Prosthetic valve endocarditis. The case for prompt surgical management.

Clinical and morphologic features are described in 27 patients with prosthetic valve endocarditis. The interval from valve replacement to onset of symptoms of prosthetic valve endocarditis was less than 2 months in 10 patients, longer than 2 months but less than 6 months in seven patients, and longer than 6 months in 10 patients. The most frequent infecting organism was Staphylococcus (11 patients). In nearly all patients, infection spread behind the site of attachment of the valve prosthesis and resulted in valve ring abscesses. Twenty-three of the 28 infected prostheses were partially or almost completely detached, and in 15 patients the infection destroyed the entire valve anulus, burrowing to adjacent structures in six. Despite prolonged bactericidal antibiotic therapy, bacterial cultures of prosthetic valves removed at operation or autopsy were positive in 14 patients. Standard valve replacement was attempted in nine patients. All were hospital survivors, but two of these patients evidenced rapid postoperative valve dehiscence and required a complex surgical procedure at reoperation. The 14 other surgically treated patients had almost complete destruction of the annular root, and surgical repair was achieved by complex surgical techniques. There were five postoperative deaths, but nine patients survived with no further evidence of infection (mean follow-up 34 months). All patients with early prosthetic valve endocarditis who recovered underwent this type of operative technique. Total exclusion of the infected annular root, as described, may offer in patients with extensive endocarditic lesions the only possibility to eradicate the infection and to reduce the mortality.

[Anesthesia for heart catheterization in children. Comparison of 3 techniques]. / Anesthésie pour cathétérisme cardiaque chez l'enfant: comparaison de trois techniques.

A study was carried out to compare the haemodynamic and respiratory effects, as well as the quality of recovery, of anaesthesia with ketamine, sodium gamma-hydroxybutyrate (GOH) and etomidate in children undergoing cardiac catheterization. Thirty children, mean age 48 +/- 35 months, ranked ASA 2 or 3 on account of congenital heart disease, were assigned to one of three groups (n = 10). They were given: in group E1, a 0.3 mg.kg-1 bolus of etomidate, followed by 0.1 mg.kg-1.min-1 for 10 minutes, and 0.026 mg.kg-1.min-1 thereafter; in group G2, a 50 mg.kg-1 bolus of GOH, and in group K3, a 4 mg.kg-1 bolus of ketamine followed by a continuous infusion of 0.083 mg.kg-1.min-1. The patients breathed spontaneously. Monitoring included heart rate, systolic, diastolic and mean blood pressure, pulse oximetry, and capnography. Femoral venous or arterial catheterization was performed after local anaesthesia (with no more than 2 mg.kg-1 of lidocaine). Measurements were performed before induction, and then 1, 10, 30 and 60 minutes afterwards. The quality of anaesthesia was assessed according to Steward's scale. The investigation lasted between 50 and 100 min in all three groups. There were no significant differences in haemodynamic and respiratory parameters during the investigation between the groups. Recovery was shorter and of better quality in group E1. On the opposite, 30 minutes after the end of the catheterization, all the patients in group K3 were stuporous, with 5 of them displaying involuntary movements. The patients of the other two groups reacted correctly to stimuli, but those in group G2 went back to sleep very rapidly. There were no complications.(ABSTRACT TRUNCATED AT 250 WORDS)

[Anaphylactic shock from succinylcholine, complicated by a rhabdomyolysis]. / Choc anaphylactique dû à la succinylcholine compliqué de rhabdomyolyse.

A young woman, with a contact dermatitis to nickel, experienced a life threatening anaphylaxis after induction of general anaesthesia for an emergency curettage. Hypersensitivity reaction involving IgE antibodies against succinylcholine was proven by positive skin test and radioimmunoassay detection of antibodies against succinylcholine and quaternary ammonium. After restoration of haemodynamics in a few hours, the patient had rhabdomyolysis predominant at lower left leg, which required a fasciotomy. An haemodialysis session was necessary, renal function being normalized thereafter. Several months later, the patient suffers from dysesthesia on the leg and foot. Muscular ischaemia was the consequence of the shock, the external compression due to the compression stockings probably being an additional factor.

