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Vascular Study Index and Classifications

Written by Betra Youhanna, a medical student and not a doctor — check every detail against your own teaching.

Pre-exam triage. Source = deck only. 61 disease entries + 17 criteria & scores.

C/P
Inves
Mng
Special — pathognomonic

A. Aneurysms & Aortic Disease

15 entries
1

Aneurysm (General & Classification)

C/P
  • Mostly incidental (U/S)
  • Pulsatile swelling
  • Back pain
  • Compression of vein / nerve / ureter / lumbar vertebrae
  • Blue toe syndrome (distal embolisation from central aneurysm)
Inves
  • Ultrasound (screening)
  • CTA / MRA (planning)
Mng
  • General principle: observe small/asymptomatic with surveillance; intervene when rupture risk > surgical risk
  • Risk factor control: smoking cessation, BP, COPD
  • Medical therapy: doxycycline (MMP inhibitor — slows wall degradation)
  • Surgical principle: channel blood from normal proximal aorta to normal distal aorta or iliacs, excluding aneurysm from circulation
  • Open repair: graft sutured to aorta with non-absorbable suture
  • EVAR: graft attached to aorta by metallic hooks
  • Choice of operation: anatomy (access + complexity), patient age, comorbidities, surgeon skills + equipment
  • Saccular shape: operate earlier (high infection + rupture risk)
Special
  • Definition: permanent localised dilation ≥1.5× normal diameter; <1.5× = ectatic artery
  • Classification: aetiology (atherosclerotic / traumatic / congenital / inflammatory / dissecting), structure (true / false), shape (fusiform / saccular), site (central / peripheral)
  • Rupture = most serious complication; aortocaval & aortoenteric fistulae life-threatening for central; thrombosis, distal embolisation, infection limb-threatening for peripheral
2

Pseudoaneurysm

C/P
  • Iatrogenic post-puncture (femoral most common)
  • Anastomotic disruption
  • IVDU infected pseudoaneurysm in superficial vessels
  • Expanding pulsatile mass
Inves
  • Duplex U/S
Mng
  • Small + asymptomatic: conservative observation
  • >2.5 cm: U/S-guided thrombin injection (closes the false sac by triggering local thrombosis)
  • Refractory / infected / IVDU / anastomotic: open surgical repair (excision + interposition graft)
  • Septic pseudoaneurysm: prolonged IV antibiotics + ligation/resection
Special
  • Haematoma communicating with arterial lumen via partial wall tear
  • Wall = adventitia + compressed surrounding structures (not all 3 layers)
3

Abdominal Aortic Aneurysm (AAA)

C/P
  • Asymptomatic (most)
  • Pulsatile abdominal mass
  • Back pain
  • Rupture triad: acute abdominal pain + back pain + hypotension (>80% mortality)
  • Retroperitoneal rupture mimics renal/ureteric colic (flank + groin pain)
Inves
  • U/S — screening & surveillance (yearly)
  • CTA — planning (shows wall calcification + intraluminal thrombus)
  • MRA if raised creatinine
  • Urgent CTA in rupture
Mng
  • Conservative (size ≤5.5 cm in men, no risk factors): close surveillance with USG or CT yearly (or more frequently); risk factor control = smoking cessation, BP control, COPD control; doxycycline as MMP inhibitor
  • Elective repair indications: size ≥5.5 cm men; 4.5–5.4 cm women; expansion >1 cm/year; saccular shape (high infection + rupture risk); symptomatic aneurysm; smaller + significant COPD / poorly controlled HTN; patient demands; atypical aneurysm (dissecting, mycotic pseudoaneurysm)
  • Decision rule: treat asymptomatic AAA when rupture risk > accepted surgical mortality of 5% (occurs at diameter 5.5 cm)
  • Choice of operation factors: anatomical considerations (access, complexity, take-off + landing zones), patient age, medical comorbidities, surgeon skill + equipment
  • Open repair approaches: transperitoneal (standard) vs retroperitoneal — retroperitoneal indicated in hostile abdomen (multiple ops/radiation), suprarenal extension / horseshoe kidney, ascites; positioning = right lateral decubitus, incision from 10th intercostal space at posterior axillary fold extending medially; left medial visceral rotation exposes entire infradiaphragmatic aorta + iliac vessels
  • Open complications: renal dysfunction, paraplegia, ischaemic colitis, prosthetic graft infection, aorto-enteric fistula (rare but more common after open); more cardiorespiratory complications
  • EVAR: graft attached by metallic hooks; preferred in older/high-risk, hostile abdomen, prohibitive comorbidities; perioperative mortality 1.2% (vs 4.6% open); late problems = device migration, iliac limb occlusion, endoleak; lifelong surveillance crucial; higher local vascular / implant-related complications
  • Rupture (rAAA): ABCDE → permissive hypotension (restrictive fluid therapy raising systemic BP without reaching normotension — avoids blowing off the unstable clot) → urgent CTA → immediate surgical intervention (only treatment offering hope of survival)
  • SVS screening: men ≥65 (all), men ≥55 (positive FHx), women ≥65 (positive FHx or personal smoking history)
Special
  • 95% infrarenal
  • Smoking RR ≈3× vs CAD, ≈5× vs cerebrovascular
  • Rupture risk by size: <0.5%/y at 3–4 cm → 30–50%/y at >8 cm
  • EVAR late problems: device migration, iliac limb occlusion, endoleak — lifelong surveillance required
  • Open complications: renal dysfunction, paraplegia, ischaemic colitis, prosthetic graft infection, aorto-enteric fistula
4

Iliac Artery Aneurysm

C/P
  • Usually associated with AAA
  • Compression: bladder / ureter / colon / rectum / lumbosacral nerves / pelvic veins
Inves
  • CTA
Mng
  • Elective repair indication: size >3.5 cm
  • Bilateral: bifurcated aortoiliac graft
  • Unilateral: iliac stent graft or open repair
  • Associated AAA: treat both during single operation if both meet threshold
Special
  • Associations: atherosclerosis, pregnancy, Marfan, Ehlers-Danlos, cystic medial necrosis
5

Splenic Artery Aneurysm

C/P
  • Most common splanchnic aneurysm; 3rd most common intra-abdominal (after aorta, iliac)
  • Multiparous women (>90% have been pregnant)
  • Rupture (main complication, esp. in pregnancy)
Inves
  • CTA / Duplex
Mng
  • Elective repair indications: presence of symptoms; documented enlargement; diameter >2.5 cm; pregnancy or anticipated pregnancy
  • Preoperative preparation: all candidates receive Hib + Pneumococcus + Meningococcus + influenza vaccination (functional asplenia after possible splenectomy)
  • Ideal surgical treatment: aneurysm repair with splenic preservation
  • Preferred percutaneous treatment: splenic artery embolisation
  • Pregnancy: repair if discovered during pregnancy because pregnancy greatly increases rupture risk
Special
  • Saccular shape predominant
  • Strong female + parity association
6

Hepatic Artery Aneurysm

C/P
  • Extrahepatic mostly true aneurysms
  • Intrahepatic mostly false aneurysms
Inves
  • CTA
Mng
  • All warrant intervention — high rupture risk
  • Preferred treatment: transcatheter embolisation
  • Open surgery if embolisation fails or anatomy unsuitable
Special
  • —
7

Renal Artery Aneurysm

C/P
  • 2nd most common visceral aneurysm
  • Multiparous women predominantly
  • Hard-to-control HTN (≥3 antihypertensives)
  • Rupture in pregnancy: fetal mortality 75%, maternal 50%
Inves
  • CTA
Mng
  • Indications for surgery: difficult-to-control HTN (on >3 anti-HTN drugs); size >2 cm generally; size >2 cm in women of childbearing age (devastating mortality if ruptures during pregnancy)
  • Treatment options: reconstruction with patch or bypass + treatment of underlying renovascular HTN
  • HTN often resolves post-repair
Special
  • Saccular, mostly at primary/secondary branch bifurcation
  • True aneurysm cause: medial fibroplasia
  • False aneurysm cause: spontaneous/traumatic dissection
8

Popliteal Artery Aneurysm

C/P
  • Acute limb ischaemia from thrombosis / distal embolisation (limb-threatening more than rupture)
  • Prominent / wide popliteal pulse (normally barely palpable)
  • Distal leg oedema (popliteal vein compression)
Inves
  • Duplex U/S (primary)
  • Imaging of distal runoff for surgical planning
Mng
  • Elective repair indication: size >2.0 cm OR thromboembolic complications
  • Preferred procedure: exclusion of aneurysm (NOT excision — dissecting out risks damage to popliteal vein + tibial nerve) + in situ saphenous vein bypass graft (helps overcome anastomotic size discrepancy)
  • Endovascular alternative: covered stent excludes aneurysm from circulation
  • Adjunctive: local thrombolysis to improve distal runoff before definitive surgery
  • Acute thrombosis with viable limb: heparin → thrombolysis → reassess → bypass
  • Always image abdomen + contralateral leg (50% bilateral, 30% associated AAA)
Special
  • 70% of all peripheral aneurysms
  • 50% bilateral
  • 30–50% associated with AAA — always image abdomen + contralateral leg
  • Exclusion preferred (excision risks popliteal vein + tibial nerve damage)
9

Femoral Artery Aneurysm

C/P
  • Palpable groin mass
  • Distal embolisation
Inves
  • Duplex U/S
Mng
  • Elective repair indication: size >2.5 cm
  • Endovascular: covered stent excluding aneurysm
  • Open: resection + interposition graft
  • Infected (IVDU): prolonged IV antibiotics + ligation/resection ± bypass via clean tissue plane
Special
  • True aneurysm: degenerative atherosclerotic, predominantly males
  • False aneurysm causes: post-catheterisation / graft anastomotic disruption / IVDU
  • Mostly associated with aortoiliac aneurysms
10

Subclavian / Upper Extremity Aneurysm

C/P
  • Limb loss risk
  • Life-threatening if delayed
Inves
  • —
Mng
  • Surgical: resection of aneurysm + interposition graft to re-establish arterial continuity
  • If thoracic outlet cause: address the compression (e.g. cervical rib excision)
Special
  • Subclavian = most common upper extremity site
  • Causes: atherosclerosis, trauma, thoracic outlet compression (cervical rib), infection
11

Berry Aneurysm

C/P
  • Subarachnoid / cerebral haemorrhage on rupture
Inves
  • CT head (rupture); CT/MR angiography for unruptured
Mng
  • Specific neurosurgical treatment not in this deck (referred from vascular block)
  • Risk factor control: BP control, smoking cessation
  • Screen ADPKD patients
Special
  • Most common type of brain aneurysm
  • Multiple small aneurysms at bifurcations in Circle of Willis
  • Weakness of media; commonest >40 years
  • Risk factors: ADPKD (10–30% association), Ehlers-Danlos type IV, Marfan, neurofibromatosis, smoking, HTN
12

Charcot-Bouchard Microaneurysm

C/P
  • Hypertensive intracerebral haemorrhage
Inves
  • CT head
Mng
  • Primary: aggressive BP control (prevents formation + rupture)
Special
  • Small penetrating brain vessels
  • Hypertension-associated
  • Most commonly lenticulostriate branch of MCA
13

