01Approach to the Critical Patient/attcp62

Immediate priorities

›Airway and breathing threats

›Blast lung (primary blast lung injury) until proven otherwise

›Dyspnea, hemoptysis, or hypoxia without external chest injury

›Bilateral perihilar infiltrates on CXR (butterfly pattern)

›Rapidly declining SpO2 before symptoms manifest

›Oxygenation failure

›SpO2 <90% or PaO2/FiO2 <300 mmHg

›Initiate 100% FiO2 via non-rebreather mask immediately

›Arterial air embolism — life-threatening early mortality cause

›Sudden neurologic deterioration, stroke-like symptoms, seizures

›Tongue blanching, livedo reticularis, air in retinal arteries

›Supine positioning; avoid Trendelenburg

›Hyperbaric oxygen therapy as soon as feasible

›Circulation threats

›Hemorrhagic shock from concomitant secondary/tertiary injuries

›SBP <90 mmHg or MAP <65 mmHg

›Permissive hypotension SBP 80–90 mmHg if no TBI component

›Vagal-mediated bradycardia and hypotension

›Transient reflex from thoracic blast overpressure

›Resolves minutes to hours; monitor and treat if persistent

›Immediate interventions

›High-flow O2 100% FiO2 via non-rebreather first-line

›Promotes air embolism reabsorption

›Treats blast-induced hypoxemia

›Tube thoracostomy for pneumothorax or hemothorax

›Consider prophylactic bilateral chest tubes before positive-pressure ventilation in severe blast lung

›Before air transport in patients with known blast lung

02History/hx52

Blast exposure details

›Mechanism of exposure

›Type of explosive — high-order vs. low-order

›High-order (TNT, C-4, dynamite) produce true blast wave causing PBI

›Low-order explosives generally do not cause primary blast injury

›Distance from detonation

›Blast overpressure decreases with distance cubed

›Proximity is the key risk determinant

›Enclosed vs. open space

›Enclosed spaces amplify blast overpressure 2–4x

›Dramatically increases PBI incidence

›Underwater exposure

›Significantly increases GI and pulmonary injury risk

›Water transmits pressure waves more efficiently than air

Symptom onset and character

›Pulmonary symptoms

›Dyspnea — onset timing relative to blast

›May be delayed hours after initially appearing well

›"Walking wounded" phenomenon — deceptively well appearance

›Hemoptysis

›Alveolar-capillary disruption marker

›Frothing at mouth with bilateral whiteout — grave prognosis

›Chest pain, cough, chest tightness

›Otologic symptoms

›Hearing loss, tinnitus, otalgia, ear fullness

›TM rupture at as little as 5 psi above atmospheric pressure

›Most common PBI finding

›Vertigo, otorrhea

03Physical Exam/exam49

Vital signs

›Hemodynamic assessment

›Tachypnea — early sensitive marker of blast lung

›Respiratory rate trend more important than single value

›Oxygen saturation — trending SpO2 critical

›Declining SpO2 may precede symptoms

›Tachycardia — hemorrhage, pain, anxiety

›Transient bradycardia — vagal reflex from thoracic overpressure

Otoscopic examination

›Tympanic membrane assessment

›TM perforation — most sensitive (though imperfect) marker of blast exposure

›Ruptures at as little as 5 psi overpressure

›Intact TMs do not exclude significant pulmonary or GI blast injury

›Hemotympanum, canal debris

›Do not probe or irrigate ear canal

›Facial nerve function — CN VII

›Vestibular assessment — nystagmus, Romberg

Pulmonary examination

›Chest auscultation and inspection

›Decreased breath sounds — pneumothorax, hemothorax

›Tension pneumothorax signs — tracheal deviation, absent unilateral breath sounds

