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A patient is admitted with a traumatic brain injury. During assessment, a nurse notes increased urinary output from the catheter. Which of the following should the nurse suspect?
brain injury (TBI) is most suggestive of central diabetes insipidus (DI). This condition is caused by damage to the hypothalamus or pituitary gland, leading to insufficient secretion of antidiuretic hormone (ADH). The result is an inability to concentrate urine, leading to polyuria (excessive urine output) and potentially significant dehydration and electrolyte imbalances if not managed appropriately. Reference: =
CCRN (Adult) Certification Review Course Online: Neurological Disorders and Endocrine Emergencies.
Adult CCRN/CCRN-E/CCRN-K Certification Review Course Online. AACN
A patient is receiving therapeutic hypothermia post-cardiac arrest. Which of the following orders should a nurse clarify?
Sequential compression devices (SCDs) are not recommended for patients receiving therapeutic hypothermia (TH) post-cardiac arrest, because they may interfere with the cooling process and increase the risk of skin injury. SCDs are used to prevent deep vein thrombosis (DVT) by applying intermittent pneumatic pressure to the lower extremities, but they may also increase peripheral blood flow and heat exchange, which can counteract the effects of TH. SCDs may also cause skin breakdown, blisters, or burns in patients with impaired sensation and reduced perfusion due to TH. Therefore, a nurse should clarify the order for SCDs and consider alternative methods of DVT prophylaxis, such as pharmacological agents or early mobilization.
A patient's blood culture report notes the presence of vancomycin resistant enterococcus. The nurse should place the patient in which type of isolation?
The nurse should place the patient in contact isolation, which is a type of precaution used to prevent the transmission of microorganisms that are spread by direct or indirect contact with the patient or the patient's environment. Contact isolation requires the use of gloves and gowns when entering the patient's room, as well as dedicated patient-care equipment and proper hand hygiene. Vancomycin resistant enterococcus (VRE) is a type of bacteria that is resistant to the antibiotic vancomycin and can cause infections in various sites, such as the urinary tract, bloodstream, or wounds. VRE can be spread by contact with contaminated surfaces, equipment, or hands.
AACN. (2023). CCRN (Adult) Exam Handbook. Retrieved from [CCRN Exam Handbook], p. 18.
AACN. (2023). CCRN (Adult) Exam Blueprint. Retrieved from [CCRN Exam Blueprint], p. 2.
CDC. (2019). Guidelines for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare Settings. Retrieved from [CDC Guidelines], p. 69-70.
CDC. (2019). Vancomycin-resistant Enterococci (VRE) and the Clinical Laboratory. Retrieved from [CDC Fact Sheet], p. 1-2.
Which of the following is most indicative of successful treatment for salicylate poisoning?
Alkalinization of urine is one of the main goals of treatment for salicylate poisoning, as it enhances the renal excretion of salicylate and reduces its reabsorption. Alkalinization of urine can be achieved by administering intravenous sodium bicarbonate and maintaining adequate hydration and urine output. Alkalinization of urine can be monitored by measuring the urine pH, which should be above 7.5. Osmotic diuresis, decrease in gastric pH, and decrease in CPK are not indicative of successful treatment for salicylate poisoning. Osmotic diuresis may occur as a result of salicylate toxicity, but it does not improve the elimination of salicylate. Decrease in gastric pH may impair the absorption of salicylate, but it does not affect the elimination of salicylate. Decrease in CPK may reflect the resolution of rhabdomyolysis, which is a possible complication of salicylate poisoning, but it does not reflect the clearance of salicylate.
Salicylate (aspirin) poisoning: Management - UpToDate1, p. 1-2.
Salicylate poisoning - Symptoms, diagnosis and treatment | BMJ Best Practice US2, p. 4-5.
A patient who survives near-drowning develops hypoxia-induced cerebral edem
a. Interventions should include
Hypoxia-induced cerebral edema after a near-drowning incident can be managed by administering osmotic diuretics like mannitol. These medications help reduce intracranial pressure by drawing fluid out of the brain tissue and into the bloodstream, thereby alleviating cerebral edema. Maintaining a MAP of 60-70 mm Hg may not be sufficient to address the elevated intracranial pressure, keeping the patient flat could worsen cerebral edema, and hyperventilation with a PaCO2 of 40-45 mm Hg is not typically recommended for managing increased intracranial pressure as it can lead to vasoconstriction and decreased cerebral perfusion. Reference: = CCRN Exam Handbook, AACN Adult CCRN Certification Review Course
