Persistent pulmonary hypertension among neonates with sepsis
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《美国医学杂志》
Department of Pediatrics, Cama and Albless Hospital,Grant Medical College, Mumbai, India
Persistent Pulmonary Hypertension of the Newborn (PPHN) is caused by a sustained elevation of pulmonary vascular resistance (PVR) at birth. A variety of events may interfere with this process of transition. Parenchymal lung disease, meconium aspiration, intrauterine/perinatal hypoxia, group B streptococcal pneumonia or sepsis, abnormal pulmonary development, severe hyaline membrane disease and cardiac diseases are known to be associated with PPHN. Sepsis is the commonest among these clinical problems. Thus in some cases of sepsis, rapid breathing may also be due to pulmonary hypertension and not due to pneumonia alone. Here is a report which records the experience of managing six newborns with sepsis and pulmonary hypertension.
The six newborns were between 34 weeks to 38 weeks gestational age and had birth weight between 1.75 kg to 2.8 kg, admitted to neonatal intensive care unit for respiratory distress since birth. Cord blood gases revealed pH between 6.8 and 7.21 and base deficit between - 8.1 and 25.8. Chest X-rays were normal in all the subjects. Complete blood counts (CBC) done on day one of life suggested sepsis in five babies.[1] I/T ratio was increased in one case (0.21); in the remaining cases the ratio ranged between 0.02 to 0.14. The blood cultures grew pseudomonas in 2, acinetobacter in 1, mixed growth of Klebsiella and coagulase negative staphylococci in 1, and coagulase negative staphylococci in 1 case. Portable echocardiographic findings included dilatation of left- sided chambers in 1, right-sided chambers in 1, all the chambers in 2 and hypocontractile heart in 1 case. Pulmonary hypertension was diagnosed from high initial pulmonary artery pressure (PAP), more than 2/3 of normal mean arterial pressure (MAP) for given birth weight in 3 cases (49,50,66)mm of Hg and from substantial increase in repeat echocardiogram in 3 cases (33 to 73, 28 to 50, 37 to 51)[2] mm of Hg. These babies received oxygen by hood, inotropes (adrenaline 0.1 mcg/kg/min + dobutamine 10 mcg/kg/min), amrinone (0.75 mg/kg bolus, followed by 10 mcg/kg/min infusion) and antibiotics in view of respiratory distress with evidence of perinatal asphyxia and sepsis. Disappearance of tachypnea and chest in drawings was taken as an indicator of decrease in PPHN, as follow-up of echocardiography was not feasible. Four babies survived.
Respiratory distress is a common neonatal problem. In presence of markers of infection like peripheral blood counts or positive blood culture, pneumonia is commonly diagnosed. Chest X-rays in neonatal pneumonia are often normal. However, in some cases of sepsis, respiratory distress may be due to PPHN. Severe infection can produce factors that cause constriction of lung vessels. Resultant hypoxia may cause further pulmonary vasoconstriction as well as decreased myocardial contractility. Early intervention may lead to favorable outcome. Specific interventions include administering oxygen; a natural pulmonary vasodilator and inotropes like dopamine, dobutamine, epinephrine, isoproterenol to decrease pulmonary blood pressure; maintain systemic blood pressure, reverse the right to left shunting and treat the underlying cause.[3] Magnesium sulphate infusion was found to be effective in PPHN in nine newborn infants with severe pulmonary hypertension, seven of which survived, suggesting a beneficial effect.[4] Magnesium sulphate infusion has been used in nonventilated babies with PPHN in lower dose of 50 mg/kg/hr without encountering respiratory depression.[5] Milrinone and amrinone are frequently used inodilators (inotrope/vasodilator) known to have favorable effect by lowering pulmonary pressure and enhancing inotropic effect.[6] Amrinone was used in the study.
Thus, it is important to keep in mind a possibility of PPHN in newborns with respiratory distress in the settings of sepsis and treat them appropriately.
References
1. Manroe BL et al. The neonatal blood count in health and diseases : reference values for neutrophilic cells. J Pediatr 1979; 95 : 89-93.
2. Versmold HT, Kitterman JA, Phibbs RH et al. Aortic blood pressure during the first 12 hours of life in infants with birth weight 610 to 4220 grams. Pediatrics 1981; 67(5) : 611.
3. Linda J Van Mater. In John P. Cloherty, Eric C Eichenwald, Ann R Stark, eds. Persistent Pulmonary Hypertension of the Newborn. Manual of Neonatal Care. Philadelphia; Lippincott Williams & Wilkins, 2004; 377-383.
4. Abu - Osba YK, Galal O, Mansara K, Rejjal A. Treatment of severe persis- tent pulmonary hypertension of the newborn with magnesium sulphate. Arch Dis Child 1992 ; 67 : 31 - 35.
5. SR Daga, B Verma, RG Lotlikar. Magnesium Sulphate for Persistent Pulmonary Hypertension in Newborns (Letter). Indian Pediatr 2000; 37 : 449-450.
