Complications Of DM PDF
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Imam Mohammad Ibn Saud Islamic University
Dr.Ihsan Nasr Eldin
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This document provides an overview of the complications of diabetes mellitus (DM). It explores acute complications like diabetic ketoacidosis and chronic issues such as macrovascular disease and microvascular complications. The document further delves into infections, diabetic foot issues, and management strategies associated with these complications.
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COMPLICATIONS OF DM Dr.IHSAN NASR ELDIN DM COMPILICATIONS Acute complications include: • Diabetic ketoacidosis • Hyperglycemia hyperosmolar state. • Hypoglycemia. • Diabetic coma :a medical emergency in which the patient of DM is un conscious. Diabetic ketoacidosis • combination of severe hype...
COMPLICATIONS OF DM Dr.IHSAN NASR ELDIN DM COMPILICATIONS Acute complications include: • Diabetic ketoacidosis • Hyperglycemia hyperosmolar state. • Hypoglycemia. • Diabetic coma :a medical emergency in which the patient of DM is un conscious. Diabetic ketoacidosis • combination of severe hyperglycemia, dehydration ,shock, and exhaustion. AG . Hyperosmolar nonketotic coma • in which extreme hyperglycemia and dehydration alone are sufficient to cause unconsciousness. • Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. • ... Diagnosis is based on blood tests finding a blood sugar greater than 30 mmol/L (600 mg/dL), • osmolarity greater than 320 mOsm/kg, and a pH above 7.3. Severe diabetic hypoglycemia. . . . . Hypoglycemia in older people with diabetes is likely to be under-recognized due to the non-specific symptoms in this age group. Also, patients who have lost the warning symptoms of hypoglycemia are vulnerable as they may not be able to recognize a hypoglycemic episode. Equally, those who cannot communicate their feelings to their carers because of cognitive impairment are at similar risk. Therefore hypoglycemia in the elderly is likely to be under -reporeted COMPLICATIONS OF HYPOGLCEMIA Seizure Loss of consciousness Death Chronic complications of DM • Macrovascular disease µvascular . • Macrovascular disease • DM leads to cardiovascular disease, to which accelerated atherosclerosis is a contributor: • Coronary artery disease, leading to angina or myocardial infarction ("heart attack").3-5 times morein DM. • Diabetic myonecrosis ('muscle wasting') • Peripheral vascular disease which contributes to intermittent claudication (exertion-related leg and foot pain) as well as diabetic foot • Stroke (mainly the ischemic type).is twice likely in DM. macrovascular • Carotid artery stenosis. • Female infertility • is more common in women with diabetes type 1. • Delayed puberty and menarche. • menstrual irregularities (especially oligomenorrhoea), polycystic ovarian syndrome, Diabetic foot • often due to a combination of sensory neuropathy (numbness or insensitivity) and vascular damage. • increases rates of skin ulcers (diabetic foot ulcers) and infection and, in serious cases, necrosis and gangrene.( clostridium perfringens, an anaerobic.),It is why it takes longer for diabetics to heal from leg and foot wounds and why diabetics are prone to leg and foot infections. • In the developed world is the most common cause of non-traumatic adult amputation, usually of toes and or feet. DSF • 10–15% of diabetic patients develop foot ulcers at some stage in their lives. • Diabetic foot problems are responsible for nearly 50% of all diabetes-related hospital admissions. • Many diabetic limb amputations could be delayed or prevented by more effective patient education and medical supervision. • Ischaemia, infection and neuropathy combine to produce tissue necrosis. Although all these factors may co-exist, the ischaemic and the neuropathic foot) can be distinguished. Management DSF • Many diabetic foot problems are avoidable, (so patients need to learn the principles of foot care). • Older patients should visit a chiropodist/podiatrist regularly and should not cut their own toenails. • Once tissue damage has occurred in the form of ulceration or gangrene, the aim is preservation of viable tissue. • The four main threats to the skin and subcutaneous tissues are: • Infection.. Early antibiotic treatment is essential, with antibiotic therapy adjusted in the light of culture results. • Ischaemia. • Abnormal pressure. An ulcerated site must be kept non-weight-bearing. • Wound environment. • Dressings are used to absorb or remove exudate, maintain moisture, and protect the wound from contaminating agents, and should be easily removable. • Expensive new dressings containing growth factors and other biologically active agents may have a role to play in future. tt DSF • When irreversible arterial insufficiency is present, it is often quicker and kinder to opt for an early major amputation rather than subject the patient to a debilitating sequence of conservative procedures. Microvscular • The damage to small blood vessels leads to a microangiopathy, which can cause one or more of the following: • • Diabetic nephropathy, damage to the kidney which can lead to chronic renal failure, eventually requiring renal dialysis. It is the most common cause of adult kidney failure in the developed world. . • Diabetic neuropathy, abnormal and decreased sensation, usually in a 'glove and stocking' distribution starting with the feet but potentially in other nerves, later often fingers and hands. When combined with damaged blood vessels this can lead to diabetic foot. . • Other forms of diabetic neuropathy may • present as mononeuritis • or autonomic neuropathy. • Diabetic amyotrophy is muscle weakness due to neuropathy. microvascular • Diabetic retinopathy • growth of friable and poor-quality new blood vessels in the retina as well as macular • • • • • • • • • • • • • • • • • edema (swelling of the macula), leads to severe vision loss or blindness. Retinopathy is the most common cause of blindness among non-elderly adults in the developed world. 