Complications of diabetes
Educator in Diabetes
Diabetes is a major and increasing health problem. It affects people at any age and in all countries. It is a disease that lasts from its inception throughout the patient’s life, usually for a few dozen years.
It is one of the main direct and indirect perpetrators of disability – blindness, kidney failure, gangrene and amputation of the lower limbs, the severity of coronary heart disease and stroke and early human mortality.
Complications of diabetes can be acute i.e. states where deep metabolic disorders appears suddenly, usually combined with disorders of fluid-electrolyte balance and acid-alkaline balance, fast leading to a significant impairment of general condition, loss of consciousness and sometimes death.
The second group of complications are chronic diseases i.e. specific groups of disorders and symptoms of being a clinical exponent of changes in vessels, nerves and other organs that appear along diabetes and contribute to disability and premature mortality.
Acute metabolic disorders – diabetic comas, in fact, is not a complication of diabetes, but the consequence of insulin deficiency. In the period before the discovery of insulin they were regarded as the final stage of the disease. Currently they appear only if there is no or improper treatment. Diabetic coma can have a different course, which results from separate pathogenic mechanisms leading to this condition.
At this time, the following types are distinguished:
- diabetic ketoacidosis
- severe diabetic hypoglycaemia
- hyperosmolar nonketotic coma
Occurs most often (mainly in patients with type 1 diabetes – juvenile diabetes, absolute insulin deficiency) and the best known. It develops in the course of diabetic ketoacidosis, which affects mainly people completely devoid of pancreatic islet beta cells.
- infections, especially purulent ones where rapidly increasing insulin resistance results in increased demand for insulin
- severe systemic diseases such as myocardial infarction, stroke, pneumonia, and major surgeries
- pregnancy with insulin resistance and increased insulin demand
- lack of patient education – often ignorant patients discontinue insulin delivery due to the loss of appetite (fever) and fear of hypoglycaemia
The clinical picture is quite diverse, and the intensity and type of common ailments and symptoms are not always formed parallel to the results of laboratory tests.
Symptoms may be presented in several groups:
Consequences of dehydration: very large thirst, polyuria reaching a few litres a day, dry tongue and mucous membranes, dry skin, soft eyeballs. Initially there is an increase in body temperature, which, if there is no infection, later turns into hypothermia, a drop in blood pressure, especially in elderly people, in extreme cases, loss of pulse and bruising of the distal parts of the body.
Gastrointestinal disorders: dreg type vomiting, abdominal pain – in extreme cases, false peritoneal symptoms (ketotic abdomen), enlargement of the liver.
Respiratory disorders: Kussmaul breath (breath of a chased dog) – deep and laboured characterised by four phases: inhale – pause – exhale – pause, acetone odour can be felt in the breath – the smell of rotten apples.
Consciousness disorders: four stages can de distinguished in the developing ketoacidosis:
- tiredness, impaired balance and vision
- state of somnolence, abnormal thinking
- deep sleep with preserved reactions to painful stimuli: the weakening of physiological reflexes
- deep neurological coma with the reduction of response to painful stimuli and physiological reflexes
Once the diabetic coma or being at risk of it is diagnosed, the patient should be immediately sent to the nearest hospital. It would be perfect if there was diabetes ward with intensive care room in the hospital.
The treatment of diabetic ketoacidosis includes:
- insulin delivery – preferably by continuous infusion by means of a pump
- supplementing fluid and electrolyte insufficiency
- use of alkalising medicines
- treatment of complications
Another condition which is a complication not of diabetes itself, but the treatment. Blood hypoglycaemia of various severity are the most common complications arising in people treated with insulin; therefore, anyone who comes into contact with diabetics, should have knowledge about hypoglycaemia.
- errors in insulin therapy: determining too much insulin, a mistake in the measurement of the dose of insulin, too late reduction of the dosage, when patient’s body weight decreased, diet therapy proved to be more accurate, infection was removed
- the pursuit of too rapid metabolic levelling out by a large increase in the dose of rapid-acting insulin, or despite the absence of conditions for this
- errors in nutrition: too long intervals between meals, too little carbohydrate in the meal, alcohol
- disorders of the gastrointestinal tract: vomiting, diarrhoea, abnormal gastric emptying
- changes in the absorption of insulin: change of injection place, the muscles in the thigh, where insulin is administered (march immediately after the administration of insulin), heating the injection site (shower after the injection), change in the depth of the puncture, accidental intramuscular or intravenous injection
- starting a new vial of insulin: the insulin may be more active than previously used, stored at room temperature
- reduced need for insulin due to emotional hyperactivity, menstruation, hormonal disorders
- intake of glucose lowering medicines: acetylsalicylic acid, beta-blockers
- increased physical activity
- natural remission of diabetes
Signs and symptoms:
There are many symptoms of hypoglycaemia. Particularly rich and varied individually is the subjective symptomatology. Symptoms are more limited objective and non-specific. Time and rate of increase of symptoms depend to a large extent on the type of insulin, the amount of injected dose and the daily dosage schedule.
