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Journal of Neurosurgery: Case Lessons logoLink to Journal of Neurosurgery: Case Lessons
. 2023 Mar 6;5(10):CASE22559. doi: 10.3171/CASE22559

Compartment syndrome associated with vascular avulsion caused by transradial access in neurointervention for unruptured intracranial aneurysm: illustrative case

Michiyasu Fuga 1,, Toshihide Tanaka 1, Rintaro Tachi 1, Kyoichi Tomoto 1, Shun Okawa 1, Toshihiro Ishibashi 2, Yuzuru Hasegawa 1, Yuichi Murayama 2
PMCID: PMC10550665  PMID: 36880514

Abstract

BACKGROUND

Transradial access (TRA) has a lower risk of access-site complications than transfemoral access but can cause major puncture-site complications, including acute compartment syndrome (ACS).

OBSERVATIONS

The authors report a case of ACS associated with radial artery avulsion after coil embolization via TRA for an unruptured intracranial aneurysm. An 83-year-old woman underwent embolization via TRA for an unruptured basilar tip aneurysm. Following embolization, strong resistance was felt during removal of the guiding sheath due to vasospasm of the radial artery. One hour after neurointervention via TRA, the patient complained of severe pain in the right forearm, with motor and sensory disturbance of the first 3 fingers. The patient was diagnosed with ACS causing diffuse swelling and tenderness over the entire right forearm due to elevated intracompartmental pressure. The patient was successfully treated by decompressive fasciotomy of the forearm and carpal tunnel release for neurolysis of the median nerve.

LESSONS

TRA operators should be aware that radial artery spasm and the brachioradial artery pose a risk of vascular avulsion and resultant ACS and warrant precautionary measures. Prompt diagnosis and treatment are essential because ACS can be treated without the sequelae of motor or sensory disturbance if properly addressed.

Keywords: access-site complication, brachioradial artery, carpal tunnel, coil embolization, radial spasm, transradial approach

ABBREVIATIONS: ACS = acute compartment syndrome, ASC = access-site complication, BRA = brachioradial artery, CT = computed tomography, DAPT = dual antiplatelet therapy, ICP = intracompartmental pressure, RA = radial artery, RAS = radial artery spasm, TFA = transfemoral access, TRA = transradial access, 3D = three-dimensional


In recent years, use of transradial access (TRA) has been expanding in neurointervention, as well as in the interventional cardiology field, because of its low risk of puncture-site complications compared with transfemoral access (TFA). A meta-analysis of 17 neurointerventional trials (2 randomized and 15 observational trials) on access-site complications (ASCs) in a total of 2767 TRA patients and 5222 TFA patients showed a composite ASC rate of 1.8% (49/2767) for TRA compared to 3.2% (168/5222) for TFA (P < .001). TRA has thus been shown to have a lower incidence of ASCs than TFA.1 However, TRA, similar to TFA, might also cause major puncture-site complications, including radial artery (RA) extravasation, delayed RA occlusion, pseudoaneurysm, infection, acute compartment syndrome (ACS), and avulsion of the RA.2 Among these, early diagnosis and treatment of ACS are particularly imperative, since delays in appropriate management can lead to permanent sequelae, such as irreversible necrosis, nerve injury, and tissue damage.3 In the field of neurointervention, although several reports have documented the frequency of postoperative ACS, few have described the clinical course and how to rescue this critical situation. Here, we present a case of ACS associated with avulsion of the RA after coil embolization of an unruptured cerebral aneurysm via TRA.

