BLASTS AND BURNS:
Don’t Feel The Heat!
Susan Marie Baro, DO, FACOS
Associate Trauma and Surgical Critical Care
Associate Director Surgical Critical Care
Physician Director Blood Conservation Program
OBJECTIVES
• Understand the injuries that result from
explosions and review current
management and treatment of Blast
Injuries
• Review Burn Injury Classifications and
Standard Treatments
• Calculate % TBSA in Burns
• Calculate IV Fluid Requirements in Burns
AMERICAN BURN ASSOCIATION
Burn Injury Severity Grading System
• Minor Burn
– 15% TBSA (Total Body Surface Area) or less
in adults
– 10% TBSA or less in children and the elderly
– 2% TBSA or less full thickness burn in
children or adults without cosmetic or
functional risk to eyes, ears, face, hands, feet
or perineum
AMERICAN BURN ASSOCIATION
Burn Injury Severity Grading System
• Moderate Burn
– 15 – 25% TBSA in adults with less than 10%
full thickness burn
– 10 – 20% TBSA partial thickness burn in
children < 10 and adults > 40 years of age
with less than 10% full thickness burn
– 10% TBSA or less full thickness burn in
children or adults without cosmetic or
functional risk to eyes, ears, face, hands, feet,
or perineum
AMERICAN BURN ASSOCIATION
Burn Injury Severity Grading System
• Major Burn
– 25% TBSA or greater
– 20% TBSA in children <10 and adults > 40
years of age
– 10% TBSA or greater full thickness burn
– All burns involving eyes, ears, face, hands,
feet, or perineum that are likely to result in
cosmetic or functional impairment
AMERICAN BURN ASSOCIATION
Burn Injury Severity Grading System
• Major Burn (cont.)
– All high voltage electrical burns
– All burn injury complicated b y major trauma
or inhalation injury
– All poor risk patients with burn injury
CLASSIFICATION OF BURNS
• Thermal
• Cold Exposure
• Chemical
• Electrical Current
• Inhalation
• Radiation
CLASSIFICATION BASED ON
DEPTH OF TISSUE INJURY
• 1st Degree – Superficial or Epidermal
• 2nd Degree – Partial Thickness
• 3rd Degree – Full Thickness
• 4th Degree – burns extending beneath the
subcutaneous tissues involving the fascia,
muscle, and /or the bone
SUPERFICIAL BURN
• Epidermal layer (ex, sunburn)
• No Blisters
• Red, painful, and dry
• Epidermal layer peels away
• Blanches with pressure
• Subsides over 2 – 3 days and heals within
6 days without scarring
PARTIAL THICKNESS:
SUPERFICIAL
• Between the epidermis and the dermis
• Forms blisters within 24 hours
• Painful, red, weeping
• Blanches with pressure
• Pigment changes can occur
• Usually heals in 7 – 21 days
• Scarring unusual
PARTIAL THICKNESS:
DEEP
• Extends deep into the dermis
• Damages hair follicles and glandular tissue
• Painful to pressure only
• Almost always blisters
• Wet, waxy, or dry
• Variable mottled coloration (Patchy cheezy
white to red)
PARTIAL THICKNESS:
DEEP (cont).
• Does not blanch
• Heals in 3 – 9 weeks if no grafting
required
• Causes hypertrophic scarring
• If involves the joint, expect dysfunction
even with aggressive physical therapy
• Hard to differentiate from Full Thickness
burn
FULL THICKNESS
• Extends through and destroys all layers of
the dermis and often injures underlying
subcutaneous tissue
• Burn eschar and denature dermis usually
intact
• Eschar compromises viability of limb and
torso if circumferential
• Anesthetic or hypoesthetic
FULL THICKNESS (cont.)
• Skin waxy white to leathery gray to
charred and black
• Dry and inelastic
• Does not blanch
• No vesicles or blisters
FULL THICKNESS (cont.)
