Skip to content.docx

50
Skip to content Patient - Trusted medical information and support On this page Epidemiology Aetiology Assessment Prehospital management Admission Patients not requiring admission Investigations Investigations for the cervical spine Indications for neurosurgical opinion Management Complications Prognosis Prevention References PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets . 403 0 0 0

Transcript of Skip to content.docx

Skip to content

Patient - Trusted medical information and support

On this page

Epidemiology

Aetiology

Assessment

Prehospital management

Admission

Patients not requiring admission

Investigations

Investigations for the cervical spine

Indications for neurosurgical opinion

Management

Complications

Prognosis

Prevention

References

PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

403

0

0

0

This article particularly refers to the National Institute for Health and Care Excellence (NICE) and Scottish Intercollegiate Guidelines Network (SIGN) clinical guidelines for head injury.[1][2]

Head injury can arise from blunt or penetrating trauma and result in direct injury at the impact site. Indirect injury may also be caused by movement of the brain within the skull, leading to contusions on the opposite side of the head from the impact, or disruptive injuries to axons and blood vessels from shearing or rotational forces as the head is accelerated and decelerated after the impact.

Traumatic brain injury may be categorised as primary (damage occurring at the time of impact) or secondary (injury as a result of neurophysiological and anatomical changes minutes to days following primary insult - eg, from cerebral oedema, haematoma or increased intracranial pressure).

Epidemiology

Hospital Episode Statistics data for the 2012-2013 annual dataset indicate that there were 171,600 admissions to hospitals in England with a primary diagnosis of head injury.[3]

70% are males.

33-50% are children under 15 years of age.[2]

There is an increasing number of patients admitted with head injuries aged 75 years (approaching 40%).[3]

Severe traumatic brain injury defined as Glasgow Coma Score (GCS) 90 mm Hg ensuring an adequate cerebral perfusion pressure - eg, boluses of 0.9% normal saline

Full cervical spine immobilisation

Attempted (unless other factors prevent this) if:[2]

GCS is 5 minutes

Anterograde or retrograde amnesia > 30 minutes

Seizures immediately prior to, or any time post injury

Any focal neurological deficit

Clinical suspicion of a possible skull fracture

Persistent vomiting (> 2) post injury

Severe Headache

Coagulopathic / bleeding disorder (including warfarin, clopidogrel, aspirin or dabigatran use)

Drug or alcohol ingestion

General observations recorded in the yellow or red zone of the NSW HealthBetween the Flags Observation charts

Additional Observations

Neurological observations including GCS, pupil size, pupil response to light, limb movement and limb strength must be completed on all patients

If indicated, commence Abbreviated Westmead Post Traumatic Amnesia Scale(A-WPTAS) assessment for patients 16 years

Additional History

1. Establish mechanism of injury

How injury was sustained

Date and time of injury

2. First aid / NSW ambulance treatment prior to arrival

Management Principles

1. Provide analgesia as required according to pain scale. Refer to Pain (any cause) NMG

2. Patient receives hourly observations as per additional observations above for 4 hours as a minimum

3. If any deterioration in patient condition is detected then medical officer must be immediately notified

4. Patient must be discharged into the care of a responsible adult or carer

5. Provide patient / carer with head injury discharge information in addition to discharge letter

6. Document assessment findings, interventions and outcomes

Updated: Jan 9, 2015

Medical Therapy

Complications

Outcome and Prognosis

Future and Controversies

Show All

Tables

References

Medical Therapy

The treatment of head injury may be divided into the treatment of closed head injury and the treatment of penetrating head injury. While significant overlap exists between the treatments of these 2 types of injury, some important differences are discussed. Closed head injury treatment is divided further into the treatment of mild, moderate, and severe head injuries.

Mild head injury

Most head injuries are mild head injuries. Most people presenting with mild head injuries will not have any progression of their head injury; however, a small percentage of mild head injuries progress to more serious injuries. Mild head injuries may be separated into low-risk and moderate-risk groups. Patients with mild-to-moderate headaches, dizziness, and nausea are considered to have low-risk injuries. Many of these patients require only minimal observation after they are assessed carefully, and many do not require radiographic evaluation. These patients may be discharged if a reliable individual can monitor them. Patients on anticoagulation therapy should have radiographic imaging performed even if they have had minimal head trauma as they can progress from a mild head injury to a catastrophic injury because their ability to coagulate blood has been medically inhibited.

Patients who are discharged after mild head injury should be given an instruction sheet for head injury care. The sheet should explain that the person with the head injury should be awakened every 2 hours and assessed neurologically. Caregivers should be instructed to seek medical attention if patients develop severe headaches, persistent nausea and vomiting, seizures, confusion or unusual behavior, or watery discharge from either the nose or the ear.

Patients with mild head injuries typically have concussions. A concussion is defined as physiologic injury to the brain without any evidence of structural alteration. Concussions are graded on a scale of I-V. A grade I concussion is one in which a person is confused temporarily but does not display any memory changes. In a grade II concussion, brief disorientation and anterograde amnesia of less than 5 minutes' duration are present. In a grade III concussion, retrograde amnesia and loss of consciousness for less than 5 minutes are present, in addition to the 2 criteria for a grade II concussion. Grade IV and grade V concussions are similar to a grade III, except that in a grade IV concussion, the duration of loss of consciousness is 5-10 minutes, and in a grade V concussion, the loss of consciousness is longer than 10 minutes.

As many as 30% of patients who experience a concussion develop postconcussive syndrome (PCS). PCS consists of a persistence of any combination of the following after a head injury: headache, nausea, emesis, memory loss, dizziness, diplopia, blurred vision, emotional lability, or sleep disturbances. Fixed neurologic deficits are not part of PCS, and any patient with a fixed deficit requires careful evaluation. PCS usually lasts 2-4 months. Typically, the symptoms peak 4-6 weeks following the injury. On occasion, the symptoms of PCS last for a year or longer. Approximately 20% of adults with PCS will not have returned to full-time work 1 year after the initial injury, and some are disabled permanently by PCS. PCS tends to be more severe in children than in adults. When PCS is severe or persistent, a multidisciplinary approach to treatment may be necessary. This includes social services, mental health services, occupational therapy, and pharmaceutical therapy.

