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GMED5002 > Acute Neurological Disturbances > Flashcards

Acute Neurological Disturbances Flashcards

1
Q

Traumatic brain injury

A
  • 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
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2
Q

Concussion

A
  • 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)
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3
Q

Pathophysiology of TBI

A
  • 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
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4
Q

Primary TBI

A
  • 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
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5
Q

Secondary brain injury

A
  • Systemic or intracranial processes that contributes to the primary brain injury cycle and causes greater tissue injury
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6
Q

Systemic insults

A
  • 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
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7
Q

Intracranial insults

A
  • intracranial HTN, cerebral oedema, extra-axial lesions
  • Leads to oxidative stress, inflammation, cell death, demyelination, neurodegeneration
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8
Q

Mechanisms of injury

A
  • Skull fractures
  • Extra-axial lesions (not in brain tissue - extra and subdural haematomas)
  • Intracranial haemorrhages
  • Subarachnoid haemorrhages (worse prognosis)
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9
Q

Clinical features of TBI

A

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)

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10
Q

Symptoms based on grade

A

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)

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11
Q

Mild TBI management

A
  • 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
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12
Q

Mod/Sev TBI Management

A
  • 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

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13
Q

Second impact syndrome

A
  • When a patient suffers a second HI before the first has resolved (impaired autoregulation)
  • Causes rapid oedema, ICP increase and death
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14
Q

Post Concussive syndrome

A
  • Symptoms that develop within 4 weeks and may persist for months
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15
Q

Post traumatic epilepsy

A
  • Seizure activity > 7 days after injury
  • Cannot be prevented with antiepiletics
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16
Q

Persistent vegetative state

A
  • Rare complication
  • Disruption of cerebral function but spared brainstem function
  • Sleep-wake cycle but no awareness or ability to interact
17
Q

Subdural haematoma

A
  • 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)
18
Q

Pathophysiology of a subdural haematoma

A

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

19
Q

Manifestations

A

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

20
Q

Full Assessment

A

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)

21
Q

Diagnostic investigations

A
  • Coag profile, FBC, U&E, LFT, crossmatch and group, ABGs, BGL, tox screen (to rule out other causes of deterioration)
  • Urgent CT
22
Q

Phenytoin

A
  • Anticonvulsant (IV/PO) that inhibits spread of seizure activity
  • HL 22h
  • SE: N&V, slurred speech, dizziness, headaches, reduced coordination
23
Q

Paeds minor head injury

A
  • Can be discharged unless there is doubt over loss of consciousness
  • If so, treat as moderate
24
Q

Paeds moderate head injury

A
  • 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
25
Q

Paeds severe head injury

A
  • 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

GMED5002 (9 decks)

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