Pituitary Surgery: Peri-operative Management

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Pituitary Surgery: Peri-operative Management Anna Boron, MD Faculty physician in Endocrinology in the Department of Internal Medicine at St. Joseph’s Hospital and Medical Center

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Pituitary Surgery: Peri-operative Management. Anna Boron, MD Faculty physician in Endocrinology in the Department of Internal Medicine at St. Joseph’s Hospital and Medical Center. What is the Likely Nature of the Sellar Mass?. Pituitary adenoma Craniopahryngioma Meningioma - PowerPoint PPT Presentation

Transcript of Pituitary Surgery: Peri-operative Management

Page 1: Pituitary Surgery: Peri-operative Management

Pituitary Surgery:Peri-operative Management

Anna Boron, MD

Faculty physician in Endocrinology in the Department of Internal Medicine at St. Joseph’s Hospital and Medical Center

Page 2: Pituitary Surgery: Peri-operative Management

What is the Likely Nature of the Sellar Mass?

• Pituitary adenoma• Craniopahryngioma• Meningioma• Pituitary hyperplasia• Infiltrative / infmammatory process• Infection• Apoplexy• Metastatic lesion /primary cancer

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Is There Any Compression (mass) Effect?

• Suprasellar, ”upward“ expansion – headache, visual field defects

• Lateral expansion – IV, V, VI cranial nerve palsy, headache, pituitary crisis (with apoplexy)

• Downward expansion – CSF leak, rarely blindness, temporal epilepsy

• Pituitary compression – hormonal deficiencies

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Which, if any, Hormone is Overproduced?

• Hyperprolactinemia – most frequent• GH hypersecretion - acromegaly• ACTH hypersecretion – Cushing’s disease• TSH hypersecretion - thyrotoxicosis• Gonadotropin producing tumors – so called

“nonfunctioning” pituitary tumors

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Which, if any, Hormone is Lacking?

• Functional suppression

• Physical suppression

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Peri~ and Postoperative Steroid Replacement

• In patients with known adrenal insufficiency “stress dose” of steroids is given, with postoperative taper to the home dose of steroids

• If postoperative cortisol level <10 mcg/dl, upon discharge - Rx hydrocortisone 15 mg q8am and 5 mg q2pm

• “Sick day” rule• Cosyntropin stimulation test • In Cushing’s disease – gradual taper from steroids

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Steroid Replacement

Every patient with central adrenal deficiency needs ID necklace or bracelet

Steroid supplementation:• Hydrocortisone• Prednisone• Dexamethasone

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Thyroid Replacement

• If hypothyroidism present pre-operatively, levothyroxine replacement should be started in dose 1.6 mcg/kg BW

• Thyroid function should be re-measured 6-8 weeks after dose initiated

• Therapy effectiveness should be assessed by plasma free T4

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Gonadotropins

1. Testosterone not routinely given before surgery

2. Testosterone replacement post surgery:– Depot testosterone 200 mg/ Q 2 weeks or 100 mg

weekly IM– Testosterone gel– Testosterone patch

3. Monitoring of hemoglobin and hematocrit, PSA, total testosterone level

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Gonadotropins

• Estradiol skin patches/ oral estrogen supplementation

• Progesterone supplementation in patients with intact uterus

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GH Deficiency

• GH supplementation in severe GH deficiency with stimulated GH <3 mcg/l or in patients with three or four other pituitary hormone deficiencies and low IGF-1 level

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Disorders of Water and Salt

1. Hypernatremia• Diabetes Insipidus (DI)• Fluid loss ( GI loss, insensible loss)

2. Hyponatremia• SIADH• Cerebral salt wasting• GI loss• Adrenal insufficiency/ hypothyroidism• edema

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Hypernatremia

• Plasma sodium >145 mmol/l• Relative sodium excess compared to whole body

water• Results either from net water loss or sodium load• Symptoms: weakness, confusion, seizures, coma• Complications: cerebral bleeding, permanent brain

damage and death, cerebral edema with overfast correction of hypernatremia

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Hypernatremia

• Prognosis - the mortality rate depends on the severity of the hypernatremia and the rapidity of its onset

• Severe hypernatremia - mortality rate of approximately 40-70% in elderly patients

• The level of consciousness is the single best prognostic indicator

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Diabetes Insipidus• Condition that occurs when the kidneys are unable to

conserve water as they perform their function of filtering blood

• The amount of water conserved is controlled by antidiuretic hormone (ADH)

• ADH is a hormone produced in the brain (hypothalamus), then stored and released from the pituitary gland

• Central DI - caused by a lack of ADH• Nephrogenic DI - caused by a failure of the kidneys to

respond to ADH

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Diabetes Insipidus

• Symptoms – excessive thirst, craving for ice water, excessive urine volume, dehydration

• Treatment – underlying condition should be treated when possible

• Central DI may be controlled with vasopressin (desmopressin, DDAVP), fluids

• If treated, diabetes insipidus does not cause severe problems or reduce life expectancy

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Hyponatremia

• Plasma sodium <135 mmol/l• Euvolemic hyponatremia - total body water

increases, but the body's sodium content stays the same

• Hypervolemic hyponatremia - both sodium and water content in the body increase, but the water gain is greater

• Hypovolemic hyponatremia - water and sodium are both lost from the body, but the sodium loss is greater

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Hyponatremia• Symptoms: abnormal mental status, confusion,

hallucinations, coma, seizures, fatigue, headache, muscle spasms or weakness, nausea, vomiting

• Treatment - depends on the type of hyponatremia and underlying cause and may include: fluids through a vein, medications (demeclocycline, vaptans, salt supplements), water restriction

• The outcome depends on the condition that is causing the low sodium

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