Complications of type 2 Diabetes mellitus


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Complications of type 2 Diabetes mellitus

  1. 1. Dr.Debajyoti Chakraborty PGT UnitII G.M.
  2. 2.       Diabetic Glomerulopathy* (including diabetic tubulopathy) Renal artery stenosis Papillary necrosis Renal tubular acidosis Urinary tract infections CIN
  3. 3.  Diabetic nephropathy is the leading cause of ESRD in the United States and a leading cause of DM-related morbidity and mortality . Both microalbuminuria and macroalbuminuria in individuals with DM are associated with increased risk of cardiovascular disease. Individuals with diabetic nephropathy comm only have diabetic retinopathy .
  4. 4. Approximately one third of type 1 diabetic patients will have a GFR higher than the upper normal range of age matched healthy nondiabetic subjects. The degree of hyperfiltration is less in type 2 diabetic patients and reported lacking in some studies. The GFR elevation is particularly pronounced in newly diagnosed diabetic patients and during other intervals with poor metabolic control. Intensified insulin treatment and nearnormal blood glucose control reduce GFR toward normal levels after a period of days to weeks in both type 1 and type 2 diabetic patients
  5. 5.  Assess urine albumin excretion annually (B) ◦ In type 1 diabetic patients with diabetes duration of ≥5 years ◦ In all type 2 diabetic patients at diagnosis  Measure serum creatinine at least annually (E) ◦ In all adults with diabetes regardless of degree of urine albumin excretion ◦ Serum creatinine should be used to estimate GFR and stage level of chronic kidney disease, if present
  6. 6. .Under most circumstances untimed (‗‗spot‘‘) urine samples should be used to detect and monitor proteinuria in children and adults. • It is usually not necessary to obtain a timed urine collection (overnight or 24hour) for these evaluations in either children or adults. • First morning specimens are preferred but random specimens are acceptable if first morning specimens are not available. • In most cases screening with urine dipsticks is acceptable for detecting proteinuria. Patients with a positive dipstick test should undergo confirmation of proteinuria by a quantitative measurement (ACR)within 3 months. • Patients with two or more +ve quantitative tests temporally spaced by1to2 weeks should be diagnosed as having persistent proteinuria and undergo further evaluation and management for ckd. • Monitoring proteinuria in patients with chronic kidney disease should be performed using quantitative measurements.
  7. 7. Kimmelstein wilson lesion
  8. 8.    Light chain deposition disease Amyloidosis Nodules may occur in advanced stages of subendothelial membranoproliferative or mesangiocapillary glomerulonephritis, also called membranoproliferative or mesangiocapillary glomerulonephritis type 1
  9. 9.   a large majority of patients have albuminuria. Lack of albuminuria may occur in DN rarely but should prompt for search of alt. cause for altered RFT the urinary sediment is characteristically unremarkable—i.e., there are usually no casts, no white blood cells, and no red blood cells—although red blood cells (2 to 15 /hpf) may be seen in up to 30% of patients , still active sediments are to be always suspected as a herald for other diseases Most common: interstitial nephritis>PIGN> memb. Neph.>FSGS
  10. 10.   the majority of patients have retinopathy before the onset of diabetic kidney disease. Lack of retinopathy in face of progressive renal injury must draw attention as previously noted, the duration of the disease is also important; it is relatively unusual to diagnose diabetic nephropathy before 5 years of diabetes.
  11. 11. There are some novel markers for estimation of stage of ckd like cystatin based GFR, urinary glycoprotein, CYP24A1, MANBA, CUNB(gene polymorphisms) but recent KDOQI guidelines have recommended that these are not required at present to include in monitoring ckd pts.
  12. 12. eGFR Recommendation for monitoring of eGFR All patients Yearly (rule out possibility of NDRD) 45-60 6 monthly 30-44 3 monthly <30 Referal to nephrologist <60 Evaluate for complications of CKD According to Kdoqi guidelines every pt. s with stage3 & above should be evaluated for bone disease by routine measurements of Ca2+ , PO43- , iPTH for evaluation of bone disease .
