VALVULAR DISORDERS 111 TABLE 3-10 NATIVE VALVE DISORDE RS (CONTINUED) VALVULAR ABNOR MALITY ETIOLOGY PR ESENTATION HEART SOUNDS NOTES Mitral valve prolapse (MVP) r The most common valvular heart abnormality in U.S. r Exact cause is uncertain but presumed to be either congenital or due to myxomatous degeneration of the mitral valve r Most cases are asymptomatic r Presenting symptoms often include atypical chest pain, dyspnea, palpitations r Increased incidence of panic disorder, TIAs, tachydysrhythmias, sudden death r Early, or mid-systolic click r Click is often followed by high-pitched late-systolic murmur r Increases in left ventricular volume (e.g., squatting, Trendelenburg) move the click/ murmur closer to S 2 and decrease the intensity/duration of the murmur r Decreases in left ventricular volume (e.g., standing, valsalva) move the click/murmur closer to S 1 and increase the intensity/ duration of the murmur r Advanced disease may be associated with MR r Treatment: beta-blocking medications relieve atypical chest pain and atrial dysrhythmias r Antibiotic prophylaxis against infective endocarditis indicated only if murmur (or echocardiographic evidence of MR) present Right-sided valvular heart disease r Isolated tricuspid valve disease is the most common right-sided valvular disorder, usually caused by intravenous drug use r Right-sided valvular disease may also be caused by rheumatic heart disease r The most common symptoms are related to infective endocarditis: fevers, myalgias, dyspnea r Tricuspid regurgitation presents with a holosystolic murmur heard best at the left lower sternal border r Treatment of tricuspid regurgitation is focused on treating underlying endocarditis, surgery if significant dysfunction occurs (Continued ) 112 CHAPTER 3 / CARDIOVASCULAR DISORDERS TABLE 3-10 NATIVE VALVE DISORDE RS (CONTINUED) VALVULAR ABNOR MALITY ETIOLOGY PR ESENTATION HEART SOUN DS NOTES Aortic stenosis (AS) r Most common causes are congenital bicuspid valve and rheumatic heart disease r Most common cause in the elderly is idiopathic calcification/ degeneration r Obstruction to outflow produces low cardiac output and leads to symptoms once the valve lumen is reduced to 25% of normal r Classic triad is angina, syncope, CHF r 5–10% incidence of sudden death r Systolic crescendo– decrescendo murmur r Paradoxical splitting of S 2 r Best heard at right upper sternal border r Usually murmur radiates to carotids r ECG usually demonstrates evidence of left ventricular hypertrophy r CXR demonstrates cardiomegaly, evidence of CHF r Narrow pulse pressure in severe disease r Best treatment is valve replacement r The use of preload reducers, afterload reducers, and inotropes must be done with extreme caution, can cause hemodynamic decompensation Aortic regurgitation (AR) r Most common causes of chronic AR are rheumatic heart disease and congenital causes r Chronic cases are associated with development of left ventricular hypertrophy and dilation, which over many year results in CHF r Chronic AR produces a high-pitched decrescendo diastolic murmur r ECG usually demonstrates evidence of left ventricular hypertrophy in chronic cases VALVULAR DISORDERS 113 TABLE 3-10 NATIVE VALVE DISORDE RS (CONTINUED) VALVULAR ABNOR MALITY ETIOLOGY PR ESENTATION HEART SOUN DS NOTES r Most common causes of acute AR are endocarditis r Proximal thoracic aortic dissection can also cause acute AR r Acute AR is the most common valvular disorder caused by blunt chest trauma r Peripheral signs of chronic AR include Water-hammer pulse, “pistol shot” femoral pulses, pulsating nail beds, and head-bobbing with systole r Acute cases are associated with chest pain and pulmonary edema; patients are sometimes hypotensive r Best heard along the left sternal border r Acute AR produces a faint short diastolic murmur, which is often