Trauma and ATLS Primary Survey

Mechanistic categories (the stem always states the mechanism first)

• Blunt trauma: motor vehicle and motorcycle collisions, pedestrian-versus-auto, falls, assault. Energy is distributed over a wide area, so deceleration and shear injuries (aortic isthmus tear, mesenteric avulsion, diffuse axonal injury) occur with little external evidence of trauma.
• Penetrating trauma: gunshot and stab wounds. Injury follows the wound tract; high-velocity rounds add cavitation injury beyond the visible tract. Trajectory across the "box" or thoracoabdominal zone predicts which cavity is violated.
• Blast injury: primary (barotrauma to air-filled organs — tympanic membrane, lung, bowel), secondary (fragments), tertiary (body thrown), quaternary (burns, inhalation).
• Crush and compartment mechanisms: prolonged entrapment causing rhabdomyolysis and hyperkalemia.
• Thermal/inhalational: fire, scald, electrical injury, with airway edema as the time-critical threat.

Non-modifiable risk factors

• Age extremes: young adult males dominate penetrating and high-speed blunt trauma; adults over 65 dominate ground-level falls, and the CDC National Guideline for the Field Triage of Injured Patients specifically lowers the triage threshold for older patients because injury severity is systematically underestimated.
• Male sex and pre-existing frailty, osteoporosis, or prior TBI, which convert low-energy mechanisms into major injury.
• Pregnancy: gravid uterus alters anatomy and masks blood loss; ACOG notes maternal vital signs may remain normal while the fetus is hypoperfused.

Modifiable risk factors examiners plant

• Alcohol and substance intoxication: the single most commonly seeded factor; also confounds GCS and abdominal exam.
• Non-use of restraints or helmets, speeding, distracted driving, and unsecured firearm access.
• Anticoagulants and antiplatelet agents: warfarin, DOACs, and dual antiplatelet therapy dramatically raise intracranial and solid-organ bleeding risk after trivial trauma.
• Beta blockers and pacemakers: blunt compensatory tachycardia, so a "normal" heart rate falsely reassures.
• Occupational and home hazards, poor lighting, and polypharmacy in the elderly faller.

• Blunt vs. Penetrating Mechanism Differences: Blunt trauma causes crushing injuries, shearing forces, and deceleration injuries affecting multiple organ systems without obvious external wounds; penetrating trauma creates direct tissue destruction along a wound tract with potential for rapid, visible hemorrhage and specific organ injury based on trajectory.

• Hemorrhagic Shock Cascade: Acute blood loss triggers activation of the sympathetic nervous system, releasing catecholamines that cause vasoconstriction, tachycardia, and increased cardiac contractility to maintain perfusion. Prolonged hypotension leads to anaerobic metabolism, lactate accumulation, metabolic acidosis, cellular dysfunction, and the development of coagulopathy through tissue factor activation, platelet consumption, and fibrinolysis impairment (the "lethal triad" of hypothermia, acidosis, and coagulopathy).

• Airway Compromise Mechanisms: Trauma causes airway obstruction through direct laryngeal/pharyngeal injury, tongue displacement from altered consciousness, aspiration of blood/vomitus, massive facial edema, or foreign body obstruction. These prevent adequate gas exchange and may necessitate emergent surgical airway establishment.

• Tension Pneumothorax Physiology: One-way valve mechanism allows air to enter the pleural space but not exit, causing progressive intrathoracic pressure elevation that compresses the lung, collapses mediastinal structures, impairs venous return, and triggers cardiovascular collapse—a true surgical emergency requiring immediate decompression.

• Spinal Cord Injury Cascade: Traumatic spinal cord injury produces initial mechanical damage followed by secondary injury through ischemia, inflammation, excitotoxicity, and apoptosis, with potential for ascending cord edema and progressive neurological deterioration if the spine is not properly immobilized.

• Traumatic Brain Injury Mechanisms: Primary injury (direct parenchymal damage, axonal shearing, contusions) is irreversible, while secondary injury (hypoxia, hypotension, increased intracranial pressure, cerebral edema) can be mitigated through aggressive resuscitation and management.