After a mild head injury, those displaying persistent emesis, severe headache, anterograde amnesia, loss of consciousness, or signs of intoxication by drugs or alcohol are considered to have a moderate-risk head injury. These patients should be evaluated with a head CT scan. Patients with moderate-risk mild head injuries can be discharged if their CT scan findings reveal no pathology, their intoxication is cleared, and they have been observed for at least 8 hours.

Moderate and severe head injury

The treatment of moderate and severe head injuries begins with initial cardiopulmonary stabilization by ATLS guidelines. The initial resuscitation of a patient with a head injury is of critical importance to prevent hypoxia and hypotension. In the Traumatic Coma Data Bank study, patients with head injury who presented to the hospital with hypotension had twice the mortality rate of patients who did not present with hypotension. The combination of hypoxia and hypotension resulted in a mortality rate 2.5 times greater than if neither of these factors was present. Of note, recent studies have demonstrated that hyperoxia in severe head injury patients who have been intubated can also be deleterious. Hyperoxia with a PaO2> 300 mm Hg in ventilated TBI patients was associated with higher in-hospital case fatality.[8]

Once a patient has been stabilized from the cardiopulmonary standpoint, evaluation of their neurologic status may begin. The initial GCS score provides a classification system for patients with head injuries but does not substitute for a neurologic examination. After assessment of the coma score, a neurologic examination should be performed. If a patient has received muscle relaxants, the only neurologic response that may be evaluated is the pupillary response.

After a thorough neurologic assessment has been performed, a CT scan of the head is obtained. The results of the CT scan help determine the next step. If a surgical lesion is present, arrangements are made for immediate transport to the operating room. Fewer than 10% of patients with TBI have an initial surgical lesion.

Although no strict guidelines exist for defining surgical lesions in persons with head injury, most neurosurgeons consider any of the following to represent indications for surgery in patients with head injuries: extra-axial hematoma with midline shift greater than 5 mm, intra-axial hematoma with volume greater than 30 mL, an open skull fracture, or a depressed skull fracture with more than 1 cm of inward displacement. In addition, any temporal or cerebellar hematoma that is larger than 3 cm in diameter is considered a high-risk hematoma because these regions of the brain are smaller and do not tolerate additional mass as well as the frontal, parietal, and occipital lobes. These high-risk temporal and cerebellar hematomas are usually evacuated immediately

If no surgical lesion is present on the CT scan image, or following surgery if one is present, treatment of the head injury begins. The first phase of treatment is to institute general measures. Once appropriate fluid resuscitation has been completed and the volume status is determined to be normal, intravenous fluids are administered to maintain the patient in a state of euvolemia or mild hypervolemia.

Another supportive measure used to treat patients with head injuries is elevation of the head. When the head of the bed is elevated to 20-30, the venous outflow from the brain is improved, thus helping to reduce ICP. If a patient is hypovolemic, elevation of the head may cause a drop in cardiac output and CBF; therefore, the head of the bed is not elevated in hypovolemic patients. In addition, the head should not be elevated (1) in patients in whom a spine injury is a possibility or (2) until an unstable spine has been stabilized.

Sedation is often necessary in patients with traumatic injury. Some patients with moderate head injuries have significant agitation and require sedation. In addition, patients with multisystem trauma often have painful systemic injuries that require pain medication, and many intubated patients require sedation. Short-acting sedatives and analgesics should be used to accomplish proper sedation without eliminating the ability to perform periodic neurologic assessments. This requires careful titration of medication doses and periodic weaning or withholding of sedation to allow periodic neurologic assessment. Intravenous lidocaine administered along with rapid sequence induction before endotracheal intubation is not associated with significant hemodynamic changes in traumatic brain injury patients.[9]

The use of anticonvulsants in patients with TBI is a controversial issue. No evidence exists that the use of anticonvulsants decreases the incidence of late-onset seizures in patients with either closed head injury or TBI. Temkin et al demonstrated that the routine use of Dilantin in the first week following TBI decreases the incidence of early-onset (within 7 d of injury) seizures but does not change the incidence of late-onset seizures.[10] In addition, the prevention of early posttraumatic seizures does not improve the outcome following TBI. Therefore, the prophylactic use of anticonvulsants is not recommended for more than 7 days following TBI and is considered optional in the first week following TBI.

After instituting general supportive measures, the issue of ICP monitoring is addressed. ICP monitoring has consistently been shown to improve outcome in patients with head injuries. ICP monitoring is indicated for any patient with a GCS score less than 9, any patient with a head injury who requires prolonged deep sedation or pharmacologic relaxants for a systemic condition, or any patient with an acute head injury who is undergoing extended general anesthesia for a nonneurosurgical procedure. Recent data from the American College of Surgeons Trauma Quality Improvement Program involving 10,628 adults with severe TBI revealed that ICP monitoring utilization was associated with lower mortality.[11]

ICP monitoring involves placement of an invasive probe to measure the ICP. Unfortunately, noninvasive means of monitoring ICP do not exist, although they are under development. ICP may be monitored by means of an intraparenchymal monitor, an intraventricular monitor (ventriculostomy), or an epidural monitor. These devices measure ICP by fluid manometry, strain-gauge technology, or fiberoptic technology.

Intraparenchymal ICP monitors are devices that are placed into the brain parenchyma to measure ICP by means of fiberoptic, strain-gauge, or other technologies. The intraparenchymal monitors are very accurate; however, they do not allow for drainage of CSF. Epidural devices measure ICP via a strain-gauge device placed through the skull into the epidural space. This is an older form of ICP measurement and is rarely used today because the other technologies available are more accurate and more reliable.

A ventriculostomy is a catheter placed through a small twist drill hole into the lateral ventricle. The ICP is measured by transducing the pressure in a fluid column. Ventriculostomies allow for drainage of CSF, which can be effective in decreasing the ICP. A risk of symptomatic hemorrhage exists with ventriculostomy placement, and Bauer et al report from a retrospective study that an international normalized ratio (INR) of 1.2-1.6 is an acceptable range for emergent ventriculostomy placement in patients with TBI.[12]

Once an ICP monitor has been placed, ICP is monitored continuously. No absolute value of ICP exists for which treatment is implemented automatically. In adults, the reference range of ICP is 0-15 mm Hg. The normal ICP waveform is a triphasic wave, in which the first peak is the largest peak and the second and third peaks are progressively smaller. When intracranial compliance is abnormal, the second and third peaks are usually larger than the first peak. In addition, when intracranial compliance is abnormal and ICP is elevated, pathologic waves may appear.

