Adrenal

Question 1

Adrenal gland role and anatomy?

Answer 1

• Maintains homeostasis
  
  • Adaption to stress
  • Control of blood pressure (RAAS system role)
  • Maintenance of water, Na+ & K+
  • Development of secondary sexual characteristics
• Anatomy
  
  • Cortex – 80%
    
    • 3 distinct layers
    • Derived from mesoderm
  • Medulla – 20%
    
    • Derived from ectoderm

Question 2

What are the layers of the cortex? Role of each and role of medulla?

Answer 2

• Outer layer: Cortex
  
  • Zona Glomerulosa (Mineralocorticoids)
  • Zona Fasciculata (Glucocorticoids)
  • Zona Reticularis (Androgens)
• Inner layer: Medulla
  
  • Catecholamines

Question 3

Synthesis of steroids? Inactivation? Secretion?

Answer 3

• All adrenocortical hormones are derived from cholesterol
• Synthesized in gland or taken up from blood stream
• ACTH – releases cholesterol from fat droplets in cytoplasm
• Cholesterol to pregnenolone in mitochondria
• Pregnenolone to the 3 main classes of steroids in smooth endoplasmic reticulum
  
  • Some final products completed back in the mitochondria (aldosterone/cortisol)
• Inactivation in liver via onjugation with glucuronide
• Secreted in urine

From picture:

• Zona glomerulosa- cholesterol–> mitochondira–> pregnenolone–> ER–> progesterone—> eventually becomes aldosterone
• Zona fasciculata- cholesterol–> pregnenolone–> ER–> MAINLY down cortisol pathway.
  
  • etomidate blocks 11- b- hydoxylase at step before cortisol/corticosterone development
• Zona reticularis–> cholesterol–> pregnenolone–> ER–> DHEA (sex steroids)

Question 4

Blood supply to adrenal gland?

Answer 4

• Arterial (don’t need specific names but just know it’s a rich vascular supply)
  
  • superior suprarenal artery
    
    • inferior phrenic artery
  • middle suprarenal artery
    
    • abdominal aorta
  • inferior suprarenal artery
    
    • renal artery
• Venous
  
  • one single vein
    
    • right- inferior VC directly
    • Left- left renal vein

Question 5

Disease classificaiton based on primary, secondary, tertiary (in general)

Answer 5

• Primary
  
  • Alteration of the gland itself
• Secondary
  
  • Disease outside of the adrenal glad that alters hormone production
    
    • tumor making ACTH
• Tertiary
  
  • Exogenous sources
    
    • Steroids

Question 6

Zona Glomerulosa location, role

Answer 6

• Directly under the capsule
• Cells contain ALDOSTERSONE SYNTHASE
• Produce aldosterone in response to
  
  • ↑ K
  • ↑ renin (angiotensin II)
  • ↓ kidney blood flow
• Aldosterone receptors located in:
  
  • Kidney
    
    • : Distal convoluted tubule & collecting duct
      
      • Principal cells (Na/K ATPase pump) & α intercalated cells (H+ ATPase proton pump)
  • sweat glands
  • alimentary tract
• Important for sodium/potassium/extra cellular fluid regulation

Question 7

RAAS system refresh?

Answer 7

• Dehydration, Na deficiency of hemoorahge–> decrease in blood volume–> decrease BP–> JG cells kidney release renin
• Renin–> Ang I via angiotensinogen
• Ang I–> Ang II via ACE
• Ang II–> vasoconstrict arteriole, also to adrenal
  
  • adrenal increase aldosterone (aldosterone also affected by increase K)
    
    • in kidneys, aldosterone causes increased Na and water reabsoprtion and increased secretion of K and H into urine
  • this, along with vasoconstriction of arteriole, increases blood volume and return BP to normal

Question 8

What are the diseases caused by mineralocorticoid excess?

S/S?

