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Year : 2012  |  Volume : 2  |  Issue : 1  |  Page : 55-57

Acute aortic syndrome in the peripartum state: Powering clinical suspicion

1 Tufts University School of Medicine; Division of Cardiology, Baystate Medical Center, SpringfIeld, Massachusetts, USA
2 Tufts University School of Medicine; Department of Medicine, Baystate Medical Center, SpringfIeld, Massachusetts, USA
3 Tufts University School of Medicine; Department of Radiology, Baystate Medical Center, SpringfIeld, Massachusetts, USA

Date of Web Publication4-Aug-2012

Correspondence Address:
Jaime A Hernandez-Montfort
Cardiovascular Disease Fellow, Division of Cardiology, Baystate Medical Center, Tufts University School of Medicine, 759 Chestnut Street, Springfield, MA 01199
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2249-4472.99337

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How to cite this article:
Hernandez-Montfort JA, Velez J, Canoy J, Giugliano GR. Acute aortic syndrome in the peripartum state: Powering clinical suspicion. J Obstet Anaesth Crit Care 2012;2:55-7

How to cite this URL:
Hernandez-Montfort JA, Velez J, Canoy J, Giugliano GR. Acute aortic syndrome in the peripartum state: Powering clinical suspicion. J Obstet Anaesth Crit Care [serial online] 2012 [cited 2022 Aug 13];2:55-7. Available from: https://www.joacc.com/text.asp?2012/2/1/55/99337


Acute aortic syndromes (AAS) are the most frequent fatal condition in the clinical spectrum of patients complaining of chest pain. AAS are a subset of the heterogeneous group of patients that present with chest discomfort and hemodynamic instability. [1],[2]

A 33-year-old G1P1 Caucasian woman with known congenital bicuspid aortic valve was initially admitted to an outlying hospital for induction of labor due to superimposed mild preeclampsia. In the labor suite, she complained of sudden, severe, pleuritic, worse-with lying chest tightness. On examination her pulse rate was 88 bpm, blood pressure was 130/80 mmHg and oxygen saturation was 98% with a respiratory rate of 22/ min. Physical examination was relevant for normal jugular venous pressure, clear lung fields with no murmurs or rubs at auscultation, along with warm, non-edematous extremities. The patient received sublingual nitrates, which relieved the intensity of chest discomfort accompanied by resolution of electrocardiographic abnormalities. Initial cardiac biomarkers were not elevated and complete blood count and basic metabolic panel were unremarkable. Several hours later, fetal tracings showed decreased variability with non-reassuring decelerations, and the patient underwent successful emergent cesarean section delivery under spinal anesthesia. The patient continued to experience chest discomfort of similar characteristics with increased intensity refractory to narcotic analgesia in the recovery area and transthoracic echocardiogram was performed showing a 5.2 cm dilated aortic root with moderate pericardial effusion and left ventricular ejection fraction of 60% without regionall wall motion abnormalities. The patient was emergently transferred to our facility via helicopter.

On arrival, CT angiography of the chest showed an ascending aortic aneurysm measuring up to 5.5 cm with an intramural aortic hematoma (IAH) gradually tapering within the aortic arch, accompanied by a large pericardial effusion [Figure 1].
Figure 1: Computed tomography angiography showing an intramural hematoma. Notice the presence of large pericardial effusion and bilateral pleural effusions, both prognostic indicators for progression to complications such as aneurysm, dissection or rupture

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The patient was brought emergently to our operating theater and Standard American Society of Anesthesiologists monitors were applied. Modified rapid sequence induction was performed with fentanyl 250 mcg, midazolam 10 mg, etomidate 20 mg and succynilcholine 120 mg. The trachea was intubated with a 7.5 mm cuffed endotracheal tube and was placed on assisted control mode of ventilation with a FiO 2 of 40%. A BIS monitor was applied. A left radial arterial line (20 G) and right internal jugular central line (7 F) were inserted with the aid of ultrasound after intubation followed by a pulmonary artery catheter which revealed an arterial blood pressure of 119/94 mmHg, cardiac index 2.0 L/min, pulmonary artery pressure 37/29 mmHg and CVP 25 mmHg. She was given 40 mg of IV furosemide. Anesthesia was maintained with isoflurane, oxygen 80% / air 20%, fentanyl and pancuronium. Mean arterial pressure throughout the procedure was maintained with 1000 mL of colloid and 25 g of albumin and a total of 300 mcg of IV phenylephrine. Transesophageal echocardiogram was made available for intraoperative hemodynamic monitoring and evaluation of ascending aortic aneurysm repair and aortic valve replacement. Total cross-clamp time was 164 min and bypass time 208 min with deep hypothermic circulatory arrest of 33 min. The patient was transferred to the cardiac intensive care unit hemodynamically stable. She was subsequently extubated within 24 h. There were no significant complications noted. Pathology reported fragments of elastic aortic artery with outer medial tearing and extensive acute hemorrhage and adventitial acute inflammation. Special stains showed areas consistent with medial degeneration. The patient was discharged home with her baby 5 days after the surgery.

