Notes for anesthesia consideration in pheochromocytoma patient

1. PHEOCHROMOCYTOMA AND ANESTHESIA
Dr. RAVIKIRAN H M
Kidwai cancer institute
The word pheochromocytoma in Greek means ―dusky coloured tumour‖ referring to the colour it
acquires when stained with chromium salts.
The morbidity and mortality in an unexpected emergency situation is quoted to be 50% but less
than 2% in planned surgery.
According to WHO: adrenal→pheochromocytoma. Exradrenal → paraganglioma
Though usually found in the adrenal medulla these tumours 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.
Highly active tumours secreting adrenaline, noradrenaline and rarely dopamine. Most
pheochromocytomas secrete norepinephrine, either alone or, more commonly, in combination
with a smaller amount of epinephrine in a ratio of 85:15—the inverse of the secretion ratio in the
normal adrenal gland. Familial phaeochromocytomas are an exception because they secrete large
amounts of adrenaline.
Phaeochromocytomas are not under neurogenic control but the trigger for catecholamine release
is not clear. hypertension can be triggered by physiological factors such as changes in
position, increased abdominal pressure (defecation, sneezing, voiding of urine and labour).
Precipitationfactors
1. Iatrogenic factors precipitating an attack include induction of anaesthesia,
2. certain opioids (eg. pethidine),
3. dopamine antagonists,
4. cold medications-sympathomimetics-salbut, terbut,
5. PCT

2. 6. radiographic contrast media and
7. drugs which inhibit catecholamine reuptake, such as tricyclic antidepressants
and cocaine catecholamine reuptake inhibitor also lignocaine).
8. MOI: antidepressants, tyrosine rich food-nuts, bananas, cheese.
9. Withdrwawal from sedative drugs, clonidine, alcohol...
PREOPERATIVE ASSESSMENT
Symptoms
Triad of headache, palpitations, and sweating
MC manifestation HTN
MC feature/symptom: headache
Classic episodes of headache (hypertension), sweating, anxiety, pallor, and palpitation
(arrythmias), provoked by posture, exercise, anxiety, pain, and drugs, occur in only 50% of
pheos. Most of these do not have elevated resting BP's; the others are found during investigation
of hypertension. Postural hypotension is common (70%) in Pheo's and suggests the diagnosis in
an untreated hypertensive. It should also be considered in pre-eclampsia, thyotoxicosis, and
malignant hypertension.
Weight loss
Dehydration
Hypercalcemia
Constipation
Visual disturbance I/V/O of papilloedema becoz of HTN
End organ damage to be assessed
Cardiovascular system: symptoms include palpitations, secondary to a tachyarrhythmia.
With noradrenaline excess secretion α adrenergic effects predominate and patients have
systolic and diastolic hypertension and a reflex bradycardia. With adrenaline secreting
tumours β effects predominate and patients have systolic hypertension and diastolic
hypotension with a tachycardia. Acute presentation can be with ventricular dysarrythmias,

3. heart failure or MI. Untreated cases can present with pulmonary oedema or
cardiomyopathy secondary to a chronic increase in vascular systemic resistance. High
catecholamine levels can cause coronary vasoconstriction by their effect on α receptors
leading 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 hematocrit 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 long term exposure to catecholamines leads to
desensitisation of the vascular system, a down regulation of adrenergic receptors or
changes in the receptor effectors coupling. HOCM.
Central nervous system manifestations include anxiety, psychosis, nervousness and
tremors. Patients can present with cerebrovascular accidents either as a cerebral
haemorrhage from uncontrolled hypertension or an embolic episode from a mural
thrombus associated with a dilated cardiomyopathy. Uncontrolled hypertension can lead to
hypertensive encephalopathy, which is characterized by an altered mental status, focal
neurologic signs and symptoms, or seizures.
Associated diseases
Medullary thyroid cancer, parathyroid adenoma, other neuromas. Von Recklinghausens in 5% of
Phaeo's, but Pheo's seen in only 1% of Von Recklinghausens. 5% inherited.
Vascular disease, HTN and it's complications, cardiac issue
Von Hippel Lindau, Mmultiple Endocrine Neoplasia type 2A and
2B , neurofibromatosis type 1, succinate dehydrogenase enzyme mutuation
Rule of 10s’
 10% are ‗extra-adrenal‘
 10% are malignant,