  13. 13. Microalbuminuria(30299mg/d)
  14. 14.     Lowering A1C to below or around 7% has been shown to reduce microvascular complications and, if implemented soon after the diagnosis of diabetes, is associated with long-term reduction in macrovascular disease (B) Therefore, a reasonable A1C goal for many nonpregnant adults is <7% (B) Providers might reasonably suggest more stringent A1C goals (such as <6.5%) for selected individual patients, if this can be achieved without significant hypoglycemia or other adverse effects of treatment (C) Appropriate patients might include those with short duration of diabetes, long life expectancy, and no significant CVD (C)
  15. 15. Less stringent A1C goals (such as <8%) may be appropriate for patients with (B) History of severe hypoglycemia, limited life expectancy, advanced microvascular or macrovascular complications, extensive comorbid conditions • Consider aspirin therapy (75–162 mg/day) (C) As a primary prevention strategy in those with type 1 or type 2 diabetes at increased cardiovascular risk (10-year risk >10%) Includes most men >50 years of age or women >60 years of age who have at least one additional major risk factor Family history of CVD Hypertension Smoking Dyslipidemia
  16. 16.     Use aspirin therapy (75–162 mg/day) ◦ Secondary prevention strategy in those with diabetes with a history of CVD (A) For patients with CVD and documented aspirin allergy ◦ Clopidogrel (75 mg/day) should be used (B) Combination therapy with aspirin (75–162 mg/day) and clopidogrel (75 mg/day) ◦ Reasonable for up to a year after an acute coronary syndrome (B) Nonpregnant patient with modestly elevated (30299 mg/day) (C) or higher levels (≥300 mg/day) (A) of urinary albumin excretion ◦ Use either ACE inhibitors or ARBs
  17. 17.     Reduction of protein intake may improve measures of renal function (urine albumin excretion rate, GFR) (B) 1. To 0.8–1.0 g/kg body wt per day in those with diabetes, earlier stages of CKD 2.To 0.8 g/kg body wt per day in later stages of CKD When ACE inhibitors, ARBs, or diuretics are used, monitor serum creatinine and potassium levels for the development of increased creatinine or changes in potassium (E)dm comp1.docx Reasonable to continue monitoring urine albumin excretion to assess both response to therapy and disease progression (E) When estimated GFR is <60 mL/min/1.73 m2, evaluate and manage potential complications of CKD (E)
  18. 18.      People with diabetes and hypertension should be treated to a systolic blood pressure goal of <140 mmHg (B) Lower systolic targets, such as <130 mmHg, may be appropriate for certain individuals, such as younger patients, if it can be achieved without undue treatment burden (C) Patients with diabetes should be treated to a diastolic blood pressure <80 mmHg (B) For BP>120/80 lifestyle & dietary changes, if BP>140/80 drugs have to be introduced along with lifestyle changes & if ne essary multiple drugs have to be used to reach BP goal In pregnant patients with diabetes and chronic hypertension, blood pressure target goals of 110– 129/65–79 mmHg are suggested in interest of longIn the UKPDS, a fetal term maternal health and minimizing impaired reduction in BP from 154 to during growth; ACE inhibitors, ARBs, contraindicated144 mm Hg was associated with a 30% reduction pregnancy (E) in microalbuminuria
  19. 19. A pure or predominant motor polyneuropathy with few or no sensory symptoms or signs is rarely due to diabetes and should trigger a search for alternative causes of weakness, such as motor neuron disease, primary muscle disease, spinal cord disease, or other potentially treatable causes of peripheral neuropathy, such as chronic inflammatory demyelinating polyneuropathy
  20. 20. Diabetic Neuropathy Symmetric 1.Distal symmetric sensorimotor polyneuropathy 2. Autonomic neuropathy 3. Acute painful neuropathy 4. Hyperglycemic neuropathy 5. Treatment-induced neuropathy 6. Symmetric proximal lower extremity neuropathy 7. CIDP Asymmetric Focal and multifocal neuropathy 1. Cranial neuropathy 2.Thoraco abdominal neuropathy 3. Focal limb neuropathy 4. Diabetic amyotrophy
  21. 21. RISK FACTORS 1.Hyperglycemia is now well established as a risk factor in both patients with type 1 diabetes and patients with type 2 diabetes. 2.Age 3.Duration of diabetes, 4. quality of metabolic control, 5. height, 6. diabetic retinopathy, 7. cigarette smoking, 8.high-density lipoprotein cholesterol, and 9.the presence of cardiovascular disease . 
