急性颈脊髓损伤并发低钠血症的机制及治疗分析

目的 :探讨急性颈脊髓损伤患者并发低钠血症的病因、发病机制和治疗方法。方法 :自2005年1月至2010年7月收治严重创伤导致急性颈脊髓损伤伴高位截瘫并发低钠血症患者57例,男46例,女11例;年龄26～69岁,平均39.5岁;颈椎骨折或脱位55例,无骨折或脱位型脊髓损伤2例;完全性损伤28例,不完全性损伤29例。神经功能损害按ASIA分级:A级28例,B级25例,C级4例。每日监测心率、血压、尿量、血钠,诊断低钠血症后即开始静脉补液、补钠,每隔2 d检测尿钠、血浆渗透压、尿渗透压,根据监测结果及治疗反应判断低钠原因是由脑性盐耗综合征(CSWS)还是由抗利尿激素不适当分泌综合征(SIADH)引起,前者继续静脉补液、补钠,后者严格限水同时静脉补钠直至低钠纠正。对治疗前后血钠等指标进行统计学分析。结果:57例中诊断CSWS者42例,SIADH者15例。治疗3周后所有患者的心率、血钠、血渗透压有明显回升(P<0.01),血压、尿渗透压升高,尿钠减少(均P<0.05),尿量未见明显减少(P>0.05)。出院时与治疗3周比较,心率、血浆渗透压、尿渗透压进一步回升,尿量减少,尿钠进一步减少(P<0.05),血压无明显改变(P>0.05)。结论:急性颈脊髓损伤后并发低钠血症受多因素影响,发病机制主要为脑性盐耗综合征(SCWS)及抗利尿激素不适当分泌综合征(SIADH),治疗时应注意鉴别,根据不同病因采取补液或限液治疗。     

急性颈脊髓损伤后低钠血症的原因及治疗

目的探讨急性颈脊髓损伤后发生低钠血症的相关因素、发病机制、诊断及治疗。方法回顾性分析2001年4月-2007年3月收治的急性颈脊髓损伤后低钠血症患者16例的临床资料。所有患者血钠〈130mmol/L,尿钠36～79mmol/L,尿渗透压390～910mmol/L,均采用3%高渗盐水静脉滴注。结果16例患者中,1例术后3天因呼吸功能衰竭死亡,2例失访,其余13例经限水、适当补钠治疗后血钠恢复正常。结论低钠血症的发生与颈脊髓损伤的程度密切相关,限水、适当补钠是有效的治疗方法。     

急性颈髓损伤后的低钠血症

[目的]探讨急性颈髓损伤后低钠血症的病因、发病机制、诊断和治疗。[方法]回顾性分析2004年-2006年收治的急性颈髓损伤后低钠血症患者15例的临床资料。[结果]全组患者入院24—72h内血钠低于130mmol／L，其中5例低于120mmol／L。14例尿钠40—68mmol／L，1例尿钠为148mmol／L；尿渗透压420～980mmol／L，12例患者经适当的补盐和限制水摄入量治疗，低钠症状2～3周内改善；2例发热患者因发热不能严格限制水摄入，其中1例2个月后恢复，另1例失访；1例患者补盐限水后病情加重，调整治疗方案后恢复。[结论]颈髓损伤越重，损伤后低钠血症发生率越高；颈髓损伤后低钠血症多由抗利尿激素分泌异常综合征引起；血钠浓度，血、尿渗透压等是诊断依据；适当补充钠盐和液体量是有效的治疗方法。     

