Ingestions, trauma, macroglossia, ankyloglossia, misc

Question 1

What is the genetic basis of Sickle Cell disease?

Answer 1

Autosomal Recessive
- Gene defect in a single nucleotide mutation (GAG codon changing to GTG) of the beta-globin gene –> results in glutamic acid (E/Glu) being substitued by valine (V/Val) at position 6 (E6V substitution)
- Allele responsible for sickle cell anemia can be found on the HBB gene, short arm of chromosome 11, more specifically 11p15.5

Carrier: HbS replaces one Hb-beta subunit
Disease: HbS replaces BOTH Hb-beta subunits

Question 2

Discuss the pre-operative, Intraoperative, and post-operative management of children with suspected sickle cell disease

Answer 2

Sickle cell disease = sickled erythrocytes in microvasculature causing decreased peripheral perfusion.
- Higher degree of perioperative morbidity and mortality (complication 30-50% higher compared to without SCD)

PRE-OPERATIVE EVALUATION
History and Exam:
- Vaso-occlusive crises (acute chest syndrome, cerebrovascular accidents, and pHTN)
- Prior transfusions
- Current analgesic regimen
- Neurologic assessment
- Oxygen saturation

Labs:
- Baseline hematocrit
- Type and rossmatch
- Polysomnography
- Sickle cell screen
- Hgb Electrophoresis (to measure sickled:non-sickled cells)

Management (to decrease risk of sickling)
- Transfuse if S:NS cells > 30:70 (ie. if >30% sickled cells) OR Hgb < 100g/L
- IV hydration
- Bronchodilators
- Hydroxyurea
- Transfusions for >30% sickled cells, and Hgb goal of over 100g/L decreases risk of vaso-occlusive crises and cerebrovascular accidents
- Exchange transfusion for patients with severe SCD phenotypes and experiencing frequent pain crises or other complications despite hemoglobin > 100g/L

INTRAOPERATIVE MANAGEMENT
- Maintain homeostasis: warm, hydrated, oxygenated

POST-OPERATIVE MANAGEMENT
- Consult hematology
- Post-operative transfusion to maintain Hgb > 100g/L
- Monitor for complications
- Keep warm
- Supplemental O2 x 24 hours
- Appropriate antibiotics
- Adequate hydration (maintenance + 50%)
- Early mobilization
- Aggressive pain management - may be difficult if chronic opioid use (chronic pain crises) –> consult chronic pain service

Question 3

Define acute chest syndrome.
What is seen on CXR?
How is it managed?

Answer 3

Acute Chest Syndrome = Hypoventilation (from pain, GA, opiates, fluid overload, etc.) results in acute sickling, especially in the lungs

CXR: Pulmonary infiltrates

Treatment:
1. O2, pain control, bronchodilators
2. Empiric IV antibiotics vs. atypicals (e.g. Mycoplasma, chlamydia –> penicilliin)
- All patients with ACS should be treated with broad spectrum antibiotics
3. Closely monitor fluids (avoid overload)
4. Blood transfusion (& consider complete exchange transfusion if symptoms severe or refractory)
5. ICU consult

Question 4

What are the AAOHNS indications for coagulation studies pre-op?

Answer 4

Only if indicated by history or if genetic information is unavailable

Question 5

What is the protein and inheritance of Hemophilia A, B, and Von Willebrand disease?

Answer 5

1. Hemophilia A: Factor VIII, X-linked recessive
2. Hemophilia B: Factor IX, X-linked recessive
3. Von Willebrand - vWD, Autosomal dominant

Question 6

Which location does airway foreign bodies preferentially go to? List 4 reasons why this occurs

Answer 6

Right mainstem bronchus

1. Wider diameter
2. Greater airflow (3 lobes on right, vs 2 on left)
3. Less acute angle of takeoff
4. Carina is positioned to the left of midline

Question 7

Describe the four mechanisms of airway obstruction from foreign body (valves of airway obstruction). What do they appear like on CXR?

