Download Introduction to Endocrine

Introduction to
Endocrine
Megan Conner, CRNA, MSN
Outline
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Acromegaly
Diabetes Insipidus
SIADH
Addison’s Disease
Cushing’s Disease
Hyperaldosteronism
Hypoaldosteronism
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Diabetes Mellitus
Hyperparathyroidism
Hypoparathyroidism
Hyperthyroidism
Hypothyroidsim
Pheochromocytoma
Acromegaly
• The excessive secretion of
growth hormone in an adult.
• Often from an adenoma in
the anterior pituitary gland
resulting in enlargement of
sella turcica.
• If hypersecretion occurs
before puberty, this is
gigantism, and the
individual grows tall,
because it occurs before
growth plate closure.
Pathophysiology
• Excessive production of growth hormone
– Does not induce bone lengthening, but rather
enhances the growth of periosteal bone.
– Bones become massive in size and thickness
leading to large hands and feet and
overgrowth of vertebrae (arthritis and
kyphoscoliosis)
– Soft tissue changes:
• Coarsened facial features: large bulbous nose,
supraorbital ridge overgrowth, dental malocclusion, and
prominent prognathic mandible
• Overgrowth of internal organs: liver, heart, spleen, and
kidneys
• Lung volume increases and may lead to V/Q mismatch
• Symptomatic cardiac disease due to cardiomyopathy,
hypertension (28%), and accelerated atherosclerosis
leading to CHF, arrhythmias, LVH, abnormal EKG
• Insulin antagonist effect of GH produce glucose
intolerance (50%) and DM (10-25%)
Clinical Manifestations
• From expanding tumor include: headaches
(55%), papilledema, visual field
defects(19%)
• Compression or destruction of normal
pituitary tissue may lead to
panhypopituitarisms
Common Features
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Skeletal overgrowth
Soft tissue overgrowth
Visceromegaly
Osteoarthritis
Glucose intolerance
Peripheral neuropathy
Skeletal muscle weakness
Extrasellar tumor extension
Treatment
• Aimed at restoring normal GH
levels
• Preferred initial: microsurgical
removal of tumor with gland
preservation via transsphenoidal
route
• Surgical ablation usually rapidly
successful at reducing tumor size,
and inhibiting GH secretion, and
alleviating some symptoms
• Administration of octreotide (a long
acting somatostatin) or
bromocriptine and gland irradiation
are treatment option for patients
who aren’t surgical candidates
Anesthetic Considerations
• Preanesthetic cardiac evaluation: assess EKG,
exercise tolerance, recent chest pain or SOB
• Due to increase risk of DM, check blood glucose
and electrolyte levels
• If impairment of adrenal or thyroid axis, then
stress-level glucocorticoid therapy and thyroid
replacement implemented preoperatively
• Entrapment neuropathies are common (CTS)
• Perform Allen’s test before placing radial a-line
to ensure adequate ulnar artery flow
Anesthetic Considerations
• May present with challenging airway so careful
examination of airway
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Prognathic mandible
Facial deformities and large nose
Large thick tongue (macroglossia)
Enlargement of thyroid tissue
Obstructive teeth
Hypertrophy epiglottis
Soft tissue overgrowth in upper airway
Subglottic narrowing
Vocal cord enlargement
Possible turbinate enlargement
Perioperative dyspnea, stridor, or hoarseness indicates airway
involvement
Transsphenoidal
hypophysectomy
• Pituitary lies in sella turcica of the
sphenoid bone
• Cavernous sinus is lateral and contains
CN III, IV, V, & VI and cavernous portion
of carotid artery
• Tumors under 10mm - if larger, will need
bifrontal craniotomy
• Transsphenoidal has lower morbidity and
mortality
• Incision in the gingival mucosa beneath
the upper lip, enters nasal cavity, dissects
through septum, and penetrates roof of
sphenoid sinus to sella turcica
Transsphenoidal
hypophysectomy
• Preoperative Preparation: replace the hormones and ameliorate
symptoms
• Problems with transsphenoidal
– Need for mucosal injections of epinephrine or use of
coccaine to reduce bleeding
– Accumulation of blood and tissue debris in pharynx and
stomach
– Risks of hemorrhage (Internal carotid art)
– Cranial nerve damage
– Pituitary hypofunction
– Venous air embolism - positioned slightly head up
– Diabetes insipidus develops postoperatively in 40% but
usually transient
• Monitoring as for craniotomies, precordial doppler for detecting
VAE, adequate venous access in event of massive hemorrhage
Diabetes Insipidus (DI)
• Reflexes the absence of antidiuretic hormone
(ADH) from one of two pathologies:
2) Failure of renal tubules
1) Destruction of
to respond to ADH
posterior pituitary
(nephrogenic DI)
(neurogenic DI)
•Hypokalemia
• Intracranial trauma
•Hypocalcaemia
• Hypophysectomy
•Sickle cell anemia
• Neoplastic invasion
•Obstructive uropathy
• Sarcoidosis
•Chronic renal
insufficiency
•Long term use of lithium
Clinical Manifestations
• Polydipsia
• Polyuria
• Poorly concentrated urine despite increase
plasma osmolarity
• Neurogenic and nephrogenic DI are
differentiated based on response to
desmopressin, which caused
concentration of urine in neurogenic DI,
but not nephrogenic DI
Treatment
• Careful monitoring of urine output, plasma
volume, plasma osmolarity.
• Isotonic fluids administered until osmolarity is
greater than 290.
• Neurogenic DI treated with desmopressin 3
mcg/kg.
• Nephrogenic DI treated with chlorpropamide, an
oral hypoglycemic drug that potentiates the
effect of ADH on renal tubules.
