WILKES CLASSIFICATION

The most widely used classification of TMJ dysfunction. It's main advantage is that it can be used to guide management. It is based upon clinical presentation, appearance on imaging and what is found at arthroscopy or surgery.

Stage 1
Clinical: Painless clicking with no restrictions in motion
Imaging: Slightly forward disc that can reduce. Normal bone contour
Surgical appearance: Normal disc.
Management: Conservative and discharge. For patients who grind or clench then refer back to dentist for lower soft mouth guard worn at night

Stage 2
Clinical: occasionally painful clicking, intermittent locking, headaches
Imaging: slightly forward disc that can reduce. Early disc deformity. Normal bone contour
Surgical appearance: thickened disc. Anterior disc displacement
Management: most difficult group to decide on management. If mildly symptomatic, treat conservatively. If any muscle pain consider physio. If parafunction then refer to dentist for soft mouthguard. If still symptomatic they perform arthrocentesis. If still symptomatic after arthrocentesis some would consider arthroscopy if available or tertiary referral. Surgery is always contraindicated in this group

Stage 3
Clinical: frequent pain, joint tenderness, headaches, closed lock, painful chewing. These patients usually progress to a stage 4 given time
Imaging: anterior disc displacement (early stages reduce, late stages don't), disc thickening, normal bone contour
Surgical appearance: disc deformed and anteriorly displaced. Sometimes adhesions, no bone changes
Management: MRI to confirm diagnosis. which will show anterior disc displacement. Most start with arthrocentesis. Arthroscopy will show a damaged disc and enable interventions such as adhesiolysis.

Stage 4
Clinical: chronic pain, headache and restricted motion
Imaging: non reducing anterior disc displacement. Disc thickening. Abnormal bone contours
Surgical appearance: gross arthritic degenerative changes 
Management: open surgery eg arthroplasty, meniscopexy

Stage 5
Clinical: variable pain, joint crepitus, painful function. Pre-ankylosis
Imaging: non reducing anterior disc displacement. Disc thickening. Abnormal bone contours
Surgical appearance: gross arthritic degenerative changes 
Management: open surgery eg arthroplasty, meniscopexy

SENTINEL NODE BIOPSY

Concept
- Identification of lymph node drainage in the order to which a tumour would drain to
- Injection of radio-labelled dye into the tumour area 1 day pre-operatively
- Followed by injection of blue dye at time of surgery
- Gamma camera used to identify lymph node which is subsequently excised
- Lymph node examined as frozen section for evidence of tumour
- If tumour found then neck dissection performed

Advantages
- May prevent unnecessary neck dissection in the cN0 neck

Disadvantages
- Doesn't account for 'skip' metastases
- Logistical difficulties in arranging the service

OSTEORADIONECROSIS

Definition:

• Multiple authors have defined ORN
• Marx 1983- greater than 1cm for longer than 6 months
• Harris 1992 (easiest definition)- exposed and necrotic bone associated with ulcerated or necrotic soft tissue that persists longer than 3 months in an area that been previously irradiated

Aetiology:

• Radiation injury to bone
• Rare if less than 60 gray given
• Lower if hyperfractionation
• IMRT may reduce it
• Addition of chemo potentially increases risk
• Brachytherapy highest risk

Epidemiology:

• Varies from 2.6-22%
• Mainly mandible- especially mylohyoid ridge
• Thought that inferior alveolar artery affected by the radiotherapy

Presentation:

• Mild asymptotic disease
• Progressive pain
• Supparation 
• Exposed bone
• Fracture

Changing concepts:

• Before 1980s it was thought that infection was the key precipitant
• In 1980s Marx suggested the 3 Hs
• 2004 onwards Delanian theory

Marx '3 H' concept:

• Hypovascularity
• Hypoxia
• Hypocellularity

Delanian theory:

• Proposed fibroatrophic theory
• Radiation produces free radicals
• This injures endothelial cells

Classification:

• Multiple authors have proposed methods of classification including Marx and Notani
• Notani most commonly used as simple and can guide treatment

Notani classification:

• Applicable to ORN in the mandible only
• Combination of clinical examination and OPG

​

ORAL PIGMENTATION

History
•    Onset
•    Drug history
•    Lesions elsewhere in body eg skin

Examination
•    Diffuse or localised
•    Peri oral pigmentation
•    Associated amalgam restoration (including previous extraction or crown)

Causes
•    Racial
•    Idiopathic
•    Addisons
•    Peutz Jeghers (not at increased risk of melanoma)
•    Heavy metal poisoning
•    Oral melanosis (usually smokers)
•    Drug induced (lead, bismuth, Mercury)
•    Melanoma (rare <1% oral cavity cancer)
•    Kaposi's sarcoma
•    Pigmented naevus 
•    Amalgam tattoo
•    Vascular malformations eg haemangioma

Investigations
•    Blood tests: check U+Es- if sodium normal then highly unlikely to be Addisons. Also for Addisons check serum cortisol and ACTH
•    Biopsy- if any concerns of melanoma

Drugs associated with oral mucosal pigmentation:
•    Antimalarials: quinacrine, chloroquine, hydroxychloroquine
•    Quinidine
•    Zidovudine (AZT) 
•    Tetracycline
•    Minocycline
•    Chlorpromazine
•    Oral contraceptives
•    Clofazimine
•    Ketoconazole
•    Amiodarone
•    Busulfan
•    Doxorubicin
•    Bleomycin
•    Cyclophosphamide
•    5-Fluorouracil

Smoker’s Melanosis
•    Smoking may cause oral pigmentation in light-skinned individuals and accentuate the pigmentation of dark- skinned patients

Peutz Jeghers
•    Pigmented mucocutaneous macules around lips and inside mouth
•    Intestinal hamartomatous polyposis
•    Increased risk of cancer in many organs