Answer 7

1. CHECK VALVE
   - Air can get in but not out (“check” in)
   - CXR: Hyperinflation on expiratory view, mediastinal shift to opposite side
2. BYPASS VALVE
   - Partial obstruction only: reduced airflow on inspiration and expiration
   - CXR: Normal
3. STOP VALVE
   - Complete obstruction: No air in or out
   - CXR: Collapse of affected segment
4. BALL VALVE
   - Air can get out but not in (rare) (“bail” out)
   - CXR: Atelectasis q

Question 8

Regarding airway foreign bodies, discuss:
1. History
2. Clinical presentation (based on location)
3. Stage
4. Work-up/diagnosis
5. Treatment
6. Post-operative considerations

Answer 8

HISTORY:
1. Most sensitive clue = paroxysmal choking episode

CLINICAL PRESENTATION:
1. LARYNGEAL = obstruction, stridor, hoarseness, “thud” on auscultation of throat
2. THORACIC = Biphasic stridor, wheeze
3. BRONCHIAL (80-90%) = cough, wheeze, decreased breath sounds
4. CHRONIC = Subacute fever/lung problems NYD (consider occult FB!)
5. Large foreign body may cause only partial obstruction - but ensuing edema will cause full obstruction!

STAGES:
1. Acute phase (minutes) = choking, gagging, coughing @ time of aspiration, most deaths happen here
2. Asymptomatic phase (days to weeks) = Symptoms subside as FB becomes lodged, reflexes fatigue
3. Complications phase (weeks) (obstruction, erosion, infection) = fever, pneumonia, hemoptysis, atelectasis, abscess

WORK-UP/DIAGNOSIS:
1. Clinical suspicion based on history
2. Respiratory examination (decreased air sounds or wheezing)
3. CXR (inspiratory & expiratory views): air trapping, hyperinflation, mediastinal shift, atelectasis
- 35% have normal CXR
4. Bronchoscopy

TREATMENT:
1. Acute foreign body = emergency (partial obstruction will quickly progress to full obstruction with progressive edema)
2. Infants: rescue breaths + chest compressions
3. Children > 1 year: abdomen thrusts while supine (only if complete! This procedure risks disloding partial to complete)
4. Older children: Heimlich maneuver
5. Endoscopic removal in OR
- NPO, Anesthesia consult, observation, steroids, transition to OR
- Once FB remove - always go back and look again!

POST-OPERATIVE CONSIDERATIONS:
1. Intubate if worried about degree of airway edema
2. ICU observation
3. Steroids
4. Epi nebs
5. Parental education on airway foreign bodies!

Question 9

What are the risks of airway foreign body removal (ie. what must you be sure to include in the consent)?

Answer 9

INTRA-OPERATIVE:
1. Anesthesic
2. Dental/laryngeal injury
3. FB impaction - worse obstruction
4. Mucosal tear - bleeding, perofration
5. Pneumothorax
6. Inability to extract - need for further surgery

EARLY POST-OPERATIVE:
1. Airway edema - obstruction
2. Post-obstructive pulmonary edema

LATE POST-OPERATIVE:
1. Pneumonia
2. Granulation tissue
3. Stricture

Question 10

When conducting airway FB removal in the OR, what are some pre-operative and pre-anesthetic considerations?

Answer 10

1. Have multiple scope sizes ready
2. Pre-test all equipment prior to induction (work out all kinks ahead of time!)
3. Have multiple back up plans
4. Patient must be spontaneously ventilating
5. Lidocaine spray to vocal folds (reduce risk of laryngospasm)
6. Observe child’s patterns: e.g. how fast do they desat, etc.?

Question 11

When conducting airway FB removal in the OR, what should be considered if there is mucosal tear or bleeding?

Answer 11

1. Epi neb through vent port
2. Epi solution squirted down airway
3. Epi bledgets
4. Direct pressure with bronchoscope

Question 12

When conducting airway FB removal in the OR, what can you do if the foreign body drops into the trachea as you’re picking it out?

Answer 12

1. Don’t try to pick it up (prolonged iatrogenic complete airway obstruction)
2. Push back down into the bronchus it came from
3. If still stable, then try again

Question 13

When conducting airway FB removal in the OR, what considerations should be made if there is a prolonged removal attempt or traumatic attempt?

Answer 13

1. Risk worsening airway edema
2. Push back into the bronchus it came from
3. Intubate if necessary
4. ICU post-op, steroids, epi nebs
5. Come back in 48 hours to retry

Question 14

When conducting airway FB removal in the OR, what happens after you fail again at the second OR and cannot remove it?

Answer 14

Consult thoracics for thoracoctomy

Question 15

What is the difference between using rigid vs. flexible bronchs for suspected pediatric airway foreign body? List some advantages and disadvantages?

