Bruising — Easy / Unexplained Algorithm

Safety

Red Flags — Exclude Serious Haematological and Safeguarding Emergencies

Done

Bruising is a symptom of a haemostatic disorder — from benign to life-threatening. Screen for the can't-miss diagnoses before anything else. Also consider safeguarding in every case.

Spontaneous large haematomas Especially if deep-tissue, no trauma, or joints/muscles — haemophilia, severe factor deficiency → Same-day haematology

Petechiae / purpura + unwell child Non-blanching rash + fever = meningococcal septicaemia until proven otherwise → 999

Thrombocytopenia <20 × 10⁹/L Platelet count critically low — high risk of intracranial or GI haemorrhage → Same-day haematology

Bruising + anaemia + lymphadenopathy Pancytopenia pattern — acute leukaemia or bone marrow failure → Same-day haematology

Unexplained bruising in child Distribution (ear, neck, buttocks, multiple stages), shape (strap marks, patterned), non-mobile child — consider NAI → Immediate safeguarding referral

Bruising + active bleeding GI bleed, haematuria, haemoptysis, intracranial bleed concurrent with bruising → 999

Warfarin/DOAC + major bruising Signs of significant anticoagulation (INR >5, haematoma at unusual site) → check INR, consider reversal agents → Same-day review

Unexplained bruising in frail elderly Consider elder abuse. Ask about safety at home, who administers medication. If concern → safeguarding referral → Safeguarding assessment

Weight loss + bruising + lymphadenopathy B-symptoms + bruising — lymphoma, leukaemia → Urgent 2WW Haematology

Non-blanching petechiae in a febrile child is meningococcal septicaemia until proven otherwise — mortality without treatment is 80%; with early treatment <10%. Intracranial haemorrhage risk rises exponentially when platelets fall below 20 × 10⁹/L — this requires same-day haematology assessment. Acute promyelocytic leukaemia (APML) presents with bruising, petechiae, and DIC — it is rapidly fatal without treatment but highly curable (90% cure rate) with urgent ATRA therapy. Non-accidental injury in children must be actively considered — bruising in non-mobile infants is pathognomonic of abuse until proven otherwise. In adults on anticoagulation, unexpected bleeding patterns may reflect drug interactions, renal impairment, or excessive dosing.

Diagnose

Focused History — Characterise the Bleeding Tendency

Done

Use history to distinguish platelet disorders (superficial, mucocutaneous) from coagulation disorders (deep, delayed) — they look and behave very differently.

Character of bleeding

Platelet disorder: petechiae, gum bleeds, epistaxis, menorrhagia — immediate on injury, superficial. Coagulation disorder: deep haematomas, haemarthroses, delayed bleeding after surgery/dental extraction

Duration

Lifelong since childhood → congenital (von Willebrand disease, haemophilia). New onset in adult → acquired (ITP, drugs, liver disease, malignancy)

Drug history

Essential: aspirin, NSAIDs, clopidogrel, warfarin, DOACs, SSRIs, steroids (skin fragility), herbal (ginkgo, fish oil). Even OTC ibuprofen causes bruising. Ask specifically — patients often don't volunteer

Family history

First-degree relatives with bleeding tendency, joint bleeds, excessive surgical bleeding → haemophilia (X-linked recessive), VWD (autosomal dominant)

Surgical/dental history

"Did you bleed a lot after tooth extraction or surgery?" — most reliable screen for congenital bleeding disorder. Prolonged post-dental bleed is specific for VWD/platelet disorders

Alcohol and liver disease

Alcohol causes thrombocytopenia (direct toxic + hypersplenism) and impairs coagulation factor synthesis. Heavy drinkers commonly bruise easily

Systemic illness

Renal failure (platelet dysfunction); HIV (ITP); autoimmune disease (ITP, lupus anticoagulant); hypothyroidism; Cushing's (skin fragility); malnutrition (vitamin K/C deficiency)

Menstrual history

Menorrhagia from puberty onwards is a classic VWD presentation. BAT (Bleeding Assessment Tool) score ≥3 in women suggests significant bleeding disorder

The Bleeding Assessment Tool (BAT) is a validated scoring instrument (ISTH-BAT) that quantifies bleeding history — a score ≥3 in women or ≥2 in men predicts a significant bleeding disorder with sensitivity 74% and specificity 88%. Von Willebrand disease affects 1 in 100 people — it is the most common inherited bleeding disorder and is frequently missed because symptoms are mild and often attributed to "normal" periods. Steroids cause skin fragility through collagen loss, producing purpura without a haemostatic defect — this is benign and requires no investigation. Drug history is the single most important first step — aspirin, NSAIDs, and SSRIs are enormously common and frequently overlooked causes.

