Intensive Care and Multimodal Monitoring in Traumatic Brain Injury (TBI)

Intensive Care and Multimodal Monitoring in Traumatic Brain Injury

• Traumatic brain injury (TBI) is a major cause of death and disability worldwide, affecting people of all ages, but increasingly affecting the elderly due to falls.

• TBI produces various lesions ranging from mild to devastating injury, which can progress over time and require specialist care in an ICU.

• Secondary injuries, caused by factors such as hypoxia and hypotension, can exacerbate primary injuries and worsen outcomes.

• Multimodal monitoring, including neurological examination, imaging, and other measures, is required to prevent secondary brain injury and optimize conditions for recovery and rehabilitation.

• TBI is not a single entity, and individualized treatment approaches based on monitoring and imaging findings, as well as pre-injury comorbidities and treatments, are necessary.

• The pathophysiology of TBI involves primary and delayed secondary injuries, including axonal injury, cerebral edema, and inflammation, which can lead to structural failure and serious disability or mortality.

• Hemorrhagic progression of a contusion (HPC) can occur in tissues with unrecoverable loss of function and is one of the most severe types of secondary injury encountered after TBI.

• Patients with severe TBI require specialized neurointensive care in the ICU, including fluid optimization, vasoactive and catecholaminergic agents, artificial ventilation, temperature control, infection control, and early enteral feeding.

• The ICU team includes intensivists, neurosurgeons, neurologists, nurses, physiotherapists, and rehabilitation specialists.

• Clinical examination remains a fundamental monitoring procedure, even in patients who undergo imaging, and is necessary for tracking recovery and assessing response to treatment.

• Age-related comorbidities and reduced physiological reserves can increase the risk of secondary brain damage and worsen outcomes in older patients with TBI.

• Multimodal monitoring and individualized treatment approaches are necessary to prevent secondary brain injury, maintain cerebral homoeostasis, and preserve rehabilitation potential in patients with TBI.Neuromonitoring and Intracranial Pressure Management in Traumatic Brain Injury

• Neurological evaluation in sedated TBI patients requires interruption of sedation, which may cause deterioration and is not without risk.

• Motor response is the most robust and important part of Glasgow Coma Scale (GCS) evaluation.

• Pupillary diameter and reactivity assessments are crucial in TBI patients, and automated pupillometry can improve accuracy.

• More than 40% of TBI patients show substantial worsening within the first 48 hours, indicating the need for immediate medical or surgical intervention.

• Intracranial pressure (ICP) monitoring using subdural or intraparenchymal probes or ventricular catheters is indicated in patients with severe TBI (GCS ≤8).

• Critical ICP thresholds may vary between young and old and male and female patients, with older patients and females having lower thresholds for prediction of poor outcome.

• The traditional approach to treat elevated ICP with head elevation, sedation, active treatment of systemic hypertension, neuromuscular blockade, cerebrospinal fluid drainage, osmotherapy, hyperventilation, and barbiturates has mainly been abandoned due to its detrimental effects.

• Cerebral perfusion pressure (CPP) is important in maintaining optimal cerebral blood flow (CBF) in TBI patients.

• The goal of CPP management is to preserve the ischemic penumbra and avoid exacerbation of secondary insults.

• The critical threshold for CPP lies between 50 and 60 mmHg, and brain monitoring techniques such as jugular venous oximetry, monitoring of brain tissue oxygen tension, and cerebral microdialysis can provide complementary and specific information.

• CPP-targeted treatment includes prevention of ICP rises and maintenance of CPP by basic measures, such as analgosedation, normocapnic mechanical ventilation, normovolemia, and normoxemia.

• If ICP increases, active interventions might be warranted, such as deepening analgosedation, detection and treatment of surgically accessible space occupying lesions, drainage of cerebrospinal fluid, and increase of mean arterial pressure.Advanced Management Strategies for Traumatic Brain Injury

• Hyperosmolar agents such as hypertonic saline, Na-lactate, and Mannitol are effective in reducing intracranial pressure (ICP), but their contribution towards better neurological outcomes remains unclear.

• Mannitol is less effective than hypertonic saline and NaCl 7.5% in reducing brain swelling after head injury and may worsen brain edema and increase ICP if excessively administered.

• Hypertonic saline seems to reduce the accumulation of excitatory amino acid (glutamate) and prevent glutamine toxicity and neuronal damage.

