Oxcarbazepine for trigeminal neuralgia may induce lower extremity weakness: A case report

BACKGROUND Although few studies have reported hyponatremia due to carbamazepine or oxcarbazepine in patients with epilepsy,no study has investigated cases of carbamazepine-or oxcarbazepine-induced hyponatremia or unsteady gait in patients with neuropathic pain.Herein,we report a case of oxcarbazepineinduced lower leg weakness in a patient with trigeminal neuralgia and summarize the diagnosis,treatment,and changes of clinical symptoms.CASE SUMMARY A 78-year-old male with a history of lumbar spinal stenosis was admitted to the hospital after he experienced lancinating pain around his right cheek,eyes,and lip,and was diagnosed with trigeminal neuralgia at the right maxillary and mandibular branch.He was prescribed oxcarbazepine(600 mg/d),milnacipran(25 mg/d),and oxycodone/naloxone(20 mg/10 mg/d)for four years.Four years later,the patient experienced symptoms associated with spinal stenosis,including pain in the lower extremities and unsteady gait.His serum sodium level was 127 mmol/L.Assuming oxcarbazepine to be the cause of the hyponatremia,oxcarbazepine administration was put on hold and the patient was switched to topiramate.At subsequent visit,the patient’s serum sodium level had normalized to 143 mmol/L and his unsteady gait had improved.CONCLUSION Oxcarbazepine-induced hyponatremia may cause lower extremity weakness and unsteady gait,which should be differentiated from those caused by spinal stenosis.     

Angiotensin-converting enzyme inhibitor-induced syndrome of inappropriate secretion of antidiuretic hormone: case report and review of the literature

Seventeen cases of severe hyponatremia induced by angiotensin-converting enzyme (ACE) inhibitor therapy have been reported in the literature. The mechanism of severe hyponatremia induced by ACE inhibitor is not clear. A 60-year-old white man with a history of idiopathic dilated cardiomyopathy was treated with enalapril, 20 mg daily, that had been started 2 weeks before heart transplantation. The serum sodium level was 138 mmol/L before initiation of enalapril therapy and 127 mmol/L just before cardiac surgery. In the post-heart transplantation period, enalapril therapy was withdrawn for the perianesthesia period, and the serum sodium level increased from 127 to 140 mmol/L. One month later, viral myocarditis developed in the patient and enalapril was reintroduced at 20 mg daily. Two weeks later, natremia decreased. Enalapril was discontinued. Three days later the serum sodium level rose to 140 mmol/L. Severe symptomatic hyponatremia induced by the syndrome of inappropriate secretion of antidiuretic hormone should be considered a rare but possible complication associated with ACE inhibitor therapy.     

Management of hyponatremic seizures in children with hypertonic saline: a safe and effective strategy

OBJECTIVE: To study efficacy and safety of hypertonic saline administration in the management of hyponatremic seizures. DESIGN: Retrospective, observational, cross-sectional study with factorial design. SETTING: In-patient population in a university hospital. PATIENTS: All children admitted with serum sodium concentrations less than 125 mmol/L. Sixty-nine episodes of severe hyponatremia in 60 children were reviewed. Forty-one of these children presented with seizures. INTERVENTIONS: Twenty-five of 41 seizure patients received an iv bolus of 4 to 6 mL/kg body weight of 3% saline. Twenty-eight patients were treated with a benzodiazepine and/or phenobarbital with or without the subsequent administration of hypertonic saline. MEASUREMENTS AND MAIN RESULTS: Thirteen treatment failures and ten instances of apnea occurred among the 28 patients treated with benzodiazepine/phenobarbital. Administration of hypertonic saline resulted in resolution of seizures and apnea in all cases. Those patients receiving 3% saline had a higher serum sodium increase rate from 0 to 4 hrs than the remaining patients (3.1 +/- 1.3 vs. 1.7 +/- 1.2 mmol/L.hr, p less than .01). None developed subsequent neurologic deterioration or clinical manifestations of osmotic demyelination syndrome. CONCLUSION: Treatment of hyponatremic seizures with routine anticonvulsants may be ineffective and is associated with a considerable incidence of apnea. A rapid increase in the serum sodium concentration by 3 to 5 mmol/L with the use of hypertonic saline is safe and efficacious in managing acute symptomatic hyponatremia.     

