ANESTHESIA FOR

PITUITARY LESIONS

Rialph Engel D. Guia

First year resident
Department of Anesthesiology
Batangas Medical Center
OBJECTIVES

1. To discuss the anatomy and physiology of the pituitary gland;

2. To enumerate the pathophysiology of pituitary lesions; and
3. To review the peri-operative management of patients with pituitary
lesions.
Anatomy
Pituitary Gland

• Glans, in quam pituita destillat, "gland in

which slime (pituita) drips”
• Pea-sized gland housed within the sella
turcica
• Weighs 0.5g
• ‘Master gland’
• Controlled by the hypothalamus
 Pituitary Gland

• Two parts:
• Front (anterior) lobe
• Back (posterior) lobe
• Connected to the
hypothalamus
• Anterior lobe: hormones
• Posterior lobe: nerve impulses
Blood Supply

• Branches of the circle of Willis

• Anterior pituitary – superior
hypophyseal artery
• Posterior pituitary – inferior
hypophyseal artery
• Venous drainage – cavernous sinuses →
petrosal sinuses → jugular vein
Physiology
Pituitary Gland Hormones

• Hormones not all produced continuously

• Anterior lobe hormones:
• ACTH, follicle-stimulating hormone and luteinizing hormone,
growth hormone, prolactin, thyroid-stimulating hormone
• Posterior lobe hormones:
• Vasopressin, oxytocin
• Other hormones
Control of Pituitary Hormone Release

Hypothalamic Factor Corresponding Anterior Pituitary

Hormone

Thyrotropin releasing hormone (TRH) TSH

Corticotropin releasing hormone (CRH) ACTH
Gonadotropin releasing hormone (GnRH) LH and FSH
Growth hormone releasing hormone (GHRH) GH
Prolactin releasing hormone (PRLH) PRL
 hypothalamus
Adrenocorticotropic Hormone
corticotropin-
releasing hormone
(CRH)

anterior pituitary

adrenocorticotropic
hormone (ACTH)

adrenal cortex
 Adrenocorticotropic Hormone

• Site of Action: adrenal cortex

• Effects: stimulates the synthesis of
glucocorticoids, synthesis of
mineralocorticoids
• Release Stimulated by: CRH, stress
(including surgery)
• Release Inhibited by: glucocorticoids
Gonadotropins

• Follicle-stimulating hormone,
luteinizing hormone
• Testes → sperm
• Ovaries → eggs
• Sex organs → sex hormones
• Placental hormone, human
chorionic gonadotropin (hCG)
FSH

Site of action testes and ovaries

Effects stimulates spermatogenesis in males;
ovarian follicle growth in females
Release stimulated by GnRH
Release inhibited by estrogen and testosterone (in men)
LH

Site of action testes and ovaries

Effects testosterone secretion in males;
luteinization of ovarian follicles and ovulation in females
Release stimulated by GnRH, estrogen
Release inhibited by estrogen and progesterone (after ovulation),
testosterone (in men)
Growth Hormone

• Somatotropin, human growth hormone (hGH)

• Stimulators: Peptide hormones, sex hormones, clonidine and L-DOPA,
nicotinic agonists, hypoglycemia, arginine, propranolol, deep sleep,
insulin, glucagon
• Inhibitors: GHIH (somatostatin), circulating concentrations of GH
and IGF-1, hyperglycemia, glucocorticoids, dihydrotestosterone,
phenothiazines
Growth Hormone

Site of action all body systems

Effects protein synthesis, lipolysis, skeletal and fetal
growth, gluconeogenesis, sodium retention and
reduced sensitivity to insulin
Release stimulated by GHRH, exercise, hypoglycaemia, stress, glucagon,
and dopamine
Release inhibited by somatostatin, GH
 Growth Hormone

• Excess
• Thickens the bones of the jaw,
fingers and toes
• Sweating, pressure on nerves,
muscle weakness, insulin resistance
• Children: gigantism
• Adults: acromegaly
Growth Hormone

• Deficiency
• Children: growth failure,
development of a short stature,
delayed sexual maturity
• Adults: increased osteoclast activity,
relative increase in fat mass, relative
decrease in muscle mass
Prolactin

hypoestrogenism, anovulatory infertility, oligomenorrhoea,

Hyperprolactinemia amenorrhoea, unexpected lactation and loss
of libido; erectile dysfunction and loss of libido
ovarian dysfunction; arteriogenic erectile dysfunction,
Hypoprolactinemia premature ejaculation, oligozoospermia, asthenospermia,
hypofunction of seminal vesicles, hypoandrogenism
Prolactin

Site of action breasts

Effects development of the breasts ready for lactation,
stimulates milk production, reduces fertility
Release stimulated by PRLH, dopamine antagonists, suckling, prolactin (positive
feedback mechanism), stress, exercise
Release inhibited by dopamine (also known as prolactin-inhibitory hormone)
Thyroid Stimulating Hormone

