Brief Reports

Acute Aortoiliac and Femoral Artery

Thrombosis Complicating Diabetic Ketoacidosis
Stan Zipser, MD, JD, Carl M. Kirsch, MD, Conway Lien, MD, Tej M. Singh, MD, and Young S. Kang, MD

Acute abdominal aortic occlusion is a devastating event with high associated rates of morbidity and mortality even
with surgical intervention. This report describes a case of acute aortoiliac and femoral artery occlusion likely resulting
from a hypercoagulable state caused by diabetic ketoacidosis (DKA). Vascular thrombosis is a little-known but
potentially devastating complication of DKA that should be considered in every patient treated for DKA and should
be added to the differential diagnoses when attempting to determine the etiology of a thrombosed vessel.
J Vasc Interv Radiol 2005; 16:17371739
Abbreviation:

DKA diabetic ketoacidosis

ACUTE abdominal aortic occlusion is

a devastating event with high associated rates of morbidity and mortality
even with surgical intervention (1,2). It
is most often caused by a cardiac embolus or in situ thrombosis from an
atherosclerotic abdominal aorta. Other
reported etiologies include sudden
thrombosis of a small abdominal aortic aneurysm, thrombosis from a hypercoagulable state, and trauma (1,2).
We present a case of acute aortoiliac
and femoral artery occlusion that we
believe was caused by a hypercoagulable state resulting from diabetic ketoacidosis (DKA).

CASE REPORT
Our institution does not require institutional review board approval for

From the Department of Diagnostic Imaging (S.Z.,

C.L., Y.S.K.); Division of Respiratory and Critical
Care Medicine, Department of Medicine (C.M.K.);
and Division of Vascular Surgery, Department of
Surgery (T.M.S.), Santa Clara Valley Medical Center;
751 Bascom Avenue, San Jose, California 95128. Received April 24, 2005; revision requested May 12;
revision received May 29; accepted June 2. Address
correspondence to S.Z.; E-mail: stanzipser@
hotmail.com
None of the authors have identified a conflict of
interest.
SIR, 2005
DOI: 10.1097/01.RVI.0000175321.56202.8D

retrospective reports. A 52-year-old

man was brought to the emergency
room by paramedics because of increasing lethargy and altered mental
status. The patients blood pressure
was 96/48 mm Hg, heart rate was 66
bpm, respiration rate was 18 breaths
per minute, and temperature was
37.2C. Additional history included 3
weeks of polydipsia and polyuria. The
patient had a history of asthma and a
remote history of smoking. There was
no history of diabetes, hypertension,
heart disease, peripheral vascular occlusive disease, or hypercoagulable
state. Initial laboratory tests revealed a
serum glucose level of 1,584 mg/dL
(normal, 70 200 mg/dL), serum acetone ratio of 1:16, and serum osmolality of 393 mOsm/kg (normal, 281297
mOsm/kg). Other laboratory results
included a creatinine level of 4.1 mg/dL
(normal, 0.71.4 mg/dL) and arterial
blood gas with a pH of 7.19. Complete
blood count showed a white blood cell
count of 14,300/L. Electrocardiography revealed sinus tachycardia.
The patient was confused and incoherent. A new diagnosis of diabetes
was made and the patient was admitted to the intensive care unit for treatment of DKA. On the morning after
the admission, the patient reported abdominal pain. He was found to have
cool lower extremities and only a right
femoral pulse was detected. The Vas-

cular surgery service was consulted

emergently who suspected acute aortoiliac thrombosis, and full-dose unfractionated peripheral intravenous
heparin drip was started. Because of
the patients increased creatinine level,
noncontrast computed tomography
(CT) and gadolinium-enhanced magnetic resonance arteriography (MRA)
of the abdominal aorta and iliac and
lower-extremity arteries were performed. CT was remarkable for distal
aorta with a normal diameter and lack
of atherosclerotic calcification. MRA
demonstrated near-complete occlusive
thrombus within the distal abdominal
aorta extending into the common iliac
arteries bilaterally. The left common
iliac artery was completely occluded
and the right was nearly completely
occluded (Fig). Flow beyond the common iliac arteries was likely from collateral flow through internal iliac arteries; however, the MR acquisition
plane did not include this entire region. Thrombus was also present in
the left common femoral artery and,
except for a short proximal segment,
the left superficial femoral artery was
completely occluded just beyond its
origin. No patent vessels were present
below the level of the knees bilaterally.
A hypercoagulability laboratory
panel was obtained, which revealed
an activated protein C concentration
of 20% (normal, 73%174%), activated

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Aortoiliac and Femoral Artery Thrombosis in Diabetic Ketoacidosis

December 2005

JVIR

Figure. Images from a 52-year-old man with DKA. (a) Gadolinium-enhanced coronal collapsed MR angiographic image (repetition
time/echo time, 5.9 msec/1.152 msec; flip angle, 45) demonstrates distal aortic, bilateral common and external iliac, and left femoral
artery occlusion. (b) Gadolinium-enhanced coronal source MR angiographic image (repetition time/echo time, 5.9 msec/1.152 msec; flip
angle, 45) demonstrates a narrow patent region through the right common iliac artery.

