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AZEEZIA MEDICAL COLLEGE
DEPARTMENT OF GENERAL MEDICINE
CUTANEOUS MANIFESTATIONS OF
DIABETES MELLITUS
Dr.Jayasoorya P G
Junior resident
Department of General medicine
Azeezia medical college
Classification
 Vascular
 Metabolic
 Necrobiotic
 Bullous
 Infection
 Neuropathic
 Treatment related
 Miscellaneous
Vascular
 Diabetic dermopathy
 Rubeosis facei(diabeticorum)
 Erysipelas-like erythema
 Pigmented Purpura
 Periungulal telangiectasia
Diabetic Dermopathy
 Aka Shin spots or pigmented pretibial papules
 Commonest cutaneous manifestation of Diabetes (70 % of diabetes)
 M>F (males diabetics over 50 years of age)
 Multiple shin spots (4 or more) have a high specificity ,indicating
microvascular complications
 Association exist between diabetic dermopathy and other diabetic
complications (DR,D neuropathy,D nephropathy)
Shin spot-morphology
 Multiple bilateral annular or irregular erythematous papules or plaques
that gradually evolve into atrophic hyperpigmented macules
 This resembles post traumatic hyperpigmentation,but no history of trauma.
 Common site-shin
 Other sites-thighs,forearm
histology
 Epidermal atrophy,mild dermal inflammation
 Microangiopathy with PAS-Positive thickening of vessel walls
 Pigmentation-d/t hemosiderin deposition
treatment
 Require no treatment
Rubeosis facei(diabeticorum)
 Rosy redness of face.More obvious in light skinned patients
 Evident in newly diagnosed diabetics
 Upto 60 % hospitalized patients with diabetes
 Associated with vascular tone and increased viscosity (functional
microangiopathy)
 Often a sign of poor glycemic control
 Yellowish discolouration of the skin,more obvious on the palms,soles and
face,may occur because of carotenemia,or with normal serum carotene
accumulation or because of nonenzymatic collagen glycosylation
 Better glucose control may improve the appearance
Erysipelas-like erythema
 Well demarcated red areas in feet and legs
 Painless,lack of systemic signs of infection
 Seen in elderly diabetics (majority >73 years, duration of diabetes 5.4
years)
 Underlying bone destruction +/-
 Compensatory increase in peripheral microcirculation caused by decreased
perfusion
 Spontaneous resolution over weeks, but may recur
Pigmented purpura
 RBC extravasation from superficial plexus
 Cayenne pepper spots (Red macules)orange tan patches
 Freequently associated with diabetic dermopathy(50 %)
 Increased incidence in elderly diabetic with cardiac failure
 Marker of microvascular disease
Periungal telangiectasia
 Seen in upto 49 % of diabetics
 Megacappillaries and irregularly elongated loops
 Often associated with nail fold erythema,accompanied by fingertip
tenderness and “ragged”cuticles
 Functional microangiopathy(engorgement of venular limbs),tortuosity
indicates structural changes
Metabolic
 Acanthosis nigricans
 Eruptive Xanthoma
 Yellow skin and nails
 Diabetic scleredema
Acanthosis Nigricans
 50 % of cases -> age >40 and 5% cases ->age <20 years
 Hyperpigmented velvety and on flexural skin
 Related to insulin binding of insulin like growth factor receptors on
keratinocyte and dermal fibroblast
 Two syndromes where AN is associated with diabetes (Type A syndrome
and Type B syndrome)
Type A syndrome (HAIR-AN syndrome)
 HA----- Hyperandrogenemia
 IR------- extreme Insulin resistance
 AN------ Acanthosis nigricans
Type B syndrome
 In middle aged women with autoimmune disease
 Circulating antibody to the insulin receptors
 Common place of AN-vulva
Eruptive xanthoma
 Occur in less than 0.1% of diabetic patients
 Crops of small (1-4 mm)yellow papules with erythematous halo
 May be pruritic and tender
 Buttock and extensor surface
 Appear in association with elevated Triglyceride
 Resolve with treatment of increase glucose and lipid
Yellow skin and nail
 Prevalence 40% in Type 2 DM,more common in elderly
 Most evident in distal end of hallux
 Cause-hypercarotinaemia,protein glycosylation end product
Diabetic scleredema
 Non enzymatic glycosyation of collagen
 Fingers and dorsum of hands,with limited joint mobility,Huntley papules
(8-50 % type 1 diabetics)
