Neurologic
Traumatic Brain Injury
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Background
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Neurologic assessment
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Glasgow Coma Score
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Orientation assessment
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Motor score
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Pupillary assessment
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Brainstem reflexes
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Critical care management
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Neuro
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Multimodal monitoring
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Sedation and Analgesia
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Seizure prophylaxis
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Hyperosmolar therapy
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Targeted temperature management
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Cardiovascular
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Pulmonary
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Gastrointestinal
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Fluids
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Infectious Disease
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DVT Prophylaxis
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References
Background
Traumatic brain injury (TBI) is an induced physiologic disruption of brain function, which can lead to temporary or permanent impairments to cognitive, physical and psychosocial functions that is caused by injury or accident. TBI is a major cause of death and disability in the United States. In 2017, the most recent year for which data is available, the CDC reports TBI accounted for 2.9 million hospital visits and 61,000 deaths.
The goal is to ensure appropriate treatment is provided to patients with acute brain injuries in a way that prevents and/or minimizes secondary CNS injury and optimize physiologic parameters. This is based on the most recent evidence-based data and practice guidelines. The foundation of the management of patients with acute brain injury is excellent critical care with attention to airway, oxygenation/ventilation, and hemodynamic support to avoid secondary injury associated with hypoxia and hypotension. In addition, there are brain-specific areas of focus, including identifying and treating intracranial hypertension and avoiding seizures, which can lead to secondary injury and worsen clinical outcomes.
Care of the patient with acute brain injury is complex. A multidisciplinary approach to care is necessary, with input from neurosurgery, trauma, critical care, nursing, pharmacy, and rehabilitation therapies. Many patients with acute brain injury have additional injuries or comorbidities, therefore a team approach to care optimizes clinical outcomes. All patients with acute brain injury will be managed in a multidisciplinary fashion.
The purpose of this document is to provide standardized guidelines for the acute care management of the head injured patient at Highland Hospital. These guidelines are based generally on the Brain Trauma Foundation guidelines, the ACS TQIP: Best Practices in the Management of Traumatic Brain Injury, and more closely on the management algorithm outlined by the Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC).
Neurologic Assessment
Glasgow Coma Scale
The Glasgow Coma Scale (GCS) allows for appropriate triage, assists in guiding therapy, and provides us with a basis for observing the depth of coma and degree of brain dysfunction. The GCS is composed of eye, verbal, and motor responses. The examiner should note the BEST score in all areas of testing. The composite GCS has been used to classify TBI into broad categories of mild, moderate, and severe injury. While the GCS is extremely helpful in the clinical management of TBI, limitations exist. It does not take into account the heterogeneity of individual cerebral physiology, nor does it provide specific information about the pathophysiology responsible for neurologic deficits after TBI.
Orientation Assessment
Disorientation is reflective of cognitive impairment. Components of a complete orientation exam include person (first and last name), place (hospital, city, state), date and circumstances (why are you here?). In assessing level of orientation, consideration should be made for a patient’s pre-injury level of orientation.
If the patient is unable to appropriately respond, the examiner should rule out the possibility of aphasia by requesting repetition of a phrase, such as “It’s a sunny day in Oakland.” An inability to accurately repeat this statement implies the presence of an aphasia and requires further detailed work-up.
Motor Response
When assessing the motor response of a head injured patient it is imperative that a focused motor exam be performed. In the unresponsive patient, the motor exam is incorporated into the GCS evaluation. If the patient is cooperative, motor strength should be tested in all four extremities with comparisons made bilaterally. The pronator drift exam is best for eliciting minor unilateral weakness often seen in patients who have a lesion pressing on the motor strip.
Pupillary Assessment
One of the most important parameters for early evaluation of increasing intracranial pressure in the TBI patient is pupillary size and reaction to light. The pupillary examination can be assessed in an unconscious patient or in a patient receiving sedation and neuromuscular blocking agents. Pupillary response should be obtained during initial resuscitation and every hour or as indicated thereafter.
The pupillometer is used to obtain accurate, objective, and consistent pupillary assessments. The Neurological Pupillary Index (NPI) is determined by pupillary size prior to light stimulation (MAX), pupillary size after light stimulus (MIN), % change of pupil, and constriction velocity (CV). NPI is obtained Q1-2 hour serially in all TBI patients with multi-modality monitoring, and after any neurologic decompensation.
