William P. Morris

Supplementing Desflurane-remifentanil Anesthesia with Small-dose Ketamine Reduces Perioperative Opioid Analgesic Requirements

Relative large-dose intraoperative remifentanil could lead to the need for more postoperative analgesics. Intraoperative N-methyl-d-aspartate receptor antagonists, such as ketamine, decrease postoperative opioid use. We therefore tested the hypothesis that intraoperative small-dose ketamine improves postoperative analgesia after major abdominal surgery with remifentanil-based anesthesia. Fifty patients undergoing abdominal surgery under remifentanil-based anesthesia were randomly assigned to intraoperative ketamine or saline (control) supplementation. The initial ketamine dose of 0.15 mg/kg was followed by 2 &mgr;g · kg−1 · min−1. In both groups, desflurane was kept constant at 0.5 minimum alveolar anesthetic concentration without N2O, and a remifentanil infusion was titrated to autonomic responses. All patients were given 0.15 mg/kg of morphine 30 min before the end of surgery. Pain scores and morphine consumption were recorded for 24 postoperative h. Less of the remifentanil was required in the Ketamine than in the Control group (P < 0.01). Pain scores were significantly larger in the Control group during the first 15 postoperative min but were subsequently similar in the two groups. The Ketamine patients required postoperative morphine later (P < 0.01) and received less morphine during the first 24 postoperative h: 46 mg (interquartile range, 34–58 mg) versus 69 mg (interquartile range, 41–87 mg, P < 0.01). No psychotomimetic symptoms were noted in either group. In conclusion, supplementing remifentanil-based anesthesia with small-dose ketamine decreases intraoperative remifentanil use and postoperative morphine consumption without increasing the incidence of side effects. Thus, intraoperative small-dose ketamine may be a useful adjuvant to intraoperative remifentanil.

Early onset pneumonia: Risk factors and consequences in head trauma patients

BackgroundEarly onset pneumonia occurs frequently in head trauma patients, but the potential consequences and the risk factors of this event have been poorly studied. MethodsThis prospective observational study was undertaken in the surgical intensive care unit of a university teaching hospital in Clichy, France. Head trauma patients requiring tracheal intubation for neurologic reasons and ventilation for at least 2 days were studied to assess the risk factors and the consequences of early onset pneumonia. ResultsDuring a 2-yr period, 109 head trauma patients were studied. The authors found an incidence of early onset pneumonia of 41.3%. Staphylococcus aureus was the most common bacteria involved in early onset pneumonia. Patients with early onset pneumonia had a lower worst arterial oxygen tension:fraction of inspired oxygen ratio, more fever, more arterial hypotension, and more intracranial hypertension, factors known to worsen the neurologic prognosis of head trauma patients. Nasal carriage of S. aureus on admission (odds ratio, 5.1; 95% confidence interval, 1.9–14.0), aspiration before intubation (odds ratio, 5.5; 95% confidence interval, 1.9–16.4) and barbiturate use (odds ratio, 3.9; 95% confidence interval, 1.2–12.8) were found to be independent risk factors of early onset pneumonia. ConclusionsThe results suggest that early onset pneumonia leads to secondary injuries in head-injured patients. Nasal carriage of S. aureus, aspiration before intubation, and use of barbiturates are specific independent risk factors for early onset pneumonia and must be assessed to find and evaluate strategies to prevent early onset pneumonia.

Effect of body repositioning after venous air embolism. An echocardiographic study

