Deck 4 Flashcards
Aneurysm definition
Arterial dilatation 1.5x normal. True has arterial wall, false has another tissue.
Can be fusiform, saccular/berry
Caused by weakening against BP
Common aneurysm sites
Aorta is most common, 60% of these are abdominal - 95% below renal artery braches. 40% thoracic.
Aneurysm RF
Atherosclerosis, male, 60+, DM, HTN, high LDL, CT disorders, coarctation of aorta, pregnancy, syphilis, infective endocarditis (mycotic aneurysm), syphilis
Aortic and popliteal are atherosclerotic
Berry aneurysms are developmental
Rupture rists are HTN, FHx of rupture, smokers and females
Aneurysm S+S
If intact, symptomless unless compressing nearby structures (e.g thoracic can compress aortic valve to give aortic regurgitation)
Ruptured causes Grey Turner (but also pancreatitis), hypotension, tachycardia, syncope, aenaemia, expansile abdomen mass, shock, severe left flank pain, vomiting, collapse
May also present with embolic events (mural thrombi)
AAA surveillance
all men >65, consider in younger if COPD, Vardio/cerebrovascular disease, european origin, FHx of AAA, hyperlipidaemia, smoking, HTN
- 0-4.5 is 2 yearly monitoring
- 5-5.4 is 3 monthly monitoring
Management
Acute: A->E, vascular team and haemorrhage protocol
USS to check for evidence of rupture
For ruptured, EVAR (balloon inflates graft, femoral access, can cause CKD through nephrotoxic contrast). Open surgery if complex.
Surgery if symptomatic, asymptomatic and >5.5cm or growing by >1cm/year
popliteal aneurysm S+S
85% of peripheral aneurysm
Normally asymptomatic, . Can be pulsatile mass behind knee, may compress tibial nerve, veins, give swelling. If ruptured, can cause acute limb ischaemia.
Could also thrombose and cause chronic limb ischaemia
Popliteal anuerysm investigation and management
Duplex USS (screen, diagnostic for patency and thrombus), CT/MRI gives true lumen. Duplex surveillance if <2cm, or EVAR/open if larger
Aortic dissection types
De bakey 1 is ascending but carries on to descending
2 is ascending only, 3 is descending only.
stanford A is 1 and 2, B is 3.
First 10cm of aorta is most common.
Aortic dissection RF
HTN (main risk), smoking, hyperlipidaemia, thoracic AA, aortic valve abnormality, FHx dissection, previous cardiac surgery, trauma, cocaine, amphetamine, CT disease, pregnancy, syphillis
dissection S+S
Sharp chest pain, radiates to back, weak downstream pulse, difference in BP between arms, hypotension/shock if ruptured
Dissection complications
Pericardial tamponade, rupture into/out of artery, false lumen compressing nearby vasculature
Dissection management
HTN control, beta blockers, resection and replacement
HTN stage 1
Clinic>140/90, abm av >135/85
HTN stage 2
Clinic >160/100, amb >150/95
Severe HTN
> 180/100
Primary HTN
Essential HTN. Most common. RF are obesity, excess salt, inactivity, excess alcohol, stress, smoking, diabetes, older age, Fhx, ethnicity, males <65, females >65
Secondary HTN causes
5-15% of HTN cases.
Can be due to pregnancy, renal disease (renal stenosis is most common, intrinsic renal disease), endocrine (thyroid, phaeochromocytima, Conns, acromegaly, Cushings), pharma (alcohol, cocaine, COC, herbal remidies, anti-depressants), aortic coarctation, sleep apnoea, CKD, neurogenic cause (raised ICP)
Malignant HTN
aka accerlerated HTN
>180/120 developed over short time with signs of end organ damage (cerebral haemorrhage, AKI, aortic dissection, HF). Must have papiloedema
May present with headache, confusion (HT encephalopathy), epistaxis, fits, LoC
Urgent Tx, but slow reduction to avoid stroke
HTN end organ damage
cardiovascular events (e.g. left ventricular hypertrophy - >CHF) Renal events (glomerular ischaemic change. Can get hyperperfusion injury once controlled (glomerulosclerosis and necrosis) Retinopathy
Retinopathy stages
1) tortuous with shiny walls (copper/silver wiring)
Stage 2: AV nipping
Stage 3)Flame haemorrhage and cotton wool spots
Stage 4)papilloedema
HTN Tx
If under 55 then ACEi/ARB
Over 55/T2DM/Afrocarribean then CCB/thiazide
Switch if not working
Then combine (ACEi+CCB+thiazide)
Can add K sparing diuretic, or alpha/beta blocker
QRISK2
Risk of CVD in 10 years, healthy person is 7%
Intervene if 10%+
Looks at age, sex, ethnicity, postcode, smoking, cholesterol, BMI, systolic, BP, diabetes, previous CVD, Fhx, HTN
HDL role
Supports transfer of non HDL cholesterol to liver for clearance. NHDL cholesterol implicated in atherosclerosis and CVD.
