Primary blast injury results from the direct interaction of the blast wave (barotrauma) with the body, preferentially damaging air-filled organs: the ear, lungs, and gastrointestinal tract. [1-2] It is distinct from secondary (projectile/fragment), tertiary (displacement/impact), and quaternary (burns/toxins) blast injuries, though these commonly coexist. [3]
The following figure illustrates the classification of blast injury types:
1. History
- Mechanism: Type of explosive (high-order vs. low-order), distance from detonation, open vs. enclosed space (enclosed spaces amplify blast overpressure 2–4×, dramatically increasing PBI incidence) [5-6]
- Timing: Onset of symptoms — immediate vs. delayed (PBI is notorious for delayed presentation, especially pulmonary and GI injuries) [1-2]
- Key symptoms to elicit:
- Hearing loss, tinnitus, ear pain, vertigo (auditory PBI)
- Dyspnea, chest pain, cough, hemoptysis (blast lung) [7]
- Abdominal pain, nausea, vomiting, hematochezia (GI PBI)
- Confusion, vision changes, focal neurologic deficits (air embolism or blast TBI) [2]
- Underwater exposure: Significantly increases GI and pulmonary injury risk [2]
- Body armor use: Protects against fragments but does NOT protect against barotrauma [1]
- Exertion after blast: Strenuous activity post-injury may increase morbidity and mortality [8]
2. Alarm Features
- Dyspnea, hemoptysis, or hypoxia without external chest injury → blast lung until proven otherwise [7]
- Frothing at the mouth with bilateral radiographic "whiteout" → grave prognosis [1]
- Sudden neurologic deterioration (stroke-like symptoms, seizures, loss of consciousness) → suspect arterial air embolism from alveolar-capillary disruption [2][8]
- Tongue blanching, livedo reticularis, air in retinal arteries → subtle signs of systemic air embolism [2]
- Acute abdomen or peritonitis developing hours to days after blast → delayed bowel perforation [2][6]
- Rapidly declining SpO₂ → early blast lung even before symptoms manifest [1]
- Facial nerve dysfunction or vestibular damage → severe otic trauma requiring urgent referral [1]
3. Medications
- High-flow O₂ (100% FiO₂): First-line; promotes absorption of air emboli and treats hypoxia [7][9]
- Analgesics: Adequate pain control to optimize spontaneous ventilation and reduce need for positive-pressure ventilation [2]
- Ototopical antibiotics: For contaminated TM perforations or debris-filled ear canals [1]
- Judicious IV fluids: Avoid crystalloid overload — damaged lung tissue is highly susceptible to pulmonary edema [1-2]
- Permissive hypotension (SBP 80–90 mmHg) may be considered in hemorrhagic shock with concomitant blast lung, but avoid in TBI [2]
- No definitive role established for prophylactic corticosteroids or systemic antibiotics in blast lung [1]
- Avoid: Excessive positive-pressure ventilation (increases risk of air embolism and pneumothorax) [2][8]
4. Diet
- NPO if any suspicion of GI blast injury or pending surgical evaluation
- Delayed bowel perforation may present days later — maintain a low threshold for NPO status in patients with abdominal complaints post-blast [10]
- Once cleared, advance diet as tolerated; no specific long-term dietary modifications for PBI
5. Review of Systems
- ENT: Hearing loss, tinnitus, otalgia, vertigo, ear fullness, otorrhea
- Pulmonary: Dyspnea, cough, hemoptysis, chest tightness, pleuritic pain
- GI: Abdominal pain, nausea, vomiting, bloody stool, tenesmus
- Neurologic: Headache, confusion, vision changes, focal weakness, seizures, amnesia
- Cardiovascular: Chest pain, palpitations, syncope
- Ophthalmologic: Vision loss, floaters, eye pain (globe rupture, hyphema, serous retinitis) [1-2]
- Skin: Burns, lacerations, subcutaneous crepitus (subcutaneous emphysema)
6. Collateral History and Family History
- Collateral: Bystander accounts of blast proximity, enclosed vs. open space, duration of exposure, loss of consciousness, extrication time
- Scene information: Type and size of explosive, number of casualties (helps estimate blast overpressure)
- Family history: Not directly relevant to acute PBI management
