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Pheochromocytoma
OdessaR.Pulido andLindseyL.Perea
67
Way Question May BeAsked?
A 27-year-old female presents as a referral from her PCP
after an incidental nding of an adrenal mass on her CT
abdomen/pelvis.
How toAnswer?
History and Physical
• Thorough history including history of multiple anti-HTN
meds with poor BP control
– Symptoms:
Hypertension
Palpitations
Headache
Anxiety
Skin ushing
Tremors
– Social history:
Substance abuse (cocaine)
– Family history:
Endocrine neoplasia
MEN 2 syndromes
von Hippel–Lindau syndrome
Neurobromatosis type 1
O. R. Pulido
Department of Surgery, Division of Trauma and Acute Care
Surgery, Cooper Medical Center, Camden, NJ, USA
L. L. Perea (
Department of Surgery, Division of Trauma and Acute Care
Surgery, Penn Medicine Lancaster General Health,
Lancaster, PA, USA
Department of Surgery, Philadelphia College of Osteopathic
Medicine, Philadelphia, PA, USA
e-mail: lindsey.perea@pennmedicine.upenn.edu
*)
• Physical ndings
– Episodic or constant hypertension, sweating,
tachycardia
– Exam neck for medullary thyroid
Workup and Treatment
• Workup
– Biochemical studies
24-h urine catecholamines and metanephrines
(including dopamine levels (malignant pheos,
paragangliomas)
• Values >2–4 times the upper limit of normal are
diagnostic
Plasma metanephrines
• Used for patients with hereditary syndromes
– Stop all interfering medications if able during workup
– Thyroid ultrasound to rule out thyroid nodules (MEN
II)
– Pre-op cardiac echo (Takotsubo cardiomyopathy)
– Images
Adrenal protocol CT (phased thin cut noncontrast
and phased IV contrast)
• HU >10 on unenhanced scan, on average it is
usually >40–50 HU
• Quick enhancement with <60% washout
MRI- bright on T2 sequences
• Superior to CT in detecting extra-adrenal lesions
FDG PET
• Used for patients whose lab studies conrm
pheochromocytoma but they are unable to be
localized using CT or MIR
• Used when there is concern for metastatic
disease
• Treatment
– Pre-op:
Alpha blocker (phenoxybenzamine) that is uptitrated should be given 14days prior to surgery.
Goal is BP <130/80.
High sodium diet (>5g/day).
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. Neff et al. (eds.), Passing the General Surgery Oral Board Exam, https://doi.org/10.1007/978-3-031-78244-2_67
209
210
O. R. Pulido and L. L. Perea
Utilize beta blockade as needed. But, only after
2 days of starting an alpha blocker. Goal HR is
60–80bpm.
– Intra-op
Discussion with anesthesia preop
• Arterial line, central line
• Meds available for BP control
• Continuous communication with anesthesia
(gland manipulation, adrenal vein ligation)
Laparoscopic adrenalectomy vs. open (depending
on size/location)
• Prone position—Right adrenalectomy exposure
– Divide right triangular ligament
• Left adrenalectomy exposure
– Mobilize splenic exure and lateral attach-
ments of spleen and tail of pancreas
• Identify adrenal gland on superior medial aspect
of kidney
• Divide adrenal vein
– Right—Junction with IVC
– Left—Junction with left renal vein
• Divide remaining vessels, lymphatics, and soft
tissues
• Remove specimen
Blood pressure management
• Treatment for hypertension: nitroprusside or
esmolol
• Treatment of hypotension: norepinephrine or
epinephrine
Common Curveballs
• Unable to localize lesion
• Recurrent postoperative symptoms
• Patient has MEN II syndrome
• Dealing with intraoperative blood pressure and heart rate
changes
• Dealing with postoperative hypotension/importance of
aggressive uid management
• Failing to ligate adrenal vein early
• Not doing an appropriate family history
• Failing to screen relatives if MENII syndrome is
suspected
Summary
Patients with pheochromocytoma present with symptoms of hypertension, headaches, palpitations, and excessive sweating. They can be found incidentally but are also
linked with MEN II syndrome. Biochemical testing
should be done rst followed by imaging for localization.
