Serum sodium and osmolal changes in tuberculous meningitis (original) (raw)

The Impact of Hyponatremia on the Severity of Childhood Tuberculous Meningitis

Frontiers in Neurology, 2022

Introduction: Hyponatremia and/or hypoglycorrhachia are commonly encountered biochemical derangements during the acute stage of childhood tuberculous meningitis (TBM). Few studies have explored the correlation between these derangements and the staging of TBM disease (severity), or explored their role as biomarkers for vascular ischemic events, hydrocephalus, or seizures.Methods: We aimed to identify the prevalence and the correlation between serum hyponatremia (mild, moderate and severe) and/or hypoglycorrhachia in relation to clinical TBM features such as stage of disease, seizures and stroke in children diagnosed with definite and probable TBM, between 1985 and 2015, at Tygerberg Hospital, Cape town, South Africa.Results: The prevalence of hyponatremia was 344 out of 481 (71.5%) patients; 169 (49.1%) had mild hyponatremia, 146 (42.4%) moderate hyponatremia and 29 (8.4%) severe hyponatremia. Children with severe hyponatremia had higher frequency of stroke [odds ratio (OR) 4.36, 95...

Raised intracranial pressure, the syndrome of inappropriate antidiuretic hormone secretion, and arginine vasopressin in tuberculous meningitis

Child's Nervous System, 1993

Intracranial pressure (ICP) monitored shortly after admission over a period of 1 h in 31 children with tuberculous meningitis (TBM) was significantly higher (median 22.5 mmHg, range 8.4-50.9 mmHg) in 19 children with laboratory evidence of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) than in 12 children without such evidence (median 16.2 mmHg, range 5.8-42.5 mmHg; P=0.027). Neither plasma nor cerebrospinal fluid arginine vasopressin (AVP) was related to ICP (r= 0.33 and 0.13 respectively). Mean arterial pressure (MAP) was measured in 23 children and a moderate correlation was found with plasma AVP (r=0.62; P=0.0019). In TBM, plasma AVP may be secreted as a response to raised ICP in an effort to raise MAP and maintain cerebral perfusion pressure. In this setting excess fluid may be inappropriately retained, leading to hyponatremia and hypo-osmolemia.

Frequency of Hyponatremia in Tuberculous Meningitis Patients

Pakistan Journal of Medical and Health Sciences

Back Ground: A severe inflammation of the meninges is often referred to as meningitis. Hyponatremia has been associated with tuberculous meningitis in numerous studies. Objective: To assess the frequency of hyponatremia in tuberculous meningitis patients Methodology: This cross sectional study was carried out at the department of Neurology Bolan Medical Complex Hospital, Fatima Jinnah Institute of Chest Diseases and Sheikh Khalifa Bin Zayyed Al Nahyan Medical Complex Quetta for duration of one year from September 2021 to September 2022. All the required data like name, gender and presence or absence of hyponatremia were documented in a special proforma designed for this research. Data analysis was carried out by using SPSS version 23. Results: In our study, totally 210 patients were included. The male participants in our study were 94 (44.76%) while female participants were 116 (55.24%). The mean sodium level in serum was observed to be 133 with SD of ± 4.29. The overall frequency o...

Cerebral salt wasting in tuberculous meningitis: Two cases and review of the literature. Case Report

PubMed, 2015

Cerebral salt wasting syndrome (CSWS) is characterized by severe natriuresis and volume depletion in the presence of cerebral pathology. In literature, there are few reports about tuberculous meningitis and cerebral CSWS. In this article, we report two tuberculous meningitis cases with CSWS and present a review of the literature on this topic. Cerebral salt wasting diagnosis was based on hyponatraemia associated with high urinary sodium excretion and inappropriately high urine output in the presence of dehydration. Treatment was made with sodium-fluid replacement plus fludrocortisone therapy in both cases. In agreement with the literature we argue that cerebral salt wasting syndrome might be more common than the syndromes of inappropriate antidiuretic hormone secretion (SIADH) in cerebral disorders. Differentiating the cerebral salt wasting syndrome from the SIADH is very important because unrecognized cerebral salt wasting syndrome can lead to inadequate management and result in unnecessary hyponatremia-related morbidity. The electrolyte and hydration status of patients should be monitored closely in patients with tuberculous meningitis.

