Immediate Recognition and Management of Life-Threatening Problems
To some, emergency medicine and dermatology may seem to be two of the most unrelated specialties in medicine, and in our daily practice dermatologic complaints most likely respresent a small percentage of our normal daily census but the emergency physician will encounter many patients presenting with dermatologic complaints. The astute clinician will realize that, although rare, some of these problems can be life-threatening. Some patients may even require emergency airway protection and vigorous resuscitation. This chapter reviews those special situations and discusses common and uncommon dermatologic complaints.
The initial evaluation begins with the primary survey and vital signs. Always focus special attention on airway, breathing, and circulation (the ABCs). Note any abnormal vital signs and oxygen saturation, and be alert to subtle changes in mental status or behavior that may indicate impending airway or cardiovascular collapse. The ABCs apply to all clinical situations, and a thorough history and examination are often the most helpful tools in arriving at any diagnosis. The dermatologic examination must be performed on a disrobed patient. Inspect all areas of the skin and mucosal surfaces before addressing specific lesions.
Parallel to the assessment of the ABCs is a thorough history that includes potential recent exposures to foods, medications, plants, insects, and the like that may have triggered the condition. An ample history, addressing the patient’s allergies, medications, medical and surgical history, last meal, and events leading up to the presentation may provide information necessary to begin appropriate management.
- Swelling of face, lips, tongue
- May lead to airway compromise
Angioedema forms in the deeper dermal and subcutaneous tissues of the distal extremities, tongue, lips, mouth, face, and neck. Particularly dangerous is the involvement of the mouth, tongue, and lower airway, which can lead to severe airway compromise. Angioedema is believed to be a similar to urticaria, which is present in half of the cases, but a deeper reaction. Two subtypes exist, the rare hereditary form and the acquired form. The autosomal dominant hereditary variant is usually due to C1-esterase deficiency or defect with 75% of patients with hereditary angioedema (HAE) having their first episode before 16 years of age. The acquired form is most commonly secondary to angiotensin-converting enzyme (ACE) inhibitors and has increased in prevalence because of widespread usage of these drugs. Patients who have been using ACE inhibitors for months or years can still develop angioedema from these agents.
Emergency airway protection is mandated if airway compromise is impending or present. Treat shock if present. Discontinue any implicated medications or substances. Supply oxygen to maintain oxygen saturation at greater than 90%. In severe angioedema with airway compromise, administer epinephrine 0.1–0.5 mg (1:1000 solution) subcutaneously or preferably intramuscularly. This may be repeated every 5–10 minutes. Give an H1 antihistamines such as diphenhydramine HCl, 1–2 mg/kg, or in adults, 25–50 mg parenterally. Consider an H2 antihistamine such as ranitidine 50 mg intravenously. Methylprednisolone sodium succinate, 125 mg intravenously, may be repeated every 6 hours. Life-threatening HAE attacks may not respond well to epinephrine in normal dosages, antihistamines, or steroids. In these cases, airway protection is mandatory and fresh frozen plasma should be considered as it contains C1 inhibitor.
Admit patients to an ICU if airway compromise is present; otherwise, they may need observation in a non-ICU hospital bed or in the emergency department. If a patient is thought to have experienced a reaction to a medication, instruct the patient to discontinue that medication and contact his or her primary-care physician to discuss an alternative medication.
- Localized areas of dermal edema
- Intense itching
Urticaria (hives) may be either acute or chronic and may appear in any age group. The condition represents one end of a continuum, ranging from urticaria to anaphylactic shock. Because various medications and foods are most often implicated as causes, take a thorough history of possible exposures. The lesions themselves represent localized areas of edema in the dermis. They appear as intensely pruritic, sharply demarcated raised circular or annular areas with either an erythematous or a blanched base and border. Their appearance may wax and wane, and individual lesions often resolve within an hour. With anaphylaxis (see Chapter 9), there may be an initial decrescendo of the presenting symptoms with early interventions. A late-phase response may occur hours later with a more severe presentation than the initial symptom complex.
If airway compromise is not present, patients can be given H1-receptor blockers (see diphenhydramine dosing, above), steroids, and even epinephrine. H2-receptor blockers, such as ranitidine, may also be added. If airway compromise is present, treat on an emergency basis as for angioedema.
Disposition is the same as for angioedema (see above). Remember the sometimes biphasic nature of anaphylactic reactions. Instruct patients to avoid any potentially responsible agents. Give any patient with a history of anaphylaxis a prescription for an autoinjector epinephrine device and instruct the patient on its proper use prior to discharge.
