a b s t r a c t

Introduction: Coronary artery bypass graft (CABG) surgery remains a high-risk procedure, and many patients re- quire emergency department (ED) management for complications after surgery.

Objective: This narrative review provides an evidence-based summary of the current data for the emergency medicine evaluation and management of post-CABG surgery complications.

Discussion: While there has been a recent decline in all cardiac revascularization procedures, there remains over 200,000 CABG surgeries performed in the United States annually, with up to 14% of these patients presenting to the ED within 30 days of discharge with post-operative complications. Risk factors for perioperative mortality and morbidity after CABG surgery can be divided into three categories: patient characteristics, clinician charac- teristics, and postoperative factors. Emergency physicians will be faced with several postoperative complications, including sternal Wound infections, pneumonia, thromboembolic phenomena, Graft failure, atrial fibrillation, pul- monary hypertension, pericardial effusion, strokes, renal injury, gastrointestinal insults, and hemodynamic insta- bility. Critical patients should be evaluated in the resuscitation bay, and consultation with the primary surgical team is needed, which improves patient outcomes. This review provides several guiding principles for manage- ment of Acute complications. Understanding these complications and an approach to the management of hemo- dynamic instability is essential to optimizing patient care.

Conclusions: postoperative complications of CABG surgery can result in significant morbidity and mortality. Phy- sicians must rapidly diagnose these conditions while evaluating for other diseases. Early Surgical consultation is imperative, as is optimizing the patient’s hemodynamics, including preload, heart rate, cardiac rhythm, contrac- tility, and afterload.

1. Introduction

While there has been a recent decline in cardiac revascularization procedures, there remains over 200,000 coronary artery bypass graft (CABG) surgeries performed in the United States annually [1]. CABG surgery is often considered a high-risk procedure, associated with a 30-day Morbidity and mortality rate up to 14.0% and 2.0%, respectively [2]. Recently, there has been a widespread institution of early extubation and fast track protocols, which has resulted in earlier hospi- tal discharge, with an average post-op length of stay of 5.4 days [3]. Many of the patients discharged after CABG surgery frequently require emergency department (ED) visits and Hospital readmissions within 30 days, often for similar diagnoses. Approximately 14% of Medicare post-CABG surgery patients are readmitted within 30 days of discharge, while an additional 10% visit the ED, many for complications from and

* Corresponding author.

E-mail address: [email protected] (B. Long).

care related to the surgery [4-6]. Overall, 7% of post-CABG surgery patients will experience more than one readmission or ED visit within 30 days of surgery [4].

Risk factors for perioperative mortality and morbidity after CABG surgery have been extensively studied and can be divided into three cat- egories: patient characteristics, Provider characteristics, and postopera- tive factors [7,8]. Patient characteristics include older age, female sex, African American race, greater body surface area, and previous myocar- dial infarction (MI) within one week. Additionally, patient comorbidi- ties associated with increased morbidity and mortality include history of femoral/popliteal disease, chronic obstructive pulmonary disease, congestive heart failure, calcified Ascending aorta, carotid/cerebrovas- cular disease, aortoiliac disease, hepatic failure, renal failure, previous MI, and previous open-heart surgery [7,8]. Provider factors include annual surgeon CABG surgery volume b 100 cases per year and hospital risk-adjusted mortality rate in the highest decile. Postoperative factors include discharge to nursing home or rehabilitation/acute care facility and length of stay during index CABG surgery admission N 5 days [9,10].

https://doi.org/10.1016/j.ajem.2018.09.014 0735-6757/

1. Discussion

Post-CABG surgery complications can affect many different systems other than the cardiovascular system, as patients are at risk for common post-surgical complications, including respiratory failure, stroke, uri- nary tract infections, renal failure, coagulopathy, Limb ischemia, wound dehiscence, pleural effusion, and hematologic abnormalities [11-17]. It is important to consider this when evaluating the patient to maintain a broad differential of the Potential causes that may lead to the patient’s presentation to the ED. Fig. 1 depicts complications based on organ system.

There are a variety of post-CABG surgery complications, and while no single diagnosis accounts for the majority of ED visits and readmissions, the three most common diagnoses include post- operative infection, congestive heart failure, and chest discomfort [6]. The term “post-operative infection” is a general term encompassing su- perficial site infections, pneumonia, urinary tract infections, and deep sternal wound infections (DSWI), which include mediastinitis, pericar- ditis, and myocarditis. DSWI is a relatively uncommon event, occurring in about 1-2% of all patients undergoing cardiac surgery [18]. However, DSWIs confer a serious risk to the post-CABG surgery patient, with a 6-30% mortality rate, much higher than the estimated mortality rate of 2% for all cardiac surgery patients [19-23]. DSWIs confer an approxi- mately 2.5-fold increase in long term mortality, even in successfully treated patients who survive for at least 6 months postoperatively [19]. Chronic post-sternotomy pain affects 21-56% of all cardiac surgery patients and remains a common presenting complaint in the ED. [24-29] Numerous etiologies for congestive heart failure (CHF) in post-CABG surgery patients are present and can be conceptually broken down into two categories: complications from the cardiac surgery itself and com- plications of the underlying disease that led to CABG surgery. Complica- tions from the surgery include graft ischemia, which may be related to increased platelet activation secondary to epinephrine, in conjunction with decreased fibrinolysis and decreased left ventricular systolic func- tion, vasospasm, or air bubbles in the graft in the immediate post-op pe- riod, which peak during the first 2 h post-reperfusion [30]. Early graft

failure due to thromboembolism has been reported up to thirty days post-surgery [31-33]. One of the most devastating complications is car- diac tamponade. The risk of pericardial effusion after cardiac surgery ap- proximates 1.5% in the immediate post-op period [34]. Of these patients, almost half have some evidence of clinically significant tamponade and require immediate intervention, and Delayed cardiac tamponade (N48 h postoperatively) is well described [35]. Cardiac surgery is inherently ar- rhythmogenic, producing a variety of electrophysiological disturbances, most commonly atrial fibrillation [36,37]. CHF can also occur secondary to the patient’s underlying disease process that led to cardiac surgery, including complications of acute MI, such as cardiogenic shock, myocar- dial rupture, or post-infarction pericarditis.

Considerations in history and physical examination

Specific historical information is needed to determine the potential cause of the patient’s presentation to the ED and potential investigations needed [38]. Elucidating information regarding the chief complaint can help focus the physician on the possible organ system involved. Addi- tionally, it is necessary to obtain a thorough surgical history with infor- mation including the date of the surgery, current postoperative day, surgical approach, and indication for surgery. Hospital course, as well as any perioperative or immediate postoperative complications includ- ing presence of a pericardial effusion, pleural effusion, or arrhythmia should be reviewed, as this may be a clue to a potential complication. Whether the surgery was elective versus emergent is important to as- certain, as emergent surgeries significantly increase mortality and mor- bidity compared to elective operations [39]. Finally, an updated medication reconciliation should be performed including any antibi- otics, analgesics, antiplatelet or anticoagulant agents, and any cardio- vascular medications the patient may be taking.

Vitals signs are crucial in the evaluation of a post-CABG patient, al- though normal vital signs do not rule out an emergent process. A post-operative fever is defined as a temperature of N100.4 ?F [40]. Tachypnea or hypoxia may suggest infection, pulmonary embolism, acute pulmonary edema, or pleural effusion. Hypotension may be

Fig. 1. Post-CABG surgery complications - common complications following CABG surgery, arranged by organ system.

suggestive of sepsis from a DSWI, cardiac tamponade, or cardiogenic shock from a variety of reasons and warrants immediate resuscitation. Tachycardia may be suggestive of pain, infection, anemia, pulmonary embolism, or delayed bleeding.

