Vascular Disease

Acute Arterial Occlusion of a Limb Essentials of Diagnosis Sudden pain in an extremity. Generally associated with some element of neurologic dysfunction with numbness, weakness, or complete paralysis. Absent extremity pulses. General Considerations Acute occlusion may be due to an embolus or to thrombosis of a diseased atherosclerotic segment. Arterial to arterial emboli such as in the cerebrovascular tree can occur, but emboli large enough to occlude proximal arteries in the lower extremities are almost always from the heart and tend to lodge at the bifurcation of major arteries. Over 50% of the emboli from cardiac sources go to the lower extremities, 20% to the cerebrovascular circulation, and the remainder to the upper extremities and mesenteric and renal circulation. Atrial fibrillation is the usual cause of the thrombus; other causes are valvular disease or ischemic heart disease where thrombus has formed on the ventricular surface of a transmural myocardial infarct. Emboli from arterial sources such as arterial ulcerations or calcified excrescences are usually small and go to the distal arterial tree (toes). The typical patient with primary thrombosis has had a history of claudication and now has an acute occlusion. If the stenosis has developed over time, collateral blood vessels will develop, and the resulting occlusion may only reduce walking distance or cause minimal increase in symptoms. Clinical Findings Symptoms and Signs The most common symptom is sudden onset of extremity pain, often accompanied by neurologic dysfunction, which can be numbness or paralysis in extreme cases. With popliteal occlusion, symptoms may only affect the foot. With proximal occlusions, the whole leg may be affected. Signs include absence of pulses in the arteries distal to the occlusion and signs of severe arterial ischemia, such as pallor on elevation, coolness of the extremity, mottling, and impaired neurologic function with hyperesthesia progressing to anesthesia accompanied with paralysis. Laboratory Findings These include little or no flow with Doppler examination of the distal vessels. Imaging, if done, shows an abrupt cutoff of the vessel involved. Blood work may indicate systemic acidosis. Imaging Whenever possible, imaging should be done in the operating room because a delay in obtaining angiography, MRA, or CTA may jeopardize the viability of the tissue at risk (see arteriogram). However, in cases with only modest symptoms and light touch of the extremity is maintained, imaging may be helpful in expediting the revascularization procedure by identifying the exact areas of occlusion and delineating distal vessel patency. Treatment Immediate revascularization is the treatment of choice in all cases of symptomatic acute arterial thrombosis. Evidence of neurologic 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 irreversible tissue damage. This risk approaches 100% at 6 hours. Heparin As soon as the diagnosis is made, heparin should be administered (5000–10,000 units) intravenously. This helps prevent propagation of the clot. Heparin may also help relieve associated spasm of the vessels. There may be some reduction in symptoms with aggressive anticoagulation, but revascularization will still be required. Patients in atrial fibrillation need to continue taking anticoagulants until cardioversion can be attempted. Surgical Intervention General anesthesia is usually indicated in these patients; local anesthesia may be used in extremely high-risk patients if the exploration is to be limited to the common femoral artery. In extreme cases, it may be necessary to perform embolectomy from the femoral popliteal and even the pedal vessels to revascularize the limb. Intraoperative thrombolysis with tissue plasminogen activator (TPA) may be used to lyse a clot in the distal arterial tree. Endovascular Techniques Chemical thrombolysis with TPA may be done but often requires 24 hours or longer to fully lyse the thrombus. This approach can be taken only in patients with an intact neurologic exam. An echocardiogram should be done to identify additional clot in the atrium. If an additional clot is found, it is a relative contraindication to thrombolysis because of the risk of subsequent emboli from the lysed cardiac clot. Catheter-based mechanical thrombolysis may be an excellent alternative. Complications Complications of revascularization of an acutely ischemic limb can include severe acidosis and myocardial arrest. In cases where several hours have elapsed but recovery of viable tissue may still possible, significant levels of lactic acid, potassium, and other harmful