Syphilitic Aneurysm

C/P
  • Thoracic aneurysm features
Inves
  • Syphilis serology + CTA
Mng
  • Treat underlying syphilis (penicillin per general principles — deck doesn't specify)
  • Surgical aneurysm repair if size warrants
Special
  • Spirochete predilection for vasa vasorum of ascending thoracic aorta
  • Mechanism: obliterative endarteritis → medial ischaemia → aneurysmal dilation
14

Mycotic / Infective Aneurysm

C/P
  • Aneurysm + signs of infection (fever, malaise)
  • May follow recent endocarditis
Inves
  • Blood cultures
  • CTA
  • Echo for source (infective endocarditis)
Mng
  • Prolonged IV antibiotics against cultured organism
  • Surgical: excision of infected aneurysm + extra-anatomic bypass through clean tissue plane (avoid synthetic graft in infected field)
  • Treat source (e.g. infective endocarditis)
Special
  • Misnomer — bacterial more common than fungal
  • Mechanisms: septic embolisation (classically from infective endocarditis), extension of adjacent suppuration, direct circulating infection
15

Aortic Dissection

C/P
  • Tearing/severe chest pain extending into abdomen as dissection progresses (MI-like)
  • Sudden onset
  • Carotid compression → stroke
  • Massive haemorrhage if rupture through adventitia
  • Can be silent if re-enters true lumen via 2nd tear
Inves
  • CTA (urgent)
Mng
  • Type A (ascending) = emergent surgery — high risk of involving coronaries / pericardium / aortic valve
  • Type B (distal to arch): medical management first (aggressive BP + HR control — IV β-blockers to ↓ shear stress)
  • Type B complications (rupture, malperfusion, persistent pain): TEVAR or open surgery
  • BP target: systolic 100–120 mmHg
  • Pain control: opioids
  • Avoid hypotension overshoot (worsens malperfusion)
Special
  • Intimal tear → blood enters media → false channel under systemic pressure
  • Stanford Type A = involves ascending aorta; Type B = distal to arch
  • Major RF = hypertension (>90% in 40–60 yr men)
  • Younger: connective tissue disorder (Marfan), bicuspid aortic valve, coarctation, pregnancy
  • NOT atherosclerosis-driven

B. Diabetic Foot

2 entries
16

Diabetic Foot Ulcer

C/P
  • 15% of diabetics develop a foot ulcer yearly
  • Plantar ulcer over metatarsal head (motor neuropathy → claw toes → pressure)
  • Trauma not felt (sensory neuropathy)
  • Dry, cracked plantar skin (autonomic neuropathy)
  • 85% of diabetic amputations preceded by ulcer
Inves
  • Deep tissue fluid aspiration (NOT just superficial swab)
  • Local wound swabs
  • Plain X-ray (osteomyelitis, soft tissue gas)
  • Duplex + CTA (vascular)
  • Bedside: 10g monofilament, pedal pulses, ankle BP
Mng
  • 6-step framework: off-loading → debridement → wound dressings → antibiotics → revascularisation → amputation
  • Step 1 — medical stabilisation: glycaemic control first (sliding scale / DKA correction) before rushing to surgery
  • Step 2 — infection control: deep tissue cultures (not superficial); empirical IV antibiotics covering Staph aureus + Strep + Pseudomonas + anaerobes; surgical drainage within 24 hours of admission
  • Step 3 — debridement: sharp surgical debridement of necrotic tissue; larval (biological) debridement as adjunct
  • Step 4 — wound care: heal by secondary intention — DO NOT suture (reduces skin edge blood flow + traps infected material → abscess); negative pressure wound therapy (removes excess fluid, ↑ microcirculatory flow, ↓ wound size)
  • Step 5 — off-loading: total contact cast (with window for wound inspection) = gold standard; specialised footwear for plantar ulcers
  • Step 6 — vascular reassessment: if not healing despite above → duplex + CTA → revascularise (endovascular ≈ surgical for limb salvage) unless foot shows signs of healing
  • Adjuncts: leg elevation to ↓ oedema; early mobilisation
  • Cardiovascular risk: PAD strongly associates with CV risk → combine BMT + exercise + intervention
  • Salvage: amputation only when revascularisation impossible / unsalvageable foot / spreading infection
Special
  • Neuropathy CAUSES the ulcer; ischaemia PREVENTS healing
  • 4× PAD risk in diabetics
  • Wagner classification (Grade 0–5)
  • Hyperglycaemia is immunosuppressive
17

Charcot Foot

C/P
  • Severely swollen, erythematous foot
  • Collapsed medial arch ("rocker bottom" deformity)
  • Bony prominences on plantar surface
  • Often misdiagnosed as cellulitis
Inves
  • X-ray (bone fragmentation, joint destruction)
Mng
  • 7-step framework: Assessment → Acute foot / treating infection → Off-loading → Vac dressing → Larvae therapy (biological debridement) → Risk factors management (BMT) → Arterial reconstruction
  • Cornerstone: rigorous off-loading (total contact cast) to halt further bony destruction
  • Acute phase: immobilise + non-weight-bearing → prevents progression
  • Chronic phase: custom footwear + bracing
  • Surgical reconstruction: for severe deformity / non-healing ulcer beneath rocker bottom
  • Multidisciplinary care
Special
  • Bone destruction + joint deformity from severe neuropathy + repetitive unperceived microtrauma
  • Rocker bottom deformity is disease-defining
  • Larvae therapy used within this framework as biological debridement

C. Cerebrovascular

1 entry
18

Carotid Artery Disease (Extracranial Cerebrovascular Disease)

C/P
  • Stroke (focal neurological loss >24h, 12% of UK deaths)
  • TIA (<24h)
  • 80% ischaemic, 20% haemorrhagic
  • Hemisensory/motor signs
  • Dysphasia (higher cortical dysfunction)
  • Amaurosis fugax (transient monocular blindness)
Inves
  • Duplex U/S (first line)
  • CTA / MRA (arch + intracranial pre-surgery)
  • CBC, lipids, coagulation, U&Cr, glucose
  • Echocardiography + 24-hour tape (cardiac source)
Mng
  • Best Medical Therapy (BMT) — essential for all: antiplatelet + statin + BP control + smoking cessation + glycaemic control
  • Symptomatic carotid disease: rapid intervention within 2 weeks (7-day recurrent stroke risk 8–10%) — CEA or CAS
  • Asymptomatic carotid disease: may benefit from intervention (per individualised risk-benefit)
  • CEA (Carotid Endarterectomy): remove part of intimal lining + any blockage; standard procedure
  • CAS (Carotid Artery Stenting): alternative — preferred in high surgical risk / hostile neck / radiation
  • CEA complications: stroke 2–3%; bleeding/haematoma; cranial nerve injury (XII, X, IX)
  • Acute stroke: FAST assessment → thrombolysis/thrombectomy pathway (per stroke team)
Special
  • Source of thromboembolism: atherosclerotic plaque at ICA origin
  • CEA complications: stroke 2–3%, bleeding/haematoma, cranial nerve injury (XII, X, IX)

D. Renovascular

1 entry
19

Atherosclerotic Renovascular Disease

C/P
  • Difficult-to-control hypertension
  • CKD progression to ESRF (association, not cause in majority)
Inves
  • Duplex
  • CTA / MRA
Mng
  • Medical therapy for ARVD: aggressive BP control (ACEi/ARB with caution + monitor renal function), statin, antiplatelet, smoking cessation, glycaemic control
  • Revascularisation: endovascular (angioplasty ± stenting) OR surgical bypass — for refractory HTN, progressive CKD, flash pulmonary oedema
  • RRT modalities (for ESRF): haemofiltration (CVVH), peritoneal dialysis, haemodialysis, transplantation
  • AV fistula access for HD: native fistula 6 months before need (allows arterialisation); graft 6–8 weeks before need; vessel mapping + education + sufficient lead time improve patency
  • "Rule of 6's" for mature AVF: flow ≥600 mL/min, depth <6 mm, diameter ≥6 mm, length adequate for 2 needles
  • Native fistula sites: wrist radiocephalic, wrist ulnobasilic, brachiobasilic (with basilic vein transposition), brachiocephalic
  • AV access complications: stenosis, thrombosis, infection, failure to mature, steal syndrome (4 stages), high-flow cardiac failure, aneurysm
Special
  • Most common pathology of renal artery
  • 1–5% prevalence in hypertensive patients
  • Mechanism: ↓ distal renal perfusion pressure → ↑ RAAS activity
  • AV fistula access: native fistula 6 months before need, graft 6–8 weeks; "Rule of 6's" — flow ≥600 mL/min, depth <6 mm, diameter ≥6 mm

E. Mesenteric

3 entries
20

Acute Mesenteric Ischemia

C/P
  • Abrupt severe abdominal pain "out of proportion" to physical signs
  • Urgent need to defecate
  • Fever, N/V
  • Complications: sepsis, irreversible bowel damage (gangrene), death
Inves
  • Raised WCC + lactate (late)
  • CTA / CT with IV contrast (investigation of choice)
Mng
  • Resuscitation first: IV fluids, O₂, NG decompression, urinary catheter, broad-spectrum antibiotics
  • Anticoagulation: IV heparin (limits thrombus propagation)
  • Revascularisation options: embolectomy, surgical bypass, catheter-directed thrombolysis, endovascular angioplasty ± stenting
  • Resection: non-viable bowel resected; second-look laparotomy at 24–48h to reassess marginally viable bowel
  • Embolic AMI: SMA embolectomy (usually distal to middle colic origin) — better survival
  • Thrombotic AMI: bypass / endovascular treatment at SMA origin; extensive bowel involvement common
  • NOMI: treat underlying cause (correct hypotension, stop vasopressors/ergotamine/cocaine/digitalis if possible)
Special
  • Embolic: lodges in SMA distal to middle colic origin; better survival
  • Thrombotic: at SMA origin (over atherosclerosis); extensive bowel involvement
  • NOMI (non-occlusive): vasopressors, ergotamines, cocaine, digitalis; or hypotension from CHF, MI, sepsis, severe liver/renal disease
  • Watershed: splenic flexure (Griffith's point), rectosigmoid junction (Sudek's point)
  • Marginal artery of Drummond = primary collateral; absent in up to 5%
21

Chronic Mesenteric Ischemia

C/P
  • Postprandial abdominal pain starting ~30 min after eating, worsens over an hour, resolves in 1–3 hours ("intestinal angina")
  • Fear of eating
  • Unintentional weight loss
  • Acute-on-chronic progression
Inves
  • CTA
Mng
  • Indication for intervention: symptomatic disease (weight loss + post-prandial pain)
  • Endovascular: angioplasty ± stenting of involved mesenteric artery (typically SMA) — first-line for most
  • Open surgical bypass: aortomesenteric or iliomesenteric bypass for complex anatomy / endovascular failure
  • Nutritional support: high-calorie diet, small frequent meals; consider TPN preoperatively if severe weight loss
  • Risk factor control: smoking cessation, statin, antiplatelet
Special
  • "Angina of the bowel" — gut O₂ demand exceeds supply after meals
22

