Psychiatric Disorders
Depression is a mood disorder characterized by sadness and pessimism. Its cause is multifactorial, but pharmacological treatment is based on the presumption that its manifestations are due to a brain deficiency of dopamine, norepinephrine, and serotonin or altered receptor activities.
Up to 50% of patients with major depression hypersecrete cortisol and have abnormal circadian secretion.
Current pharmacological therapy utilizes three classes of drugs that increase brain levels of these neurotransmitters: tricyclic antidepressants, monoamine oxidase (MAO) inhibitors, and atypical antidepressants.
The mechanisms of action of these drugs result in some potentially serious anesthetic interactions.
Electroconvulsive therapy (ECT) is increasingly used for refractory and severe cases and prophylactically once the patient returns to baseline. The use of general anesthesia for ECT is largely responsible for its safety and widespread acceptance.
All tricyclic antidepressants work at nerve synapses by blocking neuronal reuptake of catecholamines, serotonin, or both.
Desipramine (Norpramin and Pertofrane) and nortriptyline (Pamelor and Aventyl) are commonly used because they are less sedating and tend to have fewer side effects.
Other agents are generally more sedating and include amitriptyline (Elavil [withdrawn from the U.S. market]), imipramine (Tofranil and Janamine), protriptyline (Vivactil), amoxapine (Asendin), doxepin (Sinequan and Adapin), and trimipramine (Surmontil).
Clomipramine (Anafranil) is used in the treatment of obsessive–compulsive disorders.
Most tricyclic antidepressants also have significant anticholinergic (antimuscarinic) actions: dry mouth, blurred vision, prolonged gastric emptying, and urinary retention. Quinidine-like cardiac effects include tachycardia, T-wave flattening or inversion, and prolongation of the PR, QRS, and QT intervals. Amitriptyline has the most marked anticholinergic effects, whereas doxepin has the fewest cardiac effects.
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· Anti-depressant drugs are generally continued perioperatively. Increased anesthetic requirements, presumably from enhanced brain catecholamine activity, have been reported with these agents.
· Potentiation of centrally acting anticholinergic agents (atropine and scopolamine) may increase the likelihood of postoperative confusion and delirium.
· The most important interaction between anesthetic agents and tricyclic antidepressants is an exaggerated response to both indirect-acting vasopressors and sympathetic stimulation.
· Pancuronium, ketamine, meperidine, and epinephrine-containing local anesthetic solutions should be avoided (particularly during halothane anesthesia).
· Chronic therapy with tricyclic antidepressants is reported to deplete cardiac catecholamines, theoretically potentiating the cardiac depressant effects of anesthetics.
· If hypotension occurs, small doses of a direct-acting vasopressor should be used instead of an indirect-acting agent. Amitriptyline's anticholinergic action may occasionally contribute to postoperative delirium.
MAO inhibitors may be more effective for patients with depression accompanied by panic attacks and prominent anxiety. They block the oxidative deamination of naturally occurring amines.
At least two MAO isoenzymes (types A and B) with differential substrate selectivities have been identified. MAO A is selective for serotonin, dopamine, and norepinephrine, whereas MAO B is selective for tyramine and phenylethylamine.
Currently available agents that are effective in treating depression are nonselective MAO inhibitors. They include phenelzine (Nardil), isocarboxazid (Marplan), and tranylcypromine (Parnate).
Selective MAO-B inhibitors (see above) are not effective in the treatment of depression.
Nonselective agents also appear to interfere with many enzymes other than MAO.
Side effects include orthostatic hypotension, agitation, tremor, seizures, muscle spasms, urinary retention, paresthesias, and jaundice. Their hypotensive effect may be related to the accumulation of false neurotransmitters (octopamine). The most serious sequela is a hypertensive crisis that occurs following ingestion of tyramine-containing foods (cheeses and red wines).
The practice of discontinuing MAO inhibitors at least 2 weeks prior to elective surgery is no longer recommended. With the exception of tranylcypromine, these agents produce irreversible enzyme inhibition; the 2-week delay allows sufficient regeneration of new enzyme.
Studies suggest that patients may be safely anesthetized, at least for ECT, without this waiting period.
