Endocrine

Investigation and • Aldosterone secretion is under the control of the renin–

a­ ngiotensin system (see Lote, CROSS REFERENCE). It increases

management of adrenal renal reabsorption of sodium and excretion of potassium and

­hydrogen.

disease • Adrenal androgen secretion is under the control of adrenocor­

ticotropic hormone.

S P Balasubramanian The adrenal medulla synthesizes the catecholamines adrenaline,

Barney Harrison
Abstract
Disorders of the adrenal gland are rare and complex, with many ­potential
pitfalls in their management. An understanding of embryology, anatomy,
physiology and biochemistry is crucial. Surgical treatment may be ­required
for syndromes of hormonal excess and/or suspicion of ­neoplasia.
Keywords adrenal; Cushing’s syndrome; ACTH; pituitary; phaeochromo-
cytoma; MEN syndromes; adrenalectomy; Addisonian crisis
Anatomy
The adrenal glands lie within the renal fascia in relation to the
upper poles of the kidneys. The right adrenal gland is located
partly behind the inferior vena cava and superior to the kidney,
the left adrenal is anteromedial to the kidney. The arterial blood
supply arises from the abdominal aorta, phrenic and renal ves­
sels; the main adrenal vein empties into the inferior vena cava on
the right and, on the left side, the renal vein.
Each adrenal gland consists of an outer cortex derived from
mesenchymal cells and an inner medulla derived from neuro­
ectodermal cells.
• The zona glomerulosa is the outer layer, represents 15% of
the cortex and produces aldosterone.
• The zona reticularis is the middle layer, represents 70% of the
cortex, and produces cortisol, the sex steroids dehydroepiandro­
sterone (DHEA) and androstenedione.
• The zona fasciculate is the innermost layer and produces sex
steroids.
noradrenaline and dopamine. Noradrenaline has a high affinity
for α1 and β1 receptors, which are abundant in the ­cardiovascular
system, causing increased heart rate and increased myocardial
contractility. Adrenaline binds preferentially to α2 receptors in
skeletal muscle, causing vasoconstriction. Catecholamines are
metabolized to metadrenaline and normetadrenaline or via an
alternative pathway to form vanillyl mandelic acid.
Imaging
CT and MRI are commonly used in adrenal imaging to:
• localize the disease
• confirm morphological abnormalities
• identify features of malignancy.
They are also essential in the staging of adrenal cancers and to
diagnose suspected recurrence (Figure 1).
Adrenal scintigraphy is used to confirm that a morphological
abnormality found on cross-sectional imaging is the source of
a proven biochemical syndrome (e.g. metaiodobenzylguanidine
(123I-MIBG) in phaeochromocytoma; Figure 2) and to locate extra-
adrenal and metastatic phaeochromocytoma. Iodo-cholesterol
isotopes (e.g. 59NP) can be used in Cushing’s syndrome to assess
the functional significance of an adrenal nodule. Single-photon
emission computed tomography (SPECT) provides tomographic
views of an isotope scan.

Physiology
The adrenal cortex synthesizes cortisol, aldosterone and
a­ ndrogens.
• Synthesis of cortisol is controlled by corticotrophin-releasing
factor, adrenocorticotropic hormone (ACTH) and negative feed­
back. Cortisol mediates the stress response, metabolism of carbo­
hydrate, lipid and protein and, via its mineralocorticoid effects,
promotes sodium conservation in the kidney.

S P Balasubramanian MRCS is a Specialist Registrar at Northern General

Hospital, Sheffield, UK. Conflicts of interest: none declared.

Barney Harrison FRCS is a Consultant Endocrine Surgeon at Northern

General Hospital, Sheffield, UK. Conflicts of interest: none declared. Figure 1 CT of the abdomen showing a left-sided adrenal mass.

SURGERY 25:11 493 © 2007 Elsevier Ltd. All rights reserved.

 Endocrine

­ sually occurs in longstanding cases and is associated with

u
fatigue, muscle weakness, and cardiac dysrythmia.

