- Rapid Reference 🚀
- Grading scales
- Diagnostic approach
- Management: Neurologic issues
- Management: Non-neurologic issues
- Other topics
- Questions & discussion
SAH initial management:
- Coagulation labs (INR, PTT, fibrinogen).
- Review of any anticoagulant medications the patient is taking.
- CT angiography (CTA).
- Neurointerventional radiology & neurosurgery.
- Consider: aneurysm protection, external ventricular drain.
- Aggressive management of any endogenous or exogenous coagulopathy.
- See chapter on anticoagulant reversal.
blood pressure control (more)
- Usually target MAP below ~110 mm (but may be personalized, based on baseline blood pressure).
- Treat pain immediately, before starting an antihypertensive.
- Have a low threshold to start an infusion (e.g., nicardipine or clevidipine).
- Once stable, add nimodipine if tolerated to prevent vasospasm (ideally 60 mg PO q4hr).
seizure prophylaxis & diagnosis (more)
- Prophylactic levetiracetam for all patients.
- Consider vEEG for comatose patients with possible seizures.
general neurocritical care practices
- Aggressive fever management, with physical cooling if needed.
- Avoid hyponatremia (with aggressive treatment if this occurs) and hypotonic fluid.
- Target normocapnia (check blood gas & trend etCO2 if intubated).
- Chemical DVT prophylaxis is initially contraindicated; use sequential compression devices until the aneurysm is protected.
- Follow magnesium with daily labs & replete PRN.
- Nontraumatic SAH causes ~3% of all strokes.(30516599)
- The age range is broad. With an average age of only 50, SAH affects younger patients more often than most other stroke types.
- Stronger risk factors for aneurysmal SAH include:
- Hypertension, smoking, alcoholism.
- Personal or family history of SAH or another aneurysm.
- Genetic diseases, including polycystic liver/kidney disease, Ehlers-Danlos syndrome, and sickle cell disease.
- Sympathomimetic use (e.g., cocaine, amphetamine).
causes of SAH
- 85% are aneurysmal.
- 10% are perimesencephalic hemorrhages.
- 5% have other causes, including:
- Arteriovenous malformations (AVMs), dural arteriovenous fistula.
- Cerebral sinus vein thrombosis or cortical vein thrombosis.
- Reversible cerebral vasoconstriction syndrome (RCVS).
- Arterial dissection.
- Pituitary apoplexy.
- Sympathomimetic use.
- Cerebral amyloid angiopathy.
- Severe headache is the hallmark symptom.
- Most concerning is a thunderclap headache (usually defined as reaching maximal pain in <1 minute).
- Typically the headache is characterized as “worst headache of life.”
- Headache may begin during exertion or stress.
- Headache persists for hours to days.
- 20% of patients may have had a milder sentinel headache which occurred days or weeks earlier.
- Other common causes of thunderclap headache include:
- Reversible cerebral vasospasm syndrome (RCVS).
- Cervical artery dissection.
- Cerebral venous thrombosis.
- Acute hypertensive crisis.
- Intracerebral hemorrhage.
- Ischemic stroke.
- Pituitary apoplexy.
- Meningeal signs may occur, often developing more gradually (e.g., photophobia, nuchal rigidity, neck pain) and progress to low back pain and radicular pain once the blood settles in the lumbar cistern.
- Elevated intracranial pressure (ICP) is common:
- This may cause nausea/emesis, stupor, or coma.
- If these symptoms are due to hydrocephalus, this should prompt consideration for placement of an external ventricular drain. (more on this below)
- Focal neurological signs:
- These aren't typically a prominent feature, but can occur (e.g., due to mass effect of aneurysm, or dissection of blood into the parenchyma).
- Deficits may include hemiparesis, aphasia, abnormalities of pupils or extraocular movements.
- Compression of the oculomotor nerve (CN3) may result from aneurysms involving the posterior communicating artery, the superior cerebellar artery aneurysm, or the posterior cerebral artery. A frequent complaint associated with this is pulsatile tinnitus.
- Seizure (blood is a cortical irritant).
- Sudden death.
- Pulmonary edema or cardiac arrhythmias.
SAH grading scales
SAH severity is expressed using various scores as shown below. The Hunt & Hess score is easier to apply and more widely utilized than the WFNS score. A weakness of these scores is that the patient's mental status may initially be obtunded by hydrocephalus, followed by rapid improvement after insertion of a ventricular drain. Thus, neurologic status following initial resuscitation and hydrocephalus management may be more important than the patient's initial presentation.
Conventionally, clinical grades 1-3 are often referred to as “good grade” SAH, whereas grades 4-5 are referred to as “poor grade” SAH. This can be a bit misleading, because many patients with “good grade” SAH are quite sick and have a substantial mortality.
performance of noncontrast CT scan for SAH diagnosis
- Noncontrast CT is the standard initial test for possible subarachnoid hemorrhage.
