Rhabdomyolysis, literally pronounced as rhab·do·my·ol·y·sis, is a disorder which damages the integrity of the sarcolemma of skeletal muscles which results in the release of myoglobin and other breakdown products into the bloodstream. In other words, it is a condition in which injury to skeletal muscle tissue causes it to quickly break down resulting in the release of large quantities of potentially toxic muscle cell components into the circulation.
This fatal disease is often accompanied by the excretion of myoglobin in the urine. Other complication of this life threatening syndrome includes myoglobinuric acute renal failure, hyperkalaemia and cardiac arrest, disseminated intravascular coagulation, and compartment syndrome.
Any physical or non physical cause which leads to muscle tissue destruction can bring on this condition. A crush injury and trauma are believed to be the most common cause. As the muscles are destroyed myoglobin is released into the bloodstream which is filtered out of the body by the kidneys. Myoglobin breaks down into harmful compounds blocking the structure of the kidney which eventually leads to kidney failure.
Other causes are electric shock, lightning stroke, arterial thrombosis, extreme physical exercise, persistent seizures, nonketotic hyperosmolar coma, bacterial infection, foodborne toxins, ketoacidosis, mitochondrial respiratory chain defects, abuse of some drugs and medications, alcoholism (with subsequent muscle tremors), certain inherited or genetic syndromes, etc. Rhabdomyolysis brought on by physical causes tends to be restricted to one region of the patient’s body, whereas non-physical rhabdomyolysis typically harms all of the body’s muscles at once.
ATP depletion appears to be the end result of most causes of rhabdomyolysis.
The most common symptoms are muscle stiffness or aching (myalgia), muscle tenderness, weakness of the affected muscles, abnormal urine color (dark, red, or cola colored) due to the presence of myoglobin.
As the muscle tissues break down and harmful components are released into the bloodstream, certain other symptoms may occur due to the disturbances in the electrolytes and other factors. These symptoms are fatigue, joint pain, weight gain, seizures, blood clotting, etc.
Pain, paresthesias, paralysis, low blood pressure, coma, confusion, nausea and vomiting can also be seen as a result of the consequences of the condition that originally led to the muscle breakdown.
Clinical research or blood tests will show an elevated serum creatine phosphokinase (CK). Other important biochemical findings will include myoglobinuria, hyperkalemia, hypocalcaemia, hyperphosphataemia, hyperuricaemia. Pathological findings can also include an increased cellular permeability to sodium ions due to either plasma membrane disruption or reduced cellular energy (ATP) production.
The condition may be suspected in any patient who has suffered from a crush injury, lengthy period of immobilization, or trauma, deteriorating kidney function, elevated levels of creatinine and urea, failing urine output, or darkened urine. It is also possible that this condition may be present in patients without any obvious history or physical sign of rhabdomyolysis.
Physical examination of a patient includes inspection of the body, palpation, auscultation and percussion. This helps in determining the presence or absence of any physical problems related to this disease.
The most reliable clinical examination to detect rhabdomyolysis is the level of creatine kinase (ck) in the blood. Creatine phosphokinase (CPK) is an enzyme found mainly in the heart, brain, and skeletal muscle. This is the most reliable and sensitive indicator as a damaged muscles releases this enzyme and CK levels 5 times the reference range suggest rhabdomyolysis, though CK levels in rhabdomyolysis are frequently as high as 100 times the reference range or even higher.
Other useful blood tests are complete blood count (hemoglobin, hematocrit, and platelets), Serum chemistries (blood urea nitrogen (BUN), creatinine, glucose, calcium, potassium, phosphate, uric acid), liver function test, Prothrombin time (PT), Serum aldolase, Lactate dehydrogenase (LDH) and urinalysis. This disease may also alter the results of the following tests: CPK isoenzymes, urine creatinine, serum creatinine.
Urine myoglobin test: myoglobin has oxygen attached to it and is a protein in the heart and skeleton muscles. As the muscles are destroyed myoglobin is released into the bloodstream which is filtered out of the body by the kidneys. Myoglobin breaks down into harmful compounds blocking the structure of the kidney which eventually leads to kidney failure. However it should be noted that since myoglobin has a half-life of 1-3 hours and is cleared from plasma within 6 hours, it may not prove to a reliable measurement if not done at the right time.
It has also been seen that around 25% of rhabdomyolysis patients have abnormal liver function tests due to liver damage, the potassium levels are high and the calcium levels are low(hypocalcemia).
The aim for treating rhabdomyolysis sufferers is to preserve the kidney functions. Treatment varies on individual patient’s condition.
- Fluid therapy: Getting fluids that contain bicarbonate may prevent kidney damage by quickly flushing myoglobin out of the kidneys. Fluids may need to be given through a vein.
- Electrolytes: Electrolyte levels are usually abnormal in the early stages of rhabdomyolysis. Hypocalcemia is noted early in the course of rhabdomyolysis. Temporary measures can be taken to correct these problems.
- Acute Kidney failure: Renal replacement therapy (RRT) may become necessary if acute renal failure develops in the rhabdomyolysis patient. Other ways of preventing acute renal failure is by maintenance of circulating blood volume by adequate fluid replacement, alkalinization of the urine, Dialysis, etc. compartment syndrome may occur and should be treated along with the treatment of rhabdomyolysis.
Medicines that may be prescribed include diuretics and bicarbonate but only under certain conditions since bicarbonate may aggravate existing hypocalcaemia.
Surgical and orthopedic treatment may be necessary, depending on the cause of rhabdomyolysis. Dietary modification may help to reduce the symptoms associated with some of the metabolic disorders. Strenuous activities should be avoided as it may aggravate the problem. Alcohol, overdose of narcotics should be discouraged.
Prompt action must be taken to prevent these complications in a patient with rhabdomyolysis.
It was first described in the victims of crush injury during World War. The final common pathway of rhabdomyolysis may be a disturbance in myocyte calcium homeostasis. In 1944, British physician Eric Bywaters was able to demonstrate that myoglobin was the main cause of the acute kidney failure associated with rhabdomyolysis.