C r i t i c a l C a re o f t h e Va s c u l a r

Surgery Patient
a, b
Milad Sharifpour, MD, MS *, Edward A. Bittner, MD, PhD, MSEd, FCCM

KEYWORDS
 Critical care  Vascular surgery  Postoperative complications  Aortic surgery
 TEVAR

KEY POINTS
 Patients undergoing major vascular procedures often have multiple comorbidities and are
at high risk for postoperative complications.
 Major postoperative complications after vascular surgery often affect multiple organ
systems.
 Critical care of the vascular surgery patient reduces postoperative complications and im-
proves the outcome.

INTRODUCTION

Patients that have undergone major vascular surgery require admission to the ICU for
postoperative care and management of potential complications. The management of
vascular disease is complex and includes both medical and surgical interventions.
Diseases can be classified as nonocclusive, whereby there is restricted blood flow,
or occlusive, whereby the vessels are completely obstructed. Aneurysmal disease oc-
curs when vessel walls weaken. The surgical treatment of these lesions includes
replacing the diseased segment with a vascular graft or excluding it with an endovas-
cular stent. Occlusive vascular disease can occur because of atherosclerotic emboli
or thrombosis and can be treated by embolectomy, bypass, or endovascular proced-
ures. Recent advances in surgical technology have shifted treatment options from
open surgical to endovascular approach. Despite advances in patient selection, sur-
gical technique, and anesthetic management, patients who undergo major vascular
surgery, whether open or endovascular, remain at increased risk for postoperative
complications.1 The high prevalence of systemic atherosclerosis and comorbidities
(diabetes mellitus, COPD, coronary artery disease, obstructive sleep apnea (OSA),

a
Department of Anesthesiology, Cedars Sinai Medical Center, 8700 Beverly Boulevard #8211,
Los Angeles, CA 90048, USA; b Critical Care-Anesthesiology Fellowship, Department of Anes-
thesia, Critical Care and Pain Medicine, Harvard Medical School, Massachusetts General Hos-
pital, Boston MA 02114, USA
* Corresponding author.
E-mail address: Milad.sharifpour@cshs.org

Anesthesiology Clin 40 (2022) 775–790

https://doi.org/10.1016/j.anclin.2022.08.017 anesthesiology.theclinics.com
1932-2275/22/ª 2022 Elsevier Inc. All rights reserved.
776 Sharifpour & Bittner

chronic kidney disease, and so forth), prolonged surgery, large intraoperative blood
loss and the associated hemodynamic shifts, systemic inflammatory response to sur-
gery, and the ischemia-reperfusion associated with cross-clamping and unclamping
the aorta leads to increased postoperative morbidity and mortality.2 Patients who
require emergency vascular surgery are at the highest risk for perioperative morbidity
and mortality as they are often physiologically and hemodynamically not optimized.
Postoperative critical care for patients that have undergone major vascular surgery
is focused on enhancing myocardial oxygen supply, optimizing circulatory volume sta-
tus, early extubation and mobilization, achieving hemostasis, and pain control. Early
identification and management of postoperative complications is the key to improving
patient outcomes. These complications are summarized in Table 1.

Open Aortic Surgery

Cardiac Complications: Postoperative cardiac complications are common in patients
who undergo major vascular surgery due to the high prevalence of atherosclerotic dis-
ease and include myocardial ischemia, congestive heart failure, and arrhythmias.3
Postoperatively, myocardial function can change for many reasons (from systemic in-
flammatory response to new coronary ischemia). In clinical situations of low cardiac
output, a transthoracic echocardiogram (TTE) can guide therapy. Acute management
of low cardiac output involves treating the underlying cause (often ischemic), and sup-
port care (fluids, inotropes, mechanical circulatory support devices). Postoperative
EKG monitoring with two precordial leads (V3 and V5) has greater than 95% sensitivity
for detecting postoperative myocardial infarction (POMI).4

