ABSTRACT
STUDY OBJECTIVES: Obesity has many detrimental effects on the respiratory function and may lead to chronic hypoventilation in some patients, an association known as the obesity-hypoventilation syndrome (OHS). In many cases, patients with OHS also have sleep apneas. Hereafter, we describe several features of a cohort (n = 34) of patients with OHS and show the comparisons with a large cohort (n = 220) of patients with obstructive sleep apnea syndrome (OSAS). We compare also OHS patients with a group of patients with the association of OSAS and COPD, also known as "overlap" patients. DESIGN: Descriptive analysis of prospectively collected clinical data. SETTING: Respiratory care unit and sleep laboratory of university hospital. RESULTS: In OHS patients, OSAS was present in most of the cases (23 of 26 patients). However, in three patients, OHS was not associated with OSAS, showing that obesity per se may lead to chronic hypoventilation. As expected by definition, OHS patients had, on average the worst diurnal arterial blood gas measurements, compared to the other groups. For the OHS patients, the mean diurnal PaO(2) was 59 +/- 7 mm Hg, which was significantly different from the PaO(2) of the OSAS patients (75 +/- 10 mm Hg; p = 0,001) but also from the overlap patients (66 +/- 10 mm Hg; p = 0.015). Pulmonary hypertension (ie, mean pulmonary artery pressure > 20 mm Hg) was more frequent in OHS patients than in "pure" OSAS patients (58% vs 9%; p = 0.001). CONCLUSION: Patients with OSAS and chronic respiratory insufficiency had in most cases an associated OHS or COPD. Patients with OHS were older than patients with pure OSAS. They had mild-to-moderate degrees of restrictive ventilatory pattern due to obesity. Severe gas exchange impairment and pulmonary hypertension were quite frequent. The association of OHS and OSAS was the rule. However, in three patients, OHS was not associated with OSAS, suggesting that OHS is an autonomous disease.
Subject(s)
Obesity Hypoventilation Syndrome/physiopathology , Chronic Disease , Female , Humans , Hypertension, Pulmonary/complications , Lung Diseases, Obstructive/physiopathology , Male , Middle Aged , Obesity Hypoventilation Syndrome/complications , Oxygen/blood , Partial Pressure , Prospective Studies , Pulmonary Gas Exchange , Respiratory Insufficiency/complications , Sleep Apnea, Obstructive/complications , Sleep Apnea, Obstructive/physiopathologyABSTRACT
Worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease has been extensively investigated in the past 20 years owing to the development of polysomnography and to the advent of reliable transcutaneous oximeters. Sleep-related hypoxaemia is characteristic of rapid-eye-movement (REM) sleep but may be present during other sleep stages. There is a strong relationship between nocturnal O2 saturation and the level of daytime PaO2: the more pronounced daytime hypoxaemia, the more severe nocturnal hypoxaemia. Sleep-related hypoxaemia is due to a variable combination of alveolar hypoventilation and ventilation-perfusion mismatching, alveolar hypoventilation being the preponderant mechanism during REM sleep. The deleterious effects of sleep-related hypoxaemia include cardiac arrhythmias, 'hypoxaemic stress' on the coronary circulation and especially, peaks of pulmonary hypertension. The treatment of nocturnal hypoxaemia is conventional O2 therapy (both nighttime and daytime) in patients who exhibit marked daytime hypoxaemia (PaO2 < 55-60 mm Hg). At present data are not sufficient for justifying the use of isolated nocturnal O2 therapy in patients with nocturnal desaturation who do not qualify for conventional O2 therapy.
Subject(s)
Hypoxia/complications , Lung Diseases, Obstructive/complications , Oxygen/therapeutic use , Sleep Apnea Syndromes/etiology , Sleep Apnea Syndromes/therapy , Sleep, REM , Clinical Trials as Topic , Humans , Hypoxia/epidemiology , Hypoxia/physiopathology , Hypoxia/therapy , Lung Diseases, Obstructive/physiopathology , Lung Diseases, Obstructive/therapy , Oxygen Consumption , Prognosis , Pulmonary Circulation , Risk Factors , Sleep Apnea Syndromes/physiopathology , TachycardiaABSTRACT
We report a case of bilateral eosinophilic pneumonia in a 33 year old man. This case developed rapidly into acute respiratory failure and required artificial ventilation. Intravenous corticosteroid therapy produced a rapid improvement in the clinical picture. There was hyper-eosinophilia in both the blood and the alveoli which leads to a search for a parasitic aetiology. The different parasitic serologies were negative except for Toxocaracanis. The ELISA index was strongly positive at 2,597. Treatment with thiabendazole was started.
Subject(s)
Larva Migrans, Visceral/complications , Pulmonary Eosinophilia/parasitology , Respiratory Insufficiency/parasitology , Toxocara canis , Acute Disease , Adrenal Cortex Hormones/therapeutic use , Adult , Animals , Humans , Larva Migrans, Visceral/diagnosis , Larva Migrans, Visceral/drug therapy , MaleABSTRACT
Small cell carcinoma of the lung (SCLC) represents about 25% of all lung cancers. Extrapulmonary small cell carcinoma is a very uncommon feature, mostly described in the oesophagus. We report here a case of small cell carcinoma of the pleura with histopathological findings, clinical course and response to therapy typical of SCLC.