• Aggressive treatments for refractory elevated ICP include metabolic suppression, hypothermia, decompressive craniectomy, and hypnocapnic ventilation, but evidence for improved neurological outcomes is limited and carries risks of cardiovascular events and osmotic diuresis.

• The Lund concept is a therapeutic approach that focuses on reducing ICP by decreasing intracranial volumes, achieved through a flat head position, sedation, strict control of systemic hypertension, and other measures.

• The Lund concept's goals are to preserve a normal colloid osmotic pressure, reduce capillary hydrostatic pressure, and reduce cerebral blood volume.

• The Lund concept has limited evidence of superiority compared to other treatments and contradicts the common treatment goal of cerebral blood flow optimization.

• Advanced bedside physiological monitoring techniques include jugular bulb oximetry, brain tissue partial tension of oxygen, and microdialysis, which provide indirect information about pathological processes with several limitations.

• Continuous monitoring of SjVO2 allows for estimation of the balance between global cerebral oxygen delivery and utilization and reflects cerebral oxygen deficit.

• Abnormal SjVO2 can be managed with hypertonic saline, sedation, and other measures.

• Brain tissue partial tension of oxygen (PbtO2) provides a continuous measurement of extracellular oxygen tension as an indicator of the adequacy of oxygen delivery and consumption.

• A multimodal approach using various monitoring techniques and individualized targets may allow for better-tailored therapies and improved outcomes for traumatic brain injury patients.Monitoring and Assessment of Cerebral Oxygenation and Metabolism in Traumatic Brain Injury

• PbtO2 is typically in the range of 35-50 mmHg, and values below 20 mmHg indicate inadequate oxygen supply and are associated with worse outcomes in TBI.

• Oxygen diffusion in pericontusional tissue is affected not only by tissue and endothelial edema but also by microvascular collapse, which increases the mean intercapillary distance for diffusion, reducing average oxygen tension.

• Defining adequate target values for PbtO2 is difficult due to modulation by oxygen diffusion, and approaches to return PbtO2 to normal levels include increasing arterial pressure and arterial oxygen tension.

• PbtO2 increases with CPP after TBI, and the increase in PbtO2 relative to an increase in arterial PO2 is termed brain tissue oxygen reactivity.

• Manipulation of PbtO2 by increasing PO2 or altering the CPP have been investigated with the view to therapy optimization and potential prognostication, but studies have shown mixed results regarding the relationship between CPP and PbtO2.

• Microdialysis enables analysis of extracellular/interstitial biochemical changes in glucose, lactate, pyruvate, glycerol, and glutamate, and a high lactate:pyruvate ratio (LPR) is a marker of ischemia and/or diffusion hypoxia.

• CMD can be used to determine the optimal level of CPP in patients with TBI, and ischemia is defined by the combined criteria of LPR > 40 and glucose < 0.2 mmol/L.

• CMD analyses can reveal alarming levels of LPR and glucose, and changes in LPR may precede the onset of intracranial hypertension.

• Posttraumatic seizures affect 22% of patients with TBI and are associated with greater and prolonged intracranial hypertension and an increased mortality rate, and CMD allows for detection of LPR, glutamate, and glycerol increase when electrographic seizures occur.

• Cortical spreading depolarization (CSD) occurs in 50% of patients with severe TBI and is an important cause of early ischemia in TBI and SAH patients, and marked glucose depletion occurs during CSD in proportion to the number of depolarizations.

• Autoregulation is a physiological mechanism that maintains adequate cerebral perfusion in the presence of blood pressure changes, and the CPP for which the PRx is a minimum represents a state of optimum autoregulation.

• In severe TBI, autoregulation can be impaired or totally lost, and alternative measures based on assessment of blood flow or brain tissue oxygen reactivity may be needed for regional assessment.

• Simultaneous monitoring of multiple cerebral parameters, including PbtO2, CMD, and autoregulation, may provide a more comprehensive understanding of cerebral oxygenation and metabolism in TBI and help guide

Intensive Care in Traumatic Brain Injury: Multi-Modal Monitoring and Neuroprotection

• Traumatic brain injury (TBI) is a major cause of death and disability worldwide, affecting people of all ages.

• TBI produces various lesions ranging from mild to devastating injury, with secondary injuries worsening the primary injury over time.

