Acute respiratory distress syndrome in adults in colchicine poisoning

Two cases of adult respiratory distress syndrome were treated in a series of 26 patients suffering from colchicine overdose. The syndrome appeared between the 24th and 72nd hours. It was characterized by the presence of interstitial as well as alveolar oedema seen on chest roentgenograms. Haemodynamic investigation showed a hyperkinetic state with moderate precapillary pulmonary arterial hypertension. In addition, multivisceral phenomena were observed in all cases. Post-mortem examination revealed interstitial and alveolar pulmonary oedema with haemorrhagic or macrophagic alveolitis often accompanied by hyaline membrane. The physiopathology of ARDS occurring in colchicine poisoning appeared to involve such different factors as infection, the presence of a state of shock and disseminated intravascular coagulopathy. The direct toxic action of colchicine on pneumocyte microtubules and the inhibition of surfactant production were a probable cause. The responsibility of colchicine in leukocyte aggregation remains to be determined.     

Postoperative pulmonary leukostasis responsible for fatal respiratory distress

A case is reported of a 78-year-old woman with a history of chronic leukemia and who developed after emergency appendicectomy a fatal respiratory distress syndrome related to pulmonary leukostasis. Clinically, the patient had fever, dyspnea and severe hypoxaemia. Chest x-ray showed diffuse pulmonary infiltrates. The patient died from progressive respiratory failure despite ventilatory support. Post mortem lung biopsies were taken for pathologic examination. They showed thrombi composed of leukaemic blast cells which obstructed and distended the lumens of pulmonary arterioles and capillaries. The respiratory distress is attributed to pulmonary leukostasis. Toxic substances released from the leukostatic leukaemic cell or local hypoxia due to vascular occlusion produce this endothelial cell and basement membrane damage. An infectious origin or endogenous pyrogen substances released from leukaemic monocytes may explain the fever. The frequent occurrence of pulmonary leukostasis in patients with leukocyte count greater than 100,000/mm3 point out the need for prevention or therapy of pulmonary leukostasis in these high-risk patients. They need chemotherapy and, if rapid reduction is not observed, leukopheresis which may favourably influence the outcome of patients.     

Acute respiratory insufficiency caused by diffuse pulmonary hemorrhage]

Two cases of adult respiratory distress syndrome due to diffuse pulmonary haemorrhage are reported. The first patient was treated with azathioprine, prednisolone, cyclosporine and ranitidine for haemorrhagic rectocolitis; the second has untreated primary biliary cirrhosis. Haemoptysis only occurred in the latter. Both had severe isolated hypoxaemia. Chest X-rays revealed bilateral alveolar infiltrates. Bronchoscopies showed a diffusely bleeding bronchial tree. Both patients recovered after having been mechanically ventilated with positive end-expiratory pressure for six and eight days respectively. The cause of the diffuse pulmonary haemorrhage was, in the first case, severe thrombocytopaenia (17,000 G.1-1) of central origin, and, in the other patient, an unspecified vasculitis. Diffuse pulmonary haemorrhage should be added to the list of possible causes of the adult respiratory distress syndrome.     

Adult respiratory distress syndrome after cardiac surgery

Adult respiratory distress syndrome, characterized by high permeability pulmonary oedema caused by endothelial cell damage, resulting in refractory hypoxemia, has a very high mortality. Cardiopulmonary bypass is said to be responsible for the development of adult respiratory distress syndrome after cardiac surgery. The present study was performed in order to identify predicting and aetiological factors of adult respiratory distress syndrome and multiple organ failure after cardiac surgery. Between January 1984 and December 1993, 3848 patients underwent cardiac surgery with cardiopulmonary bypass in the authors' institution, and were analysed in a retrospective manner. The operations performed were 3444 coronary artery bypass grafts (CABG), 267 valve and 137 combined (CABG + valve) procedures. The incidence of adult respiratory distress syndrome was 1.0% (38 of 3848) with an overall mortality rate of 68.4% (26 patients); 24 of these died from multiple organ failure. Multivariate regression analysis identified hypertension, current smoking, emergency surgery, preoperative New York Heart Association (NYHA) class 3 and 4, low postoperative cardiac output and left ventricular ejection fraction < 40% as significant, independent predictors for adult respiratory distress syndrome. Combined cardiac surgery and diffuse coronary disease were also significant predictors; cardiopulmonary bypass time was not. Thirty-six of the 38 patients that later developed adult respiratory distress syndrome had low postoperative cardiac output, 12 requiring intra-aortic balloon pump support. The remaining two had severe hypotension caused by postoperative bleeding. Twenty-six adult respiratory distress syndrome patients (68%) had confirmed gastrointestinal complications (e.g. intestinal ischaemia). Adult repiratory distress syndrome is a rare complication after cardiac surgery but is associated with a very high mortality. Preoperative predictors were identified. Cardiopulmonary bypass alone was not found to be an important factor. Postoperative low cardiac output leading to splanchnic hypoperfusion may be the most important single factor in developing adult respiratory distress syndrome after cardiac surgery.     