Diagnose

Classify Bruising Type — Mechanism and Likely Category

Done

Classification drives investigation and urgency. Most GP bruising presentations fall into one of five categories.

Senile/steroid purpura

Atrophic skin + sun damage + extensive steroid use. Thin skin tears easily. Forearms/dorsal hands. Normal FBC + coagulation. Benign. Reassure. No investigation needed in classic presentation

Drug-induced thrombocytopenia or platelet dysfunction

Temporal relationship to new drug. Petechiae, mucosal bleeds. Platelet count low or borderline. Stop offending drug. Monitor FBC. Common culprits: quinine, heparin, valproate, trimethoprim

Immune thrombocytopenia (ITP)

Isolated thrombocytopenia (<100 × 10⁹/L), normal coagulation, no other cause. Wet purpura (oral/buccal petechiae) suggests severity. Can be primary or secondary (HIV, Hep C, SLE, CLL)

Inherited bleeding disorder

VWD (commonest; low VWF antigen + activity); haemophilia A (FVIII low, X-linked males); haemophilia B (FIX low). Lifelong history. Family history. Confirm with haematology

Systemic / acquired coagulopathy

Liver disease (all factors ↓ except FVIII + vWF); DIC (sepsis, cancer, obstetric emergency); vitamin K deficiency (malabsorption, antibiotics, poor diet). INR/PT raised

Vascular / connective tissue

Ehlers-Danlos syndrome (hyperelastic skin, hypermobile joints, normal bloods); Henoch-Schönlein purpura (palpable purpura, arthralgia, haematuria in children + young adults); scurvy (perifollicular)

Benign easy bruising

Common in young women. No bleeding history, no family history, normal FBC + coagulation. Diagnosis of exclusion. Reassure after investigation if normal

Accurate classification prevents both under- and over-investigation. Senile purpura (actinic purpura) is the most common cause of bruising in patients over 65 — requesting a full coagulation screen is unnecessary and anxiety-provoking. ITP has a 30% secondary cause rate in adults — HIV, hepatitis C, SLE, and CLL must be screened at diagnosis. Heparin-induced thrombocytopenia (HIT) is a paradoxical prothrombotic emergency despite low platelets — urgent haematology involvement is required. Scurvy (vitamin C deficiency) is under-diagnosed in the UK among elderly patients, alcohol-dependent individuals, and those with restricted diets — look for perifollicular haemorrhages and corkscrew hair.

Diagnose

Targeted Examination — Bruise Assessment and Systemic Signs

Done

Examination is not just about the bruises — look for systemic clues to the underlying cause.

Bruise characterisation

Site (sun-exposed = actinic; extensor = normal; flexor surface = suspicious); size; age (yellow = older, purple = recent); shape (geometric/patterned = NAI); number; depth (superficial = platelet; deep = coagulation)

Petechiae vs purpura

Petechiae: <2 mm pin-point, non-palpable, non-blanching — platelet disorder. Purpura: 2–10 mm, may be palpable — vasculitis (HSP). Ecchymosis: >10 mm bruise. Document and size

Skin assessment

Skin fragility/atrophy (steroid/actinic purpura). Hyperelastic skin + hypermobile joints → Ehlers-Danlos. Jaundice/spider naevi → liver disease. Cushingoid appearance

Oral cavity

Wet purpura (blood blisters on buccal mucosa) indicates platelet count <20 × 10⁹/L — immediate haematology. Gum hypertrophy with bleeding → leukaemia

Lymphadenopathy + spleen

Lymphadenopathy + bruising → lymphoma/leukaemia. Splenomegaly → portal hypertension / haematological malignancy / hypersplenism causing thrombocytopenia

Joint examination

Haemarthrosis (swollen, warm joint) without trauma → severe haemophilia. Hypermobility assessment → EDS. Arthralgia + purpura → HSP/vasculitis

Safeguarding indicators

In children: bruises on ears, neck, face, buttocks, back of legs in non-mobile child — document precisely, measure, photograph. Do not diagnose NAI — refer to safeguarding team

Nutritional assessment

Perifollicular haemorrhage + corkscrew hair → scurvy (vitamin C deficiency). Assess diet, alcohol intake, social circumstances. Check gum bleeding

The site of bruising is the most important clinical discriminator — actinic purpura on sun-exposed forearms in an elderly patient needs no investigation. Bruising on the ear, neck, or submandibular area in an infant is pathognomonic of non-accidental injury (these sites are never traumatised by accidental falls before the child can walk). Wet purpura (blood blisters in the mouth) reliably predicts platelet count below 20 × 10⁹/L and imminent serious bleeding risk — this finding mandates same-day haematology. Gum bleeding with gum hyperplasia in a young adult is leukaemia until proven otherwise — gum infiltration by leukaemic blast cells is a classic AML presentation.

