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BLASTS AND BURNS: Don’t Feel The Heat!

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1 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

2 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

3 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

4 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

5 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

6 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

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8 CLASSIFICATION OF BURNS
Thermal Cold Exposure Chemical Electrical Current Inhalation Radiation

9 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

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11 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

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13 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

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15 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)

16 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

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18 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

19 FULL THICKNESS (cont.) Skin waxy white to leathery gray to charred and black Dry and inelastic Does not blanch No vesicles or blisters

20 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

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22 FOURTH DEGREE Deep Potentially life threatening
Extend through the skin to underlying structures

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24 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

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27 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

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29 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

30 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

31 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

32 AIRWAY (cont.) RSI with Succinylcholine acceptable in the first 72 hours but no later secondary to the risk of severe hyperkalemia Significant % develop ARDS

33 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

34 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

35 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

36 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

37 TREATMENT Supplemental Oxygen and Airway Protection
Bronchodilators when bronchospasm present Avoid Corticosteroids Fluid resuscitation with aggressive monitoring

38 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 broncho-pulmonary casts

39 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

40 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

41 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

42 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

43 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

44 ESTIMATING INITIAL FLUID REQUIREMENTS (cont.)
Modified Brooke Formula Given over initial 24 hours 2 ml/kg for each % TBSA Likely reduces the overall volume

45 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

46 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

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48 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

49 CHEMOPROPHYLAXIS (cont.)
Once invasion occurs – organisms can invade the blood vessels producing secondary bacteremia Topical antibiotics are given to all patients with nonsuperficial burns

50 TETANUS Update for any burns deeper than superficial
Tetanus Immune Globulin – if patient did not receive complete set of primary immunizations

51 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

52 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

53 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

54 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)

55 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

56 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 Pulse-Ox > 90%, likely does not need escharotomy)

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61 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

62 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)

63 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

64 HARRIS BENEDICT EQUATION
Females BEE (Kcal/day) = (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) = (13.8) x Kg + (5) x Ht in cm – (6.76) x age

65 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

66 CURRERI FORMULA Age 16 – 59 Age > 60
Kcal/day = 25 kcal/Kg/day + 40 Kcal/%TBSA burned/day Age > 60 Kcal/day = 25 Kcal/Kg/day + 65 Kcal/%TBSA burned/day

67 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

68 NUTRITION IN CHILDREN RDA (RDI) – recommended daily allowance (recommended daily intake) RDI Kcal/day = 37 x Kg With a modifier based on age

69 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)

70 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

71 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

72 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

73 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

74 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

75 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)

76 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

77 ORGANISMS IN BURNS Immediately following 2 – 4 days Within 1st week
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

78 ORGANISMS IN BURNS Most Common Overall Most Predominate Gram Positives
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

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80 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

81 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

82 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

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84 TYPES OF INJURIES Primary Blast Injury Secondary Blast Injury
Tertiary Blast Injury Quaternary Blast Injury Electromagnetic Perturbations Miscellaneous Effects from the explosion

85 TYPES OF INJURIES Primary Blast Injury Secondary Blast Injury
Tertiary Blast Injury Quaternary Blast Injury Electromagnetic Perturbations Miscellaneous Effects from the explosion

86 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”

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90 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

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93 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

94 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

95 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

96 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

97 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

98 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

99 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

100 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

101 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

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105 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

106 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

107 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

108 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

109 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

110 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)

111 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

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113 bTBI: EFFECTS OF EXPOSURE (cont.)
Persistent traumatic focal cerebral vasospasm Worse outcomes noted Also noted as a common and potentially underappreciated sequellae of cTBI

114 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

115 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

116 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

117 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

118 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

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