The diagnosis of primary hyperaldosteronism should be pur­

sued in:
• patients with resistant hypertension
• hypertensive patients with hypokalemia
• hypertensive patients with adrenal incidentaloma and
• evaluation of secondary hypertension.
A raised aldosterone:renin activity ratio in plasma confirms the
biochemical diagnosis. CT/MRI is required to assess morphol­
ogy of the adrenal gland and differentiate unilateral from bilateral
gland disease. Selective adrenal vein catheterization to measure
the aldosterone–cortisol ratio is used to distinguish unilateral from
bilateral disease if imaging results are uncertain. Primary hyperal­
dosteronism must be distinguished from secondary hyperaldoste­
ronism (due to diuretic therapy, renal artery stenosis, malignant
hypertension) in which aldosterone and plasma renin concentra­
tions are raised.

Treatment of primary hyperaldosteronism is directed toward the

Figure 2 123I-MIBG scan showing uptake of radio-isotope (arrow) by a
left-sided phaeochromocytoma.
underlying disease.
Medical treatment includes the aldosterone antagonists
­spironolactone and eplerenone. The side effects of ­spironolactone
include decreased libido and gynaecomastia.
Surgery should be considered for unilateral disease. Cure
of hypertension after unilateral adrenalectomy is reported in
30–72% of cases; reduction in antihypertensive medications is
possible in the remaining patients. Factors that predict a good
response to surgery include a short duration of hypertension,
younger age and absence of family history. Surgery is contraindi­
cated in bilateral disease.

X-ray-guided selective adrenal vein sampling is often used in

Cushing’s syndrome
Conn’s syndrome to distinguish unilateral from bilateral hyper­
secretion of aldosterone. Cause: Cushing’s syndrome is caused by prolonged exposure to
high circulating concentrations of cortisol.
Primary hyperaldosteronism
Incidence: Cushing’s syndrome mainly affects adults aged
Aetiology: primary hyperaldosteronism is caused by excess 20–50 years. The annual incidence is 0.7–2.4 per million
­production of aldosterone from the adrenal cortex. The causes of ­population.
primary hyperaldosteronism are listed in Table 1.
Types: endogenous Cushing’s syndrome is ACTH-dependent
Clinical features are usually non-specific, with hypertension (85%) or ACTH-independent (15%).
being the reason for referral in most patients. Hypokalemia ACTH-dependent Cushing’s syndrome is caused by:
• pituitary adenoma (Cushing’s disease)
• ectopic secretion of adrenocorticotropic hormone (lung can­
cer, carcinoid, medullary thyroid cancer, thymoma, pancre­
Causes of primary hyperaldosteronism
atic islet cell tumour).
ACTH-independent Cushing’s syndrome is caused by:
Common
• adrenal adenoma
Adrenal adenoma (Conn’s syndrome)
• adrenal carcinoma (rare)
Bilateral adrenal hyperplasia.
• bilateral macronodular hyperplasia (rare).
Rare
Unilateral adrenal hyperplasia Clinical features are shown in Table 2.
Adrenal carcinoma
Glucocorticoid-suppressible hyperaldosteronism Diagnosis is confirmed by establishing high circulating concen­
trations of cortisol, loss of diurnal rhythm and loss of feedback
Table 1 control by the hypothalamic–pituitary–adrenal axis.

SURGERY 25:11 494 © 2007 Elsevier Ltd. All rights reserved.

