IgE-mediated hypersensitivity to latex in childhood.

A total of 267 children scheduled to receive anesthesia during a surgical, neurosurgical, or orthopedic intervention were investigated. IgE antibodies against latex were detected in serum samples of 6.4% (17/267 children) of the patients. The most important difference between sensitized and nonsensitized children was the number of surgical interventions in the past. The median of surgical interventions was 1.0 in the nonsensitized group of children and 3.0 in the sensitized group. Only 0.9% of the children with up to two surgical interventions and 34.1% with three or more procedures were sensitized to latex. Only one of the sensitized children developed intraoperative anaphylaxis during intervention after our investigation. We conclude that children with a history of three or more surgical interventions have a high risk of sensitization to latex proteins. Nevertheless, the predictive value of IgE antibodies against latex for development of anaphylaxis during anesthesia seems to be low.

The effect of general anaesthesia on breathing patterns in elderly patients during the early post-operative period.

This study was designed to investigate the incidence of critical events in breathing following light general anesthesia compared with normal sleep during the first 12 h after transfer from the recovery room. There were no significant differences in the incidence of apnoea or desaturation episodes between normal sleep and the post-operative recovery period. There was a close correlation between the pre-operative and post-operative incidence of apnoea (r = 0.93), pre-operative and post-operative desaturation periods (r = 0.81), pre-operative and post-operative mean SpO2 values (r = 0.54) and pre-operative and post-operative minimal SpO2 values (r = 0.90) in all the patients. In the early post-operative period, breathing patterns and oxygenation were similar to those observed during normal night-time sleep in elderly patients undergoing ophthalmological surgery.

Pulmonary blood flow regulation: influence of positive pressure ventilation.

Positive pressure ventilation with PEEP has been reported to reduce hypoxic pulmonary vasoconstriction (HPV) and thus increase venous admixture. This effect was investigated in six chronically instrumented unanesthetized healthy sheep. The change in left pulmonary arterial blood flow (Qlpa, ultrasonic transit time) in response to unilateral lung hypoxia (10 min of N2 alternately to the left (LLH) and right lung (RLH) was evaluated during mechanical ventilation with and without PEEP of 10 cm H2O in comparison to spontaneous breathing. In the spontaneously breathing animal and during mechanical ventilation without PEEP, Qlpa decreased during LLH from 30% to 16% of cardiac index, during RLH it increased to 51%. With 10 cm H2O of PEEP, Qlpa showed an identical reaction to hypoxia both in the left and right lung. It is concluded that mechanical ventilation and PEEP up to 10 cm H2O does not interfere with pulmonary blood flow regulation to hypoxia.

[Allergic and pseudo-allergic reactions in anesthesia. II: Symptoms, diagnosis, therapy, prevention]. / Allergische und pseudoallergische Reaktionen in der Anästhesie. Teil II: Symptomatik, Diagnose, Therapie, Prophylaxe.

In this article we present the symptomatic features and discuss relevant diagnostic and therapeutic aspects of anaphylactoid reactions. In addition we give practical advice as to how to avoid and manage allergic or pseudoallergic reactions during anaesthesia. Measurements of serum tryptase-levels and of methylhistamine in urine have been introduced in clinical diagnostic routine. Skin tests and determination of specific antibodies are essential to identify responsible substances. Preventive measures like careful premedication, calm atmosphere, slow injection of drugs, the use of diluted solutions, and the use of drugs with a low potential for anaphylactoid reactions are important. Substances like inhalation anaesthetics, propofol, etomidate, ketamine, midazolam, fentanyl, alfentanil and bupivacain without epinephrine should be used.

[Allergic and pseudo-allergic reactions in anesthesia. I: Pathogenesis, risk factors, substances]. / Allergische und pseudoallergische Reaktionen in der Anästhesie. Teil I: Pathogenese, Risikofaktoren, Substanzen.

