Clinical analysis and literature review of six cases of neurogenic pulmonary edema / 中华危重病急救医学

Objective:To explore the early diagnosis and correct treatment of neurogenic pulmonary edema (NPE) and review the literature.Method:Retrospective analysis was performed in six patients diagnosed as NPE who were admitted to the emergency department of Tianjin Third Central Hospital from March 2017 to March 2021.Results:Six patients had acute onset, presenting severe dyspnea and hypoxemia, and obvious wet rales could be heard in both lungs. The white blood cell count (WBC) increased to varying degrees (11-22)×10 9/L, procalcitonin (PCT) was normal, or slightly increased, sputum bacteriological examination was negative, and oxygenation index was < 200 mmHg (1 mmHg≈0.133 kPa). Chest CT mainly showed patchy or patchy exudation. The lesions were of different sizes and were not distributed according to lobes. By reducing intracranial pressure, ventilator assisted breathing, liquid therapy, anti-infection therapy with antibiotics, nutritional support, all six patients were well and discharged, and no one died of NPE. Conclusions:NPE has complex condition, acute onset and rapid development. Early diagnosis and correct treatment can improve the success rate of treatment and prognosis of patients with NPE.

Serum chromogranin A (CGA) level in predicting the prognosis of severe hand, foot, and mouth disease complicated with neurogenic pulmonary edema / 中华临床感染病杂志

Objective:To explore the clinical significance of serum Chromogranin A (CGA) level in predicting the prognosis of children with severe hand, foot, and mouth disease (HFMD) and complicating neurogenic pulmonary edema (NPE).Methods:A total of 162 patients with HFMD admitted in our hospital from January 2017 to December 2019 were enrolled in the study; and 40 age-matched healthy children were selected as controls. According to the disease severity and complication the patients were divided into three groups: mild group ( n=88), severe without NPE group ( n=46) and severe with NPE group ( n=28). In 72 severe HFMD patients 16 cases died (fatal group) and 56 cases survived (survival group) within 28 days of hospitalization. The serum CGA, LAC, GLU, WBC, PCT, IL-6, cTnT were measured in all subjects. SPSS 23.0 software was used for data analysis, and the receiver operating characteristic (ROC) curve was used to evaluate the various indicators for predicting the prognosis of severe HFMD combined with NPE. Results:The serum CGA, GLU, LAC, IL-6 and cTnT levels in severe HFMD group with NPE significantly higher than those in the other three group ( H=61.554, 79.031, 86.994, 36.477, 75.021, all P<0.05 ). The serum CGA, LAC, GLU and IL-6 levels in the fatal group were significantly higher than those in survival group ( Z=-6.094, -4.621, -4.283, -5.504, all P<0.05). There was no significant difference in the levels of WBC, PCT and cTnT between the survival group and the fatal group ( P>0.05). The area under the receiver operating curve (AUC) of serum CGA was 0.890 (95% CI: 0.833-0.947) for predicting the prognosis of patients and the best cut-off value was 120.59 μg/L. Conclusion:The detection of serum CGA levels may be beneficial for the early diagnosis of severe HFMD with NPE, and can be used as one of the predictors of death from severe HFMD.

Changes of vasoactive substances and adrenergic beta receptors in rabbit models of neurogenic pulmonary edema / 中国小儿急救医学