The patient should be medically optimized prior to a
planned procedure.
Bonus Points
• Patients with pheochromocytoma and MEN II, only have
symptoms half of the time
• Being able to discuss paradoxical supine hypertension in
pregnant patients with pheochromocytoma
• Knowing and applying the “rule of 10’s”
Words ofWisdom
The mainstay of addressing pheochromocytomas is biochemical diagnosis, localization with imaging, perioperative
hemodynamic control, and surgery. Care must be taken to
obtain an accurate history and physical as there are genetic
associations found in more than 50% of these tumors.
Identication of any associations with the MEN 2 gene is
especially crucial. Additionally, being able to articulate the
intraoperative management of these patients can mitigate
intraoperative complications.
Bibliography
Clean Kills
• Failing to recognize surgical causes HTN in young adults
• Not giving proper preoperative medications.
– giving a beta blocker without adequate alpha
blockade
• Doing adrenal vein sampling or adrenal biopsy when sus-
picion for pheochromocytoma and if done, relying on the
levels for diagnosis
Altieri MS, Brunt LM.Pheochromocytoma. The SCORE Portal; 2023
Mar 21. Available from: https://www.surgicalcore.org
Freel EM, Stanson AW, Thompson GB, etal. Adrenal venous sampling
for catecholamines: a normal value study. J Clin Endocrinol Metab.
2010;95(3):1328–32. https://doi.org/10.1210/jc.2009- 2253.
Mulholland M.Operative techniques in surgery. Wolters Kluwer; 2014.
p.1769–81.
Sandau AG, Sandau R. Pheochromocytoma. In: Neff MA, editor.
Passing the general surgeon oral board exam. 2nd ed. NewYork:
Springer; 2014. p.37–9.
William B, Emily M, Palmer B.Management of pheochromocytoma.
In: Cameron J, Cameron A, editors. Current surgical therapy. 13th
ed. Philadelphia, PA: Elsevier; 2019. p.750–6.
Gastrinoma
HannahShin andLindseyL.Perea
68
Way Question May BeAsked?
A 36-year-old female with a history of refractory peptic ulcer
disease presenting with persistent epigastric pain and diarrhea. The patient is on long-term proton pump inhibitor therapy with no improvement in symptoms. Recent
esophagogastroduodenoscopy (EGD) demonstrated multiple
gastric and duodenal ulcers. Biopsies were negative for
Helicobacter pylori infection.
How toAnswer?
History
• Symptoms consistent with Zollinger–Ellison syndrome
– Abdominal pain
– Severe, refractory gastroduodenal peptic ulcer disease
– Dyspepsia
– Chronic diarrhea
– Nausea or vomiting
– Weight loss
• Endoscopic ndings
– Location of ulcers:
75% D1
14% distal duodenum
11% jejunum
– Prominent gastric folds
– Reux esophagitis
H. Shin
Department of Surgery, Philadelphia College of Osteopathic
Medicine, Philadelphia, PA, USA
e-mail: Hannahsh@pcom.edu
L. L. Perea (
Department of Surgery, Philadelphia College of Osteopathic
Medicine, Philadelphia, PA, USA
Department of Surgery, Division of Trauma and Acute Care
Surgery, Penn Medicine Lancaster General Health,
Lancaster, PA, USA
e-mail: lindsey.perea@pennmedicine.upenn.edu
*)
– Esophageal, pyloric, or duodenal strictures
uncommon
– Negative H. pylori biopsy
Physical Examination
• No abnormal ndings
Diagnosis
• Screening test
– Fasting serum gastrin >1000 pg/mL AND gastric pH
<2
1. Must discontinue proton pump inhibitors 2 weeks
prior due to falsely elevated gastrin levels
2. Higher levels more often in pancreatic gastrinoma,
larger size, metastasis; can have <10 times upper
limit of normal in up to 2/3 of cases
• Elevated basal acid output
1. Normal: ≤ 15 meq/h; prior history acid-reducing
surgery ≤5meq/h
• Conrmatory test
– Secretin stimulation test
1. Administer 0.4μg/kg IV secretin
2. Positive result: Increase in gastrin >110pg/mL over
fasting serum gastrin level
• Diagnostic imaging (localization studies)
