Clinical Examination of a Diabetic Patient Er

8/13/2019 Clinical Examination of a Diabetic Patient Er

1/38

CLINICAL EXAMINATION OF

THE DIABETIC PATIENT


2/38

GENERAL EXAMINATION

Weight:Weight loss in insulin deficiency and obesitiy in

Type 2 diabetes.Check height and calculate the BMI.

General examination:ill looking?,consious? Is the patient

in any respiraory distress?Tachynoea? Some may have

Kussmauls respirations- DKA.Dry mucous membranes-

dehydration in DKA and HHS


3/38

Hands:

Dupuytren's contracture is common in diabetes Carpal tunnel syndrome is common in diabetes

and presents with wrist pain radiating into the hand.

Trigger finger (flexor tenosynovitis) may be present

in people with diabetes.It is noninfectious inflammation of the flexor

tendon sheath of the finger (or thumb). Patients

often complain of pain and a sensation of

"snapping" when they flex the affected digit; thepain radiates into the palm or the distal finger


4/38

Limited joint mobility (sometimes called

'cheiroarthropathy')

This is the inability to extend (to 180) themetacarpophalangeal or interphalangeal joints of at

least one finger bilaterally. The effect can be

demonstrated in the 'prayer sign'. It causes painless

stiffness in the hands, and occasionally affects the

wrists and shoulders


5/38


6/38

Pebbled knuckles (or Huntley papules) are

multiple minute papules, grouped on the extensor

side of the fingers and on the knuckles.This arises

as a result of thickening of the skin on the dorsum

of the hand.


7/38


8/38

Pulse: Tachycardia occurs in DKA and HHS

Blood pressure: Hypotension in DKA and HHS

Neck: Carotid pulses and bruits,Thyroid enlargement.

Head:Cranial nerve palsies,ptosis,eye movements

Examine the eyes for lens opacities,visual acuity and do

fundoscopy


9/38

Insulin Injection sites:Anterior abdominal wall Upper

thighs/buttocks ,Upper outer arms. Inspect for

bruising, Subcutaneous fat deposition(lipohypertrophy) ,Subcutaneous fat loss

(lipoatrophy),erythema, infection (rare)

Abdomen:Hepatomegaly.Due to fatty infiltration inthe liver(NAFLD). Type 2 DM is a risk factor.NAFLD

may lead to cirrhosis

Lower limbs:Muscle wasting,sensory abnormalitybytesting for sensation, tendon reflexes and

peripheral pulses .


10/38

DERMATOLOGICAL

MANIFESTATIONS OF

DIABETES MELLITUS.


11/38

Diabetes mellitus can be complicated by varietyof cutaneous manifestations. Good metabolic

control may prevent some of these

manifestations and may support cure. Almost all

diabetic patients eventually develop skin

complications from the long-term effects ofdiabetes mellitus on the microcirculation and on

skin collagen.


12/38

Patients who have had diabetes for many

years tend to develop the most devastatingskin problems. However, problems can also

develop in the short term, as insulins and

oral hypoglycemic drugs can also have

dermal side effects. Furthermore, diabetes-related cutaneous lesions may also serve as

a port of entry for secondary infection.


13/38

Poor and delayed wound healing and skin ulceration.

Insulin signaling supports normal skin proliferation,differentiation, and maintenance, and a lack of insulin

may lead to impaired wound healing.


14/38

Periungual telangiectasia:They appear as red, dilated,

capillary veins bordering the base and lateral aspects of

the nail plate. A prevalence up to 49% has been

described in all diabetic patients. In diabetes, periungual

telangiectasia is often associated with nail fold erythema,

accompanied by fingertip tenderness and ragged

cuticles.


15/38


16/38

Necrobiosis lipoidica:

The initial lesions of NLD begin as well-circumscribed

erythematous papules. Evolving radially, the sharplydefined lesions have depressed, waxy, yellow-brown,

atrophic telangiectatic centers through the underlying

dermal vessels can be visualized. The periphery is

slightly raised and erythematous. The pretibial region isthe area typically affected. Ulceration occurs in up to 35%

of cases. Women are affected more often than men.

Patients with type 1 diabetes develop necrobiosis

lipoidica at an earlier mean age than those with type 2

and those without diabetes.