In this article we present a survey on the pathogenesis of allergic or pseudoallergic reactions in anaesthesia, the risk factors and the responsible substances. The incidence of anaphylactoid reactions is between 1:3500 and 1:20,000 anaesthetic cases. The estimated mortality rate amounts to 3-6%. Neuromuscular blocking drugs account for most of the cases of significant anaphylactoid reactions (59-70%). However, the incidence of latex-related reactions in increasing. Risk factors for anaphylaxis are a history of IgE-mediated drug allergy, repeated anaesthesias, atopy, hyperventilation tetany, and the use of neuromuscular blocking drugs in females. Risk factors for pseudoallergic reactions are emotional stress, atopic predisposition, increased sensitivity for histamin, hyperventilation tetany and female gender.

[Hemo- and cardiodynamic effect of nifedipine in halothane or isoflurane anesthesia. An animal experiment study]. / Hämo- und kardiodynamische Wirkung von Nifedipin unter Halothan- oder Isoflurananästhesie. Eine tierexperimentelle Studie.

OBJECTIVE: The present experimental study on 16 acutely instrumented dogs was designed to determine the haemo- and cardiodynamic changes after an intravenous infusion of nifedipine during halothane or isoflurane anaesthesia. METHODS: General anaesthesia was induced with ketamine (10 mg/kg) and fentanyl (0.02 mg/kg) and maintained with fentanyl (0.3 micrograms/kg/min), 3:1 N2O/O2 inhalation mixture, and pancuronium (300 micrograms/kg/h). A left thoracotomy was performed and a needle force probe was placed in the left ventricular wall to measure myocardial force of contraction. A Widney gauge was placed around the left ventricle to measure left ventricular circumference changes. The animals were also monitored with left ventricular tip manometers, pulmonary arterial thermodilution catheters, and femoral arterial and venous catheters. Three hours after instrumentation baseline haemodynamic measurements were performed and repeated 30 min after either halothane 0.8 vol.% (n = 8) or isoflurane 1.5 vol.% (n = 8). Then nifedipine (10 micrograms/kg i.v.) was administered and haemodynamic measurements were repeated. RESULTS: Both volatile anaesthetic agents caused a decrease in MAP, CO, LVP, LVFS, and dP/dtmax. Heart rate, CVP, PAOP, and the diastolic diameter of the heart did not change with halothane and isoflurane. Isoflurane led to a decrease of SVR that was not seen with the administration of halothane. Nifedipine during halothane anaesthesia caused a further decrease in MAP, SVR, LVP, dP/dtmax, and LVFS compared to the already reduced values with halothane alone. However, SV did not decrease any further. If nifedipine was added to isoflurane a further decrease in CO and SV was observed despite a constant SVR. CONCLUSION: Halothane, isoflurane and nifedipine are cardiac depressant drugs. Isoflurane induces vasodilation and appears to be less cardiodepressant than halothane in the clinical situation. However, if nifedipine is added, the vasodilation caused by nifedipine offsets its own negative inotropic effect and in parts the cardiac depression of halothane. Combined with isoflurane the vasodilatory effect of nifedipine is insignificant and the negative inotropic effects of both drugs are additive resulting in a profound decrease in SV and CO.

[Eicosanoids as mediators in ARDS]. / Die Eicosanoide als Mediatoren beim ARDS.

