privacy
adequacy of time
establish understanding
don’t use jargons
come see me again (card)
compassionate
encourage to express feelings
support groups/psycology
you should be calm !
reassure that you’re there for them
documentation
Dr. Amudha Interviewing Wai Kit
how are you feeling today
i can imagine
how are you feeling after the operation
i called you to have a chat with you .. i’m afraid that this is not good news
reports have just showed you’ve got
reports and your history strongly indicate that you’ve got cancer
what do you know about this condition
am i gonna die ?
it’s too early to tell
i can assure you that we’ll do whatever we can do about that
what are you worried about
perhaps i can help you breaking this news to ....
it can be inherited .. but we can protect your children if you want to have them
Friday, May 8, 2009
Thursday, May 7, 2009
SUMMARY
Anatomy of the Skin
Largest and heaviest organ.
3 layers
- Epidermis (Stratified Squamous Epithelium)
- Dermis (Connective Tissue Layer)
- Hypodermis (Subcutaneous Tissue)
Thickness of skin
varies from 0.5mm to 6mm. Difference due mainly to variation in the thickness of the dermis.
- Thick skin covers palms, soles and surfaces of fingers/toes. has sweat glands but no hair follicles or sebaceous glands.
- Thin skin covers the rest of the body. Has hair follicles, sebaceous glands and sweat glands
Epidermis
Keratinized stratified squamous epithelium.
Layers of epidermis from the top
-stratum corneum
-stratum lucidum
-stratum granulosum-keratohyalin granules
-stratum spinosum-desmosomes attaches keratinocyte
-stratum basale
Cells of epidermis
-Stem cells
-Keratinocytes
-Melanocytes
-Tactile Cells
-Dendritic Cells/Langerhans cells
Dermis
-2 zones of dermis
- Papillary Layer
- Reticular layer
Hypodermis
-binds skin to underlying tissue
Subcutaneous fat
-energy reservoir and thermal insulation
Benign and Malignant Tumour
Benign tumours are not cancer:
• rarely life-threatening, can be removed, usually do not grow back.
• do not invade the tissues around them.
• do not spread to other parts of the body.
Malignant tumours are cancer:
• more serious. May be life-threatening, often can be removed, but sometimes they grow back.
• Cells can invade and damage nearby tissues and organs and metastasize to other parts of the body.
The two important differences between benign and malignant tumours are invasion and spread.
Confirmatory test
• By examining a small sample of cells under a microscope. This is called a biopsy.
• First, Imaging
• Then, Biopsy (removal of a small piece of tissue for lab exmination) / Tissue sampling
How to know whether the tumour is malignant or benign
- size and shape of the nucleus of a cancer cell is often abnormal and the nucleus appears darker
- overall size and shape of cancer cells are often abnormal
Cancer cells do not relate to each other normally
Incidence and prevalence
- Highest incidence in Australia and New Zealand.
- 2002, prevalence of 37.7 cases per 100,000 men and 29.4 cases per 100,000 women in Australia and New Zealand.
- America, Prevalence of 6.4 cases per 100,000 men and 11.7 cases per 100,000 women in North America.
- European countries, highest incidence rates in northern and western countries and the lowest in southern countries, with rates from three to eight times lower for men and women, respectively.
Aetiology and Pathophysiology.
Aetiology
- Can be acquired:
- Through (sporadic) somatic mutations of certain genes
- DNA can be damaged caused by chemicals or carcinogens (In melanoma is associated with DNA damage by UV radiation)
- Through (sporadic) somatic mutations of certain genes
- Can be hereditary: Caused by mutated genes passed down from the parents. In this case, it requires a germ line mutation that occurs in either one of the parents.
Pathophysiology
- Mutation in certain genes: Tumor suppressor genes, oncogenes (proto-oncogenes), apoptosis-regulating genes and mismatch repair genes.
- Mutation in these genes causes loss of function or gain in function that will predispose to cancer.
Spreading of cancer cells locally or distant (Metastasis)
Differential Diagnosis for Melanoma
Seborrheic keratosis
Diagnosis is based primarily on the appearance of the growths. A skin lesion biopsy may be used to confirm the diagnosis.
Traumatized or irritated nevus
The history of trauma or biopsy along with review of the original biopsy helps exclude a diagnosis of melanoma.
Basal cell carcinoma
grows by direct extension and appears to rely on the surrounding supportive tissue to grow – thus does not metastasize through blood vessels or lymphatics.
Lentigo
Lentigines profusa (ie, generalized lentigines) is characterized by numerous lentigines without signs of associated abnormalities or triggering factors.
Angiokeratoma
A harmless, discolored, raised skin lesion involving damaged blood capillaries.
Venous lake
Vascular thrombosis play a role in development
Hemangioma
Hemangiomas are diagnosed by a physical examination. In the case of deep or mixed lesions, a CT or MRI scan may be performed.
Dermatofibromas
Diagnosis is clinical; lesions typically dimple when grasped between the fingers
Pigmented actinic keratosis
The health care provider makes the diagnosis based on the appearance of the skin growth. A skin biopsy may reveal any cancerous changes, if they occur.
Signs and Symptoms of Melanoma
Usually detected using the ABCDE method or Glasgow 7-point checklist.
ABCDE'S of Melanoma (Asymmetry, Border, Colour, Diameter,
Elevation or Evolving)
Glasgow 7-point checklist (1985), (Change in size, Irregular shape, Irregular colour, Diameter greater than 7mm, Inflammation, Oozing, Change in sensation)
Diagnosis
Biopsy
- Types of biopsy:
- excisional biopsy
- incisional biopsy, or core biopsy
- punch biopsy
- saucerization biopsy
- fine-needle aspiration
- excisional biopsy
Staging
- Staging of primary melanoma is based on the histological features of the lesion.
- The current staging is based on measurement of the invasive component of the tumour and the presence or absence of microscopic ulceration.
Life expectancy
- 1A: 95% > 5yrs, 88%>10yrs
- 1B: 89-91% >5yrs, 79-83%>10yrs
- 2A: 77-79% >5yrs, 64%>10yrs
- 2B: 63-67%>5yrs, 51-54%>10yrs
- 2C: 45%>5yrs, 32%>10yrs
- 3A: 63-69%>5yrs, 57-63%>10yrs
- 3B: 46-53%>5yrs, 39-48%>10yrs
- 3C: 24-29%>5yrs, 15-24%>10yrs
- 4: 7-19%>5yrs
Treatment & management
Stage 1 (Wide Local Excision)
Stage II and III (Lymph Node Dissection, Adjuvant treatment, Drug – Interferon)
Stage IV (Surgery, Biological therapy, Chemotherapy, Radiotherapy)
complementary treatment :
-Nutrition therapy
-Naturopathic Medicine
-Mind-body medicine
-Oncology Rehabilitation
-Spiritual Support
-Image enhancement
Palliative care:
-improves the quality of life of patients
-can improve symptom control
-dependent on the need for intervention for physical or psychological symptoms, not the stage of the illness
-Can be given in the form of complementary medicine.
Prevention
- Primary prevention
- Limiting sun exposure
- Using sunscreens
- Limiting sun exposure
- Seeking medical attention for a suspicious and changing nevus
- Secondary prevention
- Routinely performing a total skin examination
- Routinely performing a total skin examination
Psychosocial issues on melanoma
Impact of melanoma on lifestyle of patient
- practical, emotional, psychological and physical effects of the disease & treatment
- subjected to different degrees of psychosocial distress
- depression, anxiety and deterioration in quality of life
- women have greater distress than man
Denial Patient
- The main step to cope with the emotional impact of melanoma is to:
- Talk openly about their feelings and concerns
- Ask questions they have about melanoma
- Ask about their own particular condition
- Gather as much information as possible
- Talk openly about their feelings and concerns
- Patient can promote recovery by:
- Maintaining a positive outlook
- Identifying beneficial activities
- Making changes in diet and exercise
- Reducing stress in daily life
What Physician Should Do?