Answer 8

Causes

• Primary
  
  • Conn’s Syndrome (tumors vs adrenal hyperplasia)
• Secondary
  
  • Increased renin production (CHF, Cirrhosis, nephrotic syndrome, etc)

Signs & Symptoms

• Hypertension- increase Na, H2O
• Hypokalemic (98% intracellular – large deficits can be present)– Excrete K and H
• Hypernatremia- retaining Na
• Metabolic alkalosis- increasing H excretion from kidneys, now alkalotic
• Muscle weakness
• Fatigue
• Headache

Question 9

Diagnosis of mineralocorticoid excess? Treatment?

Answer 9

Diagnosis

• Primary
  
  • Increased aldosterone and decreased renin levels
    
    • feedback loop is working. lots of aldosterone is signaling renin to be decreaesd
• Secondary
  
  • Increased aldosterone and increased renin levels
    
    • feedback loop is not working. increased aldosterone coming from somewhere that doesn’t respond to negative feedback from high renin levels

Treatment- mainly sx

• Adrenal Adenoma
  
  • Surgery
• Bilateral hyperplasia
  
  • Aldosterone antagonist (spironolactone or eplerenone)

Question 10

Proep, intraop, postop consideratiosn for mineralocorticoid excess?

Answer 10

Preoperative

• Restore intravascular volume and replace electrolyte concentrations
• Reduce hypertension
• EKG – high incidence of ischemic heart disease
• ECHO – to evaluate for cardiac remodeling (long standing HTN)

Intraoperative

• No specific anesthesia technique required
  
  • Lower dosing of NMB agents- d/t muscle weakness, monitor PNS
  • Avoid hyperventilation-don’t want to blow off excess CO2, already alkalotic
• A-line and CVP on case by case basis

Postoperative

• Manage fluid volume status and electrolyte balance

Question 11

Causes of mineralocorticoid deficiency?

Answer 11

• Isolated deficiency of mineralocorticoid almost never occurs
• Primary
  
  • Adrenal insufficiency
  • Aldosterone synthase deficiency
• Hyporeninemic hypoaldosteronism (more secondary cause)
  
  • Diabetes or chronic renal disease
    
    • Damaged Juxtaglomerular cells

Question 12

S/S and treatment of mineralocorticoid deficiency?

Answer 12

• Signs and Symptoms
  
  • Hyperkalemia
  • hyponatremia
  • metabolic acidosis
  • heart block
  • orthostatic hypotension
• Treatment
  
  • Liberal sodium intake and daily fludrocortisone

Question 13

Anesthsia implications of mineralocorticoid deficiency?

Answer 13

• Preoperative
  
  • Ensure fluid volume and electrolyte status- hyperkalemia possible, hyponatremia
  • Low threshold for EKG
• Intraoperative
  
  • No specific anesthetic technique required
  • Monitor for cardiac instability
    
    • watch K level with Succinylcholine
• Postoperative
  
  • Monitor fluid volume and electrolyte status

Question 14

What is the zona fasciculata? what does it produce?

What influences output of zona fasciculata?

Daily output amount? during stress?

Answer 14

• Middle layer
• Produces glucocorticoids and some weak androgens
  
  • Primarily cortisol
• Under control of adrenocorticotropic hormone (ACTH)
  
  • From anterior pituitary
• Typical daily output is about 20 mg
  
  • Highest levels soon after waking
• Under stress output can increase to 150 – 300 mg
• Most is bound to α globulin cortisol binding globulin
  
  • 5-10% free

Question 15

What are some actions of glucocorticoids?

Answer 15

• Liver
  
  • Protein catabolism
  • Gluconeogenesis
  • Stimulation fat breakdown
• Cardiovascular
  
  • Maintain responsiveness to catecholamines
• Kidney
  
  • Weak mineralocorticoid activity
• Immune
  
  • Immune suppression (increase anti-inflammatory (IL4/10) molecules and decrease pro-inflammatory (IL-6, IL- 1, TNF alpha) molecules)

Question 16

Primary, secondary and tertiary causes of glucocorticoid excess?

