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Acute Upper Arm Ischemia in a Patient with Human Immu-
nodeficeincy Virus Infection: Underwent Successful Surgical
Thromboembolectomy
Rehman ZU*
, Begum S, Hashmi FA
Department of Surgery, The Aga Khan University, Pakistan
Volume 1 Issue 2- 2018
Received Date: 19 Aug 2018
Accepted Date: 02 Sep 2018
Published Date: 11 Sep 2018
1. Abstract
Patients with human immunodeficiency virus (HIV) are in hypercoagulabe state due to various
coagulation abnormalities and at increased risk for thromboembolic events. We report acute
upper arm ischemia caused by spontaneous thromboembolism with no identified source in a
patient with HIV infection. Patient underwent successful surgical thromboembolectomy and
had good postoperative recovery. Physicians should be aware of thromboembolic disease as the
possible complication of HIV.
Annals of Clinical and Medical
Case Reports
Citation: Rehman ZU, Begum S, Hashmi FA, Acute Upper Arm Ischemia in a Patient with Human Immu-
nodeficeincy Virus Infection: Underwent Successful Surgical Thromboembolectomy. Annals of Clinical and
Medical Case Reports. 2018; 1(2): 1-2.
United Prime Publications: http://unitedprimepub.com
*Corresponding Author (s): Zia-Ur- Rehman, Department of Surgery, The Aga Khan Uni-
versity, Pakistan, E-mail: ziaur.rehman@aku.edu
Case Reort
3. Introduction
Increased risk of venous thromboembolism is well recognized in
patient with human immunodeficiency virus (HIV), and the dis-
ease has been suggested to represent a pre-thrombotic state. Even
so, little exist in literature concerning arterial thromboembolism
causing upper arm ischemia in patients with HIV. We report a
case report of acute embolic occlusion of non-diseased brachial
and axillary artery in a 42 years old man with HIV infection.
4. Case Report
A 42 years man with HIV infection presented to Emergency De-
partment with acute left upper arm painlasting for 6-7 hours.
Pain was acute in onset, severe in intensity, continuous and now
was associated with numbness of forearm. He was on Highly Ac-
tive Antiretroviral Therapy (HAART). There was no history of
cardiac disease. At physical examination, normal arterial pulses
were present in right (unaffected) arm, but no pulses or doppler
signals were found at or below the brachial artery in left upper
arm [1,2]. The left upper arm was cyanotic and markedly cooler
than the right arm. Capillary refill was markedly delayed and
there was evidence of sensory loss in finger tips. Patient was
accompanying adopplerultrasound showing total occlusion of
left axillary and brachial artery with acute thrombus and no vis-
ible distal flow. After blood samples were drawn for laboratory
2. Key words
HIV; Primary thrombosis;
Thromboembolectomy
studies, intravenous heparin was started. An electrocardiogram
showed normal sinus rhythm. Hemoglobin was 13.1 g/dl, WBC
10X 109/l, Platelets count were 288 x 109/l. International nor-
malized ratio (INR) and partial thromboplastin time (PTT) were
within normal laboratory limits. The patient underwent trom-
boembolectomy through lazy ‘S’ incision in left elbow fossa un-
der general anesthesia (Figure. 1). Longitudinal arteriotomy was
made just above the bifurcation of brachial artery and thrombus
was removed both proximally and distally with the help of Foga-
rty balloon catheter. After clearing the arterial tree, longitudinal
arteriotomy closed with vein patch. Grossly the arterial wall was
normal [2,3]. Postoperatively patient has palpable pulses and
hand became warmer and pink. He received postoperatively con-
tinuous intravenous heparin infusion which was overlapped with
oral anticoagulants. Patient was discharged on oral warfarin and
advises to maintain INR in therapeutic range. On follow up at 2
months, he had no recurrence of symptoms and having viable,
functional limb.
Echocardiogram showed no abnormality. Levels of Protein C,
Protein S, Antithrombin III, and Factor V Leiden were within
normal laboratory limits.
Copyright ©2018 Rehman ZU This is an open access article distributed under the terms of the Creative Commons Attribution License,
which permits unrestricted use, distribution, and build upon your work non-commercially.
