ANESTHESIA MANAGEMENT OF PATIENTS WITH COEXISTING AND ENDOCRINE DISEASES

DEPARTMENT OF
ANESTHESIOLOGY
ANESTHESIA MANAGEMENT OF PATIENTS
WITH ENDOCRINE & CO-EXISTING DISEASES
By Nurhussien
(BSc) in
Anesthsiology

Course objectives
• At the end of this course students will be able to:
-Describe the normal physiology of thyroid,
parathyroid, pancreas and adrenal glands.
-Assess the sign and symptoms of thyroid, parathyroid,
pancreatic and adrenal glands malfunctioning
-Determine the surgical complications, treatment and
anaesthesia considerations
-Describe the Pathophysiology of MH, MG,Parkinsonism,
Phaeochromocytoma, and ARDS.
-Finally determine the anaesthesia consideration and
peri opertive management of the above pathologies.

ANESTHESIA FOR PATIENTS
WITH THYROID GLAND
DISORDERS

Brain storming
What are the hormones secreted from the anterior part
of the pituitary gland?

• TSH: Controlls synthesis and secretion of thyroid hormones
• FSH: Sperm cell maturation and follicular dev’t &
estrogens synthesis in ovaries
• LH: Stimulates testosterone synthesis in testis and stimulates
ovulation
• Growth hormone: Stimulates protein synthesis and overall
body growth

Cont.
• Prolactin: Stimulates milk production and secretion
in breasts
• ACTH: Stimulates synthesis and secretion of cortisol,
androgens and aldosterone.
• MSH: Stimulates melanin synthesis

The thyroid gland
• Anatomy:
 The thyroid gland is formed by two lateral lobes connected by
the thyroid isthmus at about the second tracheal ring.
 It is situated anterior to the trachea.
 Is the first endocrine gland to appear during embryonic dev’t.
 Weight 15-25 gms in adults
 It is supplied by the superior and inferior thyroid arteries.
 Venous drainage is through superior, middle and inferior thyroid
veins

cont’d……
 It is a highly vascularised endocrine gland
 Attached to the trachea by a loose connective tissues
 Covered by:
-Anteriorly by skin and paltysma muscle
-Antero laterally by
@ Sternocleidomastoid muscle
@Sternothyroid muscle
@Sternohyoid bone
-Posteriorly parathyroid glands are located on both
sides

• Thyroid gland contains two separate hormone
producing cells.
1.Follicular cells: they synthesize, store and release
thyroid hormones(T4 and T3)
• They also trap iodide from the circulation
• The iodide is then oxidized to iodine which is
catalysed by thyroid peroxidase (organification)
takes place on the apical membrane of the
follicular cells

Cont.
• They synthesize and secrete thyroglobulin a
substance containing tyrosine.
• This tyrosine is then iodinated by the oxidized iodine
to form monoiodotyrosine(MIT) and diiodotyrosine

Cont’d……..
• MIT+DIT=T3
• DIT+DIT=T4
• This iodinated thyroglobulin is the storage form of thyroid
hormones which is kept inside the follicle

Thyroxine (T4)
3,5,3´,5´-tetraiodothyronine

 Iodide transport-trap iodide moving it into the thyroid
follicle and then oxidizes it
 Organification- iodine is combined with tyrosine to form
MIT & DIT
 Coupling- two DIT combine to make thyroxin (T4) or one
MIT combines with one DIT to form triiodotyronine (T3)
 Storage- hormones migrate to the colloid space in the
centre of the thyroid follicular cells
 Secretion- release of hormones by reversing process of
storage reversal of migration through cell membranes.

cont’d……
• TSH- it is one of the hormones produced in the anterior
part of the pituitary gland
• It controls the function of follicular cells and secretion of
thyroid hormones(T3 & T4).
• it stimulates the thyroid to release T3 & T4
• It also increases thyroglobulin synthesis & iodine uptake
• It’s secretion is regulated by TRH produced from the
hypothalamus
• Excess T3 & T4 suppress the release of TSH (-ve feedback
mechanism).

Brain(hypothalamus)
TRH
Anterior pituitary
TSH
Thyroid
Thyroid hormones
Body tissues

cont’d………
 Negative feedback mechanism
 Low blood levels of hormones stimulate hypothalamus
 Hypothalamus stimulates pituitary to release TSH
 TSH stimulates the thyroid to raise the amount of hormones
in the blood

cont’d……
NB: the over all result of any type of negative
feedback in the endocrine system is :
-inhibition when the level of the hormone in the
periphery is high
-stimulation when there is low amount of
hormones in the periphery

2. Para follicular cells:
 They secrete calcitonin which has a minor role in
maintaining calcium homeostasis.
 Two main effects of calcitonin are :
1. It enhances excretion of calcium into urine
2. Inhibition of bone resorption of calcium,
which would minimize fluxes of calcium from
bone to blood.

SPECIFIC ACTIONS OF THYROID
HORMONE: METABOLIC
• Regulation of Basal Metabolic Rate (BMR).
• Increases oxygen consumption in most target
tissues.
• Permissive actions: TH increases sensitivity of target
tissues to catecholamines, thereby elevating
lipolysis, glycogenolysis, and gluconeogenesis.
• The high sensitivity of target tissues to
cathecolamines also causes tachycardia,
palpitations and high cardiac out put.