Answer 16

• Primary – ACTH Independent<<- adrenal gland itself causing issues
  
  • Adrenocortical adenomas
  • Adrenal hyperplasia
• Secondary – ACTH Dependent (majority of causes)
  
  • Pituitary corticotrope adenoma (Cushing’s Disease)
    
    • ​pituitary causing issue
  • Non-pituitary tumors (lungs)
    
    • ​SCC
• Tertiary – Iatrogenic
  
  • Medical use of steroids
    
    • excess steroids

Question 17

S/S cushings disease?

Answer 17

• Emotional disturbance
• osteroporosis- need good padding
• buffalo hump- may make intubation difficult
• thin/wrinkled skin

Question 18

Diagnosis of glucocoritocid excess?

Answer 18

Steps are in order of how the tests should be done…

• 1. Check for exogenous glucocorticoid administration and 24 hour urine
• 2. Low dose dexamethasone test (1 mg) (give dex at 10pm and measure cortisol/acth in am)
     * Normal – decrease in CRH, ACTH, and Cortisol
     
     • ​negative feedback working, normal axis
       * Abnormal – No changes above- cortisol will be high/normal range= cushing syndrome…. not getting decrase in cortisol that you should!
• 3. High dose dexamethasone test (8 mg) (only do once low dose was abnormal!! this analyzes cause for cushing syndrome)
     * Normal – decrease in CRH, ACTH & Cortisol
     * Adrenal Gland- high cortisol, low ACTH because increased dex won’t supress tumor but will suppress pituitary
     
     • Decrease in CRH and ACTH with INCREASED Cortisol
       * Pituitary Gland-high dose dexamethasone is enough to suppress pituitary even though adenoma there
     • Decrease in CRH, ACTH & Cortisol
       
       • diagnostic of cuhsing disease (pituitary source)
         
         • Distal site (Lung cancer)
     • Decrease in CRH with INCREASE IN ACTH & CORTISOL
       
       • ​Increase ACTH from lung tumor, not respondign to dex.
• https://www.youtube.com/watch?v=ZINZOob04IY
• 4. Imaging
     * MRI/CT scan for tumor

Question 19

Treatment of glucocorticoid excess??

Answer 19

• Surgical removal
  
  • Pituitary
  • Adrenal
• Medical treatment
  
  • Steroid blockers
  • Metyrapone
  • Ketoconazole
  • Mitotane

Question 20

Anesthesia implications of glucocorticoid excess?

Answer 20

• NO contraindication to specific technique or medications
• Preoperative
  
  • Check and correct hypertension, glucose & electrolytes (potassium)
  • Continue steroid blocking drugs in perioperative period – hold AM of surgery
  • Good airway exam
• Intraoperative
  
  • Airway positioning
  • RSI as needed (obesity)
  • Induction – propofol and etomidate (ketamine contraindicated if hypertensive)
  • Maintenance – volatile or TIVA
  • Reduce doses of NMBD’s- use short acting – and monitor frequently
  • Monitor blood glucose
  • May include significant blood loss if tumors are highly vascular
    
    • A-line and central line may be indicated
• Postoperative
  
  • Monitor and correct hypertension, glucose & electrolytes
  • May require exogenous glucocorticoid and mineralocorticoid administration if bilateral adrenal glands removed

Question 21

Causes of glucocorticoid deficiency?

Answer 21

• CAN BE A MEDICAL EMERGENCY!
• Cortisol is essential for life
• Primary (Addison’s Disease)
  
  • Destruction of adrenal gland (Not apparent until 90% destroyed)
    
    • Idiopathic due to autoimmune destruction of the gland
    • Deficiency of glucocorticoid, mineralocorticoid, and androgens– destruction of gland itself, leads to deficiency in everything
• Secondary
  
  • CRH or ACTH deficiency – hypothalamus-pituitary axis failure
  • Exogenous steroid administration
  • Sepsis, cancer, stress, and infection can all play a role

Question 22

S/S Glucocorticoid deficiency? Adrenal crisis?

Answer 22

Signs and Symptoms

Primary Disease

1. Chronic fatigue
2. Anorexia and weight loss
3. Nausea/vomiting/diarrhea
4. Hyperpigmentation
5. Orthostatic hypotension
6. Hypoglycemia
7. Hypovolemia
8. Hyponatremia/hyperkalemia

Crisis

• Abdominal pain
• Severe N/V/D
• Hypotension
• Changes in LOC
• Circulatory Shock

Question 23

Diagnosis for glucocorticoid deficiency?

