[Distraction osteogenesis in the head and neck region]. / Distractieosteogenese in het hoofd-halsgebied.

Distraction osteogenesis is used in oral and maxillofacial surgery for the purpose of lengthening or widening an upper or lower jaw or to reposition the jaw to such an extent as cannot be achieved with normal osteotomy. This technique moves the parts of an osteomised bone slowly apart. Subsequently, new trabecular bone growth occurs between the separate bone parts that is then turned into bone with a normal mineralised architecture. Extraoral distractors can be fitted, activated, positioned and removed fairly easily. Distractors for intraoral placement do not cause any extraoral scars and are less burdensome in their daily use. Some distractors can impede access to the larynx and the trachea. For elective surgical procedures, the accessibility of the larynx can be judged with a laryngoscope for the induction and ending of anaesthesia. Should the intraoral or extraoral distractors form any obstruction in this process, then they should be removed. The alternatives are fibroscopic intubation and emergency tracheotomy.

Keuskamp and the Amsterdam Infant Ventilator.

At the First International Symposium on the History of Modern Anaesthesia (1982), Professor Keuskamp mentioned that the introduction of breathing machines for lung ventilation during operations had taken over 'the tiresome handwork of ventilation'. This paper traces some aspects of Keuskamp's professional career and his role in the development of the Amsterdam Infant Ventilator. In 1974, Urban and Weitzner from the State University of New York reported that the ventilator was a reliable and effective constant-volume paediatric ventilator. Other clinicians from the United States and Europe echoed this satisfactory clinical evaluation. At present, this paediatric ventilator is still in use for the initial ventilation of small infants and for the mechanical ventilation of different animal species in a variety of experimental settings.

[Physostigmine for the immediate treatment of a patient with the central anticholinergic syndrome induced by cocaine cut with atropine]. / Fysostigmine als acute behandeling van een patiënt met het centraal anticholinerg syndroom na gebruik van cocaïne versneden met atropine

A 34-year-old man was admitted in a coma after a nightlong abuse of cocaine and alcohol, whereupon he fell and convulsed at home. There was a fracture of the nose, hyperpyrexia, tachycardia and hypertension. Dry mouth and mydriasis were suggestive of anticholinergic poisoning. Physostigmine 3 mg were slowly administered intravenously, followed by complete neurological recovery and normalisation of the body temperature. There was no brain damage. Cocaine and atropine were found in the patient's urine. Several users of cocaine in various European countries have recently developed a central anticholinergic syndrome due to adulteration of cocaine with atropine. In the presence of indications for such an intoxication, physostigmine is the antidote of first choice.

[Submental intubation: surgical and anesthesiological aspects]. / Submentaal intuberen: chirurgische en anesthesiologische aspecten.

In patients with cranio-maxillofacial trauma and in corrections of cranio-facial anomalies submental intubation may be used during surgery and postoperatively. In the period June 2001-May 2002 submental intubation was performed on five patients with cranio-maxillofacial trauma and on two patients with cranio-facial anomalies (Dubowitz syndrome (LeFort II osteotomy and distraction) in one patient and cheilognathopalatoschisis (Le Fort I osteotomy and distraction) in the other). In accordance with the literature the submental intubation technique was a useful, fast and safe technique which provides a secure airway during surgery. No postoperative intubation-related complications were seen in the group of patients. It provides the surgeon with an excellent view of the operation field and permits optimal intra-operative control of the dental occlusion. Combined procedures by the surgeon and the anaesthetist must be planned beforehand.

Tramadol suppositories are less suitable for post-operative pain relief than rectal acetaminophen/codeine.

The suitability of tramadol suppositories for inclusion in our hospital formulary for the treatment of mild to moderate post-operative pain was evaluated. In an open randomized trial, rectal tramadol was compared with our standard treatment acetaminophen/codeine suppositories. We expected tramadol to be equally effective as our current standard but with fewer side effects. Forty patients were treated with either tramadol suppositories 100 mg 6 hourly (qds) or acetaminophen/codeine suppositories 1000/20 mg qds. Patients were comparable with regard to demographic data and type of surgery and anaesthesia. Post-operative pain was scored with the aid of a Visual Analogue Scale before each drug administration, at rest and during movement. Side effects, notably nausea and vomiting, were recorded by interviewing the patients and by inspecting the nursing report. There was no difference in pain scores between the two groups. The incidence of nausea and vomiting was significantly higher in the tramadol-treated (84%) than in the acetaminophen/codeine treated group (31%). The relative risk of experiencing an episode of nausea under treatment with tramadol was 2.7 (95% confidence interval: 1.3-5.3; P = 0.0001) as compared with acetaminophen/codeine. We conclude that for acute treatment of mild to moderate post-operative pain frequent nausea and vomiting makes tramadol suppositories less suitable than acetaminophen/codeine.

[Fatal arrhythmia following administration of suxamethonium in a postpartum woman subsequently found to have dystrophia myotonica]. / Fatale hartritmestoornis na toediening van suxamethonium aan een kraamvrouw die achteraf dystrophia myotonica bleek te hebben.