• Eschar usually separates from the
underlying tissue and reveals an unhealed
bed of granulation tissue
• Without surgery – they heal by wound
contracture with epithelialization around
the edges
• Scarring is severe with contractures
FOURTH DEGREE
• Deep
• Potentially life threatening
• Extend through the skin to underlying
structures
TOTAL BODY SURFACE AREA
• Size is usually underestimated
– Results in under resuscitation
• Lund-Browder
– Most accurate for both children and adults
– Takes into account the relative % of body
surface area affected by growth
• Kids have larger heads and smaller extremities
TOTAL BODY SURFACE AREA
(cont).
• Rule of Nines (adults)
– Each leg represents 18% TBSA
– Each arm represent 9% TBSA
– Anterior and Posterior Trunk each represent
18% TBSA
– Head represents 9 % TBSA
TOTAL BODY SURFACE AREA
(cont).
• Palm Method
– Used when the burn is irregular and/or patchy
– Utilizes the surface area of the patients palm
– Palm, excluding extended fingers = 0.5%
patients TBSA
– Palm, extending fingers = 1% of patients
TBSA
INITIAL MANAGEMENT
• Essentially ATLS
• Special attention to respiratory distress
and smoke inhalation
• Remove clothing promptly
• Consider early transfer to Burn Center
• History is important
– Materials, chemicals, open vs closed space,
explosion or blast involvement, associated
trauma
AIRWAY
• Inhalation injury remains a leading cause
of death in the adult burn victim
• Present in 2/3’s of patient with burns >
70% TBSA
• Supplemental oxygen, maintain airway
• Upper airway edema occurs rapidly
AIRWAY (cont.)
• RSI with Succinylcholine acceptable in the
first 72 hours but no later secondary to the
risk of severe hyperkalemia
• Significant % develop ARDS
SIGNS OF SIGNIFICANT SMOKE
INHALATION INJURY
• Persistent cough, stridor, or wheezing
• Hoarseness
• Deep facial or circumferential neck burns
• Nares with inflammation or singed hair
• Carbonaceous sputum or burnt matter in
the nose or mouth
• Blistering or edema of the oropharynx
SIGNS OF SIGNIFICANT SMOKE
INHALATION INJURY (cont.)
• Depressed mental status
• Respiratory distress
• Hypoxia or Hypercapnia
• Elevated Carbon Monoxide and/or Cyanide
levels
• Inhalation injury from hot gasses usually
occurs above the vocal cords
CARBON MONOXIDE AND
CYANIDE
• Check Carboxyhemaglobin level in all
patients with moderate to severe burns
• Standard Pulse-Ox not reliable
• Treatment with high flow oxygen alone
effectively removes CO
• Hyperbaric Oxygen Treatment if increased
CO or if treatment for Cyanide poisoning
places patient at risk for hypoxemia
CARBON MONOXIDE AND
CYANIDE (cont.)
• Check Methemaglobin if Cyanide poisoning
suspected
• Consider Cyanide toxicity in severe burn
patients with unexplained lactic acidosis
and declining EtCO2
• Treatment: Hydroxocobalamin
TREATMENT
• Supplemental Oxygen and Airway
Protection
• Bronchodilators when bronchospasm
present
• Avoid Corticosteroids
• Fluid resuscitation with aggressive
monitoring
TREATMENT (cont.)
• Vent Settings: low tidal volumes to
minimize airway pressures and to reduce
incidents of Ventilator Associated Acute
Lung Injury (ALI)
• Inhaled Nitric Oxide – may increase
hypoxic vasoconstriction
• Aerosolized Heparin and N-Acetylcysteine
(NAC) – may help to remove bronchopulmonary casts
FLUID RESUSCITATION
• Burn Shock – occurs within 24 – 48 hours
• Characterized by myocardial depression
and increased capillary permeability
• Results in large fluid shifts and depletion
of intravascular volume
• Rapid, aggressive fluid resuscitation helps
to reconstitute the intravascular volume
and maintain end organ perfusion
FLUID RESUSCITATION (cont.)
• A-line
• Foley for accurate urine outputs
• Over-resuscitation leads to ARDS,
pneumonia, MSOF, and compartment
syndromes (including abdomen, limb, and
orbit)
• Any patient with > 15% TBSA,
nonsuperficial burns (2nd/3rd Degree)
should receive formal fluid resuscitation
FLUIDS
• IV Crystalloid – typically Ringer’s Lactate
– helps to reduce incidence of hyperchloremic
acidosis associated with large volumes of
isotonic saline (NS)
– Colloid and Hypertonic Saline for initial
resuscitation not found to show any
improvement in outcomes, are more
expensive, and possibly increase renal failure
and death
FLUIDS (cont.)