Answer 15

RIGID BRONCHOSCOPY:
1. Can ventilate through bronch
2. Definitive airway
3. Can more easily suction
4. Allows instrumentation
5. BUT more traumatic
6. BUT can’t access smaller airways

FLEXIBLE BRONCHOSCOPY:
1. Less traumatic (good if low suspicion for FB)
2. Can get into small airways
3. Can see around corners

Question 16

Regarding esophageal foreign bodies, discuss:
1. Common locations of dislodgement
2. Clinical presentation
3. Work-up/diagnosis
4. Treatment

Answer 16

LOCATIONS:
At sites of natural esophageal narrowing:
1. Upper esophageal sphincter/Cricopharyngeus (most common) - C6, 15cm from upper incisor
2. Aortic arch - T4, 23cm from upper incisor
3. Crossing of left mainstem bronchus (in front of esophagus) - T6 ~25cm
4. Left atrium
5. Lower esophageal sphincter - 40cm from upper incisor

CLINICAL PRESENTATION:
1. Choking/gagging episode
2. Odynophagia, dysphagia, retching, vomiting, hypersalivation
3. If large FB, may cause tracheal compression, cough, respiratory distress

WORK-UP and DIAGNOSIS:
1. Clinical suspicion
2. CXR

Button battery:
- Halo/Double ring sign (AP view)
- Step-off sign (lateral)

TREATMENT:
- Usually not emergency, except battery or large FB causing airway obstruction

Stable:
- Observation, serial CXR (may pass)
- Young symptomatic children, FB >24h, and sharp metallic or caustic objects should undergo endoscopic removal
- Asymptomatic children, recent ingestion (< 24h), no esophageal disorders, can be observed for 8-16h
- ?Evidence that honey might lessen caustic injury

Lodged at UES:
- Endoscopic removal in OR

Options if lodged past UES:
- Observation (will likely pass)
- Push into stomach (will likely pass)
- Glucagon (increases esophageal motility)
- GI consult

5% risk of second FB, so always look for another!

Vancouver 510

Question 17

Compare and contrast airway vs. esophageal foreign bodies with respect to:
1. History
2. Physical Exam
3. Imaging
4. Treatment

Answer 17

HISTORY:
1. Airway:
- Witnessed aspiration
- Cough, dyspnea, wheezing, stridor
- Refractory asthma
2. Esophagus:
- Witnessed ingestion
- Vomiting, drooling, dysphagia, odynophagia, emesis, food refusal, chest pain

PHYSICAL EXAM:
1. Airway
- Decreased lung sounds
- Wheezing
- Crackles
- Tachypnea
- Hypoxemia
2. Esophagus:
- Drooling
- Poor feeding
- Choking

IMAGING:
1. Airway
- PA and lateral radiographs (radiopaque FB, unilateral emphysema or hyperinflation, localized atelectasis or infiltrate)
2. Esophagus
- PA and lateral radiographs (radioipaque FB, widened prevertebral shadow, loss of lordosis)

TREATMENT:
1. Airway
- Rigid bronch for removal
2. Esophagus
- Young symptomatic children, FB >24h, and sharp metallic or caustic objects should undergo endoscopic removal
- Asymptomatic children, recent ingestion (< 24h), no esophageal disorders, can be observed for 8-16h

Question 18

Describe 4 mechanisms that button batteries in the esophagus can cause damage

Answer 18

A. ELECTRICAL INJURY: ELECTROLYSIS (Mucosal burn)
- Predominant mechanism of injury
- Moist environment –> hydrolysis reaction starts on the anode (negative) surface –> electrical charge created
- Mucosa bridges the positive and negative terminals, completing the circuit, allowing current to flow –> this creates an electrical burn
- Very quick! Injury can start within 15 minutes

B. MECHANICAL INJURY: Pressure Necrosis
- Physical pressure and compression of battery on esophageal mucosa –> necrosis with increased duration of compression

C. TOXIC INJURY: Heavy metal/poison toxicity
- Rarer injuries (case reports)
- Systemic damage caused by leakage of toxins
- Lithium toxicity (e.g. weakness, ataxia, neurologic symptoms)
- Heavy metal poisoning (e.g. mercury poisoning)

D. CHEMICAL INJURY: Acidic/alkaline caustic injury

Alkaline caustic exposure:
- Discharged current from electrical circuit hydrolyzes water, creating Hydroxide Ions (OH-) and increasing pH creating alkaline environment
- Alkalis strip protons (H+) from nearby molecules –> protein denaturation and liquid saponification
- “Liquefaction Necrosis”: reacts with proteins and fats to produce proteinases and soaps (salt of a fatty acid)
- Penetrates deeper than acids (transmural injury)
- Significant injury can occur within 2 hours
- Alkaline material leakage from the battery can occur, but not as responsible for majority of caustic injury

“Negative-Narrow-Necrosis”
- Current generates hydroxide at negative terminal (anode)
- Negative terminal is narrow side of the battery
- Orientation of the battery can predict where more severe necrosis and injury will be

Acidic Caustic exposure:
- Negative electrode creates alkaline environment, while positive electrode creates an acidic environment
- “Coagulative Necrosis” (tissue ischemia)
- Less significant injury compared to alkaline environment for the following reasons:
– Forms eschar, preventing deep penetration
– Esophagus slightly alkaline at baseline –> some neutralizing effects occur against acid formed
– Squamous epithelium naturally more resistant to acids

Interesting Case Rounds 2022

Question 19

Can dead batteries cause esophageal injury?

