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8.2 Renal Complications

Acute kidney injury (AKI) is one of the most difﬁ cult-to-predict complications

occurring after cardiac surgery. Much emphasis has been placed in attempting to

elucidate the physiologic mechanisms for AKI and to develop methods to minimize

its occurrence. Because patients who develop AKI after cardiac surgery have a

signiﬁ cantly higher mortality rate than those who do not, AKI is a major focus of

current research.

8.2.1 Acute Kidney Injury

Acute kidney injury (AKI), also known as acute renal failure, after cardiac surgery

is one of the most serious complications during the postoperative period of the

patient having undergone cardiac surgery. The deﬁ nition of AKI has been quite vari-

able for many years. Recently, the Acute Kidney Injury Network (AKIN) deﬁ ned

AKI as the new need for institution of hemodialysis within 30 days of surgery.

However, other deﬁ nitions of AKI in past literature may include milder degrees of

kidney injury; these may be deﬁ ned as a 50 % drop in estimated glomerular ﬁ ltra-

tion rate (GFR) or an analogous rise in serum creatinine. Therefore, it is important

to consider the multiple deﬁ nitions that may comprise AKI when evaluating the

literature.

Although the incidence of postoperative AKI is relatively low (approximately

5–7 %), it is associated with high mortality rates during hospitalization and may

exceed 50 %. The incidence of AKI appears to be fairly stable across institutions in

the United States. Compared with patients who do not have postoperative renal dys-

function, patients with renal dysfunction (who do not need dialysis) remain twice as

long in both the intensive care unit and hospital wards and have signiﬁ cantly higher

mortality rates (1 % compared with 19 %). Furthermore, approximately 1 in 6

patients with renal dysfunction will need dialysis; 2 of 3 of these patients will not

survive their hospitalization. Finally, patients with renal dysfunction are three times

as likely to require continued, costly extended care after hospital discharge.

Etiology for AKI during cardiac surgery may be secondary to loss of pulsatile

blood ﬂ ow during CPB, increases in levels of circulating catecholamines and

inﬂ ammatory mediators, macroembolic and microembolic events to the kidney, and

release of free hemoglobin from damaged red blood cells. Patients undergoing car-

diac surgery may develop maldistribution of renal blood ﬂ ow, increases in renal

vascular resistance, and substantive decreases (25–75 %) in renal blood ﬂ ow and

glomerular ﬁ ltration rate. Predisposing factors that have been associated with acute

kidney injury in cardiac surgical patients are multifactorial, and most are indepen-

dently associated with AKI (see Table 8.3 ). Many of the conditions leading to AKI

do not occur in isolation; therefore, it is difﬁ cult to isolate a speciﬁ c critical period

or inciting event. In addition, patients undergoing valve surgery or valve surgery

with coronary artery bypass grafting (CABG) or multiple valve procedures are more

likely to sustain AKI compared to CABG alone.

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8.2.1.1 Diagnosis

Renal dysfunction after cardiac surgery is typically deﬁ ned as a postoperative serum

creatinine level of 177 micromol/L or greater and an increase in serum creatinine

level of 62 micromol/L or greater from preoperative to maximum postoperative

values. Postoperative renal failure is deﬁ ned by the need for dialysis within 30 days

after surgery. Additionally, emerging evidence is demonstrating that urinary inter-

leukin- 18 (IL-18) is an early, predictive biomarker of AKI after CPB and that uri-

nary neutrophil gelatinase-associated lipocalin (NGAL) and IL-18 are increased in

tandem after CPB. The combination of these two biomarkers may allow for the

reliable early diagnosis and prognosis of AKI at all times after CPB, much before

the rise in serum creatinine.

8.2.1.2 Management

There is currently no speciﬁ c method to prevent AKI from occurring in the postop-

erative period in patients undergoing cardiac surgery. Three major variables are

highly predictive of mortality, and those include (1) preoperative intra-aortic bal-

loon pump, (2) prolonged CPB time, and (3) emergent surgery. Unfortunately, there

is no way to alter those variables in order to mitigate AKI. However, multiple addi-

tional variables have been identiﬁ ed that may be modiﬁ able during the operative

period. These include (1) optimizing anemia preoperatively, (2) avoiding intraop-

erative red blood cell transfusions, and (3) preventing surgical re-exploration.

