An international group of 12 experts in the field of perioperative resuscitation has reviewed best available evidence on management of cardiac arrest and periprocedural crises. These experts were selected on the basis of several criteria: (1) clinical experience in anesthesiology and perioperative patient management; (2) expertise in simulation training in perioperative crises; (3) familiarity with the evidence behind current resuscitation guidelines; and (4) international representation (ensure that the recommendations are easily translatable to bedside practice in multiple clinical platforms). The group communicated via email, face-to-face meetings, and telephone. The papers selected for review were those included in the previous iteration of these guidelines (which underwent repeat scrutiny) and relevant papers that had been published since 2012 and available in PubMed on the specific topics to be discussed. For part 2, disagreements among committee member were discussed as a group in an attempt to reach consensus, and in case of ongoing dissent, adjudicated by 3 of the authors (M.D.M., V.K.M., and M.F.O.).
The scenarios were chosen through a modified Delphi technique involving several rounds of input from the group. These scenarios were chosen because they represent perioperative emergencies that are likely to be immediately life threatening. Four of the topics briefly covered in a previous publication were reanalyzed for a more in-depth discussion and updated knowledge (eg, severe anaphylaxis and hyperkalemia) or landmark publications (eg, trauma-related cardiac arrest). Due to constraints on length for the review article, the number of included scenarios was limited to 7. As such, the scenarios presented are not intended to be an exhaustive list.
Pathophysiology and Epidemiology. Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction mediated by immunoglobulins IgE and IgG and accounts for about 500–1000 deaths per year in the United States.[17,18] The causative agent is usually not obvious, and assigning causality is typically complicated in the periprocedural and hospital setting, where patients are commonly exposed to multiple agents. Furthermore, anaphylactic reactions may occur with no documented prior exposure. Hypersensitivity reactions are graded 1–5 corresponding to minor, low severity, life-threatening symptoms, cardiac or respiratory arrest, and death.[20,21] The overall incidence of hypersensitivity reactions is about 15 cases per 10,000 operations (95% confidence interval, 13–17 per 10,000). The incidence of severe hypersensitivity reactions (grade 3–5) with life-threatening symptoms is about 2 cases per 10,000 operations.
Presentation and Initial Assessment. Anaphylaxis is characterized by the rapid onset of potentially life-threatening airway, breathing, or circulatory problems. The initial symptoms are nonspecific. Rhinitis, tachycardia, confusion, altered mental status/presyncope, and skin and mucosal changes are common in the awake patient, but not always present. In addition, bronchospasm is not present in all cases and does not necessarily precede cardiovascular instability. Extensive vasodilatation and increased vascular permeability lead to decreased cardiac preload with relative hypovolemia, which can in turn cause cardiovascular depression, myocardial ischemia, acute myocardial infarction, and malignant arrhythmias (anaphylactic shock).[24,25] When hemodynamic deterioration occurs rapidly and untreated, patients can experience cardiac arrest.[24,25] Evidence in the treatment of anaphylaxis is generally limited and is mostly based on case reports and extrapolations from animal models, nonfatal cases, interpretation of pathophysiology, and consensus opinion.
Assessment and Initial Management Steps. When anaphylaxis is within the differential diagnosis, surgery should be interrupted, if possible, and the likely triggers of anaphylaxis should be immediately removed (eg, stopping an injection or infusion of medication or blood products). Administration of epinephrine is indicated in patients with clinical features of anaphylaxis.[27,28] In the setting of signs and symptoms of severe anaphylaxis, 100–300 μg epinephrine should be given intravenously (IV) immediately with repeated and escalating doses as clinically indicated. We do not recommend to use the same epinephrine doses used in pulseless cardiac arrest (1 mg IV) if the patient maintains a cardiac rhythm with a pulse. Caution is warranted, as fatal dysrhythmias to large doses of epinephrine have been reported.[27,29] In patients without an IV line, early intramuscular administration of 300–500 μg epinephrine in the anterolateral aspect of the middle third of the thigh is recommended, with this dose being repeated every 5–15 minutes in the absence of clinical improvement.[30,31] Inhaled or subcutaneous administration of epinephrine is ineffective for severe anaphylaxis. Close hemodynamic monitoring (eg, arterial blood pressure) with a goal systolic blood pressure (SBP) ≥90 mm Hg is indicated.
