Free TCRN Exam Flashcards

Prevent hypoxemia and hypotension, maintain ventilation near normocapnia unless treating imminent herniation, and trend GCS, pupils, motor findings, oxygenation, and perfusion. A normal initial scan or examination does not replace serial reassessment because deterioration may be delayed.

An epidural hematoma is typically lens-shaped on CT and often arterial; a lucid interval may occur. An acute subdural hematoma is crescent-shaped and usually reflects torn bridging veins with associated brain injury. Neurologic decline with either requires immediate neurosurgical escalation.

Hypertension with widening pulse pressure, bradycardia, and irregular respirations is a late sign of critically increased intracranial pressure and possible herniation. It is not the expected pattern of uncomplicated hemorrhagic shock and demands immediate airway and neurosurgical action.

Brief controlled hyperventilation is a rescue bridge for signs of imminent herniation while definitive treatment is arranged. Routine or prolonged prophylactic hyperventilation can reduce cerebral blood flow; prioritize oxygenation, perfusion, head-neutral positioning, and prescribed hyperosmolar therapy.

Battle sign, periorbital ecchymosis, hemotympanum, or cerebrospinal fluid leakage from the nose or ear are warning findings. Avoid blind nasal tubes or nasotracheal instrumentation when skull-base or severe midface injury is suspected; use an oral route when indicated.

Place a rigid eye shield without pressure, keep the patient NPO, control pain and vomiting, and obtain urgent ophthalmologic care. Do not patch tightly, palpate the eye, measure intraocular pressure, remove an embedded object, or perform ocular ultrasound over a suspected open globe.

Neurogenic shock is distributive circulatory failure after spinal cord injury, classically hypotension with relative bradycardia and warm skin after hemorrhage is excluded. Spinal shock is temporary loss of motor, sensory, reflex, and autonomic function below the lesion; it describes neurologic physiology, not blood pressure.

The diaphragm depends on C3-C5 innervation, while intercostal and abdominal muscle weakness impairs ventilation and cough. Trend work of breathing, voice, secretion clearance, gas exchange, and respiratory strength; apparent early stability can precede fatigue and the need for a definitive airway.

Central cord syndrome typically causes greater motor weakness in the upper extremities than the lower extremities. Anterior cord syndrome causes motor loss plus loss of pain and temperature below the lesion while dorsal-column vibration and position sense are relatively preserved.

Suspect carotid or vertebral injury with an unexplained focal neurologic deficit, arterial neck bleeding or bruit, expanding hematoma, high-risk cervical or skull-base fractures, or a concerning neck-seatbelt mechanism. Escalate for protocol-based CT angiography and antithrombotic planning when bleeding risk permits.

Active or pulsatile bleeding, expanding hematoma, shock, bruit or thrill, air bubbling from the wound, airway compromise, major hemoptysis or hematemesis, and focal neurologic deficit require immediate operative and airway escalation. Do not blindly probe or clamp the wound.

Tension pneumothorax is a clinical diagnosis when unilateral breath-sound loss and respiratory distress progress to obstructive shock. Immediate decompression is required; needle or finger decompression is a bridge and should be followed by definitive tube thoracostomy as soon as feasible.

Cover the defect with a vented chest seal and give oxygen while arranging tube thoracostomy at a separate site. Continuously reassess for tension physiology; an occlusive seal that cannot vent may convert the injury to a tension pneumothorax.

Blood in the pleural space can cause both hemorrhagic shock and ventilatory compromise. Support circulation, place a chest tube, quantify output, and escalate urgently for operative control when the initial return is massive, bleeding persists, or transfusion needs continue.

Provide oxygenation, effective multimodal analgesia, pulmonary hygiene, and close monitoring for evolving respiratory failure. Do not bind the chest. Escalate to noninvasive or invasive ventilatory support when gas exchange or work of breathing fails rather than intubating solely because a flail segment exists.

The full Beck triad is often absent, especially with hypovolemia or positive-pressure ventilation. Suspect obstructive shock with jugular venous distention, muffled heart sounds, narrow pulse pressure, or unexplained arrest; bedside ultrasound supports the diagnosis, but unstable patients need immediate decompression or operative control.

High-energy deceleration or suggestive chest imaging warrants CT angiography in a hemodynamically stable patient. Once diagnosed, reduce aortic shear with carefully titrated impulse control when not contraindicated and obtain urgent trauma and vascular input; injury grade and associated injuries determine surveillance versus endovascular repair.

