Anesthesia for Pituitary

Surgery
Speaker:- Dr. Bhaskar
Moderator:- Dr. Srilatha

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CONTENTS
• Anatomy of pituitary gland & its clinical importance
• Diseases of sellar and parasellar areas
• Indication for surgery in pituitary tumors
• Pre-operative assessment
• Airway assessment
• Premedication
• Surgical approaches to pituitary tumor
• Airway management
• Intraoperative management
• Postoperative management
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Anatomy of pituitary gland & its clinical importance
• Located in sella turcica, a saddle-like formation in the superior aspect of sphenoid
bone at the base of skull.
• Its location in the roof of the sphenoid sinus has made it amenable to surgical
approaches through that sinus.
• Composed of 3 substructures:- anterior (Rathke’s pouch); intermediate and
posterior lobes (infundibular process).
• The anterior pituitary (adenohypophysis) - glandular tissue while the posterior
pituitary gland (neurohypophysis) is neural in character.
• Cells in anterior pituitary secrete the critical trophic hormones responsible for
growth, development and the maintenance of homeostasis.

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BORDERS OF SELLA TURSICA:-
• Lateral  Cavernous sinus (venous sinuses enclosed entirely by Dura)
• Within these sinuses there are carotid arteries and CN III, IV, VI, V 1 & V2
• Lateral extension - well tolerated & seldom cause clinical symptoms - slow growth & non-
malignant nature
• Superior  Dural reflection with an opening to allow pituitary stalk known as
‘Diaphragma sella’
• Above the diaphragma lies Arachnoid space filled with CSF and inside the space lies the optic
chiasma.
• Growth of a tumor occurs through the least resistance.
• In this instance, pituitary tumor growth most commonly occurs superiorly as there is natural
opening present in the diahpragma sella and impinges on the optic chiasma
• Anterior  Dural communications between two cavernous sinus
• Posterior  Basilar sinus and the interpeduncular/prepontine cisterns, in which
reside the basilar artery and the brainstem.
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Pituitary gland and adjacent
anatomy as seen in tissue
dissection in a coronal plane

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Diseases of Sellar and parasellar area & their presentation
• Classified based on size and whether they are hormone-secreting or not

Hor
• Microadenoma (<10mm) Size mon
• Functioning
• Macroadenoma (>10mm) e • Non-functioning

• Functioning tumors present with symptoms of hormone excess while non-

functioning one present asymptomatically or with symptoms of mass effect of the
tumor.
Non functioning tumors;-
The symptoms are produced due to the pressure effect caused by tumor impinging
on the surrounding structures.

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Pressure Symptoms include:-
1. Headache/ ICP due to
compression of 3rd ventricle
2. Visual loss due to compression of
optic chiasma
3. Hypopituitarism due to
compression of anterior pituitary
4. Diabetes Insipidus due to
compression of pituitary stalk
5. Intracranial bleeding due to
artery/venous sinus erosion
6. Ophthalmoplegia/Ptosis/Horner
syndrome due to compression of
nerve bundles

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Hypersecretory pituitary adenomas
CUSHING’S DISEASE:-

• Glucocorticoid excess caused by ACTH

released by tumor in anterior pituitary
• Endogenous ACTH release suppressed
• Diffuse adrenal hyperplasia seen
• Clinical diagnostic tests include late night
salivary cortisol levels, low-dose and high
dose dexamethasone suppression test, urinary
free cortisol, serum ACTH.
• Tumor resection is the first line treatment.

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ACROMEGALY:-
• Overproduction of GH hormone 
Overproduction of IGF1
• Enlargement of visceral as well as somatic
structures
• Laboratory findings indicative of active
disease are:
• random GH ≥1 ng/mL;
• nadir GH after oral glucose tolerance test ≥0.4
ng/mL;
• Elevated ILGF-1 for age

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HORMONE HYPOSECRETION
1.Adrenocortical insufficiency:
• can be a life-threatening condition in acute setting.
• The renin-angiotensin-aldosterone axis is preserved in contrast to Addison's disease;
hence fluid and electrolyte abnormalities are less severe.
• Treated with IV hydrocortisone and fluid resuscitation.
2.Central DI:
• Due to failure of secretion of ADH.
• Treated with desmopressin; usually administered orally or intra-nasally, after
procedure it can be given as a SC or IM injection.
• Oxytocin: Failure to secrete oxytocin only becomes clinically evident during and
after childbirth

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Pituitary apoplexy:-
• Sudden onset of symptoms due to hemorrhage or infarction within the
pituitary or a pituitary tumor.
• Severe headaches associated with compromise of vision, ocular paresis, and
vomiting (mimic SAH)
• Emergent surgical decompression of the optic apparatus may be necessary.
• Also present with acute adrenal insufficiency from destruction of the
normal gland
• Requires high dose IV steroid treatment to prevent cardiovascular collapse.