- The sensitivity is nearly 100% within six hours of headache onset, after which time blood starts looking a bit more grey, so the sensitivity may decrease slightly.
- (Pseudo-subarachnoid hemorrhage may occur in patients with dramatically elevated ICP, leading to minimal intracranial blood flow. When this occurs, blood in arteries at the base of the skull can appear hyperdense on CT and mimic SAH.)
causes of diffuse or basal SAH (26046515)
- Blood near the circle of Willis suggests aneurysmal SAH (e.g., blood in the basal cisterns, sylvian fissure, interhemispheric fissure, or interpeduncular fissure).
- Perimesencephalic SAH. (specific imaging criteria suggest this; see section below).
- Arterial dissection.
- Vascular malformation:
- Arteriovenous malformation (AVM).
- Dural arteriovenous fistula.
- Pituitary apoplexy.
- Reversible Cerebral Vasoconstriction Syndrome (RCVS).
- Posterior Reversible Encephalopathy Syndrome (PRES).
- Traumatic Brain Injury (TBI).
- Cerebral venous sinus thrombosis or cortical vein thrombosis.
- Cerebral amyloid angiopathy.
- Coagulation disorders.
- Pial or dural arteriovenous malformations, cavernous malformations.
- Septic embolism from endocarditis leading to mycotic aneurysm.
- Intracranial dissection, high-grade vascular stenosis.
- Moyamoya disease.
- CT angiography (CTA) is highly sensitive and specific (~95%) for aneurysm detection, but may miss very small aneurysms.
- CTA has numerous potential roles:
- (1) For patients who have a SAH, CTA is essential to evaluate for underlying vascular anomalies (e.g., aneurysms, arteriovenous malformations).
- (2) For patients who do not have a SAH, CTA is useful to evaluate for the possibility of Reversible Cerebral Vasoconstriction Syndrome (RCVS) or cervical artery dissection.
- (3) For patients with a thunderclap headache and possible SAH, the finding of an aneurysm may indicate the need for further diagnostic testing (e.g., with lumbar puncture).
- Based on increasing appreciation of the prevalence of RCVS among patients with thunderclap headache, such patients may benefit from CTA regardless of whether the noncontrast CT scan is positive for SAH.
- Broader use of CTA may also be bolstered by evidence that contrast dye is not nephrotoxic.
- A potential drawback of CTA is that it may reveal asymptomatic unruptured aneurysms in ~2% of the population. Thus, it must be borne in mind that detecting an aneurysm without subarachnoid blood is not diagnostic of an aneurysmal subarachnoid hemorrhage. However, detecting unruptured aneurysms may provide an opportunity to advise patients regarding practices that could reduce their risk of aneurysmal rupture in the future (e.g., blood pressure control, tobacco cessation, avoidance of excessive alcohol use, and avoidance of sympathomimetics).
A traumatic tap is common and often cannot be differentiated from SAH in part because most clinical laboratories do not have validated spectrophotometry. -Maher M et al. (31964292)
- Traditionally, LP has been used to evaluate for SAH in patients with negative noncontrast head CT scan who have high suspicion for SAH (primarily if the CT scan was obtained >6 hours after headache onset). In this context, erythrocytes or xanthochromia would support a diagnosis of SAH.
- Xanthochromia refers to the yellow hue noted on CSF that occurs due to RBC breakdown. It develops within 2-4 hours after the acute hemorrhage and should be present after 12 hours. This can be very helpful to make the diagnosis of SAH when the RBC count has downtrended between the first and last tube.
- The only way an LP can be entirely reassuring is if there are zero RBCs and there is no xanthochromia.
lumbar puncture suffers from numerous drawbacks:
- LP is an invasive procedure with risks of infection and hematoma.
- LP can be technically challenging in some patients.
- LP is contraindicated in patients with coagulopathy or those taking antiplatelet agents or therapeutic anticoagulation.
- LP is time-consuming, delaying the diagnosis of SAH.
- The performance of LP is far from perfect, with sensitivity and specificity in the 85% range.
- It's unclear how to optimally differentiate between SAH and a traumatic LP (falling numbers of RBCs from tube #1 to tube #4 can be seen with both a traumatic tap and a SAH; various articles disagree about optimal RBC cutoffs for tube #4).
Due to uncertainty in the interpretation of LP results, LP for the diagnosis of SAH is controversial.(34030777) The routine use of LP is gradually falling out of favor, primarily for two reasons:
- (1) With ongoing, perpetual improvements in CT scanning technology, fewer hemorrhages will be missed by CT scan. The seminal Perry study showing that CT scan sensitivity decreased after six hours was performed between 2000-2009.(21768192) CT scanners have improved a lot in the past fifteen years, so this data probably doesn't apply to modern scanners.
