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Outmuscling rhabdomyolysis

Kring, Daria RN,BC, MSN

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Abstract

The day after his 21st birthday, James Singer decided to celebrate his official passage to legal drinking age with all the tequila shots he could muster. When he finally returned home, he passed out on the way to the bathroom. He stayed in that position on the hardwood floor until 5 p.m. the next day, when a friend discovered him unconscious, and called 911.

Mr. Singer arrived at the emergency department by ambulance and has been transferred to your intensive care unit. He has an indwelling urinary catheter, which is draining brown-colored urine. He's receiving an infusion of 0.9% sodium chloride solution through a large-bore I.V. line at a rate of 200 ml/hour, to maintain a urine output of 200 to 300 ml/hour. His admission diagnosis states, “Acute alcohol ingestion and dehydration. Rule out rhabdomyolysis.”

Muscle trouble

Rhabdomyolysis is a potentially fatal disease characterized by massive muscle tissue breakdown, such as from traumatic injury, excessive exertion, and ingestion of toxic substances, accompanied by the release of potentially toxic breakdown products into the bloodstream. See How rhabdo-myolysis threatens.

The muscle cell breakdown seen in rhabdomyolysis can be caused by any situation in which muscle cells are massively destroyed, including traumatic crush injuries, severe extensive burns, significant blunt trauma, and high-voltage electrical injuries. In fact, any time a muscle contracts for an extended time—as in status epilepticus or extreme physical effort—cells may release their contents. Muscle hypoxia from shock or hypothermia also can lead to rhabdomyolysis. Hyperthermia, as is often seen in athletes training during hot summer months, creates a need in the body for more oxygen, and may lead to hypoxia as well.

Alcohol abuse or alcohol poisoning (such as from ingestion of ethylene glycol in antifreeze or methanol in Sterno) is often seen with rhabdomyolysis. Binge alcohol drinking can be toxic to muscle cells, causing generalized destruction. Use of illegal drugs (such as cocaine, heroin, or LSD) or abuse of prescription drugs (such as barbiturates and amphetamines) are often implicated in rhabdomyolysis. Cocaine overstimulates the sympathetic nervous system, producing muscle destruction. Excessive drug and alcohol use also may be associated with long periods of immobility; this too can cause muscle breakdown. See Causes of rhabdo-myolysis for more information.

So you can see that Mr. Singer was at risk for muscle cell damage from the minute he downed his first tequila shot; the excessive alcohol consumption destroyed his myocytes. He also drank shots without other fluid intake, the root of his dehydration. That's because alcohol inhibits antidiuretic hormone (ADH) secretion. Without ADH, the kidneys get rid of water instead of reabsorbing it for use in the body, resulting in diuresis. When Mr. Singer passed out on the floor, the muscles in his left leg and arm remained compressed by his body weight for well over 14 hours, causing further damage.

One thing leads to another

Why do we need to be so concerned about rhabdomyolysis? The massive muscle cell breakdown characteristic of the disease puts a person at risk for multiple organ system failure, even death. Here's why:

Myocytes contain potassium, magnesium, phosphate ions, acids, creatinine kinase (CK), lactic dehydrogenase (LDH), and myoglobin. Paradoxically, although these substances are essential to cell function, many are toxic to the body when released into the bloodstream. For example, hyperkalemia interferes with the action potentials needed for cardiac contraction, and can lead to cardiac arrest if not treated.

About one-third of patients with rhabdomyolysis develop acute renal failure due to the release of myoglobin. Normally, myoglobin is harmless to the body and passes through the nephron, which consists in part of the renal tubules. But the dehydration common in rhabdomyolysis leads to a low urine flow rate, which, coupled with an acidic environment, causes the myoglobin to precipitate. The precipitation creates sloughing, obstruction, and edema in the renal tubules, and may eventually cause acute renal failure. This common complication must be detected and treated early to prevent death.