While the cardiopulmonary evaluation usually focuses on the heart and lungs, it should also include a broad assessment for other abnormal- ities such as auscultation for murmurs and distant heart sounds, lung sounds, perfusion status, peripheral pulses, presence or absence of jug- ular venous distension, hepatomegaly, peripheral edema, and bilateral upper extremity blood pressures. The clinician should evaluate for depth of breathing, tachypnea, splinting, and Accessory muscle use.

Careful evaluation of the surgical incision is important to evaluate for dehiscence and infection, although the examination may be normal in patients with a DSWI. Overlying erythema, warmth, or induration may suggest the presence of infection. Any fluctuance or drainage is also im- portant to note, suggesting the presence of a hematoma or abscess. Fig. 2 depicts common post-operative complications and pertinent clin- ical findings that may assist in distinguishing the etiology.

Diagnostic considerations

1. Laboratory testing

Laboratory testing should be guided by the patient’s clinical presen- tation, history, and underlying comorbidities. There are no dedicated guidelines mandating required testing. Several valuable assessments for a patient presenting with chest discomfort include an electrocardio- gram (ECG), complete blood count , type and screen, troponin, basic metabolic panel, and imaging dependent on the specific Clinical concern (Point of Care Ultrasound , computed tomography (CT), chest x-ray). A patient presenting with a fever necessitates an evaluation for infection, which can include laboratory investigations and potentially blood cultures.

Imaging

Imaging should be guided by the patient’s clinical presentation, his- tory, and underlying comorbidities. However, POCUS is an invaluable tool to evaluate a wide range of intrathoracic variables, including pres- ence of Pleural effusions, pneumothorax, global and regional wall mo- tion abnormalities, valvular dysfunction, vegetations or abscesses, and aortic dissection, as well as the presence of pericardial effusion and any associated tamponade physiology [41]. When evaluating for a peri- cardial effusion, care must be taken, as material in the retrocardiac space can be difficult to view on transthoracic echocardiography or chest x- ray [42]. Chest x-ray also provides information on the integrity of sternal closure wires, while allowing evaluation of the lung fields for a variety of pathologies [43]. CT scan of the chest is often warranted in evaluation for the various complications during the postoperative period including deep space infection, dysphagia, or surgical leak. Intravenous contrast is recommended to better evaluate the anatomic and vascular structures of interest [44].

Medication considerations

Pain is often the chief complaint that has brought the patient to the ED. A routine post-sternotomy home regimen includes opioids, acet- aminophen, and Nonsteroidal anti-inflammatory drugs for pain. However, when considering treatment in the ED, opioids remain the mainstay of treatment [45]. A variety of antiemetics are available for treatment of any nausea. Ondansetron is a common, safe, and readily available medication and is often the first line in treating nausea due to its lack of sedative quality seen in promethazine or risk for akathisias seen with metoclopramide and prochlorperazine [46]. Additional con- sideration should be given to the evaluation of any new medications the patient is taking, as post-cardiac surgery patients may begin many new medications after discharge, including anti-platelet agents, ?-

Fig. 2. Post-operative complications - common complications following CABG surgery, with associated signs, symptoms, and laboratory findings.

blockers, nitrates, angiotensin-converting enzyme inhibitors (ACE-I), lipid-lowering agents, and possibly antibiotics.

Post-surgical complication management pearls based on differential diagnosis

1. Sternal wound infections

It is important to distinguish between DSWI and superficial sternal wound infections (SSWI). A SSWI involves the skin, subcutaneous tis- sue, and/or pectoralis fascia only [47]. There is no bony or mediastinal involvement [47]. The incidence of SSWI ranges from 0.5-8%, with a combined morbidity and mortality of 0.5-9% [48]. In contrast, DSWIs are a relatively uncommon event, occurring in 1-2% of all patients un- dergoing cardiac surgery. However, DSWIs confer a serious risk to the post-CABG surgery patient, with a 6-30% mortality rate [49]. Despite the significant clinical and economic consequences of sternal wound in- fections, there are currently no specific guidelines for the prevention and treatment of sternal wound infections in the cardiac surgery pa- tient. The Centers for Disease Control and Prevention define DSWI with the presence of any one of the following: [50].

1. An organism isolated from culture of mediastinal fluid or tissue;
2. Evidence of mediastinitis seen during operation; or
3. Presence of either chest pain, sternal instability, or fever (N38 ?C), and purulent drainage from the mediastinum, or isolation of an organism present in a blood culture or a culture of the mediastinal area.

Sternal wound infections are a clinical diagnosis, although imaging support usually consists of CT of the chest, which is highly sensitive and assists in determining the depth and degree of sternal wound infec- tion and dehiscence [51]. The treatment of sternal wound infections must be individualized based on the depth of the infection, the organ- isms that are cultured, and the patient’s clinical status. Discussion with the cardiothoracic surgeon is needed when determining treatment. Treatment of SSWIs is similar to localized abscesses: incision and drain- age to allow unimpeded drainage of the purulent material and possibly packing the wound with dressing changes, as guided by the surgical team [52]. For DSWIs, management principles include debridement of all devitalized/necrotic tissue, drainage of all infected spaces, antibiotic therapy, and techniques to achieve closure of the sternal space, most commonly vacuum-assisted [53]. In a 10-year surveillance study of ster- nal wound infections, methicillin-sensitive Staphylococcus aureus accounted for 28.3% of the isolates, Pseudomonas aeruginosa 18.3%, methicillin-resistant Staphylococcus aureus 14.6%, and Enterobacter spe- cies 6.7% [54]. In terms of establishing a causative organism, superficial swabs of the sternal incision predicted the pathogen 75% of the time in DSWIs, which improved to 82% of the time when blood cultures were included [55]. While the diagnosis of DSWI is clinical in nature, imaging support mainly consists of CT of the chest with contrast, which provides measurements on the depth of infection and dehiscence, and is highly sensitive in aiding diagnosis of sternal wound infections [56]. Nuclear imaging may be of value in the early stages of DSWI, but these are typ- ically not available in the ED. [57]

Management in the ED of a suspected DSWI consists of obtaining ap- propriate imaging and cultures of the sternal wound, urine, sputum, and blood while starting empiric antibiotic therapy including broad cover- age against methicillin-resistant gram-positive, gram-negative, and an- aerobic organisms. Culture-directed therapy should be initiated as soon as microbiological analysis is available, as antibiotics are typically con- tinued for six weeks. Empiric antibiotic regimens for DSWI include a broad-spectrum beta-lactam combined with vancomycin and an ami- noglycoside [58]. Early consultation with the surgical team for possible debridement and Negative pressure wound therapy is critical [59].

Pneumonia

Postoperative cardiac surgery patients are at a markedly increased risk for developing pneumonia secondary to postoperative chest wall pain that limits their mobility, ability to cough, and inspiratory effort. In those who undergo mechanical ventilation, even for a Short period of time, risk and mortality are both increased [60]. Post-operative pneu- monia incidence can range from 6.37% to as high as 35.2% in high-risk groups, with a 30-day post-operative mortality as high as 42% [61,62]. This is dependent upon patient comorbidities, illness severity, and the causative pathogen, with ventilator-associated pneumonia having a higher mortality rate. Evaluation of possible pneumonia includes a fo- cused clinical history and physical examination, as well as laboratory as- sessment, chest x-ray, and consideration of DSWI when beginning broad-spectrum antibiotics.

Venous thromboembolism (deep vein thrombosis/pulmonary embolism)

venous thromboembolism continues to remain one of the most common preventable causes of readmission, accounting for 6.3% of all post-CABG surgery readmissions, despite the low overall cumula- tive incidence of pulmonary embolism following cardiac surgery (1.3%), and low associated mortality (0.5%) [13,63,64]. The low incidence is likely due to the high rate of anticoagulation in this population [65]. However, patients undergoing CABG surgery typically possess risk fac- tors for VTE formation, including prolonged immobilization and recov- ery, surgical trauma to the lower limbs during vein harvesting, MI, atrial fibrillation, heart failure, hyperlipidemia, obesity, and postopera- tive Heparin-induced thrombocytopenia [66-69].