Immediate endotracheal intubation is critical and should not be delayed, as oropharyngeal and laryngeal edema are likely to occur rapidly. If necessary, a surgical airway should be considered. Initial fluid resuscitation using 20 mL/kg crystalloid infusions is indicated to treat the vasodilatory component of anaphylactic shock.[34,35]
Subsequent Assessment and Treatment Steps. If hemodynamic instability persists after initial epinephrine boluses, this drug should be continued by a carefully titrated continuous IV infusion (0.05–0.3 μg/kg/min) because the plasma half-life of epinephrine is brief (<5 minutes). If epinephrine infusion fails to restore normal hemodynamic variables, continuous infusions of vasopressin,[36,37] norepinephrine, methoxamine, and metaraminol may be considered. Glucagon should be considered in patients who have taken β-blockers and who are unresponsive to combined inotrope and vasopressors management. Adjuvant use of antihistamines is appropriate,[41–43] and treatment with inhaled β2-adrenergic agents[27,44] and IV corticosteroids[28,45] should be considered in severe anaphylaxis. Extracorporeal life support (venous–arterial extracorporeal membrane oxygenation) has been successful in isolated cases and may be considered if clinical staff and equipment is immediately available. After stabilization, the patient should be monitored in an intensive care unit (ICU) for at least 24 hours due to the bimodal nature of severe anaphylaxis and a high risk of recrudescence. Finally, laboratory testing for histamine, tryptase, or IgE within 24 hours is indicated for diagnostic purposes. Table 1 provides a full list of management steps.
Epidemiology and Pathophysiology. A tension pneumothorax occurs when there is a "ball-valve effect" within the lung allowing progressive accumulation of air within the pleural space, which in turn leads to a corresponding increase in intrapleural and intrathoracic pressures. In tension pneumothorax, the intrapleural pressure is positive and exceeds the atmospheric pressure throughout the respiratory cycle. The incidence of tension pneumothorax remains poorly estimated and ranges from 1% to 3% in prehospital, major trauma, and ICU patients.
The pathophysiology of tension pneumothorax differs between patients who are spontaneously breathing versus those on positive-pressure ventilation. In spontaneously breathing patients, several compensatory mechanisms likely prevent initial hemodynamic compromise. These factors include increasing respiratory rate, decreased tidal volume and negative-pressure contralateral chest excursions. These mechanisms may maintain arterial blood pressure by limiting transmitting pleural pressure to the mediastinum and contralateral hemithorax. In patients receiving positive-pressure ventilation, increased intrapleural pressure throughout the respiratory cycle produces a marked decrease in cardiac venous return, which leads to hypotension, and, if untreated, may result in cardiac arrest.
Presentation and Initial Assessment. Spontaneously breathing patients with tension pneumothorax present with shortness of breath, dyspnea, tachypnea, respiratory distress, hypoxemia, and ipsilateral decreased air entry and percussion hyperresonance. In a large systematic review, the reported incidence of respiratory arrest (9%), hypotension (16%), and cardiac arrest (2%) were much lower compared to patients on positive-pressure ventilation. Patients on positive-pressure ventilation usually present with hypoxemia, tachycardia, sudden onset of hypotension, subcutaneous emphysema, and ipsilateral decreased air entry. These signs are followed by circulatory collapse and subsequent cardiac arrest with pulseless electrical activity (PEA). Tension pneumothorax should always be in the differential diagnosis of a patient with acute decompensation during laparoscopic surgery.
