The Centers for Disease Control and Prevention (CDC) reports that about 150 individuals die of a traumatic brain injury (TBI) daily in the United States. Advancements in medical and surgical care seemingly allow for a higher prevalence of individuals living with a disability related to a TBI—now believed to be between 3.2 and 5.3 million.1,2 Long-standing disability secondary to a TBI and the difficulty predicting the extent of recovery continue to challenge patients, families, caretakers, and medical practitioners. Clinical aspects of a TBI can aid in determining prognosis of a patient’s recovery. With such knowledge, families may be better equipped for weighing medical and surgical decisions and managing their expectations in the setting of the resultant TBI.
Because TBI is an extremely heterogeneous condition, it poses a unique set of challenges for the critical care provider. During resuscitation efforts and critical care interventions, the intensivist must consider the brain and systemic organs as a whole to prevent or minimize further brain injury resulting from secondary insults such as hypotension, hypoxia, and metabolic abnormalities. Major efforts have been put toward the development of standardized approaches that follow the recommendations from national and international societies dedicated to the management of TBI. In this chapter we briefly cover the most commonly employed strategies for the critical care management of patients with severe TBI.
Prehospital management
Currently, there is no therapy to reverse the primary injury associated with TBI. Therefore the main goals of prehospital evaluation and management are to prevent, identify, and treat secondary insults that will result in further brain injury. The two most commonly recognized secondary insults are hypotension and hypoxia, which are particularly deleterious during the first 24 hours after the initial insult. In 2007, McHugh et al. reported in a metaanalysis of clinical trials and population-based studies that hypoxia (partial pressure of oxygen [PaO 2 ] <60 mm Hg) and systolic blood pressure (SBP) less than 90 mm Hg is associated with a higher likelihood of poor outcomes. Some authors have reported that prehospital care aimed to achieve early intubation and normalize blood pressure (BP) may be associated with improved outcomes, , whereas others have found increased mortality from prehospital intubation.
Endotracheal intubation is recommended for patients with a Glasgow Coma Scale (GCS) of 8 or less or an inability to protect their airway regardless of GCS and/or oxygen saturation below 90%. Although some authors recommend prehospital intubation in patients with severe TBI, its benefit is uncertain, with several studies reporting conflicting results or no benefit, and in some cases, it was associated with decreased survival in moderate to severe TBI patients.
Initial resuscitation and management
Before arriving to the neurointensive care unit (NeuroICU), patients are usually resuscitated and stabilized in the emergency department (ED) or operating room (OR). This first contact is crucial for both treatment and prognostication. Initial approach should follow the Advanced Trauma Life Support (ATLS) guidelines, including airway, breathing, circulation, disability (including GCS), and exposure ( Table 11.1 ). Particular attention should be paid to avoiding hypoxia and hypotension. A neurological evaluation should be completed as soon as possible to determine the severity of the TBI. If intracranial hypertension is suspected, evaluation and management should be initiated in the ED/OR. If clinical signs of cerebral herniation are imminent, immediate life-saving measures should be instituted. After initial assessment and management, computed tomography (CT) scan of the head should be performed as soon as possible to detect any condition that requires immediate neurosurgical intervention.
| Glasgow Coma Scale (GCS) | Score |
|---|---|
| Motor Response | |
| Obeys commands | 6 |
| Localizes to pain | 5 |
| Withdrawal response to pain | 4 |
| Flexion to pain | 3 |
| Extension to pain | 2 |
| None | 1 |
| Verbal Response | |
| Oriented | 5 |
| Confused | 4 |
| Inappropriate words | 3 |
| Incomprehensible sounds | 2 |
| None | 1 |
| Eye Opening | |
| Spontaneously | 4 |
| To verbal commands | 3 |
| To stimulation | 2 |
| None | 1 |
If not yet secured, an endotracheal airway should quickly be placed on arrival to the ED. The primary goal during airway instrumentation is to avoid extremes of BP and hypoxia. Induction agents such as propofol should be titrated carefully to prevent excessive vasodilation and subsequent hypotension. Etomidate can be a more suitable option during rapid sequence induction because it maintains better hemodynamics. Although some evidence suggests that ketamine does not increase intracranial pressure (ICP), the authors refrain from its use when the suspicion is high for intracranial hypertension. Ventilation and oxygenation should be optimized to prevent hypoxia and extreme hypo- or hypercarbia.
Intensive care management
The main goal of critical care management in TBI patients is to limit the development of secondary brain injury, which entails maintenance of cerebral perfusion, optimization of oxygenation/ventilation and BP, and prevention of hyperthermia, seizures, glucose derangements, and other metabolic abnormalities.
