Acute Dermatology (1).docx

Hello students. Today we will be discussing dermatologic issues that can be seen in the acute care setting. Conditions to discuss: There are many dermatological issues that can be found within the acute care settings. Today we will discuss a few as noted below. Exfoliative Erythroderma: The first de...

Hello students. Today we will be discussing dermatologic issues that can be seen in the acute care setting. Conditions to discuss: There are many dermatological issues that can be found within the acute care settings. Today we will discuss a few as noted below. Exfoliative Erythroderma: The first dermatological process we will discuss will be exfoliative erythroderma. Erythroderma is a clinical finding characterized by diffuse erythema and scaling of 90% of the body surface area. It results from of underlying cutaneous disorders, drugs, and malignancies. Because erythroderma may be life-threatening, it is crucial to identify and manage this condition appropriately. The most common cause of erythroderma is preexisting cutaneous conditions, like psoriasis which accounts for roughly half of erythroderma cases. Exfoliative dermatitis may also be triggered by certain drugs. These drugs include antiepileptics like phenytoin, carbamazepine, and phenobarbital, antibiotics like sulfonamides, penicillin, and vancomycin, lithium, and allopurinol. The classical physical finding of erythroderma is bright red patches that coalesce to cover almost the entire skin surface, followed by the appearance of a white or yellow scale. The skin may appear glossy and thin, and the patient may complain of tight skin due to progressive edema and lichenification which is thick and leathery skin. Pruritis occurs in nearly all patients, and fever may be present in more than half. Lymphadenopathy, splenomegaly, and hepatomegaly may be present in almost half of patients and may suggest a drug hypersensitivity or malignancy. Some patients may also present with hair loss and dry and brittle nails. Erythroderma is a clinical finding, but correlation with laboratory studies and histopathology is common practice. Laboratory abnormalities are nonspecific, though ESR and CRP are elevated in a vast majority of cases. Anemia, leukocytosis, eosinophilia, and abnormal serum protein levels may also be present in some patients. Erythroderma can be severe and life-threatening. Management of erythroderma predominantly involves monitoring and ensuring metabolic and hemodynamic stability. Emphasis should focus on symptom management with bed rest and proper wound care, including lukewarm baths, wet dressings, mild topical corticosteroids, and bland emollients. Oral antihistamines may also be helpful. Findings suggestive of secondary infection warrant antibiotic therapy. Management of idiopathic cases may include emollients, oral or topical steroids, methotrexate, or other modalities depending on patient’s response. Erythema Multiforme (EM): Erythema multiforme or EM is a cutaneous and mucosal hypersensitivity reaction with characteristic lesions in target triggered by certain antigenic stimuli. It represents an acute condition, sometimes recurrent, of the skin and mucosal membranes manifested by papular, bullous, and necrotic lesions. Its causes are variable and numerous. Most lesions appear in 48-72 hours and favor the extremities. The lesions remain localized to one site and heal within 7-21 days. Common precipitating factors include herpes simplex virus, histoplasmosis, and Epstein Barr virus. Most cases are mild, severe cases can be life-threatening. Drugs associated with EM include antibiotics like penicillin, cephalosporins, macrolides, sulfa drugs, antipyretics and many others. In some patients contact with heavy metals, herbal agents, topical therapies and poison ivy can trigger EM. A fever and a feeling of general unease may precede and/or accompany the eruption the first days. Sometimes there is arthralgia or even joint swelling. The typical lesion of the EM described as a rounded lesion that is regular with three concentric circles and a well-defined border. The peripheral ring is erythematous, the middle zone is often clearer, edematous, and palpable, and the center is erythematous, covered by a blister. The lesions measure less than 3 centimeters. They are symmetrical in the palms and backs of the hands, the feet, and the extended faces of the limbs. The trunk is often spared, but the face and ears can be reached. There is no pruritus, but rather sensations of burning in some patients. Mucosal lesions are common, mostly in the mouth, but also be found in the genital area. They are initially bullous, then quickly turn into painful erosions. A punch biopsy can be used to confirm the diagnosis of EM. Treatment of the acute phase includes topical treatment that is based on antiseptics for bullous lesions, antiseptic mouthwashes, and anesthetic. Ocular involvement is managed by ophthalmologists. Healing is promoted by the application of Vaseline on the lips and vitamin A ointment on the eyes. Mycoplasma pneumoniae infection justifies treatment with azithromycin for three days without even waiting for the results of the bacteriological examinations, especially if there is a cough or pulmonary radiological abnormalities. Some suggest treating herpes with aciclovir or valaciclovir if herpes is suspected. Severe cases of EM will require admission to manage the complications, dehydration and any infection. These patients