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Year : 2022  |  Volume : 16  |  Issue : 4  |  Page : 485-487

Differential diagnosis of intraoperative cardiac arrest after spine surgery in prone position

Anesthesiology Department of Hospital das Clínicas da Universidade Federal de Minas Gerais (Clinic's Hospital of the Federal University of Minas Gerais, Brazil), Brazil

Correspondence Address:
Davi Brasil Khouri
Rua Monte Alverne, 90, apt 401 – Floresta. Belo Horizonte - 31015-400, MG
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/sja.sja_893_21

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Date of Submission28-Dec-2021
Date of Acceptance04-Jan-2022
Date of Web Publication03-Sep-2022


Intraoperative cardiac arrest is one of the most feared events by anesthesiologists and surgeons. Although there are many possible causes, three differential diagnoses stand out in the presented scenario: pulmonary embolism, gas embolism, and acute myocardial infarction. A 61-year-old female patient was admitted in the hospital to C2-C5 arthrodesis. Despite no major bleeding during surgery, immediately after supination the patient developed refractory hypotension, a decrease in end tidal CO2, progressive bradycardia that ultimately led to pulseless electrical activity. Resuscitation maneuvers were promptly performed, sustained return of spontaneous circulation was attained after 50 minutes, and the patient was transferred to the ICU. This paper discusses the main causes for an episode of cardiac arrest in the context of cervical arthrodesis, with a markedly prolonged resuscitation time, in which the patient survived.

Keywords: Air embolism, cardiac arrest, gas embolism, intraoperative cardiac arrest, intraoperative myocardial infarction, pulmonary embolism, spine surgery

How to cite this article:
Khouri DB, Delgado MA, Lemes JL, Afonso Cruz MM. Differential diagnosis of intraoperative cardiac arrest after spine surgery in prone position. Saudi J Anaesth 2022;16:485-7

How to cite this URL:
Khouri DB, Delgado MA, Lemes JL, Afonso Cruz MM. Differential diagnosis of intraoperative cardiac arrest after spine surgery in prone position. Saudi J Anaesth [serial online] 2022 [cited 2023 Jan 31];16:485-7. Available from:

  Introduction Top

Intraoperative cardiac arrest (IOCA) is among the most feared events by anesthesiologists. It is an ominous occurrence with a 50% lethality rate.[1] Three differential diagnoses stand out in the presented scenario: pulmonary embolism (PE), gas embolism (GE), and acute myocardial infarction (MI). Reaching a specific diagnosis is challenging, since patients cannot refer to symptoms and full physical examination is often not possible. The clinician must react quickly and decisively to emerging clues.

  Case History Top

A 61-year-old female suffering from depression, fibromyalgia, and hypertension was being treated for an L2 extramedullary plasmacytoma that had disseminated to C5-T2. She underwent arthrodesis between C5-T4 and T12-L4, during which she developed hemodynamic instability and transitory ST segment elevation, later diagnosed as a type 2 MI. Diagnostic coronary catheterization was executed, but no major issues were found. A transthoracic echocardiography reported normal right and left ventricular function.

A year later, the patient was readmitted due to upper limb weakness and a burning neck pain irradiating to both hands. An uneventful decompressive C4-T4 arthrodesis was performed but ultimately failed after a week, due to loosening of osteosynthesis material attributed to poor bone quality, ending up in cervical instability.

A new C2-C5 arthrodesis in the prone position lasting 5 hours was performed. Despite no major bleeding nor hemodynamic instability until wound closure, the patient developed sudden and refractory hypotension immediately after supination, accompanied by decreased end tidal CO2 (ETCO2) and progressive bradycardia that ultimately led to pulseless electrical activity (PEA). Resuscitation maneuvers were promptly initiated, and sustained return of spontaneous circulation was attained after 50 minutes, but the patient remained hemodynamically unstable and a deterioration in oxygenation was perceived, such that PaO2/FiO2 ratio was 60.4 and PaCO2 101.4 mmHg, despite normal tidal volumes. Point-of-care echocardiography showed marked hypocontractile left ventricle (LV) and an even worse right ventricle (RV). A poor echocardiographic window prevented more elaborated evaluation at the time. The patient was transported to intensive care receiving norepinephrine, vasopressin, epinephrine, and dobutamine.

Echocardiography performed 2 days later showed hypocontractile and dilated RV, TAPSE 13 mm, and PSAP of 37 mm. Meanwhile, LV had a mild systolic dysfunction. Five days later, LV had normal systolic function, but RV remained hypocontractile. Postoperative troponin I was 11.600 ng/L, and D-dimer was not measured due to institution limitations.

After several weeks, the patient woke up and was transferred to infirmary care, still wearing a neck brace. Upon examination, Glasgow 15/15, the patient preserved strength and sensitivity in all four limbs, except for difficulty closing her left hand. Mild respiratory effort persisted, and an oxygen flow of one liter per minute was necessary to maintain normal saturation.

