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Vertebral artery thrombosis and subsequent stroke following attempted internal jugular central venous catheterization.

Since its initial description in 1952 (1), central venous catheterization has been frequently performed, with millions of days of patient exposure to central vascular catheters in the United States each year (2). Although the procedure is common and relatively safe, several complications have been described, with a prevalence ranging from 5% to 19% depending on the definition used (3, 4). In particular, internal jugular vein (IJV) catheter insertion is prone to several unique complications, some of which can, albeit rarely, prove to be fatal. Presented here is a case of vertebral artery thrombosis with subsequent stroke and death following attempted IJV catheterization.

CASE STUDY

A 17-year-old young man with a history of idiopathic scoliosis, essential hypertension, and a patent ductus arteriosus (surgically repaired at 1 month of age) was admitted for instrumented posterior spinal fusion from T2 to L1 for treatment of his scoliosis. Intraoperatively, right IJV catheterization was attempted for vascular access. After failed attempts, central line placement was obtained through right subclavian vein catheterization. The remainder of the operative procedure was uncomplicated, and the patient was subsequently admitted to the intensive care unit for postsurgical care. Initial postoperative neurological examination showed no focal motor or sensory deficits.

Approximately 24 hours postoperatively, the patient began showing decreased mental status, progressing to an obtunded state and requiring respiratory support. A computed tomography scan showed large right occipital and bilateral cerebellar ischemic changes with mild hydrocephalus and cerebral edema. A ventriculostomy was placed to relieve elevated intracerebral pressure.

On day 3, a two-dimensional echocardiogram showed no cardiac abnormalities. A magnetic resonance imaging study showed normal blood flow in the subclavian and common carotid arteries. There was symmetric bilateral tapering of blood flow into the internal carotid arteries with apparent cessation of intracranial blood flow secondary to severe cerebral edema. The patient died on postoperative day 3.

At autopsy, external examination found a 1- to 2-mm, well-defined, circular perforation at the right anterolateral aspect of the neck consistent with attempted IJV vascular catheter placement surrounded by a few smaller puncture marks. Within the adjacent neck tissues, there was a moderate amount of hemorrhage within perivascular soft tissue along the right anterior aspect of the cervical spine. There was no gross evidence of thrombus within the right carotid, right jugular, or either vertebral artery at their entrances into the lower cervical spine or within the cranial vault, although a moderate amount of hemorrhage was noted around the right vertebral artery at its entrance into the lower cervical spine (Figure 1). The heart weighed 325 g. The brain showed cerebellar tonsillar herniation with moderate flattening of gyri and narrowing of sulci consistent with cerebral edema. There was extensive necrosis of the entire right cerebellar hemisphere, and the left cerebellar hemisphere also contained large areas of geographic necrosis. None of the cerebellar branches of the vertebrobasilar system, including the inferior and superior cerebellar arteries, contained thrombus.

Microscopically, sections of each intracranial vertebral artery near the base of the skull showed both vessels to be well formed and to contain patent lumens. Sections of the right vertebral artery at its entrance into the lower cervical spine showed extensive perivascular hemorrhage. The arterial wall was focally punctured through the intimal, elastic, medial, and adventitial layers of the vessel. Within the vessel there was definite luminal thrombosis with adjacent reactive changes involving the endothelium. The thrombotic material also focally extended through the disrupted muscular layer. These findings were further accentuated using the Russell-Movat pentachrome stain (Figure 2).

[FIGURE 1 OMITTED]

Microscopic sections of brain contained scattered "red" neurons and apoptotic nuclei consistent with diffuse and acute anoxic/ischemic encephalopathy. Blood vessels within the leptomeninges overlying the area of necrosis in the occipital lobe and left cerebellar hemisphere contained thromboemboli with microscopic features similar to the thrombus identified within the right vertebral artery (Figure 3).

[FIGURE 2 OMITTED]

[FIGRUE 3 OMITTED]

DISCUSSION

Most catheterization-related vertebral artery injuries have occurred during IJV catheterization, although injury to the carotid artery is generally more frequent (5-7). Several types of vertebral artery injuries have been described following IJV catheterization, including arteriovenous fistulas, lacerations, pseudoaneurysm formation (8), and dissection with thrombosis, with arteriovenous fistulas and pseudoaneurysm as the most common. Of note, only two cases of injury with thrombosis of the vertebral artery leading to massive posterior circulatory stroke following IJV catheterization have been reported (9, 10).

Typically, injury to the vertebral artery occurs during IJV catheterization when the needle is directed lateral to the IJV or extends too deep. The portion of vertebral artery most susceptible to injury is the V1 portion between its origin from the subclavian artery and the C6 transverse foramen (11). Patient signs and symptoms following injury are typically delayed, with most presenting with bruits or pulsating masses representing arteriovenous fistulas or pseudoaneurysm, respectively. In the two previously reported cases of vascular injury with thrombosis, patients presented with altered mental status followed by an obtunded state leading to coma, similar to the case presented here.

Iatrogenic injury to the vertebral artery can occur under other circumstances, including cervical spine surgery, chiropractic manipulation, diagnostic cerebral angiography, percutaneous nerve block, and radiation therapy (12); therefore, with this patient's history of recent spine surgery, special consideration was also given to possible vertebral artery injury secondary to the operative procedure.

Most cases of vertebral artery injury during spine surgery have occurred during cervical spine procedures. The patient presented here underwent spinal fusion from T2 to L1, a procedure that is well below the level likely to cause vertebral artery injury, in our opinion. Furthermore, even with anterior cervical spine surgery, injury to the vertebral artery is rare, with an incidence of < 1% (13). Although relatively safe, anterior cervical corpectomy has a slightly higher incidence of vertebral artery injury compared to other anterior cervical spine surgeries (such as standard anterior cervical discectomy and fusion) (13-15).

During posterior cervical spine surgery, most cases of vertebral artery injury occur during the C1-C2 transarticular screw fixation procedure for atlantoaxial instability secondary to the proximity of the artery and the blind passage of a guiding wire or transarticular screw into the C1-C2 facet joint (16-19). Additionally, most surgical injuries to the vertebral artery involve lacerations. This is distinctly different from the puncture and thrombosis seen in the present case, which is more consistent with previous reports of injury due to IJV catheterization.

The circumstances surrounding pathologic evaluation of the cervical and thoracic spine following surgical intervention present special challenges at autopsy. Admittedly, for many pathologists, involvement in such an autopsy can prove overwhelming with laborious and meticulous dissections involving complex anatomy. Preparation and detailed knowledge of the regional anatomy are essential to reach accurate conclusions, and systematic and thorough evaluation of all neck and back compartments will allow for the most complete information (20). Such efforts are certainly justified, since potentially catastrophic complications demand a thorough explanation whenever possible.

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Michael J. Van Vrancken, MD, MPH, and Joseph Guileyardo, MD

From the Department of Pathology, Baylor University Medical Center at Dallas.

Corresponding author: Joseph Guileyardo, MD, FCAP, 2911 Turtle Creek Boulevard, Suite 300, Dallas, Texas 75219 (e-mail: guileyardo@sbcglobal.net).
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Author:Van Vrancken, Michael J.; Guileyardo, Joseph
Publication:Baylor University Medical Center Proceedings
Article Type:Clinical report
Geographic Code:1USA
Date:Jul 1, 2012
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