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Delayed Ischemic Neurological Deficit After Uneventful Elective Clipping

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Delayed Ischemic Neurological Deficit After Uneventful Elective Clipping brain sciences Case Report Delayed Ischemic Neurological Deficit after Uneventful Elective Clipping of Unruptured Intracranial Aneurysms Petr Vachata 1,2,*, Jan Lodin 1, Aleš Hejˇcl 1, Filip Cihláˇr 3 and Martin Sameš 1 1 Department of Neurosurgery, J. E. PurkynˇeUniversity, Masaryk Hospital, EU 401 13 Ústí nad Labem, Czech Republic; [email protected] (J.L.); [email protected] (A.H.); [email protected] (M.S.) 2 Department of Neurosurgery, University Hospital in Pilsen, The Faculty of Medicine in Pilsen, Charles University in Prague, 30605 Prague, Czech Republic 3 Department of Radiology, J. E. PurkynˇeUniversity, Masaryk Hospital, EU 401 13 Ústí nad Labem, Czech Republic; fi[email protected] * Correspondence: [email protected]; Tel.: +420-736210076; Fax: +420-477112880 Received: 29 June 2020; Accepted: 27 July 2020; Published: 29 July 2020 Abstract: Cerebral vasospasm and subsequent delayed ischemic neurological deficit is a typical sequela of acute subarachnoid hemorrhage after aneurysm rupture. The occurrence of vasospasms after uncomplicated surgery of an unruptured aneurysm without history of suspected rupture is extremely rare. The pathogenesis and severity of cerebral vasospasms is typically correlated with the amount of blood breakdown products extravasated during subarachnoid hemorrhage. In rare cases, where vasospasms occur after unruptured aneurysm surgery, the pathogenesis is most likely multifactorial and unclear. We present two cases of vasospasms following uncomplicated clipping of middle cerebral artery (MCA) aneurysms and a review of literature. Early diagnosis and therapy of this rare complication are necessary to achieve optimal clinical outcomes. Keywords: unruptured intracranial aneurysm; vasospasm; delayed ischemic neurological deficit 1. Introduction Cerebral vasospasm (CVS) frequently complicates the course of patients with subarachnoid hemorrhage (SAH) caused by ruptured intracranial aneurysms. Delayed ischemic neurological deficit (DIND) accounts for 10–20% of mortality and morbidity in these cases [1,2]. Vasospasms after acute SAH typically begin in the first week after aneurysmatic rupture, and their severity decreases during the second week. The exact pathophysiology of cerebral vasospasms, despite intensive research over the last fifty decades, is still unknown. The generally accepted consensus focuses on the major role of blood breakdown products. This theory is supported by the relationship between the amount of the subarachnoid blood and the incidence and severity of vasospasms [3,4]. Delayed ischemic neurological deficits as a result of vasospasms after uncomplicated surgery of unruptured intracranial aneurysms (UIA) have rarely been reported (Table 1). The aim of the study was to present two cases, along with a complete review of identical cases without evidence of SAH (preoperative computed tomography (CT) scans, cerebrospinal fluid (CSF) evaluation, intraoperative findings), absence of intraoperative events (intraoperative rupture, twisting or destruction of parent vessels, diffuse bleeding), and negative postoperative CT images. Brain Sci. 2020, 10, 495; doi:10.3390/brainsci10080495 www.mdpi.com/journal/brainsci Brain Sci. 2020, 10, 495 2 of 13 Brain Sci. 2020, 10, x FOR PEER REVIEW 2 of 14 2. Case Report 1 2. Case Report 1 A 65-year old woman, non-smoker, with history of arterial hypertonic disease and cardiac atrial A 65-year old woman, non-smoker, with history of arterial hypertonic disease and cardiac atrial fibrillation, was evaluated by computed tomography angiography (CTA) due to suspected internal fibrillation, was evaluated by computed tomography angiography (CTA) due to suspected internal carotidcarotid stenosis.stenosis. ThereThere waswas no preceding headache or or symptoms symptoms associated associated with with SAH SAH in in the the patient patient history.history. CTACTAexcluded excluded internalinternal carotidcarotid artery (ICA) stenosis stenosis,, but but showed showed a a left left middle middle cerebral cerebral artery artery (MCA)(MCA) aneurysmaneurysm inin thethe M1–2M1–2 bifurcationbifurcation with a diameter of of approximately approximately 10 10 mm mm.. The The patient patient underwentunderwent uncomplicated uncomplicated surgery surgery via via a a left left lateral lateral supraorbital supraorbital craniotomy. craniotomy. There There was was no no evidence evidence of previousof previous SAH SAH during during aneurysm aneurysm dissection. dissection. The The aneurysm aneurysm waswas occludedoccluded with two two curved curved titanium titanium clipsclips without without intraoperativeintraoperative rupture.rupture. Intraoperative indocyanine indocyanine