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Head & Neck
Occlusion scenario
ICA stenosis — ECA to ICA collateral
Facial a. → angular / dorsal nasal → ophthalmic a. (ICA)
The facial artery (ECA branch) anastomoses with the ophthalmic artery (first ICA branch) at the medial canthus via the angular and dorsal nasal arteries. When the ICA is stenosed proximally, ECA blood flows retrograde into the ophthalmic artery and into the ICA, supplying the brain. Detectable by reversed supraorbital Doppler flow.
Key: ECA (facial a.) ↔ ICA (ophthalmic a.) via angular/dorsal nasal. Classic ECA-to-ICA collateral in carotid disease.
Occlusion scenario
Subclavian steal syndrome
Proximal subclavian stenosis → vertebral artery reverses flow → basilar ischemia
Subclavian stenosis proximal to the vertebral artery origin → low pressure in the arm → vertebral artery reverses flow, stealing from the basilar artery to supply the arm during exercise. Causes posterior circulation symptoms: dizziness, diplopia, ataxia provoked by arm use. BP difference >20 mmHg between arms is the clinical clue.
Key: Vertebral artery reverses flow. Arm exercise triggers posterior circulation ischemia. BP difference >20 mmHg between arms.
Clinical pearl
Scalp lacerations — profuse bleeding
Superficial temporal ↔ supraorbital ↔ supratrochlear ↔ occipital ↔ posterior auricular
The scalp has five pairs of anastomosing arteries forming a rich ring: superficial temporal and posterior auricular (ECA), occipital (ECA), supraorbital and supratrochlear (ophthalmic/ICA). These vessels are tethered by fibrous septa in the subcutaneous layer — they cannot retract when cut. The rich anastomosis also means blood can flow from all directions even under compression.
Key: 5 arterial pairs, rich ring anastomosis, vessels tethered and cannot retract → profuse bleeding from even small lacerations.
Occlusion scenario
Proximal common carotid artery occlusion
Vertebral a. → basilar → PComm → ipsilateral ICA (retrograde)
With proximal CCA occlusion, the Circle of Willis compensates: ipsilateral vertebral → basilar → PComm → ICA retrograde. ECA branches simultaneously anastomose with the ophthalmic artery (ICA branch) to provide partial retrograde ICA filling from external sources.
Key: Vertebral → basilar → PComm → ICA retrograde. The Circle of Willis rescues the hemisphere from the posterior side.
Brain — Circle of Willis
Anastomosis
Anterior communicating artery (AComm)
Right ICA → right ACA ↔ left ACA ← left ICA
The AComm bridges the two ACAs, connecting left and right ICA territories. When one ICA is occluded, the contralateral ICA can push blood across the AComm to fill the ipsilateral ACA. Most common site of berry aneurysm (30–35%). A large AComm aneurysm can compress the optic chiasm → bitemporal hemianopia.
Key: Left ↔ right ICA bridge. Most common berry aneurysm site. AComm aneurysm → bitemporal hemianopia.
Anastomosis
Posterior communicating artery (PComm)
ICA (anterior circulation) ↔ PCA (posterior circulation)
The PComm runs between the ICA and PCA on each side — the anterior-to-posterior circulation bridge. Basilar occlusion → ICA blood travels via PComm → PCA → retrograde into basilar. PComm aneurysm classically compresses CN III → ipsilateral "down-and-out" eye with dilated, fixed pupil (the "surgical pupil").
Key: Anterior ↔ posterior circulation bridge. PComm aneurysm → CN III palsy with pupil dilation ("surgical third nerve palsy").
Occlusion scenario
Basilar artery occlusion
ICA → PComm → PCA → basilar (retrograde from both sides)
Both ICAs send blood via their PComms → PCAs → retrograde into the basilar. A well-developed PComm is protective. Basilar occlusion causes "locked-in syndrome": quadriplegia, anarthria, preserved vertical eye movement and consciousness. A patent PComm is a critical lifeline.
Key: Both ICAs → both PComms → both PCAs → retrograde basilar. Well-developed PComm is a lifeline in basilar occlusion.
