“แนวทางป้องกัน VAP ”
http://www.bhumibolhospital.rtaf.mi.th/multimedia/oraeuerm/KM-VAP%20team.pdf
การพยาบาลผู้ป่วยบาดเจ็บทรวงอก
http://www.ra.mahidol.ac.th/files/file/0NS/2009/SNPR/NEWS/2009/Emergency2009/Doc/EmergecyS01.pdf
การพัฒนาระบบการดูแลต่อเนื่องในผู้ป่ วยโรคหลอดเลือดสมอง ในโรงพยาบาลนพรัตนราชธานี
http://www.bcnnv.ac.th/80bcnnv/80%20pee/Abstract_Full%20text/P.05.pdf
Fluid and Electrolyte management of surgical patient
ผู้ช่วยศาสตราจารย์ นายแพทย์วิชิต วิริยะโรจน์
การให้โภชนบำบัดในผู้ป่วยวิกฤต
http://cyberclass.msu.ac.th/cyberclass/cyberclass-uploads/libs/document/05rangsan
_d5dc.pdf
ดหมาในแวดวงการดูแลโรคหัวใจหลอดเลือเฉิน
http://www.americanheart.org/downloadable/heart/1155149431223Currents%20Winter%20Thai.pdf
การจัดการความรู้ หน่วยช่วยการหายใจ
http://www.bhumibolhospital.rtaf.mi.th/multimedia/oraeuerm/KM-CoP
http://www.vascular.co.nz/angiogram.htm
ANGIOGRAM / ANGIOPLASTY
What is an angiogram? angiogram คืออะไร?
Preparation for the angiogram เตรียม angiogram
During the angiogram ระหว่าง angiogram
After the angiogram หลังจาก angiogram
When do I know the angiogram result? ผลทำเมื่อฉัน angiogram รู้
What is an Angioplasty? Angioplasty คืออะไร?
During the angioplasty ในช่วง angioplasty
After the angioplasty หลังจาก angioplasty
What are the possible side effects/complications? อะไรคือผลข้างเคียงภาวะแทรกซ้อน /?
Can I do anything to help myself? ฉันสามารถทำอะไรเพื่อตัวเอง?
How effective is angioplasty? วิธีที่มีประสิทธิภาพเป็น angioplasty?
ANGIOGRAM / ANGIOPLASTY
What is an angiogram? angiogram คืออะไร?
Preparation for the angiogram เตรียม angiogram
During the angiogram ระหว่าง angiogram
After the angiogram หลังจาก angiogram
When do I know the angiogram result? ผลทำเมื่อฉัน angiogram รู้
What is an Angioplasty? Angioplasty คืออะไร?
During the angioplasty ในช่วง angioplasty
After the angioplasty หลังจาก angioplasty
What are the possible side effects/complications? อะไรคือผลข้างเคียงภาวะแทรกซ้อน /?
Can I do anything to help myself? ฉันสามารถทำอะไรเพื่อตัวเอง?
How effective is angioplasty? วิธีที่มีประสิทธิภาพเป็น angioplasty?
case กรณีศึกษา ที่มีปัญหาเรื่อง Vanco level มี guidline ค่ะ
VANCOMYCIN MONITORING GUIDELINES
http://www.dobugsneeddrugs.org/healthcare/antimicrobial/VancomycinMonitoringGuidelines.pdf
Evaluation of D-Dimer in the Diagnosis of Suspected Deep-Vein Thrombosis
http://content.nejm.org/cgi/content/short/349/13/1227
Ability of Different d-Dimer Tests To Exclude Deep Venous Thrombosis and Pulmonary Embolism
http://www.annals.org/content/140/8/I-42.full
Best Hospitals 2010-11: the Honor Roll
http://health.yahoo.net/articles/healthcare/best-hospitals-2010-11-honor-roll
ขอบคุณค่ะพี่ต้อม
รื่อง arterial occlusion มาช่วยกันแปลนะคะ
Acute arterial occlusion of the lower extremities (acute limb ischemia)
AuthorsMarc E Mitchell, MDEmile R Mohler, III, MDJeffrey P Carpenter, MD
Section EditorsDenis L Clement, MD, PhDJames Hoekstra, MD
Deputy EditorKathryn A Collins, MD, PhD, FACS
INTRODUCTION AND DEFINITIONS
According to the 2007 Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II), acute limb ischemia is defined as a sudden decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present within two weeks of the acute event [1]. Patients with similar manifestations who present later than two weeks are considered to have critical limb ischemia, which is by definition chronic.
The management of acute arterial occlusion remains a challenge for vascular specialists. Surgical thromboembolectomy and bypass grafting were the mainstays of therapy for many years [2]. Subsequently, thrombolytic therapy and percutaneous transluminal angioplasty (PTA) have become treatment options for selected patients.
Despite these advances, the morbidity, mortality, and limb loss rates from acute lower extremity ischemia remain high. Thus, regardless of the treatment modality used, early diagnosis and rapid initiation of therapy are essential in order to salvage the ischemic extremity.
The major causes and management approaches to acute limb ischemia will be reviewed here. Issues related to critical limb ischemia (ie, similar manifestations in patients who present more than two weeks after symptom onset) are discussed separately. (See "Clinical manifestations and evaluation of chronic critical limb ischemia" and "Treatment of chronic critical limb ischemia".)
INTRODUCTION AND DEFINITIONS
Limb-threatening ischemia occurs when arterial blood flow is insufficient to meet the metabolic demands of resting muscle or tissue; it is the most common indication for lower extremity arterial reconstruction. It has been estimated that limb-threatening ischemia occurs in 1 to 2 percent of patients with peripheral arterial disease (PAD) who are 50 years of age or older [1].
According to the 2007 Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II), acute limb ischemia is defined as a sudden decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present within two weeks of the acute event [2]. Patients with similar manifestations who present later than two weeks are considered to have critical limb ischemia, which is by definition chronic.
The natural history of critical limb ischemia usually involves inexorable progression to amputation unless there is an intervention that results in the improvement of arterial perfusion. This is in contrast to the often benign natural history of mild and moderate claudication. (See "Clinical features, diagnosis, and natural history of lower extremity peripheral arterial disease".)
This topic will review the clinical manifestations and evaluation of critical limb ischemia. The approaches to therapy of this disorder and a review of acute limb ischemic due acute arterial occlusion of the lower extremities are discussed separately. (See "Treatment of chronic critical limb ischemia" and "Acute arterial occlusion of the lower extremities (acute limb ischemia)".)
Medline ® Abstract for Reference 4
of 'Clinical manifestations and evaluation of chronic critical limb ischemia'
4
TI
Suggested standards for reports dealing with lower extremity ischemia. Prepared by the Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery/North American Chapter, International Society for Cardiovascular Surgery.
AU
SO
J Vasc Surg 1986 Jul;4(1):80-94.
Reports in the vascular surgery literature are often difficult to assess and compare with each other because of poorly defined terms, imprecise categorization, lack of indices for gauging the severity of the disease or the presence of risk factors capable of affecting outcome, and varying criteria for success or failure--in essence, a lack of standardized reporting practices. The joint councils of the Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery have appointed an ad hoc committee to deal with this problem. This report represents the recommendations of the first of its several subcommittees, that is, the one dealing with reports on lower extremity ischemia. Certain terms are defined and criteria offered for uniformly gauging the severity of disease, the findings of diagnostic studies, the types of therapeutic interventions, and the outcome of such treatments. Although future modifications may further improve on this effort, it is hoped that this committee's recommendations will help establish reporting standards for articles dealing with lower extremity ischemia.
Medline ® Abstract for Reference 8
of 'Clinical manifestations and evaluation of chronic critical limb ischemia'
8
TI
Value of arterial pressure measurements in the proximal and distal part of the thigh in arterial occlusive disease.
AU
Heintz SE; Bone GE; Slaymaker EE; Hayes AC; Barnes RW
SO
Surg Gynecol Obstet 1978 Mar;146(3):337-43.
A prospective study was carried out comparing two techniques of segmental arterial pressure measurements of the leg to detect, localize and quantify regional arterial occlusive disease. The measurement of pressures of the proximal and distal parts of the thigh with the narrow cuff technique permitted correct anatomic localization of aortoiliac, femoropopliteal or combined disease in 78 per cent of diseased extremities, including all limbs with isolated aortoiliac or femoropopliteal disease. A single wide cuff arterial pressure measurement of the thigh correctly localized arterial obstructions in only 19 per cent of diseased extremities. Although a wide cuff is associated with less artifactual elevation in measured arterial pressure at the thigh, this advantage is outweighed by the limitation of diagnostic accuracy in localizing segmental arterial occlusive disease. We recommend that segmental arterial pressure measurements of the limb be made at four levels on the lower extremity, including arterial pressures of the proximal and distal parts of the thigh to achieve maximal diagnostic accuracy.
Medline ® Abstract for Reference 7
of 'Clinical manifestations and evaluation of chronic critical limb ischemia'
7
TI
"Blue toe" syndrome. An indication for limb salvage surgery.
AU
Karmody AM; Powers SR; Monaco VJ; Leather RP
SO
Arch Surg 1976 Nov;111(11):1263-8.