- (2) There is increasing recognition that many patients with thunderclap headache have RCVS, a diagnosis that requires CT angiography. Thus, patients presenting with thunderclap headache may benefit from CT angiography even if the LP is negative. Such patients may be better served by receiving both a CT and CTA immediately. If both the CT and CTA are negative, then SAH can generally be safely excluded.(30881537) However, some centers may still complete an MRI to be entirely certain, especially in more subacute presentations.
In some patients, LP may be required to exclude CNS infection (e.g., patients presenting with a more gradual-onset headache, or other features suggestive of infection).
MRI & MRA
- MRI/MRA overall has similar performance compared to CT +/- CTA. However, MRI is limited by logistic constraints as the initial diagnostic test.
- (1) Diagnosis of subarachnoid hemorrhage:
- FLAIR is sensitive in the acute phase of SAH, showing sulcal hyperintensity.(31485117)
- Sequences that detect hemosiderin (GRE and SWI) may be better than CT scan for subacute or chronic SAH.(30516599) These sequences become more sensitive for SAH detection over a period of days, rendering MRI a potentially attractive option for patients who present late and have a negative CT scan.
- MRI sensitivity increases from ~94% in the acute phase to ~100% in the subacute phase.(11160469)
- (2) Detection of underlying pathology:
- MRI can be useful to detect subtle underlying pathology (e.g., arteriovenous malformations, infections, malignancy, or inflammatory disorders).(30516599)
- For patients with SAH near the base of the brain and no defined source of bleeding, cervical spine MRI may be useful to evaluate for a spinal source of bleeding.
- (1) Diagnostic role:
- Invasive angiography is the gold standard for detection of aneurysms or cerebral vasospasm.
- For patients with a SAH and no evidence of an aneurysm on CT angiography, an invasive angiogram may be performed to further exclude the presence of aneurysms or other vascular causes of bleeding.
- (2) Interventional role:
- Following initial SAH diagnosis, angiography may allow for interventional embolization of aneurysms, to prevent rebleeding. This can be done via coils, stent-assisted coiling (usually deferred in the acute setting due to the need for dual antiplatelet therapy), or newer WEB devices (woven mesh devices designed to minimize the need for stents).
- For patients with post-SAH vasospasm, angiography may allow for local infusion of vasodilators and angioplasty.
overall diagnostic algorithm
- For patients with thunderclap headache, a reasonable diagnostic strategy might be to perform a STAT noncontrast CT scan followed immediately by a CTA of the head and neck. CT/CTA is fast, noninvasive, and safe (remember that contrast nephropathy doesn't exist). This combination provides an immediate wealth of information about possible diagnostic possibilities (especially SAH, RCVS, arterial dissection, arteriovenous malformation, or intraparenchymal hemorrhage). For patients with SAH, immediate vascular imaging will help fast-track patients to prompt neurointervention, to prevent rebleeding.
- If CT/CTA leaves remaining confusion about the possibility of SAH, then lumbar puncture and/or MRI/MRA may be considered. MRI may be especially useful if there is concern regarding other underlying brain or cervical spine pathology, such as CNS vasculitis or malignancy.
- Traditionally, the approach to thunderclap headache has focused narrowly on ruling SAH in or out. As we learn more about other vascular pathologies (e.g., cervical arterial dissection and RCVS), it's becoming clear that simply evaluating for SAH isn't enough for these patients. With ongoing improvements in CT scanning technology, a CT/CTA strategy may offer patients a rapid evaluation for numerous vascular pathologies – not just “rule-out SAH.”
approach to neurological deterioration in a patient with known SAH
Differential diagnosis and approach need to be tailored to an individual patient, but common concerns include the following:
common causes of neurological deterioration
- Aneurysm rebleeding:
- Risk highest early on.
- Deterioration is often rapid & dramatic.
- Rebleeding increases mortality almost two-fold.
- Hydrocephalus with elevated intracranial pressure (ICP).
- Early hydrocephalus is very common, immediately following SAH.
- Late hydrocephalus may occur as well, due to dysfunction of arachnoid granulations in reabsorbing CSF.
- Delayed cerebral ischemia:
- May occur after 3-14 days, peak ~7-10 days.
- Deterioration is often gradual and somewhat subtle.
- Shock or hypotension (with subsequent inadequate cerebral perfusion pressure).
- Takotsubo cardiomyopathy.
- Central adrenal insufficiency.
- Medication effect (e.g., sedation).
- Infection (e.g., ventriculitis following ventricular drain placement).
- High fever (e.g., central fever).
