Anesth Prog 39:146-149 1992
Contemporary Anesthetic Techniques for Orthognathic Surgery Joel M. Weaver, II, DDS, PhD Section of Oral and Maxillofacial Surgery, College of Dentistry, and Department of Anesthesiology, College of Medicine, Ohio State University, Columbus, Ohio
he anesthetic management of patients having elective orthognathic surgery is dependent on a variety of factors, including the physical status of the patient, the type and anticipated duration of the surgery, and the training and experience of the surgeon, anesthesiologist, and adjunctive personnel involved in patient care. The routine preoperative evaluation and laboratory studies of the patient for general anesthesia are accomplished with special attention given to the airway and the related orofacial deformity to be corrected. Patients who have predeposited autologous blood for replacement during or after surgery should be on iron supplementation. Patients are generally encouraged to remain on most usual medications. Selection of an appropriate anesthetic plan for healthy patients should start with the type of airway. Most orthognathic surgical procedures require or at least are better accomplished via nasotracheal intubation. In the absence of unusual anticipated intubation difficulty, intubation is generally best done under general anesthesia.
berg et al1 noted a 40% decrease in whole blood loss and a 44% decrease in red cell loss utilizing double-tagged radioisotope techniques during hypotensive anesthesia for such surgery. Chan et al2 recorded a 41% decrease in blood loss utilizing 15Cr-tagged red blood cells when the mean arterial pressure (MAP) was reduced by 20%. They also calculated a 27% improvement in the relatively bloodless quality of the surgical field. Decreased blood loss reduces the incidence of transfusion of blood products, with the obvious advantages of decreased risk of transfusion reactions and associated diseases. Although Thompson and coworkers3 were able to significantly decrease operating time during total hip replacement, hypotensive anesthesia has not been shown to do that with orthognathic surgery. Risks The potential risks of hypotensive anesthesia are many, but most studies indicate that relatively few major complications occur. The majority of these are related to hypoperfusion of vital organs, especially the central nervous system (CNS), heart, kidney, and liver. Should hypoperfusion occur, significant morbidity or mortality could result. Other complications of hypoperfusion include tissue necrosis at points of pressure, such as the nasal tip from the endotracheal tube, nasogastric tube, or the esophageal stethoscope pressure, the arm from the blood pressure cuff, or the fingertip from the pulse oximeter probe. These are rarely seen during normotensive anesthesia, but the severity is magnified during induced hypotensive anesthesia. A variety of other risks include rebound hypertension, reflex tachycardia, fluid deficit or excess, and toxicity of the hypotensive drugs (eg, nitroprusside).
HYPOTENSIVE ANESTHESIA
Relatively short, uncomplicated orthognathic procedures, particularly in the mandible, do not involve significant blood loss. Longer procedures and particularly those in the maxilla have greater potential for blood loss, and thus a decision should be made, in consultation with the surgeon if possible, whether normotensive or deliberate hypotensive anesthesia is desirable. This decision should be made before entering the operating room, since it influences the selection of monitors, anesthetic drugs, and the informed consent. Benefits There are several significant benefits of intentional hypotensive anesthesia for major orthognathic surgery. Scha-
Cerebrovascular Disease. Since perfusion of the brain is maintained by an autoregulatory mechanism, it is not subject to normal fluctuations in arterial blood pressure. Normal drops in blood pressure trigger cerebral vasodilation to maintain brain perfusion. However, when the MAP falls below 50 mm Hg (or higher pressures for
Received July 1, 1991; accepted for publication September 10, 1991. Address correspondence to Dr. Joel M. Weaver, Ohio State University, College of Dentistry, 305 W. 12th Avenue, Columbus, OH 43210. © 1992 by the American Dental Society of Anesthesiology
ISSN 0003-3006/92/$6.00
146
Weaver 147
Anesth Prog 39:146-149 1992
cerebrovascular occlusive disease), autoregulation is abolished, and perfusion is dependent on blood pressure. Hypocarbia leading to arterial carbon dioxide tensions below 30 mm Hg, also inhibits autoregulation. Hyperoxia, as when ventilation occurs with 100% oxygen, may also cause a significant decrease in cerebral blood flow. The patient with preexisting cerebrovascular disease is even more likely to experience CNS damage from prolonged hypotensive anesthesia.
