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10.1 Diabetic Hand and Diabetic Foot 355
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Fig. 10.1.10. Axial
postcontrast CT of the
scrotum and the upper thighs
shows scrotal abscess with
areas of ring contrast
enhancement ( arrows ) and
gas formation ( arrowhead );
a radiological stigma of
Fournier’s gangrene
The Role of Doppler Sonography in DM
Doppler sonography is used to detect stenosis within the
arterial system of the lower extremities. Arteriosclerosis
is the most common cause of arterial stenosis with the
formation of atheromas and calcium plaques within the
arterial walls. Analysis of the Doppler wave spectrum is
essential to detect the hemodynamic abnormalities of
circulation in the lower limbs. Different spectral waves
are observed, according to the degree of stenosis.
Signs of Peripheral Vascular Disease
on Doppler Scan (Can Be Detected Even
Before the Appearance of Clinical Symptoms)
Medial arterial wall calcifi cation with acoustic shadowing
“ string of beads sign ” (Fig. 10.1.11 ).
Increased diastolic fl ow with reduced resistance index (RI) in
the spectral fl ow analysis (Fig. 10.1.12 ). The increase in
diastolic fl ow is due to arteriovenous shunting.
Spectral fl ow abnormalities.
Spectral Flow Abnormalities on Doppler Scan
of the Lower Limbs
The normal arterial spectrum is triphasic, with peak
systolic velocity (PSV) <120 cm/s.
Fig. 10.1.11. Sagittal ultrasound image of the superfi cial femoral artery in a diabetic shows multiple dense calcifi cations of the
arterial wall ( arrowheads )
0–50% stenosis: shows triphasic or biphasic arterial
spectrum (due to loss of the reversal fl ow pattern),
with PSV <180 cm/s.
50–75% stenosis: shows biphasic or monophasic arte-
rial spectrum, with PSV >180 cm/s (Fig. 10.1.13 ).
75–99% stenosis (high grade): shows biphasic or
monophasic arterial spectrum, with PSV >250 cm/s.
As the stenosis becomes generalized and affects
a long segment of the artery, the fl ow spectrum
becomes biphasic or monophasic, the acceleration
upstroke is reduced, and the systolic peak becomes
rounded (Fig. 10.1.14 ).
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Fig. 10.1.12. Sagittal
ultrasound image of the
superfi cial femoral artery in a
patient with peripheral
vascular disease due to
diabetes mellitus (DM) shows
10.1
monophasic arterial spectral
wave with increased diastolic
fl ow ( arrowhead )
Fig. 10.1.13. Sagittal
ultrasound image of the
superfi cial femoral artery in a
patient with peripheral
vascular disease due to DM
shows monophasic arterial
spectral wave with PSV >250
cm/s ( arrowhead ), represent-
ing >75–99% arterial stenosis
10.1 Diabetic Hand and Diabetic Foot 357
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Fig. 10.1.14. Sagittal
ultrasound image of the
superfi cial femoral artery in a
patient with peripheral
vascular disease due to DM
shows monophasic arterial
spectral wave with PSV <50
cm/s ( arrowhead ). As
mentioned earlier, the normal
peripheral arterial spectral
wave for the superfi cal
femoral artery is triphasic,
with PSV <120 cm/s
Signs of Diabetic Nephropathy on Doppler
Scan
Increased renal length and parenchymal thickness due to
glomerular hyperfi ltration. The normal kidney size is 10–12 cm
in the longitudinal diameter and 4–6 cm in the transverse
diameter; the normal renal parenchymal thickness is 1.6 cm.)
RI of arcuate arteries is >0.7.
In advanced renal disease, there is increased echogenicity of the
renal cortex, with reduction of its thickness.
The Role of MRI in DM
MRI is a powerful tool to detect early bone changes
that may not be seen on plain radiographs or evoke
complaints unless they are severe and destructive.
Contrast-enhanced studies should be done to detect
signs of soft tissue infl ammation, abscess formation,
sinus tract detection, and devitalization.
Signs of Diabetic Foot on MRI
A callus is detected on MRI as a soft-tissue area of low T1
signal intensity with intense contrast enhancement after
contrast injection. It is typically found at the fi rst and fi fth
metatarsal heads, the malleoli, and the calcaneus
(Fig. 10.1.15 ).
