Cerebral Salt Wasting

2017 ◽  
Author(s):  
Mark A. Henry ◽  
Avinash B. Kumar
Keyword(s):  
Serum Sodium ◽  
Extracellular Fluid ◽  
Cerebral Salt Wasting ◽  
Delivery Of Care ◽  
Salt Wasting ◽  
Neurological Illness ◽  
Assessment And Treatment ◽  
Life Threatening ◽  
Biochemical Level ◽  
Timely Delivery

Human survival (on a biochemical level) depends on the body’s critical ability to regulate the osmolality and salinity of extracellular fluid. When functioning in a normal state, the osmoregulatory system stringently maintains the serum sodium in a narrow range. Alterations in the serum sodium and water balance have significant and sometimes life-threatening impact on patients—especially when they occur in conjunction with serious intracranial pathology. This chapter, including the case discussion, illustrates the conundrum of hyponatremia and high urine output states complicating neurological illness. A thorough understanding of the pathophysiology, assessment, and treatment of these conditions is essential for the timely delivery of care and optimal patient outcomes.

scholarly journals Incidence of 1-lyponatraemia in Patients with lschemic Stroke: Our Experience at RMCH

2009 ◽  
Vol 22 (2) ◽  
pp. 212-215
Author(s):  
I Mahmood ◽  
MK Rahman ◽  
MMR Khan ◽  
MA Haque ◽  
MMH Chowdhury ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cohort Study ◽  
Ischemic Stroke ◽  
Clinical Evidence ◽  
Extracellular Fluid ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Electrolyte Disorder ◽  
Inappropriate Secretion

Hyponatraemia is a common electrolyte disorder in central nervous system (CNS) disease and is often attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). By contrast, there are patients with intracranial disease who develop hyponatraemia with similar characteristics, but differ in that there is clinical evidence of a contracted extracellular fluid (ECF) volume. This form of hyponatraemia is caused by excessive renal Na excretion, resulting from a centrally mediated process, and is termed cerebral salt wasting (CSW). Hyponatraemia, if acute that is developed within hours or days may cause confusion, coma restlessness or seizures. 72 patients with ischemic stroke admitted at RMCH were selected for this prospective cohort study. Among the subjects 34 (47.22%) cases were found to have hyponatraemia. The number was quite large and screening patients with stroke for electrolytes may be extremely helpful to reduce mortality and morbidity.TAJ 2009; 22(1): 212-215

Syndrome of alternating hypernatremia and hyponatremia after hypothalamic hamartoma surgery

2011 ◽  
Vol 30 (2) ◽  
pp. E6 ◽  
Author(s):  
Adib A. Abla ◽  
Scott D. Wait ◽  
Jonathan A. Forbes ◽  
Sandipan Pati ◽  
Roger E. Johnsonbaugh ◽  
...  
Keyword(s):  
Serum Sodium ◽  
Initial Period ◽  
Absolute Difference ◽  
Hypothalamic Hamartoma ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Patients Âgés ◽  
Type Iii ◽  
Type Iv ◽  
Total Type