Avoidance of the aforementioned variables may serve to diminish the occurrence

of AKI.

Speciﬁ c pharmacologic therapies, such as vasoactive agents (i.e., low-dose dopa-

mine, fenoldopam, or theophylline), have been utilized in the treatment of postop-

erative AKI. None of these agents has shown conclusive beneﬁ ts in ameliorating

kidney function. Diuretics (i.e., furosemide) have not been shown to improve or

protect kidney function and have, in some cases, worsened outcomes. Pro-

inﬂ ammatory cytokines have been extensively studied as mediators or markers of

acute ischemia–reperfusion injury in experimental models of AKI. Their role in

patients undergoing cardiac surgery is of particular interest due to the potential

stimulation of inﬂ ammatory mediators upon exposure to the extracorporeal circuit.

Table 8.3 Risk factors for acute kidney injury after cardiac surgery

Patient-related factors

Surgical factors

Others

Advanced age: 70–79 Cardiopulmonary bypass >3 h Left ventricular dysfunction

Severely advanced age: 80–89 Use of intra-aortic balloon pump Red blood cell transfusion

Congestive heart failure Surgical re-exploration

Diabetes mellitus

Elevated preoperative serum

creatinine (124–177 mmol/L)

Female gender

Preoperative anemia

Previous myocardial

revascularization

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Use of therapeutic agents to interfere with these mediators, however, has not been

promising in terms of reducing risk for AKI in the clinical setting of cardiac surgery.

Both steroid use and N-acetylcysteine use have been examined in cardiac surgery

patients without any conclusive beneﬁ ts.

8.3 Infectious Complications

8.3.1 Surgical Site Infections

Surgical site infections (SSIs) have been the focus of much attention during the past

30 years, and the major emphasis has been to completely prevent the occurrence of

operative-related surgical infections and their associated morbidity and mortality.

The key interventions that should be performed and subsequently monitored in the

intensive care unit include (1) the proportion of patients who have parenterally

administered antibiotics within 1 h before incision (within 2 h for vancomycin and

ﬂ uoroquinolones), (2) the proportion of patients who are given a prophylactic anti-

microbial regimen consistent with published guidelines, and (3) the proportion of

patients whose prophylactic antimicrobial is discontinued within 24 h after surgery

end time (48 h for cardiac surgical patients).

Despite multiple pharmacologic and procedural policy guidelines implemented

in the last three decades, SSIs continue to occur at a rate of 2–5 % for extra-

abdominal surgeries, inclusive of mediastinal wound infections. SSIs are among the

top three causes of nosocomial infection, accounting for 14–16 % of all nosocomial

infections among hospitalized patients. SSIs are a major source of morbidity and

mortality rendering patients 60 % more likely to spend time in ICU, ﬁ ve times more

likely to require hospital readmission, and twice as likely to die. In the United

States, the increased cost per patient who experiences an infectious complication

has been reported to be approximately $1,398 per occurrence. A recent resurgence

in SSIs may be attributable to bacterial resistance, the increased implantation of

prosthetic and foreign materials, as well as the poor immune status of many patients

undergoing surgery. The universal adoption of simple measures including frequent

hand decontamination with alcohol and appropriate administration of prophylactic

antibiotics has been emphasized as a method of dramatically decreasing the inci-

dence of SSIs.

SSIs are divided into superﬁ cial (involving skin and subcutaneous tissues), deep

(fascial and muscle layers), and organ or tissue spaces (any area opened, manipu-

lated during surgery); see Table 8.4 . S . aureus , including methicillin-resistant

S . aureus ( MRSA ), is the predominant cause of SSIs. Other causative organisms are

coagulase-negative staphylococci, enterococci, coliforms, and Clostridium perfrin-

gens . Organ or tissue space infection after gastrointestinal surgery presents as peri-

tonitis or intra-abdominal abscess. Common causative organisms are coliforms,

P . aeruginosa , Candida spp., and Bacteroides fragilis . The increased proportion of

SSIs caused by resistant pathogens and Candida spp. may reﬂ ect increasing

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numbers of severely ill and immunocompromised surgical patients and the impact

of widespread use of broad-spectrum antimicrobial agents.