Answer 23

• Low blood glucose
• High ACTH— pituitary trying it’s best to stimulate the adrenal gland, but adrenal gland not working
• Low Cortisol– because the adrenal gland isn’t responding
  
  • 8 – 9 am < 3 mg/dl
• ACTH stimulation test
  
  • Give 250 mg ACTH
  • If Cortisol fails to rise >19 mg/dl—> then adrenal gland has issues, not pituitary

Question 24

Treatment of glucocorticoid deficiency?

Answer 24

• Exogenous steroids
• Usually glucocorticoids twice a day and mineralocorticoid once daily:
  
  • AM – Prednisone 5 mg; Hydrocortisone 20 mg
    
    • also– Fludrocortisone 0.05 - 0.1 mg/day<– to replace aldosterone component
  • PM – Prednisone 2.5mg; Hydrocortisone 10 mg
• on this for rest of life

Question 25

When is steroid replacement for sx needed with glucocorticoid deficiency?

Answer 25

• Prednisone < 5 mg/day
  
  • Does not clinically depress the HPA axis <– does nto need supplementation
• Prednisone > 20 mg/day for > 3 weeks within the previous year
  
  • Should receive perioperative supplementation
  • Other:
    
    • > 2 g/day topical- creams lead to subclinical HPA depression
    • > 0.8 mg/day inhaled– big allergy dose, sublinclinical HPA depression

Question 26

What are some guidelines for steroid replacement intraop?

Answer 26

• Perioperatively
  
  • Patients should receive their baseline therapy plus supplementation
  • Controversial – multiple different regimes
  • Supplementation based on individual need and degree of surgery (table 23.9- see pic)
    
    • Hydrocortisone 100 mg IV Q8
    • Hydrocortisone 25 mg IV @ induction then 100 mg over the next 24 hours
  • Monitor fluid volume, glucose, and electrolyte status
• Hydrocortisone (1:1) vs methylprednisolone (5:0.5) vs dexamethasone (30:0)
  
  • ​if total glucocorticoid deficiency, hydrocortison has both gluco and mineralocorticoid prop
  • methylprednisolong has more glucocorticoid properties
  • dexamethasone has no mineralocorticoid properties
  • usually select hydrocortisone as replacement

Question 27

Intraop and postop anesthesia consideraiton for glucocorticoid deficiency?

Answer 27

• Intraoperative
  
  • No specific anesthesia technique or medication recommended
    
    • +/- etomidate - blocks 11-b-hydroxlyase but the adrenal gland is already not working to make steroids. we’re giving steroids exogenously. if pt condition warrants etomidate use, go ahead and give
  • Volume deficient may be substantial
  • Monitor glucose and electrolyte levels
  • May require invasive monitoring
  • May require vasopressor support- don’t have stress response needed
• Postoperative
  
  • Monitor vitals, glucose, and electrolyte levels
  • Where to send?- may need ICU after

Question 28

What is the zona reticularies?

Answer 28

• Inner most layer
• Produces precursor androgens
  
  • Dehydroepiandrosterone (DHEA)
  • Androstenedione
• Released into blood stream
  
  • Converted in secondary sex organs
• Partially regulated by ACTH
• Stress pulls to cortisol

Question 29

Causes of androgen excess?

Answer 29

• Primary/secondary disease very rare
• Tertiary disease- most common cause from abuse of steroids
  
  • Up to 40% of regular gym users abuse anabolic steroids
    
    • > 3 million use for cosmetic regions
    • All likely a gross underestimation….

Question 30

What can androgen excess cause?

Answer 30

• Anabolic steroids are derived from cholesterol and very similar to testosterone
• Therefore, they enhance male reproductive and secondary sex characteristics
  
  • Acne
  • Muscle growth
  • Facial hair
  • Impotence
  • Infertility
  • Gynecomastia

Question 31

What are some other meds that people might use if they abuse steroids?