Illustrative Case

An 83-year-old woman with a history of hypertension and dyslipidemia was referred to our institution because of a newly diagnosed, unruptured, intracranial aneurysm with a maximum diameter of 4.4 mm at the tip of the basilar artery. The irregularly shaped aneurysm with a bleb was growing, so she underwent coil embolization to prevent rupture. Preoperative angiography showed a right RA with an internal diameter of 2.0 mm and a high bifurcation origin (Fig. 1A), and treatment via TRA was planned. The patient had received dual antiplatelet therapy (DAPT) (aspirin: 100 mg/day; clopidogrel: 75 mg/day) for 14 days prior to the procedure in preparation for unscheduled stent placement. Coil embolization via TRA was performed under general anesthesia. During the procedure, heparin was administered to maintain an activated clotting time of at least 300 seconds. With ultrasound assistance, the right RA was punctured using the frontwall technique and a 4-Fr short sheath (Terumo) was inserted. This sheath was exchanged for a 6-Fr straight guiding sheath (Fubuki Dilator Kit, Asahi Intecc). The guiding sheath was then guided coaxially to the distal right vertebral artery V2 segment using a 130-cm, 5-Fr nontaper angle catheter (Glidecath II, Terumo) over a 180-cm, soft-tipped, 035-inch hydrophilic wire (Terumo). No vasodilators including calcium channel blocker and nitroglycerin or methods such as heat packs, blood pressure cuff–mediated vasodilation, and nerve blocks were taken for radial artery spasm (RAS), although mild resistance was felt when the guiding sheath was directed. A distal access catheter (Tactics, Technorat Corporation) was then guided to the basilar artery. Subsequently, a microcatheter (Excelsior SL-10, Stryker) was directed into the aneurysm over a micro-guidewire (Synchro2 soft, Stryker). The aneurysm was completely occluded by a primary coiling technique without adjunctive procedures, with a volume embolization ratio of 36.5% (Fig. 1B). Following embolization, we noticed strong resistance upon removing the guiding sheath. The successfully removed guiding sheath was damaged at 20 cm from the tip, with tissue fragments adhering to the damaged area (Fig. 1C). For hemostasis of the puncture site, the RA was compressed using a TR Band (Terumo), a TRA-specific RA compression device applied at the end of the procedure. After treatment, anticoagulants (argatroban: 60 mg/day) were administered continuously to avoid ischemic complications. One hour after completing treatment, the patient complained of severe pain in the right forearm, with motor and sensory disturbance of the first 3 fingers of the median nerve and radial nerve distribution. Physical examination revealed diffuse swelling and tenderness throughout the right forearm with pulselessness in the right RA (Fig. 1D).

FIG. 1.

FIG. 1.

A: Radial artery angiography showing the right radial artery (inner diameter 2.0 mm) and high origin of the radial artery. The arrow indicates where the brachial artery bifurcates with the radial artery proximal to the intercondylar line of the humerus (the fixed line describing the proximal end of the anterior fossa of the humerus). B: Right vertebral angiography showing an intracranial aneurysm with an irregular shape and a bleb with a maximum diameter of 4.4 mm at the tip of the basilar artery. The aneurysm was completely occluded using a primary coiling technique without adjunctive procedures, with a volume embolization ratio of 36.5%. Before embolization (upper) and after embolization (lower). C: Photograph showing that the removed guiding sheath was damaged at 20 cm from the tip, with tissue fragments adhering to the damaged area. The arrowhead indicates damaged area of the guiding sheath. Inset: General view of the guiding sheath. The dotted circle shows the enlarged area. D: Photograph showing diffuse swelling of the entire right forearm. E: Avulsion of the proximal right radial artery is evident on 3D CT angiography of the right forearm. The dotted line indicates the original route of the radial artery.

Investigations and Treatment

Three-dimensional (3D) computed tomography (CT) angiography of the right forearm revealed avulsion of the proximal right RA (Fig. 1E). Diastolic blood pressure was 45 mm Hg, and intracompartmental pressures (ICPs) were 39 and 41 mm Hg in the dorsal and lateral compartments, respectively. The pressure gradient between diastolic blood pressure and ICPs was below 30 mm Hg, the normal threshold for fasciotomy. Based on these findings, the patient was diagnosed with ACS with median nerve and radial nerve neuropathy in the right forearm caused by avulsion of the proximal right RA during removal of the guiding sheath.

After discontinuing argatroban, the patient immediately underwent fasciotomy and carpal tunnel release for neurolysis of the median nerve (Fig. 2A). The avulsed vessel was successfully anastomosed. The surgical wound for fasciotomy and carpal tunnel release was left open but sutured in a shoelace fashion with vessel loops using regular skin staples (Fig. 2B).

FIG. 2.

FIG. 2.