Aortic pain in the setting of long-standing hypertension or connective tissue disease should raise the clinical suspicion for an AAS. [2] Aortic pain is usually described as severely intense, acute, tearing, ripping, pulsating and migratory chest pain. In contrast to the more gradual increasing intensity of pain in acute coronary syndromes (ACS), pain from AAS is sudden with the maximal intensity at appearance. The migration of chest pain to the neck, throat or jaw may indicate that the segment involved is the ascending aorta, whereas pain referred in the back or abdomen suggests descending aortic disease. [3]

Physical examination findings can be related to the location and extension of the dissection. Acute aortic valve regurgitation manifested as a diastolic murmur can occur in 18-50% of proximal dissections and is the second most common cause of death (first is aortic rupture). Decreased or unequal distal pulses are also a common physical examination finding. [4] Laboratory studies might help differentiate AAS from ACS as there is usually diagnostic uncertainty between both entities. A rapid rise in D-dimer plasma concentrations in the absence of EKG changes suggests the presence of AAS. On the other hand, increase in myocardial enzymes with concomitant EKG changes suggestive of ischemia favors ACS. It is important to mention that AAS can be overlapped with ACS, as there can be concomitant decreased coronary artery perfusion or dissection involving the left main or right coronary artery ostium manifested as angina and/or ischemic EKG changes. Furthermore in 10-15% of AAS cases, echocardiography can demonstrate regional wall motion abnormalities. [5]

Plasma D-dimers are the result of a degradation product of cross-linked fibrin and is an important diagnostic test in the evaluation of suspected AAS. High D-dimer levels have a high sensitivity and correlates significantly with extension of disease, explaining its higher levels in classic aortic dissection compared with an intramural hematoma. The high negative predictive value of D-dimer offers the possibility of excluding AAS when a negative test is present. Of note, the presence of D-dimer is not exclusive for AAS and only subsequent imaging such as CT angiogram can differentiate from other clinical entities such as a pulmonary embolism. [6]

When AAS are suspected, aortic imaging ideally in the form of computed tomography, magnetic resonance or transesophageal echocardiography is necessary to confirm the diagnosis. [7] The presence of IAH has been described in 10-30% of patients with an AAS. [8] Defined as a variant of classic aortic dissection, an IAH is characterized by the absence of an entrance tear and therefore is considered a non-communicable type of aortic dissection. The false lumen is created by a hemorrhage into the aortic media, most likely after the rupture of the vasa vasorum that penetrates the outer half of the aortic media from the adventitia and branches freely at this level. [9] The key feature of IAH is its evolving pattern over time, and the lesion can be interpreted differently depending on the moment of diagnostic examination. Evolution might vary from a self-limiting contained rupture due to disintegration of the outer layers of the aortic media, to an overt aortic rupture with bleeding into the pericardial, pleural and mediastinal structures. The most important predictors of progression to complications (aneurysm, dissection and rupture) in patients with IAH are involvement of the ascending aorta and maximum aortic diameter (>50 mm). Other indicators of progression include persistent pain and/or hemodynamic instability, severe worsening of pleural or pericardial effusion, large intimal erosion, or increment of aortic thickness. [2] Our patient had several predictors of progression such as ongoing chest discomfort, a dilated ascending aorta and the presence of effusion.

AAS in pregnancy has been reported in multiple case series, leading to propose pregnancy per se as an independent risk factor. [10] However, most of the patients have preexisting risk factors such as connective tissue aortopathy (Marfan's, Ehlers Danlos, and Turner's syndromes), arterial hypertension or atherosclerosis and congenital aortic valve anomalies. [11] On the other hand, the International Registry for Acute Aortic Dissection (IRAD) study has shown a low incidence of pregnancy-related dissection with 2 cases in >1000 autopsied subjects. [12],[13] Even if the association is only a result of coincidental and selective reporting, pregnancy-associated AAS has management implications related to time, as it has been shown that there is a 1-3% increase in mortality per undiagnosed hour. [14] Our patient had a known history of a bicuspid aortic valve with aortic root enlargement which has retrospectively shown to increase the long-term risk of aortic dissection. [15]

