Anesth Analg 2003;96:168-170
© 2003 International Anesthesia Research Society
ANESTHETIC PHARMACOLOGY
An Unusual Complication of Total Intravenous Anesthesia: Mutism
Ismail Kati, MD*,
C. Bekir Demirel, MD*,
Omer Anlar, MD ,
Urfettin A. Hüseyinoglu, MD*,
Emin Silay, MD*, and
Kamuran Elcicek, MD*
Departments of *Anesthesiology and Neurology, Medical Faculty, Yuzuncu Yil University, Van, Turkey
Address correspondence and reprint requests to Ismail Kati, MD, Yüzüncü Yil Üniversitesi, Tip Fakültesi Anesteziyoloji AD, 65300 Van, Turkey. Address e-mail to ismaikati{at}hotmail.com
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Abstract
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IMPLICATIONS: We report a case of mutism secondary to total IV anesthesia with propofol, as an unusual complication that we have not found in the literature.
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Introduction
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Propofol is a total IV anesthetic with a rapid onset of action. It is metabolized in a short period (1). Propofol may cause side effects such as convulsion, seizure, opisthotonus, involuntary muscle activities, and tonic-clonic movements (2–4). A focal infarct involving the brain caused by an occluded anterior cerebral artery may cause mutism (5). Mutism occasionally is a result of a vascular lesion or other type of localized injury of the dominant frontal lobe. The patient loses all capacity to speak whereas retaining perfectly the ability to write, to understand spoken words, and read silently with comprehension (5). We report an unusual case in which the patient developed mutism without cerebral infarction probably secondary to total IV anesthetic with propofol.
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Case Report
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A 56-yr-old woman underwent an operation for left collum femoris fracture caused by a fall; she had no head trauma. She had previously been given indapamide (1.5 mg/day) for essential hypertension. With the exception of high levels of lactate dehydrogenase 873 U/L and alkaline phosphatase (354 U/L), the laboratory values, mental and psychological status, neurologic and other systematic examination findings were normal. Anesthetic induction was achieved with propofol, fentanyl, and vecuronium, and routine monitoring was used. Arterial blood pressure was 130/80 mm Hg, heart rate 78 bpm, and SpO2 96%. After endotracheal intubation, central venous and radial artery catheters were inserted. Maintenance of anesthesia was provided by O2/dry air (3:5 L/min) fentanyl, vecuronium, and propofol (of 10 mg/kg for the first 10 min, 8 mg/kg for the second 10 min, and 4 mg/kg for the duration of surgery) during the operation. Mean arterial blood pressure, heart rate, SpO2, and end-tidal carbon dioxide were between 70–86 mm Hg, 65–90/min, 96–99, and 32–39 mm Hg, respectively. Central venous pressure was 4 mm Hg at the beginning, and remained between 2–6 mm Hg during the 3-h operation. Fentanyl, vecuronium, and propofol infusion were stopped 60 and 15 min, respectively, before the operation was completed. Residual neuromuscular block was reversed with IV neostigmine and atropine. After the patient could open her eyes and respond to a simple verbal command, her trachea was extubated. During 1-h follow-up in the recovery room, the hemodynamic variables were normal.
Although the patient could respond to verbal commands for eye opening and nodding, she could not speak. Laboratory values (hematocrit, glucose, urea, Ca, Mg, K, and blood gases analysis) were obtained and were within normal range in the early postoperative period. On the first day, no change was observed in her physical examination findings. All neurologic examination findings and blood gases analysis were normal except somnolence, inability to speak, and positive Babinski sign (only partially on the left foot). Minimal brain edema was found on the computerized tomography (CT) scan (Figs. 1 and 2). Mannitol, dexamethasone, diclofenac Na+, and cephamesine were given. In repeated blood analysis, all biochemical parameters were within normal range except urea 65 mg/dL, creatine 1.2 mg/dL, LDH 695 U/L, creatine kinase 1258 U/L, and creatine kinase-myocardial band 54 U/L. Because of continuation of mutism on the second day, neurologic findings were again evaluated and no other neurologic abnormality was observed. The patient could open her eyes to verbal commands but was unable to speak until postoperative day 5. On the fifth day, a control CT was evaluated and found normal (Figs. 3 and 4); mannitol and dexamethasone were then gradually decreased and stopped. She could respond to verbal stimuli by pointing on the eighth day. On the 11th day, the patient started to speak and recovered totally, and was discharged without any neurologic sequels on the 18th day.
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Figure 1. Effacement of Sylvian fissure and cortical sulci on a study of cranial computerized tomography at transsection plane passing through Sylvian fissure.
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Figure 2. Effacement of cortical sulci on a study of cranial computerized tomography at a transsection plane passing through centrum semiovale.
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Figure 4. Fissures of cortical sulci were markedly enlarged on a study of cranial computerized tomography at a transsection plane passing through centrum semiovale after 5 days after first computerized tomography study.
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Discussion
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Short-acting anesthetics, including propofol, have become widely used because they permit neurologic assessment shortly after discontinuation and recovery time even after prolonged use (6,7). This characteristic, however, depends on rapid redistribution of propofol (8). The most commonly reported adverse effects of propofol are seizures, convulsion, opisthotonus, involuntary muscle activities, and tonic-clonic movements (2–4). Hedera et al. (9) reported two patients with good outcomes whose unresponsiveness persisted up to 48 hours after a moderate duration of small-dose propofol sedation without neurologic sequels. Patients undergoing total hip arthroplasty may rarely develop neurologic complications that may present as transient confusion or, if severe, as coma or death (10). Byrick et al. (11) reported that transpulmonary systemic fat embolism had been demonstrated in mongrel dogs. In our case, we did not observe any clinical signs of fat or air emboli. Moreover, there was no evidence of cerebral infarction revealed by CT scan on the first and fifth days. Although the CT scan was normal on the fifth day, the patient could not speak until the 11th day, and therefore we considered that it was not caused by brain edema. We do not believe that any mechanism of propofol can cause brain edema and we do not think that mutism can result from other medications except propofol.
Although there were no abnormalities in renal and hepatic functions or hemodynamic variables in the perioperative period, our patient’s mutism continued for 11 days postoperatively.
Thus, in the absence of any other predisposing factor that would explain this mutism during the postoperative period, we conclude that this neurologic complication might be attributed to an unknown effect of propofol.
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References
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- Mohr JP. Aphasia, apraxia, and agnosia. In: Rowland LP, ed. Merritt’s textbook of neurology. 9th ed. Baltimore: Williams & Wilkins, 1995: 8–19.
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- Dorr LD, Merkel C, Mellmann MF, Klein I. Fat emboli in bilateral total knee arthroplasty: predictive factors for neurologic manifestations. Clin Orthop 1989; 248: 112–8.
- Byrick RJ, Mullen JB, Mazer CD, Guest CB. Transpulmonary systemic fat embolism: studies in mongrel dogs after cemented arthroplasty. Am J Respir Crit Care Med 1994; 150: 1416–22.[Abstract]
Accepted for publication October 7, 2002.
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Abstract
Introduction
