PULMONARY HEMORRHAGE

CLINICAL DEFINITION: pulmonary hemorrhage is typically defined as the presence of

hemorrhagic fluid in the trachea accompanied by respiratory decompensation that
requires increased respiratory support or intubation within 60 minutes of the
appearance of fluid.

Pulmonary hemorrhage is defined on pathologic examination as the presence of

erythrocytes in the alveoli and/or lung interstitium (In infants who survive longer than
24 hours, interstitial hemorrhage predominates)
Bleeding is predominantly alveolar in approximately 65% of cases and interstitial in the
rest.
Confluent hemorrhage involving at least two lobes of the lung is termed massive
pulmonary hemorrhage.

INCIDENCE

 Reported incidence of PH is 1 to 12/1,000 live births.

 However, this may be much higher at 50/1,000 live births in the risk group of preterm
or fetal growth restriction (FGR) infants.
 Some degree of pulmonary hemorrhage occurs in about 10% of extremely preterm
infants
 Pulmonary hemorrhage complicates the course of 3% to 5% of preterm infants
ventilated for respiratory distress syndrome (RDS).
 Approximately 80% of pulmonary hemorrhages in preterm infants occur within
72 hours of birth

PATHOPHYSIOLOGY

Precise mechanisms underlying pulmonary hemorrhage remain uncertain

A. Based on studies of lung effluent demonstrating relatively low erythrocyte (20%)

concentration (hematocrit) compared to whole blood, pulmonary hemorrhage is
thought to result from hemorrhagic pulmonary edema rather than direct bleeding into
the lung.
 B. Acute left ventricular failure, caused by hypoxia and other conditions, may lead to
increased pulmonary capillary pressure and injury to the capillary endothelium. This
may result in increased transudation and leak into the interstitium and, ultimately,
pulmonary airspace.

C. An alternative hypothesis suggests that a fall in pulmonary vascular resistance

after birth causes increased left-to-right shunt through patent ductus arteriosus
(PDA); this in turn leads to increased pulmonary blood flow and capillary leak.

D. Other factors that alter the integrity of the epithelial–endothelial barrier in the
alveolus or that change the filtration pressure across these membranes may also
predispose infants to pulmonary hemorrhage.

E. Disorders of coagulation may worsen pulmonary hemorrhage but are not thought
to initiate the condition.

PREDISPOSING FACTORS

 Prematurity, RDS, IUGR, intrauterine and intrapartum asphyxia, male gender, multiple
gestation, infection, congenital heart disease, oxygen toxicity, maternal blood aspiration, severe
hypothermia, diffuse pulmonary emboli, polycythemia, maternal cocaine exposure, and urea
cycle defects accompanied by hyperammonemia
 Antenatal steroids may be protective,
 While thrombocytopenia and requirement of positive-pressure ventilation in the delivery room
may be predisposing to PH

PDA Increased pulmonary blood flow and compromised ventricular function

accompany decreasing pulmonary vascular resistance, leading to pulmonary
microvascular injury and hemorrhagic pulmonary edema
Exogenous  Pulmonary hemorrhage may complicate surfactant therapy,
surfactant likely related to changes in lung compliance, increased left-to-right shunting
across a PDA, and increased pulmonary blood flow.
 However, the overall benefits of surfactant treatment outweigh the risks
Sepsis As a result of increased pulmonary capillary permeability, and potentially
exacerbated by the associated thrombocytopenia and coagulopathy
CLINICAL PRESENTATION
 The typical presentation of the infant with PH is a premature infant who suddenly presents with
frothy pink tinged secretions from an ET.
 Over the next minutes to hours, the infant often requires increased ventilator support and has
increased work of breathing.
 As increasing amounts of blood are suctioned from the ET, PCO2 starts to rise, as does the need for
oxygen.
 If the PH continues, the infant will develop apnea, generalized pallor, become cyanotic, with
concomitant bradycardia and a drop in blood pressure.
 Only a small percentage of pulmonary hemorrhages observed at autopsy are evident clinically. This
is most likely due to the difficulty in diagnosing hemorrhage confined to the interstitial space without
spread to the airways.
 In the absence of hemorrhagic secretions, respiratory deterioration is usually attributed to other
causes.

EVALUATION

HISTORY AND PHYSICAL EXAMINATION: A thorough history may help identify predisposing factors such
as risks for infection or the presence of a PDA. On physical examination, infants with pulmonary
hemorrhage have pink or red frothy fluid in the airway and signs of respiratory decompensation. In
the absence of respiratory deterioration, isolated bleeding may result from erosion or ulceration in the
upper airway and not represent pulmonary hemorrhage.

