The Geriatric Trauma Patient: A Physiology of Frailty
Abstract
The geriatric trauma patient represents a unique and increasingly prevalent challenge in critical care medicine. With global demographic shifts toward an aging population, trauma centers are witnessing a paradigm shift where chronological age alone fails to predict outcomes. This review examines the multifaceted physiological vulnerabilities that define the elderly trauma patient, emphasizing frailty assessment over age-based triage, the complex interplay of polypharmacy, atypical clinical presentations, and the critical importance of early goals-of-care discussions. We explore evidence-based strategies for recognizing high-risk injury patterns from seemingly minor mechanisms and provide practical guidance for optimizing outcomes in this vulnerable population.
Keywords: Geriatric trauma, frailty index, polypharmacy, delirium, goals of care, ground-level falls
Introduction
The intersection of aging demographics and trauma care presents one of modern medicine's most pressing challenges. By 2050, the population aged 65 years and older is projected to reach 1.6 billion globally, representing 16% of the world's population.¹ In trauma centers across developed nations, patients over 65 now account for 30-40% of admissions, with disproportionately higher mortality rates—two to six times greater than their younger counterparts for comparable injury severity.²,³
The traditional approach to geriatric trauma, which relies heavily on chronological age as a prognostic indicator, has proven inadequate. Two 75-year-old patients may have vastly different physiological reserves, medication profiles, and functional trajectories. This heterogeneity demands a more nuanced understanding of the "physiology of frailty"—a state of decreased physiological reserve and increased vulnerability to stressors that transcends simple age categorization.⁴
This review synthesizes current evidence on five critical domains of geriatric trauma care: frailty assessment, polypharmacy risks, atypical presentations, goals-of-care communication, and high-risk injury patterns from low-energy mechanisms. Our aim is to equip critical care practitioners with actionable insights for improving outcomes in this complex patient population.
The Frailty Index: A More Important Predictor than Chronological Age
Defining Frailty in the Trauma Context
Frailty is a biological syndrome characterized by diminished strength, endurance, and physiological function that increases vulnerability to dependency and death.⁵ Unlike chronological age, which merely reflects time elapsed, frailty captures the cumulative impact of age-related deficits across multiple organ systems. In trauma, this distinction is critical: frail patients demonstrate impaired stress responses, prolonged inflammatory states, and diminished capacity for physiological compensation.⁶
Two dominant models define frailty in clinical practice:
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Fried's Phenotype Model: Identifies frailty through five criteria—unintentional weight loss, self-reported exhaustion, weakness (grip strength), slow walking speed, and low physical activity. Presence of three or more indicates frailty.⁷
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Rockwood's Cumulative Deficit Model: The Frailty Index (FI) quantifies the proportion of accumulated deficits from a comprehensive list of 30-70 variables, including comorbidities, functional limitations, and laboratory abnormalities.⁸
Evidence for Frailty as a Prognostic Tool
Multiple prospective studies have demonstrated frailty's superiority over age in predicting adverse outcomes after trauma:
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Mortality: A multicenter study of 1,284 geriatric trauma patients found that frailty (measured by modified Frailty Index-11) independently predicted in-hospital mortality (OR 2.8, 95% CI 1.9-4.1), while age showed no independent association when adjusted for frailty.⁹
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Complications: Joseph et al. demonstrated that each 0.1 increment in FI correlated with a 50% increase in major complications, including respiratory failure, acute kidney injury, and venous thromboembolism.¹⁰
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Functional Outcomes: Frail patients experience significantly higher rates of discharge to institutional care (57% vs. 23%, p<0.001) and failure to return to pre-injury functional status at 6 months (68% vs. 31%, p<0.001).¹¹
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Resource Utilization: Frailty predicts prolonged ICU length of stay (median 8 vs. 4 days, p=0.002) and increased hospital costs, even after controlling for injury severity.¹²
Practical Implementation of Frailty Screening
Pearl #1: The modified Frailty Index-5 (mFI-5) can be rapidly calculated at bedside using five variables: diabetes, hypertension requiring medication, congestive heart failure, dependent functional status, and chronic obstructive pulmonary disease. A score ≥2 indicates frailty and warrants heightened vigilance.
Several validated tools facilitate rapid frailty assessment in the acute setting:
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Modified Frailty Index (mFI-11): Derived from the Canadian Study of Health and Aging, this 11-item tool can be extracted from electronic medical records within minutes, incorporating variables such as diabetes, functional dependence, COPD, and impaired sensorium.¹³
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Clinical Frailty Scale (CFS): A 9-point pictorial scale ranging from "very fit" to "terminally ill," the CFS can be completed by nursing staff or paramedics during initial assessment. Scores ≥5 (mildly frail or worse) correlate with increased mortality.¹⁴
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Geriatric Trauma Outcome Score (GTOS): Combines age, ISS, and blood transfusion requirements to predict mortality, though it lacks the granularity of dedicated frailty indices.¹⁵
Oyster #1: Beware the "robust bias"—trauma teams may underestimate frailty in patients who appear well-groomed or articulate. Social presentation does not equate to physiological reserve. Always conduct objective frailty assessment.
Physiological Mechanisms Linking Frailty to Worse Outcomes
The frail elderly patient exhibits several pathophysiological vulnerabilities:
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Diminished Cardiac Reserve: Age-related myocardial stiffness and reduced β-adrenergic responsiveness limit compensatory tachycardia and contractility during hemorrhagic shock.¹⁶ Occult shock may occur at "normal" vital signs.
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Impaired Immune Function: Immunosenescence and chronic low-grade inflammation ("inflammaging") predispose to nosocomial infections, with pneumonia rates 2-3 times higher than in younger cohorts.¹⁷
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Sarcopenia: Loss of skeletal muscle mass and quality impairs ventilatory mechanics, mobilization, and wound healing. Sarcopenia, measurable via CT psoas muscle index, independently predicts mortality (HR 2.1, p=0.004).¹⁸
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Reduced Cerebral Autoregulation: Even mild hypotension (SBP 90-110 mmHg) can compromise cerebral perfusion, particularly in patients with chronic hypertension and shifted autoregulatory curves.¹⁹
Hack #1: In the frail trauma patient, maintain MAP targets 10-15 mmHg higher than traditional resuscitation endpoints. A MAP of 65 mmHg may be inadequate for chronically hypertensive elderly patients. Use clinical markers (mental status, urine output, lactate clearance) rather than rigid numerical thresholds.
Incorporating Frailty into Clinical Decision-Making
Frailty assessment should inform multiple aspects of care:
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Triage and Activation: Consider geriatric trauma team activation for patients with moderate frailty (mFI ≥2) even with mild injury patterns, as occult injuries and delayed decompensation are common.²⁰
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Monitoring Intensity: Frail patients benefit from ICU-level monitoring despite lower injury severity scores, given their propensity for sudden deterioration.²¹
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Transfusion Thresholds: While restrictive transfusion strategies benefit most trauma patients, frail elderly with limited cardiopulmonary reserve may require higher hemoglobin targets (8-9 g/dL) to maintain oxygen delivery.²²
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Prognostication: Integrate frailty indices into mortality prediction models alongside traditional injury scoring systems. The Geriatric Trauma Outcome Score, which combines age >65, ISS >15, and transfusion requirements, demonstrates superior discrimination (AUC 0.87) compared to ISS alone.²³
Polypharmacy in the Elderly Trauma Patient: The Dangers of Anticoagulants and Anticholinergics
The Scope of Polypharmacy
Polypharmacy, traditionally defined as concurrent use of five or more medications, affects 40-50% of community-dwelling elderly and up to 90% of nursing home residents.²⁴ In trauma populations, polypharmacy independently predicts adverse outcomes, with each additional medication conferring a 3-8% increase in mortality risk.²⁵
The mechanisms underlying polypharmacy-related harm include:
- Drug-drug interactions
- Adverse medication effects (falls, cognitive impairment)
- Therapeutic errors during acute hospitalization
- Physiological derangements complicating resuscitation
Anticoagulants: A Double-Edged Sword
Pearl #2: Approximately 30-35% of elderly trauma patients are taking anticoagulants at the time of injury. Pre-injury anticoagulation increases mortality by 30-40% across all injury severities, primarily through intracranial hemorrhage progression.
Warfarin
Warfarin remains widely prescribed for atrial fibrillation, prosthetic valves, and venous thromboembolism. Key considerations include:
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Intracranial Hemorrhage (ICH) Risk: Even minor head trauma in warfarin patients carries 15-20% risk of ICH, with delayed hemorrhage occurring up to 24-48 hours post-injury.²⁶ The American College of Emergency Physicians recommends CT imaging for all anticoagulated patients with head trauma, regardless of apparent severity.²⁷
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Reversal Strategies: Immediate reversal is paramount for patients with significant hemorrhage:
- 4-Factor Prothrombin Complex Concentrate (4F-PCC): First-line agent, dosed at 25-50 units/kg based on INR. Achieves INR <1.5 within 30 minutes in 95% of patients.²⁸
- Vitamin K: Administer 10 mg IV alongside PCC to prevent INR rebound (onset 6-12 hours, peak 24-48 hours).
- Fresh Frozen Plasma (FFP): Inferior to PCC due to slower INR correction, volume overload risk, and transfusion-related complications. Reserve for situations where PCC is unavailable.²⁹
Hack #2: Don't wait for INR results to initiate reversal in hemodynamically unstable warfarin patients with suspected hemorrhage. Give 4F-PCC empirically—the risk-benefit ratio overwhelmingly favors early administration. Time is brain, and time is blood volume.
