Bullous pemphigoid

Bullous pemphigoid is a chronic, inflammatory, subepidermal, blistering disease. If untreated, it can persist for
months or years, with periods of spontaneous remissions and exacerbations. The disease can be fatal, particularly
in patients who are debilitated.

Signs and symptoms

Bullous pemphigoid may present with several distinct clinical presentations, as follows:

 : The most common presentation; tense bullae arise on any part of the skin surface, with a predilection for
the flexural areas of the skin
 Vesicular form: Less common than the generalized bullous type; manifests as groups of small, tense
blisters, often on an urticarial or erythematous base
 Vegetative form: Very uncommon, with vegetating plaques in intertriginous areas of the skin, such as the
axillae, neck, groin, and inframammary areas
 Generalized erythroderma form: This rare presentation can resemble psoriasis, generalized atopic
dermatitis, or other skin conditions characterized by an exfoliative erythroderma
 Urticarial form: Some patients with bullous pemphigoid initially present with persistent urticarial lesions
that subsequently convert to bullous eruptions; in some patients, urticarial lesions are the sole
manifestations of the disease
 Nodular form: This rare form, termed pemphigoid nodularis, has clinical features that resemble prurigo
nodularis, with blisters arising on normal-appearing or nodular lesional skin
 Acral form: In childhood-onset bullous pemphigoid associated with vaccination, the bullous lesions
predominantly affect the palms, soles, and face
 Infant form: In infants affected by bullous pemphigoid, the blisters tend to occur frequently on the palms,
soles, and face, affecting the genital areas rarely; 60% of these infant patients have generalized blisters [1]

See Clinical Presentation for more detail.

Diagnosis

To establish a diagnosis of bullous pemphigoid, the following tests should be performed:

 Histopathologic analysis: From the edge of a blister; the histopathologic examination demonstrates a
subepidermal blister; the inflammatory infiltrate is typically polymorphous, with an eosinophil
predominance; mast cells and basophils may be prominent early in the disease course
 Direct immunofluorescence (DIF) studies: Performed on normal-appearing, perilesional skin (see the
image below)
 Bullous pemphigoid is a chronic inflammatory disease. If untreated, the disease can persist for months or
years, with periods of spontaneous remissions and exacerbations. In most patients who are treated, bullous
pemphigoid remits within 1.5-5 years. Patients with aggressive or widespread disease, those requiring high
doses of corticosteroids and immunosuppressive agents, and those with underlying medical problems have
increased morbidity and risk of death. Because the average age at onset of bullous pemphigoid is about 65
years, patients with bullous pemphigoid frequently have other comorbid conditions that are common in
elderly persons, thus making them more vulnerable to the adverse effects of corticosteroids and
immunosuppressive agents.
 Bullous pemphigoid may be fatal, particularly in patients who are debilitated. The proximal causes of
death are infection with sepsis and adverse events associated with treatment. Patients receiving high-dose
corticosteroids and immunosuppressants are at risk for peptic ulcer disease, GI bleeds, agranulocytosis,
and diabetes.
 Bullous pemphigoid involves the mucosa in 10-25% of patients. Patients who are affected may have
limited oral intake secondary to dysphagia. Erosions secondary to rupture of the blisters may be painful
and may limit patients' daily living activities. Blistering on the palms and the soles can severely interfere
with patients' daily functions.
 Bullous pemphigoid lesions typically heal without scarring or milia formation. In a survey of patients
conducted in a Midwest United States university medical center, no difference was noted in expected
 mortality in bullous pemphigoid 223 patients compared with the general population.[32] In a population-
based cohort study in the United Kingdom, however, the risk of death for bullous pemphigoid patients was
found to be twice as great as that for controls.[31] Furthermore, a Swiss prospective study confirmed a high-
case fatality rate, with increased 1-year mortality compared with the expected mortality rate for age-
adjusted and sex-adjusted general population.[33]
 Race
 No racial predilection is apparent.
 Sex
 The incidence of bullous pemphigoid appears to be equal in men and women.
 Age
 Bullous pemphigoid primarily affects elderly individuals in the fifth through seventh decades of life, with
an average age at onset of 65 years. Bullous pemphigoid of childhood onset has been reported in the
literature. It is suggested that the childhood-onset bullous pemphigoid may be more self-limited.[34] One
puzzling finding, however, is a report of rising incidence of infant-onset bullous pemphigoid.

