A 68-year-old male nursing home resident was brought to the emergency department by emergency medical services for altered mental status since early morning. As per nursing home staff, the patient had been experiencing poor oral intake and had been noted to be withdrawn from social activities over the past few days. Review of system was negative for nausea, vomiting, diarrhea, or fever. His medical history included hypertension, hyperlipidemia, osteoarthritis, and dementia. His medications included amlodipine, simvastatin, and multivitamins. Physical examination showed stable vital signs. However, the patient was cachectic, had dry mucous membranes, was alert and awake, and was able to follow commands but was confused. The rest of the examination was completely unremarkable. Significant laboratory data showed sodium of 167 mmol/L, chloride of 125 mmol/L, potassium of 4.0 mmol/L, and creatinine of 1.8 mg/dL (137.25 µmol/L). His cell count was normal. CT of the head showed no acute infarct, mass, or hemorrhages as well as no chronic microvascular changes. He was started on intravenous fluid and was transferred to the telemetry unit for electrolyte monitoring. How would you manage this case?
The case presents a common scenario where an elderly nursing home resident with poor oral intake is admitted with acute altered level of consciousness due to poor eating and has responded to fluids. Hypernatremia should be managed cautiously in this case, and frequent monitoring of sodium level should be performed. Rapid correction can lead to central pontine myelinolysis.
Hypernatremia is defined as a serum sodium concentration >145 mmol/L. It reflects a total body water deficit relative to total body sodium content caused by decreased water intake compared to water losses. The risk factors for development of hypernatremia include advanced age, mental or physical impairment, diuretic therapy, uncontrolled diabetes (solute diuresis), underlying polyuria disorders, nursing home resident, inadequate nursing care, and hospitalization.
Importantly, extracellular fluid (ECF) volume status should be assessed because it shows total body sodium content.
Hypovolemic hypernatremia: Decreased total body water (TBW) and sodium with a relatively greater decrease in TBW. It includes gastrointestinal losses (diarrhea, vomiting), skin losses (burns or excessive sweating), and renal loss (intrinsic renal disease, osmotic [glucose, urea, mannitol] and loop diuretics).
Euvolemic hypernatremia: Decreased TBW with near-normal total body sodium. It includes extrarenal losses from the respiratory tract (tachypnea) or skin (excessive sweating or fever), renal losses (central diabetes insipidus or nephrogenic diabetes insipidus), and other causes (inability to access water, primary hypodipsia, reset osmostat).
Hypervolemic hypernatremia: Increased sodium with normal or increased TBW. It includes hypertonic fluid administration (hypertonic saline, sodium bicarbonate, total parenteral nutrition) and mineralocorticoid excess (adrenal tumors, congenital adrenal hyperplasia).
Thirst is a major symptom with dehydration or clinical signs of volume depletion. Other symptoms include neurologic symptoms such as generalized weakness, confusion, neuromuscular excitability, hyperreflexia, seizures, and coma.
The approach to therapy is based on:
Estimating water deficit = Current TBW × [(Serum [Na]/140) – 1]
Designing the fluid repletion regimen:
Acute: Hourly infusion rate (mL/h) > Water deficit in mL ÷ 24 hours
Chronic: Desired water replacement in the first day in mL = 3 mL/kg body weight × 10 hourly infusion rate (mL/h) = Desired water replacement in the first day in mL ÷ 24 hours
Determining the appropriate rate of correction (rapid lowering of sodium concentration can lead to cerebral edema in chronic hypernatremia, and untreated acute hypernatremia can cause permanent neurologic injury):
Acute hypernatremia (<48 hours, uncommon; seen in patients with use of salt tablets, uncontrolled diabetes insipidus, severe hyperglycemia):
Goal is to lower the serum sodium by 1 to 2 mmol/L per hour and to achieve normonatremia in <24 hours.
Dextrose 5% in water intravenously (IV) at a rate of 3 to 6 mL/kg/h.
Reduce to 1 mL/kg/h once sodium concentration has reached 145 mmol/L and continue until normonatremia (140 mmol/L) is restored.
Monitor serum sodium and blood glucose every 2 to 3 hours until sodium is <145 mmol/L.
Chronic hypernatremia (>48 hours; nearly all patients with hypernatremia):
Goal is to lower the serum sodium by a maximum of 10 mmol/L in a 24-hour period.
Dextrose 5% in water IV at a rate of approximately 1.35 mL/h × patient’s weight in kilograms, or approximately 70 mL/h in a 50-kg patient and 100 mL/h in a 70-kg patient.
While correcting hypernatremia, simultaneously monitor fluid status and urine output, repeat weight (initially every 6 hours, especially for infants or those with severe hypernatremia), monitor other electrolytes and blood sugar, measure ongoing losses (ie, vomiting or diarrhea, excluding urine) and replace milliliter for milliliter with normal saline, and perform careful neurologic monitoring.
Patients with central diabetes insipidus will also require desmopressin therapy.
Key Points
Hypernatremia requires assessment of volume status and fluid deficit.
Acute hyponatremia should be treated with caution.
