Perioperative Cardiac Arrest Complicated by Acute Pulmonary Edema Following Myomectomy: A Case Report from a Resource Limited Sitting

Introduction

Perioperative cardiac arrest is an uncommon but potentially catastrophic event, defined as the sudden cessation of effective cardiac activity during anesthesia or within the first 24 hours postoperatively, requiring immediate resuscitative measures. While rare, with reported incidences ranging from 4 to 35 per 10,000 anesthetic procedures, perioperative cardiac arrest carries a high risk of morbidity and mortality, with 30-day mortality rates reported between 50% and 70% in high-risk populations.¹ Factors influencing risk include patient comorbidities, type and urgency of surgery, anesthetic technique, and availability of perioperative monitoring and resuscitation resources.

Among the precipitating causes, airway-related and respiratory complications remain significant contributors. Prospective audit data and multicenter analyses have identified failed or difficult intubation, laryngospasm, airway obstruction, and inadequate oxygenation as common precipitants of perioperative arrest.^2,3 These events often result from a combination of patient factors (eg, obesity, obstructive sleep apnea, limited cervical mobility), procedural challenges, and system-related issues such as inadequate airway planning or delayed recognition of deterioration.³ Evidence from the Seventh National Audit Project (NAP7) highlighted that poor preparation for difficult airways, failure to escalate promptly to advanced airway interventions, and delayed administration of oxygenation strategies were disproportionately associated with serious morbidity and mortality.²

Acute pulmonary edema is a life-threatening complication that may develop in the perioperative period due to multiple mechanisms, including aggressive fluid administration, myocardial dysfunction, transfusion-related reactions, or negative-pressure pulmonary edema following upper airway obstruction.⁴ Clinically, it presents with dyspnea, hypoxemia, tachypnea, frothy sputum, and diffuse alveolar infiltrates on imaging. If not promptly recognized, it may rapidly progress to acute respiratory distress syndrome (ARDS) and multiorgan failure.⁵ Optimal management relies on early recognition, supportive ventilation, judicious diuresis, and hemodynamic stabilization, but outcomes are particularly poor in patients with preexisting cardiac or pulmonary comorbidities.

Although perioperative cardiac arrest and pulmonary edema have been well described individually, the simultaneous occurrence of both complications during elective non-cardiac surgery is extremely rare. Patients with underlying comorbidities such as uncontrolled hypertension, ischemic heart disease, or limited cardiopulmonary reserve are at higher risk for fluid- and hemodynamic-related complications.⁶ This risk is further amplified in resource-limited settings where access to advanced airway equipment, invasive hemodynamic monitoring, and intensive care support is restricted, leading to worse outcomes. Understanding these rare but critical events is essential to improve perioperative risk stratification, preparedness, and early intervention strategies to reduce morbidity and mortality.

Cardiac arrest and acute pulmonary edema may coexist and precipitate one another in the perioperative setting. Hypoxemia resulting from pulmonary edema can lead to myocardial ischemia and subsequent cardiac arrest, while cardiac arrest itself may cause neurogenic pulmonary edema through a catecholamine surge and disruption of the alveolar-capillary membrane. Understanding this bidirectional relationship is essential for prompt recognition and appropriate management of both conditions simultaneously.

However, the interaction between airway failure and perioperative fluid management in precipitating cardiac arrest remains poorly understand, particularly in resource-limited setting where monitoring capabilities and advanced airway equipment may be unavailable. This case report aims to address this gap by describing a perioperative cardiac arrest complicated by acute pulmonary edema and the subsequent successful resuscitation in a resource-constrained environment.

Case Presentation

A 42-year-old multiparous woman (para 4) with a known history of poorly controlled chronic hypertension was admitted to a peripheral hospital for an elective myomectomy due to symptomatic uterine fibroids. Preoperative evaluation revealed stable vital signs with no evidence of acute cardiopulmonary compromise. Routine laboratory investigations were unremarkable, and spinal anesthesia was selected as the initial anesthetic technique.

