Journal of Clinical Neuroscience 21 (2014) 2072–2076
Contents lists available at ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Review
Iatrogenic traumatic intracranial aneurysm after endoscopic sinus surgery Joshua Wewel ⇑, Erwin Zeta Mangubat, Lorenzo Muñoz Rush Professional Office Building, 1725 W. Harrison Street, Suite 855, Chicago, IL 60612, USA
a r t i c l e
i n f o
Article history: Received 11 May 2014 Accepted 17 May 2014
Keywords: Endoscopic sinus surgery Nasal polyp Traumatic intracranial aneurysm
a b s t r a c t Iatrogenic traumatic intracranial aneurysms are rare, but their clinical impact is significant secondary to their risk of intracranial hemorrhage and in their frequent complexity in management. We report an adult patient with a history of chronic sinusitis who, while undergoing elective endoscopic polypectomy, suffered an iatrogenic injury to an A2 segment branch of the left anterior cerebral artery, resulting in a pseudoaneurysm. Management included endovascular coiling and a bicoronal craniotomy approach, using a split-thickness cranial graft and abdominal fat graft to repair the associated left cribriform plate defect. Ó 2014 Elsevier Ltd. All rights reserved.
1. Introduction A traumatic intracranial aneurysm (TICA) is considered a rare entity, constituting less than 1% of all aneurysms in large series [1–3]. Delayed intracranial hemorrhage is associated with a significant mortality rate, as high as 50% [1,3,4]. Therefore, diagnosis should be made as soon as possible when suspected to prevent delayed intracranial hemorrhage. More specifically, iatrogenic TICA occurring as a result of surgery in or around the skull base, the sinuses, and orbits are exceedingly rare, but may have devastating consequences. Vascular injuries generally involve the internal carotid artery (ICA) [5–15] and less often the anterior cerebral artery (ACA) [9,10,15,18,19], basilar artery (BA) [20,21], and middle cerebral artery (MCA) [18,22]. TICA are challenging to treat, as both perforator and distal blood supply must be maintained. We report a 66-year-old woman with diffuse subarachnoid hemorrhage (SAH) from an ACA traumatic pseudoaneurysm as result of an iatrogenic injury during endoscopic sinus surgery. An extensive literature review and discussion are provided.
2. Case report A 66-year-old woman with a history of chronic sinusitis underwent endoscopic sinus surgery for nasal polypectomy at an outpatient surgical center. A review of her MRI prior to endoscopic sinus surgery did not show skull base defects or lesions (Fig. 1). At the ⇑ Corresponding author. Tel.: +1 4026585069. E-mail address: [email protected] (J. Wewel). http://dx.doi.org/10.1016/j.jocn.2014.05.017 0967-5868/Ó 2014 Elsevier Ltd. All rights reserved.
time of procedure, there had been reported bleeding when opening the posterior ethmoids. Postoperatively, she was slow to wake up, was electively intubated in the recovery area, and brought to a community hospital emergency room for further workup. A CT scan at this facility demonstrated a Fisher grade 4 SAH (Fig. 2), which prompted a transfer to our facility. Upon presentation, she was found to be Hunt-Hess grade 5 with a Glasgow Coma Scale score (GCS) of 6T. She required an emergent right frontal external ventricular drain secondary to hydrocephalus. Further imaging included a CT scan that revealed a bony defect of the left cribriform plate and left fovea ethmoidalis (Fig. 2) and CT angiography (CTA) that demonstrated a lesion suspicious for a small pseudoaneurysm off the left orbitofrontal branch of the A2 segment of the left ACA (Fig. 3). Initial catheter-based digital subtraction angiography (DSA) was negative for any aneurysms or other vascular malformations. A follow-up DSA a week later demonstrated a left A2 aneurysm measuring 2.3 mm 1.7 mm 1.5 mm (Fig. 4). The aneurysm was coiled with a Raymond Class 1 occlusion with preservation of distal blood flow. On post-bleed day 8, the patient was evaluated and treated with intra-arterial verapamil for severe vasospasm of the bilateral A1 and proximal A2 arteries. On post-bleed day 10, once the edema was thought to have adequately subsided, she underwent repair of her skull base defect via a bicoronal craniotomy, transbasal approach, harvesting pericranium and using a split-thickness cranial graft and abdominal fat graft to repair the defect (Fig. 5). Intraoperatively, there was an oval-shaped skull base defect inclusive of the cribriform plate, but mostly localized over a very thin fovea ethmoidalis. At the time of surgery, it was difficult to delineate whether this defect and resulting brain injury was a result of an encephalocele misconstrued as a
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Fig. 1. T1-weighted contrast-enhanced sagittal (A) and T1-weighted non-contrasted coronal (B) MRI does not demonstrate an encephalocele.
