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be a better predictor [11, 12]. MELD does not account for the

presence of portal hypertension and ascites which are spe-

cically vital markers in cardiac surgery, but it does include

renal function. Common practice at present utilizes the

MELD score most frequently to predict mortality risk after

cardiac surgery (Table5.2) [13–15].

Patients with hepatic dysfunction are predisposed to mul-

tiple postoperative complications based on hepatic functional

reserve, which is difcult to predict. This is one of the main

problems of surgical intervention in liver failure patients [14].

The normal stresses of cardiac surgery include transient

hypotension, uid shifts, relative ischemia, reperfusion,

SIRS, catecholamine exposure, and potential anesthetic tox-

ins. The liver is exquisitely sensitive to these routine periop-

erative conditions. Although the GI service is often

encouraging in their recommendations to proceed if the risk

scores are low, it is critical to remember that the CPB pump is

a demanding physiologic challenge for cirrhotics.

Preoperative, intraoperative, and postoperative care must all

be carefully controlled and monitored with even more than

the usual vigilance in order to prevent the catastrophic com-

plication of fulminant hepatic failure (Table5.3). Causes of

death in cirrhotic patients post-bypass include sepsis, multi-

system organ failure, and hepatic failure [14]. More common

postoperative complications include cholestasis, hemorrhage,

and mesenteric ischemia [14]. Understanding the pathophysi-

ology of dysfunction is helpful in planning for surgery.

In addition to the basics of nonpulsatile ow and low car-

diac output that accompany heart surgery, catecholamines

and synthetic vasoconstrictors cause a specic decrease in

arterial liver perfusion. Anesthetic medications themselves

can exacerbate liver failure. Furthermore, routine volume

loading can lead to tissue edema, coagulopathy, and further

hypoxia secondary to a hepatic venous congestion that limits

oxygen delivery. Cirrhotics have low oncotic pressure based

on hypoalbuminemia; they do not tolerate large volume

shifts. In addition to the ischemic insult, there are circulating

endotoxins and translocated bacteria that also impact the

liver through the portal vein, markedly increasing the SIRS

response and directly decreasing blood ow [14]. From

there, it can be a short step to sepsis and multi-system organ

failure. Prevention with a specic strategy is necessary

(Table5.4).

A review of multiple studies published in 2015 found that

mortality rates after cardiac surgery for Childs A/B/C are

90%/37%/52%, respectively [15]. Patients with advanced-

stage liver disease and/or portal hypertensive complications

have difculty surviving the stresses of cardiac surgery. Even

without cardiac surgery, the expected 1-year survival for

Childs A/B/C are 100%/81%/45% [15]. Keeping the CPB

time to <70minutes has been shown to be helpful in prevent-

ing complications [16]. In patients with lesser stage liver dis-

ease, close evaluation of cardiac function and a good

understanding of long-term prognosis are mandatory when

choosing surgical technique. These patients must also be

monitored after surgery with careful uid resuscitation and

careful prevention of bleeding, infection, or other

complications.

Patients with advanced liver disease and little hepatic

reserve tolerate cardiac surgery poorly. Optimizing medical

management and planning for percutaneous options are often

Table 5.2 ESLD risk scores and cardiac surgery

CPT A or MELD <11

CPT B or MELD

12–14 CPT C or MELD >14

Green light (relative) Yellow light Red light

Look for red ags:

Recent GI bleed,

encephalopathy,

ascites,

thrombocytopenia

Remember that even

class A has a 7x

higher rate of death in

10years [15]

Carefully examine

cardiac anatomy

and function in

terms of complexity

of surgery to make a

decision

Consider combined

heart liver transplant

Look for red ags:

Portal HTN,

cirrhotic

complications,

bleeding

Think about medical

management or

percutaneous

therapies, not surgery

Remember any

treatment (even

minimally invasive)

that requires general

anesthesia and/or

involves hypotension

will likely affect

postoperative hepatic

function

Table 5.3 Keys to operating on cirrhoticpatients

1. Maintain splanchnic perfusion

2. Careful uid management

3. Limit coagulopathy

4. Thermoregulation

5. Avoid/limit CPB and nonpulsatile ow

6. Optimize transfusion

Table 5.4 Preoperative and intraoperative strategy for cardiac surgery

in ESLD

Preop Intraop Postop

Thorough history and

physical.Lookfor stigmata

of cirrhosis including

encephalopathy

Avoid large

volume shifts

Manage

coagulopathy

Minimize CPB

time

Minimize

transfusions

Maintain HD

support

Follow LFTs and

coagulation

studies closely

Tests: LFT, platelets,

Creatinine, coagulation

studies

Liver ultrasound

Abdominal CT

CPB: Low prime

volume

Smaller tubing

High-ow rates

Try to keep

<70min

Metabolic

support

Nutrition

Prevent sepsis

Prevent

hemorrhage

Medical management of

portal HTN with beta

blockers

Consider TIPS

Give vitamin K and nutrition

prior to surgery to improve

coagulopathy (a sign of

hepatic reserve)

Constant and

careful

monitoring of BP

5.2 Hepatic Failure

preferred. Careful consideration of cardiac function, other

comorbidities, and technical options are all necessary to

ensure a good outcome.

