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CMDT 2025
CHAPTER 13
thrombotic thrombocytopenic purpura (TTP), thereby
presenting a diagnostic challenge. However, the presence of
advanced retinal changes indicates that the likely primary
cause is hypertension, whereas the hematologic
abnormalities associated with TTP or HUS are typically
more dramatic.
B. Management of Hypertensive Emergency Based
on Type of End-Organ Damage
1. Acute hypertensive microangiopathy—In general,
the initial goal is to reduce the pressure by no more
than 25% (within minutes to 1 or 2 hours) and then
toward a level of 160/100 mm Hg within 2–6 hours.
The risk of organ ischemia from excessive reductions
in pressure is minimized by using agents that have a
predictable, dose-dependent, transient, and progressive
antihypertensive effect (Table 13–17). In that regard, the
use of sublingual or oral fast-acting nifedipine preparations
is best avoided.
2. Acute ischemic stroke—This is often associated with
marked elevation of blood pressure, which will usually fall
spontaneously. In such cases, antihypertensives should only
be used if the systolic blood pressure exceeds 180–200 mm
Hg, and blood pressure should be reduced cautiously by
10–15% over 24 hours (Table 13–17). If thrombolytics are to
be given, blood pressure should be maintained at less than
185/110 mm Hg during treatment and for 24 hours following treatment.
3. Intracerebral hemorrhage—The aim of therapy for
intracerebral hemorrhage is to minimize bleeding by
reducing the systolic blood pressure in most patients to
Table 13–17. Treatment of hypertensive emergency depending on primary site of end-organ damage.
See Table 13–18 for dosages.
Type of Hypertensive Emergency Recommended Drug Options and Combinations Drugs to Avoid
Acute hypertensive microangiopathy Labetolol
Hypertensive encephalopathy and posterior
reversible encephalopathy syndrome
Myocardial ischemia and infarction Nicardipine plus esmolol
Acute kidney injury Fenoldopam
Aortic dissection Esmolol plus nicardipine
Acute pulmonary edema, LV systolic
dysfunction
Acute pulmonary edema, diastolic
dysfunction
Ischemic stroke (systolic blood pressure
> 180–200 mm Hg)
Intracerebral hemorrhage (systolic blood
pressure > 140–160 mm Hg)
Hyperadrenergic states, including cocaine use Nicardipine plus a benzodiazepine
Preeclampsia, eclampsia Labetalol
Scleroderma renal crisis Captopril or intravenous enalaprilat
1
Avoid if there is LV systolic dysfunction.
2
Drug of choice if LV systolic dysfunction is associated with ischemia.
Nicardipine
Labetalol
Nicardipine
1
Nitroglycerin plus labetalol
Nitroglycerin plus esmolol
Nicardipine
Clevidipine
Esmolol plus clevidipine
Labetalol
Esmolol plus nitroprusside
Nicardipine plus nitroglycerin2 plus a loop diuretic
Clevidipine plus nitroglycerin2 plus a loop diuretic
Esmolol plus low-dose nitroglycerin plus a loop diuretic
Labetalol plus low-dose nitroglycerin plus a loop diuretic
Nicardipine
Clevidipine
Labetalol
Nicardipine
Clevidipine
Labetalol
Clevidipine plus a benzodiazepine
Phentolamine
Labetalol
Nicardipine
1
Nitroprusside, methyldopa,
clonidine, nitroglycerin
Hydralazine, diazoxide,
minoxidil, nitroprusside
Hydralazine, diazoxide,
minoxidil
Hydralazine, diazoxide,
beta-blockers
Nitroprusside, methyldopa,
clonidine, nitroglycerin
Nitroprusside, methyldopa,
clonidine, nitroglycerin
Beta-blockers
Diuretics, ACE inhibitors
SYSTEMIC HYPERTENSION
CMDT 2025
457
140 mm Hg within the first 6 hours. In acute subarachnoid
hemorrhage, as long as the bleeding source remains uncorrected, a compromise must be struck between preventing
further bleeding and maintaining cerebral perfusion in the
face of cerebral vasospasm. In this situation, blood pressure goals depend on the patient’s usual blood pressure. In
previously normotensive patients, the target should be a
systolic blood pressure of 110–120 mm Hg; in hypertensive patients, blood pressure should be reduced to 20%
below baseline pressure. In the treatment of hypertensive
emergencies complicated by (or precipitated by) CNS
injury, labetalol and nicardipine are good choices since
they are nonsedating and do not appear to cause significant increases in cerebral blood flow or intracranial pressure. Patients with subarachnoid hemorrhage should
receive nimodipine for 3 weeks following presentation to
minimize cerebral vasospasm. In hypertensive emergencies
arising from catecholaminergic mechanisms, such as pheochromocytoma or cocaine use, beta-blockers can worsen the
hypertension because of unopposed peripheral vasoconstriction; nicardipine, clevidipine, or phentolamine is preferred.
Labetalol is useful in these patients if the heart rate must be
controlled but should not be used as first-line therapy
because it exhibits more beta- than alpha-blockade.
4. Acute aortic dissection—Systolic blood pressure and
heart rate should be reduced within 30 minutes to below
120 mm Hg and less than 60 beats per minute, using a
combination of vasodilation and beta-blockade.
