Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 473 - файл
.pdf
352
Complications of parathyroidectomy and their management
Complications Characteristics Management
H. Hashmi and K. Patel
Hypocalcemia
Recurrent laryngeal nerve
injury
Persistent hyperparathyroidism
Mild hypocalcemia is common in the
postoperative period
May present with perioral numbness or
anxiety
Severe hypocalcemia may be the result
of permanent hypoparathyroidism (low
PTH, hyperphosphatemia) or hungry
bone syndrome (normal PTH, low/
normal phosphate)
Severe hypocalcemia may present with
ECG changes, seizures, and tetany
In experienced hands, injury to the
recurrent laryngeal nerves is rare (<1%)
Reoperative surgery increases the risk
of injury
Injury results in either temporary
dysfunction or paralysis of the vocal
cord
Traction injury to the nerve ➔result in
dysfunction, which is usually
temporary, resolving within 6months
Dened as a lack of sustained
normalization of calcium within
6months of surgery
May be due to technical error or missed
abnormal or supernumerary glands
All patients who have undergone
parathyroidectomy should be started
on calcium supplementation
Symptomatic hypocalcemia ➔
increase oral calcium and vitamin D
supplements
Severe hypocalcemia ➔IV calcium
and active vitamin D supplements
Unilateral injury➔ paralysis of the
ipsilateral cord in either the lateral or
paramedian position
Injections may be used for
medialization to improve swallowing
and vocal cord function
Bilateral injury ➔ respiratory
complications ➔ emergency
reintubation
Reoperation (by an experienced
surgeon)
Preoperative localization ➔may help
prevent this complication
Missed glands are most often found in
their appropriate anatomic location
Recurrent primary
hyperparathyroidism
Initial biochemical cure with subsequent
elevation of serum calcium after
6months of eucalcemia
Multiple Endocrine Neoplasias
Multiple endocrine neoplasia
MEN I MEN2A MEN2B
Genetics
Gene is located on 11q13 ➔
produce Menin protein
Preoperative localization and
reoperation if indicated
RET proto-oncogene located
on 10q11.21➔produce ret.
protein
RET proto-oncogene located
on 10q11.21➔produce ret.
protein
11 Endocrine
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Multiple endocrine neoplasia
MEN I MEN2A MEN2B
353
Characteristics
Management
Primary
hyperparathyroidism
➔hypercalcemia➔ most
common presenting
symptom
Pancreatic endocrine tumor
(nonfunctioning,
gastrinomas)
50% of MENI develops
Zollinger-Ellison syndrome
as a result of gastrinoma
Anterior pituitary tumors
Parathyroid imaging is not
required ➔ bilateral
exploration is required
Subtotal parathyroidectomy
versus total
parathyroidectomy with
autotransplantation ➔risk of
recurrence is greater with
subtotal rather than total
parathyroidectomy with
autotransplantation
These patients also have a
greater incidence of
supernumerary and ectopic
glands and thymic
carcinoids➔ bilateral
thymectomy
MTC➔ rst clinical
manifestation (nearly all
patients with classical
MEN2A develop MTC)
Pheochromocytomas
Hyperparathyroidism
Pheochromocytoma must be
excluded or managed prior to
surgery for MTC ➔ to
prevent potentially fatal
hypertensive crisis
Age recommendation for
prophylactic thyroidectomy
guided by the specic ret.
mutation. For patients with
the highest risk mutations➔
prophylactic thyroidectomy
is in the rst year of life or at
the time of diagnosis
Central compartment lymph
node dissection is not
required in prophylactic
thyroidectomy (except for:
hypercalcitonemia, and
highest risk ret. mutations)
MTC➔ rst clinical
manifestation (more
aggressive than MEN2A)
Pheochromocytoma➔
multiple and bilateral
Mucosal neuromas
Marfanoid habitus
Age recommendation for
prophylactic thyroidectomy
guided by the specic ret.
