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On-line version ISSN 1806-907X
Rev. Bras. Anestesiol. vol.58 no.6 Campinas Nov./Dec. 2008
Tako-Tsubo syndrome secondary to residual neuromuscular blockade. Case report*
Síndrome de Tako-Tsubo como consecuencia de bloqueo neuromuscular residual. Relato de caso
Marcos Guilherme Cunha Cruvinel, TSA, M.D.I; Fabiano Soares Carneiro, TSA, M.D.II; Roberto Cardoso Bessa Junior, TSA, M.D.III; Yerkes Pereira e Silva, M.D.IV; Mirna Bastos Marques, M.D.V
do Hospital Lifecenter; Especialista em Clínica Médica; Certificado
de Área de Atuação em Dor
IIAnestesiologista dos Hospitais Lifecenter e das Clínicas
IIIAnestesiologista dos Hospitais Lifecenter, IPSEMG e das Clínicas; Especialista em Terapia Intensiva; Certificado de Área de Atuação em Dor
IVAnestesiologista do Hospital Lifecenter; Especialista em Pediatria; Doutor em Pediatria pela UFMG
VAnestesiologista do Hospital Lifecenter; Especialista em Terapia Intensiva; Mestranda em Clínica Médica pela UFMG
OBJECTIVES: Tako-Tsubo syndrome is a rare postoperative complication with
a 5% mortality rate. The objective of this report was to present residual neuromuscular
blockade as a trigger for this syndrome, discuss this disorder, and call attention
to the risks of residual neuromuscular blockade.
CASE REPORT: A 61-year old female, physical status ASA I, who underwent general anesthesia associated with paravertebral cervical block for arthroscopic repair of a rotator cuff lesion. Physical exam after extubation detected residual neuromuscular blockade. In the post-anesthetic care unit the patient developed somnolence, tachycardia, hypertension, and severe respiratory acidosis. After reintubation the patient evolved for cardiac arrest with electrical activity without a pulse, which was reverted with the administration of adrenaline and external cardiac massage. In the postoperative period the patient presented elevation of the ST segment, increased troponin, and left ventricular medial-apical akinesia with an estimated ejection fraction of 30%. Cardiac catheterization showed absence of significant atheromatous lesions in the coronary vessels, and severe disruption of the systolic function with inferior and antero-septo-apical akinesia and compensatory basal hypercontractility. The patient had complete functional recovery with the treatment instituted.
CONCLUSIONS: Residual neuromuscular blockade associated with diaphragmatic paralysis and possible pulmonary atelectasis leading to respiratory failure, hypercapnia, and adrenergic discharge triggered the Tako-Tsubo syndrome with severe clinical repercussion.
Key Words: COMPLICATIONS: Residual neuromuscular blockade, Tako-Tsubo syndrome.
Y OBJETIVOS: El Síndrome de Tako-Tsubo es una complicación
postoperatoria rara con una mortalidad en torno de un 5%. El objetivo de este
relato es presentar el bloqueo neuromuscular residual como factor desencadenante
del referido síndrome, discutir sobre él y alertar sobre el bloqueo
RELATO DEL CASO: Paciente del sexo femenino, 61 años, estado físico ASA I, sometida a la anestesia general asociada al bloqueo paravertebral cervical para la reparación artroscópica de lesión de manguito de los rotadores. Después de la extubación, quedó demostrado el bloqueo neuromuscular residual a través del examen clínico. En la sala de recuperación postanestésica, evolucionó con somnolencia, taquicardia, hipertensión arterial y acidosis respiratoria grave. Después de la reintubación evolucionó con parada cardíaca en actividad eléctrica sin pulso, revertida con adrenalina y masaje cardíaco externo. En el postoperatorio presentó una elevación de segmento ST, aumento de troponina y acinesia de segmento medio-apical del ventrículo izquierdo, con fracción de eyección estimada en un 30%. La cineangiocoronariografía mostró coronarias exentas de ateromatosis significativa y un grave comprometimiento de la función sistólica con acinesia inferior y ántero-septo-apical, con hipercontratilidad compensatoria de sus porciones basales. Con el tratamiento iniciado, hubo una recuperación funcional completa.
CONCLUSIONES: El bloqueo neuromuscular residual asociado a la parálisis diafragmática y la posible atelectasia pulmonar, que conlleva a la insuficiencia respiratoria, hipercapnia y descarga adrenérgica, fueron los factores desencadenantes del síndrome de Tako-Tsubo con su grave repercusión clínica.
Residual neuromuscular blockade (RNB) is a relatively common complication even with intermediary-acting neuromuscular blockers 1-7, which has a high morbidity 2,3. On the other hand, Tako-Tsubo syndrome is a rare postoperative complication8. This is a transitory systolic myocardial dysfunction affecting the apex of the left ventricle. In the acute phase, the shape of the heart, during systole, is similar to a Japanese vase used to trap octopuses (Tako = Octopus, Tsubo = vase) 9-15, with a 5% mortality rate 14. The objective of this report was to present a case of RNB triggering the Tako-Tsubo syndrome.
