Postoperative analgesia in patients with substance use disorders: Part I

Postoperative analgesia in patients with substance use disorders: Part I

Revie w Article Postoperative analgesia in patients with substance use disorders Part I* Jargen Jage, M D (1) Tareg Bey, M D (2) Abstract T h e speci...

1MB Sizes 18 Downloads 135 Views

Revie w Article

Postoperative analgesia in patients with substance use disorders Part I* Jargen Jage, M D (1) Tareg Bey, M D (2) Abstract T h e specific problems related to postoperative analgesia in patients with substance use disorders (SUD) concerning opioids, alcohol, benzocliazepines, barbiturates, cocaine, crack, amphetamines, amphetamine-like designer drugs (MDMA, ecstasy), LSD, and marijuana are described. Whereas SUD with only one substance rarely occurs, the number of polysubstance abusers is increasing. Patients with SUD may have multiple organic diseases, impaired immune response, psychiatric and behavioural abnormalities and substance-induced disorders (intc0~ieation, withdrawal, delerium, psychotic disorders), often associated with low compliance and craving behaviour. T h e perioperative management should be focused on three problems: (1) on the prevention of physical withdrawal symptoms and stressful complications in patients with SUD using C N S depressants, (2) on the symptomatic treatment of the predominant affective withdrawal symptoms in patients suffering from SUD with CNS stimulants, and (3) on the effective pain treatment. T h e analgesic therapy is often difficult and required for longer periods of time than in other patients. However, the principles of multimodal analgesia are as valid as in non addicts. To be effective, systemic analgesia with paracetamol, NSAIIN and opioids has to be adapted as usual, but regional analgesia techniques should be preferred for postoperative pain relief. Patients enrolled in preoperative maintenance programmes (methadone, buprenorphine) need their daily maintenance dose as baseline. Ths baseline therapy does not, however, induce analgesia. Therefore, these patients need additional short-acting opioids which have to be administered at higher doses than usual (which do not cause respiratory depression due to opioid tolerance). T h e additional opioid does not increase the risk of relapse into active SUD. O n the other hand, regional analgesia in patients w h o are enrolled in a maintenance programme does not mean withdrawal prophylaxis. These patients have excellent analgesia, but they need their previously used maintenance opioid to prevent withdrawal. Special considerations will have to be made in patients with naltrexone. Recovering patients with a history of SUD have both an intensive fear of relapsing into the active SUD as well as fear of suffering from postoperative pain. These patients require an equally effective analgesia as other patients. Depending on the type of surgery and pain intensity they need atypical opioids (eg tramadol) or strong opioids (eg buprenorphine or morphine) as a part of balanced analgesia to the same degree as other patients. Withholding effective analgesic treatment can paradoxically lead to relapses in recovering patients. T h e c o m m o n opinion of healthcare providers to withhold strong opioids from recovering patients with SUD is obsolete. However, in order to amid psychotropic side effects the dosages of opioids, as well as the analgesic efficacy, should be monitored closely. Acute Pa/n 2000:3 (3):141 156. Keywords: substance use disorder; addiction; postoperative analgesia

(I) Dept of Anaestheslologg University Hospital Mainz, Germany (2) Division of Ernergency Medicine, University of California, lrvlne UCI Medical Centea Orange, California, USA. Address for correspondence: Prof Dr Jage, Dept of Anaestheslotogy;, University Hospital Matnz, Langenbeckstr. I, 55131 Malnz, Germany. Fax O0 49 6131 1 g 66 49 Ematl Jage@ anaesthesle,kllnl k. unt -matnz. de

Acute Pain

Introduction Postoperative analgesia in patients d e p e n d e n t on psychoactive substances poses special problems since these patients are often suffering from severe medical illness including organ damage and infectious diseases

*Part H u4tt be published in Acute Pare 2000; 3 (4).

V o l u m e 3 (3) S e p t e m b e r 2000

141

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T

s u c h as HIV, tuberculosis, hepatitis and others. Moreover, psychological disorders may be severe. F u r t h e r m o r e , d r u g specific a d a p t a t i o n s such as t o l e r a n c e , physical d e p e n d e n c e and w i t h d r a w a l symptoms may diminish the analgesic effectiveness. In order to provide effective care the following issues should be taken into consideration: • Basic aspects o f substance use disorders Criteria and definitions Prevalence • Clinical aspects S U D with CNS-depressant substances Heroin and other opioids Alcohol - Benzodiazepines and barbiturates S U D w i t h C N S - s t i m u l a n t s u b s t a n c e s and others Cocaine, amphetamines, amphetamine like designer drugs - Cannabis ( , ~ ] u a n a )

LSD General recommendations • Patients in drug-free recovery In Part 1 of this review, we kx~k at the areas of basic aspects of substance use disorders together with the clinical aspects of S U D w i t h C N S d e p r e s s a n t substances. Basic aspects o f s u b s t a n c e use disorders Criteria and definitions

A c c o r d i n g to DSM-IV1 substance use disorders ( S U D ) have b e e n classified as p s y c h o l o g i c a l d e p e n d e n c e w i t h physical d e p e n d e n c e a n d / o r tolerance (Table 1). Psychoactive substances have a w e l l - d e f i n e d a d d i c t i o n liability 2-5, however, the interactions between substances, psychological and social influences m a y be m o r e i m p o r t a n t for the d e v e l o p m e n t of an active d e p e n d e n c e t h a n the exposure to the chemical substance alone 6. E x p e r i m e n t a l results have s h o w n an addictive p a t h w a y in t h e m a m m a l i a n b r a i n via n e u r o t r a n s m i t t e r s such as d o p a m i n e and e n d o g e n o u s opioids in the nucleus accumbens 7-1°. T h e intensity of S U D differs according to the psychotropic substances 12. C N S depressants (opioids, alcohol) induce severe psychological and physical dependence associated with a high degree of tolerance, whereas C N S stimulants (eg cocaine) induce severe psychological dependence with no or

142

j u s t a l o w d e g r e e o f p h y s i c a l d e p e n d e n c e and tolerance. Helpful definitions in this context can be found in Table 2. Physical dependence Physical d e p e n d e n c e does n o t m e a n the same as psychological dependence. It can only be associated w i t h t h e a b u s e of C N S - d e p r e s s a n t s u b s t a n c e s (opioids, alcohol, benzodiazepines, and barbiturates), but n o t w i t h C N S s t i m u l a n t s (eg c o c a i n e , amphetamine) 12. T h e clinically 13 and experimentally 14 well-known latent hyperexcitability due to neuronal and subcellular counterregulationslS. 16 can, u n d e r p o s t o p e r a t i v e c o n d i t i o n s , t u r n into s y m p a t h e t i c stimulation 10, increased posttraumatic nociception, diminished endogenous pain modulation 17, and pain as a part of hyperalgesia 17. T h e nociceptive threshold can be d i m i n i s h e d by b o t h s u b s t a n c e i n d u c e d h y p e r e x c i t a b i l i t y 17 a n d the p o s t t r a u m a t i c spinal neuronal plasticity zs (which has been described in patients without SUD as well). Physical withdrawal s y m p t o m s occur if the used substance is abruptly withdrawn, its dose is too low or an antagonist is administered, yet they subside after readministration of the substance 9,13. T h e pre dominant excitatory and autonomic symptoms are conlxary to the action of the CNS-depressant substancel7, lg. T h e y are m e d i a t e d in the locus coeruleus 17 and can be accompanied by painful abdominal cramps and other pains 15,16, i n t e n s i v e s y m p a t h e t i c s t i m u l a t i o n 2°,21 including cardio-circulatory stress 21 23, other neuronal h y p e r a c t i v i t y 24, and severe m e n t a l i n s t a b i l i t y 15. Depending on the degree of maladaptive substance patterns the intensity of withdrawal symptoms varies individually. Thus, physical withdrawal symptoms rmy be stressfixl and life-threatening in some patients 1&22, w h e r e a s in s o m e patients t h e y are o n l y m i l d to moderate. T h e intensity of withdrawal s y m p t o m s should be assessed repeatedly in order to adapt the withdrawal Ixeatment 6,192526. Their onset depends on the time of the last substance exposition as well as on pharmacokinetic aspects 3,12,15,22. Administration of the lacking substance (substitution) or of a similarly acting substance (crossdependence) (%ble 2) t e r m i n a t e s w i t h d r a w a l s y m p t o m s quickly 2L28. T h e dose of the substitute depends on the dose of the substance used originally (cross-tolerance) u27-29. After discontinuation of cenlxally stimulating drugs (eg cocaine, amphetamines) predominantly affective

V o l u m e 3 (3) S e p t e m b e r 2000

Acute Pain

P o s t o p e r a t i v e a n a l g e s i a in p a t i e n t s w i t h s u b s t a n c e use d i s o r d e r s : P a r t I Jage J, Bey T

