This document summarizes information about endocrine disorders, with a focus on diabetes mellitus. It describes the different types of diabetes, including type 1, type 2, gestational diabetes, and maturity-onset diabetes of the young. The clinical features, acute and chronic complications, diagnosis, and management of diabetes are discussed in detail. Treatment involves lifestyle changes, oral medications, insulin administration, and glycemic control monitoring. Dental considerations for diabetic patients are also reviewed.

1. Endocrine disorders
Dr. Dina Hassan Al-Saidi

2. Diabetes Mellitus
• Diabetes mellitus (DM) is a disorder caused by an absolute or
relative lack of insulin: there can be a low output of insulin from the
pancreas, or the peripheral tissues may resist insulin. In diabetes,
with insulin lacking or its action blocked, glucose cannot enter cells
and, without energy, weakness results. Glucose also then
accumulates in the blood (hyperglycaemia) and spills over into the
urine (glucosuria), taking with it, osmotically, a large amount of
water (polyuria).
• This leads to dehydration and thus thirst and the need to drink
excessively (polydipsia). As glucose is then no longer a viable energy
source, fat and protein stores are metabolized with weight loss,
peripheral muscle wasting and, in type 1 diabetes, the production
of ketone bodies (acetoacetate, β-hydroxybutyrate and acetone.

3. • In severe cases, ketone bodies may be detected on the
breath (in particular acetone) and accumulate in the blood
(ketonaemia) as well as be excreted in the urine
(ketonuria). The resultant metabolic ketoacidosis leads to a
compensatory increase in respiratory rate
(hyperventilation) and a secondary respiratory alkalosis.
• Chronic hyperglycaemia causes microvascular
complications, and atherosclerosis, and is a leading cause
of death and disability. Diabetes affects about 3–4% of the
general population but may be recognized in only 75% of
those individuals, yet it is a leading cause of death and
disability.
• Risk factors for diabetes include family history; being
overweight; inactivity; age (the risk of developing type 2
diabetes rises with age, especially after age 45) and race.

4. • Diabetes may be primary, or secondary to some other factors
as shown in the Table. Type 2 is by far the most common type
of diabetes.
Primary Type 1 – insulin-dependent (IDDM);
juvenile onset
Type 2 – non-insulin-dependent
(NIDDM); maturity onset
Secondary Drugs (corticosteroids, thiazide
diuretics, beta-blockers)
Endocrine disorders
(phaeochromocytoma, acromegaly,
Cushing syndrome)
Pancreatic disease (pancreatitis),
haemochromatosis
Pregnancy (gestational diabetes)
usually represents type 2 diabetes
exposed by the increased insulin
resistance of pregnancy

5. Type 1 diabetes
• formerly termed insulin-dependent (IDDM) or
juvenile-onset diabetes – is most commonly diagnosed
at about 12 years of age and commonly presents
before the third decade, but can appear at any age.
• it is characterized by antibodies directed against
insulin and the pancreatic islets of Langerhans. It may
have a viral (possibly Coxsackie or rubella) aetiology.
• Latent autoimmune diabetes in adults (LADA) is
essentially a slow presentation of type 1 diabetes,
which is seen in slimmer patients who progress quickly
to insulin requirement. Anti-GAD (glutamic acid
decarboxylase) antibodies may be helpful in the
diagnosis.

6. Type 2 diabetes
• formerly termed non-insulin-dependent
(NIDDM) or maturity-onset diabetes – accounts
for 80–90% of diabetics. Generally it occurs in
genetically predisposed individuals over the age
of 40 who are typically overweight.
• Patients are insulin resistant and have diminished
beta-cell function.
• Maturity-onset diabetes of the young (MODY) is
caused by autosomal dominant mutations and so
there is vertical transmission of diabetes within
families. The phenotype varies from mild glucose
intolerance to insulin-requiring diabetes, typically
diagnosed before the age of 25 years.

7. Gestational diabetes
• It is basically an insulin-resistant state
exposing future risk of type 2 diabetes.
• Appears usually in second or third trimester
of pregnancy
• Affects up to 5% of pregnant women.

