Pulmonary thromboendarterectomy

Pulmonary thromboendarterectomy
ICD-9-CM 38.15

In thoracic surgery, a pulmonary thromboendarterectomy (PTE) is an operation that removes organized clotted blood (thrombus) from the pulmonary arteries, which supply blood to the lungs.

Indication

Surgery is indicated in patients with pulmonary artery emboli that are surgically accessible. Thrombi are typically the result of chronic thromboembolic pulmonary hypertension (CTEPH) (pulmonary hypertension induced by recurrent/chronic pulmonary emboli).[1] Indeed, PTE is the only definitive treatment option currently available for CTEPH.[2]

Due to the nature of the procedure patients with significant hemodynamic or ventilation complications or impairments may be unable to undergo PTE.

Description of the surgery

A PTE has significant risk; mortality for the operation is typically 5%, but less in centers with high volume and experience. Individuals with favorable hemodynamic risk profiles also demonstrate lower mortality rates (1.3%).[2] PTEs are risky because of what is done and how it is done. PTEs involve a full cardiopulmonary bypass (CPB), deep hypothermia and full cardiac arrest, with the critical procedure carried out in a standstill operation.[3] The reason for the complexity of procedure comes from the anatomy. The obvious part is that a pulmonary bypass is required. Surgeons cannot operate on something they cannot see; the blood going to the lungs has to be diverted from the pulmonary vasculature and lung function taken care of by a machine. Less obvious is that hypothermia is required. This goes back to the pathophysiology of emboli; they are organized, somewhat delicate, essentially part of the vessel wall, and hard to remove completely, unlike in an acute pulmonary embolectomy (for acute pulmonary embolism, which is done without hypothermia).[4][5] Making this task more difficult is the anatomy of the lung and pathophysiology of chronic thromboembolic pulmonary hypertension; lungs also get blood from the bronchial arteries are often enlarged. The practical implication is that a conventional cardiopulmonary bypass (CPB) is not sufficient to do the surgery because:

  1. too much blood would be in the surgical field and
  2. the delicate thrombi would be difficult to remove completely.

The solution is a full cardiac arrest, which can be done with hypothermia. So, after going on to CPB and they induce a deep hypothermia (18-20 degrees Celsius), to preserve the patient's brain. Once the patient is cooled off sufficiently the CPB machine is turned off and the surgeon has time to do the delicate work, which takes about 40 minutes, and consists of carefully removing the organized thrombus. The most challenging part of the surgery is finding the optimal plane to dissect the pulmonary artery. If the surgeon dissects too deeply into the vessel wall the pulmonary vessels may rupture. If the surgeon does not dissect deep enough the clot breaks proximally during extraction and the distal part of the pulmonary vasculture will not have its pulmonary blood flow restored. The right lung is typically done first. At the end an almost beautiful negative of the pulmonary arteries exists—as the emboli over time fill the larger vessels that feed the smaller occluded vessel.. It is not uncommon that collectively this negative almost represents the whole pulmonary tree—the only part missing being what the person was living off before the surgery. Bypass time is typically 345 minutes.[3]

Recovery/ICU

The ICU recovery involves several challenges. Some patients get significant reperfusion pulmonary edema, at places where thrombi were removed, [Levinson et al., 1986] and thus have less than ideal oxygen saturation values. This results because with the thrombus removal the surgeon strips out the pulmonary endothelium. The challenge for the ICU physician thus is getting the extra water out of the lungs, (for which they make use of the strong diuretic furosemide) to get decent oxygen saturation values, yet maintain the blood pressure. Maintaining these two parameters can be a challenge. Maintaining a good oxygen saturation can be accomplished by running the patient dry (with a diuretic) and setting a high BiPAP (bidirectional positive airway pressure). However, a high BiPAP tends to leads to poor venous return, which causes a decrease in blood pressure. Adding volume would increase blood pressure, but would this worsens the edema so it is generally avoided. Adding albumin does not help; the pulmonary arteries are too porous post-operation. With these described limitations of the available interventions, a delicate balance is required between the BiPAP setting and diuretic dosing to maintain proper blood pressure and oxygen saturation.

