Critical Care Medicine
In North America, anesthesiologists were integral to the development of critical care medicine as a specialty (Hallman M, Treggiari MA, Deem S. Critical care medicine. In: Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Ortega R, Stock MC, eds. Clinical Anesthesia. Philadelphia: Lippincott Williams & Wilkins; 2013:1580–1610). However, in contrast to other countries, in the United States, anesthesiologists have played an ever-diminishing role in the specialty, and today they make up a minority of the intensivist workforce. The driving forces behind intensive care unit (ICU) development included advances in surgical techniques, polio epidemics that resulted in widespread respiratory failure, and later the recognition of the acute respiratory distress syndrome (ARDS). In the late 1960s, a group including Dr. Safar and another anesthesiologist, Ake Grenvik, were instrumental in inaugurating the Society of Critical Care Medicine (SCCM). Anesthesiologists working through the SCCM were instrumental in developing the board certification process for critical care medicine, and in 1986, the first Critical Care Medicine Certification examination was administered by the American Board of Anesthesiology.
I. Anesthesiology and Critical Care Medicine: The Future
Forces that will shape the evolution of the specialty of critical care medicine and the contribution that anesthesiologists will make to this evolution include quality of care issues and the contribution of intensivists to improved ICU outcomes, business and economic factors, and the aging population and increasing demand for critical care services. Mortality and other intermediate end points such as ICU length of stay can be reduced when “high-intensity” physician staffing models that mandate management or co-management by intensivists are used.
II. Critical Care Medicine: A Systems and Evidence-Based Approach
Process of Care in the Intensive Care Unit
Implementation of evidence-based practices in the ICU could save up to 200,000 lives per year in the United States.
The Leapfrog Group is a coalition of more than 150 purchasers and providers of health care benefits with the
stated goal of improving health care, particularly by reducing deaths caused by medical errors.
To accomplish this aim, the Group formulated the Leapfrog Initiative, which includes a series of “safety standards” that health care providers (largely hospitals) should strive for if they are to provide care for Leapfrog.
Prompted by data associating intensivists with improved outcomes, the Leapfrog Initiative included an ICU Physician Staffing (IPS) standard that promotes the continuous involvement of intensivists in the care of critically ill patients (Table 55-1).
Table 55-1 Leapfrog ICU Physician Staffing (IPS) Standard | |||
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III. Neurologic and Neurosurgical Critical Care
Neuromonitoring devices used in the ICU setting may help in assessing pathophysiologic processes and adjusting therapy.
Transcranial Doppler (TCD) ultrasonography measures mean, peak systolic, and end-diastolic flow velocities and indirectly estimates cerebral blood flow (CBF). In patients with subarachnoid hemorrhage (SAH) or traumatic brain injury (TBI), TCD can be used as a tool to identify vasospasm. In patients with TBI, flow velocities are depressed, and impaired autoregulation and vascular reactivity are common. In these patients, monitoring of TCD and jugular venous oxygen saturation (SjO2) may be used to define the optimum cerebral perfusion pressure (CPP) level.
Brain tissue oxygenation (PbrO2) measurements are performed by introducing a small, oxygen-sensitive catheter into the brain tissue (normal PbrO2 values, 25–30 mm Hg). An increase in intracranial pressure (ICP) and a decrease in CPP or arterial oxygenation along with hyperventilation may result in decreased PbrO2. CPP above 60 mm Hg has been identified as the most important factor determining sufficient brain tissue oxygenation.
Microdialysis uses a probe as an interface to the brain to continuously monitor the chemistry of a small focal volume of the cerebral extracellular space. (This allows measurement of chemical substances such as lactate, pyruvate, glucose, glutamate, glycerol, metabolites of several biochemical pathways, and electrolytes and thus provides insight into the bioenergetic status of the brain.) Increased lactate, decreased glucose, and an elevated lactate/glucose ratio indicate accelerated anaerobic glycolysis. This metabolic pattern commonly occurs with cerebral ischemia or hypoxia, and increased glycolysis in this setting is associated with a poor outcome.
