Long-term neurologic outcome in psychogenic water drinkers with severe symptomatic hyponatremia: the effect of rapid correction

PURPOSE: The purpose of our study was to ascertain the safety of rapidly correcting acute symptomatic hyponatremia in psychogenic water drinkers, particularly in regard to any delayed adverse neurologic sequelae. PATIENTS AND METHODS: We reviewed the medical records of all known psychogenic water drinkers (34) in our hospital from 1977 to 1989. Using seizure as a marker of severity, we identified 13 patients having a total of 27 episodes associated with severe hyponatremia. We evaluated the charts of those patients in detail to assess the mode of treatment, rate of correction, and long-term neurologic outcome. None of the patients experienced respiratory arrest before treatment, which was initiated within 2 hours of seizure. RESULTS: For all 27 episodes, the initial serum sodium level (mean +/- SE) was 110.9 +/- 1.2 mmol/L, and the rate of correction (mean +/- SE) was 1.65 +/- 0.2 mmol/L/hour. All but one episode were corrected "rapidly" (initial correction rate of 0.7 or more mmol/L/hour) to 120 to 130 mmol/L within 12 hours. The absolute change in the serum sodium level was 15.1 +/- 1.2 mmol/L in 12 hours, 21.6 +/- 1.4 mmol/L in 24 hours, and 25.9 +/- 1.4 mmol/L in 48 hours. In no instance did therapy induce hypernatremia. All patients recovered immediately after treatment. There was no clinical or radiologic evidence of adverse neurologic sequelae immediately after treatment or after 6 years of follow-up. CONCLUSION: In this series of male psychogenic water drinkers, early "rapid" correction of acute symptomatic hyponatremia by raising the serum sodium level 15 mmol/L in 12 hours while maintaining an absolute change in the serum sodium level of 26 mmol/L within 48 hours produced no long-term neurologic sequelae.     

Fatal central diabetes mellitus and insipidus resulting from untreated hyponatremia: a new syndrome

After elective hospitalization, eleven healthy young women developed symptomatic hyponatremia that was rapidly followed by polyuria, hypernatremia, hyperglycemia, and death. The patients were 30 +/- 2 years old (+/- SE) with initial serum sodium of 140 +/- 1 mmol/L. They all awoke from analgesia but, 32 hours after completion of the procedure, they went from alertness to respiratory arrest in less than 1 hour. At this time, serum sodium was 116 +/- 2 mmol/L and blood glucose was 6.7 +/- 0.7 mmol/L. Without treatment for the hyponatremia, urine output spontaneously increased from 38 to 689 mL/h and urine osmolality fell from 546 to 83 mmol/kg body weight. Over the next 51 hours, blood glucose rose to a high of 24.1 +/- 2.5 mmol/L while serum sodium rose to a high of 167 +/- 2 mmol/L. None of the patients regained consciousness. At autopsy, all patients had cerebral edema with herniation along with hypoxic brain damage. The pituitary showed infarction of both anterior and posterior lobes in 7 of 7 patients examined, while 8 of 11 had necrosis of the medulla and 8 of 8 patients examined had hypothalamic necrosis. All had normal pancreas and kidneys at autopsy. Soon after respiratory arrest, all of the patients developed fixed, dilated pupils that often led to the diagnosis of brain death. Autopsy showed compression of the third cranial nerve (oculomotor) because of cerebral herniation. Thus, all of the patients were diagnosed as being brain dead when some may have been saved. These data suggest that in otherwise healthy young women, untreated symptomatic hyponatremia may lead to brain edema, cerebral herniation, and infarction of pituitary and hypothalamus, resulting in central diabetes insipidus and mellitus.     