are best managed in an ICU and treated like a burn-patient. Debridement should be avoided while the lesions are progressing. The eroded lesions should be bathed in Burrow's solution or saline with non-adherent dressings. All offending drugs must be immediately discontinued. New skin will form in about 7-21 days. Nutrition support is vital. Steven Johnson Syndrome (SJS): Stevens-Johnson syndrome or SJS is an acute, rare, and potentially fatal skin reaction involving loss of skin and, in some cases, mucosal membranes accompanied by systemic symptoms. Death is mainly due to sepsis and multiorgan failure. Medications is the culprit in over 80 percent of the cases. SJS is classified by the extent of the detached skin surface area with less than 10% body surface area. SJS can affect anyone with a genetic predisposition at any age, either sex, and all races, although it is more common in older people and women. It is much more likely to occur in people infected with HIV. The drugs that most commonly cause SJS include Anticonvulsants, Allopurinol, Sulfonamides, Antibiotics like penicillin, cephalosporins, quinolones, and minocycline; acetaminophen, NSAIDS, and contrast media. The drugs that precipitate SJS tend to have long half-lives and are nearly always taken systemically. SJS can develop within a few days to eight weeks after starting a new drug. A subsequent exposure can result in symptoms within a few hours. The illness begins with nonspecific symptoms such as fever and malaise, upper respiratory tract symptoms such as a cough, rhinitis, sore eyes, and myalgia. Over the next three to four days, a blistering rash and erosions appear on the face, trunk, limbs, and mucosal surfaces. Mucosal ulceration and erosions can involve lips, mouth, pharynx, esophagus and gastrointestinal tract, eyes, genitals, upper respiratory tract. About half of patients have involvement of three mucosal sites. The patient is very ill, anxious, and in pain. Liver, kidneys, lungs, bone marrow, and joints may be affected. Typical symptoms include fever, malaise, headache, anorexia, pharyngitis­, as well as any symptoms due to acute dysfunction of ocular, pulmonary, cardiovascular, gastrointestinal, renal, and hematological systems. Evaluation begins with a skin biopsy which will show full thickness skin necrosis. A direct immune fluorescence is negative. The provider should obtain a CBC, LFT, BMP, EKG, Chest x-ray to monitor for organ damage. Care of a patient with SJS requires supportive care including cessation of the suspected causative drug, hospital admission preferably to an intensive care and/or burn unit, fluid replacement with crystalloids, nutritional assessment, temperature control in a warm environment, pain relief, supplemental oxygen and sterile or aseptic handling. Skincare requires daily examination of skin and mucosal surfaces for infection, non-adherent dressings, and avoidance of trauma to the skin. Antibiotics may be required for secondary infection but are best avoided prophylactically. It is unknown whether systemic corticosteroids are beneficial, but they are often prescribed in high doses for the first three to five days of admission. Other drugs reported effective include systemic corticosteroids, ciclosporin, TNF-alpha inhibitors, Mucomyst, and intravenous immunoglobulins. Toxic Epidermal Necrolysis: Toxic epidermal necrolysis or TEN is like SJS but is more extensive. TEN is classified by the extent of the detached skin surface area of more than 30% body surface area, whereas SJS was less than 10%. A patient can have an overlap of SJS and TEN when 10% to 30% body surface area is affected. The etiology, symptoms, evaluation, and treatment are the same as SJS. TEN is potentially very serious with a high mortality to include 19.4% for SJS/TEN overlap, and 14.8% for TEN. Staphylococcus Aureus: Staphylococcus aureus is a gram-positive bacteria that cause a wide variety of clinical diseases. Infections caused by this pathogen are common both in community-acquired and hospital-acquired settings. The treatment remains challenging due to the emergence of multi-drug resistant strains such as MRSA or Methicillin-Resistant Staphylococcus aureus. Staph aureus does not normally cause infection on healthy skin, however, if it is allowed to enter the internal tissues or bloodstream, these bacteria may cause a variety of potentially serious infections.  Staph aureus including drug-resistant strains such as MRSA are found on the skin and mucous membranes, and humans are the major reservoir for these organisms. It is estimated that up to half of all adults are colonized, and approximately 15% of the population persistently carry Staph aureus in the anterior nares. Staph aureus is one the most common bacterial infections in humans and are the causative agents of multiple human infections, including bacteremia, infective endocarditis, skin and soft tissue infections like impetigo, folliculitis, furuncles, carbuncles, cellulitis, and scalded skin syndrome, osteomyelitis, septic arthritis, prosthetic device infections, pulmonary infections like pneumonia and empyema, gastroenteritis, meningitis, toxic shock syndrome, and urinary tract infections. Evaluation of a staph infection involves evaluation of clinical signs and symptoms as well as the history and physical findings. In many cases, routine cultures will reveal the diagnosis. Drug susceptibility testing often is required to guide treatment.  