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| CECIL |
| TEXT BOOK of MEDICINE |
Section XXVII Medical Consultation
| 460 MEDICAL CONSULTATION IN PSYCHIATRY Peter Manu • |
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HEALTH STATUS IN PSYCHIATRIC PATIENTS
The physical health of psychiatric patients is poor, with a higher risk for death at an early age than in the mentally sane. The magnitude of the problem is greatest in patients with schizophrenia, who have a 50% increased risk for death and 20% shorter lifespan. Poverty, social neglect, substandard medical care, unhealthy life habits, and complications of psychiatric treatments are major contributors to this increased morbidity and mortality. The problem is actually worsening even in First-World countries; in Stockholm County, Sweden, the standardized mortality ratio (observed/expected deaths) of 9.4 in males and 3.6 in females with schizophrenia in 1991 to 1995 was two-fold higher than in the previous decade.
MEDICAL EVALUATION IN PSYCHIATRIC SETTINGS
Requirements for medical training in psychiatry vary. In the United States, psychiatric residents have up to 4 months of inpatient medical training. Data suggest that psychiatrists have limited skills in assessing nonpsychiatric problems in terms of history taking, a reluctance to perform physical examinations, and a tendency toward premature diagnostic closure. As a result, the need for medical consultation is enormous. In one study, 1001 consecutively admitted psychiatric patients generated 2120 initial consultations (Table 460-1) and 1800 follow-up visits. The highest rate of medical utilization was for patients with dementia, schizophrenia, substance abuse disorders, and mental retardation. About 10% of patients seen by a medical consultant required transfer to a medical or surgical unit. Medical consultation in psychiatry is not more difficult than in other clinical settings but must be informed by knowledge about the serious complications of psychiatric treatments (Table 460-2). This chapter provides details about some of the most important entities specific to the psychiatric setting.
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EVALUATION OF CHIEF COMPLAINTS
Medical consultation for psychiatric patients creates unique challenges in evaluation of the chief complaint. Many patients with outpatient psychiatric disorders have somatic symptoms such as fatigue, weakness, dizziness, headache, insomnia, widespread pain, and constipation. In most of these patients, the underlying mental illnesses are mood disorders (unipolar depression and dysthymia), anxiety disorders (panic disorder and generalized anxiety disorder), somatoform disorders, substance use disorders (most often alcohol, opiates, cocaine, and benzodiazepine), and borderline personality disorder. As a group, these patients have many physical complaints and resist a psychological explanation for their symptoms even when the medical evaluation fails to identify objective abnormalities.
In contrast, patients admitted for inpatient psychiatric treatment often have psychotic disorders, developmental abnormalities, or dementia with behavioral disturbance; they are frequently vague or silent about physical suffering and only rarely voice somatic delusions. Such patients even may deny pain after bowel perforation or myocardial infarction.
A rigorous diagnostic evaluation is therefore required to avoid the errors of omission created by the weak correlation between complaints and pathology. This evaluation should include consideration of physical disorders, drug effects (adverse reaction, toxicity, or withdrawal), cognitive impairment (delirium), sensory impairment (loss of vision, hearing, speech, or postural balance), and situational maladjust-ment (isolation, overload, or loss of privacy). Attribution of symptoms to the patient's psychiatric condition should remain a diagnosis of exclusion.
