1
Q
Adrenal gland role and anatomy?
A
- 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
- Cortex – 80%
2
Q
What are the layers of the cortex? Role of each and role of medulla?
A
- Outer layer: Cortex
- Zona Glomerulosa (Mineralocorticoids)
- Zona Fasciculata (Glucocorticoids)
- Zona Reticularis (Androgens)
- Inner layer: Medulla
- Catecholamines
3
Q
Synthesis of steroids? Inactivation? Secretion?
A
- 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)
4
Q
Blood supply to adrenal gland?
A
- 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
- superior suprarenal artery
- Venous
- one single vein
- right- inferior VC directly
- Left- left renal vein
- one single vein
5
Q
Disease classificaiton based on primary, secondary, tertiary (in general)
A
- Primary
- Alteration of the gland itself
- Secondary
- Disease outside of the adrenal glad that alters hormone production
- tumor making ACTH
- Disease outside of the adrenal glad that alters hormone production
- Tertiary
- Exogenous sources
- Steroids
- Exogenous sources
6
Q
Zona Glomerulosa location, role
A
- 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)
- : Distal convoluted tubule & collecting duct
- sweat glands
- alimentary tract
- Kidney
- Important for sodium/potassium/extra cellular fluid regulation
7
Q
RAAS system refresh?
A
- 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
- adrenal increase aldosterone (aldosterone also affected by increase K)
8
Q
What are the diseases caused by mineralocorticoid excess?
S/S?
A
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
9
Q
Diagnosis of mineralocorticoid excess? Treatment?
A
Diagnosis
- Primary
- Increased aldosterone and decreased renin levels
- feedback loop is working. lots of aldosterone is signaling renin to be decreaesd
- Increased aldosterone and decreased renin levels
- 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
- Increased aldosterone and increased renin levels
Treatment- mainly sx
- Adrenal Adenoma
- Surgery
- Bilateral hyperplasia
- Aldosterone antagonist (spironolactone or eplerenone)
10
Q
Proep, intraop, postop consideratiosn for mineralocorticoid excess?
A
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
11
Q
Causes of mineralocorticoid deficiency?
A
- 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
- Diabetes or chronic renal disease
12
Q
S/S and treatment of mineralocorticoid deficiency?
A
- Signs and Symptoms
- Hyperkalemia
- hyponatremia
- metabolic acidosis
- heart block
- orthostatic hypotension
- Treatment
- Liberal sodium intake and daily fludrocortisone
13
Q
Anesthsia implications of mineralocorticoid deficiency?
A
- 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
14
Q
What is the zona fasciculata? what does it produce?
What influences output of zona fasciculata?
Daily output amount? during stress?
A
- 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
15
Q
What are some actions of glucocorticoids?
A
- 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)
16
Q
Primary, secondary and tertiary causes of glucocorticoid excess?
A
- 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
- Pituitary corticotrope adenoma (Cushing’s Disease)
- Tertiary – Iatrogenic
- Medical use of steroids
- excess steroids
- Medical use of steroids
17
Q
S/S cushings disease?
A
- Emotional disturbance
- osteroporosis- need good padding
- buffalo hump- may make intubation difficult
- thin/wrinkled skin
18
Q
Diagnosis of glucocoritocid excess?
A
Steps are in order of how the tests should be done…
- Check for exogenous glucocorticoid administration and 24 hour urine
- 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!
- negative feedback working, normal axis
- Low dose dexamethasone test (1 mg) (give dex at 10pm and measure cortisol/acth in am)
- 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)
- diagnostic of cuhsing disease (pituitary source)
- Decrease in CRH with INCREASE IN ACTH & CORTISOL
- Increase ACTH from lung tumor, not respondign to dex.
- Decrease in CRH and ACTH with INCREASED Cortisol
- High dose dexamethasone test (8 mg) (only do once low dose was abnormal!! this analyzes cause for cushing syndrome)
- https://www.youtube.com/watch?v=ZINZOob04IY
- Imaging
* MRI/CT scan for tumor
- Imaging
19
Q
Treatment of glucocorticoid excess??