mutation. For patients with the
highest risk mutations➔
prophylactic thyroidectomy is
in the rst year of life or at the
time of diagnosis
Central compartment lymph
node dissection is not required
in prophylactic thyroidectomy
(except for:
hypercalcitonemia, and
highest risk ret. mutations)
For pheochromocytoma:
Unilateral adrenalectomy for
unilateral disease; resection of
the entire gland rather than
cortical-sparing surgery
Hyperparathyroidism is
multiglandular ➔ bilateral
exploration
For pheochromocytoma:
Unilateral adrenalectomy for
unilateral disease; resection
of the entire gland rather than
cortical-sparing surgery
MTC follow-up ➔calcitonin
level
Follow-up
If calcitonin levels are
normal➔ follow-up with
calcitonin and CEA twice
yearly for 2 years and then
yearly
354
adrenal ar
Right
e
artery
artery
Adrenals
Anatomy
Arterial Supply
Three vessels
Inferior phrenic artery ➔ Superior suprarenal
artery
Aorta ➔ Middle suprarenal artery
Renal Artery➔ Inferior suprarenal artery
H. Hashmi and K. Patel
Venous drainage
Left adrenal vein:
Drains into left renal or inferior phrenic
2–3cm in length
Right adrenal vein:
Less than 1cm in length
Empties into the posterior IVC or into an
accessory right hepatic vein
Right adrenal gland
Abuts the posterolateral surface of the
retrohepatic vena cava
Bounded by the right kidney➔ inferiorly
Bounded by diaphragm ➔posteriorly
Bounded by bare area of the liver➔
anterosuperiorly
Right superior
adrenal artery
Right middle
adrenal artery
Right inferior
tery
Liver
phrenic
artery
Kidney
Left
Aorta
phrenic
artery
Left
inferior
adrenal
arteries
Left
Right
renal
renal
Adrenal gland
Inferior
vena cava
Left superior
adrenal
arteries
Left middl
adrenal
artery
11 Endocrine
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Anatomy
355
Left adrenal gland
Lies between the left kidney and the aorta
Bounded by the diaphragm➔ posteriorly
Tail of the pancreas and splenic hilum
➔anteriorly
Physiology
Physiology
Glomerulosa
Fasciculata
Adrenal cortex
Stomach
Adrenal gland
Pancreas
Spleen
Kidney
Duodenum
Aldosterone: Regulated by angiotensin II and blood potassium level
Aldosterone regulates circulating uid volume and electrolyte balance by
promoting Na resorption and secretion of K and H ions
Glucocorticoids
CRH from hypothalamus ➔ secretion of ACTH by anterior pituitary ➔release
of cortisol
Highest levels of ACTH and cortisol are detected on waking
Nadir happens early evening
Cortisol creates a catabolic state ➔Increases vascular tone, gluconeogenesis,
glycogenolysis, suppresses immune system
Reticularis
Adrenal medulla
Androgens/estrogens
Androgen secretion is regulated by ACTH
Catecholamines
Tyrosine ➔(rate limiting step) ➔ dihydroxyphenylalanine (L-dopa)
➔dopamine ➔ norepinephrine ➔ epinephrine
Epinephrine is created by the action of phenylethanolamine
N-methyltransferase (found only in medulla and organ of Zuckerkandl)
Target tissue: Myocardium, brain, and skeletal muscle are mediated through
α-adrenergic receptors (norepinephrine > epinephrine) and β-adrenergic
receptors (epinephrine > norepinephrine)
356
Hyperaldosteronism
Hyperaldosteronism
Mean age of presentation is 50years
Resistant hypertension (on at least two medications)
Presentation
Hypokalemia (cramps, weakness, and paresthesia) ➔ can be a late sign of the disease
H. Hashmi and K. Patel
Primary hyperaldosteronism Secondary hyperaldosteronism
Diagnosis
Adenoma (85%)
Hyperplasia (15%)
Low renin
Aldosterone/renin
ratio>30+aldosterone>15mg/dl
➔90% sensitive for diagnosis
Stop all medications that affect potassium, renin, angiotensin, and aldosterone levels
(spironolactone, angiotensin-converting enzyme inhibitors, diuretics, and betaadrenergic blockers) before getting labs
Conrmatory biochemical testing ➔ salt-loading suppression test (aldosterone stays
high after increasing intravascular volume ➔ support a diagnosis of primary
aldosteronism
Localizing studies:
CT of the abdomen/pelvis is performed with less than 3-mm slices
MRI
Iodocholesterol or NP-59 scintigraphy (shows hyperfunctioning adrenal tissue ➔
differentiate adenoma from hyperplasia)
Adrenal vein sampling ➔ localize an aldosterone-producing tumor when none is
visible imaging (aldosterone level in one adrenal vein that is 4x higher than the
other➔ conrms the site of the aldosteronoma)
CHF
Renal artery stenosis
Liver failure
Renin is high
Imaging
>40years old + adrenal mass ➔ need selective venous sampling (because such
patients have a higher risk of nonfunctional adrenal adenomas)
Imaging ndings Likely diagnosis
Small unilateral mass Unilateral Aldosteronoma
One gland with a large mass and
opposite gland with a small mass
Bilateral normal glands Bilateral adrenal hyperplasia
Smaller mass may represent Aldosteronoma
