Trauma bay simulator — Airway, Breathing, Circulation, Disability, Exposure per ATLS 10th edition. Toggle life-threats and apply interventions to watch vitals respond.
Airway assessment is the first and fastest action in the primary survey — it takes only a few seconds. A trauma patient who can speak clearly in a normal voice demonstrates, at that instant, a patent airway, intact ventilation, and adequate brain perfusion. Every airway maneuver in a trauma patient is performed simultaneously with manual in-line cervical spine stabilization until the c-spine is definitively cleared.
The airway is assessed before anything else because hypoxia kills faster than any other treatable process in trauma. Causes of airway compromise include:
• Direct obstruction: blood, teeth, vomitus, dentures, or foreign material in the oropharynx • Soft-tissue obstruction: the tongue falling posteriorly against the pharyngeal wall in an obtunded patient (the single most common cause of airway obstruction in an unconscious trauma patient) • Laryngeal or tracheal injury: blunt or penetrating neck trauma disrupting the airway architecture directly, often with subcutaneous emphysema or a changing voice • Expanding neck hematoma: penetrating neck injury with an enlarging hematoma that progressively compresses the airway • Maxillofacial trauma: severe midface or mandibular fractures that destabilize the airway structurally
Warning signs on exam include stridor (partial upper airway obstruction), gurgling (fluid in the airway), hoarseness (laryngeal injury), see-saw/paradoxical chest-abdominal movement, and use of accessory muscles. Agitation should be assumed to be hypoxia until proven otherwise; obtundation should be assumed to be hypercarbia until proven otherwise.
The rapid airway exam follows a look-listen-feel sequence: look for chest and abdominal movement and signs of obstruction or cyanosis, listen for air movement at the nose/mouth and abnormal breath sounds, feel for air flow against your cheek.
Basic maneuvers: • Chin lift: two fingers lift the mandible anteriorly; used when c-spine injury is not a concern • Jaw thrust: the mandible is displaced forward without extending the neck; the preferred first maneuver in trauma because it does not require neck manipulation • Suctioning clears blood/secretions; foreign bodies are manually removed • Oropharyngeal airway (OPA) in the unconscious patient without a gag reflex; nasopharyngeal airway (NPA) in the patient who still has a gag reflex — avoided with suspected basilar skull or midface fracture
Indications for a definitive (cuffed, secured, tracheal) airway: • GCS ≤ 8 ("cannot protect the airway") • Apnea or impending respiratory failure • Severe maxillofacial trauma threatening airway patency • Risk of aspiration from ongoing bleeding or vomiting • Risk of obstruction from neck hematoma, laryngeal or tracheal injury, or stridor • Inability to maintain oxygenation by other means
Rapid sequence intubation (RSI) with continued manual in-line stabilization is the standard approach for the trauma patient requiring a definitive airway.
Roughly 2–3% of blunt trauma patients have a clinically significant cervical spine injury, and this risk rises substantially with head injury, high-energy mechanism, or a distracting injury. Until imaging or clinical decision rules (NEXUS criteria or the Canadian C-Spine Rule) clear the spine, the neck is treated as unstable:
• Manual in-line stabilization is applied by a dedicated team member the instant the patient is approached — this takes priority over, and is maintained during, every airway maneuver • A properly sized rigid cervical collar is applied once manual stabilization is established • Log-roll technique (minimum three providers, one dedicated solely to the head/neck) is used for any repositioning, back inspection, or transfer • The collar and manual stabilization are not equivalent alone — a collar limits gross motion but a jaw thrust or intubation attempt can still translate significant force to an unstable segment without a hands-on second provider
The NEXUS low-risk criteria (no posterior midline tenderness, no focal neurologic deficit, normal alertness, no intoxication, no painful distracting injury) allow clinical clearance without imaging when all five are met.
Every chest is exposed and examined systematically — inspection, palpation, percussion, and auscultation — to identify the injuries that kill within minutes if missed: tension pneumothorax, open pneumothorax, massive hemothorax, and flail chest with pulmonary contusion. ATLS 10th edition revised the anatomic landmark for emergency needle decompression after data showed a high failure rate at the classic site.
Tension pneumothorax is a clinical diagnosis made at the bedside, never delayed for a chest radiograph. Air enters the pleural space through a one-way valve mechanism (lung or chest wall injury) with each breath and cannot escape, progressively raising intrapleural pressure. This compresses the ipsilateral lung, then shifts the mediastinum toward the contralateral side, kinking the vena cavae and dropping venous return to the heart.
