Long-term Complications and Management

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Chapter 30 Long-Term Complications and Management

In the modern era, the majority of cardiac surgical patients have brief stays in the intensive care unit (ICU) (<24 hours), and these stays follow a predictable pattern. During this time, most instability and morbidity are attributable to the cardiopulmonary organ systems, bleeding, hypothermia, and the emergence from anesthesia. A small minority of patients, however, have prolonged ICU stays characterized by multisystem complications involving both the cardiac and noncardiac systems. This group of patients consumes a disproportionate number of ICU resources, generates enormous hospital costs, and ultimately has a much worse prognosis (bothin-hospital and long term).1

When caring for the unfortunate minority of cardiac surgical patients requiring prolonged stays in the ICU, a distinct shift in orientation of the health care providers must occur—from a “recovery room” mode, focusing primarily on the cardiovascular organ system, to a true intensive care mode, focusing on preventing and treating dysfunction in multiple organ systems. At the same time, the physician’s decision to continue aggressive treatment must be tempered with a realistic view of the patient’s prognosis and an assessment of the “cost” of that treatment to the patient, family, and society.

SEDATION IN THE INTENSIVE CARE UNIT

The major goals of sedation in the ICU are to provide anxiolysis and to improve the patient’s perceptual experience during this physiologically and emotionally stressful period (Box 30-1). Secondarily, sedation reduces the physiologic stress response and attendant cardiovascular work, may facilitate the maintenance of circadian rhythms, and lessens delirium and agitation. These goals are distinct from those associated with analgesia, which are the alleviation of pain through nonpharmacologic and pharmacologic means and to facilitate diagnostic and therapeutic procedures. Although sedation and analgesia are separate therapeutic goals usually provided by individual drugs, there is often synergism between anxiolytic and analgesic drugs; and some newer agents provide elements of both analgesia and anxiolysis, thus blurring the distinction in clinical practice.

The Society of Critical Care Medicine (SCCM) published guidelines for sedation,2 which emphasize the need for the goal-directed delivery of psychoactive medications. Goal-directed sedation is supported by an increasing body of literature that shows that daily interruption of sedation, intermittent sedation, and sedation protocols all reduce the duration of mechanical ventilation and in some instances decrease ICU length of stay.3

There are several scoring systems available to assess a patient’s degree of sedation in the ICU and facilitate goal-directed therapy (Table 30-1). The Riker Sedation-Agitation Scale (SAS) was the first scale proved to be reliable and valid in critically ill adults. The SAS score is assigned by choosing a score from a seven-item scale that best matches a patient’s behavior. Another scale, the Motor Activity Assessment Scale (MAAS), has seven categories to describe patients’ behavior in response to stimulation. Like the SAS, it has been validated in critically ill adults. Most comparative clinical studies of sedation in critically ill patients have used the Ramsey scale. This scale is a six-point scale of motor activity that ranges from 1 (“patient anxious, agitated or restless, or both”) to 6 (“no response to light glabellar tap or loud auditory stimulus”) (Table 30-2). This scale was originally designed as a research tool but has been used for decades in clinical practice. Although no scientific consensus exists about which level of sedation using the Ramsey scale is optimal, recent literature frequently cites sedation goals of Ramsey 2 to 4, reflecting more realistic levels of sedation as part of goal-directed therapy. Other sedation scales that have been validated in critically ill adults include the Vancouver Interaction and Calmness Scale (VICS), the COMFORT Scale, and the Richmond Agitation-Sedation Scale (RASS). The SCCM’s guidelines do not advocate one specific scoring system. Instead, they advocate defining a specific sedation goal or endpoint for each patient and then regularly assessing and documenting the patient’s level of sedation in response to therapy.

Table 30-2 The Ramsey Sedation Scale

Awake levels

Asleep levels

Reprinted with permission from Young C, Knudsen N, Hilton A, Reves JG: Sedation in the intensive care unit. Crit Care Med 28:854, 2000.

Sedative Agents

Benzodiazepines

Many drugs are available for sedating patients in the cardiothoracic ICU. The most frequently used agents for sedation include benzodiazepines (midazolam, lorazepam), propofol, and the α2-agonist dexmedetomidine. While there are multiple medications that can be used to allay anxiety, the traditional approach has been to use benzodiazepines. These drugs act by binding to benzodiazepine receptors (subunits of the GABAA [γ-aminobutyric acid] receptors, in the limbic area of the brain). This binding enhances the effects of GABA in a dose-dependent fashion. Benzodiazepines can be titrated to effect, which can range from light sedation to coma. Side effects such as respiratory depression are also dose dependent and are more likely to appear in patients with comorbid conditions such as chronic obstructive pulmonary disease (COPD), in those at the extremes of age, and in patients receiving drugs with synergistic properties, such as opioids.

Midazolam is a short-acting benzodiazepine that can only be given parenterally. It is water soluble, its intravenous administration causes no pain or venous irritation (and therefore thrombosis), and its potency is two to four times that of diazepam. Midazolam is readily redistributed in tissues and is rapidly cleared by the liver and kidneys. It is enzymatically degraded in the liver to α-hydroxy-midazolam, which has minimal, if any, clinical sedative or hypnotic effects. The clinical effects of midazolam are short lived owing to an elimination half-life of 1.5 to 3.5 hours. These properties make midazolam ideal as an anxiolytic benzodiazepine for short-term use in the ICU. Depending on the situation, intermittent boluses of midazolam can be given or a continuous infusion of 0.5 to 5.0 mg/hr can be used. Higher doses may be required, and infusions of up to 20 mg/hr have been safely used in mechanically ventilated patients.

