A birthmark is a colored mark on or under the skin that’s present at birth or develops shortly after birth.Some birthmarks fade with time; others become more pronounced. Birthmarks may be caused by extra pigment in the skin or by blood vessels that do not grow normally. Most birthmarks are painless and harmless. In rare cases, they can cause complications or are associated with other conditions. All birthmarks should be checked by a doctor.
See the slideshow here: http://www.medicinenet.com/birthmarks_pictures_slideshow/article.htm
Former Soviet President Mikhail Gorbachev has a port wine stain.
Salmon patches are nests of blood vessels that appear as small, pink, flat marks on the skin. They occur in 1/3 of newborn babies. Salmon patches can appear on the back of the neck (“stork bite”), between the eyes (“angel’s kiss”), or on the forehead, nose, upper lip, or eyelids. Some fade as baby grows, but patches on the back of the neck usually don’t go away. Salmon patches require no treatment.
Port Wine Stains
A port wine stain begins as a flat, pinkish-red mark at birth and gradually becomes darker and reddish-purple with age. Most will get bigger and thicker, too. Port wine stains are caused by dilated blood capillaries. Those on the eyelid may increase the risk of glaucoma. Port wine stains may be a sign of other disorders, but usually not. Treatment includes laser therapy, skin grafts, and masking makeup.
Mongolian spots are flat, smooth marks that are present from birth. Frequently found on the buttocks or lower back, they’re typically blue, but can also be bluish gray, bluish black, or brown. They may resemble a bruise. Mongolian spots are most common on darker-skinned babies. They usually fade by school age, but may never disappear entirely. No treatment is required.
Cafe-au-lait spots are smooth and oval and range in color from light to medium brown, which is how they got their name, “coffee with milk” in French. They’re typically found on the torso, buttocks, and legs. Cafe-au-lait spots may get bigger and darker with age, but are generally not considered a problem. However, having several spots larger than a quarter is linked with neurofibromatosis and the rare McCune-Albright syndrome. Consult a doctor if your child has several spots.
Hemangiomas are a collection of small, closely packed blood vessels. Strawberry hemangiomas occur on the surface of the skin, usually on the face, scalp, back, or chest. They may be red or purple; they can be flat or slightly raised, with sharp borders. Strawberry hemangiomas usually develop a few weeks after birth. They grow rapidly through the first year before subsiding around age 9. Some slight discoloration or puckering of the skin may remain at the site. No treatment is required, but when desired, medicines and laser therapy are effective.
Present at birth, deeper cavernous hemangiomas are just under the skin and appear as a bluish spongy mass of tissue filled with blood. If they’re deep enough, the overlying skin may look normal. Cavernous hemangiomas typically appear on the head or neck. Most disappear by puberty. A combination of cavernous and strawberry hemangioma can occur.
Venous malformations are caused by abnormally formed, dilated veins. Although present at birth, they may not become apparent until later in childhood or adulthood. Venous malformations appear in 1% to 4% of babies. They are often found on the jaw, cheek, tongue, and lips. They may also appear on the limbs, trunk and internal organs, including the brain. They will continue to grow slowly, and they don’t shrink with time. Treatment — often sclerotherapy or surgery — may be necessary for pain or impaired function.
Pigmented Nevi (Moles)
Moles occur when cells in the skin grow in a cluster instead of being spread throughout the skin. They can appear anywhere on the body, alone or in groups. Moles are usually flesh-colored, brown, or black. Moles may darken with sun exposure and during pregnancy. They tend to lose color during adulthood and may disappear in old age. Most moles are not cause for alarm. However, moles may have a slightly increased risk of becoming skin cancer. Moles should be checked by a doctor if:
* They change size or shape
* They look diffrent from other moles
* They appear after age 20
Actress Eva Mendes sports a “beauty mark” on her check.
Congenital nevi are moles that appear at birth. The skin texture may range from normal to raised, or nodular to irregular. Congenital
nevi can grow anywhere on the body and vary in size –from a small 1-inch mark to a giant birthmark covering half of the body or more. Small congenital nevi occur in 1% of newborns. Most moles are not dangerous. But congenital nevi, especially large ones, should always be evaluated by a doctor since they may have an increased risk of becoming skin cancer.
