PHAEOCHROMOCYTOMA:

PERIOPERATIVE
MANAGEMENT

Dr. Satyanarayan Bhubjabal

Guided by Asso Prof Dr. K.B.Nayak
Dept.of Anaethesia and critical care
SCB MCH CTC
 INTRODUCTION
Phaeochromocytomas are catecholamine secreting
neuroendocrine tumors that arise from the chromaffin cells
of the sympathoadrenal system.
They are usually found in the adrenal gland but extra-adrenal
Phaeochromocytomas, though less common, are tumors that
originate in the ganglia of the sympathetic nervous system.
It is a rare tumor, being responsible for less than 0.1% of all
cases of hypertension.
These tumors although rare are important as they present a
great challenge to the anesthesiologist.
The condition is potentially life threatening unless diagnosed
and treated .
PATHOLOGY
The word Phaeochromocytomas in Greek means
dusky olored tu or referring to the color it
acquires when stained with chromium salts.
Phaeochromocytomas is often referred to as the
% tu or because
10% are extra adrenal .
10 % are malignant .
10% are inherited as an autosomal dominant trait .
10% present bilaterally.
10% seen in child .
 Though usually found in the adrenal medulla these
tumors can be found anywhere in association with the
sympathetic ganglia.
The Organ of Zuckerkandl near the aortic bifurcation is
the most common extra adrenal site.
Phaeochromocytomas are usually solid highly vascular
tumors.
Malignant spread can occur in 10%cases, with a
predisposition for the liver and bones.
 Familial phaeochromocytomas can be part of the multiple
endocrine neoplastic syndromes (MEN) and can also occur in
association with neuroectodermal dysplasia.(von Hipple Lindau
syndrome).
MEN2a (Sipples s syndrome) MEN2b

Phaeochromocytoma, Pheochromocytoma
Medullary carcinoma of the thyroid Medullary carcinoma thyroid
Hyperparathyroidism Mucosal neuro mas
Marfanoid body habitous

Almost 100% of patientswith MEN2a have or will develop

phaeochromocytoma and they are frequently bilateral.
The neuroectodermal dysplasias associated with
phaeochromocytomas are Von Hippel-Lindau Syndrome and Von
Re kli ghause s Disease.
 Phaeochromocytomas are not under neurogenic control and
secret catecholamines autonomously.
Phaeochromocytomas are highly active tumours secreting
adrenaline, noradrenaline and rarely dopamine.
Most tumours predominantly secrete noradrenaline.Noradr
and adr in the ratio of 85:15 (Normal adrenal secretion is 85%
adrenaline).
Familial phaeochromocytomas are an exception because they
secrete large amounts of adrenaline.
On rare occasions chromaffinomas can secrete intestinal
peptides such as VIP and somatostatins.
CLINICAL FEATURES
The clinical presentation of
pheochromocytoma is variable;attacks range
from infrquent(once in a month) to
numerous(many times per day).
Hypertension either continuous or paroxysmal
is the most frequent manifestation.
Headache,sweating,pallor and palpitations
are other classic sign and symptom.
Orthostatic hypotension is also a common
finding and is considered due to hypovolemia
and impaired vasoconstrictor reflex responses.
 If adrenaline secreting tumor - Tachycardia
Systolic hypertension
adrenergic predominance
Diastolic hypotension
.
If noradrenaline secreting tumor Systolic hypertension
adrenergic predominance Diastolic hypertension
Reflex bradycardia
.
There exists a down regulation of adrenergic receptors or
alteration in d receptor-effector coupling d/t long term exposure to
excess catecholamines leads to desensitisation of the vascular
system .It may causes discrepancy between amount of
catecholamine and the degree of hypertension.
Pt may present with ventricular arrhythmias,myocardial
infarction,heart failure.
Tumors producing dopamine. Nausea and vomiting
Cardiovascular system
Cardiovascular symptoms include palpitations secondary to a
tachyarrhythmia.
Cardiomyopathy is a complication of pheochromocytoma
Causes of cardiomyopathy
1. catecholamine induced permeability changes in the
sarcolemmal membrane leading to excess calcium influx
2. Toxicity from oxidized products of catecholamines
3. Myocardial damage from free radicals.
Both dilated ,hypertrophic cardiomyopathies have been
demonstrated.
ECG findings include
elevation or depression of ST segment
flattening or inversion of T waves
prolongation of QT interval
high or peaked P waves
LAD and arrhythmias.
Contd
Untreated cases can present with pulmonary oedema
secondary to a chronic increase in
vascular systemic resistance.
High catecholamine levels can cause coronary
aso o stri tio y their effe t o re eptors leadi g
to myocardial ischaemia.
Prolonged exposure of the circulation to
noradrenaline leads to constriction of arteriolar and
venous circulation with a marked decrease in
circulatory blood volume.
This explains the raised haematocrit and apparent
polycythemia. (Treatment often reveals an underlying
anaemia.)
 There exists a discrepancy between the degree of
hypertension and blood catecholamine
concentrations in
patients with phaeochromocytoma.
Despite a 10 fold increase in circulating
catecholamines, the degree of hypertension is not
substantially different from patients with essential
hypertension.
This is explained by the fact that
I. long term exposure to catecholamines leads to
desensitisation of the vascular system,
II. A down regulation of adrenergic receptors or
III. changes in the receptor effector coupling..
Central nervous system manifestations
anxiety,
psychosis, embolic
nervousness episode
tremors.
cerebrovascular accidents
cerebral
hemorrhage
Uncontrolled hypertension