Intraoperative Events

There was a progressive perioperative deterioration. Following induction, spinal anesthesia proved inadequate and was poorly tolerated by the patient, necessitating conversion to general anesthesia. However, general anesthesia was administered without securing the airway via endotracheal intubation. In the resource-limited setting of the referring hospital, the decision was made to maintain spontaneous ventilation rather than perform endotracheal intubation, likely due to limited airway equipment and expertise. This decision, while not consistent with standard practice, reflects the challenges commonly encountered in peripheral facilities with constrained anesthesia resources. Approximately 30–40 minutes after induction, the patient developed progressive hypoxemia, which rapidly deteriorated into cardiac arrest. The likely pathophysiological sequence was failure to secure the airway during conversion to general anesthesia, leading to progressive hypoxemia that precipitated cardiac arrest. The prolonged resuscitation period of approximately 30–40 minutes with suboptimal perfusion further compounded the hypoxic insult, contributing to post-cardiac arrest hypoxic respiratory failure and the development of acute pulmonary edema. At the referring facility, basic life support measures were initiated, including chest compressions and bag-mask ventilation; however, advanced cardiac life support (ACLS) protocols, including defibrillation and pharmacological resuscitation, were not available. Documentation of the exact resuscitation timeline and interventions from the referring hospital was incomplete. Given the limited resources and failure to achieve sustained recovery, the patient was urgently transferred to our tertiary care center while resuscitation efforts were ongoing.

Following induction, spinal anesthesia proved inadequate and was poorly tolerated by the patient, necessitating conversion to general anesthesia. However, general anesthesia was administered without securing the airway via endotracheal intubation. Approximately 30–40 minutes after induction, the patient developed progressive hypoxemia, which rapidly deteriorated into cardiac arrest. Immediate basic life support was initiated at the referring hospital. Given the limited resources and failure to achieve sustained recovery, the patient was urgently transferred to our tertiary care center while resuscitation efforts were ongoing.

Resuscitation and Initial Stabilization

Upon arrival at our emergency department, the patient was unresponsive and pulseless. Advanced cardiopulmonary resuscitation (CPR) was commenced immediately, and return of spontaneous circulation (ROSC) was achieved after several cycles. The patient was promptly intubated and placed on mechanical ventilation. Due to profound hypotension, a continuous noradrenaline infusion was initiated.

Operative and anesthesia records from the referring hospital documented significant intraoperative blood loss, managed with transfusion of approximately 1 liter of whole blood and administration of 3 liters of intravenous crystalloids. This raised concern for acute fluid overload and possible pulmonary edema contributing to her respiratory failure.

Investigations

Initial arterial blood gas analysis on 100% inspired oxygen revealed severe hypoxemia and metabolic acidosis: pH 7.26, PaCO₂ 48 mm Hg, PaO₂ 80 mm Hg (PaO₂/FiO₂ ratio ≈ 80), bicarbonate 20 mmol/L, and serum lactate 5.2 mmol/L. Laboratory investigations showed leukocytosis (WBC 15.6 × 10⁹/L), anemia (hemoglobin 8.9 g/dL), and a normal platelet count (210 × 10⁹/L). Serum electrolytes demonstrated mild hyponatremia (Na 131 mmol/L) and normokalaemia (K 3.6 mmol/L), Other laboratory investigations demonstrated with preserved renal function, normal liver enzyme levels, and coagulation parameters were within normal limits, as shown in (Table 1).

Table 1 Laboratory Investigations

An Initial chest radiograph obtained after resuscitation showing diffuse bilateral alveolar opacities consistent with acute pulmonary edema. (Figure 1).

Figure 1 Anteroposterior (AP) chest radiograph obtained upon admission to the tertiary care intensive care unit demonstrates diffuse bilateral alveolar opacities predominantly involving the mid and lower lung zones, consistent with acute pulmonary edema. Blunting of the bilateral costophrenic angles suggests associated pleural effusions.