The management of hyponatremic emergencies

Given time, the brain can tolerate extraordinarily severe hyponatremia, but it does not take well to sudden changes; both rapid onset and rapid correction of hyponatremia can be injurious. Emergency treatment of hyponatremia should be reserved for the patient who has not had time to fully adapt to the disturbance. When the clinical situation demands it, treatment can be safely initiated by infusing 3% saline at 1 to 2 mL/kg/hour for 2 to 3 hours. Once the emergency has passed, more conservative measures can be substituted so that the overall rate of correction does not exceed 12 mEq/L/day. Limiting therapy in this manner avoids the osmotic demyelination syndrome, a complication of overly rapid correction of hyponatremia.     

Citalopram-associated SIADH

OBJECTIVE: To report a case of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with use of citalopram in an elderly male patient and to review the English-language literature for any previous reports of SIADH or hyponatremia caused by citalopram. CASE SUMMARY: An 87-year-old Filipino man was admitted to the hospital reporting malaise, confusion, dizziness, and falls approximately 3 weeks following an increase in his citalopram dosage from 10 to 20 mg/d. On physical examination, the patient was euvolemic and had no evidence of malignancy, cardiac, renal, or hepatic disease. Pertinent laboratory test results revealed hyponatremia, serum hypoosmolality, urine hyperosmolality, and elevated urine sodium concentration, leading to a diagnosis of SIADH. Citalopram was discontinued and fluid restrictions were instituted. The patient was discharged after his serum sodium increased from 122 to 128 mEq/L and he reported increased strength and decreased confusion. Five days after discharge, the patient denied experiencing any new falls, weakness, confusion, or lethargy. His serum sodium measured that day was 131 mEq/L; 2 months later, it was 135 mEq/L. DISCUSSION: We report the seventh case of citalopram-induced hyponatremia published in the English language and the second in a man. Review of the cases demonstrated that the onset of citalopram-induced hyponatremia or SIADH ranged from 6 to 20 days. Potential risk factors for SIADH due to citalopram included advanced age, female gender, concomitant use of medications known to cause SIADH or hyponatremia, and, possibly, higher citalopram doses. CONCLUSIONS: Elderly patients receiving citalopram should be monitored for signs and symptoms of SIADH, especially in the first few weeks of therapy, in the presence of risk factors, and during dose escalation.     

Ten pitfalls in the proper management of patients with hyponatremia

Hyponatremia (serum sodium <135 mEq/L) is a common electrolyte disorder in community or hospitalized patients. Serum sodium levels should be corrected at a proper rate in patients with hyponatremia, since overcorrection of serum sodium levels is related to devastating neurologic consequences, such as the osmotic demyelination syndrome (ODS). However, a number of pitfalls, which could lead to undercorrection or overcorrection of hyponatremia, are common during the treatment of hyponatremic patients. Hereby, we describe ten common pitfalls that are observed during the correction of serum sodium concentration in hyponatremic patients. These refer to pitfalls in the goals and limits of the correction rate of serum sodium, pitfalls in the means (e.g. solutions but also drugs) and formulas used for achieving the desired correction rate and pitfalls associated with inadequate management or overcorrection. The knowledge of these common-in-clinical-practice pitfalls could assist clinicians in the proper management of patients with hyponatremia.     

急性颈髓损伤后低钠血症37例临床分析

目的:探讨急性颈髓损伤后低钠血症的治疗.方法:回顾性分析2008年1月-2010年12月收治的急性颈髓损伤后低钠血症患者37例的临床资料.结果:血钠在120-130 mmol/L的32例经补盐和限制水摄入量治疗2-3周后低钠症状改善;血钠<120 mmol/L的5例,治疗6-8周后恢复正常2例,死亡3例.结论:颈髓损伤后低钠血症发生率与损伤程度密切相关,及早发现并补充钠盐和控制液体量是有效的治疗方法;能量支持及维持胶体渗透压能提高疗效.     