agents may be released into the circulation during revascularization. Pretreatment of the patient with sodium bicarbonate prior to 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 acute arterial occlusion, and a 25% or higher in-hospital mortality rate. Prognosis for acute occlusion of an atherosclerotic segment is generally much better because the collateral flow can maintain extremity viability. The longer term survival reflects the overall condition of the patient. In high-risk patients, an acute arterial occlusion suggests a dismal prognosis. Occlusive Cerebrovascular Disease Essentials of Diagnosis Sudden onset of a neurologic deficit consistent with unilateral cortical ischemia; weakness and numbness of an extremity, aphasia, dysarthria, or unilateral blindness (amaurosis fugax). Bruit heard loudest in the mid neck. General Considerations Unlike the other vascular territories, symptoms of occlusive cerebrovascular disease are predominantly due to emboli. Transient ischemic attacks (TIAs) are the result of small emboli and are the earliest manifestation of carotid stenosis (see illustration). These transient symptoms are thought to demonstrate plaque instability, and the risk of additional emboli causing permanent deficits are high. Twenty-five percent or more of all strokes may be due to emboli. In the absence of atrial fibrillation, approximately 90% of these emboli originate from the proximal internal carotid artery. Lesions in the carotid siphon, the common carotid, and the proximal great vessels are far less common.  Clinical Findings Symptoms and Signs Generally, the ischemic symptoms of TIAs last only a few minutes but may continue up to 24 hours. Emboli to the retinal artery cause unilateral blindness which, when transient, is termed "amaurosis fugax." Posterior circulation symptoms referable to the brainstem, cerebellum, and visual regions of the brain are due to atherosclerosis of the vertebral basilar systems and are much less common. Signs of cerebrovascular disease include bruits in the mid-cervical area with reduced or absent arm pulses. While bruits in the neck in older patients and generalized atherosclerosis are important signs of cerebrovascular disease, they are not specific for narrowing within the vessel. There is poor correlation between the degree of stenosis and the presence of the bruit. Furthermore, absence of a bruit does not exclude the possibility of carotid stenosis. Nonfocal symptoms, such as dizziness and unsteadiness, seldom are related to cerebrovascular atherosclerosis. Imaging Duplex ultrasonography is the imaging modality of choice with a high specificity and sensitivity for detecting and grading the degree of stenosis at the carotid bifurcation (see ultrasound); (see ultrasound). Excellent depiction of the full anatomy of the cerebrovascular circulation from arch to cranium can be obtained with either MRA or CTA. Each of these 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. Cerebral angiography is reserved for cases that cannot be resolved by these less invasive imaging modalities. Treatment Asymptomatic Patients Patients with no neurologic symptoms but with carotid stenosis on imaging will benefit from carotid intervention if they are considered to be at low risk for intervention and their expected survival is greater than 5 years. Recommendation for intervention also presumes that the treating institution has a stroke rate in asymptomatic patients that is acceptable (< 3%). Large studies indicate a reduction in stroke from 11.5% to 5.0% over 5 years with surgical treatment of asymptomatic carotid stenoses of greater than 60%. However, the usual practice is to only treat those patients who have greater than 80% stenosis. Symptomatic Patients Patients with TIAs or strokes from which they have completely or nearly completely recovered will benefit from carotid intervention if the carotid stenosis, ipsilateral to the event, has a stenosis of 70%, and they are likely to derive benefit with a stenosis of 50–69%. In these situations, carotid endarterectomy has been shown to have a durable effect in preventing further events. Complications The primary complication of carotid intervention is stroke due to embolization of plaque material during the procedure. The American Heart Association has recommended upper limits of acceptable combined morbidity and mortality for these interventions: 3% for asymptomatic, 5% for those with TIAs, and 7% for patients with previous stroke. Results that do not match these guidelines will jeopardize the therapeutic benefit of carotid intervention. Carotid Endarterectomy In addition to stroke