5.3 Abdominal Compartment Syndrome

A moderately obese 78-year-old patient with a low ejec-

tion fraction undergoes a difcult CABG on-pump. His

targets are small and his CPB time is prolonged. He is

transfused two units of packed red blood cells along with

platelets and fresh frozen plasma. Despite moderate doses

of inotropes, his cardiac output remains marginal. A tense

abdominal wall is noted at the completion of the proce-

dure; this is not improved with nasogastric tube decom-

pression. Postoperatively, there is moderate postoperative

bleeding and coagulopathy that requires additional blood

transfusions.

Over the next several days, he does not progress well. He

is extubated on day 1 and placed on high-ow oxygen, but is

persistently tachypneic and tachycardic. His urine output is

marginal despite a normal cardiac index. He has a poor

response to uid administration. His abdomen is distended

and rm; abdominal lms reveal a large ileus. Also present,

and more concerning, are nonspecic changes in mental sta-

tus. Eventually, the patient goes into anuric renal failure and

his BUN rises over 100. The team is treating profound ileus,

abdominal distention, renal failure, and altered mental

status.

5.3.1 Discussion

Abdominal compartment syndrome (ACS) has been

described after extensive abdominal surgery or trauma. A

sudden increase in intra-abdominal pressure occurs after clo-

sure of the abdomen and results in new organ dysfunction,

most commonly renal and pulmonary impairment [17]. In

the setting of non-abdominal surgery, this effect is termed

secondary abdominal compartment syndrome. Although not

directly cardiac in scope, knowledge of etiology, pathology,

organ dysfunction, and available treatments need to be

understood by all surgical care teams.

ACS usually begins with a shock state, which in cardiac

surgery patients can include a CPB run with its relative

hypotension, hemodilution, vasoconstriction, decreased

osmotic pressure, and nonpulsatile ow. Blood can be redis-

tributed away from organs and lead to intestinal, renal, tis-

sue, and cellular hypoxia. Reperfusion injury occurs in the

splanchnic system. Multiple cytokines and free radicals are

released, leading to capillary leak and increased edema of

the intestinal walls [18]. This edema in itself can increase the

intra-abdominal pressure and decrease perfusion. Bowel

ischemia and hypoxia from poor ow lead to even more

edema and higher pressures. CPB is the initial injury, but

aggressive post-bypass uid administration can exacerbate

this effect.

This syndrome notably affects the kidneys, GI tract, and

lungs. The result of increased abdominal pressure is decreased

blood ow to the kidneys. This ischemic injury can be

increased by the use of inotropes, increased mechanical pres-

sure, hypotension, hemodynamic shifts, and increased renal

vascular resistance [18]. Oliguria occurs, sometimes in the

face of normal measured cardiac output, but always in the

presence of a tense, distended abdomen [18]. CPB, particu-

larly the cooling and rewarming, can affect the oxygen

demand of the gut. Mesenteric organs can incur injury through

a combination of aerobic/anaerobic conversion and endothe-

lial cell dysfunction [19]. Changes in vascular tone and vaso-

constriction at the gut mucosal level during CPB can cause

tissue hypoxia of the intestinal cells, manifesting as lactate

and putting the gut more at risk for edema [19, 20].

The effects of tight abdominal distention on the lung are

increased restriction with decreased compliance, ventilation,

lung capacity, and functional residual capacity [17]. Without

clear inltrates or pulmonary edema on CXR, these patients

are hypoxic and demonstrate increased respiratory drive with

poor gas exchange. This pulmonary status is accompanied by

increased ventilatory pressures. The patients can appear clin-

ically similar to those with acute heart failure or sepsis.

Hypotension in the setting of a large ileus can lead to uid

resuscitation that compromises the patient further. Liver and

direct bowel injury can occur in the form of ischemia, and

both cardiovascular and neurologic changes occur [18].

The immediate rst step for these patients is measurement

of bladder pressure (Table5.5) [21]. This simple monitoring

measurement can be done intermittently and can assist in deter-

mining more pointed treatments if organ dysfunction and a

tense abdominal compartment remain. This is followed by

recording and interpretation of the ndings (Table5.6) [20, 21].

