoring is required until the patient is stable.

C. Encourage ambulation: A patient with a respiratory rate of 8 is likely experiencing significant sedation and lethargy, making ambulation impossible and unsafe. Physical activity would increase oxygen demand that the compromised respiratory system cannot meet. The patient requires ventilatory support and reversal.

D. Administer naloxone: Naloxone is a competitive opioid antagonist that displaces opioids from their receptors, rapidly reversing respiratory and CNS depression. It must be administered intravenously in small, titrated doses to restore a safe respiratory rate without triggering acute withdrawal. It is the priority rescue medication.