急性颈脊髓损伤并发抗利尿激素分泌异常综合征的诊断和治疗

目的探讨急性颈脊髓损伤并发抗利尿激素分泌异常综合征的临床特点、诊断和治疗方法。方法回顾性分析8例急性颈脊髓损伤并发抗利尿激素分泌异常综合征患者的临床资料。脊髓损伤分级:FrankelA级5例,B级3例;损伤节段:C4～53例,C5～63例,C6～72例。8例于受伤后3～7d行骨折椎体次全切除椎管减压、自体髂骨植骨融合及颈椎前路钢板内固定术。3例于术前,5例于术后3～7d发生低钠血症,所有患者低钠血症发生后第2～10d确诊SIADH,根据血钠水平,采用控制每日水量、补钠进行治疗。结果7例经10～21d治愈,血钠平均恢复至138(135～142)mmol/L,血浆渗透压、尿渗透压、尿钠均正常;1例C4骨折、FrankelA级者,因截瘫平面上升并发呼吸衰竭死亡。结论急性颈脊髓损伤并发抗利尿激素分泌异常综合征的发病机制与治疗措施不同于普通低钠血症,早期正确的诊治能降低患者病残率和死亡率,严格控制入液量及补钠为主要治疗方法。     

急性颈脊髓损伤并发低钠血症的发病机制、治疗与预防

目的探讨急性颈脊髓损伤并发低钠血症的发病机制、治疗方法及预防措施。方法自2002—01—2012～12诊治急性颈脊髓损伤并发低钠血症179例。结果治疗1个月后各项指标与住院时相比较,血压、心率升高;24h尿量减少不明显（P〉0．05）;血钠、血浆渗透压、尿渗透压值升高;尿钠减少（P〈0．05）。出院时较治疗1个月时各项指标相比较,心率升高,血压无明显变化（P〉0．05）;尿量明显减少,血钠值升高,尿钠明显减少（P〈0．05）;血浆渗透压、尿渗透压值升高。结论急性颈脊髓损伤合并低钠血症的影响因素较多,发病机制为SIADH及CSWS,治疗时要鉴别,并可针对各种因素桌预防．减少低钠血症发毕率．     

颈髓损伤后抗利尿激素分泌异常综合征诊治分析

目的探讨颈髓损伤后伴发抗利尿激素分泌异常综合征的发病机制和诊疗方法。方法2004年1月至2006年12月收治的92例急性颈髓损伤患者中39例患者并发抗利尿激素分泌异常综合征。损伤节段分布,C3-4 2例,C4-5 19例,C5-6 12例,C6-7 6例;骨折26例,骨折伴脱位13例;颈髓损伤程度Frankel分级,A级28例,B级11例。监测血钠、尿钠、尿量、尿比重等变化,测量血浆抗利尿激素水平,行限水补钠治疗。结果本组39例患者,37例经限水补钠治疗3周,血钠基本恢复正常,病情好转。另2例出现顽固性低钠,多器官功能衰竭死亡。症状出现时间为（7.6±3.4）d,高峰出现时间（12.7±5.3）d,症状消失时间（45.5±16.3）d。结论急性颈髓损伤患者易并发抗利尿激素分泌异常综合征,发病隐匿,诊断相对困难,稀释性低钠血症、尿渗透压高于血浆渗透压及抗利尿激素增高是其诊断依据。治疗原则应以限水为主,严重低钠时可适当补盐,同时积极治疗原发病。     

神经外科抗利尿激素异常分泌综合征的诊治

目的探讨神经外科中抗利尿激素异常分泌综合征(SIADH)诊断、鉴别诊断及其治疗.方法对6例SIADH患者的临床表现、治疗经过、确诊过程进行回顾性分析总结.结果 SIADH病人特点(1)低血钠(血钠≤128 mmol/L),补钠越多,尿排钠越多,24 h尿钠与每日补充的钠总量持平;(2)ADH测定对SIADH与CSWS无鉴别意义;(3)无血容量增多或水肿表现;(4)限水治疗有效.结论 SIADH诊断及与CSWS的鉴别诊断十分困难,临床采用试验性限水限钠疗法,即是鉴别诊断的重要手段,又是SIADH治疗的有效方法.     

