Adrenal Flashcards

1
Q

Does abnormal renal development change adrenals?

A

Adrenal gland development occurs normally in the absence of the ipsilateral renal unit development, malrotation, or malascent.

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2
Q

What percentage of neonates have adrenal rests? What percentage of adults?

A

50% of neonates
1% of adults (it atrophies)

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3
Q

What happens to adrenal rests in CAH?

A

In congenital adrenal hyperplasia, adrenal rests within the testis may become hyperplastic and present as a testicular mass

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4
Q

What do the zona glomerulosa, fasciculata, and reticularis do?

A

zona glomerulosa: mineralocorticoid (100-50 mcg/day)–salt
zona fasciculata: glucocorticoid (10-20 mg/day)–sugar
zona reticularis: androgens (>20 mg/day)–sex

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5
Q

Up to 50% of patients with Cushing’s syndrome will get THIS common urologic issue

A

Nephrolithiasis

(NB: It is also relatively common to see Cushing’s syndrome cause hypogonadotropic hypogonadism)

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6
Q

Hyper-Aldosterone Testing

A

IV saline infusion test - 2L of 0.9% NaCl IV over 4 hours
Performed in the morning after a overnight fast, while the patient is recumbent
Draw aldosterone, >5 ng/dL is diagnostic of primary hyperaldosterone and >10 ng/dL suggestive of aldosterone-producing adenomas

Only do captopril suppression test for patients with cardiac and renal disease, which prohibits sodium loading - give 25-50 mg ACE inhibitor followed by measurement of aldosterone (again recumbent) - positive test if >15 ng/dL

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7
Q

Adrenal mass with HTN workup?

A

Morning aldosterone to renin radio (ARR) and aldosterone level
-Stop potassium sparing diuretics for 6 weeks, consider stopping beta blockers

IF result abnormal, consider confirmatory testing with endocrinology and possible adrenal vein sampling

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8
Q

What percentage of aldosterone producing tumors will be less than 1 cm in size?

A

20%!!
CT is good, MRI does not usually offer an advantage in delineating primary aldosteronism subtypes

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9
Q

Adrenal vein sampling for aldosterone

A

The value of adrenal vein sampling in evaluating the presence of lateralized aldosterone secretion
-22% of patients would have been incorrectly excluded from adrenalectomy and 25% would have been inappropriately recommended to undergo adrenalectomy based on CT findings instead of adrenal vein sampling

Make sure to do in the morning
Correct hypokalemia first
Withdraw contraindicated medicines (K sparing diuretics and beta blockers)

Make sure to evaluate cortisol ratio first, then aldosterone ratio (cortisol in the IVC should be less than the samples from the renal veins - confirms you actually got renal vein samples from the veins)

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10
Q

Antihypertensive of choice in patients with primary aldosteronism?

A

Spironolactone and epleronone
-Androgen receptor antagonists

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11
Q

List side effects of aldosterone receptor antagonists?

A

Spironolactone and Epleronone (more favorable)

gynecomastia
impotence
menstrual disturbances
hyperkalemic

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12
Q

What conditions are associated with pheochromocytomas?

A

Rearranged Transfection Protooncogene (RET) - MEN2A and MEN2B - 50% risk of pheo
-Remember MEN2A - Medullary thyroid cancer, hyperparathyroidism, and pheo
-Men2B - Medullary thyroid cancer, neuromas, marfanoid habitus, pheo
von Hippel-Lindau (VHL) - 20% risk of pheo
Neurofibromatosis type 1 (NF1)
Mitochondrial succinate dehydrogenase subtype D and B genes (SDHD, SDHB)

VHL is the most relevant syndrome (10-20% risk) as these patients are already being screened for RCC

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13
Q

Why do we measure plasma metanephrines? For pheos

A

The conversion of catecholamines to metanephrines is an uninterrupted process within pheochromocytomas, measurement of plasma metanephrines is a much more sensitive means of tumor detection than catecholamines, which may be paroxysmal.
-Measure in plasma or urine

Stop acetaminophen 5 days prior
Draw in supine position

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14
Q

Functional evaluation of adrenal tumors with suspicion for adrenal cortical carcinomas

A

Glucocorticoid excess:
-Low dose dexamethasone suppression test or late night salivary or 24 hour urine cortisol

Sexual steroids and steroid precursors:

  • DHEA
  • 17-OH-Progesterone
  • Androstenedione
  • Testosterone
  • 17Beta-estradiol (only in men and post menopausal women)

