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362
Adrenocortical carcinoma (ACC)
H. Hashmi and K. Patel
Biochemical
evaluation
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
Serum adrenal androgens
Serum estradiol in men and postmenopausal women
Imaging CT of the chest and abdomen to look for metastases to the liver, lymph nodes, and lungs;
bone scan to look for bony metastases
T N M
Staging
T1<5cm, no
invasion
T2>5cm, no
invasion
T3 tumor
invasion into fat
T4 tumor with
organ invasion
No lymph node
disease
N1 lymph node
disease
Biochemical evaluation
Fasting blood glucose
M0 no metastases
M1 metastases
Management
Stage TNM 5years survival
Stage I T1N0M0 82%
Stage II T2N0M0 61%
Stage III T1-T4, N1, M0 or
T3-T4, N0, M0
Stage IV Any M1 13%
Complete surgical excision is the only potentially curable treatment for ACC
Stages I–III disease that is potentially resectable ➔ surgical resection rst
The disease is often not curable because of occult micrometastases
Intracaval extension or tumor thrombus is not a contraindication to surgery
If nearby organs involved ➔ en bloc resection of involved organs
Suspicious lymph nodes should be resected, but benet has not been established
Debulking may play a role: For functional tumors, debulking may help control
hypersecretion
Laparoscopic resection is controversial
50%
11 Endocrine
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Adrenocortical carcinoma (ACC)
363
Mitotane Radiation Chemotherapy
Indications • Incomplete
resection
• High-grade
disease (Ki67>10% or>20
mitoses/HPF)
• Intraoperative
tumor spillage
Adjuvant therapy
Benet Improves local
Follow-up Surveillance for recurrence of disease should include CT or MRI of the chest, abdomen and
pelvis every 3months for 2years and then every 4–6months for 5years
• Vascular or
capsular invasion
• Incompletely
resected tumor
• Stage III disease
• Tumor spillage at
the time of
resection
• High-grade
disease
• Palliative
radiation for relief
of bone pain and
reduction in
paresthesia or
paralysis from
metastatic ACC
control; no survival
benet
Cisplatin-based
adjuvant regimen in
combination with
mitotane in patients
who are at higher risk
for early recurrence
Limited data exist
regarding its usefulness
Research
Reference Findings
Autorino R, Bove P, De Sio M, etal. Open
versus laparoscopic adrenalectomy for
adrenocortical carcinoma: a meta-analysis of
surgical and oncological outcomes. Ann Surg
Oncol. 2016;23(4):1195–1202
Open adrenalectomy is considered the standard for the surgical
management of ACC, as it allows proper radical extirpation of
the disease. Laparoscopic adrenalectomy offers a shorter hospital
stay, possibly allowing a quicker postoperative recovery, but
minimally invasive approach should be only offered in carefully
selected ACC cases and by centers with appropriate laparoscopic
expertise in order to avoid jeopardizing the oncological outcome
Surgical Therapy
Preoperative management
Preoperative alpha blocker (phenoxybenzamine) to control hypertension and tachycardia
(10–14days before surgery) ➔ add beta-blocker if additional antihypertensives are needed
Pheochromocytoma
Aldosterone or
cortisol-producing
adenoma
Beta-blockers should never be given before alpha-blockers because they may precipitate a
hypertensive crisis and cause acute cardiac decompensation
Volume replacement as the blockade proceeds and volume capacity expands
IV hydrocortisone preop to prevent adrenal insufciency postop
364
Preoperative management
Start antihypertensive medications that can be stopped without a taper postoperatively:
aldosterone antagonist (spironolactone), angiotensin-converting enzyme inhibitors or
Aldosteronoma
angiotensin receptor blockers, or calcium channel blockers
May have hypokalemia and hypernatremia➔ potassium-sparing diuretics can aid in
preoperative blood pressure control and counteract potassium losses
Intra-op issue Management
H. Hashmi and K. Patel
Hypertension in
pheochromocytoma
Hypotension in
pheochromocytoma
Hypertensive exacerbations may occur during surgery with anesthesia induction, carbon
dioxide insufation, and tumor manipulation ➔ nitroprusside: First line vasodilator
Transient pressor support may be needed after the tumor has been devascularized. The
surgeon should inform the anesthesia team when the adrenal vein has been
ligated➔phenylephrine: drug of choice
Laparoscopic
retroperitoneal
Open approach
Adrenal tumors demonstrating
features concerning for
malignancy
Indications
Contraindication BMI>35, especially in males,
approach
Small tumors with low risk of
malignancy
Small (<4cm) tumors with
previous abdominal surgery ➔
avoid intra-abdominal
adhesions
due to increased
retroperitoneal perinephric fat
Key steps to adrenalectomy
Laparoscopic
transabdominal
approach
Small tumors with low
risk of malignancy
Right adrenalectomy
Incise the right hepatic triangular ligament and retract the liver and colon
