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- •Preface
- •Contents
- •Contributors
- •References
- •Introduction
- •History
- •Prevalence
- •Interfering Medications
- •Lab Interpretation
- •Radiological Diagnosis
- •Introduction
- •Etiology
- •Epidemiology
- •Parathyroid Gland Anatomy
- •Clinical Evaluation
- •Historical Presentations
- •Normocalcemic Primary Hyperparathyroidism
- •Laboratory Evaluation
- •Initial Laboratory Testing
- •Calcium
- •Corrected Calcium
- •Ionized Calcium
- •Parathyroid Hormone Assays
- •First Generation Assays
- •Serum Phosphate
- •25-Hydroxyvitamin D (Vitamin D)
- •24-Hour Urine Calcium
- •Biochemical Stone Risk Analysis
- •1,25-Dihydroxy Vitamin D (Calcitriol)
- •Secondary Hyperparathyroidism
- •Medication Effects
- •Tertiary Hyperparathyroidism
- •Familial Hypocalciuric Hypercalcemia
- •Autoimmune Hypocalciuric Hypercalcemia
- •Pseudohypoparathyroidism
- •Imaging Evaluation
- •Plain Radiography
- •Dual-Energy X-ray Absorptiometry
- •Vertebral Fracture Assessment by DEXA
- •Trabecular Bone Score by DEXA
- •High-Resolution Peripheral Quantitative CT
- •Gland Localization
- •Parathyroid Ultrasound
- •SPECT-CT
- •4D Neck CT
- •Magnetic Resonance Imaging
- •Conclusions
- •References
- •Introduction
- •Etiology
- •Epidemiology
- •Pathophysiology
- •Androgen Production by Endocrine Glands
- •Clinical Evaluation
- •Laboratory Evaluation
- •Imaging Evaluation
- •Conclusion
- •References
- •Introduction
- •Etiology
- •Epidemiology
- •Pathophysiology
- •Pituitary Corticotroph Adenomas: Cushing’s Disease
- •Ectopic ACTH Syndrome
- •Unilateral Adrenal Adenoma
- •Adrenocortical Carcinoma
- •Bilateral Adrenal Nodular Disease
- •Clinical Evaluation
- •Musculoskeletal
- •Metabolic
- •Cardiovascular
- •Reproductive
- •Immune
- •Psychiatric
- •Laboratory Evaluation
- •Diagnosing Hypercortisolemia: 24-Hour Urine Free Cortisol
- •Diagnosing Hypercortisolemia: Low-Dose Dexamethasone Suppression Test
- •Diagnosing Hypercortisolemia: Late Night Salivary Free Cortisol
- •Determining ACTH Status
- •Imaging Evaluation
- •ACTH-Secreting Pituitary Adenomas
- •Ectopic ACTH Syndrome
- •ACTH-Independent Hypercortisolism
- •References
- •Introduction
- •Etiology/Physiology
- •Epidemiology
- •Insulinoma
- •Etiology/Pathophysiology
- •Epidemiology
- •Clinical Evaluation
- •Laboratory Evaluation
- •Gastrinoma
- •Etiology/Pathophysiology
- •Epidemiology
- •Clinical Evaluation
- •Laboratory Evaluation
- •Somatostatinomas
- •Etiology/Pathophysiology
- •Epidemiology
- •Clinical Evaluation
- •Laboratory Evaluation
- •VIPoma
- •Etiology/Pathophysiology
- •Epidemiology
- •Clinical Evaluation
- •Laboratory Evaluation
- •Imaging Evaluation
- •Conclusion
- •References
- •Epidemiology
- •Clinical Evaluation
- •Laboratory Evaluation
- •Glucagonomas
- •Etiology/Pathophysiology
- •Introduction
- •Primary Aldosteronism
- •Adrenal Vein Sampling
- •Anatomy
- •Embryology
- •Right Adrenal Vein
- •Left Arenal Vein
- •AVS Procedure
- •ACTH Stimulation
- •Technique
- •Rapid Cortisol Assay
- •Sequential vs. Simultaneous AVS
- •C-Arm Cone-Beam CT
- •Complications