While D-dimer demonstrates high sensitivity, it has only moderate specificity, and should not be used in the post-CABG surgery patient. There are no other differences in imaging and treatment of VTEs in the post-CABG surgery patient when compared to other patients concerning the evaluation for VTE [70]. Hemodynamically unstable pa- tients presenting with a PE without contraindications may undergo thrombolytic therapy, catheter assisted thrombectomy, or surgical pul- monary embolectomy, although discussion with the operative team should be considered in conjunction to treatment.

Coronary artery bypass graft occlusion

Postoperative graft failure and perioperative MI following CABG sur- gery are serious complications with a varying incidence. When deter- mined by elevations in cardiac biomarkers and new ECG evidence of Q waves or bundle branch blocks, the incidence of CABG surgery failure ranges from 5 to 14% [71,72], However, when determined using cardiac magnetic resonance (CMR) to detect new loss of viable myocardium, the incidence is between 20 and 30% [73]. Because graft failure is signif- icantly more common in venous compared to arterial grafts, most of the published literature regarding pathological mechanisms is from saphe- nous vein grafts [74]. The pathophysiology varies, but thrombosis, endo- thelial dysfunction, vasospasm, and oxidative stress are different mechanisms associated with graft failure. Furthermore, the target artery characteristics, including severity of stenosis, internal diameter, extent of atherosclerotic burden, and any previous endovascular interventions are important determinants of graft patency [75]. The clinical conse- quences of graft failure are reliant upon the location of the distal anasto- mosis, with failure of grafts to the left anterior descending artery more closely tied to clinical events [76]. Diagnosis of postoperative graft fail- ure and subsequent MI is analogous to the diagnosis of acute coronary syndrome in the non-cardiac surgery patient, with special attention paid to how long after surgery the patient presents [77]. Troponin levels typically rise 4-8 h after onset of myocardial ischemia, peak within 18-24 h, and normalize within 10 days [78]. Thus, it is prudent to under- stand the definitions of MI, including Type 5 MI. Type 5 MI has been de- fined in the Third Universal Definition of MI (2012) as an elevation of cardiac troponin values N 10 x 99th percentile Upper reference limit during the first 48 h following CABG surgery in patients with

normal baseline cardiac troponin values (b99th percentile URL) to- gether with either: (a) new pathological Q waves or new Left bundle branch block , or (b) angiographic documented new graft or new native coronary artery occlusion, or (c) imaging evidence of new loss of viable myocardium or new regional Wall motion abnormality \(RWMA\) [79]. An ECG is an important diagnostic tool, as new ST- segment elevation or depression may indicate regional ischemia. How- ever, caution must be used, as post-CABG surgery patients with LV an- eurysm may have sustained ST segment elevations [80]. While many cardiac imaging modalities exist for detecting loss of viable myocardium or new regional wall motion abnormalities following CABG surgery, cor- onary angiography remains the gold standard, which also drives treat- ment strategy [81]. Treatment strategies for graft occlusion parallel those of acute coronary syndrome, consisting of medical therapy, thrombectomy, bypass graft surgery, or Balloon angioplasty with or without stenting [32].

Atrial fibrillation in the postoperative period

Postoperative atrial fibrillation is common after CABG surgery. Atrial fibrillation has been reported in up to 5-40% of patients within 2-4 days postoperatively, with a peak incidence on day 2 [82,83]. Atrial fibrilla- tion worsens a patient’s hemodynamics and increases the risk of con- gestive heart failure, as well as Thromboembolic events. Apart from a higher risk of stroke, atrial fibrillation worsens survival (74% vs. 87%) at long-term follow-up (4-5 years) [84]. The postoperative recovery pe- riod is characterized by increased autonomic nervous system activity and adrenergic stress, making the ventricular rate in patients with atrial fibrillation difficult to control, especially for patients with rapid ventric- ular response [85]. Before initiating treatment for atrial fibrillation, opti- mization of underlying medical comorbidities including electrolyte imbalance, hypoxia, and infection is recommended.

The treatment of post-CABG surgery atrial fibrillation includes use of medications and electrical cardioversion. Beta blockers are the therapy of choice, particularly in patients with ischemic heart disease, but care should be taken when using them in patients with asthma, chronic ob- structive pulmonary disease, congestive heart failure, and Conduction abnormalities, in whom they are relatively contraindicated [86]. Among calcium channel blockers, verapamil and diltiazem are routinely used [87]. Likewise, digoxin is an option for patients with concomitant congestive heart failure, although it is less effective when adrenergic tone is high [88]. For Hemodynamically stable patients, Rhythm control is an acceptable alternative to Rate control and can be achieved with the use of amiodarone, which leads to cardioversion within 12-24 h in 40-90% of patients [89,90]. Additionally, it provides effective rate con- trol, has a lower risk for arrhythmias, and is easily converted to oral therapy [91]. Because of the demonstrated increased mortality in post-MI patients receiving type Vaughan Williams Class IC agents for Premature Ventricular Complexes, these medications should be avoided in post-CABG surgery patients [92].

Pulmonary hypertension

Pulmonary hypertension following CABG surgery presents a signifi- cant diagnostic and therapeutic challenge, as it is associated with high morbidity and mortality secondary to right ventricular failure, arrhyth- mias, myocardial ischemia, and intractable hypoxia [93]. While the mechanism for development of pulmonary hypertension is complex, several factors induce pulmonary hypertension in the postoperative set- ting, including left ventricular dysfunction, underlying pulmonary hy- pertension, pulmonary inflammation and ischemia, mitral or aortic patient-prosthesis-mismatch, pulmonary emboli, and mechanical com- pression of the pulmonary vessels [94]. There is a growing body of evi- dence that morbidity and mortality associated with pulmonary hypertension are dependent on the adaptation of the right ventricle to postoperative hemodynamics rather than on the absolute value of pul- monary arterial pressure [95-98]. Pulmonary hypertension should be considered in any postoperative cardiac patient with unexplained

dyspnea, syncope, or signs of right ventricular dysfunction. The best ini- tial screening modality when pulmonary hypertension is clinically suspected is echocardiography, and a definitive diagnosis requires right heart catheterization. POCUS often demonstrates evidence of ele- vated pulmonary artery systolic pressure, Right ventricular dilation or hypertrophy tricuspid regurgitation, and dilated pulmonary arteries [99]. ECG findings may include right heart strain.

Management of these patients requires an understanding of the un-

derlying pathophysiology and focus on avoiding factors which further increase peripheral vascular resistance while simultaneously maintain- ing right ventricular perfusion [100]. Additionally, it is vital to avoid pul- monary vasoconstriction. These patients are incredibly sensitive to fluid balance, and excessive fluid resuscitation should be avoided [100]. Re- spiratory failure should be treated aggressively, utilizing lung protective strategies in intubated patients, and any metabolic derangements should be optimized including acidosis, hypoxemia, and anemia. Right ventricular afterload should be reduced through the use of Pulmonary vasodilators, including intravenous epoprostenol, oral bosentan, tadalafil, and sildenafil [101,102]. Patients may already be prescribed oral therapy for pulmonary hypertension diagnosed in the post- operative period [103,104]. Concomitant pulmonary embolism should be considered as a potential complicating factor in these patients.

