History Taking:
When did the incident occur?
Was there any LOC?
Is there evidence of incontinence?
Have there been changes in symptoms?
Has this ever happened before?
Spinal emergencies:
Autonomic dysreflexia:
This is a potentially dangerous situation that occurs in patients with a spinal cord injury at T6 or above. It is usually initiated by signals from the bladder (indwelling catheter patients), or the bowel. What happens is the bladder, for example, becomes full and sends a sympathetic signal to the spinal cord to notify the brain. This impulse cannot cross the point of injury, and so the spine triggers a sympathetic NS response below the injury site. This means vasoconstriction, among other things. The result is of course, systemic HTN develops. The carotid baroreceptors pick this HTN up and say “hold up, this is a problem”, and they stimulate the vagus nerve to drop heart rate in an effort to reduce BP. The result of this is bradycardia, and a parasympathetic response above the level of the spinal cord injury.
Symptoms include:
HTN
Bradycardia
Flushing of the face (due to parasympathetic stimulation of cranial nerve VII)
Sweating above the injury site and dry skin below it.
Headache
This needs to be treated in hospital and transport is needed.
Seizure:
Seizure causes: There are 3 main categories of seizure causes:
Structural causes:Tumours, inflammation/infection, scarring, or abscesses.
Metabolic causes: Abnormally low levels of essential chemicals in the bloodstream, Ie: hypoglycemia, electrolyte disturbances, hypoxia, etc.
Febrile causes: Seen primarily in children or those with heat stroke (Temp >40 degrees celsius).
Phases of seizures:
Aura
Tonic/clonic phase
Postictal state
The physiological treat from a seizure: aside from the potential for trauma, and damage to structures like the tongue; the biggest risk with seizures is from hypoxia. During a seizure, respiratory drive is depressed; leading to anaerobic cellular metabolism, accumulation of metabolic wastes, and a state of metabolic acidosis. Additionally, tonic/clonic activity is very energy expensive, and prolonged seizures can burn up a lot of glucose, which may lead to hypoglycemia.
Treatment of seizures is aimed at 3 main goals:
Control ABCs
Protect the patient from injury
Stop the seizure (Midazolam)
Beware of status epilepticus: this is a seizure lasting >5 minutes or 2 or more seizures without a return of consciousness in between.
Strokes: There are 2 flavours of CVA: Ischemic, and Hemorrhagic. 80% of strokes are ischemic and 20% are hemorrhagic, with the latter being more severe with a much higher mortality rate. In general we don't see a lot of the second kind but it is important to recognize them.
Ischemic CVA: This occurs when a blockage, usually an embolus from one of the carotids, forms in the vasculature of the brain. The result is the cessation of O2 and glucose delivery to the cells in that area. Where the blockage is will largely determine the presentation. In general we break strokes into anterior and posterior symptom sets. Anterior strokes affect the front of the brain, and are usually unilateral. Because neurons cross over at the brainstem, we will see physical symptoms on the side of the body opposite the affected side of the brain (the exception being cranial nerves). In anterior strokes we see the classic symptoms described in the FAST exam: -Facial asymmetry -Unilateral grip and pedal deficits -Pronator drift -Slurred speech -Alterations in LOA In posterior strokes, we see ischemia in areas like the cerebellum, so we see symptoms that are more to do with coordination: -Ataxia -Vertigo -Nausea -Respiratory irregularities
Hemorrhagic CVA: These are a different animal with similar effects. Rather than a blockage, we are dealing with a rupture of cerebral vasculature. The result is twofold. First, the area distal to the rupture becomes ischemic. Second, the blood pooling in the cranial vault exerts pressure on the brain, both at the site, and on the opposite side of the brain as it is compressed against the skull. In these patients, initial symptoms may be: -”Thunderclap” headache -Nausea -Vertigo -LOC -Cheyne-Stokes or Apneustic respirations (Fish-breathing) As ICP increases we usually see some variation of Cushing's Triad: -Severe HTN with a wide pulse pressure -Irregular respirations -Tachycardia that rapidly becomes bradycardia We also may see signs of cerebral herniation: Unequal/unreactive pupils, unilateral motor response to painful stimuli, and posturing.
Treatment goals: For either type of stroke, our priority should be maintaining ABCs and getting an accurate time of onset or the last time the patient was seen normal. Depending where you work, you have between 4.5 and 6 hours from time of onset to get to a stroke centre. We also want to address vomiting. First, because vomiting causes increase in blood pressure, which will actually worsen the situation, and Second, because there is high risk of aspiration in the CVA patient.
We definitely want to do a good neurological assessment, and really pay attention for signs of increasing ICP.
Meningitis:
We don't see this very often anymore due to the success of vaccination in North America. That being said, it is not unheard of, and should be addressed. In meningitis, a pathogen, usually a bacteria, is able to exit the bloodstream and enter the CSF. Once it is there it attacks the meningeal membrane, causing inflammation and increased ICP. These patients usually have some combination of altered LOA, fever, petichae body rash, nuchal rigidity, photophobia, and nausea. You may see focal neurological deficits similar to a CVA. The treatment in the prehospital setting is essentially recognition, droplet precautions, addressing oxygenation, and management of fever or volume deficits.
Top 5 Killer causes of altered LOA: (SITES)
S- Stroke
I- Infections/Sepsis
T- Toxidromes
E- Endocrine/hypoglycemia
S- Seizure
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