S u b s t a n c e d e p e n d e n c e is a maladaptive pattern of substance abuse, leading to clinically significant impairment or distress as manifested by three or more of the following occurring at any time in the same 12 m o n t h period: - Tolerance (a need for markedly increased amounts of the substance to achieve the desired effects or intoxication) Physical dependence (typical withdrawal symptoms; the same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms) Substance is taken in larger amounts and o v e r a longer period than was intended Persistent desire to control substance abuse A great deal of time is necessary to obtain the substance or recover from its effects Important social, occupational, or recreational activities are given up or reduced due to the abuse Substance abuse despite k n o w l e d g e of harm -

-

Table I: Moddr3eddiagnostic rrtterla of substanre dependenre, rerommended by DSM-tVI Addiction

C o m m o n l y used term m e a n i n g the aberrant use of a specific psychoactive substance in a manner characterised by loss of control, compulsive use, preoccupation, and continued use despite harm; pejorative term, replaced in the D S M IV in a n o n pejorative way by the term 'substance use disorder' (SUE)) 1 with psychological and physical dependence

Dependence

(1)

Psychologicaldependence: need for a specific psychoactive substance either for its

positive effects or to avoid negative psychological or physical effects associated w i t h its withdrawal. (2) Physical dependence: A physiological state of adaptation to a specific psychoactive substance characterised by the emergence of a withdrawal syndrome during abstinence, w h i c h may be relieved in total or in part by readministration of the substance (3) O n e category of psychoactive substance use disorder

Chemical dependence

A generic term relating to psychological a n d / o r physical dependence on one or m o r e psychoactive substances (11 classes of psychoactive substances are abused: alcohol; sedatives, hypnotics and anxiolyties; cannabis; opioids; cocaine; amphetamine and other sympathicomimetics; hallucinogens; inhalants; caffeine; nicotine; phencyclidine)

S u b s t a n c e use disorders T e r m of D S M IV comprising two main groups: (1) Sub~umce dependence disorder and substance abuse disorder (2) Substance-induced disorders (eg intoxication, withdrawal,delirium, psychotic disorders) Tolerance

A state in which an increased dosage of a psychoactive substance is needed to produce a desired effect; cross tolerance: induced by repeated administration of one psychoactive substance that is manifested toward another substance to w h i c h the individual has not been recently exposed

Withdrawal syndrome

T h e onset of a predictable constellation of signs and symptoms following the abrupt discontinuation of or rapid decrease in dosage of a psychoactive substance

Polydrug dependence

C o n c o m i t a n t use of t w o or m o r e psychoactive substances in quantities and frequencies that cause individually significant physiological, psychological a n d / o r sociological distress or impairment (polysubstance abuser)

Recovery

A process of o v e r c o m i n g both physical and psychological dependence on a psychoactive substance w i t h a c o m m i t m e n t to sobriety

Abstinence

In recovery, non-use of any psychoactive substance

Maintenance

Prevention of craving behaviour and withdrawal symptoms of opioids by permanently acting opioids (eg methadone, buprenorphine)

S u b s t a n c e abuse

Use of a psychoactive substances in a m a n n e r outside of sociocultural conventions; according to this, any use of illicit and licit drugs in a manner not dictated by c o n v e n t i o n (eg according to physician's order) is abuse.

Table 2: Substanm use disorder-related deBntttor~l,~,ll,zg,58

Acute Pain

Volume

3 (3) S e p t e m b e r

2000

143

Postoperative analgesia in patients with

substance

use

withdrawal syptomsl2, 30-33 are observed. Mild physical withdrawal symptoms due to cocaine and others have low clinical significance 12. Clinical implications: Physical d e p e n d e n c e means increased neuronal excitability including higher and longer lasting pain intensities as well as a higher need for analgesics after surgery. Acute w i t h d r a w a l of CNS-depressants increases the perioperative stress and s h o u l d be a v o i d e d d u r i n g the i m m e d i a t e post operative period.

disorders: Part I Jage J, Bey T

Eff~ (m) ,, .~...-°='="~ m...-~= ..... , .~...-°=..... m

/

Tolerance Tolerance means a markedly diminished effect after repeated use of the same amount of the substance. T h e initial effect can only be reached by increasing doses (Figure 1). A high tolerance of the desired p s y c h o t r o p i c effects d u r i n g S U D (eg e u p h o r i a ) provokes an increase of substance use 13,23, p o l y substance abuse for self-treatment of w i t h d r a w a l symptoms, both logistical and financial problems as well as conflicts w i t h the law. Severe tolerance is c o n n e c t e d w i t h CNS depressant drugs 12, w h i c h means, the m o r e severe the S U B the higher the degree of tolerance 23. A certain partial tolerance can be o b s e r v e d w i t h CNS s t i m u l a t i n g substances, tcx312,30. Different n e u r o n a l adaptations c o u n t e r a c t the p r i m a r y effects of substances and cause not only p h y s i c a l d e p e n d e n c e , b u t also tolerance16,2C R e c e p t o r b i n d i n g s u b s t a n c e s (eg o p i o i d s a n d benzodiazepines) induce other adaptations than nonreceptor substances such as alcohol 34 or cocaine 31. F u r t h e r m o r e , an a c t i v a t i o n of the 'anti o p i o i d ' systems, eg N M D A receptors in the brain during opioid tolerance 16,24, has been described. Learned behavioural or conditioning processes support the p h a r m a c o d y n a m i c t o l e r a n c e 29. P h a r m a c o k i n e t i c reasons of tolerance are rare 12. Significant tolerance d e v e l o p s to c e n t r a l o p i o i d effects, eg sedation, nausea, and ventilatory depression 23,24,35. Hence, the t e r m 'opioid tolerant patient' is appropriate. Within the group of opioids (heroin, morphine, fentanyl, sufentanil, m e t h a d o n e , h y d r o m o r p h o n , oxycodon) and also within the group of alcohol and benzodiazepines cross tolerance can be observed, but not b e t w e e n b o t h groups 12. Even cross tolerance between ]a-opioidreceptor-agonists is inconsistent 36. Thus, if the opioid therapy is switched f r o m one opioid to another, the calculated new dose should initially be titrated carefully to prevent overdosing 3s.

144

Figure 1: Dyv~nlc of the dose-response curve of optolds with tolerance and higher sensttlvffy alter withdrawal. (t) Dose response curve o[ optolds eg heroin ~r methadone In patients without optod experience (optold-nalve) (2) Tolerance: In toterant patlents the dos~response curve of optolds Is shifted to the right35 meaning higher doses than initially are necessary to achieve the same effert~ eg euphoria, sedation, ventltatory depression and others. Patients with SUE) need higher closes for analgesia (cross tolerance), but without danger of ventllatory depression If dangerous drug combinations are avoided (see texO. (3) Protracted abstinence syndrome: A few days alter acute optold withdrawal tolerance Is lost. tn a period of 6 months ~ longer the dos~ response curve Is shifted to the left with increased sensitivity to optolds. Lower doses than during tolerance induce the same effects. An Increased autonotnlc instability and sensitivity to ventllatory depression and sedation due to optotd~ is observedlS,zz,29.

B e t w e e n agents w i t h no effect on the o p i o i d r e c e p t o r s ( s u c h as a l c o h o l , b a r b i t u r a t e s a n d benzcxtiazepines, cocaine and cannabis) and opioids cross tolerance 29 does not exist, therefore patients w i t h a d d i c t i o n to alcohol, b e n z o d i a z e p i n e s and barbiturates do n o t per se n e e d higher analgesic opioid doses during the postoperative phase 37-40. Clinlclal lmplicatlon~. In particular in p o l y d r u g (including opioids) users, opioid tolerance can be severe and may result in diminished efficacy of the a p p l i e d o p i o i d s e s p e c i a l l y o n p o l y d r u g users c o n s u m i n g opioids 23,29. Thus, these patients need h i g h e r doses o f o p i o i d s t h a n n o n d e p e n d e n t patients. Tolerance to central effects as well as crosst o l e r a n c e i n c r e a s e safety w i t h r e g a r d to t h e respiratory depressant effects, even during adapted analgesia with high doses of opioids. However, the lack of cross-tolerance b e t w e e n alcohol, b e n z o diazepines, cocaine, amphetamines, and cannabis on the one hand and opioid on the other explains w h y no h i g h o p i o i d dose a d j u s t m e n t s are n e e d e d in

V o l u m e 3 (3) S e p t e m b e r 2000

Acute Pain

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T

Drugs

Age 18 25 yrs

7.6 35 yrs

>.q5 yrs

Any illicit drugs

49.4 to 29.1

37.1 to 15.4

6.4

Marijuana

47.0 to 24.5

11.0 to 6.6

4.0

Cocaine

19.6 to 7.7

4.2 to 2.3

1.4

Heroin

1.3 to 0.3

0.2

0.1

Hallucinogens

9.9 to 4.7

0.8 to 0.5

0.2

Stimulants

10.8 to 3.3

2.6 to 0.9

0.5

Table 3: Annual prevalence o[11Idcttdrug abuse (percent) in relationship to age (gears) tn the US population (data from Nattonat Household Survey on Drug Abuse t9Z2 t 99 t)48 Specific dtagnost.~