Anesthetic Considerations
• Monitoring of urine output and plasma
electrolyte concentrations
• In emergency surgery, CVP monitoring
may aid in evaluation of volume status
Syndrome of Inappropriate ADH
(SIADH)
• Excessive secretion of ADH
• Causes: head injuries, intracranial tumors, pulmonary
infections, small cell carcinoma of the lung,
hypothyroidism
• Clinical Manifestations: dilutional hyponatremia,
decreased serum osmolarity, and reduced urine output
with high osmolarity  weight gain, skeletal muscle
weakness, mental confusion, convulsions
• Diagnosis: is done by exclusion of other causes of
hyponatremia
• Treatment:
– fluid restriction (800 ml/day)
– if mental confusion, then more aggressive treatment required: IV
hypertonic saline, lasix
Addison’s Disease
• Is primary adrenal insufficiency
• Reflects the absence of cortisol and aldosterone
due to destruction of adrenal cortex
• Most common cause is adrenal hemorrhage
secondary to abnormal coagulation
• Other causes include: sepsis, accidental trauma,
or surgical trauma
• Diagnosis requires measurement of
plasma cortisol concentration within
1 hour of administration of
adrenocorticotropic hormone (ACTH)
Clinical Manifestations
• Clinical symptoms reflect glucocorticoid and
mineralocorticoid deficiency
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Weakness
Fatigue
Reduce appetite with weight loss
Abdominal pain
Vomiting
Diarrhea
Volume depletion leading to orthostatic hypotension
Hypoglycemia
Hyponatremia
Hyperkalemia
Lack of catecholamines
In women, oligomenorrhea or amenorrhea
Clinical Manifestations
• The adrenal-pituitary axis is intact in
primary adrenal insufficiency, and ACTH
concentrations are elevated as a result of
reduced production of cortisol.
• Increase ACTH leads to increased
melanin formation in skin and
hyperpigmentation of knuckles, knees,
elbows, lips, buccal mucosa.
Treatment
• Normal adults secrete 15-25 mg of cortisol
(hydrocortisone) and 50 to 250 mcg of
aldosterone per day
• Therapeutic replacement of glucocorticoids is
typically 50% greater than basal adrenal output
so the patient is covered for mild stress
• Oral replacement of glucocorticoids (with
prednisone or hydrocortisone) and
mineralocorticoid (with fludrocortisone)
• Treatment entails both glucocorticoid and
mineralocorticoid replacement
• Acute adrenal insufficiency (Addisonian Crisis) is
medical emergency, and treatment includes
fluids, steroid replacement, inotropes, electrolyte
correction.
Anesthetic Considerations
• Provide exogenous corticosteroid
supplementation
• Avoid etomidate
• Sensitive to drug induced myocardial
depression
• Initial dose of muscle relaxant reduced
due to skeletal muscle weakness
• Consider monitoring glucose and
electrolytes
Cushing’s
Disease
Cushing’s Disease
• Adrenocortical hyperfunction; chronic
glucocorticoid excess.
• Clinical manifestations from excess
glucose production caused by
hypersecretion of cortisol
• Caused by adrenal neoplasms,
hypersecretion of ACTH, and ectopic
ACTH syndrome
Cushing’s Syndrome
• Caused by excess glucocorticoid hormone
• Most common cause is therapeutic
administration of supraphysiologic doses
of glucocorticoids (as in treatment of
arthritis, asthma, autoimmune disorders,
allergies, ect.)
• Endogenous Cushing’s syndrome result of
one of three pathogenic disorders:
• Pituitary tumor (Cushing’s Disease)
• Adrenal tumor
• Ectopic hormone production
• Cushing’s Disease: specifically denotes
anterior pituitary tumor cause of the
syndrome
• Pituitary tumor produces excessive
amount of adrenocorticotropic hormone
(ACTH)
• Associated with bilateral adrenal
hyperplasia
• Excess ACTH results in increase skin
pigmentation
• Most common cause of endogenous
Cushing’s syndrome
• Adrenal Cushing’s syndrome is caused
by autonomous cortisol production (ACTH
independent) by an adrenal tumor.
• Associated with suppressed plasma ACTH
levels
• Usually unilateral and can be malignant
• This form of hyperadrenalism accounts for
20-25% of patients with Cushing
syndrome
• Ectopic hormone production
Diagnosis
• By measuring plasma cortisol
concentration the morning after a dose of
dexamethasone
• Dexamethasone suppresses plasma
cortisol in physiologically normal patients,
but not in those with hyperadrenocorticism
• Also based on elevations of plasma and
urinary cortisol level and of urinary 17hydroxycorticosteroids
Clinical Manifestations
• Reflects cortisol excess from endogenous or exogenous
sources and leads to:
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Central obesity
Hypertension
Glucose intolerance
Plethoric facies
Purple striae
Muscle weakness
Bruising
Osteoporosis
Poor wound healing
Susceptibility to infection
Thin skin (atrophic unable to withstand stress of normal activity)
Weigh gain in a yoke-like pattern over clavicles, neck, trunk, abdomen, and
cheeks
• Women manifest a degree of maculinization (hirsutism, hair thinning, acne,
oligomenorrhea, amenorrhea)
• Men manifest a degree of feminization (gynecomastia, impotence)
Mnemonic
• C - Central obesity, Cervical fat pads,
Collagen fiber weakness
U - Urinary free cortisol and glucose increase
S - Striae, Suppressed immunity
H - Hypercortisolism, Hypertension,
Hyperglycemia, Hirsutism
I - Iatrogenic (Increased administration of
corticosteroids)
N – Non-iatrogenic (Neoplasms)
G - Glucose intolerance, Growth retardation
Clinical Manifestations
• Mineralocorticoid effects include:
• Fluid retention
• Hypokalemic alkalosis
Treatment
• Depends on cause of Cushing’s syndrome
• Transsphenoidal hypophysectomy is a primary treatment
for Cushing’s syndrome cause by anterior pituitary
tumor.