We describe 31 patients in whom proximal lesions in the arterial tree were identified as probable sources of emboli causing the "blue toe" syndrome. This syndrome consists of acute digital ischemia caused by microembolization to the digital arteries from a proximal source via a patent arterial tree, as evidenced by an otherwise well-perfused foot. It is closely analogous to the transient ischemic attacks of the brain, and carries the same potential for serious tissue loss because of repeated embolic showers. The prompt delineation and eradication of the embolic source is of prime importance, in addition to restoration of arterial continuity. Along with the other well-known features of chronic severe ischemia, that is, rest pain, gangrene, etc, the "blue toe" syndrome is therefore an indication for limb salvage surgery.
Clinical features, diagnosis, and natural history of lower extremity peripheral arterial disease
Patients with compromise of blood flow to the extremities as a consequence of peripheral arterial disease may present with typical ischemic pain of one or more muscle groups, atypical pain or no symptoms. Intermittent claudication (derived from the Latin word for limp) is defined as a reproducible discomfort of a defined group of muscles that is induced by exercise and relieved with rest. This disorder results from an imbalance between supply and demand of blood flow that fails to satisfy ongoing metabolic requirements.
The etiology, risk factors, and clinical manifestations of claudication are reviewed here, with emphasis upon the presentation of peripheral arterial disease (PAD) due to atherosclerosis. The frequency of asymptomatic disease will also be discussed. The noninvasive evaluation and management of this disorder by medical therapy, percutaneous intervention, and surgery are presented separately. (See "Noninvasive vascular diagnosis in lower extremity peripheral arterial disease" and "Medical management of claudication" and "Indications for surgery in the patient with claudication".)
The majority of patients with PAD have atherosclerotic disease of the lower extremity. Atherosclerotic PAD of the upper extremity is much less common and is discussed elsewhere. (See "Upper extremity peripheral arterial disease".)
ETIOLOGY
Although many diseases can cause intermittent claudication (table 1), the vast majority of patients with claudication suffer from peripheral atherosclerosis. The clinical history can help distinguish among some of the less common causes of this disorder. As examples, a history of limb trauma, radiation exposure, vasculitis, or ergot use for migraines represent some important clues to the etiology of claudication.
Popliteal entrapment syndrome can also present with intermittent claudication and should be suspected in the young patient who presents with claudication, but lacks atherosclerotic risk factors. Popliteal entrapment syndrome is due to anomalous musculoskeletal attachments which cause compression of the popliteal artery with activity.
Treatment of chronic critical limb ischemia
According to the 2007 Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II), acute limb ischemia is defined as a sudden decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present within two weeks of the acute event [1]. Patients with similar manifestations who present later than two weeks are considered to have critical limb ischemia, which is by definition chronic.
Signs of severe peripheral arterial disease (PAD) on noninvasive testing include an ankle-brachial index less than 0.4, a flat waveform on pulse volume recording, and absent pedal flow on duplex ultrasonography [2]. If these findings are not present, one should consider atheroembolism, thromboembolism, or phlegmasia cerulea dolens. (See "Acute arterial occlusion of the lower extremities (acute limb ischemia)".)
The different therapies for critical limb ischemia will be reviewed here, according to the site of the vascular lesion and the specific clinical setting. The clinical manifestations and diagnosis of this disorder and acute limb ischemia are discussed separately. (See "Clinical manifestations and evaluation of chronic critical limb ischemia" and "Acute arterial occlusion of the lower extremities (acute limb ischemia)".)
GENERAL PRINCIPLES
The 2005 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on peripheral arterial disease (PAD), which were produced in collaboration with major vascular medicine, vascular surgery, and interventional radiology societies, suggested that limb-threatening ischemia occurs in 1 to 2 percent of patients with PAD who are 50 years of age or older [2].
The natural history of critical limb ischemia usually involves inexorable progression to amputation unless there is an intervention that results in the improvement of arterial perfusion. This is in contrast to the often benign natural history of mild and moderate claudicat
Indications for surgery in the patient with claudication
Intermittent claudication, defined as a symptomatic deficiency in blood supply to exercising muscle that is relieved with rest, is generally a reliable indicator of occlusive arterial disease [1,2]. Classic claudication is a cramping pain that is consistently reproduced with exercise and relieved with rest. However, atypical leg pain is more common [2]. (See "Clinical features, diagnosis, and natural history of lower extremity peripheral arterial disease".)
The location of pain varies with the vessels that are involved. Patients with aorto-iliac arterial occlusive disease often complain of buttock and thigh claudication, whereas patients complaining of
claudication in the calf may have infrainguinal disease.
The severity of symptoms depends upon the degree of stenosis, the collateral circulation, and the vigor of exercise. (See "Clinical features, diagnosis, and natural history of lower extremity peripheral arterial disease", section on 'Symptomatic disease'.)
Most patients with intermittent claudication remain stable with medical therapy. When revascularization is required, the options are percutaneous interventional procedures and surgery.
ECG tutorial: Miscellaneous diagnoses
LOW VOLTAGE
Low voltage of the limb leads is present when the amplitude of the QRS complex in each of the three standard limb leads (1, 2, and 3) is <5 mm (figure 1). This may be due to underlying myocardial disease; pericardial disease; lung disease; or anasarca, in which the low voltage correlated with weight gain [1].
Low voltage of all leads is diagnosed when the average voltage in the three limb leads is <5 mm, and the average voltage in the chest leads is <10 mm (figure 2). This also may be due to underlying myocardial disease (particularly amyloidosis), pericardial disease, lung disease, or a thick chest wall.
EARLY REPOLARIZATION
Early repolarization is a variant seen in approximately two to five percent of the population, with predominance in young men [2]. Early repolarization is characterized by elevation of the J point, which represents the junction between the end of the QRS complex (termination of depolarization) and the beginning of the ST segment (onset of ventricular repolarization) as well as elevation of the ST segment itself (figure 3).
The pattern of ST elevation varies in degree, morphology and location and may be dynamic [3]. The ST segment may be concave up (cup-like) or concave down (dome-like). These findings are most often present in the mid to lateral precordial leads V3-V6. Although ST changes may be observed diffusely in many leads, approximately one-half of patients have no ST deviations in the limb leads.
Although early repolarization was considered a benign condition for many years, two findings raise the possibility of an adverse association:
Acute arterial occlusion of the lower extremities (acute limb ischemia)
INTRODUCTION AND DEFINITIONS
According to the 2007 Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II), acute limb ischemia is defined as a sudden decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present within two weeks of the acute event [1]. Patients with similar manifestations who present later than two weeks are considered to have critical limb ischemia, which is by definition chronic.
The management of acute arterial occlusion remains a challenge for vascular specialists. Surgical thromboembolectomy and bypass grafting were the mainstays of therapy for many years [2]. Subsequently, thrombolytic therapy and percutaneous transluminal angioplasty (PTA) have become treatment options for selected patients.
Despite these advances, the morbidity, mortality, and limb loss rates from acute lower extremity ischemia remain high. Thus, regardless of the treatment modality used, early diagnosis and rapid initiation of therapy are essential in order to salvage the ischemic extremity.
The major causes and management approaches to acute limb ischemia will be reviewed here. Issues related to critical limb ischemia (ie, similar manifestations in patients who present more than two weeks after symptom onset) are discussed separately. (See "Clinical manifestations and evaluation of chronic critical limb ischemia" and "Treatment of chronic critical limb ischemia".)
ETIOLOGY
Acute arterial occlusion can be the result of emboli from a distant source, acute thrombosis of a previously patent artery, or direct trauma to an artery (table 1)
Heparin-induced thrombocytopenia
INTRODUCTION
Thrombocytopenia is a well-recognized complication of heparin therapy, usually occurring within 5 to 10 days after heparin treatment has started [1].
• The more serious form (heparin-induced thrombocytopenia, type II; HIT-II) is an immune-mediated disorder characterized by the formation of antibodies against the heparin-platelet factor 4 complex. This disorder has also been called heparin-associated immune thrombocytopenia, heparin-associated thrombocytopenia and thrombosis (HITT), and white clot syndrome [1,2]. White clot syndrome refers to platelet-rich arterial thrombosis (rather than fibrin-rich venous thrombosis), which occurs with high frequency in patients who develop this disorder [2].
• A second form of thrombocytopenia, of no clinical consequence (type I heparin-induced thrombocytopenia), is typically characterized by a lesser fall in platelet count that occurs within the first two days after heparin initiation and often returns to normal with continued heparin administration (table 1) [1]. The mechanism of the thrombocytopenia is nonimmune and appears to be due to a direct effect of heparin on platelet activation [3,4].
For the remainder of this review, the term HIT will refer only to the immune form (ie, type II). The clinical manifestations, diagnosis, prevention, and treatment of HIT will be reviewed here [1,5-9]. The clinical use of heparin and low molecular weight heparin is discussed separately. (See "Therapeutic use of heparin and low molecular weight heparin".)
INCIDENCE
A critical assessment of immune-mediated HIT suggests a frequency of 0.2 to 5.0 percent in patients exposed to heparin for more than four days [10-15], with an overall incidence of 2.6 percent noted in a meta-analysis [10]. The incidence is closer to 0.2 percent for those treated with unfractionated heparin (UFH) for less than four days [16,17].
