20.3 Acute Severe Epistaxis & Airway Obstruction

Acute Epistaxis: Vascular Anatomy, Triage & Emergency Protocols

Epistaxis is one of the most frequent otolaryngologic emergencies encountered in primary care and emergency settings, affecting approximately 60% of individuals during their lifetime, with 6% requiring professional medical intervention. Rapid management requires localizing the bleeding source to either the anterior or posterior nasal cavity.

Vascular Anatomy: Kiesselbach's vs. Woodruff's Plexus

                         NASAL SEPTAL VASCULAR ANATOMY

                   Anterior Ethmoidal Artery (Internal Carotid)
                                       │
                                       ▼
  Posterior Ethmoidal Artery ──> ┌──────────────┐ <── Sphenopalatine Artery
  (Internal Carotid)             │ KIESSELBACH  │     (External Carotid: Terminal IMAX)
                                 │    PLEXUS    │
  Superior Labial Artery ──────> │(Little's Area│ <── Greater Palatine Artery
  (External Carotid: Facial)     └──────────────┘     (External Carotid: IMAX)
                                        │
                                        ▼
                         ANTERIOR SEPTAL HEMORRHAGE (~90%)
                    (Digital Compression / Silver Nitrate / Tampon)

  ─────────────────────────────────────────────────────────────────────────────

                         POSTERIOR VASCULAR SUPPLY

  Sphenopalatine Artery (IMAX) + Ascending Pharyngeal Artery
                                       │
                                       ▼
                               ┌────────────────┐
                               │   WOODRUFF'S   │
                               │     PLEXUS     │
                               └────────────────┘
                                       │
                                       ▼
                         POSTERIOR ARTERIAL HEMORRHAGE (~10%)
                 (Profuse / Bilateral / Down Posterior Oropharynx)
               (Mandatory Posterior Balloon Pack + Hospital Telemetry)

1. Anterior Epistaxis (~90% of cases):

   • Anatomical Site: Kiesselbach's plexus (also designated Little's area), located on the anterior inferior third of the cartilaginous nasal septum.
   • Arterial Anastomosis: Formed by the confluence of five arteries derived from both the internal and external carotid systems:
     1. Anterior ethmoidal artery (from ophthalmic artery / internal carotid);
     2. Posterior ethmoidal artery (from ophthalmic artery / internal carotid);
     3. Sphenopalatine artery (terminal branch of internal maxillary artery / external carotid);
     4. Greater palatine artery (from internal maxillary artery / external carotid);
     5. Superior labial artery (septal branch of facial artery / external carotid).
   • Clinical Features: Typically unilateral, low-pressure capillary or small arteriolar bleeding. Readily visualized via anterior rhinoscopy. Commonly triggered by digital trauma (nose picking), mucosal dryness from low ambient humidity, upper respiratory infections, allergic rhinitis, or chronic misuse of topical nasal corticosteroids directed toward the septum rather than the lateral nasal wall.

2. Posterior Epistaxis (~10% of cases):

   • Anatomical Site: Woodruff's plexus, located on the lateral nasal wall inferior to the posterior aspect of the inferior turbinate, or directly from the trunk and posterior branches of the sphenopalatine artery as it emerges from the sphenopalatine foramen.
   • Clinical Features: High-pressure arterial bleeding that flows profusely down the posterior oropharynx regardless of patient position. Difficult or impossible to visualize on anterior rhinoscopy. Typically occurs in older adults with longstanding essential hypertension, severe systemic atherosclerosis, coagulopathy, liver disease, or those receiving therapeutic anticoagulation (warfarin, direct oral anticoagulants) or antiplatelet agents.

---

Stepwise Emergency Management of Anterior Epistaxis

Step 1: Patient Positioning and Airway Protection

• Seat the patient completely upright, leaning slightly forward at the waist, with the mouth open, allowing blood to drain into an emesis basin.
• Strict Warning: The historical maneuver of tilting the head backward is dangerous and strictly obsolete. Tilting the head back diverts blood into the hypopharynx, causing blood ingestion (which produces severe gastric irritation, nausea, and hematemesis) and significantly increases the risk of tracheobronchial aspiration and airway compromise.
• Instruct the patient to gently blow the nose once to evacuate non-hemostatic, jelly-like clots that prevent direct vessel tamponade.

