Unexplained Transient Postoperative Myocardial Dysfunction in a Previously Healthy Child

Acute postoperative myocardial dysfunction in a healthy child is rare, and to our knowledge there are only a few relevant reports in the recent anesthesia literature [1,2]. We describe the case of a child who postoperatively developed acute transient cardiac failure of unknown etiology. Case Report An 8-yr-old, 23-kg active boy with no known medical or anesthesia-related problems presented for outpatient closed reduction of a traumatic nasal fracture under general anesthesia. In the operating room, monitors were placed (electrocardiogram, noninvasive blood pressure, pulse oximeter, and precordial stethoscope), anesthesia was induced by mask with nitrous oxide (N2 O) in oxygen (70%/30%) and halothane, and intravenous (IV) access was established. Three minutes later, at an end-tidal halothane concentration of 2.0%, 25 mg of lidocaine was sprayed on the trachea during laryngoscopy, and the trachea was intubated without difficulty. After intubation, anesthesia was maintained with isoflurane (1%-1.5% end-tidal concentration) and 70% N2 O. Two minutes after intubation, 5 mL of 0.25% bupivacaine with 5 micro gram/mL epinephrine was injected into the nasal mucosa with no changes in heart rate or arterial blood pressure, which were 75-80 bpm and 98/52 mm Hg, respectively. Five minutes after intubation, anesthesia was supplemented with 2.0 mg of IV morphine. The patient breathed spontaneously throughout the 30-min procedure. End-tidal CO2 concentration was measured via a side port sampler and remained between 40 and 45 mm Hg throughout the operation. Oxygen saturation was measured continuously, and at no time did it decrease to less than 98%. The initial room air oxygen saturation was 99%. There were no episodes of hyper- or hypotension, tachycardia > 120 bpm, or bradycardia intraoperatively. Ten minutes prior to completion of the surgery, 20 mg of IV ketorolac was administered. Blood loss was minimal, and the total volume infused during the case was 200 mL of crystalloid. The patient was taken to the postanesthesia care unit (PACU) while tracheally intubated, since residual anesthesia did not allow for immediate extubation. No vital signs were monitored during the less than 20-s transport time, and no supplemental oxygen was used. Immediately upon arrival in the PACU, the heart rate was 50 bpm, arterial blood pressure 115/62 mm Hg, and oxygen saturation 95% while breathing room air. Oxygen and atropine 200 micro gram IV were administered, and the heart rate increased to 130 bpm. The endotracheal tube was removed 3 min later. There was no physical evidence of upper airway obstruction, laryngospasm, or pulmonary aspiration. Within 1 min after extubation, pink frothy sputum was noticed in the patient's oropharynx and the oxygen saturation decreased from 95% to 78% (on 100% oxygen by face mask). Arterial blood pressure was 102/58 mm Hg, heart rate 140 bpm, and respirations 40-50 breaths/min. Bilateral rales were present on auscultation. The trachea was immediately reintubated after the administration of lidocaine 25 mg IV, propofol 80 mg IV, and succinylcholine 30 mg IV. A chest radiograph postintubation confirmed the diagnosis of acute pulmonary edema. A propofol infusion was begun at 25 micro gram centered dot kg-1 centered dot min-1 for sedation. Manual ventilation improved the oxygen saturation to 92%-95% while the patient was breathing 100% oxygen. Persistent hypotension and tachycardia with arterial blood pressures as low as 41/24 mm Hg and heart rates of 130-150 bpm over the next 5 min led us to discontinue the propofol infusion, and midazolam 1 mg IV was administered for sedation. No inotropes or vasopressors were given to treat the transient severe hypotensive episode. Two hours after the reintubation in the PACU, the oxygenation and blood pressure gradually improved without any pharmacologic intervention and the trachea was extubated. Arterial blood pressure prior to extubation was 82/54 mm Hg, heart rate 145 bpm, respiration 32 breaths/min, and oxygen saturation 94%-96% while breathing 30% oxygen. Because no blood gas analyzer was immediately available in the free-standing outpatient surgical center, no arterial blood gas values were obtained. The patient was admitted to the hospital and a pediatric cardiologist was consulted. The first set of cardiac enzymes (isoenzymes of creatinine phosphokinase [CPK] and lactate dehydrogenase) showed an increased total CPK (660 IU/L; normal range 30-200 IU/L) with normal values for total lactate dehydrogenase and cardiac isoenzymes. Two subsequent sets of enzymes were within the normal range. Transthoracic echocardiography on the day of admission revealed moderately