Lundberg described 3 types of abnormal ICP waves, A, B, and C waves.[13] Lundberg A waves, known as plateau waves, have a duration of 5-20 minutes and an amplitude of 50 mm Hg over the baseline ICP. After an episode of A waves dissipates, the ICP is reset to a baseline level that is higher than when the waves began. Lundberg A waves are a sign of severely compromised intracranial compliance. The rapid increase in ICP caused by these waves can result in a significant decrease in CPP and may lead to herniation. Recent data from a prospective observational study of severe blunt head injury patients demonstrated that a single episode of sustained increased ICP is an accurate predictor of poor outcome and is associated with an increased in-hospital mortality.[14]

Lundberg B waves have a duration of less than 2 minutes, and they have an amplitude of 10-20 mm Hg above the baseline ICP. B waves are also related to abnormal intracranial compliance. Because of their smaller amplitude and shorter duration, B waves are not as deleterious as A waves.

C waves, known as Hering-Traube waves, are low-amplitude waves that may be superimposed on other waves. They may be related to increased ICP; however, C waves can also occur in the setting of normal ICP and compliance.

When treating elevated ICP, remember that the goal of treatment is to optimize conditions within the brain to prevent secondary injury and to allow the brain to recover from the initial insult. Maintaining ICP within the reference range is part of an approach designed to optimize both CBF and the metabolic state of the brain. Treatment of elevated ICP is a complex process that should be tailored to each particular patient's situation and should not be approached in a "cookbook" manner. Many potential interventions are used to lower ICP, and each of these is designed to improve intracranial compliance, which results in improved CBF and decreased ICP.

Acute treatment of increased intracranial pressure

The Monro-Kellie doctrine provides the framework for understanding and organizing the various treatments of elevated ICP. In patients with head injuries, the total intracranial volume is composed of the total volume of the brain, the CSF, intravascular blood volume, and any intracranial mass lesions. The volume of one of these components must be reduced to improve intracranial compliance and to decrease ICP. The discussion of the different treatments of elevated ICP is organized according to which component of intracranial volume they affect.

The first component of total intracranial volume to consider is the blood component. This includes all intravascular blood, both venous and arterial, and comprises approximately 10% of total intracranial volume. Elevation of the head increases venous outflow and decreases the volume of venous blood within the brain. This results in a small improvement in intracranial compliance and, therefore, has only a modest effect on ICP.

The second component of intracranial vascular volume is the arterial blood volume. Hypocapnia is capable of reducing cerebral blood flow 4% for each mm Hg change in PaCO2. The control mechanism is probably extravascular pH changes in fluid bathing cerebral resistor vessels, which alter smooth muscle intracellular calcium concentrations. This may be reduced by mild-to-moderate hyperventilation, in which the PCO2 is reduced to 30-35 mm Hg. This decrease in PCO2 causes vasoconstriction at the level of the arteriole, which decreases blood volume enough to reduce ICP. The effects of hyperventilation have a duration of action of approximately 48-72 hours, at which point the brain resets to the reduced level of PCO2. This is an important point because once hyperventilation is used, the PCO2 should not be returned to normal rapidly. This may cause rebound vasodilatation, which can result in increased ICP.

Below a PaCO2 of 25-30 Torr, CBF falls much less rapidly, presumably because of severe enough vasoconstriction to induce hypoxemia in brain tissues, limiting oxygen delivery. PaCO2 tensions less than 25 Torr are sufficient to change brain metabolism into anaerobic, which increases acidosis. Low arterial O2 tensions influence CBF but to a lesser degree than PaCO2. No measurable changes in CBF occur during hypoxemia until the PaO2 drops below 50 Torr, at which time CBF gradually increases. In addition to reducing CBF, the resultant respiratory alkalosis may reverse local tissue acidosis, which develops in cerebral edema, benefiting cellular respiration and restoring autoregulation. Within 48-72 hours, renal mechanisms for handling bicarbonate excretion compensate for altered PaCO2 tensions, thereby normalizing cerebral pH and returning CBF to baseline values.

There are 3 theoretical physiologic paradoxes to hyperventilation therapy for the control of ICP.

Since cerebral vasospasm is a serious concern in subarachnoid hemorrhage (SAH), attempts to create further vessel constriction by hyperventilation in order to decrease concomitant cerebral edema are rarely indicated unless the amount of edema is clinically emergent.

Vessels in the damaged area of the brain have lost their autoregulatory control. While unaffected brain regions would vasoconstrict normally to the stimulus of decreased PaCO 2, damaged areas might vasodilate in response to diminished cerebral blood flow. This can create a reverse steal phenomenon, where blood and nutrients are diverted away from normal areas of the brain and into damaged areas. This diversion would feed the increased metabolic requirement of damaged tissues, but the sum total effect may cause more harm to the rest of the brain. In addition, the increased hydrostatic pressure combined with the capillary permeability damage might, in some cases, paradoxically increase ICP in damaged areas.

Sudden increases in PaCO 2, as a result of ventilator changes, often result in dramatic increases in CBF, and rapid deteriorations in the patients condition. During hyperventilation, the cerebral bicarbonate level gradually adjusts to offset the lower level of CO 2, maintaining normal pH. If the pCO 2 is allowed to rise suddenly, the excess CO 2 rapidly crosses the blood-brain barrier, but the bicarbonate level in the brain increases much less rapidly. The result is cerebral acidosis, with attendant cerebral vascular dilatation, increased cerebral blood volume, and elevated ICP, usually resistant to further hyperventilation.

Unfortunately, little objective evidence exists that treatment by hypocapnia has significantly improved mortality or survival. At best, it seems to be a temporary stop-gap measure until some other curative measure, such as surgery, might be attempted. Patients with the most prompt response to hyperventilation generally have the best prognosis for recovery. No evidence exists that hyperventilation therapy produces benefit in hypoxemic-anoxic encephalopathy.

