Bruno Bissonnette

Duchenne muscular dystrophy: an old anesthesia problem revisited

Patients with Duchenne and Becker muscular dystrophy suffer from a progressive deterioration in muscle secondary to a defect in the dystrophin gene. As such, they are susceptible to perioperative respiratory, cardiac and other complications, such as rhabdomyolysis. Inhalational anesthetic agents have been implicated as a cause of acute rhabdomyolysis that can resemble malignant hyperthermia (MH). This article reviews perioperative ‘MH‐like’ reactions reported in muscular dystrophy patients and groups them into three categories according to clinical presentation. The etiology and underlying pathophysiological process responsible for these reactions is discussed and recommendations are proposed for the safe anesthetic management of these patients.

Intraoperative temperature monitoring sites in infants and children and the effect of inspired gas warming on esophageal temperature.

This study tested the hypotheses that 1) temperatures of “central” sites are similar in infants and children undergoing noncardiac surgery and 2) airway heating and humidification increases distal esophageal temperature. Twenty children were randomly assigned to receive 1) active airway humidification using an airway heater and humidifier set at 37°C (N = 8), 2) passive airway humidification using a heat and moisture exchanger (N = 6), or 3) no ainvay humidification and/or heating (control, N = 6). There were no statistically significant differences between tympanic membrane, esophageal, rectal, and axillary temperatures. The temperatures of the peripheral skin surface (forearm and fingertip) were significantly lower than tympanic membrane temperature and significantly different from each other. Although esophageal and tympanic membrane temperatures in the entire group were similar, esophageal temperatures in patients receiving active and passive airway humidification were about 0.35°C above tympanic temperatures after induction of anesthesia. In contrast, esophageal temperatures in patients without airway humidification were 0.25°C below tympanic temperatures after induction of anesthesia. Esophageal-tympanic membrane temperature differences in the patients given active and passive humidification differed significantly from the corresponding sum in the control group at all times, but not from each other.

Passive or active inspired gas humidification increases thermal steady-state temperatures in anesthetized infants.

We tested the hypothesis that active and passive airway humidification minimize hypothermia in infants, but that maintaining normothermia does not decrease the duration of postoperative recovery. A circle system was used to ventilate the lungs of anesthetized, intubated infants who were randomly assigned to active airway humidification and warming with use of an MR450 Servo airway heater and humidifier set at 37°C (n = 10), passive airway humidification with use of the Humid-Vent Mini heat and moisture exchanger placed between the Y-piece of the circle and the endotracheal tube (n = 10), or no airway humidification and heating (control, n = 10). Anesthesia was induced with thiopental and maintained with isoflurane and nitrous oxide in oxygen. The relative humidity of inspired respiratory gases was ∼35% in the control group and ∼90% in the group undergoing active airway humidification. Initial inspired humidity in the passive humidification group (45%) increased to ∼80% after 1 h of anesthesia. Humidity differed significantly across groups at all times (P ≤ 0.05). Steady-state rectal temperatures (100--120 min after induction) were 36.2 ± 0.7°C in patients given active humidification and heating, 35.7 ± 0.9°C in the passively humidified group, and 35.2 ± 0.4°C in the control group (P ≤ 0.05 between each group). Recovery from general anesthesia was rapid in all patients and did not correlate with central temperature changes or type of humidification (P = NS). We conclude that heat and moisture exchangers are less effective than active heating and humidification, but significantly better than no humidification.

Awake intubation increases intracranial pressure without affecting cerebral blood flow velocity in infants