 Laboratory Studies
 To establish a diagnosis of bullous pemphigoid, the following tests should be performed: histopathologic
analysis from the edge of a blister and DIF studies on normal-appearing perilesional skin. If the DIF result
is positive, indirect immunofluorescence (IDIF) is performed using the patient's serum. The preferred
substrate for IDIF is salt-split normal human skin substrate.
 Direct immunofluorescence studies
 DIF studies demonstrate in vivo deposits of antibodies and other immunoreactants, such as complement.
DIF tests usually demonstrate IgG (70-90% of patients) and complement C3 deposition (90-100% of
patients) in a linear band at the dermal-epidermal junction. This pattern of immunoreactants is not specific
for bullous pemphigoid and may be seen in cicatricial pemphigoid and epidermolysis bullosa acquisita.
Bullous pemphigoid can be differentiated from these conditions by incubating the patient's skin biopsy
sample in 1 mol/L salt prior to performing the DIF technique. This process induces cleavage through the
lamina lucida. DIF on salt-split skin reveals IgG on the blister roof (epidermal side of split skin) in patients
with bullous pemphigoid, while, in CP and EBA, the IgG localizes to the blister floor (dermal side of split
skin).
 The optimal location for DIF testing is normal-appearing perilesional skin. False-positive results can be
observed when it is performed on lesional skin. Rarely, skin biopsy samples placed in transport media may
yield false-negative results. This observation makes the use of fresh tissue the preferred substrate for DIF
studies. See the image below.

 Direct immunofluorescence study performed on a

perilesional skin biopsy specimen from a patient with bullous pemphigoid detects a linear band of immunoglobulin
G deposit along the dermoepidermal junction.

 Indirect immunofluorescence
 IDIF studies document the presence of IgG circulating autoantibodies in the patient's serum that target the
skin basement membrane component. Seventy percent of patients with bullous pemphigoid have
circulating autoantibodies that bind to split skin. The titer of circulating antibody is not correlated with the
disease course.
  IDIF studies can be used to detect the patient's IgG circulating autoantibodies that bind to the epidermal
roof (upper part) of the salt-split skin substrate. See the image below.
 As in other autoimmune bullous diseases, the goal of therapy is to decrease blister formation, to promote
healing of blisters and erosions, and to determine the minimal dose of medication necessary to control the
disease process. Therapy must be individualized for each patient, keeping in mind preexisting conditions
and other patient-specific factors.
 Treatment is directed at reducing the inflammatory response and autoantibody production. Although
target-specific therapy is the "Holy Grail" for immunodermatologists, non–target-specific treatments are
currently used. The most commonly used medications are anti-inflammatory agents (eg, corticosteroids,
tetracyclines, dapsone) and immunosuppressants (eg, azathioprine, methotrexate, mycophenolate mofetil,
cyclophosphamide). An article from Europe provided evidence that strong topical corticosteroid treatment
may achieve disease control while avoiding systemic adverse effects from systemic corticosteroids.[44, 3, 2]
 Proper treatments of bullous pemphigoid depend on the severity of the disease. For localized disease,
topical steroids plus the systemic anti-inflammatory (tetracycline and nicotinamide) may be sufficient.
Effects of monotherapy with nicotinamide are unknown. For more severe cases, systemic steroids along
with immunosuppressives may be needed to control the disease. If the disease is difficult to control,
consider treatment with an anti-CD20 antibody (rituximab), which is relatively specific in targeting the
antibody-producing B cells.[45, 46, 47, 48, 49, 50]

 Indirect immunofluorescence study performed on

salt-split normal human skin substrate with the serum from a patient with bullous pemphigoid detects
immunoglobulin G class circulating autoantibodies that bind to the epidermal (roof) side of the skin basement
membrane.

Eczema Treatment

Patient Comments Read 24 Comments Share Your Story

Treatment for eczema can be managed at home by changing laundry detergents or soaps that may be causing the
irritant. Avoid tight-fitting or rough clothing. Avoid scratching the affected area. Medical treatment include
prescription anti-inflammatory medications, and steroid creams. Antibiotics may have to be prescribed to clear the
affected irritation.

Eczema Home Remedies

Removing exacerbating factors is a good place to start. This may be as simple as changing the laundry detergent to
one that is fragrance free or as difficult as moving to a new climate or changing jobs.

