Trauma — Primary and Secondary Survey (ATLS)

• Hemorrhagic shock and hypoperfusion cascade: Acute blood loss triggers the body's compensatory mechanisms through baroreceptor and chemoreceptor reflexes. Sympathetic nervous system activation causes catecholamine release (epinephrine and norepinephrine), resulting in tachycardia, vasoconstriction, and peripheral blood flow redistribution toward vital organs. Simultaneously, the renin-angiotensin-aldosterone system (RAAS) activates, promoting sodium and water retention to expand intravascular volume. However, in severe hemorrhage (Class III-IV shock), these compensatory mechanisms fail, leading to progressive tissue hypoxia, anaerobic metabolism, lactate accumulation, and cellular acidosis. Capillary endothelial dysfunction develops through several mechanisms: hypoxia-inducible factor (HIF-1α) activation increases vascular permeability, inflammatory mediators (TNF-α, IL-1, IL-6) amplify endothelial injury, and prolonged shock triggers apoptotic pathways in multiple organs. The consequence is the development of the "lethal triad" of hypothermia, coagulopathy, and acidosis, which perpetuates hemorrhagic shock despite resuscitation attempts if not promptly reversed.

• Traumatic brain injury (TBI) and increased intracranial pressure (ICP): Mechanical trauma causes primary brain injury through direct neuronal and axonal damage at the moment of impact, with subsequent diffuse axonal injury (DAI) from shear forces. Secondary brain injury develops over minutes to hours through multiple mechanisms: cerebral edema results from both vasogenic edema (blood-brain barrier disruption with protein extravasation into the interstitium) and cytotoxic edema (cellular swelling due to Na+/K+ ATPase failure from hypoxia and ischemia). Elevated ICP directly reduces cerebral perfusion pressure (CPP = MAP - ICP), causing progressive cerebral ischemia, metabolic failure, and herniation. Inflammatory cascade activation releases excitatory amino acids (glutamate and aspartate), which overstimulate N-methyl-D-aspartate (NMDA) receptors, causing calcium influx into neurons, mitochondrial dysfunction, and cell death. Traumatic subarachnoid hemorrhage triggers vasospasm, typically occurring 4-14 days post-injury, further compromising cerebral blood flow.

• Tension pneumothorax and impaired ventilation mechanics: Direct chest wall trauma or penetrating injury can lacerate visceral pleura, allowing air to enter the pleural space. In a simple pneumothorax, pressure equilibrates between pleural space and atmosphere, partially collapsing the lung. However, in a tension pneumothorax, a "one-way valve" mechanism develops in which air enters the pleural space during inspiration but cannot exit during expiration, leading to progressive pressure accumulation. This compresses the ipsilateral lung, causes mediastinal shift toward the contralateral side, and impairs venous return to the heart by compressing the vena cava. The resulting cardiovascular collapse occurs through decreased preload (reduced venous return), decreased cardiac output, and hypotension. Simultaneously, the contralateral lung is mechanically compressed, reducing minute ventilation and causing hypoxemia and hypercapnia. The pathophysiology combines mechanical ventilation impairment with circulatory collapse.

• Airway compromise from maxillofacial trauma and cervical spine injury: Facial trauma causes airway obstruction through blood and secretion accumulation, soft tissue edema, tongue displacement posteriorly (loss of pharyngeal muscle tone or direct displacement), and potential aspiration. Laryngeal injury from blunt anterior neck trauma causes submucosal edema and hemorrhage, progressively narrowing the already fixed airway diameter. Cervical spine injury creates a dual problem: the primary mechanical injury to neural elements requires strict immobilization to prevent secondary neurologic deterioration, yet this very immobilization (through cervical collars and spine boards) can impair mouth opening and increase aspiration risk. The challenge in the primary survey is balancing airway management with spinal precautions.

