Management of the ever-increasing number of diabetic feet is an important issue for orthopedic foot and ankle surgeons. A thorough understanding of the pathophysiology and treatment options is necessary to provide optimal care for these patients. Within the multidisciplinary team, the orthopedic surgeon has a unique opportunity to play a critical role in the care of the diabetic patient.
Globally in 2013 an estimated 382 million people had diabetes. The International Diabetes Federation states that by 2035 this number will increase to 592 million1. Diabetes is more common in developed countries. The American Diabetes Association currently estimates that more than 10% of all Americans over the age of 20 have diabetes. This number steadily increases with age, and 26% of the population older than 65 years has diabetes2. Up to 25% of diabetic patients will be affected by foot disorders at some point in their life3. Foot ulcers are the most common medical complication causing diabetics to seek medical treatment. Each year in the United States over 65 000 non-traumatic lower limb amputations are performed in diabetics. Diabetes and its complications can and should be viewed as an epidemic, with the worldwide total yearly cost of the disease topping £360 billion ($465 billion)1.
Diabetes is a metabolic disease with systemic manifestations involving the nervous, vascular, immune, and musculoskeletal systems. The etiology of diabetic foot problems is multifactorial. Sensory neuropathy is usually the underlying cause of ulceration and infection. Peripheral vascular disease is also common and hinders healing, but in itself rarely causes foot pathology4. If and when an infection does develop in the diabetic foot, the body’s immune response is weakened and less effective.
Diabetic neuropathy is described as a distal, symmetric polyneuropathy5–6. It is a length-dependent axonopathy involving both myelinated and unmyelinated nerves, with a predilection for the distal sensory and autonomic fibers, with relative sparing of motor fibers7. Metabolic, ischemic, and possibly even hormonal factors drive the nerve damage5–8. Although not fully understood the metabolic factors causing nerve damage include the intraneural accumulation of the end products of glycosylation and sorbitol, disruption of the hexosamine and protein kinase C pathways, and activation of the poly(ADP-ribose) polymerase pathway9–11. The common end pathway is the cellular build-up of reactive oxygen species, which cause metabolic neural damage.
The role of nerve ischemia in diabetic neuropathy is supported by the finding of thickened endoneural blood vessel walls in neuropathic patients12. It has also been shown that diabetic patients with advanced neuropathy have reduced oxygen tension in the peripheral nerves13.The impairment in antithrombotic mechanisms may also play a part in the pathogenesis, as there is a decreased level of thrombomodulin and tissue plasminogen activator in the peripheral nerve microvessels of diabetic patients14. It is probable that ischemic and metabolic factors work together in the development of peripheral neuropathy, but the exact interaction is not fully understood.
Risk factors for the development of diabetic neuropathy principally relate to the duration and severity of hyperglycemia15. More recent epidemiologic studies have focused on additional factors, which include hypertension, smoking, dyslipidaemia, and elevated body mass index16–17.
Neuropathy alone does not cause diabetic foot pathology, it is the insensitivity combined with abnormal foot pressures that leads to ulceration and tissue breakdown. Brand showed in animal models that with low-level repetitive trauma to tissue, inflammation followed by necrosis will develop. With the inability to sense and respond to mechanical stresses, repetitive trauma from high pressure in the diabetic foot ultimately leads to tissue breakdown. Brand concluded that there are three factors that determine the probability of actual foot ulceration: the severity and location of sensory loss, the magnitude of the forces on the foot, and the walking distance it takes for repetitive stress to induce a state of inflammation18. Skin breakdown in diabetics frequently results from deformities from conditions that create bony prominences, such as the proximal phalangeal joints of claw toes, bony ridges from arthritic joints, malunited fracture fragments, or protuberances from Charcot neuroarthropathy. These prominences are vulnerable to pressure from the floor, shoes, or braces.
Dysfunction of the autonomic nervous system compounds the pathological process. With loss of skin temperature regulation, loss of perspiration, and arteriovenous shunting, the plantar skin becomes dry, thickened, and coarse. This leads to fissures and cracks19. The fissure leaves a breach in the integument with a vulnerability to infection, but the thickened callus and fissured tissues can also result in pressure areas and shear forces that can lead to deep ulceration.