Fig. 2. A non-contrasted axial CT scan (A) demonstrates a diffuse subarachnoid hemorrhage with a focal hematoma in the posterior aspect of the interhemispheric fissure and along the anterior cranial fossa. The coronal (B) and sagittal (C) reconstructions of the CT scan demonstrate a bony defect (white arrow) in the left half of the cribriform plate and planum sphenoidale.
polyp or simply injury through the fovea ethmoidalis with an endoscopic instrument. The MRI prior to her sinus surgery suggests the latter. The patient’s hospital course included treatment with intraarterial verapamil for symptomatic vasospasm, once on post-bleed day 11 for vasospasm in the bilateral A1 and proximal A2 arteries and again on post-bleed day 14 for vasospasm in the left A1 artery and right distal A1 and middle cerebral arteries. The patient was eventually successfully extubated and underwent a percutaneous endoscopic gastrostomy tube placement. Due to an inability to wean the patient off the external ventricular drain, the patient required a right frontal ventriculoperitoneal shunt. The patient’s neurological status did improve to a GCS of 14 and she was discharged to a subacute nursing facility on post-bleed day 28. 3. Discussion The true incidence of vascular injuries during endonasal endoscopic surgery is unknown. Kassam et al. [23] reported from their early endoscopic skull base surgery experience a 0.9% incidence of
vascular complications in a series of 800 patients. However, as described here, such injuries can be devastating. The majority of TICA are pseudoaneurysms. As Sutton et al. [17] described, the two types of iatrogenic pseudoaneurysms that can be observed are fusiform and saccular. The former are caused by arterial adventitia injury of the parent vessel resulting in thinning of this layer and subsequent vessel dilation. Saccular pseudoaneurysms result from a more focal and complete laceration of the arterial wall where the apparent lumen of the opacified aneurysm is contained by an organized extra-luminal hematoma [7]. Saccular pseudoaneurysms seem to have a greater tendency to rupture. Unfortunately, only anecdotal cases of traumatic saccular aneurysms are reported in the literature, without any statistical analysis of hemorrhage risk [17,24,25]. The first step toward preventing complications is a clear understanding of the anatomic knowledge of the paranasal sinus and skull base anatomy from the endoscopic perspective. The roof of the ethmoid is particularly thin and vulnerable at the attachment point of the vertical bony shelf of the middle turbinate [26]. Similarly, in the medial ethmoid sinus, the bony roof is thin, and the
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Fig. 3. A CT angiogram demonstrates a 1–2 mm out-pouching (white arrow) along the superior aspect of the focal hematoma arising from the orbitofrontal branch of the A2 segment of the left anterior cerebral artery, suspicious for a small pseudoaneurysm.
dura may be adherent. Minimal trauma in this area may cause bleeding of the intradural meningeal branches or bleeding of subarachnoid branches of the ACA [27]. Trauma to the cribriform plate may compromise the ACA itself. Injury to the ICA can occur through penetration of the lateral sphenoid wall. As there is inadequate exposure for proximal control, intracranial bleeding as a result from injury to these vessels can prove disastrous. A thorough preoperative assessment of the bony integrity of the skull base should be obtained and understood in each individual patient with CT scans and/or MRI. Conditions predisposing to vascular damage during surgical procedures may include anatomic variants of the temporal and sphenoidal bones [28], acromegaly with distortion of the nasal sinus anatomy, tortuosity of the carotid arteries sometimes protruding into the sella [28], and encephaloceles [9,29–35]. Specifically, the diagnosis of encephalocele, albeit rare, should be considered in any patient with nasal polyps because the gross appearance is not distinctive or characteristic [32]. Although
encephaloceles are usually a congenital anomaly, they may also occur following trauma or as a result of chronic intracranial hypertension. Symptoms and clinical features of an intranasal encephalocele may mimic those of a nasal polyp. Similar to nasal polyps, patients with these lesions have been reported to present with nasal obstruction or unilateral nasal congestion [29,36,37]. According to a small number of reports available, several patients harboring an intranasal encephalocele have undergone a ‘‘polypectomy’’ with tragic results [9,29,32,34]. Typically, nasal polyps appear laterally from underneath the turbinates, while encephaloceles have a midline location [38]. In cases of unusual intraoperative hemorrhage when operating close to the anterior skull base, damage to an arterial wall should be suspected. Violation of the dura is rarely associated tactile feedback particularly when the anterior skull base floor is very thin. Furthermore, frank cerebrospinal fluid leakage is seldom seen at the