Of importance, two prospective observational studies showed a surprisingly high incidence of thrombocytopenia in patients treated with either unfractionated or low molecular weight heparin for ≥4 days, with 15 percent of patients showing a >50 percent reduction in baseline platelet counts in one study [18] and 42 percent in the other [19].
Embolism from aortic plaque: Thromboembolism
INTRODUCTION AND DEFINITIONS
Aortic atherosclerotic plaques are a manifestation of systemic atherosclerosis (figure 1 and movie 1). They are associated with risk factors for atherosclerotic disease, and are more common in patients with coronary artery disease and older individuals [1-5].
In addition aortic atherosclerotic plaques are an important cause of systemic embolization [6-9]. Embolic events in the setting of aortic atherosclerosis can occur spontaneously or they can be induced by interventions including cardiac catheterization, and cardiac surgery [10,11].
Thromboembolism from severe aortic plaques is common, whereas cholesterol crystal embolization is fairly rare. Although there is some overlap, these disorders have characteristic distinguishing features:
• Thromboembolism may occur when an atherosclerotic plaque from large or medium arteries becomes unstable, and superimposed thrombi embolize. The thromboemboli tend to be single, and to lodge in small or medium arteries, resulting most often in stroke or transient ischemic attack [6-9,12]. Limb ischemia, renal infarction, intestinal ischemia, or ischemia of other organs may also occur [9,13].
• The term atheroembolism is used synonymously with cholesterol crystal embolism or cholesterol embolism. These terms refer to arterio-arterial embolism of small pieces of atheromatous material originating from an atherosclerotic plaque of the aorta or occasionally other arteries. The result of such embolization is tissue and organ damage produced by multiple small artery occlusions (eg, "blue toe" syndrome, retinal ischemia, renal failure, livedo reticularis, and intestinal infarction).
The risk of thromboembolism or atheroembolism in patients with aortic atherosclerosis is markedly increased when the transesophageal echocardiogram (TEE) reveals protruding plaques, particularly if >4 mm in thickness or mobile. (See 'Plaque thickness' below.)
Print
Medline ® Abstract for Reference 19
of 'Acute arterial occlusion of the lower extremities (acute limb ischemia)'
19
TI
A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia.
AU
Ouriel K; Shortell CK; DeWeese JA; Green RM; Francis CW; Azodo MV; Gutierrez OH; Manzione JV; Cox C; Marder VJ
SO
J Vasc Surg 1994 Jun;19(6):1021-30.
PURPOSE: Despite the widespread use of intraarterial thrombolytic therapy for peripheral arterial occlusive disease, a randomized study comparing its efficacy with that of operative intervention has never been performed. This study evaluates the potential of intraarterial urokinase infusion to provide clinical benefits in patients with acute peripheral arterial occlusion. METHODS: Patients with limb-threatening ischemia of less than 7 days' duration were randomly assigned to intraarterial catheter-directed urokinase therapy or operative intervention. Anatomic lesions unmasked by thrombolysis were treated with balloon dilation or operation. The primary end points of the study were limb salvage and survival. RESULTS: A total of 57 patients were randomized to the thrombolytic therapy group, and 57 patients were randomized to the operative therapy group. Thrombolytic therapy resulted in dissolution of the occluding thrombus in 40 (70%) patients. Although the cumulative limb salvage rate was similar in the two treatment groups (82% at 12 months), the cumulative survival rate was significantly improved in patients randomized to the thrombolysis group (84% vs 58% at 12 months, p = 0.01). The mortality differences seemed to be primarily attributable to an increased frequency of in-hospital cardiopulmonary complications in the operative treatment group (49% vs 16%, p = 0.001). The benefits of thrombolysis were achieved without significant differences in the duration of hospitalization (median 11 days) and with only modest increases in hospital cost in the thrombolytic treatment arm (median $15,672 vs $12,253, p = 0.02). CONCLUSIONS: Intraarterial thrombolytic therapy was associated with a reduction in the incidence of in-hospital cardiopulmonary complications and a corresponding increase in patient survival rates. These benefits were achieved without an appreciable increase in the duration of hospitalization and with only modest increases in hospital cost, suggesting that thrombolytic therapy may offer a safe and effective alternative to operation in the initial treatment of patients diagnosed with acute limb-threatening peripheral arterial occlusion.
AD
Department of Surgery, University of Rochester, NY 14642.
PMID
8201703
Print
Medline ® Abstract for Reference 17
of 'Acute arterial occlusion of the lower extremities (acute limb ischemia)'
17
TI
Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity. The STILE trial.
AU
SO
Ann Surg 1994 Sep;220(3):251-66; discussion 266-8.
PURPOSE: This study was designed to evaluate intra-arterial thrombolytic therapy as part of a treatment strategy for patients requiring revascularization for lower limb ischemia caused by nonembolic arterial and graft occlusion. MATERIALS AND METHODS: Patients with native arterial or bypass graft occlusion were randomized prospectively to either optimal surgical procedure or intra-arterial, catheter-directed thrombolysis with recombinant tissue plasminogen activator (rt-PA) or urokinase (UK). Thrombolysis patients required successful catheter placement into the occlusion before infusion of either rt-PA at 0.05 mg/kg/hr for up to 12 hours or UK of 250,000 units bolus followed by 4000 units/min x 4 hours, then 2000 units/min for up to 36 hours. A composite clinical outcome of death, ongoing/recurrent ischemia, major amputation, and major morbidity was the primary endpoint. Additional endpoints were reduction in surgical procedure, clinical outcome classification, length of hospitalization, and outcome by duration of ischemia. RESULTS: Randomization was terminated at 393 patients because a significant primary endpoint occurred by the first interim analysis. Failure of catheter placement occurred in 28% of patients who were randomized to lysis, and thus, were considered treatment failures. Thirty-day outcomes demonstrated significant benefit to surgical therapy compared with thrombolysis (p<0.001), primarily because of a reduction in ongoing/recurrent ischemia (p<0.001). However, clinical outcome classification at 30 days was similar. Stratification by duration of ischemia indicated that patients with ischemic deterioration of 0 to 14 days had lower amputation rates with thrombolysis (p = 0.052) and shorter hospital stays (p<0.04). Patients with ischemic deterioration of>14 days who who were treated surgically had less ongoing/recurrent ischemia (p<0.001) and trends toward lower morbidity (p = 0.1). At 6-month follow-up, there was improved amputation-free survival in acutely ischemic patients treated with thrombolysis (p = 0.01); however, chronically ischemic patients who were treated surgically had significantly lower major amputations rates (p = 0.01). More than half of thrombolysis patients (55.8%) had a reduction in magnitude of their surgical procedure (p<0.001). There was no difference in efficacy or safety between rt-PA and UK; however, in the thrombolysis group as a whole, fibrinogen depletion predicted hemorrhagic complications (p<0.01). CONCLUSIONS: Surgical revascularization of patients with<6 months of ischemia is more effective and safer than catheter-directed thrombolysis. Although ongoing/recurrent ischemia is greater in the patients undergoing thrombolysis, 30-day clinical outcomes are similar, probably because of cross-over treatment to surgery. There is no difference in efficacy or safety between rt-PA and UK, although bleeding occurs in patients with greater fibrinogen depletion. A significant reduction in planned surgical procedure is observed after thrombolysis. Patients with acute ischemia (0-14 days) who were treated with thrombolysis had improved amputation-free survival and shorter hospital stays. However, for patients with chronic ischemia (>14 days), surgical revascularization was more effective and safer than thrombolysis. Combining a treatment strategy of catheter-directed thrombolysis for acute limb ischemia with surgical revascularization for chronic limb ischemia offers the best overall results.
AD
PMID
8092895
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Antithrombotic Therapy in Peripheral Arterial Occlusive Disease
The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy
1. G. Patrick Clagett, MD, Co-Chair,
2. Michael Sobel, MD, Co-Chair,
3. Mark R. Jackson, MD,
4. Gregory Y. H. Lip, MD,
5. Marco Tangelder, MD, and
6. Raymond Verhaeghe, MD
Next Section
Abstract
This chapter about antithrombotic therapy for peripheral arterial occlusive disease is part of the seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: Evidence Based Guidelines. Grade 1 recommendations are strong and indicate that the benefits do, or do not, outweigh risks, burden, and costs, and Grade 2 suggests that individual patients’ values may lead to different choices (for a full understanding of the grading see Guyatt et al, CHEST 2004;126:179S–187S). Among the key recommendations in this chapter are the following: For patients with chronic limb ischemia, we recommend lifelong aspirin therapy in comparison to no antiplatelet therapy in patients with clinically manifest coronary or cerebrovascular disease (Grade 1A) and in those without clinically manifest coronary or cerebrovascular disease (Grade 1C+). We recommend clopidogrel over no antiplatelet therapy (Grade 1C+) but suggest that aspirin be used instead of clopidogrel (Grade 2A). For patients with disabling intermittent claudication who do not respond to conservative measures and who are not candidates for surgical or catheter-based intervention, we suggest cilostazol (Grade 2A). We suggest that clinicians not use cilostazol in patients with less-disabling claudication (Grade 2A). In these patients, we recommend against the use of pentoxifylline (Grade 1B). We suggest clinicians not use prostaglandins (Grade 2B). In patients with intermittent claudication, we recommend against the use of anticoagulants (Grade 1A). In patients with acute arterial emboli or thrombosis, we recommend treatment with immediate systemic anticoagulation with unfractionated heparin (UFH) [Grade 1C]. We also recommend systemic anticoagulation with UFH followed by long-term vitamin K antagonist (VKA) in patients with embolsim [Grade 1C]). For patients undergoing major vascular reconstructive procedures, we recommend UFH at the time of application of vascular cross-clamps (Grade 1A). In patients undergoing prosthetic infrainguinal bypass, we recommend aspirin (Grade 1A). In patients undergoing infrainguinal femoropopliteal or distal vein bypass, we suggest that clinicians do not routinely use a VKA (Grade 2A). For routine patients undergoing infrainguinal bypass without special risk factors for occlusion, we recommend against VKA plus aspirin (Grade 1A). For those at high risk of bypass occlusion and limb loss, we suggest VKA plus aspirin (Grade 2B). In patients undergoing carotid endarterectomy, we recommend aspirin preoperatively and continued indefinitely (Grade 1A). In nonoperative patients with asymptomatic or recurrent carotid stenosis, we recommend lifelong aspirin (Grade 1C+). For all patients undergoing extremity balloon angioplasty, we recommend long-term aspirin (Grade 1C+).
