Peripheral Vascular Diseases

Friday, January 5, 2001 Hire: Melissa ICM 9am 438-0668 Dr. Jenkins Peripheral Vascular Diseases

2 handouts were given in class titled Peripheral Vascular disease and Diseases of the Aorta. Disclaimer: if this scribe reads like her handout sometimes, it’s because Dr. Jenkins just read from her notes.

 Coronary disease is the #1 killer in the U.S. The association between coronary artery disease and carotid disease is about 40%. The association between coronary disease and peripheral vascular disease (PVD) in the legs is about 70%.

 ETIOLOGY – there are many. Here are the ones she mentioned in class.  Aging  Atherosclerosis – the major etiology  Hypertension and tobacco. Dr. Jenkins really hates tobacco. Even though there is only a 5% chance that the patient will quit smoking if you (as their physician) tell them to, you should do it anyway because telling them to do it is cheap, easy and it still works no matter how infrequently. She likes to tell her patients to smoke lots everyday (jokingly) because it’s great for her business. Nicotine is extremely addictive. However, the physical addiction disappears 7-10 days after smoking cessation, so most people are really addicted in their heads. Counseling may be required since it is difficult to give up something pleasurable like smoking.

 EXAMINATION of someone with PVD.  Palpatation/auscultation. During an exam, Dr. Jenkins would listen for bruits, which can be caused by either tortuous flow or stenosis.  Elevation pallor – the leg of a CVD patient becomes white upon elevation. This tells you that the veins are properly draining the blood, but the arteries are obstructed so not enough blood is coming into the leg.  Ankle/brachial index or ABI – this the most important test. Calculated from (systolic bp of ankle)/(systolic bp of arm). . Normal value = 1. With PVD, the systolic bp in the legs will be diminished and the index will be <1  Claudication usually shows up at around ABI of 0.7  Significant claudication – at around 0.5  Threatened limb loss at ABI of 0.3 or less . Because a patient with PVD may not have an abnormal ABI at rest, it is also calculate after physical exertion to see if the ratio plummets when exercising.  Allen test – checks for functional collateral circulation to the hand. . First, take the patient’s hand and occlude both the ulnar and radial arteries at the wrist. Then, ask the patient to rapidly open and close his hand in order to void the blood. Once the hand turns pale, remove the pressure from one of the arteries and see if the patient’s hand pinks up. Repeat procedure but release the other artery. . Test should always be performed before doing all arterial sticks (such as for measuring arterial blood gas) to insure survivability of the hand. If one of the arteries is occluded and you stick the good artery, the patient will loose the hand and you will end up writing a fat check for malpractice.  Doppler ultrasound – can identify the degree of stenosis in carotid, vertebral, upper and lower extremities, and aortoiliac regions.  Angiography – reserved for patients in whom intervention is planned or if you can’t make the diagnosis non- invasively. An angiogram should not be performed on someone with claudication because we do not fix something that the patient can’t die from. The only reason Dr. Jenkins will intervene in someone with claudication is if there’s the possibility of limb loss (‘cuz limb loss can kill ya). Hence, no angiography is done in the periphery vasculature until the disease is relatively progressed.

 OCCLUSIVE PERIPHERAL ARTERIAL DISEASE – symptoms and signs depend on the location and extent of the occlusion and the adequacy of the collateral circulation. Must differentiate between acute and chronic occlusion because the therapy is different.  1) Acute occlusion . Clinical presentation – will have to know the following “5 p’s” because surgical attendings like to ask.  Pain, pallor, paresthesia, pulselessness, paralysis – these are the usual signs.  Acceleration of claudication also can occur – this occurs when there is an embolus on top of the stenosis. May cause the progression of the symptoms. . Signs  Cyanosis  Livedo reticularis – purple mottling of the skin so that “you look dead”. . Management:

1  Protect the extremity  Pain relief  Heparin – thrombolytic therapy. Dr. Jenkins’ famous saying: “our patients don’t bleed to death; they clot to death”. This is why her patients regularly receive blood thinners.  Angiography/surgery to fix the problem . Sources of acute claudication stenosis  Embolic – if you decide that the source is embolic and not from chronic claudication stenosis, then the source of the embolus must be identified. Anticoagulate the patient. Often times, it comes from the heart especially if the patient has abnormal heart rhythms like atrial fibrillation. Can use coumadin (rat poison).  Thrombotic – "embolic" means the clot came from somewhere else vs. "thrombotic," which means the clot was formed at the site it was found. Can treat with:  Thrombectomy – this is when Dr. Jenkins use a balloon to go in the artery and pull the thrombus out.  Thrombolytic therapy plus angioplasty – bust up the clot and then fix the underlying stenosis  Bypass the vessel.  2) Chronic occlusions . Atherosclerosis is the usual cause, but the ideology can also be extrinsic compression of arteries by tumors/trauma, and Buerger’s disease. Buerger’s disease is seen in smokers who end up with severe inflammation of the artery. The patient’s hand turns purple, may “fall off”, and hurts a lot. Buerger’s disease is very difficult to manage, and there is no good therapy for the afflicted. . Chronic occlusion manifests differently depending on where the occlusion is.  Upper extremity  Often from blunt palmar trauma especially found in people who use jackhammers all of the time.  Must protect these people’s hands and get them to stop smoking (nicotine is a vasoconstrictor and enhances the symptomology)  Calcium channel and alpha-1 adrenergic receptor blockers may be used to reduce the pain or risk of ischemia.  Lower extremity  Presentation  Intermittent claudication – the patient experiences pain on walking, and the pain ceases upon sitting down or standing still  Spinal stenosis – see this often. It is caused by the vertebral body squeezing on the spinal cord, which results in back and extremity pain. In contrast to intermittent claudication, spinal stenosis occurs even when the patient is standing still. The pain is relieved when patient leans over some object. This is called the “shopping-cart sign”.  Avoid vasoconstrictive agents (tobacco), cold, and drugs.  Therapy  Walk until it hurts, quit, and then walk again. This helps to develop collateral circulation.  Low fat diet  Aspirin  Platol (spp?) – a cAMP derivative. Helps to improve flow in some patients. (Trintol is the old one that doesn’t work).  Indications for revascularization – Angioplasty /Surgery/Vegf. Vegf is the substance that can be injected into patients to stimulate growth of arteries and veins. Right now, it is only used in the periphery; it might be used in the heart in the future.  Relief of disabling claudication – we want to relief this condition because the patient can’t do anything.  Improved prognosis for limb survival in diabetics – however, diabetics still die of heart disease more oftentimes than PVD. Amputation is an extremely morbid procedure causing high mortality rates especially in diabetics. Hence, it must be stressed to diabetics the importance of foot care. Diabetics are never supposed to run around bare-foot because the tinniest scratch can lead to amputation from lack of blood flow and consequent infection.  Relief of rest pain  Promote healing of ischemic ulcers

 PERIPHERAL ARTERIAL ANEURYSM  Usually progressive once they start  May contain thrombus, which are little emboli babies that can go flying out of there and cause trouble elsewhere.  Usually these patients are asymptomatic, and they were diagnosed by ultrasound when looking for something else  Usually found in femoral or popliteal arteries

2  VASOSPASTIC DISORDERS – generally uncommon.  Raynaud’s disease (NOT the same as than Raynaud’s phenomenon) – aka the “All-American Problem”, because when the patient’s hand gets cold (such as when rummaging in the refrigerator), the hand first turns white, then blue, and then red.  Raynaud’s phenomenon . Generally secondary to an underlying disease like diabetes, amyloidosis . It is transient, reversible, and precipitated by exposure to cold.  Treatment – tell patient not to expose hands to the cold. Picture: abdominal aortic stenosis. The symptom (claudication) was felt in the buttock. Usually, the symptom is distal to the stenosis. For instance, calf claudication (which is the most common claudication) is a sign of superficial femoral artery disease.

 DISEASES OF THE VEINS – pretty darn common but very difficult to deal with due to lack of effective treatment.  Varicose veins . Caused by weakness in vein walls and valves . Predisposing conditions: pregnancy, right heart failure, ascites, and obesity . Symptoms – really painful with lots of swelling in the veins and in the leg. . Therapy: elastic stockings, sclerotherapy (doesn’t really work very well), surgical stripping (“a nightmare”).  Venous thrombosis – Extraordinarily common especially in post-operative patients. . Common cause of morbidity and mortality . Incidence increased with:  Post-operative state – It is important to get the patient up and moving after surgery so venous thrombosis does not form. Heparin may also help.  Trauma  Congestive heart failure  Malignancy  Oral contraceptives  Coagulopathy  Most common group of people to get these are truck drivers . Superficial thrombosis  Red, tender cords or nodules  Threat with warm, moist hot packs and aspirin  Unlike deep vein thrombosis, this superficial type won’t kill. . Deep vein thrombosis (DVT)  Presentation is highly variable.  Diagnose with Duplex Doppler. Using a probe, the clot in the vein can be visualized.  If Doppler is not diagnostic (which is rare), a venography can be done  Most serious complication: Pulmonary embolism. This is what kills. Having a DVT is bad enough, but if it doesn’t stay where it started, that’s even worse.  Management  Get patients up and moving ASAP.  Anticoagulate – use heparin  Sequential Compression Devices (SCD’s) – little blood pressure cuffs that inflates over the patient’s leg and sequentially squeezes legs repeatedly. This stimulates venous blood flow.  May require thrombolytic therapy – usually does not work well.  Vena cava filter – an umbrella thing that goes in through the femoral v. and catches clots to prevent them from going north. Then, the body’s intrinsic mechanism breaks up the clots. Basically, this device prevents the thrombus from reaching the lungs.  Vena cava interruption – very dramatic, not done anymore.  Chronic venous insufficiency  Usually due to postphlebitic valvular incompetence – this occurs when the patient has had varicose veins for a long time.  This condition presents like varicose veins and usually the morbidly obese.  Treat with elastic stockings