Answer 31

Usually Go through cycling periods (of steroid use— so they’re not discovered)

Take multiple other drugs to help cover up

• Diuretics (mask effects)- edema
• Human chorionic gonadotropin (prevents testicular loss)
• Tamoxifen (antagonize estrogen receptors and increase testosterone levels)
• HGH (Increase muscle mass)
• B2 agonists (clebuterol/fenoterol – improve strength and performance)
• Amphetamines (decrease fatigue and appetite)
• EPO (increase red blood cell density)
• Beta Blockers (lower heart rate –steady nerves)

Question 32

What are some anabolic steroid side effects?

Answer 32

• CV
  
  • Hypertension, LVH, & arrythmias
    
    • Several case reports of sudden death with exercise
• Lipids
  
  • Increase in CAD
• Vascular thrombosis
  
  • Increase in factor VII and IX
• Hepatotoxicity
  
  • Increased AST/ALT levels
• Tendon Injury
  
  • Tendon rupture from changes in collagen structure
• Neuropsychiatric
  
  • Mood swings, manic, & violent antisocial behavior

Question 33

Preop/intraop Anesthesia considerations with androgen excess?

Answer 33

• Preoperatively
  
  • Labs – CBC, LFT, US
  • EKG/ECHO
• Intraoperatively
  
  • Increased neck/deltoid muscles may make mask ventilation/intubation difficult
  • May require increased anesthetic requirements
  • May require larger doses of NDMBD (increased nicotinic receptors)- from more muscle mass
  • Monitor for bradycardia/arrythmias from increase drug requirement?
  • Succinylcholine – intense myalgias (more muscle mass)
  • May have higher ventilation requirements – increased oxygen consumption
  • Increased potassium release following tourniquet release
  • Good padding of pressure points – especially for long cases

Question 34

Postop consideration with androgen excess?

Answer 34

• May wake up agitated and combative
• High risk of NPPE if they laryngospasm– higher muscle mass
• DVT prophylaxis
• Increased risk compartment syndrome- large muscle mass
• Case report of prolonged ventilation required following aortic valve replacement
  
  • 21 days (dependence?) d/t excess steroid use

Question 35

What is the adrenal medulla?

Answer 35

• Really an extension of the sympathetic nervous system
• Formed from neurocrest cells
  
  • Neuroblasts
  • Chromaffin cells
• Responds to stress (physical and psychological)
• Release epinephrine (80 – 85%) and nor-epinephrine (15 -20%)

Question 36

What are chromaffin cells?

Answer 36

• Most abundant cells of the medulla
• Modified neurons
  
  • Have lost their axons and dendrites
• Innervated from pre-ganglionic fibers
  
  • Splanchnic nerves

Question 37

Pathway for epinephrine synthesis?

Answer 37

• Memorize pathway
• Tyrosine w/ trysoine hydroxylase (in chromaffin cell cytoplasm)–> dopa
• dopa + l-aromatic acid decarboxylase (in chromaffin cell cytoplasm as well)–> dopamine
• dopamine+ dopamine hydroxylase–> norepinephrine (in the NE chromaffin granule)
• Norepinephrine + phenylethanolamine n- methyltransferase–> epinephrine (in the epinephrine chromaffin granule)

Question 38

What is pheochromocytoma?

Answer 38

• Rare neuroendocrine tumors of the adrenal medulla (80 -85%)
  
  • Chromaffin cells
• Outside the medulla – paraganglioma (15-20%)
• Survival rate @ 5 years is 44%
• 5-10% of benign recurrence
• Synthesize and store excess amounts of epinephrine and norepinephrine

Question 39

Causes of pheochromocytoma?

Answer 39

• Precise incidence unknown
  
  • Usually isolated findings – 90%
• Inherited or Familial – (autosomal dominant) – 10%
  
  • Usually occur as bilateral or same place generation after generation
  • Multiple Endocrine Neoplasia (MEN) – tumors of different endocrine glands
    
    • Type 2A – 30%
    • Type 2B – 50%
  • Von Hippel-Lindau Disease – (mutation of VHL tumor suppressor gene)— may also have pheo
  • Neurofibromatosis Type 1 (mutation of neurofibromin gene) may alsohave pheo!
• PATIENTS WITH THESE CONDITIONS (VHL, neurofibromatosis) PRESENTING FOR OTHER SURGERIES NEED TO BE EVALUATED FOR THE SIGNS AND SYMPTOMS OF PHEOCHROMOCYOMA

Question 40

Clinical presentation pheochromocytoma?