MECHANISMS of MUTATION
MUTATION
Learning Objectives for this Section
As we learned earlier, the sequence of deoxyribonucleotide bases in the genes (def) that make up a organism's DNA determines the order of amino acids in the proteins and polypeptides made by that organism. This order of DNA bases constitutes an organism's genotype (def). A particular organism may possess alternate forms of some genes. Such alternate forms of genes are referred to as alleles (def). The physical characteristics an organism possesses, based on its genotype and the interaction with its environment, make up its phenotype (def).
Mutation (def) is an error during DNA replication that results in a change in the sequence of deoxyribonucleotide bases (def) in the DNA. Spontaneous mutation (def) occurs naturally (a normal mistake rate) about one in every million to one in every billion divisions and is probably due to low level natural mutagens normally present in the environment. Induced mutation (def) is caused by mutagens, substances that cause a much higher rate of mutation.
A. Spontaneous Mutation (def)
1. Mechanisms of mutation
a. Substitution of a nucleotide (point mutations (def)): substitution of one deoxyribonucleotide for another during DNA replication (see Fig. 17). This is the most common mechanism of mutation. Substitution of one nucleotide for another is a result of tautomeric shift, a rare process by which the hydrogen atoms of a deoxyribonucleotide base move in a way that changes the properties of its hydrogen bonding. For example, a shift in the hydrogen atom of adenine enables it to form hydrogen bonds with cytosine rather than thymine. Likewise, a shift in the hydrogen atom in thymine allows it to bind with guanine rather than adenine.
b. Deletion or addition of a nucleotide (frameshift mutations (def)): deletion or addition of a deoxyribonucleotide during DNA replication (see Fig. 18 and Fig. 19).
2. Results of mutation
One of four things can happen as a result of these mechanisms of mutation and the resulting change in the deoxyribonucleotide base sequence mentioned above:
a. A missense mutation (def) occurs. This is usually seen with a single substitution mutation and results in one wrong codon (def) and one wrong amino acid (see Fig. 20).
b. A nonsense mutation occurs (def). If the change in the deoxyribonucleotide base sequence results in transcription (def) of a stop or nonsense codon (def), the protein would be terminated at that point in the message (see Fig. 21).
c. A sense mutation (def) occurs. This is sometimes seen with a single substitution mutation when the change in the DNA base sequence results in a new codon still coding for the same amino acid (see Fig. 22). (With the exception of methionine, all amino acids are coded for by more than one codon.)
d. A frameshift mutation occurs (def). This is seen when a number of DNA nucleotides not divisible by three is added or deleted. Remember, the genetic code is a triplet code where three consecutive nucleotides code for a specific amino acid. This causes a reading frame shift and all of the codons and all of the amino acids after that mutation are usually wrong (see Fig. 23); frequently one of the wrong codons turns out to be a stop or nonsense codon and the protein is terminated at that point.
B. Induced Mutation (def) is caused by mutagens, substances that cause a much higher rate of mutation.
Chemical mutagens generally work in one of three ways.
Some chemical mutagens, such as nitrous acid and nitrosoguanidine, work by causing chemical modifications of purine and pyrimidine bases that alter their hydrogen-bonding properties. For example, nitrous acid converts cytosine to uracil which then forms hydrogen bonds with adenine rather than guanine.
Other chemical mutagens function as base analogs. They are compounds that chemically resemble a nucleotide base closely enough that during DNA replication, they can be incorporated into the DNA in place of the natural base. Examples include 2-amino purine, a compound that resembles adenine, and 5-bromouracil, a compound that resembles thymine. The base analogs, however, do not have the hydrogen-bonding properties of the natural base.
Still other chemical mutagens function as intercalating agents. Intercalating agents are planar three-ringed molecules that are about the same size as a nucleotide base pair. During DNA replication, these compounds can insert or intercalate between adjacent base pairs thus pushing the nucleotides far enough apart that an extra nucleotide is often added to the growing chain during DNA replication. An example is ethidium bromide.
Certain types of radiation can also function as mutagens.
Ultraviolet Radiation. The ultraviolet portion of the light spectrum includes all radiations with wavelengths from 100 nm to 400 nm. It has low wave length and low energy. The microbicidal activity of ultraviolet (UV) light depends on the length of exposure: the longer the exposure the greater the cidal activity. It also depends on the wavelength of UV used. The most cidal wavelengths of UV light lie in the 260 nm - 270 nm range where it is absorbed by nucleic acid.
In terms of its mode of action, UV light is absorbed by DNA and causes adjacent thymine bases on the same DNA strand to covalently bond together, forming what are called thymine-thymine dimers (see Fig. 24). As the DNA replicates, nucleotides do not complementary base pair with the thymine dimers and this terminates the replication of that DNA strand. In the case of bacteria, however, most of the damage from UV radiation actually comes from the cell trying to repair the damage to the DNA by a process called SOS repair. In very heavily damaged DNA containing large numbers of thymine dimers, a process called SOS repair is activated as kind of a last ditch effort to repair the DNA. In this process, a gene product of the SOS system binds to DNA polymerase allowing it to synthesize new DNA across the damaged DNA. However, this altered DNA polymerase loses its proofreading ability resulting in the synthesis of DNA that itself now contains many misincorporated bases. (Most of the chemical mutagens mentioned above also activate SOS repair.)
Ionizing Radiation. Ionizing radiation, such as X-rays and gamma rays, has much more energy and penetrating power than ultraviolet radiation. It ionizes water and other molecules to form radicals (molecular fragments with unpaired electrons) that can break DNA strands and alter purine and pyrimidine bases.
Learning Objectives for this Section
As we learned earlier, the sequence of deoxyribonucleotide bases in the genes (def) that make up a organism's DNA determines the order of amino acids in the proteins and polypeptides made by that organism. This order of DNA bases constitutes an organism's genotype (def). A particular organism may possess alternate forms of some genes. Such alternate forms of genes are referred to as alleles (def). The physical characteristics an organism possesses, based on its genotype and the interaction with its environment, make up its phenotype (def).
Mutation (def) is an error during DNA replication that results in a change in the sequence of deoxyribonucleotide bases (def) in the DNA. Spontaneous mutation (def) occurs naturally (a normal mistake rate) about one in every million to one in every billion divisions and is probably due to low level natural mutagens normally present in the environment. Induced mutation (def) is caused by mutagens, substances that cause a much higher rate of mutation.
A. Spontaneous Mutation (def)
1. Mechanisms of mutation
a. Substitution of a nucleotide (point mutations (def)): substitution of one deoxyribonucleotide for another during DNA replication (see Fig. 17). This is the most common mechanism of mutation. Substitution of one nucleotide for another is a result of tautomeric shift, a rare process by which the hydrogen atoms of a deoxyribonucleotide base move in a way that changes the properties of its hydrogen bonding. For example, a shift in the hydrogen atom of adenine enables it to form hydrogen bonds with cytosine rather than thymine. Likewise, a shift in the hydrogen atom in thymine allows it to bind with guanine rather than adenine.
b. Deletion or addition of a nucleotide (frameshift mutations (def)): deletion or addition of a deoxyribonucleotide during DNA replication (see Fig. 18 and Fig. 19).