SPECIFIC ACTIONS OF THYROID
HORMONE: DEVELOPMENT
• TH is critical for normal development of the
skeletal system and musculature.
• TH is also essential for normal brain
development and regulates
synaptogenesis, neuronal integration,
myelination and cell migration.
• Cretinism is the term for the constellation of
defects resulting from untreated neonatal
hypothyroidism.

HYPERTHYROIDISM
• It is a syndrome caused by excessive secretion of TH when
there is over active thyroid gland.
• This can be due to over functioning of the entire gland or
due to the presence single or multiple adenomas of the
gland.
• Its clinical manifestation is thyrotoxicosis a syndrome
caused when the body tissues are stimulated by a high
level of TH.

• Causes :
• The most common cause is graves disease(w/c is a diffuse
enlargement of the gland)
• Thyroid adenoma
• Thyroid carcinoma
• TSH pituitary adenomas
• Iatrogenic

Pathophysiology :
• B/c the action of thyroid hormones on the body is
stimulatory, hyperthyroidism results in sympathetic over
activity.
• The excessive amount of TH stimulates the cardiac system
and increases the number and sensitivity of beta
adrenergic receptors
-tachycardia
-increased CO and stroke volume
-increased adrenergic responsiveness
-increased peripheral blood flow

cont’d
 Increased metabolism leads to:
 Negative nitrogen balance
 Lipid depletion
 Stage of nutritional deficiency
 Increased oxygen consumption
 TH and catecholamine work together in metabolic
acceleration
 Increased oxygen consumption, BMR, and heat
production
 Positive inotropic and chromo tropic effect by
increasing calcium-ATPase & beta receptors.

cont’d…..
 There is also increased GI motility.
 Increased bone and protein turn over, glycogenolysis,
hepatic gluconeogenesis, intestinal glucose absorption,
cholesterol synthesis and degradation.
 High BMR => high body temperature =>peripheral vessel
dilatation=>increased CO=> high out put failure.
 Prolonged period of hyperthyroidism leads to bone
destruction, and hunger damage due to increased
catabolism of cellular proteins and fat.

 Symptoms and signs:
 Symptoms:
Nervousness
Increased sweating ( warm and moist skin )
Heat intolerance
Palpitation
Fatigue and weakness
Weight loss
Increased appetite
Hyperdefication

 Signs:
Thyroid enlargement
Tachycardia
Atrial fibrillation
Systolic hypertension ( wide pulse pressure)
Eye signs (exophthalmus )

TESTS NORMAL
VALUES
INCREASED DECREASED
T4 60-120 nmole/L
-Hyperthyroidism
-Thyroditis
-Early hepatitis
-Pregnancy
-Oestrogen therapy
-Exogenous T4
-Hypothyroidism
-Androgens
-Salicylates
-Sulphonamides
T3 0.92-3 nmole/L Hyperthyroidism
-Hypothyroidism
-Cirrhosis
-Uraemia
-Malnutrition
TSH 0.25-8micIU/L Primary
hypothyroidism
Hyperthyroidism

TREATMENT
• Anti thyroid drugs:
o PTU, methimazole and carbimazole- these drug inhibits
the synthesis of TH by blocking the action of peroxidise
enzyme (an enzyme that converts I- to I+ )
o PTU also inhibits the peripheral conversion of T4 to T3.

CONT.
o Potassium or Sodium iodide prevent the release of
TH to the tissues
o Dosage : PTU 100-150 mg PO TID, Methimazole 15-60
mg PO BID, Carbimazole 20-40 mg PO TID for at
least 6-8 weeks and potassium or sodium iodide 100
mg PO QID for7-10 days prior to surgery.

Beta blockers:
o Propranolol 40-80 mg PO QID. This drug blocks the high
responsiveness of beta adrenergic receptors to
catecholamine there by reducing pulse rate.
o Beta blockers also have little effect on preventing
peripheral conversion of T4 to T3

• Although blockage of hormone synthesis is rapid, clinical
improvement occurs after months.
• This is b/c a large pool of stored TH continues to be
released from the gland.
• Most patients become euthyroid 2-3 months after the
beginning of anti-thyroid therapy.

• After clinical improvements, dosage should
be tapered to the minimum to maintain an
euthyroid state.
• The drug should continue up to one year.
• A free T4 level should be checked after one
month of therapy and then every 2-3
months

• Indications for surgery
 Large goitre not amendable to RAI
 Compressive symptoms
 Children and young patients
 Patients with cancer or suspicious nodule
 Allergy to anti-thyroid drugs
 Pregnant and those with a desire to conceive
soon
 Moderate to severe opthalmopathy
 Cosmetic desire of the patient

ANESTHESIA
MANAGEMENT
Preoperative preparation:
– Careful assessment of upper airway &
tracheal deviation
– Thoracic inlet X-ray, CT scan
– Patient must be rendered EUTHYROID
– Use anti-thyroid drugs and B - blockers
– Resting pulse rate 85-90 bpm

– Lugol’s iodine 3-5 drops BID for 10 days to
decrease vascularity of the gland
– Benzodiazepines premedication
– Continue the morning dose of anti thyroid and
beta blocking drugs.