Step 2: Direct Continuous Digital Compression

• Apply firm, uninterrupted manual compression directly over the soft, cartilaginous lower third of the nose, pinching both alae nasi tightly against the nasal septum.
• Compression must be held continuously for 10 to 15 full minutes by the clock without releasing pressure to check for cessation of bleeding.
• Common Error: Pinching the bridge of the nose (the rigid nasal bones of the upper third) applies zero compressive force to Kiesselbach's plexus and is completely ineffective.

Step 3: Topical Vasoconstrictors and Local Anesthesia

• If bleeding persists despite 15 minutes of firm compression: insert cotton pledgets soaked in a topical vasoconstrictor (0.05% oxymetazoline [Afrin] or 1% phenylephrine) combined with a rapid-acting topical anesthetic (4% lidocaine or cocaine solution).
• Reapply continuous digital compression over the soft lower third for an additional 10 minutes. This induces mucosal vasoconstriction and achieves anesthesia for subsequent examination and cauterization.

Step 4: Chemical Cautery with Silver Nitrate

• Remove the cotton pledgets and perform anterior rhinoscopy utilizing a nasal speculum, suction catheter, and focused headlamp.
• If an active focal bleeding point or a prominent, non-bleeding prominent vessel with surrounding clot is clearly identified:
  • Apply a silver nitrate ($AgNO_3$) applicator tip directly to the mucosa.
  • Technique: Roll the applicator tip circumferentially around the peripheral margin of the bleeding vessel first to seal the feeding vessels, and then apply it gently onto the center of the bleeding site for no more than 3 to 5 seconds until a grey-white eschar forms.

[!CAUTION] THE ABSOLUTE CONTRAINDICATION TO BILATERAL CHEMICAL CAUTERY: NEVER apply silver nitrate cautery to bilateral opposing surfaces of the nasal septum simultaneously (or during the same procedural visit). The cartilaginous nasal septum is an avascular structure that relies entirely on nutrient diffusion from the overlying mucoperichondrium on either side. Applying caustic silver nitrate to both sides of the septum simultaneously destroys the perichondrial microvasculature bilaterally, causing full-thickness ischemic chondronecrosis of the septal cartilage. This results in a permanent, irreversible septal perforation, leading to chronic whistling, crusting, turbulent airflow, and intractable recurrent epistaxis.

Step 5: Anterior Nasal Packing

• Indicated when direct compression and chemical cautery fail to achieve hemostasis, or when no discrete bleeding site can be visualized:
  1. Polyvinyl Alcohol Sponge Nasal Tampon (Merocel): Coated with water-soluble antibiotic ointment, inserted gently along the floor of the nasal cavity parallel to the hard palate, and rehydrated with 5 to 10 mL of normal saline or topical tranexamic acid (TXA, 500 mg), causing the sponge to expand and exert uniform mechanical pressure.
  2. Pneumatic Nasal Catheter (Rapid Rhino): Hydrocolloid-coated carboxymethylcellulose pack soaked in sterile water for 30 seconds, inserted along the nasal floor, and gently inflated with air via a 20-mL syringe until bleeding halts.
• Antibiotic Prophylaxis Debate: In situ nasal packing creates a stagnant, blood-filled aerobic-anaerobic medium that promotes colonization by Staphylococcus aureus capable of secreting Toxic Shock Syndrome Toxin-1 (TSST-1). To prevent Toxic Shock Syndrome (TSS), guidelines recommend prescribing oral amoxicillin-clavulanate (875/125 mg PO BID) or cephalexin (500 mg PO QID) while non-absorbable packing remains in place. Non-absorbable packing must be removed within 48 to 72 hours.

---

Management of Posterior Epistaxis

Posterior epistaxis is a true medical emergency characterized by refractory hemorrhage that continues to flow vigorously down the posterior pharynx despite correctly positioned anterior packing.

