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Diagnosis and treatment of children with severe influenza A from the 2009/2010 pandemic in Tianjin, China Jing Ning Trop Doct 2014 44: 69 originally published online 10 January 2014 DOI: 10.1177/0049475513517230 The online version of this article can be found at: http://tdo.sagepub.com/content/44/2/69
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Original Article
Diagnosis and treatment of children with severe influenza A from the 2009/2010 pandemic in Tianjin, China
Tropical Doctor 2014, Vol. 44(2) 69–70 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0049475513517230 tdo.sagepub.com
Jing Ning
Abstract The clinical characteristics and treatments of severe influenza A (H1N1) in infected children were discussed and analysed. We found that such severe cases predominantly manifested respiratory symptoms; symptoms affecting the nervous system are also rare but dangerous. The clinical data of eight children with severe influenza A (H1N1) were analysed retrospectively. These children generally manifested fever and flu-like symptoms, short-term aggravation with dyspnoea. One case exhibited neurological symptoms. After continuous positive airway pressure and immunological regulation were administered, the clinical symptoms gradually improved. Patients with severe influenza A (H1N1) manifested respiratory tract symptoms. Those exhibiting neurological symptoms were seriously affected. Physical signs were regularly monitored and laboratory examination was conducted in order to determine the causes of severe illness. The treatments were adjusted accordingly.
Keywords Children, influenza A (H1N1), severe illness
Introduction Influenza places a significant burden on young people and hospital resources in developing countries.1,2 Influenza A (H1N1) is an acute infectious disease caused by a post variation of a novel type A H1N1 influenza virus. The general population is susceptible to influenza A (H1N1), which exhibits clinical manifestations similar to those of seasonal influenza. The severity of the disease varies but many cases are characterized by fever, mild infection in the upper respiratory tract and even death.
Materials and methods General data A total of eight patients (five boys, three girls) aged between 9 months and 8 years (mean ¼ 2.2 years) were included in the study. All of the patients were Han nationals and resided in the suburbs or rural areas. None had a past history or family history of influenza A. The symptoms of each patient included fever and upper respiratory tract infection. All of the patients manifested fever, listlessness, shortness of
breath, myalgia, tachycardia, lowered oxygen saturation, low blood pressure and cyanosis. Symptoms such as spasm and coma, which affect the central nervous system, were observed in two patients. This study was conducted in accordance with the Declaration of Helsinki. This study was conducted with approval from the Ethics Committee of Tianjin Children’s Hospital. Written informed consent was obtained from all participants.
Laboratory tests The eight patients’ X-ray results revealed pneumonia and diffuse ground-glass opacities in both lungs as revealed in the chest computed tomography (CT) scan. The peripheral blood routine revealed that the median of white blood cells was 4500 (the highest value was 16,900), the median of neutrophil percentage
Associate Chief Physician, Tianjin Children’s Hospital, Tianjin, China Corresponding author: Jing Ning, Tianjin Children’s Hospital, No. 225 Machang Road, Tianjin 300074, China. Email: [email protected]
Downloaded from tdo.sagepub.com at COLUMBIA UNIV on November 7, 2014
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Tropical Doctor 44(2)
was 45%, with a peak value of 60% and the red blood cells and platelet (PLT) were in the normal range. Quick read C-reactive protein (CRP) ranges from 8–24 mg/dL (median: 14.5 mg/dL) and blood glucose ranges from 83–270 mg/dL (median: 105 mg/dL). The hepatic/renal function was generally normal. Increased levels of lactate dehydrogenase (LDH) and choline kinase (CK) were observed in four patients, who were generally normal based on the results of myocardial isodynamic enzymes. Electrocardiogram (ECG) results showed that all the patients suffered from tachycardia.
Therapy All of the patients were treated with oseltamivir (3 mg/ kg/day) by mouth, intravenous antibiotics, methylprednisolone (20 mg/kg/day) and human immunoglobulin (2 g/kg/day) for 1–2 days. Oxygen inhalation was administered to patients with minor disorders and artificial mechanical ventilation was provided for those with severe cases. Other supportive treatments were applied at the doctors’ discretion. The therapies were then adjusted according to iconographic variations and changes in vital signs.
