Management of hyponatremia

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.     

Polydipsia as another mechanism of hyponatremia after 'ecstasy' (3,4 methyldioxymethamphetamine) ingestion.

Acute symptomatic hyponatremia after ecstasy (3,4 methyldioxymethamphetamine; MDMA) ingestion is well documented and has been attributed to the syndrome of inappropriate antidiuretic hormone (SIADH). We report the case of an 18-year-old woman who took five tablets of ecstasy in a suicide attempt and drank 1700 ml water at the Emergency Department (ED). The laboratory findings obtained 5 h after ingestion showed a serum sodium concentration of 130 mmol/l, plasma osmolality of 264 mOsm/kg, urinary osmolality of 335 mOsm/kg and natriuresis of 101 mmol/l. The plasma arginine vasopressin level by radioimmunoassay was 33.7 pmol/l 5 h after ingestion. A gas chromatography-mass spectrometry assay confirmed MDMA in blood samples, with serum concentrations of 0.87 mg/l on arrival. This case report strongly suggests that MDMA reduces serum sodium levels through the dual pathways of SIADH and polydipsia. Accordingly, we believe that hyponatremia may be prevented in ED patients after MDMA ingestion by the early restriction of water intake.     

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.     

Diagnosis and management of hyponatremia in cancer patients

BACKGROUND: Hyponatremia is among the metabolic disturbances encountered in oncology. Risk factors for hyponatremia include chemotherapy, treatment-induced nausea and vomiting, hydration, pain, narcotic drugs, and physical and emotional stress. A common cause of hyponatremia in patients with cancer is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), which may result from ectopic production of arginine vasopressin (AVP) by the tumor tissue. TREATMENT: The AVP-receptor antagonists, a new class of agents, correct hyponatremia by directly blocking the binding of AVP with its receptors. In clinical trials, conivaptan, lixivaptan, tolvaptan, and satavaptan have increased serum osmolality and normalized the serum [Na(+)] in hyponatremia associated with SIADH, cirrhosis, or congestive heart failure. These drugs may have a potential in cancer-related hyponatremia as well.     

颈髓损伤后抗利尿激素分泌异常综合征的护理

目的探讨颈髓损伤抗利尿激素分泌异常综合征(syndrome of inappropriate secretion of antidiuretic hor-mone,SI-ADH)的护理方法。方法回顾性分析山东大学附属省立医院创伤骨科2006年4月至2010年3月收治的20例SIADH患者的临床资料,总结其护理方法。结果 20例SIADH患者血钠浓度为115～130mmol/L,症状持续时间为2～8d。经治疗,18例患者的低血钠症获得及时纠正,血钠水平恢复正常,临床有效率为90%。结论颈髓损伤患者护理中应重视观察血清电解质、尿钠等,对已发生的SIADH首先要明确诊断,并采取及时有效的治疗方法,大多数患者在短期内都可以得到纠正。     

Syndrome of inappropriate antidiuretic hormone secretion: recognition and management.

Older persons are at greater risk for developing hyponatremia. Renal system changes which occur with aging cause alterations in the functional balance of fluid and electrolytes, and sodium regulation is not as effective. In one form of hyponatremia seen among the elderly, total body sodium content is normal, but water is retained because of increased antidiuretic hormone (ADH) secretion. This condition, called the syndrome of inappropriate antidiuretic hormone secretion (SIADH), has many causes including chronic illnesses and various medications. The physiology behind SIADH, its causes, diagnostics, and various treatment modalities are explored.     

颈髓损伤后水电解质紊乱的临床诊断治疗

目的 探讨颈髓损伤后电解质紊乱的临床特点及诊断治疗.方法 回顾30例颈髓损伤患者（完全性损伤15例，不完全性损伤15例）血压、心率，血清钠、钾、血浆渗透压、尿量及24ｈ尿钠排出量等资料：23例患者于伤后2－8天出现低钠血症，其中完全性损伤15例全部出现，发生率100％，1例患者并发抗利尿激素分泌异常综合征 结果 根据血钠水平,经采用控制每日水量、补钠治疗5－14天后，23例均治愈,血钠平均恢复至138(135－142)mmol/l,血浆渗透压、尿钠均正常.结论 低钠血症是颈髓损伤后极为常见的并发症，但并发抗利尿激素分泌异常综合征十分少见；机体内抗利尿激素不适当分泌，导致的稀释性低钠血症可能是颈髓损伤继发低钠血症的发生机制之一。严格控制入液量及补钠为主要治疗方法.     

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。     

Tolvaptan for the treatment of hyponatremia secondary to the syndrome of inappropriate antidiuretic hormone secretion

Hyponatremia is prevalent in hospitalized patients and predicts a poor prognosis. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is perceived as one of the most frequent causes of hyponatremia. Traditionally, chronic hyponatremia has been treated with fluid restriction and demeclocycline. However, these treatment options have been unsatisfactory due to problems with treatment compliance and/or safety concerns. In recent years, several vasopressin-receptor antagonists, the vaptans, were introduced into clinical practice. One of these vaptans – tolvaptan – is an oral vasopressin V2-receptor antagonist that induces free water excretion without increasing sodium excretion. Few studies have assessed the role of vaptans in treating hyponatremia in a population with only SIADH. Current data shows that vaptans may safely correct mild or moderate hyponatremia in patients with SIADH. However, further clinical trials are needed to determine the optimal dosing, proper monitoring and adequate precautions for the use of vaptans in this patient population.     

