Acute Medicine Flashcards
(37 cards)
Headache Red Flags
Thunderclap = sudden onset, maximal within 5 minutes
New onset neurological deficit
New cognitive dysfunction/personality change
History of malignancy (especially if < 20)
Immunosuppression e.g. HIV
Impaired GCS
Recent head injury (< 3 months)
Triggered by cough/valsalva
Worse on waking/lying down
+ sudden LoV/painful eye (?GCA ?AACG)
Substantial change in usual headaches
Differentials for Thunderclap Headache
Subarachnoid haemorrhage
Internal Carotid Artery Dissection
ICH
Pituitary Apoplexy
CVST
Reversible Cerebral Vasoconstriction Syndrome
Acute hypertensive crisis
Posterior Reversible Leucoencephalopathy
Primary cough, sexual, and exertional headache
Causes/RFs for SAH
85% of non-traumatic SAH = due to aneurysms in the circle of Willis
5% = AVMs/Tumours/ Vasculitides/Arterial dissection
RFs
- FHx
- PKD
- CTD e.g. Ehler Danlos, Marfan’s, Pseudoxanthoma elasticum
- Vascular RFs = HTN, smoking
- Cocaine/meth use
- IE with mycotic aneurysms
Investigating SAH
CTH
- if <6 hours after onset and negative = excluded!
Lumbar Puncture
- >6 hours onset
CT Angiogram if xanthochromia/RBC positive LP but CTH negative
Management of SAH
ABCDE
Depends on cause
Refer to neurosurgical team - ?coil vs clip
BP control
Supportive Rx (?ICU/HDU)
Complications of SAH
Vasospasm (4-10days post)
Hydrocephalus (20%)
- Raised ICP = CN palsies, reduced GCS, Cushing’s Triad
Rebleeding (17%)
Seizuers
Arrhythmias
Hyponatraemia (SIADH vs Salt-wasting)
Death
When to perform a CT head prior to LP (for meningitis)?
Consider CTH prior to LP if:
- > 60
- Focal neurology deficit
- Reduced GCS
- Seizures
- Features of raised ICP e.g. papilloedema
- History of SoL/cancer/immunosuppression
Indications for Non Traumatic CT Head
Confusion/Reduced GCS and known ICH/cerebral infarct/SoL/CNS infection
New focal neurological deficit e.g. stroke
Thunderclap headache
New headache and features of raised ICP e.g. papilloedema
New/worsening headache and history of cancer/immunosuppresion/pregnancy or >50
1st Seizure or change in seizure pattern
Management of Migraines
CONSERVATIVE
- Avoid exacerbating factors/triggers e.g. cut out all caffeine
- Sleep hygiene
- Education/reassurance
MEDICAL
- Prophylatic Rx e.g. propanolol, candesartan, topiramate (avoid if trying to get pregnant!)
- Rescue Rx = simple analgesia, triptans (avoid if IHD)
- Do NOT give COCP
Management of Cluster Headache
Acute Attack = triptans (SC or nasal), ?high flow oxygen
Prophylaxis = verapamil or lithium
Definition of HTN
> 135/85 = Stage 1 Hypertension (confirmed with ambulatory/home BP monitoring)
> 150/95 = Stage 2 Hypertension
> 180/120 = Severe/Malignant HTN (depends if features of End Organ Damage present)
When would you treat stage 1 HTN?
1) If > 80
2) If <80 AND
- Evidence of end organ damage
- CVD
- Renal disease
- Diabetic
- Q Risk >10%
Outline the management of Stage 2 HTN
If < 55 or T2DM
- ACEI first line
If >55 / Afro-Caribbean ethnicity
- CCB first line
2nd line = ACEI + CCB / ACEI + diuretic
3rd line = ACEI + CCB + diuretic
4th line = refer to specialist ?spironolactone ?alpha blocker ?beta blocker
When should we consider Secondary HTN?
If <40 and lack risk factors for HTN (e.g. CKD) or their HTN is resistant to treatment
Causes of Secondary HTN
ENDOCRINE
- Primary hyperaldosteronism (Conn’s)
= Most common cause
- Cushing’s syndrome
- Phaeochromocytoma
- Acromegaly
- Thyrotoxicosis
- Congenital Adrenal Hyperplasia
RENAL
- Glomerulonephritis
- Adult PKD
- Renal artery stenosis
Carcinoid syndrome
How would you investigate someone for Secondary HTN?
Bedside
- ECG
- Fundoscopy
- Urine dip
Bloods
- Routine FBC, U&Es, glucose, lipids
Renal USS
Further Ix tailored by underlying suspicion of cause
- Renin:Aldosterone ratio
- Dexamethasone Suppression Test
- TFTs
- OGTT & IGF1
- ?Renal angiogram
Define Acute Severe Hypertension.
How would you manage a patient with Acute Severe HTN?
BP > 180/120
No evidence of acute end organ damage/grade III or IV retinopathy
Rx =
1) 24 hour ambulatory/home BP monitoring
2) Arrange follow up within 7 days
3) If confirmed persistent HTN = start treatment
Define Malignant HTN
How would you manage a patient with Malignant HTN?
A.k.a Accelerated HTN
BP >180/120 with signs of retinal haemorrhage +/- papilloedema
No other signs of Acute End Organ damage
Rx
1) Start treatment e.g. amlodipine
2) Shared decision making with patient - most can be discharged home with follow up e.g on ambulatory care with home BP monitoring
Outline features which would make you concerned for a Hypertensive Emergency
Chest pain (?ACS)
(?Hypertensive encephalopathy/ICH/Stroke/SAH)
- Confusion
- Seizures
- Reduced GCS
Proteinuria
New AKI/deterioration in renal function
HTN in Pregnancy
= Systolic >140 or diastolic > 90
(or increased by >30 (s) / >15 (d) since booking BP)
PRE-EXISTING HTN
- History of HTN before 20 weeks
GESTATIONAL HTN
- HTN occurring after 20 weeks
- Usually resolves after birth
PRE-ECLAMPSIA
- HTN & proteinuria > 20 weeks
- High risk pts given Aspiring 75mg OD from 12 weeks
Features of Pre-eclampsia
Hypertension
Proteinuria
Headache
Visual disturbance, papilloedema
RUQ pain
Brisk reflexes
Seizures = ECLAMPSIA
Treatment of Pre-Eclampsia
PO labetalol/nifedipine if BP >160/110
Optimum timing of delivery
If develop eclampsia = IV magnesium 4g
Well’s Score - DVT
0 - DVT unlikely
1-2 = Do d-dimer
>3 = DVT likely, request USS
Active cancer (1)
Bedridden > 3 days/Major surgery <12 weeks ago (1)
Previous DVT (1)
Paralysis/plaster cast of that leg (1)
Calf swelling > 3cm (1)
Collateral (non varicose) superficial veins (1)
Entire leg swollen (1)
Tender along deep venous system (1)
Pitting oedema (1)
If alternative diagnosis as/more likely = - 2 points
Wells Score - PE
<4 = PE unlikely, do d-dimer
>5 = PE likely, do CTPA
Previous DVT/PE = 1.5 points
Immobilisation >3 days/surgery in last 4 weeks = 1.5 points
Malignancy (received treatment in last 6 months/palliative) = 1
Clinical signs of DVT = 3
HR > 100 = 1.5
Haemoptysis = 1
If PE is number 1/equally likely diagnosis = +3