Acute pulmonary embolism (PE) during high-risk orthopedic surgery requires urgent diagnosis and treatment. End-tidal capnographic guidance may be ineffective under such circumstances as a guide for cardiopulmonary resuscitation (CPR). We report an interesting case scenario that shows the use of transesophageal echocardiography (TEE) in both the diagnosis of PE and the management of CPR. The patient gave written consent for use of his medical information.
A 70-year-old man was scheduled for open reduction and internal fixation of his right knee complex fracture of the proximal tibia and fibula extending into the joint space. His medical history included hypertension, diabetes mellitus, stroke, chronic kidney disease, chronic obstructive pulmonary disease, obstructive sleep apnea, and alcoholic liver disease. His chest radiograph was unremarkable. His complete blood count showed anemia and thrombocytosis; 7.8 g/dL and 431,000/mL, respectively. His coagulation status was altered: prothrombin time was 15.8 seconds and international normalized ratio was 1.3. A complete metabolic profile revealed elevated urea and creatinine; 41 mg/dL and 1.71 mg/dL, respectively. The preanesthesia evaluation was significant, showing a Mallampati class-4 airway.
General anesthesia was induced and maintained using etomidate, fentanyl, oxygen, air, and desflurane. Intermittent positive pressure ventilation was established after endotracheal intubation was facilitated by cisatracurium and a GlideScope (Verathon Inc., Bothell, WA). Intraoperative monitoring included noninvasive arterial blood pressure (BP), electrocardiography, pulse oximetry (SpO2), end-tidal capnography (ETCO2), end-tidal anesthetic drug concentration, bispectral index (BIS), esophageal temperature, and train-of-4 neuromuscular evaluation.
The surgeon applied a tourniquet to the right thigh to secure a bloodless operative field. After 90 minutes of tourniquet time, the surgeon requested an additional 60-minute extension. When the tourniquet was deflated after 150 minutes, a rapid reduction in SpO2 from 100% to 80% and decrease in ETCO2 from 40 to 7 mm Hg were noted. The BP and heart rate also decreased precipitously, and a presumptive diagnosis of pulseless electrical activity was established. The BIS reading decreased from 45 to 10. Surgery was immediately stopped, and CPR was initiated using the adult cardiac life support guidelines. Inhaled anesthesia was suspended, and ventilation was continued with 100% inspired oxygen. The BIS reading improved to 25 to 30, but his ETCO2 was still very low at 5 mm Hg. PE was suspected.
A TEE probe was urgently placed, and the examination showed a thrombus in the right ventricle (RV) extending into the pulmonary arteries (PAs). Small echogenic matter was noted in the right atrium (RA) and RV with intermittent bridging strands with the thrombus. The RV was severely dilated and akinetic. The left ventricle was severely hypokinetic. The RA was cannulated with an 8.5F right internal jugular venous catheter placed under ultrasound guidance. Several attempts failed to withdraw the clot and debris from the RA. Tissue thromboplastin activator was requested from the pharmacy and until it became available, a bolus dose of heparin 10,000 IU was given IV for fibrinolysis. CPR was continued. A 20-gauge left femoral arterial line was placed to guide the management of CPR. The activated clotting time was 134 seconds.
During CPR, his diastolic BP was maintained >25 mm Hg with effective cardiac compressions. The cardiologist was consulted for possible interventional embolectomy and a cardiothoracic surgeon for possible extracorporeal membrane oxygenation. TEE monitoring during the CPR revealed progressive resolution of the intracardiac thrombus and after 45 minutes complete resolution of thrombus was noted. After 59 minutes of CPR, the patient’s hemodynamic status improved with return of spontaneous circulation (ROSC). His BIS value improved to 51 and ETCO2 also improved to 39 mm Hg. The patient was treated with infusions of epinephrine 0.5 μg/kg/min, dobutamine 10 μg/kg/min, and vasopressin 12 IU/h to maintain the systolic BP 100 to 110 mm Hg. The electrocardiogram showed a sinus tachycardia of 115 to 120/min. Coronary angiogram revealed nonobstructive coronary artery disease. Pulmonary angiogram showed no thrombus in the PAs, but the segmental branches bilaterally appeared to have clots with filling defects.