Mesenteric Venous Thrombosis

C/P
  • Abdominal pain (subacute)
Inves
  • CTA / CTV
  • Hypercoagulability workup (Protein C/S, ATIII, Factor V Leiden, JAK2)
Mng
  • Anticoagulation = mainstay: IV heparin acutely → long-term warfarin/NOAC (duration depends on underlying cause — lifelong if irreversible thrombophilia)
  • Bowel resection if peritonitis / non-viable bowel
  • Thrombolysis / thrombectomy: selected cases of extensive thrombosis without peritonitis
  • Treat underlying: cancer, infection, portal hypertension
Special
  • >80% have predisposing condition
  • Hypercoagulability: Protein C/S deficiency, ATIII deficiency, polycythemia vera (most common), thrombocytosis, sickle cell, Factor V Leiden, dysfibrinogenemia
  • Tumour compression / paraneoplastic
  • Intra-abdominal infection (appendicitis, diverticulitis, abscess)
  • Cirrhosis (portal hypertension)
  • Pancreatitis
  • OCP / pregnancy

F. PAD / Chronic Arterial Occlusion

7 entries
23

Peripheral Arterial Disease (PAD)

C/P
  • Intermittent claudication (most common)
  • Critical limb ischaemia (rest pain, ulcer, gangrene)
  • Higher CV/cerebrovascular event risk (3–4× vs non-PAD)
Inves
  • ABI (screening)
  • Segmental limb pressures
  • Duplex (first-line imaging)
  • DSA / CTA / MRA — for planning revascularisation
  • Continuous-wave handheld Doppler at bedside
Mng
  • Treatment objectives: relief of symptoms + prevention of limb loss + prevent disease progression + reduce CV event risk
  • PAD is more a marker for early death than imminent limb loss — 50% mortality after peripheral reconstruction is cardiac
  • BMT (AHA guidelines) = standard for all: lipid modification + antiplatelet + antihypertensive + smoking cessation
  • BP target: 130/85 mmHg with ACEi + β-blocker (reduce mortality)
  • LDL target: <100 mg/dL via statin
  • Diabetes target: HbA1c 7%
  • Smoking cessation: counselling + adjunctive drug therapy
  • Supervised exercise: >30 min, >3×/week — significantly improves walking ability
  • Pharmacological: cilostazol / pentoxifylline (first-line for intermittent claudication after 3-month trial of exercise)
  • Intermittent claudication algorithm: no functional disability → no Rx + annual follow-up; lifestyle-limiting → 3-month trial of supervised exercise + cilostazol → if persistent → evaluate for endovascular/surgical revascularisation
  • CLI algorithm: candidate for revascularisation → imaging → revascularise; not candidate + stable pain → medical Rx; not candidate + intolerable pain / spreading infection → amputation
  • Endovascular indications: lifestyle-limiting claudication, ischaemic rest pain, tissue loss or gangrene
  • Endovascular options: balloon angioplasty (compresses plaque + widens lumen); balloon-expandable stent (overcomes arterial recoil); self-expanding stent (vessel conformability); bioabsorbable stent; cryoplasty (reduces flow-limiting dissection); cutting balloon (anastomotic segments + in-stent restenosis); mechanical atherectomy (debulks plaque without stent); laser (acute thrombotic + chronic total occlusions)
  • Unfavourable lesions for endovascular: long segment occlusion, heavily calcified, orifice lesion, lesions not crossable by guidewire
  • Surgical bypass: bioprosthetic (autograft preferred, homograft, xenograft, tissue-engineered) or synthetic (Dacron, ePTFE, polyurethane)
  • Amputation: only when no revascularisation option / spreading infection / unsalvageable
  • Concomitant CAD screening: 25% have correctable CAD
Special
  • >age 45: atherosclerosis; <45 diabetic: presenile atherosclerosis; <45 non-diabetic: Raynaud, Buerger, arteritis
  • 50% of PAD mortality is cardiac in origin
  • Untreated claudication: 5% major amputation at 5 years; 50% improve with smoking cessation + exercise
  • PAD = marker for early death more than limb loss
  • Rare causes: external compression, popliteal entrapment, thoracic outlet, cystic medial necrosis, fibromuscular dysplasia
24

Aortoiliac Disease (Leriche Syndrome)

C/P
  • Buttock, thigh, calf claudication
  • Impotence
  • Buttock muscle wasting
  • Triad: impotence + lower extremity claudication + buttock wasting
Inves
  • ABI, Duplex, CTA
Mng
  • BMT (as PAD General)
  • Endovascular: iliac angioplasty + stenting (first-line for short-segment disease)
  • Open surgery: aortobifemoral bypass (Y-graft from aorta to both femorals) — gold standard for diffuse aortoiliac disease
  • Extra-anatomic bypass (axillobifemoral, femorofemoral): high-risk patients unfit for major aortic surgery
  • Profundoplasty if disease confined to common femoral / profunda origin
Special
  • Distal abdominal aorta + iliac arteries
  • Erectile dysfunction needs bilateral hypogastric flow obstruction
25

Femoropopliteal Disease

C/P
  • Calf claudication
Inves
  • ABI, Duplex
  • Angiography for planning
Mng
  • BMT first with 3-month trial of supervised exercise + cilostazol
  • Endovascular: angioplasty ± self-expanding stent (good for short SFA lesions; less successful in long segments / heavy calcification)
  • Surgical bypass: femoropopliteal bypass with autologous saphenous vein (preferred — better patency) or prosthetic graft (ePTFE) when vein unavailable
  • Indications for intervention: lifestyle-limiting claudication despite BMT; rest pain; tissue loss
Special
  • Most common site: distal SFA at adductor hiatus (entrapment prevents compensatory dilation)
  • Often asymptomatic because PFA collateralises around distal SFA occlusion
26

Infrapopliteal (Tibioperoneal) Disease

C/P
  • Calf and sole claudication
  • Frequently limb-threatening
Inves
  • ABI, Duplex, angiography
Mng
  • Conservative management mostly (small vessels limit surgery)
  • Endovascular: tibial angioplasty (drug-coated balloons in selected cases)
  • Distal bypass: to dorsalis pedis or posterior tibial — reserved for limb salvage with adequate target vessel + good inflow
  • Treat underlying: DM (HbA1c <7%) and Buerger's (smoking cessation)
Special
  • Common in DM and Buerger's
  • Collaterals less developed than aortoiliac / femoropopliteal
27

Intermittent Claudication

C/P
  • Pain / ache / cramp / fatigue in muscles brought on by walking, relieved by rest
  • Distal to occlusive lesion ("one level downstream")
  • Aorto-iliac → buttock/thigh/calf
  • Common femoral → thigh/calf
  • SFA / popliteal → calf
  • Infrapopliteal → calf ± sole
Inves
  • ABI 0.5–0.9
  • Disappearing pulse after exercise to claudication (pulse returns after few min rest)
  • Treadmill exercise testing
  • Duplex
Mng
  • No functional disability: no specific treatment + annual follow-up + BMT
  • Lifestyle-limiting symptoms — 3-month trial of: supervised exercise (>30 min, >3×/week); cilostazol / pentoxifylline; BMT (smoking cessation, statin, antiplatelet, BP/glycaemic control)
  • If persistent disability after 3-month trial: evaluate for endovascular or surgical revascularisation
  • Outcome: 50% improve with smoking cessation + exercise alone; only 5% require major amputation at 5 years
Special
  • Mechanism: adequate perfusion at rest, but inadequate during exercise → anaerobic metabolism → painful local metabolic acidosis
  • Differentiate from neurogenic pseudoclaudication (back pain + bilateral + relieved by stooping)
28

Critical Limb Ischemia (Rest Pain)

C/P
  • Ischaemic rest pain (severe burning, forefoot/distal to metatarsals, resistant to opioids)
  • Aggravated by elevation
  • Relieved by hanging leg over bed (gravity)
  • ABI ≤0.5
  • Ankle pressure <70 mmHg / toe pressure <50 mmHg
  • Ischaemic ulceration / gangrene
  • Beurger's angle 30°
Inves
  • ABI
  • Duplex
  • CTA (preserved renal function) or MRA
Mng
  • No place for conservation when limb loss is impending — urgent revascularisation
  • Candidate for revascularisation: duplex/CTA/MRA → endovascular (angioplasty ± stent) OR surgical bypass (autologous saphenous vein preferred over prosthetic)
  • Not candidate + stable pain/lesion: medical (non-operative) — pain control, foot care, prevent infection
  • Not candidate + intolerable pain / spreading infection: amputation
  • Aggressive CV risk modification: smoking cessation, statin, antiplatelet, BP control
  • Pain control: opioids (often inadequate — neuritic component)
  • Investigate other lesions: extracranial cerebral vascular, coronary, intestinal angina, AAA, HTN, DM, hyperlipidaemia
Special
  • Hanging leg relieves ischaemic neuritis but NOT peripheral neuropathy (differentiation manoeuvre)
  • Infection ↑ resting metabolic demand → worsens rest pain
  • No place for conservation when limb loss is impending
29

Arterial Ulcer

C/P
  • Punched-out margin
  • Intensely painful
  • Base devoid of granulation tissue
  • Absent pulses
  • Lateral malleolus / dorsum of foot / distal digits
  • Thin shiny skin, absence of hair, brittle nails
Inves
  • Arterial Doppler + pulse volume recordings
  • ABI
  • X-ray (osteomyelitis)
Mng
  • Revascularisation is the only definitive treatment (healing requires higher perfusion than maintenance of intact skin)
  • Wound care: gentle dressing, avoid debridement of dry eschar before revascularisation, infection control
  • Pain control
  • Treat underlying PAD: smoking cessation, statin, antiplatelet, BP/glycaemic control
  • AVOID compression (worsens arterial ischaemia)
  • Amputation if unsalvageable
Special
  • Healing requires higher perfusion than maintenance of intact skin (CLI thresholds insufficient for healing)

G. Vasculitis

1 entry
30

Buerger's Disease (Thromboangiitis Obliterans)

C/P
  • Young men <40 with smoking
  • Triad: claudication + Raynaud's phenomenon + migratory superficial thrombophlebitis
  • Affects upper AND lower limbs
  • Tibial, plantar, radial arteries
  • Reduced/absent radial, ulnar, tibial, dorsalis pedis pulses
  • Brachial + popliteal pulses normal
  • Distal gangrene
Inves
  • Angiography of all four limbs
  • Pathological exam = confirmatory
Mng
  • Complete abstinence from smoking = cornerstone — arrests but does not reverse the disease
  • Sympathectomy for rest pain / ulceration (improves microcirculation)
  • Bypass rarely feasible due to small/medium vessels + segmental skip lesions + absence of distal target vessel
  • Endovascular: limited role for same anatomical reasons
  • Pain control + wound care
  • Amputation if gangrene develops
  • Iloprost (prostacyclin analogue) — vasodilator therapy used in some centres (not specified in deck for vascular block — use only if confirmed)
Special
  • Inflammatory occlusive disease of small/medium arteries AND veins
  • "Corkscrew collaterals" on angiography
  • Segmental "skip" lesions, distal circulation (infrapopliteal / distal to brachial)
  • Pain from lactic acid + substance P
  • Medium-vessel vasculitis classification
  • Pathology: thrombus + neutrophilic infiltration → organised thrombus + perivascular fibrosis + recanalisation

H. Venous

10 entries
31

Superficial Thrombophlebitis

C/P
  • Erythema, induration, tenderness along superficial vein
  • Triggered by: varicose veins, pregnancy, Buerger's, post-IV therapy, localised trauma
Inves
  • Clinical
Mng
  • Primary treatment: NSAIDs + limb elevation + local application of heat
  • Excision of involved vein if symptoms persist >2 weeks
  • Anticoagulation + ligation/resection if progressive proximal extension to saphenofemoral junction (risk of DVT/PE)
  • Address underlying cause (treat varicose veins, remove IV cannula, etc.)
Special
  • —
32