Myocardial Ischemia
Myocardial ischemia can manifest in several ways including acute hemodynamic
instability (from decreased cardiac output), postoperative ECG changes, or an eleva-
tion in troponin. Ischemia can be the result of coronary thrombosis, or decreased flow
across a stable fixed lesion. Troponin can also rise in response to significant myocar-
dial strain, especially in the presence of renal impairment. Echocardiography is neces-
sary for evaluating cardiac function and detecting new wall motion abnormalities. The
presence of regional wall motion abnormalities should prompt input from a cardiolo-
gist regarding the need for coronary angiography and revascularization. Maintaining
adequate organ perfusion using a combination of inotropes, vasopressors, and intra-
venous (IV) fluids when warranted reduces the risk of ischemic complications.
Perioperative myocardial infarction defined by elevated troponin levels, occurs in
3% to 12% of the patients who undergo major vascular surgery, and is associated
with a three-fold increased risk of cardiac arrest and death.5,6 The pathophysiology
of POMI is complex and poorly understood. Tachycardia plays a role in the develop-
ment of cardiac ischemia while flow-mediated hypoperfusion, exacerbated by hypo-
tension and thrombosis, secondary to hypercoagulability and inflammation are also
contributing factors. Reducing myocardial oxygen demand is key to reducing the inci-
dence of postoperative myocardial complications. Optimization of hemodynamics,
maintenance of normothermia and treatment of shivering, and adequate control of
pain are crucial. Patients should be maintained on their usual cardiac medications
perioperatively; withdrawal of ß-blockers in patients on long-term therapy is associ-
ated with increased mortality, while discontinuation of statins postoperatively is a pre-
dictor of adverse postoperative cardiac events.7,8 Antiplatelet therapy requires
individualized consideration, particularly in the presence of coronary artery stents.
Hypertension and tachycardia increase myocardial oxygen demand and the risk of
myocardial ischemia and therefore should be treated with antihypertensive agents,
 Critical Care of the Vascular Surgery Patient 777

Table 1
Postoperative complications after open aortic surgery and strategies to prevent them

Complication Management Strategy

Neurologic
Spinal Cord Ischemia Monitoring for early signs of SCI
Epidural Hematoma Maintain appropriate CSF pressure
Stroke Ensure adequate SCPP
Pain Frequent neurologic checks to assess lower extremity
strength, bowel/bladder continence
Monitoring for early signs/symptoms of CVA
Multimodal pain management strategy
Cardiovascular
Postoperative MI Monitoring for symptoms/signs of myocardial ischemia,
Arrythmias myocardial biomarker checks
Heart failure/cardiogenic shock Early resumption or initiation of aspirin, beta-blocker,
Limb ischemia and statins
Avoid hypertension/hypotension
Careful management of intravascular volume
Monitoring peripheral pulses hourly by palpation or
Doppler signals
Monitoring for compartment syndrome
Daily inspection of surgical incisions
Pulmonary
Atelectasis Postextubation incentive spirometry and noninvasive
Pleural effusions positive pressure ventilation
Pulmonary edema Diuresis when appropriate
Pneumonia Expedite ventilator weaning process
Respiratory failure Early extubation when possible
ARDS Ventilator-associated pneumonia prevention bundle
Lung protective ventilation strategy
Renal
AKI Maintain euvolemia and adequate renal perfusion
pressure
Avoid nephrotoxins
Hematologic
Hemorrhage Monitor for bleeding complications and
HIT retroperitoneal hematoma
Conservative blood transfusion strategy unless
evidence of organ ischemia or hypotension
Thromboembolic prophylaxis
Gastrointestinal
Ileus Early resumption of oral feeding or early institution of
Mesenteric ischemia enteral feeding
Stress ulceration Monitoring for early signs of mesenteric ischemia
Abdominal compartment Stress gastritis prophylaxis when indicated
syndrome Early resumption of enteral feeding
Monitoring for abdominal compartment syndrome

which commonly include short-acting calcium channel blocker (nicardipine, clevidi-

pine) or ß-blocker (esmolol) infusions. Hypertension also exacerbates the risk of
bleeding and should be treated promptly. A target systolic blood pressure within
20% of the patient’s baseline value is often recommended.
778 Sharifpour & Bittner