In patients whose condition deteriorates while in the ICU, such as the patient who develops sepsis or multiple organ dysfunction syndrome, midazolam elimination may be decreased and its clinical effect prolonged. This prolongation of effect may be due to the increased volume of distribution that occurs in patients with multiple organ dysfunction syndrome whose renal clearance is decreased.

Dexmedetomidine

Herr and colleagues conducted a multicenter trial comparing dexmedetomidine and propofol for sedation after coronary artery bypass grafting (CABG).5 In their trial there was no significant difference in time to extubation between groups but the dexmedetomidine patients had significantly reduced use of supplemental analgesics, antiemetics, epinephrine, and diuretics.

Neuromuscular Blocking Agents

Occasionally, some patients are so critically ill that they cannot be adequately sedated to receive appropriate care. This most commonly happens in an agitated patient requiring mechanical ventilation in whom the level of sedation would mimic a general anesthetic and whose hemodynamic status does not tolerate this degree of deep sedation. In these circumstances, neuromuscular blocking agents (NMBAs) are used.

If these medications are used, it cannot be overemphasized that the patient must be adequately sedated before the initiation of the NMBA. Once an adequate degree of sedation (usually to include an analgesic medication such as an opioid) is achieved, the patient is administered a bolus and then a continuous infusion of an NMBA. Although there are several drugs available, the drugs most commonly used in the ICU are the aminosteroidal compounds (pancuronium, vecuronium, and rocuronium) and the benzylisoquinolinium compounds (doxacurium, atracurium, and cisatracurium). Pancuronium and doxacurium are long-acting NMBAs, whereas rocuronium and vecuronium are intermediate-duration medications and atracurium and cisatracurium are short-acting medications, at least when given by bolus. Because these drugs are infused continuously, this attribute is not as important, but it does become important when the medication is discontinued and the physician is assessing the return of the patient’s neuromuscular function. When infusing these medications, a twitch monitor should be used and the physician should strive to achieve a train-of-four of one or two twitches.6 If there are no twitches observed, then the patient may be overdosed and may be at risk for development of acute quadriplegic myopathy syndrome (AQMS), a situation that develops in patients receiving NMBAs in which, when the medication is discontinued, the patient remains flaccid for much longer than would be predicted simply based on pharmacokinetics of the medications that were infused. The etiology of this syndrome is unknown but is most likely secondary to the destruction of myosin by the NMBA or one of its metabolites. Often, it is difficult to differentiate between AQMS and critical illness polyneuropathy, but in the latter profound muscle necrosis as is seen with AQMS would not be expected to occur.

Another way to minimize the likelihood of this syndrome is to institute a daily drug holiday. Not only is this beneficial in decreasing the incidence of AQMS, but in patients receiving opioids and benzodiazepines the incidence of drug withdrawal also decreases with the discontinuation of the medication. When using NMBAs in the ICU, the algorithm as shown in Figure 30-1 is recommended.

INFECTIONS IN THE INTENSIVE CARE UNIT

Intravascular Device-Related Infections

Virtually all adult patients having cardiac surgery are monitored with invasive intravascular devices (IVDs), such as arterial, central venous, and pulmonary artery catheters. Unfortunately, these IVDs are frequently associated with bloodstream infections (BSIs). IVD-related BSIs are associated with an attributable mortality of 12% to 15%, prolonged hospitalization (mean of 7 days), and increased hospital cost of approximately $35,000.7

Approximately 90% of all vascular catheter-related bloodstream infections (CRBSIs) occur with use of short-term central venous catheters (CVCs). CVCs that are present for a short term are most commonly colonized from the skin surrounding the insertion site. Organisms migrate along the external surface of the catheter and then the intercutaneous and subcutaneous segments, leading to colonization of the intravascular segment. Once colonized, it is difficult to eradicate organisms from the intravascular segment without catheter removal because the microbes adhere to and are covered by either a biofilm layer they produce or the thrombin layer the host forms on the device. Because the skin is the most common site of colonization, coagulase-negative staphylococci and Staphylococcus aureus from the host’s skin and the hands of hospital personnel caring for the patient are the most common infecting pathogens. However, with long-term catheters, contamination of the catheter hub also contributes to intraluminal colonization.

Several factors have been associated with a risk of CVC-related bacteremia. These include site of insertion (femoral > internal jugular > subclavian), number of lumens (multiple > single), duration of catheter in situ, established infection elsewhere in body, bacteremia, and experience of personnel placing the catheter.

In an effort to reduce IVD-related BSIs, a Centers for Disease Control and Prevention advisory committee has formulated evidence-based guidelines pertaining to the prevention of IVD-related BSIs. These guidelines are summarized in Box 30-2.8

The diagnosis of central catheter infection can be challenging. The diagnosis should be suspected in patients with evidence of infection (e.g., fever, leukocytosis, positive blood cultures) when another source is not evident. Careful inspection of the catheter site is warranted, because exit site erythema or purulence strongly supports the diagnosis. If there are no visible signs of infection, then clinical suspicion and supporting data must be used to guide therapy. The most commonly used technique to culture CVCs is the semiquantitative roll-plate technique. With this technique, the most common threshold to define colonization is the growth of a colony count greater than 15.

The first clinical decision to make when managing a suspected CVC-related BSI is whether to remove the catheter. This decision is influenced by whether the risk of CVC-related BSI is low, intermediate, or high. Risk, in turn, is determined by the infecting organism and whether the CVC-related BSI is complicated or uncomplicated. Complicated infections are those associated with shock, persistence of positive blood cultures for longer than 48 hours after appropriate antibiotics, CVC-related BSIs associated with septic thrombosis, septic emboli, or deep-seated infections (e.g., endocarditis), or a tunnel or port-pocket infection (Fig. 30-2).