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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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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