Sudden death caused by aortic dissection in a patient with polycystic kidney disease.

A 43-year-old man presented at the emergency medical unit with chest pain. The results of a clinical examination were normal, apart from sternum pain (without radiation) on palpation. The patient had no respiratory problems and the pain was relieved by paracetamol. The electrocardiogram, laboratory tests and chest X-ray were normal. However, the man was found dead the next morning. In the autopsy, we noted the presence of haemopericardium, aortic dissection (starting from the vessel's origin and extended to the aortic arch and on through the diaphragm), polycystic kidney disease and liver cysts. In adult autosomal dominant polycystic kidney disease (ADPKD) patients, the main causes of death are ruptured intracerebral aneurysms, coronary artery disease, congestive heart failure, valvular heart disease and ruptured abdominal aortic aneurysms. Aortic dissection is considered to be rare cause of sudden death in ADPKD sufferers. ADPKD can have serious consequences for the vascular system. The families of confirmed ADPKD sufferers must be informed and screened as early as possible, in order to prevent renal and cardiovascular complications.

[Intensive care anaesthesia practice in the prison environment. Can a prisoner benefit from ambulatory anaesthesia]. / Pratique de l'anesthésie réanimation en milieu pénitentiaire. Un détenu peut-il bénéficier d'une anesthésie ambulatoire ?

Ambulatory anaesthesia is an anesthesia allowing the return of the patient home the same day. Even if the ambulatory hospitalization can, in theory, be applied to a prisoner as to every patient, caution is essential in such approach. Every anaesthetist reanimator doctor practicing in public hospitals may give care to patient prisoners while he is far from dominating all features of the prison world and while he must put down his therapeutic indications. The ambulatory anaesthesia in prison environment does not guarantee full security for the patient. Procedures could be set up between hospital complexes, caretakers practicing within penal middle (Unit of Consultation and Ambulatory Care [UCAC]) the prison service and hospital, the prefecture, to identify possible ambulatory interventions for a patient prisoner and to set up all guarantees of patient follow-up care in his return in prison environment. The development of interregional secure hospital units (ISHU) within teaching hospitals, allows an easier realization of interventions to the prisoners, but exists only in seven teaching hospitals in France.

[Obstructive lung diseases in a French prison: results of systematic screening]. / Dépistage de l'asthme et de la bronchopneumopathie obstructive à la maison d'arrêt d'Amiens: étude préliminaire transversale.

BACKGROUND: French prisoners have health problems that have been inadequately treated before imprisonment. This population has insufficient access to the healthcare system. Addictive behaviours, particularly smoking, are widespread. The aim of the study is to evaluate the prevalence of airflow limitation by using a primary care screening method adapted for the correctional facility and its inmates. METHOD: The screening of airflow limitation using a mobile spirometer is carried out in inmates consulting the primary care unit (UCSA) of Amiens prison. Patients consulting the UCSA between 16 August and 17 October 2006 and providing their consent are included in the study. The criteria for exclusion are: a counter-indication for spirometry, poor compliance with the effort of forced expiry after eight efforts, as well as refusal to take part in the study. The descriptive statistical analysis includes all of the quantitative and qualitative variables. RESULTS: Among the 210 patients included in the sample, only five patients refused to take part in the study. Their mean age was 37 (range: 16-65) and 90% were men. Ninety percent of this population were active smokers. Sixty percent of these smokers would like to quit. The spirometry detected 11% undiagnosed airflow limitation: 11 prisoners suffered from chronic obstructive lung disease and 13 prisoners suffered from asthma. DISCUSSION: Given the relative youth and high risk nature of these diagnosed patients, the potential for the long or short term aggravation, and a growing recognition of the seriousness of exposure to tobacco, the authors suggest that the systematic screening of inmates for airflow limitation may be used to assist in detecting serious health issues. Along with new French antismoking legislation, this screening may enable primary care workers to better reduce smoking habits in prisons.

Increased erythropoietin synthesis in patients with COLD or left heart failure is related to alterations in renal haemodynamics.

