TRAUMA
& ITS COMPLICATIONS
Bernard Hojaili, MD, FACR
American Board of Rheumatology and Internal Medicine
Assistant Professor of Rheumatology & Immunology, LAU
[Link]
Graduate of the Albert Einstein College of Medicine, Dept Of
Rheumatology, New York city, USA
Blunt
Trauma
Penetrating
BLUNT TRAUMA
▣MVA
▣Pedestrian vs
Vehicle
▣Falls
Penetrating Trauma
▣Gun shot wounds
▣Stab wounds
▣Impalement
DO NOT PANIC!
DEATH FROM TRAUMA
1. Death may occur within seconds of the injury, usually due to massive
head injury, heart injury, or aortic injury. These deaths cannot be
prevented
2. A second peak in deaths begins an hour or two after the injury. Deaths
occurring in this second peak are usually due to subdural and
epidural hematomas, hemo- or pneumothorax, organ rupture, or
blood loss. These deaths are often preventable. This period is called the
“golden hour” during which prompt intervention can save a life
3. The third peak in deaths occurs many days after the injury, and is
usually due to sepsis or multi-organ failure. Prompt treatment of
shock and hypoxemia during the “golden hour” can reduce these deaths
SHOCK
• Shock is circulatory failure
• Inadequate perfusion of tissues with oxygenated blood
• It leads to organ damage and death from multi-organ
failure
• Management comes after attention to the airway and
breathing – unless there is catastrophic external bleeding
for which control of the bleeding takes precedence.
THERE ARE FIVE TYPES OF SHOCK
• ■ Vasoconstrictive:
• ● Hypovolemic (Hemorrhagic)
• ● Cardiogenic (e.g. pericardial tamponade)
• ■ Vasodilative:
• ● Septic: late sequela
• ● Neurogenic (e.g. spinal cord injury)
– hypotension without tachycardia
– Vasoconstrictive meds not administered until volume is restored
• ● Anaphylactic
HYPOVOLEMIC SHOCK
• Secondary to hemorrhage
• It is the most common type of shock
• As the circulating blood volume decreases,compensatory
mechanisms maintain systolic blood pressure up to
around 30% of blood loss (1.5 liters) in a fit patient
• Above this loss, compensation fails and coma followed
by death occurs after loss of around 50% of blood
volume (2.5 liters loss)
Cardiogenic shock
• Occurs in trauma patients who have suffered a
myocardial infarction
• Or direct myocardial injury
• NEUROGENIC SHOCK :
It is seen in high spinal cord transections
• SEPTIC SHOCK AND
ANAPHYLACTIC SHOCK:
are unusual in acute trauma.
RECOGNITION
• The patient becomes apathetic and thirsty
• Breathing becomes shallow and rapid
• The lips and skin are pale
• The extremities feel cold and clammy
• As compensation fails, the pulse becomes rapid
and weak, the blood pressure drops and the
patient may become confused
• Eventually renal function is impaired and urinary
output falls
HYPOVOLAEMIC SHOCK
UNRESPONSIVE TO TREATMENT
• It is commonly due to bleeding into body cavities
or potential spaces
• Identified by FAST or CT
• You should ‘Count bleeding onto the floor and
four more places: chest; abdomen;
pelvis/retroperitoneum; and long bones
MANAGEMENT
• Control bleeding: several methods are available:
• The choice depends upon the severity of blood loss
• Consider elevation and direct pressure
• Use of tourniquets
• Wound packing with haemostatic dressings
• Circumferential pressure dressings
• At all times maintain normothermia.
SECURE VASCULAR ACCESS:
• venous cannulation is usually appropriate
• Site two large-bore cannulas
• Central venous cannulation is associated with
dangerous complications and should be avoided
unless performed by an expert
• Femoral vein cannulation is an option (not the
best, because below the diaphragm)
• IO cannulation: Cannula can be inserted through
bone cortex into the marrow cavity of the tibia or
the humeral head
ADMINISTER INTRAVASCULAR FLUIDS
• Infuse blood if immediately available and bleeding has stopped
• Or give 2 Liters IV FLUIDS (20 mL/kg in children) followed by
transfusion: If bleeding is persistent and blood not immediately
available
• Give fluids in 250 mL boluses, titrated against a palpable radial pulse.