Results All of the eight patients were diagnosed with influenza A (H1N1) as revealed by a pathogenic test (reverse transcription-polymerase chain reaction (RT-PCR) of H1N1 on samples obtained from oropharyngeal swabs). After one week, their general conditions were ameliorated. Pulmonary infiltration was also alleviated and transdermal oxygen saturation was recovered (98– 100%). All eight of the patients survived.
Discussion The main pathophysiological features of influenza A (H1N1) include ulcer or exfoliation of the bronchial mucosa, alveolus capillary hyperaemia, alveolar haemorrhage, damaged endothelial barrier, alveolus gap filled with fibrin and exudates, and hyaline membrane formation and fibrosis that may occur simultaneously.3 Basic pathophysiological variation in the lungs lowers pulmonary compliance, decreases the effective aeration area and disrupts diffusive function.4–7 Glucocorticoid is used to treat acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). In theory, systematic stress response and cytokine storm may occur during acute virus infection. As the final effector in the hypothalamus-pituitaryadrenal axis, glucocorticoid is one of the most
important anti-inflammatory agents.8 Clinical reviews also support the positive function of glucocorticoid in ARDS treatment.9 Considering these data, we administered liquid in limited amounts, which is consistent with the recommended dosage for ARDS therapy. Previous reports have proved the capability of exogenous pulmonary surfactant to ameliorate oxygenation.10
Conclusion Based on pulmonary pathological variation and our previous experiences in clinical therapy, we found that the progression of infection from the lower respiratory tract to ALI or ARDS can occur gradually. Lesions in the lungs caused by a new type of influenza A (H1N1) can be treated by controlling the inflammatory response and maintaining effective oxygenation. References 1. Ampofo K, Gesteland PH, Bender J, et al. Epidemiology, complications, and cost of hospitalization in children with laboratory-confirmed influenza infection. Pediatrics 2006; 118: 2409–2417. 2. Poehling KA, Edwards KM, Weinberg GA, et al. The under recognized burden of influenza in young children. N Engl J Med 2006; 355: 31–40. 3. Rello J, Rodrı´ guez A, Iban˜ez P, et al. Intensive care adult patients with severe respiratory failure caused by influenza A (H1N1) in Spain. Crit Care 2009; 13: R148. 4. Pistolesi M, Miniati M, Milne EN and Giuntini C. The chest roentgenogram in pulmonary edema. Clin Chest Med 1985; 6: 315–344. 5. Gattinoni L and Caironi P. Refining ventilatory treatment for acute lung injury and acute respiratory distress syndrome. JAMA 2008; 299: 691–693. 6. Halter JM, Steinberg JM, Gatto LA, et al. Effect of positive end-expiratory pressure and tidal volume on lung injury induced by alveolar instability. Crit Care 2007; 11: R20. 7. Toth I, Leiner T, Mikor A, Szakmany T, Bogar L and Molnar Z. Hemodynamic and respiratory changes during lung recruitment and descending optimal positive endexpiratory pressure titration in patients with acute respiratory distress syndrome. Crit Care Med 2007; 35: 787–793. 8. Rhen T and Cidlowski JA. Anti-inflammatory action of glucocorticoids-new mechanisms for old drugs. N Engl J Med 2005; 353: 1711–1723. 9. Meduri GU, Marik PE, Chrousos GP, et al. Steroid treatment in ARDS: a critical appraisal of the ARDS network trial and the recent literature. Intensive Care Med 2008; 34: 61–69. 10. Nosal S, Durdik P, Luptakova A, et al. Therapeutic approach to a child with acute respiratory distress syndrome: a report of two cases. J Physiol Pharmacol 2008; 59: 43–51.