MEDICAL COMPLICATIONS OF PSYCHIATRIC TREATMENTS
Antipsychotic-Induced Metabolic Syndrome
Metabolic syndrome is more prevalent (range, 29 to 63%) in schizophrenic and other psychiatric patients treated with atypical antipsychotic drugs such as clozapine, olanzapine, risperidone, and quetiapine than in the general population. Clozapine and olanzapine are the worst offenders because they induce substantial weight gain, thereby leading to insulin resistance (with or without fasting hyperglycemia) and atherogenic dyslipidemia. This gain in weight may be related to affinity for the histamine H1-receptor and to neurobiologic mechanisms that regulate appetite and metabolism via the production and activity of serotonin, leptin, and tumor necrosis factor-α. Within 18 months, 30% of patients treated with olanzapine will increase their body weight by more than 7%, with an average increase of 43 mg/dL in triglycerides, 15 mg/dL in blood glucose, and 0.41% in glycosylated hemoglobin. Not surprisingly, these changes result in about a two-fold increased risk for diabetes and coronary heart disease events. Nonetheless, controlled trials have identified olanzapine and clozapine as the most effective drugs for patients with schizophrenia and other psychotic disorders, and the beneficial therapeutic response sometimes correlates with the amount of weight gained during treatment.1 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) must be used aggressively to achieve individualized low-density lipoprotein cholesterol targets (Chapter 217). Blood pressure control should be obtained with judicious use of diuretics, angiotensin-converting enzyme inhibitors, angiotension receptor blockers, or calcium-channel blockers (Chapter 66). β-Adrenergic blockers are problematic in patients with comorbid depressive disorders, and α-adrenergic blockers should be used cautiously in patients receiving neuroleptics because they increase the potential for orthostatic hypoten-sion, syncope, and falls. The glucose intolerance often seen in patients treated with antipsychotic agents is due to insulin resistance and is best treated by weight reduction (Chapter 239), metformin, thiazolidinediones (pioglitazone or rosiglitazone; Chapter 239), or any combination of these measures. Smoking cessation programs combining transdermal or transmucosal nicotine replacement, bupropion, and cognitive-behavioral therapy should be strongly recommended despite the dismally high failure rates that have been reported in patients with chronic schizophrenia (Chapter 30).
Antipsychotic-Induced Myocarditis and Cardiomyopathy
Antipsychotic-induced myocarditis and cardiomyopathy (Chapter 59) are most common in patients treated with clozapine (0.9%) and fluphenazine (0.4%). In contrast, the risk for these complications is only 0.1% in patients receiving haloperidol, thioridazine, and risperidone.
The accepted pathophysiologic explanation for myocarditis is that of an IgE-mediated acute hypersensitivity reaction, similar to the allergic myocarditis produced by penicillins, sulfonamides, and methyldopa. In a small number of patients, a competing hypothesis proposes that clozapine induces hypereosinophilic myocarditis, colitis, hepatitis, pancreatitis, alveolitis, and interstitial nephritis. A direct cardiotoxic effect of drug metabolites cannot be excluded.
In patients in whom myocarditis develops, the mortality rate is as high as 50%, with almost half the deaths occurring suddenly and unexpectedly. The average duration of exposure to clozapine before diagnosis or death is 21 days, and the dosage range is 50 to 725 mg/day. Common symptoms are fever (48%), dyspnea (35%), “flulike illness” (30%), chest pain (22%), and fatigue (17%). Laboratory features include left ventricular hypokinesia or reduced ejection fraction (48%) or pericardial effusion (17%) on echocardiography, nonspecific repolarization abnormalities on electrocardiography (35%), peripheral eosinophilia (35%), elevated creatine kinase and troponin levels (22%), and radiographic evidence of heart failure (13%). The diagnosis can be confirmed by endomyocardial biopsy showing fraying of myocytes and perivascular infiltrates with degranulated eosinophils. Among survivors, symptoms resolve or substantially improve after discontinuation of clozapine and treatment with high-dose corticosteroids (e.g., prednisone, 1 mg/kg/day for 4 days, tapered to 0.33 mg/kg/day for the following 4 days).
Clozapine-induced dilated cardiomyopathy may be caused by an evolving myocarditis or by chronic injury mediated by free radicals, similar to the myocarditis produced by doxorubicin (Chapter 59). The demographic features are similar to those of myocarditis, but the mean duration of treatment before diagnosis is much longer (9 months vs. 3 weeks) and the mortality rate is lower (22 vs. 51%). Patients have clinical or echocardiographic evidence of left ventricular dysfunction without eosinophilia or enzymatic evidence of myocardial necrosis.