Objective To establish an animal model of neurogenic pulmonary edema (NPE),and to study the role of catecholamine and beta receptors in the occurrence of NPE. Methods The NPE model was established by injecting fibrinogen and thrombin into the cerebellum medullary pool of the rabbits. Twenty-four rabbits were divided into the control group,the saline group and the experimental group by random num-ber table. In the control group,only cerebellar medullary cistern puncture was carried out,and no drug was in-jected. Cerebrospinal fluid was drew out and the same amount of saline was injected into the cerebellum me-dullary pool in the saline group. Fibrinogen and thrombin were injected into the cerebellum medullary pool in the experimental group. The animals were intubated by tracheotomy,the femoral artery and the internal jugu-lar vein were dissected and connected with the PiCCO instrument to detect the blood pressure,heart rate,and respiratory rate before puncture and at 1 min,10 min,30 min after puncture. Serum samples were collected for the determination of epinephrine,norepinephrine,acetylcholine,endothelin-1,cardiac troponin I,brain natri-uretic peptide and neuropeptide Y levels before puncture and at 1 min,10 min after puncture. The rabbits weresacrificed at 3 hours after successful modeling,the pathological examination of lung was performed. Myocar-dial samples were taken to detect adrenergic beta receptors mRNA. Results (1)The heart rate,respiratory rate and mean arterial pressure at 1 min and 10 min after puncture in experimental group were significantly higher than those in control group and saline group. (2) The pathological examination of the rabbits′ lungs in experimental group found that the lung tissue was swollen and dark red in appearance with large areas of con-gestion. Under the microscope,the lung tissue was edema,bleeding,and inflammatory cells were infiltrated in the alveolar cavity,which was consistent with characteristics of NPE. (3)There was no difference in epineph-rine and norepinephrine concentration in all groups before the cerebellar medullary pool puncture. The concen-tration of epinephrine and norepinephrine at 1 min after puncture time were (200. 0 ± 251. 7)μg/ L,(448. 9 ± 356. 7)μg/ L in the experimental group,whcih were significantly higher than those of control group[(15. 4 ± 3. 4)μg/ L,(15. 9 ± 9. 7)μg/ L] and saline group[(17. 1 ± 3. 8) μg/ L,(29. 6 ± 18. 4) μg/ L] (P < 0. 05). The concentration of epinephrine and norepinephrine at 10 min after puncture were (397. 0 ± 797. 7)μg/ L, (221. 4 ± 173. 7)μg/ L in the experimental group,whcih were significantly higher than those of control group [(23. 3 ± 6. 4) μg/ L,(18. 8 ± 3. 9) μg/ L] and saline group[(16. 7 ± 9. 1) μg/ L,(20. 3 ± 6. 5) μg/ L] (P < 0. 05). (4)There was no significant difference in the levels of serum neuropeptide Y,acetylcholine and endothelin-1 among the three groups. (5)The mRNA of adrenergic beta-1 receptor in the experimental group was 0. 37 ± 0. 12,which was significantly lower than those in the control group (0. 54 ± 0. 13) and saline group (0. 56 ± 0. 14) (P < 0. 05). There was no significant difference in adrenergic beta-3 receptor mRNA among the three groups. Conclusion The NPE animal model was constructed by injecting fibrinogen and thrombin into the cerebellum medullary pool of the rabbits. Catecholamine and beta-1 receptor play a role in the occurrence of NPE rabbit model. There is no significant correlation between neuropeptide Y,acetylcholine,en-dothelin-1 and the occurrence of NPE in rabbits.

Analysis of Factors Associated with Neurogenic Pulmonary Edema after Intracerebral Hemorrhage / 中国医科大学学报

Objective To determine the association of the oxygenation index and lactate levels with neurogenic pulmonary edema (NPE) in patients with intracerebral hemorrhage. Methods We retrospectively evaluated 116 patients with intracerebral hemorrhage, who were admitted to the First Affiliated Hospital of China Medical University between May 2014 and May 2017. Patients were divided into NPE and non-NPE groups and the groups were compared to identify the factors associated with the occurrence of NPE. Results The oxygenation index, lactate level, pH, PC02, brain natriuretic peptide (BNP) level, and Glasgow coma scale were significantly different between the NPE and non-NPE groups (all P ＜ 0. 05). Logistic regression analysis showed that the oxygenation index (B =0. 049; OR =1. 05;p =0. 04) and lactic acid level (B =-5. 855; OR =0. 003;P=0. 01) were associated with the occurrence of NPE in patients with intracerebral hemorrhage. Conclusion A decrease in oxygenation index and an increase in serum lactate level are directly associated with the occurrence of NPE in patients with intracerebral hemorrhage.

Rerecognition of neurogenic pulmonary edema / 中国小儿急救医学

Neurogenic pulmonary edema is a clinical complication caused by various central nervous system disorders.It includes a variety of pathogenic factors,however,over-activation of the sympathetic nerve is the main mechanism.The main clinical manifestations are dyspnea and hypoxemia,which may be accompa-nied by circulatory disorder. The respiratory support therapy and circulatory support therapy are the main treatment measures.It has the characteristics of rapid progress and high mortality,which should be obtained enough attention.

Neurogenic pulmonary edema due to ventriculo-atrial shunt dysfunction: a case report / Edema pulmonar neurogênico devido à disfunção da derivação ventrículo-atrial: relato de caso

ABSTRACT BACKGROUND AND OBJECTIVES: Pulmonary edema is caused by the accumulation of fluid within the air spaces and the interstitium of the lung. Neurogenic pulmonary edema is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system insult. It may be a less-recognized consequence of raised intracranial pressure due to obstructive hydrocephalus by blocked ventricular shunts. It usually appears within minutes to hours after the injury and has a high mortality rate if not recognized and treated appropriately. CASE REPORT: We report a patient with acute obstructive hydrocephalus due to ventriculo-atrial shunt dysfunction, proposed to urgent surgery for placement of external ventricular drainage, who presented with neurogenic pulmonary edema preoperatively. She was anesthetized and supportive treatment was instituted. At the end of the procedure the patient showed no clinical signs of respiratory distress, as prompt reduction in intracranial pressure facilitated the regression of the pulmonary edema. CONCLUSIONS: This report addresses the importance of recognition of neurogenic pulmonary edema as a possible perioperative complication resulting from an increase in intracranial pressure. If not recognized and treated appropriately, neurogenic pulmonary edema can lead to acute cardiopulmonary failure with global hypoperfusion and hypoxia. Therefore, awareness of and knowledge about the occurrence, clinical presentation and treatment are essential.

