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VTS(ECC) Preparation > Neurologic emergencies > Flashcards

Neurologic emergencies Flashcards

1
Q

Cheyne-stokes breathing

A

Periods of hyperpnoea followed by brief periods of apnoea

Diffuse cerebral or thalmic disease and metabolic encephalopathies

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2
Q

Central neurogenic hyperventilation

A

Persistant hyperventilation that can induce respiratory alkalosis

Midbrain lesions

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3
Q

Apneusis

A

Pauses in breathing at full inspiration

Pontine lesions

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4
Q

Irregular/ataxic breathing

A

Irregular frequency & depth of respiration before complete apnoea

Lower pons & medulla

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5
Q

Unilateral mydriatic, unresponsive pupil

A

Loss of parasympathetic innervation to the eye indicating destruction or compression of ipsilateral midbrain for CNIII.

Increased ICP, cerebral herniation

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6
Q

Bilateral miosis

A

Metabolic encephalopathies, diffuse midbrain compression with increased ICP

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7
Q

Bilateral, mydriatic, unresponsive pupils

A

Severe, bilateral compression or destruction of midbrain or CNIII

Bilateral cerebral herniation
Grave prognosis

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8
Q

In patients with traumatic brain injury, it is important to maintain a normal MAP and to closely monitor the patient’s:
a. electrocardiogram
b. ventilation
c. range of motion
d. potassium

A

B

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9
Q

Which of the following can occur after blood flow is suddenly restored after using a clot dissolution drug?
a. Hyperkalemia
b. Azotemia
c. Hypotension
d. Respiratory alkalosis

A

A

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10
Q

Patients suffering from upper motor neuron injury can also suffer dysfunction of:
a. the urinary bladder
b. the gastrointestinal system
c. the cardiac system
d. the brain

A

A

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11
Q

Which nerve fibers are responsible for sensing temperature:
a. Autonomic afferent
b. Somatic afferent
c. Autonomic efferent
d. Somatic efferent

A

B

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12
Q

A patient that responds only to noxious stimulation is:
a. comatose
b. stuporous
c. obtunded
d. lethargic

A

B

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13
Q

A clinical factor that can increase intracranial pressure is:
a. decreased PaCO2
b. hypothermia
c. increased PaO2
d. coughing

A

D

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14
Q

Cerebral blood flow is equal to which of the following?
a. CPP/CVR
b. CVR/CPP
c. MAP–ICP
d. ICP–MAP

A

A

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15
Q

Cushing’s reflex is defined as:
a. hypertension and bradycardia
b. hypotension and tachycardia
c. absent PLR and decreased level of consciousness
d. present PLR and decreased level of consciousness

A

A

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16
Q

Which toxin should be considered if a patient presents for tremor/seizure activity?
a. Ibuprofen
b. Grapes
c. Metaldehyde
d. Garlic

A

C

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17
Q

Which drug class is considered the first line of treatment in non-hypoglycemic seizures?
a. NMDA antagonists
b. Benzodiazepines
c. Phenothiazines
d. Alpha-2 agonists

A

B

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18
Q

Which drug class is considered the first line of treatment in non-hypoglycemic seizures?
a. NMDA antagonists
b. Benzodiazepines
c. Phenothiazines
d. Alpha-2 agonists

A

B

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19
Q

Serotonin

A

Serotonin actions (enterochromaffin): platelet aggregation, vasoconstriction, uterine contraction, peristalsis and bronchoconstriction. Either excreted by lungs or transported to platelets
Central serotonin: influences mood, aggression, sleep, thermoregulatiom, vomiting and pain perception.

Serotonin is formed by AA tryptophan, synthesised and stored in enterochromaffin cells and myenteric plexus in the GI tract

Synthesised in neuronal cytosol, stored in vesicles at nerve terminals and released into the synaptic cleft where it binds to post-synaptic receptor mediating transmission. It is inactivated by MAOI to form 5-HT and then eliminated by urine

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20
Q

Obtund

A

Decreased response to external stimuli

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21
Q

Stupor

A

Response only to noxious stimuli

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22
Q

Coma

A

No conscious response to stimuli.
+- cranial nerve reflexes

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23
Q

Cerebrum

A

Integrates information and planning of motor activity, specific response to information input and responsible for emotion & memory

