CRUSH SYNDROME

&
Compartment Syndrome

Buildings damaged in the 1999 Marmara

earthquake
A Case of Crush Syndrome….
 Clinical Features

 Lower limb injury with pain and swelling,

which later on developed anesthesia and
motor disturbance
 Signs of hypovolemic shock
 Tea-colored urine, maybe oliguria
 Nausea and confusion

Pathophysiology
 On Investigating further….

 Hyperkalemia & hypocalcaemia

 ECG changes secondary to hyperkalemia
 Metabolic acidosis
 Raised Creatine Kinase
 Elevated UREA and CREATININE
 Myoglobinuria
 Evidence of D.I.C.
Diagnosis: Crush Syndrome
Definition:
◦ A severe, often fatal condition that follows a severe
crushing injury, particularly involving large muscle
masses, characterized by fluid and blood loss, shock,
hematuria, and renal failure. Also known as
compression syndrome. (McGraw Hill Dictionary)

◦ In a nutshell: TRAUMATIC RHABDOMYOLYSIS

due to crushing

◦ Also known as Bywaters Syndrome/

Reperfusion injury
PATHOPHYSIOLOGY
Crushing injury

Ischaemic
damage to
muscles

Release of toxic
metabolites
Clinical
Features
KIDNEY IS IN DANGER AS SOON AS WE
RELIEVE THE COMPRESSION

Renal hypoperfusion + Renal Tubular Necrosis = Renal Failure

 Mechanisms of ARF in
rhabdomyolysis
 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
 Complications
◦ early
◦ late
Lysed cell release
 Potassium
 Phospate
 Creatine kinase
 Myoglobin

Electrolyte disturbances
 Hyperkalaemia
 Hypocalcaemia
 Hyperphosphatemia
 Hyperuricaemia
 Metabolic acidosis
Revascularization
 Fluids trapped in damaged tissue
 Oedema of affected limb
 Haemoconcentration and shock
 Myoglobin, potassium, phosphate enter
venous circulation
Musculoskeletal signs

Pain
Weakness
Swelling
 General manifestation
 Malaise
 Fever
 Tachycardia
 Nausea
 Vomiting
 Complications
Early Late(12-72hrs)
 Hypovolaemia  Acute renal failure
 Hyperkalaemia  DIC
 Hypocalcaemia  ARDS
 Cardiac arrhythmias  sepsis
 Cardiac arrest
 Compartment
syndrome
 Lab findings
 CK n 45-260U/L
 Rises within 12hours
 Peaks 1-3 days
 Declines 3-5days after cessation of muscle
injury
 CK-peak
 Huerta-Alardin et al :
CK>5000U/L serious muscle injury, related to
renal failure

 Gonzales et al:
>10000U/L related to ARF

 Brown et al :2083 trauma

ICUadmission,85%abn CK (>520)
74 of 382 <5000U/L developed RF(8%)
143 of 1701 >5000U/L developed RF(19%)
Renal failure defined peak creatinine >2mg/dl
 CK-peak
CK < 75000 45 of 115 (39%) developed RF
requiring dialysis
CK > 75000 43 of 51 (84.3%) developed
renal failure requiring dialysis

Note different definitions of renal failure

 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
 Carbonic anhydrase 3
 Aldolase
 Trop T I
 Lab tests
 Raised Ureum & Electolite
Hyperkalaemia
hypocalcaemia
hyperphosphataemia
uric acid
 MANAGEMENT
 Initial Management:

1. Follow the usual criteria of A-B-C as injuries are

massive and high chances of poly-trauma
2. Early and rapid rehydration
3. Venous access preferably before the limb is
decompressed
4. CVP and urinary catheterization for monitoring
 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%) didn’t
◦ No significant difference in renal failure ,dialysis,or
mortality between the groups.
 Dialysis
 Despite optimal treatment ,daily
haemodialysis or haemofiltration may be
necessary
 Remove urea and potassium
 Further Management
1. Large amount of saline infusion with forced
diuresis
2. Debridement of crushed tissue and a
fasciotomy for compartment syndrome
3. Dialysis if renal failure sets in
4. Amputation as the last resort if massive
limb injury is there and we have to prevent
crush syndrome
 Summary
 High index of suspicion
 On scene treatment important
 Aggressive fluid treatment
 Adequate monitoring
 Recognition and early treatment of
complications
 Compartment Syndrome is …
 ‘ … an elevation of the interstitial pressure in a closed
osseofascial compartment that results in microvascular
compromise’
Mubarak & Hargens (1983, cited Edwards 2004:32)

 ‘ … a condition in which the circulation and function of

tissues within a closed space are compromised by an
increased pressure within that space’.
Matsen (1975, cited Singh, Trikha & Lewis
2005:468)

CS originally described by Volkmann in 1872 with

reference to the forearm.
Anatomy refresher - muscle
Anatomy revision
Key Compartment
Syndrome sites
4 Lower limb
compartments
3 Thigh compartments
2 Forearm compartments

Normal Inter
Compartmental Pressure
(ICP) = 0-8mmHg
(Edwards 2004)
Is compartment syndrome acute?
 ACUTE
follows traumatic event, commonly
fractures, with worsening symptoms &
irreversible tissue damage within hours

 CHRONIC
a recurrent syndrome occurring with
exercise or work (microtrauma or repetitive
overexertion). Symptoms often resolve with
rest.
 Causes
 Intrinsic
bleeding disorders ie
post ischemic swelling
Rhabdomyolysis