RESUMO JUSTIFICATIVA E OBJETIVOS: o edema pulmonar é causado pelo acúmulo de líquido nos alvéolos e no interstício pulmonar. Edema pulmonar neurogênico é uma síndrome clínica caracterizada por edema pulmonar de início agudo após um acometimento súbito do sistema nervoso central. Pode ser uma consequência menos reconhecida de pressão intracraniana aumentada por causa da hidrocefalia obstrutiva por derivações ventriculares bloqueadas. Geralmente aparece em minutos ou horas após o insulto e tem uma alta taxa de mortalidade, caso não seja identificado e tratado adequadamente. RELATO DE CASO: relatamos o caso de paciente com hidrocefalia obstrutiva aguda por causa da disfunção da derivação ventrículo-atrial, programado para cirurgia em caráter de urgência para a colocação de derivação ventricular externa, que apresentou edema pulmonar neurogênico no pré-operatório. A paciente foi anestesiada e o tratamento de manutenção instituído. No fim do procedimento, a paciente não apresentou quaisquer sinais de distúrbio respiratório, pois a redução rápida da pressão intracraniana facilitou a regressão do edema pulmonar. CONCLUSÕES: este relato aborda a importância da identificação de um edema pulmonar neurogênico como uma possível complicação no período perioperatório resultante de um aumento da pressão intracraniana. Quando não identificado e tratado adequadamente, o edema pulmonar neurogênico pode levar à insuficiência cardiorrespiratória aguda, com hipoperfusão global e hipóxia. Portanto, a conscientização e o conhecimento de sua ocorrência, apresentação clínica e seu tratamento são essenciais.

Dynamic changes in serum inflammatory cytokines and their association with neurogenic pulmonary edema in patients with severe hand-foot-mouth disease / 中华实用儿科临床杂志

Objective To investigate the dynamic changes in the serum inflammatory cytokines and their association with neurogenic pulmonary edema (NPE) in the patients with severe hand-foot-mouth disease (HFMD).Methods Eighty-nine patients with severe HFMD from March 2010 to December 2012 were recruited in the study.The patients were divided into NPE group and central nervous system diseases (CNSD) group according whether they had NPE.The cytokines,including interleukin (IL)-4,IL-6,IL-10,IL-17,tumor necrosis factor-α (TNF-α) and interferon-γ(IFN-γ)were evaluated by using enzyme-linked immunosorbent assay on day 1,3 and 5 after admission to hospital.Risk factors for NPE involvement during hospital stay were analyzed with multivariate Logistic regression analysis.Results (1) Compared with the CNSD group,the serum levels of IL-6 (Ftime =1.876,P =0.177,Ftime* group =2.192,P =0.145,Fgroup =7.855,P =0.007),TNF-α(Ftime =13.133,P =0.001,Ftime* group =0.291,P =0.592,Fgroup =3.644,P =0.042),IL-10 (Ftime =14.580,P =0.001,Ftime* group =2.612,P =0.078,Fgroup =16.823,P =0.000),INF-γ (Ftime =3.093,P =0.045,Ftime* group =0.513,P =0.600,Fgroup =20.141,P =0.000) were significantly higher than those in NPE group.(2)The serum levels of TNF-α,IL-10,INF-γ rose to the peak on the third day.(3) By using multivariate Logistic regression analysis,age (OR =3.383,95％ CI:1.173-4.759),days of fever (OR =4.925,95％ CI:1.758-3.794),hyperglycaemia (OR =3.465,95％ CI:1.303-5.220),leucocytosis (OR =7.579,95 ％ CI:2.530-12.704) and elevation of IL-10 (OR =1.228,95 ％ CI:1.007-1.523) were entered into equation.In the risk evaluation model,these variables remained independent predictors for NPE.Conclusions Abnormal cytokine productions appear to be responsible for the pathogenesis of NPE,and might be an effective tool for predicting NPE in infants with severe HFMD.