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Indication for surgery in pituitary tumors
Primary
• Symptomatic pituitary adenomas
• Asymptomatic tumors with radiologic evidence of invasion (Knosp grading
system estimating invasiveness using MRI)
• Pituitary apoplexy with acute vision loss </= 72 hours
Secondary
• when medical treatment fails for the treatment of prolactinoma & GH adenoma
• There is evidence to suggest that debulking of medically refractory prolactinomas
and GH adenomas can return these tumors to a responsive state

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PRE-ANESTHETIC MANAGEMENT
OF SURGERY FOR PITUITARY
TUMORS

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Pre-operative evaluation
• The mainstay includes pre-operative management of symptoms caused by
hormonal excess in functional pituitary tumors.
• History and physical examination should be reviewed.
• Signs and symptoms of mass effect such as headache, loss of vision, nausea and vomitings
• Signs and symptoms of hormonal excess which include

Frailable Difficulty in
Cushing’s disease skin & easy IV
bruising canulation

Carpal Difficult in
Acromegaly Tunnel arterial
syndrome canualtion

Avoid
Use of
Hypo/Hyperthyroid thyroid
medication
storm
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Investigations
• Complete blood picture:- Patients with pituitary tumors tend to have increased
incidence of Anemia
• Metabolic Panel:-
1. HYPONATREMIA : Diabetes insipidus due to posterior pituitary dysfunction can cause
hyponatremia.
2. HYPERCALCEMIA : Pituitary tumors associated with MEN 1 syndrome (parathyroid
hyperplasia) can lead to hypercalcemia.
3. HYPERGLYCEMIA : Patients with acromegaly and cushing’s syndrome are prone for
glucose intolerance or frank diabetes mellitus.
4. HYPOKALEMIA : Cushing’s disease can cause hypokalemic alkalosis

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• Endocrine workup:-
• Thyroid profile – Patient must be euthyroid prior to the procedure.
Hypothyroidism:
• Patients show increased sensitivity to and reduced metabolism of all classes of anaesthetic drugs.
• Emergence from anaesthesia may be very prolonged, necessitating postoperative respiratory
support.
• The normal ventilatory responses to hypercapnia and hypoxia are obtunded and perioperative
hypothermia is common.
• Clinical response to thyroid replacement therapy may take 10 days or more, although rapid
correction can be achieved with IV L-iodothyronine (T3), there is a significant risk of precipitating
myocardial ischaemia and heart failure.
• Serum ADH levels to be evaluated to rule out the presence of pre-op DI.
• Serum ACTH & cortisol levels.

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Airway assessment
Changes in Acromegaly Changes in Cushing’s disease

Hypertrophy of Mandible Central Obesity

Hypertrophy of pharyngeal soft tissue Presence of Obstructive sleep apnea

Calcinosis of larynx Moon facies

Buffalo hump

• Radiograph of neck in Anterior & Lateral view; Preoperative indirect laryngoscope evaluation of glosttis
may be required in Acromegaly patients in view of increased incidence of postoperative Tracheomalacia.

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 Premedication
• Benzodiazepines and narcotics should be administered under vigilance to patients
with OSA as they are more prone for respiratory failure.
• Patients with Cushing’s disease commonly have GI reflux. H2 receptor
antagonists should be prescribed.

STEROID SUPLLEMENTATION:-
• Perioperative glucocorticoid cover in all patients with Cushing’s disease is
mandatory.
• IV Hydrocortisone 100 mg: evening before the surgery, repeated before start of
surgery.

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• In patients with ACTH deficiency, cortisol test is recommended before
administration of steroid.

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Surgical Approaches for pituitary tumors
Extracranial Transcranial
A. Trans-sphenoidal:- A. Intra-dural:-
Sublabial trans-sphenoidal Subfrontal
Trans-nasal trans-sepatal trans-sphenoidal Pterional

Trans-maxillary trans-ethmoidosphenoidal Sub temporal

Fronto orbital external trans-ethmoidal

B. Endoscopic endonasal B. Extra-dural:- Orbito zygomatic

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• Endoscopic approach is favoured as it requires less dissection and less bone
removal. It has improved tumor visualization while minimizing the risk of
nasal and dental complications and septal perforation.
• Nasal intubation or placement of a nasogastric tube is contraindicated for at
least 14 days and should always be carefully considered as the bone defect
will persist after the surgery.