 Endocrine
Clinical features of Cushing’s syndrome
Features listed in decreasing order of incidence
• Obesity including abnormal deposition of fat (upper body,
rounded face, neck)
• Decreased libido
• Thin skin
• Decreased linear growth in children
• Menstrual irregularity
• Hypertension
• Hirsutism
• Depression ± emotional lability
• Easy bruising
• Glucose intolerance
• Weakness
• Osteopenia or fracture
• Nephrolithiasis
Table 2
High concentrations of cortisol are also seen in depression,
alcoholism, anorexia nervosa and late pregnancy (pseudo-
­Cushing’s syndrome). Tests used for the secure diagnosis of
­cortisol excess include:
• 24-hour urinary free cortisol
• Midnight and morning plasma cortisol
• 1 mg overnight dexamethasone suppression test
• 48-hour low-dose dexamethasone suppression test.
When hypercortisolaemia is confirmed, plasma concentrations
of ACTH are required to distinguish ACTH-dependent disease
(high/normal ACTH levels) from ACTH-independent disease
(low ACTH levels).
In ACTH-independent Cushing’s syndrome, CT/MRI of the
adrenal glands shows the morphological abnormality responsible
for excess secretion of cortisol.
In ACTH-dependent Cushing’s syndrome, the following tests
distinguish pituitary-dependent ACTH secretion (70%) from
ectopic ACTH secretion (15%):
• non-invasive tests (e.g. high-dose dexamethasone suppres­
sion test, corticotrophin-releasing hormone test)
• imaging of the pituitary (MRI) and the chest and abdomen (CT)
• bilateral inferior petrosal sinus sampling.
Treatment: inhibitors of cortisol synthesis (metyrapone, keto­
conazole, mitotane) before definitive therapy reduce circulating
cortisol concentrations.
Pituitary adenomas are treated by trans-sphenoidal excision;
the cure rate of is ≈70–80%. Options for persistent or recurrent
pituitary disease include reoperative pituitary surgery, pituitary
radiotherapy or bilateral adrenalectomy. Pituitary radiotherapy is
effective, but has a delayed onset of action and is associated with
long-term hypopituitarism.
Laparoscopic adrenalectomy is indicated for ACTH-indepen­
dent and some ACTH-dependent (after failed pituitary surgery)
forms of the disease. Open adrenalectomy is indicated in most
cases of adrenocortical cancer. Patients with Cushing’s syndrome,
including patients with subclinical disease, require corticosteroid
SURGERY 25:11
cover after adrenalectomy (unilateral or bilateral) in accordance
with local guidelines that should be clearly defined.
In ectopic ACTH syndrome, if the tumour can be localized,
treatment options include surgery, radiotherapy, chemotherapy
or a combination of these. Drug treatment is continued and
bilateral laparoscopic adrenalectomy should be considered if the
tumour cannot be localized.
Phaeochromocytoma
The estimated annual incidence of phaeochromocytoma is 1–2
per million population. The prevalence in patients with hyper­
tension is 0.1–0.6%. The incidence of malignancy ranges is
11.6–23%; the risk is higher for tumours arising in extra-adrenal
sites.
Types: phaeochromocytomas are catecholamine-secreting neuro­
endocrine tumours arising from the chromaffin tissue of the
adrenal medulla (80–85%) and from extra-adrenal paraganglia
(15–20%)—paragangliomas. These tumours are very vascular
and stain positive for chromogranin A and synaptophysin. Most
phaeochromocytomas produce noradrenaline and adrenaline;
extra-adrenal phaeochromocytomas produce a preponderance of
noradrenaline.
Familial phaeochromocytoma should be considered in patients
aged <40 years presenting with unilateral or bilateral disease. It
occurs, even in the absence of family history, in association with
the disorders described below.
Multiple endocrine neoplasia type 2 (MEN 2) is an autoso­
mal dominant disorder caused by germline mutations in the RET
proto-oncogene on chromosome 10.
• MEN 2A is characterized by medullary thyroid carcinoma,
phaeochromocytoma, primary hyperparathyroidism and cutane­
ous lichen amyloidosis.
• MEN 2B is characterized by medullary thyroid carcinoma,
phaeochromocytoma, marfanoid habitus and ganglioneuroma of
