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NUR3310 > Wk 4: Neurology > Flashcards

Wk 4: Neurology Flashcards

1
Q

Define intracranial pressure and what is considered increased ICP?

A

= the sum of the pressure that these three volumes exert in the skull.
- raised ICP is considered to be a sustained pressure over 20mmHg.

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2
Q

What is the Monro-Kellie hypothesis theories?

A

= if the volume of one component within the skull increases, another must decrease to maintain normal ICP.

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3
Q

What is normal ICP?

A

= 0-15mmHG

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4
Q

How does the brain compensate for small and brief increases in ICP?

A
  • pushing blood into the venous sinuses in the brain
  • increasing the CSF resorption
  • moving CSF into the spinal column

= is susceptible to damage from pressure changes that can occur in systemic blood system (vaso constriction/dilation), hence the need for these.

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5
Q

Define autoregulation in the context of cerebral perfusion.

A

= the ability of blood vessels in the brain, to constrict or dilate to maintain a stable blood flow within the normal range of cerebral perfusion pressure.

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6
Q

What causes cerebral vasodilation?

A
  • hypoxia
  • hypercapnia
  • acidosis
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7
Q

What causes cerebral vasoconstriction?

A
  • hypocapnia
  • decreased ICP
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8
Q

Define cerebral perfusion pressure (CCP) and explain why it is important.

A

= the pressure needed to maintain blood flow to the brain.

Adequate perfusion is critical as it determines whether neurons receive blood (oxygen and glucose) or not.

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9
Q

What is normal CPP and what threshold is associated with ischemia and death of neurons?

A

Normal: 60-100mmHg

<50mmHg is associated with ischemia and death of neurons.

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10
Q

What is the calculation for CPP?

A

CPP is determined by the mean arterial pressure (MAP) and intracranial pressure (ICP):

CPP = *MAP minus ICP

*(MAP = Diastolic BP + 1/3 (Systolic BP minus Diastolic BP)

**think that the ICP counter blocks its equivalent in MAP and this what is left is the CPP.

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11
Q

Why is CCP important in the management of ICP?

A

= a patient who has a normal ICP but is hypotensive will have inadequate cerebral perfusion. Similarly, a patient who has a raised ICP and normal blood pressure will have decreased cerebral perfusion.

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12
Q

What are some causes of increased ICP?

A

Brain
- tumor
- infection/inflammation (meningitis, encephalitis)
- cerebral oedema (trauma, hypoxia, stroke)
- haemorrhage/haematoma

CSF
- increased production
- decreased absorption following meningitis
- impaired circulation (obstructive hydrocephalus)

Blood
- vasodilation (respiratory depression, ↑ CO2, cerebral hypoxia)
- Obstruction of venous outflow-neck surgery, jugular vein compression
- Heart failure

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13
Q

Explain the two main ‘natures’ of brain injury.

A
  1. Immediate damage as a result of injury
  2. Damage that develops from swelling or bleeding that occur in response to an injury.
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14
Q

Outline the progression of increased intracranial pressure from cranial insult to death.

A
  • Cranial injury
    -> tissue oedema
    -> increased ICP
    -> Compression of blood vessels
    -> reduced cerebral blood flow
    -> decreased O2 with death of brain cells
    -> oedema around necrotic tissue
    -> increased ICP with compression of brainstem and respiratory centre
    -> accumulation of CO2
    -> vasodilation
    -> increased ICP resulting from increased blood volume
    -> death
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15
Q

Do small ICP changes result in clinical manifestations and why?

A
  • Small immediate increases in brain volume do not lead to increases in intracranial pressure (ICP) due to autoregulation and displacement of the CSF into the spinal canal.

Similarly, small changes that occur slowly can have a small effect on ICP (for example large meningiomas).

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16
Q

What are some clinical manifestations of large or sudden increases in ICP that do decrease cerebral perfusion?

A
  • Altered level of consciousness: one of the earliest signs
    - agitated
    - irritability
    - unconious
  • Changes in speech pattern
  • Pupillary changes: unequal/ dilated/ non-reactive (compression of oculomotor nerve)
  • Neurological symptoms-weakness, numbness
  • Nausea, vomiting
  • Seizures: neuronal damage
  • Cranial nerve palsy, particularly involving the abducens (VI) nerve

Late signs
- Cushing’s triad
- Abnormal posturing
- decorticate: planta flexed, internally rotated legs, flexed arms and hands and abducted sholders.
- decerebrate: planta flexed, flexed hands, pronated hands, extended and abducted sholders.
** due toHerniation of the cerebellar tonsils due to pressure gradient

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17
Q

What is a classic triad that is a late sign of increased ICP and possible brainstem herniation?