Phenelzine can decrease plasma cholinesterase activity and prolong the duration of succinylcholine.
Opioids should generally be used with caution in patients receiving MAO inhibitors, as rare but serious reactions to opioids have been reported. Most serious reactions are associated with meperidine, resulting in hyperthermia, seizures, and coma.
As with tricyclic antidepressants, exaggerated responses to vasopressors and sympathetic stimulation should be expected. If a vasopressor is necessary, a direct-acting agent in small doses should be employed.
Drugs that enhance sympathetic activity such as ketamine, pancuronium, and epinephrine (in local anesthetic solutions) should be avoided.
These include fluoxetine (Prozac), which is available in a once-weekly preparation, sertraline (Zoloft), and paroxetine (Paxil), which some clinicians consider first-line agents of choice for depression.
These agents have little or no anticholinergic activity and do not affect cardiac conduction.
Their principal side effects are headache, agitation, and insomnia.
Other atypical agents include bupropion (Welbutrin), venlafaxine (Effexor), also available in an extended-release formulation,
trazodone (Desyrel), nefazodone (Serzone), fluvoxamine (Luvox), maprotiline (Ludiomil), and mirtazapine (Remeron), which is available in an oral-disintegrating tablet (Remeron SolTab).
Maprotiline is not commonly used because of a relatively high incidence of seizures. Bupropion may primarily inhibit dopamine reuptake.
Anesthetic interactions with atypical antidepressants are not well documented.
Mania is a mood disorder characterized by elation, hyperactivity, and flight of ideas. Manic episodes may alternate with depression in patients with a bipolar disorder. Mania is thought to be related to excessive norepinephrine activity in the brain.
· Lithium (Eskalith, Lithobid) and lamotrigine (Lamictal) are the drugs of choice for treating acute manic episodes and preventing their recurrence, as well as suppressing episodes of depression.
· Concomitant administration of an antipsychotic (haloperidol) or a benzodiazepine (lorazepam) is usually necessary during acute mania.
· Alternative treatments include valproic acid, carbamazepine, and aripiprazole (Abilify), as well as ECT.
The mechanism of action of lithium is poorly understood. It has a narrow therapeutic range, with a desirable blood concentration between 0.8 and 1.0 mEq/L.
Side effects include reversible T-wave changes, mild leukocytosis, and, on rare occasions, hypothyroidism or a vasopressin-resistant diabetes insipidus-like syndrome.
Toxic blood concentrations produce confusion, sedation, muscle weakness, tremor, and slurred speech. Still higher concentrations result in widening of the QRS complex, atrioventricular block, hypotension, and seizures.
Although lithium is reported to decrease minimum alveolar concentration and prolong the duration of some NMBAs, clinically these effects appear to be minor. Nonetheless, neuromuscular function should be closely monitored when NMBAs are used.
The greatest concern is the possibility of perioperative toxicity. Blood levels should be checked perioperatively. Sodium depletion decreases renal excretion of lithium and can lead to lithium toxicity. Fluid restriction and overdiuresis should be avoided.
Patients with schizophrenia display disordered thinking, withdrawal, paranoid delusions, and auditory hallucinations. This disorder is thought to be related to an excess of dopaminergic activity in the brain. Antipsychotic drugs remain the only effective treatment for controlling this disease.
The most commonly used antipsychotics include phenothiazines, thioxanthenes, phenylbutylpiperadines, dihydroindolones, dibenzapines, benzisoxazoles, and a quinolone derivative.
Commonly used agents include haloperidol (Haldol), chlorpromazine (Thorazine), risperidone (Risperdal), molindone (Moban), clozapine (Clozaril), fluphenazine (Prolixin), trifluoperazine (Stelazine), thiothixene (Navane), perphenazine (Trilafon), aripiprazole (Abilify), and thioridazine (Mellaril).
All these agents have similar properties with minor variations. Clozapine may be effective in patients refractory to other drugs. The antipsychotic effect of these agents appears to be due to dopamine antagonist activity. Most are sedating and mildly anxiolytic. With the exception of thioridazine, all are potent antiemetics.
Mild 
-adrenergic blockade and anticholinergic activity are also observed. Side effects include orthostatic hypotension, acute dystonic reactions, and parkinsonism-like manifestations.
