颈髓损伤后血浆心房肽动态变化与低血钠

目的:观察颈髓损伤(CSCI)患者血浆心房肽(ANP)的动态变化,探讨其与低血钠的关系。方法:采用放免分析法对15例CSCI并低血钠患者血浆心房肽水平进行测定,并与23例CSCI不伴低血钠患者及12例正常同龄组进行对照比较。同时检测血清钠和部分患者的24h尿钠及尿量。并将低血钠患者分为吸氧组和非吸氧组,观察吸氧对血浆ANP和血清钠恢复的影响。结果:⑴CSCI伴低血钠者血浆ANP水平较不伴低血钠者及正常对照组显著升高(P<0.01)。⑵CSCI急性期血浆ANP水平与CSCI程度(Frankel分级)密切相关,CSCI越重,ANP水平越高(P<0.05);ANP水平越高,血钠越低,二者呈显著负相关。⑶吸氧可加速血浆ANP的下降和血清钠的恢复。结论:⑴CSCI后低血钠患者血浆心房肽明显异常,且与CSCI的严重程度(Frankel分级)成正相关。血浆心房肽水平升高可能是导致CSCI后低血钠的一个重要因素;⑵纠正低氧血症可降低ANP水平,从而纠正CSCI后顽固性低血钠。     

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.     

颅脑损伤并发低钠血症的诊断治疗

目的探讨颅脑损伤后住院患者并发低钠血症的临床诊断与治疗。方法回顾分析急性颅脑损伤患者出现低钠血症的临床资料。结果 22例抗利尿激素分泌异常综合症患者21例血钠恢复正常,1例死于肺部感染。10例脑性耗盐综合症患者和5例营养性低钠血症患者血钠均恢复正常。结论密切监测血钠浓度,区别低钠血症的类别,将提高颅脑损伤治愈率。     

肝脏移植术后桥脑中央髓鞘溶解症的病因探讨

目的　进一步总结肝脏移植术后桥脑中央髓鞘溶解症 (centralpontinemyelinolysis,CPM )的临床特征及发病原因。方法　回顾性研究 1999年 1月至 2 0 0 3年 5月 14 2例原位肝脏移植患者的临床资料 ,比较分析移植后有无中枢神经系统并发症及有无CPM者 ,围手术期血钠、血镁、血浆渗透压及环孢素A(CsA)浓度的变化和总手术时间。结果　 14 2例肝脏移植患者中 13例 (9 2 % )出现中枢并发症 ,其中CPM 5例 (3 5 % ) ,脑出血 /脑栓塞 8例 (5 6 % )。CPM患者中 ,移植前 2例血钠 <130mmol/L ,平均 (130 6± 5 5 4 )mmol/L ,与无中枢并发症和非CPM中枢并发症者比较显著降低 (P <0 0 5 )。CPM与非CPM中枢并发症及无中枢并发症患者移植前后 4 8h血钠的变化分别为(19 5± 6 5 )mmol/L ,(10 1± 6 4 )mmol/L ,(4 5± 4 3)mmol/L(P <0 0 1)。CPM患者术后血浆渗透压显著升高。所有患者肝脏移植前后均存在低镁血症 ,但无组间差异。并发CPM患者的总手术时间为 (492± 190 )min ,显著长于无中枢并发症患者 (P <0 0 5 ) ;术后所有移植患者的血CsA浓度在正常范围 ,但有中枢并发症高于无中枢并发症者 (P <0 0 5 )。结论　肝脏移植者是CPM的易患人群。CPM的发生可能与慢性低钠血症 ,围手术期血钠大幅波动 ,术后血浆渗透     

肝移植术后的低钠血症

目的探讨肝移植术后低钠血症的原因及治疗。方法对肝移植术后发生低钠血症的27例患者的临床资料进行回顾性分析。结果25例在术后1周左右发生低钠血症,2例术前已有低钠血症,术后即发生严重低钠血症,一例患者发生急性低钠综合征;血钠为130～135mmol/L者10例,120～130mmol/L者12例,低于120mmol/L者5例;血钾、血磷及血钙均在正常范围;尿钠、钾、氯均在正常范围;5例患者测定腹水钠含量,均高于同时段血钠含量。治疗主要是通过胃肠和/或静脉补给高渗盐水。结论肝移植术后发生低钠血症的原因是多方面的,治疗上应去除导致低钠血症的原因,并持续、缓慢地补充高渗盐水。     

