SLR - June 2016 - Christopher Juels

Arterial Anatomy of the Posterior Tibial Nerve in the Tarsal Tunnel

Reference: Manske MC, McKeon KE, McCormick JJ, Johnson JE, Klein SE. Arterial Anatomy of the Posterior Tibial Nerve in the Tarsal Tunnel. J Bone Joint Surg Am. 2016 Mar 16;98(6):499–504.

Scientific Literature Review

Reviewed By: Christopher Juels, DPM
Residency Program: Wheaton Franciscan Healthcare-St. Joseph Hospital, Milwaukee, WI

Podiatric Relevance: The specific etiology of tarsal tunnel syndrome in 60 to 80 percent of cases consists of intrinsic causes (venous congestion, osteophytes, space-occupying lesions, etc.) and extrinsic causes (footwear, trauma, hindfoot deformity). The remaining 20 to 40 percent are considered idiopathic and is hypothesized by this article that a vascular etiology may be the culprit if compression is not present. This article’s purpose is to identify and describe the extraneural and intraneural arterial anatomy of the tibial nerve (TN) and its branches, with the intention of providing further insight into the role of TN vasculature on the development of tarsal tunnel syndrome. This knowledge becomes important when weighing various clinical and surgical treatment options for tarsal tunnel syndrome.

Methods: Sixty adult cadaver lower extremities (30 frozen, 30 fresh specimens) were utilized to identify, measure and describe the vascular supply to the TN macroscopically and microscopically. Limbs were excluded if there was evidence of deformity, surgery or trauma. Fresh and frozen specimens underwent a series of three injections (saline, India ink, blue latex) into the peroneal, anterior tibial and posterior tibial arteries in order to stain and help identify the vessel anatomy. Macroscopic evaluation was performed on the 30 frozen specimens. Skin and subcutaneous fat were sharply excised, then specimens were submerged in 6 percent sodium hypochlorite to chemically debride soft tissue. Location of the vessels entering the TN relative to the tip of the medial malleolus and abductor hallucis fascia was recorded.

Microscopic analysis was only performed on the 30 fresh specimens using the Spälteholz technique. The TN nerve was dissected and transected 5 cm proximal and distal to the bifurcation into the medial and lateral plantar nerves (MPN, LPN). Serial dehydration was then performed with different concentrations of ethanol. Then each nerve was evaluated using a stereoscopic microscope to identify locations of entering vessels relative to the bifurcation of the TN, as well as recording the number of vessels per centimeter entering each nerve. Student t test was performed to determine if vascular density was statistical significant between the TN, MPN and LPN.

Results: Macroscopic analysis of the vessel entry into the TN relative the medial malleolus revealed three common locations for vessels to enter (within 1 cm, between 1–3 cm and between 3–5 cm) proximal to the medial malleolus, with an average of 1.9±0.7 vessels entering per TN. The MPN was supplied by 2.6±0.5 vessels, and the LPN was supplied by 1.9±0.6 vessels. Majority of vessels entered the nerves within 1 cm of the abductor hallucis fascia. Very few specimens had vessels entering the LPN or MPN >3 cm distal to the abductor hallucis fascia. On microscopic examination, a vessel was found to enter the TN at its bifurcation in 73 percent of cases with immediate division into two branches to supply MPN and LPN. Vascular density was 0.17±0.07 for the TN, 0.31±0.13 for MPN and 0.36±0.14 for LPN, with significantly greater density (p<0.05) for MPN and LPN compared to TN.

Conclusions: Peripheral nerve function requires adequate arterial supply while limiting nerve vascular compression within a tight anatomical space. From this study, a rich vascular supply is shown to source the TN and its branches. This profuse blood supply to peripheral nerves has also been shown in median, ulnar and sciatic nerves where compression injuries also commonly occur. In this study, they conclude that this abundant blood supply may have a factor in symptomatic patients. When conditions occur to increase the contents of the canal (hemorrhage, edema, venous congestion) or decrease its volume (hypertrophic retinaculum, soft tissue mass), it may cause a shift in balance of the abundant blood supply to become a source of symptoms instead of a source of protection. This information is useful in understanding the importance of a tarsal tunnel release, the goals being to decompress the canal but being very careful not to disrupt the abundant blood supply to the nerve, which may cause ischemia leading to altered nerve response. 

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