Primary insult refers to the initial injury itself.

Secondary insult is a subsequent deviation from normal physiological conditions that can worsen the effects of the primary insult.

Common examples: hypotension, hypoxia, elevated intracranial pressure (ICP).

A recently injured brain is highly vulnerable even to mild physiological derangements that would be well tolerated by an uninjured brain.

Dozens of clinical trials have failed to identify any effective therapy for traumatic brain injury (TBI). ^, There are many possible reasons for these failures, including:

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  Lack of appreciation of the heterogeneity of TBI

  
  
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  Failure to use appropriately sophisticated statistical techniques

  
  
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  Poor adherence to complex study protocols

  
  
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  Lack of sensitivity of outcome instruments

Current treatment is limited to careful monitoring and prompt intervention when secondary insults occur.

So far, all attempts at aggressive initiation of therapies to prevent secondary insults have not only failed to improve outcomes but also have usually led to worse outcomes.

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  Examples of failed prophylactic interventions: induced hypertension, neuromuscular paralysis, barbiturate coma, hypothermia, decompressive craniectomy (DC), and many others.

Even though various treatments may lower ICP, none of these treatments has been shown to improve outcomes in TBI patients.

Because we have been largely unable to prevent secondary insults, the best we can do is to promptly recognize and treat them when they do occur.

If endotracheal intubation has not been performed in the prehospital setting, it should be performed immediately on a patient’s arrival in the emergency department (ED).

Cervical spine immobilization must be maintained.

Nasotracheal intubation or other instrumentation is generally discouraged in patients with head trauma because of the risk of passage of the inserted object through a basilar skull fracture and into the cranial vault.

Rarely, extensive injury and bleeding from the oropharynx may make it impossible to perform orotracheal intubation, in which case emergency tracheostomy may be required.

After the airway has been secured, the patient should be placed on a mechanical ventilator.

Ventilation by bag–valve–mask is discouraged because of the tendency of those who are doing the bagging to use excessive tidal volumes and respiratory rates. The reduction in partial pressure of carbon dioxide (Pa co ₂ ) and subsequent increase in arterial pH lead to constriction of the cerebral arteries, resulting in a decrease in cerebral blood flow (CBF) that may be so severe that the metabolically impaired injured brain may progress to infarction.

The goal of ventilation is to keep Pa co ₂ in the normal range of 35 to 45 mm Hg.

Although often used in the past, continuous hyperventilation is no longer recommended because of its adverse effect on outcome, presumably from reduction of CBF.

If hyperventilation is prolonged, it must be remembered that cerebral arterioles progressively dilate and return to baseline diameter within 24 hours even when Pa co ₂ is maintained at low levels. Thus, nothing has been gained by continuous hyperventilation, and the reduction in bicarbonate ions that might have served to buffer regions of cerebral acidosis could potentially cause harm.

However, as a short-term intervention during emergencies that may be caused by expansion of a mass lesion, such as sudden neurological deterioration in a patient who develops a dilated pupil and asymmetrical motor examination, hyperventilation may be used to transiently lower ICP while emergency computed tomography (CT) scanning is performed to assess for the presence of a large hematoma that requires immediate surgery. If evaluation reveals that no such hematoma is present, hyperventilation should not be maintained, as discussed earlier.

As with Pa co ₂ , normal levels are also the goal for partial pressure of oxygen (PaO ₂ ). In general, maintaining oxygen saturation above 90% is adequate, but because hypoxia is such a common and potentially devastating secondary insult, many clinicians aim for slightly higher levels, such as 92% to 94%, to create a bit of a buffer.

Driving PaO ₂ to supranormal levels confers no benefit.

Hypotension is among the most frequent and most harmful of secondary insults in TBI patients, and one-third of severe TBI patients suffer cerebral ischemia during the initial hours after injury. ^,

Traditionally, the recommended minimum systolic blood pressure for severe TBI patients was 90 mm Hg or higher. More recent evidence suggests that a goal of 100 mm Hg may be a more appropriate starting point, with some patients—such as those at the younger and older ends of the adult age spectrum—benefiting from a target of 110 mm Hg.

Another commonly measured parameter is cerebral perfusion pressure (CPP), defined as mean arterial pressure minus ICP. The recommended target range for CPP is 60 to 70 mm Hg.

Blood pressure management aims to ensure sufficient blood flow to meet the brain’s metabolic needs and avoid ischemia.

In uninjured individuals, the cerebral arteries dilate and constrict as needed to maintain CBF constant even if systemic blood pressure fluctuates widely. This process is known as autoregulation .

The impairment of autoregulation in many TBI patients causes CBF to become “pressure passive,” that is, CBF passively rises and falls in response to corresponding changes in blood pressure. As a result, some practitioners in years past routinely used pressors to artificially raise blood pressure in TBI patients because of a belief that this practice had little downside and would avoid cerebral hypoperfusion

Subsequent work, however, demonstrated that this practice actually worsens outcome, largely because of the pulmonary complications caused by the amount of fluid and pressors needed to maintain artificial elevation of blood pressure and CPP.

