11/14/24, 10\:53 AM Non-blanching Rashes

Non-blanching Rashes

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Non-blanching rashes\: caused by small bleeds beneath the skin, appearing as petechiae (\<5mm), purpura (5-10mm), or
ecchymoses (>1cm).
Common causes\: meningococcal sepsis, Henoch-Schönlein purpura, idiopathic thrombocytopaenic purpura, haemolytic
uraemic syndrome, forceful coughing/vomiting, non-accidental injury.
Meningococcal sepsis\: caused by N e i s s e r i a m e n i n g i t i d e s , common in children under 5 and 14-19-year-olds. Symptoms
include fever, neck sti
and hospital transfer needed.
Henoch-Schönlein purpura (HSP)\: IgA-mediated vasculitis, often post-infection. Common in children under 10. Symptoms
include abdominal pain, bloody diarrhoea, joint pain, and a symmetrical rash on the legs and buttocks. Diagnosis is clinical,
with supportive management.
Immune thrombocytopaenic purpura (ITP)\: purpuric rash with low platelets, often post-viral in children. Symptoms include
petechiae and epistaxis. Management involves stopping medications a
and possibly splenectomy.
Haemolytic uraemic syndrome (HUS)\: triad of microangiopathic haemolytic anaemia, acute kidney injury,
thrombocytopaenia, often post E . c o l i O157 infection. Common in children aged 6 months to 5 years. Symptoms include
bloody diarrhoea, abdominal pain, and fever. Management is supportive; notify Public Health England.
Forceful coughing/vomiting\: can cause petechiae in the head, neck, and shoulders. No speci
Non-accidental injury (NAI)\: consider in cases with suspicious distributions of rashes (e.g., hand marks, linear markings).
Requires thorough examination and safeguarding protocols.
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Introduction

Non-blanching rashes are caused by small bleeds in the vessels beneath the skin, giving a purplish discolouration.
Depending on the size of the individual lesions they can be de
Petechiae\: \<5mm diameter (
Purpura\: 5-10mm diameter (
Ecchymoses\: >1cm diameter (
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Figure 1. Petechiae
common causes of non-blanching rashes, including\:
Meningococcal sepsis
Henoch-Schönlein purpura
Idiopathic thrombocytopaenic purpura
Haemolytic uraemic syndrome
Forceful coughing/vomiting
Non-accidental injury

Meningococcal sepsis

Aetiology
Meningococcal meningitis is a central nervous system infection commonly caused by N e i s s e r i a
m e n i n g i t i d e s , a gram-negative diplococcus and commensal of the nasopharynx. Meningococcal sepsis is a complication
of meningitis which occurs when the infection moves beyond the central nervous system into the blood.
Risk factors
Meningococcal meningitis is most common in children under 5 years of age. A second smaller peak has been recognised
in 14-19-year-olds.
Clinical features
History
Typical symptoms of meningococcal sepsis include\:
Fever
Neck sti
Confusion and/or seizures
Clinical examination
If meningitis/meningococcal sepsis is suspected, patients should undergo a thorough examination and the skin should be
assessed for any rashes. Important
Kernig's sign (pain and resistance on passive knee extension with hips fully
Brudzinski’s sign (knees and hips
Non-blanching rash
Photophobia
Hypovolaemic shock\: low blood pressure, high heart rate, capillary re
Investigations
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Investigations must not delay treatment. They may include\:
Baseline blood tests (FBC, CRP, U&E, clotting)\: in
Blood cultures\: may identify a causative organism.
Pharyngeal swab\: to screen for the presence of N e i s s e r i a m e n i n g i t i d e s in the pharynx.
Lumbar puncture\: the de
Management
This is an emergency and the patient will need immediate transfer to hospital. Antibiotics need to be given immediately.
If the patient is seen in primary care intramuscular benzylpenicillin can be given whilst awaiting transfer to hospital. Local
microbiology guidelines should be followed. Generally, initial empirical therapy is\:
Intravenous cefotaxime and amoxicillin in patients under 3 months.
Intravenous ceftriaxone in patients over 3 months old.
In addition, corticosteroids (e.g\: intravenous dexamethasone) is given in those over 3 months old to reduce neurological
complications.
Complications
If not diagnosed and treated swiftly complications can include\:¹
Seizures
Raised intracranial pressure and hydrocephalus
Disseminated intravascular coagulation leading to multi-organ failure and even death
For more information on meningitis, see the Geeky Medics article here.

Henoch-Schönlein purpura (HSP)

Aetiology
Henoch-Schönlein purpura (HSP) is an IgA mediated vasculitis of unknown aetiology. It tends to occur post-
infection with the most common trigger being group A streptococci.
² Risk factors for HSP include\:
Risk factors
Age\: most cases occur in children under 10 years of age with a peak of cases between 4-6 years old.
Season\: usually occurs in autumn/winter months.
Clinical features
History
Typical symptoms of HSP include\:
A prodromal mild upper respiratory tract illness or gastrointestinal infection
Generalised abdominal pain
Bloody diarrhoea
Nausea and vomiting
Joint pain
Clinical examination
Patients with suspected HSP require an abdominal examination and examination of the a

Low-grade fever
Symmetrical rash on the back of the legs, buttocks and arms (Figure 1)
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Figure 4. Henoch Schonlein purpura
Di
In young children, consider intussusception which also presents as bloody diarrhoea and abdominal pain. Intussusception
can also be a complication secondary to HSP. Investigations
following investigations should be performed.
Urinalysis\: to test for the presence of haematuria or proteinuria.
Baseline blood tests (FBC, CRP, U&E, LFT)\: may be helpful in aiding diagnosis.
Skin biopsy\: can be considered if there is doubt surrounding the origin of the rash.
The diagnosis of HSP is mainly clinical, however, the
If there is concern regarding intussusception, an abdominal ultrasound should be arranged. Management
resolve with no intervention. However, hospital admission may be necessary for patients with renal or abdominal
Most cases
complications. of HSP include\:
Complications
It is common for HSP to recur. This can happen in one-third of patients.
² Complications
Nephrotic or nephritic syndrome
Renal failure
Intussusception