Tolvaptan for the treatment of hyponatremia secondary to the syndrome of inappropriate antidiuretic hormone secretion

Hyponatremia is prevalent in hospitalized patients and predicts a poor prognosis. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is perceived as one of the most frequent causes of hyponatremia. Traditionally, chronic hyponatremia has been treated with fluid restriction and demeclocycline. However, these treatment options have been unsatisfactory due to problems with treatment compliance and/or safety concerns. In recent years, several vasopressin-receptor antagonists, the vaptans, were introduced into clinical practice. One of these vaptans - tolvaptan - is an oral vasopressin V2-receptor antagonist that induces free water excretion without increasing sodium excretion. Few studies have assessed the role of vaptans in treating hyponatremia in a population with only SIADH. Current data shows that vaptans may safely correct mild or moderate hyponatremia in patients with SIADH. However, further clinical trials are needed to determine the optimal dosing, proper monitoring and adequate precautions for the use of vaptans in this patient population.     

Syndrome of inappropriate antidiuretic hormone secretion associated with lisinopril

OBJECTIVE: To describe a case of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with lisinopril therapy. CASE SUMMARY: A 76-year-old white woman who was being treated with lisinopril and metoprolol for hypertension presented with headaches accompanied by nausea and a tingling sensation in her arms. Her serum sodium was 109 mEq/L, with a serum osmolality of 225 mOsm/kg, urine osmolality of 414 mOsm/kg, and spot urine sodium of 122 mEq/L. Diclofenac 75 mg qd for osteoarthritic pain and lisinopril 10 mg qd for hypertension was begun in 1990. Lisinopril was increased to 20 mg qd in August 1994 and to 20 mg bid pm in August 1996 for increasing blood pressure; metoprolol 50 mg qd was added in July 1996. A diagnosis of SIADH was postulated and further evaluation was undertaken to exclude thyroid and adrenal causes. After lisinopril was discontinued and the patient restricted to 1000 mL/d of fluid, serum sodium gradually corrected to 143 mEq/L. The patient was discharged taking metoprolol alone for her hypertension; serum sodium has remained > or =138 mEq/L through April 1999, 32 months after discharge, despite daily use of diclofenac. DISCUSSION: Angiotensin-converting enzyme (ACE) inhibitors in antihypertensive doses may block conversion of angiotensin I to angiotensin II in the peripheral circulation, but not in the brain. Increased circulating angiotensin I enters the brain and is converted to angiotensin II, which may stimulate thirst and release of antidiuretic hormone from the hypothalamus, eventually leading to hyponatremia. CONCLUSIONS: SIADH should be considered a rare, but possible, complication of therapy with lisinopril and other ACE inhibitors.     

颅脑损伤后中枢性低钠血症的诊治

目的:分析颅脑损伤并发中枢性低钠血症的临床特点、诊断和治疗。方法:回顾分析近10年收治的25例颅脑损伤后中枢性低钠血症的临床资料。结果:本组抗利尿激素分泌异常综合征11例,治愈8例,死亡3例;脑耗盐综合征14例,治愈12例,死亡2例。结论:抗利尿激素分泌异常综合征和脑耗盐综合征的发病机制、临床表现和治疗都不相同,早期诊断和治疗可以降低病人的死亡率。     

Nedaplatin-induced syndrome of inappropriate secretion of antidiuretic hormone: A case report and review of the literature

BACKGROUNDSyndrome of inappropriate secretion of antidiuretic hormone (SIADH) is relatively common in several cancers, such as small cell lung cancer. However, nedaplatin-induced SIADH is rare. We describe a case of SIADH mediated by nedaplatin.CASE SUMMARYA 54-year-old female with nasopharyngeal carcinoma was treated with nedaplatin and developed severe hyponatremia due to SIADH. The side effects were successfully treated by fluid restriction and sodium supplementation.CONCLUSIONThis case report highlights the importance of cautiously treating life-threatening hyponatremia in patients treated with nedaplatin.     

Syndromes of excess antidiuretic hormone release

Hyponatremia, particularly that due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH), is common in patients seen in the critical care setting. Because of aging-associated changes in the hormonal and renal systems involved in regulation of water and sodium balance, older persons are at higher risk than the young. The high prevalence of disease states and drug use in the elderly can affect water and sodium conservation and further contribute to the risk of hyponatremia in this population. The approach to management is dependent both on the severity of hyponatremia-related symptoms and the rapidity with which hyponatremia has developed. Careful monitoring of serum sodium during treatment is essential to produce prompt resolution of symptoms while avoiding the development of central pontine myelinolysis. Several therapeutic modalities are available for the longterm management of chronic hyponatremia.     

