Neuro Flashcards
(128 cards)
1
Q
What is cerebral blood volume?
A
the amount of blood in the cranial vault (~10% of total intracranial volume)
2
Q
What is the Circle of Willis?
A
the series of interconnected vessels that ensure continual blood supply to the brain - collateral circulation. Fed via internal carotid arteries and vertebral arteries.
3
Q
What is the Monroe-Kellie Doctrine?
A
The sum of volumes of the brain tissue, CSF and intracranial blood volume is constant.
- if there is an increase in blood, there will be a decrease in CSF
- increase in brain mass = decrease in blood and/or CSF
- increase CSF = decreased blood
4
Q
What is intracranial pressure (ICP)?
A
- the combined pressure of brain tissue, blood and CSF within the cranial vault
- normally between 5 - 15mmHg
- measured by placing a catheter in the lateral ventricle
5
Q
What is the Cushing’s triad?
A
The three classic signs of increased intracranial pressure
- increased pulse pressure
- irregular breathing
- decreased pulse
6
Q
What is cerebral perfusion pressure (CPP)?
A
Blood pressure gradient across the brain
- determines if neurons receive blood or not
- CPP = MAP-ICP
- normal range = mmHg
7
Q
Cycle of ICP/CPP
A
insult contributes to increase ICP, decreases cerebral blood flow, decreases CPP, decreased blood flow to affected area of brain, causes ischaemia, leads to infarction of brain tissue, results in swelling, manifests in cerebral oedema, exacerbates/perpetuates the cycle
8
Q
types of brain herniation
A
- Cingulate Herniation – -cingulate gyrus compressed under falx cerebri
- Central Herniation – downward displacement of brain structures
- Uncal or Lateral Herniation – lateral mass displaces cerebral tissue centrally
- Infratentorial Herniation – increased pressure in infratentorial compartment. Herniation may be upwards or downwards
9
Q
Clinical management of increased ICP
A
- Mannitol
- CSF drainage
- respiratory support
- analgesics, sedatives, paralytics
- blood pressure management
- seizure prophylaxis
- hypothermia
- decompressive craniectomy
- positioning
- environmental considerations
10
Q
Define consciousness
A
a state of awareness of oneself and the environment and responding to that environment
11
Q
define arousal
A
individual’s state of awareness. impacted by the reticular activating system (RAS)
12
Q
define post coma unresponsiveness (previously known as persistent vegetative state)
A
complete lack of responses that suggest a cognitive component, preservation of sleep-wake cycles and cardiorespiratory function, partial or complete preservation of hypothalamic and brainstem autonomic functions.
13
Q
define locked in syndrome
A
syndrome indicative of damage to the brainstem without damage to the cerebrum. No abnormality in level of arousal or consciousness.
14
Q
Glasgow Coma Scale Eyes assessment readings
A
4- spontaneously
3- to speech
2- to pain
1- no response
15
Q
Glasgow Coma Scale best motor response assessment readings
A
6- obeys commands 5- localises pain 4- flexion withdrawal 3- abnormal flexion 2- abnormal extension 1- no response
16
Q
Glasgow Coma Scale best verbal response assessment readings
A
5- oriented 4- confused 3- inappropriate words 2- incomprehensible sounds 1- no response
17
Q
terms used to describe level of consciousness
A
- full consciousness (GCS 15)
- confusion (GCS 13-14)
- disorientation (GCS 13-14)
- drowsy (GCS 13-14)
- stupor (GCS 8-10)
- semicomatose (6 - 7)
- coma (GCS 4 - 6) - decorticate or decerebrate posturing
- deep coma (GCS 3)
18
Q
Altered breathing types
A
- Cheyne-Stokes breathing
- Central neurogenic hyperventilation
- apneustic breathing
- cluster breathing
- ataxic breathing
19
Q
diagnostic testing for altered cognitive function
A
- Blood Glucose
- Serum electrolytes
- Serum osmolality
- Arterial Blood Gas
- Liver Function Tests
- Toxicology screening
20
Q
Cranial nerves
A
Cerebral hemisphere - I olfactory - II optic Midbrain - III oculomotor - IV trochlear Pons - V trigeminal - Vi abducens - VII facial - VIII acoustic Medulla - IX glossopharyngeal - X vagus - XI hypglossal - XII spinal accessory
21
Q
types of seizures
A
- generalised tonic/clonic (Grand Mal)
- partial complex seizure
- absence seizures (petit mal)
- myoclonic seizure
22
Q
details of generalised tonic/clonic seizure
A
Characterised by an aura, sudden loss of consciousness and motor control
Tonic – spasm, increased muscle tone, stiffening
Clonic – muscular contractions, rapid synchronous jerking
23
Q
details of a partial complex seizure
A
Alterations in consciousness, unusual stereotyped movement, changes in temperament, confusions, feelings of unreality.
