Meningococcal septicaemia is the most rapidly fatal bacterial infection in the UK — it can kill a previously well individual within 12–24 hours of first symptoms. The classic purpuric non-blanching rash (the "glass test" rash) represents petechial and purpuric haemorrhage from septic emboli and DIC, and indicates established septicaemia. By the time the rash appears, the patient is already critically ill. NICE NG240 (2024) advises not delaying transfer to give antibiotics: when meningococcal disease is strongly suspected, give ceftriaxone (preferred when available) or benzylpenicillin as soon as possible before transfer, unless this will delay transfer. Check doses against the current BNF/BNFC and local emergency medicines protocol. Meningococcal disease can occur without a rash, and absence of fever does not exclude serious infection in an infant or immunocompromised patient. The glass test helps identify a non-blanching rash but is not diagnostic: a negative or equivocal result does not exclude serious infection, lighting and skin tone affect interpretation, and rashes may evolve from blanching to non-blanching. NICE advises that rashes may be difficult to see on brown, black or tanned skin — look for petechiae in the conjunctivae. Valsalva petechiae (from coughing, vomiting, or straining) are a benign cause of petechiae suggested by: distribution confined to the face/neck, absence of fever, a well child with normal observations, and a clear precipitating event (coughing fit, vomiting episode, prolonged crying). This is a diagnosis of exclusion — distribution alone should not be used to rule out serious disease; examine the whole child, consider thrombocytopenia, medication and safeguarding, and give explicit safety-netting.

Palpable purpura (purpuric lesions that can be felt — slightly raised, may have urticarial component) is characteristic of small-vessel vasculitis — the palpability reflects perivascular inflammation and oedema in addition to the haemorrhage. In the context of petechiae and purpura assessment, palpating the rash takes 5 seconds and provides crucial diagnostic information: flat purpura points to coagulopathy or thrombocytopenia; palpable purpura points to vasculitis. The commonest cause of palpable purpura in children is IgA vasculitis (HSP) — the classic distribution is buttocks and extensor surfaces of lower limbs (gravity-dependent). The pathophysiology is IgA immune complex deposition in small vessel walls causing leucocytoclastic vasculitis. Adult palpable purpura may need targeted tests where clinically indicated (urinalysis, renal function, FBC, CRP/ESR, liver profile, ANA, ANCA, complement, cryoglobulins, hepatitis and HIV testing) as the underlying causes are more diverse and include connective tissue disease, haematological malignancy, and drug-induced vasculitis. The TTP pentad (thrombocytopenia, microangiopathic haemolytic anaemia, renal failure, fever, neurological symptoms) is rarely complete at presentation — any two of the first three should raise TTP as a diagnostic possibility and prompt emergency hospital assessment with direct haematology contact. Plasma exchange is life-saving in TTP and must be commenced within hours.

IgA vasculitis (HSP) — renal monitoring is the most important long-term clinical task for GPs. Renal involvement (IgA nephropathy in the setting of HSP) occurs in 30–50% of cases and is the primary determinant of long-term prognosis. Blood pressure and urine dipstick for protein and blood should be performed at every consultation during the acute illness and repeated over several months per the local paediatric/nephrology pathway. Nephrotic or nephritic syndrome (heavy proteinuria, oedema, or haematuria with renal impairment) requires urgent nephrology referral. Most childhood HSP nephritis resolves without treatment — but approximately 1–2% develop chronic kidney disease or end-stage renal disease over years. Heparin-induced thrombocytopenia (HIT) is a critical drug-related thrombocytopenia — it is paradoxically associated with both thrombocytopenia (purpura, bleeding) and severe arterial and venous thrombosis. The mechanism is heparin-dependent antibodies activating platelets (HIT antibody — anti-PF4/heparin). Any patient on heparin whose platelet count falls by >50% from baseline between days 5–14 of heparin exposure must have HIT considered, heparin stopped immediately, and switched to a non-heparin anticoagulant (argatroban, fondaparinux, or DOAC). This is a haematological emergency — continuing heparin in HIT causes catastrophic arterial/venous thrombosis (limb amputation, stroke, PE).

Schistocytes on the blood film are pathognomonic of microangiopathic haemolytic anaemia (MAHA) — red blood cell fragments produced when red cells are sheared by fibrin strands in small vessels. MAHA is the defining feature of TTP, HUS, and DIC. Identifying schistocytes on a blood film is the single most important investigation in a patient with thrombocytopenia + renal impairment + anaemia — it directs the diagnosis to a thrombotic microangiopathy and mandates emergency haematology input. GPs requesting FBC in suspected TTP/HUS must specifically ask for a blood film (many labs do not automatically perform a film unless requested or unless the automated analyser detects abnormalities). Retinal haemorrhage assessment in children with unexplained petechiae and no clear benign cause is important both clinically (severe thrombocytopenia or hypertension can cause retinal haemorrhage) and in the safeguarding context (retinal haemorrhage is a significant finding in suspected shaken baby syndrome). Ophthalmology referral for fundoscopy should be arranged if the cause of petechiae/purpura is unclear in a young child.