 Extrinsic
fracture
crush injury
surgical procedures – vascular, fascial defects
surgical positioning
constriction – tight cast, compression bandages
snake venomisation, insect sting
burns
IV drug use
exercise ie excessive for a muscle group, weightlifting
Edwards (2004)
 Pathophysiology
Fluid enters fixed volume
compartment

Myocyte necrosis produces

osmotically active particles
attracting sufficient fluid to
cause further rise in tissue pressure increases,
intramuscular pressure that venous pressure rises
decreases tissue blood flow
thus increasing muscle
ischaemia & cell oedema

capillary collapse and

muscle/tissue ischemia occur. Rise in interstitial
pressure
exceeds the
arterio venous
perfusion gradient
Increasing Inter Compartmental
Pressure Raised Inter
Compartmental
Pressure
(ICP) > 30mmHg
basis for treatment

ICP > 40mmHg =

surgical emergency

(Edwards 2004)
Untreated, within 6-
10 hours, the
outcome of
persistent high
compartmental
pressures is muscle
infarction, tissue
necrosis, and nerve
injury
Single-incision
fasciotomy.
Photographs courtesy
of DG Smith, MD,
Harborview Hospital,
Seattle, WA
 Assessment
 Neurovascular Observations 5 P’s,
-Pain, parasthesiae, pallor (capillary refill), ,
paralysis, pulselessness (Altizer 2004)
+ warmth & swelling (Judge 2007)
* 5 P’s clinically unreliable, argue Wallace et al (2009)
identifying a deep, aching, ‘crescendo pain’ out of
proportion to original injury.

Issues…?
Sensory deficit, the most reliable physical finding using
two point discrimination ? (Edwards 2004)
Pulselessness, a very late sign occurring when
Inter Compartmental Pressure > than systolic
pressure, so … (Altizer 2004)
Diagnostics
Assessment…
? Frequency, ? By who, ? Recording, Action?
Professional Accountability by ‘act or omission’

Investigations:
X-ray, MRI, CT, Ultra sound
Intercompartmental measuring using,
wick catheter, simple needle manometry, infusion
technique, Slit catheter, CVP manometer, side
ported needle, fibreoptic transducer
Care management issues:
aseptic technique, equipment, location, who performs
it, consent, analgesia, timing, parameters
Conservative management
 Cast care management – split
immediately !!! Include all the
bandage inside the cast

 Elevate

 I/V Infusion
Surgery - Fasciotomy

Two-incision
posteromedial
fasciotomy.
Photographs
courtesy of DG
Smith, MD,
Department of
Orthopedics,
Harborview
Hospital, Seattle,
WA.
Post-op fasciotomy & external
fixation
Skin Grafting
 Follow-up
 The postoperative wound check is at 3-5 days.
 Suture removal occurs at 10-14 days (if the wounds are closed).
 Patients may need skin grafting or traction dermoplasty if the skin
defect is large.
 The rehabilitation protocol depends most on the underlying
mechanism of injury. For stable tibial shaft fractures treated with
closed reduction and casting, the following guidelines apply:
◦ 0-3 Weeks
 Begin quadriceps sets, hamstring sets, gluteal sets, and straight-leg raises before
hospital discharge.
 Early weightbearing is performed as tolerated.
 Ice, elevation, and anti-inflammatory drugs are recommended.
◦ 3-5 Weeks
 Increase weightbearing.
 Begin range-of-motion (ROM) exercises on knee (0-140°) and start open-chain
exercises with Thera-Band (The Hygienic Corporation, Akron, Ohio) or ankle
weights.
 Begin closed-chain exercises if patient is bearing weight.
◦ 6-8 Weeks
 Ambulate, bearing full weight.
 Continue open- and closed-chain exercises.
◦ 3-4 Months
 Discontinue cast or patellar tendon bearing (PTB).
 Begin ankle stretching, ROM exercises, and strengthening.
Complications
 Motor deficits ie foot drop, Volkmann contracture

 Infection, with potential amputation

 Hyperaesthesia & painful dysesthesia: medication

ie phenytoin, carbamazepine, gabapentin

 Recurrent CS, due to scarring - athletes

 Systemic complications: acute renal failure, sepsis,

Adult Respiratory Distress Syndrome
 References
 Oda, Jun MD; Tanaka, Hiroshi MD; Analysis of 372 Patients with
Crush Syndrome Caused by the Hanshin-Awaji Earthquake,J of
trauma:Volume 42(3), March 1997, pp 470-476

 Gonzalez, Dario MD ,Crush syndrome,J of critical care:Volume

33(1) Supplement, January 2005, pp S34-S41

 Ana L Huerta-Alardín1, Joseph Varon2 and Paul E Marik .Bench-

to-bedside review: Rhabdomyolysis – an overview for clinicians;
Critical Care 2005, 9:158-169Crush Injury and Crush Syndrome: A
Review

 Smith, Jason MD; Greaves, Ian Crush Injury and Crush Syndrome: A
Review .J of trauma:Volume 54(5) Supplement, May 2003, pp S226-
S230

 Brown,carlos V MD:Rhee,Peter MD ;Preventing Renal Failure in

Patients with Rhabdomyolysis: Do Bicarbonate and Mannitol Make a
difference . J of Trauma :Vol 56 ,June2004,pp1191-1196