Primary dyslipidaemia
Familial. Classed by Frederickson I-V. Combined hyperlipidaemia dn TGs are more common types
Secondary hypercholesterolaemia
Obesity, hypothyroidism, anorexia nervosa, obstructive jaundice, nephrotic syndrome, ciclosporin use
Secondary hypertriglycerideaemia
Obesity, diabetes, alcohol abuse, pregnancy, renal failure, hepatitis, oral contraceptives, beta blockers, isotretinoin, protease inhibitors
Mixed secondary hypertriglycerideaemia and hypercholesterolaemia
obesity, thiazides and steroids
When should you consider familial cause?
FHx of premature CVD and total cholesterol >7.5mmol
Popliteal vein is formed from
Dorsal arch giving off anterior tibial, posterior tibial (medial) and fibular vein.
Femoral vein
From popliteal vein as it enters the thigh
Great saphenous vein
Dorsal venous arch and dorsal vein of great toe give great saphenous vein.
Medial
Empties into femoral vein inferior to inguinal ligament
Small saphenous vein
Dorsal venous arch and dorsal vein of great toe give small saphenous vein.
Lateral
Passes between two heads of gastrocnemius, emptying into popliteal vein in popliteal fossa.
Veins running medial
Great saphenous vein, posterior tibial
Veins running lateral
Anterior tibial, fibular and small saphenous
Varicose veins
Superficial veins drain into deep.
Incompetent valves mean backflow into superficial - > tortuous
Varicose veins RF
- Age
- Female
- Obesity
- Sedentary lifestyle
- Pregnancy
- Smoking
Varicose veins clinical features
Tortuous veins
Pruritus
Oedema
Haemosiderin stain (red/brown/yellow - > RBC breakdown)
Generalised or local leg pain, worse standing and better with walking
Primary varicose veins
More common, esp in women and pregnancy. More likely due to primary superficial valve defect than depe venous incompetence. Often have FHx
Secondary varicose veins
Deep venous incompetence. Hx of DVT or raised systemic venous pressure (e.g. pelvic tumour, pregnancy, AV fistula, severe tricuspid incompetence)
Lipodermatosclerosis
localised chronic inflammation of skin and subcut - painful and hardened skin. Occurs due to venous insuffficiency (pooling and oedema)
“Champagne legs”
Varicose vein complications
- Venous ulcers
- Thrombophlebitis (inflammation and thrombosis of superficial vein - red and painful)
- Excessive bleeding from minor trauma
- Venous eczema (dry and scaly legs)*
Lipodermatosclerosis
Venous ulcer
Formed due to hypoxia and hypoperfusion. Shallow, sloping, minimal pain, large exudate.
Often medial malleolus. Often gauter area.
Oedema gives venous eczema lipodermatosis sclerosis -> skin breakdown
Most common ulcer out of venous and arterial
Venous
Investigations for venous disease
Clinical Hx and exam. Use Trendelenburg tourniquet to assess location.
USS for structure, valves and blood flow
Venography can be used to visualise veins
Management of venous disease
Compression stocking IF ruled out arterial disease
Surgical Tx can be ablation (First choice) - seals vein and diverts to better vessel. Can also use chemical ablation (sclerotherapy) or surgical stripping
Indications for surgical intervention in varicose veins
Grossly dilated/symptomatic, haemorrhage, concomitant deep venous insufficiency. Could also be done if just incompetent perforator veins (minimal invasion)
Trendelenburg tourniquet
Striaght leg raise and empty vein. Tie tourniquet to upper thigh and get patient to stand.
If non on standing but rapid filling on release then isolated sepheno-femoral junction defect. If filling with tourniquet then perforator valves involved too
Deep venous insuffiency
AKA postphlebetic limb
Incompetent deep venous valves and stasis gives superficial varicose veins, oedema, haemosiderin deposition, eczema, pruritus, atrophie blanche, lipodermosclerosis, ulcers
Primary lymphoedema
Intrinsic abnormality (e.g. milroy disease with deficiency in lymphatic vessels),
Secondary lymphoedema
Damage to lymphatic system. Can be cancer Tx, infection, trauma, venous oedema, immobility, obesity, HF, advanced cancer, liver disease
Investigation for lymphatic disease and management
Lymphoscintography.