– 70% located within the gastrinoma triangle bound by
the cystic duct, D2/D3, and pancreatic neck/body
– Start with CT or MRI→68Ga-DOTATATE PET→E
US+/−biopsy→Selective secretin testing
– Contrast-enhanced multidetector CT (MDCT)
1. PNETs are hypervascular compared with pancre-
atic adenocarcinoma
2. Assess in arterial phase: hyperenhancement/
hyperattenuation
– MRI:
1. T1: low signal
2. T2: high signal
3. Helps delineate primary tumors and metastases
– Somatostatin receptor scintigraphy and 68Ga-
DOTATATE PET
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. Neff et al. (eds.), Passing the General Surgery Oral Board Exam, https://doi.org/10.1007/978-3-031-78244-2_68
211
212
H. Shin and L. L. Perea
1. Display afnity for type 2 somatostatin receptors
2. Can be limited given other conditions can demonstrate uptake as well
– Endoscopic ultrasound
1. Useful when suspected tumor not localized on CT/
MRI
– Selective secretin testing
1. Selective arterial injection of secretin followed by
sequential sampling of right hepatic vein for gastrin
levels
• Screen for MEN-1
– Calcium
– Parathyroid hormone
– Pancreatic polypeptide
– Prolactin
– Genetic risk evaluation
Management
Gastrinoma in setting of MEN-1: Multiple lesions usually
<2cm in pancreas or duodenum
• Surgical resection if tumor >2 cm. Repeat imaging in
3–6months if it does not meet size criteria for resection.
• Ulcers often multifocal, small and >50% with lymph
node involvement.
• If primary hyperparathyroidism is present, perform 3½
gland or total parathyroidectomy with autotransplantation
prior to gastrinoma resection. This may aid in the management of refractory ulcer disease in patients with
MEN-1.
– Duodenotomy with internal palpation of duodenum
and periduodenal node dissection
• Wide local drainage
Recurrent gastrinoma
• Restaging with reoperation in localized and resectable
disease.
Metastatic or locally advanced disease
• Most common site of metastases
– Duodenal gastrinoma—lymph node
– Pancreatic gastrinoma—liver (poorer prognosis)
• Most important predictor of survival=Extent of hepatic
involvement
• Surgical resection if primary tumor and metastases mostly
resectable
Nonoperative management
• Recommended in the following patients:
– Unresectable locally advanced or metastatic disease
– ZES in setting of MEN-1
• High-dose proton pump inhibitor
• Octreotide or lanreotide
• Chemotherapy
• Chemo/radioembolization
• Radiofrequency ablation
Postoperative Considerations
Sporadic gastrinoma, resectable: Solitary lesion usually
>2cm most commonly in D1
• Preoperative considerations
– IV proton pump inhibitor administration
– Administer preoperative trivalent vaccines when
indicated
1. Pneumococcus
2. Haemophilus inuenzae b
3. Meningococcal group c
• Exploratory laparotomy
• Evaluation of liver +/− biopsy for occult metastases
• Intraoperative localization: inspect gastrinoma triangle
– Kocher maneuver with bimanual palpation and intra-
operative ultrasound of pancreas
– Local resection or enucleation of tumors
1. May require pancreaticoduodenectomy or distal
pancreatectomy and splenectomy inlocated in the
pancreatic head or distal pancreas, respectively
2. May require pancreaticoduodenectomy if involves
major ductal/vascular structures or bulky in nature
• PPI for 3months when hypergastrinemia is expected to
resolve.
• Persistently elevated gastrin after 3 months warrants
repeat imaging studies at 6months postoperatively.
• Consider reexploration if evidence of recurrence on
imaging.
Common Curveballs
• Presence of MEN-1
– Parathyroid adenoma/hyperplasia
– Pancreatic islet cell tumors
– Pituitary tumor
• Achlorhydria mimics ZES due to hypergastrinemia, but
lacks stomach acid production (gastric pH >2).
• Inability to localize preoperatively or intraoperatively
with usual maneuvers.
