Unsuspected concentric tracheal rings in a 14-year-old with scoliosis.

A 14-yr-old boy was first found to have tracheal stenosis when anaesthesia was induced for extensive scoliosis surgery in the prone position. There are no guidelines for airway management under these conditions. We describe how we managed the problem and suggest some useful modifications.

Preemptive analgesia in children. Does it exist?

BACKGROUND AND OBJECTIVES: Preemptive analgesia has been evident in animals, but few adult human studies exist demonstrating this concept exist, and there are fewer still in children. Caudal epidural blocks with local anesthetics are often placed for postoperative analgesia in children. This study evaluated whether these blocks are more effective when placed prior to surgical incision. METHODS: Children aged 1-6 years and ASA I and II (n = 51), undergoing elective herniorrhaphy, orchidopexy, or circumcision were randomly assigned to receive a caudal epidural block with 0.6 mL/kg of 0.25% bupivacaine with 1:200,000 epinephrine, either before incision (n = 28) or after surgery (n = 23). In all patients, anesthesia was induced and maintained with oxygen, nitrous oxide, and halothane, and caudal epidural blocks were placed. Postoperative pain was scored by a blinded observer using a Faces Pain Scale in the recovery room and was also assessed at home by the parents. Analgesic requirement during the 24-hour period was recorded. RESULTS: The Faces Pain Scale scores and analgesic requirements did not differ between the groups, either in the recovery room or at home (P > .05). CONCLUSIONS: Although preemptive analgesia has been successfully demonstrated in some earlier clinical studies, our results indicate that pre- and postincisional caudal epidural blocks with 0.25% bupivacaine were equally effective in children.

Cardiac performance preserved despite thiopental loading.

BACKGROUND: Some cerebral artery aneurysms require cardiopulmonary bypass and deep hypothermic circulatory arrest to be clipped safely. During bypass these neurosurgical patients often are given large doses of thiopental in the hope that additional cerebral protection will be provided. However, thiopental loading during bypass has been associated with subsequent cardiac dysfunction in patients with heart disease. This study was undertaken to determine how patients without concomitant heart disease would respond to thiopental loading. METHODS: Twenty-four neurosurgical patients with giant cerebral aneurysms and little or no cardiac disease were anesthetized with fentanyl, nitrous oxide, and isoflurane. Thiopental was titrated to achieve electroencephalographic burst-suppression before bypass, and the infusion was continued until after separation. Prebypass hemodynamic and echocardiographic measurements were obtained during a stable baseline and 15 min after thiopental loading began. They were repeated after bypass. RESULTS: Prebypass thiopental loading increased heart rate from 61 +/- 11 to 72 +/- 13 beats/min and decreased stroke volume from 43 +/- 10 to 38 +/- 8 ml.beat-1.m-2, but arterial and filling pressures, vascular resistance, cardiac index, and ejection fraction remained the same. Before bypass, thiopental plasma concentration measured 28 +/- 8 micrograms/ml. Loading continued for 2-3 h until after bypass was terminated, and the overall infusion rate was 18 +/- 5 mg.kg-1.h-1. All patients were easily separated from bypass without inotropic support. Following bypass, vascular resistance was decreased; heart rate, filling pressures, and cardiac index were increased; stroke volume had returned to its baseline; and ejection fraction was unchanged. CONCLUSIONS: It was concluded that if preoperative ventricular function is good, thiopental loading to electroencephalographic burst-suppression causes negligible cardiac impairment and does not impede separation from cardiopulmonary bypass.

Effect of massive intraoperative thiopental loading on cardiovascular hemodynamics and myocardial performance.

Anesthetics that protect the brain may also depress the heart. We recently anesthetized a patient with a giant cerebral aneurysm of the basilar artery who had it clipped during circulatory arrest. Thiopental loading was carried out prior to and during cardiopulmonary bypass, and we monitored transesophageal echocardiographic function and the hemodynamic profile throughout. The patient demonstrated little change in cardiovascular parameters or myocardial performance, and we conclude that the massive dose of thiopental was well tolerated.

Risk of myocardial ischaemia during anaesthesia in treated and untreated hypertensive patients.

