Charles A. Welch

Comparative effects of esmolol and labetalol to attenuate hyperdynamic states after electroconvulsive therapy

We studied 18 patients (age range, 53-90 yr) with at least one cardiovascular risk factor who were treated with electroconvulsive therapy (ECT) and compared effects of five pretreatments: no drug; esmolol, 1.3 or 4.4 mg/kg; or labetalol, 0.13 or 0.44 mg/kg. Each patient received all five treatments, during a series of five ECT sessions. Pretreatment was administered as a bolus within 10 s of induction or anesthesia. Doses of methohexital and succinylcholine were constant for the series of treatments and the assignment to no drug or to drug and dose was determined by randomized block design. Measurements of systolic and diastolic blood pressure (SBP, DBP) and heart rate (HR) were recorded during the awake state and 1, 3, 5, and 10 min after the seizure. The deviation of ST segments from baseline was measured by an electrocardiogram (ECG) monitor equipped with ST-segment analysis software. The results (mean +/- SEM) show that without pretreatment, there were significant (P<0.05) peak increases in SBP and HR (55 +/- 5 mm Hg and 37 +/- 6 bpm, respectively), recorded 1 min after the seizure. Comparable reductions (by approximately 50%) in these peak values were achieved after esmolol (1.3 mg/kg) or labetalol (0.13 mg/kg), and cardiovascular responses were nearly eliminated after the same drugs in doses of 4.4 and 0.44 mg/kg, respectively. The deviation of ST-segment values from baseline in any lead was not measurably influenced by either antihypertensive drug. SBP values were lower after labetalol 10 min after the seizure, but not after esmolol. Asystolic time after the seizure was not significantly longer with either drug. No adverse reactions were observed. Because SBP effects were still present 10 min after the seizure, esmolol may be preferred if administration of a large dose of a beta-adrenergic blocker is contemplated. (Anesth Analg 1995;80:557-61)

Depression and Costs of Health Care

BACKGROUND In spite of its global importance, the interaction between depression and chronic comorbid diseases remains incompletely understood with regard to prevalence, severity of disease, and potential causative factors mediating this interaction. OBJECTIVE The authors sought to compare overall medical costs in nondepressed and depressed individuals. METHOD Insurance claims for 618,780 patients were examined for total annual non-mental health cost of care in 11 chronic diseases. In each disease cohort, median annual non-mental health cost was calculated for individuals with and without depression. RESULTS Patients with depression had higher median per-patient annual non-mental health costs than patients without depression in all 11 diseases studied. There was a higher-than-random comorbidity between depression and all 11 chronic comorbid diseases. CONCLUSION Even when controlling for number of chronic comorbid diseases, depressed patients had significantly higher costs than non-depressed patients, in a magnitude consistent across 11 chronic comorbid diseases.

Encephalitis and catatonia treated with ECT.

ObjectiveTo describe 2 cases of encephalitis with neuropsychiatric symptoms including catatonia, compounded by neuroleptic use for delirious agitation culminating in malignant catatonia responsive to electroconvulsive therapy (ECT). BackgroundNeuropsychiatric symptoms including catatonia can be manifestations of limbic encephalitis and encephalitides of unidentified etiology, including encephalitis lethargica. Catatonic features are often difficult to appraise in this context. This can easily lead to the use of neuroleptics, which may precipitate worsening of catatonia. MethodMedical, neurologic, and psychiatric histories, physical examination findings, results of laboratory, imaging and neurophysiologic investigations, and treatment response with medications and ECT were recorded. ResultsBoth patients showed significant improvement with ECT. ConclusionsMalignant catatonia can complicate encephalitis lethargica and idiopathic limbic encephalitis, which already carry high mortality rates. When neuroleptics are used for agitation in cases of encephalitis, physicians must be wary of precipitating malignant catatonia and neuroleptics should be discontinued when such a danger emerges. Although lorazepam is helpful in treating catatonia, it may not suffice, as in the cases presented. ECT deserves serious consideration early in the course of malignant catatonia and for catatonia nested in encephalopathy secondary to encephalitis, unresolved with lorazepam.