time of intracranial injury as cerebral tissue may herniate through the defect. Because adequate visualization may become difficult, the most important management steps include ensuring hemodynamic stability and aggressive packing of the nasal cavity to help prevent further bleeding. In these cases, early neuroradiological imaging is mandatory in the form of CTA, MR angiography (MRA), or DSA. DSA is still the gold standard for aneurysm detection as the literature suggests that CTA and MRA have limited sensitivity for detection of small (65 mm) aneurysms [39–41]. If initial imaging is negative, repeated studies should be administered as TICA can become more recognizable as post-surgical changes are less evident. Additionally, these vascular abnormalities can enlarge over time, being more obvious on follow-up. It has become common practice in our institution to repeat a diagnostic DSA approximately 1 week after a negative study for subarachnoid hemorrhage patients. Ciceri et al. [25] report an iatrogenic fusiform pseudoaneurysm diagnosed 2 years after transsphenoidal approach for resection of a tuber cinereum hamartoma. However, it is still important to be aware that iatrogenic TICA may occur even without discrete bleeding at surgery. Postoperatively, clinical symptoms, including neurological deterioration ranging from headache to coma, massive post-operative epistaxis, and cranial nerve palsy, are often the first indication of an unexplained intracranial hemorrhage related to a TICA. In the trauma literature, TICA are generally treated with conservative management and close surveillance, open surgery, or endovascular repair. Fleischer et al. [4] reported that TICA patients who were managed conservatively presented a much higher mortality rate than those managed surgically (41% versus
Fig. 4. A catheter-based digital subtraction angiography (DSA) performed 1 week after an initial negative DSA demonstrates, at the A2 segment of the anterior cerebral artery, an anteriorly directed 3 3 mm dissecting cerebral aneurysm (white arrow) as seen in anteroposterior (A) and lateral (B) views. A DSA after endovascular treatment (C) demonstrates complete occlusion of the dissecting cerebral aneurysm (white arrow) with preservation of the parent vessel (black arrow).
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In contrast to peripheral aneurysms, intracavernous ICA lesions are technically more challenging through both open surgery and endovascular means. In these patients, collateral circulation must be evaluated with complete angiographic assessment of the circle of Willis and possibly with balloon test occlusion in cases in which ICA sacrifice is contemplated. Bare stents or stent grafts used for exclusion of these aneurysms from flow have been reported in the literature [54]. Iatrogenic intracranial vascular injuries are rare but dangerous complications following endoscopic endonasal surgery. Careful preoperative evaluation of the integrity of the skull base and a thorough understanding of basic skull base and paranasal sinus anatomy would help avoid these complications. Its presentation often manifests as massive intraoperative bleeding or early postoperative epistaxis, but may be delayed and atypical. When a vascular injury is suspected, careful evaluation of the vessels should be carried out along with extensive follow-up imaging. Endovascular treatment of saccular pseudoaneurysms represents a feasible and safe form of treatment. Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References
Fig. 5. Intraoperative photograph (A) demonstrates the oval-shaped skull base defect (1.2 0.4 cm) (white arrow) involving the cribriform plate, mostly localizing over the fovea ethmoidalis. Intraoperative photographs after repair show a harvested piece of bone from the inner table of the skull used to plug the defect secured with a micro-plating system (B) and subsequent onlay of harvested abdominal fat and biological glue (C). (This figure is available in colour at http:// www.sciencedirect.com.)
18%). Other reports from case series also report mortality as high as 50% in untreated TICA patients [3,42–44]. Although reported results of surgical treatment are better than those after conservative management, mortality is still high, at 18 to 29% [4,16,45,46]. TICA present a surgical challenge because of their unusual locations, thin walls, and poorly defined necks [47,48]. As most TICA are pseudoaneurysms, clipping without sacrifice of the parent artery may not be possible [45,47]. In these cases, trapping or excision of the aneurysm has become an accepted technique [3,49,50]. Endovascular approaches have emerged as therapeutic alternatives [48,51,52]. Selective management by endovascular means is becoming more frequently utilized in patients with pseudoaneurysms [8,11–14,18,25,48,51–53]. Early reports of outcomes after endovascular treatment of TICA show no mortality and no or very little morbidity [48]. In selected patients, primary coiling may allow aneurysm exclusion with parent vessel preservation [51,53].
