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398
V. J. Cabrera
ultrasonography can also reveal if there is chronic venous insufficiency and a transthoracic echocardiogram (TTE) could be obtained if history and physical are concerning for heart failure. Ultrasound examination of the inferior vena cava diameter and collapsibility may also provide informa­tion about hypervolemia.
By directing therapy at correcting the underlying capillary hemodynamic disturbance, development of edema can be stopped or reversed. Lifestyle and dietary modification in conjunction with pharmacotherapy are useful in the long­term management. For the common systemic causes, treat­ment of the underlying condition is indicated. For those with chronic venous insufficiency, mechanical therapies such as leg elevation and compression stockings, as well as judicious diuretic therapy, are useful, although caution should be taken in those with peripheral arterial disease. Deep venous throm­bosis is treated with anticoagulation therapy and cellulitis with antibiotics. In medication-induced edema, the culprit medication should be discontinued if possible, and in those with heart failure, cirrhosis, and nephrotic syndrome, cautious use of diuretics and salt restriction can be initiated. Caution to avoid volume depletion with diuretics must be exerted. Patients should be monitored for electrolyte disturbances and changes in urea and serum creatinine, watching for signs of volume depletion. For patients with nephrotic syndrome, higher doses of diuretics might be required. For those with diuretic resistance, the use of diuretic combinations could be required.
Clinical Pearls
• A thorough history and physical examination are
essential.
• Chronic venous insufficiency and cellulitis have common
manifestations: peripheral edema, increase in skin tem-
perature, and erythema. Have in mind that cellulitis is usu-
ally a unilateral process.
Chapter 19. Edema
399
Don’t Miss This!
• Deep vein thrombosis presents with acute limb swelling in
a patient with risk factors (e.g., immobilization) but could
be bilateral in patients with malignancy.
• Compartment syndrome presents with acute limb swelling,
tense skin, and decreased peripheral pulses.
• Heart failure presents with peripheral edema ± pulmonary
edema, jugular venous distention, and ascites.
• Recheck medication list and do not forget over-the-
counter medications: common things are common!
• Think of central venous stenosis causing upper extremity
edema in patients with history of central catheter
placement.
• Facial edema and dilated neck veins are findings of supe-
rior vena cava syndrome.

References

1. Cho S, Atwood JE. Peripheral edema. Am J Med.
2002;113(7):580–6.
2. Ely JW, Osheroff JA, Chambliss ML, Ebell MH. Approach
to leg edema of unclear etiology. J Am Board Fam Med.
2006;19(2):148–60.
3. Blankeld RP, Finkelhor RS, Alexander JJ, Flocke SA, Maiocco J,
Goodwin M, etal. Etiology and diagnosis of bilateral leg edema
in primary care. Am J Med. 1998;105(3):192–7.
4. Trayes KP, Studdiford JS, Pickle S, Tully AS.Edema: diagnosis and
management. Am Fam Physician. 2013;88(2):102–10.
5. Messerli FH.Vasodilatory edema: a common side effect of anti-
hypertensive therapy. Curr Cardiol Rep. 2002;4(6):479–82.
6. Frishman WH. Effects of nonsteroidal anti-inammatory drug
therapy on blood pressure and peripheral edema. Am J Cardiol.
2002;89(6A):18D–25D.
7. Nesto RW, Bell D, Bonow RO, Fonseca V, Grundy SM, Horton
ES, et al. Thiazolidinedione use, uid retention, and congestive
heart failure: a consensus statement from the American Heart
Association and American Diabetes Association. Diabetes Care.
2004;27(1):256–63.
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V. J. Cabrera
8. Stemmer R. A clinical symptom for the early and differential
diagnosis of lymphedema. Vasa. 1976;5(3):261–2.
9. Wells PS, Anderson DR, Rodger M, Forgie M, Kearon C, Dreyer
J, etal. Evaluation of D-dimer in the diagnosis of suspected deep-
vein thrombosis. N Engl J Med. 2003;349(13):1227–35.
Part V
Dermatologic
Chapter 20
Rash
AlexanderHowell andKarthikKrishnamurthy

Introduction

Rashes are common problems encountered in all facets of healthcare that often represent a diagnostic conundrum, even at times to the most experienced dermatologist. Many condi­tions produce rashes that appear very similar clinically, and the differences distinguishing them are often subtle, or only apparent on histopathology. It is important that the correct differential diagnosis be made initially. Many conditions can be exacerbated by incorrect treatments or delay of therapeu­tic intervention, leading to significant morbidity in some cases and, rarely, mortality. When approaching rashes, it is helpful to generate a good differential diagnosis by categoriz­ing the rash based on its reaction pattern. Presented here is an algorithmic approach to rashes that begins with five previously described reaction patterns: papulosquamous, eczematous, vascular, dermal, and vesiculobullous [1]. Each reaction pattern is then subcategorized based on nuances in the appearance, texture, and symptoms of various skin conditions.
A. Howell · K. Krishnamurthy (*) Department of Dermatology, Orange Park Medical Center, Orange Park, FL, USA
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022 E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-031-15353-2_20
403
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A. Howell and K. Krishnamurthy