The clinical nding of ACS should be made early. The

patients that raise concern include those who exit the operat-

ing room with a tense abdomen and/or a prolonged or dif-

cult cardiopulmonary bypass run with aggressive

intraoperative uids and an elevated lactate. An abnormal

physical exam with profound abdominal distention and an

X-ray showing multiple dilated loops of bowel is seen along

with new-onset renal dysfunction.

Table 5.5 Steps to measure bladder pressure

1. Fill the urinary catheter toward the bladder with 25cc of saline

2. Clamp the tubing

3. Transmit the pressure to a manometer positioned and zeroed at

the mid-axillary line

4. The measurement should be recorded at end expiration in the

supine position

5 Critical Postoperative Complications

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Table 5.6 Intra-abdominal pressure (World Society of Abdominal

Compartment Syndrome)

Normal

Intra-abdominal HTN

(IAH)

Abdominal compartment

syndrome

IAP 5–7mm

IAP>12mmHg IAP>20mm hg

Grade I, IAP

12–15mmHg

Grade II, IAP

16–20mmHg

Grade III, IAP

21–25mmHg

Grade IV, IAP >25mmHg

Table 5.7 Management of abdominal compartment syndrome

NGT decompression

NPO

Diuresis

CRRT negative uid balance

Rectal tube, colon decompression/enemas

Sedation

Analgesia

Neuromuscular blockades

Body position (reverse Trendelenburg)

Promotability agents/gastropyrokinetics

Cisapride, Metaclopramide, Erythromycin, Neostigmine

Percutaneous drainage of ascites

Intraperitoneal uid catheter

Decompressive laparotomy

Laparostomy (open/Bogota bag)

Some specic risk factors for IAH include age, hyperten-

sion, length of bypass, intraoperative lactate, and transfusion

[22]. Other predictors include high CVP, a markedly positive

uid balance with blood transfusion, and high-dose inotro-

pes that result in mesenteric ischemia. Age, baseline IAP,

vasoactive drugs, and AKI are also signicant [18].

Depending on ndings on exam, some general manage-

ment goals will follow. The basic themes to consider are

intraluminal, extraluminal, compliance, uids, and ow

(Table5.7) [18, 21, 23]. From a respiratory perspective, high

peak airway pressures are needed to adequately ventilate the

patient. Thus, sedation, analgesia, and paralysis are required

in the post-cardiac surgery patient with IAH.Fluid balance is

critical, as patients can be volume responsive with a large

amount of third spacing, but ultimately too much volume

will cause marked abdominal distention and increase IAH

even further [23]. Finally, surgical invasive approaches

become necessary if there is lack of improvement with con-

servative therapy. These treatments include percutaneous

drainage of intraperitoneal uid and decompressive

laparotomy.

This syndrome needs to be carefully monitored in order to

prevent major morbidity. Understanding the cause of the

underlying disease and the role that IAP is playing in the

overall picture of the patient will make a difference in subse-

quent organ dysfunction. A tense abdomen results from

increased volume or decreased compliance or both. The

timeline between the IAP and the organ dysfunction is cru-

cial. Decompressive laparotomy, performed in extreme cir-

cumstances, has the potential for other serious complications,

including enteric stula and intra-abdominal sepsis [23].

Mortality rates range from 22.2 to 71.4% in individual stud-

ies recently reviewed, with an overall mortality of 49.7%

[24]. The main cause of death is multi-system organ failure.

The second most common cause is profound intestinal isch-

emia or necrosis [24].

The key to this disease is acute awareness with early rec-

ognition, early measurement of bladder pressure, conserva-

tive therapies, and constant monitoring and re-evaluation to

determine the next escalation of treatment if indicated

(Fig.5.2) [20].

5.3 Abdominal Compartment Syndrome

Evacuate intraluminal

contents

Insert nasogastric

and/or rectal tube

Initiate gastro-/colo-

prokinetic agents

Minimize enteral

nutrition

Administer enemas

Consider

colonoscopic

decompression

Discontinue enteral

nutrition

Consider surgical

evacuation of lesions

Consider

neuromuscular

blockade

Consider

hemodialysis /

ultrafiltration

Vosoactive

medications to keep

APP

60 mmHg

Consider reverse

Trendelenberg

position

Fluid removal through

judicious diuresis

once stable

Hemodynamic

monitoring to guide

resuscitation

Resuscitate using

hypertonic fluids,

colloids

Avoid prone position

head of bed > 20

degrees

Abdominal computed

tomography to

identify lesions

Percutaneous

catheter drainage

Abdominal ultrasound

to identify lesions

Evacuate intra-

abdominal space

occupying lesions

Improve abdominal

wall compliance

Optimize fluid

administration

Optimize systemic /

regional perfusion

Goal-directed fluid

resuscitation

Patient has IAP

12 mmHg

Begin medical management to reduce IAP

Measure IAP / APP at least every 4-6 hours or continuously.