  22. 22.      Most common type of Neuropathy in Dm pt.s as a whole is Distal symmetric sensorymotor neuropathy Symmetric involvement in a length dependent manner giving rise to ―glove & stocking‖ pattern, though an asymmetric pattern due to involvement of root or nerve m/b superimposed Once developed this symm. Neuropathy is irreversible but may have intercurrent exacerbations with infections, depression This variety is often associated with autonomic involvement In more severe cases, distal portions of thoracic intercostal nerves are affected, producing an asymptomatic midline sensory loss in a teardrop distribution over the anterior thorax and abdomen that gradually spreads laterally . This thoracic and abdominal sensory loss differs from focal thoracic truncal radiculopathy in that it manifests as a painless, bilateral, symmetrical, and persistent form of neuropathy
  23. 23.          SFN involvement pattern Burning or lancinating pain Hyperesthesia, Paresthesia Loss of pain and temperature sensation Dysautonomia Foot ulceration Loss of visceral pain Early in onset with no/minimal Ncv abnormality This pattern of isolated small fiber symptoms when involves U.limbs is known as ―pseudosyringomyelia‖ pattern      LFN involvement pattern Areflexia NCV test abnormal Loss of vibration & joint position sense patients with disproportionate large-fiber involvement may manifest muscle weakness, atrophy of the intrinsic foot muscles, and weakness of the extensors and flexors of the toes and ankles with foot drop. When these deficits are combined with proprioceptive deficit in the toes and feet, a ―pseudotabetic‖ gait ataxia may result
  24. 24. Other symmetrical polyneuropathies Features Acute painful neuropathy •Diabetic neuropathic cachexia • Correlates poorly with severity of diabetes or presence of other diabetic microangiopathic complications. • Prognosis may be good in some patients, with gradual recovery over a period of months Treatment induced neuropathy •Starts with onset of t/t with insulin or OHA •Gradually improves over months, m/b reversible Hyperglycemia induced neuropathy •May occur in states of DKA/HONK •rapidly improve with control of hyperglycemia. •diffuse rather than distal distribution of paresthesias Chronic inflammatory demyelinating neuropathy • symmetric weakness with demyelination and conduction block on electromyography and demyelination on nerve biopsy. •The clinical progression is characteristically more rapid than that of diabetic polyneuropathy, weakness may be more prominent
  25. 25.      This neuropathy typically occurs with a peak incidence in the fifth or sixth decade in patients with type 2 diabetes The clinical picture is one of acute or subacute pain, weakness, and atrophy of the pelvic girdle and thigh musculature Symptoms begin unilaterally but extend to the opposite extremity within weeks or months. Most patients have weight loss, and some appear cachectic. subtle sensory symptoms and signs are commonly present. The knee jerk is nearly always reduced or absent on the affected side, whereas ankle jerks may be preserved unless compromised by a coexistent distal polyneuropathy. The prognosis is usually good, with most patients showing resolution of pain followed later by gradual return of strength over a period of 6 to 18 months.
  26. 26.    The finding of slow nerve-conduction velocities in femoral and distal nerves and of features of demyelination in nerve biopsy specimens in these patients indicates that ―diabetic amyotrophy‖ is a form of diabetic neuropathy Electromyography of patients with diabetic amyotrophy characteristically displays abundant fibrillations in the affected limb muscles and the paraspinal muscles. Nerveconduction studies are unable to differentiate patients with diabetic amyotrophy from those with a generalized polyneuropathy. Patients with unilateral and relatively focal pain and weakness seem to improve more rapidly and completely than patients with more widespread involvement.
