Commentary.

Hypokalaemic paralysis secondary to thiazide diuretic abuse: an unexpected outcome for cauda equina syndrome

Cawley et al describe an interesting case of progressive leg weakness and urinary retention caused by severe hypokalemia. The neurological presentation somewhat mimicked cauda equina syndrome, although there was no back or leg pain and no saddle anesthesia.

On a cursory review of the literature, I could find no other cases of cauda equina syndrome caused by thiazide-induced hypokalemia. However, there is a recent report1 of a patient with lower extremity weakness, sensory disturbance, and intermittent urinary incontinence from Gitelman syndrome, which is a rare inherited defect in the distal convoluted tubule of the kidneys that manifests as hypochloremic metabolic alkalosis, hypokalemia, and hypocalciuria. People with Gitelman syndrome present with a metabolic profile almost identical to those treated with thiazide diuretics.2

It is important to remember that cauda equina syndrome has a wide differential diagnosis including compressive, ischemic, and/or inflammatory neuropathy of multiple lumbar and sacral nerve roots.3 The literature is rife with examples of unusual organic explanations for this clinical presentation, including transverse myelitis, vasculitis, spinal dural arteriovenous fistula, spinal ischemic stroke, inflammatory polyradiculopathy (autoimmune or infectious), and meningeal carcinomatosis (lymphomatous or metastatic).4

Although a structural cause, such as a large lumbar disc herniation, is important to rule out, Rooney et al5 reported that 48% of patients seen in the emergency department for cauda equina syndrome turned out to have no obvious structural abnormality on magnetic resonance imaging. While some patients had an alternate organic cause, most cases were “non-organic” (ie, functional) in nature.

The authors have provided a valuable contribution to the literature, not only because they made an astute diagnosis, saving a patient who was in a “pre-arrest” state to a full recovery but also by adding to the broader differential diagnosis of cauda equina syndrome.

Editorial Perspective

EBSJ thanks the authors for providing this fascinating case and reminding us of the bewildering variety of conditions that may present as spinal disorder. The commentary provided by Dr. Fourney underscores the rarity of this disorder and adds another variant to electrophysiological imbalance mimicking neurologic dysfunction with the description of Gitelman syndrome. While there remains strong hope for increasing cost efficiency in healthcare by more widespread use of care pathways in common conditions such as low back pain, cases like these remind us that there is no substitute for practicing good medicine when encountering each individual patient.