Downloaded from tdo.sagepub.com at COLUMBIA UNIV on November 7, 2014
Diagnosis and treatment of children with severe influenza A from the 2009/2010 pandemic in Tianjin, China Jing Ning Trop Doct 2014 44: 69 originally published online 10 January 2014 DOI: 10.1177/0049475513517230 The online version of this article can be found at: http://tdo.sagepub.com/content/44/2/69
Published by: http://www.sagepublications.com
On behalf of: THET
Additional services and information for Tropical Doctor can be found at: Email Alerts: http://tdo.sagepub.com/cgi/alerts Subscriptions: http://tdo.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav
>> Version of Record - Mar 19, 2014 OnlineFirst Version of Record - Jan 10, 2014 What is This?
Downloaded from tdo.sagepub.com at COLUMBIA UNIV on November 7, 2014
Original Article
Diagnosis and treatment of children with severe influenza A from the 2009/2010 pandemic in Tianjin, China
Tropical Doctor 2014, Vol. 44(2) 69–70 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0049475513517230 tdo.sagepub.com
Jing Ning
Abstract The clinical characteristics and treatments of severe influenza A (H1N1) in infected children were discussed and analysed. We found that such severe cases predominantly manifested respiratory symptoms; symptoms affecting the nervous system are also rare but dangerous. The clinical data of eight children with severe influenza A (H1N1) were analysed retrospectively. These children generally manifested fever and flu-like symptoms, short-term aggravation with dyspnoea. One case exhibited neurological symptoms. After continuous positive airway pressure and immunological regulation were administered, the clinical symptoms gradually improved. Patients with severe influenza A (H1N1) manifested respiratory tract symptoms. Those exhibiting neurological symptoms were seriously affected. Physical signs were regularly monitored and laboratory examination was conducted in order to determine the causes of severe illness. The treatments were adjusted accordingly.
Keywords Children, influenza A (H1N1), severe illness
Introduction Influenza places a significant burden on young people and hospital resources in developing countries.1,2 Influenza A (H1N1) is an acute infectious disease caused by a post variation of a novel type A H1N1 influenza virus. The general population is susceptible to influenza A (H1N1), which exhibits clinical manifestations similar to those of seasonal influenza. The severity of the disease varies but many cases are characterized by fever, mild infection in the upper respiratory tract and even death.
Materials and methods General data A total of eight patients (five boys, three girls) aged between 9 months and 8 years (mean ¼ 2.2 years) were included in the study. All of the patients were Han nationals and resided in the suburbs or rural areas. None had a past history or family history of influenza A. The symptoms of each patient included fever and upper respiratory tract infection. All of the patients manifested fever, listlessness, shortness of
breath, myalgia, tachycardia, lowered oxygen saturation, low blood pressure and cyanosis. Symptoms such as spasm and coma, which affect the central nervous system, were observed in two patients. This study was conducted in accordance with the Declaration of Helsinki. This study was conducted with approval from the Ethics Committee of Tianjin Children’s Hospital. Written informed consent was obtained from all participants.
Laboratory tests The eight patients’ X-ray results revealed pneumonia and diffuse ground-glass opacities in both lungs as revealed in the chest computed tomography (CT) scan. The peripheral blood routine revealed that the median of white blood cells was 4500 (the highest value was 16,900), the median of neutrophil percentage
Associate Chief Physician, Tianjin Children’s Hospital, Tianjin, China Corresponding author: Jing Ning, Tianjin Children’s Hospital, No. 225 Machang Road, Tianjin 300074, China. Email: [email protected]
Downloaded from tdo.sagepub.com at COLUMBIA UNIV on November 7, 2014
70
Tropical Doctor 44(2)
was 45%, with a peak value of 60% and the red blood cells and platelet (PLT) were in the normal range. Quick read C-reactive protein (CRP) ranges from 8–24 mg/dL (median: 14.5 mg/dL) and blood glucose ranges from 83–270 mg/dL (median: 105 mg/dL). The hepatic/renal function was generally normal. Increased levels of lactate dehydrogenase (LDH) and choline kinase (CK) were observed in four patients, who were generally normal based on the results of myocardial isodynamic enzymes. Electrocardiogram (ECG) results showed that all the patients suffered from tachycardia.