Management of hyponatremia: providing treatment and avoiding harm

Hyponatremia, in its most severe form, requires urgent infusion of hypertonic saline to correct cerebral edema. However, overly rapid correction of chronic hyponatremia can cause osmotic demyelination syndrome. The authors review the treatment of hyponatremia in order to provide clinicians with a sound approach in a variety of settings in which severity, symptoms, and underlying disease states influence therapy. Also discussed is the current role of vasopressin antagonists in treatment.     

Study of brain electrolytes and organic osmolytes during correction of chronic hyponatremia. Implications for the pathogenesis of central pontine myelinolysis.

Osmotic injury induced by rapid correction of severe chronic hyponatremia has been implicated in the development of central pontine myelinolysis. Organic osmolytes known previously as "idiogenic osmoles" accumulate intracellularly to protect cells from osmotic injury. We investigated the changes of these organic osmolytes as well as electrolytes in the brain during the induction and correction of chronic hyponatremia. Using 1H-nuclear magnetic resonance spectroscopy and HPLC, we found that in rats with chronic hyponatremia (3 d, serum sodium = 109 +/- 3 meq/liter), brain concentrations of myoinositol (41%), glycerophosphorylcholine (45%), phosphocreatine/creatine (60%), glutamate (53%), glutamine (45%), and taurine (37%) were all significantly decreased compared with control values (percentage control value shown, all P less than 0.01). The contribution of measured organic osmolytes and electrolytes to the total brain osmolality change was 23 and 72%, respectively. With rapid correction by 5% NaCl infusion, significant brain dehydration and elevation of brain Na and Cl levels above the normal range occurred at 24 h. These changes were not seen with slow correction by water deprivation. Reaccumulation of most organic osmolytes except glycerophosphorylcholine is delayed during the correction of hyponatremia and is independent of the correction rate of serum sodium. It is concluded that: most of the change of brain osmolality in chronic hyponatremia can be accounted by the changes in organic osmolytes and brain electrolytes; and rapid correction of hyponatremia is associated with an overshoot of brain sodium and chloride levels along with a low organic osmolyte level. The high cerebral ion concentrations in the absence of adequate concentrations of organic osmolytes may be relevant to the development of central pontine myelinolysis.     

Disorders of water imbalance

Disorders of water imbalance manifest as hyponatremia and hypernatremia. To diagnose these disorders, emergency physicians must maintain a high index of suspicion, especially in the high-risk patient, because clinical presentations may be nonspecific. With severe water imbalance, inappropriate fluid resuscitation in the emergency department may have devastating neurological consequences. The rate of serum sodium concentration correction should be monitored closely to avoid osmotic demyelination syndrome in hyponatremic patients and cerebral edema in hypernatremic patients.     

Massive Ethylene Glycol Poisoning Triggers Osmotic Demyelination Syndrome

Background

Ethylene glycol is a toxic organic solvent implicated in thousands of accidental and intentional poisonings each year. Osmotic demyelination syndrome (ODS) is traditionally known as a complication of the rapid correction of hyponatremia.

Objective

Our aim was to describe how patients with ethylene glycol toxicity may be at risk for developing ODS in the absence of hyponatremia.

Case Report

A 64-year old female patient was comatose upon presentation and laboratory results revealed an anion gap of 39, a plasma sodium of 150 mEq/L, a plasma potassium of 3.5 mEq/L, an osmolal gap of 218, an arterial blood gas pH of 7.02, whole blood lactate of 32 mEq/L, no measurable blood ethanol, and a plasma ethylene glycol concentration of 1055.5 mg/dL. The patient was treated for ethylene glycol poisoning with fomepizole and hemodialysis. Despite having elevated serum sodium levels, the patient's hospital course was complicated by ODS.

Conclusions

Rapid changes in serum osmolality from ethylene glycol toxicity or its subsequent treatment can cause ODS independent of serum sodium levels.     