• anticoagulants
• antithrombotic
• occlusive artery disease
• peripheral artery
Patient populations with peripheral arterial occlusive disease (PAOD) are summarized in Table 1 .
Previous SectionNext Section
1.0 Chronic Limb Ischemia
Atherosclerotic PAOD is symptomatic with intermittent claudication in 2 to 3% of men and 1 to 2% of women > 60 years old.123 However, the prevalence of asymptomatic PAOD, generally proven by a reduced ankle/brachial systolic pressure index, is three to four times as great.45 After 5 to 10 years, 70 to 80% of patients remain unchanged or improved, 20 to 30% have progression of symptoms and require intervention, and 10% require amputation.67 Progression of disease is greatest in patients with multilevel arterial involvement, low ankle-to-brachial pressure indices, chronic renal insufficiency, diabetes mellitus and, possibly, heavy smoking.6
The prevalence of PAOD increases with age and is a significant cause of hospital admission and an important predicator of cardiovascular and stroke mortality, which is increased twofold to threefold.1289 Rest pain and critical ischemia are usually the result of progression of atherosclerotic disease, leading to occlusion of the distal vessels such as the popliteal and tibial arteries. There is an inverse relationship between the ankle-to-brachial pressure index and clinically manifest cardiovascular disease.5 The lower the index, the greater the occurrence of adverse cardiac events, strokes, and cardiovascular deaths.
This chapter addresses antithrombotic therapy for patients with PAOD. We note, however, that a systematic review and metaanalysis10 of randomized trials of exercise therapy in patients with claudication suggests that exercise improves maximal walking time by 150%. One must judge symptomatic antithrombotic therapy in this context. Furthermore, while risk factor modification is not well studied in patients with PAOD, observational data and generalization from trials1112 in persons with other manifestations of cardiovascular disease support the importance of treating key risk factors such as smoking, diabetes, dyslipidemia, and hypertension.
1.1 Antiplatelet therapy
Antiplatelet therapy may modify the natural history of chronic lower-extremity arterial insufficiency, as well as lower the incidence of associated cardiovascular events. No convincing data from properly designed large trials demonstrate that antithrombotic therapy will delay or prevent progression of atherosclerosis.
A compelling reason to administer antiplatelet therapy to patients with PAOD is to prevent death and disability from stroke and myocardial infarction (MI). The Antithrombotic Trialists’ Collaboration metaanalysis13 found that among 9,214 patients with PAOD in 42 trials, there was a 23% reduction in serious vascular events (p = 0.004) in patients treated with antiplatelet therapy. Patients with intermittent claudication, those having peripheral bypass, endarterectomy, and those having peripheral angioplasty all benefited to a similar degree. For all conditions, aspirin at 80 to 325 mg/d was at least as effective as any other regimen, including higher-dose aspirin therapy, which is more prone to cause side effects and GI complications.
1.1.1 Aspirin
The antiplatelet trialists analysis13 showed that for all conditions, aspirin at 80 to 325 mg/d was at least as effective as any other regimen, including higher-dose aspirin therapy, which is more prone to cause side effects and GI complications. Data from a single randomized controlled trial (RCT)14 suggest that aspirin, alone or combined with dipyridamole, will delay the progression of established arterial occlusive disease as assessed by serial angiography. This may have been an effect on inhibiting thrombotic occlusion of stenotic vessels rather than retarding stenosis progression.
In another study of 54 patients with intermittent claudication, the combination of aspirin and dipyridamole was found to increase the pain-free walking distance and resting limb blood flow.15 An RCT16 of 296 patients with intermittent claudication found an improved coagulation profile and ankle/brachial index with therapy, but did not report if walking distance improved with combined therapy. The Physicians Health Study,17 a primary prevention study, found that aspirin, 325 mg every other day, decreased the need for peripheral arterial reconstructive surgery; however, no difference was noted between the aspirin and placebo groups in the development of intermittent claudication.
Other chapters in these guidelines describe the compelling evidence for aspirin in patients with coronary artery disease and stroke. This applies to many patients with chronic arterial insufficiency who also have clinically manifest coronary or cerebrovascular disease. Almost all patients with PAOD who do not have clinically manifest disease have occult coronary or cerebrovascular disease. Aspirin is less effective than ticlopidine and clopidogrel (see below). However, the marginal benefit of these other drugs is small, and aspirin is much less expensive. These are the rationales for our recommendation for aspirin over clopidogrel.
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Recommendation
1.1.1. We recommend lifelong aspirin therapy (75 to 325 mg/d) in comparison to no antiplatelet therapy in patients with clinically manifest coronary or cerebrovascular disease (Grade 1A) and in those without clinically manifest coronary or cerebrovascular disease (Grade 1C+).
1.1.2 Ticlopidine
One metaanalysis18 demonstrated that patients with intermittent claudication treated with ticlopidine had a significant reduction in fatal and nonfatal cardiovascular events in comparison with patients treated with placebo. Ticlopidine has also shown a modest beneficial effect for relieving symptoms, increasing walking distance, and improving lower-extremity ankle pressure indices in patients with intermittent claudication (see chapter by Patrono et al in this Supplement).1920 In a multicenter, placebo-controlled RCT,21 ticlopidine, 250 mg/d, resulted in fewer vascular surgery procedures (relative risk, 0.49; p < 0.001) among patients with intermittent claudication. However, ticlopidine is associated with a substantial risk of leukopenia and thrombocytopenia, requiring close hematologic monitoring. Because of these side effects, clopidogrel has replaced ticlopidine as the thienopyridine of choice.
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Recommendation
1.1.2. We recommend clopidogrel over ticlopidine (Grade 1C+).
1.1.3 Clopidogrel
Clopidogrel is a thienopyridine, the chemical structure of which is similar to ticlopidine, that exerts an irreversible antiplatelet effect primarily directed against adenosine diphosphate-induced stimulation of platelet function (see chapter by Patrono et al in this Supplement). In a large, multicenter RCT22 of 19,185 patients, investigators compared the relative efficacy of clopidogrel and aspirin in reducing the risk of a composite end point of ischemic stroke, MI, or vascular death. The study population comprised patients with recent ischemic stroke, recent MI, or PAOD. The overall incidence of composite end points was lower in the group treated with clopidogrel (5.32%/yr) than with aspirin (5.83%; p = 0.043). A subgroup analysis suggested that a larger benefit of clopidogrel over aspirin in patients with symptomatic PAOD than those with cardiac or cerebrovascular disease. Subgroup analysis is often misleading, and we are inclined to trust the overall estimate of clopidogrel effectiveness in all patients with vascular disease.
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Recommendation
1.1.3. We recommend clopidogrel in comparison to no antiplatelet therapy (Grade 1C+) but suggest that aspirin be used instead of clopidogrel (Grade 2A).
Underlying values and preferences: This recommendation places a relatively high value on avoiding large expenditures to achieve small reductions in vascular events.
1.1.4 Cilostazol
Cilostazol is a type III phosphodiesterase inhibitor that suppresses platelet aggregation and is a direct arterial vasodilator. Its mechanism of action as a treatment for claudication is not fully understood. We found no systematic reviews on this drug for PAOD. Several published clinical trials that have evaluated the efficacy of cilostazol as a therapeutic agent for intermittent claudication.
In the first of these published trials,23 239 patients randomly assigned to receive a 16-week course of cilostazol or placebo, the cilostazol group showed an increase in absolute claudication distance (ACD) of 47%, while the control group improved by 13% (p < 0.001). Functional status assessment also showed improvement with cilostazol compared with control subjects, although there were significantly more side effects with cilostazol, most notably headache (30%) and diarrhea (12.6%).