[1] Ararbi B. Management of traumatic aneurysms caused by high-velocity missile head wounds. Neurosurg Clin N Am 1995;6:775–97. [2] Benoit BG, Wortzman G. Traumatic cerebral aneurysms. Clinical features and natural history. J Neurol Neurosurg Psychiatry 1973;36:127–38. [3] Holmes B, Harbaugh RE. Traumatic intracranial aneurysms: a contemporary review. J Trauma 1993;35:855–60. [4] Fleischer AS, Patton JM, Tindall GT. Cerebral aneurysms of traumatic origin. Surg Neurol 1975;4:233–9. [5] Ahuja A, Guterman LR, Hopkins LN. Carotid cavernous fistula and false aneurysm of the cavernous carotid artery: complications of transsphenoidal surgery. Neurosurgery 1992;31:774–8 [discussion 778-9]. [6] Awad I, Sawhny B, Little JR. Traumatic postsurgical aneurysm of the intracavernous carotid artery: a delayed presentation. Surg Neurol 1982;18:54–7. [7] Cabezudo JM, Carrillo R, Vaquero J, et al. Intracavernous aneurysm of the carotid artery following transsphenoidal surgery. Case report. J Neurosurg 1981;54:118–21. [8] Cappabianca P, Briganti F, Cavallo LM, et al. Pseudoaneurysm of the intracavernous carotid artery following endoscopic endonasal transsphenoidal surgery, treated by endovascular approach. Acta Neurochir (Wien) 2001;143:95–6. [9] Grigorian A, Rajaraman V, Hunt CD. Traumatic intracranial aneurysms complicating anterior skull base surgery. J Craniomaxillofac Surg 1998;4:10–4. [10] Hudgins PA, Browning DG, Gallups J, et al. Endoscopic paranasal sinus surgery: radiographic evaluation of severe complications. AJNR 1992;13:1161–7. [11] Kadyrov NA, Friedman JA, Nichols DA, et al. Endovascular treatment of an internal carotid artery pseudoaneurysm following transsphenoidal surgery. Case report. J Neurosurg 2002;96:624–7. [12] Lempert TE, Halbach VV, Higashida RT, et al. Endovascular treatment of pseudoaneurysms with electrolytically detachable coils. AJNR Am J Neuroradiol 1998;19:907–11. [13] Vanninen RL, Manninen HI, Rinne J. Intrasellar iatrogenic carotid pseudoaneurysm: endovascular treatment with a polytetrafluoroethylenecovered stent. Cardiovasc Intervent Radiol 2003;26:298–301. [14] Alexander MJ, Smith TP, Tucci DL. Treatment iatrogenic petrous carotid artery pseudoaneurysm with a Symbiot covered stent: technical case report. Neurosurgery 2002;50:658–62. [15] Cosgrove GR, Villemure JG, Melancon D. Traumatic intracranial aneurysm due to arterial injury at surgery. Case report. J Neurosurg 1983:291–4. [16] Parkinson D, West M. Traumatic intracranial aneurysms. J Neurosurg 1980;52:11–20. [17] Sutton LN. Vascular complications of surgery for craniopharyngioma and hypothalamic glioma. Pediatr Neurosurg 1994;21:124–8. [18] Tokunaga K, Kusaka N, Nakashima H, et al. Coil embolization of intradural pseudoaneurysms caused by arterial injury during surgery: report of two cases. AJNR AM J Neuroradiol 2001;49:1461–4. [19] Walcott BP, Nahed BV, Kahle KT, et al. Cerebrovascular bypass and aneurysm trapping for the treatment of an A2-segment anterior cerebral artery pseudoaneurysm and herniation through a skull base defect following trauma. J Clin Neurosci 2012;19:149–51.
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[20] Horowitz M, Albright AL, Jugreis C, et al. Endovascular management of a basilar artery false aneurysm secondary to endoscopic third ventriculostomy: case report. Neurosurgery 2001;49:1461–4 [discussion 1464-5]. [21] McLaughlin MR, Wahlig JB, Kaufman AM, et al. Traumatic basilar aneurysm after endoscopic third ventriculostomy: case report. Neurosurgery 1997;41:1400–4 [discussion 1403-4]. [22] Dario A, Dorizzi A, Scamoni C, et al. Iatrogenic intracranial aneurysm. Case report and review of the literature. J Neurosug Sci 1997;41:195–202. [23] Kassam AB, Prevedello DM, Carrau RL, et al. Endoscopic endonasal skull base surgery: analysis of complications in the authors’ initial 800 patients. J Neurosurg 2011;114:1544–68. [24] Dunn IF, Woodworth GF, Siddiqui AH, et al. Traumatic pericallosal artery aneurysm: a rare complication of transcallosal surgery. J Neurosurg 2007;106:153–7. [25] Cicieri EFM, Regna-Gladin C, Erbetta A, et al. Iatrogenic intracranial pseudoaneurysms: neuroradiological and therapeutical considerations, including endovascular options. Neurol Sci 2006;27:317–22. [26] Solares CA, Ong YK, Carrau RL, et al. Prevention and management of vascular injuries in endoscopic surgery of the sinonasal tract and skull base. Otolaryngol Clin N Am 2010;43:817–25. [27] Berenholz L, Kessler A, Sarfaty S, et al. Subarachnoid hemorrhage: a