Hypertensive patients were monitored for myocardial ischaemia during anaesthesia and surgery with the V5 lead of a standard electrocardiograph. Myocardial ischaemia was detected in 11 of 39 untreated hypertensive patients and in four of seven receiving therapy with a diuretic, but in none of 44 receiving atenolol. Fourteen of the atenolol-treated patients were receiving the drug on a long-term basis and the remaining 30 were treated acutely only on the morning of surgery. When myocardial ischaemia was observed, it was always associated with noxious stimulation and tachycardia, but a conspicuous increase in arterial pressure was not usually present. We conclude that myocardial ischaemia is prevalent during anaesthesia in untreated hypertensive patients, and that pretreatment with atenolol, but not diuretics, provides prophylaxis.

Is sufentanil removed by blood conservation devices?

To conserve blood during open heart surgery, cell savers and hemoconcentrators are used. Cell savers retrieve and filter shed blood from the operative field and then wash and separate reconcentrated erythrocytes from a supernatant by centrifugation. Hemoconcentrators are extracorporeal devices that extract an ultrafiltrate from the circulating perfusate during cardiopulmonary bypass. Both cell saver supernatant and hemoconcentrator ultrafiltrate are discarded. Twenty patients were anesthetized with a single dose of sufentanil, 30 microg/kg, and the cell saver supernatant and hemoconcentrator ultrafiltrate were analyzed for sufentanil. The supernatant contained only 0.1% of the total administered dose. Hemoconcentrators from two different manufacturers were tested, and 0.1% of the administered sufentanil was detected in one ultrafiltrate and none was found in the other. Thirty minutes after induction of anesthesia, the plasma sufentanil concentration was 8.5 ng/mL (1.3% of the given dose); 1 hour later, it was 4.9 ng/mL (0.8%). During cardiopulmonary bypass, the plasma level decreased to 2.5 ng/mL (0.6%); after bypass, it fell to 1.5 ng/mL (0.3%). It is concluded that intravenous (IV) sufentanil rapidly leaves the plasma compartment, and little remains available to be extracted by the devices used to process and conserve blood.

Global and regional myocardial blood flow and metabolism during equipotent halothane and isoflurane anesthesia in patients with coronary artery disease.

Global and regional myocardial blood flow and metabolism were examined in 20 patients with coronary artery disease before surgical stimulation. Half were anesthetized with halothane (0.8%) and half with isoflurane (1.2%). Coronary perfusion pressure decreased similarly in both groups. During halothane anesthesia coronary sinus blood flow, an index of global perfusion, decreased from an awake value of 129 +/- 7 to 97 +/- 7 ml/min (P less than 0.05), and great cardiac vein blood flow, an index of regional perfusion, decreased from 60 +/- 8 to 44 +/- 5 ml/min (P less than 0.05). In contrast, during isoflurane anesthesia global coronary blood flow increased from 131 +/- 13 to 153 +/- 16 ml/min (P less than 0.05), while regional blood flow decreased from 68 +/- 7 to 56 +/- 6 ml/min (P less than 0.05). Thus, the ratio of great cardiac vein blood flow to coronary sinus blood flow was unchanged during halothane anesthesia but decreased significantly during isoflurane. Neither global nor regional coronary vascular resistance was altered by halothane, whereas isoflurane decreased global coronary vascular resistance without affecting regional coronary vascular resistance. All patients receiving halothane had net myocardial lactate extraction. In the isoflurane group, four patients showed global lactate production and three regional lactate production. All patients demonstrating lactate production also developed electrocardiographic evidence of myocardial ischemia, which was not present before induction. The authors conclude that halothane is a preferable anesthetic to isoflurane in patients with coronary artery disease because the latter has the propensity to induce maldistribution of the coronary circulation and myocardial ischemia.

Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent.