3 Diseases of the Aorta

Dr. Jenkins covered this section very quickly. She prefaced this section by saying, “y’all can read, I have confidence in y’all”.  PATHOPHYSIOLOGY  Divided into four segments – because they are all treated differently . Ascending . Arch – the most difficult one to treat because of the braches coming off. Often run the risk of strokes. . Descending . Abdominal  Composition – she assumes we know this already  Aorta plays a major role in control of systemic vascular resistance and heart rate  Systolic aortic pressure is a function of the volume of blood ejected, the compliance of the aorta and the resistance to blood flow which relates to preload, afterload, heart rate and contractility. This is the basics; must know this.  Atherosclerosis is the most common cause of aortic aneurysms in adults > 50yo.  Once dilation starts (aneurysm), it will progress because wall stress at constant arterial pressure increases proportionally to chamber diameter (Law of Laplace). This basically says that the bigger the aneurysm gets, the higher the pressure becomes, so it gets even bigger.

 ANEURYSMS  Several types – the cardiologists never really know what type it is until autopsy. . True – includes all three layers of the wall . Pseudoaneurysm – disruption of the intima and media only . Usual cause of death is rupture. Thoracic aneurysm ruptures into the pleural space and abdominal aneurysms rupture into retroperitoneal space.  Marfan’s syndrome (cystic medial necrosis) – not common. We think Abe Lincoln had this. Diagnosis can be made in various ways. For instance, patients have wingspan greater than their height, and they can usually do funny things with their joints. Often, afflicted patients play professional basketball. . Degeneration of elastic and collagen fibers . Accelerated by HTN and pregnancy . Dilated ascending aorta with left ventricular dilation on CXR (chest x-ray). Scribe note: in class, she said “descending aorta” and not ascending. . Aortic regurgitation is commonly present . Widened aortic root with incomplete coaptation – this means that the valve cusps do not meet which causes the aortic regurgitation mentioned above. . Complication of aneurysms (rupture) account for 90% of deaths. . Surgical repair is indicated with root diameter > 6.0 cm or severe AI.  Mycotic aneurysms . Bacterial in origin . Requires previously damaged area of endothelium to have bacterial infection . May spread directly or hematogenously  Aortic Aneurysms (2 locations) . 1) Thoracic  Signs and symptoms depend on size and location  Most are asymptomatic and recognized by mediastinal widening on CXR  Other investigative techniques: CT, MRI, TEE (transesophageal echocardiograph)  Angiography may be required if surgical repair is considered – this is not the best form of diagnosis because it may underestimate the true size of the aorta. If the dye is injected into a clotted aorta, we will only see the size of the lumen and not the true extent of the aneurysm.  Symptoms:  Chest pain  Respiratory symptoms  Hoarseness  Dysphagia  Embolization  Management:  Depends on size, location, clinical presentation, and relative risks  Aneurysms > 6 cm should be considered for elective repair even though the repair is high risk at this location.  With signs and symptoms of expansion or sudden growth, urgent surgical repair is indicated.

4 . 2) Abdominal  Usually asymptomatic and found on routine palpation of the abdomen.  Patients may complain of low back pain or abdominal pulsations.  Diagnosis is confirmed by ultrasound.  Thrombus is present in most cases.  Indications for surgery:  Symptomatic patients – once the aortic aneurysm ruptures, the mortality rate is 90% even with emergency operation. Hence, the littlest symptom indicates surgery.  Any evidence of rapid expansion, regardless of size – this is because of Law of Laplace. Once it starts to expand, it will continue to grow at a logarithmic rate so we must fix it regardless of size.  Aneurysms > 5 cm in diameter, regardless of symptoms  Serial ultrasound is used for management.  Prognosis depends on:  Extent  Location  Severity of ASVD in vessels supplying vital organs: CAD, Carotid disease.  Elective repair mortality: 1-5%  Emergent repair mortality: 50%  Alternative treatment: aneurysm exclusion – this is where you fix the aneurysm using a Dacron graft, a balloon, and a bunch of wires. The advantage to this procedure is that you would go thru the femoral artery instead of the traditional surgical route where you cut thru the abdomen and filet open the aorta. Aneurysm exclusion is less invasive and has a much lower morbidity/mortality rate than the surgical procedure. Pictures of this were shown. Dr. Jenkins thinks this is a great advancement in cardiology; however, not everyone is a candidate for this procedure. For instance, the aneurysm has to be >1cm from the renal artery.