Coronary Artery Disease. Coronary artery perfusion is related to the MAP and the diastolic pressure, since blood flow for the heart muscle cells occurs during diastole. As the time the heart spends in diastole decreases when the heart rate increases, coronary perfusion decreases during tachycardia associated with hypotension. Myocardial oxygen consumption during tachycardia tends to increase but may be somewhat offset by the decreased inotropic response needed to empty the ventricle during afterload reduction produced by arterial dilators. Hypocapnea also produces coronary constriction. Intentional hypotensive anesthesia presents a significant risk of coronary insufficiency and myocardial ischemia. Renal Disease. Renal perfusion is determined by autoregulatory mechanisms, the autonomic nervous system, antidiuretic hormone, and aldosterone. General anesthesia abolishes autoregulation, so that perfusion is dependent on arterial blood pressure. As the systolic pressure decreases below 80 to 90 mm Hg, renal blood flow (RBF) decreases. Glomerular filtration drops at systolic pressures between 60 and 70 mm Hg, and oliguria and acute renal failure may occur if the restriction is prolonged, particularly in patients with preexisting renal disease. General anesthetics also decrease RBF independently of the blood pressure. Catecholamines released in response to induced hypotension also decrease RBF in low concentrations and decrease RBF and GFR in high concentrations. The renin-angiotension system is also actuated during hypotension and by anesthetics and causes vasoconstriction with a decrease in RBF.4 Aldosterone from the adrenal cortex and antidiuretic hormone from the pituitary further decrease urine output. Fortunately, many vasodilating hypotensive agents tend to maintain RBF by their vasodilating action. Liver Disease. Liver blood flow is not maintained by autoregulation but rather is dependent on the hepatic artery (30%) and the portal vein (70%). Catecholamines released during hypotension as well as hypoxia and acidosis may cause hepatic vasoconstriction and a decrease in perfusion.
Other Conditions. Other contraindications for intentional hypotensive anesthesia include other peripheral
vascular disease, severe anemia and hypovolemia, and
cardiomyopathy. Drugs There are a variety of drugs that can be used for hypotensive anesthesia. All have advantages and disadvantages, and none are necessarily agents of choice in many or most instances.
Potent Inhalation Anesthetics. Halothane, enflurane, and isoflurane have all been used for hypotensive anesthesia. Halothane decreases stroke volume and cardiac output. In addition to abolishing cerebral autoregulation, it sensitizes the myocardium to endogenous and exogenous epinephrine, with resulting ventricular dysrhythmias. Halothane has also a questionable association with hepatotoxicity. Enflurane not only produces myocardial depression but also significant vasodilation. High concentrations of enflurane and hypocarbia may induce seizure activity as well as elevate serum fluoride concentrations, which may approach renotoxic levels. lsoflurane has the least effect on the heart but causes significant vasodilation. Isoflurane-associated tachycardia and an increased likelihood of producing coronary steal syndrome in patients with coronary artery disease are drawbacks to its use as the sole hypotensive agent.
(3-Adrenergic Blockers. The f3-adrenergic blockers decrease heart rate, contractility, and renin release. Propranolol and other nonselective 8-blockers may cause bronchospasm and permit unopposed a-adrenergic vasoconstriction when epinephrine is released during hypotension or injected by the surgeon. Selective 31 blockers, such as the ultrashort-acting esmolol, are less likely to produce these adverse effects. Labetalol, an a blocker as well as a ,8 blocker, is an excellent hypotensive agent, but its long duration makes it less controllable than esmolol. a-Adrenergic Blockers. Drugs with a-adrenergic blocking activity produce passive vasodilation by inhibiting the vasoconstrictive a-receptors. Droperidol possesses a-blocking activity as well as antinausea and sedative properties. It may result in unopposed 8-adrenergic activity with tachycardia and hypotension when interacting with epinephrine. Its prolonged effects may slow recovery and produce an uncomfortable restless feeling postoperatively. Angiotensin-Converting Enzyme Inhibitors. Angiotension-converting enzyme (ACE) inhibitors such as enalapril block the conversion of angiotensin I to angioten-
148 Anesthesia for Orthognathic Surgery
sin II, a potent vasoconstrictor. Agents such as nitroprusside and nitroglycerin have short half-lives, and the renin that is released during hypotension has a longer half-life. Thus, the rebound hypertension that frequently occurs, especially with nitroprusside, may be due to residual renin. ACE inhibitors help reduce the severity of rebound hypertension, because they outlast the duration of the released renin.