Answer 19

Yes!

Even though battery is no longer capable of powering a device, it still has enough current to cause esophageal injury

Question 20

Are singing/musical greeting cards dangerous with respect to button battery risk?

Answer 20

This has mostly been addressed by most greeting card industries.

A few manufacturers abadoned use of lithium batteries and reintroduced alkaline batteries. Others have secured the battery compartments making it very difficult to pop out the battery.

Question 21

Why are lithium batteries particularly dangerous with respect to button battery ingestion?

Answer 21

• Most common battery type in kids’ toys
• Thin design - easier to swallow and become impacted, also resembles coin on CXR given how thin and therefore may be missed/delayed (see Interesting Case rounds comparison photo of thin batteries)
• 2x more powerful than other batteries
• Severe damage in 2 hours, ulceration by 4 hours, perforation by 6 hours

Question 22

What are the risks of esophageal foreign body extraction? (Consent for OR)

Answer 22

INTROPERATIVE:
1. Anesthetic
2. Dental/laryngeal injury
3. ETT dislodged - airway emergency
4. Mucosal tear - bleeding, perforation
5. Mediastinitis

EARLY POST-OP:
1. Vomiting
2. Aspiration
3. Missed 2nd FB
4. Retropharyngeal abscess (rare)

LATER POST-OP:
1. STricture

Question 23

Describe the grading system for Esophageal burns and caustic ingestions

Answer 23

ZARGAR’S GRADING
1 = Edema/erythema
2 = Ulceration/white exudates
3 = Necrosis
4 = Perforation

• Grade 0: No injury
• Superficial - Grade I: Mucosal edema and hyperemia
• Superficial - Grade IIa: Superficial, noncircumferential, whittish membranes, shallow ulcers, hemorrhage, friable exudates
• Transmucosal - Grade IIb: Deep, circumferential lesions with stricture formation
• Transmucosal - Grade IIIa: Small, scattered areas of necrosis
• Transmural - Grade IIIb: Extensive necrosis
• Transmural - Grade IV: Perforation

Interesting case rounds Slide 20

Question 24

What is the pathological classification of caustic esophageal injuries?

Answer 24

1st Degree
- Superficial mucosal damage
- Focal or diffuse erythema, edema, hemorrhage
- Mucosa sloughs eventually
- No scar formation

2nd Degree
- Mucosal and submucosal damage
- Ulceration, exudates, vesicle formation
- Eventually granulation tissue
- Scar possible stricture

3rd Degree
- Transmural injury
- Ulcers, black discoloration
- Perforation of the wall

Question 25

What are the possible structures that may be injured secondary to esophageal injury from perforation/button battery?

Answer 25

ANTERIOR INJURIES (Vascular & Trachea):
1. Proximal esophagus: Inferior thyroid artery, TEF, VF injury
2. Mid-esophagus: Aorto-esophageal fistula
3. Distal esophagus: Atrio-esophageal fistula

POSTERIOR INJURIES:
1. Spondylodiscitis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5425245/

Interesting Case Rounds Slide 21

Question 26

Describe the management post-operatively for a patient with esophageal injury secondary to button battery ingestion / removal

Answer 26

1. NPO, NG insertion (for stenting and enteral nutrition)
2. Second look endoscopy (controversial) - early timing may lead to false reassurance
3. Evaluate extra-esophageal injuries (e.g. vascular injuries)
   - MRI with contrast
   - CT angiography
4. Esophagram (fluoro) with water-soluble contrast (Gastrograffin): detecting perforation and stricture formation
   - First study POD1-7
   - Second study POD7-14

Question 27

Compare alkaline and acidic caustic ingestions, including mechanism of action, and sites at greatest risk.

See separate card for battery-related alkaline/acidic injury.

