term1 Definition1term2 Definition2term3 Definition3
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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
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
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
Injury caus release of proinflammatory cytokines
Detailed
Neutrophils produce reactive oxygen free radicals and protease that injure capillary endothelium
Increased permeability,
Influx of protein rich fluid in alveolar space
Increased permeability, Influx of protein rich fluid in alveolar space
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
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
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
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
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
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