Tag Archives: avascular necrosis

Talectomy (astragalectomy) and tibiocalcaneal arthrodesis following traumatic talus fracture-dislocation

The Foot and Ankle Online Journal 12 (2): 4

by Dr Alison Zander, MBBCh, BSc (hons), MSc (PHNutr)1, Mr Anirudh Gadgil, MBBS, M.S. (Orth), FRCS (Ed), FRCS (Trauma & Ortho)2, Derek Protheroe, BSc(Hons), MSc, PgDip3*

Talus fractures occur rarely but are often associated with complications and functional limitations. Urgent reduction of associated dislocations is recommended with open-reduction and internal fixation of displaced fractures when adjacent soft tissue injury permits [1]. However, it is important to remember that there is a high incidence of long term complications, along with a significant impact on activities of daily living and quality of life.  This case report describes the successful treatment of a severely comminuted talar fracture dislocation with primary talectomy and tibio-calcaneal arthrodesis. A reminder that in selected cases that the talectomy (astragalectomy) may be a viable alternative.

Keywords: talus, comminuted, tibiocalcaneal arthrodesis, fusion, talectomy, astragalectomy, trauma, avascular-necrosis, AVN

ISSN 1941-6806
doi: 10.3827/faoj.2018.1202.0004

1 – Foundation Doctor, Cardiff and Vale University Health Board, University Hospital of Wales, Heath Park, Cardiff
2 – Consultant Orthopaedic Surgeon, Cardiff and Vale University Health Board, University Hospital of Wales, Heath Park, Cardiff
3 – Advanced Podiatry Practitioner, Prince Philip Hospital, Bryngwyn Mawr, Llanelli, Wales, SA14 8QF
* – Corresponding author: Derek.Protheroe@wales.nhs.uk

Talus fractures account for less than 1% of all fractures, they may be caused by high-energy trauma, and any other form of forced dorsiflexion injury to the ankle and foot [1]. Talar fractures may be classified anatomically as head, neck, body, lateral or posterior processes, displaced or non-displaced. A range of classifications have been established such as the original Hawkins, then modified by Canale & Kelly and then the Sneppe classification [2]. These sub-classifications help to guide treatment options[3]. Non-displaced fractures may be treated conservatively with a non-weight-bearing short-leg cast, whereas displaced fractures require open-reduction and internal fixation. Reconstruction after a talus fracture poses the greater surgical challenge if restoration of the articular surfaces is precluded secondary to comminution [4]. The talus is the second largest of the tarsal bones, with more than half of its surface being covered with articular cartilage, with no muscular attachments[1]. Therefore, the vascular supply of the talus is well-known to be tenuous, therefore predisposing the talus to significant ischemic injury after fractures [5]. Risk of post-traumatic avascular necrosis (AVN) increases with the magnitude of injury [6]. Extensive intraosseous anastomoses are present throughout the talus and are responsible for its survival during severe injuries. At least one of the three main anastomoses preserved may potentially allow adequate circulation via anastomotic channels [1].

Using the Hawkins’s classification system; 0-13% for grade I, 20-50% for grade II, 83-100% for grade III, and 100% for grade IV fracture dislocations result in AVN [1,6]. 

Clinical experience of talar fracture assessment and management is limited by their infrequent incidence, which is further exacerbated by the numerous sub-classifications of fracture, as previously alluded to. Case reports, although regarded as level V evidence can aid and develop an understanding of the risks and benefits of treatment options to achieve optimal patient outcomes [7].  Clinicians should maintain a high index of suspicion for AVN, which can only be diagnosed radiographically six to eight weeks following injury [8].  Furthermore, the potential for long term issues, such as hind-foot arthrosis and further revisionary surgery must be considered, alongside risks of repeated anesthetics for multiple procedures after complications. Approximately 25% of talus dislocations treated with internal reduction require additional surgery, including secondary arthrodesis [9].

Operative treatment measures for this area may be broadly split into two categories; joint sparing procedures – such as protected weight bearing, patella loading splints and bone graft or joint sacrifice procedures – such as talectomy and arthrodesis. Total talectomy and tibiocalcaneal arthrodesis may be viewed as a salvage procedure in this case report due to the case of severe comminuted fracture, where it may be impossible to anatomically reduce the talus and allow for adequate stable fixation. 

A literature search was performed using the keywords ‘talectomy’, ‘astragalectomy’, ‘fracture’, ‘tibiocalcaneal arthrodesis’ and Boolean search terms. Ovid SP databases (including embase & medline) was used with no exclusion dates to allow for a search of all historical literature. It appears that there was only one other reference in 1955 to such a procedure following a traumatic fracture to the talus body [10]. Historically, this case involved a Royal Navy soldier, where following a dislocated fracture a primary talectomy and tibiocalcaneal arthrodesis was performed.

Figure 1 Preoperative radiographs lateral and AP views.

Case Report

A sixty eight-year-old lady with no significant past medical history presented to Accident and Emergency.  She had been a seat-belted, front-seat passenger of a car that suffered a high-speed head-on road traffic collision.  She sustained a grade I (Gustilo-Anderson) open, comminuted fracture dislocation of the talus (Figure 1) with puncture wounds on the lateral aspect of the talus.  The foot was neurovascularly intact initially. The ankle was manipulated and back-slab applied. Apart from body ache and multiple minor abrasions and bruises there were no other injuries.  Whilst she was waiting on the ward to have a CT scan performed she developed increasing pain in foot, numbness of toes and sluggish capillary refill in the toes, which were not relieved even after removing the plaster slab.  She was counselled that she would need to be rushed to the operating room to attempt to reestablish circulation to her foot with a plan to open reduce the fracture and stabilize it. She was also made aware of the possibility of having to excise the fragments if it was not possible to operatively stabilize the fracture.


Under spinal anaesthesia, antibiotic cover and usual sterile draping, the lateral puncture wounds were thoroughly debrided and lavaged with saline.  The fracture was exposed using an anterior approach between tibialis anterior and extensor hallucis longus, carefully protecting the neuro-vascular bundle throughout the procedure.  The displaced fracture fragments of the talus, the medial malleolus and the medial hematoma all appeared to have caused pressure on the posterior tibial neurovascular bundle. 

Figure 2 One year follow-up radiographs.

This was relieved after opening the fracture and the toes regained their color.  Intra-operatively, it became apparent that the fracture could not be anatomically reduced and fixated adequately due to the severe degree of comminution, and lack of any soft tissue attachments to the majority of the fragments. Hence, the original plan of anatomical reduction and internal fixation of the fracture was abandoned.  All loose fragments were excised, which involved removing all of the posterior process and body of the talus. Using the cancellous bone from the excised fragments as autogenous graft, the calcaneal and tibial articular surfaces were fused using three 7.5 mm cannulated AO screws (Figure 2). A small lateral malleolar avulsion fragment was excised.  The medial malleolus fragment was reduced and fixed with a cancellous 4mm AO screw (Figure 2). Post-operatively, the foot was observed to be well-vascularised. The lateral wounds were allowed to heal with regular dressings and a plaster of Paris splint was applied.  

Postoperative care protocol

Postoperatively, the patient received intravenous antibiotics for 24 hours, limb elevation for 48 hours and prophylactic anticoagulation for six weeks. Mobilization started with physiotherapy, consisting of non-weight bearing for six weeks, partial-weight bearing in air cast boot for two weeks and then allowed to fully-weight bear with an air cast boot.  The patient was advised to stop using the air cast boot at three months. The wounds healed well and there were no other complications.  


Due to the urgency of care required and history of trauma it was not deemed appropriate to use any form of patient reported outcome measure at the time of incident. However, the patient was reviewed frequently for eight weeks until the wounds healed. Then, accordingly, when she was allowed to weight bear, again at six months, one year and two years post-injury.  At six months, the patient had no pain or tenderness, with some dorsiflexion and plantar flexion possible at the mid-tarsal level. One-year follow-up showed that the tibio-calcaneal fusion was solid via plain x-ray (Figure 2). Final follow up at two years, she had a 2 cm shortening of her right leg measured in a weight bearing manner (measured blocks) and appropriate footwear adaptations were incorporated on the right side.  She is very happy with the outcome, has no pain and is fully mobile and weight bearing without support. 


Talus fractures occur rarely and are commonly associated with complications and functional limitations [11].  The main complication being osteonecrosis, Vallier et al reviewed 100 talus fractures and reported osteonecrosis with collapse (31%), ankle arthritis (18%), subtalar arthritis (15%). Operative intervention was complicated by superficial (3.3%) and deep infection (5%), wound dehiscence (3.3%), delayed union (1.7%) and non-union (3.3%) [11]. Restoration of the axial alignment has been recommended to ensure optimisation of ankle and hindfoot function. It has been reported that tibiotalar and subtalar ranges of motion are reduced by up to 50% and arthrosis occurs in roughly 50% of fractures classified as Hawkins type III and IV [4]. The original paper proposing Hawkins classification even stated that comminuted fractures or those involving the body of the talus, were believed to be more problematic injuries and outside the scope of his original article [12].

A range of classifications for talus fractures exist, the most famous being the original Hawkins classification [2]. 

Historically, cases of talus injuries date as far back to as 1608. Interestingly, a term was coined known as ‘aviator’s astragalus’ due to its high frequency of injury in aircraft accidents [12]. The first case of talectomy for compound fracture was reported in 1609 by Hildanus  [13]. The patient had jumped over a ditch and turned his ankle on landing, causing the talus to dislocate completely out of the skin.  The talus was removed completely, following which the man was seen walking without apparent discomfort. In 1931, Whitman reported use of astragalectomy in correction of a calcaneus deformity of the foot [14]. Although these accounts are reported anecdotally, they demonstrate that the procedures used then are used in a similar fashion to case descriptions today. Talectomy has been used as a salvage procedure in correction of pathological deformity in conditions like  Charcot-Marie-Tooth, neglected idiopathic clubfoot, neurogenic clubfoot, cerebral palsy, gunshot wound, hemiplegia secondary to head trauma, Volkmann ischaemic contracture, poliomyelitis, arthrogryposis, myelomeningocele, and Charcot arthropathy  [15-18]. Talectomy has been used for patients with osteomyelitis or osteonecrosis of the talus [19,20]. We found only one study which reported 4 cases of total talectomy for Hawkins Type III fractures dislocations of talus in 1993 [21].  However, tibiocalcaneal arthrodesis was formally not carried out in the patients in this series.

Detenbeck and Kelley (1969) reported dire results following total dislocation of the talus in nine cases, of which seven were open [22]. Eight of the nine developed sepsis; seven required secondary talectomy, five with tibio-calcaneal fusion. This report highlights the serious consequences of this kind of injury. Their recommendations were to apply a more aggressive approach to initial treatment using talectomy and some form of tibio-calcaneal arthrodesis as the primary treatment for fracture-dislocation of the talus.  

Predominantly, cases of tibio-calcaneal (TC) arthrodesis are described for treatment of post-traumatic AVN of the talus or for treatment of rheumatoid arthritis [23-25]. Authors have reported TC arthrodesis of nine ankles in eight patients; seven were for post-traumatic talar AVN and one for rheumatoid arthritis [25]. Fixation was achieved using 6.5 or 7mm cannulated screws or multiple staples, with autologous cancellous bone graft.  Fusion was achieved in all patients between 12 and 40 weeks with a 2cm leg length discrepancy. Complications included local infection, malunion, wound dehiscence, prominent fibula and two patients required supplemental external fixation.  

In 1972, Reckling reported early TC fusion after displaced talus fractures in eight feet; Steinmann pins were used to achieve fixation without the use of bone grafting [26].  No wound complications were reported and bone union was achieved within 17 weeks. 

