28/10/2012
04/06/2011
Rhytides
Wrinkles (rhytides) are partly due to the contraction of underlying muscles and partly
due to a loss of elasticity, thus paralyzing the muscles with the toxin will reduce wrinkles.
The effect of toxin A on glabellar lines was noted incidentally when it was used
therapeutically for strabismus and torticollis, and it subsequently gained FDA
approval specifically for the treatment of glabellar lines. There is extensive use in cosmetic
surgery for a wide variety of indications, generally in an ‘off label’ manner, as
the indications for which the toxin is specifically licensed are fairly limited. Botulinum
toxin is also used in conditions such as dystonias (blepharospasm and hemifacial
spasm) or hyperhidrosis (excess sweating) in the axilla or face (Frey’s syndrome).
The commonest areas treated with botulinum toxin are shown in Table 1.
Other areas include: lower and upper eyelid wrinkles, circumoral lines (orbicularis
oris), nasal lines (nasalis), marionette folds or drooping labial commissure, chin folds
or cobblestone chin (mentalis), platysmal folds or turkey neck, and decollete folds.
The toxin (about 5U per site for Botox—more is needed in men due to greater
muscle mass) is injected into muscle; some use EMG guidance. The action is delayed
for 1–3 days because the toxin needs to be internalized and cleaved to take effect. The
effects peak at 1–2 weeks and last for 8–12 weeks (if boosted, effects may last up to
9 months and may be due in part to muscle atrophy).
due to a loss of elasticity, thus paralyzing the muscles with the toxin will reduce wrinkles.
The effect of toxin A on glabellar lines was noted incidentally when it was used
therapeutically for strabismus and torticollis, and it subsequently gained FDA
approval specifically for the treatment of glabellar lines. There is extensive use in cosmetic
surgery for a wide variety of indications, generally in an ‘off label’ manner, as
the indications for which the toxin is specifically licensed are fairly limited. Botulinum
toxin is also used in conditions such as dystonias (blepharospasm and hemifacial
spasm) or hyperhidrosis (excess sweating) in the axilla or face (Frey’s syndrome).
The commonest areas treated with botulinum toxin are shown in Table 1.
Other areas include: lower and upper eyelid wrinkles, circumoral lines (orbicularis
oris), nasal lines (nasalis), marionette folds or drooping labial commissure, chin folds
or cobblestone chin (mentalis), platysmal folds or turkey neck, and decollete folds.
The toxin (about 5U per site for Botox—more is needed in men due to greater
muscle mass) is injected into muscle; some use EMG guidance. The action is delayed
for 1–3 days because the toxin needs to be internalized and cleaved to take effect. The
effects peak at 1–2 weeks and last for 8–12 weeks (if boosted, effects may last up to
9 months and may be due in part to muscle atrophy).
Botulinum toxin
Clostridium botulinum is a spore-forming, gram-positive, anaerobic rod. A number of
different potent neurotoxins (from A–G) are produced by different strains. The name
is derived from the Latin for sausage, botulus, due to its association with food poisoning
from bad sausages. Botulinum toxin A is the most widely studied; it is the easiest
to obtain from culture and was the first to be commercially prepared as Botox (Allergan).
The toxin, consisting of two subunits (light and heavy chains are connected by a
disulphide bridge), selectively inhibits acetylcholine release at the neuromuscular
junctions in a dose-dependent manner.
different potent neurotoxins (from A–G) are produced by different strains. The name
is derived from the Latin for sausage, botulus, due to its association with food poisoning
from bad sausages. Botulinum toxin A is the most widely studied; it is the easiest
to obtain from culture and was the first to be commercially prepared as Botox (Allergan).
The toxin, consisting of two subunits (light and heavy chains are connected by a
disulphide bridge), selectively inhibits acetylcholine release at the neuromuscular
junctions in a dose-dependent manner.
Treatment
Surgical excision is the standard treatment. Randomized trials of excision margins are
lacking, but generally margins of 2 mm (for well-circumscribed lesions, particularly on
the face) to 5 mm (for lesions with indistinct margins) are recommended. Four millimetre
margins give a cure rate of 94–96% according to Zitelli.
