Acute Neuro Conditions- Caused by SPI & Meds Flashcards
What type of shock is Neurogenic Shock?
Neurogenic shock is a type of DISTRIBUTIVE SHOCK (impaired distribution of blood flow from excessive vasodilation)
What is Neurogenic Shock?
Think about- who experiences it, the type of shock, what it does to the vessels
Neurogenic Shock= a type of distributive shock which causes hemodynamic instability. It occurs following a spinal cord injury at T6 or above. It results from impaired distribution of blood flow secondary to excessive vasodilation.
Describe the pathophysiology of Neurogenic Shock & the signs/symptoms which manifest throughout the process
Neurogenic Shock:
1. Spinal cord injury at T6 or above
2. This cuts off the sympathetic NS but parasympathetic remains unaffected (S/S= sweat line- sweaty above injury line, dry below injury line)
3. Sudden loss of sympathetic tone
3. Celiac Ganglion can’t receive messages & can’t stimulate adrenal glands
4. Adrenal glands can’t release adrenaline (catecholamines)
5. No adrenaline + no sympathetic tone= loss of vascular tone & massive vasodilation (S/S= hypotension, hypothermia)
6. Loss of sympathetic tone, but preservation (& exaggeration) of parasympathetic function (S/S= bradycardia)
What are the 3 key Signs/Symptoms of Neurogenic Shock?
Neurogenic Shock=
1. Hypotension
2. Hypothermia
3. Bradycardia
What is the similarities and differences between Neurogenic Shock & Spinal Shock
[hint- only 1 similarity]
Neurogenic VS Spinal Shock:
Similarity- Both occur following a spinal cord injury
Difference- Neurogenic Shock causes hemodynamic deficits/ instability (from a loss of sympathetic and vascular tone), whereas spinal shock causes musculoskeletal deficits (impaired- motor function, reflexes, sensation)
If there is adequate blood volume, what causes low blood pressure in patients with Neurogenic Shock?
Neurogenic shock causes low BP because of vasodilation (poor vascular tone) and poor cardiac contractility
Neurogenic Shock and Autonomic Dysreflexia both occur in the setting of a spinal cord injury (SCI) at T6 or above. Which condition usually occurs at the time of the SPI, and which usually occurs in the period (weeks, months, years) following the injury?
Neurogenic shock= occurs at the time of the initial spinal cord injury
Autonomic Dysreflexia= occurs in the period following the spinal cord injury (eg. In the weeks, months, years following)
Autonomic Dysreflexia & Neurogenic Shock both cause a mismatch in skin appearance above & below the injury level. Describe the expected skin appearance in each condition
- Neurogenic Shock:
Above injury= pale + sweaty
Below injury= flushed + dry - Autonomic Dysreflexia:
Above injury= flushed + sweaty
Below injury= pale + dry + goosebumps (piloerection)
[Memory hack- Below the SCI the skin reflects the sympathetic response & vasoconstriction (dry, pale), but the healthy part of the body above SCI has no idea what’s going on down below as the messages aren’t getting past the injury level so it just dilates all the vessels to try control the rapidly increasing BP, and this results in vasodilation effects (flushed, sweaty) reflects what is actually happening- sympathetic response]
What are some examples of noxious stimuli that can trigger Autonomic Dysreflexia?
[hint- think of the categories of bladder, bowel, skin, other]
Noxious Stimuli:
a) Bladder- distension, UTI, kidney stone, catheter insertion/blockage
b) Bowel- constipation, impaction, haemorrhoids
c) Skin- pressure area, burns, ingrown toenail, tight clothes
d) Other- fractures, sexual activity
Describe the pathophysiology of Autonomic Dysreflexia & the clinical manifestations at each stage of the process
Autonomic Dysreflexia:
(Previous spinal cord injury to T6 or above)
1. Noxious (strong) stimuli below level of injury
2. This stimulates the Sympathetic Nervous System
3. Sympathetic response is exaggerated, uninhibited & hyper stimulated (as the SCI impairs function of the nerves that innervate/control the sympathetic NS, & impairs the ability of the parasympathetic NS to oppose the sympathetic NS)
4. Sympathetic response= severe vasoconstriction below SCI level (S/S= Hypertension, skin- pale, dry, goosebumps)
5. Baroreceptors recognise the high BP and try to compensate by:
5a- increasing parasympathetic drive to the heart (S/S= Bradycardia)
5b- vasodilate vessels above SCI level (S/S= flushing, sweaty)
Why is GTN given to patients with Autonomic Dysreflexia?