risk, carotid endarterectomy carries a 10% risk of transient cranial nerve injury (usually the vagus or hypoglossal nerve) and 1–2% risk of permanent deficits. There is also the risk of postoperative neck hematoma, which can cause acute compromise of the airway. Coronary artery disease exists as a comorbidity in most of these patients. Myocardial infarction rates after carotid endarterectomy are approximately 5%. Angioplasty and Stenting Carotid angioplasty and stenting has been advocated as an alternative to carotid endarterectomy. Angioplasty and stenting offers the advantage of avoidance of both cranial nerve injury and neck hematoma. However, emboli are more common during angioplasty in spite of the use of embolic protection devices during the procedure. The Carotid Revascularization Endarterectomy versus Stent Trial (CREST), sponsored by the National Institutes of Health, randomized patients to undergo carotid endarterectomy or angioplasty; this study should determine the role of stenting in carotid disease. Recurrent Carotid Stenosis Scarring of the arterial wall at the site of the intervention after both angioplasty and endarterectomy may create recurrent stenosis. These lesions tend to be less embologenic, and treatment need not be as aggressive as for primary disease. The cranial nerve risk for these patients may be higher with repeat endarterectomy than with angioplasty of the narrowed segment. Prognosis Prognosis for patients with carotid stenosis who have had a TIA or small stroke is poor without treatment; 25% of these patients will have a stroke with most of the events occurring in the first year of follow-up. Patients with carotid stenosis without symptoms have an annual stroke rate of just over 2%. Risk factor modification with antiplatelet agents is not nearly as effective in preventing stroke as removing the stenosis. Symptomatic patients most likely have unstable plaques with ulceration or they have had a recent progression of the stenosis. This suggests that prospective ultrasound screening would be valuable in timing intervention in asymptomatic patients. Approximately 10% of asymptomatic patients have evidence of plaque progression in a given year. Concomitant coronary artery disease is common and is an important factor in these patients both for perioperative risk and long-term prognosis. Aggressive risk factor modification should be prescribed for patients with cerebrovascular disease regardless of planned intervention. Visceral Artery Insufficiency (Intestinal Angina) Essentials of Diagnosis Severe postprandial abdominal pain. Weight loss with a "fear of eating." General Considerations Acute visceral artery insufficiency results from either embolic occlusion or primary thrombosis of at least one major mesenteric vessel. Ischemia can also result from nonocclusive mesenteric vascular insufficiency, which is generally seen in patients with low flow states, such as congestive heart failure, or who are in shock. A chronic syndrome occurs when there is adequate perfusion for the viscera at rest but ischemia occurs with severe abdominal pain when flow demands increase with feeding. Because of the rich collateral network in the mesentery, generally at least two of the three major visceral vessels (celiac, superior mesenteric, inferior mesenteric arteries) are affected before symptoms develop. Ischemic colitis, a variant of mesenteric ischemia, usually occurs in the distribution of the inferior mesenteric artery. The intestinal mucosa is the most sensitive to low perfusion and will slough if underperfused. The clinical presentation is similar to inflammatory bowel disease. Ischemic colitis can occur postoperatively, particularly after aortic aneurysm resection or aorto-femoral bypass for occlusive disease, when there is sudden reduction in blood flow to the inferior mesenteric artery. Clinical Findings Symptoms and Signs Acute Intestinal Ischemia Patients with primary thrombosis often give an antecedent history consistent with chronic intestinal ischemia. The key finding with acute mesenteric ischemia is severe, steady epigastric and periumbilical pain with minimal or no findings on physical examination of the abdomen. A high white cell count, lactic acidosis, hypotension, and abdominal distention may aid in the diagnosis. Chronic Intestinal Ischemia Patients are generally over 45 years of age and may have evidence of atherosclerosis in other vascular beds. Symptoms consist of epigastric or periumbilical postprandial pain lasting 1–3 hours. To avoid the pain, patients limit food intake and may develop a fear of eating. Weight loss is universal. Ischemic Colitis