›Tube thoracostomy immediately without imaging if unstable

›Crackles, wheezing — blast lung

›Subcutaneous emphysema — crepitus over chest and neck

›Air leak from alveolar-bronchial disruption

›Pneumomediastinum associated finding

Abdominal examination

›Peritoneal assessment

04Differential Diagnosis/ddx35

Life-threatening mimics

›Tension pneumothorax

›ICD-10: J93.0

›May coexist with blast lung — treat immediately if suspected

›Tracheal deviation, hypotension, absent breath sounds

›Arterial gas embolism

›ICD-10: T79.0XXA

›Stroke-like presentation from coronary or cerebral air emboli

›Differentiate from blast TBI — HBOT is definitive for embolism

›Hemorrhagic shock from secondary blast injury

›ICD-10: T14.91XA

›Penetrating fragment injuries — most common cause of blast mortality

›FAST exam and surgical consultation

Pulmonary differentials

›Pulmonary contusion from blunt trauma (tertiary blast)

›ICD-10: S27.329A

›Tertiary mechanism — displacement and impact against surfaces

›Similar CXR findings but different pathophysiology

›ARDS from other etiology

›PaO2/FiO2 <300 mmHg criteria may overlap with severe blast lung

›Management similar; blast lung may progress to ARDS

›Inhalation injury from smoke or toxic gases

›Quaternary blast component — burns and chemical exposure

›CBRNE exposure — chemical, biological, radiological (quinary blast)

Neurologic differentials

›Traumatic brain injury — concussive blast TBI

›ICD-10: S09.90XA

›Blast TBI from direct pressure wave transmission to CNS

05Laboratory Tests/lt35

Arterial blood gas

›ABG — first priority in any respiratory complaint

›PaO2/FiO2 ratio — blast lung severity staging

›Mild: PaO2/FiO2 200–300 mmHg

›Moderate: PaO2/FiO2 60–200 mmHg

›Severe: PaO2/FiO2 <60 mmHg

›Respiratory acidosis — rising PaCO2 indicates ventilatory failure

›Permissive hypercapnia acceptable on lung-protective ventilation

›Metabolic acidosis — base deficit and lactate as shock markers

Hematologic and coagulation studies

›Complete blood count

›Hemoglobin baseline for hemorrhage monitoring

›Serial CBCs in hemorrhagic shock

›Leukocytosis — evolving infection or systemic inflammatory response

›Coagulation panel

›PT/INR, fibrinogen — blast-induced coagulopathy and DIC

›Hyperinflammation from blast injury activates coagulation cascade

›DIC reported in severe blast injury cases

›Fibrinogen <1.5 g/L — cryoprecipitate administration threshold

›Type and screen/crossmatch

›Anticipate transfusion in polytrauma setting

›Massive transfusion protocol activation if indicated

Metabolic and organ injury markers

›Basic metabolic panel

›Electrolytes, renal function

›Rhabdomyolysis component if crush injury (tertiary blast)

›Acute kidney injury from shock or rhabdomyolysis

›Lactate

06Diagnostic Tests/dt59

Scoring Systems

›Blast Lung Injury (BLI) Severity Score

›Uses PaO2/FiO2 ratio, CXR findings, and bronchopleural fistula presence

›Mild: PaO2/FiO2 200–300 mmHg, unilateral infiltrates, no fistula

›Moderate: PaO2/FiO2 60–200 mmHg, bilateral infiltrates, no fistula

›Severe: PaO2/FiO2 <60 mmHg, massive bilateral infiltrates, or bronchopleural fistula

›Guides ventilator management strategy selection

›Severe score — consider prophylactic bilateral chest tubes before PPV

›Severe score — ECMO or high-frequency ventilation consideration

›Blast injury classification — 4 mechanisms

›Primary — direct barotrauma from blast wave (air-filled organs)

›Lungs, ears, GI tract preferentially affected

›Secondary — fragment/projectile injuries

›Tertiary — displacement/impact injuries

›Quaternary — burns, toxins, crush

MRI

›MRI indications in blast injury

›Brain MRI for blast TBI evaluation

›Superior to CT for diffuse axonal injury and subtle parenchymal changes

›MRI after initial CT in neurologically deteriorating patients

›Diffusion-weighted imaging for early ischemia from air embolism

›Spinal MRI for suspected cord injury (tertiary blast mechanism)

