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NUR3310 > Neurological conditions > Flashcards

Neurological conditions Flashcards

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1
Q

Outline Intracranial Pressure

A

The skull is a rigid structure and contains brain tissue, cerebrospinal fluid, and blood. Intracranial pressure can be defined as the sum of the pressures that these three volumes exert in the skull. Raised intracranial pressure is considered to be a sustained pressure over 20mmHg

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2
Q

What is the monro-kellie hypothesis?

A

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

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3
Q

Define Increased intracranial pressure

A

Regular intracranial pressure is a relatively stable balance of volumes that has a relatively constant pressure of 0-15mmHg
Raised intracranial pressure is considered to be a sustained pressure over 20mmHg

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4
Q

What methods does the brain use to maintain a stable ICP?

A

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

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5
Q

What three volumes inhabit the intracranial space?

A

brain tissue (intracellular and extracellular fluids, 80%), cerebrospinal fluid (CSF, 10%) and blood (arterial, venous and capillary, 10%)

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6
Q

How does the brain protect itself from variations in blood flow (Vasoconstriction/dilation)?

A

regulation of blood flow, called cerebral autoregulation. Autoregulation is 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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7
Q

What complications can cause vasoconstriction of cerebral blood flow?

A

hypocapnia (reduced CO2 in the blood) - which reduces cerebral blood flow and decreases ICP

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8
Q

What conditions can cause vasoconstriction of cerebral blood flow?

A

Hypoxia, hypercapnia (increased CO2 in the blood) and acidosis - which increases cerebral blood flow and raises ICP

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9
Q

Define Cerebral Perfusion Pressure (CPP)

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. Normal CPP is 60-100 mmHg; less than 50 mmHg is associated with ischaemia and death of neurons

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10
Q

how is CPP calculated?

A

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)

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11
Q

What are some brain related causes of increased ICP?

A

Tumour
Infection/ inflammation (meningitis, encephalitis)
Cerebral oedema (trauma, hypoxia, stroke)
Haemorrhage/ haematoma

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12
Q

What are some CSF related causes of increased ICP?

A

Increased production
Decreased absorption-following meningitis
Impaired circulation (obstructive hydrocephalus)

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13
Q

What are some blood related causes of ICP?

A

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

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14
Q

Progression of increased ICP

A

cranial insult -> tissue oedema -> raised ICP -> compression of blood vessels -> blocked cerebral blood flow -> blocked O2 with death of brain cells -> oedema around necrotic tissue -> raised ICp with compression of brain stem and respiratory centre -> vasodilation -> raised ICP resulting from raised blood volume -> death

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15
Q

What is the general reason for clinical manifestations of ICP to appear?

A

Sudden or large increases in volume and ICP decreasing cerebral perfusion, which ultimately is responsible

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16
Q

What are some clinical manifestations of ICP?

A

altered level of conciousness, changes in speech pattern, pupillary changes, alterations in cognition, nausea, vomiting, seizures, cushings triad (late stage)

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17
Q

What are late-stage signs of ICP?

A

Known as Cushing’s triad:
>HTN with widening BP (raised systolic with dropped diastolic)
>Bradycardia
>respiratory depression
Abnormal posturing:
>Decorticate -> joints stuff and turned towards body, arms raised over chest
>Decerebrate -> joints stiff and turned away from body

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18
Q

What are the main management goals of ICP?

A

> maintain cerebral perfusion by maintaining adequate cerebral perfusion pressure (5-10mmHG)
minimise cerebral damage and complications through early recognition and management: prevent hypoxia, hypercapnia (^CO2), hypotension

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19
Q

Outline the timeline of raised ICP

A

Autoregulation of ICP fails -> raised ICP -> pathological intracranial HTN -> 20mmHg -> CPP must be 60mmHg to perfuse the brain (CPP = MAP - ICP)

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20
Q

What are some possible outcomes of raised ICP?

A

> brain herniation (pressure that moves brain tissues)
Diabetes insipidous (causes the body to make too much urine = polyuria)
syndrome of inappropriate secretion of antidiuretic hormone (SIADH) (This hormone helps the kidneys control the amount of water your body loses through the urine. SIADH causes the body to retain too much water)

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21
Q

DRSABCD of raised ICP

A

maintain airway, apply O2, avoid hypoxaemia (vasodilation = raised ICP), monitor fluid balance (avoid hypovalaemia), IVT fluids, AVOID HYPOTENSION, monitor BGLs (due to altered concious state)

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22
Q

best patient positioning for ICP

A

sedate (reduce metabolic demand), reduce environmental stressors, avoid neck tension, reduce coughing straining (raises ICP)

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23
Q

List treatments for raised ICP

A

treat cause if possible (eg. antibiotics for bacterial), lower compression (consider craniotomy if need to lower pressure urgent), ICP monitoring if available, Hypertonic solutions to lower brain volume (draw fluids out of body), loop diuretics for diuresis, dexamethasone to reduce brain fluid volume, barbituates to reduce metabolic demand, mechanical ventilation