Brainstem Reflexes
Brainstem reflexes are reflective of the functional status of the brainstem. The brainstem reflexes that are easy, quick, and safe to evaluate at any time during the workup of a TBI patient include corneal reflex, cough/gag reflex, and respiratory drive assessment. These reflexes will be impaired or unreliable if the patient has received a neuromuscular blocking agent or is on high levels of sedation or analgesia. In a patient who is awake, talking, and breathing with no difficulty, it can be assumed that these reflexes are intact.
Critical Care: Neuro
Cerebral edema, seizures, hypoxia, and ischemia are common sequelae after severe TBI that may be prevented or controlled when acted upon early and before secondary brain injury develops. Critical Care for the severe, acute brain injury patient relies heavily on the knowledge and experience of an interdisciplinary team of providers to understand the pathophysiology and progression of the injury. Rapid detection of both drastic and subtle changes in neurological status allows for prompt intervention to prevent further disability and possibly death.
All patients with acute intracranial hemorrhage on initial head CT with corresponding neurologic deficits will be admitted to the ICU. Serial neurological examinations will occur every 1-2 hours. This includes a full GCS for all patients, pupillometry readings, and brainstem reflex assessment for intubated, sedated, and/or nonresponsive patients. Any subtle or major neurological change must be reported to the neurosurgical provider immediately. Repeat head CT will be obtained for changes in neurological status, as indicated. Neurosurgical intervention will be performed as appropriate based upon findings.
Multimodal Neuro Monitoring
The objective of employing multimodality monitoring in neurocritical care is to integrate patient data to facilitate early and accurate diagnosis, management, and prediction of neurological deterioration. Multimodal monitoring encompasses standard non-invasive as well as invasive patient monitoring practices. This includes the neurological exam, telemetry (cardiac and respiratory physiology), neuroimaging, EEG monitoring, and invasive monitoring. Comprehensive monitoring is utilized to determine the physiological, functional, and metabolic status of the brain, allowing for targeted therapy for each patient.
Every patient with a GCS 8 or less on admission and evidence of an intracranial traumatic lesion will be evaluated for multi-modal intracranial monitoring to measure hourly ICP, CPP, and PbtO2. They will also undergo continuous EEG monitoring when available, whether via external leads or internally placed ECoG strip or depth electrode. The addition of jugular bulb venous oxygen monitoring and cerebral blood flow monitoring will be utilized at the discretion of the treating physician and based on availability.
Monitors will be placed and maintained in a sterile fashion, especially ventricular catheters, as conditions during placement and instrumentation are the greatest risks for inducing infection. CSF will be sent for analysis from ventricular catheters as needed for infection diagnosis. CSF will be withdrawn directly from the ventricular catheter using sterile technique and will be performed only by Neurosurgical team members. Antibiotic coverage will be initiated for treatment of suspected or confirmed ICP monitor infection, but not prophylactically.
Invasive monitoring
Intracranial Pressure (ICP)
ICP monitoring has been a cornerstone in the management of patients with severe TBI. Management of severe TBI patients using information from ICP monitoring is recommended
to reduce in-hospital and 2-week post-injury mortality. Clinicians should use their clinical judgement and perform intracranial monitoring in patients who are high risk for intracranial hypertension and clinical deterioration. Current recommendations indicate that ICP should be monitored in all patients with GCS of 8 or less.
ICP will be continuously monitored by parenchymal probe (eg Camino or bolt), external ventricular drain (EVD or ventriculostomy), or both. When an EVD is in place, this will be leveled at the external auditory canal (EAC). The height at which to drain will be determined by the attending neurosurgeon. EVD will be clamped once per hour to record an ICP value, otherwise it will be left open to drain. EVDs must also be clamped for any transport. The level at which the EVD will be placed, as well as the decision to openly drain CSF may be adjusted at the discretion of the attending neurosurgeon.
Normal ICP ranges from 10-15 mmHg. Elevated ICP above 22 mmHg sustained for more than 5 minutes necessitates treatment as sustained, elevated ICP is associated with increase mortality. A member of the neurosurgical team must be notified immediately of any elevated ICPs. The approach to treatment of elevated ICP will be addressed in a separate document.
