Head Injury in the Elderly: Role of Clinicians in Comprehensive Management

Head injury has historically been the domain of the surgeon. However, populations are aging rapidly and the number of people >85 years old is expected to double in the coming decades. Currently, in England, the majority of head injuries occur due to falls from a height of a person, generally an elderly person.

Between 2009 and 2015, the rate of patients starting oral anticoagulant treatment increased by 58%, with more than 500/100,000 people.

When the head injury is due to falls in a patient on anticoagulation or taking antiplatelet agents, complications can reach 15.9%.

Although neurosurgical teams are highly trained to treat hemorrhagic complications, age is associated with the accumulation of multiple morbidities.

Multimorbidity patients challenge traditional surgical services because the rise of superspecialization has attenuated generalist skills. Adverse outcomes in elderly surgical patients are well known. These usually occur mainly as a consequence of surgical complications.

In the modern era, it is necessary to recognize that traditional surgical services cannot offer a high quality of medical care to complex patients, without support from medical teams. Modern models of collaborative trauma care have evolved in orthopedics; but they are not yet ubiquitous.

Doctors in England are often inadequately equipped to handle what are often complicated situations, attributed in part to a lack of support from the relevant authorities. Therefore, many haemorrhagic complications of head trauma remain during complex medical admissions as a result of the 250,000 inpatient falls that occur per year in the UK.

Trauma services do not have the capacity to care for all patients hospitalized with complications from head trauma and typically only accept candidates for neurosurgery.

Therefore, physicians often have clinical responsibility for the care of patients with head injury complications, but lack the knowledge and experience to optimally manage this cohort. So it is necessary for doctors who provide support for traumatic head injuries to know more about it.

During aging, a series of physiological changes occur that predispose older patients to hemorrhagic complications of head injury.

Evidence indicates that 30% of intracranial lesions do not present reliable clinical signs.

Brain atrophy due to aging causes older patients to tolerate substantial intracranial hemorrhages better than younger patients with an equivalent injury. This may lead to underestimation of the severity of the injury and delay in presentation.

Therefore, non-contrast head CT may be appropriate for all elderly patients with head injury, especially if the imaging result will influence medical decision making.

A study from the United Kingdom showed that older people wait longer for imaging than younger patients, despite having a higher risk of bleeding and/or adverse outcomes.

Most of the common hemorrhagic consequences of head injury can be adequately visualized by CT, although MRI may have greater sensitivity in evaluating diffuse parenchymal damage, especially when the injury is small in volume and not detected on plain CT. .

In anticoagulated patients with a normal initial CT scan, there is little risk that subsequent scans will show hemorrhage. Therefore, anticoagulated patients may benefit from a period of observation and repeat CT before discharge.

The role of neurosurgery is to relieve intracranial hypertension, improve cerebral perfusion pressure, and correct depressed skull fractures. The NICE guide establishes that the presence of the following signs requires neurosurgical consultation:

•  Unexplained confusion of >4 hours

•  Persistent Glasgow Coma Score (PCG) <8

•  Deterioration of PCG after admission

•  Focal neurological signs

•  Seizure without complete recovery

•  Penetrating head injury

•  Cerebrospinal fluid leak.

North American consensus guidelines indicate that in patients with potential benefit, surgical evacuation should consider the presence of hemorrhage (regardless of PCG) when radiological parameters show:

•  Subdural hematoma with clot thickness >10 mm or midline shift >5 mm

•  Epidural hematoma with volume >30 cm.

Surgery may also be indicated when these criteria are not met and clinical signs of cerebral herniation or intracranial hypertension (e.g., anisocoria) remain, especially in the setting of clinical deterioration. Surgical results may depend on the time between the appearance of neurological signs and surgical decompression. The indication for surgery must be carried out within 4 hours.

In patients who do not meet surgical criteria but have a PCG <9, intracranial pressure monitoring in an intensive care unit is recommended. Surgery is indicated if intracranial pressure remains above 20 mmHg.