前列腺癌并SIADH 1例报告

前列腺癌伴顽固性低钠血症临床少见, 本文报道1例。患者因排尿困难入院, 住院期间出现乏力、精神淡漠、神志改变, 诊断为严重低钠血症。请内分泌科、神经内科等多学科会诊后诊断为抗利尿激素分泌异常综合征(SIADH)。完善PSA及前列腺MRI检查, PSA升高, MRI检查考虑前列腺癌, 后经前列腺穿刺确诊为前列腺癌。术前口服托伐普坦使血清钠维持正常, 行腹腔镜根治性前列腺切除术。术后1个月患者乏力、纳差症状消失, 停用托伐普坦并停止补钠, 复查血清钠恢复正常。随访6个月, 肿瘤及低钠血症未复发。     

脑外伤伴抗利尿激素分泌异常综合征

抗利尿激素(ADH)分泌异常综合征(SIADH),是脑外伤伴低血钠症的主要原因之一,严重的低血钠症往往导致脑水肿或其它脑损害,近年来有更多有关低血钠症与脑损伤互为因果的报道犤1、2犦。本文就近年来SIADH的有关研究进展,综述如下。1SIADH的命名1957年Schwaitz观察到2例支气管肺癌的病人表现出低血钠伴肾性失钠,推测其原因可能为ADH异常分泌所致。此后发现此症多见于一些中枢神经系统疾病。其它如肺部疾病、癌肿以及许多药物都可能引起这种表现犤3、4犦,遂定名为抗利尿激素分泌异常综合征(SIADH)。2SIADH的发病机制在正常生理条件…     

血钠水平与重型颅脑损伤预后相关性研究

目的探讨重型颅脑损伤不同血钠水平对患者病情及预后的影响。方法采用回顾性队列研究方法分析2020年1月—2022年10月河西学院附属张掖人民医院收治的150例重型颅脑损伤的病例资料, 根据入院后第1天及脑水肿高峰期间(伤后2～4 d)、伤后7 d检测的5次血钠值, 得出血钠代谢失调者102例, 根据血钠水平分为两组, 低钠组:血钠平均值<135 mmol/L者43例, 高钠组:血钠平均值>145 mmol/L者59例。分析患者钠离子代谢失衡特点及血钠水平与伤后2周格拉斯哥昏迷评分(GCS)、格拉斯哥预后评分(GOS)、急性生理与慢性健康评分(APACHE Ⅱ)之间的关系。正态分布的计量资料以均数±标准差(±s)表示, 组间比较采用t检验;计数资料以例数或百分率(%)表示, 组间比较采用χ²检验。结果本组患者伤后急性期钠代谢失衡率为68.00%(102/150), 其中高钠血症发生率为57.84%(59/102), 低钠血症为42.16%(43/102), 在伤后7 d时钠代谢失衡率明显高于伤后即刻, 高钠血症的发生时间早于低钠血症、持续时间长于低钠血症(...     

Atrial natriuretic polypeptide in patients with subarachnoid haemorrhage due to aneurysmal rupture

Summary Measurement of plasma alpha-humanANP (ANP) and antidiuretic hormone (ADH) in 28 cases with aneurysmal subarachnoid haemorrhage (SAH) was carried out, and then compared with control subjects who were infused with hypertonic saline.In cases with hyponatremia (HN), statistical correlation between control subjects and cases without HN was not evident with regards to ANP and plasma osmolality (Posm), excreted fraction of filtrated sodium (FENa) and urinary Na/K. Furthermore, they secreted supernumerarilly in spite of HN.Cases with HN were further subdivided into two groups, they were those cases with negative total sodium balance at the time of appearance of HN, and those cases without total negative sodium balance. In the former, central venous pressure had a tendency to decrease, however, secretion of ANP and ADH was statistically not different in either groups.It appears that ANP regulated urinary sodium excretion against an osmotic or sodium load acts as a maintenance of homeostasis as an osmotic regulator. Cases with HN in which secretion of ADH was physiological, ANP secreted supernumerarilly in spite of hypoosmonaemia and hypovolaemia.Our findings may contribute to a better understanding of the pathophysiological processes leading to hyponatremia in cases with cerebral disorders, and may help to improve the treatment possibilities.     