Catecholamine excess:
-Serum or urinary metanephrines

Mineralocorticoid excess:
-Aldosterone to renin ratio (only in patients with HTN or hypokalemia)

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15
Q

Adrenal Adenoma:
Imaging, appearance on imaging, and workup

A

Non-contrast CT
<10 HU

7% of adrenal adenomas exhibit metabolic hyperactivity
<2% gain function

Evaluate for excess cortisol (low dose dexamethasone suppression) and catecholamine secretion (urine or plasma metanephrines)
In patients with hypertension, test for hyperaldosteronism

Campbells says resect all adrenal masses >6 cm, others argue 4 cm

Reimage at 6, 12, and potentially 24 months

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16
Q

Which adrenal masses do you test?

A

The NIH consensus statement recommends metabolic testing for all adrenal incidentalomas
Test all new adrenal masses for cortisol and catecholamine hypersecretion
In a patient with hypertension, test for aldosterone hypersecretion

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17
Q

What medication can mess with a dexamethasome suppression test?

A

Oral contraceptives!
50% false positive rate because it increases total but not bioavailable cortisol levels by raising the patient’s cortisol binding globulin concentration

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18
Q

What medication can mess with a dexamethasome suppression test?

A

Oral contraceptives!
50% false positive rate because it increases total but not bioavailable cortisol levels by raising the patient’s cortisol binding globulin concentration

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19
Q

What medicine can interfere with catecholamine testing?

A

Acetaminophen (false positive result)
- Cross reactivity with plasma free metanephrines or 24 hour urinary fractionated metanephrines

Watch out for tricyclic antidepressants and phenoxybenzamine
Take off beta blockers

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20
Q

Surgical Indication for Adrenalectomy

A

Functional adrenal mass (cortisol hypersecretion, pheochromocytoma, aldosterone hypersecretion)
Mass >4 cm with the exception of myelolipoma
Mass with imaging findings suggestive of malignancy (lipid poor, heterogenous, irregular borders, infiltrates surrounding structures)
Adrenal incidentaloma with >1 cm growth on follow up
Extremely large or symptomatic myelolipomas
Isolated adrenal metastases
During radical nephrectomy if:
-Adrenal abnormal or not seen on imaging with large tumor size
-Large >7 cm upper pole mass
-Vein thrombus to the level of the adrenal vein
Failed neurosurgical treatment of Cushing’s disease, requiring bilateral adrenalectomy
Select patients with ectopic ACTH syndrome, requiring bilateral adrenalectomy
ACTH independent macronodular adrenal hyperplasia
Primary pigmented nodular adrenocortical disease

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21
Q

Once more:
Adrenal mass with benign features and mass <4 cm
Workup?

A
  1. Low dose dexamethasone suppression test or late night salivary cortisol or 24 hour urinary cortisol
  2. 24 hour urinary fractionated metanephrines or plasma free metanephrines
  3. If patient hypertensive, morning plasma aldosterone to renin radio and morning plasma aldosterone level
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22
Q

Adrenal mass with benign features <4 cm - follow up

A
  1. Repeat imaging at 6, 12, and 24 months
  2. Repeat functional workup annually for 4 years (per Campbells)
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23
Q

CAH: 21 Hydroxylase Deficiency

A

95% of CAH - elevated 17hydroxyprogesterone and progesterone (and androstendione according to the other book but not campbells)
A pelvic ultrasound demonstrating the presence of mullerian tissues is confirmatory (if female and virilized)
75% with salt wasting (hypotension) - failure to regain birth weight, progressive weight loss, dehydration
-Adrenal crisis within 10-21 days in severe forms
25% simple virilization

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24
Q

11 Beta Hydroxylase Deficiency

A

5% of CAH
High amount of deoxycorticosterone (DOC) causes high blood pressure EVEN THOUGH you don’t get all the way to cortisol on the chart of enzymes
Test 11 deoxycorisol and 11 DOC
Hypertension and virilization

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25
Q

3 Beta hydroxysteroid dehydrogenase deficiency

A

Increased 17-hydroxypregnenelone and hydroepiandrosterone (DHEA)

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26
Q

Can you do prenatal testing for CAH? What do you do if you find something?

