[Clinical analysis of community-acquired Pseudomonas aeruginosa septic shock].

OBJECTIVE: This study sought to analyze the clinical manifestations and intervention of fulminant septic shock in community-acquired Pseudomonas aeruginosa septicemia. METHODS: We retrospectively reviewed the medical records for diagnosis, antibiotic therapy, clinical course of septic shock, respiratory support, laboratory data etc. RESULTS: Eight of nine cases with P. aeruginosa septic shock died. Fever (nine cases) and cough (three cases) or diarrhea (3 cases) were the 2 most common initial symptoms, three cases developed skin gangrenosum later. Pseudomonas aeruginosa infection was not considered in any of the cases before death or blood culture showed positive result. Only 3 cases were initially treated with susceptible antibiotic regimen but no anti pseudomonas combination therapy was applied, susceptible antibiotic monotherapy was applied in 7 cases after transfer to the ICU. The mean latency of shock occurrence was 5.1 hours (range 0 to 21 hours) after admission, the mean duration from the occurrence of shock to death was 13.8 hours (range, 1 - 32 hours). All the patients were transfer red to ICU for shock, the appropriate resuscitation of shock patients was delayed by 49.3 minutes (range 25 - 80 minutes) by transfer. Only two cases were diagnosed and treated for shock on admission; after transferred to ICU, only 5 patients were diagnosed as having shock, and only 3 received anti-shock treatment. Eight of the patients died of persistent shock. In 6 patients who died, mechanical ventilation was not applied until cardiac arrest occurred. All the patients had hypoalbuminaemia, elevated serum C-reactive protein concentration, leukopenia and 6 cases had DIC. CONCLUSION: The initial presentation of the cases with community-acquired Pseudomonas aeruginosa septicemia was nonspecific with fever and cough or diarrhea. Clinicians often underestimated the severity of the infection, few patients received effective antimicrobial therapy. The authors suggest that an anti-pseudomonas antibiotic should be included in the initial empiric antibiotic regimen to cover P. aeruginosa high-risk patients; the front-line clinician should be educated for early recognition and aggressive resuscitation of P infection. aeruginosa septicemia.

[Three cases of enterovirus 71 infection with pulmonary edema or pulmonary hemorrhage as the early clinical manifestation].

OBJECTIVE: To recognize the clinical features of the enterovirus 71 (EV71) infection with pulmonary edema or pulmonary hemorrhage as a fulminant and often fatal illness. METHODS: We retrospectively reviewed the medical records of the three cases with EV71 infection for clinical manifestation, laboratory data, medications, outcome etc. RESULTS: All 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. CONCLUSION: Pulmonary 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.

[Myocardial expression and distribution of calcineurin in normal and failing human ventricular myocardium].

OBJECTIVE: To explore the expression and distribution of calcineurin (CaN) in normal and failing human myocardium. METHODS: Left and right ventricles were obtained from end-staged heart failure patients (n = 12) undergoing heart transplantation and donor hearts (n = 5) taken from victims of vehicle accidents. Immunohistochemistry and SDS-PAGE technique were used to demonstrate expression and distribution of CaN. RESULTS: Positive immunoreactive staining for CaN was detected in human cardiomyocytes, cardiac fibroblasts and epicardial mesothelial cells, but not detected in cardiac vascular endothelial cells and smooth muscle cells. There was no difference in CaN protein levels between failing hearts and donor hearts (Band intensity of right ventricle in failing hearts and donor hearts was 130.20 +/- 8.66 and 139.87 +/- 6.21, P = 0.33. Band intensity of left ventricle in failing hearts and donor hearts was 106.45 and 126.34 +/- 12.09) and between left ventricular and right ventricular myocardium (Band intensity of left and right ventricles in failing hearts was 96.99 +/- 10.67 and 104.58 +/- 13.18, P = 0.63. Band intensity of left and right ventricles in failing hearts was 132.12 and 120.74). CONCLUSIONS: CaN is expressed in human cardiomyocytes, fibroblasts and epicardial mesothelial cells and the protein level and distribution of CaN are similar in failing and donor hearts.

[The role of alveolar macrophages in airway remodeling in asthmatic rats].

OBJECTIVE: To study the role of alveolar macrophages (AM) in the processes of airway remodeling in asthmatic rats. METHODS: Forty-eight young male Sprague-Dawley rats (Grade II) were divided randomly into a control group (A group), a 3 day asthma group (B group), a 14 day asthma group (C group) and a 30 day asthma group (D group). The rats were sensitized and challenged by ovalbumin to establish the asthmatic model. AM were purified from bronchoalveolar lavage. The content of tumor necrosis factor-alpha (TNF-alpha) in AM was measured by enzyme-linked immunosorbent assay, prostaglandin E2 (PGE2) by radioimmunoassay, matrix metalloproteinase-9 mRNA (MMP-9 mRNA) and tissue inhibitor of metalloproteinase-1 mRNA (TIMP-1 mRNA) by hybridization in situ. The total bronchial wall area (WAt) and the smooth muscle area (WAm) were measured by image analysis system. The WAt and the WAm were quantified per unit length of basement membrane (Pbm). RESULTS: The bronchial wall thickness and the smooth muscle thickness of D group [(85 +/- 9) microm2/microm, (28.6 +/- 4.9) microm2/microm] were significantly higher than those of A group [(67 +/- 10) microm2/microm, (16.8 +/- 2.4) microm2/microm, t = 2.938, 3.227, all P < 0.01]. The contents of TNF-alpha and PGE2 in D group [(0.68 +/- 0.25) microg/L, (0.122 +/- 0.030) microg/L] were significantly higher than those in A group [(0.37 +/- 0.09) microg/L, (0.079 +/- 0.018) microg/L, t = 2.683, 3.016, all P < 0.01]. When A group was compared with B group [(0.74 +/- 0.29) microg/L, (0.120 +/- 0.028) microg/L] and C group [(0.71 +/- 0.23) microg/L, (0.117 +/- 0.028) microg/L], there was no significant difference (t = 1.624, 0.472, all P > 0.05) and (t = 0.935, 0.533, all P > 0.05). The contents (light density) of MMP-9 mRNA and TIMP-1 mRNA in D group (0.346 +/- 0.033, 0.361 +/- 0.040) were significantly higher than C group (0.279 +/- 0.015, 0.259 +/- 0.015, t = 2.574, 2.716, all P < 0.01), and so did D group and B group (0.183 +/- 0.025, 0.136 +/- 0.014, t = 2.913, 3.017, all P < 0.01), D group and A group (0.104 +/- 0.007, 0.109 +/- 0.008, t = 3.632, 3.487, all P < 0.01). There were significant correlations between the contents of MMP-9 mRNA and WAt (r = 0.693, P < 0.01), between MMP-9 mRNA and WAm (r = 0.738, P < 0.01), between TIMP-1 mRNA and WAt (r = 0.823, P < 0.01), and between TIMP-1 mRNA and WAm (r = 0.876, P < 0.01). CONCLUSION: AM and AM-derived cytokines are associated with airway remodeling in asthmatic rats.