Treatment of staph aureus infections depends largely on the type of infection as well as the presence or absence of drug resistant strains. When antimicrobial therapy is needed, the duration and mode of therapy are largely dependent on the infection type as well as other factors. In general, penicillin remains the drug of choice if isolates are sensitive like with MSSA, or methicillin sensitive staph aureus strains and vancomycin for MRSA strains. In some cases, alternative therapy is necessary for addition to antimicrobial therapy. For example, fluid-replacement management is often required for toxin-mediated illness. Because many MRSA strains are resistant to multiple antibiotics, MRSA infections are emerging as serious pathogens in both the hospital and the community settings. Erysipelas: Erysipelas is a skin infection involving the dermis layer of the skin, but it may also extend to the superficial cutaneous lymphatics. It is characterized by an area of erythema that is well demarcated, raised, and often affects the lower extremities, with the face being the second most commonly affected site. The primary inciting infection involves streptococci. Most facial infections are due to Group A streptococcus while non-group A streptococcus involves more of the lower extremity. Surgical incisions, insect bites, stasis ulcerations, and venous stasis are among the many entry portals. A major risk factor for developing erysipelas includes lymphatic edema, but patients at risk also include excising for saphenous vein for bypass, post-surgical, nephrotic syndrome, and patients in an immunocompromised state. Erysipelas remains a clinical diagnosis and assessing a patient for any recent skin trauma or pharyngitis is important. Patients often experience systemic symptoms, such as malaise, fever, and chills 48 hours before the onset of the skin lesion. It has been well described that erysipelas presents as an area of skin erythema that is sharply demarcated with raised edges. Often patients will complain of burning, tenderness, and itchiness at the site. More severe disease can present with vesicles, bullae, and even frank necrosis. The location of inflammation is very important. In lower extremity erysipelas, it is recommended to examine the interdigital toe spaces for fissures, scaling, or maceration.  Redness and swelling involving a joint should raise suspicion for other more serious disease processes like septic arthritis. No laboratory workup is required for the diagnosis of erysipelas. Leukocytosis, elevated ESR and C-reactive protein are common but will not change the management or the treatment plan for most otherwise healthy individuals. Blood cultures should be obtained in patients that are immunocompromised, or ill-appearing patient. Also, consider extensive workup in who may be intravenous drug abusers, patients with prosthetic heart valves, and those with other intravascular devices. Antibiotics against streptococci should be initiated when erysipelas is suspected. Penicillin as monotherapy remains the first-line antibiotic used for the treatment of erysipelas. Most patients with erysipelas can be discharged home on oral antibiotics. The recommended duration of antibiotic therapy is 5 days, but the period may be extended to 10 days if the infection does not improve. Hospitalization is recommended for concern of necrotizing infection, the immunocompromised, patients with poor adherence to medications and follow up, and for those whose outpatient treatment is failing. Cellulitis: Cellulitis typically presents as a poorly demarcated, warm, erythematous area with associated edema and tenderness to palpation. It is an acute bacterial infection causing inflammation of the deep dermis and surrounding subcutaneous tissue. The infection is without an abscess or purulent discharge. Beta-hemolytic streptococci typically cause cellulitis, generally group A streptococcus, followed by methicillin-sensitive Staphylococcus aureus or MSSA. Patients who are immunocompromised, colonized with methicillin-resistant Staphylococcus aureus or MRSA, bitten by animals, or have comorbidities such as diabetes mellitus may become infected with other bacteria. Risk factors for cellulitis include any culprit that could cause a breakdown in the skin barrier such as skin injuries, surgical incisions, intravenous site punctures, fissures between toes, insect bites, animal bites, and other skin infections. Patients with comorbidities such as diabetes mellitus, venous insufficiency, peripheral arterial disease, and lymphedema are at higher risk of developing cellulitis. Cellulitis is characterized by erythema, warmth, edema, and tenderness to palpation. The patient may present with constitutional symptoms of generalized malaise, fatigue, and fevers. It is essential to ask patients if they have recently traveled, experienced any trauma or injuries, have a history of intravenous drug use, and/or have had insect or animal bites to the affected area.  The area should be demarcated with a marker to monitor for continuous spread. The area should be palpated to feel for fluctuance that could indicate the formation of a possible abscess. When gently palpating the affected area, be sure to note any presence of warmth, tenderness, or purulent drainage. Cellulitis can present on any area of the body, but most often affects the lower extremities. It is rarely bilateral. If any extremities are affected, check for proper sensation and verify pulses are intact to monitor closely for compartment syndrome.  