hypertensive encephalopathy - altered mental status,

focal neurologic signs and symptoms
Metabolic disturbances
seizures
Glucose control is impaired because of the excessive
glycogenolysis induced by the catecholamine's, combined with an
impaired release of insulin.
Excessive adrenaline secretion can cause a state of hyper
metabolism associated with weight loss
Rare presentations
Bladder phaeochromocytomas can present with crisis
symptoms precipitated by the voiding of urine.
Phaeochromocytoma can present during pregnancy
mimicking preeclampsia.
Phaeochromocytoma is an extremely rare tumour in
children, but may be suspected in episodic
hypertension especially in association with a family
history of medullary carcinoma of the thyroid gland or
phaeochromocytoma or both.
DIAGNOSIS: CLINICAL, BIOCHEMICAL,
RADIOLOGICAL LOCALISATION
A. Urine 24 hr assay of adrenal hormones
1. Free catecholamines : best confirmatory
test.>250g/day suggests pheochromocytoma.
2. Urine metanephrine : best urinary screening
test >1.3mg/day suggests
pheochromocytoma.
3. Urinary vanillylmandellic acid (VMA):
nonspecific less expensive. >14mg/day
suggesta pheochromocytoma.
4. High performance liquid chromatography can
accurately measure the free noradrenaline,
adrenaline and dopamine.
B.Plasma -free metanephrines : most sensitive test
. pg/ml confirms.
plasma- free normetanephrine : pg/ml
confirms.
C. Clonidine suppression test: clonidine lowers
plasma catecholamines in patients without
phaeochromocytoma whilst having no effect on
patients with the tumour.
D. Provocative testings with histamine and
tyramine are not used any more due to concerns
over precipitating hypertensive crises.
E.Glucagon stimulation test now considered to b
safest and most specific provocative test.
Localisation
MRI and CT both provide accurate and consistent identification
of the majority of phaeochromocytomas.
MIBG scan. Meta-iodobenzyl guanidine is a radiopharmaceutical
agent which is an analogue of guanethedine,similar in structure to
noradrenaline and hence taken up by adrenergic neurons and
concentrated incatecholamine secreting tumours.
MIGB is detected by scintigraphy. and such scans can help to
localize recurrent tumours, metastases and tumours in unusual
sites.
Other useful tests include positron emission scans and selective
venous catheterisation ,catecholamine sampling,arteriography
also usefull.
The topographic location can b correctly found using metabolic
marker of catecholamine synthesis such as 1231-MIBG
scintigraphy and 18f-fluorodopamine PET scan.
Preoperative investigations
Complete blood count
Haematocrit
Serum electrolytes,sr urea creat
Fbs ,ppbs
Thyroid function test
ECG
Chest x-ray
2D Echo: m mode
Ophthalmological examination.
PREOPERATIVE MANAGEMENT
Early multidisciplinary involvement is recommended in
order to optimise the outcome.
The occasional management of phaeochromocytoma is
now deemed to be inappropriate and patients should
be referred to an experienced team.
Perioperative optimisation includes the use of
adrenergic receptor blocking drugs. The value of
preoperati e lo kade has ot ee su je t to a y
randomised studies, but the mortality of patients
undergoing surgery has dropped from 50% to less than
%, si e re eptor lo kade as i trodu ed.
Contd.
Induction of anaesthesia, intubation, and during tumour
handling may lead to an uncontrollable adrenergic crisis.
Proper preoperative evaluation and management
dramatically reduces the morbidity and mortality
associated with pheochromocytoma.
Adrenergic receptor blocking drugs are useed for
Perioperative optimisation of the patient.
It is conventionally done for a period of 10-14 days with -
adrenergic blockade and then, -adrenergic blocker is
added to counteract any associated tachy-arrhythmias .
If ST-T a e ha ges prese t lo g ter - blockade i.e. 1-
6 month recommended.
Use of the re eptor lo kade de reases the ortality
from 50% to less than 6% of patients undergoing tumour
resection.2
Preoperative adrenergic blockade achieves the following
objectives:
Lo ers lood pressure,
I reases i tra as ular olu e,
Redu es the ha e of hyperte si e rises duri g i du tio a d
tumour manipulation,
Allo s resensitisation of adrenergic receptors
Redu es yo ardial dysfu tio i the perioperative period.
Criteria for optimal control include:
Blood pressure readi gs o siste tly less tha /
Prese e of orthostati hypote sio ot less tha /
ECG should e free of ST-T changes
No ore tha o e pre ature e tri ular o tra tio e ery
minutes
Nasal o gestio
 Oral phenoxybenzamine