A 28-year-old woman died of irreversible ventricular fibrillation after administration of succinylcholine because of post partum curettage. Afterwards it became known she had undiagnosed myotonic dystrophy. She also had metabolic acidosis because of haemorrhagic hypovolaemia resulting in a probably elevated serum K+ concentration preoperatively. Succinylcholine given to patients with myotonic dystrophy may lead to life threatening hyperkalaemia and cardiac arrest. Therapy should be aimed at immediate lowering of serum K+ concentration with calcium, sodium bicarbonate and hyperventilation.

[Local anesthesia in dentistry. Additional techniques]. / Lokale anesthesie in de tandheelkunde. Additionele technieken.

Patients with insufficient coping abilities can yet be dentally treated by practising several additional techniques. Behaviour management should always be the starting point of all dental treatment strategies. In the end the administration of well selected drugs should lead, via anxiolysis, sedation or general anaesthesia, to a painfree and optimal treatable patient.

Effects of morphine and physostigmine on the ventilatory response to carbon dioxide.

BACKGROUND: It has been reported that physostigmine antagonizes morphine-induced respiratory depression, but it is not known whether this is due to a central chemoreceptor effect, an effect on the peripheral chemoreflex loop, or both. We therefore assessed the effect of morphine and physostigmine on the normoxic hypercapnic ventilatory response mediated by the central and peripheral chemoreceptors in ten alpha-chloralose-urethan-anesthetized cats. METHODS: The breath-by-breath ventilatory responses to stepwise changes in end-tidal CO2 tension were determined before (control), after administration of morphine hydrochloride (0.15 mg.kg-1) and during intravenous infusion of physostigmine salicylate (bolus of 0.05 mg.kg-1 followed by 0.025 mg.kg-1.h-1). Each response was separated into a central and a peripheral chemoreflex characterized by CO2 sensitivity (Sc and Sp), time constant, time delay, and apneic threshold (a single off-set B). RESULTS: Morphine increased B and decreased Sc and Sp (P < 0.01), but not the ratio Sp/Sc. Subsequent infusion of physostigmine decreased B (P < 0.01), without further change of Sp and Sc. Premedication with physostigmine decreased B, Sp and Sc (P < 0.01) vs. control, but not Sp/Sc. Subsequent administration of morphine decreased Sp and Sc further but increased B (P < 0.01), while Sp/Sc remained constant. CONCLUSIONS: Because morphine diminishes the Sc and Sp of the chemoreflex loop to the same extent this depressant effect is presumably due to an action on the respiratory integrating centers rather than on the peripheral and central chemoreceptors as such and is not antagonized by physostigmine. We argue that the increase in B may be due to changes in the amount of acetylcholine available in the brain and can be antagonized by physostigmine.

Behavioral and electrophysiological aspects of nitrous oxide dependence.

We examined the effect of 70% nitrous oxide (N2O) on locomotion and visual-evoked potentials (VEP) in rats. The animals exposed to N2O showed an initial decrease of locomotion, followed by development of tolerance and unaltered motor activity during N2O withdrawal. Similarly, an initial decrease of VEP amplitudes was followed by tolerance to N2O. In addition, some amplitudes (N2-P3, P3-N3, and N3-P4) exceeded the control values, indicating an increase of neuronal excitability of the visual system during a long lasting exposure to N2O. The increase of VEP amplitudes was further potentiated by cessation of this gas. The VEP latencies after initial increase, returned to normal and remained unaltered during N2O withdrawal suggesting that the speed of neurotransmission is not essentially changed during chronic exposure to N2O. However, a significant increase of neuronal excitability during chronic N2O exposure, which further increased by cessation of N2O, could be of clinical importance. Therefore, monitoring of VEP, particularly the amplitude values, may significantly improve a detection of altered neuronal excitability during anaesthesia and drug withdrawal.

Patient-controlled analgesia (PCA) leads to more postoperative pain relief, but also to more fatigue and less vigour.

This investigation evaluated patient-controlled analgesia (PCA) for subjective well-being and mood in the postoperative period in comparison with the intramuscular (im) administration of morphine given on demand. Patients scheduled for elective upper abdominal surgery were assigned at random to either PCA (n = 17) or im morphine (n = 14). The PCA group experienced significantly more pain relief and consumed more morphine than those who received im morphine. The PCA patients suffered from more fatigue and showed less vigour than the im group. Neither preoperative trait anxiety nor locus of control was associated with postoperative pain in either of the groups.

Effects of eseroline on the ventilatory response to CO2.

