Epistaxis & Misc Flashcards
What are the local factors that may cause epistaxis? 7
- Anatomic factors (septal deviation/spur)
- Intranasal corticosteroid use
- Septal perforation
- Mucosal dryness/inflammation
- CPAP/nasal prongs
- Digital trauma
- Intranasal subtance abuse
Describe the complete management of epistaxis
A. GENERAL STEPS
1. ABC’s
2. Large bore IV x 2
3. Vital signs ± ABGs
4. Investigations: CBC, platelets, INR, PTT, group and screen
5. Continuous oximetry
6. Suction at bedside
B. CONSERVATIVE
1. HOB elevation
2. Remove irritants such as nasal prongs
3. Sit forward
4. Apply manual pressure
5. Stop/reverse anticoagulation
C. NON-SURGICAL
1. Topical decongestion
2. Tranexamic acid (IV or topical)
3. Cauterization - silver nitrate, electrocautery
4. Packing - absorbable vs. nonabsorbable, anterior, posterior, combined, balloon packs
5. Greater palatine canal injection
6. Radiologic embolization of internal maxillary and facial arteries
D. SURGICAL
1. Sphenopalatine artery ligation - transantral vs. endoscopic
2. Ethmoid artery ligation - Lynch frontoethmoidectomy approach vs. endoscopic
3. Maxillary artery ligation - Transantral
4. External cartoid artery ligation (should see at least 3 branches to confirm its ECA before ligating - in case it could be the ICA that may also have branches)
Describe how to do an SPA ligation?
- Find attachment of middle turbinate to lateral wall
- Make a sickle shaped cut here
- Identify the crista ethmoidalis
- SPA should exit just behind the crista ethmoidalis
- Ligate/cauterize/clip the SPA and its branches here
Name the important landmarks for performing an endoscopic sphenopalatine artery ligation
- Crista Ethmoidalis, part of the perpendicular process of the palatine bone
- Seen after a vertical incision in the mucosa of the lateral wall (in the middle meatus, ~1cm anterior to the middle turbinate attachment to the lateral nasal wall, or just anterior to the posterior fontanelle) is made and the mucosa is elevated
What 2 vessels must be ligated in a transantral maxillary artery ligation to prevent recurrent epistaxis from collaterals?
- Sphenopalatine artery
- Descending palatine artery
- Both are branches from the IMAX, found in the PPF
- ECA ligation alone - ~55% success due to collaterals
- Add anterior/posterior ethmoid ligation (ICA branches)
- Ligation of both IMAX + Facial vessels = 97% success
What are the advantages and disadvantages of endoscopic SPA vs. other ligation 3, 6
ADVANTAGES:
1. Highest success rate
2. Able to control anterior and posterior branches of SPA
3. If needed, able to convert to external approach
DISADVANTAGES:
1. Periorbital ecchymosis
2. Risk of orbital hematoma
3. RIsk of optic nerve and infraorbital nerve injury
4. Dislodgement of clips possible
5. Recurrence due to collateral circulation
6. Risk of V2 numbness
What are the advantages and disadvantages of embolization for epistaxis?
ADVANTAGES:
1. Can pinpoint the site of bleeding
2. Local anesthesia
DISADVANTAGES:
1. Only for IMAX + Facial embolization
2. Cannot embolize ethmoids (risk of blindness)
3. Requires active bleeding
4. Risk of embolic event (stroke, PE)
5. Facial pain
6. Groin hematoma
7. Ophthalmoplegia
8. Hemiplegia
What are 9 complications of angioembolization in epistaxis?
