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CASE PRESENTATION

V.KRISHNACHARY. 62YR Male from AlapuzhaGoldsmith By ProffessionK/C/OType 2 Diabetes Mellitus since 20 yrs on Tab Obimet SR 1-0-0And Inj H.Mixtard 0-0-40USystemic Hypertension since 20 yrs on Tab Amlopress 5mg 1-0-0. Complaints. Lower Limb numbness since 10yrsLower Limb weakness since 10 yrsW

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CASE PRESENTATION

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    1. SKIN DEEP BY DR NAGANATH NARASIMHAN PREM CASE PRESENTATION

    2. V.KRISHNACHARY 62YR Male from Alapuzha Goldsmith By Proffession K/C/O Type 2 Diabetes Mellitus since 20 yrs on Tab Obimet SR 1-0-0 And Inj H.Mixtard 0-0-40U Systemic Hypertension since 20 yrs on Tab Amlopress 5mg 1-0-0

    3. Complaints Lower Limb numbness since 10yrs Lower Limb weakness since 10 yrs Weakness of upper limbs since 1yr Numbness of upper limbs since 1yr No c/o sensory loss over arm/thigh No c/o diplopia/deviation of angle of mouth/numbness over the face No c/o ataxia/vertigo No c/o urinary/bowel/bladder incontinence

    4. Past history Diabetes Mellitus since 20 yrs on tab Obimet Sr and Inj. H.Mixtard 0-0-40U Systemic Hypertension since 20yrs on Tab Amlopress 5mg 1-0-0

    5. Personal History Non Vegetarian Normal Sleep and Appetite Normal Bowel Habits Increase in Nocturnal micturation No hesitancy/urgency No addictions

    6. Family History Brother has Type 2 Diabetes Mellitus/Systemic Hypertension Aunt has Type 2 Diabetes Mellitus/Systemic Hypertension/Coronary Artery Disease

    7. General Examination Moderately Built Conscious,Cooperative ,Well oriented in Time,place and person Pulse-80 beats per min BP-130/90 mm of Hg RR-18 per min Temp-98.6 F JVP- not raised No pallor,icterus,cyanosis,clubbing,oedema,lymphadenopathy

    8. Examination of Thyroid normal Examination of Throat-Normal Examination of Skin-Thickening of the skin in the B/L thigh regions in the legs,Thickening of the skin in the lower back area

    9. Working Diagnosis Sensory Motor Neuropathy Diabetic Neuropathy?? Skin Manifestation??

    10. Systemic Examination Higher Mental Functions-Normal Cranial nerves-Visual Acuity 20/70 B/L Field- intact Colour Vision-intact Fundus no papilledema B/L Exudates more in Rt upper Quadrant Other Cranial Nerves within the normal limit

    11. Motor System Bulk-B/L wasting of small mucles of the hand Lower Limb wasting Left>right Tone-decreased B/L Power Upper limb-Shoulder-5/5 B/L Elbow-4/5 B/L Forearm-4/5 B/L Wrist-4/5 B/L Fingers-2/5 B/L

    12. Thumb 3/5 B/L Trunk and abdominal muscles normal Lower limb Hip-4/5 B/L Knee Right 2/5 and Left 3/5 Ankle,Foot 0/5 B/L

    13. Reflexes Biceps B/L diminished Triceps B/L ++ Supinator B/L Diminished Knee,Ankle B/L Dimished B/L- Plantars mute Cerebellar Signs Nil Menigeal Signs- Nil Gait High Stepping

    14. Sensory System UPPER LIMB Sensations decreased around 50-75% elbow downwards Palm Around 50% decreased Lower Limb 50% decreased sensations B/L below Knee Nil Sensations B/L from around Shin of tibia to entire feet

    15. Other Systems CARDIOVASCULAR-S1S2 Normal No Murmurs RESPIRATORY Normal Vesicular breath Sounds,no crepitations/wheeze PER ABDOMINAL-Soft Non tender No organomegaly

    16. Differential Diagnosis Diabetic Neuropathy Diabetic Retinopathy Sytemic Hypertension Skin manifestation??

    17. Investigations TLC-12.4 Eosinophils-31.9% Hb-12g/dl Platelets-210K/ul ESR-48 Urea-35.9 Creatinine-1.1 Sodium-136.7 Potassium-4.1

    18. LFTS normal Lipid Profile All values normal except LDL-164.3 PSA-2.279 TSH-0.71 Urine routine showed Glucose 3+,ketone negative GRBS-325 Chest Xray- Normal

    19. 2D ECHO-Normal Peripheral Smear-normocytic normochromic with luecocytosis and eosinophilia Metals Panel Urine qualitative screening-Negative USG Abdomen Both kidneys show increased cortical echotexture with corticomedullary differentiation,moderate fatty liver

    20. Nerve conduction study Lower Limb Inelicitable Conduction motor action potential amplitude from B/L peroneal and tibial nerves. Reduced Conduction motor action potential amplitude from B/L femoral nerves. Upper limb Prolonged distal latencies from both median nerves and reduced Conduction motor action potential amplitude from B/L ulnar nerves,conduction block across wrist

    21. Sensory studies Absent sensory potentials from B/L sural and prolonged peaked latencies from B/L median nerves and absent from B/L ulnar and dorsal ulnar cutaneous nerves.