Therapeutic strategies for specific end-organ damage
profiles, including those associated with cardiac injury,
preeclampsia, scleroderma renal crisis, and hyperadrenergic
states, are outlined in Table 13–17.
» Pharmacologic Management
A. Parenteral Agents
In most situations, appropriate control of blood pressure is
best achieved using combinations of nicardipine or clevidipine plus labetalol or esmolol; sodium nitroprusside is no
longer the treatment of choice for acute hypertensive problems. (Table 13–18 lists drugs, dosages, and adverse effects.)
1. Nicardipine—Intravenous nicardipine is the most
potent and longest acting parenteral calcium channel
blocker. As a primarily arterial vasodilator, it has the potential to precipitate reflex tachycardia, and for that reason, it
should be used with a beta-blocker in patients with CAD.
2. Clevidipine—Intravenous clevidipine is an L-type calcium channel blocker with a 1-minute half-life, which
facilitates swift and tight control of severe hypertension. It
acts on arterial resistance vessels and is devoid of venodilatory or cardiodepressant effects.
3. Labetalol—This combined beta- and alpha-blocking
agent is the most potent adrenergic blocker for rapid blood
pressure reduction. Other beta-blockers are far less potent.
Excessive blood pressure drops are unusual. Experience
with this agent in hypertensive syndromes associated with
pregnancy has been favorable.
4. Esmolol—This rapidly acting beta-blocker is approved
only for treatment of supraventricular tachycardia but is
often used for lowering blood pressure. It is less potent
than labetalol and should be reserved for patients in whom
there is particular concern about serious adverse events
related to beta-blockers.
5. Fenoldopam—Fenoldopam is a peripheral dopamine-1
(DA1) receptor agonist that causes a dose-dependent
reduction in arterial pressure without evidence of tolerance, rebound, withdrawal, or deterioration of kidney
function. In higher dosage ranges, tachycardia may occur.
This drug is natriuretic, which may simplify volume management in AKI.
6. Enalaprilat—This is the active form of the ACE inhibitor enalapril. The onset of action is usually within 15 minutes, but the peak effect may be delayed for up to 6 hours.
Thus, enalaprilat is used primarily as an adjunctive agent.
7. Diuretics—Intravenous loop diuretics can be helpful
when the patient has signs of HF or fluid retention, but the
onset of their hypotensive response is slow, making them
an adjunct rather than a primary agent for hypertensive
emergencies. Low dosages should be used initially (furosemide, 20 mg, or bumetanide, 0.5 mg). They facilitate the
response to vasodilators, which often stimulate fluid
retention.
8. Hydralazine—Hydralazine can be given intravenously
or intramuscularly, but its effect is less predictable than that
of other drugs in this group. It produces reflex tachycardia
and should not be given without beta-blockers in patients
with possible coronary disease or aortic dissection. Hydralazine is used primarily in pregnancy and in children, but
even in these situations, it is not a first-line drug.
9. Nitroglycerin, intravenous—This agent should be
reserved for patients with accompanying acute coronary
ischemic syndromes.
10. Nitroprusside sodium—This agent is given by controlled intravenous infusion gradually titrated to the
desired effect. It lowers blood pressure within seconds by
direct arteriolar and venous dilation. Monitoring with an
intra-arterial line avoids hypotension. Nitroprusside, in
combination with a beta-blocker, is useful in patients with
aortic dissection.
B. Oral Agents
Patients with less severe acute hypertensive syndromes can
often be treated with oral therapy. Suitable drugs will
reduce the blood pressure over hours. In those presenting
as a consequence of noncompliance, it is usually sufficient
to restore the patient’s previously established oral
regimen.
1. Clonidine—Clonidine, 0.2 mg orally initially, followed
by 0.1 mg every hour to a total of 0.8 mg, will usually lower
blood pressure over several hours. Sedation is frequent,
and rebound hypertension may occur if the drug is
stopped.
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CMDT 2025
CHAPTER 13
ischemia.
1–5 minutes 3–6 hours Hypotension, tachycardia, headache. May precipitate myocardial
in patients with allergy to soy
or egg.
2–4 minutes 5–15 minutes Headache, nausea, vomiting. Lipid emulsion: contraindicated
dysfunction, asthma. May be
continued orally.
dysfunction, asthma. Weak
Avoid in acute LV systolic
heart block.
5–10 minutes 3–6 hours Nausea, hypotension, bronchospasm, bradycardia,
antihypertensive.
May protect kidney function.
1–2 minutes 10–30 minutes Bradycardia, nausea. Avoid in acute LV systolic
continued orally.
pressure.
Excessive hypotension. Additive with diuretics; may be
more
used except in pregnancy.
primarily with myocardial
ischemia.
No longer the first-line agent.
bowel obstruction; thiocyanate and cyanide
toxicity, especially with kidney and liver
dysfunction; hypotension. Coronary steal,
decreased cerebral blood flow, increased
intracranial pressure.
10–30 minutes 2–6 hours Tachycardia, headache, vomiting, diarrhea Avoid in CAD, dissection. Rarely
30–60 minutes 6–8 hours Sedation. Rebound may occur.