Intraoperatively
- Anesthetic options:
A- No difficulty anticipated:
- usual iv induction & intubation (fentanyl, non-depolarizing
muscle relaxant
B- possible difficulty in intubation:
- iv induction, test ventilation when pt is unconscious,
intubation +- suxamethonium
C- definite intubation problem / evidence of airway obstruction
 awake fibreoptic intubation
 inhalational induction
 choice of ETT- armoured ETT (< risk of kinking)
 The size of ETT to be used should be 0.5 mm ID smaller
than the normal calculated size

cont’d……..
 Intra operatively:
 Allow safe induction and awakening
 Maintain adequate level of anaesthesia (avoid
exaggerated sympathetic response to surgical
stimulus)
Drugs of choice
• Etomidate, propofol and barbiturates for
induction
• Atracurium, vecuronium for muscle relaxation
• Isofulrane choice of inhalational.

cont’d…………..
Avoid drugs like:
oAtropine
oPancuronium
oHalothane
oketamine

 Positioning and skin preparation:
o Put an iv bag between scapulas
o Protect eyes
o ETT is strapped firmly in position
o Gentle traction the arms along the side body
o Put patient in a head up position 15-20 degrees
to facilitate venous drainage
o Surgeon stands on the opposite to the lobe to
be removed
o Skin prepared and draped
o IV line on opposite

• If a hyperthyroid patient with clinically apparent disease
requires an emergency surgery:
Propranolol 0.5 mg/kg iv is given
Or esmolol infusion 50-150 micg/kg/minute
If the site allows regional technique is preferred
but adrenalin containing LA should be
avoided.
It is also important to avoid all the causes of
sympathetic stimulations

C) POSTOPERATIVE
Possible problems
1.Thyroid storm /crisis
An acute exacerbation of hyperthyroidism
with excessive release of thyroid hormone
Onset – intraoperative or 6-24 hours after
surgery
Sign and symptom:- hyperpyrexia,
tachycardia or atrial fibrillation,
hypotension, vomiting, dehydration,
tachypnoea, acute abdominal pain
simulating an acute abdomen, agitation,
psychosis
Dx: primarily clinical
DDx: MH,Pheochromocytoma or light
anesthesia

Management:
A) Supportive and medical management.
 Investigate for precipitants – FBC, , blood
glucose, FT4, FT3
If the cause is Hyperthyroidism mange as follows:
1) Inhibition of thyroid hormone formation
 PTU 900-1200mg/day orally / NG in 3-4
divided doses
OR
 Carbimazole 60-120mg/day 3-4 divided
doses orally / NG

Precipitants
- infection, surgery, poorly prepared thyroid
surgery, diabetic ketosis, radioiodine therapy
in a poorly prepared pt, MI

2) Inhibition of thyroid hormone release:
- sodium iodide IV 1gm/24hr – slow infusion
or
- oral potassium iodide 100mg 6hrly
- Given 1hr after 1st dose PTU/carbimazole
3) Steroids - iv dexamethasone 2mg 6hrly
- inhibits thyroid hormone release & peripheral
conversion

4) Receptor blockade ( in the absence of HF)
- Iv propranolol 1-2mg slowly 4-6hrly / oral
propranolol 40-80mg 6hrly
5) Cardiac failure
- diuretics, digoxin, O2 +-propranolol if d/t
uncontrolled AF with good LV function
5) Hyperpyrexia
- fans, tepid sponge, PCM
6) Dehydration
- IV fluid replacement

2) Airway obstruction
Possible causes:
- neck hematoma with tracheal
compression
- tracheomalacia
- incomplete reversal of NDMR
- CNS depression

3) Tetany
- clinical manifestations: circumoral tingling,
paraesthesia, laryngeal spasm, (+) ve Chvostek &
Trousseau signs
- May result from respiratory alkalosis
- over-ventilation in immediate
postoperative period
- hypocalcemia from
hypoparathyroidism
Mx
- calcium replacement
- Slow injection of 10% calcium gluconate 10 mls IV

4) RLN injury
Manifestations:
1) Unilateral
 Asymptomatic unless larygoscopic examination
is done
 Weak and horse voice chocking and coughing
during drinking and aspiration
2) Bilateral
 Usually manifests immediately after extubation
 Laryngeal stridor, acute respiratory distress,
phonation lost and desaturation

• Management
 Unilateral
 Re intubation & observe for 6-12 minutes
 If normal function of cords is not returned with in
6- 12 minutes Teflon injection
 Speech therapy
 Medialization and re -innervation
 Other than the above measures there is no
definitive Rx until 6 months

Cont’d….
 Bilateral
 temporarily:
= re intubation muscle paralysis
= hydrocortisone 100 mg TID
= if extubation fails after 48 hrs Tracheostomy
is mandatory

ANESTHESIA MANAGEMENT
OF HYPOTHYROIDISM
• Definition
o It is a condition when the body tissues
are exposed to decreased circulating
concentration of thyroid hormones.

• Causes
1. Primary- b/c of destruction of thyroid gland
 Thyroid gland can be destructed by
 Chronic thyroiditis( Hash Moto's disease)
 Previous STT
 Previous RAI therapy
 Irradiation of the neck

• Hashimoto’s thyroiditis is an autoimmune
destruction of the thyroid gland in which
antibodies may either frankly destroy the
gland or block TH synthesis.
• And this remains the most common cause of
primary hypothyroidism

Cont’d….
Thyroid hormone deficiency secondary to:
 Anti thyroid drugs
 Excessive iodine ( inhibits TH release)
 Dietary iodine deficiency

Cont’d….
2. Secondary – b/c of CNS dysfunction
Hypothalamic dysfunction which causes TRH
deficiency
Anterior pituitary dysfunction which causes
TSH deficiency

• NB:
 Depending on the cause, the level of TSH
may be increased or decreased.
 If the defect is in the thyroid gland (e.g.
thyroiditis) TSH level will be increased by a
negative feedback mechanism as the low
circulating level of TH will stimulate the
pituitary to secrete more TSH
 If the defect is in the hypothalamus or in the
pituitary the level of TSH will be decreased.

