Surgical
anatomy
At birth, the adrenal glands have attained
nearly adult proportions. Fully developed, each weighs about 4 g, but the left
is a little larger than the right. A deeper yellow colour and a firmer
consistency enable the gland to be distinguished from the adjacent fat. Each
rests on the superior, anterior and medial aspects of the superior pole of the
corresponding kidney, and presents the appearance of a French Liberty cap worn
at a rakish angle.
Although
intimately related anatomically; the adrenal cortex and the adrenal medulla are
quite separate internal secretory glands.
The
adrenal glands are supplied by several adrenal arteries, rendering them
remarkably vascular, but only one vein drains each gland. On the right side the
adrenal vein is short and enters the inferior vena cava, while on the left it
empties into the left renal vein [which communicates through the azygos vein
with the left intercostal, internal mammary and vertebral veins (Anson)]. This
dissimilarity of the right and left venous flow determines, to some extent, the
location of metastases from malignant tumours of these glands.
Computerised tomography (CT) has been a
significant advance in imaging the adrenal glands and in the detection of
adrenal masses with an accuracy of 90 per cent (Fig.
45.7). Ultrasonography can
detect most adrenal masses larger than 2 cm in diameter, but is operator and
machine dependent and less accurate, especially in obese patients. CT has made
invasive techniques, such as selective retrograde venography and selective
arteriography, almost obsolete. In those cases where CT findings are
inconclusive and functional information is required, isotope scanning (see
below) and differential venous sampling for hormone levels may be indicated.
A
radiograph or CT scan of the pituitary fossa showing an enlarged pituitary fossa
is suggestive of a basophil adenomas of the pituitary gland with excess
adrenocorticotrophic hormone (ACTH) pituitary secretion.
Adrenal
gland scintigraphy using NP-59 [1311-6(-iodomethyl-19Norchest-5(10)EN-3beta-ol] is of value in addition to CT. In a benign functioning
adrenal tumour there is uptake with suppression of the contra lateral gland. By
contrast adrenocortical carcinoma does not usually concentrate the isotope and,
as a result of contra lateral gland suppression, there is little uptake.
Bilateral adrenal hyperplasia produces the opposite result with a prominent
bilateral image.
MRI
is of value particularly for small lesions.
Adrenal cortex
The adrenal cortex is made up (if the
following layers from without inwards: the zona glomerulosa, the zona
fasciculata and the zona reticularis.
Physiology.
At least 50 steroid compounds have been isolated from the adrenal cortex. These
hormones exhibit various types tif activity which, for practical purposes, can
be arranged in three groups.
Mineralocorticoids
are
concerned in the maintenance of water and electrolytic balance. A deficiency of
these hormones produces sodium diuresis, potassium retention and dehydration;
an excess results in hypertension, oedema, cardiac dilatation and hypokalaemia. Aldosterone
is the most important of these salt-regulating’ hormones (see Conn’s
syndrome later).
Glucocorticoids
are
concerned with the metabolism of proteins and carbohydrates, favouring the
formation of the latter from the body’s storehouse of the former. This
conversion is known as gluconeogenesis.
• In endocrine deficiencies. Hydrocortisone is the logical need in adrenocortical
insufficiency and after bilateral adrenalectomy.
• In nonendocrine disease. Hydrocortisone or synthetic analogues, such as prednisone and
betamethasone, are used in the treatment of a diversity of diseases, including
allergic conditions, granulomatous disorders, blood diseases and the collagenoses. Hydrocortisone is used in the treatment of hypocorticism and shock
(Chapter 4) and is an effective antiallergic agent in a number of skin diseases
and eye conditions.
Sex
hormones. Androgenic
and oestrogenic hormones are produced by the adrenal cortex. Excessive secretion
of androgens due to adrenal enzyme deficiencies or tumours causes virilism in
females or, rarely, excessive secretion of oestrogens brings about effeminacy in
males.
Interhormonic
action. The anterior lobe of the pituitary gland secretes ACTH which stimulates
the adrenal cortex, whereas the cortisol of the adrenal cortex inhibits the
secretion of ACTH. ACTH secretion is also controlled by higher cerebral centers and the hypothalamic corticotrophin-releasing hormone (CRH).
