抗利尿激素不适当综合征临床诊治

低钠血症是临床最常见的电解质紊乱,并增加患者病死率。而抗利尿激素不适当综合征(SIADH)是临床表现低钠血症的主要原因之一,其基础病因复杂且多样化,临床表现与低钠血症的程度和病程明显相关。因此,及早识别和正确诊断该病可减少误诊并降低病死率。临床上需要对该部分患者予以及时准确的诊断并制定个体化的治疗方案,而抗利尿激素受体拮抗剂在该类疾病的治疗中具有广阔的应用前景。     

急性脑血管病并发低钠血症67例临床分析

目的探讨急性脑血管病患者发生低钠血症的诊断及治疗方法。方法 67例急性脑血管病并发低钠血症患者。根据临床症状、实验室检查及中心静脉压确定低钠血症的类型并给予相应处理。结果 1例死于肺部感染,3例自动出院,63例患者低钠血症症状恢复。结论中枢性低钠血症包括脑性盐耗综合征和抗利尿激素分泌不当综合征,前者应予以充分补钠、补水;后者却需要限水治疗。     

颈椎骨折致尿崩症的诊断与治疗

目的:探讨颈椎骨折并发尿崩症的机制及临床诊断治疗经验。方法:回顾性分析18例颈椎骨折并发尿崩症患者的临床资料。结果:18例患者临床诊断为尿崩症,均出现不同程度的低钠血症,其中低氯血症15例,低钾血症13例,给予垂体后叶素治疗后尿量明显减少。结论:颈椎骨折引起颈髓的直接损伤和缺血缺氧继发颈髓及脑垂体的损伤导致抗利尿激素的异常分泌可引起尿崩症,限制水、晶体摄入,抗利尿激素的替代治疗有效。     

中枢性低钠血症的诊治体会

目的探讨中枢性低钠血症的发病机制、诊断及治疗方法。方法对该院21例中枢性低钠血症患者的临床资料进行回顾性分析。结果19例低钠血症恢复正常;2例因合并颅内感染,高热不退,1例死亡,1例经控制感染后,低钠血症恢复正常,但仍昏迷不醒。结论低血钠、高尿钠和意识状态改变是中枢性低钠血症的诊断依据,抗利尿激素分泌不当综合征（SIADH）应限水治疗,脑性盐耗综合征（CSWS）则作水化和补盐治疗。     

低钠血症诊疗中问题和处理经验

低钠血症是临床最常见的电解质紊乱之一,它也是内分泌会诊的常见疾病。血钠水平与低钠血症的症状间关系密切。抗利尿激素分泌失调综合征和脑性失盐综合征常需鉴别,它们都表现为低钠血症,但脑性失盐综合征患者尿量常较大,体液容量不足,抗利尿激素分泌失调综合征患者体液容量通常无明显不足。低钠血症的治疗将血钠纠正至130 mmol/L左右即可,24 h血钠升高不要超过10~12 mmol/L。血钠纠正过快容易引起渗透性脱髓鞘病变。V2受体拮抗剂治疗抗利尿激素分泌失调综合征时应从小量开始,且不能严格限水。     

提高抗利尿激素分泌异常综合征的诊治水平

抗利尿激素分泌异常综合征(SIADH)以稀释性低钠血症为主要表现,是住院患者等容量性低钠血症最常见的病因.SIADH的传统治疗包括限制液体入量、输注盐溶液及一些调节体液平衡的药物.由于各种原因,常规治疗的疗效欠佳.抗利尿激素受体拮抗剂是一种新型的药物,可以阻断抗利尿激素介导的受体活化,是针对SIADH的病因治疗.     

甲状腺机能减退并抗利尿激素分泌异常综合征10例分析

目的 增强对原发性甲状腺机能减退症并抗利尿激素分泌异常综合征的认识，提高其诊治水平。方法 对10例原发性甲状腺机能减退症并抗利尿激素分泌异常患者临床表现、化验检查结果、治疗及预后情况进行临床分析。结果 经甲状腺素替代治疗和及时限水对症补钠治疗，甲状腺激素水平正常后，低钠血症易纠正。结论 甲状腺机能减退症并抗利尿激素分泌异常综合征应明确低钠血症的性质，同时应该注意查甲状腺激素，考虑甲减的可能，及时补充甲状腺激素，以免漏诊、误诊和延误治疗。     

严重颈髓损伤致低钠血症36例临床分析

重症医学患者中常出现各种水、电解质紊乱,其中脑性盐耗综合征(cerebral salt wasting syndrome,CSWS)及颈髓损伤致低钠血症是中枢性神经系统损伤后严重并发症之一[1].二者均表现为低钠血症、高尿钠、低血容量,多伴有多尿.这些表现较易与抗利尿激素分泌不当综合征(syndrome of inappropriate antidiuretic hormone,SIADH)及尿崩症相混淆,如诊断、治疗不当,常加重病情[ 2].本文将我科收治严重颈髓损伤致低钠血症患者诊治情况进行临床分析.     