Devitalization is an area of soft tissue that is devoid of vascular
supply (tissue infarction). It is detected on MRI as a soft tissue
area with low T1 and low T2 signal intensities, which shows
no contrast enhancement after contrast injection (like any
other tissue infarction in the body). It is important to inform
the surgeon about devitalization areas for tissue debridement
planning.
ulcer is detected as an area of skin and soft tissue defect,
An
with low signal intensity on T1W images, and intense
enhancement after contrast administration.
Cellulitis is an area of soft tissue infl ammation, and is detected
on MRI as an ill-defi ned area of soft tissue with low T1 and
high T2 signal intensities, with ill-defi ned enhancement after
contrast administration (Fig. 10.1.16 ).
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10.1
An abscess is a localized area of pus collection, and typically
detected as acystic area of low T1 and high T2 signal
intensities, with ring enhancement after contrast administration (Fig. 10.1.17 ).
Reactive bone marrow is detected as a normal (isointense)
signal intensity of the bone marrow on T1W images, with
high signal intensity on T2W images (Fig. 10.1.18 ).
Osteomyelitis is infl ammation of the bone and the bone
marrow. It is detected on MR as areas of cortical bone defect
characterized by the following characteristics: diff use bone
marrow edema, may show sequestrum, shows no bone
deformities (unless complicated by neuropathic joint), usually
underlying an ulcer (e.g., metatarsal heads), may show sinus
formation into the skin surface, and the soft tissue around it is
usually infl amed and shows marked contrast enhancement.
(Fig. 10.1.19). Signs of periostitis may be found, which is seen
as linear contrast enhancement surrounding the outer cortical
margin. An intraosseous abscess may occur in subacute
osteomyelitis ( Brodie’s abscess ), which is characterized by the
“ penumbra sign .” The penumbra sign is detected on MRI as a
discrete zone of peripheral T2 hyperintensity signal
surrounding a high T2 signal intensity intraosseous abscess
(Fig. 10.1.19 ). Osteomyelitis is classically located in a single
focus. However, multiple lesions may be seen in 20% of cases.
is infl ammation of a joint due to infection. It is
Septic arthritis
detected on MRI as high T2 signal intensity within a joint and
its surrounded soft tissue, with signs of joint eff usion and
cartilage destruction. There is intense enhancement of the
joint and its surrounding soft tissue after contrast administration (Fig. 10.1.20 ).
A foreign body is detected on MRI as an object of low T2 signal
intensity, surrounded by a high intensity signal in the soft
tissues on T2W images (due to edema around the foreign
body). (Fig. 10.1.21 )
Neuroarthropathic joint (Charcot’s joint) has the same presenta-
tion and signal intensities as osteomyelitis, with destruction of
the subchondral cortices. Neuropathic joint is characterized by:
midfoot predominance, subchondral cyst formation, normal
surrounding tissue with intact overlying skin, juxta-articular
edema, signs of joint disorganization and deformity (5Ds), and
no signs of fl uid collection or abscess (Fig. 10.1.22 ).
Osteomyelitis, in contrast to neuropathic joint, predominates in
pressure areas such as the metatarsal heads in the forefoot and
the calcaneus in the hindfoot. The only common location for
osteomylitis in the midfoot is in the cuboid bone, which occurs
in severe midfoot neuropathic joint. However, bone biopsy
remains the defi nite diagnostic method to diff erentiate
osteomyelitis from neuropathic joints in diabetics.
Tenosynovitis
: is detected as normal tendon size, surrounded
by high T2 fl uid-signal intensity on T2W images.
Calcaneal insuffi ciency avulsion fracture : is an extra-articular
fracture aff ecting the posterior third of the calcaneus
(Fig. 10.1.23 ). It is seen almost exclusively in diabetics.
Sinus tract is detected as a hypodense line extending from
an area of bone destruction to the adjacent soft tissues
(Fig. 10.1.19 ). It is best detected on postcontrast fast-
suppressed T1W images.