Thrombophlebitis Migrans (Trousseau Sign)

C/P
  • Migratory superficial thrombophlebitis
Inves
  • Workup for occult malignancy (CT chest/abdo/pelvis, tumour markers, age-appropriate cancer screening — esp. pancreatic)
Mng
  • Treat underlying cancer (often pancreatic adenocarcinoma)
  • LMWH for thrombosis (warfarin often less effective in cancer-associated thrombosis)
  • Symptomatic: NSAIDs, warm compresses, elevation
Special
  • Trousseau's sign — paraneoplastic, classically pancreatic adenocarcinoma
  • Special variety of superficial thrombophlebitis
33

Deep Vein Thrombosis (DVT)

C/P
  • Mostly silent
  • Onset 3rd–4th post-op day
  • Triad: swelling + calf/thigh pain + tenderness
  • Massive swelling → pelvic / femoral vein involvement
  • Homans sign (obsolete)
Inves
  • Wells score (≥2 → imaging; <2 → D-dimer first)
  • Whole blood D-dimer (low risk)
  • Compression duplex ultrasonography (>95% sens/spec; lack of compressibility = principal criterion)
  • MRV for iliac veins + IVC
  • CBC, D-dimer, PT, PTT, INR, LFT, KFT
Mng
  • Goals: limit thrombus extension; prevent PE; ↓ recurrence; ↓ post-thrombotic sequelae
  • Anticoagulation = mainstay
  • UFH protocol: 80 U/kg IV bolus → 15 U/kg/hr infusion; check PTT at 6 hours, target 60–80 sec
  • Warfarin: started same day as heparin; target INR 2–3 (or 2.5–3)
  • Stop heparin when INR therapeutic
  • LMWH (outpatient option): 30 mg SC BID; combined with warfarin (LMWH stops propagation, warfarin prevents recurrence)
  • Duration of anticoagulation: per individual risk (provoked vs unprovoked; cancer-associated etc.)
  • Thrombolytics: ONLY if phlegmasia develops (otherwise high bleeding risk outweighs benefit)
  • IVC filter: if anticoagulation contraindicated OR failed (recurrent PE despite therapeutic AC)
  • Thrombectomy: phlegmasia cerulea dolens / impending venous gangrene
  • Prophylaxis (general principles): Mechanical (early mobilisation 24–48h, elastic stockings, intermittent pneumatic compression intraoperative); Pharmacological (UFH 5000 U SC BID OR LMWH 30 mg SC BID — preferred); start preoperatively, continue while at risk
  • Avoid: sitting in a chair (most thrombogenic out-of-bed position)
  • DDx: cellulitis, lymphoedema, ruptured Baker's cyst, lymphangitis, haematoma
Special
  • Virchow's triad: endothelial injury + stasis + hypercoagulability
  • LMWH advantages: longer t½, higher bioavailability, predictable response, no monitoring, safe in head injury, doesn't affect PTT
  • Sitting in a chair = most thrombogenic out-of-bed position
  • Outcomes: PE, paradoxical embolism, post-phlebitic syndrome, phlegmasia alba dolens → cerulea dolens → venous gangrene
34

Pulmonary Embolism

C/P
  • Sudden death (massive PE → right ventricular outflow obstruction → acute right HF)
  • Asymptomatic (small)
  • Haemorrhagic infarction if underlying chronic venous congestion (mitral stenosis, left HF)
  • Cor pulmonale (recurrent emboli → permanent ↑ pulmonary vascular resistance → right HF)
Inves
  • (Deck doesn't specify CTPA / V/Q for PE workup — those live in respiratory module)
Mng
  • Pharmacological: morphine + oxygen + thrombolytics + anticoagulant
  • Anticoagulation: same as DVT (UFH bolus + infusion → warfarin; or LMWH + warfarin)
  • Thrombolytics: indicated for massive PE (haemodynamic compromise)
  • Surgical embolectomy: for massive PE when thrombolytics contraindicated or failed
  • IVC filter: when anticoagulant contraindicated
  • Resuscitation: ABCDE, vasopressors for hypotension, mechanical ventilation if needed
Special
  • From systemic vein DVTs
  • Lung's dual blood supply (bronchial + pulmonary) protects healthy lungs from medium emboli; CVC removes this protection
  • Most common direct cause of death in surgical patients (autopsy studies)
35

Paradoxical Embolism

C/P
  • Systemic infarction (stroke, limb ischaemia, mesenteric ischaemia) in patient with DVT
Inves
  • Echo with bubble study for septal defect (PFO or ASD)
  • Imaging of infarcted territory
Mng
  • Anticoagulation (treat the DVT)
  • Close cardiac septal defect (percutaneous PFO/ASD closure) for recurrent paradoxical embolism
  • Treat infarcted organ (per organ — stroke pathway, limb ischaemia pathway)
Special
  • Venous embolus crosses to systemic circulation via cardiac septal defect (patent foramen ovale / ASD)
  • Lodges in any systemic organ
36

Phlegmasia Alba / Cerulea Dolens

C/P
  • Phlegmasia alba dolens (white leg) → progresses to phlegmasia cerulea dolens (blue leg, massive DVT with arterial compromise) → venous gangrene
  • Painful, cyanotic, swollen limb
Inves
  • Duplex (urgent)
Mng
  • Aggressive anticoagulation: IV heparin
  • Thrombolytics: phlegmasia is the sole DVT indication for thrombolytics in this deck
  • Thrombectomy: for phlegmasia cerulea dolens or impending venous gangrene (limb-salvage procedure)
  • Limb elevation
  • IVC filter if anticoagulation contraindicated
  • Fasciotomy if compartment pressure rises
Special
  • End-stage venous limb complication of DVT
  • Differentiates from acute arterial ischaemia (cyanotic + swollen vs pale + cold)
37

Varicose Veins

C/P
  • Aching, heaviness aggravated by prolonged standing, relieved by elevation/compression
  • Tortuous, dilated palpable subcutaneous veins (>4 mm)
  • Female predominance, prolonged-standing occupations
  • Pregnancy-aggravated
  • Complications: bleeding, superficial thrombophlebitis, eczema, lipodermatosclerosis, ulceration
Inves
  • Examined while standing
  • Duplex U/S (status of GSV, SSV, SFJ, SPJ, deep veins, perforators)
  • Trendelenburg test (SFJ vs perforator incompetence)
  • Ochsner-Mahorner / multiple tourniquet test
  • Schwartz test (tap at SFJ → impulse at lower varicose vein)
  • Fegan's test (crescentic gap in deep fascia at incompetent perforators)
Mng
  • 5 treatment categories: reassurance · compression therapy · pharmacological · surgery · minimally invasive
  • Reassurance + lifestyle: leg elevation, weight loss, avoid prolonged standing
  • Compression therapy indications: postthrombotic varicose veins, minimal symptoms, unfit/unwilling for surgery, after surgery/sclerotherapy/laser
    • Class I (18–21 mmHg) — minor varicosities
    • Class II (26–34 mmHg) — uncomplicated varicose veins
    • Class III (>34 mmHg) — complicated varicose veins / venous ulcers
    • Contraindicated in PAD + cardiac failure
  • Surgery indications: varicosities >4 mm; varicosity with complications; refractory to medical/compression
  • Trendelenburg's surgery: identify GSV + saphenofemoral junction → ligate tributaries → strip GSV from groin to knee
  • SEPS (subfascial endoscopic perforator surgery): endoscopic interruption of incompetent medial calf perforators using bipolar coagulation/clips under direct vision — difficult with lipodermatosclerosis
  • Sclerotherapy: for telangiectasias / reticular / small varices below knee; agents = 0.2% sodium tetradecyl sulfate, polidocanol, hypertonic saline; 25–30 gauge needle, ≤0.1 mL per injection; pressure dressing 72h; complications = bruising, phlebitis, ulceration
  • Endovenous laser: USG-guided cannulation → laser fibre into vein → energy ablates endothelium → vein thromboses; compression bandage for 2 days
  • Radiofrequency ablation: USG-guided → heat denatures vein wall collagen
  • Foam sclerotherapy (Tessari method): foam made by to-and-fro motion of 1% polidocanol or 1–3% sodium tetradecyl sulfate + air; ≤20 mL per sitting
  • Other minimally invasive: catheter-directed sclerotherapy; hyperheated steam obliteration
Special
  • Primary (idiopathic) = majority
  • Secondary causes: pelvic masses (pregnancy, fibroids, ovarian mass, pelvic tumour), pelvic surgery/irradiation, previous DVT
  • GSV varicosity: medial thigh + calf (60%)
  • SSV varicosity: posterolateral calf (20%)
  • Anterolateral long saphenous tributary
  • Saphena varix (groin lump at SFJ)
  • Blow outs = incompetent perforators
38

Chronic Venous Insufficiency

C/P
  • Whole-leg oedema
  • Skin pigmentation (haemosiderin), eczema, lipodermatosclerosis
  • Ankle flare (corona phlebectatica)
  • Atrophie blanche (pale area around ankle)
  • Champagne bottle sign (prominent calf, narrow ankle)
  • Brawny skin
Inves
  • Duplex (deep + superficial + perforators)
  • CEAP staging
Mng
  • Conservative + lifestyle: leg elevation, mobilise, weight loss, avoid prolonged standing
  • Compression therapy = cornerstone — graduated stockings (Class II/III depending on severity)
  • Skin care: emollients for dry skin; topical steroids for varicose eczema
  • Treat superficial / perforator incompetence: surgery / endovenous laser / RFA / sclerotherapy / SEPS
  • Treat ulceration: see Venous Ulcer entry
  • Avoid compression if PAD coexists (check ABPI >0.8 before compression)
Special
  • Failure of muscle pump, unidirectional valves, or negative intrathoracic pressure → stasis
  • Gaiter's zone = handbreadth around malleoli (where complications occur)
  • Telangiectasia <1 mm intradermal; reticular vein <4 mm non-palpable subdermal; varicose vein >4 mm palpable
39

Venous Ulcer

C/P
  • Just proximal to medial malleolus (gaiter's area, over medial calf perforators)
  • Irregular sloping white edges
  • Slough + exudate
  • Surrounding lipodermatosclerosis, pigmentation
  • Associated varicose veins
Inves
  • Duplex venous + Doppler ankle BP
  • ABPI (to exclude arterial cause; needs >0.8 for safe compression)
  • CBC, ESR, CRP, fasting lipids
  • Blood glucose
Mng
  • Compression therapy = the most important conservative treatment — Class III graduated compression stockings
  • Conservative: encourage mobilisation (venous return); leg elevation (↓ venous pressure + swelling)
  • Local ulcer management: debridement of ulcer; irrigation with NS; topical steroids if eczematous reaction around ulcer
  • AVOID topical antibiotics (encourages resistance + dermatitis)
  • Dressing changes: ulcer inspected on every change; bandages applied + frequently changed by experienced nurse
  • Surgical varicose vein treatment (Trendelenburg / endovenous laser / RFA / sclerotherapy) — if patient fit/willing + superficial venous incompetence alone (no deep vein insufficiency)
  • Surgical debridement if necrotic
  • Long-term prevention: Class I or II graduated stockings after healing
  • Antibiotics only if clinical infection (cellulitis)
Special
  • ~85% of chronic lower limb ulcers are venous
  • Mixed (venous + arterial): 15–30% of venous ulcer patients
  • Other ulcer causes: vasculitic (RA, pyoderma gangrenosum), malignant (Marjolin), infective (TB, syphilis, leprosy), traumatic, diabetic neuropathic, haemolytic anaemia (sickle, pernicious)
40