Traditionally, diagnosis relies on clinical signs and symptoms although these are unreliable (especially contralateral tracheal deviation and jugular venous distention). Thoracic ultrasonography, which is being used with increasing frequency, may be superior to chest radiography for diagnosing pneumothorax (sensitivity of approximately 80%–90% vs 50%) and can also be performed rapidly at the bedside.[51,52]
Initial Management Steps. Initial treatment should focus on maximizing oxygenation. Immediate tube thoracostomy by trained personnel is encouraged as the treatment of choice in both the ventilated and the spontaneously breathing patient. However, it should be noted that in situations of high clinical suspicion of tension pneumothorax (eg, high airway pressures, unilateral breath sounds, and circulatory instability in the setting of pneumoperitoneum), immediate needle decompression would be recommended rather than delaying treatment.
Subsequent Assessment and Treatment Steps. After initial assessment and treatment, the patient should be stabilized to prevent further respiratory or cardiovascular compromise. The tube thoracostomy is left in place until the parenchymal injury that caused the tension pneumothorax has resolved. The underlying cause for the parenchymal injury needs to be ascertained. Occasionally surgical repair may be indicated. Resolution of the pneumothorax is documented with serial chest radiographs.
Local Anesthetic Systemic Toxicity
Epidemiology and Pathophysiology. While any use of local anesthetic can potentially lead to LAST, peripheral nerve block carries the highest risk, with published rates typically ranging from 1 to 10 per 10,000 qualifying this iatrogenic complication as a "rare event." Nevertheless, the potential for severe, even fatal physiological sequelae demands that measures be taken to reduce the likelihood of LAST and that education/training include detection and treatment of this condition. In addition to using standard monitors and safety measures (eg, frequent aspiration during needle progression incremental injection), there is evidence that the use of ultrasound guidance can reduce the risk of LAST.
Presentation and Initial Assessment. A wide range of either neurological symptoms (eg, seizure, agitation, or obtundation) or cardiovascular signs (eg, arrhythmia or conduction block, hypertension, tachycardia, or progressive hypotension and bradycardia) occur with LAST. A study of LAST episodes published from 1979 to 2009 showed that >40% of cases departed from the standard text book presentation (eg, rapid-onset seizure potentially leading to cardiac arrest). In 35 of 93 patients (38%), symptoms were delayed >5 minutes, and in 10 patients (11%), cardiovascular signs occurred without a neurological prodrome. Another study from the same group indicated that there is a wide variety of clinical presentations in cases of LAST, including an increase in delayed onset (52%; >5 minutes from injection), which is likely a result of ultrasound guidance.
Initial Management Steps. The initial focus in treating LAST includes managing the airway to assure adequate oxygenation and ventilation and using a benzodiazepine to suppress seizures. Early treatment of LAST by infusion of lipid emulsion 20% can prevent progression to cardiovascular compromise possibly by reducing peak local anesthetic levels. Propofol is cardiodepressant, and its lipid content is inadequate to confer benefit. It is important to continue monitoring even after symptoms resolve because recurrence or delayed progression can occur after an interval of apparent stability.
Subsequent Assessment and Treatment Steps. If LAST progresses to cardiovascular collapse, it is important to administer high-quality cardiovascular support since improving coronary and cerebral blood flow reduces local anesthetic tissue concentrations both directly and by delivering lipid emulsion to affected sites. The main benefit of infusion of lipid emulsion in reversing LAST is accelerating redistribution of local anesthetic, rapidly shuttling drug from sites of toxicity (brain and heart) to unaffected organs (eg, liver and skeletal muscle). This scavenging effect is the result of both partitioning into the lipid phase and the direct inotropic effect of lipid emulsion infusion. The direct inotropy is seen in intact rats and isolated heart without a pharmacotoxic challenge; however, during experimental LAST, it only occurs after myocardial bupivacaine content drops below a specific (eg, channel blocking) threshold. Lipid infusion also exerts a postconditioning effect that might contribute to successful resuscitation. It is important to consider extracorporeal life support relatively early in those instances in which the patient does not respond to more conservative measures. Postevent monitoring should occur for at least 6 hours because cardiovascular instability can recur after initial recovery. Table 2 provides a full list of management steps.
