[ACE-inhibition and bradykinin-mediated angioedema]. / Cas clinique. Angioedème bradykininique induit par inhibition de l'enzyme de conversion de l'angiotensine.

Angiotensin converting enzyme inhibitors (ACE-i) are the most common cause of bradykininin angioedema. These bradykinin-mediated angioedemas are sometimes confused with histamine-induced angioedema, which may cause a late diagnosis and hence poor initial management, deleterious to the patient. This report describes a patient with a bradykinin-mediated angioedema soon after the initiation of perindopril, with laryngeal involvement requiring orotracheal intubation in emergency. The diagnosis was confirmed later and the assay of the activity of the enzymes involved in the catabolism of kinins - aminopeptidase P (APP), carboxypeptidase N (CPN) and Angiotensin-Converting Enzyme (ACE) - demonstrated a decrease of activity of both APP and ACE. As the diagnosis was not made initially, the specific treatments - concentrate of C1 inhibitor or antagonist of the B2 receptor of bradykinin (Icatibant) - were not administered. Any angioedema occurring during a treatment with ACE-i should be considered as a bradykinin-mediated angioedema.

Les inhibiteurs de l'enzyme de conversion de l'angiotensine (IEC) sont la cause la plus fréquente d'angioedème bradykininique. Ceux-ci se confondent facilement avec l'angioedème histaminique, pouvant causer un retard diagnostique et donc une mauvaise prise en charge initiale, délétère pour le patient. Nous rapportons le cas d'un patient présentant un angioedème induit par le périndopril, avec une atteinte laryngée nécessitant une intubation orotrachéale en urgence. Le diagnostic a été posé a posteriori et le dosage des activités des enzymes du catabolisme des kinines - aminopeptidase P (APP), carboxypeptidase N (CPN) et enzyme de conversion de l'angiotensine (ECA) - a démontré une diminution des activités APP et ECA. Le diagnostic n'étant pas posé initialement, les traitements spécifiques - concentré de C1 inhibiteur ou antagoniste des récepteurs B2 de la bradykinine (Icatibant) - n'ont pas été administrés. Tout angioedème sous IEC doit être considéré comme un angioedème bradykininique.

Clinical Practice: Should we Radically Alter our Sedation of Critical Care Patients, Especially Given the COVID-19 Pandemics?

The high number of patients infected with the SARS-CoV-2 virus requiring care for ARDS puts sedation in the critical care unit (CCU) to the edge. Depth of sedation has evolved over the last 40 years (no-sedation, deep sedation, daily emergence, minimal sedation, etc.). Most guidelines now recommend determining the depth of sedation and minimizing the use of benzodiazepines and opioids. The broader use of alpha-2 adrenergic agonists ('alpha-2 agonists') led to sedation regimens beginning at admission to the CCU that contrast with hypnotics+opioids ("conventional" sedation), with major consequences for cognition, ventilation and circulatory performance. The same doses of alpha-2 agonists used for 'cooperative' sedation (ataraxia, analgognosia) elicit no respiratory depression but modify the autonomic nervous system (cardiac parasympathetic activation, attenuation of excessive cardiac and vasomotor sympathetic activity). Alpha-2 agonists should be selected only in patients who benefit from their effects ('personalized' indications, as opposed to a 'one size fits all' approach). Then, titration to effect is required, especially in the setting of systemic hypotension and/or hypovolemia. Since no general guidelines exist for the use of alpha-2 agonists for CCU sedation, our clinical experience is summarized for the benefit of physicians in clinical situations in which a recommendation might never exist (refractory delirium tremens; unstable, hypovolemic, hypotensive patients, etc.). Because the physiology of alpha-2 receptors and the pharmacology of alpha-2 agonists lead to personalized indications, some details are offered. Since interactions between conventional sedatives and alpha-2 agonists have received little attention, these interactions are addressed. Within the existing guidelines for CCU sedation, this article could facilitate the use of alpha-2 agonists as effective and safe sedation while awaiting large, multicentre trials and more evidence-based medicine.

Primitive Tumour of the Pulmonary Valve: Discussion of the Differential Diagnosis.

There is a paucity of information concerning cardiac tumours of the pulmonary valve due to their rarity at this location. We report a case of a 47-year-old patient suffering from haemoptysis, asthenia, and acute kidney injury (AKI). A transthoracic echocardiography (TTE) revealed a mass on the pulmonary valve. Further diagnostic investigation was completed until he exhibited worsening hemodynamic instability. This case emphasizes the lack of information regarding the management of a pulmonary valve tumour.

Preoperative frailty assessment: a review.

Elderly surgical population is growing faster than the rate of population ageing. The risk of postoperative complication is higher in this population, the type of complication and the risk indicators are different from younger patients. There is also a huge heterogeneity in the elderly population. The concept of frailty-emerges to explain these specific aspects and to risk stratify older patients. The present work intends to help the anaesthesiologist to take into account the concept of frailty at the preoperative visit. We reviewed, in the light of surgical context, the physiopathology of ageing, the definitions of frailty concept,the current existing strategies for peri-operational optimisation and the different frailty assessment tools. Our conclusions are that preoperative frailty assessment is essential in modern perioperative medicine practice and that the Edmonton Frail Scale stands out from other tools even though it cannot yet be considered as a gold standard.

Effect of epidural morphine on post-operative pulmonary dysfunction.

The effect of post-operative epidural morphine analgesia on pulmonary function was assessed after abdominal surgery and compared to conventional analgesia. In a control group, ten patients received a parenteral analgesic, non-narcotic drug. In a second group of 11 patients, epidural morphine was injected after the operation and continuous analgesia was prolonged until the 3rd post-operative day by means of repeated injections through an epidural catheter. Analgesia was tested on a visual pain scale. Pulmonary function was evaluated by measurements of blood gases, pulmonary volumes (vital capacity, by spirometry, and functional residual capacity by helium dilution technique) and forced expiratory volume in one second. Measurements were performed on the day before the operation and on the first, third and sixth post-operative days. Pain scoring documented a better analgesia in the epidural group during the post-operative period. By contrast, epidural morphine was unable significantly to improve VC, FEV1 and FRC during the post-operative course. The results suggest that pain is not an important factor of decreased post-operative pulmonary function.