Head injury ICP management

Raised ICP

Treatment measures for elevated ICP

General information

This section presents a general protocol for treating documented (or sometimes clinically suspected) intracranial hypertension (IC-HTN).
Guidelines promulgated by the Brain Trauma Foundation are generally followed.
Unless otherwise stated, guidelines are for adult patients (≥ 18 years of age).
Dosages are given for an average adult, unless specified as mg/kg.
Treatment may be initiated prior to insertion of a monitor

If there is

Acute neurologic deterioration or
Clinical signs of IC-HTN

But continued treatment requires documentation of persistent IC-HTN.

ICP management protocol:

General care

Major goals

Avoid hypoxia (pO2 < 60mm Hg)
Avoid hypotension (SBP ≤90mm Hg): 67% positive-predictive value (PPV) for poor outcome (79% PPV when combined with hypoxia)

Details of general treatment measures

Prophylaxis against steroid ulcers (if steroids are used) and Cushing’s (stress) ulcers (seen in severe head injury and in increased ICP, accompanied by hypergastrinemia) for all patients including peds

Elevating gastric pH:

Titrated antacid and/or H2 antagonist (e.g. ranitidine 50mg IV q 8 hrs) or proton pump inhibitor.
Potential increased mortality as a result of increased gastric pH

Sucralfate

Aggressive control of fever (fever is a potent stimulus to increase CBF, and may also increase plateau waves)
Arterial line for BP monitoring and frequent ABGs
CVP or PA line if high doses of mannitol are needed (goal: keep patient euvolemic)
IV fluids

Choice of fluids:

Isolated head injury: IVF of choice is isotonic (e.g. NS+20 mEq KCl/L)
Avoid hypotonic solutions (e.g. lactated ringers) which may impair cerebral compliance

Fluid volume:

Provide adequate fluid resuscitation to avoid hypotension
Normalization of intravascular fluid volume is not detrimental to ICP
Although fluid restriction reduces the amount of mannitol needed to control ICP,

The concept of “running patients dry” is obsolete

If mannitol is required, patient should be maintained at euvolemia
Also exercise caution in restricting fluids following SAH

See Cerebral salt wasting

If injuries to other systems are present (e.g. perforated viscus), they may dictate fluid management

Pressors (e.g. dopamine) are preferable to IV fluid boluses in head injury

Measures to lower ICP

General measures that should be routine

Positioning:

Elevate HOB 30–45°

Seemingly simple, but there is still some controversy.
Early data obtained from dog studies indicated that keeping the HOB at 30–45° optimized the trade-off between the following two factors as the HOB is elevated:

Reducing ICP (by enhancing venous outflow and by promoting displacement of CSF from the intracranial compartment to the spinal compartment)

Recent data indicate that although mean carotid pressure (MCP) is reduced, the ICP is also reduced and the CBF is unaffected by elevating the HOB to 30°.

Reducing the arterial pressure (and thus CPP) at the level of the carotid arteries.

Some studies showed a deleterious effect from elevating the HOB and were used to justify nursing these patients with HOB flat.

The onset of action of raising the HOB is immediate.

Keep head midline (to prevent kinking jugular veins)

Light sedation: codeine 30–60mg IM q 4 hrs PRN, or lorazepam (Ativan®) 1–2mg IV q 4–6 hrs PRN
Avoid hypotension (SBP <90mm Hg):

Normalize intravascular volume, support with pressors if needed

Control HTN;

In ICH, aim for patient’s baseline

Prevent hyperglycemia:

Aggravates cerebral edema
Usually present in head injury, may be exacerbated by steroids

Intubation:

For GCS≤8 or respiratory distress.
Give IV lidocaine first and antibiotics

Avoid hyperventilation:

Keep PaCO2 at the low end of eucapnia (35mm Hg)

Prophylactic hypothermia:

Measures to use for documented IC-HTN

Proceed to each step if IC-HTN persists.

Heavy sedation and/or paralysis when necessary (also assists treatment of HTN)

CSF drainage (when IVC is being utilized to measure ICP):

3–5ml of CSF should be drained with the drip chamber at ≤ 10cm above EAC.
Works immediately by

Removal of CSF (reducing intracranial volume)
Possibly by allowing edema fluid to drain into ventricles (latter point is controversial)

“Osmotic therapy” when there is evidence of IC-HTN:

Hyperventilation (HPV) to PaCO2 =30–35mm Hg

❌ do not use prophylactically
❌ avoid aggressive HPV (PaCO2 ≤25mm Hg) at all times
Use only for

Short periods for acute neurologic deterioration
Chronically for documented IC-HTN unresponsive to sedation, paralytics, CSF drainage, and osmotic therapy

Avoid HPV during the first 24 hrs after injury if possible

❌ steroids:

The routine use of glucocorticoids is not recommended for treatment of patients with head injuries

“Second tier” therapy for persistent IC-HTN

General

Indicated: If IC-HTN remains refractory to the above measures, and especially if there is loss of previously controlled ICP,
Things to consider before second tier therapies

CTH
EEG to rule out subclinical status epilepticus (seizures that are not clinically evident);

“Second tier” can be either effective but with significant risks (e.g. high-dose barbiturates), or are unproven in terms of benefit on outcome.