Tracheal intubation is frequently required in neonatal anaesthetic practice. Awake intubation is one method of securing the airway and in certain circumstances, for many anaesthetists, can be preferable to intubation following induction of anaesthesia. Previous studies have inferred that the elevation in anterior fontanelle pressure observed during tracheal intubation in neonates was caused by an increase in cerebral blood flow although it was never measured. In this study, direct methods were used to observe changes in the cerebral circulation. Thirteen neonates, ASA I to III (E), aged from 1 to 34 days of age were studied. Patients were randomized to receive either tracheal intubation awake or following induction of anaesthesia with thiopentone 5 mg · kg− 1 and succinylcholine 2 mg · kg−1. Heart rate, systolic arterial blood pressure, anterior fontanelle pressure, cerebral blood flow velocity (using transcranial Doppler sonography) and oxygen saturation were recorded at the following intervals: baseline (not crying), after intravenous atropine 0.02 mg · kg− 1, during laryngoscopy, immediately after insertion of the endotracheal tube, one and five minutes later. The use of atropine masked the cardiovascular responses to intubation. Whereas the change in anterior fontanelle pressure from baseline was different between the groups (P < 0.05), the cerebral blood flow velocity variables were not. The rise in anterior fontanelle pressure seen in the awake group may be attributed to a reduction of the venous outflow from the cranium thereby increasing cerebral blood volume and sub-sequently the intracranial pressure.RésuméEn anesthésie néonatale, l’intubation endotrachéale est souvent nécessaire. L’intubation éveillée est utilisée pour le maintien de la perméabilité des voies respiratoires et dans certaines circonstances, plusieurs anesthésistes la préfèrent à l’intubation sous anesthésie générale. Auparavant des études ont conclu que l’augmentation de la pression de la fontanelle antérieure observée pendant l’intubation endotrachéale du nouveau-né était due à une augmentation du débit sanguin cérébral bien qu’on ne l’ait jamais mesurée. Dans cette étude, des méthodes directes sont utilisées pour l’observation des changements de la circulation cérébrale. Treize nouveaux-nés, ASA I à III (E), âgés de I à 34 jours font partie de l’étude. Ils sont répartis au hasard pour subir une intubation endotrachéale soit éveillés, soit sous anesthésie au thiopentone 5 mg · kg− 1et à la succinykholine 2 mg · kg− 1. La fréquence cardiaque, la tension artérielle systolique, la pression de la fontanelle antérieure, la vélocité du débit sanguin cérébral (par sonographie intracrânienne au Doppler) et la saturation en oxygène sont enregistrées aux intervals suivants: ligne de base (sans pleurs de l’enfant), après atropine iv 0,02 mg· kg− 1, pendant la laryngoscopie, immédiatement après l’insertion du tube endotrachéal et une et cinq minutes plus tard. L’utilisation de l’atropine masque la réponse cardiovasculaire à l’intubation. Alors que les variations de la pression de la fontanelle antérieure mesurées différent de la ligne de base diffèrent entre les groupes (P < 0,05), les variables de la vélocité du débit sanguin cérébral ne diffèrent pas. L’élévation de la pression de la fontanelle antérieure constatée chez le groupe éveillé est possiblement attribuable à une baisse du drainage veineux intracrânien avec augmentation consécutive du volume sanguin cérébral et subséquemment de la pression intracrânienne.

Hyperkalaemia during rapid blood transfusion and hypovolaemic cardiac arrest in children

A morbidity and mortality review documented a high occurrence of hyperkalaemia in cardiac arrests associated with rapid blood transfusion, which resulted in further study. In order to simulate events during rapid blood transfusion and cardiac arrest, the central circulation was modeled as a linear one compartment, and used to simulate a child who suffered a hypovolaemic cardiac arrest and was resuscitated with rapid blood transfusion (RBT). The simulation suggested that the combination of RBT and a low cardiac output state could be associated with hyperkalaemia, if the potassium concentration in the plasma fraction of the transfused blood was ≥10 mmol · L−1. In an associated clinical study the plasma potassium concentration during cardiac arrest was documented from a retrospective review of 138 cardiac arrests in a paediatric population. Patients were divided into two groups. The RBT-group received a rapid blood transfusion during resuscitation. The non-RBT group did not receive blood during resuscitation. During cardiac arrest the plasma [K] in the non-RBT group was 5.63 ±2.39 mmol · L−1 compared with 8.23 ±1.99 mmol · L−1 in the RBT-group (P < 0.05). The hyperkalaemia during cardiac arrest in the RBT-group could be explained as a consequence of RBT to a hypovolaemic child with a low cardiac output.RésuméDans une revue de la morbidite, nous avons détecté une prévalence élevée d’ hyperkaliémie lors des arrêts cardiaques associés à des transfusions sanguines rapides (TSR). Nous avons alors utilisé un modèle unicompartimental de la circulation centrale pour simuler un cas d’enfant en choc hypovolémique réanimé à l’aide de TSR. Nous en avons conclu que si la [K+]plasma du sang transfusé était ≥10 mmol · L−1, l’utilisation de TSR combinée à un faible débit cardiaque pouvait entraîner de l’hyperkaliémie. Nous avons alors colligé rétrospectivement la kaliémie mesurée lors de 138 cas d’arrêt cardiaque chez des enfants, pour s’apercevoir quelle s’élevait à 8,23 ±1,99 mmol · I−1 chez ceux qui avaient reçu des TSR durant la réanimation alors qu’elle n’était que de 5,63 ±2,39 chez les autres (P < 0,05). Les TSR employées chez ces enfants hypovolémiques au faible débit cardiaque ont pu contribuer à l’hyperkaliémie observée lors de ‚arrêt cardiaque.