8. Clinical features
• Patients with diabetes may be asymptomatic and detected
on routine or opportunistic screening, or present in a
variety of ways related to severity and degree of onset.
• Lethargy is the most common symptom but
hyperglycaemia, polyuria and thirst (polydipsia) are
prominent.
• Since glucose is lost as an energy source in type 1 diabetes,
fats must be metabolized, leading to weight loss from fat
breakdown to fatty acids and ketone bodies, which appear
in the blood causing acidosis and hyperventilation, and in
the urine (ketonuria) and to some extent in the breath
(acetone).
• Diabetes is also associated with immune deficiencies,
particularly polymorph dysfunction, leading to
susceptibility to infections (mainly skin infections and
mucosal candidosis).

9. • Type 1 diabetes develops most often in
children and young adults. Symptoms usually
develop over a short period. Excessive thirst
and urination, constant hunger, weight loss,
blurred vision and extreme fatigue are typical.
• Life-threatening diabetic coma (diabetic
ketoacidosis) is a significant risk. Insulin is
required daily for treatment, for life, and diet
must be controlled. Hypoglycaemia is a risk.

10. • Type 2 diabetes develops most often in
overweight patients. Symptoms usually develop
gradually.
• Fatigue, frequent urination, unusual thirst,
weight loss, blurred vision, frequent infections,
and slow healing of wounds or sores are seen.
• Most patients with type 2 diabetes can be
managed on diet and oral hypoglycaemic drugs.
Many will eventually need insulin, but are often
resistant.
• About 80% of people with type 2 diabetes have
the metabolic syndrome that includes obesity,
elevated blood pressure and high levels of blood
lipids.

11. Acute complications of diabetes
• Diabetes can lead to coma. Hypoglycaemic coma is the
main acute complication of diabetes, is growing in
frequency with the trend towards tighter metabolic
control of diabetes.
• Many insulin-treated patients are liable to
hypoglycaemia, due to an imbalance between food
intake and usage, and insulin therapy. Hypoglycaemia
can be of rapid onset, and may resemble fainting.
• There is adrenaline release, leading to a strong and
bounding pulse, sweaty skin, and often anxiety,
irritability and disorientation, before consciousness is
lost. Occasionally the patient may convulse.

12. • hypoglycaemia must be quickly corrected
with glucose or brain damage can result.
• Glucose will cause little harm in
hyperglycaemic coma but will improve
hypoglycaemia.
• Never give insulin since this can cause severe
brain damage or kill a hypoglycaemic patient.
Assess the glucose level with a testing strip.

13. • If the patient is conscious, give glucose
solution or gel (GlucoGel) immediately by
mouth or 10 g sugar.
• if the patient is comatose, give 10–20 ml of
20–50% sterile dextrose intravenously or, if a
vein cannot readily be found, glucagon 1 mg
intramuscularly.
• On arousal, the patient should also be given
glucose orally, usually in the form of longer-
acting carbohydrate (e.g. bread, biscuits).

14. • Hyperglycaemic coma usually has a slow onset over many
hours, with deepening drowsiness (but unconsciousness is
rare, so an unconscious diabetic should always be assumed
to be hypoglycaemic).
• signs of dehydration (dry skin, weak pulse, hypotension),
acidosis (deep breathing) and ketosis (acetone smell on
breath and vomiting) only in type 1 diabetes.
• If it is certain that collapse is due to hyperglycaemic
ketoacidotic coma, the first priority is to establish an
intravenous infusion line. This enables rapid rehydration to
correct dehydration and electrolyte (especially potassium)
losses, and the administration of insulin.
• Blood should be taken for baseline measurements of
glucose, electrolytes, pH and blood gases. Raised plasma
ketone body levels can be demonstrated with a testing strip
such as Ketostix (Ames). Insulin is then started, such as 20
units i.m. stat.
• Medical help should be obtained as soon as possible.

15. Chronic complications of diabetes
• Diabetes is associated with long-term
microvascular and macrovascular complications .
• Diabetes is a leading cause of death and disability
due to premature cardiovascular disease: the risk
of myocardial infarction is at least tripled.
• Renal and retinal complications are also
incapacitating, as is gangrene of toes.
• Smoking increases the risk of many chronic
complications.

