Acute rhabdomyolysis syndrome: Diagnosis and treatment

2021-09-05 10:49 AM

Rhabdomyolysis, a syndrome in which skeletal muscle cells are damaged, and destroyed, leading to the release of a variety of muscle cell substances into the bloodstream.

Acute rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle components into the circulation. Creatine kinase (CK) levels are often markedly elevated, and myalgia and myoglobinuria may be present. Disease severity ranges from asymptomatic elevations of serum muscle enzymes to life-threatening illness associated with extreme enzyme elevations, electrolyte imbalances, and acute kidney injury.

The clinical manifestations and complications of rhabdomyolysis are caused by muscle cell death, which can be triggered by any number of initiating events. The final common pathway for injury is an increase in cellular calcium and free intracellular mitochondrial ions. This can be caused by depletion of adenosine triphosphate (ATP), the cellular energy source, and/or by direct injury and rupture of the plasma membrane. The latter pathway of injury also leads to ATP depletion.

Acute rhabdomyolysis

Rhabdomyolysis

Increased intracellular calcium leads to protease activation, increased contractility of skeletal muscle cells, dysfunction of mitochondria, and production of reactive oxygen species, leading to skeletal muscle cell death. ATP depletion causes dysfunction of the Na/K-ATPase pump and Ca 2+ ATPase is essential for maintaining muscle cell integrity. ATP depletion leads to muscle cell damage and the release of intracellular muscle components, including creatine kinase (CK) and other muscle enzymes, myoglobin, and other electrolytes.

Rhabdomyolysis is a syndrome in which skeletal muscle cells are damaged and destroyed leading to the release of a variety of muscle cell substances into the blood: potassium, uric acid, myoglobin, lactic acid, enzymes: CPK, AST, ALT... lead to water-electrolyte disturbances, metabolic acidosis, shock, hyperkalemia, compartment syndrome, in addition, myoglobin also blocks renal tubules, causing acute renal failure. TCV, known since 1941 after the London bombing, has been described by Byvvaters and Beall as the "burying syndrome".

Definite diagnosis

Tests to help confirm the diagnosis:

Blood CPK enzyme over 1000 units/ml, CKMB < 5%.

Exclude other causes: myocardial infarction, cerebral infarction.

Differential diagnosis

Acute myocardial infarction: CPK-MB > 5%, troponin T increased above 0.05U/I, there are changes on electrocardiogram: ST elevation, Q wave...

New infarction: CPK is elevated, accompanied by focal neurological signs.

Diagnose the cause

Causes of trauma: severe trauma, burial syndrome, electric shock, severe thermal burns...

Medical causes: poisoning (sedation, sleeping pills, coma...) or prolonged immobility.

Generalized and prolonged convulsions or excessive muscle movement.

Alcohol poisoning, snake bites, bee stings...

Certain types of infections: tetanus, bacteria, viruses...

Acute ischemia: acute arterial occlusion due to compression, air, blood clot...

Some other cases: prolonged elevation or hypothermia, hypokalemia, hyponatremia, ketoacidosis, hyperosmotic coma, lack of some metabolic enzymes...

Symptoms

Fluid disturbance (due to water accumulation in the muscle), which can lead to hypovolemic shock and compartment syndrome.

Electrolyte disturbances (low sodium, calcium, increased potassium, phosphorus).

Transformation.

Disseminated intravascular coagulation (DIC).

Acute renal failure.

Multi-organ failure.

Risk factors for acute renal failure due to acute rhabdomyolysis

Traumatic shock.

Red-brown urine.

Systolic blood pressure < 90 mmHg.

CK > 15,000 units/ml.

Acute respiratory failure.

Late treatment >12 hours.

Tests to do:

Ure, creatinin.

CK (typically above 10,000U/I), uric acid, AST, ALT.

Blood gases (metabolic acidosis often seen: pH and HCO 3 - decreased blood)

Electrolyte: decreased sodium, calcium. Increases in potassium and phosphorus (note: a very rapid increase in potassium can lead to circulatory arrest, requiring repeated tests and continuous ECG monitoring).

Other tests serve to diagnose the cause.

Diagnostic imaging: depends on the cause of acute rhabdomyolysis.

Treatment

General treatment

Ensure steps: A (Airway) to ensure ventilation, B (Breathing), to ensure breathing; C (Circulation) to ensure circulation...

Assessment of damage, planning of temporary treatment, especially paying attention to the cervical spine, craniocerebral...

Determine the cause to address the cause, and at the same time determine whether the patient is at risk of acute renal failure or not? If available, treat immediately according to the protocol for acute renal failure in patients with acute rhabdomyolysis (next page).

Attention:

Adjust infusion rate according to central venous pressure.

Measure central venous pressure every hour to determine infusion rate.

Dialysis: until kidney recovery (average about 2 weeks).

Treatment of acute renal failure, acute hyperkalemia

If an acute renal failure (treatment according to acute renal failure protocol): balance water and electrolytes, acid-base, ensure nutrition, dialysis when indicated, use drugs that need to adjust the dose accordingly.

Treatment of compartment syndrome

Repeated examination, assessment of progress and extent of damage of vascular, neurological, software...

Incision of the fascia to reduce pressure (fasciotomy): pay attention to avoid incisions on arteries or nerves to limit the risk of infection (always present).

Amputate if no longer preserved.

Prevention

Acute rhabdomyolysis must be considered if the patient is lying down for a long time, has severe poisoning, or has elevated CK... or dark urine color.

If rhabdomyolysis is suspected, administer adequate fluids and administer diuretics to maintain a urine output of 150-200 mL/hour as soon as possible.