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Case Study
Treating Acute Bilateral Foot Compartment Syndrome From Rhabdomyolysis And Frostbite
June 2014
These authors discuss the diagnosis and treatment of a 57-year-old male who had rhabdomyolysis, an acute kidney injury and alcoholic neuropathy that masked compartment syndrome.
Acute compartment syndrome of the foot is an emergent condition, requiring surgical fasciotomies as soon as possible after one has diagnosed the condition. The most common cause is trauma such as crush injury or fracture. A study from a Level 1 trauma center over seven years showed 164 cases of acute compartment syndrome. The incidences were 7.3 per 100,000 for men and 0.7 per 100,000 for women.1 Sixty-nine percent of these cases were the result of fracture with 23 percent resulting from non-traumatic soft tissue injuries.1 These non-traumatic injuries can include vascular injuries, thermal injuries and prolonged limb compression.
In this particular case study, the patient developed bilateral frostbite in both feet, which caused rhabdomyolysis and ultimately bilateral compartment syndrome in the feet.
Rhabdomyolysis is a condition in which damaged skeletal muscle cells break down and leach toxins into systemic circulation.2,3 Acute kidney injury is a common side effect of rhabdomyolysis due to the release of myoglobin, which is nephrotoxic. Some causes include thermal injuries, compromise of blood supply to muscle, crush injuries, severe inflammation or infection.4,5 If the damaged muscle is contained within a fascial compartment, there is the risk of compartment syndrome.
An acute compartment syndrome involves cellular anoxia to a fascial compartment containing muscle. The fascial compartment prevents expansion of swollen and damaged tissues.6 This condition is best explained by the arteriovenous pressure gradient theory.7 This describes a decrease in local blood flow due to extreme swelling, causing ischemia and an inability to meet local tissue metabolic demands. As more fluid enters the compartment and cannot leave due to venous compression, the compartment pressure rises, reducing venous outflow even more. This causes a decrease in the arteriovenous pressure gradient. Finally, arteriolar pressure cannot overcome the compartment pressure so blood is shunted away from the affected tissue.
In 1990, a study by Manoli and Weber showed there are nine foot fascial compartments: lateral, medial, superficial, adductor, calcaneus compartments and four interosseous compartments.8 The calcaneal compartment communicates with the deep posterior compartment of the leg, which can potentially cause compartment syndrome of both the foot and leg.
The diagnosis of compartment syndrome is both clinical and through the use of intra-compartmental catheters. Clinically, there are the “6 Ps”: Pain out of proportion to injury, pallor, paresthesias, paralysis, poikilothermia and pulselessness. Pulselessness and paralysis are generally late findings. Clinicians can measure compartment pressures with a sharp catheter, which punctures the suspected compartment. Normal pressure is 8 mmHg or less. When compartmental pressures are above 30 mmHg or within 30 mHg of diastolic pressure, one should perform a fasciotomy as soon as possible after making the diagnosis.9 There are a variety of descriptions for the fasciotomy incisions with Myerson’s recommendation being two dorsal incisions and one medial-plantar incision.10 One should initially leave the incisions open and employ wet-to-dry dressings for the first few days, and subsequently close the incisions after swelling recedes.
Two days later, the patient began complaining of pain and swelling to both feet. Throughout his stay, his creatinine phosphokinase values were increasing and his neurovascular status had become worse. He was unable to walk due to pain. The circumferences of his feet were increasing by 0.5 cm per hour.
When we were consulted about the patient, we evaluated him and noted severe swelling to the feet, duskiness to all toes, absent sensation to the ankles, pain with passive toe dorsiflexion and painful palpation dorsally to both feet. The exam was complicated by the patient’s alcoholic neuropath as the patient’s pain did not seem to be consistent with compartment syndrome.
Using a Stryker catheter, we measured the pressure between the first and second metatarsals of both feet. The patient showed no painful reaction from the insertion of the catheter at this time. The pressure on the right side was 90 mmHg and the left side pressure was 50 mmHg, both consistent with compartment syndrome. The patient gave his consent for bilateral fasciotomies for that night.
