World j . Surg. 16, 899-903, 1992

World Journal of Surgery ¢~ 1992 by the Soei~t~

Internationale de Chirurgie

Crush Injury and Crush Syndrome

Moshe Michaelson, M.D.

Emergency Department, Rambam Medical Center, Haifa, Israel

Crush injury is caused by continuous prolonged pressure on the limbs. It ~s tOund in patients extricated after being trapped for at least 4 hours. The main injury is to the muscles of the limbs. Treatment should be conserv- ative and fasciotomy should be avoided. If fasciotomy is performed, it should be followed by radical debridement of the injured muscle in an attempt to avoid infection of the injured limb. Infection endangers the Patient,s life and is the main cause of morbidity and mortality today. The OUtcome of conservative local treatment of crush injury is much superior to that of operative treatment. The pathophysiology of crush injury is not fully understood and no good animal model is known. Crush syndrome, Which is the general manifestation of crush injury, is better understood. If not prevented, it will lead to acute renal failure. A method for preventing acute renal failure is discussed and a protocol is described. There is no doubt that prevention of acute renal failure is the goal in the treatment of crush syndrome and can be achieved.

A crush injury is caused by continuous prolonged pressure on the body. The major factor in producing this kind of injury is the length of time the pressure is applied; a crush injury is caused Only by hours of pressure. The shortest duration reported in the literature is 4 hours [1]. A crush injury occurs in limbs and is not found as a torso injury. The prolonged pressure required to Cause this syndrome is not compatible with life if applied to the torso. Crush injuries are found usually in disasters, such as earthquakes [2], bombings [3], mine accidents [4], and train accidents [5]. In all these disastrous events, extrication is a very long Procedure because of the need for highly skilled personnel and Specialized equipment which is usually not on the scene and must be brought from far away.

Crush syndromes are the systemic manifestations that follow crush injuries. Crush injury and crush syndrome were reported by the Germans during World War I, but the first to fully describe crush injury and crush syndrome was Bywaters [3, 6] during the blitz in London. Bywaters was the first to study this syndrome which occurred when people were trapped under the debris of bombardment and, although seemed to be only slightly Injured, died shortly after extrication.

BYwaters described the clinical syndrome and the changes that took place in the injured muscles, explained the events that followed the crush injury, and suggested a treatment. It should be stressed that his work gives us the basic understanding of

~eprint requests.. Moshe Michaelson, M.D., Emergency Depart- ,uent, Rambam Medical Center, P.O.B. 9602, Haifa 31096 Israel.

this injury and the keys to modern treatment. It is only the lack of technical development that prevented Bywaters and col- leagues from successfully treating crush syndrome. Since By- waters' work, there have been only sporadic reports in the English literature concerning crush injury, most of which are anecdotal reporting only one or two cases (Table 1) [2, 4, 5, 7-10]. Only in the last decade do we find a new interest in the subject, with papers reporting series of patients. One is from Italy [2] and describes 17 patients buried under debris during an earthquake. Another is from Israel, reporting on 16 patients buried under masonry debris during war [7, 8, 9]. Although earthquakes occur at least once a year, we find no reports of crush injuries occurring at such catastrophic sites [11].

Crush Injury

As described above, crush injuries are produced by continuous and prolonged pressure. By the time the patient is extricated from the rubble, he suffers no pain and has no physical complaints [12]. His main complaints are emotional, as can be expected from a person who has been buried for hours. This lack of complaint by the patient may be misleading, and his situation should be examined correctly [9].

During examination of a patient immediately following extri- cation, we find a severe neurological deficiency, mainly flaccid paralysis of the injured limb. When sensation is checked, one may find a patchy pattern of sensory loss, mainly to pain and touch [3, 9, 12]. There is no limb edema initially; the gross edema takes time to develop but, once developed, is most striking. In fact, it is so striking that it dominates the clinical picture. It should be stressed that the distal pulses are present even in the presence of gross edema, although they may be dit~cult to palpate. If the pulses are not demonstrated, an additional injury should be sought. After extrication, the hemo- dynamic status of the injured person deteriorates and, as edema develops, the patient becomes severely hypovolemic which, if not treated, may develop into severe shock.

The first urine specimen is dark, with the color ranging from pink to dark brown, depending on pH. The color results from the large amount of myoglobin found in the urine. To the physician unfamiliar with this phenomenon, the colour of the urine may lead one to suspect hematuria, an error which may be

900 World J. Surg. Vol. 16, No. 5, Sept./Oct. 1992

Table 1. Crush injury reported in the English literature since 1960.

