Acne conglobata is an extremely severe form of acne where acne nodules come together and create sinuses. Acne fulminans, on the other hand, is a rare and severe complication of acne conglobata that is accompanied by systemic symptoms. It is linked to elevated levels of androgenic hormones, specific autoimmune conditions, and a genetic predisposition.

The typical clinical characteristics of acne fulminans are as follows:

– Sudden and abrupt onset
– Inflammatory and ulcerated nodular acne primarily found on the chest and back
– Often painful lesions
– Ulcers on the upper trunk covered with bleeding crusts
– Severe acne scarring
– Fluctuating fever
– Painful joints and arthropathy
– General feeling of illness (malaise)
– Loss of appetite and weight loss
– Enlarged liver and spleen (hepatosplenomegaly)

It is crucial to refer patients immediately for a specialist evaluation and hospital admission. Treatment options for acne fulminans include systemic corticosteroids, dapsone, ciclosporin, and high-dose intravenous antibiotics.

Chickenpox is a highly contagious illness caused by the varicella-zoster virus, a DNA virus from the Herpesviridae family. Most cases are mild to moderate, and the infection usually resolves on its own. Severe complications are rare but can occur, especially in individuals with weakened immune systems or underlying health conditions.

The incubation period for chickenpox is typically between 14 to 21 days. It is contagious from a few days before the rash appears until about a week after the first lesions show up.

The common clinical features of chickenpox include:

– Fever, which lasts for approximately 3-5 days.
– The initial rash starts as flat red spots and progresses into raised bumps.
– These bumps then turn into fluid-filled blisters and eventually form pustules surrounded by redness.
– The lesions are extremely itchy.
– The rash reaches its peak around 48 hours in individuals with a healthy immune system.
– The rash tends to be more concentrated on the face and trunk, with fewer lesions on the limbs.
– The blisters eventually dry up and form crusts, which can lead to scarring if scratched.
– Headache, fatigue, and abdominal pain may also occur.

Chickenpox tends to be more severe in teenagers and adults compared to children. Antiviral treatment should be considered for these individuals if they seek medical attention within 24 hours of rash onset. The recommended oral dose of aciclovir is 800 mg taken five times a day for seven days.

Immunocompromised patients and those at higher risk, such as individuals with severe cardiovascular or respiratory disease or chronic skin disorders, should receive antiviral treatment for ten days, with at least seven days of intravenous administration.

Although most cases are relatively mild, if serious complications like pneumonia, encephalitis, or dehydration are suspected, it is important to refer the patient for hospital admission.

For more information, you can refer to the NICE Clinical Knowledge Summary on Chickenpox.
https://cks.nice.org.uk/topics/chickenpox/

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

Fifth disease, also known as ‘slapped cheek syndrome’, is a common childhood exanthem caused by parvovirus B19.

The clinical features of fifth disease include:

– A mild coryzal illness usually occurs as a prodrome.
– The classic ‘slapped cheek’ rash appears after 3-7 days, characterized by a red rash on the cheeks with pale skin around the mouth.
– A morbilliform rash develops on the extensor surfaces of the arms and legs 1-4 days after the facial rash appears.

This disease is generally harmless and resolves on its own in children. However, it can be dangerous for pregnant women who are exposed to the virus, as it can cause intrauterine infection and hydrops fetalis. Additionally, it can lead to transient aplastic crisis. Therefore, it is important to keep affected children away from pregnant women and individuals with weakened immune systems or blood disorders.

Pityriasis versicolor, also known as tinea versicolor, is a common skin condition caused by an infection with the yeasts Malassezia furfur and Malassezia globosa. It typically presents as multiple patches of altered pigmentation, primarily on the trunk. In individuals with fair skin, these patches are usually darker in color, while in those with darker skin or a tan, they may appear lighter (known as pityriasis versicolor alba). It is not uncommon for the rash to cause itching.

The recommended treatment for pityriasis versicolor involves the use of antifungal agents. One particularly effective option is ketoconazole shampoo, which is sold under the brand name Nizoral. To use this shampoo, it should be applied to the affected areas and left on for approximately five minutes before being rinsed off. This process should be repeated daily for a total of five days.

Methicillin-resistant Staphylococcus aureus (MRSA) has become a significant issue in hospitals and other healthcare facilities in recent years. MRSA refers to any strain of Staphylococcus aureus that has developed resistance to beta-lactam antibiotics, such as penicillins and cephalosporins. This resistance is caused by the presence of the mecA gene, which produces a penicillin-binding protein with low affinity. Fortunately, MRSA is typically susceptible to teicoplanin, vancomycin, daptomycin, and linezolid. On the other hand, imipenem is an intravenous beta-lactam antibiotic that belongs to the carbapenem subgroup.

Shingles is caused by the varicella-zoster virus (VZV), which primarily infects individuals during childhood as chickenpox. However, the initial infection can also be subclinical. After the primary infection, the virus remains dormant in the sensory nervous system, specifically in the geniculate, trigeminal, or dorsal root ganglia.