inaudible r CXR in chronic cases demonstrates cardiomegaly, CHF r CXR in acute cases demonstrates normal sized heart with pulmonary edema r Patients with chronic AR develop a wide pulse pressure r Treatment of chronic AR is based on treating the CHF r Acute AR requires treatment with inotropes, afterload reduction, and surgery 114 CHAPTER 3 / CARDIOVASCULAR DISORDERS TABLE 3-11 PROSTHETIC VALVE COMPLICATIONS COMPLICATION NOTES Thromboemboli r Thrombus formation can cause acute valvular dysfunction r Patients may present with acute heart failure, hypotension, loss of the expected abnormal valve sounds r More common with mechanical valves than with tissue valves Endocarditis r See section on Infective Endocarditis Hemolysis r If mild, iron supplementation is adequate treatment r If severe, consider paravalvular leak r Patients may present with anemia symptoms and jaundice r More common with mechanical valves than with tissue valves Paravalvular leak r Occurs when part of the valve becomes displaced r Patients may present with acute heart failure and/or hemolytic anemia r Regurgitant murmur is usually present r More common with mechanical valves than with tissue valves Primary valve failure r Patients may present with evidence of embolization of a prosthetic fragment, hemolysis, acute valvular occlusion FURTHER READING Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction—Executive Summary. Circulation 2004;110:588–636. Chen K, Varon J, Wenker OC, et al. Acute Thoracic Aortic Dissection: The Basics. J Emerg Med 1997;15:859–867. Fox KA. Management of Acute Coronary Syndromes: An Update. Heart 2004;90:698–706. Gropper MA, Wiener-Kronish JP, Hashimoto S. Acute Cardiogenic Pulmonary Edema. Clin Chest Med 1994;15:501–15. Lange RA, Hillis LD: Clinical practice: acute pericarditis. N Engl J Med 2004;351:2195–2202. Ma OJ, Cline DM, Tintinalli JE, et al. (eds.). Emergency Medicine: Just the Facts, 2nd ed. New York: McGraw-Hill, 2004. Marx JA, Hockberger RS, Walls RM, et al. (eds.). Rosen’s Emergency Medicine: Concepts and Clinical Practice, 5th ed. St. Louis: Mosby, 2002. Mattu A. Cardiogenic pulmonary edema. Current Opinion in Cardiovascular, Pulmonary, and Renal Investigational Drugs 2000;2:9–16. Mattu A, Brady WJ: ECGs for the Emergency Physician. London: BMJ Publishing Company, 2003. CHAPTER 4 CUTANEOUS DISORDERS GENERAL TERMINOLOGY AND DESCRIPTORS TABLE 4-1 DEFINITION OF SKIN LESIONS TERM LATIN MEANING DESCRIPTION SIZE EXAM PLE Macule Spot Flat, nonpalpable well defined <1 cm Vitiligo Papule Pimple Palpable <1 cm Mollususcum contagiousum Plaque Confluence of papules Plateau-like elevation that is well defined Psoriasis, Lichenification of atopic dermatitis Nodule Small knot Solid, palpable lesions (hard or soft) >1 cm Wart Wheal Flat-topped papule or plaque that last for 24–48 h Urticaria Vesicles Blister Elevated, superficial, fluid-filled cavities <0.5 cm Herpes zoster Bullae Bubble Elevated, superficial, fluid-filled cavities >0.5 cm Bullous impetigo Pustule Circumscribed skin cavity filled with purulent exudates, may arise from a hair follicle Variable Folliculitis Purpura Red-purple lesions that do not blanch with pressure >0.3 mm ITP, TTP, meningiococcemia Petechaie Skin spot Red-purple lesions that do not blanch with pressure <0.3 mm Seen on the arm distal to the BP cuff in patients on anticoagulants 115 Copyright © 2007 by The McGraw-Hill Companies, Inc. Click here for terms of use. 116 CHAPTER 4 / CUTANEOUS DISORDERS Specific Lesions and Management ERYTHEMA MULTIFORME Erythema multiforme (EM) is a continuum of pathology including EM minor and EM major. EM major encompasses Stevens-Johnson syndrome (SJ) and toxic epidermal necrolysis (TEN). ERYTHEMA MULTIFORME MINOR Etiology: Over 50% of cases are idiopathic. Of known etiologies, drugs are the most common cause. Common offenders