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24
Q

Reticular activating system

A

Activates the cerebral cortex and maintains consciousness

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25
Seizures indicate
Cerebral cortisol dysfunction and may be due to an extracranial or intracranial process.
26
Decerebrate activity
Opisthotonos and extensor rigidity of all four limbs; associated with stupor or coma. Indicates lesion of rostral pons and midbrain.
27
Decerebellate rigidity
Associated with acute cerebellar lesions. Opisthotonus and extensor of thoracic limbs and +- hind limbs; patient generally responsive.
28
Basic neurological evaluation
1. LOC 2. Motor activity 3. Pupil size & reactivity 4. Respiratory patterns 5. Oculocephalic reflexes * form basis for coma scales
29
Pupil size
Balance between sympathetic and parasympathetic innervation. Loss of parasympathetic innervation indicates deteriorating patient status and is identified by unilateral or bilateral mydriasis
30
Causes of pupil size changes
#1 structural lesions Other: metabolic and some drugs
31
Loss of oculocephalic reflexes
Generally associated with lesions of medial longitudinal fasciculus (pons & midbrain) which normally coordinates CN 3, 4, 6 and usually indicates poor prognosis.
32
Increase in ICP
CSF and blood compartment must reduce to compensate > reduced cerebral blood flow to prevent further increases in ICP
33
MGCS
Facilitates assessment of prognosis Assesses motor function, LOC and brainstem reflexes and scores /18 (18 normal) Doesn’t predict long-term functional outcome
34
Initially miotic pupils that become mydriatic
Indicate progressive brainstem lesion
35
PLR
Assess the optic nerve function Changes can be unilateral or bilateral
36
Fixed dilated pupils (mydriasis)
May indicate irreversible midbrain lesion or advanced herniation
37
Miosis
May still indicate adequate function of rostral brainstem, optic chiasm, optic nerve and retina
38
Seizures
Clinical manifestation of paroxysmal cerebral disorder cause by synchronous, excessive electrical neuronal discharge which comes from the cerebral cortex. They may be partial/localised or complex/generalised.
39
Types of epilepsy
Idiopathic Symptomatic Cryptogenic
40
What is termed cluster seizures
2 or more seizures within a 24h period
41
Status epilepticus
Abnormal brain homeostasis mechanisms that usually prevent seizures. Can be due to neuronal excitation, inadequate neuronal inhibition and excess neurotransmitters leading to ATP depletion and build up of lactate ultimately leading to neuronal necrosis.
42
Minimum database for seizure disorders
CBC Biochemistry 24h fasted glucose Bile acids Urinalysis +- Advanced imaging (EEG, MRI, CT)
43
Benzodiazepines for seizures
Diazepam or midazolam; 0.5-1mg/kg and 0.2mg/kg respectively Bind to GABA receptors and hyperpolarise neurons to decrease neuronal firing. Diazepam fat soluble whereas midazolam water soluble
44
Barbiturates for seizure disorders
Provided if SE non-responsive to benzodiazepines or for control of long term seizure disorders Phenobarbital and levetiracteam most common Pheno may cause sedation, respiratory depression, hypotension and death
45
Refractory seizures
Propofol and light anaesthesia/deep sedation Propofol is a GABA agonist
46
Long term anticonvulsant therapy
Phenobarbital + bromide +- levetiracetam
47
Spinal cord ischaemia
Decreased blood flow and/or loss of autoregulation, vasospasm and haemorrhage > ischaemia… cytosine oedema, axonal degeneration, demyelination, abnormal impulse transmission, conduction block and cellular death.
48
Neurological scoring
Grade 1 = no deficits Grade 2 = paresis, walking Grade 3 = paresis, non-ambulatory Grade 4 = paralysis Grade 5 = paralysis, no deep pain
49
UMN signs
In the CNS (brain, spinal cord) - hyperreflexia - increased muscle tone/spasticity - spastic paralysis
50
LMN signs
Anterior horn to the muscle - atrophy - paresis/paralysis - hyporeflexia - decreased muscle tone - flaccidity
51
S1 to S3 spinal lesion
LMN signs Sciatic, pudendal, perineal nerves involved Flaccidity, decreased segmental reflexes Urinary and faecal incontinence Pelvic limb paresis without completely absent withdrawal
