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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 muscleatrophy 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) Acutefibrillation potential, positive shock wave, decreased motor unit recruitment Chronichigh 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