Prevalence (96) Men Woman

Antisocial personality disorder

22

10

Phobic disorder

19

29

Major depression

14

28

Dysthymia

9

12

Obsessive compulsive disorder

6

9

Mania

5

7

Schizophrenia

5

8

Panic disorder

3

6

TaMe 4: Prevalence of psychiatric ddsorders tn a US population with SUE) 53 patients solely dependent on these drugs. However, psychological influences may increase the demand for analgesic opioids. Prevalence T h e data of several surveys show a highly variable prevalence of use of different substances, partially depending on the age and gender of patients 41. T h e life-time prevalence of alcohol disorders in a USpopulation amounts to 23.8% for men, and 4.7% for w o m e n 42, the one of illicit drug disorders is 7.7% for m e n and 4.8% for w o m e n 43, whereas the estimated annual prevalence of illicit drugs reveals a different o u t c o m e (Table 3). A m o n g patients with SUD the p r e v a l e n c e o f p s y c h i a t r i c illness a n d s e v e r e behavioural disturbances is high (Table 4) 44 46, and aggravations under stressful perioperative circumstances are well known6, 37. High levels of anxiety47 and other mental disturbances increase pain intensityl 7. T h e n u m b e r of polydrug abusers w i t h multiple organic diseases and an impaired immune response is increasing 32,n,4s. In patients with severe S U D a high

Acute Pain

i n c i d e n c e o f i n f e c t i o u s diseases s u c h as HIV, tuberculosis, hepatitis A, B and C (Table 5), and others can be observed, all involving an increased risk of infection for staff members. Patients with SUD to alcohol or nicotine show a higher incidence of dependence on other substances than the general population (cross addiction) s°,51. Almost 700/0 of opioid addicts in the US are cocaine dependent as well 52.

Clinical a s p e c t s Several perioperative problems should be considered. Organ damages in substance dependent patients may be serious (Table 5)4o,53.55 therefore requiring extensive preoperative diagnostic procedures including blood and urine drug screening 56. Due to their higher risks of organic and psychological complications, patients with SUD need more intensive postoperative m o n i t o r i n g d e p e n d i n g on the type of surgery or trauma4& 56 than patients without SUD 40. P s y c h o l o g i c a l a l t e r a t i o n s , severe o r g a n i c and functional disturbances, problems related to tolerance as well as prevention of withdrawal and pain are

V o l u m e 3 (3) S e p t e m b e r 2000

145

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T

System Behavioural/psychiatric disorder

Pulmonary system

Cardiovascular system

Liver Kidney Pancreas Blood vessels Skin Muscles Spine Central/peripheral nervous system Immune system Sexually transmitted diseases Nutrition Haematopoetic system

Symptom/disease Anxiety, depression, psychosis, disorientation, hallucination, schizophrenia, personality disorders; compulsive behaviour, danger of suicide; cocaine and amphetamine (after acute drug action): sleepiness, fatigue alcohol: delirium tremens Chronic obstructive/restrictive disease, pulmonary hypertension, infection; opioids: pulmonary embolism cocaine: pneumothorax, pneumomediastinum Cardiomyopathy, valvular diseases, endocarditis, coronary sclerosis, thromboembolic complications cocaine: myocardial ischaemia, infarction, aortic dissection Hepatitis A, B,C; cirrhosis; coagulopathy cocaine: cholinesterase deficiency Nephropathy, pyelonephritis Pancreatitis Thrombophlebitis, sclerosed vessels, septic embolization; accidentally intraarterial injection with severe arterial spastic reaction Abscess, scars, track marks, bums, phlebitis Myopathy opioids, cocaine (intoxication): danger of rhabdomyolysis opioids: osteomyelitis, radieular symptoms Polyneuropathy, encephalopathy, myelitis, parkinsonism cocaine: intracranial hematoma, pontine myolysis Multiple infections: abscess, endocarditis, pneumonia tuberculosis, HIV, tetanus, parasites H1V, syphilis, gonorrhoea, trichomonas Malnutrition Alcohol: anaemia (normochromic, hypochromic, megaloblastic) cocaine: thrombo cytopathy

Table 5: Preoperative morbtdiD, in patients with SUE) (opiotds, atcohot, ¢omlne/amphetamlne) i m p o r t a n t aspects in d e p e n d e n t patients 57. T h e y require a well-organised postoperative rranagement in order to adapt analgesics and dosages to the actual pain intensity. It is very c o m m o n among healthcare providers to use opioids sparingly in patients with SUD, and to withdraw opioids during the postoperative period. However, the opposite should be the case. Neither the anaesthesiologist nor the surgeon or any other specialist should intend to keep patients suffering from SUD with GNS-depressants 'opioid-free '37-39,57. T h e y can display dramatic examples of aberrant drug ingestion when undermedicated for pain 5°,58. Thus, it should be ensured that during effective substitution therapy, eg with m e t h a d o n e (SUD with opioids), clonidine (SUD w i t h alcohol) or sedatives (SUD with C N S stimulants), these patients do not develop stressful withdrawal symptorm or increasing anxiet N, w h i c h clearly means that the patient w i t h SUD should be stabilised during that time IL3L40,50. T h e perioperative management should focus on

146

three problems: (1) p r e v e n t i o n of p e r i o p e r a t i v e withdrawal symptoms with stressful complications (eg hypertension, tachyeardia, myocardial ischaemia, pain, seizures), (2) s y m p t o m a t i c t r e a t m e n t o f p s y c h o l o g i c a l a l t e r a t i o n s s u c h as anxiety, uncontrolled behaviour and other affective disorders, and (3) effective analgesic treatment (see Figure 2).

j]

Svstemic opioids + non-opioids

-I-

.

.

.

.

m,,-

-

Realonal (catheters, nerve blocks infiltrations) local anaesthetics (+ opioids) (+ clonidine)

Prevention / withdrawal (substitution, stabilization)

Figure 2: Schematic concept of postoperative pain management in patients with SUD

V o l u m e 3 (3) S e p t e m b e r 2000

Acute Pain

P o s t o p e r a t i v e a n a l g e s i a in p a t i e n t s w i t h s u b s t a n c e use d i s o r d e r s : P a r t I Jage J, Bey T

Opioids

Alcohol

Benzodiazepines, Barbiturates

Severn; cro• tolerance with other g -opiotdreceptor-agontsts, but not with benzodiazepines/ barbiturates sedation, respiratory depression, bradycardia, miosis

moderate to s e v e r e severe; n o cross tolerance with }l-optotdreceptor-agonists, but with benzodiazepines/ barbiturates Sedation, restlessness, circulatory collapse, hypothermta, dturests, metabolic disturbances

Physical withdrawal symptoms

moderate to severe

moderate to severe

Affectlve withdrawal

mild to moderate

mild to moderate

mild to severe severn; no cross tolerance p- opioidreceptor-agontsts, but with berLzodiazepines/ barbiturates Sedation (respiratory depm~ton with barbiturate), circulatory collapse, hypothermta, metabolic disturbances anxiety, agitation, Irritability, sensitivity to light and noise, tremor, nausea, vomiting, muscle cramps, my~Aontc jerk, sleep disturbances', high dose dependence: confusion, hallucinations, seizures, craving behavtour mild to moderate

Prevention/therapy of withdrawal

methadone or other p opioidreceptor agonists

Analgesia

see Table 8

long-acting benzodtazepines, clontdine, halopertdol, clomethiazol see Table 8

long-acting benzodtazepines, clonidine clontdine see Table 8

Dependence Tolerance

Signs of intoxication (examples)

severe

symptoms

Table 6: Pertoperattve management of patients with SUD (optot&, alcohol, benzoddazeplnes, barbiturates) Feeling sick Vomiting Diarrhoea Poor appetite Dry mouth Stomach cramps Restlessness Visual sensitivity to light Headache Drowsiness Dizziness or giddiness Fainting attacks or lightheadedness Stiffness of arms or legs Spontaneous twitching (contraction) of muscles Trembling Sneezing Insomnia

Trembling hands Feeling of coldness Feeling of unreality ' Gooseflesh' Hot and cold flushes Increased sweating Runny nose Trouble starting urination Passing more than usual quantity of urine Heart pounding Fatigue or tiredness Muscular tension Aches and pains Weakness Yawning Runny eyes

Table Z: Op~o~dw~thdr~w~ , ~ e (ows?~ (E.e, or the ~ = p t o ~ ~.~ t~ r~t~ ~th ,'~ (o]..e~d (1). ,~d~.te (3) and ,e~re (4)). Analgesia in these patients should be m a n a g e d by

this context, the interdisciplinary c o o p e r a t i o n w i t h an

appropriately skilled personnel (such as an acute pain service (APS)) ff major surgery or other surgery w i t h

a d d i c t i o n specialist m a y be of further help t o avoid misconceptions.

intensive n c ~ o u s stimulation is planned. T h e quality

B o t h systemic and r e g i o n a l analgesia are suitable.

