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Terminal conditions such as congenital anomalies and cancer are a significant source of infant and childhood mortality. Many terminally ill children are considered for operative procedures each year. These procedures may be palliative or elective, and the prognosis and natural course of the terminal illness play a significant role in determining the appropriateness of the surgical procedure. Providing anesthesia to a terminally ill patient is a complex task requiring an appropriate balance between adequate anesthesia and hemodynamic normality. Some children with a terminal condition will have a standing "Do-Not-Resuscitate" order that should not necessarily be reversed. Surgeons, anesthesiologists, and family members must consider a number of factors when determining the appropriateness of an operation for a dying patient, including the rights of the child.
OBJECTIVE: To evaluate the level of patient discomfort during phacoemulsification and implantation of a foldable intraocular lens (IOL) while under topical lidocaine, alone or in combination with intracameral lidocaine. DESIGN: A prospective, randomized, controlled trial. PARTICIPANTS: Between January and July 1997, a total of 162 patients (162 eyes) scheduled for cataract surgery were randomly assigned to either the placebo group (topical anesthesia with intracameral balanced salt solution [group 1, n = 81]) or the interventional group (combined topical-intracameral anesthesia [group 2, n = 81]). INTERVENTIONS: All patients underwent temporal clear corneal phacoemulsification and implantation of a foldable silicone IOL. All patients received a minimum total of five doses (two drops per dose) of 2% topical lidocaine hydrochloride. Three doses were administered before surgery into the superior and inferior cul-de-sac at 10 minutes, 5 minutes, and immediately before the initial corneal incision. One dose was administered before the commencement of phacoemulsification and another dose before implantation of the IOL. In addition, all patients received an intracameral injection immediately after entrance into the anterior chamber. Patients in group 1 received a 0.5-ml injection of balanced salt solution, and those in group 2 received a 0.5-ml injection of 1% lidocaine. MAIN OUTCOME MEASURE: A 10-point visual analogue scale was used immediately after the surgery to assess each patient's overall severity of pain intraoperatively. RESULTS: Ninety percent of patients in group 1 and 95% in group 2 assigned a score of 0 or 1 to the level of intraoperative discomfort. The mean pain score +/- 1 standard deviation for group 1 was 0.63 +/- 0.68 and for group 2 was 0.37 +/- 0.58. The difference between the pain scores for the two groups was statistically significant (P = 0.0053). A small but significant proportion (15%) of patients in group 1 expressed distress when the ciliary body was stretched or the iris was manipulated with instruments. CONCLUSION: Although topical lidocaine alone provides adequate anesthesia for phacoemulsification and implantation of a foldable IOL, combined topical and intracameral administration of lidocaine can further minimize intraoperative discomfort.
In the preparation for operation and anesthesia, as well as in the choice of drugs for premedication and actual anesthesia, the anesthesiologist should be primarily concerned about avoiding additional impairment of liver function. The result of an inquiry shows that neuroleptanalgesia is by far the most commonly used anesthetic method. In general, anesthetics that have to be detoxified in the liver microsomes are to be dispensed with. Regional anesthesia is advisable only in combination with general anesthesia. A well balanced postoperative infusion therapy is of utmost importance.
OBJECTIVE: To determine whether the routine use of supplementary intracameral lidocaine has any benefit over topical anesthesia alone when performing phacoemulsification surgery. DESIGN: A prospective single-center, randomized, double-masked, clinical trial. PARTICIPANTS: A total of 204 patients undergoing phacoemulsification surgery with lens implantation under planned topical anesthesia. METHODS: Patients were randomly allocated to receive either topical anesthesia plus 0.5 ml intracameral balanced salt solution or topical anesthesia plus 0.5 ml preservative-free 1% intracameral lidocaine. MAIN OUTCOME MEASURES: On the day after surgery, patients were asked to document the discomfort they had experienced using a visual analog scale. Intraoperative discomfort, postoperative discomfort, and discomfort caused by the microscope light were assessed. RESULTS: Multiple linear regression analysis did not show any significant relationship between the use of intracameral lidocaine and either intraoperative (P = 0.34) or postoperative (P = 0.45) pain scores. There was a small reduction in the discomfort caused by the operating microscope when intracameral lidocaine was used (P = 0.04). CONCLUSIONS: In this study, the routine use of intracameral lidocaine as a supplement to topical anesthesia was shown not to have a clinically useful role.