Background Current therapy for massive venous air embolism (VAE) may include the use of the left lateral recumbent (LLR) position, although its effectiveness has been questioned. This study used transesophageal echocardiography to evaluate the effect of body repositioning on intracardiac air and acute cardiac dimension changes. Methods Eighteen anesthetized dogs in the supine position received a venous air injection of 2.5 ml/kg at a rate of 5 ml/s. After 1 min the dogs were repositioned into either the LLR, LLR 10 degrees head down (LLR‐10 degrees), right lateral recumbence, or remained in the supine position. Results Repositioning after VAE resulted in relocation of intracardiac air to nondependent areas of the right heart. Peak right ventricular (RV) diameter increase and mean arterial pressure decrease were greater in the repositioned animals compared with those in the supine position (P < 0.05). Right ventricular diameter and mean arterial pressure showed an inverse correlation (r = 0.81). Peak left atrial diameter decrease was greater in the LLR and LLR‐10 degrees positions compared with the supine position (P < 0.05). Repositioning did not influence peak pulmonary artery pressure increase, and no correlation was found between RV diameter and pulmonary artery pressure. All animals showed electrocardiogram and echocardiographic changes reconcilable with myocardial ischemia. Conclusions In dogs, body repositioning after VAE provided no benefit in hemodynamic performance or cardiac dimension changes, although relocation of intracardiac air was demonstrated. Right ventricular air did not appear to result in significant RV outflow obstruction, as pulmonary artery pressure increased uniformly in all groups and was not influenced by the relocation of intracardiac air. The combination of increased RV afterload and arterial hypotension, possibly with subsequent RV ischemia rather than RV outflow obstruction by an airlock appeared to be the primary mechanism for cardiac dysfunction after VAE.

Brain parenchyma PO2, PCO2, and pH during and after hypoxic, ischemic brain insult in dogs

OBJECTIVES 1) The investigation of fiberoptic PO2, PCO2, and pH sensor technology as a monitor of brain parenchyma during and after brain injury, and 2) the comparison of brain parenchyma PO2, PCO2, and pH with intracranial pressure during and after hypoxic, ischemic brain insult. DESIGN Prospective, controlled, animal study in an acute experimental preparation. SETTING Physiology laboratory in a university medical school. SUBJECTS Fourteen mongrel dogs (20 to 35 kg), anesthetized, room-air ventilated. INTERVENTIONS Anesthesia was induced with thiopental and maintained after intubation using 1% to 1.5% halothane in room air (FiO2 0.21). Mechanical ventilation was established to maintain end-tidal PCO2 approximately 35 torr (-4.7 kPa). Intravenous, femoral artery, and pulmonary artery catheters were placed. The common carotid arteries were surgically exposed, and ultrasonic blood flow probes were applied. A calibrated intracranial pressure probe was placed through a right-side transcranial bolt, and a calibrated intracranial chemistry probe with optical sensors for PO2, PCO2, and pH was placed through a left-side bolt into brain parenchyma. Brain insult was induced in the experimental group (n = 6) by hypoxia (FiO2 0.1), ischemia (bilateral carotid artery occlusion), and hypotension (mean arterial pressure [MAP] approximately 40 mm Hg produced with isoflurane approximately 4%). After 45 mins, carotid artery occlusion was released, FiO2 was reset to 0.21, and anesthetic was returned to halothane (approximately 1.25%). The control group (n = 5) had the same surgical preparation and sequence of anesthetic agent exposure but no brain insult. MEASUREMENTS AND MAIN RESULTS Monitored variables included brain parenchyma PO2, PCO2, and pH, which were monitored at 1-min intervals, and intracranial pressure, MAP, arterial hemoglobin oxygen saturation (by pulse oximetry), end-tidal PCO2, and carotid artery blood flow rate, for which data were collected at 15-min intervals for 7 hrs. Arterial and mixed venous blood gas analyses were done at approximately 1-hr intervals. Baseline data agreed closely with other published results: brain parenchyma PO2 of 27 +/- 7 (SD) torr (3.6 +/- 0.9 kPa); brain parenchyma PCO2 of 69 +/- 12 torr (9.2 +/- 1.6 kPa); and brain parenchyma pH of 7.13 +/- 0.09. Postcalibration data were accurate, indicating stability and durability over several hours. In six experiments, during the brain insult, brain parenchyma PO2 decreased to 16 +/- 2 torr (2.1 +/- 0.3 kPa), brain parenchyma PCO2 increased to 105 +/- 44 torr (14 +/- 5.9 kPa) (p < .05), and brain parenchyma pH decreased to 6.75 +/- 0.08 (p < .05). Intracranial pressure (ICP) remained nearly constant (baseline 16 +/- 6 to 14 +/- 5 mm Hg at the end of the brain insult). Cerebral perfusion pressure (CPP = MAP - ICP) decreased (baseline 95 +/- 15 to 28 +/- 8 mm Hg; p < .05). On release of brain insult stresses, ICP increased to 30 +/- 9 mm Hg and CPP increased to 71 +/- 19 mm Hg (p < .05). A biphasic recovery was observed for brain parenchyma pH, which had the slowest recovery of the monitored variables. On average, brain parenchyma pH gradually returned toward baseline, and was no longer significantly different from baseline 3 hrs after release of insult stresses. Brain parenchyma PCO2 continued to decrease rapidly after brain insult and then remained approximately 52 +/- 10 torr (approximately 6.9 +/- 1.3 kPa) (p < .05). Brain parenchyma PO2 increased from a minimum at the end of brain insult to a maximum of 43 +/- 17 torr (5.7 +/- 2.3 kPa) within 1.25 hrs (p < .05), and then gradually decreased to approximately 35 +/- 10 torr (approximately 4.7 +/- 1.3 kPa). Cerebral perfusion pressure gradually decreased as ICP increased 3 to 5 hrs after insult. CONCLUSIONS Intracranial chemistry probes with optical sensors demonstrated stable, reproducible monitoring of brain parenchyma PO2, PCO2, and pH in dogs for periods lasting > 8 hrs. Significant changes in brain p