- Metabolic derangements (e.g., hypoglycemia, hyponatremia, hypercapnia, uremia).
evaluation may include:
- Review of data:
- Review recent electrolytes.
- Review fever curve.
- Review glucose trends.
- Review ICP trends if available.
- Review medication history, focusing on neuroactive medications.
- Obtain laboratory studies as appropriate:
- STAT fingerstick glucose (if a recent glucose isn't available).
- Repeat electrolytes if not recently measured.
- Consider blood gas measurement if hypercapnia or hypocapnia are suggested by a review of etCO2 trends and minute ventilation.
- Bedside examination:
- Neurological examination.
- POCUS evaluation of the optic nerve sheath diameter to evaluate for ICP (if no ICP monitor is in place).
- Studies to consider:
- CT scan is useful to evaluate for hydrocephalus, intracranial hemorrhage, or aneurysm rebleeding.
- CT scan + CT angiography may be useful if delayed cerebral ischemia is possible.
- EEG may be considered to exclude nonconvulsive status epilepticus.
prevention of rebleeding
rebleeding: the problem
- Rebleeding occurs in ~15% of patients. When it occurs, the mortality rate is enormous (~40%).
- Most rebleeding (50-90%) occurs within the first six hours following admission.(30516599)
- Risk factors for rebleeding include:
- Poor grade SAH.
- History of a sentinel bleed.
- Large aneurysm.
- Antiplatelet medications or another coagulopathy.
- Greater duration of time to aneurysm treatment.
- Laboratory studies should be obtained (e.g., INR, PTT, fibrinogen, possibly TEG with platelet mapping in more complex situations).
- Home medications should be reviewed (including over-the-counter aspirin).
- Any coagulopathy (based either on history or laboratory studies) should be aggressively reversed. More on emergent reversal of coagulopathies here.
blood pressure control
- There is no solid data on Bp targets:
- Adequate blood pressure to perfuse the brain is needed (with hypotension being particularly dangerous).
- Excess blood pressure could potentially encourage aneurysmal rebleeding.
- Adequate analgesia is always essential, both for comfort and for blood pressure control. Pain should be rapidly treated prior to initiation of antihypertensives, as analgesia alone will often reduce the blood pressure.
- Guidelines recommend typically targeting a SBP <160 (American Heart Association) or MAP < 110 mm (Neurocritical Care Society). However, these targets may be personalized when the patient's baseline blood pressure is known. If the patient is conscious, blood pressure may be correlated with mental status (e.g., if reducing the blood pressure causes a mental status deterioration, then antihypertensives may be held to determine if the mental status will improve at a slightly higher pressure).
- Continuous antihypertensive infusions may be useful initially (e.g., nicardipine or clevidipine).
- After the aneurysm has been clipped or coiled, blood pressure targets may be liberalized (e.g., allowing the SBP to rise up to <200 mm). Permissive hypertension may theoretically reduce the likelihood of symptomatic vasospasm.
antifibrinolytics (tranexamic acid)
- The ULTRA RCT of early tranexamic acid failed to show benefit in clinical outcomes (with a trend that actually seemed to favor placebo).(33357465) This is a large, modern, multicenter RCT which should guide our practice.
- Tranexamic acid may be considered for occasional patients with challenging coagulopathies (e.g., hyperfibrinolysis revealed on thromboelastography) or in those whose aneurysm management needs to be delayed (e.g., patients requiring long distance inter-hospital transfer).
- The ISAT trial demonstrated that endovascular coiling generally yields superior outcomes compared to neurosurgery.(16139655) Ongoing advances in neurointerventional radiology are continuing to improve patient outcomes following aneurysm coiling.
- In most centers, neurointerventional radiology and neurosurgery discuss the aneurysm’s amenability to coiling vs. clipping, which will depend on the aneurysm’s configuration, size, anatomy, presence of a neck, and location. Since ISAT, if the optimal management modality is equivocal, neurointervention is usually preferred.
- Clipping is sometimes completed if the surgery may offer an additional added benefit (e.g., can leave craniectomy flap off due to swelling, or for hematoma evacuation causing severe mass effect).
- Acute hydrocephalus occurs in ~20% of patients, within minutes to days after hemorrhage.(30516599)
- Clinical features may include reduced consciousness, impaired upgaze, nausea/vomiting, and hypertension. Deterioration may occur gradually, as patients appear increasingly lethargic.
- Serial CT scan can help clarify the diagnosis.
- If CT scans are not readily available (e.g., patient is too unstable to travel to the scanner), other tests may also be considered (e.g., ocular ultrasonography). More on the diagnosis of ICP elevation here.
- Hydrocephalus may resolve spontaneously in about a third of patients, but those experiencing symptoms from their hydrocephalus will need intervention.