-adrenergic blockade and anticholinergic activity are also observed. Side effects include orthostatic hypotension, acute dystonic reactions, and parkinsonism-like manifestations. Risperidone and clozapine have little extrapyramidal activity, but the latter is associated with a significant incidence of granulocytopenia. T-wave flattening, ST segment depression, and prolongation of the PR and QT intervals may be seen, particularly in patients taking thioridazine.
Generally, patients whose disease is controlled by antipsychotics present few problems. Continuing antipsychotic medication perioperatively is desirable.
Reduced anesthetic requirements may be observed in some patients. -Adrenergic blockade is usually well compensated.
-Adrenergic blockade is usually well compensated. Ketamine should probably be avoided, as antipsychotics decrease the seizure threshold.
Neuroleptic malignant syndrome is a rare complication of antipsychotic therapy that may occur hours or weeks after drug administration.
Meperidine and metoclopramide can also precipitate the disorder. The mechanism is related to dopamine blockade in the basal ganglia and hypothalamus and impairment of thermoregulation.
In its most severe form, the presentation is similar to that of malignant hyperthermia. Muscle rigidity, hyperthermia, rhabdomyolysis, autonomic instability, and altered consciousness are seen.
Creatine kinase levels are often high. The mortality rate approaches 20–30%, with deaths occurring primarily as a result of renal failure or arrhythmias.
Treatment with dantrolene appears to be effective; bromocriptine, a dopamine agonist, may also be effective.
Although muscle biopsy is often normal, patients with a history of neuroleptic malignant syndrome should be treated in the same way as patients susceptible to malignant hyperthermia.
Behavioral disorders from abuse of psychotropic (mind-altering) substances may involve a socially acceptable drug (alcohol), a medically prescribed drug (eg, diazepam), or an illegal substance (eg, cocaine). Environmental, social, and perhaps genetic factors lead to this type of behavior. A "need" for the substance develops, ranging in intensity from a simple desire to a compulsion that consumes the patient's life. Characteristically, with chronic abuse, patients develop tolerance to the drug and varying degrees of psychological and physical dependence. Physical dependence is most often seen with opioids, barbiturates, alcohol, and benzodiazepines. Life-threatening complications primarily due to sympathetic overactivity can develop during abstention. Barbiturate withdrawal is potentially the most lethal and dangerous of the withdrawal syndromes.
Knowledge of a patient's substance abuse preoperatively may prevent adverse drug interactions, predict tolerance to anesthetic agents, and facilitate the recognition of drug withdrawal. The history of substance abuse may be volunteered by the patient (usually only on direct questioning) or deliberately hidden. A high index of suspicion is often required. Sociopathic tendencies are difficult to detect during a short interview. The presence of numerous punctate scars with difficult venous access strongly suggests intravenous drug abuse. Such injecting drug users have a relatively high incidence of skin infections, thrombophlebitis, malnutrition, endocarditis, hepatitis B and C, and HIV infection.
Anesthetic requirements for substance abusers vary depending on whether the drug exposure is acute or chronic (see Table 27–4). Elective procedures should be postponed for acutely intoxicated patients and those with signs of withdrawal. When surgery is deemed necessary in patients with physical dependence, perioperative doses of the abused substance should be provided or specific agents should be given to prevent withdrawal. In the case of opioid dependence, any opioid can be used, whereas for alcohol, a benzodiazepine is usually substituted. Tolerance to most anesthetic agents is often seen but is not always predictable. Regional anesthetics should be considered whenever possible. For general anesthesia, a technique primarily relying on a volatile inhalation agent may be preferable so that anesthetic depth can be readily adjusted according to individual need. Opioids with mixed agonist–antagonist activity should be avoided in opioid-dependent patients because such agents can precipitate acute withdrawal. Clonidine is a useful adjuvant in the treatment of postoperative withdrawal syndromes.
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1  , decreases; , increases; 0, no effect; ?, unknown. 2Associated with marked sympathetic stimulation. |
source: Clinical Anesthesiology, Fourth Edition
Chapter 27. Anesthesia for Patients with Neurologic & Psychiatric Diseases
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