2. Results of mutation
One of four things can happen as a result of these mechanisms of mutation and the resulting change in the deoxyribonucleotide base sequence mentioned above:
a. A missense mutation (def) occurs. This is usually seen with a single substitution mutation and results in one wrong codon (def) and one wrong amino acid (see Fig. 20).
b. A nonsense mutation occurs (def). If the change in the deoxyribonucleotide base sequence results in transcription (def) of a stop or nonsense codon (def), the protein would be terminated at that point in the message (see Fig. 21).
c. A sense mutation (def) occurs. This is sometimes seen with a single substitution mutation when the change in the DNA base sequence results in a new codon still coding for the same amino acid (see Fig. 22). (With the exception of methionine, all amino acids are coded for by more than one codon.)
d. A frameshift mutation occurs (def). This is seen when a number of DNA nucleotides not divisible by three is added or deleted. Remember, the genetic code is a triplet code where three consecutive nucleotides code for a specific amino acid. This causes a reading frame shift and all of the codons and all of the amino acids after that mutation are usually wrong (see Fig. 23); frequently one of the wrong codons turns out to be a stop or nonsense codon and the protein is terminated at that point.
B. Induced Mutation (def) is caused by mutagens, substances that cause a much higher rate of mutation.
Chemical mutagens generally work in one of three ways.
Some chemical mutagens, such as nitrous acid and nitrosoguanidine, work by causing chemical modifications of purine and pyrimidine bases that alter their hydrogen-bonding properties. For example, nitrous acid converts cytosine to uracil which then forms hydrogen bonds with adenine rather than guanine.
Other chemical mutagens function as base analogs. They are compounds that chemically resemble a nucleotide base closely enough that during DNA replication, they can be incorporated into the DNA in place of the natural base. Examples include 2-amino purine, a compound that resembles adenine, and 5-bromouracil, a compound that resembles thymine. The base analogs, however, do not have the hydrogen-bonding properties of the natural base.
Still other chemical mutagens function as intercalating agents. Intercalating agents are planar three-ringed molecules that are about the same size as a nucleotide base pair. During DNA replication, these compounds can insert or intercalate between adjacent base pairs thus pushing the nucleotides far enough apart that an extra nucleotide is often added to the growing chain during DNA replication. An example is ethidium bromide.
Certain types of radiation can also function as mutagens.
Ultraviolet Radiation. The ultraviolet portion of the light spectrum includes all radiations with wavelengths from 100 nm to 400 nm. It has low wave length and low energy. The microbicidal activity of ultraviolet (UV) light depends on the length of exposure: the longer the exposure the greater the cidal activity. It also depends on the wavelength of UV used. The most cidal wavelengths of UV light lie in the 260 nm - 270 nm range where it is absorbed by nucleic acid.
In terms of its mode of action, UV light is absorbed by DNA and causes adjacent thymine bases on the same DNA strand to covalently bond together, forming what are called thymine-thymine dimers (see Fig. 24). As the DNA replicates, nucleotides do not complementary base pair with the thymine dimers and this terminates the replication of that DNA strand. In the case of bacteria, however, most of the damage from UV radiation actually comes from the cell trying to repair the damage to the DNA by a process called SOS repair. In very heavily damaged DNA containing large numbers of thymine dimers, a process called SOS repair is activated as kind of a last ditch effort to repair the DNA. In this process, a gene product of the SOS system binds to DNA polymerase allowing it to synthesize new DNA across the damaged DNA. However, this altered DNA polymerase loses its proofreading ability resulting in the synthesis of DNA that itself now contains many misincorporated bases. (Most of the chemical mutagens mentioned above also activate SOS repair.)
Ionizing Radiation. Ionizing radiation, such as X-rays and gamma rays, has much more energy and penetrating power than ultraviolet radiation. It ionizes water and other molecules to form radicals (molecular fragments with unpaired electrons) that can break DNA strands and alter purine and pyrimidine bases.
management and treatment of malignant melanoma
stage 1 :
-Wide Local Excision
>surgically removing the melanoma as well as a small area of skin around it
>removes at least 1cm of skin all around the melanoma
>leave significant scarring
>Skin Grafts
---removing a patch of healthy skin , it is then connected, or grafted, to the affected area.
Stage II and III
-Lymph Node Dissection
-Adjuvant treatment :Treatment after surgery to try to reduce the risk of the melanoma coming back
-Drug – Interferon
Lymph node dissection :
-an operation to remove all the lymph nodes in the area, Just in case they contain cancer cells
>>Block dissection
-Risk : disruption of the lymphatic system.leading to a build-up of fluids in your limbs ---> lymphoedema
Drug -interferon
-It is given after surgery has been completed
-is administered by injection under the skin (subcutaneously )
-require three injections a week
-helps stimulate the body’s own immune system to fight any remaining cancerous cell
-cause side effects similar to flu symptoms (fever, chills, headache, tiredness)
Stage IV
-Surgery
>Sentinel lymph node biopsy
>Lymph node dissection
-Biological therapy
>Interferon
>Interleukin
-Chemotherapy
>Isolated limb perfusion
-Radiotherapy
Surgery
-removes the tumor and some normal tissue around it (margin)
-Lymph nodes near the tumor may be removed
>Sentinel lymph node biopsy
*To determine whether further surgery is needed by checking whether there are cancer cells in the lymph nodes
>Lymph node dissection
Biological therapy
-Interferon
-Interleukin
>part of the immune system.
chemotherpy
-damage the DNA of the cancer cells, interrupting their ability to reproduce
-cancer drugs to destroy cancer cells
>dacarbazine (DTIC)
>temozolomide (Temodal)
-is given by an infusion (drip) into one of the veins in your arm (intravenously)
-three or four weeks
-Side effects of chemotherapy can include:
>nausea,
>vomiting,
>hair loss, and
>fatigue.
-weaken your immune system, making you more vulnerable to infection
-Isolated limb perfusion
>secondary melanoma is confined to just an arm or a leg
>allows chemotherapy to be given to just one limb
Radiotherapy :
-Using high speed ionising radiation to destroy cancer cells
-Most effective : the cancer cell needs to be dividing at the time of the radiotherapy
>treatments often take place daily for a number of weeks
-There are internal and external radiotherapy
-Side effects :
>tiredness,
>nausea,
>loss of appetite,
>hair loss,
>sore skin, and
>a lack of interest in sex.
complementary treatment :
-Nutrition therapy – nutrition plan, diet, supplements, education
-Pain management - pharmacological and non-pharmacological
-Naturopathic Medicine - botanical med. , eastern med., psychological med.
-Mind-body medicine - stress management, relaxation and imaginary training, spiritual meditation, support group, counseling
-Oncology Rehabilitation – physical therapy, manual therapy, occupational therapy, speech therapy
-Spiritual Support - group prayer
-Image enhancement – cosmetic image enhancement, plastic/reconstructive support
http://www.cancercenter.com/melanoma/complementary-alternative-melanoma-treatment.cfm
Palliative care :
-improves the quality of life of patients and their families facing the problem associated with life-threatening illness through the prevention and relief of suffering by means of early identification,impeccable assessment and treatment of pain and other problems, physical, psychosocial and spiritual.
-provides relief from pain and other distressing symptoms;
-affirms life and regards dying as a normal process;
-intends neither to hasten or postpone death;
-integrates the psychological and spiritual aspects of patient care;
-offers a support system to help patients live as actively as possible until death;
-offers a support system to help the family cope during the patients illness and in their own bereavement;
-uses a team approach to address the needs of patients and their families, including bereavement counselling, if indicated;
-will enhance quality of life, and may also positively influence the course of illness;
-is applicable early in the course of illness, in conjunction with other therapies that are intended to prolong life, such as chemotherapy or radiation therapy, and includes those investigations needed to better understand and manage distressing clinical complications.
http://www.who.int/cancer/palliative/definition/en/
-Wide Local Excision
>surgically removing the melanoma as well as a small area of skin around it
>removes at least 1cm of skin all around the melanoma
>leave significant scarring
>Skin Grafts
---removing a patch of healthy skin , it is then connected, or grafted, to the affected area.