1) 10-20mg TID (maximum upto 80-250mg ) usually given to achieve

alpha blockade which is a non-selective, non-competitive.
2) It takes 2 to 3 weeks to cause spontaneous volume expansion which is
gradual. Half-life of phenoxybenzamine is more than 24 hours.
3) Both supine and standing blood pressure monitoring should be done
during the therapy.
4) Hypotension,somnolence,headache,stuffy nose are the side effects
associated with it.
 some prefer selective competitive -1 antagonists as they donot produce
reflex tachycardia due to absence of -2 action, short acting and can be
adjusted rapidly before surgery to cause reduction of the duration of
postoperative hypotension.
Prazosin is preferred as it is a selective -1 blocker, shorter half life ( 2-3
hrs) and easier to titrate to the desired end point.
Starting dose is 1mg, 3 to 4 times per day and increased up to 12mg per
day gradually.
If the last dose was given on the night before surgery, it is relatively
ineffective in the intraoperative control of blood pressure.
This drug may cause profound first dose hypotension
Doxazosin and Terazosin are selective -1 blocker similar to prazosin.
It is important to start cautiously with small doses and gradually increase
until orthostatic hypotension develops which indicate adequate -
blockade.
 Tachycardia and arrhythmias see duri g - lo kade due to u opposed -
receptor activity4,13.This a e o trolled y areful i trodu tio of -
lo kers. - lo kade should t e started u til o plete -adrenergic
blockade is achieved as it may lead to severe hypertension due to
u opposed -stimulation .
In patients having myocardial dysfunction, heart failure can be precipitated
if -blockade is used as it causes the heart to cope with the elevated after
load with less contractility power .
Bisoprolol a d ate olol are sele ti e -1 antagonists given to decrease
adverse effects in the bronchi or peripheral vasculature.
In case of obstructive airway disease or peripheral vascular disease non-
sele ti e -1 antagonists like metoprolol and propranolol should be
avoided.
 Tyrosine hydroxylase enzyme inhibitor - methylparatyrosine
(Metyrosine) is used only in malignant and inoperable cases
For preoperative control of blood pressure Calcium channel blockers
and ACE inhibitors may have been used3
A 7-10 days course of Nicardipine before surgery induces arterial
vasodilatation.
Magnesium sulphate can also be used as it suppress the release of
catecholamines and adrenergic receptor response alternation.