• Thyrotropin, thyrotropic hormone, TSH

• Hypothalamus → thyrotropin-releasing hormone → anterior pituitary
→ TSH
• Stimulates the thyroid gland to produce thyroxine (T4) and
then triiodothyronine (T3) → stimulates metabolism
• Thyroxine (T4) – slight effect on metabolism
• Triiodothyronine (T3) – active hormone
 Thyroid Stimulating Hormone

Source of TSH Thyroid Disease-causing conditions

pathology level hormone level
Hypothalamus/ High High Benign tumor of the pituitary (adenoma)
pituitary or thyroid hormone resistance
Hypothalamus/ Low Low Secondary hypothyroidism or "central"
pituitary hypothyroidism
Hyperthyroidism Low High Primary hyperthyroidism i.e. Graves' disease
Congenital hypothyroidism, Primary
Hypothyroidism High Low hypothyroidism i.e. Hashimoto's thyroiditis
Thyroid Stimulating Hormone

Site of action thyroid

Effects stimulates follicular activity and the synthesis and
release of thyroid hormones (T3 and T4)
Release stimulated by TRH
Release inhibited by somatostatin, thyroid hormones
Vasopressin

• Antidiuretic hormone, arginine vasopressin, argipressin

• Regulates the amount of water excreted by the kidneys → maintain
water balance in the body (maintaining tonicity of body fluids)
• Released from the posterior pituitary in response to hypertonicity
• Low levels: diabetes insipidus
Vasopressin

Site of action distal tubule and collecting ducts in the kidney,

blood vessels
Effects water reabsorption in the kidney at the above sites,
arteriolar vasoconstriction, synthesis of Factor VIII
Release stimulated by increased osmolarity of extracellular fluid, pain,
haemorrhage, stress, thirst, activation of the renin-
angiotensin system
Release inhibited by alcohol, reduced osmolarity of extracellular fluid
Oxytocin

• Produced in the hypothalamus and stored in the Herring bodies of the

posterior pituitary
• Milk ejection reflex / Letdown reflex
• Uterine contraction
• Antidiuretic
• Cardiac
• Indirectly inhibits release of adrenocorticotropic hormone, cortisol
Oxytocin

Site of action breasts, kidneys

Effects stimulates contraction of myoepithelial cells
surrounding the milk ducts → secretion of milk;
stimulates contraction of the uterus and water
retention by the kidney
Release stimulated by suckling
Release inhibited by dopamine
Pathophysiology
Pituitary Gland Malfunction

• Usually as a result of developing a noncancerous tumor (adenoma)

• May overproduce one or more pituitary hormones
• May press on the normal pituitary cells → underproduction of
pituitary hormones
• Excess cerebrospinal fluid can fill the space around the pituitary gland
and compress it (empty sella syndrome)
Pituitary Gland Malfunction
Pituitary Gland Malfunction

• Imaging tests (computed tomography, magnetic resonance imaging)

• Levels of pituitary hormones
Pituitary Tumors

• Microadenomas (< 10mm) and macroadenomas (> 10mm)

• Macroadenomas
• Mass effect
• Microadenomas
• Unregulated amounts of anterior pituitary hormones → hormone
excess
• Prolactin (35%), GH (20%), ACTH (7%)
Anterior Pituitary Hypersecretion

• Negative-feedback loop
• Dopamine – prolactin-inhibiting hormone
• Somatostatin – GH release–inhibiting hormone
• GH-releasing hormone
• Corticotropin-releasing hormone
• Gonadotropin-releasing hormone
• Tyrotrophin-Releasing Hormone (TRH)
Anterior Pituitary Hypersecretion

• Most common disorders of pituitary hypersecretion:

• Excesses of prolactin (amenorrhea, galactorrhea, infertility)
• ACTH (Cushing syndrome)
• GH (acromegaly)
 Hyperprolactinemia

• Plasma prolactin > 390 mU/L

• Clinical Features
• Weight gain, menstrual disturbance, infertility, depression, galactorrhoea
• Men: impotence, reduced facial hair, galactorrhoea
• Diagnosis and Treatment:
• Measurement of plasma prolactin levels
• Pituitary MRI scan
 Acromegaly
Clinical Features

• Most cases diagnosed in • Prognathism

patients aged 40-60 years • Prominent supraorbital ridges due to
skull growth and kyphosis
• slow onset • Increase in the size of hands and feet
• Soft tissue changes
• Deepening of the voice
• Development of coarse oily skin
• Osteoarthritis
• Sleep apnea
• Hypertension
• Diabetes mellitus
Acromegaly

• Diagnosis and Treatment

• Oral Glucose Tolerance Test and GH measurement
• Pituitary MRI Scan
• Transsphenoidal surgery to remove the tumour +/- radiotherapy
• Somatostatin analogues
 Cushing’s Disease

Clinical Features

• Most commonly diagnosed • Weight gain and central obesity

between 30-55 years • Thin skin
• Easy bruising
• Women > men • Abdominal striae
• Proximal myopathy
• Poor wound healing
• Depression
• Hypertension
• Hyperglycemia
Cushing’s Disease

• Diagnosis and Treatment

• Dexamethasone suppression test
• Pituitary MRI
• Transsphenoidal surgery
Anterior Pituitary Hypofunction