o f postoperative analgesia carried o u t by t h e A P S is

R e g i o n a l c a t h e t e r t e c h n i q u e s s h o u l d be p r e f e r r e d

significantly better t h a n that by other clinicians 5g. In

not

Acute Pain

only

V o l u m e 3 (3) S e p t e m b e r

for anaesthesia

2000

itself but

also for

147

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T

Systemic analgesia 1. NSAID, paracetamol, dipyrone; ff necessary spasmolyttcs Application: t.v., rectal, oral 2. Additionally opioids dependent on pain intensity SUD v~th heroin Only p-agontsts as short-acting analgesics at high doses (morphine, piritramide, others) or other opioids (no partial agontsts as buprenorphine, no agontsts antagonists as pentazocine) AppLication: i.v. (i.v. PCA with background infusion, i.v. infusion), s.c./i.m., rectal, oral SUD w~th ateohot, benzodJazpine, cocaine amphetamine,cannabis

LSD

Optotds for mild to moderate pain: tramadol: optotds for severe pain: morphine, piritramid also buprenorphine is possible (at higher doses lower analgesic effectiveness compared with p-agontsts) AppLication: t.v. (i.v. PCA without background infusion), s.c./t.m., rectal, oral

Regional analgesia I. Catheter techniques whenever possible (eptdural, femoral, brachtal plexus, sciatic, others) 2. Alternatively intraoperattve infiltration/instillation (tissue, nerves) Local anaesthetics (roptvacaine, buptvacaine) plus optotds (morphine, fentanyl, 3. Drugs: sufentanfl: eptdural analgesia) plus clontdine (eptdural analgesia, peripheral nerve analgesia) AppLication: Continuous regional infusion or regional PCA with background infusion . Adapted administration of NSAID, paracetamol, dipyrone: ff nessecary spasmolyttcs AppLication: t.v., rectal, oral Table 8: Analgesic management of patients with S U D

p o s t o p e r a t i v e analgesia ( e p i d u r a l , i n t r a t h e c a l , peripheral nerves such as femoral, brachial plexus, psoas c o m p a r t m e n t blocks)37. 38. C o m p a r e d w i t h systemic analgesia, continuous regional analgesia does not only prove to be more advantageous, but may also be more effective 6° 64. Preoperatively existing neurologic deficits should be d o c u m e n t e d prior to surgery. Contraindications for regional analgesia are t h e same as usual, eg local i n f e c t i o n s , severe neuropathy, uncooperative behaviour and coagulo pathy 64. After a few days b o t h the p o s t o p e r a t i v e pain intensity and the therapeutic demand of analgesics will decrease. If possible, the opioid dose should be reduced by tapering before discharge, however, most patients with SUD are non-compliant and tend to leave the hospital as soon as possible, hence not taking advantage of further steps to become substance free.

SUD with CNS d e p r e s s a n t substances Heroin

and other opioids

T h e degree of psychological and physical dependence is usually severe (Table 6), as well as the extent of preexisting organ damage (Table 5) 53. T h e dealer's practice to dilute the drug with an unknown amount of glucose, flour, plaster or quinine in order to betray the 'customers '65,66 will result in intravenous injection o f n o n sterile particles and thus b a c t e r i a l inflammatory processes leading to acute as well as

148

chronic cardiac, renal or pulmonary problems 40. In particular in p o l y s u b s t a n c e abusers w i t h d r a w a l s y m p t o m s may be severe (Table 7), resulting in instability of the a u t o n o m o u s n e r v o u s system, increased posttraumatic n o c i c e p t i o n 17 diminished e n d o g e n o u s pain m o d u l a t i o n 17,67 and diminished efficacy of applied opioids 23,29,68. In addition to the opioid baseline therapy to prevent withdrawal, these patients also need high opioid doses for analgesia during the perioperative period. Analgesic therapy F r e q u e n t l y , t h e analgesic t h e r a p y (Table 8) is comparatively difficult and required for a longer time than with patients w i t h o u t SUD 39,40,57. R e g i o n a l analgesic techniques show some relevant advantages over systemic analgesia6L Patient controlled analgesia (PCA) (i.v. P C A with m o r p h i n e or other short acting opioids, but not with meperidine 70, or epidural P C A w i t h local a n a e s t h e t i c s plus o p i o i d s ) are preferred37. 71. Singular i.m./s.c.injections of an opioid on demand instead of i.v. PCA are possible, but only if c o m b i n e d with sufficient analgesic monitoring. Otherwise, ineffective pain relief could drive the patient into severe behavioural alterations 6. Since there is reduced risk of any accidental side effects based on the specific o p i o i d tolerance, analgesic opioids may be used generously until adequate pain relief is achieved. H o w e v e r , in o p i o i d t o l e r a n t patients with SUD severe sedation and ventilatory

V o l u m e 3 (3) S e p t e m b e r 2000

Acute Pain

P o s t o p e r a t i v e analgesia in patients with substance use disorders: Part I Jage J, Bey T

I.

Administration of m e t h a d o n e ' . a) Recovering patients enrolled in maintenance programrnes Methadone Daily dose at the same time as usual (oral or s.c./i.m.; relation oral to parenteral: 2:1,3s.n in some case reports almost I: 1) b) SLID in patients not enrolled in maintenance programmes Methadone 20 40 mg p.o. q24h 10-20 rag s.c./i.m, q24h 1.25 2.5 mg i.v. q5 10 min (start with 20 mg p.o./10 mg s.c./i.m, or 1.25 mg i.v., followed by titrated injections to diminish or to avoid withdrawal symptoms)

II. Administration of other pure p optotdreeeptor agontsts Instead of methadone (morphine, fentanyl, sufentanil and others, but not pethidine v°) (i.v., s.c., i.m.) III. Administration of the 0~2-adrenoeeptor-agontst elonidlne (i.v., p.o.) IV. Administration of huprenorphtne (only for patients enrolled in the maintenance programme with buprenorphine) Sublingual: Daily dose at the same time as usual s.c./Lm.: Relation sublingual to parenteral: 2:1 (in some countries the parenteral application of buprenorphine is not available: switching to parental methadone is advised) V. Naltrexone (p.o.) The optimum solution is to discontinue naltrexone 24-48h prior to surgery (see page 150), otherwise postoperative analgesic effectiveness of opioids is diminished and/or withdrawal symptoms may occur Careful titration of analgesic opioids is advised (see page 150) * -

Methadone - methadone racemate. This drug is indicated for prevention or therapy of withdrawal symptoms. The effective doses do not provide analgesia for acute pain. In Germany with levomethadone (p.o. or s.e./i.m./Lv.) or with methadone raeemate (only p.o. available). Relation oflevomethadone to racemate is 1:2 (range 0.6-2.41n

Table 9: Cltvdcat management of physical withdrawal symptoms (prophylactic or therapeutic) in patients with SUD (oploids)

depression is possible due to interactions between

individual unsually high opioid doses and C N S depressants 12,68,72J3. These drug combinations should be used with extreme care. T h e analgesic therapy with high opioid doses does n o t m e a n a a g g r a v a t i o n o f SUE), but a transient stabilisation o f b o t h p s y c h o l o g i c a l a n d physical dependence37. 50.

Transient (perloperatlve) administration of methadone: T h e last time of opioid exposition prior to admission has to be clarified in order to start the withdrawal p r o p h y l a x i s w i t h m e t h a d o n e as s o o n as possible (Table 9) 39.4(]. T h e transient baseline therapy w i t h

n o e i e e p t i v e substances (opioids, N S A I D s , paracetamol and dipyrone) and their additive or synergistic analgesic el~fects74,75 represent as valuable a concept here as in patients w i t h o u t dependence.

m e t h a d o n e ensures the patient's mental and physical stabflisation to an o p t i m u m extentTL M e t h a d o n e has a long half life (mean 1.5 days) 12 and a long lasting preventive effect w i t h o u t any toxic complications subsequent to administration once a day 9,28. C o n t r a r y to its use as a baseline opioid 28 m e t h a d o n e is difficult to control w h e n used as an acute analgesic opioid 35. T h e perioperatively started baseline t h e r a p y w i t h

Prevention/therapy of wlthdrawnt

m e t h a d o n e (per os, s.e./i.m, injection) (Table 9) prevents w i t h d r a w a l s y m p t o m s but w i t h o u t any

Multimodal

a n a l g e s i a 69 w i t h d i f f e r e n t a n t i -

Several effective administration administration of neuroleptics, and programmes.

A c u t e Pain

ways are possible: (1) t r a n s i e n t of methadone, (2) t r a n s i e n t trieyelie antidepressants (TCA) or (3) c o n t i n u a t i o n of m a i n t e n a n c e

r e l e v a n t a n a l g e s i c effect. A l t e r n a t i v e l y , t h e i.v. infusion of other p-opioidreeeptor agonists such as m o r p h i n e or f e n t a n y l can be applied (Table 9). T h e 0~ adrenoceptor agonist clonidine has a specific phar macodynamic

V o l u m e 3 (3) S e p t e m b e r 2000

profile

with

central

149

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T

s y m p a t h o l y t i c e f f e c t s 2~) i n c l u d i n g w i t h d r a w a l p r e v e n t i o n and therapy, sedation, and analgesia, w h i c h rmy improve the effectiveness of opioids and other analgesics TB,79.

