Loading...
Please wait, while we are loading the content...
Similar Documents
Crush syndrome due to earthquake subsidence
| Content Provider | Semantic Scholar |
|---|---|
| Author | Enç, Nuray |
| Copyright Year | 2002 |
| Abstract | Crush syndrome is one of the many types of damage encountered in the aftermath of an earthquake. It was first reported following the Messina earthquake in 1909 and during World War II in Germany. The first description of acute renal failure (ARF) caused by crush syndrome in modern English literature dates back to Bywaters and Beall’s description in bombing victims found in London during the Battle of Britain in World War II (Better, 1990; Better, 1997; Yavuz, 1999). Since then, a number of crush syndrome cases have been reported during epidemics, wars and other social incidents. During the last quarter of the 20th century, major earthquakes were the main cause of most cases of crush syndrome, including earthquakes in 1976 in Tangshan, China, in 1980 in South Italy, in 1988 in Armenia and in 1995 in Honshin-Awaji, Kobe, Japan (Abassi et al., 1998). Major earthquakes are followed by a substantial number of crush syndromes, provoking rhabdomyolysis and pigmentinduced ARF (Vanholder et al., 1999). The incidence of crush syndrome has been estimated at 2–5% (Better et al., 1992; Better et al., 1993; Better et al., 1997; Vanholder et al., 1999). Approximately 50% of patients with crush syndrome develop ARF, of whom about 50% will need dialysis (Ron et al., 1984; Vanholder et al., 1999). Table 1 summarises the reported experiences with major earthquakes during the period from 1985 to 1999 (Vanholder et al., 1999). In the Marmara earthquake, the proportion of dialysed patients with ARF was very high. The clinical crush syndrome occurs as a consequence of traumatic events, either accidents or disasters. In contrast with accidents involving only a few individuals, disasters can affect many victims simultaneously, all of whom may require medical care. As a result of compression, muscular cells are damaged, followed by the release of intracellular contents into the systemic circulation. This process is called rhabdomyolysis. One of the key compounds released is myoglobin. Myoglobin is filtered by renal glomeruli and transferred into the renal tubules, where it causes obstruction and functional failure (Yavuz, 1999). Other intracellular components, such as nucleotides, precursors of uric acid, proteins, phosphate and potassium, are also released from the damaged muscle cells. These have an important pathophysiological impact, as well as causing volume depletion of the victim. Today, rhabdomyolysis is one of the leading causes of ARF (Yavuz, 1999). However, it should be noted that most cases of rhabdomyolysis occurring during peacetime are provoked by non-traumatic processes, mainly alcohol abuse, muscular compression due to coma or seizures, electrolyte disturbances (hypokalaemia, hypophosphataemia), exertion, hyperthermia, drug ingestion and infectious diseases (Yavuz, 1999). It should also be remembered that muscular trauma does not necessarily lead to rhabdomyolysis. Similarly, rhabdomyolysis does not always result in ARF; other causes of ARF include dehydration, sepsis and drug nephrotoxicity. |
| Starting Page | 23 |
| Ending Page | 27 |
| Page Count | 5 |
| File Format | PDF HTM / HTML |
| DOI | 10.1891/1748-6254.2.1.23 |
| Volume Number | 2 |
| Alternate Webpage(s) | http://connectpublishing.org/assets/journals/2_1_4.pdf |
| Alternate Webpage(s) | https://doi.org/10.1891/1748-6254.2.1.23 |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
