A previously healthy 18-year-old woman presents to the emergency department 4 hours ago with headache and photophobia. Her parents state that her symptoms began as a mild fever and headache, and today, she appears to be a bit confused and has been urinating a lot. On physical examination, she is alert and oriented but slow to answer questions. There are no focal neurological signs. Her labs reveal elevated leukocytosis and hypernatremia. Blood cultures were sent.
What is the next BEST step in management?
Correct Answer: A
Central diabetes insipidus (DI) is a rare complication of bacterial meningitis. The presence of polyuria and hypernatremia is concerning for the development of DI in this patient. While it is important to obtain urine electrolytes and osmolality (Answer C) to confirm the diagnosis of DI, the most concerning issue here is the potential for bacterial meningitis in this patient. Therefore, prompt diagnosis and treatment are needed to prevent morbidity and mortality. According to the 2004 Infectious Diseases Society of America guidelines, a CT scan of head is indicated when a patient is immunosuppressed, has new onset of seizure, a history of an intracranial mass lesion, altered mental status, or focal neurological deficit. However, this patient does not have any of these features, making choice D incorrect.
Obtaining a sample of spinal fluid is essential for diagnosis of meningitis. However, in this case, there was a delay in antibiotics initiation since the patient has been in the emergency department for 4 hours before consultation with no antibiotics initiated. Delay in antibiotic administration is associated with worse outcomes in patients with bacterial meningitis. Retrospective data suggest a 10% increase of in-hospital mortality and risk for unfavorable outcomes with each hour of delay. Thus, antibiotic administration takes precedence in this patient.
References: Tunkel AR. Clinical Features and Diagnosis of Acute Bacterial Meningitis in Adults. Uptodate. 2018. https://www.uptodate.com/contents/clinicalfeatures-and-diagnosis-of-acute-bacterial-meningitis-in-adults.
Bichet DG. Evaluation of Patients with Polyuria. Uptodate. 2019. https://phstwlp2.partners.org:2057/contents/evaluation-of-patientswith-polyuria.
Bodilsen J, Dalager-Pedersen M, Schonheyder HC, Nielsen H. Time to antibiotic therapy and outcome in bacterial meningitis: a Danish population-based cohort study. BMC Infectious Diseases. 2016;16:392. Epub 2016/08/11. doi:10.1186/s12879 to 016 to 1711-z.
A 45-year-old man is admitted for urgent laparoscopic cholecystectomy for severe cholecystitis. His medical history was significant for chronic kidney disease and moderate to severe pulmonary hypertension which is being treated with continuous epoprostenol infusion at home. Intraoperative transesophageal echocardiogram showed depressed right ventricular systolic function. Intraoperative course was complicated by blood loss, requiring 2 units of packed red blood cells and 500 mL of lactated ringer. Postoperatively, he remained sedated and intubated and transferred to the intensive care unit (ICU) for close monitoring. His home-dose IV epoprostenol was continued intraoperatively and in the ICU. During his first postoperative day, he made minimal urine. Oxygen saturation is 100%, and estimated pulmonary artery pressure is at baseline, however, central venous pressure has increased.
Which of the following is the next BEST step in management?
Correct Answer: B
Acute right ventricular failure can occur in patients with moderate to severe pulmonary hypertension. Compared to the left ventricle, the right ventricle is more sensitive to increases in afterload. As a result, in this patient, who already has right ventricular dysfunction, efforts must be made to minimize right ventricular afterload. Factors such as hypoxemia, hypercapnia, hypothermia, high airway pressure, positive end-expiratory pressure, and acidosis can increase pulmonary vascular resistance.
Additional fluid challenge could be detrimental in this patient with depressed right ventricular function. It may increase the risk of right heart failure, especially since the increasing central venous pressure is an indicator of right heart volume overload (nswer D). Renal failure and associated metabolic acidosis will also be poorly tolerated by this patient, since acidosis will worsen pulmonary vascular resistance and right ventricular afterload. Hence, early intervention with renal replacement therapy to avoid renal acidosis is most beneficial. Moreover, renal replacement therapy will also help correct volume status, especially since he is anuric (Answer B).
The patient’s pulmonary artery pressure and pulmonary vascular resistance remained stable which indicates that the intravenous epoprostenol has been effective. Inhaled and intravenous administration of epoprostenol is similarly effective and therefore no indication to change (Answer C). While transesophageal echocardiogram allows direct assessment of ventricular function, it requires equipment and the availability of an expert who can acquire and interpret the images. As a result, in the patient with impending sign of right ventricular failure, transesophageal echocardiogram should not be a priority (Answer A).
References:
A 62-year-old woman with medical history of hypertension and smoking presents to the hospital after sudden onset of severe headache followed by collapse. In the emergency department, CT scan of the head showed diffuse subarachnoid hemorrhage and CT angiogram revealed a left middle cerebral artery aneurysm. An extraventricular drain is placed by neurosurgery team. On day 7 of hospitalization, the patient develops new aphasia. The urine output has been 1800 mL in the past 3 hours, while the serum sodium has decreased from 138 to 132 mmol/L.
What is the best next step in management to address this high urine output?
Correct Answer: E
In the setting of acute intracranial injury, both syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting (CSW) are potential causes of hyponatremia. The main difference between the two is the patient’s volume status which can be difficult to determine using clinical criteria.