Hemodynamic response and peritoneal findings drive the decision more than injury grade alone. Stable patients without peritonitis may undergo monitored nonoperative management with serial examinations and possible angioembolization; persistent instability or peritonitis requires rapid hemorrhage control.

Early CT and examination findings may be subtle. Increasing abdominal pain, guarding, fever, leukocytosis, rising lactate, free air, bowel-wall abnormality, or mesenteric injury should raise concern for leakage or ischemia and trigger urgent surgical reassessment.

Consider it after major thoracoabdominal trauma when abdominal viscera appear in the chest, bowel sounds are heard above the diaphragm, or unexplained respiratory compromise persists. Gastric decompression may improve ventilation, but definitive management is surgical repair.

Center the binder over the greater trochanters, not the iliac crests, to reduce pelvic volume and stabilize the ring. Document application time, reassess distal perfusion and skin, and avoid repeatedly releasing the binder before a definitive plan is established.

Apply a correctly positioned binder, activate balanced blood-product resuscitation, prevent hypothermia, and move rapidly to definitive hemorrhage control. Angioembolization targets arterial bleeding, while preperitoneal packing or operative strategies may be needed for venous, bony, or associated intra-abdominal bleeding.

Blood at the meatus, inability to void, or perineal or scrotal hematoma after pelvic trauma warrants retrograde urethrography before blind urethral catheterization. A 'high-riding prostate' is neither sensitive nor required; use suprapubic drainage if directed when urethral disruption is confirmed.

Gross hematuria with pelvic trauma should prompt retrograde cystography when bladder injury is suspected. Intraperitoneal rupture usually requires operative repair; uncomplicated extraperitoneal rupture is often managed with catheter drainage, while bladder-neck injury or bone fragments may require surgery.

Pain out of proportion and pain with passive stretch are early warnings, followed by tense swelling and sensory or motor change. Normal pulses do not exclude compartment syndrome because arterial flow may persist; remove constriction and obtain immediate surgical evaluation for fasciotomy.

Control hemorrhage, document distal neurovascular status, cover with a sterile dressing, align and splint as indicated, and give early protocol-directed antibiotics and tetanus prophylaxis. Do not repeatedly inspect, irrigate aggressively at bedside, or push exposed bone back through the wound.

Wrap it in sterile saline-moistened gauze, seal it in a clean watertight bag, and place that bag in a second container with ice and water. Do not place tissue directly on ice, immerse it in water, scrub it, or delay care of the patient to manage the part.

Reperfusion can release potassium, acids, and myoglobin, causing dysrhythmia, shock, and acute kidney injury. Start early isotonic fluid when appropriate, monitor ECG, potassium, urine output, creatine kinase, and renal function, and treat hyperkalemia immediately according to protocol.

Children can maintain blood pressure through vasoconstriction and tachycardia despite substantial blood loss, then deteriorate rapidly when compensation fails. Use age-adjusted vital signs, mental status, skin perfusion, pulses, and urine output, and use weight-based equipment, medications, and blood products.

Beta-blockers, pacemakers, hypertension, frailty, and limited physiologic reserve can blunt tachycardia or make an apparently normal pressure misleading. Review anticoagulants, compare with baseline, trend perfusion and mentation, and maintain a low threshold for imaging and escalation after even low-energy mechanisms.

Maternal stabilization is the best initial fetal resuscitation: manage airway, oxygenation, ventilation, and hemorrhage first. After about 20 weeks, use manual left uterine displacement or left lateral tilt to reduce aortocaval compression while preserving spinal precautions and obtain obstetric and fetal assessment when feasible.

Count partial-thickness and full-thickness burns; do not count superficial erythema. Use a Lund-Browder chart for the most age-accurate estimate, especially in children; the patient's entire palmar hand is roughly 1% for scattered burns. Titrate resuscitation to response rather than a formula alone.

Standard pulse oximetry cannot distinguish oxyhemoglobin from carboxyhemoglobin and may be falsely reassuring. Give high-concentration oxygen, obtain co-oximetry, and consider early intubation when facial burns, soot, progressive hoarseness, stridor, or edema threaten the airway.

