连续性肾脏替代疗法抢救急危重症43例疗效分析

目的 :总结连续性肾脏替代疗法 (CRRT)对各类重症疾病的疗效 ,旨在总结经验 ,提高疗效。方法 :CRRT治疗的 4 3例重症患者按病因分类 ,并分析各类疾病CRRT前后神志、肝、肾功能、电解质及生命体征的变化。结果 :8例肾移植后急性肾功能衰竭者经CRRT治疗后 8～ 16hSCr、BUN逐渐下降。 7例肝性脑病、肝肾综合征及 4例多脏器衰竭者经CRRT治疗后 ,2例肝昏迷者神志恢复 ,4例肾功改善 ,治疗中生命体征稳定。 8例因脑卒中高钠血症者在行CRRT治疗 8～12h后血钠下降。结论 :①肾移植后急性肾功能衰竭患者经CRRT治疗后肾功能恢复时间明显缩短。②对肝性脑病、肝肾综合征患者 ,CRRT可改善神志及肾功能 ,延长存活时间 ,为行肝移植赢得时间。③CRRT能降低脑卒中高钠血症 ,疗效好     

Hypernatremia in critically ill patients

Hypernatremia is common in intensive care units. It has detrimental effects on various physiologic functions and was shown to be an independent risk factor for increased mortality in critically ill patients. Mechanisms of hypernatremia include sodium gain and/or loss of free water and can be discriminated by clinical assessment and urine electrolyte analysis. Because many critically ill patients have impaired levels of consciousness, their water balance can no longer be regulated by thirst and water uptake but is managed by the physician. Therefore, the intensivists should be very careful to provide the adequate sodium and water balance for them. Hypernatremia is treated by the administration of free water and/or diuretics, which promote renal excretion of sodium. The rate of correction is critical and must be adjusted to the rapidity of the development of hypernatremia.     

肝移植术后高钠血症的原因及治疗方法(附28例报告)

目的探讨肝移植术后高钠血症的原因及治疗方法。方法对28例肝移植术后高钠血症患者的临床资料进行回顾性分析。结果患者术前均无高钠血症；21例高钠血症发生在术后48h内；16例血钠为146～150mmol／L，9例为151～155mmol／L，3例为156～160mmol／L;有18例并发低钾血症，21例并发高磷血症，13例伴有肾脏损害。对不同程度的高钠血症，采用不同的治疗方法，严格计算补液量、补液内容以及补液速度。经治疗，24例患者完全康复，3例死亡，1例致残。结论肝移植术后发生高钠血症的原因是多方面的；治疗应在处理原发病的基础上适时、适量的补充液体，并选择好补液速度。     

重症脑卒中患者并发高渗血症的危险因素

目的探讨重症脑卒中患者并发高渗血症的危险因素，为制定干预措施提供依据。方法重症脑卒中患者80例，根据评价生存与死亡的血浆渗透压界值分为高渗组（〉310mmol／L，34例）和非高渗组（≤310mmol／L，46例）。监测可能影响血浆渗透压的危险因素。结果大剂量甘露醇（〉100g／d）、高钠血症和高血糖症是导致高渗血症的3个主要危险因素。高渗组4周生存率（47．1％）明显低于非高渗组（78．3％），两组比较差异有统计学意义（P〈0．01）。结论引起高渗血症的主要危险因素是大剂量甘露醇、高钠血症和高血糖症，高渗血症患者预后差，生存率低。     

Preoptic hypernatremic syndrome and the regulation of water balance in the rat

Lesions of the medial preoptic area in rats cause a transient adipsia and aphagia, with a weight loss of 15–20%. Feeding and drinking behaviours return, with water intakes similar to sham-operated rats. However, the rats remain chronically hypernatremic for a period of at least 2 months. The hypernatremia persists during food deprivation and during stimulation of drinking by extracellular dehydration. No deficiency is evident in urinary concentrating ability or in ability to excrete sodium ions; extrarenal water loss is similar to that of sham-operated rats. The rats do not drink in response to hypertonic saline injection, and they do not retain an imposed water load. A comparison with rats with diabetes insipidus, which avoid hypernatremia by sharply increasing their water intakes, demonstrates that the hypernatremia is related to a dysfunction of intake as well as output. The findings suggest that medial preoptic lesions may reset the set-point for regulation of plasma sodium concentration; they also suggest that the lesions may cause reduced sensitivity to an increase in plasma sodium concentration.     