Thorax
Occlusion scenario
Coarctation of the aorta
Subclavian → internal thoracic → intercostal arteries → descending aorta
Coarctation at the ligamentum arteriosum forces blood via: subclavian → internal thoracic → anterior intercostals ↔ posterior intercostals (from descending aorta distal to stenosis). Posterior intercostals enlarge, eroding inferior rib borders of ribs 3–8 → "rib notching" on CXR. Associated: upper body hypertension, radio-femoral pulse delay, bicuspid aortic valve (80%).
Key: Intercostal arteries enlarge → rib notching on CXR (ribs 3–8). Only coarctation produces this pattern.
Anastomosis
Internal thoracic ↔ superior epigastric (anterior wall axis)
Subclavian → internal thoracic → superior epigastric ↔ inferior epigastric → external iliac
The internal thoracic (from subclavian) continues as the superior epigastric below the diaphragm, anastomosing with the inferior epigastric (from external iliac) deep to the rectus abdominis. This longitudinal axis bridges subclavian to iliac territory — bypassing aortic obstruction in Leriche syndrome. The internal thoracic is also the most commonly harvested vessel for CABG.
Key: Continuous axis: subclavian → internal thoracic → superior epigastric ↔ inferior epigastric → external iliac. Bridges thorax to pelvis.
Abdomen
Occlusion scenario
Celiac trunk occlusion
SMA → inferior pancreaticoduodenal ↔ superior pancreaticoduodenal (celiac)
The pancreaticoduodenal arcade bridges celiac and SMA. Superior pancreaticoduodenal (gastroduodenal → celiac) ↔ inferior pancreaticoduodenal (SMA). Celiac occlusion → SMA back-fills via inferior → superior pancreaticoduodenal → gastroduodenal → hepatic and splenic. This is the #1 most-tested abdominal anastomosis on Step 1.
Key: Superior pancreaticoduodenal (celiac) ↔ inferior pancreaticoduodenal (SMA). #1 most tested abdominal anastomosis.
Occlusion scenario
IMA occlusion — marginal artery of Drummond
SMA → middle colic ↔ left colic (IMA) via marginal artery
The marginal artery of Drummond is a continuous arcade along the inner colonic margin connecting middle colic (SMA) with left colic and sigmoid arteries (IMA). Griffith's point (splenic flexure) and Sudeck's point (rectosigmoid) are watershed danger zones where the marginal artery is most tenuous. IMA ligation during aortic aneurysm repair → sigmoid ischemia if the marginal artery is inadequate.
Key: Marginal artery = SMA ↔ IMA bridge. Griffith's point (splenic flexure) and Sudeck's point are watershed zones — highest ischemia risk.
Occlusion scenario
Abdominal aortic occlusion (Leriche syndrome)
Internal thoracic → superior epigastric ↔ inferior epigastric → external iliac → femoral
Leriche syndrome: atherosclerotic occlusion of the distal aorta at the bifurcation. Classic triad: bilateral leg claudication, impotence, absent femoral pulses. Collateral: internal thoracic → superior epigastric ↔ inferior epigastric (from external iliac) → femoral. This epigastric axis is the main rescue route keeping the legs perfused.
Key: Leriche triad = bilateral claudication + impotence + absent femoral pulses. Internal thoracic → epigastric axis is the main collateral.
Occlusion scenario
Splenic artery occlusion / splenectomy
Right gastroepiploic (gastroduodenal) ↔ left gastroepiploic (splenic) — greater curvature
Greater curvature of the stomach has a dual supply via the gastroepiploic arcade: right gastroepiploic (from gastroduodenal/celiac) and left gastroepiploic (from splenic). After splenectomy, the right gastroepiploic takes over greater curvature perfusion. Short gastric arteries supply the fundus — most vulnerable region when the splenic artery is occluded.
Key: Right gastroepiploic (celiac) ↔ left gastroepiploic (splenic). Right compensates after splenectomy.
Portosystemic Anastomoses
Portal hypertension
Esophageal varices
Left gastric vein (portal) ↔ esophageal veins → azygos (systemic)
Left gastric (coronary) vein drains to the portal system. Portal hypertension → retrograde flow through esophageal tributaries → azygos → SVC (systemic). Submucosal esophageal varices form at the gastroesophageal junction — highest risk of rupture (30% mortality per episode) of all portosystemic shunts.