Decision-Making/Differential Diagnosis

The initial step in approaching a rash is to create a detailed description of the rash. A good description includes primary morphology, secondary change, color, shape, configuration, and distribution (see H and P).
Next, categorize the reaction pattern based on your description:
• Papulosquamous rashes are red scaly rashes.
• Eczematous rashes are red and itchy and can have scale,
crust, and lichenification (accentuation and thickening of
skin markings).
• Dermal rashes are rashes with no surface (or epidermal)
change.
• Vascular rashes are red and may be blanching or
non-blanching.
• Vesiculobullous rashes are rashes with blisters of varying
sizes.
In general, consider common conditions first while at the same time ruling out life-threatening conditions promptly (i.e., severe drug reactions such as Stevens-Johnson syndrome [SJS], toxic epidermal necrolysis [TEN], drug reaction with eosinophilia and systemic symptoms, urticaria with angio­edema, staphylococcal scalded skin syndrome [SSSS], toxic shock syndrome [TSS] , erythroderma, meningococcemia, rocky mountain spotted fever [RMSF], bacterial endocarditis, necrotizing fasciitis, etc.) [2, 3].
Papulosquamous
Generally speaking, this reaction pattern includes rashes with red, scaly papules and plaques.
Chapter 20. Rash
405
Psoriasiform
Psoriasis. Well-demarcated, red plaques with thick overlying
scale. Common locations include extensor surfaces (knees,
elbows), scalp, palms, and soles. Nail findings can aid in the
diagnosis and include pitting, oil spots, and onycholysis
(Fig.20.1). Seborrheic dermatitis. Erythema with overlying greasy scale
in a “seborrheic distribution” (oil- and hair- bearing areas).
Associated with HIV, Parkinson’s disease, and other neu-
rologic conditions [4]. Pityriasis rubra pilaris. Reddish-orange scaly plaques, kera-
totic follicular papules, or palmoplantar keratoderma.
Distinct areas of uninvolved skin referred to as “islands of
sparing” are characteristic. Tinea corporis. Annular or ring-shaped red, scaly plaques.
Raised border has more scale than the clearer center of
the lesion [4].
F . Plaque psoriasis. Thick, red plaques with sharply demarcated borders and overlying silvery scale
406
A. Howell and K. Krishnamurthy
Pityriasiform
Pityriasis rosea. Oval-shaped pink to red scaly thin plaques
in “Christmas tree” distribution along the body folds.
Often a herald patch appears a few days before the other
smaller lesions. Located mostly on the trunk, it can
involve extremities. This can occur on the face in African
Americans. Secondary syphilis. Small red to brown scaly papules with
involvement of the palms and soles. Tinea versicolor. Tan to red or hypopigmented thin plaques
with fine scale. These are typically located on the upper
chest, upper back, and neck.
Lichenoid
Lichen planus (LP) five Ps. Purple, polygonal, planar, and
pruritic plaques. “Wickham striae” may be present. Lower
extremities are a common location, but some people have
mucosal and penile lesions. Drug-induced LP is associated
with NSAIDs, diuretics, ACE inhibitors, and beta-blockers
[4] (Fig.20.2).
Erythroderma
Erythroderma is generalized erythema and scaling that affects >90% of the body surface area. The underlying causes include preexisting dermatoses (atopic dermatitis, psoriasis, seborrheic dermatitis), cutaneous T-cell lymphoma, or drug reactions [4] (Fig.20.3).
Eczematous
1. Acute eczema. Weeping, vesicular erythematous papules
and plaques that are very itchy. Geometric or linear con-
guration indicates an “outside job” and is a clue to diag-
nosis [1]. Includes acute allergic/irritant contact dermatitis
and dyshidrotic eczema.
Chapter 20. Rash
407
F . Lichen planus. Purple, polygonal, planar plaques on the anterior lower extremity
408
A. Howell and K. Krishnamurthy
F . Erythroderma. Generalized erythema and exfoliative scaling in a patient with underlying psoriasis
2. Subacute eczema. Eczematous lesions that progress, form-
ing scaly crust.
3. Chronic eczema. Characterized by lichenication, hyper-
pigmentation, and thicker scaly plaques.
Atopic dermatitis. Common in children, but can also be seen in adults. Located in flexural areas. It is associated with asthma, allergies, and an “itch-scratch” cycle. A diagnostic clue is that the middle part of the back (where the patient cannot reach to scratch) will be spared (Fig.20.4).
Stasis dermatitis. Typically seen on the lower extremities in elderly individuals. Underlying venous insufficiency, varicose veins, and edema are present. Hyperpigmentation occurs from hemosiderin deposition. Itching and overlying scale occurs.