The Neurointensive Care Unit: Intracranial Pressure and Cerebral Oxygenation

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The Neurointensive Care Unit: Intracranial Pressure and Cerebral Oxygenation


Brandon A. Francis and Matthew B. Maas


GENERAL PRINCIPLES


Once a traumatic brain injury (TBI) occurs, little can be done to reverse the initial injury. The main aim of TBI management therefore focuses on minimizing secondary injury.


Secondary Brain Injury


Cerebral Vasospasm


While aneurysmal subarachnoid hemorrhage (aSAH) is the prototypic disease associated with vasospasm, the same process can occur in TBI if there is sufficient blood coating the vessels in the circle of Willis. TBI causes endothelial damage and extravasation of blood which, through a variety of mechanisms, irritates the blood vessels themselves leading to vasospasm [1]. Vasospasm can lead to downstream ischemia.


Secondary Brain Ischemia


Cerebral ischemia can occur whenever cerebral oxygen demand exceeds oxygen supply. This metabolic mismatch can occur following a TBI due to a cascade of events, including release of inflammatory cytokines, vascular abnormalities, changes in neuronal metabolism, and susceptibility to infection. These mechanisms may be related to systemic changes, intracranial changes, or both. No pharmacologic agent has proven effective at reducing secondary ischemic injury in this population [2].


Brain Compression


Intracranial pressure (ICP) values are often conceptualized as a whole brain measurement, but in reality there are regional variations and gradients of ICP. One common area for these regional variations would be the posterior fossa, where large changes in ICP locally may not be accurately captured by frontally placed bolts or external ventricular drains (EVDs). This is most apparent when one considers that herniation syndromes can occur in the setting of apparently normal ICP values. When ICP is high and compensatory mechanisms have been exhausted, herniation can occur. Emergently, herniation syndromes may be managed by providing an alternative path for the excess pressure (such as EVDs or surgical decompression), by decreasing the available fluid in the intracellular space (hyperosmolar therapy), or by decreasing cerebral blood flow (hyperventilation and hemodynamic parameter manipulation). If left untreated, acute herniation syndromes can be fatal [3].


Mechanisms of TBI Morbidity


Nosocomial Infection


Patients with TBI are considered to be at increased risk of nosocomial infections compared to general surgical patients and other types of neurosurgical patients, most commonly ventilator associated pneumonia (8.4%), surgical site infections (4.25%), and meningitis (2%) [4].


Cardiac Instability


Stress induced cardiomyopathy, or Takotsubo cardiomyopathy, is common in TBI patients [5]. The mechanism is not fully understood but appears to be related to catecholamine elaboration following brain injury. Cardiac instability may manifest as arrhythmias, diastolic or systolic heart failure, autonomic dysfunction, or pulmonary hypertension.


Seizures


Seizures are common in patients with TBI [6]. In one cohort of 94 patients, 22% of TBI patients had seizures, 52% of which had nonconvulsive seizures that were only appreciated on electroencephalography (EEG).


Pathophysiology of Cerebral Perfusion (How Are Cerebral Vasospasm, Secondary Brain Ischemia, and Brain Compression Linked?)


The intracranial compartment is composed of the following components: blood, cerebrospinal fluid (CSF), and brain parenchyma. The Monro-Kellie hypothesis states that the volume inside the skull is fixed, so that if there is an increase in the volume of any of the components, there must be a decrease in volume of another component [7]. For example, CSF may be shunted into the spinal canal in the setting of a brain mass. Once the compensatory abilities are overwhelmed, pressure in the intracranial cavity will rise rapidly. The relationship between the change in pressure (ICP) and the change in volume can be conceptualized by the cerebral compliance curve [8] (Figure 23.1).