Two of the four criteria are needed to make the diagnoses of cellulitis which include warmth, erythema, edema, or tenderness. The Infectious Disease Society of America practice guidelines recommends against imaging the infected area except in patients with febrile neutropenia. Consider blood cultures only in patients that are immunocompromised, experienced an immersion injury or animal bite, or have signs of systemic infection. Patients presenting with mild cellulitis and displaying no systemic signs of infection should be covered with antibiotics that target the treatment of streptococcal species. Though believed to be a less common cause, consider coverage of MSSA. The duration of oral antibiotic therapy should be for a minimum duration of 5 days. In nonpurulent cellulitis, patients should receive cephalexin 500 mg every 6 hours. If they have a severe allergy, treat with clindamycin 300 mg to 450 mg every 6 hours. In patients with purulent cellulitis, methicillin-resistant staph aureus colonization, cellulitis associated with an abscess or extensive puncture wounds, or a history of intravenous drug use, patients should receive antibiotics that cover against methicillin-resistant staph aureus as well. Cellulitis with MRSA risk factors should be treated with Bactrim 800 mg/160 mg twice daily for 5 days in addition to cephalexin 500 mg every 6 hours. If a patient has an allergy to Bactrim, treat with clindamycin 300 mg to 450 mg every 6 hours. A longer duration of antibiotic treatment may be a consideration in patients who show minimal improvement with antibiotic therapy within 48 hours. Intravenous antibiotics should be initiated to cover against group A strep. Absent patient risk factors for MRSA, treat with intravenous cefazolin, and when able de-escalate to cephalexin for a total of 5 days of treatment. If risk factors for MRSA are present, initiate therapy with Vancomycin with subsequent de-escalation to Bactrim. Necrotizing Fasciitis: Necrotizing fasciitis is a subset of aggressive skin and soft tissue infections that cause necrosis of the muscle fascia and subcutaneous tissues. Necrotizing fasciitis is a life-threatening disorder that carries a mortality ranging from 20% to 80%. Risk factors for adverse outcomes include advanced age, resistant organism, delay in therapy, multiorgan failure, and infection site. Initially, the overlying tissues are unaffected, potentially delaying diagnosis and surgical intervention. The infectious process can rapidly spread, causing infection of the fascia and perifascial planes as well as secondary infection of the overlying and underlying skin, soft tissue, and muscle.  Necrotizing fasciitis is typically an acute process occurring rapidly over several days. It is a direct sequela of bacterial infection introduced through a break in the skin’s integrity in approximately 80% of all cases. Gram-positive cocci specifically strains of Staphylococcus aureus and Streptococci are responsible for the majority of these single-site source infections. Polymicrobial infections occur as well because of a combination of gram-negative and anaerobic involvement. The majority of patients have diabetes and have a history of alcoholism. Patients with liver cirrhosis are also prone to necrotizing fasciitis. Necrotizing infections are more commonly present with excruciating pain out of proportion to presenting symptoms and systemic septic signs than non-necrotizing infections. Physical findings of necrotizing soft tissue infections may include tenderness to palpation beyond the erythematous border, crepitus, and cellulitis. The presence of bullae, ecchymotic changes to the skin, and dysesthesia or paresthesia should also be treated as a necrotizing infection. Subcutaneous emphysema and crepitus are almost always present. The infection can spread rapidly within hours hence suspicion should be high for necrotizing fasciitis in the presence of intense pain. Any rapidly progressing skin or soft tissue infection should be managed aggressively due to the difficulty in differentiating non-necrotizing from necrotizing skin and soft tissue infections. Imaging may be useful in providing data when the diagnosis is uncertain. The most common plain film finding is similar to cellulitis with increased soft tissue thickness and opacity. CT has greater sensitivity than plain film in identifying necrotizing soft tissue infections. These patients are extremely ill and should be transferred immediately to the intensive care unit. The sepsis causes refractory hypotension and diffuse capillary leak. Thus the patient will need aggressive resuscitation with fluids and use of inotropes to maintain blood pressure. The patient must be kept NPO until seen by the surgeon. Nutrition is vital but only after surgery has been completed.  