Key: Left gastric vein (portal) ↔ esophageal veins (systemic via azygos). Highest rupture risk. Located at gastroesophageal junction.
Portal hypertension
Caput medusae
Paraumbilical veins (portal) ↔ superficial epigastric veins (systemic)
Paraumbilical veins run in the falciform ligament and reopen under portal hypertension, connecting the portal system to superficial epigastric veins of the anterior abdominal wall. Dilated veins radiate from the umbilicus = caput medusae. Flow is away from the umbilicus (distinguishes from IVC obstruction, where flow is upward).
Key: Paraumbilical veins (falciform ligament) ↔ superficial epigastric veins. Flow is away from umbilicus in caput medusae.
Portal hypertension
Anorectal varices
Superior rectal vein (portal via IMV) ↔ middle & inferior rectal veins (systemic)
Superior rectal vein → IMV → portal. Middle and inferior rectal veins → internal iliac → systemic. Their anastomosis at the anorectal junction enlarges in portal hypertension = anorectal varices. Critical distinction: anorectal varices are NOT hemorrhoids. Hemorrhoids are arteriovenous cushions (normal structures), unrelated to portal hypertension.
Key: Superior rectal (portal) ↔ middle/inferior rectal (systemic). Anorectal varices ≠ hemorrhoids. Don't confuse them on the exam.
Portal hypertension
Retroperitoneal varices (veins of Retzius)
Mesenteric veins (portal) ↔ lumbar / renal / gonadal veins (systemic)
Veins of Retzius are embryological retroperitoneal anastomoses between mesenteric tributaries (portal) and parietal veins (lumbar, renal, gonadal — systemic). They reopen in portal hypertension, visible as retroperitoneal varices on CT. They also cause unexpected venous bleeding during retroperitoneal surgery in portal hypertension patients.
Key: Retroperitoneal mesenteric tributaries (portal) ↔ lumbar/renal/gonadal (systemic). Often invisible until portal hypertension — dangerous during retroperitoneal surgery.
Pelvis & Uterus
Surgical scenario
Internal iliac ligation — postpartum hemorrhage
Ovarian artery (abdominal aorta) ↔ uterine artery (internal iliac)
The uterus receives blood from the uterine artery (internal iliac) AND the ovarian artery (direct aortic branch). Bilateral internal iliac ligation reduces perfusion pressure ~85%, slowing bleeding — but the ovarian artery persists and anastomoses with the uterine artery in the broad ligament, preventing uterine necrosis. Also why uterine artery embolization for fibroids preserves viability.
Key: Ovarian artery (from aorta, NOT internal iliac) ↔ uterine artery. Uterus survives internal iliac ligation because the ovarian supply persists.
Occlusion scenario
Superior rectal artery occlusion — rectal supply
Middle & inferior rectal arteries (internal iliac) ↔ superior rectal (IMA)
The rectum has a triple arterial supply: superior rectal (IMA), middle rectal (internal iliac), inferior rectal (internal pudendal → internal iliac). This redundancy protects the rectum from ischemia — in contrast to the sigmoid, which depends almost entirely on IMA branches. The rectum is rarely ischemic after IMA ligation; the sigmoid is the vulnerable segment.
Key: Rectum = triple supply (superior + middle + inferior rectal). Rarely ischemic. Sigmoid = poor collateral — always vulnerable after IMA ligation.
Upper Limb
Occlusion scenario
Brachial artery occlusion at the elbow
Profunda brachii → radial/ulnar collaterals ↔ radial/ulnar recurrent arteries
The profunda brachii gives off radial and middle collaterals that anastomose with recurrent branches of the radial and ulnar arteries around the elbow. Superior and inferior ulnar collaterals (from brachial) anastomose with anterior/posterior ulnar recurrent arteries. Important: brachial occlusion below the profunda brachii origin is more ischemic than above it — the profunda collateral origin is lost.
Key: Profunda brachii provides the collateral origin. Brachial occlusion below the profunda origin = more severe ischemia.