During the dormant phase, the virus is kept under control by the immune system for many years. However, it can later become active and cause a flare-up in a specific dermatomal segment. This reactivation occurs when the virus travels down the affected nerve over a period of 3 to 5 days, leading to inflammation within and around the nerve. The decline in cell-mediated immunity is believed to trigger the virus’s reactivation.

Several factors can trigger the reactivation of the varicella-zoster virus, including advancing age (with most patients being older than 50), immunosuppressive illnesses, physical trauma, and psychological stress. In immunocompetent patients, the most common site of reactivation is the thoracic nerves, followed by the ophthalmic division of the trigeminal nerve.

Diagnosing shingles can usually be done based on the patient’s history and clinical examination alone, as it has a distinct history and appearance. While various techniques can be used to detect the virus or antibodies, they are often unnecessary. Microscopy and culture tests using scrapings and smears typically yield negative results.

Cellulitis is a common cause of swelling in one leg. It is characterized by red, hot, tender, and swollen skin, usually affecting the shin on one side. Other symptoms may include fever, fatigue, and chills. It is important to consider deep vein thrombosis (DVT) as a possible alternative diagnosis, as it can be associated with cellulitis or vice versa. Unlike cellulitis, DVT does not typically cause fever and affects the entire limb below the blood clot, resulting in swelling in the calf, ankle, and foot. Necrotizing fasciitis is a rare condition. Gout primarily affects the joints of the foot, particularly the first metatarsophalangeal joint. Erythema migrans usually produces a distinct target-shaped rash.

Further Reading:

Cellulitis is an inflammation of the skin and subcutaneous tissues caused by an infection, usually by Streptococcus pyogenes or Staphylococcus aureus. It commonly occurs on the shins and is characterized by symptoms such as erythema, pain, swelling, and heat. In some cases, there may also be systemic symptoms like fever and malaise.

The NICE Clinical Knowledge Summaries recommend using the Eron classification to determine the appropriate management of cellulitis. Class I cellulitis refers to cases without signs of systemic toxicity or uncontrolled comorbidities. Class II cellulitis involves either systemic illness or the presence of a co-morbidity that may complicate or delay the resolution of the infection. Class III cellulitis is characterized by significant systemic upset or limb-threatening infection due to vascular compromise. Class IV cellulitis involves sepsis syndrome or a severe life-threatening infection like necrotizing fasciitis.

According to the guidelines, patients with Eron Class III or Class IV cellulitis should be admitted for intravenous antibiotics. This also applies to patients with severe or rapidly deteriorating cellulitis, very young or frail individuals, immunocompromised patients, those with significant lymphedema, and those with facial or periorbital cellulitis (unless very mild). Patients with Eron Class II cellulitis may not require admission if the necessary facilities and expertise are available in the community to administer intravenous antibiotics and monitor the patient.

The recommended first-line treatment for mild to moderate cellulitis is flucloxacillin. For patients allergic to penicillin, clarithromycin or clindamycin is recommended. In cases where patients have failed to respond to flucloxacillin, local protocols may suggest the use of oral clindamycin. Severe cellulitis should be treated with intravenous benzylpenicillin and flucloxacillin.

Overall, the management of cellulitis depends on the severity of the infection and the presence of any systemic symptoms or complications. Prompt treatment with appropriate antibiotics is crucial to prevent further complications and promote healing.

Reperfusion after a frostbite injury can be extremely painful, so it is important to provide strong pain relief. If there are clear blisters, they should be opened and aloe vera should be applied every 6 hours. However, if there are blisters with blood, they should not be opened, but aloe vera can still be used topically. Taking 400 mg of ibuprofen orally, if there are no contraindications, can help reduce inflammation and improve the outcome of frostbite. Technetium-99m pertechnetate scintigraphy is the preferred method for assessing blood flow in the affected area. To treat frostbite, it is recommended to re-warm the affected areas by immersing them in warm water.

Further Reading:

Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, the basal metabolic rate decreases and cell signaling between neurons decreases, leading to reduced tissue perfusion. This can result in decreased myocardial contractility, vasoconstriction, ventilation-perfusion mismatch, and increased blood viscosity. Symptoms of hypothermia progress as the core temperature drops, starting with compensatory increases in heart rate and shivering, and eventually leading to bradyarrhythmias, prolonged PR, QRS, and QT intervals, and cardiac arrest.

In the management of hypothermic cardiac arrest, ALS should be initiated with some modifications. The pulse check during CPR should be prolonged to 1 minute due to difficulty in obtaining a pulse. Rewarming the patient is important, and mechanical ventilation may be necessary due to stiffness of the chest wall. Drug metabolism is slowed in hypothermic patients, so dosing of drugs should be adjusted or withheld. Electrolyte disturbances are common in hypothermic patients and should be corrected.