Epidemiology and Pathophysiology. MH is an extreme reaction to volatile anesthetics and succinylcholine, which is attributed to abnormalities of skeletal muscle metabolism and calcium disposition. Its occurrence is rare, ranging between 1:62,000 and 1:500,000 anesthetics, more commonly occurring in men and younger patients, but described in a wide variety of patients.[63,64] The pathophysiology of this syndrome involves mainly cytoplasmic proteins participating in the movement of calcium within skeletal muscle, most commonly the ryanodine receptor. However, many genetic abnormalities are associated with MH, both inherited or sporadic. The syndrome is marked by extreme muscle hypermetabolism, leading to muscle necrosis, hyperpyrexia, acidosis, and in extreme cases, cardiac arrest.
Presentation and Initial Assessment. Because of its rarity, MH can be a once-in-a-career event. Mortality without dantrolene treatment is as high as 80%, but with it, it may be as low as 1.4%. Because the time to dantrolene administration correlates with morbidity and mortality, early recognition is crucial to an effective response. The earliest signs of MH are hypercapnia and sinus tachycardia. Masseter muscle spasm, general muscle rigidity, tachypnea, and rising temperature (late) are additional common findings. Blood gas analysis can reveal respiratory and metabolic acidosis, especially when drawn from a vein draining a large muscle bed.
Initial Management Steps. When MH is suspected, all triggering agents should be immediately discontinued. Dantrolene 2.5 mg/kg IV is the key therapy for MH. Several formulations exist, and providers should be familiar with preparation and administration of a normal adult dose in anticipation of an MH event. Dantrolene should be available at all places that triggering anesthetic agents are available. Regular monitoring of arterial PaCO2, temperature, and lactate levels should accompany dantrolene administration, and any abnormalities should be aggressively treated with external and internal cooling, ventilation, and fluid resuscitation.
Subsequent Assessment and Treatment Steps. After initial recognition and treatment, the goals of care involve the mitigation of ongoing tissue injury, hyperthermia, and their sequelae. With extremes of temperature (median temperature, 40.3°C), disseminated intravascular coagulation may occur. Other complications can occur at any temperature, but mortality correlates with temperature. Rhabdomyolysis is common; if severe, it can lead to renal failure and hyperkalemia. Cooling and monitoring for these complications should continue for 72 hours after a suspected episode, because of the risk of recrudescence. Because dantrolene interferes with calcium disposition, patients should be monitored for muscle weakness. Importantly, calcium channel blockers are contraindicated in the setting of dysrhythmias. MH resources are available through expert groups in the United States (www.mhaus.org) and in Europe (www.emhg.org). Table 3 provides a full list of management steps.