Emergency Posterior Tamponade Techniques

1. Dual-Balloon Pneumatic Catheter (e.g., Epistat / Rapid Rhino Posterior):
   • Lubricated and inserted along the floor of the nasal cavity into the nasopharynx.
   • The posterior balloon is inflated with 5 to 10 mL of sterile water (never air, which can leak, and never saline, which can crystallize and damage the valve) and gently pulled forward until firmly lodged in the posterior choana.
   • The anterior balloon is then inflated with 10 to 15 mL of sterile water to achieve anterior tamponade.
2. Foley Catheter Technique:
   • In the absence of a dedicated commercial balloon catheter: pass a 12 to 14 French Foley catheter with a 30-mL balloon along the nasal floor until the tip is visible in the posterior oropharynx.
   • Inflate the balloon with 5 to 10 mL of sterile water, and gently traction the catheter anteriorly until the balloon wedges securely against the posterior choana.
   • While maintaining continuous forward traction, place formal anterior nasal packing.
   • Secure the catheter at the external naris using an umbilical clamp or plastic clip, placing generous gauze padding between the clamp and the nasal ala to prevent pressure-induced necrosis of the alar cartilage.

The Nasopulmonary Reflex & Mandatory Inpatient Admission

[!IMPORTANT] MANDATORY INPATIENT TELEMETRY ADMISSION FOR ALL POSTERIOR PACKS: Every patient with a posterior nasal pack must be admitted to an inpatient telemetry or step-down unit with continuous pulse oximetry and cardiac monitoring. Mechanical distension of the posterior nasopharynx stimulates sensory afferents of the trigeminal (V2) and glossopharyngeal (CN IX) nerves, triggering the nasopulmonary reflex. This profound vagal reflex produces severe central respiratory depression, arterial hypoxemia, hypercapnia, severe bradycardia, malignant cardiac dysrhythmias, and sudden cardiac arrest, especially in elderly patients with pre-existing cardiopulmonary disease.

Refractory Posterior Hemorrhage

If posterior bleeding persists despite balloon tamponade, urgent Otolaryngology consultation is mandatory for:

• Endoscopic Sphenopalatine Artery Ligation (ESPAL): Direct transantronasal clip ligation of the sphenopalatine artery branches (success rate >95%); OR
• Endovascular Interventional Embolization: Superselective catheter-directed embolization of the internal maxillary artery branches under fluoroscopy.

---

Acute Upper Airway Obstruction

Acute upper airway obstruction is a catastrophic medical emergency that can progress to complete asphyxiation, anoxic brain injury, and death within 3 to 5 minutes if untreated.

1. Foreign Body Airway Obstruction (FBAO)

• Recognition: Sudden onset of respiratory distress while eating or playing, characterized by the universal choking sign (hands clutching the neck), aphonia (inability to speak), ineffective cough, inspiratory stridor, and rapidly developing cyanosis.

Emergency Resuscitation Protocols by Patient Category

• Conscious Adult or Child >1 Year:
  • Perform subdiaphragmatic abdominal thrusts (Heimlich Maneuver): Stand behind the patient, wrap arms around the waist, make a fist with one hand, place the thumb side of the fist against the patient's abdomen midway between the umbilicus and the xiphoid process, grasp the fist with the other hand, and deliver rapid, inward and upward thrusts until the object is expelled.
  • Special Populations: In visibly pregnant women or morbidly obese patients where abdominal thrusts cannot be performed, deliver chest thrusts over the lower third of the sternum.
• Conscious Infant (<1 Year):
  • Place the infant prone along the rescuer's forearm with the head positioned lower than the trunk, supporting the infant's jaw and head with the hand.
  • Deliver 5 firm back slaps / blows between the infant's scapulae using the heel of the hand.
  • Turn the infant supine onto the opposite forearm (head still lower than trunk) and deliver 5 rapid chest thrusts over the lower half of the sternum (depressing approximately 1.5 inches / 4 cm).
  • Repeat alternating cycles of 5 back blows and 5 chest thrusts until the foreign object is dislodged or the infant loses consciousness.
  • Strict Rule: Abdominal thrusts are STRICTLY CONTRAINDICATED in infants <1 year due to the high risk of catastrophic hepatic laceration and intra-abdominal hemorrhage.
• Unconscious Choking Patient (All Ages):
  • Lower the patient gently to the ground, activate emergency medical services (call 911), and immediately initiate Cardiopulmonary Resuscitation (CPR), beginning with 30 chest compressions.
  • Each time the airway is opened to deliver rescue breaths: visually inspect the posterior oropharynx.
  • If a foreign object is clearly visualized, remove it with a targeted finger sweep.
  • NEVER perform a blind finger sweep: Blind sweeps push an unseen foreign body deeper from the hypopharynx into the laryngeal inlet, converting a partial obstruction into an irreversible complete obstruction.