Fluid management requires attention to detail both during the initial resuscitation
and on the second and third postoperative days, when the mobilization of interstitial
fluids (third space fluids) tends to occur. Patients commonly require additional fluid
resuscitation in the immediate postoperative period to maintain adequate end-organ
perfusion. However, by the second or third postoperative day, interstitial fluid shifts
back into the intravascular space and leads to volume overload and necessitates
diuresis. Hypervolemia should be treated with loop diuretics, or renal replacement
therapy if indicated, as volume overload is associated with adverse cardiac (arrhyth-
mias), respiratory (pulmonary edema), renal (AKI), and gastrointestinal (bowel edema,
delayed bowel function) outcomes. Volume status can be assessed by close moni-
toring of clinical examination, urine output, laboratory values and noninvasive cardiac
monitoring including transthoracic echocardiography.
Pulmonary complications: Postoperative pulmonary complications (PPC) are re-
ported in up to 30% of the patients undergoing open thoracoabdominal aortic repair
and are associated with increased ICU length of stay and mortality.9,10 PPCs include
atelectasis, pleural effusions, pulmonary edema, pneumonia, the need for supple-
mental oxygen, noninvasive positive pressure ventilation, reintubation, or failure to
wean from mechanical ventilator and the need for tracheostomy, and ARDS.11 Preop-
erative risk factors include tobacco use, COPD, and OSA. Intraoperative risk factors
include surgical division of the diaphragm, phrenic nerve injury, prolonged one-lung
ventilation, ischemia-reperfusion associated with aortic cross-clamping and unclamp-
ing, and the systemic release of inflammatory mediators, infusion of large volumes of
IV fluids transfusion of blood products and the associated fluid shifts.
Many patients, who undergo vascular surgery, are extubated in the operating room.
Those that remain intubated likely had complex operations with large volume fluid
resuscitation or transfusion or may have had trouble with intraoperative ventilation re-
quirements. Postoperatively, intubated patients should receive lung protective me-
chanical ventilation with tidal volumes of 6 to 8 mL/Kg of predicted body weight
and moderate amounts of PEEP, which may attenuate the risk of PPCs.12,13 Thoracic
epidural analgesia for intra- and postoperative pain control reduces intraoperative
opioid consumption, while providing superior postoperative pain control, and further
reduces the risk of PPCs.14 It is essential to achieve reversal of neuromuscular
blockade before extubation. Head of the bed should be elevated to 30 to reduce
airway edema and the risk of ventilator-associated pneumonia, and the patients
should undergo diuresis, when ready, to minimize pulmonary and airway edema
before extubation. Administration of dexamethasone, 8 to 10 mg every 8 hours for
24 hours, may be beneficial for reducing airway edema associated with fluid infusions
and prolonged double-lumen tube use. Early extubation facilitates patient mobilization
and reduces the risk of ventilator-associated pneumonia. Application of continuous
positive airway pressure or use of high flow nasal cannula after extubation has been
associated with fewer pulmonary complications. The benefit is believed to result
from maintaining functional residual capacity, which prevents atelectasis formation,
shunting, and hypoxemia, and improves the work of breathing.15 For patients who
require prolonged ventilator support, early tracheostomy can be beneficial for early
mobilization and expedited transfer out of the ICU.

Neurologic Complications
Spinal cord ischemia: Spinal cord ischemia (SCI) resulting in paraparesis, or para-
plegia is a devastating complication of surgery on the thoracoabdominal aorta. The re-
ported incidence of SCI following open thoracoabdominal aortic surgery is 2% to 8%,
compared with 4% to 7% after endovascular repair.16–18 The extent (highest risk in
 Critical Care of the Vascular Surgery Patient 779

patients with Crawford class II aneurysm) and location of the aneurysm, prior abdom-
inal aortic surgery, hypotension, duration of aortic cross-clamp, and emergent surgery
increase the risk of SCI.18,19 SCI may be identified immediately after emerging from
general anesthesia, or days to weeks later. It commonly presents as anterior spinal ar-
tery syndrome, with the loss of motor function, pain, and temperature sensation, while
vibration and proprioception may remain intact.
Frequent neurologic examinations facilitate prompt diagnosis and treatment and
reduce the risk of permanent deficit. Treatment includes increasing spinal cord perfu-
sion pressure (SCPP) by raising mean arterial pressure (MAP) to 90 mm Hg, using
phenylephrine or norepinephrine infusions, and cerebral spinal fluid (CSF) drainage
with the use of a lumbar drain.20 CSF drainage improves SCPP by decreasing CSF
pressure. It has been shown to reduce the risk of SCI and can improve or reverse a
postoperative neurologic deficit.21–24 CSF pressure is maintained below 10 mm Hg
to optimize spinal cord perfusion, as SCPP is determined by the difference between
MAP and CSF pressure (or central venous pressure, whichever is higher).

SCPP 5 MAP – CSF Pressure (or CVP)

CSF drainage should not exceed 20 mL/h as excessive drainage may increase the
risk of subdural hematoma and subarachnoid hemorrhage.20,25 CSF drainage is typi-
cally started intraoperatively and is maintained for 72 hours.2,20–22 While multiple ther-
apeutic adjuncts including barbiturates, steroids, naloxone, or free radical scavengers
have been proposed for the management of SCI after vascular surgery, strong data
supporting their benefit is lacking.
Epidural hematoma: Placement of a lumbar drain using an 14G Touhy needle may
result in bleeding and the formation of an epidural hematoma with resulting cord
compression and paraplegia. The incidence of epidural hematoma is 2 to 20 cases
per 100,000 lumbar drain insertions.26–28 A high index of clinical suspicion, combined
with diagnostic neurologic examination and a prompt MRI study are essential. It is
important to note that many lumbar drains are MRI compatible, whereas spring-
wound epidural catheters are not. Rapid surgical decompression (within 8 hours of
the onset of symptoms) is key to achieving resolving neurologic deficits.
Stroke: Patients undergoing major vascular surgical procedures are at increased
risk of stroke due to patient characteristics and conditions related to systemic athero-
sclerosis such as high blood pressure, coronary artery disease, diabetes, and proce-
dural factors such as atherosclerotic plaque embolization or profound intraoperative
hypotension. The incidence of stroke in patients undergoing noncarotid, major
vascular surgery is 0.2% to 0.6%, compared with 3% in patients undergoing carotid
endarterectomy.29 Majority of perioperative strokes are ischemic and caused by
embolic events and hypoperfusion.30,31 Perioperative stroke is associated with
increased length of ICU stay and mortality.29 Diagnostic work up includes noncontrast
head CT to rule out acute intracranial hemorrhage, followed by an MRI/MRA of head
and neck to evaluate for arterial obstruction. Treatment is focused on endovascular
embolectomy when indicated, antiplatelet and statin therapy, and preventing second-
ary injury by maintaining adequate CPP, and avoiding hyperglycemia and hyperther-
mia. A consultation with a neurocritical care specialist should be promptly obtained.
Pain: Inadequate treatment of pain related to surgery may be associated with
increased complications and prolonged recovery time. Postoperative pain is recog-
nized as one of the many factors contributing to the surgical stress response, and
pain control is known to reduce myocardial oxygen demand. Modern pain manage-
ment uses multimodal therapies; options available for postoperative analgesia depend
780 Sharifpour & Bittner