This minimizes dilutional anemia and increased bleeding as the blood
pressure is restored
• Titrate fluids against response, gauged by blood pressure, pulse rate,
peripheral perfusion, central venous pressure (CVP) and
measurement of metabolic acidosis
• The underlying cause of shock should be established and treated
alongside resuscitative measures
HEAD INJURIES
• Most head injuries result from a blow that causes either
direct damage or intracerebral movement due to rapid
acceleration or deceleration Damage may consist of:
1. minor contusion causing transient loss of consciousness
or amnesia
2. severe contusion or laceration, due either to direct injury
or to shearing forces
3. localized intracranial bleeding
4. fractures of the skull
5. diffuse edema and a rise in intracranial pressure
• High-velocity penetrating injuries (e.g. gunshot wounds)
also cause diffuse and severe brain damage as the
pressure wave moves across the brain.
• Extradural, subdural and intracerebral bleeding contribute
to the rise in ICP
• If the ICP is sustained above 20 mmHg, permanent brain
damage can result
• This is the secondary brain injury, which accounts for a
significant number of fatalities
• When pressure compensation reaches its limit, the ICP
rises exponentially causing uncal herniation with pupillary
dilatation on the side of the injury
• Ultimately, the cerebellum herniates through the foramen
magnum, leading to brainstem death
• Head injuries account for more than 50% of
trauma deaths
• These injuries can be classified into three groups
based on the GCS:
• Mild:
• GCS 13–15 (80% of cases).
• 55% have mild disability at 1 year.
• Moderate:
• GCS 9–12 (10% of cases).
• 63% have significant disability at 1 year.
• Severe:
• GCS 3–8 (10% of cases).
• 85% have significant disability at 1 year
RECOGNITION
• ABC before neurological assessment
• D: Assess the GCS
• Examine the pupils for equality, diameter, and
response to light
• Re-assess thoroughly, look for lateralizing signs
and motor and sensory deficits
• Diagnostic signs of a basal skull fracture are:
otorhinorrhoea (CSF leakage from ear or nose),
periorbital haematomas (‘raccoon eyes’),
subconjunctival haemorrhage without a posterior
margin and retromastoid bruising (Battle’s sign).
• Open wounds should be gently explored with a
gloved finger to exclude underlying skull fractures
• Patients suffering a severe head injury require an
urgent CT
• Specific indications include a drop in GCS,
suspected skull fracture, seizures, focal
neurological signs, vomiting and amnesia
BATTLE’S SIGN
SUBCONJUNCTIVAL HAEMORRHAGE WITHOUT A POSTERIOR MARGIN
Spinal Shock
▣Period immediately following injury to the spinal cord
▣characterized by:
1. Absence of all reflex activity
[Link]
[Link] of sensation below the level of the lesion
[Link] subsides within 24 hour unless the injury is
very severe like the one on the next slide
Nerve Injury
▣Nerves are fragile and can be damaged by pressure,
stretching, or cutting
Neuropraxia
▣least severe injury, is characterized by a conduction
block (focal conduction block)
▣conduction across the zone of nerve injury is
inhibited
▣conduction within the nerve
both proximal
and distal to
the lesion remains intact
Neuropraxia
▣Continuity of all structures is preserved
▣Wallerian degeneration does not occur (no axonal
loss) but there is focal demyelination
▣Complete recovery is evident in 3 to 6 weeks
▣Aftera simple crush injury function may return
within days
Axonotmesis
▣Ismore severe injury, with disruption of axons & surrounding
endoneurial sheaths
▣Perineurium and epineurimum remain intact
▣Wallerian degeneration occurs
▣After axonotmesis, conduction velocity may be preserved
distally for up to 7 days
▣ Recovery is good but may require many months
NEUROTMESIS
▣Most severe nerve
injury
▣Complete disruption
of axons, endoneurium,
perineurium, & epineurium
▣Wallerian degeneration
occurs
▣Recovery requires
operative repair and the
prognosis is variable,
ranging from complete
recovery to no recovery
ABDOMINAL INJURIES
• The immediately life-threatening injury is bleeding into the abdominal
cavity
• Blunt abdominal trauma is a cause of avoidable death but it is difficult
to detect
• Visceral rupture and laceration cause internal bleeding
• Look carefully for stab wounds; they may also be very small but they
can penetrate deeply and damage several structures
• During the primary [Link]. inspect the abdomen for wounds, abrasions
and contusions.
• Examine the flanks, posterior abdomen, back, perineum and genitalia,
and perform rectal examination
• FAST has replaced diagnostic peritoneal lavage
• Early CT is indicated, but a shocked patient may need urgent transfer
to surgery
MANAGEMENT
• Control external bleeding and manage shock.
