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doi:10.1111/jpc.12443
Letters to the Editor
17 October 2013 Dear Editor, RE: COMMUNICATION SKILLS TRAINING IN PAEDIATRICS We read with interest the article by Keir and Wilkinson and support their call for formal training in communication skills.1 Their article did not mention post-graduate university studies as a pathway for developing skills in communication. We would like to bring to their attention that from 2014 The University of Western Australia is offering a post-graduate masters degree in neonatology. Within this degree students can choose two practicum units. Each of these practicum units include a significant component of formal communication teaching. Dr Mary Sharp1,2,3 Dr Catherine Campbell1,2,3 Professor Karen Simmer1,2,3 1 Neonatal Clinical Care Unit King Edward Memorial Hospital for Women 2 UWA Centre for Neonatal Education and Research 3 School of Paediatrics and Child Health UWA Perth, Western Australia, Australia
Reference 1 Keir A, Wilkinson D. Communication skills training in paediatrics. J. Paediatr. Child Health 2013; 49: 624–8.
Conflict of interest: No conflict of interest.
23 October 2013
result, 10 mg/kg of ibuprofen (Pedea, Orphan Europe, Paris, France) was administered intravenously at 53 h of life. Three hours later, his oxygen necessity increased from FiO2 0.21 to 0.4, without any changes in the mean airway pressure. An X-ray was taken, and no atelectasis, lung condensations or air leaks were detected. Twenty-four hours later, the infant received the second ibuprofen dose (5 mg/kg), and after that, the FiO2 increased to 1 and respiratory and metabolic acidosis, oliguria and hypotension were observed, without any changes in the X-ray. By this time, a 2 mm PDA shunting mainly right to left and a type II-III ventricular septal contour were observed (the right ventricle presented flat or concave contour into the left ventricular cavity). These findings suggested high right ventricular pressure, so the ibuprofen treatment was interrupted. The infant received nitric oxide, sedation, muscle relaxants and cardiovascular support but ultimately died of refractory hypotension and hypoxemia at 5 days of life. A post-mortem arterial vessel study revealed no intimal-medial alterations. The lungs and heart showed no specific findings and no signs of infection. Pulmonary hypertension is a rare adverse reaction after ibuprofen administration. Although this effect was initially thought to be associated with prophylactic treatment or when ibuprofen was buffered with tromethamine,1 a few cases have been also observed after therapeutic use of l-Lysine ibuprofen.2,3 Placental insufficiency due to maternal hypertension could lead to vasoconstriction that predisposed to pulmonary vascular constriction.3 The serum magnesium was above the normal range. Thus, the vasoconstriction due to placental insufficiency could have been counteracted initially by the vasodilation induced by the hypermagnesemia. Finally, some reports have documented benefits of echocardiographically guided treatment of PDA.4 Thus, information about pulmonary pressures or PDA size before the second dose of ibuprofen may have helped the clinicians decide whether to continue the pharmacological treatment of PDA.
Dear Editor, LETHAL PULMONARY HYPERTENSION ASSOCIATED WITH IBUPROFEN TREATMENT IN A VERY LOW BIRTH WEIGHT INFANT An infant weighing 640 g was born at 25 1/7 weeks’ gestation. The mother received antenatal steroids before delivery and calcium channel antagonist, angiotensin II receptor antagonist and magnesium sulphate to treat severe preeclampsia. The infant was intubated at birth and was transferred to the Newborn Intensive Care Unit with a fraction of inspired oxygen (FiO2) 0.8 (Apgar scores were 4 and 7). He received surfactant that improved the oxygenation status immediately (FiO2 of 0.21). Asymptomatic hypermagnesemia was observed in the first hours of life (5.36 mg/dL) but progressively improved (4.33 mg/dL at 48 h of life). A 2.5 mm patent ductus arteriosus (PDA) shunting left to right with signs of left cardiac overload and failure to withdraw from the ventilator was observed at 48 h of life. As a Conflict of interest: None declared.
Dr María Carmen Bravo1 Dr Malaika Cordeiro1 Dr Lucía Deiros3 Dr Jesús Pérez-Rodríguez2 1 Neonatologist 2 Associate Professor in Pediatrics and Neonatologist Department of Neonatology 3 Paediatrics Cardiologist Department of Cardiology La Paz University Hospital Madrid, Spain
References 1 Gournay V, Savagner C, Thiriez G, Kuster A, Rozé JC. Pulmonary hypertension after ibuprofen prophylaxis in very preterm infants. Lancet 2002; 359: 1486–8.