Titrate therapy to maintain IAP

15 mmHg and APP 60 mmHg

Maintain abdominal

perfusion pressure

(APP)

60 mmHg

Avoid excessive fluid

resuscitation

Aim for zero to

negative fluid balance

by day 3

Remove constrictive

dressings, abdominal

eschars

Ensure adequate

sedation & analgesia

Step 1Step 2Step 3Step 4

If IAP > 25 mmHg (and/or APP < 50 mmHg) and new organ dysfunction / failure is present, patient’s IAH / ACS is refractory to medical

management. Strongly consider surgical abdominal decompression.

Fig. 5.2 Management of intra-abdominal hypertension. IAP, intra-

abdominal pressure; IAH, intra-abdominal hypertension; APP, abdom-

inal perfusion pressure. From “Nonoperative management of

intraabdominal hypertension and abdominal compartment syndrome,”

by Springer Nature BV.Reprinted with permission

5.4 Pulmonary Artery Rupture

An 85-year-old female undergoes mitral valve replacement

for mitral stenosis. She has known pulmonary hypertension

with a systolic PAP of 80 mmHg prior to surgery.

Postoperatively, the pulmonary pressure remains 60 mmHg,

and she is started on inhaled nitric oxide. Two days later, the

surgeon is called emergently to the bedside for a sudden drop

in blood pressure that occurs during PA catheter manipula-

tion. A large amount of blood is within the endotracheal

tube, and 2 liters of blood is lling the right chest tube. The

blood bank is notied and chest compressions are started.

5.4.1 Discussion

Introduced in 1970, the Swan-Ganz catheter (SGC) has a

long history in cardiac surgery. Recent literature has been

5 Critical Postoperative Complications

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mixed regarding use of this invasive monitoring, citing

decreased utility within the medical and surgical intensive

care setting. A Cochrane Review of 13 studies and over 5000

patients showed no difference in cost of care, length of stay

(LOS), or ICU LOS with use of the SGC [25].

Paradox and controversy exist regarding SGC use in car-

diac surgery. There is a lack of adequate evidence for its use,

but with limited data and no randomized controlled trials. It

makes sense that the patients who have invasive lines in

place would have longer hospital stays and higher hospital

costs, based on the rationale for monitoring. Reviews of car-

diac surgery patients alone show no difference in mortality,

except in a small group of very-high-risk patients [26].

Others support the use of PAC in terms of its ability to

provide clinically relevant, real-time information about

patients who are hemodynamically unstable [27]. This infor-

mation includes cardiac output and mixed venous measure-

ments that quickly change management, particularly if

echocardiography is not immediately available [27]. Overall,

the consensus in the modern era is that the PAC should not be

used routinely, but in complex patients with cardiac dysfunc-

tion, it can guide in management decisions [28]. Patients

with low ejection fraction and severe PH may be helped with

this monitoring in the setting of cardiogenic shock and

decreased organ function. Specically, the addition and

weaning of inotropes, vasopressors, and pulmonary vasodi-

lators can be tailored to the patient’s condition.

Complications have been well described and have been

deemed prohibitive by some, particularly when added to

arguments regarding time, cost, and potential increased LOS

(Table5.8) [29]. Complete heart block can occur with pass-

ing of the PA catheter in the setting of a bundle branch block,

and perforations of the RA or RV have been described.

Complications of SGC are most common at the time of

insertion, but improvements in imaging and monitoring have

minimized these injuries. For example, inadvertent puncture

of the carotid artery rather than the internal jugular vein

would sometimes result in case cancellation. This cancella-

tion was due to the requirement for high-dose anticoagula-

tion in cardiac surgery and thus a potential for carotid artery

hematoma or dissection. In the past, this complication had an

incidence of 1.9% [30]. The use of transducers to check pres-

sure, intraoperative echo to determine correct placement of

the wire, and site ultrasound for needle entry have all been

used to minimize this complication further. Other injuries at

the time of insertion have to do with passage of the catheter

into the pulmonary artery. Right atrial perforation can occur

during oating of the catheter, particularly if the balloon is

not fully inated or in the presence of a thin right atrial wall.

Certainly, the most serious complication is PA rupture,

which carries an incidence of 0.031% [31]. Specic guide-

lines to avoid this complication have been recommended

(Table5.9) [32]. In addition to inating the PA balloon in a

small arterial branch, this injury may occur just in the setting

of severe pulmonary hypertension, when the tip of the cath-

eter migrates to smaller, more fragile PA branches. If the bal-

loon is not inated, it is possible for the tip to spear the wall

of the pulmonary artery, particularly in elderly patients

whose pulmonary arteries are not elastic.

