Itchy Skin

Inspired by last Friday’s AMR case, I thought I’d write an overview of the causes of pruritus, particularly the causes that DON”T go along with a rash (because I hate rashes? Nah).  You can organize these causes in a few ways, but I like to think of them based on the big categories of: dermatologic, systemic disease, neurologic, and psychogenic.

Only takes a few of these guys to set off some serious itching


Most dermatologic etiologies are going to have an associated rash, but it may be subtle. Here are a few where you make have to look closely:

  • Xerosis: The most common cause of generalized pruritus, just plain old dry skin. Common in winter, often can tell skin is try just by feeling it.
  • Scabies: Regular scabies, not the Norwegian kind discussed in AMR, may not have much of a rash associated. Sometimes you can see a burrow, but rarely. I learned that the itching is a delayed hypersensitivity reaction, and may not appear for weeks after infestation.
  • Atopic Dermatitis: Think of this in a patient with other allergic phenomena (rhinitis, conjunctivitis), sx at an early age, and a family history of allergic disease. Patients also have allokinesis, when an innocuous stimuli, like temperature changes or clothing, induces itching.
  • Contact dermatitis: there are two kinds of contact dermatitis. Irritant contact dermatitis (like that caused by poison ivy) occurs when an irritant directly damages the skin.  There is often a rash in this instant.  Allergic contact dermatitis occurs when the irritant induces an allergic response. The rash here may be diffuse and obvious, or may be more subtle. Ask about anything that comes in contact with skin, including soaps, lotions, and laundry detergent.

Systemic Disease

  • Cholestasis: The first thing we think of, but pretty rare. Most commonly starts in the palms and soles before becoming more generalized. Disorders that cause cholestasis include: Primary biliary cirrhosis, cholestasis of pregnancy, viral hepatitis, and anything that causes obstructive jaundice.
  • Renal disease: We think about this in uremia, but it is actually common even in dialyzed patients. Worse at night or after a dialysis session,
  • Malignancy/hematologic disorders: More often with hematologic malignancies than with solid tumors. Think of: Hodgkin’s disease, Polycythemia vera (worse in water), Carcinoid (thank you, histamine), and cutaneous T cell lymphoma. Patients without a diagnosis for their pruritus may be at increased risk for malignancy.
  • Thyrotoxicosis: cause you can’t have a list without thyroid on it. Actually, a fairly common sx of Graves disease.  hypothyroidism can cause xerosis, which itches
  • Connective Tissue Disease: Common with dermatomyositis and scleroderma in particular.

Brachioradial pruritus


Small fiber neuropathy may be associated with pruritus, so anything that causes neuropathy could lead to itching, including diabetes.  These are typically localized to the affected area, however.

  • Post herpetic neuralgia: Up to 50% of patients with post herpetic neuralgia experience this as itching rather than pain.
  • Notalgia Paresthetica: Itching on the upper back, perhaps due to trapped nerve fibers in the T2-T6 nerve roots. Unilateral, near the medial or upper border of the scapula.
  • Brachioradial pruritis: Itching of the proximal dorsolateral forearm, but may extend up to the upper arm or even trunk. Feels better with ice application. Similar to notalgia paresthetica, this may be related to nerve root entrapment in C5-C8, but also may have something to do with sun exposure.
  • MS: Compared to the rest on this list, MS is more likely to cause generalized pruritus. Typically a relapsing, remitting type course that mirrors the rest of the disease.


  • Psychogenic excoriation: Skin is normal, but affected individuals pick and scratch at it. Lesions are all within reach of the patient, and may be precipitated by psychologic stressors.
  • Delusional parasitosis: Patients experience a firm, fixed belief that they are infested by parasites, despite a lack of evidence of infestation.  This may be secondary to another psychiatric disorder, or may be the primary disorder itself.
  • No matter the underlying etiology, pruritus may get worse under emotional stress.

For many, the itching itself causes emotional stress. It impacts sleep, work, relationships. Relief can really improve your patient’s quality of life, plus you may uncover a systemic disease earlier.

If you are itching after reading this post, that is probably psychogenic itching. Good luck!


Lumps and Bumps

So, I realize that I have a tendency to call every bump I see on a patient either a lipoma (if it’s squishy) or a sebaceous cyst (if it’s not) and tell them not to worry.  Thought it might be time to refine my diagnostic skills a little.  Thanks to Up to Date and Visual Dx for the pictures, and thanks to Ashley Haddad for inspiring this one…


We’ll talk about these “tumors” based onwhere they come from:

Dermal Tumors

Skin Tags (fancy name, Acrochordon) Single or Multiple pedunculated lesions on narrow stalks. Often grow in areas of friction: neckline, axilla, inframammary regions. Easy to remove, but bleed freely.


  • Dermatofibromas Firm, hyperpigmented lesions, most commonly on lower extremities.  Made of benign proliferation of fibroblasts. Dimple when the edges are pinched together (nevi don’t do that).  Can recur if removed, sometimes the scar looks worse than the original lesion.