Tests of
adrenocortical activity
The tests are of two types, those that confirm
the presence of a change in cortisol production and those that indicate a cause.
No tests should be interpreted in isolation but all the results of the
investigations should be considered together.
Plasma
electrolytes. Sodium levels are raised and potassium is low in a hyper functioning
adrenocortical lesion with the opposite in Addison’s disease,
but changes in Addison’s disease may not occur until the patient is
approaching crisis.
Plasma
cortisol levels. Diurnal variation with a maximum value at 8.00 am. may be lost
both in Cushing’s syndrome, where all levels are high, and in insufficiency
when levels are low.
Plasma
ACTH levels. Low plasma levels are found with adrenal tumours and high levels
with a pituitary lesion or ectopic ACTH production. The ratio of ACTH to related
peptides such as beta-lipotrophin may facilitate the distinction between pituitary
Cushing’s and ectopic ACTH production.
Plasma
aldosterone levels. The concentration of aldosterone is only one-thousandth that
of cortisol, and both dietary sodium and posture may change the value. Plasma
renin levels should be measured along with aldosterone to differentiate between
primary and secondary hyperaldosteronism.
Urinary
steroid excretion. Cortisol secretion rate. The daily output of cortisol is a precise measure of
adrenocortical activity, but is routinely performed in only a few centres. Adult
levels are reached by 18 years of age and after 40 years fall gradually, to be
halved by 70 years of age. The average excretion is higher in Caucasian males.
The daily output may be determined by the administration of a small amount of
radioactive-labelled cortisol, which is metabolised and excreted, and the
urinary radioactivity measured. The normal range is 5—28 mg per 24 hours, with
high levels in Cushing’s syndrome and low levels in adrenal insufficiency.
Urinary
cortisol excretion. The
cortisol excretion in a 24-hour urine sample is probably the best screening test
for adrenocortical over secretion.
I
7-Oxosteroids or ketosteroids. These reflect androgen output, and excretion is increased in many women
with virilising syndromes.
Dexamethasone
suppression test. Dexamethasone is 25 times more potent than cortisol.
Dexamethasone 0.5 mg is administered 6-hourly for 2 days and causes a marked
decrease in urinary steroid excretion by inhibiting ACTH production, and thus
cortisol, without contributing greatly to the total urinary steroid output. In
Cushing’s syndrome, no effect is produced by the dose. Larger doses of up to 2
mg 6-hourly will, over several days, reduce urinary steroid excretion if the
overactivity is secondary to bilateral adrenal hyperplasia, but not with an
adrenal tumour, which is autonomous. Measurement of the plasma cortisol at 9.00
a.m. after the administration of 2 mg dexamethasone the previous midnight serves
as a convenient screening test for Cushing’s syndrome.
Metyrapone
test. This differentiates between excess ACTH production and a lesion in the
adrenal cortex causing Cushing’s syndrome. Metyrapone inhibits the
biosynthesis of cortisol so plasma levels fall. If the pituitary—adrenal axis
is intact, this results in an increase in ACTH production and stimulation of the
adrenal cortex. The basal levels of 17-oxosteroids and ketosteroids in the urine
are measured for 2 days, 750 mg of
metyrapone is given per 4 hours and a 24-hour urine collection completed. A
normal response is a two to fourfold increase in the urinary steroids over basal
levels. A diminished response in Cushing’s syndrome indicates a primary
adrenal lesion.
Synacthen
test. Tetracosactrin (Synacthen) 250 pg is given intramuscularly and blood
cortisol measured at 30 and 60 minutes. In normal subjects the basal plasma
cortisol should be greater than 60 pg/litre and be at least 70 pg/litre after
stimulation. In Addison’s disease the response is impaired.
