出血性休克与脑病综合征的干预探讨

目的 探讨出血性休克与脑病综合征(HSES)有效的急救措施。方法 回顾性分析12例出血性休克与脑病综合征的临床过程，干预措施及对干预的反应。结果 HSES的主要危害是脑功能的损害。结论 改善和保护脑功能是治疗的重点，关键是迅速恢复氧通气、脑灌注，即迅速稳定呼吸和循环功能。休克纠正越快，预后越好；扩容应迅速而大胆。可尽早气管插管和正压通气，纠正低氧血症。正压通气、纠酸、抗DIC、抑制炎症反应均有利于循环功能的改善，应尽早进行。降颅压并不能改善神经系统功能的预后。     

出血性休克与脑病综合征

出血性休克与脑病综合征(HSES)于1983年由Levin首先报道并加以命名。HSES发病迅速,病死率高,生存者易留有严重的神经系统后遗症,其临床特点是突发的抽搐和昏迷、休克、弥漫性血管内凝血、水样腹泻、代谢性酸中毒、肝肾功能障碍。该文对HSES的临床研究进展作一综述,以提高对该病的认识和治疗水平。     

出血性休克与脑病综合征

出血性休克与脑病综合征(HSES)于1983年由Levin首先报道并加以命名。HSES发病迅速，病死率高，生存者易留有严重的神经系统后遗症，其临床特点是突发的抽搐和昏迷、休克、弥漫性血管内凝血、水样腹泻、代谢性酸中毒、肝肾功能障碍。该文对HSES的临床研究进展作一综述，以提高对该病的认识和治疗水平。     

出血性休克与脑病综合征患儿脑功能损害的临床特点

目的　探讨出血性休克与脑病综合征的脑功能损害的临床特点。方法　对 12例出血性休克与脑病综合征患儿的临床资料进行分析总结。结果　 12例依据脑功能损害的临床特点可分为暴发型 7例 :发病后迅速进入昏迷 ,频繁抽搐 ,肌张力显著降低 ,伴有多脏器功能衰竭 ;脑功能障碍型 5例 :入院后病情有所缓解 ,但 3～ 4d后又反复抽搐 ,持续 2d ,在此期间检查可有重度脑电图异常和CT示脑水肿。本文 7例暴发型均死亡 ,5例脑功能障碍型 ,4例留有严重的运动和语言障碍 ,1例目前判断神经功能正常。结论　出血性休克与脑病综合征可分为暴发型和脑功能障碍型 ,各有其临床特点。     

肠道感染相关性出血性休克与脑病综合征临床分析

目的探讨肠道感染相关的出血性休克与脑病综合征临床特点。方法分析12例与文献报道的出血性休克与脑病综合征相一致的患儿,均为突发昏迷和抽搐、高热、休克、水样腹泻、代谢性酸中毒、DIC、肝肾功能损害,前躯期为严重的水样便。结果大便检测3例轮状病毒阳性:高死亡率和严重的运动和语言障碍是其特点;极显著的肝酶学改变,血胆红素多正常。入院1～2d后肝转氨酶达高峰,多于1周内恢复正常;随着休克的纠正,肾功能于1～2d内转正常,病情缓解,但神经功能却发生进行性损害:发病后持续昏迷或频繁抽搐,肺出血,难以纠正的休克,持续无尿,出血不止,多于短期内死亡;本组死亡7例,4例留有严重的神经后遗症,1例神经功能正常。结论应提高对出血性休克与脑病综合征的临床认识。治疗关键是纠正休克,肠源性的全身炎症反应可能参与发病机制。     

出血性休克及脑病综合征患儿血中“葡萄状”核的白细胞

出血性休克及脑病综合征(HSES)时的高热是否在病理生理学上有重要意义尚有争论。外周血中白细胞核呈放射状分裂(即“葡萄状核”)见于成人中暑患者已有报道,并认为是该病的特征。作者曾观察4例年龄为2～4个月的HSES患儿,其中3例有高热及穿衣过多史。所有患儿发病时均有大汗湿透衣服、意识消失、休克及痉挛,其中2例于入院时外周血中检出大量带有葡萄状核的白细胞,这些白细胞于24小时后消失,另2例于起病后18小时才检测血液,未发现此种白细胞。以前在HSES患儿中尚未报道过有此种改变,作者认为于疾病早期注意寻找此种白细胞对HSES诊断     

