Fatal, Fulminant Herpetic Tracheobronchitis following Cardiac Surgery

Fatal, Fulminant Herpetic Tracheobronchitis following Cardiac Surgery ABSTRACT Nosocomial infection is a feared complication after any surgical procedure. Respiratory tract microbial colonization and development of ventilator-associated tracheobronchitis and/or pneumonia are unfortunate sequelae in mechanically ventilated patients, commonly caused by bacteria; viral etiology is seldom anticipated. We present a fatal case of fulminant herpetic tracheobronchitis in a 33-month-old patient following cardiac surgery. We intend to highlight the fact that herpetic viral etiology should be considered in post-operative respiratory infections. nosocomial infections, ventilator-associated tracheobronchitis, ventilator-associated pneumonia, herpes simplex virus INTRODUCTION Hospital-acquired or nosocomial infections are a bane to patients admitted in intensive care units. In mechanically ventilated patients, there is always a greater risk of developing lower respiratory tract microbial colonization, which can progress to a full-fledged ventilator-associated pneumonia (VAP). A process considered as an intermediate between the two (i.e. colonization and VAP) is termed as “ventilator-associated tracheobronchitis” (VAT) [1]. The VAT is diagnosed on the basis of clinical findings of infection (fever ≥38°C, leukocytosis and purulent secretions) and positive microbiologic identification of the causative organism (positive culture of, or antigen detection in, tracheobronchial secretions) in the absence of new lung opacities on imaging in patients mechanically ventilated for more than 48 h [2]. Most of the organisms isolated represent endogenous or exogenous flora and are most often bacteria such as Pseudomonas aeruginosa [3]. Viruses are usually not considered or implicated in either colonization or infections after endotracheal intubation [4]. We report an unfortunate occurrence of obliterative herpetic tracheobronchitis in a pediatric patient who was on prolonged mechanical ventilation after open heart surgery. CASE REPORT An immunocompetent girl [age, 33 months; weight, 10 kg (1st percentile); seronegative for human immunodeficiency virus (HIV), hepatitis B surface antigen (HBsAg) and hepatitis C virus [HCV] presented with symptoms of failure to thrive and cyanosis since the age of two years. She had been immunized as per protocol and showed normal developmental milestones. There was no history of any exanthematous fever. Routine hematological and biochemical investigations showed normal levels. The patient was diagnosed to have perimembranous ventricular septal defect (VSD) with valvular pulmonary stenosis. She underwent intracardiac repair of VSD using a Dacron patch and pulmonary valvotomy four days after admission. She received ceftriaxone, amikacin and dexamethasone on post-operative day zero. She was extubated on post-operative day one with satisfactory pre-extubation clinical and blood gas parameters; she was, however, electively re-intubated within 12 h because the blood gas levels were not maintained and saturation levels were decreasing. Echocardiography performed was not remarkable. On post-operative day three, the patient developed neutrophilia (total leukocyte count, 27 100/mm3). Because of the possibility of development of septicemia, the patient was administered imipenem–cilastatin and vancomycin. Blood culture for bacteria was negative. Feeding was initiated via the nasogastric tube, and inotropic supports were slowly tapered off. The patient was nasally intubated in view of prolonged ventilation due to poor blood gas levels; but, she passed away on post-operative day nine. The restricted autopsy (partial chest) revealed obliteration of the entire tracheobronchial tree caused by granular, focally laminated, pale yellowish-brown exudates (Fig. 1A). Histopathological examination showed inflammation of the tracheobronchial lining, which was focally ulcerated with a collection of necrotic slough in the lumens. The denuded areas were replaced by collections of neutrophils and histiocytes in a fibrin-rich matrix. The entrapped epithelial cells, which were scattered in the inflamed zone, showed intranuclear Cowdry type A inclusions. Similar inclusions were also observed in the nuclei of the submucosal glandular epithelium (Fig. 1B). The submucosa also showed collections of lymphocytes and histiocytes with extravasated mucin. An interesting