Therapy All of the patients were treated with oseltamivir (3 mg/ kg/day) by mouth, intravenous antibiotics, methylprednisolone (20 mg/kg/day) and human immunoglobulin (2 g/kg/day) for 1–2 days. Oxygen inhalation was administered to patients with minor disorders and artificial mechanical ventilation was provided for those with severe cases. Other supportive treatments were applied at the doctors’ discretion. The therapies were then adjusted according to iconographic variations and changes in vital signs.
Results All of the eight patients were diagnosed with influenza A (H1N1) as revealed by a pathogenic test (reverse transcription-polymerase chain reaction (RT-PCR) of H1N1 on samples obtained from oropharyngeal swabs). After one week, their general conditions were ameliorated. Pulmonary infiltration was also alleviated and transdermal oxygen saturation was recovered (98– 100%). All eight of the patients survived.
Discussion The main pathophysiological features of influenza A (H1N1) include ulcer or exfoliation of the bronchial mucosa, alveolus capillary hyperaemia, alveolar haemorrhage, damaged endothelial barrier, alveolus gap filled with fibrin and exudates, and hyaline membrane formation and fibrosis that may occur simultaneously.3 Basic pathophysiological variation in the lungs lowers pulmonary compliance, decreases the effective aeration area and disrupts diffusive function.4–7 Glucocorticoid is used to treat acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). In theory, systematic stress response and cytokine storm may occur during acute virus infection. As the final effector in the hypothalamus-pituitaryadrenal axis, glucocorticoid is one of the most
important anti-inflammatory agents.8 Clinical reviews also support the positive function of glucocorticoid in ARDS treatment.9 Considering these data, we administered liquid in limited amounts, which is consistent with the recommended dosage for ARDS therapy. Previous reports have proved the capability of exogenous pulmonary surfactant to ameliorate oxygenation.10
Conclusion Based on pulmonary pathological variation and our previous experiences in clinical therapy, we found that the progression of infection from the lower respiratory tract to ALI or ARDS can occur gradually. Lesions in the lungs caused by a new type of influenza A (H1N1) can be treated by controlling the inflammatory response and maintaining effective oxygenation. References 1. Ampofo K, Gesteland PH, Bender J, et al. Epidemiology, complications, and cost of hospitalization in children with laboratory-confirmed influenza infection. Pediatrics 2006; 118: 2409–2417. 2. Poehling KA, Edwards KM, Weinberg GA, et al. The under recognized burden of influenza in young children. N Engl J Med 2006; 355: 31–40. 3. Rello J, Rodrı´ guez A, Iban˜ez P, et al. Intensive care adult patients with severe respiratory failure caused by influenza A (H1N1) in Spain. Crit Care 2009; 13: R148. 4. Pistolesi M, Miniati M, Milne EN and Giuntini C. The chest roentgenogram in pulmonary edema. Clin Chest Med 1985; 6: 315–344. 5. Gattinoni L and Caironi P. Refining ventilatory treatment for acute lung injury and acute respiratory distress syndrome. JAMA 2008; 299: 691–693. 6. Halter JM, Steinberg JM, Gatto LA, et al. Effect of positive end-expiratory pressure and tidal volume on lung injury induced by alveolar instability. Crit Care 2007; 11: R20. 7. Toth I, Leiner T, Mikor A, Szakmany T, Bogar L and Molnar Z. Hemodynamic and respiratory changes during lung recruitment and descending optimal positive endexpiratory pressure titration in patients with acute respiratory distress syndrome. Crit Care Med 2007; 35: 787–793. 8. Rhen T and Cidlowski JA. Anti-inflammatory action of glucocorticoids-new mechanisms for old drugs. N Engl J Med 2005; 353: 1711–1723. 9. Meduri GU, Marik PE, Chrousos GP, et al. Steroid treatment in ARDS: a critical appraisal of the ARDS network trial and the recent literature. Intensive Care Med 2008; 34: 61–69. 10. Nosal S, Durdik P, Luptakova A, et al. Therapeutic approach to a child with acute respiratory distress syndrome: a report of two cases. J Physiol Pharmacol 2008; 59: 43–51.
Downloaded from tdo.sagepub.com at COLUMBIA UNIV on November 7, 2014