Peripheral vascular disease is four to six times more prevalent in the diabetic population20. In diabetics, the arterial calcification process is more diffuse than in those without the disease; it involves the entire circumference of the vessels4, 19. Furthermore, occlusive disease is rapidly progressive, which prevents compensation with the opening of the collateral circulation. In diabetics the distribution of the vascular disease also differs with more distal vascular involvement. There is commonly popliteal trifurcation and tibioperoneal disease21. Interestingly the dorsalis pedis artery is frequently spared.
Studies on the microcirculation based on histology, arterial casting, and vascular resistance show that the changes in the small vessels of the foot are not occlusive22. Although patients with diabetes have a thickened capillary basement membrane, the lumen itself is not narrowed23. A pathological vascular process at the subarteriolar level that correlates to diabetic foot pathology has not been conclusively identified4, 23. It is thought that peripheral vascular disease hinders the healing of the diabetic foot, but alone is rarely the cause of foot pathology.
Diabetics are more susceptible to infections, largely due to their impaired immune response. Leukocyte chemotaxis and function are dramatically reduced24. Thus once neuropathic and vascular factors permit pathogens to enter and colonize the foot, the diabetic host is less efficient in combating the infection. With an environment of hyperglycemia, hypoxia, hypertonicity, edema, and an impaired immune response the environment is optimal for continued bacterial growth19. A hemoglobin A1c greater than 8% is independently associated with surgical site infection25.
A thorough lower extremity physical examination is essential in the evaluation of a diabetic patient presenting with foot problems. Inspection of the affected limb alone can provide many important clues to the overall heath of the foot. This includes wear patterns on shoes, hair growth or lack thereof, erythema, edema, open wounds, and nail deformity.
The patients should be assessed in both static (seated and standing) and dynamic (walking and maneuvering) modes. The overall alignment of the foot, range of motion, and any bony prominences should be noted.
Evaluation and quantification of sensory neuropathy are critical aspects in the examination of the diabetic foot. Although light touch, two-point discrimination, and proprioception are simple and rapid assessments of neuropathy, more quantitative measures are important for prognostic value. These include vibratory testing, nerve conduction studies, temperature testing, and monofilament testing4. By far the most commonly used is the Semmes–Weinstein monofilament (Figure 19.1). The monofilament consists of nylon filaments of varying thickness that are pressed onto the skin until they bend. The smallest monofilament that the patient can feel represents the threshold of sensation. Monofilament testing has been shown to have a higher reproducibility than vibration threshold perception26. It is frequently quoted that being able to feel a 5.07 monofilament, which is equivalent to a 10 g force, is needed for protective sensation. It has been shown that failure to perceive such a monofilament is associated with an increased risk of foot ulceration and amputation27. Although the 5.07 monofilament is easy to use, economical, and widely accepted, nearly 10% of patients with sensation at this level still go on to develop ulceration and neuroarthropathy19.
Figure 19.1 Sensory examination with 10 g Semmes–Weinstein monofilament.
A vascular evaluation is necessary to inform treatment options. Beyond palpation of pulses and the timing of capillary refill, the most commonly used assessment of blood flow is with Doppler studies4. Doppler ultrasound can be used to measure arterial pressure. The ankle–brachial index (ABI) is the ratio of the systolic blood pressure measured at the ankle to the pressure in the arm. Wagner determined that an ABI of 0.45 was the minimum required for healing of diabetic foot lesions28. Although only a guideline, the prognostic value of an ABI can be strengthened with the addition of absolute toe pressures. The absolute toe pressure often quoted to achieve wound healing is 45 mmHg19. It is important to keep in mind, however, that pressure values can be falsely elevated in calcified vessels. In this setting, more pressure is required to compress the stiffened vessels. Thus an ABI of greater than 1.0 should raise the possibility of calcification4. The shape of the waveform is important and is normally bi- or triphasic. A monophasic waveform can indicate proximal disease.
Transcutaneous oxygen measurements are also used as a measure of vascularity and healing potential. Pinzur et al. found a direct correlation with healing of amputations and transcutaneous oxygen pressure (TcPO2)29. When the TcPO2 was greater than 30 mmHg over 90% of amputations healed, whereas when the TcPO2 was less than 30 mmHg only 66% healed. The measurement has also been linked to the response to hyperbaric oxygen treatments19.
If and when the patient is found to have vascular insufficiency, evaluation by a vascular surgeon or interventional radiologist is often warranted. An arteriogram can be used to localize specific points of occlusion and plan angioplasty or revascularization procedures. Coupled with local wound care and debridement, such procedures can often lead to limb salvage.
