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Year : 2019  |  Volume : 3  |  Issue : 2  |  Page : 69-72

A dreadful complication of peritonsillar abscess drainage managed endovascularly

Department of Neurointervention, Medanta, Medicity, Gurgaon, Haryana, India

Date of Submission18-Oct-2019
Date of Acceptance20-Oct-2019
Date of Web Publication25-Nov-2019

Correspondence Address:
Dr. Gaurav Goel
Medanta, Medicity, Gurgaon, Haryana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aiao.aiao_25_19

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A 11 year female presenting with sorethroat and diagnosed as peritonsillar abscess ,drained outside under aseptic precautions lead to bleeding, later presented with hemiparesis with DSA revealing a large pseudoaneurysm formation in ipsilateral carotid with patchy infarcts on CT. At emergency repeat bleeding occurred and patient started deteriorating following which the patient was managed by endovascular parent vessel occlusion following which she recovered gradually with regaining normal strength in paretic limbs within a few days . The case highlights the dreadful complication of peritonsillar abscess drainage as well as its endovascular management.

Keywords: Collaterals, parent vessel occlusion, peritonsillar abscess, stroke

How to cite this article:
Chatterjee A, Mahajan A, Banga V, Goel G. A dreadful complication of peritonsillar abscess drainage managed endovascularly. Ann Indian Acad Otorhinolaryngol Head Neck Surg 2019;3:69-72

How to cite this URL:
Chatterjee A, Mahajan A, Banga V, Goel G. A dreadful complication of peritonsillar abscess drainage managed endovascularly. Ann Indian Acad Otorhinolaryngol Head Neck Surg [serial online] 2019 [cited 2023 Mar 26];3:69-72. Available from: https://www.aiaohns.in/text.asp?2019/3/2/69/271600

  Introduction Top

Although rare, an aneurysm in the internal carotid artery (ICA) can present as a result of peritonsillar abscess drainage this presentation is lethal and correct and prompt management is crucial to save a life.

  Case Report Top

An 11-year-old female presenting with fever and sore throat for 1 week was diagnosed clinically as a case of PTA and put on oral penicillin antibiotics by local physicians. The patient had acute onset of left hemiparesis 7 days after onset of fever and had altered sensorium. She was then brought to our center for workup.

In triage, the patient had E2V2M5 status and was restless. Plan for computed tomography (CT) brain and neck along with CT angiogram [Figure 1] and [Figure 2] was taken to look for the current status of ICA occlusion and extent of infarct. Decision for sedation was taken and hence she was being intubated in the triage. Just when preparing for the same, there was a sudden spurt of a huge amount of oropharyngeal bleed. Immediate hemostasis was tried to be achieved by the otolaryngology department by nasal and pharyngeal packs, but were hardly of any use.
Figure 1: Computed tomography brain at presentation

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Figure 2: Computed tomography neck showing right cervical internal carotid artery aneurysm with bleed

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Neurointervention team immediately rushed her to digital subtraction angiography (DSA) laboratory where DSA revealed a large dissecting ruptured pseudoaneurysm of the right cervical ICA [Figure 3]. Endovasular parent vessel occlusion was done using multiple detachable coils [Figure 4] and [Figure 5]. Final check angiogram reveals complete occlusion of the right ICA (distal cervical segment) with no filling of the aneurysm. The right side of the brain parenchyma was being supplied now by anterior cerebral artery and middle cerebral artery filling from the contralateral side by anterior communicating artery and posterior communicating artery, respectively.
Figure 3: Digital subtraction angiography images showing AP and lateral views of cervical internal carotid artery aneurysm

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Figure 4: Digital subtraction angiography image showing aneurysm postcoiling and parent vessel occlusion of cervical internal carotid artery

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Figure 5: Digital subtraction angiography image showing postparent vessel occlusion filling of the right side middle cerebral artery via collaterals from posterior communicating arteries

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The patient was then given intensive care unit care and was extubated the subsequent day. CT brain revealed no increase of infarct. ENT exploration of local site did not reveal much evidence of abscess in peritonsillar area, revealing that the carotid aneurysm must have presented as the abscess. The patient was then transferred to general ward and with rehabilitation she regained her power in the left upper and lower limb and was subsequently discharged home within a week ambulatory.

  Discussion Top

The case highlights the importance of the diagnosis, the underlying etiology which can change the course of the disease. The same patient if her aneurysm would have ruptured outside hospital would have been mortal. This case also underlies the importance of carotid aneurysm as a deadly important differential of peritonsillar swelling presenting with swelling and sore throat. Furthermore, it highlights the importance of the role of a neurointerventionist in securing such a ruptured bleeding aneurysm and moreover even clogging such a major vessel did not lead to any increase in size of infarct with good patient recovery due to good collaterals. Hence, a good endovascular planning before such procedure makes so much of a difference in saving and restoring brain function.

