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. 2019 Jun 3;12(6):e229982. doi: 10.1136/bcr-2019-229982

Intravenous tPA in the treatment of acute stroke related to aortic dissection

Vikram Shivkumar 1, Dipali Nemade 1
PMCID: PMC6557344  PMID: 31164384

Abstract

A 61-year-old woman with no prior medical illness presented with acute onset stroke symptoms. She had no chest pain at the time of presentation. However, CT angiogram showed an extensive aortic dissection, resulting in hypoperfusion of the right cerebral hemisphere and thus causing stroke symptoms. Due to this finding, tissue plasminogen activator was not given and a negative outcome was avoided.

Keywords: stroke, cardiovascular medicine, neurology

Background

Aortic dissection (AD) is a life-threatening but treatable emergency. It usually presents with chest and back pain. However, 10%–55% of patients might not experience any significant pain.1 Neurological symptoms occur in 17%–40% of patients.2 This may present as transient ischaemic attack/stroke. Tissue plasminogen activator (tPA) is used to treat acute stroke in a subset of patients within 3–4.5 hours of symptom onset. Imaging guidelines necessitate only a non-contrast CT of the head to rule out haemorrhage prior to administration. However, severe complications are highly likely when it is given in patients with AD presenting with neurological symptoms. We present a case of a woman who presented with acute onset stroke symptoms in whom the diagnosis of AD was established successfully.

Case presentation

A 61-year-old woman, with no prior history of hypertension or any other significant medical illness, presented to the emergency department (ED) with complaints of facial droop and left-sided weakness. She was brought to the ED by family within 30 min of symptom onset. On initial presentation, she was afebrile with a pulse of 78/min, respiratory rate of 20/min, blood pressure was 180/95 mm Hg and 98% SpO2 on room air. She did not have any chest pain or any other symptoms. On examination, she did not have any speech deficits and was awake and alert. She was noted to have left homonymous hemianopia, left nasolabial fold flattening and 4/5 strength in left upper and lower extremities on Medical Research Council (MRC) scale.

Investigations

CT of the head and CT angiography (CTA) of the head+neck with perfusion scans were ordered as per our hospital stroke protocol. The preliminary report of the non-contrast CT of the head was called in to the ED by radiology and was reported as normal. On receiving the preliminary report, an order for tPA was placed after discussing the potential benefits and risks with the husband. Meanwhile, the CTA was completed and images were viewed by the radiologist and the on-call neurologist. CTA of the head was normal. CTA of the neck showed Stanford type A AD involving the aortic arch (figure 1) extending proximally to the origin of the right brachiocephalic artery. The common, internal and external carotids were patent bilaterally. Perfusion sequences showed prolonged mean transit time in the right hemisphere with relatively normal blood volume images (figure 2). CTA of the chest and abdomen showed that the dissection extended distally to the pararenal abdominal aorta with about 70%–80% compromise of the true lumen distally and about 20% compromise of the brachiocephalic origin.

Figure 1.

Figure 1

CT angiography showing the dissection in the aortic arch. The arrows indicate the true lumen (TL) and false lumen (FL) of the dissection.

Figure 2.

Figure 2

CT perfusion scans showing prolonged mean transit time (left) and normal blood volume (right).

Treatment

Given the presence of an AD, the tPA order was cancelled. When the patient returned from the CT suite, she was noted to be normotensive. She was then transferred to a different centre for cardiothoracic surgery.

Outcome and follow-up

We followed up with the patient and after nearly a 4-week stay in the hospital and rehab, she recovered very well and did not have any residual neurological deficits.

Discussion

ADs can present with neurological symptoms in 17%–40% of cases.2 Stroke is the most common neurological symptom in AD.2–5 Neurological symptoms can sometimes remit before presentation to the ED.3 With regard to management of acute stroke, current protocol dictates that haemorrhage must be ruled out by a non-contrast CT of the head. If the patient then meets other criteria and is within the 3-hour window6 or 4.5 hours for a certain subset,7 he/she can be given tPA. However, administration of tPA in AD has been shown to result in extension of dissection into the pericardium, leading to cardiac tamponade. A review of the literature revealed that two patients who presented with stroke symptoms due to AD died following tPA,2 8 while few others initially worsened so tPA was stopped and they underwent emergent surgery with good recovery.9 10 In another case, the patient received some tPA but then worsened with hypotension and reduced left radial pulse rate. He was found to have left common carotid dissection and left intracranial internal carotid artery (ICA) occlusion. tPA was stopped and surgery was offered but the patient declined and died.11 tPA has been previously reported to have been used in stroke from ICA dissection.12 However, it appears that the risks of using tPA in AD are much higher and have been consistently associated with adverse outcomes. A CT angiogram of the neck will certainly help to diagnose an AD as in our case. In addition, physical examination findings such as hypotension, diminished pulses and aortic regurgitation murmur might indicate the presence of an AD. However, the International Registry of Acute Aortic Dissection showed that pulse deficits might be present in less than 20% of patients with type A dissection.13 In addition, an aortic regurgitation murmur was only found in 44% of patients with type A dissection.13 A routine chest X-ray is abnormal in 60%–90% of cases but can be normal even in type A dissections.13 14 Carotid ultrasound would help only if the dissection extends to the carotids, which it did not in our patient. Therefore, a CT angiogram would likely be of more value. Acute AD is a life-threatening emergency which can present as stroke, as shown in this case. Missing the diagnosis or administration of tPA can be fatal in such cases.

