Trimethoprim-sulfamethoxazole-induced hyponatremia in an elderly lady with Achromobacter xylosoxidans pneumonia: Case report and insights into mechanism.

RATIONALE: Hyponatremia occurs frequently in the hospital setting and may be attributable to a host of etiologies. Drugs are frequently implicated. Trimethoprim-sulfamethoxazole (TMP/SMX) represents a well-recognized pharmacologic precipitant of drug-induced hyponatremia, with several reports extant in the retrievable literature. Nephrologists thus debate the mechanisms giving rise to TMP/SMX-induced hyponatremia and the precise mechanism by which treatment with TMP/SMX generates reductions of serum sodium concentration remain controversial. The agent has a well-known effect of antagonizing the effects of aldosterone upon the distal nephron. Renal salt wasting and the syndrome of inappropriate antidiuretic hormone secretion represent implicated mechanistic intermediaries in TMP/SMX-induced hyponatremia. PATIENT CONCERNS: The patient endorsed no explicit concerns. DIAGNOSES: We describe the case of an 83-year-old female clinically diagnosed with pneumonia found to have an initial serum sodium in the range of 130 to 134 mEq/L consistent with mild hyponatremia upon admission. Sputum cultures grew Achromobacter xylosoxidans susceptible to TMP/SMX. The patient's serum sodium concentration precipitously decline following institution of treatment with TMP/SMX to 112 to 114 mEq/L during the course of 5 days. INTERVENTIONS: Severe hyponatremia proved recalcitrant to initial therapy with supplemental salt tabs and standard doses of the vasopressin receptor antagonist tolvaptan. OUTCOMES: Escalating doses of tolvaptan increased the patient's sodium to 120 to 124 mEq/L. The patient was transferred to another hospital for further management. During her stay, the patient did not exhibit frank or obvious clinical features consistent with hyponatremia nor readily appreciable evidence of volume depletion. LESSONS: TMP/SMX represents a frequent, though underreported cause of hyponatremia in the hospital setting several authors believe natriuresis may represent the most common mechanism underlying TMP/SMX-induced hyponatremia. Evidence implicating natriuresis to be mechanistic in TMP/SMX-induced hyponatremia include clinically appreciable hypovolemia and resolution of hyponatremia with oral or intravenous salt repletion. Salt repletion failed to monotherapeutically enhance our patient's hyponatremiadisfavoring renal salt wasting as originately mechanistic. Contemporaneous refractoriness of serum sodium to fluid restriction nor standard doses of tolvaptan confounded our initial attempts to mechanistically attribute the patient's hyponatremia to a specific cause. Clinical euvolemia and rapid response of hyponatremia to exceptionally high doses of tolvaptan strongly favors syndrome of inappropriate antidiuretic hormone to represent the chief mechanism by which TMP/SMX exacerbates hyponatremia.

Spinal Intramedullary Tuberculosis with Concurrent Supra- and Infratentorial Intracranial Disease in a 9-Month-Old Boy: Case Report and Comprehensive Review of the Literature.

BACKGROUND: Tuberculous involvement of the spinal cord parenchyma is an exceedingly rare clinical entity; even more so is concurrent intracranial tuberculosis (TB). Spinal intramedullary TB presents with a characteristic subacute myelopathy, with slowly progressive paraplegia, sensory deficits, and/or bowel and bladder dysfunction. Diagnosis is strongly suspected with a clinical history of known TB in conjunction with characteristic findings on magnetic resonance imaging. Management involves multiagent antitubercular chemotherapy without or with operative intervention. CASE DESCRIPTION: We present a case of a 9-month-old boy with a retrospectively recognized history of pulmonary TB presenting with fever and back tenderness found to have lower-extremity hypertonia and clonus. Imaging revealed concurrent intracranial and spinal intramedullary tuberculomas. The patient was treated for hydrocephalus with external ventricular drainage followed by T8-T10 laminectomy, drainage of abscess, and duraplasty. Parietal lobe biopsies proved the tuberculous etiology of intracranial lesions. CONCLUSION: Etiopathogenesis, diagnosis, and management considerations of spinal intramedullary tuberculosis are reviewed and discussed.