 Chest,neck,shoulders-increase thickness,difficult to tent the skin (common
in older type 2 diabetics ),Peau d orange appearance
 May be subclinical
 Improve with tight glycaemic control
Necrobiotic
 Necrobiosis lipoidica
 Disseminated granuloma annulare
Necrobiosis lipoidica
 0.3%-0.7 % of diabetics
 Mean age-34 years
 F>M,Caucasians,type 1 is more associated
 In 15% patients precede the development of diabetes by about 2 years
 Well circumscribed papules ->radial expansion ->sharply-demarcated
slightly depressed yellow waxy plaques with erythematous raised border -
>central atrophy with telangiectasia
 Sites-pretibial,medial malleolus,15 % cases outside legs,ulcerate in 1/3
patients
 Persist despite glycemic control
 Chronic course ,20 % remit spontaneously
 Rx-intralesional steroids,aspirin,pentoxifylline
Granuloma Annulare
 Relationship with DM is controversial
 Generalized GA associated with DM-mainly in oldage patients
 Papular morphology and more chronic relapsing course
 Histology-foci of necrobiosis in the upper and mid-dermis surrounded by
palisaded histocytes and abundant dermal mucin
 Sporadic therapeutic success reported with intralesional /typical/systemic
steroids,isotretinoin,chlorambucil,cryotherapy,chloroquine,nicotinamide,da
psone and PUVA
Bullous
 Bullous diabeticorum
Bullous diabeticorum
 Type 1>type 2,M>F
 Sites-mainly feet,occasionally hands
 Spontaneous,not related to trauma or infection
 Blisters contain sterile fluid,rest on a non-erythematous base
 Heal in 2-3 weeks without scarring
Types
 Common type-clear sterile blisters on tip of toe/fingers.Heals without
scarring.intraepidermal cleavage
 Haemorrhagic bullae-heal with scarring,Cleavage-DEJ
 Multiple tender non-scarring blisters in sunexposed areas.IMF
(immunoflourescence) and porphyrins negative.cleavage-lamina lucida
Infection
 Bacterial infections
 Fungal infections
Bacterial infections
 Staphylococcal-furuncle,carbuncle,ecthyma
 Strept pyogenes-cellulitis,erysipelas
 Pseudomonas spp-
1)malignant otitis externa-cellulitis,osteomyelitis,meningitis,cranial nerve
palsy.and mortality 50%.treatment-IV Quinolones
2)Toe nail infection
3)Toe web infection
Other bacterial infections
 Erythrasma-
1)Chronic,asymptomatic symmetric red scaly macerated plaques in the axillae
and groin
2)Corynebacterium minutissimum
3)Rx-topical/systemic erythromycin
Non-clostridial gas gangrene
1)Develops in soft tissues near a gangrenous focus
2)E.coli,Klebsiella,Pseudomonas and bacteroids
Fungal infection
 Candida-produce oral perliche,vaginal/balanoprosthitis,intertrigenous skin
in toe web,paronychia,nail infection
 Dermatophytosis-incidence not increase in diabetes,commonly caused by
Trychophyton rubrum,T mentagrophytes,Epidermophyton floccosum
Rhinocerebral mucormycosis
 Associated with ketosis
 Black crust/pus in turbinate,nasal septum,plate and orbit
 Cerebral involvement may occur
 Treatment-debridment + IV amphotericin +treat ketosis
 High mortality
Neuropathic
 Anhidrosis/hyperhidrosis
 Neuropathic ulcers-circular,punched out ulcer in the middle of a callosity
over metatarsal heads
Treatment related
 Insulin reactions
 OHA related
OHA related
 Sulphonyl urea (chlorpropamide or tolbutamide –usually on first two
months of treatment )-maculopapular eruptions.these may clear on
continuation of therapy
 Lichenoid reactions,urticarial,erythema multiforme or erythema nodosum
may also occur
 10%-30% of those on chlorpropamide –disulfiram like reaction occur after
alcohol consumption (marked
flushing,headache,tachycardia,dyspnea,lasting for about an hour )
Insulin reactions
 Allergic reaction-insulin itself or by preservatives (parabens),addictives
(zinc),pork or beef protiens or impurities
 Erythematous,urticated nodules appear at the site of injection,immediately
or upto four hours of administration
 Adjunct to manage allergic reaction-addition of dexamethasone to insulin
injection and desensitization of insulin
 Lipodystrophy can occur(it can occur as lipoatrophy or lipohypertrophy or
both).this will reduce the insulin absorbtion.treat by rotation of insulin site.