Opioids. Fentanyl and sufentanil deepen the anesthetic state and induce mild bradycardia. Morphine also releases the vasodilator histamine and may induce bronchospasm. Opioids tend to prolong recovery and produce respiratory depression postoperatively. Ganglionic Blockers. Blockade of autonomic ganglia produces vasodilation by inhibiting sympathetic transmission. Trimethaphan produces arterial dilation as well as venous pooling. Unfortunately, parasympathetic blockade also occurs, which results in cycloplegia, mydriasis, decreased gastrointestinal motility, tachycardia, xerostomia, urinary retention, histamine release, tachyphylaxis, rebound hypertension, and decreases in hepatic, cerebral, and renal blood flow and glomerular filtration rate. Nitroprusside. Sodium nitroprusside produces direct vascular smooth muscle relaxation on resistance blood vessels and to a lesser degree on capacitance vessels. Its metabolism releases cyanide and may cause cyanide toxicity. Nitroprusside causes reflex tachycardia and rebound hypertension. At equal systolic pressure reductions, it produces more profound reductions in MAP and diastolic pressure than does nitroglycerin. Coronary ischemia is also more likely.
Nitroglycerin. Nitroglycerin produces direct relaxation of vascular smooth muscle, especially in capacitance vessels. It tends to decrease venous bleeding and causes less tachycardia compared to nitroprusside. Rebound hypertension, tachycardia, and tachyphylaxis do occur, however. A RECOMMENDED HYPOTENSIVE ANESTHETIC TECHNIQUE FOR THE HEALTHY ORTHOGNATHIC SURGERY PATIENT After a review of the chart, auscultation of the chest, and assurance of fasting status of the patient, a skin wheal of 1% lidocaine is produced, and a 16-ga intravenous catheter is placed. If the patient desires anxiolysis, conscious sedation is given with 1 mg increments of midazolam to effect. Both nostrils are sprayed with 4% cocaine or 1% phenylephrine. The patient is then taken to the operating
Anesth
Prog 39:146-149 1992
room, and the appropriate monitors are applied (electrocardiogram, automatic blood pressure monitor, and pulse oximeter). The patient is preoxygenated, and the endtidal carbon dioxide (ETCO2) monitor is checked. Fentanyl (2 gg/kg) or sufentanil (0.2 ,g/kg) is administered, followed by an induction dose of thiopental (5 mg/kg), propofol (2.5 mg/kg), or methohexital (2.5 mg/kg). Relaxation is obtained with vecuronium (0.1 mg/kg), and the patient is nasally intubated and ventilated. Bilateral breath sounds and a positive ETCO2 response assure proper placement of the nasal RAE tube or standard tube cut to 27 cm and fitted with a metal acute-angle adapter. Nitrous oxide/oxygen (65%/35%) and isoflurane are given to maintain anesthesia at normotensive levels. The patient is placed in a 20° head-up position. An appropriate dose of glucocorticosteroid and prophylactic antibiotic is given and repeated as necessary. An 18-ga nasogastric (NG) tube is placed, and auscultation of an injected air bubble confirms proper position. An esophageal stethoscope/temperature probe is also placed beside the NG tube. Both tubes are taped to the nasotracheal tube to form the same curve. The tubes are taped to the patient's head after padding with foam. The eyes are lubricated with bland ophthalmic ointment and are then taped. A foley catheter is inserted and checked for flow of urine. The surgeon injects the initial surgical site with 1% lidocaine with 1:100,000 epinephrine (up to 3,ug/kg), and incisions are begun after the appropriate preparation and draping. An infusion with fentanyl (2.5 Ag/kg/hr) or sufentanil (0.25 Ag/kg/hr) is started, and isoflurane is adjusted to moderately hypotensive levels. Tachycardia that does not respond to an increased infusion of opioid is managed with an infusion of esmolol or small incremental boluses of labetalol. Additional hypotension is attained