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FRCS Plastic Surgery > CHAPTER 06: FACIAL PALSY, SCALP RECON & VASCULAR ANOMALIES > Flashcards

CHAPTER 06: FACIAL PALSY, SCALP RECON & VASCULAR ANOMALIES Flashcards

1
Q

What is the anatomy of the facial nerve?

A

brainstem, temporal bone, internal auditory meatus, facial canal, parotid gland

Within facial canal, it gives off

  1. Greater petrosal nerve → secretomotor → lacrimal gland and palatal glands
  2. Tympanic nerve → sensory
  3. Nerve to stapedius
  4. Chorda tympani → taste to the ant 2/3 of the tongue, travels with the lingual nerve.

It then emerges from the stylomastoid foramen:

  1. Posterior auricular nerve → occipital muscles and sensation to post earlobe.
  2. Nerve to posterior belly of digastric and stylohyoid
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2
Q

What happens to the facial nerve as it emerges from the stylomastoid foramen?

A

Temporozygomatic branch & lower cervicofacial branch

  1. Temporal (frontal) branch - runs along Pitanguy’s line, at temple it lies just deep to sup temporal fascia. Supplies frontalis
  2. Zygomatic branch - orbicularis oculi
  3. Buccal branch - buccinator, upper lip muscles
  4. Marginal mandibular - just below mandible, deep to platysma, superficial to facial vein
    supplies lower lip muscles, depressors
  5. Cervical - platysma
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3
Q

What are the congenital causes of facial nerve palsy?

A

Obstetric - forceps
Möbius syndrome
Goldenhar’s syndrome

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4
Q

What is Möbius syndrome?

A 
Defect in development of facial nerve VI & VII nuclei
Bilateral facial paralysis
May also involve III, V, IX, XII
CLUFT abnormalities
C ranial nerves
L ower limb
U pper limb 
F acial
T horacic (15%)

Rx - LD direct coaptation to CN IX, V, XI

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5
Q

What is Moebius syndrome?

A

1888 Moebius
‘Congenital facial diplegia and bilateral abducens nerve palsies’

Incidence - 1: 50,000 live births

Aetiology - multifactorial

  • 2% genetic
  • hypoxic / ischaemic injury (basilar / subclavian artery)
  • intrauterine toxin exposure - ergotamine, misoprostol, cocaine

Pathogenesis
underlying problem is an inherited congenital hypoplasia or agenesis of the CN nuclei

facial nerves (CN VII) 100%
abducens nerves (CN VI) 75%
hypoglossal nerves (CN XII)
(CN VI - XII can be affected, with VIII spared)
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6
Q

What is noted in history and examination of Moebius syndrome?

A 
HISTORY
inability to suck
drooling
incomplete eye & mouth closure
lack of eye mvmt
lack of facial expression
speech problems
normal intelligence usually (autism 30-40%)

EXAMINATION

  • Bilateral incomplete facial nerve palsy (VII) → mask-like facies
  • External ocular palsies (VI) → internal strabismus
  • Dysphagia (IX & X)
  • Inability to protrude tongue (XII)

Upper limb abnormalities

  • radial club hand
  • syndactyly, brachydactyly
  • Poland’s
  • Arthrogryposis

Lower limb
- club foot (Talipes equinovarus)

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7
Q

Who is involved in the MDT?

A 
Pediatricians
Plastic surgeons
Hand surgeons
General surgeons
Pediatric dentists
Orthopedic surgeons
Ophthalmologists
Pediatric otolaryngologists
Psychologists
Occupational and physical therapists
Audiologists
Speech therapists
Dieticians
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8
Q

What are the immediate and early treatments that need to be considered in Moebius syndrome?

A

Immediate

  • eye protection
  • NG feeding
  • infections (prone to aspiration, otitis media)

Early surgical

  • tracheostomy
  • PEG
  • strabismus correction (can delay, as may improve with time)
  • gold weight upper lid insertion
  • club foot, radial club hand correction
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9
Q

What procedures may be be considered in reanimating the face in Moebius syndrome?

