Emily Downs, MD, and Gorav Ailawadi, MD
Concept
- Diagnosis of pulmonary embolism
- Indications for surgical embolectomy
- Surgical technique
- Chronic pulmonary embolus and management
Chief complaint
“You are called to see a 47-year-old woman with a recent diagnosis of localized pancreatic cancer who presented to the emergency department with a 1-week history of progressive fatigue and dyspnea on exertion. She appears short of breath, heart rate is 116 beats/min, blood pressure is 100/66, oxygen saturation is 88% on room air. CT chest with pulmonary arteriography shows a large embolus nearly occluding the right pulmonary artery.”
Differential
The diagnosis of pulmonary embolism (PE) is established from the history and high index of suspicion. A PE protocol CT with contrast during the pulmonary phase (CTPA) is diagnostic. Extent of pulmonary and hemodynamic compromise is important in determining management.
History and physical
Key points include contributing factors to thrombosis, determining clinical status and extent of hemodynamic instability. Determine patients risk profile for invasive therapeutic options such as surgery or thrombolytic therapy. Thrombosis risks are summarized by Virchow’s triad: venous stasis, endothelial injury, and hypercoagulability. History should evaluate:
- Venous stasis: recent immobility due to travel, illness, surgery, prolonged bedrest.
- Endothelial injury from surgery, trauma, venous access procedures.
- Hypercoagulable state associated with malignancy, inherited thrombophilia, use of medications (oral contraception) or history of thrombosis.
Hemodynamic stability is evaluated with close attention to signs of shock and right heart strain. Thrombolysis with tissue plasminogen activator (several formulations available) may be considered but must rule out absolute contraindications. Ask patients about history of stroke, intracranial tumors, or recent trauma or surgery.
Tests
- EKG: most common finding is tachycardia; may have T-wave abnormalities, right bundle branch pattern, atrial arrhythmias, S1Q3T3 (S wave in I, Q wave in III, inverted T wave in III—not common but highly specific).
- Echocardiogram. Transthoracic study done at bedside can detect signs of PE but cannot image the pulmonary arteries directly: evaluate for right heart strain (dilation, septal flattening), overall function, intra-atrial thrombus. Transesophageal study (TEE) can directly image the pulmonary arteries and atria.
- Pulmonary angiography: may be used to further evaluate clot extent and location.
- CTPA is the diagnostic test of choice for pulmonary embolism.
Stratification of early risk of death from PE
- Low-risk PE. Embolus identified without presence of shock/hypotension, RV dysfunction, or myocardial injury (positive troponin). Low-molecular weight heparin, unfractionated heparin infusion, or fondaparinux treatment with transition to long term oral anticoagulation.
- Intermediate-risk PE. Embolus present with RV dysfunction and/or myocardial injury, but without shock or hypotension. Options include unfractionated heparin infusion, low-molecular weight heparin or fondaparinux treatment, with transition to long term oral anticoagulation.
- High-risk PE. Presence of hemodynamic compromise (shock or hypotension) and RV dysfunction. Heparin infusion with thrombolysis or embolectomy. Risk of imminent death is ~10%, 30-day risk is ~30%.
Regardless of the risk stratification of a pulmonary embolism, it is critical to recognize this condition and initiate anticoagulation promptly. In the case of high-risk embolism, aggressive management and intensive observation is warranted. Survival rate decreases sharply if a patient requires cardiopulmonary resuscitation (CPR). In one study, patients who required CPR demonstrated mortality of 57% compared with 12% in patients who never required CPR.
Index scenario (additional information)
“Heparin infusion is initiated immediately. Echocardiogram is obtained and shows moderate dilation of the right ventricle with floating thrombus in the right atrium. The patient’s clinical condition deteriorates shortly after the study is obtained: Blood pressure 78/52, heart rate 132/min, increasing dyspnea with oxygen saturations of 84% on 100% O2 by nonrebreather mask. What are the options for management?”
Treatment/management
Hemodynamic compromise automatically classifies this as a high-risk pulmonary embolism and intervention is indicated. The recommended treatment is heparin infusion plus thrombolysis or embolectomy. Systemic administration of thrombolytic agent reduces the risk of death in patients with acute PE exhibiting signs of shock, but there is a significant risk of bleeding. Absolute contraindications to systemic thrombolysis include:
- Stroke. Any history of hemorrhagic stroke or stroke of unknown origin, ischemic stroke in the past six months.
