Download Diabetic muscle infarction

Neuromuscular
disorder
in Diabetes mellitus
R3 Kim Hyun Soo
Differential diagnosis of painful swelling of
an extremity in a patient with diabetes
Infection
Inflammatory
Vascular
Neoplastic
Miscellaneous
Cellulitis
Polymyositis
dermatomyositis
Deep venous
thrombosis
Benign: lipoma,
fibroma, or
leiomyoma
Diabetic muscle
infarction
Myositis,
inclusion body
Haemorrhage
(haematoma)
Malignant:
liposarcoma
Calcific uraemic
arteriolopathy
Soft tissue
abscess
Necrotising
fasciitis
Thrombophlebitis Neurological
Osteomyelitis
with soft
tissue
involvement
Arterial occlusion
Diabetic
lumbosacral
radiculoplexopathy
(amyotrophy)
Drug induced
(statins)
Parasitic
infestation
Post traumatic
pseudoaneurysm
Bruns-Garland
syndrome
Rhabdomyolysis
BMJ 2009;338
Trauma
2
Diabetes muscle infarction
3
Epidemiology
1. The first case was reported in 1965 by Angervall and
Stener.
2. Reported 86 cases till 2001.
1. 65 patients : type 1 diabetes, 19 patients: type 2 diabetes,
2 patients: undetermined
2. The male/female ratio: equal (44/42), In some article more
common in female
3. Age range of 19–81 years
4. Longstanding diabetes and extensive end-organ damage due to
microvascular disease
Ann Rheum Dis 2001;60:310–312
4
Am J Med. 1996; 101:245-250.
Clinical presentation
1.
2.
3.
4.
5.
6.
7.
Atraumatic swelling of the limb, most commonly the thigh.
Quadriceps(83.7%), Vastus lateralis(24%), vastus medialis(22%),
calf involvement(19.28%)
The onset of pain is usually abrupt, but can be gradual.
The local swelling, palpable painful mass
Fever was present in 10%
No skin color change
The white cell count and the level of CK are normal or slightly
raised.
Often associated with microvascular complications (nephropathy,
retinopathy, or neuropathy) of diabetes
Ann Rheum Dis 2001;60:310–312
DIABETES CARE, 26, NUMBER 1, JANUARY 2003
5
Clinical presentation
DIABETES CARE, 26, NUMBER 1, JANUARY 2003
6
pathophysiology
1.
Unclear,, several hypothesis
Most likely hypothesis- vascular disease such as
arteriosclerosis and diabetic microangiopathy
Alteration in the coagulation-fibrinolysis system, in the
form of hypercoagulability
Palmer and Greco
antiphospholipid
Gargiulo et al.
antibodies
Galtier-Dereure et al.
hypoxia-reperfusion injury- Silberstein, Britton, Marsh, et
al.
DIABETES CARE, 26, NUMBER 1, JANUARY 2003/
Ann Rheum Dis 2001;60:310–312
7
Investigations and diagnosis
Combination of clinical presentation and radiological imaging
The most valuable diagnostic technique is MRI.
Increased signal intensity in T2-weighted MRI images
with marked muscle oedema extending into the perifascicular
and subcutaneous tissues
Radiographic films, US, CT, gallium scintigraphy
Needle electromyography of the muscle
Biopsy
DIABETES CARE, 26, NUMBER 1, JANUARY 2003
8
prognosis
The short-term prognosis of diabetic muscle
infarction is good
Recurrence has been reported in a total of 55
cases (47.82%): 10 cases (8.69%) involving the
originally affected muscle and 45 cases (39.13%)
involving another muscle.
Long term prognosis is poor
DIABETES CARE, 26, NUMBER 1, JANUARY 2003
9
management
Bed rest and analgesics
Nonsteroidal anti-inflammatory drugs,
glucocorticoids, aspirin, and
pentoxyphylline
Some authors- anticoagulant agents
DIABETES CARE, 26, NUMBER 1, JANUARY 2003
10
Diabetic Muscle Infraction: An unusual cause
of muscle pain in a diabetic patient on
hemodialysis
A 36-year-old diabetic woman referred to our clinic with
severe pain in the left anteromedial thigh. She had a 15year history of Type 2 diabetes mellitus (DM). She was
complicated by diabetic nephropathy and requiring
hemodialysis.
Clinical and laboratory evaluation, and muscle biopsy
revealed the diagnosis of muscle infarctions. She did no
respond to the conservative therapy. Pain and swelling
in her thigh worsened progressively. She underwent
surgical debridment and then, her clinical status
improved.