on the type of surgery and the use of anticoagulants and antiplatelet agents that may
preclude the use of regional techniques. Epidural analgesia provides superior anal-
gesia when compared with the use of intravenous opiates, especially during move-
ment, and may reduce the duration of mechanical ventilation, overall rates of
myocardial infarction, acute respiratory failure, gastrointestinal and renal
complications.14
Renal Complications: Acute kidney injury (AKI) is a common complication after
vascular surgery and occurs in 20% to 49% of the patients undergoing aortic surgery,
depending on the criteria used to define AKI, and is associated with worse outcomes.1
Preoperative risk factors for postoperative AKI include the history of chronic kidney
disease, anemia, and emergent surgery.1 Intraoperative risk factors include hypoten-
sion, hypovolemia, embolic debris, juxta- or suprarenal aortic cross-clamping, and the
duration of cross-clamping. Intraoperative partial left heart bypass and distal perfusion
of renal arteries with cold crystalloid reduces renal ischemic time and attenuates the
risk of postoperative AKI.
Maintenance of adequate intravascular volume and cardiac output in the postoper-
ative period optimizes kidney perfusion. Nephrotoxins such as nonsteroidal anti-
inflammatory medications, aminoglycoside antibiotics, and intravenous contrast dye
should be avoided.1 Of note, perioperative infusion of dopamine, furosemide,
mannitol, and N-acetylcysteine have not been shown to reduce the risk of periopera-
tive AKI. If AKI develops, meticulous management of fluids, electrolytes, and acid–
base status is imperative. Renal replacement therapy should be instituted promptly
when clinically indicated.

Gastrointestinal Complications
Mesenteric ischemia is a potentially fatal complication of aortic surgery.32–34 It affects
2% of the patients undergoing elective aortic surgery, with mortality up to 65%.33
Mesenteric hypoperfusion may be caused by embolic, thrombotic, or mechanical
obstruction of arterial blood flow. The resulting bowel ischemia triggers a systemic in-
flammatory response leading to distant organ damage and often worsens any previ-
ously ongoing coagulopathy.33 Delayed diagnosis is associated with transmural
ischemia and increased mortality. Abdominal pain out of proportion to physical exam-
ination, persistent lactic acidosis, ongoing fluid requirement, and refractory shock are
signs of mesenteric ischemia and require immediate surgical attention.33 Workup in-
cludes serial abdominal examinations, gastric decompression, early surgical consul-
tation, and an abdomen and pelvis CT angiogram. Diagnosis can be confirmed by
flexible sigmoidoscopy or colonoscopy but should not delay surgical intervention. Pa-
tients with transmural bowel necrosis require exploratory laparotomy with the resec-
tion of the involved segment and diverting ostomy, whereas patients with reversible
mucosal ischemia are treated with bowel rest and broad-spectrum antibiotics.
Ileus: Prolonged postoperative ileus occurs in 10% of the patients who have under-
gone open aortic surgery.35 Mobilization of abdominal viscera, bowel edema from
intraoperative fluid administration, and perioperative use of opioids are risk factors
for ileus. Utilization of thoracic epidural analgesia may facilitate faster return of bowel
function by reducing perioperative opioid use and unopposed parasympathetic inner-
vation of the bowels.36,37 Prokinetic agents can be beneficial in the absence of bowel
obstruction.
Abdominal compartment syndrome (ACS): Patients who receive large volumes of
intravenous fluids, blood, and blood products intraoperatively, and those with mesen-
teric ischemia, are at increased risk for developing abdominal compartment syn-
drome.38 ACS is more common in patients who have undergone an emergency
 Critical Care of the Vascular Surgery Patient 781