Addison’s Disease 
•    Hypoadrenalism due to progressive bilateral destruction of the adrenal cortex by autoimmune disease, infection or malignancy
•    The lack of adrenocortical hormones in the blood stimulates production of ACTH by the anterior pituitary gland
•    ACTH induces melanocyte-stimulating hormone causing diffuse pigmentation of the skin and oral mucosa
•    Systemic manifestations including weakness, nausea and vomiting, abdominal pain, constipation or diarrhoea, weight loss and hypotension
•    Assess levels of ACTH, plasma cortisol and serum electrolytes
•    Addison’s disease can be fatal if left untreated
•    Management involves treatment of the underlying cause and corticosteroid replacement therapy

PRE-OPERATIVE PREPARATION OF ONCOLOGY (MAJOR CASE) PATIENTS

Anticoagulants prior to surgery (BAHNO recommendations)

• Clopidogrel should be discontinued 5 days preoperatively
• Aspirin should be continued without interruption
• Warfarin should be discontinued 5 days preoperatively 
• Warfarin given for uncomplicated atrial fibrillation can be stopped with no added precautions
• Warfarin stopped in patients with previous thromboembolic disease or artificial heart valves they require SC heparin therapy for 5 days perioperatively (self administered)

Day before surgery

• Most patients are admitted the night before
• Medications should be prescribed
• Anticoagulant management as above
• Some units start on a proton pump inhibitor pre operatively (check local protocol)
• Ensure recent bloods (generally within last 2 weeks)
• Try to avoid taking bloods for fear of damaging veins being used for flap anastamosis
• Ensure group and save in date
• If radial flap ensure that the arm is marked with a pen to ensure no one takes blood from it
• Ensure consented

Oral hypoglycaemics

• Omit on the day of surgery and restarted when normal diet is resumed.

Antihypertensives

• Omit antihypertensives on day of surgery and restart following day

Venous thromboembolism prophylaxis

• All patients should be prescribed thigh length graduated elastic compression stockings (TEDS) on admission.
• All patients should receive intraoperative intermittent pneumatic compression.
• All patients should be given prophylactic dose subcutaneous low molecular weight heparin started on admission and continued until discharge.
  

FREE FLAP MONITORING

Equipment required:  

• Suction with Yanker tip
• Gauze swabs
• Gloves
• Tongue depressors
• Light source (non LED)
• Hand held Doppler

 
Preparation: 

• Ensure good and reproducible lighting every time
• Suck out secretions and blood
• Dry and clean the flap with the gauze 
• A colleague to assist if required

Examination:  

• Colour
• Skin turgor- normal, flaccid or swollen
• Temperature- normal or cold 
• Capillary refill- should be < 2 seconds
• Hand held doppler if available
• Pin prick (registrar only- do not hit pedicle)
• Ensure no external compression- tracheostomy tapes, head in neutral position
• Repeat

Management of potential flap failure:

• Alert senior who may request you to contact theatre staff
• Evaluate and correct systemic factors (hypovolemia, hypotension) or mechanical factors (head positioning, external compression)
• Heparin +/- thrombectomy and thrombolytics
• Revise anastamosis
• Leech therapy

Buried flaps:

• Clinical assessment is not possible
• Some authors suggest a bone scan at 4 days post op

 
Important Notes:

• Venous failure is more common than arterial
• Reproducibility is the key to successful monitoring
• Avoid vasopressors during operation and postoperatively
• Micro dialysis is the gold standard but is labour intensive and expensive
• Free flap failure rates have decreased to generally less than 4% (includes successful salvage of flaps).
• The overall flap complication rate has been reported as 28-36%, with a flap takeback rate of 5-25%.
• The most critical factor in flap salvage is early detection
• Success of free tissue transfer is 95-98%
• Most failures are due to venous or arterial thrombosis
• Arterial thrombosis is responsible for 20% of failures and generally occurs within 24 hours
• Venous thrombosis is responsible for 50% of failures and generally occurs within 24-48 hours
• 80% of thrombi necessitating return to theatre occur in first 48 hours
• The probability of success of surgical salvage is low after the first 48 hours.
• Arterial problems generally present before venous

Causes of flap failure:

• Anastamotic failure- venous more common than arterial
• External compression- haematoma in neck, neck ties

Factors that may potentially affect success:

• Vein graft use
• Comorbidities (BMI, preop Hg, ASA/KFI, previous surgery, XRT, chemoXRT, smoking, diabetes)
• Previous radiotherapy
• Previous chemotherapy
• Type of anastomosis (end to end, end to side)
• Pedicle characteristics/ kinks
• Vessel selection
• Running vs. interrupted vs. anastomotic coupler
• Surgery time
• Loupes vs microscope (no evidence for this)
• Type of intraoperative fluid used
• Hypotension and vasopressor use (controversial)
• Patient age
• Osseous flaps
• Presence of infection
• Hypothermia

Oral, Head and Neck Oncology and Reconstructive Surgery, 1e 1st Edition

Oral, Head and Neck Oncology and Reconstructive Surgery is the first oral and maxillofacial surgery (OMS) text to provide you with a system for managing adult oral, head and neck cancers and reconstructive cranio-maxillofacial surgery. Using an evidence-based approach to the management and treatment of a wide variety of clinical conditions, the extensive experience of the author and contributors in head and neck/cranio-maxillofacial surgery and oncology are highlighted throughout the text. This includes computer aided surgical simulation, intraoperative navigation, robotic surgery, endoscopic surgery, microvascular surgery, molecular science, and tumor immunology. In addition, high quality photos and illustrations are accompanied by videos of surgical procedures that are easily accessible on mobile devices.

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