Eicosanoids partly develop from the metabolism of arachidonic acid through the cyclooxygenase or the lipoxygenase pathway. Lipoxygenase products are the leukotrienes (LTA4, LTB4, LTC4, LTD4, LTE4) and the 5-hydroxyeicosatetraenoic acid (5-HETE). Cyclooxygenase products are the prostanoids (prostaglandins [PG] D2, E2, F2, I2 and thromboxane A2). The other part of the eicosanoids develops from the metabolism of two other fatty acids over the same pathways; 8,11,14-eicosatrienoic acid leads to the prostaglandins D1, E1, F1, I1 and the leukotrienes A3, B3, C3, D3, E3. From 5,8,11,14,17-eicosapentaenoic acid result the prostaglandins D3, E3, F3, I3 and the leukotrienes A5, B5, C5, D5, E5. The pathophysiological changes in ARDS are mainly due to an imbalance of opposing effects of mediators. In this regard eicosanoids play an important role which has not yet been clearly determined. Bronchoconstriction and pulmonary hypertension are increased by thromboxane A2 and leukotrienes, whereas they are reduced by PGI2. Pulmonary edema is enlarged by leukotriene, especially, LTB4, whereas PGI2 has a protective effect. The aggregation of platelets is mediated through thromboxane A2, PGF2 and LTB4; PGE1 and PGI2 counteract these reactions. LTB4, in addition to 5-HETE, leads to the activation of inflammatory cells. Drug induced eicosanoid imbalances can be used for therapeutic interventions.

[An anaphylactic reaction under anesthesia due to a combined latex and ethylene oxide allergy]. / Anaphylaktische Reaktion unter Narkose aufgrund einer kombinierten Latex- und Athylenoxidallergie.

There is an increasing number of reports on anaphylactic reactions due to latex. We report on a 9-year-old boy who developed anaphylaxis shortly after induction of anaesthesia due to a combined latex and ethylene oxide allergy. Patients with multiple medical treatment and those with atopy seem to be at risk.

Ventilation with positive end-expiratory airway pressure causes leukocyte retention in human lung.

We examined the effect of assisted ventilation with different positive end-expiratory airway pressures (PEEP) on pulmonary leukocyte retention in humans after cardiopulmonary bypass. Eight patients who underwent heart surgery were ventilated in the postoperative phase briefly with 10 (39.6 +/- 0.9 s) and 20 cmH2O (40.3 +/- 1.0 s) PEEP. Before, during, and after this ventilatory maneuver, blood was withdrawn simultaneously from catheters placed in the pulmonary and radial arteries for blood cell differentials. At the same time points, pulmonary and systemic hemodynamics were recorded. During PEEP ventilation, there was a four- (10 cmH2O PEEP) and an eightfold (20 cmH2O PEEP) increase in mixed venous-arterial leukocyte cell difference compared with baseline. This phenomenon was based mainly on a transpulmonary cell difference of polymorphonuclear cells. Likewise, the lymphocytes were entrapped in the pulmonary vasculature during PEEP ventilation. During the ventilatory maneuver, the pulmonary blood flow was significantly reduced; it was indexed by a declined cardiac output. We conclude that PEEP ventilation in the post-operative phase after cardiopulmonary bypass causes pulmonary polymorphonuclear cell entrapment. The most likely mechanism for this phenomenon is the compression of alveolar capillaries and reduced pulmonary blood flow in response to the raised alveolar pressure.

The influence of different procedures of general anaesthesia on platelet function, coagulation and the fibrinolytic system.

We investigated whether different procedures during general anaesthesia alter platelet activation in vivo and/or activate coagulation and fibrinolysis. Forty-one healthy adult patients, scheduled for elective ophthalmic surgery under general anaesthesia, were studied with regard to changes of plasma beta-thromboglobulin (beta TG, index of platelet activation), thrombin-antithrombin III-complex (TAT, index of activation of coagulation) and d-dimer (index of fibrinolysis) during anaesthesia. The patients underwent either inhalation anaesthesia with enflurane and nitrous oxide or balanced anaesthesia with enflurane (0.5% end-tidal concentration) and alfentanil. Ten minutes after intubation the beta TG level was significantly reduced compared to the preoperative value in both general anaesthesia groups. Balanced anaesthesia caused a moderate but significant increase of TAT values at 10 min after extubation. No significant change in d-dimer levels was seen. Presuming a minimal effect of the surgical procedure on the determined variables, we conclude that none of the anaesthetic procedures induces platelet activation and fibrinolysis. The clinical relevance of the moderate coagulation activation during balanced anaesthesia remains to be investigated.

