Heather Lesson test 1

As soon as possible, ideally within 24 hours, for the following reasons: Coiling/clipping significantly reduces risk of early rebleed (15% within 24 hours for unsecured ruptured aneurysms) 1/3 of rebleeds occur within 3 hours 1/2 of rebleeds occur within 6 hours After the first day, the subsequent risk is 1.5% daily for 13 days Facilitates treatment of any future vasospasm by allowing higher arterial blood pressure and volume expansion without danger of aneurysm rupture Reduction in overall patient mortality and reduced likelyhood of severe neurological deficit with early intervention (see here)

Therapeutic options include: 1. Endovascular management by interventional neuroradiology Thrombosis of the aneurysm via coiling is most commonly used. Thrombosis by flow diversion, trapping and proximal ligation are other endovascular strategies for securing aneuryms (though less commonly used) 2. Microvascular neurosurgical intervention “Clipping” is the surgical gold standard and by far the most common strategy to secure and aneurysm surgically Other methods including wrapping or coating the aneurysm (not preferred and less common)

Clipping vs coiling Treatment choice will depend on aneurysm and patient characteristics Multi-disciplinary decision ideally made at centre where both options feasible within 24 hours of ictus There have been four major trials conducted comparing the two methods. The largest of these (ISAT 2002) suggested coiling is preferable (if feasible) due a reduced risk of poor outcome (MRS >2; ARR 7%) Other factors to consider include Technical complications: higher in clipping (19% versus 8%) Late re-bleeding rates: higher in coiled patients (2.9% vs 0.9% after clipping) Complete obliteration of aneurysm higher in clipping (81% versus 58% after coiling) Coiling also associated with lower risk of subsequent epilepsy and cognitive decline and decreased hospital length of stay Coiling generally prefered if: Older Patients Low neck:dome ratio (thin neck) Significant comorbidities Basilar or posterior communicating artery aneurysms (hard to clip) Patient is on anticoagulation Clipping generally preferred if: Younger patients (less risk of recurrence later in life) If a craniotomy is happening anyway e.g. for significant clot evacuation Multiple suitable aneurysms MCA, ACA, and sometimes proximal ICA (easiest to reach) Other factors to consider Health care environment / equipment available Skill set and experience of the neurosurgeon / neurointerventionalist

The basic steps are: Prepare the patient Perform a craniotomy Expose the aneurysm Insert the clip Check the clip Close the craniotomy More here Here’s one surgeon’s approach to clipping an aneurysm:

Pain and anxiety must be treated, for obvious reasons as well as to avoid hypertension and rebleeding. For non-intubated patients analgesics like paracetamol, tapentadol and opiates usually suffice; NSAIDs may be useful but the slight effect on platelet function risking bleeding should be considered. Intubated patients usually receive opiate (fentanyl) infusions titrated to pain Sedation is different to analgesia and intubated patients usually require propofol infusions to tolerate the endotracheal tube. Nausea should be aggressively treated as vomiting raises blood pressure and ICP

There is a paucity of high quality evidence guiding nutrition post-SAH. There is weak evidence that patients with SAH have an increased resting energy expenditure, with potential benefits of high protein diets with adequate minerals for neurofunctional recovery existing (1, 2). Given this, ensuring adequate caloric intake with good amounts of protein and minerals is likely suitable in post-SAH patients until better evidence becomes available.

Patients with aSAH are at increased risk of developing a DVT or PE Mechanical thromboprophylaxis is commenced in all patients prior to securing aneurysm. Subcutaneous heparin/clexane is commonly commenced after the aneurysm is secured (in consultation with Neurosurgery). Recent evidence would suggest that mechanical thromboprophylaxis (with pneumatic calf compression devices) provides no additional benefit to chemoprophylaxis alone for most ICU patients. Hence, mechanical devices can likely be ceased following commencement of chemoprophylaxis. The decisions surrounding thromboprophylaxis are centre/surgeon specific, so best to follow your instituitions practice.

Patients are commonly nursed in a head up (>30 degrees) position where possible. For Weak evidence suggests this is associated with reduced risk of ventilator associated pneumonia (VAP). There is some suggestion that having the head at 20-30 degrees improves ICP, so may have some role in patients with intracranial hypertension. Against Despite several small exploratory studies, no head position has been shown superior over another, in terms of maximising cerebral blood flow and minimisng vasospasm or most importantly – patient outcome. Similarly, there is no strong evidence demonstrating superiority of head up positions in other aspects of neurocritical care Although there is no convincing evidence for this practice, in the absence of high quality research, a head up position of 20-30 degrees is likely not to be harmful and has some potential to minimise VAP and may reduce ICP

Stress ulcer prophylaxis (SUP) with a PPI or H2RB is given to most ICU patients SUP with pantroprazole reduces clinically important GI bleeding in ICU patients (see SUP-ICU trial) H2RB may have benefits over PPI for SUP (see PEPTIC trial) though best to follow your local guidelines for which agent to choose

No strong evidence exists for BSL control in aSAH patients alone. However, strict glycaemic control has been shown to have worse outcomes for ICU patients in the landmark NICE-SUGAR trial. Extrapolating from the NICE-SUGAR trial is probably safe in the absence of alternative evidence, so best to aim between 6 mmol/L and 10 mmol/L.