Some areas such as the medical canthus, and external auditory alar base meatus
are more prone to incomplete excision as the tumour seems to extend deeper at these
locations; the usual explanation being that these areas are embryological fusion lines.
Note that only one-third of incompletely excised BCCs will show histological evidence
of residual tumour on further resection. Recurrent lesions tend to be more
aggressive in behaviour.
Mohs’ micrographic surgery (MMS)—in which successive layers are exised and the
base of the specimen is mapped out and examined histologically perioperatively—
may be most useful in complex lesions with indistinct borders and where tissue conservation
is important. It has the best reported cure rate of 99%.
lacking, but generally margins of 2 mm (for well-circumscribed lesions, particularly on
the face) to 5 mm (for lesions with indistinct margins) are recommended. Four millimetre
margins give a cure rate of 94–96% according to Zitelli.
Some areas such as the medical canthus, and external auditory alar base meatus
are more prone to incomplete excision as the tumour seems to extend deeper at these
locations; the usual explanation being that these areas are embryological fusion lines.
Note that only one-third of incompletely excised BCCs will show histological evidence
of residual tumour on further resection. Recurrent lesions tend to be more
aggressive in behaviour.
Mohs’ micrographic surgery (MMS)—in which successive layers are exised and the
base of the specimen is mapped out and examined histologically perioperatively—
may be most useful in complex lesions with indistinct borders and where tissue conservation
is important. It has the best reported cure rate of 99%.
Basal cell carcinoma
Basal cell carcinoma (BCC) is the commonest human malignancy in Caucasians, it is
less common in those with pigmented skin. The incidence varies from over 1500 in
100 000 in Queensland, Australia, to 200–300 per 100 000 in the United Kingdom, and
2–3 per 100 000 in Hong Kong Chinese. There is a male predominance, but the incidence
in females is increasing.
The tumour arises in hair-bearing skin, particularly on the face where sun exposure
is the highest; over three-quarters arise on the face, one-quarter on the nose. The
lesion is generally slow-growing, but is locally destructive, hence the common name of
‘rodent ulcer’.
Despite their name, BCCs probably do not arise from the basal cells of the epidermis
but from the pluripotential cells in the epidermis; this is supported by the occasional
observation of appendigeal differentiation in these tumours. The typical
features are raised pearly edges and telangiectasia (small blood vessels) with or
without a central ulcer. Histologically, there are undifferentiated cells in nodules with
peripheral palisading (‘picket fence pattern’).
There are a number of morphological subtypes of BCC:
• Nodular—less than 5% of BCCs in Caucasians are pigmented (can look very
similar to malignant melanoma), but pigmented carcinomas are more common
in darker-skinned races. (Three-quarters of BCCs in Chinese patients are
pigmented)
• Superficial—commoner on the trunk. Multiple lesions in a patient should raise the
possibility of arsenic poisoning as a cause
• Morpheaform/sclerosing—often a scar-like lesion with ill-defined margins
• Infiltrative.
The latter two subtypes are more aggressive in behaviour. The overall
rate of metastasis is extremely low but there have been several reports in the
literature.
Sun exposure (ultraviolet B)—the strongest association is repeated sunburn
in childhood with a lag time of 20–50 years; the field effect is demonstrated
by the almost 50% risk of developing a further BCC in the subsequent 5
years. Psoralen ultraviolet A (PUVA) treatment for psoriasis is another risk
factor.
Other risk factors include:
• immunosuppression
• exposure to carcinogens such as hydrocarbons/arsenic (occupational, medicinal
or environmental—contaminated water supplies are often implicated)
• irradiation
• genetic conditions such as xeroderma pigmentosa or syndromes such as
Gorlin’s syndrome. It has a multitude of alternative names, including BCC
syndrome which is inherited in an autosomal dominant manner. Patients
have a predisposition to developing carcinomas from puberty onward,
particularly BCCs. Other associated feature include jaw cysts, bifid ribs, pits
in the palms and soles, prominent brow with hypertelorism, partial agenesis
of the corpus callosum with learning difficulties.
