RETRACTED ARTICLE: Sudden cardiac arrest under spinal anesthesia in a mission hospital: a case report and review of the literature

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 local anesthetic, 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.


Background
Ever since August Bier administered the first clinical spinal anesthesia more than a century ago, it has become an integral part of the modern day anesthesia practice. Although considered simple to perform and a relatively safe technique, life-threatening complications do occur under spinal anesthesia [1,2]. In the literature, the reported incidence of cardiac arrest is 1.3-18 in 10,000 patients [3][4][5].
We are reporting the occurrence of unanticipated delayed cardiac arrest following spinal anesthesia in a young and healthy patient. This communication is to bring to the fore the importance of vigilant monitoring and prompt intervention in the management of sudden cardiac arrest under spinal anesthesia in a lowresource setting.

Case presentation
The patient was a 25-year-old Cameroonian man weighing 65 kg who was recently operated on for acute appendicitis in Banso Baptist Hospital, Northwest Cameroon. All the preoperative investigations, including routine blood biochemistry, chest X-ray posterior and anterior view, and 12-lead electrocardiograms were normal. The abdominal ultrasound scan was essentially normal. In the operating theater (OT), routine monitoring included heart rate 78 beats/min, electrocardiogram, noninvasive blood pressure (BP) 120/78 mmHg, and pulse oximetry with SpO 2 at 99% in room air, and these baseline parameters were recorded and were essentially normal. An intravenous (IV) access was secured with a cannula and our patient was preloaded with 500 mL of normal saline solution. Under all aseptic precautions, a subarachnoid block was performed at L3/L4 space in the left lateral position with a 25-gauge Quincke needle and 3.2 mL of hyperbaric bupivacaine was injected into the subarachnoid space after confirming a clear and free flow of cerebrospinal fluid (CSF). Five minutes after turning the patient to the supine position, the sensory level of block was found to be at T10. During skin preparation of the abdomen, and almost 25 min after the subarachnoid injection, our patient started complaining of difficulty in breathing and this was followed with a convulsion. Sensory level was rechecked and was found to be at T10. A bolus of atropine 0.6 mg was administered as his heart rate suddenly dropped to 40 beats/min, SpO 2 to 65%, while his BP became unrecordable and peripheral pulses could not be palpated. Owing to diminishing consciousness, our patient was immediately intubated with a cuffed endotracheal tube (ETT) of 7.5 mm and positive pressure ventilation initiated with Bain circuit and 100% oxygen was administered. His heart arrested and cardiopulmonary resuscitation (CPR) was started immediately with pharmacologic intervention with adrenaline and dopamine and intravenous normal saline infusion. (Other vasopressors like mephenteramine, noradrenaline etc. were not available.) Within 4 min, our patient responded with a heart rate of 140 bpm, SpO 2 of 90%, and BP of 90/60 mmHg. Our patient was restless even after administration of injection of diazepam 10 mg, and phenytoin 1.5 g in IV infusion. Considering his slow response to resuscitative measures, our patient was administered 150 mg propofol and was paralyzed with 6 mg vecuronium and electively ventilated in the OR. Apart from sinus tachycardia, all investigations results including serum electrolytes, complete blood counts and chest X-ray were normal. Arterial blood gas analysis (ABG) was not available in our facility. Our patient was adjudged by both the anesthetist and attending surgeon as being fit enough to proceed for the emergency open appendicectomy via a Lanz incision with uneventful postoperative course. After 2 h of elective ventilation and achievement of hemodynamic stability, our patient became conscious and started responding to verbal commands with good respiratory efforts, and extubation was done after reversing the relaxant effect with standard doses of neostigmine and glycopyrrolate. His postextubation hemodynamic parameters were normal, and he was transferred to the high dependency unit (HDU) for further observation. Our patient was discharged on the 4th postoperative day with an uneventful course in HDU. The follow-up visits at the 2nd, 4 th , and 10th week in the postoperative period showed satisfactory clinical status.