The management of childhood ITP is increasingly non-interventional — current UK paediatric haematology practice (BSH, formerly BCSH, and the international ITP consensus, Provan et al. 2019 — international) recommends observation without treatment for most children with acute ITP who are clinically well, regardless of platelet count. The rationale is that most childhood ITP resolves spontaneously without treatment, and the risks of treatment (IVIG infusion reactions, steroid side effects) outweigh the benefits in an otherwise well child without significant bleeding. Treatment is only indicated for: active significant bleeding (oral mucosa bleeds, heavy epistaxis, haematuria, GI bleeding), planned invasive procedure, or specialist judgement in severe thrombocytopenia — decisions are haematology-led and not based on platelet count alone. Platelet transfusion in ITP is generally reserved for life-threatening or critical-site bleeding. GPs who see a child with petechiae and a low platelet count should refer to paediatric haematology and resist the urge to immediately request hospital admission "for safety" — many of these children can be managed safely as outpatients with individualised activity advice and avoidance of NSAIDs/aspirin while platelet count recovers. This approach reflects current UK paediatric haematology practice.

Pre-hospital antibiotics for suspected meningococcal disease must never delay transfer; doses should be checked against the current BNF/BNFC and local emergency medicines protocol, and NICE NG240 gives ceftriaxone preference when available. The 1.2 g adult dose can be remembered as "one vial" (benzylpenicillin typically comes in 600 mg vials — two vials for an adult). Having these vials stocked and accessible in every GP emergency bag is a professional responsibility. The Meningitis Now charity provides a recommended GP emergency bag contents list that includes benzylpenicillin. For IgA vasculitis (HSP), the steroid decision requires nuance — the European SHARE initiative recommendations for IgA vasculitis (international, Ozen et al. 2019) indicate that prednisolone reduces the duration of abdominal pain (by approximately 24 hours) but does not prevent or treat renal involvement. Therefore, steroids are only indicated when abdominal pain is severe or incapacitating, not as a routine treatment. The key GP action for HSP is setting up the urine and BP monitoring schedule — monitoring for renal involvement over several months per the local paediatric/nephrology pathway is the most important long-term management step.

Ciprofloxacin prophylaxis for household contacts of meningococcal disease is organised by the local Health Protection Team (UKHSA) — the GP's role is to notify the HPT immediately after a case is confirmed, and the HPT will arrange contact assessment and prophylaxis. GPs should not prescribe prophylaxis independently without public-health advice — the HPT system handles this. However, knowing that ciprofloxacin 500 mg single dose is the first-line prophylaxis (preferred over rifampicin as it is single dose, single drug, available in pregnancy, and has high eradication efficacy for nasopharyngeal carriage) is important. The post-meningococcal care pathway is frequently neglected — patients who survive meningococcal disease (especially children who develop purpura fulminans and digital/limb ischaemia requiring amputation) have complex long-term physical, psychological, and social rehabilitation needs. The Meningitis Now and Meningitis Research Foundation charities provide support and advocacy. GPs should ensure these patients are referred to hearing services (sensorineural hearing loss from labyrinthitis affects 10% of survivors), clinical psychology (PTSD affects 25% of survivors and 50% of parents), and reconstructive surgical teams where needed.

The MenACWY vaccination programme for university freshers was introduced specifically because university students (particularly those living in halls of residence for the first time) have historically been at disproportionately high risk of meningococcal W disease — contact with many new individuals from different geographical backgrounds in a shared living environment creates ideal transmission conditions. The MenACWY vaccine (Menveo or Nimenrix) provides protection against serogroups A, C, W, and Y. Students who did not receive MenACWY during the Year 9 school programme (age 13–14) should be offered catch-up vaccination via GP before going to university. Checking vaccination status at university pre-registration is a high-yield opportunistic intervention. The glass test is one of the highest-impact patient safety messages in the entire RCGP curriculum — it has been directly credited with saving lives by enabling parents to identify the non-blanching rash and call 999 before the child becomes deeply shocked. It should be taught at the 8-week baby check (when MenB is first given), reinforced at subsequent baby checks, and included in written safety-netting information for any febrile illness.

Renal monitoring for IgA vasculitis (HSP) is one of the most frequently overlooked follow-up requirements in paediatric GP practice. The risk of late-presenting renal complications (hypertension, proteinuria, progressive CKD) is real — approximately 1–2% of children with HSP develop significant long-term renal disease, and some do not develop proteinuria until months after the acute episode. The GP's role is to ensure urinalysis and blood pressure are checked repeatedly over several months after the acute illness, per the local paediatric/nephrology pathway — these checks are often delegated to Health Visitors or community nurses and never actually performed. Documenting the monitoring plan in the clinical record and setting review reminders is the standard of care. For ITP patients who subsequently undergo splenectomy (for chronic refractory ITP), the pre-splenectomy and post-splenectomy vaccination programme is a critical GP responsibility — these patients are functionally asplenic and require lifelong prophylactic penicillin V (250 mg BD) + vaccination against encapsulated organisms (pneumococcal, Hib, meningococcal, influenza annually). Failure to prescribe post-splenectomy penicillin is associated with overwhelming post-splenectomy infection (OPSI) — a fulminant bacteraemia with pneumococcus or meningococcus carrying 50–70% mortality.