A: Photograph showing fasciotomy for decompression of the right forearm, including the carpal tunnel. The arrow indicates the avulsed proximal radial artery. Inset: Anastomosed avulsed radial artery. B: Photograph showing closure of the incisional wounds of the fascia and carpal tunnel on the right forearm in a shoelace-like fashion with vessel loops using skin staples. C: One week after surgery, 3D CT angiography of the right forearm shows that the anastomosed radial artery has resumed blood flow. The arrow indicates the anastomosed avulsed radial artery. D: Complete sutures and scar at after 6 months.

Outcome

Postoperatively, the motor and sensory disturbances seen in the first to third digits completely subsided without neurological sequelae. Postoperative DAPT was discontinued. One week after surgery, 3D CT angiography of the right forearm showed resumption of blood flow in the anastomosed RA (Fig. 2C). By 3 weeks after fasciotomy, edema in the right forearm had resolved. After the vessel loops and skin staples were removed, the wound was completely sutured (Fig. 2D). A year and a half following the complication, the patient remains free of neurological abnormalities.

Discussion

In the present case, prompt diagnosis of ACS caused by RA avulsion and rescue surgery including fasciotomy with release of the carpal tunnel allowed avoidance of permanent postoperative neurological deficits. ACS associated with TRA procedure for interventional endovascular surgery is a very rare but serious complication caused by increased ICP in a confined space. Of 9681 interventional cardiology procedures performed via TRA at a single, large, academic medical center in the United States, ACS occurred in only 1 case (0.01%).4 In the neurointerventional field, among 1524 TRA procedures, ACS occurred in only 1 case (0.1%).2 Regardless of the low incidence, the possibility of postoperative ACS should be taken seriously because delayed diagnosis could result in permanent sequelae, including irreversible necrosis and nerve damage in addition to tissue damage.3

Cause of Postoperative ACS

ACS is caused by increased pressure within an enclosed space comprising blood vessels, nerves, and muscles. Since the guiding sheath proved difficult to remove due to severe spasm of the RA, the efforts to pull out the catheter resulted in avulsion of the high origin of the RA in the present case. Subsequently, ACS was caused by massive bleeding from the damaged blood vessels. In addition, use of antiplatelet and anticoagulant agents might be associated with massive bleeding from avulsed vessels, resulting in the development of ACS.

Diagnosis and Treatment of Postoperative ACS

Awareness of the signs and symptoms of ACS is essential. because the diagnosis of ACS is generally based on clinical manifestations. Initial symptoms are traditionally known as the “6 Ps” (pain, pallor, poikilothermia, paraesthesia, paresis, and pulselessness).5 Once ACS is suspected, ICP should be measured to confirm diagnosis. A diastolic blood pressure – ICP (ΔP) < 30 mm Hg can be diagnosed as ACS.5 When a diagnosis of ACS is confirmed, early decompressive fasciotomy is critical. Nerves can conduct impulses for up to 1 hour, and muscles can sustain electrical responses for up to 3 hours. Nerves and muscles can withstand ischemia for up to 4 hours, but irreversible damage occurs at 8 hours.3 Therefore, delayed diagnosis might induce ischemic changes in the muscles and nerves of the forearm due to inadequate blood flow caused by compression of the blood vessels, resulting in progression to motor and sensory deficits. Specifically, these impairments include irreversible fixed flexion of the first 3 digits, loss of sensation, and complete contracture of the entire hand, known as Volkmann’s contracture. In the present case, pain and tense swelling in the right forearm, pulselessness in the right RA, and motor and sensory disturbance of the right first to third digits were observed 1 hour after treatment via TRA. Based on typical clinical symptoms and elevation of ICP (ΔP < 30 mm Hg) in the dorsal and lateral compartments, we diagnosed ACS. Decompressive fasciotomy of the right forearm with release of the carpal tunnel resulted in complete resolution of symptoms without neurological deficits. Prompt diagnosis and treatment of ACS are thus imperative to allow avoidance of severe complications.