Discussion
Spinal anesthesia is considered to be a safe procedure but complications rarely can occur in the clinical scene [1,2]. Ever since Caplan et al. [6] reported 14 cases of cardiac arrest during spinal anesthesia in an American Society of Anesthesiologists closed claim analysis, numerous case reports and reviews have been published [7,8]. The mechanism that triggers severe bradycardia [7][8][9][10] and the etiology of cardiac arrest under spinal anesthesia remain controversial and unclear. Oversedation, respiratory arrest, unintentional total spinal, myocardial infarction, and local anesthetic toxicity have all been suggested as the causative factors. However, contribution of intrinsic cardiac mechanisms and autonomic imbalance with the background of parasympathetic predominance may provide a more convincing and physiologic explanation for the occurrence of abrupt severe bradycardia and cardiac arrest under spinal anesthesia [6][7][8][9]. It is established that the final pathway is the absolute or relative increase in activity of the parasympathetic nervous system [11]. Cardiac arrest has been reported within 12-72 min of spinal anesthesia, while other cardiovascular side effects have been reported as late as 3-5 h after the administration of spinal anesthesia [12].
Our patient was hemodynamically stable and well oxygenated prior to the administration of spinal anesthesia. No ischemic changes were noticed in the electrocardiogram. Causative factors like myocardial infraction, respiratory depression, local anesthetic toxicity, subdural injection, and high level of spinal anesthesia were considered and excluded by the sequence of events and laboratory investigations. Our patient had acute appendicitis with right iliac fossa pain, leading to sympathetic stimulation to maintain BP and cardiac output with normocardia or relative tachycardia. Once the spinal analgesia was established, our patient became pain free and the sympathetic drive was aborted. Subsequently, the resulting bradycardia and hypotension occurred. The other contributory factor is that this patient with abdominal pain, nausea, and a few bouts of vomiting might have been avoiding fluids or food for some unspecified period. Hence our patient was probably in negative fluid balance. The 500 mL of fluid loading at spinal anesthesia might be inadequate to counter the vasodilator effect of the spinal anesthesia. These two factors, including aborted sympathetic overdrive and negative fluid balance, must have been the cause for sudden cardiac arrest.
Thus, contributing to autonomic imbalance was a possible primary trigger resulting in bradycardia and asystole in our patient [13][14][15].
Reports from the literature also implicate autonomic imbalance with a background of vagal dominance may intensify any tendency to bradycardia that might otherwise have been more benign, transient, or possibly unnoticed [16]. There exist a number of risk factors (Table 1) with variable impact on the occurrence of severe bradycardia and cardiac arrest under spinal anesthesia. These factors may identify vulnerable patients. However, presence of two or more listed factors may place these patients at high risk for bradycardia and cardiac arrest under spinal anesthesia [16]. Due to inconsistent reporting, risk factor association with the occurrence of bradycardia and cardiac arrest under spinal anesthesia still remains uncertain and contradictory [16].
The other mechanisms involved in cardiac arrest after spinal anesthesia include administration of excessive doses of local anesthetics in a previously hypovolemic patient, which can be secondary to preoperative fasting, malnutrition, dehydration, use of diuretics or vasodilators [17]. Even the perioperative events such as bleeding, changes in patient's positioning, placement of bone cement, light nature of anesthesia on a background of comorbidities and others can be responsible for cessation of cardiac activity [17]. It is generally recommended that the level of blockade should be limited to T6 and hemodynamic reserves should be evaluated and monitored for any complication [17]. The degree of bleeding should be observed regularly and replaced with blood whenever necessary, so as to reduce morbidity and mortality [17]. The present case report pertains to young ASA grade I patient who was preloaded with about 500 mL of fluid before administration of anesthesia. The preloading might be inadequate to offer a plausible etiology, especially with a background of vomiting and inadequate oral intake, even though the patient had been on intravenous fluids prior to the procedure. The spinal anesthesia also might have aborted the sympathetic overdrive provided by pain stimulation in a patient with abdominal pain from acute appendicitis. The resultant outcome was vagal predominance, which was a major contributor to the cardiac arrest [18][19][20].