• If unresponsive, administer further fluid and transfuse
blood
• Pass a gastric tube and a urinary catheter unless signs of
urethral injury are present
• Bleeding into the abdomen is an indication for immediate
laparotomy
• The patient will require supportive critical care, and may
require ventilation in an ICU
FOLLOW ESTABLISHED PROTOCOLS
ABCDEF
• A = Airway (with c. spine control)
• B = Breathing
• C = Circulation
• D = Disability
• E = Exposure
• F = Fracture
FRACTURES AND JOINT INJURIES
Types of Fractures
CLOSED FRACTURES OPEN FRACTURES
• Fracture is not exposed to the environment A break in the skin and
underlying soft tissue
• Do not underestimate the soft tissue injury
▣Fracture healing, infection
and amputation rate correlate
with the degree of soft tissue
injury
INTRAARTICULAR FRACTURES
crosses into the surface of a joint
cartilage damage (never heal)
bone fragments
ligament attachments
Pathophysiology of Fractures Healing
Vascular Response in Fracture Repair
▣Fracturestimulates the release of growth factors that
promote angiogenesis and vasodilation
▣Blood flow is increased substantially to the fracture
site
▣Peaks at two weeks after fracture
Stages of Fracture Healing
▣ Inflammation
▣ Repair
▣ Remodeling
INFLAMMATION
▣Tissue disruption results in hematoma at the fracture
site
▣Local vessels thrombose causing bony necrosis at the
edges of the fracture
▣Increasedcapillary permeability results in a local
inflammatory milieu
○Osteoinductive growth factors stimulate the
proliferation and differentiation of mesenchymal stem
cells
REPAIR
▣Periosteal callus forms along the periphery of
the fracture site. The ossification is initiated by
preosteoblasts
▣Intramedullary callus forms in the center of
the fracture site
▣Ossification at the site of the fracture
▣Chemical and mechanical factors stimulate
callus formation and mineralization
REMODELING
▣Woven bone is gradually converted to lamellar bone
▣Medullary cavity is reconstituted
▣Bone is restructured in response to stress and strain (Wolff’s Law)
IMAGING
▣ Xrays:
○Must have at least 2 views of the injured body part (AP/Lat) but
3 is even better
○Must include the joint above and below in evaluation
○Easy, cheap and part of the initial patient evaluation
CT scan
▣The best imaging technique in acute major trauma
▣Gives excellent visualization of intraarticular
displacement
○Gives a better 3 dimensional picture of the fracture
○Used to clear the cervical spine when adequate xrays
cannot be obtained
MRI
○Better for soft tissue evaluation
○Incertain cases like undisplaced hip fractures not seen
on Xray it is the modality of choice
○Will show bone marrow edema in the area of the
fracture
Bone Scan
○Used when other studies are negative
○Looking for stress fractures or occult fractures
○Highly sensitive but not specific
Fractures Treatment
▣Immobilization (casting or splinting)
▣Closed Reduction and Pinning
▣OpenReduction Internal Fixation
(ORIF)
▣Intramedullary Fixation
▣External Fixation
DEFINITIONS
▣ Nonunion: A fracture that has not and is
not going to heal
▣ Delayed union: A fracture that requires
more time than usual to heal. It shows
progression over time
HYPERTROPHIC HEALING
▣Vascularized
▣Callus formation present on x-
ray
▣Elephant’s foot - abundant
callus
▣Horse’s hoof - less abundant
callus
▣Typically only needs stability
to consolidate!
OLIGOTROPHIC HEALING
▣Some/minimal
callus on x-ray
○Not an aggressive
healing response
▣Vascularity is
present on bone scan
ATROPHIC HEALING
No evidence of callous formation on
▣
x-ray
▣ Ischemic or cold on bone scan
PSEUDARTHROSIS HEALING
▣Typically has adequate
vascularity
Excessive
▣
motion/instability
▣False joint forms over
significant time
ETIOLOGY OF NONUNION
▣ Host factors
▣ Fracture/Injury factors (Traumatic Soft Tissue
Disruption: Incidence of nonunion is increased with open fractures)
▣Initial treatment of injury
▣ Infection: The worst prognostic factor
ETIOLOGY OF NONUNION – HOST FACTORS
▣Smoking
▣Diabetes:Especially those with end organ disease –
neuropathy, Peripheral Vascular Disease, renal
dysfunction
▣Endocrinopathy: Thyroid, / parathyroid disorders,
hypogonadism, Vit D deficiency, others
▣Malnutrition: Adequate protein and energy is required for wound healing.