- External ventricular drain is the treatment of choice. Historically, there was some concern that drain placement could eliminate a tamponade effect of the CSF on the aneurysm, and thereby promote rebleeding. This does not seem to be the case. However, before aneurysm protection is in place, the drain will often be managed gingerly (e.g., kept at a level of 20 cm water above the tragus or outer canthus, to prevent excess drops in intracranial pressure). Practice varies between institutions, with the neurosurgical team usually managing the ventricular drain.
seizures & seizure prophylaxis
- Nonconvulsive seizures or status epilepticus may occur in ~10% of patients, especially comatose patients.
- Risk factors for seizure include:
- >65 years old.
- Thick SAH on CT scan.
- Intraparenchymal hemorrhage.
- Cerebral infarct.
- Continuous video EEG should be considered for patients with coma or evidence of seizure.
- Seizure prophylaxis should be considered initially:
- 🛑 Phenytoin has been associated with poor outcomes, so phenytoin should not be used. Phenytoin is notable among antiepileptics for its broad range of side effects, so phenytoin is not a favored antiepileptic agent in general.
- Levetiracetam is generally the preferred agent for seizure prophylaxis, based on its safety profile.(33896527)
- Seizure prophylaxis is often continued for roughly 3-7 days. For patients who don't have a seizure, prophylaxis can be discontinued after seizure has been excluded (either via EEG or clinical examination) and the aneurysm has been secured.
- Patients with seizure should be treated in the usual fashion, including longer durations of antiepileptic therapy. More on the treatment of status epilepticus here.
vasospasm & delayed cerebral ischemia
- Vasospasm is the leading cause of morbidity among patients who survive their initial SAH.(30516599)
- Vasospasm occurs 3-14 days after SAH, with a peak risk around days 7-10.
- Risk factors:
- More severe SAH (e.g., greater thickness of blood in the subarachnoid space).
- Intraventricular hemorrhage.
- Younger age.
- The Modified Fisher Scale may be used to estimate the risk of symptomatic vasospasm (table below).
- Only about half of patients with vasospasm have tissue ischemia with neurological deterioration (termed “symptomatic vasospasm” or “delayed cerebral ischemia”). If vasospasm does not cause neurological deterioration, then it can often be observed without treatment.
- Clinically, patients with delayed cerebral ischemia may deteriorate gradually with nonspecific symptoms (e.g., lethargy or behavioral changes).
prevention of delayed cerebral ischemia
- (1) Nimodipine (a calcium channel blocker):
- Class I evidence supports an improvement in clinical outcomes (although, curiously, nimodipine hasn't been shown to affect angiographic vasospasm – it's possible that it affects smaller caliber vessels).
- The usual dose of nimodipine is 60 mg q4hrs for 21 days, but this may be reduced in patients with borderline hypotension (e.g., to 30 mg q2hr or q4hr).
- (2) Maintenance of euvolemia.
- (3) Maintenance of normal magnesium levels.
diagnosis of delayed cerebral ischemia (a.k.a., symptomatic vasospasm)
- Detection of vasospasm:
- Transcranial Doppler (TCD) may be used to surveil for the development of vasospasm. Comparing flow velocities between vessels may improve specificity (Lindegaard ratio). Performance may vary between operators.
- Continuous EEG: Alpha: delta decreases, alpha power, or alpha variability have been used to predict the onset of vasospasm, up to three days before the onset of vasospasm.(9546487)
- CT angiography may be performed rapidly and noninvasively, with high sensitivity and specificity. It can simultaneously exclude many alternative diagnoses (e.g., hydrocephalus). However, travelling with the patient and cumulative radiation exposure may limit how often this can be repeated.
- Invasive angiography is the gold standard test for large-vessel vasospasm. However, this is invasive and may not be readily available.
- Diagnosis of vasospasm causing delayed cerebral ischemia
- New onset of focal neurological findings that correlates with vasospasm in the suspected vascular territory is the hallmark of diagnosing delayed cerebral ischemia. This can sometimes be extremely difficult to determine, particularly when patients are comatose.
- A thorough and frequent neurological exam is the best way to determine if vasospasm has progressed to cause delayed cerebral ischemia.
- Exclusion of alternative causes of neurologic deterioration will make it more likely that clinical deterioration is truly caused by vasospasm.
- Neurological improvement following augmentation of blood pressure may support the diagnosis of symptomatic vasospasm (see below).
- An MRI showing areas of ischemic tissue could be used to support a diagnosis of symptomatic vasospasm – however, if ischemia is evident on MRI then it is likely that the window of opportunity to intervene may have been missed already.
management of delayed cerebral ischemia (a.k.a., symptomatic vasospasm)
- Getting started: Avoid hypovolemia and hypomagnesemia.