Minor injuries to the lung that occur at the time of perfo-

ration and involve small areas of hemorrhage can self-seal by

surrounding parenchyma. These injuries are treated simply

with removal of the SGC, avoidance of high pressure on the

pulmonary bed, and close monitoring. If a focal injury is

present with ongoing hemorrhage, percutaneous treatment

with coil embolization is a minimally invasive option.

Management of massive PA rupture as described above

involves resuscitation with packed RBC during immediate

transfer to the operating room. An emergent right anterior

thoracotomy followed by placement of a large vascular

clamp onto the hilum will stop the hemorrhage after initial

immediate manual pressure is obtained. Continued resusci-

tation is necessary during this time. The lung should be

carefully examined. If a clear rupture site is able to be

exposed, it should be directly oversewn. However, a large

bleeding site within a lobe requires lobectomy or even pneu-

monectomy [32].

Table 5.8 Complications of PA catheters

1. Carotid cannulation (hematoma, AV stulas, strokes, bleeding)

2. Catheter knot

3. Arrhythmias, both atrial and ventricular, RBBB and CHB,

particularly on insertion

4. Thrombus

5. Tricuspid valve rupture/injury with tricuspid regurgitation

6. Intracardiac balloon rupture

7. Insertion complications: Pneumothorax, thoracic duct injury, air

embolism, perforation of RA, RV, PA with balloon tip

8. Limited local hemorrhage in lung parenchyma

Table 5.9 Methods to avoid PA rupture

1. Never inate the balloon without monitoring in place and stop

inating when the wedge appears or the tracing dampens

2. If there is a concern about position, pull the catheter back into the

RV or RA and reoat with the balloon up rather than inating

within the PA itself

3. Check the volume with every balloon ination and make sure that

if the waveform suddenly dampens at a lower volume, the balloon

has not migrated

4. Check catheter position daily by CXR

5. Consider positioning of the balloon without frequent ination or

documentation of wedge pressure

6. Keep stopcock off and the syringe attached to make sure no uid

lls the balloon inadvertently

5.4 Pulmonary Artery Rupture

5.5 Acute Pulmonary Embolism

A 60-year-old morbidly obese diabetic male with a normal

EF and good targets carries a STS mortality risk of 0.4% for

CABG.Thus, four patients out of every 1000 patients with

his characteristics are predicted to die within 30days of car-

diac surgery. This patient did well with surgery. The ows in

all of his grafts were excellent, and he was extubated on the

same day of surgery. He went home in 5days and looked

well in initial follow-up 2weeks later. On day #24, he died

suddenly at home.

5.5.1 Discussion

Massive pulmonary embolism is a rare complication after

cardiac surgery, although it is often the initial suspicion when

unexplained sudden death occurs. DVT alone after cardiac

surgery has a reported rate of 17% to 48% [33, 34]. A recent

review and meta-analysis of venous thromboembolism

(VTE) after cardiac surgery looked at 68 studies [35]. Of all

these studies, the median incidence of asymptomatic DVT

was 14.8%, asymptomatic PE 1.9%, and fatal PE 0.3% [35].

When reviewing only prospective studies and randomized

controlled trials, the incidence of fatal PE is reported as 0.4%

[35]. Another review found that fatal PE was present in 0.5%

of patients postoperatively, occurring mostly in the rst

2weeks after surgery [36].

A certain number of VTE are asymptomatic, and the diag-

nosis can be difcult. In a recent study of 100 patients who

received postoperative lower extremity ultrasound and CT

after CABG, PE alone was seen in 13%, PE and DVT were

seen in 8%, and DVT alone was seen in 4% in patients pro-

phylaxed only with aspirin and without SQ heparin or

mechanical compression devices [34]. This study, and the

fact that the majority of these patients would be discharged

as asymptomatic without treatment, underscores the actual

presence of this complication in the postoperative period.

Earlier, standard teaching was that patients who undergo

cardiac surgery, with its associated heparinization and car-

diopulmonary bypass, are somehow protected from DVT

and VTE.Routine aspirin use, DVT prophylaxis, inamma-

tory mediators, and potentially abnormal liver function all

contribute to this concept. Yet studies have shown increased

brin, thrombin, tissue factor, and aspirin resistance contrib-

ute to a prothrombotic state initially after surgery [37]. These

ndings occur on POD 1, peak on POD 3–5, and can be pres-

ent up to 30days postoperatively [37] (Table5.10).