急性颈髓损伤后低钠血症51例临床分析

目的探讨急性颈髓损伤后低钠血症的病因、发病机制、诊断和治疗。方法分析51例急性颈髓损伤后低钠血症患者的临床资料。10例血钠130~134 mmol/L,未予特殊处理,16例血钠120~129 mmol/L,补充等渗盐水、高钠盐饮食;25例血钠低于120 mmol/L,采用3%高渗盐水静脉滴注。结果43例患者经适当的补盐和限制水量治疗,低钠症状均有恢复;6例高热患者因发热不能严格限制水摄入,其中4例3个月后恢复,2例死亡。2例失访。Frankel分级:A级35例中25例恢复到B级,5例恢复到C级,3例恢复到D级,2例无恢复;B级5例中1例无恢复,4例恢复到D级;C、D级病例均恢复正常。结论颈髓损伤越重,损伤后低钠血症发生率越高;适当补充钠盐和液体量是有效的治疗方法。     

颅脑损伤后中枢性低钠血症的诊断及治疗

目的探讨颅脑损伤后中枢性低钠血症的诊断及治疗方法。方法回顾分析62例颅脑损伤后中枢性低钠血症患者的临床资料,CSW S患者补钠、补水,SIADH患者限水补钠,同时注意适度脱水预防脑水肿。结果 56例平均8 d血钠正常;6例伤后6 d内死于重度脑干损伤。结论准确判断颅脑损伤后中枢性低钠血症的发病原因,及时阻断发病机制是治疗该并发症的重要前提。     

急性颈髓损伤并低钠血症的临床分析

目的:探讨急性颈髓损伤并低钠血症患者血钠浓度与颈髓损伤平面、程度的关系,观察低钠血症治疗效果.方法:回顾分析2002年1月～2007年12月我院收治的256例急性颈髓损伤并低钠血症患者资料,伤后第1天入院179例,第2天入院77例.高位颈髓(C4及C4以上)损伤101例,其中完全性颈髓损伤者59例,不完全性颈髓损伤者42例;低位颈髓(C4以下)损伤155例,其中完全性颈髓损伤者67例,不完全性颈髓损伤者88例.均于入院后第1、3、5天清晨空腹抽取静脉血查血钠,取其平均值,统计分析低血钠程度与颈髓损伤平面、程度的关系,观察低钠血症的治疗效果.结果:130mmol/L≤血钠＜135mmol/L者(轻度)96例,120mmol/L≤血钠＜130m01/L者(中度)122例,＜120mmol/L者(重度)38例.高位颈髓损伤者中,完全性损伤者血钠为117.33±4.52mm01/L.不完全性损伤者为125.49±3.74mmol/L;低位颈髓损伤者中,完全性损伤者血钠为123.67±3.81mmol/L,不完全性损伤者为131.9±4.85mmol/L,同一损伤部位完全性损伤者的血钠浓度与不完全性损伤者比较有显著性差异(P＜0.05),同一损伤程度高位损伤者与低位损伤者比较有显著性差异(P＜0.05).218例轻、中度低钠血症患者经治疗血钠完全恢复正常,38例重度低钠血症患者中9例因合并高热、感染、呼吸衰竭死亡.结论:急性颈髓损伤患者低钠血症的程度与颈髓损伤平面、程度有关,且血钠浓度越低,患者预后越差,病死率越高.     

Syndrome of Inappropriate Antidiuretic Hormone in Association with Amiodarone Therapy: A Case Report and Review of Literature

Background: Amiodarone is a class III antiarrhythmic agent that is widely used in the treatment of a variety of arrhythmias. Several different systemic side effects are reported after use of this medication. In this article, we report a case that had developed syndrome of inappropriate antidiuretic hormone (SIADH) after starting treatment with this agent.?Case report:?The patient is a 66-year-old male with past medical history of hypertension, hyperlipidemia, coronary artery disease, and class III New York Heart Association congestive heart failure who presented with monomorphic nonsustained ventricular tachycardia. A loading dose of amiodarone followed by maintenance dose was started. Baseline serum sodium of 138 mmol/L on admission decreased to 119 mmol/L by day 7, and a diagnosis of SIADH was made. The patient was not taking any other medication known to cause SIADH, nor had any such comorbidity to explain it. Serum sodium increased to 133 and 138 mmol/L, respectively, after 16 and 33 days from discontinuation of amiodarone.?Conclusion:?SIADH is a rare but serious side effect of amiodarone and practicing physicians should be aware of this complication, particularly after loading dose of the medication.     

Acute symptomatic hyponatremia and cerebral salt wasting after head injury: an important clinical entity.