– Complications in 5% of patients and include transient DI, CSF
rhinorrhea, and hemorrhage.
• Adrenal Cushing’s syndrome treated by surgical removal
of adrenal adenoma. Because contralateral adrenal
gland is preoperatively suppressed, glucocorticoid
replacement may be necessary for months until adrenal
function returns. Bilateral adrenalectomy is a/w post-op
complications and permanent glucocorticoid and
mineralocorticoid deficiency results.
• For ectopic ACTH-secreting tumor, treatment of choice is
surgical removal. If surgical removal is not feasible (ex.
metastatic carcinoma), metyrapone and ketoconazole
may be used to normalize cortisol levels.
Anesthetic Considerations
• Perioperative considerations focus on
normalizing BP, blood glucose levels,
intravascular fluid volume, and electrolyte
concentrations
• Spironolactone
• Osteoporosis
• Skin damage
• Increased risk of infection
• Exaggerated effect of muscle relaxants
may be seen
Anesthetic Considerations
• With unilateral or bilateral adrenal resection,
glucocorticoids administered at dose equivalent
to adrenal output for maximum stress
(hydrocortisone 100 mg IV Q8H)
• Glucocorticoids continued post-op
• Increased frequency of thromboembolic
phenomena (DVT 11%, PE 2-3%)
• Anesthetic management should take into
account for effects of excess cortisol secretion
on BP, blood glucose, and electrolytes.
Hyperaldosteronism
• Primary hyperaldosteronism (Conn’s
syndrome) is excess secretion of
aldosterone from a functional tumor
independent of physiologic stimulus
• Secondary hyperaldosteronism is when
increased renin secretion is responsible
for excess secretion of aldosterone
Clinical Manifestations
• Hyperaldosteronism should be suspected if diastolic
hypertension (100-125 mmHg) and plasma potassium <
3.5 mEq/L
• HTN due to aldosterone-induced sodium retention and
leads to increased extracellular fluid volume
• Hypokalemic metabolic alkalosis due to aldosteroneinduced renal excretion of potassium and hydrogen
• Skeletal muscle weakness (due to hypokalemia)
• Hypokalemic nephropathy polyuria and inability to
optimally concentrate urine
Diagnosis
• Confirmed by increased plasma
concentration of aldosterone and
increased urinary potassium excretion
(greater than 30 mEq/L) despite coexisting
hypokalemia
• Measurement of plasma renin activity
permits classification of the disease as
primary (low renin activity) or secondary
(increase renin activity)
Treatment
• Supplemental potassium
• Administration of aldosterone antagonist
(spironolactone)
• Antihypertensives
• Diuresis with potassium-sparing diuretic
(triamterene) to minimize drug induced
hypokalemia
• Surgical excision is definitive treatment for
aldosterone-secreting tumor
Anesthetic Considerations
• Pre-op correction of hypokalemia and
treatment of hypertension
• Assess for hypovolemia as evidence by
orthostatic hypotension
• Consider invasive monitoring (CVP, PAC)
• Consider supplementation with exogenous
cortisol
Hypoaldosteronism
• Is suggested by hyperkalemia in the absence of renal
insufficiency
• Can be caused by:
– a congenital deficiency of aldosterone synthetase or
hyporeninemia from a defect in juxtaglomerular apparatus
– Treatment with ACE inhibitor leading to a loss of angiotensin
stimulation
• Hyporeninemic hypoaldosteronism typically occurs in
patients >45 with chronic renal disease, DM, or both.
• Indomethacin-induced prostaglandin deficiency is a
reversible cause of this syndrome.
Clinical Manifestations
• Heart block due to hyperkalemia
• Postural hypotension with or without
hyponateremia
• Hyperchloremic metabolic acidosis
Treatment
• Liberal sodium intake
• Daily administration of hydrocortisone
Anesthetic Considerations
• Pre-op check of serum potassium level (should
be less than 5.5 mEq/L for elective surgery)
• EKG to check for effects of hyperkalemia (tall T
waves, heart block)
• Avoid hypoventilation to prevent further increase
in serum potassium
• Avoid succinylcholine
• IVF without potassium
• Hypovolemia corrected with fluid
replacement possibly with help of CVP
Diabetes Mellitus
• A complex metabolic derangement caused
by relative or absolute insulin deficiency
• Affect 17 million in US (6% of population)
• Rise attributed to overweight population,
sedentary life-styles, and rise in number of
elderly people
• Insulin-dependent DM (IDDM or type 1 DM)
– Typically develops before age 16
– From autoimmune destruction of pancreatic beta
cells, may be precipitated by a viral infection
– 15% have other autoimmune diseases
– Depend on exogenous insulin to prevent ketoacidosis
• Non-insulin-dependent DM (NIDDM, adult onset
DM, or type 2 DM)
– Often develops after age 35
– Prevalence increase with age among black women
– Many may require insulin therapy, but not prone to
ketoacidosis
– Patients are typically overweight (90%)
Complications of DM
• Ketoacidosis: a serious acute metabolic
complications defined as hyperglycemia in
the presence of metabolic acidosis:
– Nausea, vomiting, lethargy, signs of
hypovolemia with dehydration d/t osmotic
effect of glucose
• Causes:
– Poor compliance with insulin therapy, insulin
resistance d/t infection, silent MI, beta 2
agonist to inhibit labor
Complication of DM
• NIDDM: macroangiopathies such as CAD,
cerebrovascular disease, PVD with sequelae of