Syndrome of inappropriate secretion of antidiuretic hormone in tuberculous meningitis

Pediatric Nephrology

We describe the first reported case of a syndrome of inappropriate secretion of antidiuretic hormone (SIADH) induced by low-dose tacrolimus in a patient with autoimmune disease. A 41-year-old man with systemic lupus erythematosus (SLE) developed hyponatremia induced by SIADH after administration of tacrolimus (0.06 mg/kg per day). In this case, the hyponatremia promptly resolved upon withdrawal of tacrolimus. This case strongly suggests that SIADH is a potentially important complication of tacrolimus administration, irrespective of dosage, and should be borne in mind whenever the drug is used.

Cerebral salt wasting following tuberculous meningoencephalitis in an infant

2012

exclusively breast fed. Her father was receiving treatment for pulmonary tuberculosis. On admission, she was in Glasgow coma scale (GCS) of 5 (Eyes 1, Motor 2, Verbal 2). Her blood pressure was 90/60 mm Hg. Her weight was 4.9 kg and length was 57 cm (both below 5 th percentile for age and sex). Mild pallor was present. She demonstrated no cranial nerve palsy. There was hypertonia in all four limbs, brisk deep tendon reflexes, and absent abdominal reflex. There were no meningeal signs or involuntary movements. Systemic examination was normal. Investigations revealed: Hemoglobin 9.8 gm/dL, total leucocyte count 12300/cumm (neutrophils 60%, lymphocyte 40%), platelet count 2.1 lakh/cumm. Cerebrospinal fluid examination showed 360 cells (neutrophils 60%, lymphocytes 40%), protein 160 mg and sugar 38 mg/dL. Liver function, renal function tests, serum electrolytes, and serum calcium were normal. Urine output on the day of admission was 2.2 mL/kg/hour. Mantoux test was positive i.e. 24 mm. Magnetic resonance imaging of the brain was s/o tuberculous meningoencephalitis [Figure 1]. Intravenous fluids, intravenous mannitol, dexamethasone, and antituberculous therapy were started. There was no improvement in her sensorium. On the fifth day of admission, she developed hyponatremia, polyuria (8.6 mL/kg/hour), and hypotension [Table 1]. A diagnosis of CSWS was made on the basis of above investigations. Mannitol was discontinued. Fluid correction was given (volume-to-volume) with normal saline. Despite volume-to-volume correction with normal saline, the serum sodium dropped to 108 mEq/L on the seventh day. Urine output was 17 mL/kg/hour and urinary sodium 190 mEq/L. Hence, sodium correction with 3% saline and fludrocortisone (0.1 mg/day) were started on the seventh day. Fludrocortisone

Cerebral salt wasting in tuberculous meningitis: treatment with fludrocortisone

Annals of Tropical Paediatrics, 2005

Three cases of cerebral salt wasting complicating tuberculous meningitis are described. Diagnosis was based on hyponatraemia associated with high urinary sodium excretion and inappropriately high urine output in the presence of dehydration. Treatment with fludrocortisone resulted in sodium and fluid homeostasis.

Cerebral salt wasting in a case of tubercular meningitis in a child

International Journal of Contemporary Pediatrics, 2017

A 12-year-old female child presented with fever, headache, vomiting since 20 days and convulsions for 1 day. She was unimmunised and BCG scar was absent. Clinical examination showed signs of meningeal irritation, Kernigs sign and Brudzinkins sign with signs of raised intracranial tension. Fundus examination was suggestive of stage 2 papilledema. Her laboratory reports were normal on admission. LP was with hold in view of raised ICT. CT brain was done. S/O meningeal enhancement, mild communicating hydrocephalus with periventricular ooze, extra axial hyper densities in bilateral sylvian fissures along the tentorium (Basal Exudates) On day 3 of admission she had low serum sodium, serum osmolality High urinary sodium. While on lumbar puncture (LP) and cerebrospinal fluid (CSF) examination, CSF protein, and total leukocyte count (predominant lymphocytes) were all increased. On his 5th day of admission, her serum sodium was low and he had a normal urine output. Fluid restriction was tried...