A

Ideally before 7yrs

Donor - unaffected accessory nerve or the masseteric branch of CN V

Gracilis muscle transfer with masseteric nerve innervation (or Pec minor, LD)

Nerve grafting, cross-face grafting, and cranial nerve (CN) substitution techniques have had poor success due to lack of functional neuromuscular system

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10
Q

What is Goldenhar’s syndrome?

A 
Oculo-auriculo-vertebral syndrome
1st & 2nd branchial arch abnormality
Hemifacial microsomia
Epibulbar dermoids
\+/- facial nerve abnormality
Clinical 
10% bilateral
Incomplete development of ear, nose, soft palate, lip, mandible (deafness, blindness)
hypoplasia of heart, kidney, lungs
scoliosis
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11
Q

What are the acquired causes of facial palsy?

A

SYSTEMIC
hypo/hyperthyroid, DM, lead, tetanus, diphtheria COHb

CENTRAL
Intracranial
CNS tumours, acoustic neuroma, MS, Polio, Mobius

Intratemporal
Bell's palsy
trauma (incl iatrogenic)
otitis media
infection (HZV - Ramsay Hunt Syndrome)
cholesteatoma
middle ear tumours

Extratemporal
trauma, tumours, parotid tumours (esp acinic cell - perineural invasion), iatrogenic

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12
Q

What is Bell’s palsy?

A

described by Charles Bell 1811
idiopathic facial palsy
e.g. viral infection, swelling of nerve within tight intratemporal course
1/60 lifetime risk, 20/100,000
90% recover fully, good sign = incomplete paralysis, recovery 4wks

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13
Q

How is facial palsy assessed?

A

House and Brackman
Grade 1 → some mimetic (spontaneous) movement
Grade 2 → no mimetic
Grade 3 → only mass action of facial muscles
Grade 4 → unable to completely close eyelids
Grade 5 → symmetry despite complete paralysis
Grade 6 → an asymmetrical face with no movement

Others
Nottingham score
MRC grade
Facial grading scale (Ross)

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14
Q

Clinical evaluation of facial palsy

A

History - insidious vs rapid
Trauma - blunt / sharp
Total / partial, uni / bilat symmetry - rest & dynamic
Synkinesis? Over innervation?
Forehead - wrinkles
Brow - lift
Eyes - ptosis, ectropion, snap test, Bell’s phenomenon
Nose - nasal tilt, nasal valving
NL fold, malar prominence
Mouth - position, occulsive cant (tongue dep)
clench teeth - test temporalis

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15
Q

Investigations for facial nerve palsy

A

Electroneuronography
Schirmer’s test 1 (2 = with LA)
Stapedius reflex test
Taste and 2/3 of tongue - chorda tympani

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16
Q

What are the principles of VII palsy treatment?

A

No op vs op
Static vs dynamic
Functional vs free muscle

Goals of treatment

  • rest symmetry
  • facial function
  • voluntary function
  • spontaneous mvmt
  • absence of synkinesis
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17
Q

What conservative treatment is there for facial palsy?

A

Protect eyes - drops, taping at night
Botox normal side to improve symmetry
Bells palsy - high dose steroids, antivirals

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18
Q

What static procedures are there for facial nerve palsy?

A

Tarsorrhaphy - perm/temp, lateral / Frost
Kuhnt-Symanowski procedure - over orbic
Gold weight / springs
Brow lifts / suspensions - endo / open
Forehead skin excision - melon slice
Unilateral facelift type procedures
Fascial slings - fascia lata - corner of mouth, nose to temporalis

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19
Q

What dynamic procedures are there for facial nerve palsy

A
  1. Nerve repair / graft
  2. Cross-facial nerve graft
  3. Nerve transfers / substitution
    - glossopharyngeal, hypoglossal, accessory, phrenic: coarse mvmts, donor defect
  4. Muscle shortening / local muscle flaps
    - masseter (3 slips above, on below commissure)
    - temporalis
  5. Cross face nerve grafting & free muscle transfer
    - 1 stage - donor muscle with long nerve pedicle - but long denervation time
    - 2 stage - reversed sural nerve graft, wait for Tinels sign, then harvest free muscle and insert onto zygomatic arch to mimic zygomaticus major (gracilis, LD, pec minor)
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20
Q

What procedures are you familiar with for dynamic correction of facial nerve palsy?

