CRUSH SYNDROME

Osman Dönmez, M.D.

Associate Professor, Department of Pediatric Nephrology,
Faculty of Medicine, Uludag University. Bursa, TURKEY

odonmez@uludag.edu.tr

INTRODUCTION

Crush syndrome (CS) is a reperfusion injury as a result of traumatic rhabdomyolysis. CS was first described in the English language literature by Bywaters and Beal¹ after several patients who had been trapped under rubble of buildings bombed in the Blitz subsequently died of acute renal failure (ARF). It has been described in numerous settings since, most commonly after natural disasters such as earthquakes, in war, and after buildings have collapsed as a result of explosion. Crush syndrome is also seen following industrial incidents such as mining and road traffic accidents^2-4.

Crush syndrome appears to be common in earthquakes of disastrous proportions. Recently, numerous patients with crush syndrome were reported after the 1976 earthquake in Tangshan, China⁵, the 1980 earthquake in southern Italy⁶, the 1988 earthquake in Armenia⁷, the 1995 earthquake in Hanshin-Awaji, Japan⁸, and the 1999 earthquake in Marmara, Turkey^9,10.

The purpose of this conference is:

• to review definition, pathogenesis, clinical features, and treatment of the crush syndrome.
• to share our experiences with crush syndrome of children in the Marmara earthquake, Turkey

DEFINITION

A crush injury is a direct injury resulting from crush.

Crush syndrome is the systemic manifestation of rhabdomyolysis caused by prolonged continuous pressure on muscle tissue^10,11.

The diagnose criterias for crush syndrome are:

• Crushing injury to a large mass of skeletal muscle.
• The sensory and motor disturbances in the compressed limps, which subsequently become tense and swollen.
• Myoglobinuria and/or hematuria.
• Peak creatine kinase (CK) > 1000 U/L.

Patients with nephrological problems are defined as crush injury and one of the following characteristics; oliguria (urine output <400 ml/24 h), elevated levels of blood urea nitrogen (BUN) (>40 mg/dl), serum creatinine (2 mg/dl), uric acid (8 mg/dl), potassium (>6 mg/dl), phosphorus (> 8 mg/dl), or decreased serum calcium (< 8 mg/dl)¹².

PATHOGENESIS AND CLINICAL FEATURES

The typical clinical features of crush syndrome are predominantly as a result of traumatic rhabdomyolysis and subsequent release of muscle cell contents. The mechanism behind the crush syndrome is the leakiness of the sarcolemmal membrane caused by pressure or stretching. As the sarcolemmal membrane is stretched, sodium, calcium and water leak into the sarcoplasm, trapping extracellular fluid inside the muscle cells (Table 1). In addition to the influx of these elements into the cell, the cell releases potassium and other toxic substances such as myoglobin, phosphate and urate into the circulation^13-16.

The result of these events is hypovolemic shock, hyperkalaemia, metabolic acidosis, compartment syndrome, and acute renal failure. The ARF is caused by a combination of hypovolemia with subsequent renal vasoconstriction, metabolic acidosis and the insult of nephrotoxic substances such as myoglobin, urate and phosphate. Major earthquakes are followed by a substantial number of crush syndromes, provoking rhabdomyolysis and pigment-induced ARF.

The incidence of CS has been estimated at 2 and 5% at least. Approximately 50% of the patients with CS develop ARF, and approximately 50% of those with ARF need dialysis¹⁴.

Compartment syndrome occurs after crush because of the uptake of fluid into muscle cells contained within a tight compartment. Once compartment pressure exceeds capillary perfusion pressure at about 30 mmHg, the tissue inside the compartment becomes ischemic, and compartment syndrome develops¹⁷.

Table 1: Flow of solutes and water across the sarcolemma in rhabdomyolysis.

Consequences
Influx from extracellular compartment into muscle cells
Water, sodium chloride, and calcium	Hypovolemia and hemodynamic shock, prerenal and acute renal failure; hypocalcemia, aggravated hyperkalemic cardiotoxicity; increased cytosolic calcium, activation of cytotoxic proteases
Efflux from damaged muscle cell
Potassium	Hyperkaliemia and cardiotoxicity aggravated by hypocalcemia and hypotension
Purines from disintegrating cell nuclei	Hyperuricemia, nephrotoxicity
Phosphate	Hyperphsphatemia, aggravation of hypercalcemia, and metastatic calcification, including the kidney
Lactic acid and other organic acids	Metabolic acidosis and aciduria
Myoglobin	Nephrotoxicity, particularly with coexisting oliguria, aciduria, and uricosuria
Thromboplastin	Disseminated intravascular coagulation
Creatine kinase	Extreme elevation of serum creatine kinase level
Creatinine	Increased serum creatinine

APPROACH TO TREATMENT

• The treatment of crushed casualties should begin as soon as they are discovered. Attention should be given to the possibility of concomitant injury such as fractures, solid organ damage, or spinal injury.
• After airway, breathing, and circulation are assessed, if possible, the oxygen and any obvious hemorrhage should be controlled.
• Intravenous access should be obtained, and the patient should receive fluid.
• Patient should be urine catheterized.
• Once in hospital, electrolytes, arterial blood gases, and muscle enzymes should be measured.