Cont’d……
• Diagnosis
 Is based on clinical signs and symptoms plus
TFT

 Signs and symptoms
 Generalized decrement in metabolic
activity
 Cold intolerance
 Lethargy
 Decreased COP ( up to 40% ) and BV
 Prolonged circulation time and narrow pulse
pressure
 PVR to decrease heat loss

Treatment
• Slow initiation
• Patients with;
-severe hypothyroidism
-older patient and
- patients CVS disease may have increased
sensitivity to TH and are at risk of acute CVS
and other complications if hypothyroidism is
corrected quickly.

Cont’d…..
• Therefore , these patients should be given a
very small dose of TH initially -25 micgm of
levo thyroxine which will gradually be
increased to a full maintenance dose every
2-4 weeks for about 6-12 weeks period

• Rapid initiation
• Younger patients, and patients with less
severe hypothyroidism may be given a
slightly higher dose of TH ( 50 micgm levo
thyroxine) & can be advanced to a full
replacement dose quickly
• For example the dose may be raised to 100
micgn in 2 weeks & 125-150 micgm in the
next 2 weeks

• Maintenance
• Most patients need 75-100 micgm of levo
thyroxine daily

Anesthetic management
• Elective surgeries should be differed in
poorly controlled hypothyroidism due to the
high risk of CVS complications
• But there are no controlled studies about
sensitivity of such patients to IAA & opioids

Cont’d….• Myxedema
• It is a severe form of hypothyroidism
characterized by
Stupor
Coma
Hypoventilation
Hypotension
Hypothermia and hypernatremia
It is a medical emergency with a mortality
rate of 25-50%

Cont’d…
• Management
• ETTI and ventilation is needed
• Sodium levo thyroxine 200-300micgm iv over
10 minutes initially and maintenance 200
micgm iv daily
• Hydrocortisone 100mg iv then 25 mg iv QID
to prevent coexisting adrenal gland
suppression.
• Fluid and electrolyte supplementation
• Avoid hypothermia

Cont’d….
• Preoperative
 Patients with uncorrected severe
hypothyroidism or with myxedema coma
should not undergo elective surgery and
should be treated with TH prior to
emergency surgery.

• Although an euthyroid state is ideal, mild to
moderate hypothyroidism are not absolute
CI to surgery
• Hypothyroid patients usually do not require
much more preoperative sedation and are
very prone to respiratory depression
• They fail to respond to hypoxia by increasing
minute ventilation

• Since patients have delayed gastric
emptying time Premedicating with
metoclopramide and H2 blockers is
important
• The normal dose of TH should be continued
in the morning of surgery
• It should however be known that half life of
most TH drug preparations is long
• For example half life of T4 is about 8 days.

 Due to their depressant effect avoid opioids
 Cortisol supplementation is considered if
there is coexisting adrenal gland
suppression.
 If possible give the premedication in OR

Cont’d…..
• Induction of anesthesia
 Ketamine is a preferable induction agent
 If no severe CVS depression, thiopental can
be used
 When using relaxants keep in mind that
there is a coexisted skeletal muscle
weakness

Cont’d…
• Maintenance of anesthesia
N2O, +- short acting opioids , BZD or
ketamine
is best
Volatiles CI in overtly hypothyroid situation
Reduce MAC if body temperature is
<37degree Celsius
CIPPV is indicated
Pancuronium is best relaxant

Cont’d….
• Regional anesthesia
 Preferable than GA
 Maintain IVFV adequately
 PNB- drug dose should be reduced

Cont’d…..
• No special consideration about the use of
reversals
• IV fluids should contain Na+
• Delay extubation until patient responds
appropriately with an accepted body
temperature
• Monitor variables repeatedly

Cont’d…
• Recovery
 Emergence is delayed from GA due to
hypothermia, respiratory depression and
slow drug biotransformation

 Prolonged post operative
somnolence(sleep)
 Inability to wean earlier => need
mechanical ventilation
 Avoid post operative hypothermia
 Give adequate anti pain
 Opioids drugs have depressant effects we
should use non opioid analgesics like
ketorolac.

THE PARATHYROID GLANDS
• ANATOMY
o Four bean shaped glands are located
behind the upper and lower poles of the
thyroid gland.
o Inferior glands are located ventral(to the
front) to RLN.
o Superior glands usually dorsal( to the back)
to the RLN at level of cricoid cartilage

Cont’d…..
• They get most of their blood supply from
branches of inferior thyroid artery, although
branches from superior thyroid supply at least
20% of upper glands.
• They drain their venous blood through
superior, middle, and inferior thyroid veins

• PHYSIOLOGY
• The main physiologic role of the parathyroid
glands is production of a polypeptide
hormone called parathyroid hormone.
• Maintenance of calcium, phosphate and
magnesium homeostasis is under the
influence of two polypeptide hormones;
parathyroid hormone(PTH), and calcitonin

Cont’d..
• These hormones regulate the flow of
minerals in and out of the extracellular fluid
compartments through their actions on
intestine, kidneys, and bones.
• The PTH acts directly on the bones and
kidneys and indirectly on the intestine
through its effect on the synthesis of 1,25
(OH)2D3. Its production is regulated by the
concentration of serum ionized calcium.

