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Welcome back to the tasty morsels of critical care podcast.
Nestled towards the end of Oh Chapter 51 we have a section dedicated to SAH. Given that a lot of ICU bed days are given over to managing SAH, I felt it might have warranted its own chapter. Indeed, looking at its prevalence in fellowship examinations it does seem that a fair deal of attention should be given to SAH. It stands apart from the usual intracranial bleeding where the typical treatment and discussions are all focussed on supportive care and the the nuance only comes in when you get to BP management. Whereas in SAH you have a whole bunch of interesting and well proven interventions that can improve outcome for the lucky patients who haven’t already prognosticated themselves by presenting with a GCS of 3.
As a starter for 10: in which meningeal space in the brain do you find an SAH? The clue, thankfully is in the name. The space between the brain adhering pia matter and the filmy arachnoid matter is where you’ll find an SAH. This is the space that CSF flows in from it’s genesis in the choroid plexi of the ventricles on its journey to reabsorption in the arachnoid granulations. Also in this space lies the cerebral vasculature that has a tendency to become aneurysmal and rupture arterial blood into this space.
Blood in the sub arachnoid space is easily seen on a simple dry CT scan, particularly in the first few hours. It has now become a test so good that people would suggest that if you have a negative CT in the first 6 hrs then you probably can skip the de rigeur LP that has been all the rage for the past century. Though i’ll admit that that question is delving much more into the realm of EM than hard core crit care.
In a critical care exam type stem you might be faced with someone in their 60s with a history of poorly controlled hypertension, who smokes, takes cocaine and has polycstic kidneys. All of these are identified as risk factors for SAH, though such a combination, i imagine only exists on exams. In the stem they’re likely to have a reduced GCS in the 13-14 range with a BP of somewhere north of 170mmHg. You’ll be given a CT scan showing some diffuse SAH but you’re waiting on an angio etc… Imagine a question like: what are your immediate priorities in management.
Given that 85% of SAH is aneurysmal, and they need definitive treatment likely not available in your hospital then getting that angio done is certainly a priority. But probably more acutely will be the basics of assessments of ABCs with particular attention to getting that BP under control. The biggest risk to life in the first few hours is going to be a rebleed which happens in maybe 20% of patients. Getting the BP down to somewhere south of 160 is likely a good idea with the ubiquitous labetalol probably being the most accessible and available option. Avoid the GTN and the foil wrapped madness of nitroprusside as both can cause a little cerebral vasodilation that you want to avoid. Bonus points for a decent analgesic (which will help the pain) and an antiemetic as vomiting does indeed tend to make the BP spike a little.
The stem continues and the plot thickens. While waiting for the CT angio the patient becomes obtunded gets intubated (where great attention was paid to the heamodynamics). Now the CT shows more blood, some hydrocephalus and a big posterior communicating aneurysm. What now genius?
Hydrocephalus is a relatively common event in SAH and the theory is that blood in the CSF space blocks up the arachnoid granulations preventing reabsorption and with ongoing production and failure to reabsorb you get hydrocephalus. There may be other reasons including a clot in one of the intricate drainage canals in the brain but either way you get more CSF than you want with a concomitant rise in ICP that quickly becomes life threatening if not drained with an EVD. Now if you’re a neurosurgeon and someone gives you the story of GCS 13-14 with SAH and an aneurysm your interest is definitely piqued but this is likely to be a transfer within 24 hrs to get some coiling done but is unlikely to require any surgery per se by the neurosurgeon at 3am. However if you give them that same story but now add some hydro and a falling GCS you have the type of thing that will buy your patient an emergency blue light transfer over to the OT in the neurosurgical centre.
So what’s going to happen with the aneurysm? Assuming we keep the BP under control and correct any coagulopathy then it needs secured. If possible this should be done by a neurointerventionalist with a coiling procedure, and not by craniotomy and clipping of aneurysm. This is now well defined and supported by randomised controlled level evidence. Given the complexity of these procedures the timescales provided for which it has to be secured is generally in the 24-48hr range and this allows them to be done as day time procedures most of the time.
The scene fades and the time jumps and the question stem now is in the ICU on day 5. On your daily sedation break it is noted the patient is not moving the left side. What pray tell is this new calamity? Has the poor soul now had a big embolic stroke in addition to his SAH? While this is definitely cerebral ischaemia it is not stroke and instead rejoices in the name of “Delayed cerebral ischaemia” or DCI to its friends or “vasospasm” to the people it knew in high school but haven’t bothered to stay in touch. DCI is a clearly recognized phenomenon in SAH patients and is typically found to co exist with the radiological phenomenon of vasospasm where the artery spasms and has reduced flow. Vasospasm itself is very common in up to 70% of SAH patients but only about 30% of vasospasm is DCI. DCI requires a focal deficit or drop in GCS in addition to imaging findings of ischaemia.
The typical response in days of yore would have been “triple H therapy” consisting of hypervolaemia, hypertension and high haemoglobin. Over the passage of years the only remaining tenet of the grlorious trio is induced hypertension which does seem to have some kind of effect on improving those ischaemic symptoms. Don’t be surprised to find your neurosurgeons requesting MAP targets like 90 or 100mmHg in these scenarios. The single best treatment for DCI we have is actually a prophylactic treatment in the form of the calcium channel blocker nimodipine. 60mg given 4 hrly is the standard recommended from day of rupture given for 3 weeks or so. It’s not entirely clear how this works but it’s fairly clear that it does. lastly it’s worth noting that DCI is not a day 1 concern for your SAH patient with incidence peaking in the 4-10 day range.
As a broad overview Oh Chapter 51 covers all the bases.