Diagnosis and Clinical Management of the Most Common Types of Neurologic Failure
Traumatic brain injury is the leading cause of death from blunt trauma, and in patients between the age of 5 and 45 years, TBI represents the leading cause of death (Table 55-2). Examination of the pupils can predict neurologic outcome.
Resuscitation. The goal of resuscitation in traumatic and other types of brain injury is to prevent continuing cerebral insult after a primary injury has occurred. A primary insult is often associated with intracranial hypertension and systemic hypotension, leading to decreased cerebral perfusion and brain ischemia. Concomitant hypoxemia aggravates brain hypoxia, especially in the presence of hyperthermia, which increases the brain’s metabolic demand. The combined effect of these factors leads to secondary brain injury characterized by excitotoxicity, oxidative stress, and inflammation. The resulting cerebral ischemia may be the single most important secondary event affecting outcome after a cerebral insult.
Prevention of secondary injury is the main goal of resuscitative efforts. Traumatized areas of the brain manifest impaired autoregulation, with increased dependency of flow on perfusion pressure and disruption of the blood–brain barrier. The goals of neuroresuscitation are oriented at restoration of CBF by maintenance of adequate CPP, reduction of ICP, evacuation of space-occupying lesions, and initiation of therapies for cerebral protection and avoidance of hypoxia (Table 55-3).
Drug-induced Sedation. A common practice is to provide sedation with propofol or benzodiazepines in patients after TBI. These agents have favorable effects on cerebral oxygen balance. Despite the induction of systemic hypotension, propofol decreases cerebral metabolism, resulting in a coupled decline in CBF with a consequent decrease in ICP. Barbiturates should be considered if ICP is not controlled by moderate doses of propofol. Although neuromuscular blockade may result in a decrease in ICP, the routine use of neuromuscular blockade is discouraged because its use has been associated with longer ICU course, a higher incidence of pneumonia, and a trend toward more frequent sepsis without any improvement in outcome.
Hyperventilation effectively reduces ICP by reducing CBF, but in small randomized trials, prophylactic hyperventilation has not proven to be beneficial in patients with TBI. Prolonged or prophylactic hyperventilation should be avoided after severe TBI. Hyperventilation may be necessary for brief periods
to reduce intracranial hypertension refractory to sedation, osmotic therapy, and cerebrospinal fluid drainage and should be guided by SjO2, PbrO2, or both (a decrease in either of these values suggests a harmful effect of hyperventilation).
Hypothermia. There is insufficient evidence to provide recommendations for the use of moderate hypothermia in patients with TBI.
Corticosteroids to reduce posttraumatic inflammatory injury should not be administered as therapy for acute TBI.
Anticonvulsants may be used to prevent early posttraumatic seizures within 7 days after head trauma. (Evidence does not indicate that prevention of early seizures improves outcome after TBI.)
Albumin as fluid replacement therapy in patients with TBI may increase mortality when compared with saline.
Subarachnoid hemorrhage is most commonly caused by the rupture of an intracranial aneurysm with only one-third of patients with SAH being functional survivors. The leading causes of death and disability are the direct effects of the initial bleed—cerebral vasospasm and rebleeding. At the time of aneurysm rupture, a critical reduction in CBF takes place because of an increase in ICP toward arterial diastolic values. The persistence of a no-flow pattern is associated with acute vasospasm. In survivors of the initial bleed, emphasis has been placed on early aneurysm securing with either surgery or interventional neuroradiology (coiling). Early aneurysm occlusion substantially reduces the risk of this rebleeding.
Cerebral vasospasm after SAH is correlated with the amount and location of subarachnoid blood. A reduction in CBF is ultimately responsible for the appearance of delayed ischemic neurologic deficits. Oral nimodipine (60 mg every 4 hours for 21 days) as prophylaxis for cerebral vasospasm is recognized as an effective treatment in improving neurologic outcome (reduction of cerebral infarction and poor outcome) and mortality from cerebral vasospasm in patients with SAH. The benefits of nimodipine have been attributed to a cytoprotective effect related to the reduced availability of intracellular calcium and improved microvascular collateral flow.
