- Email: [email protected]
Patients who abuse drugs
Vol. 91 No. 1 January 2001
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY MEDICAL MANAGEMENT UPDATES
Editor: James R. Hupp
Patients who abuse drugs Noah A. Sandler, DMD, MD,a Minneapolis, Minn UNIVERSITY OF MINNESOTA
(Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;91:12-14)
Discussion of the management of patients with a history of substance abuse often focuses on preoperative diagnosis and perioperative pain management. The avoidance of perioperative morbidity depends on understanding the pathophysiology associated with the long-standing use of drugs of abuse. The purpose of this article will be to review the long-term effects of commonly abused drugs and current concepts of the management of patients with these conditions. Many substances, including nicotine, marijuana (THC), and caffeine can be considered substances of abuse that can alter homeostasis. For purposes of this discussion, alcohol, cocaine, and heroin will be used as examples of the effects of depressants, stimulants, and narcotics on perioperative patient management.
ALCOHOL ABUSE Alcohol abusers are commonly defined by consumption of at least 5 drinks (more than 60 g of ethanol) per day.1 Evidence from different types of procedures, major and minor, elective and acute, suggest a 2-fold to 3-fold increase in postoperative morbidity in matched subjects who consume no more than 2 drinks per day.2-4 The most frequent complications seen are wound infections and impaired wound healing, cardiac compromise, bleeding, and delirium tremens. Chronic alcohol abuse leads to immune compromise by suppressing T-cell mediated responses involving cell migration, adhesion, and signal transduction.5 Tcell production of free oxygen radicals and cytotoxic activity is also affected, increasing the susceptibility of aAssistant Professor of Oral-Maxillofacial Surgery. Received for publication Jun 8, 2000; accepted for publication Jul 19, 2000. Copyright © 2001 by Mosby, Inc. 1079-2104/2001/$35.00 + 0 7/13/110307 doi:10.1067/moe.2001.110307
12
the organism to bacterial colonization and subsequent infection.6 Wound healing also depends on an appropriate inflammatory response. In a recently completed study, alcohol consumption was found to be more of a risk factor for impaired wound healing than wound contamination or duration of the surgery.7 In addition to immune dysfunction, a reduction in protein production, particularly collagen, and impaired hemostasis contributes to poor wound healing.8 Functional reversibility of immune dysfunction occurs after approximately 2 weeks of abstinence, and complete normalization occurs after 2 months.1 Minor alcohol consumption has been noted for its cardiac protective effect. Long-term abuse, however, can lead to dilated cardiomyopathy with impaired cardiac function.9 The resultant decrease in ejection fraction can result in significant postoperative cardiac complications, such as dysrhythmia and cardiac failure.10 Alcohol-induced cardiac dysfunction is improved in about half of symptomatic patients after 3 to 6 months11 and is reversible in approximately 1 month if the patient is asymptomatic early in the disease process.12 Alcohol consumption has effects on both coagulation and fibrinolysis. Platelet counts and mean platelet volume are reduced by effects on megakaryocyte maturation.13 Platelet aggregation is also affected by chronic consumption of alcohol. These effects result in a prolonged bleeding time, irrespective of the effects of liver disease.13,14 This can result in increased bleeding after surgery.1 Alcohol withdrawal is relatively common in the postoperative period because oral intake is usually restricted before the procedure. It typically develops within 6 to 24 hours after the last drink consumed. Symptoms are primarily caused by autonomic hyperactivity and can proceed to seizures or death from cardiovascular and
Sandler 13
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY Volume 91, Number 1
Table I. Acute alcohol-withdrawal symptoms Autonomic
Neuronal
Delirium tremens
Hours after last drink
12-48 h
Develops in few cases
Tremulousness, sweating, nausea/vomiting, anxiety, agitation
Grand mal seizures
Hallucinations (auditory/visual), confusion/disorientation, clouded consciousness, impaired attention, autonomic hyperactivity, death (cardiovascular, respiratory)
respiratory collapse (Table I).15 Long-acting benzodiazepines are the mainstay of the management of alcohol withdrawal syndrome in the postoperative period. Recently, symptom-triggered dosing has been shown to be as effective as the more typical fixed dosing regimens.16 This substantially reduces the amount of sedative and the duration for which it is needed but requires trained nursing care to carefully monitor the patient for the first signs of symptoms.