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Characteristic symptoms are left lower quadrant pain and tenderness, abdominal cramping, and mild diarrhea, which is often bloody.

Imaging and Colonoscopy

In patients with acute or chronic mesenteric ischemia, a CTA or MRA can demonstrate narrowing of the proximal visceral vessels. In acute mesenteric ischemia from a nonocclusive low flow state, angiography is needed to display the typical "pruned tree" appearance of the distal visceral vascular bed (see arteriogram). Ultrasound scanning of the mesenteric vessels may show proximal obstructing lesions in laboratories that have experience with this technique.

In patients with ischemic colitis, colonoscopy may reveal segmental inflammatory changes, most often in the rectal sigmoid and splenic flexure where collateral circulation may be poor. Treatment A high suspicion of acute mesenteric ischemia dictates immediate exploration to determine bowel viability. If the bowel remains viable, bypass can be done from the aorta to the celiac and the superior mesentery artery. In cases where bowel viability is questionable or bowel resection will be required, the bypass can be done with autologous vein, or with PTFE. Recent reports suggest a surprisingly low incidence of graft infection in these cases. The mainstay of treatment of ischemic colitis is maintenance of hydration until collateral circulation becomes well established. For the treatment of nonocclusive mesenteric disease, vasodilators can be delivered through a catheter in the mesenteric arteries. In chronic visceral ischemia, angioplasty and stenting of the proximal vessel may be beneficial depending on the anatomy of the stenosis. Should an endovascular solution not be available, an aorto-visceral artery bypass is the preferred management. The long-term results are highly durable. Visceral artery endarterectomy is reserved for cases with multiple lesions where bypass would be difficult. Prognosis The combined morbidity and mortality rates are 10–15% from surgical intervention in these debilitated patients. However, without intervention both acute and chronic visceral ischemia are uniformly fatal. Adequate collateral circulation usually develops in those who have ischemic colitis; the prognosis for this entity is better than chronic mesenteric insufficiency. Acosta S et al. Clinical implications for the management of acute thromboembolic occlusion of the superior mesenteric artery: autopsy findings in 213 patients. Ann Surg. 2005 Mar;241(3): 516–22. [PMID: 15729076]

Acute Mesenteric Vein Occlusion The hallmarks of acute mesenteric vein occlusion are postprandial pain and evidence of a hypercoagulable state. Acute mesenteric vein occlusion presents similarly to the arterial occlusive syndromes but is much less common. Patients at risk include those with a systemic hypercoagulable state, such as that observed with paroxysmal nocturnal hemoglobinuria or protein C, protein S, or antithrombin deficiencies. These lesions are difficult to treat surgically, and thrombolysis is the mainstay of therapy. Long-term anticoagulation is required for these patients.

Thromboangiitis Obliterans (Buerger's Disease)

Essentials of Diagnosis

• Typically occurs in young male cigarette smokers.
• Distal extremities involved with severe circulatory insufficiency.
• Thrombosis of the superficial veins may occur.
• Amputation will be necessary unless the patient stops smoking.

General Considerations

Buerger's disease is a segmental, inflammatory, and thrombotic process of the distal most arteries and occasionally veins of the extremities. Pathologic examination reveals arteritis in the affected vessels. The cause is not known but it is rarely seen in nonsmokers. Arteries most commonly affected are the plantar and digital vessels of the foot and lower leg. In advanced stages, the fingers and hands may become involved. Fortunately, the incidence of Buerger's disease seems to have decreased in the past decade.

Clinical Findings

Symptoms and Signs

Buerger's disease may be initially difficult to differentiate from routine peripheral vascular disease, but in most cases, the lesions are on the toes and the patient is younger than 40 years old. The observation of superficial thrombophlebitis may aid the diagnosis. Because the distal vessels are usually affected, intermittent claudication is not common with Buerger's disease, but rest pain, particularly pain in the distal most extremity (ie, toes), is frequent. This pain often progresses to tissue loss and amputation, unless the patient stops smoking. The progression of the disease seems to be intermittent with acute and dramatic episodes followed by some periods of remission.

Imaging

MRA or invasive angiography can demonstrate the obliteration of the distal arterial tree typical of Buerger's disease.

Differential Diagnosis

In peripheral vascular disease, the onset of tissue ischemia tends to be less traumatic than in Buerger's disease, and symptoms of proximal arterial involvement, such as claudication, predominate.

Symptoms of Raynaud's disease may be difficult to differentiate from Buerger's disease. Repetitive atheroemboli may also mimic Buerger's disease and may be difficult to differentiate. It may be necessary to image the proximal arterial tree to rule out sources of arterial emboli.

Treatment

Smoking cessation is the mainstay of therapy and will halt the disease in most cases. As the distal arterial tree is occluded, revascularization is not possible. Sympathectomy is rarely effective.

Prognosis

If smoking cessation can be achieved, the outlook for Buerger's disease may be better than in patients with premature peripheral vascular disease. If smoking cessation is not achieved, then the prognosis is generally poor, with amputation of both lower and upper extremities the eventual outcome.