Life-threatening postoperative pulmonary complications in patients with previous amiodarone pulmonary toxicity undergoing cardiothoracic operations

Amiodarone therapy for cardiac arrhythmias is increasingly being recognized to be associated with pulmonary toxicity. In this report, we describe the case histories of four patients with previously diagnosed amiodarone pulmonary toxicity in whom the adult respiratory distress syndrome developed after cardiothoracic operations for malignant ventricular arrhythmias. Three patients underwent endocardial resection (two died), and a fourth patient had implantation of an automatic defibrillator unit. Radiographic changes and results of pulmonary function testing are evaluated during initial toxicity and preoperatively. These four patients (mean amiodarone dosage of 420 mg/day for 20 months) are compared to 13 other patients undergoing cardiothoracic operations with prior amiodarone treatment (one patient with preoperative pulmonary toxicity) in whom life-threatening postoperative pulmonary complications did not develop (mean dosage of 550 mg/day for 10 months). Mean preoperative serum amiodarone levels for the four patients were 1.5 micrograms/ml. In the two patients who died, desethylamiodarone levels were 510 and 4,400 micrograms/gm in pulmonary tissue. Histologic examination showed "honeycomb" appearance of the lung with prominent septae, alveolar foamy macrophages, and hyperplasia of alveolar lining cells, consistent with amiodarone pulmonary toxicity. Causes including pump-oxygenator time, oxygen toxicity, anesthetic agents, congestive heart failure, and pulmonary infection superimposed on amiodarone pulmonary toxicity are discussed with a review of the literature.     

Tumour necrosis factor in the bronchoalveolar secretions of infants with the respiratory distress syndrome and the effect of dexamethasone treatment.

BACKGROUND: Tumour necrosis factor alpha may contribute to the lung damage that occurs in the adult respiratory distress syndrome. Whether it occurs in the lungs of preterm infants with respiratory distress syndrome is unknown. METHODS: Tumour necrosis factor alpha concentrations in the bronchopulmonary secretions of 28 ventilated preterm infants were determined by the enzyme linked immunosorbent assay. RESULTS: Concentrations were low in the first three days of life, being undetectable in nine of the 20 infants whose bronchopulmonary secretions were sampled. From day 4 concentrations were increased and detectable in all but two of 14 infants. Similar concentrations were found in samples taken on days 8-20 and 21-40. Greater mean concentrations occurred in those infants requiring oxygen for a long time. In six infants who received dexamethasone treatment for prolonged ventilator dependency treatment was associated with a reduction in tumour necrosis factor alpha concentrations. CONCLUSIONS: Tumour necrosis factor may contribute to the neonatal respiratory distress syndrome, as suggested for the adult respiratory distress syndrome. The therapeutic effects of dexamethasone treatment in neonatal respiratory distress syndrome may be mediated, at least in part, by reduced production of pulmonary tumour necrosis factor.     

体外膜肺氧合在肺移植前支持过渡中的应用

目的 探讨体外膜肺氧合(extracorporeal membrane oxygenation,ECMO)在肺移植前支持过渡中应用的可行性和疗效.方法 终末期肺病患者5例,原发病为特发性肺间质纤维化3例,结核性毁损肺1例,淹溺致吸入性肺炎合并急性呼吸窘迫综合征(ARDS)1例.药物治疗和呼吸机无法纠正呼吸衰竭,紧急行E...     

Cavitating lung infarction after bland pulmonary thromboembolism in patients with the adult respiratory distress syndrome.

