Chapter 25: Thoracic Trauma and Cardiothoracic Intensive Care Unit Management

Patients who experience thoracic trauma may present with life-threatening injuries such as a pneumothorax, hemothorax, traumatic air embolism, cardiac tamponade, major airway injury, aortic rupture, myocardial rupture, and flail chest (Figure 25-1).^1-7

A pneumothorax occurs from an injury to the chest wall or lung. As the patient inspires, gas enters the pleural space, where it is trapped. When a one-way valve mechanism occurs at the site of injury, intrapleural pressure increases with each respiratory cycle. Eventually, the ipsilateral lung is compressed and displaced to the opposite side causing a tension pneumothorax. In a tension pneumothorax, kinking of the major vessels entering the heart, decreased venous return, and hypotension occur.⁸ A hemothorax also occurs after blunt or penetrating thoracic trauma. The diagnosis isconfirmed by placement of a chest tube and drainage of blood from the thoracic cavity. A double-lumen tube can be used for lung isolation to prevent further hypoxia (Figure 25-2).

There is paradoxical motion of the chest wall in patients with a flail chest. After rib injury, free-floating segments of a loose chest wall move in response to pleural pressure instead of the mechanical positions of the rest of the chest wall. Compromised lung mechanics make inspiration difficult and lead to a pulmonary contusion as a loose chest wall collides with underlying lung tissue.

In patients who present with stridor or subcutaneous emphysema, major airway injury should be considered.⁹ There should be a low threshold to intubate patients with suspected injury of the airway. Endotracheal intubation can be difficult when there are changes in the anatomy of the airway. Damage to the bronchial tree can lead to the development of a bronchovenous fistula resulting in a massive air embolus. The presentation of this process may be delayed and unmasked by positive-pressure ventilation.

Almost all patients with an aortic or myocardial rupture die prior to transfer to the intensive care unit (ICU).^3,10

Multiple mechanisms contribute to respiratory failure after a burn injury. Most commonly, toxins contained in smoke injure and inflame the airway. Upper airway edema may completely obstruct the airway, and lower airway edema may close small airways and lead to pneumonia. Patients at risk may have stridor, wheezing, hoarseness, facial burns, or carbonaceous sputum, but these signs are not always present. In many cases, fiberoptic bronchoscopy may be necessary to reveal inhalation injury. If inhalation injury is suspected, the airway should be secured promptly by endotracheal intubation, as the progress of edema is unpredictable and may worsen with fluid resuscitation.

Intubation is considered in trauma patients who present with diminished mental status and the inability to maintain an airway or clear secretions. Patients with a Glasgow Coma Scale (GCS) score equal to or less than 8 may be intubated to prevent secondary cerebral injury from hypoxemia or hypercapnia.¹¹ Additional indications for tracheal intubation after trauma include cardiopulmonary arrest, elevated intracranial pressure, acute hypoxemia, and transport to a less monitored situation.

(Figure 25-3)

Inadequate analgesia causes splinting and respiratory compromise and may lead to mechanical ventilation of the patient's lungs. Cautious use of opioid analgesics is advised in patients whose lungs are not mechanically ventilated. Thoracic epidural analgesia with continuous infusion of local anesthesia in the epidural space effectively prevents pulmonary splinting from rib fractures.^12,13 Placement of an epidural catheter is contraindicated in patients who are coagulopathic or suffer from head injury. An anesthesiologist should be consulted to place a thoracic epidural catheter. Repeated intercostal nerve blockade (Figure 25-4) anesthetizes the nerves of the chest wall without sedation. Disadvantages of this technique include the need for repeat injections and the risk of local anesthetic toxicity from intravascular uptake of medications.

The differential diagnosis for respiratory failure 2 days after thoracic injury includes pleural effusion; pulmonary contusion; pneumonia; recurrent pneumothorax from a dislodged thoracostomy tube; splinting with atelectasis; pericardial effusion with tamponade, cardiac contusion, and myocardial stunning; and congestive heart failure in the setting of fluid mobilization after trauma. Her unilateral findings of decreased breath sounds and egophony suggest pulmonary contusion and pneumonia.