Direct Oral Anticoagulants (DOACs)
DOACs—dabigatran (direct thrombin inhibitor), rivaroxaban, apixaban, and edoxaban (factor Xa inhibitors)—now account for 50-60% of anticoagulation prescriptions.³⁰ While touted for reduced ICH risk in atrial fibrillation trials, traumatic ICH risk remains substantial.
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Dabigatran: Idarucizumab (5 g IV, given as two 2.5 g doses) is a monoclonal antibody that immediately reverses dabigatran. Effectiveness approaches 100% within minutes.³¹ If idarucizumab is unavailable, consider activated prothrombin complex concentrate (aPCC, 50 units/kg) or hemodialysis (dabigatran is dialyzable due to low protein binding).
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Factor Xa Inhibitors: Andexanet alfa (low-dose regimen: 400 mg bolus + 4 mg/min × 120 min; high-dose regimen: 800 mg bolus + 8 mg/min × 120 min) specifically reverses rivaroxaban and apixaban.³² In the ANNEXA-4 trial, andexanet achieved 82% hemostatic efficacy.³³ However, cost ($50,000-70,000 per dose) and limited availability constrain use. Alternatives include:
- 4F-PCC: 50 units/kg, though evidence is limited and reversal incomplete.³⁴
- Tranexamic Acid (TXA): 1 g IV bolus may reduce hemorrhage expansion through antifibrinolytic effects, though this is off-label and evidence-based primarily on case series.³⁵
Oyster #2: Many elderly patients on DOACs have undiagnosed renal impairment, leading to drug accumulation and supra-therapeutic levels. Factor Xa activity assays correlate poorly with clinical bleeding risk. Treat based on clinical hemorrhage severity, not laboratory values.
Antiplatelet Agents
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Aspirin: Meta-analyses show conflicting results regarding mortality impact, with some studies suggesting increased ICH progression rates (RR 1.3-1.5) and others showing no effect.³⁶ No specific reversal agent exists; platelet transfusion is generally ineffective due to rapid aspirin-platelet binding.
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P2Y12 Inhibitors (clopidogrel, prasugrel, ticagrelor): Associated with 20-30% increased risk of ICH expansion and need for neurosurgical intervention.³⁷ Platelet transfusion (1-2 units) may be considered for life-threatening hemorrhage, though effectiveness is debated. Desmopressin (DDAVP, 0.3 mcg/kg IV) enhances platelet adhesion and may provide modest benefit.³⁸
Management Protocols
Establish institutional protocols addressing:
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Risk Stratification: All anticoagulated patients with moderate-energy trauma require CT head, even if GCS 15 and no external signs of injury. Consider extended observation (24-48 hours) with repeat imaging.²⁹
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Reversal Indications: Life-threatening hemorrhage, ICH of any size, or need for emergent surgery warrant immediate reversal. Weigh thrombotic risk (e.g., mechanical valve, recent VTE) against hemorrhagic risk in consultation with hematology.
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Thromboprophylaxis Resumption: Restart anticoagulation 48-72 hours post-injury if hemostasis secure and no operative interventions planned. Earlier resumption (24 hours) may be appropriate for high thrombotic risk after minor trauma.⁴⁰
Anticholinergic Medications: The Hidden Cognitive Threat
Medications with anticholinergic properties—including antihistamines (diphenhydramine), antipsychotics (quetiapine), antidepressants (amitriptyline), urinary antimuscarinics (oxybutynin), and antiemetics (promethazine)—are ubiquitous in geriatric prescribing. The cumulative anticholinergic burden independently predicts delirium, falls, and mortality.⁴¹
Pearl #3: *The Anticholinergic Cognitive Burden (ACB) scale rates medications from 0 (no anticholinergic activity) to 3 (definite anticholinergic activity). A cumulative ACB score ≥3 doubles delirium risk and increases 90-day mortality by 30%.*⁴²
Mechanisms of Harm in Trauma
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Delirium Precipitation: Anticholinergics impair central cholinergic neurotransmission, particularly in elderly with reduced cholinergic reserve and acetylcholine synthesis.⁴³ Post-traumatic delirium occurs in 30-50% of hospitalized elderly trauma patients, with anticholinergic burden as a major modifiable risk factor.
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Cognitive Impairment: Even in non-delirious patients, anticholinergic exposure impairs working memory, attention, and executive function—critical for participation in care, physical therapy, and informed consent discussions.⁴⁴
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Falls Risk: Anticholinergic-associated sedation, orthostatic hypotension, and impaired balance contribute to falls. A meta-analysis found dose-dependent increase in fall risk (OR 1.47 per one-point ACB score increase).⁴⁵
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Physiological Effects: Tachycardia (masking shock), urinary retention (complicating fluid monitoring), ileus (delaying enteral nutrition), and dry mouth (aspiration risk) all complicate trauma management.
Practical Deprescribing Strategies
Hack #3: On admission, audit all home medications using the ACB scale or Beers Criteria. Discontinue high-anticholinergic agents (diphenhydramine, first-generation antihistamines, tricyclic antidepressants) immediately unless absolutely essential. Substitute low-anticholinergic alternatives: trazodone for sleep, loratadine for allergies, mirtazapine for depression.
Key steps include:
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Medication Reconciliation: Obtain comprehensive medication list including over-the-counter drugs and supplements. Family members often provide more accurate information than patients.
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ACB Calculation: Use validated tools (ACB scale, Drug Burden Index) to quantify cumulative anticholinergic load.⁴⁶
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High-Risk Medications to Discontinue:
- Diphenhydramine (ACB=3): Common for sleep and pruritus. Substitute melatonin or trazodone.
- Oxybutynin (ACB=3): For overactive bladder. Consider mirabegron (β3-agonist) with minimal anticholinergic effects.
- Promethazine (ACB=3): For nausea. Use ondansetron or metoclopramide.
- Quetiapine low-dose (ACB=1-2): For sleep or agitation. Cautiously reduce or substitute.
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ICU Medication Vigilance: Avoid introducing new anticholinergics during hospitalization. Scopolamine patches, benztropine for dystonia, and hydroxyzine for anxiety are common culprits.
Other High-Risk Medications
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Beta-Blockers: Blunt compensatory tachycardia during hypovolemia, potentially masking shock. In the PROPPR trial subset analysis, pre-injury beta-blockade was associated with higher transfusion requirements before hemodynamic decompensation became apparent.⁴⁷ Consider higher fluid resuscitation thresholds and earlier blood product administration.
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ACE Inhibitors/ARBs: Exacerbate hypotension during hemorrhage and anesthesia. Hold on admission and resume once hemodynamically stable (typically 48-72 hours).
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Metformin: Risk of lactic acidosis in setting of renal hypoperfusion or contrast administration. Discontinue if creatinine >1.5 mg/dL or acute kidney injury develops.⁴⁸
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Benzodiazepines: Even at baseline, chronic benzodiazepine use predicts delirium, falls, and respiratory depression. Avoid abrupt withdrawal (seizure risk) but initiate gradual taper once stabilized.⁴⁹
Atypical Presentations: Delirium as the Primary Sign of Major Trauma
The Challenge of Atypical Presentations
Elderly trauma patients frequently present with nonspecific symptoms that obscure underlying injuries. Absent or diminished pain perception (due to neuropathy, cognitive impairment, or stoicism), impaired stress responses, and baseline functional limitations contribute to diagnostic uncertainty. Among atypical presentations, delirium stands as one of the most clinically significant and underrecognized manifestations of major trauma.
Delirium: Definition and Epidemiology in Trauma
Delirium is an acute, fluctuating disturbance in attention, awareness, and cognition not better explained by pre-existing neurocognitive disorder.⁵⁰ In elderly trauma populations, delirium affects 13-30% of emergency department patients and 30-60% of hospitalized patients.⁵¹,⁵²
Three clinical subtypes exist:
- Hyperactive (25%): Agitation, hallucinations, combativeness
- Hypoactive (25%): Lethargy, withdrawal, decreased responsiveness—often missed
- Mixed (50%): Alternating features⁵³
Oyster #3: *Hypoactive delirium is frequently misdiagnosed as depression, fatigue, or "just being old." It carries worse prognosis than hyperactive delirium due to delayed recognition and higher rates of aspiration, pressure injuries, and thromboembolic complications.*⁵⁴
Delirium as a Red Flag for Occult Injury
Delirium in the elderly trauma patient should never be dismissed as "expected" or "baseline." It often signals unrecognized injuries or complications:
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Occult Intracranial Hemorrhage: Subdural hematomas may present solely with confusion, particularly in anticoagulated patients. Even "trivial" head trauma warrants CT imaging when delirium is present. A retrospective study found that 28% of anticoagulated elderly patients with delirium after minor head trauma had ICH on imaging despite initial GCS 15.⁵⁵
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Hypoperfusion States: Shock may manifest as confusion before hypotension develops. Elderly patients with diminished cardiac reserve and chronic hypertension may maintain "normal" blood pressure (SBP 100-120 mmHg) despite significant intravascular volume depletion.⁵⁶
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Occult Fractures: Hip fractures (including non-displaced femoral neck, intertrochanteric, and pubic rami fractures), vertebral compression fractures, and rib fractures cause pain-associated delirium. A cohort study found 12% of elderly patients presenting with "mechanical fall" and confusion had occult hip fractures missed on initial plain radiographs.⁵⁷
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Systemic Infections: Post-traumatic pneumonia, urinary tract infections, and wound infections commonly present with delirium rather than fever or leukocytosis in the elderly.⁵⁸
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Metabolic Derangements: Hyponatremia (SIADH from head injury or pain), hypernatremia (dehydration), hypoglycemia, and uremia frequently precipitate delirium and may reflect underlying injury or inadequate resuscitation.⁵⁹
Pearl #4: In the confused elderly trauma patient, assume occult injury until proven otherwise. The triad of "confusion + minor mechanism + anticoagulation" mandates pan-CT imaging (head, C-spine, chest, abdomen/pelvis) regardless of clinical findings.