complication of endoscopic sinus surgery using powered instrumentation. Otolaryngol Head Neck Surg 1999;121:665–7. [28] Bergland RM, Ray BS, Torack RM. Anatomical variations in the pituitary gland and adjacent structures in 225 human autopsy cases. J Neurosurg 1968;28:93–9. [29] Nishizawa S, Ohta S, Yamaguchi M, et al. Encephalocele in the ethmoid sinus presenting as a massive intracerbral hemorrhage after a ‘‘polyptectomy’’: a case report. Am J Otolaryngol 2005;26:67–70. [30] Chang GY, Calloway C, Bhatti S. Meningoencephalocele presenting as a nasal polyp. Am Fam Physician 1994;50:1223. [31] Choudhury AR, Taylor JC. Primary intranasal encephalocele. J Neurosurg 1982;57:552–5. [32] Jones RE Jr, Bennington JL, Warner NE. Encephalocele masquerading as nasal polyp. JAMA 1962;181:640–2. [33] Kumar KK, Ganapathy K, Sumathi V, et al. Adult intranasal meningoencephalocele presenting as a nasal polyp. J Clin Neurosci 2005;12:594–6. [34] Love GL, Riehl PA. Intranasal encephalocele masking as a nasal polyp in an adult patient. Arch Otolaryngol 1983;109:420–1. [35] Mukerji SS, Parmar HA, Gujar S, et al. Intranasal meningoencephalocele presenting as a nasal polyp – a case report. Clin Imaging 2011;35:309–11. [36] Davis CH Jr, Alexander E Jr. Congenital nasofrontal encephalomeningoceles and teratomas. Review of seven cases. J Neurosurg 1959;16:365–77. [37] Dodge HW Jr, Love JG, Kernohan JW. Intranasal encephalomeningoceles associated with cranium bifidum. Arch Surg 1959;79:75–84. [38] Schmidt PH, Luyendijk W. Intranasal meningoencephalocele. Arch Otolaryngol 1974;99:402–5.
[39] Romijn M, Gratama van Andel HA, van Walderveen MA, et al. Diagnostic accuracy of CT angiography with matched mask bone elimination for detection of intracranial aneurysms: comparison with digital subtraction angiography and 3D rotational angiography. AJNR Am J Neuroradiol 2008;29:134–9. [40] Young N, Dorsch NW, Kingston RJ. Pitfalls in the use of spiral CT for identification of intracranial aneurysms. Neuroradiology 1999;41:93–9. [41] White PM, Teasdale EM, Wardlaw JM. Intracranial aneurysms: CT angiography and MR angiography for detection- Prospective blinded comparison in a large patient cohort. Radiology 2001;219:739–49. [42] Aarabi B. Traumatic aneurysms of brain due to high velocity missile head wounds. Neurosurgery 1988;22:1056–63. [43] Kaufman HH, Makela ME, Lee KF, et al. Gunshot wounds to the head: a perspective. Neurosurgery 1986;18:689–95. [44] Rahimizadeh A, Abtahi H, Daylami MS, et al. Traumatic cerebral aneurysms caused by shell fragments. Report of four cases and review of literature. Acta Neurochir (Wien) 1987;84:93–8. [45] Haddad FS, Haddad GF, Taja J. Traumatic intracranial aneurysms caused by missiles: their presentation and management. Neurosurgery 1991;28:1–7. [46] Levy ML, Rezai A, Masri LS, et al. The significance of subarachnoid hemorrhage after penetrating craniocerebral injury: correlations with angiography and outcome in a civilian population. Neurosurgery 1993;32:532–40. [47] Amirjamshidi A, Rahmat H, Abbassioun K. Traumatic aneurysms and arteriovenous fistulas of intracranial vessels associated with penetrating head injuries occurring during war: principles and pitfalls in diagnosis and management. A survey of 31 cases and review of literature. J Neurosug 1996;84:769–80. [48] Uzan M, Cantasdemir M, Seckin MS, et al. Traumatic intracranial carotid tree aneurysms. Neurosurgery 1998;43:1314–22 [discussion 1320-2]. [49] Buckingham MJ, Crone KR, Ball WS, et al. Traumatic intracranial aneurysms in childhood: two cases and a review of the literature. Neurosurgery 1988;22:398–408. [50] Ventureyra EC, Higgins MJ. Traumatic intracranial aneurysms in childhood and adolescence. Case reports and review of literature. Childs Nerv Syst 1994;10:361–79. [51] Cohen JE, Gomori JM, Segal R, et al. Results of endovascular treatment of traumatic intracranial aneurysms. Neurosurgery 2008;63:476–86 [discussion 485-6]. [52] Kocer N, Kizilkilic O, Albayram S, et al. Treatment of iatrogenic internal carotid artery laceration and carotid cavernous fistula with endovascular stent-graft placement. AJNR AM J Neuroradiol 2002;23:442–6. [53] Cohen JE, Rajz G, Itshayek E, et al. Endovascular management of traumatic and iatrogenic aneurysms of the pericallosal artery. Report of two cases. J Neurosurg 2005;102:555–7. [54] Redekop G, Marotta T, Weill A. Treatment of traumatic aneurysms and arteriovenous fistulas of the skull base by using endovascular stents. J Neurosurg 2001;95:412–9.