Frostbite refers to a freezing injury to human tissue and occurs when tissue temperature drops below 0ºC. It can be classified as superficial or deep, with superficial frostbite affecting the skin and subcutaneous tissues, and deep frostbite affecting bones, joints, and tendons. Frostbite can be classified from 1st to 4th degree based on the severity of the injury. Risk factors for frostbite include environmental factors such as cold weather exposure and medical factors such as peripheral vascular disease and diabetes.

Signs and symptoms of frostbite include skin changes, cold sensation or firmness to the affected area, stinging, burning, or numbness, clumsiness of the affected extremity, and excessive sweating, hyperemia, and tissue gangrene. Frostbite is diagnosed clinically and imaging may be used in some cases to assess perfusion or visualize occluded vessels. Management involves moving the patient to a warm environment, removing wet clothing, and rapidly rewarming the affected tissue. Analgesia should be given as reperfusion is painful, and blisters should be de-roofed and aloe vera applied. Compartment syndrome is a risk and should be monitored for. Severe cases may require surgical debridement of amputation.

The scalp is composed of five layers, starting from the outermost layer, which is the skin, and moving towards the deepest layer, which is the periosteum of the skull. These layers can be remembered using the mnemonic: SCALP – Skin, Connective tissue, Aponeurosis, Loose areolar connective tissue, and Periosteum.

Further Reading:

The scalp is the area of the head that is bordered by the face in the front and the neck on the sides and back. It consists of several layers, including the skin, connective tissue, aponeurosis, loose connective tissue, and periosteum of the skull. These layers provide protection and support to the underlying structures of the head.

The blood supply to the scalp primarily comes from branches of the external carotid artery and the ophthalmic artery, which is a branch of the internal carotid artery. These arteries provide oxygen and nutrients to the scalp tissues.

The scalp also has a complex venous drainage system, which is divided into superficial and deep networks. The superficial veins correspond to the arterial branches and are responsible for draining blood from the scalp. The deep venous network is drained by the pterygoid venous plexus.

In terms of innervation, the scalp receives sensory input from branches of the trigeminal nerve and the cervical nerves. These nerves transmit sensory information from the scalp to the brain, allowing us to perceive touch, pain, and temperature in this area.

Systemic lupus erythematosus (SLE) is a connective tissue disorder that affects multiple systems in the body. It is characterized by skin rashes, joint pain, and the presence of antibodies against double-stranded DNA. SLE is more commonly seen in young women, with a ratio of 10 females to 1 male. It is also more prevalent in West Indian populations.

One of the classic signs of SLE is the presence of a butterfly rash. This rash appears as redness over the bridge of the nose and cheeks. It is often worsened by exposure to sunlight and can occur before other symptoms of SLE develop.

Joint involvement is common in SLE and can affect both large and small joints. The knee, proximal interphalangeal, wrist, and metacarpophalangeal joints are most frequently affected.

Chickenpox is a highly contagious illness caused by the varicella-zoster virus, a DNA virus from the Herpesviridae family. Most cases are mild to moderate, and the infection usually resolves on its own. Severe complications are rare but can occur, especially in individuals with weakened immune systems or underlying health conditions.

The incubation period for chickenpox is typically between 14 to 21 days. It is contagious from a few days before the rash appears until about a week after the first lesions show up.

The common clinical features of chickenpox include:

– Fever, which lasts for approximately 3-5 days.
– The initial rash starts as flat red spots and progresses into raised bumps.
– These bumps then turn into fluid-filled blisters and eventually form pustules surrounded by redness.
– The lesions are extremely itchy.
– The rash reaches its peak around 48 hours in individuals with a healthy immune system.
– The rash tends to be more concentrated on the face and trunk, with fewer lesions on the limbs.
– The blisters eventually dry up and form crusts, which can lead to scarring if scratched.
– Headache, fatigue, and abdominal pain may also occur.

Chickenpox tends to be more severe in teenagers and adults compared to children. Antiviral treatment should be considered for these individuals if they seek medical attention within 24 hours of rash onset. The recommended oral dose of aciclovir is 800 mg taken five times a day for seven days.

Immunocompromised patients and those at higher risk, such as individuals with severe cardiovascular or respiratory disease or chronic skin disorders, should receive antiviral treatment for ten days, with at least seven days of intravenous administration.

Although most cases are relatively mild, if serious complications like pneumonia, encephalitis, or dehydration are suspected, it is important to refer the patient for hospital admission.

For more information, you can refer to the NICE Clinical Knowledge Summary on Chickenpox.
https://cks.nice.org.uk/topics/chickenpox/

Erythroderma is a condition characterized by widespread redness affecting more than 90% of the body surface. It is also known as exfoliative erythroderma due to the presence of skin exfoliation. Another term used to describe this condition is the red man syndrome.

The clinical features of exfoliative erythroderma include the rapid spread of redness to cover more than 90% of the body surface. Scaling of the skin occurs between days 2 and 6, leading to thickening of the skin. Despite the skin feeling hot, patients often experience a sensation of coldness. Keratoderma, which is the thickening of the skin on the palms and soles, may develop. Over time, erythema and scaling of the scalp can result in hair loss. The nails may become thickened, ridged, and even lost. Lymphadenopathy, or enlarged lymph nodes, is a common finding. In some cases, the patient’s overall health may be compromised.