Prolonged QTc Interval and Sudden Death
Significant prolongation of the QTc interval (Chapter 64) leading to ventricular tachyarrhythmias and sudden cardiac death (Chapter 62) can occur after antipsychotic treatment with the usual doses of thioridazine, haloperidol, and sertindole. Abnormal myocardial repolarization has been observed during treatment with most antipsychotic medications and after intentional or accidental overdoses of tricyclic antidepressants, lithium, and methadone (Chapter 111). All antipsychotics affect the cardiac potassium channel by blocking the rapidly activating component of the rectifier potassium current (Chapter 60). This effect translates into a dose-dependent increase in the duration of phase 3 of the action potential. The drug concentration that produces 50% inhibition of rapid potassium outflow varies for each drug (e.g., 1 nmol/L for haloperidol and 6 nmol/L for olanzapine). For first-generation antipsychotics, the mean changes in QTc from baseline to the recommended steady-state drug dose range from 36 msec for thioridazine to 6 msec for quetiapine, 5 msec for haloperidol, and 0.2 msec for risperidone. In one study, QTc prolongation (to greater than 450 msec in males or 470 msec in females) was observed in 3% of patients treated with risperidone and quetiapine, 1% of patients receiving ziprasidone, but none of those treated with olanzapine.1 All patients about to start antipsychotic drugs should be asked about a personal history of syncope and a family history of long QT syndrome or sudden death at a young age. A baseline electrocardiogram and serum electrolytes should be obtained before starting antipsychotic drug therapy, tricyclic antidepressants, and methadone. Interval electrocardiograms should be obtained after each increase in medication in older patients, patients with known heart disease, and those starting other drugs known to produce QTc prolongation or hypokalemia (Chapter 64) A QTc interval of 500 msec or greater requires the discontinuation of all drugs that affect membrane repolarization. QTc intervals greater than 450 msec in males and 470 msec in females, QTc dispersion (difference between the longest and shortest QTc on a 12-lead electrocardiogram) greater than 100 msec, and an increase in QTc duration of more than 60 msec in comparison to the baseline measurement should prompt a re-evaluation of the risks and benefits associated with the drugs in question.
Choking and Laryngeal Dystonia
Asphyxia deaths from choking occur at a rate of 0.8% per 1000 psychiatric patients each year, a frequency that is more than 100 times greater than in the general population. In addition, videofluoroscopy demonstrates silent aspiration in 38% of psychiatric patients who survive a choking incident. Choking and silent aspiration are manifestations of dysphagia (Chapter 140), which is common in the mentally ill. Half the psychiatric patients with dysphagia have a fast-eating syndrome seen in association with restlessness, poor chewing skills, food pocketing in the cheeks, and attention deficits that characterize psychotic disorders and mental retardation. Bradykinetic dysphagia, which is seen in 25% of psychiatric patients with choking episodes, is due to the antidopaminergic and anticholinergic effects of psychotropic medications. This condition, which features reduced lingual range of motion, increased oral transit time, decreased pharyngeal peristalsis, and delayed initiation of the swallowing reflex, is seen in patients with neurologic features of drug-induced parkinsonism (Chapter 433). Dyskinetic dysphagia (7% of choking cases), which generally occurs in patients maintained on long-term antipsychotic medication, is part of the clinical spectrum of tardive dyskinesia (Chapter 434). The examination reveals involuntary contractions of the tongue and perioral musculature, clumsiness of voluntary movements of the tongue, and discontinuous bolus propulsion in the oral stage. In the remaining patients, the dysphagia is due to cerebrovascular disease (11%) or to pharyngeal or esophageal pathology (7%).