• Following initial resuscitation IV fluids
need to meet baseline fluid needs and
maintain Urine outputs
• IF UO < 0.5 ml/kg/hr – bolus with 500 to
1000 ml fluid and increase rate by 20 –
30%
• If adequate resuscitation and patient
stabilizes, change to D5 ½ NS with 20
mEq KCl per liter at maintenance to keep
UO > 0.5 ml/kg/hr
ESTIMATING INITIAL FLUID
REQUIREMENTS
• Parkland Formula – utilized in initial 24 hrs
• Includes partial and full thickness burns
• 4 ml/kg for each % of TBSA burned over
15% TBSA
• ½ volume given in 1st 8 hours and the
remaining volume given over the next 16
hours
ESTIMATING INITIAL FLUID
REQUIREMENTS (cont.)
• Modified Brooke Formula
• Given over initial 24 hours
• 2 ml/kg for each % TBSA
• Likely reduces the overall volume
BLOOD TRASFUSION
• Avoid if possible
• Associated with increased mortality
• Only if Hemoglobin < 8 gm/dL unless
patient with acute coronary syndrome
• If at risk for ACS – transfuse to 10 gm/dL
IMMEDIATE BURN CARE
• Remove clothing
• Cool burned area immediately using cool
water or saline soaked gauze
– can minimize the zone of injury in small burns
• Monitor cor body temp to prevent
hypothermia, especially if >10% TBSA
• Avoid temps below 35o C/95o F
• Aggressive Pain control with Morphine and
Benzo’s for anxiety
CHEMOPROPHYLAXIS
• Extensive burns cause immunosuppression
on basis of altered neutrophil activity, T
lymphocyte dysfunction, and imbalance in
production of cytokines
– Bacterial colonization of the burn eschar site
can result
• Burns destroy physical barrier to tissue
invasion
– Permits spread of bacteria to the dermis and
through the lymphatics along the fibrous
septae
CHEMOPROPHYLAXIS (cont.)
• Once invasion occurs – organisms can
invade the blood vessels producing
secondary bacteremia
• Topical antibiotics are given to all patients
with nonsuperficial burns
TETANUS
• Update for any burns deeper than
superficial
• Tetanus Immune Globulin – if patient did
not receive complete set of primary
immunizations
ANTIBIOTICS
• Apply topically to all nonsuperficial burns
• If transferring to Burn Center – hold on
topical coverage and cover with clean,
dry, dressings
• No Prophylactic IV antibiotics
• Silver Sulfadiazine (SSD)
– avoid near eyes and mouth, sulfonamide
hypersensitivity, pregnant women, newborns, and
nursing mothers
• Bacitracin as an alternative
WOUND
• Wash with mild soap and water
• Remove debris
• Avoid local anesthetics
• Never aspirate intact blisters
• Burn wound debridement and excision and
coverage is performed within the first 6 –
24 hours after local injury
DRESSINGS
• If transferring – clean, dry sheet
• Non-adherent mesh gauze after cleaning
with antibiotics ointment
• Avoid tape on skin
• Tubular gauze or light circumferential
wraps
• Deep wounds – biologic or biosynthetic
dressings or bismuth impregnated
petroleum gauze
ESCHAROTOMY
• Occurs with deep dermal and full
thickness burns which are circumferential
• Dermis can becomes stiff and unyielding –
referred to as an eschar
• Usually does not occur until 3 – 4 hours
following initiation of fluid resuscitation
• Utilize scalpel or electrocautery (preferred)
ESCHAROTOMY (cont.)
• Extend through the eschar to the fatty
tissue beneath – no further
• Leaves fascia intact
• If no improvement, may have developed
compartment syndrome which could
require fasciotomy, but this is a different
entity
• If signs of ischemia or respiratory distress
occur – need to perform prior to transfer
ESCHAROTOMY (cont.)