Body position does not affect the hemodynamic response to venous air embolism in dogs

Current therapy for massive venous air embolism (VAE) includes the use of the left lateral recumbent (LLR) position. This recommendation is based on animal studies, conducted 50 yr ago, which looked primarily at survival. Little is known, however, about the concomitant hemodynamic response after VAE in various body positions. The purpose of this study was to investigate the hemodynamic and cardiovascular changes in various body positions after VAE. Twenty-two mechanically ventilated supine mongrel dogs received a venous air infusion of 2.5 mL/kg at a rate of 5 mL/s. One minute after the infusion, 100% oxygen ventilation was commenced and the body position of the dogs was changed to either the LLR (n = 6), the LLR with the head 10 degrees down (LLR-10 degrees; n = 6) or the right lateral recumbent (RLR; n = 5) position. Five dogs were maintained in the supine position (SUP; n = 5). One dog died in every group except in the SUP group, where all the dogs recovered. There were no significant differences among the various body positions in terms of heart rate, mean arterial pressure, pulmonary artery pressure, central venous pressure, left ventricular end-diastolic pressure, or cardiac output. The acute hemodynamic changes occurring during the first 5-15 min after VAE recovered to 80% of control within 60 min. Our data suggest that body repositioning does not influence the cardiovascular response to VAE. Specifically, our data do not support the recommendation of repositioning into the LLR position for the treatment of VAE.

Transesophageal echocardiographic study of venous air embolism following pneumomediastinum in dogs.

BackgroundContinuous venous air emboli have been detected in the inferior vena cava and smaller veins using transesophageal echocardiography in patients with positive pressure ventilation and associated pulmonary barotrauma. The authors hypothesized that gas entered the venous circulation, following dissection of small vessels at several sites in the subcutaneous or retro-peritoneal soft tissues.ObjectiveThe present study was designed to determine if a comparable venous gas embolism occurred in anesthetized dogs, after creation of a pneumomediastinum.DesignUsing transesophageal echocardiography, we observed 11 anesthetized dogs mechanically ventilated with positive end-expiratory pressure, while mediastinal air was introduced through a catheter at a rate of 0.5 ml/kg/min.ResultsA continuous stream of bubbles appeared in the inferior vena cava in 8/11 dogs (73%) after an infusion period of 280±81 min. A surge of bubbles was commonly observed following abdominal massage and was often associated with a transient decrease of end-tidal carbon dioxide tensions. In two dogs the air infusion rate was reduced to 0.25 mg/kg/min, and bubbles were detected in the inferior vena cava for as long as 16 consecutive hours.ConclusionWe conclude that in anesthetized dogs mechanically ventilated with positive end-expiratory pressure, unremitting pneumomediastinum is usually followed by continuous venous air embolism. A mechanism hypothesized for venous gas entry in the clinical condition of positive end-expiratory pressure ventilation with subcutaneous gas is suggested by this model.