- Epidermal detachment
- Drug-induced or postviral illness
- Patients may be critically ill
A disorder of epidermal detachment was initially reported in 1922 when Stevens and Johnson published a description of two children with fever, erosive stomatitis, severe conjunctivitis, and a disseminated cutaneous eruption. It is now known to be a drug-induced state or one that follows a viral illness. Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are now thought to represent ends of a spectrum of reactions involving detachment of the epidermis. Both conditions share inciting factors and mucosal involvement. The range of disorders has been classified into three categories: SJS, involving less than 10% of body surface area (BSA); transitional cases, involving 10–30% of BSA; and TEN, with greater than 30% of BSA with detached epidermis. Mortality rates for SJS are approximately 5%; rates are much higher (30%) with TEN. Death is most commonly from sepsis secondary to infections from Staphylococcus aureus and Pseudomonas aeruginosa.
With a few exceptions, SJS/TEN results from drug exposure. The main culprits are sulfonamide antibiotics. Others on the list include aromatic anticonvulsants, β-lactam antibiotics, NSAIDs, allopurinol, tetracyclines, quinolones, and abacavir. Over 200 medications have been implicated along with vaccinations, malignancy, HIV and herpes viral infections. Patients with SJS/TEN typically present with 1- to 2-week prodrome of arthralgia, anorexia, fever, pruritus, pharyngitis, and conjunctivitis prior to skin involvement. With re-exposure of a drug, the time to onset to skin involvement is typically 1–3 days. Any mucous membrane site can be involved. Mucous membrane involvement often precedes but may accompany skin lesions. Patients with SJS/TEN present with severe, intensely painful macules and mucosal ulcerations with a truncal and occasionally facial distribution of target like lesions. The skin lesions begin as macules and are often described as burning. Over time macules coalesce into wide areas of erythema as the eruption expands. As lesions age, the skin becomes necrotic and bullae may form. The Nikolsky sign may be elicited. This refers to easy separation of the upper layers of the epidermis from the lower layers with very minor trauma, such as lateral traction or gentle rubbing on the skin. There may be eroding of the bullae, or the affected skin may slough in large sheets. This may progress over hours to days. The sloughing may involve other organ systems, including the gastrointestinal tract, genitourinary system, and the respiratory tree.
Discontinue any potentially inciting medications. This usually requires that all nonessential medications be stopped, because no tests are available to identify the offending agents. Careful correction of electrolyte abnormalities and fluid replacement are critical, because significant fluid losses occur with loss of the protective skin barrier. Airway protection and mechanical ventilation may be necessary if the trachea and upper airway are involved. Sloughing and detachment of mucosa can lead to airway compromise. Antibiosis may be necessary to avoid sepsis-related complications. Pain control is essential. For uveitis, corneal ulceration, and/or vision loss, ophthalmologic consultation is strongly encouraged. Skin biopsy can aid in ruling out other deadly bullous diseases such as pemphigus vulgaris.
In severe cases, treatment in a burn center may be necessary. Guard carefully against infection. Avoid steroids because they have not proved beneficial.
- A diffuse, generalized erythema and scaling
- Occurs secondary to many disease states
Many cutaneous diseases present with exfoliative erythroderma, or generalized redness and scaling. This condition is associated with a high risk for morbidity and mortality, independent of the inherent risks of the disease process it represents. Most commonly, this condition occurs secondary to psoriasis, atopic dermatitis, Hodgkin’s disease, or mycosis fungoides (aka cutaneous T-cell Non-Hodgkin’s lymphoma), or reactions to any of a wide range of inciting drugs. The erythrodermic state usually has a slow progression, but an acute onset may occur in patients who have cutaneous dermatoses or severe drug reactions.
Clues to the diagnosis may be from the underlying disease, such as psoriatic plaques or characteristic nail changes. Bullous pemphigoid typically exhibits tense bullae in addition to erythroderma. Long-standing erythroderma may be associated with keratoderma, alopecia, and ectropion. Peripheral edema occurs in 50% of patients. Patients with severe drug reactions may appear acutely ill with fever, malaise, and lymphadenopathy. A leukocytosis with eosinophilia, organomegaly, and hepatic or renal impairment may be present. In the most severe cases, high-output cardiac failure may occur. Severe alterations in fluid balance may occur, leading to shock. Sepsis may ensue, and hepatic necrosis may be fatal.
Correction of derangements in fluid balance must begin early. Take care with the skin, applying moist dressings to weeping areas. Low-potency topical steroids may be used. Avoid high-potency preparations, because the large surface areas involved could lead to the absorption of large doses of steroids. Treat secondary infections.