Post-Thrombotic Syndrome

C/P
  • Chronic aching + heaviness of whole leg
  • Itching from haemosiderin deposition (brown around ankle)
  • Whole-leg oedema
  • Secondary varicose veins (irregular pattern, crossing veins at groin)
  • Venous ulcer above medial malleolus
  • Venous claudication
Inves
  • Duplex (NOT plain U/S)
  • D-dimer
  • Blood tests for clotting
Mng
  • Encourage mobilisation (muscle pump)
  • Leg elevation (improves venous return)
  • Compression therapy — treats ulcer + prevents recurrence
  • Antibiotics if cellulitis
  • Long-term compression stockings post-ulcer healing
  • Skin care: emollients, topical steroids for eczema
  • Address underlying: if recurrent DVT consider long-term anticoagulation
  • Surgical varicose vein treatment if secondary varicosities symptomatic + deep system patent
Special
  • Late DVT complication from valvular damage + venous obstruction
  • Veins crossing groin to anterior abdominal wall = iliofemoral collaterals

I. Acute Limb Ischemia & Trauma

4 entries
41

Acute Limb Ischemia

C/P
  • 6 Ps: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Poikilothermia
  • Pale → cyanosed → fixed mottling & cyanosis
  • Empty veins (vs normal contralateral)
  • Sensory loss progression: light touch → vibration → proprioception → deep pain → pressure sense
  • Intrinsic foot muscles affected first
  • Late: muscle turgidity (rigor) = irreversible
  • Wet gangrene in pure acute / dry gangrene in acute-on-chronic
Inves
  • Duplex (extension of physical exam)
  • CTA = gold standard for planning (check creatinine)
  • DSA (if thrombolysis planned; "meniscus sign" at bifurcation for embolus; saddle embolus at aortic bifurcation)
  • MRA (less nephrotoxic; bilateral popliteal aneurysm detection)
Mng
  • Goals: prevent thrombus propagation + restore blood flow + preserve limb and life + prevent recurrent thrombosis
  • Immediate management (all patients): IV heparin (anti-propagation — bolus then infusion, target PTT 60–80 sec); analgesia; optimise underlying condition (treat AF, CHF, electrolytes)
  • Simple bedside measures to improve perfusion: keep foot dependent; avoid pressure over heel; avoid temperature extremes (do NOT warm — ↑ metabolic demand); maximum tissue oxygenation; correct hypotension
  • Treatment by Rutherford stage:
    • Stage I (viable) → imaging first → revascularisation
    • Stage IIA (marginally threatened) → imaging first → revascularisation
    • Stage IIB (immediately threatened) → bedside imaging only if no delay → emergency revascularisation
    • Stage III (irreversible) → amputation (revascularising dead tissue causes fatal reperfusion)
  • Embolic + viable limb: Fogarty embolectomy via common femoral arteriotomy (proximal + distal control of vessel FIRST, then arteriotomy) → balloon catheter passed through embolus, inflated, withdrawn → repeat for deep femoral + iliac arteries → post-op warfarin (target INR 2–3)
  • Thrombotic short segment: catheter-directed thrombolysis → recanalised vessel ready for balloon angioplasty or bypass
  • Thrombotic long segment: surgical bypass with autologous vein or prosthetic graft (requires satisfactory inflow + outflow vessels)
  • Revascularisation options: thromboembolectomy + catheter-directed thrombolysis + endovascular techniques + bypass surgery
  • Post-revascularisation: monitor for reperfusion syndrome (K+, CK, myoglobin, urine output, ECG); consider prophylactic fasciotomy if prolonged ischaemia
  • Treat underlying cause: AF → long-term anticoagulation; mural thrombus → echo + AC; PAD → BMT + intervention
Special
  • Tissue infarction timelines: brain 4–8 min, heart 15–20 min, limbs 5–6 hours
  • 80% of emboli are cardiac (AF most common; mural thrombus post-MI; valvular; CHF; atrial myxoma)
  • Embolic vs thrombotic: sudden vs hours/days onset; no claudication vs claudication history; no bruit (except aneurysm site) vs bruit across trunk; clinical diagnosis vs angiography
  • Other emboli: infective, parasitic, tumour, fat (long bone fractures → ARDS), air (head/neck surgery), therapeutic
  • ABI <0.9 = sensitive + specific for arterial injury
  • Rutherford Class IIB defined by motor deficit + inaudible arterial Doppler
  • DDx of acute painful extremity: ALI, compartment syndrome, phlegmasia cerulea dolens, CVA, disc herniation, spinal cord tumour
42

Vascular Trauma

C/P
  • Hard signs: pulsatile/arterial bleeding, persistent haemorrhage with shock, expanding/pulsatile haematoma, bruit/thrill, distal ischaemia
  • Soft signs: small stable haematoma, related nerve injury, unexplained hypotension, prior haemorrhage history, proximity to major vessel
  • Partial transection bleeds more than complete (cannot retract/spasm)
  • Posterior knee dislocation → popliteal artery tear (anchored across joint)
Inves
  • ABI (gatekeeper if no hard signs; <0.9 → CTA)
  • CTA (if soft signs + ABI <0.9)
  • On-table arteriogram (if hard signs)
  • Completion angiogram post-repair
Mng
  • ATLS first — ABCDE
  • Initial steps (6): control bleeding → replace volume loss → cover wounds → reduce fractures/dislocations → splint → re-evaluate
  • Ischaemia management timeline: rapid resuscitation → urgent exploration → revascularisation → ? fasciotomy
  • Hard signs algorithm: immediate OR + on-table arteriogram
  • Soft signs algorithm: ABI → if <0.9 → CTA → if positive → OR; if negative → non-operative observation
  • No hard signs + ABI ≥0.9: non-operative management
  • Surgical principles:
    • Proximal + distal control of injured artery FIRST (before opening vessel — prevents catastrophic exsanguination)
    • Minor injury: ligation / direct suture / patch angioplasty
    • Major injury: interposition grafting — autologous vein in contaminated fields (synthetic = infection risk); spiral/panel grafting to enlarge vein
    • Complex injury with soft-tissue loss: extra-anatomic bypass through clean tissue plane
    • Damage control (ligation) if unstable patient
    • Endovascular techniques (covered stents) for selected injuries
  • Completion angiogram documents distal flow + technical success
  • Prophylactic fasciotomy if lower leg injury / prolonged warm ischaemia time
  • Catheter-related complications: arterial perforation, internal dissection, pseudoaneurysm, AV fistula
Special
  • Mechanisms: blunt, penetrating (low velocity / high velocity / shotgun), iatrogenic
  • Presentation timeline: immediate exsanguination or spasm → subacute pseudoaneurysm (hours-days) → chronic AV fistula (weeks-months)
  • Synthetic grafts avoided in contaminated fields (infection risk)
  • Catheter-related: arterial perforation, internal dissection, pseudoaneurysm, AV fistula
43

Compartment Syndrome

C/P
  • Severe pain on passive stretching of involved muscles
  • Numbness in webspace between great toe + 2nd toe (deep peroneal nerve) = diagnostic
  • Tense leg oedema
  • Pulses may be present initially
  • Calf most commonly (anterior tibial compartment)
Inves
  • Clinical diagnosis (do NOT delay surgery for measurements)
  • Compartment pressure measurement (when suspicion low-moderate); diagnostic threshold typically >30 mmHg
Mng
  • Urgent fasciotomy = the only treatment
  • Calf: four-compartment fasciotomy (anterior, lateral, superficial posterior, deep posterior) via medial + lateral incisions
  • Thigh + arm: anatomy-specific fasciotomies
  • Avoid delay: irreversible muscle necrosis within hours
  • Post-fasciotomy: leave wounds open initially → delayed primary closure or split-thickness skin graft once swelling resolves
  • Treat the cause: release tight cast, remove constrictive dressings, drain haematoma
  • Monitor for reperfusion syndrome (K+, myoglobin, urine output)
  • Prevent: prophylactic fasciotomy in lower leg trauma + prolonged warm ischaemia
Special
  • Fascia doesn't stretch → swelling = tourniquet
  • Causes — decreased compartment size: plaster casts, circumferential 3rd-degree burn, external compression, military anti-shock garments, splints
  • Causes — increased compartment volume: vascular injury, blast, bone fracture, crush, electrical burns, haematoma, ischaemia/reperfusion, sepsis, large-volume resuscitation, severe exertion, severe hypotension, prolonged surgery/immobilisation
  • Local: muscle necrosis, nerve damage
  • Distal: renal failure from myoglobin
44

Reperfusion Syndrome

C/P
  • Cardiac arrhythmia (hyperkalaemia)
  • ARDS / pulmonary oedema (lung injury)
  • Acute kidney injury (myoglobin → haematin → ATN in acidic urine)
  • Mucosal oedema (GI)
  • Worsens with hypotension / hypovolaemia
Inves
  • K+, creatinine, CK, myoglobin (serum + urine), ABG, lactate
  • ECG (peaked T waves, widened QRS in hyperkalaemia)
  • Urine output monitoring
Mng
  • Aggressive IV hydration (maintain urine output >100 mL/hr)
  • Urinary alkalinisation (sodium bicarbonate IV → urine pH >6.5 prevents haematin precipitation in tubules)
  • Hyperkalaemia management: calcium gluconate IV (membrane stabilisation); insulin + glucose (shift K+ intracellularly); salbutamol nebulised; sodium bicarbonate; K+-binding resins / dialysis if refractory
  • Forced diuresis: mannitol + furosemide (controversial)
  • Dialysis if refractory hyperkalaemia / ATN with anuria
  • AVOID revascularising dead (Class III Rutherford) limbs → fatal reperfusion → primary amputation instead
  • Prophylactic fasciotomy during revascularisation of prolonged ischaemia
  • Monitor cardiac, renal, respiratory function in HDU/ICU
Special
  • Substances released: K+, lactic acid, myoglobin
  • Myocardial depressant factors: C3a, TxA2, LTD4, PAF
  • Mechanism: ischaemia → ROS + Ca²⁺ → mitochondrial permeability transition pore opens → cytochrome C → caspases → apoptosis
  • Myoglobin structurally similar to haemoglobin