Cerebral Perfusion Pressure (CPP)
Once an ICP monitor is in place, CPP must be monitored continuously. CPP is monitored to avoid secondary ischemia of traumatized brain by ensuring adequate cerebral perfusion. Current recommendations are to maintain a CPP between 60 and 70 mmHg. CPP will be documented every hour. CPP less than 55 should be avoided in order to prevent hypoperfusion, while attempts to maintain CPP greater than 70 is associated with an increased risk of ARDS. Whether or not a patient has intact cerebral autoregulation and cerebral compliance may alter the CPP goals for a patient. Management of blood pressure to maintain mean arterial pressure (MAP), and therefore CPP in goal range will be addressed in the Hemodynamics section of this document.
Brain oxygenation (PbO2)
Maintenance of adequate tissue oxygenation is one of the fundamental goals of critical care. From a simplistic point of view, low brain tissue oxygenation is indicative of cerebral ischemia.
Measuring the partial pressure of oxygen in cerebral tissue is used as a marker of ischemia and CBF, but also provides measured responses to interventions (e.g., changes in CPP, ventilator targets, pharmacologic sedation, and transfusion) and can be used to guide therapy. PbO2 can be low, despite normal ICP and CPP, therefore PbO2 measurements should be used in conjunction with ICP/CPP management. PbO2 will be recorded every hour.
PbO2 will be monitored continuously by Licox, or other similar device. Normal PbO2 is 18-30 mmHg on 40% FiO2. A drop in PbO2 to 15mm Hg or less necessitates treatment. A member of the neurosurgical team must be notified immediately of any drops in PbO2. Similarly, a rise in PbO2 to greater than 100mm Hg or a change by 50% from baseline (either increase or decrease) should prompt notification of a neurosurgery provider. The approach to management of PbO2 will be addressed in a separate document.
Additional invasive monitors
Additional invasive monitors may become available, including cerebral microdialysis, cerebral blood flow monitoring, jugular bulb venous oxygen saturation, depth electrodes, and cortical strip electrodes. These will add additional clinical data to be used in the comprehensive approach to management of patients with acute brain injury.
Non-invasive
Pupillometry
Pupillometry is now a well-established tool as a part of the neurologic assessment of patients with acute brain injury. Use of the pupillometer allows for objective assessment of pupil size and reactivity, and calculation of the Neurologic Pupillary Index (NPI). Cranial nerve dysfunction, as evidenced by a decrease in the NPI, can be an early indicator of neurologic deterioration, including worsening cerebral edema, increase in intracranial pressure, development of delayed cerebral ischemia, or identification of herniation syndromes. A change in the NPI can often be detected before there is a change in the ICP or other clinical signs of deterioration.
EEG
Studies suggest that up to nearly 50% of patients with intracranial pathology in the ICU suffer from seizures, the majority of which are non-convulsive. EEG is a simple and non-invasive way to detect abnormal cortical activity. Consensus statements strongly recommend the use of EEG in all patients with moderate to severe acute brain injury, hypoxic-ischemic injury, or any brain injury with persistent or unexplained altered level of consciousness.
Multimodal Monitoring Adjuncts
Moberg CNS allows for comprehensive collection, annotation, review, and analysis of time synchronized patient data. This comprehensive collection of data helps to guide treatment. Moberg will be utilized in all patients with acute brain injury, once this becomes available.
Sedation and Analgesia
Sedation and analgesia are important for several reasons in patients with acute brain injury. Adequate sedation and analgesia in this population has been shown to diminish pain and anxiety and improve ventilator synchrony. Unrelieved pain and anxiety can lead to increase in MAP and ICP, thereby decreasing CPP. Increased intrathoracic pressure from ventilator dysynchrony impedes cerebral venous drainage. Sedation also helps lower the cerebral metabolic rate of oxygen (CMRO2).
Selection of medications used for sedation and analgesia must also take into account the need to preserve access to a neurological examination, and also potential side effects of the medications including negative effects on hemodynamics. It is also difficult to predict the hemodynamic response to certain medications in patients with acute brain injury, until it is established whether they intact or impaired cerebral autoregulation. Medications with short half-lives are thus preferred, and it may be necessary to frequently reassess the choice of medications.