A
- Surgical removal
- Pituitary
- Adrenal
- Medical treatment
- Steroid blockers
- Metyrapone
- Ketoconazole
- Mitotane
20
Q
Anesthesia implications of glucocorticoid excess?
A
- 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
21
Q
Causes of glucocorticoid deficiency?
A
- 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
- Destruction of adrenal gland (Not apparent until 90% destroyed)
- Secondary
- CRH or ACTH deficiency – hypothalamus-pituitary axis failure
- Exogenous steroid administration
- Sepsis, cancer, stress, and infection can all play a role
22
Q
S/S Glucocorticoid deficiency? Adrenal crisis?
A
Signs and Symptoms
Primary Disease
- Chronic fatigue
- Anorexia and weight loss
- Nausea/vomiting/diarrhea
- Hyperpigmentation
- Orthostatic hypotension
- Hypoglycemia
- Hypovolemia
- Hyponatremia/hyperkalemia
Crisis
- Abdominal pain
- Severe N/V/D
- Hypotension
- Changes in LOC
- Circulatory Shock
23
Q
Diagnosis for glucocorticoid deficiency?
A
- 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
24
Q
Treatment of glucocorticoid deficiency?
A
- 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
- AM – Prednisone 5 mg; Hydrocortisone 20 mg
- on this for rest of life
25
When is steroid replacement for sx needed with glucocorticoid deficiency?
* 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*
26
What are some guidelines for steroid replacement intraop?
* 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*
27
Intraop and postop anesthesia consideraiton for glucocorticoid deficiency?
* **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*
28
What is the zona reticularies?
* 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_**
29
Causes of androgen excess?
* 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….
30
What can androgen excess cause?
* 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
31
What are some other meds that people might use if they abuse steroids?
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)
32
What are some anabolic steroid side effects?
* 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 ruptur**e from changes in collagen structure
* Neuropsychiatric
* **Mood swings**, manic, & violent antisocial behavior
33
Preop/intraop Anesthesia considerations with androgen excess?
* 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
34
Postop consideration with androgen excess?
* 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*
35
What is the adrenal medulla?
* 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%)
36
What are chromaffin cells?
* Most abundant cells of the medulla
* Modified neurons
* Have lost their axons and dendrites
* **Innervated from pre-ganglionic fibers**
* **Splanchnic nerves**
37
Pathway for epinephrine synthesis?
* 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)
38
What is pheochromocytoma?
* **_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**
39
Causes of pheochromocytoma?
* 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
40
Clinical presentation pheochromocytoma?
* Classic: paroxysms of **hypertension**, **palpitation**, diaphoresis, and **headaches**
* **ONLY 6% have symptoms**
* Other:
* warmth,
* pallor,
* tremors**,**
* **weight loss,**
* **anxie**ty,
* 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_**
41
Other clinical presentations of pheochromocytoma?
* 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
42
Diagnosis of pheochromocytoma?
* Screening test
* Urine
* Plasma
* Location
* CT/MRI
* Metaiodobenzylguanidine (MIGB) nuclear scan
* Ultrasonography
* IV pyelography
43
What are you looking for on a 24 hours urine test for pheochromocytoma?
* 24 Urine for fractionated metanephrine, normetanephrine, and vanillylmandelic acid
* Also need creatinine to determine adequate kidney function
44
What is the clonidine suppression test?
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*
45
Preop eval pheochromocytoma?
* 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/
46
What is Roizen criteria?
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**
47
Surgical approach to pheochromocytoma removal?
* 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**
48
Intraop anesthesia managment for pheochromocytoma? (monitors and induction mgmt specifically)
* 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*
49
Maintenance of anesthesia in pheo?
* 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*
50
Meds to use intraop in pheo case to address HTN/Hypotension/arrhtyhmias?
* 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
51
Blood/fluid and emergence of pheo casE?
* 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*
52
What are some reasons why a pheo case may need ICU after case?
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 blocker**s (esmolol), or **calcium channel blockers** (clevidipine/nicardipine)
53
Postop complications of pheochromocytoma?
* 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
CO-EXIST Test 4!
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