- •Conclusion
- •References
- •Introduction
- •Indications
- •Techniques
- •Anatomy
- •Approaches
- •Technical Considerations
- •Interpretation
- •Complications
- •Outcomes
- •Conclusion
- •References
- •Introduction
- •Imaging Evaluation
- •Indications
- •Contraindications
- •Technique
- •Anatomy
- •Procedure Technique
- •Challenges
- •Results Interpretation
- •Complications
- •Conclusions
- •References
- •Introduction
- •Indications
- •Contraindications
- •Technique
- •Anatomy
- •Anatomical Variations
- •Pathophysiology
- •Approach
- •Technical Considerations
- •Complications
- •Conclusion
- •References
- •Introduction
- •Indications
- •Insulinomas
- •Gastrinomas
- •Nesidioblastosis
- •Other Indications
- •Contraindications
- •Technique
- •Anatomy
- •Procedure Technique
- •Outcomes
- •Complications
- •Conclusions
- •References
- •Hyperaldosteronism
- •Surgical/Pharmacological Therapy
- •Nuclear Medicine
- •Hyperparathyroidism
- •Primary Hyperparathyroidism: Surgical/Pharmacological Therapy
- •Secondary Hyperparathyroidism: Surgical/Pharmacological Therapy
- •Tertiary Hyperparathyroidism: Surgical/Pharmacological Therapy
- •Nuclear Medicine
- •Hyperandrogenism
- •Pharmacological Therapy
- •Nuclear Medicine
- •Pancreatic Endocrine Tumors
- •Surgical/Pharmacological Therapy
- •Nuclear Medicine
- •Hypercortisolism
- •Surgical/Pharmacological Therapy
- •Nuclear Medicine
- •References
- •Introduction
- •Preoperative Optimization
- •Adrenalectomy
- •Surgical Approach
- •Open Adrenalectomy
- •Laparoscopic Adrenalectomy
- •Transperitoneal (Transabdominal) Adrenalectomy
- •Retroperitoneal Adrenalectomy
- •Robotic Adrenalectomy
- •Partial Adrenalectomy
- •Complications
- •Postoperative Care
- •References
- •Preoperative Planning
- •Imaging
- •Ultrasound Evaluation
- •Nuclear Medicine Imaging Techniques
- •Dynamic Computed Tomography
- •Preoperative Medical Optimization
- •Indications
- •Contraindications
- •Surgical Interventions
- •Bilateral Cervical Exploration
- •Minimally Invasive Techniques
- •Autotransplantation
- •Complications
- •Postoperative Care
- •References
- •Introduction
- •Surgical Technique
- •Approach
- •Tumor Resection
- •Skull Base/Sellar Repair
- •Surgical Challenges
- •Postoperative Care
- •Conclusion
- •References
- •Introduction
- •Functional PNET
- •Insulinoma
- •Gastrinoma
- •Glucagonoma
- •VIPoma
- •Somatostatinoma
- •Nonfunctional PNET
- •Hereditary Syndromes
- •MEN-1
- •Von Hippel-Lindau Syndrome
- •Preoperative Workup
- •Operative Approaches
- •Curative Intent
- •Pancreatic Resections
- •Pancreaticoduodenectomy
- •Distal Pancreatectomy
- •Total Pancreatectomy
- •Enucleation
- •Transduodenal Approach
- •Nonlocalized Lesions
- •Other Operative Considerations
- •Cholecystectomy
- •Perioperative Somatostatin Analogues
- •Postoperative Care
- •Postoperative Complications
- •Pancreatic Fistula
- •Conclusion
- •References
- •Introduction
- •Adrenal Vein Sampling
- •Ablation
- •Patient Preparation
- •Procedure
- •Follow-Up
- •Outcomes
- •Embolization
- •Patient Preparation
- •Procedure
- •Follow-Up
- •Outcomes
- •Conclusion
- •References