repair (due to a significant retroperitoneal hematoma and edema).38 ACS can impair
the function of nearly every organ system, resulting in impaired cardiac function,
decreased venous return, impaired ventilation with hypoxemia and hypercarbia, renal
impairment, diminished gut perfusion, and elevated intracranial pressure. Diagnosis of
ACS includes an intra-abdominal pressure of more than 20 mm Hg associated with ev-
idence of new organ failure. Management consists of supportive care such as using
neuromuscular blockers and early surgical decompression.39
Pancreatitis: Acute pancreatitis after open abdominal aortic repair is a rare but
serious complication that occurs in 1% to 2% of patients.40 It can result from direct
trauma and manipulation during surgical dissection or ischemia. Treatment is
supportive.

Hematologic Complications
Postoperative Hemorrhage: Postoperative hemorrhage occurs in up to 5% of patients
after aortic surgery and may require surgical reexploration, further increasing
morbidity and mortality.41
Large intraoperative blood loss, extensive surgical dissection, systemic hepariniza-
tion, mesenteric ischemia, and hypothermia all combine to increase the risk of post-
operative hemorrhage.42,43 The differential diagnosis for hemodynamic instability in
the postoperative period should include hemorrhage until proven otherwise. Bleeding
from aortotomy suture lines is a potentially devastating complication of aortic surgery.
Fluid administration and blood transfusion should be provided in conjunction with
vasopressor support as appropriate. Hypertension exacerbates the risk of bleeding
and should be promptly treated. Hypothermia, acidosis, and hypocalcemia should
also be aggressively treated, and coagulation abnormalities should be corrected
promptly, guided by thromboelastography when available.44 The attending surgeon
should be notified immediately. If the patient is hemodynamically “stable,” a CT angio-
gram to investigate the source of bleeding should be obtained.
In the absence of ongoing bleeding and hemodynamic instability (vasopressor
requirement) and ischemic signs/symptoms or concerns for SCI, a hemoglobin trans-
fusion threshold of 7 g/dL is reasonable.45,46 Patients with hemodynamic instability,
hypovolemia, or signs/symptoms of ischemia may benefit from a higher hemoglobin
target. Thrombocytopenia is common in the early postoperative period secondary
to platelet consumption in the setting of persistent bleeding or sequestration by aortic
graft material. Less commonly, heparin-induced thrombocytopenia (HIT) may result in
the development of heparin-dependent, platelet-activating antibodies. While rare, HIT
should always be considered in thrombocytopenic patients with a history of heparin
exposure.
Thromboembolism: Patients undergoing vascular surgery are at increased risk for
lower extremity deep venous thrombosis (DVT) (up to 10%) and prophylactic mea-
sures should be instituted as soon as deemed safe.47,48 Advanced age, morbid
obesity, limb ischemia, venous injury, lengthy surgery, and prolonged immobilization
are predisposing factors to DVT formation. Patients who have undergone vascular sur-
gery are often hypercoagulable, increasing their risk of DVT or arterial graft occlusion,
and should receive antithrombotic measures postoperatively. Early ambulation and
perioperative use of thoracic epidural analgesia are associated with reduced inci-
dence of perioperative lower extremity DVT.14
Lower extremity ischemia: Ischemia due to embolic or thrombotic complications
can occur in 2% to 5% of the patients undergoing aortic surgery.49 Frequent evalua-
tion of lower extremity pulses or Doppler signals facilitates early detection and
intervention.
782 Sharifpour & Bittner

Endocrinologic Complications: Postoperative hyperglycemia is common among pa-

tients undergoing vascular surgery and is associated with increased risk of wound
infection, graft failure, increased length of ICU stay, and mortality.50,51 Blood glucose
should be maintained below 180 mg/dL and blood glucose > 180 mg/dL should be
treated with intravenous insulin infusion.52

Infection
Infection of the graft, stent, or surgical site can result in major morbidity or mortality.
For this reason, correct timing, and dosing of perioperative antibiotics are important.
Postoperatively adherence to wound management, ICU “care bundles,” hand hy-
giene, general aseptic technique, and glucose control are important for preventing
infection.