Thiazide-induced hyponatremia. Reproducibility by single dose rechallenge and an analysis of pathogenesis

STUDY OBJECTIVE: To determine whether a single-dose of thiazide administered to patients with previous thiazide-induced hyponatremia will cause hyponatremia and, if so, to analyze its pathogenesis. DESIGN: Prospective controlled study comparing patients with previous thiazide-induced hyponatremia with two control groups. PATIENTS AND CONTROLS: Eleven patients with thiazide-induced (Kaluril [hydrochlorothiazide, 50 mg; amiloride, 5 mg]) hyponatremia of less than 130 mmol/L at least 1 week before the study. Two groups of controls: 10 young healthy volunteers and 11 elderly hypertensive patients previously treated uneventfully with thiazide. INTERVENTIONS: Administration of a single dose of hydrochlorothiazide, 50 mg, and amiloride, 5 mg. MEASUREMENTS: Blood pressure, pulse rate, body weight, serum urea, creatinine, sodium, potassium, magnesium, osmolality, plasma antidiuretic hormone, renin, aldosterone and also urinary sodium, potassium, osmolality, and cyclic adenosine monophosphate (cAMP) before and 6 to 8, 12, and 24 hours after drug administration. RESULTS: Within 6 to 8 hours serum sodium decreased in patients, young controls, and elderly controls by 5.5 +/- 1.1 (mean +/- SE), 1.2 +/- 0.4, and 1.8 +/- 0.9 mmol/L, respectively (Py less than 0.001 [patients versus young controls], Pe = 0.017 [patients versus elderly controls]). Serum osmolality decreased in patients, young controls, and elderly controls by 14.9 +/- 2.6, 2.8 +/- 1.6, and 6.6 +/- 1.5 mmol/kg, respectively (Py less than 0.001, Pe = 0.012). All patients and only one control subject reached osmolality of less than 280 mmol/kg. At 6 to 8 hours all patients gained weight (0.85 +/- 0.13 kg) whereas young and elderly controls lost weight (0.47 +/- 0.23 and 0.45 +/- 0.2 kg, respectively) (Py much less than 0.001, Pe much less than 0.001). Patients' responses to the drug did not differ from both control groups regarding sodium and potassium urinary excretion, osmolar and free water clearance, and antidiuretic hormone blood levels. Water restriction in one patient attenuated serum sodium reduction. CONCLUSIONS: Use of a single-dose of a thiazide diuretic may predict the development of hyponatremia. Increased body weight apparently due to polydipsia may play a major role in the pathogenesis of thiazide-induced hyponatremia.     

Hyponatremia and arginine vasopressin secretion in patients with refractory hepatic ascites undergoing peritoneovenous shunting

Seven patients with persistent hyponatremia but normal or elevated serum arginine vasopressin levels and refractory ascites undergoing peritoneovenous shunting were studied in a Metabolic Unit on a 20 mEq sodium 1200 ml fluid-restricted diet to elucidate the mechanism of this response. The intravascular volume expansion after shunt implantation resulted in improvements in cardiac output, renal plasma flow and creatinine clearance (70.7 +/- 9.5 to 140.1 +/- 18.5 ml/min, p less than 0.005). There was an immediate diuresis (632 +/- 135 to 2450 +/- 323 ml/day, p less than 0.005) and natriuresis (3 +/- 1 to 25.9 +/- 10.6 mEq/24 h, p less than 0.05), and urine osmolality decreased significantly (622 +/- 91 to 251 +/- 76 mosmol/L, p less than 0.05) with a significant rise in serum sodium concentration by 72 hr (131 +/- 2 to 135 +/- 1.6 mEq/L, p less than 0.05) and serum osmolality. Serum arginine vasopressin levels remained elevated at 3.85 +/- 0.94 microU/ml, however, although a transient depression cannot be excluded. Subsequently, a small but significant decrease in serum arginine vasopressin levels to 3.04 +/- 0.65 microU/ml (p less than 0.05) was associated with a further rise in serum sodium levels above baseline values (138 +/- 1.4 mEq/L, p less than 0.01) and in serum osmolality. In conclusion, these results indicate that in this group of cirrhotic patients with refractory ascites, intrarenal factors, such as decreased delivery of filtrate to the distal nephron as well as elevated inappropriate levels of arginine vasopressin, are important in the pathogenesis of hyponatremia.     

