An Unusual Case of Pulmonary Hemorrhage in a Term Neonate without Any Specific Risk Factor

Introduction: Pulmonary hemorrhage (PH) is a complication of prematurity and respiratory distress syndrome (RDS), but it could rarely cause respiratory distress also in term neonates. The incidence of PH is 1 to 12 per 1,000 live births. The exact pathogenesis of PH remains unknown. Recent studies suggest the presence of damage in the endothelial barrier of pulmonary capillaries resulting in leakage of hemorrhagic fluid into the alveoli. PH is associated with a high mortality rate and with significant neonatal and long-term morbidities and, until now, no consensus on treatment exists.

Materials and Methods: We report the case of a term, large for gestational age, female neonate, born by vaginal delivery at 40 weeks’ gestation. Her Apgar score was 7, 7, and 8 at 1, 5, and 10 minutes, respectively. Birth weight was 4,000 g. The newborn was admitted to the neonatal intensive care unit (NICU), Ospedale degli Infermi, ASL Biella, Italy. The capillary blood gas immediately after admission showed a pH level of 7.04, pCO₂ 65 mm Hg, pO₂ 38 mm Hg, a base excess of −14 mmol/L, and lactate of 10 mmol/L. The newborn developed a respiratory distress with rapid worsening of the respiratory function and an increase in oxygen requirement. The chest X-ray showed diffuse micronodular and upper right opacities. Blood cultures were collected and antibiotic therapy with piperacillin–tazobactam and gentamicin was started. At 2 hours of life, she developed hypotension and dopamine was administered at 5 µg/kg/min up to 10 µg/kg/min.

Soon after, large amounts of blood were retrieved in the upper airways and a difficult emergency intubation was performed following sedation with fentanyl. Abundant blood secretions were aspirated from the endotracheal tube and severe bradycardia occurred, requiring chest compressions, adrenaline plus crystalloid bolus infusion. Blood continued to be retrieved in the endotracheal tube and the newborn’s cardiovascular status remained unstable.

The infant was thus transferred to a third level NICU where she was sedated with fentanyl and midazolam and ventilated with high-frequency oscillatory ventilation (HFOV) (fraction of inspired oxygen 1, mean airway pressure 19, Hz 9, and ΔP 28) switched to synchronized intermittent positive pressure ventilation + GV with improvement of the respiratory distress. On day 8, she was extubated. Inotropic support was continued with dopamine and dobutamine that were withdrawn on days 5 and 6 from admission, respectively. An echocardiogram showed a good left ventricular function and no pulmonary hypertension. Laboratory exams revealed a total white cell count of 8.69 × 10³/μL, Hb 14.3 g/dL, Hct 42.7%, and platelet count 257 × 10³/μL. Liver enzymes were normal. Since coagulation profile was altered (prothrombin time international normalized ratio 2.31, partial thromboplastin time 69.2 seconds, and fibrinogen 125 mg/dL), plasma was administered on day 1. Her cardiovascular status remained stable. C-reactive protein, procalcitonin, and blood cultures were negative. On day 11, she was back-transported in the unit where she was born. Her head and renal ultrasound scans were negative. She was discharged home after 20 days of hospital stay.

Conclusion: The precise etiology of PH remains unclear.[1] This feature can occur without any known baseline risk factors such as prematurity, RDS, treatment with surfactant, patent ductus arteriosus, intrauterine growth retardation, birth asphyxia, meconium aspiration, pneumothorax, or pulmonary interstitial emphysema. Some 60% of survivors develop bronchopulmonary dysplasia, and 75% neurosensory deficit or death. Increased incidence of cerebral palsy, cognitive delay, and periventricular leukomalacia are also reported.[2]

Current management of PH in preterm infants includes strategies to maintain adequate gas exchanges and to prevent hemorrhagic shock such as ventilatory support (conventional or HFOV), transfusion of blood products to support the blood volume and to restore possible coagulation disorders, and treatment of patent ductus arteriosus if present.

The use of surfactant to contrast the increase in surface tension could be a promising treatment option but a recent Cochrane review does not provide any specific guidance for clinical practice due to overall lack of high-quality evidence.[3]

Additional strategies include recombinant activated factor VII or hemocoagulase through endotracheal tube as rescue therapy in case of failure of ventilation. Further researches on the pathogenesis of PH are needed to identify interventions that can improve outcomes related to this feature.

Keywords: pulmonary hemorrhage; term neonate; respiratory distress; emergency intubation

Conflict of Interest: None declared.

• References

• 1 Zahr RA, Ashfaq A, Marron-Corwin M. Neonatal pulmonary hemorrhage. Neoreviews 2012; 13 (05) e302-e306
• 2 Berger TM, Allred EN, Van Marter LJ. Antecedents of clinically significant pulmonary hemorrhage among newborn infants. J Perinatol 2000; 20 (05) 295-300
• 3 Aziz A, Ohlsson A. Surfactant for pulmonary haemorrhage in neonates. Cochrane Database Syst Rev 2012; (07) CD005254