Transcript Musculoskeletal and Spinal Trauma

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Explain common complications associated with
orthopaedic emergencies.
Discuss fracture types, shock classifications,
and hemorrhage control devices.
Identify compartment syndrome,
rhabdomyolysis, and associated treatments.
Differentiate Neurogenic and Spinal shock and
associated treatment modalities.
State the proper principles of the initial
assessment and management of
musculoskeletal injuries.
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More than half of all hospital trauma
admissions are a result of a fracture
32 million musculoskeletal injuries annually
Most common causes: MVC, falls, assaults,
sports injuries.
Musculoskeletal trauma costs $850 billion
annually
Annual lost work days totaling 440 million
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Musculoskeletal trauma, as a result of blunt
force injury, often presents on a spectrum, it
may be relatively benign or life/limb
threatening. These injuries, though often
dramatic and grotesque, are rarely life
threatening. However, pelvic and long bone
fractures are often an important source of
unrecognized hemorrhagic shock.
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Musculoskeletal trauma does not require a
reordering of the priorities of the Primary
Survey (ABCDE).
Musculoskeletal trauma is predominantly
managed in the Secondary Survey
Musculoskeletal trauma is managed in the
Primary Survey when hemorrhage control
measures are required.
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Prevent hemorrhagic shock related to
Musculosketetal trauma:
Recognize S/S of hemorrhagic Shock (LOC,
skin, pulses)
Identify the source of the ongoing hemorrhage
(chest, abdomen, pelvis, extremities, external)
Intervene appropriately
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Direct pressure
Tourniquets
Splinting (prevents further pain and blood loss)
Pelvic binders
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History to include MOI
SAMPLE
Physical examination (Head-to-toe exam)
Look, listen, & feel
Assess for pain/paresthesias
Radiological studies
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Assess all suspected orthopaedic injuries for
vascular compromise
Manage open fractures
Identify compartment syndrome
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Appropriately reduce and splint fractures
Irrigate, cleanse, and dress all wounds
Ensure appropriate antibiotic therapy
Tetanus toxoid prophylaxis
Radiologic studies (for hemodynamically
normal patients)
TIME
Orthopaedic consult early
IS
CRITICAL
Do not delay transfer
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28 y/o male “tree surgeon”. Fell approximately
20 feet while performing his job duties. Fall
onto grassy surface with a subsequent
“entrapment” by the severed 1000 lb tree limb.
No loss of consciousness. Pt reportedly
trapped, by tree limb, for > 2 hours.
Pt reportedly pale, cool, diaphoretic.
Enroute via HEMS with full spinal
immobilization.
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A: Patent airway. Speech clear and
comprehensible. No blood, vomitus, teeth, etc
B: Tachypnea noted. No accessory muscle use.
LCTAB. No chest crepitus. Equal chest rise and
fall.
C: No obvious external hemorrhage. Two large
bore IV’s infusing with isotonic crystalloid.
Skin pale, cool, and diaphoretic with weak
central pulses. Labs obtained. Pt is confused
and lethargic.
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C: Skin remains pale, cool, diaphoretic despite
4L of warmed isotonic crystalloid. O+ PRBCs
administered. Source of hemorrhage identified:
Unstable pelvis and bilateral angulated,
deformed femurs. Pelvic binder placed.
Interventions improve perfusion.
D: GCS 13. Confusion noted. PERRL.
E: Pt exposed and warmed blankets placed.
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Primary Survey adjuncts: PCXR (WNL), pelvis
radiograph (open book), FAST (negative).
Orthopaedic consult. Prepare for transfer to
OR/angio suite.
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SAMPLE history (NKA, No PMH).
Pain control measures
Head, face, neck, chest, abdomen all
atraumatic, non-tender, and non-deformed.
Pelvic binder in place. Urinary catheter
contraindicated due to blood at the urethral
meatus.
BLE closed angulated, deformed femoral areas
Posterior surfaces with superficial abrasions
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Ulna/Radius- 250 ml
Radius – 500 ml
Tibia/Fibula – 1000 ml
Femur – 1500 ml
Pelvis – 2000 ml
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Worst type of open fx
Potential for vascular compromise
High risk of wound infection
Unlikely replantation
Tourniquet???
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Lateral compression
Anterior-Posterior
Vertical sheer
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Lateral compression pelvic fractures are often a result
of motor vehicle accidents. Involved hemipelvis
internally rotates. Pelvic volume decreases. Rarely
causes life-threatening hemorrhage.
Anterior-Posterior pelvic fractures are most often
caused by pedestrian vs auto injuries, falls >12 feet,
MCC, or a direct crush injury. There is pubic diastasis,
ligamentous tearing, and hemorrhage likely from the
posterior venous complex or iliac arteries.
Vertical Sheer pelvic fractures typically result from a
high energy force as falls. This results in major pelvic
instability, ligamentous injuries, and potential for life
threatening hemorrhaging.
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Primary Survey management of a Pelvic
fracture with affiliated s/s of hemorrhagic
shock:
Stop the bleeding (compressive hemorrhage
control device-Pelvic binder/Sheet)
Assess for need to transfer (facility, OR, angio)
Get expert advice (trauma/ortho surgeon,
interventional radiologist)
Continue initial resuscitative efforts to achieve
balanced resuscitation (SBP approx 90mmHg).