Imaging studies are critical in the evaluation of the diabetic foot and its complications. The most commonly used techniques include plain radiography, ultrasonography, MRI, and bone scintigraphy.
With its wide availability and low cost, radiographs remain the staple first-line imaging for the diabetic foot. They provide baseline information on joint changes, bone infection, soft tissue gas, and foreign bodies. Although they are less sensitive and specific for many diabetic complications than other imaging modalities, they are essential in evaluating the basic foot and ankle structure. Weightbearing radiographs of the foot and ankle should be obtained in all cases if possible.
Ultrasound is another widely available, non-invasive imaging modality, which is extensively used. It is helpful in the detection of inflammatory soft tissue changes, fluid collections, joint effusions, and foreign bodies. It can also be useful in guiding diagnostic aspiration.
MRI may be the most important modality for evaluation of the diabetic foot. Its strength lies in its ability to evaluate both soft tissue and bone, detecting bone marrow changes. MRI is useful for identifying soft tissue abscesses, particularly in swollen feet with cellulitis or Charcot neuroarthropathy. The imaging is multiplanar, which allows precise identification of the involved structures, and it is invaluable for directing surgical management. Nevertheless it is important to remember that the bone edema found in osteomyelitis and neuroarthropathy remains difficult to differentiate with MRI alone30.
The most commonly used nuclear medicine techniques in the diabetic foot include three-phase bone scanning with technetium-99m (99mTc) and indium-111 (111In) labeled white blood cell (WBC) scans30. Although less expensive than MRI, a 99mTc bone scan is highly non-specific and can remain positive for over a year following fracture or surgery4. Alone the 99mTc scan cannot easily differentiate osteomyelitis from neuroarthropathy. The addition of an extra scan at 24 hours, a four-phase bone scan, has not been found to help31. The 111In white cell scan, in contrast, has a greater specificity for infection. Several studies have shown that by combining a 99mTc scan and 111In white cell scan the sensitivity and specificity for differentiating infection from neuroarthropathy can be raised to over 90% and 80% respectively.
Foot ulcers are the most common medical complication causing diabetics to seek medical attention. Fifteen percent of patients with diabetes will eventually develop an ulcer in their lifetime. Such ulcers have a tremendous impact on patients’ quality of life. The majority require an ambulatory assist device or are unable to ambulate independently, and view their condition as significantly interfering with their daily lives32. Ulceration is often the precursor to infection and osteomyelitis, and ulcers lead to over 65 000 amputations per annum in the United States alone2.
Over 70% of ulcers occur in the forefoot, followed by the heel and midfoot19. Much work has been done to identify risk factors for the development of foot ulcers. The International Working Group on the Diabetic Foot33 stratified over 200 diabetic patients into four risk groups: group 0 consisted of patients without neuropathy, group 1 consisted of patients with neuropathy but without deformity or peripheral vascular disease, group 2 consisted of patients with neuropathy and deformity or peripheral vascular disease, and group 3 consisted of patients with a history of foot ulceration or a lower extremity amputation. During a three-year follow-up period, ulceration occurred in 5%, 14%, 19%, and 56% of patients in groups 0, 1, 2, and 3, respectively. All the amputations occurred in groups 2 and 3. Additional risk factors include an abnormal tendo Achillis reflex, insensitivity to a 10 g monofilament, reduced pulses, increased age, and previous podiatric attendance. Factors associated with increased healing potential of ulcers include a serum albumin greater than 30 g/L and a total lymphocyte count of more than 1.5 × 109/L.The combination of sensory neuropathy and autonomic skin changes places soft tissue at high risk for breakdown. With continued pressure, usually over unprotected bony prominences, ulceration can develop.