Screening tests: serum albumin, total lymphocyte count, Albumin less than 3.5 and
lymphocytes less than 1,500 cells/ml is significant
Host Factors (cont)
Medications: Steroids, Chemotherapy,
▣
Bispohosphonates
▣ Bone quality, vascular status
▣Balance, compliance with weight bearing
restrictions
SMOKING
▣ Decreases peripheral oxygen saturation
▣ Decreases peripheral blood flow
▣ Higher infection and nonunion rates
▣Welldocumented difficulties in wound healing in patients who
smoke: Schmite, M.A. e.t. al. Corr 1999
Jensen J.A. e.t. al. Arch Surg 1991
INITIAL TREATMENT OF INJURY
▣Excessive soft tissue stripping
▣Improper or unstable fixation
VESSELS INJURY
• Blood loss
• Progressive ischemia
• Compartment syndrome
• Tissue necrosis
Vascular injury
• Penetrating trauma
• Blunt trauma
• Iatrogenic
Irreversible damage after 6 hours
DIAGNOSIS
• Physical exam
• Doppler/Duplex scanning
• Arteriogram
• Exploration
Careful physical exam and
high index of suspicion are
most important
SURGICAL EXPLORATION
Immediate exploration is indicated
for:
• Obvious arterial injury on exam
• No doppler signal
• Site of injury is apparent
CONTINUED EVALUATION
• Vascular injuries are dynamic
• Evaluation should continue after the initial
injury or surgery
• Additional debridement and/or fixation
undertaken after successful
revascularization
TENDON INJURIES
▣Sharp penetrating trauma (lacerations)
▣Sportstrauma
○Eccentric contraction causing avulsion or tear
○Overuse causing tendonitis
TREATMENT OF TENDON INJURIES
▣Depends on location, mechanism, and function of tendon
▣Acute repair with suturing then protection of the repair with
temporary immobilization
COMPARTMENT SYNDROME DEFINITION
Symptoms resulting from increased pressure
▣
within a limited space compromising:
■ Circulation
■ Function
ETIOLOGY
▣Fractures
▣Soft Tissue Injury (Crush)
▣Arterial Injury
○Post-ischemic swelling
○Reperfusion injury
▣Drug Overdose (limb compression)
▣Burns
Diagnosis
▣ Clinical diagnosis
○ High index of suspicion
▣ Syndrome
○History
○Physical Exam
COMPARTMENT SYNDROME DIAGNOSIS
▣5 P’s - NOT RELIABLE:
○pain
○pallor
○paralysis
○pulselessness
○paresthesias
▣(These signs may be present in the absence of compartment syndrome)
▣The most important symptom
of an impending compartment
syndrome is PAIN
DISPROPORTIONATE TO
THAT EXPECTED FOR
THE INJURY
SIGNS & SYMPTOMS
▣ Pain
○May be worse with elevation
○Patient will not initiate motion on
own
Be careful with coexisting
▣
nerve injury
▣Tense compartment on palpation
▣Elevated compartment pressure
PATHOPHYSIOLOGY
▣A continuous increase in pressure within a compartment occurs
until the low intramuscular arteriolar pressure is exceeded and
blood cannot enter the capillaries
▣Increased Volume - internal : hemmorhage, fractures,
swelling from traumatized tissue, increased fluid secondary
to burns, post-ischemic swelling
▣Decreased volume - external: tight casts, dressings
▣Most common cause: hemmorhage into a compartment:
fractures of the tibia, elbow, forearm or femur
MUSCLE ISCHEMIA
▣4 hours - reversible damage
▣8 hours - irreversible changes
▣4-8 hours - variable
Hargens JBJS 1981
MUSCLE ISCHEMIA
▣ Myoglobinuria after 4 hours
○Renal failure
○Maintain a high urinary output
○Alkalinize the urine
▣ Cell death initiates a “vicious cycle”
○increase capillary permeability
○increased muscle swelling
NERVE ISCHEMIA
▣1 hour - normal conduction
▣1- 4 hours - neuropraxic damage
reversible
▣8 hours - axonotmesis and
irreversible change
Hargens et al. JBJS 1979
Tissue Pressure
▣Normal tissue pressure
○ 0-4 mm Hg
○8-10 with exertion
TREATMENT
▣Remove restricting bandages
▣Immediate SURGICAL FASCIOTOMY
▣Serial exams
BUT
▣Fasciotomies’complications are >25%
○Chronic swelling
○Chronic pain
○Muscle weakness
○Iatrogenic Nerves and Vessels injury
○Cosmetic concerns