Internal carotid artery aneurysm is defined as a local increase in the vessel diameter of >50%, compared to reference values for appropriate vessel segment. Extracranial ICA aneurysms (EICAAs) are uncommon arterial lesions; the estimated incidence is <1% of all arterial aneurysms and exceedingly rarely may be bilateral.[1],[2],[3]

Reported etiology of EICAA varies greatly depending on the population studied. According to the three largest studies, atherosclerosis is the leading cause of EICAA (43%–91%). Other etiologies include fibromuscular dysplasia, aneurysm formation after surgical interventions, trauma, vasculitis, and infections.[1],[2],[4] The prevalence of causative factors has changed over the last 40 years and mycotic aneurysms are now sporadic; at the same time, a higher incidence of dysplastic aneurysms is reported, due to improved screening of patients with carotid dissection. The incidence of traumatic EICAA remains at a relatively constant level of around 14% and justifies the low age average of patients with EICAA: 56 years of age.[2] Manifestations of EICAA depend on the size and location and fall into three main categories: neurologic disorders caused by decreased perfusion of the central nervous system, symptoms resulting from compression of surrounding tissues, and hemorrhage. Neurologic disorders are the most common and typically include focal symptoms such as strokes, transient ischemic attacks, transient amaurosis, and anopsia. Less commonly described are Horner's syndrome, inarticulate speech, facial numbness, and retinal infarction.[2],[3],[5],[6]

Large aneurysms displace tonsillar fossa medially and trigger compression symptoms, of which dysphagia is the most common and is caused by impaired function of the glossopharyngeal nerve (n. IX). Hoarseness of voice results from compression of recurrent pharyngeal and vagus nerves (n. X); local pain and discomfort are associated with malfunction of cervical branch of facial nerve (n. VII).[1],[7] Further symptoms described include dizziness and tinnitus.[2] Hemorrhage has been described as a consequence of rupture of atherosclerotic and mycotic aneurysms.[7],[8] Often, patients present with no symptoms other than a palpable mass at mandibular angle.[3],[9]

Differential diagnosis of peritonsillar mass comprises carotid artery aneurysm and infectious and neoplastic etiologies. Patients with diabetes, the elderly, and those living in common quarters are at risk of developing infections and their complications, signs of which may be less apparent. The initially suspected PTA is the most common complication of acute tonsillitis. In a series of 15 EICAAs, Szopinski et al. mentioned a patient with recurrent tonsillitis who sustained hemorrhage after an attempt of drainage of suspected PTA.[10] Further infectious causes to be considered are retropharyngeal cellulitis, infectious mononucleosis, mycobacterial cervical lymphadenitis, and Lemierre's syndrome (also known as postanginal sepsis). Neoplastic causes to be ruled out in these clinical circumstances include oropharyngeal tumor of the tonsil or very rare primary parapharyngeal space tumor. In a case series of 24 EICAAs, an aneurysm was misdiagnosed as a neoplastic mass during otolaryngologic surgery, and the patient died of stroke, complicating emergency vascular surgical intervention. Other possible etiologies of peritonsillar mass include iatrogenic, posttraumatic, or spontaneous hematoma and ectopic thyroid gland, which may remain undiagnosed for years.[5] Duplex Doppler ultrasonography is the diagnostic method of choice in suspected EICAA. Detailed evaluation of the anomaly is obtained with the use of CT angiography and magnetic resonance imaging (MRI). In patients with neurologic symptoms, brain CT and MRI angiography may be employed to confirm or exclude ischemia.[4],[7],[11],[12] To differentiate between dissection and aneurysm, flow signal inside the vessel may be recorded with the use of transoral carotid ultrasonography.[13] Three-dimensional time-of-flight MRI angiography provides information about early stage vessel pathology and may be used for the evaluation of treatment effects, especially in patients with cardiovascular risk factors.[11] In patients with EICAA, further diagnostics should be performed to exclude concomitant cerebral and peripheral aneurysms, and chest CT angiography and duplex Doppler ultrasonography are recommended for this purpose.[4],[9]