6. Lindsay CA, Barton P, Lsawless S, Kitchen L, Zorka A, Garcia J et al. Pharmacokinetics and pharmacodynamics of milrinone lactate in pediatric patients with septic shock. J Pediatr 1998; 132; 329-334.(Verma Bela, Daga SR, Maha)
Persistent Pulmonary Hypertension of the Newborn (PPHN) is caused by a sustained elevation of pulmonary vascular resistance (PVR) at birth. A variety of events may interfere with this process of transition. Parenchymal lung disease, meconium aspiration, intrauterine/perinatal hypoxia, group B streptococcal pneumonia or sepsis, abnormal pulmonary development, severe hyaline membrane disease and cardiac diseases are known to be associated with PPHN. Sepsis is the commonest among these clinical problems. Thus in some cases of sepsis, rapid breathing may also be due to pulmonary hypertension and not due to pneumonia alone. Here is a report which records the experience of managing six newborns with sepsis and pulmonary hypertension.
The six newborns were between 34 weeks to 38 weeks gestational age and had birth weight between 1.75 kg to 2.8 kg, admitted to neonatal intensive care unit for respiratory distress since birth. Cord blood gases revealed pH between 6.8 and 7.21 and base deficit between - 8.1 and 25.8. Chest X-rays were normal in all the subjects. Complete blood counts (CBC) done on day one of life suggested sepsis in five babies.[1] I/T ratio was increased in one case (0.21); in the remaining cases the ratio ranged between 0.02 to 0.14. The blood cultures grew pseudomonas in 2, acinetobacter in 1, mixed growth of Klebsiella and coagulase negative staphylococci in 1, and coagulase negative staphylococci in 1 case. Portable echocardiographic findings included dilatation of left- sided chambers in 1, right-sided chambers in 1, all the chambers in 2 and hypocontractile heart in 1 case. Pulmonary hypertension was diagnosed from high initial pulmonary artery pressure (PAP), more than 2/3 of normal mean arterial pressure (MAP) for given birth weight in 3 cases (49,50,66)mm of Hg and from substantial increase in repeat echocardiogram in 3 cases (33 to 73, 28 to 50, 37 to 51)[2] mm of Hg. These babies received oxygen by hood, inotropes (adrenaline 0.1 mcg/kg/min + dobutamine 10 mcg/kg/min), amrinone (0.75 mg/kg bolus, followed by 10 mcg/kg/min infusion) and antibiotics in view of respiratory distress with evidence of perinatal asphyxia and sepsis. Disappearance of tachypnea and chest in drawings was taken as an indicator of decrease in PPHN, as follow-up of echocardiography was not feasible. Four babies survived.
Respiratory distress is a common neonatal problem. In presence of markers of infection like peripheral blood counts or positive blood culture, pneumonia is commonly diagnosed. Chest X-rays in neonatal pneumonia are often normal. However, in some cases of sepsis, respiratory distress may be due to PPHN. Severe infection can produce factors that cause constriction of lung vessels. Resultant hypoxia may cause further pulmonary vasoconstriction as well as decreased myocardial contractility. Early intervention may lead to favorable outcome. Specific interventions include administering oxygen; a natural pulmonary vasodilator and inotropes like dopamine, dobutamine, epinephrine, isoproterenol to decrease pulmonary blood pressure; maintain systemic blood pressure, reverse the right to left shunting and treat the underlying cause.[3] Magnesium sulphate infusion was found to be effective in PPHN in nine newborn infants with severe pulmonary hypertension, seven of which survived, suggesting a beneficial effect.[4] Magnesium sulphate infusion has been used in nonventilated babies with PPHN in lower dose of 50 mg/kg/hr without encountering respiratory depression.[5] Milrinone and amrinone are frequently used inodilators (inotrope/vasodilator) known to have favorable effect by lowering pulmonary pressure and enhancing inotropic effect.[6] Amrinone was used in the study.
Thus, it is important to keep in mind a possibility of PPHN in newborns with respiratory distress in the settings of sepsis and treat them appropriately.
References
1. Manroe BL et al. The neonatal blood count in health and diseases : reference values for neutrophilic cells. J Pediatr 1979; 95 : 89-93.
2. Versmold HT, Kitterman JA, Phibbs RH et al. Aortic blood pressure during the first 12 hours of life in infants with birth weight 610 to 4220 grams. Pediatrics 1981; 67(5) : 611.
3. Linda J Van Mater. In John P. Cloherty, Eric C Eichenwald, Ann R Stark, eds. Persistent Pulmonary Hypertension of the Newborn. Manual of Neonatal Care. Philadelphia; Lippincott Williams & Wilkins, 2004; 377-383.
4. Abu - Osba YK, Galal O, Mansara K, Rejjal A. Treatment of severe persis- tent pulmonary hypertension of the newborn with magnesium sulphate. Arch Dis Child 1992 ; 67 : 31 - 35.
5. SR Daga, B Verma, RG Lotlikar. Magnesium Sulphate for Persistent Pulmonary Hypertension in Newborns (Letter). Indian Pediatr 2000; 37 : 449-450.
6. Lindsay CA, Barton P, Lsawless S, Kitchen L, Zorka A, Garcia J et al. Pharmacokinetics and pharmacodynamics of milrinone lactate in pediatric patients with septic shock. J Pediatr 1998; 132; 329-334.(Verma Bela, Daga SR, Maha)