A study of plasma atrial natriuretic peptide, antidiuretic hormone and aldosterone levels in a series of patients with intracranial disease and hyponatremia]

For intracranial diseases, plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone were determined and their effects on the development of hyponatremia with central origin were studied. The subjects were 71 cases of intracranial diseases which were admitted to our hospital during a period of 1 year from March, 1989 to March, 1990. The diseases were broken down to subarachnoid hemorrhage 26 cases, hypertensive intracerebral hemorrhage 19 cases, head injury 12 cases, cerebral infarction 11 cases and 3 other cases. Serum-urine electrolytes, plasma ANP and ADH were determined in the acute stage on Day 1 to 4, in the hyponatremia stage on Day 5 to 14 and in the chronic stage on Day 15 downward. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less. Cases evidently having other causes such as heart failure and renal insufficiency were excluded. In the normal control group of persons who were admitted to our hospital for a close checkup (n = 20), plasma ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of 50 pg/ml or more were regarded as abnormally high. 1) Hyponatremia was found in 18 cases (25.4%), subarachnoid hemorrhage in 7 cases, hypertensive intracerebral hemorrhage in 4 cases, head injury in 5 cases and others in 2 cases. 2) The time of onset of hyponatremia was on the 8.3 hospital day. The duration was 7.2 days. The minimum serum sodium level was 124.6 mEq/l. 3) There was no significant change in the plasma aldosterone level at each stage.2+ Predicting development of hyponatremia from plasma ADH and ANP levels in the acute stage is difficult. Inadequate secretion of ANP rather than ADH appeared to be an important factor for the development of hyponatremia, but the plasma ANP level was not always abnormally high, so involvement of other sodium diuretic factors should also be kept in mind.     

The electrolytes in hyponatremia.

It is commonly taught that retention of free water is the dominant factor reducing the serum sodium concentration in hyponatremia. To determine whether the concentrations of other electrolytes are similarly diluted, we identified 51 patients with hyponatremia (Na = 121 +/- 1 mmol/L [mEq/L]) and compared electrolyte and laboratory values at the time of hyponatremia with values at a time when serum sodium was in the normal range (138 +/- 1 mmol/L). The medium interval between these measurements was 12 days. At the time of hyponatremia, serum sodium and chloride were substantially and significantly reduced by 12% to 15%. Although many hyponatremic patients had overtly increased or decreased concentrations of the other measured electrolytes, there were no significant changes in the mean concentration for any of these at the time of hyponatremia. Unchanged mean values were found for the plasma concentration of bicarbonate (26.1 +/- 0.6 normal v 25.2 +/- 0.8 mmol/L at the time of hyponatremia), potassium (4.31 +/- 0.10 v 4.33 +/- 0.15 mmol/L), albumin, phosphate, and creatinine. The stability of these laboratory values was observed both in patients with clinically normal extracellular fluid (ECF) volume and in those with true or effective ECF depletion. The urinary sodium (UNa) concentration was found to be a reliable predictor of the ECF volume status, whereas the fractional sodium excretion (FENa) was not. Electrolyte derangements are common in patients with hyponatremia, but are usually confined to patients on diuretics or who have an abnormal ECF volume. In the absence of these complicating situations, the plasma electrolytes are typically normal and are not reduced by dilution to the same extent as Na and CI. Based on a review of both the classic and recent knowledge concerning electrolyte regulation in hyponatremia, we propose that two factors explain these observations. First, the degree of dilution is overestimated because of Na losses in urine and perhaps Na shift into cells. Second, both renal and extrarenal adaptive mechanisms are activated by hyponatremia that stabilizes the concentration of other ions. One of these mechanisms is cell swelling, which triggers a volume-regulatory response leading to the release of ions and water into the ECF. Other adaptive mechanisms are mediated by antidiuretic hormone (ADH) per se, and by atrial natriuretic peptide (ANP).     