Protect staff, remove contaminated clothing and jewelry, brush away visible dry chemicals, then irrigate promptly and copiously with water unless a substance-specific protocol directs otherwise. Do not attempt bedside acid-base neutralization because the reaction can generate additional heat and injury.

Treat life threats first and obtain consent when possible. Minimize unnecessary handling, document findings and statements objectively, package dry items separately in paper rather than plastic, label and seal them, and record every transfer to maintain chain of custody under the facility's forensic protocol.

Use a rapid <C>ABCDE sequence to find and treat immediate threats: catastrophic hemorrhage, airway with spinal protection, breathing, circulation, disability, and exposure with temperature control. Interventions and reassessment occur simultaneously; any deterioration restarts the primary survey.

Begin only after immediate primary-survey threats are addressed and resuscitation is underway. Perform a head-to-toe examination and obtain AMPLE history: Allergies, Medications, Past history or Pregnancy, Last meal, and Events or Environment surrounding the injury.

Control bleeding rapidly while minimizing crystalloid, using warmed whole blood or balanced components according to the major-hemorrhage protocol. Track temperature, coagulation, fibrinogen, ionized calcium, acid-base status, and response, then transition from fixed ratios to laboratory-guided therapy when possible.

Citrate in blood products binds calcium; rapid transfusion can cause hypocalcemia, worsening hypotension, myocardial function, and coagulation. Monitor ionized calcium and ECG, and replace calcium promptly according to the massive-transfusion protocol rather than waiting for overt tetany or arrest.

Hypothermia, acidosis, coagulopathy, and hypocalcemia amplify one another during hemorrhagic shock. Break the cycle with rapid hemorrhage control, warmed blood-based resuscitation, temperature conservation, correction of calcium and coagulation deficits, and restoration of perfusion.

When protocol criteria for active or suspected major bleeding are met, give tranexamic acid as early as possible and no later than 3 hours after injury. Do not initiate it more than 3 hours after injury because late treatment may increase harm; follow the current trauma protocol for eligibility and dosing.

Restrictive pressure targets may limit bleeding before hemostasis, but inadequate pressure worsens cerebral ischemia. When significant TBI is the dominant problem, use a less restrictive strategy that preserves cerebral perfusion while pursuing hemorrhage control; individualize targets to the injury pattern and protocol.

Both can cause acute hypoxemia and bilateral pulmonary opacities. TRALI is noncardiogenic lung injury without circulatory overload; TACO reflects volume overload and more often includes hypertension, jugular venous distention, positive fluid balance, and improvement with diuresis. Stop the transfusion and initiate reaction protocol for either.

A deliberate repeat head-to-toe examination and review of imaging, laboratory results, procedures, and mechanism identifies injuries missed during resuscitation. Perform it after stabilization, commonly within 24 hours, and repeat focused examinations when the patient awakens, mobilizes, or reports new symptoms.

Treat new delirium as acute organ dysfunction: repeat the primary survey, check glucose, perform a focused neurologic assessment, and evaluate hypoxemia, hypoperfusion, intracranial complications, infection, withdrawal, medications, pain, retention, constipation, and other metabolic causes. Pair cause-directed treatment with orientation, sleep protection, sensory aids, early mobility, hydration, and avoidance of unnecessary restraints or sedatives.

Stabilize immediate airway, breathing, and hemorrhage threats without delaying definitive care for nonessential tests. Confirm acceptance, use direct clinician handoff, send imaging and records, secure tubes and lines, match transport capability to risk, and continue monitoring and resuscitation en route.

Confirm safe mobility, pain and medication plans, wound or device care, equipment, transport, caregiver capacity, and follow-up. Give written return precautions for worsening breathing, bleeding, fever, neurologic change, uncontrolled pain, or device problems, using teach-back and language-access support.

Triage categories are temporary because physiology, resources, hazards, and treatment capacity change. Reassess after movement or intervention and as resources evolve; the goal is the greatest overall survival benefit, not first-come-first-served care.

Identify a case through registry data, audit filters, event reports, or outcome review; analyze contributing system factors; implement a measurable corrective action; then monitor whether compliance and outcomes improve. Education without documented follow-up does not complete the loop.

Provide an appropriate medical screening examination and stabilizing treatment within the hospital's capability, regardless of insurance or ability to pay. If needed care exceeds capability, arrange an appropriate transfer with acceptance, records, qualified transport, and treatment to reduce transfer risk.