Abstract

We report an 82-year-old male patient who developed complete atrioventricular block (CAVB) with severe bradycardia 1 hour after craniotomy. After emergency placement of a transvenous pacemaker, the patient's heart rate was restored. Serial assays of serum cardiac enzymes, echocardiography and serum digoxin concentration did not show evidence of myocardial infarction, myocardial injury, or drug toxicity. Tracing back past history, neither syncope nor arrhythmia of any form was noted. A neurogenic heart disorder, high vagal tone, and aging possibly contributed to this cardiac event in this patient. CAVB, although uncommon, is a disastrous complication following craniotomy, and needs aggressive and instantaneous management.

Keywords

atrioventricular block; craniotomy;

1. Introduction

Craniotomy is a surgery for treatment of cerebral disorders such as brain tumors or subdural hematoma. We present an elderly male patient who, while undergoing emergency craniotomy because of subdural hematoma associated with increased intracranial pressure (ICP), developed complete atrioventricular block (CAVB) 1 hour after completion of surgery. The etiology of CAVB includes a myriad of causes such as ischemic heart disease, myocardial infarction, increased vagal tone, infection, metabolic imbalance, and drug effects.¹ We highlight the clinical course of the event and the potential effects of brain insults and surgery on CAVB.

2. Case Report

An 82-year-old male came to our emergency service unconscious after a fall at home. The patient’s medical history included rheumatic heart disease (for which he had undergone mitral valve replacement), hypertension, diabetes, chronic obstructive pulmonary disease, and cerebrovascular accident with consequent left hemiparesis for 2 years. Neither a history of syncope nor arrhythmia was confirmed by the patient’s family. The patient had been taking regular medication of coumadin 5 mg and digoxin 0.125 mg.

Physical examination showed that he was unconscious with a Glasgow Coma Scale score of E₁V₁M₂.

The vital signs were relatively stable except for hypertension (blood pressure, 190/78 mmHg; pulse, 65 beats/min; respiration, 16 breaths/min), and neither fever nor a skin rash were found. Electrocardiography (ECG) revealed a sinus rhythm with a borderline first-degree AVB and ST depression and inverted T wave on leads II, III and aVF (Figure 1).

Laboratory findings were unremarkable except for anemia with hemoglobin of 10.5 g/dL, blood urea nitrogen of 31 mg/dL, marginal creatinine of 1.4 mg/dL, and serum glucose of 206 mg/dL. An assay of cardiac enzymes showed an acceptable creatine kinase-MB level of 7 U/L and troponin I of 0.06 ng/mL.

Chest roentgenography showed mild cardiomegaly with chronic reticulonodular opacities in both lungs, and computed tomography of the brain demonstrated a subdural hematoma 2.7 cm in diameter in the left frontotemporoparietal area with a shift of the midline to the right.

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Figure 1 Preoperative electrocardiogram shows ST-T change at leads II, III, and aVF.

He was sent to the operating room for emergency craniotomy to remove the hematoma. Physiological surveillance, including a radial arterial line, revealed hypertension (210/70 mmHg), sinus rhythm (85 beats/min), and steady respiratory rate (16 breaths/min). General anesthesia was induced with 0.5 mg atropine, 6 mg/kg thiopental, 3 μg/kg fentanyl and 1 mg/kg rocuronium. After tracheal intubation, anesthesia was maintained with isoflurane in O₂ (1%), rocuronium, and continuous infusion of fentanyl (3−5 μg/kg/hr). Ventilation was set to maintain end-tidal CO₂ at around 26−30 mmHg. Blood pressure could be maintained around 120/50 mmHg and heart rate around 60 beats/min without resorting to the use of inotropics during the operation. The whole surgical procedure including installation of a continuous ICP monitoring device was completed in 3.5 hours, and the estimated blood loss was 200 mL. The patient endured the surgical procedure well with stable hemodynamics (blood pressure, 121/52 mmHg; heart rate, 61 beats/min) and normothermia. He was transferred to the postanesthetic care unit for mechanical ventilatory support and intensive care.

