anaes&DM
anaes&DM
Dr G C Werrett
Christchurch Hospital
New Zealand
Self Assessment
1. What are the adverse metabolic consequences of insulin deficiency?
a. Increased glycogenolysis and gluconeogenesis
b. Ketogenesis and metabolic acidaemia
c. Protein synthesis
d. Dehydration
e. Lipolysis
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
Diabetes Mellitus
Fasting or ≥ 7.0 ≥ 6.1
2hrs post load/ “Random” ≥ 11.1 ≥ 10.0
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).
*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
Minor surgery, type 2 diabetes NOT on insulin (diet/tablet controlled), 1st on list
Preoperative blood sugar <10mmol/l Take normal medication inc. evening dose
Preoperative blood sugar >10mmol/l Treat as if “Major” surgery
Monitor blood glucose 1 hour preop; intraoperatively if over 1 hour; and 4hourly
postop until eating.
Monitor blood glucose 1 hour preop; intraoperatively at least once; 2 hourly until
eating and then 4 hourly.
*If taking a long acting insulin, either convert to short/intermediate acting several
days prior or ½ 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)
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)
<4 0 0
4.1 – 9 1 2
9.1-13 2 3
13.1-17 3 4
17.1-28 4 6
>28 6 (check infusion running) 8
Postoperatively – if usually on insulin, stop the infusion when eating and drinking.
Calculate the total daily dose of insulin (units) taken usually and administer as S/C
soluble insulin (Actrapid), divided into 3-4 doses over 24hours.Adjust as required.
If usually diet/tablet controlled, stop infusion and restart oral hypoglycaemics once
eating.
Major surgery, all types of diabetes, 1st on list, NO infusion pump
available:
Start intravenous infusion of 500ml 5% or 10% dextrose solution with insulin and
potassium added as below according to blood glucose and potassium measurements
<4 0
4-6 5 <3 20
6-10 10 3-5 10
10-20 15 >5 0
>20 20
*If blood potassium level unavailable, add 10mmol KCL per bag
Hypoglycaemia
Defined as blood glucose less than 4mmol/l, hypoglycaemia is one of the main dangers to
patients in the perioperative period. In the awake patient, the usual warning symptoms
and signs include profuse sweating, pallor, light-headedness, tachycardia, confusion and
incomprehensible speech progressing to convulsions and coma.
Irreversible brain damage can occur. Alcohol consumption, liver disease, fasting and
sepsis exacerbate hypoglycaemia. Hypoglycaemia may also result inadvertently by poor
blood glucose monitoring or equipment failure.
The best warning sign, that of the conscious patient detecting a forthcoming “Hypo”, is
lost under general anaesthesia together with most of the other signs.
Frequent monitoring of blood glucose, and appropriate adjustments to therapy is the key
in prevention
Once detected, give 25ml of 50% dextrose intravenously and repeat if blood sugar
measurement doesn’t increase. Glucagon 1mg IM or IV is an alternative but slower
strategy. If the patient is awake, try any sugary food/solution to hand
Conclusion
The diabetic patient provides many challenges to the anaesthetist, most of which can be
anticipated with good preoperative assessment, careful monitoring and an understanding
of the relevant pathophysiological features. Regional techniques might reduce some of
the associated risks but require similar vigilance.
2. T T T T T
a. Heart rate variability to assess for autonomic neuropathy
b. Glycosylated haemoglobin is used to measure recent glucose control. Levels are less
than 6.2% in normal subjects. A level of 7% or under indicates good recent control in a
diabetic patient. If the level is over 9% then control has been poor and thus the metabolic
consequences are likely to be more pronounced with associated dehydration and
electrolyte loss. Levels over 12% indicate incipient ketoacidosis. Correcting electrolyte
and water losses preoperatively and “shutting off” lipolysis and proteolysis with insulin
should improve outcome.
c. See text – may herald a difficult airway/intubation
d. Diabetes is associated with obstructive spirometry and altered diffusing capacity
e. Documentation of pre-existing neuropathy is vital if considering a regional technique.
Neuropathic patients are particularly liable to further neuropathy –position and pad with
care. Significant neuropathy should warn of system involvement elsewhere e.g.
cardiac/renal
3. T T T F T
a-c. See Text
d.e. Hyperthroidism is associated with diabetes as is phaeochromocytoma