Year Author (reference) No. of pts. Died Cause of injury

1968 Bentley & Jeffreys (7) 3 1 Coal mine 1977 Brown & Nicholls (5) 2 2 Train disaster 1982 Santangelo et al. (12) 19 5 Earthquake 1984 Michaelson et at. (8) 8 0 Bomb I984 Ron et al. (9) 7 1 Bomb 1984 Jones (4) 1 0 Tin mine 1987 Kikta et al. (10) 4 0 Bomb

Table 2. Blood chemistry anomalies found in crush syndrome patients.

Laboratory value Anomaly Normal range

Hematocrit t 44~c--55% Myoglobulin t t <0.1 ug/ml Potassium (initially) 1' 5.4-8.3 mg Calcium t 7.5-10.1 mg/DL Phosporus t 6.9-10.2 mg CPK t t 1" 730,000 u

CPK: Creatinine phosphokinase.

reinforced by a false positive result if checked with a lab stick for hemoglobin.

The skin and subcutis layers are not injured, but the muscles are severely damaged with necrosis and are pale in color. They do not contract to physical or electrical stimuli, and have lost their elastic component, feeling rather like cooked meat. If cut, they bleed profusely. The blood biochemical changes are de- scribed in the section on crush syndrome (Table 2).

Pathophysiology

The pathophysiology of crush injury is still not clear. What is known is that to produce this kind of injury one must be subjected to continuous pressure for several hours and that, after the insult, the main injury is to the muscles [3, 5, 6]. When trying to understand the injury by comparing it to other known pathologies, we can eliminate arterial occlusion as a factor. One of the first signs of arterial occlusion is discoloration of the skin, with eventual necrosis of skin and, obviously, disappearance of the distal pulses. These two major signs are missing in crush injury. If compared to a direct pressure insult, as in injuries resulting from being run-over by the wheel of a truck, we find the main damage in such an injury is to the cutis and subcutis layers, while the muscle is relatively undamaged, contrary to crush injury.

The syndrome most similar to crush injury is compartment syndrome [CS], and this similarity should be clarified, as it is very important in the understanding of the treatment advo- cated. CS is a well-described and well-understood injury [13- 15] caused by elevation of the pressure in the muscle compart- ments. This elevation of pressure causes occlusion of the venous drainage from the compartments and this, in turn, further elevates the compartment pressure, with the end result being necrosis of the muscle in the compartment [13, 15]. Because the elevation of pressure is gradual and, up to a certain pressure, reversible, the best treatment is to release the pres- sure in the compartment by facsiotomy. Today, this pressure

can be measured directly by the introduction of a catheter into the compartment, and decisions can be made in time to avoid irreversible damage to the suffering muscle.

As the clinical signs of CS are the same as the late signs of crush injury, it was once thought that they shared the same pathophysiology, but this is not so. In CS, the elevation of the pressure in the compartment is the cause of muscle damage and necrosis [t5] but, in crush injury, the damage to the muscle is caused by continuous pressure. As a result of this damage, the muscle cell loses its ability to control fluids and swells, causing an elevation in the compartment pressure. Therefore, the elevation of pressure in crush injury is secondary to the muscle damage, and not the cause of it.

The only explainable damage in this injury is the nerve damage, which is the same as that seen in vasonervosum occlusion, and which is completely reversible, although it may take up to a year for the nerve to recover completely. It may be that the massive damage to the muscle in crush injury is a combination of nerve injury and direct pressure on the muscle, and may have something to do with capillary tone regulation.

Treatment

Treatment of the crush injured patient should be aimed at preventing crush syndrome, which has a high mortality and morbidity rate [2, 5, 8].

The treatment of injuries of the limbs is controversial. The textbooks and the literature [2, 4, 5, t0, 16, 17] still believe that the similarity in signs between crush injury and compartment syndrome calls for the same treatment, i.e., early fasciotomY- However, fasciotomy does not give good results and the few deaths that are reported in the literature following crush injury are directly related to fasciotomy [1].