Dysplastic Nevi (Atypical Moles)
Atypical moles are generally larger (one-quarter inch across or more) than ordinary moles and have irregular and indistinct borders. They may resemble cancerous moles. They may have a mix of colors including pink, red, tan and brown.These moles tend to be hereditary. Atypical moles have an increased chance of developing into melanoma skin cancer. Have a doctor evaluate all moles that look unusual, grow larger, or change in any way.
Our skin is host to a number of bacteria, most of which are beneficial. Including the friendly flora in our gut, more than 200 species of bacteria reside within the tissues exposed to the external environment. Skin infections result from these bacteria when the integrity of the skin breaks down or when the immune defense system is weak.
Skin infections can occur on the skin surface or deeper within the skin tissue. The most common bacteria that infect the skin are Staphylococcus aureus and Streptococcus pyogenes. Read more about bacterial infections on www.skincareguide.ca/conditions/bacterial_infections
TYPES OF BACTERIAL INFECTIONS:
Impetigo and Ecthyma
Impetigo begins with a redness of the skin and progresses to blisters that fill with fluid and itch, and then produce honey-colored crusts. Lesions usually form around the nose and face. Ecthyma is a deeper version of impetigo that usually forms on the legs. It causes large boils, crusts, and deep sores that leave scars.
Folliculitis is an infection of the hair follicles. It produces pimplelike skin bumps and small blisters with pus. Folliculitis occurs on the face, upper trunk, arms, and buttocks. When the infection goes deeper, feels tender, and produces more pus, it is furunculosis. Carbuncles are furuncles that have fused.
An abscess is a deep infection that appears like a closed blister or an open hole with pus. It is usually tender and becomes sore and painful as the infection progresses.
Erysipelas and Cellulitis
Erysipelas is a superficial infection that tends to occur in young children and the elderly. It is also seen in those who have chronic swelling of the limbs, are addicted to alcohol, have diabetes mellitus, or have experienced trauma. Erysipelas mostly occurs on the face or legs. A fever occurs abruptly, the cheeks become red, and the skin feels hot, tense, and swollen. Cellulitis is a deeper form of this infection.
Bacterial skin infections are treated according to their severity. Your physician may incise and drain deeper infections and abscesses, and recommend that you apply warm compresses. Creams such as Fucidin® or Bactroban® are prescribed for mild stages of:
If the infection is more extensive, oral antibiotics such as Cloxacillin or Cephalexin are used as well as those in the erythromycin family. Penicillin is often used to treat for strep.
Antibiotic resistance is an increasing problem so it is best to have early adequate proper treatment to minimize risk of exposure to antibiotics and lower the risk of transmission to others.
During treatment, remember to wash your hands daily with an antibacterial solution such as Trisan®, Tersaseptic® or Hibitane®, or use a product like Safe4Hours® (www.invisicare.com) which kills bacteria for four hours. Hand washing is the most important thing you can do to minimize the spread of infection.
If you suspect a bacterial skin infection, see your doctor before it becomes severe. Due to the increase of bacterial resistance to drugs in general, it is important to take the full course of your prescribed medicines.
Milia are very common, benign, keratin-filled cysts. Primary milia are typically seen in infants but also may occur in children and adults. Secondary milia are observed in a number of blistering disorders and following dermabrasion. Milia en plaque and multiple eruptive milia are distinct entities.
The eMedicine Pediatrics article Milia may be of interest, as may the Medscape Dermatologic Surgery Resource Center.
Pathophysiology: Milia are tiny epidermoid cysts. The cysts may be derived from the pilosebaceous follicle. Primary milia arise on facial skin bearing vellus hair follicles. Secondary milia result from damage to the pilosebaceous unit.
Frequency in the United States:
Primary milia in newborns are so common that they can be considered normal (occurring in approximately half of all infants). Multiple eruptive milia and milia en plaque are rare entities.
Race : No racial predilection is recognized.
Sex : Sexual prevalence is equal for primary and secondary milia. Eruptive milia and milia en plaque occur more frequently in women.
Age : Milia occur in persons of all ages but are typically found in infants.
Milia are asymptomatic. In children and adults, they usually arise around the eye. Eruptive milia, as the name suggests, have a rapid onset, often within a few weeks.
* Skin lesions
o Milia are superficial, uniform, pearly white to yellowish, domed lesions measuring 1-2 mm in diameter.
o In milia en plaque, multiple milia arise on an erythematous plaque.