the lips, tongue and gastrointestinal tract.
Screening for RET mutations in family members of the gene-
positive index case allows diagnosis of the familial syndrome
before the onset of symptoms and facilitates prophylactic sur­
gery for medullary thyroid carcinoma (total thyroidectomy)
but not for phaeochromocytoma (occurs in ≈50% of gene
­carriers).
von Hippel-Lindau disease (autosomal dominant) occurs
due to mutations in the VHL gene on chromosome 3 and is
characterized by renal cancers and cysts, CNS/retinal heman­
gioblastomas, pancreatic tumours and phaeochromocytomas
(10–20%).
Neurofibromatosis type I (autosomal dominant; von Reck­
linghausen’s disease) occurs due to mutations in the NF1 gene
on chromosome 17 and is characterized by café au lait spots,
neurofibromas, axillary or inguinal freckling, optic nerve gliomas
and phaeochromocytoma (<5%).
Paraganglioma syndromes include mutations in succinate dehy­
drogenase B and D genes on chromosomes 8 and 4, respectively.
They are characterized by paragangliomas of the head, neck, chest
and abdomen. SDH B mutation-associated tumours have a signifi­
cantly higher risk of malignant phaeochromocytoma (≈50%).
495 © 2007 Elsevier Ltd. All rights reserved.
 Endocrine
Clinical features (Table 3) are very variable (phaeochromocytoma
is called the ‘great mimic’) and can involve many different organ
systems. Classic features include severe hypertension with head­
ache, palpitations and sweating. Most patients have persistent or
intermittent hypertension that is difficult to control; the absence of
hypertension does not exclude ­phaeochromocytoma.
The sudden release of catecholamines can cause life-­threatening
crises with pulmonary oedema, myocardial infarction or cerebro­
vascular accident. Adrenal biopsy, induction of anaesthesia and
various drugs may also precipitate these symptoms.
Diagnosis: phaeochromocytoma is suspected in patients with:
• paroxysmal signs or symptoms suggestive of a
­phaeochromocytoma
• treatment-resistant or labile hypertension
• a paradoxical blood pressure response during surgery and
­anaesthesia
• a family history of phaeochromocytoma
• an adrenal incidentaloma.
Investigations: biochemical confirmation of catecholamine
excess and localization of the adrenal (or extra-adrenal) tumour
are the objectives. Investigations include:
• 24-hour urinary fractionated catecholamines (epinephrine,
norepinephrine) and their metabolites (metanephrine, nor­
metanephrine, vanillylmandelic acid).
• plasma-free metanephrines is a highly accurate test for the
diagnosis of a phaeochromocytoma
• CT/MRI confirms the morphological abnormality of the
­adrenal gland.
• 123I-MIBG scan combines functional and anatomical ­imaging;
it is recommended in those at high risk of extra-adrenal
and ­ metastatic disease (i.e. large tumours and familial
­syndromes).
Management: resection is the only cure for phaeochromocy­
toma. Preoperative adrenergic blockade with an α-blocker (e.g.
phenoxybenzamine) is essential, with gradual dose increments
until control of blood pressure and development of ­ tolerable
Clinical features of phaeochromacytoma
Features listed in decreasing order of incidence
• Sustained or paroxysmal hypertension
• Headache
• Palpitations
• Sweating
• Pallor
• Nausea
• Flushing
• Weight loss
• Tiredness
• Psychological symptoms (anxiety, panic)
• Orthostatic hypotension
• Hyperglycaemia
Table 3
SURGERY 25:11
postural hypotension is achieved. β-blockers are required
only if tachycardia develops in an α-blocked patient: their use
before complete α-blockade can precipitate a hypertensive
­crisis. Adequate preoperative hydration prevents postoperative
­hypotension.
Laparoscopic adrenalectomy is the procedure for phaeochro­
mocytoma. In bilateral disease, cortical-sparing adrenalectomy
may minimize (or totally obviate) lifelong dependence on corti­
costeroid replacement, but is associated with an increased risk of
recurrence. Intraoperative hypertensive crisis and hypotension
can complicate the perioperative course; an anaesthetist with