2
Volume 1 Issue 2 -2018 Case Report
Figure 1: Thrombus extracted from the brachial artery with the help of Foga-
rty Catheter.
5. Discussion
Patients with human immunodeficiency virus (HIV) have vari-
ous coagulation abnormalities as well as increased risk for devel-
opment of clinical thrombosis and subsequent embolic events.
Abnormalities predisposing to ahypercoagulablestate that have
been detected in HIV patients includeantiphospholipid anti-
bodies , lupus anticoagulants , increased von Will brand factor,
deficiency in Protein C and S, antithrombin and heparin cofac-
tor. Factors such as opportunistic infections and neoplasm may
also contribute to the hypercoagulable state and hence to throm-
botic events.
HIV/ AIDS associated vasculopathy was first recognized as an
entity in 1987. Since then there has been several reports on large
vessel vasculopathy associated with HIV/AIDS and few of these
have dealt with peripheral arterial thrombosis and its manage-
ment. Pathogenesis of HIV/ AIDS associated vasculopathyis
multifactorial. HIV may produce protein –wasting nephropathy
or endothelial cell injury, both of which may possibly contribute
to alterations in circulating levels of anticoagulant proteins. Fur-
thermore, reduction in CD 4+ cell count to less than 200cellss/
mm3has been observed in patients with thromboembolic com-
plication. Nair et al. [4] first described the pathology in detail,
which was regarded as unique to HIV/AIDS vasculopathy. They
noted that inflammation was centered on the vasa vasora in the
adventitia and was characterized by a vasculitis in which the ves-
sels were surrounded by acuff of neutrophils, monocytes and
plasma cells, which ultimately lead to occlusion of vasa vasora
with resultant transmural fibrosis and necrosis. This either leads
to HIV associated aneurysm formation or localized thrombosis.
HIV-related thrombosis, which is segmental, shows a histological
picture with inflammatory changes confined to the vasavasora
with bland organizing luminal thrombus. The striking feature
of this disease is the normality of the arterial tree proximal to
the thrombosed arteries by duplex ultrasonography, angiography
and macroscopic appearance. The other remarkable feature is the
thrombosis of all distal vessels with no demonstrable runoff. Du-
plex ultrasound also showed hypoechoic ‘spotting’ in the arterial
wall, the’ string of pearls sign’, which also has been observed in
patients with HIV associated arterial aneurysm [5,6].
Surgical thromboembolectomy is effective is restoring the circu-
lation as was this case. Percutaneous mechanical thrombectomy
and thrombolysis has been also found effective in various case
reports.
The duration of necessary anticoagulation is unknown, but gen-
erally these are candidates for prolong anticoagulation due co-
agulation abnormalities present in a patient of HIV/AIDS.
6. Conclusion
This case highlight arterial ischemia caused by spontaneous
thrombosis is a patient with HIV. The clinical diagnosis of limb
threatening ischemia was prompt, as was intervention. Surgical
embolectomy restored upper extremity circulation. Physicians
should be aware of thromboembolic disease as the possible com-
plication of HIV.
References
1. Saber A, Aboolian A, Laraja R, Baron H, Hanna K. HIV/AIDS and
the risk of deep venous thrombosis: a study of 45 patients with lower
extremity involvement. Am Surg. 2001; 67: 645-7.
2. Joshi VV, Pawel B, Connor E. Arteriopathy in children with acquired
immunodeficiency syndrome. PediatrPathol. 1987; 7: 261- 275.
3. Copur A, Smith P, Gomez V, Bergman M, Homel P. HIV infection is
a risk factor for venous thromboembolism. AIDS Patient Care STDs.
2002; 16: 205-9.
4. Nair R, Abdool Carrim ATO, Chetty R, Robbs JV. Arterial aneurysms
in patients infected with human immunodeficiency virus: a distinct clin-
icopathological entity? J VascSurg. 1999; 29: 600-7.
5. Woolgan JD, Ray R, Maraj K, Robbs JV. Colourdoppler and grey scale
ultrasound features of HIV- related vascular aneurysms. Br J Radiol
2002; 75:884-888.
6. Bush RL, Bianco CC, Bixler TJ, Lin PH, Lumsden AB. Spontaneous
arterial thrombosis in a patient with human immunodeficiency virus in-
fection: Successful treatment with pharamcomechanical thrombectomy.