11 Endocrine
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Hyperaldosteronism
357
Untreated hyperaldosteronism ➔ increased risk of stroke, myocardial infarction,
arrhythmias, and heart failure
Bilateral adrenal hyperplasia ➔ medical management
Management
Postoperative care Discontinue all antihypertensive medications and potassium supplements
Unilateral aldosteronoma ➔ surgical resection
Risk factors for incomplete resolution of their symptoms after adrenalectomy: male,
age>45years old, family history of hypertension, long-standing hypertension, need
>2 antihypertensive medications, and nonresponse to spironolactone
postoperatively except beta-blockers and clonidine ➔ wean beta-blockers and
clonidine
Adrenal Insuciency (Addison’s Disease)
Adrenal Insufciency
Causes Primary adrenal insufciency (Addison
Disease)
Intrinsic adrenal disease (Congenital
adrenal dysgenesis), defective
steroidogenesis, adrenal destruction,
pituitary disease, adrenal infection,
hemorrhage, and metastasis
Autoimmune destruction is the most
common mechanism
Increased ACTH Decreased or normal ACTH
Secondary adrenal insufciency
Due to withdrawal of exogenous steroids
Presentation Acute: Refractory hypotension, fever, lethargy, abdominal pain, nausea, vomiting; hypoglycemia,
and hyperkalemia
Chronic: Hyperpigmentation, weakness, weight loss, GI symptoms, hyperkalemia, and
hyponatremia
Diagnosis
Management Daily dose of a glucocorticoid and mineralocorticoid
Serum cortisol 15mg/dL or salivary cortisol 5 hg/ml is concerning for adrenal insufciency ➔ If
levels below threshold ➔ provocative testing through administration of 250mg cosyntropin with
serum cortisol levels measured within 30–60min (cortisol <18mg ➔ adrenal insufciency)
358
H. Hashmi and K. Patel
Pheochromocytoma
Pheochromocytoma
Arise from sympathetic ganglia or ectopic neural crest cells
Most Common location: Adrenal gland (90%) ➔ right side predominance
Extra-anatomic sites: near the renal hilum (most common), organ of Zuckerkandl (inferior aorta
Characteristics
Associated with MEN IIa, MEN IIb, von Recklinghausen’s disease, tuberous sclerosis, Sturge Weber disease,
Presentation Hypertension, tachycardia, palpitations, headache, sweating, anxiety, and malignant hypertension
near bifurcation), bladder, and along the sympathetic chain ➔ extra-adrenal tumors are more
likely malignant
Pheochromocytomas tend to be larger tumors (>3cm) that may appear heterogenous with cystic
areas
10% rule: malignant, bilateral, in children, familial, extra-adrenal
succinate dehydrogenase gene mutations, and neurobromatosis type 1
Initial screening test: Plasma fractionated metanephrines if positive ➔ conrm by 24-hour
urine for catecholamines and metanephrines (99% specicity)
Diagnosis
Management
Urine vanillylmandelic acid test ➔ is no longer used because it is less specic for the diagnosis
Falsely elevated plasma fractionated metanephrines due to decongestants, acetaminophen, and
tricyclic antidepressants
If biochemical testing conrms pheochromocytoma ➔ CT or MRI for localization ➔ of
nonlocalizing or metastatic disease suspected ➔
(FDG) positron emission tomography, or 18F-dihydroxyphenylalanine (DOPA)
Adrenalectomy
Ligate adrenal vein rst to avoid spilling catecholamines during tumor manipulation
123
I-MIBG scanning, 18F-uorodeoxyglucose
Hypercortisolism (Cushing’s Disease)
Hypercortisolism
Most common cause of hypercortisolism➔ exogenous steroid use
Characteristics
Presentation Central obesity, moon facies, striae, ecchymosis, acne, fatigue, muscle weakness, and poor
Cushing syndrome refers to endogenous hypercortisolism
Solitary adrenal adenoma ➔ causes atrophy of adjacent adrenal tissue and the contralateral
adrenal gland
wound healing
11 Endocrine
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Hypercortisolism
Diagnosis
359
Screening tests: 24-hour urine collection of free cortisol and a low-dose dexamethasone
suppression test
If any of the screening tests are elevated ➔ ACTH level should be determined
Random salivary or plasma cortisol ➔ not enough to rule out hypercortisolism
ACTH High-dose dexamethasone
Adrenal adenoma (10%) Decreased(<10pg/ml)
Pituitary adenoma (80%) Increased Suppressed
Ectopic ACTH (non-small cell
lung cancer; bronchial
carcinoids)
Low-dose dexamethasone suppression test (administer 1mg dexamethasone orally at
11pm; plasma cortisol is obtained at 8am); cortisol >5μg/dL ➔ Cushing
High-dose dexamethasone suppression test (administer 2mg dexamethasone orally every
6h for 2days. Take 24-hour urine collection for free cortisol on day 2)
Management Case Management
Adrenal adenoma (10%) Surgical removal of the affected adrenal gland
Pituitary adenoma (80%) Surgery, radiation, or medication to lower cortisol levels
