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Diabetic Emergencies and Anaesthesia

by Pat Neligan

All tutorials located on this site are the property of Patrick Neligan and are for personal study purposes only. They are not peer reviewed and no responsibility is taken for inaccuracies. These tutorials must not be reproduced without permission or used in any other publication.

Type 1 Diabetes (IDDM) involves:

  • Autoimmune destruction of b islet cells of the pancreas leading to an absolute deficiency of insulin.
  • There is probably a genetic susceptibility to the disease, and some environmental event initiates the process in such susceptible individuals (e.g. viral infection). The best evidence that an environmental insult is required comes from studies in monozygotic twins, in whom the concordance rate for diabetes is less than 50 percent. If diabetes were a purely genetic illness, concordance rates should approximate 100 percent.
  • Autoimmune attack then follows ® destruction of most of beta islet cells.

Type II Diabetes (NIDDM) is:

  • Aetiologically diverse (multifactorial)
  • Two physiologic defects: abnormal insulin secretion and resistance to insulin action in target tissues. Most authorities believe that insulin resistance is primary and that hyperinsulinemia is secondary; i.e., insulin secretion increases to compensate for the resistance state. Although insulin resistance in type 2 NIDDM is associated with decreased numbers of insulin receptors, most of the resistance is postreceptor in nature.
  • Associated with familial clustering and obesity.

Treatment of Diabetes:

Diet: low in fat high in complex carbohydrates.

Type 1: Insulin - combination of short acting and intermediate acting human insulins given subcutaneously two to four times a day.

Type 2: diet ® oral hypoglycaemic agents (OHAs) ® insulin.

OHAs:

  • Sulphonyureas (glicazide) ® increase beta cell sensitivity to insulin (can cause hypoglycaemia).
  • Metformin ® reduce hepatic glucose production (do not cause hypoglycaemia)
  • Acarbose ® inhibits a glucosidases in the brush border of the small intestine, inhibiting glucose absorption.

Diabetic emergencies

Patients with diabetes are susceptible to two major acute metabolic complications: diabetic ketoacidosis and hyperosmolar, nonketotic coma (HONC). The former is a complication of IDDM, while the latter usually occurs in the setting of NIDDM. Ketoacidosis is rare in true NIDDM, although it can occur in that setting

Ketoacidosis

Diabetic patients present to anaesthetists with ketoacidosis usually in the setting of trauma or sepsis, for surgical intervention. The worst case scenario would be a young diabetic with necrotising fasciitis.

The problem lies in that, in many cases, the metabolic upset cannot be resolved without surgical intervention, and the perioperative course carries a high risk.

Clinical Picture:

  • Ketoacidosis begins with anorexia, nausea, and vomiting, polyuria and polydipsia.
  • Abdominal pain may be present.
  • Subsequent progression to altered consciousness or frank coma may occur.
  • The initial examination usually shows Kussmaul respiration (gasping for breath - which also smells of acetone) together with signs of dehydration.
  • Body temperature is normal ® fever suggests the presence of infection. Leukocytosis is a feature of diabetic acidosis per se and may not indicate infection.
  • Metabolic acidosis and widened anion gap (almost totally accounted for by the elevated plasma levels of acetoacetate and beta-hydroxybutyrate, although other acids (e.g., lactate, free fatty acids, phosphates) contribute).
  • Initial potassium concentrations that are normal to high, there is a total-body potassium deficit of several hundred millimoles.
  • Similarly, initial serum phosphorus levels may be high despite depletion of body stores. Magnesium deficiency also may be present.
  • "Spurious Hyponatraemia" ® the serum sodium concentration tends to be low in the face of a modest osmolar concentration because the hyperglycemia draws intracellular water into the plasma space. A very low serum sodium level (e.g., 110 mmol/L) suggests vomiting with water drinking, or else pseudohyponatremia due to severe hypertriglyceridemia if the assays were done in autoanalyzers that do not remove fat prior to assay.
  • Hypertriglyceridemia
  • Prerenal failure, reflecting volume depletion, is usually modest in degree and reverses with treatment.
  • The serum amylase level may be elevated, and frank pancreatitis can occur.

Management

These are the mainstays of treatment:

  • Diabetic ketoacidosis cannot be reversed without insulin: insulin is administered until the acidosis has been reversed and the urine ketone negative.
  • The patient is profoundly volume depleted (usually 3 - 8 litres) and requires aggressive volume resuscitation.
  • The acidosis is more important than the hyperglycaemia, more difficult to treat and lasts longer.

Plan:

  1. ABC
  2. Intravenous access, blood sampling (FBC, renal, liver, bone profile, ABG, blood cultures), urine for ketones, glucose and microbiology, CXR
  3. Actrapid 10 to 20 iu iv stat
  4. Commence iv insulin infusion, using hourly sliding scale.
  5. IV Fluid: 1 litre NaCl 0.9% stat, then 1 L over 30 mins, 1L over 1 hour, 1L over 2 hours, 4 hours and then 8 hourly.
  6. Add 10 - 20 mmol KCL or KPO4 to 2nd and subsequent litres of fluid.
  7. When blood glucose < 15 mmol/l replace NaCL with Solution 18, as glucose is required to metabolise the ketone bodies.
  8. Administer broad spectrum antimicrobial agents (e.g. augmentin)
  9. Bicarbonate is not usually required for reversal of the acidosis.
  • The plasma glucose level invariably falls more rapidly than the plasma ketone level. Insulin administration should not be stopped because glucose concentrations approach normal; rather, as mentioned, glucose should be infused and insulin continued until the ketosis has cleared.
  • The key parameters to follow are the pH and the calculated anion gap, since these give a more accurate assessment of response. The usual picture is for the pH to rise and the anion gap to narrow even though the plasma bicarbonate level remains low.
  • The persistently low bicarbonate level is the consequence of hyperchloremia, which develops because of rapid infusion of sodium chloride, the loss of potential bicarbonate from the body in urine as ketones, and exchanges with intracellular buffers.
  • An anion gap that remains elevated and a pH that is persistently low indicate insulin resistance and mandate an aggressive increase in the amount of insulin administered.