COCAINE USE The clinical effects of cocaine are primarily caused by the inhibition of the normal uptake of catecholamines at the sympathetic nerve endings. The neurologic system is the most common site of morbidity in cocaine abusers. Seizures result from a decrease in the seizure threshold, similar to other local anesthetics, and tend to be more lethal because of the potentiation of catecholamines. Cerebrovascular accidents can result from hypertension, cerebral vasospasm, and ischemia.17 Manifestations of cocaine toxicity on the cardiovascular system primarily result from the elevated levels of adrenergic molecules. Hypertension, tachycardia, dysrhythmias, coronary artery constriction, or myocardial infarction can occur. Dysrhythmias include sinus tachycardia, ventricular premature contractions, ventricular tachycardia, ventricular fibrillation, and asystole.18 Dysrhythmias can also occur through a condition called contraction-band necrosis. This is caused by a local increase in catecholamines with a resultant sudden increase in intracellular calcium, causing overcontraction of the myocardial muscle fibers. In addition to rhythm changes, this condition can cause scarring, resulting in interstitial fibrosis.17,19 A direct toxic effect on cardiac muscle cells can also occur. Cocaine also alters platelet and endothelial function, predisposing an individual to acute thrombosis.17 Preoperative workup should include a review of vital signs, including a measurement of blood pressure and heart rate. A 12-lead electrocardiogram should be performed to look for the presence of occult dysrhythmias, silent ischemias, or previous myocardial infarc-
tions. Management of the patient who abuses cocaine includes the avoidance of endogenous adrenergic stimulation or excessive exogenous catecholamine introduction. In particular, the use of ketamine, epinephrine, and succinylcholine should be avoided or used with caution.17
HEROIN USE Heroin is converted in the bloodstream through hydrolysis into an active intermediate metabolite, monoacetyl morphine, and then to morphine. Interactions of these 2 molecules in the central nervous system cause analgesia, euphoria, drowsiness, and respiratory depression.20 Respiratory depression is characterized by a decreased response to carbon dioxide. Muscular rigidity, including the muscles of respiration, can occur with higher doses. Pulmonary disease, such as lung abscesses, pneumonia, pneumonitis, and fibrosis, occur frequently in heroin abusers and can contribute to respiratory compromise. Repeated injections with unclean needles can lead to complications. Hepatitis, human immunodeficiency virus, or endocarditis can result in a compromise of liver function, blood coagulation, immune function, or cardiac function. Preoperative examination with necessary laboratory tests is indicated when potential compromise exists. Before any procedure, any question regarding recent narcotic use warrants postponement of the planned procedure. Consideration should be given to a toxicology screen test. Tolerance can develop to the effects of narcotic drugs, making titration of anesthetic agents potentially more difficult. Often hypotension is seen on induction of anesthesia. Consideration should be given to administration of a vasopressor.20,21 Postoperatively, pain medication should be prescribed for a set period that has been established with the patient before the procedure. Patients who abuse narcotics who remain abstinent for 12 to 14 hours might have symptoms develop, including lacrimation, yawning, restless sleep, rhinorrhea, diaphoresis, or a combination of these. In the next 24 to 36 hours, the patient might experience increased
14 Sandler
restlessness, diarrhea, nausea and vomiting (resulting in dehydration), electrolyte abnormalities, and in severe cases, acidosis and cardiovascular collapse. Usual treatment consists of 1 mg of methadone for every 2 mg of heroin used. Sometimes 0.1 to 0.2 mg clonidine is added to the daily dose of methadone in an attempt to control cravings and other symptoms.20 Unfortunately, drug abuse is a reality of our time. The intent of this review is to discuss aspects of management of the dental or surgical patient who is known to abuse drugs. It is important to note that the effects of the abused drug or withdrawal of the agent can have consequences relevant to the homeostasis of the abuser. Alcoholics might require the administration of a benzodiazepine drug if a period is anticipated in which the patient will not be able to consume any alcohol. Drugs administered by the practitioner, including local anesthesia can cause potentially harmful interactions affecting this delicate balance. For a patient who admits recent (within 24 hours) cocaine abuse, the procedure should be deferred until a 24-hour abstinence period has passed. A patient who is a heroin abuser, other intravenous drug abuser, or prolonged alcohol abuser with cirrhosis might demonstrate liver failure. A prothrombin time/partial thromboplastin time test and bleeding time test to screen for an undetected coagulopathy should be performed on patients with suspected liver problems or platelet defects resulting from drug abuse. Analgesics should still be provided and tailored to the surgical procedure and to the personality of the individual. Narcotics should be avoided if possible; however, if they are necessary for pain management, they might be prescribed in the same manner as they would be for any other patient undergoing the same procedure. This should be discussed before surgery with the patient and with any individuals assisting with the patient’s rehabilitation. REFERENCES 1. Tonnesen H, Kehlet H. Preoperative alcoholism and postoperative morbidity. Br J Surg 1999;86:869-74. 2. Tonnesen H, Schutten BT, Jorgensen BB. Influence of alcohol on morbidity after colonic surgery. Dis Colon Rectum 1987; 30:549-51. 3. Tonnesen H, Pedersen AE, Jensen MR, Moller A, Madsen JC. Ankle fractures and alcoholism. The influence of alcoholism on
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY January 2001
4. 5. 6. 7. 8. 9. 10. 11.