Hyponatremia is a well known complication of traumatic and nontraumatic cerebral injury, often related to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Nonetheless, it also can be associated with a different entity, the syndrome of cerebral salt wasting (CSW). The authors report the case of a 4.5-year-old boy presenting with major head injury who at day 6 after admission had generalized tonic-clonic seizures caused by severe acute hyponatremia (serum sodium level, 119 mmol/L) and signs of dehydration. Despite initial isotonic rehydration, hyponatremia persisted because of excessive renal salt losses and concomitant enormous water losses, necessitating increasing amounts of sodium, up to 160 mmol/kg/d, and large amounts of intravenous fluids, up to 27 L/d. Highly increased levels of atrial natriuretic peptide (ANP) confirmed the diagnosis of CSW. The occurrence of a CSW has to be recognized early in the clinical course for adequate treatment and remains one of the important differential diagnosis of SIADH in hyponatremic states in patients with cerebral disorders, especially after head injury.     

Demeclocycline in the treatment of the syndrome of inappropriate secretion of antidiuretic hormone.

Fourteen patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been treated with demethylchlortetracycline (demeclocycline) 1200 mg daily. In 12 patients the underlying lesion was malignant. The serum sodium returned to normal (greater than 135 mmol/l) in all patients after a mean of 8.6 days (SD +/- 5.3 days). Blood urea rose significantly from the pretreatment level of 4.2 +/- 2.3 mmol/l to 10.1 +/- 5.1 mmol/l at ten days (P less than 0.001). The average maximum blood urea was 13.4 +/- 6.8 mmol/l. In four patients the urea rose above 20 mmol/l, and in two of these demecyocycline was discontinued because of thie rise. The azotaemia could be attributed to a combination of increased urea producation and a mild specific drug-induced nephrotoxicity. Discontinuation of demeclocycline in six patients led to a fall in serum sodium, in one case precipitously, and return of the urea towards normal levels. Demeclocycline appears therefore to be an effective maintenance treatment of SIADH, and the azotaemia that occurs is reversible and probably dose dependent.     

Hyponatremia in patients with the acquired immunodeficiency syndrome

Of 103 patients with the acquired immunodeficiency syndrome (AIDS) admitted for acute opportunistic infections, 36 had serum sodium less than or equal to 130 mEq/l (130 mmol/l). In 12 the hyponatremia was associated with volume depletion and corrected with saline replacement therapy. In 23 it was associated with the syndrome of inappropriate antidiuretic hormones secretion (SIADH). One patient had adrenal insufficiency and the serum sodium corrected after steroid replacement. We conclude that hyponatremia is a common electrolyte abnormality in AIDS patients suffering acutely from opportunistic infections and that SIADH and volume depletion are important contributing factors.     

Utility and limitations of biochemical parameters in the evaluation of hyponatremia in the elderly