Answer 27

ALKALINE = LIQUEFACTION NECROSIS
1. Mechanism of Action
- Alkali or Hydroxide Ions (OH-) strip protons (H+) from nearby molecules –> protein denaturation and liquid saponification of cell membranes
- “Liquefaction Necrosis”: reacts with proteins and cell membrane components and fats to produce proteinases and soaps (salt of a fatty acid) –> forms caustic protein matter
- Solubility allows for deeper tissue penetration compared to acids (transmural injury)
- Significant injury can occur within 2 hours

2. Esophageal narrowings at greatest risk: areas of slower passage, prolonged contact time
   - UES
   - Aortic arch
   - LMSB
   - Diaphragm/LES
   - GE Junction

ACIDIC = COAGULATIVE NECRORIS
1. Mechanism of Action
- “Coagulative Necrosis” (tissue ischemia) = eschar formation, which prevents deep tissue penetration
- Less significant injury compared to alkaline environment for the following reasons:
– Forms eschar, preventing deep penetration
– Esophagus slightly alkaline at baseline –> some neutralizing effects occur against acid formed
– Squamous epithelium naturally more resistant to acids

2. Locations at greatest risk:
   - Gastric antrum (site of acid pooling - long contact time)

Question 28

What are the symptoms of caustic ingestion? What are key history points that should be asked?

Answer 28

SYMPTOMS:
1. Oral mucosal edema/erythema
2. Drooling
3. Tongue edema
4. Hoarseness
5. Stridor
6. Odynophagia
7. Dysphagia
8. Vomiting
9. Hematemesis
10. Epigastric/chest/back pain
11. Peritonitis
12. Sepsis

KEY HISTORY POINTS:
1. What was ingested? (pH, consistency)
2. When was it ingested?
3. How much? (volume)
4. Other co-ingestions?
5. Is bottle available (for review of labels)?

Question 29

What is the initial management of caustic ingestions?

What are the medical and surgical options for caustic ingestions?

What is the definitive treatment algorithm for caustic ingestions?

Answer 29

INITIAL MANAGEMENT:
1. ABCs
2. FNL ± secure airway if necessary
3. CXR: r/o pulmonary infiltrates, mediastinitis, perforation (Free air)
4. Esophagoscopy in OR

MEDICAL CONSIDERATIONS:
1. Do NOT provoke emesis (double burn!)
2. Do NOT dilute/buffer (risk emesis or aspiration)
3. Secure airway
4. Analgesia
5. NPO, IVF
6. Antibiotics (e.g. ampicillin) x 3-6 weeks (possible increases epithelialization and reduces granulation tissue)
7. Steroids x 3-6 weeks (decreases stricture formation)
8. PPI
9. Lathyrogens - reduce collagen cross binding to decrease esophageal stricture, unproven benefit (e.g. penicillamine, beta-aminoproprionitrile, acetylcysteine)
10. Sucralfate - protects esophageal mucosa against gastric acid, and reduces granulation

SURGICAL CONSIDERATIONS:
1. Endoscopy in OR at 24-48 hours (timing and frequency controversial)
2. Determine degree of injury (may need VATS or thoracotomy for mural exam if cannot determine transmural injury or not)
3. STOP if further endoscopy risks perforation
4. Place NG intra-operatively and leave for 7-10 days
5. Gastrograffin swallow at day 7-10 to check for perforation
6. Esophagectomy may be required if severe damage (blunt vs. thoracotomy) - early with reconstruction
7. Possible gastrectomy with exploratory laparotomy to remove necrotic tissue

DEFINITIVE TREATMENT ALGORITHM
Caustic ingestion –> < 48 hours vs. > 48 hours

If >48 hours, then gastrograffin esophagram.
- Normal = Repeat in 3 weeks, and if normal observe
- Stricture = dilatation

If < 48 hours, then determine whether airway emergency or not
- If yes, secure airway then go down admission pathway
- If no, then determine extent of symptoms, type of substance ingested, and whether there are oropharyngeal lesions or not

If no symptoms/issues with substance/no lesions, then observe < 24 hours and discharge

If symptoms/lesions/strong substance, then admission pathway:
1. Admit, NPO, IV fluids, Esophagoscopy in 24-48 hours

Based on esophagoscopy, determine extent of esophageal injury based on grading system:
1. Grade 0 and 1: Discharge, follow up as needed
2. Grade 2: Feeding tube, possible steroids, dilate stricture if present
3. Grade 3: Feeding tube or stent, IV antibiotics, dilate stricture if present
4. Grade 4: Esophageal replacement, IV antibiotics
If no stricture - repeat esophagram in 3 weeks

Kevan Peds Question 183 - flow chart

Question 30

List the complications of caustic ingestion (13)

Answer 30

1. Fibrosis and stricture (most common)
2. Mucosal burn
3. Perforation
4. Mediastinitis
5. Pneumonia
6. Tracheoesophageal fistula
7. Aortoesophageal fistula
8. Airway obstruction (secondary to inflammation/edema)
9. Gastric outlet obstruction (3-5%)
10. Gastric perforation –> peritonitis
11. Sepsis
12. Death
13. Higher risk for esophageal carcinoma (?1000x)

Late complications:
1. Schatzki’s ring
2. Complete stenosis
3. Barrett’s esophagus
4. Esophageal carcinoma

Question 31

What is the prognosis for esophageal caustic ingestion?