A – AIRWAY (with C-spine Protection)

• Stridor, gurgling, or absent air movement indicating airway obstruction
• Blood, vomitus, or secretions in oropharynx
• Trismus (jaw clenching) from temporomandibular joint injury
• Inability to speak full sentences or phonation changes
• Pearl: Any patient with altered mental status or facial/neck trauma requires immediate c-spine immobilization regardless of mechanism clarity

B – BREATHING (Ventilation and Oxygenation)

• Tachypnea, bradypnea, or apnea indicating respiratory compromise
• Asymmetrical breath sounds suggesting pneumothorax or hemothorax
• Subcutaneous emphysema (crepitus) indicating pneumothorax
• Accessory muscle use, nasal flaring, intercostal retractions
• Cyanosis (late sign), pale skin from shock
• Tension pneumothorax classic presentation: Hypotension, JVD, tracheal deviation, absent breath sounds on affected side—this is clinical diagnosis requiring immediate decompression without waiting for imaging
• Flail chest with paradoxical movement and severe pain with breathing

C – CIRCULATION (Hemorrhage Control and Perfusion)

• Tachycardia (early sign of shock—may be absent in athletes or elderly)
• Hypotension indicating significant blood loss
• Weak or absent pulses suggesting profound shock or exsanguination
• Pale, cool, clammy skin with delayed capillary refill (>2 seconds) indicating poor perfusion
• Massive external hemorrhage visible at wound sites
• Distended abdomen suggesting intra-abdominal bleeding
• Pericardial ultrasound findings: Beck's triad (hypotension, JVD, muffled heart sounds) indicating cardiac tamponade from hemopericardium

D – DISABILITY (Neurological Status)

• Altered consciousness using Glasgow Coma Scale (GCS)—score <8 requires airway protection consideration
• Pupillary changes: Anisocoria, blown pupil (ipsilateral to epidural hematoma), pinpoint pupils (brainstem injury)
• Focal neurological deficits suggesting spinal cord injury or intracranial pathology
• Incontinence or lack of anal tone indicating spinal shock

E – EXPOSURE (Complete Assessment with Hypothermia Prevention)

• Full body examination for additional injuries while maintaining core temperature
• Petechial rash suggesting crush syndrome or fat embolism
• Pearl: Prevent hypothermia (heat loss through radiation, evaporation, conduction) which worsens coagulopathy and mortality

• Airway Assessment: Direct visualization of the oropharynx; ability to speak, swallow, and maintain patency. Imaging (CT of neck) indicated only after stabilization if injury suspected.

• Breathing Evaluation: Auscultation for bilateral breath sounds; percussion for hyperresonance (pneumothorax) or dullness (hemothorax). Chest X-ray (CXR) confirms pneumothorax, hemothorax, and rib fractures; however, tension pneumothorax is a clinical diagnosis and treatment should not be delayed for imaging.

• Circulation Assessment: Blood pressure, heart rate, skin perfusion, and capillary refill provide clinical estimate of shock severity. FAST exam (Focused Assessment with Sonography for Trauma) rapidly identifies free intraperitoneal fluid (blood) in Morrison's pouch, pericardium, and pelvis—performed during Primary Survey. Pelvic X-ray identifies pelvic fractures associated with retroperitoneal hemorrhage.

• Disability Evaluation: Glasgow Coma Scale (GCS) quantifies consciousness; normal is 15, coma is ≤8. Pupil examination and basic neurological testing (motor/sensory). CT head performed only after stabilization if intracranial injury suspected.

• Exposure/Complete Exam: Systematic examination of all body surfaces with particular attention to wounds, deformities, and signs of injury.

• Diagnostic Considerations: Labs including CBC, CMP, coagulation studies, lactate, type and cross, and pregnancy test for females of childbearing age should be ordered early. Mechanism and clinical suspicion guide selective imaging (CT trauma pan-scan vs. targeted imaging).

A – AIRWAY MANAGEMENT

• First-line: Positioning (head-tilt/chin-lift in trauma-neutral position without c-spine compromise), suctioning of secretions/blood, supplemental oxygen
• Second-line: Bag-valve-mask (BVM) ventilation if inadequate spontaneous breathing; nasopharyngeal airway for conscious patients; oropharyngeal airway for unconscious patients
• Definitive airway (when GCS ≤8, inability to protect airway, apnea, or severe maxillofacial trauma): Rapid sequence intubation (RSI) with inline c-spine stabilization by second provider; agents include propofol (1-2 mg/kg IV) or etomidate (0.2-0.3 mg/kg IV) for induction plus succinylcholine (1-1.5 mg/kg IV) or rocuronium (1.2 mg/kg IV) for paralysis. Surgical airway (cricothyrotomy) required if RSI fails and