J. Gangrene / Infarction

6 entries
45

Dry (Senile) Gangrene

C/P
  • Blackened, mummified skin in limb
  • Starts at big toe (senile)
  • Conical stump line of separation
  • Red zone of acute inflammation at margin (line of demarcation)
  • Progresses proximally until reaches good collateral circulation (e.g. ankle)
Inves
  • ABI, Duplex, CTA (assess proximal arterial supply for surgical planning)
Mng
  • Wait for autoamputation (allows natural separation at level of good collaterals — conical stump)
  • Surgical amputation at level of healthy collateral flow (must be above demarcation line for stump to heal)
  • Address underlying atherosclerosis: smoking cessation, statin, antiplatelet, BP/glycaemic control
  • Revascularisation if feasible (proximal target available) to halt progression
  • Wound care: keep dry, prevent secondary infection (which converts to moist gangrene)
  • Pain control
  • No sepsis risk in true dry gangrene (mild toxaemia)
Special
  • Arterial occlusion + patent veins
  • Limbs only (surface evaporation + venous drainage of existing fluid)
  • Slow putrefaction, mild toxaemia
  • Underlying: atherosclerosis (senile)
  • Conical stump because muscles/bones have better collaterals than skin distally
  • No sepsis risk
46

Moist (Wet) Gangrene

C/P
  • Oedematous, swollen, blackened gangrene
  • Poor demarcation
  • No line of separation
  • Rapid putrefaction, severe toxaemia
Inves
  • Bloods: CBC, CRP, lactate, U&Cr, blood cultures
  • X-ray (soft tissue gas)
  • CTA if revascularisation considered
Mng
  • Urgent surgical debridement / amputation (limb-saving if possible, life-saving if not)
  • Broad-spectrum IV antibiotics (cover anaerobes + Gram-negatives)
  • IV fluid resuscitation + sepsis bundle
  • Treat underlying cause: remove tourniquet, decompress crushed limb, treat bed sores
  • Internal organ moist gangrene (intestine): emergency laparotomy + resection
  • Higher-level amputation than initially apparent — extent often greater than externally visible
Special
  • Occlusion of BOTH artery AND vein
  • Causes: crush injuries, tight tourniquet, bed sores, diabetic gangrene
  • Internal organs (intestine) more serious — rich tissue fluid, intraluminal saprophytes in large numbers
47

Diabetic Gangrene

C/P
  • Starts dry in big toes → rapidly becomes moist/infective from secondary infection → oedematous + moist
  • Rapid putrefaction, severe toxaemia
  • Poor demarcation, no line of separation
Inves
  • Glucose, HbA1c, CBC, CRP, lactate, blood cultures
  • X-ray (soft tissue gas, osteomyelitis)
  • Duplex + CTA (assess perfusion for revascularisation)
  • Deep tissue cultures (NOT superficial swabs)
Mng
  • Sepsis bundle: IV fluids, broad-spectrum antibiotics (covering Staph aureus + Strep + Pseudomonas + anaerobes), source control
  • Glycaemic control: sliding scale insulin / DKA correction
  • Urgent surgical debridement / amputation (often higher level than expected)
  • Revascularisation if proximal target available and limb potentially salvageable
  • Wound left open to heal by secondary intention
  • Off-loading if any salvageable foot
  • Multidisciplinary: vascular surgery + endocrine + microbiology + podiatry + plastic surgery
  • Prevention: foot screening, footwear, glycaemic control, PAD treatment
Special
  • Mechanism: DM → atherosclerosis → thrombosis + neuropathy (unfelt injury) + high tissue sugar + low immunity favouring infection
  • Conversion from dry to moist is what makes diabetic gangrene dangerous
48

Gas Gangrene

C/P
  • Swollen, oedematous, painful, crepitant limb
  • Deep wound especially in muscles
  • Often post-trauma / war injury / deep contamination
Inves
  • Soft tissue X-ray (gas in tissues)
  • Wound culture (Clostridium)
  • Bloods: CBC, lactate, CK
Mng
  • Emergency surgical debridement — extensive, often multiple returns to theatre
  • Amputation if widespread / unable to control
  • High-dose IV antibiotics: penicillin + clindamycin (deck doesn't specify regimen — general clostridial cover)
  • Wound left open (anaerobes flourish in closed/anoxic environments)
  • Hyperbaric oxygen therapy if available (toxic to anaerobes)
  • Aggressive fluid resuscitation + sepsis management
  • Tetanus prophylaxis
Special
  • Gas-forming Clostridia (Gram +ve anaerobic)
  • Powerful toxins → tissue necrosis + putrefaction
  • Crepitus from CO₂ (carbohydrate fermentation)
  • Doesn't complicate superficial wounds (anaerobes need O₂-poor environment)
49

Infective Gangrene (Cancrum Oris)

C/P
  • Lung gangrene on top of lung abscess
  • Cancrum oris: massive destructive necrosis of cheek in debilitated children
  • Severe toxaemia
Inves
  • Bloods, blood cultures, wound swabs
  • Imaging of affected area (CT for lung)
Mng
  • High-dose IV antibiotics (broad-spectrum covering anaerobes; penicillin G for Treponema)
  • Surgical debridement of necrotic tissue
  • Nutritional support (esp. cancrum oris in debilitated children)
  • Treat underlying: lung abscess drainage, malnutrition correction
  • Reconstructive surgery later for facial defects in cancrum oris survivors
Special
  • Cancrum oris caused by Treponema vincenti
  • Cheeks of debilitated children
50

Infarction — Pale & Red

C/P
  • Pale infarct: solid organ (heart, spleen, kidney) — wedge-shaped pale area
  • Red infarct: loose tissue (lung) or dual-supply (lung, small intestine) — wedge of dark red consolidation
  • Brain: wedge of liquefaction → residual cystic space (no scar)
  • Small bowel: extensive dark/black loops
Inves
  • Per organ (ECG/troponin for cardiac, CT for stroke/PE/mesenteric, etc.)
Mng
  • Revascularisation per organ (thrombolysis, embolectomy, bypass, PCI, etc.)
  • Treat underlying: anticoagulation for thromboembolism, address atherosclerosis
  • Supportive care per affected organ
  • Resection of non-viable bowel (mesenteric infarct)
  • Healing: pale infarcts heal by fibrosis + dystrophic calcification → depressed organ surface; brain infarcts → cystic space (no fibrous stroma to scar)
Special
  • 99% arterial occlusion (thrombus/embolus); rarely prolonged venous obstruction
  • Coagulative necrosis (exception: liquefactive in CNS)
  • Pale: end-arterial circulation + dense tissue squeezes blood out
  • Red causes: venous occlusion (ovarian torsion, strangulated intestine, jugular vein), loose tissue, dual blood supply, previously congested tissue, reperfusion
  • Wedge shape from fan-shaped end-artery distribution (apex at occlusion, base at organ surface)
  • Healing: fibrosis + dystrophic calcification + depressed organ surface
  • Brain: liquefactive → cystic space (no fibrous stroma to scar)
  • Lines of Zahn = alternating platelet/fibrin + RBC layers (pre-mortem thrombus marker)

K. Lymphatic & Limb Swelling

5 entries
51

Primary Lymphedema

C/P
  • Lymphoedema congenita: shortly after birth (within 2 yr), males > females, mostly bilateral whole limb
  • Lymphoedema praecox: 2–35 years (peak post-menarche), females (3× male), usually unilateral, limited to knee
  • Lymphoedema tarda: onset after age 35, associated with obesity
  • Milroy's disease: congenital + hereditary; slanting of nails
Inves
  • Duplex (rule out venous)
  • Lymphoscintigraphy (radionuclide tracer to 1st web space, gamma camera)
  • Pelvic U/S / CT / MRI for underlying cause
Mng
  • Conservative / medical (cornerstone):
    • Light exercise (moving limb encourages lymph drainage)
    • Wrapping / bandaging (encourages flow toward trunk)
    • Manual lymph drainage massage (contraindicated in infection / clots / active disease)
    • Pneumatic compression (intermittent sleeve → moves lymph proximally)
    • Compression garments during exercise
    • Skin care + hygiene (oedematous limb prone to bacterial infection)
  • Complete Decongestive Therapy (CDT): combines lifestyle + manual drainage + compression + exercise
  • CDT contraindications: HTN, DM, paralysis, HF, blood clots, active infection
  • Antibiotics: for any superimposed cellulitis (low threshold)
  • Surgery (for severe / refractory): lymphatic-to-venous anastomosis; lymph node transplant
  • Weight management: obesity worsens outcomes
Special
  • <10% of primary lymphedema is congenital
  • Distinguished from secondary by age of onset and absence of identifiable cause
  • Praecox triggered by hormonal changes at puberty
52

Secondary Lymphedema

C/P
  • Slowly progressive limb swelling
  • Post-mastectomy / axillary clearance arm swelling
  • Triggered by minor trauma
  • Early signs: achiness, tingling, bursting/shooting pain, slight puffiness with pitting, tighter clothing/jewelry
  • Elephantiasis (chronic, advanced — hyperkeratotic, papillomatous, indurated)
Inves
  • Same as primary
  • Rule out tumour recurrence (brachial plexus involvement → radicular pain)
Mng
  • Same conservative + surgical principles as primary lymphedema (CDT, compression, surgery if refractory)
  • Skin protection (critical — oedematous limb is bacterial culture medium):
    • Protect hands when washing / gardening
    • Never walk barefoot
    • Use electric razor (no nicks)
    • Never let skin macerate
    • Wash + dry + antiseptic + plaster cuts immediately
    • Insect repellent sprays
    • Sun block
    • Seek medical attention if swollen / hot / painful
    • AVOID injections / blood tests / BP measurement on affected arm
    • Consider prophylactic antibiotics for travel
  • Avoid extremes: overuse, excessive pressure, hot/cold temperatures (heat ↑ blood flow → ↑ lymph production)
  • Gradual exercise programme with lymphedema specialist
  • Weight loss (obesity ↑ risk + severity)
  • Antibiotics with low threshold for cellulitis
  • Prevention post-axillary clearance: skin protection + early gentle exercise + monitoring
Special
  • Developed world: malignancy, post-surgical (mastectomy), radiotherapy
  • Less-developed world: filariasis (Wuchereria bancrofti)
  • Causes (broad): infection, parasites, mechanical injury including surgery, postphlebitic syndrome, neoplasms
  • Specifics: lymph node excision, RT, burns, varicose vein surgery, large wounds, scarring, metastases, infiltrative carcinoma, lymphoma, tumour pressure, chronic venous insufficiency, IVDU, cellulitis/erysipelas, lymphadenitis, TB, RA, dermatitis, psoriasis, sarcoidosis, pretibial myxoedema, paralysis, self-harm
53

Lymphangiosarcoma (Stewart-Treves)

C/P
  • Multiple subcutaneous nodules in upper limb
  • Years post-mastectomy/lymphedema
Inves
  • Biopsy (DDx: recurrent breast carcinoma)
  • Staging: CT chest/abdo/pelvis
Mng
  • Cytotoxic chemotherapy (some response)
  • Irradiation (some response)
  • Wide local excision if localised
  • Amputation sometimes required for limb-confined disease
  • Palliative care if metastatic (poor prognosis)
Special
  • Rare complication of chronic lymphedema (Stewart-Treves syndrome)
  • Prognosis usually poor
54

Klippel-Trenaunay Syndrome

C/P
  • Present at birth / early childhood
  • Abnormal lateral venous complex
  • Capillary naevus
  • Bony abnormalities
  • Hypo/aplasia of deep veins + limb lengthening
  • Coexisting lymphatic abnormalities common
Inves
  • Duplex, MRV (assess deep venous system before any venous surgery)
  • Plain X-ray + scanogram (limb length discrepancy)
Mng
  • Compression therapy (manage venous + lymphatic component)
  • Sclerotherapy / endovenous laser for symptomatic abnormal superficial veins — only if deep system is patent (deep system may be aplastic — removing collaterals → catastrophic)
  • Orthotic shoe lift for limb length discrepancy
  • Orthopaedic intervention for severe length discrepancy (epiphysiodesis)
  • Multidisciplinary: vascular surgery + orthopaedics + genetics + interventional radiology
Special
  • AGGF1 mutation
  • Vascular malformation cause of limb swelling
55