GTN is a vasodilator which dilates coronary arteries, as well as systemic veins & arteries
Giving GTN to patients with Autonomic Dysreflexia allows for the reversal of the severe (& uninhibited) sympathetic response of vasoconstriction, achieved by dilating their vessels and bringing down the increasing BP
(Remember to always check for use of erectile dysfunction drugs [contraindication] as they are commonly used in SCI pts)
Other than pharmacological interventions (GTN), what other management can you provide for patients with Autonomic Dysreflexia
Therapeutic Interventions for Autonomic Dysreflexia:
1. Position upright (to orthostatically reduce BP)
2. Search for the causative noxious stimuli & manage/remove it if possible
What is Malignant Hyperthermia? And what medication usually causes it?
Malignant Hyperthermia is a life threatening medication reaction which occurs in individuals who have an underlying genetic mutation that causes abnormal composition of muscular tissue. When these genetically susceptible individuals are exposed to certain IV or inhaled medications (eg. Methoxyflurane), they experience malignant hyperthermia
What are the key signs and symptoms of Malignant Hyperthermia?
Malignant Hyperthermia:
= Muscular rigidity
Increases metabolism:
= Hyperthermia (temp usually >40)
= Tachycardia
= Increased RR
Extra Pyramidal Reactions impair function of the extrapyramidal tract. Q- What is the extrapyramidal tract?
Extra Pyramidal Reactions are drug induced reactions which impair function of the extrapyramidal tract.
A- The extrapyramidal tract is one of the pathways from the brain which carry’s motor signals (the other one being the pyramidal tract). It controls reflexes, complicated movements (walking, posture), and fine motor movements (of face, hands, fingers)
What 2 types of medications can trigger Extra Pyramidal Reactions?
Extra Pyramidal Reactions often occur in the setting of:
1. Antipsychotics (eg. Olanzapine, quetiapine, droperidol, haloperidol)
2. Dopamine Blocking Agents (eg. metoclopramide)
There are 4 groups of Extra Pyramidal Reactions. These often occur at different time periods following initiation of antipsychotics (eg. After 4hrs, 4 days, 4 weeks, 4 months)
Q- which group of reactions occur at each stage?
Extra Pyramidal Reactions:
After 4hrs- DYSTONIA
After 4 days- AKINESIA / PSEUDO PARKINSONISM
After 4 weeks- AKATHESIA
After 4 months- TARDIVE DYSKINESIA
Extra Pyramidal Reactions can include ‘Akinesia’/ ‘Pseudo Parkinsonism’ (both occur after 4 days). How do these conditions present? What medication can be used to treat this?
Akinesia= absence of movement (or slow movement)
Pseudo Parkinsonism= shuffling gait, stooped posture, tremor
Medication= Dopamine agonist
Extra Pyramidal Reactions can include ‘Akathesia’. How does this present?
Akathesia= inability to sit still. Pts will present with psychomotor restlessness such as constant foot/leg movements
Extra Pyramidal Reactions can include ‘Tardive Dyskinesia’. How does this present?
Tardive Dyskinesia= involuntary movements of face. Pts will present with chewing motions, sticking out tongue, smacking lip movements
Extra Pyramidal Reactions will often first manifest as ‘Acute Dystonia’. How does this present?
Acute Dystonia= involuntary muscular contraction & posturing. Dystonia can be sustained or intermittent
What must paramedics remain vigilant for when someone is experiencing acute dystonia (a type of extra pyramidal reaction)?
[hint- think of an area of the body where muscular contraction could cause fatal consequences]
Acute Dystonia can cause laryngospasm (spasm of the vocal cords) and failure of the respiratory muscles. This can cause pts to feel like they are choking, can impair breathing, and cause respiratory failure/depression/arrest
What medication can ICPs administer to stop acute dystonic reactions? What two classes of drugs make up this medication?
ICPs can give Benztropine to stop acute dystonia.
Benztropine= anti-cholinergic + anti-histamine
What is the management for acute dystonia that is usually implemented by intensive care paramedics?
Management of Acute Dystonia:
= Benztropine (anti-cholinergic + antihistamine)
= Intubation (if dystonia causes laryngospasm/ failure of respiratory muscles)
What is ‘Neuroleptic Malignant Syndrome’? What medication can trigger it?
Neuroleptic Malignant Syndrome= a drug induced neurological reaction which can occur following administration of antipsychotics, especially Haloperidol. It causes altered mental status, rigidity, fever, & dysautonomia
What are the key signs & symptoms of Neuroleptic Malignant Syndrome?
[Hint- think of S/S in the categories of motor, mental status, body temp, autonomic nervous system]
Neuroleptic Malignant Syndrome:
Motor= Severe tremor, muscular rigidity
Mental Status= Agitated delirium, progress to lethargy & unresponsiveness
Body Temp= Hyperthermia
Autonomic NS= Hyperactivity of ANS= tachycardia, arrhythmia, tachyponea, hypertension
What is the prehospital management of Neuroleptic Malignant Syndrome?
Neuroleptic Malignant Syndrome Management= aggressive cooling
(in-hospital they will cease the culprit drug)