Response unpredictable.
angina, MI, stroke.
15 minutes 2–6 hours Excessive hypotension, tachycardia, headache,
Table 13–18. Drugs for hypertensive emergencies and urgencies (in descending order of preference).
Agent Action Dosage Onset Duration Adverse Effects Comments
5 mg/hour intravenously; may
Hypertensive Emergencies
Nicardipine (Cardene) Calcium channel
increase by 1–2.5 mg/hour every
15 minutes to 15 mg/hour
1–2 mg/hour intravenously initially;
blocker
Clevidipine (Cleviprex) Calcium channel
double rate every 90 seconds until
near goal, then by smaller
amounts every 5–10 minutes to a
maximum of 32 mg/hour
blocker
10 minutes to 300 mg; 2 mg/min
infusion
nously over 1 minute; mainte-
20–40 mg intravenously every
alpha-blocker
Labetalol (Trandate) Beta- and
nance, 25–200 mcg/kg/min
0.1–1.6 mcg/kg/min intravenously 4–5 minutes < 10 minutes Reflex tachycardia, hypotension, increased intraocular
tor agonist
Dopamine recep-
Esmolol (Brevibloc) Beta-blocker Loading dose 500 mcg/kg intrave-
Fenoldopam
(Corlopam)
Enalaprilat (Vasotec) ACE inhibitor 1.25 mg intravenously every 6 hours 15 minutes 6 hours or
after 20 minutes
Vasodilator 5–20 mg intravenously; may repeat
(Apresoline)
Furosemide (Lasix) Diuretic 10–80 mg orally or intravenously 15 minutes 4 hours Hypokalemia, hypotension. Adjunct to vasodilator.
Hydralazine
Nitroglycerin Vasodilator 0.25–5 mcg/kg/min intravenously 2–5 minutes 3–5 minutes Headache, nausea, hypotension, bradycardia. Tolerance may develop. Useful
Vasodilator 0.25–10 mcg/kg/min intravenously Seconds 3–5 minutes Anxiety, increased intracranial pressure, vomiting,
(Nitropress)
Nitroprusside
0.1–0.2 mg orally initially; then
Hypertensive Urgencies
Clonidine (Catapres) Central
0.1 mg every hour to 0.8 mg orally
sympatholytic
Captopril (Capoten) ACE inhibitor 12.5–25 mg orally 15–30 minutes 4–6 hours Excessive hypotension.
repeated after 30 minutes
10 mg orally initially; may be
blocker
Calcium channel
Procardia)
Nifedipine (Adalat,
SYSTEMIC HYPERTENSION
CMDT 2025
459
2. Captopril—Captopril, 12.5–25 mg orally, lowers blood
pressure in 15–30 minutes. The response is variable and
may be excessive. Captopril is the drug of choice for treating systemic sclerosis hypertensive crisis.
3. Nifedipine—The effect of fast-acting nifedipine capsules is unpredictable and may be excessive, resulting in
hypotension and reflex tachycardia. Because MI and stroke
have been reported in this setting, the use of sublingual
nifedipine is not advised. Nifedipine retard, 20 mg orally,
appears to be safe and effective.
C. Subsequent Therapy
When the blood pressure has been brought under control,
combinations of oral antihypertensive agents can be
added as parenteral drugs are tapered off over a period of
2–3 days.
Rossi GP et al. Modern management of hypertensive emergen-
cies. High Blood Press Cardiovasc Prev. 2022;29:33. [PMID:
34813055]
460
CMDT 2025
14
Blood Vessel & Lymphatic Disorders
Warren J. Gasper, MD
James C. Iannuzzi, MD, MPH
Meshell D. Johnson, MD
º
ATHEROSCLEROTIC PERIPHERAL
VASCULAR DISEASE
Occlusive atherosclerotic lesions in the extremities, or
peripheral artery disease (PAD), is evidence of a systemic
atherosclerotic process. The prevalence of PAD is 30% in
patients who are 70 years old without other risk factors, or
50 years old with risk factors such as diabetes mellitus or
tobacco use. Pathologic changes of atherosclerosis may be
diffuse, but flow-limiting stenoses occur segmentally. In
the lower extremities, stenoses classically occur in three
anatomic segments: the aortoiliac segment, femoralpopliteal segment, and the infrapopliteal or tibial segment
of the arterial tree.
OCCLUSIVE DISEASE: AORTA &
ILIAC ARTERIES
ESSENTIALS OF DIAGNOSIS
»
Claudication: cramping pain or tiredness in the
calf, thigh, or hip while walking.
»
Diminished femoral pulses.
»
Tissue loss (ulceration, gangrene) or rest pain.
only leg weakness when walking, or extreme limb fatigue.
The symptoms are relieved with rest and are reproducible
when the patient walks again. Femoral pulses and distal
pulses are absent or very weak. Bruits may be heard over
the aorta, iliac, and femoral arteries.