feature noted was the presence of focal squamous metaplasia (Fig. 1C). Antibodies to herpes simplex virus (HSV) 1 (polyclonal) focally labeled the epithelial cells and the lining cells of the mucous glands (Fig. 1B). The involvement of the airways was also accompanied by herpetic esophagitis. There was no pulmonary involvement. Fig. 1. View largeDownload slide (A) The transverse sections of the trachea and both main bronchi were completely filled with inflammatory exudates; (B) The lining was completely ulcerated. A group of glandular epithelial cells (arrow) showed intra-nuclear inclusions (hematoxylin and eosin [H&E]; original magnification, 400×); (C) At places, the respiratory lining was replaced by metaplastic squamous epithelium (H&E; original magnification, 400×); (D). Antibodies to HSV 1 labeling the lining cells of the mucous glands (original magnification, 400×). Fig. 1. View largeDownload slide (A) The transverse sections of the trachea and both main bronchi were completely filled with inflammatory exudates; (B) The lining was completely ulcerated. A group of glandular epithelial cells (arrow) showed intra-nuclear inclusions (hematoxylin and eosin [H&E]; original magnification, 400×); (C) At places, the respiratory lining was replaced by metaplastic squamous epithelium (H&E; original magnification, 400×); (D). Antibodies to HSV 1 labeling the lining cells of the mucous glands (original magnification, 400×). DISCUSSION Unexpected and unsuspected obliterative tracheobronchitis lead to postoperative deterioration and fatality in a child. The circumstances leading to this pathway appeared to be nosocomial in nature and related to endotracheal and esophageal intubations. Both VAP and VAT share similar etiopathogenetic mechanisms and begin with colonization of the upper aerodigestive tracts by endogenous or exogenous flora. The colonization and subsequent infection results from the disruption or bypass of mechanical and immunological natural defense mechanisms [5]. The intraluminal tubes potentiate biofilm formation and permit aspiration of the pooled contaminated secretions. Additional risk factors would be the presence of certain comorbid conditions and overall immune status of the patients. Although the incidence of VAP is fairly well established, little is known about the incidence of VAT in not only adults (estimated to be around 12% [6]) but also children; again, the major thrust is on the isolation of bacteria. In our case, the causative agent was HSV. Although this case does not fit into the definition of VAT, we believe that intubation exacerbated the inflammation, considering the magnitude of the response that led to luminal occlusion. HSV, a double-stranded DNA virus, is capable of producing an infection that is frequently asymptomatic and has a life-long latency because of viral persistence in the neurons of the dorsal root ganglia and autonomic nervous system. Hence, there can be asymptomatic shedding in some individuals, which can be detected in the respiratory secretions [7]. In addition, reactivation mediated by a variety of local or systemic factors can also occur in not only critically ill patients but also those in the intensive care units [8]. In our patient, we speculated if the flaring of the latent infection could have been potentiated by the cardiopulmonary bypass, probably because of the post-bypass immunosuppression or immunoparalysis [9]. HSV has a propensity to affect the squamous epithelia, and this patient also had herpetic esophagitis. The tracheobronchial tree involvement could be explained by the presence of squamous metaplasia, which may have been induced by underlying nutritional deficiency or even prolonged intubation [10]. A post-cardiac surgery respiratory tract infection can be caused by a variety of etiological agents. A virus is rarely a primary suspect, not commonly looked for, sometimes leading to a catastrophic turn of events. Because judicious use of antiviral agents may be therapeutic, HSV VAT should be considered in mechanically ventilated patients with prolonged or explained respiratory symptoms. It should be noted that diagnosis is not easy despite the availability of routine or sophisticated techniques. ACKNOWLEDGEMENTS The authors would like to thank Dr. Anita Mahadevan, Additional Professor, Department of Neuropathology, National Institute of Mental Health and Neuro Sciences, Bengaluru, Karnataka, India, for the HSV immunohistochemistry. REFERENCES 1 