---

2. Acute Epiglottitis (Supraglottitis)

Acute epiglottitis is a rapidly progressive bacterial cellulitis and edema of the supraglottic structures, including the epiglottis, aryepiglottic folds, and arytenoid soft tissues.

Etiology and Microbiology

• Historically driven by Haemophilus influenzae type b (Hib) in young children. Following widespread routine Hib conjugate vaccination, the pediatric incidence declined by >90%.
• Current cases occur primarily in unvaccinated children and adults (mean age 45 to 55 years).
• Dominant pathogens: Streptococcus pneumoniae, Haemophilus influenzae (non-typeable and Hib), Staphylococcus aureus (including MRSA), and Group A Streptococcus (Streptococcus pyogenes).

Clinical Presentation: The Cardinal "3 D's"

• Rapid onset of severe sore throat, high fever, toxic appearance, and severe odynophagia that is dramatically out of proportion to mild pharyngeal erythema on superficial inspection.
• The Classic Triad of the "3 D's":
  1. Drooling: Inability to swallow oral secretions due to excruciating odynophagia;
  2. Dysphagia;
  3. Distress: Severe inspiratory stridor, tachypnea, and accessory muscle use.
• Voice Changes: Muffled "hot potato" voice (supraglottic fullness dampens vocal resonance; vocal cords are unaffected, so hoarseness is typically absent).
• Characteristic Posture: The tripod position (patient sits upright, leaning forward with arms braced on knees, neck hyperextended, and chin thrust forward to maintain maximal supraglottic airway diameter).

Diagnostic Imaging: The "Thumbprint Sign"

• In a hemodynamically stable patient with a secure airway, a lateral soft tissue radiograph of the neck demonstrates:
  • The "Thumbprint Sign": A rounded, enlarged, edematous epiglottis resembling the silhouette of an adult human thumb projecting into the hypopharynx, with obliteration of the vallecular air space.
  • Safety Rule: Radiographs should NEVER be performed if the patient is in severe respiratory distress or shows signs of airway compromise; imaging must never delay definitive airway management.

[!WARNING] STRICT PROHIBITION OF ORAL EXAMINATION (THE FATAL LARYNGOSPASM WARNING): DO NOT use a wooden tongue depressor, attempt indirect laryngoscopy, or perform oral swabs in a patient with suspected epiglottitis outside of an operating room. Mechanical irritation of the inflamed, hypersensitive supraglottic tissues or acute patient distress can precipitate sudden, catastrophic reflex laryngospasm, resulting in complete, irreversible airway obstruction and immediate cardiac arrest.