Object In this paper, the authors' goal was to describe the occurrence of alternating hypernatremia and hyponatremia in pediatric patients who underwent resection of hypothalamic hamartomas (HHs) for epilepsy. Hypernatremia in patients after pituitary or hypothalamic surgery can be caused by diabetes insipidus (DI), whereas hyponatremia can occur due to a syndrome of inappropriate antidiuretic hormone, cerebral salt wasting, or excessive administration of desmopressin (DDAVP). The triphasic response after surgery in the pituitary region can also explain variations in sodium parameters in such cases. Methods One hundred fifty-three patients with HH who underwent surgery were enrolled in a prospective study to monitor outcomes. Of these, 4 patients (2.6%) were noted to experience dramatic alterations in serum sodium values. The medical records of these patients were identified and evaluated. Results Patients' ages at surgery ranged from 1.2 to 6.0 years. All patients were girls. Two patients had Delalande Type IV lesions (of 16 total Type IV lesions surgically treated) and 2 had Type III lesions (of 39 total Type III lesions). All patients had a history of gelastic seizures refractory to medication. Seizure frequency ranged from 3 to 300 per day. After surgery, all patients experienced hypernatremia and hyponatremia. The largest fluctuation in serum sodium concentration during hospitalization in a single patient was 53 mEq/L (range 123–176 mEq/L). The mean absolute difference in maximum and minimum sodium values was 38.2 mEq/L. All patients exhibited an initial period of immediate DI (independent of treatment) after surgery followed by a period of hyponatremia (independent of treatment), with a minimum value occurring between postoperative Days 5 and 8. All patients then returned to a hypernatremic state of DI, and 3 patients still require DDAVP for DI management. A second occurrence of hyponatremia lasting several days without DDAVP administration occurred in 2 patients during their hospitalization between periods of hypernatremia. One patient stabilized in the normal range of sodium values prior to discharge from rehabilitation without the need for further intervention. At last follow-up, 3 patients are seizure-free. Conclusions Severe instability of sodium homeostasis with hypernatremia and hyponatremia is seen in up to 2.6% of children undergoing open resection of HH. This risk appears to be related to HH type, with a higher risk for Types III (2 [5.1%] of 39) and IV (2 [12.5%] of 16) lesions. Here, the authors describe alternating episodes of hypernatremia and hyponatremia in the postoperative period following HH surgery. Management of this entity requires careful serial assessment of volume status and urine concentration and will often require alternating salt replacement therapy with DDAVP administration.

scholarly journals Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis

2019 ◽  
Vol 4 ◽  
pp. 189
Author(s):  
Usha K. Misra ◽  
Jayantee Kalita ◽  
Keyword(s):  
Natriuretic Peptide ◽  
Serum Sodium ◽  
Venous Pressure ◽  
Border Zone ◽  
Rapid Decline ◽  
Fluid Restriction ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Inappropriate Secretion ◽  
V2 Receptor

Hyponatremia is the commonest electrolyte abnormality in hospitalized patients and is associated with poor outcome. Hyponatremia is categorized on the basis of serum sodium into severe (< 120 mEq/L), moderate (120-129 mEq/L) and mild (130-134mEq/L) groups. Serum sodium has an important role in maintaining serum osmolality, which is maintained by the action of antidiuretic hormone (ADH) secreted from the posterior pituitary, and natriuretic peptides such as atrial natriuretic peptide and brain natriuretic peptide. These peptides act on kidney tubules via the renin angiotensin aldosterone system. Hyponatremia <120mEq/L or a rapid decline in serum sodium can result in neurological manifestations, ranging from confusion to coma and seizure. Cerebral salt wasting (CSW) and syndrome of inappropriate secretion of ADH (SIADH) are important causes of hyponatremia in tuberculosis meningitis (TBM). CSW is more common than SIADH. The differentiation between CSW and SIADH is important because treatment of one may be detrimental for the other; evidence of hypovolemia in CSW and euvolemia or hypervolemia in SIADH is used for differentiation. In addition, evidence of dehydration, polyuria, negative fluid balance as assessed by intake output chart, weight loss, laboratory evidence and sometimes central venous pressure are helpful in the diagnosis of these disorders. Volume contraction in CSW may be more protracted than hyponatremia and may contribute to border zone infarctions in TBM. Hyponatremia should be promptly and carefully treated by saline and oral salt, while 3% saline should be used in severe hyponatremia with coma and seizure. In refractory patients with hyponatremia, fludrocortisone helps in early normalization of serum sodium without affecting polyuria or functional outcome. In SIADH, V2 receptor antagonist conivaptan or tolvaptan may be used if the patient is not responding to fluid restriction. Fluid restriction in SIADH has not been found to be beneficial in TBM and should be avoided.