Olin JW. Thromboangiitis obliterans (Buerger's disease). N Engl J Med. 2000 Sep 21;343(12):864–9. [PMID: 10995867]

Abdominal Aortic Aneurysms

Essentials of Diagnosis

• Most aortic aneurysms are asymptomatic until rupture.
• Abdominal aortic aneurysms measuring 5 cm are palpable in 80% of patients.
• Back or abdominal pain with aneurysmal tenderness may precede rupture.
• Rupture is catastrophic; hypotension; excruciating abdominal pain that radiates the back.

General Considerations

Dilatation of the infrarenal aorta is a normal part of aging. The aorta of a healthy young man measures approximately 2 cm. An aneurysm is considered present when the aortic diameter exceeds 3 cm, but aneurysms rarely cause any problems until their diameter exceeds 5 cm. Abdominal aortic aneurysms are found in 2% of men over 55 years of age; the male to female ratio is 8:1. Ninety percent of abdominal atherosclerotic aneurysms originate below the renal arteries. The aneurysms usually involve the aortic bifurcation and often involve the common iliac arteries.

Inflammatory aneurysms happen when an inflammatory peel, similar to the inflammation that occurs with retroperitoneal fibrosis, surrounds the aneurysm and encases the retroperitoneal structures, which include the duodenum and, occasionally, the ureters (see photograph).

Clinical Findings

Symptoms and Signs

Asymptomatic

Although 80% of 5-cm infrarenal aneurysms are palpable on routine physical examination, most aneurysms are discovered as incidental findings on ultrasound or CT imaging during the evaluation of unrelated abdominal symptoms.

Symptomatic

Pain

Aneurysmal expansion may be accompanied by pain that is mild to severe midabdominal discomfort often radiating to the lower back. The pain may be constant or intermittent and is exacerbated by even gentle pressure on the aneurysm sack. The pain may also accompany inflammatory aneurysms.

Rupture

The sudden escape of blood into the retroperitoneal space causes severe pain, a palpable abdominal mass, and hypotension. Free rupture into the peritoneal cavity is a lethal event. Most aneurysms have a thick lining of blood clot, which can break away, float with the blood to a small peripheral artery where it occludes blood flow (embolism). Although this phenomenon is rare, multiple localized areas of poor peripheral blood flow (blue toe syndrome), should prompt a search for an aneurysm.

Laboratory Findings

Even with a contained rupture, there may be little change in routine laboratory findings. The hematocrit will be normal, since there has been no opportunity for hemodilution.

Aneurysms are associated with the cardiopulmonary diseases of elderly male smokers, which include coronary artery disease, carotid disease, renal impairment, and emphysema. Preoperative testing may indicate the presence of these comorbid conditions.

Imaging

Abdominal ultrasonography is the diagnostic study of choice for initial diagnosis (see ultrasound). In approximately three-quarters of patients with aneurysms, curvilinear calcifications outlining portions of the aneurysm wall may be visible on plain films of the abdomen or back. CT scans provide a more reliable assessment of aneurysm diameter and should be done when the aneurysm nears the diameter threshold for treatment. Contrast-enhanced CT scans show the arteries above and below the aneurysm (see CT Scan). The visualization of this vasculature is essential for planning repair. 

Screening

There are now data to support using abdominal ultrasound to screen 65- to 74-year-old men, but not women, who have a history of smoking. Repeated screening does not appear to be needed.

Treatment

Aneurysmal Rupture

If the rupture and bleeding are confined to the retroperitoneum, the combination of low blood pressure and retroperitoneal containment may arrest the blood loss long enough for the patient to undergo urgent operation. Endovascular repair represents the best opportunity for survival because the retroperitoneal blood clot is left intact. Patients who have free rupture of the aneurysm into the peritoneum do not survive long enough to undergo surgical repair.

Elective Repair

In general, elective repair is indicated for aortic aneurysms > 5.5 cm in diameter or aneurysms that have undergone rapid expansion (> 5 mm in 6 months). Symptoms such as pain or tenderness may indicate impending rupture. These patients need to undergo aneurysm repair regardless of the aneurysm's diameter. Improving outcomes with endovascular techniques have caused some experts to recommend treatment of smaller aneurysms. Current studies are ongoing to determine whether this may be appropriate.

