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Cardiovascular examination should also include peripheral arterial evaluation for COVID-19 patients
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body
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The global impact of coronavirus disease (COVID-19) on vascular surgical services has been initially addressed by Ng et al.1 This change in how vascular surgery departments are adapting to the ongoing scenario reveals a clear trend toward providing urgent care, as previously suggested by some vascular communities.2 In addition, along that line, an “endovascular first-line approach” seems reasonable because less in-hospital resources are required.
Spain has been especially affected, with nearly 15,000 deaths and 1,500,000 positive cases. Interestingly, nearly 20% of the affected cases are health care workers, which is due to an extreme lack of personal protection equipment and protection strategies. All Spanish national efforts are currently directed toward stopping the disease propagation and diminishing the disease impact, leading to unprecedented cooperation between public and private centers in attempts to provide care to all who need it.
The cardiovascular effect of COVID-19 is currently under study. Some reports describe acute coronary syndromes, arrhythmias, and/or myocarditis due to the systemic inflammatory response as well as localized vascular inflammation.3
Although substantial attention is directed toward evaluating the relationship between COVID-19 and myocardial disease,4 , 5 we should not forget the global picture of the cardiovascular pathology and its potential inducement of peripheral arterial disease (PAD).
Tables I and II summarize four cases presenting with acute critical limb ischemia in patients testing COVID-19 (+) with no previous vascular consultations or symptoms. We identified a delayed diagnosis for the entire group. The patients were either extremely fearful about coming to the hospital or underdiagnosed during hospitalization, as confirmed with written commentary from nurses. An arterial thrombotic event presented in two COVID-19 patients who were asymptomatic despite testing positive for the disease. Blood testing demonstrated a high inflammatory response in all of these patients (D-dimer, C-reactive protein) that was significantly higher in those who were hospitalized with active and severe pneumonia. Interestingly, procalcitonin values were normal in all of these patients, indicating an evolving inflammatory condition. Although no strong conclusions can be drawn from this initial description, it may serve as guidance for future studies seeking to improve PAD identification.
Table I Clinical data and outcomes of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
Age, years Other COVID-19 symptomsa Vascular bed affected Treatment Outcome
1 72 COPD, HT + Popliteal artery (right) LMWH alone Death 1 day after consultationDIC + MOF
2 53 – – Iliac and popliteal artery (left) LMWH and delayed thrombectomy at day 7 Clinical improvement
3 72 DM – SFA, popliteal with distal thrombosis (right) Thrombectomy + LMWH + prostaglandins 10-day limb salvage, 50% ischemic neuropathy
4 70 PV + Infragenicular (right) LMWH alone 2 days—clinical improvement
COPD, Chronic obstructive pulmonary disease; DIC, disseminated intravascular coagulopathy; DM, diabetes mellitus; HT, hypertension; LMWH, low-molecular-weight heparin; MOF, multiorgan failure; PV, polycythemia; SFA, superficial femoral artery.
a Includes respiratory or fever.
Table II Blood test data of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
D-dimer, ng/mL Platelet count, 109 L Lymphocytes count, /mm3 CRP, mg/dL
1 6531 50 900 184
2 1415 335 800 9.1
3 3235 228 1800 58.9
4 7528 121 400 77.7
CRP, C-reactive protein.
Clinicians involved in PAD care understand that timing is a key factor in limb salvage and acute critical limb ischemia patient survival. These delayed presentations clearly demonstrate a population that is in fear of presenting to an overwhelmed health system. The underdiagnoses in hospitalized patients could be related to incomplete physical examinations in poorly communicating isolated elderly patients (who may already have oxygen support and painkillers to treat high-grade fever). These underdiagnoses could also be related to the aforementioned lack of personal protection equipment that currently affects the entire health care system.
We recognize the difficulty in diagnosis and therefore the late timing of disease identification for those who are confined at home. Telemedicine and teleconsultations may be a game changer for those patients.
Further studies should focus on (1) the real rate and association (if there is any) of thromboembolic (both venous and arterial) events in COVID-19 patients and (2) identifying the patients who are at risk for thrombosis to determine the best preventive maneuvers (ie, aggressive anticoagulation therapies), thereby counterbalancing the risk of bleeding in such a high-risk population.
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p
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The global impact of coronavirus disease (COVID-19) on vascular surgical services has been initially addressed by Ng et al.1 This change in how vascular surgery departments are adapting to the ongoing scenario reveals a clear trend toward providing urgent care, as previously suggested by some vascular communities.2 In addition, along that line, an “endovascular first-line approach” seems reasonable because less in-hospital resources are required.
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|
p
|
Spain has been especially affected, with nearly 15,000 deaths and 1,500,000 positive cases. Interestingly, nearly 20% of the affected cases are health care workers, which is due to an extreme lack of personal protection equipment and protection strategies. All Spanish national efforts are currently directed toward stopping the disease propagation and diminishing the disease impact, leading to unprecedented cooperation between public and private centers in attempts to provide care to all who need it.