The main draw-back of TC fusion is the shortening of 2 to 3 cm that is produced in the limb.  It is also possible that secondary arthrosis of other joints of the foot may occur over time after TC fusion.

Using the technique of tibio-calcaneal fusion there is a potential to increase the calcaneal pitch angle. Intra-operatively, the surgeon must be careful to keep this in mind and achieve a well-aligned position of the foot. 7.5 mm cannulated AO screws were utilised providing stable compression across the fusion surfaces and encouraged rapid fusion of the inferior tibial surface to calcaneal articular surface.  There are other modes of fixation discussed within the literature such as intramedullary nail, pre-contoured plates or an external fixator. This would depend not only the surgeon’s experience and preference but in this case the setting (trauma) and clinical scenario due to the compromised blood supply.

Dennison et al treated six patients who had previous failed surgery and suffered post-traumatic AVN of the talus [27]. The necrotic body of the talus was excised and TC fusion achieved using an Ilizarov frame, combined with corticotomy and a lengthening procedure.   Patients were aged between 27 and 67 years. Shortening was corrected in four patients, and bony fusion achieved in all. Four out of six patients reported good or excellent results. 

Thomas and Daniels in 2003 reported using talonavicular and subtalar arthrodesis as a primary fusion to treat a three week old Hawkins type IV traumatic comminuted neck of talus fracture in a 29-year-old man [28]. Their case had similarities to ours, in that open reduction internal fixation had been planned, however, this was not possible anatomically due to the degree of comminution.  The patient underwent 16 months of follow-up and despite successful fusion without avascular necrosis, he was unable to return to his job as a roofer. 

Hantira et al reported treating a comminuted open fracture of the body of the talus on the same day of injury by tibio-talar fusion using the Blair technique [29].  Küntscher nails and cancellous screws remained in situ while the graft healed and they were removed at four and eight weeks post-surgery, respectively.  The patient started active and assisted foot exercises 14 weeks following surgery, with partial-weight bearing on crutches 20 weeks after the injury.  Fusion was complete at 10 months after injury and the patient was reportedly almost pain free.


The severity of talus fractures has increased over the last 3 decades due to modern safety equipment resulting in higher survival rates from serious accidents [2]. Due to recent advances in surgical and fixation techniques, the tendency is to reduce the talar fractures as anatomically as possible and stabilize them with screws.  

It is worthwhile considering the option of a talectomy in conjunction with a primary tibiocalcaneal arthrodesis. although cases of talus fractures with comminuted dislocations are rare. In this particular case study, to attempt to perform an open reduction and internal fixation procedure may have increased the potential risk and complications associated with these procedures, mainly AVN, traumatic hind foot arthrosis both potentially requiring further surgery. Ultimately, increasing the potential for a high rate of long-term complications and a significant impact on activities of daily living and quality of life after such treatment [30].

In summary, surgeons should be flexible in their approach in regards to consideration of treatment options in order to maximise patient outcomes.  This case highlights that the procedure choice of a primary talectomy and tibio-calcaneal arthrodesis is a viable treatment option for traumatic dislocated comminuted talar fractures, which intra-operatively was unable to be anatomically reduced and fixated.

Funding declaration: None  

Conflict of interest declaration: None


  1. Fortin PT and Balazsy JE.  Talus Fractures: Evaluation and Treatment. Journal of the American Academy of Orthopaedic Surgeons. 2001; 9(2):114-127. 
  2. Dale JD, Ha AS, Chew FS (2013). Update on Talar Fracture Patterns. A Large Level 1 Trauma Center Study. American Journal of Roentgenology. 201:1087-1092.
  3. Lamothe JM and Buckley RE. Talus fractures: a current concepts review of diagnoses, treatments, and outcomes. Acta Chir Orthop Traumatol Cech. 2012; 79(2):97-106.
  4. Ptaszek, A (1999) Immediate Tibiocalcaneal Arthrodesis with Interposition Fibular Autograph for Salvage After Talus Fracture: A Case Report. Journal of Orthopaedic Trauma. 13(8): 589-592.
  5. Pearce DH, Mongiardi CN, Fornasier VL, Daniels TR. Avascular necrosis of the Talus: A pictorial essay. RadioGraphics. 2005; 25(2):399-410. 
  6. Balaji GG and Arockiaraj J. Bilateral talus fracture dislocation: is avascular necrosis inevitable? BMJ Case Rep. Aug 25;2014. pii: bcr2014205367. doi: 10.1136/bcr-2014-205367
  7. Cutler L and Boot DA. Complex fractures, do we operate on enough to gain and maintain experience? Injury. 2003; 34(12):888-91.
  8. Melenevsky Y, Mackey RA, Abrahams RB, Thomson NB. Talar Fractures and Dislocations: A Radiologist’s Guide to Timely Diagnosis and Classification. Radiographics. 2015; 35(3):765-79.
  9. Weston JT, Liu X, Wandtke ME, Liu J, Ebraheim NE.  A Systematic Review of Total Dislocation of the Talus. Orthop Surg. 2015; 7(2):97-101. 
  10. Marsden CM (1955). Ankle fusion after complete talectomy in fracture dislocation of the talus. Journal of the Royal Army Medical Corps. 101(1):60-2.
  11. Vallier HA, Nork SE, Barei DP, Benirschke SK, Sangeorzan BJ. Talar neck fractures: results and outcomes. Journal of Bone & Joint Surgery. 86: 1616-1624.
  12. Alton T, Patton DJ, O.Gee A (2015) Classification in Brief: The Hawkins Classification for Talus Fractures. Clinical Orthopaedics and Related Research. 473(9): 3046-49.
  13. Hilandus F (1608): Report quoted in Opera, quae extant omnia (1946), Obs. 67, p. 140. Francofurti ad Moenum : Beyer.
  14. Whitman A , Astragalectomy – Ultimate Result.  Americal Journal of Surgery. 1931; 11(2):357–358.
  15. Gursu S, Bahar H, Camurcu Y, Yildirim T, Buyuk F, Ozcan C, et al.  Talectomy and Tibiocalcaneal Arthrodesis with Intramedullary Nail Fixation for Treatment of Equinus Deformity in Adults. Foot Ankle Int. 2015 Jan; 36(1):46-50. doi: 10.1177/1071100714550649
  16. Ruet A, Desroches A, Pansard E, Schnitzler A, Denormandie P.  Role of talectomy in management of severe equinovarus deformity in adults. Annals of Physical and Rehabilitation Medicine. 2014 May; 57:e197. doi: 10.1016/j.rehab.2014.03.719
  17. Joseph TN and Myerson MS. Use of talectomy in modern foot and ankle surgery  Foot Ankle. Clin N Am. 2004; 9:775–785.
  18. Daghino W, Di Gregorio G, Cerlon R. Surgical reconstruction of a crush injury of the talar body: a case report. J Bone Joint Surg Am. 2011 Jul; 93(14):e80.
  19. Stapleton JJ, Zgonis T. Concomitant Osteomyelitis and Avascular Necrosis of the Talus Treated with Talectomy and Tibiocalcaneal Arthrodesis. Clin Podiatr Med Surg. 2013 Apr; 30(2):251-6. doi: 10.1016/j.cpm.2013.01.001
  20. Kharwadkar N, Nand S, Walker AP. Primary talectomy for severe fracture-dislocation of the talus with a 15-year follow up: case report. Foot Ankle Int. 2007; 28(2):272-275.
  21. Gunal I, Atilla S, Araç S, Gürsoy Y, Karagözlu H. A new technique of talectomy for severe fracture-dislocation of the talus. J Bone Joint Surg Br. 1993 Jan; 75(1):69-71.
  22. Detenbeck LC and Kelly PJ. Total Dislocation of the Talus. J Bone Joint Surg Am. 1969 Mar; 51(2):283-288.
  23. Cinar M, Derincek A, Akpinar S. Tibiocalcaneal arthrodesis with posterior blade plate in diabetic neuroarthropathy. Foot Ankle Int. 2010; 31(6):511-516
  24. Clements JR. Use of allograft cellular bone matrix in multi-stage talectomy with tibiocalcaneal arthrodesis: a case report. J Foot Ankle Surg. 2012; 51(1):83-86.
  25. Mann RA, Chou LB. Tibiocalcaneal arthrodesis. Foot Ankle Int. 1995; 16(7):401–405.
  26. Reckling FW. Early tibiocalcaneal fusion in the treatment of severe injuries of the talus. J Trauma. 1972; 12(5):390–396.
  27. Dennison MG, Pool RD, Simonis RB, Singh BS. Tibiocalcaneal fusion for avascular necrosis of the talus. J Bone Joint Surg Br. 2001; 83(2):199–203.
  28. Thomas RH, Daniels TR. Primary fusion as salvage following talar neck fracture: a case report. Foot Ankle Int. 2003 Apr; 24(4):368-71. 
  29. Hantira H, Al Sayed H, Barghash I. Primary ankle fusion using Blair technique for severely comminuted fracture of the talus. Med Princ Pract. 2003 Jan-Mar; 12(1):47-50E
  30. Stake IK, Madesan JE, Hvaal K, Johnsen E. Surgically treated talar fractures. A retrospective study of 50 patients. Foot and Ankle Surg. 2016; 22:85-9.

Dextrose Prolotherapy Treatment for Unresolved “Morton’s Neuroma” Pain

by Ross A. Hauser, MD1, Wayne A. Feister2, DO, Debra K. Brinker, RN3

The Foot and Ankle Online Journal 5 (6): 1

This study investigates the effectiveness of Dextrose Prolotherapy injections on a group of patients with “Morton’s neuroma.” These patients had failed previous conservative therapies, including surgical and non-surgical procedures as well as steroid injections. In this study, seventeen patients with neuroma pain were treated for six months. Every month, 10 to 20 injections containing 0.5 to 1 milliliter of Dextrose solution were given based on patient response. Pre- and post-treatment surveys utilized both objective data (i.e., solutions used, length and number of treatments, etc.) and subjective data (post-treatment visual analog scale or VAS ratings of pain relief/reduction). The results of this short-term study suggest that Prolotherapy, using injections of Dextrose into weakened ligaments, tendons, and joints, is a promising option among current treatment choices. Prolotherapy works by stimulating the body to repair these soft tissues. Future studies must confirm not only the efficacy but also the reduced risks of Dextrose Prolotherapy for one of the most common foot ailments.

Key words: Morton’s neuroma, neuralgia, metatarsalgia, paresthesias, intermetatarsal bursitis, inflammatory arthritis, osteomyelitis, rheumatoid arthritis, localized vasculitis, ischemia, tarsal tunnel syndrome, peripheral neuritis, synovitis, tendonitis, avascular necrosis, metatarsophalangeal joint capsulitis, Hackett-Hemwall Dextrose Prolotherapy

Accepted: March, 2012
Published: June, 2012

ISSN 1941-6806
doi: 10.3827/faoj.2012.0506.0001

Morton’s neuroma (MN) is a painful condition that affects the ball of the foot. First described in the 1800s, this affliction continues to be a common cause of forefoot pain [1]. Seemingly benign, MN pain can cause extreme discomfort, making it difficult to walk. Those affected become so cautious that they are afraid to place the afflicted foot (or feet) on the ground to take a step.

The word “neuroma” suggests a tumor of the nerve; however, the term is actually a misnomer since the condition is not necessarily an abnormal growth of the nerve [2, 3]. Also, the term neuroma does not describe what is seen with a microscope. Over time, other terms have been used to describe aspects of this pathology. Based on the shape, size, and structure (morphology) of tissues noted under the microscope, other terms may apply: perineural fibrosis, endoneural edema, neurofibromata, angioneurofibromata, local demyelination, and local vascular degeneration [4, 5] (Fig. 1).