The two major complications of fasciotomy in these patients are recurrent bleeding from the fasciotomy site [ t ] and infection [5, 7, 8]. Bleeding from the fasciotomy site is uncontrollable oozing from the muscle surface and the subcutaneous layers. This is due to loss of tone in the capillary wall as a result of the injury and the acidemic environment, This kind of bleeding is very hard to control surgically, and local infection of the fasciotomy site is very hard to prevent. The incision of the ski0 which, in most cases, cannot be closed primarily due to the bulging of the edematous muscle, brings the dead muscle into direct contact with room air. This dead muscle has no means bY which to combat infection, which may spread and endanger the life of the patient. At best, antibiotics can only prevent the sepsis for a short time; they cannot control the local infection-

If fasciotomy is carried out on a patient with crush injury, the muscle is found to be grey and lifeless. When cut, the muscle bleeds profusely, which may confuse the surgeon who is conditioned to believe that dead muscle does not bleed. This belief is based on experience obtained in performing amputa" tions on arteriosclerotic limbs, when the height of the amputa" tion is decided by reaching a good bleeding muscle.

As explained, fasciotomy should not be carried out in crush injury. However, if fasciotomy is carried out neverthelesS, radical resection of all dead muscle should be performed at the first operation [18], as the dead muscle cannot be identified bY lack of bleeding Or histology. The best method for identifying dead muscle is by its reaction to direct physical or electrical

M. Michaelson: Crush Injury and Crush Syndrome 901

stimuli. Muscle that does not contract to direct physical or electrical stimuli should be considered dead and should be removed. Failure to recognize dead muscle at the first operation will lead to recurrent surgical debridements and danger of severe infection, with attendant high mortality and morbidity [8]. The only indication for fasciotomy in crush injury is in open crush injury, where aggressive radical debridement should be performed in an attempt to avoid infection of the injured limb.

The morbidity and mortality rates of crush injury are still high [1, 2, 5, 7], but there is very little data on the functional outcome of the limbs suffering from crush injury [10, 11]. Our experience !n treating two groups of crush-injured patients [I 8] is that there xs a recuperation of the sensory loss after the acute phase, accompanied by a transient period of parasthesia with pain so severe that it may necessitate continuous analgesic treatment. The end result is restoration of the feelings of touch and pain while, in patients who have fasciotomy and debridement, the limb becomes lifeless, and arthrodesis of the ankle may need to be carried out so that the leg can function as a living prosthesis. It is agreed that, although the leg may be motionless below the knee, arthrodesis is superior to amputation, as the leg maintains its feelings of touch and pain.

The outcome for crush-injured limbs not treated by fasciot- orny is good. In the follow-up of our group a year after the injury, all patients could walk freely without any orthopedic harnesses (except for one patient who had a proven sciatic lesion). All had returned to work and felt free from disability, although physical examination revealed residual disabilities ranging from mild weakness to loss of motion of 5 ° of the knee [181.

Crush Syndrome

Crush syndrome is the general manifestation of crush injury. If not treated, it will cause acute renal failure (ARF) or even death [3, 4, 5, 6, 8]. The severity of the clinical manifestations of the syndrome is proportional to the amount of injured muscle. Therefore, although crush syndrome can be seen in a mild form When the upper extremities are injured, the full-blown picture Will present itself only when the lower limbs are involved, as the amount of injured muscle is much greater.

The pathophysiology of crush syndrome is clearly under- Stood and much research on it has been done, revealing the Same mechanism as in rhabdomyolysis [19-21]; actually, crush syndrome may be labelled traumatic rhabdomyolysis [9, 22]. After extrication of the damaged limb, the membrane of the injured muscle cell losses its ability to actively control and protect the cell and becomes permeable. Thereafter, water can enter the cell freely, which results in severe muscle edema and xs responsible for the outstanding edematous appearance of the entire limb. On the other hand, it may cause hypovolemia and Shock as fluids come primarily from the intervascular space.

In addition, the breakdown products of the damaged cells can no longer be contained and pour into the blood stream. Among the most important of these are potassium, phosphorus, and rnyoglobin, which is the basic pigment of the muscular ceils. These ingredients, flushed in a large amount into the blood Stream, may cause severe damage, In the first hour, the most dangerous among them is the potassium, a rise in potassium

Table 3. Treatment protocol to prevent acute renal failure in crush syndrome.

1. Combat hypovolemia with crystaloids. 2. Infuse hourly 500 ml of crystaloids and 22.4 meq bicarbonate. 3. If diuresis is <300 ml/hour, give mannitol 1 g/kg per dose~ 4. If blood pH is >7.45, give 250 mg acetazolamide. 5. Monitor vital signs hourly, plus urine pH and volume. 6. Monitor every 6 hours osmolarity and electrolytes in blood and

blood gases.

ions in the blood may cause electrical heart disturbances, followed by death.