Emergency Airway & Medical Management

1. Maintain Calm: Keep the patient in their chosen position of comfort (allow children to remain in a parent's lap). Avoid invasive procedures, blood draws, or IV lines until the airway is secure.
2. Controlled Airway Control in the Operating Room:
   • Immediate mobilization of a multidisciplinary emergency team: Otolaryngology (ENT) and Anesthesiology.
   • Transport the patient directly to the operating room; perform inhalational induction (sevoflurane) in the sitting position, followed by gentle endotracheal intubation utilizing a flexible fiberoptic bronchoscope or video laryngoscope with an endotracheal tube sized 0.5 to 1.0 mm smaller than normal.
   • Equipment for an emergent surgical airway (cricothyrotomy / tracheostomy) must be open and immediately available at the bedside prior to induction.
3. Parenteral Antimicrobial Therapy:
   • Once the airway is secured, obtain blood cultures and initiate high-dose IV antibiotics: $\mathbf{Ceftriaxone\text{ }2\text{ g IV daily}} \quad + \quad \mathbf{Vancomycin\text{ }15\text{ to }20\text{ mg/kg IV q8-12h}}$
   • Intravenous Dexamethasone ($0.15\text{ mg/kg}$) is frequently administered as an adjunctive anti-inflammatory agent to hasten resolution of supraglottic edema.

---

3. Ludwig's Angina

Ludwig's angina is a rapidly expanding, potentially gangrenous, non-suppurative cellulitis involving the bilateral submandibular, sublingual, and submental fascial spaces.

Pathogenesis & Odontogenic Origin

• Odontogenic Source: Over $70%\text{ to }90%$ of cases originate from an infected mandibular molar—specifically the second or third mandibular molars.
• Anatomical Basis: The roots of the second and third lower molars extend inferiorly below the insertion of the mylohyoid muscle on the lingual aspect of the mandible. Periapical dental abscesses or periodontitis in these teeth directly penetrate the thin lingual cortical plate, gaining unimpeded access to both the sublingual space (above the mylohyoid) and the submandibular space (below the mylohyoid).
• Microbiology: Virulent polymicrobial oral flora consisting of oral streptococci (Streptococcus viridans, Streptococcus anginosus), Staphylococcus aureus, and oral anaerobes (Peptostreptococcus, Fusobacterium nucleatum, Bacteroides species, and Prevotella).

Physical Examination Findings

• Massive, symmetric, tense, brawny swelling of the bilateral anterior neck and submandibular regions, displaying a firm, unyielding texture ("woody induration" or "bull neck" appearance).
• Elevation and Posterior Displacement of the Tongue: The tongue is pushed superiorly and posteriorly against the hard palate, resulting in severe airway narrowing, severe drooling, inability to swallow secretions, muffled voice, and trismus (inability to open the jaw).
• Important Diagnostic Pearl: Ludwig's angina is primarily a rapidly spreading phlegmonous cellulitis rather than an abscess; palpable fluctuance is characteristically ABSENT in the early stages.

Emergency Airway Management

• Leading Cause of Death: Asphyxiation caused by the progressive superior-posterior displacement of the tongue occluding the hypopharynx.
• Airway Management Mandate:
  • Standard direct laryngoscopy and blind oral or nasotracheal intubation are strictly contraindicated due to distorted anatomy, severe trismus, tissue rigidity, and the extreme risk of precipitating total airway collapse or laryngospasm.
  • Gold Standard: Awake flexible fiberoptic nasotracheal intubation performed by an expert airway specialist in the operating room.
  • If fiberoptic intubation is unsuccessful or anatomically impossible, emergent awake tracheostomy or cricothyrotomy under local anesthesia must be performed immediately.
• Pharmacotherapy & Surgical Decompression:
  • High-dose broad-spectrum intravenous antibiotics initiated immediately:
    • Ampicillin-sulbactam (Unasyn) $3\text{ g}$ IV every 6 hours; OR
    • Ceftriaxone $2\text{ g}$ IV daily PLUS Metronidazole $500\text{ mg}$ IV every 8 hours; OR
    • In penicillin-allergic or septic patients: Vancomycin $15\text{ to }20\text{ mg/kg}$ IV q12h PLUS Meropenem $1\text{ g}$ IV q8h.
  • Urgent surgical consultation for wide surgical incision, drainage, and bilateral fascial decompression if purulent collections or tissue tension fail to resolve rapidly with antibiotics.

---

4. Acute Angioedema: Histaminergic vs. Bradykinin-Mediated

Angioedema is characterized by sudden, localized, non-pitting, transient swelling of the deep dermis, subcutaneous tissue, or submucosal tissues. Rapidly identifying the underlying biochemical mediator is life-saving, as medical treatments are entirely different.