4.  10% are bilateral,
 10% are found in normotensive patients,
 10% are familial.
However, this statement probably no longer holds true as there appears to be a significantly
higher proportion of tumours that are malignant (29%), extra-adrenal (24%), and/or familial
(32%).
PATHOPHYSIOLOGY
 Catecholamines mediate effects through adrenergic receptors
 α adrenergic receptors (α1 &α2)
 β adrenergic receptors (β1,β2,β3).
 Activity of catecholamines at different adrenergic receptors.
 Adrenaline: α1, α2, β1, β2 & weak β3 action. Predominantly beta.
 Noradrenalin: α1, α2, β1 & β3 but NO β2 action. Predominantly alpha.
 Hemodynamic effects depends on predominant catecholamine secreted by the tumour.
 With NE, α adrenergic effects predominate → systolic & diastolic hypertension with reflex
bradycardia.
 With Epinephrine, β adrenergic effects predominate→ systolic hypertension, diastolic
hypotension & tachycardia.
Phenylalanine
↓
Tyrosine
↓ Tyrosine hydrolase
DOPA
↓
Dopamine
↓
Norepinephrin
↓PNMT
Epinephrine

5. COMT, MAO degrade epi to metanephrine, norephi to normetaneph, finally VMA
Tyrosine hydrolase is rate limiting enzyme
PNMT:paraethanalamine N-methyl transferase: - present only in adrenal cortex which enters
adrenal medulla to convert NE to E. So extra adrenal tumor lacks PNMT →no epinephrine
secretion from extra adrenal pheo.
If big size tumor PNMT cannot diffuse into adrenal medulla.
In MEN pheo is small so Epinep.
Adrenal average size 5cm
↓
←----------→
↓ ↓
<3cm >3cm
↓ ↓
Epinephrine norephin
Benign versus malignant
Capsular invasion
Nuclear cytoplasmic ratio
Number of mitotic spindles
All this features can be seen in both.
So to say malignant metastasis to be present
↑ DOPA[precursor] : malignant
During treatment
Do not give β blocker first
Becoz if β blocked →↓contraction→↓Cardiac output
And α active→↑vasoconstriction→↑HTN[paradoxical HTN]
Thus ↓perfusion→MODS
So first give α-block
But if α-blocked alone→hypotension→reflex tachycardia→so danger in MI patient. So
here both started together.
Phenoxybenzamine

6. ι
2weeks↓ prazosin/phentolamine(short acting use when spikes)
Proper α-blockade
↓
β-blocker
↓
Surgery
DIAGNOSIS
IOC: 24hr urine fractionated metanephrine + catecholamine
most sensitive test: plasma metanephrines
1. Urine metanephrine, VMA and catecholamines
2. Plasma catecholamines, free metanephrine, chromagranin A
3. Provocation test: Glucagon or histamine or tyramine provocation of catechol release then
blood levels taken - little used these days. Glucagon is safest and most specific provocative
test.
4. Suppression test: Clonidine 300μg has no effect on plasma Nad in phaeo but suppresses
normal.
5. Tumour localisation
1. IVP: Positive in only 40%
2. Ultrasound: Positive in 85%
3. Angiography: Selective angio has risks of GA but localises 90% - DSA better
4. Selective renal venography
5. CT Scan: As good as the selective angios, but may miss the smaller phaeos
6. Scintiscan: Meta iodo benzyl guanidine 90% accuracy. less sensitive for
dopamine-secreting tumours.
MRI sensitivity 98%
MIBG sensitivity 81%
Best/most accurate for localizing : DOPA PET, PET CT > MRI
IOC for localizing: MRI
IOC for recurrence: PET