Additionally, the combination of hypovolemia, acidemia, and myoglobinemia may cause acute anuric renal failure [23]. This is a vicious circle, as the body suffering from ARF cannot excrete the very large amount of cell breakdown products, and the danger of death from hyperkalemia increases. The mecha- nism by which ARF is caused is well-known and well-docu- mented [19, 23] and will not be discussed here, but the enor- mous amount of research which went into understanding the mechanism of ARF in rhabdomyolysis gave us the tools to prevent it in crush injury.

The important facts are that a urinary pH of > 6.5 will protect the kidney cell from the poisonous effects of myoglobin and that diuresis by itself has a protective quality on the kidney. These two facts enabled us to develop a treatment protocol which will prevent ARF in crush syndrome [9, 21, 22, 23]. The aim of the treatment is to produce diuresis of 300 cc per hour, with a urinary pH of not below 6.5. This was achieved by introducing large amounts of crystaloids and bicarbonates and causing diuresis with mannitol. This protocol is described in Table 3.

It should be stressed that crush syndrome patients are very severely injured and should be treated in an intensive care unit. The clinical picture presented in the first few hours may be misleading and can lead to grave consequences, as the success of the preventive treatment of ARF is directly related to early initiation [19, 23]. This protocol, if applied in the early stages, will prevent the appearance of ARF [9].

Our experience with 16 patients treated for crush injury consists of two separate groups [1, 8, 9, t8]. One group was treated in 1978 by the methods understood at that time. Of 7 patients, 5 had fasciotomies performed on both legs. All had recurrent debridements of the wound and necrotic muscle removed, leaving healthy cutaneous and subcutaneous tissue. Eventually, the wounds were dosed secondarily or skin- grafted. There was no follow-up, except for 2 patients who regained full sensation in the legs but had no motion. In 5 patients, severe infection developed in the fasciotomy sites with septicemia, necessitating amputation of 3 limbs as the infection could not be controlled and was endangering the patient's life. As to the crush syndrome in this group, treatment was started only 12 hours after extrication and all the patients developed ARF, 5 of whom were treated by hemodialysis and 2 by peritoneal dialysis. There was no mortality but the stay in intensive care was 12-39 days. All recovered normal renal function.

The second group, treated in 1982, consisted of 8 patients. Treatment was started immediately, even before full extrica- tion, according to a policy developed after our previous expe-

902 World J. Surg. Vol. 16, No. 5, Sept./Oct. 1992

rience, and only 1 fasciotomy was performed. This fasciotomy lead to unnecessary bilateral amputations and local complica- tions, which eventually resulted in death. In the other patients, there were no local complications and no infections, and the results were good [18]. As to crush syndrome in this group [9], except for 1 patient who was not diagnosed as a crush injury for the first 24 hours, all received treatment according to the protocol described above and none developed ARF. Their stay in intensive care was a brief 5-7 days.

Discussion

There are few reports on crush injury and crush syndrome in the English literature. Even when these injuries are mentioned, they are not described at length, so that no conclusion can be drawn from the treatment indicated. This is surprising, as earthquakes occur every year and account for many deaths and injuries [11], and it can be presumed that at least some of the victims suffered from crush injury and crush syndrome. It may be that the bigger the earthquake, the greater the disruption of the medical layout, and all efforts are centered on saving lives and rebuilding the medical foundation, leaving no time for the gathering and publishing of data.

The description of many kinds of local injuries under the title of crush injury and the lack of publication of large series with follow-up of treated crush injuries makes it difficult to draw any conclusions as to the best treatment for crush injury, i.e., fasciotomy versus conservative treatment (non-fasciotomy). Our experience with two groups of patients, one treated with fasciotomy and one treated conservatively with follow-up for one year, lead to the following principles:

1. Crush injury should not be fasciotomized. 2. Skin over a crush injury site should never be debrided. 3. If the crush injury is open, radical debridement of all dead

muscle should be carried out. 4. Fasciotomy on a closed crush injury should be performed

only if distal gangrene is imminent. 5. Amputate only if infection of the limb endangers the pa-

tient's life.

These principles were developed after critically examining the results on our first group of patients, those treated by fasciot- omy.