- (1) MAP elevation to ~20 mm above baseline using norepinephrine or phenylephrine may increase cerebral blood flow.
- If possible, neurological exams should be followed, to determine if this causes clinical improvement.
- (2) Interventional radiology therapy with intra-arterial vasodilator administration and/or angioplasty may be helpful.
- (3) Intrathecal infusion of a calcium-channel blocker (e.g., nicardipine) has been used for refractory vasospasm, although no high-quality randomized data are available regarding this.(30607826)
- Unfortunately, trials involving statins, magnesium, or endothelin-1 antagonists have not shown benefit from these therapies.(24837690, 22633825, 22403047)
- Potential indications for intubation may include:
- Inability to protect the airway.
- Rapidly deteriorating mental status.
- Status epilepticus.
- Refractory agitation, with a need for intubation in order to expedite a safe diagnostic work-up.
- Intubation should be performed with efforts to avoid elevating the intracranial pressure or causing hemodynamic instability. (more on this here)
- SAH may be painful, with ongoing meningeal irritation causing headache.
- NSAIDs should generally be avoided due to risks of coagulopathy and renal dysfunction (at least until the aneurysm is secured).
- Scheduled acetaminophen may be helpful (e.g., 1 gram q6hrs).
- Gabapentin may be useful for the pain of meningeal irritation (within a dosing range of ~300-900 mg TID).(25403765)
- Migraine therapies are often useful as well, including antiemetics such as metoclopramide or prochlorperazine, in combination with magnesium infusions and/or diphenhydramine.
- Valproic acid 500 mg IV over 15 minutes may be beneficial in refractory psatients.
- Opioid should be minimized as they are not effective for meningeal pain (e.g., by using PRN boluses for breakthrough pain only).
- More on pain management in critical care here.
- This is very common in patients with SAH, especially more severe SAH.
- More on takotsubo cardiomyopathy here.
neurogenic pulmonary edema
- Intense sympathetic stimulation may promote pulmonary edema via several mechanisms:
- i) Systemic vasoconstriction increases left ventricular afterload.
- ii) Vasoconstriction of pulmonary veins increases hydrostatic pressure within alveolar capillaries.(30516599)
- iii) Takotsubo cardiomyopathy may occur, causing reduced ejection fraction.
- Treatment is generally supportive. Sympathetic tone should normalize over a period of days.
- Central fever (a.k.a., neurogenic fever) is common in SAH. However, SAH remains a diagnosis of exclusion, following evaluation for infection.
- Regardless of the etiology, fever should always be treated aggressively to reduce secondary brain injury (e.g., using acetaminophen +/- physical cooling, as needed).
- Further discussion in the section on central fever.
deep vein thrombosis prophylaxis
prior to aneurysm protection
- Chemical DVT prophylaxis is contraindicated.
- Pneumatic compression devices should be used for DVT prophylaxis.
after aneurysm protection
- When to initiate DVT prophylaxis:
- After aneurysm coiling: chemical DVT prophylaxis may usually be started immediately (but confirm this with the neurointerventional team).
- After surgical clipping: chemical DVT prophylaxis may usually be started after >24 hours (but confirm this with the neurosurgery team).
- Heparin-induced thrombocytopenia is relatively common in this context, with some series reporting rates of 6%.(30516599) The use of low-molecular-weight heparin may be preferable in patients with adequate renal function, because low-molecular-weight heparin causes less heparin-induced thrombocytopenia than unfractionated heparin.
Hyponatremia following aneurysmal SAH is very common, and often a presage to the start of cerebral vasospasm.
potential causes of hyponatremia after SAH
- Cerebral salt wasting.
- Hypovolemia – including cerebral salt-wasting syndrome.
- Adrenal insufficiency due to hypothalamic/pituitary axis dysfunction.
- Pseudohyponatremia (due to mannitol, uncontrolled hyperglycemia, or hypertriglyceridemia from propofol infusion).
- Multifactorial combination of the above etiologies.
- Evaluate volume status.
- Check serum osmolality and cortisol level.
- Check urine sodium and urine osmolality.
- 🛑 Because hypovolemia can precipitate vasospasm, fluid restriction or diuretics should generally be avoided among patients who are within the vasospasm window.
- 🔑 Hypertonic therapy is the front-line therapy for all hyponatremic SAH patients (e.g., 3% saline or ampules of hypertonic bicarbonate, depending on the patient's acid/base status).(18216309)
- Worsening hyponatremia represents a threat to the brain, so this requires a prompt and definitive therapy.
- Hypertonic therapy will be effective regardless of the etiology of the hyponatremia (unlike, for example, isotonic saline – which may work for patients with isolated hypovolemia, but will exacerbate hyponatremia among patients with SIADH).
