67

Chapter

Crush Syndrome

V Paramshetti

History Stretching of cell membranes causes influx of Ca. The

In 1910, Meyer Betz reported “rhabdomyolysis with the triple
symptoms of myalgia, loss of muscle power and dark brown urine”
observed following the Sicily earthquake in 1909.1,2
Bywaters in the UK first used the English term “crush
syndrome” (CS) in his 1941 paper that delineated the pathogenesis
of crush syndrome and established guidelines for the management
of casualties.3,4
Japanese used the term “atsuza” for cases related to crush
syndrome.5
Epidemiology
Majority of reported crush syndrome cases are associated
with disasters involving collapse of heavy masses. But crush
syndrome may also be seen in daily practice in road-traffic
accidents, complications with the use of pneumatic antishock
suits, injury from using immobilizing bandaging and injury due
to automatically cycled blood pressure cuff.
increase in intracellular Ca level causes the activation wide
variety of enzymes resulting in cellular edema
• Ischemic injury to skeletal muscles. Ischemic injury results
in anaerobic metabolism in the muscle. Hence, anaerobic
byproducts further damage cell membrane resulting in cellular
edema
TABLE 1: Flow of solutes and water across skeletal-muscle-cell
membranes in rhabdomyolysis
Influx from extracellular compartment into muscle cells
Water, sodium chloride, Hypovolemia and hypodynamic shock, prerenal
and calcium and later acute renal failure; hypocalcemia,
aggravated hyperkalemic cardiotoxicity;
increased cytosolic calcium; activation of
cytotoxic proteases
Efflux from damaged muscle cell
Potassium Hyperkalemia and cardiotoxicity aggravated by
hypocalcemia and hypotension

Definition Purines from Hyperuricemia, nephrotoxicity

disintegrating cell
Crush syndrome is a condition in which rhabdomyolysis develops nuclei
rapidly after the skeletal muscles are released from prolonged Phosphate Hyperphosphatemia, aggravation of
pressure, resulting in shock, acute renal failure and other systemic hypocalcemia, and metastatic calcification
symptoms (Table 1). including the kidney
Lactic and other organic Metabolic acidosis and aciduria
5 acids
Pathophysiology (Fig. 1)
Myoglobin Nephrotoxicity, particularly with coexisting
Pathophysiology of crush syndrome involves following events oliguria, aciduria, and hyperuricosuria
mainly: Thromboplastin Disseminated intravascular coagulation
• Compression injury to the skeletal muscles: Stretch myopathy.
Creatine kinase Extreme elevation of serum creatine kinase level
Compression injury to skeletal muscle results in stretching of
cell membranes. Creatinine Increased serum creatinine-urea ratio
 CRUSH SYNDROME 473

