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ICP Monitoring in TBI Dr Swapnil Pawar
TBI remains a major cause of death and disability worldwide. Poor outcome is associated in part with the primary insult and importantly from secondary brain injury, which is a complex series of pathologic events triggered in the early phase after TBI that then evolve over time. Apart from treating Primary pathology, modern TBI management focuses on the prevention, identification and management of SBI.
Neuromonitoring is central to SBI management. This includes serial clinical examination, imaging and the use of invasive and non-invasive devices that allow cerebral physiology to be assessed over time. Traditionally neuromonitoring has focussed on ICP monitoring which in turn used to quantify CPP.
What are the indications of ICP monitoring in ICU?
Earlier guidelines by the Brain Trauma Foundation and the American Association of Neurosurgeons (2007) suggested ICP monitoring in TBI with a Glasgow Coma Scale (GCS) score ≤8 with an abnormal CT showing evidence of mass effect due to hematomas, contusions, or swelling. They also suggested ICP monitoring in patients with severe TBI with a normal CT if two of the following were present: age >40 years, motor posturing, systolic blood pressure (BP) <90 mmHg. However, the current Brain Trauma Foundation (BTF) guidelines (2017) do not support these specific indications. They suggest ICP monitoring to guide the management of severe TBI, to reduce in-hospital and two-week mortality after injury. At a practical level, ICP monitoring would be helpful if sedation interruption to check neurological function is inappropriate, e.g., respiratory failure from lung contusions and flail chest and when the neurological examination may be unreliable, e.g., maxillofacial trauma or spinal cord injury. Cessation of sedation and neuromuscular blockade might lead to agitation, coughing etc., that may lead to an increase in the ICP.
2. What are the options available, relative advantages vs. disadvantages?
Currently, intraparenchymal pressure measurement using a strain gauge or a fibreoptic monitor or an intraventricular catheter using a ventriculostomy is preferred. The external ventricular drain was the first monitor to be tried out. The advantage of using an EVD is is that cerebrospinal fluid (CSF) can be drained and ICP reduced in case of intracranial hypertension. However, intraventricular catheters are difficult to insert if the brain is swollen and the ventricles are squashed. Infections are relatively common (20%), with the incidence directly related to the duration of insertion. Hemorrhage can occur during insertion. Intra-parenchymal monitors are relatively easy to insert, as the presence of brain swelling or small-sized ventricles does not affect insertion. The incidence of infection and haemorrhage are less than with intraventricular catheters. Besides, blockage by hemorrhage or debris does not happen. Intraparenchymal devices may become inaccurate over several days; recalibration is not possible after insertion.
In the presence of hydrocephalus, however, an EVD is preferred because it can also be used for treatment.
Transcranial doppler with measurement of the pulsatility index and optic nerve sheath diameter are non-invasive methods to measure the ICP.
Besides catheter-related harm, aggressive interventions to normalize ICP, including the excessive use of mannitol and hypertonic saline in elderly patients, with compromised cardiovascular and renal function, may lead to harm. Decompressive craniectomy aimed at alleviating intracranial hypertension may also lead to poor functional outcomes in patients with TBI. Although ICP monitoring is recommended by the Brain Trauma Foundation guidelines, in the Trauma Quality Improvement Program database study that included 13,188 patients, only 11.5% of eligible patients underwent ICP monitoring.
As I mentioned before the aim for neuromonitoring is to prevent SBI caused by ischemia, hypoxia and cellular dysfunction. Current TBI management is mainly based on ICP and CPP monitoring, as it helps us to predict cerebral autoregulation in a very primitive way. However, after TBI, there is great heterogeneity in the autoregulatory capacity. In addition, it helps us to predict macro-vascular dysfunction and there is growing evidence to suggest that microvascular dysfunction such as diffusion abnormalities rather perfusion abnormalities, alteration of glucose utilisation or mitochondrial dysfunction all of which can not be predicted with ICP or CPP monitoring.
The current consensus is to treat ICP greater than 22 mmHg which is mainly based on our understanding of Munro-Kelly doctrine. However, this is an oversimplification as cellular dysfunction or brain hypoxia can occur even with normal ICP. There is growing evidence that ICP may be better managed when considered in the setting of compliance, ICP waveform morphology, cerebral autoregulation and brain metabolism. And I guess we need to switch to the multi-modal approach of neuromonitoring rather than relying on the single number displayed on the monitor. However, the use of other monitoring devices is often more expensive and need expertise, which limits its generalisability.
4) What’s the evidence out there either in favour of or against the routine use of ICP monitoring in patients with TBI
ICP monitoring is commonly used to titrate interventions including osmotherapy, optimize sedation and ventilator management, and for decision making regarding surgical intervention such as decompressive craniectomy. Most of the information available regarding the efficacy of ICP monitoring and its impact on clinical outcomes is based on observational studies.
The relationship between ICP monitoring and mortality was evaluated among centres participating in the American College of Surgeons Trauma Quality Improvement Program (TQIP). After adjustment for possible confounders, mortality was significantly lower in patients who underwent ICP-guided management. Besides, centres that performed ICP monitoring more often revealed lower mortality. A 2-year observational study was performed in patients with severe TBI (GCS of 8 or less) from 14 trauma centers in the US. In-hospital mortality was evaluated after adjusting for confounders using propensity score matching. On both unadjusted and propensity-matched analysis, ICP-based care resulted in a significantly lower in-hospital mortality compared to patients who did not receive ICP monitoring.