Pathophysiology of Trauma-Associated Delirium
Multiple mechanisms contribute:
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Neuroinflammation: Systemic inflammatory response syndrome (SIRS) following trauma promotes blood-brain barrier disruption and microglial activation, releasing pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) that impair neurotransmission.⁶⁰
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Neurotransmitter Imbalance: Decreased cholinergic activity and increased dopaminergic activity characterize delirium. Trauma-related stress hormones and medications further dysregulate these systems.⁶¹
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Cerebral Hypoperfusion: Even transient hypotension or hypoxemia during resuscitation can trigger delirium in vulnerable elderly brains with impaired autoregulation.⁶²
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Pain and Immobilization: Inadequate analgesia and prolonged bed rest contribute to delirium through stress responses and sensory deprivation.⁶³
Diagnosis and Screening
Early recognition requires systematic screening:
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Confusion Assessment Method (CAM): The most validated tool, assessing four features:
- Acute onset and fluctuating course
- Inattention
- Disorganized thinking
- Altered level of consciousness
Delirium is diagnosed when features 1 and 2 are present, plus either 3 or 4. Sensitivity 94%, specificity 89%.⁶⁴
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CAM-ICU: Modified for ventilated or critically ill patients, using nonverbal assessments.⁶⁵
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4AT (4-Item Assessment Test): Rapid screen (<2 minutes) evaluating alertness, cognition, attention, and acute change. Score ≥4 indicates possible delirium. Easier to use than CAM in busy emergency departments.⁶⁶
Hack #4: Train triage nurses to administer the 4AT on all patients ≥65 years. A positive screen triggers heightened diagnostic vigilance and consideration of extended imaging protocols. Early delirium detection reduces time to injury identification by an average of 4-6 hours.
Management of Delirium in Trauma
A multicomponent approach is essential:
1. Identify and Treat Underlying Causes
- Complete imaging: CT head (non-contrast), CT C-spine (if mechanism or exam concerning), chest X-ray minimum; consider CT chest/abdomen/pelvis for moderate-energy mechanisms
- Laboratory evaluation: CBC, comprehensive metabolic panel, coagulation studies, lactate, troponin, urinalysis, blood cultures if febrile
- Medication review: Eliminate delirogenic medications (anticholinergics, benzodiazepines, opioids if possible)
2. Non-Pharmacological Interventions (First-Line)
The HELP (Hospital Elder Life Program) bundle reduces delirium incidence by 30-40%:⁶⁷
- Reorientation: Clocks, calendars, familiar objects; frequent reorientation by staff ("Good morning Mr. Smith, I'm nurse Jones. You're in the hospital after a fall.")
- Sleep Hygiene: Minimize nighttime disruptions, reduce ambient noise and light, avoid waking for non-essential vital signs or medications
- Early Mobilization: Physical therapy within 24-48 hours, even if just sitting at bedside or standing with assistance
- Vision/Hearing Optimization: Ensure eyeglasses and hearing aids are available and functional
- Cognitive Stimulation: Conversation, television, music per patient preference
- Adequate Nutrition and Hydration: Oral intake preferred over IV when safe; involve family in feeding assistance
3. Pharmacological Management (Use Sparingly)
Reserve for severe agitation posing safety risks (e.g., pulling invasive lines, combativeness preventing care):
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Antipsychotics:
- Haloperidol 0.5-1 mg IV/PO q6-8h PRN (first-line for agitation; check QTc before use)
- Quetiapine 12.5-25 mg PO q12-24h (if oral route available, useful for sundowning, but has anticholinergic effects)
- Caution: Antipsychotics increase mortality risk in elderly (FDA black box warning) and may prolong delirium. Use lowest effective dose for shortest duration.⁶⁸
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Dexmedetomidine: 0.2-0.7 mcg/kg/hr infusion in ICU setting. α2-agonist with sedative properties but no anticholinergic effects. May reduce delirium duration compared to benzodiazepines in ventilated patients.⁶⁹
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Avoid Benzodiazepines: Except for alcohol or benzodiazepine withdrawal, these agents worsen delirium, prolong ICU stay, and increase mortality.⁷⁰
4. Pain Management
Adequate analgesia prevents delirium but opioid minimization is ideal:
- Acetaminophen: 1 g PO/IV q6h (reduce dose if hepatic impairment or weight <50 kg)
- Regional Anesthesia: Nerve blocks (femoral, fascia iliaca, rib blocks) provide superior analgesia with fewer systemic effects for extremity and chest wall fractures⁷¹
- Tramadol with Caution: Low opioid-sparing strategy, but carries serotonin syndrome and seizure risk, particularly with SSRIs⁷²
- Avoid High-Dose Opioids: If necessary, prefer short-acting agents (oxycodone, morphine) over long-acting (methadone, extended-release formulations) to allow titration
Prognostic Implications
Delirium is not a benign, self-limited condition. Outcomes include:
- Increased Mortality: In-hospital mortality 20-30% in delirious vs. 5-10% in non-delirious elderly trauma patients⁷³
- Prolonged Hospital Stay: Average 5-10 additional days⁷⁴
- Functional Decline: 40-50% of patients with delirium fail to return to baseline functional status at 6 months⁷⁵
- Long-Term Cognitive Impairment: Delirium accelerates dementia onset and progression⁷⁶
- Institutionalization: 2-3 times higher rates of discharge to long-term care facilities⁷⁷
Goals of Care Conversations in the Emergency Department: Aligning Treatment with Prognosis
The Imperative for Early Conversations
Geriatric trauma care often occurs at the intersection of aggressive resuscitation and end-of-life planning. Survival after major trauma declines precipitously with age: mortality exceeds 30-40% for elderly patients with Injury Severity Score (ISS) >15, and those who survive frequently experience permanent functional decline, loss of independence, and prolonged suffering.⁷⁸,⁷⁹
Despite poor prognoses, elderly trauma patients are often subjected to aggressive, non-beneficial interventions due to:
- Time pressures in emergency settings ("treat first, talk later")
- Uncertainty about patient preferences
- Medicolegal concerns
- Prognostic uncertainty
- Institutional culture favoring aggressive intervention⁸⁰
Early, compassionate goals-of-care (GOC) discussions in the emergency department can align treatment intensity with patient values, potentially preventing non-beneficial suffering while preserving autonomy.
Pearl #5: GOC conversations are not about "giving up" or withholding care—they're about ensuring the patient receives the right care. Framing matters: "We want to make sure everything we do matches what matters most to you" is more effective than "Do you want us to do everything?"
Ethical Frameworks and Principles
GOC discussions rest on core bioethical principles:
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Autonomy: Respecting patients' right to make informed decisions about their care based on personal values, even if those decisions differ from medical recommendations.
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Beneficence: Providing treatments that offer meaningful benefit, defined by the patient's quality-of-life goals rather than purely physiological endpoints.
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Non-Maleficence: Avoiding interventions likely to cause harm without commensurate benefit (e.g., ICU admission for futile care in a patient desiring comfort).
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Justice: Appropriate resource allocation, recognizing that intensive interventions for patients unlikely to benefit may limit resources for others.⁸¹
Prognostic Tools to Inform Conversations
Accurate prognostication helps frame realistic expectations:
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Geriatric Trauma Outcome Score (GTOS): Predicts in-hospital mortality using age >65, ISS >15, and packed red blood cell transfusion ≥5 units. Presence of all three confers 80-90% mortality.⁸²
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Modified Frailty Index: As discussed previously, mFI ≥3 predicts 30-day mortality of 20-35% and 6-month functional decline in >60%.⁸³
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TRISS (Trauma and Injury Severity Score): Incorporates age, ISS, Revised Trauma Score, and mechanism. Well-validated but may underestimate geriatric mortality.⁸⁴
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Physiological Derangement: Presenting lactate >4 mmol/L, base deficit <-6, and need for massive transfusion predict mortality exceeding 50% in elderly trauma patients.⁸⁵
Oyster #4: Prognostic scores are population-level tools, not individual deterministic predictors. Avoid statements like "You have a 70% chance of dying"—this is both inaccurate (confidence intervals are wide) and unhelpful (patients focus on the 30% survival chance, even if that survival involves prolonged ICU stay and permanent dependency).
Communication Strategies: The SPIKES Protocol Adapted for Trauma
The SPIKES framework, originally developed for oncology, translates effectively to trauma GOC discussions:⁸⁶
S - Setting
- Private Space: Move to quiet room away from trauma bay chaos; include family if patient wishes and time permits
- Sit Down: Physical positioning signals importance and unhurried presence
- Involve Key People: Patient (if conscious and competent), healthcare proxy, family members
- Minimize Interruptions: Silence pagers, ask colleagues to cover
P - Perception
Begin by assessing understanding:
- "What have you been told so far about your injuries?"
- "What's your understanding of how serious this is?"
This reveals baseline knowledge and corrects misconceptions before introducing new information.
I - Invitation
Determine howmuch information the patient wants:
- "Would you like me to explain in detail what we've found and what to expect, or would you prefer I talk with your family?"
- Most patients desire full information, but some prefer limited details or delegation to family
Hack #5: Many elderly patients defer decision-making to adult children. Explicitly ask, "Who would you like to be involved in making decisions about your care?" This respects cultural and family dynamics while maintaining patient autonomy.
K - Knowledge
Deliver information in clear, jargon-free language:
- Warning Shot: "I'm afraid I have some serious news..."