One hour after surgery, the patient unexpectedly developed severe bradycardia with a ventricular rate around 23 beats/min and CAVB. In spite of intravenous administration of atropine up to a total dose of 3 mg, the effect was poor (Figure 2). On physical examination, the function of the surgical drain was good and the amount of drainage was only about 20 mL. ICP was around 11−13 mmHg and no pupillary dilatation was found. Although arterial blood pressure was stable at 130/65 mmHg and central venous pressure was around 16−18 mmHg, temporary placement of a transvenous pacemaker was contemplated and accordingly performed. It gave a satisfactory pacing rhythm of 80 beats/min (Figure 3). In addition, the possibilities of myocardial infarction, sepsis, infection, or drug toxicity were carefully investigated. ECG revealed a functioning mechanical mitral valve, concentric left ventricular hypertrophy, mild hypokinesia in the inferior wall of the left ventricle, but no intracardiac masses or valvular vegetation. Sequential assays of serum concentrations of cardiac enzymes and digoxin within 24 hours postoperatively revealed that all were within normal limits. Repeated blood culture and laboratory examinations were negative for bacterial growth. Although his coma scale slightly improved to E₃V_TM₄, his renal function deteriorated and complicated his cardiac condition. Because of his family’s refusal of aggressive treatment, the patient died on postoperative day 15.

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Figure 2 Electrocardiogram shows complete heart block 1 hour after craniotomy.

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Figure 3 Electrocardiogram shows pacemaker rhythm after placement of a transvenous pacemaker.

3. Discussion

The etiology of complete AVB encompasses a myriad of causes including cardiac events, such as myocardial infarction, myocardial ischemia, infective endocarditis and hypertrophic cardiomyopathy, aging, high vagal tone, infection, surgery, and drug toxicity.¹ A patient with a brain injury and preexisting first-degree AVB, and newly-developed CAVB, but without evidence of sepsis, cardiac events and drug intoxication, should alert the clinician to consider a contributory effect from the brain.

An ECG, knowledge of a history of cardiac disorders, and cardiac enzyme analysis are useful in evaluating cardiac events. In the present case, CAVB occurred at the post-anesthetic care unit 1 hour after craniotomy. Although no evidence of newly developed myocardial injury or infarction was found after sequential analysis of the ECG and cardiac enzymes, a history of rheumatic heart disease with mitral valve replacement, borderline first-degree AVB and myocardial ischemia could not negate the possibility of a cardiac etiology. In addition, there was no evidence to indicate there was an existing infection, sepsis, or metabolic disturbance. CAVB has been ascribed to brain events, such as treatment with phenytoin alone or in combination with ephedrine during craniotomy,^2,3 pituitary apoplexy after total hip replacement surgery,⁴ or stimulation of left temporal epileptic activity.⁵ The serum concentrations of digoxin and other medications did not support the existence of drug toxicity.

The incidences of ECG changes and AVB have been reported to be 12% and 1%, respectively, following head injury.^6,7 CAVB might be attributed to the combined effect of neurological pathology, craniotomy and aging. Unexplained bradycardia has been reported during craniotomy or after connection of an extradural drain to negative-pressure suction after craniotomy to relieve intracranial hypotension.⁸⁻¹¹ In addition, bradydysrhythmia might indicate neurogenic events and increased ICP. Although we did not apply negative-pressure suction on the extradural drain in the present case, the function of the extradural drain was serviceable without occlusion when bradydysrhythmia occurred. The presence of a normal ICP level (around 11−13 mmHg), absence of papillary dilation, and good function of the extradural drain could exclude the probability of increased ICP. Although a high vagal tone with a vasovagal reflex might contribute to the bradycardia, it is usually accompanied by hypotension.¹² In contrast, our case developed bradycardia and CAVB without hypotension after craniotomy. Since the patient had previously sustained cerebrovascular accident and subdural hematoma, focal brain ischemia or an infarct could have occurred. Although no seizure-related motor responses were found after admission in our patient, we could not exclude the effect of cerebral events which would exacerbate the preexisting borderline first-degree AVB. Furthermore, stress and secretion of catecholamines, either induced by surgery or pain, could also contribute to the development of neurogenic heart disease.¹³ The neurogenic effects, such as postoperative pain and stress could also induce bradydysrhythmia. Accordingly, neurogenic heart disease was the most likely cause of CAVB in the present case, and the possibilities of high vagal tone and age factors could not be excluded.

In conclusion, we have presented a patient who developed postoperative CAVB after craniotomy. The causes of heart block were discussed. Neurogenic cardiac arrhythmia and conduction block in patients with brain injury could be a problem in anesthetic management.