Transient (perloperatlve) administration of TCA and/or neuroleptlcs: A n o t h e r possibility to m a n a g e peri o p e r a t i v e p r o b l e m s , is t o w a i t for d e v e l o p i n g withdrawal symptoms, and then to treat with T C A and n e u r o leptics only. T h i s a p p r o a c h p r o v o k e s unneccessary risks following surgical and withdrawal stress in patients w i t h severe organic and m e n t a l alterations. Moreover, T C A and neuroleptics may induce circulatory depression, cardiac arrhythmia, and sedation79; these symptoms inhibit mobilisation and rehabilitation and are undesirable postoperatively69. In a d d i t i o n w i t h d r a w a l of opioids d u r i n g the immediate postoperative period gives rise to further problems. T h e more acute the physical dependence and the higher the dosages of the abused substances, the more severe are the withdrawal symptoms 13,z523. W i t h i n a few clays following the last injection of heroin, symptoms disappear, the acute withdrawal syndrome has passed, and the tolerance is predominantly gone 23. However, a persistent and significant a u t o n o m i c nervous system instability, diminished pain tolerance, increased pain intensity, and increased sensitivity to exogenous opioids may persist throughout the following six months (protracted abstinence syndrome) 1~,22,29, resulting in mental and physical instability and requiring careful titration of analgesic opioids in order to avoid accidental side effects. Continuation of maintenance programmes: A n o t h e r group of patients has been enrolled preoperatively in the Methadone Maintenance Program (MMP) 28 or in maintenance with buprenorphine 80 which both have to be continued as a baseline therapy3L Additionally, these patients need an effective analgesic opioid. In patients enrolled in M M P morphine is the opioid of analgesic choice, whereas in patients w i t h buprenorphine maintenance only buprenorphine should be u s e d for b a s e l i n e plus analgesic therapy. If t h e analgesic control proves to be insufficient, a switch from buprenorphine to methadone plus morphine is possible. Equianalgesic doses are 0.8 m g b u p r e n o r p h i n e ( s u b l i n g u a l ) a n d 20 m g m e t h a d o n e (racemate) per os 36. M a i n t e n a n c e therapy needs to be c o n t i n u e d in patients under regional analgesia even if analgesia is e x c e l l e n t , o t h e r w i s e w i t h d r a w a l s y m p t o m s can develop.

150

Instead of methadone other bl agonists (eg fentanyl) may be used as an i.v. infusion as baseline therapy, T h e additional opioid doses w i t h the i.v. P C A is calculated by t a k i n g 50% of the h o u r l y baseline infusion, and w h e n c o m p a r i n g it to c u m u l a t i v e amount of the analgesic needed of over a period of four hours alternatively as s.c./i.m, injection. Optotd antagonists (naloxone, naltrexone)

Naloxone is an i.v. injectable, short acting antagonist. It has to be strictly avoided at the end of anaesthesia in o p i o i d - d e p e n d e n t patients, o t h e r w i s e h y p e r algesia 81 with severe postoperative pain ~7 and intense stimulation of catecholamine release 21 with high risk of cardiac complications may occur 82,83. N o t only the administration of pure antagonists, but also of mixed agonists antagonists, eg pentazocine, in addition to methadone or morphine may precipitate withdrawal symptorm 68. T h e higher the opioid dose, the higher the sensitivity to naloxone 84. Therefore, only in lifet h r e a t e n i n g t o x i c i t y n a l o x o n e m a y be t i t r a t e d carefully at low doses of 0.02 0.04 m g every 2 3 minutes until the ventilation is no longer depressed. A subsequent i.v. infusion of naloxone (2/3 of initial i.v. dosage per hour) is possible in opioid tolerant patients 85. Naltrexone is an oral long-acting opioid receptor antagonist. T h e l o n g - t e r m treatment appears to be useful in r e c o v e r i n g patients w h o participate in medically supervised behavioural programmes. In addition, it also prevents euphoric opioid effects after opioid detoxification 8H8 as well as psychological effects of alcohol 89. Naltrexone inhibits the analgesic a c t i o n of p e r i o p e r a t i v e l y a d m i n i s t e r e d 1.l o p i o i d r e c e p t o r - a g o n i s t s w i t h m a r k e d l y e n h a n c e d postoperative opioid requirements 9D. In addition, opioid w i t h d r a w a l s y m p t o m s 25,26 resulting f r o m residual naltrexone activity can be observed during analgesic opioid therapy. Naltrexone has a half-life of 3-4 hour (its active metabolite 6 naltrexone one of 9 h) sT. Therefore, naltrexone should be discontinued at least 24 hours prior to selective surgery requiring anaesthesia and analgesia. After discontinuation it should be taken into a c c o u n t that a selective up regulation of bl opioidreceptors with increasing opioid sensivity may have developed due to the previous blockade of tlo p i o i d r e c e p t o r s w i t h n a l t r e x o n e 91. T h e r e f o r e , postoperative opioids should be titrated carefully to avoid potential side effects.

V o l u m e 3 (3) S e p t e m b e r 2000

Acute Pain

P o s t o p e r a t i v e a n a l g e s i a in p a t i e n t s w i t h s u b s t a n c e use d i s o r d e r s : P a r t I Jage J, Bey T

Symptoms

Rating

Nausea/vomiting

0 - none

Tremor

7 - constant nausea, frequent dry heaves and vomiting 0 - none 7 - severe, even with arms not extended

Paroxysmal sweats Anxiety Agitation Tactile disturbances Auditory disturbances Visual disturbances Headache Orientation

0 - no sweat visible 7 drenching sweats 0 -- none 7 -- state of severe delirium/acute schizophrenic reactions 0 - normal activity 7 - permanently in movement 0 - none 7 - continuous hallucinations 0 7 0 7 0 7

-

none continuous hallucinations none continuous hallucinations none extremely severe

0 - yes, can do serial additions 4 - disoriented for place, time, date and person

Table 10: Withdrawal stole (alcohol)(CIWA-Ar)lOz. (Eachsymptom wilt be rated dependent on its intensity between 0 -7 and between 0-4 (only "ortentaUon')) Alcohol

of substance-induced mental disorders 46,1°4 associated

O r g a n d a m a g e due to alcohol is considerable (Table

w i t h a l o w e r e d n o c i c e p t i v e t h r e s h o l d a n d increased

5) a n d m a y r e s u l t in h i g h risks o f p o s t o p e r a t i v e c o m p l i c a t i o n s 92. A l c o h o l a b u s e o f t e n p l a y s an

pain 6,17. Pure ~ agonists are m o r e effective analgesics than partial agonists. Initial o p i o i d doses are the same

i m p o r t a n t role in further SUD, eg nicotine, heroin or

as in patients w i t h o u t SUD, and increasing doses of bl-

cannabis abuse. Psychological dependence, tolerance,

agonists should be tilzated as usual.

p h y s i c a l d e p e n d e n c e a n d p s y c h i a t r i c d i s o r d e r s are o f t e n severe46.9~.93. S e i z u r e s a n d d e l i r i u m as

t o l e r a n c e , a l c o h o l i c s m a y have a h i g h e r n e e d o f

manifestations of withdrawal can become lifethreatening. Thus, the prevention of w i t h d r a w a l has

analgesics. The whole spectrum of multimodal analgesia 69,1° should be used 37. T h e therapeutic goal o f

p r i o r i t y in the perioperative m a n a g e m e n t (Tables 10 a n d l l)g4 gT. T h e n e u r o n a l h y p e r e x c i t a b i l i t y in

an e f f e c t i v e a n a l g e s i a in a l c o h o l i c s s h o u l d h a v e p r i o r i t y over fears o f i n d u c t i o n of cross-addiction to

a l c o h o l i c s a n d its i n c r e a s e d u r i n g c l i n i c a l o r e x p e r i m e n t a l withdrawallT.34.93.9s can result in difficult

analgesic opioids 6.

pain c o n t r o l r e q u i r i n g h i g h doses o f o p i o i d s in t h e p o s t o p e r a t i v e phase, a l t h o u g h t h e r e is n o c r o s s -

analgesia. In s o m e patients w i t h m o d e r a t e S U D t o alcohol u n d e r g o i n g m i n o r surgery, the atypical o p i o i d

from physical dependence

However,

resulting

and not from opioid

R e g i o n a l analgesia is m o r e effective than systemic

However,

t r a m a d o l r m y be used if N S A I D s or paracetamol are

low doses o f opioids may be administered successfia_lly

ineffective. Alternatively, and d e p e n d i n g on the pain

in the t r e a t m e n t of alcohol withdrawal 9g. In o r d e r to improve the p u l m o n a r y it°, cardiac81-,101,102 and gastro-

intensity, t h e partial agonist b u p r e n o r p h i n e m a y be

t o l e r a n c e b e t w e e n a l c o h o l and o p i o i d s 12.

adequate.

intestinal 1°3 fianctions after surgery, effective analgesia is as i m p o r t a n t as in other patients w i t h o u t S U D 69.