green green angiography angiography (ICG) (ICG) and and direct direct micro-Dopplermicro-Doppler evaluation evaluation were were performed performed to to exclude exclude stenosis stenosis of of both both M2 M2 segments. segments. The The aneurysm aneurysm sac wassac perforatedwas perforated after verifiedafter verified exclusion, exclusion and a, veryand a small very amount small amount of blood of was blood immediately was immediately aspirated (Figureaspirated1). (Figure 1). FigureFigure 1.1. PreoperativePreoperative computed tomography angiography angiography ( (CTA)CTA) and and perioperative perioperative microscope microscope imageimage together together with with indocyanine indocyanine green green angiography angiography (ICG) (ICG evaluation) evaluation following following application application of tandem of curvedtandem clips. curved (A ,clipsB) Preoperative. (A,B) Preoperative CTA of the CTA left of middle the left cerebral middle artery cerebral (MCA) artery bifurcation (MCA) bifurcation aneurysm. (Caneurysm.) Application (C) Application of the first clip. of the (D first) Persistent clip. (D) filling Persistent of aneurysm filling of on aneurysm ICG angiography. on ICG angiography. (E) Application (E) ofApplication the second of curved the second tandem curved clip fortandem total clip closure for total and theclosure resection and the of theresection sac. of the sac. TheThe applicationapplication ofof temporary clips was not not necessary. necessary. The The postoperative postoperative course course was was uneventful. uneventful. PostoperativePostoperative CTCT andand CTACTA performedperformed 1 day after the surgical procedure procedure were were without without evidence evidence of of hemorrhagehemorrhage oror otherother complications.complications. The aneurysmatic sac sac was was completely completely excluded, excluded, without without any any residuumresiduum oror signssigns ofof parenteralparenteral vesselvessel stenosisstenosis (Figure(Figure2 2).). Brain Sci. 2020, 10, 495 3 of 13 Brain Sci. 2020, 10, x FOR PEER REVIEW 3 of 14 FigureFigure 2.2. PostoperativePostoperative CT and CTA evaluation one one day day after after surgery. surgery. (A (A,B,B) )Postoperative Postoperative CT CT scan. scan. (C(C,D,D))Postoperative Postoperative CTA.CTA. OnOn thethe 5th5th day,day, duringduring thethe dischargedischarge process, the patient developed developed aphasia aphasia and and right right sided sided motormotor epileptic seizures. seizures. An An acutely acutely performed performed CT excluded CT excluded any major any major complications complications;; however however,, CTA CTArevealed revealed vasospasms vasospasms in both in M2 both segments M2 segments of the left of middle the left cerebral middle artery. cerebral Mean artery. velocity Mean measured velocity measuredby Transcranial by Transcranial Doppler (TCD) Doppler was (TCD)150 cm/s was on 150the left cm /M1s on segment. the left M1The segment.patient was The transferred patient wasto transferredthe angiography to the unit angiography, and chemical unit, andintra chemical-arterial angioplasty intra-arterial was angioplasty performed was with performed nimodipine with nimodipineaccording to according our previously to our published previously protocol published [5]. The protocol diameter [5]. of The both diameter M2 segments of both, as M2 well segments, as the asclinical well as status the clinical of the patient status of improved the patient immediately improved immediatelyduring the procedure. during the Mean procedure. velocity Mean decreased velocity decreasedto 125 cm/s. to 125Nimodipine cm/s. Nimodipine was then administered was then administered intravenously intravenously (1 mg/h), and (1 mg mean/h), andarterial mean pressure arterial pressurewas maint wasained maintained above 90 above mmHg. 90 mmHg. Chemical Chemical angioplasty angioplasty was repeated was repeated on the on thethird third day day,, due due to to anotheranother episodeepisode ofof clinicalclinical deteriorationdeterioration and increased mean velocity velocity of of 170 170 cm/s cm/s ( (FigureFigure 33).). Milrinone was used for the second angioplasty and continued intravenously for six days, after which the medication was switched to an oral form of nimodipine. The patient’s clinical status improved throughout the two days after the second angioplasty. MR evaluation with diffusion-weighted images did not reveal any acute ischemic lesions. The patient was discharged home 16 days after clinical Brain Sci. 2020, 10, 495 4 of 13 manifestation of vasospasm. She was without any neurological deterioration or other pathologies on follow-up CT and CTA one year after the procedure (Figure4). Brain Sci. 2020, 10, x FOR PEER REVIEW 4 of 14 Figure 3.FigureChemical 3. Chemical intra-arterial intra-arterial angioplasty. angioplasty. ( A)) DSA DSA before before the
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