Analgesia
Short acting opioids can be used for analgesia as follows. A bolus dose strategy is encouraged to best preserve the neurological exam, starting at 25-50 mcg/hr. If repeated bolus doses of opioids are ineffective in providing adequate pain management, then a continuous infusion may be initiated. For patients with oral access, oral opioids may be considered (ie oxycodone). Analgesia should be titrated to the lowest dose necessary to meet the analgesia goal. Analgesia is not ICP directed.
When possible, multimodal analgesia should be utilized. Acetaminophen is a preferred non-opioid adjunct for TBI patients. NSAIDs should be avoided in the acute phase of TBI management but may be considered upon clinical improvement if cleared with the Neurosurgery Attending. Other non-opioid adjuncts (i.e. gabapentin, baclofen, etc) may be considered based on the perceived or described type of pain a patient may be experiencing.
Sedation
For severe TBI patients with ICP elevations, sedation can be used to help reduce ICPs in conjunction with other ICP control measures, such as CSF drainage and hyperosmolar therapies. For patients without ICP issues, sedative use should be minimized unless needed for seizure management, paroxysmal sympathetic hyperactivity and/or to facilitate critical care interventions (e.g. mechanical ventilation, line placement, endotracheal suctioning, patient safety and restraint). Indication for use of sedative infusions and the targeted sedation goal should be evaluated at least daily but is encouraged more frequently.
First line approach to sedation is as follows, with titration to the lowest dose necessary to meet the sedation goal. Propofol is the preferred sedative for use in TBI patients due to its favorable kinetic profile (i.e. fast onset, fast offset) which allows for neurological examination. Infusion rates up to 80mcg/kg/min are acceptable. Any changes in the sedative regimen in patients with ICP monitors must be discussed with the Neurosurgery Attending.
Additional agents that can be utilized for sedation and analgesia include: midazolam, precedex, ketamine, and barbiturates. Depending on the patient and their intracranial injury, these medications may be utilized to achieve the analgesia or sedation goal. Benzodiazepine infusions have a prolonged offset of clinical effect compared to propofol, making neurologic assessment less reliable. They can be considered for patients with ICP elevations as they have been shown to reduce both ICP and cerebral metabolic rate of oxygenation, though less pronounced than propofol.
Dexmedetomidine has no documented effect on ICP and cerebral metabolism to date, and may be considered for patients without concern for ICP elevations. It is an ideal sedative agent for patients who are nearing liberation from the ventilator and/or those warranting light sedation. Regarding ketamine, recent systematic reviews provided low-level evidence that ketamine does not increase, but might even lower ICP in brain injured patients who are sedated and mechanically ventilated. Ketamine may have a neuroprotective role in acute brain injury by suppressing cortical spreading depolarizations.
Propofol and dexmedetomidine can cause significant hemodynamic compromise (i.e. hypotension, bradycardia). When used for sedation in ICU TBI patients, close attention to a patient’s hemodynamic status is indicated to ensure that the patient is still achieving the targeted CPP goal.
Neuromuscular Blockade
If a patient is having persistently elevated ICPs despite sedation and other interventions, paralysis can be considered. The decision to initiate or discontinue paralytics in patients with ICP monitors must be cleared by the Neurosurgery Attending. The following criteria must be satisfied prior to the initiation of paralysis:
- Mechanically ventilated on a volume control or pressure control mode
- Patient is on a continuous analgesic infusion
- Patient is receiving a continuous sedative infusion with propofol or midazolam, and sedated to a RASS of -5.
Train-of-four should be used to monitor the depth of paralysis in conjunction with clinical assessment (i.e. respiratory effort, skeletal muscle movement). A trial dose of a paralytic can be given, and only if this is effective in lowering ICP can an infusion be initiated.
Seizure Prophylaxis
Posttraumatic seizures may occur within seven days of injury (early), or after seven days (late). Seizures complicate ICP control and may worsen secondary brain injury especially if status epilepticus occurs. Prospective randomized trials have shown that prophylactic anticonvulsants may prevent the occurrence of early, but not late posttraumatic seizures. Anticonvulsants will be administered to any patient with intracranial hemorrhage for 7 days. There are two exceptions to this. First, the patient with isolated traumatic subarachnoid hemorrhage. The decision to provide seizure prophylaxis will be at the discretion of the attending neurosurgeon. Second, the patient with penetrating TBI (for example gunshot wound), may be treated with seizure prophylaxis for a duration of 3 months.