A

Royal Free - Pec minor to upper, lower lip & alar base. 2 stage
EG - Nduka - Labbe temporalis lengthening myoplasty & lip reanimation
Chester - temporalis turndown?

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21
Q

What are the eye problems and assessment in facial nerve palsy?

A 
Problems
 Corneal exposure
 Paralytic ectropion
 Epiphora
 Poor cosmesis
Assessment
 Vertical palpebral aperture
 Lagophthalmos – inability to close eye completely
 Lid position
 Lower lid laxity
 Corneal exposure
 Corneal sensation
 Bell's Phenomenon
 Brow ptosis
22
Q

What are the different flaps for scalp reconstruction?

A 
LOCAL FLAPS
Rotational flap
- Ortichochea 3 or 4 flap techniques
Transposition flap
Advancement flap
Crane principle
REGIONAL FLAPS
Washio flap
Superficial temporal / parieto-occipital flap
FREE FLAPS
LD, scapular, RFF, rectus abdo
23
Q

What is the sensory innervation of the scalp?

A

Sensory innervation

  • supraorbital
  • supratrochlear
  • trigeminal branches
  • temporal (auriculotemporal?)
  • auricular (great auricular?)
  • occipital (lesser?)
24
Q

What is the blood supply of the scalp?

A

External carotid

  • superficial temporal ant & post branches
  • occipital

Internal carotid

  • supratrochlear
  • supraorbital
  • posterior auricular
25
Q

What are the layers of the scalp?

A 
SCALP
Skin
SubCutaneous tissue
Galea Aponeurotica
Loose areolar tissue
Pericranium
26
Q

What are the priniciples of scalp recon?

A
  1. provide durable cover to pericranium
  2. restore hairline
  3. maintain contour of scalp
27
Q

What are the advantages and disadvantages of tissue expansion in scalp recon?

A

Advantages

  1. like for like, contains skin adnexal structures
  2. increased vascularity of flap

Disadvantages

  1. discomfort
  2. long duration
  3. multiple surgeries
  4. temporary deformity
  5. only on stable healed wounds or before scalp lesion is excised (trauma and most oncological excisions unsuitable)
28
Q

How was vascular anomalies first classified?

A

Mulliken and Glowacki PRS 1982
- classification based on endothelial characteristics
Vascular tumours
- Infantile haemangioma

Vascular malformations
Slow-flow
- Capillary Malformation
- Venous Malformation
- Lymphatic Malformation

Fast-flow

  • Arterial Malformation
  • Arteriovenous fistula
  • AV Malformation

Vascular malformations may be a combination of the above, especially syndromic cases

28
Q

How has the classification of vascular anomalies changed?

A

Enjolras & Mulliken 2002
International Society for the Study of Vascular Anomalies (ISSVA)

  • Vascular Tumours vs. Vascular malformations

Vascular tumours

  • Infantile haemangiomas
  • Congenital haemangiomas
  • Tufted angiomas (+/- KMP)
  • Kaposiform haemangioendothelioma (+/- KHP)
  • Spindle cell haemangioendothelioma
  • Other HE’s
  • Dermatologic acquired vascular tumours (pyogenic granuloma, other haemangiomas)

Vascular Malformations
Slow flow
- Capillary malformation (PWS, telangiectasia angiokeratoma)
- Venous malformation (common sporadic VM, Bean syndrome, Familial cutaneous and mucosal VM
- Glomuvenous malformation
- Maffucci snydrome
- Lymphatic Malformation

Fast flow
- AM, AVF, AVM

Complex combined vascular malformations
- CVM, CLM- LVM, CLVM, ACM-LM, CM-AVM

Syndromes

29
Q

What is a haemangioma?

A
  • benign, usually self-involuting neoplasm of endothelial cells (vasoformative tissue)
  • characterised by increased number of normal or abnormal vessels filled with blood
  • most common vascular tumour of childhood
  • 1 in 10 Caucasian children by 1yr
  • 60% H&N
  • F:M 3:2
  • 80% solitary
  • more common in premature infants
30
Q

How do haemangiomas present?

