A young man with a cough, an abnormal chest radiograph, and multiple skin lesions.
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Biomedical subjects
Publications and source records attributed to Loutfi S Aboussouan.
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Theophylline has been shown to have beneficial effects on phrenic nerve and diaphragm activation. This case report involves a C5-C6 chronic tetraplegic patient with acute respiratory failure and ventilator dependence. IV aminophylline was administered in increasing doses (2 mg/kg, 4 mg/kg, and 6 mg/kg) over the course of 1 day. Diaphragm surface electromyography (sEMG), measures of respiration (tidal volume, minute ventilation, and frequency), and serum theophylline levels were captured. Diaphragm sEMG activity increased by a maximum of 50% at therapeutic levels. The rapid shallow breathing index dropped from 112 to 86. The subject was successfully weaned from ventilatory support. We conclude that administration of aminophylline facilitated weaning from ventilatory support in this tetraplegic patient.
BACKGROUND: As the decision-making process in long-term respiratory care units often depends on time-based outcomes, we sought to identify independent predictors of time-to-weaning (TTW) in a hospital-based specialized respiratory care unit. METHODS: Characteristics that were identified in previous studies as predictors of weaning success in ICUs and long-term ventilator units were prospectively collected on 113 consecutive admissions to our unit. TTW analyses were performed with Kaplan-Meier curves, log rank test, and Cox proportional regression. RESULTS: The TTW was shorter in patients with static lung compliance (Cst) of > 20 mL/cm H(2)O, a normal creatinine level (0.6 to 1.4 mg/dL), a rapid shallow breathing index (RSBI) of < or = 105, intact skin, and in those patients from a surgical referral source. We found an interaction between RSBI and Cst (p = 0.02) such that patients with an RSBI of < or = 105, regardless of Cst, had a median TTW of 11 days, those with an RSBI of > 105 and a Cst of > 20 had a median TTW of 31 days, and those with an RSBI of > 105 and a Cst of < or = 20 mL/cm H(2)O had not reached a median TTW by 60 days (p = 0.007 [log rank for linear trend]). In a Cox-proportional hazard model, both this categorization model of RSBI and Cst, and renal function had a significant impact on TTW. CONCLUSIONS: In a multivariate model incorporating the variables reviewed, only the lung parameters (RSBI combined with Cst) and renal function remained independently associated with TTW.
Various neurologic diseases such as multiple sclerosis and Parkinson disease can cause pulmonary complications. Pulmonary disorders often manifest late in a neuromuscular disease, but occasionally a respiratory problem may be the first sign. Often the first signs are sleep disturbances and nocturnal desaturation. Although the diseases are diverse, common principles apply in their management.
We wished to determine the severity of posthypoxic ventilatory decline in patients with sleep apnea relative to normal subjects during sleep. We studied 11 men with sleep apnea/hypopnea syndrome and 11 normal men during non-rapid eye movement sleep. We measured EEG, electrooculogram, arterial O(2) saturation, and end-tidal P(CO2). To maintain upper airway patency in patients with sleep apnea, nasal continuous positive pressure was applied at a level sufficient to eliminate apneas and hypopneas. We compared the prehypoxic control (C) with posthypoxic recovery breaths. Nadir minute ventilation in normal subjects was 6.3 +/- 0.5 l/min (83.8 +/- 5.7% of room air control) vs. 6.7 +/- 0.9 l/min, 69.1 +/- 8.5% of room air control in obstructive sleep apnea (OSA) patients; nadir minute ventilation (% of control) was lower in patients with OSA relative to normal subjects (P < 0.05). Nadir tidal volume was 0.55 +/- 0.05 liter (80.0 +/- 6.6% of room air control) in OSA patients vs. 0.42 +/- 0.03 liter, 86.5 +/- 5.2% of room air control in normal subjects. In addition, prolongation of expiratory time (Te) occurred in the recovery period. There was a significant difference in Te prolongation between normal subjects (2.61 +/- 0.3 s, 120 +/- 11.2% of C) and OSA patients (5.6 +/- 1.5 s, 292 +/- 127.6% of C) (P < 0.006). In conclusion, 1) posthypoxic ventilatory decline occurred after termination of hypocapnic hypoxia in normal subjects and patients with sleep apnea and manifested as decreased tidal volume and prolongation of Te; and 2) posthypoxic ventilatory prolongation of Te was more pronounced in patients with sleep apnea relative to normal subjects.
OBJECTIVE: To describe the pathogenesis of chronic obstructive pulmonary disease (COPD) and mechanisms of benefit, formulations available, drug costs, pharmacokinetic profiles, and pertinent clinical studies for long-acting beta(2)-agonists. DATA SOURCES: A MEDLINE search was conducted from July 1966 through October 2002. STUDY SELECTION AND DATA EXTRACTION: Pertinent articles related to COPD and long-acting beta(2)-agonists. DATA SYNTHESIS: The incidence and subsequent morbidity and mortality of COPD have increased during the last 4 decades, prompting worldwide initiatives to formulate guidelines to decrease the burden of this disease. COPD is a progressive, irreversible disease state characterized by chronic cough, dyspnea, sputum production, and wheezing, in which no medication has been shown to decrease mortality, excluding oxygen supplementation. Bronchodilators have been a mainstay of COPD treatment through their ability to work by both smooth- and non-smooth-muscle mechanisms. Long-acting beta(2)-agonists (i.e., formoterol, salmeterol) dosed twice daily provide more convenient dosing than 4-times-daily regimens of traditional short-acting bronchodilators. Both formoterol and salmeterol have acceptable adverse event profiles when used at recommended doses. There have been no direct clinical outcome studies comparing formoterol and salmeterol, but both have shown some benefits over ipratropium and theophylline in improving the symptoms, spirometric indices, exacerbations, and quality of life of patients with COPD. CONCLUSIONS: Based on current evidence, long-acting beta(2)-agonists are acceptable first-line agents for patients with COPD.
Alpha1-antitrypsin deficiency is a genetic disorder that affects about one in 2000-5000 individuals. It is clinically characterised by liver disease and early-onset emphysema. Although alpha1 antitrypsin is mainly produced in the liver, its main function is to protect the lung against proteolytic damage from neutrophil elastase. The most frequent mutation that causes severe alpha1-antitrypsin deficiency arises in the SERPINA 1 gene and gives rise to the Z allele. This mutation reduces concentrations in serum of alpha1 antitrypsin by retaining polymerised molecules within hepatocytes: an amount below the serum protective threshold of 11 micromol/L increases risk for emphysema. In addition to the usual treatments for emphysema, infusion of purified alpha1 antitrypsin from pooled human plasma represents a specific treatment and raises the concentrations in serum and epithelial-lining fluid above the protective threshold. Evidence suggests that this approach is safe, slows the decline of lung function, could reduce infection rates, and might enhance survival. However, uncertainty about the cost-effectiveness of this expensive treatment remains.