重型颅脑损伤低钠血症患者48例临床分析

重症颅脑损伤患者在治疗过程中合并低钠血症非常多见,但因下丘脑-垂体激素轴损伤引起中枢性低钠血症则少见,主要包括抗利尿激素分泌不当综合征（SIADH）和脑性盐耗综合征（CSWS）,二者易混淆。本研究对我院收治的重型颅脑损伤所致低钠血症的48例患者临床资料分析报告如下。     

重型颅脑损伤并发中枢性低钠血症67例诊治分析

目的探讨重型颅脑损伤后中枢性低钠血症的发病机制、诊断及治疗方法。方法对67例中枢性低钠血症患者的临床表现、实验室检查、治疗方法及疗效进行回顾性分析。结果重型颅脑损伤后发生中枢性低钠血症有两种因素:(1)抗利尿激素不适当分泌引起的综合征(SIADH),主要行限水治疗;(2)脑性盐耗引起的综合征(CSWS),主要给予补充盐水治疗。本组病例上述二种治疗后,全部患者低钠血症均得到纠正。结论引起中枢性低钠血症有两种不同原因,且治疗方法也不同。     

Early hyponatraemia after pituitary surgery: cerebral salt-wasting syndrome

Hyponatraemia is a common complication in patients undergoing neurosurgery. It can be caused either by the syndrome of inappropriate secretion of antidiuretic hormone or by the cerebral salt-wasting syndrome (CSWS). CSWS frequently occurs in patients suffering from subarachnoid haemorrhage and brain injury, but it is rare after pituitary tumour surgery. However, this diagnostic possibility should be considered as these disorders require specific treatment and have different prognoses. In this article, we present a case of acute and early hyponatraemia caused by CSWS after pituitary tumour surgery. We also revise the aetiology, mechanisms, differential diagnosis and treatment of hyponatraemia after pituitary surgery.     

Hyponatremia and antidiuresis syndrome

Antidiuretic hormone (ADH), or arginine vasopressin (AVP), is primarily regulated through plasma osmolarity, as well as non-osmotic stimuli including blood volume and stress. Links between water-electrolyte and carbohydrate metabolism have also been recently demonstrated. AVP acts via the intermediary of three types of receptors: V1a, or V1, which exerts vasoconstrictive effects; pituitary gland V1b, or V3, which participates in the secretion of ACTH; and renal V2, which reduces the excretion of pure water by combining with water channels (aquaporin 2). Antidiuresis syndrome is a form of euvolaemic, hypoosmolar hyponatraemia, which is characterised by a negative free water clearance with inappropriate urine osmolality and intracellular hyper-hydration in the absence of renal, adrenal and thyroid insufficiency. Ninety percent of cases of antidiuresis syndrome occur in association with hypersecretion of vasopressin, while vasopressin is undetectable in 10% of cases. Thus the term “antidiuresis syndrome” is more appropriate than the classic name “syndrome of inappropriate ADH secretion” (SIADH). The clinical symptoms, morbidity and mortality of hyponatraemia are related to its severity, as well as to the rapidity of its onset and duration. Even in cases of moderate hyponatraemia that are considered asymptomatic, there is a very high risk of falls due to gait and attention disorders, as well as rhabdomyolysis, which increases the fracture risk. The aetiological diagnosis of hyponatraemia is based on the analysis of calculated or measured plasma osmolality (POsm), as well as blood volume (skin tenting of dehydration, oedema). Hyperglycaemia and hypertriglyceridaemia lead to hyper- and normoosmolar hyponatraemia, respectively. Salt loss of gastrointestinal, renal, cutaneous and sometimes cerebral origin is hypovolaemic, hypoosmolar hyponatraemia (skin tenting), whereas oedema is present with hypervolaemic, hypoosmolar hyponatraemia of heart failure, nephrotic syndrome and cirrhosis. Some endocrinopathies (glucocorticoid deficiency and hypothyroidism) are associated with euvolaemic, hypoosmolar hyponatraemia, which must be distinguished from SIADH. Independent of adrenal insufficiency, isolated hypoaldosteronism can also be accompanied by hypersecretion of vasopressin secondary to hypovolaemia, which responds to mineralocorticoid administration. The causes of SIADH are classic: neoplastic (notably small-cell lung cancer), iatrogenic (particularly psychoactive drugs, chemotherapy), lung and cerebral. Some causes have been recently described: familial hyponatraemia via X-linked recessive disease caused by an activating mutation of the vasopressin 2 receptor; and corticotropin insufficiency related to drug interference between some inhaled glucocorticoids and cytochrome p450 inhibitors, such as the antiretroviral drugs and itraconazole, etc. SIADH in marathon runners exposes them to a risk of hypotonic encephalopathy with fatal cerebral oedema. SIADH treatment is based on water restriction and demeclocycline. V2 receptor antagonists are still not marketed in France. These aquaretics seem effective clinically and biologically, without demonstrated improvement to date of mortality in eu- and hypervolaemic hyponatraemia. Obviously treatment of a corticotropic deficit, even subtle, should not be overlooked, as well as the introduction of fludrocortisone in isolated hypoaldosteronism and discontinuation of iatrogenic drugs.     