experience in the care of these patients is essential.
Histological differentiation of benign from malignant tumours
is difficult and relies on operative findings of local invasion
or metastasis. Vascular invasion may be seen in tumours that
behave in a benign fashion. Lifelong follow-up (including annual
biochemical screening) is recommended to exclude recurrent or
metachronous phaeochromocytoma.
Malignant phaeochromocytoma – high-dose 131I-MIBG may
relieve symptoms. Combination chemotherapy with cyclophos­
phamide, vincristine and dacarbazine has a response rate of
57%. The five-year survival rate is ≈20%.
Adrenal ‘incidentaloma’
Definition: an adrenal incidentaloma is an adrenal mass >1 cm
in diameter that is discovered incidentally on cross-sectional
imaging; widespread use of CT and MRI has led to increased
detection of such tumours.
Incidence: incidentalomas are present in ≈2.1% of individuals
from autopsy series and the incidence rises with age. About 95%
of incidentalomas are non-functioning.
Pathology includes benign cortical adenomas, cysts, lipomas,
myelolipomas, haematomas, adrenal cancer, metastases and
tumours arising from the adrenal medulla.
Investigations: if an incidentaloma is discovered, biochemical
tests are done to confirm or exclude the hormonal syndromes
discussed above:
• overnight 1 mg dexamethasone suppression test
• plasma DHEA
• 24-hour urinary metanephrines and fractionated catecholamines
• serum potassium, plasma aldosterone, and plasma renin
­activity.
Percutaneous biopsy of an adrenal tumour should not be per­
formed unless biochemical tests have excluded phaeochromo­
cytoma. The only indication for biopsy of an incidentaloma is
if adrenal metastasis is suspected in a patient with a history of
epithelial cancer.
Needle biopsy can precipitate a life threatening cardiovascular
crisis if the tumour is an undiagnosed phaeochromocytoma.
Management: incidentalomas that are hormonally active should
be treated like their symptomatic counterparts. Non-­functioning
incidentalomas should be considered for resection if there is
­suspicion of malignancy based on size (>4 cm) or appear­ance on
imaging (including evidence of growth on sequential scans).
496 © 2007 Elsevier Ltd. All rights reserved.
 Endocrine
Adrenocortical carcinoma
Incidence: adrenocortical cancer is a highly malignant but
uncommon tumour with an age-adjusted annual incidence of 1.5
per million. It causes 0.2% of cancer deaths. Genetically deter­
mined adrenocortical cancer is a component of the Li Fraumeni,
Beckwith Wiedemann, and MEN 1 syndromes.
Types: adrenocortical carcinomas can be functioning or non-
functioning. The former present at an earlier age and are more
common in women; non-functioning tumours are more common
in men.
Presentations
• Hormone excess is a presenting feature in 50% of patients.
The common manifestations are virilization, Cushing’s syn­
drome or a mixture. Excess of pure aldosterone and feminization
are ­uncommon.
• Asymptomatic—incidentaloma.
• Local or systemic symptoms (abdominal mass, pain, weight
loss, fever, symptoms due to metastases).
Rapid progression of symptoms and high concentrations of
hormones suggest malignancy.
Investigations: malignancy is a strong possibility if preopera­
tive CT or MRI show a large adrenal tumour (>5 cm). Imag­
ing may also reveal extra-adrenal invasion, intracaval extension
of tumour or distant metastasis. The investigations listed in the
adrenal incidentaloma section are appropriate to confirm or
exclude biochemical abnormalities in functioning tumours.
Management: en bloc resection of the tumour and lymph nodes
is the only chance of cure. Resection in early-stage disease is
potentially curative; resection of locally advanced disease in
patients with functioning tumours provides better palliation.
Mitotane is the most effective systemic agent against adre­
nocortical carcinoma, and is often used in metastatic disease for
symptom control or after incomplete resection of the tumour.
Radiotherapy may be used in the adjuvant setting after sur­
