Petechiae, purpura and vasculitic rashes — branching viva

Opening question

Examiner: Take me through this child. What is your immediate frame? [8]

Candidate: This is a sick child with a rapidly progressive non-blanching rash and signs of septic shock — meningococcal septicaemia or purpura fulminans until proven otherwise. My first split is sick versus well, and this child is unwell: the fever, irritability, cool peripheries, prolonged capillary refill and the spreading dark purpuric rash all place her in the emergency pathway. My immediate frame is the first-hour sepsis bundle: oxygen, access, blood cultures, a broad-spectrum parenteral antibiotic such as ceftriaxone, and a fluid bolus, with escalation to intensive care. [8] [9]

Examiner: How do you confirm the rash is non-blanching? [8]

Candidate: With the glass test. I press a clear glass or transparent tumbler firmly over a lesion; petechiae and purpura remain visible through the glass because the blood is extravascular, whereas an erythematous inflammatory rash would fade. A non-blanching rash means blood outside the vessel lumen, which points me to a platelet, vessel-wall or coagulation problem. [8]

Branch 1 — the emergency pathway and disseminated intravascular coagulation

Examiner: Walk me through the first hour in detail. [9]

Candidate: I give high-flow oxygen, establish intravenous or intraosseous access, take blood cultures, a full blood count and film, coagulation, lactate and a blood gas, and give a broad-spectrum parenteral antibiotic such as ceftriaxone within the first hour. For shock I give a 10 to 20 mL per kilogram crystalloid bolus, reassess, and repeat with escalation to intensive care for refractory shock. The antibiotic comes before the cultures return, because antibiotic delay is the preventable cause of death in meningococcal disease. [8]

Examiner: Her coagulation shows a low fibrinogen and a raised D-dimer. What is this and how do you grade it? [9]

Candidate: This is disseminated intravascular coagulation driving the purpura fulminans. I grade it with the ISTH overt disseminated intravascular coagulation score, which scores the platelet count, the fibrin-related markers such as D-dimer, the prothrombin time and the fibrinogen. I manage it with haematology-guided fresh-frozen plasma, platelets and, in selected inherited cases, protein C concentrate, alongside treating the sepsis and the underlying cause. [9]

Branch 2 — immune thrombocytopenia and the leukaemia differential

Examiner: Suppose instead this were a well, afebrile four-year-old with bruising and a platelet count of 12 × 10⁹ per litre. What is the diagnosis and how do you exclude leukaemia? [3]

Candidate: The most likely diagnosis is acute immune thrombocytopenia, defined by a platelet count under 100 × 10⁹ per litre with isolated thrombocytopenia and a normal film in an otherwise well child. I exclude leukaemia by confirming the haemoglobin, white-cell and neutrophil counts are normal, that the film shows no blasts, and that there is no hepatosplenomegaly or lymphadenopathy. Isolated thrombocytopenia with pancytopenia, blasts or organomegaly is not primary ITP — it points to leukaemia, aplasia or a secondary cause. Looking at the film is non-negotiable. [3] [4]

Examiner: How does the pathophysiology of ITP explain a low count with little bleeding? [1]

Candidate: In ITP, IgG autoantibodies — often against glycoprotein IIb/IIIa — coat the platelets, which are then cleared by splenic macrophages. The marrow responds normally with large young platelets, which is why the bleeding is often mild relative to the count and why the film shows isolated thrombocytopenia with normal red and white cells. [1]

Examiner: When would you treat, and with what? [1]

Candidate: ITP treatment is risk-based, matched to the bleeding rather than the count alone. For dry purpura with an acceptable count, observation and safety-netting may suffice. When treatment is indicated — active or wet bleeding, a very low count, or high-risk activities — first-line options are a short course of corticosteroids, intravenous immunoglobulin, or anti-D immunoglobulin in an Rh-positive, non-splenectomised child. I avoid steroids if any atypical feature is present, because they can mask leukaemia; here the film is clean, so treatment is appropriate if the bleeding warrants it. For life-threatening bleeding such as an intracranial haemorrhage, I give urgent intravenous immunoglobulin, high-dose corticosteroids and a platelet transfusion. [1]

Branch 3 — IgA vasculitis

Examiner: If the child instead had palpable purple spots on the legs and buttocks with ankle swelling and colicky abdominal pain, what would you think of? [5]

Candidate: IgA vasculitis, Henoch-Schönlein purpura, the commonest childhood vasculitis. The palpable dependent purpura is the signature, and the EULAR/PRINTO/PRES criteria require palpable purpura or petechiae plus at least one of abdominal pain, arthritis or arthralgia, renal involvement, or IgA deposition on biopsy. It usually follows an upper-respiratory infection in a young child, and the tetrad is palpable purpura, abdominal pain, arthritis and renal involvement. [5]

Examiner: What is the long-term priority, and how do you manage it? [5]

Candidate: The kidney. IgA nephritis can appear weeks after the rash and is what determines the long-term outcome, so I check the urinalysis and blood pressure at presentation and monitor them regularly for six to twelve months. Management is predominantly supportive — analgesia, hydration, rest, and monitoring of the abdomen, joints, blood pressure and urinalysis — with corticosteroids reserved for severe gastrointestinal or renal disease under specialist guidance. I warn the family about intussusception and about late nephritis. [5]

Branch 4 — safeguarding

Examiner: Now suppose the child is a four-month-old who is not yet mobile, with a bruise on the arm. How do you approach this? [12]

Candidate: Any bruise in a non-mobile infant is abnormal and warrants a safeguarding assessment. I apply the TEN-4 FACES pattern: bruising on the Torso, Ear or Neck; any bruise in an infant four months or younger; and Facial bruising at the Frenum, Angle of the mouth, Cheek, Eyelid or Subconjunctiva. A positive pattern escalates to a child-protection referral. I take a careful, non-judgemental history, examine fully for other injuries, and involve the child-protection team for the workup, because bruising in a pre-mobile infant is almost never accidental. [12]

Examiner: What is your role as the clinician? [12]

Candidate: To recognise the pattern, document it contemporaneously, and refer — not to adjudicate. The validated bruising literature shows that the distribution and the developmental stage of the child discriminate abuse from accidental injury, so a bruise in the wrong place on a non-mobile infant is a referral, not a reassurance. My role is to raise the concern and let the multi-disciplinary child-protection team take the assessment forward. [12]

Wrap

Examiner: Summarise the non-blanching rash stance in one sentence. [8]

Candidate: A non-blanching rash in a child is a triage problem whose first split is sick versus well: the febrile toxic child gets a glass-test confirmation, a first-hour antibiotic and resuscitation for suspected meningococcaemia or purpura fulminans, the well child gets a full blood count and a film to confirm ITP and exclude leukaemia, the vasculitis child gets palpable-purpura recognition with six to twelve months of renal monitoring, and the bruised non-mobile infant gets a TEN-4 FACES safeguarding referral — because the dangerous diagnoses are caught and the common ones are managed calmly. [8] [3]