Given this prothrombotic state, systemic prophylaxis dur-

ing this high-risk period should be considered, particularly if a

patient has multiple risk factors (Table 5.11) [35]. Previous

DVT, age, obesity, bed rest, and respiratory failure are risk fac-

tors in this patient population [35]. The risk of DVT/PE with

heart surgery is not the same as in general surgery. Cardiac

surgery involves blood with foreign body interference, coagu-

lopathy, platelet dysfunction, and thrombocytopenia. Each

patient does have a risk of bleeding, based on the type of sur-

gery performed. Individual risk factors need to be considered

when determining choice of anticoagulation and dosing.

Patients who are treated with ultrafractionated heparin

(UFH) or LMWH have not been shown to have a signi-

cantly increased rate of pericardial effusion, postoperative

pericardial effusion, GIbleeding, mediastinal hemorrhage,

or cardiac tamponade [35]. That being said, these complica-

tions must be monitored and the real risk-benet ratio indi-

vidualized for each patient. Not one method of anticoagulation

has been found to be superior [35]. Anti-platelet agents,

commonly used in CABG patients, also help in preventing

VTE in the preoperative period.

Controversy continues to exist about the timing and choice

of medications for prophylaxis. Guidelines are conicting

between the European Association for Cardio- Thoracic

Surgery that recommends pharmacologicprophylaxis start-

ing on POD 1 [38] and the American College of Chest

Physicians that has concerns about risk for bleeding in the

immediate postoperative period and favors mechanical com-

pression stockings alone unless the patient is at high risk for

VTE[39]. A morerecent study of 331,950 CABG patients

found the incidence of VTE with PE to be 1.3% and with

DVT alone to be 0.9% [40]. Despite this low number, these

patients had signicantly higher mortality, morbidity, and

cost [40]. The mortality in particular was striking: 6.8% vs

1.7% [40]. Specic risk factors included coagulopathy, obe-

sity, COPD, prior DVT, heart failure, and increased age [40].

Sudden unexplained death in the postoperative period is

often thought to be PE.Autopsy studies reviewing sudden

death in cardiac surgery report fatal PE occurs in 11–20% of

studied cases [41, 42]. In actuality, nearly 50% of deaths are

of cardiac origin [41]. These numbers are not helpful in any

Table 5.10 Etiology of prothrombotic state post-cardiac surgery

Aspirin resistance

Increased brinogen

Decreased brinolysis

Platelets normalize

Tissue factor activation

Thrombin production

Table 5.11 Pulmonary embolism risk factors

RV or LV failure

Obesity

History of DVT

Increased age

Preoperative immobility

Blood transfusion

Respiratory failure or reintubation

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individual case unless an autopsy has been performed. In

summary and practice, risks and benets must be weighed to

protect each patient from VTE/PE carefully in the postopera-

tive period after cardiac surgery.

5.6 Postoperative Bleeding

A 78-year-old male undergoes an uneventful coronary

bypass X 3 and is extubated at 3pm. He remains stable but at

11pm is found to have 300ml of bleeding in the previous

5minutes. An additional 300ml is recorded in the drains,

and the vasopressor requirements are increasing. On the sur-

geon’s arrival into the ICU, the patient is peri-arrest with 2

liters of the blood in the drainage chamber. The surgeon

opens the chest rapidly and there is relief of some degree of

tamponade. The source of bleeding is unclear as there is a

large volume of clotted and fresh blood present. Careful

inspection in the operating room reveals that a clip from a

venous graft to the RCA was dislodged, leading to immedi-

ate blood loss and tamponade.

5.6.1 Discussion

Postoperative bleeding presents in two categories—cata-

strophic acute bleeding after many hours of stability or con-

tinuous bleeding after leaving the OR. The former is

mechanical in nature, while the latter is often related to coag-

ulopathy. All bleeding is considered to be from a surgical

source until proven otherwise.

Denitions of signicant bleeding in the literature relate

to drain output in the rst 4–12hours or a threshold value of

red cell transfusion. The risk of major bleeding increases

with the complexity of surgery including multiple valves,

aortic/arch replacement, aortic dissections, redo operations,

renal or liver dysfunction, and the use of preoperative anti-

platelets or anticoagulants. Postoperative bleeding requires

careful assessment, management, and treatments (Tables

5.12, 5.13, 5.14 and 5.15).

Ongoing high-volume bleeding does not always man-

date urgent return to the OR, particularly in the setting of

known and documented coagulopathy. However, this sce-

nario involves very close attention to the patient with cor-

rection of all reversible causes of coagulopathy and keeping

the option open for an urgent return to the OR.Monitoring

includes:

Every 15min—review drain output and hemodynamics.

Every 60 min—arterial blood gas—Hb drop, pH, BE,

lactate.

Every 4h—CXR for retained intrapleural clot.

Maintain Hb>90in a bleeding patient.