Contents lists available at ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Review
Iatrogenic traumatic intracranial aneurysm after endoscopic sinus surgery Joshua Wewel ⇑, Erwin Zeta Mangubat, Lorenzo Muñoz Rush Professional Office Building, 1725 W. Harrison Street, Suite 855, Chicago, IL 60612, USA
a r t i c l e
i n f o
Article history: Received 11 May 2014 Accepted 17 May 2014
Keywords: Endoscopic sinus surgery Nasal polyp Traumatic intracranial aneurysm
a b s t r a c t Iatrogenic traumatic intracranial aneurysms are rare, but their clinical impact is significant secondary to their risk of intracranial hemorrhage and in their frequent complexity in management. We report an adult patient with a history of chronic sinusitis who, while undergoing elective endoscopic polypectomy, suffered an iatrogenic injury to an A2 segment branch of the left anterior cerebral artery, resulting in a pseudoaneurysm. Management included endovascular coiling and a bicoronal craniotomy approach, using a split-thickness cranial graft and abdominal fat graft to repair the associated left cribriform plate defect. Ó 2014 Elsevier Ltd. All rights reserved.
1. Introduction A traumatic intracranial aneurysm (TICA) is considered a rare entity, constituting less than 1% of all aneurysms in large series [1–3]. Delayed intracranial hemorrhage is associated with a significant mortality rate, as high as 50% [1,3,4]. Therefore, diagnosis should be made as soon as possible when suspected to prevent delayed intracranial hemorrhage. More specifically, iatrogenic TICA occurring as a result of surgery in or around the skull base, the sinuses, and orbits are exceedingly rare, but may have devastating consequences. Vascular injuries generally involve the internal carotid artery (ICA) [5–15] and less often the anterior cerebral artery (ACA) [9,10,15,18,19], basilar artery (BA) [20,21], and middle cerebral artery (MCA) [18,22]. TICA are challenging to treat, as both perforator and distal blood supply must be maintained. We report a 66-year-old woman with diffuse subarachnoid hemorrhage (SAH) from an ACA traumatic pseudoaneurysm as result of an iatrogenic injury during endoscopic sinus surgery. An extensive literature review and discussion are provided.
2. Case report A 66-year-old woman with a history of chronic sinusitis underwent endoscopic sinus surgery for nasal polypectomy at an outpatient surgical center. A review of her MRI prior to endoscopic sinus surgery did not show skull base defects or lesions (Fig. 1). At the ⇑ Corresponding author. Tel.: +1 4026585069. E-mail address: [email protected] (J. Wewel). http://dx.doi.org/10.1016/j.jocn.2014.05.017 0967-5868/Ó 2014 Elsevier Ltd. All rights reserved.
time of procedure, there had been reported bleeding when opening the posterior ethmoids. Postoperatively, she was slow to wake up, was electively intubated in the recovery area, and brought to a community hospital emergency room for further workup. A CT scan at this facility demonstrated a Fisher grade 4 SAH (Fig. 2), which prompted a transfer to our facility. Upon presentation, she was found to be Hunt-Hess grade 5 with a Glasgow Coma Scale score (GCS) of 6T. She required an emergent right frontal external ventricular drain secondary to hydrocephalus. Further imaging included a CT scan that revealed a bony defect of the left cribriform plate and left fovea ethmoidalis (Fig. 2) and CT angiography (CTA) that demonstrated a lesion suspicious for a small pseudoaneurysm off the left orbitofrontal branch of the A2 segment of the left ACA (Fig. 3). Initial catheter-based digital subtraction angiography (DSA) was negative for any aneurysms or other vascular malformations. A follow-up DSA a week later demonstrated a left A2 aneurysm measuring 2.3 mm 1.7 mm 1.5 mm (Fig. 4). The aneurysm was coiled with a Raymond Class 1 occlusion with preservation of distal blood flow. On post-bleed day 8, the patient was evaluated and treated with intra-arterial verapamil for severe vasospasm of the bilateral A1 and proximal A2 arteries. On post-bleed day 10, once the edema was thought to have adequately subsided, she underwent repair of her skull base defect via a bicoronal craniotomy, transbasal approach, harvesting pericranium and using a split-thickness cranial graft and abdominal fat graft to repair the defect (Fig. 5). Intraoperatively, there was an oval-shaped skull base defect inclusive of the cribriform plate, but mostly localized over a very thin fovea ethmoidalis. At the time of surgery, it was difficult to delineate whether this defect and resulting brain injury was a result of an encephalocele misconstrued as a
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Fig. 1. T1-weighted contrast-enhanced sagittal (A) and T1-weighted non-contrasted coronal (B) MRI does not demonstrate an encephalocele.
