Prognosis after recovery from adult respiratory distress syndrome.

Ten patients who survived an acute episode of the adult respiratory distress syndrome were studied on recovery. Serial pulmonary function tests performed in 3 subjects revealed a tendency toward normalization of values at 4 to 6 months after the episode, with a subsequent serial decrease in maximal mid-expiratory flow rates, and a partial reversal by bronchodilators. Of the 10 patients, 6 had dyspnea on exertion and all but one of the 6 were smokers. The ventilatory tests revealed a predominantly restrictive pattern in 2 patients and an obstructive pattern in 4. The 4 asymptomatic patients had essentially normal pulmonary function. Pathologic features of the lung, available in 3 cases, are discussed.     

Reversible platypnea and orthodeoxia following recovery from adult respiratory distress syndrome.

Platypnea nad orthodeoxia developed during an episode of adult respiratory distress syndrome in a previously healthy individual. An outstanding feature of the patient's illness was the development of numerous pneumatoceles secondary to necrotizing pneumonia. These abnormalities spontaneously improved with improvement of the underlying parenchymal lung disease.     

Resolution of the adult respiratory distress syndrome following colectomy and liver transplantation

A 32-year-old woman with liver failure from end-stage cirrhosis and ulcerative colitis developed septicemia and severe ARDS. Subtotal colectomy and a successful liver transplantation resulted in complete resolution of the ARDS.     

Clinical and pathologic comparison of adult respiratory distress syndrome and infant respiratory distress syndrome

The authors compared the clinical and pathological findings between adult respiratory distress syndrome (ARDS), and infant respiratory distress syndrome (IRDS). In ARDS, the most common causes were injury, infection, shock and acidosis. The clinical course was longer. The weight of the lungs increased markedly, the hyaline membrane formation in the alveoli was late in the clinical course, and the degree of edema in the interstitium of the lungs and microthrombosis within the blood vessels was more serious. The pathogenesis of ARDS was related to the activation of the complements and neutrophils by inflammation in which proteinase, oxygen radical, thromboxane, leukotriene and prostaglandin were released. Thus the endothelial cells of the blood vessels and capillary-alveoli membrane were damaged by these mediators. On the other hand, the main contributory factors of IRDS were suffocation of premature fetus by various reasons in the uterus and aspiration of meconium during delivery by the infant. The clinical course was shorter, alveolar hemorrhage and collapse were severe and hyaline membrane in alveoli was formed in early stage of the clinical course. Insufficiency of surfactant in premature fetus, damage of the surfactant system by hypoxia, aspiration of foreign materials and defect of the epithelial cells of infant were the pathogenic factors of IRDS, they resulted in increase of permeability of fluid and, as a result, led to pulmonary edema and atelectasis.     

Budd-Chiari syndrome presenting as fulminant hepatic failure.

Two cases of the Budd-Chiari syndrome are described in whom the diagnosis was finally confirmed at necropsy. The presentation was with encephalopathy, occurring within eight weeks of first symptoms and coming therefore within the definition of fulminant hepatic failure. In one, thought to have non-A, non-B hepatitis, encephalopathy progressed to grade 4 coma with death 12 days after presentation. In the other, mistakenly thought to have intra-abdominal malignancy, an exploratory laparotomy exacerbated the encephalopathy with death three weeks later. In neither case were non-invasive investigations, such as ultrasound and isotope scanning, carried out which might have facilitated an earlier diagnosis and consideration for orthotopic liver transplantation, probably the most appropriate form of therapy for these very severe cases.     

Acute respiratory distress syndrome of the adult

In a 43-year-old female patient after a bland influenzal infection suddenly an acute life-threatening picture of a disease with severe dyspnoea developed. Radiologically a distinct interstitial oedema was to be seen. According to the clinical and paraclinical data the case in question was the benign for of an acute dyspnoea syndrome of the adult. Etiology and therapy of the acute dyspnoea syndrome are shown. This picture of a disease should be included into the differential-diagnostic consideration in acute conditions of dyspnoea.     

