Brain Edema ; etiology ; Female ; Heart Failure ; etiology ; Humans ; Infant ; Pneumonia ; complications ; Pulmonary Edema ; etiology

Central Nervous System Diseases ; complications ; Humans ; Pulmonary Edema ; etiology

Enterovirus A, Human ; Enterovirus Infections ; pathology ; Female ; Hemorrhage ; etiology ; virology ; Humans ; Infant ; Male ; Pulmonary Edema ; etiology ; virology

Bulbar Palsy, Progressive ; etiology ; Child, Preschool ; Hand, Foot and Mouth Disease ; complications ; Humans ; Male ; Pulmonary Edema ; etiology

OBJECTIVETo identify the causes of respiratory complications following liver transplantation (LT) and to discuss the management of these complications.

METHODSOne hundred and twenty four cases with pulmonary complications in the first two weeks after LT were identified among 163 patients admitted to the First Affiliated Hospital, College of Medicine, Zhejiang University from February, 1999 to March, 2003.

RESULTSThe incidence rate of complications was 76%(124/163) with the total cure rate of 92%(114/124). The cure rates of the various complications were as follows: pleural effusion 100%(113/113), pneumonia 92%(76/83), respiratory insufficiency 91%(59/65), pulmonary hypertension 98%(101/103), pulmonary edema 98(58/59), atelectasis 100%(4/4) and pneumothorax 100%(2/2).

CONCLUSIONTo drainage the pleural effusion with an unicameral venous catheter is safety and effective. To cure or prevent pneumonia and atelectasis, aseptic manipulating, aspiration of sputum and keeping respiratory channel open were the key measurements of treatment. Restrictive ventilatory functional disturbance (RVFD) and dysfunction of ventilation are two major types of respiratory insufficiency in early stage of post-transplantation. The causes of pulmonary hypertension and edema are associated with pulmonary angiotasis and blood flow volume, and the vasodilator and diuretic often introduced in the therapy.

Female ; Humans ; Hypertension, Pulmonary ; etiology ; therapy ; Liver Transplantation ; adverse effects ; Male ; Pleural Effusion ; etiology ; therapy ; Pneumonia ; etiology ; therapy ; Postoperative Complications ; etiology ; therapy ; Pulmonary Atelectasis ; etiology ; therapy ; Pulmonary Edema ; etiology ; therapy ; Respiratory Insufficiency ; etiology ; therapy ; Respiratory Tract Diseases ; etiology ; therapy

Enterovirus A, Human ; pathogenicity ; Enterovirus Infections ; complications ; Humans ; Pulmonary Edema ; etiology ; virology

OBJECTIVETo observe and compare the effects of natural colloid and artificial colloid on pulmonary edema of swine during shock stage of severe burn injury.

METHODSTwelve Guangxi Bama miniature swine were inflicted with 40% TBSA full-thickness burn on the back, and then they were divided into natural colloid group (N) and artificial colloid group (A) according to the random number table, with six swine in each group. At post injury hour (PIH) 2, fluid resuscitation was begun. The main part of electrolyte was lactic acid Ringer's solution. The colloids included swine plasma and hydroxyethyl starch 130/0.4. Before injury and at every hour within PIH 48, heart rate, blood pressure, urine volume, central venous pressure (CVP), and pulmonary arterial wedge pressure (PAWP) were recorded. The mean heart rate, blood pressure, urine volume per hour per kg of body weight, CVP, PAWP, resuscitation liquid volume, and the ratio of fluid intake to output during the first and second PIH 24 were calculated. At PIH 48, lung tissue was harvested for histopathological observation and calculation of lung water ratio. Data were processed with one-way analysis of variance, analysis of variance of repeated measurement, LSD test and independent sample t test.

RESULTS(1) There were no statistically significant differences between two groups in heart rate, blood pressure, and urine volume before injury and during the first and second PIH 24 (P values all above 0.05); during the first PIH 24, the CVP and PAWP of group A were significantly higher than those of group N (P values all below 0.05). Compared with those before injury, the heart rate, CVP and PAWP of two groups during the first and second PIH 24 were significantly higher (P < 0.05 or P < 0.01); the urine volume of group N was decreased during the first PIH 24 (P < 0.05), while there was no significant change in group A (P > 0.05); the urine volumes of two groups during the second PIH 24 were increased, while no statistically significant differences were observed (P values all above 0.05). There were no statistically significant differences in blood pressure of two groups between the first, second PIH 24 and before injury (P values all above 0.05). (2) There were no statistically significant differences in the resuscitation liquid volume and fluid intake to output ratio between two groups during the first and second PIH 24 (P values all above 0.05). (3) The alveolar septum was found widened in varying degrees, and there were edema fluid accumulating and inflammatory cell infiltrating within the pulmonary interstitial of lung tissue sections in both two groups. (4) The lung water ratio of group N [(71 ± 10)%] was not statistically significant different from that of group A [(79 ± 4)%, t = -1.753, P > 0.05].