J VascSurg. 2003; 38: 392-5.

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Acute Upper Arm Ischemia in a Patient with Human Immunodeficeincy Virus Infection: Underwent Successful Surgical Thromboembolectomy

  • 1. Acute Upper Arm Ischemia in a Patient with Human Immu- nodeficeincy Virus Infection: Underwent Successful Surgical Thromboembolectomy Rehman ZU* , Begum S, Hashmi FA Department of Surgery, The Aga Khan University, Pakistan Volume 1 Issue 2- 2018 Received Date: 19 Aug 2018 Accepted Date: 02 Sep 2018 Published Date: 11 Sep 2018 1. Abstract Patients with human immunodeficiency virus (HIV) are in hypercoagulabe state due to various coagulation abnormalities and at increased risk for thromboembolic events. We report acute upper arm ischemia caused by spontaneous thromboembolism with no identified source in a patient with HIV infection. Patient underwent successful surgical thromboembolectomy and had good postoperative recovery. Physicians should be aware of thromboembolic disease as the possible complication of HIV. Annals of Clinical and Medical Case Reports Citation: Rehman ZU, Begum S, Hashmi FA, Acute Upper Arm Ischemia in a Patient with Human Immu- nodeficeincy Virus Infection: Underwent Successful Surgical Thromboembolectomy. Annals of Clinical and Medical Case Reports. 2018; 1(2): 1-2. United Prime Publications: http://unitedprimepub.com *Corresponding Author (s): Zia-Ur- Rehman, Department of Surgery, The Aga Khan Uni- versity, Pakistan, E-mail: ziaur.rehman@aku.edu Case Reort 3. Introduction Increased risk of venous thromboembolism is well recognized in patient with human immunodeficiency virus (HIV), and the dis- ease has been suggested to represent a pre-thrombotic state. Even so, little exist in literature concerning arterial thromboembolism causing upper arm ischemia in patients with HIV. We report a case report of acute embolic occlusion of non-diseased brachial and axillary artery in a 42 years old man with HIV infection. 4. Case Report A 42 years man with HIV infection presented to Emergency De- partment with acute left upper arm painlasting for 6-7 hours. Pain was acute in onset, severe in intensity, continuous and now was associated with numbness of forearm. He was on Highly Ac- tive Antiretroviral Therapy (HAART). There was no history of cardiac disease. At physical examination, normal arterial pulses were present in right (unaffected) arm, but no pulses or doppler signals were found at or below the brachial artery in left upper arm [1,2]. The left upper arm was cyanotic and markedly cooler than the right arm. Capillary refill was markedly delayed and there was evidence of sensory loss in finger tips. Patient was accompanying adopplerultrasound showing total occlusion of left axillary and brachial artery with acute thrombus and no vis- ible distal flow. After blood samples were drawn for laboratory 2. Key words HIV; Primary thrombosis; Thromboembolectomy studies, intravenous heparin was started. An electrocardiogram showed normal sinus rhythm. Hemoglobin was 13.1 g/dl, WBC 10X 109/l, Platelets count were 288 x 109/l. International nor- malized ratio (INR) and partial thromboplastin time (PTT) were within normal laboratory limits. The patient underwent trom- boembolectomy through lazy ‘S’ incision in left elbow fossa un- der general anesthesia (Figure. 1). Longitudinal arteriotomy was made just above the bifurcation of brachial artery and thrombus was removed both proximally and distally with the help of Foga- rty balloon catheter. After clearing the arterial tree, longitudinal arteriotomy closed with vein patch. Grossly the arterial wall was normal [2,3]. Postoperatively patient has palpable pulses and hand became warmer and pink. He received postoperatively con- tinuous intravenous heparin infusion which was overlapped with oral anticoagulants. Patient was discharged on oral warfarin and advises to maintain INR in therapeutic range. On follow up at 2 months, he had no recurrence of symptoms and having viable, functional limb. Echocardiogram showed no abnormality. Levels of Protein C, Protein S, Antithrombin III, and Factor V Leiden were within normal laboratory limits.