Fig. 10.1.15. Sagittal T1W ( a ) and STIR ( b ) ankle MR illustra-
tions demonstrate callus seen as an area of soft tissue with low
T1 signal intensity in ( a ) and with high T2 signal intensity in ( b )
( arrowheads )
10.1 Diabetic Hand and Diabetic Foot 359
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Fig. 10.1.16. Sagittal T1W
( a ) and STIR ( b ) ankle MRI
show areas of low T1 and
high T2 signal intensity
lesions confi ned to the skin
and the subcutaneous tissue,
without signs of bone marrow
edema or joint effusion
( arrowheads ), representing
cellulites
Fig. 10.1.17. Sagittal T1W
postcontrast ( a ) and STIR ( b )
ankle MR illustrations
demonstrate abscess
formation, seen as a cystic
area surrounded by rim
contrast enhancement in ( a ),
and seen as an area of cystic
fl uid collection in ( b )
Fig. 10.1.18. Sagittal T1W
( a ) and STIR ( b ) ankle MR
illustrations demonstrate
reactive bone edema affecting
the posterior third of the
calcaneus
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10.1
Fig. 10.1.19. Sagittal T1W postcontrast ( a ) and STIR ( b ) ankle
MR illustrations show signs of osteomyelitis. Notice the calcaneal ulcer with edema ( white arrowhead ), the penumbra sign
( black arrowhead ), sinus tract from the osteomyelitis spreading
infection to the nearby soft tissues ( arrow ), and signs of perios-
titis seen as linear high signal intensities located around the cortex of the calcaneus ( hollow arrowhead )
Fig. 10.1.21. Sagittal STIR ankle MR illustration demonstrates
a foreign body surrounded by tissue edema located within the
infracalcaneal soft tissue region
Fig. 10.1.20. Sagittal STIR ankle MRillustration demonstrates
talo-navicular joint septic arthritis, seen as bone marrow edema
affecting the articular bones with joint effusion
10.1 Diabetic Hand and Diabetic Foot 361
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inability to perceive pain stimuli due to peripheral
autonomic nervous system demyelination and reduced
fi ber caliber. CIPA patients respond to normal pain
stimuli, but not to painful stimuli. Early symptoms
include decreased sweating (anhydrosis), which causes
episodes with extreme hyperpyrexia, multiple healed
tongue bites since infancy, and multiple missing teeth
due to auto-extraction (50% of cases). Characteristically,
CIPA patients present with multiple bony features at
varying stages of the healing process. Interestingly,
patients with CIPA develop aseptic necrosis and osteochondritis in the juxta-articular regions of the weightbearing long bones (hip, knees, and ankles). Joint
radiographs of CIPA patients show changes similar to
those of chronic Charcot’s joint and osteomyelitis.
Fig. 10.1.22. Sagittal STIR ankle MR illustration demonstrates
talo-navicular Charcot’s joint. Notice the midfoot location, the
joint deformity ( arrow ), the subchondral cysts ( arrowhead ), and
the mild joint effusion due to reactive infl ammation
Fig. 10.1.23. Sagittal T1W ankle MR illustration demonstrates
avulsion fracture of the posterior third of the calcaneus
( arrowheads )
Diff erential Diagnoses and Related Diseases
Congenital insensitivity to pain (CIPA) : CIPA, also
referred to as hereditary sensory and autonomic neu-
ropathy type IV , is a rare disorder characterized by the
For Further Reading
1 . Chatha DS et al MR imaging of the diabetic foot: diagnostic
challenges. Radiol Clin N Am. 2005;43:747–59
2 . Puttemans T et al Diabetes: the use of color Doppler sonog-
raphy for the assessment of vascular complications. Eur J
Ultrasound. 1998;7:15–22
3 . Beltran J et al The diabetic foot: magnetic resonance imag-
ing evaluation. Skeletal Radiol. 1990;19:37–41
4 . Gefen A et al Integration of plantar soft tissue stiffness
measurements in routine MRI of the diabetic foot. Clin
Biomech. 2001;16:921–25
5 . Marcus CD et al MR imaging of osteomyelitis and neuro-
pathic osteoarthropathy in the feet of diabetics. RadioGraphics. 1996;16:1337–48
6 . Biswal N et al Congenital indifference to pain. Indian J
Pediatr. 1988;65:755–69
7 . Abdel-Hafez HZ et al Congenital insensitivity to pain with
anhidrosis (CIPA). Egyptian Dermatol Online J. 2007; 3(1):5
8 . Purewal TS. Charcot’s diabetic neuroarthropathy: patho-
genesis, diagnosis and management. Pract Diab Int. 1996;
13(3):88–91
9 . Chuter V et al Limited joint mobility and plantar fascia func-
tion in Charcot’s neuroarthropathy. Diabet Med. (2001);18,
558–61
10 . Tiwari S et al Tropical diabetic hand syndrome. Int J Diab
Dev Ctries. 2008;28(4):130–31
11 . Jung Y et al Diabetic hand syndrome. Metabolism. 1971; 20
(11), 1008–1015
12 . Peyri J et al Necrobiosis Lipoidica. Semin Cutan Med Surg.