24
Q
details of an absence seizure (petit mal)
A
Temporary lapses of consciousness that last a few seconds
25
details of myoclonic seizures
Bilaterally symmetrical muscle jerks
26
what is the characteristics of the ideal antiepileptic (anticonvulsant)
- Highly effective but with a low incidence of toxicity
- Effective against more than one type of seizure and for mixed seizures
- Long acting and non-sedating
- Inexpensive
- Does not result in the development of tolerance
27
What are the main types of antiepilectic medications?
- Drugs that enhance GABA inhibition (eg Clonazepam, phenobarbitone, topiramate)
- Drugs that inhibit sodium channel function (eg. Phenytoin, carbamazepine, sodium valproate)
- Drugs inhibiting calcium channel function
28
drugs for treating generalised seizures
- Hydantoins (Phenytoin)
- Stabilises nerve membrane throughout CNS by influencing ionic channels in cell membrane, decreases excitability
- Decreasing conduction through nerve pathways it reduces tonic-clonic, muscular and emotional responses to stimulation
- Barbiturates (phenobarbitone)
- Inhibit impulse conduction in the ascending reticular activating system, depresses the cerebral cortex, alter cerebellar function and depress motor nerve output
- Reduce tonic-clonic, muscular and emotional responses to stimulation.
- Benzodiazepines (Clonazepam, diazepam)
29
Drugs for treating partial seizures
- Carbamazepine, Lamotrigine, Gabapentin and Topiramate
Directly – by altering sodium and calcium channels
Indirectly – by increasing activity of GABA and thereby decreasing excessive activity
Carbamazepine – ability to inhibit polysynaptic responses and to block sodium channels to prevent formation of repetitive action potentials
Gabapentin – inhibits polysynaptic responses and blocks stimulus increases in certain situations.
Lamotrigine – inhibit voltage sensitive sodium and calcium channels, stabilise nerve membranes and modulate release of excitatory neurotransmitters
30
Indications for phenytoin
Indications – control of tonic-clonic and psychomotor seizures, prevention of seizures during neurosurgery, control of status epilepticus
31
adverse effects of phenytoin
Adverse Effects – nystagmus, ataxia, dysarthria, slurred speech, mental confusion, dizziness, fatigue, tremor, headache, dermatitis, nausea, Stevens-Johnson syndrome, gingival hyperplasia, liver damage, haematopoietic complications, sometimes fatal.
32
Phenytoin routes, timings, metabolisation
Route – oral or IV
Onset of action – slow (oral), 1-2 hours (IV)
Duration of action – 6-12 hours (oral), 12-24 hours (IV)
Half Life – 6 to 24 hours
Metabolised in the liver, excreted in the urine
33
Indications for carbamazepine
Treatment of partial disorders, including partial seizures with complex patterns, tonic-clonic seizures, mixed seizures, trigeminal neuralgia
34
adverse effects of carbamazepine
drowsiness, ataxia, dizziness, N&V, CV complications, hepatitis, haematological disorders, Stevens-Johnson syndrome
35
carbamezapine route, timings and metabolisation
Route – Immediate release and slow release oral
Onset of Action – Slow
Half Life – 25-65 hours
Metabolised in the liver, excreted in the urine and faeces
36
Two main forms of stroke
- heamorrhagic
| - ischaemic
37
what is cerebrovascular disease (CVD)?
- CVD is a general term encompassing different conditions
- One condition can be a predisposing factor towards developing another condition underlying pathology:
- Atherosclerosis - Fat deposits on arterial walls narrow blood vessels reducing cerebral blood supply
- Cerebral Haemorrhage
- Subarachnoid
- Haemorrhage
- Vascular Lesions
- Weakening of Blood Vessels
- Aneurism
- Stroke
- Ischaemic
- Haemorrhagic
- Transient Ischaemic Attack (TIA)
38
What is a stroke
- Involves sudden interruption in the blood supply to the brain
- Brain cells die due to lack of oxygen following disruption of blood supply leading cause of morbidity and mortality.
- Australia's 3rd largest medical killer after cancer and heart disease colloquially used to be known as “brain attack”.
