Blast and crush injury

• An explosion does not produce one "blast injury"; it can injure a casualty through the pressure wave, flying fragments, being thrown or crushed, and everything that follows (burns, smoke and toxins, and psychological shock).
• The lung is the organ most at risk from the pressure wave, because gas-filled tissue is torn at air-fluid interfaces; a person who was close to the explosion and is short of breath may have "blast lung" even without obvious wounds.
• Crush syndrome begins when a limb or the torso is compressed for long enough to kill muscle; once the pressure is released, potassium, myoglobin and acid pour into the circulation and can cause sudden cardiac arrest, acute kidney injury and death. ^[6]
• Crush syndrome can be prevented or softened by starting intravenous fluids early, even before the casualty is freed, and by running enough fluid to keep the urine flowing.
• A tourniquet stops life-threatening limb bleeding but is a second injury; record the time it is applied, do not loosen it at intervals, and manage conversion according to the expected time to surgery.
• Care runs from scene safety and haemorrhage control through extrication, fluids, hyperkalaemia treatment, wound care and dialysis; low-resource settings can apply almost all of it with oral instructions, a drip set and a watch.

By the end of this page you should be able to:

1. Define a blast injury and assign a wound to one of the four recognised blast mechanisms, explaining the physics behind each.
2. Explain the pathophysiology of primary blast lung injury and state its presentation, imaging and immediate management.
3. Distinguish a simple crush injury from crush syndrome and describe the events from muscle compression to acute kidney injury.
4. Use the commonly applied creatine kinase threshold for rhabdomyolysis and state what the result does and does not tell you about kidney injury.
5. Diagnose hyperkalaemia in this setting, including the serum potassium levels at which symptoms and ECG changes appear.
6. Apply safe tourniquet practice: indications, placement, timing, conversion and recorded handover.
7. Carry out the field and hospital sequence for a crush casualty, including fluid rates, urine targets, alkalinisation and dialysis indications.
8. List the complications, prognosis and prevention measures described in current major trauma and blast guidance.

Explosions produce several quite different injury mechanisms at once, and the same casualty often has more than one. The four categories below describe what caused the wound, which is what guides management.^[2]

A simple way to remember the order is the medium: pressure first, then flying objects, then the person moving, then everything else.^[2] Real casualties have mixtures: a building collapse can produce a tertiary crush injury with secondary contamination and quaternary smoke inhalation in the same patient.

Explosions harm many people at the same time. Because numerous casualties arrive together, blast injuries test the whole trauma system, from triage through critical care, and survivors often need long stays in intensive care.^[1] In one large paediatric data set of blast injuries, the reported mortality was about 8%, matching the 6 to 9% reported for paediatric trauma deaths from conflict zones.^[2]

Most topics in this site are hospital diseases; this one is managed first at the roadside, often in a mass-casualty scene, and only later in hospital. The guidance base for deployed practice (Joint Trauma System and Tactical Combat Casualty Care) and for civilian major trauma differs, but the underlying physiology is the same.

The explosion releases energy as an expanding gas cloud, producing an initial positive pressure (overpressure) phase followed by a negative pressure (underpressure or suction) phase, with gas flow, debris and heat. The lethality and the pattern of injury reflect how much energy is delivered, how it is focused, and how long it acts.^[1]

Primary blast injury happens because tissues are distorted where they meet gas. The pressure change across the wavefront is hundreds to thousands of times faster than in a normal breath or heartbeat. Low-density and air-containing tissues experience the greatest shear and tearing, which is why the lung, the middle ear and the bowel are the index organs. Spallation (the ejection of fragments of a dense medium into a less dense one), implosion (pressure-driven bubbles in fluid) and inertia (differential acceleration of tissues of different density) are the three physical mechanisms most commonly invoked for lung injury. Hard surfaces reflect the wave and can amplify the effect, so a person in a closed space or against a wall is more likely to have primary injury than one in open air at the same distance.

Blast lung is the pulmonary form of primary blast injury. It is not a contusion in the ordinary sense: the pressure wave tears the alveolar walls and the vessels, producing haemorrhage and oedema, with damage strongest at the air-tissue interfaces. Ventilation, perfusion and compliance all fall; hypoxaemia and shock follow. It can occur with no visible external chest injury, which is why the chest must be assessed in everyone removed from an enclosed or near explosion even when the surface looks intact.