Inflammatory Aneurysm

The presence of peri-aortic inflammation (inflammatory aneurysm) is not an indication for surgical treatment, unless there is associated compression of retroperitoneal structures, such as the ureter. Interestingly, the inflammation that encases an inflammatory aneurysm recedes after either endovascular or surgical aneurysmal repair.

Assessment of Operative Risk

Aneurysms appear to be a variant presentation of systemic atherosclerosis. Some assessment of coronary risk for aneurysm intervention is essential prior to planning procedures. A 2004 trial demonstrated minimal value in addressing stable coronary artery disease prior to aneurysm resection. However, in patients with significant symptoms of coronary disease, the coronary disease should be treated first. Aneurysm resection should follow shortly thereafter because there is a significant increase risk in aneurysm rupture after the coronary procedures. In patients with concomitant carotid stenosis, there is no benefit in repairing asymptomatic carotid disease prior to aneurysm resection.

Open Surgical Resection versus Endovascular Repair

In open surgical aneurysm repair, a graft is sutured to the non-dilated aorta above and below the aneurysm. This involves an abdominal incision, extensive dissection, and interruption of aortic blood flow. The mortality rate is low in centers that have a high volume for this procedure and it is performed in good risk patients. Older, sicker patients may not tolerate the cardiopulmonary stresses of the operation. With endovascular repair, a stent-graft is used to line the aorta and exclude the aneurysm. The anatomic requirements to securely achieve aneurysm exclusion vary according to the performance characteristics of the specific stent-graft device. In general, successful attachment requires a segment of non-dilated aorta (neck) between the renal arteries and the aneurysm to be at least 15 mm in length, and device insertion requires iliac arteries to be at least 7 mm in diameter.

Complications

Myocardial infarction, the most common complication, occurs in up to 10% of patients who undergo open aneurismal repair. The incidence of myocardial infarction is substantially lower with endovascular repair. For routine infrarenal aneurysms, renal injury is unusual; however, when it does occur, it is a significant complicating factor in the postoperative period. Respiratory complications are similar to those seen in most major abdominal surgery. Gastrointestinal hemorrhage, even years after aortic surgeries, may suggest the possibility of graft enteric fistula; the incidence of this complication is higher when the initial surgery is performed on an emergency basis.

Prognosis

The mortality rate for an open elective surgical resection is 1–5%. Of those who survive surgery, approximately 60% are alive at 5 years; myocardial infarction is the leading cause of death. The decision to repair aneurysms in high-risk patients has been made easier with the reduced perioperative morbidity and mortality of the endovascular approach. In the long-term, difference between open and endovascular repair in perioperative mortality are relatively small compared with the mortality rates associated with the usual comorbid conditions.

Mortality rates of untreated aneurysms vary with aneurysm diameter. The mortality rate among patients with large aneurysms who have not undergone surgery, has been defined as follows: 12% annual risk of rupture with an aneurysm 6 cm in diameter and a 25% annual risk of rupture in aneurysms of 7 cm diameter. In general, a patient with an aortic aneurysm has a threefold greater chance of dying of a consequence of rupture of the aneurysm than of dying of the surgical resection.

At present, endovascular aneurysm repair may be less definitive than open surgical repair. The subsequent behavior of the endovascularly repaired aneurysm depends on how successfully it has been excluded from the circulation, as demonstrated by the absence of contrast-enhanced blood on CT within the space between the stent-graft and the aneurysm wall. Complete exclusion lowers the pressure in the aneurysm sac, which causes the aneurysm to shrink. On the other hand, direct leakage of contrast-enhanced blood into the aneurysm (endoleak, types 1 and 3) is associated with high aneurysm sac pressure, a low rate of aneurysm shrinkage, and a persistent risk of rupture. Indirect leakage of blood through persistent lumbar and inferior mesenteric branches of the aneurysm (endoleak, type 2) produces an intermediate picture with somewhat reduced pressure, slow shrinkage and low rupture risk. However, type 2 endoleak warrants close observation because aneurysm dilatation and rupture can occur.

Recources: Current Medical Diagnosis & Treatment 2008

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