- Social context: Military vs. civilian, occupational exposure (industrial explosions), terrorism context (consider CBRNE contamination — quinary blast injury)
7. Risk Factors
- Enclosed-space detonation: Single most important risk factor — blast waves reflect off walls, amplifying overpressure [5-6]
- Underwater explosion: Dramatically increases GI and pulmonary injury [2]
- Proximity to blast center: Overpressure decreases with distance cubed [1]
- High-order explosives (TNT, C-4, dynamite) produce true blast waves; low-order explosives generally do not cause PBI [7]
- Body armor: Paradoxically may increase blast lung injury while protecting against fragments [1][8]
- Pre-existing pulmonary disease: May worsen blast lung outcomes
- Strenuous exertion post-blast: Increases morbidity [8]
8. Differential Diagnosis
- Pneumothorax from other causes (traumatic, tension) — may coexist
- Pulmonary contusion from blunt trauma (secondary/tertiary mechanism)
- Hemorrhagic shock from penetrating fragment injuries (secondary blast)
- Traumatic brain injury (concussive vs. air embolism — must differentiate) [1]
- Myocardial contusion or acute MI from coronary air embolism [2]
- Inhalation injury from smoke/toxic gases (quaternary)
- CBRNE exposure (chemical, biological, radiological — quinary blast)
- Perforated viscus from penetrating abdominal trauma vs. primary blast bowel perforation
9. Past Medical History
- Pre-existing COPD, asthma, or restrictive lung disease — increases vulnerability to blast lung and complicates ventilator management
- Prior ear surgery or TM perforation — alters otologic assessment
- Anticoagulant use — increases hemorrhagic risk from pulmonary and GI blast injury
- Cardiac disease — relevant if air embolism causes coronary occlusion
- Prior abdominal surgery — adhesions may alter GI injury patterns
10. Physical Exam
- Vitals: Tachypnea, hypoxia (SpO₂ trending), tachycardia; transient bradycardia and hypotension may occur from vagal reflex mediated by pulmonary C fibers [2][11]
- Otoscopic exam: TM perforation (most common PBI finding; ruptures at as little as 5 psi above atmospheric pressure). Hemotympanum, canal debris [1]
- Pulmonary: Decreased breath sounds, crackles, wheezing; subcutaneous emphysema (crepitus) over chest/neck
- Abdomen: Tenderness, guarding, rigidity, rebound (may be initially absent with delayed perforation) [2]
- Neurologic: GCS, pupillary response, focal deficits (air embolism vs. TBI)
- Eyes: Visual acuity, pupil exam, slit lamp if available (hyphema, globe rupture) [2]
- Skin: Livedo reticularis, tongue blanching (air embolism signs); burns, blast tattoo [2]
11. Lab Studies
- ABG: PaO₂/FiO₂ ratio is critical for blast lung severity scoring and monitoring; expect hypoxemia, possible respiratory acidosis [2][7]
- CBC: Baseline hemoglobin for hemorrhage monitoring
- BMP/CMP: Electrolytes, renal function (crush injury, rhabdomyolysis if tertiary component)
- Lactate: Marker of tissue hypoperfusion/shock
- Type and screen/crossmatch: Anticipate need for transfusion
- Coagulation studies (PT/INR, fibrinogen): Blast-induced coagulopathy and DIC can occur [12]
- Troponin: If cardiac contusion or coronary air embolism suspected
- CK/myoglobin: If crush injury component present
12. Imaging
- Chest X-ray (CXR): First-line screening — classic finding is bilateral "butterfly" or "bat-wing" perihilar infiltrates. May also show pneumothorax, hemothorax, pneumomediastinum, subcutaneous emphysema [1-2]
- Chest CT: More sensitive than CXR; obtain if symptoms persist with normal CXR or if substantial pulmonary complaints — can detect consolidations missed on plain film [2]
- FAST exam: Rapid bedside assessment for intraperitoneal free fluid; however, a negative FAST does not exclude abdominal PBI [2]
- Abdominal CT: For hemodynamically stable patients with abdominal pain — specific for solid organ injury and perforation but lacks sensitivity for intestinal contusions and mesenteric injury [2]
