Rhabdomyolysis is a condition in which skeletal muscle cells break down and leak their contents into the extracellular space and bloodstream. We can break down the causes of rhabdomyolysis into two broad categories –  physical and non-physical.

Physical causes are usually related to prolonged physical pressure placed on blood vessels, leading to tissue ischemia. This can be due to prolonged immobilization, crush injuries, and prolonged use of surgical tourniquets. Other physical causes are very strenuous exercise, status epilepticus and high-voltage injuries. 

Non-physical causes can be due to things like infection, septic shock, electrolyte imbalances, and snake venom. Medication-induced rhabdomyolysis can be caused by several drugs including statins, corticosteroids, diuretics, antimalarial drugs and illicit drugs administered intramuscularly or IV.  

Rhabdomyolysis = the breakdown of striated muscle

The most common causes of rhabdomyolysis are trauma, overexertion, toxic substances and medication. Overall, rhabdomyolysis caused by physical factors results in poorer outcomes than when caused by non-physical factors.

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Rhabdomyolysis pathophysiology

Rhabdomyolysis occurs when there is direct physical damage to the muscle tissue, depletion of ATP, and damage to the muscle tissue membrane (sarcolemma). 

In cases of physical damage, as the muscle reperfuses (such as when a patient who fell is lifted off the ground), leukocytes find their way to the damaged cells, which brings along a host of other components that further damage the fibers. 

Regardless of the cause, when a muscle cell membrane is injured, there’s an influx of sodium and calcium into the cell. Water follows and is drawn into the cell, leading to cellular edema and disruption of cell structures. The excessive intracellular calcium leads to further cell damage, disruption of ion channels, and depletion of ATP. Once ATP is depleted and calcium reaches a critical level, the cell is unable to compensate, resulting in cellular death. 

When the cell dies it breaks apart sending potassium, calcium, myoglobin, uric acid, creatine kinase, and other materials into circulation.

Let’s talk about each of these in more detail:

  • Potassium – Hyperkalemia causes serious cardiac dysfunction ranging from palpitations to ventricular fibrillation. Additionally, hyperkalemia causes significant muscle weakness that can progress to total paralysis. 
  • Calcium – Hypercalcemia causes a range of problems including bradycardia, hypertension, acute renal insufficiency, nephrolithiasis, muscle weakness, vomiting, and a short QT-interval (which can lead to arrhythmias and sudden cardiac death).
  • Myoglobin – Excess myoglobin precipitates in the renal glomeruli causing damage. The heme in myoglobin is broken down into free iron, which also damages the renal tubules. Additionally, it reacts negatively with the lipid membrane, causing even more renal damage. The presence of myoglobin in the urine is what causes the characteristic dark, “tea-colored” urine of rhabdomyolysis.
  • Uric acid – When muscle cells are damaged, uric acid is released and forms crystals which damage renal tubules.
  • Creatine kinase – Found primarily in heart and skeletal muscle, levels will rise when muscle injury is present. 

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What are the complications of rhabdomyolysis?

Acute kidney injury – Up to 58% of patients with rhabdomyolysis will suffer from acute kidney injury (AKI). Renal injury is associated with a higher incidence of mortality and increased usage of renal replacement therapy.

Electrolyte imbalances – At the time of injury, calcium first shifts into the muscle cell resulting in hypocalcemia. As the cells lyse, calcium and potassium are released, leading to hypercalcemia and hyperkalemia. The most important consideration with these electrolyte imbalances is their effect on cardiac electrophysiology.

Disseminated intravascular coagulation (DIC) – Thought to be caused by the release of thromboplastin, DIC is a late complication of rhabdomyolysis. You can learn more about DIC here.

Compartment syndrome – The release of intracellular components and fluid leads to edema which can be further compounded by aggressive fluid resuscitation. The edema can be significant, putting pressure on vasculature within the confined space and significantly impeding blood flow. Learn more about compartment syndrome here.

If left untreated, rhabdomyolysis can be fatal. In severe cases, mortality rates can be as high as 59%.

Now that you have some background understanding of rhabdomyolysis, let’s go through how to care for these patients using the Straight A Nursing LATTE method

L: How does the patient with rhabdomyolysis LOOK?

The classic triad of symptoms for rhabdomyolysis are muscle pain, weakness, and dark “tea colored” urine. However, it is important to note that only about 10% of patients actually present with all three symptoms. 

Other signs and symptoms include swelling, stiffness and/or cramping, presence of a pressure injury, reduced urine output, malaise, fever, nausea/vomiting, abdominal pain, palpitations and abnormal ECG.

A: How do you ASSESS the patient with rhabdomyolysis?

Due to the high risk for acute kidney injury, monitoring urine output and urine characteristics are vital nursing assessments. With that, you’ll also monitor the patient for signs of fluid volume overload, namely edema and pulmonary congestion. 

