You and your partner respond to a private residence for a fall. You’re met at the door by the patient’s son, who reports that he found his father on the floor this morning after no one answered the door.
You find the patient on the ground in a kneeling position. He’s awake, alert and oriented with no complaints besides, “I’m unable to get up.” Upon further questioning, you determine that he had a mechanical fall 18 hours earlier (with no prodrome, i.e., early sign of disorder or disease) that caused him to collapse onto his knees. He lives independently and was unable to call for help or get up on his own.
Initial vital signs include a heart rate of 88, blood pressure is 124/76, respiratory rate of 16 and SpO2 of 99% on room air. His exam is most notable for his lower extremities, which include bilateral edema extending to knees, tense anterior compartments, loss of sensation, dusky skin with delayed capillary refill and without palpable dorsalis pedal pulses of either foot. Due to his concerning physical exam, he’s transported to the closest medical center to be evaluated for bilateral lower leg ischemia.
En route, his blood sugar is 98 mg/dL and his ECG shows sinus rhythm with a right bundle branch block and QTc prolongation of 533 milliseconds.
Upon arrival to the ED, the patient continues mentating normally and confirms the history of recent events. A chest X-ray is performed and shows small bilateral effusions. His labs reveal multiple abnormalities most notable for hyperkalemia (potassium of 5.4 mEg/L), acute kidney failure, rhabdomyolysis (creatinine kinase 63,308 units/L), liver function derangement and metabolic acidosis. He’s treated with calcium gluconate, insulin/glucose, sodium bicarbonate IV push, and IV fluids for his hyperkalemia. He’s also started on a sodium bicarbonate drip.
He’s evaluated by the orthopedic surgery team and taken to the operating room for a fasciotomy of both lower legs, monitored in the surgical ICU for more than a week, and received several sessions of intermittent dialysis before ultimately being discharged to a residential rehabilitation facility for aggressive physical therapy and wound care.
This patient has a classic presentation for rhabdomyolysis and acute compartment syndrome, a clinical condition rare enough to be overlooked but dangerous enough to be never forgotten. Rhabdomyolysis is estimated to have an annual occurrence of 26,000 cases and occurs more frequently in adults and in males.1 In this case, the patient’s prolonged period of immobility led to limb ischemia, which led to muscle cell breakdown. As the myocytes break down, they release intracellular contents (including potassium, creatinine kinase and massive amounts of myoglobin) into plasma, overwhelming the body’s mechanisms to combat it.2,3
Elevated potassium (i.e., hyperkalemia) poses an immediate life threat due to cardiac dysrhythmias and can lead to cardiac arrest. (See Table 1.) Serum potassium levels are regulated by the kidneys; the release of myoglobin precipitates in the glomeruli, leading to renal dysfunction, which further hinders the ability to excrete excess potassium.1
Rhabdomyolysis can cause a multitude of other problems such as hypovolemia from either dehydration or loss to the interstitial space, other electrolyte derangements (such as hypocalcemia and hyperphosphatemia), liver injury, compartment syndrome, metabolic acidosis and coagulopathy.
In the hospital, rhabdomyolysis is diagnosed by measurement of creatinine kinase, which will usually be elevated, to at least five times the upper limit of normal. However, the condition can be suspected if the patient reports, or you observe, very dark “Coca-Cola” urine, which is caused by the myoglobin leaked into the urine. (See Figure 1, top).
Acute compartment syndrome and rhabdomyolysis can occur independently or simultaneously (as in this case). Compartment syndrome occurs most commonly in the lower leg or forearm, but can happen whenever localized pressure inside a “compartment” interferes with blood flow and perfusion.
The lower leg is divided into four compartments formed by the tibia, fibula and dense fibrous connective tissue bands (i.e., fascia). Lower leg compartment syndrome is usually seen after a fracture or other trauma that causes bleeding and soft tissue swelling; as the pressure in the compartment builds, blood flow is reduced, causing ischemia and ultimately infarction of the muscle tissue. Of course, the ischemia and cell damage causes more inflammation and soft tissue swelling, further increasing compartment pressure and decreased perfusion, setting up a vicious cycle that can ultimately threaten the viability of the limb.