The mechanisms controlling erythropoietin (EPO) synthesis by the kidney in patients with chronic obstructive lung disease (COLD) or congestive left heart failure (CLHF) remain incompletely understood. Renal dysfunction occurs as a consequence of decreased renal blood flow (RBF) in these diseases. Because alterations in renal haemodynamics may affect EPO synthesis and red blood cell production, we investigated the potential relationships between renal function and plasma EPO synthesis in patients with COLD or CLHF. Thirty-two patients with COLD and 13 with CLHF underwent determination of renal physiology parameters, plasma EPO levels and haemoglobin levels. Plasma EPO concentrations were increased in patients with COLD or CLHF as compared to normal subjects, and were inversely correlated to haemoglobin concentrations. In patients with COLD or CLHF, plasma EPO was negatively correlated with both RBF and renal oxygen delivery (ROD) and positively correlated with filtration fraction. Plasma EPO was not correlated with glomerular filtration rate, fractional excretion of sodium, PO2 or PCO2. Among the patients with COLD, those with polycythemia (haemoglobin > 150 g L-1) had lower plasma EPO and higher RBF and ROD values than those with normocythemia (haemoglobin < or = 150 g L-1). Taken together, our data suggest that in patients with COLD or CLHF the critical determinant for EPO production is impairment of renal haemodynamics.

Polycythemia impairs vasodilator response to acetylcholine in patients with chronic hypoxemic lung disease.

To investigate whether polycythemia associated with chronic hypoxemic lung disease (CHLD) increases vascular resistance by altering endothelium-derived nitric oxide (NO), we examined the responses to acetylcholine (ACh) infusions (5, 10, and 15 mg/min) on hemodynamics and gas exchange in 21 patients with CHLD of varying severity. Patients were classified into two groups based on whether their hemoglobin (Hb) level was less or greater than 15.5 g/dl. In the normocythemic patients (Hb = 13.6 +/- 0.3 g/100 ml, n = 10), ACh decreased pulmonary artery pressure (Ppa) from 30 +/- 2 mm Hg 26 +/- 2 mm Hg (p < 0.01); pulmonary vascular resistance (PVR), from 5.1 +/- 0.4 U/m2 to 3.4 +/- 0.3 U/m2 (p < 0.001); systemic arterial pressure (Psa), from 111 +/- 4 mm Hg to 108 +/- 4 mm Hg (p < 0.05); and systemic vascular resistance (SVR), from 27 +/- 2 U/m2 to 22 +/- 2 U/m2 (p < 0.01); and also increased the cardiac index (CI), from 3.8 +/- 0.2 to 4.7 +/- 0.3 L/min/m2 (p < 0.001). PaO2 fell from 59 +/- 3 mm Hg to 48 +/- 3 mm Hg (p < 0.001) whereas venous admixture (Qs/Qt) rose from 32 +/- 4% to 44 +/- 4% (p < 0.01). In contrast, in patients with polycythemia (17.7 +/- 0.5 g/100 ml, n = 11) ACh failed to produce any changes in PaO2 (49 +/- 2 mm Hg versus 51 +/- 2 mm Hg, p = NS), Ppa (34 +/- 1 mm Hg versus 33 +/- 1 mm Hg, p = NS), PVR (6.7 +/- 0.9 U/m2 versus 6.9 +/- 0.8 U/m2, p = NS) or Psa, but slightly increased the CI, from 3.6 +/- 0.3 L/min/m2 to 3.9 +/- 0.3 L/min/m2 (p < 0.01), and Qs/Qt, from 40 +/- 4% to 45 +/- 3% (p < 0.05). In the 21 patients, negative correlations with Hb concentrations were found for ACh-induced changes in PVR (r = -0.57, p < 0.01), Ppa (r = -0.46, p < 0.01), CI (r = -0.5, p < 0.05), PaO2 (r = -0.79, p < 0.01), and Qs/Qt (r = -0.79, p < 0.01). In the six polycythemic patients who received isovolemic hemodilution, with a decrease in Hb concentration from 18.6 +/- 0.9 g/dl to 15.3 +/- 0.3 g/dl as a result, infusion of ACh, which was without effect before hemodilution, caused decreases in Ppa from 28 +/- 1 mm Hg to 23 +/- 1 mm Hg (p < 0.05) and in PVR from 5.7 +/- 0.8 U/m2 to 3.6 +/- 0.5 U/m2 (p < 0.02), as well as an increase in CI from 3.4 +/- 0.4 L/min/ m2 to 4.1 +/- 0.4 L/min/m2 (p < 0.05). In contrast to ACh, inhaled NO (40 ppm) induced pulmonary vasodilation in both the normocythemic and polycythemic groups. Our results show that high hematocrit (Hct) levels inhibit endothelium-dependent vasodilation in response to ACh in patients with CHLD, possibly through inactivation of endothelial-derived NO by Hb.