Other key assessments include: 

  • Get a full set of vital signs. You are likely to see elevated HR, RR and BP due to pain and inflammatory response.
  • Assess for the 5 Ps of limb ischemia. Compartment syndrome can be severe enough to cause limb ischemia. Assess for pulselessness, pallor, paresthesia, poikilothermia and paralysis.
  • Neuromuscular assessment, looking for signs of muscle weakness and tenderness.
  • Assess for localized and systemic edema, especially when giving fluid boluses.
  • Assess cardiac function with continuous ECG monitoring. 
  • Ask the patient/family about recent trauma, infections, periods of immobilization, intense seizure activity or exercise, and medications.
  • Assess neurological status as drugs and toxins can induce rhabdomyolysis.
  • Perform a thorough skin assessment. Illicit drug use, injuries, bites and stings can cause rhabdomyolysis.
  • Ask the patient about their drug and alcohol use. Common culprit substances are alcohol, cocaine, marijuana, amphetamines, and ecstasy.
  • Ask about recent illness or exposure to infection. Assess the patient for signs of infection such as swollen lymph nodes, cough, fever, and rash. Common viral causes are influenza, Epstein-Barr virus and cytomegalovirus. Common bacterial causes include group A strep and salmonella. Malaria is also a culprit, so inquire about recent travel to locations where malaria is prevalent. Viral infections are the leading cause of rhabdomyolysis in children.

T: What TESTS will be ordered for a patient with rhabdomyolysis?

  • 12-lead ECG: Used to identify cardiac arrhythmias which may be present due to electrolyte imbalances.
  • Creatine kinase: Highly sensitive to muscle injury and will begin to rise within 2 to 12 hours of the onset of injury and will reach its maximum in 24 to 72 hours. Serum CK levels are typically at least five times the normal value, with typical ranges between 1,500 and 100,000 units/L. This is the primary diagnostic lab test used to identify rhabdomyolysis.
  • Myoglobin: May be used to confirm diagnosis, but because it has such a short half-life, it is not sensitive enough to be used on its own. Myoglobin will begin to rise before CK and return to baseline while CK is still continuing to increase. When plasma myoglobin levels exceed 1.5 mg/dL, you’ll see the tea-colored urine that is a hallmark sign of rhabdomyolysis. Myoglobin can also be detected in the urine with a dipstick test.
  • BUN/Cr: These tests tell us about renal function and will be elevated in AKI.
  • Uric acid: Will be elevated in rhabdomyolysis.
  • Other tests will be conducted to monitor for complications or determine the underlying cause: 
    • WBC, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are likely to be elevated when the rhabdomyolysis is due to an infection or crush injury.
    • CBC, urinalysis and cultures to monitor the infectious process.
    • Toxicology for medication or drug-induced rhabdomyolysis.
    • Electrolytes due to the high risk for severe imbalances.
    • Albumin levels will be monitored as low levels are correlated with high risk for AKI and more severe disease.
    • Coagulation studies to assess for DIC.
    • CT and MRI may be helpful in identifying the underlying cause and identify the presence of compartment syndrome.

T: What TREATMENTS will be provided?

The key goals of treatment are to prevent the continued release of myoglobin into the bloodstream and to preserve renal function. 

Address the underlying cause – A vital component of rhabdomyolysis treatment is identifying and addressing the underlying cause to stop the release of myoglobin and other substances into circulation. 

Fluid resuscitation – Early fluid resuscitation restores renal perfusion, increases GFR and helps flush myoglobin and other substances from the kidneys. While there are no standard guidelines on the amount of fluid to administer, the consensus is that “normal saline” is preferred over Lactated ringers due to the lack of potassium in 0.9% NaCl. Patients may receive up to 10 liters of fluid per day to maintain a urine output of 200 -300 ml per hour until CK levels stabilize.

Bicarbonate administration – A sodium bicarbonate infusion may be utilized in patients with severe rhabdomyolysis (CK above 5,000 unit/L or evidence of a significant muscle injury). Sodium bicarbonate raises the pH of the urine and may help prevent AKI by diminishing the harmful effects of myoglobin on the kidneys. However, it is not used in all patients and is only used when arterial pH is less than 7.5, serum bicarbonate is less than 30 mEq/L and the patient does not have hypocalcemia.

Loop diuretics – Not given unless the patient has fluid volume overload and may actually cause hypocalcemia and promote cast formation in the kidneys.

Mannitol – Not routinely given but may be utilized if urine output is not adequate relative to the amount of fluid being administered.

Address hyperkalemia – Because hyperkalemia can cause significantly dangerous cardiac arrhythmias, it will be treated pharmacologically or with dialysis. The pharmacologic treatment for hyperkalemia is to give insulin plus dextrose. This combination causes a potassium shift into the intracellular environment. Patients with significant hyperkalemia may also receive calcium gluconate as it makes the heart less irritable and less likely to go into a dysrhythmia. 

Hemodialysis – In severe cases of rhabdomyolysis where the kidney injury is extensive and when patients have significant fluid volume overload, dialysis will be needed. 

Treat secondary complications – For example, a patient with compartment syndrome may require a fasciotomy and patients with DIC will receive platelets, cryoprecipitate, fresh frozen plasma and possibly PRBCs.

E: How do you EDUCATE the patient/family?

The important education components for your patient are to help them recognize the cause of rhabdomyolysis and any steps they can take to prevent future occurrences. This may include getting vaccinations to avoid infection, avoiding overexertion, abstaining from illicit drug use, or avoiding certain medications.

Other key teachings include: 

  • Individuals can reduce their risk for exercise-induced rhabdomyolysis by starting new exercise routines gradually, staying hydrated and avoiding excessive heat exposure. 
  • Know the signs of rhabdomyolysis – fatigue, weakness, muscle aches and tea-colored urine. 
  • Individuals who have suffered AKI should avoid nephrotoxic medications, including NSAIDs until their MD states it is safe to do so.
  • The individual will need to return to activity slowly. Swimming and other water exercises are good choices to prevent muscle strain and heat exposure.

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References:
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