Stage II and III
-Lymph Node Dissection
-Adjuvant treatment :Treatment after surgery to try to reduce the risk of the melanoma coming back
-Drug – Interferon
Lymph node dissection :
-an operation to remove all the lymph nodes in the area, Just in case they contain cancer cells
>>Block dissection
-Risk : disruption of the lymphatic system.leading to a build-up of fluids in your limbs ---> lymphoedema
Drug -interferon
-It is given after surgery has been completed
-is administered by injection under the skin (subcutaneously )
-require three injections a week
-helps stimulate the body’s own immune system to fight any remaining cancerous cell
-cause side effects similar to flu symptoms (fever, chills, headache, tiredness)
Stage IV
-Surgery
>Sentinel lymph node biopsy
>Lymph node dissection
-Biological therapy
>Interferon
>Interleukin
-Chemotherapy
>Isolated limb perfusion
-Radiotherapy
Surgery
-removes the tumor and some normal tissue around it (margin)
-Lymph nodes near the tumor may be removed
>Sentinel lymph node biopsy
*To determine whether further surgery is needed by checking whether there are cancer cells in the lymph nodes
>Lymph node dissection
Biological therapy
-Interferon
-Interleukin
>part of the immune system.
chemotherpy
-damage the DNA of the cancer cells, interrupting their ability to reproduce
-cancer drugs to destroy cancer cells
>dacarbazine (DTIC)
>temozolomide (Temodal)
-is given by an infusion (drip) into one of the veins in your arm (intravenously)
-three or four weeks
-Side effects of chemotherapy can include:
>nausea,
>vomiting,
>hair loss, and
>fatigue.
-weaken your immune system, making you more vulnerable to infection
-Isolated limb perfusion
>secondary melanoma is confined to just an arm or a leg
>allows chemotherapy to be given to just one limb
Radiotherapy :
-Using high speed ionising radiation to destroy cancer cells
-Most effective : the cancer cell needs to be dividing at the time of the radiotherapy
>treatments often take place daily for a number of weeks
-There are internal and external radiotherapy
-Side effects :
>tiredness,
>nausea,
>loss of appetite,
>hair loss,
>sore skin, and
>a lack of interest in sex.
complementary treatment :
-Nutrition therapy – nutrition plan, diet, supplements, education
-Pain management - pharmacological and non-pharmacological
-Naturopathic Medicine - botanical med. , eastern med., psychological med.
-Mind-body medicine - stress management, relaxation and imaginary training, spiritual meditation, support group, counseling
-Oncology Rehabilitation – physical therapy, manual therapy, occupational therapy, speech therapy
-Spiritual Support - group prayer
-Image enhancement – cosmetic image enhancement, plastic/reconstructive support
http://www.cancercenter.com/melanoma/complementary-alternative-melanoma-treatment.cfm
Palliative care :
-improves the quality of life of patients and their families facing the problem associated with life-threatening illness through the prevention and relief of suffering by means of early identification,impeccable assessment and treatment of pain and other problems, physical, psychosocial and spiritual.
-provides relief from pain and other distressing symptoms;
-affirms life and regards dying as a normal process;
-intends neither to hasten or postpone death;
-integrates the psychological and spiritual aspects of patient care;
-offers a support system to help patients live as actively as possible until death;
-offers a support system to help the family cope during the patients illness and in their own bereavement;
-uses a team approach to address the needs of patients and their families, including bereavement counselling, if indicated;
-will enhance quality of life, and may also positively influence the course of illness;
-is applicable early in the course of illness, in conjunction with other therapies that are intended to prolong life, such as chemotherapy or radiation therapy, and includes those investigations needed to better understand and manage distressing clinical complications.
http://www.who.int/cancer/palliative/definition/en/
Wednesday, May 6, 2009
Summary for incidence and prevalence
Malignant melanoma incidence has continued to increase worldwide, with the highest incidence in Australia and New Zealand. From 2002, a prevalence of 37.7 cases per 100,000 men and 29.4 cases per 100,000 women in Australia and New Zealand is demonstrated. America has a lower incidence compared to Aus-NZ, with a prevalence of 6.4 cases per 100,000 men and 11.7 cases per 100,000 women in North America. In the European countries, the highest incidence rates are found in northern and western countries and the lowest in southern countries, with rates from three to eight times lower for men and women, respectively.
DIfferential Diagnosis for Melanoma
Seborrheic keratosis
- benign wart-like growths on the surface of the skin.
- cause is unknown. The condition commonly appears after age 40.
Symptoms:
1) located on the face, chest, shoulders, back, or other areas
2) usually painless, but may become irritated and itch
3) yellow, brown, black, or other colors
4) slightly elevated, flat surface
5) May have a rough or wart-like texture
6) Often have a waxy surface
7) Have a round-to-oval shape
8) May have a "pasted-on" appearance
9) May be single, but are usually multiple growths
Diagnosis is based primarily on the appearance of the growths. A skin lesion biopsy may be used to confirm the diagnosis.
Traumatized or irritated nevus
- may be partially avulsed and/or have hemorrhagic crusting suggesting ulceration.
- Melanocyte hyperplasia develops superficial to the scar resulting in uneven pigmentation and irregular outlines as pigment extends into the surrounding skin (quite suggestive of melanoma)
- recurrent nevus phenomenon can resemble melanoma histologically, as well.
- The history of trauma or biopsy along with review of the original biopsy helps exclude a diagnosis of melanoma.
Basal cell carcinoma
- grows by direct extension and appears to rely on the surrounding supportive tissue to grow – thus does not metastasize through blood vessels or lymphatics.
- starts in the top layer of the skin called the epidermis.
- grows slowly and is painless.
- A new skin growth that bleeds easily or does not heal well may suggest basal cell carcinoma.
- The majority of these cancers occur on areas of skin that are regularly exposed to sunlight or other ultraviolet radiation, may also appear on the scalp.
Features:
Pearly or waxy
White or light pink
Flesh-colored or brown
In some cases the skin may be just slightly raised or even flat.
May have:
A skin sore that bleeds easily
A sore that does not heal
Oozing or crusting spots in a sore
Appearance of a scar-like sore without having injured the area
Irregular blood vessels in or around the spot
A sore with a depressed (sunken) area in the middle
Lentigo
- a spot on the skin that is darker (usually brown) than the surrounding skin. Lentigines are more common among whites, especially those with fair skin.
- sometimes called an age spot or freckle
Types:
Lentigo simplex (eg, simple lentigo, juvenile lentigo) is the most common form of lentigo
Solar lentigo (eg, actinic lentigo, senile lentigo, sun spot, liver spot) is the most common benign sun-induced lesion that occurs in sun-exposed areas.
Ink-spot lentigo (ie, reticulated black solar lentigo) can be distinguished by a wiry or beaded, markedly irregular outline; these lesions occur in patients of Celtic ancestry.
PUVA lentigo is a persistent, pale brown macule appearing 6 months or longer after the start of PUVA therapy for psoriasis.
Radiation lentigo resembles UV-induced lentigo, but it often includes other histopathologic signs of long-term cutaneous radiation damage such as epidermal atrophy, subcutaneous fibrosis, keratosis, and telangiectasias.
Tanning-bed lentigines usually occur in women with a history of tanning-bed use.
Vulvar and penile lentigo are benign lesions similar to labial melanotic macules.
Lentigines profusa (ie, generalized lentigines) is characterized by numerous lentigines without signs of associated abnormalities or triggering factors.
Angiokeratoma
- A harmless, discolored, raised skin lesion involving damaged blood capillaries.
- The lesion ranges in color from red to blue and the skin involved is usually thickened.
