Anaesthesia and Diabetes Mellitus Key Points · Diabetics are at increased risk of perioperative complications · Cardiac, renal and neurological manifestations are common · Aim for a stable plasma glucose and avoid hypo/hyperglycaemia · Tight glycaemic control can impove perioperative outcome Biochemical classification of Diabetes Mellitus WHO guidelines Diabetes Mellitus Fasting Glucose conc (mmol/l) Plasma Venous =7 Whole Blood Venous=6.1 2hrs post load/ “Random” Glucose conc (mmol/l) Plasma venous= 11.1 Whole blood venous= 10.0 Aetiological Classification of Disorders of Glycaemia Type 1 - Autoimmune/non-immune forms. Early onset. Beta-cell destruction. Genetic susceptibility and environmental factors implicated. Ketosis occurs with absolute lack of insulin, so previously known as “Insulin-dependent” diabetes mellitus (IDDM). Type 2 – Previously known as “Non-insulin-dependent” diabetes (NIDDM) or “Maturity-onset”. Encompasses a spectrum of insulin hyposecretion and insulin resistance. Ketosis rare. Risk factors include obesity (especially abdominal), reduced exercise and racial origin. Others -where the cause is known – such as gestational diabetes, drug-induced diabetes, pancreatic diseases, endocrinopathies like acromegaly/Cushing’s Introduction Diabetes is a multisystem disorder caused by a relative or absolute lack of insulin. The prevalence of diabetes is approximately 7%. The majority (85%) have type 2 diabetes. With increasing obesity, reduced exercise and alterations in dietary habits, the prevalence of diabetes is increasing. For every case of diagnosed type 2 diabetes, there is another undiagnosed individual. Pathophysiology The cleaving of proinsulin from the beta cells of the pancreas produces the peptide hormone insulin. Insulin has both excitatory and inhibitory effects. For example, it simultaneously stimulates lipogenesis from glucose whilst inhibiting lipolysis. It is the inhibitory actions, such as the tonic inhibition of lipolysis, proteolysis, glyogenolysis, gluconeogenesis and ketogenesis, that are the physiologically more important. Thus, the fasting hyperglycaemia of diabetes is due predominantly to overproduction of glucose by the liver as opposed to the commonly thought, underutilisation of glucose by peripheral tissues. In effect, insulin “keeps the brakes on” a number of key metabolic processes and prevents over-secretion of the “anti-insulin” hormones -glucagon, cortisol, growth hormone and catecholamines. These hormones also happen to be released as part of the “stress response” to surgery. In the absence of insulin, the “brake” is removed and a sort of metabolic mayhem ensues. The resulting hyperglycaemia leads to an osmotic diuresis and dehydration with associated sodium and potassium loss. In the absence of insulin (type 1 DM), ketogeneis also occurs with associated metabolic acidaemia – a state of diabetic ketoacidosis (DKA). If there is some residual insulin activity (type 2 DM), enough to inhibit lipolysis and ketogenesis but not gluconeogenesis, then a hyperosmolar non-ketotic (HONK) diabetic coma can ensue. Both states are medical emergencies with a high mortality; the specific treatments are beyond this review. Chronic hyperglycaemia results in microvascular (including proliferative retinopathy and diabetic nephropathy), neuropathic (autonomic and peripheral neuropathies) and macrovascular (accelerated atherosclerosis) complications. Improved glycaemic control has a beneficial effect on the microvascular and neuropathic complications in type 2 diabetes. Blood pressure control is particularly important to help prevent macrovascular complications. It is the chronic complications that need careful assessment in the preoperative period. Preoperative Assessment A standard assessment is required with specific attention to the following details: Autonomic Neuropathy Autonomic dysfunction is detectable in up to 40% of type 1 diabetics. Only a few have the typical symptoms and signs of postural hypotension, gastroparesis, gustatory sweating, and nocturnal diarrhoea. It is worth assessing all diabetic patients for autonomic neuropathy. The easiest way is to assess heart rate variability. The normal heart rate should increase by over 15 