Craven DE. Ventilator-associated tracheo-bronchitis (VAT): questions, answers, and a new paradigm? Critical Care 2008 ; 12 : 157. Google Scholar CrossRef Search ADS PubMed 2 Niederman MS. Hospital-acquired pneumonia, health care - associated pneumonia, ventilator-associated pneumonia, and ventilator-associated tracheo-bronchitis: definitions and challenges in trial design . Clin Infect Dis 2010 ; 51 : S12 – 17 . Google Scholar CrossRef Search ADS PubMed 3 Cavalcanti M , Valencia M , Torres A. Respiratory nosocomial infections in the medical intensive care unit . Microbes Infect 2005 ; 7 : 292 – 301 . Google Scholar CrossRef Search ADS PubMed 4 Hauptmeier BM , Borg I , Rohde G , et al. Viral colonization in intubated patients: initial pathogen pattern and follow-up . Clin Respir J 2010 ; 4 : 139 – 46 . Google Scholar CrossRef Search ADS PubMed 5 Mehta A , Bhagat R. Preventing ventilator-associated infections . Clin Chest Med 2016 ; 37 : 683 – 92 . Google Scholar CrossRef Search ADS PubMed 6 Agrafiotis M , Biempos II , Falagas ME. Frequency, prevention, outcome and treatment of ventilator-associated tracheo-bronchitis: systemtic review and meta-analysis . Respir Med 2010 ; 104 : 325 – 36 . Google Scholar CrossRef Search ADS PubMed 7 Bruynseels P , Jorens PG , Demey HE , et al. Herpes simplex virus in the respiratory tract of critical care patients: a prospective study . Lancet 2003 ; 362 : 1536 – 41 . Google Scholar CrossRef Search ADS PubMed 8 Engelmann I , Gottlieb J , Meier A , et al. Clinical relevance of and risk factors for HSV-related tracheo-bronchitis or pneumonia: results of an outbreak investigation . Crit Care 2007 ; 11 : R119. Google Scholar CrossRef Search ADS PubMed 9 Allen ML , Hoschtitzky JA , Peters MJ , et al. role in clinical immunoparalysis following pediatric cardiac surgery . Crit Care Med 2006 ; 34 : 2658 – 65 . Google Scholar CrossRef Search ADS PubMed 10 Kim D , Kim S , Lee Y , et al. A case report of tracheo-bronchitis by herpes simplex virus type 1 . Korean J Int Med 1986 ; 1 : 249 – 53 . Google Scholar CrossRef Search ADS © The Author(s) [2018]. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Tropical Pediatrics Oxford University Press

Fatal, Fulminant Herpetic Tracheobronchitis following Cardiac Surgery

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Abstract

ABSTRACT Nosocomial infection is a feared complication after any surgical procedure. Respiratory tract microbial colonization and development of ventilator-associated tracheobronchitis and/or pneumonia are unfortunate sequelae in mechanically ventilated patients, commonly caused by bacteria; viral etiology is seldom anticipated. We present a fatal case of fulminant herpetic tracheobronchitis in a 33-month-old patient following cardiac surgery. We intend to highlight the fact that herpetic viral etiology should be considered in post-operative respiratory infections. nosocomial infections, ventilator-associated tracheobronchitis, ventilator-associated pneumonia, herpes simplex virus INTRODUCTION Hospital-acquired or nosocomial infections are a bane to patients admitted in intensive care units. In mechanically ventilated patients, there is always a greater risk of developing lower respiratory tract microbial colonization, which can progress to a full-fledged ventilator-associated pneumonia (VAP). A process considered as an intermediate between the two (i.e. colonization and VAP) is termed as “ventilator-associated tracheobronchitis” (VAT) [1]. The VAT is diagnosed on the basis of clinical findings of infection (fever ≥38°C, leukocytosis and purulent secretions) and positive microbiologic identification of the causative organism (positive culture of, or antigen detection in, tracheobronchial secretions) in the absence of new lung opacities on imaging in patients mechanically ventilated for more than 48 h [2]. Most of the organisms isolated represent endogenous or exogenous flora and are most often bacteria such as Pseudomonas aeruginosa [3]. Viruses are usually not considered or implicated in either colonization or infections after endotracheal intubation [4]. We report an unfortunate occurrence of obliterative herpetic tracheobronchitis in a pediatric patient who was on prolonged mechanical ventilation after open heart surgery. CASE REPORT An immunocompetent girl [age, 33 months; weight, 10 kg (1st percentile); seronegative for human immunodeficiency virus (HIV), hepatitis B surface antigen (HBsAg) and hepatitis C