• Breathlessness (sometimes out of proportion to visible injury), cough, chest tightness and haemoptysis.
• Hypoxaemia, tachypnoea, respiratory distress and cyanosis.
• Signs may be delayed; deterioration over hours is common, and bilateral infiltrates can track the shock front across the chest.
• Associated findings from the same wave: tympanic membrane perforation, abdominal pain and occult pneumothorax.

• Chest radiograph and (where available) CT thorax for bilateral infiltrates, haemothorax or pneumothorax. Findings can be patchy and basal, and they may worsen over the first 24 hours.
• Arterial blood gas and pulse oximetry to follow hypoxaemia and the degree of respiratory failure.
• ECG and troponin where there is chest pain or circulatory compromise, to exclude cardiac blast injury.
• Ears and abdomen should be checked even when the chest is the main complaint, because the auditory and hollow organs are air-containing and vulnerable.

• Oxygen early and generously. Many patients need high-flow oxygen; a lower threshold for intubation is appropriate because pulmonary compliance is poor and deterioration is sudden. Protective (low-tidal-volume) ventilation is preferred.
• Treat pneumothorax and haemothorax. A pneumothorax after blast may become rapidly fatal under positive pressure, so intercostal drainage should be placed and a one-way valve or closed water-seal used. Tension should be recognised early and decompressed (needle or finger thoracostomy as locally trained) before positive-pressure ventilation.
• Keep fluids cautious. Over-resuscitation worsens pulmonary oedema; use the minimum compatible with a normal blood pressure, and let haemorrhagic shock from other injuries guide volume rather than the blast lung alone.
• Avoid unnecessary bronchoscopy unless there is a foreign body or heavy haemoptysis that needs control.
• Observe. Patients with an abnormal chest radiograph, hypoxia or haemoptysis need admission and repeated imaging, because infiltrates may worsen over the first 24 hours.

• Secondary wounds are the commonest reason casualties require surgery. Control the haemorrhage and ask about eye pain, because small metal fragments are easily missed in the cornea and sclera.
• Tertiary falls and impacts produce the head, spine and limb fractures that dominate the second and third hours of care; follow usual trauma imaging pathways.
• Quaternary burns and inhalation (including dust, combustion products and toxic industrial chemicals) can produce acute respiratory distress without external burns, and psychological shock (post-traumatic stress) is a common long-term quaternary injury. Early, simple information and support reduce later morbidity.

A crush injury is sometimes hidden: a casualty pinned by rubble may talk and have normal observations for an hour, then deteriorate the moment they are freed. Crush syndrome develops in roughly 30 to 50% of people who have had significant rhabdomyolysis, and it is the second most frequent cause of death in survivors of mass disasters after direct trauma itself.^[7]

• Muscle under sustained pressure becomes ischaemic. The higher the pressure and the longer it is maintained, the more tissue dies: pressures well above capillary and tissue perfusion levels produce hypoxia, necrosis and breakdown of muscle fibre membranes.
• Pressure is not the only cause of damage. When the load is lifted, reperfusion delivers oxygen to damaged cells, generates reactive oxygen species and releases potassium, phosphate, myoglobin, creatine kinase, lactic acid, uric acid and inflammatory mediators.
• The muscle compartment becomes oedematous and interstitial pressure rises in its own non-compliant fascial envelope, so intracompartmental pressure can keep climbing (compartment syndrome).
• Myoglobin precipitates in the renal tubules when urine is concentrated and acidic, producing pigment nephropathy and acute tubular injury. Hypovolaemia from third spacing adds a pre-renal insult.
• Hyperkalaemia (potassium leaking from dead cells, worsened by acidosis) is the most immediately lethal event, because of ventricular arrhythmia.

