Ch75 Critical care for aneurysm patients Flashcards
(22 cards)
What is the evidence for Nimodipine in SAH?
British Aneurysm Trial 1989. Compared placebo with oral nimodipine 60mg 4 hourly and started within 4 days of SAH. Rate of cerebral infarction and mortality fell from 33% with placebo to 22% with nimodipine.
What are risk factor for rebleeding?
Hypertension >175 mmHg systolic Female Large aneurysm
What is the equation for cerebral O2 delivery (DO2)?
DO2 = CBF x arterial blood oxygen content
What is the equation for arterial blood oxygen content?
= Sats x Hb x 1.34
What is the equation for cerebral perfusion?
CPP = MAP - ICP
What is the equation for cerebral blood flow?
CBF = CPP / CVR (cerebral vascular resistance)
How can CBF be optimised following SAH?
Due to autoregulation increasing CPP does not improve CBF. Avoid hypotension using NorAd (if low HR) or Phenylephrine (if normal HR). Maintain euvolaemia Maintain normal ICP Sats 100% Hb 8-10
What was the NEWTON-2 trial?
RCT comparison of sustained-release intrathecal Nimodipine vs oral nimodipine. No difference in outcomes.
What is the SAHaRA trial?
Comparison of Hb >8 vs Hb>10 for SAH. Still on-going.
How do you manage SAH?
Admit to ICU HOB 30 and bed rest Fluids 3L AEDs 7 days if aneurysm unsecured Laxative Analgesia Antiemetics BP control Nimodipine PPI
What is the evidence for statins in SAH?
STASH trial 2014. No benefit with simvastatin 40 mg
What increases the risk of DNID?
Hyponatraemia by 3x
What is the cause of low Na in SAH?
Cerebral Salt Wasting
Are seizures a predictor of outcome following SAH?
Yes, 65% with seizures compared to 23% without. Treat with AEDs for one week until aneurysm secure.
What is the rebleed rate of an unsecured aneurysm?
20% @ 14 days and 50% @ 6 months
What is the evidence for TXA in SAH?
Reduces the rebleed rate prior to definitive treatment from 10% to 2%. Hillman et al JNS 2002. Dose of TXA is 1 gram every 6 hours.
What is the action of E-aminocaproic acid?
Reduces conversion of plasminogen to plasmin. Reduces the risk of rebleed but increases DNID rate.
What is neurogenic stress cardiomyopathy?
AKA stunned myocardium due to catecholamine surge resulting in reduced cardiac contractility and output. 10% may progress to MI.
What proportion of SAH patients have ECG changes?
50% - thought to be due to subendocardial ischaemia or coronary artery spasm from catecholamine surge
What is the treatment for neurogenic pulmonary oedema?
Ventilation with low PEEP and normalisation of ICP
What is the main time of risk for vasospasm?
3-17 days (peak incidence 6-8 days)
What are the clinical features of vasospasm?
Non-localising = headache / reduced conciousness / confusion ACA syndrome = incontinence confusion leg weakness MCA syndrome = hemiparesis aphasia and parietal lobe syndromes