Cont’d..
• Lowering of the serum calcium levels will
induce an increased rate of parathyroid
hormone secretion
• Calcitonin is released by the “C” cells (Para
follicular cells in the thyroid gland) in
response to small increases in plasma ionic
calcium. It acts on the kidney and bones to
restore the level of calcium to just below a
normal set point which in turn inhibits
secretion of the hormone

Cont’d…
• Calcitonin is therefore the physiological
antagonist of PTH. The two hormones act in
concert to maintain normal concentration
of calcium ion in the extracellular fluid.
• The total calcium concentration in the
blood is 10mg/dl
• Of this 40% is bound to plasma proteins
mainly albumin

• The remaining 60% is found in two different
forms
• The first is complexed with anions ( sulfate,
phosphate and citrate) which accounts
about 10%
• About 50% is found as free ionized calcium
and this is the only form of calcium which is
biologically active.

• This free Ca++ is important for
o Skeletal muscle contraction
o coagulation,
o neurotransmitter release,
o endocrine function, other intracellular
functions

Actions of major calcium regulating hormonesHORMONE BONE KIDNEY INTESTINE
PTH
Increase
resorption of
calcium and
phosphate
 Incr. reabsorption of
calcium
 Decr. reabsorption of
phosphate
 Incr. conversion of
25OHD3
 to 1,25(OH) 2 D3
No direct
effect
Calcitonin
Decr.
Resorption
of calcium &
phosphate
Decr. Reabsorption of
calcium & phosphate
No direct
effect
VtD
Maintains
calcium
transport
system
Decr. Reabsorption of
calcium
Incr.
reabsorption of
calcium &
phosphate

DISORDERS OF THE
PARATHYROID GLAND

PRIMARY HPT
• Primary HPT is due to excessive production
of PTH by one or more of hyper functioning
parathyroid glands.
• This leads to Hypercalcemia and hypo
phosphatemia
• It affects patients older than 40 years
• Female to male ratio is 3:1

• 85% caused by isolated adenoma, 14% by
diffuse hyperplasia, 1% by parathyroid CA

HPT CONT’D….
• C/M
• Clinical manifestations are mostly due to
Hypercalcemia.
• CVS: HTN, arrhythmias, short QT, prolonged
PR
• Renal: impaired renal concentration,
metabolic acidosis ,polyuria, dehydration,
polydipsia, renal stones (nephrolithiasis),
renal failure
• GI: ileus, nausea & vomiting, pancreatitis,

Cont’d…
• Musculoskeletal: weakness, osteoporosis(a
fragile bone) & pathological fractures
• CNS: mental status changes(delirium,
psychosis and coma)
• Eyes- calcification, conjunctivitis

SECONDARY HPT
• An increase in PTH secretion which is
adaptive and unrelated to intrinsic disease
of the parathyroid glands is called
secondary hyperparathyroidism.
• This is due to chronic stimulation of the
parathyroid glands by a chronic decrease in
the ionic calcium level in the blood

SECONDARY HPT CONT’D..
• Is a compensatory hyper functioning of the
parathyroid glands caused by
hypocalcemia or peripheral resistance to
PTH
• Treating the underlying cause can reverse
secondary HPT
• It is commonly seen in a patient with an end
organ failure e.g. in chronic renal
insufficiency

TERITIARY HPT
• It occurs in previous secondary HPT
• In such conditions the glandular hyper
functioning continues despite correction of
the underlying problem.
• Most of the c/m of secondary & tertiary HPT
are the same as that of primary HPT as they
are caused by Hypercalcemia

• DIAGNOSIS
• The presence of established Hypercalcemia
in more than one serum measurement
accompanied by elevated immunoreactive
PTH is characteristic feature of HPT
o Marked increase in Ca++ usually b/o
cancer
o Serum Ca++>2.8mmol/L; (NR=2.13-2.55)
o Ionized Ca++>1.25mmol/L (NR=1.1-1.25)

Cont’d…
• Less commonly caused by
 calcium malabsorption
 VtD. Deficiency or deranged VtD
metabolism

MEDICAL MG’T & ANESTHESIA
CONSIDERATIONS
o Medical mg’t
o Saline infusion & loop diuretics
o Biphosphonates(cause binding &inhibit
bone resorption) that may be
administered IV when levels are life
threatening
o Calcitonin produces transient results

• In acute severe forms the main stay of
therapy is adequate hydration with saline
and forced diuresis by diuretics to increase
the urinary excretion of calcium rapidly
along with sodium and prevent its
reabsorption by the renal tubules

Cont’d…
o Hem dialysis
o SURGERY. Resection of the parathyroid
lesion is curative with recurrences
observed mainly in the multiple glandular
disease.

CONT’D…..
• Anesthesia mg’t
Pre operative evaluation should include ass’t
of volume status to avoid hypotension
during induction.
• Hydration with normal saline and diuresis
with furosemide usually decreases serum
calcium to acceptable levels.
• Check labs
• Evaluate status of co morbidities
• Any issues with bone fragility?