Criteria for optimal control include : as per ROIZENs criteria

18(Roizen et al in 1982 )
Blood pressure should e u der / of hg hr prior to
surgery
Orthostati hypote sio ith sta di g BP > / of hg
ECG should e free of ST-T changes for 1 weak prior to surgery
Pre ature e tri ular o tra tio should t e ore tha i e ery
5 minutes.
Nasal o gestio
Anaesthetic Management

Premedication:
NPO for at least 8 hrs
informed consent
Alprazolam 0.5 mg given orally
Prazocin at night before sx.
Oral metoprolol is also prescribed on the morning
of surgery.
In patients with catecholamine induced
ardio yopathy -adrenergic blockade should be
avoided as it may cause bradycardia,intractable
hypotension and asystolic arrest
 . An intravenous drip is started night before sx.
But according to Desmont & Marty intraoperative
fluid administration is as effective as preoperative
fluid infusion in reference to haemodynamic
control.
Venous thromboprophylaxis is essential with
Dalteparin 5000 IU subcutaneous or Enoxaparin
0.4mg subcutaneous evening before surgery and
12 hrs postoperatively is given.
Steroid supplementation given if bilateral
adrenalectomy planned.
Periods of instability include:

Induction and intubation

Surgical incision
Abdominal exploration and tumour manipulation
Pneumoperitoneum if done laparoscopically
Ligation of venous drainage
Monitoring
Two large bore peripheral venous access
Pulse oximeter
NIBP
ECG monitoring
EtCO2
Temperature probe
Arterial line (inserted prior to induction of anaesthesia) for
invasive blood pressure
CVP monitoring
Pulmonary artery catheter and TOE in patient with left
ventricular dysfunction
In cardiomyopathy patients - Cardiac output monitoring
should be done.
ABG
Drugs to be avoided

Morphine,pethidine,curare,atracurium avoided
due to histamine release.
Succinylcholine avoided due to catecholamine
release by virtue of muscle fasciculation
Metoclopramide and droperidol as they cause
catecholamine release
Atropine as parasympathetic block causes
unimposed sympathetic overactivity
Pancuronium avoided as it has sympathomimetic
effect
Halothane as it sensitises myocardium to
catecholamines
Anaesthetic techniques
General epidural anaesthesia have been
successfully used.
Epidural catheter inserted at T10-11 to T12 L1
level after proper positioning of the
patientl4,11.
Epidural analgesia should be used for both
intraoperative and postoperative period as it
can prevent sensory and sympathetic
discharge in the surgical field, but during
surgical manipulation of the tumour it cant
able to block the release of catecholamines.
.
The following drugs should be prepared and
kept ready for immediate uses are-