* Slurred speech
* Facial droop
* Arm drop/downward drift
39
Stroke outcomes are influenced by:
- Duration of ischaemia
- Magnitude of loss of flow
- Rapidity of development
- Collateral supply
40
Most common causes of stroke
1 - Thrombus formation in an area narrowed by vascular disease
2 - Embolus formation from the thrombus (or debris from the atheroma)
3 - A haemorrhage in the cerebrum (cerebral haemorrhage) as a result of both vascular disease and hypertension, or by a congenital aneurysm.
41
Definition of ischaemic stroke?
- sudden blockage or occlusion of cerebrovascular blood flow.
- Caused by thrombosis or emboli of large or small blood vessels of the brain
- Most common variety of stroke
- 3 major categories of ischaemic stroke
* thrombotic
* embolic
* thrombo-embolic
42
Definition of thrombus?
- aggregation of blood factors (clot or plaque) causing vascular occlusion.
- most common cause of Ischaemic stroke
- typically occurs when flow in a blood vessel in the brain is obstructed by atherosclerotic plaques
- usually occurs in:
* large vessels of the brain
* older people
- often associated with:
* atherosclerotic heart diseases or
* peripheral artery disease
- not associated with activity and can occur at rest
43
Definition of embolic ischaemic stroke?
- Cardiogenic embolic stroke
- Movement of the blood clot from the heart to the brain
- Blocks small blood vessels
- Usually originate from thrombus in the left heart
44
Definition of thrombo-embolic ischaemic stroke?
- Occurs following dislodgement of a clot from an atherosclerotic plaque in the carotid arteries
- Lodges in a downstream blood vessel & blocks blood flow
- Rx and prevention = Carotid endarterectomy, carotid stents
45
What is a carotid endarterectomy?
- Surgical excision of atheromatous segments of the endothelium and tunica media of the carotid artery.
- Results in smooth tissue lining and facilitating blood flow through the vessel reducing risk of stroke.
46
What is a transient ischaemic attack (TIA)?
- also termed “mini stroke”
- temporary disturbance in cerebral blood flow
- Focal or localised
- usually reverse before infarction occurs
- causes include:
* Atherosclerosis
* emboli
- may provide a warning of impending stroke.
47
Definition of a haemorrhagic stroke?
- Is the most frequently fatal stroke
- Rupture of blood vessel results in:
* Oedema
* Compression & increased ICP
* Spasms of adjacent blood vessels
* Leading to worsening oedema and possible eventual brain death
- Two major types:
1. Intracerebral haemorrhage
2. Subarachnoid haemorrhage
48
What is an intracerebral haemorrhage (ICH)?
- Occurs when a blood vessel bursts within the brain
- Sudden build-up in pressure causes damage to brain cells
- Usually large single bleeds and often catastrophic
- most common cause of spontaneous ICH is hypertension
* Results in micro-aneurysms at bifurcation of arterioles
* Persistently raised blood pressure damages small vessel walls
- Other Causes:
* Brain tumours
* Aneurysms
* AV Malformations
* Angiomas
* AV fistulae
49
What is a sub-arachnoid haemorrhage?
- Occurs when a blood vessel bursts immediately outside the brain
- Subarachnoid space suddenly fills with blood & pressure increases
- Symptoms include:
* Neck or sudden severe back pain
* Nausea
* Intense migraine-like headache
* Weakness
- Most common cause are cerebral aneurysms of arteries at the base of the brain.
- One-third of patients who suffer an SAH will survive with good recovery; one-third will survive with a disability; and one-third will die.
- Treatment focuses on stopping the bleeding, restoring normal blood flow, relieving the pressure on the brain, and preventing vasospasm.
* When RBCs breakdown and form a clot, they trigger the release of prostaglandins which result in vasospasm, leading to reduced arterial blood supply and ischaemia leading to secondary stroke!
* The greatest risk of vasospasm is 5-10 days after a bleed.
* Prevented with drug called nimodipine – given IV initially then orally.
50
What is an aneurysm?
- Focal dilation of arteries occurring in about 5% of people.
- r/t:
* Hypertension
* Arteriosclerosis
* Genetic factors i.e.:
+ Inherited connective tissue disorders
+ Autosomal dominant PCKD
+ Ehlers-Danlos syndrome
- Most occur along middle or anterior communicating arteries of the Circle of Willis.
51
What are arteriovenous malformations?
- Also known as AVMs
- Present as tangled, dilated blood vessels in which arteries flow directly into veins.