premature MI, angina pectoris or peripheral vascular
insufficiency
• IDDM: microvascular complications and disorders of the
nervous system such as retinopathy, nephropathy,
autonomic and peripheral nervous system dysfunction
• May also have:
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Arterial disease
Cataracts
Peripheral neuropathies
Arterial thrombotic lesions
Delayed wound healing
Stiff joint syndrome (affecting laryngoscopy)
Treatment
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Diet
Oral hypoglycemic drugs
Exogenous insulin
For NIDDM: treatment or avoidance of
obesity
• Transplantation of pancreatic tissue
Anesthetic Considerations
• DM patients have a higher morbidity and
mortality in perioperative period due to
organ damage a/w with long-term disease
• Ischemic heart disease is the most
common cause of perioperative mortality
• Schedule DM patients early in the day
• Careful pre-op assessment:
– HTN, CAD, ANS dysfunction result in a labile
cardiovascular course
– Assess cardiovascular and volume status
– EKG
• Autonomic dysfunction
– Delayed gastric emptying (gastroparesis) 20-30%
– Prone to N/V, aspiration, abdominal distension
– Consider treatment with H2 blockers, reglan,
preinduction antacids, ETT over LMA for GA
– May have impaired respiratory response to hypoxia
– Sensitive to respiratory depressant effects of
sedatives and anesthetic and require vigilance in
perioperative period
• Restrict joint mobility: limited motion of
atlanto-occipital joint  difficult intubation
– Prayer sign: inability to approximate palms of hands
and fingers
Prayer sign
• Check for kidney disease (urinalysis, serum
creatinine, BUN) and results may affect
anesthetic drug selection
• Pre-op blood glucose, and possible A1C
• Check electrolytes
• Sustain hyperglycemia with osmotic diuresis
may indicated fluid deficits and electrolyte
depletion
• Adequate hydration and good urine output
maintained
• Avoided lactate-containing solution d/t lactate
conversion to glucose and contribute to
hyperglycemia
• Assess oral hypoglycemia and insulin regimens
Oral hypoglycemic agents
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Sulfonylureas:
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Increase secretion of insulin from the pancreas and improve tissue sensitivity
to insulin
Require functioning beta cells so not for IDDM patients
SE: hypoglycemia, cholestatic jaundice, rashes, GI symptoms
Chlorpropamide SE include: SIADH and hyponatremia
Alpha glycosidase inhibitors (Acarbose and Miglitol):
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Blocks intestinal enzymes that digest starches into absorbable
monosaccharides resulting in slower and lower rise in plasma glucose
Thiazolidinediones (Rosiglitazone and Pioglitazone):
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Decrease hepatic glucose output and reduce insulin resistance in the patient
with NIDDM by sensitizing the insulin receptor for glucose uptake
Liver enzymes must be monitored closely
Biguanides (Metformin):
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Decreases hepatic glucose production and increases peripheral insulin
sensitivity
Lactic acidosis is a potentially fatal problem, it is precipitated by drug
accumulation so mild renal impairment is a contraindication
Nonsulfonylurea secretagogues (meglitinides and D-phenylalanine):
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Increase insulin production by pancreatic beta cells similar to sulfonylureas
Must be taken before each meal, and if a meal is missed the drug should be
omitted
Insulin Preparations
• Differ in onset and duration after SQ administration, can
use implantable pumps or syringes
• Greatest risk is hypoglycemia
• Three classes: short-acting, intermediate-acting, and
long-acting
• Imperative know the patient’s normal insulin dosage
regimen and treatment compliance
• Most diabetics are on a regimen that consists of both
rapid and intermediate acting insulin taken before
breakfast and at evening meal
• Long-acting is discouraged in the perioperative period
• Lantus:
– a recombinant DNA analogue of human insulin, and taken once
a day
– Forms micro-precipitates in SQ tissue that delays its absorption
and prolongs its effect
– Has no peak effect, but behaves like an insulin infusion
Characteristics of Insulin
Preparations
Type of Insulin
Onset of
Action
Peak
Action
Duration
Route
30-60 min
1-2 hr
5-12 hr
IV, SC, IM
10-30 min
10-30 min
30-60 min
30-60 min
3-5 hr
3-5 hr
SC
SC
1-2 hr
4-8 hr
10-20 hr
SC
2-4 hr
1-2 hr
8-20 hr
No peak
16-24 hr
24 hr
SC
SC
Short-acting
Regular
Rapid-acting
Aspart (Novolog)
Lispro (Humalog)
Intermediateacting
NPH/ Lente
Long-acting
Ultralente
Glargine
Time course is based on SC administration.
Intraoperative Management
• Surgery produces a catabolic stress response and
elevates stress-induced counter-regulatory hormones.
• Hyperglycemic, ketogenic, lipolytic effects of counterregulatory hormones in the diabetic patient compound
the state of insulin deficiency.
• Therefore, hyperglycemia is common in the surgical
period.
• Regional and general anesthesia have been used safely.
However, general anesthesia has been shown to induce
hormonal changes that accentuate glycogenolysis and
gluconeogenesis  hyperglycemia.