The problem not yet solved in crush injury is understanding of the pathophysiology. Evidence shows that there is transient nerve injury but no large artery injury, yet there must be a component of direct muscle injury. More understanding of the crush injury mechanism will surface once a good laboratory model of crush injury is found.

Our recommendation for conservative treatment is based on our follow-up and our belief that, although crush injury portrays the same clinical picture as compartment syndrome, the patho- physiology is different and the two conditions should not be treated in the same way, i.e., by fasciotomy. This is still not accepted by the literature and the recommendation in most textbooks is for amputation and fasciotomy [16, 17].

We recommend that, if fasciotomy is done, then radical muscle debridement should be done also. This may cause a problem for the operating surgeon who is accustomed to identifying dead muscle as non-bleeding muscle, while in crush

injury the muscle, although dead, still bleeds. The only way to solve this problem is to treat the muscle which reacts to neither electrical nor mechanical stimuli as dead muscle. Failure to do so will endanger the patient through local infection and the need for recurrent debridement.

The amazing recovery of crush injured limbs is not well understood and the best explanation is that there are some fibers which recuperate in the "dead" and non-reactive muscle. This was described by Brown [5] who found some live fibers which escaped damage in crush injured muscles.

The treatment of crush syndrome is less controversial, be- cause of the better understanding of the pathophysiology, and because of the great amount of research done on rhabdomyol- ysis. The aim of treatment is to prevent ARF and, if started early, this treatment can prevent ARF. Since the prevention of ARF, mortality and morbidity rates have lessened [8, 9, 10, 24] and, today, most of the mortality and morbidity is directly caused by complications of the local treatment of crush injury, i.e., fasciotomy.

R~sum~

Les lSsions par 6crasement sont d6finies comme celles provo- qu6es par une compression prolong6e des membres. Elles se voient surtout lorsqu'une victime a 6t6 ensevelie pendant au moins 4 heures. La 16sion principale int6resse les muscles. Le traitement dolt 6tre conservateur et il faut 6viter l'apon6vroto- mie. Toutefois, si une apon6vrotomie dolt 6tre effectu6e, il faut pratiquer une excision complSte de tousles tissus bless6s afin de pr6venir l'infection. L'infection en effet est un facteur de pronostic vital et constitue de nos jours la cause principale de mortalit6 et de morbiditY. Les r6sultats du traitement local conservateur des 16sions par 6crasement sont bien sup6rieurs ceux obtenus apr6s traitement chirurgical. La physiopathologie des 16sions par 6crasement n'est toujours pas compl~tement 61ucid6e et il n'existe pas de mod~,le animal satisfaisant. Le crush syndrome, la manifestation g6n6rale des 16sions par 6crasement, est mieux compris actuellement. S'il n'est pas pr6venu, il en r6sulte une insuffisance r6nale aigu~. La meilteure fagon ~ pr6venir cette insuffisance est discut6e et un protocole est d6crit. It n'existe pas de doute que la pr6vention de l'insuffisance r6nale dolt 6tre le but du traitement du crush syndrome et peut souvent 6tre atteint.

Resumen

Las lesiones de machacamiento son causados por presi6n continua y prolongada sobre una extremidad. Con frecuencia se encuentran en pacientes que se resctan despu6s de estar atra- pados por no menos de 4 horas. La injuria principal ocurre en los mt~sculos de la extremidad afectada. El tratamieno debe set conservador y la fasciotomia debe ser evitada, por el riesgo de sangrado y de infecci6n. Si se practica fasciotomia, 6sta debe acompafiarse de desbridamiento radical de los mtasculos lesion- ados con el objeto de evitar infecci6n en el miembro trauma- tizado. La infecci6n puede poner en peligro la vida del paciente, y hoy en dfa constituye la principal causa de morbilidad Y mortalidad. E1 resultado final del tratamiento conservador local

M. Miehaelson: Crush Injury and Crush Syndrome 903

es muy superior al del t ratamiento operatorio. La fisiopatologfa de la lesi6n de machacamiento no ha sido totalmente dilucidada Y no se dispone de un buen modelo animal para su estudio. El sfndrome de machacamiento, que representa la manifestaci6n general de la lesi6n de machacamiento, es mejor conocido; si no se lo previene, da lugar a falla renal antlrica aguda, eomo resultado de hipovolemia, acidemia y mioglobinemia. Se de- scribe un mr todo para la prevenci6n de la falla renal aguda y se presenta el protocolo correspondiente. No hay duda de que la prevensi6n de la falla renal aguda es el objetivo del tratamiento del sindrome de machacamiento, y tal objetivo puede ser logrado mediante un manejo racional.

