Alegbeleye Journal of Medical Case Reports (2018) 12:144 https://doi.org/10.1186/s13256-018-1648-5

CASEREPORT Open Access Sudden cardiac arrest under spinal in a mission hospital: a case report and review of the literature Bamidele Johnson Alegbeleye

Abstract Background: Sudden cardiac arrest following spinal anesthesia is relatively uncommon and a matter of grave concern for any anesthesiologist as well as clinicians in general. There have been, however, several reports of such cases in the literature. Careful patient selection, appropriate dosing of the , volume loading, close monitoring, and prompt intervention at the first sign of cardiovascular instability should improve outcomes. The rarity of occurrence and clinical curiosity of this entity suggest reporting of this unusual and possibly avoidable clinical event. Case presentation: We report the occurrence of unanticipated delayed cardiac arrest following spinal anesthesia in a 25-year-old Cameroonian man. Incidentally, the index patient was successfully resuscitated with timely and appropriate cardiopulmonary resuscitative measures. He went ahead to have emergency open appendectomy with good post-operative outcome and recovery. Conclusions: The management of such cardiac arrest under spinal anesthesia is very challenging in resource- limited settings such as ours. Anesthetists and clinicians need to be well informed of this grave complication. A good understanding of the physiologic changes caused by spinal anesthesia and its complications, adequate patient selection, respecting the contraindications of the procedure, adequate monitoring, and constant vigilance are of paramount importance to the eventual outcome. Keywords: Anesthesia-spinal, Cardiac arrest, Intraoperative complications, Resuscitation

Background and prompt intervention in the management of sud- Ever since August Bier administered the first clinical den cardiac arrest under spinal anesthesia in a low- spinal anesthesia more than a century ago, it has become resource setting. an integral part of the modern day anesthesia practice. Although considered simple to perform and a relatively Case presentation safe technique, life-threatening complications do occur The patient was a 25-year-old Cameroonian man weigh- under spinal anesthesia [1, 2]. In the literature, the re- ing 65 kg who was recently operated on for acute appen- ported incidence of cardiac arrest is 1.3–18 in 10,000 dicitis in Banso Baptist Hospital, Northwest Cameroon. patients [3–5]. All the preoperative investigations, including routine We are reporting the occurrence of unanticipated de- blood biochemistry, chest X-ray posterior and anterior layed cardiac arrest following spinal anesthesia in a view, and 12-lead electrocardiograms were normal. The young and healthy patient. This communication is to abdominal ultrasound scan was essentially normal. In bring to the fore the importance of vigilant monitoring the operating theater (OT), routine monitoring included heart rate 78 beats/min, electrocardiogram, noninvasive blood pressure (BP) 120/78 mmHg, and pulse oximetry with SpO2 at 99% in room air, and these baseline param- Correspondence: [email protected] Department of , Banso Baptist Hospital, P.O Box 9, Nso-Kumbo, eters were recorded and were essentially normal. An Northwestern Region, Cameroon intravenous (IV) access was secured with a cannula and

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our patient was preloaded with 500 mL of normal saline Discussion solution. Under all aseptic precautions, a subarachnoid Spinal anesthesia is considered to be a safe procedure block was performed at L3/L4 space in the left lateral but complications rarely can occur in the clinical scene position with a 25-gauge Quincke needle and 3.2 mL of [1, 2]. Ever since Caplan et al. [6] reported 14 cases of hyperbaric bupivacaine was injected into the subarach- cardiac arrest during spinal anesthesia in an American noid space after confirming a clear and free flow of Society of Anesthesiologists closed claim analysis, numer- cerebrospinal fluid (CSF). Five minutes after turning ous case reports and reviews have been published [7, 8]. the patient to the supine position, the sensory level of The mechanism that triggers severe bradycardia [7–10] block was found to be at T10. During skin preparation and the etiology of cardiac arrest under spinal anesthesia of the abdomen, and almost 25 min after the subarach- remain controversial and unclear. Oversedation, respira- noid injection, our patient started complaining of tory arrest, unintentional