Classic findings: absent or markedly diminished breath sounds on the affected side, hyper-resonance to percussion, tracheal deviation away from the affected side (a late and inconsistent sign), distended neck veins, and progressive hypotension with tachycardia. Untreated, it progresses to obstructive shock and cardiac arrest via pulseless electrical activity.
Immediate management is needle decompression, a temporizing measure, not definitive treatment:
• Historic landmark: 2nd intercostal space, midclavicular line, over the superior border of the 3rd rib (to avoid the neurovascular bundle running along the inferior rib border) • ATLS 10th-edition preferred site: 5th intercostal space, anterior axillary line (roughly the nipple line in males) — imaging studies demonstrated chest wall thickness at the 2nd ICS/MCL frequently exceeds standard needle-catheter length (~5 cm), causing a high failure rate; the lateral chest wall is thinner at this second site • A large-bore (10–14 gauge), long (≥8 cm) angiocatheter is used; a rush of air confirms correct placement and immediate decompression • Needle decompression is always followed by definitive management: tube thoracostomy (chest tube), typically placed at the 5th intercostal space, anterior to the mid-axillary line
Failure to convert to a chest tube risks re-accumulation and recurrent tension physiology.
Open pneumothorax ("sucking chest wound") occurs when a chest wall defect larger than roughly two-thirds the diameter of the trachea allows air to preferentially enter the pleural space through the wound rather than through the airway. Management is a sterile occlusive dressing taped on three sides, creating a flutter-valve effect that allows air to escape but not enter — taping all four sides risks converting it into a tension pneumothorax. A chest tube is placed remote from the wound, and the wound is often closed formally in the operating room.
Massive hemothorax is defined as ≥1500 mL of blood in the pleural space on initial chest tube output, or ongoing output >200 mL/hr for 2–4 consecutive hours — either threshold prompts urgent thoracotomy. It presents with the combination of shock plus absent breath sounds and dullness to percussion on the affected side (the opposite exam finding pattern from tension pneumothorax, which is hyper-resonant). Simultaneous volume resuscitation and tube thoracostomy are required; autotransfusion of shed blood may be used when available.
A flail segment occurs when three or more contiguous ribs are each fractured in two or more places, creating a free-floating segment that moves paradoxically — inward on inspiration, outward on expiration — opposite to the rest of the chest wall. The clinical danger is rarely the flail segment's mechanics themselves, but the underlying pulmonary contusion, which frequently worsens over the first 24–48 hours and can precipitate respiratory failure.
Management centers on aggressive pulmonary toilet, adequate analgesia (including regional techniques such as epidural or paravertebral blocks to enable effective coughing and deep breathing), judicious fluid administration (over-resuscitation worsens the contused lung), and early consideration of positive-pressure ventilatory support if oxygenation deteriorates.
Needle decompression buys minutes, not a cure. Every needle decompression must be followed by a definitive tube thoracostomy — treat it as a bridge, not a destination.
Hemorrhage is the leading cause of preventable death after trauma. Circulation assessment identifies shock early — often before a systolic blood pressure fall, which is a late finding masked by physiologic compensation — and immediately controls any identifiable source of bleeding while resuscitation proceeds in parallel.
Hypotension after injury is hemorrhage until proven otherwise. External bleeding is controlled on sight; occult bleeding is sought systematically using the mnemonic "blood on the floor and four more" — the four internal cavities that can conceal life-threatening blood loss without any external sign: the chest (hemothorax), the abdomen, the pelvis and retroperitoneum, and the long bones (particularly bilateral femur fractures, each capable of concealing 1–1.5 L).
FAST ultrasound (Focused Assessment with Sonography in Trauma) rapidly screens the pericardium and the four abdominal quadrants for free fluid; pelvic radiograph and clinical exam screen for pelvic ring disruption; chest radiograph screens for hemothorax.
Class I (<15% blood volume, <750 mL): heart rate normal or minimally elevated, blood pressure normal, pulse pressure normal, mental status normal — often clinically silent.
Class II (15–30%, 750–1500 mL): heart rate 100–120, blood pressure normal to minimally decreased, pulse pressure narrowed (diastolic rises as catecholamines vasoconstrict), respiratory rate mildly increased, mild anxiety.
Class III (30–40%, 1500–2000 mL): heart rate 120–140, blood pressure begins to fall, pulse pressure narrowed, respiratory rate 30–40, mental status confused — this is the threshold at which decompensation becomes clinically obvious and transfusion is almost always required.
Class IV (>40%, >2000 mL): heart rate >140, blood pressure markedly decreased, pulse pressure very narrow, respiratory rate >35, mental status confused to lethargic — immediately life-threatening and requires massive transfusion.