• Blast injury pathophysiology: Explosions generate multiple injury mechanisms: primary blast injury (pressure wave effects on air-filled organs), secondary blast injury (projectiles penetrating tissues), tertiary blast injury (patient displacement and blunt impact), and quaternary blast injury (burns, inhalation injuries, crush syndrome). Primary blast injury particularly affects the lungs (blast lung with pulmonary contusion, hemoptysis, and respiratory failure), ears (tympanic membrane rupture), and gastrointestinal tract. The mechanism involves rapid pressure changes that cause tissue disruption, cavitation formation, and internal hemorrhage in areas of different tissue density (air-fluid interfaces).

• Blunt trauma mechanisms: Motor vehicle collisions (highest mortality cause of trauma in most developed countries) generate high-energy transfer injuries; severity correlates with vehicle deceleration, intrusion distance, and ejection. Falls from heights >20 feet (>6 meters) in adults or >10 feet in children predictably cause severe injuries; the mechanism involves conversion of gravitational potential energy into tissue-destructive kinetic energy. Pedestrian-vehicle collisions create predictable injury patterns: initial contact injures the lower extremities, hood contact injures the torso, and windshield contact injures the head. Assaults with blunt objects cause focal tissue destruction; the mechanism varies by object shape and impact velocity. Sports injuries and high-velocity recreational accidents (skiing, mountaineering) cause increasingly recognized morbidity in younger populations.

• Penetrating trauma mechanisms: Gunshot wounds create tissue injury through both temporary and permanent cavity formation; temporary cavities produce tissue stretch and damage extending centimeters from the projectile tract (particularly damaging to solid organs), while permanent cavities are the actual tissue destroyed by the projectile. Handgun wounds typically cause lower-velocity injury with less cavitation effect, whereas rifle rounds cause extensive cavitation. Stab wounds create injury limited primarily to structures in the direct path of the blade; the depth of penetration determines injury severity. The type of weapon (caliber, velocity, distance) directly predicts injury pattern and severity.

• Environmental and systemic risk factors: Age extremes confer vulnerability; pediatric patients have different anatomy (proportionally larger head, more anterior larynx) and physiology (higher metabolic demands, limited physiologic reserve), while elderly patients have reduced compensatory capacity, polypharmacy (anticoagulation), and comorbidities. Alcohol and drug intoxication impair protective reflexes and mask injury severity through pain suppression. Preexisting anticoagulation (warfarin, direct oral anticoagulants) or coagulopathy dramatically increases bleeding risk and complicates resuscitation. Obesity creates anatomic challenges for airway management and vascular access while increasing metabolic stress. Pregnancy alters physiology (increased circulating volume, left uterine displacement concerns, altered drug metabolism) and introduces fetal considerations.

• High-energy mechanisms warranting trauma center referral: Mechanisms predicting severe injury include ejection from vehicles, death of another occupant in the same vehicle, rollover accidents, falls >20 feet, pedestrians struck at speeds >20 mph, motorcycle crashes at speeds >20 mph, penetrating trauma to head/neck/torso/extremity proximal to elbow or knee, blast injuries, and crush injuries. These mechanisms trigger automatic trauma activation protocols regardless of initial vital signs.

• Shock and hypoperfusion signs: Tachycardia develops early as a compensatory response to blood loss or pain, with heart rates >120 bpm suggesting significant hemorrhage. Hypotension is a late finding in hemorrhagic shock; normotensive patients may still have Class II-III hemorrhage with significant blood loss (750-1500 mL or 15-30% blood volume). Cool, clammy skin reflects peripheral vasoconstriction and sympathetic activation. Altered mental status (confusion, anxiety, combativeness) indicates either direct brain injury or systemic hypoperfusion with cerebral hypoxia. Tachypnea (>20 breaths/minute) serves dual purposes: compensation for metabolic acidosis and response to pain/anxiety. Weak or absent pulses in unresponsive trauma patients suggest Class IV hemorrhage and mandate emergency resuscitation or pronouncement depending on context.