Complications of the injury itself

• Exsanguination and the lethal triad (hypothermia, acidosis, coagulopathy): each element inhibits clotting factor kinetics and platelet function, creating a self-amplifying bleeding loop. Signal: rising lactate and base deficit with diffuse oozing from puncture sites. Emergency — activate massive transfusion.
• Tension pneumothorax and cardiac tamponade: obstructive shock from impaired venous return. Signal: hypotension with distended neck veins and clear or unilaterally absent breath sounds. Both are immediate emergencies treated before imaging.
• Secondary brain injury: a single episode of hypoxia or hypotension markedly worsens outcome after TBI; the Brain Trauma Foundation guidelines therefore center management on avoiding hypoxemia and hypotension. Signal: falling GCS, unilateral blown pupil, Cushing reflex (hypertension, bradycardia, irregular respirations). Emergency — restore oxygenation and MAP, temporize elevated ICP (head-of-bed elevation, hyperosmolar therapy), and obtain emergent CT with neurosurgical consultation for possible decompression of a mass lesion.
• Missed injury: the classic reason ATLS mandates a tertiary survey after resuscitation. Signal: new pain or deformity 24–48 hours later.
• Abdominal compartment syndrome: bowel edema plus over-resuscitation raises intra-abdominal pressure, causing oliguria, high peak airway pressures, and hypotension. Emergency — decompressive laparotomy.
• Late systemic complications: ARDS, fat embolism syndrome after long-bone fracture (hypoxia, petechiae, confusion), rhabdomyolysis-induced AKI, VTE, and sepsis/MODS.

Complications of treatment

• Airway management: failed or esophageal intubation, aspiration, and cricothyrotomy bleeding or tracheal stenosis.
• Succinylcholine after burns: acceptable within roughly the first 24 hours, then avoided for up to about a year, because extrajunctional acetylcholine receptors upregulate over days and produce massive potassium efflux.
• Succinylcholine after crush injury: avoid whenever rhabdomyolysis or hyperkalemia is known or suspected — hyperkalemia is often already present on arrival and depolarization can precipitate hyperkalemic cardiac arrest immediately. Use rocuronium 1.2 mg/kg IV instead.
• Needle decompression and tube thoracostomy: lung laceration, intraparenchymal or subdiaphragmatic tube placement, empyema, and re-expansion pulmonary edema.
• Massive transfusion: citrate chelation causing ionized hypocalcemia (hypotension, prolonged QT), hyperkalemia, hypothermia, dilutional coagulopathy, TRALI, and TACO.
• Excess crystalloid: hyperchloremic metabolic acidosis, clot dilution, and worsened edema — the rationale for balanced blood-product resuscitation over large-volume saline.

• Treat as you go: the primary survey is not "assess then treat." A problem found at A is fixed before moving to B. The commonest wrong answer is ordering a CT scan while an ABC problem is unaddressed.
• Tension pneumothorax is a clinical diagnosis: hypotension, distended neck veins, unilateral absent breath sounds, tracheal deviation (a late sign). Best next step is immediate needle decompression followed by tube thoracostomy — never a chest x-ray first. ATLS now favors the 5th intercostal space just anterior to the midaxillary line in adults because chest wall thickness often defeats a needle at the 2nd interspace.
• Hypotension in trauma is hemorrhage until proven otherwise. Blood hides in five places: chest, abdomen, retroperitoneum/pelvis, thighs (long bones), and "on the floor."
• Unstable patient with a positive FAST goes to the operating room, not the CT scanner. A hemodynamically normal patient with a positive FAST can be imaged. FAST does not exclude retroperitoneal or hollow-viscus injury.
• Hemostatic resuscitation: the ACS Committee on Trauma supports balanced product transfusion in approximately equal ratios of plasma, platelets, and red cells. PROPPR did not show a difference in its primary mortality endpoints, but 1:1:1 achieved hemostasis more often and reduced early deaths from exsanguination — the basis for current balanced-ratio practice. Add tranexamic acid early: TXA started more than 3 hours after injury is not beneficial and may increase bleeding-related mortality (CRASH-2), with benefit greatest within the first hour.
• Distinguish neurogenic from hemorrhagic shock: neurogenic shock after cervical/high thoracic cord injury gives hypotension with bradycardia and warm, dry skin from lost sympathetic tone. Hemorrhagic shock gives tachycardia and cool, clammy skin. Do not confuse either with spinal shock, which is areflexia, not a blood-pressure diagnosis.
• GCS ≤ 8 — intubate, with manual inline cervical stabilization. Calculate GCS before sedation and paralysis, and record the pre-intubation number.
• Common distractor: the dramatic open femur fracture or amputated digit in the stem. Airway, breathing, and circulation always outrank the visually impressive injury; only exsanguinating external hemorrhage (control with direct pressure or tourniquet) preempts the airway.