Conditions List Flashcards
(122 cards)
What are the causes of Stroke?
-Vessel occlusion or thrombosis in situ
-Cardiac emboli (AF, endocarditis)
-Atherothromboembolism (eg from carotids)
-CNS bleeds (HTN, trauma, aneurysm rupture, anticoagulation, thrombolysis)
-Sudden BP drop
-Carotid artery dissection
-Vasculitis
-SAH
-Venous sinus thrombosis
-Antiphospholipid syndrome
-Thrombophilia
-Fabry disease
What are the risk factors for developing a stroke?
-HTN
-Smoking
-DM
-CV disease (valvular, IHD, AF)
-Increased clotting
-Increased homocysteine
-Syphilis
How do you manage an acute stroke?
- Protect the airway
- Maintain homeostasis: blood glucose (check signs are not due to hypoglycaemia), BP (only treat if hypertensive emergency such as encephalopathy or aortic dissection because lowering BP may affect cerebral perfusion
- CT/MRI immediately: diffusion-weighted MRI is gold standard, CT helps to rule out primary intracerebral haemorrhage
ONLY IF HAEMORRHAGE IS EXCLUDED:
4. Antiplatelet - give aspirin 300mg stat and continue for 2 weeks
5. Thrombolysis - If onset of symptoms was <4.5 hours ago, give alteplase (tissue plasminogen activator) with close monitoring (incl repeated CT 24 hours post lysis to check for bleeds)
6. Thrombectomy - if the area of infarction is confirmed and depending on the location of the infarct and the time since stroke (not used >24 hours after event). For those with large artery occlusion in the proximal anterior circulation
What are the contraindications to thrombolysis treatment of acute stroke?
-Major infarct or haemorrhage on CT
-Mild/non-disabling deficit
-Recent surgery, trauma, or artery or vein puncture at uncompressible site
-Previous CNS bleed
-AVM/aneurysm
-Severe liver disease, varices or portal hypertension
-Seizures at presentation
-Very low or very high blood glucose
-Stroke or serious head injury in last 3 months
-GI or urinary tract haemorrhage in last 21 days
-Known clotting disorder
-On anticoagulants or INR>1.7
-Low platelets
-History of intracranial neoplasm
-Rapidly improving symptoms
-BP> 180/105
What secondary preventative measures should be started after the acute management of a stroke?
-Control risk factors: eg lowering BP, most patients should be started on atorvastatin 80mg
-Start Antiplatelets: After 2 weeks of 300mg aspirin, switch patients to clopidogrel 75mg monotherapy. If this is CI or not tolerated, give low dose aspirin and slow release dipyridamole
What tests should be carried out following a stroke (post-acute phase)?
- Check BP: look for retinopathy, nephropathy or cardiomegaly on CXR
- Cardiac sources of emboli: 24hr ECG to check for AF. CXR may show large left atrium. Echo may show mural thrombosis due to AF or hypokinetic segment of cardiac muscle post-MI, valvular lesions in infective endocarditis or rheumatic heart disease. TOE more sensitive than TTO
- Carotid artery stenosis: Do carotid doppler ultrasound +/- CT?MRI angiography. (Carotid endarterectomy may be indicated)
- Check for hyper/hypoglycaemia, dyslipidaemia or hyperhomocysteinaemia
-Vasculitis: increased ESR, ANCA, check for active untreated syphilis
-Prothrombotic states: thrombophilia, antiphospholipid syndrome
-Hyperviscosity: polycythaemia, sickle-cell disease
-Thrombocytopaenia and other bleeding disorders
-Genetic tests eg CADASIL and Fabry disease
What treatment should be given to a stroke patient found to have AF?
Anticoagulation with a DOAC or Warfarin from 2 weeks (or from 7-10 days if clinically and radiologically small embolus).
What is the mechanism of action of aspirin?
Inhibits cox-1, suppressing prostaglandin and thromboxane synthesis
What is the mechanism of action of clopidogrel?
A thienopyridine that inhibits platelet aggregation by modifying platelet adenosine diphosphate (ADP) receptors
What is the mechanism of action of dipyridamole?
Increases cAMP and decreases thromboxane A2
What is vertigo?
Vertigo is a descriptive term for a sensation that there is movement between the patient and their environment. They may feel they are moving or that the room is moving. Often this is a horizontal spinning sensation, similar to how you feel after turning in circles then stopping abruptly.