include penicillin, sulfonamides, and anticonvulsants. Infections are also a common cause and are more commonly the etiology in children. HSV I and II, Influenza A, and mycoplasma have been implicated in EM. Recurrent EM has been associated with HSV I and II. It may present with mucosal lesions, possibly causing confusion with EM major. Clinical Presentation: EM Minor is an acute, self-limited process. An inflammatory process yields the pathognomonic target, or “iris” lesion. The lesions evolve over 1–2 days, are symmetrically distributed and are found on the hands, feet, and extensor surfaces of the extremities. Lesions persist for about 7 days and tend to resolve after 1 to 2 weeks with minimal or no sequelae. EM Minor has little or no mucus membrane involvement. Diagnosis: Clinical. Treatment: Supportive care and symptomatic treatment. Discontinue offending agent if possible. Topical steroids may be used on all lesions except eroded areas. Control of HSV using oral antiviral therapy when indicated may prevent recurrent EM. FIGURE 4-1. ERYTHEMA MULTIFORME MINOR. ERYTHEMA MULTIFORME MAJOR Two main syndromes include SJS and TEN (see Figure 4-2). Etiology: The same drugs have been implicated as the cause of EM major as in EM minor, though some cases are idiopathic. SJS is considered a maximal variant of EM Major, while TEN is considered a maximal variant of SJS. Clinical Presentation: With EM major, the patient is clinically ill appearing. A prodrome of fever and flu-like symptoms occur for 1–3 days prior to mucocutaneous manifestations. Target lesions become confluent, progress to diffuse erythema, and later become bullous. Necrosis of epidermis occurs followed by sheet-like loss of the epidermis. The epidermis of bullous lesions will dislodge with minimal lateral pressure (positive Nikolsky sign). EM Major is associated with mucus membrane lesions in all cases. It may present with odynophagia or dysuria secondary to oropharyngeal and genital involvement. Epithelial erosions of trachea, bronchi, and GI tract may also occur. Fever is usually higher with TEN. Diagnosis: The diagnosis is made clinically. A differential diagnosis includes graft-versus-host-disease, ther- mal burns, toxic shock syndrome (TSS), scarlet fever, and staphylococcal scalded-skin syndrome (SSSS) (children). GENERAL TERMINOLOGY AND DESCRIPTORS 117 –FIGURE4-1— Erythema multiforme minor—Iris and target-like lesions with concentric macules and papules on the palm. Reprinted from Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology. 5th ed. New York: McGraw Hill, 2005, Fig. 7-20, p. 141. Treatment: Despite aggressive treatment, SJS and TEN have a mortality rate anywhere from 5–30%, de- pending on severity. Early withdrawal of the suspected drug is essential. IV fluids and electrolyte management is done similar to a burn victim, thus patients with SJS or TEN with diffuse skin involvement are probably best cared for in the ICU or burn care center setting. Administration of systemic glucocorticoids has not been proven to be beneficial, although it is recommended. Intravenous immunoglobulin (IVIG) has been shown to be beneficial in TEN if given early. TOXIC SHOCK SYNDROME Etiology: The source of infection is often a foreign body such as a tampon (85%), nasal packing, or indwelling catheter. Staph aureus produces an exotoxin that is responsible for the clinical syndrome. Nearly one-third of reported patients with TSS are men. Clinical Presentation: Patients generally have a history of indwelling foreign body. Fever, hypotension, and diffuse erythroderma should prompt clinical suspicion for TSS. Multiorgan dysfunction is common with severe laboratory abnormalities noted. The rash has been described as “painless sunburn” that fades and is followed by full-thickness desquamation, especially on the palms and soles. There