%% -*

Fig. 1 Pathophysiology of crush syndrome

Abbreviations: SIRS, systemic inflammatory response syndrome; MOF, multiorgan failure;
ARF, acute renal failure; DIC, disseminated intravascular coagulation.
 474 TEXTBOOK OF ORTHOPEDICS AND TRAUMA
• Propagation of intracompartmental pressure: Localized
compression may cause a substantial increase in intra-
compartmental pressure (ICP) due to edema in myocytes
leading to widespread muscle injury.
Changes Seen after Release of Pressure
Local Changes
Following the release of pressure, reperfusion results in further
damage to myocytes.
• Ischemia reperfusion injury: Reperfusion results in release
reactive oxygen radicals which damage skeletal cells and
vascular endothelium. Leukocytes adhere to the damaged
endothelial cells and impair microcirculation, aggravating the
hypoxic condition of myocytes.
• Involvement of compartment syndrome: Cellular edema and the
increase in vascular permeability cause the rapid rise in ICP
and compartment syndrome develops in the parts that have
not shown overt signs of injury.
Systemic Changes
• Fluid shift and electrolytes imbalances: Sudden electrolyte
abnormalities and fluid shifts may result in hypovolemic shock
and myocardial function abnormalities.
• Development of acute renal failure: Multiple factors including
a drop in renal blood flow and renal tubular ischemia due
to dehydration, myoglobin, acidosis, tension of the renal
nerves, azotemia and hyperphosphatemia contribute to the
development of acute renal failure. Myoglobinuria is the major
cause of acute renal failure.
Systemic Inflammatory Response Syndrome or Sepsis:
This can result in multiorgan failure.
Clinical Features5
See Box 1
Laboratory Evaluation2,5
Laboratory evaluation is of utmost importance in diagnosis and
treatment of crush syndrome. Blood parameters that need to be
monitored are creatine kinase more than 10,000 U/L, oliguria
(urine output <400 mL/24 hours), elevated blood urea nitrogen
(>40 mg/dL), serum creatinine (>2 mg/dL), uric acid (>8 mg/dL),
potassium (>6 mg/dL) or phosphorus (>8 mg/dL) and a decreased
serum calcium (<8 mg/dL).
The extent of injury can be evaluated by creatine kinase level,
blood myoglobin level, the number of parts with compartment
syndrome, and the number of limbs affected by compression.
Treatment
Fluid therapy is the first choice in the management of crush
syndrome, because the development of shock and acute renal
failure can be avoided by the early provision of fluid resuscitation.
It should be started within 6 hours postinjury.
The purposes of fluid therapy in crush syndrome are:
• To replenish the shortage of extracellular fluid
• To promote the renal excretion of potassium
• To avoid acute renal failure.
is
Box 1: Clinical feature
Immediately following extrication (on the spot)
•  Stable vital sign
•  Clear consciousness, unless head injury
•  Emotional complaint, but no physical complaint
•   Numbness of the involved limbs, exception for a short time of 
pain after extrication
•  Flaccid paralysis of the injured limb
•  A patchy pattern of sensory loss, mainly to pain and touch
•   Patches of erythematous skin, delineating accurately the areas of 
compression
•  No limb edemia initially
Several hours to a couple of days after extrication (e.g. on admission)
•  Hypovolemia and hypodynamic shock; hemoconcentration
•  Hyperkalemic cardiotoxity
•  Metabolic acidosis
•  Oliguria, myoglobinuria; prerenal and later acute renal failure
•  Insensitive and paralyzed limbs
•   Compartment syndrome following gross edema of the injured limb
•  Present distal pulses of the edematous limb
•  Blister formation of the erythematous skin, mistaken for burns
Following fluid therapy
•   Hemodilution 
•    eight gian and sequestration of external cellular fluid
W
•   Congestive lung, ARDS
•   DIC
•   SIRS
•   Sepsis
Abbreviations: ARDS, adult respiratory distress syndrome; DIC, disseminated
intravascular coagulation; SIRS, systemic inflammatory response syndrome.
Box 2: Infusion therapy
On the spot
•  Normal saline should be incused at 1.5 liter/hour
•   Continuous infusion should be secured by the time of arrival at a hospital
In the hospital
•  A   standard solution of 75 mEq/L NaCl in 5% dextrose should be 
started at 500 mL/hour
•   It a diuretic response of more than 300 mL/hour is not achieved, 
and CVP rises by more than 5 cm H2O, the infusion should be
stopped and mannitol, 1 g/kg of body weight, as a 20% solution 
should be administered IV.
•   Once a diuresis of more 300 mL is established, fluids excreted 
in the urine should be replaced with a solution of 5% dextrose 
with the sodium and potassium content adjusted, on the basis of 
measurements made on the previous six-hour urinary collection.
•   Sodium  bicarbonate,  44  mEq/L,  should  be  added  to  every  other 
500  mL  bottle  of  the  standard  NaCl  in  5%  dextrose  solution.  The 
dose of sodium bicarbonate will be adjusted to maintain urinary pH 
above 6.5
•   Acetazolamide (Diamox) should be administered in a dose of 
250 mg IV, if plasma pH approaches 7.45.
•   Disappearance of visible myoglobinuria and a leveling off of 
the negative potassium balance will indicate a cessation of this
treatment protocol.
(The urinary pH is measured hourly. Six hourly collections of urine should
be assayed for sodium content, potassium content blood gases, plasma
pH, and serum electrolytes are similary measured every six hours).
 CRUSH SYNDROME
A protocol modified from the formula of Ron et al.6 may be
considered for fluid-electrolyte balance therapy (Box 2). The
principle of this protocol is the use of a starting fluid to avoid
potassium load and the use of an alkaline isotonic electrolyte fluid
with sodium bicarbonate adjustment. The goals of fluid therapy
are stabilization of circulation, hourly urine volume of 200–300
mL, blood pH 7.5, and urine pH between 6 and 7.
←Use of Hemodialysis
Hemodialysis in crush syndrome is important in treating acute
renal failure and elimination of myoglobin.
Treatment of Compartment Syndrome
No consensus has been reached concerning whether or not
fasciotomy should be performed to treat compartment syndrome
in crush syndrome. Early treatment certainly improves chances of
preservation of the functions of affected limbs and avoidance of
amputation, but the inevitable development of infection worsens
life prognosis. Numerous studies have indicated fasciotomy is a
factor inducing sepsis. Therefore, judicial decision is required.
475
Conclusion
Crush syndrome is a serious injury and should be identified in
early hours.
Fluid and electrolyte maintenance remains the mainstay of
treatment.
References
1. Better OS. History of the crush syndrome: from the earthquakes
of Messina, Sicily 1909 to Spitak, Armenia 1988. Am J Nephrol.
1997;17(3-4):392-4.
2. Gonzalez D. Crush syndrome. Crit Care Med. 2005;33
(1 Suppl):S34-41.
3. Bywaters EG. 50 years on: the crush syndrome. BMJ. 1990;301
(6766):1412-5.
4. Bywaters EG, Beall D. Crush injuries with impairment of renal
function. 1941. J Am Soc Nephrol. 1998;9(2):322-32.
5. Yokota J. Crush syndrome in disaster. JMAJ. 2005;48:341-52.
6. Ron D, Taitelman U, Michaelson M, et al. Prevention of acute
renal failure in traumatic rhabdomyolysis. Arch Intern Med.
1984;144(2):277-80.