Pt w/ Collapse Flashcards
List some important question to ask in the history of a patient presenting with collapse
BEFORE (how did they feel)
- Palpitations, dizzy, chest pain, breathlessness, headache, nausea, last time they ate or drank, any illegal drugs or alcohol, past hx of collapse, pale and clammy, weakness
DURING THE COLLAPSE
- do they remember falling or did they black out before
- did they hit their head
- did anyone else see (collateral hx)
- did they seize/shake/twitch
- how long were they unconscious for?
- did they bite their tongue?
- were they incontinent or urine or faeces
AFTER
- How did they feel after (sleepy, sick)
- How do they feel now?
- Any ongoing chest pain or breathlessness
Presenting features of an AAA
Depends very much on whether it has ruptured…
UNRUPTURED:
- usually asx
- Only known as aneurysm when increased by >50% (>3cm across)
- MAY cause abdominal or back pain
RUPTURED:
- intermittent or continuous abdominal pain that might radiate to back, iliac fossa or groin. COLLAPSE IS COMMON
Examination features of ruptured AAA
Rigid abdomen, pt in shock (tachycardia, hypotension, pale, clammy and low CRT)
Presence of PULSATILE, EXPANSIVE MASS in stomach
Where is the most common site for a AAA to form?
Just below the renal arteries (infrarenal)
What are some common causes of AAA?
Spontaneous main RF is AGE (main over 60 at high risk and are regularly screened)
Other causes include syphilis, Ehlers Danlos and Marfans
Investigations for AAA
USS is diagnostic (if already ruptured do not waste time doing this) ECG BLOODS (amylase is important and get a group and save and cross match for 10U)
Management of AAA
If you suspect rupture immediately inform theatres - will need surgical repair
- high flow O2
- IV access and give some O- blood while waiting for cross match AIM FOR SYSTOLIC <100mmHg (too high BP might rupture a contain leak)
Prophylactic METRONIDAZOLE AND CEFUROXIME
Unruptured are only repaired when they reach >5.5cm in diameter
When do symptoms of alcohol withdrawal commonly occur?
12 hours after stopping or considerably reducing the alcohol intake
What are some features of alcohol withdrawal? How quickly will they occur?
Will usually occur just 6-8 hours after alcohol withdrawal
D = Delirium, which is often worse at night T = Tremor (aka “the shakes”) S = Sympathetic overactivity (i.e. fever, tachycardia, hypertension, sweating)
H = Hallucinations (which are often visual or tactile) E = ESR (raised) L = Leucocytosis L = LFTs (impaired)
Which syndrome is suggestive of withdrawal from chronic alcohol use, when does it occur and what are its symptoms?
DELIRIUM TREMENS Usually occur 2-3 days after alcohol withdrawal PHYSICAL SIGNS: - Shaking - Sweating - Increased heart rate - Seizures - Pseudohallucinations
What investigations are important in someone with alcohol withdrawal?
Baseline bloods: FBC, U&E, Glucose (check thiamine - often deficient and can be corrected easily)
ECG
Monitor obs
ABG (monitor for metabolic acidosis)
Initial management for alcohol withdrawal
the benzodiazepine CHLORDIAZEPOXIDE (10-30mg) is very useful in the treatment of alcohol withdrawal
PABRINEX Is a thiamine-corrective solution that should also be given
What are some common cardiac causes of collapse?
COMPLETE HEART BLOCK
What is complete heart block?
Where there is incomplete or lack of conduction between the SAN and the AVN meaning the heart doesn’t beat properly and cardiac output drops
- there are many different types and degrees of heart block but complete (or third degree) heart block is the most serious and most likely to cause collapse
Why might there still be heart beat in someone with complete heart block? How will this appear on ECG
Sometimes there is some accessory pacemaker tissue that generates and conducts a signal - known as an ESCAPE RHYTHM
- will cause NARROW QRS COMPLEXES
What are some others symptoms of complete heart block?
Bradycardia
Hypotension
COLLAPSE
Haemodynamic instability
What are some common causes of complete heart block?
CORONARY ISCHAEMIA
INFERIOR WALL MI are the ones that are most likely to disturb the AVN and therefore ruin conduction and lead to heart block
What are some relevant investigations for patients with heart block and what might you find?
ECG: lack of relationship between p waves and QRS complexes - remember spotting the pattern in the relationships between the two tells us what degree of heart block it is.
Also look for LBBB as evidence of old MI
FBC, U&E, Trop
How does DKA typically present?