total spinal, myocardial infarc- difficulty in breathing and this was followed with a con- tion, and local anesthetic toxicity have all been suggested vulsion. Sensory level was rechecked and was found to as the causative factors. However, contribution of intrinsic be at T10. A bolus of atropine 0.6 mg was administered cardiac mechanisms and autonomic imbalance with the as his heart rate suddenly dropped to 40 beats/min, background of parasympathetic predominance may pro- SpO2 to 65%, while his BP became unrecordable and vide a more convincing and physiologic explanation for peripheral pulses could not be palpated. Owing to the occurrence of abrupt severe bradycardia and cardiac diminishing consciousness, our patient was immedi- arrest under spinal anesthesia [6–9]. It is established that ately intubated with a cuffed endotracheal tube (ETT) the final pathway is the absolute or relative increase in ac- of 7.5 mm and positive pressure ventilation initiated tivity of the parasympathetic nervous system [11]. Cardiac with Bain circuit and 100% oxygen was administered. arrest has been reported within 12–72 min of spinal His heart arrested and cardiopulmonary resuscitation anesthesia, while other cardiovascular side effects have (CPR) was started immediately with pharmacologic been reported as late as 3–5 h after the administration of intervention with adrenaline and dopamine and intra- spinal anesthesia [12]. venous normal saline infusion. (Other vasopressors like Our patient was hemodynamically stable and well oxy- mephenteramine, noradrenaline etc. were not available.) genated prior to the administration of spinal anesthesia. Within 4 min, our patient responded with a heart rate No ischemic changes were noticed in the electrocardio- of 140 bpm, SpO2 of 90%, and BP of 90/60 mmHg. Our gram. Causative factors like myocardial infraction, re- patient was restless even after administration of injec- spiratory depression, local anesthetic toxicity, subdural tion of diazepam 10 mg, and phenytoin 1.5 g in IV infu- injection, and high level of spinal anesthesia were con- sion. Considering his slow response to resuscitative sidered and excluded by the sequence of events and la- measures, our patient was administered 150 mg propo- boratory investigations. Our patient had acute fol and was paralyzed with 6 mg vecuronium and with right iliac fossa pain, leading to sympathetic stimula- electively ventilated in the OR. Apart from sinus tachy- tion to maintain BP and cardiac output with normocardia cardia, all investigations results including serum elec- or relative tachycardia. Once the spinal analgesia was trolytes, complete blood counts and chest X-ray were established, our patient became pain free and the sympa- normal. Arterial blood gas analysis (ABG) was not thetic drive was aborted. Subsequently, the resulting available in our facility. Our patient was adjudged by bradycardia and hypotension occurred. The other con- both the anesthetist and attending surgeon as being fit tributory factor is that this patient with abdominal pain, enough to proceed for the emergency open appendicec- nausea, and a few bouts of might have been tomy via a Lanz incision with uneventful postoperative avoiding fluids or food for some unspecified period. Hence course. After 2 h of elective ventilation and achieve- our patient was probably in negative fluid balance. The ment of hemodynamic stability, our patient became 500 mL of fluid loading at spinal anesthesia might be conscious and started responding to verbal commands inadequate to counter the vasodilator effect of the spinal with good respiratory efforts, and extubation was done anesthesia. These two factors, including aborted sympa- after reversing the relaxant effect with standard doses thetic overdrive and negative fluid balance, must have of neostigmine and glycopyrrolate. His postextubation been the cause for sudden cardiac arrest. hemodynamic parameters were normal, and he was Thus, contributing to autonomic imbalance was a pos- transferred to the high dependency unit (HDU) for fur- sible primary trigger resulting in bradycardia and asys- ther observation. Our patient was discharged on the tole in our patient [13–15]. 4th postoperative day with an uneventful course in Reports from the literature also implicate autonomic HDU. The follow-up visits at the 2nd, 4th, and 10th imbalance with a background of vagal dominance may week in the postoperative period showed satisfactory intensify any tendency to bradycardia that might other- clinical status. wise have been more benign, transient, or possibly Alegbeleye Journal of Medical Case Reports (2018) 12:144 Page 3 of 5