High dose barbiturate therapy: initiate if ICP remains >20–25mm Hg

Hyperventilate to PaCO2 = 25–30mm Hg.

Monitoring SjVO2, AVdO2, and/or CBF is recommended

Hypothermia:

Patients must be monitored for a drop in cardiac index, thrombocytopenia, elevated creatinine clearance, and pancreatitis.
Avoid shivering which raises ICP

Decompressive surgery:

Lumbar drainage: showing some promise. Watch for “cerebral sag”

Hypertensive therapy

Adjunctive measures

Lidocaine:

1.5 mg/kg IVP at least one minute before endotracheal intubation or suctioning.
Watch for hypotension, reduce dose if necessary
Blunts the rise in ICP as well as tachycardia and systemic HTN

Based on patients with brain tumors undergoing intubation under light barbiturate-nitrous oxide anesthesia; extrapolation to trauma patients is unproven

High frequency (jet) ventilation:

Consider if high levels of positive end-expiratory pressure (PEEP) are required
NB: patients with reduced lung compliance, e.g. pulmonary edema, transmit more of PEEP through lungs to thoracic vessels and may raise ICP
PEEP ≤ 10cm H2O does not cause clinically significant increases in ICP.
Higher levels of PEEP > 15–20 are not recommended.
Also, rapid elimination of PEEP may cause a sudden increase in circulating blood volume which may exacerbate cerebral edema and also elevate ICP

Details of some measures employed in treating increased ICP

Trial Wilberger et al

Trend for earlier surgery to improve mortality and functional recovery, but only significant in patients having surgery >12h post injury (p=0.05)

Poor pre-operative neurological status (GCS<5) significantly associated with high mortality (>75%, p<0.05)

ICP control:

Mortality 40% with ICP <20 mmHg
Mortality >95% with ICP >45mmHg (p<0.05)
No patient with ICP>45mmHg had functional recovery (p<0.05)

Relationship between mortality, functional recovery and timing of surgery post injury in the study by Wilberger et al.

ICP monitoring in head injury

Introduced into clinical practice as early as 1950s (Guillame and Hanny, 1951; Lundberg, 1960).

Two studies from Richmond in 70s and 80s firmly established its role in head injury management – Miller et al., 1977 and Miller et al., 1981 (one retrospective and one prospective case series, Class III evidence)

These two studies so influential that ICP monitoring became standard of care for severe TBI despite lack of supporting trial data

Chesnut et al 2012 – landmark trial of ICP monitoring in TBI in centres in Bolivia and Ecuador (BEST:TRIP) (multicentre RCT, Class I)

ICP recordings in the studies by Miller et al. were made by transducing from a ventricular catheter placed in the frontal horn of one of the lateral ventricles.

In the first study by Miller et al. the initial threshold for treating raised ICP was a sustained rise over 40 mmHg. However, by the end of the study this was reduced to 30 mmHg and in the later studies the threshold was set at an ICP of 25 mmHg for over 15 min.

Outcomes in the studies by Miller et al. were assessed using the 5-point GOS with a good outcome being defined as moderate disability or good recovery and a poor outcome being defined as a significant disability, vegetative state, or death.

In the BEST:TRIP trial by Chestnut et al. an intraparenchymal ICP monitor was placed and ICP was maintained <20 mmHg in accordance with the Brain Trauma Foundation/ American Association of Neurological Surgeons guidelines.

The composite primary outcome in the BEST:TRIP trial was a composite of 21 components including measures of survival time, impaired consciousness, and functional and neuropsychological measures. The primary outcome was a composite score of 0–100.