CSF represents the third component of total intracranial volume and accounts for 2-3% of total intracranial volume. In adults, total CSF production is approximately 20 mL/h or 500 mL/d. In many patients with TBI who have elevated ICP, a ventriculostomy may be placed and CSF may be drained. Removal of small amounts of CSF hourly can result in improvements in compliance that result in significant improvements in ICP.

The fourth and largest component of total intracranial volume is the brain or tissue component, which comprises 85-90% of the total intracranial volume. When significant brain edema is present, it causes an increase in the tissue component of the total intracranial volume and results in decreased compliance and increased ICP. Treatments of elevated ICP that reduce total brain volume include diuretics, perfusion augmentation (CPP strategies), metabolic suppression, and decompressive procedures.

Diuresis and brain edema

Diuretics are powerful in their ability to decrease brain volume and, therefore, to decrease ICP. No single diuretic has been established in randomized controlled trials to be superior to another. Mannitol, an osmotic diuretic, is the most common diuretic used. Mannitol is a sugar alcohol that draws water out from the brain into the intravascular compartment. It has a rapid onset of action and a duration of action of 2-8 hours. Mannitol is usually administered as a bolus because it is much more effective when given in intermittent boluses than when used as a continuous infusion. The standard dose ranges from 0.25-1 g/kg, administered every 4-6 hours.

Because mannitol causes significant diuresis, electrolytes and serum osmolality must be monitored carefully during its use. In addition, careful attention must be given to providing sufficient hydration to maintain euvolemia. The limit for mannitol is 4 g/kg/d. At daily doses higher than this, mannitol can cause renal toxicity. Mannitol should not be given if the patient's serum sodium level is greater than 145 or serum osmolality is greater than 315 mOsm.

Other diuretics that sometimes are used in patients with TBI include furosemide, glycerol, and urea. Mannitol is preferred over furosemide because it tends to cause less severe electrolyte imbalances than a loop diuretic. Interestingly, mannitol and furosemide have a synergistic effect when combined; however, this combination tends to cause severe electrolyte disturbances. Urea and glycerol have also been used as osmotic diuretics. Both of these compounds are smaller molecules than mannitol and, as a result, tend to equilibrate within the brain sooner than mannitol; therefore, they have a shorter duration of action than mannitol. Urea has the additional problem that it can cause severe skin sloughing if it infiltrates into the skin.

Boluses of mannitol can generate a dramatic diuresis, resulting in rapid intravascular depletion and potential kidney damage. Mannitol can cause as much as 1500 cc of fluid to diurese in the space of 2 hours, as intravascular fluid depletion occurs, hematocrit can rise,and blood viscosity can increase. This makes the area of brain irritation much more amenable to stroke.

Hypertonic saline (3-23%) has generated some interest in the treatment of intracranial hypertension secondary to brain edema because it is thought to be less disruptive to fluid and electrolyte balance than other diuretic agents. In a recent review of the literature, 23% saline was noted to decrease elevated ICP by nearly 50% an hour after administration in patients with life-threatening elevations in ICP.[15]

Saline 3% or 7.5% administered in continuous infusion generates a more predictable and gentle osmotic flow of brain intracellular water into the interstitial space. The maximum effect occurs after the end of infusion and is visible over 4 hours. Therapeutically, the limits of serum sodium and osmolality are in the range of 155 and 320 respectively. More research is needed to elucidate the exact method of action of hypertonic saline, the optimal dosing and timing and the contraindications.[15]

Other supportive treatments

While awaiting possible operative therapy, other supportive treatments are as follows:

Early extraventricular drainage of CSF is sometimes of value in controlling brain edema if there is a suspicion that the ventricles will progressively diminish in size because edema cannot be cannulated from a burr hole.

Coughing and straining increase venous pressure, restricting drainage and backing up blood into the head, thereby increasing ICP. Neuromuscular paralysis may decrease ICP by preventing sudden changes related to coughing or straining and by promoting systemic venous pooling that increases venous drainage from the head. Any other restrictions to jugular blood drainage, such as a kinked neck from positioning in bed, increase ICP by retarding jugular drainage, transmitting pressure back into the brain.

Trying to differentiate a drug-induced coma from an increased ICPinduced coma with a trial of naloxone (Narcan) is contraindicated, as it invariably induces agitation if the stupor is narcotic induced. Agitation increases catecholamine response, increases cardiac output, and increases blood flow to the head, thereby increasing hydrostatic pressure and ICP.

Use of positive end-expiratory pressure (PEEP) for mechanical ventilation is controversial in TBI patients with acute lung injury/acute respiratory distress syndrome. Zhang et al found that PEEP can have a varied impact on blood, intracranial, and cerebral perfusion pressure in patients with cerebral injury. When applying this technique, mean arterial and intracranial pressure monitoring appears beneficial. [16]

Management of cerebral perfusion pressure

CPP management involves artificially elevating the blood pressure to increase the MAP and the CPP. Because autoregulation is impaired in the injured brain, pressure-passive CBF develops within these injured areas. As a result, these injured areas of the brain often have insufficient blood flow, and tissue acidosis and lactate accumulation occur. This causes vasodilation, which increases cerebral edema and ICP. When the CPP is raised to greater than 65-70 mm Hg, the ICP is often lowered because increased blood flow to injured areas of the brain decreases the tissue acidosis. This often results in a significant decrease in ICP.

Metabolic therapies are designed to decrease the cerebral metabolic rate, which decreases ICP. Metabolic therapies are powerful means of reducing ICP, but they are reserved for situations in which other therapies have failed to control ICP. This is because metabolic therapies have diffuse systemic effects and often result in severe adverse effects, including hypotension, immunosuppression, coagulopathies, arrhythmias, and myocardial suppression. Metabolic suppression may be achieved through drug therapies or induced hypothermia.

Barbiturates are the most common class of drugs used to suppress cerebral metabolism. Barbiturate coma is typically induced with pentobarbital. A loading dose of 10 mg/kg is administered over 30 minutes, and then 5 mg/kg/h is administered for 3 hours. A maintenance infusion of 1-2 mg/kg/h is begun after loading is completed. The infusion is titrated to provide burst suppression on continuous electroencephalogram monitoring and a serum level of 3-4 mg/dL. Typically, the barbiturate infusion is continued for 48 hours, and then the patient is weaned off the barbiturates. If the ICP again escapes control, the patient may be reloaded with pentobarbital and weaned again in several days.