急性呼吸窘迫综合征的肺开放策略

机械通气是抢救急性呼吸窘迫综合征的最关键措施,开放塌陷肺泡的压力高达60cmH2O,而维持肺泡开放的压力即呼气末正压应大于20cmH2O。数分钟内维持极高的气道压力来开放已塌陷的肺泡即肺开放策略,有短时高压力控制通气、叹息通气和短时高持续气道正压通气,它们并无气压伤和持久的循环影响,但肺开放策略并不常规用于每个急性呼吸窘迫综合征患者。     

失血性休克小容量复苏治疗进展

失血性休克发生后 ,心脏输出量减少 ,脏器血流灌注不足 ;氧供减少 ,微循环紊乱 ,造成脏器不同程度的损伤 ,甚至导致多器官功能衰竭 (MODS)。尽早进行液体治疗是失血性休克复苏的重要措施 ,通过补充液体达到恢复血容量 ,维持循环功能 ,保证器官、组织灌注和氧供的目的。等渗晶体溶液和胶体溶液大量输注是临床常采用的失血性休克复苏方法 ,但是其易导致肺水肿等不良反应。近年来的研究表明 ,高渗溶液复苏可以迅速改善循环功能 ,增加血流灌注 ,减轻组织损伤 ,降低急性呼吸窘迫综合征 (ARDS)和MODS的发生率 ,具有一定的脏器保护作用。本文…     

急性呼吸窘迫综合征的肺开放策略

机械通气是抢救急性呼吸窘迫综合征的最关键措施，开放塌陷肺泡的压力高达60cmH2O，而维持肺泡开放的压力即呼气末正压应大于20cmH2O。数分钟内维持极高的气道压力来开放已塌陷的肺泡即肺开放策略，有短时高压力控制通气、叹息通气和短时高持续气道正压通气，它们并无气压伤和持久的循环影响，但肺开放策略并不常规用于每个急性呼吸窘迫综合征患者。     

出血性休克和脑病综合征

出血性休克和脑病综合征(Heamorrhagic Shock and Eecephalopathy syndrom, HSE)起病突然,发生于婴儿期,以高热、脑病、严重休克和DIC、水样或血水样腹泻伴肝肾功能不全为特征。Levin等于1983年报道10例,并首次将本病命名为HSE。     

小儿心源性休克的诊断和治疗

心源性休克是由于心脏泵功能障碍导致的全身多器官功能衰竭和代谢紊乱,起病急骤,表现多样,进展迅速,病死率高,是儿科临床危重症之一.早期诊断和积极治疗是改善预后的关键.血流动力学监测和机械循环辅助装置的应用在小儿心源性休克的救治中发挥日益重要的作用.     

Case control study of thermal environment preceding haemorrhagic shock encephalopathy syndrome

The purpose of the study was to investigate whether the thermal environment in which babies slept before developing haemorrhagic shock encephalopathy syndrome (HSES) differed from that of other babies. Data were collected by standardised interview from parents of 31 babies who had had HSES before the age of 7 months and compared with equivalent data for 124 control babies, with matching for outside temperature on the relevant night and for age. Multivariate analysis showed a strong association between HSES and covering of the baby''s head by bedding, the odds ratio being 30.7 (95% confidence interval, 2.5 to 384). There were weaker associations with other aspects of the thermal environment. This suggests a link between HSES and some cases of cot death, supports the suggestion that HSES may be caused by overheating, and reinforces advice that babies should be placed to sleep in such a way that they are less likely to become totally covered.     

Case control study of thermal environment preceding haemorrhagic shock encephalopathy syndrome.