A

= Cushing’s triad
- hypertension with widening pulse pressure (↑ systolic pressure with ↓ diastolic pressure)
- Bradycardia
- Respiratory depression/ agonal breathing

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18
Q

What are the goals of managing raised ICP?

A
  • maintain cerebral perfusion by maintaining adequate cerebral perfusion pressure
  • minimise cerebral damage and complications through early recognition and intervention
  • prevent secondary injury (by controlling hypotension, hypoxia and hyercarpia)
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19
Q

Describe the nature of the skull and its components and then what the significance there relationship has in the context of ICP.

A

Skull= rigid structure
Holds;
- brain tissue (80%)
- CSF (10%)
- Blood (10%)

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20
Q

What are the two processes of autoregulation?

A
  • vasoconstriction of cerebral vessels
  • cerebrospinal fluid (CSF) displaced into spinal column to reduce volume and thus pressure

**when autoregulation processes fail then ICP rises.

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21
Q

What is margin for intracranial hypertension

A

= >20mmHg

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22
Q

What are some outcomes of increased ICP?

A
  • brain herniation

if pituitary involvement
- diabetes inspects
- Syndrome of inappropriate secretion of antidiuretic hormone (SIADH)

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23
Q

What may the primary assessment findings of a pt with suspected neurological decline be nd how would you manage these?

A

Danger

Response
- AVPU
- A: alert
- V: response to verbal stimula
- P: response to painful stimuli
- U: unresponsive

Send for help
- MET or code blue

Airway
- ?are they conscious enough to maintain and protect their own airway

Management: if needed protect with adjuncts, hea tilt/chin life maneuvers or jaw thrust
- consider intubation if drop in GCS
- ?entering oma if GCS <9.

Breathing
- looking at trends and changes
- ?decrease sats
- ?decrease rate
- agonal breathing

Management: apply O2 and ongoing management of O2
Avoid hypoxemia: as this causes vasodilation which increased ICP

Circulation
- normotensive/hypotensive (if sepsis)
- (late signs) Hypertensive, bradycardia (Cushing’s triad)
- Skin hot (if infection) -> cool, clammy

Manage:
- Vital signs
- IVC
- monitor fluid status (avoid hypovolemia)
- IVT (Normal saline/ Hartmanns, not Dextrose)
- Avoid hypotension CPP = MAP – ICP, vasopressors

Disability
- Irritable/ confused/ somnolence/ changes in behaviour
- Slowed speech/ comprehension
- Headache
- Febrile
- Blurred vision/ unequal pupils/ sluggish
- Limb weakness
- Seizures (focal/ generalised)

Management:
- Maintain safety
- maintain BGL
- monitor GCS (ensure to reassess)
- pain management (as stress then increases HR and BP)
- ↓ fever (reduce risk of brain injruy)
- anticonvulsants

All patients with an altered conscious state should have a blood glucose performed.

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24
Q

How do we reduce ICP or minimise further elevations of ICP?

A
  • Sedate/ paralyse
    - to ↓metabolic demand of the body and thus brain to decrease level of injury
  • ↓ noxious stimuli (noise, clustering procedures)
  • Position with raised head of 30o – 40o angle (↓ ICP as helps with blood decrease from head)
  • Avoid neck flexion (to optimise outflow of blood from head)
  • reduce coughing/ straining (↑ ICP)
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25
Q

What are some treatments for those with increased ICP?

A
  • treat and relive the cause
  • ↓Compression- burr holes/ craniotomy (risk of herniation)
  • ICP monitoring if available: guides treatment
  • Hypertonic solutions (Mannitol 20%, saline 23.4%): ↓ brain volume (osmotic diuresis)
  • +/- Loop diuretics -> diuresis (we are trying to avoid hypotension but may be indicated in some cases)
  • ? Dexamethasone (↓ inflammation-meningitis, tumours. Not indicated in traumatic brain injuries)
  • Barbiturates (↓ metabolic demand brain) especially pr pts who are combative
  • Mechanical ventilation
    - we can institute hyperventilate to ↓PCO2 (26-30 mmHg)
    - ↓vasodilation, ↓cerebral blood flow= <ICP
    - Cooling:↓ brain metabolism, neuroprotective
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26
Q

What are the two broard categories of CNS infections?