• Treatment of TBI requires a multidisciplinary team, including intensivists, neurosurgeons, neurologists, and skilled nurses, among others.

• Individual and tailored treatment approaches are necessary, based on monitoring and findings in imaging, respecting pre-injury comorbidities and their therapies.

• Age-related comorbidities increase the risk of disability and mortality, especially in older patients who suffer from low-energy impacts.

• Multimodal monitoring and treatment in the ICU aim to prevent secondary brain injury, maintain cerebral homoeostasis, and preserve rehabilitation potential.

• Clinical examination remains a fundamental monitoring procedure, even in patients who undergo imaging.

• Imaging techniques, such as CT and MRI, are used to diagnose and monitor TBI, with MRI being more sensitive in detecting subtle lesions.

• Hemorrhagic progression of a contusion (HPC) is one of the most severe types of secondary injury encountered following TBI and involves delayed, progressive microvascular failure in the region of injury.

• Treatment guidelines frequently applied to all patients are usually derived from cohort studies but ignore differences in underlying pathological features and the influence of pre-injury conditions.

• Neuroprotection strategies, such as hypothermia, hyperbaric oxygen therapy, and pharmacological interventions, aim to reduce secondary brain injury and improve outcomes.

• Rehabilitation strategies, such as early mobilization, cognitive stimulation, and physical therapy, aim to optimize frame conditions for recovery and early rehabilitation.Neurological Evaluation and Management of Traumatic Brain Injury

• Neurological evaluation of TBI patients relies on GCS assessment, investigation of pupil diameter and reactivity to light.

• GCS assessment performed on the site of the accident may overestimate degree of disturbance of consciousness.

• Motor response is the most important part of GCS evaluation in TBI patients who are comatose or sedated.

• Wake-up test may help to identify important clinical changes in deeply sedated patients.

• Assessments of pupillary diameter and reactivity are crucial in identifying neurological deterioration.

• More than 40% of TBI patients show substantial worsening during the first 48 hours in the ICU, significantly associated with high ICP and poor outcome.

• Intracranial pressure (ICP) monitoring has been the cornerstone of TBI care since the 1980s.

• Available data suggest that critical ICP thresholds may vary between young and old and male and female patients.

• Three main strategies proposed by the scientific community for ICP therapy are traditional approach, Rosner concept, and Lund concept.

• Maintenance of cerebral perfusion pressure (CPP) is important to meet the metabolic needs of the injured brain.

• A CPP above 70 mmHg should be avoided, as it is associated with five times greater risk of acute respiratory distress syndrome (ARDS).

• CPP-targeted treatment concept includes prevention of ICP rises and maintenance of CPP, and active interventions if ICP increases.Advanced Management of Elevated Intracranial Pressure in Traumatic Brain Injury

• Hyperosmolar agents (such as hypertonic saline, Na-lactate, and mannitol) are effective in reducing intracranial pressure (ICP) but their contribution to better neurological outcomes is unclear.

• Mannitol is less effective than hypertonic saline and may cause rebound edema and worsen brain edema.

• Hypertonic saline reduces the accumulation of extracellular excitatory amino acid (glutamate) and improves tissue oxygenation.

• Aggressive treatments for refractory elevated ICP include metabolic suppression, hypothermia, decompressive craniectomy, and hypnocapnic ventilation.

• The Lund concept focuses on reducing ICP by decreasing intracranial volumes through a reduction in microvascular pressures.

• The goals of the Lund concept are to preserve a normal colloid osmotic pressure, reduce capillary hydrostatic pressure, and reduce cerebral blood volume.

• The Lund concept includes analgosedation with low-dose thiopental, use of beta-1-antagonist metoprolol, and use of alpha-2-agonist clonidine, among other interventions.

• The Lund concept has limited evidence of superiority compared to a cerebral perfusion pressure (CPP)-targeted protocol and has several controversial issues.

• Advanced bedside physiological monitoring using techniques such as jugular bulb oximetry, brain tissue partial tension of oxygen (PbtO2), and microdialysis can allow for individual targeted interventions.

• SjVO2 (jugular bulb oximetry) allows for estimation of the balance between global cerebral oxygen delivery and utilization and reflects cerebral oxygen deficit.

• Brain tissue PbtO2 provides a continuous measurement of extracellular oxygen tension as an indicator of the adequacy of oxygen delivery and consumption.

