Everything that makes this room hard is about distance — from the patient, from help, from the drugs you did not bring. And when the catastrophe comes it arrives in one of two forms that look identical and want opposite blood pressures. The good news is that you are standing in the only place in the hospital where the test that tells them apart is already inside the patient.
An intracranial catastrophe in the angiography suite is either haemorrhagic or occlusive, and the two managements are opposites. Haemorrhagic: reverse the heparin immediately — 1 mg protamine per 100 units of heparin given — and hold a low-normal mean arterial pressure. Occlusive: deliberate hypertension, titrated to the neurological examination or the angiogram. Guessing has a fifty per cent chance of making it worse, which is why the first action is not a drug but a question to the team running the images that will answer it.
Neuro 2 day 05 already brought you here once, for thrombectomy. This day is about the room itself — the other procedures done in it, and the fact that the room is the problem.
The chapter names what an anaesthetist is for in this suite, and the list is short: keep the patient immobile so the images are usable and catheter-related complications are avoided; manage the physiology the procedure requires; and be ready for the complications, which are the ones a catheter in a cerebral vessel can cause.
Everything below is one of those three.
Assume the X-ray machine is always on. The practical rule that follows is specific and easy to forget: ask the interventionalist whether fluoroscopy is running before you reach toward the patient’s head.
Three sources of exposure: direct radiation from the tube, leakage through the collimators’ shielding, and scatter reflected off the patient and the surrounding area. Exposure falls with the inverse square of distance, which makes distance the single best protection available — and it is the one thing the layout of the room usually gives you for free.
Digital subtraction angiography delivers considerably more radiation than fluoroscopy, so the moments when the pictures matter most are the moments to step back.
Protection is a lead apron, thyroid shield, eye protection and an exposure badge, with a movable lead glass screen if the suite has one. Aprons need periodic inspection for cracks in the lining. Eye protection deserves particular thought for anyone working regularly in the suite. And clear communication between the two teams is named as crucial to limiting exposure — with proper precautions, the anaesthesia team should be well under the annual recommended limit.
Every practical decision here is shaped by distance.
Intravenous access needs extension tubing long enough to give drugs and fluid at maximal distance from the C-arm and the detector during fluoroscopy.
Airway access is limited by table and room logistics, so a sedation case requires an honest assessment of how you would perform laryngoscopy here rather than in an operating theatre. One specific trap: a recent pterional craniotomy can impair temporomandibular joint mobility, so a patient who was easy last month may not be.
Monitoring is standard, with capnography sampled from the nasal cannula port during sedation. For intracranial work, an arterial line for beat-to-beat pressure and sampling. The femoral sheath side port can be used, but the sheath usually comes out at the end of the case, so a separate radial line is convenient if pressure monitoring will be needed afterwards. A reasonable compromise is to use the side port immediately to avoid delay and place a conventional line during the procedure.
A useful piece of interpretation: with a coaxial or triaxial system, pressures can be measured at the carotid, the vertebral and the distal cerebral circulation. Those distal catheters underestimate systolic and overestimate diastolic pressure — but the mean is reliable. Use the mean.
A bladder catheter earns its place, because a significant volume of heparinised flush and contrast goes in.
Practice varies among centres with no clear superior method. General anaesthesia is chosen to minimise motion artifact, improve image quality and reduce catheter-induced complications. Sedation is chosen to permit neurological assessment — and can be converted to general anaesthesia if further treatment is needed or the patient cannot stay still.
If the patient is sedated, they will feel things: contrast injected into the cerebral arteries burns, and distension or traction on the vessels causes headache. Lying motionless for a long period is itself uncomfortable, so pressure points are padded and positioning is negotiated with the patient before the drapes go on.
Under general anaesthesia, ventilate to normocapnia or modest hypocapnia consistent with safe positive-pressure ventilation, unless intracranial pressure is a concern. There is no clear superiority of one modern anaesthetic over another for pharmacologic protection against neuronal injury; total intravenous or combined techniques may optimise rapid emergence.
There is a case for avoiding nitrous oxide: the possibility of introducing air emboli into the cerebral circulation, and reports that it worsens outcome after experimental brain injury.
And a rule for patients who arrive already hyperventilating — whether by the intensive care unit’s design or their own injury: maintain PaCO₂ at or below the pre-procedure level. Do not “correct” it upward.
Heparin at approximately 70 units/kg after a baseline activated clotting time, targeting 2 to 3 times baseline, then infusion or intermittent bolus with hourly activated clotting times.
Two failure modes worth recognising rather than fighting. Apparent refractoriness may resolve by switching bovine heparin to porcine or the reverse. Suspected antithrombin III deficiency may need fresh frozen plasma.
Heparin-induced thrombocytopenia turns anticoagulation into a prothrombotic syndrome, and the alternative is a direct thrombin inhibitor — which inhibits both free and clot-bound thrombin and can be monitored by activated partial thromboplastin time or activated clotting time. Bivalirudin has a half-life of about 25 minutes and lepirudin 40 to 120; both are renally eliminated and need adjustment in renal dysfunction. Argatroban is the hepatically metabolised alternative. Anaphylaxis is an inherent risk of the class.