Intravenous albumin infusion is an effective therapy for hyponatraemia in cirrhotic patients with ascites.

The treatment of moderate to severe hyponatraemia in patients with decompensated liver disease is unsatisfactory. We report our preliminary experience using intravenous infusion of albumin to treat this condition. Three patients with cirrhosis, ascites, and hyponatraemia responded satisfactorily to treatment; one patient with fulminant hepatitis B did not respond. Intravenous albumin infusion is a safe and effective therapy for patients with cirrhosis complicated by hyponatraemia. Its main role may be in preparing patients for surgery, particularly liver transplantation.     

Electrolyte derangement in cerebral malaria: a case for a more aggressive approach to the management of hyponatraemia

Although hyponatraemia has been consistently shown to occur in a large proportion of children with cerebral malaria, no statistical relationship has been established between the incidence of hyponatraemia and that of malaria-attributable mortality. However, hyponatraemia is not a benign state in other conditions (such as meningitis) or in surgical patients, and is likely to add to malarial deaths. The high mortality rate seen among cases of cerebral malaria, despite all efforts to curb it, therefore calls for a more aggressive approach to the management of hyponatraemia. Current methods for the administration of hypotonic saline and isotonic glucose solutions need review. In addition, children admitted with cerebral malaria should have their electrolyte status monitored to identify new or ongoing hyponatraemia. When hyponatraemia is discovered, it should be quickly and actively corrected.     

Severe hyperhomocysteinaemia and 5-oxoprolinuria secondary to antiproliferative and antimicrobial drug treatment

Summary A hitherto healthy 7-year-old girl underwent antiproliferative and antibiotic treatment owing to the diagnosis of T-cell lymphoma and concomitant bacterial infection. She developed an encephalopathic crisis associated with metabolic acidosis, hyponatraemia and severe hyperhomocysteinaemia and 5-oxoprolinuria. Laboratory tests normalized completely after recovery. Primary defects in glutathione metabolism could be excluded.     

Risk factors for symptomatic hyponatraemia: the role of pre-existing asymptomatic hyponatraemia

Background: Hyponatraemia is associated with substantial morbidity and mortality. Identification of the risk factors associated with the development of symptomatic hyponatraemia is important in determining preventive strategies. Methods: A retrospective analysis of the risks factors associated with the development of severe, symptomatic hyponatraemia requiring hospital admission over the past 3 years at our institution was carried out. Results: Forty‐seven patients (26 women, 21 men) with a hospital admission serum sodium <134 mmol/L were identified. Of these patients, 31 (65.9%) had associated changes in the mental status that improved with the treatment of the hyponatraemia suggesting causality. The average admission sodium level of this cohort was 118.8 mmol/L. Symptomatic hyponatraemia was associated with volume depletion (32.6%), congestive heart failure (26%), syndrome of inappropriate antidiuretic hormone (26%), thiazide diuretic use (26%) and selective serotonin re‐uptake inhibitor use (26%). In 21.7% of cases, the cause was multifactorial (congestive heart failure, syndrome of inappropriate antidiuretic hormone or medication use with volume depletion). In 11% of cases, patients were taking both thiazide diuretics and serotonin re‐uptake inhibitors. Most importantly, 70.9% of all patients admitted with symptomatic hyponatraemia had pre‐existing hyponatraemia that was untreated and believed to be asymptomatic (P < 0.05). This was the most common risk factor identified. We next investigated the prevalence of presumed asymptomatic hyponatraemia in the outpatient setting. Out of 27 496 patients analysed, 14% had serum sodium levels less than or equal to 134 mEq/L and 4% had values less than 130 mEq/L. Conclusion: Pre‐existing asymptomatic hyponatraemia is a common finding and is associated with a high risk for the development of worsening hyponatraemia with altered mental status.     