A
  • usu appears during the first weeks of life
  • grows rapidly b/t 5-8mths
  • proliferate, plateau and involute
  • small bright red, slightly bosselated surfaces, blanch with pressure with well
    defined borders
  • deep = bluish, dermal = red
  • rubbery, firm and rapidly refills, soft and doughy
  • can outgrow its blood supply, ulcerate
  • multiple haemangiomas - may also be intraoral, gut, CNS, liver, lungs
  • intravascular thrombosis and fibrosis result in regression (corresponds with mast cell infiltrate)
  • 50% resolve by 5yrs, 60% 6 yrs, 70% 7 yrs
31
Q

What is the clinical course of haemangiomas?

A

Cycle of growth and involution classified into 7 stages
1. Origin (Herald patch)
2. Initial growth
3. Intermediate growth
4. Completed growth
5. Initial involution
6. Intermediate involution
7. Completed involution
• Proliferative → stages 1-4 → 6 – 18 months
• Involutional → stages 5-7 → usu complete by 9 yrs old
• Some fibrofatty swelling remains esp lip and oral mucosa tend to undergo less regression

32
Q

What is the pathogenesis of haemangiomas?

A

Masses of thin walled endothelium lined channels, rapid endothelial turnover (24hrs) increased mast cells, progressive maturation to capillary or cavernous channels
Theories
o ?VEGF and bFGF over-expression
o ?hormone responsive → angiogenic stimulus
o ?fibroblast growth factors
o ?Insulin like growth factor 2 → vascular sprouting
o ? heparin from the mast cells

33
Q

How are haemangiomas treated?

A

Vast majority - conservative
Indications: obstruction, Kassabach-Merritt, ulceration/bleeding, aesthetic, psychiatric

Non-invasive:
PROPRANOLOL - 1st line
- 2-3mg - current European studies to look at ideal dose
- started in hospital setting: risks bradycardia, hypotension, hypoglycaemia
- steroids
- interferon alpha 2a
- vincristine (ITU setting, spastic diplegia)
- antiplatelet agents (Aspirin for KM)
- Compression, DXT, chemo

Invasive

  • intralesional steroid, OK432 (denatured streptococcal protein)
  • intralesional sclerosant
  • surgical debulking
  • pulse dye laser (early)
34
Q

What are the complications associated with haemangioma?

A
  • Obstruction → vision/airway (subglottic)
  • Ulceration, bleeding, infection
  • Skeletal distortion
  • High output cardiac failure
  • Late = scarring, residual colour, mass, redundant skin
35
Q

What is Kasabach-Merritt phenomenon?

A
  • described 1940
  • associated with kaposiform hemangioendothelioma (or tufted angioma)
  • characterised by profound thrombocytopenia, microangiopathic hemolytic anemia, a consumptive coagulopathy, and an enlarging vascular lesion (KHE / TA or a mixture of both)
  • mortality rate ~ 30%

Presentation

  • M>F (unlike haemangiomas)
  • reddish brown / blue tender skin lesion, rapidly evolves into violaceous bulging mass with petchiae and purport

Sequelae
o Sequestration of platelets
o Fibrinogen consumed → prolonged PT & APTT
o DIC, haemorrhage, airway compression, high output cardiac failure → can be fatal
o DIC Rx = aspirin, ticlopidine, corticosteroids, interferon alpha-2a
o Selective embolisation (usu lesions are too large for surgery)
o Early intervention before established coagulopathy better.
o Mortality = 77% without / 27% with treatment. Overall 30-40% †

36
Q

What is congenital haemangioma?

A

Present fully grown at birth & grows with child
Negative for Glut-1marker
M=F

RICH – Rapidly Involuting Congenital Haemangioma
• Rapid regression - 50% involute <7 mths

NICH – Non-Involuting CH – never disappear
• Well circumscribed, plaque-like tumour
• Pink, blue or purple hue
• Central, course telangiectasia
• Pale rim
37
Q

What are vascular malformations?