Disorders of
adrenocortical function
Acute hypocorticism. Adrenal apoplexy in the newborn. Extensive
haemorrhage into one or both adrenals may be a cause of death in infants within
the first few days of birth. The condition may occur after a long and difficult
labour, and particularly when resuscitative procedures have to be employed to
combat asphyxia neonatorum. The haemorrhage into the adrenals follows necrosis
of the innermost layer of the cortex, which always occurs at birth, possibly as
a result of sudden withdrawal of the female sex hormone (oestrogen). Adrenal
crisis in the newborn produces signs of profound shock. A mass may be palpable
in one or hoth renal regions. Intravenous fluid therapy with hydrocortisone, or
failing the latter, cortisone intramuscularly, offers the only hope.
Waterhouse—Friderichsen
syndrome. Massive
bilateral adrenal cortical haemorrhage occurs in eases of fulminating meningococcal
septicaemia and in some cases of streptococcal, staphylococcal or pneumococcal septicaemia. Most cases occur in infants and young children, but it
can happen in adults with severe haemorrhage or burns. The onset is
catastrophic, with rigors, hyperpyrexia, cyanosis and vomiting. Petechial
haemorrhages into the skin which coalesce rapidly into purpuric blotches are a
constant feature. Profound shock follows, and before long the patient passes
into coma. The condition is one of overwhelming sepsis that pursues a galloping
course, death occurring in most eases within 48 hours of the onset of symptoms
unless correct treatment is given without delay.
Unilateral
haemorrhage causing a lesser degree of systemic upset and not associated with
infections has been described. This type of case resembles a perinephric abscess
or other upper abdominal acute condition.
Confirming the diagnosis. It is futile to await the result of a blood culture.
Bilateral tenderness 5 cm below the
costal margin, clear urine (oliguria is often present) and an absence of signs
in the lungs help to call attention to the adrenal glands. In meningoccocal
infection the diplococcus may be demonstrated by smears obtained from a
punctured petechial spot in the skin.
Treatment. Antibiotic therapy must be given intensively by the intravenous route.
Hydrocortisone 100 mg is given intravenously (i.v.), or intramuscularly (i.m.)
if venous access is difficult. Up to 400 mg hydrocortisone may be required in
the first 24 hours. No mineralocorticoid is needed as the weak intrinsic
salt-retaining action of hydrocortisone suffices at this dosage. Oral
medication may be commenced after the first day and then over about 4 days
reduced to a maintenance level. Oxygen should also be administered. Following
such treatment, improvement often sets in within 3 hours, and a number of
patients has recovered.
Crises
of infantile hypercortism. See later.
Following
bilateral adrenalectomy. If precautions are taken, acute hypocorticism is unusual in the
postoperative period. Treatment is to give 300 mg hydrocortisone on the first
day. Most patients achieve a maintenance dose of 30 mg/day. After about 3 weeks
fludrocortisone 0.1 mg may be given.
Postoperative
adrenal haemorrhage. Adrenal haemorrhage is a rare unexpected cause of deterioration and
sudden death in the postoperative period. In some cases the left adrenal gland
is damaged during radical gastrectomy for carcinoma (Fox). In other cases, when
adrenal haemorrhage is bilateral, there is no evidence of operative injury, they
are usually associated with intra-abdominal sepsis, pneumonia, coagulation
defects and cancer. Thrombosis of the adrenal veins is the cause of infarction
of glands.
Chronic
hypocorticism (Addison’s disease)
This is due to adrenocortical insufficiency
consequent upon progressive destruction with lymphocytic infiltration of the
zona reticularis, the zona fasciculata, the zona glomerulosa and the medulla of
the adrenal glands, in that order. In about 60 per cent of cases the condition
is believed to be due to an autoimmune disease, sometimes in association with
autoimmune thyroiditis (Chapter 44) and pernicious anaemia. Tuberculosis, metastatic
carcinoma and amyloidosis account for the remaining 40 per cent.
Clinical
features
Addison’s disease usually commences in the
third or fourth decade. Sometimes it is the terminal event in cases of
adrenogenital hyperplasia. The sex distribution is about equal. The leading
features are muscular weakness and a low blood pressure. Irregular dusky
pigmentation of the skin, due to deposits of melanin, appears at points of
pressure, e.g. garter or belt, and in the flexion creases. Pigmentation of
mucous membranes, particularly of the mouth, is often striking. When fully
established, the course of the disease is punctuated by crises of acute
adrenocortical insufficiency (see above).