Mediastinitis is a particularly concerning postoperative infectious complication

and may occur with or without sternal wound dehiscence. The STS database indi-

cates that 25 % of wound infections in cardiac patients are related to mediastinal

wounds. Clinical predictors of sternal infections are diabetes, obesity, preoperative

hemodynamic instability, preoperative renal failure on dialysis, use of bilateral

internal mammary arteries, sepsis, and transfusions of more than four units of

packed red blood cells after surgery. Preoperative patient management and optimi-

zation may lessen the impact of these risk factors.

8.3.1.1 Risk Factors for Surgical Site Infections

The risk of SSI is a multifactorial issue and is related to the following factors:

Patient-Related Factors

Chronic illness, extremes of age, baseline immune- competence or inherent/

acquired immunocompromise, diabetes mellitus, and corticosteroid therapy are

associated with an increased risk of developing an SSI. The American Society of

Anesthesiologists’ Risk Stratiﬁ cation Classiﬁ cation score of 2 or more when

combined with the type and duration of surgery has been shown to be predictive

of an increased rate of SSIs.

Microbial Factors

Enzyme production ( S . aureus ), possession of polysaccharide capsule

( B . fragilis ), and the ability to bind to ﬁ bronectin in blood clots ( S . aureus and

Staphylococcus epidermidis ) are mechanisms by which microorganisms exploit

weakened host defenses and initiate infection. Bioﬁ lm formation, exempliﬁ ed by

S . epidermidis , is particularly important in the etiology of prosthetic material

infections (i.e., prosthetic joint infection). Coagulase- negative staphylococci

Table 8.4 Types of surgical site infections

Type of SSI

Time course

Criteria (at least one)

Superﬁ cial

incisional SSI

Within 30 days

of surgery

Superﬁ cial pus drainage

Organisms from superﬁ cial tissue or ﬂ uid

Signs and symptoms (pain, redness, swelling, heat)

Diagnosis by surgeon

Deep incisional SSI Within 30 days

of surgery or

within 1 year if

prosthetic implant

is present

Deep pus drainage

Dehiscence or wound opened by surgeon (for fever

>38 °C, pain, tenderness)

Abscess (e.g., radiographically diagnosed)

Diagnosis by surgeon or attending physician

Organ/space SSI Within 30 days

of surgery or

within 1 year if

prosthetic implant

is present

Pus from a drain in the organ/space

Organisms from aseptically obtained culture of ﬂ uid

or tissue in the organ/space

Abscess involving the organ/space

Diagnosis by a surgeon or attending physician

SSI surgical site infection

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produce glycocalyx and an associated component called “slime,” which

physically shields bacteria from phagocytes or inhibits the binding or penetration

of antimicrobial agents.

Wound-Related Factors

Devitalized tissue, dead space, and hematoma formation are factors associated

with the development of SSI. Historically, wounds have been described as

clean , contaminated , and dirty according to the expected number of bacteria

entering the surgical site. The presence of a foreign body (i.e., sutures, mesh)

reduces the burden of organisms required to induce SSI; however, the implanta-

tion of major devices such as foreign material and cardiac devices does not

necessarily yield expected SSIs. Risk factors for SSIs are summarized in

Table

8.5 .

8.3.1.2 Signs and Symptoms

SSIs typically present within 30 days of surgery with localized inﬂ ammation of the

surgical site and evidence of poor healing. Systemic features of infection, such as

fever and malaise, may occur soon thereafter. Erythema, pain, and purulent dis-

charge may develop at the sternal site; dressings should be routinely removed from

the sternum to inspect for possible development of mediastinitis.