In a smaller trial24 of 12 weeks of cilostazol or placebo, the ACD increased 31% with cilostazol, vs a drop of 9% with placebo (p < 0.01). In another study,25 45 patients with claudication were randomly assigned to one of three groups, cilostazol, pentoxifylline, or placebo for 24 weeks; at 24 weeks, the treatment was changed to placebo for all groups, and follow-up was continued for 6 more weeks. There was a more significant decrease in ACD after cessation of cilostazol therapy than with either pentoxifylline or placebo. The increase in ACD from baseline was similar in both the cilostazol and pentoxifylline groups (109% and 94%, respectively).
In a trial26 of 516 patients randomly assigned to cilostazol (100 mg bid or 50 mg bid) or placebo therapy for 24 weeks, those receiving 50 mg bid had a 38% and 48% mean improvement in maximal and pain-free walking distance, respectively, while with a dose of 100 mg bid showed a 51% and 59% improvement, respectively, compared to placebo. Benefit was noted as early as 4 weeks, with progressive improvement over the 24-week period of the trial. There was also a significant improvement in functional outcomes with cilostazol, and no difference in the incidence of adverse events in the three groups. Side effects noted in each of the studies included headache, loose and soft stools, diarrhea, dizziness, and palpitations.
Cilostazol is more effective than pentoxifylline, as illustrated in a study of 698 patients randomized to pentoxifylline (400 mg tid), cilostazol (100 mg bid), or placebo for 24 weeks.27 In comparison to pentoxifylline, cilostazol produced a significant increase in walking distance for onset of claudication (218 m for cilostazol vs 202 m for pentoxifylline, p = 0.0001) and ACD (350 m for cilostazol vs 308 m for pentoxifylline, p = 0.0005). In addition, there were fewer patients who had no change or deterioration in walking distance (23% for cilostazol vs 34% with pentoxifylline).
Cilostazol thus appears to be an appropriate therapy for patients with disabling claudication who are not candidates for revascularization. However, its high cost, modest effect on walking distance, lack of demonstrated benefit in improving health-related quality of life, and the salutary effects of exercise therapy and risk factor modification argue against its routine use in patients with less-disabling intermittent claudication.
Cilostazol has weak platelet inhibitory effects, and there are no data to support its use as an antiplatelet agent. Antiplatelet therapy with aspirin or clopidogrel should be continued in patients receiving cilostazol.
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Recommendation
1.1.4. For patients with disabling intermittent claudication who do not respond to conservative measures (risk factor modification and exercise therapy) and who are not candidates for surgical or catheter-based intervention, we suggest cilostazol (Grade 2A). We suggest that clinicians notuse cilostazol in those with less-disabling claudication (Grade 2A).
Underlying values and preferences: The recommendation against cilostazol for those with less-disabling claudication places a relatively low value on small possible improvements in function in the absence of clear improvement in health-related quality of life.
1.1.5 Pentoxifylline
Pentoxifylline is a weak antithrombotic agent; its putative mechanisms of action include an increase in RBC deformity, and decreases in fibrinogen concentration, platelet adhesiveness, and whole-blood viscosity.282930 One metaanalysis31 suggests that pentoxifylline improves walking distance by 29 m compared with placebo, although the improvement was approximately 50% in the placebo group, and use of pentoxifylline improved walking distance by an additional 30%. Moreover, clinical trials have shown conflicting results. Some323334353637 have concluded that pentoxifylline was significantly more effective than placebo in improving treadmill-walking distance, but others383940414243 could not demonstrate consistent benefit. In many trials, patients treated with placebo also demonstrated significant improvement. Thus, the actual improvement in walking distance attributable to pentoxifylline is often unpredictable and may not be clinically important compared with the effects of placebo.44 In summary, the evidence for a beneficial effect of pentoxifylline is not strong enough to suggest an important role in the treatment of patients with PAOD.4546
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Recommendation
1.1.5. We recommend againstthe use of pentoxifylline (Grade 1B).
1.1.6 Prostaglandins
Prostaglandins with antiplatelet and vasodilatory effects, such as prostaglandin E1 (PGE1) and prostaglandin I2 (PGI2), have been administered IV or intra-arterially to patients with advanced chronic arterial insufficiency in hopes of relieving rest pain and healing ischemic ulcers. In a study47 of 80 patients with intermittent claudication, IV administration of a PGE1 produced a dose-related improvement in walking distance and quality of life at 4 weeks and 8 weeks. In an older but larger randomized, blinded, multicenter trial48 of patients with one to three ischemic ulcers not healing for 3 weeks with standard care who were randomized to receive either PGE1 or a placebo for 72 h through a central venous catheter, PGE1 was found to be ineffective. In a small, randomized open study,49 PGE1 administered IV and combined with an intensive exercise regimen produced dramatic and sustained improvement in symptom-free walking distance in comparison with exercise alone or exercise combined with IV-administered pentoxifylline. The largest data set comes from a multicenter RCT50 in which 1,560 patients with chronic critical ischemia of the leg were randomly assigned to receive either a daily IV infusion of PGE1 or nothing (open-label study) during their hospital stay. At discharge, there was a greater reduction in composite outcome events in the PGE1 group than in the control subjects (63.9% vs 73.6%; relative risk, 0.87; p < 0.001), but this difference was not statistically significant at 6 months (52.6% vs 57.5%; relative risk, 0.92; p = 0.074). AS-013, a PGE1 prodrug, was evaluated in a small randomized trial51 of 80 patients with claudication, and was associated with an increase of 35 m in maximal walking distance after 8 weeks of treatment, compared with a slight decrease in placebo-treated control subjects. This difference was statistically significant (p < 0.01), although the clinical significance of the increase was marginal.
A blinded trial that contained a high proportion of diabetics showed no beneficial effect of IV PGI2 on ulcer healing or rest pain.52 However, selective intra-arterial PGI2 was found to relieve rest pain and promote healing of ulcers to a significantly greater degree than did placebo treatment in 30 nondiabetic patients, half of whom had thromboangiitis obliterans (Buerger disease).53 In another double-blind trial,54 PGI2 administered IV to nondiabetic patients with severe arterial insufficiency produced significantly greater relief (lasting up to 1 month) of rest pain than did placebo, but there was no correlation with changes in ankle-to-brachial pressure index, or ulcer healing.
Beraprost, an orally active PGI2 analog, was evaluated in the Beraprost et Claudication Intermittente-2 trial55 of 549 patients with a pain-free walking distance of 50 to 300 m. After 6 months, more patients receiving beraprost (40 μg tid) compared to placebo had an increase in walking distance on a treadmill (44% vs 33%), and pain-free walking distances (82% vs 53%), and maximum walking distances (60% vs 35%). These benefits were modest and probably not clinically significant. The incidence of cardiac death, MI, coronary revascularization, stroke, transient ischemic attack (TIA), or leg ischemia requiring intervention was similar in both groups.
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Recommendation
1.1.6. For limb ischemia, we suggest clinicians notuse prostaglandins (Grade 2B).
Underlying values and preferences: The recommendation places a low value on achieving small gains in walking distance in the absence of demonstrated improvement in quality of life.
1.1.7 Other agents
Other agents with putative antithrombotic activity that have been subjected to RCTs but were found to be ineffective in the treatment of intermittent claudication include the following: the antiserotonin agent ketanserin,56 suloctidil,57 fish oil supplementation,58 and naftidrofuryl.5960 Other ineffective drugs for intermittent claudication (such as nifedipine, l-carnitine, etc) are not discussed, as there is little evidence for the role as antithrombotic agents.
Picotamide, an antiplatelet agent that inhibits thromboxane-A2 synthase and antagonizes thromboxane-A2 receptors, has been evaluated in one, small, blinded RCT61 in patients with PAOD. Treatment with picotamide significantly reduced the overall incidence of major and minor cardiovascular events. In a blinded, placebocontrolled RCT,62 patients treated with picotamide showed no progression of carotid atherosclerosis (as measured by B-mode ultrasound) compared with placebo-treated control subjects. There are no data on whether this agent is superior or equivalent to aspirin or other agents.63 “Hemodilution therapy” for reducing the plasma viscosity involves the removal of blood and replacing it with a colloidal solution such as hydroxyethyl starch or a low molecular weight dextran one or twice weekly for several weeks, resulting in small improvement in pain-free walking distance in two studies.6465
A Cochrane review66 assessed the effects of anticoagulant drugs (unfractionated heparin [UFH], low molecular weight heparin [LMWH], and vitamin K antagonists [VKAs]) in patients with PAOD. End points included walking capacity (pain-free walking distance or absolute walking distance), mortality, cardiovascular events, ankle/brachial pressure index, progression to surgery, amputation-free survival, and side effects. Thirteen trials were initially considered eligible for inclusion in the review. Only three studies (two evaluating VKA, one evaluating UFH) met the high quality methodologic inclusion criteria and were included in the primary analysis, while four other studies were included in the sensitivity analysis. No significant difference was observed between UFH treatment and control groups for pain-free walking distance or maximum walking distance at the end of treatment. The review found no data to indicate that LMWHs benefit walking distance. No study reported a significant effect on overall mortality or cardiovascular events, and the pooled odds ratios were not significant for these outcomes. Major and minor bleeding events were significantly more frequent in patients treated with VKAs compared to control, with a nonsignificant increase in fatal bleeding events. No major bleeding events were reported in the study evaluating UFH, while a nonsignificant increase in minor bleeding events was reported. In conclusion, no benefit of UFH, LMWH, or VKA has been established for intermittent claudication. An increased risk of major bleeding events has been observed especially with VKAs. The Cochrane review66 concluded that the use of anticoagulants for intermittent claudication cannot be recommended.
