Diabetes - Presenting problems Flashcards
In a patient with newly discovered hyperglycaemia, what is the key goal?
The key goals are to establish whether the patient has diabetes, what type of diabetes it is, and how it should be treated.
How is the diagnosis of diabetes established in a patient with newly discovered hyperglycaemia?
If the patient is symptomatic (i.e. polyuria, polydipsia, fatigue, dehydration etc), then the diagnosis can be confirmed by a random plasma glucose concentration of >11.1 mmol/l or a fasting plasma glucose concentration of >7 mmol/l. In an asymptomatic patient two samples are required.
An oral glucose tolerance test (OGTT) is indicated when plasma glucose levels are elevated but not diagnostic of diabetes: fasting range 6.1-7 mmol/l, or random plasma glucose range 7.8-11.0 mmol/l. These values come from the WHO diagnostic criteria for diabetes and are based on the risk of developing microvascular disease.
Patients who do not meet the criteria for diabetes may have “impaired glucose tolerance” (IGT) or “impaired fasting glucose”. These patients have an increased risk of progression to frank diabetes and of macrovascular disease.
What is stress hyperglycaemia?
Stress hyperglycaemia occurs when conditions impose a burden on the pancreatic beta cells - e.g. during pregnancy, infection or treatment with corticosteroids. It usually disappears after the acute illness has resolved, but blood glucose should be measured.
When diabetes is confirmed what other investigations should be considered?
U&Es Creatinine LFTs and TFTs Lipids Urine testing for protein or microalbuminaemia
How should a patient with newly discovered hyperglycaemia be assessed clinically?
Hyperglycaemia causes: thirst, polyuria, fatigue, bluured vision, pruritis vulvae/ balanitis, nasuea, hyperphagia, irritability, poor concentration, headache
Uncontrolled diabetes is associated with an increased susceptibility to infection and patients may present with skin infections. A history of pancreatic disease (particularly with alcohol excess) makes insulin deficiency more likely.
The clinical features of the 2 main types of diabetes can overlap. This occurs particularly at age of onset, duration of symptoms and family history. Typical type 2 diabetes increasingly occurs in obese young people. Older adults may have evidence of autoimmune activity against B cells, a slowly evolving variant of type 1 diabetes (LADA). More than 70% of patients with type 2 diabetes are overweight, 50% have hypertension and hyperlipidaemia are common.
Summarise the typical features of type 1 diabetes
Typical age at onset: <40 years Duration of symptoms: weeks Body weight: normal or low Ketonuria: Yes Rapid death without insulin treatment: Yes Autoantibodies: Yes Diabetic complications at diagnosis: No Family history of diabetes: Uncommon Other autoimmune diseases: Common
How should a patient with newly discovered hyperglycaemia be managed?
- Dietary/ lifestyle modification
- Oral anti-diabetic agents
- Insulin by injection
- Suspected type 1 diabetes: urgent therapy with insulin and prompt referral to a specialist
- Suspected type 2 diabetes: advice about dietary and lifestyle modification, followed by initiation of oral anti-diabetic drugs if needed
- Hypertension, dyslipidaemia and smoking cessation need to be addressed
What are the key aspects of educating patients with newly diagnosed diabetes?
This can be achieved by a multidisciplinary team (doctor, dietition, specialist nurse and podiatrist) in the outpatient setting. However, patients requiring insulin initially need daily advice and possibly admission to hospital. They need to learn how to measure insulin doses, give their own injections and adjust the dose depending on glucose monitoring, excecise, illness and hypoglycaemia. They must understand the principles of diabetes, recognise the symptoms of hypoglycaemia, and receive advice about risks of driving with diabetes.
How should patients with newly diagnosed diabetes self monitor?
Urine testing has limitations, as persistent hyperglycaemia may be masked and hypoglycaemia not detected. However, it is inexpensive and may suffice for those with well controlled type 2 diabetes or those treated with diet alone. Those treated with insulin should be taught to perform capillary blood glucose measurements at home. This allows patients to make appropriate adjustments in treatment on a day-to-day basis. Thus, changes in routine can be accommodated, ketoacidosis avoided and dietary compliance encouraged while avoiding hypoglycaemia.
What advice should be given to patients with impaired glucose tolerance?
The same lifestyle advice recommended for type 2 patients may reduce the risk of progression ofIGT to diabetes.
Treat other cardiovascular risk factors reduces the risk of macrovascular disease.
Patients with IGT should be monitored - e.g. with annual fasting blood glucose
Outline a checklist for follow up of patients with diabetes
1) Body weight (BMI)
2) Urinalysis (fasting) - glucose, ketones, macro and microalbuminaemia
3) Glycaemic control - HbA1c, inspection of home blood glucose monitoring record
4) Hypoglycaemic episodes - number and time of day, severe and mild episodes, nature of symptoms, awareness
5) BP
6) Eye examination - visual acuity, ophthalmoscopy, digital photography
7) Lower limbs - peripheral pulses, tendon reflexes, sensory: proprioception, vibration, light touch
8) Feet - callus skin indicating pressure areas, nails, podiatry, ulceration, deformity
What are the therapeutic goals for long term diabetic patients?