Prevention/therapy of withdrawal

Analgesic therapy

T h e cross t o l e r a n c e b e t w e e n a l c o h o l a n d b e n z o d i a z e p i n e s 12 m a k e s it possible t o a c c o m p l i s h b o t h

T h e analgesic therapy is difficult and partially differs

prevention and treatment of alcohol withdrawal

from the therapy in patients suffering from S U D w i t h

symptoms

by substituting a long acting benzo

opioids (Table 8). Alcoholics show a high prevalence

diazepine

s u c h as f l u n i t r a z e p a m

Acute Pain

V o l u m e 3 (3) S e p t e m b e r

2000

(Table

11) 4°. 151

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T Prophylactic (median, range)

Therapeutic (median, range)

1.0 (0.5-2.0) 6 (1.0-61)

4.0 (0.5-16.0) 19 (2-290)

bolus [mg] iN.infusion [pg kg-1 h-l] Haloperidol

0.15 (0.075-0.30) 0.83 (0.07 3.39)

0.3 (0.15-1.2)

bolus [mg] i.v.infusion [t16kg] h ]] Clomethiazol bolus [mg] i.v.infusion [mg kgl h 11

10 (5-20) 29 (9 99)

20 (10-40) 53 (5 355)

Flunitrazepam bolus [mg] i.v. infusion [ ~ kg-~ h-q Clonidine

0.9 (0.14 4.7)

150 (25 500)

375 (45 500)

2.5 (0.6 8.9)

8 (1.5 12.0)

Table 11: CllmrM management of physlrM withdrawal symptoms (prophylactic or therapeutic) in patients with SUD ( atmhot)ge Flunilxazepam has recently been banned in the US because of its misuse for 'date rape '1°5, but remains available in many other countries. Flunitrazepam can be easily substituted with alternative longer-acting benzodiazepines such as diazepam or lorazepam. Adjuvant drugs are r e c o m m e n d e d to reduce the intensive sympathetic stimulation, eg clonidine 78,95,g6 or ~]-blockers 95 and h a l o p e r i d o l d u r i n g hallucinations 95,91. In some counlxies clomethiazo196, z0e has b e e n used successfully (Table 11), w h e r e a s the s u b s t i t u t i o n w i t h b a r b i t u r a t e s is n o l o n g e r recommended 97. However, during the administration of c l o m e t h i a z o l and haloperidol, significantly more patients developed bronchial hypersecretion followed by increased incidence of pulmonary complications and the need for artificial mechanical ventilationZ0k These side effects are not seen with clonidine 96,m7. T h e prophylactic i.v. infusion of low doses of ethyl alcohol to prevent withdrawal symptoms in alcoholics may be effective, but recently published evidence based guidelines do not recommend this therapeutic approach 95. Since both clonidine and neuroleptics may decrease the seizure threshold, they should only be a d m i n i s t e r e d in c o m b i n a t i o n w i t h b e n z o diazepines 95. Here, low p o t e n t aliphatic p h e n o t h i a z i n e s (eg c h l o r p r o m a z i n e , t h i o x a n t h e n e , chlorprothixene) diminish the seizure threshold more t h a n o t h e r n e u r o l e p t i c s 79. For t e r m i n a t i o n o f w i t h d r a w a l p r o p h y l a x i s / t h e r a p y w i t h clonidine, benzodiazepines and clomethiazol, these drugs should be tapered slowly over days (clonidine) to weeks (benzodiazepines) to prevent withdrawal symptoms to the substitutes.

152

Benzodtazepines and barbiturates Polysubstance abusers prefer long acting benzo diazepines such as flunitrazepam or diazepam, or else b a r b i t u r a t e s for s e l f - t r e a t m e n t of w i t h d r a w a l symptoms clue to alcohol or opioids 12,39,40,109-111. Isolated SUD with low doses of benzodiazepines is also seen lc~.

Analgesia and prevention/therapy of withdrawal The initial opioid doses are the same as in patients without SUD; increasing doses of p-agonists should be titrated carefully since there is no cross-tolerance to opioids 12. Patients with polysubstance dependence ( w i t h o u t opioids) o f t e n have a higher n e e d of analgesics which is based on physical dependence, m e n t a l alterations or u n r e c o g n i s e d w i t h d r a w a l symptoms but not on opioid tolerance. The whole spectrum of muki modal analgesia69 should be used (Table 8). B e n z o d i a z e p i n e s s h o w c r o s s - t o l e r a n c e to barbiturates and alcohol and cause similar withdrawal symptoms (Table 6) 12,2g. T h e r e f o r e , long acting b e n z o d i a z e p i n e s are suitable for w i t h d r a w a l p r o p h y l a x i s or t h e r a p y in d r u g addicts and alcoholics 3L39,40,56,93. T h e antidote flumazenfl should be strictly avoided 11&112. A b r u p t t e r m i n a t i o n of regularly used benzodiazepines can produce serious and o c c a s i o n a l l y l i f e - t h r e a t e n i n g w i t h d r a w a l symptoms29,111 After the e n d of acute therapy, the doses of substituted benzodiazepines should be tapered very slowly over weeks to avoid withdrawal symptoms to the d i s c o n t i n u e d benzodiazepines lll,ll2. N e u r o leptics 7g should be used cautiously

V o l u m e 3 (3) S e p t e m b e r 2000

Acute Pain

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T

Part 2 of this review will go on to look at the areas of clinical aspects of SUD with CNS s t i m u l a n t substances and patients in drug-free recovery.

References 1.

2.

3.

.

5.

.

.

.

.

10. 11.

12.

13.

14.

DSM IV. Diagnostic and statistical manual of mental disorders. Washington DC: American Psychiatric Association, 1994 (4th ed). Eddy NB, Halbach H, Braenden OJ. Synthetic substances with m o r p h i n e - l i k e effect. Clinical experience: potency, side effects, addiction liability. Bu//WHO 1957; 17: 569~63. ]sbell H, Eisenman AJ. The addiction liability of some drugs of the methadon series. J Pharmacot Exptt Therap

1948, 93:305 312. Jasinski DR. Assessment of the abuse potentiality of morphinelike drugs (methods used in man). In: Martin W R (ed). Drug Addiction [. Handbook of Experimental Pharmacology. New York: Springer-Verlag 1977; 45/I: 197 258. Zacny JP, Galinkin JL. Psychotropic drugs used in anesthesia practice. Abuse liability and epidemiology of abuse. Anesthesiology 1999; 90:269 288. Savage S R. Addiction in the treatment of pain: Significance, recognition and treatment. J Pain Sympt Manage1993; 8:265 278. Bond C, LaForge KS, Tian M. Single nucleotide polymorphism in the human mu opioid receptor gone alters B endorphine binding and activity: possible implications for opioid addiction. Pro¢ Natt Acad Sci 1998; 95: 9608-9613. Gardner EL. Brain reward mechanisms. In: Lowinson ]H, Ruiz P, Millman RB (eds). Comprehensive textlr~ok of Substance Abuse. 3rd edn. Baltimore: Williams & Willdns 1997; 514~5. I~eek MJ, Koob GF. Drug dependence: stress and dysregulation of brain reward pathways. Drug Alcohol Depend 1998; 51: 23-47. K o o b GF, Le Moal M. Drug abuse: hedonic homeostasis dysregulation. Scienoe 1997; 278: 52-58. Steindler EM. ASAM addiciton terminology. In: Graham AW, Schultz TK (eds). Principles of Addiction Medicine. 2nd edn. Chevy Chase, MD: American Society of Addition Medicine, 1998; 1301-1304. Jaffe JH. Drug addiction and drug abuse. In: Gilman AG, Rail TW, Nies AS, Taylor P (eds). ~ and Gilman "s The Pharmacological Basis of Therapeutics. 8th ed. New York: Pergamon Press 1990; 522 573. Wilder A. R e c e n t progress in research on the neurophysiologic basis of morphine additiction. Am J Psy~atr 1948; 329 338. Ayesta FJ. Tolerance and physical dependence: Physiological manifestations of chronic exposure to opioids. In: Herz A (ed). Neurobtotogy of Optolds. New York: Springer-Veflag 1991; 387-405.

Acute Pain

15. Martin W R , Sloan JW. Morphine dependence. In: Martin W R (ed). Drug Addiction I. Handbook of Experimental Pharmacology. New York: Springer Veflag 1977; 45/I: 43-158. 16. Nestler EJ, Hope BT, Widnell KL. Drug addiction: A model for the molecular basis of neuronal plasticity. Neuron 1993; 11: 995-1006. 17. Compton P, Gebhardt GF. The neurophysiology of pain in addiction. In: Graham AW, Schultz TK (eds). Principles of Addiction Mediane. 2nd edn. Chevy Chase, MD: American Society of Addiction Medicine, Inc.

1998; 901 917 18. Woolf CJ, Chong MS. Preemptive analgesia- treating postoperative pain by preventing the establishment of

central sensitization. Anesth Analg 1993; 77; 362 379. 19. Bradley BP, Gossop M, Phillips GT, Legarda ]]. The development of an opiate withdrawal scale (OWS). Br HAddia 1987; 82:1139 1142. 20. Aghajanian GK, Wang YY. Common alpha 2- and opiate-effector mechanisms in the locus coeruleus: intracellular studies in brain slices. Neuropharmacot 1987; 26:793 799. 21. Kienbaum P, Thfirauf N, Michel MS, et al. Profound increase in epinephrine concentration in plasma and cardiovascular stimulation after mu opioid receptor blockade in opioid-addicted patients during barbiturate induced anesthesia for acute detoxification. Anesgnesiotogy 1998; 88:1154 1161. 22. Martin WR, Jasinski DR. Physiological parameters of morphine dependence in man: tolerance, early abstinence, protracted abstinence. J Psychlatr Res 19691

7: 9-17. 23. Seevers M H , W o o d s LA. T h e p h e n o m e n a of tolerance. AmJMed 1953; 546 557. 24. Cox BM. Mechanisms of tolerance. In: Stein Ch (ed).