Distinguishing cerebral salt wasting syndrome and syndrome of inappropriate ADH in a patient with traumatic brain injury

2021 ◽  
Vol 14 (3) ◽  
pp. e237027
Author(s):  
Hassan Mohamed ◽  
George Shorten
Keyword(s):  
Serum Sodium ◽  
Road Traffic ◽  
Clinical Impression ◽  
Cerebral Salt Wasting Syndrome ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Wasting Syndrome ◽  
Conscious Level ◽  
Ct Brain ◽  
Salt Wasting Syndrome

A previously healthy 48-year-old woman was referred to our intensive care unit (ICU) from a neurosurgical ward due to deterioration of her conscious level. She had a road traffic accident 6 days earlier. On admission to the hospital, a brain CT demonstrated subarachnoid haemorrhage which was considered not amenable to surgical intervention. A second CT brain performed shortly after admission to ICU showed no change in comparison to the initial CT. Serum sodium level on ICU admission was 108 mEq/L; serum and urine osmolalities were 223 mOsm/kg and 438 mOsm/kg, respectively. Her hyponatraemia was initially attributed to syndrome of inappropriate antidiuretic hormone. However, a clinical impression of low volume status raised the suspicion of cerebral salt wasting syndrome. She was managed by infusion of hypertonic saline and fluids for 5 days and discharged from ICU after improvement of her conscious level and normalisation of serum sodium.

Diagnosis and Management of Sodium Disorders in the Neurosurgical Patient

2019 ◽  
pp. 156-174
Author(s):  
Jesse Edwards ◽  
Sharad Sharma ◽  
Rakesh Gulati
Keyword(s):  
Serum Sodium ◽  
Patient Population ◽  
Free Water ◽  
Diagnosis And Treatment ◽  
Fluid Shift ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Neurosurgical Patient ◽  
Neurosurgical Patients ◽  
Osmotic Demyelinating Syndrome

Sodium disorders are the most common electrolyte abnormality among hospitalized patients and even more common in the neurosurgical patient population. Timely diagnosis and careful correction of serum sodium is an essential skill for the neurosurgical hospitalist and may greatly mitigate the risk of significant harm to the patient. Water dysregulation is the primary feature of sodium abnormalities and may manifest as hyponatremia due to syndrome of inappropriate antidiuretic hormone (SIADH) secretion or hypernatremia due to central diabetes insipidus (DI). Therapy for the correction of serum sodium must take into consideration the etiology of dysregulation, unique risks associated with different neurologic pathologies, and the risk of osmotic fluid shift associated with fluctuations in serum sodium. Rapidly correcting sodium levels may lead to a variety of unintended sequelae, including osmotic demyelinating syndrome (ODS), cerebral edema, seizure, pulmonary edema, and death. Since neurosurgical patients are at elevated risk for severe morbidity due to osmotic fluid shift, it is crucial that neurosurgical hospitalists have a firm understanding of water and sodium pathophysiology, expertise in the diagnosis and treatment of sodium abnormalities, and nuanced appreciation for the risks and features unique to neurosurgical diseases. This chapter outlines the most common etiologies of sodium disorders in the neurosurgical patient population and offers recommendations for their diagnosis and treatment. Hyponatremia due to hypovolemia, cerebral salt wasting (CSW), SIADH, and adrenal insufficiency (AI) will be highlighted first, followed by hypernatremia due to free water deficit in the setting of central DI and inadequate oral fluid intake.

A method to estimate urinary electrolyte excretion in patients at risk for developing cerebral salt wasting

2001 ◽  
Vol 95 (3) ◽  
pp. 420-424 ◽  
Author(s):  
Ana P. C. P. Carlotti ◽  
Desmond Bohn ◽  
James T. Rutka ◽  
Sheila Singh ◽  
W. A. David Berry ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Extracellular Fluid ◽  
Mass Balances ◽  
Electrolyte Excretion ◽  
Cerebral Salt Wasting ◽  
Content Type ◽  
Salt Wasting ◽  
Prospective Comparison ◽  
Patients At Risk ◽  
Fine Print

