(medicine) A severe, often fatal condition that follows a severe crushing injury, particularly involving large muscle masses, characterized by fluid and blood loss, shock, hematuria, and renal failure. Also known as compression syndrome.
| Sci-Tech Dictionary: crush syndrome |
(medicine) A severe, often fatal condition that follows a severe crushing injury, particularly involving large muscle masses, characterized by fluid and blood loss, shock, hematuria, and renal failure. Also known as compression syndrome.
| 5min Related Video: Crush syndrome |
| Sports Science and Medicine: compression syndrome |
An overuse injury characterized by pain and muscle stiffness in areas where the space available for tissues (e.g. muscles, nerves, and blood vessels) is limited. During exercise, the tissue is pressed against another structure and becomes inflamed or damaged. See also compartment syndrome, compression neuropathy.
| Medical Dictionary: crush syndrome |
A severe shocklike condition that follows release of a limb or other large body part after a prolonged period of compression, characterized by edema, hematuria, and renal failure. Also called compression syndrome.
| Veterinary Dictionary: crush syndrome |
The edema, oliguria and other clinical signs of renal failure that follow crushing of a part, especially a large muscle mass, causing the release of myoglobin. See also lower nephron nephrosis.
| Wikipedia: Crush syndrome |
| Crush syndrome | |
|---|---|
| Classification and external resources | |
| ICD-10 | T79.5 |
| ICD-9 | 958.5 |
| DiseasesDB | 13135 |
| MeSH | [1] |
Crush syndrome (also traumatic rhabdomyolysis or Bywaters' syndrome) is a serious medical condition characterized by major shock and renal failure following a crushing injury to skeletal muscle. Cases commonly occur in catastrophes such as earthquakes or war, where victims have been trapped under fallen masonry.
Contents |
The syndrome was discovered by British physician Eric Bywaters in patients during the 1941 London Blitz.[1][2]
It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products - notably myoglobin, potassium and phosphorus - that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions).
The specific action on the kidneys is not fully understood, but may be due in part to nephrotoxic metabolites of myoglobin.
Treatment should begin at the time of extrication and anticipate the syndrome. In adults, a saline infusion of 1000-1500 ml/h should be initiated during extrication. When a urine flow has been established, a forced mannitol-alkaline diuresis up to 8 L/d should be maintained (urine pH greater than 6.5). Once the patient reaches hospital, 5% dextrose should be alternated with normal saline to reduce the potential sodium load.
Alkalinization increases the urine solubility of acid hematin and aids in its excretion. This may protect against renal failure and should be continued until myoglobin is no longer detectable in the urine. In addition to its protective effect as an osmotic diuretic, mannitol also is an effective scavenger of oxygen free radicals and may help reduce the reperfusion component of this injury by this mechanism.
In view of the risk of crush syndrome, current recommendation to lay first-aiders (in the UK) is to not release victims of crush injury who have been trapped for more than 15 minutes.
This treatment has some opposition. The Australian Resuscitation Council recommends in Guideline 8.20 "If safe and physically possible, all crushing forces should be removed as soon as possible after the crush injury" [3]
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