52
L4 to S1 spinal lesion
Femoral, sciatic, pupendal, obturator & pelvic nerves involved Pelvic limb, tail & anus dysfunction. Normal thoracic function. Short-strided gait and shuffling paws Plato grade or weak stance Diminished or absent pelvic reactions
53
T3 to L3 spinal lesion
UMN signs caudal to the lesion Paresis/paralysis/spasticity Exaggerated reflexes, cross-extensor Limited to the pelvic limbs Urinary retention and faecal incontinence Abnormal cutaneous trunchi reflex approx. L3 Schiff-Sherrington phenomenon
54
C6 to T2 spinal lesion
UMN signs to the pelvic limbs and LMN to the thoracic limbs Subscapular, suprascapula, musculocutaneous, axillary, radial, median and ulna nerves Neuropathic lameness Absent cutaneous trunchi reflex Decreased thoracic movement
55
C1 to C5 spinal lesion
UMN in all limbs and respiration may be shallow or absent due to loss of phrenic and intercostal nerve function
56
Treatment for spinal cord injury
1. IVFT to support spinal cord vasculature and optimise arterial blood flow 2. Stabilise F# and keep patient immobile where indicated 3. Refer to surgeon and have surgery performed if indicated 4. General supportive care measures I.e. pain relief, antispasmodics, nutrition, comfort, wounds etc
57
ICH
Intracranial hypertension When the ICP increases above its range of 5-12mmHg resulting in neurological abnormalities
58
CSF
Ultrafiltration of fluid from the blood volume of choroid plexus
59
BBB
Tightly regulates solutes entering the brain but is permeable to water
60
Cerebral perfusion pressure
CPP = MAP - ICP
61
An increase in cerebral blood flow due to dilation
Increases cerebral blood volume leading to increased ICP
62
A decrease in cerebral blood flow due to constriction
Leads to decreased cerebral blood volume and reduced ICP
63
3 homeostatic mechanisms to maintain normal ICP
1. Volume buffering; intracranial volume fixed so increases in one compartment means a compensatory fall in others 2. Autoregulation; arteriole resistance changes and operates between 50-150mmHg 3. Cushing response; bradycardia and severe hypertension, as well as mentation abnormalities
64
Neurological exam
1. LOC 2. Brainstem reflexes 3. Motor function 4. Respiration
65
Treatment of ICH
HTS/Mannitol Furosemide Head elevation 30 degrees Avoid jugular compression Oxygen therapy IVFT Prevent hypotension & hypoxia Manage neurological and inflammatory signs Other supportive therapies
66
Mannitol
Immediately induces plasma volume expansion and increases CBF resulting in better delivery of oxygen to the brain due to osmotic shifts (takes 15-30 min). Recommended 0.5-1g/kg of 20% over 20min and lasts 1-3 hours
67
HTS 7%
Similar effects as mannitol but less likely to induce hypotension and also has benefits on the excitatory neurotransmitters and the immune system 4ml/kg over 10min
68
Minimum database for patients suspected to motor unit disease
CBC & Biochemistry T4 Cortisol/ACTH stim Glucose Urinalysis, C&S CK Tox screening Advanced imaging
69
Neurapraxia
Loss of nerve conduction without structural changes (transient loss of blood supply)
70
Axonotmesis
Axonal damage without loss of supporting structures (axonal regeneration required)
71
Neurotmesis
Complete severance of a nerve
72
Tetanus
Caused by bacterium clostridium tetani (G+ anaerobe, spore-forming, motile, non-encapsulated) that releases neurotoxins tetanospasm & tetanolysin during its vegetative stage which inhibits motor neurons, affects inhibitory control (GABA) and dyregulates autonomacity. Neuronal binding leads to sympathetic over-reactivity and once bound to neurons cannot be reversed and new terminals must be created (prolonged recovery).
73
Tetanus signs
Sardonic grin Localised signs proximal to entry site Muscle rigidity and spasms, increased muscle tone Trismus Dyspnoea Stiff gait Opisthotonus Seizures Respiratory paralysis Dysphagia Autonomic dysregulation (HR, BP, temp)
74
Treatment of tetanus
Neutralise unbound toxin (100-1000U/kg max 20000U) Remove source of infection Control rigidity & spasms Aggressive supportive care I.e. nutrition, comfort etc
75
Dysfunction to vestibular system
Disequilibrium and clinical signs usually point to side of brain affected
76
Horners