Exfoliative erythroderma can be caused by various factors, including eczema (with atopic dermatitis being the most common underlying cause), psoriasis, lymphoma and leukemia (with cutaneous T-cell lymphoma and Hodgkin lymphoma being the most common malignant causes), certain drugs (more than 60 drugs have been implicated, with sulphonamides, isoniazid, penicillin, antimalarials, phenytoin, captopril, and cimetidine being the most commonly associated), idiopathic (unknown cause), and rare conditions such as pityriasis rubra pilaris and pemphigus foliaceus. Withdrawal of corticosteroids, underlying infections, hypocalcemia, and the use of strong coal tar preparations can also precipitate exfoliative erythroderma.

Potential complications of exfoliative erythroderma include dehydration, hypothermia, cardiac failure, overwhelming secondary infection, protein loss and edema, anemia (due to loss of iron, B12, and folate), and lymphadenopathy.

Management of exfoliative erythroderma should involve referring the patient to the medical on-call team and dermatology for admission. It is important to keep the patient warm and start intravenous fluids, such as warmed 0.9% saline. Applying generous amounts of emollients and wet dressings can help alleviate

Eczema herpeticum occurs when an individual with atopic eczema comes into contact with the herpes simplex virus. While some patients may only experience typical cold sores, others may develop a more extensive infection. This condition is often accompanied by systemic disturbance and can be quite painful. Administering antiviral treatment can help reduce the duration of the illness. In cases where the rash is widespread or there are concerns about eye complications, hospital admission may be necessary for intravenous antiviral therapy.

Dermovate (Clobetasol propionate) is a strong steroid used for treating skin conditions. It is important to continue using emollients alongside steroid treatment. If the flare-ups are not effectively controlled by steroids, Tacrolimus can be considered as a secondary treatment option.

Further Reading:

Eczema is a chronic inflammatory skin disease characterized by dry, itchy skin with eczematous lesions. It often follows a chronic relapsing course and can lead to chronic skin changes such as lichenification and pigment changes. The term eczema is often used interchangeably with dermatitis, but strictly speaking, dermatitis refers to inflammation of the skin while eczema refers to specific conditions where skin inflammation is a feature.

Atopic eczema, also known as atopic dermatitis, is the most common type of eczema. It is usually first diagnosed in young children, with 90% of cases diagnosed before the age of 5. However, it can affect individuals of any age. Symptoms often improve as patients progress into their teens and adulthood. Around 10-20% of children are affected by atopic eczema, but only 3% of adults experience symptoms.

The exact cause of atopic eczema is not fully understood, but it is believed to be multifactorial, with both genetic and environmental factors playing a role. Genetic defects in genes that aid in the functioning of the skin barrier have been identified, which may predispose individuals to breaks in the skin barrier and increased exposure to antigens. Environmental factors such as pollution, allergen exposure, climate, and others also contribute to the development of the disease.

Diagnosing atopic eczema involves assessing the presence of key clinical features, such as pruritus (itching), eczema/dermatitis in a pattern appropriate for age, early age of onset, and personal or family history of atopy. Various diagnostic criteria have been established to aid in the diagnosis, including those set out by the American Academy of Dermatology and the UK working party.

The severity of atopic eczema can vary, and treatment options depend on the severity. Mild cases may be managed with emollients (moisturizers) and mild potency topical corticosteroids. Moderate cases may require moderate potency topical corticosteroids, topical calcineurin inhibitors, and bandages. Severe cases may necessitate the use of potent topical corticosteroids, topical calcineurin inhibitors, bandages, phototherapy, and systemic therapy.

In addition to medical treatment, identifying and avoiding triggers is an important aspect of managing atopic eczema. Common triggers include irritants, contact allergens, certain foods, skin infections, inhalant triggers, stress and infection.

Toxic epidermal necrolysis is a severe and potentially life-threatening form of erythema multiforme. This condition leads to the detachment of the dermis from the lower layers of the skin. In some cases, it can result in death due to sepsis and failure of multiple organs.

Stevens-Johnson syndrome and toxic epidermal necrolysis are considered to be different stages of the same mucocutaneous disease, with toxic epidermal necrolysis being more severe. The degree of epidermal detachment is used to differentiate between the two conditions. In Stevens-Johnson syndrome, less than 10% of the body surface area is affected by epidermal detachment, while in toxic epidermal necrolysis, it is greater than 30%. An overlap syndrome occurs when the detachment is between 10-30% of the body surface area.

Certain medications can trigger Stevens-Johnson syndrome and toxic epidermal necrolysis. These include tetracyclines, penicillins, vancomycin, sulphonamides, NSAIDs, and barbiturates. It is important to be aware of these potential triggers and seek medical attention if any symptoms or signs of these conditions develop.

