A Case of Hypokalemic Paralysis in a Patient With Neurogenic Diabetes Insipidus

Abstract

Acute hypokalemic paralysis is characterized by muscle weakness or paralysis secondary to low serum potassium levels. Neurogenic diabetes insipidus (DI) is a condition where the patient excretes large volume of dilute urine due to low levels of antidiuretic hormone. Here, we describe a patient with neurogenic DI who developed hypokalemic paralysis without a prior history of periodic paralysis. A 30-year-old right-handed Hispanic male was admitted for refractory seizures and acute DI after developing a dental abscess. He had a history of pituitary adenoma resection at the age of 13 with subsequent pan-hypopituitarism and was noncompliant with hormonal supplementation. On hospital day 3, he developed sudden onset of quadriplegia with motor strength of 0 of 5 in the upper extremities bilaterally and 1 of 5 in both lower extremities with absent deep tendon reflexes. His routine laboratory studies revealed severe hypokalemia of 1.6 mEq/dL. Nerve Conduction Study (NCS) revealed absent compound motor action potentials (CMAPs) with normal sensory potentials. Electromyography (EMG) did not reveal any abnormal insertional or spontaneous activity. He regained full strength within 36 hours following aggressive correction of the hypokalemia. Repeat NCS showed return of CMAPs in all nerves tested and EMG revealed normal motor units and normal recruitment without myotonic discharges. In patients with central DI with polyuria, hypokalemia can result in sudden paralysis. Hypokalemic paralysis remains an important differential in an acute case of paralysis and early recognition and appropriate management is key. Keywords hypokalemia, paralysis, diabetes insipidus Case ReportA 30-year-old Hispanic male with a history of pituitary adenoma resection at the age of 13, with subsequent pan-hypopituitarism, epilepsy, and medication noncompliance was admitted with seizures and acute diabetes insipidus (DI). During the hospitalization, he remained seizure free on levetiracetam 1 g q12H and was treated with appropriate antibiotics for a dental abscess. He was initiated on a stress dose steroid taper, restarted on hormone replacement and desmopressin replacement therapy for DI.The patient's initial hospital stay was without complication until hospital day 3 when a dose of desmopressin acetate (DDAVP) was delayed, and he developed acute quadriplegia. Magnetic resonance imaging (MRI) brain and computed tomography (CT) brain did not reveal any acute abnormalities. Routine laboratory studies were notable for acute hypokalemia from 3.8 to 1.6 mEq/dL (Table 1), which he developed over 12 hours. His thyroid studies were suggestive of secondary hypothyroidism with low thyroid-stimulating hormone level, free T3, total T3 level, and normal free T4 level (Table 1).On examination, he was afebrile and in no apparent distress. He was fully oriented with intact cranial nerves. Muscle strength was 0 of 5 in the bilateral upper extremities, 0 of 5 in the proximal lower extremities, and 1 of 5 in the distal lower extremities. Sensory evaluation of la...

Effects of the Experiment Conditions on the Nerve Action Potential: A Model Study

“…Interestingly, not only the potassium channel conductivity but also sodium channel conductivity has found to be effected from this conduction. In agreement with the current literature extracellular potassium concentration restriction is important, if not results in many problems such as nerve dysfunction or paralysis [20,21].…”

Diverse phenotype of hypokalaemic periodic paralysis within a family

“…Episodic flaccid weakness occurs based on the concentration of extracellular potassium ions, which are decisive for membrane excitability 1. Acquired causes include renal tubular acidosis, diabetes insipidus,4 coeliac disease5 and thyrotoxicosis6 and these should be ruled out. We describe a case presenting with late-onset myopathy and various phenotypes in the same family with a heterozygous pathogenic mutation in CACNA1S gene (figure 1 shows the pedigree).…”

A case of acute areflexic, flaccid quadriplegia resulting from acute hypophysitis

“…Although further testing on plasma and urine osmolalities could have been performed, such as the water deprivation test or the desmopressin challenge test, our patient's severe hypernatremia precluded such assessments. The use of desmopressin was essential for the alleviation of weakness [18], which was demonstrated by our case; the delay in diagnosis and treatment with desmopressin led to the worsening of her condition and ultimately required the use of ventilatory support. Panhypopituitarism with hypokalemic paralysis and neurogenic diabetes insipidus is rare [18].…”

“…The use of desmopressin was essential for the alleviation of weakness [18], which was demonstrated by our case; the delay in diagnosis and treatment with desmopressin led to the worsening of her condition and ultimately required the use of ventilatory support. Panhypopituitarism with hypokalemic paralysis and neurogenic diabetes insipidus is rare [18]. From the observation of an enlarged pituitary gland with a thickening of the pituitary stalk found on MRI, one can postulate a diagnosis of acute hypophysitis in the absence of other causative factors [19,20]; however, a transsphenoidal biopsy remains the best method for the diagnosis of hypophysitis [19,21].…”