To further characterize the extent of pulmonary involvement and exclude alternative causes, contrast-enhanced computed tomography (CT) of the thorax demonstrated diffuse bilateral alveolar infiltrates with interstitial thickening and dependent ground-glass opacities, consistent with acute pulmonary edema. (Figure 2A and B). Transthoracic echocardiography revealed preserved left ventricular systolic function with an estimated ejection fraction of approximately 60%, along with concentric left ventricular hypertrophy, in keeping with long-standing hypertension.

Figure 2 (A and B) Contrast-enhanced computed tomography (CT) of the thorax. (A) Axial CT scan demonstrates diffuse bilateral alveolar infiltrates with interstitial thickening and dependent ground-glass opacities, consistent with acute pulmonary edema. (B) A large right-sided pleural effusion is identified, with bilateral dependent ground-glass opacities. The red arrow indicates areas of dependent ground-glass opacification.

Intensive Care Management

The patient was admitted to the intensive care unit (ICU) with diagnoses of post–cardiac arrest hypoxic respiratory failure, acute pulmonary edema secondary to fluid overload, and hemodynamic instability. Management included lung-protective mechanical ventilation under sedation with midazolam and fentanyl. Aggressive diuresis was initiated using a continuous intravenous furosemide infusion (100 mg in 100 mL normal saline at 6 mL/hour), with strict fluid balance monitoring.

Empiric broad-spectrum antibiotic therapy with intravenous meropenem was started due to concern for aspiration pneumonia. Inhaled bronchodilators were administered via the ventilator circuit. Noradrenaline infusion was titrated to maintain a mean arterial pressure above 65 mmHg and was gradually weaned off by the third ICU Day. Thromboprophylaxis was provided with subcutaneous enoxaparin (0.6 mL once daily). Electrolyte abnormalities were corrected during diuresis, and oral antihypertensive therapy was introduced once hemodynamic stability was achieved.

Clinical Course

During ICU Days 1 and 2, the patient remained sedated and mechanically ventilated. A net negative fluid balance was achieved, accompanied by significant radiological and clinical improvement. Oxygenation progressively improved, with the PaO₂/FiO₂ ratio increasing from approximately 80 to 200. Vasopressor requirements steadily decreased.

By Day 3, hemodynamic stability had been restored, sedation was tapered, and spontaneous breathing trials were initiated. On Day 4, the patient was successfully extubated and maintained oxygen saturation above 95% on room air, with marked resolution of dyspnea and cough. A follow-up chest radiograph obtained on ICU Day 4 demonstrated near-complete resolution of the previously observed bilateral pulmonary infiltrates, with restoration of normal lung fields (Figure 3). By Day 5, she was fully conscious, hemodynamically stable, mobilizing with assistance, and tolerating oral intake.

Figure 3 Follow-up posteroanterior (PA) chest radiograph obtained during the recovery period demonstrates significant interval improvement with near-complete resolution of previously noted bilateral alveolar opacities, indicating clearing of pulmonary edema. The bilateral costophrenic angles are now sharp, confirming resolution of pleural effusions. The cardiac silhouette is within normal limits, consistent with successful post-resuscitation recovery.

Ward Course and Outcome

Following stabilization, the patient was transferred from the ICU to the general gynecology ward, where she remained for an additional three days. Her recovery was uneventful, with continued clinical improvement. She ambulated independently, tolerated a full oral diet, and maintained well-controlled blood pressure on oral antihypertensive medications.

The patient was discharged home in good condition after a total hospital stay of eight days. At weekly outpatient follow-up visits, she remained clinically stable with no residual respiratory or neurological deficits.

