Adrenal Crisis in a Delayed Diagnosis of Sheehan Syndrome.

Sheehan syndrome is a well-documented endocrinological disorder that appears to be closely associated as a secondary sequela to postpartum hemorrhage. Due to pregnancy-related physiological adaptations, namely the increase in blood volume but lack of hypertrophic or hyperplastic growth within the pituitary, pregnancy increases the likelihood of infarction of the pituitary. This, coupled with other complications, such as postpartum hemorrhage, can lead to ischemia and permanent damage to the pituitary, and thus, all the downstream endocrinological pathways regulated by the pituitary. Namely, this can include, but is not limited to, adrenal crisis from improper stimulation of steroid secretion. Individuals who have been diagnosed with Sheehan syndrome require lifelong steroid supplementation for appropriate regulation of multiple systems, specifically circulatory. Without appropriate steroid supplementation exogenously, patients can rapidly decline with adverse hypotension, altered mental status, and loss of vascular tone. This case presents a case of a patient who, after extensive chart review and history taking, was found to have had a complicated pregnancy many years ago with multiple transfusions needed to stabilize her and was placed on exogenous steroid management, presenting for adrenal crisis, hypotension, and altered mental status after not taking her home steroid medication.

Levetiracetam-Induced Rhabdomyolysis Following Medication Re-Initiation.

Rhabdomyolysis is a potentially life-threatening condition in which skeletal muscle breaks down, resulting in the release of myoglobin and creatine kinase (CK) in the blood; CK accumulation can lead to kidney failure and death. Several case reports have reported incidences of levetiracetam (LEV)-induced rhabdomyolysis. However, there are currently no reports of new-onset rhabdomyolysis after restarting LEV in a patient who previously tolerated the medication with no side effects. In this report, we present the case of a 35-year-old male who developed rhabdomyolysis after being restarted on LEV following a generalized tonic-clonic seizure. The patient was loaded with LEV 1 g IV and subsequently restarted on LEV 500 mg PO BID immediately after admission, from which time his serum CK level began to steadily rise to a maximum of 47,078 U/L despite aggressive intravenous hydration. LEV was discontinued on day five of admission when it was suspected to be the cause of the elevated CK levels in the absence of other contributing factors. The patient's CK level decreased to 35,635 U/L on day six of admission and continued to decrease before reaching 5,556 U/L at discharge. It is important to closely monitor serum CK in patients initiating or restarting LEV. Other antiepileptic medications should be considered if CK levels remain persistently elevated without other inciting factors.