A

Meningitis: those primarily involving the meninges.
Encephalitis: those primarily confined to the brain parenchyma.

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27
Q

Define Meningitis

A

= an acute inflammation of the meningeal tissues surrounding the brain and the spinal cord.

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28
Q

Define Leptomeningitis

A

= inflammation of the arachnoid tissue and subarachnoid space.

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29
Q

Is meningitis or leptomeningitis more common?

A

= Leptomeningitis

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30
Q

What are some causes of meningitis?

A
  • Bacterial
  • Aseptic
    - Viral (most common)
    - Other causes:
    - Head injury (penetrating wound, skull #)
    - Cancer (Leptomeningeal cancer)
    - Drug induced (hypersensitive reaction)
    - Other types of infection (fungal, Tuberculosis, parasite)
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31
Q

Describe the nature of viral meningitis

A
  • most commonly affects children and young adults
  • clinical manifestations are similar to bacterial however are less severe
  • symptoms usually last 7-10 days
  • self liminiting= no matter the treatment these pts will get better.
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32
Q

What are common viral causative agents for meningitis?

A
  • most common=enteroviruses
  • Epstein-Barr
  • herpes simplex 2

*Often the causative agent is not identified.

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33
Q

How do enteroviruses the most common causes of viral meningitis spread?

A

Enteroviruses are present in the;
- respiratory secretions
- saliva
- faeces
of an infected person and spread through close contact.

34
Q

Is bacterial meningitis significant and what is the mortality rates?

A

= yes, it is a neurological and infectious disease emergency.

Mortality;
- Adults= about 25% of cases

61% of infants who survive have significant developmental and neurological issues.

35
Q

What is the most common means of transmission of bacteria that causes bacterial meningitis?

A
  • those most commonly linked reside in the nose and throat, and are passed on through coughing and sneezing.
36
Q

What are the most common bacterial causes of bacterial meningitis?

A
  1. Streptococcus pneumonia
    - a widespread bacterium
    - incidence of severe pneumococcal infection, including meningitis, has decreased significantly since the introduction of the pneumococcal vaccine onto the Australian National Immunisation Plan in 2005; the vaccine is given to babies, at risk groups and seniors.
  2. Neisseria meningitides
    - responsible for meningococcal disease which includes meningococcal meningitis and septicaemia.
    - The infection can develop quickly
    - is fatal in 5-10% of cases.
    - It is believed 10-20% of the population carries the Neisseria meningitides bacteria in the back of our nose and throat without being aware of it.
    - Mode of transmission is by respiratory droplets from the upper respiratory tract.

Others include;
- GBS
- Gram neg bacteria
- Haemophilus influenza (vaccine)

37
Q

What are some risk factors for bacterial meningitis?

A
  • head trauma with a skull fracture
  • otitis media
  • mastoiditis
  • systemic sepsis
  • immunocompromised
38
Q

Explain the pathophysiological process of viral/bacterial meningitis.

A
  • infectious agent invades CNS via;
    - Haematogenous spread (via blood supply) is the most common route and upper respiratory tract the most common source of entry of microorganisms
    - Direct inoculation of brain parenchyma (penetrating injuries, skull fractures)
    - From adjacent structures (middle ear, mastoid and paranasal sinuses)
    - Spread of infection from outside the CNS (respiratory or gastrointestinal tracts)
  • once the blood-brain barrier is breached infection multiplies due to the lack of immunological components in the CSF.
39
Q

What is the impact of meningitis on ICP? and how do it have this impact?

A
  • The presence of bacteria induces an inflammatory response by the meninges, CSF and ventricles, with cytokine release and increased permeability.
  • A series of injuries occur to the endothelium of the blood brain barrier leading to impairment:
    - Separation of the tight junctions allows protein, water and white blood cells to migrate into the subarachnoid space
    - Autoregulation of cerebral perfusion pressure is impaired and cerebral blood flow disrupted causing areas of ischaemia

Results in
= raised ICP due to cerebral oedema (vasogenic), ischaemia due to impaired cerebral blood flow and cytotoxic damage to neurons and brain cells due to leukocytes (neutrophils) and bacteria invasion, and ischaemia.
- Further inflammation continues as purulent secretions spread to other areas of the brain compounding the injuries caused by the host inflammatory response.