26:87–89
13 . McGuinness M et al Necrobiosis Lipoidica diabeticorum.
Foot. 1997;7:47–51
14 . Nguyen K et al Necrobiosis Lipoidica diabeticorum treated
with chloroquine. J Am Acad Dermatol. 2002;46:S34–6
15 . Naderi ASA et al Diabetic muscle necrosis. J Diabet
Complications. 2008;22:150–52
16 . Glauser SR et al Diabetic muscle infarction: a rare compli-
cation of advanced diabetes mellitus. Emerg Radiol 2008;15:
61–65
362 Chapter 10 Diabetology
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10.1
17 . Gold RH et al Imaging the diabetic foot. Skeletal Radiol.
1995;24:563–71
18 . Beltran J et al The diabetic foot: magnetic resonance imag-
ing evaluation. Skeletal Radiol. 1990;19:37–41
19 . Reinhardt K. The radiological residua of healed diabetic
arthropathies. Skeletal Radiol. 1981;7:167–72
20 . Chantelau E et al “Silent” bone stress injuries in the feet of
diabetic patients with polyneuropathy: a report on 12 cases.
Arch Orthop Trauma Surg. 2007;127:171–77
21 . Erickson SJ et al MR imaging of the tarsal tunnel syndrome
and related spaces: normal and abnormal fi ndings with
anatomic correlation. AJR. 155:323–28
22 . Bhute D et al Dermatographism. Ind J Dermatol Venerol
Leprol. 2008;74:177–79
23 . Piedra T et al Fournier’s gangrene: a radiologic emergency.
Abdom Imaging. 2006;31:500–502
24 . Bhanushali MJ et al Diabetic and non-diabetic lumbosacral
radiculoplexus neuropathy. Neurology India. 2008;56(4):
420–25
25 . Nguyen VD et al Freiberg’s disease in diabetes mellitus.
Skeletal Radiol. 1991;20:425–28
26 . Tan PL et al MRI of the diabetic foot: differentiation of infec-
tion from neuropathic change. Br J Radiol. 2007;80: 939–48
27 . Singson RD et al Postamputation neuromas and other
symptomatic stump abnormalities: detection with CT.
Radiology. 1987;162:743–45
28 . Singson RD et al Postamputation neuromas. Skeletal Radiol.
1990;19:259–62
10.2 Diabetic Brain and Nervous System 363
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10.2
Diabetic Brain and Nervous System
In advanced stages, diabetes mellitus (DM) can affect
the brain, due to microangiopathy and prolonged exposure to hypoglycemia. Over the past decade, many
researches have evaluated the anatomical and functional status of the brain in diabetics compared to the
normal population. This topic presents the most common, well-documented brain changes in diabetics, as
reported in the medical and radiological literature.
DM type 1 can be associated (rarely) with chorea-ballismus episodes due to nonketotic hyperglycemia (NKH).
The cause of these chorea-ballismus episodes is unknown,
but it is believed that they are vascular in origin.
Chorea is defi ned as involuntary, continuous, ran-
dom, fast, jerking, dance-like movements in the distal
parts of the limbs. Ballismus shows a picture similar to
chorea, but the movements are more irregular, of large
amplitude, and violent, affecting the proximal portion
of limbs.
Nonketotic hyperglycemia (NKH) is a severe form of
hyperglycemia with hyperosmolarity and intracellular
dehydration, with little or no ketoacidosis. It is typically
observed in diabetic patients >50 years of age. NKH is
characterized by partial insulin defi ciency with enough
insulin to inhibit ketoacidosis, but not enough to transport glucose into the cells. Hyperglycemia causes an
osmotic diuresis, with progressive dehydration, resulting in NKH. Up to 40% of patients with NKH develop
seizures beside the chorea-ballismus episodes.
The incidence of stroke is six times higher in patients
with DM than in nondiabetics. This high stroke risk can
be explained by the high incidence of atherosclerosis of
the internal carotid artery in diabetics.
Many researchers reported high cerebral brain atrophy among long-term diabetics. Patients with DM type
2 were found to have an increased risk of Alzheimer’s
disease (AD) and vascular dementia. AD in diabetics
is believed to be due to the increase in advanced glycation end products, which increase aggregation of proteins involved in AD development. Furthermore,
dysfunction of insulin signaling in the brain has been
implicated in the pathogenesis of AD. Subcortical
arteriosclerosis encephalopathy can develop in diabetics due to brain vessel atherosclerosis.