Acute complications of Ketoacidosis:

  • Vascular thrombosis induced by volume depletion, hyperosmolality, increased viscosity of blood, and changes in clotting factors favoring
  • ARDS and sepsis syndrome
  • Acute gastric dilation / acute gastritis
  • Cerebral oedema
  • Myocardial infarction

Hyperosmolar Coma

  • Hyperosmolar, nonketotic diabetic coma is usually a complication of NIDDM. It is a syndrome of profound dehydration resulting from a sustained hyperglycemic diuresis under circumstances in which the patient is unable to drink enough water to keep up with urinary fluid losses.
  • The absence of ketoacidosis is important in the pathophysiology of this condition.
  • When ketoacidosis develops, nausea, vomiting, and air hunger bring the patient to the physician before extreme dehydration can occur.
  • Such a protective mechanism is not operative in these cases.
  • Hyperosmolar syndrome can occur in insulin-dependent diabetic patients who are given enough insulin to prevent ketosis but not enough to control hyperglycemia.
  • The reason for the absence of ketoacidosis in maturity-onset diabetes is not known ® insulin levels in the portal vein in IDDM are higher than those of insulin-dependent subjects and prevent full activation of the hepatic carnitine palmitoyltransferase system ® production of ketone bodies

Clinical Picture

Patients present with:

  • Extreme hyperglycemia (40 - 100 mmol/L ® much higher than DKA) Hyperosmolality
  • Severe volume depletion
  • Central nervous system signs ranging from drowsiness to coma.
  • A high index of suspicion for infection should be maintained.
  • Plasma viscosity is high ® thrombosis
  • Bleeding (caused by disseminated intravascular coagulation)
  • Acute pancreatitis.
  • Metabolic acidosis may be present and is usually mild, plasma bicarbonate on average being about 20 mmol/L.
  • The acidosis is due to a combination of starvation ketosis, retention of inorganic acids secondary to renal hypoperfusion, and elevation of plasma lactate, the latter due to volume depletion.
  • If the bicarbonate level is less than 10 mmol/L and plasma ketones are not elevated, lactic acidosis is assumed to be present.

Management:

  1. The most important measure is rapid administration of large amounts of intravenous fluids. The average fluid deficit is 10 to 11 L.
  2. ABC
  3. IV access and bloods as before
  4. Fluid resuscitation as before, but replace NaCl with 0.45% saline
  5. Intravenous insulin 10 iu actrapid stat.
  6. Insulin infusion according to sliding scale.
  7. Broad spectrum antibiotics.

Serum osmolality can be estimated from the following formula: Serum osmolality (mosmol/L) = 2([Na+] + [K+] +[glucose] (mmol/L) + Urea (mmol/L).

Key Points for anaesthetists:

If you're taking the patient to theatre, resuscitate the patient yourself in a HDU if possible and delay surgery for as long as possible to allow adequate resuscitation. At the very least, volume resuscitation and correction of the acidosis should be achieved. Intravenous insulin should continue throughout the operation and into the post-op period.

A few thoughts on the conventional perioperative management of diabetics

Hypoglycaemia is much more dangerous in a patient rendered unconscious than hyperglycaemia

Therefore it is safer to err on the side of hyperglycaemia in patients undergoing surgery.

Nevertheless ketoacidosis must be avoided.

IDDM require insulin constantly or they will become ketoacidotic. Depending on the metabolic upset associated with surgery (i.e. stress response), the patient will require either a intravenous infusion or iv pump with sliding scale.

The "Alberti" solution of combining insulin and glucose in a single bag of fluid has the advantage of safety (you can't get too much of either).

The local modification of this regime is: 1/3 of total morning dose (or 40% of total daily dose) of insulin as actrapid in 1L Solution 18 + 10 mmol KCl over 8 hours; an additional subcutaneous sliding scale of actrapid can be added for tighter perioperative control. Intermediate duration-depot insulin (insulatard) should be avoided during the perioperative period.

For most well controlled Type II diabetics, hypoglycaemia caused by OHAs and insulin pose a higher risk in the perioperative period than hyperglycaemia.

"No glucose no insulin" BMJ 1996; 76; 198-202

OHAs should be withheld on the morning of surgery and on the evening before. It is the sulphonyureas that cause hypoglycaemia.

Take special precaution with chlorpropamide (diabenase) and glibenclamide (daonil) as these have a very long duration of action, and should be stopped a couple of days in advance.

Take home message: be paranoid of hypoglycaemia in patients on OHAs and remember that blood sugar levels that constitute euglycaemia for non diabetics will cause symptoms of hypoglycaemia in diabetic patients.

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