Intrapericardial fibrinolysis: a useful treatment in the management of purulent pericarditis.

Since the introduction of antibiotics into clinical practice, purulent pericarditis has become a rare disease. The major complication of the standard management for this condition is constrictive pericarditis. We report two cases of purulent pericarditis in which intrapericardial fibrinolysis was performed in order to minimize this complication. The first case was a 38-year-old man admitted to our intensive care unit (ICU) for management of constrictive pericarditis complicating purulent pericarditis diagnosed 17 days previously. The patient was treated with four intrapericardial injections of streptokinase (250,000 IU each). Fluid drainage and cardiac output were improved. No change in clotting parameters was noted. Pericardiectomy and esophagectomy were then performed for a diagnosis of esophageal neoplasm. The postoperative course was uneventful. The second case was a 16-year-old boy admitted with loss of consciousness due to cardiac tamponade. Percutaneous pericardiocentesis drained 900 ml of cloudy fluid. Two intrapericardial injections were performed (day 1 and day 5) without any complication. Pericardial drainage was withdrawn on day 13 and the patient was discharged from ICU on the same day. Six months later, there was no evidence of constrictive pericarditis. Intrapericardial fibrinolysis appears to be safe and effective when prescribed rapidly in the course of purulent pericarditis.

Lack of a relationship of elastin peptide level to emphysema assessed by CT scans.

Clinical reports suggest that peptide (EP) concentration may be used as a subclinical marker of pulmonary emphysema. This hypothesis was tested in a clinical study by comparing EP concentration in male emphysematous patients with the level in two control groups, and by exploring the relation of elastin peptide level to high-resolution computed tomography (HRCT) scan emphysema score among emphysematous patients. Serum EP level was determined among male emphysematous patients with at least 20% of emphysema (n = 27) and in two populations of male workers, drawn from epidemiologic studies (227 coal miners and 310 policemen). No difference in elastin peptide concentration was observed between emphysematous patients and control subjects (mean +/- SD = 2.39 +/- 1.18 micrograms/ml in patients versus 2.55 +/- 1.34 micrograms/ml in policemen and 2.59 +/- 1.20 micrograms/ml in coal miners). The correlation of elastin peptide concentration with percentage of pulmonary emphysema was negative and of borderline significance (r = -0.36; p = 0.06). These results cast doubts on the usefulness of elastin peptide level as a predictive marker of pulmonary emphysema.

Epidurual pneumatosis: a benign complication of benign pneumomediastinum.

Subcutaneous emphysema and pneumomediastinum are well-known complications of barotrauma. There are no fascial barriers between the posterior mediastinum and the retropharyngeal and epidural spaces; thus, air can diffuse freely to the epidural space and produce an epidural pneumatosis. We report a case of epidural pneumatosis caused by a pneumomediastinum following nasotracheal intubation for an attempted suicide. This benign complication of air leakage was easily recognized on computed tomography (CT) scan.

Intravenously administered atrial natriuretic factor in patients with COPD. Effects on ventilation-perfusion relationships and pulmonary hemodynamics.