Endovascular Aneurysm Repair and Hybrid Operations

EVAR has emerged as a less invasive and potentially safer alternative to open surgical
repair. EVAR avoids thoracotomy or laparotomy, aortic cross-clamping, and is gener-
ally associated with reduced blood loss, less postoperative pain, and a shorter recov-
ery. EVAR was initially limited to patients considered to be at high risk for conventional
open surgical repair. However, increased clinical experience, together with improve-
ments in endograft design and delivery techniques have expanded its application.
Today, EVAR is used for elective and emergent repair of thoracic and abdominal an-
eurysms, pseudoaneurysms, aortic dissections, and traumatic aortic injuries if there
are suitable “landing zones” for the stents that do not compromise other major ves-
sels, and the size of the femoral and common iliac arteries needs to be assessed to
ensure access. The procedure involves the delivery and deployment of one or more
self-expanding aortic grafts within the aorta under fluoroscopic guidance, through
percutaneous access via the femoral artery or, less frequently, the brachial artery.
Fenestrated and branched stent grafts are used to maintain perfusion of the visceral
arteries that originate from the covered aortic segment. Hybrid procedures, which
combine open surgery and endovascular stenting, use the creation of an extra-
anatomical bypass to the branch arteries of the aorta and expand the indications
for endovascular stenting. For example, in patients undergoing thoracic endovascular
aortic repair (TEVAR), an open left carotid-subclavian bypass is performed to prevent
upper extremity ischemia in patients when the repair requires covering the ostium of
the left subclavian artery.
Much of the postoperative critical care provided for an open aortic repair applies to
an endovascular repair as well. Complications associated with EVAR are summarized
in Table 2 and include:
Vascular access injury: Frequent injuries include iliofemoral lacerations and rupture,
pseudoaneurysm formation, and retroperitoneal hematoma. The sheath size can be
large and, in some patients, can constitute a sizable part of the femoral artery,
increasing the risk of injury. Consequently, large hematomas can develop, leading
to anemia and hemodynamic instability. Occasionally these hematomas can be mask-
ing false aneurysms created by the puncture. Ultrasound and further vascular inter-
vention may be required.
Device-related problems: Malposition, migration, or embolization of the graft can
occur. Malposition is the most common of these problems and can result in organ
ischemia (commonly renal). Device-related problems require urgent intervention in
the interventional suite.
Hemorrhage: There can be unrecognized blood loss “under the drapes” from the
femoral access site, resulting in hypovolemia. Endoleak, defined as persistent blood
 Critical Care of the Vascular Surgery Patient 783

Table 2
Postoperative complications after TEVAR/EVAR and mitigation strategies

Early Complications
Vascular access site injury Assessment of thigh hematoma formation,
Stroke assessment of distal pulses
SCI Frequent neurologic checks for S/Sx of stroke
AKI Maintaining MAP > 80 mm Hg and adequate CPP.
Post implantation syndrome CSF drainage as indicated
Maintaining euvolemia and avoiding nephrotoxins
Supportive care
Late Complications
Device-related problems:
malposition, migration
Endoleak
Stent graft infection
Aorto-esophageal fistula

flow outside the lumen of the endoprosthesis and within the aneurysm sac following
endovascular graft stenting, can occur in up to 30% of cases and result in drops in he-
moglobin (or if serious may result in sudden hemodynamic instability). Hypothermia
resulting from the patient spending prolonged time in a cold interventional suite may
worsen coagulopathy and hemorrhage.
Acute kidney injury: The incidence of AKI after elective EVAR is 0.7% to 2.0%.53,54
This can result from hypovolemia, bleeding, contrast-induced nephropathy, or malpo-
sition of a stent occluding renal artery. Hydration during and after the procedure may
help reduce the risk.
Spinal cord ischemia: Placement of thoracic aortic stents can be associated with
SCI. The longer the length of the segment of aorta stented, the greater the risk of
cord ischemia.
Infection: The endovascular graft is foreign material and can become infected
following an episode of bacteremia. The groin puncture site (or any hybrid operation
wounds around this area) can also become infected. Infected pseudoaneurysms
can be particularly difficult to manage, involving surgery and continued antibiotics.
Postimplantation syndrome: A clinical syndrome that is thought to result from endo-
thelial activation by the endograft. It manifests as a mild leukocytosis, fever, and eleva-
tion of C-reactive protein. Postimplantation syndrome is commonly associated with
large segment coverage and the use of multiple stent devices. Post implantation syn-
drome is associated with prolonged length of stay.55

Carotid Endarterectomy
Most patients do not require admission to ICU after undergoing carotid endarterec-
tomy. However, patients undergoing CEA suffer from widespread atherosclerosis
and are at increased risk for neurologic and cardiac complications. Potential postop-
erative complications after CEA include hypo- or hypertension, myocardial infarction,
stroke, postoperative bleeding, cervical hematoma, and nerve injury and are summa-
rized in Table 3.
Hypotension: Removal of the carotid plaque, and the associated stenosis, during
surgery results in transmission of increased arterial pulsation to the carotid baro-
ceptor, which can result in reflex bradycardia and hypotension. Postoperative vaso-
pressor support may be necessary. If such support is required, it typically lasts no
784 Sharifpour & Bittner

Table 3
Postoperative complications after carotid endarterectomy and strategies to prevent them