• Respiratory distress and hypoxemia: Severe dyspnea with accessory muscle use suggests airway compromise, pneumothorax, or massive hemothorax. Stridor (high-pitched breathing sound) indicates upper airway obstruction from laryngeal edema, vocal cord injury, or foreign material. Unilateral absence of breath sounds suggests pneumothorax, hemothorax, or mainstem intubation (if intubated). Subcutaneous emphysema (crepitus under the skin) indicates air in subcutaneous tissues, suggesting pneumothorax with air leaking into fascial planes or tracheal/laryngeal injury. Tension pneumothorax presents with sudden cardiovascular collapse, unilateral absent breath sounds, tracheal deviation (late finding), elevated jugular venous pressure (JVP), and hypotension; this is a clinical diagnosis requiring immediate decompression without awaiting imaging.

• Neurologic presentation: Glasgow Coma Scale (GCS) score provides standardized assessment of consciousness: Eye Opening (E1-4), Verbal response (V1-5), Motor response (M1-6), with total ranging from 3-15. GCS ≤8 indicates severe TBI requiring airway protection. Focal neurologic deficits (hemiparesis, hemisensory loss, pupillary abnormality) localize brain injury. Blown pupil (unilateral pupillary dilation unresponsive to light) suggests ipsilateral epidural hematoma with uncal herniation; this is a neurosurgical emergency. Cerebrospinal fluid (CSF) rhinorrhea or otorrhea suggests basilar skull fracture. Raccoon eyes (periorbital ecchymosis) and Battle's sign (mastoid ecchymosis) indicate anterior and posterior basilar skull fractures, respectively. Seizure activity in the acute phase suggests significant intracranial injury or metabolic derangement.

• Abdominal and pelvic trauma signs: Abdominal distension suggests intra-abdominal bleeding; the finding is usually absent until significant volume (>1500 mL) has accumulated. Positive Focused Assessment with Sonography for Trauma (FAST) exam or physical exam findings (bruising, tenderness, rebound, guarding) indicate peritoneal irritation from solid organ injury or hollow viscus perforation. Flank ecchymosis (Turner's sign) suggests retroperitoneal bleeding from renal or duodenal injury. Pelvic fractures, particularly unstable ones (involving disruption of pelvic ring), can cause massive retroperitoneal hemorrhage; pelvic instability is assessed by manual compression of the iliac wings (should be painless and stable). Absent bowel sounds suggest bowel injury but have poor sensitivity.

• Extremity trauma: Limb deformity indicates fracture; angulation and shortening are classic signs. Compartment syndrome develops over hours from soft tissue swelling within fascial compartments; classic signs include pain out of proportion to exam findings, pain with passive stretch of muscles in the compartment, and sensory/motor changes (late findings). Open fractures with visible bone or associated wounds carry high infection risk and require urgent surgical consultation. Vascular injury presents with distal ischemia: absence of distal pulses, cool skin, cyanosis, pain, and potential compartment syndrome if reperfusion is delayed.

• Hemorrhage classification (American College of Surgeons): Class I hemorrhage (<750 mL or <15% blood volume) causes minimal vital sign changes; compensation is adequate. Class II (750-1500 mL or 15-30% blood volume) causes tachycardia >100 bpm, tachypnea 20-30, mild anxiety. Class III (1500-2000 mL or 30-40% blood volume) causes tachycardia >120, tachypnea >30, hypotension, confusion, possible oliguria. Class IV (>2000 mL or >40% blood volume) causes profound shock with hypotension, marked tachycardia, marked tachypnea, confusion/lethargy, and minimal urine output; survival without resuscitation is unlikely.

• Primary Survey findings: The primary survey employs a mnemonic approach—ABCDE—which guides both assessment and immediate interventions: Airway assessment includes determining if the airway is patent and if the patient can maintain it; signs of obstruction include stridor, inability to speak, pooled secretions, or altered mental status. Breathing assessment includes bilateral auscultation for breath sounds (presence, symmetry), respiratory rate and effort, oxygen saturation, and jugular venous pressure (should not be grossly distended unless tension pneumothorax or cardiac injury is present). Circulation assessment includes pulse check (carotid pulse for central circulation), blood pressure, skin perfusion (color, temperature, capillary refill), and external hemorrhage control. Disability assessment uses GCS score and pupils. Exposure involves undressing the patient completely to identify all injuries while maintaining normothermia.