Beyond a reasonable doubt

Although the health care provider suspects Mr. Singer has rhabdomyolysis because of his history and physical assessment, the actual diagnosis is made through lab findings. The hallmark for rhabdomyolysis is an elevated serum CK level. A normal level is 45 to 260 units/liter; in patients with rhabdomyolysis, it may be as high as 200,000 units/liter. Suspect rhabdomyolysis in patients with risk factors for the disorder and serum CK levels two to three times the reference range.

The presence of dark urine (usually brown) is often the first clue to rhabdomyolysis and indicates myoglobin in the urine. A urine dipstick test also can help make the diagnosis. A patient with rhabdomyolysis typically has a hemoglobin-positive reading. However, urinalysis will show few, if any, red blood cells (RBCs). The absence of RBCs means that myoglobin, not hemoglobin, is reacting to the dipstick reagent.

Urinalysis shows the presence of brown casts, which form in the nephrons and produce blockage. The brown color of the casts comes from the pigment in myoglobin.

In addition to hyperkalemia, hyperphosphatemia is another possible sign of rhabdomyolysis. Both are due to the large release of muscle cell contents into the bloodstream.

Patients with rhabdomyolysis are at increased risk for disseminated intravascular coagulation (DIC), which, if left untreated, can lead to profuse hemorrhaging. If you suspect DIC, obtain prothrombin time, activated partial thromboplastin time, platelet count, and fibrinogen level.

Putting the lid back on

Once rhabdomyolysis is suspected, your main treatment goal is to aggressively hydrate the patient to increase the glomerular filtration rate and dilute and clear toxic substances from the blood and kidneys. Start an infusion of 0.9% sodium chloride solution through a large-bore I.V. line to maintain urine output of 200 to 300 ml/hour. Place an indwelling urinary catheter to ensure accurate measurement. If urine output is too low, expect an order for an osmotic diuretic such as mannitol or a loop diuretic such as furosemide.

The health care provider may also order an I.V. infusion of sodium bicarbonate to alkalinize the urine and reduce the toxic effects of myoglobin on the nephrons. Sodium bicarbonate also controls the acidosis and hyperkalemia associated with rhabdomyolysis.

Closely monitor the patient's blood urea nitrogen (BUN) and creatinine levels. Increases may signal acute renal failure, which usually requires emergency hemodialysis to clear the body of toxic substances and prevent further kidney damage. This may be only a temporary measure until the kidneys can regain function. However, in a 2002 analysis of 84 patients with rhabdomyolysis that led to acute renal failure in 78 patients, 49 recovered, 5 required maintenance dialysis, and 30 died. Although these outcomes may reflect the degree of trauma that led to the rhabdomyolysis in the first place, be aware that your patients with acute renal failure caused by rhabdomyolysis are at high risk of dying.

Watch it!

Although Mr. Singer seems relatively stable on arrival to your unit, vigilant monitoring is in order. Life-threatening electrolyte imbalances, metabolic acidosis, acute renal failure, and DIC are possible within the next 24 hours. Aggressive I.V. therapy is crucial to ensure adequate hydration and urinary output. Monitor fluid status carefully to avoid fluid overload. Check his intake and output hourly, weigh him daily, and assess for neck vein distension and abnormal breath sounds. He may need a pulmonary artery catheter to more closely monitor fluid status.

Immediately contact his health care provider if his urine output drops below 200 to 300 ml/hour. Protect Mr. Singer's kidneys at this vulnerable time. Limit the use of nephrotoxic agents, such as certain drugs (for example, gentamicin) and I.V. contrast medium. Keep a watchful eye on lab values. Draw blood for a CK level every 6 to 12 hours to monitor the progression of rhabdomyolysis. Check electrolyte levels and arterial blood gas results; they can alert you to potential life-threatening imbalances. Monitor him for cardiac arrhythmias secondary to electrolyte imbalances, especially acute hyperkalemia. Obtain a 12-lead ECG at least daily to monitor for signs of hyperkalemia, such as peaked T-waves.