›Not first-line in acute resuscitation phase

›Delayed imaging when patient stabilized

›Limitations in acute blast setting

›Time-consuming — not appropriate in unstable patients

›CT remains first-line for acute phase

07Disposition/dispo38

ICU admission indications

›ICU-level care criteria

›Blast lung with persistent hypoxia

›SpO2 <92% despite supplemental oxygen

›PaO2/FiO2 <200 mmHg (moderate-severe BLI score)

›Mechanical ventilation requirement

›All intubated blast lung patients

›Arterial air embolism confirmed or suspected

›Continuous monitoring pending hyperbaric transfer

›GI perforation requiring operative management

›Hemodynamic instability from any blast mechanism

›Polytrauma with multiple blast injury types

Ward admission and observation

›Observation admission indications

›TM perforation with any pulmonary symptoms

›Even mild dyspnea or cough warrants admission

›Abnormal CXR without hypoxia

›Declining SpO2 trend even within normal range

›All patients with known TM rupture

›Minimum 6–8 hours observation before any discharge decision

›Minimum observation period

›All patients with TM rupture, pulmonary symptoms, or significant blast exposure

›6–8 hours minimum even with initially normal CXR

›Delayed blast lung presentation is well-documented

Discharge criteria

›Safe discharge requirements

›Intact tympanic membranes bilaterally

›Intact TMs make significant pulmonary PBI unlikely

08Treatment/t81

Oxygen therapy and airway management

›High-flow oxygen — first-line intervention

›100% FiO2 via non-rebreather mask

›Promotes nitrogen washout and air embolism bubble reabsorption

›Treats blast-induced hypoxemia

›Maximize spontaneous ventilation

›Positive-pressure ventilation increases air embolism and barotrauma risk

›Avoid intubation if at all possible in blast lung

Mechanical ventilation strategy

›Lung-protective ventilation protocol — if intubation unavoidable

›Tidal volume 5–7 mL/kg ideal body weight

›Pressure-controlled mode preferred to limit peak pressures

›Low peak inspiratory pressure to minimize barotrauma

›PEEP — individualized based on oxygenation and compliance

›Avoid excessive PEEP — increases air embolism risk

›Target: minimum effective PEEP to maintain SpO2 ≥90%

›Permissive hypercapnia — accept rising PaCO2 to limit pressures

›Target SpO2 ≥90% as minimum acceptable

›Prophylactic bilateral chest tubes before PPV in severe BLI

›Before air transport in severe blast lung

›Refractory hypoxemia

›High-frequency oscillatory ventilation consideration

›Avoids large tidal pressure swings

›ECMO — salvage therapy for refractory blast lung

›Specialist center referral required

›Bridge to recovery or transplant evaluation

Arterial air embolism treatment

›Positioning and immediate management

›Supine positioning — Trendelenburg no longer recommended

›May worsen cerebral edema without proven embolism benefit

›100% O2 to maximize bubble reabsorption

›Accelerates bubble resolution via nitrogen washout

›Hyperbaric oxygen therapy — definitive treatment

›Initiate as soon as clinically feasible

›Benefits reported even with delays up to 60 hours post-injury

›Do not delay HBOT for diagnostic workup if clinical diagnosis clear

›Monoplace or multiplace chamber — 2.8 ATA standard protocol

›Coordinate transfer early — HBOT availability may require transport

›Compression accelerates bubble reabsorption and reverses ischemia

›Class I recommendation for arterial gas embolism

Fluid management

›Judicious crystalloid resuscitation

›Avoid crystalloid overload — damaged blast lung is highly edema-prone

›Preferential crystalloid accumulation in disrupted alveoli

›Target euvolemia, not aggressive volume expansion

›Balance against hemorrhagic shock resuscitation needs

›Invasive hemodynamic monitoring in complex cases

›Permissive hypotension SBP 80–90 mmHg if hemorrhagic shock without TBI

›Do not apply permissive hypotension if TBI suspected

GI blast injury treatment

›NPO for all suspected GI blast injury

›Maintain NPO if any abdominal complaints post-blast

›Delayed bowel perforation may present days after blast

›Low threshold for NPO status in mechanism-positive patients

›Serial abdominal examinations every 2–4 hours

›Peritonitis development — emergent surgical indication

›Operative management

›Emergent laparotomy for peritonitis or hemodynamic instability from abdominal hemorrhage