Cont’d….
Intraoperatively
• Routine monitors
• Titration of muscle relaxants(pre existing
muscle weakness)
• Issues of positioning
• If preoperative LOC decrease dose of
anesthetic agents
• Protect the eyes

cont’d….
• Avoid hypoventilation as acidosis can cause
an increase in ionized calcium which in turn
causes cardiac dysrhythmias.
• Tracheal manipulation during dissection
• Proper patient positioning is important b/c
osteoporosis predisposes patients to
vertebral compression during laryngoscopy
and bone fractures during transfer

Cont’d….
Post operatively
•
• Smooth emergence
• Evaluate for recurrent laryngeal n. damage
• Pain control

Cont’d…..
• Postop complications
• Worry about
o Neck hematoma
o Laryngeal swelling/ glottis edema
o Recurrent laryngeal n. damage
o Hypocalcemia= tetany
o Acute arthritis
o Metabolic acidosis with deterioration of
renal function (transient)

• PARATHYROID CRISIS:
o CA++ >15 mg/dl
o Requires hydration (dilutes Ca++) followed
by diuresis with loop diuretic (promote
Ca++ & H2O excretion)
o May also be given,glucocorticoids,
calcitonin, dialysis

HYPOPARATHYROIDISM
• Most common cause: accidental excision of
all glands during thyroidectomy
• Also due to: neck trauma, neoplasia
• CRF
• Hypomagnesaemia
• Vt D deficiency

Cont’d…..
• Clinical manifestations
• CVS: hypotension, CHF, prolonged QT
interval
• Musculoskeletal system: muscle weakness &
cramps

Cont’d….
• Neurologic
 Neuro muscular irritability(e.g. laryngeal
spasm, inspiratory stridor, tetany and seizures)
+Chvosteks sign
o Tap facial n at angle of mandible = facial
muscle twitch
+Trousseau sign
o Carpopedal spasm after applying a
tourniquet for 3 min
 Perioral parasthesia mental status changes
(e.g. dementia, depression and psychosis)

• Dx:
o Serum Ca++<4.0 mEq/L, ionized fractions
<2.0 mEq/L

Cont’d…
• RX includes:
o Calcium IV in acute conditions until
neuromuscular signs are controlled
o Correction resp/metabolic alkalosis
o Hypoparathyroid without
hypocalcemia=oral Ca++ and Vit D
o Thiazides tend to increase serum Ca++
concentration

Cont’d..
Treatment of acute episode
o Prevent laryngospasm & seizures
o Secure airway
o IV Calcium slowly
o Anticonvulsants

ANESTHESIA CONSIDERATIONS
• PREOP EVALUATION
o Check Ca++ and Mg levels
o Evaluate EKG ; how is the QT?
o Replace Ca++ if necessary

Cont’d…
• Intraoperatively
o Anesthetics that depress the myocardium
should be avoided.
o Increased sensitivity to Sux
o Titrate muscle relaxants slowly and monitor
response
o Positioning considerations

Cont’d…
o Keep them warm b/c hypothermia may
impair drug elimination & metabolism
o Remember co morbidities
o Avoid hyperventilation ( or anything that will
change Ca++ level) as alkalosis will further
decrease ionized calcium level

• Post operatively
o Assess for changes of serum calcium level
o Pain control
o Close air way follow up

THE ADRENAL GLANDS
• ANATOMY
• Anatomy was first described in 1563.
• Consists of the adrenal cortex and adrenal
medulla

CONT’D….
• PHYSIOLOGY
 Activities are regulation of fluid volume and
stress response
• Adrenal Cortex: The cortex synthesizes &
secretes 30+ different steroids.
o Glucocorticoids
o Mineralocorticoids
o Androgens

cont’d…
o Mineralocorticoids
 Aldosterone
Function: Regulates electrolyte & fluid
homeostasis

Cont’d…
o Glucocorticoids
 Cortisol
 Hydrocortisone
Function:
Stim. gluconeogenesis & h blood
glucose
Anti-inflammatory
Anti-immunity
Anti- allergy

Cont’d…
o Androgen
• Sex hormones
Function: Female= Stim. Sex drive
Men = Negligible

• Adrenal Medulla
o Epinephrine(Adrenaline)
o Function
• Prolong & h SNS (sympathetic nervous
system) response to stress

• Norepinephrine(noradrenaline) and
dopamine.
o Function= the same as that of epinephrine

Adrenal Medulla:
A Modified Sympathetic Ganglion
• Sympathetic stimulation
o Catecholamine release to blood
• Epinephrine
• Norepinephrine
o Travel to:
• Multiple targets
• Distant targets

Review of Efferent Pathways: Motor and
Autonomic

Mechanism: Norepinephrine Release
and Recycling

Catechalomines: Activity
• Stimulate the “fight or flight” reaction
• Increase plasma glucose levels
• Increase cardiovascular function
• Increase metabolic function
• Decrease gastrointestinal and genitourinary
function

DISORDERS OF THE ADRENAL
GLAND
1. Pheochromocytoma( catecholamine excess)
2. Addisons’s disease(adrenal cortex
insufficiency)
3. Conn’s syndrome (mineralocorticoid excess)
4. Cushing’s syndrome (glucocorticoid excess)

PHEOCHROMOCYTOMA
• History
• First recognized by Von Frankel
• Pheochromocytoma= dusky colored tumor
• Name coined by Pick in 1912
• Successful surgery for excision of tumor-
Roux & Mayo ( 1926-27)

Cont’d…
• Neuroendocrine tumour of the medulla of
the adrenal glands
• Originates from the chromaffin cells along
the paravertebral sympathetic chain
extending from pelvis to base of skull
• >95% are abdominal
• >90% in adrenal medulla