Cerebral perfusion pressure (CPP; CPP = mean arterial pressure [MAP]—ICP) is the pressure gradient driving blood into the brain [1]. If CPP is too low, the brain can become ischemic. When cerebral autoregulation is intact, blood vessels will constrict or dilate in order to keep cerebral blood flow constant. After TBI, cerebral autoregulation is often dysfunctional, so ICP measurement is often utilized to accurately determine CPP and prevent cerebral ischemia. Hypercapnia strongly stimulates cerebral vasodilation and an increase in cerebral blood flow. Conversely, hypocapnia (hyperventilation) leads to cerebral vasoconstriction. If the hyperventilation is prolonged or severe, it can lead to cerebral ischemia, which ultimately can worsen neurologic outcomes [9].


Frequent causes of elevated ICP in TBI are impaired autoregulation, diffuse cerebral edema, focal brain contusion, intracerebral hemorrhage, epidural hematoma or subdural hematoma, hydrocephalus, and venous sinus thrombosis. Additionally, if there is associated intraventricular hemorrhage (IVH), obstructive hydrocephalus may develop and may present another cause of elevated ICP.


Image


FIGURE 23.1    Cerebral compliance curve. In a simple model, pulse amplitude of intracranial pressure (ICP) (expressed along the y-axis on the right side of the panel) results from pulsatile changes in cerebral blood volume (expressed along the x-axis) transformed by the pressure–volume curve. This curve has three zones: a flat zone, expressing good compensatory reserve, an exponential zone, depicting poor compensatory reserve, and a flat zone again, seen at very high ICP (above the “critical” ICP) depicting derangement of normal cerebrovascular responses. The pulse amplitude of ICP is low and does not depend on mean ICP in the first zone. The pulse amplitude increases linearly with mean ICP in the zone of poor compensatory reserve. In the third zone, the pulse amplitude starts to decrease with rising ICP. RAP, index of compensatory reserve. Source: From Ref. [8]. Czosnyka M, Pickard JD. Monitoring and interpretation of intracranial pressure. J Neurol Neurosurg Psychiatry. 2004;75:813-821. Used with permission from BMJ Publishing Group Ltd.


DIAGNOSIS AND MONITORING


Clinical Presentation of Elevated ICP


Initial presentation is variable but can include agitation, somnolence, confusion, vomiting, unilaterally or bilaterally dilated pupils, sluggish or absent reaction of pupil to light, and motor posturing.


Blood pressure may be elevated as a reflex to maintain CPP. The Cushing reflex may be observed—the triad of hypertension, bradycardia, and irregular breathing [10].


Papilledema or absent venous pulsations may be observed on fundoscopic exam. Additionally, there has been some data to support optic nerve sheath ultrasound measurements as a method for evaluation for elevated ICP, although the stretch in the optic nerve sheath may remain even after the ICP crisis has resolved [11]. The utility of serial optic nerve sheath diameter measurement needs further study. Papilledema, absence of venous pulsations, and increased optic nerve sheath diameter may all occur at different points in time and may not all be apparent in the hyperacute setting.


Radiographic Assessments


CT scan is indicated to evaluate for:



A.   Intra- and extra-axial hemorrhage


B.   Cerebral edema


C.   Hydrocephalus or compression of ventricles


D.   Midline shift


E.   Effacement of the suprasellar or quadrigeminal plate cisterns


F.   Effacement of sulci and gyri


G.   Infarction, such as a large ischemic middle cerebral artery (MCA) syndrome or an infarction in the posterior fossa (where even a small increase in pressure can result in dramatic neurological consequences given the limited space).


Neuromonitoring Approaches


Rationale for Neuromonitoring


Invasive and noninvasive neuromonitoring for the critically ill patient, in addition to frequent and active clinical assessment, is often necessary to optimize evaluation and treatment (see Table 23.1) [12]. Advanced or multimodality monitoring (MMM) can assist the clinicians’ decision-making process by tracking biomarkers associated with complicated physiologic derangements.


Surveillance Neurologic Exams and Neuroimaging


Patients with severe neurologic injury are often best managed in an intensive care unit setting, where appropriate hemodynamic and neurologic monitoring can be performed. Surveillance neurologic assessment (“neurochecks”) consists of consistent, regular, reproducible evaluations by trained staff to monitor and in some cases quantify neurologic clinical parameters. They have been shown to reliably detect neurologic changes in patients with neurologic injury and can be considered a clinically meaningful biomarker [13]. When combined with appropriate neuroimaging, neurochecks have been shown to detect clinically meaningful neurologic changes [14]. Similarly, neuroimaging repeated at regular intervals can be used to monitor changes in cerebral edema, brain compression, and focal hematomas.