Anastomosis
Palmar arches — radial ↔ ulnar anastomosis
Superficial arch (mainly ulnar) ↔ deep arch (mainly radial)
Superficial palmar arch = mainly ulnar; deep palmar arch = mainly radial. They anastomose, so occlusion of one vessel alone is usually tolerated. Allen test: compress both vessels → fist → release one → hand should flush within 5–7 seconds if arch is complete. An incomplete arch means the hand depends on that vessel — radial artery harvest or cannulation is contraindicated.
Key: Superficial arch = mainly ulnar; deep arch = mainly radial. Allen test checks adequacy before radial artery cannulation or CABG harvest.
Lower Limb
Occlusion scenario
Superficial femoral artery occlusion
Profunda femoris → perforating branches → geniculate network
The profunda femoris (deep femoral artery) is the main collateral for SFA disease — the most common site of peripheral arterial disease. Profunda perforating branches anastomose with geniculate arteries around the knee. Classic presentation: calf claudication with palpable femoral pulse but absent popliteal and pedal pulses. Normal resting perfusion (supplied by profunda) but claudication on exertion.
Key: Profunda femoris = main collateral for SFA occlusion. Palpable femoral pulse + absent popliteal/pedal pulses = SFA occlusion.
Occlusion scenario
Popliteal artery occlusion
5 geniculate arteries form an anastomotic ring around the knee
The geniculate ring: superior medial, superior lateral, inferior medial, inferior lateral, and middle geniculate arteries — all popliteal branches. They connect above the knee (popliteal and profunda branches) to below (tibial vessels). Popliteal aneurysm (most common peripheral aneurysm) thrombosis is particularly dangerous because it can simultaneously clot the geniculate ring.
Key: 5 geniculate arteries form the ring. Popliteal aneurysm thrombosis = threatened limb if geniculate network is also occluded.
Surgical scenario
Medial circumflex femoral artery occlusion — femoral head AVN
Lateral circumflex femoral ↔ medial circumflex femoral via trochanteric anastomosis
The medial circumflex femoral artery (MCFA) is the dominant supply to the femoral head via retinacular vessels in the femoral neck. The trochanteric anastomosis (MCFA, lateral circumflex femoral, inferior gluteal, obturator branch) exists but is insufficient to prevent AVN when the MCFA is disrupted. A displaced femoral neck fracture tears the retinacular vessels → avascular necrosis of the femoral head.
Key: MCFA = dominant femoral head supply via retinacular vessels. Femoral neck fracture → disruption → AVN. Trochanteric anastomosis cannot rescue it.
Heart — Coronary Collaterals
Occlusion scenario
LAD occlusion — RCA collateral (right-dominant heart)
RCA → PDA septal branches ↔ LAD septal perforators
Right dominant (85%): RCA → PDA → septal perforators (from below) ↔ LAD septal perforators (from above) within the interventricular septum. LAD occlusion = anterior STEMI (ST elevation V1–V4). Pre-existing RCA collaterals can limit infarct size. The LAD supplies the anterior wall, anterior 2/3 of septum, and apex.
Key: RCA (PDA) septal perforators ↔ LAD septal perforators. Right dominant = RCA gives PDA (85%). LAD occlusion → anterior STEMI.
Occlusion scenario
RCA occlusion — inferior MI and heart block
RCA → inferior wall LV + AV node (90%) + SA node (60%)
Proximal RCA occlusion (right dominant): inferior MI (ST elevation II, III, aVF), RV infarction, and AV block (AV nodal artery = RCA branch in 90%). Inferior MI + bradycardia/heart block = think RCA. Nitrates are cautious in RV infarction — preload reduction can precipitate severe hypotension. The LCx via obtuse marginal branches provides some collateral to the posterior territory.
Key: RCA occlusion → inferior MI + AV block. AV nodal artery is RCA branch in 90%. Inferior MI + bradycardia = RCA until proven otherwise.
Coronary dominance
Left-dominant heart — LCx gives PDA (~15%)
LCx → PDA → inferior wall LV + AV node
In ~10–15% of people, the LCx supplies the PDA → inferior wall of LV, posterior septum, and AV node. LCx occlusion in these patients causes inferior MI + AV block — the same pattern usually attributed to the RCA. This is why the culprit vessel for inferior MI may be the LCx in 15% of cases — angiography confirms dominance, not the ECG alone.
