Department of Anaesthesia

University of Cape Town

Lecture 20
Anaesthesia and Endocrine Disease

Diabetes mellitus
Diabetes exists in 5 % of the population. Type II or non-insulin dependent diabetes is the most
common type. Type I diabetics have an absolute deficiency in Insulin. Both the hyperglycaemia and
deficiency in Insulin is responsible for the pathophysiology of the disease.
There are three diabetic emergencies. These require immediate resuscitation and patients should
not have any surgery until they have been stabilised.
Ketoacidosis Need fluid resuscitation with normal saline and Insulin infusion. Consider surgery
when glucose is <

20 mmol l
-1
, normal K
+
, ketones clearing from the urine and pH is >

7,2.
Non ketotic hyperosmolar coma Require large fluid resuscitation and an Insulin infusion.
Lower the glucose slowly at 3

5 mmol hr
-1
.
Hypoglycaemia (glucose <

4 mmol l
-1
) Give 50 ml of 50 % dextrose IV and re-check glucose in
30 minutes.

Pathophysiology of diabetes
Hyperglycaemia
Can cause osmotic diuresis and dehydration
In Type I diabetes, intracellular hypoglycaemia results in fat metabolism and ketone
production causing metabolic acidosis.
Glycosolation and thickening of tissues occurs with chronic hyperglycaemia. This may limit
mouth opening and neck extension.
Increased risk of sepsis due to impaired leucocyte function.
Concurrent sepsis, the surgical stress response, corticosteroids and pregnancy can all
exacerbate hyperglycaemia.
Whilst trying to treat and correct any hyperglycaemia one must monitor the glucose level carefully
and avoid hypoglycaemia, which can result in severe cerebral damage or death. Aim for a glucose
of 4

8 mmol l
-1
.

The long term complications of diabetes are vasculopathy, nephropathy and neuropathy.
Vasculopathy manifests with hypertension, ischaemic heart disease and cerebro-vascular
events. Many patients have silent ischaemia and do not have classic anginal pain (because
of the autonomic neuropathy). The retinopathy of diabetes is also a consequence of the
vasculopathy.
Renal disease is common with many patients developing micro-albuminuria and some
progressing to renal failure.
Peripheral sensory neuropathy is common. Autonomic neuropathy may cause
dysrhythmias, labile blood pressure, delayed stomach emptying and reflux.

Pre-operative assessment
Perioperative morbidity is related to pre-existing organ damage. The pulmonary,
cardiovascular (CVS) and renal systems must be critically assessed.
Ascertain the type of diabetes, type of treatment and glucose control.
Check for other risk factors including smoking, hypercholesterolaemia and obesity.
Haemoglobin, U & E & Creatinine, glucose and urinary ketones should be mandatory.
Haemoglobin A
1C
will give you an indication of control over the past 3 months.
Should be <

6 % if normal.
Electro cardiogram (ECG) and chest X-ray in all diabetics.

Type II diabetics who are usually well controlled, for minor surgery, may simply omit their morning
oral hypoglycaemic agents and should preferably be first on the list.
Type I and poorly controlled

or sick Type II diabetics should be on an Insulin sliding scale. Whilst
fasting, patients should receive 5 % dextrose containing solution as IV maintenance. Small
amounts of glucose prevent excessive gluconeogenesis; the source of the disease process.
Anaesthesia and endocrine disease

20 - 2
Intra-operative and post-operative management
Check the glucose pre-operatively and at least 2-hourly intra-operatively
Some patients may require an Insulin infusion
Post-operative checks can be 4-hourly until the patient is eating again.
Choosing an induction technique may be difficult. One must balance the risk of aspiration
(delayed gastric emptying and reflux), with the presence of CVS disease and autonomic
neuropathy and the requirement for a cardiovascularly stable induction.
Etomidate is useful as a CVS stable drug.
Avoid tachycardia in patients with ischaemic hearts. Ensure good anaesthesia during airway
manipulation and good analgesia intra- and post- operatively.
Blood pressures may be labile during GA or with spinal

/

epidural so have vasopressors ready.
If the patient has renal impairment, modify your drug selection.
Check and document any nerve impairment before performing regional blockade.

Thyroid disease
Thyroid disease can manifest as either hyper- or hypo- thyroidism. Thyroid hormone is integral to
growth, metabolism and Oxygen consumption. It also indirectly increases heart rate and contractility.
An excess or deficiency causes abnormal physiology. Hypertrophy of the gland itself can cause
airway compromise via tracheal compression and tracheomalacia.