12. 13. 14. 15. 16.
17. 18. 19. 20. 21.
morbidity after malleolar fractures. J Bone Joint Surg 1991; 73:511-3. Sonne NM, Tonessen H. The influence of alcoholism on outcome after evacuation of subdural haematoma. Br J Neurosurg 1992;6:125-30. Chiapelli F, Kung M, Lee P, Pham L, Manfrini E, Villanueva P. Alcohol modulation of human normal T-cell activation, maturation, and migration. Alcohol Clin Exp Res 1995;19:539-44. Watson RR, Borgs P, Witte M, McCuskey RS, Lantz C, Johnson MI, et al. Alcohol, immunomodulation and disease. Alcohol Alcohol 1994;29:131-9. Rantala A, Lehtonen O-P, Niinikoski J. Alcohol abuse: a risk factor for surgical wound infections? Am J Infect Control 1997;25:381-6. Jorgensen LN, Tonnesen H, Pedersen S, Laursen M, Tuxoe J, Gottrup F. Reduced amounts of total protein in artificial wounds of alcohol abusers. Br J Surg 1998;85(Suppl 2):152-3. Patel VB, Why HJ, Richardson PJ, Preedy VR. The effects of alcohol on the heart. Adverse Drug React Toxicol Rev 1997;16:15-43. Tonnesen H, Petersen KR, Hojgaard L, Stokholm KH, Nielsen HJ, Knigge U, et al. Postoperative morbidity among symptomfree alcohol misusers. Lancet 1992;340:334-7. La Vecchia LL, Bedogni F, Bozzola L, Bevilacqua P, Ometto R, Vincenzi M. Prediction of recovery after abstinence in alcoholic cardiomyopathy: Role of hemodynamic and morphometric parameters. Clin Cardiol 1996;19:45-50. Kelbaek H, Nielsen BM, Eriksen J, Rabol A, Christensen NJ, Lund JO, et al. Left ventricular performance in alcoholic patients without chronic liver disease. Br Heart J 1987;58:352-7. Rubin R, Rand ML. Alcohol and platelet function. Alcohol Clin Exp Res 1994;18:105-10. McGarry GW, Gatehouse S, Vernham G. Idiopathic epistaxis, haemostasis and alcohol. Clin Otolaryngol 1995;20:174-7. Hall W, Zador D. The alcohol withdrawal patient. Lancet 1997;349:1897-900. Saitz R, Mayo-Smith MF, Roberts MS, Redmond HA, Bernard DR, Calkins DR. Individualized treatment for alcohol withdrawal: a randomized double-blind controlled trial. JAMA 1994;272:519-23. Goupil MT. Anesthetic management of the substance abuse patient. Oral Maxillofac Surg Clin NA 1999;11:583-7. Nanji AA, Filipenko JD. Asystole and ventricular fibrillation associated with cocaine intoxication. Chest 1985;85:132-3. Laposata EA. Cocaine-induced heart disease: mechanisms and pathology. J Thorac Imaging 1991;6:68-75. Cook H, Peoples J, Paden M. Management of the oral surgery patient addicted to heroin. J Oral Maxillofac Surg 1989;47: 281-5. Eisman B, Lam R, Rush B. Surgery on the narcotic addict. Ann Surg 1964;159:784.
