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Ards

Respiratory pathology

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0% found this document useful (0 votes)
11 views20 pages

Ards

Respiratory pathology

Uploaded by

sahilshroff012
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

ACUTE RESPIRATORY

DISTRESS SYNDROMES:
NEWBORN +ADULT
Definition:
 Respiratory failure occuring within 1 week of a known
clinical insult with bilateral opacities on chest imaging, not
fully explained by effusions, atelectasis, cardiac failure, or
fluid overload.

 It is graded based on the severity of the changes in arterial


blood oxygenation.
 It is a disease of prematurity in newborn
 Characterized by deficiency of pulmonary surfactant
(produced by Type II pneumocytes)
 Risk factors
◦ Premature birth
 <28 wks – 60% incidence
 >37 wks - <5% incidence
◦ Excessive sedation of the mother,
◦ Fetal head injury during delivery,
◦ Aspiration of blood or amniotic fluid,
◦ Intrauterine hypoxia
◦ Maternal diabetes
◦ Twin gestation
◦ Male baby > female baby
 Deficiency of Surfactant → alveoli tend to collapse →
more inspiratory effort required → baby rapidly tires from
breathing → generalized atelectasis sets in → Hypoxemia
and acidosis → Pulmonary vasoconstriction → This leads
to damage
◦ to endothelium → leakage of plasma protein
◦ to epithelium → necrosed epithelial cells
 Hyaline membrane formed
Deficiency of Surfactant

Alveoli Collapse

Atelectasis

Hypoxemia and Acidosis

Pulmonary Vasoconstriction
Damage to Damage to
Epithelium Endothelium

Necrosed epithelial cells Leakage of plasma protein

HYALINE MEMBRANE FORMED


GROSS
• Normal size but are heavy and airless
• Mottled purple color

MICROSCOPICALLY
• Alternative atelectatic and dilated alveoli.
• Characteristic eosinophilic hyaline membranes
– Necrotic epithelial cells admixed with extravasated plasma proteins
– Lining the respiratory bronchioles, alveolar ducts and alveoli
• Congestion and hemorrhage
• Inflammation is minimal
HMD
 Often normal at birth
 Severe respiratory distress develops within a few hours
 Tachypnea, Hypoxemia, Cyanosis, Acidosis
 Prevention
◦ Amniotic fluid L/S ratio >2 = fetal maturity
◦ Corticosteroid for lung maturity
◦ Delay birth till lung maturity
 Treatment
◦ Surfactant replacement and 100% O2
 Prognosis
◦ Overall – good after prompt treatment
Acute Respiratory Distress
Syndrome
(ARDS )
Synonym –
◦ Diffuse alveolar damage,
◦ Shock lung syndrome,
◦ Acute alveolar injury

Definition –
It is a clinical syndrome characterized by
–Diffuse damage of alveolar epithelium or capillaries or
both
–Clinically resulting in acute progressive respiratory
failure that is often unresponsive to O2 treatment
 Pulmonary infections
 Shock due to
◦ Sepsis by Gm negative bacteria
◦ Severe Trauma
◦ Burn
 Aspiration of gastric contents
 DIC
 Radiation injury
 Oxygen toxicity
 Inhalation of toxic gas
 Drugs – e.g., narcotics
 Injury → Macrophage activated:
◦ Release IL8, IL1 , TNF
◦ Neutrophils come from capillaries to alveoli
(chemotaxis)
◦ Damage and activation of capillary endothelium
◦ Activation of Neutrophils

 Activated Neutrophils (main role in tissue injury) release:


◦ Protease , Leukotriene, O2 radicals, PAF
◦ Damage to the alveolar epithelium and maintain the
inflammation
 Some role of inactivation of anti-inflammatory mediators
 In one word - pathogenesis is based on
imbalance between pro-inflammatory and anti-
inflammatory mediators
 As a result ,
◦ Increased capillary permeability
◦ Pulmonary edema
◦ Damage to Type I and II pneumocytes
◦ Loss of surfactant
◦ Alveoli unable to expand – “collapse”
 If patient survives
◦ Attempts at regeneration by proliferation of Type II
cells
◦ Fibrosis – intra-alveolar & inter-alveolar ( interstitial )
NORMAL ALVEOLUS ACUTE LUNG INJURY
GROSS
• Heavy, Airless, Firm, Noncompliant
• Dark red due to congestion
• At autopsy – lung sinks in water
MICRO
• Inter-Alveoli and Intra-Alveoli -
–Edema, Inflammation, Congestion, H’ge, Necrosis
• HYALINE MEMBRANE formation – characteristic
–Lining the distended alveolar duct
–fibrin-rich edema fluid + necrotic epithelial cells
• Later in the course – fibrosis
10X

40X
 Acute onset of dyspnea
 Hypoxemia
 Cyanosis
 Tachypnea
 Pulmonary edema (without left heart failure)
 Chest X-ray - bilateral pulmonary infiltrates
 Prognosis – grim – more than 50% - death
 Treatment by
◦ PEEP ( positive end expiratory pressure) and ventilation support
◦ Initiating cause – e.g. sepsis - should be treated

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