There is considerable debate and controversy regarding the indication and outcome of decompressive neurosurgery in patients who do not fit the aforementioned hematoma criteria. Several studies suggest that these patients tend to have longer survival but potentially worse neurological outcomes, so decompressive craniectomy in patients with advanced frailty is generally less accepted.

Nonsurgical treatment is appropriate for small hematomas or when intracranial pressure is <20 mmHg. Nonsurgical interventions include: head elevation, sedation, analgesia, mechanical hyperventilation to maintain normal pCO2, euthermia, antiepileptics, mannitol (or hypertonics, saline), and intracranial pressure monitoring.

In patients who are potentially surgical candidates, the risk of hematoma expansion indicates serial CT, 8-12 hours after injury. Ventricular catheters, considered the gold standard in the US, are used to monitor intracranial pressure. These devices allow therapeutic drainage of cerebrospinal fluid if necessary, although they carry a greater risk of infection. In the UK, monitoring is most commonly done with intraparenchymal devices.

Better outcomes of intracranial hemorrhage have been demonstrated in patients transferred to a neurology or neurosurgery service, even if immediate surgical intervention is not required. In symptomatic patients who may be good candidates for surgery if they develop deterioration, transfer to a neurosurgical center may be appropriate for medical follow-up and treatment (e.g., for severe hypertension).

Despite the availability of consensus guidelines, older patients are less likely to undergo neurosurgical intervention than younger patients with equivalent injury. This may be because older patients treated surgically have inferior outcomes.

In one study, survival after surgery for traumatic brain injury was 59.3% for patients aged 65 to 74 years and only 32.4% for those aged >75 years. However, compared with age-matched peers treated conservatively, older people who underwent surgery after head trauma had significantly reduced mortality, with better functional outcomes.

Debate still persists about the benefits and role of decompressive neurosurgery in the elderly patient with hemorrhagic complications of head injury. This is complicated by difficulties in interpreting the literature when it is known that older patients tend to tolerate intracranial injury before reflecting the severity of their injury through the PCG. Therefore, in older patients with PCG similar to that of younger patients, adverse outcomes may represent a more severe injury.

The balance between risk and benefit in older patients with complications of traumatic brain injury is therefore complex. Careful consideration of postoperative outcomes is required on an individual basis. Age and fragility are not synonyms. In older people there may be wide functional heterogeneity.

Emerging evidence indicates that frailty assessment provides a more accurate prediction of surgical risk than age, while frailty appears to intuitively influence the decision to operate on patients undergoing oncologic neurosurgery. There is some evidence that frailty is associated with poor outcomes from geriatric trauma, but there is little specific data published for older adults with traumatic brain injury.

Sarcopenia defined by CT criteria is emerging as a potential surrogate for frailty assessment, which may be useful in predicting future outcomes.

Importantly, the UK’s trauma center and spoke model means that many decisions whether to operate or not are currently made without direct assessment from an experienced neurosurgeon. Therefore, the decision to offer surgery or not depends on the collection of information and communication between doctors and surgeons, based on the baseline evaluation.

Combined with the severity of the injury, this determines the potential for recovery and allows for neurosurgical prognosis. However, subsequent communication with the patient and family is often the responsibility of the referring medical team, especially when surgery is not indicated. This emphasizes the need for clinicians to understand the basis and rationale for decision making. In addition to reviewing the mechanism of injury and optimizing comorbidity, the responsibility of physicians is also to treat complications and promote rehabilitation.

> Management of anticoagulation

Many older people regularly take anticoagulants and antiplatelet medications, which contribute to bleeding complications from head injury. Challenging decisions related to reversal of anticoagulant and antiplatelet effect are often required. The programmed reintroduction of these drugs after hemorrhage resulting from head trauma is also complex. In these cases, a risk assessment criteria is required.

In each individual, the risk of thrombosis must be weighed against the risk of recurrent intracranial hemorrhage. These risks are often difficult to estimate for general practitioners without experience in managing head trauma. This can lead to poor decision making, so specialist advice is recommended. Mortality due to hemorrhagic complications of traumatic brain injury in the presence of continuous anticoagulation is surprisingly high, and can reach 80.6%.