During one year five patients were observed with the adult respiratory distress syndrome who were found at necropsy to have cavitated lung infarcts following bland (non-infected) pulmonary thromboembolism. There were three instances of bronchopleural fistula and in one person a tension pneumothorax was the immediate cause of death. Four of the five patients had severe lung infections. In all patients airway pressure was raised as a result of positive pressure mechanical ventilation. It is postulated that diffuse microvascular injury, bacterial pneumonia, and high airway pressures may be important factors predisposing patients with adult respiratory distress syndrome to develop lung necrosis, cavitation, and bronchopleural fistula after bland pulmonary thromboembolism. This complication may occur more frequently than has been previously recognised.     

Pulmonary vascular permeability to transferrin in the pulmonary oedema of renal failure.

Thirteen patients with renal failure and pulmonary oedema were assessed for evidence of increased pulmonary vascular permeability to protein by a double isotope technique. Comparison was made with 10 patients with cardiogenic pulmonary oedema, 11 healthy volunteers, and 10 patients with the adult respiratory distress syndrome. There was no significant difference in the accumulation of a radiolabelled plasma protein (transferrin) in patients with renal or cardiogenic pulmonary oedema and normal volunteers. Patients with adult respiratory distress syndrome showed significantly greater protein permeability (p less than 0.001). In pulmonary oedema associated with renal failure managed by current regimens there was no evidence of increased permeability to transferrin.     

Whole-body inflammation in trauma patients. An autopsy study

In a review of autopsy specimens and reports in 35 trauma cases, we found signs of generalized inflammation and tissue damage with increases in organ weights in organs not primarily injured. These abnormalities occurred independent of the time of death and were also found in patients who died of brain injury alone. The most pronounced signs of inflammation and increases in organ weights were found when the adult respiratory distress syndrome, hypovolemic shock, or multiple organ failure were the causes of death. These findings are similar to those found in several organs of rabbits after four hours of complement activation in combination with 20 minutes of hypoxia. Therefore, the autopsy findings in this series of trauma patients might represent the morphologic features of adult respiratory distress syndrome and multiple organ failure in an early, preclinical stage.     

Type I collagen content is increased in lungs of patients with adult respiratory distress syndrome.

Collagen in lung tissue was examined from patients with adult respiratory distress syndrome, from patients who did not have this disease but required mechanical ventilation and oxygen treatment, and from patients without overt lung disease. Cyanogen bromide peptide mapping techniques were used to determine the ratio of type I to type III collagen present in these lungs. In the fibrotic lungs from patients with adult respiratory distress syndrome a shift was found in the ratio of type I to type III from the normal value of 2:1 to a mean value of 3.4:1. In patients with normal lungs and those with other lung diseases collagen type ratios were normal. Our data suggest that (i) changes in lung collagen of patients with adult respiratory distress syndrome resemble those previously described in patients with idiopathic pulmonary fibrosis, although the changes occur much more rapidly in the former; (ii) the increased content of collagen in lungs of patients with adult respiratory distress syndrome shown by others is predominantly of type I collagen; and (iii) the stimulus to the lung to produce excess type I collagen relative to type III is not solely of iatrogenic origin--that is, resulting from oxygen or ventilator treatment.     

Adult respiratory distress syndrome following cardiopulmonary bypass: incidence and prediction

The outcome of adult respiratory distress syndrome complicating cardiopulmonary bypass has changed little in recent years. A retrospective, case-controlled study was designed to assess the incidence of the adult respiratory distress syndrome in these circumstances and the extent to which it could be linked with pre and peri-operative predictive factors. Eleven patients who developed the syndrome out of 840 who underwent cardiopulmonary bypass over a 9 month period were compared with 53 controls matched for sex, operation and surgeon. The incidence of adult respiratory distress syndrome and its mortality were 1.3% and 53% respectively. Significant predictors were a high intra and postoperative intervention score, the total volume of blood pumped during bypass (greater than 300 l) and age (greater than 60 years). These risk factors should alert the clinician to the possibility of severe postoperative pulmonary complications.     