with increases in isoflurane or by adding low-dose nitroglycerin infusion. Physiologic parameters for the major portion of the surgery consist of the following: (1) Systolic pressure between 80 and 100 mm Hg, depending on the field; (2) MAP above 60 mm Hg; (3) ETCO2 above 35 mm Hg; (4) heart rate below 100 beats/min; (5) urine output of 1 mL/kg/hr; and (6) body temperature above 35° C. Appropriate fluid management is essential. Hypotensive anesthesia can mask hypovolemia. Fluid overload can negate vasodilatory hypotensive drugs. The preoperative fluid deficit is replaced during the first 2 hr, and intraoperative needs are provided during the hour they occur. A basal crystalloid formula for hourly requirements is: 4 mL/kg/hr for the first 10 kg of body weight plus 2 mL/kg/hr for the second 10 kg, plus 1 mL/kg/hr for the remainder. A running estimation of blood loss and irrigation fluid used is recorded, and blood is replaced by three
Weaver 149
Anesth Prog 39:146-149 1992
times the volume of crystalloid. Autologous blood is not given intraoperatively unless major blood loss is encountered, since mislabeled blood could cause problems. Additional crystalloid is given if urine output is inadequate. After adequate hydration is assured, a 5-mg dose of furosemide is usually sufficient to yield adequate urine. Blood pressure must be increased and other appropriate measures taken if urine output fails to respond. When the surgery has progressed to the final stages (wiring, plating for rigid fixation, suturing), the administration of opioid and isoflurane are significantly reduced, and the patient is allowed to resume spontaneous ventilation. The patient is maintained on nitrous oxide and oxygen alone or with 0.25% or less isoflurane for the last 30 to 40 min. Intravenous lidocaine (1.5 mg/kg) may be given to prolong the anesthetic state for a few extra minutes. An intramuscular nonsteroidal antiinflammatory drug (ketorolac) is administered within the last hour for postoperative pain control. Additional small doses of morphine may be given later in the postanesthesia care unit if necessary. After several minutes of 100% oxygen administration, the patient is extubated when he or she responds to verbal commands, such as, "Open your eyes." As the endotracheal tube is withdrawn from the trachea after maximal inhalation, suction is applied to the acute-angle connector to suction blood, blood clots, and other debris from the pharynx and nose. A soft nasopharyngeal tube may be necessary if ventilation is modestly impaired. Extubation is best accomplished in the operating room where reintu-
bation or other procedures are most readily completed in an emergency. Adequate attention to small details, preparation for unexpected occurrences, and communication with the surgical team will increase the likelihood of a successful and safe anesthetic course for the orthognathic surgery patient.
REFERENCES 1. Schaberg SJ, Kelly JF, Terry BC, Posner MA, Anderson EF: Blood loss and hypotensive anesthesia in oral-facial corrective surgery. J Oral Surg 1976;34:147-156. 2. Chan W, Smith DE, Ware WH: Effects of hypotensive anesthesia in anterior maxillary osteotomy. J Oral Surg 1980;38:504-508. 3. Thompson GE, Miller R, Stevens WC, Murray WR: Hypotensive anesthesia for total hip arthroplasty: a study of blood loss and organ function (brain, heart, liver and kidney). Anesthesiology 1978;48:91-96. 4. Fukayama H, Ito H, Shimada M, Kubota Y, Fukunaga A: Effects of hypotensive anesthesia on endocrine systems in oral surgery. Anesth Prog 1989;36:175-177. 5. Anderson JA: Deliberate hypotensive anesthesia for orthognathic surgery: controlled pharmacologic manipulation of cardiovascular physiology. Int J Adult Orthodon Orthognath Surg 1986;1: 133-159. 6. Hegtvedt AK: Orthognathic surgery: intraoperative and postoperative patient care. Oral Maxillofac Surg Clin North Am 1990;2:857-868.