In a non-double-blind, prospective, randomized study, the intra-operative electrocardiograms of 128 mildly hypertensive surgical patients were examined in order to determine the incidence of myocardial ischemia during anesthesia. No patient had been receiving chronic antihypertensive therapy prior to the study, but a single small oral dose of a beta-adrenergic blocking agent (labetalol, atenolol, or oxprenolol) was given to 89 of them along with premedication. Forty-four per cent of the untreated control patients and 61% of the patients pretreated with a beta-adrenergic blocking agent had normal preoperative electrocardiograms and no risk factors for coronary artery disease other than hypertension (this difference between groups was not statistically significant). During tracheal intubation and/or emergence from anesthesia, a brief, self-limited episode of myocardial ischemia was detected in 11 of 39 untreated control patients, and in two of 89 patients pretreated with a beta-adrenergic blocking agent (P less than 0.001). Tachycardia always accompanied the ischemic events, but a conspicuous increase in blood pressure did not. The authors conclude that mild hypertension, when untreated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beta-adrenergic blocking agent, given with pre-medication, can significantly reduce that risk.

Propranolol increases oxygen utilization during hypoxia.

The effects of propranolol on whole body oxygen consumption and blood oxygen content were measured in the dog during extreme hypoxic conditions. At 9% inspired oxygen four of eight control animals died within 40 min. An identical second group was pretreated with propranolol and none died during the same hypoxic stress. Hypoxia decreased oxygen consumption in both groups, but the decrease was less in the propranolol-pretreated dogs. A second set of 16 dogs was ventilated with 10% oxygen and all animals survived. A similar, although less pronounced, effect on oxygen consumption was noted and propranolol once again lessened the hypoxia-induced decrease in oxygen consumption. With hypoxaemia, metabolic acidosis developed in all animals and the arterio-venous oxygen content difference decreased; however, propranolol lessened the acidosis and the decrease in arterio-venous oxygen content difference. We conclude that, during hypoxia, propranolol increases oxygen utilization by the tissues and this might account for better survival.

Effects of propofol on cardiovascular dynamics, myocardial blood flow and myocardial metabolism in patients with coronary artery disease.

The effects of propofol (emulsion formulation) on cardiovascular dynamics, myocardial blood flow and myocardial metabolism were studied in 12 patients scheduled for elective coronary artery bypass surgery. Measurements were performed with the patient awake, during steady-state maintenance anaesthesia with propofol 200 micrograms kg-1 min-1 at rest, and during sternotomy when the propofol was supplemented with fentanyl 10 micrograms kg-1. Propofol alone decreased mean arterial pressure and cardiac index; heart rate was increased. Myocardial blood flow and myocardial oxygen consumption were decreased by 26% and 31%, respectively. Myocardial lactate production was seen in one patient during this period. Surgical stimulation, under propofol-fentanyl anaesthesia, led to the return of arterial pressure and heart rate towards baseline; cardiac index decreased further. Myocardial blood flow and oxygen consumption increased such that they almost achieved their baseline values. Myocardial lactate production was seen in one patient. These results suggest that propofol may on occasions, lead to myocardial ischaemia in patients with coronary artery disease, but that it is able to block the sympathetic responses to surgical stimulation when combined with a suitable analgesic.

Temporary unilateral pulmonary artery occlusion: a method for controlling Swan-Ganz catheter-induced hemoptysis.

A patient undergoing mitral and aortic valve replacement suffered catheter-induced pulmonary artery trauma and massive hemoptysis during weaning from cardiopulmonary bypass. Hemorrhage ceased when the ipsilateral pulmonary artery was occluded. Forty-eight hours later the temporary band was removed, and the patient did well without further bleeding.

Propranolol premedication blunts stress response to nitroprusside hypotension.

Hypotension was induced in sixteen patients with nitroprusside during anesthesia for surgical correction of cerebral aneurysms. Eight patients were premedicated with propranolol (180 mg orally) for one day and the other eight were not. Before the start of anesthesia, the untreated patients had a mean arterial pressure of 102 +/- 3 mm Hg, a heart rate of 76 +/- 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 114 +/- 21 and 258 +/- 34 pg/ml, respectively. The propranolol-premedicated patients came to the operating room in a significantly different clinical state with a mean arterial pressure of 92 +/- 3 mm Hg, a heart rate of 71 +/- 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 76 +/- 28 and 144 +/- 28 pg/ml. During induced hypotension, plasma epinephrine and norepinephrine concentrations increased significantly in both groups (454 +/- 42 and 730 +/- 58 pg/ml in the untreated patients, 160 +/- 48 and 419 +/- 67 pg/ml in the propranolol premedicated patients), but the increase in catecholamines was significantly greater in the untreated patients. Thirty minutes after nitroprusside was discontinued, epinephrine and norepinephrine concentrations were higher than in the awake state in untreated patients and were associated with rebound hypertension and tachycardia. In contrast, in propranolol-premedicated patients, plasma epinephrine and norepinephrine concentrations decreased towards the preanesthesia values, mean arterial pressure gradually returned to the prehypotension level, and heart rate remained unchanged. This study thus demonstrates that propranolol premedication attenuates the release of catecholamines in response to nitroprusside-induced hypotension.