Intracranial haemodynamics during attenuated responses to electroconvulsive therapy in the presence of an intracerebral aneurysm

OBJECTIVES This report describes successful anaesthesia and electroconvulsive therapy (ECT) in a patient with an unruptured basilar artery aneurysm. ECT is associated with a hyperdynamic state characterised by arterial hypertension, tachycardia, and considerably increased cerebral blood flow rate and velocity. These responses pose an increased risk for subarachnoid haemorrhage when an intracranial aneurysm coexists. METHODS A 54 year old woman presented for ECT. She had a 20 year history of major depression which was unresponsive to three different antidepressant drugs. There was also an unruptured 5 mm saccular aneurysm at the basilar tip, which had been documented by cerebral angiography, but its size had remained unchanged for the previous four years. After she declined surgical intervention, she gave informed consent for ECT. During a series of seven ECT sessions middle cerebral artery flow velocity was recorded by a pulsed transcranial Doppler ultrasonography system. She was pretreated with 50 mg oral atenolol daily, continuing up to the day of the last ECT and immediately before each treatment, sodium nitroprusside was infused at a rate of 30 μg/min, to reduce systolic arterial pressure to 90–95 mm Hg. RESULTS Systolic flow velocity during the awake state ranged from 62–75 cm/s, remaining initially unchanged with sodium nitroprusside infusion. After induction of anaesthesia (0.5 mg/kg methohexitone and 0.9 mg/kg succinylcholine), flow velocities decreased to 39–54 cm/s, reaching maximal values of 90 cm/s (only 20% above baseline) after ECT. These flow velocities recorded post-ECT were considerably below the more than twofold increase recorded when no attenuating drugs were used. Systolic arterial blood pressure reached maximal values of 110–140 mm Hg and heart rate did not exceed 66 bpm. Rapid awakening followed each treatment, no focal or global neurological signs were apparent, and the patient was discharged in remission. CONCLUSION In a patient with major depression and a coexisting intracerebral saccular aneurysm who was treated with ECT, the combination of β blockade with atenolol and intravenous infusion of sodium nitroprusside prevented tachycardia and hypertension, and greatly attenuated the expected increase in flow velocity in the middle cerebral artery.

Neuromuscular blocking agents for electroconvulsive therapy: a systematic review

Electroconvulsive therapy (ECT) is the transcutaneous application of small electrical stimuli to the brain to induce generalised seizures for the treatment of selected psychiatric disorders. The clinical indications for ECT as an effective therapeutic modality have been considerably expanded since its introduction. Anaesthesia and neuromuscular blocking agents (NMBAs) are required to ensure patients’ safety during ECT. The optimal dose of muscle relaxant for ECT reduces muscle contractions without inducing complete paralysis. Slight residual motor convulsive activity is helpful in ascertaining that a seizure has occurred, while total paralysis prolongs the procedure unnecessarily. Suxamethonium is commonly used, but nondepolarising NMBAs are indicated in patients with certain comorbidities. In this review, we summarise current concepts of NMBA management for ECT.

A double-blind, placebo-controlled study of the impact of galantamine on anterograde memory impairment during electroconvulsive therapy.

Background Electroconvulsive therapy (ECT) continues to be an effective treatment option for patients who fail to respond to pharmacological interventions, are unable to tolerate medications, and show a suboptimal response to behavioral and psychotherapeutic treatments. However, risks for cognitive impairment may contribute to some patients’ refusal of ECT. Methods The present study examined galantamine as a pharmacological intervention to reduce cognitive adverse effects from ECT. Thirty-nine inpatients diagnosed with major depressive disorder; bipolar disorder, depressed type; or schizoaffective disorder, depressed type and admitted for ECT were randomized to galantamine or placebo. Study drugs were initiated 24 to 48 hours before starting ECT and continued throughout the course of ECT. A neuropsychological test battery was administered at baseline and 24 to 48 hours after completing a course of ECT treatments. Depression severity was monitored using the 17-item Hamilton Rating Scale for Depression and Clinical Global Impression Scale at baseline, weekly, and end point. Self-rated adverse effects were monitored weekly. Results Thirty participants (12 patients in the galantamine group, 18 patients in the placebo group) had both pretreatment and posttreatment neuropsychological ratings. Those in the galantamine group scored significantly higher at discharge for delayed memory (t28 = 2.44, P < 0.05). Hierarchical regressions examined if treatment condition predicted changes in delayed memory scores from baseline to discharge. Inclusion of the treatment condition in the final model made a significant incremental improvement in prediction (&Dgr;R2 = 0.12, F1,27 change = 4.65, P < 0.05; &bgr; = 0.37, t = 2.16, P < 0.05). Galantamine was well tolerated with no clinically significant bradycardia or prolonged paralysis when administered with ECT. Conclusions Galantamine may be protective against impairment in retention of new learning. Galantamine exhibited minimal adverse effects and was safe when administered during ECT. The present findings require replication by future researchers using larger samples before broad conclusions can be drawn.

Rapid improvement of depression and psychotic symptoms in Huntington's disease: a retrospective chart review of seven patients treated with electroconvulsive therapy.

