A 78-year-old man is brought to the hospital after being found down by his daughter at his home this morning. He was functional at baseline and last seen normal yesterday. He is a life-time smoker with chronic obstructive pulmonary disease (COPD) and was recently diagnosed with lung cancer. On physical examination, he is lethargic, has unsteady gait, and is confused. His temperature is 37.4°C, blood pressure is 127/94 mm Hg, pulse rate is 74 beats/min, and respiratory rate is 11 breaths/min. On examination, he has a normal jugular venous pressure, but he has decreased air entry at the lung bases. A CT head obtained shows age-related atrophic changes. Laboratory studies obtained are as follows:
Which of the following is the MOST appropriate next step in management of this patient?
Correct Answer: E
The patient’s history and laboratory studies are consistent with hypotonic euvolemic hyponatremia. The important differentials are SIADH, adrenocortical insufficiency, polydipsia, physiological stimulus antidiuretic hormone (ADH) release (nausea, pain, anxiety), and hypothyroidism. Based on presentation, the most likely etiology of hyponatremia in this patient is SIADH. Patients with lung cancer, particularly small cell lung cancer, have a reported incidence of up 18.9%. SIADH is caused by the secretion of ADH from the posterior pituitary gland or unregulated ectopic production by tumor cells. Elevated levels of ADH lead to hyponatremia and hypoosmolality by decreasing the renal excretion of free water. While not all cases of hyponatremia require correction with hypertonic saline, this patient has acute onset, severe hyponatremia and has moderate symptoms. Symptoms of hyponatremia include headache, nausea, vomiting, confusion, disorientation, and seizures. Though his sodium needs correction with hypertonic saline, the sodium should not be corrected by more than 9 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). It is important to note that neurological effects related to ODS can take up to 1 week to manifest, including dysarthria and dysphagia.
A 17-year-old college student is admitted to the hospital after sustaining a traumatic hit to the head during football practice, resulting in subdural hemorrhage. Upon arrival, his Glasgow Coma Scale is 4. He is started on hypertonic saline and undergoes emergent neurosurgical intervention. His exam remains unchanged overnight, but during morning rounds, the nurse reports that his urine output increased to over 300 mL/h.
Laboratory studies obtained show:
Which is the MOST likely cause of his increased urine output?
Correct Answer: B
Central DI occurs in the setting of inadequate production of ADH. Normally, ADH is secreted by the posterior pituitary gland. However, in patients who sustained traumatic brain injury, a decrease or cessation of ADH production can occur, thereby decreasing reabsorption of water leading to hypernatremia. In otherwise healthy patients, the lack of ADH will cause increased thirst and lead to polydipsia. These symptoms might not be apparent in a critically ill patient.
Water deprivation test and administration of desmopressin, as depicted in the flowchart below, may be used to confirm the diagnosis. However, the test is relatively contraindicated in hypovolemic and hypernatremic patients due to risk of exacerbating these. Further testing is not needed in our patient, since the clinical presentation and laboratory studies are consistent with central DI. Diagnostic evaluation for suspected DI includes serum sodium, serum, and urine osmolality, which are expected to show hypernatremia with decreased urine osmolality <600 mOsm/kg and serum osmolality of >295 mOsm/kg. In patients with central DI, the urine osmolality is expected to increase by >100% after administration of desmopressin.
A 68-year-old man presents to his primary care physician complaining of frequent urination at night. He reports a strong urinary stream without any feeling of incomplete emptying. His medications include aspirin, pravastatin, lithium, and amlodipine. On physical examination, he is afebrile, his blood pressure 138/75 mm Hg, pulse rate 74 beats/min, and respiratory rate 18 breaths/min.
Which of the following laboratory studies are MOST consistent with the patient’s clinical presentation?
Correct Answer: C
The patient’s history and presentation is consistent with lithium-induced NDI. In NDI, the kidney’s ability to concentrate the urine is decreased despite the presence of sufficient ADH, due to insufficient water reabsorption in the collecting duct. Vasopressin is responsible for regulating the water permeability in the collecting duct and water reabsorption based on the tonicity of the medullary interstitium. Lithium causes NDI by entering the principal cells in the collecting tubules and interfering with aquaporin function, thereby decreasing the ability to concentrate urine.