• Risk of death and of requiring dialysis rises with the duration of crushing.
• Risk is higher in enclosed spaces, in patients with pre-existing kidney disease and in mass-casualty situations, where delays multiply.
• Crush syndrome features described in the disaster literature include tense, oedematous and painful muscles; hypovolaemic shock; acute kidney injury; hyperkalaemia; acidosis; cardiac and respiratory failure; and sepsis.^[7]

Rhabdomyolysis is the dissolution of skeletal muscle, with leakage of muscle cell contents (myoglobin, sarcoplasmic proteins and electrolytes) into the extracellular fluid and circulation. Crush injury is one of the commonest causes; others are extreme exertion, drugs and toxins, infections, electrolyte imbalance and metabolic myopathy.^[4]

• Muscle pain, weakness, tenderness and local swelling; dark reddish "tea-coloured" urine from myoglobin.
• Oedema, fever and nausea are common.
• Complications range from mild (asymptomatic creatine kinase elevation) to life-threatening: compartment syndrome, intravascular fluid depletion, disseminated intravascular coagulation, pigment-induced acute kidney injury and arrhythmias from potassium release.

There is no single diagnostic cut-off for creatine kinase (CK). The commonly used working definition is CK elevated to 3 to 5 times the upper limit of normal (100 to 400 U/L in most laboratories), about 1000 U/L.^[4] CK is the most sensitive marker of muscle injury, but its height does not tell you how much the kidneys have been injured, and it must be read beside renal function, potassium, calcium, phosphate and urinalysis. Myoglobin in the urine is supportive, but it peaks early and can be cleared before the patient arrives.

Other blood results in established rhabdomyolysis include raised urea and creatinine, raised phosphate, low calcium, and metabolic acidosis; the urine may be positive for blood on dipstick with few red cells (myoglobin is mistaken for blood). An ECG should be checked because, in crush, the potassium rather than the CK determines the immediate risk.

• Early volume resuscitation is the treatment. Give generous intravenous crystalloid, avoid potassium-containing solutions, and aim for a target urine output of at least 300 mL per hour in adults, starting the fluid before extrication where the situation allows.^[3][7]
• Severity-guided fluid rate. If no intravenous fluid has been given before rescue, protocols in the disaster literature use 1000 mL per hour of isotonic saline in adults (15 to 20 mL per kg per hour in children) until the first 6 litres have been given, then re-assess urine output and volume status.^[7]
• Alkalinisation. Sodium bicarbonate added to half-isotonic fluid (and given only when systemic acidosis is present) alkalinises the urine (pH above 6.5) and limits myoglobin precipitation in the tubules; the average requirement is 200 to 300 mEq per day.^[7] Modern reviews caution that no randomised trial has shown that bicarbonate or mannitol, added to fluids, improves outcome beyond fluids alone; give them when acidosis or oliguria persists, not by default.^[3]
• Mannitol. Reserve for when urine output remains under target despite adequate fluid (one formula combines 40 mEq sodium bicarbonate and 50 mL of 20% mannitol in 1000 mL of 0.45% sodium chloride with 5% dextrose).^[3] It is not routine first-line treatment.
• Avoid nephrotoxic insults and monitor electrolytes and fluid balance closely. Maintain pressure relief, wound care and sepsis precautions.

Hyperkalaemia means a serum or plasma potassium above the upper limit of normal, typically above 5.0 to 5.5 mEq per L. Clinical manifestations generally appear at above 6.0 mEq per L, and severe hyperkalaemia can precipitate life-threatening arrhythmias, muscle weakness and paralysis.^[5]

In crush and severe rhabdomyolysis, hyperkalaemia is the most immediately dangerous laboratory finding and the main reason patients die.^[7] Potassium arrives with acidosis, in proportion to the amount of necrotic muscle, and worsens when kidney function falls.

Principles (actual drug doses depend on your local guideline and senior clinician):

• A 12-lead ECG is mandatory in anyone with a potassium above 6.0 mEq per L; manage according to ECG appearance and level, not the number alone.
• Stabilise the cardiac membrane first when ECG changes are present.
• Shift potassium into cells (insulin with glucose, inhaled beta-2 agonist) as a temporising measure.
• Remove potassium by renal excretion (fluids, diuretics if renal function allows), by dialysis or (in selected cases) by exchange resin therapy.
• Treat the underlying cause: relieve compression, flush muscles, rehydrate, correct acidosis and drain urine flow.
• Admit to monitored care. Hyponatraemia, hypocalcaemia and acidosis often accompany severe rhabdomyolysis and should be corrected alongside.

