Acute Neurological Disturbances Flashcards
Traumatic brain injury
- Spectrum of intracranial injury resulting from direct (strike/penetration) or indirect (brain impacts the skull) trauma, leading to alterations in neuro function
- GCS 30min after used to classify
- 14-15 mild, 9-13 moderate, < 8 severe
Concussion
- Subset of mild TBI, where the head and brain moves rapidly back and forth, causing immediate impairment of neural function
- Includes alteration of consciousness, disturbance in vision or equilibrium
- Symptoms are usually shortlived and resolve spontaneously (within 7-10days: simple, more than that is complex)
Pathophysiology of TBI
- Cerebral autoregulation is a mechanism that controls blood flow to the brain despite changes to systemic artieral pressure and ICP, through constriction and dilation of vessels and maintenance of the BBB
- Changes in volume must be compensated, such as CSF redistribution
- Direct or systemic injury to the brain can disrupt blood flow and regulatory processes
- Increased brain tissue, blood or CSF causes vessel compression, loss of O2, compression on brainstem (loss of resp function), rise in CO2 and herniation
Primary TBI
- Direct or indirect forces to brain tissue causing cellular injury (fractures, intracranial haemorrhage, extra-axial fluid, acceleration/rotation)
Grey matter injury
* Coup injury: moving object strikes stationary head
* Contrecoup: moving head strikes a stationary object (both cause oedema and increased ICP)
Diffuse axonal injury: from shearing strains, usually rotational forces (seen in shaken baby syndrome) that causes small focal haemorrhages and diffuse oedema
- Neurotransmitter storm from cellular injury (high glutamate, calcium, ROS) that causes cellular death
Secondary brain injury
- Systemic or intracranial processes that contributes to the primary brain injury cycle and causes greater tissue injury
Systemic insults
- Hypoxia (most common), hypotension (usually from haemorrhage, cardiac contusion, pneumothorax), anaemia (blood loss) hyper/hypocapnia (hypervention leads to cerebral vasoC)
- Others incluse electrolyte abnormalities, infection, hyperthermia
Intracranial insults
- intracranial HTN, cerebral oedema, extra-axial lesions
- Leads to oxidative stress, inflammation, cell death, demyelination, neurodegeneration
Mechanisms of injury
- Skull fractures
- Extra-axial lesions (not in brain tissue - extra and subdural haematomas)
- Intracranial haemorrhages
- Subarachnoid haemorrhages (worse prognosis)
Clinical features of TBI
Confusion: distractibility, non-coherent train of thought, unable to carry out sequence of movements
Amnesia: repeated questioning, unable to follow commands (decreases slowly over time)
LOC: due to rotational forces near upper midbrain and thalamus (not a predictor of long term problems)
Symptoms based on grade
Mild: confusion, amnesia, foggy, slurred speech, headache, photophobia, N&V (GCS13-15)
Moderate: GCS 9-13, may have ‘talk and die’ syndrome where they present talkative then rapidly deteriorate within 48 hours, usualy an epidural haematoma
Severe: severe neuro defects and pupil response, usually requires airway control, resus, ICU, surgery
* Cushings triad: progressive HTN, brady, impaired resp pattern (response to poor perfusion)
Mild TBI management
- Observe for 24hours after injury
- Treat symptoms and prevent secondary injury
- Monitor haematoma risks: coagulopathy, drugs/alcohol, prev neuro procedures, epilepsy
- Educate about warning signs post-discharge: worsening headache, confusion, visual difficulties, N&V, numbness –> return for repeat neuro exam
- Pt doesnt have to stay awake
Mod/Sev TBI Management
- CT imaging
- Stabilisation and prevention of secondary insults (airway management for hypoxia and hypoventilation)
- ETT for GCS < 9
- Maintain cervical spine immobilisation
- Monitor CO2 (hypercapnia causes vasoD and increases ICP) - consider arterial catheter
- Maintain MAP and fluid balance (autoregulation is lost and cant regulate ICP well)