Organ interactions in sepsis. Host defense and the hepatic-pulmonary macrophage axis

Endotoxin (lipopolysaccharide [LPS]) and tumor necrosis factor (TNF-alpha) have been implicated in the pathogenesis of sepsis-induced adult respiratory distress syndrome. To evaluate the possible interaction of the hepatic-pulmonary macrophage axis in the adult respiratory distress syndrome, we compared the kinetics of immunosuppressive prostaglandin E2, TNF-alpha, and interleukin 6 production in LPS-stimulated Kupffer cells and alveolar macrophages (AMs). Interleukin 6 production by Kupffer cells was significantly higher than for equal numbers of AMs. Kupffer cell TNF-alpha levels peaked early before decreasing as regulatory prostaglandin E2 levels rose. In contrast, AM TNF-alpha levels rose sharply and remained significantly higher than for Kupffer cells throughout culture coincident with negligible prostaglandin E2 production. Kupffer cell sequestration of LPS may normally invoke a coordinated cytokine response able to locally induce acute-phase hepatocytes. In hepatic failure, however, LPS spillover to the lung may promote adult respiratory distress syndrome by inducing unregulated AM TNF-alpha production within the pulmonary microenvironment.     

Surgical management of resistant mycobacterial tuberculosis and other mycobacterial pulmonary infections

Between August 1983 and October 1990, 42 patients with resistant Mycobacterium tuberculosis underwent 44 pulmonary resections. During the same time, 38 patients with mycobacterial infections other than tuberculosis had 41 pulmonary resections. All patients either were poor candidates for medical therapy alone or had existing complications requiring surgical intervention. There was one operative death in each group, both from adult respiratory distress syndrome (postpneumonectomy pulmonary edema). Complications were high, with bronchopleural fistula most commonly occurring after right pneumonectomy in patients infected with Mycobacterium avium with superimposed infection with nonmycobacterial pathogens. In patients undergoing pneumonectomy for resistant Mycobacterium tuberculosis, the left lung was most often resected. It is recommended that if localized disease is present and medical treatment is likely to fail, pulmonary resection should be performed for resistant Mycobacterium tuberculosis infection after 3 months of drug-specific therapy. Muscle flaps were used frequently to avoid residual space and bronchial stump problems. Earlier resection in patients with indolent nontuberculous mycobacterial pulmonary infections is advocated before extensive polymicrobial contamination and right lung destruction.     

Early identification of patients prone to develop adult respiratory distress syndrome

Fifty-nine intubated nonhypoxic patients with clinical criteria associated with adult respiratory distress syndrome were studied. Clinical measurements were sought to identify patients before severe hypoxemia occurred. Etiologic factors, chest roentgenography, effective static compliance, intrapulmonary shunt and arterial blood gases on 40 and 100 percent inspired oxygen were analyzed. Pulmonary failure occurred in 22 patients, while 37 had minimal pulmonary difficulties. Comparison of these two groups revealed that only sequential arterial oxygen tensions accurately predicted pulmonary deterioration. A 40 percent arterial oxygen pressure below 100 torr and a 100 percent oxygen pressure below 350 torr indicated a 95 percent probability of pulmonary deterioration. When either determination was above these levels, the probability of pulmonary deterioration was 10 percent. The use of sequential arterial blood gases allows the selection of high risk patients for adult respiratory distress syndrome. This ensures that therapy is offered at the most beneficial time.     

Acute respiratory distress syndrome caused by tuberculosis

The adult respiratory distress syndrome (ARDS) is rarely due to tuberculosis. Two new cases are reported here. Both were female patients, aged 33 and 41 years. The first, of North African origin, was admitted for epigastralgia, hyperpyrexia and intestinal problems. She underwent an exploratory laparotomy, which only showed oedematous mesenteries. Hepatic and lymph node biopsies revealed an ongoing tuberculosis. On the 4th postoperative day, she developed ARDS. Despite an initial period of improvement after proper treatment (antituberculous drugs, steroids, positive pressure ventilation) had been started, she died 27 days later. In the other patient, smoker and alcoholic, the diagnosis of tuberculosis relied only on bacterial culture of various excretions. She also died after 8 days of treatment. In both patients, the symptoms were atypical. The febrile non cardiogenic pulmonary oedema of sudden onset masked the typical miliary mottling pattern on chest X-rays. The life-threatening character of this condition requires that rapid histological studies are carried out to obtain an early diagnosis. Indeed, the precociousness of appropriate treatment seems to be the essential element of the prognosis.     