- Recurrence of bleeding (10-20%)
- Cerebrovascular accident with permanent neurologic deficit (4%)
- Pulmonary embolus
- Blindness
- Temporal facial pain and paresthesia
- Trismus
- Skin necrosis
- Groin infection or hematoma
- Death
What are the advantages and disdvantages/complications of using posterior nasal packing for Epistaxis management? 10
ADVANTAGES:
1. Can be done in ED
2. Does not need General anesthesia (least invasive)
DISADVANTAGES:
1. Airway obstruction and exacerbation of OSA
2. Dyspena
3. Nasopulmonary reflex: pressure on nasal side wall causes Bronchoconstriction, hypoxemia, apnea, and cardiac dysrhythmia
4. Vagal bradycardia
5. Sinusitis
6. Otitis media
7. Toxic shock syndrome
8. Septal or alar necrosis
9. Soft palate necrosis
10. Synechiae
11. Recurrence of bleeding and need for further intervention
Regarding Hereditary Hemorrhagic Telangiectasia, discuss:
1. What is another name for this?
2. What is the genetics mutations and penetration?
3. Clinical presentation?
4. What is the diagnostic criteria?
Aka. Osler-Weber-Rendu Syndrome
- Disorder characterized by ectasias of the skin, mucous membranes, and viscera
Genetics:
- Inheritance: Autosomal dominant, varying pentrance and expression
- Chromosome: 9
- Genes: >600 mutations identified; most common = ENG (Endoglin protein mutation, part of TGF beta complex) or ACVRL1 genes
- Involved in VEGF pathways (Vascular endothelial growth factor)
- Results in: abnormal tissue repair and angiogenesis, weakened vasculature / vessel walls
Presentation:
1. Telangiectasias
2. Recurrent epistaxis
3. Pulmonary, GI, CNS bleeds possible
4. Complications: morbidity and mortality due to multiorgan AV malformations and associated hemorrhages
Diagnosis: Curacao Criteria
1. Epistaxis: Spontaneous and recurrent epistaxis
2. Telangiectasias: Multiple telangiectasias at characteristic sites including the lips, oral cavity, fingers, and nose
3. Visceral Lesions/AVMs: Including GI telangiectasias, pulmonary AVMs, hepatic AVMs, cerebral AVMs, or spinal AVMs
4. Family history: A first-degree relative with HHT meeting these criteria
Definite HHT requires at least 3 criteria
Suspected/possible HHT requires 2 criteria
Unlikely HHT if 0-1 criteria
Vancouver 458
Describe a management plan for HHT
SCREENING/COUNSELLING:
1. Consider genetic counselling
2. Evaluation of anemia and iron deficienty
3. Pulmonary AVM screening: TTE, Non-contrast CT chest
4. Screening for Cerebral AVMs, hepatic AVMs, Spinal AVMs (controversial)
LOCAL EPISTAXIS MANAGEMENT
1. Conservative: Humidification, lubricants, saline sprays/irrigation
2. Medical: Topical or PO TXA (high dose), topical estrogen
3. Procedural: Cauterization (ideally not, disturbs more)
4. Procedural: Lasers with wavelengths absorbed by hemoglobin (450-600nm, 800-950nm)
- Nd:YAG argon laser
- KTP (potassium titanyl phosphate) laser (532nm)
- Argon laser (514nm)
SYSTEMIC EPISTAXIS THERAPY
1. Tamoxifen (selective estrogen receptor modulator)
2. TXA
3. Evolving modalities: Bevacizumab - Avastin (Anti-VEGF antibody); Thalidomide
PROCEDURAL/SURGICAL
1. Saunders septodermoplasty (gold standard): excising septal mucosa in the supraperichondrial plane (cannot graft over cartilage only) and covering it with a skin graft
2. Local rotation flaps
3. Embolization (only for severe and unresponsive epistaxis, potential for severe complications - i.e. cerebrovascular events)
4. Young’s procedure (last resort): Septodermoplasty + closure of the nostril with vestibular skin
Vancouver 459
What is nasal folliculitis and furuncle? What are the possible complications?