unnoticed [16]. There exist a number of risk factors Table 2 Management strategies for bradycardia and cardiac (Table 1) with variable impact on the occurrence of arrest during spinal anesthesia severe bradycardia and cardiac arrest under spinal Prevention: anesthesia. These factors may identify vulnerable pa- 1. Appropriate patient selection for spinal anesthesia when two or tients. However, presence of two or more listed factors more risk factors are present (Table 1) may place these patients at high risk for bradycardia and 2. Maintaining adequate preload cardiac arrest under spinal anesthesia [16]. Due to in- 3. Prompt replacement of fluid and blood loss. consistent reporting, risk factor association with the oc- 4. Vigilance during patient positioning currence of bradycardia and cardiac arrest under spinal Treatment of bradycardia: anesthesia still remains uncertain and contradictory [16]. The other mechanisms involved in cardiac arrest after 1. Mild to moderate bradycardia (HR 30–60/min) - stepwise escalation of therapy spinal anesthesia include administration of excessive – doses of local anesthetics in a previously hypovolemic a. Atropine 0.4 0.6 mg, IV patient, which can be secondary to preoperative fasting, b. Ephedrine 25-50 mg, IV malnutrition, dehydration, use of diuretics or vasodila- c. Epinephrine 0.2–0.3 mg, IV tors [17]. Even the perioperative events such as bleeding, 2. Severe bradycardia or cardiac arrest ’ changes in patient s positioning, placement of bone ce- a. Advanced Cardiac Life Support guidelines to be followed ment, light nature of anesthesia on a background of co- b. Early administration of epinephrine known to improve morbidities and others can be responsible for cessation outcome of cardiac activity [17]. It is generally recommended that Management of associated factors: the level of blockade should be limited to T6 and 1. Rapid fluid infusion hemodynamic reserves should be evaluated and moni- tored for any complication [17]. The degree of bleeding 2. Patient repositioning should be observed regularly and replaced with blood 3. Avoid surgical manipulation. whenever necessary, so as to reduce morbidity and mor- HR Heart Rate, IV Intravenous Route, Min Minute, Mg Milligram tality [17]. The present case report pertains to young ASA grade I patient who was preloaded with about 500 in patients at risk must be evaluated carefully. Alternative mL of fluid before administration of anesthesia. The pre- anesthetic techniques should be considered whenever intra- loading might be inadequate to offer a plausible etiology, operative massive blood loss or vasodilatation is anticipated. especially with a background of vomiting and inadequate Adequate preloading and replacement of volume loss has oral intake, even though the patient had been on been emphasized in a number of studies [18–20]. intravenous fluids prior to the procedure. The spinal Local anesthetics are widely used in modern medical anesthesia also might have aborted the sympathetic over- procedures. Though the incidence of reported adverse drive provided by pain stimulation in a patient with ab- effects of local anesthetics is low, occasional severe tox- dominal pain from acute appendicitis. The resultant icity and deaths have been reported [21]. Among all, outcome was vagal predominance, which was a major bupivacaine is considered to be 4–16 times more cardio- contributor to the cardiac arrest [18–20]. toxic than lignocaine [22]. Delayed cardiac arrests have Specific strategies to anticipate and prevent vagal predom- been reported after 20 min of spinal anesthesia [21, 22]. inance forms the mainstay in the management of severe This possibility was also being considered in the present bradycardia and cardiac arrest under spinal anesthesia are scenario as our patient developed breathlessness and presented in Table 2. Appropriateness of spinal anesthesia convulsions before cardiac arrest, almost 20 min after administration of spinal anesthesia. Table 1 Risk factors for bradycardia and cardiac arrest during Circulatory or respiratory insufficiency can occur after spinal anesthesia inducing sedation for the purpose of giving comfort 1. Age < 50 years and relieving anxiety related to a surgical procedure. 2. Baseline heart rate < 60/min The sedated state can result in loss of spontaneous verbalization for a brief period of time before detection 3. ASA physical status I and II of cardiac arrest. Major hypoxic events (SpO2 < 85% for 4. Use of beta blockers > 30 s) have been reported without apparent cyanosis 5. Sensory level blockade above T6 or changes in the respiratory pattern. Thus it is possible 6. Prolonged PR interval that respiratory insufficiency may have been present 7. Vagotonia but clinically unrecognized [23]. It has been suggested Min Minute, ASA American Society of Anesthesiologists, T6 Intervertebral disc recently that the combination of sympathetic blockade space no 6, PR P and R wave as per Electrocardiogram (ECG) waves produced by high spinal anesthesia and the vagolytic Alegbeleye Journal of Medical Case Reports (2018) 12:144 Page 4 of 5

