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3 Cards in this Set
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Non cardiogenic pulmonary edema
Abrupt onset of hypoxemia and diffuse pul infiltrate Absence of cardiac failure
ARDS is severe ALI
Both with inflammation associated increase in pul vascular permeability , epithelial and endothelial cells death
ARDS - acute diffuse inflammatory lung injury leading to increased pul vascular permeability, increased lung lung weight, loss of aerated lung tissue with hypoxemia and bilateral radiogenic opacities associated with increased venous admixture, increased physiological dead space and decreased lung compliance
Clinical presentation
Acute dyspnea Hypoxemia Bilateral pulmonary infiltrate on radiograph No clinical evidence of primary left heart failure
Conditions associated with devt of ARDS
Infections -. Sepsis, gastric aspiration, diffuse pulmonary infections eg miliary TB
Physical injury - head injury, burns, fracture with fat embolism, near drowning Inhaled irritants - oxygen toxicity, smoke, irritants gas
Chemical injury - heroine, methadone, acetylsalicylic acid, barbiturates
Others - DIC, multiple transfusion, uraemia, pancreatitis, hypersensitivity reaction
Exudative phase
Inflammation damage Endo and epithelial cells - increase permeability
Inhaled irritants - oxygen toxicity, smoke, irritants gas
Chemical injury - heroine, methadone, acetylsalicylic acid, barbiturates
Others - DIC, multiple transfusion, uraemia, pancreatitis, hypersensitivity reaction
Pathogenesis
Alveolar capillary membrane has two separate barriers - microvascular endothelium and alveolar epithelium
Integrity of this barriers compromised by endothelial or epithelium injury o both
Injury due to imbalance btwn proinflammatory and anti Inflammatory mediators
Exudative phase
Inflammation damage Endo and epithelial cells - increase permeability
Exudate fill the alveoli
Alveolar epithelial cells injured, basement membrane denuded, surfactant production and fluid resorption inhibited
Hyaline membrane form( cellular debris, fibrin)
Endothelial damage triggers coagulation pathway, micro emboli form
DetailedInjury caus release of proinflammatory cytokines
Activated neutrophils secret TNF Alpha, interleukins to increase inflammatory reaction
Neutrophils produce reactive oxygen free radicals and protease that injure capillary endotheliumIncreased permeability, Influx of protein rich fluid in alveolar space
Exudate fill the alveoli
Alveolar epithelial cells injured, basement membrane denuded, surfactant production and fluid resorption inhibited
Hyaline membrane form( cellular debris, fibrin)
Endothelial damage triggers coagulation pathway, micro emboli form
Injury caus release of proinflammatory cytokines
Activated neutrophils secret TNF Alpha, interleukins to increase inflammatory reaction
Detailed
Injury caus release of proinflammatory cytokines
Activated neutrophils secret TNF Alpha, interleukins to increase inflammatory reaction
Neutrophils produce reactive oxygen free radicals and protease that injure capillary endothelium
Increased permeability,
Influx of protein rich fluid in alveolar space Neutrophils produce reactive oxygen free radicals and protease that injure capillary endothelium
Increased permeability, Influx of protein rich fluid in alveolar space
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Morphology
Acute - heavy,firm red boggy lungs
Exhibit congestion, interstitial and intraalveolar edema, Inflammation, fibrin deposit, diffuse alveolar damage
Alveolar walls lined with waxy hyaline membrane Hyaline membrane ( fibrin, rich edema fluid mixed with cytoplasmic and lipid remnants of necrotic epithelial cells)
Organizing stage- type 2 pneumocytes proliferation, granulation tissue in alveolar walls and space
Granulation tissue resolves in most cases
Fibrotic thickening of alveolar septa , by proliferation of of interstitial cells and collagen deposit
Gross
Acute Heavy, firm, dark red
Proliferation phase Firm pale gray( fibroblast)
Fibrotic Firm, gray white, cystic changes ie honey comb
Histopathological change
Diffuse alveolar damage ( marked desquamation of type I epithelial cells
Pathological stages
Exudative -. Diffuse alveolar damage in first week
Proliferative -. Resolution of pulmonary edema, poliferation of type 2 pneumocytes, squamous metaplasia, interstitial infiltration of myofibroblasts, early collagen deposit
Fibrotic- obliteration of normal lung architecture, diffuse fibrosis, cystic formation
Resolution
Removal of exudate, dear cells and replacement By macrophages Replacement by type 2 pneumocytes |
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Clinical features Tachypnea, tachycardia in 12-24hrs Ventilation perfusion mismatch due to alveolar flooding Reduced lung compliance Respiratory failure in 48 hrs of onset Treatment Patient die from multiple organs failure Minimize condition like nosocomial infections, Gi bleeding, thromboembolism Stress ulcers prophylaxis Nutrition |
Hyaline membrane disease Disease of premature infants 60% of infants less than 28 week, 15-20% on 32-36 week, less than 5% for 37 week Manifest within 48 hrs of birth Deficiency of surfactant in alveoli Leads to acute respiratory distress with fatal termination Etiology - def of surfactant in the alveoli Surfactant Seen in fetal lung 16 week, proper at 24 week, abundant at 35 week By type 2 pneumocytes Lower surface tension decreasing pressure required to keep alveoli open Alveolar collapse in lack of surfactant, greater inspiration effort needed Risk factor Premature Multiple births Maternal diabetes CS without labour Prenatal asphyxia White race, male Hypothermia |
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Pathophysiology Prematurity ( immature lung with underdeveloped and un inflated alveoli) Decreased surfactant Increased alveolar surface tension Atelectasis - CO2 retention; hypoxemia Acidosis Pul vasoconstriction and hypo profusion Capillary damage Plasma leak Fibrinogen Hyaline membrane Morphology Gross Solid, red airless lungs resemble liver Beefy lungs Heavy and will sink in cup of water Chest x-ray No any black air spaces - only whitish areas Ground glass picture Clinical features Appear in minutes after birth Tachypnea greater than 60 Nasal flaring Subcostal and intercostal retraction, cyanosis, expiratory grunting Apnea Irregular respiration Diminished breath sounds, fine rales |
Diagnosis Antenatal Examination of amniotic fluid ie lecithin sphingomyelin ratio If greater than 2 full maturation 1.5-1.99 borderline maturation Less - severe ARDS Lab tests Paco2 elevated Partial pressure of oxygen low Blood pH low due to metabolic acidosis Calcium low Serum glucose low Management Antenatal corticosteroids therapy Beta methasone Induce surfactant production Surfactant replacement therapy |