RADIOGRAPHIC EVALUATION: The clinical diagnosis of pulmonary hemorrhage may be facilitated by

the radiographic changes that accompany it. Nonspecific changes on chest radiograph include diffuse
fluffy infiltrates or opacification of one or both lungs with air bronchograms.

LABORATORY STUDIES: The laboratory evaluation reflects the cardiopulmonary compromise with
associated metabolic or mixed acidosis, a drop in hematocrit, and sometimes evidence of coagulopathy.
TREATMENT
The general approach involves clearing the airways of hemorrhagic fluid and restoring adequate
ventilation
A. Provide positive end-expiratory pressure (PEEP): The use of elevated PEEP of 6 to 8 cm H2O
helps to decrease the efflux of interstitial fluid into the alveolar space. (PEEP may provide
tamponade of the pulmonary capillaries)
B. Restore hemodynamic stability: Correct hemodynamic instability with volume resuscitation,
including packed red blood cell replacement, and consider the addition of vasoactive
medications as needed. ( ? PROPHYLACTIC DOPAMINE)
C. Correct acidosis: Restore both adequate ventilation and blood pressure to improve acidosis.
D. Consider echocardiogram: An echocardiographic evaluation may assist in the evaluation of
ventricular function, need for vasoactive medications, and the possible contribution of a PDA.
Consider pharmacologic or surgical closure of the PDA if hemodynamically significant. ( ??
PROPHYLACTIC INDOMETHACIN) _
E. Identify other predisposing factors: Additional potential contributing factors such as sepsis
and coagulopathy must be addressed.
F. Strategy for ventilation: Using high-frequency ventilation to provide, increase Inspiratory
time, high MAP while limiting tidal volume excursions is more effective than conventional
ventilation to minimize further interstitial and alveolar fluid accumulation.
G. Limit aggressive airway suctioning.
(The trachea should first be suctioned to ensure that blood clots have not obstructed the ET. A
number 6.5F catheter should be used for a 2.5-mm ET and an 8.0F catheter if the ET is 3.0 or
3.5 mm)

ROLE OF SURFACTANT THERAPY

 Surfactant therapy after pulmonary hemorrhage has been considered for continued
treatment of primary surfactant deficiency in RDS or for treatment of secondary
surfactant deficiency resulting from hemorrhagic airway edema.
 Following pulmonary hemorrhage, hemoglobin, plasma proteins, and cell membrane
lipids present in the airspace may inactivate the surfactant. Exogenous surfactant
replacement may reverse the inhibition, as demonstrated in the setting of meconium
aspiration.
 Case reports and case series suggest that a surfactant may reduce mortality and
morbidity from pulmonary hemorrhage. However, a 2020 Cochrane Review failed to
identify any randomized controlled trials that address the use of a surfactant to treat
pulmonary hemorrhage.
 Given the positive results from nonrandomized studies, it suggests further research.
Treatment should be decided on a case-by-case basis.

EPINEPHRINE: Endotracheal or nebulized epinephrine at a dose of 0.1 mL/kg of 1: 10,000

dilutions may be useful due to its vasoconstrictive action.

ACTIVATED RECOMBINANT FACTOR VII (RFVIIA): It works by activating the extrinsic pathway
and promoting hemostasis. Used in hemophilia patients, there are anecdotal reports of use in
newborns with refractory pulmonary hemorrhage. Risk of thromboembolism is high and use in
newborns has a higher risk, but that is likely to benefit.

HEMOCOAGULASE: It is derived from the venom of Bothrops atrox. It promotes conversion of

prothrombin to thrombin and fibrinogen to fibrin. In a prospective study of 48 preterm
newborns with pulmonary hemorrhage on ventilator, babies who received endotracheal
hemocoagulase (28 babies) had significant reduction in PH and lower mortality. The study has
many limitations, and routine use cannot be recommended

PROGNOSIS

 The prognosis is difficult to establish in part due to the difficulty in establishing a clinical
diagnosis for this condition
 The risks of death or survival with neurosensory impairment at 18 months of age were
increased in infants with serious pulmonary hemorrhage.
 Overall mortality rate has been reported up to 50%.
 PH survivors have a higher incidence of bronchopulmonary dysplasia, seizures, cerebral
palsy, and periventricular leukomalacia on follow-up.

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