16. General management
• Glycosuria is usually indicative of diabetes,
but absence of glycosuria does not completely
exclude it, and confirmation by blood glucose
levels is essential.
• Diagnosis is from the presence of raised blood
(venous plasma) glucose level

17. Test Confirms Diabetes Excludes Diabetes
Fasting plasma glucose
(after a person has
fasted for 8 h)
> 7.0 mmol/L < 6 mmol/L
Random blood glucose
(taken any time of day)
≥ 11.1 mmol/L < 8 mmol/Lb
Plasma glucose taken 2 h
after a person has
consumed a drink
containing 75 g of
glucose in oral glucose
tolerance test (OGTT)
> 11.1 mmol/L < 11.1 mmol/L

18. • A diagnosis of diabetes is made when any one of the above
three tests is positive, with a second test positive on a
different day (not needed if symptomatic).
• Pre-diabetes is the term given when there is either of the
following:
1. An impaired glucose tolerance (IGT) test – blood glucose
during the oral glucose tolerance test is higher than
normal but not high enough for a diagnosis of diabetes
(7.8–11.0 mmol/L).
2. An impaired fasting glucose (IFG; impaired fasting
glycaemia) – fasting plasma glucose is higher than normal
(6.1–6.9 mmol/L) but less than the level confirming the
presence of diabetes.
• Patients with IGT and IFG are more likely to develop type
2 diabetes, and have an increased risk of cardiovascular
disease.

19. Diabetes prevention
1. Weight reduction and greater physical
activity.
2. Diet may help diabetic control;
recommendations are to eat more starches
such as bread, cereal and starchy vegetables.
eat five portions of fruits and vegetables
every day.
3. eat fewer sugars and sweets.

20. • Long-term assessment of glucose control is made
by estimation of the blood level of glycosylated
haemoglobin (HbA1c).
• HbA1c is normal adult haemoglobin that binds
glucose, remains in the circulation for the life of
the erythrocyte and therefore acts as a
cumulative index of diabetic control over the
preceding 3 months; the higher the glycosylated
haemoglobin level, the greater the risk of chronic
complications.
• Patients should have an HbA1c test every 3–6
months; glycosylated haemoglobin below 4.8% of
total haemoglobin is normal. Fructosamine is an
alternative assay of long-term diabetic control.

21. • Optimum control would be to aim to keep
blood glucose levels at 4–7 mmol/L before
meals (preprandial) and at no higher than 10
mmol/L 2 h after meals (postprandial) and
HbA1c (long-term glucose level) optimally at
7% or less.

22. Treatment
Type 1 diabetes
• Basic treatment of type 1 diabetes is
subcutaneous insulin administration, the amount
being balanced against food intake and daily
activities, and home blood glucose testing.
• Insulin may be of human or animal (pork or beef)
origin, and comes in various forms: short-acting,
intermediate-acting or long-acting insulins;
insulin analogues have been modified so as to
produce very rapid-onset and very long duration
of activity.

23. • Insulin is given by injection. There is no single
standard for patterns of insulin
administration. The dose varies widely
between patients and also depends on the
type of preparation, diet and exercise.
Infections or traumas also raise insulin
requirements.

24. The following three insulin regimes are in common use.
• 1. Twice-daily doses of short- and intermediate-acting
insulin, often pre-mixed, given before breakfast and
before the evening meal. The short-acting doses cover
the insulin needs of the morning and evening. The
intermediate-acting doses cover the afternoon and
overnight.
• 2. Three times a day dosing; short-acting and
intermediateacting insulin before breakfast, short-
acting insulin before the evening meal and
intermediate-acting insulin before bed.
• 3. Multiple daily doses: short-acting insulin used
before each main meal and an intermediate- or long-
acting insulin used before bedtime to give coverage
overnight.

25. Type 2 diabetes
• Basic treatment of type 2 diabetes is by controlled
eating and physical activity, and home blood glucose
testing.
• In some patients, hypoglycaemic drugs may also be
needed, which may be used as monotherapy or in
certain combinations such as dual therapy (e.g.
metformin plus a sulfonylurea or sitagliptin; or a
glitazone plus sitagliptin).
• Intensive control of blood glucose and blood pressure
lowers the risk of blindness, renal disease, stroke and
myocardial infarction.
• Gastric bypass surgery provides long-term control for
obesity and diabetes in adult-onset diabetes, and also
alleviates some of the complications.

