[Mediastinitis during oesophageal stenosis dilation].
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Biomedical subjects
Publications and source records attributed to E Wiel.
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We report the case of a 64-year-old man without hemorrhagic history experiencing epistaxis. The standard hemostasis assessment including prothrombin index, activated partial thromboplastin time (APTT) and platelet count found an isolated abnormal APTT (105 sec vs 33 sec). Therefore, coagulation factors were explored. An acquired factor VIII deficiency (5%) with anti-FVIII antibody (4.5 Bethesda unit.mL-1) was recognised. This anti-FVIII antibody was related to a Chlamydia pneumoniae pulmonary infection. Treatment consisted of: i) Four successive anterior packing and activated factor VII infusion (Novoseven); ii) steroids injection and bi-antibiotherapy. The time course of the epistaxis was favourable under treatment.
From 1980 to 1998, 65 patients whose glottic lesions were classified T1 or T2 were operated with a reconstructive anterior frontal laryngectomy with epiglottoplasty such as described by Tucker (Arch Otolaryngol Head Neck Surg 115:1341-1344). This procedure consists of resection of the two vocal cords, in some cases one arytenoid, the anterior commissure with a part of the thyroid cartilage, the anterior part of both false vocal cords, and of 1 cm of the subglottis. The epiglottis is grasped downward to close the larynx. There were no per or postoperative deaths. Our functional results confirm those reported in the previous publications. The mean time of removal of the nasogastric tube was about 12 days and the patients were generally satisfied about their residual voice. Decannulation was performed after satisfactory peroral feeding, generally about 2 weeks postoperatively. Three patients only required subsequent procedures which can be considered due to functional failures. There were four recurrences, which means a 5-year actuarial local control rate of 94%. This operation takes place as part of our surgical treatment policy of laryngeal carcinomas, considering that this surgery is like an extensive frontolateral laryngectomy. In case of an infiltrating tumor or in case of invasion to the arytenoid cartilage, we perform a supracricoid partial laryngectomy with crico-hyoido-epiglottopexy (the Majer-Piquet's procedure).
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OBJECTIVE: To investigate the effects of AZ-1, a murine monoclonal antiglycoprotein-IIb/IIIa antibody, on endothelium and on hemostasis in a rabbit endotoxic shock model. DESIGN: Prospective laboratory study. SETTING: University laboratory. SUBJECTS: Thirty-five male New-Zealand rabbits. INTERVENTIONS: In vitro vascular reactivity, endothelium CD31-PECAM1 immunohistochemistry, plasma coagulation factors, and monocyte tissue factor determination were performed 1 day and/or 5 days after onset of endotoxic shock (0.5 mg/kg, intravenous bolus,Escherichia coli lipopolysaccharide) with or without treatment by AZ-1 (0.5 mg/kg intravenously) given 1 hr after lipopolysaccharide injection. MEASUREMENTS AND MAIN RESULTS: Metabolic acidosis and coagulation activation confirmed the presence of shock. AZ-1 treatment improved endothelial-dependent relaxation at 1 day (maximal effect = 87.2 +/- 4.0% vs. 60.9 +/- 5.2% in the nontreated group, p <.05) and at 5 days (maximal effect = 84.5 +/- 3.5% vs. 56.6 +/- 8.2% in the nontreated group, p <.05). Endotoxin-induced endothelial injury was decreased significantly by AZ-1 at 1 day (6.4 +/- 1.9% vs. 10.3 +/- 0.8% in the nontreated group, p <.05) and at 5 days (6.3 +/- 2.0% vs. 20.2 +/- 1.2% in the nontreated group, p <.05). Monocyte tissue factor expression was significantly reduced at 5 days. CONCLUSIONS: These data indicate that potent inhibition of platelet function via antiglycoprotein-IIb/IIIa receptor blockade can inhibit coagulation activation and protect against endothelial dysfunction and histologic injury in endotoxin-induced shock.
OBJECTIVES: a) To review endothelial properties and to establish how these unperturbed properties contribute to the maintenance of endothelium anticoagulant activity; b) to better understand the relative contributions of endothelial cells and monocytes in sepsis-induced altered coagulation. DATA SOURCES: A summary of published literature from MEDLINE search files and other original articles and reviews published on endothelial cell and monocyte functions and modifications owing to sepsis. DATA EXTRACTION AND SYNTHESIS: Unperturbed endothelial cells provide anticoagulant properties; exposure to inflammatory and/or septic stimuli can rapidly lead to procoagulant behavior. Sepsis alters endothelial cell surface and induces tissue factor synthesis at the endothelial and subendothelial levels. During endotoxemia, endothelial cells generate adhesion molecules that bind leukocytes and monocytes, increasing local procoagulant reactions. Tissue factor expression is also increased at the level of the monocyte; the relative importance of endothelial injury and monocyte activation in coagulation disorders was recently assessed. Endothelium protection before induction of septic shock was not associated with any reduction in monocyte tissue factor expression, suggesting that altered coagulation was present despite normal endothelial cell function. On the other hand, decreased monocyte tissue factor expression was associated with a marked reduction in endothelial injury, increased endothelium-derived relaxation, and improved survival rate in treated animals. CONCLUSIONS: This review suggests that monocyte activation and tissue factor expression may be of paramount importance in sepsis-associated injuries and that coagulation activation may contribute to the endothelial cell injury observed during sepsis. Endothelial injury, in turn, exacerbates sepsis-induced coagulation abnormalities.