The purpose of the study was to investigate whether the thermal environment in which babies slept before developing haemorrhagic shock encephalopathy syndrome (HSES) differed from that of other babies. Data were collected by standardised interview from parents of 31 babies who had had HSES before the age of 7 months and compared with equivalent data for 124 control babies, with matching for outside temperature on the relevant night and for age. Multivariate analysis showed a strong association between HSES and covering of the baby's head by bedding, the odds ratio being 30.7 (95% confidence interval, 2.5 to 384). There were weaker associations with other aspects of the thermal environment. This suggests a link between HSES and some cases of cot death, supports the suggestion that HSES may be caused by overheating, and reinforces advice that babies should be placed to sleep in such a way that they are less likely to become totally covered.     

Management of dengue fever in ICU

Dengue virus infection can cause a wide spectrum of illness. Thrombocytopenia with concurrent haemoconcentration differentiates dengue haemorrhagic fever from classical dengue fever. Only cases with shock or unstable vitals signs need admission in the pediatric intensive care. The management is essentially supportive and symptomatic. The key to success is frequent monitoring and changing strategies. A rise in hematocrit of 20% along with a continuing drop in platelet count is an important indicator for the onset of shock. Patients in grade I and II should be closely monitored for signs of shock. The management of dengue shock syndrome (grade III and IV) is a medical emergency needing prompt and adequate fluid replacement for the rapid and massive plasma losses through increased capillary permeability. Early and effective replacement of plasma losses with plasma expanders or fluid and electrolyte solutions results in a favourable outcome in most cases. The ideal fluid management should include both cystalloids and colloids (including albumin). Cystalloids are given as boluses as rapidly as possible, and as many as 2 to 3 boluses may be needed in profound shock. Colloidal fluids are indicated in patients with massive plasma leakage and in whom a large volume of cystalloids has been given. Frequent recording of vital signs and determinations of haematocrit are important in evaluating the results of treatment. Apart from correction of electrolyte and metabolic disturbances, oxygen is mandatory in all patients of shock. Some patients develop DIC and need supportive therapy with blood products (blood, FFP and platelet transfusions). Polyserositis, in the form of pleural effusion and ascitis, are common in cases of dengue shock syndrome, and if possible, drainage should be avoided as it can lead to severe hemorrhages and sudden circulatory collapse. The prognosis depends mainly on the early recognition and treatment of shock.     

Haemorrhagic shock encephalopathy syndrome presenting with myoglobinuria.

An infant with haemorrhagic shock encephalopathy syndrome (HSES) who in addition presented with hyperpyrexia and myoglobinuria is reported. As rhabdomyolysis is a feature of heat stroke and malignant hyperthermia, the association of HSES with myoglobinuria supports the hypothesis that HSES may be a form of hypermetabolic state triggered by hyperthermia.     

Sepsis und septischer Schock in der Pädiatrie

Background

Sepsis and septic shock are important causes of pediatric morbidity and mortality. Early recognition of the critically ill patient followed by immediate and aggressive treatment is the hallmark of survival and prevention of organ dysfunction.

Therapy

Fluid resuscitation in order to counteract sepsis-induced capillary leak remains the cornerstone of therapy. Three boluses of 20 ml/kg of isotonic full electrolyte solution should be administered within the first 15 min. If shock persists, inotropes should be started within the first 15–30 min. Respiratory therapy includes oxygen administration and mechanical ventilation according to ARDS guidelines (high peep, low tidal volume). Further ICU management aims at secondary organ protection. Invasive monitoring is mandatory. Metabolic acidosis and hypo- or hyperglycemia should be corrected aiming at high-normal blood sugar levels and providing the patient with 2–3 g/kg/day of glucose. Antibiotics are given as a combination therapy and should be chosen according to the most probable site of infection. The clinical course within the first 24–48 h may require significant changes and intensification of therapy. Early contact with a tertiary level care center and careful planning of transfer is recommended.     