• The sublabial approach enters the nasal antrum through an incision below
the upper lip and above the teeth.
• Visualization is achieved via an operating microscope, which allows for
significant magnification and illumination
• The sublabial approach may be required in children or adults with very
large tumors.
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Airway management
• Airway management may be particularly challenging in patients with acromegaly
or Cushing’s disease.
• Many studies suggest that acromegaly is associated with a high incidence of
unanticipated difficult intubation, despite a reassuring preoperative airway
examination (like Mallampatti grade 1 or 2)
• Difficult airway trolley should be thoroughly checked for various adjuncts
required to secure airway and it is recommended to keep a secondary technique
ready (eg. Video laryngoscope, Fiberoptic bronchoscope)
• In cases of anticipated difficult intubation, awake orotracheal fiberoptic intubation
is the technique of choice.
• After the airway is secured, oropharynx is packed with saline soaked gauze to
stabilise the tube and to protect the lower airway from accumulation of blood and
secretions which many precipitate post operative nausea vomiting.

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INTRAOPERATIVE ANESTHETIC
MANAGEMENT OF SURGERY FOR
PITUITARY TUMORS

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Goals of Anesthesia
• Optimization of Cerebral oxygenation
• Maintenance of Hemodynamic Stability
• Providing conditions that facilitate surgical exposure
• Rapid and smooth emergence

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Positioning of the patient
• The patient is positioned in a semi recumbent beach chair position with the
operative field above the heart to facilitate venous drainage and prevent venous
engorgement.

• The neck is extended and head is turned slightly to facilitate surgical access to
both the nares.

• Cushing’s disease is associated with diffuse osteoporosis and proximal myopathy.

Careful positioning & padding is important to prevent pathological fractures.

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Preparation for surgery
1. Injection of lignocaine with epinephrine is given by surgeon at the nasal mucosa
of incision site. Xylometazoline is also a safer alternative.

2. Routine use of large quantities can result in significant systemic effects.

HYPERTENSION and cardiac dysrhythmias are most frequently observed.

3. Hypertension is transient and should be treated with short acting agents like
nitroglycerine, sodium nitroprusside.

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Intraoperative monitors
• Routine monitors are used during induction and maintenance of anesthesia,
including
• ECG,
• Pulse oximetry,
• Temperature, and
• Noninvasive blood pressure monitoring.
• If invasive monitoring is indicated, it is important to remember that acromegalic
patients with carpal tunnel syndrome may suffer from ulnar artery compression.

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Induction and maintenance of anesthesia
• Antibiotics and IV hydrocortisone(100 mg) are administered during induction of
anesthesia.
• Short acting agents are preferred for hemodynamic stability and to facilitate rapid
recovery.
• The suggested sequence :
1. PREMEDICATION : Fentanyl- 1 to 2 mcg/kg/Remifentanil 0.5 to 1 mcg/kg
2. PREOXYGENATION and VOLUNTARY HYPERVENTILATION
3. INDUCTION : Propofol : 1.25 to 2.5 mg/kg (or) Thiopentone- 3 to 6 mg/kg
4. NON DEPOLARISING MUSCLE RELAXANT : Vecuronium, Rocuronium
or Cisatracurium.
5. VENTILATION : adjusted to a PaCO2 of 35 mm of hg.
6. MAINTENANCE : Sevoflurane 0.5 to 1.5 % (or) Propofol 50 to 150
mcg/kg/min along with fentanyl(or remifentanil,sufentanyl) 1 to 2 mcg/kg/hr.

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• In a study conducted by Ali Z et al, of 90 patients undergoing transsphenoidal
pituitary surgery, patients were randomized to received propofol, isoflurane, or
sevoflurane maintenance with anesthetic level titrated to a bispectral index score
between 40 and 60.
• While time to emergence & to tracheal extubation were comparable; postoperative
cognition function was better in patients receiving propofol.
• Chowdhury et al. [22] investigated 26 patients undergoing pituitary surgery and
compared the effects of propofol versus sevoflurane on thermoregulation in
patients undergoing pituitary surgery.
• The aim was to determine which agent better preserved thermoregulation, as both
general anesthesia and pituitary tumors are known to impair thermoregulation and
predispose patients to hypothermia.
• The authors found no difference in the time for the temperature to fall 18 0C or in
the time to return to baseline in either group, suggesting equivalence.