Relationship between intracranial pressure, mild hypothermia and temperature-corrected PaCO2 in patients with traumatic brain injury.

Objective: To study the effects of mild hypothermia and associated changes in temperature-corrected PaCO2 (cPaCO2) on intracranial pressure (ICP), mean velocity of the middle cerebral artery (Vm), and venous jugular saturation in O2 (SjvO2) in patients with severe traumatic brain injury (TBI).¶Design: Prospective, observational study.¶Setting: Intensive care unit.¶Patients: Severe TBI patients mechanically ventilated, sedated and paralyzed.¶Interventions: Twenty patients were subjected to four consecutive periods: (a) normocapnia-normothermia; (b) hypocapnia-normothermia, where hypocapnia was induced by an increase in minute volume; (c) hypocapnia-hypothermia, where hypocapnia was induced by hypothermia maintaining the ventilatory settings constant; (d) normocapnia-hypothermia, where normocapnia was achieved by a decrease in minute volume.¶Measurements and results: cPaCO2 was 41 ± 8 mmHg in periods 1 and 4, and 31 ± 7 mmHg in periods 2 and 3. Core temperature was 37.1 ± 0.8 °C in periods 1 and 2, and 34.1 ± 1.1 °C in periods 3 and 4. End-tidal CO2 and cPaCO2 values showed no difference between periods 1 and 4 and periods 2 and 3. ICP and Vm were dependent on cPaCO2 but independent of core temperature values. SjvO2 was related to cPaCO2 and was significantly higher during period 3 than during period 2 (P < 0.05).¶Conclusion: The decrease in ICP was similar when hypocapnia was induced by hyperventilation or as a result of hypothermia alone. The relationship between cPaCO2 and ICP might predict variations in ICP during changes in core temperature. Further studies are needed to confirm the cerebral metabolic effects of moderate hypothermia in TBI patients.

Cerebral Hyperthermia in Children after Cardiopulmonary Bypass

BACKGROUND Cerebral hyperthermia after hypothermic cardiopulmonary bypass has been poorly documented for adults and never in children. This study was designed to monitor brain temperature during and up to 6 h after cardiopulmonary bypass in infants and children. METHODS Fifteen infants and children, between 3 months and 6 yr of age, were studied. A right retrograde jugular bulb catheter was used to measure the jugular venous bulb temperature (JVBT) during the procedure and the first 6 h in the critical care unit. The temperature of the blood from the bypass machine was measured at the aorta through the cannula using an indwelling temperature probe. All data were acquired every minute. RESULTS The age of the patients ranged from 3 to 71 months (median, 15 months). The mean weight was 11.5 +/- 8.4 kg. The mean JVBT recorded at the end of cardiopulmonary bypass was 36.9 +/- 1.4 degrees C but reached 39.6 +/- 0.8 degrees C after six h (P < 0.01). The kinetics of brain rewarming was determined by the slope of the mean JVBT and corresponded to y +/- 0.006x + 37.21 (r2 = 0.97). The JVBT differed from the tympanic temperature after 200 min (P < 0.01) and the lower esophageal (P < 0.05) and rectal (P < 0.001) temperatures after 300 min. After 6 h, the tympanic, rectal, and lower esophageal temperatures were 37.8 +/- 0.9, 37.7 +/- 0.6, and 38.4 +/- 0.7 degrees C, respectively, whereas the JVBT was 39.6 +/- 0.8 degrees C (P < 0.001). However, the correlation coefficients between the JVBT and the tympanic, rectal, and esophageal temperatures were 0.98, 0. 85, and 0.97, respectively. No complications were recorded with placement of the jugular bulb catheter. CONCLUSIONS Mean JVBT was significantly increased over the mean core temperature at all times from rewarming by cardiopulmonary bypass onward. Although the lower esophageal, rectal, and tympanic temperatures correlated well with JVBT, all three failed to reflect JVBT during recovery. This observation might help to elucidate factors involved in the functional and structural neurologic injury known to occur in pediatric patients.