- Lung ultrasound: Emerging evidence supports handheld ultrasound for early detection of moderate-severe blast lung injury, with effective mortality prediction as early as 0.5 hours post-injury [13]
- When imaging is unnecessary: Asymptomatic patients with intact TMs and normal SpO₂ after adequate observation period [1]
13. Special Tests
- BLI Severity Score: Uses PaO₂/FiO₂ ratio, CXR findings, and presence of bronchopleural fistula to stratify blast lung into mild/moderate/severe and guide ventilator management: [2]
- Otoscopic examination: Essential screening tool — TM rupture is the most sensitive (though imperfect) marker of blast exposure [1][5]
- Serial pulse oximetry: Continuous monitoring; declining SpO₂ may be the earliest sign of blast lung before symptoms develop [1]
- Hyperbaric oxygen therapy (HBOT): Definitive treatment for arterial air embolism — should be initiated as soon as clinically feasible; benefits reported even with delays up to 60 hours [2][14]
- FAST/E-FAST: Point-of-care ultrasound for pneumothorax and free fluid
14. ECG
- Indications: All patients with significant blast exposure, chest pain, hemodynamic instability, or suspected air embolism
- Findings to watch for:
- Bradycardia: Vagal-mediated reflex from thoracic blast overpressure (transient, resolves minutes to hours) [2][11]
- ST changes/ischemia: Coronary air embolism can cause acute MI [2]
- Arrhythmias: Cardiac contusion may produce dysrhythmias [2]
- PEA/asystole: Massive air embolism or tension pneumothorax
- Pearl: New ST elevation or cardiac arrest in a blast victim without obvious chest wall trauma should raise suspicion for coronary air embolism [8]
15. Assessment
Primary blast injury is a barotrauma-mediated condition affecting air-filled organs, with the ear being most commonly injured (lowest threshold at ~5 psi), the lung being the most life-threatening target organ, and the colon/ileocecal region being the most commonly affected abdominal structure. [1-2]
Severity stratification
- Mild: Isolated TM perforation, no pulmonary or abdominal symptoms
- Moderate: Blast lung with localized infiltrates, PaO₂/FiO₂ >200, no bronchopleural fistula
- Severe: Massive bilateral infiltrates, PaO₂/FiO₂ <60, bronchopleural fistula, arterial air embolism, or bowel perforation [2]
Key complications: Arterial air embolism (principal cause of early mortality), ARDS, delayed bowel perforation (days after exposure), tension pneumothorax, DIC [8][10][12]
Atypical presentations: Patients may appear initially well ("walking wounded") and deteriorate hours later — PBI has a notoriously delayed onset [1-2]
16. Treatment Plan
Initial stabilization (ABCDE approach)
- High-flow O₂ (100% FiO₂) via non-rebreather [7]
- Maximize spontaneous ventilation; avoid intubation if possible
- Immediate tube thoracostomy for pneumothorax/hemothorax [2]
Ventilator management (if intubation required)
- Lung-protective ventilation: Low tidal volumes (5–7 mL/kg IBW), pressure-controlled mode, low peak inspiratory pressures, PEEP, permissive hypercapnia [1-2]
- Accept SpO₂ ≥90% [2]
- Avoid high peak pressures → increases risk of air embolism and worsening barotrauma [1]
- Consider prophylactic bilateral chest tubes before positive-pressure ventilation or air transport in severe blast lung [2]
- Refractory cases: High-frequency oscillatory ventilation, ECMO [15]
Fluid management
- Judicious crystalloid — avoid overload (damaged lungs are edema-prone) [1-2]
- Balance with hemorrhagic shock resuscitation needs; consider invasive hemodynamic monitoring [2]
- Permissive hypotension (SBP 80–90) if hemorrhagic shock without TBI [2]
Arterial air embolism
- Position supine (Trendelenburg no longer recommended) [9][16]
- 100% O₂ to promote bubble reabsorption
- Hyperbaric oxygen therapy as soon as feasible — definitive treatment [2][14]
GI blast injury
- Emergent laparotomy for peritonitis or hemodynamic instability from abdominal hemorrhage [2]
- Serial abdominal exams for delayed perforation [10]
Otic injury
- Expectant management for small TM perforations (most heal in weeks) [1]
- Ototopical antibiotics for contaminated canals
- Avoid ear canal irrigation or probing