- Red to blue skin lump
- Localized thickening of skin
Causes of Angiokeratoma
Fucosidosis
GM1 gangliosidosis, type 2
Fabry's disease
Angiokeratoma circumscriptum
Angiokeratoma of Fordyce
Venous lake
- manifest as dark blue-to-violaceous compressible papules caused by dilation of venules.
- exacerbated by solar exposure and damage
- Vascular thrombosis play a role in development
Hemangioma
- an abnormal buildup of blood vessels in the skin or internal organs.
- About 30% of hemangiomas are present at birth. The rest appear in the first several months of life.
May be:
In the top skin layers (capillary hemangioma)
Deeper in the skin (cavernous hemangioma)
A mixture of both
- A red to reddish-purple, raised sore (lesion) on the skin
- A massive, raised tumor with blood vessels
- Most hemangiomas are on the face and neck.
Hemangiomas are diagnosed by a physical examination. In the case of deep or mixed lesions, a CT or MRI scan may be performed.
Dermatofibromas
- a firm, red-to-brown, small papule or nodule composed of fibroblastic tissue. It usually occurs on the thighs or legs.
- Benign tumour
- Cause is unknown
- Most are asymptomatic, but some itch or ulcerate following minor trauma.
- Diagnosis is clinical; lesions typically dimple when grasped between the fingers
Pigmented actinic keratosis
- a precancerous growth on the skin.
- caused by sun exposure.
- occurs most commonly in fair skin, especially in the elderly and in young people who have light skin.
- Rough and dry skin lesion
- patch or growth on the skin
- Limited to one area (localized)
- Located on the face, scalp, back of the hands, chest, or other sun-exposed areas
- Gray, pink, red (erythematous), or the same color as the skin
- Begins as flat and scaly areas
- Later develops a hard and wart-like or gritty, rough, and "sandpapery" surface -- may develop a horn-like texture
- The skin lesion may be easier to feel than to see.
The health care provider makes the diagnosis based on the appearance of the skin growth. A skin biopsy may reveal any cancerous changes, if they occur.
Reference:
http://www.aafp.org/afp/20010401/1359.html
http://www.merriam-webster.com/medical/seborrheic%20keratosis
http://www.wrongdiagnosis.com/a/angiokeratoma/intro.htm
http://emedicine.medscape.com/article/1056397-overview
http://www.childrenshospital.org/az/Site998/mainpageS998P0.html
http://emedicine.medscape.com/article/1085199-overview
http://www.aad.org/public/publications/pamphlets/common_growths.html
http://www.merck.com/mmpe/sec10/ch127/ch127b.html
- benign wart-like growths on the surface of the skin.
- cause is unknown. The condition commonly appears after age 40.
Symptoms:
1) located on the face, chest, shoulders, back, or other areas
2) usually painless, but may become irritated and itch
3) yellow, brown, black, or other colors
4) slightly elevated, flat surface
5) May have a rough or wart-like texture
6) Often have a waxy surface
7) Have a round-to-oval shape
8) May have a "pasted-on" appearance
9) May be single, but are usually multiple growths
Diagnosis is based primarily on the appearance of the growths. A skin lesion biopsy may be used to confirm the diagnosis.
Traumatized or irritated nevus
- may be partially avulsed and/or have hemorrhagic crusting suggesting ulceration.
- Melanocyte hyperplasia develops superficial to the scar resulting in uneven pigmentation and irregular outlines as pigment extends into the surrounding skin (quite suggestive of melanoma)
- recurrent nevus phenomenon can resemble melanoma histologically, as well.
- The history of trauma or biopsy along with review of the original biopsy helps exclude a diagnosis of melanoma.
Basal cell carcinoma
- grows by direct extension and appears to rely on the surrounding supportive tissue to grow – thus does not metastasize through blood vessels or lymphatics.
- starts in the top layer of the skin called the epidermis.
- grows slowly and is painless.
- A new skin growth that bleeds easily or does not heal well may suggest basal cell carcinoma.
- The majority of these cancers occur on areas of skin that are regularly exposed to sunlight or other ultraviolet radiation, may also appear on the scalp.
Features:
Pearly or waxy
White or light pink
Flesh-colored or brown
In some cases the skin may be just slightly raised or even flat.
May have:
A skin sore that bleeds easily
A sore that does not heal
Oozing or crusting spots in a sore
Appearance of a scar-like sore without having injured the area
Irregular blood vessels in or around the spot
A sore with a depressed (sunken) area in the middle
Lentigo
- a spot on the skin that is darker (usually brown) than the surrounding skin. Lentigines are more common among whites, especially those with fair skin.
- sometimes called an age spot or freckle
Types:
Lentigo simplex (eg, simple lentigo, juvenile lentigo) is the most common form of lentigo
Solar lentigo (eg, actinic lentigo, senile lentigo, sun spot, liver spot) is the most common benign sun-induced lesion that occurs in sun-exposed areas.
Ink-spot lentigo (ie, reticulated black solar lentigo) can be distinguished by a wiry or beaded, markedly irregular outline; these lesions occur in patients of Celtic ancestry.
PUVA lentigo is a persistent, pale brown macule appearing 6 months or longer after the start of PUVA therapy for psoriasis.
Radiation lentigo resembles UV-induced lentigo, but it often includes other histopathologic signs of long-term cutaneous radiation damage such as epidermal atrophy, subcutaneous fibrosis, keratosis, and telangiectasias.
Tanning-bed lentigines usually occur in women with a history of tanning-bed use.
Vulvar and penile lentigo are benign lesions similar to labial melanotic macules.
Lentigines profusa (ie, generalized lentigines) is characterized by numerous lentigines without signs of associated abnormalities or triggering factors.
Angiokeratoma
- A harmless, discolored, raised skin lesion involving damaged blood capillaries.
- The lesion ranges in color from red to blue and the skin involved is usually thickened.
- Red to blue skin lump
- Localized thickening of skin
Causes of Angiokeratoma
Fucosidosis
GM1 gangliosidosis, type 2
Fabry's disease
Angiokeratoma circumscriptum
Angiokeratoma of Fordyce
Venous lake
- manifest as dark blue-to-violaceous compressible papules caused by dilation of venules.
- exacerbated by solar exposure and damage
- Vascular thrombosis play a role in development
Hemangioma
- an abnormal buildup of blood vessels in the skin or internal organs.
- About 30% of hemangiomas are present at birth. The rest appear in the first several months of life.
May be:
In the top skin layers (capillary hemangioma)
Deeper in the skin (cavernous hemangioma)
A mixture of both
- A red to reddish-purple, raised sore (lesion) on the skin
- A massive, raised tumor with blood vessels
- Most hemangiomas are on the face and neck.
Hemangiomas are diagnosed by a physical examination. In the case of deep or mixed lesions, a CT or MRI scan may be performed.
Dermatofibromas
- a firm, red-to-brown, small papule or nodule composed of fibroblastic tissue. It usually occurs on the thighs or legs.
- Benign tumour
- Cause is unknown
- Most are asymptomatic, but some itch or ulcerate following minor trauma.
- Diagnosis is clinical; lesions typically dimple when grasped between the fingers
Pigmented actinic keratosis
- a precancerous growth on the skin.
- caused by sun exposure.
- occurs most commonly in fair skin, especially in the elderly and in young people who have light skin.
- Rough and dry skin lesion
- patch or growth on the skin
- Limited to one area (localized)
- Located on the face, scalp, back of the hands, chest, or other sun-exposed areas
- Gray, pink, red (erythematous), or the same color as the skin
- Begins as flat and scaly areas
- Later develops a hard and wart-like or gritty, rough, and "sandpapery" surface -- may develop a horn-like texture
- The skin lesion may be easier to feel than to see.