International Urology and
Nephrology (2005) 37:629–632
11
Diabetic lumbosacral
radiculoplexopathy
(amyotrophy)
12
overview of diabetic neuropathy
involvement of peripheral and autonomic nervous
system
 probably the most common complication of diabetes
occurs in ~50% of individuals with long-standing type 1
or type 2 DM
Prevalence is a function of disease duration and of
glycemic control.
BMI and smoking are known to be another risk factors.
13
Risk factors
14
Classification
15
DLRPN
subtype of diabetic polyradiculopathy
aka Bruns-Garland syndrome, diabetic myelopathy,
diabetic amyotrophy, diabetic mononeuritis multiplex,
diabetic polyradiculopathy, femoral or femoral–sciatic
neuropathy of diabetes, diabetic motor or paralytic
neuropathy, proximal diabetic neuropathy
Involvement : nerve root, lumbosacral plexus, peripheral
nerve
most common type: high lumbar radiculopathy involving L2, L3
and L4 roots
16
Comparison
DLRPN
Polyneuropathy
Onset
Abrupt
Insidual
Location
Focal
Diffuse
Initial symptome
Unilateral
Symmetrical
Complication
Rare
Often
Glycermic control
Well controlled
Not well controlled
Weight loss
Frequent
Not frequent
DM duration
Short
Long
17
Clinical features
initially asymmetrical/unilateral involvement in hip and
thigh
 quickly spreading to unaffected/contralateral side
Although pain is the most prominent early symptom,
weakness soon becomes the major symptom.
The average of bilateral disease: 3 months
Early wasting of Quadriceps muscleatrophy
Autonomic impairment such as orthostatic intolerance
and sphincter control
Muscle Nerve 25:477-491, 2002 ,
Neurol India. 2008;56(4):420-5
18
Prognosis
Although substantial improvement could be expected, recovery is
usually delayed and incomplete.
Persistent pain and weakness tend to remain.
 m/c long-term problem : foot drop
Jeniffer et al. 33 patients with DLRPN,
only one did not develop bilateral involvement
one-half require the use of a wheelchair
16 require ongoing assistive aids at long-term F/U (2 years)
Pascoe et al. 21 patients
three years from the onset of symptoms
12 had resumed normal walking, seven ambulated with an aid
and two were wheelchair-bound
Phys Med Rehabil Clin N Am. 2009
Mayo Clin Proc 1997;72:1123-3
19
pathophysiology
an immune attack and probably microvasculitis of nerve
some degree of inflammation, mostly surrounding
epineurial microvessels
inflammatory cells disrupted vessel walls, possibly
causing microvasculitis
evidence of bleeding due to vessel
 damage: hemosiderin-laden macrophage
Muscle Nerve 25:477-491, 2002
20
pathophysiology
normal
A
B
C
D
E
F
microvasculitis
Muscle Nerve 25:477-491, 2002
21
Diagnosis
mainly based upon the presence of suggestive clinical
features
MR-r/o compression, hematoma, tumor
electrodiagnositic studies
1. nerve conduction study
 reduced amplitude of the muscle/sensory nerve action potential
 only mild slowing of conduction velocity
2. needle electromyelography (EMG)
 Acutefibrillation potential, positive shock wave, decreased
motor unit recruitment
 Chronichigh amplitude, long duration motor unit action
potential
Mayo Clin Proc 56:725-735, 1981
treatment
Immune suppression
Symptomatic treatment
narcotic medications (TCA or anti-seizure
agents)
anti-depressants may be helpful.
exercise, gait training, equipment/orthotics
23
Immunotherapy
A retrospective study by Pascoe et al (1997)
Treated or untreated with immunosuppressive
agents (either steroids, intravenous immune
globulin or plasma exchange).
higher rate of improvement (9 of 12 patients) in
the treated group compared to the untreated
group (17 of the 29 patients )
Mayo Clin Proc 1997;72(12):1123–32.
24
Immunotherapy
A randomized double-blinded placebo-controlled prospective
treatment trial Seventy-five patients
placebo or IV methylprednisolone
at baseline, and at weeks 1, 6, 12, 24, 36, 52, and 104.
The primary outcome -time to improvement in NIS(LL) by four
points.
No significant difference between the two groups in time to
improvement in the NIS(LL) by four points
the decision to initiate immunosuppression
individualized considering the clinical presentation, relative
acuity and time between symptom onset (less than three
months), extent of disability and severity of symptoms, as well
as the risks and benefits in a given patient
Neurology 2006;662):A191
25