TABLE 23.1    Reasons Why We Monitor Patients With Neurologic Disorders Who Require Critical Care












Detect early neurological worsening before irreversible brain damage occurs


Individualize patient care decisions


Guide patient management


Monitor the physiologic response to treatment and to avoid any adverse effects


Allow clinicians to better understand the pathophysiology of complex disorders


Design and implement management protocols


Improve neurological outcomes and quality of life in survivors of severe brain injuries


Through understanding disease pathophysiology begin to develop new mechanistically-oriented therapies where treatments currently are lacking or are empiric in nature






Source: From Ref. [12]. Le Roux P, Memon DK, Citerio G, et al. Consensus summary statement of the International Multidisciplinary Conference on multimodality monitoring in neurocritical care: a list of recommendations and additional conclusions: a statement for healthcare professionals from the Neurocritical Care Society and the European Society of Intensive Care Medicine. Intensive Care Med. September 2014;40(9):1189–1209. Used with permission.


Invasive ICP Monitoring


The Brain Trauma Foundation (BTF) guideline recommends ICP monitors in patients with Glasgow Coma Scale (GCS) of ≤8 with an abnormal head CT scan as well as patients with GCS ≤8 with normal head CT but age greater than 40 years, systolic blood pressure (SBP) less than 90 mmHg, or motor posturing [15].


The Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury was designed to detect whether or not protocol-guided management using ICP monitors impacted the primary outcome of survival time, impaired consciousness, and functional status versus neurochecks and surveillance neuroimaging alone [16]. They found that ICP guided care with a goal ICP of ≤20 mmHg did not improve outcomes (functional status p = 0.49; 6-month mortality p = 0.6; length of stay p = 0.25).


Cerebral Oxygenation Monitoring


There are multiple known methods to measure cerebral perfusion. Some measure cerebral blood flow directly, but the more commonly used technologies measure delivery of oxygen to the brain. Low cerebral oxygen tension has been associated with poor outcomes, but therapy guided by brain oxygenation measurements has not been shown to improve outcomes. This may be in part due to regional differences in oxygen tension between the sampling site and other injured regions. To date, there are no prospective, randomized trials to offer guidance in this regard [17].


EEG Monitoring


Seizures can occur in approximately 8% of the general intensive care unit (ICU) population while seizures can occur in upwards of 30% in the neuro-ICU [18]. EEG monitoring can be used to diagnose seizure activity and response to treatment. If a seizure is detected, a diagnostic workup should be performed to evaluate for causes other than the primary brain injury such as toxins, medications or in the right clinical scenario, infections. There are also a host of other metabolic and physiologic derangements that can occur in the setting of seizures including acid–base disturbances, respiratory compromise, and cardiac arrhythmias—all of which require close monitoring. As discussed earlier, seizures in TBI patients are common, especially in the acute setting. The European Society of Intensive Care Medicine (ESICM) strongly recommends continuous EEG monitoring in TBI patients with persistent and unexplained altered consciousness [19]. Nonconvulsive status epilepticus (NCSE) is difficult to diagnose clinically, and given that up to 48% of comatose patients in an ICU have been found to be in NCSE it is important to consider as an etiology for persistent altered consciousness. In a study of 110 ICU patients, continuous EEG (cEEG) found that 95% of conscious patients had their first seizures within 24 hours; however, only 80% of comatose patients had their first seizures by that same time. By the 48-hour mark, 98% of comatose patients had their first seizures. It therefore may require longer than 24 hours to diagnose NCSE in the comatose patient [20].