medially
Mobilize the second portion of the duodenum to expose the right adrenal gland
Dissect superiorly along the IVC to the level of the right diaphragmatic crus
Divide the adrenal vein and inferior phrenic vein
Divide and ligate the small-caliber arterial branches
Circumferential dissection of the adrenal gland
11 Endocrine
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Key steps to adrenalectomy
Left adrenalectomy
365
Take down the lateral splenic attachments
Spleen and pancreatic tail can be retracted gently anteriorly
Dissect in the avascular plane between the posterior surface of the pancreas and
the anterior surface of Gerota fascia
Divide and ligate adrenal vein and its associated phrenic vein
Divide and ligate the small-caliber arterial branches (avoid the superior pole
renal artery branch that can lie inferior to the gland)
Dissect the medial edge of the gland from the diaphragm en bloc
Case scenario Management/prevention
Intraoperative decision making
Splenic capsule tearing ➔
bleeding
Injury to the IVC Hold pressure above and below the injury to
Mistaken removal of distal
pancreas during attempted
laparoscopic adrenalectomy
Tumor invades solid organs
(i.e., liver, kidney, pancreas)
The adrenal gland can lie very close to the
splenic hilum and the tail of the pancreas.
Avoid injury to these structures by staying
close to the adrenal capsule with dissection
slow blood loss. Attempt at primary repair for
a small injury
Left adrenalectomy should entail positive
identication of both the distal pancreas and
the adrenal gland to ensure the correct organ
is removed
En bloc resection should be performed
Vascular Access
Surgical Intensive Care
12
AmirH.Sohail, YeshaManiar, RandiHarris,
AmauryMartinez, andJamesMaurer
Ultrasound use for intravascular access
Depth of Penetration is inversely
related to ultrasound frequency
General Information
Resolution of images is directly
related to ultrasound frequency
Vascular access
A. H. Sohail (*) · Y. Maniar
General Surgery Residency, NYU Long Island
School of Medicine, NYU Langone—Long Island
Hospital, Mineola, NY, USA
e-mail: amir.sohail@nyulangone.org;
yesha.maniar@nyulangone.org
R. Harris
Department of Vascular and Endovascular Surgery,
Mayo School of Graduate Medical Education, Mayo
Clinic, Rochester, MN, USA
e-mail: harris.randi@mayo.edu
High-frequency linear transducer (5–10MHz) is selected for the identication of vascular
structures
Lower frequencies: higher tissue
penetration; lower resolution
Higher frequencies: lower tissue
penetration; higher resolution
A. Martinez
Saint Joseph’s University Medical Center,
Paterson, NJ, USA
J. Maurer
Department of Surgery, Mount Sinai South Nassau,
Oceanside, NY, USA
e-mail: james@mailmaurer.com
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
H. Ajouz et al. (eds.), The ABSITE Blueprints, https://doi.org/10.1007/978-3-031-32643-1_12
367
368
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A. H. Sohail et al.
Choosing central venous catheterization site
Clinical scenario Management
Patient with arteriovenous stula Do not place central venous catheter on the side of an arteriovenous
stula
Patient has pacemaker or AICD Do not place central venous catheter on the side of a pacemaker
Patient had previous lung surgery
Trauma patient that needs resuscitation Subclavian approach preferred if no torso trauma
During CPR Preferred site is femoral
Possible intra-thoracic adhesions ➔ avoid iatrogenic pneumothorax/
hemothorax on the same (ipsilateral) side
Central venous catheterization
Site Anatomy Advantages Disadvantages
• Highest failure rate
Subclavian
Internal
jugular
Femoral
Subclavian vein lies posterior to the clavicle
after crossing the rst rib
Internal jugular vein is anterolateral to the
common carotid artery
Femoral vein lies medial to the femoral artery
(NAVEL—Nerve—Artery—Vein—Empty—
Lymphatic)
** Greater saphenous vein (GSV) can be an
anatomic marker (medial on the inner upper
leg and identifying GSV and then follow it
proximally to the femoral vein)
Lowest
infection rate
Lowest rate of
thrombosis
Commonly used
with sonography
Highest success
rate
• Highest risk of pneumothorax
• Non-compressible bleeding
• If used for temporary
hemodialysis access ➔ stenosis
➔negatively affect potential for
future permanent access
Difcult with tracheostomy
Highest risk of DVT
Highest risk of infection
No CVP monitoring
Avoid if IVC lter
Complications of central venous catheterization
Risk factors and
Complication
Venous air
embolism
presentation Diagnosis and prevention Management
Occurs when as little as
20mL of air is aspirated;
lethal dose is 3–5mL/kg
Place patient in Trendelenburg
position during insertion, Valsalva
maneuver during placement
Remove the catheter during
expiration and with the patient
supine / Trendelenburg (positive
intra-thoracic pressure). Hold
pressure over area for 1min after
removal.