7. Imaging
↓
Abdominal MRI
↓
←---------------→
↓ ↓
Negative positive
↓ ↓
MIBG MIBG
MIBG in negative : to search in thorax and Head and Neck
MIBG in positive: to search mets.
PREOPERATIVE DRUG MANAGEMENT
Alpha blockers
Phenoxybenzamine : non-selective, non-competitive, long-acting {24-48hr} α-blocker.
Its non-competitive antagonism may reduce the effects of catecholamine surges, but may
be implicated in postoperative refractory (catecholamine-resistant) hypotension. It should
therefore be stopped 24–48 h before surgery due to its long half-life. Its non-specific
nature also allows pre-synaptic α2-blockade which interferes with the norepinephrine
negative feedback loop that regulates norepinephrine release. The resulting uninhibited
release of norepinephrine from cardiac sympathetic neurones causes a reflex tachycardia
via β1 stimulation. Central α2-blockade also results in somnolence, headache, and nasal
congestion. Allows plasma volume re-expansion, but some hypertension on handling may
still occur. Dose is 20 mg/day orally, increasing by 10-20mg/day, until desired effect.
Overdose causes toxic megacolon and postural hypotension. This confers a degree of
protection against blood pressure surges during tumour manipulation when
catecholamine levels can rise by a factor of several hundred. (A competitive reversible
blockade would be overwhelmed by this catecholamine surge!)
Prazosin: 6-10mg of this α-1 selective blocker used with propranolol in high doses (120-
480 mg/day). at least 7–14 days before surgery. not block the α2 receptors and therefore
do not induce a tachycardia as a side effect. Doxazosin same as Prazosin.
Doxazosin had less preoperative postural hypotension,
required less fluid administration after the effluent vein was clamped (phase II), a
nd rec vered to normal BP more rapidly at the end of surgery.

8. Urapidil is a selective alpha
adrenergic blocker with a central sympatholytic effect mediated by
stimulation of serotonin 5HT receptors, and is available in some countries.
β-Blockers:
Added to manage persistent tachycardia, arrythmias, angina. Most tumours, however,
are predominantly adrenaline secreting and β blockers are added to counteract the
side effects of non selective α blockade. In a pure noradrenaline secreting tumour
con trolled by a selective α1 blocker such as doxazosin, β blockers are not
necessary.The removal of β1 stimulation following β blockade means the heart has
to cope with an increased after load with less ability to contract and this can
precipitate heart failure in patients with myocardial dysfunction. This is another
reason why β blockade should only be started after appropriate arteriolar dilatation
has been achieved with α blockers. May worsen BP and LV performance unless
adequately α-blocked.
Labetolol: Has been decribed but is probably inadequate alone. Good for resting rather
than paroxysmal hypertension; frequently need Nad postop.
Calcium channel blockers:
inhibit norepinephrine-induced calcium influx and have been utilized for haemodynamic
control before surgery, mainly as an additional drug class to further improve control in
those already α-blocked. They are not recommended for monotherapy unless patients
have very mild hypertension or develop severe orthostatic hypotension with α-blockers.
Sustained-release nicardipine 30 mg twice daily is a commonly used preparation. An α1-
blocker plus a calcium channel blocker is an effective combination in treatment-resistant
cases.
Magnesium:
MgSO4 > 2g IV may be useful for managing acute episodes. inhibits adrenal
catecholamine release and reduces α-adrenergic receptor sensitivity to catecholamines. It
also dilates predominantly arteriolar vessels, reducing left ventricular afterload while

9. maintaining preload and exerts anti-arrhythmic effects via antagonism of L-type calcium
channels. Useful for intubation also.
High sodium diet and fluid intake are also recommended to help restore blood volume
Alpha methyparatyrosin/ Metyrosine
Inhibits the rate-limiting enzyme tyrosine hydroxylase and decreases catecholamine
production by 50% to 80%.
DOSAGE- 250 mg BD to 3 to 4 g/day.
Useful for malignant and inoperable tumors.
Side effects : extrapyramidal reactions and crystalluria.
ANAESTHETIC MANAGEMENT
Aim is to avoid excessive sympathetic stimulation, hypoxia, and hypercarbia, and to be able to
cope with the acute changes (ie, hypertension, arrythmias, etc) which may arise. Several weeks
of bedrest and preoperative drug treatment in hospital are usually required.
The objectives of preoperative care include:
 arterial pressure control,
 reversal of chronic circulating volume depletion,
 heart rate and arrhythmia control,
 assessment and optimization of myocardial function,
 Reversal of glucose and electrolyte disturbances.
Goals of anesthesia:
1. avoid drug-induced catecholamine release,
2. avoid catecholamine release induced by anaesthetic or surgical manoeuvres,
3. minimize haemodynamic responses to tumour handling,
4. treat episodes of hypotension, particularly after tumour devascularization