The optimal haemoglobin threshold for transfusion in SAH is still under investigation and will hopefully be clarified in the SAHARA trial which is ongoing at present Current thinking (in absence of SAHARA trial data) <80 transfuse (to increase DO2) 80-100 site/clinician/patient factor dependant >100 avoid tranfusion: liberal transfusion may be associated with worse outcomes (secondary to increased blood viscosity and cerebrovascular ressistance) Watch this space!

Aim  for high normal oxygen saturations in all patients, particularly if at risk of vasospasm. Aim for normocarbia in ventilated patients (prophylactic hyperventilation may exacerbate cerebral vasospasm) For some patients with chronic respiratory disease and a hypoxic respiratory drive, a lower oxygen saturation target may be appropriate

Corticosteroids Corticosteroids are not required unless there is evidence of adrenocortical insufficiency Statins No evidence of benefit Magnesium No evidence of benefit

Trial eligibility Its always good to check with your department whether the patient is appropriate for enrolling in trials Ceilings of care Always important to have ongoing conversations surrounding goals of treatment / ceilings of care.

The only medication that has been shown to improve neurological outcomes following aSAH (33% RRR of poor neurological outcome). So great we’ve made a separate page about it if you’re interested: NIMODIPINE In brief Can be given orally or intravenously Standard nimodipine dosing is 60mg every 4 hours PO or 20 mcg/kg/hr (1 ml/10 kg body weight) IV for 21 days Although preferentially selective for cerebral vessels, patients often  have some hypotension related to peripheral vasodilation. Hence patients may require noradrenaline and intravenous fluids to maintain blood pressure targets whilst on nimodipine. Nimodipine is not indicated in traumatic SAH.

Aim: Avoid hypotension to prevent vasospasm and maintain cerebral perfusion pressure Avoid hypertension which will increase the risk rebleeding from an unsecured aneurysm There is no firm evidence for optimal BP targets, however the values below are reasonable aims 100-140 mmHg prior to securing aneurysm 120-150mmHg following securing of aneurysm 140-160mmHg if radiological vasospasm confirmed on DSA For hypotension Use isotonic crystalloid to achieve euvolemia If low BP and euvolemic then IV noradrenaline is appropriate For hypertension Short acting anti-hypertensives including hydralazine and clevidipine are reasonable agents. Avoid glyceryl trinitrate and other vasodilators which may increase ICP As always, follow local guidelines/policies.

Aims: Maintain euvolemia Avoid hypovolemia: increased risk of vasospasm Avoid fluid overload which worsens mortality, causes pulmonary oedema and other organ dysfunction Choice of fluid 0.9% saline or other isotonic fluids such as Plasma-Lyte 148 are reasonable fluid choices Hartman’s (CSL) and other hypotonic fluids should be avoided. Adjust for fluid balance, fluid status and electrolytes.

Hyponatraemia commonly occurs post SAH (up to 50% patients) and most likely causes are cerebral salt wasting and SIADH, although differentiating these makes little difference Hyponatraemic patients have increased relative risk (x3) of DCI Given how common hypontraemia is and the associated complications, sodium need to be monitored closely. Na is often monitored daily following an acute aSAH though may be monitored more frequently if hyponatraemia ensues. Aim: Prevent serum Na < 135 mmol/L while maintaining euvoleamia Management strategies Minimise free water intake (e.g. allow only fluids containing sodium) Aim for euvolemia (note: fluid restriction increases risk of hypotension and vasospasm and has no role in post SAH hyponatraemia) Replace sodium with hypertonic saline (e.g. 30 ml/h 3% HTS) or salt tablets (e.g. 1200 mg TDS) Fludrocortisone (e.g. 0.1-0.2 mg BD) may prevent natriuresis if hyponatremia persists. For refractory cerebral salt wasting consider oral urea (e.g. 15 g PO BD)

Fever is an independent risk factor for poor outcomes and development of secondary brain injury. Aim Normothermia (36-38C) Management strategies Paracetamol Exposure and surface cooling techniques (e.g ice packs, fans, cooling blankets, non-invasive precision temperature management systems) Consider NSAIDS, taking into account potential for anti-platelet effects affecting intracranial bleeding, renal injury and GI bleeding risks Note: fever may also represent infection and septic workups should be completed for febrile patients.