  27. 27. Fda apprvd. Management of painful neuropathy
  28. 28.       Intensive glycemic control Stop smoking & alcohol addiction Management of dyslipidemia α tocopherol can be used as antioxidant Aldose reductase inhibitors Supplementation with methylcobalamin
  29. 29. Autonomic neuropathy Cardiovascular involvement Sudomotor g.i. involvemennt Orthostatic hypotension Fludroco rt & Midodrin e, Genitourinary involvement Diabetic gastroparesis Erectile dysfunction Erythro mycin & domperi done PDE5 inh. hyperhydrosis Topical anticholi nergic & botulinu
  30. 30. Rheumatological manifestations of DM Rheumatic syndromes uniquely or commonly associated with diabetes mellitus Adhesive capsulitis Common rheumatological diseases associated with diabetes Osteoarthritis Dupuytren's disease Gout and hyperuricemia Calcium pyrophosphate deposition arthropathy Osteopenia Neuroarthropathy Osteolysis of forefoot Shoulder-hand syndrome Diabetic hand syndrome Migratory osteolysis of
  31. 31.      The usual presentation is that of a patient with longstanding diabetes with complications present with an unilateral painless Jt. Swelling. The foot is most commonly involved, followed in frequency by the ankle and knee. Rarely, upper extremity joints are involved. Warmth and erythema may be present. When they are present, the differential diagnosis includes gout, pseudogout, osteomyelitis, or septic arthritis. Typically, there are few systemic symptoms and no documented fever and leukocytosis. ―claw toe‖ arises as chronic motor neuropathy affects the small intrinsic muscles of the feet. When the larger muscles of the anterior tibial compartment are unopposed, subluxation of the proximal interphalangeal metatarsal joints may result, leading to a claw-toe appearance. This may lead to excessive pressure on the metatarsal heads and thus the tendency to form skin ulcers.
  32. 32. phase manifestations acute edema, localized warmth, erythema, and joint crepitus with range-of-motion examination Radiographs are normal but MRI may suggest NA coalescence skin temp. begins to equilibrate and jt. Crepitus diminishes. Plain radiographs will show resorption of osseous fragments and the laying down of new bone Reconstruction This can eventually lead to a stable foot devoid of / remodelling significant motion. Unfortunately, in many cases, the foot can be severely deformed, with obvious bony prominences susceptible to ulceration (e.g., the rocker-bottom foot)
  33. 33. Claw toe
  34. 34.    Diagnostic criteria typically require the new bone formation to bridge four contiguous vertebral bodies in the absence of degenerative disc disease and the absence of inflammatory sacroiliac or facet joint changes The condition is characterized by widespread new bone formation ,specifically the presence of new bone growth into the entheseal regions Osseous changes are found around the acetabulum where fluffy new bone is formed, but similar changes around the knees and wrists have been documented.
  35. 35. Lateral view CXR DISH changes are most characteristic in the thoracic spine, where uninterrupted new bone may ―flow‖ from one vertebra to another more prominent on the right side of the thoracic vertebra, thought to be a consequence of the pressure effect of the left-sided aorta. The presence of the anterior longitudinal ligament over the anterior two thirds of the vertebral bodies dictates the distribution of the new bone formation
  36. 36. Patients with diabetes mellitus commonly suffer from a wide variety of cutaneous maladies. Estimates of the frequency of skin disease in people with diabetes range from 30% overall to 71% of patients with type 1 diabetes mellitus . While several skin conditions are specific to diabetes, most of them also occur in individuals without diabetes. The clinical manifestations and complications of skin disease are frequently more severe in the setting of diabetes medicineJoslin's Diabetes 14e.chm
  37. 37. ACANTHOSIS NIGRICANS: Eruptive xanthoma: present as 1-4 mm papules on buttock and extensor surface of extremities, indicates severe hypertriglyceridemia associated with uncontrolled diabetes . Does‘nt correlate with microvascular complications