Epidemiology and Pathophysiology. The exact cutoff for moderate or severe hyperkalemia is inconsistently described in the literature. However, recent reports note that initiation of emergency therapies are recommended for serum potassium levels >6.0 or 6.5 or electrocardiographic (ECG) manifestations of hyperkalemia, regardless of potassium level. Of note, a potassium level of ≥6.5 mmol/L occurs in only 0.1% of hospitalized patients. Acidosis (primarily metabolic), for example, promotes an extracellular potassium shift; each 0.1 unit decrease in pH is accompanied by an increase of ~0.6 mmol/L in serum potassium.[69,70] The most common causes of hyperkalemia are renal pathology and drug therapy.[68,71,72] There are limited data on the prevalence of hyperkalemia in adult patients undergoing surgery and anesthesia. However, hyperkalemia is consistently estimated to be the cause of death in 1%–2% of cases of anesthesia-related cardiac arrests in children.[73–75]
Presentation and Initial Assessment. Clinical manifestations of this potentially life-threatening electrolyte disorder are mostly insidious and nonspecific. Thus, preoperative assessment of patients at risk should include timely blood testing. There is a common misconception that the cardiac manifestations of hyperkalemia are well known and occur in an orderly fashion. On the contrary, the cardiac clinical symptoms of hyperkalemia may randomly range from nonexistent to vertigo, chest pain, and presyncope to syncope and cardiac arrest. Physical examination may reveal bradycardia and/or bradyarrhythmia and hypotension. Accompanying ECG changes include peaked T-waves, QRS widening, diminished P waves,[77,78] and/or a range of arrhythmias including bradycardia, atrioventricular blocks at different conduction levels,[80–82] ventricular tachycardia, and ventricular fibrillation.[84–86] Absence of ECG changes should not be taken to indicate that blood potassium levels are normal; some patients with end-stage renal disease do not exhibit ECG changes in the presence of hyperkalemia because of a protective effect of calcium fluctuations.[87–89] Neurological manifestations include generalized muscle weakness and respiratory failure due to flaccid muscle paralyses.[90–92]
Abnormal ECG findings should command immediate attention and treatment when highly suggestive of severe hyperkalemia. Cardiac arrest caused by hyperkalemia has been shown to be associated with accompanying ECG changes, multiorgan system failure, and emergent admission. Therefore, perioperative management of life-threatening hyperkalemia depends on whether surgery is elective or urgent and on the perioperative timing of the finding. With the widespread availability of sugammadex, succinylcholine should be avoided or used with great caution if there is any concern for the acute development of hyperkalemia (eg, patients with muscle wasting from neurological injury or those who have been immobile for days in the ICU).
Initial Management Steps. The first management step is avoidance of hyperkalemia and thus postponing of elective surgical cases in the setting of this condition and avoiding succinylcholine and prolonged propofol infusions for urgent/emergent cases with known hyperkalemia.[86,95–97] Respiratory acidosis should be corrected normalizing ventilation. Acute hyperventilation is to be avoided because it can contribute to hypotension by reducing venous return. Treatment with β-2 agonists (eg, salbuterol) and glucose with insulin can be initiated to promote potassium shift toward the intracellular compartment.[98–101] Combined therapy with β-2 agonists and insulin is more effective than a single agent. The literature supports administration of calcium as a membrane stabilizer when ECG changes are present. In the setting of ongoing hemorrhage and blood administration (with citrate), preventative therapy with calcium may also be deemed justifiable.
Subsequent Assessment and Treatment Steps. If patient volume status is considered adequate and his or her renal function permits, loop diuretics may be administered in the hope of inducing potassium loss. Early and aggressive correction of potassium is important to avoid deterioration to cardiac arrest. Moderate quality evidence (retrospective observation) supports treatment with IV calcium chloride during adult hyperkalemic cardiac arrest. The use of bicarbonate to enhance intracellular shift of potassium is controversial.[103,104] Selection bias may underlie the association of both therapies with poor cardiopulmonary resuscitation (CPR) outcomes, since both drugs are more likely to be used in critically ill patients and after prolonged CPR. If hyperkalemia is considered reversible, bridging therapy with extracorporeal life support should be considered. Hemodialysis should be initiated as soon as possible after return of spontaneous circulation.[106,107] There have been reports of successful outcome from hyperkalemic cardiac arrest with hemodialysis being initiated even during CPR.[108–111] Given that vascular access is often easily available in the operating room, blood purification is a pertinent option should hyperkalemic cardiac arrest occur perioperatively. Table 4 provides a full list of management steps.
Traumatic Cardiac Arrest
Epidemiology and Pathophysiology. Traumatic cardiac arrest (TCA) carries a high mortality rate, but in survivors, the neurological outcome appears to be much better than in other causes of cardiac arrest.[112,113] Uncontrolled hemorrhage is the main cause of death (48%), followed by tension pneumothorax (13%), asphyxia (13%), and pericardial tamponade (10%). A large systematic review reported an overall survival rate of 3.3% in blunt and 3.7% in penetrating trauma, with good neurological outcome in 1.6% of all cases.