The potent pulmonary vasodilating property of atrial natriuretic factor (ANF) may alter gas exchange in patients with COPD. We examined the hemodynamic and gas exchange responses to intravenous infusion of ANF (0.01 and 0.03 ng/min/kg body weight) in eight stable patients with COPD studied during spontaneous breathing, using the inert gas elimination technique. When compared with baseline, ANF infusion was associated with a dose-dependent decrease in pulmonary artery pressure (from 27.3 +/- 2.5 to 23.9 +/- 1.8 and 20.2 +/- 1.7 mm Hg, respectively) and a dose-dependent increase in blood flow perfusing poorly ventilated and unventilated units (VA/Q < 0.1: from 5.80 +/- 2.05 to 7.25 +/- 2.5 and 12.0 +/- 5.4 percent of total blood flow, respectively; p = 0.02). However, PaO2 remained unchanged (70.2 +/- 3.6, 68.1 +/- 3.8 65.4 +/- 3.5 mm Hg, respectively) because of a significant increase in minute ventilation (VE) from 8.6 +/- 0.8 to 9.6 +/- 0.8 and 10.3 +/- 0.7 L/min (p < 0.002). Six additional COPD patients receiving intravenously administered ANF at the same dosages were studied during controlled mechanical ventilation using right heart catheterization. In these patients, pulmonary vasodilation was associated with a significant increase in venous admixture (from 12.7 +/- 2.4 to 14.4 +/- 2.9 and 17.5 +/- 3.5 percent of total blood flow, respectively; p < 0.02), and a dose-dependent reduction in arterial PO2 (from 117 +/- 17 to 110 +/- 15 and 96.4 +/- 8.8 mm Hg, respectively; p < 0.05). The present results show that ANF infusion is associated with alterations in the VA/Q relationship in patients with COPD. However, a decrease in arterial oxygenation may be prevented by an increase in VE.

[Resistance of Streptococcus pneumoniae to penicillin. "Bacteriological" resistance/"clinical" resistance]. / La résistance de Streptococcus pneumoniae à la pénicilline résistance "bactériologique"/résistance "clinique".

From January 1988 to December 1992, 143 Streptococcus pneumoniae strains have been isolated at a significant level from 136 patients hospitalized in the pulmonary care unit of CHI Créteil. The clinical presentations were: 83 pneumonia (P), 48 acute bronchitis (B) and 12 colonizations (C). Fourteen strains were found to be penicillin resistant (MIC > 0.125 mg. l-1): 11 P, 2 B, 1 C. Two patients were lost of view after the beginning of the treatment: a pneumonia (Serotype 23F, MIC = 2 mg. l-1) and a bronchitis (Serotype 23F, MIC = 2 mg. l-1). Treatment was pristinamycine for one and amoxicilline alone or associated to clavulanic acid for the other 13. We observed the failure of the treatment in two. A pneumonia (Serotype 23, MIC = 2 mg. l-1) was treated before hospitalization by josamycine (3 days), then cefpodoxime (4 days) and amoxicillin-clavulanic acid (1.5 gr/d during 7 days). Healing was obtained with the increase to 3 gr/d. The other failure was a pneumonia without improvement after 11 days with 3 gr/d of amoxicilline. The treatment was stopped during 5 days and a protected brushing was performed. A Streptococcus Pneumoniae (Serotype 23F, MIC = 8 mg. l-1) was isolated. The clinical status rapidly improved with erythromycine (3 gr/d) to which the strain was susceptible. "Bacteriological" Resistance to penicillin is demonstrated (10 percent in our sample, 17 percent in France during 1991). However amoxicillin to a sufficient dosage is still enough ("Clinical" Resistance < 1 percent in our sample) for the treatment of respiratory infections except when the MIC is at a high level.

Weaning criteria from mechanical ventilation.

Although the majority of mechanically-ventilated patients can be rapidly transferred to spontaneous breathing, a substantial minority of them develop difficulties during weaning attempts, prolonging the length of hospital stay and increasing the risk of complications. Inversely, excessively early weaning and extubation increase the morbidity of ventilated patients. It is, therefore, essential to be able to determine the ideal time of weaning for each patient, more particularly for those likely to develop difficulties. Various clinical and laboratory criteria of weaning, or, more precisely, predictive factors of weaning, may therefore help the intensive care physician to precisely evaluate the suitability of disconnecting a patient from a ventilator. Many of the classical criteria used are frequently inaccurate in predicting the outcome of weaning, and new criteria have been described and designed to be more objective and discriminant in predicting the suitability of weaning. The authors make a critical review and analyse the limitations of these different criteria.