17/38


18/38

Bullosis Diabeticorum (Diabetic bullae)

This develops in approximately 0.5% of diabetic patients,but more often in those with type 1 diabetes, and more

often in men and in patients with long-standing diabetes

with peripheral neuropathy. It presents as asymptomatic

bullae containing sterile fluid on a noninflamed base,

usually arising spontaneously on the dorsa and sides of

the lower legs and feet, sometimes on the hands or the

forearms. The cause is unknown, and it is a diagnosis of

exclusion.


19/38


20/38

Vitiligo

Vitiligo vulgaris, or skin depigmentation, occurs more

often in type 1 diabetic patients. From 1% to 7% of alldiabetic patients have vitiligo vs 0.2% to 1% of the

general population.


21/38


22/38

Lichen planus

Clinically, lichen planus presents as polygonal

erythematous flat lesions. Most often affected are thewrists, the dorsa of the feet, and the lower legs. Oral

lichen planus presents as white stripes in a reticular

pattern and may occur in some diabetic patients.


23/38


24/38

Scleroderma diabeticorum

Scleredema diabeticorum is characterized by thickening

of the skin of the posterior neck and upper back,occasionally extending to the deltoid and lumbar regions.

A peau dorangeappearance of the skin can occur, often

with decreased sensitivity to pain and touch.It almost

exclusively occurs in long-standing diabetes, is usuallypermanent, is not related to previous infection, and

usually occurs in middle aged,overweight poorly

controlled type 2 diabetes.


25/38


26/38

Acanthosis nigricans

Acanthosis nigricans presents as hyperpigmented,

velvety plaques in body folds. The dark color is due to

thickening of keratin-containing superficial epithelium.

The pathogenesis is most likely related to high levels of

circulating insulin, which binds to insulin-like growth

factor receptors to stimulate the growth of keratinocytes

and dermal fibroblasts.Although the lesions are generally asymptomatic, they

can be painful, malodorous, or macerated.


27/38


28/38

Granuloma annulare

The cause is not known. The lesions are oval or ring-

shaped, with a raised border of skin-colored or

erythematous papules. The size varies from millimeters

to centimeters. The dorsa of the hands and arms are the

areas usually affected.This skin manifestation has no

direct association with diabetes but may be seen in somediabetics.


29/38


30/38

Diabetic dermopathy

Diabetic dermopathy (ie, shin spots and pigmented

pretibial papules) affects 7% to 70% of all diabetic

patients and has been termed the most common

cutaneous finding in diabetes. It is usually noted as

asymptomatic atrophic, scarred, hyperpigmented, finely

scaled macules, which are usually bilateral but notsymmetrically distributed.Lesions may also be found on

the forearms, thighs, and lateral malleoli. Several studies

found severe microvascular complications in patients with

diabetic dermopathy, indicating a close association with ahigh risk of accelerated diabetes complications.


31/38


32/38

Yellow Skin and nails

The possible cause of yellow skin and nails might

be glycosylation end products. It is known thatproteins which have a long turnover time, such as

dermal collagen, undergo glycosylation and

become yellow. Yellow skin is a common finding

among patients with diabetes, probably bestappreciated on the palms and soles because of

sparse competition with melanocytic pigment in

these areas


33/38

WHEREASKERATINOFTHEEPIDERMISISONLYPRESENT

FORONEMONTHBEFOREBEINGSHED, THATOFTHENAIL

PLATEMAYBEPRESENTFORGREATERTHANAYEAR. THEPROTEIN- GLUCOSE REACTION PRESUMABLY CONTINUES

TOEVOLVE INTHEAGINGNAILRESULTING INTHEMOST

YELLOWPIGMENTATTHEDISTALASPECTNAIL.


34/38

Insulin lipoatrophy and lipodystrophy.

Lipoatrophy presents as circumscribed, depressed areas

of skin at the insulin injection site 6 to 24 months after thestart of therapy. Children and obese women are affected

most often. It may be caused by lipolytic components in

the insulin preparation or by an inflammatory process

mediated by immune complex.


35/38

Other theories involve cryotrauma from refrigerated

insulin, mechanical trauma due to the angle ofinjection, surface alcohol contamination, or local

hyperproduction of tumor necrosis factor alpha from

macrophages induced by injected insulin.


36/38


37/38

Lipohypertrophy clinically resembles lipoma and

presents as soft dermal nodules at the site offrequent injections. Lipohypertrophy is regarded as

a local response to the lipogenic action of insulin

and can be prevented by rotation of the injection

site


38/38

Clinical Examination of a Diabetic Patient Er

Documents