The health care provider makes the diagnosis based on the appearance of the skin growth. A skin biopsy may reveal any cancerous changes, if they occur.
Reference:
http://www.aafp.org/afp/20010401/1359.html
http://www.merriam-webster.com/medical/seborrheic%20keratosis
http://www.wrongdiagnosis.com/a/angiokeratoma/intro.htm
http://emedicine.medscape.com/article/1056397-overview
http://www.childrenshospital.org/az/Site998/mainpageS998P0.html
http://emedicine.medscape.com/article/1085199-overview
http://www.aad.org/public/publications/pamphlets/common_growths.html
http://www.merck.com/mmpe/sec10/ch127/ch127b.html
Diagnosis
A biopsy is the only certain way of diagnosing melanoma. In a biopsy, the doctor removes an area of the suspicious growth. Biopsies usually are done after the skin is numbed with a local anesthetic so there is almost no pain. Once the tissue sample is removed, a specialist examines it for cancer cells under a microscope.
The type of biopsy depends on the size of the skin growth and its location on the body. Several types of biopsy can be done when the doctor suspects melanoma:
An excisional biopsy excises, or cuts away, the entire growth with a margin of normal surrounding skin. The skin may be stitched together to close the hole. This procedure is more time-consuming and therefore usually needs to be scheduled. Generally, an additional wide local excision of normal surrounding skin will be required if the biopsy is positive. The width of the margin will depend on the thickness of the cancer.
An incisional biopsy, or core biopsy, removes only a sample of the growth, and the resulting hole is closed with stitches. Further treatment is necessary if the microscopic examination reveals cancer cells.
A punch biopsy removes a small, cylindrical shaped sample of skin. It includes the epidermis, dermis, and parts of the underlying tissue. It is done with a surgical tool that looks like a round hollow tube with sharp edges.
A saucerization biopsy removes the entire lesion by cutting under the lesion in a "scoop like" manner. This leaves a large, deep depression in the skin, but can be performed immediately and provides the dermatopathologist with a complete specimen to better analyze the tumors architecture.
A shave biopsy is shaving the top layer of skin (epidermis)Diagnosing many types of skin diseases and in sampling moles when the risk of melanoma is very LOW. May not be thick enough to measure how deeply the melanoma has invaded the skin.
A fine-needle aspiration biopsy is done with a very thin needle and syringe that looks like a hypodermic syringe used for giving injections. It removes a very small sample of tissue. This type of biopsy is not done on a suspicious mole or skin growth. Rather, it is done on other deeper tissue, such as nearby lymph nodes or an internal organ, to see if melanoma has spread.
Lymphoscintigraphy - A tiny dose of radioactive tracer is injected into the skin. The first lymph node which drains the melanoma is called the sentinel node. A gamma camera is used to identify the relevant lymph channels and lymph nodes. it is also called the sentinel node biopsy.
After biopsy, the tissue removed will then be sliced, stained and looked at under a microscope. This comes under histopathology.
to check for metastasis:
blood test
MRI/NMR
Radiology
Ultrasound
PREVENTION OF MALIGNANT MELANOMA
- Primary prevention
- Limiting sun exposure
- Avoid the strong midday sun between the hours of 10 a.m. and 3 p.m.
- When outdoors, seek out shaded areas
- Wear wide-brimmed hats ( to protect the ears), long-sleeved shirts and long pants ( tightly woven clothing is more protective)
- Wear sunglasses
- Do not use sunbeds or tanning salons
- UV can cause skin cancer and wrinkling
- The amount of radiation is similar to the sun and in some cases may be stronger
- UV can cause skin cancer and wrinkling
- Sunburn or excessive exposure to the sun in childhood is thought to be the biggest risk factor to the developing of skin cancer as an adult.
- People with a family history of melanoma should take extra care to protect their skin from the sun.
- Avoid the strong midday sun between the hours of 10 a.m. and 3 p.m.
- Using sunscreens
- Use a sunscreen with at least SPF 15(Sun Protecting Factor)
- Provide broad spectrum coverage against both UVA and UVB rays
- SPF
- Calculated by the amount of time needed to produce a sunburn on sunscreen protected skin to the amount of time needed to cause a sunburn on unprotected skin.
- E.g. if a person would turn red after ten minutes of exposure in the sun, SPF 2 will give protection for 20 minutes, while SPF 15 will give him protection for 150 minutes against to the exposure to the sun.
- Calculated by the amount of time needed to produce a sunburn on sunscreen protected skin to the amount of time needed to cause a sunburn on unprotected skin.
- Actually, SPF no. on sunscreen only reflects the product's screening ability for UVB rays. No FDA-approved rating system that identifies UVA protection have yet been made
- apply to dry skin 15-30 minutes before going outdoors
- reapplying the product every two to three hours and after sweating and swimming
- Should be applied everyday to exposed skin, not just if you are gioing to be in the sun.
- UVB rays cannot penetrate galss windows, UVA rays can
- UVB rays cannot penetrate galss windows, UVA rays can
- Don't reserve the use of sunscreen only for sunny days.
- Even on a cloudy days, 80% of the sun's ultraviolet rays can pass through the cloud
- Sand reflects 25% of the sun rays
- Snow reflects 80% of the sun rays
- Increase the chances of sunburn
- Even on a cloudy days, 80% of the sun's ultraviolet rays can pass through the cloud
- Concerns
- May provide a false sense of security. No products can give 100% UVB protection
- Users may spend excessive amount of time under the sun
- May provide a false sense of security. No products can give 100% UVB protection
- Use a sunscreen with at least SPF 15(Sun Protecting Factor)
- Seeking medical attention for a suspicious and changing nevus
- 46% of patients with melanoma did not seek medical attention until they found ulceration, bleeding or a lump in the pigmented lesion (late signs of melanoma)
- 46% of patients with melanoma did not seek medical attention until they found ulceration, bleeding or a lump in the pigmented lesion (late signs of melanoma)
- Secondary prevention
- Routinely performing a total skin examination for a specific segments of the population
- Routine screening for melanoma could save lives because earlier detection of thinner tumours is associated with better survival rates.
- Routine screening for melanoma could save lives because earlier detection of thinner tumours is associated with better survival rates.
Staging
The concept of stage is applicable to almost all cancers except for most forms of leukemia. Since leukemias involve all of the blood, they are not anatomically localized like other cancers, so the concept of staging doesn't make as much sense for them. A few forms of leukemia do have staging systems which reflect various measures of how advanced the disease is. For most solid tumors, there are two related cancer staging systems, the Overall Stage Grouping, and the TNM system.
Staging11
- Staging of primary melanoma is based on the histological features of the lesion. Accurate staging is vital to determine appropriate treatment, follow-up, and calculation of risk of recurrence.
- In 2001 the American Joint Committee on Cancer staging system for cutaneous melanoma was published.12
- The current American Joint Committee on Cancer (AJCC) staging is based on measurement of the invasive component of the tumour (the Breslow thickness) and the presence or absence of microscopic ulceration.
- The staging system is in the process of being revised and an update is expected in 2009.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
For Survival Rates according to stages please feel free to look up the following sites.
http://www.cancerhelp.org.uk/help/default.asp?page=3015
http://www.cancerhelp.org.uk/help/default.asp?page=5436
http://www.cancerguide.org/basic.html
http://jco.ascopubs.org/cgi/reprint/19/16/3635.pdf
I'd reccomend going through the fourth link for information on the staging system as well as the survival rates. the other three links give you the information in an easy to understand way. the first gives the information on the different staging while the second gives the survival rates, the third gives an account of the staging system.