B. Doppler and Vascular Findings
By Doppler examination, the ratio of systolic blood pressure at the ankle compared with the brachial artery (anklebrachial index [ABI]) is reduced to below 0.9 (normal ratio
is 0.9–1.2); this difference is exaggerated by exercise. Both
the dorsalis pedis and the posterior tibial arteries are measured and the higher of the two artery pressures is used for
calculation. Segmental waveforms or pulse volume recordings obtained by strain gauge technology through blood
pressure cuffs demonstrate blunting of the arterial waveform throughout the lower extremity.
C. Imaging
CT angiography (CTA) and magnetic resonance angiography (MRA) can identify the anatomic location of disease.
Due to overlying bowel gas, duplex ultrasonography has
limited utility for aortoiliac imaging. Imaging is required
only when symptoms necessitate intervention, since a
history and physical examination with vascular testing can
locate the involved levels of the arterial tree.
» General Considerations
Lesions in the distal aorta and proximal common iliac
arteries classically occur in White men aged 50–60 years
who smoke cigarettes. Disease progression may lead to
complete occlusion of one or both common iliac arteries,
which can precipitate occlusion of the entire abdominal
aorta to the level of the renal arteries.
» Clinical Findings
A. Symptoms and Signs
The pain from aortoiliac lesions may extend into the thigh
and buttocks and erectile dysfunction may occur with
bilateral common iliac disease. Rarely, patients experience
» Treatment
A. Medical and Exercise Therapy
The cornerstones of aortoiliac disease treatment are cardiovascular risk factor reduction and an exercise program.
1. Risk factor reduction—Essential elements include
cigarette smoking cessation, antiplatelet therapy, weight
loss, and lipid and blood pressure management. Nicotine
replacement therapy, bupropion, varenicline, and counseling have established benefits in cigarette smoking cessation (see Chapter 1). While no longer recommended
for primary prevention of CVD, antiplatelet agents (aspirin [81 mg orally daily] or clopidogrel [75 mg orally
daily]) are important for secondary prevention of cardiovascular events in those with PAD and to reduce
BLOOD VESSEL & LYMPHATIC DISORDERS
CMDT 2025
461
peripheral vascular morbidity. Low-dose rivaroxaban
(2.5 mg orally twice daily) with aspirin 81 mg orally daily
reduces major cardiovascular and limb-related adverse
events in symptomatic patients. All patients with PAD
should receive a high-dose statin (eg, atorvastatin 80 mg
daily if tolerated) to treat hypercholesterolemia and arterial inflammation. Cilostazol, 100 mg orally twice a day,
improves walking distance in approximately two-thirds
of patients but may take 2–4 weeks to be effective and
12 weeks until full effect.
2. Exercise programs—Supervised exercise programs for
PAD provide significant improvements in pain, walking
distance, and quality of life and may be more effective than
endovascular treatment alone. A minimum training goal is
a walking session of 30–45 minutes at least 3 days per week
for a minimum of 12 weeks. Structured community or
home-based exercise programs as well as alternative exercises (cycling, upper-body ergometry) may also be effective. Digital apps show promise in pilot studies to improve
walking distance and patients coping with their disease.
B. Endovascular Therapy
Focal atherosclerotic lesions in the aorta or iliac arteries
can be effectively treated with angioplasty and stenting,
matching the results of surgery for single stenoses, but
effectiveness and durability decrease with longer or multiple stenoses.
C. Surgical Intervention
A prosthetic aortofemoral bypass graft that bypasses the
diseased aorta or iliac artery segments is a highly effective
and durable treatment. Patients may also be treated with a
graft from the axillary artery to the femoral arteries (axillofemoral bypass graft) or with a graft from the contralateral femoral artery (femoral–femoral bypass) when iliac
disease is unilateral. The operative risk of axillofemoral and
femoral–femoral bypass grafts is lower because the abdominal cavity is not entered and the aorta is not crossclamped, but the grafts are less durable.
» Complications
The complications of aortofemoral bypass are those of any
major abdominal surgery in a patient population with a
high prevalence of CVD. Mortality is low (2–3%), but morbidity is higher and includes a 5–10% rate of MI. While
endovascular approaches are safer and the complication
rate is 1–3%, they are less durable with extensive disease.
» Prognosis
Patients with isolated aortoiliac disease may have a further
reduction in walking distance without intervention, but
symptoms rarely progress to rest pain or limb threat. Life
expectancy is limited by attendant CVD, with 5-year mortality of 25–40%.
Symptomatic relief is generally excellent with supervised exercise or after intervention. Aortofemoral bypass
5-year patency is 90%. In short stenoses, endovascular
patency and symptom relief also are good, with 80% of
patients symptom free at 3 years. In more extensive disease,
recurrence rates increase to 30–50%.
» When to Refer
Patients with progressive reduction in walking distance
despite risk factor modification, consistent exercise, or
limitations that interfere with activities of daily living
should be referred for vascular surgical evaluation.
» When to Admit
• Patients with acute limb ischemia for treatment with
intravenous anticoagulation, pain control, and surgical
evaluation.
• Patients with evidence of chronic limb-threatening
ischemia, including lower extremity rest pain and tissue
loss, since these may quickly progress to amputation of
the foot or leg.