10. Critical events:
a. Intubation
b. Surgical incision
c. Abdominal exploration, particularly during tumor manipulation
d. Secondary hypotension following ligation of tumor‘s venous drainage.
e. Pneumoperitoneum during laparoscopic approach
Phases
Phase I
includes the portion of surgery during which the tumor is dissected and the
vascularsupply isolated, before clamping of the effluent vein. This phase is
often characterized by periods of severeepisodic hypertension and arrhythmias
as adrenal manipulation releases catecholamines. Phase I also includesendotrac
heal intubation and insufflationof the abdomenwith CO2for laparoscopy, both of
which can also result in marked hypertension & arrhythmias
Phase II
is the portion of surgery after the effluent vein is clamped. Precipitous hyp
otension canoccur because of the sudden drop in endogenous catecholamine
levels, the chronic downregulation of alphaadrenergic receptors, the presence
of alphablocking medication, and intravascular volume depletion. Vasopressor
support is often necessary.
a) Assessment
Roizens criteria for adequate preoperative control are:
1. Blood pressure < 165/90for 48hrs before surgery
2. Postural BP fall to not below 80/45
3. ECG free of ST changes for two weeks

11. 4. < 1 VPC over 5 minutes
5. Nasal congestion
Cardia: Look for significant LV compromise or dysfunction, and consider S-G catheterisation if
present. Book an ICU bed postop. Check RBS, K+. Crossmatch blood. ST or T wave changes
may reflect inverted Takotsubo cardiomyopathy rather than ischaemia.
Catecholamine-induced cardiomyopathy
Etiology
1. Permeability changes of the sarcolemmal membranes → to excess calcium influx
2. Toxicity from oxidized products of catecholamines
3. Damage by free radicals
4. High catecholamines lead to coronary vasoconstrictioncoronary ischemia
Reversal of glucose and electrolyte disturbances::
Hyperglycaemia can occur due to increased glycogenolysis (α1 receptors), impaired insulin
release (α2 receptors), lipolysis (β1 receptors), and increased glucagon release coupled with
peripheral insulin resistance (β2 receptors) and is treated with standard therapies.
Electrolyte measurements will identify catecholamine-induced renal impairment.
Hypercalcaemia occurs when a neuroendocrine tumour is associated with a parathyroid adenoma
(e.g. as occurs in MEN 2A).
Risk factors for intraoperative haemodynamic instability include high pre-induction plasma
norepinephrine levels, large tumour size, profound postural drop after commencement of α-
blockade, and a pre-induction mean arterial pressure (MAP) above 100 mm Hg
b) Premedication

12. Relief of anxiety is important, deep premeds usually advocated. Almost all drugs have been used
without problems, however Droperidol has been associated with some idiosyncratic responses,
and Atropine is often not recommended. α-blockers and other short acting drugs are usually
given on the same day, but not phenoxybenzamine (long acting , non specific non competition).
Drugs to consider avoiding on this basis include desflurane, ketamine, morphine, pethidine,
atracurium, pancuronium, ephedrine, droperidol, metoclopramide, and cocaine.
c) Choice of anaesthesia
Intubation and muscle relaxation is required for access, and anaesthesia with volatile agents,
narcotic, and neurolept techniques have all been used. Gallamine, pancuronium, and
suxamethonium have disadvantages, and Halothane may worsen arrythmias. Agents that release
Histamine best avoided (morphine). Relaxant, nitrous, narcotic, and Enflurane or Isoflurane
supplementation are recommended.
Inhalation agents: Sevoflurane is preferred because it is cardio-stability and lack of
arrhythmogenic potential. Isoflurane lowers peripheral vascular resistance and blood pressure
and can be used. Halothane (arrhythmia potential) and desflurane (sympathetic stimulation) are
not preferred in pheochromocytoma
Avoid hypoxia, hypercarbia, pain, fear, hypothermia
Tumour handling induces by far the most significant haemodynamic responses, catecholamine
release is also provoked by tracheal intubation and the raised intra-abdominal pressure associated
with capnoperitoneum or coughing. Capnoperitoneal pressures of up to 28 mm Hg have been
advocated to both improve surgical access and reduce venous bleeding without any apparent
increase in cardiovascular instability, although the supporting evidence is sparse. The arterial
pressure response to pain is also likely to be exaggerated. Hypercarbia releases catecholamines.
Auscultation for pulmonary edema at end
d) Monitoring equipment