Tracheocutaneous fistula is seen frequently in decannulated children and respiratory complications associated with primary surgical closure can be potentially fatal. Cough is a precipitating factor for an air leak and we report two cases in which this occurred. A tracheotomy was performed on a 5-month-old girl for mechanical ventilation. Decannulation was successful at the first attempt. One year later, she presented with a persistent tracheo-cutaneous fistula. After surgical closure without drainage, she developed subcutaneous emphysema during a coughing episode. Sutures were removed. A 9-month-old boy presented with oxygen-dependence after lung disease and a tracheotomy was performed for respiratory support. Decannulation was successful at the first attempt 6 months later. He developed a pneumomediastinum after surgical closure of a tracheo-cutaneous fistula. Sutures were removed but replacement of a tracheotomy tube was required. In both cases the wounds were allowed to heal by secondary intention.
To investigate whether impaired endothelial function was related to alteration of nitric oxide (NO) formation during endotoxic shock, we studied the effects of supplementation of L-arginine (L-Arg), D-arginine (D-Arg), and N(G)-nitro-L-arginine methyl ester (L-NAME), on endothelial function and structure in a rabbit model. Endotoxic shock was induced by a single lipopolysaccharide bolus (0.5 mg/kg i.v., Escherichia coli endotoxin). Coagulation factors and expression of monocyte tissue factor were determined by functional assays. Endothelium-dependent vascular relaxation was assessed by in vitro vascular reactivity. Immunohistochemical staining (CD31) was performed to assess damaged endothelial cell surface of the abdominal aorta. These parameters were studied 5 days after the onset of endotoxic shock and were compared under three conditions: in absence of treatment, with L-Arg or D-Arg supplementation, or with L-NAME. Both L-Arg and D-Arg significantly improved endothelium-dependent relaxation and endothelial morphological injury. L-NAME did not alter endothelial histological injury induced by lipopolysaccharide. These data indicate that arginine supplementation nonspecifically prevents endothelial dysfunction and histological injury in rabbit endotoxic shock. Moreover, L-Arg has no effect on coagulation activation and expression of monocyte tissue factor induced by endotoxic shock.
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The authors report the case of a 22-month-old boy experiencing a voluminous subcutaneous haematoma, 72 hours after a head trauma. Two subsequent drainages of this haematoma were required because of its recurrence. The child, whose parents had blood relations, suffered from recurrent bleeding since his birth. A standard haemostasis assessment including prothrombin time, activated partial thrombopiastin time, bleeding time, concentration of fibrinogen and platelet count was unremarkable. Therefore, coagulation factors were explored. An inherited factor XIII deficiency (less than 2%) was recognized. A new drain was inserted, after administration of factor XIII concentrate. The time course of the haematoma was favourable. After discharge, the prophylactic therapy consisted of an injection of factor XIII concentrate (50 Ul.kg-1) every 5 weeks.
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Partial avulsion of the middle turbinate is an unusual complication of nasotracheal intubation, while minor nasal mucosal trauma is common. We report a case in a 25 year-old healthy-woman, diagnosed four years after nasotracheal intubation for removal of wisdom teeth under general anaesthesia, consisting in a unilateral nasal obstruction related to partial avulsion of the middle turbinate.
A 21-year-old man sustained a closed fracture of the leg from an industrial accident, without associated head trauma. The orthopaedic treatment consisted of immediate immobilization by setting leg in plaster. Two hours after admission, the Glasgow coma scale score was 10. Four hours after admission he developed a coma (Glasgow coma scale score = 7) with repetitive seizures. No lesion was visible on cerebral CT scan. Chest X-ray was unremarkable. Petechiae on the anterior chest wall and abdomen with bilateral mydriasis occurred. Thrombocytopenia with prothrombine time increase were observed. Magnetic resonance imaging, 27 hours after admission, showed high-intensity areas on T2 weighted views due to fat embolism. Retinal haemorrhages were observed. The bronchoalveolar lavage showing fat staining of tracheal aspirates confirmed the diagnosis of fat embolism. This case report emphasizes the possibility of predominant neurologic manifestations of a fat embolism and the diagnostic help of cerebral magnetic resonance imaging.
Chondronecrosis of the cricoid cartilage is a rare complication of intubation. The records of two children were reviewed. An 8-month-old girl with myelomonocytic leukaemia developed chondronecrosis 10 days after a 2-day period of ventilation. A 4-year-old girl comatose after poisoning by the histamine antagonist, alimemazine, developed chondronecrosis after a 2-day period of intubation. The complication was suspected when extubation led to dyspnoea owing to laryngeal stridor and was confirmed by direct laryngoscopy. We review the development of the condition, the causative factors, treatment and prevention.
Acquired laryngotracheal stenosis is a serious long term complication of tracheal intubation with an incidence of 0.7 to 8% in intubated children. We report five cases of subglottic stenosis over a 4.5-year period and review the pathology and pathogenesis of the condition. A diagnosis of subglottic stenosis was suspected when extubation failed due to the onset of dyspnoea or laryngeal stridor. An incidence of 0.9% of all intubated children was observed. We conclude that the main components contributing to stenosis are pathologies with decreased mucosal capillary perfusion pressure and intubation conditions.
The aim of this study was to analyse the follow-up of patients with a history of endotracheal intubation and/or tracheotomy because of respiratory distress, surgical necessity or long-term resuscitation. Twenty adults were followed up in a ENT facility for laryngeal or tracheal stenosis, of which 7 cases were diagnosed during 1994. This study shows that, in patients with a history of intubation, or intubation followed by tracheotomy, the stenosis developed within two months after resuscitation with a favourable outcome. After tracheotomy only, the stenosis developed later (2 months or more) with more recurrences. The diagnosis of stenosis was made on gradual or acute dyspnea. While respiratory resuscitation methods are essential and often life-saving, they are not without complications. Laryngeal and tracheal stenosis could be largely prevented by more careful techniques of endotracheal intubation and tracheotomy. Periodic endoscopic airway surveillance is useful to detect stenosis even when there is no clinical symptom.