Oplolds In Pain Control. Basis and clinical aspects. Cambridge: Cambridge University Press 1999, 109 130. 25. Bradley BP, Gossop M, Phillips GT, Legarda JJ. The development of an opiate withdrawal scale (OWS). [Jr J Addia 1987;82:1139-1142. 26. Loimer N, Linzmayer L, Grtmberger J. Comparison between observer assessment and itsself rating of withdrawal distress during opiate detoxification. Drag

Alcohol Depend 1991; 28:265 268. 27. Kreek MJ. Exogenous opioid: drug disease interactions. In: Foley KM, Inturrisi CE (eds). Adv Pain Res Thor 1986; 8:201 210. 28. Kreek MJ. Long term pharmacotherapy for opiate (primarily heroin) addiction: Opioid agonists. In: Schuster C R , Kuhar MJ (eds). Handbook of Experimental Pharmacology. New York: Springer Vedag 1996; 118: 487-562. 29. O'Brien CP. Drug addiction and drug abuse. In: Mardman JG, Limbird LE, Molinoff PB, Ruddon RW, Gilman AG (eds) Goodman and Gihnan's. The

V o l u m e 3 (3) S e p t e m b e r 2000

153

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T

30.

31. 32.

33.

34.

35.

36.

37.

38.

39.

40.

41.

42.

43.

154

Pharmacological Basis of Therapeutics. 9th edn. New York: Pergamon Press 1996; 557-577. Fisehman MW, Johanson C E. Cocaine. In: Schuster CR, Kuhar MJ (eds). Handbook of Experimental Pharmacology. New York: Springer 1996; 118: 159195. Hyman SE. Addiction to cocaine and amphetamine. Neuron 1993; 16:901-904. Mendelsohn JH, Mello NK. Management of cocaine abuse and dependence. New Engt J Med 1996; 334: 965-972. Withers NW, Pulvirenti L, Koob GF, Gillin JC. Cocaine abuse and dependence. J Clgn Psychopharmacot 1995; 15: 63-78. Hobbs WR, Rail TW, Verdoom TA. Hypnotics and sedatives; ethanol. In: Hardman JG, Limbird LE, Molinoff PB, R u d d o n RW, Gilman AG (eds). Goodman and Gilman "s The Pharmacological Basis of Therapeutics. 9th edn. New York: Pergamon Press 1996; 361-396. Foley KM. Clinical tolerance to opioids. In: Basbaum AI, Besson JM (eds). Towards a New Pharmacotherapy of Pa/n. Chichester: Wiley 1991; 181-204. Foley KM. Opioid analgesics in clinical pain management. In: Herz A (ed). Optolds ~L. Handbook of Experimental Pharmacology. New York: SpringerVerlag. 104/II: 697 743. Beattie Ch, Mark L, Umbricht Schneiter A. Evaluation of the patient with alcoholism and other dependencies. In: Longnecker DE, Tinker JH, Morgan Jr GE (eds). Principles and Practice of Anesthesiology. 2nd edn. Boston: Mosby 1998; 537565. Jage J. Anaesthesia and analgesia in drug addicts. Anaesabes/st 1988; 37: 470-482. McCammon RL. Anesthesia for the chemically dependent patient. Intern Anesthesia Res Soc Anes~ Ana/g ~Suppl: Review Course Lectures) 1986; 47-55. Caldwell Ill TB. Anesthesia for patients with behavioral and environmental disorders. In: Katz J, Benumof JL, Kadis LB (eds). Anesthesia and Uncommon Diseases. 3rd edn. Philadelphia: WB Saunders 1990; 792 922. Winick C. Epidemiology. In: Lowinson JH, Ruiz P, Millman RB, Langrod JG (eds). Substance Abuse. 3rd edn. Baltimore: Williams & Wilkins 1997; 10 16. Helzer JE, Burnam A, McEvoy. Alcocol abuse and dependence. In: Robins LN, Regier DA (eds). PsycNatr/c Disorders in America: The eptderalogtc catchment gea study. New York: The Free Press, MacMillan Inc. 1991; 81 115. Anthony JC, Helzer JE. Syndromes of drug abuse and dependence. In: Robins LN, Regier DA (eds). Psychiatric Disorders In America: The epldemlologlc catchment area study. New York: The Free Press, MacMillan Inc. 1991; 116-154.

44. Kandal DB. Epidemiological trends and implications for understanding the nature of addiction. In: O'Brian CP, Jaffe JIt (eds). Addtc~e States. New York: Raven Press 1992; 23-40. 45. Lellan AT, Woody GE, O'Brian CP. Development of psychiatric illness in drug abusers. N EngtJMed 1979; 301: 1310-1314. 46. Rounsaville BJ, Zelig SD, Babor TF, Meyer ER. Psychopathology as a predictor of treatment outcome in alcoholics. Arch Gen Psy~atry 1987; 44: 505-513. 47. Scott LE. Clum GA, Peoples JB. Preoperative predictors of postoperative pain. Pain 1983; 15:283 293. 48. National Household Survey on Drug Abuse: 19721991 (ages 12 17). Rockville, MD: US Deparmaent of Health and Human Services 1993. 49. Moss AR. AIDS and intravenous drug use: the real heterosexual epidemic. Br MedJ 1987: 294: 389. 50. Savage SR. Principles of pain treatment in the addicted patient. In: Graham AW, Schultz TK (eds). Principlesof Addiction Medicine. 2nd edn. Chevy Chase, MD: American Society of Addiction Medicine, Inc. 1998, 919-944. 51. Simon R, Tauscher M, Gessler A. Suchtbericht Deutschland 1997. Schneider Verlag Hohengehren GmbH. 52. Kosten TR, Rounsa~ille BJ, Kleber HD. Antecedents and consequences of cocaine abuse among opioid addicts: A 2.5 year follow-up. J Nerv Ment Dis 1988; 176:176 181. 53. Cisek JE. Substance users. In:Goldfrank LR, Flomenbaum NE, Lewin NA, Weisman RS, Howland MA, Hoffman RS (eds). Gotdfrank's Toxicologic Emergencies. 6th edn. Stanford, Conneticutl Appleton & Lange, 1998; 1729-1740. 54. Sapira JD. The narcotic addict as a medical patient. Am JMed 1968; 45:555 588. 55. Cushman P. The major medical sequelae of opioid addiction. Drug Alcohol Depend 1980; 5:239 254. 56. Wood PR, Soni N. Anaesthesia and substance abuse. Anaesthesia 1989, 44: 672-680. 57. Latasch I, Christ R. Anaesthetic problems in drug addicts. Anaesthes/st1988; 37:123 139. 58. Passik SD, Portenoy RK (1998) Substance abuse issues. In: Ashbum MA, Rice LJ (eds). The Management afPatn. New York: Churchill Livingstone 1998; 51431 59. Miaskowski C, Crews J, Ready LB, Paul SM, Ginsberg B. Anesthesia based pain services improve the quality of postoperative pain management. Pain 1999; 80: 23-29. 60. Jage J, Faust P, Strecker U, et aL Clinical efficiency of postoperative analgesia with i.v. PCA or continuous epidural analgesia. Anaestheslot I_ntenslvmed 1996; 9: 459 475. 61. De Leon Casasola OA, Lema MJ, Karabella D, Harrison P. Postoperative myocardial ischemia:

V o l u m e 3 (3) S e p t e m b e r 2000

Acute Pain

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T

62.

63.

64.