Key concepts for treatment and management of necrotizing fasciitis include early diagnosis, starting appropriate empiric antibacterial coverage, adequate control of infection sources such as aggressive surgical intervention for abscess drainage, and identification of infection-causing pathogen and applicable adjustment of antimicrobial coverage. Antimicrobial therapy of necrotizing fasciitis includes Linezolid and Zosyn daily or Daptomycin and Zosyn and Clindamycin The treatment of necrotizing fasciitis is surgery and no time should be wasted calling for a surgical consult. The earlier the surgery is undertaken the better the outcome. The surgery requires extensive, wide debridement of all necrotic tissues. Early surgery may help minimize tissue loss and eliminate the need for amputation of a gangrenous extremity. the wounds need to be left open and are packed with wet gauze. Daily dressing changes are mandatory. Psoriatic Urgencies: Psoriasis is not generally thought of as a life-threatening condition, but there are certain kinds of flare-ups that can become life-and-death emergencies. Two very rare types of psoriasis, erythrodermic psoriasis and generalized pustular psoriasis which can cause fever, fluid loss and other dangerous problems. Erythrodermic psoriasis tends to produce large, red patches, often covering nearly all of the skin surface. It may be accompanied by severe itching and pain. It can occur suddenly as the first sign that a person has psoriasis or occur more gradually and affect people who already have plaque psoriasis. It can be triggered by an infection including HIV, stress, alcohol, suddenly stopping psoriasis medications, some medications including TNF-alpha inhibitors, Bactrim, and Wellbutrin. Erythrodermic psoriasis is dangerous because it can disrupt your body's ability to control its temperature and can lead to dehydration and heart failure. Pustular psoriasis comes on quickly in as little as a few hours and produces the following symptoms including widespread areas of erythema, pain, tenderness, white blisters filled with non-infectious pus that will dry and peel within a day or two which leaves the skin smooth and shiny, fever, chills, pruritis, tachycardia, thirst, dehydration, muscle weakness, loss of appetite, nausea, and edema. Some possible triggers include infection, suddenly stopping psoriasis medications, pregnancy, medications such as amoxicillin, terbinafine, codeine, ceftriaxone, oxacillin and rituximab, and topical medications used for psoriasis treatments. Erythrodermic psoriasis is usually treated first from the outside in – wet compresses, moisturizers and steroids applied to the skin, and bed rest while in the hospital. Usually, a systemic medication (taken by mouth or injection) such as acitretin, cyclosporine, and methotrexate is started to control the psoriasis quickly. It is important to avoid using oral steroids since they can trigger psoriasis flares. Phototherapy with an ultraviolet light should be avoided in the early stages, as they may make it worse, but they can be used after the inflammation has gone down. Generalized pustular psoriasis is treated with hospitalization, bed rest, fluids, and measures to bring the body temperature back to normal. The affected areas of the skin are treated with bland compresses. Systemic drugs including acitretin, cyclosporine, and methotrexate, are often started first. Medications applied to the skin may not be helpful if the symptoms are widespread. If an infection has occurred, antibiotics can be used to treat it. If it’s suspected that the episode was caused by a medication used to treat psoriasis, the causative medication can be switched to that of another class. Phototherapy may be used once the condition has become less severe. Bullous Dermatoses: Bullous pemphigoid or BP is the most common autoimmune subepidermal blistering disorder, representing 80% of cases. Bullous pemphigoid most commonly affects elderly patients between the ages of 60 to 80 years.  While the clinical presentation of BP presents with tense bullae and intense generalized pruritus. While most bullous pemphigoid cases are due to autoantibodies against certain proteins, some cases of bullous pemphigoid are caused by systemic medications that are initiated around three months prior. The drugs reported in the literature to cause BP like eruptions include diuretics such as furosemide and spironolactone, NSAIDs, amoxicillin, gliptins, and TNF-alpha inhibitors. In the prodromal phase, patients may experience moderate-to-severe pruritus alone or associated with urticarial, papular lesions. This later evolves to bullae in weeks to months, typically present in the axilla, forearms, medial thighs, trunk, and abdomen. The blisters are tense, up to 1 to 4 centimeters in diameter, and sometimes hemorrhagic. They typically contain clear fluid and may persist for several days before leaving erosions and crusts.  Histology with direct and indirect immunofluorescence studies aid in diagnosis. The mainstay of treatment for bullous pemphigoid is systemic corticosteroids, but treatment ultimately depends on comorbidities and the extent of the disease. For extensive disease, systemic prednisone at a dose of 0.5 to 1.0mg/kg per day is recommended. This dose of systemic corticosteroids controls the disease within approximately two weeks and can be slowly tapered over six to nine months or longer.  