Hyponatremia and hyperreninemic hypoaldosteronism in a critically ill patient: combination of insensitivity to angiotensin II and tubular unresponsiveness to mineralocorticoid

A 62-year-old man with pneumonia and left flank pain had a clinical syndrome of hyponatremia, hypotension, dehydration, and high urinary sodium excretion in the presence of a normal glomerular filtration rate. The plasma level of antidiuretic hormone was relatively high despite decreased serum osmolality. Thyroid function and excretion of glucocorticoid and sex steroids were normal. The serum aldosterone level was very low despite elevated plasma renin activity. Angiotensin II failed to stimulate any secretion of aldosterone, despite the occurrence of a progressive rise in blood pressure. On the other hand, rapid ACTH administration increased both serum aldosterone and cortisol. The patient showed no effective response to increased salt intake, but large doses of mineralocorticoid resulted in a normal serum sodium level without dehydration. Subsequently, he suffered cardiac arrest secondary to ventricular tachycardia. Postmortem examination showed well differentiated adenocarcinoma in the left pleura and an intact, histologically normal adrenal zona glomerulosa and kidney. This is the first reported case of a critically ill patient with hyponatremia caused by hyperreninemic hypoaldosteronism possibly due to angiotensin II insensitivity and tubular unresponsiveness to mineralocorticoid.     

Urinary sodium and chloride during renal salt retention

One hundred ten episodes of renal salt retention (urinary sodium and/or chloride less than 10 mEq/L) were studied retrospectively to determine the significance of discordance of urinary sodium from chloride. In 16 episodes the urinary sodium exceeded chloride by at least 15 mEq/L. This disparity was associated with the necessity for urinary excretion of substantial quantities of poorly reabsorbed anions (penicillin, ketones, or diatrizoate), a rapidly falling serum bicarbonate level (due to resolving metabolic or developing respiratory alkalosis), or substantial renal insufficiency (serum creatinine greater than 3 mg/dL). In 14 of 110 episodes, urinary chloride exceeded urinary sodium by at least 15 mEq/L. These patients were more often oliguric and had a higher mean serum chloride than patients without this dissociation. In patients with oliguria, hyponatremia, or metabolic alkalosis, measurement of urinary sodium or chloride alone will, in a substantial number of cases, fail to detect renal salt retention. When evidence is sought for renal salt retention, both urinary sodium and chloride should be determined.     

Hyponatremia with high plasma ANP level--report of two cases with emphasis on the pathophysiology of cerebral salt wasting

Two cases of hyponatremia with intracranial lesions are reported with emphasis on diagnostic value of measurement of antidiuretic hormone (ADH) and atrial natriuretic polypeptide (ANP). Case 1. A 77-year-old female was transferred to our hospital for further care of vegetative state after subarachnoid bleeding on May 23, 1986. She was operated by neck clipping of rt-IC bifurcation aneurysm and lt-internal carotid-posterior communicating aneurysm at another hospital. On admission, computed tomography showed diffuse low density at bilateral thalamus and centrum semiovale. Biochemical analysis revealed hyponatremia (120 mEq/t) with increased natriuresis. Endocrinological date revealed normal plasma ADH and high plasma ANP levels. Patient was treated with infusion of 1% NaCl. Case 2. A 65-year-old male was admitted to our department because of gradual impairment of consciousness and generalized convulsion. Computed tomography showed small low density area at rt-thalamus and lt-cerebellar hemisphere. Biochemical date revealed severe hyponatremia (91 mEq/t) with normal plasma level of ADH and high plasma ANP. He was treated with infusion of 3% NaCl and hyponatremia was improved. The hyponatremia is frequently associated with intracranial disorders such as brain tumor, subarachnoid hemorrhage and head injury. Originally, hyponatremia with natriuresis was thought to be caused by salt wasting. This syndrome was defined as the inability to prevent salt loss in the urine due to undefined natriuretic factor in the brain. However, since 1957, because of introduction of concept of SIADH, it has generally become accepted that patients with natriuresis had SIADH. (ABSTRACT TRUNCATED AT 250 WORDS)     

