Page 60 - JSOM Summer 2022

decreasing CPP and resulting brain dysfunction, as dis- FIGURE 2 Cushing triad is associated with elevated intracranial
cussed above. Isolated blown pupil or cranial nerve deficit pressure (ICP).
in an otherwise intact person is unlikely to be from high The triad consists of increase in systolic blood
ICP, but in the presence of an unconscious patient, these pressure (SBP) and pulse pressure, reduction in
indicate imminent death without intervention (Table 3). heart rate (HR), and irregular respiratory rhythm
and rate (RR). Cushing triad is only seen in patients
with intracranial hypertension, and it indicates a
TABLE 3 General Measures to Reduce Intracranial Pressure in high probability of imminent herniation and death.
Traumatic Brain Injury Patients Although not part of the triad, a blown pupil may
Treatment Rationale be seen.
Keep the head above the level of Improves venous drainage
the heart from the head and neck skull fractures, intracranial hemorrhages, pneumocephalus
Maintain neutral neck position Improves venous drainage (intracranial air), contusions, hydrocephalus (enlarged ventri-
and ensure the cervical collar/ from the head and neck cles), CSF leak, and brain shifts. However, CT is suboptimal
anything compressing against the for detecting microscopic injuries such as diffuse axonal in-
neck is not too tight jury (DAI) or stroke soon after the injury, and therefore an
Maintain EtCO 35–40mmHg Optimizes cerebral blood flow MRI is needed. However, neither CT nor MRI are available
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and volume
Maintain normothermia/core Shivering and fever both in the field. Numerous technologies based on electromagnetic
temperature worsen intracranial pressure and sound waves have been developed to enable prehospital
96–99.5°F (35.5–37.5°C) providers to image the brain. However, currently there is no
Treat pain, anxiety, agitation Pain, anxiety, and agitation widely used portable device that can deliver high resolution
worsen intracranial pressure images of the whole brain in the field. Therefore, clinical ex-
through increased sympathetic amination remains the most important diagnostic tool in TBI
activity, cerebral metabolic patients.
demand, and increased
intrathoracic pressure
Minimize noxious stimulus (bright Prevent increasing ICP Ultrasound-based optic nerve sheath diameter (ONSD) mea-
lights, loud sounds, unnecessary surement has emerged as a useful imaging tool in patients with
sudden movements) and spikes in suspected high ICP. The optic nerve is a direct extension of the
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ICP (vomiting, coughing) brain and it is bathed with CSF, just like the brain. Therefore,
EtCO = end-tidal CO , ICP = intracranial pressure. when the ICP goes up, CSF gets displaced into the optic nerve
2 2
sheath and causes the ONSD to increase. The slightly dilated
• TBI patients with temporal lobe and posterior fossa (i.e., portion of the optic nerve, which is approximately 3mm be-
cerebellum) injuries are at a higher risk for rapid deteri- hind the globe, is the most distensible and therefore sensitive
oration and herniation because of these structures’ prox- to ICP changes. ONSD cutoff of 5.2 mm in adults has been
imity to the brainstem. Younger patients have fuller brain associated with excellent (greater than 90%) sensitivity (i.e.,
inside the cranial vault in comparison to the elderly (whose true positive) and specificity (i.e., true negative) for elevated
brains atrophy with age); as such, the young may deterio- ICP that can be detected on a CT scan. 17,18 Therefore, ONSD
rate faster than the elderly. may be useful in checking for high ICP in patients who is un-
• Clinical signs of high ICP, also known as intracranial hy- conscious or altered. ONSD number does not translate to an
pertension, are 1) unilateral or bilateral blown pupil, 2) absolute ICP and not everyone’s baseline ONSDs are the same.
asymmetric pupillary reaction to light, 3) decerebrate or Therefore, ONSD trends in a patient may be more informative
decorticate posturing (often on opposite side to the blown than comparing one patient’s ONSD to that of another. Ulti-
pupil), and 4) progressive decline of the neurological exam. mately, one should consider ONSD measurement as a useful
Development of one or more of these signs strongly suggest adjunct that must be interpreted within the clinical context
high ICP and indicates the need for emergent intervention and patient status.
(see “Treatment”).
• The Cushing reflex or the Cushing triad is associated with Treatment
high ICP and consists of 1) increase in systolic and pulse
pressure, 2) reduction in heart rate, and 3) irregular res- Establishing and optimizing airway, breathing, and circulation
piration (in rhythm and rate). Cushing reflex is only seen (ABC) is the cornerstone of advanced trauma life support.
with ICP crisis and no other known condition. It is asso- ABC is also paramount in prehospital TBI management. As
ciated with CPP < 15mmHg, and indicates a high proba- discussed in “Normal Physiology,” the brain is exquisitely sen-
bility of imminent herniation and death. Cushing reflex sitive to any disturbances in CBF and it works hard to main-
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develops over three stages – hypertension and tachycardia tain it through autoregulation. It is important to understand
due to increased sympathetic activity (Stage 1), followed by that cerebral autoregulation may become dysfunctional after
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bradycardia due to counteractive parasympathetic activity TBI and the brain may fail to maintain its own blood supply.
(Stage 2), and lastly abnormal respiration that is often slow Therefore, TBI patients can depend heavily on their systemic
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and irregular (Stage 3) (Figure 2). Do not wait for the full blood pressure to keep the brain alive. As the injured brain
Triad to develop, because some patients may not make it to begins to develop swelling and inflammation, it becomes crit-
Stage 3 without permanent brain damage or death. Initiate ical that we help the TBI brain optimize and stabilize its CBF.
treatment immediately when high ICP is suspected! Hypotension or hypoxemia during this time can significantly
worsen the injuries and lead to worse outcomes. Again, there
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Imaging is no practical way to measure CBF in the field. Therefore, we
The gold standard of diagnostic imaging in TBI is the com- must rely on CPP. Also, remember that once the secondary
puted tomography (CT) scan. Head CT can rapidly detect injury process begins, the brain’s CBF need may evolve with

58 | JSOM Volume 22, Edition 2 / Summer 2022