Tourniquets save lives in life-threatening limb haemorrhage (battlefield and civilian major trauma), but a tourniquet converts a bleeding problem into an ischaemia problem. The evidence base summarised below comes from a widely cited prehospital review of civilian tourniquet use.^[6]

• Indication: arterial bleeding from a limb that cannot be controlled by direct pressure.
• Position: as distal as possible but at least 5 cm proximal to the wound; avoid placing directly across a joint; apply onto exposed skin where possible so it does not slip. Record the time. ^[6]
• Tighten until bleeding stops and re-assess distal pulses and bleeding. A loose tourniquet is worse than none because it venously obstructs without stopping arterial flow.

• Continuous application beyond 2 hours risks permanent nerve, muscle (contracture, rhabdomyolysis, compartment syndrome), vascular and skin damage. ^[6]
• Muscle damage is nearly complete by 6 hours, with likely need for amputation. ^[6]
• If the expected transport time to theatre is under 1 hour, leave the tourniquet in place until direct surgical control can be achieved. ^[6]
• If expected transport is longer than 1 hour and the casualty is otherwise stable with an isolated injury (or other life-threatening injuries have been managed), a trial of tourniquet conversion (release with wound packing or direct pressure and close monitoring) may be attempted. ^[6]
• Never loosen a tourniquet at intervals to "let the blood through": this practice is commonly fatal because of incremental exsanguination. If conversion fails, reapply and leave it in place.
• In the review, 5.5% of 110 pre-hospital tourniquet applications caused neurological complications, with ischaemic times between 109 and 187 minutes; none lost the limb. The mean ischaemic time without complications was 78 minutes. These figures are small, single-centre data and should be read as a warning rather than as rules. ^[6]

Record the time of application and the limb, and hand it over verbally and in writing to receiving emergency department staff. Time pressure matters: once the casualty arrives, the clock that started at the roadside decides how much muscle can still be saved.

Wounding in these events is multi-factorial: crush plus burns plus smoke plus psychological shock. The following sequence adapts the Joint Trauma System field and prolonged field care approach to a single casualty; in a mass-casualty event triage, safety and the number of casualties modify every step.^[8]

• Primary survey. ABCDE with spine protection; reassess after imaging, because blast and crush injuries evolve. Tetanus and antimicrobial prophylaxis as indicated by the Joint Trauma System infection prevention guidance, with wound debridement and irrigation.

• Laboratory and monitoring panel. Full blood count, urea and electrolytes, creatinine, arterial blood gas, calcium, phosphate, creatine kinase, glucose, coagulation, troponin, ECG and urinalysis. A dipstick positive for blood with few red cells supports myoglobinuria. Consider compartment pressure monitoring when pain or swelling is out of proportion; a delta pressure of 30 mm Hg or below suggests compartment syndrome.^[9]

• Fluids and urine output. Admit to a monitored bed and continue aggressive but not blind fluid therapy. Target at least 300 mL of urine per hour in adults for the first 24 hours, adjusting for children and for cardiac or renal limits.^[3][7]

• Alkalinisation and mannitol as above, with the caveat that the evidence is not decisive; add bicarbonate when acidosis or oliguria persists and monitor serum calcium.

• Dialysis. Indications are the standard ones (oliguria or anuria, life-threatening hyperkalaemia, severe acidosis, fluid overload or uraemic complications) and, in this cohort, prophylactic renal replacement therapy for casualties judged at high risk of dangerous hyperkalaemia even before it develops. In the Marmara earthquake, 477 casualties needed renal replacement therapy from a crush cohort.^[7]

• Acute kidney injury from myoglobin pigment nephropathy, hypovolaemia and acidosis.
• Life-threatening hyperkalaemia and cardiac arrhythmia; this is the most common immediate cause of death.
• Acute compartment syndrome, requiring fasciotomy when the pressure remains elevated.
• Hypovolaemic and haemorrhagic shock from crush and associated injuries.
• Sepsis from contaminated wounds, and late multi-organ dysfunction.
• Disseminated intravascular coagulation and rhabdomyolysis-related hyperphosphataemia and hypocalcaemia.
• Amputation when muscle is irreversibly damaged after prolonged ischaemia.
• Long-term: post-traumatic stress, chronic pain and disability from limb loss or nerve injury; children have additional growth and longer-term rehabilitation needs.