Resuscitate and replace volume loss.

Be ready to rapidly reopen in the ICU.

Return to the OR is indicated if there is a rapid increase in

drain output, signs of tamponade, or ongoing bleeding

despite correction of a coagulopathy (Table5.14). The surgi-

cal team should be activated and a decision made whether a

perfusionist is required. At all times, the patient’s volume

Table 5.12 Initial assessment and management of postoperative

bleeding

Drain output per hour

Hemodynamics—Heart rate, rhythm, arterial pressure, venous

pressures, inotropic support, vasopressors

Respiratory—Lung volumes and pressures, gas exchange

End organ function—pH, base excess, urine output, lactate

Hemoglobin: Absolute value, trend, red cell transfusion required

Basic coagulation prole: INR, APTT, platelet count, brinogen

Advanced coagulation prole: ACT, TEG/ROTEM

Temperature

Remainder of lab values (including calcium)

Table 5.13 Initial treatment of postoperative bleeding with sudden

increase in drain output

Urgent return to the OR

Activate surgical team—Anesthesia, nursing, assistant, operating

room available

Ensure perfusionist and cell salvage available

Prepare for possible reopening in ICU

4units of red cells X-matched, plus platelets and clotting factors

Delegate where possible

Inform the family

Table 5.14 Correction of reversible non-surgical causes for bleeding

Correct coagulopathy Non-surgical options

Low brinogen: Fibrinogen

concentrate or cryoprecipitate

Correct hypocalcemia

High INR/PR: Clotting factors Maintain normothermia

High ACT: Protamine (25–50mg at a

time)

Consider prothrombin-X

Recent anti-platelets: Platelet

transfusion

Consider recombinant

activated factor VII

Table 5.15 Systematic assessment of potential bleeding sites

Common sites of bleeding

Less common sites

of bleeding

Mammary harvest bed Coronary sinus tear

Pericardial and thymic branches Left atrial appendage

Cannulation sites—Arterial, venous, vent

sites, retrograde cardioplegia site

Drain entry sites

Aortotomy or atriotomy LV apex from vent

Proximal/distal anastomoses Pacing wires

Conduit side branches

Sternum—Wire holes, periosteum, marrow,

fractures

5.6 Postoperative Bleeding

status and hemodynamics should be maintained, ideally with

volume resuscitation and early use of packed red cell

transfusion.

Once in the OR, the anesthesia team must resuscitate the

patient and correct any coagulopathy. The surgeon needs to

open the chest and reopen the pericardium as soon as possi-

ble—there is often a degree of cardiac tamponade that

accompanies any major bleeding episode. Catastrophic

bleeding sources are usually identied quickly and at least

temporarily managed with nger pressure and then denitive

management. For most bleeding patients, the source is not

immediately clear, and a systematic approach to all potential

bleeding sites should be used (Table5.15).

The lateral wall of the left ventricle can be difcult to

visualize in the bleeding patient without cardiopulmonary

bypass. The best approach to inspecting the lateral wall is to

use the techniques used in off-pump. Opening the right

pleura widely is a simple technique to improve exposure.

Once the bleeding has been identied and corrected, the

patient should be packed temporarily, while resuscitation is

continued. The volume status should be restored, coagulopa-

thy corrected, and the patient warmed before contemplating

sternal closure. If there is a profound coagulopathy or hemo-

dynamic instability, the chest can be packed for 24 hours

until some degree of stability has been achieved.

5.7 Cardiac Tamponade

A 55-year-old female undergoes an elective mitral valve

repair and initially has high drain output which settled after

transfusion of clotting factors. At the end of day, the patient

is noted to have sudden escalating vasoconstrictor require-

ments and a fall in urine output. An urgent bedside transtho-

racic echocardiogram was ordered, but the views were

suboptimal. The report shows good ventricular function and

possible intrapericardial clot.

5.7.1 Discussion

Cardiac tamponade in the postoperative setting is relatively

common and usually occurs in the rst few hours after

returning to the ICU.

Findings include:

• Increasing vasoconstrictor and inotrope requirements.

• Raised lling pressures (CVP and PA pressures).

• Low cardiac output state.

• Low urine output.

• Decreased mixed venous saturation.

• Metabolic acidosis.

• Pericardial effusion and features of tamponade visible on

echocardiography.

Not all tamponade patients have such a classic presenta-

tion. The mentioned ndings are typical for a circumferential

pericardial effusion. However, in the postoperative setting,

there can also be a localized tamponade of the right atrium,

the right ventricular free wall, or the left atrium (clot in the

oblique sinus). Localized tamponade will present with a low

cardiac output state, rising inotrope requirements, and low

urine output. The lling pressures and echocardiogram are

sometimes difcult to interpret. Any postoperative patient

with falling cardiac output and oliguria should have tampon-

ade excluded.