Anesthetic Considerations
• Careful positioning and padding in the diabetic patient d/t
decreased tissue perfusion and peripheral sympathetic
neuropathy  skin breakdown and ulceration
• Checking glucose is central to safe practice: pre-op,
post-op, and intra-op for long procedures
• Hyperglycemia: impair wound healing, impair wound
strength, increased with risk of infection, worsens
neurologic outcome after ischemic brain injury
• Goal to avoid hypoglycemia and metabolic
derangements
• Patients under GA usually maintain with mild transient
hyperglycemia to avoid catastrophic effects of
hypoglycemia
• There is a debate over tight versus non-tight blood
glucose control
Non-Tight Control
• Less intensive control, but avoids marked
hyperglycemia and dangerous hypoglycemia
• This is the traditional approach for stable
diabetic patient undergoing elective operations
• Technique:
– DOS fasting blood glucose level measured
– IV infusion 5% Dextrose at 125ml/ 70 kg body weight
– After infusion started, 30-50% of patient’s normal
intermediate insulin (NPH or Lente) is administered
– Glucose containing infusion continued throughout
surgery. Additional fluid requirement with
administration of second glucose-free solution
– Glucose checked every 1-2 hours during surgery
– If glucose >200, treated with a IV bolus of regular
insulin
• On average, 1 unit of regular insulin can be
expected to decrease blood glucose level 50
mg/dL
• Advantages: easy to implement, successful in
preventing significant hypoglycemia and other
metabolic extremes, diabetic ketoacidosis, and
hyperosmolar states
• Absorption of SQ insulin is unpredictable and
erratic d/t BP, blood flow, and temperature
variations that occur with anesthesia
• Onset and peak of pre-op intermediate-acting
insulin may not correspond with time of surgical
stress, especially if there is a delay in surgery
• Half life of regular insulin is short and a roller
coaster profile may develop
Tight control
• Maintains blood glucose within narrow range of 100-180
mg/dL
• Require infusion pumps and more frequent blood
glucose checks
• Recommended for IDDM patient having major surgery
and for patient with poorly controlled NIDDM
• Technique:
– Infusion of 5% dextrose with 0.32 units regular insulin/g of
dextrose (16 units/L), with 20 mEq KCL at 100 ml/hr
– Infusion started when glucose >200
– Glucose checked every hour, and potassium checked after first
hour
– If patient has higher insulin needs, an additional 1-2 units of
insulin can be added to bag
– Additional fluid requirement with administration of second
glucose-free solution
• Blood glucose levels less than 80 mg/dL treated with
D50W, and rechecked in 30 minutes
• 70 kg patient, 15 ml of D50W expected to raise
blood glucose concentration by about 30 mg/dL
• Higher insulin infusion requirement are usually
required in renal transplantation, CABG, obese
patients, septic patients, and those on steroid
therapy
• Advantages of tight control: insulin infusion can be
finely regulated on a hourly basis, periods of
hyperglycemia are less likely, deleterious effect of
hyperglycemia may be prevented, continued until
the patient is ready to eat and SQ insulin or oral
agent can be restarted
NIDDM and Oral Hypoglycemic
Agents
• Note duration of action for oral agents
• Discontinuing long-acting agents 2 to 3 days before
surgery and converting to shorter-acting agents or insulin
affords better perioperative glucose control
• Metformin should be discontinued 2 days before surgery
d/t surgical risks of hypotension and renal hypoperfusion
place patients at risk for lactic acidosis
• For well-controlled NIDDM patient in for minor to
moderate surgery may continued until the evening of
surgery
• Regardless of the technique, glucose measured
frequently and hyperglycemia treated
Hyperparathyroidism
• Increased parathormone
• Serum calcium may be
increased, decreased, or
unchanged
• Classified as primary,
secondary, or ectopic
• Can result from
parathyroid adenoma,
gland hyperplasia, or
parathyroid cancer
• Primary hyperparathyroidism
– Excessive secretion of parathormone by a benign
parathyroid adenoma
– Carcinoma of a parathyroid gland
– Hyperplasia of parathyroid glands
• Secondary hyperparathyroidism
– Compensatory response of parathyroid glands to
secrete more parathormone to counteract a disease
process that produces hypocalcemia
• Ectopic hyperparathyroidism
– Secretion of parathormone by tissues other than the
parathyroid glands (occurs with carcinomas of the
lung, breast, pancreas, kidney, and
lymphoproliferative diseases)
Clinical Manifestations
• Overactivity leads to high serum calcium
– Usually asymptomatic until level more than 11-12 mg/dL
– Greater than 14 mg/dL is life-threatening and demands
immediate treatment
– Patients with carcinomas usually have increased levels greater
than 7.5 mEq/L
• Clinical signs and symptoms of hypercalcemia
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Early: N/V, skeletal muscle weakness, hypotonia
Inability to concentrate urine, polyuria
Oliguric renal failure can occur in advanced cases
Renal stones, peptic ulcer disease, HTN, bone pain, pathologic
fractures hallucinations, mood disturbances, and acute or
chronic pancreatitis
“Stones, Bones, & Groans”
• Stones
– Nephrolithiasis, nephrocalcinosis, polyuria
• Bones
– Osteoclastic absorption of bone overwhelms osteoblastic
deposition
– Weakened bones filled with decalcified cavities painful and
susceptible to fracture
– Destructive bone disease a/w hyperparathyroidism is osteitis
fibrosa cystica
– Despite increased mobilization of phosphorus from bone, serum
phosphate concentration remains normal to low d/t increased
urinary excretion
• Groans
– Pancreatitis
– Peptic ulcer disease
• HTN
• Heart: shortened ventricular refractory
period, bradyarrhythmias, BBB, heart
block
• Other features: muscle weakness,
anorexia, confusion, N/V, lethargy
• Patients with CRF or gastrointestinal
malabsorption, may develop
compensatory parathyroid gland
hyperplasia or secondary
hyperparathyroidism in response to
hypocalcemia
• Clinical course still includes skeletal
symptoms in primary disorder, but is
seldom a/w hypercalcemia
Treatment
• Saline infusion (150 ml/hr)
• Loop diuretics (lasix 40-80 mg IV Q2-4hrs)
• Thiazide diuretics not used, because enhance renal
tubular reabsorption of Ca
• Bisphosphonates (disodium etidronate) is the drug of
choice in life-threatening hypercalcemia. These drugs
bind to hydroxyapatite in bone and act as potent
inhibitors of osteoclastic bone resorption.