* Skin distribution
o Primary milia, in term infants, occur on the face, especially the nose. They also may be found on the mucosa (Epstein pearls) and palate (Bohn nodules).
o Primary milia in older children and adults develop on the face, particularly around the eyes.
o Milia have been observed to occur in a transverse, linear distribution along the nasal groove in some children.
o Secondary milia are found anywhere on the body at the sites affected by the predisposing condition.
o Eruptive milia occur on the head, neck, and upper body.
o Milia en plaque manifests as distinct plaques on the head and neck. Plaques have been described in the postauricular area, unilaterally or bilaterally, the cheeks, the submandibular plaques, and on the pinna.
* Primary milia are believed to arise in sebaceous glands that are not fully developed, explaining the high prevalence in newborn infants.
* Secondary lesions arise following blistering or trauma due to disruption of the sweat ducts. Milia have been described in association with many disorders, including bullous pemphigoid, inherited and acquired epidermolysis bullosa, bullous lichen planus, porphyria cutanea tarda, and burns. Skin trauma from dermabrasion or radiotherapy can result in milia formation.
* Secondary milia have arisen from a bullous contact dermatitis and a photocontact allergy to sunscreen.
They have also arisen following treatment of cutaneous leishmaniasis and after topical nitrogen mustard ointment for plaque stage mycosis fungoides.
* Secondary milia have been described following potent topical corticosteroid use.
* Milia are a feature of a number of very rare genodermatoses (eg, Bazex-Dupré -Christol syndrome). Both primary milia and multiple eruptive milia have been reported as familial disorders with autosomal dominant inheritance.
* The etiology of milia en plaque is unknown.
No topical or systemic medications are effective on primary and secondary milia. Single case reports have demonstrated the success of topical isotretinoin, oral etretinate and minocycline in treating patients with milia en plaque.
Milia can be safely left alone, but if the patient requests treatment, then incision with a cutting-edge needle and manual expression of the contents are effective. This can be performed without local anesthetic. A paper clip has been successfully used to express the contents of the cyst. Milia en plaque has been treated effectively with electrodesiccation, carbon dioxide laser, dermabrasion, and cryosurgery.
Milia, also known as milk spots or oil seeds, are benign, keratin-filled cysts that can appear just under the epidermis or on the roof of the mouth. They are commonly associated with newborn babies but can appear on people of all ages. They are usually found around the nose and eyes, and sometimes on the genitalia, often mistaken by those infected as warts or other STDs.
In children milia often disappears within two to four weeks. In adults it may require removal by a physician or an esthetician. Milia can sometimes be a result of harsh face washes or from repeated heat stress from hot showering on people with sensitive skins. Milia can be confused with stubborn whiteheads.
A seborrheic keratosis (also known as “Seborrheic verruca,” “Senile keratosis,” and “Senile wart”) is a noncancerous benign skin growth that originates in keratinocytes. Like liver spots, seborrheic keratoses are seen more often as people age. In fact they are sometimes humorously referred to as the “barnacles of old age”.
They appear in various colors, from light tan to black. They are round or oval, feel flat or slightly elevated (like the scab from a healing wound), and range in size from very small to more than 2.5 centimetres (1.0 in) across. They can resemble warts, though they have no viral origins. They can also resemble melanoma skin cancer, though they are unrelated to melanoma as well. Because only the top layers of the epidermis are involved, seborrheic keratoses are often described as having a “pasted on” appearance. Some dermatologists refer to seborrheic keratoses as “seborrheic warts”, however these lesions are usually not associated with HPV, and therefore such nomenclature should be discouraged.
Seborrheic keratoses may be divided into the following types:
* Common seborrheic keratosis (Basal cell papilloma, Solid seborrheic keratosis)
* Reticulated seborrheic keratosis (Adenoid seborrheic keratosis)
Reticulated seborrheic keratosis (also known as “Adenoid seborrheic keratosis”) is a common benign cutaneous condition characterized by a skin lesion with a dull or lackluster surface, and with keratin cysts seen histologically.
* Stucco keratosis (Digitate seborrheic keratosis, Hyperkeratotic seborrheic keratosis, Serrated seborrheic keratosis, Verrucous seborrheic
keratosis) Stucco keratosis (also known as “Digitate seborrheic keratosis,” “Hyperkeratotic seborrheic keratosis,” “Serrated seborrheic keratosis,” and “Verrucous seborrheic keratosis”) is a common benign cutaneous condition characterized by a skin lesion with a dull or lackluster surface, and with church-spire-like projections of epidermal cells around collagen seen histologically.