Immune thrombocytopenic purpura (ITP)

Immune thrombocytopaenic purpura (ITP) involves the development of a purpuric rash in those with low circulating
platelets (\<100 x 10⁹/L) in the absence of any clear cause. 3 Risk factors
ITP usually follows a viral illness in children
however, there are no known speci
Clinical features
History
Typical symptoms of ITP include\:
Prodromal viral illness in children
Epistaxis
Many patients may be asymptomatic.
Clinical examination
Typical clinical
Petechiae and/or bruising
Di
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Meningococcal sepsis
Aplastic anaemia
Leukaemia
Non-accidental injury
Disseminated intravascular coagulation
Investigations
Investigations may include\:
Baseline blood tests (FBC) and blood
Bloodborne virus screen (HIV, hepatitis C)\: to exclude secondary cause of ITP.
Bone marrow biopsy\: if the diagnosis is uncertain.
Management
haematology.
In children, ITP is usually self-limiting. Treatment is based upon symptoms, rather than the absolute
platelet count. In practice, active treatment is rarely needed for platelet counts of >50x10⁹/L. Patients should be referred to
Medical management
Medical management of ITP may include\:⁴
Stopping any medications which may a
Oral prednisolone is regarded as the
Other treatments that may be o
rituximab.
Surgical management in the form of a splenectomy can be considered once all medical treatment options have been
exhausted.
⁴

Haemolytic uraemic syndrome (HUS)

Haemolytic uraemic syndrome (HUS) is de
Microangiopathic haemolytic uraemia
Acute kidney injury
Thrombocytopaenia
5
Aetiology
HUS occurs after infection with E s c h e r i c h i a c o l i O157; this pathogen is commonly found in the faeces of
sheep, cows and goats. A potential source of infection is petting zoos, improper hand hygiene during these visits can lead
to infection with E.Coli O157. Risk factors
Common risk factors for HUS include\:
Age\: young children are by far the most commonly a
years.
Immunocompromised adults and the elderly population are also at increased risk.
The number of infections tends to peak in the summer months.
Clinical features
History
Typical symptoms of HUS include\:
Diarrhoea, which typically turns bloody around day three
Abdominal pain
Fever
Vomiting
school or playgroup.
During history taking it is also important that you cover any recent exposure to farm animals and if the child attends
Clinical examination
Patients with suspected HUS require an abdominal examination and examination of the a

Abdominal tenderness
Hypertension secondary to acute kidney injury
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Small petechiae on the skin can occur due to low platelet count
Di
Acute gastroenteritis
Intussusception
HUS can appear similar to several conditions including\:
Disseminated intravascular coagulation
Investigations
Investigations may include\:
injury.
Urinalysis\: to screen for haematuria and proteinuria.
Stool cultures\: to screen for the presence of E.Coli O157.
Baseline blood tests (FBC, U&E, CRP, clotting)\: may show thrombocytopenia, raised WCC, anaemia and acute kidney
Management
The treatment of HUS is mainly supportive, the mainstay of treatment is the maintenance of
balance and correction of electrolyte abnormalities. Severe cases may lead to the development of renal failure requiring
dialysis. HUS is a noti
⁶

Forceful coughing and/or vomiting

Forceful coughing or vomiting can cause petechiae to appear on the skin in the superior vena cava distribution, which is
the head, neck and the top of the shoulders. Other serious causes of petechiae should be excluded before they are
attributed to forceful coughing or vomiting. No management is needed and the petechiae should self-resolve.

Non-accidental injury

When assessing children with non-blanching rashes it is important to consider the possibility of a non-accidental injury
(NAI). Certain distributions of ‘rashes’ should be suspicious for this such as hand marks, linear markings and those on the
face/ears. They usually occur with other signs of NAI so careful examination is necessary.
⁷ For more information on NAI,
see the Geeky Medics article here.

References

Text references
Patient Professional. M e n i n g i t i s . Last updated July 2019. Available from\: [LINK]
Patient Professional. H e n o c h-S c h o n l e i n P u r p u r a . Last updated June 2019. Available from\: [LINK]
Patient Professional. I m m u n e T h r o m b o c y t o p a e n i a . Last updated February 2015. Available from\: [LINK]
NICE. Immune (idiopathic) thrombocytopenic purpura\: rituximab - Evidence Summary. Last updated October 2014.
Available from\: [LINK]
Patient Professional. H a e m o l y t i c U r a e m i c S y n d r o m e . Last updated February 2016. Available from\: [LINK]
Public Health England. L i s t o f N o t i LINK]
DermNet. S k i n s i g n s o f N o n-A c c i d e n t a l I n j u r y . Last updated in 2010. Available from\: [LINK]
Image references
Figure 1. Hektor. P u r p u r a . License\: [CC-BY-SA]. Available from\: [LINK]
Figure 2. DrFO.Jr.Tn. P e t e c h i a l r a s h . License\: [CC-BY-SA]. Available from\: [LINK]
Figure 3. Rosetheboston. P o s t g a l l b l a d d e r s u r g e r y b r u i s e . License\: [CC-BY-SA]. Available from\: [LINK]
Figure 4. Madhero88. H e n o c h-S c h o n l e i n p u r p u r a . License\: [CC-BY-SA]. Available from\: [LINK]

Reviewer

Dr Thomas King
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Dermatology SpR

Acne vulgaris
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