40
Q

Link the clinical manifestation of petechial rash of meningococcal meningitis to the pathophysiology of bacterial meningitis

A

Bacterial meningitis can trigger a systemic inflammatory response
= increased capillary permeability
= contributes to fluid shifts between intra-and extravascular compartments
= resulting in hypovolemia
- As the infection progresses and blood vessels are damaged, blood leaks from the capillaries as seen in the characteristic petechial rash of meningococcal meningitis.

41
Q

What are some complications of bacterial meningitis?

A
  • seizures
  • bradycardia
  • hypertensive coma
  • death
    *this is due to acute cerebral oedema which leads to increased ICP
42
Q

Define cerebral oedema and why does it occur?

A

= is the excess accumulation of fluid in the intracellular or extravascular spaces of the brain
- usually occurs in response to a brain insult such as trauma, stroke, haemorrhage, contusion or inflammation

43
Q

What are the two categories of cerebral oedema? and what is the goal of management of it?

A

Localised (focal): around the area of injury
Diffuse: as a result of hypoxia or hypotension.

44
Q

What is the goal of management of cerebral oedema and how is it achieved?

A

Goal: reduce pressure on the brain and prevent secondary injury.

Achieved by;
- use of an intravenous hypertonic solution (Mannitol/ Saline) which draws fluid from the cells into the circulating volume, causing diuresis.
- Steroids have also been used with varying degrees of success.

45
Q

In basic terms, how does meningitis occur?

A
  • causative agent must come in contact with the meninges.

to do this it must breach the skull via abnormality or breach in skull or must develop a primary infection elsewhere.

46
Q

What are the vimulvent factors that

A
  • colonisation
  • invasion
  • immune evasion
  • meningeal invasion
47
Q

What are some complications of meningitis?

A
  • increased ICP from cerebral oedema
  • altered mental state
  • seizures

if left untreated;
- permanent brain damage
- seizures are more common with pneumococcal meningitis
- septic shock
- Irritation of the cranial nerves from the raised ICP= disturbance in auditory and visual senses.

48
Q

What are the clinical manifestations of meningitis?

A

*classic presentation of 3 signs and most commonly the last two
- sever headache
- N + V
- Nuchal rigidity (neck stiffness)
- fever

Other signs may include
Systemic infection
- fever
- chills
- tachy
- generalised back, abdominal or limb pain
- malaise

Neuro signs
- altered conscious state (drowsy, confused, coma)
- focal neurological deficits
- N + V
- seizures ~30%

Meningeal irritation
- sever headache
- neck stiffness
- photophobia
- phonophabia
- Kernig’s sign (resistance to leg extension)
- Brudzinski’s sign (neck flexion causes hip and knee flexion)

Other (specific to causative agent):
- Petechial rash (meningococcal disease)
- Sore throat (virus)

49
Q

Outline key points about bacterial meningitis

A
  • medical emergency (fatal if not treated quickly)
  • rapid onset (hrs to 1-2 days), slow recovery
  • death ~5-10%
  • can result in permanent disabilities including cerebral palsy and deafness.
50
Q

How is meningitis diagnosed and types differentiated?

A
  • History: helps differentiate
  • Physical examination
  • Lumbar puncture for CSF specimen:
    - Bacterial: cloudy, purulent, under increased pressure ↑ WBC, ↑ Protein, ↓Glucose
    - Viral: ↑ lymphocytes, moderate ↑ protein, normal glucose
    - Relative contraindications: coagulopathy, ↑ ICP so ?CT or MRI as there is a rick of herniation
  • +/- CT/ neuroimaging
  • Blood cultures
  • Pathology: ……… (CRP etc distinguish between bacterial & non-bacterial)
51
Q

What are the classic signs of bacterial meningitis?

A

Classic triad
- sever headache
- N + V
- changes in mental status
*less than half pts present with all three but most present with at least one

  • Nuchal rigidity (neck stiffness) *
  • Fever (mostly present) *
52
Q

What are the clinical manifestations of bacterial meningitis?