Cerebral Hemodynamics in Neonates and Infants Undergoing Cardiopulmonary Bypass and Profound Hypothermic Circulatory Arrest: Assessment by Transcranial Doppler Sonography

Profound hypothermic circulatory arrest (PHCA) is followed by a transient period of increased intracranial pressure and a longer period of neurophysiologic dysfunction. To investigate the effect of cardiopulmonary bypass (CPB) with PHCA on cerebral hemodynamics, we used transcranial Doppler sonography to measure cerebral blood flow velocity in 10 neonates and infants before and after PHCA. Cerebral blood flow velocity was compared before and after PHCA during normothermic cardiopulmonary bypass at the same mean arterial pressure, central venous pressure, hematocrit, and arterial carbon dioxide tension. Cerebral blood flow velocity decreased exponentially with decreasing nasopharyngeal temperature before PHCA (P < 0.05) and remained decreased after PHCA during normothermic CPB, compared with values for normothermic CPB before PHCA (P < 0.005). During normothermic CPB after PHCA, the modified cerebral vascular resistance (mm Hg-cm-s−1) was increased above values for normothermic CPB before PHCA (P < 0.05). The results of this study suggest that the observed increase in intracranial pressure during PHCA is not caused by increased cerebral perfusion, but rather that cerebral perfusion is reduced in response to a decreased demand for cerebral metabolic oxygen.

Early SjvO2 monitoring in patients with severe brain trauma.

Objective: To investigate early cerebral variables after minimal resuscitation and to compare the adequacy of a cerebral perfusion pressure (CPP) guideline above 70 mmHg, with jugular bulb venous oxygen saturation (SjvO2) monitoring in a patient with traumatic brain injury (TBI). Design: Prospective, observational study. Setting: Anesthesiological intensive care unit. Patients: 27 TBI patients with a postresuscitation Glasgow Coma Scale score less than 8. Intervention: After initial resuscitation, cerebral monitoring was performed and CPP increased to 70 mmHg by an increase in mean arterial pressure (MAP) with volume expansion and vasopressors as needed. Measurements and results: MAP, intracranial pressure (ICP), CPP, and simultaneous arterial and venous blood gases were measured at baseline and after treatment. Before treatment, 37 % of patients had an SjvO2 below 55 %, and SjvO2 was significantly correlated with CPP (r = 0.73, p < 0.0001). After treatment, we observed a significant increase (p < 0,0001) in CPP (78 ± 10 vs 53 ± 15 mmHg), MAP (103 ± 10 vs 79 ± 9 mmHg) and SvjO2 (72 ± 7 vs 56 ± 12), without a significant change in ICP (25 ± 14 vs 25 ± 11 mmHg). Conclusion: The present study shows that early cerebral monitoring with SjvO2 is critical to assess cerebral ischemic risk and that MAP monitoring alone is not sensitive enough to determine the state of oxygenation of the brain. SjvO2 monitoring permits the early identification of patients with low CPP and high risk of cerebral ischemia. In emergency situations it can be used alone when ICP monitoring is contraindicated or not readily available. However, ICP monitoring gives complementary information necessary to adapt treatment.

Airway management in children: ultrasonography assessment of tracheal intubation in real time?

BACKGROUND: Pediatric tracheal intubation requires considerable expertise and can represent a challenge to many anesthesiologists. Confirmation of correct tracheal tube position relies on direct visualization or indirect measures, such as auscultation and capnography. These methods have varying sensitivity and specificity, especially in the infant and young child. Ultrasonography is noninvasive and is becoming more readily available to the anesthesiologist. In this study, we investigated the characteristic real-time ultrasonographic findings of the normal pediatric airway during tracheal intubation and its suitability for clinical use. METHODS: Thirty healthy children with normal airways requiring tracheal intubation were studied. Ultrasonographic measurements of the pediatric airway during tracheal intubation under deep inhaled anesthesia were performed using a Sonosite Titan® (Sonosite, Bothell, WA) scanner while recording characteristic images during this process. Correct tracheal tube placement was further confirmed using auscultation and satisfactory end-tidal capnography. RESULTS: The mean (± sd) age of studied patients was 48 ± 37 mo, weight was 19.7. ± 8.6 kg and the sex ratio (m/f) was 1:2. Successful tracheal intubation was verified using the following criteria: 1) identification of the trachea and tracheal rings, 2) visualization of vocal cords, 3) widening of glottis as the tracheal tube passes through, and 4) tracheal tube position above carina and demonstration of movement of the chest wall visceroparietal pleural interface (i.e., sliding sign) after manual ventilation of the lungs. One esophageal intubation was readily recognized by visualization of the tube in the left paratracheal space. CONCLUSION: This study describes characteristic ultrasonographic findings of the pediatric airway during tracheal intubation. It suggests that ultrasonography may be useful for airway management in children.