TRAUMATIC

CRUSH SYNDROME

Yoyos Dias Ismiarto, dr., SpOT(K),

M.Kes, FICS., CCD.

Department of Orthopaedics & Traumatology

Hasan Sadikin Hospital
Faculty of Medicine Universitas Padjadjaran
DEFINITIONS

Rhabdomyolysis - destruction of striated

muscle

A crush injury is direct injury resulting from a

crush

A crush syndrome is the systemic manifestation

of muscle cell damage, resulting from pressure
or crushing.
Also known as traumatic rhabdomyolysis
 CRUSH SYNDROME

The systemic manifestations of muscle injury

after direct trauma or ischemia-reperfusion
injury. Commonly found in victims of
earthquakes who have been caught under the
rubble of collapsed buildings.

SIGNS AND SYMPTOMS:

Tense, edematous, painful muscles
Dark tea-colored urine
Shock
Acidosis
Acute renal failure
 Based on 3 criteria:
1. Involvement of a muscle mass
2. Prolonged compression
3. Compromised local circular
HISTORY OF RHABDOMYOLYSIS
1880s : first reported in the German
Literature

1911 : Meyer-Betz described a clinical

syndrome consisting of dark brown urine,
muscle pain, and weakness

1941 : Bywaters and Beall report 4 cases

of crush syndrome during the bombing of
London during WWII. They recognized the
association between swollen extremities,
hypovolemia, vaso-constriction, and
eventual oliguria / renal failure.
CAUSES - TRAUMATIC
Trauma and compression
Crush injuries
MVA
Long-term confinement without changing
position
Physical torture and abuse
Prolonged hours of surgery without
changing position
PATHOPHYSIOLOGY OF MUSCLE
INJURY
Immediate cell disruption
Direct pressure on muscles
Stretch-activated channels opened Ca +
+ influx

Ischemia/Anaerobic metabolism
Loss of cellular membrane integrity
Vascular compromise
Prolonged compression vs. vascular
injury
Histologic changes at 2 hours
Necrosis at 6-8 hours
 ISCHEMIA-REPERFUSION INJURY

Occurs when patients are extricated from

collapsed buildings or when vascular flow is
re-established:
Swelling of affected extremities / Compartment
Syndrome
Hypovolemia / Shock
Free Radical formation
Lipid Peroxidation cell lysis
Toxin release: lactic acidosis, aciduria,
myoglobinemia, CK, and thromboplastin (can
DIC)
Electrolyte abnormalities: K, Phos, Ca
SCHEME OF PATHOPHYSIOLOGY

-Malinoski, Slater, Mullins. Crit Care Clin, 2004.

MECHANISMS OF ARF IN CRUSH SYNDROME

Renal vasoconstriction with diminished

renal perfusion
Cast formation leads to tubular
obstruction

Direct Myoglobin nephrotoxicity

- Haeme produced free radicles
CLINICAL MANIFESTATIONS
Range from asymptomatic to acute
renal failure and DIC
Triad : muscle pain, weakness ,dark
urine
Musculoskeletal signs
General manifestations
MUSCULOSKELETAL SIGNS
Pain
Weakness
Swelling
GENERAL MANIFESTATION
Malaise
Fever
Tachycardia
Nausea
vomiting
LABORATORY FINDINGS
CK n 45-260U/L
Rises within 12hours
Peaks 1-3 days
Declines 3-5days after cessation of
muscle injury
OTHER MUSCLE MARKERS
Measuring myoglobin level in serum or urine
Appears in urine when plasma concentration
exceeds 1.5mg/dl
Urine becomes dark red brown colour
>100mg/dl
Myoglobin has short T1/2 (2-3hours)
Serum level return to normal after 6-8hours
Myoglobin cast formation in renal tubules
TREATMENT

ABCDE (A T L S)
Fluids
Treat hyperkalaemia
FLUIDS
When
if possible before the crush is relieved
What
isotonic crystalloids are favoured normal saline preferred
(consensus meeting crush syndrome 2001-Edinburgh) (R/L
have 4 mEq K )
How much
Gonzalez et al:adult
extrication 1.5l/hr
postextrication .5l/hr alternating with D5W
Children 10-20ml/kg/hr
Urine output -.50ml/hr -200mls/hr
Children 2mls/kg/hr

CVP Smith et al suggest fluid bolus until a sustained increase

in CVP (>3mmhg after 15 min )
Stop fluids if patient oliguric, fluid overloaded, consider dialysis
ALKALINISATION OF URINE
Alkalinisation increases the solubility of myoglobin
and promotes its excretion .
Bicarbonate is used to raise the urine pH to 6.5
thereby increasing solubility of Haeme pigments
Add 50 ml 8.5%sodium bicarbonate to each litre
HOWEVER little clinical evidence to support use
Brown and colleagues CK >5000U/L
154(40%) received mannitol and bicarbonate
228 (60%) didnt
No significant difference in renal failure ,dialysis,or
mortality between the groups.
MANNITOL
 It was postulated that treatment with mannitol
was more efficacious than isotonic volume
expansion alone.

It is argued that it forces an osmotic diuresis,

thereby diluting nephrotoxic agents and
encouraging their excretion.

Little evidence to prove mannitol alone

Brown et al Failed to show benefit of bic/man

DIALYSIS
Despite optimal treatment ,daily
haemodialysis or haemofiltration may
be necessary
Remove urea and potassium
 FREE RADICAL SCAVENGERS AND ANTIOXIDANTS
The magnitude of muscle necrosis caused by ischemia-
reperfusion injury has been reduced in experimental models
by the administration of free-radical scavengers .

Many of these agents have been used in the early treatment

of crush syndrome to minimize the amount of nephrotoxic
material released from the muscle

Pentoxyphylline is a xanthine derivative used to improve

microvascular blood flow. In addition, pentoxyphylline acts to
decrease neutrophil adhesion and cytokine release

Vitamin E , vitamin C , lazaroids (21-aminosteroids) and

minerals such as zinc, manganese and selenium all have
antioxidant activity and may have a role in the treatment of
the patient with rhabdomyolysis
BETTER OS, STEIN JH. EARLY MANAGEMENT OF SHOCK AND PROPHYLAXIS OF
ACUTE RENAL FAILURE IN TRAUMATIC RHABDOMYOLYSIS. NEW ENGLAND
JOURNAL OF MEDICINE 1990; 322 (12): 825-829

Hypothesis: Shock occurs only after extrication,

when compressed extremities are released,
resulting in ischemia-reperfusion injury
1979: 7 men with rhabdo due to building collapse
who did not receive IV fluid for at least 6 hours; all
7 developed ARF
1982: 7 men with traumatic rhabdo who received
IV fluid before extrication and forced mannitol-
alkaline diuresis within 2 hours of extrication;
none developed ARF
TAKE HOME MESSAGE
High index of suspicion
On scene treatment important
Aggressive fluid treatment
Adequate monitoring
Recognition and early treatment of
complications
THANK YOU