Learning points.

  • Intravenous tissue plasminogen activator (tPA) is given for certain patients with acute ischaemic stroke.

  • Aortic dissection (AD) can present as a stroke without typical symptoms of pain.

  • Use of tPA in AD can be fatal.

  • Being aware of this aetiology and testing for it will prevent mortality.

Footnotes

Contributors: VS and DN were involved in the care of the patient in the emergency room. VS and DN performed the literature review. DN obtained the images and wrote the case history. VS was responsible for the discussion and the other parts of the manuscript. Both authors have reviewed the manuscript. VS is the corresponding author and also obtained the consent from the patient.

Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests: None declared.

Provenance and peer review: Not commissioned; externally peer reviewed.

Patient consent for publication: Obtained.

References

  • 1. Grupper M, Eran A, Shifrin A. Ischemic stroke, aortic dissection, and thrombolytic therapy--the importance of basic clinical skills. J Gen Intern Med 2007;22:1370–2. 10.1007/s11606-007-0269-2 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2. Gaul C, Dietrich W, Friedrich I, et al. Neurological symptoms in type A aortic dissections. Stroke 2007;38:292–7. 10.1161/01.STR.0000254594.33408.b1 [DOI] [PubMed] [Google Scholar]
  • 3. Gaul C, Dietrich W, Erbguth FJ. Neurological symptoms in aortic dissection: a challenge for neurologists. Cerebrovasc Dis 2008;26:1–8. 10.1159/000135646 [DOI] [PubMed] [Google Scholar]
  • 4. Gerber O, Heyer EJ, Vieux U. Painless dissections of the aorta presenting as acute neurologic syndromes. Stroke 1986;17:644–7. 10.1161/01.STR.17.4.644 [DOI] [PubMed] [Google Scholar]
  • 5. Blanco M, Díez-Tejedor E, Larrea JL, et al. Neurologic complications of type I aortic dissection. Acta Neurol Scand 1999;99:232–5. 10.1111/j.1600-0404.1999.tb07352.x [DOI] [PubMed] [Google Scholar]
  • 6. National Institute of Neurological D, Stroke rt PASSG. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995;333:1581–7. [DOI] [PubMed] [Google Scholar]
  • 7. Del Zoppo GJ, Saver JL, Jauch EC, et al. Expansion of the time window for treatment of acute ischemic stroke with intravenous tissue plasminogen activator: a science advisory from the American Heart Association/American Stroke Association. Stroke 2009;40:2945–8. 10.1161/STROKEAHA.109.192535 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8. Fessler AJ, Alberts MJ. Stroke treatment with tissue plasminogen activator in the setting of aortic dissection. Neurology 2000;54:1010 10.1212/WNL.54.4.1010 [DOI] [PubMed] [Google Scholar]
  • 9. Chua CH, Lien LM, Lin CH, et al. Emergency surgical intervention in a patient with delayed diagnosis of aortic dissection presenting with acute ischemic stroke and undergoing thrombolytic therapy. J Thorac Cardiovasc Surg 2005;130:1222–4. 10.1016/j.jtcvs.2005.06.023 [DOI] [PubMed] [Google Scholar]
  • 10. Hong KS, Park SY, Whang SI, et al. Intravenous recombinant tissue plasminogen activator thrombolysis in a patient with acute ischemic stroke secondary to aortic dissection. J Clin Neurol 2009;5:49–52. 10.3988/jcn.2009.5.1.49 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11. Rodríguez-Luna D, Vilar RM, Peinazo M, et al. Intravenous thrombolysis in an elderly patient with acute ischemic stroke masking aortic dissection. J Stroke Cerebrovasc Dis 2011;20:559–61. 10.1016/j.jstrokecerebrovasdis.2010.02.023 [DOI] [PubMed] [Google Scholar]
  • 12. Derex L, Nighoghossian N, Turjman F, et al. Intravenous tPA in acute ischemic stroke related to internal carotid artery dissection. Neurology 2000;54:2159–61. 10.1212/WNL.54.11.2159 [DOI] [PubMed] [Google Scholar]
  • 13. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000;283:897–903. [DOI] [PubMed] [Google Scholar]
  • 14. Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management: Part I: from etiology to diagnostic strategies. Circulation 2003;108:628–35. 10.1161/01.CIR.0000087009.16755.E4 [DOI] [PubMed] [Google Scholar]

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