effect of fentanyl might account for the sudden appear- seen. Disbelief and insecurity are common patterns of this ance of bradycardia [24].Drugssuchasdroperidolcan situation and may influence the final outcome [1, 32]. also lead to severe hypotension and sudden cardiac ar- Therefore, the knowledge of the physiologic changes rest during spinal anesthesia on account of their α- caused by spinal anesthesia and its complications, ad- blocking effect [25]. Patients on beta blockers and other equate patient selection, respecting the contraindica- alternative medicines provide another challenging situ- tions of the procedure, adequate monitoring, and ation as the cardiac arrest in these patients can be refrac- constant vigilance are of paramount importance to the tory as vasoconstriction mechanisms in the peripheral eventual outcome. vasculature may be impaired [3, 11, 26]. But in the present Acknowledgments clinical situation, our patient did not receive any beta Dr. Benjamin Kakule Malikidogo MD, PAACS, General Surgeon, Department of blockers or other medications nor was any sedation ad- General Surgery, Banso Baptist Hospital, Cameroon, who provided professional ministered before the occurrence of cardiac arrest. support during the writing of this case report and also read and approved the “ ” final manuscript. The term vagotonia describes the clinical situation Mr. Samuel Yengong SRN, Dip. Anaesthesia, Anaesthesiologist, Department of resting bradycardia, atrioventricular (AV) block, or of Anaesthesia, Banso Baptist Hospital, Cameroon, who provided professional complete AV dissociation that is normally present in support during the writing of this case report and also read and approved 7% of the population [27]. In such population, inci- the final manuscript. dence of asystole is higher during performance of pro- Funding cedures, which can enhance vagolytic activity [28, 29]. No record of funding for this case report declared. Cardiac arrest is more common in young individuals Availability of data and materials with an established fact that vagal tone is greater in the All data generated or analysed during this study are included in this patient and increase in parasympathetic activity further published article and can also be accessed via http://dx.doi.org/10.6084/ enhances exaggerated vagal tone [11, 30]. This could be m9.figshare.6220241. one of the plausible causes in our patient. Unexpected Disclosures cardiac arrest has been reported after small postural The authors have no disclosures. changes of the patient including placing a leg in the holder and turning the patient to the left lateral or Author’s contributions BJA conceived of the study and participated in its design and coordination, prone position, and in some cases the arrest has been helped to draft the manuscript, read and approved the final manuscript. reported even after the surgical procedure had already finished [31]. It seems difficult to explain these situa- Ethics approval and consent to participate tions based only on preload changes. Maybe they are Not applicable. due to reflex phenomena similar to those of auto- Consent for publication nomic dysfunction or hyperreflexia described in pa- Written informed consent was obtained from the patient for publication of tients with a spinal cord section. Thus, there should this case report and any accompanying images. A copy of the written be minimal movement or mobilization of the patient consent is available for review by the Editor-in-Chief of this journal. after spinal anesthesia [31]. However, in the present Competing interests clinical scenario, our patient had cardiac arrest in a The author declares that he has no competing interests. supine position, which excludes the above-mentioned plausible cause, while the likely indicators have already Publisher’sNote been described. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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