part 3 crush injury

The second stage of rhabdomyolysis entails how the normal muscle cellular function is disrupted from the injury. The sarcoplasmic reticulum, which is involved in calcium transport, now has an “effusion of extracellular calcium that has diffused across the damaged cell membrane and into the intracellular space” (Childs, 2005, p.444). This intracellular calcium stimulates enzymes and proteases to break down the membrane. The destruction of the muscle cell membrane releases creatine kinase (CK), lactate dehydrogenase (LDH), alanine transaminase, calcium, myoglogin, potassium, uric acid, and phosphorus into the systemic circulation (Childs, 2005). 

The thirds stage of rhabdomyolysis involves the side effects of the cellular dysfunction.  As the calcium channels are opened, sodium and water also enters the cell. The integrity of the cell wall is thus lost, and cellular edema leads to muscle fiber necrosis and cellular death (Childs, 2005). The client also develops third spacing and hypovolemia, which will be discussed later (Wilson, 2006).

The fourth stage of rhabdomyolysis is when the “muscle cell death and systemic complications may lead to renal dysfunction” (Wilson, 2006, p. 22). The main cause for myoglobinuria is due to the following four components; intravascular volume depletion, renal vasoconstriction, and the presence of myoglobin in the systemic circulation and the urine (Russell, 2005). Myoglobin may not always be detected in the urine, however, that should not rule out the possibility of rhabdomyolysis. The capillaries of the nephron in the kidney are not always able to pass the large proteins that are often attached to the myoglobin (Wilson, 2006). The glomerular filtration rate (GFR) also has to be considered. If the rate is slow, then the myoglobin will not be able to be pushed through the nephron’s filter, and will instead end up in the systemic blood volume.  Hypovolemia is typically what lowers the GFR (Wilson, 2006). The rate of urine flow also has to be taken into consideration. If the client is not passing much urine, then myoglobin may not be able to be detected (Wilson, 2006). When myoglobin is present in the urine, the urine is referred to as being tea-colored. When a urinalysis is done, “the urine tests positive for blood and has an acid pH, but when sent to the laboratory, no red blood cells are present (Wilson, 2006, p.22).

Another likely factor in diagnosing rhabdomyolysis is that CK levels are typically five times or more than their normal range (Wilson, 2006).  This is due to the CK being leaked into the bloodstream from the damaged muscle cell membranes.  This factor should be considered, especially if myoglobin is not detected in the urine (Childs, 2005).

Hyperkalemia Caused By Tissue Damage

When an insult to the body occurs, musculoskeletal cells are damaged. For this reason, hyperkalemia is one of the most life-threatening complications of rhabdomyolysis. More than 98 % of potassium resides within the intracellular space and because of the high concentration, even a small amount of muscle damage can cause large amounts of potassium to be released into the extracellular compartment (Russell, 2005). 

Hyperkalemia is an electrolyte imbalance that is in an excess of 5.0 mEq/liter (Porth, 2004). Tissue injuries, such as burns or crush injuries, causes a transcellular shift of potassium from the intracellular to the extracellular compartments which results in elevated serum potassium levels. The same tissue injuries often cause a decrease in renal function, which is another potential source of hyperkalemia (Porth, 2004).