- Other identifiable problems should be treated as well. However, treating these issues will not lead to prompt and reliable resolution of hyponatremia, so these treatments should not be utilized as the sole therapy for hyponatremia:
- Evaluate and treat for adrenal insufficiency as appropriate. (more on the investigation and treatment of adrenal insufficiency here).
- If there is evidence of hypovolemia, this may be treated with additional administration of isotonic crystalloid (e.g., Plasmalyte). If patients appear to have ongoing salt wasting that requires persistent and large-volume crystalloid resuscitation, then the addition of fludrocortisone may be trialed in efforts to simplify their fluid management, at a dose of 0.1-0.2 mg PO BID. (more on cerebral salt wasting below).
- Sodium levels should be frequently monitored, until stable improvement has been achieved.
cerebral salt wasting syndrome
- Following SAH, some patients develop cerebral salt wasting, which is marked by a combination of:
- (1) Hyponatremia.
- (2) Polyuria causing volume depletion.
- (3) Urine with high osmolality and high sodium concentration.
- The existence of cerebral salt wasting is controversial.(32611661) In particular, it's difficult to sort out this phenomenon from SIADH (which will cause a nearly identical laboratory profile). Different authors have provided drastically different estimations regarding the prevalence of SIADH versus cerebral salt wasting (e.g., some authors state that cerebral salt wasting is common, whereas one series of 100 patients failed to diagnose a single case).(24248182)
- Cerebral salt wasting does seem to be a real clinical phenomenon. The most likely pathophysiology may be aldosterone deficiency, which occurs in some patients with SAH.(12030914, 32501957, 9014912) This would explain the efficacy of exogenous fludrocortisone or hydrocortisone for these patients (as both medications possess mineralocorticoid effects).(17585086, 18268175)
- Treatment of cerebral salt wasting may thus involve a combination of approaches:
- (1) Hyponatremia may be treated with hypertonic therapy (e.g., 3% NaCl).
- (2) Hypovolemia may be managed with simultaneous administration of isotonic fluid and fludrocortisone, as needed to achieve euvolemia. The use of fludrocortisone is recommended by AHA/ACC and NCS guidelines as a strategy to limit natriuresis. The dose range may be 0.1-0.2 mg PO BID. Fludrocortisone can cause hypokalemia, so this may require appropriate potassium repletion.
- Numerous articles claim that the treatment of SIADH involves water restriction +/- diuresis, such that the treatment of SIADH is “opposite” to that of cerebral salt wasting syndrome. This is dangerously misleading. In fact, both SIADH and cerebral salt wasting can be managed with hypertonic therapy – allowing prompt initiation of hypertonic therapy without knowing the precise etiology.(18216309)
perimesencephalic subarachnoid hemorrhage
- Perimesencephalic SAH constitute 10% of all SAH. They result from bleeding from a venous origin, which is centered in the perimesencephalic area.
- These are sometimes referred to as “benign perimesencephalic subarachnoid hemorrhages,” since they do not rebleed and carry a better prognosis than aneurysmal SAH. However, these are quite serious bleeds.
- Findings on noncontrast head CT:(26046515)
- Hemorrhage should be centered anterior to the midbrain or within the quadrigeminal plate cistern.
- Hemorrhage should not extend to the lateral portions of the Sylvian fissure, or to the anterior part of the interhemispheric fissure.
- Some layering of blood in the lateral ventricles may occur, but frank intraventricular hemorrhage should not be seen.
- No parenchymal hematoma should occur.
- Aneurysm should be excluded with CT angiography and/or digital subtraction angiography.
- Management is generally similar to that of a subarachnoid hemorrhage. Initially it may be difficult to differentiate an aneurysmal SAH from a perimesencephalic SAH. Until an aneurysmal SAH has been excluded, it may be wise to treat the patient as if they have an aneurysmal SAH.
- Once a perimesencephalic SAH has been definitively diagnosed, the patient may be treated similarly to a patient with aneurysmal SAH whose aneurysm has been protected (e.g., coiled).
- About 10-20% of SAH patients are not found to have an aneurysm or other vascular process.
- These patients should continue to be managed under the assumption that they have an unidentified aneurysm that ruptured.
- Recent data suggests that up to 10% of those with no identified aneurysm will subsequently be found to have an aneurysm on repeat angiogram.(34184178)
- MRI brain and cervical spine (with and without contrast) can be completed in between angiograms, to continue to search for other underlying pathologies.
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questions & discussion
To keep this page small and fast, questions & discussion about this post can be found on another page here.
- When evaluating a patient with thunderclap headache, be careful of falling into the binary trap of simply excluding SAH. There are other important causes of thunderclap headache (e.g., RCVS).