不同程度颈脊髓损伤后低钠血症的临床分析

 目的回顾性总结急性颈脊髓损伤后低钠血症的发生特点,并分析其可能的发生原因,以及脊髓损伤严重程度、性别、年龄等因素对血钠变化的影响。方法研究对象为2005年6月至2011年3月急诊收治的一组颈椎外伤患者,排除合并颅脑外伤及慢性疾病的患者,入选病例分为完全性脊髓损伤组、不完全性脊髓损伤组及无神经功能障碍组,回顾性分析各组病例的血钠变化情况。结果入选病例共102例,男83例,女19例;年龄17~68岁,平均45.6岁。完全性脊髓损伤组23例,不完全性脊髓损伤组60例,无神经功能障碍组19例。共发生低钠血症共39例,完全性脊髓损伤组15例(65%),不完全性脊髓损伤组23例(38%),无神经功能障碍组1例(5%)。低钠血症发生率在三组间两两比较,差异有统计学意义,完全性脊髓损伤组低钠血症的发生率明显高于不完全性脊髓损伤组和无神经功能障碍组。Logistic逐步回归分析结果显示低钠血症与患者脊髓损伤程度有明确相关关系,而与患者的年龄、性别、脊髓损伤节段无相关关系。结论急性颈脊髓损伤后具有较高的低钠血症发生率,虽然影响钠盐平衡的因素及相互作用非常复杂,但颈脊髓损伤致自主神经功能障碍、神经内分泌功能异常以及血液动力学改变可能是导致颈脊髓损伤后电解质系统异常的重要原因。     

Elevation of plasma atrial natriuretic peptide in a neurosurgical patient with the syndrome of inappropriate secretion of antidiuretic hormone--case report

The authors describe a case of subarachnoid hemorrhage with hyponatremia accompanied by elevation of plasma atrial natriuretic peptide (ANP). The early phase of hyponatremia was classified as the syndrome of inappropriate secretion of antidiuretic hormone (ADH) due to subarachnoid hemorrhage. However, in the later phase, hyponatremia and natriuresis were accompanied by suppression of ADH while plasma ANP remained elevated. The patient was effectively treated with demeclocycline and hypertonic saline. The significance of ANP in the pathophysiology of increased natriuresis is discussed.     

Three cases of severe hyponatremia under taking selective serotonin reuptake inhibitor (SSRI)

The association between selective serotonin reuptake inhibitors(SSRIs) and hyponatremia has been documented throughout the world. In Japan, since SSRIs have recently come into use for patients with depression, there are only a few reports of hyponatremia associated with SSRIs. We present here three cases of the syndrome of inappropriate secretion of antidiuretic hormone(SIADH) associated with the administration of fluvoxamine for depression. They were admitted to our hospital because of deep coma, and revealed severe hyponatremia. Their serum sodium levels were 103-112 mEq/l, serum osmolalities were 227-241 mmol/kg, urine sodium levels were 38-107 mEq/l, and urine osmolalities were 352-781 mmol/kg. These patients were started on fluvoxamine 3 days-3 months previously. The diagnosis of SIADH in these patients was made based on hyponatremia, and low serum and high urine osmolalities. The fluvoxamine treatment was discontinued, and hypertonic saline was infused. Their serum sodium levels and osmolalities were subsequently normalized. None of the other known causes of hyponatremia, including diuretic therapy, tumors, and respiratory and central nervous system diseases, were present. High plasma AVP levels observed in the two cases suggest that SSRIs stimulate AVP secretion, thereby causing SIADH. Many reports have shown that people older than 70 years were at a particularly high risk of developing hyponatremia when SSRIs were used. In the future, since the use of SSRIs will be increasing, the water and electrolyte balance of elderly patients should be monitored carefully during SSRIs therapy.