26. Dental Aspects
• There are no specific oral manifestations of diabetes
mellitus but, even if well controlled, patients are
predisposed to infections, and diabetics have more
severe periodontal disease than controls
• If diabetic control is poor, oral candidosis can develop
and cause, for example, angular stomatitis.
• Severe dentoalveolar abscesses with fascial space
involvement in seemingly healthy individuals may
indicate diabetes. Any such patients should be
investigated to exclude it and other immune defects.

27. • In patients with insulin-treated diabetes,
circumoral paraesthesia is a common and
important sign of impending hypoglycaemia.
• Neuropathy may occasionally cause cranial
nerve deficits and occasionally there is
swelling of the salivary glands (sialosis) due to
autonomic neuropathy.
• A burning mouth sensation in the absence of
physical changes may be possible. A dry
mouth may result from dehydration.

28. • The main hazard is hypoglycaemia, as dental disease
and treatment may disrupt the normal pattern of food
intake.
• Prevent this by planning, such as by administering oral
glucose just before the appointment if a patient has
taken his or her medication but has not had the
appropriate meal.
• Furthermore, particularly before surgical procedures,
the patient’s blood glucose level may be tested using a
point of care device prior to treatment, and oral
glucose given if the level is too low – less than about 5
mmol/L (180 mg/dl).
• If normal eating will not be resumed at lunchtime, a
post-operative blood glucose level may be taken and
further glucose given.

29. • In a well-controlled diabetic patient, providing
that normal diet has, and can, be taken, it is
feasible to carry out even minor surgical
procedures, such as simple single extractions
under LA, as long as the procedure is carried out
within 2 h of breakfast and the morning insulin
injection.
• More protracted procedures, such as multiple
extractions, must only be carried out in hospital.
• Poorly controlled diabetics (whether type 1 or 2)
should also be referred for improved control of
their blood glucose before non-emergency
treatment is performed.

30. • Drugs should be sugar-free, avoiding those that can
disturb diabetic control: steroids, which increase blood
glucose; and doxycycline, tetracyclines and
ciprofloxacin, which enhance insulin hypoglycaemia.
• Acetaminophen/paracetamol or codeine are the
analgesics of choice.
• Non- steroidal anti-inflammatory drugs (NSAIDs)
should be used with caution in view of renal damage
and risk of gastrointestinal bleeding, especially as many
diabetics are already on low-dose aspirin for
prophylaxis of ischaemic heart disease.
• The dentist should manage infections aggressively, as
people with diabetes may be immunocompromised
• Amoxicillin is the antibiotic of choice.

31. • Local analgesia can usually be safely used in
diabetics; the dose of adrenaline is unlikely to
increase blood glucose levels significantly.
• Conscious sedation with benzodiazepines can
usually be safely used.
• Autonomic neuropathy in diabetes can cause
orthostatic hypotension; therefore the supine
patient should be slowly raised upright in the
dental chair.
• Routine non-surgical procedures or short minor
surgical procedures under LA can be carried out
with no special precautions apart from ensuring
that treatment does not interfere with eating.

32. More protracted procedures, such as multiple extractions, must only
be carried out in hospital, with the following precautions
• Pre-operative assessment : before the operation, the patient
should be put on soluble insulin and stabilized. Insulin may need to
be given twice or three times daily, and control is confirmed by
estimation of blood glucose
• The operation should be carried out early in the morning and
booked first in the list, so that any delays in the operation schedule
will not impair diabetic control
• At 8.00–9.00 am blood should be taken for glucose estimation and
an intravenous infusion set up giving glucose 10 g, soluble insulin 2
units and potassium 2 mmol/h (GIK infusion), until normal oral
feeding is resumed – at which time the patient can be returned to
the pre-operative insulin regimen
• Blood glucose should be monitored at 2–4-hour intervals until the
patient is feeding normally
• The patient is put on an insulin sliding scale from the morning of
the day of operation until the normal feeding regimen is possible.

33. • General anaesthesia for the diabetic patient
may be complicated especially by
hypoglycaemia, chronic renal failure,
ischaemic heart disease or autonomic
neuropathy. Severe autonomic neuropathy
can lead to postural hypotension and impaired
ability to respond to hypoglycaemia, and
carries a risk of cardiorespiratory arrest under
GA.