A

YES
Measure amniotic fluid for 17 hydroxyprogesterone (or during chorionic villus sampling)
Treat mother with dexamethasone, which suppresses fetal production of ACTH, which prevents virilization of the genitalia

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27
Q

Complete Androgen Insensitivity

A

46XY
Bilateral testes
Female appearing genitalia
Absence of mullerian derivates

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28
Q

5 Alpha Reductase Deficiency

A

Male undervirilization
46XY
Penoscrotal hypospadias or markedly ambiguous genitalia
Elevated testosterone, low DHT

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29
Q

Test for Cushing’s

A

Overnight low-dose (1-mg) dexamethasone suppression test (OST)
Late-night salivary cortisol test (SCT)
24-hour urinary-free cortisol evaluation (UFC)

To perform the OST, a dose of 1 mg dexamethasone is given at 23:00 hours followed by measurement of serum cortisol and dexamethasone the following morning at 08:00.

A putative diagnosis of Cushing Syndrome is made if the serum cortisol level is > 5 micrograms/dL following an OST.

An ACTH level can be checked to ascertain whether it is ACTH-independent or -dependent.

A low/suppressed ACTH or DHEA-sulfate support an adrenal source.

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30
Q

Who to screen for hyperaldosteronism? (Conn’s syndrome)

A

Any patient with sustained blood pressure above 150/100 on three separate measurements taken on different days
Hypertension resistant to 3 antihypertensives
Hypertension controlled with four or more medications
Hypertension and low potassium
Hypertension and a newly diagnosed adrenal incidentaloma
Hypertension and concomitant sleep apnea
Hypertension and a family history of early onset hypertension or stroke before age 40
All first-degree relatives of patients with a diagnosis of primary aldosteronism

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31
Q

What do you do if you have elevated aldosterone or an elevated aldosterone renin ratio to confirm hyperaldosteronism?

A

A positive ARR screen should prompt a confirmatory 24-hour urine study with salt loading to assess for primary aldosteronism.

It is also important to note that positive testing for aldosterone hypersecretion does not guarantee a unilateral source, and therefore, adrenal venous sampling is recommended prior to surgical intervention.

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32
Q

For those patients with pheochromocytoma and age < 50, family history, or extra-adrenal pheochromocytoma….

A

Investigation for familial syndromes with genetic testing is warranted, with emphasis on mutation of the RET proto-oncogene (multiple endocrine neoplasia type 2), VHL (von Hippel-Lindau disease), or succinate dehydrogenase genes

33
Q

What is an adrenal protocol CT?

A

An adrenal protocol CT scan is a triphasic study. The first phase of the study is without contrast. This is followed by imaging immediately after intravenous administration of contrast. The final phase is imaging after 10 to 15 minutes. Adrenal washout can be presented as absolute percentage contrast-washout ((enhanced HU – 15-min delayed HU)/(enhanced HU – unenhanced HU) x 100%) or as relative percentage contrast washout ((enhanced HU – 15-min delayed HU)/enhanced HU x 100%).

The 2017 ACR guidelines denote thresholds of
> 60% absolute percentage washout or
> 40% relative percentage washout as characteristic of benign incidentalomas.

34
Q

Pheochromocytoma Imaging

A

Pheochromocytomas measure greater than 10 HU on unenhanced CT scans and will enhance to more than 100 HU on contrast studies, often exhibiting a well-circumscribed appearance with or without necrotic or cystic elements.

Recent data suggest that if HU are <10 then biochemical testing for pheochromocytoma is not necessary.

The classic “light bulb” signal on T2-weighted MRI may be helpful, but recent studies suggest that this sign is less sensitive and specific than previously thought.

Additional imaging, such as meta-iodobenzylguanidine (MIBG) scanning may also be warranted in this setting, especially if assessing for an extra-adrenal, metastatic, or recurrent pheochromocytoma.

35
Q

Adrenocortical carcinomas on imaging

A

Adrenocortical carcinomas typically are larger than 4 cm and exhibit a heterogeneous appearance on CT, with calcifications and necrosis often present.

HU measurement on non-contrast CT are typically >25 HU with <50% washout demonstrated at 10 minutes post-contrast imaging.

Adrenal metastasis may also have a similar appearance, which belies the importance of clinical history in this setting.

Lipid-poor adenomas may have attenuation values of 20-40 HU, but a washout of >50% is believed to distinguish these lesions from adrenal carcinomas.

36
Q

How do you distinguish lipid-poor adenomas from adrenal carcinomas?

A

Lipid-poor adenomas may have attenuation values of 20-40 HU, but a washout of >50% is believed to distinguish these lesions from adrenal carcinomas.

37
Q

If an adrenal is _____ (size), it should be removed regardless of function.