Figure 1 Possible tissue pathologies that explain interdigital pain.

What circumstances give rise to the onset of neuromas in the foot? Chronic irritation, trauma, or excessive motion induces a severe, intermittent pain between a pair of the five metatarsal heads in the bones of the fore foot. MN pain may then radiate through the nerves to the tip of the toes [6]. The shooting pain follows a path from that web space to the touching halves of adjacent toes. Seen most commonly in the second and third web space—any interdigital space between toes can be affected [7-9] (Fig. 2).

Figure 2 Interdigital spaces.

Typical symptoms in the region of the intermetatarsal spaces include sharp pains, burning sensations, and paresthesias (abnormal sensation) with weight-bearing activity. (Fig. 3) In fact, the sensation is often described as walking with a stone in the shoe or on a folded or creased sock. As the condition progresses, the pain becomes debilitating; and walking becomes more apprehensive, even to an observer. Noting these typical symptoms, an accurate diagnosis can then be made after a thorough review of the patient’s history and a physical assessment.

Figure 3 Inflamed interdigital nerve.

Evidence on the frequency of this condition is minimal; however, a foot clinic computed the incidence of patients diagnosed with a “neuroma” at a rate of 9.3% of 4000 patients who complained of foot pain [10-12]. Although neuromas in both feet and multiple neuromas in one foot occur, both conditions are rare [13, 14]. Furthermore, neuromas are seen among patients of all ages; even so, they are more prevalent in middle-aged adults [15-17]. The condition most often affects women who frequently wear pointed, high-heeled, close-toed, ill-fitting shoes poorly designed for foot mechanics [18]. Footwear that transfers body weight to the metatarsal heads may be the reason women suffer from MN more frequently than men at a documented rate of eighteen to one [19]. The pain generally intensifies with walking, weight-bearing movement, and tight-fitting shoes.

The discomfort, however, eases with rest and the removal or change of footwear [20, 21] At the onset of the condition, additional relief may be gained by removing the shoe, massaging the foot, and wiggling the toes.

The etiology (cause) of Morton’s neuroma is controversial. A longstanding entrapment theory maintains that the third digital nerve, which is large and formed by a branch of the medial and lateral plantar nerves, is compromised by mechanical irritation. With dorsiflexion—when the toes or foot are bent upward toward the nose—the unyielding transverse ligament fixates the proximal end of the digital nerve [22, 23] (Fig. 4). However, this pinching does not always occur in one nerve; other intermetatarsal spaces can be affected [24]. Since it is not a true neuroma (tumorous nerve), some refer to the condition as Morton’s metatarsalgia [25]. Metatarsalgia is pain related to the metatarsal bones of the foot [26]. Another explanation for the pain is an ischemia or lack of blood flow through the plantar digital artery, which precedes a fibrous thickening around the nerve, called a perineural fibrosis [27]. In addition, a pathophysiological theory for MN claims that the intermetatarsal bursa—distally located to the transverse metatarsal ligament and close to the neurovascular bundles—is irritated. Thus inflamed, secondary fibrosis in the bursa can lead to the symptoms of neuroma. Lateral compression of the foot will then invariably cause pain, probably due to the inflamed bursa—not the nerve—being squeezed between the metatarsal heads [28] (Fig. 4).

Figure 4 Cross sectional view of the fore foot displaying the interdigital points of irritation/inflammation.

The inflamed and enlarged bursa causes a click when the metatarsals are squeezed. This distinctive click, called “Mulder sign,” can be used when diagnosing Morton’s neuroma [29].

A clear knowledge of conditions that affect the metatarsal region is critical to making a definitive diagnosis. Initially, possible diagnoses include metatarsal stress fracture, intermetatarsal bursitis, inflammatory arthritis, osteomyelitis, rheumatoid arthritis, localized vasculitis, ischemia, tarsal tunnel syndrome, peripheral neuritis, synovitis, tendonitis, avascular necrosis, metatarsophalangeal joint capsulitis, and others [30-32] (Fig. 5).

Figure 5 Diagnoses to consider when interdigital pain is the main symptom.

Many treatments have been developed for relief of the symptoms of Morton’s neuroma, but initially, non-surgical approaches are preferred. Among these conservative treatments from simple to complex are changing the footwear; avoiding high-heeled shoes; resting the feet; applying ice; elevating the foot; taking anti-inflammatory medications; taping and strapping, padding, and immobilizing the foot; receiving physical therapy; wearing orthotics or other shoe gear; and injecting steroids. When conservative approaches are unsuccessful, surgery is generally sought as the next step. Surgical approaches include resection, transection, decompression, excision of the involved nerve, and cryogenic nerve ablation.

Another conservative treatment for Morton’s neuroma pain is Prolotherapy, which has a longstanding record of success with hypermobility, when joints are unusually loose or abnormally flexible.

If the goal of padding and strapping is to reduce forefoot motion and pain, it is reasonable to utilize a treatment, such as Prolotherapy, that not only reduces hypermobility, but also results in joint stabilization [33].

Additionally, recent studies demonstrate that injection therapy, utilizing 4% sclerosing alcohol, has success rates of 84 – 89% [34-36]. Dextrose Prolotherapy injections will induce a proliferative response without the risk of alcohol infiltrating the surrounding tissue. The overall purpose of this study was to record the outcomes of Dextrose Prolotherapy on a group of patients with Morton’s neuroma in a private pain clinic.

Patients and Methods

In the study, an attending physician treated seventeen patients with Morton’s neuroma at a private medical clinic. All subjects signed a consent form, stating that a minimum of three and a maximum of six monthly treatments might be needed.

To meet the criteria for inclusion in the study, patients had to be at least 18-years-old, to have suffered unresolved Morton’s neuroma at any intermetatarsal space, and to have failed previous conservative treatment.

At the clinic, a search of electronic medical records (EMR) to find patients with the diagnosis of Morton’s neuroma was conducted.

To be included in the study, two criteria were paramount: 1) a diagnosis of Morton’s neuroma, which had to be the primary condition, and 2) a six-month time lapse, since the patient’s last Prolotherapy injections. The search revealed 31 patients diagnosed with Morton’s neuroma; of these, five could not be contacted by phone (three attempts were made before discontinuing phone calls). Two patients chose not to participate.

Five patients were excluded because of multiple foot problems that took priority over Morton’s neuroma: previous surgeries, osteoarthritis, and ankle problems. Two patients were excluded because not enough time had elapsed—at least six months—since their last Prolotherapy session.

Patients selected for the study had to complete preliminary oral, written, and visual surveys. Demographic information was obtained. Then the patient completed a visual analog scale (VAS), which includes ratings of pain at rest; pain with normal activities; pain while walking barefoot; ability to walk distances without pain; as well as stiffness and numbness/burning (Fig. 6). Finally, an assessment interview with clinical staff members collected both subjective and objective data, such as the type and duration of symptoms, previous treatments and tests, limitations to activity, and previous medical opinion.

Figure 6 Questionnaire used by patients to assess levels of pain.

Next, a physical examination determined objective data by checking for the following: the precise location of the pathology or point of maximal tenderness by palpating (light and/or deep touch) the affected web space; the presence or absence of Mulder’s click; and the severe pain that results with lateral compression of the forefoot.

The end of the Prolotherapy treatment was determined when patients indicated a zero to 1 on the pain scale, or their personal goals for pain relief or for the ability to function were met. Although some had little pain, their main goal was to eradicate numbness, which they found disturbing. Some patients wanted to achieve a zero to 1 level of pain while walking, even with level 4 pain while jumping. Therefore, they would stop treatment with a low level of walking discomfort.

Following treatment, interviews and surveys were completed on a monthly basis. Monthly data collection included the total percentage of improvement; VAS score of pain; level of pain intensity; level of stiffness; degree of crepitation (grating sensations from a joint); range of motion; ability to perform the ADLs (activities of daily living) and to exercise the affected body part.

Six months after the last visit, patients were called to obtain information and answered detailed questions. Interviews provided data on the level of foot/toe pain (VAS scale), percent of overall improvement, limitations/improvements in activities and walking, duration of post-treatment pain relief, and assessment of the treatment by the patient.

For data analysis, patient responses were collected, calculated, and compared at three different times: prior to Prolotherapy, during monthly visits, and in phone interviews conducted six months after Prolotherapy. Statistical analysis using Graph Pad Software calculated the paired student t-test before and after Prolotherapy.


The Hackett-Hemwall technique of Prolotherapy (www.hacketthemwall.org) was used. Each patient received 10 – 20 injections of 15% Dextrose, 0.2% Procaine, and a 10% Sarapin solution, for a total of 10 to 20 cubic centimeters of solution per foot. Each injection consisted of 0.5 to 1 cubic centimeter of solution and used a two-inch, 27-gauge needle. Injected areas were web spaces one through four—with attention given to metatarsophalangeal joints, dorsal and plantar surfaces, and joint capsules and ligaments (Fig. 7). If applicable, patients were advised to reduce or discontinue non-steroidal anti-inflammatory (NSAID), steroidal and narcotic medications, and other therapies. Prolotherapy treatments were discontinued, once a patient reached a clinical resolution of symptoms.

Figure 7 Prolotherapist injecting the third interdigital space with sclerosant solution.


The final study group included 17 patients but 19 feet, since some patients suffered from MN in both feet. Ten right feet and nine left feet were treated. The average age of the 17 patients was 57 years: eleven were women, and six were men.

Before introducing Prolotherapy, study patients reported previous treatments. No one used pain medications for their symptoms. Some patients had tried wide-toed shoes, orthotics, padding, chiropractics, acupuncture, and steroid injections. Some patients had had MRI and radiographic diagnosis. One of seventeen had seen a podiatrist. A physician told three patients that surgery was required, but only one had surgery to remedy the pain on the other foot.

From patient questionnaires, averages were determined for periods of time. The average length of time patients experienced the pain of Morton’s neuroma was 20 months before entering the clinic. Patients received an average of 3.7 Prolotherapy treatments.

The average time of follow-up was 13.3 months. To determine the efficacy of treatments, only those patients with follow-up more than 6 months were included.

Patients’ subjective experience of pain offers the best measure for statistical accuracy. Patients were asked to rate their pain levels on a scale of 0 to 10—with 0 being no pain and 10 being severe crippling pain. All 17 patients reported pain as a symptom. Thus, patients were asked to report pain levels before and after Prolotherapy in these four categories: 1) pain at rest; 2) pain with normal activities; 3) pain with exercise, and 4) pain while walking barefoot.

Concerning 1) pain at rest: prior to Prolotherapy treatment, VAS pain levels averaged 4.68. None of the patients had a starting pain of less than three. After Prolotherapy treatment, VAS pain levels averaged 0.95.

Concerning 2) pain with normal activity and mobility: prior to Prolotherapy treatment, 15 of the 17 participants reported walking with some degree of pain, and a VAS pain level of 6.89. Eleven of 17 patients were unable to walk fifty feet without pain; 14 of 17 could not walk a half-mile without pain. Four of 17 patients reported an inability to walk barefoot. After Prolotherapy, all patients reported improvements in walking without pain, and a VAS pain level of 1.89. Fourteen of the 17 participants walked normally again and rated their pain relief at greater than 74%. Sixteen of the 17 could walk one block or more.

Concerning 3) pain with exercise: prior to Prolotherapy, 15 of the 17 patients reported decreased ability to exercise, and a VAS pain level of 7.27. Of those 15, eight were totally compromised and unable to exercise; five were moderately (only 30 to 60 minutes possible) to severely compromised (only 0 to 30 minutes possible). Nearly half of the patients were totally compromised in their athletic abilities prior to treatment. After Prolotherapy, 5 of the 17 patients reported being able to exercise as much as they wanted without impediments and with satisfaction, with a VAS pain level of 1.73. Other physical improvements occurred, notably, decreases in stiffness and numbness (burning). Thirteen to 14 patients reported a 100% improvement in the activities of daily living that continued to the end of the study. None reported an inability to exercise.