Object. Two major criteria are necessary to diagnose cerebral salt wasting (CSW): a cerebral lesion and a large urinary excretion of Na+ and Cl− at a time when the extracellular fluid (ECF) volume is contracted. Nevertheless, it is difficult for the physician to confirm from bedside observation that a patient has a contracted ECF volume. Hyponatremia, although frequently present, should not be a criterion for a diagnosis of salt wasting. A contracted ECF volume is unlikely if there are positive balances of Na+ and Cl−. The goal of this study was to assess the accuracy of calculating balances for Na+ plus K+ and of Cl− over 1 to 10 days in an intensive care unit (ICU) setting. Methods. A prospective comparison of measured and estimated quantities of Na+ plus K+ and of Cl− excreted over 1 to 10 days in 10 children and 12 adults who had recently received a traumatic brain injury or undergone recent neurosurgery. Plasma concentrations of electrolytes were recorded at the beginning and end of the study period. The total volumes infused and excreted and the concentrations of Na+, K+, and Cl− in the infusate were obtained from each patient's ICU chart. The electrolytes in the patients' urine were measured and calculated. Correlations between measured and calculated values for excretions of Cl− and of Na+ plus K+ were excellent. Conclusions. Mass balances for Na+ plus K+ and for Cl− can be accurately estimated. These data provide information to support or refute a clinical diagnosis of CSW. The danger of relying on balances for these electrolytes measured within a single day to diagnose CSW is illustrated.

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

2017 ◽  
Vol 4 (6) ◽  
pp. 2217
Author(s):  
Kapil Bainade ◽  
V. Kotrashetti ◽  
Vijay Sonwane ◽  
Rizwan Ahmed ◽  
Prashant Abusaria
Keyword(s):  
Serum Sodium ◽  
Hormone Secretion ◽  
Final Diagnosis ◽  
Total Leukocyte Count ◽  
Fluid Restriction ◽  
Communicating Hydrocephalus ◽  
Cerebral Salt Wasting ◽  
Meningeal Enhancement ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting

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 in order to rule out syndrome of inappropriate antidiuretic hormone secretion (SIADH) but the patient did not respond to it. Keeping in view the above findings, a final diagnosis of tuberculous meningitis leading to cerebral salt wasting syndrome was made. The patient was started on anti-tuberculous therapy (ATT), IV Steroids, anticonvulsants, 3% NaCl and supportive treatment, to which she responded favourably and was later discharged. 

scholarly journals Cerebral Salt-Wasting Syndrome Caused by Minor Head Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-3 ◽  
Author(s):  
Toshiki Fukuoka ◽  
Yuko Tsurumi ◽  
Arihito Tsurumi
Keyword(s):  
Head Injury ◽  
Serum Sodium ◽  
Motor Vehicle ◽  
Skull Fracture ◽  
Minor Head Injury ◽  
Cerebral Salt Wasting Syndrome ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Wasting Syndrome ◽  
Salt Wasting Syndrome

A 34-year-old woman was admitted to hospital after sustaining a head injury in a motor vehicle accident (day 1). No signs of neurological deficit, skull fracture, brain contusion, or intracranial bleeding were evident. She was discharged without symptoms on day 4. However, headache and nausea worsened on day 8, at which time serum sodium level was noted to be 121 mEq/L. Treatment with sodium chloride was initiated, but serum sodium decreased to 116 mEq/L on day 9. Body weight decreased in proportion to the decrease in serum sodium. Cerebral salt-wasting syndrome was diagnosed. This case represents the first illustration of severe hyponatremia related to cerebral salt-wasting syndrome caused by a minor head injury.

scholarly journals Renal salt wasting syndrome in a patient with COVID-19; a case report and review of the literature

2020 ◽  
Vol 7 (1) ◽  
pp. e02-e02
Author(s):  
Bassam Al-Helal ◽  
Emad Abdallah ◽  
Altayyeb Yousef ◽  
Reem Asad ◽  
Mahmoud Reda
Keyword(s):  
Uric Acid ◽  
Serum Sodium ◽  
Hormone Secretion ◽  
Lower Limbs ◽  
Cerebral Salt Wasting ◽  
Cerebral Disease ◽  
Salt Wasting ◽  
Renal Salt Wasting ◽  
First Case ◽  
Disease Case

