Management of aortic dissection

Management of aortic dissection


Aortic dissection is the most common aortic emergency. It is one of the three acute aortic syndromes, the others being aortic intramural hematoma and penetrating aortic ulcer. It has a grave prognosis with 20% pre hospital and 30% in hospital mortality. Aortic dissection is generally considered as acute when diagnosis is made within 14 days of onset and chronic after that. An intimal and medial tear in the aorta causes blood to seep into the media and the false lumen usually progresses along a variable extend of the aorta. Important risk factors for aortic dissection are hypertension, Marfan syndrome and bicuspid aortic valve [1].

Management of aortic dissection is according to its anatomical extend and duration. Pain is the most common presenting symptom which initiates imaging studies. Computed tomography is the first line investigation in suspected aortic dissection. Other modalities are transesophageal echocardiography and magnetic resonance imaging [2]. Early diagnosis and management is key to improving outcome in aortic dissection. Surgical repair if feasible is considered in proximal dissections. Distal dissections call for endovascular repair in the presence of malperfusion or imminent rupture. Uncomplicated distal dissections may be managed medically [2].

Severe pain in the chest or back with migration down as dissection progresses, is classical of aortic dissection. History of recent strenuous exercise or use of drugs like cocaine or amphetamines may be there. Neurological symptoms like loss of consciousness, paraparesis or paraplegia may occur. New onset aortic regurgitation, pericardial effusion and myocardial ischemia may occur with proximal dissection [3].

Even though aortic dissection is classically divided into acute and chronic based on duration, another classification by Booher AM et al divides it into four time domains, based on data from International Registry of Aortic Dissection (IRAD) [4]. From symptom onset to 24 hours it was named hyperacute, acute between 2 -7 days, subacute between 8-30 days and chronic if it is more than 30 days.

Traditional anatomical classifications are DeBakey classification and Stanford classification [3]. In DeBakey category I, dissection tear in ascending aorta propagates distally to include at least the aortic arch and typically the descending aorta. DeBakey category II is dissection only in the ascending aorta. Category III is dissection tear in the descending aorta propagating most often distally. It is subdivided into category IIIa in which it is confined to descending thoracic aorta and IIIb in which the tear extends below the diaphragm. In Stanford classification, all dissections involving the ascending aorta are type A, irrespective of the site of tear. All dissections that do not involve the ascending aorta are classified as Stanford type B. PENN ABC and DISSECT are other classification systems.

Though several biomarkers have been evaluated in aortic dissection, only D-dimer is considered clinically feasible. It is markedly elevated in aortic dissection. Cut off value of 500 ng/mL can be used to rule out aortic dissection with a negative likelihood ratio of 0.07 within the first 24 hours [5]. In a study of 113 cases, it was found that those with younger age, thrombosed false lumen without ulcer like projections and shorter dissection length were likely to have false negative D-dimer values [6].

Initial management of acute aortic dissection is to control blood pressure and reduce dP/dt which is linked to the ventricular ejectile force, to reduce propagation of dissection. Blood pressure is reduced to the levels just enough for end organ perfusion. Intravenous beta blocker is the most important medical management for reducing dP/dt. Labetalol which blocks both alpha and beta receptors lowers blood pressure and dP/dt. Use of vasodilators without beta blockade should be avoided as they can increase dP/dt. Sedation with opiates will be useful in reducing the sympathetic discharge [3].

Mortality of type A dissection has been reported as 26% in those managed surgically and 58% in those not receiving surgery, typically because of advanced age and comorbidity. Type B dissection had a mortality of 10.7% on medical management. In those 20% of type B dissection patients who underwent surgery, mortality was 31.4% [7].

Prompt surgical treatment aims to remove the entry into the false lumen and reconstitute the true lumen with a synthetic graft with or without reimplantation of coronary arteries. Resuspension of native aortic valve is preferred to replacement for associated aortic regurgitation [3]. Endovascular repair is considered for descending thoracic aortic dissection. Open surgical repair requires single lung ventilation, left heart bypass, profound hypothermia and cerebrospinal fluid drainage. Hence endovascular repair has a class I indication in type B dissection. For type A dissection, though endovascular repair is technically feasible in some cases, surgical repair is the standard option. In type B dissection, if malperfusion of a branch persists, then branch vessel stenting or PETTICOAT (provisional extension to induce complete attachment) technique with open bare metal stents can be used [8].

References

  1. Thrumurthy SG, Karthikesalingam A, Patterson BO, Holt PJ, Thompson MM. The diagnosis and management of aortic dissection. BMJ. 2011 Jan 11;344:d8290.
  2. Nienaber CA, Powell JT. Management of acute aortic syndromes. Eur Heart J. 2012 Jan;33(1):26-35b.
  3. Nienaber CA, Clough RE. Management of acute aortic dissection. Lancet. 2015 Feb 28;385(9970):800-11.
  4. Booher AM, Isselbacher EM, Nienaber CA, Trimarchi S, Evangelista A, Montgomery DG, Froehlich JB, Ehrlich MP, Oh JK, Januzzi JL, O’Gara P, Sundt TM, Harris KM, Bossone E, Pyeritz RE, Eagle KA; IRAD Investigators. The IRAD classification system for characterizing survival after aortic dissection. Am J Med. 2013 Aug;126(8):730.e19-24.
  5. Suzuki T, Distante A, Zizza A, Trimarchi S, Villani M, Salerno Uriarte JA, De Luca Tupputi Schinosa L, Renzulli A, Sabino F, Nowak R, Birkhahn R, Hollander JE, Counselman F, Vijayendran R, Bossone E, Eagle K; IRAD-Bio Investigators. Diagnosis of acute aortic dissection by D-dimer: the International Registry of Acute Aortic Dissection Substudy on Biomarkers (IRAD-Bio) experience. Circulation. 2009 May 26;119(20):2702-7.
  6. Hazui H, Nishimoto M, Hoshiga M, Negoro N, Muraoka H, Murai M, Ohishi Y, Fukumoto H, Morita H. Young adult patients with short dissection length and thrombosed false lumen without ulcer-like projections are liable to have false-negative results of D-dimer testing for acute aortic dissection based on a study of 113 cases. Circ J. 2006 Dec;70(12):1598-601.
  7. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, Evangelista A, Fattori R, Suzuki T, Oh JK, Moore AG, Malouf JF, Pape LA, Gaca C, Sechtem U, Lenferink S, Deutsch HJ, Diedrichs H, Marcos y Robles J, Llovet A, Gilon D, Das SK, Armstrong WF, Deeb GM, Eagle KA. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000 Feb 16;283(7):897-903.
  8. Nienaber CA, Kische S, Zeller T, Rehders TC, Schneider H, Lorenzen B, B√ľnger C, Ince H. Provisional extension to induce complete attachment after stent-graft placement in type B aortic dissection: the PETTICOAT concept. J Endovasc Ther. 2006 Dec;13(6):738-46.
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