Antiplatelet agents are increasingly used in cerebrovascular disease and may have a role in treating thromboembolic complications acutely, though this remains controversial. Abciximab has been used for that purpose.
Reversal, which is the part to know cold before the case rather than during it:
| Agent | Reversal |
|---|---|
| Heparin | Protamine, 1 mg per 100 units of heparin given |
| Dabigatran | Idarucizumab |
| Apixaban, rivaroxaban | Andexanet alfa |
With the caveat the source attaches: expense and availability limit these in many countries, and their safety and efficacy remain to be further investigated.
Allergy. There is no difference between older and newer agents in the propensity to cause anaphylactoid reactions. A significant history is pretreated with steroids and both H₁ and H₂ blockers.
Kidneys. This is a place where the honest answer changed. Renal function should still be evaluated, because contrast agents are nephrotoxic, particularly where function is already impaired. But routine prophylaxis has been abandoned on trial evidence:
Current guidance from the American College of Radiology and the National Kidney Foundation, and from the Canadian Association of Radiologists, suggests 0.9% saline as an option only for non-dialysis patients with eGFR below 30 mL/min/1.73 m² or acute kidney injury, with bicarbonate equivalently supported by local protocol or convenience, and discretionary prophylaxis for high-risk individuals with eGFR 30 to 44.
The wider lesson is one this curriculum keeps meeting: a plausible mechanism, a long-standing habit, and a trial that removed it.
Deliberate hypotension has exactly two indications here:
The agent matters less than the ability to reach the target quickly and safely while keeping the patient stable — and, if the patient is awake, without interfering with neurological assessment. Nicardipine or sodium nitroprusside infusions are typical. Adenosine, used in aneurysm surgery to induce a transient cardiac pause, is a viable method of partial flow arrest. Direct intra-arterial pressure monitoring is required throughout.
Deliberate hypertension is used when a vessel is acutely occluded or in vasospasm, because raising the systemic pressure is the only practical way to raise collateral perfusion pressure — during emergency thrombolysis, for instance.
Deliberate hypercapnia has one specific indication that is worth knowing because it inverts everything else in this curriculum: embolisation of extracranial vascular malformations that drain into the intracranial venous system. Inducing hypercapnia promotes high venous outflow from the cerebral venous system and helps keep embolic material from moving the wrong way, into the intracranial compartment.
The collateral supply is central to this day and to Neuro 2 day 08, and the book’s two chapters give different numbers for it.
Chapter 16 states that a complete circle of Willis is present in only 15 to 20% of people. Chapter 14 states that in as many as 21% of otherwise normal subjects the circle may not be complete. Those are close to being reciprocals of each other: one implies most people lack a complete circle, the other implies most people have one.
Neither matches the primary literature. MR angiography in 150 healthy volunteers found an entirely complete circle — both anterior and posterior parts — in 42%, slightly more often in younger people and in women.
Three numbers for one anatomical question, and the resolution is almost certainly definitional: “complete” is not one thing. Whether a component need only be present or must also be of normal calibre; whether the anterior and posterior parts are scored separately or both required; and what the imaging can resolve — each moves the figure, and none of the three sources states its criterion in the same terms as the others. Neither chapter says which it used, so this curriculum quotes the primary study and declines to arbitrate between two textbook paragraphs that do not define their term.
What both chapters agree on is the part that governs behaviour: the circle of Willis is the primary collateral pathway, its configuration varies, and you cannot assume this patient’s works. There are also secondary collateral channels bridging adjacent vascular territories — the pial-to-pial or leptomeningeal pathways carried by the long circumferential arteries over the hemispheric convexities — which are part of why some patients tolerate occlusion better than their circle would predict.
The practical instruction survives the disagreement intact: look at this patient’s imaging, and discuss the collateral supply with the person who has seen it.
The femoral route has limitations that shape the aftercare: bed rest for 5 to 6 hours unless a percutaneous closure device is used, and the risks of retroperitoneal haematoma, femoral nerve damage, pseudoaneurysm and limb claudication. Those limitations are what have driven interest in radial and direct carotid access.
And one late complication belongs to the arteriovenous malformation patient specifically: normal perfusion pressure breakthrough, where territory that has been chronically hypoperfused around a shunt is suddenly exposed to normal pressure after the shunt is closed. It is the reason blood pressure after AVM embolisation is a managed variable rather than a number to leave alone.
The environment is the hazard: radiation you cannot see, a patient you cannot reach, and help that is further away than it would be in theatre. All three are addressed before the case rather than during it.
And the crisis has a shape. One appearance, two mechanisms, opposite treatments, and a diagnostic test already threaded into the vessel. The discipline is to spend the first ten seconds asking which one it is, while starting everything that is true of both.
No randomized trial addresses this.