• A proposed algorithm for managing abnormal SjVO2 includes interventions such as hypertonic saline, increasing CPP, and improving oxygen delivery. However, SjVO2 measurement is not frequently used in clinical routine.Assessing Brain Injury: Techniques and Considerations

• PbtO2 range is 35-50 mmHg, with ischemic thresholds between 5-20 mmHg.

• Reduced PbtO2 is associated with poor neurotrauma outcomes and is modulated by oxygen diffusion affected by tissue and endothelial edema and microvascular collapse.

• Defining adequate target values for PbtO2 is difficult, but values below 20 mmHg are typically accepted as thresholds for inadequate oxygen supply in TBI.

• Therapeutic approaches to return PbtO2 to normal levels include increasing arterial pressure, arterial oxygen tension, and/or carbon dioxide partial pressure to enhance CBF.

• PbtO2-directed therapy has led to improved outcomes, but CPP and ICP are not surrogates for PbtO2 and evidence for guided therapy using brain tissue oxygenation in addition to ICP and CPP monitoring is increasing.

• Cerebral microdialysis (CMD) enables online analysis of extracellular/interstitial biochemical changes in glucose, lactate, pyruvate, glycerol, and glutamate.

• High lactate:pyruvate ratio is a marker of ischemia and/or diffusion hypoxia and is an independent predictor of mortality.

• CMD can be used to determine optimal CPP levels, and ischemia is defined as LPR > 40 and glucose < 0.2 mmol/L.

• Changes in LPR may precede the onset of intracranial hypertension, and low PbtO2 and high LPR are associated with high ICP and low CPP.

• CMD has shown increased glutamate after TBI, which may lead to cellular swelling and increased ICP.

• CMD allows for detection of electrographic seizures, and high LPR persists longer and occurs more frequently in patients with electrographic seizures.

• Autoregulation can be assessed through the pressure-reactivity index (PRx), with the CPP for which the PRx is a minimum representing a state of optimum autoregulation. Prospective evidence from clinical studies is needed.

Intensive Care in Traumatic Brain Injury: Multi-Modal Monitoring and Neuroprotection

• Traumatic brain injury (TBI) is a major cause of death and disability worldwide, affecting people of all ages.

• TBI produces various lesions ranging from mild to devastating injury, with secondary injuries worsening the primary injury over time.

• Treatment of TBI requires a multidisciplinary team, including intensivists, neurosurgeons, neurologists, and skilled nurses, among others.

• Individual and tailored treatment approaches are necessary, based on monitoring and findings in imaging, respecting pre-injury comorbidities and their therapies.

• Age-related comorbidities increase the risk of disability and mortality, especially in older patients who suffer from low-energy impacts.

• Multimodal monitoring and treatment in the ICU aim to prevent secondary brain injury, maintain cerebral homoeostasis, and preserve rehabilitation potential.

• Clinical examination remains a fundamental monitoring procedure, even in patients who undergo imaging.

• Imaging techniques, such as CT and MRI, are used to diagnose and monitor TBI, with MRI being more sensitive in detecting subtle lesions.

• Hemorrhagic progression of a contusion (HPC) is one of the most severe types of secondary injury encountered following TBI and involves delayed, progressive microvascular failure in the region of injury.

• Treatment guidelines frequently applied to all patients are usually derived from cohort studies but ignore differences in underlying pathological features and the influence of pre-injury conditions.

• Neuroprotection strategies, such as hypothermia, hyperbaric oxygen therapy, and pharmacological interventions, aim to reduce secondary brain injury and improve outcomes.

• Rehabilitation strategies, such as early mobilization, cognitive stimulation, and physical therapy, aim to optimize frame conditions for recovery and early rehabilitation.Neurological Evaluation and Management of Traumatic Brain Injury

• Neurological evaluation of TBI patients relies on GCS assessment, investigation of pupil diameter and reactivity to light.

• GCS assessment performed on the site of the accident may overestimate degree of disturbance of consciousness.

• Motor response is the most important part of GCS evaluation in TBI patients who are comatose or sedated.

• Wake-up test may help to identify important clinical changes in deeply sedated patients.

• Assessments of pupillary diameter and reactivity are crucial in identifying neurological deterioration.

• More than 40% of TBI patients show substantial worsening during the first 48 hours in the ICU, significantly associated with high ICP and poor outcome.