In blood hypoglycaemia we can distinguish:
Neurovegetative symptoms (catecholamine): agitation, fatigue, skin pallor, sweating, dilated pupils, tachycardia, a moderate increase in pressure. Symptoms present at glucose concentration of 65 – 55 mg/dl.
Neuroglycopenia symptoms are caused by a reduction of transmission of glucose to the brain. They can be divided into mental symptoms: anxiety, abnormal thinking, cognitive disorders, inability to concentrate, personality changes, amnesia, manic behaviour, delirium, and neurological symptoms: slurred speech, vision, clonic and tonic spasms, overactive tendon reflexes, positive Babinski sign, loss of consciousness. These symptoms occur when the glucose concentration reached approximately 45 mg/dl.
The neurovegetative symptoms are a warning to the patient of threatening neuroglycopenia and are indication for acute prophylactic – eating a meal or sugar. Within time these symptoms of diabetes are reduced or even disappear.
The treatment deals with immediate administration of carbohydrate in an amount increasing blood glucose. Mild hypoglycaemic states are treated by the consumption of additional food, if necessary, a few lumps of sugar that a diabetic patient should always have on him/her.
In states of unconsciousness 1 mg of glucagon should be injected. Upon regaining the consciousness, the patient should be fed and watered with sweet liquid until return to normal glucose level. If we are able to give drugs intravenously, the patient should get 1 mg of glucagon subcutaneously, then we give 5 or 10% glucose until the glycaemic stabilises. In case of insulin overdose, after transient improvement the hypoglycaemia may occur again. Such a patient requires hospitalisation. In most cases of hypoglycaemia the prognosis is good. It can be quickly and easily controlled. However, repeated hypoglycaemic states can cause chronic threat due to the extinction of warning signs and abnormal neurohormonal regulation of glycaemic homeostasis.
Very severe hypoglycaemic shock can lead to death or cause permanent damage to the central nervous system and permanent maintenance of mental and neurological symptoms. In diabetic patients treated with insulin, the appearance of hypoglycaemia state is an alarming condition and requires prompt clarification of the cause of this complication, and if necessary correction of the treatment. Appropriate therapeutic programs should implement, taking into account the patient’s involvement in order to minimise the risk of this complications.
CHRONIC COMPLICATIONS OF DIABETES
The characteristic feature of organ changes, referred to as chronic complications of diabetes, is their slow and long-term development. Therefore, they disclose as well-defined clinical syndromes or less specific symptoms of the disease at a later stage, and only then they can cause disability and life threat. For these reasons they are called late complications of diabetes. Long-term asymptomatic evolution of the changes bears the danger of underestimating the negative impact on the prognosis of diabetes.
The major chronic complications of diabetes include:
- changes in the vessels – angiopathia diabetica, changes affect both large vessels – macroangiopathy, and small vessels and capillaries – microangiopathy
- changes in peripheral nerves – neuropathy
- changes outside the circulatory and nervous system: gastrointestinal tract, skin, motor organ, lens
Small vessel disease are diabetes-specific changes in the capillaries, which are present in all organs, in which the vessels have a basal membrane e.g. changes to the capillaries in the eyes and kidneys cause such significant damage to these organs that it is disclosed in the form of characteristic clinical syndromes. These syndromes are the cause of disability, and even premature death.
The treatment should be initiated by the correction and providing the best possible clinical and biochemical indicators. It is important to introduce the change relatively slowly. Too violent attempts to stabilise the diabetes may lead to accelerate the progress of changes. In the symptomatic treatment vessel sealing preparations are used.
Prevention refers to optimal diabetes treatment from the beginning of the disease with the use of contemporary therapies. It is recommended to take early prevention in form of regular evaluation of the ocular fundus and kidney function.
Large vessel disease whose anatomical substrate is atherosclerosis, and to a lower extent – hardening of arterioles. Changes in the arteries and arterioles are very common in diabetes and appear earlier and are more intensive, which in turn causes premature death or disability. They are especially common among patients with type 2 diabetes, especially in the elderly.
Characteristic features of the large vessel disease in people with diabetes:
Coronary heart disease is most common and is the leading cause of death in diabetic patients. A characteristic feature is asymptomatic and painless myocardial infarction. Approximately in 8% of people with diabetes, both women and men, an ECG test shows abnormalities that might be the evidence of past cardiac necrosis. This applies mainly to patients with long-lasting diabetes, in whom coronary artery disease coexists with other late complications of diabetes, especially diabetic nephropathy.