颅脑损伤并发抗利尿激素异常分泌综合征机制和临床分析

目的：探讨颅脑损伤并发抗利尿激素异常分泌综合征（SIADH）机制。临床特征及治疗转归。方法：回顾分析总结1992年1月-2001年2月我院收治的23例颅脑损伤并发SIADH资料，23例均有临床表现，CT及实验室检查完整资料。结果：23例均有不同程度的脑挫裂伤和低钠，低氯血症，低渗血症及高尿钠症，其中19例早期诊断，预后好，4例误诊误治，预后差。结论：SIADH是由于下丘脑直接或间接损伤所致，临床特征为难以纠正的低钠，低渗血症，治疗关键是严控摄入水量。适量补盐，将血钠控制在安全水平（125mmol/L)以上。     

Normo-osmolar, nonketotic, hyponatremic diabetic syndrome associated with impaired renal function

A case is reported of a nonketotic woman with diabetes who presented with a blood glucose of 72.8 mmol/L (1310 mg/dl), plasma sodium of 92 mmol/L, normal osmolality, impaired renal function, and alert clinical state. Before the implication of the unusual nature of the metabolic disturbance was fully considered, the initial treatment was with a rapid infusion of saline. On consideration, however, it was postulated that as her hyperglycemia had developed, the expected osmotic diuresis was prevented by the impairment of her renal function. This had allowed compensatory hyponatremia to develop to maintain normal osmolality and protect the patient from coma. The high-dose saline infusion was stopped, and she was successfully treated with insulin and potassium but only minimal saline. The use of large quantities of saline in normo-osmolar, nonketotic, hyponatremic diabetic syndrome associated with impaired renal function and alert mental state is unnecessary and potentially dangerous.     

Central pontine myelinolysis

Central pontine myelinolysis (CPM), a neurologic disorder caused most frequently by rapid correction of hyponatremia, is characterized by demyelination that affects the central portion of the base of the pons. There are no inflammatory changes, and blood vessels are normal. Clinical features usually reflect damage to the descending motor tracts and include spastic tetraparesis, pseudobulbar paralysis, and the locked-in syndrome. Magnetic resonance imaging of the brain, the imaging procedure of choice, shows an area of prolonged T1 and T2 relaxation in the central pons, which may have a characteristic shape. Recovery varies, ranging from no improvement to substantial improvement. To avoid CPM, correction of serum sodium in patients with hyponatremia should not exceed 12 mEq/24 h. We describe a case of CPM in a hyponatremic patient who presented with a cerebellar syndrome with no pyramidal tract involvement and in whom the rate of correction of serum sodium was within the recommended limits.     

急性脊髓损伤后并发重度低钠血症的临床分析

目的:探讨急性脊髓损伤后并发重度低钠血症的临床特点和治疗方法。方法:1997年10月至2005年12月间我科共收治358例急性脊髓损伤患者,其中121例(33.8%)发生低钠血症(血清钠<135mmol/L),对其中8例重度低钠血症(血清钠<120mmol/L)患者资料进行回顾性分析。结果:8例中男5例,女3例,年龄25～51岁,平均36岁,均因车祸或高处坠落致伤,7例为颈脊髓损伤,1例为胸髓损伤,均为完全性脊髓损伤(AsiaA级),2例合并有轻度闭合型颅脑损伤。平均出现低钠血症时间为伤后(5.7±1.8)d,最低血清钠浓度为(111.6±4.0)mmol/L,出现低钠高峰时间为伤后(8.1±2.0)d,低钠持续时间(20.9±5.9)d。8例均给予深静脉插管,行中心静脉压监测。6例经限水、补钠等治疗后低钠血症纠正,2例低钠血症进行性加重,出现呼吸、循环衰竭死亡。2例合并有肺部感染。结论:急性脊髓损伤后早期易并发低钠血症,由于其症状隐匿,常不被重视,一旦出现重度低钠血症,治疗非常棘手,死亡率高。     