34. Adrenal Cortex
• The adrenal cortex produces a series of
corticosteroids, mainly cortisol (hydrocortisone)
and corticosterone (the glucocorticoids), and
aldosterone (the mineralocorticoid).
• Corticosteroids are an essential part of the body’s
response to stresses such as trauma, infection,
GA or operation, pain, stress, fever, burns and
hypoglycaemia.
• At such times, there is normally raised adrenal
corticosteroid production and the size of the
response is proportional to the degree of stress.

35. ADRENOCORTICAL DISORDERS
• Adrenocortical hyperfunction may lead to
release of excessive:
1. glucocorticoids (Cushing disease)
2. mineralocorticoids (Conn syndrome or
hyperaldosteronism)
3. androgens (congenital adrenal hyperplasia).

36. CUSHING DISEASE
• Cushing disease is caused by excess aglucocorticoid
production by adrenal hyperplasia secondary to excess
ACTH production by pituitary basophil adenomas.
• The most obvious feature is central obesity, affecting
the abdomen and also the face (moon face).
interscapular region (buffalo hump) and trunk, but
with relative sparing of the limbs.
• Hypertension is common. Breakdown of proteins with
conversion to glucose (gluconeogenesis) leads to
hyperglycaemia and possibly diabetes mellitus,
osteoporosis, muscle weakness, thinning of the skin,
purpura and purplish skin striae .

37. • The diagnosis is confirmed by a raised plasma
cortisol level and absence of the normal
diurnal variation in cortisol levels, normally
highest in the morning around 8.00 am and
lowest at midnight.
• Another useful screening test is to measure
plasma cortisol at 8.00–9.00 am after giving 1
mg dexamethasone orally at midnight to
suppress the adrenal glands temporarily; in
health, cortisol levels fall but in Cushing
syndrome there is no such fall (low-dose
overnight dexamethasone suppression test).

38. Dental aspects
• Local analgesia is preferred for pain control. Conscious
sedation can be given, preferably with nitrous oxide and
oxygen. GA must be carried out in hospital. Management
complications may include:
1. the need for corticosteroid cover; patients, once treated,
are maintained on corticosteroid replacement therapy
and then are at risk from an adrenal crisis if subjected to
operation, anaesthesia or trauma
2. hypertension
3. cardiovascular disease
4. diabetes mellitus
5. psychosis
6. vertebral collapse or myopathy causing limited mobility
7. multiple endocrine adenomatosis (MEA)

39. • There are no specific oral manifestations of
Cushing disease, but patients have been
referred for a suspected dental cause of the
swollen face

40. HYPERALDOSTERONISM
• Primary hyperaldosteronism (Conn syndrome) arises
from an adrenal cortex benign tumour or hyperplasia.
• Secondary hyperaldosteronism arises from activation
of the renin–angiotensin system in cirrhosis, nephrotic
syndrome, severe cardiac failure or renal artery
stenosis.
• High aldosterone secretion leads to potassium loss
(hypokalaemia) – causing muscle weakness and
cramps, paraesthesia, polyuria and polydipsia, and,
since it is associated with a metabolic alkalosis, may
lead to tetany – and sodium retention (causing
hypertension but rarely oedema).

41. • Amiloride, or the aldosterone antagonist
spironolactone, is given until the affected adrenal gland
can be excised.
• Dental aspects :
- Local analgesia is used for pain control. Conscious
sedation may be helpful, especially if there is
hypertension.
- GA must as always be carried out in hospital. In the
untreated patient, hypertension and muscle weakness
are the main complications.
-Competitive muscle relaxants may be dangerous, as
they can cause profound paralysis.
- If bilateral adrenalectomy has been carried out, the
patient is at risk from collapse during dental treatment
and therefore requires corticosteroid cover.