ALWAYS CONSIDER THIS IS THE COLLAPSED YOUNG PERSON
Can present in a large variety of ways that can be quite non specific:
- GI: nausea, vomiting, abdominal pain
- D: polyuria, polydipsia, sweet smelling breath, recent weight loss, recent fatigue, decreased skin turgor and dry mucus membranes, altered conscious state, focal neurology. HIGH BLOOD GLUCOSE
- HD: tachycardia and hypotension, hyperventilation (to blow off CO2 to compensate for metabolic acidosis)
Causes of DKA (explanation of symptoms)
Often happens in the young person who does not know they are diabetic.
Without insulin body draws of reserves of glycogen and liver breaks down fats and proteins during gluconeogenesis - breaking down fatty acids to produce glucose leads to KETONE RELEASE - ACIDOTIC
- very high levels of plasma glucose leads to diuretic osmosis and water and sodium are drawn out of cells leading to the polyuria and polydipsia
Initial management of DKA
If the patient has altered mental state consider airway preservation and breathing support etc.
FLUIDS IMPORTANT - 0.9% NaCl IV infusion over 0.5-1hr and then give constant bags until the BP is corrected
INSULIN INFUSION pump at 6U/hr
Potassium correction (insulin drives K into IC comp)
- Consider monitoring urine output (?catheter)
What condition occurs when blood glucose is high but there isn’t a considerable ketoacidosis?
HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS)
What are some clinical features of HHS?
Glucose >30mmol LACK of urinary ketones Increased blood osmolality leading to sx of polydipsia and polyuria Dehydration Weakness Leg cramps Vision problems Altered consciousness
What causes HHS?
Can just happen with inter-current illness
OR
Can happen in someone who had diabetes that is poorly controlled
Can occur in dehydration
What investigations are relevant in HHS?
Blood glucose
FBC,U&E, CRP
ECG
CXR
What is the management of HHS?
VERY SIMILAR TO DKA
- Insulin infusion 6U/hr
- Monitor potassium
- Keep hydrated with salt boosts - NaCl 0.9%
What is classed as high blood glucose and what are some general symptoms?
BM >11.1mmmol
Classic triad of sx: polyphagia, polyuria and polydipsia
Sx of CHRONIC POOR GLUCOSE CONTROL:
- ED, blurred vision, poor kidney function, weight loss, restlessness, fatigue, poor wound healing, dry mouth, itchy skin
What factors in the history are important to ascertain in someone presenting with seizures?
BEFORE
- any aura (visual, auditory, gustatory, olfactory, tactile), headaches, feeling unwell - familiar to pt?
DURING
- were the jerking/twitching (tonic clonic), were they unconscious/how long for, did they bite their tongue, were they incontinent?
AFTER
- are they sleep/confused/drowsy and how long for
- Do they have headache
How do we classify seizures?
Firstly they are either PARTIAL OR GENERALISED
- SIMPLE PARTIAL - awareness is unimpaired, focal motor and sensory /autonomic symptoms
- COMPLEX PARTIAL - awareness is impaired. Usually temporal lobe. Post-ictal confusion is common but fast to resolve
- PARTIAL WITH 2RY GENERALISATION - seizure starts with focal motor or sensory deficits and then will become convulsions (2/3 of pt with partial seizures)
- ABSENCE SEIZURES: more common in children - unresponsive for several seconds
- TONIC-CLONIC SEIZURES: classical jerking seizures, pt will collapse. Post octal period is considerable with dizziness and confusion
- MYOCLONIC - sudden jerking of a limb or trunk may cause patient to fall to ground
- ATONIC SEIZURES - pt goes completely floppy (no LOC)
Causes of seizures
EPILEPSY Hypoglycaemia Strokes/TIAs/SAH Drugs/alcohol Arrhythmias Head injuries Medication Pregnancy
What investigations should be done in someone with seizures?
Glucose FBC, U&E, cultures (if indicated) ECG CXR Cranial nerve exam Peripheral nerve exam
What is the management of someone with a seizure?
Most people will present post-seizure and so investigations and hx most important
For those in STATUS EPILEPTICUS (>30min)
- A-E
- Monitor ECG
- Gain IV access –> IV LORAZEPAM 4mg INTO LARGE VEIN
- BUCCAL MIDAZOLAM
- If alcohol misuse suspected or malnutrition give PABRINEX
- ABG
What is the difference between stroke and TIA?
Sx lasting less than 24h = TIA
What are the brain 2 initial blood supplies and what do these feed into?
- Where are strokes more common?
Internal carotids (supply anterior and medial cerebral arteries) and basilar arteries (supply posterior cerebral arteries) - Strokes more common in there anterior circulation
What are the two main types of stroke and what are the proportions of their occurrence?