Other causes for NDI include hypercalcemia, hypercalciuria, and obstructive uropathy. In the setting of a positive water deprivation test, the administration of desmopressin can further differentiate primary polydipsia from central and nephrogenic DI. Patients with NDI will not respond to the administration of desmopressin, whereas patients with central DI will have an increased urine osmolality.
In NDI, the urine osmolarity is typically lower than serum osmolarity (option C). Since water intake is maintained by compensatory polydipsia, patients do not typically develop overt hypernatremia.
A 58-year-old woman with past medical history of alcohol abuse and bipolar schizophrenia presents to the hospital after a fall complicated by numerous rib fractures seen on chest x-ray. She is currently not taking any medications. On physical examination, her temperature is 37.1°C, blood pressure is 138/88 mm Hg, pulse rate is 99 beats/min, and respiratory rate is 14 breaths/min, oxygen saturation is 95% on room air. Her neurological, cardiovascular, and abdominal examinations are normal. She exhibits tenderness to palpation over the left chest wall with decreased bibasilar breath sounds. Her chemistry panel is as follows:
What is the MOST appropriate management of her hyponatremia?
Correct Answer: D
This patient’s hyponatremia is due to low solute intake associated with increased consumption of beer which is also known as beer potomania. Beer is low in solutes and electrolytes. Excessive consumption with an otherwise nutritionally poor diet leads to impaired water clearance and therefore dilutional hyponatremia. Typical laboratory findings include low urine sodium, low urine osmolality, and low ADH levels. However, it should be noted, that the concomitant use of diuretics can make the diagnosis of beer potomania more difficult as diuretics will cause increased sodium excretion in urine and thus result in higher than expected urine sodium and osmolality concentrations.
A 62-year-old woman is brought to the hospital with sudden onset headache followed by nausea and vomiting. Upon arrival to the emergency room, she is lethargic with a Glasgow Coma Scale of 5. Significant vital signs include a blood pressure of 220/130 mm Hg. She is emergently intubated. CT scan of the head reveals subarachnoid hemorrhage in the basilar cisterns. She undergoes placement of a right frontal extraventricular device and coiling with improvement of her neurological examination. Over the following days, she is weaned off propofol. However, on the seventh day, her urine output increases to 4 L/d and she becomes hypotensive with blood pressure of 89/60 mm Hg and pulse rate of 118 beats/min. Laboratory data show:
What is the MOST likely cause for the patient’s acute changes?
Correct Answer: A
The pathophysiology of CSW syndrome remains poorly understood. There are two proposed mechanisms that lead to CSW. One of the mechanisms involves the disruption of the sympathetic neural input which normally promotes the reabsorption of sodium. The other mechanism is natriuresis induced by natriuretic peptides that are released in patients with brain injury. Both of these mechanisms lead to decreased activation of the renin-angiotensin-aldosterone system, leading to decreased sodium absorption at the proximal tubules.
CSW syndrome and SIADH both have similar laboratory values, including low serum osmolality, high urine osmolality, and high urine sodium levels. The most important distinguishing feature is the extracellular fluid volume status. Patients with CSW will have low extracellular fluid, reflected by their hypotension, whereas SIADH patients are generally euvolemic.
Evaluation of 24 hour uric acid excretion may also aid in the diagnosis as patients with SIADH. Uric acid is normally resorbed in the proximal tubule along with sodium. Both SIADH and CSW results in loss of uric acid via urine. However, an important differentiating feature is that in patients with SIADH, serum uric acid level and fractional excretion of uric acid normalize after correction of the serum sodium level, whereas the uric acid level remains low and uric acid excretion remains elevated in patients with CSW, despite correction of hyponatremia.
Common causes for CSW include subarachnoid hemorrhage, intracranial tumors and infections. Overall, the prevalence of CSW is less common than SIADH, but it is important to exclude as the treatment for CSW and SIADH vary vastly. The treatment for CSW includes administration of fluids and mineralocorticoids. In contrast, SIADH is treated with water restriction.
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