13. CVP (for monitoring and vasoactive infusions) and Arterial line (essential).Invasive arterial
monitoring should be obtained before induction of anaesthesia. Central venous access is
necessary, if only for drug infusions, and can usually be inserted after induction.
Swan-Ganz / TEE if LV dysfunction or other indications present.
Oesophageal Doppler has been used in the paediatric population
Usual equipment for a long case with bloodloss, ie 5lead ECG, IV, warming blanket, blood
warmer, humidifier, temperature probe, HiLo cuffed ETT with pressure monitor, NGT, Urinary
catheter, etc.
e) Induction
Major danger period, requiring profound reflex supression prior to intubation. Insert arterial line
prior to induction and ensure an adequate CVP. Avoid Ketamine; use a large dose of thiopentone,
+/- Fentanyl, Diazepam, IV or topical lignocaine, MgSO4 etc.
f) Hypertensive crises
Provoked by noxious stimuli or tumour palpation, usually best managed by removing the
stimulus. SNP bolus, Phentolamine 1-5 mg IV bolus or by infusion, MgSO4 2g IV, Lignocaine
1-2 mg/kg, Esmolol, Labetalol, etc are all useful.
SNP causes predominantly arteriolar dilatation while GTN is principally a venodilator. Although
both have rapid onset and offset of action, the decrease in arterial pressure seen with SNP is
more rapid which probably explains its preferential use as the first-line vasodilator for
phaeochromocytomasurgery.infusion at 0.5to 5mcg/kg/minute. Not exceed 3mcg/kg/min. Reflex
tachycardia is often treated with infusion of a short acting beta blocker(esmolol ).
Phentolamine is a reversible non-selective α-receptor antagonist, which primarily results in
vasodilatation and can lead to reflex tachycardia. It is usually administered as a bolus of 1–2 mg,
has a short duration of action, but may demonstrate tachyphylaxis. It can be used as the sole
vasodilator, but is particularly useful to control surges in arterial pressure while establishing

14. desired infusion rates of other drugs. An
initial test dose of 1 mg is administered, followed by a 5mg bolus and/or continuous inf
usion (0.5 to1 mg/minute IV).
Nicardipine, a dihydropyridine calcium channel antagonist, is a potent arterial vasodilator and
can be administered by infusion intraoperatively. It is initiated at a rate of 3–5 mg h−1
for 15 min
and adjusted by increments of 0.5 or 1 mg h−1
every 15 min. Once the target pressure is achieved,
the infusion should be gradually reduced to 2–4 mg h−1
. Hypertensive crises can be treated with
boluses of 1–2 mg. Cardiac output is maintained without the tachycardia seen with SNP and
GTN, making it the preferred choice of some authors. However, clinical experience is still
limited and its elimination half-life of 40–60 min can result in persistent hypotension.
Clevidipine is a novel alternative of the same class which achieves a shorter half-life via plasma
and tissue esterase hydrolysis and has been successfully used in phaeochromocytoma surgery.
Esmolol is a selective β1 antagonist with a rapid action and short duration. These properties
make it the ideal β-blocker for these cases. The initial loading dose is 500 μg kg−1
over 1 min,
followed by a 4 min maintenance infusion of 50 μg kg−1
min−1
, which is subsequently titrated to
clinical effect. Bolus (10 to 50 mg IV) or by infusion (25 to 250 mcg/kg/minute)
g)Treatment of hypotension —
Hypotension should be treated with aggressive administration of IV fluid,
discontinuation of vasodilator infusions, and administration of rapidly acting vasopressors.
Drugs commonly used to support BP in this setting include the following:
 Phenylephrine – drug of choice for the management of hypotension during these
procedures. It is a pure alpha agonist with a short halflife that can be given by b
olus (40 to 160 mcg IV)or infusion (wide range of dosing; 10 to 200 mcg/minute IV
), titrated to effect.
 Ephedrine – an indirect
acting alpha and beta agonist. It should be avoided before tumor
removal. When hypotension occurs after tumor resection, ephedrine can be given b
y bolus (5to 25 mg IV,repeated as needed). Ephedrine should not be administered d