Diagnose

Investigations — Haematological Workup

Done

First-line tests are simple, cheap, and highly informative. Do not withhold first-line bloods in a patient with concerning bruising.

FBC + blood film All new unexplained bruising

Platelets: normal ≥150 × 10⁹/L; borderline 100–150; thrombocytopenic <100. Blood film: blast cells (leukaemia), schistocytes (TTP/DIC), atypical lymphocytes (viral/CLL)

Coagulation screen All significant bruising

PT/INR (extrinsic pathway: liver, vitamin K, warfarin, factor VII). APTT (intrinsic pathway: haemophilia A/B, heparin, lupus anticoagulant). Fibrinogen (DIC, liver failure)

U&E + LFTs

Renal failure (platelet dysfunction, uraemic bleeding). Liver disease (↓ albumin, ↑ bilirubin, ↑ LFTs, impaired factor synthesis). GGT as alcohol marker

TFTs

Hypothyroidism causes both thrombocytopenia and coagulation abnormalities. Thyroid disease is common and frequently missed as a cause of bruising

Vitamin B12, folate

Macrocytic anaemia + thrombocytopenia → consider B12/folate deficiency, bone marrow pathology, or excess alcohol

von Willebrand studies Specialist

VWF antigen, VWF ristocetin cofactor activity, FVIII — haematology arranges. Consider if: prolonged post-dental bleed, menorrhagia since menarche, family history, APTT borderline raised

HIV, Hep C serology

Request if ITP diagnosis likely (both cause secondary ITP and must be excluded before starting treatment). HIV test should be offered universally in line with BHIVA guidelines

Do NOT routinely order

Platelet function analyser (PFA-100) — primary care cannot interpret. D-dimer — non-specific. ANA without clinical indication. Bone marrow biopsy without haematology input

A normal FBC and coagulation screen in a patient with easy bruising, no relevant history, and normal examination makes a serious haematological disorder very unlikely (negative predictive value >98%). The blood film is cheap and profoundly informative — it must be specifically requested with FBC; automated analysers alone cannot reliably detect blast cells, schistocytes, or atypical lymphocytes. ISTH guidance recommends von Willebrand studies for all patients with BAT score ≥3 — VWD is significantly underdiagnosed in women with heavy periods, with average time to diagnosis of 16 years. Hypothyroidism is a reversible cause of both thrombocytopenia and coagulopathy that is frequently not screened in a bruising work-up.

Refer

Referral Criteria — Urgency and Destination

Done

Haematological referral thresholds are specific. Use blood results alongside clinical picture to determine urgency.

999

Non-blanching rash + fever + unwell child (meningococcal). Active major bleed (intracranial, GI haemorrhage). Severe pancytopenia with systemic compromise. DIC with haemodynamic instability

Same-day haematology

Platelet count <20 × 10⁹/L on first presentation. Blast cells on blood film (AML/ALL). Wet purpura (oral blood blisters). INR >5 with bleeding. Suspected HIT (heparin + falling platelets + thrombosis)

2WW Haematology

Platelet count <100 × 10⁹/L with no drug cause. Unexplained pancytopenia. Lymphocytosis >10 × 10⁹/L. B-symptoms + bruising. Suspected leukaemia/lymphoma. Progressive thrombocytopenia

Urgent haematology (1–2 wk)

Isolated thrombocytopenia 50–100 × 10⁹/L stable, no active bleeding. Suspected ITP (refer before starting steroids). Abnormal APTT/PT without anticoagulants and no obvious cause

Routine haematology

Stable VWD (diagnosed / screening). Mild haemophilia (carrier status investigation). Investigation of menorrhagia with bleeding history. Confirmed ITP (stable platelet >50) for surveillance

Safeguarding referral

Any suspicion of NAI in child or elder abuse — local safeguarding pathway. Document meticulously. Do not confront the suspected abuser. Inform safeguarding lead. May require immediate MASH referral