Two commonly cited classification systems of diabetic ulcers are the Wagner classification28 and the Brodsky depth–ischemia classification34. The Wagner classification, developed at Rancho Los Amigos Hospital, has historically served as a basis for evaluation. There are six grades, 0 to 5, based on depth of lesion and presence of gangrene (Table 19.1). There is an important divide in the system between the first four grades and the final two, with grades 4 and 5 being related to loss of vascularity, rather than depth of lesion.
|0||Foot at risk||Thick callus, no break in skin, prominent bony lesion|
|1||Superficial ulcer||Full thickness destruction of skin|
|2||Deep ulcer||Penetrates through skin, fat, tendons, and ligaments but not through bone. Includes penetration into a joint|
|3||Abscess and deep ulcer||Localized osteomyelitis or abscess|
|4||Limited gangrene||Limited necrosis in toes or forefoot|
|5||Extensive gangrene||Necrosis of complete foot with systemic effects|
The Brodsky depth–ischemia classification (Table 19.2) is a modification of the Wagner classification, with an alphanumeric system to separate the classification of the depth of the foot wound from the vascularity of the foot. The soft tissue is given a numbered depth (Grade 0–3). The perfusion of the foot is examined and given a letter (Grade A–D). This combination of soft tissue and vascularity assessment better helps guide prognosis and treatment (Figures 19.2 to 19.5). Brodsky outlines a logical, stepwise approach for treating diabetic ulcers34. The surgeon first assesses the soft tissue wound using the numeric, depth component of the depth–ischemia classification system. This includes visual inspection and palpation of the wound with a probe to determine which, if any, underlying deep structures are exposed. The typical grade 1 lesion, superficial ulceration with healthy granulation tissue, is treated as an outpatient, whereas the deeper grades usually require surgical care. Following this the ischemic component, A to D, of the depth–ischemia classification system is used to determine if there is adequate vascularity to allow healing. If palpable pulses are absent, vascular studies are carried out. This is critical, as vascular reconstruction is often needed for wound healing. Finally, the ulcer is assessed for infection. If more than simple superficial colonization, the patient should be admitted to hospital for intravenous antibiotics. These ulcers often require surgical debridement to clear the ulcer bed of infected tissue. The ultimate goal of debridement is to achieve a wound with healthy granulation tissue with no infected or non-viable tissue.
|0||At-risk foot, no ulcer (Figure 19.2)|
|1||Superficial ulcer, not infected (Figure 19.3)|
|2||Deep ulceration exposing tendon or joint, with or without superficial infection (Figure 19. 4)|
|3||Extensive ulceration with exposed bone and deep infection (Figure 19.5)|
|B||Ischemia without gangrene|
|C||Partial (forefoot) gangrene of the foot|
|D||Complete gangrene of the foot|
Figure 19.2 Grade 0 ulcer: foot at risk for ulceration, note the subcutaneous hemosiderin.
Figure 19.3 Grade 1 ulcer: superficial ulceration.
Figure 19.4 Grade 2 ulcer: deep ulceration.
Figure 19.5 Grade 3 ulcer: extensive ulceration with exposed bone and deep infection.
Once the above steps have been taken, the ultimate treatment in ulcer care can be initiated – pressure relief. This comes in many forms, both non-operative and operative. Non-operative pressure relief includes footwear modification, total contact casts, and walking boots. Although the specific pressure-relieving device is chosen based on both provider and patient preference, a few points are worth mentioning here. Firstly, total contact casting, changed at two- to four-weekly intervals, remains the “gold standard” for most plantar sided ulcers, with an 85 to 90% healing rate of grade 1 and 2 ulcers35–36. These casts are not without problems. Guyton37 found an overall complication rate of 30% per patient and 5% per cast. Although most of the complications were new abrasions or ulcers, which healed spontaneously, patients should be made aware of this before cast application. Prefabricated walking boots also reduce plantar foot pressure. The reduction in pressure is equal to, or can be greater than, that achieved by total contact casting38–39. The advantage of cost and ease of application must be weighed against the risk of patient non-compliance.
Sometimes pressure relief requires surgical intervention, with the creation of a plantigrade foot with no bony prominences. Sometimes this is simply achieved with tendo Achillis lengthening, to correct equinus and unload the forefoot, followed by total contact casting. This combination has been found to be very effective in the treatment of recurrent forefoot ulcers40. Other procedures are tailored to the specific ulcer and its location, but there are unifying surgical concepts4. The majority of procedures focus on resection of the bone causing the excessive pressure, as well as removal of non-viable and infected tissue. It is important that the incision for bone resection should be distinct from the ulcer. For example, with a plantar ulcer the incision for bone resection, or exostectomy, can be made on the medial or lateral border of the foot, and the ulcer is debrided directly. Once the underlying pressure has been relieved and the ulcer is clean and non-infected, the treatment returns to casting or shoe modification until healing is complete.
