COMPLICATIONS OF DIABETES

Patients with diabetes have a reduced life expectancy. Cardiovascular prob-lems (70%) followed by chronic kidney disease (10%) and infections (6%) are the most common causes of premature death in treated patients. Com-plications are directly related to the degree and duration of hyperglycaemia and can be reduced by improved diabetic control.

Vascular

Macrovascular complications

Diabetes is a risk factor for atherosclerosis and this is additive with other risk factors for large vessel disease, e.g. smoking, hypertension and hyper-lipidaemia. Atherosclerosis results in stroke, ischaemic heart disease and peripheral vascular disease. The risk is reduced not only by good diabetic control but also modification of other risk factors. This includes aggressive control of blood pressure (target <130/80 mmHg), cessation of smoking, treatment with a statin for most type 2 diabetics irrespective of serum cho-lesterol, and treatment with an angiotensin-converting enzyme (ACE) inihibi-tor (or angiotensin II receptor antagonist in the event of ACE inhibitor intolerance, usually a cough) for patients with one other major cardiovascular risk factor. Some patients depending on age and other cardiovascular risk factors are also treated with low-dose aspirin.

Microvascular complications

In contrast to macrovascular disease, microvascular disease is specific to diabetes. Small vessels throughout the body are affected, but the disease process is of particular danger in three sites: the retina, the renal glomerulus and the nerve sheath. Diabetic retinopathy, nephropathy and neuropathy tend to manifest 10-20 years after diagnosis in young patients. They present earlier in older patients, probably because they have had unrecognized dia-betes for months or even years before diagnosis.

Diabetic eye disease

About one-third of young diabetics develop visual problems, and in the UK 5% have become blind after 30 years of diabetes. However, the prevalence is falling. Diabetes affects the eye in a variety of ways:

■ Diabetic retinopathy with lesions developing in the retina and the iris

■ Cataracts develop earlier in diabetics than in the general population. Temporary blurred vision also occurs caused by reversible osmotic changes in the lens in patients with acute hyperglycaemia

■ External ocular palsies - the sixth and third nerve are most commonly affected (p. 731).

Retinopathy

Diabetes is the most common cause of blindness in people under 65 years old. At diagnosis almost 30% of people with diabetes have early retinal damage (background retinopathy) which increases as the duration of diabetes increases. Diabetic retinopathy is divided into two major forms: non-proliferative and proliferative, named for the absence or presence of abnor-mal new blood vessels (neovascularization) arising from the retina (Table 15.6

Table 15.6 Classification of diabetic retinopathy

Retinopathy grade

Retinal abnormality (cause of abnormality)

Peripheral retina

Non-proliferative/background

Tiny red dots (capillary microaneurysms)

Larger red spots (intraretinal ‘blot’ haemorrhages)

*Hard exudates (capillary leaks of plasma rich in lipids and protein)

Pre-proliferative

Venous beading/loops

Growth of intraretinal new vessels

*Multiple cotton wool spots (oedema from retinal

infarcts)

Proliferative

Preretinal new (fragile) blood vessel formation Preretinal or subhyaloid haemorrhage (from above)

Vitreous haemorrhage

Advanced retinopathy

Retinal íibrosis Traction retinal detatchment

Central retina

Maculopathy

Macula oedema Perimacular hard exudates

NB: *hard exudates have a bright yellowish white colour and are often irregular in outline with a sharply defined margin. Cotton-wool spots are greyish white, have indistinct margins and a dull matt surface, unlike the glossy appearance of hard exudates.

Fig. 15.2 Some features of diabetic eye disease. (A) The normal macula (centre) and optic disc. (B) Dot and blot haemorrhages (early background retinopathy). (C) Multiple frond-like new vessels, the hallmark of proliferative retinopathy. White fibrous tissue is forming near the new vessels, a feature of advanced retinopathy (this eye also illustrates multiple xenon arc laser burns superiorly). (D) Exudates appearing within a disc-width of the macula are a feature of an exudative maculopathy.

and Fig. 15.2). Proliferative retinopathy develops as a consequence of damage to retinal blood vessels and the resultant retinal ischaemia which occurs in non-proliferative retinopathy. Most patients are asymptomatic until the late (and often untreatable) stages. Retinal screening programmes for people with diabetes perform annual assessment of visual acuity and digital retinal photography by trained staff. Patients with background retinopathy need annual review only to look for progression to maculopathy or prolifera-tive retinopathy. All other forms of retinopathy require referral to an ophthal-mologist, urgently in the case of proliferative and advanced retinopathy as vision is immediately threatened. New vessel formation and maculopathy are treated by laser photocoagulation of the retina. The development and pro-gression of retinopathy is accelerated by poor glycaemic control, hyper-tension and smoking.

The diabetic kidney

The kidney may be damaged by diabetes as a result of:

■ Glomerular disease

■ Ischaemic renal lesions

■ Ascending urinary tract infection.