Second degree frostbite is characterized by tissue necrosis that affects both the epidermis and a variable depth of the dermis. However, there is still some healthy dermis present, which allows for regeneration and recovery of the skin. This type of frostbite is often referred to as partial thickness. Clinically, it is observed as the formation of blisters filled with clear or milky fluid on the surface of the skin, accompanied by redness and swelling.

Further Reading:

Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, the basal metabolic rate decreases and cell signaling between neurons decreases, leading to reduced tissue perfusion. This can result in decreased myocardial contractility, vasoconstriction, ventilation-perfusion mismatch, and increased blood viscosity. Symptoms of hypothermia progress as the core temperature drops, starting with compensatory increases in heart rate and shivering, and eventually leading to bradyarrhythmias, prolonged PR, QRS, and QT intervals, and cardiac arrest.

In the management of hypothermic cardiac arrest, ALS should be initiated with some modifications. The pulse check during CPR should be prolonged to 1 minute due to difficulty in obtaining a pulse. Rewarming the patient is important, and mechanical ventilation may be necessary due to stiffness of the chest wall. Drug metabolism is slowed in hypothermic patients, so dosing of drugs should be adjusted or withheld. Electrolyte disturbances are common in hypothermic patients and should be corrected.

Frostbite refers to a freezing injury to human tissue and occurs when tissue temperature drops below 0ºC. It can be classified as superficial or deep, with superficial frostbite affecting the skin and subcutaneous tissues, and deep frostbite affecting bones, joints, and tendons. Frostbite can be classified from 1st to 4th degree based on the severity of the injury. Risk factors for frostbite include environmental factors such as cold weather exposure and medical factors such as peripheral vascular disease and diabetes.

Signs and symptoms of frostbite include skin changes, cold sensation or firmness to the affected area, stinging, burning, or numbness, clumsiness of the affected extremity, and excessive sweating, hyperemia, and tissue gangrene. Frostbite is diagnosed clinically and imaging may be used in some cases to assess perfusion or visualize occluded vessels. Management involves moving the patient to a warm environment, removing wet clothing, and rapidly rewarming the affected tissue. Analgesia should be given as reperfusion is painful, and blisters should be de-roofed and aloe vera applied. Compartment syndrome is a risk and should be monitored for. Severe cases may require surgical debridement of amputation.

Technetium 99 (Tc-99) pertechnetate scintigraphy is the preferred imaging method for evaluating frostbite. This technique is highly accurate in detecting tissue damage and provides both sensitivity and specificity.

Further Reading:

Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, the basal metabolic rate decreases and cell signaling between neurons decreases, leading to reduced tissue perfusion. This can result in decreased myocardial contractility, vasoconstriction, ventilation-perfusion mismatch, and increased blood viscosity. Symptoms of hypothermia progress as the core temperature drops, starting with compensatory increases in heart rate and shivering, and eventually leading to bradyarrhythmias, prolonged PR, QRS, and QT intervals, and cardiac arrest.

In the management of hypothermic cardiac arrest, ALS should be initiated with some modifications. The pulse check during CPR should be prolonged to 1 minute due to difficulty in obtaining a pulse. Rewarming the patient is important, and mechanical ventilation may be necessary due to stiffness of the chest wall. Drug metabolism is slowed in hypothermic patients, so dosing of drugs should be adjusted or withheld. Electrolyte disturbances are common in hypothermic patients and should be corrected.

Frostbite refers to a freezing injury to human tissue and occurs when tissue temperature drops below 0ºC. It can be classified as superficial or deep, with superficial frostbite affecting the skin and subcutaneous tissues, and deep frostbite affecting bones, joints, and tendons. Frostbite can be classified from 1st to 4th degree based on the severity of the injury. Risk factors for frostbite include environmental factors such as cold weather exposure and medical factors such as peripheral vascular disease and diabetes.

Signs and symptoms of frostbite include skin changes, cold sensation or firmness to the affected area, stinging, burning, or numbness, clumsiness of the affected extremity, and excessive sweating, hyperemia, and tissue gangrene. Frostbite is diagnosed clinically and imaging may be used in some cases to assess perfusion or visualize occluded vessels. Management involves moving the patient to a warm environment, removing wet clothing, and rapidly rewarming the affected tissue. Analgesia should be given as reperfusion is painful, and blisters should be de-roofed and aloe vera applied. Compartment syndrome is a risk and should be monitored for. Severe cases may require surgical debridement of amputation.

Onchocerciasis is a parasitic disease caused by the filarial nematode Onchocerca volvulus. It is transmitted through the bites of infected blackflies of Simulium species, which carry immature larval forms of the parasite from human to human.

In the human body, the larvae form nodules in the subcutaneous tissue, where they mature to adult worms. After mating, the female adult worm can release up to 1000 microfilariae a day.

Onchocerciasis is currently endemic in 30 African countries, Yemen, and a few isolated regions of South America. Approximately 37 million people worldwide are currently infected.