The best score is used when an examination fluctuates or when the two sides are asymmetrical.

Each component should be recorded separately, but a single sum score is often used to summarize a patient’s neurological status.

Any right–left asymmetry should be noted.

Generally, a score of 3 to 8 is described as a severe injury, 9 to 12 is moderate, and 13 to 15 is mild.

Accurate assessment may be compromised by the presence of alcohol, other drugs, hypothermia, hypotension, and many other factors.

A dilated pupil may indicate the presence of a large mass lesion that is exerting pressure on the third cranial nerve. The pupilloconstrictor fibers on the periphery of the nerve are vulnerable to compression by large hematomas or edematous brain.

Bilaterally dilated pupils may indicate the presence of diffuse cerebral edema and high ICP. This is an ominous finding.

It must be remembered that, in a sizeable minority of cases, a dilated pupil is caused by local ocular trauma and does not indicate an intracranial emergency. However, the burden is on the treating physician to obtain an emergency CT scan to verify that an expanding intracranial hematoma is not present.

Complete Blood Count, Basic Chemistries, Coagulation Studies, Alcohol Level and Toxicology Screens, Blood Type and Crossmatch, Pregnancy Level as Appropriate, Urinalysis, Additional Studies as Appropriate

Significant comorbidities

Medications, especially anticoagulants and/or antiplatelet agents

Severe TBI rarely occurs in isolation. Significant associated systemic injuries are the rule rather than the exception.

Chest x-ray in resuscitation bay

Head CT scan

Cervical spine CT scan, and other studies as needed

Most severe TBI patients receive anticonvulsant prophylaxis.

The highest-quality studies find that phenytoin prophylaxis prevented seizures during the first 8 days after injury but not later.

Many clinicians have substituted levetiracetam for a 7-day course of prophylaxis because it is not necessary to check serum levels and because of a perceived lower rate of adverse events.

Of note: The decrease in seizures during the first week has not been shown to improve long-term outcomes.

Steroids were often administered to TBI patients in the past.

The rationale was that steroids were known to reduce edema associated with brain tumors, and it was assumed the same would be true for trauma.

However, large clinical trials have demonstrated that steroids increase the mortality rate after TBI.

Steroids are no longer given to TBI patients unless a patient has been on steroids for another reason.

The only level 1 recommendation in the Brain Trauma Foundation’s Guidelines for the Management of Severe Traumatic Brain Injury is that use of steroids is not recommended for improving outcome or reducing ICP in TBI patients.

For many years, TBI patients were given red blood cells whenever their hemoglobin dropped below 10 g/dL.

That level represents the theoretical point at which blood oxygen–carrying capacity (which increases at a higher hemoglobin concentration) and blood viscosity (which decreases at a lower hemoglobin concentration) come into optimal balance.

However, a large body of literature demonstrated the many adverse effects of blood transfusions, and a hemoglobin transfusion threshold of 7 g/dL was widely adopted for most nonneurologically injured patients.

It remained unclear whether TBI patients could safely tolerate a hemoglobin transfusion of 7 g/dL until a prospective clinical trial demonstrated lack of benefit and an increase in thromboembolic events by keeping TBI patients at a hemoglobin concentration of 10 g/dL.

Midline shift >5 mm in patients with GCS score ≤8

Significant enlargement of a mass lesion or surrounding edema on repeat CT scanning

Inability to control ICP in patients with moderate-sized mass lesions who are being managed nonoperatively

Decrease in GCS score of 2 or more points in patients with moderate-sized mass lesions who are being managed nonoperatively

Bilateral subfrontal (anterior inferior frontal lobe) contusions: Many patients can tolerate very large contusions in this area surprisingly well.

Cerebral atrophy: Elderly patients and others with significant atrophy have a relatively large amount of intracranial volume that can accommodate sizeable acute mass lesions that might require immediate surgery in younger or nonatrophied patients.

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  Acute subdural hematoma in elderly patients: In asymptomatic patients with significant atrophy, even large acute subdural hematomas can be managed without surgery while they gradually evolve from a solid hematoma to a liquid subacute hematoma, which will resolve spontaneously or drain easily through a bur hole.

Diffuse brain injury: In the past, some neurosurgeons performed DC in severe TBI patients whose CT scans showed only diffuse injury. The rationale was that removal of a large portion of the skull would permit the brain to swell without the harmful elevation of ICP that would occur if the brain were confined within the rigid skull. The randomized, prospective DEcompressive CRAniectomy (DECRA) trial demonstrated that such a practice actually worsened outcomes in the patients who had surgery. Although the results generated some controversy, it is clear that the operated patients did not experience any benefit from surgery but were still exposed to the many complications of this procedure.