- ENT referral for large perforations, ossicular disruption, or vestibular/CN VII dysfunction [1]
17. Disposition
- Admit (ICU): Blast lung with hypoxia, hemodynamic instability, arterial air embolism, GI perforation, polytrauma, need for mechanical ventilation [1-2]
- Admit (observation/floor): TM perforation with any pulmonary symptoms, abnormal CXR, declining SpO₂
- Observe minimum 6–8 hours: All patients with TM rupture, pulmonary symptoms, or significant blast exposure — even with initially normal CXR [1-2]
- Discharge criteria: Intact TMs, no respiratory symptoms, normal SpO₂ trending, no abdominal complaints, normal CXR after adequate observation period, reliable follow-up [1]
- Specialist consultation triggers:
- Trauma surgery: All significant blast injuries, abdominal complaints
- Cardiothoracic surgery: Massive hemothorax, bronchopleural fistula
- ENT: Significant TM perforation, vestibular symptoms, CN VII dysfunction
- Ophthalmology: Globe rupture, hyphema, vision changes
- Hyperbaric medicine: Suspected arterial air embolism [2]
- Neurosurgery: Blast TBI with focal deficits or declining GCS
18. Follow Up / Return Precautions
- Follow-up timing:
- ENT within 1–2 weeks for TM perforation reassessment [1]
- Pulmonary follow-up if blast lung — monitor for late ARDS or fibrosis
- Surgical follow-up if abdominal PBI managed non-operatively
- TBI/concussion clinic if blast brain injury suspected [1]
- Return immediately for:
- New or worsening shortness of breath, chest pain, or cough with blood
- Abdominal pain, vomiting, bloody stool (delayed bowel perforation may present days after blast) [10]
- Confusion, vision changes, weakness, seizures
- Fever or signs of infection
- Patient counseling:
- Avoid strenuous exertion after blast exposure [8]
- Keep ears dry; avoid swimming or submerging head if TM perforated [1]
- Do not probe or irrigate ears
- Expect temporary hearing loss/tinnitus — most small TM perforations heal spontaneously
- Psychological screening — high rates of PTSD, anxiety, and depression after blast exposure
References
1. Blast Injuries. — DePalma RG, Burris DG, Champion HR, Hodgson MJ. The New England Journal of Medicine. 2005.
2. Blast Injuries. — Wolf SJ, Bebarta VS, Bonnett CJ, Pons PT, Cantrill SV. Lancet. 2009.
3. High Risk and Low Prevalence Diseases: Blast Injuries. — Bukowski J, Nowadly CD, Schauer SG, Koyfman A, Long B. The American Journal of Emergency Medicine. 2023.
4. Blast Injuries. — Ortega R, Vietor R, Arbelaez C, et al. The New England Journal of Medicine. 2024.
5. Primary Blast Injuries--an Updated Concise Review. — Yeh DD, Schecter WP. World Journal of Surgery. 2012.
6. Primary Blast Injury After a Bomb Explosion in a Civilian Bus. — Katz E, Ofek B, Adler J, Abramowitz HB, Krausz MM. Annals of Surgery. 1989.
7. Blast Lung Injury. — Sasser SM, Sattin RW, Hunt RC, Krohmer J. Prehospital Emergency Care. 2006.
8. Primary Blast Injuries. — Phillips YY. Annals of Emergency Medicine. 1986.
9. Gas Embolism. — Muth CM, Shank ES. The New England Journal of Medicine. 2000.
10. Abdominal Trauma in Primary Blast Injury. — Owers C, Morgan JL, Garner JP. The British Journal of Surgery. 2011.
11. Characterization of the Response to Primary Blast Injury. — Kirkman E, Watts S. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 2011.
12. Crosstalk Between Inflammation and Hemorrhage/Coagulation Disorders in Primary Blast Lung Injury. — Li J, Zhang J, Shi M, et al. Biomolecules. 2023.
13. Evaluating the Effectiveness of Handheld Ultrasound in Primary Blast Lung Injury: A Comprehensive Study. — Shao S, Wu Z, Liu J, et al. Scientific Reports. 2025.
14. Decompression Sickness and Arterial Gas Embolism. — Mitchell SJ, Bennett MH, Moon RE. The New England Journal of Medicine. 2022.
15. Thoracic Injury in Patients Injured by Explosions on the Battlefield and in Terrorist Incidents. — McDonald Johnston A, Alderman JE. Chest. 2020.
16. Part 10: Adult and Pediatric Special Circumstances of Resuscitation: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. — Cao D, Arens AM, Chow SL, et al. Circulation. 2025.