The aim of treatment is as near normal metabolism as is practical. Recommended target HbA1c is <7% to minimise vascular complications. However, type 2 diabetes progresses in severity with time, making this target difficult to achieve. In addition, strict control in type 1 diabetes increases the risk of hypoglycaemia. Glycaemic targets should therefore be appropriate: strict control may be inappropriate in the very young, the elderly and people with cancer.
Blood glucose targets are:
- fasting <6 mmol/l in type 2
- pre prandial 5-8 mmol/l in type 1
Treatment of hypertension and dyslipidaemia is often required following assessment of cardiovascular risk. Targets are:
- BP < 140/80 mmHg
- Total cholesterol <5.0 mmol/l
- LDL cholesterol <3.0 mmol/l
What is diabetic ketoacidosis (DKA)?
Ketoacidosis is a major medical emergency, principally occuring in patients with type 1 diabetes. A significant number of newly diagnosed diabetic patients present with ketoacidosis. In established disease, any form of stress, particularly infection, can precipitate DKA. Patients lose their appetite, and stop or reduce their dose of insulin in the mistaken belief that less insulin is required. No obvious precipitating cause can be found in many cases. The average mortality in developed countries is 5-10%.
Ketoacidosis occurs because insufficient insulin prevents glucose uptake into cells. This produces a catabolic state, where fats and proteins are broken down to provide substrates for gluconeogenesis. Ketone bodies are produced as a biproduct of lipid breakdown and when supply outweighs demand hyperketonaemia occurs. This produces an acidosis.
What are the cardinal biochemical abnormalities in DKA? What are the consequences of this?
Hyperglycaemia
Hyperketonaemia
Metabolic acidosis
Hyperglycaemia causes an osmotic diuresis leading to dehydration and electrolyte loss. Ketosis is caused by insulin deficiency, exacerbated by stress hormones resulting in unrestrained lipolysis supply FFAs for hepatic ketogenesis. When this exceeds the capacity to metabolise acidic ketones, these accumulate in the blood. The resulting acidosis forces hydrogen ions into cells, displacing potassium ions, which are lost in urine or through vomiting.
Patients with DKA have a total body potassium deficit but this is not reflected by plasma potassium levels, which may initially be raised due to disproportionate water loss. However, once insulin is started, plasma potassium levels can fall precipitously, due to dilution by iv fluids, potassium movement into cells and continuing renal loss of potassium.
What are the symptoms of DKA?
Polyuria, thirst Weight loss Weakness Nausea, vomiting Blurred vision Abdominal pain (especially in children)
Signs of DKA
Dehydration Tachycardia, hypotension (supine/ erect) Cold extremities/ peripheral cyanosis Air hunger (Kussmaul breathing) Smell of acetone Hypothermia Apathy, confusion, drowsiness, coma (10%)
What is the average fluid and electrolyte loss in adult DKA of moderate severity?
Water: 6 litres
Sodium: 500 mmol
Potassium: 350 mmol
Chloride: 400 mmol
These need to be replenished differently. Water and sodium are principally extracellular so should be replaced with normal saline. Potassium and chloride and intracellular, so need to be replaced with dextrose (dextrose is metabolised by the liver to give free water which is distributed evenly across all compartments). But beware! Do not give dextrose to a patient with DKA straight away as this will feed the ketogenesis. Give insulin first (see management questions).
What investigations are required in DKA?
The following investigations are important, but should NOT delay iv fluid and insulin replacement:
- U&Es, blood glucose, plasma bicarbonate (at admission and at 1, 2, 3, 6, 12, 24 hours)
- ABG to assess severity of acidosis (rapid assessment by plasma bicarbonate: <12 mmol/l is severe)
- Urine and plasma for ketones
- ECG
- Infection screen: FBC, blood/ urine culture, CRP, CXR (leucocytosis invariably occurs, representing a stress response rather than an infection)
- Serum amylase may be elevated, but rarely indicates pancreatitis
How should DKA be managed? How much insulin should be administered?
DKA should be treated in hospital, preferably in a high-dependency unit. Regular clinical and biochemical monitoring is essential, particularly during the first 24 hours. The principles of management are insulin, fluid and potassium.
If iv insulin is not possible, 10-20 U can be given i.m. followed by 5 U i.m. hourly thereafter. A rapid fall in blood glucose can cause cerebral oedema, particularly in children. The half life of i.v. insulin is short so the infusion should not be interrupted. Restoration of the usual subcutaneous insulin regimen should be delayed until the patient is eating and drinking normally.
Infusions are normally set up for 50 U soluble insulin in 50ml 0.9% saline and given i.v. via infusion pump. The rate is 6 U/hr initially, followed by 3 U/hr when blood glucose is <15 mmol/l, and 2 U/hr if blood glucose <10 mmol/l.
Blood glucose should be checked hourly initially, and if no reduction in first hr increase the infusion rate. Aim for a fall in blood glucose of 3-6 mmol/l per hour.
