Anaesthesia for the porphyric patient.
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Biomedical subjects
Publications and source records attributed to H Böhrer.
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The muscle relaxant atracurium is known to undergo extrahepatic degradation via Hofmann elimination and ester hydrolysis. The purpose of the present study was to evaluate the effects of atracurium on hepatic P450-dependent enzyme activities. Thirty-two male Sprague-Dawley rats were anaesthetized, mechanically ventilated, and randomly allocated to one of four study groups: group 1 received saline, group 2 atracurium, group 3 vecuronium, and group 4 pancuronium intravenously for a period of 3 hr. Equipotent doses of the muscle relaxants were applied; the doses had been obtained in a pilot study using evoked electromyography. At the end of the study period, the livers were removed and analyzed. All three muscle relaxants may lead to inhibition of hepatic drug metabolism. Atracurium influences hepatic P450, although it is predominantly degraded in extrahepatic tissues. Further studies are needed to evaluate the contribution of the major metabolite laudanosine to this inhibitory action.
Familial dysautonomia (Riley-Day syndrome) is a rare genetic disorder that is transmitted via an autosomal recessive gene. The disease, typically involving Jewish children, affects the central nervous system and can be characterised by pathological deficits in peripheral autonomic and sensory neurones. The signs, which begin in early childhood, include poor perception of pain and temperature, poor co-ordination of muscles, emotional crises with hypertension and profound sweating, postural hypotension, and excessive vagal reflexes. We present the case of a 1.5-year-old child who underwent general anaesthesia for gastrostomy and fundoplication because of chronic aspiration. The technique consisted of balanced anaesthesia with invasive monitoring: intra-arterial line, central venous catheter, pulse oximetry, capnography, and monitoring of urinary output, temperature, and metabolic changes. Pulmonary problems included a dramatic decrease in SaO2 during intubation, massive bronchial secretions, and a high fluid requirement. The haemodynamic parameters remained stable. In the postoperative period, pulmonary problems included severe pneumonia with variable pulmonary shunting and requiring an inspired oxygen fraction of between 0.5 and 1.0, accompanied by bronchoconstriction, atelectasis, and profuse bronchial secretions. Controlled ventilation had to be maintained for 4 days. The cardiovascular system was unstable with intermittent episodes of bradycardia, tachycardia, and hypo- or hypertension. The patient also showed signs of autonomic crises, which were treated with diazepam. Although patients with autonomic dysfunction are at high risk in the perioperative period, they can be managed safely when therapeutic efforts are optimised.
Since there will be an increase in the number of geriatric patients who undergo surgery and anesthesia over the next few years, studies comparing the effects of general and local anesthesia on cognitive functioning in elderly persons are mandatory. One hundred eleven ophthalmological patients, all over the age of 64 years, were assessed preoperatively, on the first and on the fourth postoperative day using a battery of standardized cognitive tests. Of the initial sample, 47 patients undergoing local and 54 undergoing general anesthesia completed the assessment. The performance of the patients in six tests did not change perioperatively. In both anesthesia groups, two tests revealed a cognitive deficit postoperatively, which only became evident on the first postoperative day. The two other tests showed a significant difference between the two anesthesia groups on the first postoperative day. The performance of patients with general anesthesia decreased transiently and returned to the initial levels within 3 days. We conclude from our results that postoperative cognitive deficits may occur in geriatric patients. However, general anesthesia poses no more risk to cognitive function than local anesthesia.
The clinical syndrome sepsis has been redefined recently, and the SIRS (systemic inflammatory response syndrome) concept has been developed. In the initial phase of sepsis, different mediator systems are activated finally resulting in a generalized endothelial inflammatory reaction. This reaction may lead to a vicious circle with subsequent multiple organ failure. Standard therapeutic regimen include the surgical removal of the source of sepsis, antimicrobial therapy, optimizing oxygenation, volume resuscitation, and treatment with catecholamines. Recently, new treatment modalities have become available. Replacement of antithrombin III, continuous venovenous hemofiltration, application of high doses of immunoglobulins and of low doses of hydrocortisone have been used. A monoclonal antibody against endotoxin (Centoxin) was taken from the German market in January 1993. Experimental aspects of treatment include the administration of C1 esterase inhibitor, pharmacological inhibition of nitric oxide (NO), plasmapheresis, the application of non-steroidal anti-inflammatory agents and of high-dose naloxone as well as manipulation of cytokines.
Muscle relaxants are essential in anaesthesia for neuroradiological diagnosis. In addition, neurosurgical and neurological patients often face, because of their basic illness, respiratory danger, which can increase postoperatively through the use of muscle relaxants during anaesthesia. Because of their pharmacodynamic properties and side-effects, muscle relaxants must be clearly differentiated from one another and used selectively for the different phases of anaesthesia-intubation, calmness during examination and recovery from neuromuscular block with extubation. During planned extubation in particular, no residual relaxation or danger of recurarization must exist during the recovery stage from neuromuscular block. For investigations with planned extubation, only the muscle relaxants atracurium and vecuronium with their medium-long effect should be applied. A high degree of safety is provided by neuromuscular block and especially in the recovery phase. Using relaxometers it is possible to determine individual relaxant requirements, avoid under- and overdoses, carry out an antagonism at the correct time and prevent residual relaxation situations so that respiratory insufficiency can be reliably excluded.