Hypothermia may also be used to suppress cerebral metabolism. The use of mild hypothermia involves decreasing the core temperature to 34-35C for 24-48 hours and then slowly rewarming the patient over 2-3 days. Patients with hypothermia are also at risk for hypotension and systemic infections. This therapy remains controversial because of the lack of high quality trials that have clearly established neurologic benefits or mortality reduction.[17] There are no known randomized controlled trials of modest cooling therapies (35-37.5 degrees Celcius).[18]

Another treatment that may be used in patients with TBI with refractory ICP elevation is decompressive craniectomy. In this surgical procedure, a large section of the skull is removed and the dura is expanded. This increases the total intracranial volume and, therefore, decreases ICP. Which patients benefit from decompressive craniectomy has not been established. Some believe that patients with refractory ICP elevation who have diffuse injury but do not have significant contusions or infarctions will benefit from decompressive craniectomy. Nirula and colleagues investigated whether early decompressive craniotomy, done within 48 hours of TBI was associated with improved survival in patients with refractory intracranial hypertension. Their results did not demonstrate a survival benefit when compared to patients treated with standard medical therapy. This led the authors to recommend that neurosurgeons pause before considering this "resource-demanding form of therapy."[19]

Management of elevated ICP involves using a combination of treatments. Each patient represents a slightly different set of circumstances, and treatment must be tailored to each patient. Although no rigid protocols have been established for the treatment of head injury, many published algorithms provide treatment schemas.

The American Association of Neurologic Surgeons published a comprehensive evidence-based review of the treatment of TBI, called the Guidelines for the Management of Severe Head Injury. In these guidelines, 3 different categories of treatments, standards, guidelines, and options are outlined. Standards are the accepted principles of management that reflect a high degree of clinical certainty. Guidelines are a particular strategy or a range of management options that reflect a high degree of clinical certainty. Options are strategies for patient management for which clinical certainty is unclear.

Penetrating trauma

The treatment of penetrating brain injuries involves 2 main aspects. The first is the treatment of the TBI caused by a penetrating object. Penetrating brain injuries, especially from high-velocity missiles, frequently result in severe ICP elevations. This aspect of penetrating brain injury treatment is identical to the treatment of closed head injuries.

The second aspect of penetrating head injury treatment involves debridement and removal of the penetrating objects. Penetrating injuries require careful debridement because these wounds are frequently dirty. When objects penetrate the brain, they introduce pathogens into the brain from the scalp surface and from the surface of the penetrating object.

Penetrating injuries may be caused by high-velocity missiles (eg, bullets), penetrating objects (eg, knives, tools), or fragments of bone driven into the brain. Bullet wounds are treated with debridement of as much of the bullet tract as possible, dural closure, and reconstruction of the skull as needed. If the bullet can be removed without significant risk of neurologic injury, it should be removed to decrease the risk of subsequent infection. Penetrating objects, such as knives, require removal to prevent further injury and infection. If the penetrating object either is near or traverses a major vascular structure, an angiogram is necessary to assess for potential vascular injury. When the risk of vascular injury is present, penetrating objects should be removed only after appropriate access has been obtained to ensure that vascular control is easily achieved.

Penetrating brain injuries are associated with a high rate of infection, both early infections and delayed abscesses. Appropriate debridement and irrigation of wounds helps to decrease the infection rate. Some of the risk factors for infection following penetrating brain injury include extensive bony destruction, persistent CSF leak, and an injury pathway that violates an air sinus.

Late-onset epilepsy is a common consequence of penetrating brain injuries and can occur in up to 50% of patients with penetrating brain injuries. No evidence exists that prophylactic anticonvulsants decrease the development of late-onset epilepsy. During the Vietnam War, prophylactic anticonvulsants were used, and the rate of late-onset epilepsy was not different from that of previous wars, when prophylactic anticonvulsants were not used

Assessing and Treating Head Injuries

Although they look gruesome, superficial cuts to the scalp without underlying skull or brain injury are relatively benign injuries. However, head wounds should be treated with care. In rare cases, especially when there are other sources of blood loss, severe bleeding can cause hypovolemic shock. Skull fractures and brain injuries are cause for much greater concern.

This paper examines three major topics: Lacerations of the Scalp, Skull Fractures and Brain Injuries. The third topic is examined in depth

Topic 1: Lacerations of the Scalp

Treat lacerations by applying direct pressure with your gloved hand using a dry, sterile dressing. If the skin is avulsed (torn into a flap which remains connected) flush the area clean with water, fold the flap back down, and apply pressure with a dressing. Secure dressings to the head with roller gauze. If dressings become saturated with blood, do not remove them, but add more dressings on top. If you suspect an underlying skull fracture, apply very gentle pressure, being careful not to compress the fracture or push bone fragments into the brain. There are several different types of soft tissue injuries.

Topic 2: Skull Fractures

Fractures may be open, if the skin above the fracture is broken allowing access to the bone, or closed, if the overlying skin is intact. Suspect a fracture if there is point tenderness (pain) when you palpate (press) the skull or face bones or if there is substantial swelling or skull deformity. Raccoon eyes (bruising around the eyes) and Battle's Sign (bruising behind the ear) suggest a fracture to the base of the skull, but these usually develop some time after the initial injury. Clear fluid from the nose or ear may be cerebrospinal fluid leakage and indicates a skull fracture.

Topic 3: Brain Injuries

A concussion occurs when head trauma causes a temporary change in brain function without perceptible physical damage to the brain. Concussions can involve minor changes (e.g. seeing stars) or serious changes (loss of consciousness) in brain function.

A contusion is the bruising of brain tissue and is more serious. The skull is essentially a sealed compartment. Because of associated swelling and bleeding, increased pressure and distortion of the brain tissue can result in serious and life-threatening symptoms.

Intracranial hemorrhage refers to bleeding from vessels within the brain or its covering. If your patient is deteriorating rapidly and showing poor neurological signs, suspect intracranial bleeding. It is very important to assess patients with suspected brain injury for their Level of Responsiveness (LOR). LOR is measured using the AVPU scale, which refers to the patient's ability to remain awake and responsive.