A

Systemic infection:
- Fever
- Chills
- Tachycardia
- Petechial rash
- Generalised back, abdominal or limb pain
- Malaise

Neurological signs:
- Altered conscious state (drowsy, confused, coma)
- Focal neurological deficits
- Nausea & vomiting
- Seizures~30%

Meningeal irritation:
- Severe headache
- Neck stiffness (Nuchal rigidity)
- Photophobia
- Kernig’s sign
- Brudzinski’s sign

Other (specific to causative agent):
- Petechial rash (meningococcal disease)
- Sore throat (virus)

53
Q

What is the management of viral meninigitis?

A
  • Isolation not required
    - Hand washing & precautions handling of stools when enterovirus suspected
  • If causative agent mumps, varicella
    - usual precaution of isolating from susceptible individuals

Goal of management: symptom management as it is self limiting: paracetamol-temperature, headache, antiemetic
- AB (IV 3rd gen Cephalosporin) until bacterial meningitis ruled out
- Antivirals: for Herpes simplex virus 2 (HSV-2) (Acyclovir)/ encephalitis
- Steroids
- Dexamethasone if signs of ↑ ICP
- Management of seizures if develop (↑ ICP)
- Phenytoin

54
Q

What would your likley assessment findings be and the subsequent management?

A

Danger
A: Organism spread through close contact/ coughing/ sneezing, ?seziure injury
M:
- Droplet precautions x 24 hours
- Report incidence to Office of Health - Protection (communicable diseases)
- Seizures: minimise injury

Response
A: Alert/ ↓ level of consciousness (↑ ICP)/ lethargic/ seizures
M:
- AVPU
- Send for help
- Maintain safety/ anticonvulsants

Airway
A: Patent/ speaking in sentences/ partial obstruction
M:
- Monitor for deterioration (can be sudden)
- Support airway as required

Breathing
A: Tachypnoea
M:
- Apply O2 to maintain saturations
- Monitor for deterioration
- Position patient upright

Circulation
A: Hypotensive Tachycardia (septic shock), fever, diaphoresis, cool and clammy skin
M:
- Monitor BP and HR (deterioration can be sudden)
- IVC x 2
- IVT (shock, rehydration)
- Pathology: CSF, PCR (polymerase chain reaction- can pick up on dead bacteria and comes back before lumbar puncture), ABGs, FBC, U&E, coagulation, blood cultures, throat/ nasal swabs
- Fluid balance: SIADH (syndrome of inappropriate antidiuretic hormone)
- BGL: accurate CSF: blood ratio

Disability
A: confusion/ irritability, rash (meningococcal septicaemia), nausea & vomiting, pain-severe headache/ neck stiffness/ joint pain, photophobia, seizures (15-30%)
M:
- Monitor GCS
- Provide reassurance
- Pain management/ position
- Dark, quiet room
- Antiemetic
- Monitor BGL
- Anticonvulsants/ prevent injury
- Minimise interruptions/ group procedures
- Prepare for lumbar puncture

55
Q

What are some systemic complications of meningitis?

A

Risk of developing complications
- Age and general health
- The causative pathogen
- Severity and duration of illness at time of presentation

Systemic complications: bacteremia
- Septic shock
- Disseminated intravascular coagulation (DIC)
- Acute respiratory distress syndrome (ARDS)

56
Q

What are some neurological complications of viral meningitis?

A

*Neurologic complications: not uncommon, but many transient
- Altered mental status:
- ↑ ICP and cerebral oedema
- Seizures
- Cerebrovascular abnormalities: thrombosis, acute cerebral haemorrhage
- Focal neurologic deficits: hemiparesis, visual field deficits (CNII), aphasia. Cranial nerve
palsy-
- Cranial nerves VII (taste, eyelid closing, facial expression)
- Ocular movements affected with irritation to cranial nerves III, IV, and VI (ptosis, diplopia, unequal pupils)
- Hearing loss (CN VIII)

57
Q

Define a head injury

A

= any alteration in mental or physical functioning related to a blow to the head.

58
Q

What are the most common causes of head injuries?

A
  • falls
  • roads/MVA
59
Q

What are risk factors for head injuries?

A
  • age >65
60
Q

What are the classifications of head injury?

A
  • mild: (GCS 13-15) e.g. concussion
  • moderate: (GCS 9-12) e.g. contusion
  • severe: (GCS 3-8) e.g. intracranial haemorrhage, epidural haematoma, subdural haematoma, subarachnoid haemorrhage
61
Q

What are the four ways a head injury can be described?