Answer 31

Grade 1/2A: Will heal fully, no scarring
Grade 2B/3A: 70-100% stricture
Grade 3B: 65% risk of death

Question 32

In what situations should esophagoscopy be aborted in esophageal burn injury?

Answer 32

1. Cannot see the lumen
2. Severe, third degree burn (Risk of perforation)

Question 33

Where do the vertical and horizontal height and projection of the nose originate?

Answer 33

Osseous and cartilaginous growth centers of the nasal septum and lateral nasal wall

Question 34

What are the most common pediatric fractures of the head/neck, in order of frequency?

Answer 34

1. Nasal
2. Orbital
3. Mandible (40-70% condyle) - Panorex best for kids

30% associated with another injury

Question 35

What is necessary for the work up of significant pediatric facial trauma?

Answer 35

1. Ophthalmology consult - ex/enopthalmos, vertical dystopia, globe rupture, and increased IOP
2. Forced duction for globe mobility
3. Intra/supraorbital nerve
4. Intercanthal distance
5. Medial canthal ligament integrity

Question 36

What are the different types of pediatric nasal septal injuries?

Answer 36

1. Perichondrium - Hematoma
2. Bone displacement - obstruction and long term hypertrophic growth disturbance
3. Caudal septal - obstruction
4. Twisted nose deformity

Question 37

Outline the treatment of pediatric mandible fractures

Answer 37

• < 2 = Splint, no IMF, soft diet
• 2-5 = Arch bars + IMF
• 6-12 = Arch bars with piriform aperture suspension, circumdental wire due to foreshortened teeth roots
• Over 12 = same as adult if permanent teeth
• Condyle (unilateral or bilateral) - soft diet, intermaxillary fixation (IMF)

Arch fractures:
- < 7 years old = splint, IMF
- Over 7 years old = wire mini plate in all ages, or if unstable

Question 38

Discuss the management for pediatric midface, zygomaticomalar, and nasoethmoid fractures

Answer 38

• CT needed for pre-op planning
• Severity dictates management
• Overall similar to that of adults
• After 5 years, maxillary sinus pneumatization favours zygomaticomalar fractures over malar and mandible arch fractures

Question 39

Discuss the management for pediatric orbital fractures

Answer 39

• Unlikely < 5 years due to small maxillary sinus
• Most common isolated fracture > 7yrs
• Coronal CT and Ophthalmology consult are needed
• Isolated blowout – observe 7-10 days
• Surgery if enophthalmos, diplopia, pain with motion
• Small orbital floor defects repaired with absorbable gelatin foam
• Large defect requires split calvarial graft (Bone graft technique < 10 years old – full thickness with reimplantation of outer cortex)

Question 40

Regarding congenital epulis, discuss:
1. What is it?
2. What is the epidemiology?
3. Where is the typical location?
4. What is the treatment?

Answer 40

What is it?
- Granular cell tumor or congenital gingival granular cell tumor (different from adult granular tumors)
- Rare benign tumor of newborns or mesenchymal origin

Epidemiology:
- Female:Male 8:1

Location:
- Anterior maxillary alveolus tumor, usually solitary

Treatment:
- Surgical excision to assist with feeding and breathing

Question 41

What are all the important lymph nodes in the head and neck named?

Answer 41

1. Node of Star (Submandibular)
2. Node of Rouvier (retropharyngeal)
3. Delphian node (Pre-tracheal)
4. Virchow’s node (Supraclavicular)

Question 42

What are the bugs that are common in odontogenic (bite) wounds and their treatment?

Answer 42

BACTERIA:
1. Eikenella
2. Group A Strep
3. Fusobacterium
4. Peptostreptococcus
5. Prevotella
6. Porphyromanoas

TREATMENT:
- Wound care, leave to heal by secondary intention
- Prophylactic antibiotics: Amoxicillin-Clavulanate

Question 43

What is the differential of chronic drooling/sialorrhea?