• Neck and Chest – can lead to respiratory
compromise
• Abdomen – leads to Abdominal
compartment syndrome
• Extremities – ischemia with decreased
pulses, capillary refill, pulse-ox (if PulseOx > 90%, likely does not need
escharotomy)
GI
• Shock from thermal burn injuries results in
mesenteric vasoconstriction predisposing
to gastric distention, ulceration (Cushing’s
Ulcer) and aspiration
• NGT if > 20% TBSA
• Stress ulcer prophylaxis
NUTRITION
• Early feeding: within 24 – 48 hours
• Meet basic patient energy needs to
attenuate the catabolic response to burns
• Hypermetabolic
• Enteral preferred
• Indication for Nutritional Support – failure
to maintain LBM (Lean Body Mass) and
body weight (dry body weight on day 5
post burn)
HARRIS BENEDICT EQUATION
• Estimates basal energy expenditure
• For burn patients the BEE is multiplied by
an arbitrary activity or stress factor of 1.2
to 2.0 (usually 1.2 to 1.5)
• Useful for initial estimate of energy
demand
• Usually overestimates caloric requirements
HARRIS BENEDICT EQUATION
• Females
– BEE (Kcal/day) = 655 + (9.6) x Kg + (1.85) x
Ht in cm – (4.68) x Age
– Then multiply by 1.2 to 2.0
• Males
– BEE (Kcal/day) = 66.5 + (13.8) x Kg + (5) x
Ht in cm – (6.76) x age
– Then multiply by 1.2 to 2.0
CURRERI FORMULA
• Takes into account TBSA and Body Weight
prior to burn
• Estimates the energy required by linear
regression analysis based on the number
of calories required to prevent weight loss
• Still likely overfeeds
CURRERI FORMULA
• Age 16 – 59
– Kcal/day = 25 kcal/Kg/day + 40 Kcal/%TBSA
burned/day
• Age > 60
– Kcal/day = 25 Kcal/Kg/day + 65 Kcal/%TBSA
burned/day
GOLD STANDARD
• Preferred method to estimate caloric
requirements in burn patient is by Indirect
Calorimetry (IDC)
• Uses respiratory gas exchange to estimate
fuel consumption
• Results affected by oxygen therapy,
hemodynamic instability, fever, sepsis,
ongoing procedures
NUTRITION IN CHILDREN
• RDA (RDI) – recommended daily
allowance (recommended daily intake)
• RDI Kcal/day = 37 x Kg
• With a modifier based on age
NUTRITIONAL FORMULA
• At least 50% calories as Carbohydrates
• 35% as Protein
• No more than 15% as Fat
• Supplement with micro and macro
nutrients
• Add Glutamine to standard formulas
(decreased Gran Negative Bacteremia)
FORMULA (cont.)
• 1.5 to 2.0 grams protein/kg/day
• 5 to 7 mg/kg/min of glucose/day
representing ~ 50% of total calories
• No more than 15% non-protein calories
from fats
• Vitamin A,C, and D
• Trace Minerals (selenium, zinc, copper)
• Glutamine
THROMBOEBMOLIC PROPHYLAXIS
• Burn patients are at an increased risk for
thromboembolic complications
• Initial prophylaxis on arrival to ICU
– Enoxaparin 40 mg q day
– Enoxaparin 30 mg q day if < 40 Kg or with creatinine
clearance < 30 mL/min
– Enoxaparin 40 mg q day if > 100 Kg
– Enoxaparin 30 mg bid with associated lower extremity
or pelvic orthopedic injuries or burn
– Heparin 5000 mg q 8 if not a candidate for
Enoxaparin
SEPSIS
• > 20% TBSA Burns – increased risk for an
invasive burn wound infection
• Referred to as “Burn Wound Sepsis”
• Often lead to MOF and death
• 75% of the mortality following thermal
injuries is related directly to infection
• Different criteria than non-burn patients
– Takes into account the changing metabolism
and altered inflammatory response in burns
BACTERIAL BURN WOUND
SEPSIS
• Non-Invasive burn wound infection
– > 105 bacteria per gram of tissue
• Invasive burn wound infection
– Defined as the presence of micororganisms in
the adjacent unburned tissue
FUNGAL BURN WOUND INFECTION
• Non-Invasive fungal infection
– Defined as the recovery of mold or yeast by
culture of a specimen obtained from a burn
wound or eschar
• Invasive fungal infection
– Need to identify hyphae or melanized yeast-like
forms utilizing histopath/cytopath, or by direct
microscopic exam of a needle aspirate or
biopsy specimen, or by associated tissue
damage or recovery of mold/yeast by culture of
a specimen from a normally sterile site
ABA CRITERIA FOR DEFINITION
OF SEPSIS & INFECTION
• Most include three of the following
–
–
–
–
–
–
–
–
Temp > 102.2oF/39oC
Progressive tachycardia
Progressive tachypnea
Refractory hypotension
Leukocytosis or Leukopenia
Thrombocytopenia
Hyperglycemia (in the absence of DM)
Inability to tolerate enteral feeds for > 24 hours
(strict criteria for failure)
SEPSIS AND INFECTION (cont.)