8.3.1.3 Diagnosis

There may be nonspeciﬁ c evidence of infection in patients with surgical site infec-

tions, including but not limited to elevated white blood count, poor blood glucose

control, and elevation of inﬂ ammatory markers, such as C-reactive protein and pro-

calcitonin. However, surgery itself is a great confounder leading to inﬂ ammation,

thus rendering surrogate markers of infection unreliable. Purulence at the wound

sight is suggestive, but not invariable. The “gold standard” in documenting infection

is by growing organisms from an aseptically obtained culture. Approximately one

third of organisms cultured are staphylococci ( S . aureus and S . epidermidis ),

Enterococcus spp. makes up more than 10 %, and Enterobacteriaceae ( Escherichia

coli , P . aeruginosa , Enterobacter spp., Proteus mirabilis , and K . pneumoniae ) make

up the bulk of the remaining culprits.

Table 8.5 Risk factors for surgical site infections (SSIs)

Patient-related factors

Microbial factors

Wound-related factors

Age Enzyme production Devitalized tissue

Nutritional status Polysaccharide capsule Dead space

ASA score >2 Bind to ﬁ bronectin Hematoma

Diabetes Bioﬁ lm and slime Contaminated

Smoking Foreign material

Coexisting infections

Bacterial colonization

Immunocompromise

Length of preoperative hospital stay

ASA American Society of Anesthesiologists

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8.3.1.4 Treatment

It was recognized many years ago that prophylactic antimicrobial agents prevent

postoperative wound infections. The organisms that are implicated in SSIs are usu-

ally those that are carried as colonizers, for example, in the nose or on the skin, by

the patient at the time of surgery. Unless the patient has been in the hospital for

some time prior to surgery, these are usually community organisms that have not

developed multiple drug resistance; gram-positive organisms are typical. Timing of

antibiotic prophylaxis (within 1 h) of surgical incision is important as these organ-

isms are introduced into the bloodstream at the time of incision. Ideally, antibiotics

should be given within 30 min of surgical incision to achieve peak effect. Currently,

this recommendation is being evaluated as part of surveillance measures by the

CDC as there is tremendous variation in the timing of prophylactic antibiotics. For

most procedures, a single dose is adequate. Prolonged surgery (>4 h) may necessi-

tate a second dose. Prophylaxis should usually be discontinued within 24 h of the

procedure. For cardiac surgery, the Joint Commission on Accreditation of Healthcare

Organizations (TJC) has recommended that the duration of prophylaxis be increased

to 48 h. A ﬁ rst-generation cephalosporin such as cefazolin is effective for many

types of surgery. In general, the antibacterial spectrum, low incidence of side effects,

and tolerability of cephalosporins have made them the ideal choice for prophylaxis.

Refer to Boxes 8.2 and 8.3 for surgical infection prevention guidelines and methods

to decrease surgical site infections.

Box 8.2. Surgical Infection Prevention Guidelines

• Prophylactic antibiotics received within 1 h of surgical incision.

• Stop prophylactic antibiotics at 24 h (or 48 h for cardiac surgery).

• Increase dose of antibiotics for larger patients.

• Repeat dose when surgery exceeds 4 h.

• Administer antibiotic(s) appropriate for local resistance patterns.

• Follow American Heart Association guidelines for patients at risk for

endocarditis, regardless of surgery.

• Adhere to procedure-speciﬁ c antibiotic recommendations.

Box 8.3. Methods to Decrease Surgical Site Infection

• Ensure hand hygiene with alcohol.

• Observe strict asepsis.

• Mask, sterile gloves, and sterile gown for invasive procedures.

• Perform proper hair removal (use of hair clippers only, no razors, or no hair

removal).

• Maintain tight glucose control, especially in patients undergoing cardiac

surgery.

• Maintain normothermia via active measures.

• Promote adequate tissue oxygenation.

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8.3.2 Bloodstream Infections

Bloodstream infections (BSIs) are among the top three nosocomial infections.