Symptoms start to occur around a year after the patient is infected. The earliest symptom is usually an intensely itchy rash. Various skin manifestations occur, including scattered, red, pruritic papules (acute papular onchodermatitis), larger, chronic, hyperpigmented papules (chronic papular onchodermatitis), lichenified, oedematous, hyperpigmented papules and plaques (lichenified onchodermatitis), areas of skin atrophy with loss of elasticity (‘Lizard skin’), and depigmented areas with a ‘leopard skin appearance, usually on shins.

Ocular involvement provides the common name associated with onchocerciasis, river blindness, and it can involve any part of the eye. Almost a million people worldwide have at least a partial degree of vision loss caused by onchocerciasis. Initially, there may be intense watering, foreign body sensation, and photophobia. This can progress to conjunctivitis, iridocyclitis, and chorioretinitis. Secondary glaucoma and optic atrophy may also occur.

In a number of countries, onchocerciasis has been controlled through spraying of blackfly breeding sites with insecticide. The drug ivermectin is the preferred treatment for onchocerciasis.

A non-blanching rash in a child should always raise suspicion of meningococcal septicaemia, especially if the child appears unwell, has purpura lesions larger than 2 mm in diameter, a capillary refill time of more than 3 seconds, or neck stiffness. In the UK, most cases of meningococcal septicaemia are caused by Neisseria meningitidis group B.

In this particular case, the child is clearly very sick and showing signs of septic shock. It is crucial to administer a single dose of benzylpenicillin without delay and arrange for immediate transfer to the nearest Emergency Department via ambulance.

The recommended doses of benzylpenicillin based on age are as follows:
– Infants under 1 year of age: 300 mg of IM or IV benzylpenicillin
– Children aged 1 to 9 years: 600 mg of IM or IV benzylpenicillin
– Children and adults aged 10 years or older: 1.2 g of IM or IV benzylpenicillin.

Tinea cruris, commonly known as ‘jock itch’, is a fungal infection that affects the groin area. It is primarily caused by Trichophyton rubrum and is more prevalent in young men, particularly athletes. The typical symptoms include a reddish or brownish rash that is accompanied by intense itching. Pustules and vesicles may also develop, and there is often a raised border with a clear center. Notably, the infection usually does not affect the penis and scrotum.

It is worth mentioning that patients with tinea cruris often have concurrent tinea pedis, also known as athlete’s foot, which may have served as the source of the infection. The infection can be transmitted through sharing towels or by using towels that have come into contact with infected feet, leading to the spread of the fungus to the groin area.

Fortunately, treatment for tinea cruris typically involves the use of topical imidazole creams, such as clotrimazole. This is usually sufficient to alleviate the symptoms and eradicate the infection. Alternatively, terbinafine cream can be used as an alternative treatment option.

This child has been clinically diagnosed with measles. The typical presentation includes a high fever accompanied by symptoms of a runny nose and sensitivity to light. Conjunctivitis, or pink eye, is often present as well. The associated rash is a widespread red rash with raised bumps. Koplik spots, which are white lesions on the inside of the cheeks, are a telltale sign of measles.

According to Public Health England, it is recommended that children with measles stay away from school, nursery, or childminders for four days starting from when the rash first appears.

For more information, you can refer to the Guidance on Infection Control in Schools and other Childcare Settings.
https://www.publichealth.hscni.net/sites/default/files/Guidance_on_infection_control_in%20schools_poster.pdf

Bullous pemphigoid (BP) is a chronic autoimmune disorder that affects the skin, causing blistering. It occurs when the immune system mistakenly attacks the basement membrane of the epidermis. This attack is carried out by immunoglobulins (IgG and sometimes IgE) and activated T lymphocytes. The autoantibodies bind to proteins and release cytokines, leading to complement activation, neutrophil recruitment, and the release of enzymes that destroy the hemidesmosomes. As a result, subepidermal blisters form.

Pemphigus, on the other hand, is a group of autoimmune disorders characterized by blistering of the skin and mucosal surfaces. The most common type, pemphigus vulgaris (PV), accounts for about 70% of cases worldwide. PV is also autoimmune in nature, with autoantibodies targeting cell surface antigens on keratinocytes (desmogleins 1 and 3). This leads to a loss of adhesion between cells and their separation.

Here is a comparison of the key differences between pemphigus vulgaris and bullous pemphigoid:

Pemphigus vulgaris:
– Age: Middle-aged people (average age 50)
– Oral involvement: Common
– Blister type: Large, flaccid, and painful
– Blister content: Fluid-filled, often haemorrhagic
– Areas commonly affected: Initially face and scalp, then spread to the chest and back
– Nikolsky sign: Usually positive
– Pruritus: Rare
– Skin biopsy: Intra-epidermal deposition of IgG between cells throughout the epidermis

Bullous pemphigoid:
– Age: Elderly people (average age 80)
– Oral involvement: Rare
– Blister type: Large and tense
– Blister content: Fluid-filled
– Areas commonly affected: Upper arms, thighs, and skin flexures
– Nikolsky sign: Usually negative
– Pruritus: Common
– Skin biopsy: A band of IgG and/or C3 at the dermo-epidermal junction

Slapped cheek syndrome, also known as fifth disease or erythema infectiosum, is caused by parvovirus B19. It is most commonly seen in children aged 4-12, but can affect individuals of any age. In the UK, the peak occurrence of this condition is in April and May. Slapped cheek syndrome is contagious, with the period of infectivity occurring before the appearance of the characteristic rash. The rash itself is painless.