Specific strategies to anticipate and prevent vagal predominance forms the mainstay in the management of severe bradycardia and cardiac arrest under spinal anesthesia are presented in Table 2. Appropriateness of spinal anesthesia in patients at risk must be evaluated carefully. Alternative anesthetic techniques should be considered whenever intraoperative massive blood loss or vasodilatation is anticipated. Adequate preloading and replacement of volume loss has been emphasized in a number of studies [18][19][20].
Local anesthetics are widely used in modern medical procedures. Though the incidence of reported adverse effects of local anesthetics is low, occasional severe toxicity and deaths have been reported [21]. Among all, bupivacaine is considered to be 4-16 times more cardiotoxic than lignocaine [22]. Delayed cardiac arrests have been reported after 20 min of spinal anesthesia [21,22]. This possibility was also being considered in the present scenario as our patient developed breathlessness and convulsions before cardiac arrest, almost 20 min after administration of spinal anesthesia.
Circulatory or respiratory insufficiency can occur after inducing sedation for the purpose of giving comfort and relieving anxiety related to a surgical procedure. The sedated state can result in loss of spontaneous verbalization for a brief period of time before detection of cardiac arrest. Major hypoxic events (SpO 2 < 85% for > 30 s) have been reported without apparent cyanosis or changes in the respiratory pattern. Thus it is possible that respiratory insufficiency may have been present but clinically unrecognized [23]. It has been suggested recently that the combination of sympathetic blockade produced by high spinal anesthesia and the vagolytic   [24]. Drugs such as droperidol can also lead to severe hypotension and sudden cardiac arrest during spinal anesthesia on account of their αblocking effect [25]. Patients on beta blockers and other alternative medicines provide another challenging situation as the cardiac arrest in these patients can be refractory as vasoconstriction mechanisms in the peripheral vasculature may be impaired [3,11,26]. But in the present clinical situation, our patient did not receive any beta blockers or other medications nor was any sedation administered before the occurrence of cardiac arrest. The term "vagotonia" describes the clinical situation of resting bradycardia, atrioventricular (AV) block, or complete AV dissociation that is normally present in 7% of the population [27]. In such population, incidence of asystole is higher during performance of procedures, which can enhance vagolytic activity [28,29]. Cardiac arrest is more common in young individuals with an established fact that vagal tone is greater in the patient and increase in parasympathetic activity further enhances exaggerated vagal tone [11,30]. This could be one of the plausible causes in our patient. Unexpected cardiac arrest has been reported after small postural changes of the patient including placing a leg in the holder and turning the patient to the left lateral or prone position, and in some cases the arrest has been reported even after the surgical procedure had already finished [31]. It seems difficult to explain these situations based only on preload changes. Maybe they are due to reflex phenomena similar to those of autonomic dysfunction or hyperreflexia described in patients with a spinal cord section. Thus, there should be minimal movement or mobilization of the patient after spinal anesthesia [31]. However, in the present clinical scenario, our patient had cardiac arrest in a supine position, which excludes the above-mentioned plausible cause, while the likely indicators have already been described.

Conclusions
Finally, Banso Baptist Hospital is a mission hospital with limited facilities. The hospital intensive care unit has very limited facilities and therefore can best be described as a high dependency unit (HDU). This index patient had a good postoperative outcome. We must reiterate that the significance and management of such clinical situations depends upon the anesthesiologist's acumen and a high index of suspicion in order to detect early that something is "going wrong". The experience-based empirical anesthesia practice should always consider the evidence-based approach in such clinical situations [32]. The best clinical pearl in such situations is to believe and to intervene immediately any detectable abnormalities are seen. Disbelief and insecurity are common patterns of this situation and may influence the final outcome [1,32]. Therefore, the knowledge 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.