Place the patient in the left
lateral decubitus position
and Trendelenburg to trap
air in right ventricular apex
Attempt aspiration of the
air
Place patient on a FiO2 of
1.0
12 Surgical Intensive Care
Complications of central venous catheterization
Risk factors and
Complication
Pneumothorax
Central lineassociated blood
stream infection
Arterial puncture
presentation Diagnosis and prevention Management
Ultrasound use lowers
Risk higher with subclavian
catheters than internal
jugular
See CLASBI section below See CLASBI section below See CLABSI section below
Risk is higher if ultrasound
is not used
pneumothorax rate
Aspiration of air does not
necessarily mean pleural puncture
Ultrasound-guided placement
369
Pigtail catheter if
pneumothorax on imaging,
especially if patient is
symptomatic
May lead to tension
pneumothorax, particularly
in mechanically ventilated
patients
• Hold manual nonocclusive pressure for
15min
• If cannulated by a
large-bore catheter (> 7
French), vascular surgery
consultation for removal
and/or repair
Higher risk with placement
in the left IJ or subclavian
vein, longer dwell time, use
Central vein
stenosis
Catheter related
thrombosis
Arrhythmias
of dialysis catheters
Mostly asymptomatic, can
cause edema, SVC
syndrome, high venous
pressures in case of an AV
stula on ipsilateral side
Mostly in upper extremities
Usually from irritation of
right atrium from the wire/
catheter
Duplex or venogram
• Duplex: initial study of choice
• Prophylactic anticoagulation is
not recommended, even with a
history of DVT
Do not advance wire >20cm
• Appropriate catheter length
• Fluoroscopic visualization
during placement, if possible
Research
Reference Conclusion
American Society of Anesthesiologists Task Force on Central
Venous Access, Rupp SM, Apfelbaum JL, Blitt C, etal.
Practice guidelines for central venous access: a report by the
American Society of Anesthesiologists task force on central
venous access. Anesthesiology. 2012;116(3):539–573
Asymptomatic stenosis
should not be treated
Can perform angioplasty/
stenting
High rate of re-stenosis
after endovascular
intervention
Treat with anticoagulation
Removal of catheter is not
required
Repositioning of catheter or
retrieving wire/catheter in
case of arrhythmia
The best way to conrm correct wire location is
to use the ultrasound in both cross-sectional and
longitudinal views to show that the wire is in the
vein, not in the artery
370
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Shock
Septic shock
A. H. Sohail et al.
Systemic inammatory response syndrome (SIRS)
Diagnosed based upon the following criteria:
• Temperature<36°C or>38°C
• Heart rate>90 beats per minute
• Respiratory rate>20 breaths per minute or PaCO2<32mm Hg
• White blood cell count >12,000 or<4000 or>10% bands
Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to
infection
Denitions
Presentation
Management
Septic shock: Sepsis + persisting hypotension requiring vasopressors to maintain MAP
≥65mm hg and lactate level>2mmol/L despite adequate volume resuscitation
SOFA (sepsis-related organ failure assessment score)
Calculated using P/F ratio, platelets, bilirubin, MAP, GCS, creatinine, and urine output
Organ dysfunction: Acute change in SOFA score≥2 points consequent to the infection
A SOFA score≥2 ➔ mortality risk of 10%
qSOFA (quick SOFA)
Calculated based upon RR≥22/min, GCS<15, and systolic BP (≤ 100mm Hg)
Each abnormality is worth one point. Patients with a qSOFA ≥2 are likely to have a
prolonged ICU stay or to die in the hospital
Early symptoms include confusion, sudden unexplained dyspnea, fever, hypothermia,
decreased urine output, cholestatic jaundice, metabolic acidosis, excessive bleeding, or
unexplained hypotension
Patients with hypoperfusion should receive at least 30mL/kg of IV crystalloid within 3h
For patients who require vasopressors, the initial target MAP≥65mm Hg
Norepinephrine is the recommended rst choice for patients who need vasopressors
Vasopressin or epinephrine can be added or used as second line therapy
Intravenous broad-spectrum antibiotics should be started within 1h of sepsis recognition
Steroids: IV hydrocortisone (200mg/day) for patients who remain hemodynamically
unstable despite uids and vasopressors
Sodium bicarbonate ➔ only for patients with pH<7.15
Glucose control: Blood glucose management should be used targeting a blood glucose
level>140 and≤180mg/dL