Hemodynamic management
Blood pressure and cerebral perfusion pressure
The Avoidance of Hypotension Remains a Priority in Traumatic Brain Injury. SBP below 90 mm Hg is an independent predictor of poor outcomes and has been associated with increased mortality. Although hypotension is easily prevented and treated, it has been shown that close to 75% of patients present with at least one episode of hypotension during their intensive care unit (ICU) stay.
Neurogenic and hypovolemic shock account for the most common etiologies of hypotension after severe TBI. Unless significant blood loss associated with scalp laceration or spinal cord injury exists, it is uncommon for isolated head trauma to present with severe hypotension. Consequently, other sources of hypotension should be sought, such as intrathoracic or abdominopelvic trauma or long bone fractures. Occasionally, hypotension can be masked by the Cushing response to intracranial hypertension.
Current recommendation is to maintain SBP 100 mm Hg or higher for patients 50 to 69 years old or at 110 mm Hg or higher for patients 15 to 49 or 70 years or older to decrease mortality and improve outcomes. Optimal cerebral perfusion pressure (CPP) is discussed in the Intracranial Hypertension Management section. One must be aware that the location of the arterial transducer (heart or brain) can have significant effects on CPP determination. In 2013, Kosty et al. surveyed practices at different NeuroICUs across the United States regarding arterial transducer location to determine CPP, and a wide variation in practice was found. The authors recommend placing an arterial transducer at the level of the tragus to estimate the CPP accurately.
Adequate intravenous access should be obtained, including at least two large-bore peripheral intravenous catheters (14–16 gauge) and a central venous catheter as soon as possible. Subclavian venous access is preferable in patients with TBI to minimize the risk of cerebral venous obstruction and vein thrombosis associated with internal jugular vein catheters. Additionally, internal jugular vein cannulation carries a higher likelihood for infection. Ultrasound-guided cannulation is recommended to increase success rate and decrease risk of arterial puncture, pneumothorax, and catheter malposition.
Radial or femoral arterial cannulation should be achieved to actively guide fluid resuscitation with dynamic tests of fluid responsiveness such as pulse pressure variation and stroke volume variation. These variables can be calculated from commercially available minimally invasive devices such as EV1000 and FloTrac/Vigileo. There is good evidence that static measures of volume status such as central venous pressure should no longer be used when guiding fluid resuscitation. , Pulmonary artery catheter might incur undue risk and is no longer recommended as a first-line intervention.
Resuscitation fluids
Normal (0.9%) saline is the resuscitation fluid of choice in neurotrauma. Albumin was associated with increased mortality rate in a subset of TBI patients enrolled in the SAFE trial and is typically avoided. Hypotonic solutions (e.g., 5% dextrose, 0.45% saline) should be avoided in the acute setting because they can decrease plasma osmolarity and worsen cerebral edema. Although hypertonic saline can quickly restore BP and improve intracranial hypertension, no survival benefit has been identified, and its routine use is not recommended for resuscitation purposes. Although balanced crystalloid solutions (i.e., Ringer’s lactate, PlasmaLyte) are associated with less risk of acute kidney injury in critically ill patients, no benefit was seen among the TBI patients enrolled in the SMART ICU trial. Overall, providers in the NeuroICU should become familiar with the most commonly used resuscitation fluids because the fluid of choice is often based on the individual’s hemodynamic and clinical profile ( Table 11.2 ).
| mEq/L | g/L | ||||||
|---|---|---|---|---|---|---|---|
| Fluid | Osm | Na | Cl | K | Ca | Lactate | Dextrose |
| Normal saline 0.9% | 308 | 154 | 154 | ||||
| Lactated Ringer’s solution | 275 | 130 | 109 | 4 | 3 | 28 | |
| D5W | 278 | 50 | |||||
| 0.45% NaCl | 154 | 77 | 77 | ||||
| 3% NaCl | 1026 | 513 | 513 | ||||
| 5% NaCl | 1710 | 855 | 855 | ||||
| 23.4% NaCl | 8008 | 4004 | |||||
| 5% Dextrose LR | 525 | 130 | 109 | 4 | 3 | 50 | |
| 5% Dextrose 0.9% NaCl | 561 | 154 | 154 | 50 | |||
| 5% Dextrose 0.45% NaCl | 405 | 77 | 77 | 50 | |||
Ventilation and oxygenation
Endotracheal intubation after severe TBI provides airway protection to reduce the risk of aspiration and subsequent development of pneumonia. In addition, it helps to control partial pressure of carbon dioxide (Pa co 2 ) and minimize changes to cerebral blood flow (CBF) and ICP. Pa co 2 and/or end-tidal CO 2 monitoring throughout the acute care phase is recommended with an initial target of normocarbia (35–45 mm Hg). In addition, hypoxia should be avoided and plateau pressure maintained less than 30 mm Hg.
