A patient presents with a rash. In emergency medicine we often recognize certain rashes at a glance, like urticaria or a viral exanthem. This does not fit any of those. The patient is scratching vigorously. Is this atopic dermatitis, commonly known as eczema?


Eczema might be the most common rash we see in the emergency department but its presentations are diverse so it is not always a “know it at a glance” diagnosis. We can get tricked. The etymology of eczema is “out boiling.” which describes that rash that is papulovesicular with erythema and weeping and crusting. A lot of rashes do that of course.


Atopic dermatitis is a special disease that arises from a defect in the epithelial connections between cells. When you understand that, you can diagnose it, and you can treat it.


The epithelial defect leads to microscopic “holes” in the skin. Water gets out, and irritants get in. Itching is dramatic.


Here is how you diagnose atopic dermatitis in the emergency department:

-Pruritus is a must

-The classic inflammatory rash of eczema (papulovesicular with erythema and weeping)

Allow for hyperkeratosis if the lesions are subacute or chronic

Allow for findings of excoriation


So far that hasn’t nailed down the specificity yet. Any inflammatory rash will do all that. Poison oak, for example will do the same thing.


Add in the specificity with:

dry skin by history or current presentation (defect in skin barrier)

distribution is flexural or hands by history or current presentation (areas of trauma and friction)

-history of atopic diseases or childhood onset


Now that you have the diagnosis, it is all about restoring hydration, and restoring the skin barrier. Have them take baths, hydrate the skin, and then lock it in with ointment. Teaching that will empower them to be less reliant on steroids.



-Suspect atopic dermatitis by severe itching and an inflammatory rash

-Localizes to areas of friction (hands or flexural areas)

-Dry skin prominent

-History of allergies or asthma

-Usually childhood onset




Cellulitis, when you think about it, is probably not the most helpful term. Literally, it means “infection of cells.” What cells? The anatomical area is actually the dermis, as well as the subcutaneous tissue.


A patient presenting with “dermitis” has a lesion that is clearly confined to the skin. A patient presenting with significant edema has involvement of subcutaneous tissues. These are the patients where we need to consider the surgical diseases: necrotizing fasciitis, pyomyositis, and abscess.


There is very little in the literature about palpation of the erythematous lesion. However, extensive induration might be the trigger that leads you to perform an ultrasound, and find an abscess.


The other traditional role for palpation is with erysipelas. This streptococcal infection is most commonly encountered in the lower extremities. Traditionally it was thought of as confined to the epidermis, palpable, with sharp borders. But now it is believed that erysipelas and cellulitis are the same disease, on a spectrum depending on how superficial the infection is.[Kilburn Cochrane Database Syst Rev. 2010]


Palpation in cellulitis probably does not receive enough attention in the medical literature. The next time you have a patient with cellulitis, pay particular attention to palpation. It may signal to you that there is something deeper to find on ultrasound.


Take home points:

Erythema of the skin sometimes hides something below

Use palpation to better understand where the inflammation is located


A young child presents with blistering exfoliation over the face and neck. It started around the mouth. It has the appearance of impetigo, with the honey crusted lesions, but other areas have confluent denuding of the skin. You wonder whether this could be staphylococcal scalded skin syndrome (SSSS) or toxic epidermal necrolysis(TEN). How can these be differentiated at the bedside?


These diseases can be differentiated by the thickness of the skin. The toxin of SSSS cleaves at the stratum granulosum so the exfoliation is a very thin layer. TEN is full thickness. An online images search reveals how differently these diseases appear.


You look again at the child and see that the blistering reveals a very thin layer. That, in addition to the lack of mucus membrane involvement, and the confluent erythema of surrounding areas suggests that this is not TEN, but is staphylococcal. The toxin of impetigo and SSSS is the same. Given that this started around the mouth and spread from there, you diagnose severe impetigo.


Take Home Points

The toxin of SSSS (and impetigo) cleaves superficially, leaving thin blisters or flaking

TEN causes full thickness blistering



If atopic dermatitis is an atopic disease, why does it only proceed to asthma and allergic rhinitis in 30 and 35% of cases, respectively?(Williams, NEJM 2005)  And why would an allergic disease tend to present at areas of friction or moisture, the extensor surfaces in babies (the friction is from crawling) and in flexural areas in adults?  Or the somewhat peculiar hands and feet eczema?


Atopic dermatis is now believed to be a disease of the epidermal barrier. Breaches in the skin can introduce allergens that secondarily produce an atopic response. This understanding offers much better explanatory power, and helps make sense of the disparate bedside findings. For example, hand eczema is often provoked by occupational hazards, such as the wet hands of one who works for a restaurant. It also explains why eczema patients have dry skin – the epidermal integrity is breached, and water loss occurs.