Prevention of Postoperative ACS

Management of RAS

Preventing and managing RAS are very important in endovascular treatment via TRA. The incidence of RAS can be affected by multiple factors, including vascular tortuosity, pain, younger age, repeated punctures, procedure duration, female sex, small arteries, and increased arterial sheath diameter.6 In the present case, the patient was a woman with a small-caliber RA who underwent endovascular surgery using a large guiding sheath, suggesting that she had many predisposing factors for RAS. The incidence of RAS via TRA can be up to 20% in patients without premedication, but decreases to approximately 4% when antispasmodic prophylaxis is administered.7 Previous reports have recommended appropriate prevention and management for RAS, including adequate sedation and analgesia,8 administration of prophylactic vasodilators,9 local warm compress to cause vasodilation,10 flow-mediated dilatation (i.e., inflation of the sphygmomanometer above systolic blood pressure for 5 minutes and then rapid deflation),11 and axillary brachial plexus nerve or radial nerve block.12,13 Although the present patient had several predisposing factors for RAS, we did not consider the administration of vasodilators or the above-mentioned management for RAS. This is because the ACS occurred in the second month after we started neurointervention via TRA at our institution, and before we had yet to recognize the importance of preventing RAS. After experiencing this complication, prophylactic vasodilators were routinely administered following sheath insertion at our institution for the prevention of RAS. Since then, no complications associated with RAS have been observed. Without precautions for RAS and appropriate management, RAS and catheter trapping could not be avoided.

High Origin of the RA

A high origin of the RA, referred to as the brachioradial artery (BRA), could be a risk factor for vascular complications via TRA.14 The BRA is defined as the bifurcation of the brachial artery into the radial and ulnar arteries proximal to the intercondylar line of the humerus—namely, the fixed line describing the proximal end of the anterior fossa of the humerus.15 The prevalence of the BRA is estimated to be 9.2%.16 BRA is longer than a normal RA due to its confluence with the more proximal side of the brachial artery, suggesting that the luminal side of the vessel wall would become longer under friction from the guiding catheter. BRA would be more likely to be affected by RAS, raising the risk of vascular injury. Due to the longer range of the BRA involved in vasospasm compared with the normal RA, the risk of RA avulsion would have been increased when the guiding catheter was removed at the end of the neurointervention. The preoperative diagnostic angiography failed to recognize the BRA, even though vascular rundown from the RA to the brachial artery was well visualized. Preoperative imaging of anomalies in forearm arteries, including the BRA, and selection of an appropriate device may help prevent RA avulsion.

Antithrombotic Agents

Antithrombotic agents should be considered a risk for hematoma expansion and deterioration of ACS.17,18 Recently, in the field of neurointervention, stents (including flow diverter stents) have tended to be used, which leads to routine usage of DAPT for endovascular surgery. In the present case, DAPT was started 2 weeks prior to the procedure to allow for possible stenting. In addition, anticoagulants were continuously administered intra- and postoperatively to prevent perioperative ischemic complications. These may have inhibited hemostasis of the avulsed RA and may have caused an increase in hematoma and progression to ACS. Postoperatively, a high degree of suspicion is required for swelling and pain in the forearm used for TRA procedures, especially in patients taking antiplatelet or anticoagulant agents.

Observations

Consequently, in patients who have many predisposing risk factors for RAS and show RA anomalies, including BRA, or in treatments requiring DAPT, neurointervention via TFA may be an alternative option if TRA appears more likely to cause an ASC than TFA.

Lessons

TRA operators should be aware that RAS and the BRA pose a risk of vascular avulsion and resultant ACS and warrant precautionary measures. Prompt diagnosis and treatment are essential because ACS can be treated without the sequelae of motor or sensory disturbance if properly addressed.

Disclosures

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author Contributions

Conception and design: Fuga, Tanaka. Acquisition of data: Fuga, Tachi, Okawa. Analysis and interpretation of data: Fuga, Tachi, Hasegawa. Drafting of the article: Fuga, Tanaka, Tachi. Critically revising the article: Tachi, Ishibashi, Hasegawa, Murayama. Reviewed submitted version of the manuscript: Tachi, Okawa, Hasegawa, Murayama. Approved the final version of the manuscript on behalf of all authors: Fuga. Administrative/technical/material support: Fuga, Tomoto. Study supervision: Tanaka, Murayama.

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