Neonatal respiratory distress syndrome pathophysiology

Revision as of 20:16, 13 February 2013 by Prashanthsaddala (talk | contribs)
Jump to navigation Jump to search

Neonatal respiratory distress syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Neonatal respiratory distress syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Interventions

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Neonatal respiratory distress syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Neonatal respiratory distress syndrome pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Neonatal respiratory distress syndrome pathophysiology

CDC on Neonatal respiratory distress syndrome pathophysiology

Neonatal respiratory distress syndrome pathophysiology in the news

Blogs on Neonatal respiratory distress syndrome pathophysiology

Directions to Hospitals Treating Neonatal respiratory distress syndrome

Risk calculators and risk factors for Neonatal respiratory distress syndrome pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

The lungs are developmentally deficient in a material called surfactant, which allows the alveoli to remain open throughout the normal cycle of inhalation and exhalation. Surfactant is a complex system of lipids, proteins and glycoproteins which are produced in specialized lung cells called Type II cells or Type II pneumocytes. The surfactant is packaged by the cell in structures called lamellar bodies, and extruded into the alveoli. The lamellar bodies then unfold into a complex lining of the alveoli. This layer reduces the surface tension of the fluid that lines the alveolar walls. During exhalation the walls of the alveoli come in contact and surface tension tends to cause them to stick together, preventing re-inflation. By reducing surface tension, surfactant allows the alveoli to re-expand with inspiration. Without adequate amounts of surfactant, the alveoli collapse and are very difficult to expand. Microscopically, a surfactant deficient lung is characterized by collapsed alveoli alternating with hyperaerated alveoli, vascular congestion and, in time, hyaline membranes. Hyaline membranes are composed of fibrin, cellular debris, red blood cells, rare neutrophils and macrophages. They appear as an eosinophilic, amorphous material, lining or filling the alveolar spaces and blocking gas exchange. As a result, blood passing through the lungs is unable to pick up oxgen and unload carbon dioxide from the alveolar spaces. Blood oxygen levels fall and carbon dioxide rises, resulting in rising blood acid levels and hypoxia. Structural immaturity, as manifest by low numbers of alveoli, also contributes to the disease process. Therapeutic oxygen and positive-pressure ventilation, while potentially life-saving, can also damage the lung. The diagnosis is made by the clinical picture and the chest xray, which demonstrates decreased lung volumes (bell-shaped chest), absence of the thymus (after about 6 hours), a small (0.5-1 mm), discrete, uniform infiltrate (sometimes described as a "ground glass" appearance) that involves all lobes of the lung, and air-bronchograms (ie the infiltrate will outline the larger airways passages which remain air-filled). In severe cases, this becomes exaggerated until the cardiac borders become inapparent (a 'white-out' appearance).

Gross Pathology

The characteristic pathology seen in babies who die from RDS was the source of the name "hyaline membrane disease". These waxy-appearing layers line the collapsed tiny air sacs ("alveoli") of the lung. In addition, the lungs show bleeding, over-distention of airways and damage to the lining cells.

The organs generally showed no abnormalities other than those of immaturity expected at this gestational age. There was moderate diffuse subarachnoid hemorrhage and a small amount of blood in the pleural and pericardial cavities.

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Microscopic Pathology

References

Template:WH Template:WS