Discussion

Perioperative cardiac arrest remains one of the most catastrophic complications of anesthesia and surgery, particularly in low- and middle-income countries, where limitations in infrastructure, monitoring, and trained personnel may substantially increase risk and hinder timely rescue interventions.^7,8 This case highlights the convergence of multiple well-recognized risk factors conversion to general anesthesia without definitive airway protection, liberal fluid and blood administration, and uncontrolled chronic hypertension culminating in hypoxia-induced cardiac arrest complicated by acute pulmonary edema.^9–11

The reported incidence of perioperative cardiac arrest ranges from approximately 2 to 13 per 10,000 anesthetic procedures, with mortality rates exceeding 30%, especially when arrests occur intraoperatively or are precipitated by hypoxemia.^12,13 Airway-related complications are consistently identified as among the most preventable contributors to anesthesia-related cardiac arrest.^14,15 Large audits and observational studies have demonstrated that delayed or failed airway protection, inadequate oxygenation, and unrecognized aspiration can rapidly progress to severe hypoxemia, bradyarrhythmia’s, and circulatory collapse.^10,14 In the present case, the decision to convert from spinal to general anesthesia without securing the airway may have contributed to progressive hypoxia, ultimately leading to cardiac arrest, consistent with findings from the NAP7 audit where delayed airway control was associated with adverse outcomes. This sequence is well documented in the literature.^9,14 This reinforces the fundamental principle that any conversion to general anesthesia should be accompanied by prompt airway protection with endotracheal intubation whenever feasible, particularly in high-risk or unstable patients.^10,14

Acute pulmonary edema following perioperative cardiac arrest is a complex entity with multifactorial pathophysiology. Potential mechanisms include cardiogenic causes related to transient myocardial dysfunction or hypertensive heart disease, as well as non-cardiogenic causes such as negative-pressure pulmonary edema, aspiration-related lung injury, post-resuscitation inflammatory response, and fluid overload.^11,12,15 In this patient, preserved left ventricular systolic function on echocardiography made primary cardiogenic pulmonary edema less likely. Instead, the combination of large-volume crystalloid infusion, whole-blood transfusion, and post-arrest inflammatory lung injury likely played a dominant role.^10,11 Radiological findings of bilateral alveolar infiltrates and dependent ground-glass opacities, together with profound hypoxemia, were consistent with acute pulmonary edema progressing toward acute respiratory distress syndrome.^11,16

Transfusion-related acute lung injury (TRALI) was considered as a differential diagnosis given the administration of whole blood during surgery. However, the temporal sequence of events with hypoxemia and cardiac arrest developing prior to completion of blood transfusion and the clinical presentation being more consistent with fluid overload and hypoxic injury make TRALI a less likely etiology. Furthermore, preserved left ventricular function on echocardiography supports a non-cardiogenic mechanism, and the rapid clinical response to diuresis further favors fluid overload as the primary contributor to the pulmonary edema.

Fluid management during major surgery and resuscitation represents a delicate balance. While hemorrhage and hypovolemia require prompt correction, liberal fluid strategies have been consistently associated with pulmonary complications, prolonged mechanical ventilation, and increased ICU length of stay.^8,11 Patients with chronic hypertension frequently exhibit diastolic dysfunction and reduced ventricular compliance, rendering them particularly vulnerable to fluid overload even in the presence of preserved systolic function.¹¹ This case underscores the importance of goal-directed fluid therapy, careful estimation of blood loss, and early use of vasopressors rather than excessive fluid administration to manage perioperative hypotension.^8,11

Post–cardiac arrest care played a central role in the favorable outcome observed. Early airway control, lung-protective mechanical ventilation, and aggressive yet carefully monitored diuresis resulted in rapid improvement in oxygenation and respiratory mechanics.^10,11,17 Lung-protective ventilation strategies, including low tidal volumes and appropriate positive end-expiratory pressure, are well established in reducing ventilator-induced lung injury in patients with acute hypoxemic respiratory failure.^11,16 Continuous furosemide infusion facilitated controlled negative fluid balance, which has been shown to improve pulmonary function and oxygenation in fluid-overloaded critically ill patients.¹¹

Empiric broad-spectrum antibiotic therapy was initiated due to concern for aspiration pneumonia, a frequent complication of perioperative hypoxic events,^14. Although microbiological confirmation is often unavailable, early empiric treatment in high-risk clinical scenarios is commonly justified, particularly in resource-limited settings where delayed therapy may worsen outcomes.^8,15 Importantly, antimicrobial therapy was used as an adjunct to, rather than a substitute for, definitive supportive management.