- Central nervous system neoplasm.
- Past three weeks: major trauma, surgery, or head injury.
Additionally, approximately 8% of patients who receive thrombolysis fail this treatment and continue to experience hemodynamic instability with persistent clot burden. In hemodynamically compromised patients with absolute contraindications to thrombolysis or a failed attempt at systemic thrombolysis, surgical intervention should be considered. Patients who have already experienced a code event (pulseless electrical activity or other arrhythmia) have higher mortality rates than those who are hemodynamically unstable but have not experienced PEA. This has led some to advocate more aggressive approach to hemodynamically unstable patients with PE, and even consideration of surgical intervention for intermediate-risk patients without hypotension but already with right ventricular dysfunction and significant clot burden if there is a contraindication to early thrombolysis.
Catheter-based embolectomy has been used in place of surgical intervention in unstable patients with contraindication to systemic thrombolysis or failed attempt at systemic thrombolysis. At centers where this technique is available, it may be used as an alternative to open surgical procedure, but some concern remains that catheter-based technique may cause fragmentation of proximal clot and showering to more distal arteries. This approach is highly dependent on the skill of the operator.
Another approach in the case of significant hemodynamic compromise and poor oxygenation is to utilize extracorporeal membrane oxygenation (ECMO) via peripheral cannulation. This provides support while heparin therapy takes place and may be a viable alternative for poor surgical candidates or those whose burden of clot requires more time for resolution. It may be used as a backup for catheter-based embolectomy. ECMO does not fully unload the RV and thus it will help with systemic perfusion, but myocardial injury may persist until the clot burden is relieved.
Surgical embolectomy has been described in the literature with varying success rates, though there is little data comparing this strategy to medical management. A series of 47 patients by Leacche et al describes prompt surgical intervention in patients with large clot burden and contraindications to thrombolysis or failure of medical therapy. Operative mortality was 6% and 1-year survival was 86% for this series.
Operative steps
Goals – remove clot from pulmonary arteries, remove clot in transit in the right atrium, explore smaller segmental arteries to remove more distal clot.
- Large-bore IV access, arterial line, general endotracheal anesthesia, TEE probe in place, foley catheter.
- Evaluate extent of clot with TEE, examine right atrium and ventricle for clot in transit, evaluate for patent foramen ovale (PFO) as clot has been documented extruding through PFO during embolectomy. Some centers also use epicardial echo to locate emboli and determine cannulation sites.
- Median sternotomy, pericardial stay sutures.
- Heparinization, cannulation for cardiopulmonary bypass with attention to locations of emboli visualized on TEE.
- Normothermia if the thrombus is known to be in the main trunk of the PA. If more extensive thrombectomy is anticipated, cool patient depending on plan for circulatory arrest. Cardiac arrest is generally not necessary unless repair of PFO or ASD is needed.
- Longitudinal arteriotomy incision of main pulmonary artery (PA), may extend transversely onto right or left PA, some also perform arteriotomy of the right PA between the ascending aorta and the superior vena cava if preop evaluation indicated presence of clot accessible from this location.
- Removal of clot with suction and gallbladder stone forceps. Intermittent reduction in bypass flow aids visualization of emboli. In some cases, with extensive clot distally in branch pulmonary arteries, circulatory arrest may be required to create a bloodless field. Prepare for this ahead of time.
- Removal of distal clot—methods vary; may use a choledochoscope to visualize distal clot, also reports of opening pleura and using gentle lung massage to evacuate clot (careful as this may cause pulmonary hemorrhage; not all centers advocate entering the pleura for this purpose).
- IVC filter placement within 24 hours of surgery if not placed intraoperatively. Some centers report using right atrial purse-string cannulation site to place the IVC filter after performing the embolectomy.
