Xenon-enhanced CT scanning is a method of computed tomography (CT scanning) used for neuroimaging in which the subject inhales xenon gas while CT images are made.[1] The method can be used to assess changes in cerebral blood flow in the period shortly after a traumatic brain injury.[1] The diffusion of the gas into the tissues shows how much blood flow each area is getting.[1]
Rehabilitation is the treatment for the subacute and chronic stages of recovery.[57] Once medically stable, patients may be transferred to a subacute nursing unit of the medical center or to an independent rehabilitation hospital.[57] After discharge from the inpatient rehabilitation treatment unit, care may be given on an outpatient basis. Respite care, including day centers and leisure facilities for the disabled, offers time off for caregivers and activities for people with TBI.[67] People with TBI who cannot live independently or with family may be cared for in supported living facilities such as group homes.[67] People who cannot return to regular employment may be given vocational rehabilitation; this supportive employment matches job demands to the worker’s abilities.[67]
Rehabilitation aims to improve independent function at home and in society and to help adapt to disabilities or change living conditions to accommodate impairments[57] and has demostrated its general effectiveness, when conducted by a team of specialists, in head trauma.[68] As for any patient with neurologic deficits, a multidisciplinary approach is key to limiting and overcoming disability. Neurologists will be the main physicians involved, but depending on the symptom, doctors of other medical specialties may also be helpful. Allied treatments such as physiotherapy, speech and language therapy or occupational therapy can also help to manage some symptoms and maintain quality of life. Treatment of neuropsychiatric symptoms such as emotional distress and clinical depression may involve mental health professionals such as therapists, psychologists, and psychiatrists, while neuropsychologists can help to evaluate and manage cognitive deficits.[57] Those who show psychiatric or behavioral problems may also be helped with medication.[69]
The primary concerns are ensuring proper oxygen supply, maintaining adequate cerebral blood flow, and controlling raised intracranial pressure (ICP).[3] Since high ICP deprives the brain of badly needed blood flow[56] and can cause deadly brain herniation, special care is taken to maintain intracranial pressure within normal limits where possible. Other methods to prevent damage include management of other injuries through surgery and prevention of seizures.[48][15]
People with moderate to severe injuries are likely to receive treatment in an intensive care unit, followed by a neurosurgical ward.[57] Medical personnel try to stabilize the patient and focus on preventing further injury because little can be done to reverse the initial damage caused by trauma.[57] Certain facilities are equipped to handle TBI better than others; initial measures include transporting patients to an appropriate treatment center.[27][58]
Neuroimaging is helpful but not flawless in detecting raised ICP.[59] A more accurate way to measure ICP is to place a catheter into a ventricle of the brain.[26] This has the added benefit of allowing drainage of cerebrospinal fluid which immediately releases pressure from inside the skull.[26] Treatment of raised ICP may be as simple as tilting the patient’s bed and straightening the head to promote blood flow through the veins of the neck. Sedatives and paralytic agents are often used.[27] Hypertonic saline can improve ICP by reducing the amount of cerebral water (swelling), though it is used with caution to avoid electrolyte imbalances or heart failure.[2] Mannitol, an osmotic diuretic,[2] was also studied for this use,[60][61][62] but such studies have been heavily questioned. [63] Hypertonic saline may be more effective.[47] Diuretics, drugs that increase urine output to reduce excessive fluid in the system, may be used to treat high intracranial pressures, but may cause hypovolemia (insufficient blood volume).[26] Hyperventilation, causing the patient to breathe more than normal, causes blood vessels to constrict; this decreases blood flow to the brain and reduces ICP, but it potentially causes ischemia.[3][26] Thus it is only used in the short term and as a last resort.[3]
Endotracheal intubation and mechanical ventilation may be used to ensure proper oxygen supply and provide a secure airway.[48] Hypotension (low blood pressure), which has a devastating outcome in TBI, can be prevented by giving intravenous fluids to maintain a normal or even high blood pressure. Failing to maintain blood pressure can result in inadequate blood flow to the brain.[15] It is also important to regulate body temperature, because increased temperature raises the brain’s metabolic needs, potentially depriving it of nutrients.[64] Seizures are common. While they can be treated with benzodiazepines, these drugs are used carefully because they can depress breathing and lower blood pressure.[27] Drug therapy may also include sedation, pain control, and drugs to prevent delirium.[3] TBI patients are more susceptible to side effects and may react adversely or be inordinately sensitive to some pharmacological agents.[57] It is important to monitor for signs of deterioration such as a decreasing level of consciousness.[2][3]
