Rajesh K Singh

A study of hyponatremia in tuberculous meningitis.

SETTING In view of paucity of studies on predictors of hyponatremia in tuberculous meningitis (TBM) and its influence on outcome, this study was undertaken. OBJECTIVE To study the frequency, predictors and prognosis of hyponatremia in TBM. DESIGN In this prospective hospital based study, 76 patients with TBM (definite 18 and probable 58) were enrolled. The severity of meningitis was graded as I-III and hyponatremia as severe (<120mEq/L), moderate (120-129mEq/L) or mild (130-134mEq/L). Hospital death was noted and functional outcome was assessed by modified Rankin Scale (mRS) on discharge. RESULTS 34 (44.7%) TBM patients had hyponatremia (mild 3, moderate 23 and severe 8). Hyponatremia was due to cerebral salt wasting in 17, syndrome of inappropriate secretion of antidiuretic hormone in 3 and miscellaneous causes in 14 patients. Hyponatremia was related to GCS score and basal exudates. Outcome of TBM was related to duration of hospitalization, GCS score, focal deficit, mechanical ventilation, severity of TBM, age and comorbidities. Cerebral salt wasting was related to severity of TBM. CONCLUSION Hyponatremia occurred in 44.7% of TBM patients. Cerebral salt wasting was the commonest cause of hyponatremia and was related to the severity of TBM.

Cerebral Salt Wasting Is the Most Common Cause of Hyponatremia in Stroke

OBJECTIVE The study aimed to evaluate the frequency, severity, and causes of hyponatremia in stroke and its influence on outcome. MATERIALS AND METHODS Consecutive computed tomography- or magnetic resonance imaging-proven stroke patients within 7 days of stroke were included. Severity of stroke was assessed using the National Institute of Health Stroke Scale and consciousness using the Glasgow Coma Scale. Hyponatremia was defined if 2 consecutive serum sodium levels were <135 mEq/L and hypernatremia if >145 mEq/L. Causes of hyponatremia, such as cerebral salt wasting (CSW) and syndrome of inappropriate secretion of antidiuretic hormone (SIADH), were based on predefined criteria. Patients with CSW were managed by salt supplementation and normal saline, and fludrocortisone was used in refractory cases. In SIADH, fluid was restricted. Outcome on discharge was defined using the modified Rankin Scale (mRS). RESULTS One hundred patients with stroke were included: 47% had ischemic stroke and 53% had intracerebral hemorrhage. Forty-three percent of the patients had hyponatremia, 6% had hypernatremia, and 4% had both. Hyponatremia was due to CSW in 19 (44.2%), SIADH in 3 (7%), miscellaneous causes in 14 (32.6%), and indeterminate in 7 (16.3%) patients. Duration of hospitalization was the independent predictor of hyponatremia and CSW. Fourteen patients died, whereas 15 had good outcome (mRS score of ≤2) and 71 had poor outcome (mRS score of 3-5). Hypernatremia was associated with high mortality compared with eunatremia and hyponatremia. CONCLUSION Hyponatremia occurred in 43% of stroke patients. CSW was the most common cause of hyponatremia. Hyponatremia, however, was not related to death or disability.

Multidrug-resistant Acinetobacter meningitis treated by intrathecal colistin

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Cerebral Venous Sinus Thrombosis Presenting Feature of Systemic Lupus Erythematosus

BACKGROUND CVST (cerebral venous sinus thrombosis) may sometimes be associated with autoimmune disorders that require specific treatment. The clinical and magnetic resonance imaging (MRI) findings of systemic lupus erythematosus (SLE) patients with CVST are presented and contrasted with CVST without SLE. METHODS Consecutive patients with CVST admitted in neurology service during 2012-2016 were included. The diagnosis of CVST was confirmed by MR venography or digital subtraction angiography. SLE was diagnosed according to American College of Rheumatology criteria. The clinical and MRI findings of CVST with SLE and those without SLE were compared. RESULTS Forty-three consecutive patients with CVST were included during the study period, 3 of whom had SLE .Their age ranged between 20 and 35 years and all were females. The clinical markers of SLE were present in all and included oral ulceration in 3 patients, serositis in 2 patients, and arthritis and psychosis in 1 patient. The SLE patients did not have antiphospholipid antibodies or lupus anticoagulant. The manifestation of CVST in SLE was similar to the other patients with CVST. The CVST in SLE required long-term anticoagulation and immunosuppression with cyclophosphamide pulse in 1 patient and oral prednisolone in 2 patients. The outcome was good, partial, and poor in 1 patient each. CONCLUSIONS CVST may be the presenting feature of SLE, but these patients often have clinical clues to SLE. These patients need prolonged anticoagulation and immunosuppression.

A Study of Hyponatremia in Acute Encephalitis Syndrome: A Prospective Study From a Tertiary Care Center in India

Purpose: To evaluate the frequency and causes of hyponatremia in acute encephalitis syndrome (AES) and its effect on outcome. Patients and Methods: Consecutive patients with AES were subjected to neurological evaluation including Glasgow Coma Scale, focal weakness, movement disorder, and reflex changes. The etiology of AES was based on blood and cerebrospinal fluid enzyme-linked immunosorbent assay and polymerase chain reaction. We have categorized patients into neurological or systemic AES. Hyponatremia was diagnosed if 2 consecutive serum sodium levels were below 135 mEq/L, 24 hours apart. Serum and urinary osmolality and electrolytes were measured on alternate days. Fluid intake, output, and body weight were measured daily. The hyponatremia was categorized into syndrome of inappropriate secretion of antidiuretic hormone (SIADH), cerebral salt wasting (CSW), or miscellaneous group. Outcome at 1 month was assessed by modified Rankin scale. Results: Of 79 patients, 34 had neurologic AES and 45 had systemic AES; 22 (27.8%) patients had hyponatremia. The neurologic AES as compared to systemic AES was more commonly associated with hyponatremia (38.2% vs 20%, P = .07), need longer hospitalization (25.0 vs 12.5 days, P = .003), and longer time for sodium correction (13.3 vs 8.2 days, P = .05). The hyponatremia was due to CSW in 12 patients, SIADH in 2 patients, and indeterminate in 8 patients. Thirty-six patients had poor outcome (15 died) and 43 had good outcome which was not related to hyponatremia. Conclusion: Hyponatremia occurs in one-third of patients with AES, being commoner in neurologic AES, and CSW is the commonest cause.