5.5 Vascular Emergencies, Wound Care, & Shock Recognition

Vascular Emergencies, Wound Care, & Shock Recognition

Vascular emergencies are rapidly fatal if not diagnosed and intervened upon immediately. Systemic hypoperfusion (shock) demands rapid hemodynamic profiling to guide fluid resuscitation, inotropic support, vasopressors, or surgical control.

Vascular Catastrophes: AAA & Aortic Dissection

Abdominal Aortic Aneurysm (AAA)

• Definition & Screening: Dilatation of the abdominal aorta $\ge 3.0\text{ cm}$. Screening via one-time abdominal ultrasound is recommended for men aged 65–75 years who have ever smoked.
• Elective Repair Threshold: Dilatation $\ge 5.5\text{ cm}$ in men, $\ge 5.0\text{ cm}$ in women, or rapid expansion $> 0.5\text{ cm}$ in 6 months.
• Ruptured AAA: Classic Clinical Triad: Hypotension, flank/back pain, and a pulsatile abdominal mass.
• Management Algorithm:
  • Hemodynamically Unstable: Transfer directly to the operating room for emergent open surgical repair or endovascular aneurysm repair (EVAR). Diagnostic CT is strictly contraindicated.
  • Hemodynamically Stable: Perform an emergency CT Angiogram of abdomen and pelvis to confirm rupture and evaluate anatomical suitability for EVAR.

Acute Aortic Dissection

Tear in the aortic intima allowing blood to surge into the media, creating a false lumen.

• Classification & Management:
  • Stanford Type A: Involves the ascending aorta (proximal to left subclavian artery). MANAGEMENT: EMERGENCY SURGICAL REPAIR (high risk of aortic rupture, pericardial tamponade, or acute aortic regurgitation).
  • Stanford Type B: Involves descending aorta only (distal to left subclavian artery). MANAGEMENT: MEDICAL THERAPY with IV beta-blockers (target SBP $100\text{--}120\text{ mmHg}$ and HR $< 60\text{ bpm}$). Endovascular repair (TEVAR) reserved for complicated cases (ischemia, progression, rupture).
• Clinical Presentation: Sudden onset of severe, tearing or ripping chest pain radiating to the interscapular back. Physical findings: Pulse deficits, asymmetric blood pressure between arms ($> 20\text{ mmHg}$ difference), or new aortic regurgitation murmur.
• Medical Therapy for Dissection: IV Labetalol or Esmolol as first-line agents to lower heart rate ($dp/dt$) and blood pressure. Vasodilators (nitroprusside) must NEVER be given without prior beta-blockade because reflex tachycardia increases aortic wall shear stress.

Acute Limb Ischemia (ALI)

Acute drop in limb perfusion threatening tissue viability. Symptoms progress rapidly over $< 2\text{ weeks}$.

• Etiology:
  • Embolus (50%): Cardiac origin (Afib, post-MI mural thrombus). Sudden onset severe pain in a limb with normal contralateral pulses.
  • Thrombus (40%): In-situ thrombosis over pre-existing peripheral arterial disease (PAD). Insidious onset, history of claudication, absent contralateral pulses.
• The 6 Ps of Acute Limb Ischemia:
  1. Pain (Sudden, severe, distal to occlusion)
  2. Pallor (Pale, mottled skin)
  3. Pulselessness (Loss of Doppler signals)
  4. Paresthesia (Loss of sensory function; key indicator of advanced ischemia)
  5. Paralysis (Loss of motor function; indicates impending non-viability)
  6. Poikilothermia ('Perishingly cold' extremity)
• Rutherford Classification & Management:
  • Category I (Viable): No sensory loss or muscle weakness. Arterial Doppler audible. Urgent imaging (CT angiogram) and revascularization.
  • Category IIa (Marginally Threatened): Minimal sensory loss (toes). Revascularizable if treated promptly.
  • Category IIb (Immediately Threatened): Sensory loss above toes, mild-to-moderate motor weakness. EMERGENT OPERATIVE REVASCULARIZATION $< 6\text{ hours}$ (Catheter-directed thrombolysis or open balloon catheter embolectomy).
  • Category III (Irreversible): Complete anesthesia, paralysis, rigor, marbled skin. Requires amputation to prevent lethal reperfusion metabolic syndrome.
• Initial Emergency Order: Administer an immediate IV unfractionated heparin bolus ($80\text{ units/kg}$) to prevent thrombus propagation.

Shock Classification & Hemodynamic Profiling

Shock is defined as systemic tissue hypoperfusion causing cellular hypoxia and lactic acidosis.

💡 Resuscitation Endpoint Targets: Mean Arterial Pressure (MAP) $\ge 65\text{ mmHg}$, Urine output $\ge 0.5\text{ mL/kg/h}$, Serum lactate normalization ($< 2.0\text{ mmol/L}$).

Wound Healing & Necrotizing Soft Tissue Infections

Phases of Normal Wound Healing

1. Hemostasis (Minutes): Platelet aggregation, fibrin clot formation.
2. Inflammation (Days 1–4): Neutrophils followed by macrophages clear debris and bacteria.
3. Proliferation (Days 4–21): Fibroblasts deposit collagen III, angiogenesis, granulation tissue formation.
4. Remodeling (Day 21 – 1 Year): Collagen III converted to stronger collagen I. Tensile strength reaches maximum $80%$ of uninjured tissue.

Types of Wound Closure

• Primary Intention: Surgical incision closed directly with sutures/staples. Minimal scar.
• Secondary Intention: Wound left open to heal by granulation and contraction (e.g., contaminated abscess cavity).
• Tertiary Intention (Delayed Primary): Wound initially left open, debrided, then closed surgically 3–5 days later after infection is controlled.

Necrotizing Fasciitis

Life-threatening, rapidly progressive infection of subcutaneous tissue and fascia.

• Microbiology:
  • Type I (Polymicrobial - 80%): Mixed anaerobes (Bacteroides), E. coli, Peptostreptococcus. Common in diabetics/immunocompromised.
  • Type II (Monomicrobial): Streptococcus pyogenes (Group A Strep) +/- Staphylococcus aureus. Occurs in healthy individuals following minor trauma.
• Clinical Presentation:
  • Pain out of proportion to physical exam findings early.
  • Rapidly spreading skin erythema, warmth, and edema.
  • Hard signs: Subcutaneous crepitus, gas on X-ray/CT, violaceous bullae, skin necrosis, and septic shock.
• Management:
  • IMMEDIATE EMERGENCY SURGICAL DEBRIDEMENT (Resect all necrotic tissue down to viable bleeding fascia; repeat debridement in 24 hours).
  • Empiric Triple Antibiotic Therapy: Vancomycin (covers MRSA) + Piperacillin-Tazobactam (covers Pseudomonas and Gram-negatives) + Clindamycin (inhibits bacterial protein synthesis and toxin production in Group A Strep).