Notably, the patient achieved full neurological recovery despite cardiac arrest and severe hypoxemia. Early return of spontaneous circulation, prompt restoration of oxygenation, and avoidance of prolonged hypotension likely preserved cerebral perfusion.^9,12 While advanced neuroprotective strategies such as targeted temperature management were not employed, this outcome highlights the effectiveness of timely basic resuscitative and post-arrest care.^9,12

From a systems perspective, this case exposes vulnerabilities common in peripheral hospitals, including limited airway resources, variable anesthesia expertise, and challenges in perioperative monitoring. The literature consistently demonstrates higher anesthesia-related mortality in resource-limited settings, often driven by preventable factors such as airway mismanagement and delayed recognition of deterioration.^7,8 Strengthening perioperative safety therefore requires not only individual vigilance but also institutional measures, including standardized airway protocols, routine availability of essential airway equipment, crisis resource management training, and clear referral pathways to higher-level centers.^7,18 This case also highlights potentially preventable factors, particularly delayed definitive airway management and the absence of structured escalation protocols, which in resource-limited settings may significantly increase the risk of adverse perioperative events.

Finally, this case underscores the importance of multidisciplinary collaboration. The coordinated efforts of anesthesiologists, intensivists, nurses, and surgeons during resuscitation and post-arrest care were instrumental in achieving full recovery.^8,9,18 In settings where advanced technology may be limited, teamwork, clinical judgment, and adherence to evidence-based principles remain critical determinants of outcome.

In summary, this case illustrates three key clinical lessons: first, early definitive airway management during conversion from spinal to general anesthesia is critical and should never be deferred, consistent with findings from the NAP7 audit where delayed airway control contributed to adverse outcomes.¹⁹ Second, fluid resuscitation in hypotensive perioperative patients should be cautious and goal-directed, as liberal crystalloid administration in patients with reduced ventricular compliance can precipitate pulmonary edema; and third, structured post-cardiac arrest care, including lung-protective ventilation and controlled diuresis, can achieve favorable outcomes even in resource-limited settings.²⁰ In contrast to cardiogenic causes, preserved ejection fraction on echocardiography in this patient supports a non-cardiogenic etiology of the pulmonary edema, reinforcing the role of fluid overload and hypoxic lung injury as the dominant mechanisms.

Limitations

This report has several important limitations. As a single case report, the findings are not generalizable and cannot establish definitive causality, first, incomplete documentation from the referring hospital limited our ability to fully reconstruct the timeline and exact interventions performed during the initial resuscitation. Second, the findings from a single case cannot be generalized to all perioperative settings. Third, objective hemodynamic monitoring data (eg, arterial blood pressure, central venous pressure) were not available at the referring facility, which limits our ability to fully analyze the fluid management decisions. Finally, advanced neuroprotective strategies such as targeted temperature management were not employed, and their potential impact on outcome cannot be assessed. Despite these limitations, this case provides valuable learning points for perioperative care in resource-limited settings.

Conclusion

This case demonstrates that perioperative cardiac arrest complicated by acute pulmonary edema, although rare and life-threatening, can be survivable with favorable functional outcomes when appropriate interventions are implemented promptly, the event was likely multifactorial, with airway management challenges and perioperative fluid administration acting as contributing factors rather than definitive causes. The event was likely precipitated by preventable airway and fluid management factors. Three critical clinical lessons emerge for perioperative care, particularly in resource-limited settings: (1) early definitive airway management with endotracheal intubation must be prioritized during conversion from regional to general anesthesia; (2) fluid resuscitation in hypotensive perioperative patients should be goal-directed and judicious, avoiding liberal crystalloid administration without hemodynamic guidance; and (3) early recognition of hypoxemia and timely initiation of structured post-cardiac arrest care, including lung-protective ventilation and controlled diuresis, can lead to favorable outcomes even in resource-constrained environments. While these findings cannot be generalized from a single case, this report contributes valuable insights into achievable outcomes and highlights key targets for system-level improvement in similar low-resource settings.