Severe diuretic-induced hyponatremia in the elderly. A series of eight patients

Eight elderly patients with severe diuretic-induced hyponatremia (mean serum sodium level [+/- SD], 110 +/- 2 mEq/L [110 +/- 2 mmol/L]) and overt neurological manifestations were treated with 3% sodium chloride. Within 28.8 +/- 6 hours of treatment, the serum sodium level was corrected to 132 +/- 5.6 mEq/L (132 +/- 5.6 mmol/L), indicating a correction rate of 0.78 +/- 0.26 mEq/L/h (0.78 +/- 0.26 mmol/L/h). Seven of the eight patients recovered from the neurological insult and were discharged from the hospital. One patient died of an unrelated illness. Severe diuretic-induced hyponatremia seems to be predisposed by age, sex, and body weight. Patients with this entity are usually old, female, and underweight. Associated conditions (eg, intractable diarrhea, tube feeding, hypoglycemic drugs, polydipsia, and cerebrovascular accidents) may play a role in the pathogenesis of the syndrome.     

Hyponatremic encephalopathy: is central pontine myelinolysis a component?

PURPOSE: Severe hyponatremia is often associated with permanent brain damage. There has been substantial controversy about whether central pontine myelinolysis (CPM), a rare neurologic disorder of uncertain etiology, can complicate either hyponatremia or its therapy. This study was undertaken to determine how often hyponatremic patients with the clinical diagnosis of CPM actually have the disorder as an integral structural component of their encephalopathy. PATIENTS: Analyses were carried out in 20 patients who had severe symptomatic hyponatremia and a presumptive diagnosis of CPM, based on clinical and/or neuroradiologic findings. All had been referred for neuroradiology consultation. The mean age (+/- SD) was 47 +/- 14 years, the lowest serum sodium level was 104 +/- 8 mM, and 85% of the patients were female. The etiologies were diverse and included postoperative status, thiazide diuretics, polydipsia, infection, acute renal failure, chronic alcoholism with emesis, and beer potomania. METHODS: The original and subsequent films of 20 patients were reevaluated retrospectively by two neuroradiologists. The clinical course was also reevaluated, and in eight patients, the postmortem brain findings were reviewed. The diagnosis of CPM was made only on the basis of strict criteria relating to either (1) pathologic findings of CPM on postmortem examination; or (2) computed tomographic scan and/or magnetic resonance imaging findings diagnostic of CPM. RESULTS: No pontine lesions were present in 15 of 20 patients in whom the diagnosis of CPM had initially been made. All 15 had extrapontine demyelinating lesions but the pons was normal. Two others had only lateral pontine lesions, so that only three of 20 patients had definite CPM. All but one of the 20 hyponatremic patients had a definite hypoxic event prior to any therapy with intravenous sodium chloride. The involved brain areas included basal ganglia, thalamus, cortical gray matter, and periventricular white matter, areas often affected by hypoxia. Each of the three patients in whom unequivocal findings of CPM were present had long histories of chronic alcoholism and hepatic cirrhosis. CONCLUSIONS: These results suggest that: (1) Neither hyponatremic encephalopathy nor its therapy is commonly associated with CPM; (2) Patients with chronic alcoholism who also become hyponatremic can develop pontine demyelinating lesions; (3) Most patients with symptomatic hyponatremia who are diagnosed as having CPM in fact have diffuse cerebral demyelinating lesions with a normal pons; (4) The distribution of cerebral demyelinating lesions in patients with hyponatremic encephalopathy is compatible with hypoxic damage.     

