13.3 Thoracic & Abdominal Trauma Management

13.3 Thoracic & Abdominal Trauma Management

Life-Threatening Thoracic Trauma & Pathophysiology

Thoracic injuries account for up to 25% of all trauma-related fatalities. Under the Canadian Paramedic Competence Framework (CPCF Appendix A #4 & #7), primary care paramedics must rapidly identify and intervene against life-threatening chest injuries during the primary survey. The thoracic cavity houses the cardiac pump, great vessels, and pulmonary arborization; disruption of chest wall integrity, pleural negative pressure, or pericardial dynamics rapidly precipitates irreversible shock or asphyxia.

1. Open Pneumothorax ('Sucking Chest Wound')

An open chest wall defect communicating directly with the pleural space disrupts normal pulmonary mechanics. When the chest wall opening is approximately two-thirds or more of the diameter of the trachea (roughly the size of the patient's thumb or nickle/quarter coin), air preferentially follows the path of least resistance through the wound rather than through the tracheobronchial tree during inspiration.

• Pathophysiology: Ambient atmospheric air rushes into the hemithorax on inspiration, collapsing the ipsilateral lung and impairing ventilation. On expiration, air escapes through the defect.
• Prehospital Management:
  • Immediately seal the wound with a gloved hand during the primary survey.
  • Apply a commercial vented chest seal (e.g., Bolin, Asherman, Chest Seal with hydrogel adhesive and one-way valves/channels). The vented design allows air and blood to escape during expiration while preventing atmospheric air ingress during inspiration.
  • If commercial seals are unavailable, apply an improvised three-sided occlusive dressing (sterile plastic/foil taped on three sides, creating a flutter valve).
  • The Tension Conversion Risk: Any occlusive dressing can become clogged with coagulated blood or tissue, transforming an open defect into a lethal tension pneumothorax. Paramedics must continuously monitor breath sounds and hemodynamics. If respiratory distress worsens or obstructive shock develops, the dressing must be immediately 'burped' (peeled back during expiration to release trapped intrapleural tension).

2. Tension Pneumothorax & Obstructive Shock

Tension pneumothorax develops when a parenchymal or chest wall laceration creates a 'one-way valve' mechanism: air enters the pleural space during inspiration or positive-pressure ventilation but cannot escape during expiration.

• Pathophysiology: Intrapleural pressure progressively climbs, exceeding atmospheric pressure. The ipsilateral lung collapses completely. The expanding pressure pushes the mediastinum and trachea toward the contralateral hemithorax, compressing the contralateral lung and, most critically, kinking and mechanically compressing the superior and inferior vena cava. Venous return (preload) to the right heart collapses precipitously, dropping cardiac output and inducing severe obstructive shock and cardiac arrest.
• Clinical Manifestations:
  • Severe respiratory distress, air hunger, tachypnea, and cyanosis.
  • Unilateral absent or markedly diminished breath sounds on the affected side.
  • Hyperresonance to percussion over the affected hemithorax.
  • Jugular Venous Distention (JVD) due to vena cava outflow obstruction (may be absent in severe hypovolemia).
  • Hemodynamic collapse: tachycardia, thready pulses, and severe hypotension (narrow pulse pressure).
  • Subcutaneous emphysema across the chest wall, neck, and face.
  • Tracheal Deviation: A late, pre-terminal finding where the trachea deviates away from the affected side.
• Paramedic Intervention: Recognition of tension pneumothorax with hemodynamic instability is an absolute indication for emergency pleural decompression (needle thoracostomy: 14- or 10-gauge needle catheter placed in the 2nd intercostal space at the midclavicular line or 4th/5th intercostal space at the anterior axillary line, per regional ALS/PCP expanded scope).

3. Flail Chest & Paradoxical Breathing

A flail chest occurs when two or more contiguous ribs are fractured in two or more places each, detaching a free-floating segment of the thoracic bony cage.