Effect of Propranolol and Phentolamine on neurogenic pulmonary edema in rats / 中华实用儿科临床杂志

Objective To investigate the effect of Propranolol and Phentolamine on neurogenic pulmonary ede-ma(NPE)in rats. Methods One hundred and twenty male Wistar rats were randomly divided into 4 groups:the con-trol group(group A),the NPE group(group B),the Propranolol treatment group(group C)and the Phentolamine treatment group(group D),30 cases in each group. Diffuse brain injury was induced in the latter 3 groups. The lung wet/ dry ratio was calculated. HE staining was used to measure the histological changes in the lung tissues. The levels of neuropeptide Y(NPY)and substance P(SP)in the serum and the bronchoalveolar lavage fluid(BALF)were detected by enzyme - linked immunosorbent assay(ELISA). The expressions of NPY and SP in the lung tissues were demonstra-ted by immunohistochemical staining,and immunohistochemical scores(IHS)were measured after scarifying the ani-mals at different time points(0. 5,6. 0 and 24. 0 h after injury). Results Compared with group A,water volume in the lungs in group B increased at 24. 0 h(P ﹤ 0. 05);NPY content in the serum was elevated at 6. 0 h,while that in BALF was elevated at 6. 0 h and 24. 0 h(all P ﹤ 0. 05);SP content in the serum was elevated at 0. 5 h and 6. 0 h(all P ﹤0. 05),while that in BALF was elevated at 0. 5 h(P ﹤ 0. 05);The expression of NPY protein in the lung tissue in-creased at 0. 5 h,6. 0 h and 24. 0 h(all P ﹤ 0. 05),while the level of SP protein increased at 0. 5 h(P ﹤ 0. 05). Com-pared with group B,water volume in the lungs in group C was higher at 6. 0 h and 24. 0 h(all P ﹤ 0. 05);NPY concen-trations in the serum were higher at 6. 0 h and 24. 0 h(all P ﹤ 0. 05),while those in BALF were higher at 0. 5 h, 6. 0 h,and 24. 0 h(all P ﹤ 0. 05);SP concentrations in serum and BALF were higher at 0. 5 h(all P ﹤ 0. 05). The ex-pression of NPY protein increased at 6. 0 h(P ﹤ 0. 05),while the levels of SP protein increased at 0. 5 h,6. 0 h and 24. 0 h(all P ﹤ 0. 05). Compared with group B,the level of NPY in serum in group D was lower at 6. 0 h,and that in BALF was lower at 6. 0 h and 24. 0 h(all P ﹤ 0. 05). The level of SP in serum was lower at 0. 5 h(P ﹤ 0. 05). The ex-pression of NPY protein decreased at 6. 0 h and 24. 0 h(all P ﹤ 0. 05),while the levels of SP protein decreased at 0. 5 h(P ﹤ 0. 05). Conclusions Phentolamine is effective in reducing NPE through reduction of NPY and SP,while propranolol can stimulate the release of NPY and SP to aggravate NPE following traumatic brain injury in rats.

Pathogenesis of severe hand-food-mouth disease complicated with neurogenic pulmonary edema / 国际儿科学杂志

Severe hand-food-mouth disease can be accompanied by neurogenic pulmonary edema,whicn can rapidly lead to death.The pathogenesis of neurogenic pulmonary edema may be related to the comprehensive influences on neural factors,humoral factors and multiple bioactive substances after the central nervous system is damaged.It is of great impotance to investingate the pathogenesis of neurogenic pulmonary edema,which facilitates timely treatment and prevention of the complications.

Expression of influence of continuous blood purification on the endothelin-1 and prognosis value in the neurogenic pulmonary edema / 中华急诊医学杂志

Objective To explore the influnce on the endothelin-1 (ET-1) and clinical application value of continuous blood purification (CBP) on the treatment of severe craniocerebral injury with the neurogenic pulmonary edema (NPE).Methods All data about sixty patients with NPE were prospectively studied.These 60 patients were randomly (random number) divided into control group (n =30) and treatment group (n =30).In control group,patients were rapidly given with lowering intracranial pressure,mechanical ventilation,calming,antibiotic therapy and so on.In the treatment group,patients received CBP integrated with routine treatment.On admission and 72 h posttreatment,ET-1,static lung compliance and oxygenation index were observed.Time of mechanical ventilation support,incidence rates of multipal organ dysfunction syndrome (MODS) were compared between two groups.The paired t-test was used for the amount data within the group.Chi-square was used for the constitute ratio and incidence ratio of the each relevant information.P ＜ 0.05 was considered statistically significant.Results Compared to the control group,the level of ET-1 was decreased significantly in the treatment group [(48 ± 10) ng/L vs.(85 ± 14) ng/L] after 72 h post-treatment,while static lung compliance [(60.9 ± 2.3) mL/cmH2O vs.(31.4 ±4.8) mL/cmH2O] and oxygenation index [(317 ± 11) mmHg vs.(192 ± 14) mmHg] increased significantly (P ＜ 0.05).In treatment group and control group,the time of respirator intervention were [(6.0 ± 2.1) d vs.(11 ± 3.2) d],and the statistical significance was shown (P ＜ 0.05).Compared to the control group [56.7％ (17/30)],incidence rate of MODS [20.0％ (6/30)] was lower in treatment group (P ＜ 0.05).Conclusions CBP combined with routine treatment,which can remove ET-1 effectively,improve oxygenation,reduce the time of mechanical ventilation support and incidence rate of MODS.