Prevent dry skin by taking short, lukewarm showers or baths. Use a mild soap or body cleanser. Prior to drying
off, apply an effective emollient to wet skin. Emollients are substances that inhibit the evaporation of water.
Generally, they are available in jars and have a "stiff" consistency. They do not flow and ought to leave a shine
with a slightly greasy feel on the skin. Most good emollients contain petroleum jelly although certain solid
vegetable shortenings do a more than creditable job. The thicker, the better, although patient preference is usually
toward thinner lotions because of ease of application and avoidance of a greasy feel.

A patient with longstanding eczema may become sensitized to the products they are putting on the skin and
develop allergic contact dermatitis that may be identical in clinical appearance. Skin allergy may develop to over-
the-counter (OTC) products such as topical anesthetics, topical diphenhydramine (Benadryl), lanolin, coconut oil,
and tea tree oil or even prescription medications such as topical steroid creams.

Avoid wearing tight-fitting, rough, or scratchy clothing.

Avoid scratching the rash. If it's not possible to stop scratching, cover the area with a dressing. Wear gloves at
night to minimize skin damage from scratching.

Anything that causes sweating can irritate the rash. Avoid strenuous exercise during a flare.

An anti-inflammatory topical cream may be necessary to control a flare of atopic dermatitis.

 Apply a nonprescription steroid cream (1% hydrocortisone). The cream must be applied two to four times a day
without skipping days until the rash is gone.
 Diphenhydramine (Benadryl) in pill form may be taken for the itching. Caution: This medication may make people
too drowsy to drive a car or operate machinery safely. The topical form may sensitize people and cause allergic
contact dermatitis.
 Clean the area with a hypoallergenic soap as necessary. Most antibacterial soaps are too irritating for eczema
patients. Apply an emollient over the topical steroid.

Avoid physical and mental stress. Eating right, light activity, and adequate sleep will help someone stay healthy,
which can help prevent flares.

Do not expect a quick response. Atopic dermatitis is controllable but consistency in application of treatment
products is necessary. Continue Reading

Henoch–Schönlein purpura
From Wikipedia, the free encyclopedia
Henoch-Schönlein purpura

Typical purpura on lower legs and buttocks

Classification and external resources
Specialty Dermatology
ICD-10 D69.0
 (ILDS D69.010)
ICD-9-CM 287.0
DiseasesDB 5705
MedlinePlus 000425
derm/177 emerg/767 emerg/845
eMedicine
ped/3020
MeSH D011695

Henoch–Schönlein purpura (HSP, also known as anaphylactoid purpura,[1] purpura rheumatica,[1] and
Schönlein–Henoch purpura)[1] is a disease of the skin and other organs that most commonly affects children. In
the skin, the disease causes palpable purpura (small hemorrhages); often with joint and abdominal pain. With
kidney involvement, there may be a loss of small amounts of blood and protein in the urine, but this usually goes
unnoticed; in a small proportion of cases, the kidney involvement proceeds to chronic kidney disease. HSP is often
preceded by an infection, such as a throat infection.

HSP is a systemic vasculitis (inflammation of blood vessels) and is characterized by deposition of immune
complexes containing the antibody IgA; the exact cause for this phenomenon is unknown. It usually resolves
within several weeks and requires no treatment apart from symptom control, but may relapse in a third of the cases
and cause irreversible kidney damage in about one in a hundred cases.

Contents
 1 Signs and symptoms
 2 Pathophysiology
 3 Diagnosis
o 3.1 Classification
 4 Treatment
 5 Prognosis
o 5.1 Kidney involvement
 6 Epidemiology
 7 History
 8 See also
 9 References

Signs and symptoms

Typical purpura on lower leg

More severe case of HSP on child's foot, leg, and arm

Purpura, arthritis and abdominal pain are known as the "classic triad" of Henoch–Schönlein purpura.[2] Purpura
occur in all cases, joint pains and arthritis in 80%, and abdominal pain in 62%. Some include gastrointestinal
hemorrhage as a fourth criterion; this occurs in 33% of cases, sometimes, but not necessarily always, due to
intussusception.[3] The purpura typically appear on the legs and buttocks, but may also be seen on the arms, face
and trunk. The abdominal pain is colicky in character, and may be accompanied by nausea, vomiting, constipation
or diarrhea. There may be blood or mucus in the stools.[4] The joints involved tend to be the ankles, knees, and
elbows, but arthritis in the hands and feet is possible; the arthritis is nonerosive and hence causes no permanent
deformity.[2] Forty percent have evidence of kidney involvement, mainly in the form of hematuria (blood in the
urine), but only a quarter will have this in sufficient quantities to be noticeable without laboratory tests.[3]
Problems in other organs, such as the central nervous system (brain and spinal cord) and lungs may occur, but is
much less common than in the skin, bowel and kidneys.[5]