Although therapeutic hyperventilation can be employed to decrease ICP, current guidelines recommend its use only as a temporizing measure, and it should be avoided during the first 24 hours after the initial injury when CBF is critically reduced. Hyperventilation decreases Pa co 2 , leading to cerebral vasoconstriction that may cause secondary ischemia and increased levels of extracellular glutamate and lactate. If hyperventilation is used, multimodal neuromonitoring with jugular venous oxygen saturation (SjvO 2 ) and/or partial brain tissue oxygenation (PbtO 2 ) measurement is recommended to monitor oxygen delivery. Although hyperoxia can be employed in select patients to improve brain tissue oxygenation, its routine use is not recommended because of risk for oxygen toxicity.
TBI is frequently complicated by acute respiratory distress syndrome (ARDS), which requires specific ventilatory therapy, including high levels of positive end-expiratory pressure (PEEP). Historically, elevated intrathoracic pressure resultant from high PEEP has been associated with impaired venous return from the brain and worsened ICP. Recent studies of applied PEEP up to 20 cm H 2 O have not revealed significant effect on ICP, and most important, high PEEP in TBI patients who develop ARDS seems to improve brain tissue oxygenation. In conclusion, high PEEP use is reasonable when clinically indicated for management of ARDS in conjunction with invasive ICP monitoring.
Seizure prophylaxis
Convulsive and nonconvulsive seizures may worsen neurological examination and raise ICP, especially when associated with status epilepticus. Additionally, seizures increase metabolic demand on damaged brain tissue, which could lead to secondary injury. The incidence of posttraumatic seizures (PTSs) may be as high as 30% after severe TBI, and up to 20% to 25% of patients may experience some variation of subclinical nonconvulsive seizures. Thus antiseizure medications are recommended to prevent the onset of early PTS after severe TBI. Although the clinical significance of electrographic silent seizures is unclear, continuous electroencephalogram (EEG) monitoring is a reasonable intervention when the neurological examination is disproportionate to the extent of the injury seen on imaging.
Current guidelines recommend prophylactic phenytoin for 7 days after injury. Levetiracetam is another alternative that has shown improved functional outcomes at 6 months after injury and fewer adverse events compared with phenytoin. , Antiseizure drugs should be continued indefinitely if the patient presents with clinical or electrographic seizures during the acute phase of treatment.
Status epilepticus is a condition that results either from failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms that lead to prolonged seizures. It is defined as more than 5 minutes of continuous clinical or 10 minutes of subclinical or electrographic seizures and/or recurrent clinical seizures without recovery to baseline in between episodes. The main goal is to terminate the seizure activity as soon as possible while concurrently initiating long-term antiseizure therapy. Benzodiazepines such as lorazepam and midazolam represent first-line therapy, whereas CBF-decreasing drugs such as propofol or pentobarbital are reserved for refractory status epilepticus.
Venous thromboembolism prophylaxis
Severe TBI patients commonly develop hypercoagulable state and are at higher risk for venous thromboembolism (VTE). The risk of VTE in TBI patients without any prophylaxis has been reported as high as 53% and decreases to around 10% when sequential compression stockings are employed. Certainly, pharmacological VTE prophylaxis can further reduce VTE risk, but it has to be weighed against the risk for hemorrhage expansion, which is greatest within the first 24 to 48 hours. ,
Studies are conflicting regarding VTE prophylaxis and hemorrhage expansion. A metaanalysis reported that VTE prophylaxis is safe when initiated within 24 to 48 hours of TBI with bleeding stability demonstrated on imaging. The risk of hemorrhage expansion can be stratified using the modified Berne-Norwood Guide recommended by the American College of Surgeons ( Table 11.3 ). Although currently there is insufficient evidence to support recommendations regarding specific agent, dosing, or timing of chemical VTE prophylaxis, unfractionated heparin or enoxaparin plus compression stockings can be used in most patients, and the benefit is considered to outweigh the risks of hemorrhage expansion. If VTE is identified in patients for whom anticoagulation is contraindicated, an inferior vena cava (IVC) filter should be placed.
| Low Risk | Moderate Risk | High Risk |
|---|---|---|
| No moderate or high risk |
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| Or | Or | |
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| |
| Or | Or | |
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| |
| Or | ||
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| Treatment | ||
| Start pharmacological VTE prophylaxis if CT stable at 24 h | Initiate pharmacological prophylaxis if CT stable at 72 h | Consider inferior vena cava filter placement |
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