• pre-existing sebaceous naevus.
less common in those with pigmented skin. The incidence varies from over 1500 in
100 000 in Queensland, Australia, to 200–300 per 100 000 in the United Kingdom, and
2–3 per 100 000 in Hong Kong Chinese. There is a male predominance, but the incidence
in females is increasing.
The tumour arises in hair-bearing skin, particularly on the face where sun exposure
is the highest; over three-quarters arise on the face, one-quarter on the nose. The
lesion is generally slow-growing, but is locally destructive, hence the common name of
‘rodent ulcer’.
Despite their name, BCCs probably do not arise from the basal cells of the epidermis
but from the pluripotential cells in the epidermis; this is supported by the occasional
observation of appendigeal differentiation in these tumours. The typical
features are raised pearly edges and telangiectasia (small blood vessels) with or
without a central ulcer. Histologically, there are undifferentiated cells in nodules with
peripheral palisading (‘picket fence pattern’).
There are a number of morphological subtypes of BCC:
• Nodular—less than 5% of BCCs in Caucasians are pigmented (can look very
similar to malignant melanoma), but pigmented carcinomas are more common
in darker-skinned races. (Three-quarters of BCCs in Chinese patients are
pigmented)
• Superficial—commoner on the trunk. Multiple lesions in a patient should raise the
possibility of arsenic poisoning as a cause
• Morpheaform/sclerosing—often a scar-like lesion with ill-defined margins
• Infiltrative.
The latter two subtypes are more aggressive in behaviour. The overall
rate of metastasis is extremely low but there have been several reports in the
literature.
Sun exposure (ultraviolet B)—the strongest association is repeated sunburn
in childhood with a lag time of 20–50 years; the field effect is demonstrated
by the almost 50% risk of developing a further BCC in the subsequent 5
years. Psoralen ultraviolet A (PUVA) treatment for psoriasis is another risk
factor.
Other risk factors include:
• immunosuppression
• exposure to carcinogens such as hydrocarbons/arsenic (occupational, medicinal
or environmental—contaminated water supplies are often implicated)
• irradiation
• genetic conditions such as xeroderma pigmentosa or syndromes such as
Gorlin’s syndrome. It has a multitude of alternative names, including BCC
syndrome which is inherited in an autosomal dominant manner. Patients
have a predisposition to developing carcinomas from puberty onward,
particularly BCCs. Other associated feature include jaw cysts, bifid ribs, pits
in the palms and soles, prominent brow with hypertelorism, partial agenesis
of the corpus callosum with learning difficulties.
• pre-existing sebaceous naevus.
Infection
Burn patients are at risk of infection, but prophylactic antibiotics are generally not
given.
There is a decrease in both cellular and humoral immunity:
• decreased total lymphocyte numbers
• prolonged survival of allografts
• reduction of immunoglobulin levels
• serum from burn patients is immunosuppressive in vitro.
Dressings with physical cleansing of the wound and the use of tropical antimicrobials
are the mainstay of reducing infection. Tetanus prophylaxis is given depending on the
patient’s immunization status.
given.
There is a decrease in both cellular and humoral immunity:
• decreased total lymphocyte numbers
• prolonged survival of allografts
• reduction of immunoglobulin levels
• serum from burn patients is immunosuppressive in vitro.
Dressings with physical cleansing of the wound and the use of tropical antimicrobials
are the mainstay of reducing infection. Tetanus prophylaxis is given depending on the
patient’s immunization status.
Pain relief
Adequate pain relief is important. Keeping the patient comfortable will reduce catabolic
requirements. Opiates are best given intravenously as absorption from intramuscular
administration is unpredictable. Additional analgesia should be given before
dressing changes.
requirements. Opiates are best given intravenously as absorption from intramuscular
administration is unpredictable. Additional analgesia should be given before
dressing changes.
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