Current concepts regarding adult respiratory distress syndrome

Adult respiratory distress syndrome (ARDS) is a multietiologic acute and progressive pulmonary dysfunction that may be precipitated by any of a number of pathogenic agents. Clinical and experimental studies suggest that activation of complement and blood neutrophils plays a significant role in the development of pulmonary vascular injury, which is an important pathophysiological feature of ARDS. Although the specific cellular and biochemical mechanisms resulting in the development of ARDS are unknown, it has been suggested that oxygen-derived free radicals generated from complement-activated granulocytes may be involved, directly or indirectly, in the destruction of lung vascular endothelium and alveolar tissue matrix. This hypothesis is supported by recent experimental studies showing that acute lung injury secondary to systemic complement activation can largely be prevented by interventions that scavenge for hydroxyl radicals or restrict availability of ionic iron.     

Neutrophil oxidative burst activation and the pattern of respiratory physiologic abnormalities in the fulminant post-traumatic adult respiratory distress syndrome.

The role of neutrophil oxidative burst activation (OBA) in the development of fulminant post-trauma adult respiratory distress syndrome (ARDS) was studied in 30 patients. Neutrophil (PMN) chemiluminescence (LE) was used as the index of OBA. Serially, for 8 days post-trauma, patient neutrophils (Pc) were studied in their own serum (Ps) normal serum (Ns), or Gey's solution (G). Ps was checked against normal neutrophils (Nc) for inhibition. LE was initiated by the addition of preopsonized zymosan to 1 x 10(6) PMN, the LE response monitored by luminometer, and the peak of the integral of LE recorded. Seven developed ARDS within the first 4 days; 12 patients developed sepsis (TS) but no ARDS, and 11 patients had uncomplicated trauma (TR). All ARDS showed increased LE (P less than 0.0001), at 48-96 hr. Patients without ARDS showed no significant increase in LE, although their mean injury severity (ISS) was the same. The ARDS LE response was mediated by activation of Pc [74%] with only a small but significant additional effect (6%) by ARDS serum (Ps): LE = 0.672 (Pc) + 0.24 [ARDS(Ps)] + 1343; N = 146, r2 0.733, P less than 0.0001. However, sera (Ps or Ns) was required, as incubation in G inhibited LE; [cells + s] greater than [cells + G], P less than 0.0001. LE is a biologic marker of ARDS, and the delay between injury and the LE indicated that initiation of ARDS may have therapeutic importance. Neutrophil activation in ARDS requires sera, but the ARDS effect appears mainly due to cells with only a small ARDS-specific serum-mediated role. The physiologic response to ARDS was evaluated by serial 8-hr studies of blood gases and pH; the respiratory index (RI) to pulmonary shunt (QS/QT) relationship, compliance (COMPL), and net fluid balance (DFLUID) PMN and platelet (PLAT) counts were also measured. Compared with TR and TS, the ARDS patients at 48-96 hr, showed increased RI, QS/QT, and DFluid requiring increased FiO2 and PEEP as COMPL and PLAT fell and LE rose. These changes were all simultaneously significant (P less than 0.05 to P less than 0.0001) by Bonferroni t-statistic applied to ANOVA. The clinical importance of these physiologic and biochemical responses was emphasized by the significantly (P less than 0.005) increased mortality in the ARDS patients. These data suggest that PMN LE and simple measures of respiratory function are early biologic markers of the development of fulminant post-traumatic ARDS and can be used to predict ARDS severity.     

Dress syndrome and fulminant hepatic failure induced by lamotrigine

Lamotrigine is a non-aromatic antiepileptic drug. Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is a severe idiosyncratic reaction to drugs, especially anti-epileptic drugs. Associated clinical features include cutaneous eruption, fever, multiple peripheral lymphadenopathies, and potentially life-threatening damage of one or more organs. We report a case of DRESS syndrome induced by lamotrigine presenting with a hypersensitivity syndrome and fulminant hepatic failure requiring liver transplant. A 21-year old female patient presented an episode of seizure with loss of conscience. CT and EEG studies performed were normal. Treatment with lamotrigine was prescribed. In the course of 30 days, the patient developed skin lesions, pruritus, cholestatic hepatitis, and systemic symptoms-fever, lymphadenopathies, extensive exfoliative erythematous maculopapular rash, and jaundice. Serologic and laboratory tests showed no other causes responsible for the clinical spectrum. Hematologic tests revealed peripheral eosinophilia. Fulminant hepatic failure was diagnosed and an orthotopic liver transplant was performed. Histologic sections of the ex-planted liver demonstrated submassive hepatic necrosis, with the remnant portal spaces and lobules showing a mixed inflammatory infiltrate with lymphocytes and eosinophils. Lamotrigine treatment has been associated with multiorgan failure, DRESS syndrome, acute hepatic failure, and disseminated intravascular coagulation. In conclusion, we suggest that these potentially fatal side effects should be considered in any patient with clinical deterioration following administration of this drug.     