Lipoedema

C/P
  • Always bilateral
  • Symmetrical
  • Feet/toe sparing
Inves
  • Clinical diagnosis (rule out lymphedema with Stemmer's sign — negative in lipoedema)
Mng
  • Lifestyle: diet + exercise (though typical pattern persists)
  • Compression garments (may help associated venous insufficiency)
  • Manual lymph drainage
  • Liposuction (specialist centres) for refractory disabling cases
Special
  • Distinguishing feature: foot/toe sparing (vs lymphoedema which involves dorsum of foot, positive Stemmer's sign)

L. Pathology Entities

5 entries
56

Atherosclerosis

C/P
  • Asymptomatic until complicated
  • Stenosis → angina / claudication
  • Acute occlusion → MI / stroke / gangrene
  • TIA (cerebral, <1 hour, focal, resolves)
  • Cerebral infarction (persistent)
  • Intermittent claudication (femoral)
  • Abdominal claudication / small bowel infarction (mesenteric)
  • Erectile dysfunction (bilateral hypogastric)
  • Aneurysm (abdominal aorta dominant)
Inves
  • Lipid profile (LDL, HDL, triglycerides)
  • Imaging of affected vessel (Duplex / CTA / MRA / angiography)
  • Risk stratification (QRISK / Framingham used outside this deck)
Mng
  • Primary prevention — risk factor modification:
    • Smoking cessation (single most important modifiable factor)
    • BP <130/85 mmHg (ACEi + β-blocker preferred)
    • LDL <100 mg/dL via statin
    • HbA1c 7% in diabetics
    • Weight loss, exercise (>30 min, >3×/week)
    • Mediterranean diet
  • Secondary prevention:
    • Antiplatelet (aspirin / clopidogrel)
    • High-intensity statin
    • BP + glycaemic control
    • Cardiac rehab
  • Per-organ revascularisation:
    • Coronary: PCI / CABG (cardiology block)
    • Carotid: CEA / CAS (within 2 weeks of symptoms)
    • Peripheral: endovascular / bypass per Rutherford / Fontaine stage
    • Renal: angioplasty + stent if refractory HTN / progressive CKD
    • Mesenteric: angioplasty + stent / bypass
  • Acute coronary syndrome / stroke: per emergency pathways (thrombolysis, PCI, thrombectomy)
  • Aneurysm management: see AAA entry
Special
  • Definition: patchy intimal thickening by lipid deposits + proliferated CT ("athere" = deposition, "sclerosis" = hardening)
  • Stages: fatty streak (precursor, infancy, reversible, foam cells, asymptomatic) → simple plaque (basic, white-yellow nodule, eccentric, partial obstruction, slow growth → collaterals) → complicated plaque (pathogenic, rupture/ulceration/thrombus/haemorrhage/aneurysm)
  • Distribution descending: lower abdominal aorta > coronary > popliteal > internal carotid > Circle of Willis
  • Targets: heart, brain, kidneys, lower limbs
  • Spares: upper limbs, mesenteric
  • Major RFs: age, male sex (M:F = 5:1 <55, 1:1 >70), FHx, genetic, hyperlipidaemia, smoking, HTN, DM
  • Protective: moderate alcohol, antioxidants (estrogen pre-menopausal)
  • Risk factors are additive
  • Pathogenesis (Response to Injury): endothelial injury → ↑ permeability + adhesion molecules → LDL accumulation → monocyte adhesion → macrophages → oxidised LDL engulfment → foam cells → IL-1/TNF/MCP-1/GFs → SMC proliferation → fibrous cap
  • Complications mechanism for aneurysm: ↑ MMP from plaque macrophages + medial ischaemia (thick intima ↑ diffusion distance) + HTN-related vasa vasorum narrowing → loss of SMCs + fibrosis + amorphous proteoglycan accumulation
57

Pulmonary Congestion

C/P
  • Dyspnoea
  • Heavy, moist, dark red lung
  • Frothy blood-tinged fluid on cut section
Inves
  • Chest X-ray (Kerley B lines, perihilar oedema, pleural effusions)
  • Echo (LV function, mitral valve)
Mng
  • Treat underlying cardiac cause:
    • Left HF: diuretics (furosemide), ACEi/ARB, β-blocker, MRA per HF protocols
    • Mitral stenosis: rate control, anticoagulation (AF common), balloon mitral valvotomy / surgical valve replacement
  • Acute pulmonary oedema: sit up, high-flow O₂, IV diuretic, IV nitrate, morphine, consider CPAP / mechanical ventilation
  • Long-term: salt + fluid restriction, weight monitoring
Special
  • Causes: mitral stenosis, left-sided heart failure
  • Early: engorged interalveolar capillaries + intra-alveolar oedema + haemorrhage
  • Late: heart failure cells (macrophages engulfing hemosiderin) + thickened/fibrotic septa
58

Hepatic Congestion (Nutmeg Liver)

C/P
  • "Nutmeg" gross appearance (dark red spots vs yellow fatty background)
  • Late: shrunken, firm, irregular surface (cardiac cirrhosis)
  • Hepatomegaly, RUQ discomfort, raised JVP
Inves
  • LFTs (raised AST/ALT, raised bilirubin, prolonged PT)
  • US abdomen (hepatic vein dilatation)
  • Echo (right HF)
Mng
  • Treat right HF: diuretics, salt restriction, fluid restriction
  • Treat underlying cause: cor pulmonale → treat lung disease; left-sided HF causing biventricular failure → optimise; constrictive pericarditis → pericardiectomy
  • Avoid hepatotoxic drugs
  • Manage cardiac cirrhosis complications: ascites (diuretics, paracentesis), encephalopathy, varices
Special
  • Right-sided heart failure
  • Microscopy: centrilobular (Zone 3) necrosis + peripheral (Zone 1) steatosis + congested central veins/sinusoids
  • Late: hemosiderin in Kupffer cells + central fibrosis (cardiac cirrhosis)
  • Zone 3 most vulnerable (closest to central vein, furthest from arterial O₂)
59

Splenic Congestion

C/P
  • Splenomegaly (enlarged, heavy, dark cut section)
  • Hypersplenism (cytopenias)
Inves
  • US abdomen (splenomegaly + portal vein dilatation)
  • LFTs, clotting (cirrhosis)
  • Doppler portal vein
Mng
  • Treat portal hypertension: β-blocker (propranolol) for variceal prevention; TIPS / surgical shunt for refractory; treat underlying liver disease
  • Splenectomy: reserved for refractory hypersplenism or hypersplenism-related complications
  • Manage cirrhosis (alcohol cessation, hepatitis treatment, transplantation)
  • Vaccinate against encapsulated organisms if splenectomy planned
Special
  • Cause: liver cirrhosis → portal hypertension
  • Congested sinusoids + atrophic follicles
  • Gammna-Gandy bodies (fibrosiderotic nodules) = hemosiderin leak + fibrosis
60

Thrombosis (Virchow's Triad / Lines of Zahn)

C/P
  • Arterial: ischaemia / infarction
  • Venous: stasis, oedema, embolisation
  • DVT: swollen, stiff, painful, tender, cord-like vein
Inves
  • Duplex (venous)
  • CTA / angiography (arterial)
  • Thrombophilia screen (Protein C/S, ATIII, Factor V Leiden, antiphospholipid Abs, prothrombin gene)
Mng
  • Anticoagulation = mainstay:
    • Acute: heparin (UFH bolus + infusion, target PTT 60–80 sec; or LMWH 30 mg SC BID)
    • Long-term: warfarin (target INR 2–3) or NOAC
    • Cancer-associated: LMWH preferred over warfarin
  • Thrombolysis in selected cases (massive PE, phlegmasia cerulea dolens, ischaemic stroke per pathway)
  • Mechanical thrombectomy for selected cases
  • IVC filter if anticoagulation contraindicated / failed
  • Address Virchow's triad components:
    • Endothelial: smoking cessation, statin, BP control, treat infection
    • Stasis: early mobilisation, compression stockings, IPC during surgery
    • Hypercoagulability: thrombophilia workup; lifelong AC if irreversible
  • Prophylaxis (perioperative): LMWH + mechanical methods per risk stratification
  • Treat consequence: PE pathway, DVT pathway, arterial occlusion pathway
Special
  • Virchow's triad: endothelial injury + altered blood flow + hypercoagulability
  • Normal hemostasis sequence: transient vasoconstriction (reflex neurogenic + endothelin) → primary hemostasis (VWF + collagen → platelet plug; ADP + TxA₂ recruit more platelets) → secondary hemostasis (tissue factor → extrinsic pathway → fibrin) → counter-regulation (t-PA)
  • Coagulation: intrinsic (XII), extrinsic (TF, starts hemostasis); thrombin amplifies V, VIII, XI
  • Anticoagulant inhibitors: antithrombin III (inactivates thrombin, IXa, Xa, XIa, XIIa), Protein C + S (inactivate Va, VIIIa; vitamin K-dependent)
  • Endothelial: normal = antiplatelet/anticoagulant/fibrinolytic; activated = procoagulant
  • Endothelial injury causes: atherosclerosis, endocarditis, vasculitis, prosthetic valves, hyperlipidaemia, HTN, hemodynamic, smoking, toxins, viruses, immune reactions
  • Stasis (DVT, right HF) vs turbulence (aneurysms, AF)
  • Hereditary hypercoagulable: Factor V Leiden, Protein C/S deficiency, antithrombin III deficiency
  • Acquired hypercoagulable: OCPs, pregnancy, postoperative, malignancy (pancreatic adenoca → Trousseau)
  • Arterial thrombi: usually over ruptured atherosclerotic plaques; mural (aorta/cardiac, don't occlude, embolise) vs occlusive (small arteries, wall-adherent, seldom embolise)
  • Cardiac thrombi: mural (don't occlude lumen) or vegetations (on valves)
  • Venous thrombi: thin-walled, easily injured, stasis-prone → occlude + embolise; subdivided into thrombophlebitis (inflammation-initiated, septic in suppurative areas / aseptic in trauma/radiation) vs phlebothrombosis (cardiac patients, post-op, post-labour)
  • Lines of Zahn = pre-mortem thrombus marker
  • Fates: lysis, fragmentation (septic emboli → pyaemia), occlusion, organisation (recanalisation + incorporation)
  • Propagating thrombus extends proximally until next venous tributary with normal flow, then platelets stick → process repeats toward heart