• Secretes excessive amounts of adrenaline
and noradrenaline
• 80% occur unilateral

Called “tumor of ten per cent”
• 10% extra-adrenal (closer to 15%)
• 10% occur in children
• 10% familial (closer to 20%)
• 10% bilateral or multiple (more if familial)
• 10% recur (more if extra-adrenal)
• 10% malignant
• 10% discovered incidentally

 Tumor Secretion:
• Large Pheo: more metabolites
(metabolized within tumor before release)
• Small Pheo: more catecholamines
• Sporadic Pheo: Norepi > Epi
• Familial Pheo: Epi > Norepi
• Malignant Pheo: Dopamine

• Epidemiology
 0.01-0.1% of population with HT
 Found in 10% of those screened
 M = F
 Common between 3rd and 5th decades of
life but can occur at any age.
 Rare

• Clinical manifestations
• The five P’s:
• Pressure (HTN)
• Pain (Headache)
• Perspiration(diaphoresis)
• Palpitation
• Pallor(there is a decrease in red cell
mass)

• The Classical Triad:
1. Pain (Headache)
2. Diaphoresis (excessive sweating)
3. Palpitations

• Cardiac manifestations
• Sinus tachy, ventricular ectopic,
• Catecholemine induced increased
myocardial oxygen consumption, coronary
vasospasm
o Angina/MI
o Cardiomyopathy- hypertrophic
Cardiomyopathy- diastolic dysfn- norepi
induced
o Dilated cardiomyopathy- systolic dysfn-
epi induced

• Neurologic manifestations
o Hypertensive encephalopathy (altered
mental status, focal neurological s/s,
seizures)
o Stroke – cerebral infarction/ embolus
o Intracranial bleeding

Diagnosis
1. Biochemical
2. Localization

1. Biochemical
• 24h Urine Collection
Positive results show 2-3 fold elevation from the
normal value
Normal values:
-Dopa=424-2612nmol/d
-Epi=10-110nmol/d,
-Norepi=12-85.5micg/d
-Metanephrine=0-4.9mivmol/d
-Normetanephrine=573-933nmol/d

• Test Characteristics:
• 24h urinary catechol Sen 83% Spec 88%
• 24h U total metanephrine Sen 76% Spec
94%
• 24h Ucatechols + Utotal metanephrines Sen 90%
Spec 98%
• Sensitivity increased if 24h urine collection
begun at onset of a paroxysm

• Plasma free metanephrines sensitivity = 99%
specificity = 89%
• Plasma catecholamine sensitivity 84% and
specificity = 81%

2. Localization: Imaging
• CT abdomen
• Adrenal pheo sensitivity 93-100%
• Extra-adrenal pheo sensitivity 90%
• MRI
• > sensitive than CT for extra-adrenal
pheo
• Abdominal U/S and x-ray

ANESTHESIA MANAGEMENT
• Prior to 1951, reported mortality rate for
excision of pheochromoyctoma was 24 - 50
% due to
• HTN crisis, arrhythmia, MI, stroke
• Hypotensive shock

Cont’d….
• Currently, mortality: 0 - 2.7 %
• The reasons are:
• Preoperative preparation, -blockade
• New anesthetic techniques
• Anesthetic agents
• Intraoperative monitoring: arterial
line, EKG monitor, CVP line
• Presence of experienced & coordinated
team:
• Endocrinologist, Anesthesiologist and
Surgeon

• Preoperative preparation
• Preoperative work up
- CBC, electrolytes, creatinine
- CXR
- EKG
- Echo (r/o CMY 2º to catechols)

• Preoperative & β blockade
• Start at least 10-14d preoperatively
• Allow sufficient time for ECF re-expansion
• There must also be dose increments with time until
there is optimal control of paroxysms

• Adrenergic Receptors
• Alpha-Adrenergic Receptors
• 1= vasoconstriction, intestinal relaxation,
uterine contraction, pupillary dilation
• 2=  presynaptic NE (clonidine), platelet
aggregation,
vasoconstriction,  insulin secretion
• Beta-Adrenergic Receptors
• 1=  HR/contractility,  lipolysis,  renin
secretion
• 2= vasodilation, bronchodilation, 
glycogenolysis
• 3:= lipolysis

Alpha blockade
• Phenoxybenzamine (Dibenzyline) a non
selective blocker.
• Drug of choice
• Covalently binds -receptors (1 > 2)
• Start 10 mg PO BID  increase by 10-20
mg/d PO BID
• Maintenance 40-80 mg/d (some need
> 200 mg/d)

• Phenoxybenzamine (cont’d)
• Side-effect: orthostasis with dosage
required to normalized seated BP, reflex
tachycardia
• Drawback: periop hypotension/shock
unlikely to respond to pressor agents.
• Prevents 2 mediated inhibition of
catecholamine release
• Thus beta blockers needed to be given
alongside

• -blockade
• Used to control reflex tachycardia and
prophylaxis against arrhythmia during
surgery
• Start only after effective -blockade
(may ppt HTN)
• If suspect CHF/dilated CMY  start low
dose
• Propanolol most studied in pheo prep
• Start 10 mg PO BID  increase to
control HR
• Initial dose 80-120 mg/d
• IV 1-10 mg

• Propranolol ( cont’d)
o Side effects- may induce cardiac failure,
bronchospasm
o Oral bioavailability 25% (extensive 1st pass
metabolism)
• Atenolol- selective B1
o Dose 50- 100 mg/d PO
o Max 300 mg/d
o IV 2.5 to 10 mg/d