Pericardial effusion and cardiac tamponade

Despite recent improvements in intraoperative management, surgi- cal technique, and postoperative care, pericardial effusions continue to be a significant cause of morbidity after CABG surgery. While these peri- cardial effusions may delay recovery, they can be life-threatening with tamponade and Hemodynamic compromise [105]. Additionally, there has been an increase in the incidence of postoperative pericardial effu- sions, likely due to the widespread use of chronic anticoagulation and increased complexity of cardiothoracic operations [106]. Present in up to 84% of patients after surgery, most pericardial effusions are small, asymptomatic, and clinically inconsequential [107]. The effusion usually reaches its maximum size by postoperative day ten, typically resolving spontaneously thereafter [108]. However, approximately one-fifth of cardiac surgery patients have a pericardial effusion on postoperative day 20, with an incidence of cardiac tamponade between 1 and 2.6% [109]. While early cardiac tamponade in the postoperative period is caused by surgical bleeding, late tamponade, which more commonly presents to the ED, is closely tied to postpericardiotomy syndrome, an inflammatory reaction of the pericardium secondary to surgical proce- dures [110]. This insipient diagnosis is complicated by the insidious onset and nonspecific symptoms, most commonly dyspnea, fatigue, chest pain, edema, presyncope, and nausea or vomiting [111]. Many pa- tients presenting with cardiac tamponade have tachycardia, hypoten- sion, oliguria, and increased jugular venous distention [111]. While diagnosis of cardiac tamponade is primarily clinical, POCUS plays an im- portant role. Signs of cardiac tamponade on bedside ultrasound include the presence of pericardial effusion, right atrial and ventricular diastolic collapse, left ventricular diastolic collapse, and distension of the inferior vena cava [112,113]. However, the sensitivity and specificity of trans- thoracic echocardiography for diagnosing pericardial effusion may be limited in patients after open heart surgery, likely due to potential clots in the pericardial space. Sensitivity and specificity have been re- ported as low as 75% and 64%, respectively [114]. Therefore, CT imaging is reasonable to perform after transthoracic echocardiography to assess for suspected delayed cardiac tamponade in high-risk patients after open heart surgery.

Management of pericardial effusion is dependent on the patient’s

hemodynamic status and echocardiographic findings. In the hemody- namically stable patient, early surgical consultation is critical for guid- ance on Anticoagulation management. In patients without prominent symptoms or clinical findings, decisions on interventions are deter- mined by echocardiographic features of the pericardial effusion and the amount and accessibility of the fluid. In the hemodynamically

unstable patient, decompression of the tamponade is key, as is early consultation with the primary surgical team. Options for drainage in- clude surgical operation or the use of a percutaneous catheter [115]. Furthermore, it is imperative to correct any underlying coagulopathy, as many of these patients are on anticoagulants.

Cerebrovascular accident

Stroke is widely recognized as one of the most devastating complica- tions of CABG surgery, occurring in 1.6-8.4% of patients [116]. Of note, 65% of these patients experience “delayed strokes”, defined as a stroke occurring after an initial uneventful neurological recovery from surgery [117]. Risk factors for delayed stroke include prior neurological events, diabetes, aortic atherosclerosis, low cardiac output, and atrial fibrillation [118]. The majority of strokes during the perioperative and postopera- tive periods are ischemic in nature, with atrial fibrillation playing an im- portant role [119]. While the diagnosis of acute cerebrovascular accident in post-CABG surgery patients is similar to non-cardiac surgery patients, it is important to recognize that short- and long-term cognitive changes, manifested as short-term memory loss, executive dysfunction, encephalopathy, and psychomotor slowing, are becoming increasingly common in the postoperative period, occurring in up to 32% of patients, and may mimic an acute stroke [120]. The multifactorial causes of this encephalopathy include microembolization causing Ischemic injury, surgical trauma, preexisting vascular disease, and hypothermia during surgery [121]. Regarding treatment of ischemic stroke, intravenous tis- sue plasminogen activator (tPA) is contraindicated in patients who have recently undergone major surgery, secondary to an increased risk of bleeding. However, intra-arterial administration of tPA [122], as well as endovascular mechanical clot retrieval, remain viable treatment options [123]. A retrospective case series suggests that the use of intra- arterial tPa is relatively safe within 6 h after completion of surgery [124].

Renal dysfunction

Acute kidney injury and acute renal failure (ARF) remain seri- ous complications of cardiac surgery and are important contributors of short- and long-term mortality, occurring in 5-42% of patients accord- ing to recent literature [125]. The underlying insult is often multifacto- rial, including ischemia, toxicity from antibiotics, Anesthetic agents, contrast media, diuretics, myoglobin, and embolic events [126,127]. A Prompt diagnosis of ARF provides physicians with the opportunity to implement the few strategies that may improve renal function in the post-operative period. The diagnosis of AKI typically includes the mea- surement of serum creatinine concentrations and urine output, with Consensus guidelines favoring the Kidney Disease: Improving Global Outcomes (KDIGO) criteria [128]. These criteria define AKI by any of the following: an increase in serum creatinine by >=0.3mg/dL (N26.5 umol/L) within 48 h, an increase in serum creatinine to >=1.5 times the patient’s baseline occurring within the prior seven days, or a urine volume b 0.5 mL/kg/h for 6 h [128]. Early recognition of these at-risk pa- tients and prompt resuscitation with fluids and Vasoactive medications as necessary to prevent any further renal insults are imperative. Ideally, balanced crystalloid solutions should be used, as 0.9% saline has been as- sociated with Hyperchloremic metabolic acidosis, worsening acid-base balance, and adverse renal outcomes [129]. In critically ill patients, par- ticularly those in septic shock, derangements in microcirculation, vasoreactivity, and renal blood flow autoregulation lead to ARF by way of ischemic hypoperfusion. While data on the optimal mean arterial pressure (MAP) to prevent the development and/or progression of ARF are conflicting, current recommendations propose a target MAP

>= 65 mm Hg but state that the target MAP should be individualized, es-

pecially in patients with pre-existing chronic hypertension [130].

Gastrointestinal complications

Gastrointestinal (GI) complications are relatively uncommon after cardiac surgery, occurring in 1.2% of patients undergoing cardiac sur- gery, a rate that has not decreased significantly in recent years [131-

133]. A wide range of GI complications are reported with bleeding, mes- enteric ischemia, pancreatitis, cholecystitis, Peptic ulcer perforation, he- patic dysfunction, and ileus being the most common presenting diagnoses in the ED. [131] While ischemia is thought to be the main cause of GI complications during cardiac surgery, systemic inflamma- tion, medical comorbidities, and Drug therapies play an important role [132]. Clinical presentation varies with pathology, and no single diag- nostic test has been shown to reliably diagnose or exclude intra- Abdominal pathology [133]. Investigation should be guided by patient history and presentation. Initial investigations may include biochemical and hematological blood analysis including serum lactate, glucose, liver function tests (transaminases, bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase), Coagulation studies, and CBC includ- ing white blood cell count. These may be augmented by abdominal radi- ography, ultrasound, or CT, as indicated. Likewise, management and disposition should be dictated by the clinical presentation and underly- ing pathophysiology.

Approach to the hemodynamically unstable cardiac surgery patient The hemodynamically unstable post cardiac surgery patient pro- vides a diagnostic and therapeutic challenge due to the numerous po- tential underlying mechanisms and pathophysiology. These patients may present in any combination of obstructive, cardiogenic, septic, or hypovolemic shock. Conceptually, causes of instability may be divided into two categories to aid in their diagnosis: those causes immediately recognizable on direct inspection and those immediately recognizable

on routine investigation (Fig. 3).

In addition to the standard history and physical examination ob- tained on every patient, the following simple evaluations should be per- formed on the hemodynamically unstable post-CABG surgery patient: blood glucose measurement; assessment of hands and feet for abnormal vasodilation and symmetric bilateral pulses; assessment of skin for urti- caria, facial swelling, and angioedema present in anaphylactic shock; cardiopulmonary examination for any tracheal deviation, new mur- murs, decreased or absent breath sounds, and increased jugular venous distention; and the patient should be placed on a cardiac monitor to evaluate for arrhythmias.