1. Miosis 2. Enopthalmos 3. Ptosis 4. Protrusion of the third eyelid
77
HE
Hepatic encephalopathy Accumulation of ammonia in systemic circulation due to severe liver insufficiency such as PSS. The accumulation of ammonia passes the BBB decreasing excitory neuro transmission by downregulatimg NMDA receptors and chloride extrusion from post-synaptic neurons. Induces seizures and neurotoxicity
78
Treatment of HE
IVFT Attenuation of PSS if present Reduce ICP Seizure control Colloids Glucose Electrolyte supplementation Broad spectrum AB Lactulose/enemas Low protein (14-17%) diet that is high in carbs GI protectants
79
Diagnosis of HE
Bile acids Ammonia Liver function test Imaging
80
Traumatic brain injury pathophysiology
Primary injury +- results in displacement of the brain within the skull (concussion less severe, laceration most severe) leading to haemorrhage and oedema > secondary injury involves a cascade of biochemical events including massive catecholamine/neuroexcitory release, N.O production, compression of the brain > there is influx of Na, Cl and Ca into brain cells, free radical release, influx of inflammatory mediators > disruption of the BBB occurs and there is increased ICP as well as ATP depletion (vasodilation and inflammatory response), activation of coagulation > neuronal death as CPP worsens and cycle continues
81
Systemic and intracranial injuries that perpetuate TBI
Systemic: hypoxaemia, hypo- or hyper- capnoea, hypo- or hyper- thermia, hyper- or hypo- tension, hypo- or hyper- glycaemia, SIRS Intracranial: increased ICP, compromised BBB, oedema, mass lesions, vasospasm, seizures, infection
82
Cerebral blood flow
Ability to maintain constant between MAP 50-150mmHg CBV = CPP and CR This is impaired in TBI so ischaemia more likely * CPP = MAP -ICP
83
Monro-kellie doctrine
V intracranial - V brain + V CSF + V blood + V mass lesion Increases in one area increase ICP and try to counter regulate that increase by decreasing There is a fixed amount of volume in the brain so increases can be a risk factor for poor CBF and herniation
84
Considerations for TBI patients
Avoid jugular compression Watch and treat cushings reflex Elevate head 15-30 degrees Maintain CO2 25-35mmHg Prevent hypoxaemia and hypotension 0.9% NaCl fluid of choice because of the least amount of free water Mydriasis +- strabismus associated with grave to poor outcome Avoid furosemide to avoid IV depletion
85
Treatment for TBI
Mannitol: reduces ICP, improves CBF, free radical scavenging, decreases blood viscosity, lasts 1.5-6h (blouses > CRI) HTS: reduces ICP, improves CBF, less risk of hypotension compared to mannitol, vasoregulates, immunomodulatory, improves haemodynamic status Oxygen +- ventilation Head elevation +- therapeutic hypothermia +- anti seizure meds Fluid resuscitation to maintain MAP 80-100mmHg
86
Which cranial nerve helps control eye movement? a. CN I b. CN III c. CN V d. CN VIII
B
87
What is the correct term for dilation of the pupils? a. Anisocoria b. Blepharospasm c. Miosis d. Mydriasis
D
88
Which disease does not typically result in anterior uveitis? a. Panleukopenia b. FeLV c. FIV d. Toxoplasmosis
A
89
Hyphema refers to the collection of blood in which area of the eye? a. Cornea b. Anterior chamber c. Posterior chamber d. Sclera
B
90
What is a full-thickness defect of the cornea called? a. Descemetocele b. Corneal abrasion c. Corneal ulcer d. Proptosis
A
91
An IOP reading of greater than 25^mmHg suggests what disease process? a. Anterior uveitis b. Lens luxation c. Acute glaucoma d. Progressive retinal atrophy
C
92
Retinal detachment is often a sequela of what process? a. Increased IOP b. Respiratory distress c. Distemper d. Systemic hypertension
D
93
Anterior flare may be present in a patient suffering from which condition? a. Proptosis b. Uveitis c. Anisocoria d. Corneal ulceration
B
94
The pigmented portion of the eye that surrounds the pupil is which structure? a. Lens b. Ciliary body c. Iris d. Retina
C
95
Which cranial nerve is responsible for sending images to the brain for processing? a. CN I b. CN II c. CN VI d. CN X
B
96
Normal ICP
5-12mmHg

VTS(ECC) Preparation (21 decks)

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