Level of Responsiveness Scale

Alert: patient is awake and responsive without any prompting or stimulationVerbal: patient requires verbal prompting to stay responsive ("Hey!")Pain: patient requires painful stimulation to stay responsive (e.g. pinching an earlobe)Unresponsive: patient does not respond at all.

Also assess the patient's orientation - the awareness of his/her name, location, date/time, and circumstances. Each of these is called a sphere, and the patient can be oriented in 0, 1, 2, 3, or 4 spheres. When you report to the ambulance crew, specifically state the status of each sphere (oriented or not) and what the course of the LOR has been (e.g. responsive only to pain).

Indications of Traumatic Brain Injury

Obvious damage to helmet or head (fractures, bleeding, bruising, deformities etc.)

Clear or blood-tinged fluid from the nose or ears

Pupils of different size or that don't respond to changes in light

Loss of memory

Reduction in orientation or level of responsiveness (e.g. confused, "spacey," disoriented)

Increased blood pressure, irregular respirations, and lowered pulse

Changes in sensation in or ability to move the extremities

Dizziness

Repetitive speech

Convulsions

Nausea and vomiting

Poor coordination

Steps for Treating a Brain Injury

1. As with any injury, first assess and immediately provide care for any problems with airway, breathing, and circulation (ABC's):

a. Keep the airway open

b. Provide supplemental high-flow oxygen if available

c. Control any serious external bleeding

d. Rescue breathing or CPR if indicated

2. Helmet removal: Safe helmet removal requires proper instruction and practice. A helmet needs to be removed only if it:

. Impedes assessment or treatment of ABC's

. Prevents proper immobilization of the spine

. Is loose and prevents the head from being stabilized or secured to a backboard

Conduct a rapid body survey and locate other significant injuries. A significant head injury is likely to have an associated spinal injury, so take spinal precautions beginning with your initial assessment. See "Handling Suspected Spinal Injuries." Head injury patients require a cervical collar and a backboard. Minimize movement.

Call for immediate evacuation

Do not give anything to the patient by mouth.

Monitor vital signs and level of responsiveness every 15 minutes for stable patients and every 5 for unstable patients.

All head injuries should be evaluated by a physician. Serious symptoms can develop over the following 48-72 hours.

Because patients can lose consciousness, obtain information regarding identity, emergency contacts, allergies, medical problems and medications taken and last time they ate and drank while waiting for evacuation.

is an Emergency Medical Technician and an Outdoor Emergency Care instructor for the National Ski Patrol. He welcomes your questions on first aid practices.

head injury

A head injury is any trauma to the scalp, skull, or brain. The injury may be only a minor bump on the skull or a serious brain injury. Head injury can be either closed or open (penetrating). A closed head injury means you received a hard blow to the head from striking an object, but the object did not break the skull.

Head injury facts

Brain injuries account for thousands of deaths each year in the U.S. As well, significant numbers of people suffer temporary and permanent disability due to brain injury.

Head injury does not necessarily mean brain injury.

Bleeding in the brain usually occurs at the time of injury and can continue increasing pressure within the skull. However, symptoms may develop immediately or progress gradually over time.

Medical care should be sought for any patient who is not fully awake after an injury. Activate emergency medical services or call 9-1-1.

Computerized tomography is used to look for bleeding and swelling in the brain.

Not all patients with minor head injuries require CT scanning.

Bleeding in the brain may require neurosurgery to remove blood clots and relieve pressure on the brain.

Not all brain injuries require neurosurgery.

Prevention is key to avoiding head injury, especially in motor vehicle accidents and sports injuries.

Head injury introduction

While head injuries are one of the most common causes of death and disability in the United States. A majority of patients with head injuries are treated and released from the emergency room.

Blows to the head most often cause brain injury, but shaking may also cause damage. The face and jaw are located in the front of the head, and brain injury may also be associated with injuries to these structures. It is also important to note that a head injury does not always mean that there is also a brain injury.

The brain is a soft and pliable material, almost jelly-like in feel, and is surrounded by a thin layer of cerebrospinal fluid (CSF). The brain is lined by thin layers of tissue called the meninges; 1) the pia mater, 2) the arachnoid mater, and 3) the dura mater. The cerebrospinal fluid is present in the space beneath the arachnoid layer called the subarachnoid space.

The dura mater is very thick and has septae, or partitions, that help support the brain within the skull. The septae attach to the inner lining of the bones of the skull. The dura mater also helps support the large veins that return blood from the brain to the heart.

The spaces between the meninges are usually very small but they can fill with blood when trauma occurs, and this buildup of blood can potentially press into the brain tissue and cause damage.

The skull protects the brain from trauma but it does not absorb any of the impact from a blow. Direct blows may cause fractures of the skull. There can be a contusion or bruising and bleeding to the brain tissue directly beneath the injury site. However, the brain can bounce around, or slosh, inside the skull and because of this, the brain injury may not necessarily be located directly below the trauma site. A contre-coup injury describes the situation in which the initial blow causes the brain to bounce away from that blow and is damaged by hitting the skull directly opposite the trauma site. Acceleration/deceleration and rotation are the common types of forces that can cause injuries away from the area of the skull that received the trauma.

Picture of the brain and potential brain injury areas

Picture of the brain and potential brain injury areas.

Head injuries due to bleeding are often classified by the location of the blood within the skull.

Epidural hematoma: With an epidural hematoma, the bleeding is located between the dura mater and the skull (epi=outside). This injury often occurs along the side of the head where the middle meningeal artery runs in a groove along the temporal bone. This bone is relatively thin and offers less protection than other parts of the skull. As the bleeding continues, the hematoma or clot expands. There is little space in the skull for the hematoma to grow and as it expands, the adjacent brain tissue is compressed. With increased pressure the brain begins to shift and becomes compressed against the bones of the skull. The pressure tends to build quickly because the septae that attach the dura to the skull bones create small spaces that trap blood. Symptoms of head injury and decreased level of consciousness occur as the pressure increases.

Subdural hematoma: A subdural hematoma is located beneath the dura mater (sub=below), between it and the arachnoid layer. Blood in this space is able to dissipate into a larger space because there are no septae limiting the blood flow. However, after a period of time, the amount of bleeding may cause increased pressure and cause symptoms similar to those seen with an epidural hematoma.