ㅤ	Miller et al. (1977)	Miller et al. (1981)	Chestnut et al. (1981) BEST:TRIP
Class of evidence	III	III	I
Randomization	None	None	ICP monitoring versus imaging and clinical examination
Number of patients	160	225	324
Follow-up	Retrospective analysis	1 year	6 months (92%)
Outcomes	Death and disability	Death and disability	Composite outcome of 21 components based on survival time, impaired consciousness, functional status, and neuropsychological status
Eligibility	- Blunt head injury - Motor score <6 on GCS - No evidence of brain death	- Severe head injury - V2, M3 or less on the GCS - No evidence of brain death - Gunshot wounds and patients without spontaneous respiration were excluded	- GCS 3–8 (M ≤ 5 if intubated) within 48 h of injury - Age >13 years - Patients with bilateral fixed dilated pupils were excluded
Number of centres	1	1	6
Stratification	None	None	- Site - Severity of injury - Age

Miller et al. (1977)

Results

ICP >40 mmHg on admission was associated with a poor outcome: 69% mortality and only 25% good outcome (p < 0.01).
Low ICP on admission (<10 mmHg) was associated with much better outcomes: 14% mortality and 78% survived to a good outcome (p < 0.05).
These findings of early ICP recording were even more significant when applied to patients with diffuse brain injury. In patients with mass lesions, only very high ICP (>40 mmHg) was associated with a poor outcome.
Patients with diffuse injuries who experienced delayed elevations in ICP >20 mmHg had a greater proportion of poor outcomes (46%) compared to those whose ICP remained <20 mmHg (21%, p < 0.02).
50% of fatalities were associated with uncontrolled intracranial hypertension.

Conclusions

Elevated ICP is related to poor outcome in severely head-injured patients.

Miller et al. (1981)

Results

The authors reported a significant correlation between ICP control and outcome (p < 0.001: more patients with a well-controlled ICP (<20 mmHg) throughout had a much better outcome (74% good outcome, 18% mortality) compared to patients with raised but reducible ICPs (55% good outcome, 26% mortality) and those with uncontrolled ICP rises (only 3% good outcome, and 92% mortality).

Conclusions

Even moderate intracranial hypertension is associated with a poor outcome in patients with severe head injuries.

Chesnut et al. (2012)

Results

The study reached the planned samples size of 324 determined by a power calculation and analysis was done on an intention-to-treat basis.
There was no significant difference between the two groups in the primary outcome: composite score of 56/100 in the ICP monitored group compared to 53 in the imaging-clinical examination group (p = 0.49).
There were no differences in 6-month mortality between the two groups: 41% in the ICP monitored group compared to 39% in the imaging-clinical examination group (p = 0.60).

Conclusions

Care focused on ICP monitoring is no better than care based on imaging and clinical examination in patients with severe TBI.

Critique of ICP papers

Virginia studies are landmark because led to widespread use of ICP-M in TBI patients

Nonetheless, ICPM questioned, especially as outcomes appear similar in patients managed without it (Stuart et al 1983)

Survey of 67 centres in 12 European countries, patients with ICPM seemed to have more interventions and poorer outcomes (Stochetti et al 2001)…

BEST:TRIP done in Ecuador and Bolivia – limits generalisation to other patient populations

Furthermore poorer pre hospital care in those countries may lead to less severe injuries being included (more severe ones dead). However, ICU care and criteria for severe TBI similar to wealthier countries

Chesnut et al accept value of ICPM but argue their date support reassessing treatments to manipulate ICP recordings

For high income countries SIBCC 1 see Hawryluk 2019

Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC)

Consensus-based algorithm for the management of severe traumatic brain injury guided by intracranial pressure measurements. Upper right box presents the principles for navigating through the treatments and tiers. Lower tier treatments are viewed as having a more favorable side effect profile than higher tiers and generally should be employed first. Inter-tier recommendations encourage patient reassessment for remediable causes of treatment resistance. See text for details. CPP cerebral perfusion pressure, EEG electroencephalogram, EVD external ventricular drain, ICP intracranial pressure, Kpa kiloPascals, MAP mean arterial pressure, PaCO₂ arterial partial pressure of carbon dioxide.

For MAP challenge see 2nd injury autoregulation

Critical neuroworsening

A serious deterioration in clinical neurologic status such as:

Spontaneous decrease in the GCS motor score of ≥ 1 points (compared with the previous examination)
New decrease in pupillary reactivity
New pupillary asymmetry or bilateral mydriasis
New focal motor deficit
Herniation syndrome or Cushing’s Triad which requires an immediate physician response

Response to critical neuroworsening

Emergent evaluation to identify possible cause of neuroworsening

If herniation is suspected:

Empiric treatment

Hyperventilation**
Bolus of hypertonic solution

Consider emergent imaging or other testing
Rapid escalation of treatment

Possible causes of neuroworsening include:

Expanding intracranial mass lesion

Cerebral edema

Elevated ICP

Stroke

Electrolyte or other metabolic disturbance

Medical comorbidity

Medication effect

Impaired renal or hepatic function

Systemic hypotension

Seizure or post-ictal state

Hypoxemia/tissue hypoxia

CNS infection

Infection or sepsis

Substance withdrawal

Dehydration

Hyper or hypothermia

** the hyperventilation PaCO₂ limit of 30 mmHg/4.0 kPa does not apply here

SIBICC 2

See Chesnut 2020