Influence of volume loading on intraoperative hemodynamics and perioperative fluid retention in patients with valvular regurgitation undergoing prosthetic replacement.

Preload and afterload were controlled intraoperatively in 2 groups of patients with valvular regurgitation and congestive heart failure in order to determine the effect of fluid loading on weight gain and subsequent recovery. As a part of their anesthetic management before cardiopulmonary bypass, 16 patients were given 1 liter of crystalloid with nitroprusside infused at 1 microgram/kg/min and 16 received 4 liters of crystalloid with nitroprusside at 4 micrograms/kg/min. Arterial and filling pressures were kept the same in both groups. Heart rate and vascular resistance became significantly lower and cardiac index and stroke volume significantly higher in the fluid-augmented group. The transition to cardiopulmonary bypass was smoother for the fluid-augmented patients. All patients survived, and 2 in each group were ventilated beyond 24 hours. The mean weight gain at surgery was the same in the 2 groups (3 kg). For the first 2 postoperative days, body weight remained unchanged and thereafter, both groups lost weight at 0.6 kg/day. Preoperative weight was reached on day 7 and discharge occurred on day 15, 2 kg below control. Thus, a modest operative weight gain in these patients is inevitable, benign, and independent of the volume of fluid infused before bypass.

Catheter-induced pulmonary arterial trauma: can it always be averted?

Catheter-induced pulmonary arterial hemorrhage is a serious and still recurring complication. This report describes our experience with 200 cases managed successfully by a prophylactic approach to the problem. The technique involves partial withdrawal of the pulmonary arterial catheter into a sterile protective sleeve during cardiopulmonary bypass and subsequent reinsertion when the normal circulation is restored.

Propranolol alters renin release during nitroprusside-induced hypotension and prevents hypertension on discontinuation of nitroprusside.

Ten patients who received hypotensive anesthesia for surgical correction of a cerebral aneurysm were pretreated for 1 day with propranolol. In the awake state, before start of anesthesia, mean arterial pressure was 91 +/- 3 torr and plasma renin activity 3.0 +/- 0.1 ng/ml/hr. Thirty minutes after the induction of anesthesia mean arterial pressure decreased to 79 +/- 2 torr and plasma renin activity increased to 3.5 +/- 0.1 ng/ml/hr. There was no further significant change in either measurement with surgical stimulation. During sodium nitroprusside-induced hypotension (the dose used was 0.35 +/- 0.02 mg/kg) mean arterial pressure was reduced to 53 +/- 2 torr, and plasma renin activity increased to 8.8 +/- 0.9 ng/ml/hr. Heart rate did not change. Discontinuation of sodium nitroprusside resulted in a gradual reduction of plasma renin activity to the awake level and concurrent gradual increase in mean arterial pressure to its basal anesthetic value. When compared with previous work, these results indicate that propranolol attenuates nitroprusside-induced renin release, reduces the dosage of nitroprusside required to induce hypotension, suppresses reflex tachycardia, and prevents overshoot hypertension on discontinuation of nitroprusside.

Catheter-induced pulmonary artery hemorrhage. Diagnosis and management in cardiac operations.

Three case reports describing catheter-induced pulmonary artery hemorrhage in patients having cardiac operations are presented--a 0.2% incidence of this complication. One patient exsanguinated and died, another survived after undergoing an emergency lobectomy, and the third escaped without surgical intervention. As a result of this experience and the recommendations in the literature, we have developed and describe herein a rational therapy for this highly lethal complication.