Diagnosing slapped cheek syndrome is typically based on clinical presentation, characterized by the sudden onset of bright red cheeks resembling a slap mark. In some cases, a faint rash may also appear on other parts of the body. The rash usually lasts for a few days, but in rare instances, it may persist for a few weeks. Treatment for this condition is usually focused on managing symptoms. Additional symptoms that may accompany the rash include a mild fever and joint pain.

While slapped cheek syndrome is generally mild and resolves on its own, certain groups of individuals require extra caution. Pregnant women, for instance, are at an increased risk of miscarriage if exposed to fifth disease. Patients with sickle cell disease or weakened immune systems also need to take extra precautions.

In the UK, the most commonly used treatment for acute exacerbations of hereditary angioedema (HAE) in emergency departments is C1-Esterase inhibitor. However, there are alternative options available. Icatibant acetate, sold under the brand name Firazyr®, is a bradykinin receptor antagonist that is licensed in the UK and Europe and can be used as an alternative treatment. Another alternative is the transfusion of fresh frozen plasma.

Further Reading:

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

Based on the child’s medical history, it appears that they have multiple areas of infected eczema. In such cases, the NICE guidelines recommend starting treatment with flucloxacillin as the first-line option for bacterial infections. This is because staphylococcus and/or streptococcus bacteria are the most common causes of these infections. Swabs should only be taken if there is a likelihood of antibiotic resistance or if a different pathogen is suspected. In cases where the child is allergic to flucloxacillin, erythromycin can be used as an alternative. If the child cannot tolerate erythromycin, clarithromycin is the recommended option. For more information, you can refer to the NICE Clinical Knowledge Summary on the management of infected eczema.

Patients who have Eron class III or IV cellulitis should be hospitalized and treated with intravenous antibiotics. In this case, the patient is experiencing cellulitis along with symptoms of significant systemic distress, such as rapid heart rate and breathing. This places the patient in the Eron Class III category, which necessitates admission for intravenous antibiotic therapy.

Further Reading:

Cellulitis is an inflammation of the skin and subcutaneous tissues caused by an infection, usually by Streptococcus pyogenes or Staphylococcus aureus. It commonly occurs on the shins and is characterized by symptoms such as erythema, pain, swelling, and heat. In some cases, there may also be systemic symptoms like fever and malaise.

The NICE Clinical Knowledge Summaries recommend using the Eron classification to determine the appropriate management of cellulitis. Class I cellulitis refers to cases without signs of systemic toxicity or uncontrolled comorbidities. Class II cellulitis involves either systemic illness or the presence of a co-morbidity that may complicate or delay the resolution of the infection. Class III cellulitis is characterized by significant systemic upset or limb-threatening infection due to vascular compromise. Class IV cellulitis involves sepsis syndrome or a severe life-threatening infection like necrotizing fasciitis.

According to the guidelines, patients with Eron Class III or Class IV cellulitis should be admitted for intravenous antibiotics. This also applies to patients with severe or rapidly deteriorating cellulitis, very young or frail individuals, immunocompromised patients, those with significant lymphedema, and those with facial or periorbital cellulitis (unless very mild). Patients with Eron Class II cellulitis may not require admission if the necessary facilities and expertise are available in the community to administer intravenous antibiotics and monitor the patient.

The recommended first-line treatment for mild to moderate cellulitis is flucloxacillin. For patients allergic to penicillin, clarithromycin or clindamycin is recommended. In cases where patients have failed to respond to flucloxacillin, local protocols may suggest the use of oral clindamycin. Severe cellulitis should be treated with intravenous benzylpenicillin and flucloxacillin.

Overall, the management of cellulitis depends on the severity of the infection and the presence of any systemic symptoms or complications. Prompt treatment with appropriate antibiotics is crucial to prevent further complications and promote healing.

Pemphigus, derived from the Greek word for bubble ‘pemphix’, refers to a group of autoimmune disorders that cause blistering of the skin and/or mucosal surfaces. The most common subset is pemphigus vulgaris (PV), which accounts for approximately 70% of cases worldwide. PV is characterized by an autoimmune response where autoantibodies target cell surface antigens on keratinocytes, specifically desmogleins 1 and 3. This leads to a loss of cell-to-cell adhesion and separation, resulting in blister formation.