• Requires infection be documented by one
of the following
– Confirmed on cultures (wound, blood, urine)
– Pathologic tissue source identified (> 105
bacteria on quantitative wound tissue biopsy
or microbial invasion on surrounding tissue
biopsy
– Documentation of clinical response to
antimicrobial administration
ORGANISMS IN BURNS
• Immediately following
– Predominately Gram Positive bacteria
• Staph aureus, Pseudomonas aeruginosa, Serratia
marcescens
• 2 – 4 days
– Gram Negative bacteria
• Within 1st week
– Burns colonized with GP’s, GN’s, Fungi
• > 5 days
– Gram Negatives with abx resistant traits
ORGANISMS IN BURNS
• Most Common Overall
– MSSA, MRSA, and Pseudomonas
• Most Predominate Gram Positives
– Staph aureus and enterococcus
• Most Predominate Gram Negatives
– Pseudomonas and E coli
• Candida is the most common fungal
infection (4th most common cause overall)
• HSV-1 – most common viral organism
BLAST INJURIES - PHYSICS
• Explosive detonations differ from collisions or
impacts
• High-order explosive detonations cause a near
instantaneous transformation of the explosive
material into a highly pressurized gas
• Releases energy at supersonic speeds
• Transient shock waves travel in excess of the speed
of sound
• Results in formation of a blast wave that travels
out from the epicenter of the blast
PHYSICS (cont.)
• Simply put - an explosion is caused by the rapid
chemical conversion of a solid or liquid into a
gas with resultant energy release
• An idealized free-field spherical blast creates a
temporal pressure transient (Friedlander
Function) that has a leading overpressure phase
followed by an under pressure phase all
occurring within milliseconds
• Rarely the common clinical explosion scenario
PHYSICS (cont.)
• Explosives do not always combust
instantaneously and multiple shock waves
can occur
• This is very frequent with improvised
explosive devices (IED’s)
• In addition, the blast wave is affected by
reflection from nearby surfaces, potentially
causing a merger of the initial pressure
wave and the reflected wave or waves
TYPES OF INJURIES
• Primary Blast Injury
• Secondary Blast Injury
• Tertiary Blast Injury
• Quaternary Blast Injury
• Electromagnetic Perturbations
• Miscellaneous Effects from the explosion
TYPES OF INJURIES
• Primary Blast Injury
• Secondary Blast Injury
• Tertiary Blast Injury
• Quaternary Blast Injury
• Electromagnetic Perturbations
• Miscellaneous Effects from the explosion
PRIMARY BLAST INJURY (PBI)
• Caused by the direct effect of the blast
•
•
•
•
overpressure on organs
Characterized by anatomical and physiological
changes from the force generated by the blast
wave impacting the body’s surface
Affect primarily gas-containing structures (lungs,
GI tract, middle ear)
Consequence of extreme pressure differentials
developed at the body surfaces
Leading edge of a blast wave is call the “Blast
Front”
SECONDARY BLAST INJURY
• Results from shrapnel, objects or materials
•
•
•
•
hurled at the victim
Secondary missiles created by container
fragments or nearby shattered objects have the
longest range
Like sound waves, blast waves do not move
mass, however, an additional “dynamic
pressure” is created by the net motion of air
molecules responding to blast-inducted
differentials in static pressure
Individuals far from the scene can be injured
Penetrating neck and torso trauma is common
with this force
TERTIARY BLAST INJURY
• Occurs when the victims are flung through
the air and strike other objects
