Traumatic Brain Injury Guide
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Management and approach of cases based on NICE guidelines
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Traumatic Brain Injury Guide
- 2. Definition • is a nondegenerative, noncongenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness. • Often, the term brain injury is used synonymously with head injury, which may not be associated with neurologic deficits
- 3. Types • Primary brain injury - the initial injury to the brain as a direct result of the trauma • Secondary brain -any subsequent injury to the brain after the initial insult -eg; Hypoxia and hypotension • The treatment of head injury is directed at either preventing or minimizing secondary brain injury
- 5. Causes of Secondary Brain Injury • Hypoxia ; PaO2 < 8kPa(60mmHg) • Hypotension; SBP < 90mmHg • Raised ICP ; ICP > 20mmHg • Low Cerebral Perfusion Pressure (CPP) CPP < 65mmHg • Pyrexia • Seizures • Metabolic Disturbances
- 6. Classification of severity of head injury The GCS is often used to help define the severity of TBI Mild ; GCS 13 – 15 Moderate ; 9-12 Severe ; 8 and below -a general guide to the level of injury.
- 7. Monro-Kellie Doctrine  The total volume ofThe total volume of intracranial contentintracranial content must remainmust remain constant as theconstant as the cranium is non-cranium is non- expansile boxexpansile box Normal cerebral blood flow is 55 ml/100gm/min Normal ICP is 8-12 mmHg
- 8. Relationship between Intracranial pressure and intracranial volume
- 9. Pathophysiology • A second crucial concept in TBI pathophysiology is the concept of cerebral perfusion pressure (CPP). • CPP = MAP - ICP • In the noninjured brain in individuals without long-standing hypertension, cerebral blood flow (CBF) is constant in the range of MAPs of 50-150 mm Hg.
- 10. Taking a history • Mechanism of injury • Loss of consciousness or amnesia • Level of consciousness at the scene and on transfer • Evidence of seizures • Probable hypoxia or hypotension • Pre-existing medical conditions, insulin use • Medications esp Anticoagulants • Illicit drugs and alcohol
- 11. On Examination • Glasgow coma scale • Pupil size and response • Lateralising signs • Signs of basal skull fracture -Bilateral periorbital oedema(raccoon eyes) - Battle’s sign(bruising over mastoid) -Cerebrospinal fluid rhinorrrhoea or otorrhoea -Haemotympanum or bleeding from ear • Full neurological examination ; tone , power, sensation , reflexes
- 13. Battle’s sign
- 15. Investigations • Blood I/X > Standard - FBC , RP, coagulation profile - ABG -Drug toxicology -Blood alcohol level • Computerised Tomography(CT) Scanning -The standard CT scan > non-contrast scan --identify an intracranial haematoma, scalp soft tissue injury, skull # including bass of skull #, small contusions(lesions which may not need op)
- 16. • Magnetic Resonance Imaging(MRI) -long acquisition times -difficulty in obtaining MRIs in persons who are critically ill. -It is superior to CT scan for helping identify diffuse axonal injury (DAI) and small intraparenchymal contusions.
- 18. SDH and EDH
- 19. Management of Moderate to severe head injury • Begins with Resuscitation and a primary survey • Aim ; prevention of the secondary brain injury -Avoidance of hypoxia and hypotension • Cervical spine must be immobilised till Cervical spine # has been ruled out (request for CT cervical spine in cases of doubt) • Done primary survey >> established presence of moderate to severe head injury >> CT scan • CT scan aims Early consultation to neurosurgical team • Simple measures to reduce ICP eg. Positioning
- 20. Primary survey • Airway assessments with C-Spine control • Breathing and ventilation • Circulation and Haemorrhage control • Disability and Neurological deficit - AVPU • Exposure /Environmental Control
- 21. Secondary Survey • History : AMPLE • Neurological Assessment - GCS -pupils • Head-to-toe examination -Head and face -Neck -Chest -Abdomen -Limbs -Back -Buttocks, perineum, genitalia
- 22. 15 History Examination LOC > 5 min ? Depressed skull # Lateralising signs Observe for 6 hours No Discharge with Head chart Yes 14 13 CT Head (Non-contrast)
- 23. GCS 12 or less Multiple System Injuries Isolated head injury Check and clear A & B C If haemodynamically unstableIf haemodynamically unstable CXRCXR FAST or DPL FAST or DPL PXRPXR LimbsLimbs SurgerySurgery Angioembolisation +/- Ext Fixation Angioembolisation +/- Ext Fixation SplintSplint Once C fixed Then D CT Brain and C-Spine < 20 min
- 24. NICE GUIDELINES
- 25. CT Brain in Head Injury A head injury + any of the following risk factors ; perform a CT head scan within 1 hour of the risk factor being identified: •GCS less than 13 on initial assessment in the emergency department. •GCS less than 15 at 2 hours after the injury on assessment in the emergency department. •Suspected open or depressed skull fracture. •Any sign of basal skull fracture •Post-traumatic seizure. •Focal neurological deficit. •More than 1 episode of vomiting.