Cerebrovascular disease is a collection of non-specific for diabetes neurological syndromes, which are the clinical expression of brain ischemia as a result of atherosclerosis and hardening of the arterioles. Cerebral haemorrhages rarely occur in diabetic patients. Thromboembolic changes prevail, which can cause cerebral infarction and softening. Approximately in half of the diabetic patients after stroke also microangiopathic, retinopathic and nephropathic changes appear.
Leg artery disease is the equivalent of arterial occlusive atherosclerosis. The name “leg artery disease” was introduced the WHO Expert Committee on Diabetes to note that:
- vessel changes in diabetic patients are more varied and apart from the atherosclerosis of large vessels include also the sclerosis of arterioles and small vessel disease, and therefore are more extensive and reach the end of the limb
- in diabetes the changes in a specific way focus in the lower limbs; the changes are here more advanced than in other sections of the vascular system.
Occlusion of bigger arteries or arterioles by a sudden or more slowly forming clot causes the necrosis of the most remote sections of the foot or foot gangrene – gangrene pedis diabetica that due to the complexity of its pathogenesis, should be treated as a separate clinical syndrome. Leg artery disease can result in severe disability.
Various kinds of damage to the peripheral nervous system, and its clinical forms are:
Symmetrical sensorimotor peripheral neuropathy characterised by the earlier damage of sensory nerve, lower – of the motor nerves; the lower limbs are predisposed to these changes, and rarely the upper limbs.
The clinical picture
In the initial period: tingling, burning, less impetuous and burning pain in the feet. The symptoms are at rest, intensifying at night under the influence of heat. Sometimes there may appear thermal paraesthesia and the sensation of cold, despite the fact that the feet are warm. Often the „restless legs” symptom appears, forcing them to constant move and change of position.
Mild neuropathy, in which symptoms intensify. Particularly troublesome is the sensation of burning feet. At the same time there are areas with reduced surface sensation, localised mainly in distal sections of the limbs, resembling due to its scope „gloves” or „socks”.
Severe neuropathy causing all forms of disorders to superficial sensation and vibrations. The sensory disturbance is accompanied by physiological reflexes. There appear areas of pain hypoaesthesia, favouring painless injuries. Later on, paresis and muscular atrophy appear, usually affecting foot extensors, small foot muscles, while in the upper limb they affect muscles innervated by the ulnar nerve. The changes in the muscle are accompanied by neurotrophic changes in osteoarthritis.
Focal neuropathy (mononeuropathy) – this complication involves damage to a single sensory or motor nerve, or to several nerves simultaneously, but then these changes are not symmetric and affect nerves in different areas of the body. It is assumed that its immediate cause is sudden ischemia resulting from closure of a nutrient vessel. The main symptoms of mononeuropathy are very strong radiating pain characteristic of the busy nerve and paresis. Mostly the changes affect: the femoral, sciatic, peroneal, median and ulnar nerve. Despite dramatic progress complete recovery can be seen within a few weeks or months.
Autonomic neuropathy is a group of symptoms affecting the autonomic neurons of either or both of the parasympathetic and sympathetic nervous systems.
The clinical picture consists of various syndromes reflecting dysfunctions of individual organs and systems.
Diabetic foot syndrome is a collective term for changes that occur on feet in patients with long-standing diabetes. Their main reason is diabetic specific damage to foot nerves – diabetic neuropathy. It is accompanied by changes in the joints, ligaments and foot bones as well as vascular changes, with causes that the foot is shortened, widened, the longitudinal arch gets deeper. Pressure places appear on the sole, and the reaction of the skin to them is the creation of calluses and cracks in the skin, which are the starting point for infection and foot ulcers.
Pathological changes and clinical symptoms on the lower limbs and feet:
- Changes in the vasculature: atherosclerosis, hardening of the arterioles, microangiopathy of foot tissues, ischemia of soft tissues and bones, formation of infected or not infected necrosis.
- Changes in the innervation of the foot: the loss or impairment of sensory innervation (decrease or loss of pain sensation of pain, temperature, touch, vibration), motor activity (impairment of muscle tension and foot movements, muscle atrophy), autonomic activity (impaired regulation of blood flow through the foot); trophic disorders in the joints (formation of deformations, impaired sweating).
- Skin changes: pale or grey-blue skin, papery, dry, cracked, non-elastic, hair loss, abnormal growth of nails, calluses, necrosis and ulceration.
- Changes in the muscle: muscle weakness, changes in tension, muscle atrophy, contracture.
- Bone abnormalities: bone loss, necrosis, deformations.
Treatment depends on the degree of foot damage. The diagnosis of diabetes begins with conservative treatment. The aim is to metabolic equalisation of the disease, avoid, and preferably completely give up smoking and alcohol consumption, implement an intensive program of general physical exercise and especially foot exercise and their care.