virus [HCV] presented with symptoms of failure to thrive and cyanosis since the age of two years. She had been immunized as per protocol and showed normal developmental milestones. There was no history of any exanthematous fever. Routine hematological and biochemical investigations showed normal levels. The patient was diagnosed to have perimembranous ventricular septal defect (VSD) with valvular pulmonary stenosis. She underwent intracardiac repair of VSD using a Dacron patch and pulmonary valvotomy four days after admission. She received ceftriaxone, amikacin and dexamethasone on post-operative day zero. She was extubated on post-operative day one with satisfactory pre-extubation clinical and blood gas parameters; she was, however, electively re-intubated within 12 h because the blood gas levels were not maintained and saturation levels were decreasing. Echocardiography performed was not remarkable. On post-operative day three, the patient developed neutrophilia (total leukocyte count, 27 100/mm3). Because of the possibility of development of septicemia, the patient was administered imipenem–cilastatin and vancomycin. Blood culture for bacteria was negative. Feeding was initiated via the nasogastric tube, and inotropic supports were slowly tapered off. The patient was nasally intubated in view of prolonged ventilation due to poor blood gas levels; but, she passed away on post-operative day nine. The restricted autopsy (partial chest) revealed obliteration of the entire tracheobronchial tree caused by granular, focally laminated, pale yellowish-brown exudates (Fig. 1A). Histopathological examination showed inflammation of the tracheobronchial lining, which was focally ulcerated with a collection of necrotic slough in the lumens. The denuded areas were replaced by collections of neutrophils and histiocytes in a fibrin-rich matrix. The entrapped epithelial cells, which were scattered in the inflamed zone, showed intranuclear Cowdry type A inclusions. Similar inclusions were also observed in the nuclei of the submucosal glandular epithelium (Fig. 1B). The submucosa also showed collections of lymphocytes and histiocytes with extravasated mucin. An interesting feature noted was the presence of focal squamous metaplasia (Fig. 1C). Antibodies to herpes simplex virus (HSV) 1 (polyclonal) focally labeled the epithelial cells and the lining cells of the mucous glands (Fig. 1B). The involvement of the airways was also accompanied by herpetic esophagitis. There was no pulmonary involvement. Fig. 1. View largeDownload slide (A) The transverse sections of the trachea and both main bronchi were completely filled with inflammatory exudates; (B) The lining was completely ulcerated. A group of glandular epithelial cells (arrow) showed intra-nuclear inclusions (hematoxylin and eosin [H&E]; original magnification, 400×); (C) At places, the respiratory lining was replaced by metaplastic squamous epithelium (H&E; original magnification, 400×); (D). Antibodies to HSV 1 labeling the lining cells of the mucous glands (original magnification, 400×). Fig. 1. View largeDownload slide (A) The transverse sections of the trachea and both main bronchi were completely filled with inflammatory exudates; (B) The lining was completely ulcerated. A group of glandular epithelial cells (arrow) showed intra-nuclear inclusions (hematoxylin and eosin [H&E]; original magnification, 400×); (C) At places, the respiratory lining was replaced by metaplastic squamous epithelium (H&E; original magnification, 400×); (D). Antibodies to HSV 1 labeling the lining cells of the mucous glands (original magnification, 400×). DISCUSSION Unexpected and unsuspected obliterative tracheobronchitis lead to postoperative deterioration and fatality in a child. The circumstances leading to this pathway appeared to be nosocomial in nature and related to endotracheal and esophageal intubations. Both VAP and VAT share similar etiopathogenetic mechanisms and begin with colonization of the upper aerodigestive tracts by endogenous or exogenous flora. The colonization and subsequent infection results from the disruption or bypass of mechanical and immunological natural defense mechanisms [5]. The intraluminal tubes potentiate biofilm formation and permit aspiration of the pooled contaminated secretions. Additional risk factors would be the presence of certain comorbid conditions and overall immune status of the patients. Although the incidence of VAP is fairly well established, little