is a spectrum of this illness that ranges from mild illness with no organ involvement to the severe cases that meet the strict diagnostic criteria for TSS. 118 CHAPTER 4 / CUTANEOUS DISORDERS – FIGURE 4-2 — Erythema multiforme major (toxic epidermal necrolysis)—Generalized, macular eruption with some target-like lesions which rapidly developed epidermal necrosis, positive Nikolsky sign, bulla formation, and denuded erosive areas. On the back this eruption looks like scalding. It was due to a sulfonamide. Reprinted from Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology. 5th ed. New York: McGraw Hill, 2005, Fig. 7-24, p. 147. Diagnosis: The CDC maintains strict criteria for the diagnosis of TSS: including fever over 102 ◦ F, multi- organ involvement, hypotension, and a rash that desquamates 1–2 weeks following onset of disease. Treatment: Treatment should include removal of the foreign body. Parenteral antibiotic administration is indicated although they have not been shown to affect outcomes. A reasonable treatment could include dicloxacillin and vancomycin for MRSA coverage. In penicillin allergic patients, clindamycin is an alternative to dicloxacillin. IV steroids and IVIG have been used with some success in severe cases. Care depends largely on the severity of disease. STREPTOCOCCAL TOXIC SHOCK SYNDROME Etiology: Less common than TSS caused by Staph. aureus, Group A streptoccocus (GAS) also known as Strep. pyogenes, produces an exotoxin that is responsible for the clinical syndrome. Invasive soft tissue streptococcal infections such as cellulitis are common precipitating factors. Clinical Presentation: Patients present with fever, hypotension, skin edema, erythema, or bullae. Multi- system organ involvement is the rule. Desquamation occurs less commonly than with Staph TSS. The criteria used to diagnose Staph TSS are applicable to the GAS variant. A thorough search for inciting infections such as myositis, fasciitis, or cellulitis is essential. Diagnosis: Clinical. See criteria for TSS. GENERAL TERMINOLOGY AND DESCRIPTORS 119 Treatment: Supportive care and antibiotic therapy similar to staph TSS. If deep soft tissue infection is the inciting cause, incision and drainage may be indicated. STAPHYLOCOCCAL SCALDED SKIN SYNDROME Etiology: Stap. aureus produces exfoliative toxins responsible for the clinical syndrome. This most com- monly occurs in infants <3 months of age but can occur in children up to 5 years old. It is considered a severe variant of bullous impetigo. Clinical Presentation: The site of the Staphylococcus infection is often not obvious. Conjunctivitis, occult nasopharyngeal infection, or umbilical stump infection are common sites. Localized exfoliative toxin is responsible for the lesions of bullous impetigo, while SSSS is secondary to hematogenous spread of toxin with diffuse skin effects. The skin manifestations of SSSS classically start in the perioral area. Diffuse, tender erythroderma with a sandpaper appearance progress to large, fluid-filled bullae with a positive Nikolsky sign. Desquamation then follows though mucus membranes are spared. Diagnosis: Clinical findings followed by bacterial cultures and skin biopsy. Treatment: Fluid resuscitation is the top priority. An attempt should be made to localize the source of infection and antistaphylococcal antibiotics should be given. NECROTIZING FASCIITIS Etiology: Aerobic and anaerobic bacteria in the polymicrobial form or Group A streptococcus can cause this infection. There is an increased risk in the immunocompromised patient population. Fournier’s gangrene is a severe variant involving the perineum. Concomitant Varicella infection increases the risk of GAS type infection. Clinical Presentation: With the polymicrobial form pain out of proportion to exam is the classic pre- sentation. Erythema and edema are