• A blast causing peak static overpressures
of 5 psi (strong enough to rupture ½ of
exposed TM’s) can generate a “blast wind”
of up to 145 mph
• this can propel objects and people a
considerable distance
• The wind from a blast significant enough
to cause Pulmonary PBI may exceed 831
mph
QUATERNARY BLAST INJURY
• Characterized by burns produced from the
thermal effects of the detonation itself
• Adds difficulty to the resuscitation –
requiring additional fluids not likely
beneficial with PBI to the lungs
ELECTROMAGNETIC
PERTURBANCES
• These occur with some types of
explosions, in particular, those generated
by IED’s that have metallic casings
• These events result in the generation of
small and brief radio-frequency pulses for
which the physiologic impact is unclear
MISCELLANEOUS EFFECTS
• Inhalations of dust, smoke, carbon
monoxide and other chemicals
• Burns from hot gasses or other fires
• Crushing injuries from collapsed buildings
• Accidental injuries not related to the
explosion itself but to the rescue efforts
still count as casualties
PRIMARY BLAST INJURIES: LUNG
• Clinical diagnosis
• Usually manifests as pulmonary contusions
• Worse on the side of approach of open-air
blasts
• B/l and diffuse in confined space blasts
• Characterized as respiratory difficulty and
hypoxia without evidence of obvious
external trauma or injury to the chest
PBI LUNG (cont.)
• May be complicated by pneumothoraces and air
•
•
•
emboli, as well as suffocation from massive
hemoptysis
Can see pleural and subpleural petechiae and
ecchymosis in parallel bands corresponding to
intercostal spaces
May be associated with multiple other injuries
Presents with a variety of symptoms: dyspnea,
chest pain, cough, hemoptysis
PBI LUNG PHYSICAL EXAM
• May reveal tachypnea, hypoxia, cyanosis and
•
•
decreased breath sounds
Can have sub-pleural multifocal hemorrhages
near the cheat wall, diaphragm, and
mediastinum
Hemo-pneumothoraces, traumatic emphysema,
alveolovenous fistulas from stress-induced tears
of the air tissue interface
• Can lead to Broncho-Pleural fistulas (BPF) or Arterial
Air Fistulas (AAE)
• Occurs following low vascular pressure after
hemorrhage or high airway pressure during PPV
ARTERIAL AIR EMBOLISM (AAE)
• AAE – most common cause of rapid death solely
•
•
•
•
caused by PBI in immediate survivors
Occurs at first moment of PPV
Pulmonary barotrauma, not from PBI, can lead
to venous air emboli
Long bone fractures lead to venous fat emboli
Both have same clinical picture as AAE: sudden
hypoxemia and mental status changes
ARTERIAL AIR EMBOLUS (AAE)
• Visualization of air in the retinal vessels, mottling
•
of nondependent areas of skin, or demarcated
tongue blanching are insensitive but rather
specific indicators for systemic AAE
No specific findings to detect MI and Coronary
AAE other than profound shock and bradycardia
with no other sources identified
LUNG PBI TREATMENT
• CXR, CT, ABG, etc…can assist in diagnosis
but should not delay treatment
• Tx: high flow oxygen, airway
management, chest tubes if needed,
mechanical vent if needed, permissive
hypercapnia (provided no additional TBI),
and judicious utilization of fluids
PULM E & M
• Lung PBI acts like severe pulmonary
contusions with impaired oxygen diffusion
• Give highest FiO2 possible
• If problems soley with oxygenation and not
ventilation – try NRB or CPAP
• No CPAP if suspect facial trauma/skull fx’s
• Spontaneous respirations desired for PBI
lung to lessen likelihood of AAE, but may
require PPV
PULM E & M (cont.)