Twenty-five percent of patients who suffer from blunt force thoracic trauma are diagnosed with a pulmonary contusion.¹⁴ Contusions develop over 24 to 48 hours, worsen with time, and resolve within 2 weeks. Initial chest radiography may be unremarkable or show unilateral infiltrates from capillary leak and edema (Figure 25-5). Compared to chest radiography, CT scans have a higher sensitivity (Figure 25-6).¹⁵

Complications of pulmonary contusions are common. Pulmonary contusion may progress to parenchymal lung injury or noncardiogenic pulmonary edema (Figure 25-7). Noncardiogenic pulmonary edema results from increased permeability of the alveolar capillary membrane, creating a capillary leak syndrome with exudation of water and protein into the alveolar space. In its most dramatic form, it presents as the acute onset of a massive outpouring of proteinaceous fluid from the endotracheal tube. Noncardiogenic pulmonary edema is distinguished from cardiac failure by the finding of normal or low left atrial or pulmonary artery wedge pressures and a high protein concentration in the edema fluid (albumin concentration 90% or greater than that of serum albumin).

Pneumonia occurs after airway edema obstructs the airway. Chest radiography may not be diagnostic in the setting of a preexisting opacification from the pulmonary contusion. Prophylactic antibiotics are not recommended in the treatment of pulmonary contusions, but aggressive treatment of pneumonia after presumptive diagnosis is warranted since it is a prime cause of increased morbidity and mortality.

(Figure 25-8)

ECMO is a device therapy which circulates blood extracorporeally through an oxygenator, ie, "an artificial lung" that removes carbon dioxide, and returns blood to the body via venous or arterial cannulas. Cannulation can occur centrally or peripherally (Figure 25-9).¹⁶ ECMO therapy is used for both respiratory (ie, ARDS/acute lung injury [ALI],^17,18 pulmonary hemorrhage, ischemia reperfusion injury, or primary graft failure after lung transplant¹⁹) and hemodynamic support (ie, severe congestive heart failure with cardiogenic shock, failure to wean off of cardiopulmonary bypass during cardiacsurgery, acute pulmonary embolus²⁰). In venovenous ECMO (VV-ECMO), blood is returned to the circulation via a venous cannula to provide respiratory support. In veno-arterial ECMO (VA-ECMO), blood is returned to the circulation via an arterial cannula to provide respiratory and cardiac support. During ECMO therapy, consumption of clotting factors, contact activation, and platelet dysfunction cause coagulopathy and bleeding. At the same time microthrombi form, and low doses of heparinization are required to prevent clotting of the cannula and oxygenator.¹⁶ In this trauma patient with single-organ failure and ARDS, VV-ECMO therapy should be considered if conventional mechanical ventilation is unsuccessful and the patient is not actively bleeding.

During cardiac surgery, the metabolic and endocrine function of patients can range from mild hyperglycemia of no clinical consequence to the altered neuroendocrine responses of chronic critical illness. The postoperative management of metabolic derangements can be challenging because multiple factors compromise neuroendocrine function, including the inflammatory response to cardiac surgery and cardiac bypass. Cardiac surgery and cardiopulmonary bypass provoke acute inflammation. A cascade of stress responses is elicited, mediated by the release of various cytokines and stress hormones (systemic inflammatory response syndrome). The inflammatory cascade may be activated to a variable degree in all patients who undergo cardiopulmonary bypass (CPB) and perhaps even in those who undergo other major operations without bypass.^21-23 Activation of white blood cells releases metabolites of arachidonic acid, proteases, cytokines, and reactive oxygen species into the blood stream. Production of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and IL-8 increases after CPB. Anti-inflammatory mediators such as IL-10 also are produced. Characterized by vascular permeability, leukocytosis, and vasodilation, the inflammatory response to cardiac surgery influences postoperative outcomes. Concentrations of complement in plasma, the degree to which complement levels have risen, and duration of CPB are correlated with postoperative organ dysfunction.²⁴ In a prospective observational study, an increased level of IL-6 in plasma after CPB was predictive for infection, often pulmonary in origin.²⁵ Nonpulsatile flow and contact activation on CPB provoke the release of vasoconstrictor hormones (epinephrine, angiotensin) as well as inflammatory cytokines that may induce acute kidney injury.^21,22 The kidneys, which sequester proinflammatory cytokines, may be damaged by them. Increases in inflammatory mediators such as C-reactive protein and cytokines are associated with postoperative atrial fibrillation.