Reprint requests: Noah A Sandler, DMD, MD Assistant Professor of Oral-Maxillofacial Surgery University of Minnesota 7-174 Moos Tower 515 Delaware St SE Minneapolis, MN 55455
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY MEDICAL MANAGEMENT UPDATES
Editor: James R. Hupp
Patients who abuse drugs Noah A. Sandler, DMD, MD,a Minneapolis, Minn UNIVERSITY OF MINNESOTA
(Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;91:12-14)
Discussion of the management of patients with a history of substance abuse often focuses on preoperative diagnosis and perioperative pain management. The avoidance of perioperative morbidity depends on understanding the pathophysiology associated with the long-standing use of drugs of abuse. The purpose of this article will be to review the long-term effects of commonly abused drugs and current concepts of the management of patients with these conditions. Many substances, including nicotine, marijuana (THC), and caffeine can be considered substances of abuse that can alter homeostasis. For purposes of this discussion, alcohol, cocaine, and heroin will be used as examples of the effects of depressants, stimulants, and narcotics on perioperative patient management.
ALCOHOL ABUSE Alcohol abusers are commonly defined by consumption of at least 5 drinks (more than 60 g of ethanol) per day.1 Evidence from different types of procedures, major and minor, elective and acute, suggest a 2-fold to 3-fold increase in postoperative morbidity in matched subjects who consume no more than 2 drinks per day.2-4 The most frequent complications seen are wound infections and impaired wound healing, cardiac compromise, bleeding, and delirium tremens. Chronic alcohol abuse leads to immune compromise by suppressing T-cell mediated responses involving cell migration, adhesion, and signal transduction.5 Tcell production of free oxygen radicals and cytotoxic activity is also affected, increasing the susceptibility of aAssistant Professor of Oral-Maxillofacial Surgery. Received for publication Jun 8, 2000; accepted for publication Jul 19, 2000. Copyright © 2001 by Mosby, Inc. 1079-2104/2001/$35.00 + 0 7/13/110307 doi:10.1067/moe.2001.110307
12
the organism to bacterial colonization and subsequent infection.6 Wound healing also depends on an appropriate inflammatory response. In a recently completed study, alcohol consumption was found to be more of a risk factor for impaired wound healing than wound contamination or duration of the surgery.7 In addition to immune dysfunction, a reduction in protein production, particularly collagen, and impaired hemostasis contributes to poor wound healing.8 Functional reversibility of immune dysfunction occurs after approximately 2 weeks of abstinence, and complete normalization occurs after 2 months.1 Minor alcohol consumption has been noted for its cardiac protective effect. Long-term abuse, however, can lead to dilated cardiomyopathy with impaired cardiac function.9 The resultant decrease in ejection fraction can result in significant postoperative cardiac complications, such as dysrhythmia and cardiac failure.10 Alcohol-induced cardiac dysfunction is improved in about half of symptomatic patients after 3 to 6 months11 and is reversible in approximately 1 month if the patient is asymptomatic early in the disease process.12 Alcohol consumption has effects on both coagulation and fibrinolysis. Platelet counts and mean platelet volume are reduced by effects on megakaryocyte maturation.13 Platelet aggregation is also affected by chronic consumption of alcohol. These effects result in a prolonged bleeding time, irrespective of the effects of liver disease.13,14 This can result in increased bleeding after surgery.1 Alcohol withdrawal is relatively common in the postoperative period because oral intake is usually restricted before the procedure. It typically develops within 6 to 24 hours after the last drink consumed. Symptoms are primarily caused by autonomic hyperactivity and can proceed to seizures or death from cardiovascular and
Sandler 13
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY Volume 91, Number 1
Table I. Acute alcohol-withdrawal symptoms Autonomic
Neuronal
Delirium tremens
Hours after last drink
12-48 h
Develops in few cases
Tremulousness, sweating, nausea/vomiting, anxiety, agitation
Grand mal seizures
Hallucinations (auditory/visual), confusion/disorientation, clouded consciousness, impaired attention, autonomic hyperactivity, death (cardiovascular, respiratory)
respiratory collapse (Table I).15 Long-acting benzodiazepines are the mainstay of the management of alcohol withdrawal syndrome in the postoperative period. Recently, symptom-triggered dosing has been shown to be as effective as the more typical fixed dosing regimens.16 This substantially reduces the amount of sedative and the duration for which it is needed but requires trained nursing care to carefully monitor the patient for the first signs of symptoms.