15. uring paraganglioma resection or duringincomplete pheochromocytoma resection to a
void release of catecholamines and severe hypertension.
 Norepinephrine is a combined alpha and beta agonist that is given by infusion (
wide range of dosing; 2 to 20 mcg/minute IV), titrated to effect.
 Vasopressininfusion (initial dose 0.01 to 0.03 units/minute; maintenance dose 0.03 to0.0
4 units/minute) has been used in cases of refractory hypotension after tumor removal, co
mmonly aftersignificant blood loss or in patients with extremely high preoperative levels
of catecholamines, tosupplement other vasopressors
h) Medications to avoid —
A number of medications commonly used in anesthesia should be avoided or used
cautiously in patients with pheochromocytoma. When patients having anesthesia for other
procedures exhibitsevere hypertension, arrhythmias, or other unexplained adverse reactions
to these medications, occult pheochromocytoma should be suspected.
 Dopamineblocking drugs –
Metoclopramideis contraindicated for patients with pheochromocytoma.
Metoclopramide has been reported to induce hypertensive crisis and, in some case
s, adrenergicmyocarditis with cardiogenic shock in patients with pheochromocytoma .
Mechanismislikely multifactorial; metoclopramide inhibits dopaminergic suppression
of presynaptic norepinephrinerelease and has also been shown to directly stimulate
release of catecholamines frompheochromocytoma cells .
There are case reports of hypertensive crisis when large doses of droperidol
were administered topatients with pheochromocytoma without alpha blockade. Small
doses (0.625 mg IV) of droperidol, aswell as droperidol used as part of neuroleptic a
nesthesia, have been used safely in patients with preoperative alpha blockade .
 Glucagon
Glucagon is contraindicated in patients with pheochromocytoma. It has been shown
torelease catecholamines from these tumors and has been associated with hyperten
sive crisis past, glucagon stimulation was used as part of a diagnostic test for phe
ochromocytoma.

16.  Sympathomimetic drugs –
Ketamine,halothane,ephedrine,cocaine...
should be avoided for these patients because of their
sympathomimetic properties and the potential to exacerbate hypertension and arrhyt
hmias. Halothanesensitizes the myocardium to catecholamines, is associated with arr
hythmias, and should be avoided for these patients. Ephedrine is an indirect
acting alpha and beta agonist used to treat hypotension. It should
be avoided until the tumor is excised in order to prevent an exaggerated response
via release of catecholamines from the tumor.
 Histaminereleasing medications –
Drugs that release histamine when given in large doses (eg, morphine,
atrac ) should theoretically be avoided for patients with pheochromocytoma. Howev
er,when given slowly, histamine release can be minimized, and both morphine and
atracurium have been used safely in these patients.
POSTOPERATIVE PERIOD
Postoperative hypotension
Very common, due to combination of residual α and β blockade, fall in circulating catecholamine
levels, receptor downgrading, and diminished blood volume. 50% have significant hypotension
for 3 days.
hypotensive agents should be stopped and fluid balance optimized taking into account the
possibility of ongoing postoperative haemorrhage, myocardial dysfunction, or both.
Norepinephrine can initially be used to increase peripheral vascular resistance and vasopressin
should be considered if hypotension is refractory
Management requires good pain relief, adequate fluid load, IV infusions of catecholamines, ICU
observation and monitoring. Always be wary of an Addisonian crisis. Addisonian crisis have
hyperkalemia, hyponatremia, metabolic acidosis, hypoglycemia, hypotension...treat with
hydrocortisone.... seen commonly if bilateral adrenalectomy...rare if unilateral