Vertigo is often associated with nausea, vomiting, sweating and feeling generally unwell. There may be decreased balance, hearing loss, tinnitus and nystagmus.
What is the pathophysiology of vertigo?
The sensory inputs that are responsible for maintaining balance and posture are:
1. Vision
2. Proprioception
3. Signals from the vestibular system
Vertigo is caused by a mismatch between these sensory inputs.
The vestibular system is the most important sensory system to understand when learning about vertigo. The vestibular apparatus is located in the inner ear. It consists of three loops called the semicircular canals that are filled with a fluid called endolymph. These semicircular canals are oriented in different directions to detect various movements of the head. As the head turns, the fluid shifts inside the canals. This fluid shift is detected by tiny hairs called stereocilia found in a section of the canal called the ampulla. This sensory input of shifting fluid is transmitted to the brain by the vestibular nerve and lets the brain know that the head is moving in a particular direction.
The vestibular nerve carries signals from the vestibular apparatus to the vestibular nucleus in the brainstem and the cerebellum. The vestibular nucleus then sends signals to the oculomotor, trochlear and abducens nuclei that control eye movements and the thalamus, spinal cord and cerebellum. The cerebellum is responsible for coordinating movement throughout the body. Therefore, the vestibular signals help the central nervous system coordinate eye movements and other movements throughout the body.
Vertigo can be caused by either a:
-Peripheral problem, usually affecting the vestibular system
-Central problem, usually involving the brainstem or the cerebellum
What are the four common types of peripheral (vestibular) vertigo? What other causes may be possible?
- Benign paroxysmal positional vertigo
- Ménière’s disease
- Vestibular neuronitis
- Labyrinthitis
There are several other peripheral causes of vertigo. These are:
-Trauma to the vestibular nerve
-Vestibular nerve tumours (acoustic neuromas)
-Otosclerosis
-Hyperviscosity syndromes
-Varicella zoster infection (often with facial nerve weakness and vesicles around the ear – Ramsay Hunt syndrome)
What is benign paroxysmal positional vertigo?
Benign paroxysmal positional vertigo (BPPV) is caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. They may be displaced by a viral infection, head trauma, ageing or without a clear cause. The crystals disrupt the normal flow through the canals and therefore disrupt the function of the system. The symptoms are usually positional, because movement is required to confuse the system. Therefore, attacks of vertigo are triggered by movement and can last around a minute before the symptoms settle. Often symptoms occur over several weeks and then resolve, then can reoccur weeks or months later. A special test called the Dix-Hallpike manoeuvre can be used to diagnose BPPV.
What is Meniere’s disease?
Ménière’s disease is caused by an excessive buildup of endolymph in the semicircular canals, causing a higher pressure than normal, disrupting the sensory signals. It causes attacks of hearing loss, tinnitus, vertigo and a sensation of fullness in the ear. These attacks typically last several hours before settling. It most often occurs in middle-aged adults and is not associated with movement. The symptoms are not positional. Patients will have spontaneous nystagmus during attacks (nystagmus is discussed in more detail later). Over time, the patient’s hearing will gradually deteriorate.
What is acute vestibular neuronitis?
Acute vestibular neuronitis describes inflammation of the vestibular nerve. This is usually attributed to a viral infection. Typically, the history is of acute onset of vertigo that improves within a few weeks.
What is Labrynthitis?
Labyrinthitis describes inflammation of the structures of the inner ear. This is usually attributed to a viral infection. Usually the history is of acute onset of vertigo that improves within a few weeks. Labyrinthitis can cause hearing loss, which distinguishes it from vestibular neuronitis.
What are the common causes of central vertigo?
Pathology that affects the cerebellum or the brainstem disrupt the signals from the vestibular system and cause vertigo. The most common pathology that results in a central cause of vertigo are:
- Posterior circulation infarction (stroke): will have a sudden onset and may be associated with other symptoms, such as ataxia, diplopia, cranial nerve defects or limb symptoms.
- Tumour: in the cerebellum or brainstem will have a gradual onset with associated symptoms of cerebellar or brainstem dysfunction.
- Multiple sclerosis: may cause relapsing and remitting symptoms, with other associated features of multiple sclerosis, such as optic neuritis or transverse myelitis.