Bonaca M P et al. Rivaroxaban in peripheral artery disease after
revascularization. N Engl J Med. 2020;382:1994. [PMID:
32222135]
Dittman JM et al. Medical optimization of the peripheral artery
disease patient. Semin Vasc Surg. 2022;35:113. [PMID:
35672101]
OCCLUSIVE DISEASE: FEMORAL &
POPLITEAL ARTERIES
ESSENTIALS OF DIAGNOSIS
»
Cramping pain or tiredness in the calf with
exercise.
»
Reduced popliteal and pedal pulses.
»
Foot pain at rest, relieved by dependency.
»
Foot gangrene or ischemic ulcers.
» General Considerations
The superficial femoral artery is the peripheral artery most
commonly occluded by atherosclerosis. Atherosclerosis of
the femoral-popliteal segment usually occurs about a
decade after the development of aortoiliac disease, has an
even gender distribution, and commonly affects Black and
Latino/Latina patients. The disease frequently occurs
where the superficial femoral artery passes through the
abductor magnus tendon in the distal thigh (Hunter canal).
The common femoral artery and the popliteal artery are
less often diseased but lesions in these vessels are debilitating, resulting in short-distance claudication.
» Clinical Findings
A. Symptoms and Signs
Symptoms of intermittent claudication caused by lesions of
the common femoral artery, superficial femoral artery, and
popliteal artery are confined to the calf. Claudication
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CHAPTER 14
occurs at 2–4 blocks when there is occlusion or stenosis of
the superficial femoral artery at the adductor canal, provided good collateral vessels from the profunda femoris are
maintained. However, with concomitant disease of the
profunda femoris or the popliteal artery, much shorter
distances may trigger symptoms. With short-distance
claudication, dependent rubor of the foot may be present;
pallor on elevation distinguishes rubor from erythema.
Chronic low blood flow states will also cause atrophic
changes in the lower leg and foot with loss of hair, thinning
of the skin and subcutaneous tissues, and disuse atrophy of
the muscles. With segmental occlusive disease of the
superficial femoral artery, the common femoral pulsation
is normal, but the popliteal and pedal pulses are reduced.
B. Doppler and Vascular Findings
ABI values less than 0.9 are diagnostic of PAD and levels
below 0.4 coincide with chronic limb-threatening ischemia
(formerly critical limb ischemia). ABI readings depend on
arterial compression; since vessels may be calcified in diabetes mellitus, CKD, and in older adults, ABIs can be misleading. In such patients, the toe-brachial index is usually
reliable with a value less than 0.7 considered diagnostic of
PAD. Pulse volume recordings with cuffs placed at the high
thigh, mid-thigh, calf, and ankle will delineate the levels of
obstruction with reduced pressures and blunted waveforms.
C. Imaging
Duplex ultrasonography, CTA, and MRA all adequately
show the anatomic location of the obstructive lesions and
are performed only if revascularization is planned. After
revascularization, patients can be monitored with annual
ultrasonograms.
2. Endovascular techniques—Endovascular techniques,
such as angioplasty and stenting, are often used for lesions
in the superficial femoral artery. These techniques have
lower morbidity than bypass surgery but also have decreased
durability and may limit future options for bypass.
Endovascular therapy is most effective in patients
undergoing aggressive risk factor modification in whom
lesions measure less than 10 cm long. Paclitaxel-eluting
stents or paclitaxel-coated balloons offer modest improvement over bare metal stents and noncoated balloons. The
1-year patency rate is 50% for balloon angioplasty, 70% for
drug-coated balloons, 80% for bare metal stents, and 90%
for drug-eluting stents. However, by 3 years, patency is
significantly worse than bypass for all four techniques and
reintervention for restenosis is common. While a metaanalysis of clinical trial data showed increased mortality at
3–5 years after treatment with paclitaxel-coated devices,
subsequent analyses in the SWEDEPAD and VOYAGER
PAD trials found no mortality difference between drugcoated devices and angioplasty.
3. Thromboendarterectomy—Removal of the atherosclerotic plaque is limited to common femoral and profunda
femoris artery lesions where endovascular techniques have
limited efficacy.
» Complications
Open surgical procedures of the lower extremities, particularly long bypasses with vein harvest, have a risk of wound
infection that is higher than in other areas of the body. Wound
infection or seroma can occur in as many as 10–15% of cases.
MI rates after open surgery are 5–10%, with 1–4% mortality.
Complication rates of endovascular surgery are 1–5%, making these therapies attractive despite their lower durability.
» Treatment
A. Medical and Exercise Therapy
As with aortoiliac disease, risk factor reduction, medical
optimization with an antiplatelet agent, high-dose statin, and
exercise treatment are the cornerstone of therapy and can
reduce 5-year mortality by two-thirds. Dual treatment with
rivaroxaban (2.5 mg orally twice daily) and aspirin (81 mg
orally daily) reduces limb-related events, major amputation,
and cardiovascular events. Cilostazol, 100 mg orally twice a
day, may improve intermittent claudication symptoms.
B. Surgical Intervention
Intervention is indicated if claudication is progressive, is
incapacitating, or interferes significantly with activities of
daily living, employment, or quality of life. Intervention is
critical if there is ischemic rest pain or if ischemic ulcers
threaten the foot.