Treatment
Treatment is medical. In long-term management,
most patients require 20—3 0 mg hydrocortisone in divided doses, with
fludrocortisone 0.1 mg daily as mineralocorticoid replacement. Signs of
overtreatment include hypertension, hypokalaemia and oedema; those of under treatment, fatigue and hypotension. Where relevant, chemotherapy is mandatory
for tuberculosis (Chapter 8).
Prognosis
By the use of replacement corticosteroids, the
expectation of life of a patient suffering from Addison’s disease has been
extended from up to 3 years to many years.
Hypercorticism
The various forms of adrenal cortical
hyperfunction are classified according to the age at onset:
•
infantile;
• prepubertal;
•
adult, otherwise known as Cushing’s syndrome — the commonest type;
• postmenopausal;
•
primary aldosteronism (Conn’s syndrome) can occur at any age.
Infantile
hypercorticism
Androgenic excess during intrauterine life is
one form of pseudohermaphroditism in the female
child. The condition is present at birth; sometimes the enlarged clitoris
and a varying degree of hypospadias make it difficult to determine the
infant’s sex. The 17-ketosteroid content of the urine may be sufficiently
elevated to substantiate a diagnosis of a female with adrenal hyper function. If
this is not the case, it is justifiable to perform sex determination by a skin
biopsy before the age of 1 year. Female pseudohermaphroditism with virilism is
invariably associated with disease of the adrenal cortex, usually bilateral
hyperplasia of the cortex. Hormonal studies have shown that there is a
congenital failure of the adrenal glands to synthesise glcocorticoids. Owing to
this lack, these infants are liable to acute phases of adrenal insufficiency
during stress or infection, or to suffer from periodic hypoglycemic attacks.
They need corticosteroid replacement, not only in the emergency, but as
long-term therapy, thereby inhibiting the secretion of excessive androgens. In
the absence of such treatment, the epiphyses join early, the patients are
dwarfed, menstruation does not occur and the breasts do not develop. These
tendencies are corrected by hydrocortisone given orally, 25 mg or more daily,
the dose being determined by 17-ketosteroid estimations (Simpson). Hirsutism is
moderated, but not necessarily abolished. The treatment should be commenced
early if good results are to be obtained.
Prepubertal
hypercorticism
There is never any doubt as to the sex of the
infant at birth and during the very early years of life the child is normal. The
symptoms commence at about the age of 5 or
6 years.
In
the female. Pubic and axillary hair appear, but there is no gross enlargement of
the clitoris. The child is short in stature, the legs being especially stunted,
but she looks much older than she is. Puberty is often precocious, menstruation,
if it occurs, being scanty. There is a deepening of the voice at this time.
In
the male. The term ‘infant Hercules’ is descriptive. He is extremely short,
muscular and hirsute. The genitalia assume adult proportions and spermatozoa are
often present in the seminal fluid.
In
both sexes, 17-ketosteroid content of the urine is increased. A very high
reading supports the diagnosis of an adrenocortical tumour, which must always be
excluded. In both males and females, with a later onset or the passage of time,
the features of Cushing’s syndrome become superadded.
Treatment.
This is identical to that of Cushing’s syndrome.
Postpubertal or
adult hypercorticism (Cushing’s syndrome)
Postpubertal or adult hypercorticism
(Cushing’s syndrome) is due to an excessive endogenous production of glucocorticoids,
mainly hydrocortisone. It is an uncommon condition, often suspected but seldom
confirmed. Pituitary-dependent Cushing’s syndrome is the commonest form of
endogenous hypercorticism accounting for up to two-thirds of all cases. An
adrenal adenoma accounts for 20 per cent and carcinoma (which may be bilateral) 5
per cent. In the remainder there is no discernible structural alteration in
the glands and the condition is due to an ectopic source of an ACTH-like
substance being secreted, by either a benign tumour (e.g. bronchial carcinoid)
or a malignant tumour of bronchus, mediastinum or pancreas. NonACTH-dependent
primary adrenocortical hyperplasia is a rare cause of Cushing’s syndrome.