Fig. 2. A non-contrasted axial CT scan (A) demonstrates a diffuse subarachnoid hemorrhage with a focal hematoma in the posterior aspect of the interhemispheric fissure and along the anterior cranial fossa. The coronal (B) and sagittal (C) reconstructions of the CT scan demonstrate a bony defect (white arrow) in the left half of the cribriform plate and planum sphenoidale.
polyp or simply injury through the fovea ethmoidalis with an endoscopic instrument. The MRI prior to her sinus surgery suggests the latter. The patient’s hospital course included treatment with intraarterial verapamil for symptomatic vasospasm, once on post-bleed day 11 for vasospasm in the bilateral A1 and proximal A2 arteries and again on post-bleed day 14 for vasospasm in the left A1 artery and right distal A1 and middle cerebral arteries. The patient was eventually successfully extubated and underwent a percutaneous endoscopic gastrostomy tube placement. Due to an inability to wean the patient off the external ventricular drain, the patient required a right frontal ventriculoperitoneal shunt. The patient’s neurological status did improve to a GCS of 14 and she was discharged to a subacute nursing facility on post-bleed day 28. 3. Discussion The true incidence of vascular injuries during endonasal endoscopic surgery is unknown. Kassam et al. [23] reported from their early endoscopic skull base surgery experience a 0.9% incidence of
vascular complications in a series of 800 patients. However, as described here, such injuries can be devastating. The majority of TICA are pseudoaneurysms. As Sutton et al. [17] described, the two types of iatrogenic pseudoaneurysms that can be observed are fusiform and saccular. The former are caused by arterial adventitia injury of the parent vessel resulting in thinning of this layer and subsequent vessel dilation. Saccular pseudoaneurysms result from a more focal and complete laceration of the arterial wall where the apparent lumen of the opacified aneurysm is contained by an organized extra-luminal hematoma [7]. Saccular pseudoaneurysms seem to have a greater tendency to rupture. Unfortunately, only anecdotal cases of traumatic saccular aneurysms are reported in the literature, without any statistical analysis of hemorrhage risk [17,24,25]. The first step toward preventing complications is a clear understanding of the anatomic knowledge of the paranasal sinus and skull base anatomy from the endoscopic perspective. The roof of the ethmoid is particularly thin and vulnerable at the attachment point of the vertical bony shelf of the middle turbinate [26]. Similarly, in the medial ethmoid sinus, the bony roof is thin, and the
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Fig. 3. A CT angiogram demonstrates a 1–2 mm out-pouching (white arrow) along the superior aspect of the focal hematoma arising from the orbitofrontal branch of the A2 segment of the left anterior cerebral artery, suspicious for a small pseudoaneurysm.