17. POST OPERATIVE HYPERTENSION
Plasma catecholamine levels do not return to normal until 7 to 10 days after surgery.
D/D for persistent hypertension –
1. A missed pheochromocytoma
2. Surgical complications with subsequent renal ischemia,
3. Underlying essential hypertension.
4. pain,
5. renal artery ligation,
6. Urine retention,
7. fluid overload
POST OP HYPOGLYCEMIA:
due to rebound hyper-insulinism can occur when the inhibitory effect of norepinephrine on
insulin producing cells is eliminated and its presentation may be masked by concurrent β-
receptor blockade. Regular blood glucose monitoring and appropriate titration of dextrose
infusions is therefore recommended
Causes:
Excess insulin release following the resection of the tumour
Inadequate lipolysis and glycogenolysis
Nonselective β-blockers decrease sympathetic tone and mask signs of hypoglycemia.
Dextrose-containing solutions should be included in fluid therapy
Plasma glucose levels should be monitored for 24 hours.
Adrenal insufficiency –

18. Patients who undergo bilateral adrenalectomy are at risk for acute postoperative
adrenal insufficiency and therefore require glucocorticoid replacement. Regimens for replac
ement vary among institutions.
Typical regimen is as follows:
1. Hydrocortisone 100 mg IV with induction of anesthesia
2. Hydrocortisone 100 mg IV every eight hours for 24 hours
3. Hydrocortisonetaper over three days to maintenance dose (eg, hydrocortisone 2
5 mg IV or by mouth [PO] twice daily, or prednisone 10 mg PO daily
PHAEOCHROMOCYTOMA IN PREGNANCY
25-50% mortality if untreated in 1967;
tumour excision mid-pregnancy or simultaneous Caesarian Section and excision have been
advocated,
although several cases of successful epidural C.S. and vaginal delivery with later excision have
been described.
Caution with hemodynamic agents that cross placenta (esmolol, propanolol)
Same optimization with alpha blockade followed by beta blockade applies but some suggest
having hemodynamic goals even lower than Roizen criteria (e.g. upper limit 150/80mmHg but
avoid orthostatic hypotension to prevent uteroplacental malperfusion)
Pregnancy specific management:
Controversial, based on case reports:
 If gestational age <24 weeks: may undergo open or laparascopic resection of
pheochromocytoma

19.  If gestational age >24 weeks: medical management, & may wait until fetal maturity & do
combined cesarean section & tumor resection (the problem is that gravid uterus >24
weeks obstructs access to tumor resection)
 Cesarean section is preferred as abdominal squeeze during labour can precipitate a
hypertensive crisis
 General anesthesia or epidural anesthesia > spinal anesthesia probably best NOT TO
ALLOW LABOR
Increased incidence of intrauterine fetal demise, growth restriction, abruption Often
misdiagnosed as preeclampsia

20. Check list
Prep:
1. Roizen criteria
2. HTN complications
3. Family history
4. Weight
5. HB and HCT
6. RBS
7. Serum electrolyte
8. ECG and echo
Instruments:
1. Epidural
2. Central line-double/triple lumen for inotropes
3. Infusion sets 2
4. 50cc syringe 3
5. IV extension 5
6. Arterial line set
7. Defib
8. Glucometer
9. Colloid, blood
Drugs:
1. SNP, NTG
2. Esmolol
3. Diltiazem
4. Noradrenaline
5. Dopamine
6. Adrenaline
7. Vasopressin

21. 8. Mephentermine
9. Isoprenaline
10. MgSO4
Plan
1. High dose midaz
2. Preload with crystalloids
3. Epidural-no test dose
4. Arterial line
5. High dose fentanyl
6. Propofol
7. Xylocard
8. High dose Rocuronium
9. Swift intubation
10. Central line
11. Maintenance: O2+ N2O+ Iso, vec/roc
12. Before shifting: Urine output, GRBs, ABG, auscultate for pulmonary edema
References:
1. Stoelting coexisting
2. IJA
3. Millers 8th edition
4. Anesthesia considerations
5. Open anesthesia
6. BJA