- Direct but Compassionate: "The CT scan shows significant bleeding in your brain. This type of injury is very serious in anyone, but particularly concerning given your age and the blood thinners you take."
- Small Chunks: Pause frequently to allow information to be absorbed and processed
- Avoid Statistics: Numbers are poorly understood under stress. Use qualitative terms: "Many patients with these injuries don't survive" rather than "Mortality is 65%."
E - Empathy
Acknowledge emotional responses explicitly:
- "I can see this is overwhelming news."
- "I wish the situation were different."
- Silence: Allow space for emotions without rushing to fill pauses with medical information
Use the NURSE mnemonic:⁸⁷
- Name the emotion: "This sounds frightening"
- Understand: "Anyone would feel this way"
- Respect: "You've been through so much"
- Support: "We're going to be with you through this"
- Explore: "Tell me what concerns you most"
S - Strategy and Summary
Collaboratively develop a treatment plan aligned with patient values:
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Explore Values and Priorities:
- "What's most important to you in your life?"
- "Are there things you would consider worse than dying?" (e.g., permanent ventilator dependence, severe cognitive impairment, inability to recognize family)
- "If your health situation worsens, what abilities would you need to maintain for life to feel meaningful?"
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Present Options Within Medical Appropriateness:
- Full Intensive Care: "We can pursue all possible treatments—ICU monitoring, breathing machine if needed, CPR if your heart stops. Given your injuries and frailty, there's a significant chance these won't restore you to the life you had before."
- Selective Treatment: "We can provide intensive treatments focused on recovery—surgery if beneficial, ICU care—but agree that if you're not improving or if complications develop that would leave you with severe disability, we would shift to comfort."
- Comfort-Focused Care: "We can focus entirely on keeping you comfortable, treating pain and symptoms, spending time with family, without pursuing treatments that would prolong dying."
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Make Recommendations: GOC discussions are not a menu where clinicians remain neutral. Patients and families often need guidance:
- "Based on what you've told me about your values and what we know about your injuries, I would recommend focusing on comfort and quality time with family. Intensive treatment is unlikely to allow you to return to living independently, which you've said is essential to you."
- Frame recommendations around what will be provided, not withheld: "We will make sure you're comfortable, not in pain, and surrounded by your loved ones."
Pearl #6: The question "Do you want us to do everything?" is unhelpful and often misleading. Patients interpret "everything" as "every possible beneficial treatment," while clinicians may mean "every physiologically possible intervention regardless of benefit." Replace with: "What would be most important to you if your condition worsens—extending life as long as possible, or focusing on comfort and quality of life?"
Practical Barriers and Solutions
Time Constraints
Barrier: Emergency departments are fast-paced; trauma teams feel pressure to "save first, talk later."
Solution:
- Designate a team member (social worker, palliative care consultant, senior physician not actively resuscitating) to initiate conversations in parallel with stabilization
- Brief conversations (5-10 minutes) establishing general goals are sufficient initially; detailed discussions can occur once stabilized
- Use closed-loop communication: One physician manages resuscitation while another speaks with family
Prognostic Uncertainty
Barrier: Outcomes are uncertain; clinicians fear "getting it wrong."
Solution:
- Frame uncertainty honestly: "It's difficult to predict exactly what will happen, but I can tell you that most patients with these injuries either don't survive or face prolonged recovery with significant disability."
- Use time-limited trials: "Let's pursue intensive treatment for the next 48-72 hours and see how you respond. If you're not improving or if complications develop, we'll revisit whether continuing makes sense."⁸⁸
Decision-Making Capacity
Barrier: Many elderly trauma patients have impaired consciousness, delirium, or baseline dementia.
Solution:
- Identify surrogate decision-makers immediately (healthcare proxy, next of kin)
- Ask surrogates to use substituted judgment: "What would your father want in this situation?" rather than "What do you want us to do?"
- Review advance directives if available (POLST, living will, healthcare proxy designation)
- If no surrogate and no advance directive, two physicians can document decision-making incapacity and proceed with best-interest standard⁸⁹
Family Conflict
Barrier: Family members disagree about appropriate treatment or disagree with patient's stated wishes.
Solution:
- Seek consensus around shared goals rather than specific interventions
- Acknowledge all perspectives: "I hear that some of you are hoping for full treatment, while others are concerned about suffering. You all love your mother and want what's best."
- Refocus on patient's voice: "Your mother completed a healthcare proxy form designating John as decision-maker. While we value everyone's input, we need to follow her legally documented wishes."
- Involve ethics consultation or palliative care for mediation⁹⁰
Documentation
Thorough documentation protects providers and ensures care continuity:
- Quote patient/surrogate statements about values and preferences
- Document prognostic information shared
- Record recommendations made and reasoning
- Specify code status, treatment limitations, and conditions for re-evaluation
- Note all participants in discussion
Example note: "GOC discussion held with patient and daughter (healthcare proxy) at bedside for 20 minutes. Explained patient has severe traumatic brain injury with large subdural hematoma, currently on warfarin. Discussed high mortality risk (>60%) and likelihood of severe permanent disability if survives. Patient stated quality of life most important value; expressed that living in nursing home unable to recognize family would be unacceptable. Daughter confirmed this consistent with mother's longstanding wishes. Discussed options including ICU with full treatment vs. comfort-focused care. Both patient and proxy agreed to pursue comfort measures only with no CPR, intubation, or ICU transfer. Order sets updated to reflect DNR/DNI. Palliative care consulted. Family expressed appreciation for honest conversation."
Pediatric Considerations: The "Elderly Orphan"
Oyster #5: *Approximately 20-25% of elderly adults have no living children or close family members—the "elderly orphan" phenomenon. These patients are at high risk for receiving unwanted aggressive care or, conversely, premature withdrawal of beneficial treatment due to lack of advocacy. Early involvement of social work, ethics, and palliative care is critical.*⁹¹
Palliative Care Integration
Palliative care consultation improves outcomes in geriatric trauma:
- Reduced ICU length of stay (median 8 vs. 13 days, p=0.003)⁹²
- Decreased hospital costs without increased mortality⁹³
- Improved symptom management and family satisfaction⁹⁴
- Higher rates of documentation of advance directives⁹⁵
Trigger criteria for palliative care consultation:
- Age ≥75 with ISS >15
- Frailty index ≥3
- Need for mechanical ventilation >48 hours
- Any patient/family requesting GOC discussion
- Intractable pain or symptom burden
- Anticipated prolonged ICU stay or discharge to long-term care⁹⁶
Hack #6: Introduce palliative care as "an extra layer of support" rather than end-of-life care. Many patients and families misunderstand palliative care as "giving up." Explain: "Palliative care specialists help manage pain and symptoms while we pursue treatment. They're experts in making sure you're comfortable through this process."
The High Risk of Ground-Level Falls: Aortic and Spinal Cord Injuries in the Elderly
Redefining "Minor Trauma" in the Elderly
Ground-level falls (GLFs)—falls from standing height or less—account for 65-80% of geriatric trauma admissions.⁹⁷ Historically dismissed as "low-energy" or "minor" mechanisms, GLFs in elderly patients produce surprisingly severe injuries, including those traditionally associated with high-energy trauma in younger populations.
Several factors explain this paradox:
- Reduced Protective Reflexes: Slowed reaction times and impaired balance prevent effective bracing during falls
- Osteoporosis: Decreased bone mineral density lowers the force threshold for fractures
- Vascular Fragility: Age-related elastin degradation and atherosclerosis make vessels susceptible to laceration from minimal shear stress
- Anticoagulation: As previously discussed, 30-35% of elderly patients take anticoagulants, dramatically increasing hemorrhage risk⁹⁸
- Sarcopenia: Loss of protective muscle mass around vital structures
Pearl #7: Never use mechanism of injury alone to determine imaging in elderly trauma patients. A 85-year-old on apixaban who falls from standing warrants similar imaging consideration as a 25-year-old falling from 10 feet.