• Elevated gastrin levels after resection- management with
prolonged antisecretory therapy.
68 Gastrinoma
213
Clean Kills
• Performing secretin stimulation test when discontinuation
of PPI (required for test) could be life-threatening.
• Failure to exclude other conditions associated with
increased gastric acid hypersecretion.
• Failure to exclude MEN-1 in workup of suspected
gastrinoma.
• Failure to screen for gastrinoma in patients with MEN-1.
Bonus Points
• Gastrin-producing tumors must be associated with clinical symptoms of ZES to be classied as a gastrinoma.
• Can consider alternate criteria for ZES in patients with
fasting hypergastrinemia that are unable to discontinue
PPI for screening tests due to severe peptic
complications.
– Likely diagnosis of ZES if the following are present:
1. History of PUD
2. Improvement in diarrhea with PPI
3. Positive biopsy or cytology of PNET
4. Positive 68Ga-DOTATATE PET/CT
Words ofWisdom
Gastrinoma should be considered in patients with severe,
refractory gastroesophageal reux disease, especially those
with abnormal location of ulcers on EGD.Due to the high
incidence of malignancy (60–90%), patients should be thoroughly evaluated for the presence of metastatic disease,
which is an important predictor of survival. About 20–60%
of patients with MEN-1 present with a gastrinoma. Therefore,
appropriate screening and genetic risk evaluation should also
be included in the initial workup.
Bibliography
Arrington AK, Riall TS.Endocrine pancreas. In: Townsend CM, edi-
tor. Sabiston textbook of surgery: the biological basis of modern
surgical practice. 21st ed. St. Louis, MO: Elsevier; 2022. p.941–63.
Bergsland E.Zollinger–Ellison syndrome (gastrinoma): clinical mani-
festations and diagnosis. In: Post TW, editor. UpToDate. UpToDate:
Waltham, MA; 2023.
Dream S, Chen H. Endocrine pancreatic neoplasms. SCORE; 2023
[cited 2023 Aug 1]. Available from: https://www.surgicalcore.org/
modulecontent.aspx?id=144977
Metz DC, Cadiot G, Poitras P, Ito T, Jensen RT.Diagnosis of Zollinger–
Ellison syndrome in the era of PPIs, faulty gastrin assays, sensitive
imaging and limited access to acid secretory testing. Int J Endocr
Oncol. 2017;4:167–85.
National Comprehensive Cancer Network. NCCN clinical practice
guidelines in oncology (NCCN guidelines) neuroendocrine and
adrenal tumors. In: Neuroendocrine and adrenal tumors. 2023 [cited
2023 Aug 1]. Available from: https://www.nccn.org/professionals/
physician_gls/pdf/neuroendocrine.pdf
Thornblade LW, Park JO. Endocrine pancreatic neoplasms. SCORE;
2023 [cited 2023 Aug 15]. Available from: https://www.surgical-
core.org/modulecontent.aspx?id=1000377
Townsend CM, Arrington AK, Riall TS. Endocrine pancreas. In:
Sabiston textbook of surgery: the biological basis of modern surgical practice. 21st ed. St. Louis, MO: Elsevier; 2022. p.941–63.
Primary Hyperaldosteronism
VictoriaSharp
69
Concept
Patients will typically present with uncontrolled hypertension, refractory to multiple medications, with or without
hypokalemia.
There are three main causes of primary
hyperaldosteronism:
• Aldosterone-producing adenoma.
– Unilateral, the most common cause.
• Bilateral adrenal hyperplasia (idiopathic
hyperaldosteronism).
– Second most common cause.
• Familial hyperaldosteronism.
– Type 1 (glucocorticoid-remediable aldosteronism).
Rare autosomal dominant condition resulting in abnor-
mal regulation of aldosterone synthesis by ACTH.
– Type 2 (non-glucocorticoid-remediable aldosteron-
ism).
Way Question May BeAsked?
A 42-year-old man is being referred to your clinic after failing multiple antihypertensive medications. He experiences
muscle cramps, weakness, and intermittent paresthesias. He
was started on Spironolactone, which helped briey, but his
hypertension continued so his PCP has sent him for a routine
CT scan of the abdomen and pelvis, which showed a right
adrenal mass, and to you for further evaluation. He also has
chronic hypokalemia.