• Intracranial pressure (ICP) monitoring has been the cornerstone of TBI care since the 1980s.

• Available data suggest that critical ICP thresholds may vary between young and old and male and female patients.

• Three main strategies proposed by the scientific community for ICP therapy are traditional approach, Rosner concept, and Lund concept.

• Maintenance of cerebral perfusion pressure (CPP) is important to meet the metabolic needs of the injured brain.

• A CPP above 70 mmHg should be avoided, as it is associated with five times greater risk of acute respiratory distress syndrome (ARDS).

• CPP-targeted treatment concept includes prevention of ICP rises and maintenance of CPP, and active interventions if ICP increases.Advanced Management of Elevated Intracranial Pressure in Traumatic Brain Injury

• Hyperosmolar agents (such as hypertonic saline, Na-lactate, and mannitol) are effective in reducing intracranial pressure (ICP) but their contribution to better neurological outcomes is unclear.

• Mannitol is less effective than hypertonic saline and may cause rebound edema and worsen brain edema.

• Hypertonic saline reduces the accumulation of extracellular excitatory amino acid (glutamate) and improves tissue oxygenation.

• Aggressive treatments for refractory elevated ICP include metabolic suppression, hypothermia, decompressive craniectomy, and hypnocapnic ventilation.

• The Lund concept focuses on reducing ICP by decreasing intracranial volumes through a reduction in microvascular pressures.

• The goals of the Lund concept are to preserve a normal colloid osmotic pressure, reduce capillary hydrostatic pressure, and reduce cerebral blood volume.

• The Lund concept includes analgosedation with low-dose thiopental, use of beta-1-antagonist metoprolol, and use of alpha-2-agonist clonidine, among other interventions.

• The Lund concept has limited evidence of superiority compared to a cerebral perfusion pressure (CPP)-targeted protocol and has several controversial issues.

• Advanced bedside physiological monitoring using techniques such as jugular bulb oximetry, brain tissue partial tension of oxygen (PbtO2), and microdialysis can allow for individual targeted interventions.

• SjVO2 (jugular bulb oximetry) allows for estimation of the balance between global cerebral oxygen delivery and utilization and reflects cerebral oxygen deficit.

• Brain tissue PbtO2 provides a continuous measurement of extracellular oxygen tension as an indicator of the adequacy of oxygen delivery and consumption.

• A proposed algorithm for managing abnormal SjVO2 includes interventions such as hypertonic saline, increasing CPP, and improving oxygen delivery. However, SjVO2 measurement is not frequently used in clinical routine.Assessing Brain Injury: Techniques and Considerations

• PbtO2 range is 35-50 mmHg, with ischemic thresholds between 5-20 mmHg.

• Reduced PbtO2 is associated with poor neurotrauma outcomes and is modulated by oxygen diffusion affected by tissue and endothelial edema and microvascular collapse.

• Defining adequate target values for PbtO2 is difficult, but values below 20 mmHg are typically accepted as thresholds for inadequate oxygen supply in TBI.

• Therapeutic approaches to return PbtO2 to normal levels include increasing arterial pressure, arterial oxygen tension, and/or carbon dioxide partial pressure to enhance CBF.

• PbtO2-directed therapy has led to improved outcomes, but CPP and ICP are not surrogates for PbtO2 and evidence for guided therapy using brain tissue oxygenation in addition to ICP and CPP monitoring is increasing.

• Cerebral microdialysis (CMD) enables online analysis of extracellular/interstitial biochemical changes in glucose, lactate, pyruvate, glycerol, and glutamate.

• High lactate:pyruvate ratio is a marker of ischemia and/or diffusion hypoxia and is an independent predictor of mortality.

• CMD can be used to determine optimal CPP levels, and ischemia is defined as LPR > 40 and glucose < 0.2 mmol/L.

• Changes in LPR may precede the onset of intracranial hypertension, and low PbtO2 and high LPR are associated with high ICP and low CPP.

• CMD has shown increased glutamate after TBI, which may lead to cellular swelling and increased ICP.

• CMD allows for detection of electrographic seizures, and high LPR persists longer and occurs more frequently in patients with electrographic seizures.

• Autoregulation can be assessed through the pressure-reactivity index (PRx), with the CPP for which the PRx is a minimum representing a state of optimum autoregulation. Prospective evidence from clinical studies is needed.