  38. 38. CHEIROPAT HY: •Starts with DIP of 5th finger gen. •Correlated with HbA1c% & prevalence of nephropath y •Inversely correlated with insulin therapy
  39. 39. Scleredema: Abrupt onset non pitting induration of skin. Skin appears as smooth and waxy with dense dermal infiltration with prominent follicular ostia , ―peau – de- orange‖ appearance Nephrogenic fibrosing dermatopathy Perforating dermatoses: umbillicated papules with keratinized plaques, koebnerisation+ve
  40. 40. Fibrosing: Sclerosing: Scleroderm a Fibroblast disorders Peyronies disease Fibrosc lerosis: Dupuytrens contr. Juvenile hyaline fibromatos es Morphea Eosinophilli c fascitis lipodermat osclerosis Gingival fibromatos Scleromucinosi es s scleredema Mucinosis: Fibromucinosis: Scleromyxedema Nefrogenic fibrosing dermatopathy Toxic oil syndrome Eosinophillia myalgia syndrome Pretibial myx. Gen. myx. CTD Degos disease
  41. 41. Necrobiosis lipoidica
  42. 42. Granuloma annulare (GA) is characterized by an annular configuration of flesh colored or pale red papule and plaques that occur in a localized or generalized (disseminated) pattern The lesions of GA may vary in size upto 5 cm . Localized GA is most characteristically located on the dorsa of the hands and feet. A single lesion is present in one half of patients with GA . The papules develop and enlarge slowly in a centrifugal fashion over a period of months to years. Generalized GA is characterized by a symmetrical eruption of hundreds of tiny papules, which can occur all over the body surface. Localized GA eventually undergoes spontaneous resolution usually within 2 years. Lesions often recur at the same site.
  43. 43. Diabetic dermopathy: small atrophied pink to brown skin lesions over lower limbs which disappear on own Bullous diabeticorum : painless, non pruritic bullae over lower limbs arising in normal skin abruptly and heal spontaneously gen. without scarring
  45. 45.  Delayed emptying of solid or nutrient meals is found in up to 50% of patients with type 1 diabetes and in 30% of patients with type 2 diabetes . However, the degree of delay for various constituents of food, i.e., liquids, digestible solids, and indigestible solids, is not the same. Simultaneous assessment of gastric emptying of liquids and digestible solids using dual markers (99Tc-labeled solid phase and 111Inlabeled liquid phase) showed that indigestible solids are particularly delayed in persons with diabetes.
  46. 46.      Patients have symptoms of anorexia, early satiety, and postprandial abdominal fullness and discomfort that resemble simple dyspepsia. Vomiting of old food, however, is indicative of gastroparesis. Nausea and vomiting are common when gastric distention is associated with obstruction and vigorous gastric contractions. In some patients, atonic dilation of the stomach, even when massive, may not be associated with nausea or vomiting. Nausea and reflex vomiting may be elicited by the stimulation of the gastric afferents carried via vagal and sympathetic nerves to the vomiting center in the brainstem. If gastric stasis and distention are primary causes of nausea and vomiting in diabetic gastroparesis, these symptoms should respond to gastric decompression by either vomiting or by insertion of a nasogastric tube.
  47. 47. Symptomatic diabetic gastropathy Delayed emptying Excitatory motor neuropathy Prokin etics Avoid antiAch Normal gastric emptying Inhibitory motor neuropathy AntiAch Fast gastric emptying Sensory hyperalgesia Fundal inhibitory motor neuropathy Antie metics clonidi ne AntiAch
  48. 48.    Erythromycin at a dose of 3 mg/kg bw i.v. every 8 hours can accelerate gastric emptying . When oral intake is resumed, treatment with oral 250 mg erythromycin t.i.d. for 2 weeks is worthwhile. Thereafter, the prokinetic effects of erythromycin are limited by Tachyphylaxis. Anecdotal findings suggest that erythromycin may be effective if courses are separated by a drug - free period (e.g. lasting 2 weeks). Decompression of stomach using endoscopy with dislodging of bezoar if any. Insulin theapy reqd.
  49. 49. Others include: PTB test +ve Traumatic foot wound Ulceration>30 days Previous lower limb amputation
  50. 50.       PEDIS: Perfusion, Extent (size), Depth (tissue loss), Infection, Sensation (neuropathy)