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p
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The cardiovascular effect of COVID-19 is currently under study. Some reports describe acute coronary syndromes, arrhythmias, and/or myocarditis due to the systemic inflammatory response as well as localized vascular inflammation.3
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p
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Although substantial attention is directed toward evaluating the relationship between COVID-19 and myocardial disease,4 , 5 we should not forget the global picture of the cardiovascular pathology and its potential inducement of peripheral arterial disease (PAD).
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p
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Tables I and II summarize four cases presenting with acute critical limb ischemia in patients testing COVID-19 (+) with no previous vascular consultations or symptoms. We identified a delayed diagnosis for the entire group. The patients were either extremely fearful about coming to the hospital or underdiagnosed during hospitalization, as confirmed with written commentary from nurses. An arterial thrombotic event presented in two COVID-19 patients who were asymptomatic despite testing positive for the disease. Blood testing demonstrated a high inflammatory response in all of these patients (D-dimer, C-reactive protein) that was significantly higher in those who were hospitalized with active and severe pneumonia. Interestingly, procalcitonin values were normal in all of these patients, indicating an evolving inflammatory condition. Although no strong conclusions can be drawn from this initial description, it may serve as guidance for future studies seeking to improve PAD identification.
Table I Clinical data and outcomes of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
Age, years Other COVID-19 symptomsa Vascular bed affected Treatment Outcome
1 72 COPD, HT + Popliteal artery (right) LMWH alone Death 1 day after consultationDIC + MOF
2 53 – – Iliac and popliteal artery (left) LMWH and delayed thrombectomy at day 7 Clinical improvement
3 72 DM – SFA, popliteal with distal thrombosis (right) Thrombectomy + LMWH + prostaglandins 10-day limb salvage, 50% ischemic neuropathy
4 70 PV + Infragenicular (right) LMWH alone 2 days—clinical improvement
COPD, Chronic obstructive pulmonary disease; DIC, disseminated intravascular coagulopathy; DM, diabetes mellitus; HT, hypertension; LMWH, low-molecular-weight heparin; MOF, multiorgan failure; PV, polycythemia; SFA, superficial femoral artery.
a Includes respiratory or fever.
Table II Blood test data of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
D-dimer, ng/mL Platelet count, 109 L Lymphocytes count, /mm3 CRP, mg/dL
1 6531 50 900 184
2 1415 335 800 9.1
3 3235 228 1800 58.9
4 7528 121 400 77.7
CRP, C-reactive protein.
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table-wrap
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Table I Clinical data and outcomes of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
Age, years Other COVID-19 symptomsa Vascular bed affected Treatment Outcome
1 72 COPD, HT + Popliteal artery (right) LMWH alone Death 1 day after consultationDIC + MOF
2 53 – – Iliac and popliteal artery (left) LMWH and delayed thrombectomy at day 7 Clinical improvement
3 72 DM – SFA, popliteal with distal thrombosis (right) Thrombectomy + LMWH + prostaglandins 10-day limb salvage, 50% ischemic neuropathy
4 70 PV + Infragenicular (right) LMWH alone 2 days—clinical improvement
COPD, Chronic obstructive pulmonary disease; DIC, disseminated intravascular coagulopathy; DM, diabetes mellitus; HT, hypertension; LMWH, low-molecular-weight heparin; MOF, multiorgan failure; PV, polycythemia; SFA, superficial femoral artery.
a Includes respiratory or fever.
