A b s t r a c t s From the L i t e r a t u r e

Selec ted by Mar t i n J. Tob in

Adult Respiratory I~istress Syndrome: Prognosis After Onset. Fowler AA. Itamrnan RF. Zerbe GO. et el. Am Rev Respir Dis 132:472, 1985.

In 88 patients with the adult respiratory distress syqdrome, clinical, laboratory, cardiopulmonary, and demographic data collected on the day of the onset of the syndrome were used to identify predictors of survivorship and mortality. Variables that individually were associated with mortality were then analyzed simultaneously by the Cox proportional hazards function and by multiple discriminant function using a step-up procedure. I'-our variables taken singly were signifi- cantly associated with mortality. These were the presence of less than 10% band forms on the initial peripheral blood smear, persistent acidemia with arterial pH less than 7.40, calculated I-iCO~ less than 20 mg/dL, and blood urea nitro- gen greater than 65 mg/dL. After eliminating those variables that did not comributc significantly to mortality in the presence of the others, only low band forms, low pH, and low HCO~ were significantly associated with increased mortality. These findings illustrate the continued high mortality rate in the syndrome and indicate possible systemic aberrations that contribute to its severity.

Collagenese in the Lower Respiratory Tract of Patients With Adult Respiratory Distresis Syndrome. Christner P, Fein A. Golaherg S. et al, Am Rev Respir Dis 131:690, 1985.

Collagenasc activity in the bronchoalveolar lavage (BAL) of patients with adult respiratory distress syndrome (ARDS) was measured against Type i collagen (17 patients) and against Type II! collagen (13 patients). Serin¢ protease activity was also measured against Type III collagen (13 patients). Type I collagcnase activity was detectable in 12 of 17 and Type II! collagenase was detectable in 12 of 13 patients with ARDS. The ten control subjects had no detect- able Type I or Type i[I eollagenase activity. Total and differential white cell counts were analyzed in the lavage fluid, AIIhough the total counts did not differ between patients with ARDS and control subjects, the percentage of neutrophils was increased more than 25-fold, and the per- centage of macroph;tges was reduced almost tenfold it, the ARDS patients. Serial collagenase activity was followed in one ARDS survivor, In this patient Type ill collagenase activity peaked before the Type I coltagenase activity or serine proteasc activity reached their maximums. Both the latter enzyme activities paralleled the total recoverable cells in the BAL.

Causes of Mortality in Patients With the Adult Respiratory Distress Syndrome, Montgonler)" AB. Stager A~A. Carrico CJ. et el. Am Rev Respir Dis 132:485, 1985.

This study analyzed the factors causing and contributing to death in patients with the adult respiratory distress syndrome (ARDS). Two hundred seven patients were pro- spectively identified as being at risk for development of ARDS. Forty-seven patients developed ARDS, and the remaining 160 patients were used as a comparison control group. The severity of dysfunction in eight organ systems and the presence of sepsis syndrome were determined by chart review after discharge or death. Sepsis syndrome was specifi- cally defined by signs and laboratory tests reflecting infection or inflammation plus evidence of a deleterious systemic effect (hypotension, reduced systemic vascular resistance, or unex- plained metabolic acidosis). Mortality was 68% in the ARDS group compared to 34% in the control group (P < .005). Only 16% (5 of 32) of deaths in the ARDS group were from irreversible respiratory failure. Most deaths in the first 32 days after entry into the study could be attributed to the underlying illness or injury. The majority of late deaths were related to sepsis syndrome, Of the 22 patients with ARDS who died after three days, 16 (73%) met our criteria for sepsis syndrome. There was a sixfold increase in sepsis syndrome after ARDS compared with that in the control group (P < .001 ), When sepsis syndrome preceded the ARDS, the abdo- men was the predominant source, but when sepsis syndrome occurred after the onset of ARDS there was usually a pulmonary source. Our findings indicate that sepsis syn- drome, rather than respiratory failure, is the leading cause of death in patients with ARDS.

Complications of Right Heart Catheterization: A Prospec- tive Autopsy Study. Conners AFJr , C'asteh" RJ. Farhat NZ. et el. Chest 88:4;567. 1985.

The purpose of this study was to characterize the type and prevalence of abnormalities associated with right heart cath- eterization. We performed detailed postmortem examina- tions of 32 consecutive patiepts brought to autopsy with a right heart catheter in the pulmonary artery. Thrombosis (17 patients, 53%), hemorrhagic lesions (25 patients. 78%), and intimal fibrin deposition (21 patients, 66%) were found at sites along the entire path of the catheter. Twenty-nine patients (91%) had either thrombosis, hemorrhage, or both. While the superior vena cave was the most common site for all lesions, seven patients had thrombosis involving the cham- bers and valves of the heart, and four had thrombosis involving the pulmonary artery. The incidence of thrombosis was significantly higher after 36 hours of catheterization (P < .05). All five patients with thromboemboli in the more proximal pulmonary arteries had catheter-related thrombo- sis. We conclude that there is a high prevalence of thrombotic and hemorrhagic lesions in patients dying with pulmonary catheters in place; that the risk of thrombotic complications increases with duration of catheterization; and that patients with catheter-related thrombosis are at increased risk of thromboemboli to the proximal pulmonary arteries.

Evaluation of the Portable Chest Roentgenogram for Quan- titettng Extravascular Lung Water in Critically III Adults. Halperin BD, Fee/e), TI'Y, Mihm FG, et aL Chest 88:5;649, 1985.

The diagnosis of pulmonary edema is frequently made from characteristic findings on the chest roentgenogram that

Journal of Critical Care, Vet 1, No 1 (March), 1986: pp 57-63 57