Anesthesiologists have an important role in the prevention and often the treatment

of BSIs. Central venous catheters are the predominant cause of nosocomial bactere-

mia and fungemia. Catheter-related bloodstream infections are common, costly, and

potentially lethal; these infections are monitored by the National Nosocomial

Infections Surveillance (NNIS) system of the CDC. A total of 80,000 cases of cen-

tral venous catheter-associated BSIs have been estimated to occur annually in the

United States with an attributable mortality rate estimated at 12–25 % for each

infection with an average cost of $45,000.00 per infection per patient. The NNIS

recommends that the rate of catheter-associated BSIs be expressed as the number of

catheter-associated BSIs per 1,000 central venous catheter days. This parameter is

more useful than the rate expressed as the number of catheter-associated infections

per 100 catheters (or percentage of catheters studied) because it accounts for BSIs

over time and, therefore, adjusts risk of the number of days that the catheter is

in use.

8.3.2.1 Signs and Symptoms

Patients typically have nonspeciﬁ c signs of infection with no obvious candidate

source, no cloudy urine, purulent sputum, pus drainage, wound inﬂ ammation, other

than an indwelling infected catheter. Inﬂ ammation at the catheter insertion site is

suggestive. A sudden change in a patient’s condition should alert an astute clinician

to the possibility of a BSI. Important signs include mental status changes, hemody-

namic instability, altered tolerance for nutrition, and generalized malaise.

8.3.2.2 Diagnosis

Catheter-associated BSIs are deﬁ ned as bacteremia/fungemia in a patient with an

intravascular catheter with at least one positive blood culture with a recognized

pathogen not related to another separate infection, clinical manifestations of infec-

tion, and no other apparent source for the BSI except the catheter. Bloodstream

infections are considered to be associated with a central line if the line was in use

during the 48-h period before the development of the BSI. If the time interval

between the onset of infection and device use is greater than 48 h, there should be

compelling evidence that the infection is related to the central line; however, other

sources must always be considered. The diagnosis is more compelling if, when a

catheter is removed, the same organisms that grow from blood grow abundantly

from the catheter tip.

8.3.2.3 Treatment

The best treatment of central venous catheter-related BSIs is prevention; see Box 8.4

for overview of BSIs. The source of the bloodstream infection, usually a central

venous catheter, should be removed as soon as possible, and broad-spectrum empir-

ical antimicrobial therapy should be initiated pending the results of the cultures, at

which point therapy should be appropriately narrowed and targeted. Resistance

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patterns (both in general and in individual hospitals) may dictate initial therapy.

Data from the United States are very concerning. Most coagulase-negative

staphylococci and more than 50 % of S . aureus from ICUs are oxacillin resistant.

More than 25 % of enterococci isolates from ICUs are vancomycin resistant, and

this proportion is increasing. As for the gram-negative ICU isolates, many of them

produce extended-spectrum β-lactamases, particularly K . pneumoniae , rendering

them resistant to most antibiotics including even fourth-generation cephalosporins

and extended-spectrum penicillins, such as piperacillin/tazobactam. Half of the

Candida BSIs are associated with non- Albicans species, such as Candida glabrata ,

Candida tropicalis , Candida parapsilosis , and Candida krusei , which are likely to

be resistant to ﬂ uconazole and itraconazole. Based on these resistance patterns, it is

difﬁ cult to strike a compromise between appropriate initial empirical coverage and

not exhausting the last-line antimicrobial agents with the ﬁ rst salvo. Clinical judg-

ment should be based on the severity of the patient’s condition, the known suscepti-

bility patterns of organisms at a particular institution, and the organisms that are

currently implicated in infection in a particular environment. In order to delay

widespread resistance to all antimicrobial agents, therapy must be narrowed as soon

as organisms are identiﬁ ed and susceptibility is known. The principles of manage-

ment for patients with BSIs are as for other causes of sepsis.

8.3.2.4 Central Venous Catheter Insertion Strategies

Anesthesiologists have an essential role to play in the prevention of BSIs. Many

central venous catheters are placed by anesthesiologists who may be unaware about

BSIs that develop days later. Therefore, anesthesiologists may often be unaware that

a particular erroneous practice pattern is contributing to the development of BSIs.

Preventing BSIs related to central venous catheters can be minimized by imple-

menting a series of evidence-based steps shown to reduce infections as well as fos-

tering an environment of teamwork and safety.

