FLASHPATHH a z e m A l i

BRONCHOPULMONARY

DYSPLASIAH a z e m A l i

CLINICAL• Chronic lung damage that develops in preterm neonates

suffered from respiratory distress syndrome and treated with high concentration of ventilator-administered oxygen for prolonged time

– Other complication of highly concentrated oxygen administration is retrolental fibroplasia (retinopathy of prematurity)

• Pathogenesis remains complex and poorly understood– Free radicals (from high O2)– Barotrauma– Inflammatory cytokines (TNF, interleukin-1β, IL-6, IL-8)

CLINICAL

• It had many complications:– Unimproved respiratory distress– Marked lung fibrosis– Recurrent infections– Pulmonary hypertension and core pulmonale– Respiratory failure and Death

GROSS• Early stages:

– Firm, heavy lungs– Dark red (congested)

• Late stages:– Firm, tan lungs– Pleural nodularity “cobblestoning”

• Alternation between collapsed and hyperinflated“compensatory emphysema” areas

MICROSCOPYEarly stages:• Features of Hyaline membrane disease:

– Congestion, edema, hemorrhage– Hyaline membrane formation– Necrosis of bronchiolar mucosa– Atelectasis

• Features of Early “reparative” lung changes:– Early metaplastic & reparative changes of airway– Early alveolar septal & interstitial fibroplasia

MICROSCOPYLate stagesFeatures of ”fibroproliferative” lung disease:• General architecture:

– Irregular aeration with alternating hyperinflation and atelectasis• Bronchi:

– Squamous metaplasia– Submucosal muscular hyperplasia– Obliterative bronchiolitis

• Alveoli & interstitial tissues:– Alveoli re-epithelization with type 2 cell hyperplasia– Thickened alveolar walls and interstitial fibrosis

• Blood vessels:– Decrease alveolar capillaries count– Hyperplasia of pulmonary arterial smooth muscle

DIFFERENTIAL DIAGNOSIS

• Early BPD is similar to DAD

• Late BPD has features of emphysema, interstitial fibrosis, constrictive bronchiolitis

• “ New “ BPD ??

CHRONIC LUNG DISEASE OF

PREMATURITY“NEW” BPD

H A Z E M A L I

CLINICAL• Fortunately, Improved management of premature infants

reduced incidence of BPD by using:– Modern gentler ventilation techniques– Antenatal glucocorticoid therapy– Surfactant replacement therapy

• So BPD is transformed from a severe fibrosing condition into a milderone, where continued respiratory support is still required (but at a much diminished level)

– Now it is called “chronic lung disease of prematurity” or “new BPD”

CLINICALFeatures of “New BPD”• Chronic lung disease

• Affects extremely premature infants– Almost always infants < 30 weeks of gestation– Almost always infants < 1200 g of birth weight

• Creates a need for continued ventilatory support for a certain time

– O2 supplement for longer than 28 days– O2 supplement a 36 weeks post-menstrual age

• The initial acute lung disease is not even required for diagnosis

CLINICAL• The period between 22 and 32 weeks’ gestation

encompasses the change from the canalicular to the saccular phase of lung development

• The pathogenesis in “New BPD” may be due to interference with normal lung development (arrested in saccular phase)

– Decreased alveolar septation– Dysmorphic alveolar capillary (secondary to arrested septation)

MICROSCOPY• Decreased alveolarization (alveolar septation)

– Fewer but larger and simple airspaces– Lined by undifferentiated cuboidal cells– Have cellular fibroelastic septa of even thickness

• Dysmorphic capillary configuration– Decreased alveolar capillaries– Abnormal “distant” distribution of capillaries from air surface

• Absence / Less prominence of the following– Alternating areas of collapse and overinflation – Airway epithelial lesions and smooth muscle hyperplasia– Interstitial fibrosis– Vascular hypertensive changes

WWW.

DO NOT FORGET TO SEARCH FOR MORE PICS AND VIRTUAL SLIDES

THANK YOUH a z e m A l i