Concerning 4) pain while walking in bare feet: prior to Prolotherapy treatment, 10 of 17 patients could not walk barefooted without severe pain at levels eight, nine, or ten, and an average VAS pain level of 6.47. Furthermore, 12 of 17 patients could walk less than 50 feet before they experienced noticeable pain, with or without shoes. Only 3 of the 17 patients could walk more than a half-mile without pain.

After Prolotherapy, all patients had a pain level of four or less walking barefooted, and a VAS pain level of 1.65. As for walking distances without pain, all patients could walk at least one block or more. One patient was restricted to walking between 50 feet and one block. Among the 19 treated feet of the 17 patients in the study, eighteen feet could manage walking a half-mile or more, eight of the treated feet reported no walking restrictions.

When comparing the four previous categories before and after Prolotherapy, all reached a statistically significant outcome with a paired student t-test of p = <0.0001. This p-value confirms that the numerical results, when compared and tallied, exceed the mathematical probability of mere chance.

Thus, this prospective, non-controlled study demonstrates that Hackett-Hemwall Dextrose Prolotherapy decreases pain and improves the quality of life for patients with Morton’s neuroma, which was unresolved by previous therapies, medications, and interventions. Prolotherapy provided a relief of 74% for 14 out of 17 of the patients. Among the three patients who were told they needed surgery, two patients felt sufficient pain relief with Prolotherapy to avoid surgery. After the study period, patients experienced overall improvement in range of motion, ability to walk and exercise, as well as relief of stiffness and numbness/burning (Fig. 8).

Figure 8 Survey responses before and after Prolotherapy on levels of pain with various activities.


This study should not be compared to a clinical trial in which a treatment is studied under controlled conditions. Instead, the projected goal was to document the responses of patients with unresolved Morton’s neuroma pain to the Hackett-Hemwall technique of Dextrose Prolotherapy. Clearly, the study’s strength was the number of quality of life parameters examined. Quality of life conditions—such as the ability to walk and exercise, enhanced range of motion, reduced stiffness, enjoyment of activities of daily life, and reduced levels of pain—are all important factors affecting the person with Morton’s neuroma.

Improvements in a large number of variables were most likely the result of Prolotherapy treatment. There is no medical test to quantify pain relief. However, observable, documented changes—such as the ability to walk or walk barefoot, to exercise, to work, and to use less pain therapies—are valid measures of success for patients whose health and vitality have considerably improved.

This study noted two empirical shortcomings. One is the subjective nature of the data gathered by the most reliable methods available. Surveys, for instance, relied on the patients to rate their pain, stiffness, and degree of disability. A second obvious weakness is the small number of patients involved in the study. However, on the positive side, this small study group made it possible to see results in a relatively short time span.

Many treatments for the relief of Morton’s neuroma symptoms have developed over time. Although conservative, non-surgical, and surgical approaches have been used, their effectiveness as a treatment is variable, often leaving patients with mixed results and questionable improvement.

A review of three trials that involved 121 people was not able to determine the effectiveness of conservative, surgical, and non-surgical interventions because, as the authors noted, there was insufficient evidence and research flaws. For instance, there were only three randomized controlled studies of the various treatments. The authors were also unable to find any studies to identify the incidence or prevalence of this condition. In the review of the three trials, researchers found no evidence to support the use of pronation insoles, which are routinely used as a conservative approach. Furthermore, they found no evidence supporting the effectiveness of corticosteroids (non-surgical); and they gave a poor grade to the surgical approach due to high risks of amputation neuroma (minimum of 20%), painful plantar scars, and postoperative complications [37].

Histomorphological findings are accepted as the gold standard for diagnosing Morton’s neuroma. Of consequence is a histomorphologic study of 23 nerve biopsies from patients with typical Morton’s neuroma symptoms compared to 25 plantar nerve autopsies of individuals with no record of forefoot problems. The study revealed that nerve biopsies from MN patients had the same characteristics as those removed from autopsies. Tissue samples were identical and could not be distinguished one from the other. However, none of the excised tissue in this study was found to be normal; all had the pathological features of fibrotic tissue (thickened, scarred) [38]. Another study found identical histology when comparing Morton’s neuroma and control patients, observing the same fibrotic changes in the symptomatic patients as in the asymptomatic patients [39] From this research , the question arises as to whether the “neuroma” is actually the cause of the condition, caused by other conditions, or present in normal plantar nerves?

Searches with magnetic resonance imaging (MRI) for typical pathologies of Morton’s neuroma did not discover any diagnostic features (symptomatology). In a retrospective study of 85 foot MRI examinations, 33% of patients with no clinical evidence of Morton’s neuroma showed diagnostic “lesions” suggestive of the condition [40] In a study of 70 asymptomatic volunteers, 30% were diagnosed with Morton’s neuromas [41].

In MR imaging after neuroma resection, a neuroma was found in 26% of the asymptomatic and 50% in the symptomatic web spaces [42]. Thus, MRI reveals neuroma-like abnormalities in both symptomatic and asymptomatic patients [43].

Another retrospective study of steroid injections showed a 47% improvement in the recipients [44]. A study gauging symptom relief from a series of corticosteroid injections reported that 30% of the patients attested to total symptom relief [45]. In another study involving 60 patients, the results of conservative treatment were considered poor in 73% of the cases; thus, the authors recommended surgery as the initial treatment of choice [46].

Surgical removal of the neuroma is reported to provide satisfactory relief in 76 – 85% of the patients [47, 48]. Nonetheless, there were exceptions. In a study of 56 patients with excised neuromas, two thirds of the satisfied patients continued to have tenderness at the cut end of the common digital nerve; 75% were still limited in their choice of footwear; and 14% failed to demonstrate any notable improvement. Those who did not respond to surgery continued their pre-surgical use of steroids, lidocaine, and broad-toed shoes [49]. Other complications of surgery include numbness of the affected toes, postoperative infection, tenderness at the incision, keratosis (scarring) of the sole of the foot, recurrence of pain, and an amputation neuroma. Nearly 20% of the patients continued to feel pain after the first surgery, and few found pain relief with additional surgery [50]. In view of these findings, patients should be informed of the possible results of surgery, since adverse outcomes are common.

Patients searching for alternatives to the mainstream medical care are prudent to consider Prolotherapy for reasons of which practitioners of Prolotherapy are aware. First, Prolotherapists know that ligaments need to be tighter, shorter, and stronger. If the intermetatarsal ligament is weak and loose, however, the interdigital nerve rises up between the metatarsal heads where they can be compressed and, thereby, traumatized [51]. Abnormal metatarsal mobility that results from such weakened ligaments inflames the bursa (cushioning sac) between the heads, creating a space into which tissue from the plantar side of the foot can enter and is subsequently pinched by the metatarsal heads [52]. A fibrous build-up can occur when the weak ligaments allow tissue between bones to be rubbed and irritated. Because Prolotherapy strengthens weakened ligaments and connective tissues, it is a viable treatment option.

For Prolotherapists, Morton’s “neuroma” is most likely mechanically-induced from excessive motion between the metatarsals, combined with excessive weight-bearing stress on the forefoot [53]. Hypermobility of the forefoot predisposes a person to this condition, and Prolotherapy injections at the plantar and dorsal structures of the affected metatarsals will benefit the patient [54].

Prolotherapy has a long history of being utilized for unresolved foot and toe pain [55]. In a study of 19 patients with unresolved foot and toe pain, 63% of patients noted 75% pain relief from Prolotherapy [56] In a study undertaken precisely to evaluate the effectiveness of Dextrose Prolotherapy on Morton’s neuroma pain, 16 of the 20 patients with chronic plantar fasciitis who had failed previous conservative treatment reported good to excellent results from the Prolotherapy [57].

As a treatment, Prolotherapy has been utilized for approximately 100 years, with its modern injection protocols being formalized by George S. Hackett, MD in the 1950s [58, 59]. Increasingly popular in the US, Prolotherapy is used nationally and internationally in both alternative (integrative) and allopathic (orthodox) medical practice [60] The treatment is simple. When therapeutic solutions are injected into painful and tender ligaments, tendons, and joints—an inflammation develops, which causes healing cells to proliferate and strengthen damaged ligament, tendon, and joint structures [61], These injections improve both joint stability and biomechanics, ultimately decreasing pain [62]. In this way, Prolotherapy is a safe and practical option for hypermobile joints of the foot that cause persistent pain [63].


While the exact cause of Morton’s neuroma (MN) is still debated, this study confirms that the Hackett-Hemwall technique of Dextrose Prolotherapy not only reduces levels of pain for patients with MN, but also enhances other quality of life concerns. Conventional therapies, on the other hand—rest, weight loss, exercises for muscle strengthening, orthotics, massage therapy, physiotherapy, manipulation, analgesics, non-steroidal anti-inflammatory drugs, anti-depressant medications, trigger point and steroid injections, and various surgical treatments—often result in residual pain for the patients [64-66]. Patients with MN, therefore, are searching for alternative treatments to relieve the pain [67]. Patients unable to find relief with traditional treatments are also hesitant to use options like surgery.

Surgery for Morton’s neuroma, for instance, presents these significant risks: numbness of the affected toe, postoperative infection, incisional soreness, scarring, and recurring stump neuromas [68, 69]. Instead of these traditional options, patients dealing with Morton’s neuroma are now trying Prolotherapy [70]

As a promising option, Prolotherapy—using injections of an irritant—tightens, shortens, and strengthens ligaments, tendons, and joints. Prolotherapy works by stimulating the body to repair these soft tissues. The solution starts and accelerates healing through inflammation, triggering a healing cascade of effects. Initially, fibroblasts—immature cells capable of producing collagen fibers—proliferate. Hence, the term Prolotherapy arose from this observable process. Once collagen forms, it is woven (reticulated) into ligament and tendon tissue. In this manner, Prolotherapy has the potential to stop the disease process.

In some cases, preliminary, anecdotal evidence suggests that Prolotherapy can reverse Morton’s neuroma. In one double-blind animal study over a six-week period, for instance, Prolotherapy was shown to increase ligament mass by 44%, ligament thickness by 27%, and ligament-bone attachment by 28% [71]. In human studies on Prolotherapy, biopsies performed after the completion of Prolotherapy showed significant increases in collagen fiber and ligament diameter of 60% [72, 73]. These finding are especially significant since a potential cause of Morton’s neuroma is weakened ligaments [74, 75].

In this prospective study, the Hackett-Hemwall technique of Dextrose Prolotherapy used on patients averaging 1.5 years of unresolved pain with Morton’s neuroma was shown to improve their quality of life, which continued 13.3 months after their last session. The 17 patients treated with Prolotherapy reported significantly less pain, stiffness, disability, or use of other pain therapies, as well as improvements in walking, range of motion, ability to exercise, and performing activities of daily living.

Patients told that there were no other treatments for pain or that surgery was their only option achieved the same positive results. This study justifies the desirability and use of Prolotherapy for Morton’s neuroma pain. Future studies need to further substantiate these findings, especially if Prolotherapy enables Morton’s neuroma sufferers to avoid surgery and its possible adverse effects. Although a study with more patients in a controlled empirical setting is needed to document the efficacy of Hackett-Hemwall Dextrose Prolotherapy, this treatment should be considered, based on the substantial advantages and minimal drawbacks (e.g., aversion to needles), as well as the reduced risks and increased rewards of Prolotherapy over conventional treatments.