1. Bypass surgery—The most effective and durable treatment for superficial femoral artery lesions is a femoralpopliteal bypass with autologous saphenous vein. Synthetic
material, usually polytetrafluoroethylene, can be used, but
these grafts do not have the durability of single segment
vein bypass.
» Prognosis
The prognosis for motivated patients with isolated superficial
femoral artery disease is excellent, and surgery is not recommended for mild or moderate claudication in these patients.
However, when claudication significantly limits daily activity
and cardiovascular health, intervention may be warranted.
All interventions require close postprocedure follow-up with
repeated ultrasound surveillance so that recurrent narrowing
can be detected and treated promptly with angioplasty or
bypass to prevent complete occlusion. The reported 3-year
patency rate of bypass grafts of the femoral artery, superficial
femoral artery, and popliteal artery is 65–70%, whereas the
patency of angioplasty is less than 50%.
Because of the extensive atherosclerotic disease, including associated coronary lesions, 5-year survival with lower
extremity PAD is 70% and decreases to 50% when there is
involvement of the tibial arteries. However, with aggressive
risk factor modification, substantial improvement in
longevity has been reported.
» When to Refer
Patients with progressive symptoms, short-distance claudication, rest pain, or any ulceration should be referred to a
peripheral vascular specialist.
BLOOD VESSEL & LYMPHATIC DISORDERS
CMDT 2025
463
» When to Admit
Individuals with chronic limb-threatening ischemia (eg,
ischemic rest pain, tissue loss) warrant admission
because of a high risk for rapid progression to limb loss.
If there is concern for a foot infection, particularly in
patients with diabetes, admission for broad-spectrum
antibiotics and emergent surgical evaluation should be
considered since emergent debridement may be necessary to prevent ascending infections that could be limband life-threatening.
Bauersachs RM et al. Total ischemic event reduction with
rivaroxaban after peripheral arterial revascularization in the
VOYAGER PAD Trial. J Am Coll Cardiol. 2021;78:317.
[PMID: 34010631]
Nordanstig J et al. Mortality with paclitaxel-coated devices in
peripheral artery disease. N Engl J Med. 2020;383:2538.
[PMID: 33296560]
OCCLUSIVE DISEASE: TIBIAL &
PEDAL ARTERIES
ESSENTIALS OF DIAGNOSIS
»
Severe pain of the forefoot that is relieved by
dependency (ischemic rest pain).
»
Pain or numbness of the foot with walking.
»
Ulcer or gangrene, and not claudication, is a
frequent initial manifestation.
»
Rubor when the foot is dependent and pallor
when the foot is elevated.
» General Considerations
Occlusive processes of the tibial arteries of the lower leg
and pedal arteries in the foot occur primarily in patients
with diabetes. There often is extensive calcification of the
artery wall.
B. Doppler and Vascular Findings
The ABI is often below 0.4; however, the ABI may be falsely
elevated due to calcification of the arterial media layer from
diabetes or CKD (Mönckeberg medial calcific sclerosis) and
may not be compressible. Toe-brachial indexes are preferred
for assessing perfusion and predicting wound healing.
C. Imaging
Digital subtraction angiography is the gold standard
method to delineate the anatomy of the tibial-popliteal
segment. MRA or CTA is less helpful for detection of
lesions in this location due to the small vasculature and
other technical issues related to image resolution.
» Differential Diagnosis
It is important to differentiate rest pain from diabetic neuropathic dysesthesia. Neuropathic pain is often described as
plantar surface burning and is not relieved with leg dependency. Similarly, leg night cramps should not be confused
with ischemic rest pain. Dependent rubor in the presence of
a toe wound can often be mistaken for cellulitis; pallor on
elevation helps confirm the diagnosis of rubor.
» Treatment
Good foot care may prevent ulcers, and most patients with
diabetes will do well with a conservative regimen and podiatric
care. However, if ulcerations appear and there is no significant
healing within 2–3 weeks, blood flow studies (ankle-brachial
index/toe-brachial index) are indicated. Poor blood flow and a
foot ulcer or nightly ischemic rest pain requires expeditious
revascularization to avoid a major amputation.
A. Bypass and Endovascular Techniques
Bypass with a saphenous vein to treat rest pain and heal
ischemic foot ulcers provides significantly better survival
and limb preservation rates than endovascular therapies.
However, an endovascular therapy–first strategy has similar
survival and limb preservation rates compared to bypass
with a conduit other than a single segment saphenous vein.
» Clinical Findings
A. Symptoms and Signs
Isolated tibial disease will manifest as rest pain, an ulcer, or
gangrene rather than claudication. Chronic limb-threatening ischemia is defined as the presence of ischemic rest
pain or ulcers and is associated with the highest rate of
amputation. Classically, ischemic rest pain is confined to
the dorsum of the forefoot and is relieved with dependency: the pain does not occur with standing, sitting, or
dangling the leg over the edge of the bed. It is severe and
burning in character and experienced when recumbent,
possibly awakening the patient.
On examination, femoral and popliteal pulses may or
may not be present depending on disease extent, but palpable pedal pulses will be absent. Dependent rubor may be
prominent with pallor on elevation. The skin of the foot is
generally cool, atrophic, and hairless.