A

There is some controversy over the management of masses between 4-6 cm.

The American Association of Clinical Endocrinologists/American Association of Endocrine Surgeons (AACE/AAES) guidelines recommend removal of all masses over 4 cm regardless of functional status or imaging characteristics, unless it is clearly a myelolipoma.

38
Q

What are medical options for patients with Cushing’s syndrome who are not candidates for surgery?

A

Patients with excessive glucocorticoid production are at risk for development of the metabolic syndrome, including hypertension, medical issues related to obesity, cardiovascular disease and diabetes.

If a patient is not a candidate for adrenalectomy, medical treatment such as
-aminoglutethimide
-metyrapone
-ketoconazole
should be initiated while simultaneously monitoring for adrenal insufficiency.

For patients with sub-clinical Cushing syndrome, surgical resection is reserved for those with worsening hypertension, dyslipidemia, abnormal glucose tolerance, or osteoporosis.

39
Q

Adrenal Vein Sampling.- when do you do it?

A

For those patients with primary aldosteronism, excess plasma aldosterone is harmful and can lead to myocardial fibrosis, left ventricular hypertrophy, cardiac ischemic events, and clotting abnormalities, even if blood pressure is controlled.

Therefore, adrenalectomy is preferred unless the patient is not an operative candidate.

Adrenal vein sampling is nearly universally performed prior to surgery to identify laterality, even in the case of micronodularity or bilateral adrenal masses.

However, in the setting of a unilateral hyperdense nodule > 1cm with a positive aldosteronoma screen, unilateral adrenalectomy is indicated.

40
Q

What do you give a patient with hyperaldosteronism prior to surgery?

A

Prior to surgery, patients are given

  • A mineralocorticoid receptor antagonist (epleronone, spironolactone)
  • Antihypertensive
  • Potassium repletion

Following surgery, antihypertensives are weaned slowly.

Almost all patients will exhibit improvement in hypertension following adrenalectomy with complete normalization seen in approximately 60%.

41
Q

Follow up for adrenal masses

(Core curriculum)

A

AACE/AAES recommendd radiographic re-evaluation at 3-6 months and then annually for 1-2 years for all adrenal incidentalomas, even in the setting of benign radiographic characteristics initially.

Hormonal evaluation should be performed at time of diagnosis and annually for 5 years.

If the lesion size increases by ≥ 1 cm or develops functionality, surgery should be considered.

However, 75-95% of incidentalomas remain stable in size while 2-8% of previously non-functioning lesions develop functionality, with hypersecretion of cortisol being the most common finding.

CONTROVERSIAL
However, in 2016 the European Society of Endocrinology and European Network for the Study of Adrenal Tumors guidelines recommended no further follow-up imaging for an incidentaloma that showed benign imaging (non-contrast HU <10) and was under 4 cm in size.

For tumors greater than 4 cm or with indeterminate imaging characteristics, additional imaging was recommended at 6-12 months.

Similar recommendations were put forth in 2017 by the American College of Radiology, which recommended against follow-up imaging for incidentalomas with unequivocally benign characteristics, regardless of size on initial imaging including the presence of macroscopic fat, low CT density (non-contrast HU <10), cystic features, hemorrhage, absence of enhancement, and loss of MRI signal between in-phase and opposed-phase images on chemical shift MRI. However, for masses measuring 1-4 cm with indeterminate radiographic features, additional risk-stratified imaging follow-up vs. advanced imaging (e.g. PET-CT), biopsy, or extirpation are recommended accordingly.

42
Q

Metastatic Pheochromocytoma Sites

A

The most common sites of pheochromocytoma spread are bone, liver, regional lymph nodes, lung, and peritoneum.

43
Q

Pheochromocytoma Recurrence

A

Most metachronous metastases will present within the first 5 years of diagnosis; however, lifelong annual biochemical follow-up is recommended as recurrences have been noted to occur more than 15 years following surgery.

44
Q

What do you give prior to surgery for pheochromocytoma?

A

Alpha-adrenergic blockade, typically with phenoxybenzamine (an irreversible non-selective alpha blocker), is started 7-14 days prior to surgery and titrated to a blood pressure of 120-130/80mmHg.

This is followed by beta blockade with atenolol or metoprolol if tachycardia or arrhythmias develop.

Use of metyrosine to block catecholamine synthesis is not commonly needed but can be used in combination with alpha-blockade.

Calcium channel blockers have been advocated by some as an adjunct to or in lieu of traditional alpha blockade.