                   DIAGNOSTIC & THERAPEUTIC DIFFERENTIATION
                             OF ACUTE ANGIOEDEMA

  ┌─────────────────────────────────────────┐   ┌─────────────────────────────────────────┐
  │     HISTAMINERGIC ANGIOEDEMA            │   │      BRADYKININ-MEDIATED ANGIOEDEMA     │
  ├─────────────────────────────────────────┤   ├─────────────────────────────────────────┤
  │ • Mast cell degranulation (IgE / Type I)│   │ • Kininase II (ACE) block or C1-INH def │
  │ • Rapid onset (minutes to 1-2 hours)    │   │ • Indolent onset (hours, peaks 12-24h)  │
  │ • URTICARIA (HIVES) & PRURITUS PRESENT  │   │ • NO URTICARIA; NO PRURITUS             │
  │ • Often wheezing / bronchospasm / shock │   │ • Bowel edema (severe abdominal colic)  │
  │                                         │   │                                         │
  │ HIGHLY RESPONSIVE TO:                   │   │ COMPLETELY REFRACTORY TO:               │
  │ 1. IM Epinephrine 0.3 mg (1:1,000)      │   │ • Epinephrine                           │
  │ 2. IV Diphenhydramine 50 mg (H1)        │   │ • Antihistamines                        │
  │ 3. IV Famotidine 20 mg (H2)             │   │ • Corticosteroids                       │
  │ 4. IV Methylprednisolone 125 mg         │   │                                         │
  │                                         │   │ TARGETED RESCUE THERAPY:                │
  │                                         │   │ 1. C1-INH Concentrate (Berinert 20 U/kg)│
  │                                         │   │ 2. Icatibant (Firazyr 30 mg SubQ)       │
  │                                         │   │ 3. Ecallantide (Kalbitor 30 mg SubQ)    │
  │                                         │   │ 4. Fresh Frozen Plasma (FFP 2-4 units)  │
  └─────────────────────────────────────────┘   └─────────────────────────────────────────┘

Bradykinin-Mediated Angioedema Mechanisms

1. ACE Inhibitor-Induced Angioedema:
   • Angiotensin-converting enzyme (ACE) is identical to kininase II, the primary endogenous metalloproteinase that degrades bradykinin.
   • Pharmacological ACE inhibition halts bradykinin breakdown. Accumulated bradykinin binds to endothelial bradykinin $B_2$ receptors, triggering massive release of nitric oxide and prostacyclin, producing dramatic post-capillary venular vasodilation and increased microvascular permeability.
   • Occurs in $0.1%\text{ to }0.7%$ of patients receiving ACE inhibitors (with a 5-fold higher incidence in African Americans due to genetic polymorphisms in alternative kinin breakdown enzymes).
   • Timing Phenomenon: Can manifest within hours of the initial dose, or after months to years of completely uneventful chronic ACE inhibitor therapy.
2. Hereditary Angioedema (HAE):
   • Autosomal dominant deficiency (Type 1, ~85% of cases; low antigenic C1-INH level) or dysfunction (Type 2, ~15% of cases; normal/elevated antigenic level but low functional activity) of C1-esterase inhibitor (C1-INH).
   • C1-INH regulates the contact (kallikrein-kinin) system; its absence allows uncontrolled conversion of prekallikrein to kallikrein, generating massive quantities of bradykinin.
   • Diagnostic Screening: Serum complement C4 concentration is the best initial screening test, remaining persistently low (<50% of normal) even during asymptomatic remission periods.

Emergency Airway Protection in Angioedema

• Immediate bedside flexible fiberoptic nasopharyngoscopy must be performed to inspect the uvula, base of the tongue, epiglottis, and false/true vocal cords.
• Indications for Prophylactic Awake Fiberoptic Intubation:
  • Stridor, hoarseness, dyspnea, progressive posterior tongue enlargement, or supraglottic / epiglottic edema.
  • Intubation must be executed proactively while the airway remains partially open; waiting until full glottic closure transforms a manageable intubation into an emergency surgical airway.