A 39-year-old woman is admitted to the gynecology service for hysterectomy for symptomatic uterine fibroids. Postoperatively the patient develops an ileus accompanied by severe nausea and vomiting; ondansetron is piggybacked into an IV of D5 ½ normal saline running at 125 cc/h. On the second postoperative day the patient becomes drowsy and displays a few myoclonic jerks. Stat labs reveal Na 118, K 3.2, Cl 88 HCO3 22, BUN 3, and creatinine 0.9. Urine studies for Na and osmolality are sent to the lab.
What is the most appropriate next step?
The patient has acute symptomatic hyponatremia, a life-threatening condition. Although some controversy persists as to whether chronic hyponatremia should be rapidly corrected, acute symptomatic hyponatremia should be rapidly treated with hypertonic saline. This patient is at high risk of seizure and respiratory arrest, the main cause of permanent CNS damage in hyponatremia. ICU care, with frequent monitoring of the serum sodium level and CNS status, is critical. Once the Na has risen 4 to 8 mEq/L and the symptoms have improved, the rate of hypertonic saline infusion can be decreased. Less aggressive methods of treating her free-water overload, such as fluid restriction alone or in combination with furosemide, are not appropriate for this acute emergency. Isotonic fluids such as normal saline and lactated Ringer solution are useful in volume depletion but will not treat this patient’s free-water excess. Postoperative hyponatremia is particularly common in premenopausal women. The nausea and pain sometimes associated with surgery are very potent stimulators of vasopressin (ADH) release by the neurohypophysis. If hypotonic fluids are used at all in this setting, the serum sodium level should be closely monitored, and isotonic fluids used if there is any trend toward free-water retention (ie, hyponatremia).
You evaluate a 48-year-old man for chronic renal insufficiency. He has a history of hypertension, osteoarthritis, and gout. He currently has no complaints. His medical regimen includes lisinopril 40 mg daily, hydro-chlorothiazide 25 mg daily, allopurinol 300 mg daily, and acetaminophen for his joint pains. He does not smoke but drinks 8 oz of wine on a daily basis. Examination shows BP 146/86, pulse 76, a soft S4 gallop, and mild peripheral edema. There is no abdominal bruit. His UA reveals 1+ proteinuria and no cellular elements. Serum creatinine is 2.2 mg/dL and his estimated GFR from the MDRD formula is 42 mL/minute.
What is the most important element is preventing progression of his renal disease?
This patient has stage III chronic kidney disease (estimated GFR 30-60 mL/minute). At this stage it is crucial for the internist to prevent progression to end-stage renal disease. Blood pressure control, with a target blood pressure of less than 130 systolic and less than 80 diastolic, is a critical element in his management. The patient is on maximal doses of thiazide and angiotensin-converting inhibitor (ACEI), so the addition of a calcium channel blocker is appropriate. Other important management issues include avoiding nephrotoxins (such as NSAIDs and IV contrast agents), if possible, modest dietary protein restriction, and atherosclerotic risk factor management. If the patient progresses to stage IV CKD (estimated GFR 15-30 mL/minute), he should be referred to a nephrologist. Modest ethanol consumption is not a renal or cardiovascular risk factor and need not be modified unless you believe the patient is consuming much more alcohol than he admits. Acetaminophen in usual therapeutic doses is the safest agent to control DJD pain and certainly is preferable to nonsteroidals. Angiotensin receptor blockers (such as losartan) can be substituted for ACEIs if side effects such as cough occur, but ARBs have no advantage over ACEIs in preventing progression of CKD. The critical element is tighter blood pressure control.
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