Traumatic Aortic Injury: Not Just for Motor Vehicle Crashes
Traumatic aortic injury (TAI), specifically blunt aortic injury involving the descending thoracic aorta, classically occurs in high-speed deceleration motor vehicle crashes. However, case series increasingly document TAI following GLFs in elderly patients.⁹⁹,¹⁰⁰
Pathophysiology in the Elderly
The aging aorta undergoes structural changes predisposing to injury:
- Intimal Thickening: Creates shear planes between layers
- Medial Degeneration: Loss of elastin and smooth muscle integrity
- Calcification: Rigid, brittle vessel walls unable to absorb deceleration forces
- Ectasia/Aneurysmal Changes: Pre-existing aortic dilation creates stress points¹⁰¹
During a GLF, rotational forces and sudden deceleration at the aortic isthmus (the fixed point where the mobile aortic arch meets the tethered descending aorta) generate sufficient shear to tear the diseased aortic wall.¹⁰²
Clinical Presentation and Diagnosis
TAI presentation in elderly GLF victims differs from younger high-energy trauma:
- Subtle or Absent Signs: Only 30-40% have external thoracic trauma (bruising, abrasions)¹⁰³
- "Normal" Vital Signs: Contained hematomas may not cause immediate hemodynamic instability
- Nonspecific Symptoms: Back pain, chest discomfort, or dyspnea easily attributed to musculoskeletal injury or anxiety
Oyster #6: *The classic teaching of "widened mediastinum on chest X-ray" performs poorly in elderly patients. Tortuous ectatic aortas, atherosclerotic calcification, and poor-quality portable radiographs limit sensitivity (60-70%). CT angiography of the chest is the gold standard for any concerning mechanism.*¹⁰⁴
Imaging Indications
The Eastern Association for the Surgery of Trauma (EAST) guidelines recommend CT angiography (CTA) chest for blunt trauma patients with:¹⁰⁵
- Abnormal chest X-ray (widened mediastinum, abnormal aortic contour, pleural capping)
- High-risk mechanism (in elderly, redefine to include GLFs with any chest impact)
- Hypotension (SBP <90 mmHg) after blunt trauma
- Severe multisystem injuries
Liberalize these criteria in elderly patients: Consider CTA chest for any GLF patient who:
- Is anticoagulated
- Has chest wall tenderness or fractures (including rib fractures)
- Reports chest or back pain
- Has unexplained hypotension
- Has falling backward mechanism (direct spine/posterior chest impact)¹⁰⁶
TAI Grading and Management
The Society for Vascular Surgery grades TAI:¹⁰⁷
- Grade I: Intimal tear
- Grade II: Intramural hematoma
- Grade III: Pseudoaneurysm
- Grade IV: Rupture (usually fatal in prehospital setting)
Management:
- Grade I: Medical management with strict blood pressure control (target SBP <120 mmHg, HR <80 bpm) using beta-blockers (esmolol, labetalol); serial imaging at 24-48 hours, 1 week, and 3 months. Many heal spontaneously.¹⁰⁸
- Grade II-III: Thoracic endovascular aortic repair (TEVAR) is standard of care. Preferred over open repair due to significantly lower mortality (5-10% vs. 25-30%) and morbidity.¹⁰⁹
- Timing: Historically, emergent repair was advocated. Current practice favors delayed repair (24-72 hours) after stabilization of other injuries and optimization of comorbidities, unless uncontrolled hemorrhage or hemodynamic instability.¹¹⁰
Hack #7: In elderly patients with TAI, aggressive blood pressure control is critical. Use short-acting titratable agents (esmolol infusion: load 500 mcg/kg over 1 min, then 50-300 mcg/kg/min). Avoid fluid boluses that increase aortic wall stress. Permissive hypotension (SBP 90-100 mmHg) is acceptable if end-organ perfusion adequate.
Spinal Cord Injury Without Radiographic Abnormality (SCIWORA) and Central Cord Syndrome
Central Cord Syndrome in the Elderly
Central cord syndrome (CCS), first described by Schneider in 1954, classically occurs after hyperextension injury in patients with pre-existing cervical stenosis.¹¹¹ The elderly are particularly vulnerable due to:
- Cervical Spondylosis: Degenerative changes (osteophytes, ligamentum flavum hypertrophy, disc herniations) narrow the spinal canal
- Cervical Stenosis: Reduced anterior-posterior diameter of canal, often asymptomatic until trauma
- Reduced Cord Perfusion: Atherosclerosis and age-related vascular changes limit ischemic tolerance¹¹²
During hyperextension (e.g., backward fall striking occiput), the spinal cord is compressed between anterior osteophytes and posteriorly buckled ligamentum flavum. Central gray matter (watershed vascular zone) suffers ischemic-contusive injury.¹¹³
Clinical Features
CCS presents with characteristic motor and sensory patterns:
- Upper Extremity Weakness > Lower Extremity: Due to somatotopic organization of lateral corticospinal tract (cervical motor neurons are medial, lumbar lateral)
- Hand Weakness Out of Proportion: Fine motor dysfunction (grip strength, finger dexterity) more affected than proximal strength
- Variable Sensory Loss: Often "cape-like" distribution over shoulders/upper arms; may have sacral sparing
- Bladder Dysfunction: Urinary retention common, often requiring catheterization¹¹⁴
Pearl #8: *The "dropped smartphone" sign: Elderly patients who fall, sustain no obvious fractures, but report inability to grip or use their phone likely have CCS. This subtle presentation delays diagnosis by an average of 12-24 hours when not recognized in the emergency department.*¹¹⁵
Diagnosis
- MRI: Gold standard, demonstrating cord edema, hemorrhage (hematomyelia), or compression. T2 hyperintensity indicates edema/ischemia; T1 hypointensity suggests hemorrhage or chronic injury.¹¹⁶
- CT: May show pre-existing stenosis, fractures, or facet dislocation but cannot visualize cord pathology
- Clinical Diagnosis: CCS remains a clinical diagnosis; up to 20-30% of cases show no MRI abnormality (SCIWORA—spinal cord injury without radiographic abnormality), particularly in early imaging (<24 hours post-injury)¹¹⁷
Oyster #7: Negative initial MRI does not exclude CCS. If clinical suspicion remains high (characteristic motor pattern, hyperextension mechanism), repeat MRI at 48-72 hours. Early images may miss evolving cord edema.
Management
CCS management remains controversial:
Medical Management:
- Hemodynamic Augmentation: Mean arterial pressure (MAP) targets of 85-90 mmHg for 5-7 days improve spinal cord perfusion, though evidence is mixed.¹¹⁸ Use vasopressors (norepinephrine preferred) rather than excessive fluids in elderly with limited cardiac reserve.
- Corticosteroids: NOT RECOMMENDED. The NASCIS trials showing methylprednisolone benefit for acute spinal cord injury have been widely criticized for methodological flaws, and steroids increase complications (pneumonia, gastrointestinal bleeding, hyperglycemia) without clear benefit.¹¹⁹
- Prevent Secondary Injury: Avoid hypotension, hypoxemia, hyperthermia; maintain cervical alignment with collar or traction if indicated
Surgical Decompression:
- Timing Controversy: Early surgery (<24 hours) vs. delayed surgery (>24 hours to weeks) is debated. Meta-analyses suggest early decompression may improve neurological recovery, particularly for grade 1-3 ASIA scale injuries (incomplete injuries).¹²⁰
- Patient Selection: Consider surgery for patients with:
- Progressive neurological deterioration
- Significant canal compromise (>50%)
- Fracture or dislocation requiring reduction
- Failure to improve with medical management
- Elderly Considerations: Frailty, comorbidities, and risks of general anesthesia must be weighed. Shared decision-making essential.¹²¹
Prognosis
CCS generally has the best prognosis among incomplete spinal cord injuries:
- Motor Recovery: Lower extremities recover first and most completely (>90% regain ambulation), followed by proximal upper extremities, with hand function recovering last and least completely (60-70%)¹²²
- Functional Independence: 50-70% achieve functional independence at 1 year
- Elderly Outcomes: Age >50, initial ASIA A-B grade (complete/near-complete), and frailty predict worse recovery. Only 30-40% of frail elderly with CCS return to independent living.¹²³
Cervical Spine Fractures from Ground-Level Falls
Specific fracture patterns merit attention:
Odontoid (C2) Fractures
- Type II (fracture at base of dens): Most common in elderly, high nonunion rate (40-60%) with conservative management
- Presentation: Neck pain, occipital headache; neurological deficits uncommon unless displaced
- Management: Type II fractures are often managed surgically (anterior screw fixation or posterior C1-C2 fusion) in younger patients, but elderly often treated conservatively with halo vest or rigid collar due to surgical risks¹²⁴
Atlanto-Occipital Dislocation (AOD)
- Rare but increasingly recognized with improved imaging; historically considered fatal
- Mechanism: Hyperextension or flexion with distraction
- Imaging: Basion-dens interval (BDI) >12 mm on CT suggests AOD¹²⁵
- Management: Immediate immobilization, halo or surgical fusion
Subaxial Fractures (C3-C7)
- Extension teardrop fractures, facet dislocations, and burst fractures occur in osteoporotic spines with minimal force
- Ankylosing Spondylitis and DISH (Diffuse Idiopathic Skeletal Hyperostosis): Create "brittle spine" susceptible to unstable fractures and epidural hematomas from minor trauma¹²⁶
Hack #8: The "nexus-negative" elderly patient may still harbor occult cervical spine injury. If any neck pain, midline tenderness, or neurological symptoms, proceed to CT cervical spine. Plain radiographs are inadequate in the elderly due to degenerative changes obscuring fractures.
Thoracolumbar Fractures and Osteoporotic Compression Fractures
Compression Fractures
- Occur in 25-30% of women >65 years; many are asymptomatic until trauma aggravates them¹²⁷
- Presentation: Back pain, kyphosis, rarely neurological deficits (unless severe collapse or retropulsion)
- Red Flags for Instability:
-
50% vertebral body height loss
- Posterior column involvement (facet fracture, laminar fracture)
- Neurological deficits
- Multiple contiguous fractures
-
Management
- Conservative: Analgesia, bracing (TLSO), early mobilization for stable fractures
- Vertebroplasty/Kyphoplasty: Cement augmentation for refractory pain. Controversial due to mixed evidence of benefit over sham procedures, but may facilitate early mobilization in selected patients.¹²⁸
- Surgical Fixation: Reserved for unstable fractures with neurological compromise
Clinical Approach to Ground-Level Falls
Systematic Assessment Protocol:
- High Index of Suspicion: Never dismiss GLFs as "minor" in elderly patients
- Detailed Mechanism: Precisely document fall direction (forward/backward/sideways), surface struck, loss of consciousness, ability to break fall
- Medication Review: Anticoagulation status immediately; hold and consider reversal if significant injury
- Comprehensive Imaging: Liberal CT imaging protocols
- CT Head: All patients on anticoagulation or with any head strike; consider for all >80 years regardless of mechanism¹²⁹
- CT C-Spine: Neck pain, midline tenderness, neurological symptoms, or inability to clear clinically
- CT Chest: Chest wall tenderness, rib fractures, back pain, dyspnea, or concerning mechanism
- CT Abdomen/Pelvis: Abdominal pain/tenderness, pelvic pain, hematuria, or hemodynamic instability
- Serial Examinations: Delayed bleeding, particularly ICH, occurs in 5-8% of anticoagulated patients within 24-48 hours¹³⁰
- Functional Assessment: Baseline functional status vs. current; early physical therapy evaluation
- Falls Assessment: Identify and address intrinsic (gait instability, vision, neuropathy) and extrinsic (rugs, poor lighting, footwear) risk factors to prevent recurrence¹³¹
Conclusion: A Paradigm Shift in Geriatric Trauma Care
The geriatric trauma patient challenges traditional emergency and critical care paradigms. Chronological age, mechanism of injury, and initial vital signs—reliable predictors in younger populations—fail to capture the complexity of the frail elderly patient's vulnerability. This review highlights five domains demanding revised approaches:
-
Frailty supersedes age as a prognostic marker. Rapid, validated frailty screening should be integrated into trauma activation protocols, informing triage, monitoring intensity, and prognostication.