Laryngeal dystonia, which is a life-threatening complication of antipsychotic drug therapy, primarily with haloperidol and phenothiazines, is produced by acute spasmodic contraction of the adductor laryngeal muscles. Symptoms include respiratory distress, dysphonia, and stridor. Neuroleptic-induced bronchospasm may precede the onset of stridor. Patients typically indicate extreme subjective distress by clutching their anterior cervical area. The majority of patients also have other dystonias involving the head and neck, including torticollis, retrocollis, trismus, tongue protrusion, and deviation of the eyes up, down, or sideward. In general, the symptoms and signs develop in the first week after starting or rapidly increasing the dose of neuroleptic medications. Similar dystonic phenomena have been described after treatment with the antiemetics promethazine, prochlorperazine, and metoclopramide. A reduction in the dose of anticholinergic or antiparkinsonian medication used to prevent or treat extrapyramidal symptoms can also precipitate laryngeal dystonia. The condition is more common in young males and must be distinguished from epiglottitis, allergic/anaphylactic laryngeal edema or laryngospasm, mechanical obstruction, and psychogenic stridor. Intravenous administration of diphenhydramine (initial dose, 25 mg; may repeat after 5 minutes if symptoms persist) is the treatment of choice, and endotracheal intubation is seldom required.
Drug-Induced Neutropenia and Agranulocytosis
Drug-induced neutropenia with absolute neutrophil counts of less than 1500/mL has been observed during treatment with most second-generation antipsychotics (clozapine, olanzapine, risperidone, and quetiapine) and mood stabilizers (carbamazepine, valproic acid, and lamotrigine), as well as some antidepressant drugs (tricyclic antidepressants and mirtazapine). Clozapine-induced neutropenia occurs in 4 to 5% of patients within 6 months after starting treatment and progresses to agranulocytosis in 10% or more of neutropenic patients if the drug is continued. In vitro, clozapine toxicity requires peroxide and peroxidase, and the defect in oxidation is related to abnormalities in the NQO2 (quinone oxidoreductase) gene involved in drug detoxification. The cytotoxic effect can be blocked in vitro by exogenous glutathione, N-acetylcysteine, and ascorbic acid, but the therapeutic effect of these agents has not yet been studied. Treatment with clozapine should be started only if the baseline absolute neutrophil count is greater than 1500/μL. The concomitant use of carbamazepine, angiotensin-converting enzyme inhibitors, sulfonamides, and propylthiouracil should be avoided. Clozapine should be stopped and the patient evaluated immediately for fever, oral ulcerations, and symptoms or signs of infection. Complete blood counts should be obtained once a week for the first 26 weeks and every other week thereafter, and clozapine should be stopped and all medications reassessed if the absolute neutrophil count drops below 1500/μL. Clozapine-related agranulocytosis has been treated successfully with colony-stimulating factors (either granulocyte or granulocyte-macrophage colony-stimulating factor).
Neutropenia has also been associated with olanzapine, risperidone, and quetiapine in patients who have never received clozapine. Treatment with anticonvulsant mood stabilizers, particularly carbamazepine, is associated with a dose-dependent neutropenia and thrombocytopenia in approximately 10% of patients in the first 6 months of treatment and should be monitored with complete blood counts twice each month during this period.
Neuroleptic Malignant Syndrome
Neuroleptic malignant syndrome, which occurs in approximately 0.2% of patients receiving neuroleptics, must be part of the differential diagnosis of fever and rhabdomyolysis (Chapter 114) in a psychiatric patient (Table 460-3). The frequency is greater in young males and patients who are malnourished or dehydrated, have Parkinson's disease, or are treated parenterally with large doses of neuroleptics over short periods. The main diagnostic criteria are elevated temperature (higher than 104° F in 40% of patients) and diffuse muscle rigidity (ranging from mild hypertonicity to severe “lead pipe” stiffness). In addition, two or more of the following are required for a definitive diagnosis: (1) autonomic instability (tachycardia, elevated or labile blood pressure, postural hypotension, diaphoresis, sialorrhea, and urinary incontinence), (2) changes in mental status (ranging from confusion to mutism or coma), (3) leukocytosis (up to 20,000/mL), and (4) elevated creatine kinase (up to 100,000 IU/L). Other clinical manifestations include bradykinesia, chorea, dystonias, dysphagia, dysarthria or aphonia, seizures, and tremor. The severity of rhabdomyolysis correlates with the creatine kinase level and with the presence of myoglobinemia, myoglobinuria, metabolic acidosis, and azotemia. The electroencephalogram shows nonspecific slowing in slightly more than half of patients.
