Intensive Care in Traumatic Brain Injury Including Multi-Modal Monitoring and Neuroprotection
Abstract
:1. Background
2. Pathological and Pathophysiological Features
3. Traumatic Brain Injury Is Not a Single Entity
4. Multimodal Monitoring and Treatment of Patients with Moderate to Severe TBI
4.1. Neurological Clinical Examination and Early Imaging
4.2. Intracranial Pressure and Cerebral Perfusion Pressure
4.2.1. Intracranial Pressure
4.2.2. Intracranial Pressure Guided “Traditional” Approach
4.2.3. Cerebral Perfusion Pressure Guided Therapy
4.2.4. Rationale for Cerebral Perfusion Pressure Directed Therapy in Traumatic Brain Injuries
- Prevention of ICP rises and maintenance of CPP by basic measures:
- Analgosedation;
- Normocapnic mechanical ventilation;
- Mean systolic arterial pressure of ≥100 mmHg;
- Maintenance of a cerebral perfusion pressure of 60–70 mmHg if autoregulation is preserved;
- Maintenance of a normal body temperature;
- Normoxemia;
- Enteral feeding,
- If ICP increases, active interventions might be warranted:
- Deepening analgosedation;
- Detection and treatment or exclusion of surgically accessible space occupying lesions with imaging;
- Drainage of cerebrospinal fluid (insertion of a ventricular catheter if ventricles are not already fully compressed; risk of infection);
- Increase of mean arterial pressure if autoregulation is preserved in order to reduce cerebral blood volume without compromising cerebral blood flow (risk of cardiovascular side effects, risk of promoting edema formation);
- Use of hyperosmolar solutions (NaCl 3–7.5% (HTS; hypertonic saline), Na–lactate 1100 mosm/L, Mannitol 20%;Hyperosmolar agents are effective in reducing ICP. What remains unanswered is whether these agents contribute toward better neurological outcomes; tiered, algorithmic approaches employed in many trials make it difficult to determine which therapy is beneficial or potentially harmful. Mannitol seems to be less effective than NaCl 7.5% and hypertonic Na–lactate in reducing brain swelling after head injury. Moreover, there is evidence that excessive administration of mannitol may be harmful, because mannitol might pass from the bloodstream into the brain, where it worsens brain edema and increases ICP (rebound edema). In contrast to NaCl 7.5%, mannitol does not improve tissue oxygenation [57]. While both osmolar agents increase cerebral blood flow, the magnitude of augmentation seems to be greater in HTS treatment and HTS seems to reduce the accumulation of extracellular excitatory amino acid (glutamate), thus preventing glutamine toxicity and neuronal damage [58]. However, there is no difference in neurologic outcome between the treatments at 6 months using the Glasgow outcome score [59]. In general, evidence for improved neurological outcome for all these interventions is still very limited, and they bear a risk of fluid overload including cardiovascular events and risks of osmotic diuresis, including dehydration [60].
- Aggressive treatment of refractory elevated intracranial pressure:
- Metabolic suppression (e.g., burst suppression targeted EEG-guided barbiturate coma). Lowers oxygen consumption of the brain by approximately 50% and thus decreases cerebral blood flow and cerebral blood volume, especially if autoregulation is preserved. No proof of improved outcome; risk of cardiovascular depression, risk of infections);
- Hypothermia (e.g., 34 °C; lowers oxygen consumption of the brain and thus cerebral blood flow and cerebral blood volume). Evidence comes mainly from animal experiments; there is no solid beneficial evidence in humans, but an elevated risk for cardiovascular compromise and infections. In a recent multicenter study, it could be shown that in patients with an intracranial pressure of more than 20 mmHg, therapeutic hypothermia plus standard of care to reduce intracranial pressure did not result in better outcomes than standard care alone [61]. Therefore, therapeutic hypothermia is not recommended by the newest guidelines [2];
- Decompressive craniectomy (DC) for selected cases only as DC is a last-resort treatment for severe refractory ICP, reducing ICP and mortality while increasing incidence of unfavorable outcome at six months [62];
- Hypnocapnic ventilation (rescue therapy only; high risk of cerebral ischemia).
4.2.5. Lund Concept: Background and Clinical Application
- Reduction of stress and brain metabolism by analgosedation with low-dose thiopental (0.5–3 mg/kg/h), use of beta-1-antagonist metoprolol, and use of alpha-2-agonist clonidine;
- Reduction of hydrostatic capillary pressure with metoprolol and clonidine;
- Maintenance of colloid-oncotic pressure, control of fluid balance with blood/albumin transfusions and use of furosemide.
- ICP <20–22 mmHg;
- CPP 50–70 mmHg.
4.3. Advanced Bedside Physiological Monitoring for Tailored Management of Cerebral Perfusion Pressure
4.3.1. Jugular Bulb Oximetry, Arteriovenous Difference in Lactate
4.3.2. Brain Tissue Partial Tension of Oxygen (PbtO2)
4.3.3. Cerebral Microdialysis
4.3.4. Clinical Use of Cerebral Microdialysis
4.3.5. Cerebral Microdialysis and Seizures, Cortical Spreading Depolarization
4.4. Assessment of Autoregulation
4.5. Simultaneous Multimodal Monitoring for Individualised Management
5. Specific Considerations in Traumatic Brain Injury in the Elderly
6. Conclusions
Funding
Conflicts of Interest
References
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Intervention | Effect | Pot. Benefit | Pot. Risk |
---|---|---|---|
(Deepening of) Analgosedation, Barbiturates | Decrease of brain metabolism and therefore oxygen consumption | Decrease in CBF, CBV and ICP | Adverse effects of long-term sedation, impaired neurological assessment |
Osmotherapy with Mannitol | Reduction in brain tissue volume, increase in CBF | Decreases ICP, no improvement of tissue oxygenation | Fluid overload, osmotic diuresis leading to hypovolemia, hyperosmolarity, rebound brain edema |
Osmotherapy with hypertonic saline | Reduction in brain tissue volume, increase in CBF | Decreases ICP, improvement of tissue oxygenation | Fluid overload, osmotic diuresis leading to hypovolemia, hyperosmolarity |
CSF drainage | Allows for expansion of brain tissue by reducing CSF volume | Lowers ICP | Transcerebral ventricular drainage required, risk of ventriculitis, meningitis |
Hyperventilation | Cerebral vasoconstriction leading to reduced CBV | Lowers ICP if autoregulation is intact | Reduction in CBF leading to brain tissue ischemia |
Decompressive craniectomy | Allows for expansion of the edematous brain | Decreases ICP, may improve tissue perfusion | Aggravation of brain edema, unfavorable outcome after 6 months |
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Stocker, R.A. Intensive Care in Traumatic Brain Injury Including Multi-Modal Monitoring and Neuroprotection. Med. Sci. 2019, 7, 37. https://doi.org/10.3390/medsci7030037
Stocker RA. Intensive Care in Traumatic Brain Injury Including Multi-Modal Monitoring and Neuroprotection. Medical Sciences. 2019; 7(3):37. https://doi.org/10.3390/medsci7030037
Chicago/Turabian StyleStocker, Reto A. 2019. "Intensive Care in Traumatic Brain Injury Including Multi-Modal Monitoring and Neuroprotection" Medical Sciences 7, no. 3: 37. https://doi.org/10.3390/medsci7030037
APA StyleStocker, R. A. (2019). Intensive Care in Traumatic Brain Injury Including Multi-Modal Monitoring and Neuroprotection. Medical Sciences, 7(3), 37. https://doi.org/10.3390/medsci7030037