急性心肌梗死低钠血症的预后价值

目的探讨急性心肌梗死(AMI)低钠血症的预后价值。方法对我院心内科CCU病房2003年1月至2004年12月670例资料完整的AMI患者进行了回顾性分析,根据患者入院后即刻、24、48h血清钠离子浓度最低值共分为三组:A组Na+≥135mmol/L;B组Na+120~135mmol/L;C组Na+≤120mmol/L。比较各组心肌酶、心肌梗死面积、心功能及住院病死率。结果(1)三组住院病死率分别为:A组7·6%(17/225),B组8·1%(34/421),C组33·3%(8/24),C组分别与A组和B组比较,差异具有统计学意义(P<0·05)。(2)三组肌酸激酶(CK),肌酸激酶同工酶(CK-MB)及心肌梗死面积(S)进行比较,C组分别与A组和B组比较差异有统计学意义(P<0·05)。(3)住院期间死亡59例,存活611例,存活组与死亡组血清钠离子浓度分别为(133·00±5·25)mmol/L和(122·00±7·25)mmol/L,两组比较差异有统计学意义(P<0·01)。(4)对AMI后30天住院期间死亡危险因素进行多因素logistic回归分析,血清钠离子浓度降低与AMI后30天住院期间病死率相关。并且30天住院期间病死率随着血清钠离子浓度降低而升高。结论低钠血症可能是AMI预后不良的标志之一。     

Terlipressin-induced hyponatremic encephalopathy in a noncirrhotic patient

Terlipressin, an analogue of vasopressin, is frequently used for the management of esophageal varices bleeding and hepatorenal syndrome. Terlipressin therapy in portal hypertensive patients is frequently associated with hyponatremia, but is rarely accompanied with serious neurological manifestations. A 39-year-old female with pancreatic neuroendocrine tumor, liver metastasis, main portal vein thrombosis, and a history of esophageal varices presented to the emergency room because of hematemesis. Terlipressin was given with a loading dose of 2 mg followed by 1 mg every 6 hours. After a total of 6 mg terlipressin injection, she suffered from acute delirium. Pertinent examinations showed there was no gross brain lesion by computed tomography, whereas her serum sodium level dropped from baseline (136 mmol/L) to 116 mmol/L with a serum osmolality of 256 mOsm/kg. At that time, urine sodium and urine osmolality were 142 mmol/L and 488 mOsm/kg, respectively. Under the tentative diagnosis of terlipressin-induced hyponatremic encephalopathy, terlipressin was withheld and hypertonic saline infusion was given. Within 12 hours, her serum sodium level recovered to 130 mmol/L and she gradually regained her cognitive functions. Although symptomatic hyponatremic encephalopathy is a rare complication of terlipressin treatment, close monitoring of serum electrolyte level is warranted in patients receiving terlipressin.     

连续性静脉-静脉血液滤过治疗急性严重低钠血症六例

目的　观察连续性静脉 静脉血液滤过 (CVVH)治疗急性严重低钠血症的疗效。方法急性严重低钠血症 6例 ,基础病变分别为慢性肾功能衰竭 3例 ,急性肾功能衰竭、妊娠子痫及骨科手术后各 1例。所有患者血钠均低于 115mmol/L ,均为 4 8h内发生。采用中心静脉留置导管建立血管通路行CVVH。滤器为AN6 9及AV6 0 0各 2例 ,HF12 0 0及FH6 6各 1例 ,每 2 4h更换 1次 ,低分子肝素抗凝。结果　CVVH平均治疗时间为 5 9 7h。CVVH治疗中 ,患者血流动力学稳定 ,6例意识模糊者 ,5例治疗 12h后意识有所好转 ;3例嗜睡及谵妄者治疗 2 4h后症状消失 ;1例抽搐者治疗 2 4h后症状消失 ;1例昏迷者治疗 96h后神志完全恢复正常。CVVH治疗后 4 8h血钠上升至 (14 0 3± 1 6 )mmol/L ,纠正速度为 (0 82± 0 10 )mmol·L-1·h-1;血渗量水平为 (2 95 0± 4 2 )mOsm/kgH2 O ,纠正速度为 (1 6 3± 0 2 0 )mOsm·kgH2 O-1·h-1。CVVH开始置换液钠比血钠高 (16 0± 6 0 )mmol/L。CVVH治疗 4 8h后Glasgow评分较治疗前有显著升高 (P <0 0 5 ) ,APACHEⅡ评分较治疗前有显著降低 (P <0 0 5 )。 6例患者全部存活 ,3例转为维持性血液透析 ,3例完全康复。结论　CVVH治疗严重急性低钠血症是有效的 ,为严重急性低钠血症的救治提供了新的治疗     

Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist: a randomized double-blind multicenter trial

BACKGROUND & AIMS: Dilutional hyponatremia is a frequent complication of cirrhosis partly because of nonosmotic vasopressin release. No effective therapy exists for this complication. Therefore, we investigated the effects of VPA-985, an orally active vasopressin V2 receptor antagonist, in patients with cirrhosis and dilutional hyponatremia. Primary endpoint was normalization of serum sodium (serum sodium >or=136 mmol/L). METHODS: Sixty patients with cirrhosis and dilutional hyponatremia were randomly assigned to 100 or 200 mg/day of VPA-985 or placebo in a double-blind study. Treatment was given with fluid restriction (1000 mL/day) until normalization of serum sodium or for 7 days. RESULTS: Normalization of serum sodium concentration was achieved in 27% and 50% of patients in the VPA-985 100 mg/day and 200 mg/day groups, respectively, but in none of the patients in the placebo group (P < 0.05 and P < 0.001, respectively). Treatment with VPA-985 was associated with a significant reduction in urine osmolality and body weight. Thirst sensation increased significantly in the VPA 200 mg group but not in the VPA 100 mg or placebo group. Serious adverse events were similar among the 3 groups. CONCLUSIONS: An orally active vasopressin receptor antagonist can correct hyponatremia in patients with cirrhosis and ascites. This represents a novel therapy of water retention in cirrhosis.     

慢性心力衰竭伴低钠血症患者102例临床分析

目的 探讨3%氯化钠治疗慢性心力衰竭伴低钠血症患者的临床疗效.方法 对102例慢性心力衰竭(纽约心功能分级Ⅲ-Ⅳ级)伴低钠血症患者,给予限水、扩张血管、强心、利尿、血管紧张素转换酶抑制剂/血管紧张素II受体拮抗剂等常规治疗外,同时给予3%氯化钠.比较治疗前后患者的心功能分级、治疗效果及血钠水平.结果 102例患者治疗后,心功能恢复至Ⅰ级39例,心功能恢复至Ⅱ级47例,心功能Ⅲ级11例,心功能Ⅳ级5例.与治疗前心功能Ⅲ级45例,Ⅳ级者57例比较,差异有统计学意义(χ2=150.26,P＜0.05).治疗后显效58例,37例有效,7例无效,总有效率93.1%.治疗后心功能Ⅲ级、Ⅳ级患者的血钠分别(139.4±22.6) mmol/L、(138.2±23.3)mmol/L,与治疗前心功能Ⅲ级、Ⅳ级患者的血钠(122.9±20.5)mmol/L、(120.5±26.8)mmol/L比较,差异有统计学意义(t=2.02、2.04,均P＜0.05).结论 合理利尿、适当补充钠盐有助于减少慢性心力衰竭伴低钠血症患者不良事件的发生,改善患者预后.