Ischaemia (80-85%) and haemorrhage (15-20%)
What are the symptoms of anterior circulation stroke?
- Unilateral weakness (limb and facial droop)
- Difficult speaking
- Numbness and loss of sensation
- Cognitive impairment
What are some symptoms of posterior circulation strokes?
Nausea, dizziness, vertigo, lack of coordination, memory loss, limb weakness - ataxia
Sensory deficits
CEREBELLAR SYMPTOMS (DANISH)
Causes of stroke / TIA
Most common is atherosclerotic plaque aetiology
Haemorrhage: aneurysm rupture, SAH
Carotid artery dissection
Cerebral embolism from AF
Investigations for stroke/TIA
CT head
Carotid dopplers
Initial management of stroke
Carotid endarterectomy
If haemorrhage is excluded:
- 300mg ASPIRIN followed by 6 weeks of 75mg doses
- Consider ALTEPLASE given within 4 hours of onset of symptoms
What are some symptoms of SAH?
THUNDERCLAP HEADACHE
- LOC, neck stiffness, vomiting, photophobia, dizziness and confusion
What is the cause of SAH?
Most commonly is ruptured berry aneurysm on the circle of willis
- ask about FH because these are familial
What investigations are important in SAH
MONITOR OBS - this is really important because as with any case of increased intracranial pressure there is a chance of developing CUSHINGS TRIAD (hypertension, bradycardia and irregular breathing)
Full cranial nerve exam important
- OCULOMOTOR NERVE PALSY is classic of berry aneurysm rupture in the posterior communicating circulation
LP will show xanthochromia
Initial management of SAH
- A-E
- IV access: FBC, U&E, BMG, clotting
- ECG
- Emergency CT
- Inform neurosurgical team
- Analgesia and anti-emetic (codeine)
If there are evidence of ICP increase can give MANNITOL 200mL 10%
What is mannitol?
osmotic diuretic that forces protein out of the blood causes a drop in pressure - it temporarily decreases ICP until more definitive measures can be found
What is the typical history of a VASOVAGAL SYNCOPE?
Sudden, transient loss of consciousness/collapse with a quick recovery and other vasovagal symptoms such as sweating, flushing, dizziness, feeling sick and visual sensory symptoms (lights flashing in eyes)
Causes of vasovagal syncope
Due to neurological increase in vagal tone which causes a drop in BP and hence collapse
Important investigations in someone with vasovagal syncope
Lying and standing BP (low BP can be a cause) Blood glucose FBC, U&E ECG Monitor obs
Initial management of vasovagal
Likely to be able to be discharged quickly as long as they have a normal examination and investigations and have fully recovered
If episodes are frequent might consider referral to neurology
What factors of a collapse history would make you start considering seizures?
Presence of aura (changes in vision, smell, headache)
Jerking / twitching - TONIC-CLONIC in appearance
Tongue biting
Incontinence
Post-ictal period of drowsiness, headache or weakness
What are the two main types of seizure?
Partial and generalised?
What further sub-types are there of partial seizures?
SIMPLE PARTIAL - awareness unimpaired, focal motor sensory or autonomic symptoms and no post-octal sx
COMPLEX PARTIAL - awareness is impaired. Commonly arise from temporal lobe. Focal symptoms (poss within aura). Post-ictal is possible but if temporal lobe recovery will be rapid
PARTIAL W/ 2RY GENERALISATION: 2/3 will have generalising features (typically tonic-clonic convulsions)
What are some further sub-types of generalised seizures?
ABSENCE: unresponsive and unaware for up to 10s. Common in children
TONIC-CLONIC: MOST COMMON. Limbs jerk, LOC, considerable post-octal period with confusion and drowsiness
MYOCLONIC JERK: single jerking of limbs face or trunk - may cause person to fall
ATONIC: sudden loss of muscle tone and fall to ground
If it is someone’s first seizure what common causes/risk factors might you try and identify?
Hypoglycaemia - always check glucose Strokes/TIAs Vasovagal (people often twitch which can be confusing) Drugs and alcohol Arrhythmias Head injuries SAH
Also consider infection, pregnancy and new epilepsy
What investigations should you consider in someone presenting with seizures?
FBC, U&E, GLUCOSE ECG Cultures (if indicated) CNS PNS
How should someone with stroke initially be managed?
CT head, consult neurology if no cause found
How should status epilepticus be managed?
A-E
Monitor ECG
Secure airway and delivery oxygen
Get IV access and give IV lorazepam 4mg slow into large vein
IF alcohol or malnutrition co-existing give PABRINEX
ABG
Search for features of injury or rash