42. ADRENOCORTICAL HYPOFUNCTION
• Adrenocortical hypofunction is due most
commonly to adrenocorticotropic hormone
(corticotropin) deficiency caused by the
suppression of adrenocortical function
following the use of systemic corticosteroids
(secondary hypoadrenocorticism);
occasionally by acquired adrenal disease
(primary hypoadrenocorticism); and rarely,
due to a congenital defect in corticosteroid
biosynthesis (congenital adrenal hyperplasia)

43. Primary hypoadrenocorticism (Addison disease)
• Primary hypoadrenocorticism is rare and caused by
autoantibodies to the adrenal cortex, causing
adrenocortical atrophy and failed hormone secretion –
cortisol (hydrocortisone) and aldosterone.
• Lack of cortisol predisposes to hypotension and
hypoglycaemia, but stimulates the
hypothalamopituitary axis causing release of pro-
opiomelanocortin which has ACTH and melanocyte-
stimulating hormone (MSH) activity and can cause
hyperpigmentation.
• Lack of aldosterone leads to sodium depletion,
reduced extracellular fluid volume and hypotension

44. • The lack of adrenocortical reserve makes
patients vulnerable to any stress such as
infection, trauma, surgery or anaesthesia,
though they may be asymptomatic otherwise.
• An acute adrenal crisis (Addisonian crisis or
shock) is thus characterized by collapse,
bradycardia, hypotension, profound
weakness, hypoglycaemia, vomiting and
dehydration.

45. • Patients with hypoadrenocorticism also suffer
from fatigue and weakness, lethargy, weight
loss, anorexia, nausea, vomiting, diarrhoea,
hyperpigmentation, dizziness and postural
hypotension.
• Diagnosis of hypoadrenocorticism is
confirmed by: hypotension; sometimes low
plasma sodium and raised potassium; plasma
glucose assay (hypoglycaemia is common);
and low plasma cortisol levels and depressed
cortisol responses to ACTH stimulation.

46. • In hypoadrenocorticism the basal plasma
cortisol level is usually lower than 6 mg/100
ml.
• Most patients are treated with oral
hydrocortisone and fludrocortisone.
• Dental aspects:
• Conscious sedation should generally be
avoided unless the patient has had
corticosteroid cover. GA is obviously a matter
for the expert anaesthetist in hospital.

47. • Brown or black pigmentation of the mucosa is
seen in over 75% of patients with Addison
disease, but is not a feature of corticosteroid-
induced hypoadrenocorticism or of
hypoadrenocorticism secondary to
hypothalamopituitary disease.
• Hyperpigmentation is related to high levels of
MSH and affects particularly areas normally
pigmented or exposed to trauma (e.g. in the
buccal mucosa at the occlusal line, or the
tongue, but also the gingivae

48. SYSTEMIC CORTICOSTEROID THERAPY
• Corticosteroids have a negative feedback
control on hypothalamic activity and ACTH
production and there is thus suppression of
the HPA axis and the adrenals may become
unable to produce a steroid response to
stress. When the adrenal cortex is unable to
produce the necessary steroid response to
stress, acute adrenal insufficiency (adrenal
crisis) can result, with rapidly developing
hypotension, collapse and possibly death.

49. • Suppression of the HPA axis becomes profound if
corticosteroid treatment has been prolonged
and/or the dose of steroids exceeds physiological
levels (more than about 7.5 mg/day of
prednisolone). Adrenal suppression is less when
the exogenous steroid is given on alternate days
or as a single morning dose (rather than as
divided doses through the day)
• However, adrenal function may even be
suppressed for up to a week after cessation of
steroid treatment lasting only 5 days. If steroid
treatment is for longer periods, adrenal function
may be suppressed for at least 30 days and
perhaps for 2–24 months after the cessation of
treatment.

50. • Patients on, or who have been on,
corticosteroid therapy within the past 30 days
may be at risk from adrenal crisis, and those
who have been on them during the previous
24 months may also be at risk, if they are not
given supplementary corticosteroids before
and during periods of stress such as operation,
GA, infection or trauma.

51. • Although the evidence for the need for
steroid cover may be questionable,
medicolegal and other considerations suggest
that one should act on the side of caution and
fully inform and discuss with the patient, take
medical advice in any case of doubt and give
steroid cover unless confident that collapse is
unlikely.

52. Dental Aspects
• Adrenocortical function may be suppressed if:
• the patient is currently on daily systemic
corticosteroids at doses above 5 mg
prednisolone
• corticosteroids have been taken regularly
during the previous 30 days
• corticosteroids have been taken for more
than 1 month during the past year.