Surgery can be performed on mass lesions or to eliminate objects that have penetrated into the brain. Mass lesions such as contusions or hematomas causing a significant mass effect (shift of intracranial structures) are emergencies and need to be removed surgically.[15] For intracranial hematomas, the collected blood may be removed using suction or forceps or it may be floated off with water.[15] It may also be necessary to locate hemorrhaging vessels and control bleeding.[15] In penetrating brain injury, damaged tissue is surgically debrided, and craniotomy may be needed.[15] Craniotomy, in which part of the skull is removed, is required in about a third of severe TBIs.[26] It may be needed to remove pieces of fractured skull or other objects that have become embedded in the brain.[65] Decompressive craniectomy (DC) is performed routinely in the very short period following TBI during operations to treat hematomas; part of the skull is removed temporarily (primary DC).[66] DC performed hours or days after TBI in order to control high intracranial pressures (secondary DC) has not been shown to improve outcome in some trials and may be associated with severe side effects.[66][2]
The type, direction, intensity, and duration of forces all contribute to the characteristics and severity TBI.[2] Forces that may contribute to TBI include angular, rotational, shear, and translational forces.[21] Even in the absence of an impact, significant acceleration or deceleration of the head can cause TBI; however in most cases a combination of impact and acceleration is probably to blame.[21] Forces involving the head striking or being struck by something, termed contact or impact loading, are the cause of most focal injuries, and movement of the brain within the skull, termed noncontact or inertial loading, usually causes diffuse injuries.[12] The violent shaking of an infant that causes shaken baby syndrome commonly manifests as diffuse injury.[40] In impact loading, the force sends shock waves through the skull and brain, resulting in tissue damage.[21] Shock waves caused by penetrating injuries can also destroy tissue along the path of a projectile, compounding the damage caused by the missile itself.[15]
Damage may occur directly under the site of impact, or it may occur on the side opposite the impact (coup and contrecoup injury, respectively).[39] When a moving object impacts the stationary head, coup injuries are typical,[41] while contrecoup injuries are usually produced when the moving head strikes a stationary object.[42]
Subdural hematomas are divided into acute, subacute, and chronic, depending on their speed of onset. Acute subdural hematomas that are due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression.
Acute bleeds develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. They are most severe if associated with cerebral contusions.[2] Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the usually arterial bleeding of an epidural hemorrhage. Acute subdural bleeds have a high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the velocities necessary to cause them cause other severe injuries as well.[4] The mortality rate associated with acute subdural hematoma is around 60 to 80% [5]
Chronic subdural bleeds develop over the period of days to weeks, often after minor head trauma, though such a cause is not identifiable in 50% of patients.[6] They may not be discovered until they present clinically months or years after a head injury.[7] The bleeding from a chronic bleed is slow, probably from repeated minor bleeds, and usually stops by itself.[1][8] Since these bleeds progress slowly, they present the chance to be stopped before they cause significant damage. Small subdural hematomas, those less than a centimeter wide, have much better outcomes than acute subdural bleeds: in one study, only 22% of patients with chronic subdural bleeds had outcomes worse than “good” or “complete recovery”.[2] Chronic subdural hematomas are common in the elderly.[7]
While the clinical picture of subarachnoid hemorrhage may have been recognized by Hippocrates, the existence of cerebral aneurysms and the fact that they could rupture was not established until the 18th century.[48] The associated symptoms were described in more detail in 1886 by Edinburgh physician Dr Byrom Bramwell.[49] In 1924, London neurologist Sir Dr Charles P. Symonds (1890–1978) gave a complete account of all major symptoms of subarachnoid hemorrhage, and he coined the term “spontaneous subarachnoid hemorrhage”.[48][50][51] Symonds also described the use of lumbar puncture and xanthochromia in diagnosis.[52]
The first surgical intervention was performed by Mr Norman Dott, who was a pupil of Dr Harvey Cushing then working in Edinburgh. He introduced the wrapping of aneurysms in the 1930s, and was an early pioneer in the use of angiograms.[51] American neurosurgeon Dr Walter Dandy, working in Baltimore, was the first to introduce clips in 1938.[22] Microsurgery was applied to aneurysm treatment in 1972 in order to further improve outcomes.[53] The 1980s saw the introduction of triple H therapy[32] as a treatment for delayed ischemia due to vasospasm, and trials with nimodipine[30][54] in an attempt to prevent this complication. The Italian neurosurgeon Dr Guido Guiglielmi introduced his endovascular coil treatment in 1991.[23][55]
Screening for aneurysms is not performed on a population level; because they are relatively rare, it would not be cost-effective. If someone has two or more first-degree relatives who have suffered an aneurysmal subarachnoid hemorrhage, screening may be worthwhile.[1][46]
Autosomal dominant polycystic kidney disease (ADPKD), a hereditary kidney condition, is known to be associated with cerebral aneurysms in 8% of cases, but most such aneurysms are small and therefore unlikely to rupture. As a result, screening is only recommended in families with ADPKD where one family member has suffered a ruptured aneurysm.[47]