beats/minute in response to deep breathing. Neuropathy is likely is there is less than 10 beats/minute increase. Peripheral Neuropathy The commonest type of peripheral neuropathy is the “glove and stocking” type. However diabetics are also prone to mononeuritis multiplex and some particularly painful sensory neuropathies. Poor patient positioning is more likely to result in pressure sores that are often slow to heal given poor peripheral blood flow. Documentation of existing neuropathy is prudent, especially if considering a regional technique. Cardiovascular Diabetics are more prone to ischaemic heart disease (IHD), hypertension, peripheral vascular disease, cerebrovascular disease, cardiomyopathy and perioperative myocardial infarction. Ischaemia may be “silent” as a result of neuropathy. Routine ECG should be performed and appropriate stress testing if in doubt. Autonomic neuropathy can result in sudden tachycardia, bradycardia, postural hypotension and profound hypotension after central neuraxial blockade. Respiratory Diabetics, especially the obese and smokers are more prone to respiratory infections and might also have abnormal spirometry. Chest physiotherapy, humidified oxygen and bronchodilators should be considered. Gastrointestinal Gastroparesis is characterised by a delay in gastric emptying without any gastric outlet obstruction. Increased gastric contents increase the risk of aspiration. Always ask about symptoms of reflux and consider a rapid sequence induction with cricoid pressure even in elective procedures. If available prescribe an H2 antagonist such as ranitidine150mg plus metoclopramide 10mg, at least 2 hours preoperatively. Airway Glycosylation of collagen in the cervical and temporo-mandibular joints can cause difficulty in intubation. To test if a patient is at risk, ask them to bring their hands together, as if praying, and simultaneously hyperextend to 90 degrees at the wrist joint. If the little fingers do not oppose, anticipate difficulty in intubation. Renal Diabetes is one of the commonest causes of end-stage renal failure. Check urea, creatinine and electrolytes. Specifically check the potassium especially in view of the possible need for suxamethonium as a result of gastroparesis. If unavailable, proteinuria is likely to indicate kidney damage. Ensure adequate hydration to reduce postoperative renal dysfunction. Immune system Diabetics are prone to all types of infection. Indeed an infection might actually worsen diabetic control. Tight glycaemic control will reduce the incidence and severity of infections and is routine practice in the management of sepsis and diabetic foot infections. Perform all invasive procedures with full asepsis. Other Autonomic neuropathy predisposes to hypothermia under anaesthesia Diabetics are prone to cataracts and retinopathy. Prevent surges in blood pressure, for example at induction, as this might cause rupture of the new retinal vessels. Hypoglycaemic Therapy Type 1 diabetics always require insulin. Insulin can be extracted from bovine or porcine pancreas, or more commonly now, synthesised using recombinant DNA technology. There are three types of insulin preparation, each classified by its duration of action. Soluble insulin has a rapid onset and short duration of action. Intermediate and longer acting insulins are mixed with protamine or zinc to delay absorption, are insoluble and should only be given S/C. Type 2 diabetics can be managed with diet alone, diet and oral agents or insulin, depending on the degree of insulin resistance and residual insulin activity. Dietary advice and weight loss is the mainstay of therapy There are four groups of oral hypoglycaemics (see table below). Oral Agent Example Mechanism of action Usage Watch for Sulphonylureas Gliclazide, Tolbutamide Increases insulin release Variable half- lives. Common Drug interaction Biguanides* Metformin Potentiates insulin Commonest 1st line if obese Lactic acidosis Thiazolidinediones Rosiglitazone Peripheral insulin action Add on therapy Liver function Glucosidase Inhibitors Acarbose Delays rise in postprandial glucose conc. Add on therapy Liver function *Risk of acidosis is not as great as was thought. More likely to occur in the elderly, with