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24
Q

Outline Meningitis

A

Protection for the central nervous system (CNS) is provided by the skull and vertebral column, the meninges and the blood brain barrier. Any breach can lead to infection
Meningitis is an acute inflammation of the meningeal tissues surrounding the brain and the spinal cord

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25
What are the two broad categories of CNS infections?
those primarily involving the meninges (protective brain membranes) (MENINGITIS) and those primarily confined to the brain parenchyma (brain tissues) (ENCEPHALITIS)
26
Outline Leptomeningitis
More common than meningitis and is defined as inflammation of the arachnoid tissue and subarachnoid space
27
What is the aetiology (causes) of CNS infections
>Bacterial, >Aseptic (Viral ->most common) Other causes> head injury (skull penetrating trauma), cancer, drug induced, other types of infection (fungal, parasite, ect)
28
Define viral meningitis
most commonly affects children and young adults. Clinical signs similar to bacterial meningitis but usually less severe with symptoms lasting 7-10 days Common causative agents include enteroviruses, present in the respiratory secretions, saliva, and faeces of an infected person. Causative agent often not identified
29
Define Bacterial meningitis
a neurological and infectious disease emergency. Mortality is estimated to be about 25% in adults and 61% of infants who survive have significant developmental issues. The bacteria responsible most commonly resides in the nose and throat, and are passed on through coughing and sneezing
30
Meningitis and reporting
Incidences of meningitis are reportable to the Department of Health and Australia's National Immunisation Program includes vaccines for pneumococcal disease and meningococcal disease
31
what are risk factors for bacterial meningitis?
head trauma with skull fracture, otitis media (ear infection), mastoiditis (ear infection -> bone infection), systemic sepsis and immunocompromise
32
What is the pathophysiology of bacterial/viral meningitis?
The pathophysiology of bacterial or viral meningitis begins when an infectious agent invades the central nervous system (CNS)
33
What are some common ways viruses/bacteria gain access to the CNS to cause meningitis?
>Haematogenous spread (via blood supply) the most common route (upper respiratory tract the most common source of entry) >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)
34
How does meningitis progress once the CNS is breached?
the virus/bacteria multiples due to a lack of immune response in the CNS, an inflammatory response is induced by the meninges, CSF and ventricles, cytokine is released and increases permeability, injuries occur to the endothelium of the blood brain barrier, leading to impairment
35
What injuries occur to the endothelium (lining) of the blood brain barrier when meningitis is contracted?
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
36
What happens once the blood brain barrier is damaged?
Raised ICP due to cerebral oedema (vasogenic), ischaemia due to impaired cerebral blood flow and cytotoxic damage to neurons and brain cells due to leukocyte (neutrophils) and bacteria invasion, and ischaemia. further inflammation continues
37
How does bacterial meningitis affect the whole body?
It can trigger a systemic inflammatory response; increased capillary permeability contributes to fluid shifts and hypovolaemia, as infection progresses and blood vessels damages can cause a characteristic petechial (spotty) rash
38
What is the major cause of raised ICP in bacterial meningitis?
Acute cerebral oedema, excess accumulation of fluid in the intracellular or extravascular spaces of the brain. It can be localised (focal) around the area of injury or diffuse as a result of hypoxia or hypotension. management is to reduce pressure on the brain and prevent secondary injury
39
How is acute cerebral oedema treated?
intravenous hypertonic solution (Mannitol/ Saline) which draws fluid from the cells into the circulating volume, causing diuresis Steroids can also be used, with more mixed success
40
What are the clinical manifestations of meningitis?
severe headache, nausea and vomiting, neck stiffness, fever can also include fever, chills, tachycardia, malaise, altered conscious state, rash
41
What are some acute complications of meningitis?
Associated with increased ICP as a result of cerebral oedema. This may manifest as altered mental status and seizures, and if left untreated can lead to permanent brain damage septic shock may also be present
42
Give an overview of viral meningitis
Usually children or young adults, slow onset (days), lasts 7-10 days, self-limiting common viral agents include enterovirus-coxsackievirus, Epstein-Barr virus
43
Give an overview of bacterial meningitis
Medical emergency, rapid onset (hours), slow recovery. death rate 5-10%. permanent disabilities can include cerebral palsy and deafness causative agents: pneumococcal, meningococcal, Hib)
44
How is meningitis diagnosed?
Lumbar puncture for CSF specimen >bacterial: cloudy, purulent, ICP, raised WBC, raised protein, low glucose >viral: raised lymphocytes, raised protein, normal glucose CT/neuroimaging, blood cultures, pathology
45
outline viral meningitis management
isolation not required symptom control: paracetamol for fever, headache, antiemetic AB until bacterial meningitis riled out antivirals steroids: dexamethasone if signs of raised ICP