is known about the incidence of VAT in not only adults (estimated to be around 12% [6]) but also children; again, the major thrust is on the isolation of bacteria. In our case, the causative agent was HSV. Although this case does not fit into the definition of VAT, we believe that intubation exacerbated the inflammation, considering the magnitude of the response that led to luminal occlusion. HSV, a double-stranded DNA virus, is capable of producing an infection that is frequently asymptomatic and has a life-long latency because of viral persistence in the neurons of the dorsal root ganglia and autonomic nervous system. Hence, there can be asymptomatic shedding in some individuals, which can be detected in the respiratory secretions [7]. In addition, reactivation mediated by a variety of local or systemic factors can also occur in not only critically ill patients but also those in the intensive care units [8]. In our patient, we speculated if the flaring of the latent infection could have been potentiated by the cardiopulmonary bypass, probably because of the post-bypass immunosuppression or immunoparalysis [9]. HSV has a propensity to affect the squamous epithelia, and this patient also had herpetic esophagitis. The tracheobronchial tree involvement could be explained by the presence of squamous metaplasia, which may have been induced by underlying nutritional deficiency or even prolonged intubation [10]. A post-cardiac surgery respiratory tract infection can be caused by a variety of etiological agents. A virus is rarely a primary suspect, not commonly looked for, sometimes leading to a catastrophic turn of events. Because judicious use of antiviral agents may be therapeutic, HSV VAT should be considered in mechanically ventilated patients with prolonged or explained respiratory symptoms. It should be noted that diagnosis is not easy despite the availability of routine or sophisticated techniques. ACKNOWLEDGEMENTS The authors would like to thank Dr. Anita Mahadevan, Additional Professor, Department of Neuropathology, National Institute of Mental Health and Neuro Sciences, Bengaluru, Karnataka, India, for the HSV immunohistochemistry. REFERENCES 1 Craven DE. Ventilator-associated tracheo-bronchitis (VAT): questions, answers, and a new paradigm? Critical Care 2008 ; 12 : 157. Google Scholar CrossRef Search ADS PubMed 2 Niederman MS. Hospital-acquired pneumonia, health care - associated pneumonia, ventilator-associated pneumonia, and ventilator-associated tracheo-bronchitis: definitions and challenges in trial design . Clin Infect Dis 2010 ; 51 : S12 – 17 . Google Scholar CrossRef Search ADS PubMed 3 Cavalcanti M , Valencia M , Torres A. Respiratory nosocomial infections in the medical intensive care unit . Microbes Infect 2005 ; 7 : 292 – 301 . Google Scholar CrossRef Search ADS PubMed 4 Hauptmeier BM , Borg I , Rohde G , et al. Viral colonization in intubated patients: initial pathogen pattern and follow-up . Clin Respir J 2010 ; 4 : 139 – 46 . Google Scholar CrossRef Search ADS PubMed 5 Mehta A , Bhagat R. Preventing ventilator-associated infections . Clin Chest Med 2016 ; 37 : 683 – 92 . Google Scholar CrossRef Search ADS PubMed 6 Agrafiotis M , Biempos II , Falagas ME. Frequency, prevention, outcome and treatment of ventilator-associated tracheo-bronchitis: systemtic review and meta-analysis . Respir Med 2010 ; 104 : 325 – 36 . Google Scholar CrossRef Search ADS PubMed 7 Bruynseels P , Jorens PG , Demey HE , et al. Herpes simplex virus in the respiratory tract of critical care patients: a prospective study . Lancet 2003 ; 362 : 1536 – 41 . Google Scholar CrossRef Search ADS PubMed 8 Engelmann I , Gottlieb J , Meier A , et al. Clinical relevance of and risk factors for HSV-related tracheo-bronchitis or pneumonia: results of an outbreak investigation . Crit Care 2007 ; 11 : R119. Google Scholar CrossRef Search ADS PubMed 9 Allen ML , Hoschtitzky JA , Peters MJ , et al. role in clinical immunoparalysis following pediatric cardiac surgery . Crit Care Med 2006 ; 34 : 2658 – 65 . Google Scholar CrossRef Search ADS PubMed 10 Kim D , Kim S , Lee Y , et al. A case report of tracheo-bronchitis by herpes simplex virus type 1 . Korean J Int Med 1986 ; 1 : 249 – 53 . Google Scholar CrossRef Search ADS © The Author(s) [2018]. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

Journal of Tropical PediatricsOxford University Press

Published: May 25, 2018

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