- AVMs occur most often at the junction of cerebral arteries:
* Fronto-parietal region
* Frontal lobe
* Lateral cerebellum
* Occipital lobe
* Within the dura
52
Risk factors associated with stroke
- high blood pressure
- smoking
- high blood cholesterol
- diabetes
- poor diet, inactivity, overweight
- excessive alcohol
- atrial fibrillation
53
Modifiable risk factors
- smoking
- obesity
- high risk diet (high in saturated fats, trans fats, caloric excess)
- substance abuse (marijuana, anabolic steroids, heroin, amphetamines, cocaine)
54
What is the FAST campaign?
Face (has their mouth drooped?)
Arms (can they lift both arms)
Speech (slurred? Can they understand you?)
Time (call 000 asap)
55
Manifestations of acute stroke
- Sudden weakness or paralysis of the face arm or leg usually on one side (unilateral) of the body (hemiplegia)
- Slurred speech
- Unilateral vision loss
- Sudden confusion
- Sudden trouble walking
- Sudden headache
56
Sequelae of stroke (pathological conditions resulting from a disease process)
- Depend on size & location of infarct
- Motor deficits
* Decreased or absent muscle tone
* Usually contralateral to the side of the brain affected
- Sensory deficits
* Usually in same location as motor paralysis
Communication deficits
* Aphasia- integrated speech & language disorder
* Follows damage to the (usually) left hemisphere
- Cognitive deficits
* Vary according to the area of brain affected
* Attention & reason deficits
57
Communication deficits that may arise from stroke?
- Aphasia – the inability to use of understand language
* Expressive – once can understand what is being said but cannot respond verbally
* Receptive - Once cannot understand the spoken work however speech may be fluent
* Mixed or Global – dysfunction in both understanding and expression
- Dysarthria – any disturbance in muscular control of speech
58
How stroke is diagnosed
- Medical history
* Focal symptoms
* Previous TIA’s
* Co-existing disease
- Common diagnostic methods
* Imaging of the brain (CT scan, MRI)
* Imaging of blood vessels (cerebral angiogram)
* Heart function (ECG)
* Nerve function (brain waves, nerve conduction)
* Blood tests (cell count, blood clotting, glucose, cholesterol
59
What is a stroke clinical pathway?
- “Code STROKE” called by ambulance or emergency department activates pathway in hospital.
- Treatment varies depending upon ischaemic or haemorrhagic
* Needs neuroimaging
+ If bleeding, contact neurosurgeon and/or interventional neuroradiologist [aneurysm]
* If ischaemic, follow stroke care pathway
+ More imaging - Carotid Doppler to determine carotid arterial blood flow
+ May necessitate carotid endarterectomy once stabilised.
60
Immediate teatment of ischaemic stroke
Essential to know it is an ischaemic stroke, as if haemorrhagic, these treatments could kill the patient
- Treatment aim is to minimise infarct size & preserve neurological function
- Medications (*** Ischaemic stroke only***)
* Antiplatelets (aspirin)- immediate response
* Thrombolytic agents
+ Streptokinase, urokinase
+ Tissue plasminogen activator (TPA)
* Anticoagulants (heparin, warfarin)
* Do not use in conjunction with thrombolytic (high bleed risk)
61
Post-stroke treatment
- Prevention of cerebral hypoxia
- Maintain blood pressure & prevent obstruction
- Identify & remove sources of emboli
- Improve left ventricle function
- Anti-thrombotics/antiplatelets – aspirin, clopidogrel
- Serum lipid lowering agents – satins
- Anti-hypertensives - betablockers
- Anti-arrthymics – digoxin, amiodarone
- risk reduction
* Smoking, diet, lifestyle factors….
* Serum lipids
62
Treatment of haemorrhagic stroke
- Treatment aim is to reduce blood pressure without inducing ischaemia.
- “HHH therapy” - Hypervolaemia, hypertension [mild ~130mmHg], and haemodilution
- Surgical evacuation of the clot (Craniotomy)
- Evacuation of bleeding if in ventricles, evacuation of excess CSF to reduce ICP (EVD – external ventricular drain)
- Maintain ICP <15mmHg
* Invasive – Codman catheter, EVD [attached to manometry]
* Risk of increased ICP following haemorrhagic stroke
* 2* - blood and/or oedema
* Elevated ICP results in worsening brain injury
63
Drugs that effect thrombosis and haemostasis
- anticoagulants - inhibit specific clotting factors
- antiplatelets - inhibit platelet action
- thrombolytics - clot dissolving
- haemostatics - inhibit fibrin destruction
- clotting factor concentrates - missing clotting factors
64
What is a thrombus
an aggregation of platelets, fibrin, clotting factors and the cellular elements of blood
65
What is an embolus?
mass of undissolved matter that breaks off from the thrombus, can travel in the vascular system and lodge in a vital area (lungs, brain, heart, deep vein)
66
What is coagulation?
the process of blood’s changing from a fluid state to a solid state to plug injuries to the vascular system
67
What is haemostasis?
arrests bleeding from an injured site and maintains blood in a fluid state in normal vessel
68
What is arterial thrombus?