- 26. For adults with any of the following risk factors + LOC or amnesia > perform a CT head scan within 8 hours of the head injury •Age 65 years or older. •Any history of bleeding or clotting disorders. •Dangerous mechanism of injury •More than 30 minutes' retrograde amnesia of events immediately before the head injury.
- 27. When to intubate? •Coma (GCS 8 or less) •Loss of protective laryngeal reflexes. •Ventilatory insufficiency as judged by blood gases: hypoxaemia (PaO2 < 13 kPa on oxygen) or hypercarbia (PaCO2 > 6 kPa). •Spontaneous hyperventilation causing PaCO2 < 4 kPa. •Irregular respirations.
- 28. Admission • new, clinically significant abnormalities on imaging. • GCS has not returned to 15 after imaging, regardless of the imaging results. • has indications for CT scanning but cannot be done within the Eg . CT is not available , or pt not cooperative • Continuing worrying signs Eg persistent vomiting, severe headaches • Other sources of concern Eg. drug or alcohol intoxication, shock, suspected non-accidental injury, meningism, cerebrospinal fluid leak
- 29. Observation in ward Document GCS; pupil size and reactivity; limb movements; RR, PR, BP, T, SpO2 Perform and record observations on a half-hourly basis until GCS equal to 15 has been achieved. The minimum frequency of observations for patients with GCS equal to 15 should be as follows, starting after the initial assessment in the emergency department: •Half-hourly for 2 hours. •Then 1-hourly for 4 hours. •
- 30. Extradural Haematoma • A neurosurgical emergency • Almost always associated with skull fracture • Tearing of the meningeal artery and the haematoma accumulates in the space between the bone and the dura • Most common site ; temporal ( pterion) • Classical presentation ; Initial LOC may be there (cerebral concussion) at the time of injury • followed by lucid interval ( all vital signs are normal, GCS is 15) (=compensatory phase) • subsequent rapid deterioration of conscious level due to enlarging haematoma causing brain herniation may be associated with contralateral hemiplegia and ipsilateral pupil dilatation
- 31. Hutchinson’s pupil  pupil on the side of an intracranial mass lesion is dilated and unreactive to light, due to compression of the oculomotor nerve on that side.
- 32. • Early recognition and treatment >> likely full recovery • Delay in d/x >> death d/t secondary brain injury • CT scan ; lentiform, hyperdense lesion, associated mass effect, with or without MLS • Treatment ; immediate surgical evacuation via a craniotomy
- 33. Acute Subdural Haematoma • Blood accumulates in the space between the dura and the arachnoid • Disruption of a cortical vessel or brain laceration • impaired conscious level from time of injury, but can further deteriorate as the haematoma expands • CT scan: hyperdense lesion, diffuse and concave shape • T/x ; evacuation via a craniotomy • Small haematomas with little mass effect ; conservative
- 34. Subarachnoid Haemorrrhage • Traumatic SAH > managed conservatively
- 35. Cerebral contusions • brain being damaged by impacting against the skull either at the point of impact (coup) or on the other side of the head(counter-coup) • or as the brain slides forwards and backwards over the ridged cranial fossa floor • CT scan; Heterogenous with mixed areas of high and low density, may be an associated mass effect • Rarely require immediate surgical treatment • Must be admitted for observation > as the lesions tend to mature and expand for 48 to 72 hours PT • delayed evacuation to reduce the mass effect (small proportion)
- 36. When to re-evaluate? • Development of agitation or abnormal behaviour. • A sustained (for at least 30 minutes) drop of 1 point in GCS score (Esp . the motor response) • Any drop of 3 or more points in the eye-opening or verbal response scores of the GCS, or 2 or more points in the motor response score. • Development of severe or increasing headache or persisting vomiting. • New or evolving neurological symptoms or signs such as pupil inequality or asymmetry of limb or facial movement
- 37. Role of A repeat Brain CT Scan • If the first CT demonstrates an intracranial lesion then apply the BTF criteria for surgical intervention • In no surgical intervention is indicated, repeat CT should be performed between 6 to 12 hours after initial trauma – regardless of the patient’s clinical exam. • If on repeat CT > stable or improved > no further imaging is required, and can follow clinical exam. • If there is deterioration > BTF criteria for surgical intervention • 2 sequential studies stable > > no further imaging is required, and can follow clinical exam.