Primary care manage

Actinic purpura: reassure and educate. Aspirin/NSAID-induced: review drug necessity. Drug-induced (non-serious): stop drug, monitor FBC. Vitamin C deficiency: replace, dietary advice

ITP should be referred to haematology before initiating corticosteroid treatment — secondary causes must be excluded first, and bone marrow biopsy may be needed in patients >60 to exclude MDS. Starting steroids empirically in AML can cause dangerous delays. HIT (type II) is a life-threatening prothrombotic complication of heparin — platelet count falling >50% from baseline on heparin exposure requires immediate specialist input as all heparin products must be stopped and alternative anticoagulation started. The 4T score (Thrombocytopenia, Timing, Thrombosis, oTher causes) is a validated tool for estimating HIT probability. Elder abuse (physical) has a prevalence of 2–4% in community-dwelling UK adults over 65 — clinicians must be vigilant at every presentation of bruising in this group.

Treat

Treatment — Primary Care Manageable Causes

Done

Definitive treatment of most coagulopathies requires haematology. Primary care manages modifiable causes, anticoagulation, and DINT.

Warfarin — supratherapeutic INR

INR 5–8, no bleeding: omit 1–2 doses

Recheck INR in 48h. If INR >8 or bleeding: phytomenadione (vitamin K1) 1–5 mg oral. If major bleed + INR >4: 999 for IV vitamin K + PCC (Beriplex). Review dose and interactions.

DOAC — bleeding on therapeutic dose

Minor bleed: supportive

Delay next dose. If major bleed: 999 + specific reversal agents (idarucizumab for dabigatran; andexanet alfa for Xa inhibitors). Review indication and renal function.

Vitamin C deficiency (scurvy)

Ascorbic acid 250 mg QDS × 1 month curative

Resolution of bruising within 2–4 weeks. Dietary advice: citrus fruit, kiwi, peppers. Address underlying social causes (poverty, food insecurity, alcohol dependence).

Drug-induced (aspirin/NSAID)

Medication review

Assess necessity vs risk. If aspirin not indicated: stop. If NSAID: switch to paracetamol where possible. SSRIs + anticoagulants: monitor closely. Review 4–6 weeks.

ITP (mild)Haematology initiates treatment. Platelets 30–50 with no bleeding: observation. Platelets <30 or bleeding: prednisolone 1 mg/kg/day (initiated by haematology). Do NOT start steroids in primary care before diagnosis confirmed.

VWD (Type 1)Desmopressin (DDAVP) 0.3 mcg/kg IV/SC for minor procedures — haematology to prescribe and monitor. Tranexamic acid 1 g TDS for mucosal bleeding / menorrhagia — can be initiated in primary care (unlicensed but supported by RCOG).

HaemophiliaFactor replacement managed entirely by haemophilia centre. Primary care role: avoid aspirin/NSAIDs; avoid IM injections; prescribe factor infusion products as directed by centre; provide emergency letter.

Liver disease coagulopathyTreat underlying liver disease. Vitamin K 10 mg PO daily × 3 days if vitamin K deficiency component suspected. Severe coagulopathy with bleeding → 999 (FFP/PCC required).

Tranexamic acid (antifibrinolytic) is safe, cheap, and effective for mucosal bleeding in VWD and ITP — the RCOG recommends it for menorrhagia associated with bleeding disorders as first-line alongside hormonal therapy. Scurvy is treatable and curable within weeks — failure to diagnose it in socially isolated elderly patients and those with alcohol dependence is a recurrent Serious Incident finding in the UK. Andexanet alfa (Ondexxya) was approved by NICE in 2020 for reversal of factor Xa inhibitors (rivaroxaban, apixaban) in major bleeding — available in UK emergency departments. Idarucizumab (Praxbind) reverses dabigatran within minutes. Primary care GPs must never start steroids for presumed ITP without haematology input — the clinical and diagnostic consequences of treating AML or lymphoma with immunosuppression are catastrophic.

Lifestyle

Non-Pharmacological Interventions and Patient Education

Done

Lifestyle advice is essential regardless of cause — for safety, treatment optimisation, and preventing further injury.

Alcohol reduction / cessation Alcohol directly suppresses platelet production (thrombocytopenic within days of binge), impairs coagulation factor synthesis, and increases falls/injury risk. Target <14 units/week. AUDIT score. Refer if dependent.

Falls prevention Patients on anticoagulation with bruising are at high risk from falls. Refer to falls prevention service. Home hazard assessment. Review medications causing postural hypotension. Hip protectors if osteoporotic.