protein S concentration of 19% (normal, 63%155%), antithrombin III function of 24% (normal, 80%131%), and
fibrinogen level of 151 mg/dL (normal,
200 400 mg/dL). Cardiolipin screen,
lupus anticoagulant, factor V Leiden,
and prothrombin 20210A were negative. No echocardiogram was obtained.
The patient underwent an emergent
aortic and bilateral iliofemoral artery
embolectomy and bilateral below-knee
amputations. On postoperative day 1,
the patient developed worsening hypotension despite three vasopressive
agents. Creatinine kinase measured
150,000 U/L and renal function worsened rapidly with corresponding hyperkalemia and increasing metabolic acidosis consistent with rhabdomyolysis and
reperfusion injury. Hemodialysis was
initiated. On postoperative day 4, after
all resuscitative measures were exhausted, the patient died. No autopsy
was performed.

DISCUSSION
DKA has been found to promote a
prothrombotic state and to activate the
vascular endothelium. Free protein S

and protein C activity levels have been

shown to decrease, and von Willebrand factor has been shown to increase, during DKA and its treatment,
raising the risk of vascular thrombosis
(3). The metabolic insult of DKA may
also initiate or perturb the steady state
of vascular endothelial cells, changing
the hemostatic profile and resulting in
a prothrombotic state (3). In addition,
even in the absence of DKA, diabetes
mellitus has been asserted to present a
hypercoagulable state. Coagulation
markers and multiple clotting factors,
including factors VII, VIII, XI and XII,
and von Willebrand factor, are increased in diabetes (4). Protein C has
also been shown to be decreased, and
there is increased platelet aggregation
in diabetes. Various investigators have
found normal, increased, and decreased levels of antithrombin III in
uncomplicated diabetes (4).
For review, von Willebrand factor
is synthesized and secreted by endothelial cells, facilitates platelet adhesion, and serves as a carrier protein for
factor VIII. Proteins C and S and antithrombin III are inhibitors that limit
thrombin generation and fibrin forma-

tion. Defects in any of these proteins

predispose patients to thrombus formation. Heparin enhances the inhibitory effects of antithrombin III. Activated protein C may also stimulate
fibrinolysis and accelerate clot lysis
(35).
Many clinical instances of hypercoagulability and vascular thrombus formation in the setting of DKA have
been reported in the literature. In a
study of 610 patients with DKA or
hyperosmolar coma during a 16-year
period, six of 38 deaths were attributed to mesenteric or iliac artery
thromboses (6). No discussion about
etiology was presented in this study.
Two studies (7,8) have shown an increased incidence of deep venous
thrombosis (DVT) in pediatric patients
with femoral vein catheters in DKA
compared with age-matched control
patients with circulatory shock who
also had femoral vein catheters but not
in DKA. In these studies, the authors
conjectured that the increase in thrombotic events may be a result of hyperglycemia and DKA causing an increase in platelet aggregability, red
blood cell rigidity, resistance to blood

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Number 12

flow, and possibly dehydration (7,8).

Interestingly, in two of three patients,
all 18 months of age or younger, protein S levels were decreased, but protein C, antithrombin III, homocysteine,
and factor VIII concentrations were
normal. Pediatric patients with DKA
are also known to be at risk for cerebral ischemic events (3). Additionally,
in a case report (9) in which DKA was
implicated as the cause of pulmonary
thromboembolism in an adult, the authors proposed that patients with
DKA be routinely evaluated for lowerextremity DVT because of their increased risk of thromboembolic complications.
Our patients hypercoagulability
profile comports with the studies asserting that DKA and diabetes promote a prothrombotic state. The patients protein S, protein C, and
antithrombin III levels were decreased
whereas the remainder of the hypercoagulability laboratory panel results,
assessing for an inherited hypercoagulable state, was negative. The patient
had no clinical history of a clotting
disorder or peripheral arterial occlusive disease significantly decreasing
the likelihood this event was a result
of in situ thrombosis from one of these
causes. Although no echocardiogram
was obtained, there was no history of
cardiac disease including arrhythmia.
The patient was in sinus rhythm during the period before the thrombosis

Zipser et al

was diagnosed, which makes cardiac

embolus an unlikely cause for this
event.
As exemplified by this case, imaging findings of a thrombosed vessel as
a result of DKA are nonspecific. Establishing DKA as the etiology of the
thrombosis involves excluding other
causes of thrombosis such as other
prothrombotic states and a cardiac
source. As in other cases of vascular
thrombosis, in addition to correcting
the DKA, treatment will vary with the
location and severity of the thrombosis. Anticoagulation, catheter-directed
pharmacologic or mechanical thrombolysis, or surgical thrombectomy
may be undertaken as indicated.

CONCLUSION
In conclusion, we present a case of
acute aortoiliac and lower-extremity
arterial thrombosis in a patient with
DKA. We believe that DKA caused a
prothrombotic, hypercoagulable state
that led to the acute thrombotic event.
Acute vascular thrombosis from DKA
in the adult population is a littleknown but potentially devastating
complication of DKA that should be
considered in every patient treated for
DKA. In addition, the interventional
radiologist should add this entity to
the differential diagnosis when encountering an acutely thrombosed
vessel.

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