• Paradoxical Motion: During spontaneous inspiration, negative intrathoracic pressure pulls the flail segment inward, while the rest of the chest expands outward. During expiration, positive intrathoracic pressure pushes the flail segment outward, while the chest collapses inward.
• The True Killer: Pulmonary Contusion: The skeletal instability itself rarely kills the patient; the primary driver of mortality is the massive underlying pulmonary contusion (alveolar hemorrhage, capillary disruption, and interstitial edema) caused by the blunt kinetic energy transfer. This leads to profound ventilation-perfusion ($V/Q$) mismatch, shunting, and severe refractory hypoxemia.
• Management: Provide high-flow oxygen. If respiratory failure or profound hypoventilation occurs, initiate positive pressure ventilation (PPV) via BVM or continuous positive airway pressure (CPAP, if hemodynamically stable). Positive pressure acts as an 'internal pneumatic splint', pushing the collapsed lung and flail segment outward synchronously. Provide analgesia via ALS intercept. Never tape sandbags or apply restrictive circumferential taping to the chest wall, as this severely impairs lung volumes.

4. Pericardial Tamponade

Blunt or penetrating trauma to the 'cardiac box' (sternal notch to xiphoid, between bilateral midclavicular lines) can lacerate epicardial coronary vessels or the myocardium. Because the fibrous pericardial sac is inelastic, rapid accumulation of as little as 100 to 200 mL of blood creates acute intrapericardial hypertension that exceeds right ventricular diastolic filling pressure.

• Beck's Triad:
  1. Hypotension with narrow pulse pressure (due to collapsed left ventricular stroke volume).
  2. Muffled/distant heart tones (fluid layer dampening acoustic transmission).
  3. Jugular Venous Distention (JVD) (impaired right atrial filling leading to central venous congestion).
• Pulsus Paradoxus: An exaggerated drop in systolic blood pressure (>10 mmHg) during spontaneous inspiration.
• Differential Diagnosis: Tamponade vs Tension Pneumothorax:

5. Traumatic Aortic Disruption

High-energy rapid deceleration mechanisms—such as high-speed frontal or lateral motor vehicle collisions or falls from >5 metres—induce severe violent shearing forces across the thoracic aorta. The aorta is relatively mobile, except at the aortic isthmus, where it is tethered to the thoracic wall by the ligamentum arteriosum. Shearing tears the vessel, causing immediate fatal transection in 80–90% of cases. In survivors, bleeding is temporarily contained by a fragile adventitial pseudoaneurysm.

• Clinical Signs: Tearing midscapular back pain, retrosternal chest pain, harsh systolic murmur, differential blood pressures (>15–20 mmHg) or pulse deficits between right and left upper extremities, or loss of lower extremity pulses.
• Management: Rapid non-emergent handling (avoid jarring), high-flow oxygen, judicious fluid resuscitation adhering to permissive hypotension (target SBP ~90 mmHg to avoid bursting the adventitial bubble), and priority bypass transport to a cardiothoracic surgical centre.

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Abdominal Trauma: Visceral Rupture & Evisceration

The abdomen is vulnerable to both blunt kinetic trauma and penetrating ballistic/stab wounds. Abdominal trauma is categorized into solid organ injury, hollow organ injury, and evisceration:

Solid Organ vs Hollow Organ Injury

• Solid Organs (Spleen, Liver, Kidneys): Highly vascular parenchyma. Injury results in massive, occult intra-abdominal hemorrhage leading to hypovolemic shock. Splenic laceration frequently triggers diaphragmatic peritoneal irritation, manifesting as referred left shoulder pain (Kehr's sign) mediated by the phrenic nerve (C3–C5). Liver rupture manifests with right upper quadrant guarding and hypovolemia.
• Hollow Organs (Stomach, Small/Large Intestine, Bladder): Injury spills acidic digestive enzymes, bile, bacteria, and feces into the peritoneal cavity. This induces chemical and bacterial peritonitis, presenting with severe diffuse abdominal tenderness, rigidity, involuntary board-like guarding, and rebound tenderness, progressing to septic shock.

Prehospital Management of Abdominal Evisceration

Abdominal evisceration occurs when penetrating trauma creates a full-thickness rupture of the abdominal musculature, allowing intra-abdominal viscera (most commonly loops of small bowel or greater omentum) to protrude outside the abdominal cavity.