References

1. Michaelson, M., Taitelman, U., Bshouty, Z., Bar-Joseph, G., Bursztein, S.: Crush syndrome: Experience from the Lebanon War 1982. Isr. J. Med. Sci. 20:305, 1984

2. Santangelo, M.L., Usberti, M., Di Salvo, E.: A study of the pathology of crush syndrome. Surg. Gynecol. Obstet. 154:372, 1982

3. Bywaters, E.G.L., Beall, D.: Crush injuries with impairment of renal function. Br. Med. J. 1:427, 1941

4. Jones, R.N.: Crush syndrome in a Cornish tin mine. Injury 15:282, 1984

5. Brown, A.A., Nicholls, R.J.: Crush syndrome: A report of two Cases and a review of the literature. Br. J. Surg. 64:397, 1977

6. Bywaters, E.G.L.: lschemic muscle necrosis. J.A.M.A. 124:1103, 1944

7. Bentley, G., Jeffreys, T.L,: The crush syndrome in coal miners. J. Bone Joint Surg. [Br.] 50B:588, 1968

8. Michaelson, M., Taitelman, U,, Bursztein, S.: Management of crush syndrome. Resuscitation 12:141, 1984

9. Ron, D., Taitelman, U., Michaelson, M., Bar-Joseph, G., Bursz- tein, S., Better, O,S,: Prevention of acute renal failure in traumatic rhabdomyolysis. Arch. Intern. Med. 144:277, 1984

10. Kikta, M.J., Meyer, J.P., Bishara, R.A., Goodson, S.F., Schuler,

J.J., Flanigan, D.P.: Crush syndrome due to limb compression. Arch. Surg. 122:1078, 1987

11. Zui-Yong, Z.: Medical support in the Tangshan earthquake: A review of the managment of mass casualties and certain major injuries. J. Trauma 27:1130, 1987

12. Michaelson, M., Reis, N.D.: Crush injury and crush syndrome. Unfallchirurg 91:330, 1988

13. Bourne, R.B,, Rorabeck, C.H.: Compartment syndrome of the lower leg. Clinical Orthopaedics and Related Research. 240:97, 1989

14. Schwartz, J.T., Brumback, R.J., Lakatos, R., Poka, A., Bathon, H., Burgess, A,R.: Acute compartment syndrome of the thigh. J. Bone Joint Surg. [Am.] 71A:392, 1989

15. Owen, C.A., Mubarak, S.J., Hargens, A.R., Rutherford, L., Ga- retto, L.P., Akeson, W.H.: Intramuscular pressures with limb compression. N. Engl. J. Med. 21:1169, 1979

16. Crush Injury. In: Emergency War Surgery. T.E. Bowen, R.E. Bellamy, editors, Washington, D.C. United States Government Printing Office, 1988, p. 241

17. Explosions and Explosive Device-Related Injuries. In: Crush Syn- drome: Trauma Management for Civilians and Military Physicians. S.L. Wiener, J. Barrett, editors, Philadelphia, W.B. Saunders Company, 1986, pp. 23-25

18. Reis, N.D., Michaelson, M.: Crush injury to lower limbs: Treat- ment of the local injury. J. Bone Joint Surg. [Am.] 68A:414, 1986

19. Kurokawa, K.: Acute renal failure and rhabdomyolysis. Kidney Int. 23:888, 1983

20. Gabow, P.A., Kaehny, W.D., Kelleher, S.P.: The spectrum of rhabdomyolysis. Medicine 61:141, 1982

21. Mueller, C.B.: The mechanism of acute renal failure after injury and transfusion reaction and its prevention by solute diuresis. Surg. Clin. North Am. 45:499, 1965

22. Better, O.S.: Traumatic rhabdomyolysis ("crush syndrome"): Up- dated 1989. Isr. J. Med. Sci. 25:69, 1989

23. Better, O.S., Stein, J.H.: Early management of shock and prophy- laxis of acute renal failure in traumatic rhabdomyolysis. N. Engl. J. Med. 322:825, 1990

24. Michaelson, M., Reis, N.D.: Crush injuries and crush syndrome. In Manual of Disaster Medicine. N.D. Reis, E. Dolev, editors, Berlin- Heidelberg-New York, Springer-Verlag, 1989, pp. 106-112