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Unlike adults, neonates tolerate high thoracic spinal anesthesia with minimal changes in heart rate (HR) and arterial blood pressure. To examine the potential autonomic regulatory mechanisms which may account for these findings, the relation between short-term heart rate variability (HRV) and respiratory activity was analyzed in a group of eight ASA grade II former premature infants undergoing high thoracic spinal anesthesia for inguinal hernia repairs. Quantitative measures of sympathetic (As) and parasympathetic (Ap) modulation of HR were derived. HR, arterial blood pressure, and a calibrated respiratory signal were recorded during 4.4-min stable epochs in eight subjects 1) preoperatively, 2) postincision after high thoracic spinal anesthesia, and 3) during an active sleep state in the postoperative period. Power spectral analysis of HRV and respiratory power yielded measures of low-frequency power (LFP: 0.02-0.15 Hz) and high-frequency power (HFP: 0.15-0.8 Hz). Transfer function analysis between respiratory activity and HR were used to quantify As and Ap. All subjects had successful high thoracic spinal anesthesia with highest levels ranging from C7-T4. Mean HR, blood pressure, and respiratory power did not change significantly with high thoracic spinal anesthesia. LFP and HFP both decreased significantly, whereas the LFP/HFP ratio remained stable. Group mean As and Ap both decreased, but the changes were not significant. Despite overall cardiovascular stability, HRV decreased with high thoracic spinal anesthesia, but the balance between LFP and HFP remained stable, suggesting that the reflex response to high thoracic spinal anesthesia was predominantly diminished parasympathetic modulation of cardiac function. The expected decrease in HR and blood pressure from the sympatholysis which results from high thoracic spinal anesthesia were apparently offset by withdrawal of cardiac vagal activity.
OBJECTIVES: The aim of this study was to evaluate the effect of cortical spreading depression (CSD) on the metabolic, hemodynamic, electrical and ionic properties during anesthesia as compared with the awake state. METHODS: The mitochondrial NADH redox state, reflected light, direct current (DC) potential, electrocorticography (ECoG), cerebral blood flow (CBF) and volume (CBV), and extracellular K(+) concentrations ([K(+)](e)), were measured continuously and simultaneously in real time using two unique monitoring systems that evaluate brain function. Three consecutive CSD waves were initiated using a KCl solution in both awake and anesthetized rats. RESULTS AND DISCUSSION: CSD caused typical amplitude changes: biphasic waves in reflectance, oxidation cycles in NADH, an increase in CBF, CBV and in [K(+)](e), a negative shift in DC potential and depression in ECoG. Anesthesia by equithesin decreased significantly the baseline levels of CBF and [K(+)](e), showing a reduction in oxygen supply and demand. After anesthesia, CSD significantly decreased [K(+)](e) and NADH oxidation cycles, indicating a reduction in oxygen demand and in oxygen balance, respectively. Furthermore, anesthesia reduced CSD wave frequencies by slowing the recovery period, showing a decline in energy production during brain activation, or by changing electrophysiological properties of the tissue. No changes were found in the propagation rate and in the initiation period of CSD, which may indicate that equithesin does not block CSD initiation. In addition, we found that the whole cerebral cortex reacts homogenously to CSD and that equithesin may reduce oxygen demand and energy production, which may have a protective effect on the brain exposed to pathophysiological conditions.
