- CRUSH INJURIES -

PRESENTATION BY DR
MAKOJOA K
INTERN DR – FMMED
MOTEBANG HOSPITAL
NOVEMBER 2022
 CRUSH INJURY
PRESENTATION LAYOUT
 JUSTIFICATION
 DEFINITIONS
 APPROACH
 CONCLUSION
 REFERENCES
JUSTIFICATION
 Festive Season and Trauma in Lesotho
 Gaps recognized in the management
DEFINITIONS
 Crush Injury - result of physical trauma from prolonged compression of torso, limbs or other
parts of the body (with possible tissue necrosis and neurologic dysfunction)
 Crush Syndrome – systemic manifestations resulting from crush injury which can result in
organ dysfunction (eg AKI), multisystem organ injury or death
 Mechanism of Injury:
 Compressive forces( be it getting trapped under a vehicle, industrial injuries, construction,
agricultural accidents)cause direct tissue damage
 Occluding venous outflow
 Prolonged compression results in cellular death-myonecrosis resulting in Crush Syndrome
APPROACH - CLINICAL
FEATURES
 APPROACH
Clinical Manifestations
 Attributed to by direct crushing force, prevention of venous outflow leading to accumulation of potassium,
phosphorus and myoglobin as well as extremity oedema

- Traumatic Asphyxia – due to severe crush injury to chest, results in significant increase in the
thoracic pressure, pressure within superior vena cava and attempts at inspiration against closed
epiglottis can lead to capillary rupture in the head and neck. This results in cervicofacial cyanosis,
oedema, subconjunctival haemorrhage, petechial eruptions on face, neck, torso. TA may be combined
with liver and spleen lacerations, rib fractures, pulmonary contusions and anoxic brain injury
- Hypovolaemia due to external haemorrhage, distributive shock (3rd spacing), inflammatory
response to reperfusion injury and cell death
 APPROACH
- Extremity Crush Injury – generalized swelling, erythema to blisters and purpura to
open fractures and mangled extremities with ischaemia, then acute compartment
syndrome and rhabdomyolysis
- Organ Injury - blunt injury to thorax or abdomen which can also result in pulmonary
contusion, cardiac contusion, rib fractures, pelvic fracture, haemothorax, pneumothorax,
other blunt solid or hollow viscus injuries
SEQUELAE OF CRUSH
INJURY
Acute Kidney Injury – multifactorial aetiology:
- nephrotoxic effects of haeme products
- tubular obstruction by myoglobin and urate crystals
- hypotension & hypoperfusion could cause ATN Crush-related AKI ,manifests as rhabdomyolysis and
myoglobinaemia, hyperkalaemia, hyperphosphataemia, myoglobinuria
Acute Respiratory Distress Syndrome: due in part to large-volume crystalloid resuscitation,
inflammatory response to
injury, tissue necrosis, distributive shock or fat embolism syndrome associated with long-bone fractures
WORK-UP
 General Laboratory studies on admission and monitoring:
 Urine myoglobin
 Full Blood Count
 Arterial Blood Gases
 Electrolytes
 Creatine Kinase Muscle - CKMM (> 1000 IU/l, indicator of crush syndrome)
 Coagulation studies

 Search for potential injuries and perform diagnostic studies:

 Portable radiographs
 Electrocardiogram (ECG)
 FAST (Focused Assessment with Sonography in Trauma)
 Emergency CT
 MANAGEMENT
PRINCIPLES N JURY
NE Y I
KID
HYPOVOLAEMIC ACUTE
SHOCK

METABOLIC
ABNORMALITIES
MANAGEMENT – IV FLUIDS
Can IV Access be established prior to extrication

yes no

Start IV isotonic solution saline (1 L/hr) Start isotonic saline as soon as possible after extraction
Continue during extraction (1L/hr)

Is victim still under rubble after 2 hours

yes no
MANAGEMENT – IV FLUIDS CONT

Reduce rate to 0.5L/hr Continue 1L/hr

Monitor for 6 hrs since inititation of fluids

Total Fluids during this time is 3 – 6 L

Is patient anuric

yes no

Give IV fluids 0.5 – 1 L/day

Can patient be closely monitored
Plus losses of the previous day
MANAGEMENT – IV FLUIDS CONT

Can patient be closely be monitored

yes no

Is patient older or has hx of heart failure

no yes

Give > 6L /day IV fluids Give IV Fluids 3 – 6L/day

Stop all IV Fluids when patient is able to take orally to keep up with requirement
MANAGEMENT –
ELECTROLYTE
ABNORMALITIES
1. Correct Electrolytes eg hyperkalaemia, hypercalcaemia
 Serum K+ > 5.0 mEq/L should be treated. NB: hyperkalaemia > 7 mEq/L causes cardiac arrhythmias
 ECG: peaked T-Waves and prolonged PR Interval
 Rx: - stabilise myocardium (decrease extracellular K + and enhance K + removal from
the body
- NaHCO3, albuterol & insulin are indicated
 Serum Ca2+ < 2.2 mmol/L or < 8.5 mg/dL. Hypocalcaemia ≤ 7.5 mg/dL causes arrhythmias, seizures,
tetany.
 Rx: calcium replacement
 Hyperuricaemia due to accelerated purine degradation as in rhabdomyolysis causing acute renal injury
 Rx: aggressive IV hydration
MANAGEMENT –
ELECTROLYTE
ABNORMALITIES & OTHER
ASPECTS
 2. Address metabolic abnormalities eg alkalinisation of urine in acidosis (eg use

of NaHCO3 44 or 88mEq mixed with 1l D5W)

 3. Analgesia (ketamine 0.3 – 0.5mg/kg IV or 1-2mg/kg IM). Beware of ketamine’s

symphathetic response, high BP & pulse). Alternatives are fentanyl & morphine
 4. Injury-specific treatment:
 Treat open wounds (eg wound care, antibiotics, tetanus toxoid, debridement as per indication)
 Compartment syndrome: pain, pallor, pulselessness, paraesthesia, poikilothermia,
paralysis……………Fasciotomy
 5. Management of organ injuries and fractures
TAKE-HOME
 The hospital management of crush injuries is essentially that of rhabdomyolysis
 Surgical management is akin to that of a case of trauma
 Very energetic fluid replacement and diuresis with timely fasciotomies and monitoring
enzymes and electrolytes will salvage many limbs and lives
REFERENCES
 Haines L. N. & Doucet J.J, 2022. Severe Crush Injury in Adults. Wolters Kluwer in
Update.17032:11.0
 Lecturio. 2022. Crush Syndrome
 Rajagoplalan C.S. Crush Injuries and Crush Syndrome. Symposium: Combat Casualty
Care. 2010; 66: 317 - 320