  • 2. Copyright ©2018 Rehman ZU This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and build upon your work non-commercially. 2 Volume 1 Issue 2 -2018 Case Report Figure 1: Thrombus extracted from the brachial artery with the help of Foga- rty Catheter. 5. Discussion Patients with human immunodeficiency virus (HIV) have vari- ous coagulation abnormalities as well as increased risk for devel- opment of clinical thrombosis and subsequent embolic events. Abnormalities predisposing to ahypercoagulablestate that have been detected in HIV patients includeantiphospholipid anti- bodies , lupus anticoagulants , increased von Will brand factor, deficiency in Protein C and S, antithrombin and heparin cofac- tor. Factors such as opportunistic infections and neoplasm may also contribute to the hypercoagulable state and hence to throm- botic events. HIV/ AIDS associated vasculopathy was first recognized as an entity in 1987. Since then there has been several reports on large vessel vasculopathy associated with HIV/AIDS and few of these have dealt with peripheral arterial thrombosis and its manage- ment. Pathogenesis of HIV/ AIDS associated vasculopathyis multifactorial. HIV may produce protein –wasting nephropathy or endothelial cell injury, both of which may possibly contribute to alterations in circulating levels of anticoagulant proteins. Fur- thermore, reduction in CD 4+ cell count to less than 200cellss/ mm3has been observed in patients with thromboembolic com- plication. Nair et al. [4] first described the pathology in detail, which was regarded as unique to HIV/AIDS vasculopathy. They noted that inflammation was centered on the vasa vasora in the adventitia and was characterized by a vasculitis in which the ves- sels were surrounded by acuff of neutrophils, monocytes and plasma cells, which ultimately lead to occlusion of vasa vasora with resultant transmural fibrosis and necrosis. This either leads to HIV associated aneurysm formation or localized thrombosis. HIV-related thrombosis, which is segmental, shows a histological picture with inflammatory changes confined to the vasavasora with bland organizing luminal thrombus. The striking feature of this disease is the normality of the arterial tree proximal to the thrombosed arteries by duplex ultrasonography, angiography and macroscopic appearance. The other remarkable feature is the thrombosis of all distal vessels with no demonstrable runoff. Du- plex ultrasound also showed hypoechoic ‘spotting’ in the arterial wall, the’ string of pearls sign’, which also has been observed in patients with HIV associated arterial aneurysm [5,6]. Surgical thromboembolectomy is effective is restoring the circu- lation as was this case. Percutaneous mechanical thrombectomy and thrombolysis has been also found effective in various case reports. The duration of necessary anticoagulation is unknown, but gen- erally these are candidates for prolong anticoagulation due co- agulation abnormalities present in a patient of HIV/AIDS. 6. Conclusion This case highlight arterial ischemia caused by spontaneous thrombosis is a patient with HIV. The clinical diagnosis of limb threatening ischemia was prompt, as was intervention. Surgical embolectomy restored upper extremity circulation. Physicians should be aware of thromboembolic disease as the possible com- plication of HIV. References 1. Saber A, Aboolian A, Laraja R, Baron H, Hanna K. HIV/AIDS and the risk of deep venous thrombosis: a study of 45 patients with lower extremity involvement. Am Surg. 2001; 67: 645-7. 2. Joshi VV, Pawel B, Connor E. Arteriopathy in children with acquired immunodeficiency syndrome. PediatrPathol. 1987; 7: 261- 275. 3. Copur A, Smith P, Gomez V, Bergman M, Homel P. HIV infection is a risk factor for venous thromboembolism. AIDS Patient Care STDs. 2002; 16: 205-9. 4. Nair R, Abdool Carrim ATO, Chetty R, Robbs JV. Arterial aneurysms in patients infected with human immunodeficiency virus: a distinct clin- icopathological entity? J VascSurg. 1999; 29: 600-7. 5. Woolgan JD, Ray R, Maraj K, Robbs JV. Colourdoppler and grey scale ultrasound features of HIV- related vascular aneurysms. Br J Radiol 2002; 75:884-888. 6. Bush RL, Bianco CC, Bixler TJ, Lin PH, Lumsden AB. Spontaneous arterial thrombosis in a patient with human immunodeficiency virus in- fection: Successful treatment with pharamcomechanical thrombectomy. J VascSurg. 2003; 38: 392-5.