If identified early, acute kidney injury from rhabdomyolysis has a relatively benign prognosis.^[4] Once established, the need for dialysis, the number of trapped hours and the development of refractory hyperkalaemia or sepsis drive mortality. The crush syndrome itself accounts for a large share of delayed deaths in survivors of mass disasters.

Blast and crush injury is an event, not a disease, so prevention is engineering and behaviour change rather than screening.

• Engineering: blast-mitigating architecture and vehicles, safe storage of explosives and combustible gases, controlled demolition practices, seismic-resistant building codes and clearance of mines and unexploded ordnance.
• Training: scene safety, tourniquet use, recognition of crush syndrome and early fluid therapy for rescuers and pre-hospital clinicians.
• Mass-casualty planning: drills that include triage, tourniquet stations, fluid resuscitation circuits, dialysis surge planning and recorded tourniquet times reduce deaths when an event occurs.
• Psychological follow-up: early debriefing and referral pathways for post-traumatic stress in casualties and responders.

• Children. Crush and blast injuries differ in children (smaller circulating volume, higher relative surface area, different injury heights and airway anatomy). Paediatric blast mortality and injury patterns are summarised in the narrative review cited above, and one large data set quotes an overall mortality near 8%.^[2]
• Pregnancy. Maternal shock threatens fetal perfusion immediately; a trapped pregnant person should be extricated with simultaneous maternal fluid resuscitation, left uterine displacement where possible, and urgent obstetric and trauma discussion.
• Older adults and those with kidney disease. Pre-existing renal impairment or cardiovascular disease lowers the safety margin for both fluids and hyperkalaemia; use measured, often reduced, fluid volumes and early senior or renal advice.
• Long compressed time. As the period of crushing extends, the chance of limb survival falls and mortality rises; the six-hour mark (muscle damage near complete) should be treated as a hard physiological limit rather than a guideline.

Most of the above is transferable:

• Use, where available: a wide-bore cannula, isotonic saline, a urinary catheter or measured urine pot, a wristwatch, and oral instruction cards for fluid rates.
• If pumps are unavailable, count drops using standard giving sets and record cumulative volume on a chart; drop rates vary by set and must be calculated from the giving-set specification.
• Use potassium-containing fluids only if they are all that is available, and otherwise avoid them.
• Alkalinisation can be started with intravenous sodium bicarbonate if available, but do not delay transfer to obtain it.
• Decisions about amputation, compartment syndrome and dialysis should be made with the nearest surgical and renal team, with the receiving hospital notified early.

• Blast injury is classified by four mechanisms (primary, secondary, tertiary, quaternary), and the same casualty often has several.^[2]
• Primary blast injury damages gas-containing organs and can present with few external wounds.^[2]
• Blast lung is a pulmonary primary blast injury: alveolar tearing, haemorrhage and hypoxaemia, worsened by positive pressure ventilation and fluid overload.^[1]
• Crush injury and crush syndrome are separated by reperfusion: the danger begins when the weight is lifted.
• Crush syndrome develops in roughly 30 to 50% of rhabdomyolysis cases and is a leading cause of delayed death in mass disasters.^[7]
• Early fluids, started before extrication where feasible, with a urine-output target, are the mainstay of prevention.
• Creatine kinase around 1000 U per L (3 to 5 times the upper limit of normal) is commonly used to define rhabdomyolysis, but its height does not predict renal injury.^[4]
• Hyperkalaemia is the most immediately lethal finding; symptoms appear above about 6.0 mEq per L, with the condition defined as above 5.0 to 5.5 mEq per L.^[5]
• Tourniquets save lives but place a limb at risk: do not release them at intervals, record the time, and manage conversion by expected transport time.
• Dialysis is needed by a substantial minority of mass-disaster crush cohorts (477 casualties in Marmara).
• Most of this management (fluids, urine target, tourniquet discipline) works in low-resource settings.

Acute kidney injury; hyperkalaemia; hypomagnesaemia and calcium disorders; traumatic brain injury; shock and sepsis; burns; thoracic trauma; abdominal and pelvic trauma; vascular trauma; trauma resuscitation and massive transfusion; acute extremity compartment syndrome; acute limb ischaemia.