Pulmonary function in patients after CPB is consistently altered, ranging from microscopic atelectasis of no clinical consequence to fulminant ARDS.¹³ Perioperative management of oxygenation and ventilation can be challenging because multiple factors compromise pulmonary function, including atelectasis, pleural disruption, impaired lung compliance, and the systemic inflammatory response to extracorporeal circulation. CPB represents a particular challenge to the patient with limited pulmonary reserve, who has a particularly high risk of postoperative pulmonary complications. Recruitment maneuvers and lung-protective ventilation should be performed in hypoxic patients with lung injury after cardiopulmonary bypass.

Hyperglycemia is a ubiquitous phenomenon after cardiac surgery. The metabolic consequences of cardiac surgery and cardiopulmonary bypass, characterized by elevations in circulating catecholamines, growth hormone, glucagon, and cortisol levels with a concomitant depression in insulin levels, promote hepatic glycogenolysis and gluconeogenesis. Hyperglycemia and insulin resistance marks this metabolic profile. Impaired skeletal muscle utilization of glucose (secondary to increased insulin resistance) and decreased entry into the liver reduce glucose clearance.^26,27

The degree of postoperative hyperglycemia may be dependent on the duration of surgery, intraoperative medications (eg, steroids, epinephrine, or IV fluids containing dextrose), anesthetic agents, and dextrose in pump prime fluid.^28-32 Patients who undergo cardiac surgery with CPB under deep hypothermic circulatory arrest frequently develop hyperglycemia.³³ This is due to the profound inflammatory and stress response of CPB and/or hypothermia, which decreases insulin secretion and further augments insulin resistance.²⁹ Hyperglycemia after CPB may also reflect an increased reabsorption of glucose in the renal tubules.³⁴

Significant insulin resistance develops intraoperatively during cardiac surgery and continues in the postoperative period.³⁵ This resistance is mediated by proinflammatory molecules, free fatty acids, and counterregulatory hormones.³⁶ In patients who develop postoperative infections, endotoxin potentiates hyperglycemia by stimulating the adrenergic system and increasing the levels of cytokines that cause insulin resistance.³⁷

Varying recommendations have been proposed by professional organizations (American College of Endocrinology, Canadian Diabetes Association, American Diabetes Association, and the Society of Thoracic Surgeons).^38-41 A general theme of these guidelines is to maintain glucose levels <180 mg/dL perioperatively and between 140 and 180 mg/dL postoperatively. Although the Society of Thoracic Surgeons recommends to maintain a glucose level of <150 mg/dL in cardiac surgery patients with a complicated ICU course, it should be recognized that the recommendation is not based on a high level of evidence.⁴¹ Maintaining glucose levels to < 180 mg/dL is a reasonable goal in most situations. Insulin should be administered preferably by IV infusion, and glucose should be monitored consistently by established monitors.⁴²

Immediately after cardiac surgery, patients have chest tubes. Chest tubes are connected to pleurovacs, which are connected to wall suction. Occasionally, these connections become loose or suction is not applied. Large clots can form in the chest tube preventing drainage of blood or air from the patient's chest. The result is a hemothorax or pneumothorax causing hypoxia from atelectasis and shunt physiology.