inj Phentolamine 10 mg/ml

inj Nitroglycerine 5 mg/ml
inj nitroprusside 50mg /ml;
inj dopamine 40 mg/ml
inj norepinephrine 2mg/ml
inj lidocaine
inj amiodarone
inj esmolol
 Factors like pain, anxiety, stress, hypoxia
and hypercarbia which causes more
catecholamines release should be avoided.
Consider premedication with midazolam 1-2
mg and radial artery cannulation is performed
under local anaesthesia.
Arterial cannulation can be done after
induction in apprehensive patients.
A large bore peripheral IV catheter is to be
inserted routinely in preinduction period.
 Histamine receptor 2 antagonist are also indicated
in appropriate patients.
Metocloppamide may induces hypertensive crisis
so best avoided.
Adequate depth of anaesthesia should be achieved
to prevent exaggerated pressor response due to
release of catecholamines from stored nerve
terminals during endotracheal intubation.
Drugs stimulating the sympathetic nervous system
like ketamine,ephedrine should be avoided.
Drugs like benzodiazepines, fentanyl, alfentanil,
remifentanil, propofol, etomidate, vecuronium,
rocuronium considered to be safe3.
 Attenuation of pressure response to laryngoscopy can be done with
small dose of fentanyl,IV lidocaine, esmolol 0.5 mg/kg bolus and infusion
as required.
A central venous line inserted for hemodynamic monitoring and
administration of fluid,it is to be maintained around 8-9 mm hg.
Etco2 to be kept within normal range by adjusting respiratory rate rather
than tidal volume.
Anesthesia is maintained with O2 ,N2O and isoflurane or sevoflurane with
intermittent doses of fentanyl citrate.
Fluids should be considered as the first line of management in these
patients as large amounts of fluid is generally required after tumour
resection.
Management of hypotension by fluids like ringer lactate and normal saline
replacement is believed to lower postoperative mortality. But some studies
suggest that the predominant mechanism of severe hypotension following
tumour resection is likely to be a decrease in arterial tone and that severe
hypotension may occur in normovolemic patients .
.
 After tumour removal there is more chance of hypoglycaemia so closely
monitoring of blood glucose should be done3,21.
So dextrose containing fluid to be started after tumour removal
depending on blood sugar3.

Forced air warming devices used to maintain normothermia. In case of

laparoscopic removal of tumour surgeons are asked for slow insufflation
of CO2 and to keep Intra abdominal pressure low at 8-10 mm hg.
Epidural infusion of 0.125% bupivacaine with fentany l - 2 g/ml at the
rate of 0.1 0.2 ml/kg/hour, is administered after an initial bolus of 8-10
ml to achieve adequate intraoperative and postoperative analgesia .
So further doses of fentanyl or any other opioid are usually not required.
Control of intraoperative
haemodyanamic response :-
Most of the patients shows haemodynamic
instability during tumour manipulation despite
preoperative blockade.
Tachycardia is predominant in adrenaline secreting
and hypertensive response is mostly seen in
noradrenaline secreting tumours.
Vasodilators must be kept ready in hand to control
these surges6,7,15.
Tumour manipulation may cause increase in blood
catecholamines concentration as high as 200 to
1000 ng/ml2. Close monitoring should be done to
avoid myocardial dysfunction as a result of this
huge surge.
Pharmacological options for intraop
haemodynamic control.
Phentolamine: A competitive blocker and
direct vasodilator, given as boluses of 1-5 mg
for controlling surges in blood pressure.
Tachyphylaxis and tachycardia are common.
Phentolamine can be used on its own or in
combination with labetalol.
Sodium nitroprusside: A direct potent,
vasodilator with an immediate onset and
short duration of action make it a favourite of
many clinicians. The toxicity of SNP is not
seen at normal clinical doses.
 Glyceryl TriNitrate: A venodilator. Larger
doses are generally required and the reflex
tachycardia may present a problem
Magnesium sulphate: Direct vasodilator,
inhibits catecholamines from the adrenal
medulla and nerve terminals, reduces
sensitivity of receptors and is a useful
antiarrythmic.
A loading dose of 40-60mg/kg followed by 1-
2g/hr has been described
Cont

Volatile anaesthetics: Increasing the depth of

anaesthesia using volatile agents works at a cost
of a persisting hypotension after tumour removal.
Calcium channel blockers: Calcium ion transfer
is needed for the release of catecholamines from
the adrenal medulla. Nicardipine is the drug of
choice from this group..
blockers: the selective, short acting blocker,
esmolol is useful for isolated tachyarrythmias and
tachycardia without hypertension. The rapid onset
and offset of esmolol makes it the drug of choice
in such situations.
 Labetalol: predominantly a blocker
with some blocking effect, it is used to
control blood pressure as well as
tachycardias in adrenaline secreting
tumours. When administered with
phentolamine, the effects are
synergistic.
Antiarrhythmics: Lidocaine is useful for
ventricular arrhythmias with amiodarone
is an alternative..
 Catecholamine withdrawal
following venous ligation :-