While this is the pathognomonic presentation, many
patients will not have hypokalemia and most will be
asymptomatic.
V. Sharp (*)
Trauma, Acute, and Critical Care Surgery, Trinity Health Ann
Arbor, Ypsilanti, MI, USA
e-mail: victoria_sharp@ihacares.com
How toAnswer?
History
• History of multiple antihypertensive medication use (two
• Family history of any familial hyperaldosteronism or
• Family or personal history of stroke, MI, Ab, or LV
out other possibilities:
• Pheochromocytoma.
• Adrenal cancer—primary or metastatic.
• Myelolipoma.
• Hemorrhage.
• Renal tumor/malignancy.
• Medication effect (i.e., diuretics).
Physical Examination
• Check vital signs i.e. blood pressure.
• Palpate for any tumors/masses/lymphadenopathy to indi-
Diagnostic Tests
• Potassium level.
• Step 1=Biochemical screening for hyperaldosteronism.
to four medications without improvement).
uncontrolled hypertension.
hypertrophy, all common sequelae of primary
hyperaldosteronism.
History should also focus on symptoms, being sure to rule
cate underlying malignancy.
– Ratio of plasma aldosterone (PAC) to plasma renin
activity (PRA).
Discontinue interfering medications rst.
• I.e. Spironolactone, ACE inhibitors, diuretics,
and beta-adrenergic blockers.
Positive if PAC/PRA >30ng/dL.
If ratio is positive and patient <30yo, screen for
glucocorticoid-remediable aldosteronism (familial
hyperaldosteronism type 1).
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. Neff et al. (eds.), Passing the General Surgery Oral Board Exam, https://doi.org/10.1007/978-3-031-78244-2_69
215
216
V. Sharp
If renin is high, suspect other etiology (renal artery
stenosis, secondary disease).
– Absolute aldosterone concentration >15mg/dL.
• Step 2=Biochemical conrmatory testing.
– Option 1 = Give Captopril and measure aldosterone
level before and after.
If decreases=bilateral hyperplasia.
– Option 2 = IV or PO salt load then measure aldoste-
rone=high means hyperaldosteronism.
• Step 3=Localization.
– First line =Thin-cut adrenal CT scan =preferred ini-
tial localization test.
If unilateral mass is present and >1cm, with normal
contralateral adrenal, and age <40 = perform
adrenalectomy.
– Second line=Selective adrenal venous sampling.
Measures cortisol and aldosterone levels in the
peripheral circulation and the left and right adrenal
veins.
Greater than vefold elevation in cortisol concentration in a sample relative to peripheral blood indicates successful cannulation of the adrenal vein.
Fourfold greater ratio of aldosterone to cortisol on
one side indicates the positive location.
Only used when biochemical diagnosis is conrmed but CT shows no abnormalities or bilateral
abnormalities.
– Third line = Functional scanning with radiolabeled
131
I-6-β-iodomethylnorcholesterol (NP-59).
Sensitivity is low in small tumors—only used if the
rst two methods do not help.
Treatment
• Nonoperative management: Spironolactone.
• Operative management:
– Preferred=Laparoscopic adrenalectomy.
• Cure is conrmed by clinical and biochemical endpoints
(reduction in BP/antihypertensive med needs), improved
plasma/urine aldosterone levels, and resolution of hypoK
(if seen prior) as soon as 24h after surgery.
– Overall cure rate=75–95%.
Surgery (Right Adrenalectomy)
• Lateral position.
• Mobilize the hepatic exure of the colon.
• Incise peritoneal reection of the right triangular ligament
and retract liver and colon medially.
• Open Gerota’s fascia over the kidney.
• Identify the inferior vena cava.
• Dissect superior and lateral aspects of the adrenal gland
rst.
• Gently retract the adrenal gland laterally.
• Divide adrenal vein and remove the adrenal gland.
• Important anatomy points:
– Right adrenal vein enters posteriorly into the IVC.
– Left adrenal vein empties into the renal vein.
Common Curveballs
• Patients will have persistent hyperaldosteronism after
unilateral adrenalectomy.