The risks associated with cessation of anticoagulants are generally extrapolated from population annualized risks and therefore may be higher in acute cases. Despite this observation, the risks of thrombosis are usually substantially lower than those of acute bleeding, even for patients considered at high risk for thrombosis. Therefore, discontinuation of anticoagulants is almost always required; this should be discussed with a hematologist with experience in coagulation.

A management plan and risk-benefit analysis must be clearly documented and reviewed periodically. In the United Kingdom, it is recommended that warfariin be discontinued in patients with suspected or confirmed intracranial bleeding and immediate initiation of prothrombin complex concentrate.

It is likely that patients admitted with anticoagulation will require a CT scan, determination of the INR (International Normalized Ratio) and, if there is a strong suspicion of head injury, determination of the INR and the concentration of the prothrombin complex. The use of factor VIIa Recombinant or fresh frozen plasma are not acceptable treatments.

Other measures should include 5-10 mg of intravenous vitamin K, immediate cessation of all anticoagulant therapy, and serial measurement of INR at 30 minutes, 4 to 6 hours, and 24 hours, if new doses of concentrate are administered. of the prothrombin complex.

Reversal of direct oral anticoagulants (DOAs) is more complex. The factor II inhibitor dabigatran can be effectively reversed with idarucizumab. Andexenant, a specific reversal agent for factor X inhibitors, is in development.

Meanwhile, the consensus currently advises that suspected intracranial hemorrhage in patients taking a factor Tranexamic acid can be used as an adjunct and limited risk of thrombosis.

There is some evidence indicating that clopidogrel may predispose to traumatic intracranial hemorrhage, to a greater extent than warfarin. There is little evidence to determine the risks of modern potent antiplatelet agents.

Strategies to reverse the antiplatelet effect include regular tranexamic acid, platelet infusion (typically 2 pools) and, in extreme cases, recombinant activated factor VIIa.

Of note, although 2 pools of platelets would be expected to largely reverse the effect of aspirin, the prolonged pharmacodynamics of clopidogrel (washout period: 5 to 7 days) limits the effectiveness of platelet transfusions and is often require several pools. However, none of these interventions improve outcome after intracerebral hemorrhage.

> Restart of anticoagulants and antiplatelet agents

Although hematoma expansion and rebleeding are important risks after intracerebral hemorrhage, there is also an increased risk of thromboembolism, precipitated by immobility, the inflammatory response to trauma, and the procoagulant effects of reversal agents.

Non-pharmacological prophylaxis of venous thromboembolism should be performed and understanding the evolution with this risk profile allows for timely reestablishment of anticoagulant therapy when the risk of thrombosis is considered high. Current evidence regarding patients at high risk of thrombosis indicates that anticoagulant therapy can be reinstated after 10 days, with a modest risk of rebleeding. However, the risks of reinstating anticoagulation will vary, depending on the extent and site of the intracranial hemorrhage.

Currently, there is no consensus on what the ideal interval is, and what prospective studies should be done to answer this question. Many surgeons prefer to delay reinstitution of anticoagulation until brain CT indicates complete resolution of the hemorrhage. Inevitably, this requires a very careful appreciation of the risks of continuing to discontinue anticoagulation.

However, it should also be noted that the risks of discontinuing anticoagulant therapy are modest, even in the presence of modern metal heart valves. In these cases, the rate of valve thrombosis is 4% per year in patients who do not take anticoagulants. In patients with metallic heart valves, in whom anticoagulants were discontinued, a thrombosis rate of 4% and a variable risk of thrombosis (0–4%, at 30 days) were found.

Guidelines recommend stopping anticoagulation 7 to 10 days after bleeding complications from head trauma.

