Traumatic Brain Injury (Head Injury)*

The following article has been written for the General Practice/Family Physician community, and for nursing and paramedical staff and medical students.

Introduction

Traumatic brain injury (TBI), which can be associated with mortality and long-term morbidity, results from an external force to the brain causing transient or permanent neurological dysfunction. It is most common in young people, thereby causing a significant social and financial burden for the individual and society. The purpose of this editorial is to provide an overview of the epidemiology, pathogenesis and complications associated with TBI as well as to briefly outline some of the investigation and management recommendations relevant to the General Practice community.

Epidemiology (statistics) of Traumatic Brain Injury

It is estimated that around 200 people are admitted to hospital with a TBI per 100,000 population per year. This figure is likely to be an underestimate of the true incidence due to the underreporting of mild TBI. The incidence of TBI peaks in the age group of 15–35 years, and is 3 to 4 times more common in males than females. Motor vehicle-related trauma accounts for about two-thirds of moderate and severe TBI and alcohol is associated with up to one-half of all cases.

Pathogenesis (mechanism) of Traumatic Brain Injury

TBI is divided into primary and secondary injury. Primary brain injury is where brain damage (neuroglial cell trauma and cell death) is inflicted at the time of impact. This is typically irreversible as cell components are sheared or severed, but the brain’s adaptability (its “plasticity”) at a microscopic level may allow some degree of functional compensation to occur via neighboring intact cell groups. Secondary brain injury follows usually hours to days after the impact and is due to potentially reversible factors such as hypoxemia, systemic hypotension, intracranial haematoma, infection and intracranial hypertension. Thus, the aim of early treatment is to prevent secondary injury.

Assessing the severity of TBI

The severity of TBI is best measured by the Glasgow Coma Score (GCS) and the duration of Post-Traumatic Amnesia (PTA) period. The GCS is an objective method of following the patient’s neurological status, and a score for “normal” is 15. Eye movements are scored from 1 to 4, voice responses from 1 to 5, and limb motor responses from 1 to 6. The acute application of the GCS does have some limitations. For example, hypoxia, hypotension and intoxication can all falsely lower the GCS. On the other hand, PTA is defined as that period of time after the injury in which the brain is unable to lay down new and continuous day-to-day memories. Approximately 70% of patients with TBI will experience PTA. In Australia, the Westmead PTA Scale is commonly used. It consists of orientation and memory items and used to assess the patient daily. Patients are deemed to be “out of PTA” once a score of 12/12 is achieved on three consecutive days. As a rule of thumb, the lower the GCS and the longer the PTA period, the worse the severity of the TBI. The length of the period of PTA is a strong predictor of functional outcome.

By definition, the severity of a TBI can be classified as follows: “Mild” = PTA period of < 1 hour; “moderate” = PTA Period of 1-24 hours; “severe” = PTA period of 1-7 days; “very severe” = PTA period of > 7 days; and “chronic amnestic state” = PTA period of > 6 months.

Complications Associated with TBI and Their Management

Skull fractures: These can be simple-linear, comminuted (multiple fragments), depressed, open or a combination of these, and some involve the skull base. Skull fractures can cause haematomas, cranial nerve damage, cerebrospinal fluid (CSF) leakage and meningitis, seizures and brain tissue (parenchymal) injury. Linear skull fractures (Fig. 1A) account for up to 80% of all skull fractures. These fractures occur at the point of contact and fracture lines may radiate away from this point. Most heal without complication or intervention. Depressed fractures (Fig. 1B) involve displacement of the skull or skull fragments inward below the plane of skull, and require urgent neurosurgical intervention (Fig. 1C) particularly when open to the outside world or when the depression is equal to or greater than the thickness of the overlying skull. Basilar fractures (Fig. 1D) are fractures that occur at the base of the skull. Such fractures can involve the numerous neurovascular structures at the skull base, imply significant force, and may cause leakage of tear-like CSF from the nose or ear, in which case the patient should be referred for urgent neurosurgical evaluation.
Intracranial hematomas: Compartmentalised blood collections are commonly associated with TBI. The symptoms and signs are due to raised intracranial pressure (ICP) essentially through the progressive occupation of space in a rigid box, the skull. Hematomas may occur in the extradural, subdural, subarachnoid or intracerebral compartments. Their radiological appearance is shown in Figure 2. Such haematomas frequently warrant operative intervention.
Cerebral contusions: These can be thought of as a “bruise” of the brain parenchyma (Fig. 3A). The brain has the ability to move independently within the cranium, despite its surrounding thin cushion of CSF. Thus, acceleration-deceleration forces can cause the brain to impact the jagged inner table of the skull. Coup contusions occur at the area of direct impact to the skull and contrecoup are located opposite to the site of direct impact. Contusions can markedly expand or “blossom” in the first several hours after injury, and this effect may cause neurological decline warranting neurosurgical intervention (Fig. 3B).
Diffuse axonal injury (DAI): DAI is another common and potentially devastating type of brain injury occurring in almost half of all cases of severe head trauma. It is a major cause of unconsciousness and persistent vegetative state after a head injury. DAI refers to the damage triggered by traumatic shearing forces which occur when the head is rapidly accelerated-decelerated (whiplash type injury) and/or rapidly rotated, leading to stretching or severing of axons that traverse junctions between different areas of density in the brain, including the cortical mantle, brainstem and corpus callosum (Figs 3C & D). It is thought that axonal damage is actually largely due to secondary biochemical cascades triggered by linear and rotational forces thereby leading to a delayed onset of symptoms. DAI is difficult to detect as it does not show up on CT and requires an MRI. It should be suspected in any patient with a normal head CT yet significantly impaired level of consciousness. DAI seldom leads to death, however the outcome can be poor, particularly in older patients. There is no specific neurosurgical role in DAI alone, except supportive in the intensive care unit environment, with subsequent input from TBI rehabilitation staff. For comatose DAI patients, an ICP monitor may be inserted by a neurosurgeon to measure brain pressures in the absence of a reliable clinical exam.
Postconcussion syndrome: While the term concussion could refer to any type of TBI event, it is frequently used in the setting of non-severe brain injury. In postconcussion syndrome, TBI patients can present with headache, nausea and vomiting, loss of appetite, “dizziness”, irritability, problems with concentration, fatigue and depression. While many symptoms resolve in the first few weeks after the injury, they can persist for a few months, and during this time should be gradually improving. Post-TBI patients presenting to their local physicians should not have new or progressive mental status impairment or new or progressive neurological dysfunction, and at no time should CSF leakage be expected.