SIADH and hyponatremia with theophylline

OBJECTIVE: To report a case of possible theophylline-induced hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SIADH). CASE SUMMARY: An 88-year-old man developed severe symptomatic hyponatremia (serum sodium 112 mEq/L) associated with inappropriate natriuresis (urinary sodium 58 mEq/L) temporally related to the initiation of theophylline. The patient fulfilled the criteria for the diagnosis of SIADH after all other causes of hyponatremia were excluded. Furthermore, no other drugs or conditions that could have evoked SIADH were found. DISCUSSION: Theophylline has rarely been associated with hyponatremia. A thiazide-like action of the drug on the stimulation of SIADH could be the underlying mechanism for SIADH. CONCLUSIONS: Theophylline should be considered as a possible cause of hyponatremia.     

颅脑损伤并发低钠血症的补液护理

目的探讨颅脑外伤并发低钠血症患者的观察护理。方法回顾性分析42例颅脑损伤并发低钠血症病例,通过正确合理补液和口服或鼻饲盐水,动态监测血钠的变化。结果患者血清钠均小于130mmol／L,尿钠大于20mmol／L。经正确的补钠治疗和全面的护理,均在2周左右得到纠正。结论密切观察患者意识、生命体征,监测血清钠,有助于低钠血症的早期诊断和治疗,强调低钠血症患者的全面护理,可降低病残率和病死率。     

Negative anion gap in a young adult with multiple myeloma.

A young patient with multiple myeloma was found to have a negative anion gap, with marked asymptomatic hyponatremia. The cause for his negative anion gap is thought to be the myeloma protein, which acts as a cation at physiological pH. Such a hyponatremia responds to reduction in serum concentration of paraprotein and should not be treated by sodium replacement.     

Chlorpropamide-induced hyponatremia in the veteran population.

OBJECTIVE: To determine the incidence and possible risk factors associated with chlorpropamide (CPA)-induced hyponatremia in the veteran population. DESIGN: Retrospective cohort study. SETTING: Federal tertiary care medical center. PATIENTS: Veterans receiving CPA from our facility with at least one serum sodium concentration below 135 mmol/L within the past year were eligible. A randomly selected control group consisting of patients taking CPA with normal sodium concentrations was also chosen. One hundred forty-five of 799 patients who had received CPA were included in the study. RESULTS: The average daily dose of CPA was 425 +/- 207 mg (+/- SD). The incidence of hyponatremia associated with CPA was 7.1 percent (57/799 patients). The majority of patients were mildly hyponatremic (48/57 patients, 84 percent) with serum sodium concentrations between 130 and 134 mmol/L. The incidence of CPA-induced syndrome of inappropriate antidiuretic hormone was 2.1 percent. Concurrent angiotensin-converting enzyme (ACE) inhibitor use was identified as a risk factor; thiazide diuretic use was not. CONCLUSIONS: The incidence of hyponatremia related to CPA use in elderly veterans is consistent with other reports in the literature. ACE inhibitors may be a predisposing factor for CPA-induced hyponatremia.     

口服食盐胶囊和静脉补钠对充血性心力衰竭患者低钠血症的疗效观察

目的 观察口服食盐胶囊和静脉补钠两种方法对充血性心力衰竭(congestive heart failure,CHF)患者合并低钠血症的疗效.方法 对43例CHF合并低钠血症的住院患者血钠进行分析,了解血钠与纽约心脏协会(NYHA)心功能分级的关系,并根据补钠方法随机分为口服食盐胶囊组(21例)和静脉补钠组(22例),检测每组治疗前后血钠的水平及NYHA心功能分级.结果 NYHA心功能不同分级患者血钠水平差异有统计学意义,NYHAⅢ级血钠(125.12±2.88)mmol/L,NYHAⅣ级血钠(121.87±3.49)mmol/L(P＜0.01),连续观察治疗3天,静脉补钠组患者血钠水平和心功能改善率明显高于口服食盐胶囊组(P＜0.05或＜0.01).结论 CHF患者低钠程度重者心力衰竭亦严重,且静脉补钠是纠正CHF患者低钠血症、改善心功能较好的一种方法.