Risk factors for hepatic encephalopathy in patients with cirrhosis and refractory ascites: relevance of serum sodium concentration

2010 ◽  
Vol 30 (8) ◽  
pp. 1137-1142 ◽  
Author(s):  
Mónica Guevara ◽  
María E. Baccaro ◽  
Jose Ríos ◽  
Marta Martín-Llahí ◽  
Juan Uriz ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatic Encephalopathy ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Refractory Ascites

Case Report of SIADH Associated With Escitalopram Use

2009 ◽  
Vol 22 (6) ◽  
pp. 594-599 ◽  
Author(s):  
Renee R. Koski ◽  
Jill A. Covyeou ◽  
Michelle Morissette
Keyword(s):  
Risk Factors ◽  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Case Reports ◽  
Treatment Options ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
White Female ◽  
Fluid Restriction

The authors report a case of syndrome of inappropriate antidiuretic hormone (SIADH) associated with the use of escitalopram in an elderly female patient. A 97-year-old white female was admitted to the hospital for a suspected vertebral fracture and hyponatremia. Her serum sodium concentration was 113 mEq/L (113 mmol/L) at admission. She was started on escitalopram 5 mg daily 1 week prior to admission for anxiety. During admission, her laboratory tests revealed serum hyponatremia and hypo-osmolality and urine hyperosmolality and hypernatremia. Her escitalopram was stopped, and she was diagnosed with syndrome of inappropriate antidiuretic hormone. She was treated with hypertonic (3%) saline. She was discharged 1 week later with a serum sodium concentration of 121 mEq/L (121 mmol/L). There have been hundreds of case reports of SIADH associated with selective serotonin reuptake inhibitors (SSRIs), including 5 cases associating escitalopram with syndrome of inappropriate antidiuretic hormone. The median time to onset of SIADH after initiating SSRIs is approximately 2 weeks. Risk factors include advanced age, concomitant diuretic use, low baseline sodium, and low body mass index. Treatment options include fluid restriction, normal saline, diuretics, hypertonic saline, and discontinuing the SSRI. The authors conclude that elderly patients receiving escitalopram or other SSRIs should be monitored carefully for SIADH in the first couple of weeks of treatment and with dose increases, especially if other risk factors are present.

scholarly journals Correlation of Serum Sodium with Severity of Hepatic Encephalopathy

2016 ◽  
Vol 3 (01) ◽  
pp. 3-10
Author(s):  
Muhammad Arshad ◽  
Shah Zeb ◽  
Muhammad Atif Tauseef ◽  
Najeeb Ullah
Keyword(s):  
Hepatic Encephalopathy ◽  
Serum Sodium ◽  
Sodium Level ◽  
Serum Sodium Level ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Common Finding ◽  
Decompensated Cirrhosis ◽  
Grade Ii ◽  
Grade Iii