Anatomy of Skin
Anatomy of the Skin
Largest and heaviest organ
3 layers
-Epidermis (Stratified Squamous Epithelium)
-Dermis (Connective Tissue Layer)
-Hypodermis (Subcutaneous Tissue)
Thickness of skin
Skin thickness varies from 0.5mm to 6mm. Difference due mainly to variation in the thickness of the dermis. However, skin is classified as thick or thin based on thickness of epidermis alone.
Thick skin covers palms, soles and surfaces of fingers/toes. (Epidermis alone is 0.5mm due to thick surface of dead cells called stratum corneum). Thick skin has sweat glands but no hair follicles or sebaceous glands.
Thin skin covers the rest of the body. (0.1mm thick epidermis with thin stratum corneum). Has hair follicles, sebaceous glands and sweat glands
Epidermis
Keratinized stratified squamous epithelium.
Layers of epidermis from the top
-stratum corneum
-stratum lucidum
-stratum granulosum-keratohyalin granules
-stratum spinosum-desmosomes attaches keratinocyte
-stratum basale
Cells of epidermis
Stem cells
-undifferentiated cells that divide and give rise to keratinocytes. Found in stratum basale.
Keratinocytes
-makes up most of epidermal cells
-synthesize keratin
Melanocytes
-found in stratum basale
-synthesize brown to black pigment called melanin (shields DNA from UV radiation)
Tactile Cells
-receptors for sense of touch
Dendritic Cells/Langerhans cells
-found in stratum granulosum and stratum spinosum
-originate in bone marrow but migrates to epidermis
-guard against toxins, microbes and other pathogens by alerting immune system
Dermis
-composed of collagen, elastic and reticular fibers, fibroblasts
-rich with blood vessels, sweat glands, sebaceous glands and nerve endings
-hair follicles and nail roots are embedded in dermis
-smooth muscles associated with hair follicles contract in response to stimuli which causes the hair to stand, goosebumps and wrinkles.
-skeletal muscles on face attach to dermal collagen fibres-wrinkle,lifting eyebrow, smiling
2 zones of dermis
Papillary Layer
-thin zone of areolar tissue in and near dermal papillae
-mobility of leucocytes and other defenses against foreign substances
-rich in small blood vessels
Reticular layer
-deeper and much thicker
-consists dense irregular connective tissue
-collagen forms thicker bundles-less room for ground substance
-small clusters of adipocytes
Hypodermis
-has more areolar and adipose tissue
-binds skin to underlying tissue
Subcutaneous fat
-hypodermis composed of adipose tissue
-energy reservoir and thermal insulation
Largest and heaviest organ
3 layers
-Epidermis (Stratified Squamous Epithelium)
-Dermis (Connective Tissue Layer)
-Hypodermis (Subcutaneous Tissue)
Thickness of skin
Skin thickness varies from 0.5mm to 6mm. Difference due mainly to variation in the thickness of the dermis. However, skin is classified as thick or thin based on thickness of epidermis alone.
Thick skin covers palms, soles and surfaces of fingers/toes. (Epidermis alone is 0.5mm due to thick surface of dead cells called stratum corneum). Thick skin has sweat glands but no hair follicles or sebaceous glands.
Thin skin covers the rest of the body. (0.1mm thick epidermis with thin stratum corneum). Has hair follicles, sebaceous glands and sweat glands
Epidermis
Keratinized stratified squamous epithelium.
Layers of epidermis from the top
-stratum corneum
-stratum lucidum
-stratum granulosum-keratohyalin granules
-stratum spinosum-desmosomes attaches keratinocyte
-stratum basale
Cells of epidermis
Stem cells
-undifferentiated cells that divide and give rise to keratinocytes. Found in stratum basale.
Keratinocytes
-makes up most of epidermal cells
-synthesize keratin
Melanocytes
-found in stratum basale
-synthesize brown to black pigment called melanin (shields DNA from UV radiation)
Tactile Cells
-receptors for sense of touch
Dendritic Cells/Langerhans cells
-found in stratum granulosum and stratum spinosum
-originate in bone marrow but migrates to epidermis
-guard against toxins, microbes and other pathogens by alerting immune system
Dermis
-composed of collagen, elastic and reticular fibers, fibroblasts
-rich with blood vessels, sweat glands, sebaceous glands and nerve endings
-hair follicles and nail roots are embedded in dermis
-smooth muscles associated with hair follicles contract in response to stimuli which causes the hair to stand, goosebumps and wrinkles.
-skeletal muscles on face attach to dermal collagen fibres-wrinkle,lifting eyebrow, smiling
2 zones of dermis
Papillary Layer
-thin zone of areolar tissue in and near dermal papillae
-mobility of leucocytes and other defenses against foreign substances
-rich in small blood vessels
Reticular layer
-deeper and much thicker
-consists dense irregular connective tissue
-collagen forms thicker bundles-less room for ground substance
-small clusters of adipocytes
Hypodermis
-has more areolar and adipose tissue
-binds skin to underlying tissue
Subcutaneous fat
-hypodermis composed of adipose tissue
-energy reservoir and thermal insulation
Current concepts in wound dressings
| Current concepts in wound dressings |
Peter G. Hayward and Wayne A. Morrison, Plastic and Reconstructive Surgeons, St Vincent's Hospital, Melbourne
Summary
Wound management has recently become more complex because of new insights into wound healing and the increasing need to manage complex wounds outside hospital. The wound is a synthetic environment in which numerous cellular processes are interlinked in the process of repair. Modern dressings are designed to facilitate the function of the wound rather than just to cover it. Principles of wound dressings are changing, especially in relation to debridement of wounds and control of the wound environment. Occlusive dressings which allow debridement in a fluid environment are equal to traditional wet or dry dressings. There are some advantages in allowing wounds to heal in a moist environment which facilitates cellular migration and epithelialisation. Straightforward surgical and traumatic wounds require low cost and low technology dressings. The place of more costly and complicated wound dressings has to be defined in terms of cost, labour saving and patient comfort, in addition to any putative advantages in the speed of wound healing.
Key words: healing process, alginates, hydrogels, hydrocolloids
(Aust Prescr 1996;19:11-3)
Wound management is a significant clinical and economic problem. Pressure sores alone account for a significant amount of health expenditure. A myriad of dressings have been applied to wounds since ancient times1 and, today, many more new dressing materials are available.
Wound healing
Immediately after wounding, tissue repair begins with haemostasis. Healing then involves a complex chain of events coordinated by key cells, principally macrophages, which use an array of polypeptide growth factors. These newly identified factors act to induce migration and multiplication of cells, as well as the production of other growth factors. The interrelated processes of epithelialisation, angiogenesis, fibroplasia and collagen synthesis occur only when appropriate cells receive growth factor encoded signals.2 The modern view of the wound considers it to be a temporary 'organ' established to effect healing. Following this view, modern dressings are designed to nurture the cellular environment of the wound. Ultimately, dressing design may resemble the technology of tissue culture.
Function of a dressing
Traditionally, dressings fulfilled a number of functions: cosmesis, haemostasis, protection, support and absorption.
Previously, prolonged hospital stays for chronic wound treatment with multiple (and frequently painful) dressing changes were not unusual. Currently, there are insufficient resources to allow chronic inpatient treatment of all wounds and patients are less prepared to accept prolonged morbidity. New parameters for dressings have emerged. A dressing is no longer a passive adjunct to healing, but is an active element of wound management designed to debride the wound, control infection and promote healing. The ideal dressing must be easy to apply, painless to remove and require fewer changes (and less human resources). It must be robust enough to be used by outpatients.
Wound management
Comprehensive wound management includes prevention. Patients at risk of developing chronic wounds such as pressure sores or venous ulcers should be watched and receive appropriate preventive measures.3 Grading scales have been developed to estimate the risk, and surveillance of inpatients at risk has reduced the incidence of pressure sores.