Another hurdle

With all the damage to his muscle cells and the aggressive I.V. therapy required to manage rhabdomyolysis, Mr. Singer may develop significant edema in his muscles. Although more common in crush injuries, compartment syndrome is a possible complication. This limb-threatening and life-threatening condition is observed when pressure builds up in a closed anatomic space.

Untreated, compartment syndrome can lead to tissue necrosis, permanent functional impairment, and, if severe, renal failure and death.

In compartment syndrome, the fascia surrounding a muscle doesn't allow for much expansion. If muscle cells swell, the fascia becomes very tight, pressure builds within the compartment, and arterial flow is occluded. Fasciotomy is the definitive therapy for compartment syndrome to prevent further local tissue necrosis.

The finish line

About 5% of patients with rhabdomyolysis die. Given Mr. Singer's age, early intervention, and diligent monitoring, he'll likely make a full recovery. To prevent future episodes of rhabdomyolysis, however, he should be advised to drink alcohol in moderation and to drink at least two glasses of water for every alcoholic beverage.

How rhabdomyolysis threatens

Figure
Figure

Myoglobin released by damaged muscles is filtered in the glomerulus and reabsorbed in the proximal renal tubule. As myoglobin is degraded, toxic metabolites form myoglobin-protein casts that clog the tubules, decreasing renal perfusion and potentially leading to acute tubular necrosis and renal failure.

Causes of rhabdomyolysis

Anything that destroys large numbers of muscle cells can lead to rhabdomyolysis. Here are some causes:

  • Direct muscle injury, such as from animal bites, burns, crush injuries, electrocution, fights or beatings, or high-impact trauma
  • Drugs or toxins, including illegal drugs, alcohol, caffeine, venom, and adverse reactions to statins. (Patients taking statins for hyperlipidemia should have their CK levels carefully monitored along with their blood lipids and liver enzymes. Patients are at higher risk for statin-induced rhabdomyolysis if they have renal impairment, hypothyroidism, a personal or family history of hereditary muscle disorders, history or muscular toxicity with another statin or a fibrate, abuse alcohol, are of Japanese or Chinese ethnicity, or also take a fibrate.)
  • Hypoxia, such as from arterial embolism, carbon monoxide poisoning, compartment syndrome, constrictive dressings or casts, drowning, hypotension, prolonged immobility, shock, sickle-cell crisis, or tourniquet use
  • Infection, including human immunodeficiency virus, influenza virus, sepsis, tetanus, or toxic shock syndrome
  • Muscle overuse, as from delirium tremens, seizures, severe agitation, strenuous exercise, or tetany
  • Systemic imbalances such as hyperosmolar hyperglycemic nonketotic coma, hypokalemia, hyponatremia, or thyroid storm
  • Temperature extremes, such as frostbite, hyperthermia, hypothermia, or malignant hyperthermia.

Daria Kring is a clinical nurse specialist at Moses Cone Health System in Greensboro, N.C. This article was adapted from Kring D, Rhabdomyolysis: Out-muscling a life-threatening illness, Nursing made Incredibly Easy! November/December 2004.

SELECTED REFERENCES

Criddle L. Rhabdomyolysis: Pathophysiology, recognition, and management. Critical Care Nurse, 23(6):14–30. December 2003.
Criner J, et al. Rhabdomyolysis: The hidden killer. Medsurg Nursing, 11(3):138–143, 155. June 2002.
Ravnan S, et al. Cerivastatin-induced rhabdomyolysis: 11 case reports. Pharmacotherapy, 22(4):533–537. April 2002.
Sulowicz W, et al. Acute renal failure in patients with rhabdomyolysis. Medical Science Monitor, 8A(1):CR24–CR27. January 2002.
© 2005 Lippincott Williams & Wilkins, Inc.