Haemorrhagic shock encephalopathy syndrome presenting with myoglobinuria

An infant with haemorrhagic shock encephalopathy syndrome (HSES) who in addition presented with hyperpyrexia and myoglobinuria is reported. As rhabdomyolysis is a feature of heat stroke and malignant hyperthermia, the association of HSES with myoglobinuria supports the hypothesis that HSES may be a form of hypermetabolic state triggered by hyperthermia.     

Peripheral circulatory failure

Shock is a syndrome arising from any of several initiating causes, resulting in inadequate tissue perfusion. Untreated shock due to any cause can lead to irreversible cellular damage. Early diagnosis and intervention are, therefore, key to improved outcomes. In children, hypotension is not a sensitive marker for diagnosing peripheral circulatory failure. A detailed evaluation to assess perfusion particularly estimating capillary refill time and end organ perfusion is required. Septic shock is a complex condition with varying contribution of hypovolemia, cardiac dysfunction and distributive shock. Aggressive fluid therapy in the early stages is essential to recovery. Understanding the pathophysiology will help in judicious use of vasoactive drugs. Newer modalities of treatment for severe sepsis and septic shock still need evaluation in children.     

Management of septic shock and acquired respiratory distress syndrome in pediatric cancer patients

Septic shock occurs in 6 % of paediatric cancer patients with neutropenia and fever. The mortality of the septic shock is 40 % in BMT patients and 5 % in others. One third of paediatric ARDS cases affect immunocompromised individuals with a total mortality of 45 % and 80 % after BMT. Septic shock is caused by gram-negative bacteria in more than 75 %. ARDS is due to pneumonia in more than 50 %, sepsis in about 25 %. This article provides the recommendations of the Infectious Diseases Working Party of the German Society for Pediatric Infectious Diseases (DGPI) and the German Society for Pediatric Hematology/Oncology (GPOH) for treatment of septic shock and ARDS. Therapy of septic shock includes early antibiotic therapy and volume expansion (> or = 40 ml/kg initially). Refractory shock requires vasopressors (noradrenaline), followed by a judicious circulatory management. Hydrocortisone is indicated in patients with high probability of adrenal insufficiency. Mainstay of ARDS therapy is ventilation with sufficient end-expiratory pressure (PEEP) to prevent loss of functional residual capacity and with limited tidal volumes (< or = 6 ml/kg) and limited inspiratory pressure (< 35 cm H(2)O) respectively, to minimize ventilator induced lung injury. Volume therapy consists of maintenance of sufficient preload to counteract the impaired venous return, induced by positive pressure ventilation. Diuretics and eventually veno-venous haemofiltration are used to reduce free lung water. Surfactant application may be considered in severe cases. Steroids are indicated in pneumocystis carinii pneumonia and in engraftment pneumonitis.     

CT scan abnormalities in a series of patients with hemorrhagic shock and encephalopathy syndrome

Background. Hemorrhagic shock and encephalopathy syndrome (HSES) affects children under 1 year of age and is characterized by seizures, shock and certain laboratory abnormalities, including coagulation abnormalities. It has a high mortality and many of the survivors are neurologically abnormal. Objective. To describe abnormalities observed on initial and follow-up CT scans in a group of patients suffering from HSES. Materials and methods. Retrospective review of records and CT scans of ten patients with HSES who were admitted to the intensive care unit of the Children's Hospital and Medical Center, Seattle. Results. Cerebral edema was seen in all cases when the CT scan was obtained between 1 and 7 days after onset of HSES. The basal ganglia and cerebellum were relatively spared, and no hemorrhage was seen. Patients with moderate or marked cerebral edema usually had a poor prognosis. All survivors had significant neurologic sequelae. CT scans obtained after 7 days often showed encephalomalacia with ex vacuo ventricular enlargement. CT scans obtained between 24 h and 4 days after onset will show the acute changes of HSES. CT scans during the initial and convalescent stages of HSES can provide useful information about cerebral edema and encephalomalacia, which occur frequently with this illness. Received: 25 March 1996 Accepted: 6 November 1996