Intra-vascular volume expansion is also necessary due to the chronically vasoconstricted state. This can be achieved through preoperative and intraoperative hydration and a high salt diet.

This should be initiated 7-14 days prior to surgery.

45
Q

Adrenocortical Carcinoma TNM Staging

A

Primary Tumor (T)
pTx Primary tumor cannot be assessed
pT0 No evidence of primary tumor
pT1 Tumor ≤ 5cm in greatest dimension, no extra-adrenal invasion
pT2 Tumor > 5cm in greatest dimension, no extra-adrenal invasion
pT3
Tumor of any size with extra-adrenal invasion, but not invading adjacent organs
pT4
Tumor of any size with invasion of adjacent organs (kidney, diaphragm, spleen, liver, etc)

Regional Lymph Nodes (N)
Nx Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastases in regional lymph node(s) (retroperitoneal)

Distant Metastasis (M)
Mx Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis

46
Q

Staging for Adenocortical Carcinoma

A

Stage T N M
Stage I pT1 N0 M0
Stage II pT2 N0 M0
Stage III pT1-2 N1 M0
pT3-4 N0-1 M0
Stage IV Any T Any N M1

47
Q

5 Year Survival Rates for Stages of Adrenocortical Carcinoma and Sites of Metastasis

A

The reported 5-year survival rates are 30-45%, 13-57%, 5-18%, and 0% for stages I through IV, respectively.

The most common sites for metastases are liver (48%), lung (45%), lymph nodes (29%), and bone (13%).

Local invasion into the kidney (26%) and IVC (9-19%) can also occur.

48
Q

Chemotherapy Regimen for Adrenocortical Carcinoma

A

Cisplatin + etoposide +/- doxorubicin +/- mitotane

Just say “Resection; mitotane +/- cytotoxic chemotherapy”

49
Q

Algorithm for Workup and Management of Adrenal Incidentalomas

A
50
Q

Biochemical Testing for Functional Adrenal Adenomas:

A
51
Q

Adrenal Pathology and Associated Characteristics

A
52
Q

What are important questions to ask when evaluating a patient with an adrenal incidentaloma?

A

headache
palpitations
sweating
easy bruisability
muscular weakness
recent weight loss or gain
high blood pressure
flushing

53
Q

What are key elements of PE for adrenal incidentaloma?

A

central obesity
moon face
buffalo hump
abdominal striae
virilization
BP
body weight (BMI)

54
Q

What is ddx of adrenal incidentaloma?

A

non-functional adenoma
functional adenoma
Pheochromocytoma
Aldosteronoma (Conn’s)
Cortisoloma (Cushing’s)
Adrenal Cancer (ACC)
Myelolipoma
Adrenal mets from another cancer
Adrenal hyperplasia
Adrenal infection (Tb)
Sarcoma
Oncocytoma
Adrenal Cyst
Infarct

55
Q

If a dexamethasone suppression test yields a Cortisol (am) > 5 mcg, what is the next test?

A

ACTH

56
Q

Categories of Cushing’s Syndrome?

A

ACTH dependent → excessive secretion of ACTH from pituitary (70%), ectopic ACTH production (10-15%), ectopic production CRH (bronchogenic carcinoma < 1%)

ACTH independent → cortisol-secreting adenomas of adrenal gland or ACC (10%)

57
Q

What do you do in a patient with elevated ACTH?

A
  1. Heat CT/MRI
  2. Inferior petrosal vein sampling for ACTH (if elevated, NSG)
  3. Trans-sphenoidal hypophysectomy for pituitary adenoma
58
Q

POD 0 night s/p unilateral adrenalectomy for functional adenoma, patient is confused, nauseous, hypotensive, and tachycardic, not responding to fluids, what is concern? Tx?

A

excess cortisol secretion, suppressed HPA axis → adrenocortical insufficiency

Administer glucocorticoid replacement, hydrocortisone 100 mg IV or dexamethasone 4 mg IV
**Mineralocorticoid replacement is not necessary in acute setting

59
Q

If adenoma is not functional, what do you do?

A

CT re-evaluation at 3-6 months and then annually for 1-2 years

* even in the setting of benign radiographic characteristics initially

Hormonal evaluation should be performed annually for 5 years

If the lesion size increases by ≥ 1 cm or develops functionality, surgery should be considered.

60
Q

If you have a pancreatic injury during adrenalectomy, what do you do?