On the other hand, bullous pemphigoid (BP) is a chronic autoimmune blistering skin disorder that affects the subepidermal layer. It occurs when the basement membrane of the epidermis is attacked by IgG and sometimes IgE immunoglobulins, as well as activated T lymphocytes. The binding of autoantibodies to proteins and the release of cytokines from T cells trigger complement activation, neutrophil recruitment, and the release of proteolytic enzymes. These enzymes destroy the hemidesmosomes, leading to the formation of subepidermal blisters.

To summarize the differences between pemphigus vulgaris and bullous pemphigoid, the following provides a comparison:

Pemphigus Vulgaris:
– Age: Middle-aged people (mean age 50)
– Oral involvement: Common
– Blister type: Large, flaccid, and painful
– Blister content: Fluid-filled, often haemorrhagic
– Areas commonly affected: Initially face and scalp, then spread to the chest and back
– Nikolsky sign: Usually positive
– Pruritus: Rare
– Skin biopsy: Intra-epidermal deposition of IgG between cells throughout the epidermis

Bullous Pemphigoid:
– Age: Elderly people (mean age 80)
– Oral involvement: Rare
– Blister type: Large and tense
– Blister content: Fluid-filled
– Areas commonly affected: Upper arms, thighs, and skin flexures
– Nikolsky sign: Usually negative
– Pruritus: Common
– Skin biopsy: A band of IgG and/or C3 at the dermo-epidermal junction

Onchocerciasis is a parasitic disease caused by the filarial nematode Onchocerca volvulus. It is transmitted through the bites of infected blackflies of Simulium species, which carry immature larval forms of the parasite from human to human.

In the human body, the larvae form nodules in the subcutaneous tissue, where they mature to adult worms. After mating, the female adult worm can release up to 1000 microfilariae a day.

Onchocerciasis is currently endemic in 30 African countries, Yemen, and a few isolated regions of South America. Approximately 37 million people worldwide are currently infected.

Symptoms start to occur around a year after the patient is infected. The earliest symptom is usually an intensely itchy rash. Various skin manifestations occur, including scattered, red, pruritic papules (acute papular onchodermatitis), larger, chronic, hyperpigmented papules (chronic papular onchodermatitis), lichenified, oedematous, hyperpigmented papules and plaques (lichenified onchodermatitis), areas of skin atrophy with loss of elasticity (‘Lizard skin’), and depigmented areas with a ‘leopard skin’ appearance, usually on the shins.

Ocular involvement provides the common name associated with onchocerciasis, river blindness, and it can involve any part of the eye. Almost a million people worldwide have at least a partial degree of vision loss caused by onchocerciasis. Initially, there may be intense watering, a foreign body sensation, and photophobia. This can progress to conjunctivitis, iridocyclitis, and chorioretinitis. Secondary glaucoma and optic atrophy may also occur.

In a number of countries, onchocerciasis has been controlled through the spraying of blackfly breeding sites with insecticide. The drug ivermectin is the preferred treatment for onchocerciasis.

Atopic dermatitis is a long-lasting inflammatory skin condition that is linked to increased levels of IgE in the bloodstream. It is also characterized by sensitivity to various allergens found in the air, food, and microorganisms.

Further Reading:

Eczema is a chronic inflammatory skin disease characterized by dry, itchy skin with eczematous lesions. It often follows a chronic relapsing course and can lead to chronic skin changes such as lichenification and pigment changes. The term eczema is often used interchangeably with dermatitis, but strictly speaking, dermatitis refers to inflammation of the skin while eczema refers to specific conditions where skin inflammation is a feature.

Atopic eczema, also known as atopic dermatitis, is the most common type of eczema. It is usually first diagnosed in young children, with 90% of cases diagnosed before the age of 5. However, it can affect individuals of any age. Symptoms often improve as patients progress into their teens and adulthood. Around 10-20% of children are affected by atopic eczema, but only 3% of adults experience symptoms.

The exact cause of atopic eczema is not fully understood, but it is believed to be multifactorial, with both genetic and environmental factors playing a role. Genetic defects in genes that aid in the functioning of the skin barrier have been identified, which may predispose individuals to breaks in the skin barrier and increased exposure to antigens. Environmental factors such as pollution, allergen exposure, climate, and others also contribute to the development of the disease.

Diagnosing atopic eczema involves assessing the presence of key clinical features, such as pruritus (itching), eczema/dermatitis in a pattern appropriate for age, early age of onset, and personal or family history of atopy. Various diagnostic criteria have been established to aid in the diagnosis, including those set out by the American Academy of Dermatology and the UK working party.

The severity of atopic eczema can vary, and treatment options depend on the severity. Mild cases may be managed with emollients (moisturizers) and mild potency topical corticosteroids. Moderate cases may require moderate potency topical corticosteroids, topical calcineurin inhibitors, and bandages. Severe cases may necessitate the use of potent topical corticosteroids, topical calcineurin inhibitors, bandages, phototherapy, and systemic therapy.

In addition to medical treatment, identifying and avoiding triggers is an important aspect of managing atopic eczema. Common triggers include irritants, contact allergens, certain foods, skin infections, inhalant triggers, stress and infection.