Key: Left dominant: LCx → PDA → inferior wall + AV node. Inferior MI with AV block does NOT always mean RCA — LCx in 15%.
Anastomosis
Kugel's artery — atrial anastomosis
Proximal RCA ↔ proximal LCx via atrial anastomotic branch
Kugel's artery connects the proximal RCA with the proximal LCx through the atrial septum, running toward the AV node. Present in a significant proportion of hearts, it can enlarge in coronary artery disease to protect the AV node and posterior atria when either parent vessel occludes — explaining why some patients with severe RCA or LCx disease don't develop complete AV block.
Key: Kugel's artery = proximal RCA ↔ proximal LCx (atrial). Protects the AV node when either parent vessel occludes.
End Arteries — No Collateral Rescue
End artery — no anastomosis
Central retinal artery occlusion
Central retinal artery — true end artery, no anastomotic connections within the retina
The central retinal artery is the classic true end artery tested on Step 1. Occlusion causes sudden, painless, complete monocular vision loss. Fundoscopy: pale retina + cherry-red spot at the macula (the fovea retains color via the choroidal supply beneath it, which has some anastomoses). There is no collateral rescue because the retinal vessels don't anastomose with each other. Compare: the choroid has anastomoses, so isolated choroidal ischemia is less severe.
Key: True end artery = no collateral. Central retinal occlusion → sudden painless monocular blindness + cherry-red spot. Irreversible.
End artery — no anastomosis
Labyrinthine (internal auditory) artery occlusion
Labyrinthine artery (AICA branch) — true end artery, no collaterals to inner ear
The labyrinthine artery (internal auditory artery) is a branch of the AICA (anterior inferior cerebellar artery). It is a true end artery with no anastomoses within the inner ear. Occlusion causes sudden sensorineural hearing loss + vertigo — a classic AICA stroke presentation. Because there are no collaterals, the hearing loss is permanent. This distinguishes it from external ear pathology (conductive loss) and from Meniere's disease (episodic/fluctuating).
Key: Labyrinthine artery = AICA branch = true end artery. Occlusion → sudden sensorineural hearing loss + vertigo. Permanent — no collateral rescue.
Functional end arteries
Segmental renal arteries — wedge infarcts
Segmental renal arteries — no anastomoses between segments → wedge-shaped cortical infarcts
Segmental renal arteries are functional end arteries — they do not anastomose with each other within the parenchyma. Occlusion of a segmental artery (from embolism, vasculitis, trauma) causes a wedge-shaped (triangular base at cortex, apex pointing to hilum) cortical infarct. The entire kidney does not infarct because the renal hilum has a single artery — only the supplied segment is lost. Contrast with the liver: hepatic artery occlusion rarely causes infarct because the portal vein provides a dual supply.
Key: Segmental renal arteries = functional end arteries → wedge-shaped cortical infarcts. Unlike the liver (dual supply), kidneys have no backup per segment.
Concepts & High-Yield Distinctions
Concept
Foregut / midgut / hindgut blood supply
Celiac (foregut) · SMA (midgut) · IMA (hindgut)
The embryological gut divisions define arterial supply, venous drainage, lymphatics, autonomic innervation, and referred pain patterns. Foregut (esophagus → duodenum at ligament of Treitz) = celiac trunk; pain referred to epigastrium. Midgut (ligament of Treitz → proximal 2/3 of transverse colon) = SMA; pain referred to periumbilical region. Hindgut (distal 1/3 transverse colon → upper rectum) = IMA; pain referred to hypogastrium/suprapubic. The splenic flexure marks the midgut–hindgut transition = SMA–IMA watershed.
Key: Celiac = foregut (epigastric pain). SMA = midgut (periumbilical). IMA = hindgut (hypogastric). Splenic flexure = SMA–IMA watershed.