A

Place a drain

can close pancreatic capsule with non-absorbable sutures

distal tail w/ductal injury → resection of distal portion of pancreas with suture ligate of duct

61
Q

If you have a >50% avulsion of splenic hilum during adrenalectomy, how do you manage? small tears of capsule? minor/moderate lacerations?

A

Splenectomy
splenic artery ligated at superior border of pancreas
splenocolic ligaments dissected
Elevate spleen and ligate segmental splenic artery/veins close to capsule
short gastric vessels dissected
cut retroperitoneal attachments
remove spleen

**POST OP

Vax pneumococcus/meningococcus/HIB

small tears to capsule → fulgurate/argon beam, gelfoam/fibrin glue

minor → surgicel/avitene

moderate → close with bolster and surgicel/avitene

62
Q

For ACC or suspected adrenal cancer, do you perform a regional LN dissection?

A

Yes

63
Q

What characteristics on imaging help differentiate between benign adrenal lesions and malignant?

A

Adrenal adenoma on Ct washout
Benign have < 10 HU on non-contrast CT
>60% absolute washout or >40% relative washout

Malignant tumors and functional tumors have lesser washout, hold on to contrast

non-contrast MRI, masses that demonstrate loss of signal intensity on out of phase sequences are adenomas

64
Q

Absolute contraindications to adrenalectomy?

A

severe coagulopathy
poor cardiopulmonary performance

65
Q

Key steps of adrenalectomy?

A

Minimal manipulation of mass “no touch”

Ligate or clip adrenal arteries

Ligate adrenal vein

Inspect adrenal fossa for bleeding

Perform regional LND (if suspect ACC)

No drain necessary

Deliver carefully via lap bag

66
Q

Blood supply to adrenal gland

A

inferior phrenic artery
aorta
renal artery

67
Q

During adrenalectomy, when clamping adrenal vein, patient becomes hypotensive, now what?

A

this is normal
replace volume with NS
pressors rarely needed

68
Q

During adrenalectomy, adrenal vein is avulsed from IVC, now what?

A

Compression
Suction
Proximal and distal control
Oversew hole with 4-0 Prolene

69
Q

During adrenalectomy, IVC lacerated, now what?

A

proximal and distal control
oppose caval edges (“satinsky”)
oversew injury 4-0 Prolene

70
Q

During adrenalectomy, pleural leak, now what?

A

Insert Robinson catheter into injury
purse string with 3-0 suture
evacuate air from pleura by suction or water seal
remove tube quickly under neg pressure and tie purse string

71
Q

After adrenalectomy, PTX on CXR, now what?

A

>15% Chest tube

<15% w/o distress, no shift, manage expectantly, O2

72
Q

During adrenalectomy, duodenal injury, now what?

A

lacerations repaired in multiple layers, 4-0 silk, omental wrap, NGT

hemotomas observed, identify and control bleeding

73
Q

During adrenalectomy, liver injury, now what?

A

liver lac → mattress sutures, surgicel bolster

deep lac with bile leak → drained

significant hemorrhage → pringle maneuver (cross clamp porta hepatis until stable) call GS

74
Q

What does elevated renin activity mean?

A

renin-mediated htn
RAS
cirrhosis
heart failure
reninoma/juxtaglomerular cell tumor

75
Q

What are clinical signs of pheochromocytoma?

A

headache
palpitations
sweating
sustained HTN
pallor
hyperglycemia
paroxysmal HTN
chronic weakness, tiredness
anxiety/panic

76
Q

Where does pheochromocytoma arise?

A

adrenal medulla (75-90%)
extra-adrenal (10-25%) = paragangliomas (neural crest)
head, neck, thorax, abdomen, pelvis
can arise between aortic bifurcation and root of IMA (organ of Zuckerkandl)

77
Q

Potential risks of untreated pheochromcytoma?

A

CHF (catecholamine induce cardiomyopathy)
malignant htn
tachyarrhythmia
CVA
hypertensive encephalopathy
renal failure/renal infarction
tumor hemorrhage

78
Q

Preoperative meds for pheochromocytoma

A

ALSO aggressive peri-operative hydration

79
Q

How is heart failure associated with elevated renin?

A

Heart failure can lead to decreased cardiac output, which reduces blood flow to the kidneys. This decrease in renal perfusion leads to an increase in renin secretion as a compensatory mechanism to maintain blood pressure and blood flow to the kidneys. Elevated renin levels can also occur in response to decreased blood volume and low systemic pressure in heart failure, leading to activation of the renin-angiotensin-aldosterone system.