NASAL FOLLICULITIS/FURUNCLE:
- Infections of the hair follicle caused by Staph aureus or strep
COMPLICAITONS:
1. Septal chondritis
2. Septal abscess
3. Saddle-nose deformity/septal perforation
4. Cavernous sinus thrombosis
Describe the anatomy of the nasolacrimal duct
- Lacrimal sac ~10mm long
- Lacrimal duct ~12mm long
- Valve of Rosenmuller = junction of the lacrimal sac to the common canaliculus
- Hassner’s valve = valve that opens duct into nasal cavity
Vancouver 459 image
List a complete differential for enlarging lacrimal gland pathology 6
Most common epithelial
Most common malignancy
A. INFECTIOUS
1. Acute bacterial (Staph, Strep)
2. Chronic bacterial (trachoma, syphillis, TB)
3. Viral (HSV, EBV, mumps)
B. EPITHELIAL
1. Pleomorphic adenoma most common (50%)
2. Other 50% malignant (adenoid cystic, MEC, malignant mixed, adenocarcinoma)
C. HEMATOPOIETIC
1. Benign lymphoid hyperplasia (20% get systemic lymphoma)
2. Atypical lymphoid hyperplasia (40% get systemic lymphom)
3. Lymphoma (50% localized)
4. Leukemia
D. IDIOPATHIC
1. Sarcoid
What is the differential diagnosis of nasolacrimal duct malignancy? 5
- Squamous cell carcinoma
- Oncocytoma
- Adenoid cystic carcinoma
- Adenocarcinoma
- Melanoma
SAMOA
What is the differential for lacrimal sac pathology? 2
- Dacryocystitis
- Nasolacrimal sac malignancy
Vancouver 460
Regarding sinonasal barotrauma, discuss:
1. What is it?
2. Prevalence of sinus type affected 3
3. Epidemiology, Causes
4. Risk factors
5. Symptoms/features
6. Pathophysiology
SINONASAL BAROTRAUMA:
- Caused when sudden changes in ambient pressure are not compensated for by force equalization mechanisms within the paranasal sinuses
LOCATION:
1. Frontal (68%)
2. Ethmoid (16%)
3. Maxillary (8%)
CAUSES:
1. Most common: Sudden shifts in barometric pressure due to altitude changes during flight and resurfacing diving
2. Descent, increased gravity (ie. going lower), diving, decompression, and HBO therapy - twice as more common than ascent, compression, and reverse squeeze
RISK FACTORS: Any etiology that would narrow or obstruct the natural sinus ostia, thereby increasing risk with underwater diving or flying
1. Nasal polyposis
2. Stenosis of sinus ostia
3. Obstruction with mucous or fungus ball
4. Sinusitis
5. URTI
6. History of middle ear barostruma
NOT related to:
1. Alcohol or tobacco use
2. Gender
3. Mild nasal septal deviation
4. Inability to perform Valsalva maneuvers
SYMPTOMS:
1. Facial pain
2. Headache
3. Lacrimation
4. Epistaxis
PATHOPHYSIOLOGY:
- Normally, air pressure within sinus cavities equilibrates with surrounding nasal passages via ostia
- Small changes in volume of gas within sinuses are compensated by passageways between central nasal cavity and sinuses = pressure equalization
- In sinus barotrauma, the ostial diameter is narrowed either due to anatomic stenosis or reversible obstruction –> impairs ability to equilibrate, leading to mucosal injuries seen in barosinusitis
- Shallow waters more common (rapid 5m underwater dive is equivalent to 5500m descent above sea level)
- Presence of the following may increase intensity (more aerated): (1) concha bullosa, (2) large maxillary sinus, (3) sphenoethmoidal cells
ASCENT:
- Surrounding pressure decreases, allowing for gas expansion within nasal sinuses and increased sinus pressure
- This process slows due to slow pressure equalization, keeping high pressure within the sinus and causing pain, headache, and mucosal damage
- “Reverse squeeze” = increased sinus pressure with uncompensated pressure release
- “Trapping pressure” = pressure unable to be equalized causes an outward, expansile compression injury of the sinus mucosa against the bony sinus outer walls
- 150mmHg = mucosal hyperaemia, seromucous, effusion
- >300mmHg = interstitial hemorrhage
DESCENT:
- Increased surrounding pressure compresses gas within the sinuses causing negative pressure - creating a “pulling effect” on the mucosa, causing edema, tearing, or hematoma formation
- “Squeeze” phenomenon