Hospital admission is often required, preferentially in an ICU, depending on the needs of the patient.
- Skin appears scalded and blistered
- Affects primarily children
- Skin barrier is broken and leads to S. aureus infection
Primarily a disease of children, staphylococcal scalded skin syndrome (SSSS) refers to a series of toxin-induced blistering dermatoses. SSSS lies within a spectrum of blistering skin disorders beginning with localized bullous impetigo. The exfoliative toxins, collectively known as exfoliatin, are primarily attributed to S. aureus, and page group 2 exotoxin-producing staphylococci are most implicated. Mortality rates are low (2–3%) in children but can reach as high as 60% in adults who have comorbidities or preexisting conditions.
The clinical presentation ranges from a milder form with localized eruption of a few fragile fluid-filled bullae surrounded by normal skin, to a more involved state. The more widespread form is often associated with fever, generalized erythema, and poor feeding in infants. Subsequently, large bullae form with a predilection for sites of friction. Erosion can occur in large areas, resulting in open, painful lesions. The Nikolsky sign is present. Unlike in SJS or TEN, mucous membranes are spared in SSSS. This may be a helpful distinguishing factor. The process is thought to result from a break in the protective skin barrier, which leads to S. aureus infection. Typical areas involved in the primary infection include the umbilicus in neonates, as well as the nasopharynx, urinary tract, and other sites.
Cases of localized eruptions may be treated with oral antibiotics. The widespread form usually requires parenteral antibiotics to cover penicillin-resistant S. aureus. Treatment for adults is nafcillin, 1.5 g, or oxacillin, 2 g intravenously every 4 hours. For pediatric patients, treatment is nafcillin or oxacillin, 150 mg/kg/d intravenously in divided doses for 5–7 days. If superinfection is suspected, an aminoglycoside may be needed. Vancomycin or clindamycin should be considered. Rehydration and thermoregulation are essential, as is adequate pain control.
Severe cases require treatment in an ICU or burn center. Because the cleavage of the epidermis and exfoliation are extremely superficial, the lesions typically heal with little or no residual scarring.
1This chapter is a revision of the chapter by: Ben H. Chlapek, DO, FACEP, FACOEP from the 6th edition.
Recognition and Management of Potentially Life-Threatening Problems
Cellulitis
- Deeper infection
- Affects skin and subcutaneous tissues
Erysipelas
- Well-demarcated, superficial, erythematous infection
- Often affects face and extremities
Cellulitis and erysipelas refer to infections of the subcutaneous tissues. Erysipelas involves the more superficial upper dermis, and cellulitis is deeper, with more extensive involvement of the subcutaneous tissues and fat. Both conditions are acute and related to a breach in the skin’s protective barrier function. This can be secondary to fissuring and maceration, burns, venous stasis, malnutrition, lymphedema, or any of a number of other factors. The primary causative agent is group A β-hemolytic streptococcus. Other causes include streptococci B, C, and G and staphylococci infection. Other causative organisms associated with cellulitis include S. aureus, H. influenzae, Streptococcus pneumoniae, and Pseudomonas. If untreated, both conditions can lead to devastating complications such as local abscesses and gangrene with severe cellulitis. Facial erysipelas may lead to cavernous sinus thrombosis. Both cellulitis and erysipelas may lead to septicemia.
Erysipelas is characterized by well-demarcated, erythematous, indurated plaques. The borders may be palpable. Primary sites include the face, scalp, and lower extremities. Patients are usually in the extremes of age. Cellulitis is usually associated with painful swelling and erythema of the involved area. The borders are usually less well defined, and the affected area is typically warm.
Although many cases can be managed on an outpatient basis, patients may have constitutional symptoms, and those with comorbid conditions may be quite ill and require hospitalization. Antibiotics are used empirically to cover streptococci and S. aureus. Recommended therapies include penicillin G, 600,000 to 2 million units intravenously every 6 hours, for streptococci; and nafcillin, 1.5–2 g intravenously every 4 hours, for staphylococci. Treat methicillin-resistant cases with vancomycin 1.5–2 g intravenous q day. Patients who appear well and without constitutional symptoms may be given oral therapy. This includes dicloxacillin, 250–500 mg orally four times daily, or erythromycin, 0.25–0.5 g orally four times daily, in the penicillin-allergic patient. If methicillin-resistant staphylococcus is suspected treat with trimethoprim–sulfamethoxazole or minocycline. Simple measures may be helpful in both conditions, including rest, cool compresses, elevation of the affected part, and antibacterial soaks. Debridement is used in secondary abscesses.
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