- Vestibular migraine: will cause symptoms lasting minutes to hours, often associated with visual aura and headache. Attacks may be triggered by stress, bright lights, strong smells, certain foods (e.g. chocolate, cheese and caffeine), dehydration, menstruation, abnormal sleep patterns
All the central causes of vertigo will cause sustained, non-positional vertigo.
What key features in a history might point to the cause of vertigo?
When a patient presents with “dizziness’, it is important to first distinguish between vertigo and light-headedness. Ask whether the “room is moving” (vertigo) or whether they feel more of a light-headedness.
Ask about symptoms that will help you differentiate between central and peripheral vertigo:
1. Onset: Sudden onset (P), Gradual onset (C - except stroke)
2. Duration: Short (seconds or minutes -P), Persistent (C)
3. Hearing loss or tinnitus: Often present (P - except BPPV), Usually not (C)
4. Coordination: Intact (P), Impaired (C)
5. Nausea: More severe (P), Mild (C)
Key features that may point to a specific cause are:
-Recent viral illness (labyrinthitis or vestibular neuronitis)
-Headache (vestibular migraine, cerebrovascular accident or brain tumour)
-Typical triggers (vestibular migraine)
-Ear symptoms, such as pain or discharge (infection)
-Acute onset neurological symptoms (stroke)
What are the 4 things to examine when assessing a patient presenting with vertigo?
- Ear examination to look for signs of infection or other pathology
- Neurological examination to assess for central causes of vertigo (e.g., stroke or multiple sclerosis).
Cerebellar examination is an important part of a full neurological examination in patients with vertigo. The components can be remembered with the DANISH mnemonic:
D – Dysdiadochokinesia
A – Ataxic gait (ask the patient to walk heel-to-toe)
N – Nystagmus (see below for more detail)
I – Intention tremor
S – Speech (slurred)
H – Heel-shin test
- Cardiovascular examination to assess for cardiovascular causes of dizziness (e.g., arrhythmias or valve disease)
- Special tests
-Romberg’s test (screens for problems with proprioception or vestibular function)
-Dix-Hallpike manoeuvre (to diagnose BPPV)
-HINTS examination (to distinguish between central and peripheral vertigo). It stands for:
HI – Head Impulse
N – Nystagmus
TS – Test of Skew
Head Impulse Test
The head impulse test involves the patient sitting upright and fixing their gaze on the examiner’s nose. The examiner holds the patient’s head and rapidly jerks it 10-20 degrees in one direction while the patient continues looking at the examiner’s nose. The head is moved slowly back to the centre before repeating in the opposite direction. Ensure they have no neck pain or pathology before performing the test.
A patient with a normally functioning vestibular system will keep their eyes fixed on the examiner’s nose.
In a patient with an abnormally functioning vestibular system (e.g., vestibular neuronitis or labyrinthitis), the eyes will saccade (rapidly move back and forth) as they eventually fix back on the examiner.
The head impulse test helps diagnose a peripheral cause of vertigo but will be normal if the patient has no current symptoms or a central cause of vertigo.
Nystagmus
Nystagmus can be demonstrated by having the patient look left and right. The eyes rapidly saccade or oscillate, meaning they shake side to side as they try to settle into place. A few beats can be normal. Unilateral horizontal nystagmus is more likely to be a peripheral cause. Bilateral or vertical nystagmus suggests a central cause.
Test of Skew
The test of skew (also called the alternate cover test) involves the patient sitting upright and fixing their gaze on the examiner’s nose. The examiner covers one eye at a time, alternating between covering either eye. The eyes should remain fixed on the examiner’s nose with no deviation. If there is a vertical correction when an eye is uncovered (the eye has drifted up or down and needs to move vertically to fix on the nose when uncovered), this indicates a central cause of vertigo.
How is vertigo due to peripheral causes managed?
For peripheral vertigo, short-term options for managing symptoms include:
-Prochlorperazine/Buccastem (A vestibular suppressant)
-Antihistamines (e.g., cyclizine, cinnarizine and promethazine)
What can be used as prophylaxis in Meniere’s disease?
Betahistine
Vestibular suppressants do not stop the vertigo in BPPV. How can this condition be managed?
- Epley manoeuvre
How is vestibular migraine managed?
Usually managed by avoiding triggers and lifestyle changes (e.g., getting enough sleep and staying hydrated).
Medical management is similar to migraines, with triptans for the acute symptoms and propranolol, topiramate or amitriptyline to prevent attacks.