Lipoatrophy
 Circumscribed cutanious depressions at insulin injection sites and
occasionally at distant sites,appearing 6-24 months after starting treatment
 Cause-mechanical trauma of injection,cryotrauma from refrigerated
insulin,contamination with alcohol used for cleansing,lipolytic component
in preparation or local inflammation with lysosomal enzyme release.
 Repeated use of same injection site increase the risk of lipoatrophy
 Measures-injecting insulin at edge of atrophic area,coadministration of
dexamethasone with insulin,switching over to insulin pump
Lipohypertrophy
 Soft dermal nodules resembling lipomas
 At site of injection –d/t lipogenic action of insulin
 Most common cutaneous manifestation of insulin therapy
 Other complications of insulin therapy-keloid,purpura,hyperkeratotic
papules,hyperpigmentation
Miscellaneous
 Acquired perforating dermatoses
 Vitiligo
 Lichen planus
 Pruritis
Acquired perforating dermatosis
 Umbilicated hyperpigmented papules with a central keratotic plug
 Common site-extensor surface of extremities
 Major symptom-pruritis
 Strong association with chronic renal failure (ESRD)
 Histology-transepidermal elimination of degenerative elastic /collagen
fibres
 Treatment-topical tretinoin,phototherapy
vitiligo
 Localized/generalized forms
 1%-7 % in type 1 diabetics (0.2-1% in general population)
 May be a part of polyglandular syndrome type 1
 Rx-sun protection,topical/systemic steroids,phototherapy
Lichen planus
 Polyerythematous flat lesions
 Sites-wrist,dorsal part of feet,lower leg
 Oral/genital lesions-white lacy pattern
 DD-lichenoid drug reactions
 Treatment-topical steroids
Thank you

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Cutaneous manifestations of diabetes mellitus

  • 2. CUTANEOUS MANIFESTATIONS OF DIABETES MELLITUS Dr.Jayasoorya P G Junior resident Department of General medicine Azeezia medical college
  • 3. Classification  Vascular  Metabolic  Necrobiotic  Bullous  Infection  Neuropathic  Treatment related  Miscellaneous
  • 4. Vascular  Diabetic dermopathy  Rubeosis facei(diabeticorum)  Erysipelas-like erythema  Pigmented Purpura  Periungulal telangiectasia
  • 5. Diabetic Dermopathy  Aka Shin spots or pigmented pretibial papules  Commonest cutaneous manifestation of Diabetes (70 % of diabetes)  M>F (males diabetics over 50 years of age)  Multiple shin spots (4 or more) have a high specificity ,indicating microvascular complications  Association exist between diabetic dermopathy and other diabetic complications (DR,D neuropathy,D nephropathy)
  • 6.
  • 7.
  • 8. Shin spot-morphology  Multiple bilateral annular or irregular erythematous papules or plaques that gradually evolve into atrophic hyperpigmented macules  This resembles post traumatic hyperpigmentation,but no history of trauma.  Common site-shin  Other sites-thighs,forearm
  • 9. histology  Epidermal atrophy,mild dermal inflammation  Microangiopathy with PAS-Positive thickening of vessel walls  Pigmentation-d/t hemosiderin deposition
  • 11. Rubeosis facei(diabeticorum)  Rosy redness of face.More obvious in light skinned patients  Evident in newly diagnosed diabetics  Upto 60 % hospitalized patients with diabetes  Associated with vascular tone and increased viscosity (functional microangiopathy)  Often a sign of poor glycemic control  Yellowish discolouration of the skin,more obvious on the palms,soles and face,may occur because of carotenemia,or with normal serum carotene accumulation or because of nonenzymatic collagen glycosylation  Better glucose control may improve the appearance
  • 12.
  • 13. Erysipelas-like erythema  Well demarcated red areas in feet and legs  Painless,lack of systemic signs of infection  Seen in elderly diabetics (majority >73 years, duration of diabetes 5.4 years)  Underlying bone destruction +/-  Compensatory increase in peripheral microcirculation caused by decreased perfusion  Spontaneous resolution over weeks, but may recur
  • 14.