- •Preprocedural Evaluation
- •Contraindications:
- •Preparation Before Thermal Ablation
- •Equipment Preparation
- •Patient Preparation
- •Thermal Ablation Procedure
- •Patient Position
- •Ultrasound Evaluation Before Ablation
- •Local Anesthesia
- •Liquid Isolation
- •Thermal Ablation
- •Percutaneous Parathyroid Injection
- •Indications
- •Contraindications
- •Preparation Before Treatment
- •Procedure
- •Treatment Strategy
- •References
- •Workups
- •Serum Thyroid Stimulation Hormone (TSH)
- •Thyroid Sonography
- •Bethesda System
- •Treatment
- •Benign Lesion
- •Malignant Lesion
- •Thyroid Radiofrequency Ablation
- •Indications
- •Indications
- •Contraindications
- •Anatomy
- •The Thyroid Gland
- •Vessels
- •Muscles
- •Nerves
- •Procedure
- •Preprocedural Workup
- •The Procedure
- •Results
- •Nonfunctioning Thyroid Nodules
- •Autonomously Functioning Thyroid Nodules
- •Marginal Regrowth
- •Complications
- •Pain
- •Voice Change
- •Hemorrhage
- •Hypothyroidism
- •Rupture
- •Tracheal Injury
- •Esophageal Injury
- •References
- •Introduction
- •Goiter Embolization
- •Summary
- •References
- •Introduction
- •Transarterial Embolization (TAE or “Bland” Embolization)
- •Basic Principles
- •Technique
- •Gelatin Sponge
- •Polyvinyl Alcohol Particles (PVA)
- •Microspheres
- •n-Butyl Cyanoacrylate
- •Transarterial Chemoembolization (TACE)
- •Conventional TACE
- •Drug-Eluting Beads TACE
- •Outcomes
- •TAE vs. TACE
- •Selective Internal Radiation Therapy (SIRT)
- •Technique
- •Outcomes
- •Percutaneous Ablation
- •Summary
- •References
- •Introduction
- •Pediatric Hypertension
- •Pathophysiology
- •Pediatric Fibromuscular Dysplasia
- •Pediatric Renal Vein Sampling
- •Preprocedural Preparation
- •Procedure Technique
- •Summary
- •References
- •Index

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J. Kearney et al.

Part V
Interventional Treatment of Endocrine
Disorders

Chapter 16
Interventional Treatment ofPrimary
Aldosteronism
ChristosGeorgiades, PanagiotisLiasides, andKelvinHong
Introduction
Primary aldosteronism (PA) is the excessive production of aldosterone by one or
both adrenal glands resulting in related clinical signs and symptoms. It is an underappreciated cause of hypertension with a reported prevalence between 2.7% and
10% among the hypertensive population [1–3]. Considering there are more than 65
million Americans diagnosed with hypertension (HTN) [4], PA is the causative factor in two to seven million patients who are mislabeled as “essential” hypertensives.
In approximately one-third of these, PA is due to a unilateral functioning adrenal
adenoma, while the rest are due to bilateral hyperplasia or bilateral adenomas [5]. It
is staggering then to consider that one to two million Americans are suffering from
a more virulent form of HTN compared to its “essential” counterpart one that can
potentially be cured if diagnosed and treated. Indeed, it has been shown that PA is
associated with accelerated and worse cardiovascular outcomes compared to those
from primary hypertension, including the risk of coronary artery disease and cerebrovascular stroke [6].