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The time lag from starting the drug to the onset of neuroleptic malignant syndrome is generally short, with 30% of cases developing within 48 hours and 96% within the first month of treatment. The exception appears to be clozapine-associated neuroleptic malignant syndrome, which has an average time lag of 50 days. Neuroleptic syndrome is sometimes confused with severe catatonia (Chapter 420), but the catatonic signs in neuroleptic malignant syndrome are usually restricted to mutism and akinesia. Furthermore, hyperthermia, rigidity, tremor, and rhabdomyolysis are not present in patients with catatonia. Nonetheless, close medical follow-up of severely catatonic patients is warranted because they are at very high risk (22%) for neuroleptic malignant syndrome.
Untreated, neuroleptic malignant syndrome has a mortality of 10% as a result of acute renal failure, aspiration pneumonia, adult respiratory distress syndrome, disseminated intravascular coagulation, and cerebellar neuronal degeneration. Most fatalities are avoidable if the diagnosis is made early, the neuroleptic agent is discontinued rapidly, and the patient is immediately transferred to an intensive care setting for supportive and specific therapy. Bromocriptine (2.5 mg three times daily orally or through a nasogastric tube; may increase by 2.5 mg three times daily to a maximum daily dose of 40 mg) or amantidine (100 mg orally or through a nasogastric tube twice daily; may increase to 300 mg/day in divided doses) should be used in moderately severe cases and continued until the muscle rigidity and metabolic abnormalities have significantly improved. The skeletal muscle relaxant dantrolene (starting with a dose of 1 mg/kg intravenously and titrated to a maximum of 10 mg/kg/day divided into three intravenous or oral doses) should be added to bromocriptine or amantidine in patients with fulminant hypermetabolic features and those with persistent muscle rigidity despite treatment with dopamine agonists. Refractory neuroleptic malignant syndrome improves after electroconvulsive therapy (ECT).
Serotonin Syndrome
Serotonin syndrome (Chapters 7 and 458) is an adverse drug reaction primarily produced by excess serotonergic agonism of central nervous system and peripheral serotonin receptors. The complication is induced by selective serotonin re-uptake inhibitors (SSRIs; sertraline, fluoxetine, paroxetine, and citalopram), monoamine oxidase inhibitors (phenelzine, moclobemide clorgiline), heterocyclic antidepressants (trazodone and nefazodone), dual-uptake inhibitors (venlafaxine), psychostimulants (amphetamines and cocaine), and buspirone. Other causative drugs in psychiatric patients include mood stabilizers (lithium and valproic acid), analgesics (tramadol, meperidine, and fentanyl), antiemetics (metoclopramide), cough suppressants (dextromethorphan), and dietary supplements (tryptophan, St. John's wort, and ginseng). In postmarketing surveillance studies of the newer antidepressants, the syndrome has an incidence of four cases per 10,000 patient months in patients who start taking nefazodone and has been shown to occur in 15% of patients with intentional overdose of SSRIs. The etiology of serotonin syndrome is overstimulation of 5-HT1A and possibly also 5-HT2 receptors through excess of serotonin precursors or agonists, increased serotonin release, reduced serotonin uptake, and decreased serotonin metabolism. Severe cases of the syndrome have been more frequently reported in patients treated with monoamine oxidase inhibitors who took over-the-counter dextromethorphan or the illegal methylenedioxymethamphetamine (Ecstasy) or who started treatment with serotonin re-uptake inhibitors or meperidine.