Of the 40% of patients who develop kidney involvement, almost all have evidence (visible or on urinalysis) of
blood in the urine. More than half also have proteinuria (protein in the urine), which in one eighth is severe
enough to cause nephrotic syndrome (generalised swelling due to low protein content of the blood). While
abnormalities on urinalysis may continue for a long time, only 1% of all HSP patients develop chronic kidney
disease.[5] Hypertension (high blood pressure) may occur. Protein loss and high blood pressure, as well as the
features on biopsy of the kidney if performed, may predict progression to advanced kidney disease. Adults are
more likely than children to develop advanced kidney disease.[5][6]

Pathophysiology
Henoch–Schönlein purpura is a small-vessel vasculitis in which complexes of immunoglobulin A (IgA) and
complement component 3 (C3) are deposited on arterioles, capillaries, and venules. As with IgA nephropathy,
serum levels of IgA are high in HSP and there are identical findings on renal biopsy; however, IgA nephropathy
has a predilection for young adults while HSP is more predominant among children. Further, IgA nephropathy
typically only affects the kidneys while HSP is a systemic disease. HSP involves the skin and connective tissues,
scrotum, joints, gastrointestinal tract and kidneys.[7]

Diagnosis

Immunostaining showing IgA in the glomerulus of a patient with Henoch-Schönlein nephritis

The diagnosis is based on the combination of the symptoms, as very few other diseases cause the same symptoms
together. Blood tests may show elevated creatinine and urea levels (in kidney involvement), raised IgA levels (in
about 50%[7]), and raised C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) results; none are
specific for Henoch–Schönlein purpura. The platelet count may be raised, and distinguishes it from diseases where
low platelets are the cause of the purpura, such as idiopathic thrombocytopenic purpura and thrombotic
thrombocytopenic purpura.[2]

If there is doubt about the cause of the skin lesions, a biopsy of the skin may be performed to distinguish the
purpura from other diseases that cause it, such as vasculitis due to cryoglobulinemia; on microscopy the
appearances are of a hypersensitivity vasculitis, and immunofluorescence demonstrates IgA and C3 (a protein of
the complement system) in the blood vessel wall.[2] However, overall serum complement levels are normal.

On the basis of symptoms, it is possible to distinguish HSP from hypersensitivity vasculitis (HV). In a series
comparing 85 HSP patients with 93 HV patients, five symptoms were found to be indicative of HSP: palpable
purpura, abdominal angina, digestive tract hemorrhage (not due to intussussception), hematuria and age less than
20. The presence of three or more of these indicators has an 87% sensitivity for predicting HSP.[8]

Biopsy of the kidney may be performed both to establish the diagnosis or to assess the severity of already
suspected kidney disease. The main findings on kidney biopsy are increased cells and Ig deposition in the
mesangium (part of the glomerulus, where blood is filtered), white blood cells, and the development of crescents.
The changes are indistinguishable from those observed in IgA nephropathy.[7]

Microphotograph of a histological section of human skin prepared for direct immunofluorescence using an anti-
IgA antibody, the skin is a biopsy of a patient with Henoch-Schönlein purpura. IgA deposits are found in the walls
of small superficial capillaries (yellow arrows). The pale wavy green area on top is the epidermis, the bottom
fibrous area is the dermis.

HSP can develop after infections with streptococci (β-haemolytic, Lancefield group A), hepatitis B, herpes
simplex virus, parvovirus B19, Coxsackievirus, adenovirus, Helicobacter pylori,[5] measles, mumps, rubella,
Mycoplasma and numerous others.[7] Drugs linked to HSP, usually as an idiosyncratic reaction, include the
antibiotics vancomycin and cefuroxime, ACE inhibitors enalapril and captopril, anti-inflammatory agent
diclofenac, as well as ranitidine and streptokinase. Several diseases have been reported to be associated with HSP,
often without a causative link. Only in about 35% of cases can HSP be traced to any of these causes. [7]