Medication awareness Educate: avoid aspirin, NSAIDs, ibuprofen (OTC) unless prescribed. Check interactions with anticoagulants (antibiotics, antifungals). Carry anticoagulant alert card (warfarin) or medical ID (haemophilia).

Skin protection Actinic/steroid purpura: protective clothing (long sleeves), SPF 50+ on exposed skin, moisturisers to reduce fragility. Avoid skin trauma. Barrier creams for forearm protection in elderly.

Dietary optimisation Vitamin K food sources (leafy greens) — counsel warfarin patients on consistent dietary intake, not avoidance. Vitamin C: ensure adequate dietary intake (citrus, peppers, kiwi). Balanced diet reduces multiple deficiencies.

Activity modification (haemophilia) Contact sports and IM injections are contraindicated. Swimming, cycling, and walking are safe. Joint protection advice. Physiotherapy for joint management. Inform haemophilia centre of any planned procedure.

Anticoagulation monitoring Warfarin: consistent INR check schedule; 4-weekly if stable. DOAC: annual renal function (reduce dose if eGFR falls). Avoid grapefruit juice with DOACs. Alert to bleeding symptoms.

Psychological impact Unexplained bruising causes significant anxiety. Bruising from haematological malignancy treatment causes body image distress. Address these explicitly. Haemophilia societies provide peer support (Haemophilia Society UK).

Alcohol-related thrombocytopenia is directly dose-dependent — complete abstinence can normalise platelet count within 1–2 weeks. Falls in patients on anticoagulation are responsible for 40% of major haemorrhage admissions in the UK — falls prevention is a critical safety intervention. NICE TA249 recommends dabigatran, rivaroxaban, and apixaban do not require routine monitoring — but annual renal function checks are essential as dose reduction thresholds are based on CrCl (rivaroxaban: reduce to 15 mg OD if CrCl 15–50; apixaban: specific criteria based on weight + creatinine). All patients with a diagnosed bleeding disorder should receive a haemophilia society information pack and emergency management instructions to present to any emergency clinician.

Safety

Follow-Up, Monitoring and Safety-Netting

Done

Follow-up interval depends on the underlying cause and the severity of thrombocytopenia or coagulopathy.

1 week

Drug-withdrawn thrombocytopenia: repeat FBC — platelet count should be rising. Warfarin dose adjustment: recheck INR. Any patient awaiting 2WW haematology: confirm appointment received

2–4 weeks

Suspected drug-induced: FBC + LFTs — confirm resolution. Scurvy: symptomatic improvement expected. Vitamin B12 replacement initiated: early FBC improvement

3 months

Stable ITP under haematology: GP to be kept in loop. Anticoagulation review: bleeding events? Falls? Dose adherence? Annual renal function for DOAC patients

Annual

DOAC: U&E + eGFR. Warfarin: INR stability review, liver function, check indications still valid. VWD under haematology: bleeding symptom review. Haemophilia: joint surveillance

FBC threshold to act

Platelets <50 × 10⁹/L: same-day haematology discussion. Platelets 50–100 declining: urgent referral. Stable platelets 100–150: monitor FBC 4-weekly

Safety-net 999

Severe headache (intracranial bleed — especially if thrombocytopenic/anticoagulated); haematemesis or melaena; collapse; haematuria with clots; severe joint bleed with neurovascular compromise

Safety-net same-day

New or worsening bruising despite treatment; new oral blood blisters; spontaneous epistaxis >20 minutes; new petechial rash; any bleeding not stopping with pressure

Patient card / alert

All patients on anticoagulants or with known bleeding disorder should carry an anticoagulant card and MHRA yellow anticoagulant booklet. Haemophilia patients: emergency management card from haemophilia centre

Thrombocytopenia from drug withdrawal typically recovers within 5–14 days — a failure to improve after drug cessation should prompt urgent re-evaluation and haematology referral. Intracranial haemorrhage in thrombocytopenic patients (<20 × 10⁹/L) has a mortality of 40–60% — any severe headache in this context is a neurosurgical emergency. The MHRA anticoagulant booklet (yellow book) is a nationally standardised patient record that should be issued to all new warfarin patients — it documents INR values and enables safe cross-prescribing between healthcare professionals. DOAC renal monitoring is mandated by manufacturers but frequently omitted — apixaban requires dose reduction to 2.5 mg BD if 2 of 3 criteria met: age ≥80, weight ≤60 kg, or creatinine ≥133 µmol/L.