Potentially life-threatening, the syndrome is characterized by changes in mental status (ranging from agitation to confusion and coma), autonomic instability (tachycardia, labile or high blood pressure, diaphoresis, and diarrhea), neuromuscular abnormalities (myoclonus, mydriasis, ocular clonus, rigidity, hyperreflexia, tremors, and shivering), and hyperthermia. Death may occur as a consequence of rhabdomyolysis with renal failure, hyperkalemia, disseminated intravascular coagulation, and acute respiratory distress syndrome. The symptoms occur within the first 24 hours and sometimes within minutes after the initial use of medication, a change in dose, addition of a new drug, or overdose attempt. The differential diagnosis includes neuroleptic malignant syndrome, viral or bacterial meningitis or encephalitis, heat stroke, anticholinergic “toxidrome,” and drug or alcohol withdrawal.
General management includes immediate discontinuation of serotonergic drugs, comprehensive supportive therapy, and benzodiazepines for control of agitation and myoclonus. Specific therapy relies on the use of cyproheptadine (an H1-receptor antagonist with antiserotonergic and anticholinergic properties) and chlorpromazine (a 5-HT1A and 5-HT2 receptor antagonist). Cyproheptadine should be started at a dose of 12 mg administered orally or through a nasogastric tube and additional 2-mg doses given every 2 hours until symptoms improve or the maximum dose of 32 mg has been reached. The usual maintenance dose of cyproheptadine is 8 mg three times daily. Chlorpromazine (50 mg intramuscularly; may repeat three or four times daily and increase gradually to 400 mg/day in divided doses) is indicated in patients with severe symptoms who must be treated parenterally. Rapid improvement has also been observed after single doses of olanzapine (10 mg administered sublingually). Chlorpromazine and olanzapine should be used only after the possibility of neuroleptic malignant syndrome has been excluded.
Antipsychotic-Induced Hyperprolactinemia
Drug-induced hyperprolactinemia is produced by first-generation antipsychotic medications and by risperidone, but it is quite rare with other atypical antipsychotics such as aripiprazole, olanzapine, and ziprasidone. In patients treated with prolactin-raising antipsychotic medications, hormone levels are above the normal limit in 60% of females and 40% of males. Symptomatic hyperprolactinemia (Chapter 242) occurs in about a third of these patients and is generally associated with a 10-fold increase above baseline levels. Excess prolactin leads to dysfunction of target tissues (galactorrhea, oligomenorrhea and amenorrhea, infertility, sexual impairment, and gynecomastia), as well as an increased risk for breast cancer, osteoporosis, and cardiovascular disease. The mechanism of antipsychotic-related hyperprolactinemia is suppression of dopamine inhibition of lactotroph cells in the hypothalamus. Brain imaging is required in symptomatic patients and those with significant elevated prolactin levels to exclude tumors of the pituitary and hypothalamus.
Psychogenic Polydipsia and Drug-Induced Hyponatremia
Hyponatremia is common in psychiatric patients and can lead to severe complications, including seizure, coma, brain stem herniation, and death (Chapter 117). The diagnosis is often delayed because traditional manifestations of hyponatremia such as lethargy, restlessness, weakness, and disorientation overlap with features of psychiatric disorders. The differential diagnosis in psychiatric settings must emphasize psychogenic polydipsia and the drug-induced syndrome of inappropriate secretion of antidiuretic hormone (SIADH) (Chapter 117).