Isotonic versus hypotonic fluid supplementation in term neonates with severe hyperbilirubinemia - a double-blind, randomized, controlled trial

Aim: To compare the incidence of hyponatremia in full‐term neonates with severe hyperbilirubinemia, receiving intravenous fluid supplementation with 0.2% saline in 5% dextrose versus 0.9% saline in 5% dextrose, to prevent blood exchange transfusion (BET). Methods: In this double‐blind, randomized, controlled trial, full ‐ term newborns (≥37 weeks), appropriate for gestational age, with severe non‐haemolytic hyperbilirubinemia (serum bilirubin ≥ 20 mg/dL) were enrolled. Eligible neonates were randomized to receive either 0.2% saline in 5% dextrose (hypotonic fluid group) or 0.9% saline in 5% dextrose (isotonic fluid group) over 8 hrs, in addition to phototherapy. The primary outcome was proportion of neonates developing hyponatremia (serum Na < 135 mmol/L) after 8 h. Results: Forty‐two neonates were analysed in each group. Proportion of neonates developing hyponatremia after 8 h was higher in hypotonic fluid group as compared to isotonic fluid group (48.8% vs. 10.5%, p < 0.001). However, a larger proportion in isotonic fluid group developed hypernatremia (39.5% vs. 12.2%, p < 0.001). The rate of BET was similar in both groups. Conclusion: In full‐term neonates with severe hyperbilirubinemia, administration of hypotonic fluid to prevent BET was associated with a higher incidence of hyponatremia while isotonic fluid was associated with an increased incidence of hypernatremia.     

去氨加压素治疗重度颅脑损伤并发高钠血症的疗效观察及护理

目的探讨去氨加压素治疗重度颅脑损伤并发高钠血症的疗效及护理措施。方法回顾性分析使用去氨加压素治疗30例重度颅脑损伤并发高钠血症患者的临床资料。结果30例患者经过治疗与护理,所有患者24 h后血钠较前明显下降或逐渐恢复正常,有效率达100%,治疗14 d后死亡8例,死亡率26.7%;21 d后共死亡12例,死亡率40%。结论常规治疗护理加去氨加压素能有效治疗重度颅脑损伤并发高钠血症,降低死亡率。     

Dural Sinus Thrombosis with Severe Hypernatremia Developing in a Patient on Long-Term Lithium Therapy

Dural sinus thrombosis has not been described in a patient with hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus. A 63-year-old man on chronic lithium therapy for schizoaffective disorder was transferred to the Emergency Department with dehydration and signs of central nervous system dysfunction after a 3-week isolation in a room in a psychiatric hospital due to exacerbation of psychiatric disorder, during which he refused to eat. Laboratory examination revealed hypertonic hypernatremia (osmolality, 359 mOsm/kg and Na, 171 mEq/L) and hyposthenuria (specific gravity, 1.010 and osmolality, 249 mOsm/kg), with normal serum endogenous vasopressin concentration (2.3 pg/mL). The serum lithium concentration was within the therapeutic range (0.94 mEq/L). Cranial computed tomography demonstrated subarachnoid hemorrhage and suggested dural sinus thrombosis. Although treatment with indomethacin (25 mg parenterally at 8-hour intervals) was somewhat effective in restoring renal concentrating capacity, he died of massive hemorrhagic infarction on the sixth hospital day, probably secondary to dural sinus thrombosis. The clinical diagnosis was confirmed by postmortem examination. Physicians should be alert for the possibility of dural sinus thrombosis as a complication of hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus.     

Central diabetes insipidus related to anti-programmed cell-death 1 protein active immunotherapy

Cancer immunotherapy is a breakthrough strategy entwined with toxicity. Immune-related hypophysitis is conventionally considered distinctive of cytotoxic T-lymphocyte antigen 4 (CTLA-4) inhibitors. Immune-related central diabetes insipidus (CDI) is exceptional. CDI rarely manifests as hypernatremia, which is almost always euvolemic. We report a 71-years-old male patient with advanced lung cancer who experienced severe chronic hypernatremia presented as alterations in mental status five months after initiation of treatment with the anti-PD-1 checkpoint inhibitor nivolumab. Combination of persistent hypernatremia, polyuria, high plasma osmolality and hyposthenuria raised suspicion of diabetes insipidus, prompting measurement of serum concentration of arginine vasopressin (AVP). The inappropriately undetectable serum levels of AVP confirmed central diabetes insipidus (CDI). Nivolumab-related hypophysitis was recognized as possible cause of CDI. Further hormonal assessment excluded any endocrinopathy indicating disorder of posterior pituitary. Pituitary MRI was normal with persistence of hyperintensity of posterior pituitary on T1-weighted images (bright spot). The patient was scheduled to receive 1-deamino-8-D-arginine vasopressin (DDAVP), but he died suddenly due to cardiac arrest before initiation of treatment. Our report describes the first case of nivolumab related CDI, building on existing literature through: (I) underscoring hypovolemic hypernatremia as CDI manifestation; (ii) bringing into spotlight the rare anti-PD-1 treatment related hypophysitis; (iii) enriching the limited evidence on immune-related CDI. Increased awareness of nivolumab related CDI will enable prompt recognition and therapeutic intervention.