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label
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Table I
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caption
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Clinical data and outcomes of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
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p
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Clinical data and outcomes of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
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table
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Age, years Other COVID-19 symptomsa Vascular bed affected Treatment Outcome
1 72 COPD, HT + Popliteal artery (right) LMWH alone Death 1 day after consultationDIC + MOF
2 53 – – Iliac and popliteal artery (left) LMWH and delayed thrombectomy at day 7 Clinical improvement
3 72 DM – SFA, popliteal with distal thrombosis (right) Thrombectomy + LMWH + prostaglandins 10-day limb salvage, 50% ischemic neuropathy
4 70 PV + Infragenicular (right) LMWH alone 2 days—clinical improvement
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tr
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Age, years Other COVID-19 symptomsa Vascular bed affected Treatment Outcome
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th
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Age, years
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th
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Other
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th
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COVID-19 symptomsa
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th
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Vascular bed affected
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th
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Treatment
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th
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Outcome
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tr
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1 72 COPD, HT + Popliteal artery (right) LMWH alone Death 1 day after consultationDIC + MOF
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td
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1
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td
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72
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td
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COPD, HT
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td
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+
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td
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Popliteal artery (right)
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td
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LMWH alone
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td
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Death 1 day after consultationDIC + MOF
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tr
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2 53 – – Iliac and popliteal artery (left) LMWH and delayed thrombectomy at day 7 Clinical improvement
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td
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2
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td
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53
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td
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–
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td
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–
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td
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Iliac and popliteal artery (left)
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td
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LMWH and delayed thrombectomy at day 7
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td
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Clinical improvement
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tr
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3 72 DM – SFA, popliteal with distal thrombosis (right) Thrombectomy + LMWH + prostaglandins 10-day limb salvage, 50% ischemic neuropathy
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td
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3
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td
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72
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td
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DM
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td
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–
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td
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SFA, popliteal with distal thrombosis (right)
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td
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Thrombectomy + LMWH + prostaglandins
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td
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10-day limb salvage, 50% ischemic neuropathy
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tr
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4 70 PV + Infragenicular (right) LMWH alone 2 days—clinical improvement
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td
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4
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td
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70
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td
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PV
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td
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+
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td
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Infragenicular (right)
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td
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LMWH alone
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td
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2 days—clinical improvement
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table-wrap-foot
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COPD, Chronic obstructive pulmonary disease; DIC, disseminated intravascular coagulopathy; DM, diabetes mellitus; HT, hypertension; LMWH, low-molecular-weight heparin; MOF, multiorgan failure; PV, polycythemia; SFA, superficial femoral artery.
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footnote
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COPD, Chronic obstructive pulmonary disease; DIC, disseminated intravascular coagulopathy; DM, diabetes mellitus; HT, hypertension; LMWH, low-molecular-weight heparin; MOF, multiorgan failure; PV, polycythemia; SFA, superficial femoral artery.
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p
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COPD, Chronic obstructive pulmonary disease; DIC, disseminated intravascular coagulopathy; DM, diabetes mellitus; HT, hypertension; LMWH, low-molecular-weight heparin; MOF, multiorgan failure; PV, polycythemia; SFA, superficial femoral artery.
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table-wrap-foot
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a Includes respiratory or fever.
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footnote
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a Includes respiratory or fever.
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label
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a
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p
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Includes respiratory or fever.
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table-wrap
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Table II Blood test data of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
D-dimer, ng/mL Platelet count, 109 L Lymphocytes count, /mm3 CRP, mg/dL
1 6531 50 900 184
2 1415 335 800 9.1
3 3235 228 1800 58.9
4 7528 121 400 77.7
CRP, C-reactive protein.
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label
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Table II
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caption
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Blood test data of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
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p
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Blood test data of patients with acute critical limb ischemia (ACLI) and COVID-19 (+)
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table
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D-dimer, ng/mL Platelet count, 109 L Lymphocytes count, /mm3 CRP, mg/dL
1 6531 50 900 184
2 1415 335 800 9.1
3 3235 228 1800 58.9
4 7528 121 400 77.7
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tr
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D-dimer, ng/mL Platelet count, 109 L Lymphocytes count, /mm3 CRP, mg/dL
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th
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D-dimer, ng/mL
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th
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Platelet count, 109 L
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th
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Lymphocytes count, /mm3
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th
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CRP, mg/dL
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tr
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1 6531 50 900 184
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td
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1
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td
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6531
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td
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50
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td
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900
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td
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184
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tr
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2 1415 335 800 9.1
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td
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2
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td
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1415
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td
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335
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td
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800
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td
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9.1
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tr
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3 3235 228 1800 58.9
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td
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3
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td
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3235
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td
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228
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td
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1800
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td
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58.9
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tr
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4 7528 121 400 77.7
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td
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4
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td
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7528
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td
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121
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td
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400
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td
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77.7
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table-wrap-foot
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CRP, C-reactive protein.
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footnote
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CRP, C-reactive protein.
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p
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CRP, C-reactive protein.
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p
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Clinicians involved in PAD care understand that timing is a key factor in limb salvage and acute critical limb ischemia patient survival. These delayed presentations clearly demonstrate a population that is in fear of presenting to an overwhelmed health system. The underdiagnoses in hospitalized patients could be related to incomplete physical examinations in poorly communicating isolated elderly patients (who may already have oxygen support and painkillers to treat high-grade fever). These underdiagnoses could also be related to the aforementioned lack of personal protection equipment that currently affects the entire health care system.
|
|
p
|
We recognize the difficulty in diagnosis and therefore the late timing of disease identification for those who are confined at home. Telemedicine and teleconsultations may be a game changer for those patients.
|
|
p
|
Further studies should focus on (1) the real rate and association (if there is any) of thromboembolic (both venous and arterial) events in COVID-19 patients and (2) identifying the patients who are at risk for thrombosis to determine the best preventive maneuvers (ie, aggressive anticoagulation therapies), thereby counterbalancing the risk of bleeding in such a high-risk population.
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