B. Amputation
Patients with ischemic rest pain or ulcers have a 30–40%
1-year risk for major amputation. Patients with diabetes
and tibial disease can be asymptomatic due to peripheral
neuropathy, presenting more frequently with tissue loss.
Patients with diabetes and PAD have a 4-fold risk of
chronic limb-threatening ischemia compared with nondiabetic patients with PAD and have a risk of amputation up
to 20-fold when compared to an age-matched population.
Tibial artery disease is a major risk factor for amputation
and is included as a factor in the Global Limb Anatomic
Staging System (GLASS) vascular guidelines.
» Complications
The complications of intervention are similar to those listed
for superficial femoral artery disease; the overall cardiovascular risk of intervention increases with decreasing ABI.
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CHAPTER 14
Patients with chronic limb-threatening ischemia require
aggressive risk factor modification. Wound infection risk
after bypass is higher if there is an open foot wound.
» Prognosis
Patients with tibial atherosclerosis have extensive atherosclerotic burden and a high prevalence of diabetes. Their
prognosis without intervention is poor and complicated by
the risk of amputation.
» When to Refer
Patients with diabetes and foot ulcers should be referred
for a formal vascular evaluation and podiatric care.
» When to Admit
Any patient with diabetes and a foot ulcer and foot infection
should be evaluated for an emergent operative incision and
drainage. Empiric broad-spectrum intravenous antibiotics
should be given (eg, vancomycin for methicillin-resistant
Staphylococcus aureus [MRSA] plus either ertapenem or
piperacillin/tazobactam for gram-negative and anaerobic
organisms). Multidisciplinary limb preservation centers,
staffed with vascular surgeons, podiatrists, plastic and
orthopedic surgeons, prosthetics and orthotic specialists,
and diabetes specialists, have improved limb salvage rates.
Conte MS et al. Global vascular guidelines on the management
of chronic limb-threatening ischemia. J Vasc Surg. 2019;69:3.
[PMID: 31159978]
Farber A et al. Surgery or endovascular therapy for chronic limb-
threatening ischemia. N Engl J Med. 2022;387:2305. [PMID:
36342173]
Gallagher KA et al. Current status and principles for the treat-
ment and prevention of diabetic foot ulcers in the cardiovascular patient population: a scientific statement from the
American Heart Association. Circulation. 2024;149:e232.
[PMID: 38095068]
ACUTE ARTERIAL OCCLUSION OF A LIMB
ESSENTIALS OF DIAGNOSIS
»
Sudden pain in a limb with absent limb pulses.
»
Usually some neurologic dysfunction with
numbness, weakness, or complete paralysis.
»
Loss of light touch sensation requires revascularization within 3 hours for limb viability.
» General Considerations
Acute occlusion may be due to an embolus or to thrombosis
of a diseased atherosclerotic segment. Emboli large enough
to occlude proximal arteries in the lower extremities are
almost always cardiac in origin. Atrial fibrillation is the
most common cause of cardiac thrombus formation; other
causes are valvular disease or thrombus formation on the
ventricular surface of a large anterior myocardial infarct.
Emboli from arterial sources such as endoluminal
ulcerations or calcified excrescences are usually small and
go to the distal arterial tree (toes).
Typically, a patient with primary thrombosis will have a
history of claudication and an abrupt worsening of symptoms. If the stenosis is chronic, collateral blood vessels will
develop, and the resulting occlusion may cause only a
minimal increase in symptoms.
» Clinical Findings
A. Symptoms and Signs
The sudden onset of extremity pain, with loss or reduction
in pulses, is diagnostic of acute arterial occlusion. This
often will be accompanied by neurologic dysfunction, such
as numbness or paralysis in extreme cases. With popliteal
occlusion, symptoms may affect only the foot. With proximal occlusions, the whole leg may be affected. Signs of
severe arterial ischemia include pallor, coolness of the
extremity, and mottling. Impaired neurologic function
progressing to anesthesia with paralysis indicates irreversible injury requiring amputation.
B. Doppler and Laboratory Findings
There will be little or no flow on Doppler examination of
the distal vessels. Imaging, if done, may show an abrupt
cutoff of contrast with embolic occlusion. Blood work may
show myoglobinemia and metabolic acidosis.
C. Imaging
Whenever possible, imaging should be done in the operating room because obtaining angiography, MRA, or CTA
may delay revascularization and jeopardize the viability of
the extremity. However, in cases with only modest symptoms and where light touch of the extremity is maintained,
imaging may be helpful in planning revascularization.
» Treatment
Immediate revascularization is required in all cases of
symptomatic acute arterial thrombosis. Evidence of neuro-
logic injury, including loss of light touch sensation, indicates
that collateral flow is inadequate to maintain limb viability
and revascularization should be accomplished within
3 hours. Longer delays carry a significant risk of irrevers-
ible tissue damage approaching 100% at 6 hours.
A. Heparin
As soon as the diagnosis is made, an initial intravenous
bolus of unfractionated heparin (80 U/kg) should be given
followed by a continuous heparin infusion to maintain the
activated partial thromboplastin time (aPTT) in the therapeutic range (60–85 seconds) (12–18 units/kg/hour). This
helps prevent clot propagation and may also relieve associated vessel spasm. Anticoagulation may improve symptoms, but revascularization will still be required.