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Recommendation
1.1.7. In patients with intermittent claudication, we recommend againstthe use of anticoagulants (Grade 1A).
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2.0 Acute Limb Ischemia
The major causes of acute arterial insufficiency are arterial thrombosis, embolus, and trauma. Extreme vasospasm (eg, ergot induced) and arterial dissection are unusual causes. Most traumatic occlusive events are associated with transection, laceration, or occlusion from external compression such as a fracture or dislocation; but in some instances, thrombosis occurs from blunt trauma. Iatrogenic vascular trauma, most often from diagnostic and therapeutic catheter placement, is a common cause of acute arterial occlusion. In most patients early surgery is required, with appropriate repair of the injured vessel. If thrombosis occurred, use of the Fogarty balloon catheter to remove thrombi is often required and is usually effective. Anticoagulation with UFH is variably used at the time of operation, but may be contraindicated because of other injuries. Outcome is related to the seriousness of associated injuries and duration of ischemia; successful vascular repair can be achieved in most cases.
Nontraumatic acute occlusion is mainly embolic or thrombotic. The large majority of emboli arise from the heart in patients with valvular disease and/or atrial fibrillation, with prosthetic valves, or with mural thrombi in an infarcted or dilated left ventricle. Noncardiac sources of embolism include arterial aneurysms, ulcerated atherosclerotic plaque, recent (endo)vascular procedures, paradoxic emboli from venous thrombi, and rarely arteritis or vascular trauma. Approximately two thirds of noncerebral emboli enter vessels of the lower extremity and half of these obstruct the iliofemoral segment, while the remainder involve the popliteal and tibial vessels. The upper-extremity and renal plus visceral vessels each receive approximately 15% of emboli.6768
Thrombotic occlusions of arteries are usually associated with advanced atherosclerosis, and arteries often have preexisting and developed collateral blood supply. For this reason, final occlusion may not be a dramatic event and is sometimes silent; it is not an emergent process in many patients. Thrombosis also occurs in vascular grafts and with other degenerative or inflammatory diseases or with trauma. The upper extremity better tolerates arterial occlusion because of rich collateral blood supply: gangrene or ischemic rest pain is rare in the absence of distal embolization. Hypovolemia, hyperviscosity, and hypercoagulability as observed in shock, thrombocytosis, polycythemia, and malignant disorders predispose to thrombotic arterial occlusion. Arterial thrombosis most frequently involves the lower extremities.
Therapeutic management will depend on whether the occlusion is caused by embolism in a healthy artery vs thromboembolism in an atheromatous artery. Prompt embolectomy through surgical intervention is the usual technique to remove emboli from healthy arteries. The introduction of the Fogarty balloon catheter 40 years ago dramatically decreased the mortality and the amputation rate from arterial embolism. Percutaneous thromboembolectomy with the aid of an aspiration catheter or of a thrombectomy device is a recent alternative. Literature on either of these new techniques is descriptive and was recently reviewed.6970 No randomized comparison between the different options is available. Traditionally, thromboembolism in a severely diseased artery or in a vascular graft causing acute ischemia symptoms has been the domain of the vascular surgeon as well, but optimal management needs to be determined.
2.1 Heparin
Patients presenting with acute limb ischemia secondary to thromboembolic arterial occlusion usually receive prompt anticoagulation with therapeutic dosages of UFH in order to prevent clot propagation and to obviate further embolism. The logic of this common clinical practice is not questioned, even though no formal studies have established unequivocally a beneficial role of any antithrombotic agent in patients with acute embolic occlusion. The expected adverse effect of perioperative anticoagulant therapy is an increased risk of wound complications, particularly hematomas. The major role for continued anticoagulant therapy (UFH followed by VKA) after embolization is to prevent embolic recurrence if the source of embolism cannot be eradicated or corrected.
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Recommendation
2.1. In patients with acute arterial emboli or thrombosis, we recommend treatment with immediate systemic anticoagulation with UFH to prevent thrombotic propagation (Grade 1C). We also recommend systemic anticoagulation with UFH followed by long-term VKA to prevent recurrent embolism in patients undergoing embolectomy (Grade 1C).
2.2 Thrombolysis
Initial intervention with thrombolysis with the aim of eliminating all thrombotic and embolic material and restore perfusion is a potential alternative to surgical revascularization in acute limb ischemia of thromboembolic origin. Systemic thrombolysis with IV administration of a thrombolytic agent was used in the 1960s and 1970s and has been completely abandoned and replaced by catheter-directed thrombolysis. With this technique, a catheter is positioned intra-arterially and advanced into the thrombus for local delivery of the thrombolytic agent. Several infusion methods can be used. Initially, streptokinase was the most widely used agent, but later it was superseded in clinical use by urokinase and recombinant tissue-type plasminogen activator (rt-PA). Dosages schemes vary considerably; an overview of reported dosages was published in a recent consensus document.71 rt-PA was mainly used in Europe, but since the suspension of urokinase sales in 1998, it has been administered in the United States as well. In addition, new agents are being investigated. For instance, reteplase, a nonglycosylated mutant of alteplase, was tested in a few small series:7273 doses of 0.5 up to 2 U/h produced thrombus dissolution rates and bleeding rates that appear comparable to published data with other thrombolytic agents, but a direct comparison is not available.
A new approach is the use of the platelet glycoprotein IIb-IIIa antagonist abciximab as adjuvant therapy to thrombolysis with the hope of improving lytic efficacy and clinical outcome. A pilot trial74 randomized 70 patients to urokinase plus abciximab or to urokinase plus placebo. At 90 days, amputation-free survival was 96% in the urokinase-abciximab group vs 80% in the urokinase-placebo group. Thrombolysis occurred faster in the former group, but the rate of nonfatal major bleeding was also higher.74
Only a few randomized studies compared thrombolytic agents directly. An open trial75 compared intra-arterial streptokinase to intra-arterial and IV rt-PA in 60 patients with recent onset or deterioration of limb ischemia; initial angiographic success was superior with intra-arterial rt-PA (100%) than with intra-arterial streptokinase (80%; p < 0.04) or IV rt-PA (45%; p < 0.01), the 30-day limb salvage rates being 80%, 60%, and 45%, respectively. Another randomized trial76 in 32 patients showed significantly faster lysis with rt-PA than with urokinase, but the 24-h lysis rate and the 30-day clinical success rate were similar. The Surgery vs Thrombolysis for Ischemia of the Lower Extremity (STILE) study77 included a comparison of rt-PA and urokinase; patients assigned to thrombolytic treatment received at random one of the two drugs, and the main report mentions similar efficacy and safety for both agents.
A German study78 randomized 120 patients with thrombotic infrainguinal arterial occlusion to treatment with urokinase or rt-PA, and noted a slight improvement in successful lysis in all segments treated with rt-PA(p < 0.05), but local hematomas were more common. The Prourokinase Versus Urokinase for Recanalization of Peripheral Occlusions, Safety and Efficacy trial79 compared three doses of recombinant prourokinase to tissue culture urokinase with complete lysis as a primary end point; the highest lysis rate was obtained with the highest dose tested (8 mg/h for 8 h, then 0.5 mg/h), at the expense of a slightly increased frequency of bleeding and decrement in fibrinogen level. In assessing all of these data, there is at present no convincing scientific proof of superiority of any agent for catheter-directed thrombolysis in terms of efficacy and safety.
Although the extensive literature on catheter-directed thrombolysis is largely descriptive, five prospective randomized studies compared this treatment method to surgical intervention.7780818485 Two meta-analyses8687 are available and conclude that there is a similar mortality and amputation rate for thrombolysis and surgery; thrombolysis reduces the need for open major surgical procedures but causes more bleeding and distal embolization.
In a small trial,80 surgical thrombectomy was compared to an intra-arterial continuous infusion of 30 mg of alteplase over 3 h in 20 patients with acute (> 24 h but < 14 days) arterial occlusion and severe leg ischemia. Only patients with a need for intervention were included. Considerable lysis was obtained in six of nine patients treated with alteplase, and half of them subsequently underwent percutaneous transluminal angioplasty. Two early reocclusions occurred. Thrombectomy also resulted in an immediate restitution of blood flow in six of nine cases.
Ouriel et al81 compared initial thrombolysis complemented with percutaneous transluminal angioplasty or/and surgery vs immediate surgery in 114 patients with limb-threatening ischemia of < 7 days in duration, due to native artery or graft occlusion. Thrombolysis resulted in dissolution of the occluding thrombus in 70% of the patients. Limb salvage rate was similar in the two groups (82% at 1 year), but cumulative survival was significantly improved in patients randomized to thrombolysis due to fewer cardiopulmonary complications in hospital (84% vs 58% at 1 year, p = 0.01).
