Clinical Pharmacology and Therapeutics

306 ADRENAL HORMONES
Key points
Adrenal cortex and medulla – pharmacology
• The adrenal cortex secretes three major hormones.
• Glucocorticosteroids, primarily in the form of
hydrocortisone (cortisol), are secreted in a diurnal
pattern from the zona fasciculata.
• Aldosterone controls Na /K ion exchange in the distal
nephron and is secreted from the zona glomerulosa.
• Small amounts of reproductive steroids are produced.
• The adrenal medulla secretes adrenaline (epinephrine)
and smaller amounts of noradrenaline
(norepinephrine).
Case history
A 32-year-old man presents after collapsing in the street
complaining of severe lower abdominal pain.
His relevant past medical history is that for 10 years he
has had chronic asthma, which is normally controlled with
β 2 -agonists and inhaled beclometasone 2000 μg/day. Initial
assessment shows that he has peritonitis, and emergency
laparotomy reveals a perforated appendix and associated
peritonitis. His immediate post-operative state is stable,
but approximately 12 hours post-operatively he becomes
hypotensive and oliguric. The hypotension does not
respond well to intravenous dobutamine and dopamine
and extending the spectrum of his antibiotics. By 16 hours
post-operatively, he remains hypotensive on pressor agents
(blood pressure 85/50 mmHg) and he becomes hypoglycaemic
(blood glucose 2.5 mM). His other blood biochemistry
shows Na 124 mM, K 5.2 mM and urea 15 mM.
Question
What is the diagnosis here and how could you confirm it?
What is the correct acute and further management of this
patient?
Answer
In a chronic asthmatic patient who is receiving high-dose
inhaled steroids (and may have received oral glucocorticosteroids
periodically), any severe stress (e.g. infection or
surgery) could precipitate acute adrenal insufficiency.
In this case, the development of refractory hypotension in a
patient who is on antibiotics and pressors, and the subsequent
hypoglycaemia, should alert one to the probability of
adrenal insufficiency. This possibility is further supported by
the low sodium, slightly increased potassium and elevated
urea levels. This could be confirmed by sending plasma
immediately for ACTH and cortisol estimation, although the
results would not be available in the short term.
The treatment consists of immediate administration of
intravenous hydrocortisone and intravenous glucose. Hydrocortisone
should then be given eight hourly for 24–48 hours,
together with intravenous 0.9% sodium chloride, 1L every
three to six hours initially (to correct hypotension and sodium
losses). Glucose should be carefully monitored further. With
improvement, the patient could then be given twice his normal
dose of prednisolone or its parenteral equivalent for five
to seven days. This unfortunate clinical scenario could have
been avoided if parenteral hydrocortisone was given preoperatively
and every eight hours for the first 24 hours postoperatively.
Glucocorticosteroids should be continued at
approximately twice their normal dose for the next two to
three days post-operatively, before reverting to his usual dose
(clinical state permitting).
FURTHER READING
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