长期服用丙戊酸钠引起抗利尿激素不适当分泌综合征一例并文献复习

目的 探讨服用丙戊酸钠（VPA）引起抗利尿激素不适当分泌综合征（SIADH）的发病机制、诊治方法,提高临床医师的认识水平。方法 总结1例长期服用VPA引起SIADH患者的临床资料,并以“丙戊酸钠”和“抗利尿激素不适当分泌综合征”（包括中英文）为关键词对PubMed和CNKI数据库收录的文献进行检索分析。结果 该例患者为62岁男性,以全身乏力、下肢水肿、低钠血症为主要表现,既往因继发性癫痫长期服用VPA。排除可能引起低钠血症的其他病因后被确诊为VPA所致SIADH,遂停用VPA并加用托伐普坦卡,其后患者血钠水平逐渐恢复正常。随访结果显示患者症状好转,多次复查血钠水平正常。检索数据库后共收集到 5 篇相关病例报道的8例患者资料,其中6例为中老年患者,在逐步停用VPA后症状均好转。结论 临床上因服用VPA引起SIADH的病例较少见,容易漏诊或误诊,该文提示对出现顽固性低钠血症且诊断考虑为SIADH的患者,需要关注是否为服用VPA所致,以便及时调整治疗方案以改善患者的症状及预后。     

鞍区肿瘤术后低钠血症原因诊断及处理对策

目的探讨鞍区肿瘤手术后并发低钠血症的病因、发病机制、诊断及治疗方法。方法回顾性分析32例鞍区肿瘤术后低钠血症患者的临床表现和实验室检查，总结有效的诊断及治疗方法。结果32例中临床诊断抗利尿激素分泌异常综合征12例，脑性盐耗综合征18例，余2例因连续数日尿量／d〉5000ml而诊断为尿崩症未列入统计范围；均恢复良好。结论鞍区肿瘤术后低钠血症出现后，尿量、尿比重的变化以及试验性限水治疗有助于鉴别抗利尿激素分泌异常综合征和脑性盐耗综合征；病因未明时，应首选限水治疗。     

Treatment of euvolemic hyponatremia in the intensive care unit by urea

Introduction  

Hyponatremia in the intensive care unit (ICU) is most commonly related to inappropriate secretion of antidiuretic hormone (SIADH). Fluid restriction is difficult to apply in these patients. We wanted to report the treatment of hyponatremia with urea in these patients.     

Central neurogenic diabetes insipidus, syndrome of inappropriate secretion of antidiuretic hormone, and cerebral salt-wasting syndrome in traumatic brain injury

Central neurogenic diabetes insipidus, syndrome of inappropriate secretion of antidiuretic hormone, and cerebral salt-wasting syndrome are secondary events that affect patients with traumatic brain injury. All 3 syndromes affect both sodium and water balance; however, they have differences in pathophysiology, diagnosis, and treatment. Differentiating between hypernatremia (central neurogenic diabetes insipidus) and the 2 hyponatremia syndromes (syndrome of inappropriate secretion of antidiuretic hormone, and cerebral salt-wasting syndrome) is critical for preventing worsening neurological outcomes in patients with head injuries.     

重型颅脑损伤合并抗利尿激素分泌不当综合征的临床特点及护理

抗利尿激素分泌不当综合征(SIADH),是由于颅脑损伤后影响下丘脑—神经垂体功能,促使精氨酸加压素释放而不受渗透压等正常调节机制的控制,从而导致水潴留,尿排钠增多,出现以稀释性低钠血症等临床表现为主的一组综合征[1]。SIADH在1957年首先由Schwaytz和Batter提出,目前国内也有     

Natural killer/T-cell lymphoma with concomitant syndrome of inappropriate antidiuretic hormone secretion: A case report and review of literature

We report a case of natural killer (NK)/T-cell lymphoma with concomitant syndrome of inappropriate antidiuretic hormone secretion (SIADH). The patient was a 64-year-old woman with a history of nasopharyngeal carcinoma of over 30 years. She was admitted with a chief complaint of intermittent fever for 2 mo. Palpation after admission indicated a swollen lymph node below the left jaw. Multiple imaging examinations on admission indicated multiple enlarged lymph nodes throughout the body. We performed a left submandibular lymph node biopsy, and the results revealed NK/T-cell lymphoma. A biochemical examination indicated Epstein-Barr virus positivity. At the same time, the patient developed hyponatremia. Based on her laboratory examination and clinical manifestation, decreased plasma osmolality, urine osmolality greater than plasma osmolality, lack of skin swelling, normal blood pressure, normal renal function, no adrenal function detected on serology, and no abnormalities in imaging examination of the adrenal glands, the likelihood of SIADH in the patient was high. After fluid restriction and administration of sodium chloride, the patient’s blood sodium level gradually increased. Subsequently, the immune function of the patient declined, there were severe symptoms of infection, and she died of respiratory failure. NK/T-cell lymphoma associated with SIADH has not, to our knowledge, been previously reported in PubMed. This case emphasizes the importance of monitoring serum ion levels, especially serum sodium, in patients with NK/T-cell lymphoma.