Role of atrial natriuretic factor in impaired sodium excretion of normocapnic and hypercapnic patients with chronic obstructive lung disease.

To investigate the mechanisms of sodium retention in patients with chronic obstructive lung disease (COLD), we examined the renal and hormonal responses to volume expansion with isotonic saline and to infusion of atrial natriuretic factor (ANF) in 10 hypercapnic (PaCO2 52 +/- 2 mm Hg) and 12 normocapnic patients (PaCO2 39 +/- 1 mm Hg). Sodium excreted within 4 h of loading (expressed as % sodium load) was 23.5 +/- 2.5% (p < 0.05) in normocapnic and 8.5 +/- 1.5% (p < 0.001) in hypercapnic patients, compared with 32.5 +/- 3.0% in 11 age-matched control subjects. Sodium excretion and renal blood flow correlated negatively with arterial PCO2 and positively with FEV1. Basal plasma ANF concentrations were 72 +/- 5 pg/ml in controls, 100 +/- 14 pg/ml in normocapnic patients, and 230 +/- 52 pg/ml in hypercapnic patients (p < 0.001). Plasma renin activity and aldosterone did not differ between groups. In response to volume expansion, plasma ANF increased in both normocapnic and controls (with a greater increase in normocapnic patients) but remained unchanged in hypercapnic patients. Exogenous ANF increased glomerular filtration rate, renal plasma flow, natriuresis, and diuresis in both groups of patients. Patients with COLD have depressed renal function that appears unrelated to activation of the renin-angiotensin-aldosterone system. An increased secretory response of ANF to volume expansion may help to maintain volume homeostasis in normocapnic patients, while a blunted secretory response of ANF may contribute to sodium retention in hypercapnic patients.

Hemodynamic and gas exchange responses to infusion of acetylcholine and inhalation of nitric oxide in patients with chronic obstructive lung disease and pulmonary hypertension.

To investigate endothelium-dependent and endothelium-independent nitric oxide (NO) mediated pulmonary vasodilation in patients with chronic obstructive lung disease (COLD), we examined the responses to incremental infusion rates of acetylcholine (ACh) or inhaled NO on hemodynamic and gas exchange. In 13 patients, ACh (15 mg/min) decreased pulmonary artery pressure (Ppa) from 31 +/- 1 to 28 +/- 1 mm Hg (p < 0.01) and systemic arterial pressure while increasing cardiac index from 3.7 +/- 0.4 to 4.7 +/- 0.4 L/min/m2 (p < 0.01). Inhaling 40 parts per million (ppm) NO decreased Ppa from 32 +/- 1 to 26 +/- 1 mm Hg (p < 0.001) with no associated hemodynamic change. ACh reduced PaO2 from 57 +/- 3 to 48 +/- 2 mm Hg (p < 0.01) and increased venous admixture (QVA/QT) from 35 +/- 3 to 45 +/- 3% (p < 0.01). Inhaling 40 ppm NO increased PaO2 from 57 +/- 3 to 60 +/- 3 mm Hg (p < 0.01) and decreased QVA/QT from 36 +/- 3 to 32 +/- 3% (p < 0.01). Pulmonary vascular resistance changes were similar in response to 40 ppm NO or 15 mg/min ACh. In COLD patients, ACh produces both pulmonary and systemic vasodilation but impairs arterial oxygenation whereas inhaled NO induces selective pulmonary vasodilation while improving gas exchange. The resistance to ACh in some patients could be related to pulmonary endothelial dysfunction.

[The quality of oxygen therapy delivery systems using oxygen-saving valves. A multicenter study. The ANTADIR Medico-Technical Commission]. / Qualité de l'oxygénothérapie délivrée avec les valves économiseuses d'oxygène. Une étude multicentrique. Commission médico-technique ANTADIR.