Presentation and Initial Assessment. Patients in TCA present with loss of consciousness, agonal or absent spontaneous respiration, and absence of a femoral or carotid pulse. The prearrest state is characterized by tachycardia, tachypnea, decreased pulse pressure, and a deteriorating conscious level. Hypotension may present late and beyond 1500 mL of blood loss. Beyond this stage (class III hemorrhagic shock), peripheral pulses will become absent, and the patient left untreated will typically proceed to pulseless electrical dissociation or asystolic cardiac arrest. Resuscitative efforts in TCA should focus on immediate assessment and simultaneous treatment of the hemorrhage and surgical control of the reversible causes (Figure 1).[113,115]
This figure illustrates the appropriate steps in the assessment and management of a patient experiencing traumatic cardiac arrest. ACLS indicates advanced cardiac life support; BP, blood pressure; CT, computed tomography; FFP, fresh frozen plasma; PEEP, positive endexpiratory pressure; pRBC, packed red blood cell.
Initial Management Steps. Short prehospital times are associated with increased survival rates for major trauma and TCA. The time elapsed between injury and surgical control of bleeding should be minimized. When feasible, the patient should be immediately transferred to a designated trauma center for damage control resuscitation (DCR). "Scoop and run" for these patients may be a better choice for survival than engaging on a long resuscitation on the field. While anesthesiologists in many international settings may be involved with prehospital care, being prepared to manage the airway and provide aggressive fluid resuscitation on patient arrival to the emergency room is also paramount. Successful treatment of TCA requires a team approach with all measures carried out rather in parallel than sequentially. The emphasis lies on rapid treatment of all potentially reversible pathology. In cardiac arrest caused by hypovolemia, cardiac tamponade, or tension pneumothorax, chest compressions alone are unlikely to be as effective as in normovolemic cardiac arrest.[115,117–119] Therefore, chest compressions take a lower priority than the immediate treatment of reversible causes.
Ultrasonography should be used in the evaluation of the compromised trauma patient to target life-saving interventions if the cause of shock cannot be established clinically.[116,120] Hemoperitoneum, hemothorax or pneumothorax, and cardiac tamponade can be diagnosed reliably in minutes. Early whole-body computed tomography scanning as part of the primary survey may improve outcome in major trauma. Whole-body computed tomography is increasingly employed to identify the source of shock and to guide subsequent hemorrhage control. Figure 1 shows the traumatic cardiac (peri-) arrest algorithm of the European Resuscitation Council, which is based on the universal ALS algorithm.
Hypovolemia: The treatment of severe hypovolemic shock has several elements. The main principle is to achieve immediate hemostasis. Temporary hemorrhage source control can be lifesaving. External hemorrhage can be treated with direct or indirect compression, pressure dressings, tourniquets, and topical hemostatic agents. Noncompressible hemorrhage is more difficult to control. External splints/pressure, blood and blood products, IV fluids, and tranexamic acid (TXA) can be used during patient transport and until hemorrhage is controlled surgically. Resuscitative endovascular balloon occlusion is a promising alternative to aortic cross-clamping or manual aortic compression in patients exsanguinating from noncompressible torso injuries and can serve as a bridge to definitive hemorrhage control.[123,124] If the patient is in hypovolemic TCA, immediate restoration of the circulating blood volume with blood products is mandatory. Hyperventilation should be avoided in hypovolemic patients since positive-pressure ventilation may worsen hypotension by impeding venous return to the heart. Therefore, low tidal volumes and slow respiratory rates may be associated with a more acceptable circulation.
Hypoxemia: Hypoxemia due to airway obstruction and loss of ventilator drive has been reported as the cause of 13% of all TCAs. Immediate control of the airway and effective invasive ventilation can reverse hypoxic cardiac arrest. However, positive-pressure ventilation should be applied with caution to limit its deleterious effect on venous return. Oxygen should be delivered at a fraction of 1.0, and ventilation should be monitored with capnography to avoid hyperventilation.