- 38. When to go conservative? • Patients with good GCS -showing progressive improvement -static with normal coma score • Patients with haematoma with poor GCS -ICP shows normal pressure • Multiple small contusions or haematoma -none of them individually producing mass effect • Patients with haematoma in -Brain death -Impending brain death
- 39. Indications for surgery in head injury • In acute head injury 1) Large intracranial haematoma producing mass effect and raised ICP -patient is deteriorating etc 2) Compound head injury -scalp laceration with comminuted # , or CSF leak -Surgery for foreign body eg bullet etc -Profuse CSF leak not controlled on conservative management in 2-3 weeks time • Chronic head injury eg.CSF fistulae, hydrocephalus,abscess etc
- 40. Surgical management of Head Injury • Early Evacuation of focal haematomas; EDH, ASDH • CSF drainage via ventriculostomy • Delayed evacuation of swelling contusion • Decompressive craniectomy - to control the ICP in pt without a focal Intracerebral haematoma in whom the ICP is refractory to maximal medical therapy
- 41. Craniotomy
- 42. Raising the skin flap & making the Burr – holes prior to doing a Craniotomy
- 43. Medical Management of Severe Head Injury • Aim : control of ICP ( Normal ICP is 8-12mmHg) • A sustained ICP of > 20mmHg ; poor outcome 1)Positioning 2)Avoid obstruction of venous drainage from head 3)Sedation +/- muscle relaxant 4)Normocapnia 4.5-5.0 kPa 5)Diuretics : Furosemide, mannitol 6)Seizure control 7)Normothermia 8)Sodium Balance 9)Barbiturates
- 44. •Head up 30’ if spinal clearance allows > venous return •Ensure that Cervical immobilisation collar does not obstruct venous return from the head •A definitive airway •Hypoxia and hypercapnia >> increase brain ischaemia and secondary brain injury •Once intubated ;normocapnia is maintained (PaCO2 4.5-5 kPa) •The cerebral vasculature is reactive to CO2 levels. A rise in PaCO2 in + high ICP >> generalised cerebral vasodilatation >> increased IC Blood volume >> further raise ICP >> reduced cerebral perfusion •Cerebral perfusion pressure should be maintained at >65mmHg
- 45. ICP monitoring • An ICP monitor may be parenchymal or ventricular
- 46. • Sedation , with or without muscle relaxants • Use of diuretics – Eg Mannitol and furosemide will temporarily reduce the cerebral swelling and ICP • Thermoregulation ; Pyrexia increases brain metabolic rate. Active cooling is used in some centres. • Barbiturates ; Eg Thiopentone reduces Brain Metabolic rate and helps reduce ICP. • Maintaining fluid and electrolyte balance – susceptible to disturbances of Na haemostasis eg Diabetes insipidus and SIADH) • Seizure control ; Prophylactic anticonvulsants
- 47. Role of Anti-epileptics in TBI • Had a seizure after a head injury > continued for 6 months to 1 year • Phenytoin 15-18 mg/kg IV bolus followed by 200 mg IV q12h) • Prophylactic anticonvulsants to all patients with significant head injury for at least 1st few days after injury • If seizures are not evident in the acute phase, anticonvulsants are discontinued in 1 week
- 48. Role of Antibiotics in TBI • Broad-spectrum antibiotics ; A cephalosporin or Augmentin is recommended. • Indications ; -post-operatively -Skull base fracture with CSF leak -Pneumocephalus • Usually IV Ceftriaxone 2g BD(anti-meningitis dose) or just 1g BD for 1 week
- 49. The stress of ICP • Prophylaxis with histamine blockers and/or antacids should be implemented. • stress of head injury ; leads to increased energy consumption by the injured patient's body • thus, Enteral nutrition is employed if no contraindications exist, in the 1st few days; whereas, parenteral nutrition is reserved for patients with associated abdominal injuries
- 50. Complications • Insomnia • Cognitive decline • Posttraumatic headache • Posttraumatic depression • Posttraumatic seizures • Hydrocephalus • Deep vein thrombosis • Spasticity • Gastrointestinal complications:cushing’s ulcers. • Gait abnormalities
- 51. Discharge criteria - GCS 15/15 with no focal neurological deficit - patient must be accompanied by a responsible adult and should not be under the influence of alcohol or other drugs -Verbal and written head injury advice must be given to both patient and their accompanying adult >> ssx that warrant TCA STAT to ED Eg Persistent or worsening headache despite analgesia, persistent vomiting, drowsiness, visual disturbance, development of weakness or numbness in the limbs