Alcoholism also must be considered.
In its most typical form, Cushing’s syndrome is exogenous and is seen in
patients treated with large doses of cortisone over long periods for
nonendocrine diseases, particularly rheumatoid arthritis, and in patients
receiving transplants.
Clinical
features. The female to male ratio is at least 3:1. The great majority of cases
(excluding those induced by cortisone therapy) occurs in females between 15 and
30 years of age, in whom it produces highly characteristic features. Although
the patient’s weight is not necessarily increased, there is a deposition of
fat in certain situations. The face becomes rubicund, rounded like a full moon,
and the lips are pursed. The abdomen becomes protuberant, the neck thick, the
supraclavicular fossae obliterated and a roll of fat appears over the region of
the vertebra prominens (buffalo hump). The arms, and especially the legs, are
relatively thin, the muscular development is poor, and the patient complains of
increasing weakness. As the disease progresses, so the general contour becomes
more and more that of a ‘lemon on match-sticks’ (Fig. 45.8). Consequent upon the inhibitory effect of the hypercorticism
on fibrous tissue, the skin becomes of tissue-paper consistency and inelastic.
Exceedingly
Cushing’s
syndrome is rare in children; when it occurs, the patient is nearly always a
female and an adrenal tumour is usually the cause.
A
subgroup, probably due to an excessive secretion of adrenal androgens (adrenogenital syndrome), commences between the ages of 15 and 25
and is confined to females. One of the first indications of its onset is amenorrhoea
or oligomenorrhoea. There follows an excessive growth of hair on
the face (Fig. 45.10),
acne, atrophy
of the breasts, alteration in bodily contour and muscular development, deepening
of the voice and enlargement of the clitoris. Jewish and Spanish women are more
prone to this affliction than those of other races.
Arrhenoblastoma
of the ovary
This rare condition occurs between puberty and
the menopause and also causes hirsutism. It may also arise in a suprarenal
‘rest’.
Screening
tests. There are three simple tests (see above) which may be used to screen
patients suspected to have Cushing’s syndrome:
•
24-hour urinary free cortisol excretion;
•
overnight dexamethasone suppression test.
Definitive
diagnosis. Suspected Cushing’s syndrome may be confirmed by the low-dose
dexamethasone suppression test (see above), which is highly reliable.
Differential
diagnosis. After the diagnosis of Cushing’s syndrome has been established,
it is necessary to determine the cause of adrenocortical hyperfunction. In
general, adrenal hyperfunctioning tumours and ectopic ACTH-secreting tumours
function autonomously and are unaffected by
Localisation
studies. CT accurately identifies virtually all adrenal tumours in patients with
Cushing’s syndrome and has replaced other techniques. It is also the most
reliable method of detecting nodules in the lungs, mediastinum and pancreas,
which are potential sites of ectopic ACTH production. Pituitary CT has also
replaced other techniques for the detection of pituitary microadenomas in
Cushing’s disease, although only 50 per cent of such adenomas are identified.
Bilateral selective inferior petrosal venous sampling for ACTH levels is a
valuable but technically difficult method of confirming and localising
pituitary-dependent Cushing’s disease if CT is unhelpful.
Treatment.
Trans-sphenoidal pituitary adenectomy in skilled hands is now the treatment of
choice for pituitary lesions. External pituitary irradiation is less reliable in
terms of long-term remission but is more successful in children. Yttrium-90
implantation is an alternative form of pituitary irradiation. Bilateral total
adrenalectomy is a reliable procedure for patients with Cushing’s disease in
whom pituitary treatment has failed.
The
treatment of an adrenal tumour is surgical resection and resection of benign
ectopic ACTH-secreting tumour is curative. Many, however, are malignant and
widely disseminated when Cushing’s syndrome becomes clinically apparent.
Nelson’s
syndrome
Hyperpigmentation and pituitary enlargement
occur in about 20 per cent of cases after bilateral adrenalectomy and are
avoided by selective pituitary microsurgery.
Prognosis.