Levetiracetam will be considered first line for post-traumatic seizure prophylaxis. Dosing will be per attending Neurosurgeon preference. Levetiracetam will also be used in patients who have experienced significant hemodynamic compromise or other side effects from fosphenytoin/phenytoin, are on levetiracetam as an outpatient, those with decompensated liver failure or if there are concerns related to drug interactions with fosphenytoin/phenytoin (e.g. antiretrovirals, etc).
Fosphenytoin, with an IV loading dose of 15-20 mg/kg and maintenance dose of 100 mg IV every 8 hours will be a second line or alternative medication. Fosphenytoin IV will be changed to phenytoin ER if patients are able to take medications via the PO route. Vimpat is an acceptable alternative if a patient does not tolerate or has contraindications to keppra or fosphenytoin. If a patient takes an alternative antiepileptic than what is mentioned for a primary seizure disorder, the Neurosurgical attending will determine whether continuing the outpatient antiepileptic regimen is sufficient for early seizure prophylaxis or if an alternative therapy is recommended.
If a patient has a seizure (clinical or electrographic) in the first seven days following their injury, the duration of treatment will be extending. Neurology consultation will be obtained and dose escalation and/or additional of a second antiepileptic drug (AED) will be done according to their recommendations. Similarly, weaning of AED’s will occur on an outpatient basis and guided by Neurology. If a patient suffers a penetrating TBI, the duration of treatment for seizure prophylaxis will be three months, regardless of whether or not the patient has a seizure.
Hyperosmolar Therapy for ICP Control
Hyperosmolar therapy is used to treat acutely elevated ICP while avoiding the potential undesirable complications of such therapy (hypovolemia, hypernatremia, etc). Clinical signs of cerebral herniation prior to ICP monitoring, or if ICP does not reflect focal tissue shifts (e.g. focal temporal lobe pathology), require rapid treatment. Mannitol or hypertonic saline solution (HTS) may be used as hyperosmolar therapies to reduce ICP in adult TBI patients. There is insufficient evidence available from comparative studies to support a formal recommendation of one over another.
Hypertonic saline should be administered as 250mL of 3% infusion administered over 30 minutes. This will be given on an as needed basis. In certain cases, 3% saline may be run as a continuous infusion. For patients requiring or who have the potential to require multiple doses of hypertonic saline, serum sodium and osmolarity should be checked at least every 6 hours. HTS should not be administered if the sodium is ≥ 155 mmol/L, or if the serum osmolarity is >320
Mannitol should be administered as a 1 gm/kg IV bolus. For patients requiring or who have the potential to require multiple doses of mannitol, serum osmolality should be checked at least every 6 hours. Mannitol should be used with caution if the serum osmolality is ≥ 320 mOsm/L, especially in patients with renal impairment. Although mannitol is effective for ICP management, it can also induce profound diuresis which may be undesirable. Intravascular volume depletion and electrolyte losses may occur after administration. Fluid balance should be monitored closely, and fluid should be replaced if significant volume losses occur.
Targeted Temperature Management
Fever in TBI patients should be avoided as much as possible to prevent secondary brain injury. The use of prophylactic hypothermia in the early phase of TBI management is not supported by clinical evidence and is not recommended.
Acetaminophen will be initiated in all patients, unless a contraindication exists. Measures such as cooling blankets, ice, and fans will be used to maintain a core temperature less than 38.3o C. When more advanced capabilities become available, such as Arctic Sun, these will also be utilized. The source of the fever will be thoroughly investigated, and only after an infectious etiology has been ruled out can the fever be considered central. As central fever tends to respond poorly to conventional antipyretics, bromocriptine can be considered as an adjunct medication for persistent central fevers.
Therapeutic hypothermia may be considered for patients with refractory elevated ICPs, according to a tiered therapy guideline. Goal temperature is 36-38oC. The duration of hypothermia should be individualized per patient based on ICPs. Patients should be slowly rewarmed (0.1-0.2 C/hr) to avoid a rebound increase in ICP.