53. • During intercurrent illness or infection, after
trauma, or before operation or anaesthesia,
these patients may require a higher steroid
dosage.
• Steroid supplementation should be
considered before stressful procedures. It is
recognized that dentoalveolar or maxillofacial
surgery may result in stress, but most other
forms of dental treatment cause little
response.

54. • The blood pressure must be carefully watched
during surgery and especially during recovery,
and steroid supplementation given immediately if
the blood pressure starts to fall.
• Minor operations under LA may be covered by
giving the usual oral steroid dose in the morning
and giving oral steroids 2–4 h pre- and post-
operatively (25–50 mg hydrocortisone or 20 mg
prednisolone or 4 mg dexamethasone) or by
giving intravenous 25–50 mg hydrocortisone
immediately before operation.
• Intravenous hydrocortisone must be immediately
available for use if the blood pressure falls or the
patient collapses.

55. • Cover for major operations can be provided by
giving at least 25–50 mg hydrocortisone
sodium succinate intramuscularly or
intravenously (with the pre-medication) and
then 6-hourly for a further 24–72 h.
• Drugs, especially sedatives and general
anaesthetics, are a hazard and it is extremely
important to avoid hypoxia, hypotension or
haemorrhage. Patients may also require
special management as a result of diabetes,
hypertension, poor wound healing or
infections.

56. • Aspirin and other NSAIDs should be avoided
as they may increase the risk of peptic
ulceration.
• Topical corticosteroids for use in the mouth
are unlikely to have any systemic effect but
predispose to oral candidosis.
• Susceptibility to infection is increased by
systemic steroid use and there is a
predisposition to herpes virus infections
(particularly herpes simplex).

57. • Passive immunization with varicella zoster
immunoglobulin is indicated for non-immune
patients on systemic corticosteroids (or who
have been on them within the previous 3
months), if exposed to chickenpox or zoster.
Immunization should be given within 3 days of
exposure.
• Long-term and profound immunosuppression
may lead to the appearance of hairy
leukoplakia, Kaposi sarcoma, lymphomas, lip
cancer or oral keratosis or other oral
complications

58. SECONDARY ADRENOCORTICAL INSUFFICIENCY
Secondary adrenocortical insufficiency can
also be caused by ACTH deficiency as a result
of hypothalamic or pituitary disease. It is then
associated with other endocrine defects, but
no hyperpigmentation (ACTH levels are low)
and blood pressure is virtually normal
(aldosterone secretion is normal).

59. Adrenal Medulla
• The adrenal medulla secretes the
catecholamines norepinephrine
(noradrenaline) and epinephrine (adrenaline)
in response to hypotension, hypoglycaemia
and other stress, their release being regulated
by the central nervous system.

60. PHAEOCHROMOCYTOMA
• Phaeochromocytomas are rare, usually benign
tumours, most commonly in the adrenal medulla
(producing epinephrine) but others arise in other
neuroectodermal tissues such as paraganglia or
the sympathetic chain and produce
norepinephrine or dopamine.
• Typical features are episodes of anxiety,
headache, epigastric discomfort, palpitations,
tachycardia, arrhythmias, hypertension, sweating,
pyrexia, flushing and glycosuria.

61. • Diagnosis is supported by finding excessive
urinary catecholamines and their metabolites
such as vanillylmandelic acid (VMA) or
metanephrines.
• The tumour is excised after the blood pressure
has been controlled with an alpha- blocking
agent (e.g. phenoxybenzamine) and a beta-
blocker.

62. • Dental aspects :
• Acute hypertension and arrhythmias may
complicate dental treatment.
• Elective treatment should therefore be
deferred until after surgical treatment of the
phaeochromocytoma.
• If emergency care is required, the blood
pressure should first be controlled with alpha-
(such as phenoxybenzamine or prazosin) and
then beta-adrenergic (such as propanolol)
blockers.

63. • Patients who have had adrenal surgery may
suffer from hypoadrenocorticism, since the
adrenal cortex is inevitably damaged at
operation. These patients therefore require
steroid cover at operation.
• Local analgesia is then generally safe and
epinephrine in modest amounts is unlikely to
have any significant adverse effect. Conscious
sedation may be desirable to control anxiety
and endogenous epinephrine production.

64. • General anaesthesia must only be given in
hospital; neuroleptanalgesia using a
combination such as droperidol, fentanyl and
midazolam may be the most satisfactory
choice.