No! An acute increase in central venous pressure (CVP) after cardiac surgery is cardiac tamponade until proven otherwise. The cardiac surgeon should immediately open the chest to decrease extracardiac pressure in unstable patients. Acute increases in CVP also occur with right ventricular infarction or pulmonary hypertensive crisis. Echocardiography is useful to determine the etiology of the patient's changing hemodynamics. Sudden increases in CVP impair venous return and increase intracranial pressure and cerebral edema in patients with cerebral injury.

The development of acute kidney injury (AKI) is a major cause of increased morbidity and mortality rates after cardiac surgery. AKI after cardiac surgery is associated with the initiation of renal replacement therapy and an increased incidence of gastrointestinal bleeding, respiratory infections, and sepsis.^43,44 In this setting, postoperative AKI leads to increased intensive care and hospital length of stay. Preventative strategies focus on preoperative optimization of renal function, judicious perioperative fluid balance, and "renoprotective" pharmacologic agents. These strategies appear to have only limited benefit because the incidence of postoperative renal failure has remained constant over the last two decades. Nevertheless, considerable research has been marshaled to protect the kidneys during the high-risk perioperative period when the kidney is placed at risk through preexisting impairment, nephrotoxins, renal ischemia, and the inflammatory process.

Several patient-specific risk factors are associated with the development of renal dysfunction after cardiac surgery: female gender, age, hypertension, diabetes mellitus, ventricular dysfunction, left main coronary artery disease, chronic obstructive pulmonary disease, sepsis, hepatic failure, and chronic kidney disease (CKD).⁴⁵ Because CKD also has various definitions, the association between preoperative CKD and postoperative renal injury is difficult to quantify accurately. Nevertheless, there is no doubt that the correlation is strong.^46-48 Recently, pulse pressure hypertension has been shown to precipitate worsening renal function in the setting of cardiac surgery.⁴⁹ Interestingly, there appears to be a complex relationship between apolipoprotein E (ApoE) and postoperative AKI. ApoE polymorphisms, although associated with atherosclerotic disease, may confer a degree of renal protection.^50,51

Controversial procedure-related risk factors associated with kidney injury in the setting of cardiac surgery include length of CPB, cross-clamp time, off-pump versus on-pump, nonpulsatile flow, hemolysis, and hemodilution.⁴⁵ The occurrence, alone or in combination, of compromised hemodynamics, surgery, nephrotoxins, or an inflammatory process from CPB may precipitate perioperative AKI, particularly in the patient predisposed by preexisting renal insufficiency or a genetic predisposition. Although the renal medulla receives the minority of renal blood flow, the medullary process of urinary concentration has a high metabolic requirement. Any compromise to renal blood flow increases the regional perfusion imbalance and renders the medulla ischemic. Compromise may result from aortic occlusion, atheromatous embolism, hypotension, low blood flow states, and hypovolemia. Ultimately the pathophysiologic lesion characterizing the AKI of the perioperative cardiac period may be acute tubular necrosis.⁴⁵

CPB and the interaction between blood components and the extracorporeal circuit can diminish renal blood flow through the release of vasoconstrictive compounds. It is important to note, however, that the development of AKI after cardiac surgery appears to vary with the type of surgery. Patients undergoing coronary artery bypass grafting (CABG) have the lowest incidence of injury followed by those undergoing valvular surgery. The highest incidence of renal dysfunction occurs in patients undergoing combined CABG and valvular surgery.^45,52

This patient's clinical picture is consistent with a low cardiac output. An elevation in CVP is concerning for a decrease in right ventricular cardiac output. Continuous renal replacement therapy (CRRT) is used in patients who are critically ill, unstable, and unable to tolerate the blood pressure variations of intermittent hemodialysis. Traditionally, renal replacement therapy is considered for patients with uremia, electrolyte abnormalities, acidosis, intoxication, and volume overload. After cardiac surgery, CRRT decreases myocardial edema, removes myocardial depressants, and optimizes the Starling relationship. In patients with evidence of right ventricular pressure overload who do not respond to diuretic therapy, removing intravascular volume via CRRT can improve blood pressure and cardiac output.