46
Danger in terms of meningitis
Organism spread through close contact/ coughing/ sneezing, Droplet precautions x 24 hours Report incidence to Office of Health Protection (communicable diseases) Seizures: minimise injury deterioration of pt can be sudden
47
Outline disability management of meningitis
Monitor GCS Provide reassurance Pain management/ position Dark, quiet room Antiemetic Monitor BGL Anticonvulsants/ prevent injury Minimise interruptions/ group procedures prepare for lumbar puncture
48
Define a head injury
any alteration in mental or physical functioning related to a blow to the head. The most important consideration in any head injury is whether or not the brain is injured Can be classified as mild (GCS 13-15), to moderate (GCS 9-12) to severe (GCS 3-8) Can be diffuse (generalised) or focal (localised) and can be a primary or secondary injury
49
what is a primary brain injury
the damage that occurs to the brain, at the time of injury/ impact common mechanisms include direct impact, rapid acceleration/deceleration, penetrating injury and blast injury
50
What is a secondary brain injury
the damage that occurs to the brain as a result of the natural evolution of the primary injury examples include cerebral swelling, infection and raised intracranial pressure can occur as a result of HTN, cerebral oedema, hypoxia, fever, raised ICP, ect.
51
What is the primary goal of managing head injury?
Secondary injury can impair the brain's ability to autoregulate cerebral blood flow (and pressure), one of the primary goals therefore is to prevent secondary injury
52
Define an intracranial bleed
can result in serious brain injuries; intracranial pressure (ICP). When an intracranial bleed occurs normal brain metabolism is disrupted due to the brain being exposed to blood, an increased ICP or secondary ischaemia. Symptoms may be delayed until the bleed or haematoma is large enough to cause distortion
53
How are intracranial bleeds characterised?
Axial (within the brain tissue): Intracerebral haemorrhage (ICH) Extra-axial (within the cranium but outside brain tissue): Epidural haematoma (EDH), Subdural haematoma (SDH), Subarachnoid haemorrhage (SAH)
54
Define an Intracerebral Haemorrhage (ICH)
>can be spontaneous or the result of trauma >is 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) and the use of anticoagulant therapy
55
Define an Epidural Haematoma (EDH)
>results from bleeding that occurs, in the potential space, between the skull and the dura >is a high pressure, arterial bleed (most commonly the middle meningeal artery) >is a neurological emergency >is most commonly associated with a skull fracture classic presentation: loss of consciousness followed by a lucid interval and rapid deterioration (increased ICP)
56
Define a Subdural Haematoma (SDH)
>results from bleeding that occurs between the dura mater and the arachnoid mater >can be arterial but usually low pressure, venous bleed as a result of damage to bridging veins (that drain the brain parenchyma) >most commonly due to an acceleration--> deceleration action (fall, motor vehicle accident) >can be arbitrarily divided into three types: acute (< 2 days), subacute (3-14 days) and chronic (> 14 days). >elderly and heavy users of alcohol at risk due to cerebral atrophy (shrinking) and increased tension on bridging veins
57
Define a subarachnoid haemorrhage (SAH)
>is a bleed that occurs in the subarachnoid space (normally filled with CSF), between the arachnoid mater and pia mater >most commonly caused by a spontaneous rupture of a saccular (berry) aneurysm; intracranial arteries lack an external elastic lamina and have a very thin adventitia >rapid onset 'thunder clap' headache, neck stiffness (blood irritation of meninges) >has cerebral vasospasm as a serious complication (resulting in ischaemic stroke) >requires surgical intervention to 'clip' or 'coil' the aneurysm
58
What is an example of a mild head injury?
Concussion
59
What is an example of a moderate head injury?
Contusion
60
What are examples of severe head injuries?
Epidural haematoma Subdural haematoma Subarachnoid haemorrhage Intracerebral bleed
61
What are clinical manifestations of a concussion?
Altered conscious state (i.e dizziness, confusion, drowsiness), headache, vomiting, aggression, sensory disturbances changes to vital signs rare
62
What are clinical manifestations of contusion?
altered conscious state, nausea, vomiting, visual disturbances, speech difficulty, limb weakness
63
What are clinical manifestations of Epidural haematoma?
Loss of consciousness (LOC) -> consciousness -> LOC Severe headache, vomiting, drowsiness, confusion Hemiparesis Ipsilateral pupil dilation, Cushing reflex (↑ ICP)
64
What are clinical manifestations of a subdural haematoma?
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
65
What are clinical manifestations of a subarachnoid haemorrhage?
Severe headache ‘thunderclap’ Nausea & vomiting, brief LOC
66
What are clinical manifestations of an intracerebral haemorrhage?
Manifestations vary according to size & location Primary injury (expanding bleed ↑ ICP) Secondary injury (ischaemia)
67
Assessment and management of head injuries
observe for signs of LOC or airway obstruction, monitor for deterioration, observe for respiratory depression, observe for hypotension/HTN, pale and clammy skin, monitor for changes in cognition

NUR3310 (9 decks)

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