Graft vs Host Graft-versus-host disease or GVHD occurs due to the presence of immunocompetent T lymphocytes in the graft attacking the immunodeficient recipient tissue due to histocompatibility differences within 100 days, causing tissue damage. “Graft” refers to transplanted, or donated tissue, and “host” refers to the tissues of the recipient. It is a common complication after allogeneic hematopoietic stem cell transplant. Acute GVHD presents within 100 days of transplantation, and chronic presents after 100 days of transplantation. GvHD occurs following bone transplantation most commonly, followed by transplantation of solid organs like the liver, and transfusion of un-irradiated blood. The incidence of GVHD increases with unmatched donor transplants, HLA disparity, sex mismatching. Acute GVHD usually involves the skin but can affect the gastrointestinal tract, and liver. The most common skin manifestation is a pruritic or painful maculopapular rash that initially involves the palms, soles shoulders, and nape of the neck. In severe GVHD, bullous lesions with toxic epidermal necrolysis mimicking TEN can develop. All patients receiving HCT should undergo prophylactic treatment for GVHD. Treatment protocols differ by institution, but most commonly use a combination of cyclosporine and methotrexate is continued for several months post-transplantation. Antibacterial, antiviral, and antifungal prophylaxis is typically added post HCT to mitigate the risk of infections. Most treatment options focus on immunosuppression of donor T cells and must be balanced to reduce the symptoms of GVHD while avoiding decreasing the beneficial graft. Corticosteroids remain the most commonly used treatment. Toxic Shock Syndrome Toxic shock syndrome (TSS) is an acute-onset illness characterized by fever, hypotension, sunburn-like rash, and end-organ damage. TSS was classically associated with high absorbency tampon use in menstruating women until eventually, these were taken off the market. Since that time, it has become important to also consider non-menstrual cases. TSS is most commonly caused by a toxigenic strain of Staphylococcus aureus or Group A Strep. Other strains of streptococci can lead to TSS. The disease occurs most often in the setting of menstruation despite the discontinuation of high absorbency tampons. However, TSS can also present in non-menstrual settings such as in soft tissue infections, post-surgical infections, burns, retained foreign bodies such as nasal packing, and dialysis catheters. Staphylococcal TSS is typically the result of a localized infection such as an abscess, whereas streptococcal TSS may result from bacteremia, necrotizing fasciitis, or cellulitis. TSS typically presents with rapid onset of fever, rash, and hypotension. It may be preceded by a prodrome of fever and chills with nausea and vomiting as well as nonspecific symptoms such as myalgias, headache, or symptoms of pharyngitis which then progresses to sepsis and organ dysfunction. Risk factors include superabsorbent tampon use, nasal packing, post-operative wound infections, recent influenza infection, as well as immunocompromised states. Classically, the rash is a diffuse, blanching, macular erythroderma. Initially it may be a transient macular rash, predominantly on the chest. The rash desquamates one to two weeks later followed by full-thickness peeling. There may be mucosal involvement with strawberry tongue and ulceration of the vaginal mucosa or conjunctival erythema. Patients may exhibit disorientation or altered mental status without focal deficits. There is no specific lab test to identify TSS. A complete blood count (CBC) may show leukocytosis or leukopenia. Bandemia is common. Evaluation of multisystem organ involvement including CBC, CMP, CK, and coagulation studies should be drawn to evaluate for the clinical criteria of TSS.  Patients should receive aggressive intravenous (IV) fluid hydration with crystalloids. Soft tissue infections, especially necrotizing fasciitis should be sought out and managed. Any source of bacteria such as tampons or nasal packing should immediately be removed. Emergent surgical consultation should be obtained for any wound debridement or surgical cause. This is critical in the early management of toxic shock syndrome. Broad-spectrum antibiotics should be administered for those with an unidentified organism, if possible after blood cultures and cultures from the suspected source have been drawn. For most institutions, this will include vancomycin or linezolid given the high prevalence of methicillin-resistant Staphylococcus aureus (MRSA). Clindamycin should also be administered to suppress toxin production. Once the organism is identified, and sensitivities have been determined, antibiotics should be optimized and narrowed in the spectrum. Penicillin is the preferred antibiotic for group A strep. For MSSA, clindamycin is recommended, plus flucloxacillin or a beta-lactamase-resistant penicillin such as nafcillin. Current recommendations are to treat for seven to 14 days. Urticaria / Angioedema: Contact urticaria or CU is a transient wheal and flare reaction that occurs within 10 to 60 minutes at the site of contact of the offending agent and completely resolves within 24 hours. Contact urticaria is a transient wheal and flare response on exposure to specific agents, especially in the work environment. The occupations at the most risk of developing CU are healthcare, lab work, agriculture, hairdressers, cosmetic industry, chemical industry, cleaning, construction, catering, cooking, electronics, machinery, and metal products. Urticaria and angioedema can be a part of systemic diseases like autoimmune disorders, endocrinopathies, malignancy, and hemolytic disease. Chronic idiopathic urticaria is usually associated with autoimmune disease. Angioedema is non-pitting edema that involves subcutaneous and/or submucosal layers of tissue that affects the face, lips, neck, and extremities, oral cavity, larynx, and/or gut. It becomes life-threatening when it involves the larynx. With general history-taking, the clinician should focus particular attention on the history of exposure to potential causative agents in food, home, work environment, cosmetics, and personal care products. Obtain details on the specific skin symptoms like wheals, tingling, burning, itching and progression of symptoms. Clinical presentation is commonly a wheal and flare response and urticarial swelling. Patients affected by CU can present with hives called urticaria or dermatitis like eczema. The urticarial response appears as an erythematous swelling with surrounding pallor.  