Hypernatremia Case Study



Diabetes insipidus (DI) presents with hypernatremia and consequent hyperosmolality in individuals with an impaired thirst mechanism or no free access to water. Hyperosmolality was found to be associated with rhabdomyolisis, a disease consist of elevated serum creatinine kinase (CPK) and myoglobinuria. Fluid resuscitation is the mainstay of the treatment to prevent life-threatening complications including acute hyperkalemia and acute kidney injury (AKI). We presents herein a first human case of nephrogenic DI who presented with rhabdomyolisis.

Case presentation

A 74 year old man with multiple comorbidities was transferred to emergency department for subjective fever,
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Hypernatremia and hyperosmolality is a significant predisposing factor for non-traumatic rhabdomyolysis. Along with other hyperosmolar states, nephrogenic DI should be considered in differentials. Early recognition and implementation of treatment is important to decrease mortality and morbidity. …show more content…
EMS at the site checked finger stick blood glucose which was 440 mg/dl and 8 gm of naloxone was given to the patient. Her mental status did not improve and she was transferred to emergency department. Upon her arrival, she was hypotensive to 96/54 mmHg with a heart rate of 101 beats per minute. Respiratory rate was 10 per minute, Oxygen (02) saturation was 99% on 6L of 02 via nasal cannula. Temperature was 96.8 F rectally. Initial assessment revealed unresponsive patient with pinpoint pupils bilaterally. Arterial blood gas (ABG) was reported as pH of 7.35, pC02 of 36 mmHg, p02 of 65 mmHg and bicarbonate of 19.9 mmol/L. Her mentation started to improve after additional 2 gm of naloxone administration, and she was placed on non-rebreather mask. She was transferred to intensive care unit for continuation of naloxone drip and close monitoring. Initial blood work up showed WBC count of 34.2 Thou/uL and lactate of 9.9 mmol/L which returned to normal range in 6 hours with fluid resuscitation. Repeat blood glucose level was 318 mg/dl which trended down and maintained in the range of 80-110 mg/dL without insulin use. Her BMI was 22.1 kg/m2 and HBA1C was only 5.4 %. Patient was not on steroids, thiazide or any sympathomimetic. Elevation in liver enzymes ALT of 170 U/L, AST of 288 U/L, ALP of 117 U/L trended down to normal range in a day. TSH was 0.38 uIU/ml, chest X-ray and urinalysis showed

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