OBJECTIVE: To test if hypothermia, induced by a sustained pentobarbital anesthesia, in rats can reduce ventilatory demands without compromising pulmonary gas-exchange efficiency. DESIGN: Prospective study. SETTING: Research laboratory in a hospital. SUBJECTS: One group of 11 female Sprague Dawley rats. INTERVENTIONS: The rats were anesthetized with 45 mg/kg pentobarbital, tracheostomized and intubated; their femoral veins and arteries were cannulated. After surgery, anesthesia and fluid balance were maintained (10 mg/kg per h pentobarbital, and 5 ml/kg per h saline, i.v.). Rectal temperature, mean arterial blood pressure (MAP), and heart rate (HR) were continuously monitored. The respiratory variables and gas-exchange profiles were determined at 38 degrees C (normothermia), and during stepwise hypothermia at 37, 35, 33, 31 and 29 degrees C. The arterial pressure of carbon dioxide (PaCO2), pH and arterial pressure of oxygen (PaO2) during hypothermia were corrected at body temperature. MEASUREMENTS AND RESULTS: Graded systemic hypothermia, with maintained anesthesia, produced a strong correlation between reduction in the respiratory frequency and rectal temperature (r2 = 0.55; p < 0.0001; n = 66). The minute volume was significantly reduced, starting at 35 degrees C, without significant changes in the tidal volume (repeated measures of analyses of variance followed by Dunnett multiple comparisons test). No significant changes occurred in the PaCO2, pH, PaO2, hemoglobin oxygen saturation, the calculated arterial oxygen content and estimated alveolar-arterial oxygen difference during mild hypothermia (37-33 degrees C). The PaO2, however, was significantly reduced below 31 degrees C. The MAP remained stable at different levels of hypothermia, whereas HR was significantly reduced below 33 degrees C. CONCLUSIONS: Mild hypothermia in rats, induced by a sustained pentobarbital anesthesia, reduces ventilation without compromising arterial oxygenation or acid-base balance, as measured at body temperature. Theoretically, our observations in spontaneously breathing rats imply that a combination of mild hypothermia with anesthesia could be safely utilized to maintain adequate ventilation, using relatively low minute ventilation. We speculate that such a maneuver, if applied during mechanical ventilation, may prevent secondary pulmonary damage by allowing the use of lower ventilator volume-pressure settings.
In summary, HRV is a useful tool for cardiovascular risk stratification and assessment of sympathovagal balance. It has been shown to be a useful investigative tool in anesthesia to study autonomic balance and dysfunction but has limitations with regard to a depth-of-anesthesia monitor because of the confounding effects of multiple drugs and surgical stimuli. When assessing HRV, it is important to understand the limitations of the methodology. In particular, absolute power is not a surrogate of autonomic tone, but the relationship between the power in the different frequency bands may better reflect autonomic balance.
It has been estimated that approximately 30,000 patients a year suffer awareness or consciousness during anesthesia. This paper reviews existing knowledge of the psychological impact and psychiatric sequelae of awareness during anesthesia. Literature on awareness and memory during anesthesia, traumatic memory, and posttraumatic stress disorder (PTSD) was reviewed using computer searches, books, and referenced articles. Few case reports of awareness have identified the accompanying psychological trauma and resulting PTSD. Five published cases illustrating relevant material were selected for inclusion. Waking up during anesthesia, especially if the patient experienced pain, is a traumatic event which places the patient at risk for developing PTSD. Awareness-induced PTSD must be considered for patients who present for mental health treatment following surgery. The advantages of light anesthesia must be balanced against the risk of awareness-induced PTSD.
Hypothermia during general anesthesia develops with a characteristic three-phase pattern. The initial rapid reduction in core temperature after induction of anesthesia results from an internal redistribution of body heat. Redistribution results because anesthetics inhibit the tonic vasoconstriction that normally maintains a large core-to-peripheral temperature gradient. Core temperature then decreases linearly at a rate determined by the difference between heat loss and production. However, when surgical patients become sufficiently hypothermic, they again trigger thermoregulatory vasoconstriction, which restricts core-to-peripheral flow of heat. Constraint of metabolic heat, in turn, maintains a core temperature plateau (despite continued systemic heat loss) and eventually reestablishes the normal core-to-peripheral temperature gradient. Together, these mechanisms indicate that alterations in the distribution of body heat contribute more to changes in core temperature than to systemic heat imbalance in most patients. Just as with general anesthesia, redistribution of body heat is the major initial cause of hypothermia in patients administered spinal or epidural anesthesia. However, redistribution during neuraxial anesthesia is typically restricted to the legs. Consequently, redistribution decreases core temperature about half as much during major conduction anesthesia. As during general anesthesia, core temperature subsequently decreases linearly at a rate determined by the inequality between heat loss and production. The major difference, however, is that the linear hypothermia phase is not discontinued by reemergence of thermoregulatory vasoconstriction because constriction in the legs is blocked peripherally. As a result, in patients undergoing large operations with neuraxial anesthesia, there is the potential of development of serious hypothermia. Hypothermic cardiopulmonary bypass is associated with enormous changes in body heat content. Furthermore, rapid cooling and rewarming produces large core-to-peripheral, longitudinal, and radial tissue temperature gradients. Inadequate rewarming of peripheral tissues typically produces a considerable core-to-peripheral gradient at the end of bypass. Subsequently, redistribution of heat from the core to the cooler arms and legs produces an afterdrop. Afterdrop magnitude can be reduced by prolonging rewarming, pharmacologic vasodilation, or peripheral warming. Postoperative return to normothermia occurs when brain anesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. However, residual anesthesia and opioids given for treatment of postoperative pain decreases the effectiveness of these responses. Consequently, return to normothermia often needs 2-5 h, depending on the degree of hypothermia and the age of the patient.