Avoidance of the offending substance is the cornerstone of management. Protective gear like gloves, skin conditioning creams or emollients, and cotton liners are necessary when the exposure at work is unavoidable. Second-generation H1-receptor blockers like Benadryl, hydroxyzine, or Claritin are the first-line treatment. Leukotriene inhibitors like Singular inhibit the inflammatory component. Self-administered subcutaneous epinephrine pens should be available at all times to the patient. Steroids are second-line treatment options and help to prevent the delayed phase of an anaphylactic reaction.  Immunosuppressive drugs like cyclosporine and methotrexate are options in severe cases. If the angioedema progresses you want to treat the airway with intubation or surgical airway intervention.  Leukocytoclastic Vasculitis: Leukocytoclastic vasculitis is a cutaneous, small-vessel vasculitis of the dermal capillaries and venules. This condition can be idiopathic or can be associated with infections, neoplasms, autoimmune disorders, and drugs. Infectious triggers include Mycobacterium, Staphylococcus aureus, Chlamydia, and HIV.  Chronic infections with hepatitis B, hepatitis C, and syphilis can be associated with leukocytoclastic vasculitis as well. Several drugs have been associated with leukocytoclastic vasculitis. The onset is typically 1 to 3 weeks after drug initiation. These include beta-lactams, erythromycin, clindamycin, vancomycin, sulfonamides, furosemide, allopurinol, NSAIDs, amiodarone, thiazides, beta-blockers, TNF-alpha inhibitors, SSRIs, metformin, warfarin, and valproic acid. Neoplastic or hematologic triggers of leukocytoclastic vasculitis include lymphomas, leukemias, visceral tumors such as intestinal adenocarcinoma and lung cancer.  Systemic diseases including connective tissue diseases like lupus and Sjogren syndrome, inflammatory bowel disease, and rheumatoid arthritis. Key clinical features of leukocytoclastic vasculitis include palpable purpura on the lower extremity and small vessel involvement. Hemorrhagic vesicles and bulla, pustules, nodules, crusted ulcers, or livedo reticularis may also be present on physical exam. The lesions can range in size from 1 mm to 1 cm in diameter. The lesions can appear at once in crops, or various crops may cycle and produce lesions with different stages of evolution.  Skin biopsy with direct immunofluorescence is the cornerstone for the diagnosis of leukocytoclastic vasculitis. Treatment depends on the severity of disease and can range from an oral corticosteroid taper to various steroid-sparing immunosuppressive agents. DRESS: Drug rash with eosinophilia and systemic symptoms or DRESS syndrome is a severe systemic hypersensitivity drug reaction. It typically develops 2 to 6 weeks after exposure to a culprit medication and presents with widespread rash, facial edema, systemic symptoms like fever, rigors, hypotension, lymphadenopathy with evidence of visceral organ involvement, and often eosinophilia. The syndrome may have overlapping features with SJS and TEN. The most common drugs to cause this reaction are a number of anticonvulsant drugs like phenobarbital and phenytoin, allopurinol, olanzapine, and the sulfa drugs. Drug hypersensitivity syndrome occurring within 2 weeks of starting the responsible drug is most likely with beta-lactam antibiotics or contrast media. Onset is delayed more than 2 weeks with anticonvulsants and allopurinol. A high fever of 38–40 C is usually noticed first. This is quickly followed by a widespread skin rash that can last many weeks. Characteristics of the rash are diverse. Morbilliform eruption affects 80% of cases with lesions, blisters, and pustules. Erythroderma or exfoliative dermatitis, facial swelling, and mucosal involvement can also be seen. Symptoms may worsen after stopping the drug and may continue for weeks, or even months, despite drug withdrawal. The severity of the rash does not necessarily correlate with the extent of internal organ involvement. Later symptoms depend on the internal organs affected. They may include enlarged lymph nodes in several sites, hematological findings like an increased white count, eosinophilia, atypical lymphocytes, thrombocytopenia, and anemia. The patient may have liver enlargement and hepatitis, mild interstitial nephritis, myocarditis or pericarditis which can cause chest pain, breathlessness, and lowered blood pressure. Neurological involvement may lead to meningitis and encephalitis, seizures, and coma. Gastrointestinal symptoms include gastroenteritis, pancreatitis, bleeding and dehydration. Causes of death from drug hypersensitivity syndrome include acute liver failure causing coagulation problems, jaundice, and impaired consciousness, multiorgan failure, myocarditis, and Hemophagocytosis. The diagnosis of drug hypersensitivity syndrome is based on the clinical triad of high fever, extensive skin rash, and organ involvement. It is supported by eosinophilia and abnormal liver function tests. Treatment consists of immediate withdrawal of all suspect medicines, followed by careful monitoring and supportive care. It is very important for patients presenting with a high fever and a rash to have blood tests as soon as possible. Systemic corticosteroids like prednisone are generally used in the more severe cases of drug hypersensitivity syndrome, pneumonitis, and/or hepatitis. Ciclosporin has been reported to be an alternative and effective treatment for drug hypersensitivity syndrome. Additional treatment may include intravenous immunoglobulin, plasmapheresis, mycophenolate, and rituximab.   