  1. Morris MA. Morton’s metatarsalgia.clinical orthopaedics and related research. 1977 127: 203-207. [PubMed]
  2. Spina R, et al. The effects of functional fascial taping on Morton’s neuroma: A case report. Australasian Chiropractic July 2002 10: 45-50. [Website]
  3. Hassouna H, Singh D. Morton’s metatarsalgia: pathogenesis, aetiology and current management. Acta Orthop Belg 2005 71: 646-655. [PubMed]
  4. Rout R, Tedd H, Lloyd R, Ostlere S, Lavis GJ, Cooke PH, Sharp RJ. Morton’s neuroma: diagnostic accuracy, effect on treatment time and costs of direct referral to ultrasound by primary care physicians. Pual Prim Care 2009 17: 277-282. [PubMed]
  5. Morscher E. Ulrich J, Dick W. Morton’s intermetatarsal neuroma: morphology and histological substrate. Foot Ankle Int 2000 21: 558-562. [PubMed]
  6. Decherchi P. Thomas George Morton’s metatarsalgia. Presse Med 2007 36: 1098-1103. [PubMed]
  7. Pastides P, El-Sallakh S, Charalambides C. Morton’s neuroma: A clinical versus radiological diagnosis. Foot Ankle Surg. 2012 18 :22-4. [PubMed]
  8. Beltran LS, Bencardino J, Ghazikhanian V, Beltran J. Entrapment neuropathies III; lower limb. Semin Musculoskelet Radiol 2010 14: 501-111. [PubMed]
  9. Nissen Kl. Plantar digital neuritis: Morton’s metatarsalgia. JBJS 1948 30: 84-93. [PubMed]
  10. Pace A, Scammell B, Dhar S. The outcome of Morton’s neurectomy in the treatment of metatarsalgia. Int Orthop. 2010 April; 34:511-5. [PubMed]
  11. Hassouna H, Singh D. Morton’s metatarsalgia: pathogenesis, aetiology and current management. Acta Orthop Belg 2005 71: 646-655. [PDF]
  12. Banks A, et al. McGlamry’s comprehensive textbook of foot and ankle surgery. Vol 2.Philadelphia,PA. Lippincott, Williams, and Wilkins 2001.
  13. Lee KT, Lee YK, Young KW, Kim HJ, Park SY. Results of operative treatment of double Morton’s neuroma in the same foot. 2009, J Orthop Sci 2009 14: 574-578. [PubMed]
  14. Kay D, Bennett GL. Morton’s neuroma. Foot Ankle Clin. 2003 Mar;8(1):49-59. [PubMed]
  15. Thomas JL, Blitch EL 4th, Chaney DM, Dinucci KA, Eickmeier K, Rubin LG, Stapp MD, Vanore JV. Diagnosis and treatment of forefoot disorders. Morton’s intermetatarsal neuroma. J Foot & Ankle Surgery 2009 48: 251-256. [PubMed]
  16. Adams WR 2nd. Morton’s neuroma. Clin Podiatr Med Surg. 2010 27: 535-545. [PubMed]
  17. MollicaMB. Morton’s neuroma: Getting patients back on track. Physician Sportsmedicine 1997 25: 76-82. [PubMed]
  18. Wu KK. Morton neuroma and metatarsalgia. Current Opinion Rheumatology 2000 12: 131-142.[PubMed]
  19. Terk M, Kwong PK, Suthar M, Horvath BC, Colletti PM. Morton neuroma: Evaluation with MR imaging performed with contrast enhancement and fat Suppression Radiology 1993 189:239-241. [PubMed]
  20. Clinical Practice Guideline Forefoot Disorders Panel, Thomas JL, Blitch EL 4th, Chaney DM, Dinucci KA, Eickmeier K, Rubin LG, Stapp MD, Vanore JV. Diagnosis and treatment of forefoot disorders. Morton’s intermetatarsal neuroma. J Foot & Ankle Surgery 2009 4: 251-256. [PubMed]
  21. Coady CM, Gow N, Stanish W. Foot problems in middle-aged patients: keeping active people up to speed. Phys Sportsmed 1998  26: 31-42. [PubMed]
  22. Lee KS. Musculoskeletal ultrasound: how to evaluate for Morton’s neuroma. AJR Am J Roentgenol. 2009 Sep; 193(3):W172. [PubMed]
  23. Fabie F, Accadbled F, Tricoire JL, Puget J. Anatomic danger of percutaneous section of the inter-metatarsal ligament for the treatment of Morton’s neuroma. Rev Chir Orthop Reparatrice Appar Mot 2007 93: 720-724.French. [Pubmed]
  24. Bossley CJ, Cairney PC. The intermetatarsophalangeal bursa – its significance in Morton’s metatarsalgia. JBJS 980 62B: 184-187. [PubMed]
  25. Schuh R, Trnka HJ. Metatarsalgia: distal metatarsal osteotomies Foot Ankle Clin. 2011 16: 583-595. [PubMed]
  26. Birbilis T, Theodoropoulou E, Koulalis D. Forefoot complaints-the Morton’s metatarsalgia. The role of MR imaging. Acta Medica (Hradec Kralove) 2007 50: 221-222. [PubMed]
  27. Nissen Kl. Plantar digital neuritis: Morton’s metatarsalgia. JBJS 1948 30: 84-93. [PubMed]
  28. Claustre J, Bonnel F, Constans JP, Simon L. The intercapital metatarsal space: anatomical and pathological aspects. Rev Rhum Mal Osteoartic 1983 50: 435-440. [PubMed]
  29. Mendicino SS, Rockett MS. Morton’s neuroma. Update on diagnosis and imaging. Clin Podiatr Med Surg 1997 14: 303-311. [PubMed]
  30. Schreiber K, Khodaee M, Poddar S, TweedEM. Clinical Inquiry. What is the best way to treat Morton’s neuroma? 2011 60: 157-158. [PubMed]
  31. Lee M, Kim S, Huh YM, Song HT, Lee SA, Lee JW, Suh JS. Morton neuroma: Evaluated with ultrasonography and MR imaging. Korean J Radiolog 2007 8: 148-155. [PubMed]
  32. Summers A. Diagnosis and treatment of Morton’s neuroma. Emerg Nurse  2010 18: 16-17. [PubMed]
  33. Hackett GS, Henderson DG. Joint stabilization: An experimental, histologic study with comments on the clinical application in ligament proliferation. Amer J Surg 1955 89: 968-973. [PubMed]
  34. Hughes R; Ali K; Jones H; Kendal S; Connell D. Treatment of  Morton’s neuroma with alcohol injection under sonographic guidance: Follow-up of 101 cases. Am J Roentgenology 2007 188:1535-1539.[PubMed]
  35. Hyer C, Mehl LR, Block AJ, Vancourt RB. Treatment of recalcitrant intermetatarsal neuroma with 4% sclerosing alcohol injection: A pilot study. J Foot & Ankle Surgery 2005 44: 287-291. [PubMed]
  36. Dockery GL. The treatment of intermetatarsal neuromas with 4% alcohol sclerosing injections. Journal of Foot and Ankle Surgery 1999 38:403-408. [PubMed]
  37. Thomas CE, et al. Interventions for the treatment of Morton’s neuroma (review). The Cochrane Library 2005 Issue 2:1-14.
  38. Morscher  E, Ulrich J, Dick W. Morton’s intermetatarsal neuroma: Morphology and histological substrate. Foot Ankle Int 2000 21: 558-562. [PubMed]
  39. Bourke G, Owen J, Machet D. Histological comparison of the third interdigital nerve in patients with Morton’s metatarsalgia and control patients. Aust NZ J Surg 64: 421-424. [PubMed]
  40. Bencardino J, Rosenberg ZS, Beltran J, Liu X, Marty-Delfaut E. Morton’s neuroma: Is it always symptomatic? Am J Roentgenology 2000 175: 649-653. [PubMed]
  41. Zanetti M, Strehle JK, Zollinger H, Hodler J. Morton neuroma and fluid in the intermetatarsal bursae on MR images of 70 asymptomatic volunteers. Radiology 1997 203: 516-120. [PubMed]
  42. Espinosa N, Schmitt JW, Saupe N, Maquieira GJ, Bode B, Vienne P, Zanetti M. Morton neuroma: MR imaging after resection—postoperative MR and histologic findings in asymptomatic and symptomatic intermetatarsal spaces. Radiology 2010 255: 850-856. [PubMed]
  43. Resch S, Stenstrom A, Jonsson A, Jonsson K.  The diagnostic efficacy of magnetic resonance imaging and ultrasonography in Morton’s neuroma: a radiological-surgical correlation. Foot Ankle Int 1994 15: 88-92. [PubMed]
  44. Bennett GL, Graham CE, Mauldin DM. Morton’s interdigital neuroma: A comprehensive treatment protocol. Foot Ankle Int 1995 16: 760-763. [PubMed]
  45. GreenfieldJ,  Rea J Jr, Ilfeld FW. Morton’s interdigital neuroma: Indications for treatment by local injections versus surgery. Clinical Orthopaedics Rel Research 1984 185:142-144. [PubMed]
  46. Gaynor R, Hake D, Spinner SM, Tomczak RL. A comparative analysis of conservative versus surgical treatment of Morton’s neuroma JAPMA  1989 79: 27-30. [PubMed]
  47. Monacelli G, Cascioli I, Prezzemolo G, Spagnoli A, Irace S. Surgical treatment of Morton’s neuroma: our experience and literature review. Clin Ter 2008 159: 165-167. Article in Italian. [PubMed]
  48. Faraj A, Hosur A.  The outcomes after using two different approaches for excision of Morton’s neuroma. Chinese Medical Journal 2010 123: 2195-2198. [PubMed]
  49. Mann R, Reynolds JC. Interdigital neuroma-a critical clinical analysis. Foot & Ankle 1983 3: 238-243. [PubMed]
  50. Johnson J, Johnson KA, Unni KK. Persistent pain after excision of an interdigital neuroma – results of reoperation. JBJS 1988 70A: 651-657. [PubMed]
  51. Read JW, Noakes JB, Kerr D, Crichton KJ, Slater HK, Bonar F. Morton’s metatarsalgia: sonographic findings and correlated histopathology. Foot Ankle Int. 1999  2093:153-161. [PubMed]
  52. Mulder JD. The causative mechanism in Morton’s metatarsalgia. JBJS 1951 33B: 94-95. [PubMed]
  53. Wu KK. Morton interdigital neuroma: A clinical review of it etiology, treatment and results. J of Foot and Ankle Surgery 1996 35(2): 112-119; discussion 187-8. [PubMed]
  54. Hackett G, et al. Ligament and tendon relaxation treated by prolotherapy. 5th ed.Oak Park,IL. Gustav A. Hemwall 1992
  55. Hauser R, et al. Prolo your pain away! 3rd edition.Oak Park,IL.BeulahLand Press 2007 139-147.
  56. Hauser R,  A retrospective observational study on Hackett-Hemwall dextrose prolotherapy for unresolved foot and toe pain at an outpatient charity clinical in rural Illinois. J of Prolotherapy 2011 3: 543-551. [Website]
  57. Ryan M. Sonographically guided intratendinous injections of hyperosmolar dextrose/lidocaine: A pilot study for the treatment of chronic plantar fasciitis. Brit J Sports Medicine 2009 43: 303-306.  [Website]
  58. Hauser RA. Punishing the pain. Treating chronic pain with Prolotherapy. Rehab Manag 1999 12: 26-28. [PubMed]
  59. Rabago D. Prolotherapy in primary care practice. Primary Care 2010 37: 65-80. [PubMed]
  60. Schnirring L. Are your patients asking about prolotherapy? Physician Sportsmedicine 2000 28:15-17.
  61. Rabago D, Best TM, Beamsley M, Patterson J. A systematic review of prolotherapy for chronic musculoskeletal pain. Clin J Sports Medicine 2005 15: 376-380. [PubMed]
  62. Centeno CJ, Elliott J, Elkins WL, Freeman M. Fluoroscopically guided cervical prolotherapy for instability with blinded pre and post radiographic reading. Pain Physician 2005 8: 67-72.  [PubMed]
  63. Tsatsos G. Prolotherapy in the treatment of foot problems. JAPMA 2002  92: 366-368. [PubMed]
  64. Martin E. Pharmacologic management of foot pain in the older patient. J Am Podiatr Med Assoc 2004 94(2):98-103.
  65. Drury AL. Use of homeopathic injection therapy in treatment of Morton’s neuroma. Altern Ther Health Med. 2011 17:48. [PubMed]
  66. Jannink M. Effectiveness of custom-made orthopaedic shoes in the reduction of foot pain and pressure in patients with degenerative disorders of the foot. Foot Ankle Int 2006 27: 974-979. [PubMed]
  67. Kay D, Bennett GL. Morton’s neuroma Foot Ankle Clin. 2003  8: 49-59. [PubMed]
  68. Singh SK, Loli JP, Chiodo CP. The surgical treatment of Morton’s neuroma. Current Orthopaedics 2005: 19 379-384.
  69. Hughes R; Ali K; Jones H; Kendal S; Connell D. Treatment of Morton’s neuroma with alcohol injection under sonographic guidance: Follow-up of 101 cases. American Journal of Roentgenology 2007 188: 1535-1539. [PubMed]
  70. Hauser, RA, Hauser, MA. Prolo Your Pain Away!, 2007 3rd edition Beulah Land Press,Oak ParkIL pg 144-145.
  71. Liu Y. An in situ study of the influence of a sclerosing solution in rabbit medial collateral ligaments and its junction strength. Connective Tissue Research1983 2: 95-102. [PubMed]
  72. Maynard JA, Pedrini VA, Pedrini-Mille A, Romanus B, Ohlerking F. Morphological and biochemical effects of sodium morrhuate on tendons. J  Orthopaedic Research. 1985 3: 236-248.  [PubMed]
  73. Hauser R, et al. Prolo your pain away! 3rd edition.Oak Park,IL.BeulahLand Press 2007 139-147.
  74. Wu KK. Morton’s interdigital neuroma: a clinical review of its etiology, treatment and results. J Foot Ankle Surg 1996 35:187-188. [PubMed]
  75. Hauser RA, Hauser MA, Cukla JK. A retrospective observational study on Hackett-Hemwall Dextrose Prolotherapy for unresolved foot and toe pain at an outpatient charity clinic in rural Illinois. J Prolotherapy. 2011 3: 543-551.  [Website]
  76. Ravin T, Cantieri M, Pasquarello G. Principles of Prolotherapy. Denver,CO:AmericanAcademy of Musculoskeletal Medicine; 2008.