Answer 40

• Classic: paroxysms of hypertension, palpitation, diaphoresis, and headaches
  
  • ONLY 6% have symptoms
• Other:
  
  • warmth,
  • pallor,
  • tremors,
  • weight loss,
  • anxiety,
  • diabetes, &
  • vision changes
• Variable levels of occurence – multiple times per day to very infrequent
• May occur spontaneously or precipitated by stress/life events
• Very few present in pheochromocytoma multisystem crisis:
  
  • Hypertension/hypotension,
  • hyperthermia,
  • altered mental status, &
  • end organ dysfunction

Question 41

Other clinical presentations of pheochromocytoma?

Answer 41

• Tachycardia
  
  • Beta stimulation
• Cardiomyopathy
  
  • Dilated and hypertrophic
• Ischemia
  
  • Alpha adrenergic stimulation leads to intense vasoconstriction
• ECG abnormalities
  
  • ST segment changes, flattening of T waves, prolonged QT interval, peaked P waves, left axis deviation, and dysrhythmias
• Diabetes
  
  • Glycogenolysis and inhibition of insulin release

Question 42

Diagnosis of pheochromocytoma?

Answer 42

• Screening test
  
  • Urine
  • Plasma
• Location
  
  • CT/MRI
  • Metaiodobenzylguanidine (MIGB) nuclear scan
  • Ultrasonography
  • IV pyelography

Question 43

What are you looking for on a 24 hours urine test for pheochromocytoma?

Answer 43

• 24 Urine for fractionated metanephrine, normetanephrine, and vanillylmandelic acid
• Also need creatinine to determine adequate kidney function

Question 44

What is the clonidine suppression test?

Answer 44

detect pheochromocytoma

• Clonidine suppression test
  
  • 0.3 mg PO clonidine in AM- should block alpha 2 and decrease NE release (normal)
• Serial lab draws
  
  • Baseline, Q2, Q3 hours
• Normal response (varies by lab)
  
  • Total plasma catecholamines
    
    • < 50 pg/ml
  • >50% reduction in norepi levels
  • Minimum plasma norepi < 500 pg/ml
• Abnormal response
  
  • No change- because negative feedback doesn’t work

Question 45

Preop eval pheochromocytoma?

Answer 45

• Multidisciplinary approach (surgeon, anesthesia & endocrinologist)
• Extensive preoperative preparation
  
  • May require 10 – 14 days (some say even out to 6 weeks)
  • Initiation of α adrenergic blockade
    
    • Phenoxybenzamine – long acting, non-selective alpha receptor antagonist
    • Prazosin – short acting, A1 receptor antagonist
    • Depends on surgeon preference – (no superior treatment )
  • Β blockers (propranolol) for persistent tachycardia/arrythmias
    
    • only once alpha is blocked!!! can’t have someone with HTN get BB!
  • Labs/EKG/ECHO/

Question 46

What is Roizen criteria?

Answer 46

Roizen Criteria to assess adequate α blockade

1. No blood pressure reading >160/90 in the 24 to 48 hour prior to surgery
   
   • Some institutions use an a-line in a stressful environment with minute by minute measurement over a few hours
2. Orthostatic pressures > 80/45 should be present- alpha blocker cause orthostatic hypotension. want good blockade but still want them to respond to SNS
3. ECG should be free of ST-T changes for > 1 week
4. No more than 1 PVC every 5 minutes

Question 47

Surgical approach to pheochromocytoma removal?