20 years after initial diagnosis of diabetes mellitus, almost all patients with Type I diabetes and 60% of patients with Type II diabetes will show signs of retinopathy on examination, although not all of these patients will be symptomatic. 30 years after diagnosis of diabetes, 30% of Type I diabetics and 3% of Type II diabetics will have : proliferative diabetic retinopathy. Risk factors: Duration of diabetes Glycaemic control Renal disease Systemic hypertension Hyperlipidaemia Pregnancy Laser treatment Previous diabetic eye disease Diabetic retinopathy • Visual loss may occur gradually (due to the maculopathy) or suddenly (due to vitreous hemorrhage). • Progression of diabetic retinopathy • Diabetic retinopathy can be divided into 3 stages: • non-proliferative (background) retinopathy • pre-proliferative retinopathy • proliferative retinopathy • Maculopathy (macular edema), describes the presence of non-proliferative changes in the macula. This is the leading cause of visual loss in patients with diabetic retinopathy. • . • Complications of proliferative retinopathy • Rubeosis iridis - neovascularisation of the iris, may cause a rise in intraocular pressure, resulting in • neovascular glaucoma. • Vitreous haemorrhage • Traction retinal detachment - oedema may separate the retinal pigment epithelium from the retina, resulting in retinal detachment. • Treatment Proliferative retinopathy is treated with laser photocoagulation therapy. Maculopathy is also treated using laser therapy directed at the points of leakage. If effective, the retinal oedema and exudate will resorb. .Vitrectomy may be indicated for patients with vitreous haemmorhage. Screening for diabetic retinopathy • A National Screening programme for diabetic retinopathy has been set up by the Department of Health. • It offers annual screening with digital photography of the fundus of patients over the age of 11 with diabetes. • Patients with signs of maculopathy, preproliferative or proliferative changes should be referred to an ophthalmologist. microangiopathy • Diabetic encephalopathy: • is the increased cognitive decline and risk of dementia, including : the Alzheimer's type. • Various mechanisms are proposed, like alterations to the vascular supply of the brain and the interaction of insulin with the brain itself. Microangiopathy • Diabetic cardiomyopathy, • damage to the heart muscle, leading to impaired relaxation and filling of the heart with blood (diastolic dysfunction) and eventually heart failure. • this condition can occur independent of damage done to the blood vessels over time from high levels of blood glucose. • Erectile Dysfunction: • Among men with erectile dysfunction, those with diabetes are likely to have experienced the problem as much as 10 to 15 years earlier than men without diabetes. • Periodontal disease (gum disease) is associated with diabetes • which may make diabetes more difficult to treat. • A number of trials have found improved blood sugar levels in type 2 diabetics who have undergone peridontal treatment. Infections • There is no evidence that diabetic patients with good glycaemic control are more prone to infection than normal subjects. • poorly-controlled diabetes entails increased susceptibility to the following infections: • Foot: Staphylococcus aureus and Staphylococcus epidermidis,anerobic • Skin – staphylococcal infections (boils, abscesses, carbuncles) – mucocutaneous candidiasis . • Gastrointestinal tract – periodontal disease gram-negative anaerobic bacteria – rectal and ischiorectal abscess formation (when control very poor) k. pneumonia. • Urinary tract – urinary tract infections Ecoli– pyelonephritis – perinephric abscess. • Lungs – staphylococcal and pneumococcal pneumonia – Gram-negative bacterial pneumonia – tuberculosis . • Bone – spontaneous staphylococcal spinal osteomyelitis. • infection • One reason why poor control leads to infection is that chemotaxis and phagocytosis by polymorph nuclear leucocytes are impaired because at highblood glucose concentrations .neutrophil superoxide generation is impaired. • Conversely, infections may lead to loss of glycemic control, and are a common cause of ketoacidosis. • • Insulin treated patients need to increase their dose by up to 25% in the face • of infection, and non-insulin-treated patients may need insulin cover while the infection lasts. • patient should be told , never to omit their insulin dose, even if they are nauseated and unable to eat; instead they should test their blood glucose frequently and seek urgent medical advice. • Diabetic patients should receive pneumococcal vaccine and yearly influenza vaccine. Thank you•