In SIADH, the patient is typically in an euvolemic or hypervolemic state, while in CSW, the patient is hypovolemic. Consistent with the above description, CSW is associated with large urine output volumes, whereas SIADH is associated with low to normal amounts of urine output volumes. Evaluation for CSW begins with a basic metabolic panel to identify the hyponatremia (serum sodium less than 135 mEq/L). Urine studies are commonly checked for urine sodium and osmolality. Urine sodium is typically elevated above 40 mEq/L. Urine osmolality is elevated above 100 mosmol/kg. The patient must also have signs or symptoms of hypovolemia such as hypotension, decreased central venous pressure, lack of skin turgor, or elevated hematocrit. Laboratory parameters common between SIADH and CSW are hyponatremia and increased urine sodium. However, with SIADH, the patient is euvolemic to hypervolemic from the retained free water, compared to the hypovolemic picture of CSW.
High urine output with reduction in serum sodium, in a patient with subarachnoid hemorrhage, likely suggests CSW syndrome. The treatment for CSW involves repletion of fluid and salt to prevent volume contraction (Answer E). Additionally, in subarachnoid hemorrhage, the risk of vasospasm is increased with hypovolemia. Answer A is incorrect because this case scenario does not describe SIADH. Answer B does not address the decrease in sodium. Answer C may be a step in management of neurogenic hyponatremia seen in SAH patients but is not typically done until later in the course. Further, this answer choice does not immediately address the volume or sodium deficit. Answer D does not address the fluid deficit.
Reference:
A 52-year-old man with history of bipolar disorder and headaches is admitted for elective pituitary macroadenoma resection in the early morning. Following the otherwise uncomplicated neurosurgical procedure, he is admitted to the ICU for postoperative observation. You receive a call near midnight reporting that urine output has increased to 1000 mL in the past 3 hours while serum sodium increased from 142 to 146 mmol/L.
What are the next steps you should take to prevent worsening of hypernatremia?
Low urine specific gravity in the context of polyuria and a rise in serum sodium are sufficient to make the diagnosis of DI. This postoperative neurosurgical patient is most likely experiencing central DI. Here, there is a decrease in antidiuretic hormone (ADH) which leads to polyuria (urine output >30 mL/kg body weight or >200 mL/h for 2 hours), a hallmark of DI. Additional tests that help confirm the diagnosis are measurement of urine specific gravity and serum sodium. In DI, urine will be dilute, evidenced by low urine specific gravity <1.005. With loss of dilute urine, serum sodium is expected to rise. A patient with adequate mental status may demonstrate polydipsia due to significant thirst.
Desmopressin (DDAVP) is a synthetic vasopressin analog, which acts specifically on the V2 receptor. Administration of desmopressin in central DI to replace the lack of ADH reverses the effects of central DI and thereby prevents rise in serum sodium (Answer B).
Answer A is incorrect because the relative hyponatremia is not causing clinical signs or symptoms, at this time. It is also preferable to avoid hypotonic fluids such as D5W in immediate postoperative neurosurgical or other patients with potential for cerebral edema. Answer C is not correct because increasing the rate of maintenance IV fluids (normal saline) with hypotonic fluid loss in urine (seen in DI) may further increase serum sodium. Fluid restriction (Answer D) would cause hypovolemia and may raise serum sodium.
A 75 kg, 70-year-old male with a history of hypertension, coronary artery disease, and benign prostatic hypertrophy gets admitted to the ICU after a partial colectomy and liver resection for colon cancer. Placement of indwelling urinary catheter placement was challenging due to his enlarged prostate causing some hematuria. The operative procedure was complicated by bleeding, requiring 4 units of packed red blood cell transfusion. Postoperative hemoglobin was 8.2 g/dL.
Over the next 12 hours, his abdominal drain produced 700 mL of sanguineous output and his urine output decreases from 80 mL/h in immediate postoperative period to 20, 10, and 5 mL, respectively, in the last 3 consecutive hours. His vitals 12 hours after admission are now:
Which of the following would be LEAST likely in this patient?
Correct Answer: D
Important causes for low urine output may be classified into prerenal, intrarenal, and postrenal causes. Based on presentation sanguineous output from abdominal drain, hypotension, and tachycardia are consistent with a prerenal etiology. A common cause of prerenal disease is volume depletion, which may occur from hypovolemia caused by hemorrhage, dehydration, diuretics, or gastrointestinal fluid losses (vomiting/diarrhea). Prerenal physiology and renal hypoperfusion may also occur due to heart failure causing poor cardiac output, or cirrhosis causing splanchnic venous pooling and systemic vasodilation. Prerenal physiology is often characterized by azotemia, caused by increased sodium and urea absorption in the proximal tubule in an attempt to increase circulating blood volume. In such patients, the BUN is often increased to a greater proportion than the creatinine such that the serum BUN:Cr ratio is greater than 20:1 (Answer A). In prerenal disease, the FENa is typically less than 1% due to decreased urinary sodium excretion (due to reabsorption of sodium) in an attempt to retain water and circulating blood volume (Answer B). Urine with a high specific gravity (Answer C) indicates very concentrated urine, which occurs when the kidney is trying to retain additional free water. RBC casts in the urine (Answer D) are virtually diagnostic of some form of glomerulonephritis or vasculitis and indicate microscopic bleeding in the kidney. They are not associated with trauma to an enlarge prostate on insertion of a foley catheter and are not associated with prerenal or acute tubular necrosis. Acute tubular necrosis typically results in “muddy brown casts” consisting of renal tubular epithelial cells.
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