Foot infection is common in the diabetic patient, with foot infections accounting for the largest number of diabetes-related inpatient hospital days. They are often pivotal events leading to progressive clinical deterioration41.
Diabetic foot infections are usually polymicrobial. Ge et al.42 looked at the microbiological profiles of 825 infected diabetic foot ulcers and found an average of 2.4 organisms per ulcer. Gram-positive cocci (staphylococci, group B streptococci, enterococci), gram-negative rods (Escherichia coli, Enterobacter, Proteus, Pseudomonas), and anaerobes (Bacteroides, Clostridium) are commonly found together. Antibiotic-resistant organisms such as methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococcus and staphylococcus (VRSA) are now becoming more frequent and are associated with poorer outcomes in patients with diabetic foot infections41.
A diabetic foot infection can present with a number of clinical scenarios, including cellulitis, abscesses, and osteomyelitis. A thorough examination of the foot is essential. The ability to probe to bone through an ulcer alone has a positive predictive value of 89% for the presence of underlying osteomyelitis43. In addition to a white blood cell count with differential, laboratory studies should include an ESR, CRP, albumin, and prealbumin. It should be remembered that fewer than 50% of diabetic patients with infections have leukocytosis3. Deep cultures of soft tissue and bone are paramount in typing the microorganisms and their antibiotic sensitivity. Superficial swabs are notoriously inaccurate4. In imaging the foot MRI is most useful, as it allows the extent of bone and soft tissue involvement to be determined.
Treatment of diabetic foot infections is both non-operative and operative and often overlaps with the ulcer care discussed above. Most superficial infections are treated with a course of antibiotics. The choice and duration of antibiotic treatment depend on the severity of infection and the patient. Often broad-spectrum antibiotics are initiated, until specific microorganisms have been cultured, and antibiotic sensitivities determined.
Abscesses and osteomyelitis usually require surgical debridement. Despite the case series of Embril et al.44, where 80% of cases of diabetic foot osteomyelitis went into remission with antibiotic treatment alone, the classic teaching remains that complete eradication of infection requires surgical intervention.
Forefoot osteomyelitis is usually treated with ablative surgery of the toes, including transection or disarticulation. Infection can travel along the flexor and extensor tendons, thus it is important to inspect the remaining proximal tissues, with this in mind, at the time of surgery. There is always a balance to be struck between removing all the involved tissue and retaining enough skin and subcutaneous tissue to allow primary closure of the wound.
Ulceration under prominent metatarsal heads is common, and leads to metatarsal osteomyelitis. Metatarsal head resection can be considered if the infection is localized to the head alone. Head resection is effective, although it is common for the adjacent metatarsal head to develop a transfer lesions and ulcerate, requiring an additional head resection. If head resection is not sufficient, partial or complete ray resection may be necessary. Multiple ray resections are a favorable option over transmetatarsal amputation as they allow for better postoperative shoe options, although a forefoot with three or fewer rays is prone to further ulceration as result of the high pressure under the remaining heads.
Midfoot osteomyelitis is commonly seen at the base of the fifth metatarsal in the varus hindfoot. Debridement is the standard treatment for this, but it is important to attempt to reattach the peroneus brevis to prevent worsening of the hindfoot varus. If reattachment is not possible, future triple, or even pantalar, arthrodesis may be necessary.
Hindfoot osteomyelitis is usually addressed through partial or total calcanectomies. This can be approached though a longitudinal, midline posterior and plantar incision. These procedures often require the use of negative-pressure dressings to assist with wound healing and carry a high failure rate. Revision to a below-knee amputation is sometimes required.
Nearly 50% of diabetic patients with foot infections eventually end up with an amputation45. A thorough discussion of amputations is beyond the scope of this review; however, a few important points are worth mentioning. Amputation should be viewed as a reconstructive procedure to regain energy-efficient ambulation. With advancements in surgery and prosthetics the outcomes for diabetic amputees have improved. Before any amputation a complete clinical evaluation should be undertaken including a vascular and nutritional assessment. A TcPO2 level greater than 30 mmHg and a toe pressure greater than 45 mmHg are associated with a healing rate of approximately 90%19. A serum albumin greater than 30 g/L and a total lymphocyte count of more than 1.5 × 109/L is also associated with better wound healing3. Resection should be at, or above, the level of viable soft tissue and bone. There are numerous amputation levels, which include partial digital, digital, ray, transmetatarsal, Chopart (midtarsal), Syme, below the knee, and above the knee. The length of the residual limb is inversely proportional to the patient’s energy expenditure during ambulation3.