A 61-year old female, physical status ASA I, 65 kg, 1.63 m, was admitted for arthroscopic repair of a rotator cuff lesion on the right shoulder. Monitoring with electrocardiograph (DII and V5), pulse oximeter, automatic non-invasive blood pressure, nasopharyngeal temperature, and capnography/gas analyzer (after intubation) was instituted. Clonidine, 1 µg.kg-1, and fentanyl, 1 µg.kg-1, were administered, followed by a paravertebral cervical block (posterior brachial plexus block) with 20 mL of 1% ropivacaine. After the blockade, which was free of intercurrences, general anesthesia was induced with 3.8 µg.kg-1 of fentanyl, 1.9 mg.kg-1 of propofol, and 0.76 mg.kg-1 of rocuronium. Sevoflurane (expired fraction of 0.8 to 1%) was used for anesthesia maintenance. Intraoperative intercurrences were not observed. Dexamethasone, 10 mg, ondansetron, 4 mg, ketoprofen, 100 mg, and dypirone, 2 g, were administered. At the end of surgery, 75 minutes after induction, the administration of sevoflurane was discontinued and neostigmine, 46.2 µg.kg-1, and atropine, 23.1 µg.kg-1, were administered. Ninety minutes after anesthetic induction, with the patient in dorsal decubitus and head elevated 45°, with expired fraction of sevoflurane of 0.1%, the patient opened her eyes spontaneously. The patient was extubated and afterwards the physical exam detected RNB (incapable to sustain her head for 5 seconds). Since she was not complaining of dyspnea the patient remained in the operating room for about 30 minutes during which time she was breathing oxygen (6 L.min-1) via a face mask spontaneously, pulse oximetry varied from 93% to 98%, and she was hemodynamically stable. The patient was transferred to the post-anesthetic care unit (PACU) approximately 120 minutes after anesthetic induction. The patient became progressively somnolent, with an increase in blood pressure and heart rate. Arterial blood gas analysis demonstrated severe hypercapnia (PaCO2 = 101 mmHg). Propofol, 2 mg.kg-1, was administered and the patient was reintubated 150 minutes after anesthetic induction. The patient became hypotensive and 15 minutes later she evolved to cardiac arrest with electrical activity without pulse which was reverted with 1 mg of adrenaline and external cardiac massage.
She was transferred to the intensive care unit (ICU) intubated and on mechanical ventilation, hemodynamically stable, awake, and without neurological deficits. Electrocardiogram upon admission to the ICU revealed elevation of the ST segment from V3 to V6. Troponin (10 ng.mL-1 - normal < 1.5) and CK-MB (23 U.L-1 - Normal up to 6) were increased. The echocardiogram showed akinesia of the left ventricular walls with an ejection fraction of 30% and the following conclusion: left ventricular ischemic cardiomyopathy with important disruption in systolic function. Cardiac catheterization showed severely disruption in systolic function, with antero-septo-apical and inferior akinesia and compensatory hypercontractility of the basal portions (left ventricular apical ballooning), and coronary arteries free of significant atheromatous diseases (Figures 1 and 2). The patient showed good response to 10 µg.kg-1.min-1 of dobutamine and was extubated 22 hours after anesthetic induction. Her condition improved progressively, and she was discharged from the hospital on 4 mg of candesartan, and outpatient follow-up by the cardiologist. She had complete recovery of the functional capacity, and an echocardiogram done 30 days after discharge from the hospital showed normal contractility of the left ventricle, with an ejection fraction of 63%, allowing the discontinuation of the medication. The patient does not have recollections of the day of the surgery.
Tako-Tsubo Syndrome is extremely rare, but it might have been underdiagnosed since it was described recently (1990) 9. It has also been called transitory ventricular apical ballooning syndrome. It affects mainly women (6:1) above 60 years of age, postmenopausal, without history of cardiac disease 10-15. The presentation in the majority o cases is suggestive of acute myocardial infarction (AMI), and this is typically the initial diagnosis. Electrocardiographic (elevation of the ST segment + inversion of the T wave) and cardiac enzymes (troponin and CK-MB) changes lead to this diagnosis 8. Left ventricular dysfunction with low ejection fraction on echocardiogram contributes for this diagnosis. However, coronary lesions that could justify the diagnosis of AMI are not seen in the hemodynamics laboratory, and ventriculography shows an image typical of this syndrome (Chart I) 16. Its pathophysiology is not well defined. The main hypotheses include microvascular spasm and direct myocardial damage caused by catecholamines from adrenergic receptors 13. Most cases are related with a phenomenon that generates severe physical or emotional stress (e.g., death in the family, exacerbation of chronic systemic diseases, or invasive procedure). It can cause, among other complications, pulmonary edema, cardiogenic shock, and atrial and ventricular fibrillation 8. It has a good prognosis after the acute phase, and ventricular recovery is seen in two to three weeks. Recurrences are rare.