seen initially, followed by discoloration, vesicles, and crepitus later on with development of reddish-purple patches and bullae. Low-grade fever and tachycardia are common. This infection can progress within hours. The GAS form has a similar presentation to the polymicrobial form, but is usually more rapidly progressive and associated with higher mortality due to more virulent bacteria. Diagnosis: Wound and blood cultures. Lack of bleeding and presence of cloudy, foul fluid after incision into wound suggests this disease process. Finger or surgical instrument passes easily through planes of fascia and soft tissue is easily dissected away from the fascia. X-ray or CT may demonstrate subcutaneous gas, but may be normal. MRI is more sensitive for detecting deep soft-tissue infection. Treatment: Early surgical consultation is essential. Antibiotics should be initiated early in suspected cases. Penicillin alone is often not adequate in severe cases. Broad-spectrum antibiotic administration is indicated to cover anaerobes as well. Vancomycin and pipericillin/tazobactam would be a good choice for empiric coverage. A floroquinolone with clindamycin is an alternative for penicillin allergic patients. Hyperbaric oxygen therapy (HBO) following surgical therapy may be beneficial. GAS GANGRENE (CLOSTRIDIAL AND NONCLOSTRIDIAL MYONECROSIS) Etiology: The majority of cases are caused by the spore-forming clostridial species. Clostridium perfringens is responsible for most. The nonclostridial form is caused by a mixed infection of anaerobic and aerobic organisms. This infection can be avoided by proper wound care with crushed or dead-tissue debridement at initial evaluation of a wound. 120 CHAPTER 4 / CUTANEOUS DISORDERS Clinical Presentation: Gangrene is a rapidly progressive infection of the deep subcutaneous tissues with severe myonecrosis and sepsis. Physical examination is significant for pain out of proportion to examination. Patients may report a sensation of heaviness in affected part. Edema and crepitance appear with progression of infection. Brown discoloration, bullae, and serosanguinous discharge may be present. Low-grade fever and tachycardia are common. The patient with gas gangrene may develop irritability, confusion, anddeterioration of mental status. Diagnosis: Gram stain of bullae may reveal pleomorphic gram-positive bacilli with or without spores. X-ray or CT may reveal gas in the muscle and surrounding soft tissue. Surgical exploration may reveal nonbleeding muscle in later stages of disease as well as loss of contractility and presence of gas bubbles. Treatment: Early surgical intervention is a necessity. Early antibiotic therapy should be started with peni- cillin G plus clindamycin. Ceftriaxone or erythromycin are alternative choices. HBO following surgical therapy may be beneficial. RASHES ASSOCIATED WITH BACTERIAL INFECTIONS TABLE 4-2. RASHES WITH ASSOCIATED BACTERIAL INFECTIONS (OUTPATIENT TREATMENT) FIGURE 4-3. IMPETIGO (HONEY CRUSTED LESIONS). [...]... Written Board Exam in Emergency Medicine Ohio: Emergency Medicine Educational Enterprises, Inc., 2001 Fleisher GR, Ludwig S, Henretig FM, et al Textbook of Pediatric Emergency Medicine Philadelphia: Lippincott Williams and Wilkins, 2000 Schofield JK, Tatnall FM, Leigh IM Recurrent Erythema Multiforme: Clinical Features and Treatment in a Large Series of Patients Br J Dermatol 19 93; 128(5):542–545 CHAPTER... is a life-threatening hypermetabolic state It likely represents the addition of adrenergic hyperactivity, induced by stress, onto the setting of unrecognized or undertreated hyperthyroidism Etiology: TABLE 5-1 CAUSES OF HYPERTHYROIDISM Clinical Presentation: TABLE 5-2 SIGNS AND SYMPTOMS OF HYPERTHYROIDISM 132 Copyright © 2007 by The McGraw-Hill Companies, Inc Click here for terms of use  133 ENDOCRINE... Hill, 2000 