Hyponatraemia in heart failure

Hyponatraemia is common in heart failure (HF). It is estimated that over 20% of patients admitted to hospital with HF have hyponatraemia. It has also been repeatedly shown to be a surrogate marker of increased morbidity and mortality in this specific population. This review focuses on the pathophysiology of hyponatraemia through the activation of neurohormonal cascades in HF, the clinical implications of sustained hyponatraemia and treatment options in the management of this challenging phenomenon.     

Diuretic induced hyponatraemia in elderly hypertensive women

Diuretics are recommended as first-line antihypertensive treatment in elderly patients. Although attention is usually paid to prevent hypokalaemia with diuretic therapy, risk of hyponatraemia is often ignored. We performed this study to characterise hypertensive patients at increased risk to develop hyponatraemia. We reviewed charts of hypertensive patients hospitalised in Chaim Sheba Medical Center for hyponatraemia from 1990 to 1997. Patients with other causes of hyponatraemia were excluded. The General Practice Maccabi database was used to estimate age and sex distribution of patients prescribed diuretics for hypertension. We identified 180 hypertensive patients (149 F, 31 M; mean age 76.4 +/- 9.2 years) hospitalised because of hyponatraemia. Across all age groups, odds ratio (OR) to develop hyponatraemia was three times higher for women vs men (OR 3.10, 95% confidence interval (CI): 2.07-4.67). One hundred and sixty-two patients (90%) were older than 65 years. Patients of both sexes older than 65 years were 10 times (and if they were older than 75 years 16 times) more likely to develop hyponatraemia than those younger than 65 years (OR 9.87, 95%, CI: 5.93-16.64). Most patients (74.5%) used a thiazide-based diuretic; only 10% used a low dose (<25 mg/day). In 37% of patients diuretics were used for more than 1 year before hyponatraemia developed. Diuretic-induced hyponatraemia may be insidious and appear even after prolonged diuretics use. Elderly women seem to be at particularly high risk. In this population diuretic use should be associated with close monitoring of sodium and potassium levels.     

A systematic review of known interventions for the treatment of chronic nonhypovolaemic hypotonic hyponatraemia and a meta‐analysis of the vaptans

International and national guidelines on the treatment of chronic nonhypovolaemic hypotonic hyponatraemia differ; therefore, we have undertaken this systematic review and meta‐analysis to investigate the efficacy and safety of interventions for the treatment of chronic nonhypovolaemic hypotonic hyponatraemia. Following registration of the review protocol with PROSPERO, systematic literature searches were conducted to identify randomized and quasi‐randomized controlled trials assessing any degree of fluid restriction or any drug treatment with the aim of increasing serum sodium concentration in patients with chronic nonhypovolaemic hypotonic hyponatraemia. Where appropriate, outcome data were synthesized in a meta‐analysis. A total of 45 716 bibliographic records were identified from the searches and 18 trials (assessing conivaptan, lixivaptan, tolvaptan and satavaptan) met the eligibility criteria. Results suggest that all four vasopressin receptor agonists (“vaptans”) significantly improve serum sodium concentration. Lixivaptan, satavaptan and tolvaptan were associated with greater rates of response versus placebo. There was no evidence of a difference between each of the vaptans compared with placebo for mortality, discontinuation and rates of hypernatraemia. No RCT evidence of treatments other than the vaptans for hyponatraemia such as oral urea, salt tablets, mannitol, loop diuretics demeclocycline or lithium was identified. Vaptans demonstrated superiority over placebo for outcomes relating to serum sodium correction. Few trials documented the potential benefit of vaptans on change in health‐related quality of life as a result of treatment. There was also a lack of high‐quality RCT evidence on the comparative efficacy of the vaptans and other treatment strategies for the treatment of chronic nonhypovolaemic hypotonic hyponatraemia.     

Beer drinker's hyponatraemia: a case report

Beer drinker's hyponatraemia, also called beer potomania, is a syndrome of hyponatraemia in patients who consume excessive amounts of beer and have a poor dietary intake. We describe a patient with chronic asymptomatic hyponatraemia due to beer potomania. The pathophysiology of this syndrome, the treatment and prevention are reviewed.