Patients with psychogenic polydipsia typically have serum hypo-osmolality and a maximally dilute urine (urine osmolality less than 100 mOsm/L). The incidence of polydipsia is 20% and the incidence of water intoxication is 5% in inpatient psychiatric facilities. Urinary incontinence and nocturnal enuresis may be part of the clinical manifestation. The mechanism of increased thirst is poorly understood but may involve incomplete suppression of antidiuretic hormone (ADH) by the hypothalamus, as well as response to the mouth dryness produced by the anticholinergic effect of many psychotropic drugs. The differential diagnosis includes diuretic effect, renal insufficiency, glucocorticoid deficiency, and hypothyroidism. Stringent measures to restrict fluid intake are generally effective in patients with moderate hyponatremia, and clozapine limits polydipsia and improves water intoxication in refractory cases.
Drug-induced SIADH is predominantly related to SSRIs, and animal experiments have suggested that the excess serotonin stimulates release of ADH and will lead to hyponatremia, provided that water intake is sufficient. Other drugs commonly used by psychiatric patients that may produce SIADH include tricyclic antidepressants, monoamine oxidase inhibitors, carbamazepine, first-generation antipsychotic medications, benzodiazepines, methadone, and nicotine. Elderly patients, patients with a lower body mass index, and those with a baseline plasma sodium level less than 138 mEq/L are at higher risk. The median time to diagnosis after starting SSRIs is 9 days. Urinary excretion of sodium usually is greater than 20 mEq/L, and urine osmolality is higher than 300 mOsm/L. In patients with mild asymptomatic hyponatremia, SSRIs can be continued with careful monitoring while the patient is placed on supervised fluid restriction.
Risk Assessment before Electroconvulsive Therapy
ECT is highly effective for the treatment of drug-refractory major depression and other psychiatric disorders. The procedure requires a brief period of general anesthesia with sodium penthothal, etomidate, or propofol, as well as muscle paralysis with succinylcholine, during which the patient receives bag-valve-mask ventilation with supplemental oxygen and is monitored with continuous electrocardiography and pulse oximetry. Bronchospasm may follow induction of anesthesia, particularly in patients already at risk for respiratory compromise. During electrical stimulation of the brain, parasympathetic activation can lead to bradycardia or several seconds of asystole, which can be avoided by premedicating the patient with intravenous glycopyrrolate. The parasympathetic effect lasts until onset of the akinetic seizure, when sympathetic tone increases and produces tachycardia, an elevation in blood pressure, and increased myocardial demand for oxygen. These changes can be corrected with intravenous esmolol. At the same time, because of the enhanced neuronal metabolic rate, augmented blood flow to the brain increases intracranial pressure. This elevated sympathetic tone causes ECT-related myocardial ischemia, tachyarrhythmias, and potential rupture of aortic or intracranial aneurysms. The elevated intracranial pressure may lead to brain herniation in patients with a space-occupying lesion. Older patients have a high rate of prolonged confusion, arrhythmias, and falls after ECT. A structured medical evaluation before ECT can address risks and the potential for complications (Fig. 460-1). All effort must be made to optimize the patient's active medical conditions before ECT. For high-risk patients one must require that ECT be performed in a setting that allows immediate access to an intensive care unit rather than in the ECT suite of a self-standing psychiatric hospital. Essential medications should be administered with a small amount of fluid 6 hours before ECT. Drugs that can increase or decrease the seizure threshold, such as lidocaine, theophylline, phenothiazine, tricyclic antidepressants, and benzodiazepines, must be discontinued before ECT. Optimal pre-ECT risk assessment, careful anesthesia, and post-ECT monitoring result in a serious complication rate of only 0.9% and essentially no fatalities.
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| FIGURE 460-1 Risk assessment before electroconvulsive therapy. BP = blood pressure; CAD = coronary artery disease; CHF = congestive heart failure; COPD = chronic obstructive pulmonary disease; DM = diabetes mellitus; HTN = hypertension. (Modified after Frederickson A, Manu P: Risk assessment prior to electroconvulsive therapy. In Manu P, Suarez RE, Barnett BJ [eds]: Handbook of Medicine in Psychiatry. Washington, DC, American Psychiatric Publishing, 2006, pp 687-700.) |
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