Tachycardia typically precedes hypotension by a significant margin; waiting for a falling blood pressure to diagnose shock means the diagnosis arrives late.
Direct manual pressure controls the majority of external bleeding and is always the first maneuver. Where pressure alone is insufficient:
• Tourniquets: applied "high and tight" 5–7 cm proximal to the wound (never directly over a joint) for exsanguinating extremity hemorrhage, tightened until bleeding stops and distal pulse is absent, with the application time clearly marked on the patient — prolonged tourniquet time raises ischemia risk, but the mortality benefit of stopping exsanguination outweighs this in the acute setting • Hemostatic dressings (e.g., kaolin- or chitosan-impregnated gauze) are wound-packed for junctional or non-tourniquetable hemorrhage (groin, axilla, neck) • Pelvic binders are applied at the level of the greater trochanters for suspected pelvic ring disruption to reduce pelvic volume and tamponade retroperitoneal bleeding • Two large-bore (14–16 gauge) peripheral IVs are established for volume and blood product access; intraosseous access is used when peripheral access fails
Modern trauma resuscitation favors early balanced blood product transfusion over large-volume crystalloid, which dilutes clotting factors and worsens the "lethal triad" of hypothermia, acidosis, and coagulopathy. A massive transfusion protocol delivers packed red blood cells, fresh frozen plasma, and platelets in a roughly 1:1:1 ratio, approximating whole blood composition.
Tranexamic acid (TXA), an antifibrinolytic, reduces mortality from hemorrhage when given within 3 hours of injury (CRASH-2 trial, >20,000 patients) — but administration after 3 hours may increase mortality, making this a strictly time-critical intervention.
Permissive hypotension targets a systolic blood pressure of roughly 80–90 mmHg (or a palpable radial pulse) until surgical or angiographic hemorrhage control is achieved, avoiding the higher pressures that can dislodge early clot and accelerate blood loss — this strategy is avoided in patients with concomitant traumatic brain injury, where adequate cerebral perfusion pressure takes priority.
TXA is a race against the clock: proven mortality benefit inside the first 3 hours after injury, and potential harm beyond it. Time of injury must be established as early as possible.
The "D" step is a rapid, reproducible neurologic snapshot: level of consciousness by the Glasgow Coma Scale, pupillary size and reactivity, and any lateralizing motor or sensory deficit. It takes under a minute and drives immediate decisions about airway protection and the urgency of neuroimaging.
The GCS is the sum of three independently scored components, always documented individually (e.g., "E3V4M5 = 12") as well as by total:
Eye opening (4–1): 4 = spontaneous; 3 = to voice; 2 = to pain; 1 = none.
Verbal response (5–1): 5 = oriented and appropriate; 4 = confused conversation; 3 = inappropriate words; 2 = incomprehensible sounds; 1 = none.
Motor response (6–1): 6 = obeys commands; 5 = localizes to painful stimulus; 4 = normal flexion/withdrawal from pain; 3 = abnormal flexion (decorticate posturing — cortical/subcortical injury); 2 = abnormal extension (decerebrate posturing — brainstem injury, worse prognosis); 1 = none.
Severity bands: mild TBI GCS 13–15; moderate TBI GCS 9–12; severe TBI GCS ≤8. A GCS of 8 or less is the standard threshold at which the patient is assumed unable to protect their own airway and a definitive airway is secured, independent of respiratory rate or oxygenation at that moment.
Pupils are assessed for size (in millimeters), symmetry, and direct/consensual reactivity to light. A resting size difference greater than roughly 1 mm (anisocoria) in a patient with altered consciousness is a critical warning sign of an expanding intracranial mass lesion causing uncal (transtentorial) herniation — the herniating temporal lobe compresses the ipsilateral oculomotor (CN III) nerve, producing a unilateral fixed and dilated ("blown") pupil, classically on the same side as the mass lesion.
A fixed, dilated pupil in the setting of trauma is a neurosurgical emergency: it demands immediate neuroimaging, neurosurgical consultation, and temporizing measures to reduce intracranial pressure (head-of-bed elevation, adequate sedation/analgesia, brief hyperventilation only as a bridge if herniation is actively occurring, and hyperosmolar therapy such as mannitol or hypertonic saline).
AVPU (Alert / responds to Verbal / responds to Pain / Unresponsive) is a faster, coarser alternative useful in the earliest seconds of assessment, before a full GCS can be calculated.
The primary brain injury occurs at the moment of impact and cannot be reversed; the goal of the entire trauma resuscitation is to prevent secondary brain injury — additional neuronal damage from hypoxia, hypotension, hypercarbia, or hyperthermia layered on top of the initial insult.