Contemporary Anesthetic Techniques for Orthognathic Surgery Joel M. Weaver, II, DDS, PhD Section of Oral and Maxillofacial Surgery, College of Dentistry, and Department of Anesthesiology, College of Medicine, Ohio State University, Columbus, Ohio
he anesthetic management of patients having elective orthognathic surgery is dependent on a variety of factors, including the physical status of the patient, the type and anticipated duration of the surgery, and the training and experience of the surgeon, anesthesiologist, and adjunctive personnel involved in patient care. The routine preoperative evaluation and laboratory studies of the patient for general anesthesia are accomplished with special attention given to the airway and the related orofacial deformity to be corrected. Patients who have predeposited autologous blood for replacement during or after surgery should be on iron supplementation. Patients are generally encouraged to remain on most usual medications. Selection of an appropriate anesthetic plan for healthy patients should start with the type of airway. Most orthognathic surgical procedures require or at least are better accomplished via nasotracheal intubation. In the absence of unusual anticipated intubation difficulty, intubation is generally best done under general anesthesia.
berg et al1 noted a 40% decrease in whole blood loss and a 44% decrease in red cell loss utilizing double-tagged radioisotope techniques during hypotensive anesthesia for such surgery. Chan et al2 recorded a 41% decrease in blood loss utilizing 15Cr-tagged red blood cells when the mean arterial pressure (MAP) was reduced by 20%. They also calculated a 27% improvement in the relatively bloodless quality of the surgical field. Decreased blood loss reduces the incidence of transfusion of blood products, with the obvious advantages of decreased risk of transfusion reactions and associated diseases. Although Thompson and coworkers3 were able to significantly decrease operating time during total hip replacement, hypotensive anesthesia has not been shown to do that with orthognathic surgery. Risks The potential risks of hypotensive anesthesia are many, but most studies indicate that relatively few major complications occur. The majority of these are related to hypoperfusion of vital organs, especially the central nervous system (CNS), heart, kidney, and liver. Should hypoperfusion occur, significant morbidity or mortality could result. Other complications of hypoperfusion include tissue necrosis at points of pressure, such as the nasal tip from the endotracheal tube, nasogastric tube, or the esophageal stethoscope pressure, the arm from the blood pressure cuff, or the fingertip from the pulse oximeter probe. These are rarely seen during normotensive anesthesia, but the severity is magnified during induced hypotensive anesthesia. A variety of other risks include rebound hypertension, reflex tachycardia, fluid deficit or excess, and toxicity of the hypotensive drugs (eg, nitroprusside).
HYPOTENSIVE ANESTHESIA
Relatively short, uncomplicated orthognathic procedures, particularly in the mandible, do not involve significant blood loss. Longer procedures and particularly those in the maxilla have greater potential for blood loss, and thus a decision should be made, in consultation with the surgeon if possible, whether normotensive or deliberate hypotensive anesthesia is desirable. This decision should be made before entering the operating room, since it influences the selection of monitors, anesthetic drugs, and the informed consent. Benefits There are several significant benefits of intentional hypotensive anesthesia for major orthognathic surgery. Scha-
Cerebrovascular Disease. Since perfusion of the brain is maintained by an autoregulatory mechanism, it is not subject to normal fluctuations in arterial blood pressure. Normal drops in blood pressure trigger cerebral vasodilation to maintain brain perfusion. However, when the MAP falls below 50 mm Hg (or higher pressures for
Received July 1, 1991; accepted for publication September 10, 1991. Address correspondence to Dr. Joel M. Weaver, Ohio State University, College of Dentistry, 305 W. 12th Avenue, Columbus, OH 43210. © 1992 by the American Dental Society of Anesthesiology
ISSN 0003-3006/92/$6.00
146
Weaver 147
Anesth Prog 39:146-149 1992
cerebrovascular occlusive disease), autoregulation is abolished, and perfusion is dependent on blood pressure. Hypocarbia leading to arterial carbon dioxide tensions below 30 mm Hg, also inhibits autoregulation. Hyperoxia, as when ventilation occurs with 100% oxygen, may also cause a significant decrease in cerebral blood flow. The patient with preexisting cerebrovascular disease is even more likely to experience CNS damage from prolonged hypotensive anesthesia.