INTRODUCTIONHepatic encephalopathy (HE) is neuropsychiatric syndrome for which symptoms, manifested on a continuum, is deterioration in mental status, with psychomotor dysfunction, impaired memory, increase reaction time, poor concentration, disorientation, and in severe form coma and may develop at an annual rate of 8% in cirrhotic patients in Far Eastern studies. Fluctuation in serum sodium level is a frequent complication of advanced cirrhosis related to impairment in the renal capacity to eliminate solute-free water that causes retention of water that is disproportionate to the retention of sodium, thus causing a reduction in serum sodium concentration and hypo-osmolality. Hyponatremia is a common finding in patients with decompensated cirrhosis due to an abnormal regulation of body fluid homeostasis.OBJECTIVETo determine the correlation of serum sodium with severity of hepatic encephalopathyMATERIAL AND METHODSThis study was conducted at Naseer Teaching Hospital Peshawar. Duration of the study was 01 year and the study design was cross sectional (Correlation) study in which a total of 408 patients were observed by using – 0.1411 of correlation coefficient between serum sodium and hepatic encephalopathy 95% confidence level and 80% power of test. More over non probability consecutive sampling was used for sample collection.RESULTSIn this study mean age was 65 years with SD ± 0.315. Sixty two percent patients were male and 38% patients were female. Mean serum sodium level was 123 meq/L with SD ± 0.21. Five percent patients had severity of grade I, 39% patients had severity of grade II, 48% patients had severity of grade III and 8% patients had severity of grade IV. Correlation of severity of hepatic encephalopathy with serum sodium level was analyzed as all the 20 patients with severity of grade I had serum sodium level ranged 131-133 meq/L. All the 159 patients with severity of grade II had serum sodium level ranged 126-130 meq/L. In 196 patients with severity of grade III, 45 patients had serum sodium level ranged 126-130 meq/L while 151 patients had serum sodium level ranged 120-125 meq/L where as all the 33 patients with severity of grade IV had serum sodium level ranged 120-125 meq/L.CONCLUSIONHyponatremia was a common feature in patients with cirrhosis and its severity increased with the severity of liver disease. The existence of serum sodium concentration < 135 mmol/L was associated with greater frequency of hepatic encephalopathy. It was also noticed that more severe the hyponatremia, greater will be the grade of hepatic encephalopathy. Close monitoring of serum sodium concentration should be performed in patients with cirrhosis in order to prevent the rapid development of cirrhosis related complications.

Serum Sodium Concentration Changes Are Related to Fluid Balance and Sweat Sodium Loss

2010 ◽  
Vol 42 (9) ◽  
pp. 1669-1674 ◽  
Author(s):  
MATTHEW D. PAHNKE ◽  
JOEL D. TRINITY ◽  
JEFFREY J. ZACHWIEJA ◽  
JOHN R. STOFAN ◽  
W. DOUGLAS HILLER ◽  
...  
Keyword(s):  
Fluid Balance ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Concentration Changes ◽  
Sodium Loss ◽  
Sweat Sodium

Disorders of Water Balance

2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress
Keyword(s):  
Water Balance ◽  
Water Intake ◽  
Serum Sodium ◽  
Water Conservation ◽  
Free Water ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Water Losses ◽  
Water Excretion ◽  
Impaired Water

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.

scholarly journals Hyperosmolar Non-Ketotic Diabetic Coma — Less Sodium in Therapy?

1980 ◽  
Vol 8 (3) ◽  
pp. 349-352 ◽  
Author(s):  
Luen Bik To ◽  
P. J. Phillips
Keyword(s):  
Older Women ◽  
Water Deficit ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Diabetic Coma ◽  
Factors Affecting ◽  
Serum Osmolarity

Eighteen patients with hyperosmolar non-ketotic diabetic coma were studied retrospectively to identify factors affecting prognosis and to review treatment. This condition affected older women two-thirds of whom were unrecognised diabetics. Eight (44%) died. Mortality correlated with age above 60, uraemia and hyperosmolarity, but not with the degree or rate of fall of hyperglycaemia. Hyperglycaemia responded to rehydration and insulin, but in all patients serum osmolarity remained high for several days. In 14 patients (78%) the serum sodium concentration initially increased and in four (22 %) serum osmolarity increased. This persistence or worsening of the hyperosmolar state can be avoided without the risk of cerebal oedema by replacing the fluid and electrolyte deficits over 48 hours and using 5% dextrose for the water deficit.

scholarly journals Syndrome of Inappropriate Secretion of Antidiuretic Hormone due to Selective Serotonin Reuptake Inhibitors After Pancreaticoduodenectomy for Carcinoma of the Ampulla of Vater: Case Report

2013 ◽  
Vol 98 (4) ◽  
pp. 289-291
Author(s):  
Ryota Iwase ◽  
Hiroaki Shiba ◽  
Takeshi Gocho ◽  
Yasuro Futagawa ◽  
Shigeki Wakiyama ◽  
...  
Keyword(s):  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Ampulla Of Vater ◽  
Serum Sodium Concentration ◽  
Selective Serotonin ◽  
Inappropriate Secretion