Table 57-1. Summary of treatment options for high-risk pulmonary embolism.
| Systemic thrombolysis | Catheter-based technique | Surgical embolectomy | |
| Patient candidates | Poor operative candidates; no contraindications to thrombolysis | Poor operative candidates, proximal clot accessible via catheter, contraindication to systemic thrombolysis | Patients with high-risk emboli, significant proximal clot burden, contraindication to thrombolysis |
| Mortality rate* | 7-30% | 10-20% | 14-27% |
| Major risks | Bleeding, failure of treatment in 8% with persistent clot burden | Distal showering of clot, damage to vessels from mechanical thrombectomy | Risks associated with bypass, sequelae of distal clot burden |
* Mortality rate for acute massive pulmonary embolism with any management strategy is approximately 30% at one month after diagnosis.
Potential questions/alternative scenarios
“Chronic pulmonary embolism and pulmonary hypertension: A 58-year-old man presents to clinic with chief complaint of progressive shortness of breath. Three years ago, he underwent hip surgery complicated by a large pulmonary embolus one month postoperatively and was treated with thrombolysis. He recovered from this event but over the past several months has had increasing dyspnea. Echocardiogram demonstrates pulmonary artery pressure of 64 mmHg. What are the next diagnostic steps?”
The patient presents with symptoms and echocardiogram findings consistent with chronic thromboembolic pulmonary hypertension (CTEPH). Approximately 1-5% of patients who experience acute pulmonary embolism go on to develop this complication, presenting with vague dyspnea and fatigue after initially recovering from the acute embolic event. Further workup includes pulmonary angiography to assess the location of the vasculopathy causing pulmonary hypertension. Right heart catheterization provides helpful hemodynamic information, but wedge pressures may be difficult to obtain due to irregular contour of pulmonary arteries. Pulmonary function testing should be used to evaluate coexisting obstructive or restrictive lung disease, which if severe would steer away from surgical intervention.
If a patient is evaluated and felt to be a good candidate for surgery for CTEPH, there are some key differences between the surgical procedure for acute massive pulmonary embolus versus CTEPH. For patients with chronic disease, the intervention is a pulmonary artery endarterectomy with removal of thickened scar-like tissue from the vessel intima, in addition to removal of the gross thrombus which characterizes the procedure for acute PE. Pulmonary endarterectomy is performed under hypothermia with intermittent circulatory arrest to facilitate thorough removal of intraluminal fibrinous material and optimally reduce pulmonary hypertension. This procedure has a mortality rate of 4-7% when performed at high-volume centers.
“TEE performed just prior to pulmonary endarterectomy for CTEPH demonstrates moderate to severe tricuspid regurgitation. How should this be addressed?”
Many patients with CTEPH will exhibit some degree of tricuspid regurgitation. In general, once the pulmonary arterial pressure is reduced and the right ventricle is unloaded, the valvular insufficiency resolves. One option is to wean bypass support and evaluate valve function after the embolic burden is relieved, then repair the valve if regurgitation warrants this. Consider repair for severe tricuspid regurge with structural damage to the tricuspid valve or annular dilation (> 40 mm).
“72 hours after pulmonary endarterectomy the patient is noted to have a diffuse opacity in the right middle and lower lobes.”
Reperfusion syndrome occurs in 8-10 percent of patients after endarterectomy. Treatment is mainly supportive with ventilation and pressors as needed. Patients should be diuresed and FiO2 should be weaned. Rarely inhaled NO or ECMO are required. The syndrome tends to resolve after 7-10 days.
Pearls/pitfalls
- Diagnosis of PE with hemodynamic instability (shock, signs of RV dysfunction), contraindication to thrombolysis or failure of initial attempt at thrombolysis—consider surgical embolectomy.
- Chronic thromboembolic pulmonary hypertension—thorough endarterectomy can help reduce pulmonary hypertension and symptoms.
- Tricuspid regurgitation with CTEPH—repair usually not needed; regurgitation decreases as right ventricle remodels postoperatively.
Suggested readings
- Leacche M et al. Modern surgical treatment of massive pulmonary embolism: Results in 47 consecutive patients after rapid diagnosis and aggressive surgical approach. Journal of Thoracic and Cardiovascular Surgery 2005; 129: 1018-1023.
- Madani MM, Jamieson SW. Pulmonary Endarterectomy for Chronic Thromboembolic Disease. Operative Techniques in Thoracic and Cardiovascular Surgery. 2006; 264-274.