Unilateral total, or when feasible partial, adrenalectomy is the standard of care
for a functioning adrenal adenoma causing medication-resistant PA. Minimally
invasive, image-guided treatments have recently become available to the wider
C. Georgiades (*) · K. Hong
Department of Radiology & Radiological Sciences, Johns Hopkins University,
Baltimore, MD, USA
e-mail: Khong1@jhmi.edu
P. Liasides
USC Medical Center, Los Angeles, CA, USA
Division of Trauma and Surgical Critical Care, University of Southern California Keck
School of Medicine, Los Angeles, CA, USA
Switzerland AG 2022
H. Yu et al. (eds.), Diagnosis and Management of Endocrine Disorders in
Interventional Radiology, https://doi.org/10.1007/978-3-030-87189-5_16
233© The Author(s), under exclusive license to Springer Nature

234
public, and accumulating evidence points to high efcacy and an excellent safety
prole. These image-guided treatments include percutaneous ablation and endovascular embolization of the unilateral functioning adrenal adenoma.
C. Georgiades et al.
Adrenal Vein Sampling
Prior to any non-pharmaceutical denitive treatment, conrmation of a unilateral
source of independent and excessive aldosterone production as well as lateralization is necessary [7]. This is achieved with adrenal vein sampling (AVS). Rarely,
unilateral adrenal hyperplasia and contralateral nonfunctioning adenoma can
coexist. If resection of the adenoma is performed without prior AVS conrmation,
the patient will continue to suffer from PA and miss the opportunity for curative
resection. There exist different technical protocols on how to perform AVS.The
most rigorous, sensitive, and specic one includes pre- and post-adrenocorticotropic hormone (ACTH) stimulation sampling and the use of C-arm CT to conrm
selectivity in order to render biochemical lateralization reliable [3, 8]. Briey,
both adrenal veins are selected with catheters from a common femoral vein
approach (Fig.16.1cand d). A C-arm CT is performed during contrast injection
to conrm selectivity (Fig.16.1cand d). Venous blood sampling is performed,
followed by ACTH administration. Sampling is repeated 30 min post-ACTH
stimulation. Cortisol adrenal vein levels are compared to that from inferior vena
cava (IVC) levels to conrm catheter selectivity. Once selectivity is conrmed,
aldosterone levels are compared between adrenal vein samples to conrm lateralization. If both catheter selectivity and biochemical lateralization are conrmed,
surgical or image-guided treatment can be undertaken. Less rigorous protocols
sample the adrenal veins only post- ACTH stimulation. Though less time-consuming, this protocol can result in false- negative results in approximately 22% of
patients tested [8].
Ablation
Ablation refers to the destruction of targeted tissue by way of heating (radiofrequency ablation [RFA] or microwave ablation [MWA]) or freezing (cryoablation).
Current technology allows effective ablation for lesions up to around 3–4 cm in
diameter, which is inclusive of the majority of functioning adrenal adenomas. The
technical objective of ablation is to kill the entire targeted functioning adrenal tissue
without damaging nearby collateral structures such as the bowel, pancreas, kidney,
etc. The clinical objective is to signicantly reduce the patient’s blood pressure,
eliminate/reduce the number of antihypertensive medications, and eliminate hypokalemia and the need for potassium supplementation.

16 Interventional Treatment ofPrimary Aldosteronism
235
a
c d
b
Fig. 16.1 Adrenal vein sampling in a patient with PA and a left adrenal adenoma noted on diagnostic MRI.Right adrenal venogram (a) via a catheter shows the classic “feathery” appearance of
the adrenal gland (white arrowhead). Coronal C-arm CT during the venogram (b) shows diffuse
parenchymal enhancement of the right adrenal gland (white arrowhead), conrming catheter selectivity. Digital subtraction venogram of the left adrenal gland (c) via a super-selective microcatheter
(white arrow) shows enhancement of the left adrenal nodule (white arrowhead). Axial C-arm CT
during the left adrenal venogram (d) shows enhancement of the left adrenal adenoma (white arrowhead), conrming catheter selectivity
Patient Preparation
Unilateral functioning aldosteronoma is conrmed by AVS.A cross-sectional imaging study (CT or MRI, Fig.16.2a) is reviewed to ensure there is a safe ablation
window. Eight-hour fasting is required as the procedure is performed with the
patient under conscious sedation or possibly general anesthesia. One of the perioperative risks is catecholamine shock, which manifests as severe hypertension and/or
arrhythmia and can be life-threatening. To reduce this risk, a 5-day premedication