The assessment of existing wounds includes consideration of factors which can affect healing, such as diabetes or ischaemia. Management consists of debridement, the control of infection and the promotion of natural healing.
Debridement
Not all wounds require surgical debridement, but necrotic tissue should be removed from the wound edges and cavity. Traditionally, wounds were debrided with 'wet to dry' dressings where layered gauze was allowed to dry and then removed with necrotic material attached. These dressings required frequent changes which were often painful. Recent developments in dressing technology have introduced hydrogels and other occlusive dressings. These allow in situ degradation of necrotic material which is then absorbed into the fluid phase of the dressing.
Control of infection
Great confusion arises in clinical practice between the significance of a positive wound swab and the risk of invasive infection. Wound healing is only significantly ret arded when a sufficient bacterial load (>105 bacteria/g of tissue) is present.4 In practical terms, an open draining wound without necrotic tissue will be colonised, but the bacteria present are usually insufficient in number to affect healing.5 In contrast to colonisation, invasive infection retards healing and leads to wound breakdown.
For most wounds, all that is required to reduce bacterial counts to tolerable levels is to clean away accumulated debris. Topical antiseptics can be used to irrigate, cleanse and debride wounds. In general, they do not promote the development of drug resistance, but they vary in antibacterial effect, and some species, especially pseudomonas, are resistant.
Cleansing noninfected 'clean' wounds is best carried out with saline. For purulent wounds, a range of antiseptics is available6,7, but some have been suggested to delay healing. Chlorhexidine 0.05% is the most widely used antiseptic. It has a lower incidence of contact dermatitis and less tissue toxicity. Cetrimide 1% has a marked detergent action and is often used for soiled traumatic wounds. Its in vitro cytotoxicity makes it unpopular for routine use. Povidone-iodine is particularly useful against staphylococci, but is less effective against pseudomonas species. It is associated with contact hypersensitivity as well as toxicity from systemic absorption which limits its use as an irrigant in large, deep cavities. The use of hypochlorite solutions, such as Eusol, has declined due to concerns about tissue toxicity. The 'hypochlorite debate' is an example of how conclusions drawn from animal and in vitro data are occasionally mistakenly applied to human wound healing. Hypochlorite was found to be toxic to fibroblasts in vitro, but subsequent studies8 showed that the toxicity was concentrationdependent and that lower concentrations were not toxic.
Systemic antibiotics do not penetrate necrotic tissue and have little to offer in the management of chronic wounds. Topical antibiotic applications should also be avoided since they are ineffective and foster multiple drugresistant strains of bacteria. Antibiotics are only appropriate when there is invasive infection, such as cellulitis.
Dressings (table 1)
An active dressing aims to establish an optimum microenvironment for healing the wound. It must maintain the wound temperature and moisture level, permit respiration and allow epithelial migration. Optimal wound temperature is required for the function of cells such as macrophages, neutrophils and fibroblasts. The respiration of these cells also requires adequate transfer of oxygen and carbon dioxide across the wound surface. The most favourable environment for the mobility and respiration of cells is a moist wound. Studies of the moist wound environment have shown enhanced epithelial migration, fibroblast function and collagen production. These findings supported the development of occlusive dressings.5
Semipermeable adhesive films
These dressings, including Opsite and Tegaderm, are permeable to gas and water vapour, but are a barrier to bacteria and water. They are generally reserved for the definitive closure of superficial, partial thickness wounds where comfort and ease of management are important. The dressings can be left in place for several days, but usually leak if exudate builds up. Removal is easier if the film is stretched before being pulled off.
Hydrocolloids
Dressings such as Comfeel and Duoderm are adhesive, water and gas impermeable membranes. When the inner layer comes into contact with exudate, it forms a gel. They provide an excellent seal around the edges of the wound and can protect pressure areas. The hydrocolloids absorb exudate and help to debride the wound. Patients should be warned that the wound may, at first, become smelly and appear to enlarge. The dressing needs to be changed when the gel leaks out, so to avoid frequent changes, the dressing should have a diameter at least 2 cm bigger than the wound.
The hydrocolloids can be used in the presence of necrotic material, but tend to have problems with overwhelming exudate buildup in large wounds or those where there is anaerobic colonisation.
Alginates
Kaltostat and other alginates are derivatives of seaweed. They are activated by wound exudate to produce a hydrophilic gel. Like hydrocolloids, alginates absorb the noncellular components of the exudate. Alginates provide a satisfactory dressing for lightly contaminated wounds and cavities. They are generally unsatisfactory in the presence of dry, necrotic tissue as there is no exudate to activate them. As alginates are not adhesive, they are easily removed by lavage, but must be held in place by another dressing. Depending on the amount of exudate, alginates can be changed twice a week.
| Table 1 | |
| Dressings | |
| Wound assessment | Suitable dressing |
| Superficial partial thickness | Adhesive film |
| Mild to moderate exudate | Hydrocolloid |
| Contaminated, moderate to Heavy exudate | Alginate |
| Heavy exudate | Foam |
| Dry necrotic | Hydrogel |
Hydrogels
These gels include Intrasite and are based on starch polyme rs. They provide moisture to the wound and encourage debridement. Hydrogels are best suited to dry necrotic wounds, but they also absorb exudate while maintaining the products of tissue repair and degradation, including growth factors and lysosomes, in contact with the wound. If the wound is clean, the gel only needs to be replaced once or twice a week. Daily dressings may be needed if the wound is necrotic or infected.
Foams
Dressings such as Lyofoam and Alleryn are highly absorbent synthetic foams. Currently, their main applications are to absorb large volumes of exudate from discharging wounds, reducing the need for dressing changes. They can be used in combination with a hydrogel for necrotic wounds which require debriding.
Conclusion
Definitive protocols for these dressings have not yet developed. Currently, adhesive films are used for superficial wounds with hydrocolloids being used for shallow ulcers and alginates for the deep cavities. Foams are used as an adjunct for heavily exudative wounds. Hydrogels are used increasingly in the debridement of dry or necrotic ulcers, particularly when used with an adhesive film to retain the gel at the wound surface.
Straightforward surgical and traumatic wounds require simple, lowcost dressings since healing is likely to be rapid and uncomplicated. Dressing choices for complicated wounds reflect a growing understanding of wound healing physiology. However, comparison of dressings continues to be largely anecdotal and management protocols are still evolving. Choices of dressings increasingly represent a cost/benefit analysis where the high cost of the latest dressing is balanced against savings in time and labour involved in dressing changes.
References
1. Majno G. The healing hand: man and wound in the ancient world. Cambridge, Massachusetts: Harvard University Press, 1991.
2. Cohen IK, Diegelmann RF, Lindblad WJ, editors. Wound healing: biochemical and clinical aspects. Philadelphia: W.B. Saunders, 1992.
3. Rowland J. Pressure ulcers: a literature review and a treatment scheme. Aust Fam Physician 1993;22:1819, 1822-7.
4. Heggers JP, Robson MC, editors. Quantitative bacteriology: its role in the armamentarium of the surgeon. Boca Raton: CRC Press, 1991.
5. Ryan TJ, editor. An environment for healing: the role of occlusion. London: Royal Society of Medicine, 1985.
6. Local applications to wounds - I. Cleansers, antibacterials, debriders. Drug Ther Bull 1991;29:93-5.
7. Local applications to wounds - II. Dressings for wounds and ulcers. Drug Ther Bull 1991;29:97-100.
8. Heggers JP, Sazy JA, Stenberg BD, Strock LL, McCauley RL, Herndon DN, et al. Bactericidal and wound-healing properties of sodium hypochlorite solutions: the 1991 Lindberg Award. J Burn Care Rehabil 1991;12:420-4.
Subscribe to:
Posts (Atom)