The exact cause of HSP is unknown, but most of its features are due to the deposition of abnormal antibodies in
the wall of blood vessels, leading to vasculitis. These antibodies are of the subclass IgA1 in polymers; it is
uncertain whether the main cause is overproduction (in the digestive tract or the bone marrow) or decreased
removal of abnormal IgA from the circulation.[7] It is suspected that abnormalities in the IgA1 molecule may
provide an explanation for its abnormal behaviour in both HSP and the related condition IgA nephropathy. One of
the characteristics of IgA1 (and IgD) is the presence of an 18 amino acid-long "hinge region" between
complement-fixating regions 1 and 2. Of the amino acids, half is proline, while the others are mainly serine and
threonine. The majority of the serines and the threonines have elaborate sugar chains, connected through oxygen
atoms (O-glycosylation). This process is thought to stabilise the IgA molecule and make it less prone to
proteolysis. The first sugar is always N-acetyl-galactosamine (GalNAc), followed by other galactoses and sialic
acid. In HSP and IgAN, these sugar chains appear to be deficient. The exact reason for these abnormalities is not
known.[5][7]

Classification

Multiple standards exist for defining Henoch–Schönlein purpura, including the 1990 American College of
Rheumatology (ACR) classification[9][10] and the 1994 Chapel Hill Consensus Conference (CHCC).[11] Some have
reported the ACR criteria to be more sensitive than those of the CHCC.[12]
More recent classifications, the 2006 European League Against Rheumatism (EULAR) and Pediatric
Rheumatology Society (PReS) classification, include palpable purpura as a mandatory criterion, together with at
least one of the following findings: diffuse abdominal pain, predominant IgA deposition (confirmed on skin
biopsy), acute arthritis in any joint, and renal involvement (as evidenced by the presence of blood and/or protein in
the urine).[13]

Treatment
Analgesics may be needed for the abdominal and joint pains. It is uncertain as to whether HSP needs treatment
beyond controlling the symptoms. Most patients do not receive therapy because of the high spontaneous recovery
rate. Steroids are generally avoided.[5] However, if they are given early in the disease episode, the duration of
symptoms may be shortened, and abdominal pain can improve significantly. Moreover, the chance of severe
kidney problems may be reduced.[14] However, some evidence suggests that steroids do not decrease the likelihood
of developing long-term kidney disease.[15]

Evidence of worsening kidney damage would normally prompt a kidney biopsy. Treatment may be indicated on
the basis of the appearance of the biopsy sample; various treatments may be used, ranging from oral steroids to a
combination of intravenous methylprednisolone (steroid), cyclophosphamide and dipyridamole followed by
prednisone. Other regimens include steroids/azathioprine, and steroids/cyclophosphamide (with or without heparin
and warfarin). Intravenous immunoglobulin (IVIG) is occasionally used.[7]

Prognosis
Overall prognosis is good in most patients, with one study showing recovery occurring in 94% and 89% of
children and adults, respectively (some having needed treatment).[16] In children under ten, the condition recurs in
about a third of all cases and usually within the first four months after the initial attack.[3] Recurrence is more
common in older children and adults.[5]

Kidney involvement

In adults, kidney involvement progresses to end-stage renal disease (ESRD) more often than in children. In a UK
series of 37 patients, 10 (27%) developed advanced kidney disease. Proteinuria, hypertension at presentation, and
pathology features (crescentic changes, interstitial fibrosis and tubular atrophy) predicted progression.[6] About
20% of children that exhibit nephrotic or nephritic features experience long permanent renal impairment.[17]

The findings on renal biopsy correlate with the severity of symptoms: those with asymptomatic hematuria may
only have focal mesangial proliferation while those with proteinuria may have marked cellular proliferation or
even crescent formation. The number of crescentic glomeruli is an important prognostic factor in determining
whether the patient will develop chronic renal disease.[5]

In ESRD, some eventually need hemodialysis or equivalent renal replacement therapy (RRT). If a kidney
transplant is found for a patient on RRT, the disease will recur in the graft (transplanted kidney) in about 35% of
cases, and in 11%, the graft will fail completely (requiring resumption of the RRT and a further transplant).[7]

Epidemiology
HSP occurs more often in children than in adults,[16] and usually follows an upper respiratory tract infection. Half
of affected patients are below the age of six, and 90% are under ten. It occurs about twice as often in boys as in
girls.[5] The incidence of HSP in children is about 20 per 100,000 children per year, making it the most common
vasculitis in children.[18]