236
a
b
C. Georgiades et al.
c
d
e
Fig. 16.2 A 55-year-old male with severe chronic hypertension resistant to ve antihypertensive
medications and with hypokalemia. The plasma aldosterone-to-renin ratio was elevated. The
patient had a prior AVS, which conrmed a functioning aldosteronoma in the left adrenal gland.
Contrast-enhanced, T1-weighted, fat-suppressed MR image (a) shows a 2.5cm hyper-vascular left
adrenal mass (white arrow). Axial CT image during cryoablation (b) shows the cryo-needle penetrating the left adrenal mass (white arrowheads). Post-cryoablation CT (c) shows the still frozen
left adrenal mass (white arrowheads) and the “ghost” trajectory of the removed cryo-needle (white
arrow). Within days post-cryoablation, the patient’s blood pressure showed a signicant reduction,
the number of antihypertensive medications dropped from 5 to 2, and the patient no longer required
potassium supplementation. One-month post-cryoablation, coronal, contrast-enhanced MR image
(d) shows a complete devascularization (lack of contrast enhancement) of the ablated adrenal
nodule (white arrowheads). One-year, axial, post-ablation, contrast-enhanced CT image (e) shows
size reduction and persistent devascularization (lack of enhancement) of the left adrenal nodule
(white arrowheads)

16 Interventional Treatment ofPrimary Aldosteronism
with both alpha- and beta-blockers is strongly recommended. Ablation is performed
with the patient in the prone position and in the CT scanner. In addition, if cryoablation is chosen, it should be remembered that in case of emergency, the cryoprobes
will take 2–3min to be adequately thawed for removal. To further reduce the risk of
adverse outcomes from possible arrhythmia, the placement of external pacing pads
is also recommended.
237
Procedure
The procedure is performed under continuous patient monitoring. After sedation
induction and aseptic preparation, a baseline CT is obtained to plan probe access/
trajectory. The probe is inserted into the targeted lesion (Fig.16.2b). After ablation
is completed, the probe is removed, and a repeat non-contrast CT is obtained to
exclude immediate complications, such as hemorrhage or pneumothorax
(Fig. 16.2c). The patient is recovered, observed for a minimum of 3h, and discharged to home.
Follow-Up
Because of the possibility of the post-ablation precipitous blood pressure drop as
aldosterone levels drop, the patient is advised to monitor blood pressure at home
and consult his/her primary care or interventionalist for a possible reduction of the
number or dosages of his/her antihypertensive medications. Long-term follow-up
relies solely on the stability or recurrence of symptoms and/or signs of hyperaldosteronism and not on imaging response, though the latter can be conrmatory for
complete tissue ablation (Fig.16.2d and e).
Outcomes
An important meta-analysis by Liang etal. included a total of 89 patients (7 studies)
with clinical symptoms from PA who were treated with thermal ablation. During the
nearly 4-year follow-up, 75% of patients saw signicant and sustained improvement or the resolution of their HTN with a mean systolic blood pressure reduction
of 29.06mm Hg (95% condence interval [CI], −33.93 to −24.19) and mean diastolic blood pressure reduction of 16.03mm Hg (95% CI, −18.33 to −13.73). All
patients saw a reduction in the number of antihypertensives used and potassium
levels normalized in all seven studies [9]. Though not as important as clinical follow-up, imaging response can also provide evidence as to the efcacy of percutaneous ablation. In a prospective study, Nunes TF etal. reported a 94% (16/17) complete
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