```
- Adherence of platelets
to arterial walls
- White in color
- Often associated with
MI, stroke and ischemia
```
69
What is venous thrombosis?
```
- Develops in areas of
stagnated blood flow
(deep vein thrombosis),
- Red in color
- Associated
with Congestive Heart
Failure, Cancer, Surgery
```
70
Clotting factors
```
I - fibrinogen
II - prothrombin
III - tissue factor
IV - Ca2+
VI - proaccelerin
VII - proconvertin
VIII - antihemophilic factor
IX - christmas factor
X - stuart factor
XI - plasma thromboplastin antecedent
XII - hageman factor
XIII - fibrin stabilising factor
```
71
What is platelet aggregation?
- Platelet adhesion is mediated by von Willibrands Factor.
- During activation, a receptor for fibrinogen becomes exposed on the platelet membrane.
- Activated platelets release:
* Fibrinogen
* ADP/ATP
* vWF
* Seretonin
* Factor V
* Ca2+
* Factor VIII
* Platelet derived growth factor (PDGF) ~ promotes healing
* Platelet factor IV – prevents formation of active thrombin
* inhibitor from heparin and anti-thrombin III.
72
Groups of anticoagulants
- heparin
- low molecular weight heparin - enoxaparin
- warfarin
73
What is heparin
- Block formation of thrombin from prothrombin and fibrinogen to fibrin
- Heparin not available orally therefore not drug of choice for outpatients – only IV or SC
- Indications
* Acute treatment and prevention of venous thrombosis and pulmonary embolism
* Treatment of atrial fibrillation with embolisation
* Prevention of clotting in blood samples and in dialysis and venous tubing
* Diagnosis and treatment of disseminated intravascular coagulation
74
Pharmacokinetics of heparin
- Onset of action – Immediate (IV), 20-60mins (SC)
- Peak – Minutes (IV), 2-4 hours (SC)
- Duration – 26 hours (IV), 8-12 hours (SC)
- Half Life – 30-180 minutes
- Metabolised in cells and excreted in urine
- Adverse Effects – loss of hair, bruising, chills, fever, osteoporosis, suppression of renal function (with long term use)
75
What is heparin induced thrombocytopaenia (HIT)?
- More severe symptoms occur 5-10 days into therapy
- Causes an increase in adverse thrombotic events
* Increases platelet aggregation
* Patient may experience life threatening thrombosis
- Can take up to a week after discontinuation for platelets to recover.
76
What is enoxaparin (low molecular weight heparin)?
- Indications
* After Surgery – hip replacement
* Prolonged bed rest
- Considered safer and required less monitoring
* Less systemic side effects
- Contraindicated in renal impairment
* Increase bleeding time due to renal excretion
* Predictable clearance and increased bioavailability
* Longer half life and duration of action
77
What is protamine (heparin antagonist)?
- antidote for abnormal bleeding from heparin
- Very weak anticoagulant when used alone
- Protamine sulfate given in conjunction with heparin a complex is formed - reduces anticoagulant effect of heparin
- Indicated for overdose of heparin of LMWH
- Administered IV, onset of action 1 minutes and duration of action is 2 hours.
78
What is warfarin?
- Currently only oral anticoagulant on the market in Australia
- Decrease in the production of vitamin K – dependent clotting factors in the liver
- Depletion of these factors which leads to prolonged clotting time
- Indications
* Treatment of AF,
* Patients with artificial heart valves or valvular damage that makes them susceptible to thrombus and emboli formation
* Prevention and treatment of venous thrombosis, pulmonary embolism, embolus with atrial fibrillation
* Systemic emboli after myocardial infarction
79
What is the pharmacokinetics of warfarin?
- Onset of action -3 days
- Duration of Effects – 4-5 days
- Readily absorbed through GI tract, metabolised in the liver and excreted in the urine and faeces
- Contraindicated in pregnancy – foetal injuries and deaths have occurred.
80
What is Vitamin K as a warfarin antagonist?