Management involves elevation, compression stockings and physical massage. May need Abx due to cellulitis risk
PAD definition
Narrowing/occlusion of peripheral arteries, affecting blood supply to the lower limbs
Chronic limb ischaemia types
- Intermittent claudication (ischaemic walking pain, rest relief)
- Critical limb ischaemia (imminent limb loss risk)
Chronic limb threatening ischaemia (end stage PAD, threatened limb viability relayed to several factors)
- Critical limb ischaemia (imminent limb loss risk)
Acute limb ischaemia
Sudden perfusion decrease due to thrombus/embolus
Classification of PAD chronic limb ischaemia
Fontaine classification has 4 stages: 1) Asymptomatic 2) Intermittent claudication 3) Ischaemic rest pain Ulceration/gangrene
Atheroma sequalae
- Weakened vessel wall (aneurysm/dissection)
- Demand/supply mismatch (angina, PAD, vascular dementia)
- Thrombosis (ACS, stroke, acute limb ischaemia)
Renovascular HTN
Common atheroma sites mnemonic
Wills catches perceptive criminal hAns
Circle of willis, carotid arteries, popliteal arteries, coronary arteries, abdominal aorta
Chronic PAD RF
- Weakened vessel wall (aneurysm/dissection)
- Demand/supply mismatch (angina, PAD, vascular dementia)
- Thrombosis (ACS, stroke, acute limb ischaemia)
Renovascular HTN
Causes of chronic PAD
Mainly atherosclerosis, but can be vasculitis (inflammatory) and fibromuscular dysplasia (non-inflammatory)
Can also be Buerger’s disease (thromboangiitis obliterans)- > acute inflammation and thrombosis of lower limb arteries/veins - more common in young, heavy smokers
Intermittent claudication
Angina of the limb. Pain on exercise, relieved by rest. Generally femoral artery atheroma, with collateral from produnda femoris.
Usually predominates in one leg.
Reproduced on walking same distance.
Pain in calf implies occlusion in thigh.
Can get bilateral in internal iliacs (ED)
Leriche syndrome
Bilateral occlusion in internal iliacs, associated with ED
Distinguishing Intermittent claudication from cauda equina
CE worse downhill, IC worse uphill
CE variable distance, IC fixed distance
CE pain stays 15-30 mins, IC pain relief after 1-2 mins
CE pulses present, but LMN findings. IC pulses absent, reduced ABPI, no neuro
DDx for intermittent claudication
spinal stenosis (due to spinal osteophyte formation), cauda equina, venous cladication (obstruction of venous outflow leads to pain on initiating walking (typically whole leg and “bursting” in nature - may have DVT Hx and venous disease Hx)
Critical limb ischaemia
Circulation so impaired that imminent risk of limb loss. Requires rest pain or tissue loss
Critical limb ischaemia S+S
Pale, cold, hairless leg, reduced capillary refil, weak/absent pulse, arterial bruit, arterial ulceration (deep, punched out, painful, small over pressure points or lateral leg)
Investigation of Critical limb ischaemia
Obs, ECG, FBC, ESR, thrombophilia screen, lipid profile, BM, scans (ABPI, duplex, MRI/CT angiography)
ABPI
Take highest in foot and arm.
>1.2 is abnormal (calcified vessel)
1.0-1.2 is normal
0.8-0.9 is mild disease (manage risk)
0.5-0.79 is moderate disease/severe claudication (routine referral)
<0.5 is severe disease and critical limb ischaemia (urgent referral)
ABPI of 0.8-0.9
Mild disease/claudication - just manage RF
ABPI 0.5-0.79
Moderate disease/severe claudication - routine referral
ABPI <0.5
Severe disease with critical limb ischaemia
Management of PAD
Conservative: smoking cessation, diet/exercise, lipid modifications, manage comorbidities, antiplatelets, peripheral vasodilators
Surgery (angioplasty, surfgcal reconstruction, sympathectomy, amputation)
Acute limb ischaemia types
85% are thrombotic (clot forms around ruptured atherosclerotic plaque)
15% are embolic
Embolic acute limb ischaemia
Sudden and severe (lack of collaterals). RF are endocarditis, mitral stenosis, aneurysm, atherosclerotic disease, graft presence
Thrombotic acute limb ischaemia
Acute on chronic. Generally less severe. RF are PAD, IHD, CVD, graft presence, blood disorders.