Many patients with Huntingtons disease (HD) develop psychiatric symptoms such as depression and psychosis. For severe symptoms, electroconvulsive therapy (ECT) can be a valuable treatment. In this case series, we identified seven patients with HD who received ECT at Massachusetts General Hospital in the past 20 years. In all cases, ECT was well tolerated and produced improvement in psychiatric and behavioral symptoms. Our case series supports the hypothesis of a positive risk-benefit ratio for ECT in patients with HD and severe depression or psychosis.

Minimum Effective Doses of Succinylcholine and Rocuronium During Electroconvulsive Therapy: A Prospective, Randomized, Crossover Trial.

BACKGROUND: Neuromuscular blockade is required to control excessive muscle contractions during electroconvulsive therapy (ECT). In a crossover, assessor-blinded, prospective randomized study, we studied the minimum effective dose (MED) of succinylcholine and rocuronium for ECT. The MED was the lowest dose to provide a predefined qualitative measure of acceptable control of muscle strength during induced convulsions. METHODS: Succinylcholine (0.8 mg kg−1) or rocuronium (0.4 mg kg−1) was randomly administered in 227 ECT sessions to 45 patients. The dose was incrementally increased or decreased by 10% based on 2 psychiatrists’ (blinded to treatment) assessment of “acceptable” or “not acceptable” control of evoked muscle contractions (sufficient versus insufficient or excessive paralysis). The neuromuscular transmission was monitored quantitatively until full recovery. RESULTS: In our study, the MEDs of succinylcholine and rocuronium to produce acceptable ECT conditions in 50% of patients (MED50ECT) were 0.85 mg kg−1 (95% confidence interval [CI], 0.77–0.94) and 0.41 mg kg−1 (95% CI, 0.36–0.46) and in 90% of patients (MED90ECT) were 1.06 mg kg−1 (95% CI, 1.0–1.27) and 0.57 mg kg−1 (95% CI, 0.5–0.6), respectively. Nadir twitch height for acceptable muscle activity was 0% (0–4) and 4% (0–30; P < 0.001), respectively, and the time to recovery of the neuromuscular transmission was 9.7 ± 3.5 and 19.5 ± 5.7 minutes, respectively. CONCLUSIONS: A twitch suppression of >90% is needed for control of motor contractions during ECT. The initial ECT dose of succinylcholine should be selected based on each patient’s preprocedural condition, ranging between 0.77 and 1.27 mg kg−1 to produce acceptable muscle blockade in 50% to 90% of patients. Rocuronium–neostigmine combination is a safe alternative if appropriately dosed (0.36–0.6 mg kg−1) and monitored.

The safety and efficacy of ECT and anesthesia in the setting of multiple sclerosis.

Multiple sclerosis (MS), a demyelinating disorder characterized by relapsing and remitting symptoms of weakness and paresthesias, often worsens after surgery and the administration of anesthesia; whether recurrence is due to the surgery, to the use of anesthetics, or to hyperpyrexia remains unclear.1 Therefore, referring psychiatrists and anesthesiologists should understand the potential complications when patients with MS are referred for treatment. We present the case of a young woman with MS and unstable bipolar disorder who received numerous treatments with electroconvulsive therapy (ECT) that involved use of brief general anesthesia and discuss the relationship between ECT, anesthetics, and recurrence of MS. No exacerbation of MS arose despite repeated anesthetic challenges associated with ECT.

Hemodynamic responses to electroconvulsive therapy in a hypertensive patient with end-stage pulmonary fibrosis

T he autonomic nervous system contributes significantly to the control of pulmonary circulation, and both (Yand p-adrenoreceptors are distributed throughout the pulmonary vessels for effective stress responses (1). Characteristic of stress is an increase in catecholamines locally released by sympathetic stimulation or reaching the pulmonary bed via the circulating blood (2). In normal humans, the resulting increase in pulmonary vasomotor tone leads to only a very small increase in pulmonary artery (PA) pressure (l), even in the presence of large increases in blood flow. In contrast, the PA pressure may markedly increase in response to increased pulmonary blood flow when pulmonary hypertension preexists (3), with important consequences for right ventricular (RV) performance. This combination is of special interest when electroconvulsive therapy (ECT) is planned in a patient with pulmonary hypertension. ECT is characterized by a twofold increase in cardiac output (4), a 34% increase in arterial pressure (5), and a massive catecholamine surge (6). Severe pulmonary hypertension is a hallmark of idiopathic pulmonary fibrosis (IPF) (7). The consequences of this condition in combination with ECT, however, are unknown. In a series of seven treatments, we documented the hemodynamic responses to ECT in a patient with severe IPF.