Address Correspondence to: : Ross Hauser, MD, Caring Medical, 715 Lake St., Suite 600, Oak Park, IL 60301

1Medical Director, Caring Medical & Rehabilitation Services; Editor-in-Chief, Journal of Prolotherapy
2Private Practice, Medical Editor, Ohio University Clinical Assistant Professor, Bowling Green State University Adjunct Assistant Professor
3Registered Nurse, Caring Medical & Rehabilitation Services

© The Foot and Ankle Online Journal, 2012

Talar Neck Fracture Reduced and Stabilized with an Ilizarov External Fixator: A case report with three year follow up

by Sutpal Singh, DPM, FACFAS, FAPWCA1 , Chih-Hui (Jimmy) Tsai, DPM2,
Albert Kim, DPM3, Timothy Dailey, DPM4

The Foot and Ankle Online Journal 3 (7): 1

The authors report a case of a Grade 3 Tscherne, isolated Hawkins Type III fracture that was treated with open reduction and external fixation. The Ilizarov technique simplified the surgery by allowing the reduction of the diastasis using a tensioned olive wire, providing distraction of fracture bones externally, and aid in reduction of the talus without the need for multiple, extensive dissection. The patient responded very well to the surgery, despite occurrence of avascular necrosis of the talus and three years status post surgery. The patient has good range of motion, is pain-free, and ambulates without difficulty despite having avascular necrosis.

Key words: Talar fracture, Hawkins classification, Hawkins sign, Ilizarov technique, diastasis, avascular necrosis.

Accepted: June, 2010
Published: July, 2010

ISSN 1941-6806
doi: 10.3827/faoj.2010.0307.0001

Talar fractures have been described since the early 1600’s. [1] In early literature, open talar fractures had an 84% mortality rate. [3] Due to the high mortality rate, surgeons advised extreme measures such as below knee amputations or talectomy. [1] Since then, the surgical technique for these fractures has vastly improved. However, these types of fractures, thought not fatal, still prove to be very challenging today. Talar fractures are rare, making up only 3% of all foot fractures.

Talar fractures can be classified as open or closed. The Tscherne soft tissue classification system describes both open and closed fractures. [9,17] (Table 1) For the closed soft tissue injuries, Tscherne uses a grading system from 0-3 and is based on the amount of the injury. Grade 0 is minimal soft tissue damage from indirect violence. Grade 1 is a superficial abrasion or contusion caused by pressure from within. Grade 2 is a deep contaminated abrasion associated with local skin or muscle contusion and may encompass a compartment syndrome. Grade 3 consists of extensive skin contusion or crushing, underlying severe muscle injury, decompensated compartment syndrome, and associated vascular injury. [9]

Table 1  Tscherne Classification.

Talar fractures can be further divided into three anatomical locations: neck, body and head. Talar neck fractures comprised of 50% of all talar fractures. [2] The most commonly used classification system for talar neck fractures is Hawkin’s Classification (Table 2). This classification has four types, which are differentiated by the degree of displacement. Type I is a non-displaced talar neck fracture. Type II is a talar neck fracture with mild displacement and subluxing from the subtalar joint. Type III is displacement of the talar body with dislocation of subtalar and ankle joint. Type IV is a combination of Type III with dislocation of the talonavicular joint. [1] The higher the grade, the greater the risk is for complications.

Table 2  Hawkins Classification. (AVN – avascular necrosis)

Blood supply to the talus may be an issue if one delays reduction or inadequately treats these fractures. [3] Avascular necrosis (AVN) of the talar body and arthrosis after displaced talar neck fractures is quite common; the higher the grade, the larger chance of AVN. In an article by Gholam et al, they described nine cases of Hawkins Type III fractures, and eight of the nine developed arthrosis.3 In Hawkins Type I fractures, it is quite rare to see AVN. However in Hawkins Type II, there is a 15.8%-75% chance. [1] In Hawkins Type III, the chance of AVN increases to 33-75%. [1]

Hawkins Type IV has the highest chance, reaching almost 100% due to the amount of displacement and disruption of the blood supply to the talus. [1] Subchondral atrophy of the talar dome, also called Hawkins Sign, indicates an intact blood supply to the talus. [3] It is essential to be aware of AVN so it can be treated promptly.

Various treatment options exist for talar neck fractures. Some surgeons prefer using a compression screw across the fracture fragment, while others prefer a plate. In a study performed by Charlson, et al., plate fixation and screw fixation were compared. No statistical difference between either method was found. Plate fixation may provide more control of the anatomical alignment, but has no biomechanical advantage over screws alone. [4] There are very few cases reported in the literature of an isolated talar neck fractures treated with external fixation. However, there are many cases of multiple fractures (talus with calcaneus or talus with medial/lateral malleolus) successfully treated with external fixation. The purpose of this paper is to report a Grade 3 Tscherne, isolated and displaced Hawkins Type III talar neck fracture that was specifically treated with open reduction and external fixation. By determining how much soft tissue injury and the extent of talar fracture, external fixation can be more superior to internal fixation. In this case, the Ilizarov technique is ideal when there is soft tissue injury, vascular compromise, and displaced talar neck fracture.

Case Report

The patient is a 40 year-old correctional officer who was riding a recreational vehicle at the time of his injury. (Fig. 1A and B) He reported jumping off the vehicle due to faulty breaks, resulting in a severe talar neck fracture. (Fig. 2A and B). The mechanism of the traumatic injury was that of hyperdorsiflexion of the foot against the tibia in an axial force with impingement of the talar neck.


Figure 1A and B  Note the severe contracture of all the toes. (A) Note the contracted hallux and lack of blood flow to the medial ankle where the talar body is compressing the skin and posterior tibial artery. (B)


Figure 2A and B Non-weight bearing lateral view.  Note the overlap of the talus onto the calcaneus. (A) Note the fracture fragments in the ankle. (B)

As the force continued, there was a medial and dorsal displacement fracture of the talus, and disruption of the interosseous talocalcaneal ligament. Also, the posterior and subtalar joint capsule were disrupted. As the ankle supinated, there was increased force of the talar neck against the medial malleolus resulting in subluxation of the subtalar joint and ankle joint. It was quite severe such that the medial ankle was blanching and becoming necrotic.

The flexor hallucis longus (FHL) and flexor digitorum longus (FDL) tendons were also contracted, such that the hallux and lesser toes were severely plantarflexed.

The dorsalis pedis artery was palpable, but the posterior tibial (PT) artery was being compressed and not palpable or heard using a Doppler. There was soft tissue damage and vascular supply was compromised. The patient opted to have surgery and informed consent was obtained from him to allow us to study and present this case. An open reduction was performed with the use on an Ilizarov frame immediately.

Surgical Technique

A large curvilinear incision was made on the medial ankle overlying the talus, extending distally and proximally from the area of blanching. (Fig. 3) The incision was deepened to the subcutaneous tissue and then to the deep tissue. The entire talar dome was noted at the incision site. (Fig. 4) The deep tissue was retracted. Once past the deep tissue, we noted that the posterior tibial artery was being compressed by the talar body. The talar body was exposed, and it was completely displaced and rotated out of the ankle and subtalar joint. There was a large hematoma and multiple small fracture fragments in the ankle joint. The hematoma was evacuated, and the small fracture fragments were removed. The wound was also copiously irrigated with bacitracin-impregnated saline. Then, attempt at relocating the dislocated and fractured talus was performed; however, there was much contraction of the tibia onto the calcaneus that it was extremely difficult to retract. Thus an external fixator was employed to distract the tibia from the calcaneus in order to relocate the talus.

Figure 3  1)  Medial surface of the talus.  2) Anterior or distal surface of the talus.  3) Lateral surface of the talus.    4) Posterior process of the talus with entrapped flexor hallucis longus (FHL) and  posterior tibial (PT) tendons and PT artery.   Note that the toes are at the upper left and the leg is at the lower right.

Figure 4  Dislocated and rotated talus.  1) Medial surface of the talus where the deltoid ligament is shown to be torn.  2) The posterior aspect of the talus: The posterior tibial tendon, posterior tibial artery and FHL are entrapped.  3) Lateral surface of the talus.  4) Talar dome.  5) Anterior surface of the talus.

First, two tibial rings were applied to the lower leg. Then a foot plate was applied, and all the wires were appropriately tensioned. Several distraction rods were used to connect the tibial rings to the foot plate, and then the foot was distracted. By distracting the tibia from the calcaneus, it made it much easier to rotate the talus and slide it between the tibia and calcaneus back into anatomical alignment. The fractured talus was anatomically reduced and held in place by an external fixator. Once the fracture was reduced, the severe skin tension on the medial side of the foot decreased.