- Vitamin K essential to hepatic synthesis of prothrombin
- Antidote for excessive coagulation with warfarin when withholding warfarin is not enough.
- Onset of action – 6-12 hours (orally), 1-2 hours (IV)
- Metabolised in the liver, excreted via kidneys and in the bile.
81
what are the 4 clotting studies?
1 - aPTT –Activated partial thromboplastin time
* Activity of the intrinsic pathway of coagulation
* Therapeutic range – 1.5-2.5 times baseline
* Dose adjustment of heparin and low molecular weight heparin
2 - PTT – partial thromboplastin time
3 - INR – International normalised ratio
* Standardised measure of prothrombin levels
* Therapeutic range – 2-3.5
* Warfarin dose adjustment
4 - PT – Prothrombin time
* Time required for clotting to occur, extrinsic pathway activity
* Therapeutic range – 1.3-1.5
* Warfarin dose adjustment
82
What are the nursing care considerations for anticoagulation administration?
- Evaluate patient regularly for any signs of blood loss (petechiae, bleeding gums, bruises, dark coloured stools, dark coloured urine) – evaluate effectiveness of drug dose and possible need for titration
- Educate on safety precautions- need to use an electric razor or avoid contact sports
- Mark medication chart – to ensure all staff are aware of potential for increased bleeding
- Avoid intramuscular injections – may causes serious bruising, bleeding or haematoma.
- Maintain antidotes nearby – to ensure ready access if need arises
- Ensure appropriate patient education – including warning signs of medication, need for periodic monitoring and evaluation, need to wear a medic-alert bracelet, ensure knowledge about drug regimen.
83
What are ADP receptor blockers?
- ADP released from platelets following vessel injury (Promote platelet aggregation)
- ADP receptor blockers irreversibly alter plasma membrane of platelets
- Increase the risk of bleeding should the patient experience trauma of require dental or surgical procedures.
84
What is clopidogrel
- antiplatelet medication
- Indications
* Prevention of arterial thromboembolism to reduce the chance of MI or stroke
* Prevent thrombi formation in patients with unstable angina or coronary artery stents
* Prevent post operative DVT
- Dosage – Oral, once daily
- Onset of Action – 1-2 hours
- Duration of Action - 5 days
- Adverse Effects – Excessive Bleeding, flulike syndrome, headache, diarrhoea, dizziness, bruising, URTI, rash
85
What are the types of antiplatelet medications?
- ADP receptor-blockers
| * clopidogrel
86
Mechanism of action of thrombolytics
- Alter haemostatic capability more profoundly than anticoagulants
- When bleeding occurs it is more profound and harder to control
- eg. Alteplase, streptokinase, urokinase
- Convert plasminogen in the blood to plasmin
- Plasmin – fibrinolytic enzyme that digests or dissolves fibrin clots where they exist and can be reached.
87
indications for thrombolytics
- St segment elevation myocardial infarction (STEMI)
- Pulmonary embolism
- Acute ischaemic stroke
- Peripheral arterial embolisation
- Thrombosed cannula (IV cannula, CVC, haemodialysis shunts)
88
Pharmacokinetics of thrombolytics
- Administered IV
- Half Life – Alteplase (35 mins), streptokinase (23 mins)
- Peak effect – 20mins and 2 hours
- Duration of action – 4 hours
- Adverse Reactions – Bleeding, including ICH
89
absolute contraindications of thrombolytics
- Active internal bleeding
- Recent major trauma or surgery
- Recent CVA
- Bleeding disorder
- Haemorrhagic retinopathy
- Intracranial neoplasm or prior intracranial haemorrhage
- Bacterial endocarditis or pericarditis
- Uncontrolled hypertension.
90
Nursing care considerations of thrombolytics administration
- Must be administered as soon as possible following acute MI to reduce mortality – resolve the clot before permanent damage to myocardial cells
- Evaluate for signs of blood loss
- Regularly monitor coagulation studies
- Arrange to type and cross match blood – in case of excessive bleeding.
- Mark medication chart and medical notes
- Provide increased precautions against bleeding during invasive procedures – may need pressure dressing, avoid IM injection, do not rub SC injection sites.
91
What is an acquired brain injury (ABI)?
Brain Injury is the “multiple disabilities arising from damage to the brain acquired after birth. It results in deterioration in cognitive, physical, emotional or independent functioning. It can be as a result of accidents, stroke, brain tumours, infection, poisoning, lack of oxygen, degenerative neurological disease etc.”