• Deficiency of one or more of the following: GH, TSH, ACTH, prolactin,

or gonadotropin
• No special preoperative and preprocedure preparation for prolactin or
gonadotropin deficiency
• Deficiency in GH → atrophy of cardiac muscle
Posterior Pituitary Hormone Excess and
Deficiency

• Vasopressin / antidiuretic hormone (ADH): enhanced by ↑ serum

osmolality or hypotension
• Preoperative and preprocedure management: appropriate treatment
of the causative disorders + restriction of water
• Drugs that inhibit the renal response to ADH (e.g., lithium or
demeclocycline)
Posterior Pituitary Hormone Excess and
Deficiency

• SIADH should be suspected in any patient with hyponatremia + the

following laboratory findings:
• Urinary sodium >20 mEq/L
• Low serum levels of BUN, creatinine, uric acid, and albumin
• Serum sodium <130 mEq/L
• Plasma osmolality <270 mOsm/L
• Urine hypertonic relative to plasma
Posterior Pituitary Hormone Excess and
Deficiency

• Too vigorous treatment of chronic hyponatremia → osmotic

demyelination syndrome
• Increase in serum sodium should not be >1 mEq/L/h
• Mild to moderate symptoms of water intoxication: restriction of fluid
intake to ~500 to 1000 mL/day
• Severe water intoxication + CNS symptoms: IV hypertonic saline
solutions → fluid restriction
Posterior Pituitary Hormone Excess and
Deficiency

• Treatment should be directed at the underlying problem

• Drugs that block the effect of ADH on renal tubules:
• Lithium
• Demethylchlortetracycline 900 to 1200 mg/day
• Operating room:
• Fluids are managed by measuring volume status
Posterior Pituitary Hormone Excess and
Deficiency

• Lack of ADH → diabetes insipidus

• Preoperative or preprocedure treatment:
• Restoring normal intravascular volume by replacing urinary losses,
administering desmopressin acetate (DDAVP) nasally, giving daily
fluid requirements intravenously
Posterior Pituitary Hormone Excess and
Deficiency

• Complete diabetes insipidus + total lack of ADH

• Usual dose of DDAVP (100 milliunits aqueous vasopressin) →
infusion of 100 to 200 milliunits/h
• All intravenous fluids given intraoperatively should be isotonic
• Plasma osmolality should be frequently measured
• >300 mOsm/L: hypotonic fluids + intraoperative vasopressin
infusion can be increased to >200 milliunits/h
Patient Management
Pre-Operative Assessment

• Airway and respiratory system assessment

• Cardiovascular system assessment
• Neurological assessment
• Endocrine assessment
• Full blood count, urea and electrolytes, calcium, blood glucose
Pre-Medication

• Antihypertensive, heart failure, bronchodilator and antacid

medications (except angiotensin converting enzyme inhibitors and
diuretics)
• Diabetics: regular blood sugar measurements
• Benzodiazepines and other sedative pre-medications should be
avoided
Peri-Operative Glucocorticoid Cover
Peri-Operative Glucocorticoid Cover

• All patients with Cushing’s disease

• 100mg hydrocortisone given at induction of anesthesia → 50 mg BID
on the first postoperative day → 25 mg BID on the second post-
operative day → 20 mg in the morning and 10mg in the evening on
the third and subsequent days
• May need to continue with glucocorticoid replacement for several
weeks
Perioperative management of patients with
Pituitary Tumours

• Thorough endocrinological evaluation in the pre-operative period +

follow-up in the post-operative period (hormone replacement)
• Visual function evaluation including visual field testing
• The treatment goals for secretory adenomas are 3-fold:
• Suppression of hormone secretion
• Decrease tumour size
• Restore normal pituitary function
Perioperative Management of Endoscopic
Transsphenoidal Pituitary Surgery

• Multi-disciplinary disease management approach

• History, Physical examination
• Pre-surgical testing and pre-anesthetic evaluation
• Imaging
• Optimization of comorbidities
• Continue systemic corticosteroids or levothyroxine perioperatively
• Antiplatelets and anti-coagulants is continued prior to surgery
 REFERENCES

• Abraham, M. Perioperative management of patients with pituitary tumours. Journal of

Neuroanaesthesiology and Critical Care. Wolters Kluwer 2016
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Clinical Anesthesia 8th edition. Wolters Kluwer 2017
• Griffiths, S. The Hypothalamic-Pituitary Axis. World Federation of Societies of Anesthesiologists, 2010.
https://resources.wfsahq.org/
• Gropper, M., Eriksson, L., Fleisher, L., Wiener-Kronish, J., Cohen, N., and K. Leslie. Miller's Anesthesia, 9th
Edition. Elsevier 2019
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transsphenoidal pituitary surgery. World Journal of Otorhinolaryngology - Head and Neck Surgery Volume
6, Issue 2, June 2020, Pages 84-93
• Yao, F.F., Fontes, M.L., and V. Malhotra. Yao & Artusio’s Anesthesiology: Problem Oriented Management,
7th edition. Wolters Kluwer 2012