Fluid resuscitation
Treatment should begin at the time of extrication and anticipate in this syndrome.
In the adult, 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^13,15,18.

In children, there is a little evidence, in the literature, to guide the treatment of crush injuries. The fluid therapy should be already started at the rescue area. The fluid resuscitation of an initial bolus 20 ml/kg should be followed in these patients. These patients received 2500-3000 ml/m2 per day of intravenous fluid infusion, diuretics and alkaline therapy^9,15.

The treatment of compartment syndrome is still the subject of debate, although evidence would point to a trial of conservative management before fasciotomy^10,13,15.

CONCLUSIONS

• The development of CS after crush injury is preventable and treatable.
• The mainstay of treatment is the prevention of renal failure by adequate rehydration and alkalinization of urine.
• The traditional treatment of compartment syndrome is fasciotomy. However, the complication rate for this procedure is high, with the most serious hemorrhage and sepsis.

OUR PEDIATRIC PATIENTS WITH CRUSH SYNDROME IN THE MARMARA EARTHQUAKE, TURKEY

At 03:01:37 am, on August 17, 1999, a catastrophic earthquake registering 7.4 magnitude on the Richter scale struck the north-west of Turkey. It affected the Marmara region, which is a densely populated industrial area of the country. This earthquake, subsequently known as 'Izmit (Kocaeli)' caused about more than 17.000 deaths, 40.000 serious injuries and completely destroyed approximately 75.000 buildings⁹.

We evaluated 20 children with crush syndrome transferred to our center during Marmara earthquake⁹.

The conclusions of our patients that we obtained in Marmara earthquake about crush syndrome in children.

• All patients received 2500-3000 cc/m2 per day of intravenous fluid infusion, diuretics and alkaline therapy.
• Serum peak CK levels were correlated with serum potassium (K), phosphorus, creatinine, aspartate aminotransferase (AST) and inversely correlated serum calcium.
• These findings showed that serum CK concentration is an important indicator of predicting the severity of renal disorders in CS.
• No correlation was detected between the muscle injury parameters (serum K, CK, AST, LDH) and the time period under rubble. This indicated that crush injury could happen even in people extricated in a short time.
• ARF occurred in 35% though they received intravenous and alkaline therapy. Four of them required hemodialysis.
• Some patients with ARF were required hemodialysis more than 2 or 3 per day due to hyperkalemia. The serum K levels were positively correlated peak serum CK, AST, urea and creatinine levels. This also supported that CS was more severe in these children.

References

1. Bywaters EGL, Beall D. Crush injuries with impairment of renal function. BMJ 1941; 1: 427-32.

2. Pellegrini VD, Reid JS, Evarts CM. Crush syndrome. In:Rockwood CA, Green DP, Bucholz RW, Heckman JD (eds). Rockwood and Green's Fractures in Adults, 4th edn. Lippincott-Raven, New York, 1996; 450-1.

3. Better OS. The Crush syndrome revisited (1940-90). Nephron 1990; 55: 97-103.

4. Bywaters EGL. 50 years on: The crush syndrome. BMJ 1990; 301: 1412-15.

5. Zhi-Yong Z. Medical support in the Tangshan earthquake: A review of the management of mass casualities and certain major injuries. J Trauma 1987; 27: 1130.

6. Santangelo ML, Usberti M, Di Salvo E et al. A study of the pathology of the crush syndrome. Surg. Gynecol. Obst. 1982; 154: 372-4.

7. Collins AJ. Kidney dialysis treatment for victims of the Armenian earthquake. N. Engl. J. Med. 1989; 320: 1291-2.

8. Oda J, Tanaka H, Yashioka T, et al. Analysis of 372 patients with crush syndrome caused by the Hanshin-Awaji Earthquake. J. Trauma 1997; 42: 470-5.

9. Dönmez O, Meral A, Yavuz M, Durmaz O. Crush syndrome of children in the Marmara earthquake, Turkey. Pediatr Intern 2001; 43: 678-682

10. Sever MS, Erek E, Vanholder R, et al. Clinical findings in the renal victims of a catastrophic disaster: in the Marmara earthquake. Nehrol Dial Transplant 2002; 17: 1942-1949.

11. Visweswaran P, Guntupalli J. Rhabdomyolysis. Crit. Care Clin. 1999; 15: 415-28.

12. Vanholder R, Sever MS, Erek E, Lameire N. Acute renal failure related to the crush syndrome: towards an era of seismo-nephrology?. Nephrol Dial Transplant 2000; 15: 1517-1521.

13. Better OS. Rescue and salvage of casualties suffering from the crush syndrome after mass disasters. Military Medicine 1999 164; 366-369.

14. Erek E, Sever MS, Serdengeçti K, et al. An overview of morbidity and mortality in patients with acute renal failure due to crush syndrome: the Marmara earthquake experience. Nephrol Dial Transplant 2002; 17: 33-40.

15. Smith J, Greaves I. Crush injury and crush syndrome: a review. J Trauma 2003; 54: S226-S230.