• Secondary Survey systematic approach: After primary survey stabilization, a head-to-toe examination proceeds: Head and face inspection for lacerations, bone step-offs, raccoon eyes, Battle's sign, CSF leakage. Eyes assessment includes visual acuity, pupillary size and reactivity, extraocular motion (may be impaired with retrobulbar hematoma or orbital fracture), hyphema (blood in anterior chamber suggesting significant ocular trauma). Ears examined for hemotympanum (suggests basilar skull fracture) and canal bleeding. Nose assessed for septal hematoma (requires urgent drainage if present to prevent necrosis), CSF leakage. Mouth examined for loose/broken teeth, tongue lacerations, palatal fractures. Neck palpated for tenderness, step-off in spinous processes, tracheal deviation; should maintain c-spine precautions until cleared. Chest examination includes inspection for bruising, palpation for crepitus and rib fractures, auscultation bilaterally. Abdomen examined for bruising, palpation for rebound/guarding, FAST ultrasound (assesses fluid in pericardium, perihepatic, perisplenic, and pelvic spaces). Pelvis palpated for instability. Extremities examined for deformity, neurovascular status. Back examined by log-rolling (maintains spinal precautions).

• Imaging modality selection: Portable chest radiograph rapidly identifies pneumothorax, hemothorax, mediastinal widening, rib fractures; performed during primary survey if respiratory compromise is present. Portable pelvis radiograph identifies pelvic fractures and is particularly important if hemorrhagic shock is present without clear source. FAST exam (bedside ultrasound) provides rapid assessment of free fluid in pericardium (pericardial window at xiphoid), perihepatic space (Morrison's pouch), perisplenic space, and pelvis; has >90% sensitivity for hemoperitoneum >250 mL. Computed tomography (CT) with IV contrast is the gold standard for identifying specific injuries but requires patient transport out of resuscitation area; reserved for hemodynamically stable patients. CT head is indicated for GCS ≤13, focal neurologic deficits, altered mental status, severe headache, or mechanism concerning for intracranial injury; Canadian Head CT Rules help guide use. CT cervical spine clears cervical injury in compliant, alert patients without midline tenderness or neurologic findings; has high sensitivity (>99%) for significant injury. NEXUS criteria

Immediate stabilisation (primary survey interventions)

• Airway: suction, jaw thrust (not head tilt) with manual in-line stabilisation, then definitive airway — orotracheal rapid-sequence intubation — for GCS ≤8, expanding neck hematoma, or inhalation/laryngeal injury. Failed airway → surgical cricothyrotomy (needle cricothyrotomy in children under ~12).
• Breathing: tension pneumothorax is decompressed clinically without imaging — finger thoracostomy or needle decompression at the 5th intercostal space, anterior axillary line in adults (ATLS 10th edition moved away from the 2nd interspace), followed by tube thoracostomy. Open pneumothorax gets a three-sided occlusive dressing; massive hemothorax gets a chest tube.
• Circulation: direct pressure, then junctional/extremity tourniquet; pelvic binder at the greater trochanters for suspected unstable pelvic ring injury. Two large-bore peripheral IVs; if access fails, intraosseous.

Resuscitation pharmacology

• Balanced blood product resuscitation: activate massive transfusion protocol with plasma:platelets:RBC near 1:1:1 (PROPPR); ATLS limits initial warmed crystalloid to about one litre because large-volume saline worsens dilutional coagulopathy and acidosis.
• Antifibrinolytic — tranexamic acid: 1 g IV over 10 minutes then 1 g over 8 hours, started within 3 hours of injury (CRASH-2; endorsed by ACS TQIP).
• Calcium salts (calcium chloride/gluconate) for citrate-induced hypocalcemia during massive transfusion.
• Hyperosmolar therapy — mannitol or hypertonic saline — plus head elevation and short-term hyperventilation only as a bridge for herniation; Brain Trauma Foundation guidance stresses avoiding hypotension and hypoxia, which drive secondary injury.