Abstract：

Objective To summarize the clinical experience of 3% sodium chloride in treatment of chronic heart failure with hyponatremia. Methods The 102 patients suffering from chronic heart failure with hyponatremia were treated with water limit, vasodilator, cardiotonic, diuretics, angiotensin-converting enzyme inhibitor, angiotensin Ⅱ receptor antagonist and 3% sodium chloride. Cardiac functional capacity classification (NYHA), treatment effect and hyponatremia level were compared between pre- and post- treatment. Results After treatment, heart function was statistically different as compared with that of pre-treatment (χ2=150.26, P＜0.05). The 58 cases showed distinct effect, 37 cases moderate effect, 7 cases no effect, and the percentage of total effect was 93.1%. The hyponatremia of patients with different level of heart function were (139.4±22.6) mmol/L, (138.2±23.3) mmol/L, the difference had a statistics significance compared with pre-treatment hyponatremia which were (122.9±20.5) mmol/L, (120.5±26.8) mmol/L (t=2.02, 2.04, P＜0.05). Conclusions Proper diuresis and sodium salt supplement could help to reduce the malignant risk of the patients suffering from chronic heart failure with hyponatremia and to improve the prognosis.     

SIADH closely associated with non-functioning pituitary adenoma

We demonstrated severe hyponatremia in a 68 year-old man who had pituitary tumor. He had poor appetite and was disoriented. Tests revealed hyponatremia of 110 mmol/l, and he was admitted to Jichi Medical School Omiya Medical Center to undergo further tests. Physical findings revealed disturbance of consciousness with Japan Coma Scale I-2. There was neither dehydration nor edema. Laboratory data showed a serum sodium level of 112 mmol/l; plasma osmolality, 219 mmol/kg; and urinary osmolality, 555 mmol/kg. Plasma arginine vasopressin (AVP) level was 1.6 pmol/l despite the marked hypoosmolality. Anterior pituitary function was normal. Brain magnetic resonance imaging showed a pituitary tumor of 20 x 18 x 20 mm in size, which pushed the pituitary stalk upward. After the adenomectomy, serum sodium level was kept normal without any treatment. Histology showed basophilic adenoma. These findings indicate that local pituitary tumor may cause exaggerated secretion of AVP, resulting in the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).     

Central pontine and extrapontine myelinolysis associated with type 2 diabetic patient with hypokalemia

Central pontine myelinolysis (CPM) is a demyelinating disease of the pons often associated with the demyelination of extrapontine areas of the central nervous system. Although the etiology and pathogenesis are unclear, CPM is usually associated with hyponatremia or its rapid correction, and chronic alcoholism is also a common underlying condition. We observed a 43-year-old man with diabetes mellitus who developed central pontine and extrapontine myelinolysis with no apparent evidence of hyponatremia, serum hyperosmolality or associated rapid correction, or history of alcohol abuse. On admission, the patient was lethargic with dysarthria, dysphagia, and mild tetraparesis and his face and lower extremities were severely edematous. Laboratory examination showed normoglycemia and normonatremia, although hypokalemia, elevated HbA1c, and nephrotic syndrome were also present. Magnetic resonance imaging (MRI) revealed abnormal signal intensity in the pons, the deep layers of the cerebral cortex, and the adjacent white matter consistent with central pontine and extrapontine myelinolysis. Generalized edema was reduced by the use of diuretics and extracorporeal ultrafiltration without significant changes of serum sodium or osmolality. His consciousness level and paresis gradually improved within a few weeks. Our patient is a rare case of CPM associated with diabetes without apparent evidence of sodium or glucose imbalances.     

脑出血患者载脂蛋白E基因型分布及相关研究

目的研究脑出血患者载脂蛋白E(apoE)基因多态性分布特点,探讨脑出血患者apoE基因型与神经功能缺损和血清高敏C反应蛋白(hs-CRP)水平的关系。方法选择脑出血患者78例(脑出血组)和健康体检者91例(对照组),利用PCR-RFLP技术,测定apoE基因型;采用生化全自动仪分别对TC、TG、LDL-C、HDL-C、空腹血糖和血清hs-CRP水平等进行测定;脑出血患者入院时采用美国国立卫生研究院卒中量表(NIHSS)进行神经功能缺损评分。结果脑出血组apoEε4基因频率明显高于对照组,apoEε2基因频率明显低于对照组(P<0.05,P<0.01);脑出血组TC、TG、LDL-C、空腹血糖水平明显高于对照组,HDL-C水平明显低于对照组(P<0.05);脑出血组apoEε4携带者NIHSS评分明显高于非apoEε4携带者(P<0.05);脑出血组apoEε2和apoEε4携带者血清hs-CRP水平明显高于非apoEε2和非apoEε4携带者(P<0.05)。结论 apoEε4可能是脑出血的危险因素;脑出血急性期炎性反应可能与apoEε2和apoEε4有关。     