These simple actions will help evaluate for the presence of anaphy- laxis, arrhythmias, valve failure, and pneumothorax/tension pneumo- thorax. However, there are critical investigations necessary to further assess for the presence of ischemia, tamponade, hemorrhage, cardio- genic shock, PE, and septic shock including ECG to evaluate for myocar- dial ischemia and arrhythmias; chest x-ray or point of care ultrasound to evaluate for the presence of pneumothorax, Tension pneumothorax, pulmonary edema, or underlying pneumonia; CBC; and echocardiogra- phy to assess for valve dysfunction, myocardial contractility, presence of right heart strain, left ventricular (LV) outflow tract obstruction, right ventricular (RV) failure, or presence of cardiac tamponade.

Immediate management is focused on the basics of resuscitation: airway, breathing, and circulation, with optimization of preload, rate, rhythm, contractility, and afterload [134,135]. With these critically ill surgical patients, it is prudent to consult the appropriate surgical team early in order to facilitate diagnosis and aid management.

Though the literature is not strong pertaining to a specific transfu- sion threshold, most guidelines recommend a hemoglobin of 8.0 g/dL in patients after cardiac surgery or those at risk for acute coronary syn- drome [136]. Anemia may result in tissue hypoxia, especially with fluc- tuating cardiac output; however, too much hemoglobin adds to the myocardial workload by increasing the mass of the blood, which may result in decreased cardiac output and poor perfusion.

Disposition

Early consultation with the operative team can help the clinician clarify the patient’s operative course, as well as the desired Diagnostic approach. Additionally, early consultation facilitates timely

Fig. 3. Hemodynamic decompensation in post-CABG surgery - common etiologies of hemodynamic instability immediately recognizable by direct inspection or routine investigations.

management and coordinated handoff to ensure the best patient care possible. Level of care is dependent on the patient’s underlying patho- physiology, hemodynamic status, need for invasive monitoring, and un- derlying comorbidities. Recent literature has shown that when complications occur after a major surgical procedure, returning the pa- tient to the index hospital to be cared for by the original surgical team significantly improves 90-day survival, compared to admission at a non-index hospital [137].

1. Conclusions

Post-CABG surgery patients are increasingly presenting to the ED for care. The most common issues include post-operative infections, conges- tive heart failure, and chest discomfort. Risk factors for perioperative mor- tality and morbidity after CABG surgery can be divided into three categories: patient characteristics, provider characteristics, and postoper- ative factors. Several of these complications are associated with severe morbidity. DSWIs occur in about 1-2% of all patients undergoing cardiac surgery, but have up to a 30% mortality rate. Other significant complica- tions include pneumonia, VTE, graft failure, atrial fibrillation, pulmonary hypertension, pericardial effusion, Cerebrovascular accidents, renal injury, and hemodynamic instability. Critical patients should be evaluated in the resuscitation bay, and consultation with the primary surgical team is needed. These patients require immediate consultation, which improves outcomes, and evaluation for a potentially dangerous condition. Under- standing these complications and an approach to the management of he- modynamically instability are essential to optimizing patient care.

Conflicts of interest

None.

Acknowledgements

TM, BL, and AK conceived the idea for this manuscript and contributed substantially to the writing and editing of the review. This manuscript did not utilize any grants, and it has not been presented in abstract form. This clinical review has not been published, it is not under consideration for publication elsewhere, its publication is approved by all authors and tac- itly or explicitly by the responsible authorities where the work was car- ried out, and that, if accepted, it will not be published elsewhere in the same form, in English or in any other language, including electronically without the written consent of the copyright-holder. This review does not reflect the views or opinions of the U.S. government, Department of Defense, U.S. Army, U.S. Air Force, or SAUSHEC EM Residency Program.

References

1. Riley RF, Don CW, Powell W, et al. Trends in coronary revascularization in the United States from 2001 to 2009: recent declines in percutaneous coronary inter- vention volumes. Circ Cardiovasc Qual Outcomes 2011 Mar;4(2):193-7.
2. Lazar HL, Fitzgerald CA, Ahmad T, et al. early discharge after coronary artery bypass graft surgery: are patients really going home earlier? J Thorac Cardiovasc Surg 2001;121(5):943-50.
3. Shahian DM, O’Brien SM, Normand SL, et al. Association of hospital coronary artery by- pass volume with Processes of care, mortality, morbidity, and the Society of Thoracic Surgeons composite quality score. J Thorac Cardiovasc Surg 2010;139(2):273-82.
4. Hannan EL, Zhong Y, Lahey SJ, et al. 30-day readmissions after coronary artery by- passes graft surgery in New York state. JACC Cardiovasc Interv 2011 May;4(5): 569-76.
5. Li Z, Armstrong EJ, Parker JP, Danielsen B, Romano PS. Hospital variation in read- mission after coronary artery bypass surgery in California. Circ Cardiovasc Qual Outcomes 2012 Sep;5(5):729-37.
6. Fox JP, Suter LG, Wang K, et al. Hospital-based, acute care use among patients within 30 days of discharge after Coronary artery bypass surgery. Ann Thorac Surg 2013;96(1):96-104.
7. Shahian DM, O’Brien SM, Normand SL, et al. Association of hospital coronary artery bypass volume with processes of care, mortality, morbidity, and the Society of Tho- racic Surgeons composite quality score. J Thorac Cardiovasc Surg 2010;139(2): 273-82.
8. Slamowicz R, Erbas B, Sundararajan V, Dharmage S. Predictors of readmission after elective coronary artery bypass graft surgery. Aust Health Rev 2008 Nov;32(4): 677-83.
9. Hannan EL, Wu C, Ryan TJ, et al. Do hospitals and surgeons with higher coronary artery bypass graft surgery volumes still have lower risk-adjusted mortality rates? Circulation 2003;108(7):795-801.
10. Peterson ED, Coombs LP, Delong ER, et al. Procedural volume as a marker of quality for CABG surgery. JAMA 2004;291(2):195-201.
11. Sachdev G, Napolitano LM. Postoperative pulmonary complications: pneumonia and acute respiratory failure. Surg Clin N Am 2012;92(2):321-44.
12. Le Tanneur C, Mongardon N, Haouache H, et al. Acute lower limb ischemia after Coronary artery bypass grafting. J Cardiothorac Vasc Anesth 2015;29(6):1624-6.
13. Hannan EL, Racz MJ, Walford G, et al. Predictors of readmission for complications of coronary artery bypass graft surgery. JAMA 2003;290(6):773-80.
14. Lorusso R, Mariscalco G, Vizzardi E, et al. Acute Bowel ischemia after heart opera- tions. Ann Thorac Surg 2014;97(6):2219-27.
15. Chaudhry R, Zaki J, Wegner R, et al. Gastrointestinal complications after cardiac sur- gery: a nationwide population-based analysis of morbidity and mortality predic- tors. J Cardiothorac Vasc Anesth 2017;31(4):1268-74.
16. Labidi M, Baillot R, Dionne B, et al. Pleural effusions following cardiac surgery. Chest

2009;136(6):1604-11.

