What is crush syndrome?
In some cases crush injuries can cause severe life threatening condition called crush syndrome. Crush syndrome is a systemic reaction to breakdown of muscles. When muscle cells are injured, they let out components that can lead to kidney failure. Crush syndrome is characterized by:
- Shock due to sequestration of the blood flow
- High level of potassium
These two characteristics can lead to metabolic acidosis, acute kidney failure and disseminated intravascular coagulation syndrome (DIC) .
Crush injuries that cause this syndrome are often due to rubble falling on a person- for example in case of an earthquake (also read: post concussion syndrome). In some cases crush syndrome can also be seen in persons after car crashes, especially if the extraction time is prolonged. It can also be seen in persons who have compressed a part of their body for too long.
This scenario sometimes happens to persons who have fallen down due to intoxication, stroke or mental illness. Heroin and alcohol have been found as the most common causes for intoxication leading to crush syndrome. In some cases a person can regain consciousness, but the muscle pain is too severe for them to get up, leading to even more damage .
The injury to the muscle cells is caused by compression of muscle fibers due to direct trauma as well as deprivation of blood to the area. The tissue start to lack oxygen and it causes rapid breakdown of muscle cells. The injury disrupts the proper functions of potassium and sodium channels in the cell, which allows calcium to move freely in the cell. Increased level of calcium stimulates chemicals in the cell which leads to its breakdown.
Skeletal muscle can tolerate around 2 hours of compression, without being permanently damaged, but more than 4-6 hours can cause necrosis. When the circulation of the damaged area is restored, it causes reperfusion injury. Large quantities of potassium, myoglobin, creatine kinase and urate go into blood stream and they can have toxic effects. Myogobin usually is in the blood stream in minor levels, but if more than 100 g of muscles are damaged, it causes excess myoglobin. It is filtrated by the kidneys and it can cause obstruction of kidney tubules with subsequential damage .
Symptoms & Signs
Heart and vascular system
- Dysrythmia- due to increased level of potassium
- Shock- due to hypovolemia
- Acidemia- low blood pH; it can cause headaches, confusion, tremor and coma [1,2]
- Hypovolemia, release of myoglobin and other toxic agents causes kidney damage
- Tea or cola colored urine
- Oliguria- small amounts of urine[1,2]
- Acute respiratory distress syndrome
- Pulmonary edema due to large amounts of crystalloid fluids used in treatment
- Fat emboli in lungs caused by bone fractures due to injury [1,2]
- Infection due to initial trauma and open wounds (also read toxic shock syndrome)
- Increased risk of infection due to fasciotomy- treatment for compartment syndrome[1,2]
- Absence of pain (severe pain in affected area is a sign of compartment syndrome)
- Skin is pale in the area of compartment
- Loss of sensation in the affected area (read about cauda equine syndrome)
- Loss of pulse distant from the injury[1,2]
Crush syndrome Vs. compartment syndrome
Crush syndrome is caused by an external force. Once it has been removed, the affected area starts to swell. Compartment syndrome is caused by excessive perfusion pressure in the area. When the pressure is increased in a closed space, the perfusion is lost and it can cause muscle death. This syndrome is often seen in crush syndrome patients.
The diagnosis of crush syndrome should be made prior to any action is taken to transport the patient to a hospital. Initial assessment includes:
- ABCs- assessing airways, breathing and circulation
- Monitoring vital signs and levels of oxygen in the blood
- Oxygen administration
- Assessing 5 Ps in the affected area- pain, paraesthesia, paralysis, pallor and pulse (for other causes of sudden paralysis read: Guilian-Barre syndrome)
- Preserve body heat
- Initiate infusion of saline during extraction
- Insert urinary catheter and monitor urine output 
After the initial assessment is done and measures taken, the patient can be extracted.
In hospital environment, the following tests should be done:
- blood tests
- phosphate levels
- creatine kinase (death of muscle cells is suggested when this level is 5-10 times higher than normal)
- uric acid
- full blood count, clotting studies
- blood gases
- liver enzymes
- urine dipstick test for myoglobin
- ECG to monitor arrhythmias
- Trauma assessment- X-rays, CT 
- Initial fluid replacement before the patient is moved
- Usually central line is used
- In some cases up to 25l of intravenous fluids are given
- Saline, glucose drip and bicarbonate are used
- Patients urine output should be 300ml/hr
- Mannitol is often used
- In case of kidney failure, dialysis is used 
- High pressure physically dissolves oxygen in the blood
- Enhances tissue oxygenation
- Vasoconstriction occurs, lowering edema
- Assists wound healing
- Also used to treat Steven-Johnson syndrome
Usually wide spectrum and anti-necrotic antibiotics are used.
- Compartment can be treated by fasciotomy
- Amputation can prevent crush syndrome
There is a lot of the outcomes of crush syndrome. It has been reported that 4 to 33% of patients develop kidney failure that requires dialysis. Mortality rate has been reported to be 3 to 50%. These results are mostly affected by the first response. For example in remote areas where the treatment is not available straight away, the mortality rates are higher .
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- General information: http://patient.info/doctor/crush-syndrome
- Causes: http://www.medscape.com/viewarticle/819850
- Pathophysiology: http://www.emsworld.com/article/10321291/beyond-the-basics-crush-injuries-and-compartment-syndrome
- Initial assessment: https://www.ems1.com/patient-handling/articles/767352-4-things-EMS-providers-must-know-about-crush-syndrome/
- Diagnosis and other information for health professionals: http://www.med.or.jp/english/pdf/2005_07/341_352.pdf
- Treatment: http://medind.nic.in/maa/t10/i4/maat10i4p317.pdf