›Trauma surgery consultation for all significant blast injuries

›Damage control surgery principles in polytrauma

›Staged approach — abbreviated laparotomy, temporary closure

Otic blast injury treatment

›Tympanic membrane perforation management

›Expectant management for small TM perforations

›Most heal spontaneously within weeks

›No surgical intervention for small uncomplicated perforations

›Avoid ear canal irrigation or probing

›Risk of introducing infection and worsening injury

›Keep ears dry — no swimming or submerging head

›Ototopical antibiotics

›Ofloxacin otic 0.3% solution — 10 drops twice daily for 7 days

›For contaminated TM perforations or debris-filled canals

›Not for all TM perforations — only contaminated cases

›ENT referral indications

›Large perforations, ossicular disruption

›Urgent referral within 1–2 weeks

›CN VII dysfunction, vestibular symptoms

›May require surgical exploration

Analgesia

›Pain management — optimize spontaneous ventilation

›Adequate analgesia reduces splinting and improves respiratory mechanics

›Reduces need for positive-pressure ventilation

›IV opioids — titrated to effect

›Morphine 0.05–0.1 mg/kg IV every 4 hours as needed

›Avoid respiratory depression — monitor closely in blast lung

›Regional anesthesia consideration for thoracic pain

›Intercostal nerve blocks or thoracic epidural

›Avoids systemic opioid effects

09Special Populations/sp59

Pregnancy

›Maternal blast injury considerations

›Uterus and amniotic fluid transmit blast pressure to fetus

›Placental abruption — most common fetal injury from blast

›Occurs at lower maternal injury severity than expected

›Fetal monitoring mandatory for all pregnant blast injury patients

›Continuous electronic fetal monitoring minimum 4–6 hours

›Kleihauer-Betke test for fetomaternal hemorrhage

›Rh immunoglobulin — Rh-negative mothers within 72 hours

›Treatment modifications in pregnancy

›100% O2 therapy — safe and indicated

›Promotes fetal oxygen delivery

›Permissive hypotension — avoid in pregnancy

›Uteroplacental perfusion requires adequate maternal BP

›Target MAP ≥65 mmHg to maintain placental perfusion

›Positioning — left lateral decubitus for >20 weeks gestation

›Relieves aortocaval compression

›Obstetric consultation mandatory for any pregnant blast casualty

›Emergency cesarean section if fetal distress unresponsive to maternal resuscitation

›Radiation exposure — CT justified if life-threatening injury suspected

›Benefits of diagnosis outweigh fetal radiation risk in major trauma

Geriatric

›Age-related vulnerability

›Reduced physiologic reserve — less tolerance of hypoxia and hemorrhage

›Earlier deterioration at lower injury severity

›Baseline SpO2 may already be <95% in comorbid patients

›Pre-existing COPD, CAD, cardiac disease increase vulnerability

›Blast lung on background COPD — dramatically worse prognosis

10Background/b58

Epidemiology

›Incidence and setting

›Primary blast injury predominantly military and terrorism settings

›Increasing civilian incidence — industrial explosions, terrorism

›Oklahoma City bombing (1995) and London 7/7 bombings established civilian PBI epidemiology

›Enclosed-space blasts — dramatically higher PBI incidence

›Bus bombings — GI and pulmonary PBI rates markedly elevated vs. open-air

›Katz et al. 1989 — civilian bus bombing described high rates of GI PBI

›TM rupture most common PBI finding — incidence in blast-exposed survivors

›Up to 60% of blast-exposed casualties have TM rupture

›Blast lung incidence in survivors — 0.6–8% overall; up to 37% in enclosed space

›Mortality and morbidity

›Arterial air embolism — principal cause of early blast-related mortality

›Rapid death from coronary or cerebral air embolism

›Delayed bowel perforation — significant cause of preventable mortality if missed

›Reported days after blast exposure

›DIC — reported complication of severe blast injury

Pathophysiology

›Blast wave physics

›High-order explosives generate Friedlander wave — rapid overpressure then underpressure