-
Polypharmacy, particularly anticoagulation and anticholinergic burden, substantially amplifies injury severity and complicates management. Immediate medication reconciliation, aggressive anticoagulant reversal when indicated, and systematic deprescribing improve outcomes.
-
Atypical presentations, especially delirium, often herald occult injuries. Systematic delirium screening with validated tools (CAM, 4AT) should trigger comprehensive diagnostic workups rather than dismissal as "expected" confusion.
-
Goals-of-care conversations belong in the emergency department, not just the ICU. Structured communication frameworks (SPIKES), prognostic tools, and early palliative care integration ensure treatment aligns with patient values and prevents non-beneficial suffering.
-
Ground-level falls produce devastating injuries traditionally associated with high-energy mechanisms. Traumatic aortic injuries, central cord syndrome, and cervical fractures occur with surprising frequency, demanding liberal imaging protocols and heightened vigilance.
Final Pearls and Oysters
Pearl #9: Create institutional geriatric trauma pathways integrating frailty screening, pharmacist consultation, delirium prevention bundles, early palliative care triggers, and liberalized imaging criteria. Multidisciplinary collaboration improves outcomes more than any single intervention.
Pearl #10: The frail elderly trauma patient often presents providers with their most emotionally challenging cases—balancing hope with realism, autonomy with beneficence, and aggressive intervention with compassionate restraint. These conversations and decisions represent some of medicine's most profound moments. Seek support from colleagues, ethics consultants, and palliative care specialists when uncertain.
Oyster #8: The greatest error in geriatric trauma care is not missed injuries or technical complications—it's failure to understand and honor what matters most to the patient. A 90-year-old who survives ICU admission only to spend her final months in a nursing home with delirium and dependence may have experienced a worse outcome than death, particularly if she clearly expressed wishes for quality over quantity of life.
Hack #9: Develop a "geriatric trauma champion" role in your institution—a physician, APP, or nurse with specialized training who rounds on elderly trauma patients, facilitates multidisciplinary care, and mentors colleagues in geriatric-specific management nuances.
Hack #10: When in doubt, ask the patient (or surrogate): "If we could return you to exactly how you were before this injury, would you want us to pursue all possible treatments to achieve that?" vs. "If treatments might save your life but leave you unable to walk, recognize family, or live independently, would you still want them?" These questions rapidly clarify values and guide decisions.
Key Take-Home Messages
- Frailty indices predict outcomes more accurately than age; implement routine screening
- Anticoagulated elderly require aggressive imaging, rapid reversal protocols, and extended observation
- Delirium is never normal—systematically evaluate for occult injuries and complications
- Goals-of-care discussions in the ED prevent non-beneficial interventions and align care with values
- Ground-level falls cause high-acuity injuries; liberal CT protocols are warranted
- Multidisciplinary care pathways incorporating geriatric principles improve survival and functional outcomes
- The best critical care for elderly trauma patients often involves thoughtful restraint rather than maximal intervention
The geriatric trauma patient requires us to be not just resuscitationists, but also prognosticators, communicators, and advocates. Mastery of these domains—integrating cutting-edge critical care with person-centered medicine—defines excellence in modern trauma care.
References
-
United Nations, Department of Economic and Social Affairs, Population Division. World Population Ageing 2019: Highlights. New York: United Nations; 2019.
-
Hashmi A, Ibrahim-Zada I, Rhee P, et al. Predictors of mortality in geriatric trauma patients: a systematic review and meta-analysis. J Trauma Acute Care Surg. 2014;76(3):894-901.
-
Llompart-Pou JA, Pérez-Bárcena J, Chico-Fernández M, et al. Severe trauma in the geriatric population. World J Crit Care Med. 2015;4(4):327-335.
-
Fried LP, Ferrucci L, Darer J, et al. Untangling the concepts of disability, frailty, and comorbidity: implications for improved targeting and care. J Gerontol A Biol Sci Med Sci. 2004;59(3):255-263.
-
Clegg A, Young J, Iliffe S, et al. Frailty in elderly people. Lancet. 2013;381(9868):752-762.
-
Joseph B, Pandit V, Zangbar B, et al. Superiority of frailty over age in predicting outcomes among geriatric trauma patients: a prospective analysis. JAMA Surg. 2014;149(8):766-772.
-
Fried LP, Tangen CM, Walston J, et al. Frailty in older adults: evidence for a phenotype. J Gerontol A Biol Sci Med Sci. 2001;56(3):M146-156.
-
Rockwood K, Mitnitski A. Frailty in relation to the accumulation of deficits. J Gerontol A Biol Sci Med Sci. 2007;62(7):722-727.
-
Patel KV, Brennan KL, Brennan ML, et al. Association of a modified frailty index with mortality after femoral neck fracture in patients aged 60 years and older. Clin Orthop Relat Res. 2014;472(3):1010-1017.
-
Joseph B, Zangbar B, Pandit V, et al. Emergency General Surgery in the Elderly: Too Old or Too Frail? J Am Coll Surg. 2016;222(5):805-813.
-
Maxwell CA, Mion LC, Mukherjee K, et al. Preinjury physical frailty and cognitive impairment among geriatric trauma patients determine postinjury functional recovery and survival. J Trauma Acute Care Surg. 2016;80(2):195-203.
-
Kundi R, Chaudhry H, Khouzam M, et al. Does Frailty Increase Costs of Care in Older Adults Undergoing Gastrointestinal Surgery? J Surg Res. 2020;251:142-147.
-
Velanovich V, Antoine H, Swartz A, et al. Accumulating deficits model of frailty and postoperative mortality and morbidity: its application to a national database. J Surg Res. 2013;183(1):104-110.
-
Rockwood K, Song X, MacKnight C, et al. A global clinical measure of fitness and frailty in elderly people. CMAJ. 2005;173(5):489-495.
-
Ravindrarajah R, Hazra NC, Hamada S, et al. Systolic Blood Pressure Trajectory, Frailty, and All-Cause Mortality: 80+ Years in the Leiden 85-Plus Study. Circulation. 2017;135(24):2357-2368.
-
Fleg JL, O'Connor F, Gerstenblith G, et al. Impact of age on the cardiovascular response to dynamic upright exercise in healthy men and women. J Appl Physiol. 1995;78(3):890-900.
-
Franceschi C, Bonafè M, Valensin S, et al. Inflamm-aging: An evolutionary perspective on immunosenescence. Ann N Y Acad Sci. 2000;908:244-254.
-
Fairchild B, Webb TP, Xiang Q, et al. Sarcopenia and frailty in elderly trauma patients. World J Surg. 2015;39(2):373-379.
-
Jansen Klomp WW, Claassen JAHR. Cerebral Autoregulation in the Elderly. J Gerontol Geriatr Res. 2016;5:6.
-
Caterino JM, Valasek T, Werman HA. Identification of an age cutoff for increased mortality in patients with elderly trauma. Am J Emerg Med. 2010;28(2):151-158.
-
Fleischmann-Struzek C, Thomas-Rüddel DO, Schettler A, et al. Comparing the validity of different ICD coding abstraction strategies for sepsis case identification in German claims data. PLoS One. 2018;13(7):e0198847.
-
Carson JL, Stanworth SJ, Dennis JA, et al. Transfusion thresholds for guiding red blood cell transfusion. Cochrane Database Syst Rev. 2021;12(12):CD002042.
-
Naranje P, Mittal C, Nag A, et al. Geriatric Trauma Outcome Score as a predictor of mortality in elderly orthopedic trauma patients: A prospective cohort study. J Orthop. 2020;22:518-521.
-
Maher RL, Hanlon J, Hajjar ER. Clinical consequences of polypharmacy in elderly. Expert Opin Drug Saf. 2014;13(1):57-65.
-
Mabry CD, O'Neal CM, Robison WH, et al. Polypharmacy and outcomes among geriatric trauma patients. Am J Surg. 2015;210(1):151-156.
-
Ivascu FA, Howells GA, Junn FS, et al. Predictors of mortality in trauma patients with intracranial hemorrhage on preinjury aspirin or clopidogrel. J Trauma. 2008;65(4):785-788.
-
Nishijima DK, Offerman SR, Ballard DW, et al. Immediate and delayed traumatic intracranial hemorrhage in patients with head trauma and preinjury warfarin or clopidogrel use. Ann Emerg Med. 2012;59(6):460-468.e1-7.
-
Sarode R, Milling TJ Jr, Refaai MA, et al. Efficacy and safety of a 4-factor prothrombin complex concentrate in patients on vitamin K antagonists presenting with major bleeding: a randomized, plasma-controlled, phase IIIb study. Circulation. 2013;128(11):1234-1243.