Following ligation of the venous drainage of the tumour, there is

increase chance of refractory hypotension. This is because of
1. sudden fall in the catecholamine concentration,
2. suppression of normal contralateral adrenal gland due to excessive
catecholamines,
3. residual blockade from phenoxybenzamine,
4. adreno-receptors down regulation,
5. catecholamine induced myocardial dysfunction and
6. hypovolemia from blood and fluid loss.
 A preventative measure involves volume loading before tumour ligation
and fluid boluses should be tried before initiating vasoactive
medications23.
This can be prevented by volume loading to a pulmonary capillary
wedge pressure of 16 to 18 mm hg before tumour ligation .
Colloids,plasma expanders, blood products are arranged as indicated.
If ineffective, noradrenaline, adrenaline and phenylephrine with
milrinone in the setting of right ventricular dysfunction will be the next
treatment modality.
In refractory cases drug of choice is vasopressin at a rate of 0.04U/m and
can be increased as per requirement.
Glucocorticoids is indicated in bilateral adrenalectomy cases and if
hypoadrenalism is suspected3.
Extubation is done after ensuring haemodynamic stability of the patient.
ABG is done perioperatively and at the end of surgery to study the
metabolic status of patient..
IMAGE -1(Surgical removal of tumor)

IMAGE -2 Interior of tumor (cut section)

Post op management
These patients should be shifted to a ICU/HDU
for better post operative management.
The main post operative complications are
refractory hypotension and hypoglycaemia as a
result of excess release of insulin and
insufficient glycogenolysis8.
Refractory hypotension should be managed by
large amount of fluid and vasopressors therapy.
Most of the patients are remain normotensive
instead of elevated plasma catecholamine
concentration as a result of their slow release
from the nerve terminals.
 50% of pts are hypertensive for several days after
surgery.
25% to 30% pt remain hypertensive indefinitely.in
these pt hypertension
1. Sustained rather than paroxysmal
2. Lower than before sx
3. Accompanied by the classic features of
hypercatecholaminemia.

The d/d includes

Missed pheochromocytoma
Surgical complications with subsequent renal
ischemia
Underlying essential hypertension.
 Hypotension is the frequent cause of
death in the period immediately after sx.
large vol of fluid are necessary since the
peripheral vasculature is poorly
responsive to reduced levels of
catecholamines.
steroid supplementation may b necessary
if hypoadrenalism present.
Cont..
The recurrence rate of tumor is around 14% in primary adrenal
disease and 30% in extrea adrenal disease. so long term follow up
needed for all patients24 .

Electrolyte and endocrine abnormalities must be

ruled out in drowsy and unresponsive patients.
Appropriate blood glucose and electrolyte
monitoring are indicated.Careful attention to be
given in fluid management.
Lifelong follow up may require due to late relapse
of tumour in some cases. Genetic testing should be
carried out in first-degree relatives of confirmed
cases.
This is also done in suspected cases of
hyperparathyroidism, medullary carcinoma of
thyroid, caf au lait spots and cerebellar tumor3.
Post op analgesia
Laparoscopic approach has the advantage of minimal
pain.
Local anaesthetics with opioid is given epidurally for
better pain relief post operatively.
This may be supplemented by NSAIDS, Paracetamol,
opioid like morphine and local anaesthetic infiltration.
pregnancy

The mortality from phaeochromocytoma in pregnancy is high.

Undiagnosed cases can mimic preeclampsia.
Labour can also precipitate crises and hence an elective Caesarean
Section should be planned
if the condition isdiagnosed late in pregnancy. If diagnosed early,
resection of the tumour can be considered before the second trimester
with the risk of miscarriage.
Phenoxybenzamine can be safely used during pregnancy..
Conclusion

The perioperative mortality associated with

phaeochromocytoma is around 2%.
A thorough grasp of the pathophysiology and
pharmacology will enable one to develop an
anaesthetic plan tailored to suit each patient.
Good preoperative preparation and the judicial use of
a combination of vasodilatory and vasoactive
medications help in reducing the mortality and
morbidity associated with surgery.
Good communication between the surgeon,
endocrinologist and anaesthesiologist is crucial for the
safe management of these patients.
Patients with this condition are best managed by a
team experienced in dealing with such cases
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