Cardiac Tamponade and Resuscitative Thoracotomy: Cardiac tamponade is the underlying cause of approximately 10% of cardiac arrests in trauma. Where there is TCA and penetrating trauma to the chest or epigastrium, immediate resuscitative thoracotomy (RT; via a clamshell incision) can be life saving.[126,127] The chance of survival from cardiac injury is about 4 times higher for stab wounds than for a gunshot wounds. In 2012, an evidence review with resultant guidelines stated that RT should also be applied for 3 other categories of life-threatening injuries after arrival in hospital, which include blunt trauma with <10 minutes of prehospital CPR, penetrating torso trauma with <15 minutes of CPR, and penetrating trauma to the neck or extremity with <5 minutes of prehospital CPR. The guidelines estimate survival rates of approximately 15% for RT in patients with penetrating wounds and 35% for patients with a penetrating cardiac wound. In contrast, survival from RT after blunt trauma is dismal, with reported survival rates of 0%–2%.[129,130] In the setting of the above presentation (ie, cardiac arrest with penetrating trauma), the prerequisites for a successful RT can be summarized as "4 Es rule" (4E):
Expertise: RT teams must be led by a highly trained and competent health care practitioner.
Equipment: adequate equipment to carry out RT and to deal with the intrathoracic findings is mandatory.
Environment: ideally, RT should be carried out in an operating theatre; RT should not be carried out if there is inadequate physical access to the patient or if the receiving hospital is not easy to reach.
Elapsed time: the time from loss of vital signs to commencing an RT should not be >10 minutes.
If any of the 4 criteria are not met, RT is likely less effective and exposes the team to unnecessary risks.
Subsequent Management and Treatment. Damage control resuscitation is a term recently adopted in trauma resuscitation to improve outcome of uncontrolled hemorrhages. DCR combines permissive hypotension and hemostatic resuscitation with limited (damage control) surgical repair. Limited evidence and general consensus (https://www.nice.org.uk/guidance/ta74) have supported a conservative approach to IV fluid infusion, with permissive hypotension until surgical hemostasis is achieved. In the absence of invasive monitoring, fluid resuscitation is titrated to maintain a radial pulse.[133,134] Hemostatic resuscitation with blood and blood products is used as primary resuscitation fluids to prevent exsanguination, dilution of hemostatic blood components, and trauma-induced coagulopathy. The typical massive transfusion protocol recommends packed red blood cells, fresh frozen plasma, and platelets ratio of 1–2:1:1.
Simultaneous damage control surgery and hemostatic resuscitation using massive transfusion protocol are the principles of DCR in patients with exsanguinating injuries.[116,135] Although the evidence for permissive hypotension during resuscitation is limited, particularly with regards to blunt trauma, permissive hypotension has been endorsed in both civilian (https://www.nice.org.uk/guidance/ta74) and military care, generally aiming for an SBP of 80–90 mm Hg. Caution is advised for patients with traumatic brain injury in whom a raised intracranial pressure may require a higher cerebral perfusion pressure. Specifically, the most recent Brain Trauma Foundation Guidelines for severe traumatic brain injury recommend maintaining an SBP ≥100 mm Hg for patients 50–69 years of age or ≥110 mm Hg for patients 15–49 years of age or older than 70 to improve outcomes and reduce mortality.
Finally, TXA (loading dose 1 g over 10 minutes followed by infusion of 1 g over 8 hours) increases survival from traumatic hemorrhage.[139,140] It is effective when administered within the first 3 hours after trauma; however, TXA should not be started any later than 4 hours after the injury because late dosing is associated with increased mortality.
Epidemiology and Pathophysiology. Thromboembolism, venous gas embolism, and fat embolism are all well-recognized complications that can occur during anesthesia and surgery. Venous thromboembolism is the most common cause of PE in periprocedural patients. Prophylaxis reduces its incidence, but cannot entirely prevent its occurrence. Thromboembolism causes circulatory crisis via a combination of mechanical obstruction and the release of inflammatory mediators, both of which increase the right ventricular (RV) afterload. In severe cases, the associated increase in pulmonary vascular resistance is so great that the right ventricle is unable to maintain the cardiac output. As the RV fails, it typically dilates, and the interventricular septum flattens and shifts toward the left ventricle.