1. Schimmer C, Reents W, Berneder S, et al. Prevention of sternal dehiscence and in- fection in high-risk patients: a prospective randomized multicenter trial. Ann Thorac Surg 2008;86(6):1897-904.
2. Filsoufi F, Castillo JG, Rahmanian PB, et al. Epidemiology of deep sternal wound in- fection in cardiac surgery. J Cardiothorac Vasc Anesth 2009;23(4):488-94.
3. Mauermann WJ, Sampathkumar P, Thompson RL. Sternal wound infections. Best Pract Res Clin Anaesthesiol 2008;22(3):423-36.
4. Salehi Omran A, Karimi A, Ahmadi SH, et al. Superficial and deep sternal wound in- fection after more than 9000 coronary artery bypass graft (CABG): incidence, risk factors and mortality. BMC Infect Dis 2007;7:112.
5. Toumpoulis IK, Anagnostopoulos CE, Derose JJ, Swistel DG. The impact of deep ster- nal wound infection on long-term survival after coronary artery bypass grafting. Chest 2005;127(2):464-71.
6. De Feo M, Renzulli A, Ismeno G, et al. Variables predicting adverse outcome in pa- tients with deep sternal wound infection. Ann Thorac Surg 2001;71(1):324-31.
7. Wouters R, Wellens F, Vanermen H, et al. Sternitis and mediastinitis after coronary artery bypass grafting. Analysis of risk factors. Tex Heart Inst J 1994;21(3):183-8.
8. Kalso E, Mennander S, Tasmuth T, Nilsson E. Chronic post-sternotomy pain. Acta Anaesthesiol Scand 2001;45:935-9.
9. Meyerson J, Thelin S, Gordh T, Karlsten R. The incidence of chronic post-sternotomy pain after cardiac surgery: a prospective study. Acta Anaesthesiol Scand 2001;45: 940-4.
10. Meyerson J, Thelin S, Gordh, et al. Prevalence and characteristics of post coronary artery bypass graft surgery pain (PCP). Pain 2001;92:11-7.
11. Eisenberg E, Pultorak Y, Pud, et al. The prevalence of chronic chest and leg pain fol- lowing cardiac surgery: a historical cohort study. Pain 2003;104:265-73.
12. Bruce J, Drury N, Poobalan, et al. Persistent pain after cardiac surgery: an audit of high thoracic epidural and primary Opioid analgesia therapies. Anesth Analg 2002;95:820-3.
13. Jensen MK, Andersen C. Can chronic poststernotomy pain after cardiac valve re- placement be reduced using thoracic epidural analgesia? Acta Anaesthesiol Scand 2004;48(7):871-4.
14. Smith RC, Leung JM, Mangano DT. Postoperative myocardial ischemia in patients undergoing coronary artery bypass graft surgery. S.P.I. research group. Anesthesiol- ogy 1991;74(3):464-73.
15. Szavits-Nossan J, Stipic H, Sesto I, et al. Angiographic control and percutaneous treatment of myocardial ischemia immediately after CABG. Coll Antropol 2012; 36(4):1391-4.
16. Laflamme M, DeMey N, Bouchard D, et al. Management of early postoperative cor- onary artery bypass graft failure. Interact Cardiovasc Thorac Surg 2012;14(4): 452-6.
17. Gukop P, Momin A. Early saphenous vein graft disease following coronary artery bypass grafting. Surgery (Oxford) 2018;36(2):83-5.
18. Ashikhmina EA, Schaff HV, Sinak LJ, et al. Pericardial effusion after cardiac surgery: risk factors, patient profiles, and contemporary management. Ann Thorac Surg 2010;89(1):112-8.
19. Leiva EH, Carreno M, Bucheli FR, et al. Factors associated with delayed cardiac tamponade after cardiac surgery. Ann Card Anaesth 2018;21(2):158-66.
20. Current Readings: An Update on Prevention and Management of Atrial Fibrillation Post Cardiac Surgery. Seminars in Thoracic and Cardiovascular Surgery; 2018. https://doi.org/10.1053/j.semtcvs.2018.02.007, Accessed date: 22 March 2018.
21. Khan J, Khan N, Loisa E, Sutinen J, Laurikka J. Increasing occurrence of postoperative atrial fibrillation in contemporary cardiac surgery. J Cardiothorac Vasc Anesth 2016;30(5):1302-7.
22. Narayan M, Medinilla SP. Fever in the postoperative patient. Emerg Med Clin North

Am 2013;31(4):1045-58.