The application value of pulse induced contour cardiac output monitoring in diagnosis and treatment of neurogenic pulmonary edema: a report of 4 cases and review of literature / 中国中西医结合急救杂志

Objective To explore the application value of pulse induced contour cardiac output (PiCCO) monitoring in diagnosis and treatment of patients with neurogenic pulmonary edema (NPE).Methods With review of literature, the data of 4 patients of severe neurological disease complicated by NPE admitted into Department of Critical Care Medicine of Huangshan People's Hospital Affiliated to Wannan Medical College from 2011 to 2013 were retrospectively analyzed and discussed in their PiCCO hemodynamic characteristics and processes of treatment.Results The PiCCO of 4 patients with NPE showed that the extravascular lung water index (EVLWI) was increased significantly (EVLWI was 12 - 42 mL/kg on admission and 10 - 22 mL/kg after hospitalization for 24 hours), all revealing a high permeability pulmonary edema type. The capacity balance of the first 24 hours in the 4 cases was all of positive balance (+1 130, +1 200, +1 750, +1 120 mL respectively). In the treatment, the supplementary colloid was strengthened, the vasoactive drugs such as, dopamine, dobutamine, milrinone, etc were applied to improve the circulatory oxygenation, then the EVLWI was declined; finally the disease situation in 3 cases was improved and one died.Conclusions The clinical diagnosis and treatment of NPE is complex, and many contradictions appear in the therapeutic course. PiCCO monitoring is valuable in early diagnosis, identification of pulmonary edema type, guidance in fluid supplement and vascular active drug application, and assessment of disease severity and prognosis.

Padronização e avaliação histológica de um modelo experimental de lesão medular / Standardization and histological evaluation of an experimental model of spinal cord injury

A lesão medular é incapacitante, irreversível e de custo econômico e social elevado. Neste estudo, objetivou-se padronizar um modelo de lesão medular, que produza paraplegia, com o uso de cateter e avaliar histologicamente a efetividade da lesão para estudos com terapia celular. Foram realizadas as lesões medulares em ratos Wistar, utilizando-se o cateter Fogarty n.3 e compressão na região toracolombar (T8-T9) durante 5 minutos. Foram estudados três grupos: grupo A, animais controle sem lesão medular; grupo B, animais submetidos à lesão, utilizando-se 50µL de compressão; grupo C, animais submetidos à lesão, utilizando-se 80µL de compressão. Foi realizada avaliação motora pela aplicação da escala BBB, antes da compressão, após recuperação anestésica, 24 e 72 horas depois da compressão e sete dias após a compressão. Após o sétimo dia da lesão, os animais foram submetidos à eutanásia, foi feita a retirada da medula espinhal, fígado e rins e realizada a análise histológica com a coloração hematoxilina-eosina. A mortalidade variou entre os grupos, com 0% no grupo A, 38,5% no B e 48% no C. Nesses dois últimos grupos, a causa da morte foi edema pulmonar neurogênico, confirmado clínica e histologicamente. As medulas espinhais histologicamente apresentaram diferentes graus de edema, congestão vascular e hemorragia, enquanto que os fígados e os rins apresentaram diferentes graus de congestão vascular e necrose. Em relação à recuperação dos movimentos, no grupo A, verificou-se 100% de escore 21; no B, 25% de escore 21; 37,5% de escore 11; e 37,5% de escore 0; enquanto, no grupo C, verificou-se 100% de escore 0. Conclui-se que o procedimento realizado utilizando-se 80µL de solução salina para preencher o balão do cateter foi mais eficiente, apesar de maior mortalidade, pois apresentou maior porcentagem de animais com lesão completa (paraplegia).

Spinal cord injury is disabling, irreversible and with high economic and social cost. This study aimed to standardize a model of spinal cord injury to induce paraplegia, with a catheter and to evaluate the effectiveness of the histological lesion for further studies with cell therapy. Cord lesions were performed in Wistar rats using the Fogarty catheter n.3 and compression in the thoracolumbar region (T8-T9) for 5 minutes. We studied three groups: A control group without spinal cord injury, B group subjected to 50?L compression injury, C group with animals subjected to 80?L compression injury. Motor evaluation was performed by applying the BBB scale, before compression, after recovery from anesthesia, 24 and 72 hours after compression and 7 days after compression. At the seventh day after injury, the animals were euthanized. The spinal cord, liver and kidneys were removed and a histological analysis was performed with hematoxylin-eosin staining. Mortality varied among groups, it was 0% in group A, 38.5% in group B and 48% in group C. In the latter two groups the cause of death was neurogenic pulmonary edema, clinically and histologically confirmed. Histologically the spinal cord showed different degrees of edema, hemorrhage and vascular congestion, while the liver and kidneys showed different degrees of vascular congestion and necrosis. Regarding movement recovery, in group A it was found a 100% score 21, in group B 25% of score 21, 37.5% score 11 and 37.5% of score zero, whereas in group C there was a 100% of score zero. It is concluded that the procedure performed using 80?L of saline to fill the balloon catheter was more efficient because, although the higher percentage of mortality, it induced a higher percentage of animals with complete injury (paraplegia).