COCAINE USE The clinical effects of cocaine are primarily caused by the inhibition of the normal uptake of catecholamines at the sympathetic nerve endings. The neurologic system is the most common site of morbidity in cocaine abusers. Seizures result from a decrease in the seizure threshold, similar to other local anesthetics, and tend to be more lethal because of the potentiation of catecholamines. Cerebrovascular accidents can result from hypertension, cerebral vasospasm, and ischemia.17 Manifestations of cocaine toxicity on the cardiovascular system primarily result from the elevated levels of adrenergic molecules. Hypertension, tachycardia, dysrhythmias, coronary artery constriction, or myocardial infarction can occur. Dysrhythmias include sinus tachycardia, ventricular premature contractions, ventricular tachycardia, ventricular fibrillation, and asystole.18 Dysrhythmias can also occur through a condition called contraction-band necrosis. This is caused by a local increase in catecholamines with a resultant sudden increase in intracellular calcium, causing overcontraction of the myocardial muscle fibers. In addition to rhythm changes, this condition can cause scarring, resulting in interstitial fibrosis.17,19 A direct toxic effect on cardiac muscle cells can also occur. Cocaine also alters platelet and endothelial function, predisposing an individual to acute thrombosis.17 Preoperative workup should include a review of vital signs, including a measurement of blood pressure and heart rate. A 12-lead electrocardiogram should be performed to look for the presence of occult dysrhythmias, silent ischemias, or previous myocardial infarc-
tions. Management of the patient who abuses cocaine includes the avoidance of endogenous adrenergic stimulation or excessive exogenous catecholamine introduction. In particular, the use of ketamine, epinephrine, and succinylcholine should be avoided or used with caution.17
HEROIN USE Heroin is converted in the bloodstream through hydrolysis into an active intermediate metabolite, monoacetyl morphine, and then to morphine. Interactions of these 2 molecules in the central nervous system cause analgesia, euphoria, drowsiness, and respiratory depression.20 Respiratory depression is characterized by a decreased response to carbon dioxide. Muscular rigidity, including the muscles of respiration, can occur with higher doses. Pulmonary disease, such as lung abscesses, pneumonia, pneumonitis, and fibrosis, occur frequently in heroin abusers and can contribute to respiratory compromise. Repeated injections with unclean needles can lead to complications. Hepatitis, human immunodeficiency virus, or endocarditis can result in a compromise of liver function, blood coagulation, immune function, or cardiac function. Preoperative examination with necessary laboratory tests is indicated when potential compromise exists. Before any procedure, any question regarding recent narcotic use warrants postponement of the planned procedure. Consideration should be given to a toxicology screen test. Tolerance can develop to the effects of narcotic drugs, making titration of anesthetic agents potentially more difficult. Often hypotension is seen on induction of anesthesia. Consideration should be given to administration of a vasopressor.20,21 Postoperatively, pain medication should be prescribed for a set period that has been established with the patient before the procedure. Patients who abuse narcotics who remain abstinent for 12 to 14 hours might have symptoms develop, including lacrimation, yawning, restless sleep, rhinorrhea, diaphoresis, or a combination of these. In the next 24 to 36 hours, the patient might experience increased
14 Sandler
restlessness, diarrhea, nausea and vomiting (resulting in dehydration), electrolyte abnormalities, and in severe cases, acidosis and cardiovascular collapse. Usual treatment consists of 1 mg of methadone for every 2 mg of heroin used. Sometimes 0.1 to 0.2 mg clonidine is added to the daily dose of methadone in an attempt to control cravings and other symptoms.20 Unfortunately, drug abuse is a reality of our time. The intent of this review is to discuss aspects of management of the dental or surgical patient who is known to abuse drugs. It is important to note that the effects of the abused drug or withdrawal of the agent can have consequences relevant to the homeostasis of the abuser. Alcoholics might require the administration of a benzodiazepine drug if a period is anticipated in which the patient will not be able to consume any alcohol. Drugs administered by the practitioner, including local anesthesia can cause potentially harmful interactions affecting this delicate balance. For a patient who admits recent (within 24 hours) cocaine abuse, the procedure should be deferred until a 24-hour abstinence period has passed. A patient who is a heroin abuser, other intravenous drug abuser, or prolonged alcohol abuser with cirrhosis might demonstrate liver failure. A prothrombin time/partial thromboplastin time test and bleeding time test to screen for an undetected coagulopathy should be performed on patients with suspected liver problems or platelet defects resulting from drug abuse. Analgesics should still be provided and tailored to the surgical procedure and to the personality of the individual. Narcotics should be avoided if possible; however, if they are necessary for pain management, they might be prescribed in the same manner as they would be for any other patient undergoing the same procedure. This should be discussed before surgery with the patient and with any individuals assisting with the patient’s rehabilitation. REFERENCES 1. Tonnesen H, Kehlet H. Preoperative alcoholism and postoperative morbidity. Br J Surg 1999;86:869-74. 2. Tonnesen H, Schutten BT, Jorgensen BB. Influence of alcohol on morbidity after colonic surgery. Dis Colon Rectum 1987; 30:549-51. 3. Tonnesen H, Pedersen AE, Jensen MR, Moller A, Madsen JC. Ankle fractures and alcoholism. The influence of alcoholism on
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY January 2001
4. 5. 6. 7. 8. 9. 10. 11.
