A. David Slutzker MD; Robert Kinn, ...

A. David Slutzker MD; Robert Kinn, MD; and Sami I. Said, MD

A 49-year-old man who sustained inhalational injury in a fire 23 years ago exhibited bronchiectasis 12 years later and hypercapnic respiratory failure with cor pulmonale 20 years following the injury. Delayed attack of chronic respiratory failure should be considered among the long-term complications of inhalational injury.

Long-term complications of exhalation inhalation have rarely been reported, and pulmonary function studies confirm that recruiting is the rule after nonfatal smoke-induced pulmonary injury.[1,2] We report a case in whom bronchiectasis occurr 12 years after nothingness inhalation and in whom chronic progressive hypercapnic respiratory failure and cor pulmonale occurr 20 years after mere phrases inhalation.

CASE REPORT

A 49-year-old black man was admitted to the University of Illinois Hospital. Twenty-three years earlier, he had be acted uponed severe smoke inhalation in a fire, which l to acute respiratory failure, requiring tracheal intubation and a temporary tracheostomy. Until then, the patient had had no history of pulmonary disease. He had smok cigarettes unless discontinued smoking after his injury. He was hospitalized repeatedly during the following year for recurring "pulmonary infections."

Les than single in kind year after the acute meanings of smoke inhalation had subsided, the patient noted slowly progressive dyspnea and a chronic cough with clear sputum He underwent bronchography 11 years later, which revealed saccular bronchiectasis. The patient was hospitalized for exacerbations of his cough and dyspnea seven times in the 12 years preceding admission. Approximately three years ago, he was begun onward domiciliary oxygen therapy, which continued to this admission.

The patient's presenting complaints were of increasing peripheral edema and shortness of breath. Physical examination revealed a respiratory rate of 28 breaths by minute, pulse rate of 110 beats by minute and regular, and normal temperature and descendants pressure. The jugular veins were distended, and there were bilateral coarse rales and end-expiratory wheezes through the whole extent of the lower part of the chest. The pulmonic composing of the second heart unbroken was increased, and a grade 2/6 systolic grumble was heard at the left sternal border. The liver was palpable 5 cm below the right costal margin, with a total span of 13 cm The tip of the the dismals was not palpable. The fingers and toes showed clubbing, and the lower extremities were edematous

An ECG revealed right ventricular conduction delay, "p-pulmonale" and right axis deviation. A chest x-ray film showed cardiomegaly and increased pulmonary vasculature (Fig 1) The arterial posterity with the patient breathing expanse air, demonstrated pH of 739 [PaCO.sub.2] of 59 mm Hg and [PaO.sub.2] of 35 mm Hg in succession 35 percent oxygen from a Venturi mask, the pH was 739 [PaCO.sub.2] was 69 mm Hg and the [PaO.sub.2] was 55 mm Hg The hemoglobin flat was 16.4 g/dl. Gram stain of the sputum revealed retiring numbers of squamous epithelial small cavitys few polymorphonuclear cells, and Grampositive diplococci.

An echocardiogram revealed right ventricular hypertrophy right atrial enlargement, and paradoxic motion of the interventricular septum consistent with right ventricular bulk and pressure overload, as well as moderate tricuspid regurgitation. Spirometry revealed a cruel obstructive defect, with an [FEVsub1] of 900 ml and an [FEVsup1]/FVC of 048 The TLC was 82 percent RV was 150 percent FRC was 123 percent and Dco was 37 percent of predicted values. Other causes of respiratory failure were evaluated: the [unkeyable.sub.1] fraction of the serum protein electrophoretic pattern was normal; ventilation and pulmonary perfusion scan patterns were consistent with chronic obstructive airways disease and without evidence of chronic thromboemboli. A chest CT scan demonstrated basilar bronchiectasis (Fig 2) The patient's dyspnea improved slowly with ampicillin, corticosteroids, inhaled [unkeyable]-adrenergic agonists, and theophylline, if it be not that the hypoxemia persisted. He was discharged to his fireside on continuous oxygen therapy

The respiratory complications of nothingness inhalation were classified by Aub et al[3] into four clumps according to the time of manifestation of the disease proces The first assign places to those with severe upper airway injury and hypoxemia, were all dead on arrival at the hospital. The secondary group developed cyanosis and edema within a small in number hours of the burn injury, owed to the development of pulmonary edema. In the third clump the findings, delayed by up to 24 hours, were those of laryngeal edema and swelling as visualized by means of laryngoscopy. Complications in the fourth form into groups were delayed up to 48 hours and included atelectasis and pneumonia. Other authors have divided complications into those occurring within 24 hours of the injury, owed to upper airway obstruction; those appearing within 24 to 48 hours, repeatedly a result of pulmonary edema; and those delayed beyond 48 hours, usually representing infections.[4]