Subarachnoid bleed: Subarachnoid bleeding occurs in the space beneath the arachnoid layer where the cerebrospinal fluid is located. Often there is intense headache and vomiting with subarachnoid bleeding. Because this space connects with the spinal canal, pressure buildup tends not to occur. However, this injury often occurs in combination with the other types of bleeding in the brain and the symptoms may be compounded.

Intracerebral bleed: Intracerebral bleeding occurs within the brain tissue itself. Sometimes the amount of bleeding is small, but like bruising in any other part of the body, swelling or edema may occur over a period of time, causing a progressive decrease in the level of consciousness and other symptoms of head injury.

Sheer injury: Sometimes, the damage is due to sheer injury, where there is no obvious bleeding in the brain, but instead the nerve fibers within the brain are stretched or torn. Another term for this type of injury is diffuse axonal injury.

Edema: All injuries to the brain may also cause swelling or edema, no different than the swelling that surrounds a bruise on an arm or leg. However, because the bones of the skull cannot stretch to accommodate the extra volume caused by swelling, the pressure increases inside the skull and causes the brain to compress against the skull.

Skull fracture: The bones of the skull are classified as flat bones, meaning that they do not have an inside marrow. It takes a significant amount of force to break the skull, and the skull does not absorb any of that impact. It is often transmitted directly to the brain.

Picture of epidural, subdural, and intracerebral hematomas.

Skull fractures are described by which bone is broken, whether there is an associated laceration of the scalp (open fracture), and whether the bone is depressed and potentially pushed into the brain tissue.

Brain injuries often occur in combination with one another. The effects of brain injury depend upon the amount of brain tissue damaged and the level of pressure within the skull and its effects on the brain.Continue Reading

Medically Reviewed by a Doctor on 5/11/2015

What are the causes of head injury?

Reader Stories

Read 21 Stories

Share Your Story

By definition, trauma is required to cause a head injury, but that trauma does not necessarily need to be violent. Falling down a few steps or falling into a hard object may be enough to cause damage. Motor vehicle crashes account for about 17% of traumatic brain injuries, while 35% are from falls. The majority of head injuries occur in males.

Penetrating head injuries describe those situations in which the injury occurs due to a projectile, for example a bullet, or when an object is impaled though the skull into the brain.

Closed head injuries refer to injuries in which no lacerations are present.

The brain may also be injured without a direct blow to the skull. The head sits on the neck allowing it to shake, causing the brain to slosh inside the skull and become injured.

What are the symptoms of a head injury?

Reader Stories

Read 5 Stories

Share Your Story

The symptoms of head injury can vary from almost none to loss of consciousness and coma. As well, the symptoms may not necessarily occur immediately at the time of injury. While a brain injury occurs at the time of trauma, it may take time for enough swelling or bleeding to occur to cause symptoms that are recognizable.

Initial symptoms may include a change in mental status, meaning an alteration in the wakefulness of the patient. There may be loss of consciousness, lethargy, and confusion.

Head injury symptoms may also include:

vomiting,

difficulty tolerating bright lights,

leaking cerebrospinal fluide from the ear or nose,

bleeding from the ear,

speech difficulty,

paralysis,

difficulty swallowing, and

numbness of the body.

Other symptoms may be more subtle and include:

nausea,

dizziness,

irritability,

difficulty concentrating and thinking, and

amnesia.

Late signs of significant head injury and raised pressure within the brain and skull include a dilated pupil, high blood pressure, low pulse rate, and abnormal breathing pattern.

What is the Glasgow Coma Scale?

The Glasgow Coma Scale was developed to provide health care practitioners a simple way of measuring the depth of coma based upon observations of eye opening, speech, and movement. Patients in the deepest level of coma:

do not respond with any body movement to pain,

do not have any speech, and

do not open their eyes.

Those in lighter comas may offer some response, to the point they may even seem awake, yet meet the criteria of coma because they do not respond to their environment.

Glasgow Coma Scale

Eye Opening

Spontaneous

4

To loud voice

3

To pain

2

None

1

Verbal Response

Oriented

5

Confused, Disoriented

4

Inappropriate words

3

Incomprehensible words

2

None

1

Motor Response

Obeys commands

6

Localizes pain

5

Withdraws from pain

4

Abnormal flexion posturing

3

Extensor posturing

2

None

1

An awake person has a Glasgow Coma Scale of 15, while a person who is dead would have a score of 3. The abnormal motor responses of flexion and extension describe arm and leg movement when a painful stimulus is applied. The term "decorticate" means that the cortex of the brain, the part that deals with movement, sensation, and thinking, is not working. "Decerebrate" means that the cerebrum (the whole brain), the cortex, and the brainstem that controls basic bodily functions like breathing and heartbeat, is not working.

The scale is used as part of the initial evaluation of a patient, but does not assist in making the diagnosis as to the cause of coma. Since it "scores" the level of coma, the Glasgow Coma Scale can be used as a standard method for pre-hospital emergency providers to determine the severity of head injury. It also allows the next provider in the chain of care to compare their assessment to the previous one. In this way, there is a standard score to determine whether the patient is improving or decompensating from the injury scene during the transitions to the ER, to the operating room, or ICU.Continue Reading

When should I contact a doctor about a head injury?

It is not normal to be unconscious or not fully awake. Emergency medical services (call 9-1-1 in your areas if it is available) should be activated for persons who have sustained an injury.

Because head injuries may also be associated with neck injuries, victims should not be moved unless they are in harm's way. If possible, it is important to wait for trained medical personnel to help with immobilizing and moving the patient.

If the patient is awake and feeling normal, it may be worthwhile seeking medical care if there was significant trauma. These patients may be considered to have minor head injury or concussion, and there is a significant amount of research that has been done to decide which persons with head injury should be admitted to the hospital for observation or have a CT (computerized tomography) scan of the head to look for bleeding.

While there are many guidelines from which to choose, recent literature suggests that any of them work well to help a physician decide who might have a brain injury associated with a head injury. These guidelines apply to people ages 16 to 65 who are fully awake and have a Glasgow Coma Scale of 15. Potential brain injury may exist if the patient had any of the following:

amnesia to events preceding the injury,

vomiting,

alcohol or drug intoxication,

seizure,

trauma above the collarbones,

significant headache, and

dangerous mechanism of injury like a fall from more than five stairs or being hit by a car.