Coronary Artery Disease. Coronary artery perfusion is related to the MAP and the diastolic pressure, since blood flow for the heart muscle cells occurs during diastole. As the time the heart spends in diastole decreases when the heart rate increases, coronary perfusion decreases during tachycardia associated with hypotension. Myocardial oxygen consumption during tachycardia tends to increase but may be somewhat offset by the decreased inotropic response needed to empty the ventricle during afterload reduction produced by arterial dilators. Hypocapnea also produces coronary constriction. Intentional hypotensive anesthesia presents a significant risk of coronary insufficiency and myocardial ischemia. Renal Disease. Renal perfusion is determined by autoregulatory mechanisms, the autonomic nervous system, antidiuretic hormone, and aldosterone. General anesthesia abolishes autoregulation, so that perfusion is dependent on arterial blood pressure. As the systolic pressure decreases below 80 to 90 mm Hg, renal blood flow (RBF) decreases. Glomerular filtration drops at systolic pressures between 60 and 70 mm Hg, and oliguria and acute renal failure may occur if the restriction is prolonged, particularly in patients with preexisting renal disease. General anesthetics also decrease RBF independently of the blood pressure. Catecholamines released in response to induced hypotension also decrease RBF in low concentrations and decrease RBF and GFR in high concentrations. The renin-angiotension system is also actuated during hypotension and by anesthetics and causes vasoconstriction with a decrease in RBF.4 Aldosterone from the adrenal cortex and antidiuretic hormone from the pituitary further decrease urine output. Fortunately, many vasodilating hypotensive agents tend to maintain RBF by their vasodilating action. Liver Disease. Liver blood flow is not maintained by autoregulation but rather is dependent on the hepatic artery (30%) and the portal vein (70%). Catecholamines released during hypotension as well as hypoxia and acidosis may cause hepatic vasoconstriction and a decrease in perfusion.
Other Conditions. Other contraindications for intentional hypotensive anesthesia include other peripheral
vascular disease, severe anemia and hypovolemia, and
cardiomyopathy. Drugs There are a variety of drugs that can be used for hypotensive anesthesia. All have advantages and disadvantages, and none are necessarily agents of choice in many or most instances.
Potent Inhalation Anesthetics. Halothane, enflurane, and isoflurane have all been used for hypotensive anesthesia. Halothane decreases stroke volume and cardiac output. In addition to abolishing cerebral autoregulation, it sensitizes the myocardium to endogenous and exogenous epinephrine, with resulting ventricular dysrhythmias. Halothane has also a questionable association with hepatotoxicity. Enflurane not only produces myocardial depression but also significant vasodilation. High concentrations of enflurane and hypocarbia may induce seizure activity as well as elevate serum fluoride concentrations, which may approach renotoxic levels. lsoflurane has the least effect on the heart but causes significant vasodilation. Isoflurane-associated tachycardia and an increased likelihood of producing coronary steal syndrome in patients with coronary artery disease are drawbacks to its use as the sole hypotensive agent.
(3-Adrenergic Blockers. The f3-adrenergic blockers decrease heart rate, contractility, and renin release. Propranolol and other nonselective 8-blockers may cause bronchospasm and permit unopposed a-adrenergic vasoconstriction when epinephrine is released during hypotension or injected by the surgeon. Selective 31 blockers, such as the ultrashort-acting esmolol, are less likely to produce these adverse effects. Labetalol, an a blocker as well as a ,8 blocker, is an excellent hypotensive agent, but its long duration makes it less controllable than esmolol. a-Adrenergic Blockers. Drugs with a-adrenergic blocking activity produce passive vasodilation by inhibiting the vasoconstrictive a-receptors. Droperidol possesses a-blocking activity as well as antinausea and sedative properties. It may result in unopposed 8-adrenergic activity with tachycardia and hypotension when interacting with epinephrine. Its prolonged effects may slow recovery and produce an uncomfortable restless feeling postoperatively. Angiotensin-Converting Enzyme Inhibitors. Angiotension-converting enzyme (ACE) inhibitors such as enalapril block the conversion of angiotensin I to angioten-
148 Anesthesia for Orthognathic Surgery
sin II, a potent vasoconstrictor. Agents such as nitroprusside and nitroglycerin have short half-lives, and the renin that is released during hypotension has a longer half-life. Thus, the rebound hypertension that frequently occurs, especially with nitroprusside, may be due to residual renin. ACE inhibitors help reduce the severity of rebound hypertension, because they outlast the duration of the released renin.