- Closely monitor ICP (5-10mmHg)
If ICP increases
* First raise head of bed
* Short term hyperventilation, osmotic diuretic
* Mild hypothermia, barbituates, craniotomy
Second impact syndrome
- When a patient suffers a second HI before the first has resolved (impaired autoregulation)
- Causes rapid oedema, ICP increase and death
Post Concussive syndrome
- Symptoms that develop within 4 weeks and may persist for months
Post traumatic epilepsy
- Seizure activity > 7 days after injury
- Cannot be prevented with antiepiletics
Persistent vegetative state
- Rare complication
- Disruption of cerebral function but spared brainstem function
- Sleep-wake cycle but no awareness or ability to interact
Subdural haematoma
- Localised mass of venous blood between the dura mater and arachnoid mater (30% of head injuries)
- Cresent shaped, slowly expanding (epidural is circular, rapidly expanding, arterial blood)
- Caused by head trauma, anticoagulation, intracranial HoTN, surgery, spontaneous
- The haematoma causes increased ICP, leading to hypoxia (and oedema around dead tissue), pressure on the resp centre, rise in O2 (results in further increase in blood) and herniation
- Acute: < 72h
- Chronic: slowly over weeks, common in infants, individuals with brain atrophy (elderly, alcoholics) as bridging veins are stretches and more prone to tearing)
Pathophysiology of a subdural haematoma
Follows the same process as a TBI - initial injury and secondary injury
Initial
* high impact trauma causing acceleration and tearing vessels (usually bidging veins) which are already stretched due to atrophy in elderly or alcoholics
* Subacute (3-7d) remains liquid, chronic (2-3w) forms a serous fluid that is hypodense on a CT
* Small SDHs reabsorb on their own, largers often encapsulate and continue to bleed and expand
Secondary
* progression of initial injury resulting from altered perfusion and oxygenation
* increasing SDH and ICP causes hypoxic and ischaemic changes, electrophysiological alterations, oedema, hydrocephlus, HoTN, and herniation
Manifestations
Acute
* Presents following a TBI
* May be LOC or lucid, but as ICP increases the patient shows papillary and visual dysfunction, motor impairment, headache, vomiting, cushing triad
Chronic
* Presents 2-3wks following TBI
* Gradual symptoms, usually anorexia, N/V, growing neuro deficit, confusion, personality changes, speech issues
Full Assessment
Resp: low O2, high RR, impaired gag reflex, monitor CO2 (hypercapnia will cause vasoD & increased ICP, hypocapnia will cause vasoC & impaired cerebral perfusion)
CNS: FNO using GCS to assess signs of increasing ICP, esp pupils (1hrly of 1/2 if concerns)
* Monitor neuro deterioration, CSF leak, vomiting, headache
CVS: check for brady/tachy, HTN, pulse pressures, impaired breathing, monitor MAP as autoregulation is lost
Renal: incontinence
GIT: N/V, sluggish bowels, incontinent
Also take AMPLE (allergies, meds, PMH, last ate/last period, events) or MIVT (mechanism of injury, injuries, vitals, treatment)
Diagnostic investigations
- Coag profile, FBC, U&E, LFT, crossmatch and group, ABGs, BGL, tox screen (to rule out other causes of deterioration)
- Urgent CT
Phenytoin
- Anticonvulsant (IV/PO) that inhibits spread of seizure activity
- HL 22h
- SE: N&V, slurred speech, dizziness, headaches, reduced coordination
Paeds minor head injury
- Can be discharged unless there is doubt over loss of consciousness
- If so, treat as moderate
Paeds moderate head injury
- if stable, neuro obs every 30 minutes for 4 hours
- Discharged if improvements in consciousness, no vomiting and toleration of diet
- Headache, haematoma or wounds need to be investigated
Paeds severe head injury
- AIM: prevent secondary brain damage by maintaining O2, ventilation and circulation and decreasing ICP
- Urgent CT and spine immobilisation regardless if cleared
- Intubate is unresponsive, GCS < 8, loss of resp reflexes
- Decrease ICP by increasing head of bed, ventilate to pCO2 to 35mmHg, maintain BP
- Consider mannitol