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This term refers to the clinical effects of crush
injury, compartment syndrome,
rhabdomyolysis, and acute renal failure.
Often described as a localized injury with
generalized effects.
Most common injury types are lower extremity
injuries ( tibia/fibula are the most
common)and upper extremity injuries
(ulna/radius are the most common)
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Pressure within the fascial compartment
occludes distal perfusion therefore depriving
the muscle of necessary oxygen and nutrients.
Ischemia > 6 hours causes necrosis
Devastating effects of muscle necrosis cause the
cellular release of myoglobin and potassium,
hyperkalemia, acidosis, coagulopathies, and
subsequent acute renal failure.
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Severe crush injuries
Burns
Fractures or associated vascular injuries
Constrictive splints, dressings, casts
Tibia and radius fractures the most common
injuries associated with compartment
syndrome. Other injury types include foot,
hand, gluteal, and thigh injuries.
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6 P’s (disproportionate PAIN, PALLOR,
PULSELESSNESS (late sign), PARESTHESIA,
PARALYSIS, and PRESSURE.
Asymmetrical, firm, swollen extremity
Intracompartmental pressure > 35-45 mmHg
(delta-P = DBP - compartment pressure) DeltaP of 30 mmHg or less is suggestive of
compartment syndrome.
Patient’s with altered sensorium may require
more objective assessments (pale, cool, swollen,
bruised, or pulseless extremities).
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Remove all potentially constricitve dressings,
casts, and splints.
If no improvement, a fasciotomy is required
Frequent neurovascular assessments
OR for fascial decompression and debridement
of necrotic muscle tissue.
Prevent the progression to traumatic
rhabdomyolysis.
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Muscular trauma is the most common cause
Ischemic muscle tissue releases myoglobin,
Potassium, and creatine kinase (CK).
Myoglobin and CK accumulate in the renal
tubules producing dark amber urine which
tests positive for hemoglobin (myoglobin assay
is necessary to confirm the presence of
myoglobin).
If untreated, this leads to acute renal failure,
metabolic acidosis, and coagulopathies.
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EARLY and AGGRESSIVE IV fluid
administration.
Prevent hypotension (utilizing IV fluids)
Goal is to achieve 100 ml/hr of urinary output.
Consider osmotic diuresis (caution in trauma
patients) to achieve goal urinary output.
Prevent hypothermia
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Rhabdomyolysis associated hyperkalemia
treatment:
Sodium Bicarbonate (1mEq/Kg)
Calcium chloride IVP
Regular Insulin 10 units IVP followed by 25
grams of D50.
Kayexalate
Hemodialysis or CRRT.
Closely monitor EKG and be wary of cardiac
dysrhythmias.
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TRADITIONAL thoughts on Rhabdomyolysis:
Crush injuries cause skeletal muscle damage
Damaged skeletal muscle releases myoglobin
Myoglobin lodges in the renal tubules
Acute renal failure ensues due to the
accumulation of myoglobin
Treatment includes: copious amounts of IVF,
Sodium Bicarbonate, dialysis (HD of CRRT),
prevention of hyperkalemia, acidosis,
coagulopathies, and hypothermia.
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Vanderbilt study on Rhabdomyolysis:
Crush injuries cause skeletal muscle damage
Damaged skeletal muscle releases myoglobin
Myoglobin lodges in the renal tubules
Myoglobin undergoes “Redox-cycling”
Release of oxidative free radicals
Acute renal failure caused by oxidative free
radical damage
Treatment includes all traditional options with
Acetaminophen
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Signs & Symptoms:
Loss of muscle tone
Loss of reflexes below the level of the injury
Loss of sensation
Treatment:
No specific treatment
Transient in nature
Symptomatology is often self limiting
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Almost always occurs in injuries above T6
Loss of descending sympathetic pathways
Loss of vasomotor tone and sympathetic
innervation to the heart.
Loss of vasomotor tone results in peripheral
vasodilation, pooling of blood, and subsequent
hypotension.
Loss of sympathetic innervation to the heart
results in bradycardia or the loss of the
reflexive tachycardia.
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Customary hypovolemia treatment is often
unsuccessful
Judicious IV fluid administration
Vasopressors
Atropine (for hemodynamically significant
bradycardia)
Airway support due to potential for phrenic
nerve paralysis (injuries at or above C5)
Support hemodynamics.
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Musculoskeletal trauma does not require a
reordering of the priorities of the Primary
Survey (ABCDE).
Musculoskeletal trauma is managed in the
Primary Survey when hemorrhage control
measures are required.
Musculoskeletal trauma is typically managed
in the Secondary Survey with splinting, wound
care, orthopedic consults, radiological studies,
antibiotics, tetanus toxoid, & transfer
consideration.
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Identify symptomatology related Crush
injuries, compartment syndrome, and
rhabdomyolysis.
Provide appropriate treatment related to these
injuries.
Differentiate Spinal and Neurogenic Shock
Provide appropriate treatment for these
injuries.