dura may be adherent. Minimal trauma in this area may cause bleeding of the intradural meningeal branches or bleeding of subarachnoid branches of the ACA [27]. Trauma to the cribriform plate may compromise the ACA itself. Injury to the ICA can occur through penetration of the lateral sphenoid wall. As there is inadequate exposure for proximal control, intracranial bleeding as a result from injury to these vessels can prove disastrous. A thorough preoperative assessment of the bony integrity of the skull base should be obtained and understood in each individual patient with CT scans and/or MRI. Conditions predisposing to vascular damage during surgical procedures may include anatomic variants of the temporal and sphenoidal bones [28], acromegaly with distortion of the nasal sinus anatomy, tortuosity of the carotid arteries sometimes protruding into the sella [28], and encephaloceles [9,29–35]. Specifically, the diagnosis of encephalocele, albeit rare, should be considered in any patient with nasal polyps because the gross appearance is not distinctive or characteristic [32]. Although
encephaloceles are usually a congenital anomaly, they may also occur following trauma or as a result of chronic intracranial hypertension. Symptoms and clinical features of an intranasal encephalocele may mimic those of a nasal polyp. Similar to nasal polyps, patients with these lesions have been reported to present with nasal obstruction or unilateral nasal congestion [29,36,37]. According to a small number of reports available, several patients harboring an intranasal encephalocele have undergone a ‘‘polypectomy’’ with tragic results [9,29,32,34]. Typically, nasal polyps appear laterally from underneath the turbinates, while encephaloceles have a midline location [38]. In cases of unusual intraoperative hemorrhage when operating close to the anterior skull base, damage to an arterial wall should be suspected. Violation of the dura is rarely associated tactile feedback particularly when the anterior skull base floor is very thin. Furthermore, frank cerebrospinal fluid leakage is seldom seen at the time of intracranial injury as cerebral tissue may herniate through the defect. Because adequate visualization may become difficult, the most important management steps include ensuring hemodynamic stability and aggressive packing of the nasal cavity to help prevent further bleeding. In these cases, early neuroradiological imaging is mandatory in the form of CTA, MR angiography (MRA), or DSA. DSA is still the gold standard for aneurysm detection as the literature suggests that CTA and MRA have limited sensitivity for detection of small (65 mm) aneurysms [39–41]. If initial imaging is negative, repeated studies should be administered as TICA can become more recognizable as post-surgical changes are less evident. Additionally, these vascular abnormalities can enlarge over time, being more obvious on follow-up. It has become common practice in our institution to repeat a diagnostic DSA approximately 1 week after a negative study for subarachnoid hemorrhage patients. Ciceri et al. [25] report an iatrogenic fusiform pseudoaneurysm diagnosed 2 years after transsphenoidal approach for resection of a tuber cinereum hamartoma. However, it is still important to be aware that iatrogenic TICA may occur even without discrete bleeding at surgery. Postoperatively, clinical symptoms, including neurological deterioration ranging from headache to coma, massive post-operative epistaxis, and cranial nerve palsy, are often the first indication of an unexplained intracranial hemorrhage related to a TICA. In the trauma literature, TICA are generally treated with conservative management and close surveillance, open surgery, or endovascular repair. Fleischer et al. [4] reported that TICA patients who were managed conservatively presented a much higher mortality rate than those managed surgically (41% versus
Fig. 4. A catheter-based digital subtraction angiography (DSA) performed 1 week after an initial negative DSA demonstrates, at the A2 segment of the anterior cerebral artery, an anteriorly directed 3 3 mm dissecting cerebral aneurysm (white arrow) as seen in anteroposterior (A) and lateral (B) views. A DSA after endovascular treatment (C) demonstrates complete occlusion of the dissecting cerebral aneurysm (white arrow) with preservation of the parent vessel (black arrow).
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In contrast to peripheral aneurysms, intracavernous ICA lesions are technically more challenging through both open surgery and endovascular means. In these patients, collateral circulation must be evaluated with complete angiographic assessment of the circle of Willis and possibly with balloon test occlusion in cases in which ICA sacrifice is contemplated. Bare stents or stent grafts used for exclusion of these aneurysms from flow have been reported in the literature [54]. Iatrogenic intracranial vascular injuries are rare but dangerous complications following endoscopic endonasal surgery. Careful preoperative evaluation of the integrity of the skull base and a thorough understanding of basic skull base and paranasal sinus anatomy would help avoid these complications. Its presentation often manifests as massive intraoperative bleeding or early postoperative epistaxis, but may be delayed and atypical. When a vascular injury is suspected, careful evaluation of the vessels should be carried out along with extensive follow-up imaging. Endovascular treatment of saccular pseudoaneurysms represents a feasible and safe form of treatment. Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References
Fig. 5. Intraoperative photograph (A) demonstrates the oval-shaped skull base defect (1.2 0.4 cm) (white arrow) involving the cribriform plate, mostly localizing over the fovea ethmoidalis. Intraoperative photographs after repair show a harvested piece of bone from the inner table of the skull used to plug the defect secured with a micro-plating system (B) and subsequent onlay of harvested abdominal fat and biological glue (C). (This figure is available in colour at http:// www.sciencedirect.com.)
18%). Other reports from case series also report mortality as high as 50% in untreated TICA patients [3,42–44]. Although reported results of surgical treatment are better than those after conservative management, mortality is still high, at 18 to 29% [4,16,45,46]. TICA present a surgical challenge because of their unusual locations, thin walls, and poorly defined necks [47,48]. As most TICA are pseudoaneurysms, clipping without sacrifice of the parent artery may not be possible [45,47]. In these cases, trapping or excision of the aneurysm has become an accepted technique [3,49,50]. Endovascular approaches have emerged as therapeutic alternatives [48,51,52]. Selective management by endovascular means is becoming more frequently utilized in patients with pseudoaneurysms [8,11–14,18,25,48,51–53]. Early reports of outcomes after endovascular treatment of TICA show no mortality and no or very little morbidity [48]. In selected patients, primary coiling may allow aneurysm exclusion with parent vessel preservation [51,53].
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