In both rhabdomyolysis and acute compartment syndrome, patients may report muscle tenderness or swelling. Swelling over the extremity may not be present until fluid resuscitation has been initiated. Approximately 10% of patients will have skin discoloration or blisters indicative of ischemic injury.2 Up to 50% of patients will present asymptomatically or with non-specific findings.2
Because the physical exam may not be revealing, it’s imperative that a provider considers the history that precedes their patient’s presentation for possible exposures or events. A history of prolonged immobilization or compression, traumatic injury, electrical injury, comatose with or without drugs or alcohol, severe agitation, heat stroke, strenuous exercise, fasting, viral illness, medications (e.g., statins for high cholesterol) or family history would be concerning.4
As with all patients, the initial management should include assessment and treatment of airway, breathing and circulation. Patients should receive an IV, possibly two, with early and aggressive fluid resuscitation and frequent re-evaluation for volume overload such as pulmonary edema. Initial fluid use has been recommended as 20 mL/kg in children and 1–2 L/hr in adults.1 Especially in cases with concern for limb ischemia, re-evaluation of the limb’s pulse, motor function and sensation is paramount.
These patients should be assessed for evidence of cardiac arrhythmia or hyperkalemia with peaked T waves, prolongation of PR and QRS intervals, loss of P waves or sine waves. (See Table 1, above.)
If any of these ECG abnormalities are present, the patient should be treated quickly by first receiving calcium gluconate or calcium chloride (if available) followed by continuous albuterol and sodium bicarbonate until the QRS narrows. Calcium is thought to stabilize the heart’s electrical conduction system and reduce the likelihood of dysrhythmia. Albuterol and sodium bicarbonate transiently move potassium out of the serum and into cells, which reduces the likelihood of dysrhythmia.
Aside from hyperkalemia detection and treatment, these patients may benefit from forced alkaline diuresis with a dedicated line (due to inadvertent precipitation with other medications) for a sodium bicarbonate drip 100 mEq/L 8.4% sodium bicarb (2 ampules of standard bicarbonate) added to 1 L of 0.9% normal saline and infused at a rate of 200 mL/hr.2 The evidence for use of Lasix and mannitol is unclear. Although these patients may initially be hypocalcemic, it’s not advised to empirically treat them, unless there’s either a cardiac dysrhythmia or a seizure, because of development of hypercalcemia in the recovery. Local EMS protocols for rhabdomyolysis and hyperkalemia should be followed, and contacting on-line medical control can be helpful.
The potential serious complications of rhabdomyolysis and acute compartment syndrome should drive transport destination decisions. When either of the conditions are suspected, the patient should be transported to a facility capable of emergent hemodialysis (for hyperkalemia and/or acute kidney failure) and fasciotomy (to relieve pressure in the compartments and restore perfusion to the limb). Many community hospitals may not have these capabilities.
Early recognition of rhabdomylolysis, aggressive management of fluid and electrolyte abnormalities, and identification of other complications such as acute compartment syndrome are paramount in the care of these patients.
1. Muscal E. (June 22, 2015.) Rhabdomyolysis. Medscape. Retrieved Oct. 20, 2016, from http://emedicine.medscape.com/article/1007814-overview.
2. Miller ML. (Oct. 13, 2016.) Clinical manifestations and diagnosis of rhabdomyolysis. UpToDate. Retrieved Oct. 20, 2016, from www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-rhabdomyolysis?.
3. Eustace JA. (Nov. 16, 2015.) Prevention and treatment of heme pigment-induced acute kidney injury (acute renal failure). UpToDate. Retrieved Oct. 20, 2016, from http://www.uptodate.com/contents/prevention-and-treatment-of-heme-pigment-induced-acute-kidney-injury-acute-renal-failure?.
4. Miller ML. (Oct. 21, 2016.) Causes of rhabdomyolysis. UpToDate. Retrieved Oct. 28, 2016, from www.uptodate.com/contents/causes-of-rhabdomyolysis?.