Severe symptomatic hyponatremia in elderly outpatients: the role of thiazide therapy and stress

Severe symptomatic hyponatremia (serum sodium level 112 +/- 5.5 mEq/l) was encountered in six elderly outpatients within four days of the onset of thiazide therapy. Associated polydipsia was present in two of these patients, but the thiazides alone appeared responsible in the others. In three other elderly outpatients, severe hyponatremia (serum sodium level 112 +/- 5.25 mEq/l) developed after the acute emotional stress of relocation from their place of abode to a nursing home or hospital. Recurrent episodes of hyponatremia occurred in two patients following reinstitution of diuretic therapy, and, in two other patients, was precipitated by thiazides and stress on different occasions. Severe neurologic manifestations occurred in all patients and were mostly attributed to atherosclerotic dementia or stroke. Two patients died with severe hyponatremia, although all patients in whom cessation of thiazide therapy and water restriction were instituted promptly recovered without permanent sequelae.     

Management of severe hyponatremia: rapid or slow correction?

Case reports and the literature on the treatment of severe hyponatremia were reviewed. It appeared that the conflicting opinions with respect to the rate of correction of severe hyponatremia could be reduced to not differentiating between acute and chronic hyponatremia, to using different criteria for this distinction, and to differences in treatment strategy. After reviewing the available data in the literature, it is suggested that hyponatremia should be classified as acute whenever the rate of decrease of serum sodium exceeds 0.5 mmol/L/hour. If it is unknown at which rate the hyponatremia has developed, it can be assumed to be acute if within a short period of time (two to three days), large quantities of fluid are ingested orally or administered parenterally, especially hypotonic fluids in the presence of impaired water excretion. In other cases, chronic hyponatremia is probable. It is concluded that acute hyponatremia should be treated without delay and rapidly at a rate of at least 1 mmol/L/hour, to prevent severe neurologic damage or death. With respect to chronic hyponatremia, it appeared that severe neurologic complications almost exclusively occurred in patients who were treated with hypertonic or isotonic saline without the addition of furosemide or an osmotic diuretic agent, resulting in a (rapid) correction rate of 0.5 mmol/L/hour or more. In contrast, patients with severe chronic hyponatremia treated with furosemide and isotonic or hypertonic saline almost uniformly did well after rapid correction. Uneventful recovery is also the rule when severe chronic hyponatremia is corrected slowly, at a rate less than 0.5 mmol/L/hour. On pathophysiologic grounds, and bearing in mind that slow correction was used in the majority of reported patients in the literature with severe chronic hyponatremia who recovered without neurologic complications, this treatment modality is preferable. Whenever the available data do not permit a differentiation between acute or chronic hyponatremia, rapid correction has to be pursued by means of administration of hypertonic or isotonic saline together with furosemide.     

小细胞肺癌合并低钠血症的临床特点研究

目的:探讨小细胞肺癌(SCLC)患者合并低钠血症的临床表现及其预后的关系。方法:收集我院2001年1月至2011年12月明确诊断为SCLC患者180例,比较初治时血钠正常患者(A组)与合并低钠血症患者(B组)临床分期、血钠水平、临床症状、病情进展程度和疗效。结果:SCLC合并低钠血症的发生率为12.2%。总体中位生存期是8.89个月,A组患者的1年和2年生存率分别为77.8%(123/158)和22.8%(36/158),而B组患者的1年和2年生存率分别为22.7%(5/22)和4.5%(1/22),2组比较差异有统计学意义(P=0.001 8)。2组SCLC患者血钠值水平存在统计学差异[(142.11±2.12)mmol/L比(111.22±2.67)mmol/L,P0.05];B组出现胸腔积液和多部位转移的比例显著高于A组(54.5%比9.5%和31.8%比8.9%,均P0.05)。结论:SCLC合并低钠血症的发生率为10%左右,并发低钠血症的SCLC患者可能预后更差。     