12. 13. 14. 15. 16.
17. 18. 19. 20. 21.
morbidity after malleolar fractures. J Bone Joint Surg 1991; 73:511-3. Sonne NM, Tonessen H. The influence of alcoholism on outcome after evacuation of subdural haematoma. Br J Neurosurg 1992;6:125-30. Chiapelli F, Kung M, Lee P, Pham L, Manfrini E, Villanueva P. Alcohol modulation of human normal T-cell activation, maturation, and migration. Alcohol Clin Exp Res 1995;19:539-44. Watson RR, Borgs P, Witte M, McCuskey RS, Lantz C, Johnson MI, et al. Alcohol, immunomodulation and disease. Alcohol Alcohol 1994;29:131-9. Rantala A, Lehtonen O-P, Niinikoski J. Alcohol abuse: a risk factor for surgical wound infections? Am J Infect Control 1997;25:381-6. Jorgensen LN, Tonnesen H, Pedersen S, Laursen M, Tuxoe J, Gottrup F. Reduced amounts of total protein in artificial wounds of alcohol abusers. Br J Surg 1998;85(Suppl 2):152-3. Patel VB, Why HJ, Richardson PJ, Preedy VR. The effects of alcohol on the heart. Adverse Drug React Toxicol Rev 1997;16:15-43. Tonnesen H, Petersen KR, Hojgaard L, Stokholm KH, Nielsen HJ, Knigge U, et al. Postoperative morbidity among symptomfree alcohol misusers. Lancet 1992;340:334-7. La Vecchia LL, Bedogni F, Bozzola L, Bevilacqua P, Ometto R, Vincenzi M. Prediction of recovery after abstinence in alcoholic cardiomyopathy: Role of hemodynamic and morphometric parameters. Clin Cardiol 1996;19:45-50. Kelbaek H, Nielsen BM, Eriksen J, Rabol A, Christensen NJ, Lund JO, et al. Left ventricular performance in alcoholic patients without chronic liver disease. Br Heart J 1987;58:352-7. Rubin R, Rand ML. Alcohol and platelet function. Alcohol Clin Exp Res 1994;18:105-10. McGarry GW, Gatehouse S, Vernham G. Idiopathic epistaxis, haemostasis and alcohol. Clin Otolaryngol 1995;20:174-7. Hall W, Zador D. The alcohol withdrawal patient. Lancet 1997;349:1897-900. Saitz R, Mayo-Smith MF, Roberts MS, Redmond HA, Bernard DR, Calkins DR. Individualized treatment for alcohol withdrawal: a randomized double-blind controlled trial. JAMA 1994;272:519-23. Goupil MT. Anesthetic management of the substance abuse patient. Oral Maxillofac Surg Clin NA 1999;11:583-7. Nanji AA, Filipenko JD. Asystole and ventricular fibrillation associated with cocaine intoxication. Chest 1985;85:132-3. Laposata EA. Cocaine-induced heart disease: mechanisms and pathology. J Thorac Imaging 1991;6:68-75. Cook H, Peoples J, Paden M. Management of the oral surgery patient addicted to heroin. J Oral Maxillofac Surg 1989;47: 281-5. Eisman B, Lam R, Rush B. Surgery on the narcotic addict. Ann Surg 1964;159:784.
Reprint requests: Noah A Sandler, DMD, MD Assistant Professor of Oral-Maxillofacial Surgery University of Minnesota 7-174 Moos Tower 515 Delaware St SE Minneapolis, MN 55455