A recent interventional study targeted ﬁ v e evidence-based procedures recom-

mended by the CDC and identiﬁ ed as having the greatest effect on the rate of

Box 8.4. Bloodstream Infections (BSIs)

• Bloodstream infections are among the top three causes of nosocomial

infections.

• Central venous catheters are the predominant cause of BSIs.

• Resistant organisms are commonly implicated in BSIs.

• Asepsis, masks, sterile gowns, and gloves during central line insertion

decrease the likelihood of BSI.

• Blood component transfusion causes immunosuppression and often leads

to BSIs; avoid blood component transfusion if possible.

• Remove sources of possible infection (i.e., invasive catheters) as soon as

possible.

• Management principles are same as for general sepsis.

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catheter-related BSIs and the lowest barriers to implementation. The ﬁ ve interven-

tions were (1) hand washing with soap and water or an alcohol cleanser, (2) the use

of full-barrier precautions (hat, mask and sterile gown, sterile area covering) during

central venous catheter insertion, (3) cleaning the skin with chlorhexidine, (4)

avoiding the femoral site and peripheral arms if possible, and (5) routine daily

inspection of catheters with removal as soon as deemed unnecessary. This evidence-

based interventional study resulted in a large and sustained reduction (up to 66 %)

in rates of catheter-related BSIs that was maintained throughout the 18-month study

period. The subclavian and internal jugular venous routes carry less risk of infection

than the femoral route, but the decision regarding anatomic location selection has to

be balanced against the higher risk of pneumothorax with a subclavian catheter.

During insertion, catheter contamination rates can be further reduced by rinsing

gloved hands in a solution of chlorhexidine in alcohol prior to handling the catheter.

Sterility must be maintained with frequent hand decontamination and cleaning cath-

eter ports each time with alcohol prior to accessing them. Central venous catheters

may be coated or impregnated with antimicrobial or antiseptic agents, such as sil-

ver/platinum/carbon impregnation or chlorhexidine/silver sulfadiazine or rifampi-

cin/minocycline coating; these catheters have been associated with a lower incidence

of BSIs. Concerns about widespread adoption of drug-impregnated catheters are

increased costs and promotion of further microbial resistance; however, such cath-

eters and their associated costs may be indicated for the most vulnerable patients,

such as those with severe immunocompromise.

8.3.3 Sternal Wound Infections

Deep sternal wound infection and dehiscence occurs in up to 5 % of patients under-

going median sternotomy and cardiac surgery and contributes to signiﬁ cant morbid-

ity and mortality. A superﬁ cial sternal wound infection (limited to skin and

subcutaneous tissue) may be accompanied by sternal instability, purulent discharge,

and signs of sepsis. Risk factors for developing sternal wound infection include

diabetes, renal failure, and prolonged mechanical intubation. If purulent discharge

is evident from a sternal wound infection, cultures should be immediately per-

formed to treat the speciﬁ c pathogen. Close follow-up by the surgical team is neces-

sary in order to prevent further infectious complications by other potential infectious

sites.

Noninfectious sternal dehiscence may occur secondary to obesity, chronic pul-

monary disease, osteoporotic sternum, inaccurate technique and ﬁ xation of ster-

num, excess bone wax use, steroid therapy, and history of chest radiation. In this

condition, wound reopening, debridement, and primary sternal rewiring is an ade-

quate treatment whenever the sternal bone remains intact. If the sternum has multi-

ple fractures, bone excision and defect closure by pectoral ﬂ ap is suitable treatment.

In cases of deep sternal wound infection and bony nonunion, sternal wound recon-

struction is performed with continuous antibiotic mediastinal irrigation, extensive

serial sternal debridement, plate ﬁ xation, and delay closure by using pectoral

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muscle or omental ﬂ ap. In addition, should wound dehiscence lead to breakdown of

muscle tissue, muscle ﬂ aps may be indicated. Utilization of a wound vacuum device

may assist in wound healing and prevention of entry of exogenous organisms.

Reference

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tiﬁ cation and management of ventilator-associated pneumonia. Intensive Care Med 30:

844–852