Abstract A 68-year-old man underwent pancreaticoduodenectomy with lymph nodes dissection for carcinoma of the ampulla of Vater. The patient had anxiety neurosis and had been treated with a selective serotonin reuptake inhibitor (SSRI). Postoperatively, SSRI was resumed on postoperative day 2. His serum sodium concentration gradually decreased, and the patient was given a sodium supplement. However, 11 days after the operation, laboratory findings included serum sodium concentration of 117 mEq/L, serum vasopressin of 2.0 pg/mL, plasma osmolality of 238 mOsm/kg, urine osmolality of 645 mOsm/kg, urine sodium concentration of 66 mEq/L, serum creatinine concentration of 0.54 mg/dL, and serum cortisol concentration of 29.1 μg/dL. With a diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH), the antianxiety neurosis medication was changed from the SSRI to another type of drug. After switching the medication, the patient made a satisfactory recovery with normalization of serum sodium by postoperative day 20.

Delayed postoperative hyponatremia after transsphenoidal surgery: prevalence and associated factors

2013 ◽  
Vol 119 (6) ◽  
pp. 1453-1460 ◽  
Author(s):  
Namath S. Hussain ◽  
Mackenzie Piper ◽  
W. Grant Ludlam ◽  
William H. Ludlam ◽  
Cindy J. Fuller ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Serum Sodium ◽  
Transsphenoidal Surgery ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Fisher Exact Test ◽  
Inverse Association ◽  
Large Patient ◽  
Low Bmi ◽  
Postoperative Hyponatremia

Object Transient delayed postoperative hyponatremia (DPH) after transsphenoidal surgery (TSS) is common and can have potentially devastating consequences. However, the true prevalence of transient symptomatic and asymptomatic DPH has not been studied in a large patient cohort with close and accurate follow-up. Methods A retrospective analysis of a single-institution prospective database was conducted; all patients undergoing TSS for lesions involving the pituitary gland were followed up in a multidisciplinary neuroendocrine clinic, and demographic, imaging, and clinical data were prospectively collected. Patients were examined preoperatively and followed up postoperatively in a standardized fashion, and their postoperative sodium levels were measured at Weeks 1 and 2 postoperatively. Levels of hyponatremia were rated as mild (serum sodium concentration 130–134 mEq/L), moderate (125–129 mEq/L), or severe (< 125 mEq/L). Routine clinical questionnaires were administered at all postoperative office visits. Postoperative hyponatremia was analyzed for correlations with demographic and clinical features and with immediate postoperative physiological characteristics. Results Over a 4-year interval, 373 procedures were performed in 339 patients who underwent TSS for sellar and parasellar lesions involving the pituitary gland. The mean (± SD) age of patients was 48 ± 18 years; 61.3% of the patients were female and 46.1% were obese (defined as a body mass index [BMI] ≥ 30). The overall prevalence of DPH within the first 30 days postoperatively was 15.0%; 7.2% of the patients had mild, 3.8% moderate, and 3.8% severe hyponatremia. The incidence of symptomatic hyponatremia requiring hospitalization was 6.4%. The Fisher exact test detected a statistically significant association of DPH with female sex (p = 0.027) and a low BMI (p = 0.001). Spearman rank correlation detected a statistically significant association between BMI and nadir serum sodium concentration (r = 0.158, p = 0.002) and an inverse association for age (r = −0.113, p = 0.031). Multivariate analyses revealed a positive correlation between postoperative hyponatremia and a low BMI and a trend toward association with age; there were no associations between other preoperative demographic or perioperative risk factors, including immediate postoperative alterations in serum sodium concentration. Patients were treated with standardized protocols for hyponatremia, and DPH was not associated with permanent morbidity or mortality. Conclusions Delayed postoperative hyponatremia was a common result of TSS; a low BMI was the only clear predictor of which patients will develop DPH. Alterations in immediate postoperative sodium levels did not predict DPH. Therefore, an appropriate index of suspicion and close postoperative monitoring of serum sodium concentration should be maintained for these patients, and an appropriate treatment should be undertaken when hyponatremia is identified.

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