  • 15. Pigmented purpura  RBC extravasation from superficial plexus  Cayenne pepper spots (Red macules)orange tan patches  Freequently associated with diabetic dermopathy(50 %)  Increased incidence in elderly diabetic with cardiac failure  Marker of microvascular disease
  • 16.
  • 17. Periungal telangiectasia  Seen in upto 49 % of diabetics  Megacappillaries and irregularly elongated loops  Often associated with nail fold erythema,accompanied by fingertip tenderness and “ragged”cuticles  Functional microangiopathy(engorgement of venular limbs),tortuosity indicates structural changes
  • 18. Metabolic  Acanthosis nigricans  Eruptive Xanthoma  Yellow skin and nails  Diabetic scleredema
  • 19. Acanthosis Nigricans  50 % of cases -> age >40 and 5% cases ->age <20 years  Hyperpigmented velvety and on flexural skin  Related to insulin binding of insulin like growth factor receptors on keratinocyte and dermal fibroblast  Two syndromes where AN is associated with diabetes (Type A syndrome and Type B syndrome)
  • 20.
  • 21.
  • 22. Type A syndrome (HAIR-AN syndrome)  HA----- Hyperandrogenemia  IR------- extreme Insulin resistance  AN------ Acanthosis nigricans
  • 23. Type B syndrome  In middle aged women with autoimmune disease  Circulating antibody to the insulin receptors  Common place of AN-vulva
  • 24. Eruptive xanthoma  Occur in less than 0.1% of diabetic patients  Crops of small (1-4 mm)yellow papules with erythematous halo  May be pruritic and tender  Buttock and extensor surface  Appear in association with elevated Triglyceride  Resolve with treatment of increase glucose and lipid
  • 25.
  • 26. Yellow skin and nail  Prevalence 40% in Type 2 DM,more common in elderly  Most evident in distal end of hallux  Cause-hypercarotinaemia,protein glycosylation end product
  • 27. Diabetic scleredema  Non enzymatic glycosyation of collagen  Fingers and dorsum of hands,with limited joint mobility,Huntley papules (8-50 % type 1 diabetics)  Chest,neck,shoulders-increase thickness,difficult to tent the skin (common in older type 2 diabetics ),Peau d orange appearance  May be subclinical  Improve with tight glycaemic control
  • 28. Necrobiotic  Necrobiosis lipoidica  Disseminated granuloma annulare
  • 29. Necrobiosis lipoidica  0.3%-0.7 % of diabetics  Mean age-34 years  F>M,Caucasians,type 1 is more associated  In 15% patients precede the development of diabetes by about 2 years
  • 30.  Well circumscribed papules ->radial expansion ->sharply-demarcated slightly depressed yellow waxy plaques with erythematous raised border - >central atrophy with telangiectasia  Sites-pretibial,medial malleolus,15 % cases outside legs,ulcerate in 1/3 patients  Persist despite glycemic control  Chronic course ,20 % remit spontaneously  Rx-intralesional steroids,aspirin,pentoxifylline
  • 31.
  • 32.
  • 33.
  • 34. Granuloma Annulare  Relationship with DM is controversial  Generalized GA associated with DM-mainly in oldage patients  Papular morphology and more chronic relapsing course  Histology-foci of necrobiosis in the upper and mid-dermis surrounded by palisaded histocytes and abundant dermal mucin  Sporadic therapeutic success reported with intralesional /typical/systemic steroids,isotretinoin,chlorambucil,cryotherapy,chloroquine,nicotinamide,da psone and PUVA
  • 35.
  • 37. Bullous diabeticorum  Type 1>type 2,M>F  Sites-mainly feet,occasionally hands  Spontaneous,not related to trauma or infection  Blisters contain sterile fluid,rest on a non-erythematous base  Heal in 2-3 weeks without scarring
  • 38.