Shivering associated with fever and/or cooling can lead to a significant increase in systemic and cerebral energy consumption and potentially increased ICP, thus should be avoided as much as possible. Patients with shivering from fever or hypothermia measures should be treated accordingly. Skin counter warming (eg Bair Hugger) should be used when possible. Shivering can be treated with scheduled acetaminophen 650-1000mg q 6 hours, buspirone 10-30mg q 8 hours, or with merperidine 25-100 mg q 4 hours as needed. Meperidine should be used with caution as it can lower seizure threshold.
Critical Care: Cardiovascular
The purpose of cardiovascular support in acute brain injury is to optimize and maintain blood flow to the brain. As previously stated, goal CPP should be maintained at 60-70. Once the patient has demonstrated intact cerebral autoregulation, or is out of the window for ICP elevation, CPP goals may be liberalized to greater than 55. Systemic hypertension generally should not be treated in the acute setting of TBI, since this may reflect intact autoregulation, the body’s natural response to protecting the brain during periods of intracranial hypertension. If the patient has undergone surgical intervention, maintaining a goal systolic blood pressure less than 140 is preferred.
If vasoactive medications are necessary to increase the mean arterial pressure to maintain adequate CPP, norepinephrine is considered the initial pressor of choice, with phenylephrine considered a second line choice. If diabetes insipidus (DI) is confirmed or suspected, consider using vasopressin to treat both DI and hypotension. Antihypertensive medications may be administered if the systolic blood pressure is greater than 180 mmHg, with beta blockers as the drug of choice in the absence of bradycardia. Hydralazine should not be used since it has been found to uncouple cerebral blood flow from metabolism, disrupting autoregulation. If an infusion is needed to treat persistent hypertension, a calcium channel blocker should be initiated, favoring nicardipine or clevidipine.
Due to the need for blood pressure modulation, all patients with moderate to severe TBI should have an arterial line and a central venous line in place. Subclavian or femoral central venous access is preferred due to the potential for compromise of cerebral venous outflow with an internal jugular catheter. Central lines can be swapped out for a PICC line when appropriate.
Critical Care: Pulmonary
The purpose of mechanical ventilation in severe brain injury is to ensure adequate systemic and cerebral oxygenation, ventilation, and airway protection. The injured brain has increased metabolic demand resulting in an increased oxygen demand. Furthermore, hypoxemia (defined as a PaO2 of < 60mmHg or oxygen saturation of <90%) may lead to secondary injury to the brain, and a single episode of hypoxemia is associated with the two-fold increase in mortality in severe TBI. Thus, the recommendation for early intubation and effective oxygenation for the TBI patient is crucial for prevention of secondary brain injury.
Initial target in all severe TBI patients is normo-ventilation, recognizing that pH defines ventilatory status as driven by the medulla. ABGs will be obtained on every intubated patient daily and PRN. ICP control can be optimized by fine-tuning ventilator control.
-Maintenance of pH 7.35-7.45mmHg
-Maintenance of a PaO2 95-105mmHg (Goal 100mmHg)
-Maintenance of a PaCO2 35-45mmHg (Goal 40mmHg)
Aggressive hyperventilation to decrease ICP by decreasing cerebral blood volume via hypocapnic cerebral vasoconstriction worsens outcome after severe head trauma. Hyperventilation may be used as a temporizing measure to temporarily lower ICP in patients with evidence of acute brain herniation while the patient is being transported to CT, OR, or while other interventions such as ventriculostomy placement are being instituted. Target PaCO2 for signs of herniation is 25 mm Hg. If hyperventilation has been used, it will be withdrawn slowly in a stepwise fashion over 2-4 hours to avoid a rebound increase in ICP.
Initial ventilator settings will involve volume-controlled ventilation (AC) with PEEP of 5. Recognizing that patients set their own minute ventilation via their medullary respiratory drive, patients that exhibit neurogenic hyperventilation will be allowed to do so. Changing the mode of ventilation will not affect this and it is currently unclear if neurogenic hyperventilation is deleterious or compensatory. PEEP of < 10 cm H2O will be tolerated without concern for exacerbation of ICP. On an individual basis, the effect of PEEP on ICP will be considered.