Question: An 18-year-old man with epilepsy controlled with medication develops fever, lymphadenopathy, a generalized maculopapular rash, elevated transaminases, and arthralgias. He reports having been bitten by ticks while working in the yard outside. Which of the following is the most likely etiology? A Severe poison ivy dermatitis B Reaction to anticonvulsant medication C Acute human immunodeficiency virus (HIV) infection D Lyme disease Answer: The correct answer is B. This is a common presentation of hypersensitivity syndrome associated with aromatic anticonvulsants (phenytoin, carbamazepine, phenobarbital). Poison ivy (answer A) is not associated with fever and lymphadenopathy. Lyme disease (answer D) is associated with erythema migrans, an erythematous annular rash with a central clearing (target lesion) developing within days of infection. HIV (answer C) is a less likely answer considering that a history of risk factors is not being presented. Question: A 34-year-old man is brought to the emergency department for a severe allergic reaction caused by fire ant bites. He is treated with intramuscular epinephrine and intravenous corticosteroids. His oxygen saturation falls to 80%, and he becomes apneic. Which of the following is the best next step? A Intravenous Benadryl B Intravenous epinephrine C Oxygen by nasal cannula D Endotracheal intubation E Electrical cardioversion Answer: The correct answer is D. This patient has developed airway obstruction due to an anaphylactic reaction. He requires intubation and mechanical ventilation to maintain oxygenation. The first step in treating anaphylaxis is assessing the ABCs. Intubation, if required, should not be delayed. Second, epinephrine should be administered to help control symptoms and blood pressure. Additional treatment measures include placing the patient in a recumbent position, elevating the legs, administration of oxygen as needed, NS volume replacement and/or use of vasopressors as required, and administration of Benadryl 50 mg orally or intravenously every 4 hours as needed. Question: A 38-year-old man with a history of injection heroin abuse presents to the emergency center with tenderness and swelling that extends circumferentially around his left upper arm. The entire area is minimally erythematous, but it is tense and swollen. The patient indicates that he had injected some “black tar heroin” into the area 6 days ago. His temperature is 39.5 °C (103 °F), heart rate is 125 beats per minute, and white blood cell (WBC) count is 46,000 cells/mm3. Computed tomography (CT) scan of the arm reveals no evidence of abscess or venous thrombosis, but there is extensive tissue stranding along the muscle fascia and in the muscles. Which of the following is the most appropriate treatment? A Intravenous (IV) antibiotics, and if no improvement, CT imaging B Radical debridement and IV antibiotics C Transesophageal echocardiography to assess for valvular lesion D IV antibiotics and hyperbaric oxygen treatment E Radical debridement of the affected area Answer: The correct answer is B. Based on the history of black tar heroin injection, the infection is likely a polymicrobial. Early, aggressive surgical debridement and broad-spectrum antimicrobial therapy are the keys to reduce mortality associated with this process. IV antibiotic treatment alone is not sufficient. Echocardiography may be obtained if there is suspicion on physical exam for endocarditis. Radical surgical debridement alone is not sufficient to treat this infection as antibiotics are also important. Question: A 35-year-old HIV-positive injection drug user presents, complaining of a hip abscess where he injects heroin. The temperature is 38.1°C, and there is a 10 × 10 cm circular area of erythema and induration on the lateral buttock without fluctuance. Which is the correct management? A Prescribe oral cephalexin for cellulitis and instruct the patient to return in 24 hours to assess whether an abscess has developed. B Attempt needle aspiration at the center of the infection, and if negative, cover with oral antibiotics. C Search for an abscess with bedside ultrasound and establish an IV in anticipation of a drainage procedure and admission for IV antibiotics. D Consult a surgeon immediately for suspected necrotizing SSTI. Answer: This case is a classic presentation for a deep buttock or thigh abscess related to heroin injection. A septic hip or necrotizing infection should also be considered. Nonpurulent cellulitis is very unlikely, and simply treating with antibiotics is incorrect management. These abscesses can be very large and may cause a low-grade fever. When there is no obvious fluctuance, imaging should be pursued with ultrasound, or occasionally CT, to confirm the diagnosis and guide drainage. Given the fever and immunocompromise from HIV, this patient will likely require IV antibiotics and admission. References: Thank your listening to this lecture.