gery; it has a palliative role in the management of unresectable
adrenocortical carcinoma.
Locoregional recurrence occurs in 75% of patients; further
resection is the best treatment for locoregional recurrence and
metastasis. The five-year survival rates are ≈38%.
Adrenal insufficiency and Addison’s disease
Definition: adrenocortical insufficiency is due to inadequate
secretion of glucocorticoid and mineralocorticoid hormones.
Types: adrenal insufficiency may be primary (inability of the
adrenal gland to synthesize and secrete glucocorticoid or miner­
alocorticoid hormones) or secondary to ACTH deficiency.
Primary adrenal insufficiency is usually due to Addison’s
disease, an autoimmune disorder; other causes are tumour,
tuberculosis or other infections, adrenal haemorrhage and surgi­
cal removal of adrenal tissue.
Secondary adrenal insufficiency results from pituitary or hypo­
thalamic disorders and withdrawal of exogenous ­corticosteroids.
SURGERY 25:11
Clinical features: chronic adrenal insufficiency causes progres­
sive fatigue, chronic weakness and weight loss. Pigmentation
of the skin and mucous membranes (not seen with hypopitu­
itarism), diarrhoea, vomiting and abdominal pain may be pres­
ent. Acute adrenal insufficiency results in a poor stress response;
hypovolaemia, hypotension refractory to fluid loading; hypogly­
caemia and hyperkalaemia. It is a medical emergency.
Investigations: adrenal insufficiency is associated with low serum
sodium, raised serum potassium, raised urea, raised serum cal­
cium and, in primary insufficiency, raised plasma ACTH. ­Random
serum cortisol >580 nmol/l excludes Addison’s disease.
A short synacthen test helps to exclude Addison’s disease:
1 μg of ACTH (i.v.) is given and cortisol measured at 0 and 30
minutes. Addison’s disease is excluded if, after 30 minutes,
serum cortisol is >500 nmol/l and >200 nmol/l greater than
baseline. Serum ACTH should be measured if this does not
exclude Addison’s disease. The combination of low cortisol and
high ACTH strongly suggests Addison’s disease. There is no role
for imaging.
Management
Glucocorticoid replacement – hydrocortisone is the first-
line treatment for replacement therapy and allows monitoring
of ­ cortisol concentrations. The total daily replacement dose of
hydrocortisone is 20–30 mg. Prednisolone is an alternative, but
cortisol concentrations cannot be monitored.
Mineralocorticoid replacement – fludrocortisone is given as a
single dose of 100 μg daily.
Addisonian crisis (acute adrenal insufficiency) may follow
acute withdrawal of cortisosteroids or be caused by infection,
surgery, trauma, severe sepsis, disseminated intravascular coag­
ulation or burns.
Presentation is typically:
• a history of malaise, tiredness, weakness, anorexia and ab­
dominal pain
• severe dehydration, hypotension and circulatory failure that is
refractory to treatment without corticosteroid administration.
Management – standard resuscitation procedures should be
employed (airway, breathing, circulation) including hydration
with 0.9% saline and hydrocortisone (i.v., 100 mg, 6-hourly).
Prevention – education is the crucial factor; patients should:
• know the importance of compliance with their hydrocortisone
medication
• wear a Medic Alert bracelet
• carry a steroid card
• know how to increase the dose of corticosteroid during other
illnesses
• be supplied with a predosed syringe containing 100 mg of
hydrocortisone to self-administer if cannot tolerate cortico­
steroids (p.o.) at a normal or increasing dose.
Surgical approaches to the adrenal glands
The adrenal glands can be approached through the anterior,
­posterior and lateral abdominal wall. They are removed at
open surgery or by laparoscopy. Factors to be considered in
­determining which approach to choose are listed in Table 4.
497 © 2007 Elsevier Ltd. All rights reserved.
 Endocrine
Factors determining the surgical approach to
adrenalectomy
• Unilateral versus bilateral disease
• Likelihood of malignancy
• Tumour size
• Other abdominal disease,
• Previous surgery