Hyperthyroidism
Causes include Graves disease, multinodular goitre, thyroiditis and toxic adenomas. Patients
present with loss of weight, tremor, heat intolerance and palpitations.
Anaesthetic implications are
Tachycardia and atrial fibrillation
High output cardiac failure
Proximal muscle weakness, with potentially increases sensitivity to muscle relaxants
Corneal lesions from inadequate protection of patients with proptosis (Graves).
All elective procedures should be postponed until the patient is euthyroid on medical management
(propylthiouracil, iodine, and -blockers). Resting heart rate should be <

85 beats min
-1
.
Benzodiazepines are good as an anxiolytic premed.
Avoid eliciting tachycardia by adequate anaesthetic depth during airway management and surgical
stimulation. Avoid using sympathomimetic drugs.
Thyroid storm usually occurs post-operatively but may occur intra-operatively. Secondary to
massive release of Thyroxine on manipulation of the gland or to stress. Mimics malignant
hyperthermia with tachycardia, hyperthermia, decreased level of consciousness and hypotension,
but NOT associated with muscle rigidity. Treat with cooling, antithyroid drugs, Esmolol and fluids.

Hypothyroidism
Causes include autoimmune thyroiditis, previous radiotherapy or thyroidectomy.
Anaesthetic implications relate to
Hypothermia
Hypoglycaemia
Anaemia
Low blood volume, low BP and blunted baroreceptor function
Bradycardia, reduced cardiac output and failure
Cerebral obtundation with sensitivity to sedatives and anaesthetic agents
Muscle weakness and respiratory insufficiency
Pleural, pericardial and abdominal effusions
Large tongue may cause difficulty with intubation
Patients should be clinically euthyroid on oral Thyroxine pre-operatively. They are especially
sensitive to all induction agents, opioids and sedatives. Recovery from anaesthesia can be
delayed and they must only be extubated when awake and breathing adequately.
Myxoedema coma is extreme hypothyroidism and is characterised by impaired cognition,
hypoventilation, hypothermia and congestive cardiac failure. It can be precipitated by infection,
trauma or surgery. It is life threatening.
Anaesthesia and endocrine disease

20 - 3
Adrenal disease

Adrenal insufficiency
Primary adrenal insufficiency (AI) is usually due to destruction or malfunction of more than 90 % of the
adrenal cortex. Secondary AI is the consequence of pituitary disease with reduced ACTH production.
Tertiary AI (depression of ACTH production) is usually iatrogenic but may be caused by hypothalamic
disease. Aldosterone is usually unaffected in secondary and tertiary disease.

Primary Adrenal Insufficiency
Tuberculosis
Autoimmune adrenalitis
30 % of patients with advanced HIV (Coursin D, Wood K. JAMA 2002)
Aldosterone is often also deficient and may have hyponatraemia and hyperkalaemia

Hypothalamic-pituitary axis (H-P A) suppression Steroid replacement
Medical or surgical stress Corticosteroid dosage
Minor: e.g. Inguinal hernia repair, colonoscopy,
gastroenteritis
25 mg of Hydrocortisone or 5 mg of
Methylprednisolone intravenous (IV) on day of
procedure only
Moderate: e.g. Open cholecystectomy,
hemicolectomy, pneumonia, severe
gastroenteritis
50

75 mg of Hydrocortisone or 10

15 mg of
Methylprednisolone IV on day of procedure.
Taper quickly over 1

2 days to usual dose
Severe: Major cardiothoracic surgery, Whipple
procedure, liver resection, pancreatitis
100

150 mg of Hydrocortisone or 25

30 mg
of Methylprednisolone IV on day of procedure.
Rapid taper to usual dose over next 1

2 days

Steroid equivalents
Steroid preparation Glucocorticoid Mineralocorticoid Half-life (hr) Available as
Hydrocortisone 1 1 6