Most patients are alive 20 years after successful resection of an adrenal
adenoma, but survival beyond 5 years
is rare with a carcinoma (Welbourn). Pituitary microadenectomy in expert hands
results in cure in about 80 per cent of patients very rarely, the adrenogenital syndrome appears in youths and men. Owing to excessive
production of oestrogenic hormones by the adrenal cortex, gynaecomastia, atrophy
of the testicles and psychical signs of effeminacy appear (adrenal feminism).
Postmenopausal
hypercorticism
Postmenopausal hypercorticism is usually
characterised by the growth of a beard (the bearded woman of the circus) and is
often accompanied by mental aberration. A lesser degree of hirsutism is almost a
natural accompaniment of the ageing process, particularly in dark-haired
females, and it is difficult to draw the line between the normal and the
pathological. Thus it is that operative treatment is usually disappointing.
Primary
aldosteronism
Primary aldosteronism (Coon’s syndrome) is a
surgically correctable type of hypertension found in 1—2 per cent of all
hypertensive patients. It is characterised by autonomous excessive aldosterone
secretion which leads to sodium retention and a fall in serum potassium. The
latter causes the typical associated features of the syndrome, namely episodes
of muscular weakness associated with polyuria and polydipsia. The plasma sodium
is high and the potassium is low, but simple administration of potassium does
not relieve the condition. Renin and angiotensin levels are depressed. The cause
is either an aldosteronesecreting adrenal adenoma or bilateral adrenocortical
hyperplasia (less common). CT and adrenal scanning with radioactive-labelled
cholesterol are the appropriate localisation tests to distinguish between them.
When these fail, adrenal venous sampling with measurement of aldosterone to
cortisol ratios is the next step. Unilateral adrenalectomy is the treatment for
an aldosterone-producing adenoma and has a high cure rate, whereas surgery has
been disappointing in adrenocortical hyperplasia and these patients are
generally managed medically.
Secondary aldosteronism is associated with
cirrhosis of the liver, and renal artery stenosis with high levels of renin and
angiotensin.
The incidental
adrenal mass —
‘incidentaloma’
CT and
MRI have resulted in increasing numbers (up to 1 per cent) of adrenal tumours
being identified in the course of abdominal imaging for the investigation of
other conditions. The finding may represent an adrenal tumour but more probably
a benign lesion. Opinion is divided about management but essentially functioning
lesions are excised whereas nonfunctioning lesions are managed according to
size. Lesions less than 3 cm in size should be followed 3-monthly for a time by
CT and excised if they enlarge, whereas those larger than 3 cm should be excised to
exclude malignancy.
Adrenalectomy
for hypercorticism
It is essential that all patients who are to
be subjected to adrenalectomy are supported intra operatively and
postoperatively
by adrenocortical hormone replacement therapy, irrespective of the extent of
adrenal resection.
Corticosteroid
therapy
Corticosteroids are started when anaesthesia
is induced. There is no advantage of one steroid over another except for their
different durations of action. Hydrocortisone is very short
acting, prednisolone intermediate and dexamethasone long acting. Each may be
given intravenously or intramuscularly.
During
the first 24 hours after induction of anaesthesia, the patient should receive no
more than 300 mg hydrocortisone, 60 mg prednisolone or 6 mg dexamethasone. The
dosage should be halved each day until a maintenance dose orally (hydrocortisone
30 mg, prednisolone 5 mg or
dexamethasone 0.5 mg) is reached.
Fludrocortisone 0.1 mg daily (replacing aldosterone) is usually added to the
maintenance dose of corticosteroid to regulate fluid and salt balance.
After
total adrenalectomy the patient should always carry a card stating the dosage of
corticosteroid being received. Any stress (e.g. further operation or infection)
is an indication to increase the dosage.
Operation
When an adrenal tumour has been demonstrated
preoperatively, excision of that adrenal gland alone is carried out.
Posterior approach
An ample posterolateral incision, such as is
used for nephrectomy (Chapter 64), is used. After subperiosteal resection of the
12th rib, the lower border of the pleura is defined and protected. The incision
is extended through the bed of the 12th rib to reveal the perinephric fat,
within which the adrenal gland is identified, as described below. Sometimes an
approach through the bed of the 11th rib, reflecting the pleura upwards, is
preferred. (See also Anterior approach, below.)