Post-surgery

The benefits of PTEs are significant. Most patients after surgery no longer suffer from shortness of breath and therefore have a much improved quality of life. Further, pulmonary vascular resistance usually drops back to close normal levels. Since the pulmonary resistance is proportional to the pressure driving the pulmonary flow (P=Q*R), it follows that the pulmonary pressure decreases. This in turn means that the work per time (power) decreases because it is equal to the pressure gradient times the volumetric flow, which in this case is the cardiac output. As a result of the operation, patients are spared from pulmonary hypertension and further right ventricular hypertrophy. Most pleasing is that patients who previously had right heart dysfunction often recover function.[6]

History and development

The UCSD Medical Center's cardiothoracic surgery department, led by Dr. Stuart Jamieson, is widely recognized as a pioneer in the relatively new surgery, having performed more PTEs than the rest of the world combined (over 3000 since 1970 out of a total of 4500 worldwide) with the lowest mortality rate.[7]

Papworth Hospital is the only center in the UK offering this surgery,[8] led by surgeon Mr David Jenkins.

Relation to pulmonary thrombectomies

PTEs and pulmonary thrombectomies are both operations that removed thrombus from the lung's arterial vasculature. Aside from this similarity they differ in many ways.

See also

References

  1. ↑ Pulmonary endarterectomy: Part II. Operation, anesthetic management, and postoperative care. Banks DA, Pretorius GV, Kerr KM, Manecke GR Semin Cardiothorac Vasc Anesth. 2014 Dec;18(4):331-40. Epub 2014 Jul 7. 
  2. 1 2 Chronic thromboembolic pulmonary hypertension. Fedullo P, Kerr KM, Kim NH, Auger WR Am J Respir Crit Care Med. 2011;183(12):1605. 
  3. 1 2 Dahm M, Mayer E, Eberle B, et al. (1997). "[Surgical aspects of pulmonary thrombendarterectomy]". Zentralbl Chir (in German). 122 (8): 649–54. PMID 9412095.
  4. ↑ Guilmet D, Arnaud-Crozat E, Bachet J, et al. (1989). "[Surgical treatment of chronic pulmonary embolism using thromboembolectomy under extracorporeal circulation and deep hypothermia--a new approach route. 3 cases]". Arch Mal Coeur Vaiss (in French). 82 (10): 1719–25. PMID 2512873.
  5. ↑ Moser KM, Auger WR, Fedullo PF, Jamieson SW (1992). "Chronic thromboembolic pulmonary hypertension: clinical picture and surgical treatment". Eur. Respir. J. 5 (3): 334–42. PMID 1572447.
  6. ↑ Kramm T, Mayer E, Dahm M, et al. (1999). "Long-term results after thromboendarterectomy for chronic pulmonary embolism". Eur J Cardiothorac Surg. 15 (5): 579–83; discussion 583–4. PMID 10386400. doi:10.1016/S1010-7940(99)00076-7.
  7. ↑ Thistlethwaite PA, Kaneko K, Madani M, Jamieson SW (2008). "Technique and Outcomes of Pulmonary Endarterectomy Surgery". Ann Thorac Cardiovasc Surg. 14 (5): 274–282. PMID 18989242.
  8. ↑ http://www.papworthhospital.nhs.uk/content.php?/our_services/thoracic_services_lungs/pulmonary_vascular_disease_unit_pvdu/Pulmonary_Hypertension_Service
  9. ↑ Augustinos P, Ouriel K (2004). "Invasive approaches to treatment of venous thromboembolism". Circulation. 110 (9 Suppl 1): I27–34. PMID 15339878. doi:10.1161/01.CIR.0000140900.64198.f4.
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