S+S of acute limb ischaemia
Pain (not relieved by analgesia), paralysis (nerve damage), pulseless, pallor (cyanosed, +/- mottled skin), paraesthesia, perishingly cold.
If irreversible, see fixed mottling, blisters and hard, woody muscles
DDx for acute limb ischaemia
- Chronic peripheral neuropathy (e.g. diabetic, but see normal temp and pulse)
- Compartment syndrome (hard muscles)
- DVT (red, hot swollen calf, pulses present)
Management of acute limb ischaemia
Surgical emergency (6h to save limb). Tx with heparin.
If embolus, surgical embolectomy with balloon catheter in femoral artery
If thrombus, angioplasty, bypass surgery or intra-arterial thrombolysis
Acute limb ischaemia complications
Reperfusion can cause oedema, might lead to compartment syndrome
Products of cell dealth (myoglobin, potassium phyosphate) can give rhabdomyolysis and AKI
Risk of amputation after 6h due to necrosis
Marjolin’s ulcer
SCC progression from arterial ulcer.
Vasospastic disorder
Arterial spasms cause vasoconstriction, tissue ischaemia and necrosis
- Raynaud’s
- Acrocyanosis
- Livedo Reticularis
Raynaud’s
Toes and fingers, thumb normally spared. Clear demarcation. Precipitated by cold/emotion/trauma/smoking/overuse.
Ischaemia - >cyanosis - > reactive hyperaemia.
Can manage with CCB and peripheral dilators.
Raynaud’s phenomenon
primary disease. More common in young females. Genetic cause? No underlying vascular disease
Raynaud’s syndrome
Secondary. Generally older patient and has presence of severe symptoms (scaring, ulceration, gangrene, nail changes).
Seen in SLE, scleroderma, RA, smoking, trauma, vibration, chemical, DM, hypothyroidism, Beurger’s disease, lymphoma, polycythaemia, beta blockers, CoC and cytotoxic drugs
Buerger’s disease
Thromboangiitis obliterans
Acute inflammation and thrombosis of lower limb arteries and veins. More common in young, heavy smokers
Acrocyanosis
Peristent mottled/reticular pattern on extremities and face
Livedo reticularis
Persistent mottled/reticular pattern on extremities and trunk - may have pain.
Anaemia symptoms
SOB,fatigue, dizziness, palpitations, pounding in ears, pale
Erythropoesis reduced in
reduced haematinics, bone marrow disorders, myelosuppressive drugs, CKD, anaemia of chronic disease, endocrine (hypothyroid, reduced testosterone)
Pancytopoenia
Bone marrow disorder
Microcytic anaemia
Thalassaemia, IDA and anaemia of chronic disease
Normocytic anaemia
Anaemia of chronic disease, haemolysis, combined iron/B12 deficiency, acute blood losss
Macrocytic anaemia
B12/folate deficiency, myelodysplasia, alcohol, haemolysis, DNA synthesis defect (chemo), hypothyroid
Anaemia of chronic disease
Can be microcytic or normocytic
Serum iron decreased, TIBC decreased, STR normal, ferritin raised
Seen in RA, lupus, CKD, malignancy, IBD
Distinguishing IDA from anaemia of chronic disease in microcytic anaemia
IDA has low iron, raised TIBC, ferritin decreased
ACD has low iron, high ferritin and low TIBC
Haemolysis markers
High LDH, low haptoglobin, high bilirubin and positive DAT
IDA
Iron absorbed in duodenum, needs acidification. Protein bound as free is toxic (Hb, myoglobin, transferrin, ferritin, haemosiderin).
Deficiency can be reduced intake, pregnancy, malabsorption (coeliac, gastrectomy), chronic haemorrhage,
Get pallor, tachycardia koilonychia
Ferritin and haemosiderin solubility
Ferritin is soluble, haemosiderin is insoluble
IDA diagnosis
Microcytic, hypochromic, pencil cells. GSTD is Fe stain on bone marrow but not needed.
Ferritin should be low, but can increase in inflammation/malignancy so may be normal. Transferrin saturation is better measure as not impacted by inflammation
IDA management and Tx
Hx of blood loss, weight loss and bowel change
Refer for upper/lower GI endoscopy if no cause found
\
Tx with oral iron if ferritin <25 or TF sat <20.