A
  • diffuse (generalised) or focal (localised)
  • primary and secondary injury
62
Q

Define a primary brain injury and the most common causes

A

= refers to the damage that occurs to the brain, at the time of injury/ impact.
- The damage can be focal or diffuse and the severity depends on the extent of the initial injury.

Common mechanisms include direct impact, rapid acceleration/deceleration, penetrating injury and blast injury.

63
Q

Define secondary brain injury

A

= is the damage that occurs to the brain as a result of the natural evolution of the primary injury.
- can occur hours to days after the initial injury

Examples of the natural evolution of a primary brain injury include cerebral swelling, infection and raised intracranial pressure.

64
Q

What causes a secondary brain injury?

A

= due to inadequate delivery of nutrients and oxygen as a result of:
- Haemorrhage
- Cerebral oedema
- Hypoxia
- Hypo/Hypercapnia
- Hypotension
- Fever
- Increased intracranial pressure (ICP)
- Hypo/Hyperglycaemia

65
Q

What are the complications of a secondary brain injury?

A

= can impair the brain’s ability to autoregulate cerebral blood flow (and pressure), and one of the primary goals of management of head injuries is to prevent secondary injury.

66
Q

What is the main complications caused by an intracranial bleed/heamatoma?

A
  • impacts on normal brain metabolism is disrupted due to the brains exposure to blood, increased ICP or secondary injury
  • Symptoms may be delayed until the bleed or haematoma is large enough to cause distortion of the brain and increased ICP.
67
Q

What are the classifications of intracranial bleeds and what specific bleeds are included within these?

A

Axial (within the brain tissue):
- Intracerebral haemorrhage (ICH)

Extra-axial (within the cranial vault but outside the brain tissue):
- Epidural haematoma (EDH)
- Subdural haematoma (SDH)
- Subarachnoid haemorrhage (SAH)E

68
Q

What are the locations of brain bleeds?

A

Intracranial
Axial
- intracerebral
- intraventricular

Extra-axial
- epidural
- subdural
- Subarachnoid

69
Q

Describe an intracerebral haemorrhage, location, cause, complications and risk factors

A

= haemorrhage within the brain
- can be spontaneous or the result of trauma
i- s the second most common cause of stroke after ischaemic stroke

Risk factors for spontaneous ICH include;
- hypertension
- cerebral atherosclerosis
- older age
- the presence of cerebral amyloid angiopathy (amyloid deposits weaken blood vessels)
- the use of anticoagulant therapy

70
Q

Define an epidural haematoma, the causes, cause and classic presentation.

A

= bleed in to the space between the dura and the skull
- is a high pressure, arterial bleed (most commonly the middle meningeal artery)

Cause: results from bleeding that occurs, in the potential space, between the skull and the dura.
- most commonly associated with skull fractures
- is a neurological emergency

Classic presentation: loss of consciousness followed by a lucid interval and rapid deterioration (increased ICP)

71
Q

Define a subdural haematoma, the causes, the types and risk factors

A

= bleeding into the space between the dura mater and arachnoid mater/the brain itself
- can be arterial but usually low pressure, venous bleed as a result of damage to bridging veins (that drain the brain parenchyma)

Cause: most commonly due to an acceleration–> deceleration action (fall, motor vehicle accident)

Arbitrarily divided into three types:
- acute (< 2 days)
- subacute (3-14 days)
- chronic (> 14 days).

Risk factors
- elderly
- heavy users of alcohol
* due to the risk due to cerebral atrophy (shrinking) and increased tension on bridging veins

72
Q

Describe a subarachnoid haemorrhage, common causes, complications, clinical manifestations and surgical management

A

= is a bleed that occurs in the subarachnoid space (normally filled with CSF), between the arachnoid mater and pia mater

Cause: a spontaneous rupture of a saccular (berry) aneurysm; intracranial arteries lack an external elastic lamina and have a very thin adventitia.

CMs: rapid onset ‘thunder clap’ headache, neck stiffness (blood irritation of meninges)

Complications
- has cerebral vasospasm as a serious complication (resulting in ischaemic stroke)

Intervention
- requires surgical intervention to ‘clip’ or ‘coil’ the aneurysm

73
Q

Define extra-axial haemorrhage

A
  • bleeding that occurs within the skull but outside the brain tissue.
74
Q

What are the clinical manifestations of a head injury causing concussion?