Presentation and Initial Assessment. Signs of PE under general anesthesia include the following: unexplained hypotension with concurrent decrease in EtCO2; desaturation that is only moderately responsive to increased FIO2; transitory bronchospasm with increased airway resistance; rapid changes of heart rhythm (often dysrhythmias or bradycardia after a transitory tachycardia); unexplained increased of central venous pressure or all pulmonary pressures; and rapid progression to nonshockable cardiac arrest (usually PEA).
Management Steps. A strategy for managing RV shock in this situation is proposed in Figure 2. In approximately 5% of cases, acute thromboembolism causes cardiac arrest, most often PEA.[143,144] Echocardiography of the patient with RV shock will typically reveal RV dilation and dysfunction, with an underfilled left ventricle.
An assessment and management algorithm of right heart failure, which should be followed in the case of suspected thrombotic or gaseous pulmonary embolism. CVP indicates central venous pressure; ECMO, extracorporeal membrane oxygenation; Hct, hematocrit; IABP, intra-aortic balloon pump; iNO, inhaled nitric oxide; PEEP, positive end-expiratory pressure; pRBC, packed red blood cells; PVR, pulmonary vascular resistance; RV, right ventricular; RVAD, right ventricular assist device; Scvo2, central venous oxygen saturation; Spo2, peripheral oxygen saturation; SVO2, venous oxygen saturation; TEE, transesophageal echocardiography.
The management of intraoperative or perioperative thromboembolism is highly dependent on the procedure and patient. Therapeutic options range from supportive measures only to anticoagulation to thrombolysis.[143,144,146,147]
Epidemiology and Pathophysiology. Gas embolism is an important cause of circulatory crisis and cardiac arrest in perioperative patients. As the number of procedures in which minimally invasive techniques involving gas insufflation increases, the frequency of intraoperative gas embolisms will likely increase. The risk for a venous air embolism increases when the surgical field is above the right atrium, particularly in patients with central venous pressure. The focus of hemodynamic support is on improving RV function.
Common causes of gas embolism include laparoscopy, endobronchial laser procedures, central venous catheterization or catheter removal, hysteroscopy, pressurized wound irrigation, prone spinal surgery, posterior fossa surgery in the sitting position, and endoscopic retrograde cholangiopancreatography. Nonoperative cause of vascular air embolism includes direct vascular access procedures and pressurized hemoperfusion.
Management Steps. All surgical procedures at risk of venous gas embolism should be specifically monitored. Right parasternal precordial Doppler ultrasound has very high sensitivity for air embolism (88%). Transesophageal echocardiography allows for recognition of air embolism size and location and assessment of ventricular function, but can be difficult or impossible to perform with some patient positions (eg, sitting) or procedures (eg, endoscopic retrograde cholangiopancreatography). Massive gas embolisms in awake patients have been characterized by breathlessness, continuous coughing, arrhythmias, myocardial ischemia, acute hypotension with loss of end-tidal carbon dioxide, and cardiac arrest. Patients who survive any kind of an embolic event are likely to require continued evaluation and management for several hours in an ICU setting. Table 5 provides a full list of management steps.
It is beyond the scope of this article to detail the appropriate steps of postresuscitation management. Current guidelines are available that specify the appropriate management steps to maximize discharge from the hospital with a favorable neurological function as most important outcome parameters. Neurological, cardiovascular, and respiratory dysfunction are best managed in specialized ICUs where monitoring of electroencephalogram, targeted temperature management, glucose management, correction of electrolytes, and management of blood gas parameters are all promptly available.[151–153]
Anesth Analg. 2018;126(3):889-903. © 2018 International Anesthesia Research Society