Opioids. Fentanyl and sufentanil deepen the anesthetic state and induce mild bradycardia. Morphine also releases the vasodilator histamine and may induce bronchospasm. Opioids tend to prolong recovery and produce respiratory depression postoperatively. Ganglionic Blockers. Blockade of autonomic ganglia produces vasodilation by inhibiting sympathetic transmission. Trimethaphan produces arterial dilation as well as venous pooling. Unfortunately, parasympathetic blockade also occurs, which results in cycloplegia, mydriasis, decreased gastrointestinal motility, tachycardia, xerostomia, urinary retention, histamine release, tachyphylaxis, rebound hypertension, and decreases in hepatic, cerebral, and renal blood flow and glomerular filtration rate. Nitroprusside. Sodium nitroprusside produces direct vascular smooth muscle relaxation on resistance blood vessels and to a lesser degree on capacitance vessels. Its metabolism releases cyanide and may cause cyanide toxicity. Nitroprusside causes reflex tachycardia and rebound hypertension. At equal systolic pressure reductions, it produces more profound reductions in MAP and diastolic pressure than does nitroglycerin. Coronary ischemia is also more likely.
Nitroglycerin. Nitroglycerin produces direct relaxation of vascular smooth muscle, especially in capacitance vessels. It tends to decrease venous bleeding and causes less tachycardia compared to nitroprusside. Rebound hypertension, tachycardia, and tachyphylaxis do occur, however. A RECOMMENDED HYPOTENSIVE ANESTHETIC TECHNIQUE FOR THE HEALTHY ORTHOGNATHIC SURGERY PATIENT After a review of the chart, auscultation of the chest, and assurance of fasting status of the patient, a skin wheal of 1% lidocaine is produced, and a 16-ga intravenous catheter is placed. If the patient desires anxiolysis, conscious sedation is given with 1 mg increments of midazolam to effect. Both nostrils are sprayed with 4% cocaine or 1% phenylephrine. The patient is then taken to the operating
Anesth
Prog 39:146-149 1992
room, and the appropriate monitors are applied (electrocardiogram, automatic blood pressure monitor, and pulse oximeter). The patient is preoxygenated, and the endtidal carbon dioxide (ETCO2) monitor is checked. Fentanyl (2 gg/kg) or sufentanil (0.2 ,g/kg) is administered, followed by an induction dose of thiopental (5 mg/kg), propofol (2.5 mg/kg), or methohexital (2.5 mg/kg). Relaxation is obtained with vecuronium (0.1 mg/kg), and the patient is nasally intubated and ventilated. Bilateral breath sounds and a positive ETCO2 response assure proper placement of the nasal RAE tube or standard tube cut to 27 cm and fitted with a metal acute-angle adapter. Nitrous oxide/oxygen (65%/35%) and isoflurane are given to maintain anesthesia at normotensive levels. The patient is placed in a 20° head-up position. An appropriate dose of glucocorticosteroid and prophylactic antibiotic is given and repeated as necessary. An 18-ga nasogastric (NG) tube is placed, and auscultation of an injected air bubble confirms proper position. An esophageal stethoscope/temperature probe is also placed beside the NG tube. Both tubes are taped to the nasotracheal tube to form the same curve. The tubes are taped to the patient's head after padding with foam. The eyes are lubricated with bland ophthalmic ointment and are then taped. A foley catheter is inserted and checked for flow of urine. The surgeon injects the initial surgical site with 1% lidocaine with 1:100,000 epinephrine (up to 3,ug/kg), and incisions are begun after the appropriate preparation and draping. An infusion with fentanyl (2.5 Ag/kg/hr) or sufentanil (0.25 Ag/kg/hr) is started, and isoflurane is adjusted to moderately hypotensive levels. Tachycardia that does not respond to an increased infusion of opioid is managed with an infusion of esmolol or small incremental boluses of labetalol. Additional hypotension is attained