The evidence regarding reintroduction of ODAs after post-head injury hemorrhage is limited, but rebleeding after intracerebral injury hemorrhage is rarer with ODAs, compared with warfarin, and is probably safer. Therefore, when the risk of thrombosis is high, expert consensus also recommends restarting ODAs after 7 to 10 days of discontinuation.

The evidence regarding the reinstatement of antiplatelet agents is limited. However, after intracerebral hemorrhage, these agents are safer than anticoagulants. Expert consensus indicates that a cessation period of 7 to 10 days may be appropriate.

For patients at extremely high risk of thrombosis in whom reinstitution of early anticoagulation was considered before 7 days, or when the risk of bleeding is higher, standard practice is gradual reintroduction, with escalating doses, twice daily, low molecular weight heparin (LMWH). This is generally considered safer and more effective than unfractionated heparin. It is noted that in the case of new bleeding, up to 60% of the effect of LMWH can be antagonized by protamine. Embolization of recent venous thrombosis of the lower extremity can be mitigated by inserting a filter into the inferior vena cava.

> Management of thrombocytopenia

Thrombocytopenia carries a 12-fold increased risk of hematoma expansion. Patients presenting with a platelet count <135 x 109/L are 31.5 times more likely to require neurosurgical intervention. Thrombocytopenic patients with intracranial hemorrhage should receive a platelet transfusion to maintain platelets >100 x 109/L.

> Prophylaxis

and increased pressure Early seizures occur in 30% of patients after traumatic brain injury. Most seizures occur within the first 24 hours after the injury. Seizures are thought to increase the risks of secondary brain diseases through functional intracranial hypoxia.

Anticonvulsant prophylaxis has been shown to reduce the frequency of early seizures, although these agents have no effect on the long-term development of epilepsy after brain injury. Current evidence indicates that levetiracetam has a better safety profile and equal efficacy than phenytoin. It has also been associated with better functional outcomes. Therefore, prophylaxis with 500–1000 mg, 2 times/day, for 7 days is recommended.

In patients who have not had a seizure during this period, no advantage of long-term anticonvulsant therapy has been observed. In elderly patients, lower doses should be considered, and it is important that the duration of therapy be confirmed before discharge.

In patients who experience seizures after a traumatic brain injury, the long-term risk of seizures depends on the severity of the injury. Approximately 8% to 16% will suffer from post-traumatic epilepsy by age 2 years.

On the other hand, patients with a persistent reduction in consciousness, considered disproportionate to the neurological lesion, 15-20% will show signs of non-convulsive seizures on the electroencephalogram. In general, anticonvulsants are continued throughout the hospitalization of patients who have suffered a seizure and are gradually weaned after discharge, under neurological supervision.

> Hyponatremia

Hyponatremia is a common complication of intracranial injury. Careful clinical evaluation is required to differentiate between syndromes of inappropriate antidiuretic hormone secretion, cerebral salt wasting, and other causes such as hypoadrenalism or drug effects. Inappropriate secretion of antidiuretic hormone is the most common electrolyte disorder after head injury, but it can be confused with cerebral salt wasting, the pathophysiology of which is poorly understood, although it is known to produce excessive renal excretion of sodium and subsequent dehydration.

The evaluation of hyponatremia is complicated by the fact that both electrolyte disturbances usually manifest with similar laboratory parameters. However, the treatment is diametrically opposed and incorrect treatment risks deterioration of hyponatremia. Therefore, differentiation requires careful evaluation of fluid status.

Patients suffering from cerebral salt wasting have intravascular depletion and require intravenous volume replacement. Patients with inadequate antidiuretic hormone secretion are euvolemic and require fluid restriction. Generally, resolution of brain salt wasting occurs within 2 to 4 weeks after head trauma.

After an injury, elderly patients have high mortality and greater functional reduction than younger patients.

Among hospitalized patients in the United Kingdom mortality was reported to be 22.9%; 10.8% suffered moderate long-term disability and 5.3% suffered severe disability requiring permanent help in activities of daily living.

Outcomes are considerably worse for severe traumatic brain injury, with in-hospital mortality of 70-80%.