  • 39. Types  Common type-clear sterile blisters on tip of toe/fingers.Heals without scarring.intraepidermal cleavage  Haemorrhagic bullae-heal with scarring,Cleavage-DEJ  Multiple tender non-scarring blisters in sunexposed areas.IMF (immunoflourescence) and porphyrins negative.cleavage-lamina lucida
  • 41. Bacterial infections  Staphylococcal-furuncle,carbuncle,ecthyma  Strept pyogenes-cellulitis,erysipelas  Pseudomonas spp- 1)malignant otitis externa-cellulitis,osteomyelitis,meningitis,cranial nerve palsy.and mortality 50%.treatment-IV Quinolones 2)Toe nail infection 3)Toe web infection
  • 42. Other bacterial infections  Erythrasma- 1)Chronic,asymptomatic symmetric red scaly macerated plaques in the axillae and groin 2)Corynebacterium minutissimum 3)Rx-topical/systemic erythromycin Non-clostridial gas gangrene 1)Develops in soft tissues near a gangrenous focus 2)E.coli,Klebsiella,Pseudomonas and bacteroids
  • 43.
  • 44. Fungal infection  Candida-produce oral perliche,vaginal/balanoprosthitis,intertrigenous skin in toe web,paronychia,nail infection  Dermatophytosis-incidence not increase in diabetes,commonly caused by Trychophyton rubrum,T mentagrophytes,Epidermophyton floccosum
  • 45. Rhinocerebral mucormycosis  Associated with ketosis  Black crust/pus in turbinate,nasal septum,plate and orbit  Cerebral involvement may occur  Treatment-debridment + IV amphotericin +treat ketosis  High mortality
  • 46.
  • 47. Neuropathic  Anhidrosis/hyperhidrosis  Neuropathic ulcers-circular,punched out ulcer in the middle of a callosity over metatarsal heads
  • 48.
  • 49. Treatment related  Insulin reactions  OHA related
  • 50. OHA related  Sulphonyl urea (chlorpropamide or tolbutamide –usually on first two months of treatment )-maculopapular eruptions.these may clear on continuation of therapy  Lichenoid reactions,urticarial,erythema multiforme or erythema nodosum may also occur  10%-30% of those on chlorpropamide –disulfiram like reaction occur after alcohol consumption (marked flushing,headache,tachycardia,dyspnea,lasting for about an hour )
  • 51. Insulin reactions  Allergic reaction-insulin itself or by preservatives (parabens),addictives (zinc),pork or beef protiens or impurities  Erythematous,urticated nodules appear at the site of injection,immediately or upto four hours of administration  Adjunct to manage allergic reaction-addition of dexamethasone to insulin injection and desensitization of insulin  Lipodystrophy can occur(it can occur as lipoatrophy or lipohypertrophy or both).this will reduce the insulin absorbtion.treat by rotation of insulin site.
  • 52. Lipoatrophy  Circumscribed cutanious depressions at insulin injection sites and occasionally at distant sites,appearing 6-24 months after starting treatment  Cause-mechanical trauma of injection,cryotrauma from refrigerated insulin,contamination with alcohol used for cleansing,lipolytic component in preparation or local inflammation with lysosomal enzyme release.  Repeated use of same injection site increase the risk of lipoatrophy  Measures-injecting insulin at edge of atrophic area,coadministration of dexamethasone with insulin,switching over to insulin pump
  • 53.
  • 54. Lipohypertrophy  Soft dermal nodules resembling lipomas  At site of injection –d/t lipogenic action of insulin  Most common cutaneous manifestation of insulin therapy  Other complications of insulin therapy-keloid,purpura,hyperkeratotic papules,hyperpigmentation
  • 55.
  • 56. Miscellaneous  Acquired perforating dermatoses  Vitiligo  Lichen planus  Pruritis
  • 57. Acquired perforating dermatosis  Umbilicated hyperpigmented papules with a central keratotic plug  Common site-extensor surface of extremities  Major symptom-pruritis  Strong association with chronic renal failure (ESRD)  Histology-transepidermal elimination of degenerative elastic /collagen fibres  Treatment-topical tretinoin,phototherapy
  • 58.
  • 59. vitiligo  Localized/generalized forms  1%-7 % in type 1 diabetics (0.2-1% in general population)  May be a part of polyglandular syndrome type 1  Rx-sun protection,topical/systemic steroids,phototherapy
  • 60. Lichen planus  Polyerythematous flat lesions  Sites-wrist,dorsal part of feet,lower leg  Oral/genital lesions-white lacy pattern  DD-lichenoid drug reactions  Treatment-topical steroids