Adenosine protects ultrastrueture of isolated rat lungs against fat emulsion injury

In isolated rat lungs subjected to fat emulsion damage, a model simulating adult respiratory distress syndrome, we have previously reported that adenosine (ADO) reduces pulmonary vascular resistance (PVR) and the fluid filtration rate (FFR). In the present study the aim was to examine morphologically this effect of ADO. Two groups of isolated rat lungs were subjected to the injury. Marked and significant differences were found between the groups; in lungs not given ADO, FFR and airway pressure were higher and, as evaluated by electron microscopy, the endothelial lining was thin and partly disrupted. The epithelial cells of the alveolar walls were also partly disrupted and the alveolar septa were split enclosing interstitial edema. In lungs receiving ADO from the onset of exposure to fat emulsion, FFR was lower and ultrastructure did not differ from non–injured non–treated controls perfused for the same length of time.     

Stress failure of the blood-gas barrier

The blood-gas barrier must be extremely thin because oxygen and carbon dioxide cross the alveolar-capillary membrane by passive diffusion, and the diffusion resistance is proportional to thickness. Despite its remarkable size (harmonic mean thickness approximately 0.6 microm) the membrane must be immensely strong, because maintenance of its integrity is fundamental for pulmonary gas exchange. The basement membrane is probably the principal anatomical structure providing the strength of the blood-gas barrier. Experimental studies have demonstrated that wall stress of the capillaries can become very high when perfusion pressure is increased to 5.2 kPa (39 mmHg) or more, which was associated with breaks of the capillary endothelium, the alveolar epithelium, or both. These values are potentially reached or exceeded in different cardiac or pulmonary diseases, or in healthy humans subjected to heavy exercise. Stress failure of pulmonary capillaries may play a role in neurogenic pulmonary oedema, high-altitude pulmonary oedema, re-expansion pulmonary oedema, and some forms of the adult respiratory distress syndrome. Increased alveolar pressure due to lung inflation potentiates damage of the blood-gas barrier, suggesting that increases in capillary transmural pressure and transpulmonary pressure are equivalent in terms of their effects on capillary wall stress. These data may have importance for the management of patients with acute respiratory failure requiring mechanical ventilation.     

Mechanical ventilation in the management of acute respiratory distress syndrome

The occurrence of acute respiratory distress syndrome (ARDS), is now common in intensive care units throughout the world. The diagnosis of ARDS is based on a definition that includes bilateral pulmonary infiltrates on chest radiographs, impaired oxygenation, and the absence of clinical evidence of elevated left atrial pressure. ARDS is the clinical result of a group of diverse processes, which range from physical or chemical injury, to extensive activation of innate inflammatory response. All these processes damage the integrity of the alveolar-capillary barrier causing increased alveolar-capillary permeability and an influx of protein-rich fluid into the alveolar space. This alveolar flooding results in hypoxemia, inactivated surfactant, intrapulmonary shunt, and impaired alveolar ventilation. The treatment of acute respiratory distress syndrome is largely supportive in nature, keeping patients alive while allowing their lungs to heal, and minimizing further pulmonary insult. In 1994 the National Heart, Lung, and Blood Institute (NHLBI) established the ARDS Network for the conduct of clinical trials. This is a network, supported by the National Institutes of Health, that provided the infrastructure for well-designed, multicenter, randomized trials of therapies for ARDS. The first study from this group in 2001 produced landmark data demonstrating mortality improvements in ARDS with particular mechanical ventilation strategies. Specifically, low tidal volume mechanical ventilation was demonstrated to reduce mortality by 22%. Other strategies such as high positive end expiratory pressure and prone positioning have not been shown to reduce mortality. Clinicians who are involved in the care of patients with ARDS should have a basic understanding of mechanical ventilation and the evidence guiding the mechanical ventilation strategies of these patients. Until further evidence is published, providers should adopt the use of a volume and pressure limited approach to mechanical ventilation.     

Zur Gefahr eines Fettemboliesyndroms nach Marknagelung bei Femurfraktur und Thoraxverletzung

Following the insertion of an intramedullary nail, the fat embolism is a frequent complication in patients with long bone fractures. The respiratory function of patients with fractures of the femur and accompaning severe chest injuries was improved. In general these patients have a high risk to develop a respiratory distress syndrome. The average age of the 22 polytrauma patients studied was 40 years. The injury's severity as assessed using the Hannover Polytrauma-Score (PTS) and the average score was 29 points. Using Suter's scoring system the severity of the respiratory distress syndrome was assessed (Table 3). The insertion of an intramedullary nail was performed on 18 patients. Four of them developed an ARDS (adult respiratory distress syndrome) up to grade IV for a period of 5 days. Two patients suffered an ARDS grade I for a period of 2 days. In the study no typical features of fat embolism syndrom were found in any of these patients.