A Doppler placed over the PT artery now showed good blood flow. Also, the FHL and FDL tendons became more relaxed, and the contracture over the hallux and lesser toes were reduced. A series of photographs shows the alignment of the Ilizarov frame directly after surgery (Figs. 5A and B, 6) and at 3 weeks after surgery. (Figs. 7A and B)


Figure 5A and B  Post-operative site with the Ilizarov Frame.

Figure 6  Post-operative reduction of the talar fracture in good alignment.


Figure 7A and B  Three weeks post- operative view.


A one year follow-up showed that his hallux range of motion was normal and his ankle healed in good alignment and anatomical position. This was accompanied with good range of motion, without pain, and with normal ambulation. However, despite the proper care and good post operative alignment, there was still sclerosis of the talar body which indicated that there was indeed avascular necrosis present. He remained non-weight bearing for 6 months and then weight bearing using a pneumatic cam walker for an additional 6 months. After this the patient went back to working 8 hours a day as a corrections officer and it was explained to him of the possible collapse and further complications from the osteonecrosis of the talus and to limit any vigorous activities. He was again followed up at 2 years and at 3 years after the initial traumatic event. He did have an increase in plantar flexion, and adequate dorsiflexion towards the end of the follow-up. He had no pain and was satisfied with the surgical outcome. He however, did have sclerosis of the talus but without any evidence of collapse. (Table 3)

Table 3  Patient 3 year follow-up results. (DF – dorsiflexion, PF – plantarflexion, AVN – avascular necrosis)


The complex nature of high energy talus fractures can pose complications that can challenge most foot and ankle surgeons. The complexity arises because of the blood supply to the talus being extremely vulnerable after a traumatic injury. [10] Short term complications can result in skin necrosis, wound dehiscence, and infection. [11,12] Additional complications of comminuted fractures involving the talar neck and body carry a risk of AVN due to the retrograde blood supply. [13] Injury to the joints surrounding the talus can cause irreversible osteochondral damage that could lead to possible early post traumatic arthritis or arthrosis. In this report, we have a patient with a closed talar neck fracture with vascular comprise. The case is further complicated by additional factors that included the medial ankle developing blanching and ultimately becoming necrotic, the posterior tibial artery being compressed, and the FHL and FDL tendons being contracted such that the hallux and lesser digits were severely plantarflexed.

Treatment options evolved from reduction and immobilization, to limited fixation, and currently, open reduction internal fixation being performed on most talar fractures. [14] Included in the literature are recommendations for primary arthrodesis or talectomy for severe talar fractures. [15] In this case, an external fixator was applied due to the severe contracture of the tibia onto the calcaneus. The Ilizarov external fixator allowed for distraction of the tibia from the calcaneus and this allowed for reduction and rotation of the talar body in its anatomical location.

Also, because of the volatile nature of the fracture and the additional soft tissue complications and its increased probability for an osteonecrosis sequelae, external fixation was utilized because it is commonly implemented and indicated for compromised soft tissue structures and gross instability. [16]

In this case, the patient was destined to have avascular necrosis due to the talar neck fracture which according to the literature has up to a 75% chance to develop the condition even with the utmost care and precautions. [1,14] This was exacerbated by the ruptured medial deltoid ligaments causing a dislocation of the talus. In examining the talus, it is a unique bone in the foot in that it has no muscular attachments with about 60% of the talus is covered with articular cartilage. These anatomical features make the talus vulnerable to dislocation. Extreme forces can cause dislocation of the talus out of the ankle mortise with disruption of the strong ligamentous attachments and this may have accounted for the medial deltoid ligament ruptures present in this patient.

This dislocation most likely caused tremendous vascular damage to this already intricate arrangement of vessels that are highly vulnerable to injury. The anterior tibial, PT, and perforating peroneal arteries serve as the vascular supply to the talus. The artery of the tarsal canal is a branch of the PT, and it supplies most of the talar body, the medial talar wall, and the undersurface of the talar neck. The artery of the tarsal canal anastamoses with the artery of the sinus tarsi, which is a branch of the perforating peroneal artery, and these vessels supply the inferior aspect of the talar body and neck. [18]

As the talus dislocates from the ankle mortise, there is sequential failure of the talar blood supply. Since the blood supply to bone and soft tissue are so intertwined, it has been noted that osteonecrosis was highest in cases in which no soft tissues remained attached to the talus. [19]

In this patient, this risk of avascular necrosis was increased and seen when the soft tissue along the medial aspect of the foot became de-vascularized and necrotic.

It is recommended that the patient should be non-weight bearing or protected weight bearing until the avascular necrosis resolves, [19,20] however there is no definitive evidence to suggest that full weight bearing with avascular necrosis leads to secondary complications such as collapse of the talar dome and tibiotalar arthritis. [21] This is further exemplified by this case where the patient, even at a three year follow up with avascular necrosis of the body of the talus, shows that his ankle is in good alignment, has not collapsed, shows no evidence of varus or valgus, has good range of motion, no pain, and ambulates normally. (Figs. 8A and B, 9, 10A and B)


Figure 8A and B   Six months after surgery.

Figure 9 Three years after the initial injury.


Figure 10A and B  Weight-bearing lateral view of the ankle, three years status post-operative, shows AVN of the talus, but good alignment.  There is no pain, no collapse of the talus, and the patient has good ankle range of motion. (A) Weight-bearing anterior posterior view of the ankle, three years status post-operative shows AVN of the talus, but good ankle joint congruity. (B)

By using the Ilizarov External Fixator, the talus was immobilized and held in place such that no axial pressure was placed onto the talus while healing took place.


Talar fractures are very complicated with a high incidence of AVN. We feel that if there is much difficulty in reducing the talar fracture from the tight tibial collapse onto the calcaneal surface, an external fixator is very beneficial in distracting the tibia from the calcaneus. In the above case, we used the multiplaner Ilizarov external fixator. He did have a severe fracture and dislocation of the talus which eventually resulted in AVN. At this moment, the patient states that he is pain free, and examination showed good ankle and subtalar joint range of motion. It is very important to have the patient frequently visit the office to make sure the talus is not collapsing and to explain to the patient that possible future surgeries, such as total ankle joint implant, subtalar joint arthrodesis, triple arthrodesis, or ankle fusion, may be necessary if the talus collapses as a consequence of AVN.


1. Banks AS, Downey MS, Martin DE, Miller SJ. McGlamry’s Comprehensive Textbook of Foot and Ankle Surgery. Vol 1, 3rd edition. Philadelphia: Lippincott Williams and Wilkins; 2001.
2. Juliano P, Dabbah M, Harris TG. Talar neck fractures. Foot Ankle Clinics 2004 9: 723-736.
3. Pajenda G, Vecsei V, Reddy B, Heinz T: Treatment of talar neck fractures: Clinical results of 50 patients. J Foot & Ankle Surg 2000 39(6) 365-375.
4. Charlson MD, Parks BG, Weber TG, Guyton GP. Comparison of plate and screw fixation and screw fixation alone in a comminuted talar neck fracture model. Foot Ankle Int 2006 27 (5): 340-343.
5. Marion H. Talar Shift: The stabilizing role of the medial, lateral and posterior ankle structures. Clinical Orthopedics Rel Res 1990 257: 177-183
6. Comfort TH, Behrens F, Gaither DW, Denis F, Sigmond M. Long term results of displaced talar neck fractures. Clin Orthopedics Rel Res 1985 199: 81-87.
7. Grob D, Simpson LA, Weber BG. Operative treatment of displaced talus fractures. Clin Orthopedics Rel Res 1985 199: 88-96.
8. Greenleaf J, Berkowitz RD, Whitelaw GP, Seidman GD. Hawkins Type III Fracture – Dislocation of the talus and diastasis of the tibiofibular joint without concomitant fracture of the malleolei. Clin Orthopedics Rel Res 1992 279: 254-57.
9. Frank T, Joseph B. Soft-tissue injury associated with closed fractures: Evaluation and management. J Am Academy of Orthopedic Surgeons. 2003 V:11 N:6, 431-438.
10. Baumhauer JF, Alvarez RG. Controversies in treating talus fractures. Orthop Clin North Am 1995 26(2): 335-351.
11. Fulkerson EW, Egol KA: Timing issues in fracture Management: a review of current concepts. Bulletin of the NYU hospital for joint diseases 67(1): 58-67, 2009.
12. Roberts C, Pape H, Jones A, Malkani A, Rodriguez J, Giannoudis P: Damage control orthopaedics evolving concepts in the treatment of patients who have sustained orthopaedic trauma. JBJS 2005 87(2): 434-449.
13. Elgafy H, Ebraheim NA, Tile M, Stephen D, Kase J. Fractures of the talus: experience of two level 1 trauma centers. Foot Ankle Int 2000 21(12):1023-1029.
14. Vallier HA, Nork SE, Barei DP, Benirschke SK, Sangeorzan BJ: Talar neck fractures: results and outcomes. JBJS 2004 86A(8): 1616-1624.
15. Gunal I, Atilla S, Arac S, Gursoy Y, Karagozlu H: A new technique of talectomy for severe fracture-dislocation of the talus. JBJS 1993 75B (1): 69-71.
16. Sirkin M, Sanders R, DiPasquale T, Herscovici D: A staged protocol for soft tissue management in the treatment of complex pilon fractures. J Orthopaedic Trauma 2004 18 (8 Suppl): S32-38.
17. Tscherne H, Schatzker J (editors). Major Fractures of the Pilon, the Talus, and the Calcaneus: Current Concepts of Treatment. Berlin, Germany: Springer-Verlag, 1993.
18. Schuberth J, Alder D. Talar fractures. In: Banks A, Downey M, Martin D, Miller S editor. McGlamry’s Comprehensive Textbook of Foot & Ankle Surgery. Philadelphia: Lippincott Williams and Wilkins; 2002, 1866-1867.
19. Hiraizumi Y, Hara T, Takahashi M, Mayehiyo S. Open total dislocation of the talus with extrusion: A report of two cases. Foot Ankle Int 1992 13: 473-477.
20. Brewster N, Maffulli N. Reimplantation of the totally extruded talus. J Orthop Trauma 1997 11: 42–45.
21. Vallier H, Barei D, Bernischke S, Sangeorzan B. Surgical treatment of talar body fractures. JBJS 2003 85A: 1716-1724.

Address Correspondence to: Sutpal Singh, DPM. FACFAS. FAPWCA

1  Chief Ilizarov Surgical Instructor at Doctors Hospital West Covina, Fellow of the American College of Foot and Ankle Surgeons, Fellow American Professional Wound Care Association. Private practice in Southern California.
2  Doctor of Podiatric Medicine (R3) ,Foot and Ankle Medicine and Surgery, Doctors Hospital of West Covina (PM&S-36), West Covina, CA
3  Doctor of Podiatric Medicine (R2) Foot and Ankle Medicine and Surgery, Doctors Hospital of West Covina (PM&S-36), West Covina, CA
Doctor of Podiatric Medicine (R1) Foot and Ankle Medicine and Surgery, Doctors Hospital of West Covina (PM&S-36), West Covina, CA

© The Foot and Ankle Online Journal, 2010

Open Extrusion of the Talus: A case report

by Mark A. Hardy, DPM, FACFAS1 , Stella Chuida, DPM2

The Foot & Ankle Journal 1 (12): 1

Open talar extrusion is an uncommon injury that the foot and ankle surgeon may encounter. Possible sequelae of this injury include arthrosis, osteomyelitis and avascular necrosis (AVN). The authors present a case involving an open lateral talar extrusion, with further discussion including mechanism of injury, anatomical considerations, incidence of AVN and perioperative concerns.