We evaluated in 110 consecutive elderly hyponatremic patients the value of traditional clinical and biochemical data and the place of a test infusion of 2 liters isotonic saline over 24 hours, in establishing the etiology of the hyponatremia. The causes of hyponatremia were as follows: 31% SIADH patients, 23% patients with hyponatremia due to diuretics, 18% potomania patients, 15%salt depleted patients, 5% salt depleted SIADH patients, 5%patients with a salt loosing syndrome and 3% patients with hyponatremia of unknown origin. Several salt depleted (SD) and SIADH patients could be confounded. Usually, adults with SIADH show plasma uric acid values <4 mg/dL. In our elderly population, 41% of SD patients presented plasma uric acid <4mg/dL, while 27% of SIADH patients showed plasma uric acid >4mg/dL. Eighty-two percent of SD patients appeared to have plasma urea levels >30 mg/dL, but this was also the case in 21% of SIADH patients. Twenty-nine of the SD patients presented a urinary sodium >30 mEq/L, but all had fractional sodium excretion (FENa) lower than 0.5%. However, in SIADH, 42% of the patients presented also FENa <0.5%. Fractional excretion of urea (FE urea) below 50%was encountered in 82% of SD patients and FE urea above 50% in only 52% of the SIADH patients. Plasma renin and aldosterone values were poorly discriminative. A test infusion with 2 liters isotonic saline over 24 hours allowed a correct classification of all the patients. In about 2/3 of the population, administration of isotonic saline could be considered as useful (SD, most diuretic patients, potomania patients, salt loosing syndrome patients and some SD SIADH patients). A plasma sodium (Pna) increase of at least 5 mEq/L 24 hours after saline infusion has been suggested as highly suggestive of SD. Nevertheless, 29% of our SD patients did not increase their PNa level by 5 mEq/L or more,while 30% of our SIADH patients did. PNa improved after 2 liters isotonic saline over 24 hours in 90 patients (85%) as opposed to12 others (9 SIADH and 3 diuretic patients), decreasing their plasma sodium. The isotonic saline infusion test, only allows a reliable classification of hyponatremia, as far as both PNa and sodium excretion were taken into account. In the SIADH group, 6 patients (5%) presented initially manifest solute depletion and retained the 2 liters isotonic saline before developping inappropriate natriuresis. Six patients showed a transient salt loosing syndrome with high fractional potassium excretion (FEK) and high calciuria, which differentiates them from thiazide patients presenting also high FEK, but low calciuria. These patients were also polyuric at admission. The saline infusion was well tolerated in all but 2 patients, developping mild pulmonary congestion at the end of the test infusion. This revised version was published online in September 2006 with corrections to the Cover Date.     

Serum and urine responses to the aquaretic agent tolvaptan in hospitalized hyponatremic patients

Tolvaptan, an oral, selective arginine vasopressin (AVP) V2 receptor antagonist has been approved for the treatment of euvolemic and hypervolemic hyponatremia in the United States. This report summarizes our center's experience with thirteen patients treated for hyponatremia with one 15-mg dose of tolvaptan. The patients had euvolemic or hypervolemic hyponatremia with decreased serum osmolality and serum sodium (SNa) levels less than 129 mEq/L. Eight patients had a diagnosis of the syndrome of inappropriate antidiuretic hormone (SIADH), and five patients had a diagnosis of congestive heart failure (CHF). Results revealed an increase in SNa in all patients from 122.5 ± 4.2 to 128.9 ± 4.1 mEq/L (P < 0.05). The mean increase in SNa of 6.4 mEq/L (range 2-10 mEq/L) 24 h post-tolvaptan was not different in the two groups of patients, but SIADH patients had higher pre and post-tolvaptan SNa levels than CHF patients. Urine osmolalities (UOsm) decreased in all patients, and the patients with SIADH had significantly higher baseline UOsm and a larger decrease in UOsm 12 h post-tolvaptan administration when compared with the CHF patients. AVP levels did not change post-tolvaptan administration. However, the magnitude of increase in SNa levels was inversely related to pretolvaptan AVP levels in the SIADH subgroup (r = -0.7, P = 0.01). Three SIADH patients received small amounts of D5W to attenuate changes in SNa. No significant changes in mean arterial pressure, serum potassium, serum glucose, and blood urea nitrogen or serum creatinine were observed. The data show that tolvaptan is effective for the treatment of hyponatremia and may produce differing responses in disparate patient groups.     

Human herpesvirus 6 (HHV-6) associated permanent hyponatremia in umbilical cord blood transplant recipient

Long-term neurocognitive deficits after human herpesvirus-6 (HHV-6) infection are common in stem-cell transplant recipients, but SIADH (Syndrome of inappropriate antidiuretic hormone secretion) with persistent hyponatremia is rare. A 51-year-old woman presented with somnolence, hyponatremia (121 mmol/L) and HHV-6 viremia (80,330 copies/ml) on day +22 post umbilical cord blood transplant (UCBT). With waterrestriction, tolvaptan and combination of foscarnet and ganciclovir, patient's hyponatremia and HHV-6 viremia improved. On day +94 UCBT, hyponatremia and HHV-6 viremia recurred. Foscarnet was restarted and continued until day +269 UCBT due to multiple HHV-6 recurrences with persistent hyponatremia. At day +712, patient remains on water-restriction, tolvaptan for continuous hyponatremia from SIADH.