Attenuation of the baroreceptor reflex by propofol anesthesia in the rat.

The effect of the intravenous (i.v.) short-acting anesthetic propofol on baroreflex control of heart rate (HR) was examined in normotensive rats. Propofol was infused at a fixed rate of 9 mg/kg.h immediately after a bolus dose of 10 mg/kg. Blood pressure (BP) was maintained with a plasma substitute. Conscious rats were used for comparisons. Reflex HR response were recorded after i.v. doses of the pressor agent phenylephrine and the depressor agent sodium nitroprusside. Baroreceptor reflex parameters were determined by sigmoidal computerized curve-fitting. Propofol produced tachycardia at rest and atropine increased HR only moderately. In addition, a limitation in the bradycardiac response to artificial BP increases (lower plateau) was shown. This set of data indicated a vagal depression. The sympathetic component of the baroreflex was equally affected, since the maximal tachycardia resulting from artificial BP decreases (higher plateau) was shifted toward lower values. A marked diminution of the baroreflex gain resulted from the reduced activity of both vagal and sympathetic components. The mechanism for this decrease in the baroreflex-dependent total autonomic effector output (HR range) probably reflects the interaction of propofol with the baroreceptor pathways.

Beta-adrenergic receptor function is acutely altered in surgical patients.

Catecholamine-induced desensitization of beta-adrenergic receptors resulting in hyporesponsiveness to further stimulation has been frequently reported after an increase in endogenous catecholamines. To examine the possibility of beta-adrenoceptor desensitization due to intraoperative adrenergic activation (surgical stress), the alterations of human lymphocyte beta-adrenergic receptor density and affinity observed after anesthesia and surgery were studied using (-)125I-iodocyanopindolol binding in 19 patients undergoing noncardiac surgical procedures with general anesthesia (thiopental, fentanyl, and halothane or isoflurane). In 13 patients, repeated determinations of plasma levels of norepinephrine and epinephrine showed an increase during the surgical procedure (norepinephrine +60%; epinephrine +60%); this change was not observed in the remaining patients. A significant postoperative increase in receptor density (Bmax +25%) and a significant decrease of receptor affinity for isoproterenol (IC50 +22%) were found in the patients who experienced intraoperative adrenergic activation. By contrast, no significant change in beta-receptor density or affinity was found in the patients who had normal intraoperative adrenergic activation. In addition, heart rate responses to the postoperative changes in plasma catecholamines (an index of cardiac sensitivity to agonist) were significantly attenuated in patients who experienced both intraoperative adrenergic activation and a decrease in affinity of beta-receptor for agonist, suggesting hyporesponsiveness to beta stimulation. We conclude that beta-adrenergic receptors and, consequently, beta-adrenergic responsiveness might be altered by perioperative adrenergic activation in surgical patients.

The effects of halothane on the human beta-adrenergic receptor of lymphocyte membranes.

The effects of halothane on beta-adrenergic receptor antagonist interaction were studied using the membranes of human lymphocytes as a model. Membrane preparations of lymphocytes were obtained from blood samples withdrawn from seven healthy young volunteers. Beta-receptor studies were performed using (-)125I iodocyanopindolol (125ICP) binding. Non-specific binding was determined in the presence of (-)isoproterenol. Beta-receptor density (Bmax) and the dissociation constant (KD) for 125ICP were determined from saturation curves. Beta-receptor affinity for agonists evaluated by the IC50 (the concentration of isoproterenol required to inhibit 50% of specific 125ICP binding) and the dissociation constant (KL) for isoproterenol was established from competition curves. The effect of halothane 1%, in an air oxygen mixture (oxygen fraction: 0.3) administered by tonometry during ligand membrane incubation, on beta-adrenergic receptor, was compared to that of control experiments not exposed to halothane. Halothane produced a moderate but significant decrease of Bmax (-10%) and a significant increase in non-specific binding (+30%), while KD, IC50, and KL were unchanged. The authors conclude that halothane, in vitro, decreases beta-adrenergic receptor density. This effect could be mediated by an alteration of the receptor in the membrane due to action of halothane on the lipid phase of the membrane.