  Discussion Top

Among the many possible causes for IOCA, three stand out here: pulmonary embolism, gas embolism, and myocardial infarction.

Prone position creates a state of blood stasis and decreased venous return in lower extremities. The cushions used keep the legs below the heart, and the flexed position of the hips and knees also interferes with blood circulation. Abdominal compression further exacerbates this process. Thus, it is no surprise that PTE after spinal surgery has an incidence of 19–25%.[2] Its intraoperative diagnosis, however, is challenging, given that classic signs such as tachypnea and dyspnea are absent. When there is sufficient magnitude, clues include sudden ETCO2 reduction, increased PaCO2, and appearance of hemodynamic instability.[3] Lethality rates of cardiac arrest due to pulmonary embolism are very high, 65–90%. PEA is observed in up to 50% of patients, and shockable rhythms are rarely seen.[4]

GE can occur in any procedure where the surgical site is located above the heart. Besides, many veins in the cervical vertebrae are devoid of valves, so their intraluminal pressure is directly dependent on their relation to the heart position. Although GE is common in cervical surgery in the prone position, it is usually asymptomatic. Nevertheless, significant air volumes can precipitate right ventricular outflow tract obstruction, causing dramatic drops in cardiac output, with consequent hemodynamic instability, abrupt reduction in ETCO2, and oxygen saturation.[5] Lethality rates are about 20%.[6] The lethal volume is around 200–300 ml or 3–5 ml/kg, and the closer the vein of entrainment is to the right heart, the smaller the expected lethal volume.[7] The main therapeutic interventions are: interrupting air entrainment by flooding the surgical site, placing the patient in the Trendelenburg position to increase venous pressure, and forcing the exit of air emboli from the heart through inotropic stimulation. There are few reports in the literature of GE cases during spinal surgery with major hemodynamic repercussions.[5]

As for MI, there are two main mechanisms: Type 1 occurs due to unstable or vulnerable plaque, whereas type 2 implies oxygen supply–demand imbalance.[8]

Given that our patient had ordinary preoperative echocardiography and coronary angiography, type 1 MI was ruled out. Furthermore, since there was minimal blood loss and hemodynamic stability was maintained up until supination, type 2 MI was considered less likely as a primary cause for the sudden hemodynamic instability. Therefore, the high troponin levels later obtained were attributed to ischemic insult secondary to the cardiac arrest combined with the trauma from chest compressions. Thus, although type 2 MI could be a cause, it was more likely a consequence.

PE and GE share several clinical and laboratorial manifestations. Both are compatible with the cardiovascular instability that developed upon supination, both can explain hypoxemia, elevated ETCO2–PaCO2 gap, and right heart failure, and either could justify PEA.

Therefore, in this scenario, we cannot assertively rule out either of them. Perhaps, the return to spontaneous circulation without thrombolysis and the extremely high lethality of PE-related cardiac arrests might suggest gas embolism as a primary hypothesis.

The author's aim is to raise awareness toward the main causes of IOCA, so that prompt interventions can be undertaken, and lives can be saved.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Han F, Wang Y, Wang Y, Dong J, Nie C, Chen M, et al. Intraoperative cardiac arrest: A 10-year study of patients undergoing tumorous surgery in a tertiary referral cancer center in China. Medicine (Baltimore) 2017;96:e6794.  Back to cited text no. 1
Hong B, Yoon SH, Park SY, Song S, Youn A, Hwang JG. Cardiac arrest from patient position change after spine surgery on a Jackson table. Acute Crit Care 2019;34:86-91.  Back to cited text no. 2
Mao Y, Wen S, Chen G, Zhang W, Ai Y, Yuan J. Management of intra-operative acute pulmonary embolism during general anesthesia: A case report. BMC Anesthesiol 2017;17:67.  Back to cited text no. 3
Sun SQ, Li KP, Zhi J. Multiple cardiac arrests induced by pulmonary embolism in a traumatically injured patient: A case report and review of the literature. Medicine (Baltimore) 2017;96:e9016.  Back to cited text no. 4
Cruz AS, Moisi M, Page J, Tubbs RS, Paulson D, Zwillman M, et al. Venous air embolus during prone cervical spine fusion: Case report. J Neurosurg Spine 2016;25:681-4.  Back to cited text no. 5
McCarthy CJ, Behravesh S, Naidu SG, Oklu R. Air embolism: Diagnosis, clinical management and outcomes. Diagnostics 2017;7:5.  Back to cited text no. 6
Mirski MA, Lele AV, Fitzsimmons L, Toung TJK. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007;106:164-77.  Back to cited text no. 7
Landesberg G, Beattie WS, Mosseri M, Jaffe AS, Alpert JS. Perioperative myocardial infarction. Circulation 2009;119:2936-44.  Back to cited text no. 8


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