Effect of high positive end-expiratory pressure for mechanical ventilation in the treatment of neurological pulmonary edema / 中华危重病急救医学

Objective To explore the effect of high positive end-expiratory pressure (PEEP) for the treatment of neurological pulmonary edema (NPE) in patients undergoing mechanical ventilation,and to look for the best mechanical ventilation strategy to improve the prognosis.Methods A prospective study was conducted,and 120 patients with NEP admitted to Department of Critical Care Medicine of the First Affiliated Hospital of Guangxi Traditional Chinese Medical University from January 2010 to August 2013 were enrolled and divided into two groups according to random number table (n=60 in each group).The patients in two groups were given empiric treatment for the disease,and they underwent mechanical ventilation.In the normal PEEP group PEEP was 3-10 cmH2O (1 cmH2O =0.098 kPa),and in the high PEEP group PEEP was 11-30 cmH2O,and all the rest parameters were the same.Clinical indices before and 7 days after treatment,and 28-day morality rate were compared between two groups.Results The 28-day morality rate in high PEEP group was obviously lower than that in the normal PEEP group [25.0％ (15/60) vs.65.0％ (39/60),x2=6.465,P=0.011].The clinical signs in both groups were improved after treatment.Compared with the normal PEEP group,the clinical indices in high PEEP group were more significantly improved.There were significant differences in body temperature (℃ 37.4 ± 0.5 vs.38.5 ± 0.6),respiratory rate (times/min 18.3 ± 3.1 vs.23.3 ±3.5),heart rate (beats/min 94.7 ±8.5 vs.113.5 ±8.0),white blood cell count [WBC (× 109/L) 12.5 ±2.1 vs.17.1 ± 1.7],acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score (15.6 ± 3.2 vs.19.8 ± 3.7),Glasgow coma score (GCS 12.5 ± 2.1 vs.8.5 ± 2.9),gastrointestinal dysfunction score (3.9 ± 3.0 vs.3.6 ± 2.4),oxygenation index [PaO2/FiO2 (mmHg,1 mmHg=0.133 kPa) 196.5 ± 45.1 vs.134.1 ± 22.3],serum creatinine [SCr (μmol/L) 86.5 ± 35.6 vs.98.5 ± 37.7],total bilirubin [TBil (μmol/L) 39.7 ± 23.5 vs.41.5 ± 16.2],C-reacting protein [CRP (mmol/L) 53.7 ± 21.4 vs.108.4 ± 26.3],prothrombin time [PT (s) 15.0 ± 2.1 vs.20.4 ± 2.2],activated partial thromboplastin time [APTT (s):37.3 ±4.9 vs.56.7 ± 13.6],international normalized ratio (INR 2.52 ±0.64 vs.4.01 ±0.77),extra vascular lung water index [EVLWI (mL/kg) 7.53 ± 1.21 vs.15.85 ±3.41],pulmonary vascular permeability index (PVPI 6.07 ± 0.89 vs.9.47 ± 1.26),mean arterial pressure [MAP (mmHg) 87.3 ± 10.9 vs.98.7 ± 13.6],cardiac output [CO (L/min) 7.15 ± 1.42 vs.5.65 ± 1.82],systemic vascular resistance index [SVRI (KP) 112.4 ± 9.5 vs.136.5 ± 11.9],and blood lactate (mmol/L:2.53 ± 1.23 vs.5.81 ± 2.17) between high PEEP group and normal PEEP group (P＜0.05 or P＜0.01).Conclusion Prognosis can be improved in NPE patients with the use of high PEEP in mechanical ventilation.

Muerte súbita e inesperada en la epilepsia (sudep) / Sudden unexpected death in epilepsy

El SUDEP se refiere a la muerte súbita e inesperada con o sin testigos, no traumática, y no por ahogamientos en un paciente epiléptico, con o sin evidencia de que haya sufrido una crisis epiléptica al morir, en el que se haya descartado un estado convulsivo como causa de muerte y en el que la autopsia no proporcione evidencia alguna de una causa anatómica o tóxica de la muerte. Aunque SUDEP ha sido reconocida desde el siglo XIX, sólo en las últimas dos décadas se le ha dado la importancia que ¨¦sta requiere. La frecuencia de SUDEP depende de la severidad de la epilepsia pero en general el riesgo de muerte súbita es de 20 veces mayor que el de la población en general. El edema pulmonar neurógeno, la apnea central y la arritmia cardiaca, inducidos por una descarga Á-adrenérgica de origen central, constituyen los tres mecanismos fisiopatogínicos más estrechamente relacionados con la SUDEP. Por lo anterior obliga al clínico a realizar una minuciosa autopsia la cual deber¨ªa incluir un examen neuropatol¨®gico que documente los cambios cerebrales que subyacen a la epilepsia, toxicología y el examen del corazón, los pulmones y otros órganos.