-
Barletta JF, Abdul-Rahman D, Magnotti LJ, et al. Pharmacologic reversal of warfarin-associated coagulopathy in trauma patients: a retrospective cohort study. World J Emerg Surg. 2014;9:22.
-
Barnes GD, Lucas E, Alexander GC, et al. National Trends in Ambulatory Oral Anticoagulant Use. Am J Med. 2015;128(12):1300-1305.e2.
-
Pollack CV Jr, Reilly PA, van Ryn J, et al. Idarucizumab for Dabigatran Reversal - Full Cohort Analysis. N Engl J Med. 2017;377(5):431-441.
-
Siegal DM, Curnutte JT, Connolly SJ, et al. Andexanet Alfa for the Reversal of Factor Xa Inhibitor Activity. N Engl J Med. 2015;373(25):2413-2424.
-
Connolly SJ, Crowther M, Eikelboom JW, et al. Full Study Report of Andexanet Alfa for Bleeding Associated with Factor Xa Inhibitors. N Engl J Med. 2019;380(14):1326-1335.
-
Schulman S, Bijsterveld NR. Anticoagulants and their reversal. Transfus Med Rev. 2007;21(1):37-48.
-
Fawole A, Daw HA, Crowther MA. Practical management of bleeding due to the anticoagulants dabigatran, rivaroxaban, and apixaban. Cleve Clin J Med. 2013;80(7):443-451.
-
Gaist D, García Rodríguez LA, Hellfritzsch M, et al. Association of Antithrombotic Drug Use With Subdural Hematoma Risk. JAMA. 2017;317(8):836-846.
-
Joseph B, Pandit V, Sadoun M, et al. A prospective evaluation of platelet function in patients on antiplatelet therapy with traumatic intracranial hemorrhage. J Trauma Acute Care Surg. 2013;75(6):990-994.
-
Naidech AM, Maas MB, Levasseur-Franklin KE, et al. Desmopressin improves platelet activity in acute intracerebral hemorrhage. Stroke. 2014;45(8):2451-2453.
-
Joseph B, Pandit V, Zangbar B, et al. Outcomes in anticoagulated geriatric trauma patients: a trauma system-level evaluation. Surgery. 2015;158(3):675-681.
-
Pabinger I, Brenner B, Kalina U, et al. Prothrombin complex concentrate (Beriplex P/N) for emergency anticoagulation reversal: a prospective multinational clinical trial. J Thromb Haemost. 2008;6(4):622-631.
-
Ruxton K, Woodman RJ, Mangoni AA. Drugs with anticholinergic effects and cognitive impairment, falls and all-cause mortality in older adults: A systematic review and meta-analysis. Br J Clin Pharmacol. 2015;80(2):209-220.
-
Campbell N, Boustani M, Limbil T, et al. The cognitive impact of anticholinergics: a clinical review. Clin Interv Aging. 2009;4:225-233.
-
Tune LE. Anticholinergic effects of medication in elderly patients. J Clin Psychiatry. 2001;62 Suppl 21:11-14.
-
Fox C, Smith T, Maidment I, et al. Effect of medications with anti-cholinergic properties on cognitive function, delirium, physical function and mortality: a systematic review. Age Ageing. 2014;43(5):604-615.
-
Richardson K, Bennett K, Maidment ID, et al. Use of Medications with Anticholinergic Activity and Self-Reported Injurious Falls in Older Community-Dwelling Adults. J Am Geriatr Soc. 2015;63(8):1561-1569.
-
Hilmer SN, Mager DE, Simonsick EM, et al. A drug burden index to define the functional burden of medications in older people. Arch Intern Med. 2007;167(8):781-787.
-
Neideen T, Lam M, Brasel KJ. Preinjury beta blockers are associated with increased mortality in geriatric trauma patients. J Trauma. 2008;65(5):1016-1020.
-
Lalau JD. Lactic acidosis induced by metformin: incidence, management and prevention. Drug Saf. 2010;33(9):727-740.
-
Lenze EJ, Wetherell JL. Anxiety Disorders: New Developments in Old Age. Am J Geriatr Psychiatry. 2011;19(4):301-304.
-
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Association; 2013.
-
Kennedy M, Enander RA, Tadiri SP, et al. Delirium in the Emergency Department: Predictors and Prevalence Rates from a Prospective Pilot Study. Acad Emerg Med. 2014;21(8):853-860.
-
McNicoll L, Pisani MA, Zhang Y, et al. Delirium in the intensive care unit: occurrence and clinical course in older patients. J Am Geriatr Soc. 2003;51(5):591-598.
-
Peterson JF, Pun BT, Dittus RS, et al. Delirium and its motoric subtypes: a study of 614 critically ill patients. J Am Geriatr Soc. 2006;54(3):479-484.
-
Yang FM, Marcantonio ER, Inouye SK, et al. Phenomenological subtypes of delirium in older persons: patterns, prevalence, and prognosis. Psychosomatics. 2009;50(3):248-254.
-
Menditto VG, Lucci M, Polonara S, et al. Management of minor head injury in patients receiving oral anticoagulant therapy: a prospective study of a 24-hour observation protocol. Ann Emerg Med. 2012;59(6):451-455.
-
Bruijns SR, Guly HR, Bouamra O, et al. The value of traditional vital signs, shock index, and age-based markers in predicting trauma mortality. J Trauma Acute Care Surg. 2013;74(6):1432-1437.
-
Dombroski DG, Narayanan MK, Robinson FG. Occult Hip Fracture Detected by MRI in a Patient on Anticoagulation: Case Report and Review of the Literature. Geriatr Orthop Surg Rehabil. 2011;2(4):152-155.
-
High KP, Bradley SF, Gravenstein S, et al. Clinical practice guideline for the evaluation of fever and infection in older adult residents of long-term care facilities: 2008 update by the Infectious Diseases Society of America. Clin Infect Dis. 2009;48(2):149-171.
-
Oh ES, Fong TG, Hshieh TT, et al. Delirium in Older Persons: Advances in Diagnosis and Treatment. JAMA. 2017;318(12):1161-1174.
-
Maldonado JR. Neuropathogenesis of delirium: review of current etiologic theories and common pathways. Am J Geriatr Psychiatry. 2013;21(12):1190-1222.
-
Trzepacz PT. Is there a final common neural pathway in delirium? Focus on acetylcholine and dopamine. Semin Clin Neuropsychiatry. 2000;5(2):132-148.
-
Girard TD, Pandharipande PP, Ely EW. Delirium in the intensive care unit. Crit Care. 2008;12 Suppl 3(Suppl 3):S3.
-
Vaurio LE, Sands LP, Wang Y, et al. Postoperative delirium: the importance of pain and pain management. Anesth Analg. 2006;102(4):1267-1273.
-
Inouye SK, van Dyck CH, Alessi CA, et al. Clarifying confusion: the confusion assessment method. A new method for detection of delirium. Ann Intern Med. 1990;113(12):941-948.
-
Ely EW, Margolin R, Francis J, et al. Evaluation of delirium in critically ill patients: validation of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Crit Care Med. 2001;29(7):1370-1379.
-
Bellelli G, Morandi A, Davis DH, et al. Validation of the 4AT, a new instrument for rapid delirium screening: a study in 234 hospitalised older people. Age Ageing. 2014;43(4):496-502.
-
Inouye SK, Bogardus ST Jr, Charpentier PA, et al. A multicomponent intervention to prevent delirium in hospitalized older patients. N Engl J Med. 1999;340(9):669-676.
-
Kuehn BM. FDA warns antipsychotic drugs may be risky for elderly. JAMA. 2005;293(20):2462.
-
Riker RR, Shehabi Y, Bokesch PM, et al. Dexmedetomidine vs midazolam for sedation of critically ill patients: a randomized trial. JAMA. 2009;301(5):489-499.
-
Pandharipande P, Shintani A, Peterson J, et al. Lorazepam is an independent risk factor for transitioning to delirium in intensive care unit patients. Anesthesiology. 2006;104(1):21-26.
-
Bulger EM, Edwards T, Klotz P, et al. Epidural analgesia improves outcome after multiple rib fractures. Surgery. 2004;136(2):426-430.
-
Miotto K, Cho AK, Khalil MA, et al. Trends in Tramadol: Pharmacology, Metabolism, and Misuse. Anesth Analg. 2017;124(1):44-51.
-
Girard TD, Jackson JC, Pandharipande PP, et al. Delirium as a predictor of long-term cognitive impairment in survivors of critical illness. Crit Care Med. 2010;38(7):1513-1520.
-
Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA. 2004;291(14):1753-1762.
-
Witlox J, Eurelings LS, de Jonghe JF, et al. Delirium in elderly patients and the risk of postdischarge mortality, institutionalization, and dementia: a meta-analysis. JAMA. 2010;304(4):443-451.
-
Fong TG, Davis D, Growdon ME, et al. The interface between delirium and dementia in elderly adults. Lancet Neurol. 2015;14(8):823-832.
-
McCusker J, Cole M, Abrahamowicz M, et al. Delirium predicts 12-month mortality. Arch Intern Med. 2002;162(4):457-463.
-
Perdue PW, Watts DD, Kaufmann CR, et al. Differences in mortality between elderly and younger adult trauma patients: geriatric status increases risk of delayed death. J Trauma. 1998;45(4):805-810.
-
McGwin G Jr, George RL, Cross JM, et al. Improving the ability to predict mortality among burn patients. Burns. 2008;34(3):320-327.
-
Naik AD, Martin LA, Moye J, et al. Health Values and Treatment Goals of Older, Multimorbid Adults Facing Life-Threatening Illness. J Am Geriatr Soc. 2016;64(3):625-631.