The authors report their experience with regional anaesthesia in carotid surgery. They performed 80 carotid endarterectomies in 79 patients. Thirty-three patients were at high surgical risk because of contralateral internal carotid artery occlusion or bilateral stenosis (greater than 70%) or ischemic brain areas for past stroke. In this high risk group 4 strokes were registered in the postoperative period, while no strokes appeared in patients non at risk.
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Microdialysis of the striatum of halothane-anesthetized rats was used to study the participation of local cholinergic and GABAergic neurotransmission in NMDA receptor-modulated striatal dopamine release and metabolism. Reverse dialysis.of NMDA (1 mM) evoked a 10-fold increase in dopamine efflux and reduced DOPAC and HVA to > 20% of basal values. The effect of NMDA on dopamine efflux was abolished by atropine (10 microM) but unaffected by (+)-bicuculline (50 microM). NMDA-induced decrease in DOPAC (but not HVA) efflux was potentiated by atropine, whereas (+)-bicuculline attenuated the decrease in DOPAC and HVA. Compared to our previous studies in unanesthetised rats, our data suggest that halothane anesthesia alters the balance between NMDA-stimulated cholinergic and GABAergic influences on striatal dopamine release and metabolism. Differential sensitivity to halothane of NMDA receptors expressed by the neurones mediating these modulatory influences, or loss of specific NMDA receptor populations through voltage-dependent Mg2+ block under anesthesia, could underlie these observations.
To investigate the endocrine stress response in patients undergoing major surgery with general anesthesia using a balanced technique with sufentanil, isoflurane and midazolam up to the second postoperative day, blood levels of cortisol, epinephrine, norepinephrine, prolactin and growth hormone were determined in 68 males for elective coronary artery bypass grafting (CABG) surgery. Intraoperatively, during extracorporeal circulation none of the measured parameters were significantly increased compared to preoperative values. The endocrine response of patients with perioperative epinephrine medication (n = 32) was not significant different to patients that did not receive exogenous epinephrine (n = 36). On the evening of the day of surgery, levels of cortisol (3 fold), epinephrine (4.7 fold), norepinephrine (1.7 fold) and growth hormone (16.5 fold) were significantly increased. Compared to preoperative values levels of cortisol (3.3 fold), growth hormone (5.5 fold) and norepinephrine (1.8 fold) remained elevated up to the evening of the second postoperative day. In conclusion, the endocrine stress response in patients undergoing CABG-surgery under general anesthesia with sufentanil, midazolam, isoflurane is intraoperatively prevented by anesthesia. Although hemodilution or hormone degradation might be responsible for the lack of an increase in endocrine parameters during CPB, this study indicates that a balanced technique with isoflurane, sufentanil and midazolam is more effective in blocking the endocrine stress response than previously described anesthetic techniques. In the early postoperative period, a sharp increase in cortisol, epinephrine, norepinephrine and growth hormone occurred suggesting that the predominant endocrine stress response begins in the intensive care unit with end of anesthesia. The postoperative elevated levels of cortisol, growth hormone and norepinephrine indicate a persisting stress-response for more than two days after surgical trauma.
The physiologic effects of surgery as well as anesthesia on fluid balance have been discussed. Detailed discussions of some types of surgery and patient populations were included to clarify situations in which fluid management may be unusually difficult. Principles derived from the examination of these situations should make fluid management during the perioperative period easier.