Journal of Paediatrics and Child Health 50 (2014) 85–86 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
85
doi:10.1111/jpc.12443
Letters to the Editor
17 October 2013 Dear Editor, RE: COMMUNICATION SKILLS TRAINING IN PAEDIATRICS We read with interest the article by Keir and Wilkinson and support their call for formal training in communication skills.1 Their article did not mention post-graduate university studies as a pathway for developing skills in communication. We would like to bring to their attention that from 2014 The University of Western Australia is offering a post-graduate masters degree in neonatology. Within this degree students can choose two practicum units. Each of these practicum units include a significant component of formal communication teaching. Dr Mary Sharp1,2,3 Dr Catherine Campbell1,2,3 Professor Karen Simmer1,2,3 1 Neonatal Clinical Care Unit King Edward Memorial Hospital for Women 2 UWA Centre for Neonatal Education and Research 3 School of Paediatrics and Child Health UWA Perth, Western Australia, Australia
Reference 1 Keir A, Wilkinson D. Communication skills training in paediatrics. J. Paediatr. Child Health 2013; 49: 624–8.
Conflict of interest: No conflict of interest.
23 October 2013
result, 10 mg/kg of ibuprofen (Pedea, Orphan Europe, Paris, France) was administered intravenously at 53 h of life. Three hours later, his oxygen necessity increased from FiO2 0.21 to 0.4, without any changes in the mean airway pressure. An X-ray was taken, and no atelectasis, lung condensations or air leaks were detected. Twenty-four hours later, the infant received the second ibuprofen dose (5 mg/kg), and after that, the FiO2 increased to 1 and respiratory and metabolic acidosis, oliguria and hypotension were observed, without any changes in the X-ray. By this time, a 2 mm PDA shunting mainly right to left and a type II-III ventricular septal contour were observed (the right ventricle presented flat or concave contour into the left ventricular cavity). These findings suggested high right ventricular pressure, so the ibuprofen treatment was interrupted. The infant received nitric oxide, sedation, muscle relaxants and cardiovascular support but ultimately died of refractory hypotension and hypoxemia at 5 days of life. A post-mortem arterial vessel study revealed no intimal-medial alterations. The lungs and heart showed no specific findings and no signs of infection. Pulmonary hypertension is a rare adverse reaction after ibuprofen administration. Although this effect was initially thought to be associated with prophylactic treatment or when ibuprofen was buffered with tromethamine,1 a few cases have been also observed after therapeutic use of l-Lysine ibuprofen.2,3 Placental insufficiency due to maternal hypertension could lead to vasoconstriction that predisposed to pulmonary vascular constriction.3 The serum magnesium was above the normal range. Thus, the vasoconstriction due to placental insufficiency could have been counteracted initially by the vasodilation induced by the hypermagnesemia. Finally, some reports have documented benefits of echocardiographically guided treatment of PDA.4 Thus, information about pulmonary pressures or PDA size before the second dose of ibuprofen may have helped the clinicians decide whether to continue the pharmacological treatment of PDA.
Dear Editor, LETHAL PULMONARY HYPERTENSION ASSOCIATED WITH IBUPROFEN TREATMENT IN A VERY LOW BIRTH WEIGHT INFANT An infant weighing 640 g was born at 25 1/7 weeks’ gestation. The mother received antenatal steroids before delivery and calcium channel antagonist, angiotensin II receptor antagonist and magnesium sulphate to treat severe preeclampsia. The infant was intubated at birth and was transferred to the Newborn Intensive Care Unit with a fraction of inspired oxygen (FiO2) 0.8 (Apgar scores were 4 and 7). He received surfactant that improved the oxygenation status immediately (FiO2 of 0.21). Asymptomatic hypermagnesemia was observed in the first hours of life (5.36 mg/dL) but progressively improved (4.33 mg/dL at 48 h of life). A 2.5 mm patent ductus arteriosus (PDA) shunting left to right with signs of left cardiac overload and failure to withdraw from the ventilator was observed at 48 h of life. As a Conflict of interest: None declared.
Dr María Carmen Bravo1 Dr Malaika Cordeiro1 Dr Lucía Deiros3 Dr Jesús Pérez-Rodríguez2 1 Neonatologist 2 Associate Professor in Pediatrics and Neonatologist Department of Neonatology 3 Paediatrics Cardiologist Department of Cardiology La Paz University Hospital Madrid, Spain
References 1 Gournay V, Savagner C, Thiriez G, Kuster A, Rozé JC. Pulmonary hypertension after ibuprofen prophylaxis in very preterm infants. Lancet 2002; 359: 1486–8.
Journal of Paediatrics and Child Health 50 (2014) 85–86 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
85