Complication Management Strategy

Neurologic
Stroke Monitoring for early signs of CVA
Cerebral Hyperperfusion syndrome Maintain appropriate cerebral perfusion pressure
Cranial nerve injury Frequent neurologic examinations
Cardiovascular
Postoperative MI Monitoring for symptoms/signs of myocardial
Arrythmias ischemia, check myocardial biomarkers
Heart failure Early resumption or initiation of aspirin, beta-
Postoperative hypotension blocker, and statins
Postoperative hypertension Avoid hypertension/hypotension
Early resumption of beta-blockers
Judicious fluid management
Vasopressor infusions
Early resumption of home antihypertensive agents
Pulmonary
Airway compromise (neck hematoma) Correction of coagulopathies, early surgical
Vocal cord dysfunction/aspiration decompression
Monitoring for hoarseness and signs/symptoms of
aspiration

longer than 6 to 24 hours. It is important to remember that CEA is typically performed

with little blood loss and does not result in significant fluid shifts. Therefore, treating
postoperative hypotension with fluids is often inappropriate and can result in conges-
tive heart failure. Persistent hypotension should prompt further diagnostic workup,
including invasive hemodynamic monitoring and echocardiography to assess cardiac
function.
Hypertension: Carotid sinus damage during surgical dissection or its infiltration by
local anesthetics can impair the normal baroreceptor sensitivity of the carotid sinus,
resulting in postoperative hypertension. Patients with poorly controlled preoperative
hypertension are at increased risk for postoperative hypertension. Severe hyperten-
sion increases the risk of bleeding, wound hematoma, and cardiac and neurologic
complications, such as cerebral hyperperfusion syndrome. Perioperative hyperten-
sion should be promptly treated with infusion of short-acting antihypertensive agents
(eg, nicardipine, clevidipine) until baroreceptor function is restored.
Cervical hematoma: Postoperative neck hematoma occurs in 3.4% of the patients
undergoing CEA and may lead to airway compromise.56 Immediate intubation and
decompression of the neck in the operating room or postanesthesia care unit may
be necessary to prevent airway compromise. Intubation will often be more difficult
than the previous intubation in the OR due to the distortion of the airway anatomy
and edema. Coagulopathy and uncontrolled hypertension increase the risk of hema-
toma formation and should be corrected immediately. A large cervical hematoma may
also compress the internal carotid artery and adjacent cranial nerves.
Myocardial Infarction: Postoperative MI occurs in up to 2% of the patients undergo-
ing CEA and is associated with increased short- and long-term mortality.57–59 Man-
agement is focused on optimizing myocardial oxygen supply and demand,
antiplatelet and statin therapy, and percutaneous coronary intervention to restore
blood flow if indicated.
 Critical Care of the Vascular Surgery Patient 785

Stroke: Postoperative stroke occurs in 3% to 5% of the patients undergoing carotid

endarterectomy and is the second most common cause of death after CEA.60–62 Ma-
jority of strokes are ischemic in nature and are due to embolic or thrombotic events.
Postoperative stroke can also be secondary to global hypoperfusion or hemorrhage.
Strict blood pressure control is of utmost importance as hypotension may lead to
global hypoperfusion and ischemia, and uncontrolled hypertension increases the
risk of hemorrhage and cerebral hyperperfusion syndrome (CHS). Hypotension should
primarily be treated with vasopressor infusions (phenylephrine, norepinephrine, vaso-
pressin), and fluids only when warranted, and hypertension should be treated with in-
fusions of short-acting calcium channel blockers (nicardipine, clevidipine). Any
changes in the neurologic examination should be immediately investigated by CT/
CT angiography of the brain or MRI/MRA of the brain. A neurology or neurocritical
care consultation should be obtained to further direct patient care (thrombectomy
or intra-arterial thrombolytic therapy). Patients should receive antiplatelet and statin
therapy.
Cerebral hyperperfusion syndrome: CHS occurs in 0% to 3% of the patients after
CEA. It is characterized by ipsilateral headache, hypertension, seizure, and altered
mental status.63,64 CHS is caused by impaired cerebral autoregulation of the surgically
reperfused cerebral hemisphere, which is exposed postoperatively to higher cerebral
perfusion resulting from improved arterial inflow. High-grade carotid stenosis, severe
bilateral carotid disease, and postoperative hypertension are major risk factors for the
development of cerebral hyperperfusion. If not treated promptly, it progresses to intra-
cerebral hemorrhage, cerebral edema, and death.65 Postoperative hypertension in-
creases the risk of CHS, and strict blood pressure control is of utmost importance.
A noncontrast head CT should be obtained to rule out hemorrhage and evaluate for
cerebral edema. Critical care treatment is focused on the control of blood pressure.
Antihypertensives that do not cause vasodilation (labetalol, clonidine) are favored.
Cranial nerve injury: Cranial nerve injury is common after CEA, occurring in up to
39% of the patients, with only a small proportion being permanent. Most cranial nerve
injuries are secondary to retraction trauma; less frequently, they are the result of nerve
transection.66,67 The recurrent laryngeal nerve, hypoglossal nerve, and marginal
mandibular nerve are most affected. Injury to vagus nerve and branches (recurrent
and superior laryngeal nerves) can result in paralysis of the ipsilateral vocal cord,
resulting in hoarseness and the loss of effective cough. Fortunately, the injury is tem-
porary in most cases. If a nerve injury is clinically suspected, phonation and swallow-
ing should be evaluated before the institution of oral intake to prevent aspiration. When
vocal cord dysfunction is suspected, fiberoptic examination by an otolaryngologist
should be completed to assess the need for further treatment.