Intubated patients will receive regular CXRs to assess ETT placement and assess pulmonary status. End-tidal CO2 (EtCO2) monitor will be placed on all intubated patients and/or patients with ICP monitoring. The goal EtCO2 is 1-5 points below pCO2 as determined by correlating the patient’s ABG. Patients will receive nebulizer treatments as indicated to assure effective ventilation.
Management of severe oxygenation/ventilation problems associated with ARDS (or other conditions) includes higher levels of PEEP, pulmonary recruitment maneuvers, aerosolized prostacyclin, use of neuromuscular blocking agents and/or prone positioning. Use of these therapies (as well as the order and combination) should be addressed in a multidisciplinary discussion weighing the risk/benefit at that particular time point in a patient’s disease progression.
Tracheostomy
Tracheostomy can speed liberation from mechanical ventilation and decrease risk of both pneumonia and ventilator-induced lung injury. TBI patients not deemed likely to improve rapidly should undergo tracheostomy within 8 days. There are no absolute contraindications, but relative contraindications to this procedure include active management of elevated intracranial pressure, hemodynamic instability, and severe respiratory failure.
Critical Care: Nutrition
Enteral feeding will be initiated as early as possible, preferably within 24 hours post-trauma. All patients will need a Nutrition consultation. Bearing in mind the increased metabolic demands of TBI, 140% of resting metabolism is the recommendation for most patients. In patients receiving neuromuscular blockade, 100% of resting metabolism is recommend. For patients who cannot receive enteral feeding, TPN will be initiated.
For patients with anterior skull base fractures, feeding should be via orogastric tube only. If nasal access is necessary, a feeding tube will only be placed under direct visualization by ENT. In patients with severe TBI, consideration should be given to early placement of a gastrostomy tube.
GI prophylaxis should be initiated upon admission. Either an H2 blocker (famotidine) or a PPI (omeprazole, pantoprazole) should be ordered. These will be continued at least until enteral feeding is started.
A bowel regimen will also be initiated within 24 hours of admission. This will consist of scheduled and as needed medications. Constipation may increase intraabdominal pressure and thus lead to increase in ICP.
Critical Care: Fluids
All infusions will be mixed in 0.9% NS, with Plasmalyte or other isotonic solutions as an alternative isotonic IV fluid. Volume resuscitation with 0.9%NS or blood (when appropriate) is preferred. Plasmalyte may be considered as an alternative resuscitation fluid, especially in patients with a metabolic acidosis. Hypotonic (lactated ringers) or D5-containing solutions should NOT be given to patients with acute brain injury. Euvolemia is the goal for all patients.
Critical Care: Infectious Disease
The patient with TBI has an increased susceptibility to infectious processes due to impaired consciousness, decreased mobility, prolonged ventilatory support, and multiple invasive procedures. The development of such infections leads to prolonged ICU and hospital stays. Commonly identified sources of infection include meningitis, pneumonia, and urinary tract infections. Patients who will undergo, or who have undergone an invasive cranial procedure will receive appropriate surgical prophylactic antibiotics. This will consist of a single dose of ancef for ventriculostomy placement, and 24 hours of post-operative ancef for craniotomy and craniectomy. Empiric antibiotics will not be used for prophylaxis against infection after ventriculostomy or other drain placement. If a patient has a documented penicillin allergy, an alternative antibiotic will be used as appropriate.
For patients with penetrating brain injuries, they will be treated with broad spectrum antibiotics for 7 days. This will consist of vancomycin and cefepime at CNS dosing. If the missile tract crosses an air sinus, add metronidazole to this regimen. If the patient undergoes craniotomy or craniectomy, this will be for a total of 7 days following surgery. If there is concern for meningitis, antibiotics may be continued beyond 7 days, or may be adjusted based on culture results. If there is concern for fungal or anaerobic infection, additional antibiotics will be added as indicated.
Critical Care: VTE Prophylaxis
Sequential compression devices (SCDs) will be the preferred method of VTE prophylaxis and will be initiated at time of admission. Initiation of low-molecular weight heparin or heparin will depend on the patient’s pathology and plans for surgical intervention. In general, if there is no plan for operative intervention, chemoprophylaxis may be initiated after two stable head CTs have been obtained. If the patient has undergone surgical intervention, or if intervention is planned, chemoprophylaxis can be initiated after 24 hours.
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