• Poorly compliant blast-injured lungs need to be
ventilated with techniques similar to those used
with severe contusions or ARDS
• Pressure controlled ventilation with permissive
hypercapnia to facilitate adequate oxygen exchange
but keep transalveolar pressure less than 35 cm H2O
• Initial PEEP of 10 cm H2O
• Refractory hypoxemia or with associated bTBI
• Need to be managed with inverse I:E ratios,
independent lung ventilation, high-frequency jet vent,
and nitric oxide inhalation, even ECMO if needed
PULM E & M (cont.)
• ABG
• Check PaO2/FiO2 ration
• Blast injury patients with initial ratio’s of > 200
mm Hg do not require mechanical vent for
respiratory failure
• Moderately impaired: PFR 60 – 200 mm Hg –
generally require vent assistance for at least one
day with PEEP > 5 cm H2O
• PFR < 60 mm Hg (often have b/l pneumo’s,
bronchopleural fistulas) – usually require PEEP >
10 cm H2O and unconventional vent strategies
BLAST INDUCED TBI (bTBI)
• Most common cause of death
• SAH and SDH – most common findings in
fatalities
• “Signature Wound” of the Afghanistan and
Iraq wars
• Vulnerable target, but the primary
transduction pathway of blast energy to
the brain is not well understood
PRIMARY bTBI
• 3 ways transduction can occur
• Through direct transcranial propagation
• Via the vascular system
• From the CSF in the spinal cord to the
Foramen Magnum
(4th Controversial mechanism – possible
transmission via peripheral vasculature)
bTBI: EFFECTS OF EXPOSURE ON
NEUROLOGIC FUNCTION
• Spectrum of injury severities ranging from
mild effects to fatal injuries
• Edema, contusions, DAI, hematoma,
hemorrhage
• Brain swelling occurs much soon after
blasts (within hours) than routine trauma
• Mortality decreased substantially with early
decompressive craniectomies
bTBI: EFFECTS OF EXPOSURE
(cont.)
• Persistent traumatic focal cerebral
vasospasm
• Worse outcomes noted
• Also noted as a common and potentially
underappreciated sequellae of cTBI
bTBI
• Milder end of the spectrum – “shell shock” or
•
•
•
“blast concussion”
Symptoms include: physical (somatic),
behavioral, psychological, and cognitive deficits
Symptoms often referred to as Post Concussive
Syndrome or PCS
Includes retrograde amnesia, compromised
executive function, headaches, confusion,
amnesia, difficulty concentrating, mood
disturbances, alterations in sleep patterns, and
anxiety
cTBI and bTBI
• Similar symptoms as far as cognitive impairment
• Disturbances in pain, balance, equilibrium,
•
•
•
motor functioning, vision, depression or
communicative abilities
Frequently both occur at the same time
secondary to event
Can add penetrating trauma to the mix as well
bTBI – increased risk for hearing loss and
tinnitus as well as PTSD
PE FOR bTBI
• Subtle dysfunction to profound
•
unresponsiveness
Causes of Altered Mental Status/Seizures
• Hypoxemia from acute lung injury
• Shock from tension pneumo, hemorrhage or AAE
induced MI
• Conventional blunt or penetrating head injury
• Cerebral AAE
• Brain lesions resulting in focal deficits will most
likely be related to severe intracerebral
hemorrhage or AAE induced stroke
DIAGNOSITC APPROACH TO bTBI
• Significant correlation between tympanic
•
•
•
•
membrane perforation and LOC
Also good correlation between occulo-motor
dysfunction and bTBI
Biochemical markers being developed
CT, MRI, DTI for diagnosis
DTI – Diffusion Tensor Imaging – detects white
matter damage by measuring diffusion of water
in parallel tracts
CLINICAL CONSIDERATIONS IN
bTBI
• More injuries with higher severity of injury noted
in closed vs open blast settings
• Up to 36% can have delayed finding on CT
scans 48 hours later
• 30 – 44% have abdominal injuries as well
• Up to 50% have lung related PBI
• Best practice guidelines difficult to follow with lung and brain
injuries – contradictory
• Rec’s: Inhaled Nitric Oxide to overcome severe hypoxemia and
raise O2 saturation to at least 95% in brain injury patient while
also ameliorating the inflammatory effects in the lung
• Polytrauma likely