Introduction: Cerebral salt wasting or renal salt wasting (RSW) syndrome, may be more common than syndrome of inappropriate antidiuretic hormone secretion (SIADH) and may even occur in the absence of cerebral disease. We report a case of RSW in a Bangladeshi patient positive for COVID-19 without clinical cerebral disease. Case Presentation: A 53 years-old Bangladeshi patient presented with history of chest pain and acute MI. On examination, the patient was conscious, alert, vitally stable, chest with fine bilateral basal crepitation and heart with additional S3 sound and abdomen was lax with no organomegaly. There was no lower limbs oedema. His serum creatinine; 68 umol/L, urea; 3.4 mmol/L, K; 4.7 mmol/L, sodium; 135 mmol/L, uric acid; 141 mmol/L and phosphate was 1.3 mmol./L. Echocardiography (ECG) revealed anterior lateral wall STEMI. PCI was done for LAD. ECG revealed ejection fraction (EF) 10-15 %. Nasopharyngeal swab for COVID-19 was positive. Serum sodium decreased from 135 to 108 with signs of hypovolemia. Work up for hyponatremia revealed serum osmolality of 237 mOsm/kg, urine NA; 109 mmol/L, urine osmolality; 295 mOsm/kg, urine uric acid; 685 umol/L, and urine phosphate; 6.5 mmol/L. Additionally serum T3, T4, TSH and serum basal cortisol were normal. The patient received normal saline infusion and fludrocortisone and serum sodium increased to 134 mmol/L. Our patient had all the important clinical and laboratory characteristics of RSW in the absence of cerebral disease which include hyponatremia associated with hypovolemia, high urinary sodium excretion, increased fraction excretion of phosphate and persistent hypouricemia with increased fractional excretion of urate after correction of hyponatremia and with normal renal, adrenal and thyroid functions. Furthermore, there was a prompt response to saline replacement and fludrocortisone and steady improvement in serum sodium with negativity and improvement of COVID-19. Our diagnosis was RSW in the absence of cerebral disease and to our knowledge; this is the first case of RSW in a patient with COVID-19 in the literature. Conclusion: RSW should be considered in patients with COVID-19 with hyponatremia and absence of cerebral disease. We suggest changing cerebral salt wasting to the more appropriate term RSW.

scholarly journals EVALUATION OF SODIUM LEVELS IN CHILDRENS SUFFERED FROM PNEUMONIA IN HOSPITAL FROM BIHAR REGION

2018 ◽  
Author(s):  
Dr. Mohan Kejriwal ◽  
Dr. Ramjee Prasad Gupta ◽  
Dr. Alka Singh
Keyword(s):  
Serum Sodium ◽  
Sodium Level ◽  
Early Stage ◽  
Clinical History ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Medical College ◽  
Wasting Syndrome ◽  
Time Of Admission

Hyponatremia is the most common electrolyte abnormality. Patho physiologically, hyponatremia are classified into two groups: hyponatremia due to non-osmotic hypersecretion of vasopressin (hypovolemic, hypervolemic, euvolemic) and hyponatremia of non-hyper vasopressinemic origin (pseudo hyponatremia, water intoxication, cerebral salt wasting syndrome). The aim of this study was to identify the incidence of hyponatremia in children with pneumonia and to investigated whether there is a link between hyponatremia and the severity and outcome of pneumonia. The present study was planned on 25 children diagnosed with pneumonia in department of Paediatrics in Nalanda Medical College and Hospital, Patna, from March 2016 to Dec 2016.  At the time of admission, the patient’s clinical history was recorded in prefixed proforma. Serum sodium was measured by a process known as potentiometry. This method measures the voltage that develops between the inner and outer surfaces of an ion selective electrode. Based on the above findings it can be concluded that serum electrolytes should be measured in children hospitalized for pneumonia; the appropriate fluid therapy must be carefully arranged in children with hyponatremia, and both serum and urine sodium levels should be closely monitored. Regular follow up of serum sodium level during the period of hospital stay should be considered to pick up the high risk cases at an early stage. Keywords: pneumonia, sodium level, Hyponatremia, etc.

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