– The one removed was a nonfunctioning cortical
adenoma.
– There is either a contralateral microaldosteronoma or
bilateral adrenal hyperplasia (latter doesn’t require
surgery).
• There’s an injury to the renal vein or spleen (if left adre-
nalectomy) or to the inferior vena cava (if right
adrenalectomy).
• Patients will have no tumor on CT so know other localiz-
ing studies listed above.
• Patients will have RAS or bromuscular dysplasia if you
don’t check renin levels.
• Will have postop hypotension from adrenal insufciency.
Clean Kills
• Performing adrenalectomy without localization rst.
• Not checking potassium, aldosterone, and renin levels.
• Not being able to describe the surgical approach.
• Not ruling out other causes of surgically correctable HTN.
• Not knowing medical treatment for bilateral hyperplasia
and performing bilateral adrenalectomy.
• Misdiagnosing patient as a pheochromocytoma.
• Not knowing the mechanism of action of aldosterone or
renin-angiotensin-aldosterone axis.
• Not knowing that the syndrome is nicknamed “Conn’s
Syndrome.”
Bonus Points
• Can describe right and left adrenalectomy, open and lapa-
roscopic techniques.
• Understands CT/MRI characteristics and how this pro-
cess is different from a pheo.
• Is prepared to manage/monitor for postoperative
hypotension.
69 Primary Hyperaldosteronism
217
Words ofWisdom
Primary hyperaldosteronism AKA “Conn” syndrome is most
commonly a result of an aldosterone-producing adenoma or
bilateral adrenal hyperplasia. Work-up begins with biochemical screening then biochemical conrmation followed by
localization and is typically cured with unilateral adrenalectomy. Bilateral disease is usually treated medically. Be pre-
pared for bleeding intraoperatively and postoperative
hypotension.
Bibliography
Scott-Conner C, Dawson D. Operative anatomy. Philadelphia:
Lippincott Williams & Wilkins; 2009.
Townsend JCM, Beauchamp RD, Evers BM, Mattox KL.Sabiston text-
book of surgery. 21st ed. Elsevier– Health Sciences Division; 2022.
Insulinoma
JereyBaron andLindseyL.Perea
70
Concept
The way insulinoma can be tested can range from the typical
presentation of a patient with this type of disease to an incidental imaging nding. It will be important to also ensure
that potential for malignancy, although low, is discussed and
how management strategies change.
Way Question May BeAsked?
An otherwise healthy 53-year-old woman who works as an
ICU nurse is brought to the emergency department after feeling lightheaded and was found to have a low blood glucose
level (<50mg/dL). Her symptoms improved with a glucose
tablet. She informs you that this is not the rst time that this
has happened to her both at work and at home.
This patient scenario may include a healthcare provider as
mentioned above. This may be intentional with the attempt
to make the examinee differentiate between a self-induced
hypoglycemic state versus the presentation of insulinoma.
How toAnswer?
History
• Hypoglycemic symptoms
– Syncope, sweating, blurred vision, palpitations, weak-
ness, seizures, altered mental status
J. Baron
Department of Surgery, Cooper University Hospital,
Camden, NJ, USA
e-mail: jeffreybar@pcom.edu
L. L. Perea (
Department of Surgery, Division of Trauma and Acute Care
Surgery, Penn Medicine Lancaster General Health,
Lancaster, PA, USA
Department of Surgery, Philadelphia College of Osteopathic
Medicine, Philadelphia, PA, USA
e-mail: lindsey.perea@pennmedicine.upenn.edu
*)
• Presentation with Whipple’s triad (not as prominent as
initially thought)
– Hypoglycemia (<55mg/dL)
– Symptoms of hypoglycemia
– Relief of symptoms with glucose
• History of weight gain
• Exogenous insulin use
• Family history
– Include endocrine history along with history of
MEN-1
• Rule out other causes of hypoglycemia
– Exogenous insulin use, liver disease, diabetes,
pregnancy
Physical Examination
• Although there are no specic physical examination ndings exclusively associated with the diagnosis of insulinoma, patients may be obese.