Answer 43

1. Medications
2. Neurologic

Indirect causes:
1. Nasal obstruction
2. Head position
3. Malocclusion
4. Tongue size
5. Sitting position
6. Emotional state

Question 44

Describe complications for HYPOsalivation

Answer 44

1. Dental caries
2. Recurrent aphthous ulcers
3. Burning mouth syndrome
4. Lichen planus
5. Oral candidiasis

Question 45

Describe complications for HYPERsalivation

Answer 45

Anterior (saliva spills out oral cavity and visible leakage over lips and chin) - pathologic after age 4:
1. Social stigma
2. Skin breakdown
3. Yeast infection
4. Dehydration

Posterior (saliva spills over posterior tongue into airway):
1. Aspiration
2. Pneumonia
3. Chronic lung disease

Question 46

Outline the management for sialorrhea

Answer 46

A. CONSERVATIVE OPTIONS (OT/PT/SLP)
1. Posture adjustment
2. Oral-motor or sensory therapy to improve oral control and sensitivity
3. Tongue strengthening
4. Behavioural modifications, with 4 categories:
a. Instruction, prompting, positive reinforcement
b. Negative social reinforcement and declarative procedures
c. Cueing techniques
d. Self-management procedures

B. MEDICAL OPTIONS (Anticholinergics)
1. Benztropine
- Children >3yo and adolescent: 0.02-0.05mg/kg/dose 1-2x/day
- Adults: 1-4mg 1-2x/day, max 6mg/day
2. Atropine
- 1-2 drops 0.5% ophthalmic solution
3. Glycopyrrolate
- Children ≥3 years and adolescents ≤16 years: PO 20mcg/kg/dose (= 0.02mg/kg/dose) TID; max 100mcg/kg/dose TID, not to exceed 1500-3000mcg/dose
- Adults: 1-2mg 1-2x/day, up to 6-8mg/day
4. Scopolamine
- 15mg transdermal patch once every 3 days
5. Benzhexol Hydrochloride
- Children and adolescents: 0.1-0.2 mg/kg/day in 2-3 divided doses; maximum daily dose of 0.75mg/kg/day
- Adults: 1mg/day increase to 5-15mg/day

Side effects: Drowsiness, irritability, mood changes, restlessness, xerostomia, urinary retention, flushing, constipation, tachycardia, blurred vision

C. PROCEDURAL OPTIONS
1. Botox injections (100 units in 4mL NS –> 25units/gland every 3-6 months) under utlrasound guidance
- Inhibits Acetylcholine release at neuromuscular junction –> blocks parasympathetic stimulation
- 75% reduction in salivary flow rate
- 7-10 days to onset, peak at 2-3 months, lasts 4-6 months

D. SURGICAL OPTIONS (Salivary reduction vs. salivary diversion procedures)

SALIVARY REDUCTION:

1. Nerve sectioning (tympanic neurectomy - Jacobsen’s nerve/tympanic plexus)
   - Advantages: Can be done under local anesthesia
   - Disadvantages: High recurrence rate
2. Ductal ligation
   - Advantages: Simple
   - Disadvantages: Sialocele or Sialoliths
3. Gland excision
   - Advantages: Very good outcomes
   - Disadvantages: Xerostomia, nerve injury (facial, lingual, hypoglossal nerve)

SALIVARY DIVERSION:

1. Submandibular duct rerouting (to posterior if problem is anterior)
   - Advantages: Decreases anterior pooling of saliva
   - Disadvantages: Ranula if sublingual gland is not excised, obstructive duct
2. Parotid duct rerouting
   - Advantages: Decreases anterior pooling of saliva
   - Disadvantages: Obstructive duct and sialocele

Question 47

What is the diagnostic criteria for Macroglossia?

Answer 47

Any 3 of the following criteria:
1. Extravasation of lingual apex or lingual border onto or outside the dentition
2. Impression of ≥1 teeth on lingual border visualized when mouth is open
3. Following surgical correction, a relapse of increased interdental space, open bite deformity, and/or jaw deformation with malocclusion occurs

Question 48

What are 3 common syndromes with macroglossia?

Answer 48

1. Trisomy 21
2. Mucopolysaccharideosis
3. Beckwidth Wiedeman

Question 49

Define the triad of signs of macroglossia

Answer 49

1. Open bite deformity
2. Mandibular prognathism
3. Malalignment

Question 50

What is the classification of local causes of macroglossia?