Get 10hb rise 1-2 weeks.
Can also give IV
Hb rule of 10
Max rise in Hb/week is 10g/L
If >10g/L lost/week then blood lost
If transfusing, 1 bag raises Hb by 10g/L
Thalassaemia
Hb synthesis defect - more common in middle east.
Beta thalassaemia minor
Mild/asymptomatic carrier
Beta thalassaemia major
Cooley’s. Presents in first year with severe anaemia and splenomegaly and FTL. Can have facial abnormality. Needs transfusions
Alpha thalassaemia
Range from 1 (normal) 2 genes (carrier state, reduced MCV), 3 genes (mod microcytic anaemia and haemolysis) and 4 genes (death in utero)
Sideroblastic anaemia
Bone marrow makes sideroblasts rather than erythrocytes
B12 defieicny
Causes
S+S
Needs IF for absorption in terminal ileum. 2 year store in body.
Causes are reduced intake, gastrectomy, PA, Crohns, ileal resection. May appear low in Coc, HRT
Causes peripheral neuropathy, extensor plantars, brisk knee jerl but ankle jerk absent
Diagnosis of B12 deficiency
Management
Oval macrocytes, tear drop cells, hypersegmented nuclei, low B12, IF antibodies, gastric parietal cell antibodies (but not specific), raised bilirubin
Oral B12 or IM hydroxocobalamin
Folate deficiency
Converted to folate in upper GI, absorbed in jejunum. Stores for 6 months.
Destroyed by cooking
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Rhesus
IgG antibodies, only present in RhD negative people via exposure
Group and save
Test ABO/RhD but also antibodies against other antigens.
Indirect antibody test uses Coombs reagent (antiglobulin) used to screen patient serum against donor RBCs
Transfusion reactions
Shock, renal failure, DIC, death
Acute neutrophilia
Infection, inflammation, neoplasia, bleeding, smoking, steroid
Chronic neutrophilia
Reactive, drugs, metabolic syndrome, CML/myeloproliferative disorder
Neutropoenia
Viral infection, carbimazole, chemotherapy, Felty syndrome, cyclical (?young women), acute leukaemia, myelodysplasia, hereditary, Kostmann’s syndrome, neutropoenic sepsis
Felty syndrome
RA, neutropoenia and splenomegaly
Kostmann’s syndromeq
Congenital neutrophil defect
Lymphocytosis
Lymphoid malignancy (CLL, lymphoma), reactive (viral, whooping cough, TB, brucellosis, stress), drug induced (phenytoin), septic shock, MI, trauma, Chronic raise in smoking, autoimmune, chronic inflammation, sarcoid, metabolic syndrome. if Clonal then ?malignancy
Lymphocyte make up
80% T cells, circulate.few ER
20% B cells, mainly in lymph nodes. Also get NKs
Lymphocytopoenia
bone marrow failure, steroids, SLE, uraemia, HIV, cytotoxic drugs
monocytosis
atypical infections (TB, inflammation, autoimmune disease, haemoatoligical malignancy,
Eosinophilcytosis
Parasitic infections, asthma, drugs, eczema, Hodhkings, CML
Basophilcytosis
Very rare, usually only in CML
Haematological Urgent referral
WCC>50
Blood film suggest CML/CMML
Mention of blasts
Neutrophils <0.5
Consider referral if Chronic neutrophilia, lymphocytosis, persistent basophilia (?CML) or neutrophils <1.0 with no clear cause
Leukostasis
High WCC, medical emergency. Needs urgent chemo
Papilledema and retinal venous distension
CML
raised myeloid cells, see immature myelocytes and metamyelocytes in blood (instead of marrow.). Philadelphia chromosome (9-21_. Insiduous. splenomegaly
Aplastic anaemia
pancytopoenia but no blasts. Can be idiopathic or drug induced
Glandular fever
EBV infects B cells, allowing them to circulate. Confirm with monospot test (heterophile antibodies).
Can reactive during immunosuppression
Leukaemia Acute vs chronic
Acute has no differentiation (blast cells).
Bone marrow failure over 1-2 weeks. Anaemia, neutropoenia, infection, thrombocytopoenia, bruising.
