This article is more than 5 years old. Information may no longer be current.
Spontaneous bleeding of the foot…is it so?
Click Here to Manage Email Alerts
A 76-year-old woman presented in distress with chief complaint of left heel bleeding and pain. She has an underlying history of poorly healing, non-painful bilateral heel ulcers.
Upon arrival, the patient related that she was arising from the commode when her left foot felt as though she stepped into a foam-filled box. She noted immediate pain to her left heel with inability to bear weight. Shortly thereafter, she and her husband noticed bleeding. When the bleeding failed to stop, roughly eight hours after the incidence of “heal wound began bleeding,” they phoned the office and were told to promptly come in. The patient’s past medical history included diabetes, hypertension, hypercholesterolemia, nephropathy (on dialysis), neuropathy, coronary artery disease, peripheral arterial disease and obesity. The patient’s medications were quite extensive.
Physical examination revealed the patient to not only be in intense pain and greatly distressed, but also tachycardic, diaphoretic, pale, nauseated, hyperventilating, tearful, incoherent, and very anxious. Lower extremity examination revealed absent pedal pulses (dorsalis pedis, posterior tibial, peroneal).
A heel wound to the affected area was noted with admixture of necrotic, hemorrhagic and salmon-colored granular wound tissue (see figure A). Although absent sensation via Semmes Weinstein monofilament, considerable pain was reproducible upon palpation and probing of left heel. Active bleeding was also seen with dressing removal and wound probing.
|
|
Based on the past medical history and physical examination, what is your diagnosis?
- Heel spur.
- Plantar fascial band rupture.
- Calcaneal heel fracture.
- Puncture wound.
CASE DISCUSSION
Even though radiographs were not readily available, it was evident that the patient suffered a left calcaneal heel fracture with penetration through the wound bed (see figures B and C). Initial treatment in the office comprised dry dressing with silver non-adherent contact layer. Given the patient’s disposition, the patient was sent to the hospital for admission and immediately transferred to the ER via EMS for more emergent workup. Orders were sent requesting radiographs of the left heel as well as consultation for further care by the on-call podiatrist. Unfortunately for the patient, she was further diagnosed with acute coronary syndrome.
Patris ToneyRadiographs and MRI revealed comminuted avulsion fracture of the posterior calcaneus with underlying osteomyelitis. Antibiosis with cephalosporin and aminoglycoside was instituted upon admission. Regarding surgical treatment, major reconstructive surgery was cancelled until cardiac clearance is obtained. However, infection developed and a below knee amputation was offered by outside services, but the patient refused. To treat the acute problem of spreading infection, surgical intervention posing minimal cardiac risk was decided upon and employed using only a sciatic nerve block for anesthesia to facilitate surgical placement of gentamycin-impregnated polymethyl methacrylate beads to the fracture wound site. The beads were removed four days later. With cardiac clearance not in the foreseeable future, wound stabilization and infection control are the mainstay of treatment. At present, the left heel wound is stable with necrotic eschar, no acute infection or pain (see figure D). The patient is primarily non-ambulatory due to her left calcaneal fracture and her extensive, poorly healing right heel wound (see figure E).
Figure B: Area of injury (blue circle) with visualization of the fracture (red arrow) with soft tissue penetration.
Figure D: Left heel 2 months later. Stable dry necrotic eschar, non-painful. Note wound size expansion prior to stabilization when compared to Figure C.
Figure C: Close up of the fracture (dotted blue arrow) visualized which appears slit-like, but probes 4 cm into heel with pain elicited. Note the remnant of bleeding periwound. Also, better visualization of necrotic tissue (solid blue arrow) to preexisting non-healing wound.
Figure E: Right heel wound. Note the extensive focal wound tissue necrosis and involvement of the Achilles region (arrows). Patient remains adamant against amputation yet remains poor candidate for revascularization.
Gustillo described open fractures as “one in which the bone ends have penetrated to the outside skin and there is injury to the underlying soft tissue of varying severity.” The currently used classification system takes into account the presentation of the wound. Type I wounds involve open fractures with clean wounds < 1 cm long. Type II open fractures demonstrate lacerations > 1 cm long without extensive soft tissue involvement, moderate crush injuries, moderate comminution, and moderate contamination. Type III open fractures demonstrate extensive soft tissue damage including muscle, skin, and neurovascular structures, traumatic amputation, or open segmental fracture and high contamination. Type III open fractures are further sub-characterized. Type III-A demonstrate adequate bony soft tissue coverage and include gunshot wounds. Type III-B includes farm injuries and involves periosteal stripping with exposed bone. Type III-C are associated with arterial injuries necessitating repair and include traumatic amputations. In addition, open fractures greater than eight hours old are typically considered as Type III-C.
Type III and some type II open fracture wounds need to be closely monitored within the 24 to 48 hours following injury, and initial wound debridement as further tissue necrosis may occur secondary to unfolding damage from circulatory embarrassment. Prevention of wound sepsis, fracture healing and return to normal function are the three main goals that direct the treatment of open fractures.
Treatment involves treating all open fractures as emergencies, in addition to thorough full body assessment, appropriate antibiotic coverage, debridement and irrigation, along with stabilization of the fracture, appropriate wound coverage, early cancellous bone grafting, and rehabilitation of the affected extremity as well as the patient. Above all, debridement and irrigation are considered to be most important and the first step in treatment of open fractures. To further optimize wound healing and minimize infection, soft tissue coverage is ideal within seven to 10 days and may employ primary or delayed primary closure. In certain circumstances, early amputation is deemed acceptable.
Since the risk for infection is of concern in these injuries, early antibiosis is important. For Type I fractures, Ancef is the cephalosporin of choice. Ancef, 2 g intravenously, is given and continued for at least two to three days and is given every six hours. Type II and Type III open fractures are treated with Ancef plus an aminoglycoside such as Tobramycin or Gentamycin to ensure adequate coverage of gram-negative organisms. In healthy individuals, aminoglycosides are administered intravenously with 1.5 mg/per kg administered initially and 3 mg/kg to 5 mg/pr kg given each subsequent day for three days total. Of course, as with our patient, dosages in renally compromised patients are adjusted accordingly. In addition, tetanus status is also assessed.
Open fractures are traumatic, devastating and painful injuries with great potential for debilitation, especially in the already compromised individual. Despite the devastation of the injury/situation, the limb may be salvageable, albeit demanding of time and patience.
Patris Toney, DPM, MPH, is an Attending Staff Physician at Mount Sinai Hospital in Chicago, Ill. and Past Fellow at the Center for Lower Extremity Ambulatory Research/National Center for Limb Preservation, Ill.