92
Main causes of ABI
- Accidents/Trauma
- Stroke
- Tumour
- Infection
- Poisoning/Toxins (including excessive alcohol)
- Hypoxia/anoxia
- Degenerative neurological diseases
93
What is a traumatic brain injury?
Penetrating (Open) or Closed Head Injury
Specific damage following injury is related to a combination of factors
- Mechanism of Injury
- Nature of the Injury
- Location of Injury
94
Pathophysiology of TBI
```
brain suffers traumatic injury
↓
brain swelling or bleeding increases intracranial volume
↓
intracranial pressure increases
↓
blood flow to brain slows down due to increased pressure on vessels
↓
cerebral hypoxia and ischaemia occur
↓
ICP continues to rise. Brain may herniate
↓
cerebral blood flow ceases
```
95
types of TBI injuries
- Acceleration Injury – head struck by a moving object
- Deceleration Injury – head hits a stationary object
- Acceleration-Deceleration Injury (Coup-Contrecoup) head hits and object and brain rebounds within the skull
- Deformation Injury – interruption to integrity of body part (ie skull fracture)
96
types of haematomas (blood pooling in the intracranial space)
- Epidural Haematoma (between the dura and the skull)
- Subdural Haematoma (between the dura mater and the pia mater)
* Acute or
* Chronic
- Intracerebral Haematoma (any location within the brain tissue)
97
Clinical manifestations of epidural haematoma
- Loss of consciousness on injury (may return to normal cognitive function for a few minutes or days)
- As haematoma accumulates (increase in size) – headache, vomiting, drowsiness, confusion, seizure and hemiparesis
- This is a medical emergency
98
Clinical manifestations of acute subdural haematoma
- Initially – headache, drowsiness, restlessness or agitation, slowed cognition and confusion
- Progress to unconsciousness, respiratory pattern changes and pupillary dilation
99
Clinical manifestations of chronic subdural haematoma
- Chronic headaches
- Tenderness over the haematoma
- Progressive dementia with paratonia (involuntary resistance during passive movement)
100
Clinical manifestations of intracerebral haematoma
- Decreasing consciousness and GCS
- Contralateral hemiplegia may occur
- Delayed ICH
* sudden rapid decrease in level of consciousness with pupillary dilation
* Breathing pattern changes
* Hemiplegia
* Positive Babinski reflex
101
Clinical manifestations of intraventricular haematoma
- Altered level of consciousness
- Hemiparesis
- Ipsilateral pupil dilation (on same side as haematoma)
- Intracranial hypertension
102
Grades of concussion
- mild (temporary axonal disturbance, no loss of consciousness)
- grade I (confusion and disorientation with momentary amnesia)
- grade II (momentary confusion and retrograde amnesia up to 5-10 minutes)
- grade III (confusion and retrograde amnesia from impact, also anterograde amnesia
- grade IV, aka classic cerebral concussion (immediate loss of consciousness lasting less than 6 hours, retrograde and anterograde amnesia)
103
Indicators of concussion
- Observed and documented disorientation or confusion immediately
after the event
- Impaired balance within 1 day after injury,
- Slower reaction time within 2 days after injury, and/or
- Impaired verbal learning and memory within 2 days after injury.
104
Nursing assessment of TBI
Be alert for the following signs and symptoms of possible TBI (or a worsening of an already diagnosed injury):
- Altered level of consciousness
- Confusion
- Pupillary abnormalities
- Alteration or absence of gag reflex
- Absent corneal reflex
- Sudden onset of neurological deficits
- Changes in vital signs
- Vision and hearing impairment
- Sensory dysfunction
- Spasticity
- Headache
- Vertigo
- Seizures
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Spinal vertebrae
```
cervical C1 - C8
thoracic T1 - T12
lumbar L1 - L5
sacral S1 - S5
coccyx
```
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main causes of spinal cord injury
- Traumatic
- Non- Traumatic
* Degenerative
* Infectious
* Oncogenic
* Vascular
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Mechanisms of injury for traumatic spinal injury
- Flexion
- Extension
- Compression
- Penetration
- Rotation
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types of spinal cord injury
- Cord Concussion – temporary disruption of cord-mediated function
- Cord Contusion – bruising of neural tissue causing swelling, temporary loss of function
- Cord Compression – pressure on the cord causing ischaemia to tissue, must be relieved to prevent permanent damage
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Incomplete vs complete spinal cord injury?
