脑性盐耗综合征与抗利尿激素异常分泌综合征的鉴别

脑性盐耗综合征和抗利尿激素异常分泌综合征在颅脑疾病相关的低钠血症中均占用一定比例.两种疾病临床表现极为相似,且易混淆,而治疗原则却大不相同.因此,正确鉴别两种疾病,对于临床患者的治疗及预后意义重大.该文从发病机制、诊断及治疗等方面对两种疾病进行鉴别.     

Oral urea for the treatment of chronic syndrome of inappropriate antidiuresis in children

We report the successful use of oral urea in the management of children with chronic syndrome of inappropriate antidiuretic hormone secretion (SIAD). We performed a retrospective review of four children with chronic SIAD. After initial attempts at management with fluid restriction, each was started on a 30% to 50% oral urea solution, and the dose was titrated until normal serum sodium was achieved. Fluid intake was liberalized after serum sodium normalization. All four children normalized their serum sodium. No side effects or toxicities were experienced. Oral urea is a safe, effective treatment for chronic SIAD in children.     

小儿重型颅脑损伤后脑性盐耗综合征

目的探讨小儿重型颅脑损伤后并发脑性盐耗综合征的发病机制、临床诊断及治疗。方法回顾性分析我院1990年1月~2003年12月收治18例小儿重型颅脑损伤(Glasgow昏迷分级标准评分3~8分)后并发脑性盐耗综合征的临床资料。结果18例据临床表现和实验室检查被确诊。经补钠和输液治疗,低钠血症和低血容量均得以纠正。结论低血钠、高尿钠、低血容量及意识状态改变是脑性盐耗综合征的临床诊断依据,补钠和补足血容量治疗安全有效,对预后至关重要。     

小儿重型颅脑损伤后脑性盐耗综合征

目的探讨小儿重型颅脑损伤后并发脑性盐耗综合征的发病机制、临床诊断及治疗。方法回颐性分析我院1990年1月～2003年12月收治18例小儿重型颅脑损伤（Glasgow昏迷分级标准评分3～8分）后并发脑性盐耗综合征的临床资料。结果18例据临床表现和实验室检查被确诊。经补钠和输液治疗，低钠血症和低血容量均得以纠正。结论低血钠、高尿钠、低血容量及意识状态改变是脑性盐耗综合征的临床诊断依据，补钠和补足血容量治疗安全有效，对预后至关重要。     

The syndrome of inappropriate secretion of antidiuretic hormone in children with bacterial meningitis

Plasma concentrations of arginine vasopressin were determined by radioimmunoassay in 13 normal children, 21 patients with febrile illnesses (not bacterial meningitis), and 17 patients with bacterial meningitis. The mean +/- 1 SD concentrations of AVP in the normal children and patients with various febrile illnesses were 0.7 +/- 0.6 and 1.0 +/- 1.2 muU/ml, respectively. The mean +/- 1 SD concentration of AVP in patients with bacterial meningitis was 3.3 +/- 2.3 muU/ml. The concentrations of AVP in the patients with bacterial meningitis were significantly greater (P less than 0.001) than those noted in the normal children or children with other febrile diseases.     

Syndrome of inappropriate anti‐diuretic hormone in Kawasaki disease

Background: The pathogenesis of hyponatremia in acute Kawasaki disease (KD) remains unclear. A recent case report of KD complicated by syndrome of inappropriate anti‐diuretic hormone (SIADH) led us to determine the prevalence of SIADH in acute KD patients. Methods: Subjects were 39 Japanese KD patients (2–84 months of age, 25 males and 14 females) treated with intravenous immunoglobulin (IVIG), 2 g/kg/day and oral aspirin. SIADH was defined when hyponatremic patients (serum sodium concentration <135 mEq/L) had decreased serum osmolality <280 mOsm/kg H₂O, elevated urine sodium concentration >20 mEq/L and elevated urine osmolality >100 mOsm/kg H₂O without dysfunctions of renal, thyroid or adrenal gland. We also studied the relation between clinical course of SIADH and the amount of infused fluid during IVIG. Results: Before IVIG, 27 patients (69%) had hyponatremia and 11 (28% of total; 41% of hyponatremic patients) had SIADH while after IVIG, 13 (33%) hyponatremia and four (10%; 31% of hyponatremic patients) SIADH. Among 11 patients with SIADH before IVIG, SIADH improved in 10 after IVIG, but hyponatremia persisted in five. Significant correlation was observed between serum sodium concentration after IVIG and infusion amount in SIADH patients (r=?0.64, P= 0.03), but not in non‐SIADH patients. Conclusions: This is the first report to show that SIADH is common as a cause of hyponatremia in acute KD and hence careful management of water and sodium is warranted.