The SUDEP refers to the sudden and unexpected death with or without witnesses, non-traumatic, and not drowning in an epileptic patient, with or without evidence that he suffered a seizure at death, in which a state is ruled seizure as the cause of death in the autopsy did not provide evidence of a toxic or anatomic cause of death. Although SUDEP has been recognized since the nineteenth century, only in the last two decades has been given the importance it requires. SUDEP frequency depends on the severity of epilepsy but in general the risk of sudden death is 20 times higher than the general population. Neurogenic pulmonary edema, central apnea and cardiac arrhythmias induced by ¦Á-adrenergic shock of central origin, pathophysiologic mechanisms are the three most closely related to SUDEP. Therefore forcing the clinician to perform a thorough autopsy, which should include neuropathological examination to document brain changes that underlie epilepsy, toxicology and examination of the heart, lungs and other organs.

Edema agudo de pulmón neurogénico como complicación de traumatismo encéfalocraneano / Acute neurogenic pulmonary edema as a complication of head trauma

La insuficiencia respiratoria observada tras una injuria cerebral aguda es un fenómeno común que puede debersea múltiples causas, como broncoaspiración, neumonía, atelectasia, embolismo pulmonar y, raramente, edemapulmonar neurogénico. Esta última entidad se encuentra subdiagnosticada y sería un potencial contribuyente dela disfunción pulmonar temprana en pacientes con injurias cerebrales. La misma se ha asociado a convulsiones,accidentes cerebrovasculares, infecciones, traumatismos encéfalocraneanos, entre otros. Se origina por una lesióngrave del sistema nervioso central en ausencia de cardiopatías o neumopatías previas. La gravedad es directamenteproporcional a la lesión cerebral y se produciría por una disfunción del centro vasomotor hipotalámico. Se caracterizapor un incremento en el contenido de agua intersticial pulmonar. Los cambios hemodinámicos son sugestivosde disfunción cardíaca. El análisis temprano del fluido pulmonar revela un cociente de proteínas líquido/suerobajo, compatible con edema hidrostático. El tratamiento incluye oxígenoterapia, asistencia respiratoria mecánicay manejo hemodinámico. Presentamos a una paciente de 20 años, sin antecedentes patológicos, que ingresa portraumatismo encéfalocraneano moderado tras accidente en la vía pública y que posteriormente desarrolla una descompensacióncardiorrespiratoria interpretada como edema pulmonar neurogénico (EPN).

Respiratory distress observed following an acute brain injury is a common phenomenon which could suggest multiplecauses, such as bronchoaspiration, pneumonia, atelectasis, pulmonary embolism and, rarely, neurogenic pulmonary edema(NPE). NPE is usually under-diagnosed and could be a potential contributor to early pulmonary failure in patients whosuffer brain injuries. NPE has been associated, among others, to seizures, strokes, infections, and head trauma. It appearsas a result of a severe injury of the central nervous system (CNS), in absence of previous heart or lung diseases. Its severityis directly proportional to the brain injury and would be a consequence of a failure of the hypothalamic vasomotor center.It is characterized by an increase in the lung interstitial fluid content. The hemodynamic changes suggest heart failure. Theearly assessment of lung fluid reveals a low ratio of liquid/serum proteins compatible with hydrostatic edema. Treatmentinvolves oxygen therapy, mechanical ventilation and hemodynamic monitoring. We present a 20-year old female patient,with no pathologic history, who is admitted due to moderate head trauma after a street accident and who later developscardiopulmonary failure interpreted as a neurogenic pulmonary edema (NPE).

Muerte súbita e inesperada en la epilepsia (SUDEP) / Sudden unexpected death in epilepsy (SUDEP)

El SUDEP se refiere a la muerte súbita e inesperada con o sin testigos, no traumática, y no por ahogamientos en un paciente epiléptico, con o sin evidencia de que haya sufrido una crisis epiléptica al morir, en el que se haya descartado un estado convulsivo como causa de muerte y en el que la autopsia no proporcione evidencia alguna de una causa anatómica o tóxica de la muerte. Aunque SUDEP ha sido reconocido desde el siglo XIX, solo en las últimas dos décadas se le ha dado la importancia que ésta requiere. La frecuencia de SUDEP depende de la severidad de la epilepsia pero en general el riesgo de muerte súbita es de 20 veces mayor que el de la población en general. El edema pulmonar neurógeno, la apnea central y la arritmia cardiaca, inducidos por una descarga a-adrenérgica de origen central, constituyen los tres mecanismos fisiopatogénicos más estrechamente relacionados con la SUDEP. Por lo anterior obliga al clínico a realizar una minuciosa autopsia la cual debería incluir un examen neuropatológico que documente los cambios cerebrales que subyacen a la epilepsia, toxicología y el examen del corazón, los pulmones y otros órganos...