Diabetic nephropathies Clinical nephropathy secondary to glomerular disease usually manifests 15-25 years after diagnosis and affects 25-35% of patients diagnosed under the age of 30 years. On microscopy there is thickening of the glomerular basement membrane and later glomerulo-sclerosis, which may be a diffuse or nodular form (Kimmelstiel-Wilson lesion). The earliest clinical evidence of glomerular damage is ‘microalbu-minuria' - an increase above the normal range in urinary albumin excretion but undetectable by conventional dipsticks (p. 358). This may, after some years, progress to intermittent albuminuria followed by persistent proteinuria, sometimes with a frank nephrotic syndrome. At the stage of persistent pro-teinuria the plasma creatinine is normal but the average patient is only some 5-10 years from end-stage kidney disease.

The urine of all patients should be checked at least once a year by dip-sticks for the presence of protein. Most centres also screen for micro-albuminuria, because meticulous glycaemic control and treatment with angiotensin-converting enzyme (ACE) inhibitors at this stage (even in the absence of hypertension) may delay the onset of frank proteinuria. Aggressive control of blood pressure (target below 130/80 mmHg) is the most important factor to reduce disease progression in those with established proteinuria- ACE inhibitors (or angiotensin receptor II antagonists for those intolerant) are the treatment of choice. Many will develop end-stage kidney disease and need dialysis and eventually renal transplantation. A segmental pancreatic graft is sometimes performed at the same time as a renal graft.

Ischaemic lesions Arteriolar lesions with hypertrophy and hyalinization of the vessels affect both afferent and efferent arterioles. The appearances are similar to those of hypertensive disease but are not necessarily related to the blood pressure in patients with diabetes.

Infective lesions Urinary tract infections are common (p. 370). A rare complication is renal papillary necrosis, in which renal papillae are shed in the urine and may cause ureteral obstruction.

Diabetic neuropathy

The types of diabetic neuropathy are summarized in Table 15.7. Isolated mononeuropathies are thought to result from occlusion of the vasa nervorum (the small arteries that provide blood supply to the peripheral nerves) while the other more diffuse neuropathies may arise from accumulation of fructose

Table 15.7 Diabetic neuropathies

Progressive

Symmetrical sensory polyneuropathy

Autonomic neuropathy

Reversible

Acute painíul neuropathy

Mononeuropathy and mononeuritis multiplex
Cranial nerve lesions
Isolated peripheral nerve lesions

Isolated peripheral nerve lesions

Diabetic amyotrophy

and sorbitol (metabolized from glucose in peripheral nerves) which disrupts the structure and function of the nerve.

Symmetrical mainly sensory neuropathy This is the most common form of neuropathy and affects the feet first. It is often unrecognized by the patient in the early stages. Early clinical signs are loss of vibration sense, pain sensation (deep before superficial) and temperature sensation in the feet. At later stages patients may complain of ‘walking on cotton wool' and may lose their balance when walking in the dark or while washing the face due to impaired proprioception. Involvement of the hands is uncommon. Complications include unrecognized trauma, beginning as blistering caused by an ill-fitting shoe or a hot-water bottle, and leading to ulceration. Abnormal mechanical stress and repeated minor trauma, usually prevented by pain, may lead to the development of a neuropathic arthropathy (Charcot's joints) in the ankle and knee, where the joint is grossly deformed and swollen. Involvement of the motor nerves may lead to wasting of the small muscles of the hand and a distorted foot with a high arch and clawing of the toes. All patients with diabetic sensory neuropathy are at risk of insensitive foot ulceration. They should learn the principles of foot care (p. 686) and visit a chiropodist regularly.

Acute painful neuropathy The patient describes burning or crawling pains in the lower limbs. Symptoms are typically worse at night, and pressure from bedclothes may be intolerable. Treatment is with good diabetic control, tricyclic antidepressants, gabapentin or carbamazepine.

Mononeuritis and mononeuritis multiplex (multiple mononeuro-pathy) One or more individual nerves are affected including involvement of a spinal root (radiculopathy). Onset may be abrupt and painful. Lesions are more likely to occur at common sites for external pressure, e.g. carpal tunnel syndrome. The most common cranial mononeuropathies are the third and sixth nerves supplying the extraocular muscles. Presentation is with unilateral pain, ptosis, and diplopia, with sparing of pupillary function.

Diabetic amyotrophy presents with painful wasting, usually asymmet-rical, of the quadriceps muscles. The wasting may be marked and knee reflexes are diminished or absent.

Autonomic neuropathy affects the cardiovascular system (resting tachy-cardia and loss of sinus arrhythmia, postural hypotension and peripheral vasodilation with a warm foot and bounding pulse), gastrointestinal tract (diarrhoea and gastroparesis leading to intractable vomiting), bladder (incom-plete emptying followed by an atonic painless distended bladder) and male erectile dysfunction. There is no specific treatment and management is based on a symptom approach.

