Primary Blast InjuryUpdate on diagnosis and treatmentCrit Care Med 2008; 36:[Suppl.]:S311–S317
1. Primary blast injuries: injuries due solely to theblast wave2. Secondary blast or explosive injury: primarilyballistic trauma resulting from fragmentationwounds from the explosive device or theenvironment3. Tertiary blast or explosive injury: result ofdisplacement of the victim or environmentalstructures, is largely blunt traumatic injuries4. Quaternary explosive injuries: burns, toxins, andradiologic contamination
The blast wave enters the body creating two typesof energy, stress waves and shear waves. Stress waves are longitudinal pressure forcesthat move at supersonic speeds and create a“spalling” effect at air–tissue interfaces, much likeboiling water, resulting in severe microvasculardamage and tissue disruption. Shear waves are transverse waves that causeasynchronous movement of tissue and possibledisruption of attachments.
The organs most likely affected by primary blastinjury are the ears, lungs, and colon or gas-filledorgans with the damage originating at the tissue–gas interface. Ruptured tympanic membrane, ossiculardisruption, alveolar hemorrhage, cerebral,coronary, retinal and lingual air emboli, rupturedviscus with pneumoperitoneum, and vagallymediated bradycardia, apnea, and hypotensionare among the early signs of severe primary blastinjury.
The absence of perforation of the tympanicmembrane and lack of petechiae in theoropharynx have been said to mediate againstprimary blast injury of internal organs in themajority of cases. The presence of oral petechiae and perforatedtympanic membrane together, this can be avaluable triage tool to alert the physician to keepa patient for further observation.
10% of all blast survivors have significant eyeinjuries. Symptoms of ocular injury include pain or irritation,altered vision, periorbital swelling, contusion, orforeign body sensation in the case of injuryresulting from fragments. Ophthalmic physical examination findings includeconjunctival hemorrhage, diminished visual acuity,hyphema, globe rupture, presence of foreign body,or lid lacerations.
Ophthalmology consultation should be obtainedfor suspected globe injuries, corneal foreignbodies or abrasions, orbital fractures, retinaldetachments, hyphema, intraocular foreign bodies,corneal or eyelid burns, lid lacerations,subconjunctival hemorrhage, or head injuries thatinvolve the orbit or may compromise vision
Tympanic membrane rupture is the most commonprimary blast injury, 9－47% of explosion-injuredpatients had tympanic membrane rupture. The most common symptoms of auditory injuryare hearing loss, tinnitus, pain, and dizziness. All explosion victims should be evaluated with anotoscopic examination not as a means ofscreening for other primary blast injuries, butsimply to diagnose tympanic membrane ruptureand ensure proper evaluation and treatment.
Blast lung injury is the most common fatal injuryamong initial survivors of explosions. The incidence of pulmonary blast injury ranging from3% to 14%. This may result in minor or massive parenchymalhemorrhage, pulmonary edema, pneumothorax, or airembolism from alveolovenous fistulas. Symptoms and signs include tachypnea, dyspnea,cyanosis, and hemoptysis. On physical examination, the patient may havediminished breath sounds and crepitance resultingfrom subcutaneous air. Hypoxia (oxygen saturation<90% on room air) is present and reaches its nadirwithin the first 24 hrs.
Clinical diagnosis of blast lung injury is based onthe presence of respiratory distress, hypoxia, and“butterfly” or batwing infiltrates. CXR findings of the batwing (bilateral central) lunginfiltrates were the most common radiographicfinding. The central location of infiltrates may helpdistinguish blast lung injury from blunt etiologies ofpulmonary contusion, which usually causesperipheral lesions. Additionally, radiographs mayreveal pneumothorax or pneumomediastinum
The management of blast lung injury are to avoidpositive pressure ventilation, if possible, minimizepositive end-expiratory pressure ventilation, and usejudicious fluid resuscitation strategies. Pressure-limited, volume-controlled ventilation withpermissive hypercapnia has been advocated inpatients sustaining blast lung to minimize mean airwaypressure and the chance of air embolism as well as toreduce the risk of further pulmonary trauma. When all else fails, the physician may resort tosalvage methods like ECMO.
Primary blast injury to the gastrointestinal tract israre with an incidence of 0.3% to 0.6%. Patients with primary blast injury to abdominalviscera may present with abdominal pain, nausea,vomiting, hematemesis, melena, and peritonealsigns of injury. Hemodynamic instability may also be seen in thecase of mesenteric hemorrhage or solid organinjury.
Radiographic evidence of abdominal blast injury oncomputed tomography includes pneumoperitoneum, freeintraperitoneal fluid not consistent with blood, and a“sentinel clot” seen adjacent to bowel wall or mesentery. Mesenteric or mural hematoma in hemodynamicallystable patients without peritoneal signs may bemanaged with NPO, NG tube decompression, andresuscitation. Massive hemorrhage or obvious hollow viscusperforation should be treated with laparotomy forhemostasis and control of spillage of enteric contents.
Triad of immediate bradycardia, hypotension, andapnea that is a partially vagally mediatedresponse to thoracic blast. The most common blast-induced arrhythmias arebradycardia, premature ventricular contractionsand asystole. Hypotension has been associated with low cardiacindex and stroke volume but normal systemicvascular resistance.
Physician should be aware that hemorrhagingexplosion-injured patients may not have theexpected compensatory tachycardia and maybecome hypotensive without rapid resuscitation. Atropine may be a useful adjunct in patients withblast-induced bradycardia who do not respond aspredicted to resuscitation efforts.
Principles of management of the combat-injuredextremity such as early tourniquet use should beapplied in the care of these patients regardless ofprecise mechanism of injury. Clinicians should have a high clinical suspicion foroccult explosive injuries to the CNS, thorax, andabdomen in these patients and should search forthem in the patient who does not respondappropriately to resuscitation once control ofextremity hemorrhage is achieved.
Kinetic energy of the blast wave transferred to theCNS causes shearing, resulting in diffuse or focalaxonal injury and initiating secondary injurymechanisms that may result in both acute and delayedsymptoms of post-concussion syndrome or PTSD. Symptoms of CNS injury may be psychologic, such asexcitability, irrationality, retrograde amnesia, apathy,lethargy, poor concentration, insomnia, psychomotoragitation, depression, anxiety, or physical such asfatigue, headache, back and diffuse pains, vertigo,transient paralysis, and “heavy” feeling extremities.
Physical examination should include a thoroughneurologic examination to include checking forpositive Romberg’s sign as well as funduscopy tolook for evidence of air emboli. CT scan should be used to search for evidence ofblunt head injury and ICH.
Focused history to risk stratification for primary blast injury1. Explosive device details: type and weight of explosive,improvised vs. commercially available, suicide bomber,time of detonation2. Geography: device location, open vs. closed spacedetonation, surrounding structures (urban vs. rural setting)3. Victim: distance of the victim from the detonation center,specific location of the victim with orientation of body inrelation to explosive and surrounding structures, personalprotective equipment4. Status of other casualties: cause of any on-scene deaths,primary blast injury in other surviving victims
Reference:Crit Care Med 2008; 36:[Suppl.]:S311–S317 Photo:http://www.boston.com/bigpicture/2013/04/terror_at_the_boston_marathon.html
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