Treating acute aortic dissection in pregnancy depends on the location and viability of the fetus. Type A dissections (involving ascending aorta) are considered a surgical emergency, where if the fetus is considered viable (>28 weeks), a cesarean section followed by aortic repair in the same operation is the recommended approach. [16] The management of patients undergoing cardiothoracic surgery following cesarian section (CS) must account the increased risk of bleeding from the CS wound, placental site and the recently contracted uterus. Prior case reports have used intraoperative uterotonics and adjustments of cardiopulmonary bypass (CB) techniques with favorable outcomes however there is no consensus in this regard. [11]

This case shows the importance of rapid diagnostic reasoning in any patient with chest discomfort as the appropriate diagnostic workup for AAS depends highly on clinical suspicion particularly in the setting of pre-existing risk factors such as a bicuspid aortic valve with aortic root enlargement and Marfan syndrome. In retrospect, a plasma D-dimer level could have been an important test that will have included AAS as a potential diagnosis. Patients in the peripartum period require a broader multidisciplinary approach and achieving coordination of care between delivery and surgery in a timely manner might become a challenge as cardiothoracic surgery is not readily available at all medical facilities. Therefore, increasing awareness of the risk factors and clinical presentation of AAS among clinicians dealing with acute chest pain syndromes is a paramount skill to develop particularly in non-cardiovascular centers and clinical scenarios, such as the peripartum state.

  References Top

1.Vilacosta I, San Roman JA. Acute aortic syndrome. Heart 2001;85:365-8.  Back to cited text no. 1
2.Vilacosta I, Aragoncillo P, Cañadas V, San Román JA, Ferreirós J, Rodríguez E. Acute aortic syndrome: A new look at an old conundrum. Heart 2009;95;1130-9.  Back to cited text no. 2
3.Wooley CF, Sparks EH, Boudoulas H. Aortic pain. Prog Cardiovasc Dis 1998;40:563-89.  Back to cited text no. 3
4.Von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection. Arch Intern Med 2000;160:2977-82.  Back to cited text no. 4
5.Eisenberg MJ, Rice SA, Paraschos A. The clinical spectrum of patients with aneurysms of the ascending aorta. Am Heart J 1993;125:1380-5.  Back to cited text no. 5
6.Eggebrecht H, Naber CK, Bruch C, Kröger K, Von Birgelen C, Schmermund A, et al. Value of plasma fibrin D-dimers for detection of acute aortic dissection. J Am Coll Cardiol 2004;44:804-9.  Back to cited text no. 6
7.Urbania TH, Hope MD, Huffaker, Gautham PR. Role of computed tomography in the evaluation of acute chest pain. J Cardiovasc Comput Tomogr 2009;3:S13-22.  Back to cited text no. 7
8.Evangelista A, Dominguez R, Sebastia C, Salas A, Permanyer-Miralda G, Avegliano G, et al. Prognostic value of clinical and morphologic findings in short-term evolution of aortic intramural haematoma. Eur Heart J 2004;25:81-7.  Back to cited text no. 8
9.Vilacosta I, San Roman JA, Ferreirós J, Aragoncillo P, Méndez R, Castillo JA, et al. Natural history and serial morphology of aortic intramural hematoma: A novel variant of aortic dissection.Am Heart J 1997;134:495-507.  Back to cited text no. 9
10.Gelpi G, Pettinari M, Lemma M, Mangini A, Vanelli P, Antona C. Should pregnancy be considered a risk factor for aortic dissection? J Cardiovasc Surg (Torino) 2008;49:389-91.  Back to cited text no. 10
11.Johnston C, Schroeder SN, Fletcher C, Bigham C, Wendler R. Type A aortic dissections in pregnancy. Int J Obstet Anesth 2012;21:75-9.  Back to cited text no. 11
12.Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, et al. The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease. JAMA 2000;283:897-903.  Back to cited text no. 12
13.Nienaber CA, Fattori R, Mehta RH, Richartz BM, Evangelista A, Petzsch M, et al. Gender-related differences in acute aortic dissection. Circulation 2004;109;3014-21.  Back to cited text no. 13
14.Oskoui R, Lindsay J Jr. Aortic dissection in women <40 years of age and the unimportance of pregnancy. Am J Cardiol 1994;73:821-3.  Back to cited text no. 14
15.Michelena H, Khanna A, Mahoney D, Margaryan E, Topilsky Y, Suri RM, et al. Incidence of aortic complications in patients with bicuspid aortic valves. JAMA 2011;306:1104-12.  Back to cited text no. 15
16.Zeebregts CJ, Schepens MA, Hameeteman TM, Morshuis WJ, De La Riviere AB. Acute aortic dissection complicating pregnancy. Ann Thorac Surg 1997;64:1345-8.  Back to cited text no. 16


  [Figure 1]

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