1. Schumer EM, Chaney JH, Trivedi JR, et al. Emergency coronary artery bypass grafting: indications and outcomes from 2003 through 2013. Tex Heart Inst J 2016;43(3):214-9.
2. Pile JC. Evaluating postoperative fever: a focused approach. Cleve Clin J Med Mar 2006;73(Suppl. 1):S62-6.
3. Heiberg J, El-Ansary D, Royse CF, et al. Transthoracic and transoesophageal echo- cardiography: a systematic review of feasibility and impact on diagnosis, manage- ment and outcome after cardiac surgery. Anaesthesia 2016;71(10):1210-21.
4. Hamid M, Khan MU, Bashour AC. Diagnostic value of chest X-ray and echocardiog- raphy for cardiac tamponade in post cardiac surgery patients. J Pak Med Assoc 2006;56(3):104-7.
5. Forouzannia SK, Sarvi A, Sarebanhassanabadi M, Nafisi-Moghadam R. Elimination of routine chest radiographs following off-pump coronary artery bypass surgery: a randomized controlled trial study. Adv Biomed Res 2015;4:236.
6. Mueller J, Jeudy J, Poston R, White CS. Cardiac CT angiography after coronary by- pass surgery: prevalence of incidental findings. AJR Am J Roentgenol 2007;189 (2):414-9.
7. Lahtinen P, Kokki H, Hynynen M. Pain after cardiac surgery: a prospective cohort study of 1-year incidence and intensity. Anesthesiology 2006;105(4):794-800.
8. Choi DK, Chin JH, Lee EH, et al. Prophylactic control of post-operative nausea and vomiting using ondansetron and ramosetron after cardiac surgery. Acta Anaesthesiol Scand 2010;54(8):962-9.
9. Ridderstolpe L, Gill H, Granfeldt H, et al. Superficial and deep sternal wound com- plications: incidence, risk factors, and mortality. Eur J Cardiothorac Surg 2001;20: 1168-75.
10. Lepelletier D, Perron S, Bizouarn P, et al. Surgical-site infection after cardiac sur- gery: incidence, microbiology, and risk factors. Infect Control Hosp Epidemiol 2005;26(5):466-72.
11. Lemaignen A, Birgand G, Ghodhbane W, et al. Sternal wound infection after cardiac surgery: incidence and risk factors according to clinical presentation. Clin Microbiol Infect 2015;21(7):674.e11-8.
12. Mangram AJ, Horan TC, Pearson ML, et al. Guideline for prevention of surgical site infection, 1999. Centers for Disease Control and Prevention (CDC) hospital infec- tion control practices advisory committee. Am J Infect Control 1999;27(2):97-132.
13. Gur E, Stern D, Weiss J, et al. Clinical-radiological evaluation of poststernotomy wound infection. Plast Reconstr Surg 1998;101:348-55.
14. Lazar HL, Salm TV, Engelman R, Orgill D, Gordon S. Prevention and management of sternal wound infections. J Thorac Cardiovasc Surg 2016;152(4):962-72.
15. Cotogni P, Barbero C, Rinaldi M. Deep sternal wound infection after cardiac surgery: evidences and controversies. World J Crit Care Med 2015;4(4):265-73.
16. Si D, Rajmokan M, Lakhan P, Marquess J, Coulter C, Paterson D. Surgical site infec- tions following coronary artery bypass graft procedures: 10 years of surveillance data. BMC Infect Dis 2014;14:318.
17. Chaudhuri A, Shekar K, Coulter C. Post-operative deep sternal wound infections: making an early microbiological diagnosis. Eur J Cardiothorac Surg 2012;41(6): 1304-8.
18. Gur E, Stern D, Weiss J, et al. Clinical-radiological evaluation of poststernotomy wound infection. Plast Reconstr Surg 1998;101:348-55.
19. Quirce R, Carril JM, Gutierrez-Mendiguchia C, et al. Assessment of the diagnostic ca- pacity of planar scintigraphy and SPECT with 99mTc-HMPAO-labelled leukocytes in superficial and deep sternal infections after median sternotomy. Nucl Med Commun 2002;23:453-9.
20. Molina JE, Nelson EC, Smith RR. Treatment of postoperative sternal dehiscence with mediastinitis: twenty-four-year use of a single method. J Thorac Cardiovasc Surg 2006;132(4):782.
21. Singh K, Anderson E, Harper JG. Overview and management of sternal wound in- fection. Semin Plast Surg 2011;25(1):25-33.
22. Sachdev G, Napolitano LM. Postoperative pulmonary complications: pneumonia and acute respiratory failure. Surg Clin N Am 2012;92(2):321-44.
23. Allou N, Allyn J, Snauwaert A, et al. Postoperative pneumonia following cardiac sur- gery in non-ventilated patients versus Mechanically ventilated patients: is there any difference? Crit Care 2015;19:116.
24. He S, Chen B, Li W, et al. Ventilator-associated pneumonia after cardiac surgery: a meta-analysis and systematic review. J Thorac Cardiovasc Surg 2014;148(6): 3148-55 (e1-5).
25. Protopapas AD, Baig K, Mukherjee D, Athanasiou T. Pulmonary embolism following coronary artery bypass grafting. J Card Surg 2011;26(2):181-8.
26. Shammas NW. Pulmonary embolus after coronary artery bypass surgery: a review of the literature. Clin Cardiol 2000;23:637-44.
27. Ho KM, Bham E, Pavey W. Incidence of venous thromboembolism and benefits and risks of thromboprophylaxis after cardiac surgery: a systematic review and meta- analysis. J Am Heart Assoc 2015;4(10):e002652.
28. Edelman JJ, Reddel CJ, Kritharides L, et al. Natural history of hypercoagulability in patients undergoing coronary revascularization and effect of preoperative MI. J Thorac Cardiovasc Surg 2014;148(2):536-43.
29. Vallely MP, Bannon PG, Bayfield MS, et al. Quantitative and temporal differences in coagulation, fibrinolysis and platelet activation after on-pump and off-pump coro- nary artery bypass surgery. Heart Lung Circ 2009;18(2):123-30.
30. Lison S, Dietrich W, Braun S, et al. Enhanced thrombin generation after cardiopul- monary bypass surgery. Anesth Analg 2011;112(1):37-45.
31. Parolari A, Mussoni L, Frigerio M, et al. Increased prothrombotic state lasting as long as one month after on-pump and off-pump coronary surgery. J Thorac Cardiovasc Surg 2005;130(2):303-8.
32. Wolf SJ, Hahn SA, Nentwich LM, et al. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with suspected acute Venous thromboembolic disease. Ann Emerg Med 2018;71(5): e59-109.
33. Hirsch WS, Ledley GS, Kotler MN. Acute ischemic syndromes following coronary ar- tery bypass graft surgery. Clin Cardiol 1998;21(9):625-32.
34. Thielmann M, Sharma V, Al-Attar N, et al. ESC joint working groups on cardiovas- cular surgery and the cellular biology of the heart position paper: perioperative myocardial injury and infarction in patients undergoing coronary artery bypass graft surgery. Eur Heart J 2017;38(31):2392-407.
35. Hueb W, Gersh BJ, Alves Da Costa LM, et al. Accuracy of myocardial biomarkers in the diagnosis of MI after revascularization as assessed by cardiac resonance: the medicine, angioplasty, surgery study V (MASS-V) trial. Ann Thorac Surg 2016; 101(6):2202-8.
36. Gaudino M, Antoniades C, Benedetto U, et al. Mechanisms, consequences, and pre- vention of coronary graft failure. Circulation 2017;136(18):1749-64.
37. De Vries MR, Simons KH, Jukema JW, Braun J, Quax PH. Vein graft failure: from pathophysiology to clinical outcomes. Nat Rev Cardiol 2016;13(8):451-70.
38. Harskamp RE, Alexander JH, Ferguson TB, et al. Frequency and predictors of inter- nal mammary artery graft failure and subsequent clinical outcomes: insights from the project of ex-vivo vein graft engineering via transfection (PREVENT) IV trial. Circulation 2016;133(2):131-8.
39. Van Beek D, Van Zaane B, Looije M, et al. Typical rise and fall of troponin in (peri- procedural) MI: a systematic review. World J Cardiol 2016;8(3):293-301.
40. Januzzi JL. Troponin testing after cardiac surgery. HSR Proc Intensive Care Cardiovasc Anesth 2009;1(3):22-32.
41. White H, Thygesen K, Alpert JS, Jaffe A. Universal MI definition update for cardio- vascular disease. Curr Cardiol Rep 2014;16:492.
42. Pierard LA. ST elevation after MI: what does it mean? Heart 2007;93(11):1329-30.
43. Flachskampf FA, Schmid M, Rost C, et al. Cardiac imaging after MI. Eur Heart J 2011;

32(3):272-83.