Both a single episode of hypoxia (SpO₂ <90%) and a single episode of hypotension (SBP <90 mmHg) have each been independently shown to roughly double mortality in severe traumatic brain injury. This is why oxygenation and blood pressure targets in a head-injured patient are often held higher than the "permissive hypotension" strategy used for isolated hemorrhagic shock — adequate cerebral perfusion pressure takes priority once major hemorrhage is controlled.
The disability assessment also screens for spinal cord injury: gross motor and sensory function in all four limbs, rectal tone, and priapism (a specific sign of cord injury). High cervical or upper thoracic cord injury can produce neurogenic shock — hypotension with a paradoxical bradycardia or normal heart rate, from loss of sympathetic vascular tone — which must be distinguished from hemorrhagic shock, in which tachycardia is expected. Treating neurogenic shock with aggressive fluid resuscitation alone can cause pulmonary edema; vasopressor support is often required to restore vascular tone.
GCS ≤ 8 means "coma," and coma means the airway is assumed unprotected. Secure a definitive airway before the patient decompensates, not after.
The final primary-survey step requires completely undressing the patient and performing a log-roll to inspect the back, perineum, and axillae for missed injuries — then immediately and aggressively preventing hypothermia, which is common, iatrogenic, and directly worsens survival by disrupting coagulation.
All clothing is removed — typically cut away rather than pulled, to avoid unnecessary movement of an unstable patient — so that every body surface can be inspected directly. Missed injuries hidden by clothing (stab wounds, gunshot entry/exit sites, impaled objects, burns) are a recognized and preventable cause of delayed diagnosis.
The log-roll, performed with a minimum of three to four providers (one dedicated exclusively to maintaining cervical alignment, the others rolling the torso and pelvis as a single unit), allows inspection and palpation of the entire posterior surface: the thoracolumbar spine for step-offs or tenderness, the flanks, the buttocks and perineum for blood at the urethral meatus or perineal injury, and the skin for pressure injury risk. Digital rectal exam is performed selectively based on mechanism and exam findings (assessing sphincter tone, blood, and prostate position).
Trauma patients lose heat rapidly: prehospital exposure to ambient temperature, wet clothing, cold IV fluids, exposed body cavities in the operating room, and vasodilation from hemorrhagic shock all contribute. Once core temperature falls, three interlinked derangements form a self-reinforcing, often fatal cycle:
• Hypothermia directly impairs the enzymatic clotting cascade — coagulation factor enzyme kinetics slow measurably below approximately 35°C, and platelet function is impaired independent of factor levels • Acidosis (from hypoperfusion and lactate accumulation) further impairs clotting enzyme function and myocardial contractility • Coagulopathy causes ongoing, difficult-to-control hemorrhage, which worsens hypoperfusion, which deepens both hypothermia and acidosis
Each element of the triad independently worsens the other two, and mortality rises sharply once all three are present simultaneously — this combination is a primary target of "damage control resuscitation" strategies.
Hypothermia in trauma is largely iatrogenic and therefore preventable — it should be treated as seriously as any other deranged vital sign:
• Remove wet clothing promptly and dry the patient • Warm blankets and forced-air warming devices (e.g., Bair Hugger) applied as soon as the exposure exam is complete • Fluid and blood product warmers (level-1 rapid infusers) heat resuscitation fluids to approximately 39°C before infusion — infusing large volumes of room-temperature or refrigerated blood products directly worsens core temperature • Increasing ambient room/trauma-bay temperature • Minimizing the total time the patient remains exposed once the exam is complete — re-cover promptly
Core temperature should be measured directly (esophageal, bladder, or rectal probe) rather than estimated, since peripheral skin temperature is an unreliable surrogate in a vasoconstricted, shocked patient.
Once exposure and environmental control are complete, the primary survey (A through E) is finished, and resuscitation continues in parallel with the secondary survey — a systematic head-to-toe examination and focused history (commonly using the AMPLE mnemonic: Allergies, Medications, Past medical history, Last meal, Events/environment of injury).
A tertiary survey, repeating the full examination at approximately 24 hours (or once the patient can meaningfully participate), is standard practice — studies consistently show that 2–10% of trauma patients have at least one clinically significant injury missed on the initial primary and secondary surveys, most commonly musculoskeletal injuries obscured by higher-priority life threats during the initial resuscitation.
Hypothermia is not an inevitable side effect of trauma care — it is largely preventable, and every degree of core temperature lost measurably compounds coagulopathy and mortality risk.