Delirium is common and preventative strategies should be implemented. Delirious patients are at greater risk of pulling out their essential lines and tubes or causing these to become infected. Management of delirium may require physical and pharmacological measures.

Seizure Prophylaxis Seizure-like episodes are common (up to 1/3), though are thought to not be epileptiform in origin and may be the result of the sudden rise in ICP No RCT has been performed to help guide decisions on prophylaxis or treatment of seizures. As such, there is no consensus regarding The need for anti-epileptic drugs (AEDs) The best AED to use Which patients should receive prophylactic AEDs The optimal dose or duration of treatment. Risk factors for post-SAH seizures: Increasing age (> 65 years) MCA aneurysm Volume of subarachnoid blood/thickness of clot Associated intracerebral or subdural hematoma Poor neurological grade Rebleeding Cerebral infarction Vasospasm Hyponatremia Hydrocephalus Hypertension Treatment modality, see coiling vs. clipping Which anti-epileptic drug? Levetiracetam is slightly less effective than phenytoin for short term seizure control but may carry better long term outcomes and fewer side effects. If a prophylactic AED is deemed appropriate, levetiracetam 500 mg BD for 7 days is a popular, albeit non-evidence based regimen.

The risk of rebleeding is greatest within the first 24 hours (up to 15%) for unsecured aneurysms The mainstay of prevention is therefore prompt securing of the aneurysm (clipping or coiling) as previously discussed Bed rest and hyperdynamic therapy (hypertension, haemodilution, hypervolaemia)  does not prevent this Antifibrinolytic therapy (e.g. tranexamic acid) has been shown in one non randomised study to reduce incidence of early rebleeding when there is a delay in securing an aneurysm (e.g. patient transfer to a neurosurgical centre). Currently there is not enough evidence to given this as routine, so have this discussion with the accepting neurosurgical team and follow local practice.

Raised ICP may occur in patients with SAH and is associated with adverse outcome in small studies What is raised ICP? ICP is commonly considered raised if > 22 mmhg Surgical management options for raised ICP Drainage of large blood clots Insertion of an EVD Decompressive craniectomy Medical management options for raised ICP Head positioning, as previously discussed, may have some role. Avoiding jugular compression by maintaining inline head position, avoiding restricting neck ties etc Sedation and paralysis Osmotherapy (mannitol, hypertonic saline) Barbituate coma The specifics of each of these are beyond the scope of this module, though are covered in depth in the Elevated Intracranial Pressure Module.

A radiological diagnosis showing dynamic narrowing of intracerebral vessels Common: occurs in about 50% of patients admitted to hospital with aSAH (Reference) Peak timing days 3-14 post ictus (days 6-8 highest incidence) Gold standard for diagnosis is by digital subtraction angiogram (DSA) Can also be seen on CT and MR angiography and suspected with transcranial doppler measurement Risk factors include radiological grade of SAH, location and extent of blood, younger age and smoking. May be treated to prevent ischaemia, see DCI below Treatment: Hypertensive therapy, usually with noradrenaline (e.g. Target NISBP 140-160 mmHg); if DCI present, BP target may be guided by symptoms resolution. Intra-arterial verapamil. Allows dynamic assessment of spasm reversibility Less commonly Balloon angioplasty for large vessel spasm refractory to treatment, performed with DSA Intra-arterial papaverine, targeted injection at time of DSA

***to be finished*** A more in depth overview of delayed cerebral ischaemia is covered elsewhere. In brief…

Hydrocephalus is a common complication (approximately 20%) and may be present at admission or occur later on. Acutely it may present with decreased level of conciousness, though many show no signs of this. Factors associated with acute hydrocephalus include Increasing age intraventicular blood, thick focal accumulations of subarachnoid blood posterior circulation aneurysm hyponatraemia, hypertension Management of acute hydrocephalus is usually with EVD insertion, with an ICP aim of 15-25mmHg. Chronic hydrocephalus secondary to aSAH is beyond the scope of this module

What is it? Inflammation of the ventricular drainage systems, usually secondary to bacterial infection of the CSF Patients with an EVD post aSAH, who undergo intracranial surgery, or who have an intraventricular haemorrhage are at increased risk of ventriculitis EVD ventriculitis Increased risk with increased length of insertion usually due to s. aureus and other coagula negative staph. Symptoms/Signs? headache Fever Nausea/vomting Raised ICP / focal neurological signs Investigations Bloods including cultures, CRP, WCC CSF culture and analysis Brain imaging (CT/MRI) Management Removal +/- replacement of EVD if present Intravenous antibiotics according to sensitivies, local antibiotics resistence, micro/ID input Prevention Remove EVDs ASAP Only access the EVD when absolutely necesary with meticulous sterility Antibiotics impregnated EVD catheters may reduce risk.

Treat all acute seizures, as previously covered in this module. If seizures occur, consider future prophylaxis as previously discussed.

To be finished