Neuromonitoring Controversies and Uncertainties


A.   Does invasive ICP monitoring have a role?


      1.   Currently, there are no definitive prospective, randomized-controlled trials that demonstrate improvement in mortality by managing TBI patients with invasive ICP monitors. Recently, TBI experts met to discuss the BEST TRIP ICP Trial (Benchmark Evidence from South American Trials: Treatment of Intracranial Pressure) and offer their interpretations of the evidence on the utility of ICP monitors in TBI patients [21]. The group issued seven statements that highlighted the concept that, while elevated ICP has been associated with worse outcomes, the benefit of basing intervention on ICP in TBI patients remains unclear.


B.   What is the ideal protocol for clinical-radiologic monitoring?


      1.   Currently, there is no evidence-based optimal protocol for clinical-radiologic monitoring. Most experts would agree that neurochecks and surveillance neuroimaging at regular intervals is reasonable during the acute period following the injury. Beyond the acute phase, it is reasonable to pursue additional imaging based on clinical exam changes.


TREATMENT


Initial Management of Elevated ICP


Position


Optimal head position improves cerebral venous drainage and consequently prevents venous congestion, which increases ICP. Raise the head of bed to at least 30°, keep the head midline, and make sure the cervical collar (if present) is not too tight. Proper head positioning may reduce aspiration risk as well.


Access


All patients undergoing ICP management should have a central venous catheter placed for the administration of medications and monitoring of central venous pressure. Arterial catheters are helpful in closely monitoring MAP and calculating CPP.


Respiration


Patients with inability to protect the airway for a variety of reasons such as altered sensorium, or head or neck trauma, should be intubated and mechanically ventilated.


Hyperventilation (target PaCO2 30–35 mmHg) decreases ICP by causing cerebral vasoconstriction, thereby decreasing cerebral blood volume. Hyperventilation is associated with diminished cerebral perfusion and should be used cautiously. Hyperventilation is an acute treatment and will only work for a short time. Acute elevations in PaCO2 should be prevented.


The exact arterial partial pressure of oxygen (PaO2) goal is unknown for this patient population, but oxyhemoglobin saturation less than 90% correlates with worse outcome. Some data suggests that a minimum PaO2 of 100 mmHg should be maintained to prevent cerebral hypoxia [22].


Blood Pressure


A SBP less than 90 mmHg should be avoided. Even a single episode of SBP less than 90 mmHg doubles mortality [23].


MAP goal is greater than 80 mmHg until CPP can be measured.


CPP goal is 50 to 70 mmHg. CPP of greater than 70 mmHg has been associated with an increased risk of acute respiratory distress syndrome, and is not routinely indicated [24,25]. If fluid resuscitation does not meet MAP or CPP goals, vasopressors should be started.


CSF Drainage


If an EVD is in place, CSF can be drained to reduce ICP. EVD placement may be considered in severely impaired patients, especially in the context of high ICP.


Osmotherapy


Either mannitol or hypertonic saline are equally efficacious as osmotic diuretics in TBI. It should be noted that the reflection coefficient (the marker of a substance’s ability to cross the blood–brain barrier [BBB]) suggests hypertonic saline would be superior, however, and it may be the preferred agent in certain clinical situations such as in the setting of renal failure [26].


Mannitol


  1.   Initially, 1 to 2 g/kg initial bolus, then 0.25 to 1 g/kg ever 4 to 6 hours. Serum osmolality and the osmolar gap should be assessed prior to initiating therapy to determine therapeutic need and assess for incomplete clearance (elevated osmolar gap), which increases the risk for acute tubular necrosis and resulting renal failure. Mannitol is a diuretic and may cause hypovolemia.


Hypertonic Saline


30 mL of 23.4% NaCl over 10 minutes or 250 mL of 3% NaCl over 30 minutes every 4 to 6 hours for bolus dosing, or a continuous infusion of 3% NaCl. Serum sodium should be assessed regularly to determine therapeutic efficacy targeting a clinical marker such as ICP or neurologic exam. Serum sodium levels must be monitored carefully in the context of renal replacement. Iso-osmolar dialysate used with hemodialysis and continuous veno-venous hemofiltration will work to normalize the sodium concentration, and the resulting decrease in serum osmolality may exacerbate cerebral edema.