• Hemodialysis
• Calcitonin (inhibits of osteoclastic bone resorption)
• Surgical removal is treatment in symptomatic primary
hyperparathyroidism.
Anesthetic Considerations
• Done under GA
• Cervical plexus block has been used, especially
in elderly and medically compromised patients
• Parathyroid tissue can be in ectopic places
(mediastinum, carotid sheath, or thymus gland)
• Minimal EBL
• Monitor serum Ca, Mg, and Phos post-op
• Ca usually returns to normal in 3-4 days
Anesthetic Considerations
• Treat of hypercalcemia pre-op (saline hydration,
lasix, inhibitors of osteoclastic bone resorption)
• Dehydrated d/t anorexia, vomiting, impaired
ability of kidneys to concentrate urine
– Hydration with non-calcium containing solutions to
dilute serum Ca, maintain adequate GFR and Ca
clearance, and to ensure adequate intravascular
volume
– Foley, CVP, frequent assessment of serum
electrolytes
• Elevated Ca depresses central and peripheral nervous
systems.
• Avoid pre-op sedatives if patient appears lethargic or
confused.
• May have decrease GA requirements.
• EKG changes with hypercalcemia: shortened QT interval and
prolonged PR interval.
• Dysrhythmias and HTN may respond to Ca channel blockers
(verapamil 5-10mg IV).
• Due to significant bone disease, patients are susceptible to
fractures and requires careful padding and positioning.
• Muscle weakness, hypotonia, and muscle atrophy increase
sensitivity to NDMR. Titrate MR with PNS.
• Prophylactic antiemetics, because these patients are prone to
N/V.
• With secondary hyperparathyroidism, assess renal status,
and associated complication of CRI (volume overload,
anemia, abnormal electrolytes).
• Alkalosis protects against hypercalcemia by shifting the
ionized calcium to the protein-bound form.
Hypoparathyroidism
• The deficient or absent secretion of parathyroid
hormone or a peripheral resistance to its effect
• Pseudohypoparathyroidism: a congenital
disorder in which the release of parathormone is
intact but kidneys are unable to respond to the
hormone
• Causes: inadvertent removal of parathyroid
tissue, irradiation, autoimmune destruction,
chronic severe Mg deficiency (alcohol abuse,
poor nutrition, malabsorption)
Clinical Manifestations
• Low serum Ca
• Elevated Phos d/t decreased renal excretion of
phosphate
• Clinical signs correlate with degree of hypocalcemia and
rate of calcium decline (sudden drop = more severe
symptoms)
• Cardinal features: neuromuscular excitability, muscle
spasms, hypocalcemic tetany
– Muscle cramps, perioral paresthesias, numbness in feet and
toes, hyperactive deep tendon reflexes
– Feeling of restlessness or hyperirritable
– Life threatening laryngospasm can occur stridor, labored
respirations, asphyxia
Clinical Manifestations
• Classic manifestations of hypocalcemic tetany:
– Chvostek’s sign: contracture or twitching of ipsilateral
facial muscles when the facial nerve is tapped at the
jaw ankle
– Trousseau’s sign: elicited by inflations of BP cuff
slightly above systolic level. Ischemia aggravates
muscle irritability in presence of decreased Ca and
caused flexion of wrist and thumb with extension of
fingers (carpopedal spasm)
Treatment
• IV infusion of calcium (calcium gluconate)
until signs of neuromuscular irritability
disappear
• Correct any coexisting respiratory or
metabolic alkalosis
• Asymptomatic hypocalcemia corrected
with oral Ca and vitamin D
• Thiazide diuretics
• Causes:
– Transient post-op hypocalcemia result from
parathyroid gland suppression (by pre-op
hypercalemia)
– Rapid bone uptake of calcium (“hungry bone
syndrome”)
– Inadvertent removal of all parathyroid gland
tissue
Anesthetic Considerations
• Goal to prevent further decrease in serum calcium
concentrations and treat adverse effects of
hypocalcemia
– Avoid hyperventilation
– Watch for musculoskeletal irritability (seen at serum Ca 67mg/dL)
– May have altered response to MR
– Periodic measurement of serum Ca and iCa
– Risk of laryngeal muscle spasm that may cause life-threatening
airway compromise
– EKG changes: prolonged QT interval reflecting delayed
ventricular repolarization and a predisposition to ventricular
dysrhythmias
– Decreased cardiac contractility
– Hypotension
– Vigorous diuretics can augment Ca loss
• Respiratory stress following parathyroid
surgery may be d/t laryngeal muscle
spasm, edema, bleeding in the neck or
bilateral recurrent laryngeal nerve injury
– Unilateral RLN injury produces hoarseness
usually requires observations
– Bilateral RLN injury cause aphonia and
requires immediate airway support and
intubation
• Circulating levels of ionized calcium can decline
in perioperative period:
– Increases in circulating anions (bicarb, phos, citrate)
lower iCa and result in tetany, so avoid:
• Hyperventilation
• Rapid transfusion of citrated blood
• Rapid administration of bicarb
• Initial treatment: 100-200 mg of elemental Ca
over 10 minutes
• For maintenance: 1-2 mg/kg/hr of elemental Ca
diluted in 50-100 ml of saline
• Continue monitoring electrolytes during
replacement: Ca, Mg, Phos, K, and creatinine
Hyperthyroidism
• Increased in thyroid function d/t and excess
supply of thyroid hormones, and associated with:
–
–
–
–
Grave’s Disease
TSH overproduction
Pregnancy
Subacute thyroiditis (excess hormone leaks out d/t