A 47-year-old woman was brought to the hospital by a friend for generalized fatigue, myalgia, and lethargy after running a marathon. As per the patient, she was in her usual state of health that morning prior to the marathon and was a healthy and physically active woman. She denied skipping a meal, nausea, vomiting, or neurologic deficit. She had no significant medical comorbidities and only took over-the-counter multivitamins. The patient denied any alcohol, tobacco, or illicit drug use. No significant family history was noted. In the emergency department, her vitals were noted as blood pressure of 120/83 mm Hg, heart rate of 103 bpm, respiratory rate of 20 breaths/min, and temperature of 98.6°F. Her physical examination, including a complete neurologic examination, was unremarkable. Chest x-ray was normal. Initial laboratory data showed hemoglobin of 11 g/dL, blood urea nitrogen of 20 mg/dL, creatinine of 0.9 mg/dL, sodium of 120 mmol/L (120 mEq/L), chloride of 80 mmol/L (80 mEq/L), potassium of 3.9 mmol/L (3.9 mEq/L), and creatinine kinase of 300 mg/dL. Urine drug screen was negative, and urine specific gravity was 1.10. She was started on normal saline bolus and was transferred to the telemetry floor. How would you manage this case?
This case presents a healthy adult athlete with acute asymptomatic hyponatremia. Further assessment of volume status and urine and serum osmolarity should be performed, and careful correction of sodium should be initiated. Sodium levels should be monitored frequently, and the correction should not exceed 4 to 6 mmol/L in the first 24 hours. The cause of her hyponatremia was most likely water intoxication in the setting of marathon and free water intake. Hypertonic saline can be used in acute symptomatic hyponatremia.
Hyponatremia is defined as serum sodium <135 mmol/L, representing a relative excess of water in relation to sodium. Volume assessment along with serum and urine osmolarity should be performed to identify the etiology. Common causes include heart failure, renal failure, hypothyroidism, syndrome of inappropriate antidiuretic hormone secretion (SIADH), psychogenic polydipsia, diuretic use, hypercortisolism, and poor oral intake.
It can be either acute or chronic (development of hyponatremia over ≥48 hours).
Symptoms include nausea, vomiting, dizziness, headache, muscle cramps, fatigue, gait disturbances, forgetfulness, confusion and lethargy, obtundation, coma, seizures, and respiratory arrest.
The treatment depends on the duration of the hyponatremia (acute or chronic). Patients with acute symptomatic hyponatremia should receive management in hospital settings for frequent assessments of neurologic status, accurate serum sodium concentration, and urine output.
In hospitalized patients, the treatment goal is to prevent further decrease in the serum sodium concentration, to relieve symptoms of hyponatremia, to decrease intracerebral pressure in those at risk for development of brain herniation, and to avoid excessive correction of hyponatremia in patients at risk for osmotic demyelination syndrome (ODS).
The goal of initial therapy is to raise the serum sodium concentration by 4 to 6 mmol/L in a 24-hour period.
Acute hyponatremia can be corrected by using a bolus of 3% saline (ie, hypertonic saline) to prevent a decrease in the serum sodium.
Chronic hyponatremia can be corrected by identification of the offending cause and its reversal such as medication. In symptomatic cases, 3% saline can be used with simultaneous use of desmopressin to prevent rapid correction among those who are at high risk of developing ODS.
Hypertonic saline should be discontinued once the daily correction goal of 4 to 6 mmol/L has been achieved and can be resumed as needed to preserve the desired increase in serum sodium for the day if it begins to fall again.
In addition to the specific therapies that are aimed at correcting the hyponatremia, therapy should also be directed at the underlying disease.
Fluid restriction below the level of urine output is indicated in edematous states such as heart failure, cirrhosis, advanced renal impairment, SIADH, and primary polydipsia.
Other therapies may include oral salt tablets, loop diuretics, potassium supplementation, urea, or vasopressin receptor antagonists depending on the etiology of hyponatremia.
Key Points
Symptomatic hyponatremia should be treated with hypertonic saline and slow correction of sodium levels.
Identification of etiology and reversal of offending agents are key in management.
A 58-year-old man presented to the emergency department (ED) with complaints of malaise and weakness since the morning. He reported using ibuprofen for knee pain for the past 2 days and had missed his last 2 hemodialysis sessions because he was not feeling good. His medical history included hypertension, end-stage renal disease (on hemodialysis), diabetes mellitus, and osteoarthritis of the knees. Medications included aspirin, atorvastatin, losartan, sevelamer, and carvedilol. In the ED, he was vitally stable. Physical examination revealed bibasilar crackles and pitting edema of the bilateral lower extremities. Laboratory results showed serum potassium of 7.9 mmol/L and creatinine of 11 mg/dL. His ECG (shown in the Figure 9.3.1) showed normal sinus rhythm with tall T waves in anterior precordial leads. The patient received calcium chloride, insulin, and dextrose. Emergent hemodialysis was planned. How would you manage this case?
This case describes the management of hyperkalemia. Missed hemodialysis can lead to hyperkalemia, which can present as malaise, weakness, and bradycardia. Intravenous calcium chloride, potassium-binding resins, and insulin therapy can be used to treat hyperkalemia. Any offending medication should be stopped. If unresponsive to medical therapy, emergent hemodialysis should be performed.
Potassium level >5.5 mmol/L is considered hyperkalemia. The severity is classified as follows: mild, 5.5 to 5.9 mmol/L; moderate, 6.0 to 6.4 mmol/L; and severe, >6.5 mmol/L. It is caused by impaired urinary potassium excretion due to acute or chronic kidney disease or disorders or drugs that inhibit the renin-angiotensin-aldosterone system.
Common causes include kidney failure, hypoaldosteronism, and rhabdomyolysis. Medications that cause high blood potassium include spironolactone, nonsteroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors. Pseudo-hyperkalemia, due to breakdown of cells during or after taking the blood sample, should be ruled out.
Diagnosis is usually made based on laboratory and ECG finding (prolongation of the PR interval, development of peaked T waves, widening of the QRS complex, and ECG complex that evolved to a sinusoidal shape).
Symptoms include malaise, weakness, paralysis, arrhythmias, and cardiac arrest.
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