 At this point Dr. Jenkins showed slides and angiograms of clinical aneurysms.

 DISSECTION  Pathophysiology . Usually initiated by a tear in the intima, separating intima from adventitia. It usually spirals down the aorta instead of coming straight down. . Most occur in men (ratio of 3:1), ages 40-60 yo . Predisposing factors:  Hypertension  Atherosclerosis  Trauma  Tobacco abuse  Pregnancy  Cystic medial necrosis  2 Classifications (therapy is different between the two) . DeBakey  Type I – (60%) originates in the ascending and extends into descending. This is the only one that involves the aortic arch.  Type II – (10%) affects ascending only.  Types I and II are treated with surgery.  Type III – (30%) originates upper descending and extends distally. Treated with medical management. . Stanford  Type A – Proximal (ascending aorta + arch)  Type B – Distal (beyond the ligamentum arteriosum). Ligamentum arteriosum fixes the aorta in the thorax, and this is where the aorta is most likely to break following trauma since it can’t move around there. More later  Symptoms . Chest pain – Sudden. Patients often complain of a “tearing” sensation in the chest.  Ascending – chest, neck, jaw  Descending – back . Compression of adjacent structures  See above  Horner’s syndrome – develops from the superior cervical ganglia is being squashed.  Superior vena cava syndrome . Occlusion of major branch vessels

5  CVA  MI – usually from occlusion of the right coronary artery, which means the inferior wall is infracted.  Bowel infarction  Renal hypertension . Retrograde extension into aortic valve (AI). . Rupture (shock) – the patient will usually die from this  Physical exam – “y’all can read that"  Diagnostic tests . EKG – acute myocardial infarction . CXR – widened mediastinum . Echocardiography – TTE and TEE (transthoracic and transesophageal, respectively). TEE can be performed at bedside, which is better than CT or MRI for that reason. Also, this procedure does not require any dye so it does not run the risk of renal insufficiency. Radiology is not a place you want to run a code so you don’t want to order a CT or MRI in the middle of the night with no nurse around. “It’s really uncool to take an unstable patient to radiology for a catscan or MRI.”  TTE – widened aortic root, false lumen  TEE – performed at bedside, requires less than 20 min., no dye. . CT . MRI  Prognosis – Horrible, 9 or 10 may not survive one year  2 Therapies . Medical therapy – Reduce cardiac contractility and blood pressure. We want to reduce shear stress.  Beta-blockers - #1 drug. Keep throwing these at the patients even above max dose if the heart rate and blood pressure is not controlled.  Sodium Nitroprusside – good for short term. Cannot give continuously longer than a couple of days or will cause cyanide toxicity. . Surgical therapy  Type A  Try to limit dissecting process and correct complications  May require aortic valve replacement  Type B – usually treated medically because the dissection is so extensive that you would have to replace the entire aorta to treat surgically and that’s not possible.

Dr. Jenkins doesn’t feel like talking about aortitis. She said to read it.

 OCCLUSIVE DISEASE – this is common  Chronic aortic obstruction (Leriche syndrome) . Usually a triad  Occlusion, or stenosis in the distant aorta or bilateral iliac  Buttock claudication  Impotence  Acute aortic obstruction . Usually due to emboli, commonly from heart . Cardiac conditions: atrial fibrillation, mitral stenosis, CMP, valve prostheses, recent MI . Sudden onset . Exclude aortic dissection and then heparinize . Consider angiography and surgical intervention.

 AORTIC TRAUMA  Most common location is just distal to origin of left subclavian, where mobile and fixed segments adjoin.  May be completely or incompletely transected.  Usually a deceleration injury – meaning that the patient did not have seatbelt on and flew out of the car hitting the ground at full speed.  Suspect aortic trauma if the patient has arm hypertension and leg hypotension with no lower pulses  May develop pseudoaneurysm, requiring surgical repair.

Show and Tell: She showed a movie. Femoral stent was placed in a “freedom impaired” patient. It was interesting but low yield as far as the test goes and not feasible to scribe without everyone having the movie to follow along. Thus, the end.