One of the key findings in atopic dermatitis is pruritus. It has been called not an eruption that itches but an itch that erupts.


Here are a number of additional findings:

Itch when sweating

Intolerance to wool and lipid solvents

Cutaneous infections


Pityriasis alba

Hyperkeratosis, palmar hyperlinearity



Take Home Points:

Atopic dermatitis is a disease of the epidermal barrier

Pruritus is the hallmark

The distribution reflects vulnerabilities to epidermal breakdown (eg friction and moisture)


A patient presents with pruritus and excoriations.  He has a poor social situation and appears disheveled.  Could this be scabies?


Although some diagnostic algorithms are as simple as finding itching in 2 areas of the body (Mahé Trans R Soc Trop Med Hyg 2005) a closer look may prove rewarding.


Distribution: Infection is spread by direct contact, so regardless of where the infection started, the hands and wrists tend eventually to become infected.(Fathy J Egypt Soc Parasitol 2010) Other prominently affected areas include extensor surfaces, the genitalia, and axillary skin. The head and neck generally are spared.



The lesions eventually just look like excoriations. However, in earlier stages they are papulovesicular or nodular.


A closer look

Burrows are pathognomonic.  The term burrow seems to imply that the mites go deep.  They do not. These are just epidermal tunnels. The mite makes a serpiginous run through the stratum corneum, chewing up dead skin cells along the way.  A silvery burrow can sometimes be seen on close examination with a 0.3mm mite at the very end. They look like a tiny splinter hemorrhage.


Burrow ink test

The original burrow ink test was intended to reveal occult burrows. Rub low viscosity ink on the affected area, wipe off with alcohol, and the tract might be revealed. Tetracycline is used if you intend to cover a large area.  The tracts are then visible in ultraviolet light.


Diagnosis can be confirmed with scraping and slide review.  The diagnosis is made by finding eggs, mites, or feces. Dermatologists can do this at the bedside using dermoscopy.  Generally though this is a clinical diagnosis and such studies are not necessary in the emergency department.



-Scabies prominently affects the hands and avoids the head and neck

-Lesions can be nodular or papulovesicular before being excoriated

-Epidermal burrows are pathognomonic, and sometimes the mite is seen at the end

-The burrow ink test can be used to reveal occult burrows


A patient presents with extensive burns to the left hand.  None of the fingers have circumferential burns, but both volar and dorsal aspects do have larger territories affected, with extensive skin sloughing.  How do we use bedside physical examination to guide prognosis and treatment?

The physical examination of burns is essentially a microcirculatory examination for signs of viability.  We are evaluating the viability of the dermis, because this is the organ thath will help mediate wound healing.  It has a plexus of vessels and nerves, so the burn examination assesses neurological and circulatory function of the dermis.

First degree burns are easily defined.  Everything is viable.  It hurts and it is red or pink with normal blanching, which is a sign of increased blood flow.  Every aspect of neurological sensation is normal.  Furthermore, the skin is intact, without blistering.

Third degree burns are, sadly, also quite clear.  The dermis is dead.  The skin is white and leathery.  Sensation to light touch is absent. There are no signs of viability, whether of sensation or of circulation.  Skin that is red but does not blanch means the blood is extravascular, and this is consistent with a third degree burn.  The patient will generally need skin grafting, except for some very small burns <1cm.

Second degree burns, also called partial thickness burns, pose more subtle complexity, and an astute physical examination is needed.  We differentiate superficial partial thickness from deep partial thickness burns.

Superficial partial thickness burns basically just mean first degree viability, but there is some blistering.  The stratum corneum was breached, which separates as a thin blister.  If the tissue beneath has good signs of circulation then this is a superficial partial thickness burn. Signs of good circulation include a healthy pink appearance, normal capillary refill, and normal sensation.  The prognostic importance of a superficial partial thickness burn is that the stratum corneum defense layer has been breached, and topical antibiotics will be needed when the blister breaks.

Deep partial thickness burns mean there are signs of both life and death. On neurological examination, sensation might be present but subjectively diminished.  On circulatory examination, areas are white, but areas are also pink or red and blanch on pressure.   The prognostic importance of a deep partial thickness burn is that prolonged healing is expected and skin grafting may be needed.

The examination changes with time

Because of the intermediate zone of stasis, the classification of the injury may require repeat examination in 1-2 days.  In a full thickness burn, the zone of coagulation looks dead and is dead.  But the intermediate zone of stasis is red, blanches with pressure on day 1, but stops blanching or turns white on day 2 or 3.  Only on day 2 or 3 can we confirm that this is a deep partial thickness burn.  Clues that this might turn out to be the case include early petechiae, a sign that the vessel integrity is compromised.