Cases of HSP may occur anytime throughout the year, but some studies have found that fewer cases occur during
the summer months.[19]

History
The disease is named after Eduard Heinrich Henoch (1820–1910), a German pediatrician (nephew of Moritz
Heinrich Romberg) and his teacher Johann Lukas Schönlein (1793–1864), who described it in the 1860s.
Schönlein associated the purpura and arthritis, and Henoch the purpura and gastrointestinal involvement. The
English physician William Heberden (1710–1801) and the dermatologist Robert Willan (1757–1812) had already
described the disease in 1802 and 1808, respectively, but the name Heberden–Willan disease has fallen into
disuse. William Osler was the first to recognise the underlying allergic mechanism of HSP.[20]

Emergency Department The Royal Hospital for Sick Children • Yorkhill

Medical Illustr ation Depar tment• Yor khill 178755

Management of the child with a non-blanching rash

Children commonly present with a non blanching rash +/- fever. The important diagnosis to exclude in these
patients is meningococcal disease. However, most (> 90%) of these children who are well with the rash will
have viral infections that require no treatment. They have long presented a diagnostic dilemma to
paediatricians.

Diagnosis
There are a group of conditions which present with a non blanching rash, but have specific features which
will identify them easily:
• Henoch Schonlein purpura (HSP}
• Idiopathic thrombocytopenia (ITP)
• Acute leukaemia
• Haemolytic uraemic syndrome (HUS)
They have other specific signs or symptoms:
HSP
Usually a classical distribution of purpura, bruising and urticaria on the buttocks and extensor surfaces of the
limbs, sometimes associated with joint or abdominal pain
ITP
Usually well children with multiple bruises and petechiae noted over several days
Acute Leukaemia
Symptoms of slower onset associated with anaemia, lymphadenopathy or hepatosplenomegaly
HUS
Oliguria/anuria associated with anaemia, usually following a diarrhoeal illness n
Once the above conditions are ruled out clinically, (see individual guidelines for
assessment and management), we are left with a differential diagnosis as follows: o
n-
• Meningococcal disease (MCD)
• Sepsis with other bacteria (uncommon)
• Viral illnesses

bl
• Trauma//NAI
• Mechanical e.g. due to raised intrathoracic pressure from coughing or vomiting in
superior vena caval distribution (above nipple line).
Evidence is based on retrospective and prospective observational studies, specific points
include:
a
• It is highly unlikely significant bacteraemia is present if the rash is localised to a superior
vena-caval distribution. n
• No single factor, i.e. fbc, CRP can rule out significant bacterial illness on its own.
• Observation of 4 hours is recommended in the majority of cases where diagnosis is
uncertain. c
• The presence of purpura make meningococcal disease more likely. (Petechiae are
pinpoint non-blanching spots. Purpura are larger non-blanching spots (>2mm).
hi
n
g rashEmergency Department Medical Illustr ation

Depar tment• Yor khill 178755 The Royal Hospital for Sick Children • Yorkhill
Management of the child with a non-blanching rash
Use the following algorithm to help discriminate who needs admission and IV antibiotics and who can be
discharged. If in doubt TREAT AS MENINGOCOCCAL SEPSIS.

References
1 Brogan P, Raffles A. The management of fever and petechiae: making sense of rash decisions. Arch
n
o
Dis Child 2000;83:506-507.
2 Nielson HE et al. Diagnostic assessment of haemorrhagic rash and fever. Arch Dis Child 2001
85:160-165.
3 Wells LC, Smith JC, Weston V, Collier J, Rutter N. The child with a non-blanching rash: How likely is
meningococcal disease? Arch Dis Child 2001 85:218-222. n-
bl
4 Van Nguyen Q, Nguyen EA, Weiner LB. Incidence of invasive bacterial disease in children with fever
and petechiae. Pediatrics 1984; 74:77-80.
5 Mandl KD, Stack AM, Fleisher GR. Incidence of bacteremia in infants and children with fever and
petechiae. J Pediatr 1997;131:398-404.
6 Klinkhammer M. Colletti J. Pediatric myth: fever and petechiae. CJEM 2008;10(5):479-82 a
Non Blanching Rash Algorithm
n
c
hing rashEmergency Department
Medical Illustr ation Depar tment• Yor khill 178755 The Royal Hospital for Sick Children • Yorkhill
Purpura
Petechiae
non-blanching rash