  • Neurofibromas We are used to thinking about 100s of lesions in patients with NF, but can occur as sporadic lesions in healthy adults.  Soft, usually flesh colored papules- less than 3cm. Some will retract when pushed (Button-hole sign).

Cutaneous_neurofibromaneurofibroma button hole

Epidermal Tumors

  • Seborrheic Keratosis Hyperpigmented, waxy, “stuck on” papules. Often warty or scaly in appearance. Looks like you could just scrape it off.  Don’t forget the “sign of Leser-Trelat,” which is the sudden appearance of 100s of SKs, acrochordons, and acathosis nigricans.  This is associated with underlying malignancy, often lung or GI.


  • Epidermoid Cyst  This is the all too common “sebaceous cyst.”  It is actually a cyst of normal epidermal tissue that has somehow gotten down into the dermis.  The cyst is filled with keratin produced by the epidermis- not sebum.  There is often (but not always) a punctum, and the cyst can drain a thick, cheesy, foul smelling material.  They can become inflamed or infected.

epidermoid cyst 3 epidermoid cyst2 epidermoid cyst

Appendage Tumors (Appendages? Skin appendages include hair, nails, glands, arrector pili muscles)

  • Pilar Cysts These come from the hair follicle, often grow on the scalp.  They are filled with keratin, may not have a punctum.  They tend to calcify and feel very firm, more than epidermoid cysts. They get tender if they rupture.


  • Pilomatricoma Probably come from certain cells in the hair follicle.  Smaller than Pilar cysts, often bluish or reddish discoloration.  These can also become calcified and feel quite hard.


Vascular Tumors

  • Cherry angioma Capillary proliferation, most commonly found on the trunk.  Dome shaped, blanch with pressure.


  • Pyogenic granuloma can occur on skin or mucus membranes, grows quickly and has a friable surface that bleeds profusely. Bigger than cherry angiomata.


Fatty tumors

  • Lipomas collection of mature fat cells. Often looks like a “ball” under the skin. Is soft, not painful, slow growing.  Biopsy if it is painful, restricts movement, or is growing quickly.


  • Angiolipoma  Looks like a lipoma, but is a collection of fat cells and capillaries. These may occur in groups, and are painful. May occur in HIV patients after starting anti-retroviral therapy.


Dermoid Cysts I gave these their own category. They are embryonic remnants of skin formation- with epithelial, glandular, and hair elements, and may communicate with the central nervous system.  They occur along the embryonic lines of cleavage. Most  common spot is on the eyebrow, also on forehead, scalp, floor of the mouth.  As these may communicate with the CNS- don’t attempt to excise scalp lesions without imaging. dermoid cyst

Skin Deep

It’s time for this blog to live up to its name and do a dermatology post.   Today… topical steroids.  This was always kind of a black box for me, I never knew which steroid to pick, and sort of did so randomly.  But there is some method to the madness if you understand relative potency.  Target the condition and the location with the right potency and you will be in good shape.  The thicker the skin or the “thicker” the dermatitis, the higher potency medicine you will need to penetrate it.  Also, higher potency creams come with higher risk for side effects- thinning skin, telangiectasias, and even systemic absorption.  So use them sparingly and for a short a time as possible.
A word about vehicles.  The more “goopy” an agent is, the more potent.

There are some other interesting vehicles available.  In general, a gel will give the potency of the ointment without the grease factor.  Foams are handy for hairy areas- Clobetasol (Olux) foam is
useful for thick seborrheic dermatitis or psoriasis in the hairline. 

You can also increase the potency by putting something under occlusion, either by covering it with an emollient like Vaseline or by simply covering it with a bandage, or the ever helpful white cotton sock.

On with the list. I would suggest learning one or two choices for a super high, high, and low potency steroid and just stick to those.  I’ve added some brand names below because those are easier to remember. Simplify, simplify, simplify…

Super High Potency: Class 1 
Think thick: thick skin or thick plaques of dermatitis
Location: palms and soles
Disease: severe dermatitis (contact or allergic/eczema), psoriasis
Duration: less than 3 weeks
Agents: Betamethasone diproprionate(Diprolene), Clobetasol proprionate (Temovate or Olux foam)
High Potency: Classes 2-3 
Location: arms/legs, back, trunk
Duration: 6-8 weeks
Agents: 0.5% triamcinolone ointment (Kenalog), Fluocinonide (Lidex)
Medium Potency: Classes 4-5
Location: face, intertriginous areas, large areas (risk of systemic absorbtion)
Agents: 0.1% triamcinolone ointment (Aristocort), 0.1% Hydrocortisone butyrate (Locoid)
Low Potency: Classes 6-7. 
Think thin: thin skin, not much disease. This is where the OTC steroid creams are.  
Location: eyelid, genitalia 
Agents: 0.5% Hydrocortisone base (Cortaid)