Where do atherosclerotic plaques typically occur?
At arterial bifurcations, suggesting that their formation may be related to shear stress phenomena.
Which locations in the vascular tree are most often affected by atheroscleotic lesions?
Proximal internal carotid artery
Infrarenal aorta
Superficial femoral artery
***The supraceliac aorta and deep femoral arteries are rarely diseased
Pathology of development of atherosclerotic lesions
Fill in with information from Mod 2
Which are the two mechanisms via which atherosclerogic lesions cause symptoms?
Stenosis/occlusion
Embolism (atheroembolism or thromboembolism)
Collateral circulation for the internal carotid artery is usuallu provided by…
External carotid artery
Collateral circulation for aortoiliac occlusive disease is usually provided by…
Internal iliac and lumbar artery
Internal mammary a. (via the superior and inferior epigastric a.s)
Collateral circulation for the superficial femoral artery (SFA) is usually provided by…
Deep (profunda) femoral artery
Collateral circulation to supply the lower leg in the case of popliteal disease is usuallu provided by…
Geniculate collaterals around the knee
Risk factors for peripheral arterial disease secondary to atherosclerosis include:
Tobacco abuse
Diabetes mellitus
Hypelipidemia
Family history if atherosclerosis
Which two sites of atherosclerosis are uncommon except in diabetic patients?
Profunda femoral artey
Tibial artery
Besides atherosclerosis, what are two causes of oclusive disease in the popliteal artery?
Hint: these rare conditions are usually only seen in younger patients
Popliteal entrapment (entrapment of popliteal a. by the gastrocnemius m.)
Cystic adventitial disease (cysts in the adventitia of the artery)
What is the clinical presentation of symptomatic lower extremity occlusive disease/atherosclerosis?
In order from earliest to latest (and most severe) presentation:
- Claudication (blood flow through collaterals is adequate at rest but insufficient for increased metabolic demand of exercise) - NOT limb threatening
- Ischemic rest pain (collateral blood supply is inadequate to supply metabolic demands of tissues, even at rest) - LIMB THREATENING!
- Gangrene (tissue necrosis occurring when blood flow is inadequate to maintain tissue viability - classified as wet gangrene if there is an infection within the nonviable tissues) - LIMB THREATENING!
Complications of arteriography
- Contrast media: Dye-induced nephrotoxicity (ATN) and dye allergy
- Arterial complications: thrombosis (pericatheter or direct trauma to diseased wall) and atheroembolization
- Puncture site complications: hematoma (if large, may result in adjacent nerve compression and damage or necrosis of overlying skin) and pseudoaneurysm (false aneurysm, at risk for rupture if > 2cm)
Anatomy of the femoral artery
The common femoral artery is the continuation of the external iliac artery once it crosses under the inguinal ligament.
The common femoral artery quickly gives rise to the profunda/deep femoral artery, which supplies the muscles of the thigh.
The superficial femoral artery runs down the thigh until it enters the adductor hiatus. Upon emerging from there, it is the above the knee popliteal artery.
Arteries of the leg
The below the knee popliteal artery (which is posterior to the knee) gives rise to the anterior tibial artery (which goes above/pierces the interosseus membrane between the tibia and the fibula to emerge on the anterior side of the leg, and courses to the foot to give rise to the dorsalis pedis artery) and the posterior tibial artery, which runs posterior to the tibia and courses to the foot by rounding the medial malleolus posteriorly.
About 1/4-1/5 of the way along its course down the tibia, the posterior tibial artery gives rise to the peroneal/fibular artery, which courses on more laterally down the leg between the tibialis posterior muscle and the flexor hallucis longus. It courses down to the foot along the lateral malleolus.
Clinical indicators of amputation-level healing
- Pulses: in general, should have a palpable pulse at least one level above proposed amputation site
- Skin temperature and capillary refill: skin of proposed amputation site should be soft, warm, and well-perfused. The presence of gangrenous changes or dependent rubor precludes healing at that level.
- Noninvasive tests: good pulse-volume recording waveform or pressure > 50 mmHg at level of amputation predicts healing
Tradeoff for amputating more distally vs. proximally
The more DISTAL the amputation, the more functional a person gait will be.
BUT, the more PROXIMAL an amputation, the better chance or healing without significant complications.
5 Ps of acute limb ischemia
- Pain (acute and unrellenting, ALWAYS present, may become anesthetic as neural function is lost)
- Pallor (+ mottling, + flat veins, usually one level below acute arterial occlusion)
- Paralysis (heralds limb loss)
- Paresthesias (signify severe neural dysfunction and also herald impending limb loss. Insensate limb = non-viable)
- Pulselessness (and undetectable Doppler signals)
How to manage acute LE ischemia
- Heparin
- Hydration (and means to protect kidney from myoglobinuria, namely maintaining high urine output)
- Revascularization (surgically via embolectomy or bypass, or thrombolytic therapy - tPA or urokinase)
- Post-operative care - complete cardiac evaluation, anticoagulation tx, watch for complications (compartment syndrome, myoglobinuria)
What is Virchow’s triad.
Stasis
Hypercoagulability (neoplasms, hematologic abnormalities, OCP)
Endothelial injury
In a patient with severe abdominal pain out of proportion to physical findings, what should you be worried about?
ACUTE MESENTERIC ISCHEMIA
Patient writhing in agony without signs of peritonitis.
However, if diagnosis or tx is delayed, transmural infarction of the bowel CAN result in peritoneal irritation and more pronounced physical findings.
Which triad of symptoms characterizes chronic mesenteric ischemia?
Posprandial epigastric pain (basically like claudications)
“Food fear”
Weight loss
(Also, GI dysmotility)
What might mesenteric vein thrombosis be confused for?
Intestinal obstruction (because they share the symptoms of progressive abdominal pain and distention)
Why does renal artery stenosis cause systemic hypertension (usually very severe, precipitous in onset, and refractory to multiple medications), renal insufficiency, and pulmonary edema?
RAS leads to decreased perfusion of kidneys. The juxtaglomerular apparatus interprets this as volume depleted status (as supposed to a volume distribution issue), and thus is stimulated the RAAS by releasing renin, which leads to the formation of angiotensin, a potent vasocontrictor that stimulates the release of of adrenal aldosterone, which in turn leads to sodium retention.
Increased vasoconstriction (by angiotensin) and increased water retention (water follows Na+ because of aldosterone) leads to systemic HTN.
Renal insufficiency results from ?renal hypoperfusion.
Pulmonary edema (because of volume overloaded status because of H2O following Na+ reabsorption due to actions of aldosterone. ALSO, if there is systolic LV dysfunction, effects will propagate back to cause pulmonary ?HTN.