Complications of the injury itself

• Lethal triad (hypothermia, acidosis, coagulopathy) — emergency: hypoperfusion drives lactic acidosis while heat loss from exposure and cold fluids impairs enzymatic clotting factor function; signalled by diffuse oozing from puncture sites and a non-surgical bleeding pattern despite hemostasis.
• Herniation from expanding intracranial hematoma — emergency: mass effect displaces the uncus across the tentorium, compressing CN III and the brainstem; signalled by a blown pupil, contralateral hemiparesis, and Cushing reflex (hypertension, bradycardia, irregular respirations).
• Missed injury: up to a meaningful fraction of injuries are found only on the tertiary survey (repeat head-to-toe exam within 24 hours) — classically small bowel injury, scaphoid and other extremity fractures, and thoracolumbar fractures in the obtunded patient.
• Compartment syndrome and rhabdomyolysis — emergency: swelling within a non-compliant fascial compartment exceeds capillary perfusion pressure; signalled by pain out of proportion and pain on passive stretch, with tea-coloured urine and a markedly elevated creatine kinase when myonecrosis occurs. Hyperkalemia after reperfusion can precipitate arrest.
• Delayed splenic rupture, ARDS from pulmonary contusion, fat embolism syndrome after long-bone fracture (petechiae, hypoxemia, confusion), and VTE, for which EAST recommends early chemoprophylaxis once bleeding is controlled.

Complications of treatment

• Transfusion-related: citrate binds ionised calcium (hypocalcemia → hypotension and worsened coagulopathy), potassium load from stored red cells, TACO from volume, and TRALI — emergency — presenting as hypoxemia with bilateral infiltrates within hours of transfusion.
• Airway-related: aspiration during RSI, esophageal or right mainstem intubation (unilateral absent breath sounds), and cricothyrotomy bleeding or subglottic stenosis.
• Procedure-related: iatrogenic pneumothorax or arterial puncture from subclavian access; lung, diaphragm, or intra-abdominal injury from a low chest tube.
• Abdominal compartment syndrome — emergency: massive crystalloid and bowel edema raise intra-abdominal pressure; signalled by a tense abdomen, rising peak airway pressures, and oliguria, requiring decompressive laparotomy.

• The answer is almost always the next letter of ABCDE: if the stem describes an unprotected airway, securing the airway beats ordering any imaging. Do not skip ahead to CT in an unstable patient — the CT scanner is the place trauma patients go to die.
• Tension pneumothorax is a clinical diagnosis: hypotension plus unilateral absent breath sounds plus distended neck veins → immediate decompression, never a chest radiograph first. Tracheal deviation is a late and unreliable sign. ATLS 10th edition places needle decompression at the 5th intercostal space, anterior axillary line.
• Unstable + positive FAST → operating room; unstable + negative FAST → look elsewhere (chest, pelvis, retroperitoneum, external, or "on the floor"). FAST does not exclude retroperitoneal or hollow viscus injury; a hemodynamically stable patient gets CT instead.
• Hypotension in trauma is hemorrhagic until proven otherwise. The classic distractors: neurogenic shock (hypotension with bradycardia and warm, dry, well-perfused skin after cervical/high thoracic cord injury) and cardiac tamponade (Beck triad — hypotension, distended neck veins, muffled heart sounds; pulsus paradoxus).
• Tachycardia may be absent in patients on beta blockers, in the elderly, in athletes, and in pregnancy where maternal vitals stay normal while the fetus is hypoperfused — hence left uterine displacement and fetal monitoring after 20 weeks (ACOG).
• GCS ≤8, intubate. Hypoxia and a single episode of hypotension both independently worsen outcome in TBI (Brain Trauma Foundation); steroids are harmful, not helpful.
• Tranexamic acid must be started within 3 hours of injury (CRASH-2) — later administration is not beneficial.
• Basilar skull fracture signs (raccoon eyes, Battle sign, hemotympanum, CSF otorrhea) forbid nasogastric and nasotracheal tubes — use the oral route.