- Hyponatremia in the context of SAH should be treated promptly with hypertonic saline (with or without additional treatments). Simply providing isotonic fluid or fluid restriction can exacerbate hyponatremia in some patients.
- Connolly et al. 2012 – AHA/ACC guideline on subarachnoid hemorrhage.
- Diringer et al. 2011 – Neurocritical Care Society guidelines on subarachnoid hemorrhage.
- ULTRA (2021) – TXA failed to show benefit in subarachnoid hemorrhage.
- Bradford (2013) – Hypermagnesemia didn't improve vasospasm.
Acknowledgement: Thanks to Dr. Richard Choi (@rkchoi) for thoughtful comments on this chapter.
- 12030914 Espiner EA, Leikis R, Ferch RD, MacFarlane MR, Bonkowski JA, Frampton CM, Richards AM. The neuro-cardio-endocrine response to acute subarachnoid haemorrhage. Clin Endocrinol (Oxf). 2002 May;56(5):629-35. doi: 10.1046/j.1365-2265.2002.01285.x [PubMed]
- 16139655 Molyneux AJ, Kerr RS, Yu LM, et al.; International Subarachnoid Aneurysm Trial (ISAT) Collaborative Group. International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet. 2005 Sep 3-9;366(9488):809-17. doi: 10.1016/S0140-6736(05)67214-5 [PubMed]
- 18216309 Sterns RH, Silver SM. Cerebral salt wasting versus SIADH: what difference? J Am Soc Nephrol. 2008 Feb;19(2):194-6. doi: 10.1681/ASN.2007101118 [PubMed]
- 24248182 Hannon MJ, Behan LA, O'Brien MM, Tormey W, Ball SG, Javadpour M, Sherlock M, Thompson CJ. Hyponatremia following mild/moderate subarachnoid hemorrhage is due to SIAD and glucocorticoid deficiency and not cerebral salt wasting. J Clin Endocrinol Metab. 2014 Jan;99(1):291-8. doi: 10.1210/jc.2013-3032 [PubMed]
- 26046515 Fink KR, Benjert JL. Imaging of Nontraumatic Neuroradiology Emergencies. Radiol Clin North Am. 2015 Jul;53(4):871-90, x. doi: 10.1016/j.rcl.2015.02.004 [PubMed]
- 30516599 Muehlschlegel S. Subarachnoid Hemorrhage. Continuum (Minneap Minn). 2018 Dec;24(6):1623-1657. doi: 10.1212/CON.0000000000000679 [PubMed]
- 30881537 Marcolini E, Hine J. Approach to the Diagnosis and Management of Subarachnoid Hemorrhage. West J Emerg Med. 2019 Mar;20(2):203-211. doi: 10.5811/westjem.2019.1.37352 [PubMed]
- 31485117 Patra A, Janu A, Sahu A. MR Imaging in Neurocritical Care. Indian J Crit Care Med. 2019 Jun;23(Suppl 2):S104-S114. doi: 10.5005/jp-journals-10071-23186 [PubMed]
- 31964292 Maher M, Schweizer TA, Macdonald RL. Treatment of Spontaneous Subarachnoid Hemorrhage: Guidelines and Gaps. Stroke. 2020 Apr;51(4):1326-1332. doi: 10.1161/STROKEAHA.119.025997 [PubMed]
- 32501957 Nethathe GD, Cohen J, Lipman J, Anderson R, Feldman C. Mineralocorticoid Dysfunction during Critical Illness: A Review of the Evidence. Anesthesiology. 2020 Aug;133(2):439-457. doi: 10.1097/ALN.0000000000003365 [PubMed]
- 32611661 Verbalis JG. The Curious Story of Cerebral Salt Wasting: Fact or Fiction? Clin J Am Soc Nephrol. 2020 Nov 6;15(11):1666-1668. doi: 10.2215/CJN.00070120 [PubMed]
- 33357465 Post R, Germans MR, Tjerkstra MA, et al.; ULTRA Investigators. Ultra-early tranexamic acid after subarachnoid haemorrhage (ULTRA): a randomised controlled trial. Lancet. 2021 Jan 9;397(10269):112-118. doi: 10.1016/S0140-6736(20)32518-6 [PubMed]
- 33896527 Chung DY, Abdalkader M, Nguyen TN. Aneurysmal Subarachnoid Hemorrhage. Neurol Clin. 2021 May;39(2):419-442. doi: 10.1016/j.ncl.2021.02.006 [PubMed]
- 34030777 Gottlieb M, Morgenstern J. Lumbar Puncture Should Not Be Routinely Performed For Subarachnoid Hemorrhage After A Negative Head Ct. Ann Emerg Med. 2021 Jun;77(6):643-645. doi: 10.1016/j.annemergmed.2020.11.018 [PubMed]