An aneurysm may be detected incidentally on brain imaging; this presents a conundrum, as all treatments for cerebral aneurysms are associated with potential complications. The International Study of Unruptured Intracranial Aneurysms (ISUIA) provided prognostic data both in people who had previously suffered a subarachnoid hemorrhage and people who had aneurysms detected by other means. Those who had previously suffered SAH were more likely to bleed from other aneurysms. In contrast, those who had never bled and had small aneurysms (smaller than 10 mm) were very unlikely to suffer SAH and were likely to sustain harm from attempts to repair these aneurysms.[45] On the basis of the ISUIA and other studies, it is now recommended that people are only considered for preventative treatment if they have a reasonable life expectancy and have aneurysms that are highly likely to rupture.[46]
According to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000 annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.[44]
Although the group of people at risk for SAH is younger than the population usually affected by stroke,[2] the risk still increases with age. Young people are much much less likely than middle-aged people (risk ratio 0.1, or 10%) to suffer a subarachnoid hemorrhage.[44] The risk continues to rise with age and is 60% higher in the very elderly (over 85) than in those between 45 and 55.[44] Risk of SAH is about 25% higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause, such as a decrease in estrogen levels.[44]
Genetics may play a role in a person’s disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people who have suffered a subarachnoid hemorrhage.[4] However, lifestyle factors are more important in determining overall risk.[2] These risk factors are smoking, hypertension (high blood pressure) and excessive alcohol intake.[12] Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked.[2] Some protection of uncertain significance is conferred by Caucasian ethnicity, hormone replacement therapy, diabetes mellitus and higher than normal levels of cholesterol.[2] Approximately 4% of aneurysmal bleeds occur after sexual intercourse and 10% of people with SAH are bending over or lifting heavy objects at the onset of their symptoms.[5]
Overall, about 1% of all people have one or more cerebral aneurysms. Most of these, however, are small and unlikely to rupture.[45]
SAH is often associated with a poor outcome.[2] The death rate (mortality) for SAH is between 40 and 50%,[12] but trends for survival are improving.[1] Of those who survive hospitalization, more than a quarter have significant restrictions in their lifestyle, and less than a fifth have no residual symptoms whatsoever.[24] Delay in diagnosis of minor SAH (mistaking the sudden headache for migraine) contributes to poor outcome.[13] Factors found on admission that are associated with poorer outcome include poorer neurological grade; systolic hypertension; a previous diagnosis of heart attack or SAH; liver disease; more blood and larger aneurysm on the initial CT scan; location of an aneurysm in the posterior circulation; and higher age.[37] Factors that carry a worse prognosis during the hospital stay include occurrence of delayed ischemia resulting from vasospasm, development of intracerebral hematoma or intraventricular hemorrhage (bleeding into the ventricles of the brain) and presence of fever on the eighth day of admission.[37]
So-called “angiogram-negative subarachnoid hemorrhage”, SAH that does not show an aneurysm with four-vessel angiography, carries a better prognosis than SAH with aneurysm; however, it is still associated with a risk of ischemia, rebleeding and hydrocephalus.[14] Perimesencephalic SAH (bleeding around the mesencephalon in the brain), however, has a very low rate of rebleeding or delayed ischemia, and the prognosis of this subtype is excellent.[40]
The prognosis of head trauma is thought to be influenced in part by the location and amount of subarachnoid bleeding.[15] It is difficult to isolate the effects of SAH from those of other aspects of traumatic brain injury; it is unknown whether the presence of subarachnoid blood actually worsens the prognosis or whether it is merely a sign that a significant trauma has occurred.[15] People with moderate and severe traumatic brain injury who have SAH when admitted to a hospital have as much as twice the risk of dying as those who do not.[15] They also have a higher risk of severe disability and persistent vegetative state, and traumatic SAH has been correlated with other markers of poor outcome such as post traumatic epilepsy, hydrocephalus, and longer stays in the intensive care unit.[15] However, more than 90% of people with traumatic subarachnoid bleeding and a Glasgow Coma Score over 12 have a good outcome.[15]
There is also modest evidence that genetic factors influence the prognosis in SAH. For example, having two copies of ApoE4 (a variant of the gene encoding apolipoprotein E that also plays a role in Alzheimer’s disease) seems to increase risk for delayed ischemia and a worse outcome.[41]
Hydrocephalus (obstruction of the flow of cerebrospinal fluid) may complicate SAH in both the short- and long term. It is detected on CT scanning, on which there is enlargement of the lateral ventricles. If the level of consciousness is decreased, drainage of the excess fluid is performed by therapeutic lumbar puncture, extraventricular drain (a temporary device inserted into the one of the ventricles) or occasionally a permanent shunt.[1][3] Relief of hydrocephalus can lead to an enormous improvement in a person’s condition.[5] Fluctuations in blood pressure and electrolyte disturbances, as well as pneumonia and cardiac decompensation occur in about half the hospitalized persons with SAH and may worsen prognosis.[1] Seizures occur during the hospital stay in about a third of cases.[3] Many believe that patients might benefit from prevention with antiepileptic drugs.[3] Although this is widely practiced,[34] it is controversial and not based on good evidence.[35][36] In some studies, use of these drugs was associated with a worse prognosis; this might be because they actually cause harm, or because they are used more often in persons with a poorer prognosis.[37][38] There is a possibility of a gastric hemorrhage due to stress ulcers.[39]