CONCLUSIONSThe natural colloid or artificial colloid (hydroxyethyl starch 130/0.4) applied during shock stage had similar effects on pulmonary edema in swine with severe burn.

Animals ; Burns ; complications ; Disease Models, Animal ; Fluid Therapy ; methods ; Pulmonary Edema ; etiology ; Shock ; complications ; therapy ; Swine

Animals ; Humans ; Hypertension, Pulmonary ; etiology ; Inflammation Mediators ; physiology ; Neutrophil Activation ; Platelet Activating Factor ; antagonists & inhibitors ; physiology ; Pulmonary Edema ; etiology ; Respiratory Distress Syndrome, Adult ; drug therapy ; etiology

AIMTo investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema.

METHODSThe levels of endothelin-1 in plasma and lung were measured in rats which suffered from diffuse brain injury on Marmarous' model. The changes of endothelin-1 in the lungs were also detected using an immunohistochemical method.

RESULTSAfter heavy diffuse brain injury in rats, the levels of endothelin-1 in plasma and lung began increasing at 1 hour, and peaked at 6 hour. Though a little declining at 24 hour, it maintained a higher level within 48 hours (P < 0.05). Pulmonary pathology showed that after brain injury there were congestion, swelling in pulmonary microvessels with broadened pulmonary interstitial tissue, and leucocyte infiltration was dominated by neutrophils and monocytes from 1 hour on, which peaked at 6 hour. More serious congestion, swelling and protein effusion in pulmonary alveoli were observed at both 24 h and 48 h. Immunohistochemically, endothelin-1 had more significant expression and higher levels of OD in the experimental groups than that in the control's, the most significance of which was at 6 hour.

CONCLUSIONThe inflammatory injury mechanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.

Animals ; Endothelin-1 ; metabolism ; Lung ; metabolism ; Male ; Pulmonary Alveoli ; metabolism ; Pulmonary Edema ; etiology ; metabolism ; Rats ; Rats, Wistar

OBJECTIVETo recognize the clinical features of the enterovirus 71 (EV71) infection with pulmonary edema or pulmonary hemorrhage as a fulminant and often fatal illness.

METHODSWe retrospectively reviewed the medical records of the three cases with EV71 infection for clinical manifestation, laboratory data, medications, outcome etc.

RESULTSAll the cases were infants and they all died. These infants had no skin or mucosal lesions, however, they had sudden onset of cyanosis and tachypnea 1 to 2 days after the onset of the febrile disease with vomiting. All these 3 cases were misdiagnosed and were treated for shock on admission. Pulmonary hemorrhage was not considered in any of the cases on admission. All the cases received tracheal intubation when foamy secretions were discharged from mouth and nose of the patients and notable cyanosis was noted. After intubation, all had pink foamy fluid flew out from the endotracheal tube. The patients had hyperglycemia and limb weakness, two had tachycardia, and hypertension was found in one case. Chest X-ray showed bilateral or unilateral widespread air space opacity, but the cardiac size and shape were normal. All the patients had leucocytosis. EV71 infection was confirmed by detection of specific sequences of the virus in throat swab and tracheal secretions samples and in one case in cerebrospinal fluid sample.

CONCLUSIONPulmonary edema or pulmonary hemorrhage occurred in the 3 cases with EV71-infected infants. The initial presentation was often nonspecific with fever and vomiting, and sudden appearances of cyanosis, tachypnea, tachycardia, hypertension or hypotension, limb weakness may suggest pulmonary edema or hemorrhage. Excessive fluid resuscitation may deteriorate the illness, on the contrary, fluid restriction and inotropic agents, and early intubation with positive pressure mechanical ventilation may be the proper treatment.

Enterovirus A, Human ; Enterovirus Infections ; pathology ; Female ; Hemorrhage ; etiology ; virology ; Humans ; Infant ; Male ; Pulmonary Edema ; etiology ; virology ; Retrospective Studies