- 53. References • Medscape references on Traumatic Brain Injury, penetrating head trauma etc • Bailey and Love’s Short Practice of Surgery 25th edition • NICE guidelines Head Injury ; Assessment and Early Management Recommendations (January 2014) • Manual of Definitive Surgical Trauma Care by Kenneth D.Boffard , Publication of International Association for the Surgery of Trauma and Surgical Intensive Care • Handbook of Trauma Care 6th edition ; The Liverpool Hospital Trauma Manual • Guidelines for the management of Severe Traumatic Brain Injury 3rd edition, Journal of Neurotrauma by Brain Trauma Foundation, US • Guidelines for the Surgical Management of Traumatic Brain Injury , by BTF. 2006
Editor's Notes
- -continues to be an enormous public health problem, even with modern medicine in the 21st century.
- Primary ; the initial structural injury caused by the impact on the brain, and, like other forms of neural injury, patients recover poorly. Secondary ; can result from systemic hypotension, hypoxia, elevated ICP, or as the biochemical result of a series of physiologic changes initiated by the original trauma
- kPa &gt;&gt; mmHg ( x7.5)
- . Mild head injuries are generally defined as those associated with a GCS score of 13-15, and moderate head injuries are those associated with a GCS score of 9-12. A GCS score of 8 or less defines a severe head injury. These definitions are not rigid and should be considered as a general guide to the level of injury.
- This concept is defined by the Monro-Kellie doctrine, which states that the total intracranial volume is fixed because of the inelastic nature of the skull. When a significant head injury occurs, cerebral edema often develops, which increases the relative volume of the brain. Because the intracranial volume is fixed, the pressure within this compartment rises unless some compensatory action occurs, such as a decrease in the volume of one of the other intracranial components. The rationale for each treatment of head injury is based on the concept of the Monro-Kellie doctrine and how a particular intervention affects the intracranial compliance. When the volume of any of the components of the total intracranial volume is decreased, the ICP may be decreased.
- The addition of a mass lesion can initially be compensated for by the displacement of CSF and venous blood out of the intracranial cavity. During this period ICP remains at normal levels. On further expansion, quite small increases in volume of mass lesion results in relatively large increases in ICP ; brain herniation and rapid clinical deterioration
- This is due to autoregulation by the arterioles, which will constrict or dilate within a specific range of blood pressure to maintain a constant amount of blood flow to the brain. When the MAP is less than 50 mm Hg or greater than 150 mm Hg, the arterioles are unable to autoregulate and blood flow becomes entirely dependent on the blood pressure, a situation defined as pressure-passive flow. Thus, when the MAP falls below 50 mm Hg, the brain is at risk of ischemia due to insufficient blood flow, while a MAP greater than 160 mm Hg causes excess CBF that may result in increased ICP. While autoregulation works well in the noninjured brain, it is impaired in the injured brain. As a result, pressure-passive flow occurs within and around injured areas and, perhaps, globally in the injured brain.
- Once an important part of the head injury evaluation, skull radiographs have been replaced by CT scans and are rarely used in patients with closed head injury. -spans from the base of the occiput to the top of the vertex in 5-mm increments. -CT scan aim&gt;&gt;-aim at identifying an intracranial haematoma, the evacuation of which will reduce ICP and the likelihood of Secondary brain injury
- Majority of mild head injury are discharged after history, examination and a period of observation.Will explain about discharge criteria laterSome are at significant risk of intracranial haematoma and require a CT. -NICE guidelines -Ix eg CT scan are of secondary importance to restoring normal oxygenation and blood pressure, even if it means going to OT to prevent on-going abdominal and pelvic blood loss &gt;&gt; Thus if patient has an intra-abdominal trauma , settle that 1st before getting a CT Scan Other long term m/x include referral to Physio, OCT and Rehab
- In patients with anterior skull base fractures, nasogastric tubes always should be avoided because of the increased risk of intracranial tube insertions. An orogastric tube can be placed carefully under direct vision. During and after resuscitation, a history is taken, and physical and neurological examinations are performed.