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Fluid Management
• Hyperglycemia and hypoosmolality worsen brain edema and should be avoided.
• Target osmolality : 290 to 320 mOsm/kg
• Fluids of choice:-
• 0.9 % NaCl
• 6% Hydroxyethyl starch (304 mOsm/kg)
• Avoid glucose containing or hypo-osmolar solutions (eg. Ringer’s Lactate- 254
mOsm/kg)
• Hematocrit should be kept above 28%.
• Warm fluids should be administered to maintain normothermia for emergence
from anesthesia.

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FACILITATION OF SURGICAL EXPOSURE
1.LUMBAR CSF DRAIN:
• Indication of lumbar CSF drain is massive suprasellar extension of tumor.
• The catheter is introduced in a cephalad direction and 5-10 ml of normal saline is
pushed into the subarachnoid space, which by pressure effect pushes the
suprasellar extension of the tumor into the surgical field
• In addition, should the dura be breached during the procedure, the catheter can be
left in place postoperatively to act as a CSF drain to control any leak of CSF.
• A valsalva manoeuvre is a satisfactory alternative in case there is no lumbar drain.

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2.CONTROLLED HYPERCAPNIA:
• A permissive hypercapnia with PaCO2 of 60 mm Hg is recommended to increase
the ICP to shift the suprasellar part of a tumor into the sella for easy surgical
excision.
• A high normocapnia (40-45 mm Hg) is also recommended for the purpose.
• However, hypercarbia may result in hypertension, tachycardia and a reduced
myocardial perfusion.

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INTRAOPERATIVE COMPLICATIONS:
• Despite the semi-sitting position, air embolism is infrequent.
• Bleeding from carotid artery damage is not common but is a serious complication
if it takes place.
• Other structures likely to be damaged are cranial nerves II to VI, optic
nerves/chiasm and venous sinuses.
• Transcranial approach may result in all the complications like any other
craniotomies.
• Anticonvulsant prophylaxis is a must.

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 Emergence from Anesthesia
• The proximity of the pituitary to CN 2-6 makes assessment of cranial nerve
integrity an early postoperative goal; therefore rapid emergence is extremely
important.
• Pharyngeal packs are removed at the end of the procedure and suctioning of
mouth cavity is carried out.
• Coughing or bucking is avoided as it may precipitate hemorrhage, dislodge the
nasal pack and may cause CSF leakage.

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Postoperative Analgesia
• A retrospective study of nearly 900 patients found that the median postoperative
opioid requirements was less than 4mg of morphine.
• Endogenous opioids in CNS released due to manipulation of pituitary may be the
reason for lower requirement.
• The perioperative use of acetaminophen (or paracetamol) is opioid-sparing and
will not impair postoperative neurologic assessment.
• Bilateral infraorbital nerve blocks reduce postoperative pain in patients
undergoing endonasal approach.

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ENDOCRINE DISTURBANCES POST-
OP

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Postoperative hypopituitarism
Hypercortisolism is caused due to supraphysiologic ACTH secretion by the pituitary
tumor which in turns suppresses the release of ACTH from the normal gland.
• Risk for severe adrenal insufficiency present postoperatively due to removal of
tumor
• Steroid therapy  intra and postoperatively  Normal gland is chronically
suppressed

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Diabetus Insipidus

Retrograde damage to the

hypothalamic nuclei
Onset of DI in 0.5 to 1%
patients undergoing Sx
Impairment of transport
Post trans-sphenoidal
from hypothalamus to
surgery
posterior pituitary

Impairement of ADH
release from posterior
pitutary

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• DIAGNOSTIC CRITERIA :
• Hypotonic urine : <300 mosm, Specific gravity : <1.005
• High urine output : 4-18 L/day

• Occurs within 24-48 hours post operatively

S
FIRST • Classical symptoms of polyuria and polydipsia occur.
E
PHASE
C
O
N • Occurs one week after surgery
D
T • This is characterized by antidiuresis.
H
P
I
H
R • PERSISTENT DI
A
D • This is due to axonal death and cessation of ADH
S production
E
P
H
A
S 40
E
• Treatment: Most borderline cases of DI resolve spontaneously over a few days,
as posterior lobe function recovers.
• If the patient is awake and has a normal thirst mechanism, it is safest to allow free
access to fluid rather than attempt overzealous i.v. fluid and
DDAVP(Desmopressin acetate) replacement.
• Comatose patients, those with no thirst response, careful treatment with DDAVP
will usually be required under such circumstances.
• The recommended iv/im dose of DDAVP is 0.1 µg repeated as required.

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THANK YOU

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