Sedation and Analgesia


Adequate sedation and analgesia can decrease cerebral metabolism and therefore oxygen demand. One should consider the concept of context-sensitive half-time, which describes the elimination of an infused drug based on the duration of time it has been administered. For example, fentanyl may have a relatively short half-life; however, if that infusion is continuous for over an hour, the context (the hour it was infusing) dramatically increases the half-time from 10 minutes to over 100 minutes [27]. First-line sedatives include lorazepam, midazolam, morphine, fentanyl, and propofol. Because of their adverse properties (long half life, hypotension, myocardial depression), barbiturates are often reserved for management of elevated ICP refractory to other medical treatment. Barbiturates (often pentobarbital) are often used with continuous EEG and titrated to burst suppression.


Chemical Paralysis


Chemical paralysis is used for refractory ICP elevations, especially in patients with significant shivering or ventilator dyssynchrony. Neuromuscular blockade may decrease metabolic rate and lower intrathroracic pressure, thereby reducing intracranial blood volume. Daily holidays from sedation are advised as it improves outcomes [28], but adequate sedation is recommended in patients who are chemically paralyzed. Train-of-four peripheral nerve stimulation monitoring should be employed for a goal of 1 to 2 of 4 twitches during the use of neuromuscular blocking agents as the fewer the twitches the greater the neuromuscular blockade. The greater the blockade, the longer it will take to reverse [29].


Intra-Abdominal Hypertension


Intra-abdominal hypertension should be avoided. This may require medications to promote adequate bowel motility. There are case series indicating efficacy of decompressive laparotomy in reducing refractory ICP [30].


Craniectomy


Surgical removal of part of the skull, which can reduce ICP and allow the brain to expand. For patients with diffuse, severe TBI who have refractory ICP elevation, bifrontal decompressive craniectomy has been shown to decrease ICP and hospital length of stay but was associated with worse outcomes and no improvement in mortality [31]. However, there is some controversy with respect to how to interpret the study’s findings. Evacuation of blood clots or damaged tissue may also be indicated.


Temperature Management


Fever control helps lower ICP. Normothermia should be the therapeutic goal. Cooling measures include acetaminophen 650 mg every 6 hours, intravenous cooled saline, and surface cooling devices. For every 1°C cooler the core gets, the brain decreases metabolism by 3% to 7% [32]. This is hypothesized to decrease risk of supply-demand mismatch, which can lead to apoptosis [33,34].


Seizure Prophylaxis and Treatment


Seizures worsen outcomes in patients with traumatic brain injury. The American Academy of Neurology recommends providing seizure prophylaxis for 7 days to prevent early posttraumatic seizures [35]. Prophylaxis beyond the first 7 days is not recommended due to decreased risk of seizures. Phenytoin has been associated with fevers and worse outcomes after brain hemorrhage, and is generally avoided in TBI for similar concerns [36]. (See also Chapter 46 for a more detailed discussion of post-traumatic seizures.)


Cerebral Oxygenation Management


Brain tissue oxygen monitors are intraparenchymal probes inserted via a burr hole into the white matter of the brain. A treatment threshold of less than 15 mmHg is affirmed by the latest BTF guidelines [15], although as previously discussed there is no direct evidence that management by intraparenchymal oxygen monitors improves outcomes. Treatment options for low brain oxygen include lowering ICP, increasing CPP (some patients do require CPP values above 70 mmHg for adequate perfusion), decreasing PaCO2, increasing PaO2, and increasing hemoglobin. Maintaining PaO2 greater than 90 mmHg is recommended, as lower levels are associated with higher mortality. Jugular vein oxygen saturation less than 50% is likewise associated with worse outcomes, although placement requires a fiberoptic catheter and the incremental benefit of jugular oxygen monitoring is not established [37].


May 29, 2017 | Posted by in PSYCHIATRY | Comments Off on The Neurointensive Care Unit: Intracranial Pressure and Cerebral Oxygenation

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