Carbon monoxide and pulmonary circulation in an ovine model.

The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output.

The effect of dopamine on pulmonary hemodynamics and tissue damage after inhalation injury in an ovine model.

Hypoxic pulmonary vasoconstriction and reduced blood flow occur as a result of smoke inhalation. The aim of this study was to investigate how the amelioration of blood flow reduction by the vasodilator dopamine affects histopathologic outcome. We exposed the left lungs of chronically instrumented sheep (n = 12) to smoke, awakened them, and studied them for 24 hours. Six hours after inhalation injury, the sheep received randomized infusions of dopamine (9 micrograms/kg/min) or equal volumes of 0.9% saline solution. Pulmonary resistance in the left lungs of animals in the group that received saline solution rose continuously throughout the study period (624 +/- 48 dyne.sec.cm-5/m2 to 1747 +/- 140 dyne.sec.cm-5/m2, baseline to 24 hours after injury). Dopamine treatment caused a significantly lower vascular resistance in the injured lung than did saline solution between 8 and 24 hours after injury. The histologic evaluation of the injured lungs showed epithelial necrosis and cast formation in both groups in addition to an increased wet/dry ratio. No difference in lung injury between the groups could be distinguished. We conclude that the amelioration of blood flow reduction by treatment with dopamine in the lungs that were exposed to smoke did not affect pulmonary damage after inhalation injury.

[Prophylactic administration of glucocorticoids prior to microlaryngoscopies?]. / Prophylaktische Glukokortikoidgabe vor Mikrolaryngoskopien?

Intravenous glucocorticoids before direct laryngoscopy? The necessity of a preventive injection of corticoids before direct laryngoscopy was determined in a prospective, double blind study. 51 patients, who underwent direct laryngoscopy under general anaesthesia, received either 250 mg methylprednisolone in 10 ml NaCl 0.9% (corticoid group) or 10 ml NaCl (NaCl group) intravenously one hour before laryngoscopy. Oedema formation and the degree of inflammation in the pharynx and hypopharynx were examined on the day prior to surgery and three to four hours postoperatively. Complications of the airways were noted in the immediate postoperative phase and at the time of the second examination. Direct laryngoscopy did not induce any significant change in oedema formation or degree of inflammation in both groups. However, there was a correlation between the duration of surgery and the degree of increase in oedema and inflammation in the NaCl group but not in the corticoid group. No difference between the groups was noted with regard to postoperative complications of the airways. Based on the present study, routine application of corticoids to prevent oedema after direct laryngoscopy cannot be recommended.

Time course of hypoxic pulmonary vasoconstriction after endotoxin infusion in unanesthetized sheep.

Endotoxin [lipopolysaccharide (LPS)] has been reported to reduce hypoxic pulmonary vasoconstriction and thus increases venous admixture. The time course of this failure of pulmonary blood flow regulation was investigated in six chronically instrumented unanesthetized sheep after infusion of Escherichia coli LPS (1 microgram/kg). The change in left pulmonary arterial blood flow (LPBF, ultrasonic transit time) in response to unilateral lung hypoxia (10 min of N2 alternately to the left and right lungs) was compared before and at various time intervals after the administration of LPS. During baseline conditions, LPBF was 33% of total cardiac output and decreased to 15% when the left lung was ventilated with a hypoxic gas mixture. One hour after endotoxin infusion, LPBF remained at 33% of total cardiac output yet only decreased to 28% during the hypoxic challenge. The response to one-lung hypoxia was still significantly depressed 10 h post-LPS administration. It is concluded that hypoxic pulmonary vasoconstriction is almost completely abolished for a prolonged time period after a small dose of LPS.

[The effect of halothane anesthesia on pulmonary circulation regulation during unilateral hypoxic ventilation]. / Einfluss einer Halothannarkose auf die pulmonale Kreislaufumstellung bei einseitiger Sauerstoffmangelatmung.