• Esmolol – selective B1 for rapid intraop BP
control
o Bolus IV 500 µ/kg/min
o Infusion 50 to200 µ/kg/min
• Labetolol –mixed ɑ+β
o Dose- 50- 100 mg/d PO
o IV 0.25 mg/kg
o Not used as a sole drug due to
unpredictable control of BP

• If BP is still not controlled despite  + 
blockade
 Add Prazosin to Phenoxybenzamine
 Prazosin – competitive, selective 1 blocker
o T1/2- 2-3 Hrs.
o Dose -1-5 mg PO BD
o Side effects- postural hypotension reflex
tachycardia
o Other selective 1 blockers- terazosin,
doxazocin

• Other antihypertensives
• CCB-
oDiltiazem 60- 120mg/d, max 360mg/d
oT1/2- 3 to 5 hrs
oSide effects- bradycardia, exacerbates
cardiac failure
oNifedipine – 30mg/d PO Max. 360mg/d
oT1/2-1 to 2 hrs
oSide effects- hypotension, peripheral
edema
• Avoid diuretics as already ECF contracted

• Nicardipine
• Started PO 24 Hrs to few weeks preop to
control BP and allow ECFV restoration
• After intubation  IV Nicardipine (start 2.5
ug/kg/min)
• IV Nicardipine adjusted to SBP
• Stopped prior to ligation of vein
• Tachycardia Rx with concurrent IV esmolol
• Advantage: periop hypotension may still respond
to pressor agents as opposed to those patients
who are completely -blocked

• Evaluation of  adrenergic blockade
• Roizen’s criteria
o Arterial BP < 160/95 mm Hg in the last 48
hrs prior to surgery. Recommended to
measure in stressful environment
o Mild orthostatic hypotension indicates
optimal  adrenergic blockade but not <
80/45.
o ECG- free of ST changes for > 2 wks,
o Ventricular ectopic < 1 over 5 min

• Premedication
• If patient is anxious give appropriate dose of
BDZ in the night prior to the day of surgery

• Monitoring
 ECG
 CVP
 Direct arterial pressure measurements
 Capnograph
 Temperature
 Arterial blood gas analysis
 Blood glucose levels

• Anesthetic technique
• General anesthesia
• Regional anesthesia- mid to low thoracic
• Combined regional and general anesthesia
• Preferred- combined regional and general
anesthesia technique
o Here although regional anesthesia protects
against stresses of surgery, it cannot prevent
catecholamine surges due to tumor
manipulation.
o In extensive sympathetic blockade, severe
hypotension after tumor removal,

• INDUCTION
• Essentially important to give induction
agents slowly along with close monitoring of
HR and arterial pressure
• Thiopentone / propofol widely used
• Etomidate –causes pain/ involuntary mov’t
• Ketamine – should be avoided
• Multimodal – BZD+ opioid(avoid pethidine &
morphine)+ induction agent

• Attenuate pressor response
 Important for laryngoscopy and tracheal
intubation
 2% lignocaine(with out adrenaline) – 1-
1.5mg/kg one minute before laryngoscopy
 Esmolol – 50- 100 µg/kg/min
 During laryngoscopy catecholamine levels ↑
o Normally- 200- 2000 pg/ml
o During laryngoscopy - 2000- 20,000 pg/ml

• Neuromuscular blockade
 NDMR drugs= vecuronium
 Suxamethonium- avoided causes
fasciculation and rise in intra abdominal
pressure
 Atracurium/ mivacurium- best avoided due
to release of histamine
 Cisatracurium/rocuronium- safe cardio
stable and least histamine release

• Maintenance
• Inhalational agent- isoflurane used
extensively b/c it does not sensitize the
myocardium to catecholamines
• Halothane undesirable due to it’s
arrhythmogenic properties
• Sevoflurane used successfully (fast onset
…..fast offset)

• During surgery
• Have ready: IV phentolamine, IV NTP, IV
esmolol
• Very high uncontrolled BP- tell surgeons
to stop manipulation of the gland
• Ligation of adrenal vein- care for
sudden hypotension
• Rx hypotension with crystalloid +/-
colloid 1st
• may need dopamine/ noradrenaline/
phenylephrine

• Postoperative
• Post op ventilation / ICU stay- depends upon
the hemodynamic status…. Preferably ICU
stay for 24 Hrs
• Hypoglycemia post op due to disinhibition of
B cell supression….. Increased insulin
secretion
• Glucose supplementation at end of surgery

• Post op( cont’d)
• Most cases can stop all BP meds postop
• Postop hypotension: IV crystalloid
• HTN free: 5 years 74% 10 years 45%
• 24h urine collection 2 week postop
• Surveillance:
• 24 h urine collections every year for at
least 10years
• Lifelong follow up
• 5 year survival- non malignant pheo- 95%
• Malignant- < 50 %

 Conclusion
• Long term outlook very good
• Managed by an experienced team of
anesthesiologist, surgeon, endocrinologist &
cardiologist
• Principles of anesthetic management
o Good adrenergic blockade preop
o Vigilant intraop monitoring and treatment
of hyper/ hypotension
o Post op ICU care
• Antihypertensive for a prolonged period

ANESTHESIA MANAGEMENT OF PATIENTS WITH COEXISTING AND ENDOCRINE DISEASES

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