A
  • Inborn errors of vascular morphogenesis, permanent and progressive
  • Capillary, lymphatic, venous, (low flow)
  • Arterial, arteriovenous (high flow)
  • Congenital anomalies of vasculature (NOT TUMOURS) - present at birth
  • Capillary = port wine stain esp. trigeminal area
  • Venous = dilated venous channels, lined with normal endothelium (aka cavernous haemangioma)
  • Lymphangiomas = lymphatic channels (=cystic hygromas in H&N)
  • DO NOT undergo hyperplasia or regression
  • Slow progressive dilatation of vessels but no cellular proliferation
  • most common lips, tongue, cheeks, muscle
  • Bone commonly involved - bone hypertrophy (inc teeth)
  • Soft, compressible, refill slowly
  • Grow in proportion with the child
  • Difficult to remove - vague edges and may infiltrate important nerves and vessels.
38
Q

Venous and mixed vascular malformations - presentation and management

A

present at birth, grows slowly, does not expand beyond local region
pain, bleeding, facial asymmetry
initially blue patch (cutaneous / visceral), compressible mass, dependant swelling
may develop phleboliths / thrombosis
Rx - if bleeding / obstruction
- Sclerotherapy - ethanol, bleomycin, sodium tetradecyl sulphate +/- with imaging +/- surgery
- Risks: necrosis, oedema, extravasation, beware ophthalmic circulation

39
Q

Lymphatic malformations - presentation and management

A 
micro / macrocystic / mixed
lymphangioma = microcystic
cystic hygroma (H&N) = macrocystic
present at birth / appear over 2yrs
do not involute
bleed, ulcerate, infected, painful
may cause airway obstruction / distortion of post triangle of neck

MRI
o Type I = non-invasive - most common in neck = macrocystic
o Type II = invasive - diffuse, H&N

Rx

  • supportive (treat infection, pain)
  • intralesional OK432
  • excision - symptomatic
  • Nd:Yag laser
  • complications: recurrence, poor wound healing
40
Q

What are capillary vascular malformations also know as?

What is the pathogenesis and clinical presentation?

A

Port wine stains
Pathogenesis
- Developmental vessel wall weakness → progressive ectatic dilatation of mature superficial dermal vessels
- In distribution of CN V → ? neurogenic (Sturge Weber Syndrome) - ophth and leptomeningeal abnormalities
- deficiency of sympathetic innervation
- Relative deficiency = slow growing
- Absolute deficiency = rapid growing

M=F
deep red/ purple lesion, present at birth
face, upper trunk
grows in proportion to child
flat → cobblestoning → hypertrophy → fade / deepen in colour
Rx - Pulsed dye, Nd YAG, KTP laser, multiple treatments (6-8)

41
Q

High flow vascular malformations - presentation

A

Arterial Malformation
• Aneurysms, stenosis, tortuous arteries
• rarely occur as isolated abnormalities

Arteriovenous Malformations (AVM)
• High flow lesions, interconnections between venous and arterial systems
• Most common - intracranial
• Usually present at birth but only become clinically apparent in infancy or
childhood.
• Trauma or puberty → expansion (darkens, enlarge and develop bruit / thrill)
• May rapidly expand beyond borders → ischaemic skin changes, ulceration,
pain and bleeding, bone destruction.
• Can get heart failure due to high flow shunt

42
Q

What syndromes are associated with PWS?

A 
Sturge-Weber Syndrome
• Port wine stains in ophthalmic and maxillary regions of trigeminal nerve +/-
• Meningeal vascular malformations
• Motor seizures including epilepsy
• low IQ
• Eye abnormalities inc glaucoma

Klippel Trenaunay Syndrome
• PWS of extremity (usually leg) with underlying venous or lymphatic malformation +/- abnormal lateral vein (do not ligate). May get limb hypertrophy with bony enlargement.

Parkes-Weber Syndrome
• Similar to Klippel-Trenaunay but have AV fistula.

43
Q

What other syndromes are associated with vascular lesions?