inflammation)
– Ovarian tumors and metastatic thyroid carcinoma can
produce extrathyroid hormone
– Exogenous consumption of thyroid hormone
Etiology
•
•
•
•
TSH released from anterior pituitary 
Iodine taken up into thyroid gland
Iodine incorporate into tyrosine residue 
Hormones triiodothyronine (T3) and thyroxine
(T4) are formed and stored
– Peripheral tissues convert T4 to T3
• T3 is three times more potent than T4, and has a shorter half
life
• Both T3 and T4 are partially bound to plasma protein thyroidbinding globulin (TBG); only unbound forms are
pharmacologically active
• TBG levels can increase with:
–
–
–
–
Acute liver disease
Pregnancy
Acute intermittent porphyria
Medications (oral hyoglycemics, exogenous
estrogens, clofibrate, opiods)
• TBG levels can decrease with:
–
–
–
–
Chronic liver disease
Nephrotic syndrome
Anabolic steroids
Acromegaly
• TBG has no direct role in cell metabolism, but its
concentration can alter diagnostic tests for
thyroid disease
Clinical Manifestations
• Lab findings:
– Elevated T3 and T4
– TSH may be normal or decreased
•
•
•
•
•
•
•
•
•
Nervousness
Tachycardia
Goiter
Tremors
Muscle weakness
Heat Intolerance
Weight loss despite high caloric intake
Exophthalmos
Cardiac: worsening angina, unexpected onset of CHF, or Afib may
indicate hyperthyroidism, especially in elderly d/t increase hormones
aggravate underlying heart disease
Clinical Manifestations
• Thyroid storm (thyroidtoxicosis): an abrupt
exacerbation of hyperthyroidism caused by a
sudden excessive release of thyroid gland
hormones into circulation
• Hyperthermia, tachycardia, CHF, dehydration,
and shock commonly occur
• Precipitated by surgical stress, but usually seen
6-18 hrs post-op
• Mimics MH, sepsis, hemorrhage, or transfusion
or drug reaction
Treatment
• Treatment of hyperthyroidism: antithyroid drugs,
subtotal thyroidectomy, or radioactive iodine
• Treatment of thyroid storm (thyrotoxicosis):
active cooling, hydration, Beta blockade,
steroids if indication of adrenal insufficiency, and
initiation of long term therapy
• Six weeks are required to become euthyroid
Anesthetic Considerations
•
•
•
•
•
•
•
•
Premed: consider Beta blockers
Avoid sympathetic stimulation
Eyes protected if exophthalmos
Drug metabolism and anesthetic requirements
increased
Titrate MR with PNS, d/t presence of muscle
weakness
Treat hypotension with direct-acting agents
Regional anesthesia may be beneficial, b/c
blocks sympathetic response
Local anesthetics with epi may lead to
arrhythmias
Hypothyroidism
• Primary: destruction of the thyroid gland and
there is an adequate level of TSH
–
–
–
–
Chronic thyroiditis
Subtotal thyroidectomy
Radioactive iodine therapy
Irradiation of neck
• Secondary: d/t CNS dysfunction and results in
decreased TSH
– Hypothalamic dysfunction (leading to a
thyrotropin-releasing deficiency
– Anterior pituitary dysfunction (TSH deficiency)
Clinical Manifestations
• Primary: decreased T3 and T4, increased
TSH
• Secondary: decreased T3,T4, TSH
• Resin T3 uptake decreased in both
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Lethargy
Constipation
Cold intolerance
Facial edema with enlarged tongue
Reversible cardiomyopathy
Pericardial effusion
Dilutional hyponatremia
Ascites
Anemia
Adynamic ileus with delayed gastric empting
Adrenal atrophy with decrease cortisol production
Decreased water excretion
Decreased cardiac output
Bradycardia
Hypovolemia
Diminished baroreceptors reflexes
Myexdema coma (profound hypothyroidism)
Anesthetic Considerations
• Treatment requires exogenous supplementation
• T4 requires 10 days to have an effect and T3 begins to
have an effect in 6 hours
• Treatment of myxedema coma: IV administration of T3,
and if adrenal insufficiency suspected, cortisol
• Digitalis should be used sparingly to treat CHF, b/c it is
not well tolerated by patients with hypothyroidism
• Careful fluid replacement is important, but these patient
may be vulnerable to water intoxications and
hyponatremia
• If emergency surgery is necessary:
– Avoidance of pre-op sedation d/t profound
CNS and respiratory sensitivity to depression
– Cortisol supplementation considered
– Intravascular volume optimized
– Anemia corrected
– Airway problems r/t to large tongue
– Poor gastric empting
– Increased sensitivity to all depressants
medications
Pheochromocytoma
•
•
•
•
Catecholamine-secreting tumors derived most
commonly (90%) form adrenomedullary
chromaffin cells
Extraadrenal pheochromocytomas have been
found anywhere from the pelvis to the skull
bases
They are most often extraadrenal and secrete
dopamine
Malignant pheochromocytomas usually spread
through venous lymphatic channels to the liver
Etiology
• Rare, occur less than 0.5% of
hypertensive patients
• Usually occurs in 3rd to 5th decade
• Maybe associated with neurocutaneous
syndromes (von Hippel-Lindau teberous
sclerosis, Sturge-Weber syndrome,
multiple endocrine neoplasia (MEN) type
2A or 2B)
• Pheochromocytomas produce, store, and
secrete catecholamines (mostly Norepi
and epi)
Clinical Manifestations
• Diagnosis is made by a 24 hour urine test to
measure “free” norepinephrine
• Normotension despite increase plasma
concentration of catecholamines is thought to
reflect a down regulation of alpha receptors