However, other studies have revealed conflicting results. In a two-centre Dutch study, one of the study centres used therapeutic interventions based on clinical features and computed tomography (CT) findings. The other study centre utilized interventions to maintain an ICP of less than 20 mm Hg and CPP of more than 70 mm Hg. The Glasgow outcome score was used to assess functional outcomes after 12 months. After adjustment for confounders, there was no difference in functional outcomes between centers. The median duration of ventilator support was significantly lower among patients who did not undergo ICP-based management. A large US National Trauma Databank (NTDB) study compared patients with TBI who underwent ICP monitoring with those who did not. Patients with blunt TBI with a GCS of 8 or less, with an abnormal brain CT scan, and ICU stay of 3 days or more were included. On multivariate analysis, after adjustment for possible confounders, ICP monitoring resulted in a 45% reduction in survival.
In a study based on the Trauma Quality Improvement Program (TQIP) database, the investigators assessed compliance with the BTF guidelines for ICP monitoring and the impact of ICP monitoring on clinical outcomes. The study included patients with isolated TBI with a GCS of less than 9 and a score of 3 or more on the head Abbreviated Injury Scale (AIS). This study included 13,188 patients. ICP monitoring was carried out only in 11.5% of eligible patients. Overall, no mortality benefit was discernible among patients who underwent ICP monitoring. Placement of an ICP monitor was an independent predictor of overall complications, infectious complications, and was associated with poor functional outcomes. In the subgroup of patients with the most severe injuries according to the AIS, ICP monitoring was an independent predictor of mortality.
The only randomized controlled trial comparing ICP-based vs. clinical assessment and imaging-based management was conducted in 324 patients who had suffered severe TBI. The study was conducted across six centers in Bolivia and Ecuador. The composite primary outcome included the duration of survival, the level and duration of impairment of conscious level, the functional status at 3 and 6 months, and the neuropsychological state at 6 months. There was no significant difference in the composite primary outcome between groups. The 6-month mortality and the median duration of ICU stay were also similar in both groups. The duration of cerebral protective therapy was longer in the clinical assessment and imaging-based group; the incidence of adverse events was similar in both groups. Thus, ICP-guided management of severe TBI was not superior to clinical assessment and imaging-based management in this study. This study has evoked intense debate and may need to be interpreted against the background of a clinical setting in which ICP monitoring may not be the standard of care.
I agree..BEST-TRIp was controversial in many regards. The important thing to realise that it was not the trial of ICP monitoring or trial testing the efficacy of ICP monitoring. Indeed it was a trail of two management strategies for TBI. It has definitely challenged our complacency about ICP monitoring but clearly it failed to change the practices due to its limitations and lack of external validity.
There is another study in JAMA Pediatrics published in 2017, which looked at functional outcomes after ICP monitoring in children with severe TBI. They analysed two large databases in the US and studied 3084 children out of which only 1002 underwent ICP monitoring. Ad there was no difference in functional survival between these groups.
Another important publication is from Centre-TBI, the group led by Prof David Menon and his team. In the study published by his group in J Neurosurgical Anaesthesia this year, they highlighted a very important point. The key finding is that each patient with TBI has individual specific ICP threshold which can be predicted using the relationship between pressure reactivity index and ICP. And more importantly, mean hourly dose of ICP above individual threshold has stronger correlation with mortality compared with BTF threshold of 20 or 22 mm Hg. And that’s why personalised medicine is more important than using one size fits all approach.
5) What’s your current practice
· We rely on serial CT imaging and clinical examination in most situations.
· We use ultrasonography to measure the optic nerve sheath diameter to monitor ICP. There is ongoing debate regarding absolute values; however, an increase in the ONSD compared to baseline would call for CT imaging without delay.
· Intraventricular catheters are preferred if the ventricles are accessible; intraparenchymal catheters are used less often.
That’s interesting. We rely heavily on ICP monitoring mainly EVDs here in Australia and it’s too early to discard ICP monitoring completely. However, I strongly believe that we need to adopt multi-modal approach in order to identify individual ICP thresholds so as to offer specific treatment measures. Also, its important to identify different phenotypes within TBI, similar to ARDS in order to develop better prognostication models.
· Aiolfi A, Benjamin E, Khor D, Inaba K, Lam L, Demetriades D. Brain Trauma Foundation Guidelines for Intracranial Pressure Monitoring: Compliance and Effect on Outcome. World J Surg. 2017;41(6):1543-1549. doi:10.1007/s00268-017-3898-6
· Alali AS, Fowler RA, Mainprize TG, et al. Intracranial pressure monitoring in severe traumatic brain injury: results from the American College of Surgeons Trauma Quality Improvement Program. J Neurotrauma. 2013;30(20):1737-1746. doi:10.1089/neu.2012.2802
· Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2012;367(26):2471-2481. doi:10.1056/NEJMoa12073637
· Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364(16):1493-1502. doi:10.1056/NEJMoa1102077
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· Dawes AJ, Sacks GD, Cryer HG, et al. Intracranial pressure monitoring and inpatient mortality in severe traumatic brain injury: A propensity score-matched analysis. J Trauma Acute Care Surg. 2015;78(3):492-501; discussion 501-502. doi:10.1097/TA.0000000000000559
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· Lundberg N, Troupp H, Lorin H. Continuous Recording of the Ventricular-Fluid Pressure in Patients with Severe Acute Traumatic Brain Injury. J Neurosurg. 1965;22(6):581-590. doi:10.3171/jns.1965.22.6.0581
· Miller JD, Becker DP, Ward JD, Sullivan HG, Adams WE, Rosner MJ. Significance of intracranial hypertension in severe head injury. J Neurosurg. 1977;47(4):503-516. doi:10.3171/jns.1977.47.4.0503
· Shafi S, Diaz-Arrastia R, Madden C, Gentilello L. Intracranial pressure monitoring in brain-injured patients is associated with worsening of survival. J Trauma. 2008;64(2):335-340. doi:10.1097/TA.0b013e31815dd01
Dr Swapnil Pawar November 24, 2019
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