* Clonal seborrheic keratosis
Clonal seborrheic keratosis is a common benign cutaneous condition characterized by a skin lesion with a dull or lackluster surface, and with round, loosely packed nests of cells seen histologically.
* Irritated seborrheic keratosis (Basosquamous cell acanthoma, Inflamed seborrheic keratosis)
* Seborrheic keratosis with squamous atypia
Seborrheic keratosis with squamous atypia is a less common cutaneous condition characterized by a skin lesion with a dull or lackluster surface, and with round, loosely packed nests of cells seen histologically.
* Melanoacanthoma (Pigmented seborrheic keratosis)
Melanoacanthoma (also known as “Pigmented seborrheic keratosis”) is a common, benign, darkly pigmented cutaneous condition characterized by a skin lesion with a dull or lackluster surface.
* Dermatosis papulosa nigra
Dermatosis papulosa nigra (DPN) is a condition of many small, benign skin lesions on that face that closely simulate seborrheic keratoses, a condition generally presenting on dark-skinned individuals.
They should not be confused for Leser-Trélat sign, a sudden explosion of lesions due to a growing tumor.
* The sign of Leser-Trélat
The Leser-Trélat sign is the explosive onset of multiple seborrheic keratoses (many pigmented skin lesions), often with an inflammatory base. This can be an ominous sign of internal malignancy as part of a paraneoplastic syndrome. In addition to the development of new lesions, preexisting ones frequently increase in size and become symptomatic. It is named for Edmund Leser and Ulysse Trélat.
Although most associated neoplasms are gastrointestinal adenocarcinomas (stomach, liver, colorectal and pancreas), breast, lung, and urinary tract cancers, as well as lymphoid malignancies are associated with this impressive rash. It is likely that various cytokines and other growth factors produced by the neoplasm are responsible for the abrupt appearance of the seborrheic keratoses. In some cases, paraneoplastic acanthosis nigricans accompanies the sign of Leser-Trélat.
Variances of Seborrheic Keratosis:
Dermatosis Papulosis Nigra: Often are small papules. Pinpoint to a few millimeters in size. More commonly found in dark-skinned persons.
Stucco Keratosis: Often are light brown to off-white. Pinpoint to a few millimeters in size. Often found on the distal tibia, ankle, and foot.
Diagnosis: Visual diagnosis is made by the “stuck on” appearance, horny pearls or cysts embedded in the structure. Darkly pigmented lesions can be hard to distinguish from nodular melanomas. If in doubt, a skin biopsy should be performed. Thin seborrheic keratoses on facial skin can be very difficult to differentiate from lentigo maligna even with dermatoscopy.
Clinically, epidermal nevi are similar to seborrheic keratoses in appearance. Epidermal nevi are usually present at or near birth. Condylomas and warts can clinically resemble seborrheic keratoses, and dermatoscopy can be helpful. On the penis and genital skin, differentiation between condylomas and seborrheic keratoses can be difficult and may require a skin biopsy.
When correctly diagnosed, no treatment is necessary. There is a small risk of localized infection caused by picking at the lesion. If a growth becomes excessively itchy or is irritated by clothing or jewelry, it can be removed by cryosurgery.
Small lesions can be treated with light electrocautery. Larger lesions can be treated with electrodessication and curettage, shave excision, or cryotherapy. When correctly performed, removal of seborrheic keratoses will not cause much visible scarring except in darkly colored persons.
The cause of seborrheic keratosis is unclear. Because they are common on sun-exposed areas such as the back, arms, face, and neck, ultraviolet light
may play a role, as may genetics. A mutation of a gene coding for a growth factor receptor, (FGFR3), has been associated with seborrheic keratosis.
The term “seborrheic keratosis” combines the adjective form of seborrhea, keratinocyte (referring to the part of the epidermis that produces keratin), and the suffix -osis, meaning abnormal.
Staph Wound Infections and Methicillin Resistant Staphylococcus aureus
Staphylococcus aureus, also called S. aureus or “staph,” is a bacterium that frequently colonizes the human skin and is present in the nose of about 25-30% of U.S. adults. S. aureus can exist in this form without harming its host or causing symptoms. However, if there is a break in the patient’s skin from a wound or surgery, or if there is a depression in the person’s immune system, then colonizing S. aureus can cause an infection. Staph frequently causes localized skin infections, such as folliculitis, furuncles, and impetigo. It can also cause abscesses and spread into the bones (osteomyelitis), lungs (staphylococcal pneumonia), blood (bacteremia or sepsis), heart (endocarditis – which can damage the heart valves), and other organs. Staph may also infect others as it can be passed from both infected and colonized people to other people through skin contact or through sharing contaminated objects, such as towels or razors.