A

Osler-Weber-Rendu Syndrome (Hereditary haemorrhagic telangiectasia)
• AD inheritance.
• Bright red AVMs in the skin, mucous membranes, lungs and abdo viscera

Maffucci’s Syndrome
• Multiple enchondromas and venous malformations. Usually on enchondromas
on hands.

Blue Rubber bleb syndrome (Bean syndrome)
• Multiple venous malformations of the skin (hand and feet usually) and GI tract.

Proteus Syndrome
• Symmetrical overgrowth of bone and soft tissues and development of vascular malformations

44
Q

How are high flow vascular lesions staged and managed?

A

Staging (Schobinger)
o Stage 1 QUIESCENT blue skin-blush
o Stage 2 EXPANSILE Mass assoc with bruit and thrill
o Stage 3 DESTRUCTIVE Mass + ulceration, bleeding & pain
o Stage 4 DECOMPENSATORY stage 3 lesion + heart failure

Treatment is difficult - MDT
PLASTIC, PAEDS, CARDIAC SURGEONS, PERFUSIONISTS, ANAESTHETISTS, ITU, HAEMATOLOGISTS, BLOOD BANK, RADIOLOGIST, SPECIALIST NURSES,
• MRI angiography and arteriography
• Correct any clotting abnormality
• Embolisation into nidus of malformation 24hrs pre-op
• Attempt to resect whole lesion. Limits of
resection guided by pre-op MRI, angiography, intraoperative Doppler, frozen section and pattern of bleeding at wound edges.
• Minimise intraoperative bleeding by permissive hypotension, quilting mattress sutures, bypass / circulatory arrest & diversion, cell salvage
• Reconstruct defect

  • Ligation or embolisation of feeding vessels is absolutely contraindicated as increases collateral supply and results in enlargement of lesion.
  • Recurrence common often † from bleed or airway obstruction
45
Q

What is PHACES syndrome?

A 
Posterior fossa malformations
hemangiomas
arterial anomalies
cardiac defects
eye abnormalities
sternal cleft and supraumbilical raphe syndrome
46
Q

treatment of venous malformations

A

bleomycin - risk of pulmonary fibroses
percutaneous injection into loculae under duplex scan under GA

ethanol

venous - sodium tetradecyl sulphate

surgical debulking

lymphangitis circumscripta
orthopaedic input for bone
high risk of wound healing

47
Q

How are vascular anomalies classified?

A

They are classified into vascular tumours and vascular malformations based on their

  • clinical appearance
  • radiological features
  • pathological features
  • biological behaviour
48
Q

Vascular tumours

A

Vascular tumour:

  • grow by cellular hyperplasia
  • can regress or persist

Vascular malformation:

  • localised defect of vascular morphogenesis, likely caused by dysfunction in pathways regulating embryogenesis and vasculogenesis + has quiescent endothelium
  • never regress
  • commensurate growth during childhood
  • worsen with time if not treated
50
Q

What are the main differences b/t infantile haemangioma and VM?

A

Age of occurrence and course - infancy & childhood
Course - 3 stages: proliferating, involuting, involuted
Prevalence - 3-9:1 girl:boy
Cellular - increased endothelia cellular turnover, inc mastocytes, thick basement membrane
Immunohistochemistry - VEGF, bFGF, PCNA, collagenase
Pathology - GLUT1 +
MRI - well delineated tumour w flow voids
Treatment - spontaneous involution, pharmacological treatment, surgery, lasers

VM
everlasting
commensurate growth or slow progression
1:1 girl:boy
Normal cellular turnover & mastocytes no., thin BM
IHC undetectable
Trauma, hormonal changes may cause flareup
MRI hypersignal T2
Treatment: lasers, surgery, embolisation / scelerotherapy

51
Q

What is the theory behind the therapeutic effect of propranolol in infantile haemangiomas?

A
  1. Vasoconstriction with immediate change in colour (red to purple) and palpable softening.
  2. Decreased expression of VEGF and bFGF genes through down-regulation of RAF mitogen- activated protein kinase pathway.
  3. Apoptosis of capillary endothelial cells triggered by propranolol.

Taieb et al, Bordeaux, NEJM 2008.

FRCS Plastic Surgery (63 decks)

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