Source control: Identify source and determine whether a surgical intervention is required
Hypovolemic shock
Blood loss (hemorrhagic shock) most common type
Causes
Pathophysiology
Gastrointestinal bleeding
Increased insensible losses (emesis, diarrhea)
Peripheral and splanchnic vasoconstriction occurs to preserve blood ow to vital organs ➔
hemorrhagic shock pathophysiology
Hemorrhagic shock, resuscitation, and reperfusion ➔ release of inammatory mediators➔
distant organ injury through the systemic activation of other immune cells
12 Surgical Intensive Care
Hypovolemic shock
Presentation Hypotension, tachycardia, narrow pulse pressure, and cold clammy skin
371
Classication
Management
Outcome
Blood loss Systolic
Ml %
(pneumonic–
Tennis scoring)
Class 1 750 15% Normal Normal <100
Class 2 750–1500 15–30% Normal Decreased >100
Class 3 1500–2000 30–40% Decreased Decreased >120
Class 4 >2000 >40% Decreased Decreased >140
Blood and blood products ➔ used when the etiology of hypovolemic shock is bleeding
Balanced ratio of blood products: Packed red blood cells, plasma, and platelets are given
in a 1:1:1 ratio ➔ to avoid coagulopathy
A massive transfusion protocol is triggered when a patient is anticipated to receive
>10units of red blood cells
TEG is able to direct resuscitation based on the values obtained
A lactic acid level is an important prognostic factor for patients in shock
Failure to correct high lactate value within the initial 24h ➔ higher mortality in trauma
patients
Initial base decit value and its time to normalization ➔ predict patient outcomes
pressure
Pulse pressure Heart rate
Cardiogenic shock
Denitions
Signs and symptoms
Base decit can be affected not only by anaerobic metabolism but also by administration
of chloride-containing resuscitative uids ➔ decreased utility outside of the initial
resuscitation
Left-sided heart failure:
Systolic dysfunction ➔ reduced ejection fraction
Diastolic dysfunction ➔ inability of ventricle to relax
Right-sided heart failure: inability of the right ventricle to overcome pulmonary vascular
resistance, resulting in decreased cardiac output
Diaphoresis, cold/clammy extremities, decreased capillary rell, jugular venous distention,
pulmonary congestion, and S3 gallop
372
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Cardiogenic shock
A. H. Sohail et al.
Modality Findings
CXR Pulmonary vascular congestion
Echocardiography Dilated ventricles with decreased ejection function
Diagnosis
Management
Neurogenic shock
Pathophysiology
Lactic acid Elevated secondary to right-sided heart failure and congestive
hepatopathy
BNP Elevated in conditions that increase right side heart pressure
Decreased cardiac output; increased right heart lling pressures; and decreased myocardial
oxygen consumption
Manage underlying cause
Cardiac ischemia ➔ PCI
Hypervolemia ➔ diuretics
The best initial treatment is administration of an inotrope with a goal to raise CI>2
Dobutamine at doses (5–20μg/kg/min) ➔enhances myocardial contractility with mild to
moderate changes in heart rate
A vasopressor should be initiated when mean arterial pressure MAP<60mmHg
Neurogenic shock is a distributive form of shock that occurs after injury to the cervical or high
thoracic spinal cord ➔ results in the lack of sympathetic input from the peripheral nerves and
unopposed parasympathetic activation
The sympathetic bers to the heart exit the spinal cord at the T1 to T4 level, with injuries at or
above this level resulting in decreased myocardial contractility and heart rate ➔ bradycardia is
less severe when the injury is in the thoracic spinal cord rather than the cervical spinal cord
Hypotension in patients with acute spinal cord injury ➔ decreased spinal cord perfusion ➔
further ischemic injury
Presentation Bradycardia, hypotension, and warm extremities
Physical exam (motor / sensory loss below level, priapism, lack of rectal tone)
Diagnosis
Management
CT scan to look for bony abnormalities
MRI if a spinal cord injury is suspected
Signs Management
• Resolves within 2–5weeks after the injury
Bradycardia
Hypotension
• Scheduled oral albuterol
• Dopamine
• Pacemaker placement
Initial treatment of hypotension is with uid
Vasopressors may be considered after appropriate uid resuscitation
Norepinephrine is recommended as the initial pressor for alpha and beta
activation
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