Answer 50

1. Congenital
   - Hemangioma
   - Lymphagioma
   - Lingual thyroid
2. Inflammatory/infectious
   - Angioedema
   - TB
   - Actinomycosis
   - Dental infection
   - Syphilitic gumma
   - Riga disease
   - Ranula
3. Traumatic
   - Dental irritation
   - Hematoma
   - Postoperative edema
   - Sublingual calculus
4. Neoplastic
   - Benign: Granular cell tumor, neurofibroma, leiomyoma, lipoma
   - Malignant: Carcinoma, sarcoma

Question 51

What is the classification of geeneralized causes of macroglossia?

Answer 51

1. Congenital
   - Primary idiopathic macroglossia
   - Beckwith wiedemann syndrome
   - Down syndrome
   - Trisomy 4P syndrome
   - Mucopolysaccharidosis
2. Inflammatory
   - Chronic glossitis
3. Toxic
   - Amyloidosis
   - Lipid proteinosis
   - Chronic steroid therapy
4. Endocrine
   - Acromegaly
   - Myxedema
   - Cretinism

Question 52

What are 3 causes of pseudo-macroglossia?

Answer 52

1. Habitual tongue posturing
2. Retrognathia/micrognathia
3. Hypotonia of tongue

Question 53

What are four treatment options for macroglossia?

Answer 53

1. Observation
2. Orofacial therapy: for hypotonia, or lingual malposition
3. Surgery
4. Submucosal minimally invasive lingual excision (SMILE)

Question 54

What are five indications for macroglossia surgery?

Answer 54

1. Airway obstruction (e.g. base of tongue macroglossia)
2. Speech impediment (particularly consonants requiring tip contact with alveolar ridge/palate)
3. Dysphagia (failure to thrive)
4. Maxillofacial abnormalities (anterior open bite, prognathism, increased ramus-body angle)
5. Cosmesis

Question 55

What are the surgical options for macroglossia?

Answer 55

1. Anterior wedge
2. Tip amputation
3. Dorsum and tip
4. Central reduction
5. Tip preservation - Kruchinsky
6. Horizontal filleting
7. Dorsal flap

Question 56

Regarding Ankyloglossia, discuss:
1. What is the definition?
2. What are non-surgical options?
3. What are the indications and contraindications for surgery?
4. Complications of surgery?
5. How should parents be counselled about tongue ties?

Answer 56

ANKYLOGLOSSIA:
- Limited tongue mobiliity due to a restrictive lingual frenulum (includes tight maxillary and mandibular frenulums)
- Increased awareness and diagnosis due to promotion of breastfeeding benefits, increased awareness by lactation consultants and dentists

NON-SURGICAL OPTIONS:
1. Observation
2. Lactation consultants
3. SLP

INDICATIONS FOR SURGERY:
1. Poor feeding/sucking - first few months
2. Impaired speech - 2-3 years
3. Social norms (older kids) - French kissing, sticking tongue out, etc.

CONTRAINDICATIONS:
1. Micrognathia/retrognathia
2. Hypotonia
3. Coagulopathy
4. Neuromuscular disorder

COMPLICATIONS:
1. Scarring
2. Obstruction
3. Salivary duct injury
4. Hemorrhage

COUNSEL:
- With minimal movement restriction, speceh and feeding difficulties are unlikely
- Not a cause for OSA

Question 57

Regarding pedatric eosinophilic esophagitis, discuss:
1. How does it present in comparison to adults?
2. Diagnosis?
3. Treatment options?

Answer 57

CLINICAL PRESENTATION:
- Failure to thrive
- Food aversion
- Regurgitation/vomiting
- Impaction
- Epigastric pain
- Males 4:1
- Young atopic teens
- Usually multi-year history of asthma/allergy

DIAGNOSIS:
1. Esophagoscopy: Furrows, rings/trachealization, white exudates, strictures
2. Biopsy - eosinophilic infiltrate (> 15/hpf)
3. Allergy testing: Allergic & non-allergic subtypes

CONSERVATIVE TREATMENT:
- Food allergy evaluation
- Hypoallergenic diet (e.g. Six-food elimination diet)

MEDICAL:
- Swallowed topical steroids (e.g. fluticasone/budesonide)

SURGICAL:
- Dilation of strictures

Question 58

What are the features of autism?

Answer 58

• Developmental regression
• Absence of protodeclarative pointing
• Abnormal reactions to environment stimuli
• Abnormal social interactions
• Absence of smiling when greeted by parents and other familiar people
• Absence of typical responses to pain and physical injury
• Language delay and deviations
• Susceptibility to infections and febrile illnesses
• Absence of symbolic play
• Repetitive and stereotyped behaviour