Diagnostic Tests
• Laboratory Analysis
– (Note: Initial evaluation is through biochemical testing
and a 72h fast.)
– Biochemical hypoglycemia (<55mg/dL)
– Beta hydroxybutyrate (≤ 2.7mmol/L)
– Elevated proinsulin level (≥5pmol/L)
– Elevated plasma insulin levels (≥6 μU/mL)
– Elevated C-peptide level (≥0.2nmol/L)
• Imaging/Localization
– It is important to recognize that insulinomas may not
be able to be localized pre-operatively via traditional
imaging and may require further invasive studies or
operative exploration
– Cross sectional imaging: CT/MRI
Majority located within the pancreas where there is
an equal distribution.
Due to the majority of insulinomas being relatively
small in size (<2 cm), they often require further
imaging studies for workup.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. Neff et al. (eds.), Passing the General Surgery Oral Board Exam, https://doi.org/10.1007/978-3-031-78244-2_70
219
220
J. Baron and L. L. Perea
Extra-pancreatic lesions most commonly within the
duodenum, splenic hilum, and gastrocolic
ligament.
– Arteriography/portosplenic vein sampling with cal-
cium injections.
Injection of calcium will stimulate the release of
insulin.
– Endoscopic ultrasound
Relatively successful in detection of insulinoma.
Should be used in combination with cross-sectional
imaging.
– Nuclear medicine scan
Radioisotope targeting GLP-1 receptor.
Less successful in malignant disease process.
Treatment
• Medical management
– The usage of medication in the treatment of insulin-
oma is limited to certain situations.
– Glucagon
Can be used as an adjunct to help reduce incidence
of hypoglycemia and management of hypoglycemic episode.
Best used as bridge to denitive treatment or in
patients unable to undergo surgical resection.
– Octreotide
May also have benet in certain patients in decreasing episodes of hypoglycemia.
– Diazoxide
Functions to reduce the secretion of insulin. Can be
used for initial management and as a bridge to
denitive care. If there is high suspicion for insulinoma, treatment should be initiated.
Also serves a role in management of malignant and
metastatic insulinoma.
Must be used cautiously in patients with underlying
medical conditions, especially heart disease, as this
can result in congestive heart failure.
– Chemotherapy
Chemotherapy use in insulinoma is reserved for
progressive disease, malignant/metastatic disease,
and in patients that are unable to undergo surgical
resection.
Typically used with combination therapy.
• 5-uorouracil (5FU)
• Streptozotocin or doxorubicin
Other therapies have been studied and are continually evolving to include monoclonal antibody
studies.
• Surgical treatment
– Need to perform complete examination of the
pancreas
This includes gastrohepatic ligament mobilization,
Kocher maneuver, lateral mobilization and inspection along with evaluation of the superior and inferior aspects of the pancreas.
– After initial mobilization
Tumor not able to be located
• Intraoperative palpation of the pancreas.
• Perform intraoperative ultrasound for further
localization.
• If unable to identify with ultrasound, can also
perform additional venous sampling.
Supercial and small lesions
• Enucleation procedure
– Should check for leak along with considering
a buttress and drain placement.
– Pancreatic leak is a common complication
even if not identied intraoperatively with
provocative maneuvers. Pancreatic leak management may be presented in follow up to
initial treatment management with
enucleation.
– Exceptions:
Lesions within 2mm of the main pancreatic duct.
Deep lesions.
Concern for malignancy (see below).
Distal lesions
• Can perform open or laparoscopic distal
pancreatectomy.
Malignancy
• Formal oncologic resection should be performed
with either Whipple procedure of distal
pancreatectomy.
• If there is evidence of gross metastatic disease→
should perform tumor debulking.
– Medical management with diazoxide and
chemotherapy (see above).
Special situations
• MEN-1: Can suggest performing a subtotal pancreatectomy because of the high incidence of
islet cell hyperplasia.
Patients may have mild hyperglycemia for 2–3days
postoperatively.
Common Curveballs
• Lesion not identied on initial imaging.
• Lesion not able to be identied on initial operative evaluation which can then be further elicited to reveal a lesion
unable to be identied on ultrasound and subsequent
steps.