Pulmonary embolism must often be considered as a differential diagnosis, especially in the perioperative period. Only prompt therapeutic measures can reduce the high early mortality in the acute phase of this condition. Diagnostic and therapeutic measures are dependent on the severity of the symptoms. If pulmonary embolism is suspected, heparin is administered. In the case of cardiovascular deterioration, other measures have to be taken. Following confirmation of the diagnosis of pulmonary embolism, several thrombolytic regimens are applicable. Low-dose urokinase (bolus 250,000 U followed by 60,000-80,000 U/h) is associated with a relatively low incidence of bleeding complications. A more rapid reduction of the right ventricular afterload will be achieved via short-term thrombolysis. Newer findings suggest that bolus thrombolysis with 3 million U urokinase is as effective as 100 mg tissue plasminogen activator (rt-PA) administered over a 2-h period. When the patient is found to be in a state of shock, confirmation of the diagnosis has to be delayed. Recommendations include the bolus application of 1.5-3 million U urokinase when right ventricular decompensation is prominent or during cardiopulmonary resuscitation. In case of existing contraindications or postoperatively, low-dose urokinase treatment (bolus 250,000 U followed by 40,000-60,000 U/h, rarely up to 2,200 U/kg per hour) may be initiated when the situation is urgent and there are no treatment alternatives. Bolus application of 1-2 million U urokinase should be considered depending on the severity of the symptoms and the underlying disease. In some hospitals, alternative treatment modalities include catheter-assisted procedures with subsequent local thrombolysis and surgical embolectomy. Pathophysiological aspects as well as therapeutic options in the intensive care unit are discussed in depth. In addition to adequate oxygenation, right ventricular coronary perfusion and contractility may be maintained using various catecholamine infusions. The importance of phosphodiesterase inhibitors, mediator antagonists such as acetylsalicylic acid or ketanserin, and dilators of the pulmonary vascular bed are discussed.
The objective of the study was to assess the effects of premedication with clonidine on intraocular pressure (IOP) after the administration of succinylcholine. Fifty elderly patients undergoing ophthalmic surgery were randomly allocated to two study groups. Group 1 patients (n = 25) received clonidine, 300 micrograms p.o. In group 2 (n = 25), the benzodiazepine dipotassium clorazepate was given p.o. at a dose of 0.3 mg.kg-1. Anesthesia was induced with thiopental 3-4 mg.kg-1, alfentanil 10 micrograms.kg-1, atracurium 0.07 mg.kg-1, and succinylcholine 1 mg.kg-1. Nine IOP measurements were taken in each patient starting before premedication and ending 3 min after endotracheal intubation. In both groups, there was a decrease in IOP after induction of anesthesia with thiopental and alfentanil. Succinylcholine administration and endotracheal intubation had no further effect on IOP in the clonidine group. In group 2, succinylcholine caused an increase in IOP when compared with the post induction value. We conclude that clonidine premedication can prevent the increase in IOP following succinylcholine administration.
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The effects of pretreatment with alfentanil on intraocular pressure (IOP) were investigated in 40 patients undergoing ophthalmic surgery. Patients were randomly allocated to two study groups. Group 1 patients (n = 20) received alfentanil 15 micrograms.kg-1, vecuronium 0.01 mg.kg-1, thiopentone 3-4 mg.kg-1, and suxamethonium 1 mg.kg-1 for anaesthetic induction, whereas patients in group 2 (n = 20) received vecuronium 0.01 mg.kg-1, thiopentone 3-4 mg.kg-1, and suxamethonium 1 mg.kg-1. A total of seven measurements of intraocular pressure were taken in each patient, starting before premedication and ending after extubation of the trachea. In group 2 patients, there was an increase in IOP after endotracheal intubation. In group 1 patients, a decrease in IOP occurred which was related to the decrease in arterial blood pressure. We conclude that alfentanil pretreatment can prevent the increase in IOP following suxamethonium administration.
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The purpose of this study was to determine if a guidewire change from a pulmonary artery catheter (PAC) to a central venous catheter (CVC) poses a significant infection risk. A total of 128 consecutive cardiac surgical patients with PACs inserted in the operating room were entered into this study. Postoperatively, patients were randomly allocated to receive a double-lumen CVC, either at the initial introducer insertion site over a guidewire, or at a new site with de novo catheterization. The tips of all introducers, PACs, and CVCs were cut off, cultured, and semi-quantitatively analyzed. The results show that insertion of CVCs over a guidewire within 48 hours after initial venapuncture is no more likely to be associated with catheter colonization than is de novo percutaneous insertion at a different site. From 48 hours up to 72 hours following initial insertion of the PAC, an incidence of catheter-related infection of 35.3% was observed in the guidewire group, as opposed to 12.5% in the de novo group. It is recommended that the use of a guidewire technique for catheter replacement (PAC to CVC) is a safe alternative to de novo insertion of a CVC within 48 hours after initial insertion of the PAC. In order to minimize the potential risk of catheter-related infection and bacteremia in cardiac surgical patients, de novo catheterization beyond 48 hours after initial venapuncture is suggested.
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Acute hepatic porphyrias are inherited disorders of heme biosynthesis. A characteristic feature of acute porphyrias is the occurrence of acute attacks which are often precipitated by drugs. Many of the commonly used anaesthetic agents may trigger such a potentially lethal attack. Thus, only safe agents should be administered to predisposed patients. Recommendations given are based on results from animal experiments and on a series of anecdotal reports. Regional anaesthesia is presented as anaesthetic technique of choice. General anaesthesia should be based on a fentanyl-nitrous oxide regimen, with propofol as induction agent. In the case of an acute attack, treatment consists of glucose and haematin administration.
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