Incomplete
- Some tracts remain intact together with functions mediated by those tracts
- Potential for recovery although function is temporarily lost
Complete
- All tracts are completely disrupted
- All cord-mediated function below transection are completely and permanently lost
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levels of spinal cord injury
- tetraplegia/quadriplegia (injury to the cervical spine. arms and legs non-function)
- paraplegia (damage to thoracic or lumbar. legs non-functional)
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Anterior cord syndrome
- Cause – acute disc herniation, hyperflexion injuries, injury to anterior spinal artery
- Characteristics – loss of pain, temperature and motor function below level of injury. Light touch, position and vibration sensation remain intact
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central cord syndrome
- Cause – injury or oedema to the central cord, usually cervical area
- Characteristics – motor deficits (upper extremities compared to lower), sensory loss varies but usually more pronounced in upper extremities, bowel/bladder function variable although may remain intact.
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Brown-Sequard Syndrome
- Lateral Cord Syndrome
- Cause – transverse hemisection of the cord, fracture-dislocation of a unilateral articular process or acute ruptured disc
- Characteristics – ipsilateral paralysis together with loss of touch, pressure or vibration. Contralateral loss of pain and temperature
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diagnostic tests for spinal cord injury
- Physical examination
- CT
- MRI
- Myelography
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emergency management for spinal cord injury
- DR ABC (Primary Survey)
- Immediate immobilisation of the spine to limit further trauma
- Decompression and surgical fixation may be necessary
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effect of spinal cord injury above C3
- diaphragm paralysed
- accessory muscles may be weakened or paralysed
- intercostal and abdominal muscles paralysed
- loss of inspiratory and expiratory capacity
- no cough effort
- mechanical ventilation required
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effect of spinal cord injury between C3 and C5
- diaphragm may be weakened and/or paralysed
- intercostal and abdominal muscles paralysed
- decreased tidal volume and vital capacity
- limited inspiratory and expiratory capacity
- ineffective cough
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effect of spinal cord injury between C5 and C8
- diaphragmatic function intact
- intercostal and abdominal muscles paralysed
- decreased total lung function
- ineffective cough
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effect of spinal cord injury between T1 and T6
- weakened and/or paralysed intercostals
- paralysis of abdominal muscles
- limted expiratory capacity
- weak cough
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effect of spinal cord injury between T7 and T12
- abdominal muscles weakened and/or paralysed
- reduced expiratory effort
- variable cough effort
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what is spinal shock?
- Occurs when normal activity of spinal cord cells cease below the level of injury
- Reflex function is completely lost in all segments below the injury
- Severe impairment is obvious and includes muscle paralysis and loss of sensation
- Generally lasts days to months
- Terminates with the reappearance of reflex activity
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what is autonomic dysreflexia?
- Massive cardiovascular response to stimulation of the sympathetic nervous system
- Life-threatening and requires immediate treatment
- Characterised by – hypertension, pounding headache, blurred vision, sweating and flushed skin above level of lesion, nasal congestion, nausea and piloerection and bradycardia
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Normal response pathway
1 - stimulus occurs, sensory nerve reacts
2 - spinothalamic tracts carry impulse to the brain
3 - brain interprets sensory input, course of action determined
4 - corticospinal tracts carry motor impulses to appropriate muscle
-5 - motor output, eliminates stimulus to sensory nerve
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autonomic hyperreflexia pathway
1 - stimulus occurs, sensory nerve reacts
2 - spinothalamic tracts carry sensory impulses to level of lesion
3 - reflex stimulus to major sympathetic outflow resulting in vasospasm, hypertension skin pallor, pilomotor spasms
4 - increased blood pressure stimulates carotid sinus receptors
5- 9th cranial nerve stimulated by carotic receptors send message to vasomotor centre of medulla, vagus nerve stimulated, impulse sent to SA node, results in bradycardia
6 - automatic response to hypertension down to level of cord injury. Arterial dilation, flushed skin, headache, sweating.
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Clinical manifestations of Alzheimers
- Progressively forgetful over time
- Increasing disorientation, confusion
- Difficulty concentrating
- Deterioration in abstraction, problem solving and judgement
- Behavioural changes – irritability, agitation, restlessness
- Mood changes – anxiety, depression, hostility, mood swings
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What is sundowning?
- Increased agitation, time disorientation and wandering behaviour
- Prevalent in afternoon and evening hours
- Also acceleration on overcast days
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Diagnosing Alzheimers
- History and course of illness
- Mental Status examination
- Brain imaging
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Treatment for Alzheimers
- Memory aids
- Maintaining unimpaired cognitive functioning
- Ensuring appropriate assistance with ADLs
- Medication – increase concentration of acetylcholine