Research in variation of C-reactive protein and glycoprotein KL-6 in children patients with handfoot and mouth disease complicated with neurogenic pulmonary edema and nursing / 中国实用护理杂志

ObjectiveTo discuss the content of serum C-reactive protein and the glycoprotein KL- 6 in hand-foot and mouth disease complicated with neurogenic pulmonary edema children,and discuss related nursing measures,in order to provide the basis for diagnosis of hand-foot and mouth disease complicated with neurogenic pulmonary edema. Methods96 cases of children patients with hand- foot and mouth disease complicated with neurogenic pulmonary edema from January 2010 to June 2011 were selected at random in our hospital,56 cases were heavy patients,40 patients were common type.Another 48 cases were randomly selected healthy volunteers.Using the turbidity to determine the content of C-reactive protein in serum,the Elisa method to determine the content of glycoprotein KL-6.The results were compared and the related nursing measures were summarized. ResultsThe results of the turbidity for C-reactive protein showed that heavy patients were with the highest levels of CRP,common type followed subsequently,while the healthy group was normal.The results of Elisa for glycoprotein KL-6 showed that heavy patients were with the highest levels of glycoprotein KL-6,Common type followed subsequently,the healthy group was normal.By data analysis,we found that the two kinds of test results between three groups were obviously different. ConclusionsThrough comparative analysis,we found that the content of C- reactive protein and the glycoprotein KL-6 were positively correlated with the order of severity of hand-foot and mouth disease complicated with neurogenic pulmonary edema,which can be used as index of clinical judgment of the severity of the disease.Reasonable care measures are very impartant for recovery of the patients.

Individualized monitoring and treatment for children with severe enterovirus 71 infection of different stages / 中国小儿急救医学

Objective To investigate the clinicalmanifestation,monitoring and therapeutic measure of severe enterovirus 71 ( EV71 ) infection in children.MethodsForty-five cases of severe EV71 infectionwere admitted in our PICU from May 2010 to Sep 2011.The vital sign and arterial blood pressure,central venous pressure,mixed venous oxygen saturation,dynamic non-invasive heart function and urine volume were monitored.Forty-five cases were divided into 3 stages according to clinical manifestation:( 1 ) nervous system involvement stage; (2) respiratory system involvement stage; ( 3 ) circulatory system involvement stage ( compensation and decompensation).We adopted individualized remedy measure according to different stages.ResultsIn 45 cases,38 cases discharged from hospital,the cure rate was 84.4％.Among all the 38 cases,nervous system involvement was found in 19 cases,respiratory system involvement was found in 12 cases,circulatory system involvement was found in 7 cases.Seven cases died,who had circulation failure.ConclusionWe should identify severe EV71 infection early.Positive control of high fever,appropriate liquid treatment,control of high blood pressure,early respiratory support,preventment of circulation failure are the key measures for treatment.Individualized monitoring and treatment are effective in children with severe EV71 infection.

Diagnosis and treatment of neurogenic pulmonary edema in children with severe hand, foot and mouth disease / 中国小儿急救医学

Severe hand foot and mouth disease can lead to death when accompanied by neurogenic pulmonary edema. Early identifying involvement of central nervous system, focusing on the evidences of excited sympathetic nerve tension and high risks of neurogenic pulmonary edema, monitoring respiratory rate,dyspnea, cyanosis, fine and medium rales in lungs are critical to prognosis. Managing fluid loading strictly, decreasing intracranial hypertension, supporting actively respiratory function and strengthening airway management are key points for the treatment of neurogenic pulmonary edema.

Recognition and experience in diagnosis and treatment of severe hand, foot and mouth disease / 中国小儿急救医学

Severe hand,foot and mouth disease has emerged as the important threat to lives of children in China in recent years. Enterovirus especially EV 71 is neurotropic pathogen, can cause encephalitis,brainstem encephalitis, which are considered to be related to some severe complications such as pulmonary edema and cardiovascular failure. Autonomic nervous system dysregulation and secondary excessive catecholamine release are thought to be the main mechanism. The key measures for decreasing mortality include optimal ventilatory and cardiovascular support as well as prevention of further brain injuries. The guideline should be used with cautions and clinical practice should be based on patient's conditions.