                    [ Abdominal Evisceration Protocol ]
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            | 1. Expose wound & inspect for hemorrhage       |
            | 2. DO NOT ATTEMPT TO PUSH OR REINSERT ORGANS!  |
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            | 3. Apply large sterile dressings soaked with   |
            |    WARM, STERILE SALINE directly over viscera  |
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                                     |
                                     v
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            | 4. Cover with an airtight occlusive barrier     |
            |    (plastic wrap / sterile foil) to retain     |
            |    moisture and prevent heat loss              |
            +------------------------------------------------+
                                     |
                                     v
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            | 5. Position patient supine with KNEES FLEXED   |
            |    to relax the anterior abdominal wall        |
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Mandatory Evisceration Protocols

1. Prohibition of Reinsertion: Primary care paramedics must NEVER attempt to reinsert, replace, or push protruding viscera back into the abdominal cavity. Reinsertion introduces massive bacterial contamination, risks strangulation or laceration of ischemic bowel, and increases intra-abdominal pressure.
2. Sterile Moist Dressings: Apply large, sterile, non-adherent surgical dressings or laparotomy pads soaked in warm, sterile normal saline directly over the exposed viscera. Dry gauze must never touch exposed bowel, as it adheres to the delicate serosa and strips the bowel wall upon removal.
3. Occlusive Moisture Barrier: Cover the saline-moistened dressings with a clean, impermeable occlusive layer—such as sterile plastic wrap, sterile foil, or a taped impervious drape. This seals in moisture, prevents evaporation, and halts catastrophic evaporative heat loss (which rapidly triggers hypothermia).
4. Patient Positioning: Transport the patient supine with knees and hips flexed (place pillows or rolled blankets beneath the knees). Flexing the legs takes tension off the rectus abdominis and oblique muscles, decreasing intra-abdominal pressure and preventing further extrusion of bowel.

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Clinical Scenario: Sucking Chest Wound with Tension Conversion

A 22-year-old male is stabbed in the right anterior chest during an altercation. Paramedics arrive to find the patient sitting on a curb, tachypneic at 32/min, pale, and clutching his chest. A 3 cm bubbling, whistling wound is noted in the right 4th intercostal space at the anterior axillary line.

1. Primary Assessment & Initial Seal: The paramedic immediately covers the wound with a gloved hand, noting an immediate improvement in air exchange. A commercial vented chest seal is wiped onto the dried skin.
2. Sudden Deterioration: Three minutes into transport, the patient suddenly exhibits profound agitation, severe cyanosis, and air hunger. The SpO2 drops from 94% to 81%, BP plunges from 116/74 to 76/40 mmHg, and heart rate jumps to 142 bpm. Auscultation reveals completely absent breath sounds across the right chest, marked hyperresonance to percussion, and prominent jugular venous distention.
3. Recognition of Tension Conversion: The paramedic immediately recognizes that the open defect has converted into a tension pneumothorax due to internal clotting of the vent.
4. Emergency 'Burping' Intervention: The paramedic instantly peels back one corner of the vented chest seal. A dramatic rush of high-pressure air and blood escapes from the pleural defect. Within 30 seconds, the patient's breath sounds partially return, radial pulse volume improves, BP rises to 98/62 mmHg, and SpO2 climbs to 91% on high-flow oxygen.
5. Re-sealing & Level 1 Transport: The chest seal is cleaned of clots and resealed, and the paramedic monitors the patient continuously for recurring tension physiology during emergency transport to the trauma surgical centre.

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Exam Pitfalls & High-Yield Thoracoabdominal Pearls

• Applying Dry Dressings to an Evisceration: Applying dry gauze directly to exposed intestines causes the delicate bowel serosa to desiccate and adhere to the dressing, tearing the visceral wall upon removal; always apply sterile saline-moistened non-adherent dressings followed by an occlusive moisture barrier.
• Pushing Eviscerated Bowel Back In: Attempting to force protruding bowel loops back through an abdominal wall defect increases intra-abdominal pressure, causes ischemic strangulation, and contaminates the peritoneal cavity.
• Failing to Reassess Chest Seals: Always maintain a high index of suspicion for tension pneumothorax after placing an occlusive dressing or chest seal. If hemodynamics collapse, immediately 'burp' the dressing.
• Confusing Tamponade with Tension Pneumothorax: Both present with hypotension and JVD. Always check breath sounds and chest percussion: clear bilateral breath sounds point to cardiac tamponade, whereas absent unilateral sounds with hyperresonance confirm tension pneumothorax.
• Aggressively Restoring Normal Blood Pressure in Traumatic Aortic Rupture: Infusing large crystalloid volumes to achieve 'normal' blood pressure (e.g., SBP >120 mmHg) blows out the fragile adventitial hematoma containing an aortic tear, causing instant exsanguination; maintain permissive hypotension (SBP ~90 mmHg).