The treatment for a genuine suspicion of tamponade

should be an urgent return to the operating room for surgical

drainage. For any cardiac arrest in the postoperative period,

tamponade is the diagnosis of exclusion, and the chest and

pericardium must be opened immediately at the bedside.

Emergency reopening of the lower aspect of the wound and

entering the pericardium inferiorly (as per a subxiphoid win-

dow) can often provide excellent initial drainage if the patient

is a week or 2 post-surgery. For very early tamponade, how-

ever, complete sternal reopening is required to drain the effu-

sion and correct the bleeding source.

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References

Neurologic Complications

6.1 Stroke after CPB

The patient is a 55-year-old male transferred in from an out-

side hospital for a 95% left main lesion and a NSTEMI.He

appears otherwise well, except for a long history of diabetes.

A noncontrast CT of the chest shows no arterial calcica-

tions, and the patient undergoes an off-pump CABGx 3,

clampless, with a heartstring device utilized for the proximal

anastomosis. Epiaortic ultrasound shows only Grade 1 dis-

ease. He is extubated and doing well postoperatively.

During his second walk around the ICU, the patient suf-

fers acute left hemiparesis. CTA head shows an acute right-

sided stroke. The next day, he is aphasic, and repeat CT

shows an acute left-sided CVA.TEE demonstrates no intra-

cardiac source of emboli. There are no signicant carotid

lesions or evidence of large, retrievable thrombus. MRI con-

rms the stroke and also shows signicant intracerebral ath-

erosclerotic changes including an occluded vertebral artery.

6.1.1 Discussion

Stroke is a devastating complication in cardiac surgery,

increasing morbidity, length of stay, mortality, and long-term

survival [1, 2]. Nearly all strokes after heart surgery are

thought to be embolic. Stroke is not surprising in a patient

with severe atheroma in the ascending aorta or arch. But

sometimes stroke patients have none of those ndings and

undergo surgery with minimal aortic manipulation. A strat-

egy to prevent stroke has to move beyond diseased carotid

arteries and visualized plaque in the aorta by epiaortic ultra-

sound/CT.

A critical factor for intraoperative stroke is not always

embolizing atheroma, but may also involve cerebral hypo-

perfusion. A recent functional evaluation of cerebral perfu-

sion used SPECT to nd that adequate pulsatile ows with

off-pump CABG or IABP with conventional CABG made a

signicant impact on cerebral hypoperfusion [3]. What we

learn from this is something we already suspected; stroke

can be a systemic problem. Lack of pulsatile ow during car-

diopulmonary bypass and episodes of hypotension can play

critical roles in this process. Aside from signicant stenosis

or occlusion, patients can have other diagnoses that predis-

pose them to this complication. A history of stroke is one key

factor. A high degree of peripheral vascular disease is another

marker [3].

The main causes of stroke after cardiac surgery are throm-

boembolism and/or intraoperative hypoperfusion [4]. The

incidence rates of these mechanisms have been reported as

embolism (62.1%), multiple etiologies (10.1%), and hypo-

perfusion (8.8%) [5]. Hemorrhage or unknown etiologies are

other mechanisms [5].

The majority of strokes are thought to be embolic, due to

the vascular manipulation required in cardiac surgery; one

study cited embolic disease in 83% and watershed infarcts

in 24% [1]. Most strokes occur on the rst postoperative

day (41.7%), and an additional 20.4% occurred on the sec-

ond postoperative day [5]. The instantaneous risk of post-

operative stroke has been reported to peak at 40hours after

surgery [6].

There are areas in the brain that can have chronic hypo-

perfusion due to lack of collaterals. Multiple severe stenoses

or occlusions in the same system can also predispose to

hypoperfusion in the carotid or vertebral arteries. The pres-

ence of these intracranial occlusions also play a role in peri-

operative stroke [7, 8]. In the smaller regions of the brain,

tiny emboli can cause both ischemic and hemodynamic

changes. Low BP can cause prothrombotic conditions and

prevent washout.

Some of the data from TAVR has been revelatory regard-

ing the importance of anatomy and the location of cerebro-

vascular disease; the absence of signicant carotid stenosis is

not necessarily protective in terms of CVA. One study in

TAVR patients found vertebral artery stenosis to be a signi-

cant risk factor with 60% of new CVA lesions to be located

in the posterior circulation by MRI [9].

Specic predictors for stroke include advanced age, previ-

ous CVA or TIA, carotid artery stenosis, PVD, postop atrial

S. K. Balaram, L. Bassin, Cardiac Surgical Complications, https://doi.org/10.1007/978-3-030-71563-2_6

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