with increases in isoflurane or by adding low-dose nitroglycerin infusion. Physiologic parameters for the major portion of the surgery consist of the following: (1) Systolic pressure between 80 and 100 mm Hg, depending on the field; (2) MAP above 60 mm Hg; (3) ETCO2 above 35 mm Hg; (4) heart rate below 100 beats/min; (5) urine output of 1 mL/kg/hr; and (6) body temperature above 35° C. Appropriate fluid management is essential. Hypotensive anesthesia can mask hypovolemia. Fluid overload can negate vasodilatory hypotensive drugs. The preoperative fluid deficit is replaced during the first 2 hr, and intraoperative needs are provided during the hour they occur. A basal crystalloid formula for hourly requirements is: 4 mL/kg/hr for the first 10 kg of body weight plus 2 mL/kg/hr for the second 10 kg, plus 1 mL/kg/hr for the remainder. A running estimation of blood loss and irrigation fluid used is recorded, and blood is replaced by three
Weaver 149
Anesth Prog 39:146-149 1992
times the volume of crystalloid. Autologous blood is not given intraoperatively unless major blood loss is encountered, since mislabeled blood could cause problems. Additional crystalloid is given if urine output is inadequate. After adequate hydration is assured, a 5-mg dose of furosemide is usually sufficient to yield adequate urine. Blood pressure must be increased and other appropriate measures taken if urine output fails to respond. When the surgery has progressed to the final stages (wiring, plating for rigid fixation, suturing), the administration of opioid and isoflurane are significantly reduced, and the patient is allowed to resume spontaneous ventilation. The patient is maintained on nitrous oxide and oxygen alone or with 0.25% or less isoflurane for the last 30 to 40 min. Intravenous lidocaine (1.5 mg/kg) may be given to prolong the anesthetic state for a few extra minutes. An intramuscular nonsteroidal antiinflammatory drug (ketorolac) is administered within the last hour for postoperative pain control. Additional small doses of morphine may be given later in the postanesthesia care unit if necessary. After several minutes of 100% oxygen administration, the patient is extubated when he or she responds to verbal commands, such as, "Open your eyes." As the endotracheal tube is withdrawn from the trachea after maximal inhalation, suction is applied to the acute-angle connector to suction blood, blood clots, and other debris from the pharynx and nose. A soft nasopharyngeal tube may be necessary if ventilation is modestly impaired. Extubation is best accomplished in the operating room where reintu-
bation or other procedures are most readily completed in an emergency. Adequate attention to small details, preparation for unexpected occurrences, and communication with the surgical team will increase the likelihood of a successful and safe anesthetic course for the orthognathic surgery patient.
REFERENCES 1. Schaberg SJ, Kelly JF, Terry BC, Posner MA, Anderson EF: Blood loss and hypotensive anesthesia in oral-facial corrective surgery. J Oral Surg 1976;34:147-156. 2. Chan W, Smith DE, Ware WH: Effects of hypotensive anesthesia in anterior maxillary osteotomy. J Oral Surg 1980;38:504-508. 3. Thompson GE, Miller R, Stevens WC, Murray WR: Hypotensive anesthesia for total hip arthroplasty: a study of blood loss and organ function (brain, heart, liver and kidney). Anesthesiology 1978;48:91-96. 4. Fukayama H, Ito H, Shimada M, Kubota Y, Fukunaga A: Effects of hypotensive anesthesia on endocrine systems in oral surgery. Anesth Prog 1989;36:175-177. 5. Anderson JA: Deliberate hypotensive anesthesia for orthognathic surgery: controlled pharmacologic manipulation of cardiovascular physiology. Int J Adult Orthodon Orthognath Surg 1986;1: 133-159. 6. Hegtvedt AK: Orthognathic surgery: intraoperative and postoperative patient care. Oral Maxillofac Surg Clin North Am 1990;2:857-868.