The heparin infusion was continued, and an inferior vena cava filter was placed to avoid recurrence of PE. The patient was transferred to the intensive care unit for initiation of a post-cardiac arrest–induced hypothermia protocol. The patient was sedated with midazolam and fentanyl infusions 1 mg/h and 50 μg/h, respectively. After 24 hours, the patient was rewarmed. He continued to improve over the next 48 hours with successful discontinuation of all inotropic support. A computed tomography scan of his head showed no evidence of an acute intracranial event. The patient woke up once sedation was stopped. He was successfully weaned off ventilatory support on postoperative day 4. A neurological examination showed no evidence of neurocognitive deficit.
The American Society of Anesthesiologist’s Practice Guideline for Perioperative TEE states: “If equipment and expertise are available, TEE should be used when unexplained life-threatening circulatory instability persists despite corrective therapy.”1 This case report highlights the use of intraoperative TEE in patients undergoing high-risk orthopedic surgery with a potential for the development of deep vein thrombosis (DVT) and PE. TEE examination clearly showed the cause of this patient’s sudden cardiac arrest after the release of tourniquet. The TEE evaluation continued to display the intracardiac events during CPR and alerted those caring for the patient of his possible ROSC before he improved hemodynamically. It also allowed appropriate decision making by the cardiothoracic surgeon and the cardiologist during CPR. Based on TEE evaluation, extracorporeal membrane oxygenation was not used. Treatment with tissue thromboplastin activator was not commenced because the TEE showed resolution of the intracardiac thrombus after heparin was administered. The effectiveness of the chest compressions was also visible during TEE examination. Feedback from the TEE imaging improved the quality of chest compressions and motivated the resuscitation team to maintain the diastolic BP >25 mm Hg. A previous study has shown that when the diastolic BP >25 mm Hg, CPR chest compressions appear effective.2
This was associated with BIS monitor values of 25 to 30 during CPR, indicating the likelihood of adequate cerebral circulation. Previous studies have also shown that a good neurological outcome both immediately after ROSC and 6 months later is associated with BIS values >23 and 45, respectively.3,4 This patient had a BIS reading of 25 to 30 during the entire time of CPR. After ROSC, the BIS improved to 40 to 50. Although the patient required prolonged CPR, the BIS monitoring values provided positive feedback and encouraged continued effective chest compressions.
We believe that waveform ETCO2 guidance was ineffective because of a massive PE, and it was the TEE monitoring that was very helpful as a guide to the quality of the chest compressions. The ETCO2 improved from 5 to 39 mm Hg, with ROSC suggesting maintenance of adequate cardiac output during CPR. The likelihood of a good outcome after sudden cardiac arrest in the operating room may be expected if the reversible causes of the cardiac event are promptly treated. For this patient, timely administration of unfractionated heparin produced therapeutic fibrinolysis.5 The slow circulation time during CPR delayed resolution of the clot. The clot in the main PAs may also have disintegrated because of effective cardiac compressions during CPR.
This patient had multiple comorbidities that could increase the risk of DVT and PE. He met Well’s criteria, with a score of 5 indicating high probability of forming DVT6 after a tibial fracture requiring immobilization of a limb.7 However, the Doppler scan was negative for DVT. Although treatment with low-molecular-weight heparin (Lovenox; Sanofi-Aventis US LLC, Bridgewater, NJ) was started for DVT prophylaxis,8,9 the current guidelines do not provide complete safety.10 Using a tourniquet for an extended time increases the likelihood of DVT.11 Clinical suspicion for DVT and PE should always be anticipated in high-risk cases. Release of the tourniquet is usually associated with mild to moderate hypotension. This decrease in BP is explained by a variety of factors; response to decreased systemic vascular resistance upon removal of the arterial occlusion, operative bleeding, and the release of ischemic tissue metabolites.12,13 Other important causes include bone cement implantation syndrome14 and fat embolism syndrome15 because of either an allergic reaction or dislodgement of the free particulate matter into the systemic circulation causing an inflammatory response. These causes are usually corrected with fluid resuscitation and vasoactive medication. Our patient had a rapid deterioration of BP and heart rate manifested as pulseless electrical activity resulting in minimal time for the medications and fluids to be effective. TEE can provide valuable information underlying the pathophysiology of an unexpected cardiac event during noncardiac surgery. Further studies are needed to determine the relationship between qualitatively measured cardiac compressions and BP during actual resuscitation attempts.
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