• Clonidine suppresses hypertension from
neurogenic release but not from a
pheochromocytoma
• CT to localize and diagnosis pheochromocytoma
•
•
•
•
•
•
•
•
•
•
•
•
Hypertension
Diaphoresis*
Tachycardia*
Headache*
Tremulousness
Palpitations
Weight loss
Sense of doom
Anxiety
Pallor
Orthostatic hypotension
Hct >45
• Paroxysm can be triggered by:
– Acute physical stress
– Abdominal palpitation
– Defecation
– Hypotension
– Activations of sympathetic NS
– Micturition (if in urinary bladder)
• Not usually triggered by mental or
psychological stress
• Symptoms usually reflect predominance of alpha
adrenergic activity over beta adrenergic effects
– Alpha adrenergic inhibition of insulin, mild
hyperglycemia
– Increased cardiac output and heart rate
– Increased metabolism
– Increased oxygen consumption
– Hyperthermia
– Vasoconstriction in extremities may produce pain,
paresthesias, intermittent claudication or ischemia
• Hypertension is most common symptom (90%),
and paroxysmal hypertension (40-50%)
• Sustained HTN resistant to conventional
treatment
• If pheochromocytoma are predominately epi
secreting, HTN can alternate with periods of
hypotension a/w syncope
• Coronary artery spasm can  to MI or CHF
• EKG changes
• Death d/t CHF, MI, or intracerebral hemorrhage
Treatment
• Surgical excision of tumor after medical
control is optimized
– Alpha blockade to normalize BP 
– Normotension facilitates and increase in
intravascular fluid volume  decreased
hematocrit
– If cardiac arrhythmias or tachycardia persist
after alpha blockade, then beta blockade is
indicated in the absence of CHF
• Pre-op aims at reversed effect of excessive
adrenergic stimulation.
– Antihypertensive therapy
• Alpha adrenergic antagonist or calcium channel blockers
– Volume replacement
• End points for patients awaiting surgery:
– BP should not be >165/90
– BP on standing should not be lower than 80/45
– ECG with no ST segment or T-wave abnormality that
can not be attributed to a permanent defect
– No symptoms of catecholamine excess
– No more than one PVC every 5 minutes
Anesthetic Considerations
• Select drugs that do not stimulate
catecholamine release
• Avoiding sympathetic nervous system
activation
• Implement monitor techniques that
facilitate early and appropriate intervention
when catecholamine-induced changes in
cardiovascular function occur
• Done with an open laparotomy
• Avoid:
–
–
–
–
–
–
–
–
–
Dopamine antagonist
Contrast media
Indirect-acting agents
Drugs that block neuronal catecholamine reuptake
Histamine
Glucagon
Pancuronium
Hypoxia and hypercapnia
Succinycholine d/t increased intra-abdominal
pressure with fasciculation
• Pre-op sedation to decrease anxiety and
prevent activation of SNS (Benzos)
• Avoid pre-op atropine or robinul  lead to
tachydysrhythmias
• Large bore IVs, PAC, CVP, and A-line to
help with fluid management, intervention
with inotrope or vasodilating drugs, ABGs,
frequent labs
• Keep rate of fluid replacement with rate of
loss
3 Critical Junctures
1- Induction and intubation
– Barbiturates, benzos, or propofol, mask with
volatile agent or N2O, lidocaine, fentanyl or
sufentanil
– SNP and phentolamine readily available to
treat HTN
– Select anesthetic agent based on ability to
decrease SNS activity and low likelihood of
sensitizing the myocardium to dysrhythmic
effects of catecholamines
3 Critical Junctures
2 - Manipulation of tumor  HTN and
dysrhythmias
– SNP*, phentolamine*, increased anesthetic agent,
propranolol, lidocaine, labetalol, esmolol*
– Use beta blockers cautiously b/c accentuate left
ventricular dysfunction in patient with cardiomyopathy
– Correct hypotension with neo or norepi, avoid
indirect-acting sympathomimetics b/c these are
unpredictable
– Magnesium Sulfate may be useful: inhibits
catecholamine release from adrenal medulla and
peripheral adrenergic nerve terminals, decrease
sensitivity of alpha adrenergic receptors to
catecholamines, to exert a direct vasodilators effect
3 Critical Junctures
3 - After ligation of tumor’s venous drainage
– Decreased catecholamines and the down regulation
of adrenergic receptors  decrease BP
– Decrease anesthetic level, increase IVF
administration, neo or norepi for BP
– Hyperglycemia common before excision, and
hypoglycemia after excision
• Beta blockade impairs hepatic glucose production and
glucagon secretion mechanism
• Beta blockade may also mask hypoglycemic signs by
preventing tachycardia and tremor
• Check glucose frequently
• Pheochromocytoma may present as a
hypermetabolic state and mimic light
anesthesia, thyroid crisis, MH, or sepsis
– HTN, tachycardia, hypertension, respiratory
acidosis
• Post Op
– Fluid shifts, pain, hypoxia, hypercapnia,
autonomic instability, urinary retention, and
residual tumor are all potential causes of postop hypertension
– 50% of patients remain hypertensive
– Post-op catecholamines levels decrease over
several days
– Normal BP returns in about 10 days in 75% of
patients
– Post op pain can be accomplished with
neuraxial opiods and help with early tracheal
extubation
References
• Clinical Anesthesia, 5th Edition by
Barash, Cullen, et al
• Anesthesiologist’s Manual of Surgical
Procedures 3rd Edition by Jaffe
• Handbook of Nurse Anesthesia 3rd Edition
by Nagelhout & Plaus