Tintinalli JE, Kelen GD, Stapczinski JS Emergency Medicine A Comprehensive Study Guide 6th ed New York: McGraw Hill, 2004 Cline DM, Ma OJ, Tintinalli JE, et al Just the Facts in Emergency Medicine New York: McGraw Hill, 2001 Cydulka RK, Stewart MH Dermatologic Presentations In Marx JA, Hockberger RS, Walls RM, et al (eds) Rosen’s Emergency Medicine Concepts and Clinical Practice 5th ed St... confluent on the nose, cheek, lips, and chin in a child with nasal carriage of Staph aureus and mild facial eczema – FIGURE 4 -3 Reprinted from Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology 5th ed New York: McGraw Hill, 2005, Fig 2 2-1 0, p 589 VIRAL EXANTHEMS TA B L E 4 - 3 VIRAL DISEASE AND ASSOCIATED RASH DISEASE ETIOLOGY CHARACTERISTIC RASH PRESENTATION COMMENTS Varicella Varicella zoster... risk for aplastic anemia Fading macular rash will appear “lace-like” (Continued ) 124 TA B L E 4 - 3 CHAPTER 4 / CUTANEOUS DISORDERS VIRAL DISEASE AND ASSOCIATED RASH (CONTINUED) DISEASE ETIOLOGY CHARACTERISTIC RASH PRESENTATION COMMENTS Roseola (Exanthem subitum) Human herpesvirus 6 Pink maculopapular beginning on the trunk and spreading outward High fever (up to 105◦ C) in a classically well-appearing... infarction of the leg in a child with NM meningitis and disseminated intravascular coagulation with purpura fulminans – FIGURE 4-6 Reprinted from Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology 5th ed New York: McGraw Hill, 2005, Fig 2 2-4 3, p 6 43 FURTHER READING 131 vomiting, and possibly with meningeal signs Petechial rash classically found on the extremities and trunk and progress to... viral infection ᭺ Usually self-limiting r Factitious thyrotoxicosis ᭺ Exogenous thyroid hormone r Metastatic follicular thyroid carcinoma r TSH producing pituitary tumors r Iodide-induced hyperthyroidism (Jod-Basedow syndrome) ᭺ Excess iodine intake ᭺ Found in a number of medications (Continued ) 134 CHAPTER 5 / ENDOCRINE, METABOLIC, AND NUTRITIONAL DISORDERS TA B L E 5 - 1 CAUSES OF HYPERTHYROIDISM... Lymphocytosis Eosinophilia Cortisol levels are drawn at time zero, 1-hour, and then at 6–8-hour intervals The normal response is for cortisol to increase by at least 10 mg/dL or to three times baseline levels A 24-hour urine sample must also be obtained for 17-hydroxy steroid This confirms the diagnosis suggested by the cortisol levels A 48-hour stimulation test can both confirm the diagnosis and differentiate... petechiae Treatment will not decrease incidence of nephritis Desquamation occurs after rash fades Topical mupirocin Associated post-streptococcus GN Erythromycin Petechiae and red macules on hard palate Associated post-streptococcus GN Circumoral pallor Impetigo (Figure 4 -3 ) Small pustules or Group A Streptococcus vesicles with erythematous margins (nephrogenic strain) After rupture, “honey crusted”... widespread disease OTHER COMMON CHILDHOOD RASHES TABLE 4-4 OTHER COMMON CHILDHOOD RASHES FIGURE 4-4 PITYRIASIS ROSEA (HERALD PATCH) Lesions and Pearls HERPES SIMPLEX HSV-1 Involves the lips (herpes labialis), tip of the finger (herpetic whitlow), and the eyes (herpetic keratitis) and is also responsible for the minority of urogenital lesions HSV-2 Usually involves the genital area Skin lesions begin . graft-versus-host-disease, ther- mal burns, toxic shock syndrome (TSS), scarlet fever, and staphylococcal scalded-skin syndrome (SSSS) (children). GENERAL TERMINOLOGY AND DESCRIPTORS 117 –FIGURE 4-1 —. Tintinalli JE, et al. (eds.). Emergency Medicine: Just the Facts, 2nd ed. New York: McGraw-Hill, 2004. Marx JA, Hockberger RS, Walls RM, et al. (eds.). Rosen’s Emergency Medicine: Concepts and Clinical. Folliculitis Purpura Red-purple lesions that do not blanch with pressure >0 .3 mm ITP, TTP, meningiococcemia Petechaie Skin spot Red-purple lesions that do not blanch with pressure <0 .3 mm Seen on