A
  • Altered conscious state +/- LOC: Dizziness, drowsiness, confusion, retrograde amnesia
  • Headache, vomiting, combativeness
  • Transient visual disturbances, transient hearing disturbance
  • Changes to vital signs are rare but possible
75
Q

What are the clinical manifestations of a head injury causing contusion?

A
  • Altered conscious state
  • Nausea, vomiting
  • Visual disturbances
  • Speech difficulty (slurred speech/ aphasia)
  • Limb weakness
76
Q

What are the clinical manifestations of an epidural heamorrhage?

A
  • Loss of consciousness (LOC) -> consciousness/lucid period -> LOC
  • Severe headache, vomiting, drowsiness, confusion
  • Hemiparesis
  • Ipsilateral pupil dilation, Cushing reflex (↑ ICP)
77
Q

What are the clinical manifestations of an subdural heamorrhage?

A
  • Loss of consciousness often present, hemiparesis, signs of ↑ ICP
    - Acute – 1 to 2 days after injury
    - Subacute – 3 to 14 days after injury
    - Chronic – 15 or more days after injury
78
Q

What are the clinical manifestations of a subarachnoid heamorrhage?

A
  • Severe headache ‘thunderclap’
    • can present days or week before other symptoms
  • Nausea & vomiting
  • brief LOC
79
Q

What would be the likley primary assessment findings and subsequent management for a head injury?

A

Danger:
A: ?seziures, am I at risk?
M: Maintain safety for self and patient (seizures)

Response:
A: Observe for Alert/ ↓ level of consciousness (↑ ICP)/ unresponsive/ seizures
- AVPU
M: Send for help (MET/ Code Blue)

Airway:
A: Patency (speaking in words or short sentences)
- Observe signs of ↓ conscious level for (drowsy, difficult to wake), airway obstruction (vomitus/ sputum)
M:
- Airway adjuncts (oro-/naso-pharyngeal)
- Airway support (chin lift/ head tilt, jaw thrust)
- Suction
- Monitor for deterioration (can be sudden)
- Intubate if GCS < 9
*note nasal pharyngeal airways may be contraindicated in some traumas

Breathing
A: Look, listen, feel
- Observe for respiratory depression (hypoxia, hypercapnia), peripheral/ central cyanosis
M:
- Apply O2 to maintain saturations (hypoxaemia  cerebral vasodilation)
- Position patient upright (facilitate lung expansion)
- Obtain oxygen saturation level
- Arterial blood gases (ABGs)
- Auscultate

Circulation
A:
- Observe for adequate cardiac output and tissue perfusion
- Observe for hypertension/ hypotension, bradycardia, arrhythmia, cool and clammy skin
M:
- Check BP & HR frequently (CPP = MAP minus ICP)
- ECG & cardiac monitoring
- IV cannula insertion
- IVT
- Pathology (ABGs, U&Es, coagulation…)/ reversal agents for anticoagulation
- Assess pain
- Fluid balance-urine output

Disability
A: : CNS assessment
- Observe for altered mental status (confusion/ agitation/ somnolence), signs of raised ICP (pupillary changes/ motor deficits/ vomiting/ abnormal posturing), pain (headache/ other),
temperature, seizures, patient distress
M:
- Check GCS as frequently as required (lower scores -> poorer prognosis)
- BGL
- Patient position
- Pain management
- Anticonvulsants
- Provide reassurance

79
Q

What are the clinical manifestations of a intracerebral heamorrhage?

A

*Manifestations vary according to size & location
- Primary injury (expanding bleed ↑ ICP)
- Secondary injury (ischaemia)

80
Q

What is the general management of a pt with head injury?

A

Management of ICP (maintain CPP)/ prevent secondary brain injury
- Continued assessment & reassessment
- Head elevation
- Mannitol/ Hypertonic Saline/ Diuretic: Furosemide
- Sedation
- Hyperventilation
- Surgical intervention

Safety
- Reversal agents for anticoagulation
- Nil by mouth/ dysphagia screen

Referrals
- Speech therapist/ Physiotherapist/ OT/ Dietitian/ Social worker-

NUR3310 (9 decks)

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