›Peak overpressure determines injury severity

›Overpressure decreases proportionally with distance cubed

›Enclosed spaces cause wave reflection and summation

›Amplifies peak overpressure 2–4x compared to open air

›Underwater propagation — water transmits pressure with minimal decay

›Dramatically greater GI and pulmonary injury potential

›Organ-specific mechanisms

›Lungs — air-tissue interface disruption

11Patient Discharge Instructions/pdi23

copy discharge instructions

›Discharge instructions for blast injury

›Your injury was caused by a pressure wave from an explosion (primary blast injury)

›This type of injury can affect your ears, lungs, and intestines

›Some symptoms may not appear until hours or even days after exposure

›Ear care instructions

›Keep your ears completely dry — no swimming, submerging head, or water in ears

›Do not probe, clean, or irrigate inside your ear canal

›Expect some temporary hearing loss and ringing — most small eardrum tears heal on their own

›ENT follow-up appointment within 1–2 weeks is mandatory

›Activity restrictions

›No strenuous physical exertion until cleared by your doctor

›Avoid heavy lifting, running, or vigorous exercise

›Strenuous activity after blast injury can worsen your condition

›Return to emergency department immediately for

›New or worsening shortness of breath, chest pain, or coughing up blood

›Abdominal pain, vomiting, or blood in your stool (can appear days after blast)

›Confusion, vision changes, weakness, or seizures

›Fever or signs of infection — redness, swelling, discharge from ears

›Any sudden worsening of symptoms

›Mental health

›Exposure to explosions carries high risk of PTSD, anxiety, and depression

›Seek mental health support — counseling is a normal and important part of recovery

›Contact your doctor if you experience nightmares, flashbacks, or severe anxiety

12References/r28

Guidelines and key sources

›Primary references

›DePalma RG, Burris DG, Champion HR, Hodgson MJ. Blast Injuries. N Engl J Med. 2005;352:1335-1342

›Foundational review of blast injury classification and management

›Principal source for clinical epidemiology and treatment evidence

›Wolf SJ, Bebarta VS, Bonnett CJ, Pons PT, Cantrill SV. Blast Injuries. Lancet. 2009;374:405-415

›Comprehensive civilian and military blast injury review

›Enclosed space amplification and risk factor evidence

›Bukowski J, Nowadly CD, Schauer SG, Koyfman A, Long B. High Risk and Low Prevalence Diseases: Blast Injuries. Am J Emerg Med. 2023

›Emergency medicine-focused blast injury management

›Ortega R, Vietor R, Arbelaez C, et al. Blast Injuries. N Engl J Med. 2024

›Updated NEJM review including post-exposure exertion and HBOT

›Additional key references

›Yeh DD, Schecter WP. Primary Blast Injuries — an Updated Concise Review. World J Surg. 2012;36:966-972

›Delayed GI perforation and NPO management evidence

›Sasser SM, Sattin RW, Hunt RC, Krohmer J. Blast Lung Injury. Prehosp Emerg Care. 2006;10:165-172

›BLI severity scoring system description and ventilator guidance

›Muth CM, Shank ES. Gas Embolism. N Engl J Med. 2000;342:476-482

›HBOT positioning and treatment protocol for arterial gas embolism

›Mitchell SJ, Bennett MH, Moon RE. Decompression Sickness and Arterial Gas Embolism. N Engl J Med. 2022;386:1254-1264

›HBOT evidence including delayed treatment efficacy up to 60 hours

›Shao S, Wu Z, Liu J, et al. Evaluating the Effectiveness of Handheld Ultrasound in Primary Blast Lung Injury. Sci Rep. 2025

›Handheld ultrasound mortality prediction at 0.5 hours post-blast

›Cao D, et al. 2025 AHA Guidelines for CPR and Emergency Cardiovascular Care, Part 10: Special Circumstances

›Blast injury resuscitation guidelines including HBOT recommendations

›Kirkman E, Watts S. Characterization of the Response to Primary Blast Injury. Philos Trans R Soc Lond B Biol Sci. 2011

›Vagal reflex mechanism and cardiovascular response pathophysiology

›Owers C, Morgan JL, Garner JP. Abdominal Trauma in Primary Blast Injury. Br J Surg. 2011;98:168-179

Evidence & Review

Evidence & Review