depressed global left ventricular dysfunction with an M-mode shortening fraction of only 16% (normal 28%-44%). No abnormalities in cardiac chamber size or valvular function were noted Table 1. The electrocardiogram was remarkable only for sinus tachycardia at 115 bpm. Adenovirus and Coxsackievirus antibody screens (acute and convalescent phase) were not suggestive of an acute infection.Table 1: Transthoracic Echocardiographic ResultsThe patient's condition improved progressively over the hospital stay, and the initial chest radiographic findings resolved by postoperative Day 1. Left ventricular dysfunction resolved Table 1, and the child was discharged from the hospital 2 days after the operation. A follow-up examination on postoperative Day 5 confirmed the resolution of the transient myocardial dysfunction, and transthoracic echocardiography on this day revealed normal left ventricular function. Discussion The presentation of pulmonary edema in the PACU after tracheal extubation in this healthy child was unexpected. Our first assumption was that the patient had developed postobstructive pulmonary edema [3]. However, there was never any evidence of airway obstruction or hypoxia, even during the brief transport to the PACU (respirations were monitored with a precordial stethoscope, and the first oxygen saturation in the PACU was 95%), nor was there pulmonary aspiration after extubation. The persistant hypotension and tachycardia in the PACU led us to believe that this patient had developed pulmonary edema secondary to cardiac dysfunction. The echocardiographic results showed the patient had global left ventricular dysfunction with no right ventricular involvement. We searched for reasons why this child may have developed heart failure. This was an active, healthy child with no known cardiac risk factors. There was no intraoperative hypertension, hypotension, hypoxemia, or acidosis that could have depressed the myocardium. There was no evidence that the volatile anesthetics had unmasked an undiagnosed myopathy causing cardiac compromise in this child; the initial increase in total CPK is consistent with the administration of succinylcholine in the PACU. Anticholinesterase drugs, which can cause coronary vasospasm and myocardial ischemia, were not administered, and the CPK results were not suggestive of myocardial ischemia [4]. There was no clinical or echocardiographic evidence of pulmonary embolism. Excessive intravascular volume was not an issue in this patient and, although an allergic or idiosyncratic reaction to a specific drug is possible, this seems unlikely since no medications were given to the patient 10 min prior to the event, and there were no other clinical signs (bronchospasm, rash, urticaria, angioneurotic edema) that would suggest massive mediator release. There are no reports that implicate morphine, ketorolac, atropine, or propofol in precipitating transient acute myocardial failure in a healthy patient. However, propofol has negative inotropic effects, and after the pulmonary edema was manifest in the PACU, the propofol infusion may have exacerbated the myocardial depression and led to the temporary severe hypotension before the infusion was discontinued. One report links the development of pulmonary edema in a 9-yr-old child to the combined effects of severe hypertension and tachycardia from the local injection of epinephrine and the cardiac depressant effects of sevoflurane [1]. Other reports link the administration of topical epinephrine alone with subsequent hypertension and tachycardia to the development of transient myocardial dysfunction resulting in postoperative pulmonary edema [5]. In all these cases, the administration of the local epinephrine was associated with immediate intraoperative hypertension and/or tachycardia. In our case, less than 1 micro gram/kg of topical epinephrine was injected with no changes in blood pressure or heart rate. In conclusion, we believe this is a case of unexplained acute postoperative myocardial dysfunction in a previously healthy child after uneventful general anesthesia. We are unable to explain the cause of the child's myocardial failure. A transient viral cardiomyopathy that coincided with the perioperative period, but was not detected with the limited viral serology titers, could perhaps be an explanation. An episode of coronary vasospasm could also precipitate transient global myocardial dysfunction and explain the clinical picture. This case illustrates that when diagnosing postoperative pulmonary edema in a child with no cardiac risk factors a noncardiogenic etiology should not automatically be assumed. As in our case, a pediatric cardiology consultation and transthoracic echocardiography may provide valuable information.