    22. Opthalmology Right Eye Proliferative Diabetic Retinopathy Left Eye Proliferative Diabetic Retinopathy with Vitreous Haemorrhage FFA(Fundus Fluorescein Angiogram) Right Eye- Multiple Small Neovascularisations in all areas Few focal leaks away from the fovea No neovascularisation of the disc Light eye-Multiple Neovascularisations in all areas Few focal leaks away from the fovea Optical Coherence Tomography-No oedema

    23. Dermatology Skin biopsy was taken PHYSIOTHERAPHY For providing patient proper chappals and crutches for support in walking

    24. Differential Diagnosis for skin thickening Lupus Erythematosus Systemic Scleroderma Myxedema, Generalized Connective Tissue Nevi Scleredema

    25. Skin Biopsy Sections from the skin show hyperkeratosis with irregular acanthosis. Dermis shows perivascular chronic inflammation with increase in deposition of homogenous eosinophilic material Superficial dermis lack hair adnexae & eccrine elements Deep dermis-sweat glands with a rim of hyalinisation.No hair follicles seen Special stains non contributory Impression-Scleredema

    26. Complete Diagnosis TYPE 2 DIABETES MELLITUS DIABETIC NEUROPATHY-Affecting the Ulnar,median,radial,sural,deep peroneal nerves B/L,B/l femoral neve DIABETIC RETINOPATHY SYSTEMIC HYPERTENSION DYSLIPIDEMA SCLEREDEMA

    27. Diabetic Skin Thickening

    28. Scleredema Scleredema, a rare collagen disorder First reported by Piffard in 1876 It is a misnomer because neither sclerosis nor edema is found on microscopic examination. Clinically, symmetric diffuse induration of the upper part of the body due to deposition of hyaluronic acid in the dermis. Graff described three types of scleredema

    29. Type 1 is the classic type, which was first described by Buschke in 1902,follows a febrile illness.(resolve in several months to years) Type 2 and 3 not associated with febrile illness(slow,progressive course) Type 2-Multiple myeloma Type 3-Diabetes Mellitus

    30. Type 3 Risk Factors in diabetes Long standing disease Presence of Microangiopathy Overweight Need for insulin Induration non pitting with no demarcation between normal and abnormal skin. Consequences of long standing scleredema Decrease in motility of the shoulders, Impairment of respiratory function , sleep apnea syndrome.

    31. Rho et al reported a series of 11patients with diabetes-associated scleredema,where lesions improved partially in 5 patients with well-controlled diabetes. Poor diabetic control may be an etiologic factor in scleredema. Diabetic scleredema is usually refractory to treatment with long protracted course Literature says corticosteroids,methotrexate,cyclosporine have been used.

    32. Diabetic Thick Skin Three main categories First- Scleroderma-like changes of the hand associated with stiff joints ,limited mobility Second- Measurable skin thickness (insignificant clinically) Third- Scleredema Diabeticorum Thickening of the dorsum of the hands Pebbled / rough skin, known as Huntley's papules, over the interphalangeal joints, particularly the knuckles. Waxy skin and stiff joints

    33. Scleredema-thickening of skin and non pitting induration Two types Scleredema of Buschke-occurs at any age ,secondary to viral/streptococcal infection. Affects Posterior neck and upper part of back Scleredema diabeticorum-same as former except also includes upper extremities including the hands. Has to be differentiated from scleroderma There is increased hyaloronic acid in scleredema whereas increase in dermatan sulphate in Scleroderma Supposed hydration of collagen secondary to polyol formation

    34. ACANTHOSIS NIGRICANS

    35. Acanthosis Nigricans A velvety, light brown to black hyperpigmented, cutaneous thickening Areas-back, the sides of the neck, the axillae, flexural surfaces. Show marked hyperkeratosis ,papillomatosis with mild acanthosis , hyperpigmentation. Insulin at high concentrations may stimulate insulin-like growth factor receptors on keratinocytes,[thereby promoting epidermal cell proliferation.