On
the right side the suprarenal vein is short and may be torn from the vena cava
if it is not identified and ligated at an early stage of the dissection. By
finger and gauze dissection, keeping close to the gland, the gland is freed from
below and behind, upwards, ligating and dividing bleeding vessels as they are
encountered, until it is suspended only by its main vascular pedicle near its
apex.
Anterior
approach
The adrenal glands are approached through
either a curved transverse incision or a long midline incision. The left
adrenal gland is approached first by cutting along the lateral leaf of the
lienorenal ligament and then curving downwards and medially, so as to enable a
wide peritoneal flap to be reflected. By retracting the spleen downwards and
medially, the
Thoracoabdominal
approach
For removal of a large adrenal tumour (>10—15
cm in diameter) a thoracoabdominal incision gives the wide exposure
necessary for radical resection en bloc which
may involve removal of the ipsilateral kidney or spleen and tail of the
pancreas.
Laparoscopic
adrenalectomy
Laparoscopic adrenalectomy is a developing
technique which may in selected patients, particularly patients with Coon’s
syndrome, provide an alternative operative approach using a full lateral
decubitus transperitoneal flank approach. It is claimed that such a technique
offers a less painful postoperative recovery, with the in-patient stay reduced
from a mean of 8 days for open surgery to 3—4 days. This must be offset
against a doubling of the operating time, a possible increased incidence of
wound infection and port site hernia formation.
Left
adrenalectomy. Start by dissecting the splenoparietal ligament close to the
diaphragm to permit a complete mobilisation of the spleen to the right with the
tail of the pancreas. Dissection of 5 cm
of the splenic vein, when used as a landmark, permits exposure of the renal
vein: which leads to the main and accessory adrenal veins. They can be safely
divided between clips. The right side of the gland is dissected up to the
diaphragm with clipping of the middle and upper arterial pedicles. The
adrenalectomy is achieved by dissection of the fat and the gland is extracted in
a bag.
Right
adrenalectomy. The fundamental step of the procedure is the section of the
hepatoparietal ligament far to the right allowing an upwards mobilisation of the
liver. Then dissect towards the vena cava using this structure as a landmark to
find the renal vein which is the inferior limit of the dissection. The main
adrenal vein is doubly clipped and divided. The third step is to look for an
accessory adrenal vein joining a subhepatic vein above the main adrenal vein.
The adrenal arteries, superior, middle and the main inferior one coming from the
renal artery, are dissected on the right side of the vena cava. The last step is
straightforward coagulation, vessel clipping and dividing as on the left side.
Adrenal medulla
Physiology. The medulla of the adrenal glands
(chromaffin tissue), which is developed, together with sympathetic nerves, from
ectoderm, is grey in colour and connected intimately, both anatomically and
functionally, with splanchnic nerves. Chromaffin tissue is so called because the
large polyhedral cells of which it is composed contain granules that stain
An
amino acid peptide adrenomedullin has recently been isolated from human
phaeochromocytoma. It has a structure similar to calcitonin gene-related peptide
and amylin. Intravenous administration elicits a strong, long-lasting
hypotensive effect. It has been detected in human plasma and vascular smooth
muscle cells with specific receptors. It decreases blood pressure by lowering
total peripheral resistance and increasing urine flow and urinary sodium
excretion.
Actions of catecholamines. Catecholamines exert their effects through specific
cell-surface receptors: alpha-receptors and beta-receptors (Table 45.1).
These mediate the actions of the endogenously released catecholamines,
noradrenaline and adrenaline, and some of the actions of dopamine. The receptors
have quite different pharmacological properties and an organ may have more than
one type. The complex actions of catecholamines include altering enzyme
activity, metabolic pathways and the permeability of cell membranes to ions.
Pharmacological
inhibitors of alpha stimulation (alpha-blockers) include the long-acting
phenoxybenzamine (Dibenyline) and short-acting phentolamine (Rogitine).
Beta-blockers include propranolol (Inderal) and practolol (Eraldin).