Staph infections acquired while a patient is in a hospital, long-term care facility, or other health care setting have been a challenge for many years. The confined population and the widespread use of antibiotics have led to the development of antibiotic-resistant strains of S. aureus. These strains are called methicillin resistant staphylococcus aureus (MRSA), named after the antibiotic treatment that was developed in 1960 to treat penicillin-resistant strains. Infections caused by MRSA are frequently resistant to a wide variety of antibiotics and are associated with ignificantly higher rates of morbidity and mortality, higher health care costs, and longer hospital stays than infections caused by methicillin susceptible S. aureus. Risk factors for MRSA infection in the hospital include surgery, prior antibiotic therapy, admission to intensive care, exposure to a MRSA-colonized patient or health care worker, being in the hospital more than 48 hours, and having an indwelling catheter or other medical device that goes through the skin.
One strategy that may be used in an effort to control the spread of infection includes active surveillance for the detection of MRSA in patients admitted to intensive care units (ICUs) and other high risk areas. Another approach is to screen all patients admitted to a health care facility. Community-acquired infections
MRSA infections have increased in importance in the community in recent years because they have been associated with a growing number of outbreaks and deaths in non-medical settings where individuals are in close contact such as prisons, day care facilities, military units, and contact sports. These infections are occurring in people who do not have classic MRSA risk factors as described above. A significant number of those affected have had to be hospitalized for what appears to be a simple but persistent skin infection or for pneumonia that develops after a bout of influenza.
Until recently, part of the problem with community-acquired MRSA (CA-MRSA) has been a lack of awareness in the medical community and the community at large. Historically, physicians have treated staph infections, based on their severity, with either over-the-counter triple-antibiotic ointments or with a standard course of antibiotics. They did not routinely order cultures to identify the organism and its antibiotic susceptibility profile unless the infection appeared extensive or the initial treatment was unsuccessful. With CA-MRSA, however, these conventional therapy options have frequently failed. A significant number of those affected have been hospitalized and a few previously healthy patients have died.
Investigations of these outbreaks have revealed that the CA-MRSA was spread from infected or colonized patients to those around them through skin contact (such as sports-related cuts and abrasions), through droplets from the respiratory tract, or through exposure to contaminated objects, such as shared sports equipment, towels, toys, or playground equipment. Investigations have also revealed that the S. aureus strains involved in CA-MRSA are genetically distinct from those that have been causing hospital-acquired MRSA. The CA-MRSA are resistant to methicillin and related antibiotics (oxacillin, dicloxacillin, nafcillin) and erythromycin but remain susceptible to many other antibiotics.
The purpose of culturing wound infections is to identify the bacteria causing the infection and to determine the susceptibility of the microorganism to available antibiotics. If an infection is due to MRSA, it should be investigated to determine the source of the infection. This is especially important in CA-MRSA to prevent further cases from occurring.
The primary laboratory tests performed are:
* Cultures of the affected areas. Fluid or pus from a wound, sputum, blood, joint fluid, or even breast milk (in the case of an infected breast) is collected and spread onto a thin layer of nutrient gel and/or grown in a nutrient broth. Sometimes, multiple samples are collected to evaluate different body sites or to attempt to detect bacteria that may be present in small numbers.
* Nasal cultures (collected by inserting a swab inside the nose) used to screen healthy people may also be ordered to determine whether someone has been colonized with MRSA and is a carrier. The cultured samples are incubated and examined for the growth of characteristic S. aureus colonies. If they are present, susceptibility testing is performed to determine whether the strain is MRSA.
* Nasal swabs may be collected to detect MRSA colonization based on rapid molecular tests, which do not grow the bacteria but detect their presence and antibiotic resistance by detecting the genes responsible for the methicillin resistance.
Identifying MRSA can sometimes be challenging. The population of staph that a person has tends to be mixed. This means that even if a patient has CA-MRSA or hospital-acquired MRSA, not all of the staph present will be equally resistant. Since resistant strains may grow more slowly than susceptible strains, there is the potential for missing them.
A variety of methods may be used to track different strains of MRSA. These are used in the investigation of the spread of MRSA within a community or region but are not used in the treatment of an individual patient.