The STILE trial77 randomized 393 patients with nonembolic native artery or bypass graft occlusion in the lower limbs within the past 6 months to either optimal surgical procedure or intra-arterial catheter-directed thrombolysis with rt-PA or urokinase. The primary end point was a composite outcome of death, major amputation, ongoing or recurrent ischemia, and major morbidity. At 1 month, the primary end point was reached for 36.1% of surgical patients and 61.7% of thrombolysis patients (p < 0.0001). This difference was primarily due to ongoing/recurrent ischemia (25.7% vs 54.0%; p < 0.0001); lysis was unsuccessful in 28% of the patients assigned to thrombolysis because of failure of proper catheter placement, an inexplicably high rate. However, in a secondary analysis that stratified patients by duration of ischemia, thrombolysis resulted in improved amputation-free survival at 6 months and shorter hospital stay in patients with acutely ischemic limbs (< 14 days), whereas surgical revascularization was more effective for more chronic ischemia (> 14 days).77
Two additional publications8283 analyzed the STILE trial on an intention-to-treat basis for the 30-day, 6-month, and 1-year results in patients with native artery and graft occlusion separately. For 237 patients with native artery occlusion, the composite clinical outcome was in favor of surgery because of a lower incidence of major amputation (0% vs 10% at 1 year, p = 0.0024) and recurrent ischemia (35% vs 64% at 1 year, p < 0.0001). Factors predictive of a poor outcome with lysis were femoropopliteal occlusion, diabetes, and critical ischemia. Only 20% of those patients had an onset or progression of ischemic symptoms of < 14 days in duration; in these patients, the 1-year death/amputation rate was similar for surgery and thrombolysis. Overall, lysis failed to reestablish patency in 45% of patients, but 22% did not receive a lytic agent because of problems with catheter positioning.82 For 124 patients with bypass graft occlusion, there was also a better overall composite clinical outcome at 30 days and 1 year in the surgical group compared to lysis, predominantly due to a reduction in ongoing/recurrent ischemia. However, 39% randomized to lysis failed catheter placement and required surgery. Following successful catheter placement, patency was reestablished by lysis in 84%. A poststudy analysis indicated that limb loss at 1 year was significantly lower in patients with ischemia for < 14 days if treated with thrombolysis compared with those treated surgically (20% vs 48%; p = 0.026).83
The Thrombolysis or Peripheral Arterial Surgery (TOPAS)8485 investigators prospectively compared recombinant urokinase vs surgery in acute arterial occlusion
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Epidemiology and Outcome of Klebsiella Species Bloodstream Infection: A Population-Based Study
1.Majdi N. Al-Hasan, MBBS,
2.Brian D. Lahr, MS,
3.Jeanette E. Eckel-Passow, PhD and
4.Larry M. Baddour, MD
+ Author Affiliations
1.From the Department of Medicine, Division of Infectious Diseases, University of Kentucky, Lexington (M.N.A.-H.); Division of Infectious Diseases (M.N.A.-H., L.M.B.) and Division of Biomedical Statistics and Informatics (B.D.L., J.E.E.-P.), Mayo Clinic, Rochester, MN
1.Individual reprints of this article are not available. Address correspondence to Majdi N. Al-Hasan, MBBS, University of Kentucky Chandler Medical Center, 800 Rose St, Room MN 672, Lexington, KY 40536 ([email protected]).
Abstract
OBJECTIVE: To determine incidence rate, seasonal variation, and short- and long-term outcomes of Klebsiella species bloodstream infection (BSI) in a population-based setting.
PATIENTS AND METHODS: We identified 127 unique patients in Olmsted County, Minnesota, from January 1, 1998, to December 31, 2007, who had Klebsiella spp BSI. Multivariable Poisson regression was used to examine temporal change and seasonal variation in incidence rate, and Cox proportional hazards regression was used to determine predictors of mortality.
RESULTS: The age-adjusted incidence rate of Klebsiella spp BSI per 100,000 person-years was 15.4 (95% confidence interval [CI], 11.6-19.2) in men and 9.4 (95% CI, 7.0-11.8) in women. There was no linear increase in incidence rate of Klebsiella spp BSI during the study period (P=.55). The incidence rate of Klebsiella spp BSI increased at quadratic rate with age (P=.005). No significant difference was noted in incidence rate of Klebsiella spp BSI during the warmest 4 months compared to the rest of the year (incidence rate ratio, 0.97; 95% CI, 0.66-1.38; P=.95). The overall 28-day and 1-year all-cause mortality rates of Klebsiella spp BSI were 14% (95% CI, 9%-22%) and 35% (95% CI, 27%-44%), respectively. Respiratory source of BSI was associated with a higher 28-day mortality (hazard ratio, 4.90; 95% CI, 1.73-13.84; P=.003).
CONCLUSION: The incidence rate of Klebsiella spp BSI increased with age. There was no temporal change or seasonal variation in incidence rate of Klebsiella spp BSI during the past decade. The 28-day all-cause mortality rate of Klebsiella spp BSI was relatively low; however, a respiratory source of BSI was associated with a poorer outcome.
Venous Thromboembolism Associated With Long-Term Use of Central Venous Catheters in Cancer Patients
Melina Verso , Giancarlo Agnelli
From the Division of Internal and Cardiovascular Medicine, Department of Internal Medicine, University of Perugia, Perugia, Italy.
Address reprint requests to Melina Verso, MD, Sezione di Medicina Interna e Cardiovascolare, Dipartimento di Medicina Interna, Università di Perugia, Via Enrico dal Pozzo, 06123 Perugia, Italy; e-mail: [email protected] .
Long-term central venous catheters (CVCs) have considerably improved the management of cancer patients because they facilitate chemotherapy, transfusions, parenteral nutrition, and blood sampling. However, the use of long-term CVCs, especially for chemotherapy, has been associated with the occurrence of upper-limb deep venous thrombosis (UL-DVT). The incidence of clinically overt UL-DVT related to CVCs has been reported to vary between 0.3% and 28.3%. The incidence of CVC-related UL-DVT screened by venography reportedly varies between 27% and 66%. The incidence of clinically overt pulmonary embolism (PE) in patients with CVC-related UL-DVT ranges from 15% to 25%, but an autopsy-proven PE rate of up to 50% has been reported. Vessel injury caused by the procedure of CVC insertion, venous stasis caused by the indwelling CVC, and cancer-related hypercoagulability are the main pathogenetic factors for CVC-related venous thromboembolism (VTE). Several studies have assessed the benefit of the prophylaxis of UL-DVT after CVC insertion in cancer patients. According to the results of these studies, prophylaxis with low molecular weight heparin or a low fixed dose of warfarin has been recently proposed. However, the limitations of the experimental design of the prophylactic studies do not allow definitive recommendations. The recommended therapy for UL-DVT associated with CVC is based on anticoagulant therapy with or without catheter removal. This review focuses on the epidemiology, pathogenesis, diagnosis, prevention, and treatment of VTE in cancer patients with long-term CVC.
Titre du document / Document title
Use of central venous catheter-related bloodstream infection prevention practices by US hospitals
Auteur(s) / Author(s)
SNYDMAN David R. (1) ; KREIN Sarah L. (2 3) ; HOFER Timothy P. (2 3) ; KOWALSKI Christine P. (2) ; OLMSTED Russell N. (4) ; KAUFFMAN Carol A. (3 5) ; FORMAN Jane H. (2) ; BANASZAK-HOLL Jane (6) ; SAINT Sanjay (2 3) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Medicine and Division of Geographic Medicine and Infectious Diseases Tufts New England Medical Center and Tufts University School of Medicine Boston, Mass, ETATS-UNIS
(2) Center for Practice Management and Outcomes Research, ETATS-UNIS
(3) Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, ETATS-UNIS
(4) Infection Control Services, Saint Joseph Mercy Health System, Ann Arbor, Mich, ETATS-UNIS
(5) Infectious Diseases Section, Veterans Affairs Ann Arbor Healthcare System, Ann Arbor, Mich, ETATS-UNIS
(6) Health Management and Policy, School of Public Health, University of Michigan, Ann Arbor, ETATS-UNIS
Résumé / Abstract
OBJECTIVE: To examine the extent to which US acute care hospitals have adopted recommended practices to prevent central venous catheter-related bloodstream infections (CR-BSIs). PARTICIPANTS AND METHODS: Between March 16, 2005, and August 1, 2005, a survey of infection control coordinators was conducted at a national random sample of nonfederal hospitals with an Intensive care unit and more than 50 hospital beds (n=600) and at all Department of Veterans Affairs (VA) medical centers (n=119). Primary outcomes were regular use of 5 specific practices and a composite approach for preventing CR-BSls. RESULTS: The overall survey response rate was 72% (n=516). A higher percentage of VA compared to non-VA hospitals reported using maximal sterile barrier precautions (84% vs 71%; P=.01); chlorhexidine gluconate for insertion site antisepsis (91% vs 69%; P<.001); and a composite approach (62% vs 44%; P=.003) combining concurrent use of maximal sterile barrier precautions, chlorhexidine gluconate, and avoidance of routine central line changes. Those hospitals having a higher safety culture score, having a certified Infection control professional, and participating In an infection prevention collaborative were more likely to use CR-BSI prevention practices. CONCLUSION: Most US hospitals are using maximal sterile barrier precautions and chlorhexidine gluconate, 2 of the most strongly recommended practices to prevent CR-BSIs. However, fewer than half of non-VA US hospitals reported concurrent use of maximal sterile barrier precautions, chlorhexidine gluconate, and avoidance of routine central line changes. Wider use of CR-BSI prevention practices by hospitals could be encouraged by fostering a culture of safety, participating in Infection prevention collaboratives, and promoting infection control professional certification.
