Page 445 - Medicine and Surgery

P1: FAW
BLUK007-11 BLUK007-Kendall May 25, 2005 8:5 Char Count= 0

Chapter 11: Adrenal axis 441

extracellular fluid volume. Failure to exchange Na + samples over a 24-hour period is used to distinguish
for H ions can lead to a mild acidosis. between Addison’s disease (primary adrenal failure)
+
The glucocorticoids (cortisol) allow gluconeogenesis
and adrenal suppression.
to maintain glucose concentrations between meals,
and mediate protein and fat mobilisation from the Management
tissues. Reduced cortisol may lead to symptomatic hy- Chronic adrenal insufficiency is treated with glucocor-
poglycaemia. ticoids and mineralocorticoids. Patients require signif-
Lack of cortisol feedback leads to increased ACTH icant education about the illness and how to manage

(adrenocorticotrophin) secretion from the anterior co-existing illness or stress, such as at the time of op-
pituitary. When ACTH is secreted by the anterior erations when increased steroids may be required. Par-
pituitary, other hormones are also secreted such as enteral steroids are needed if vomiting occurs. All pa-
β-endorphin and melanocyte-stimulating hormone tients requiring replacement steroids should carry a
(MSH) causing skin pigmentation. steroid (blue) card.
Once mineralocorticoid secretion ceases completely,

the patient will die within 2 weeks if not treated, from Addisonian crisis
progressive weakness and eventual shock.
Definition
Clinical features Acute presentation of complete adrenal failure.
Patients present with gradual onset of weakness, tired-
ness and fatigue. There are often gastrointestinal com- Aetiology
plaints such as anorexia, nausea, vomiting, abdominal Patients may already be diagnosed with Addison’s Dis-
pain, constipation or diarrhoea. The patient may report ease or may present in crisis for the first time. Pre-
salt craving. cipitating factors include trauma, illness or surgery. It
Examination reveals weight loss, hyperpigmentation may also be caused acutely by bilateral adrenal haemor-
especially in mouth, skin creases and pressure areas. rhage, due to meningococcal septicaemia (Waterhouse-
Chronic dehydration leads to general and especially pos- Friderichsen syndrome) or anti-coagulant therapy. An
tural hypotension. Addisonian crisis may also occur on cessation of gluco-
corticoid treatment including inhaled glucocorticoids in
Complications children.
Renal failure due to decreased perfusion. Sudden cardiac
arrest or arrhythmias due to electrolyte imbalance. Pathophysiology
In adrenal failure, there is no glucocorticoid response to
Investigations stress. If exogenous high-dose steroids are not provided
Hyponatremia, hyperkalemia and a hyperchloraemic the condition is fatal.

acidosis due to mineralocorticoid deficiency. Glucose
should be measured to detect hypoglycaemia. Clinical features
Screening can be performed by measurement of early The patient is ill with anorexia, vomiting and abdominal

morning cortisol and 24 hour urinary cortisol. pain. This may suggest an acute abdomen. Signs include
Primary adrenal insufficiency is confirmed by use of pyrexia and dehydration with tachycardia, hypotension

the short Synacthen (ACTH analogue) test. Cortisol (postural drop) decreased skin turgor and sunken eyes.
levels are measured before and 30 mins after admin- Increased pigmentation may be noticed, especially in
istration of synacthen and show a low base line and a mouth, skin creases and pressure areas.
lack of rise in Addison’s Disease. Adrenal insufficiency
thatresultsfromACTHdeficiency(secondaryandter- Investigations
tiary adrenal insufficiency) will result in an appropri- Urgent cortisol and ACTH if possible.
ate rise in cortisol following Synacthen. A long Synac- U&Es (hyponatraemia, hyperkalaemia and hyper-
then test using a depot injection and repeated cortisol chloraemia).