Lower Limb Revascularization Procedures

Lower extremity ischemia is a common result of generalized atherosclerosis and is
characterized by claudication, a lower extremity muscular pain that is induced by
increased physical exertion and is relieved by rest. Critical limb ischemia, which re-
sults from the progression of chronic atherosclerotic disease, presents with pain at
rest and may present with nonhealing ulceration or gangrene of the lower extremity.
A sudden decrease in limb perfusion from embolism or plaque rupture with thrombosis
presents more acutely, with severe pain and a pale extremity with absent pulses. Sur-
gical bypasses (aortofemoral, femoropopliteal, and femorodistal bypass grafting) and
endovascular procedures are performed to reestablish blood flow. The optimal
bypass grafting technique is based on the location and the morphology of the obstruc-
tive lesions. However, there is an increasing tendency toward endovascular
786 Sharifpour & Bittner

procedures. Patients who undergo lower extremity bypass are managed in a moni-
tored setting for 24 to 48 hours. Complications associated with lower extremity revas-
cularization procedures are similar to those associated with other major vascular
procedures. Mortality after peripheral bypass surgery ranges between 2% and 8%
and is primarily related to myocardial ischemia.68
Graft failure: Graft patency is monitored by routine evaluation of distal pulses and
perfusion every hour for six to 8 hours, then every four to 6 hours. Loss of a palpable
pulse or a Doppler signal, a cool pale extremity, or severe pain are signs of graft failure
and warrant immediate attention. Graft failure can occur due to technical complica-
tions, or because of hypoperfusion from hypotension, due to an adverse cardiac
event, bleeding, or sepsis, or from a hypercoagulable state. In case of suspected graft
failure, imaging should be performed emergently, and reintervention should be
considered.
Compartment syndrome: Reperfusion of an ischemic extremity after revasculariza-
tion can result in compartment syndrome. Frequent monitoring of the reperfused ex-
tremity is essential for the early detection of compartment syndrome. Affected limb
should be treated with fasciotomy. Creatine phosphokinase (CPK) levels should be fol-
lowed for evidence of rhabdomyolysis, and patients should be kept euvolemic to mini-
mize the risk of postoperative renal failure.
Bleeding: Both elective and emergency procedures need monitoring for potential
bleeding, hematoma, or pseudoaneurysm development.

SUMMARY

Postoperative management of the patient undergoing major vascular surgery presents

unique and complex challenges for the critical care provider. Patients undergoing
vascular surgery commonly have multiple comorbidities and the surgical procedure
impacts every major organ system. Postoperative complications after major vascular
surgery are common and associated with increased morbidity and mortality. The
spectrum of complications depends on the disease itself, its urgency, and the surgical
procedure. Critical care management of these patients requires an understanding of
the underlying disease process, surgical procedure, and a high index of suspicion
for procedure-specific complications. A multidisciplinary approach is most likely to
optimize the quality of postoperative care which is essential for successful recovery.

CLINICS CARE POINTS

 Persistent lactic acidosis, hypotension, and fluid requirement in patients who have
undergone open thoracoabdominal aortic repair should prompt an evaluation for bowel
ischemia. Surgical consultation and a CT scan maybe required for further evaluation.
 Changes in lower extremity motor strength (weakness, paraplegia), pain, or temperature
sensation in patients who have undergone open or endovascular repair of
thoracoabdominal aorta indicates spinal cord ischemia. MAP should be raised to 90 mm Hg
and CSF drainage should be instituted immediately.
 Many patients who have undergone noncarotid major vascular surgery may require volume
resuscitation in the immediate postoperative period. Volume resuscitation should be guided
by clinical signs/symptoms (mentation, urine output, skin temperature), vital signs
(normotension), and laboratory values such as lactic acid or based deficit. Transthoracic
echocardiography, when available, should be utilized to guide fluid resuscitation.
 Critical Care of the Vascular Surgery Patient 787

DISCLOSURE

The authors have nothing to disclose.

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