Molly A. Judge
Over time, there has been far more literature produced in addressing hallux abductus and undercorrection of the hallux abducto valgus (HAV) deformity than that for hallux varus despite the fact that iatrogenic hallux varus in particular can have a devastating impact on function and quality of life. The importance of hallux varus deformity resulting from failed HAV surgery is that it is commonly more painful and debilitating than the original condition. When clinically significant residual incongruity of the metatarsophalangeal joint (MTPJ) develops, it provokes a cycle of osteoarthritis that will prove irreversible if not corrected. This may be the result of stretching the indications for the McBride or modified McBride technique in an attempt to correct deformities with moderate to high intermetatarsal angles (IMAs). Expanding the indications for these procedures is often associated with an overly aggressive lateral release and similarly aggressive medial plication of capsular structures to correct IMAs greater than 10 degrees. Although iatrogenic forms of hallux varus have resulted from a variety of soft tissue and osseous procedures, it is understood that even overaggressive splintage of the hallux postoperatively may shift the muscle tendon balance to favor the pull of the abductor hallucis (ABH) and the medial head of the flexor hallucis brevis (FHB) and creates a varus deforming force.
Historically, the incidence of hallux varus as a complication of HAV surgery has been reported from less than 2% to 17% of cases performed (1,2,3,4,5,6,7,8 and 9).
Although many have discussed the etiology and mechanics of hallux varus, there is a paucity of literature documenting its incidence, and so the true incidence of this condition may not be accurately estimated. McBride’s own account of the incidence of hallux varus was 5.1%, which constituted only 2 cases from his original work in 39 patients. He suggested lengthening of the abductor tendon and supplementing that with plication of the surrounding deep fascial structures. In a much larger series, Hansen reviewed 139 patients that underwent HAV surgery and reported a 12.9% complication rate due to hallux varus (7). Joplin reported 1% incidence after performing HAV surgery with the benefit of an adductor transfer and EDL transfer from the fifth digit, and this is the largest series identified prior to 1970 (8). In Hawkins review of 300 cases of the modified McBride procedure, only 1% was documented as resulting in symptomatic hallux varus. Interestingly, each of these three had radiographic evidence that correlated with violation of the lateral head of the FHB tendon—absence of the fibular sesamoid (2). He suggested correcting the deformity by transfer of the ABH to the plantar-medial aspect of the lateral base of the proximal phalanx with good results although he only reported follow-up on three patients with bilateral conditions. In the most recent report, the incidence of hallux varus was reported as 4.71% resultant from 646 procedures including the chevron osteotomy, closing base wedge osteotomy, and the
Lapidus arthrodesis procedures performed for the correction of HAV deformity. Of the three procedure types, the incidence of hallux varus varied from 1.48%, 2.94%, and 0.29%, respectively, with the closing base wedge procedure associated with the highest incidence of occurrence (10). In light of the gravity of the diagnosis, the literature reflects a growing appreciation for the condition over time detailing the nature of the deformity, biomechanical implications, and describing a detailed surgical approach to correction (2,3 and 4,9,11,12).
Hallux varus, as it applies to a complication of HAV surgery, can be divided into two categories of deformity: static and dynamic.
When Hawkins reviewed his cases of hallux varus (3 of 300 cases of McBride bunionectomy), he believed that the static deformities—those resultant of osteotomies, Silver bunionectomies, and MTPJ arthroplasty—would realign with time and in a sense were considered the less severe of these conditions. The dynamic deformity on the other hand was considered the more disastrous of the two outcomes and is associated with recalcitrance to the conservative effort such as prolonged splintage of the hallux. The natural history of a dynamic hallux varus is well understood and is the result of musculotendinous imbalance and dysfunction about the first MTPJ, which predictably progresses to include deformity of the hallux interphalangeal joint (HIPJ). When the abductor is unopposed by the adductor and the lateral capsular structures, the normal stabilizing pull of the ABH becomes a deforming force pulling the hallux beyond neutral position destabilizing the great toe. Once the hallux translocates medialward beyond neutral position on the metatarsal head, the hallux begins to flex at the HIPJ in an attempt to maintain weight-bearing function. The hallux deviates both in the transverse and sagittal planes, medially deviating at the MTPJ and flexing at the HIPJ, resulting in hallux adductus (with or without varus rotation) with a concomitant hallux malleus deformity. The more medial the hallux deviates, the more the flexor power of the FHB is converted into a varus, producing pull as the origin of the FHB rotates into a more dorsomedial position. As the hallux rotates into varus, the pull of the flexor hallucis longus (FHL) tendon is medialized and prompts retrograde buckling of the hallux at the HIPJ. As the hallux continues to drift into varus, the base of the hallux forces the metatarsal head to translate laterally resulting in increased tension along the distal course of the extensor hallucis longus (EHL) tendon aggravating extension at the MTPJ level and further perpetuates flexion at the HIPJ. This can be seen in severe cases in which the hallux is subluxed so far medially that there is a wide gap between the hallux and second digit with bowstringing of the EHL tendon along the first ray (see Fig. 36.2A in Chap. 36).
The dynamic deformity may be the result of congenital conditions that give increased muscle tone to the lower extremity, in particular the intrinsic muscles of the foot (12,13 and 14). The development of lower extremity paralysis has been shown to disrupt the natural balance across the first MTPJ leaving the joint to drift into varus (15). If hypertonicity or spasticity of the intrinsic or extrinsic muscles of the first ray is present, then even conservative bunion surgery may result in the development of a hallux varus due to adverse neuromuscular influence. Further, there are some neuromuscular conditions that may well be exacerbated by the trauma of surgical procedures such as muscular dystrophy or multiple sclerosis. To avoid increased morbidity or even exacerbation of a stable or quiescent neuromuscular condition, it is important to complete a thorough clinical evaluation to ensure that such conditions are not overlooked. Because of the genetics of the disease, some neuromuscular conditions can present across a large spectrum of ages. Patients of any age can be affected, while the disease may not manifest until after being stimulated by the trauma of surgery. A good example would be the child that develops proximal leg weakness after heel cord lengthening to correct an equinus associated with flatfoot and HAV. Muscular dystrophy can present in this manner and in fact there are many categories of this disease defined primarily by the age groups that they attack. Such conditions are associated with spasticity in the lower extremity and can be identified with basic clinical screening. Cursory deep tendon reflex testing could rule in such confounding dysfunction and may be the first test leading to such an important diagnosis. It is unwise to perform elective surgery on patients with neuromuscular dysfunction until the entirety of their condition is understood. Appropriate neurologic consultations should always be pursued in advance of surgical consultations for elective foot surgery. Only then can all the medical specialties involved take the team approach to determine if palliative foot surgery has a role in management.
The complexities of iatrogenic or acquired hallux varus have been well documented, and it is most often due to the destabilization of the MTPJ by an overaggressive lateral release with or without lateral sesamoidectomy (1,2,3,4,5,6,7,8 and 9,11,12). This is the case when the adductor tendon is released along with the lateral head of the FHB tendon with or without removal of the fibular sesamoid. An overly tense plication of the medial joint capsule can create this condition when performed alone or in combination with an osseous procedure. An aggressive release of the lateral structures of the MTPJ leaves the medial intrinsics and ligamentous structures unopposed resulting in the medial deviation of the hallux and loss of joint congruity. Other factors may contribute to the occurrence of hallux varus such as a long or short first metatarsal segment, a rounded first metatarsal head, an abnormally low first-second IMA, ligamentous laxity, the inadvertent staking of the sagittal groove of the first metatarsal head, as well as overly aggressive bandaging after HAV surgery.