Answer 47

• Open
  
  • Transpertoneal
  • Retroperitoneal flank approach
• Laparoscopy
  
  • Most common – some may add hand assist
• Phases
  
  • Phase I – Tumor is dissected and vascular supply is isolated –BEFORE clamping the effluent vein – SEVERE HYPERTENSION AND ARRHYTHMIAS
  • Phase II – After the effluent vein is clamped – Precipitous HYPOTENSION

Question 48

Intraop anesthesia managment for pheochromocytoma? (monitors and induction mgmt specifically)

Answer 48

• Intraoperative Anesthesia Management (GETA +/- Epidural)

Monitors:

• Arterial (femoral vs. axillary BEFORE INDUCTION (AUC monitoring)– some say radial has issue and femoral preverred
  
  • +/- central line (30-60%) (for vasoactive meds) vs. multiple large IV’s
• TEE (with severe cardiac disease)

Induction

• Propofol +/- high dose narcotic and muscle relaxants
  
  • Avoid ketamine
  • Potential for succinylcholine induced tachycardia/hypertension from myalgia/ganglia stimulation- because of fasciculations, can cause tumor to release more NE/Epi
• Ensure adequate depth of anesthesia prior to laryngoscopy
  
  • Slow and gentle….
  • prop, roc, OPA/jawthrust–> more agent until no resposne–> slowly put blade in, see response–> add more agents if needed–> use esmolol to decrease HR/BP

Question 49

Maintenance of anesthesia in pheo?

Answer 49

• Volatile – sevoflurane most commonly used (most avoid desflurane)
• TIVA – Propofol/remifentanil/dexmedetomidine
• Opioids
  
  • Avoid those that release histamine
• Muscle relaxants
  
  • Avoid pancuronium
• Epidural
  
  • Most commonly used for postoperative pain control
  • Test dose?- will you use epi? how will you know if test dose worked?
  • When to bolus?- do you bolus after tumor removal? otherwise complicate picture intraop with HTN/HoTN

Question 50

Meds to use intraop in pheo case to address HTN/Hypotension/arrhtyhmias?

Answer 50

• HTN
  
  • Phentolamine (primarily α1 with weak α2 - classic)
    
    • ​nonselective competitive alpha adrenergic blockade (normal dose pharm 1-5 mg IV)
    • classive answer but there are other choices
  • Nitric oxide modulators (nitroprusside/nitroglycerin)
  • Calcium Channel Blockers (nicardipine/clividipine)
  • Magnesium (4gm loading with 2 gm/hr)- smooth muscle relaxant
• Hypo
  
  • Fluids
  • Phenylephrine
  • Norepinephrine
  • Vasopressin
  • Methylene blue
• Arrhythmia
  
  • Amiodarone –especially with epinephrine tumors

Question 51

Blood/fluid and emergence of pheo casE?

Answer 51

• Blood/Fluid
  
  • May have significant fluid volume deficit and blood loss
  • Multiple large bore IV’s
• Emergence
  
  • Most cases are extubated at the end of the case–> may go to ICU after

Question 52

What are some reasons why a pheo case may need ICU after case?

Answer 52

May require 24 hour ICU monitoring for Hemodynamic instability

• Profound hypotension
  
  • Residual preoperative blockade- from phenoxybenzamine, prazosin
  • Loss of vasoconstriction
  • Down regulation of alpha and beta receptors
  • Adequate volume expansion to include transfusion
  • May require phenylephrine or vasopressin therapy
• Severe hypertension
  
  • Catecholamines do not return to normal for 7-10 days
  • Short-acting agents – may require multiple
  • Nitric oxide modulators (nitroprusside/nitroglycerin), opioids (remifentanil), beta blockers (esmolol), or calcium channel blockers (clevidipine/nicardipine)

Question 53

Postop complications of pheochromocytoma?

Answer 53

• Hypoglycemia
  
  • Increased insulin production from Beta stimulation
  • Hourly FSBS checks for the first 12 – 24 hours
• Adrenal insufficiency
  
  • Especially with bilateral adrenalectomy
  • Hydrocortisone 100 mg IV @ induction and every 8 hours for 24 hours
• Reoccurrence
  
  • 14-30%
  • Recheck metanephrine levels in 2-6 weeks
  • Follow for 10 years