- Source : Primary and Secondary Surveys according to Trauma Guidelines - TBI ( Victoria, Australia)
- Source : Handbook of Trauma Care , The Liverpool Hospital Trauma Manual , 6th Edition Head injury &gt; in mild ones
- Head injury &gt; Severe GCS 12 or less The investigations&gt;&gt;&gt;&gt; Respective m/x (if positive)
- A provisional written radiology report should be made available within 1Â hour of the scan being performed.Â
- (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1Â metre or 5Â stairs). A provisional written radiology report should be made available within 1 hour of the scan being performed.
- PaO2 – 10.7 – 13.3kPa (80-100) PaCO2 – 4.7 -6 kPa (35-45) kPa x 7.5 (mmHg)
- Should the patient with GCS equal to 15 deteriorate at any time after the initial 2-hour period, observations should revert to half-hourly and follow the original frequency schedule.Â
- Pterion – the thinnest part and overlies the largest meningeal artery ; middle meningeal artery May also occur in other regions ; frontal , posterior fossa Not always arterial ; disruption of the major dural venous sinus can result in EDH Small force is adequate ; eg A fall from standing or a single blow to the head Lucid interval – may be just c/o headache, but fully alert and orientated with no focal neurological deficit. Deterioration can occur in minutes to hours ; this reinforces that there may be no primary brain injury with EDH A pt with EDH may also sustain a primary brain injury and have a reduced conscious level from the time of injury. Headache, nausea, vomiting are early warning signs of increased ICP Convulsion, loss of consciousness, pupil change ,neurological deficits (contralateral) Signs of Increased ICP- Cushing’s triad ( High BP, Bradycardia, irregular respiration)
- The overall mortality for all cases of EDH is about 18% but for isolated EDH cases it is about 2%. Expedite the transfer to neurosurgical services to prevent delay
- Nearly always associated with a significant primary brain injury The diffuse shape is because there is less resistance to blood moving through the subdural space then the extradural space Factors eg Best GCS, pupillary reactivity, age and presence of anticoagulants must be taken into account Mortality rate from ASDH is much higher ; 40% in some
- Aneurysms are the most common cause of spontaneous SAH, but trauma is by far the commonest cause overall. In rare cases, a spontaneous aneurysmal haemorrhage immediately precedes a head injury.
- Common in head injury Ridged cranial fossa floor – most often ; inferior frontal lobes and temporal poles A contusion may be described as an intracerebral haematoma if the lesion contains a large amount of fresh haemorrhage and therefore appears uniformly hyperdense.
- By supervising doctor. To reduce inter-observer variability and unnecessary referrals, a second member of staff competent to perform observation should confirm deterioration before involving the supervising doctor If any of the changes noted in recommendations above are confirmed, an immediate CT scan should be considered, and the patient&apos;s clinical condition re‑assessed and managed appropriately.Â
- In trauma practice, there are no guidelines on the necessity or value of repeat CT scan. Indications for Routine Repeat Head Computed Tomography (CT) Stratified by Severity of Traumatic Brain Injury Brown et al , The Journal Of Trauma and Acute Care Surgery, by Wolters Kluwer publication Conclusions of a study : Patients with any head injury (mild, moderate, or severe) should undergo a repeat head CT after neurologic deterioration, because it leads to intervention in over one-third of patients. Routine repeat head CT is indicated for patients with a GCS score ≤8, as results might lead to intervention without neurologic change Delayed traumatic intracerebral hemorrhage refers to the appearance of hemorrhage (usually within 48 hours of head trauma) in areas of the brain that were normal in appearance or nearly so on the CT scan taken shortly after injury. Neurologic deterioration is common but is not universally the rule. The frequency of delayed traumatic intracerebral hemorrhage is variable but is reported to occur in 1% to 8% of patients with severe head injury. The pathogenesis is multifactorial and may result from one or more of the following: coagulation abnormalities, necrosis of blood vessels in areas of brain injury, dysautoregulation, and release of tamponade effect with evacuation of extra-axial hematomas. Outcome is poor, and most series report a mortality of 50% or higher.