Key words: Open dislocation, talus dislocation, avascular necrosis, Hawkin’s sign

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Accepted: November, 2008
Published: December, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0112.0001

Case Report

A 41-year-old male with past medical history of hypertension presented to the emergency department after sustaining a right ankle injury while playing basketball. He reported landing on an inverted foot after attempting a ‘dunk’ shot during the game. He then noted exposure of bone at the lateral aspect of his ankle. He denied losing consciousness or sustaining any other injuries. He did admit to having consumed moderate amounts of alcohol prior to the injury.

At presentation, he was in moderate distress due to pain, found to be alert and oriented to person, place and time. Vital signs were stable.

Examination of the right foot and ankle revealed medial dislocation of the foot on the ankle and a 15cm wound to the lateral aspect of the ankle. (Figs.1 and 2) At the proximal aspect of the wound, the distal fibula, talar dome and posterolateral talar body could be visualized.


Figures 1 and 2   Gustillo-Anderson Type III open talar extrusion injury.

The base of the wound was beefy red and the wound margins viable. The open wound appeared relatively clean except for a sock embedded in the wound and was without debris or foreign bodies. There was no evidence of neurovascular compromise. Pedal pulses were palpable, capillary refill time was brisk and protective sensation intact.

Radiograph of the right ankle revealed complete dislocation of the talus from the tibiotalar, subtalar and talonavicular articulations. (Fig. 3)

Figure 3   Plain film radiographs demonstrating talar extrusion with disruption of the tibiotalar, subtalar and talonavicular joints.

The talus was dislocated laterally and anteriorly extruded through the skin and rotated approximately 90 degrees clockwise. The calcaneus was displaced medially and appeared to retain its normal relationship with the remaining portions of the midfoot. No definitive or occult fracture was identified. The tibia and fibula were intact and demonstrated a normal relationship, suggesting that the inferior tibiofibular ligaments were maintained. A computed tomography (CT) scan of the right ankle was also performed which confirmed the absence of any definitive fractures and the complete dislocation of the talus. (Figs. 4 and 5)


Figures 4 and 5   CT scans demonstrating the talar extrusion and absence of fracture(s).

Upon admission, the patient received Ancef and Gentamycin per the senior author’s open fracture protocol, in addition to ensuring tetanus prophylaxis was up to date. He was given intravenous Morphine for pain control. Dosing of aminoglycosides is not well defined in regards to Gustillo-Anderson type II and III open injuries11 – it is generally 3-5 mg/kg of body weight in divided doses for 3 days. However, high single dosing of aminoglycosides has been shown to be more effective than divided low dosing (6mg/kg given once daily). This is because the bacteriocidal effect is a result of the peak aminoglycoside concentration to minimum inhibitory concentration, not the trough levels. Moreover, nephrotoxicity and ototoxicty are a result of sustained trough concentration and not the peak concentration.

He was taken to the operating room for emergent irrigation, debridement and relocation of the talus. The wound was irrigated with 10 liter of normal saline under pulsatile lavage and wound debridement was performed appropriately. A small osteochondral depression was noted at the lateral shoulder of the talus. This was excised along with any remaining loose cartilage. The talus was then relocated with relative ease by mild plantarflexion of the forefoot and inversion of the heel.

This was performed after the calcaneus and distal foot had been relocated under the tibia and fibula. Next, a Jet X™ (Smith and Nephew, Memphis, TN) external fixator was applied in a delta configuration to the right lower extremity. (Figs. 6 and 7)


Figures 6 and 7   Intraoperative and postoperative images after reduction and stabilization with a Jet X™ (Smith and Nephew, Memphis, TN) external fixator in a simple delta frame configuration.

A Steinman pin was driven from the dorsal distal navicular into the talus to maintain the reduction. (Fig. 8) The wound was then irrigated with another 6 liter of normal saline with wound cultures taken. The wound was left open with plans for delayed primary closure in approximately three days.

Figure 8   Postoperative radiographs after reduction and stabilization with a Jet X™ external fixator in a simple delta frame configuration.  The large Steinman pin is seen through the calcaneus after reduction of the body of the talus.

The patient was admitted to the surgical floor. During his hospital stay, he had a low grade fever and mild leukocytosis during the first 24 hours, but was afebrible with a normal white count thereafter. Wound cultures were negative over three days. The wound was then closed four days later after further irrigation, at which time antibiotics were discontinued.

Postoperatively, the patient was kept non-weight bearing to the right lower extremity. The wound healed uneventfully without any signs of superficial or deep infection.

Serial radiographs showed no evidence of osteolysis or sclerotic changes of the talus. He began using an Exogen™ bone growth stimulator (Smith and Nephew, Memphis, TN) one and half months after the initial surgery. At two months, the external fixator was removed and the patient was allowed gradual weight bearing in a fracture boot for an additional six weeks. However, he did develop superficial soft tissue infections of the transcalcaneal and distal tibial pin sites.

The calcaneal wound resolved with oral antibiotic therapy and the distal tibia pin sites healed after curettage and packing with vancomycin impregnated beads.

A positive Hawkins sign was noted on radiographs three months after the initial injury (Figs.9 and 10) 3½ months postoperatively, he began ambulating in an ankle stirrup and proceeded to heal uneventfully with a full return to activities.

Figure 9   One month after removal of the external fixator demonstrating an early Hawkin’s sign, as best seen on the mortise view.

Figure 10   Another radiographic view one month after removal of the external fixator demonstrating an early Hawkins sign.


According to Wagner, et al, [1] the talus forms the peak of the hindfoot skeleton and transfers the whole weight of the body by itself onto the foot bones. The talus is responsible for the transfer of weight from the tibia to the foot via dissipation of forces to the subtalar, the calcaneocuboid and talonavicular joints. Three-fifths of the talus is covered by articular cartilage.

It is the only bone in the lower extremity without any muscular attachments, making it somewhat vulnerable in the presence of injury. [2] Despite this, pure total dislocation without any associated fractures is rare due to the strong ligamentous attachment of the talus to adjoining midfoot bones [3] and probably due to the amount of force necessary for such an injury.[4] Seventy five percent of these injuries are usually open injuries or the skin may be so tented over the talus that sloughing ultimately results.[5]

No specific mechanism of injury has been described. It is thought that total talar dislocation is the end point of maximum pronation or supination injuries; the final point of a continuum of forces that begin with dislocation of the subtalar joint.[5] A stronger injuring force applied over a long period of time eventually forces the talus out of the mortise. Injuries can occur after falling from a height, in motor vehicle accidents or sometimes during normal physical activities.

Osteomyelitis and AVN of the talus are legitimate concerns that can affect patient morbidity when treating these injuries. Other considerations include disruption to the vascular supply of surrounding soft tissue, possible damage to lymphatics, ligaments, joint capsule and tendons; all of which increase the risk of infection of both the bone and soft tissue. The vascular supply of the talus has been well described. Although there is variation in anatomy, five major vessels supply the talus. The extraosseous vascular supply comes from the anterior tibial, the posterior tibial and the perforating peroneal arteries. The artery of the sinus tarsi is an anastamosis of the lateral tarsal artery and the perforating peroneal artery. This in turn, anastamoses with the artery of the tarsal canal, a branch of the posterior tibial artery – forming an anastamotic ring about the talar neck.

The talar body is mainly supplied by the artery of the tarsal canal as well as the deltoid artery, a branch of the posterior tibial artery. [6] The posterior process is supplied by small branches of the peroneal artery and calcaneal branches from the posterior tibal artery.

The amount of articular cartilage covering the talus limits the area that remains for penetration of nutrient arteries. The likelihood of AVN is determined by the amount of soft tissue damage about the talus and how much of the numerous anastamoses as described by Mulfinger and Tureta [7] remain intact. Much of the talus is supplied by separate variable intraosseous anastamoses. Numerous anastamoses among all the arteries in the talus is one reason talar AVN is relatively uncommon. The occurrence of AVN is determined by how complete the intraosseous anastamoses are among the remaining intact vessels and the amount of damage to the soft tissue.

Treatment recommendations have evolved from primary amputation, to talectomy with tibiocalcaneal arthrodesis [8] and most recently, with reinsertion of the talus. According to Huang, et al., [9] reinsertion is preferable provided the wound is relatively clean and talus is still attached – even if by a soft tissue strand. Palomo-Traver, et al., [3] also suggested the deformity be reduced with the exception of gross contamination or complete extrusion, as he suggested the risk of infection and AVN correlates with the degree of extrusion of the bone. Primary subtalar joint or pantalar arthrodesis has been recommended in cases of failed reduction in an effort to facilitate revascularization of the talus. Care should be taken to ensure adequate debridement of all non-viable tissue. This decreases the chances of soft tissue infection which could propagate to the bone.

In our case, the wound was not grossly contaminated with debris and there was no involvement of tendinous structures that could have tracked infection more proximally. Appropriate irrigation and debridement was performed. There was adequate soft tissue for wound closure after negative cultures; all of which helped decrease the likelihood of soft tissue or bone infection. A complete Hawkin’s sign was noted at three months post injury indicating full preservation of blood supply to the talus.

A Hawkin’s sign is typically seen between six to eight weeks10, but has been reported as late as two years. [4] A partial Hawkin’s sign has also been reported which is associated with partial AVN of the talus. [6] Our patient experienced none of the major complications associated with total talar dislocation. He returned to pre-injury function levels, walking and running 1-2 miles per day and reporting only occasional pain. He may not however, escape post traumatic arthritis which may develop in any or all of the joints disrupted by the injury.


1. Wagner, et al. Injury, Int J. Car Injured, 2004: 35, S-B36- S-B45.
2. Hiraizumi Y, Hara T, Takahashi M. Mayehi S. Open total dislocation of the talus with extrusion (missing talus): Report of two cases. Foot and Ankle Int. October 13(8): 473 – 477. 1992.
3. Palomo-Traver JM, Cruz-Renovell E, Granell-Beltran V, Monzonís-García J. Open total talus dislocation: case report and review of the literature. J Ortho Trauma 11 (1): 4 5 – 49, 1997.
4. Maffulli N, Francobandiera C, Lepore L, Cifarelli V. Total dislocation of the talus. J Foot Surg, 28(3): 208-211, 1989.
5. Ries M, Healy WA Jr. Total dislocation of the talus: Case report with a 13-year follow up and review of the literature. Ortho Rev 17(1): 76-80, 1988.
6. Tehranzadeh J, Stuffman E, Ross SD. Partial Hawkins sign in fracture of the talus: a report of 3 cases. AJR Am J Roentgenol 18 (6): 1559-1563, 2003.
7. Mulfinger GL, Trueta J. The blood supply of the talus. J Bone Joint Surg 52B (1):160-7, 1970.
8. Detenberg LC, Kelly PJ. Total dislocation of the talus. JBJS 51A (2): 283-88, 1969.
9. Huang PJ, Fu YC, Tien YC, Lin GT, Lin SY et al. Open total talar dislocations – a report of 2 cases. Kaohsiung J Med Sci 16 (4): 214-218, 2000.
10. Donnelly EF. The Hawkins sign. Radiology 210 (1): 195 – 196, 1999.
11. Zalavras CG, Patzakis MJ, Holtom P. Local antibiotic therapy in the treatment of open fractures and osteomyelitis. Clin Orthop Rel Res 427: 86-93, 2004.

Address correspondence to: Mark A. Hardy, DPM, FACFAS
Kaiser Permanente Foundation Department of Podiatric Surgery
12301 Snow Road Parma, OH 44130
Email: markhardy@sbcglobal.net

1 Director, Cleveland Clinic/Kaiser Permanente. Foot & Ankle Residency Program. Director, Foot and Ankle Trauma Service. Kaiser Permanente – Ohio Region.
2 Senior Resident, Kaiser Permanente/Cleveland Clinic Foundation Residency Program, Cleveland, Ohio.

© The Foot & Ankle Journal, 2008