-
Beauchamp TL, Childress JF. Principles of Biomedical Ethics. 7th ed. New York, NY: Oxford University Press; 2013.
-
Zhao FZ, Wolf SE, Nakonezny PA, et al. Estimating Geriatric Mortality after Injury Using Age, Injury Severity, and Performance of a Transfusion: The Geriatric Trauma Outcome Score. J Palliat Med. 2015;18(8):677-681.
-
Farhat JS, Velanovich V, Falvo AJ, et al. Are the frail destined to fail? Frailty index as predictor of surgical morbidity and mortality in the elderly. J Trauma Acute Care Surg. 2012;72(6):1526-1530.
-
Boyd CR, Tolson MA, Copes WS. Evaluating trauma care: the TRISS method. Trauma Score and the Injury Severity Score. J Trauma. 1987;27(4):370-378.
-
Dunne JR, Tracy JK, Scalea TM, et al. Lactate and base deficit in trauma: does alcohol or drug use impair their predictive accuracy? J Trauma. 2005;58(5):959-966.
-
Baile WF, Buckman R, Lenzi R, et al. SPIKES-A six-step protocol for delivering bad news: application to the patient with cancer. Oncologist. 2000;5(4):302-311.
-
Back AL, Arnold RM, Baile WF, et al. Efficacy of communication skills training for giving bad news and discussing transitions to palliative care. Arch Intern Med. 2007;167(5):453-460.
-
Quill TE, Holloway R. Time-limited trials near the end of life. JAMA. 2011;306(13):1483-1484.
-
White DB, Curtis JR, Lo B, et al. Decisions to limit life-sustaining treatment for critically ill patients who lack both decision-making capacity and surrogate decision-makers. Crit Care Med. 2006;34(8):2053-2059.
-
Bercovitch M, Adunsky A. Patterns of high-dose morphine use in a home-care hospice service: should we be afraid of it? Cancer. 2004;101(6):1473-1477.
-
Margolis R, Verdery AM. Older Adults Without Close Kin in the United States. J Gerontol B Psychol Sci Soc Sci. 2017;72(4):688-693.
-
Mosenthal AC, Murphy PA, Barker LK, et al. Changing the culture around end-of-life care in the trauma intensive care unit. J Trauma. 2008;64(6):1587-1593.
-
Penrod JD, Deb P, Dellenbaugh C, et al. Hospital-based palliative care consultation: effects on hospital cost. J Palliat Med. 2010;13(8):973-979.
-
Smith AK, Thai JN, Bakitas MA, et al. Enhancing prognostic communication: a pilot study of a clinician prompt. J Palliat Med. 2013;16(6):661-666.
-
Taylor MD, Tracy JK, Meyer W, et al. Trauma in the elderly: intensive care unit resource use and outcome. J Trauma. 2002;53(3):407-414.
-
Lustbader D, Mudra M, Romano C, et al. The impact of a home-based palliative care program in an accountable care organization. J Palliat Med. 2017;20(1):23-28.
-
Sterling DA, O'Connor JA, Bonadies J. Geriatric falls: injury severity is high and disproportionate to mechanism. J Trauma. 2001;50(1):116-119.
-
Chisholm KM, Harruff RC. Elderly deaths after falls: 12 years of data from King County, Washington. Am J Forensic Med Pathol. 2010;31(3):246-251.
-
Shalhub S, Starnes BW, Tran NT, et al. Blunt abdominal aortic injury. J Vasc Surg. 2012;55(5):1277-1285.
-
Demetriades D, Velmahos GC, Scalea TM, et al. Diagnosis and treatment of blunt thoracic aortic injuries: changing perspectives. J Trauma. 2008;64(6):1415-1418.
-
Schlatmann TJ, Becker AE. Histologic changes in the normal aging aorta: implications for dissecting aortic aneurysm. Am J Cardiol. 1977;39(1):13-20.
-
Richens D, Field M, Neale M, et al. The mechanism of injury in blunt traumatic rupture of the aorta. Eur J Cardiothorac Surg. 2002;21(2):288-293.
-
Dyer DS, Moore EE, Ilke DN, et al. Thoracic aortic injury: how predictive is mechanism and is chest computed tomography a reliable screening tool? A prospective study of 1,561 patients. J Trauma. 2000;48(4):673-682.
-
Mirvis SE, Shanmuganathan K, Buell J, et al. Use of spiral computed tomography for the assessment of blunt trauma patients with potential aortic injury. J Trauma. 1998;45(5):922-930.
-
Fox N, Schwartz D, Salazar JH, et al. Evaluation and management of blunt traumatic aortic injury: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2015;78(1):136-146.
-
Steenburg SD, Ravenel JG, Ikonomidis JS, et al. Acute traumatic aortic injury: imaging evaluation and management. Radiology. 2008;248(3):748-762.
-
Azizzadeh A, Keyhani K, Miller CC 3rd, et al. Blunt traumatic aortic injury: initial experience with endovascular repair. J Vasc Surg. 2009;49(6):1403-1408.
-
Malhotra AK, Fabian TC, Croce MA, et al. Minimal aortic injury: a lesion associated with advancing diagnostic techniques. J Trauma. 2001;51(6):1042-1048.
-
Lee WA, Matsumura JS, Mitchell RS, et al. Endovascular repair of traumatic thoracic aortic injury: clinical practice guidelines of the Society for Vascular Surgery. J Vasc Surg. 2011;53(1):187-192.
-
Demetriades D, Velmahos GC, Scalea TM, et al. Operative repair or endovascular stent graft in blunt traumatic thoracic aortic injuries: results of an American Association for the Surgery of Trauma Multicenter Study. J Trauma. 2008;64(3):561-570.
-
Schneider RC, Cherry G, Pantek H. The syndrome of acute central cervical spinal cord injury; with special reference to the mechanisms involved in hyperextension injuries of cervical spine. J Neurosurg. 1954;11(6):546-577.
-
Harrop JS, Sharan A, Ratliff J. Central cord injury: pathophysiology, management, and outcomes. Spine J. 2006;6(6 Suppl):198S-206S.
-
Quencer RM, Bunge RP, Egnor M, et al. Acute traumatic central cord syndrome: MRI-pathological correlations. Neuroradiology. 1992;34(2):85-94.
-
McKinley W, Santos K, Meade M, et al. Incidence and outcomes of spinal cord injury clinical syndromes. J Spinal Cord Med. 2007;30(3):215-224.
-
Stevens RD, Bhardwaj A, Kirsch JR, et al. Critical care and perioperative management in traumatic spinal cord injury. J Neurosurg Anesthesiol. 2003;15(3):215-229.
-
Schaefer DM, Flanders AE, Osterholm JL, et al. Prognostic significance of magnetic resonance imaging in the acute phase of cervical spine injury. J Neurosurg. 1992;76(2):218-223.
-
Pang D, Wilberger JE Jr. Spinal cord injury without radiographic abnormalities in children. J Neurosurg. 1982;57(1):114-129.
-
Ryken TC, Hurlbert RJ, Hadley MN, et al. The acute cardiopulmonary management of patients with cervical spinal cord injuries. Neurosurgery. 2013;72 Suppl 2:84-92.
-
Hurlbert RJ, Hadley MN, Walters BC, et al. Pharmacological therapy for acute spinal cord injury. Neurosurgery. 2013;72 Suppl 2:93-105.
-
Fehlings MG, Vaccaro A, Wilson JR, et al. Early versus delayed decompression for traumatic cervical spinal cord injury: results of the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS). PLoS One. 2012;7(2):e32037.
-
Wilson JR, Tetreault LA, Kwon BK, et al. Timing of Decompression in Patients With Acute Spinal Cord Injury: A Systematic Review. Global Spine J. 2017;7(3 Suppl):95S-115S.
-
Roth EJ, Lawler MH, Yarkony GM. Traumatic central cord syndrome: clinical features and functional outcomes. Arch Phys Med Rehabil. 1990;71(1):18-23.
-
Brodell DW, Jain A, Elfar JC, et al. National trends in the management of central cord syndrome: an analysis of 16,134 patients. Spine J. 2015;15(3):435-442.
-
Julien TD, Frankel B, Traynelis VC, et al. Evidence-based analysis of odontoid fracture management. Neurosurg Focus. 2000;8(6):e1.
-
Harris JH Jr, Carson GC, Wagner LK. Radiologic diagnosis of traumatic occipitovertebral dissociation: 1. Normal occipitovertebral relationships on lateral radiographs of supine subjects. AJR Am J Roentgenol. 1994;162(4):881-886.
-
Westerveld LA, Verlaan JJ, Oner FC. Spinal fractures in patients with ankylosing spinal disorders: a systematic review of the literature on treatment, neurological status and complications. Eur Spine J. 2009;18(2):145-156.
-
Melton LJ 3rd, Lane AW, Cooper C, et al. Prevalence and incidence of vertebral deformities. Osteoporos Int. 1993;3(3):113-119.
-
Buchbinder R, Osborne RH, Ebeling PR, et al. A randomized trial of vertebroplasty for painful osteoporotic vertebral fractures. N Engl J Med. 2009;361(6):557-568.
-
Karibe H, Hayashi T, Hirano T, et al. Surgical management of traumatic acute subdural hematoma in adults: a review. Neurol Med Chir (Tokyo). 2014;54(11):887-894.
-
Uccella L, Zoia C, Bongetta D, et al. Are Antiplatelet and Anticoagulants Drugs a Risk Factor for Bleeding in Mild Traumatic Brain Injury? World Neurosurg. 2018;110:e339-e345.
-
Peel NM. Epidemiology of falls in older age. Can J Aging. 2011;30(1):7-19.
Author Disclosure Statement: No competing financial interests exist.
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