Ectopic ACTH (non-small cell
lung cancer; bronchial
carcinoids)
Postoperative care Steroid replacement may be necessary in patients with low cortisol levels
Increased Not suppressed
Surgical removal or medications that reduce adrenal
cortisol production (ketoconazole and metyrapone)
Adrenal Incidentalomas
Adrenal incidentalomas
1–4% of abdominal CT scans show incidentalomas
5% of Incidentalomas are metastases
10% prevalence in patients >60years old
30% of patients with pheochromocytomas present with incidentalomas
Characteristics
In patients with a history of malignant disease, metastatic disease is a more likely cause of adrenal
masses, particularly when the masses are bilateral
Common metastases to adrenals: lung cancer, renal cell carcinoma, melanoma, breast cancer, and
colorectal cancer
Tumor size is the most important predictor if <3cm ➔ benign; > 6cm ➔ malignant
The risk of malignancy in tumors >6cm in size is >25%
Most patients with an adrenal incidentaloma have no signs of hormonal excess
Presentation
Suggestive features of a functioning tumor include hypertension, especially if difcult to control,
or signs or symptoms of excess glucocorticoid or androgen secretion
360
H. Hashmi and K. Patel
Adrenal incidentalomas
Management 60% of adrenal incidentalomas are nonfunctional cortical adenomas, but all incidentalomas should
be evaluated for functional status and malignant potential:
Evaluating malignant potential: Radiographic characteristics assist in determining malignant
potential. Size and Hounseld units (HU) on CT scan are signicant predictors of malignant
potential
Features of benign lesions Features of malignant lesions
<10 HU (non-contrast CT) ➔ 100% benign
Size <4–5cm
Homogenous appearance
Low attenuation on CT
Washout rapid
Loss of signal on opposed-phase MRI
sequences➔ highly specic for cortical adenoma
due to the intracellular lipid present within an
adenoma
Axial abdominal CT image with IV contrast
demonstrates an incidental right 4.2cm
adrenal mass (arrow) that measures –5HU,
which although relatively large is still highly
consistent with an adrenal adenoma
>10 Hounseld units
>5–6cm in size
Irregular borders
Calcication
Higher attenuation
Delayed washout <50% contrast washout
No loss of signal on opposed-phase MRI
Axial abdominal CT image with IV contrast
demonstrates an 11.8cm lobulated,
heterogenous mass (arrow) with internal
areas of necrosis arising from the right
adrenal, a known adrenocortical carcinoma
Lesion Imaging characteristic
Aldosteronomas Small tumors (< 1.5–2cm)
Low attenuation on CT
Show loss of signal on opposed-phase MRI
Adenoma Loss of signal intensity on magnetic resonance
imaging
Myelolipomas May be larger in size (> 4–5cm)
Have a characteristic appearance with
macroscopic fat
Adrenal metastases Higher attenuation
Do not lose signal intensity on opposed-phase
MRI
Pheochromocytoma Hyperintense on T2 weighting
11 Endocrine
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Adrenal incidentalomas
Check for functioning tumor before biopsy or surgery
FNA is not helpful in differentiating between benign and malignant lesions because malignancy is
determined by mitotic rate or capsular invasion➔ biopsy is only indicated for unresectable primary
or metastatic malignant tumors
Functional activity evaluation:
361
Biochemical evaluation Reason
Plasma fractionated metanephrines ➔ if
positive ➔ 24-hour urine free metanephrines
for conrmation
Salivary levels at night (bedtime) or 24- hour
urine collection ➔ high suspicion ➔ overnight
dexamethasone test
Plasma aldosterone/renin Exclude Aldosteronoma
Surgery is indicated if the mass has ominous CT scan characteristics (nonhomogeneous, >4–6cm,
functioning tumor or is enlarging)
Management
Follow-up
Laparoscopic adrenalectomy is gold standard (except if local invasion or a high suspicion of
adrenal cortical carcinoma)
Suspected adrenal myelolipomas ➔ no surgery + follow-up (except if symptomatic or the
radiographic diagnosis is uncertain)
Incidentaloma ➔ repeat imaging every 6months for 1year then annually for 1–2years
Repeat biochemical testing at 1year and annually for up to 5years
Adrenal Cancer
Adrenocortical carcinoma (ACC)
0.5–2% cases per million
Characteristics
Distant metastases develop in 40% of patients in 2years
Exclude pheochromocytoma
Exclude Hypercortisolism
Associated with a p53 mutation (Li-Fraumeni syndrome)
Hormone overproduction is common (60%)
Hypercortisolism, hyperaldosteronism, or virilization may occur
Presentation
Rapidly progressive Cushing syndrome is suspicious for carcinoma
Nonfunctioning carcinomas have a vague presentation: Abdominal pain, nausea, weight
loss, and fatigue
Most patients present with advanced disease
Соседние файлы в папке @xirurgi_2025