Those older than 65 years of age are at increased risk of bleeding from head injury because the aging brain shrinks away from the skull, causing the veins that bridge from the skull to the brain surface to be more easily torn.

If a person is taking a blood-thinning medication such as warfarin (Coumadin), clopidogrel (Plavix), prasugrel (Effient), or rivaroxaban (Xarelto), they are also at an increased risk of a brain injury, even if there is relatively minor trauma

How is a head injury diagnosed?

As with most injuries and illnesses, finding out what happened to the patient is very important. The health care professional will take a history of the events. The information may be provided by the patient, people who witnessed the event, emergency medical personnel, and if applicable, the police. The circumstances are very important since it is important to find out the severity and intensity of the trauma sustained by the head. Please be aware, even small head bumps or shaking can cause a brain injury.

Physical examination begins with assessing the ABCs (airway, breathing, circulation) to make certain that the patient is stable and does not need emergent life-saving interventions. This is especially important in those patients who are unconscious and may not be able to maintain their own airway or breathe on their own.

If the patient is not fully awake, the examination will initially try to determine the level of coma. The Glasgow Coma Scale number is useful in tracking whether the patient is improving or declining in function over time.

If no other injuries are found on examining the body, attention will be paid to the head and the neurologic exam.

The skull may be examined for signs of trauma, including bruising (contusion) and swelling (hematoma). Palpating or feeling the skull may find evidence of a fracture. If a laceration is present, it is important to know if there is a broken bone beneath it. The face may be examined as well, since the face provides protection to the front of the head.

The health care professional may also examine the patient for evidence of a basilar skull fracture, in which an injury has occurred to the bones that support the brain. Signs of this type of fracture include:

bruising of the tissues around the eyes (called raccoon eyes),

bruising behind the ear (Battle's sign),

bleeding from the ear canal, or

cerebrospinal fluid leaking from the ear or nose.

The neurologic exam may include evaluation of the cranial nerves, the short nerves that leave the brain and control the face muscles, eye movements, swallowing, hearing, and sight, among other functions.

The exam may include evaluation of muscle tone and strength of the arms and legs; sensation in the extremities (including light touch, pain, and vibration); and if the neck is determined not to be injured, the patient's ability to walk may be assessed.

Depending upon the findings of the physical examination, a CT scan may be needed to look for bleeding in the brain.

It is important to remember that injuries to other parts of the body may also be present, and the evaluation of the head injury may occur at the same time as the evaluation of other injuries.

How is a head injury treated?

Reader Stories

Read 1 Story

Share Your Story

The treatment of a head injury depends upon the type of injury. For patients with minor head injuries (concussions), nothing more may be needed other than observation and symptom control. Headache may require pain medication. Nausea and vomiting may require medications to control these symptoms.

Bleeding

Intracerebral bleeding or bleeding in the spaces surrounding the brain are neurosurgical emergencies, although not all bleeding requires an operation. The decision to operate will be individualized based upon the injury and the patient's medical status.

One option may include craniotomy, drilling a hole into the skull or removing part of one of the skull bones to remove or drain a blood clot, and thereby relieve pressure on brain tissue.

Other times, the treatment is supportive, and there may be a need to monitor the pressure within the brain. The neurosurgeon may place a pressure monitor through a drilled hole through the skull to monitor the pressure. The slang term for this procedure is "placing a bolt."

Supportive care is often required for those patients with significant amounts of bleeding in their brain and who are in coma. Many times, the patient requires intubation to help control breathing and to protect them from vomiting and aspirating vomit into the lungs. Medications may be used to sedate the patient for comfort and to prevent injury if the bleeding causes combativeness. Medications may also be used to try to control swelling in the brain if necessary.

What is the prognosis for a head injury?

Reader Stories

Share Your Story

The goal for the treatment of any patient is to return to the level of function that they had prior to the injury. This maybe a challenge with head injury, and the return of function depends upon the severity of the injury to the brain.Continue Reading

How can a head injury be prevented?

Reader Stories

Share Your Story

Prevention is the best way to treat a head injury.

In sporting activities, the use of a helmet may help decrease the risk of injury. Similarly, wearing a helmet while riding a motorcycle or bicycle helps minimize the risk of brain injury. Seatbelts can help prevent a head injury during a motor vehicle crash.

Since alcohol is a risk factor for falls and other injuries, it should be used responsibly.

Falls are a concern in the elderly. Homes can be made less fall-prone by installing assist devices on walls and in bathrooms. Loose floor coverings such as area rugs should be avoided, since walking from one floor covering to another increases the risk of falls. If needed, canes and walkers may be helpful as walking assistive devices.

What about a head injury in infants and young children?

Reader Stories

Read 1 Story

Share Your Story

A minor head injury in an infant is described by the American Academy of Pediatrics as the following, "A history or physical signs of blunt trauma to the scalp, skull, or brain in an infant or child who is alert or awakens to voice or light touch."

In children and infants younger than 2 years of age, it is more difficult to assess their mental status and guidelines that work for adults do not necessarily apply to this age group. The Pediatric Emergency Care Applied Research Network (PECARN) has developed an algorithm that helps decide when a CT scan of the head might be appropriate.

For children younger than 2 years of age:

CT scan is recommended for those patients with a Glasgow Coma Scale of less than 15, altered mental status, or a palpable skull fracture.

For those with a Glasgow Coma Scale of 15 but with an occipital, temporal, or parietal hematoma (that is swelling on the back or side of the head), significant trauma, or loss of consciousness for greater than 5 seconds, or for those not acting normally according to their parents, a CT scan may be considered based upon the following:

physician experience,

multiple physical findings,

worsening symptoms during observation in the ER,

age less than 3 months, or

parental preference.

For all others, CT scan is not recommended.

For children older than 2 years of age:

CT scan is recommended for those patients with a Glasgow Coma Scale of less than 15, altered mental status, or a basilar skull fracture.

For patients with loss of consciousness, vomiting, severe headache, or a severe mechanism of injury, a CT scan may be considered based upon the following:

physician experience,

multiple physical findings,

worsening symptoms during observation in the ER, or

parental preference.

For all others, CT scan is not recommended