8 PO, IV, IM
Prednisone 4 0,1

0,2 18

36 PO
Methylprednisolone 5 0,1

0,2 18

36 IV
Dexamethasone 30 <

0,1 36

54 PO, IV
Fludrocortisone 0 20 18

36 PO

Addisonian crisis (acute adrenal insufficiency)
Failure of adrenals to meet stress-induced demand for increased glucocorticoids. Seen in patients
with H-P A suppression and in patients with primary AI undergoing surgery even if on adequate
supplementation, since they may not be able to mount an increased stress response.
Characterised by nausea, vomiting and hypotension. With primary AI there may also be
hyponatraemia and hyperkalaemia. Shock is typically distributive with a low vascular resistance,
frequently unresponsive to catecholamines. Can mimic septic shock and may be hypovolaemic.
Management Hydrocortisone 200 mg IV immediately, followed by 200 mg per 24 hours IV, until oral
steroid administration is possible. Aggressive fluid resuscitation with central venous central venous
pressure monitoring and correction of hypoglycaemia and hyponatraemia (slowly). Inotropic support
may be required

Phaeochromocytoma
Presentation:
CCF without apparent cause; cardiogenic shock; uncontrolled hypertension
Sweating, headaches, palpitations
GIT manifestations (nausea and vomiting)

May present as a phaeochromocytoma crisis under anaesthesia. A life-threatening complication!
Intra-operative diagnosis
Unexplained hypertension
Dysrhythmias
Cardiogenic shock
Clinical suspicion
Anaesthesia and endocrine disease

20 - 4
Management
Control peripheral vasoconstriction:
Magnesium sulphate, as below.
Phentolamine
Sodium nitroprusside (SNP)
Calcium channel blockers
NO BETA BLOCKERS!
Careful fluid therapy. May be intensely volume depleted
If intra-operative:
Stop surgery!!
Deepen anaesthesia with a volatile (not Desflurane may stimulate catecholamine release)
Magnesium 4 g bolus and an infusion of 2 g hr
-1
, with additional boli as needed, is the treatment
of choice. Once haemodynamic control is achieved, reconsider surgery. If the tumour is readily
accessible, and haemodynamic control can be established proceed with the operation.
Otherwise consider abandoning the procedure, while good alpha blockade is established.
If surgery is continued, these patients will need aggressive fluid replacement and may need
post-operative support following the sudden withdrawal of catecholamines.
Hypertensive crisis
Magnesium sulphate as described above.

Obesity
Not an endocrine disease per se, but a result of many contributing factors diet, exercise, genetics.
In a small minority there may be an endocrine aetiology (e.g. Cushings disease). Conversely, obesity
is implicated as a cause of Type II diabetes in susceptible individuals and the metabolic syndrome.
Body mass index (BMI)
Weight (kg)
BMI =
Height (m)
2

Obesity is defined as a BMI >

30 kg m
-
. Morbidly obese is a BMI > 35 kg m
-
. These patients are at
increased risk of hypertension, ischaemic heart disease, type II diabetes and peripheral vascular
disease. They may also have gastro-oesophageal reflux and hiatus herniae.

Intra-operative and post-operative considerations
The obese airway can be difficult to manage with a short neck and large breasts. Call for help
early. Position the patient well in a ramped up position, pre-oxygenate and be prepared with
an airway management plan.
Respiratory physiology is altered with a decrease in functional residual capacity (FRC),
decrease in pulmonary compliance and an increase in Oxygen consumption. These patients
desaturate rapidly, hence the need for pre-oxygenation. Ventilate with positive end-expiratory
pressure (PEEP) up to 10 hPa (cmH
2
O) to prevent atelectasis.
Obstructive sleep apnoea is common. A suggestive history includes snoring, apnoea with
rousing from sleep, morning headaches and daytime somnolence. Hypoventilation and
obstructive sleep apnoea can result in chronic hypoxia and pulmonary hypertension with cor
pulmonale. These patients are very high risk and should be managed by an experienced
anaesthetist and have a post-operative high care bed. They may be on nasal continuous
positive airway pressure (CPAP) pre-operatively and this should continue post-operatively.
Analgesia must be carefully considered to avoid sedation; however adequate analgesia is
imperative in order to enable good respiration and early mobilisation. Pain prevents patients
from breathing properly and coughing post-operatively, putting them at risk for pneumonias.
Regional anaesthesia is ideal but technically difficult.
Obese patients are twice as likely to develop deep vein thromboses (DVTs) and, potentially,
pulmonary emboli; mechanical and pharmacological prophylaxis should be considered in all.
Mobilise early.
Practical issues include using an obese BP cuff or one may have to insert an arterial line for
accurate and reliable measurement. Most operating tables have a weight limit of 150 kg,
beyond which they will not be able to elevate.
Surgical complications are also increased and include intra-operative technical difficulty, post-
operative wound sepsis and dehiscence.