- There is criteria given in BTF
- -involves removing a large section of skull and opening the dura, allowing the swollen brain to expand underneath the scalp-bone flap is stored and replaced 3 to 6 months later when pt made a good neurosurgical recovery and brain swelling has resolved
- -A single episode of hypoxia associated with a worse outcome in traumatic coma A definitive airway required ; patient in traumatic coma is unable to protect their airway, and is at risk of aspiration. -Conversely a fall in PaCO2 will result in generalised vasoconstriction, a fall in cerebral blood volume &gt;&gt; drop in ICP may seem beneficial but occurs at the expense of perfusion of ischaemic areas of the brain and thus will result in a higher likelihood of cerebral infarction than recovery from ischaemia (hyperventilation to induce hypocapnia is used only by experienced anaesthetists) -A single episode of hypotension with a systolic BP of &lt; 90mmHg is associated with worse outcome in Traumatic coma
- Useful adjuct in the management of unconscious patients with head injury A tunnelled parenchymal ICP monitor can be inserted through a twist drill burr hole, in this case into the left frontal lobe
- Mannitol ; 1.5g/kg over 20 minutes Barbiturates are associated with respiratory and metabolic complications and can take days to clear from the body.Dosage is guided by burst supression on EEG monitoring. Eg.Thiopentone . Fluids – preferably NS.avoid dextrose ; hypotonic and can cause hyperglycaemia.HM is also hypotonic Steroids should not be used &gt;&gt; associated with increased mortality Role of mannitol&gt; advocated for 2 circumstances A single administration can have short term beneficial effects (at most 2 hours) during which further diagnostic procedures (eg.CT scan) and intervention (eg. Evacuation of intracranial mass lesion) can be accomplished. A prolonged therapy for raised ICP. Precautions before use of mannitol -insert CBD -Ensure he/she is not hypotensive -Ensure pt does not have CRF
- Source ; medscape and Manual of Definitive Surgical Trauma Care Seizure activity in the early post-traumatic period following head injury may cause secondary brain damage as a result of increased metabolic demands, raised ICP and excess NT release. Here after loading dose : IV phenytoin 100mg TDS then oralised to 300mg OD to complete for 1 week. There are certain studies (Cochrane Database – Schierhout ) &gt; concluded that whereas prophylactic anti-epileptics are effective in reducing early seizures, there is no evidence that treatment with prophylactic anti-epileptics reduces the occurrence of late seizures or has any effect on death and neurological disability.
- Source : Manual of Definitive Surgical Trauma Care, medscape, article (refer below) Articles on Biomed Central by Eftekhar et al Prophylactic antibiotic for prevention of posttraumatic meningitis after traumatic pneumocephalus ; design and rationale of a placebo-controlled randomised multicenter trial Published on 18 Jan 2006 Post traumatic meningitis is one of the potentially serious diseases. Incidence significantly increases in the presence of the skull base #, pneumocephalus or CSF leak. After a pneumocephalus, microorganisms enter the CSF from the outside mainly the air sinuses. Pneumococci are the major causative microorganism. Meningitis happened almost always in the 1st week PT , so abx continued for 7 days. Duration remains controversial , often is based on the experience of the surgeon.
- A Cushing ulcer, named after Harvey Cushing,[1][2] is a gastric ulcer associated with elevated intracranial pressure. It is also called von Rokitansky-Cushing syndrome. Apart from in the stomach, ulcers may also develop in the proximal duodenum and distalesophagus The mechanism of development of Cushing ulcers is thought to be due to direct stimulation of vagal nuclei as a result of increasedintracranial pressure. Alternatively, it may also be a direct result of Cushing reaction. Efferent fibers of the vagus nerve then releaseacetylcholine onto gastric parietal cell M3 receptors, causing insertion of hydrogen potassium ATPase vesicles into the apical plasma membrane. The end result is increased secretion of gastric acid with eventual ulceration of the gastric mucosa. Source ; medscape
- -Risks of epilepsy and Alzheimer’s -Explanations in Medscape
- From NICE guidelines as well
- low initial GCS advanced age pupillary size and response development of hypoxia, pyrexia, and high intracranial pressure following initial presentation Factors associated with poor initial and long-term outcomes.