Concept
Arc of Riolan vs. marginal artery of Drummond
Arc of Riolan = short central anastomosis · Drummond = peripheral continuous arcade
Both connect SMA and IMA territories, but they are anatomically distinct. The marginal artery of Drummond is a continuous peripheral arcade along the inner colonic border from cecum to rectosigmoid. The Arc of Riolan (meandering mesenteric artery) is a short, central, variable anastomosis running directly between the middle colic (SMA) and left colic (IMA) in the transverse mesocolon. The Arc of Riolan enlarges and becomes visible on CT/angiography as a tortuous central vessel when either SMA or IMA is critically stenosed. Ligation of an enlarged Arc of Riolan during sigmoid resection in an SMA-stenosed patient → catastrophic small bowel ischemia.
Key: Arc of Riolan = central, short, variable (enlarges in SMA/IMA stenosis). Drummond = peripheral, continuous arcade. Both connect SMA ↔ IMA.
Surgical anatomy
Corona mortis — "crown of death"
Inferior epigastric (external iliac) ↔ obturator artery (internal iliac) — crosses superior pubic ramus
The corona mortis is the anastomosis between the pubic branch of the inferior epigastric artery (external iliac territory) and the pubic branch of the obturator artery (internal iliac territory), crossing the superior pubic ramus. It is present in ~70% of people. It is surgically dangerous during pelvic fracture fixation, inguinal/femoral hernia repair, and pubic symphysis surgery — inadvertent ligation or laceration causes brisk hemorrhage that is difficult to control given its deep pelvic location. It earns its name: "crown of death."
Key: Inferior epigastric (external iliac) ↔ obturator (internal iliac) at the superior pubic ramus. Present in ~70%. Hazardous in pelvic and hernia surgery.
Concept
Why does the liver rarely infarct despite hepatic artery occlusion?
Dual supply: hepatic artery (~30% flow) + portal vein (~70% flow)
The liver receives ~70% of its blood flow and ~50% of its oxygen from the portal vein, independent of the hepatic artery. When the hepatic artery occludes, portal venous flow maintains viability. The kidneys, by contrast, have segmental arteries that are functional end arteries with no dual supply — occlusion causes permanent wedge infarcts. Clinically: hepatic artery aneurysm, celiac occlusion, or accidental hepatic artery ligation is often survivable; renal artery embolism causes permanent infarction. This hepatic dual supply concept is also why TIPS (creating a portohepatic shunt) can reduce hepatic parenchymal oxygenation.
Key: Liver = dual supply (hepatic artery + portal vein). Hepatic artery occlusion alone → rarely infarcts. Kidney = end arteries → always infarcts per segment.
Surgical concept
TIPS — transjugular intrahepatic portosystemic shunt
Portal vein branch ↔ hepatic vein (artificial intrahepatic anastomosis)
TIPS creates an artificial stented channel between a portal vein branch and a hepatic vein within the liver parenchyma, bypassing the high-resistance hepatic sinusoids. This directly decompresses the portal system → reduces variceal pressure and ascites. Because portal blood now bypasses the liver's detoxification (urea cycle, first-pass metabolism), ammonia and gut-derived toxins accumulate → hepatic encephalopathy is the main complication. TIPS is an artificial application of the same portosystemic shunting that occurs spontaneously at the four natural anastomotic sites in portal hypertension.
Key: TIPS = portal vein ↔ hepatic vein (artificial shunt). Decompresses portal HTN. Main complication = hepatic encephalopathy (ammonia bypasses liver).
Surgical concept
Posterior duodenal ulcer — gastroduodenal artery erosion
Posterior duodenal bulb → gastroduodenal artery (celiac trunk branch)
The posterior wall of the first part of the duodenum (duodenal bulb) is directly related to the gastroduodenal artery (GDA), a branch of the common hepatic artery from the celiac trunk. A penetrating posterior duodenal ulcer (typically H. pylori-related) erodes into the GDA, causing massive upper GI hemorrhage — one of the most feared peptic ulcer complications. The anterior duodenal ulcer, by contrast, perforates into the peritoneal cavity (peritonitis), not into a vessel. This anatomical relationship is a Step 1 classic.
Key: Posterior duodenal ulcer → erodes GDA (celiac branch) → massive hematemesis. Anterior duodenal ulcer → perforates → peritonitis.