The diabetic foot

Foot problems are a major cause of morbidity and mortality in patients with diabetes mellitus, with infection, ischaemia and neuropathy all contributing to produce tissue necrosis. On physical examination evidence of a neuropathy is demonstrated by reduced sensation to vibration, temperature and pin-prick. There may be evidence of Charcot arthropathy. Signs of vascular disease in the lower leg include thin skin and absence of hair, bluish discol-oration of the skin, reduced skin temperature and absent foot pulses. Many diabetic foot ulcers are avoidable, so patients need to learn the principles of foot care: well-fitting lace-up shoes, regular chiropody, no ‘bathroom' surgery, daily inspection of feet and early advice for any damage, and finally avoiding sources of heat, such as radiators and hot bath water. Management of foot lesions involves:

■ Swabbing of ulcers for bacterial culture and early antibiotic treatment

■ Good local wound care and, if necessary, surgical debridement of ulcers

■ Evaluation for peripheral vascular disease by clinical examination, meas-urement of blood flow (by Doppler probe) and femoral angiography if clinically indicated

■ Reconstructive vascular surgery for localized areas of arterial occlusion.

Infections

Poorly controlled diabetes impairs the function of polymorphonuclear leuco-cytes and confers an increased risk of infection, particularly of the urinary tract and skin, e.g. cellulitis, boils and abscesses. Tuberculosis and muco-cutaneous candidiasis are more common in diabetic individuals. Infections may lead to loss of glycaemic control and are a common cause of keto-acidosis. Insulin-treated patients may need to increase their insulin therapy even if they feel nauseated and unable to eat. Non-insulin-treated patients may need insulin for the same reasons.

The skin

■ Lipohypertrophy (fat lumps at frequently used insulin injection sites) are avoided by varying the injection site from day to day.

■ Necrobiosis lipoidica diabeticorum is an unusual complication of diabetes characterized by erythematous plaques, often over the shins, which gradually develop a brown waxy discoloration.

■ Vitiligo is symmetrical white patches seen in diabetes mellitus and other organ-specific autoimmune diseases.

■ Granuloma annulare - flesh-coloured rings and nodules, principally over the extensor surfaces of the fingers.

Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

2. Infectious diseases

Infectious diseases

3. Gastroenterology and nutrition

Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
JAUNDICE
HEPATITIS
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
CIRRHOSIS
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
LIVER TRANSPLANTATION
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER ABSCESS
LIVER DISEASE IN PREGNANCY
LIVER TUMOURS
GALLSTONES
THE PANCREAS
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS

5. Haematological disease

Haematological disease
ANAEMIA
Assessment and treatment of suspected neutropenic sepsis
HAEMOLYTIC ANAEMIA
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
MYELOPROLIFERATIVE DISORDERS
THE SPLEEN
BLOOD TRANSFUSION
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
THROMBOSIS
THERAPEUTICS

6. Malignant disease

Malignant disease
MYELOABLATIVE THERAPY AND HAEMOPOIETIC STEM CELL TRANSPLANTATION
THE LYMPHOMAS
THE PARAPROTEINAEMIAS
PALLIATIVE MEDICINE AND SYMPTOM CONTROL

7. Rheumatology

Rheumatology
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
BACK PAIN
OSTEOARTHRITIS
INFLAMMATORY ARTHRITIS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
THERAPEUTICS

8. Water, electrolytes and acid–base balance

WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
THERAPEUTICS

9. Renal disease

Renal disease
INVESTIGATION OF RENAL DISEASE
GLOMERULAR DISEASES
NEPHROTIC SYNDROME
URINARY TRACT INFECTION
TUBULOINTERSTITIAL NEPHRITIS
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
TESTICULAR TUMOUR
URINARY INCONTINENCE

10. Cardiovascular disease

COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
CARDIAC ARRHYTHMIAS
HEART FAILURE
ISCHAEMIC HEART DISEASE
RHEUMATIC FEVER
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
MYOCARDIAL DISEASE
CARDIOMYOPATHY
PERICARDIAL DISEASE
SYSTEMIC HYPERTENSION
ARTERIAL AND VENOUS DISEASE
ELECTRICAL CARDIOVERSION
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS

11. Respiratory disease


Respiratory disease
TUBERCULOSISnd
DIFFUSE DISEASES OF THE LUNG PARENCHYMA
OCCUPATIONAL LUNG DISEASE
CARCINOMA OF THE LUNG
DISEASES OF THE CHEST WALL AND PLEURA
DISORDERS OF THE DIAPHRAGM

12. Intensive care medicine

Intensive care medicine

13. Drug therapy, poisoning, and alcohol misuse

Drug therapy, poisoning, and alcohol misuse

14. Endocrine disease

Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
THERAPEUTICS

15. Diabetes mellitus and other disorders of metabolism

DIABETES MELLITUS
DIABETIC METABOLIC EMERGENCIES
COMPLICATIONS OF DIABETES
SPECIAL SITUATIONS
HYPOGLYCAEMIA IN THE NON - DIABETIC
DISORDERS OF LIPID METABOLISM
THE PORPHYRIAS

16. The special senses

THE EAR
THE NOSE AND NASAL CAVITY
THE THROAT
THE EYE

17. Neurology

COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HYDROCEPHALUS
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES
MUSCLE DISEASES
MYOTONIAS
DELIRIUM
THERAPEUTICS

18. Dermatology

Dermatology



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