associated dehydration and with higher doses. Reduce dose with renal impairment. Metformin is well tolerated, causes beneficial weight loss, has been unequivocally shown to reduce mortality and is less likely to cause hypoglycaemia than sulphonylureas. Thus it is the first choice agent if diet therapy alone fails. Anaesthetic Management General Principles Avoid hypoglycaemia (under 4mmol/l) as this can cause irreversible cerebral damage Avoid severe hyperglycaemia (over 14mmol/l) to minimise dehydration and metabolic upset Type 1 diabetics need insulin to prevent ketogenesis and “metabolic mayhem” Aim for a blood glucose between 6 and 10mmol/l Accurate, easy-to-use glucose monitors, make the practice of “permissive hyperglycaemia” unacceptable given the known outcome benefits of tight control Diabetic patients should be placed first on the operating list to shorten the preoperative fast and potentially allow normal oral intake later that same day Tight metabolic control is important for both type 1 and type 2 patients. If control has been tight in the preceding weeks then fluid and electrolyte balance will be essentially normal. The best marker for recent control is the percentage of glycosylated haemoglobin (HbA1C). If available, levels less than 7% indicate good control whilst levels over 9% and particularly 12%, indicate poor control and likely associated electrolyte and water loss. These patients should be admitted preoperatively for correction of these abnormalities and stabilisation of blood sugar levels before the addition of surgical stressors. If this is unavailable, try to assess control by looking at the patient’s own log of urine or blood glucose. Continue all diabetic medication until the day of surgery except: a.) Chlorpropamide (stop 3 days prior as long acting, substitute with a shorter acting sulphonylurea) b.) Metformin only if major surgery as risk of lactic acidosis c.) Glitazones c.) Long acting insulin – substitute with short/intermediate acting Measure blood sugar preoperatively – 4 hourly if on insulin, 8 hourly if not If the patient is expected to eat within 4 hours of the operation then treat this group as having “Minor” surgery. Otherwise, surgery is “Major” If local guidelines exist, follow those for continuity of practice. Below are some examples of diabetic protocols Minor surgery, type 2 diabetes NOT on insulin (diet/tablet controlled), 1st on list Preoperative blood sugar 10mmol/l Treat as if “Major” surgery Omit oral hypoglycaemic on morning of surgery Monitor blood glucose 1 hour preop; intraoperatively if over 1 hour; and 4hourly postop until eating. Recommence oral hypoglycaemics with first meal Minor surgery, type 2 diabetes ON insulin/type 1 diabetes, 1st on list Take normal medication on day prior* Omit morning SC insulin if glucose < 7 mmol/l Give half normal insulin if glucose >7 mmol/l Monitor blood glucose 1 hour preop; intraoperatively at least once; 2 hourly until eating and then 4 hourly. Recommence normal SC insulin with first meal *If taking a long acting insulin, either convert to short/intermediate acting several days prior or _ the dose the day prior to surgery Major surgery, all types of diabetes, 1st on list, infusion pump available: Normal medication on day prior (unless very poorly controlled, in which case, establish sliding scale below 3 days prior) Day of surgery, omit oral hypoglycaemics/ normal SC insulin Check blood glucose 1 hour preop; hourly intraop until 4 hours postop; 2 hrly thereafter and 4 hourly once stabilised. Insulin is the key infusion. With close monitoring, and adjustment according to a sliding scale, there is no absolute requirement for concurrent dextrose containing solutions, as the tendency will be purely towards hyperglycaemia. However, commonly 5% or 10% dextrose solutions containing 20mmol/l of potassium are infused at a steady rate of 100ml/hr to provide carbohydrate substrate. Titrate the insulin infusion (through a dedicated line with one-way valve) as below. Blood glucose (mmol/l) Insulin infusion rate (unit/hr) If poor control* (unit/hr) 28 6 (check infusion running) 8 *If glucose not maintained
Posted on: Thu, 15 Jan 2015 20:40:47 +0000
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