The crisis algorithm is consensus, and the source says so of itself. Box 14.1's own footnote states that these are only general recommendations and doses that must be adapted to the clinical situation and the patient's pre-existing condition, and that less aggressive management may be appropriate for an asymptomatic or minor vessel puncture. It is a structure for thinking under pressure, not a protocol.
The physiology underneath it is not in doubt. That an occluded vessel's territory depends on collateral perfusion pressure, and that raising systemic pressure is the only practical way to raise it, follows directly from the anatomy. So does the reverse: that a ruptured vessel bleeds harder at higher pressure and while heparinised.
One half of this day was overturned by randomized trials, and the reversal is the interesting part. Prophylaxis against contrast-induced kidney injury used to be routine. AMACING found prophylactic hydration non-inferior to none in high-risk patients; PRESERVE found sodium bicarbonate no better than saline and acetylcysteine no better than placebo. The American College of Radiology and National Kidney Foundation now suggest saline prophylaxis only as an option for non-dialysis patients with eGFR below 30 mL/min/1.73 m² or acute kidney injury, with discretionary use between 30 and 44.
And the choice of anaesthetic technique is explicitly undetermined. Practice varies among centres with no clear superior method, and there is no clear superiority of one modern anaesthetic over another for pharmacologic protection against neuronal injury.
The patient deteriorates. Or the interventionalist's face changes. Or the monitor does something. Whatever the trigger, you now have seconds and one decision, and it is not which drug — it is which problem.
If the vessel has ruptured, the patient is anticoagulated to two or three times a normal activated clotting time and every millimetre of mercury is driving blood into the subarachnoid space or the parenchyma. The management is immediate heparin reversal — 1 mg of protamine for every 100 units of heparin given — and a low-normal mean arterial pressure.
If a vessel has occluded, the territory beyond it is alive only on collateral flow, and collateral flow is a function of perfusion pressure. The management is deliberate hypertension, titrated to the neurological examination, the angiogram, or physiologic imaging.
Read those two paragraphs again and notice that every element inverts. Reverse the anticoagulant or leave it. Lower the pressure or raise it. Give each treatment to the other patient and you have chosen the worst available option, twice.
Now the thing that makes this survivable, and it is genuinely unusual.
The diagnostic test is already inside the patient. In almost every other emergency in this curriculum, distinguishing the two possibilities means moving the patient to a scanner. Here the catheter is in the vessel, the contrast is loaded, and the team beside you can see the answer on the screen in under a minute. The source's own algorithm reflects this: the first step is not a drug, it is communicate with the endovascular therapy team, assess whether you need help, and call for it — and then, second, determine whether the problem is haemorrhagic or occlusive.
So the pitfall is not ignorance of the two treatments. It is acting before the question is answered, which is exactly what training pushes you toward. A neurological deterioration produces an immediate urge to raise the blood pressure, and in half of these cases that urge is the injury.
Two smaller traps sit inside the same moment.
The pressure decision is not free in either direction. After subarachnoid haemorrhage, perfusion of an at-risk territory may be critically dependent on collateral pressure, so the source says regimens that may lower blood pressure should be used with great caution even when lowering is correct. And head elevation, the reflex manoeuvre for raised intracranial pressure, lowers cerebral perfusion pressure by the height of the head above the right atrium.
The rest of the algorithm is shared, so start it while you wait. Secure the airway and ventilate with 100% oxygen. Then PaCO₂ appropriate to the setting or otherwise normocapnia, mannitol 0.5 g/kg by rapid infusion, an intravenous agent titrated to burst suppression on EEG, and consideration of a ventriculostomy for treatment or monitoring and of an anticonvulsant. None of that depends on which catastrophe it is, so none of it needs to wait for the answer — and doing it buys the time in which the answer arrives.
One last calibration, from the source's own footnote to the algorithm: these are general recommendations, and for an asymptomatic or minor vessel puncture or occlusion, less aggressive management may be appropriate. Not every event on the screen is a catastrophe. The skill is holding the full response ready while asking whether it is needed.
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During endovascular coiling of an aneurysm under general anaesthesia, the interventionalist reports a problem and the patient's blood pressure rises sharply. What should you do first?
A patient with an eGFR of 55 mL/min/1.73 m² is scheduled for diagnostic cerebral angiography. What prophylaxis against contrast nephropathy is indicated?
During embolisation of an extracranial vascular malformation that drains into the intracranial venous system, the interventionalist asks you to allow the CO₂ to rise. What is the rationale?
That is the whole orientation rule. Fat is bright on T1 and intermediate on T2, cortical bone gives no signal, and flowing blood produces a signal void. The practical summary is that anatomy is better seen on T1 and pathology on T2 — and post-contrast sequences are T1 weighted for exactly the reason given.
Ferromagnetic aneurysm clips are a contraindication; non-ferromagnetic ones are not. The risk from a ferromagnetic object is magnetically induced movement, with dislodgement and injury, and heating — image artefact is the secondary concern. The information you need is in the old operation note, not on any current imaging.