M. Procedures

1 entry
61

Amputation

C/P
  • Indications: critical limb ischaemia (rest pain + tissue loss), sepsis ± gangrene, trauma, neoplasm, congenital
  • Diabetic foot is the most common sepsis setting
  • Digital gangrene → amputation of digit + metatarsal head, wound left open
Inves
  • Vascular supply evaluation (mandatory pre-toe amputation)
  • Pre-op MDT assessment
  • Imaging if revascularisation considered
  • Pre-op anaesthetic + cardiac risk assessment
Mng
  • Critical limb ischaemia approach:
    • First-line = revascularisation (angioplasty / bypass)
    • Indications for primary amputation: unsuccessful revascularisation; primary option to control symptoms; patient choice over complex surgery; significant comorbidities
    • Primary aim: improve function + quality of life
  • Sepsis (diabetic foot) approach:
    • Glycaemic + sepsis control
    • Surgical drainage within 24h
    • Digital gangrene → amputation of digit + metatarsal head, wound left open
    • Revascularisation before surgery if pulses absent
  • Pre-op: determine level based on rehabilitative potential (more proximal = ↑ energy expenditure); MDT input essential (vascular, anaesthesia, physio, prosthetics, psychology); optimise comorbidities
  • Surgical principles (general):
    • Avoid undermining / devitalising skin flaps
    • Tourniquet to control haemorrhage (reduces blood loss without compromising healing)
    • Ligate vessels as encountered
    • Divide nerves cleanly + away from bone ends (avoid neuroma formation)
    • Test muscle viability with diathermy (bleeds / contracts = viable; if not → higher level)
    • Avoid unnecessary tension on flaps + unnecessary stump bulk
    • Suction drains
    • Avoid bandaging (can cause skin breakdown)
  • Severe sepsis: guillotine amputation of highly infected tissue with later definitive stage completion
  • Specific level techniques:
    • Toe: fishmouth or circular incisions
    • Ray: through metatarsal bone, tennis-racquet incision
    • Transmetatarsal: mid-metatarsal, plantar flap (excellent ambulation)
    • Mid-foot: proximal to metatarsals
    • Ankle: Syme + Pirogoff (seldom used in vascular practice)
    • BKA: long posterior flap technique (Burgess and Romano, 1967); tibia divided 14 cm below knee joint / 10–12 cm below tibial tuberosity (minimum 7.5 cm for limb fitting); rule of thirds for flap; tibia bevelled smoothly 1 cm proximal to skin wound; fibula divided 2 cm proximal to tibia; alternative = skew flaps
    • AKA: mid-femoral level, ≥15 cm above tibial plateau, ≥8 cm below inferior pubic ramus; fishmouth incision; equal anterior + posterior myoplastic flaps
    • Hip disarticulation / hindquarter: severe ischaemia extending proximally (aortoiliac inflow); high mortality, exceedingly poor ambulation
    • Upper limb: rare in vascular — trauma, failed/delayed revascularisation, infection
  • Post-op early management:
    • Pain control (epidural superior peri-op but doesn't prevent phantom pain)
    • Stump elevation + observation for haematoma
    • Antibiotics if infection
    • DVT prophylaxis
    • Refer to multidisciplinary pain team if refractory pain
  • Rehabilitation (start ASAP post-op):
    • Early physiotherapy: prevent flexion contractures + practice transfers
    • Stump shaping: elasticated graduated compression stump socks once healed
    • Early walking aids: Pneumatic Post Amputation Mobility Aid (max 40 mmHg)
    • Limb fitting delayed until ~6 weeks post-op (oedema subsided + stump shrunk)
  • Prosthesis selection: young athletic = sophisticated microchip-based limbs; elderly = simpler + lighter modular components
  • Phantom limb pain (~70%) + post-amputation pain (~80%): multidisciplinary pain management; no proven prevention
Special
  • Early complications: DVT, flap necrosis, wound infection, post-amputation pain, stump haematoma, flexion contractures, psychological
  • Late: excess stump bulbosity, bone erosion through skin, neuroma, ischaemia, osteomyelitis, adherent scar, ulceration
  • Post-amputation pain ~80%; phantom limb pain ~70%; no proven prevention; epidural superior peri-op but doesn't prevent phantom
  • Rehab + pneumatic post-amputation mobility aid (40 mmHg)
  • Limb fitting delayed to ~6 weeks post-op
  • Microchip prosthesis for young athletic; modular for elderly

Disease Classifications

8 entries
1

Wagner's Classification (Diabetic Foot Ulcer)

Grades (0–5)

GradeDescription
0Intact skin (impending ulcer)
1Superficial ulcer
2Deep ulcer to tendon, bone, or ligament
3Osteomyelitis
4Gangrene of toes or forefoot
5Gangrene of entire foot
2

CEAP Classification (Chronic Venous Disease)

C (Clinical)

ClassSigns
C0No visible or palpable signs
C1Telangiectasias, reticular veins
C2Varicose veins
C3Oedema
C4APigmentation + eczema
C4BLipodermatosclerosis + white atrophy
C5Skin changes with healed ulceration
C6Skin changes with active ulceration

E (Etiological)

  • Congenital · Primary · Secondary

A (Anatomical)

  • Anatomical distribution

P (Pathophysiological)

  • Reflux · Obstruction
3

Fontaine Classification (Chronic PAD)

StageClinical
IAsymptomatic
IIaMild claudication
IIbModerate to severe claudication
IIIIschaemic rest pain
IVUlceration or gangrene
4

Rutherford Classification — Chronic PAD

GradeCategoryClinical
00Asymptomatic
I1Mild claudication
I2Moderate claudication
I3Severe claudication
II4Ischaemic rest pain
III5Minor tissue loss
III6Major tissue loss
5

Stanford Classification (Aortic Dissection)

TypeDefinition
Type AInvolves ascending aorta
Type BDistal to aortic arch
  • Type A = emergent surgery (high risk of involving coronaries / pericardium)
  • Major RF = hypertension (NOT atherosclerosis)
6

Aneurysm Classification

By Domain

DomainCategories
AetiologyAtherosclerotic / Traumatic / Congenital / Inflammatory / Dissecting
StructureTrue (all 3 layers) / False (pseudoaneurysm)
ShapeFusiform / Saccular
Central siteAortic (commonest) / Splanchnic
Peripheral head & neckExtracranial / Intracranial
Peripheral limbUpper / Lower

Non-atherosclerotic Types

  • Berry · Charcot-Bouchard · Ventricular · Syphilitic · Connective tissue (Marfan, Ehlers-Danlos) · Mycotic · Vasculitic · Aortic dissection
7

Vasculitis Classification (by Vessel Size)

SizeDiseases
LargeTakayasu's arteritis · Giant cell arteritis · Behçet's disease
MediumPolyarteritis nodosa · Kawasaki's disease · Buerger's disease
SmallHypersensitivity angiitis
8

Lymphedema Clinical Stages

StageReversibilityTissueEdema
1ReversibleLittle/no hardnessSoft pitting, resolves with elevation
2IrreversibleHardStrong pressure produces pitting; doesn't resolve with elevation
3Irreversible (elephantiasis)Hard, skin papillomas—

Acute Assessment

5 entries
9

Wells Score (DVT)

+1 each

  • Active cancer (treatment within 6 months or palliative)
  • Paralysis / paresis / recent plaster immobilisation of lower extremities
  • Bedridden ≥3 days or major surgery within 12 weeks
  • Localised tenderness along deep venous distribution
  • Entire leg swollen
  • Calf swelling ≥3 cm larger than asymptomatic side (10 cm below tibial tuberosity)
  • Pitting oedema confined to symptomatic leg
  • Collateral superficial veins (non-varicose)
  • Previously documented DVT

−2

  • Alternative diagnosis at least as likely as DVT

Stratification

  • <2 → Low risk: D-dimer first; if positive → compression U/S
  • ≥2 → Intermediate/high risk: Compression U/S first; if positive → treat
10

Rutherford Classification — Acute Limb Ischaemia

ClassDescriptionSensoryMotorArterial DopplerVenous Doppler
IViableNoneNoneAudibleAudible
IIAMarginally threatenedMinimal / toesNoneMay / may notAudible
IIBImmediately threatenedModerate (>toes / rest pain)Mild–moderateNoneAudible
IIIIrreversibleProfound / anaestheticProfound (rigor)NoneNone
  • Class IIB = motor deficit + inaudible arterial Doppler → emergency revascularisation, no delay for imaging
  • Class III → amputation (revascularising dead tissue → fatal reperfusion)
11

6 Ps of Acute Limb Ischaemia

  • Pain (foot / calf, at rest)
  • Pallor (early sign)
  • Pulselessness (defining feature)
  • Paraesthesia (>50% of ALI patients)
  • Paralysis (most ominous; severe ischaemia)
  • Poikilothermia (perishingly cold)
12

Ankle-Brachial Index (ABI)

Calculation

  • Right ABI = higher right ankle systolic ÷ higher arm systolic
  • Left ABI = higher left ankle systolic ÷ higher arm systolic

Interpretation

ABIIndication
>1.2Noncompressible / severely calcified (DM)
1.0–1.2Normal
0.5–0.9Intermittent claudication (mild-moderate ischaemia)
0.1–0.4Critical limb ischaemia (ulceration, gangrene)
  • Critical limb ischaemia: ankle pressure <70 mmHg / toe pressure <50 mmHg
  • Vascular trauma: ABI <0.9 → CTA (highly sensitive and specific for arterial injury)
13

Hard vs Soft Signs (Vascular Trauma)

Hard signs (→ immediate OR)

  • Arterial / pulsatile bleeding
  • Persistent haemorrhage with shock
  • Expanding or pulsatile haematoma
  • Palpable thrill
  • Audible bruit
  • Absent pulse (or distal ischaemia: pain / pallor / paralysis / paresthesias / coolness)

Soft signs (→ further investigation)

  • Small, stable, non-pulsatile haematoma
  • Injury to anatomically related nerve
  • Unexplained hypotension
  • History of haemorrhage no longer present
  • Penetrating wound in proximity to major vessel
  • Diminished or unequal pulses

Pathophysiology Frameworks

3 entries
14

Virchow's Triad

  • Endothelial dysfunction / injury (vessel wall)
  • Alteration in normal blood flow (stasis or turbulence)
  • Hypercoagulability (blood composition)
15

Edema — Exudate vs Transudate

FeatureExudate (inflammatory)Transudate (non-inflammatory)
ProteinHigh (>3 g%)Low (<3 g%)
Specific gravity>1015<1015
Fibrinogen / clottingHigh (clots)None (no clot)
CellularityRich in inflammatory cellsLow
GrossCloudyClear
MechanismIncreased vascular permeabilityIncreased hydrostatic / decreased osmotic pressure
16

Compression Stocking Classes

ClassPressureIndication
Class I18–21 mmHgMinor varicosities, prevention
Class II26–34 mmHgUncomplicated varicose veins
Class III>34 mmHgComplicated varicose veins / venous ulcers
  • Contraindications: PAD, cardiac failure
  • Indications: post-thrombotic varicose veins, minimal symptoms, unfit/unwilling for surgery, post-surgery/sclerotherapy/laser
  • Min ABPI >0.8 for safe compression

AAA-Specific

1 entry
17

AAA Screening & Size/Rupture Risk

SVS Screening

  • Men ≥65: all
  • Men ≥55: positive family history
  • Women ≥65: positive family history or personal smoking history

Rupture risk by size

SizeRupture risk
3–4 cm<0.5%
4–5 cm0.5–5%
5–6 cm3–15%
6–7 cm10–20%
7–8 cm20–40%
>8 cm30–50%

Elective repair indications

  • Men ≥5.5 cm; women 4.5–5.4 cm
  • Expansion >1 cm/year
  • Saccular shape
  • Symptomatic
  • Atypical (dissecting, mycotic pseudoaneurysm)