The foot fasciotomy incisions were located dorsally in the first and third intermetatarsal spaces. We were able to release all intermetatarsal spaces as well as the medial and lateral compartments from these incisions. Draining a large amount of serosanguinous fluid from each incision, we took care to express as much fluid as possible. We packed the wounds, left them open to drain, and subsequently changed the packing and dressings daily for the next four days.
After the fasciotomies, the creatine phosphokinase levels decreased and then normalized a few days later. Within 48 hours of the surgery, sensation returned to the metatarsal heads bilaterally. The swelling markedly decreased and the patient had pain-free passive toe dorsiflexion. After four days, the edema had decreased enough to allow for fasciotomy closure in the OR. We only closed the skin.
The patient remained in the hospital for the next several weeks due to trouble finding a shelter or a family member who could provide him housing. We saw him daily to continue regular dressing changes and removed the sutures at two weeks. During that time, he continued to improve clinically with complete reduction of pain and swelling to the feet. The patient was able to walk again and tolerate physical therapy. By the time of discharge, he was walking pain-free in surgical shoes as he was admitted to the hospital without shoes.
Acute compartment syndrome of the foot is an emergent condition, requiring surgical fasciotomies as soon as possible after one has diagnosed the condition. The most common cause is trauma such as crush injury or fracture. A study from a Level 1 trauma center over seven years showed 164 cases of acute compartment syndrome. The incidences were 7.3 per 100,000 for men and 0.7 per 100,000 for women.1 Sixty-nine percent of these cases were the result of fracture with 23 percent resulting from non-traumatic soft tissue injuries.1 These non-traumatic injuries can include vascular injuries, thermal injuries and prolonged limb compression.
In this particular case study, the patient developed bilateral frostbite in both feet, which caused rhabdomyolysis and ultimately bilateral compartment syndrome in the feet.
Rhabdomyolysis is a condition in which damaged skeletal muscle cells break down and leach toxins into systemic circulation.2,3 Acute kidney injury is a common side effect of rhabdomyolysis due to the release of myoglobin, which is nephrotoxic. Some causes include thermal injuries, compromise of blood supply to muscle, crush injuries, severe inflammation or infection.4,5 If the damaged muscle is contained within a fascial compartment, there is the risk of compartment syndrome.
An acute compartment syndrome involves cellular anoxia to a fascial compartment containing muscle. The fascial compartment prevents expansion of swollen and damaged tissues.6 This condition is best explained by the arteriovenous pressure gradient theory.7 This describes a decrease in local blood flow due to extreme swelling, causing ischemia and an inability to meet local tissue metabolic demands. As more fluid enters the compartment and cannot leave due to venous compression, the compartment pressure rises, reducing venous outflow even more. This causes a decrease in the arteriovenous pressure gradient. Finally, arteriolar pressure cannot overcome the compartment pressure so blood is shunted away from the affected tissue.
In 1990, a study by Manoli and Weber showed there are nine foot fascial compartments: lateral, medial, superficial, adductor, calcaneus compartments and four interosseous compartments.8 The calcaneal compartment communicates with the deep posterior compartment of the leg, which can potentially cause compartment syndrome of both the foot and leg.
The diagnosis of compartment syndrome is both clinical and through the use of intra-compartmental catheters. Clinically, there are the “6 Ps”: Pain out of proportion to injury, pallor, paresthesias, paralysis, poikilothermia and pulselessness. Pulselessness and paralysis are generally late findings. Clinicians can measure compartment pressures with a sharp catheter, which punctures the suspected compartment. Normal pressure is 8 mmHg or less. When compartmental pressures are above 30 mmHg or within 30 mHg of diastolic pressure, one should perform a fasciotomy as soon as possible after making the diagnosis.9 There are a variety of descriptions for the fasciotomy incisions with Myerson’s recommendation being two dorsal incisions and one medial-plantar incision.10 One should initially leave the incisions open and employ wet-to-dry dressings for the first few days, and subsequently close the incisions after swelling recedes.