Controversies exist over the influence of inhalation anaesthesia on blood flow regulation in response to local alveolar hypoxia. This study investigates the blood flow diversion from a hypoxic to an oxygenated lung in anaesthetized and ventilated animals in comparison to unanaesthetized animals. Chronically instrumented adult ewes (n = 14, 32-45 kg) were intubated one week after surgery with a modified Carlen's tube, allowing separate ventilation of the left and right lung. In the awake state (n = 7) or after one hour of constant anaesthetic conditions (n = 7, halothane 1.6% and 2.4%), cardiac output (thermodilution) and left pulmonary blood flow (ultrasonic transit time) were evaluated. Then, under identical ventilatory conditions, the left or right lung, alternately, was rendered hypoxic for 10 min by ventilation with nitrogen. The contralateral lung was ventilated with oxygen. After 10 min, haemodynamics were again recorded. The changes in left pulmonary blood flow under unilateral lung hypoxia were similar either in the awake or the anaesthetized state. Thus, we conclude that, under these experimental conditions, halothane anaesthesia and mechanical ventilation have no influence on blood flow regulation under unilateral lung hypoxia.

Hydroxyethyl starch pretreatment in bacteremic sheep.

Live bacteria were infused in a chronic ovine lung lymph model to determine if a preceding infusion of the colloid, hydroxyethyl starch (HES), exaggerated the cardiopulmonary dysfunction or impaired removal of bacteria by macrophages in the pulmonary circulation. HES was infused (3 mL/kg/hr; n = 6) from 24 to 12 hr before the bacteria and decreased plasma protein content and increased pulmonary lymph to plasma protein concentration because of its oncotic properties. Ringer's lactate (2 mL/kg/hr) was given after stopping HES and also to the control group (n = 6). Infusion of live Ps. aeruginosa (2.5 x 10(8) Ps./min for approximately 30 min) induced equivalent pulmonary hypertension, increased pulmonary microvascular permeability, and cardiovascular depression in the two groups. The removal of bacteria in the lungs was not affected, indicating that this measurement of the function of the mononuclear phagocytic system was not impaired by the preceding HES.

[Hemo- and cardiodynamic action of halothane or isoflurane following peroral long-term pretreatment with nifedipine. An animal experimental study]. / Hämo- und kardiodynamische Wirkung von Halothan oder Isofluran nach peroraler Langzeitvorbehandlung mit Nifedipin. Eine tierexperimentelle Studie.

This study investigated the influence of chronic oral nifedipine on the hemodynamic effects of halothane or isoflurane anesthesia in dogs. Under general anesthesia with fentanyl 0.3 microgram/kg/min i.v. and 3:1 N2O/O2 inhalation mixture a left thoracotomy was performed and two needle force probes were placed in the left ventricular wall to measure myocardial force of contraction. In the halothane group (n = 12) a Hall-effect sensor was placed on the anterior surface of the left ventricle, which in combination with a magnet on the posterior surface allowed measurements of left ventricular diameter. In the isoflurane group (n = 15) a Widney gauge was placed around the left ventricle to measure left ventricular circumference changes. The dogs were also monitored with left ventricular tip manometers, pulmonary arterial thermodilution catheters, and femoral arterial and venous catheters. Prior to surgery, in the halothane group 6 dogs were pretreated with nifedipine 6 mg/kg p.o. for 10 days; the other 6 served as controls. In the isoflurane group, 8 dogs were pretreated with nifedipine in the same way and 7 served as controls. Three hours after instrumentation baseline hemodynamic measurements were performed and repeated 15 min after adding 1 MAC and then 2 MAC halothane or isoflurane. Oral pretreatment with nifedipine caused vasodilation with a significant decrease in systemic vascular resistance (SVR) and mean arterial pressure (MAP); heart rate (HR) and dp/dt max were unchanged in comparison to the control group. The cardiac output (CO) increased. Halothane (1 MAC/2 MAC) had a dose-related circulatory depressant effect. This occurred to the same extent in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)