Diagnostic criteria (Chart I) confirmed the diagnosis of Tako-Tsubo syndrome in the case presented here. Besides, she has the most common profile of patients who develop this syndrome, and her evolution was typical: initial clinical signs suggestive of AMI, cardiac catheterization showed absence of coronary artery lesions, ventriculography showing an image characteristic of this syndrome, and good evolution with complete recovery.
The cardiac arrest with pulseless electrical activity developed by the patient was probably secondary to a combination of the following factors: severe ventricular dysfunction caused by the Tako-Tsubo syndrome, aggravated by respiratory acidosis, reduced myocardial contractility, vasodilation triggered by propofol, and interruption of the existing adrenergic discharge. Immediate return of normal sinus rhythm after the administration of adrenaline makes it unlikely that involvement of other causes of cardiac arrest, such as: pulmonary thromboembolism, pneumothorax, anaphylaxis, hypercalemia, and hypovolemia related to prolonged resuscitation maneuvers. The brief period of cardiac arrest and elevated inspired fraction of oxygen explain neurological recovery without sequelae.
Tako-Tsubo syndrome is secondary to severe sympathetic discharge triggered by physical or emotional stress. It is likely that both were present in the case presented here. The fact that the patient did not recall what happened and the absence of dyspnea do not exclude the possibility of severe emotional stress. The association of the residual effect of anesthetic drugs, prostration secondary to hypercapnia, and cardiac arrest could explain the amnesia. On the other hand, the patient was under physical stress triggered by hypercapnia, which was reflected on the tachycardia and hypertension that seem to be the main factors responsible for the development of this syndrome.
Cases of Tako-Tsubo syndrome secondary to respiratory difficulty, such as asthma exacerbation, spontaneous pneumothorax, and after bronchoscopy have been reported 8,14. In the present case, respiratory difficulty was a consequence of associated factors that caused severe hypoventilation. Paralysis of the diaphragm was the first factor. Although it was not diagnosed by an imaging exam (ultrasound, radioscopy, or chest X-ray), we think that it was present due to its high prevalence (up to 100%) after high brachial plexus blocks 17.
Residual neuromuscular blockade, diagnosed clinically, was the second factor. The main clinical tests include elevation of the head for 5 seconds, hand squeeze, elevation of the legs from the surgical bed, and maintenance of the tongue between the incisive teeth. They are accompanied by a wide variation on the train-of-four (TOF) and, due to their limitations, should be used with caution. Even with T4/T1 ratios to TOF as low as 0.5, a patient is capable of maintaining the head elevated for 5 seconds and to show a strong hand grip 18. Respiratory function monitors also do not indicate the return of muscular function, since they reflect the recovery of centrally-located muscles, especially the diaphragm 18. Due to the reasons exposed here, monitoring with acceleromyography would have been important, not only for the diagnosis of RNB, but also for its quantification.
Despite the seemingly adequate reversal of the neuromuscular blockade with anti-cholinesteratic agents, the rate of RNB after the use of intermediate-action neuromuscular blockers is considerable (8 to 9%), when one considers a minimal T4/T1 ratio to TOF > 0.719. Since a growing consensus suggests that full recovery only happens with T4/T1 > 0.9, this incidence tends to be even more elevated 19. Although one cannot exclude the importance of the clinical evaluation of RNB, this can only be ruled out with objective methods that provide a quantitative measure of neuromuscular recovery 20. More important that the evidence of RNB in this case, monitoring would have been fundamental for the diagnosis of deep neuromuscular blockade that was not readily reversible. Due to the lack of monitoring, the neuromuscular blockade was not reversed at the appropriate time or the correct dose for the degree of the blockade was not used, resulting in RNB when the patient awakened. In the absence of TOF stimulation one should wait instead of stimulating the reversal of the neuromuscular blockade21. In the presence of only one or two stimuli, the dose of neostigmine to revert the blockade is 70 µg.kg-1. In the presence of three or four stimuli, a dose of 40 µg.kg-1 is adequate. In the presence of RNB after reversion, a complementary dose of neostigmine was indicated, and the patient should have been reintubated immediately with persistence of the RNB, but, in the present case, it was done later 18.
Pulmonary atelectasis was the third possible factor. Despite not being diagnosed, it should be considered since it is a frequent complication, especially in the presence of RNB and paralysis of the diaphragm.
Therefore, one should remember the importance of monitoring the neuromuscular function, and RNB as a cause of morbidity, especially if associated with other factors that cause respiratory difficulties. In the case presented here, the association of RNB, paralysis of the diaphragm, and possible pulmonary atelectasis, led to respiratory insufficiency, hypercapnia, and adrenergic discharge, triggering the onset of Tako-Tsubo syndrome and its clinical repercussions.
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Correspondence to: Submitted em 6
de março de 2008 *
Received from Hospital Lifecenter - Belo Horizonte, MG
Dr. Marcos Guilherme Cunha Cruvinel
Rua Simão Irffi, 86/301
30380-270 Belo Horizonte, MG
Accepted para publicação em 18 de agosto de 2008
Submitted em 6
de março de 2008
* Received from Hospital Lifecenter - Belo Horizonte, MG