    36. Diabetic Bullae

    37. Diabetic Bullae Areas-hands, feet Three types of diabetic bullae First-Most common, sterile , fluid-containing , heals without scarring. Histology - intraepidermal cleavage without acantholysis Second-hemorrhagic ,heals with scarring Histology-cleavage below the dermoepidermal junction with destruction of anchoring fibrils Third-multiple nonscarring bullae on sun-exposed, tanned skin. Histology-cleavage at the lamina lucida. Theraphy-treatment of infection

    38. Spontaneous Blister

    39. Necrobiosis Lipoidica

    40. Necrobiosis Lipoidica Diabeticorum

    41. Necrobiosis Lipoidica Diabeticorum Degenerative disease of collagen in the dermis , subcutaneous fat with an atrophic epidermis and granulomatous dermis. Microangiopathic basis with neuropathy leads to the degradation of collagen. Immunological role also explored T/t- NSAIDS and steroids

    42. Candida Infection

    43. Candida Infection

    44. Candida Infection

    45. Staphlococcus Infection

    46. Acute Bacterial paronychia

    47. Dermatophyte Infection

    48. Malignant Otitis Externa

    49. Infections More so in uncontrolled diabetes mellitus Staph aureus and Beta hemolytic Streptococci -Impetigo, Erysipelas, Cellulitis, necrotizing fasciitis Obese Patients with Diabetes-Erythrasma-Corynebacteria minutissimum Candida-Nail folds and web spaces of skin folds Rhinocerebral mucormycosis Malignant external otitis ( Pseudomonas aeruginosa )

    50. Diabetic Hand Syndrome Joint limitations (inability to fully extend a finger) Thickened skin of the hand, especially involving the dorsum of the fingers

    51. Prayers Sign

    52. Palpably Thickened Skin

    53. Yellow Nails

    54. Yellow Nails

    55. Yellow Skin

    57. Yellow Skin Benign condition with no known significance Cause-elevated levels of carotene or nonenzymatic glycosylation of dermal collagen. One glycosylation end product, 2-(2-furoyl)-4(5)-(2-furanyl)-1H-imidazole, has a yellow hue, which could provide the characteristic color of yellow skin No current T/t

    58. Sensory Neuropathy

    59. Diabetic Ulcer

    60. Diabetic Ulcer Ischaemic and neuropathic ulcer Most common Neuropathy- mixed distal motor and sensory neuropathy. Ulceration occurs as a consequence of the loss of protective sensation. Motor and sensory neuropathy along with mechanical factors plays a role in the pathogenesis of neuropathic ulcers Ischemic patient -disproportionately excruciating pain associated with a superficial ulcer, while the neuropathic patient is unaware of a large, deep ulcer. Education in foot care,proper footwear important. Treatment and Dressing of ulcer important.

    61. Pigmented Purpura

    62. Pigmented Purpura Skin on the lower extremities resulting from red blood cell extravasation from the superficial vascular plexus. Multiple tan to reddish small macules -called cayenne pepper spots.

    63. Motor Neuropathy

    64. Motor Neuropathy Results in weakened intrinsic foot muscles Toes dorsiflex and the foot splays (becomes wider) on weight bearing Combined with sensory neuropathy it potentiates trauma and ulceration

    65. Charcot Foot

    66. Charcot Foot With loss of sensation,weak intrinsic muscles, the foot may fracture when stressed Multiple fractures allowed to heal without realignment result in the distortion of shape.

    68. Diabetic Dermopathy

    69. Dermopathy

    71. Diabetic Dermopathy Known as shin spots Round to oval atrophic hyperpigmented lesions on the pretibial areas of the lower extremities. B/L and have an aymmetric distribution. Histology Edema of the papillary dermis, thickened superficial blood vessels, extravasation of erythrocytes, mild lymphocytic infiltrate Extravasated erythrocytes leave hemosiderin deposits, which provide the brownish hyperpigmentation

    72. Periungual Erthyema

    73. Nailfold Capillaries

    74. Perforating Dermatosis

    75. Kyrle's disease

    76. Perforating Dermatosis Kidney failure associated with diabetes Kyrle's disease or reactive perforating collagenosis. Areas-extensor surfaces of lower Extremities,can involve trunk,face Histology-hyperplastic epidermis surrounding a plug of degenerated material, which has elements of leukocytes, collagen, and nuclear debris. Difficult to treat

    77. Eruptive Xanthomas

    78. Eruptive Xanthomas Hyperlipidemic ,hyperglycemic states Waxy, yellow papules surrounded by an erythematous rim Extensor surfaces ,popliteal region Histology-lipid-laden histiocytes ,a mixed lymphoneutrophilic infiltrate in the dermis. T/T- Strict Control of Hyperlipidemia,hyperglycemia

    79. Vitiligo

    80. Granuloma Annulare

    81. Other Dermatosis Vitiligo can be associated with DIABETES Mellitus Granuloma Annulare Asymptomatic dermatosis with a predilection for the dorsum of the hands, feet, and elbow. One-fourth of porphyria cutanea tarda patients have diabetes Association between Psoriasis and diabetes Mellitus has also been told

    82. THANK YOU

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