A Closer Look At The Case Study
Our case involves a 57-year-old male presenting to an urban hospital in the winter. The patient had a history of homelessness, alcoholic neuropathy and polysubstance abuse. He was found agitated and barefoot outside of a liquor store. Due to his behavior, he was brought to the emergency department. At this time, there were no pedal complaints. However, the patient’s lab tests were concerning for rhabdomyolysis and acute kidney injury so the patient was admitted. The baseline alcoholic neuropathy likely masked any pedal complaints at this time.
Two days later, the patient began complaining of pain and swelling to both feet. Throughout his stay, his creatinine phosphokinase values were increasing and his neurovascular status had become worse. He was unable to walk due to pain. The circumferences of his feet were increasing by 0.5 cm per hour.
When we were consulted about the patient, we evaluated him and noted severe swelling to the feet, duskiness to all toes, absent sensation to the ankles, pain with passive toe dorsiflexion and painful palpation dorsally to both feet. The exam was complicated by the patient’s alcoholic neuropath as the patient’s pain did not seem to be consistent with compartment syndrome.
Using a Stryker catheter, we measured the pressure between the first and second metatarsals of both feet. The patient showed no painful reaction from the insertion of the catheter at this time. The pressure on the right side was 90 mmHg and the left side pressure was 50 mmHg, both consistent with compartment syndrome. The patient gave his consent for bilateral fasciotomies for that night.
The foot fasciotomy incisions were located dorsally in the first and third intermetatarsal spaces. We were able to release all intermetatarsal spaces as well as the medial and lateral compartments from these incisions. Draining a large amount of serosanguinous fluid from each incision, we took care to express as much fluid as possible. We packed the wounds, left them open to drain, and subsequently changed the packing and dressings daily for the next four days.
After the fasciotomies, the creatine phosphokinase levels decreased and then normalized a few days later. Within 48 hours of the surgery, sensation returned to the metatarsal heads bilaterally. The swelling markedly decreased and the patient had pain-free passive toe dorsiflexion. After four days, the edema had decreased enough to allow for fasciotomy closure in the OR. We only closed the skin.
The patient remained in the hospital for the next several weeks due to trouble finding a shelter or a family member who could provide him housing. We saw him daily to continue regular dressing changes and removed the sutures at two weeks. During that time, he continued to improve clinically with complete reduction of pain and swelling to the feet. The patient was able to walk again and tolerate physical therapy. By the time of discharge, he was walking pain-free in surgical shoes as he was admitted to the hospital without shoes.
In Conclusion
This was a case of compartment syndrome with an unusual etiology and a diagnosis that was complicated by the patient’s baseline alcoholic neuropathy. However, we were able to make the diagnosis and initiate proper therapy in time to ensure a full recovery. References 1. McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk? J Bone J Surg Br. 2000;82(3):200-3. 2. Malinoski DJ, Slater MS, Mullins RJ. Crush injury and rhabdomyolysis. Crit Care Clin. 2004;20(1):171-92. 3. Heurta-Alardin AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis – an overview for clinicians. Crit Care. 2005; 9(2):158-69. 4. Melli G, Chaudry V, Cornblath DR. Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicine (Baltimore). 2005;84(6):377-85. 5. Efstratiadis G, Voulgaridou, Nikiforou D, et al. Rhabdomyolysis updated. Hippokratia. 2007;11(3):129–137. 6. Frink M, Hildebrand F, Krettek C, et al. Compartment syndrome of the lower leg and foot. Clin Orthop Relat Res. 2010;468(4):940-50. 7. Vollmar B, Westermann S, Menger MD. Microvascular response to compartment syndrome-like external pressure elevation: an in vivo fluorescencevmicroscopic study in the hamster striated muscle. J Trauma. 1999;46(1):91-6. 8. Manoli A, Weber TG. Fasciotomy of the foot: an anatomical study with special reference to release of the calcaneal compartment. Foot Ankle. 1990;10(5): 267-75. 9. Frink M, Hildebrand F, Krettek C, et al. Compartment syndrome of the lower leg and foot. Clin Orthop Relat Res. 2010;468(4):940–950. 10. Myerson MS. Experimental decompression of the fascial compartments of the foot — the basis for fasciotomy in acute compartment syndromes. Foot Ankle. 1988; 8(6):308-14.
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