The effect of eseroline on the normoxic hypercapnic ventilatory response was assessed in nine alpha-chloralose-urethane-anaesthetized cats. The ventilatory responses to step changes in end-tidal PCO2 were determined before (control), during i.v. infusion of eseroline (bolus of 1.2 mg.kg-1 followed by 0.65 mg.kg-1 x h-1) and 1 h after the end of the infusion. Each response was separated into central and peripheral chemoreflexes, characterized by CO2 sensitivity, time constant, time delay and apnoeic threshold. We found that eseroline depressed ventilation by affecting both tidal volume and breathing frequency. The ventilatory response to CO2 was depressed due to a decrease in the CO2 sensitivity of peripheral chemoreceptors from 0.20 to 0.12 l.min-1 x kPa-1 and in the CO2 sensitivity of central chemoreceptors from 1.04 to 0.50 l.min-1 x kPa-1 (P < 0.01). However, the ratio of these sensitivities was not changed, like the apnoeic threshold. The depressant effect was reversed by naloxone. We conclude that the depressant effect of eseroline on ventilatory response to CO2 is mainly due to an action on the respiratory integrating centres in the brainstem rather than on the CO2 sensitivity of peripheral and central chemoreceptors.

The effects of orally active enkephalinase inhibitors on morphine withdrawal syndrome.

Considerable evidence has accumulated to suggest that intracerebroventricular administration of enkephalinase inhibitors, which do not penetrate the blood-brain barrier, significantly attenuates opioid withdrawal syndrome. Therefore, the aim of this study was to examine the effect of intraperitoneal (i.p.) administration of orally active enkephalinase inhibitors, acetorphan (2.5-20 mg kg-1) and SCH 34826 (15-120 mg kg-1). These drugs significantly decreased the severity of the naloxone precipitated withdrawal syndrome in morphine dependent rats and mice. It therefore appears that these orally active enkephalinase inhibitors are promising tools in studying modulation of opioid dependence phenomena.

Effect of aminophylline or physostigmine on recovery from nitrous oxide-enflurane anaesthesia.

If facilities for recovery are limited, shortening the recovery time from general anaesthesia is important. A comparative study on the effect of 3 mg.kg-1 aminophylline or 0.04 mg.kg-1 physostigmine on duration and quality of the recovery time from nitrous oxide-enflurane anaesthesia is presented. Three groups of 35 patients were observed, placebo being included for comparison in this double-blind study. Without treatment, recovery from nitrous oxide-enflurane inhalation anaesthesia lasted 18.8 +/- 5.80 min. Aminophylline considerably shortened the recovery time (12.06 +/- 3.52 min), whereas physostigmine did not (18.97 +/- 9.18 min). In the physostigmine group, however, a remarkably calm recovery and early return of protective reflexes was observed. Although aminophylline shortens the recovery time, due to earlier incidence of pain and other disturbances, it cannot be recommended for general improvement of recovery, whereas physostigmine clearly improves the quality of recovery from nitrous oxide-enflurane anaesthesia.

Monitoring cobalamin inactivation during nitrous oxide anesthesia by determination of homocysteine and folate in plasma and urine.

The effects of nitrous oxide-induced cobalamin inactivation on homocysteine and folate metabolism have been investigated. Plasma levels of cobalamin, folate, homocysteine, and methionine were determined in 40 patients before and after operation under nitrous oxide anesthesia (range of exposure time, 70 to 720 minutes). Twelve patients anesthetized with total intravenous anesthesia served as control subjects (range of exposure time, 115 to 600 minutes). Postoperative plasma levels of folate and homocysteine increased (p less than 0.001) up to 220% and 310%, respectively, in nitrous oxide-exposed patients, whereas plasma levels of methionine decreased (p less than 0.025). Response occurred after 75 minutes of nitrous oxide exposure. The percentage increase of plasma folate and homocysteine correlated significantly with exposure time (p less than 0.025 and p less than 0.0001, respectively). In eight patients receiving nitrous oxide anesthesia plasma homocysteine levels had not returned to preoperative levels within 1 week (p less than 0.01). Urinary excretion of folate and homocysteine increased during and after nitrous oxide exposure (p less than 0.01 and p less than 0.002, respectively) and correlated with exposure time (p less than 0.01 and p less than 0.005, respectively). It can be concluded that disturbance of homocysteine and folate metabolism by nitrous oxide develops with little delay and return to normal levels requires several days. Elevation of plasma homocysteine levels may therefore be used for monitoring nitrous oxide-induced cobalamin inactivation.

The central muscarinic transmission during anaesthesia and recovery--the central anticholinergic syndrome.

Clinically relevant aspects of the muscarinic transmission in the CNS are mentioned. This transmission depends on the action of acetylcholine (ACh) on the muscarinic receptor and has been better elucidated than the CNS-cholinergic transmission subserved by the nicotinic receptor. Sub-types of the muscarinic receptor have been demonstrated. They are involved in many functions of the CNS. Therefore, disturbance of the CNS muscarinic transmission by ACh-antagonists or lack of ACh results in a colorful but unpredictable behavioural syndrome which is known as the central anticholinergic syndrome (CAS). To a certain degree, the CAS follows all forms of general anaesthesia. It can be prevented or treated by physostigmine which can elevate ACh-levels in the CNS. Postoperative restitution of the CNS-muscarinic transmission results in appropriate behavioural functioning early recovery. Normalization of ACh in the CNS also enhances analgesia and helps to sustain adequate breathing, heart rate and cardiovascular tone.