• Body habitus
• Surgeon’s familiarity with the various procedures
Table 4
Laparoscopic adrenalectomy
Laparoscopic adrenalectomy is associated with reduced wound,
chest and gastrointestinal complications compared with open
surgery. The view of the operative field obtained during a trans­
peritoneal or retroperitoneal laparoscopic approach is far supe­
rior to that obtained by other approaches to the adrenal glands. A
laparoscopic approach for the adrenal gland is sometimes techni­
cally difficult and a hand-assisted approach is a useful adjunct,
providing intraoperative manipulation of large tumours. A mini-
incision is required for insertion of the hand-port, but the ­benefits
of a laparoscopic approach are retained.
Contraindications: malignancy is a relative contraindication to
the laparoscopic approach, as are large tumours and previous
abdominal surgery.
Open approaches
The anterior approach (via a midline or bilateral subcostal inci­
sion) allows access to both adrenal glands simultaneously and
if necessary resection of other diseased organs. The anterior
approach is used for malignant and some extra-adrenal tumours.
The main disadvantages are postoperative ileus, adhesions,
poor wound healing in Cushing’s syndrome, and respiratory
­complications.
The posterior approach is the most direct route to the adrenal
glands and is suitable for removal of glands <5 cm in diameter;
exposure is inadequate for larger glands, and two separate inci­
sions are required for bilateral disease.
The advantages of the posterior approach compared with an
open anterior approach are:
• shorter operating time
• less ileus
• less operative blood loss
• fewer postoperative respiratory complications.
SURGERY 25:11
Procedure – the patient is placed in the prone jackknife posi­
tion. A hockeystick skin incision is made over the twelfth rib, the
latissimus dorsi and sacrospinalis muscles are divided to expose
the periosteum and the rib divided. After dividing the perinephric
fat, the adrenal is freed on all aspects, its vascular connections
divided and the gland removed. A chest drain may be necessary
if the pleura has been breached.
The lateral approach is another extraperitoneal approach to
the adrenal glands. The main indications are a large unilateral
tumour, or if the anterior approach is contraindicated because of
previous surgery or obesity. Gravity allows intraperitoneal struc­
tures to fall away from the operating field.
Procedure – the patient is placed in the lateral position with
the diseased side uppermost. Subcostal, intercostal or transcostal
incisions can be used to enter the retroperitoneum; the incision
is centred on the mid-axillary line. The intercostal and transcos­
tal incisions provide better exposure to the adrenal glands than
the subcostal approach; dissection continues as in the posterior
approach.
The thoracoabdominal approach to the adrenal glands provides
the widest exposure and is used for very large tumours and/or
if excision of adjacent organs is anticipated. The disadvantages
of this approach are those of the anterior and lateral approaches;
postoperative respiratory complications are a major concern. ◆
Cross reference
Lote C. The renin–angiotensin system and regulation of fluid volume.
Surgery 2006; 24(5): 154–9.
Further reading
Doherty GM, Skogseid B, eds. Surgical endocrinology. Philadelphia:
Lippincott, Williams and Wilkins, 2001.
Grumbach MM, Biller BM, Braunstein GD, et al. Management of the
clinically inapparent adrenal mass (“incidentaloma”). Ann Intern
Med 2003; 138: 424–9.
Lenders JW, Eisenhofer G, Mannelli M, Pacak K. Phaeochromocytoma.
Lancet 2005; 366: 665–75.
Newell-Price J, Bertagna X, Grossman AB, Nieman LK. Cushing’s
syndrome. Lancet 2006; 367: 1605–17.
Wajchenberg BL, Albergaria Pereira MA, Medonca BB, et al.
Adrenocortical carcinoma: clinical and laboratory observations.
Cancer 2000; 88: 711–36.
Young Jr WF. Minireview: primary aldosteronism—changing concepts in
diagnosis and treatment. Endocrinology 2003; 144: 2208–13.
498 © 2007 Elsevier Ltd. All rights reserved.