Techniques to Prevent Central Venous Catheter Infections: Products, Research, and Recommendations
Jane Banton, RN, BSN, CRNI
University of Wisconsin Hospital and Clinics, Nursing Education and Development, Clinical Coordinator IV Therapy, Madison, Wisconsin
Correspondence: Correspondence: Jane Banton, RN, BSN, CRNI, University of Wisconsin Hospital and Clinics, 600 Highland Ave., Madison, WI 53792. Electronic mail may be sent to [email protected] .
Central venous catheters (CVCs) are commonly used to deliver a variety of therapies such as chemotherapy and parenteral nutrition. It is well known that there are complications associated with CVCs; a major complication is catheter-related bloodstream infection (CRBSI). Many strategies exist to prevent CVC complications and CRBSI. This paper will focus on the fight against CRBSI using 3 products at the catheter insertion site: 2% chlorhexidine, BioPatch, and transparent split dressings. Lists of key recommendations from national organizations for infection prevention are included.
Nutrition in
Catheter Associated BSI
Catheter Associated BSI
--------------------------------------------------------------------------------
BSI Prevention Project
PI: Trish M. Perl, MD, MSc & Sara Cosgrove, M.D., M.S.;
Sponsor: Centers for Disease Control and Prevention (CDC)
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Central venous catheters have become indispensable in the care of critically ill patients and have made the modern discipline of critical care medicine possible. As the severity of illness and complexity of therapeutic measures in the intensive care unit (ICU) setting has increased, the chance for complications from the use of medical devices has increased, the most serious of which is infection. Catheter-related bloodstream infection (CRBSI) is one of the most common nosocomial infections in ICU patients. Catheter-related bloodstream infections have been estimated to occur in 3 to 7% of catheters used, and affect more than 200,000 patients in the United States annually. Previous studies have shown nosocomial bloodstream infections to be associated with increased attributable mortality, length of hospital stay, and cost.
Prevention of nosocomial infections is primarily a function of hospital infection control programs. Several modifiable factors have been shown to increase the risk of catheter-related bloodstream infection. These include lapses in the use of strict sterile technique in the insertion of central venous catheters and insertion of catheters into internal jugular or femoral vein sites, compared to the subclavian vein. In 1996, the CDC developed guidelines for the prevention of intravascular device-related nosocomial infections. In these guidelines, the CDC strongly recommended the “ongoing education and training of health care workers regarding… procedures for the insertion and maintenance of intravascular devices and appropriate infection control measures to prevent intravascular device-related infections.” The studies below are multi-center studies coordinated by Washington University.
Data collection for all parts of the BSI Prevention Project concluded 12/31/03. Abstracts will be submitted for review as soon as data analysis is complete.
Surveillance Protocol for the Evaluation of Catheter-associated Bloodstream Infections (CABSI) and Central Venous Catheter Insertion Site Care
The purpose of this part of the above multicenter study is to determine the incidence of catheter-associated bloodstream infections and the processes of central venous catheter site care among hospitalized patients. This surveillance will include regular observations of central venous catheter insertion sites, plus daily determinations of patient census and total number of catheterized patients. Also, microbiologic data will be reviewed on patients admitted to study units to determine the presence of catheter-associated bloodstream infection. This study is the first part of a larger project, BSI Prevention Project, which purposes to determine if an educational intervention based on CDC guidelines can be implemented throughout multiple hospitals in various regions of the United States. This surveillance data will be used to determine the effectiveness of an intervention designed to reduce the incidence of catheter-associated bloodstream infections. Surveillance data will be collected from 1/1/02 through 12/31/03. This data will establish baseline and post-intervention BSI rates in the units involved.
The impact of an intervention designed to reduce the incidence of nosocomial catheter-associated bloodstream infections.
Hypothesis: An educational intervention, aimed at changing the process of central venous catheter insertion and care, based on CDC guidelines to prevent catheter-associated bloodstream infections, can be successfully implemented within multiple intensive care units within a multicenter framework. Secondarily, this intervention may result in a significant reduction in the incidence of catheter-associated bloodstream infections within these units.
Staff education module: A standard, self-study, educational module on the prevention of catheter-associated bloodstream infection with pre- and post-tests will be used as the primary educational tool. This would be administered to all nurses in the study units and all housestaff, fellow, and attending physicians within the intervention period (7/1/2002- 9/30/2002). The module will be accompanied by in-service sessions for nursing and a didactic slide presentation for physicians.
Posters/ Fact sheets: Posters highlighting proper central venous catheter insertion and care techniques will be placed in areas where they can be viewed by unit personnel.
Central venous catheter insertion checklist: A checklist of the process of central venous catheter insertion (type of catheter, anatomic insertion site, prep used, etc.) will be completed for all catheters inserted in the study units by unit nursing staff. The purpose of this checklist is to reinforce proper central line insertion technique in the post-intervention period. The checklists will be collected on a regular basis from the study units.
For more information on these studies please email Kathleen
Risk of Catheter-Related Bloodstream Infection With Peripherally Inserted Central Venous Catheters Used in Hospitalized Patients*
1.Nasia Safdar, MD, MS and
2.Dennis G. Maki, MD
+ Author Affiliations
1.*From the Section of Infectious Diseases, Department of Medicine, University of Wisconsin Medical School, Madison, WI.
1.Correspondence to: Dennis G. Maki, MD, H5/574, University of Wisconsin Hospital and Clinics, Madison, WI 53792; e-mail: [email protected]
Abstract
Background: Peripherally inserted central venous catheters (PICCs) are now widely used for intermediate and long-term access in current-day health care, especially in the inpatient setting, where they are increasingly supplanting conventional central venous catheters (CVCs) placed percutaneously into the internal jugular, subclavian, or femoral veins. Data on the risk of PICC-related bloodstream infection (BSI) with PICCs used in hospitalized patients are limited.
Study objectives: To determine the risk of PICC-related BSI in hospitalized patients.
Study design: Prospective cohort study using data from two randomized trials assessing the efficacy of chlorhexidine-impregnated sponge dressing and chlorhexidine for cutaneous antisepsis.
Methods: PICCs inserted into the antecubital vein in two randomized trials during from 1998 to 2000 were prospectively studied; most patients were in an ICU. PICC-related BSI was confirmed in each case by demonstrating concordance between isolates colonizing the PICC at the time of removal and from blood cultures by restriction-fragment DNA subtyping.
Results: Overall, 115 patients had 251 PICCs placed. Mean duration of catheterization was 11.3 days (total, 2,832 PICC-days); 42% of the patients were in an ICU at some time, 62% had urinary catheters, and 49% had received mechanical ventilation. Six PICC-related BSIs were identified (2.4%), four with coagulase-negative staphylococcus, one with Staphylococcus aureus, and one with Klebsiella pneumoniae, a rate of 2.1 per 1,000 catheter-days.
Conclusion: This prospective study shows that PICCs used in high-risk hospitalized patients are associated with a rate of catheter-related BSI similar to conventional CVCs placed in the internal jugular or subclavian veins (2 to 5 per 1,000 catheter-days), much higher than with PICCs used exclusively in the outpatient setting (approximately 0.4 per 1,000 catheter-days), and higher than with cuffed and tunneled Hickman-like CVCs (approximately 1 per 1,000 catheter-days). A randomized trial of PICCs and conventional CVCs in hospitalized patients requiring central access is needed. Our data raise the question of whether the growing trend in many hospital hematology and oncology services to switch from use of cuffed and tunneled CVCs to PICCs is justified, particularly since PICCs are more vulnerable to thrombosis and dislodgment, and are less useful for drawing blood specimens. Moreover, PICCs are not advisable in patients with renal failure and impending need for dialysis, in whom preservation of upper-extremity veins is needed for fistula or graft implantation.
•bacteremia
•bloodstream infection
•catheter-related bloodstream infection
•cross-infection
•intravascular catheters
•nosocomial bacteremia
•nosocomial infection
•peripherally inserted central catheters
‹ Review Articles/บทฟื้นฟูวิชาการ: ภาวะฉุกเฉินของความผิดปกติของเกลือแร่ในร่างกาย (Electrolyte disturbance emergency
Home » วารสารเวชศาสตร์ฉุกเฉินไทย ฉบับที่ 2: เมษายน-มิถุนายน 2552 » Review Articles/บทฟื้นฟูวิชาการ: ภาวะฉุกเฉินของความผิดปกติของเกลือแร่ในร่างกาย (Electrolyte disturbance emergency)
Review Articles/บทฟื้นฟูวิชาการ: ภาวะฉุกเฉินของความผิดปกติของเกลือแร่ในร่างกาย (Electrolyte disturbance emergency)
Wed, 08/05/2009 - 16:15 — zybernav
•electrolyte |
•วารสารเวชศาสตร์ฉุกเฉินไทย ฉบับที่ 2
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