B. Endovascular Techniques
Pharmacomechanical thrombectomy catheters can achieve
rapid revascularization and are most effective for the smaller
BLOOD VESSEL & LYMPHATIC DISORDERS
CMDT 2025
465
arteries of the lower leg. Catheter-directed chemical thrombolysis into the clot with tissue plasminogen activator (TPA)
may be done but often requires 24 hours or longer to fully
lyse the thrombus. TPA can only be used in patients with
mild ischemia, as determined by an intact neurologic examination. Patients with moderate to severe ischemia require
immediate revascularization. Absolute contraindications for
TPA include bleeding diathesis, GI bleeding, intracranial
trauma, or neurosurgery within the past 3 months. Frequent
vascular and access site examinations are required during the
thrombolytic procedure to guard against the development of
a hematoma.
C. Surgical Intervention
General anesthesia is usually indicated for surgical exploration of an acute arterial occlusion of a limb; local anesthesia may be used in high-risk patients if the exploration is
limited to the common femoral artery. In extreme cases, it
may be necessary to perform thrombo-embolectomy from
the femoral, popliteal, and even the pedal vessels to revascularize the limb. The combined use of devices that pulverize and aspirate clot and intraoperative thrombolysis with
TPA improves outcomes.
» Complications
Complications of revascularization of an acutely ischemic
limb include severe metabolic acidosis, hyperkalemia, AKI,
and cardiac arrest. When several hours have elapsed but
recovery of viable tissue may still be possible, significant
levels of lactic acid, potassium, and other harmful agents
such as myoglobin may be released into the circulation during revascularization. Administering sodium bicarbonate
(150 mEq NaHCO3 in 1 L of dextrose 5% in water at a rate
of 1–1.5 L in the first hour and then adjust the rate to manage acidosis) before reestablishing arterial flow is required.
Surgery in the presence of thrombolytic agents and heparin
carries a high risk of postoperative wound hematoma.
» Prognosis
There is a 10–25% risk of amputation with an acute arterial
embolic occlusion, and a 25% or higher in-hospital mortality rate. Prognosis for acute thrombotic occlusion of an
atherosclerotic segment is generally better because the collateral flow can maintain extremity viability. The longerterm survival reflects the overall condition of the patient.
In high-risk patients, an acute arterial occlusion is associated with a dismal prognosis.
OCCLUSIVE CEREBROVASCULAR DISEASE
ESSENTIALS OF DIAGNOSIS
»
Sudden onset of weakness and numbness of an
extremity or the face, aphasia, dysarthria, or unilateral blindness (amaurosis fugax).
»
Bruit heard loudest in the mid neck.
» General Considerations
Unlike the other vascular territories, symptoms of ischemic
cerebrovascular disease are predominantly due to emboli.
When collateral flow reestablishes perfusion, ischemia
reverses (transient ischemic attacks [TIAs]) but signals a
high risk for additional emboli and stroke. The origins of
emboli that cause ischemic strokes are the heart (most
commonly) and an arterial source (25% of ischemic
strokes). Approximately 90% of emboli from an arterial
source originate from the proximal internal carotid artery,
an area uniquely prone to the development of atherosclerosis. The aortic arch may also be an atheroembolic source.
Intracranial atherosclerotic lesions are uncommon in western populations but are the most frequent location of cerebrovascular disease in Asian populations.
» Clinical Findings
A. Symptoms and Signs
Generally, the symptoms of a TIA last only a few seconds
to minutes (but may continue up to 24 hours) while a
stroke is defined as persistent symptoms beyond 24 hours.
The most common lesions associated with carotid disease
involve the anterior circulation in the cortex with both
motor and sensory involvement. Emboli to the retinal
artery cause unilateral blindness; transient monocular
blindness is termed “amaurosis fugax.” Posterior circulation symptoms referable to the brainstem, cerebellum,
and visual regions of the brain may be due to atherosclerosis of the vertebral basilar systems and are much less
common.
Signs of cerebrovascular disease may include carotid
artery bruits. However, there is poor correlation between
the degree of stenosis and the presence of the bruit. Furthermore, the presence of a bruit does not correlate with
stroke risk. Nonfocal symptoms, such as dizziness and
unsteadiness, seldom are related to cerebrovascular
atherosclerosis.
B. Imaging
Duplex ultrasonography is the imaging modality of choice
with high specificity and sensitivity for detecting and
grading the degree of stenosis at the carotid bifurcation
(see Chapter 26).
Excellent depiction of the full anatomy of the cerebrovascular circulation from aortic arch to cranium can be
obtained with MRA or CTA (Figure 14–1). Each of the
modalities may have false-positive or false-negative findings. Since the decision to intervene in cases of carotid
stenosis depends on an accurate assessment of the degree
of stenosis, it is recommended that at least two modalities
be used to confirm the degree of stenosis. Diagnostic cerebral angiography is reserved when carotid artery stenting is
planned or other imaging modalities are contraindicated.
» Treatment
See Chapter 26 for a discussion of the medical management of occlusive cerebrovascular disease.