1. Maisel WH, Rawn JD, Stevenson WG. Atrial fibrillation after cardiac surgery. Ann Intern Med 2001;135(12):1061-73.
2. Villareal RP, Hariharan R, Liu BC, et al. Postoperative atrial fibrillation and mortality after coronary artery bypass surgery. J Am Coll Cardiol 2004;43:742-8.
3. Blomstrom Lundqvist C. In: Raviele A, editor. Post CABG atrial fibrillation: what are the incidence, predictors, treatment, and long-term outcome? Venice, Italy: Springer; 2005.
4. Attaran S, Shaw M, Bond L, et al. Atrial fibrillation postcardiac surgery: a common but a morbid complication. Interact Cardiovasc Thorac Surg 2011;12(5):772-7.
5. Echahidi N, Pibarot P, O’Hara G, Mathieu P. Mechanisms, prevention, and treatment of atrial fibrillation after cardiac surgery. J Am Coll Cardiol 2008;51(8):793-801.
6. Wijeysundera DN, Beattie WS, Rao V, Karski J. Calcium antagonists reduce cardio- vascular complications after cardiac surgery: a meta-analysis. J Am Coll Cardiol 2003;41(9):1496-505.
7. Ismail MF, El-Mahrouk AF, Hamouda TH, et al. Factors influencing postoperative atrial fibrillation in patients undergoing on-pump coronary artery bypass grafting, single center experience. J Cardiothorac Surg 2017;12(1):40.
8. Alawami M, Chatfield A, Ghashi R, Walker L. Atrial fibrillation after cardiac surgery: prevention and management: the Australasian experience. J Saudi Heart Assoc 2018;30(1):40-6.
9. Lomivorotov VV, Efremov SM, Pokushalov EA, Karaskov AM. New-onset atrial fi- brillation after cardiac surgery: pathophysiology, prophylaxis, and treatment. J Cardiothorac Vasc Anesth 2016;30(1):200-16.
10. Gillinov AM, Bagiella E, Moskowitz AJ, et al. Rate control versus rhythm control for atrial fibrillation after cardiac surgery. N Engl J Med 2016;374(20):1911-21.
11. Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The cardiac arrhythmia suppression trial. N Engl J Med 1991;324(12):781-8.
12. Sarkar MS, Desai PM. Pulmonary hypertension and cardiac anesthesia: anesthesiologist’s perspective. Ann Card Anaesth 2018;21(2):116-22.
13. Denault A, Ferraro P, Couture P, et al. Transesophageal echocardiography monitor- ing in the intensive care department: the management of hemodynamic instability secondary to thoracic tamponade after single lung transplantation. J Am Soc Echocardiogr 2003;16(6):688-92.
14. Ramakrishna G, Sprung J, Ravi BS, Chandrasekaran K, McGoon MD. Impact of pul- monary hypertension on the outcomes of noncardiac surgery: predictors of periop- erative morbidity and mortality. J Am Coll Cardiol 2005;45(10):1691-9.
15. Voelkel NF, Quaife RA, Leinwand LA, et al. right ventricular function and failure: re- port of a National Heart, Lung, and Blood Institute working group on cellular and molecular mechanisms of Right heart failure. Circulation 2006;114(17):1883-91.
16. Haddad F, Couture P, Tousignant C, Denault AY. The right ventricle in cardiac sur- gery, a perioperative perspective: II. Pathophysiology, clinical importance, and management. Anesth Analg 2009;108(2):422-33.
17. Chin KM, Kim NH, Rubin LJ. The right ventricle in pulmonary hypertension. Coron Artery Dis 2005;16(1):13-8.
18. Wilcox SR, Kabrhel C, Channick RN. Pulmonary hypertension and right ventricular failure in emergency medicine. Ann Emerg Med 2015;66(6):619-28.
19. Hoeper MM, Bogaard HJ, Condliffe R, et al. Definitions and diagnosis of pulmonary hypertension. J Am Coll Cardiol 2013;62:42-50.
20. Price LC, Wort SJ, Finney SJ, et al. Pulmonary vascular and right ventricular dysfunc- tion in adult critical care: current and emerging options for management: a sys- tematic literature review. Crit Care 2010;14(5):R169.
21. Michelakis E, Tymchak W, Lien D, et al. Oral sildenafil is an effective and specific pulmonary vasodilator in patients with pulmonary Arterial hypertension: compar- ison with inhaled nitric oxide. Circulation 2002;105(20):2398-403.
22. Hill NS, Roberts KR, Preston IR. Postoperative pulmonary hypertension: etiology and treatment of a dangerous complication. Respir Care 2009;54(7):958-68.
23. Trachte AL, Lobato EB, Urdaneta F, et al. Oral sildenafil reduces pulmonary hyper- tension after cardiac surgery. Ann Thorac Surg 2005;79(1):194-7.
24. Price S, Prout J, Jaggar SI, et al. Tamponade’ following cardiac surgery: terminology and echocardiography may both mislead. Eur J Cardiothorac Surg 2004;26: 1156-60.
25. Kulik A, Rubens FD, Wells PS, et al. Early postoperative anticoagulation after me- chanical valve replacement: a systematic review. Ann Thorac Surg 2006;81: 770-81.
26. Pepi M, Muratori M, Barbier P, et al. Pericardial effusion after cardiac surgery: inci- dence, site, size, and haemodynamic consequences. Br Heart J 1994;72(4):327-31.
27. Meurin P, Weber H, Renaud N, et al. Evolution of the postoperative pericardial ef- fusion after day 15: the problem of the late tamponade. Chest 2004;125(6): 2182-7.
28. Alraies MC, Aljaroudi W, Shabrang C, et al. Clinical features associated with adverse events in patients with post-pericardiotomy syndrome following cardiac surgery. Am J Cardiol 2014;114(9):1426-30.
29. Ashikhmina EA, Schaff HV, Sinak LJ, et al. Pericardial effusion after cardiac surgery: risk factors, patient profiles, and contemporary management. Ann Thorac Surg 2010;89(1):112-8.
30. Tsang TS, Barnes ME, Hayes SN, et al. Clinical and echocardiographic characteristics of significant pericardial effusions following cardiothoracic surgery and outcomes of echo-guided pericardiocentesis for management: Mayo Clinic experience, 1979-1998. Chest 1999;116:322-31.
31. Tsang TS, Enriquez-Sarano M, Freeman WK, et al. Consecutive 1127 thera- peutic echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and outcomes spanning 21 years. Mayo Clin Proc 2002; 77:429-36.
32. Aksoyek A, Tutun U, Ulus T, et al. surgical drainage of late cardiac tamponade fol- lowing open heart surgery. Thorac Cardiovasc Surg 2005;53(5):285-90.
33. Floerchinger B, Camboni D, Schopka S, et al. Delayed cardiac tamponade after open heart surgery - is supplemental CT imaging reasonable? J Cardiothorac Surg 2013; 8:158.
34. Ashikhmina EA, Schaff HV, Sinak LJ, et al. Pericardial effusion after cardiac surgery: risk factors, patient profiles, and contemporary management. Ann Thorac Surg 2010;89(1):112-8.
35. Wolman RL, Nussmeier NA, Aggarwal A, et al. Cerebral injury after cardiac surgery: identification of a group at extraordinary risk. Multicenter study of perioperative ischemia research group (McSPI) and the ischemia research Education Foundation (IREF) investigators. Stroke 1999;30(3):514-22.
36. Hogue CW, Murphy SF, Schechtman KB, Davila-Roman VG. Risk factors for early or delayed stroke after cardiac surgery. Circulation 1999;100(6):642-7.
37. Lee EJ, Choi KH, Ryu JS, et al. stroke risk after coronary artery bypass graft surgery and extent of cerebral artery atherosclerosis. J Am Coll Cardiol 2011;57:1811-8.
38. Bucerius J, Gummert JF, Borger MA, et al. Stroke after cardiac surgery: a risk factor analysis of 16,184 consecutive adult patients. Ann Thorac Surg 2003;75:472-8.
39. McKhann GM, Grega MA, Borowicz Jr LM, et al. Stroke and encephalopathy after cardiac surgery: an update. Stroke 2006;37:562-71.
40. Moazami N, Smedira NG, McCarthy PM, et al. Safety and efficacy of intraarterial thrombolysis for perioperative stroke after cardiac operation. Ann Thorac Surg 2001;72:1933-7.
41. Chalela JA, Katzan I, Liebeskind DS, et al. Safety of intra-arterial thrombolysis in the postoperative period. Stroke 2001;32:1365-9.
42. Premat K, Clovet O, Frasca Polara G, et al. Mechanical thrombectomy in periopera- tive strokes: a case-control study. Stroke 2017;48(11):3149-51.
43. Chalela JA, Katzan I, Liebeskind DS, et al. Safety of intra-arterial thrombolysis in the postoperative period. Stroke 2001;32(6):1365-9.
44. Bove T, Monaco F, Covello RD, et al. Acute renal failure and cardiac surgery. HSR Proc Intensive Care Cardiovasc Anesth 2009;1(3):13-21.
45. O’Neal JB, Shaw AD, Billings FT. Acute kidney injury following cardiac surgery: cur- rent understanding and future directions. Crit Care 2016;20(1):187.
46. Olivero JJ, Nguyen PT, Kagan A. Acute kidney injury after cardiovascular surgery: an overview. Methodist Debakey Cardiovasc J 2012;8(3):31-6.
47. Khwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract 2012;120(4):c179-84.
48. Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in crit- ically ill adults. N Engl J Med 2018;378(9):829-39.
49. Joannidis M, Druml W, Forni LG, et al. Prevention of acute kidney injury and protec- tion of renal function in the intensive care unit. Expert opinion of the Working Group for Nephrology, ESICM. Intensive Care Med 2010;36(3):392-411.
50. Allen SJ. Gastrointestinal complications and cardiac surgery. J Extra Corpor Technol 2014;46(2):142-9.
51. Mangi AA, Christison-Lagay ER, Torchiana DF, et al. Gastrointestinal complications in patients undergoing heart operation: an analysis of 8709 consecutive cardiac surgical patients. Ann Surg 2005;241(6):895-901.
52. Rodriguez R, Robich MP, Plate JF, et al. Gastrointestinal complications following car- diac surgery: a comprehensive review. J Card Surg 2010;25:188-97.
53. Yarsev A. Approach to the haemodynamically unstable cardiac surgical patient. Deranged Physiology 2017 https://derangedphysiology.com/main/required- reading/cardiothoracic-intensive-care/Chapter8.3.1/approach-haemodynamically- unstable-cardiac-surgical-patient, Accessed date: 20 July 2018.
54. Alsaddique AA, Royse AG, Royse CF, Fouda MA. Management of diastolic heart fail- ure following cardiac surgery. Eur J Cardiothorac Surg 2009;35(2):241-9.
55. Carson JL, Guyatt G, Heddle NM, et al. Clinical practice guidelines from the AABB: red blood cell transfusion thresholds and storage. JAMA 2016;315(19):2025-35.
56. Brooke BS, Goodney PP, Kraiss LW, et al. Readmission destination and risk of mor- tality after major surgery: an observational cohort study. Lancet 2015;386(9996): 884-95.