ABSTRACT
In congenital diaphragmatic hernia (CDH), chest tube insertion at repair could determine rapid overexpansion of hypoplastic lungs, increasing the risk of pneumothorax. Therefore, in our institution no drainage tube at CDH repair was inserted after 1997. Afterwards several patients needed chest drainage for cardiopulmonary distress due to pleural effusion (PE) during the postoperative course. The aims of this study are to establish the incidence of PE requiring drainage for cardiopulmonary distress during postoperative course in CDH and to assess its eventual increase in patients with patch repair. Furthermore, the aetiology and treatment of PE are highlighted. Records of high-risk CDH operated on from 1998 to 2004 were reviewed. No chest tube was inserted at repair. Drainage was accomplished postoperatively if a cardiopulmonary distress due to PE occurred. Groups with and without patch were compared on gender, gestational age, birth weight, side of hernia, PE, hernial sac, central venous line and venous thrombosis, using the chi(2) and Student's t tests. Overall mortality rate was recorded. Out of 76 patients, 23 (30%) required patch repair. The PE occurred in 22 out of 76 patients, and in 68% of cases a chylothorax resulted. Birth weight was significantly lower, and the PE rate was significantly higher in patients with patch. Pleural drainage yielded improvement of ventilatory and respiratory parameters in all cases. Overall mortality rate was 16 and 23% in patients that required chest drain. The incidence of PE was 30% in CDH and significantly higher in patients with patch. The increased mortality rate in patients with PE causing cardiopulmonary distress warrants chest tube drainage before instability occurs.
Subject(s)
Drainage , Hernia, Diaphragmatic/surgery , Hernias, Diaphragmatic, Congenital , Pleural Effusion/therapy , Postoperative Complications/therapy , Female , Humans , Incidence , Infant, Newborn , Male , Pleural Effusion/epidemiology , Pleural Effusion/etiology , Postoperative Complications/epidemiology , Postoperative Complications/etiologyABSTRACT
AIM: To investigate whether children with cystic fibrosis under 3 years of age have disordered breathing and episodes of oxygen desaturation during sleep. METHODS: We studied 19 infants (9 boys and 10 girls) with cystic fibrosis, mean age 13.1 months (range 3-36 months) and 20 age and sex matched healthy subjects. Patients and controls underwent an overnight polysomnographic study and respiratory function testing on the following morning. RESULTS: Seven patients with ongoing respiratory tract inflammation had disordered breathing and episodes of oxygen desaturation during sleep. Pulse oximetry showed a significantly lower mean oxygen saturation (SaO(2)) and a higher percentage of total sleep time spent with SaO(2) less than 93% in symptomatic children than in controls. CONCLUSION: Results suggest that infants and young children with cystic fibrosis and mild airways inflammation (rhinitis, cough, red throat) have episodes of oxygen desaturation during sleep.
Subject(s)
Cystic Fibrosis/blood , Oximetry , Oxygen/blood , Sleep/physiology , Acute Disease , Anthropometry , Case-Control Studies , Child, Preschool , Cystic Fibrosis/complications , Cystic Fibrosis/physiopathology , Female , Humans , Hypoxia/etiology , Infant , Inflammation/complications , Male , Polysomnography , Respiratory Mechanics , Respiratory Tract Diseases/complicationsABSTRACT
A 4-month-old baby girl, after a period of apparent good health, began to have aphonia, dyspnea, difficulties with swallowing, cyanosis, apnea, and hypopnea during sleep that resulted in admission to an intensive care unit for intubation and mechanical ventilation. At the age of 9 months she was admitted to our hospital with a possible diagnosis of central hypoventilation syndrome. A polysomnographic study showed apnea and hypopnea (apnea + hypopnea index = 47.1), hypercapnia (mean end-tidal PCO2 89 +/- 15.0 mmHg), and arterial desaturation (mean SaO2 91 +/- 1.7%; lowest SaO2 < 50%; 68% of total sleep time at SaO2 below 93%); the study also showed an absent ventilatory response to CO2, absent cardiac responses to apnea during sleep, and right ventricular hypertrophy. Nocturnal nasal bi-level positive airway pressure (BIPAP), applied initially at 6 cmH2O and gradually increased to 16 cmH2O, caused the sleep-related abnormal respiratory events to disappear. End-tidal PCO2 decreased to 39 mmHg, and SaO2 increased to 94%. After 6 months of nocturnal BiPAP ventricular right hypertrophy reversed and arrested growth and hypotonia normalized. The child has tolerated and has remained on BiPAP support up to her current age of 3 years and continues to use this form of ventilatory assistance without difficulties.