65.

epidural versus intravenous patient controlled analgesia. RegAnesth 1995; 20:105-112 Liu S, Carpenter RL, Neal JM. Epidural anesthesia and analgesia. Their role in postoperative outcome. Anesthesi0/ogy 1995; 82: 1474-506. Schug SA, Fry RA. Continuous regional analgesia in comparison with intravenous opioid administration for routine postoperative pain control. Anaesthesia 1994; 49:528 532. Wulf H, Schug S, Allvin R, Kehlet H. Postoperative patient management- how can we make progress? Acute Pain 1998; 1:32 44. Louria DB, Hensle T, Rose J. The major medical complications of heroin addiction. Ann Intern Med

1967; 67:1 22. 66. Douglas FG, Kaffflrnout KJ, Patt NL. Foreign particle embolism in drug addicts: Respiratory pathophysiology. Ann Jrntern Med 1971; 75:865 872. 67. Gianoulakis C, Drouin IN, Seidah NG, et al. Effect of chronic morphine treatment on beta-endorphin biosynthesis by the rat neurointermediate lobe. Eur J Pt~arrnamt1981; 72:313 316. 68. St.immel B. Pain and its Relief without Addiction. Clinical issues In the use of oplotds and otheranalgesics. New York: Haworth Medical Press, 1997. 69. Kehlet H, Dab1 JB. The value of 'multimodal' or 'balanced analgesia' in postoperative pain treatment. Anesth Analg 1993; 77:1048 1056. 70. Hagmeyer KO, Mauro LS, Mauro VF. Meperidinerelated seizures associated with patient controlled analgesia pumps. Arm Pbarmac0ther 19931 27:29 32. 71. Stacey BR, Brody MC, Burke DF. Patients with substance abuse history can effectively use PCA. Anesthesiology 1990; 73: A759. 72. Bailey PL, Pace NL, Ashbum MA, et at. Frequent hypoxemia and apnea after sedation with midazolam and fentanyl. Anesthesiology 1990; 73:826 73. Reisine T, Pasternak G. Opioid analgesics and antagonists. In: Hardman JG, Limbird LE, Molinoff PB, Ruddon RW, Gilman AG (eds). Goodman and Gilman "s The Pharmamlogimt Basis of Therapeutics. 9th edn. New York: Pergamon Press 1996; 521 555. 74. Steffen P, Schuhmacher, Weichsel T, el at. Investigations on the use of non-opioid analgesics in postoperative pain therapy I: Quantification of the analgesic efficacy of metamizol (dipyrone) using patient-controlled analgesia. An~stheslol Intenslvmed Notfaltmed Schmerzther 1996; 31:143 147. 75. Steffen P, Drfick A, Krinn E, et al. Investigations on the use of non-opioid analgesics in postoperative pain therapy [I Quantification of the analgesic efficacy of metamizol (dipyrone) in combination with diclofenac using p a t i e n t - c o n t r o l l e d analgesia. Anastheslol ]nter~ivmed Notfallmed Schmerzther 1996; 31: 216-221. 76. Eap CB, Finkbeiner T, Gastpar M, et al. Replacement of ( R ) - m e t h a d o n e by a double dose of (R,S)-

Acute Pain

77. 78.

79.

80.

81.

82.

83. 84.

85.

86. 87.

88.

89.

90.

91.

methadone in addicts: interindividual variability of the (R) /(S) ratios and evidence of adaptive changes in methadone pharmacokinetics. Eur J Clin Pharmamt 1996; 50: 385-389. Jage J. Methadone pharmacokinetics and pharmaco dynamics of an opiate. Anaestheslst 1988; 38:159 166. Maze M, Tranquili W. A l p h a 2 - a d r e n o c e p t o r agonists: Defining the role in clinical anesthesia. Anesthesiology 1991; 74:581 605. Baldessarini RJ. Drugs and the t r e a t m e n t of psychiatric disorders. In: Hardman JG, Limbird LE, Molinoff PB, R u d d o n RW, Gilman AG (eds). Goodman and Gilman "s The Pharmacological Basis of Therapeutics. 9th edn. New York: Pergamon Press 1996; 399 430. Johnson RE, Jaffe JH, Fudala PJ. A controlled trial of buprenorphine treatment for opioid dependence. ]AMA 1992; 287:2750 2755. Bederson J, Field H, Barbaro N. Hyperalgesia during naloxone precipitated withdrawal from morphine is associated with increased on,:ell activity in the rostral ventromedial medulla. Somato~en~ Mot~ Res 1990; 2: 185-188. Levin ER, Sharp B, Drayer JIM, Weber MA. Case report. Severe hypertension induced by naloxone. A m J M e d S a 1985; 290: 70-72. Andree RA. Sudden death following naloxone administration. Anesth Analg 1980; 59: 782-784. Way EL, Loh HH, Fu-hsiung Shen. Simultaneous quantitative assessrnemt of morphine tolerance and physical dependence. J Pharmacol Exptt Therap 1969; 167:1-28. Manfredi PL, l~dbeiro S, Cahndler SW, Payne R. Inappropriate use of naloxone in cancer patients with pain. J Pam Sympt Manage 1996; 11: 131-134. Brewer C. Opiate detoxification under anaesthesia. BrMedy 1998; 316: 1983-1984. G o n ~ e s JP, Brogden I~N. Naltrexone: a review of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy in the treatment of opioid dependence. Drugs 1988; 35: 192-213. Kreek MJ. Long term pharmacotherapy for opiate (primarily heroin) addiction: Opioid antagonists and partial agonists. In: Schuster CR, Kuhar MJ (eds). Handbook of Experimental Pharmacology New York: Springer 1996; 118: 563-598. Volpicelli JR, Alterman AI, Hayashida M, O'Brian CP. N a l t r e x o n e in the t r e a t m e n t of alcohol dependence. Arch Gen Psych/arty 1992; 49: 8764~80. American Hospital Formulary Service (AHFS). American Society of Health System Pharmacists, Inc. Bethesda, Maryland 1999; 1839-1846. MiUan MJ, Morris BJ, Herz A. Antagonist-induced opioid receptor up regulation: characterization of supersensitivity to selective mu and delta agonists. J Pharmamt Expt Ther 1988; 247: 721-727.

V o l u m e 3 (3) S e p t e m b e r 2000

155

Postoperative analgesia in patients with substance use disorders: Part I Jage J, Bey T

92. Bruce DL. Alcoholism and anesthesia. Anesth Anatg 1983; 62: 84-89. 93. Samson HH, Harris RA. Neurobiology of alcohol abuse. TIPS 1992: 13:206 211. 94. Tabakoff B, Hellevuo K, Hoffman PL. Alcohol. In: Schuster C R , Kuhar MJ (eds). Handbook of Experimental Pbarmamtotly. New York: Springer 1996: 373-458. 95. Mayo Smith MF for the American Society of Addiction Medicine W o r k i n g Group on pharmacological management of alcohol withdrawal. JAMA 1997: 278:144 151. 96. Spie~ CD, Rornmelspacher H. Alcohol withdrawal in the surgical patient: Preventiion and treatment. Anesth Ana/g 1999; 88:946 954. 97. Plinius Major Society. Guidelines on evaluation of treatment of alcohol dependence. Alcoholism 1994; 30: S1 8. 98. Burchfiel J-L, Duchowny MS, Dully FH. Neuronal supersensitivity to acetylcholine induced by kindling in the rat hippocampus. Sclente 1979; 204:1096 1098. 99. Tsueda K, Lloyd GE, Heine MF, et at. Opiates in ethanol withdrawal. Anestb Ana/g 1995; 81: 874477. 100.Ballantyne JC, Carr DB, deFerranti S, et at. C o m p a r a t i v e effects of postoperative analgesic therapies in pulmonary outcome: Cumulative metaanalyses of randomized, controlled trials. Anes/h Ana//~ 1998: 86:598 612. 101.Mangano DT, Siliciano D, Hollenberg M, et at. Postoperative myocardial isehemia. Therapeutic trials using intensive analgesia following surgery. Anes~eslotogy 1992; 76: 342-353.

102.Beattie WS, Buckley DN, Forrest JB. Epidural m o r p h i n e reduces the risk of p o s t o p e r a t i v e myocardial ischemia in patients with cardiac risk

156

factors. CanJAnaesth 1993; 40:532 541. 103.Liu SS, Carpenter t ~ , Mackey DC, et aL Effects of perioperative analgesic techniques on rate of recovery after colon surgery, anestbestotog g 1995: 83:757 765. 104. Regier DA, Farmer ME, Rae DS, et al. Comorbidity of mental disorders with alcohol and other drug abuse. Results from the Epidemiologic Catchment Area (ECA) ~udy. J A M A 1990; 264: 2511-2518. 105.Saum CA, Inciardi JA. Rohypnol misuse in the United States. Substanae Use Misuse 1997; 32:723 731. 106.Spies C, Rommelspacher H, Schaffartzik W. Chronic alcoholics: high risk patients in intensive care units. In: Vincent JL (ed) Yearbook ff Inter~We Care Medicine. New York: Springer-Verlag 1995; 777-788. 107.Schinzel H, W e i l e m a n n LS, Swars H, et at. Experiences in treatment of acute alcohol withdrawal syndrome with clonidine in an intensive care unit. [ntemtvraediztn 1993; 30:79 83. 108.Sullivan JT, Sykora K, Schneiderman J, et at. Assessment of alcohol withdrawal: the revised clinical institute withdrawal assessment of alcohol scale (ClWAAr). BrJAddlct 1989; 84:1353 1357. 109.Owen RT, Tyrer P. Benzodiazepine dependence. Drugs 1983; 25:385 398. 110.Woods JH, Katz ~ , Winger G. Benzodiazepines: use, abuse and consequences. Pbarraacol Rev 1992; 44: 151 347. 111.Eickelberg SJ, Mayo Smith M. Management of sedative-hypnotic intoxication and withdrawal. In: Graham AW, Schultz TK (eds). Principles of Addiction Medicine. 2nd edn. Chevy Chase, MD: American Society of Addition Medicine, Inc. 1998; 441-455. ll2.Derlet R W , Albertson TE. Flumazenil induces seizures and death in mixed cocaine diazepam intoxications. Ann Eraerg Med 1994; 23: 494-498.

V o l u m e 3 (3) S e p t e m b e r 2000

Acute Pain