Chronic has normal maturation
Children -acute is more common (esp ALL), AML is most common adult acute. CLL most common chronic
Platelet homeostasis
Endothelium secretes PGI2 (prostacyclin) and NO to prevent adhesion. Damage exposes collagen and vWF. platelets adhere and degranulate, release ADP and aggregate more
Platelets also synthesis TXA2 (vasoconstriction and aggregation)
Thrombocytoponeia
Can be increased destruction (ITP, SLE, CLL, viruses, TTP, HUS), reduced production (aplastic anaemia, marrow infiltration, marrow suppression) - epistaxis, menorrhagia, bruising
ITA
immune thrombocytic anaemia. Can be acute in children following virus or vaccine. In adults, less acute and generaly women with autoimmune disorder
TTP
Thrombotic thrombocytopoenic purpura. Widespread clotting and petichial rash. Can be congenital or acquired
HUS
Haemolytic uraemic syndrome. Can occur post E coli. Causes haemolysis, clots and AKI
DVT
Thrombi form at venous valve sites (as they disturb flow). Grow via Virchow’s triad (stasis, vessel wall damage and hypercoagulable state)
Thrombus sequalae
Lye and resolve (fibrinolytic plasmin)
Organisation (scars and collateral circulation)
Recanalisation (thrombus remains in lumen)
Embolism (can be numerous small, or larger)
Hypercoagulable state RF
oestrogen therapy, pregnancy, sepsis, malignancy, nephrotic syndrome, myeloproliferative disorders, CHF, thrombophilia (factor V leiden, antithrombin deficiency, protein C/S deficiency), aquired antiphospholipid/lupus anticoagulant
Stasis RF
- Older age
- Venous insufficiency/varicose veins
- Obesity
- Immobility (>3 days bed rest)
- Continuous travel
- Hospitalisation
Vessel wall injury RF
Trauma/surgery (esp leg surgery), indwelling venous catheter, chemical irritation (e.g. chemo)
DVT S+S
To examine leg - use 10cm distal to tibial tuberosity
Generally unilateral leg, but can be bilateral leg or can be arms.
Often throbbing pain, oedema, swelling, tenderness, erythema, warmth and venous distension.
Hofman’s sign (pain on dorsiflexion of the ankle - but unreliable and may dislodge thrombus so should not be used).
Wells score for DVT
Clinical features (tenderness, swelling (esp unilateral), collateral veins, pitting oedema), RF (cancer, bed rest, surgery, previous DVT). Each worth 1 point. 2 points if alterative likely diagnosis Score 2 is likely, 1 unlikely. D dimer to rule out if not likely
Diagnosis of DVT
Doppler USS (request if Wells>2 or low wells and positive D dimer)
May Thurner
Compression of left common iliac vein by right common iliac artery
PE S+S
dyspnoea, pleuritic chest pain, DVT signs, cough, fever, haemoptysis, syncope
Wells score for PE
Uses:
- clinical features (dVT signs, tachycardia, haemoptsis)
- RF (immobilisation, previous DVT/PE, malignancy)
Clinical judgement (3 points for no more likely diagnosis)
4 or less is unlikely (D dimer to rule out within 4 hours). If positive then CTPA
Above 4 is likely (CTPA or VQ).
CTPA
Definitive diagnosis. Can see right heart strain.Ok in pregnancy, not ok in renail impairment
V/Q
not suitable for pregnancy
ECG changes in PE
Not specific or sensitive for PE. Most common finding is sinus tachycardia.
Mat get dominant R wave in V1, T wave insersion in V1-V4, or RBBB
Slurred S in lead 1, Q wave and T inversion in III (cor pulmonale - rare)
CXR in PE
OFten normal. May have exudate, may see Westermark sign (fewer lung markings, enlarged pulmonary trunk)
PE classification ; Massive
Acute PE, sustained hypotension (<90 sys or 40 below basline or <40bpm for 15 mins)
PE classification: submassive
Submassive (40%. Right heart strain). Acute PE, no hypotension. RB dysfunction or myocardial necrosis - ECG abnormality/echo changes/elevated troponins. May have tachycardia.
PE classification (low risk)
Low risk (55%). Acute PE, no clinical markers of massive or submassive. May have tachycardia. Can be asymptomatic, but common to have pleuritic chest pain, SOB and DVT
PE management
anticoagulation, thrombolysis if haemodynamic compromise. If failed then interventional radiology or endovascular techniques.
Distinguishing embolic and thrombosis occlusion
Embolic is sudden onset and severe, thrombosis is insidious
Source in embolis is often identifiable (AF/AAA) but not in thrombosis
Pulses previously normal in embolis, now absent, but contralateral normal. Thrombosis has progressive bilateral decline.
In embolus, Hx often absent, but thrombosis often has Hx of stroke, MI