Cranial nerve involvement in DM is a rare complication. A single cranial nerve ( diabetic mononeuritis ) or
multiple cranial nerves ( mononeuritis multiplex ) can be
involved. DM classically affects the cranial nerves CN
III, CN IV, CN VI, and CN VII. Cranial nerve involvement in diabetes is thought to be a result of microvasculitis and resultant ischemic injury to the nerves.
Patients with diabetic ketoacidosis (DKA) can
develop subclinical cerebral edema for unknown reasons. The brain edema can start before or after treatment
initiation. Patients with DM type 1 are most commonly
affected, and it occurs in > 1% of cases. Typically,
patients present with severe headaches that can progress
(rarely) into brain herniation. Other manifestations of
symptomatic brain edema due to DKA include a drop in
heart rate, altered mental status that ranges from dizziness to coma, and increased blood pressure.
Signs on CT and MRI
Stroke is seen as a hypodense area on CT or a hyperintense
area on T2W MR images. Focal neurological defi cits and the
clinical picture suggest the diagnosis.
In NKH-ballismus episode , CT scan of the basal ganglia
(caudate and putamen) are hyperdense compared to the rest
of the brain parenchyma (Fig. 10.2.1 ). Normal basal ganglia
attenuation is between 33 and 36 HU. In diabetic chorea, the
basal ganglia show attenuation between 40 and 51 HU. This
fi nding is believed to be caused by multiple petechial
hemorrhages within the basal ganglia. On MRI, the basal
ganglia show hyperintense signal intensity on both T1W and
T2W images (Fig. 10.2.1 ). This sign is not specifi c, and can be
observed in cases of hepatic encephalopathy, carbon
monoxide toxicity, Wilson disease, and neurofi bromatosis.
Generalized brain atrophy is seen in diabetics with signs of
dementia. The hippocampus and the amygdale volume are
reduced in diabetics who develop signs of dementia.
Signs of subcortical arteriosclerosis encephalopathy may be
seen when the clinical status of the patient suggests
dementia.
Diabetic mononeuritis is detected as enhancement of the
aff ected cranial nerve after contrast injection ipsilateral to the
site of cranial nerve clinical defi cits. Multiple cranial nerve
enhancements are seen in mononeuritis multiplex.
Diabetic ketoacidosis brain edema often shows signs of loss of
gray-white matter diff erentiation, eff acement of the sulci,
and decrease in ventricular size
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Fig. 10.2.1. Axial nonenhanced brain CT ( a ) and MR
( b ) illustrations demonstrate
high density basal ganglia ( a )
and high intensity signal of
the basal ganglia ( b ), which
10.2
is a sign detected in patients
with ballismus episodes and
in patients with nonketotic
hyperglycemia
For Further Reading
1 . Araki Y et al MRI of the brain in diabetes mellitus.
Neuroradiology. 1994;36:101–3
2 . Lai PH et al Chorea-ballismus with nonketotic hyperglyce-
mia in primary diabetes mellitus. AJNR Am J Neuroradiol.
1996;17:1057–64
3 . Lavin PJM. Hyperglycemic hemianopia: a reversible com-
plication of non-ketotic hyperglycemia. Neurolog y. 2005;65:
616–19
4 . den Heijer T et al Type 2 diabetes and atrophy of medial
temporal lobe structures on brain MRI. Diabetologia. 2003;
46:1604–10
5 . Harten BV et al Brain imaging in patients with diabetes.
A systematic review. Diabetes Care. 2006;29(11):2539–46
6 . Brands AMA et al Cognitive functioning and brain MRI in
patients with type 1 and type 2 diabetes mellitus: a comparative study. Dement Geriatr Cogn Disord. 2007;23:
343–50
7 . Kelkar P et al Mononeuritic multiplex in diabetes mellitus:
evidence for underlying immune pathogenesis. J Neurol
Neurosurg Psychiatry. 2003;74;803–6
8 . Witzke KA et al Diabetic neuropathy in older adults. Rev
Endocr Metab Disord. 2005;6:117–27
9 . Pacheco E et al Pathophysiology and computed tomogra-
phy fi ndings in a case of diabetic ketoacidosis. Int Pediatr.
1999;14(2):118–20
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