Recommendations for the Investigation and Management of TBI for the General Practice Community

TBI is generally managed in the acute care setting (this may include surgical treatment of the injured brain and/or craniofacial skeleton) followed by a rehabilitation unit setting. However for patients presenting to General Practioners with a postconcussion syndrome including the aforementioned symptoms, usually reassurance, and recommendations for adequate rest, good hydration and mild analgesia will suffice. Such symptoms should settle. However, if they do not, or if a post-TBI patient presents with new or progressive worrisome symptoms and signs (Table 1), referral to a local emergency department is warranted. A noncontrast head CT (with both soft tissue and bone windows) is a good screening tool for such patients, and such concerns can be discussed with a neurosurgeon. Finally, despite the long-term physical disability that can be caused by TBI, the associated complex psychological changes in fact cause the greatest impact on quality of life for some patients. Cognitive, personality and behavioral changes are reported by survivors and their family members to be more disabling than any physical deficits (Table 2). Patience and serial counseling, and the input of community services associated with brain injury units are generally required to optimise outcomes in such patients.

Table 1. “TBI red flags” in the GP setting – a possible neurosurgical problem?

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Watch for any of these in TBI patients following hospital dismissal:

Worsening headaches
Worsening nausea and vomiting with poor oral intake
New or progressive neurological symptoms and signs
Unexplained fevers, neck stiffness
CSF leakage from the nose or ear or down the back of the throat

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Table 2: Common rehabilitation problems following TBI

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The following problems are often complex and chronic and impact on both the patient and family. They are best managed in conjunction with a multidisciplinary rehabilitation team:

Affective disturbances - depression, anxiety, and mood swings
Behavioural disturbances - problems with agitation, aggression, distractibility, and impulsivity.
Cognitive problems - short term memory loss, dyspraxias, visuospatial problems, frontal lobe executive dysfunction (i.e., impaired planning, sequencing, and judgement skills)
Post-traumatic epilepsy - approximately 5% of all TBI patients will develop epilepsy, with the highest risk in those with depressed skull fractures, intracranial haematomas or early seizures.
Limb contractures and spasticity - as a result of damage to the central nervous system
Heterotopic ossification
Electrolyte disturbances - syndrome of inappropriate antidiuretic hormone secretion (SIADH); watch for low serum sodium
Vocational and avocational problems - return to work issues, driving, sexuality problems, drug and alcohol dependence

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Figure 1. CT scan images of skull fractures

A. Linear fractures (frontal bone). B. Depressed fracture of the parietal and temporal bones prior to surgery. C. The same patient’s skull after surgical reconstruction with titanium mesh. D. Skull base fracture (occipital bone).

Figure 2. CT scan images of haematomas

A. Epidural haematoma (uniformly lens-shaped). B. Acute-on-chronic subdural haematoma (heterogeneous contents and irregular shape; follows the brain’s gyral pattern). C. Traumatic subarachnoid haemorrhage. D. Intraparenchymal haematoma (nontraumatic in this instance).

Figure 3. CT & MR scan images of other brain injuries

A. Simple contusions ("bruised" brain regions) at the time of presentation. B. A “blossomed” contusion, 6 hours post-injury. C & D. MR images of diffuse axonal injury (DAI). Common DAI sites in the brain include the gray-white junction of the cortex (circles in C) and the corpus callosum (arrow heads in C), and the upper brainstem (circle in D).

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