Treatment of symptomatic hyponatremia

Inadequate treatment of severe hyponatremia (<120 mEq/L) can be associated with severe neurological damage. In acute (<48 hours) hyponatremia, usually observed in the postoperative period, prompt treatment with hypertonic saline (3%) can prevent seizures and respiratory arrest. For patients with chronic (>48-72 hours) symptomatic hyponatremia, correction must be rapid during the first few hours (to decrease brain edema) followed by a slow correction limited to 10 mmol/L over 24 hours to avoid the development of osmotic demyelinating syndrome. In patients with asymptomatic hyponatremia, slow correction is the appropriate approach. When patients are overtreated, neurologic damage can be prevented by relowering the serum sodium (SNa) so that the daily increase in SNa remains below 10 mmol/L/24 hours. Frequent measurements of SNa during the correction phase of SNa are mandatory to avoid overcorrection. The use of urea to treat hyponatremia represents an advantageous alternative to hypertonic saline.     

Close association of severe hyponatremia with exaggerated release of arginine vasopressin in elderly subjects with secondary adrenal insufficiency

OBJECTIVE: Hyponatremia occurs not infrequently in hypopituitarism. Arginine vasopressin (AVP)-induced impaired water excretion is found in patients with hypopituitarism and experimental models of glucocorticoid deficiency. DESIGN: The present study was undertaken to determine whether augmented release of AVP is involved in the development of hyponatremia in elderly subjects with secondary adrenal insufficiency. METHODS: Forty patients with ACTH-deficient, secondary adrenal insufficiency were examined. They were divided into three groups according to the age at which diagnosis was ascertained (group A <20 Years, group B 20-64 Years, and group C>or=65 Years). RESULTS: Hyponatremia was more manifest in the elderly group than in the other two groups, serum sodium (Na) levels being 124.7 mmol/l in the elderly group, a value significantly less than 141.5 and 133.5 mmol/l in groups A and B. Plasma AVP levels seemed likely to be high compared with the respective hypo-osmolality in plasma in the elderly group, as plasma AVP levels were 1.7 pmol/l despite a mean plasma osmolality of 259 mmol/kg. Such an alteration was less clear in group B and was not found in group A. Therefore, elevation of plasma AVP was apparent in the elderly patients. Hydrocortisone replacement promptly normalized serum Na levels from 125 to 142 mmol/l (P<0.01) and reduced plasma AVP levels from 1.7 to 0.9 pmol/l (P<0.05), which were comparable to the respective plasma osmolality in the elderly patients. CONCLUSION: These results indicate that non-suppressible release of AVP is crucially involved in the impaired water excretion and hyponatremia seen in elderly patients with secondary adrenal insufficiency compared with the younger patients, and that exaggerated release of AVP becomes manifest as the subjects grow older.     

低钠血症诊断思路

低钠血症(血清钠<135 mmol/L)是临床最常见的电解质紊乱之一，临床表现主要包括神经系统和肌肉系统表现两个方面。首先应该查血渗透压水平除外假性低钠血症，尿渗透压检查可以鉴别大量饮用低渗液体或其他肾外失钠的情况，容量判断有助于进一步鉴别低钠血症原因。利尿剂过量、脑耗盐综合征和盐皮质激素减少都能造成低容性低钠血症。而等容或高容性低钠血症则常常因为抗利尿激素不适当分泌综合征、甲状腺激素不足、糖皮质激素缺乏或心、肝、肾功能不全引起。