The saturation of oxygen (SaO2) using oxygen therapy with an oxygen saving system, Optimox (CFPO) or COS 5 (Puritan, Bennett) has been compared to the SaO2 using continuous oxygen therapy. The oxygen output using the oxygen saving system was regulated in such a way as to be equivalent to the oxygen flow without the economiser. Three situations were studied: the day, the night and during effort. Ninety four patients (84 men and 10 women), aged 65.3 +/- 9.7), who were hypoxaemic (SaO2: 84.5 +/- 6.4%) coming from twelve pneumology units were included in the study. The percentage of time spent above SaO2 (T greater than 90) was used to judge the criteria of the efficacy of the oxygen therapy. T greater than 90 without (SSECO) and with the oxygen saving system (AVECO) were compared in each subject. T greater than 90 AVECO was below T greater than 90 SSECO in 52% of patients and was greater in 23% of subjects. The nasal, auditory and respiratory comfort was good whatever the period of examination for more than half of the subjects. In conclusion for an equivalent oxygen flow the addition of an oxygen saving device significantly alters the quality of diurnal and nocturnal oxygen therapy in one patient out of two.

Determinants of immediate survival among chronic respiratory insufficiency patients admitted to an intensive care unit for acute respiratory failure. A prospective multicenter study. The French Task Group for Acute Respiratory Failure in Chronic Respiratory insufficiency.

In this study, 322 patients were evaluated with two aims: determination of identifiable factors at the time of admission to an ICU that predict short-term survival. Application of the SAPS to this population. Characteristics of patients were as follows: age, 65.5 +/- 14.5 years; COLD, 45 percent; restrictive, 13.4 percent; obstructive and restrictive CRI, 13 percent; asthma progressing to CRI, 11.2 percent; diffuse bronchiectasis, 7.2 percent; neuromuscular diseases, 2.2 percent; others, 8 percent. Cachectic patients, those confined to home, those with initial coma or those who required MV had a higher percentage of M. The SAPS at admission was higher in those patients who died; however, there was no link between the SAPS and M. Prognostic factors in ARF complicating CRI and identifiable at the time of admission to an ICU are few and reflect severity of chronic respiratory disease; SAPS appears to be less useful in ARF complicating CRI.

Plasma levels of atrial natriuretic factor, renin activity, and aldosterone in patients with chronic obstructive pulmonary disease. Response to O2 removal and to hyperoxia.

To examine the interrelations between humoral systems involved in the circulatory and body fluid volume homeostasis of patients with chronic obstructive pulmonary disease (COPD), we measured plasma levels of renin activity (PRA), aldosterone (Aldo), and atrial natriuretic factor (ANF) in 14 patients with stable COPD who used continuous O2 therapy. Hemodynamics, blood gases, and plasma hormone levels were measured (1) while patients received supplemental O2; (2) after 30 min O2 discontinuation; and (3) after a 30-min period of 96% O2 breathing. Plasma immunoreactive ANF concentrations were 196 +/- 50 pg/ml during O2 breathing and were positively related to transmural pulmonary arterial wedge pressure (tPpaw, r = 0.90, p less than 0.001) and to PaCO2 (r = 0.57, p less than 0.02). Compared to normal subjects matched for age and sex, patients had higher plasma ANF levels (196 +/- 52 versus 72 +/- 6 pg/ml, p less than 0.01), similar PRA (2.1 +/- 0.5 versus 1.3 +/- 0.3 ng/ml/h, NS), and slightly lower plasma Aldo (98 +/- 17 versus 156 +/- 19 pg/ml, p less than 0.05). Discontinuation of O2 while decreasing PaO2 from 70 +/- 3 to 50 +/- 3 mm Hg resulted in a significant increase in pulmonary arterial pressure (Ppa) from 29 +/- 2 to 32.5 +/- 3 mm Hg (p less than 0.01) and cardiac index (Cl) from 3.6 +/- 0.1 to 3.9 +/- 0.1 L/min/m2 (p less than 0.01) and a decrease in systemic arterial pressure (Psa) from 96 +/- 3 to 91 +/- 2 mm Hg (p less than 0.05); transmural cardiac filling pressures and pulmonary vascular resistance (PVR) were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)