The first line of treatment in EICAA is open aneurysmectomy with end-to-end anastomosis or graft interposition.[1],[4] Other surgical modalities include recently described endovascular treatment and carotid ligation.[10],[14],[15] Operative technique depends on anatomic type of the aneurysm, as classified by Attigah et al.[1],[4] Operation can be performed in general or regional anesthesia.[4],[15] Conservative treatment carries a high risk of thromboembolic events and aneurysm rupture and thus is applicable in selected groups of patients only.[2],[6]

  Conclusion Top

Typical manifestations of EICAA are neurologic; however, signs and symptoms observed most commonly by ENT specialists, such as neck mass, mass in the parapharyngeal space, dysphagia, dysphonia, and local pain, may be in the foreground. Most importantly correct diagnosis and management as elucidated in this case is crucial and timely intervention if well planned as in this case would lead to avoidance of mortality.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Attigah N, Külkens S, Zausig N, Hansmann J, Ringleb P, Hakimi M, et al. Surgical therapy of extracranial carotid artery aneurysms: Long-term results over a 24-year period. Eur J Vasc Endovasc Surg 2009;37:127-33.  Back to cited text no. 1
El-Sabrout R, Cooley DA. Extracranial carotid artery aneurysms: Texas Heart Institute experience. J Vasc Surg 2000;31:702-12.  Back to cited text no. 2
Rosset E, Albertini JN, Magnan PE, Ede B, Thomassin JM, Branchereau A. Surgical treatment of extracranial internal carotid artery aneurysms. J Vascu Surg 2000;31:713-23.  Back to cited text no. 3
Radak D, Davidovic L, Tanaskovic S, Banzic I, Matic P, Babic S, et al. A tailored approach to operative repair of extracranial carotid aneurysms based on anatomic types and kinks. Am J Surg 2014;208:235-42.  Back to cited text no. 4
Faggioli GL, Freyrie A, Stella A, Pedrini L, Gargiulo M, Tarantini S, et al. Extracranial internal carotid artery aneurysms: Results of a surgical series with long-term follow-up. J Vasc Surg 1996;23:587-94.  Back to cited text no. 5
Zwolak RM, Whitehouse WM Jr., Knake JE, Knake JE, Bernfeld BD, Zelenock GB, et al. Atherosclerotic extracranial carotid artery aneurysms. J Vascu Surg 1984;1:415-22.  Back to cited text no. 6
Kaczynski J, Wilczynska M, Blaszczynski M, Fligelstone L. Extracranial saccular atherosclerotic aneurysm of the internal carotid artery (ICA) treated by an oblique end-to-end primary anastomosis. BMJ Case Rep 2013;2013:bcr2012007705.  Back to cited text no. 7
O'Connell JB, Darcy S, Reil T. Extracranial internal carotid artery mycotic aneurysm: Case report and review. Vasc Endovascular Surg 2009;43:410-5.  Back to cited text no. 8
Ktenidis K, Lioupis A, Megalopoulos A, Antoniadis K, Kiskinis D. New exposure technique for management of giant internal carotid artery aneurysm. J Vasc Surg 2011;54:522-5.  Back to cited text no. 9
Szopinski P, Ciostek P, Kielar M, Myrcha P, Pleban E, Noszczyk W, et al. A series of 15 patients with extracranial carotid artery aneurysms: Surgical and endovascular treatment. Eur J Vasc Endovasc Surg 2005;29:256-61.  Back to cited text no. 10
Galletti B, Bucolo S, Abbate G, Calabrese G, Romano G, Quattrocchi C, et al. Internal carotid artery transposition as risk factor in pharyngeal surgery. Laryngoscope 2002;112:1845-8.  Back to cited text no. 11
Alpagut U, Ugurlucan M, Kafali E, Ali Sayin O, Demir T, Basaran M, et al. Aneurysm of the kinked extracranial internal carotid artery case report and review of the literature. Acta Chir Belg 2005;105:407-9.  Back to cited text no. 12
Ohara N, Sakaguchi M, Okazaki S, Nagano K, Kitagawa K. Internal carotid artery dissection caused by an elongated styloid process: Usefulness of transoral ultrasonography. J Stroke Cerebrovasc Dis 2012;21:918.e7-8.  Back to cited text no. 13
Donas KP, Schulte S, Pitoulias GA, Siebertz S, Horsch S. Surgical outcome of degenerative versus postreconstructive extracranial carotid artery aneurysms. J Vasc Surg 2009;49:93-8.  Back to cited text no. 14
Garg K, Rockman CB, Lee V, Maldonado TS, Jacobowitz GR, Adelman MA, et al. Presentation and management of carotid artery aneurysms and pseudoaneurysms. J Vasc Surg 2012;55:1618-22.  Back to cited text no. 15


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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