Hypervolemic, hypertensive, and hemodilution (“triple-H”) therapy is one of the mainstays of treatment for cerebral ischemia associated with SAH-induced vasospasm despite the lack of evidence for its effectiveness. The rationale for hypertension derives from the concept that a loss of cerebral autoregulation associated with vasospasm results in pressure-dependent blood flow. Hemodilution is a consequence of hypervolemic therapy and is thought to optimize the rheologic properties of the blood and thereby improve microcirculatory flow. Common complications of treatment are pulmonary edema and myocardial ischemia.
Interventional neuroradiology with the use of balloon angioplasty (within 6–12 hours) can reverse or improve vasospasm-induced neurologic deficits.
Acute Ischemic Stroke. More than half of strokes can be attributed to a thrombotic mechanism. Transient ischemic attacks may precede stroke and thus should be considered a warning sign.
Thrombolysis. Rapid clot lysis and restoration of circulation using alteplase (rt-PA) should be provided within 3 hours of stroke onset. Patients receiving systemic rt-PA should not receive aspirin, heparin, warfarin, clonidine, or other antithrombotic or antiplatelet aggregating drugs within 24 hours of treatment. Because hyperglycemia is associated with poor outcome in patients with ischemic stroke, tight glucose control is recommended. (The mortality benefit at 90 days has not been demonstrated.)
Anoxic brain injury most commonly occurs as a result of cardiac arrest. The pathophysiology of anoxic brain injury is multifactorial and includes excitatory neurotransmitter release, accumulation of intracellular calcium, and oxygen free radical generation. A strong experimental literature supports a role for mild therapeutic hypothermia in anoxic brain injury (temperature, 32°C–34°C). Hypothermia is recommended in neonatal hypoxic encephalopathy.
Table 55-2 Predictors of Poor Outcome After Traumatic Brain Injury | ||
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Table 55-3 ICU Management of Patients with Severe Traumatic Brain Injury (Assuming Initial Surgical Management) | ||
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IV. Cardiovascular and Hemodynamic Aspects of Critical Care
Principles of Monitoring and Resuscitation. Shock states are associated with impairment of adequate oxygen delivery, resulting in decreased tissue perfusion and tissue hypoxia. (Global hemodynamic monitoring may not reflect regional perfusion or the peripheral tissue energy status.) Invasive monitoring in shock states provides insight into the circulatory status, organ perfusion, tissue microcirculation, and cellular metabolic status of the critically ill patient.
Functional Hemodynamic Monitoring
Pulmonary Artery Catheter (PAC). The information provided by the PAC may assist in the differentiation of cardiogenic and noncardiogenic circulatory and respiratory failure and may help guide fluid, inotropic, and vasopressor therapy.
Despite the theoretical benefits of pulmonary artery catheterization, little data support a positive effect of
PACs on mortality or other substantive outcome variables. A trial conducted in patients assigned to receive PAC-guided or central venous catheter–guided therapy did not find any survival or organ function differences between the two groups, and there was an equal number of catheter-related complications (dysrhythmias).
Studies do not support the routine use of the PAC for the management of acute lung injury (ALI) or septic shock.
Arterial Pressure Waveform Analysis. The variation in systolic blood pressure and pulse pressure during positive-pressure ventilation is highly predictive of the response to intravascular fluid administration in both normal subjects and critically ill patients. Cardiac output derived using pulse contour analysis correlates well with thermodilution cardiac output in a variety of conditions and has the advantage of providing continuous measurement without necessitating the placement of a PAC. The use of pulse contour analysis may potentially obviate the need for pulmonary artery catheterization to measure cardiac output, particularly if combined with the measurement of ScvO2 as an indicator of the balance between oxygen delivery and consumption.