Herpes simplex virus from the lower respiratory tract in adult respiratory distress syndrome

Herpes simplex virus (HSV) was found in the tracheobronchial secretions of 14 of 46 (30%) consecutive patients with the adult respiratory distress syndrome (ARDS). The HSV has not hitherto been associated with ARDS, and most previous reports of HSV in the lower respiratory tract have come from autopsy material. In the present study, the diagnosis during life was initially made by identification of the characteristic inclusion bodies of HSV in bronchial epithelial cells obtained from tracheobronchial aspiration. The presence of HSV in the lower respiratory tract was associated with the need for more prolonged respiratory support and an increased late mortality.     

Indomethacin treatment of human adult respiratory distress syndrome

The purpose of this investigation was to evaluate the magnitude and duration of changes in lung function and oxygen transport in patients with adult respiratory distress syndrome (ARDS) receiving indomethacin. Ten patients with ARDS were randomized to receive intravenously either a single 50 mg dose of indomethacin or placebo. Comparing 1 hr postinfusion levels to baseline observations in the indomethacin group, PaO2 increased to 125 +/- 13 torr from 93 +/- 8 torr, PaO2/FIO2 ratio increased to 223 +/- 24 from 160 +/- 5, and Qs/Qt dropped to 0.20 +/- 0.03 from 0.27 +/- 0.03 (all P less than 0.05). These alterations in oxygenation gradually returned to baseline levels over the ensuing 8 hr. No such changes were noted in the placebo group.     

The incidence of the adult respiratory distress syndrome

Although adult respiratory distress syndrome (ARDS) has been a recognized entity for over 20 years, estimates of its incidence have been very controversial. The most quoted figure is from a 1972 National Heart and Lung Institute Task Force, which estimated 150,000 cases/year in the United States, an incidence of about 75 cases/100,000 population. No experimental study, however, has adequately addressed this issue. We were in a unique position to answer this controversy because the hospital of one of the investigators is located on an island (Las Palmas, Canary Islands, population 700,000). All patients who required mechanical ventilation (other than during anesthesia and immediate postoperative care) were admitted to the same adult intensive care unit. A prospective study to determine the incidence of ARDS was carried out over a 3-yr period. Inclusion criteria were: (1) a known predisposing illness for ARDS; (2) PaO2 less than or equal to 55 mm Hg with FIO2 greater than 0.5 with 5 cm H2O PEEP, without improvement in 24 h; (3) bilateral pulmonary infiltrates; (4) no evidence of left ventricular failure. An average of ten patients per year, representing an incidence of 1.5 cases/100,000 population, were diagnosed as having ARDS and the mortality rate was 70%. Using a more liberal clinical criterion of PaO2 less than or equal to 75 mm Hg with FIO2 greater than or equal to 0.5, 44 more patients with ARDS, representing a total incidence of 3.5 cases/100,000 population, were identified. In conclusion, the overall incidence of ARDS was 1.5 to 3.5 cases/100,000 population, an incidence that is much lower than most previously published estimates.     

Clinical prediction of the adult respiratory distress syndrome

The use of clinical, physiologic, and laboratory parameters in the prediction or early detection of ARDS has been reviewed. From both a clinical and research standpoint, the ability to identify patients at risk is extremely important. The selection of patients according to predisposing clinical events has been the most successful thus far. The use of physiologic variables and gauges of injury severity have been of limited value, particularly for assessing ARDS risk in the individual patient. Only a handful of the proposed mediators or markers of acute lung injury have been studied prospectively in patients at risk. Of these, factor VIII antigen, lactoferrin, and phospholipase A2 appear the most promising as laboratory tests for selecting patients at risk. In the future it may be possible by using sophisticated statistical analysis techniques to combine important clinical, physiologic, and laboratory information into a numerical ARDS risk index, essentially assigning a probability of ARDS in individual patients.