Additionally, a first degree burn on day 1 might blister by day 2, and then reveal a second degree burn.  Interval follow-up is indicated in all burns where there is any doubt.

Back to the case:

At the bedside, you take a closer look and find areas of pallid appearance, and areas of blanching red.  Sensation is intact and normal.  There are signs of death, and signs of life.  This is a deep partial thickness burn.  Because it affects a critical area (the hand), the patient requires transfer to a burn center.

Take home points:

-repeat examination in 1-2 days is required to reliably classify a burn

-Skin uniformly alive: first degree or superficial partial thickness, excellent prognosis

-Skin uniformly dead: 3rd degree, generally requires skin grafting

-Skin has mix of circulatory/neurologic life and death: deep partial thickness burn, may need skin grafting if wound not expected to heal within 3 weeks


You evaluate a patient with a rash, and as you look, you notice small patches of purple lesions that are circular in distribution.  You recognize what appears to be purpura.  The differential diagnosis is long, and includes hematologic, infectious, and immune mediated conditions.  How can we use physical diagnosis to narrow the differential diagnosis at the bedside?

Blanching: Intravascular vrs extravascular

First, apply pressure to see if it blanches.  Dermatologists use glass and call it diascopy.  In the ED we just press, let go, and we have a quick look to see if it had blanched.  Blanching indicates the color is intravascular, like erythema from a rash.  If it blanches, it is not purpura.  Nonblanching indicates the problem is extravascular.  Your patient’s lesion does not blanch.

Palpable purpura: Inflammation

Next, is it palpable? Nonpalpable purpura is caused by blood leaking out of a normal blood vessel, either because of trauma or a hematologic problem.  The most common benign cause is senile or actinic purpura in the elderly, where a thin dermis renders the capillaries vulnerable to minor trauma.  A normal bruise is not palpable, nor is the purpura from thrombocytopenia and coagulation defects.

In contrast, palpable purpura means there is inflammation around the blood vessels.  Your patient’s lesions are palpable.  You have now narrowed the differential diagnosis to a vasculitis, or an infection causing inflammation around the blood vessels.  The most common cause in children is Henoch-Schonlein purpura.  The most common in adults is leukocytoclastic vasculitis, a small vessel vasculitis with various causes.

Meningococcemia is palpable in later stages of the disease but in the early stages may not be palpable, and in very early stages may actually blanch (Riordan 1996).  Petechial lesions restricted to the area above the clavicles generally signifies a benign cause, generally precipitated by coughing or vomiting (Wells 2001).

Physical diagnosis narrows the differential diagnosis of purpura to a more manageable degree. With the use of pressure to check for blanching, one can confirm whether the purple hue is intravascular or extravascular.  If it is extravascular then this suggests purpura. One can then check for palpable purpura to decide if inflammation is present.  In this manner, one can pursue this diagnosis to the highest degree at the bedside.  Depending on the findings, a phone call to the local dermatologist, rheumatologist, or hematologist and oncologist can expedite this patient’s definitive care.


-Blanching suggests a vascular cause.  Nonblanching supports purpura.

-Palpable purpura supports an inflammatory cause such as vasculitis or a systemic infection


A patient recently presented with a subcutaneous nodule that appeared to be an abscess.  It was raised, erythematous, tender, indurated, and had a central plug…wait, no, it had a central hole.  And he just got back from Belize.  We put a transparent membrane on it to see if there was a creature in there.  Sure enough, a snout pushed at the membrane, seeking air.  This established the diagnosis – myiasis, secondary to a bot fly bite.

Trying to remove that larvae was an ordeal.  These creatures don’t want to leave their cubby, and trying to pull them out is like trying to give a cat a bath.  We finally decided to leave the membrane in place.  The next morning the larva was dead, and my colleague removed it.

Other skin lesions that can be confused with an abscess include a brown recluse bite.  Reportedly a blue lesion, surrounded by concentric rings of pallor (ischemia) and then erythema (vasodilation) are classic for the brown recluse bite (Rogers 2011).


A patient presents with a chronic diabetic heel ulcer that has worsened over the past few weeks.  Could this be osteomyelitis?

It turns out that physical examination findings can significantly raise or lower the probability of this diagnosis. According to JAMA’s rational clinical examination series (Butalia 2008), 2 findings on physical examination have more powerful likelihood ratios than MRI:

-A crater breadth of 2 square cm or more has a positive LR of 7.2.

-Probing to bone has a positive LR of 6.4.

Take Home Points:

Osteomyelitis is more likely when the chronic wound is more deep and more broad