Charcot neuroarthropathy is a chronic and progressive disease following the loss of protective sensation. It is characterized by joint destruction and fragmentation and can result in significant foot deformity. The resulting deformity hinders shoe and brace use, and the bony malalignment may lead to ulceration and eventual infection. Diabetes is the leading cause of Charcot neuroarthropathy in the twenty-first century, with the incidence in the diabetic population ranging from 1 to 37%3. The feet are the most common location for neuroarthropathy, and it is bilateral in approximately 30% of patients4. Interestingly, there does not appear to be a direct relationship between the severity of the diabetic neuropathy and neuroarthropathy, which is even seen in very mild type II diabetes.
There are two major theories that exist for the pathogenesis of Charcot neuroarthropathy. The first postulates underlying neurotraumatic destruction. It is thought that with loss of protective sensation, repetitive, mechanical micro-trauma in the insensate foot leads to joint destruction and collapse. The second is neurovascular destruction. It is postulated that autonomic dysfunction increases blood flow through arteriovenous shunting. The high blood flow leads to bone resorption, weakening, and eventually failure. In all probability the two theories play a combined role in the ultimate pathogenesis of the neuroarthropathy.
More recent studies suggest that inflammatory cytokines may have a role in the development of Charcot neuroarthropathy. It is proposed that an increase in the expression of cytokines, such as tumor necrosis factor and interleukin-1, stimulates osteoclast formation and bone resorption. Baumhauer et al.46 confirmed an increase in both inflammatory markers and osteoclasts in pathologic specimens using immunologic staining.
Eichenholtz described the staging system of Charcot neuroarthropathy.
Stage I, the development phase, is characterized radiologically by osteopenia, fragmentation, and joint subluxation or dislocation. Clinically there is edema, warmth, and erythema. Osseous fragmentation and joint dislocation are seen on radiographs. Stage I usually lasts for two to six months.
Stage II, the coalescence phase, marks the initiation of the reparative process. Radiographs show coalescence of the fragments, sclerosis, and absorption of fine bone debris. Clinically there is decrease in erythema, temperature, and swelling.
Stage III is the reconstruction phase. Radiologically there is arthrosis and fibrous ankylosis, with the bone fragments becoming rounded. Clinically the foot cools and stabilizes, with or without deformity. Stage II and III usually last for a combined period of 18 to 24 months.
Brodsky classified Charcot neuroarthropathy into four anatomic regions of involvement4. Type 1 (midfoot) involves the metatarsocuneiform and naviculocuneiform joints and is the most common presentation, accounting for 60% of cases. Type 2 (hindfoot) involves the subtalar, talonavicular, or calcaneocuboid joints. There are two subgroups of type 3. Type 3A (ankle) involves the tibiotalar joint. Type 3B (os calcis) is a small group in whom the tendo Achillis avulses the calcaneal tubercle, in the so called “parrot-beak.” Over 90% of Charcot neuroarthropathy is of type 1 and 2.
The Schon classification reflects the anatomic location (I to IV), severity of the collapse (A to C), and radiographic severity (α and β)47–48. The classification has been found to be reliable and reproducible. It can be used for diagnosis, planning, treatment, and prognosis (Figures 19.6 to 19.10). Type I involves the metatarsocuneiform joints. A plantar prominence develops medially under either the first metatarsal base or the medial cuneiform. Most type I feet then abduct, with the collapse progressing plantar-laterally. Type II involves the naviculocuneiform joint and extends laterally to the fourth and fifth metatarsal-cuboid joints. A lateral rocker bottom deformity typically develops under the subluxed cuboid. Type III involves the perinavicular region with fragmentation, fracture, or osteonecrosis of the navicular. There is shortening of the medial column with supination and adduction of the foot. These feet ulcerate under the fifth metatarsal tuberosity or the cuboid. Type IV involves the midtarsal joint. The navicular subluxes laterally on the talus, with abduction of the midfoot and the calcaneus moving into valgus. The calcaneal pitch decreases and a rocker bottom deformity develops at the calcaneocuboid joint. Type IV injuries ulcerate under the talar head, the navicular, and the plantar aspect of the distal calcaneus.