202406262102

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Tags: Neurosurgery

Subarachnoid haemorrhage

aSAH accounts for only 2–5% of all strokes, and global incidence declined from 10.2 per 100,000 person-years in 1980 to 6.1 in 2010, with significant variabilities across regions, age, and sex

The global decrease in aSAH incidence paralleled a global reduction in prevalence of hypertension and smoking

Although the prognosis of aSAH has improved over the last decades, 12% of patients die before reaching the hospital, and the 90-day case-fatality of patients hospitalized for aSAH is approximately 30%

Major determinants of poor functional outcome & case fatality are

• early brain injury
• rebleeding of the ruptured aneurysm
• delayed cerebral ischaemia (DCI)

After the rupture of an intracranial aneurysm, a cascade of events ensues. Arterial blood under pressure enters the subarachnoid space, inducing swift mechanical effects, such as abrupt increases in intracranial pressure and related cerebral impact. This sets off intracranial repercussions in the form of early brain injury, accompanied by immediate systemic consequences, impacting cardiovascular and respiratory functions. The presence of blood in the subarachnoid space may contribute to cerebral vasospasm, delayed cerebral ischemia, hydrocephalus, and seizures. Systemically, there can be hyperglycaemia, an inflammatory response, electrolyte imbalances (primarily hypo/hypernatremia), and hormonal disturbances.

Severity scales

The most widely utilized clinical assessment scale to capture clinical severity in patients with aSAH is the World Federation of Neurosurgical Societies (WFNS) scale

The WFNS scale (full range 0–5) transforms the Glasgow Coma Scale (GCS) score into different levels (3–6, 7–12, 13–14 with/without motor deficit, and 15)

Hunt and Hess Scale is a clinical grading system ranging from a score of 1 to 5, based on neurological symptoms and signs ranging from mild headache to a comatose state

Imaging-based scales such as the Fisher scale or modified Fisher scale quantify the extent of subarachnoid, intraventricular, and intraparenchymal haemorrhage and are associated with outcomes

Early complications before aneurysm securing

Early brain injury

• defined as a cascade of events that develop in the first hours after SAH
• pathophysiological mechanisms leading to neuronal damage
  • cerebral oedema from bleeding
  • microcirculatory alterations
  • oxidative and inflammatory cascade
  • blood–brain-barrier breakdown

Early Mx

Comatose → intubation + MV to protect AW + optimise ventilation
neuroimaging

• to establish Dx
• guide intervention
  • treatment modality
  • need for diversion of CSF
    treat haemodynamic instability
    reversal of coagulopathy

Rebleeding

• markedly ↑ risk of poor outcome
• occurs in ~3–6% of patients w/i first 24 h
  • risk rapidly declines afterwards
• The only effective way to ↓ risk of rebleeding = secure the ruptured aneurysm
  • ∴ guidelines recommend aneurysm repair by surgical or endovascular means as soon as feasible
    • preferably w/i 24 h
      • may be difficult ∵ logistical challenges
    • patients should be haemodynamically stable before aneurysm treatment can be safely pursued
  • studies found no benefit with repair w/i 24h cf 24–72h

antifibrinolytics

The initial instability of the blood clot sealing the defect in the aneurysm is the target of antifibrinolytics

Controversial

in several initial RCT

• ↓ rebleeding
• longer-term use (wks) a/w ↑ DCI
  a recent large, adequately powered RCT that investigated ultra-early and short-term treatment w/ TXA found no difference in outcome
  → antifibrinolytic use has since been widely abandoned

while potential benefits of fibrinolytic treatment of intraventricular haemorrhage have been demonstrated for primary intracranial haemorrhage, there are no data to support this for the aSAH population

BP

• ↑BP from sympathetic response (∵SAH) ↑ risk of rebleeding
  • no high-quality data exist that treatment of HT ↓ risk of rebleeding
• ↓BP should be avoided
  • ∵ risk of ↓perfusion → acute cerebral ischaemic
• thresholds to lower SBP commonly set at a goal of < 160 mmHg
  • ideally should be individualised

Hydrocephalus

• usually an acute Cx
• can develop in the absence of visible intraventricular extension of bleeding on CT
  Mechanism
• obstructive
  • typically by clot impeding CSF through the aqueduct
• malabsorptive
  • from lack of CSF absorption by the arachnoid granulations
    Clinical presentation
• depressed level of alertness
• in severe cases
  • downgaze deviation
    • ∵ compression of mesencephalic tectum by dilated third ventricle
  • Cushing reflex: bradycardia + hypertension

CSF drainage by external ventricular drain (EVD), lumbar drain or lumbar puncture should be performed in patients with hydrocephalus to ↓ICP, thereby improving cerebral perfusion

Ventriculostomy is the method of choice in aSAH patients with obstructive hydrocephalus and those with extensive intraventricular haemorrhage

Inserting an EVD before aneurysm occlusion can protect against abrupt ICP ↑ from rebleeding
excessive ventricular drainage before aneurysm obliteration could → rerupture.

Treatment of aneurysm

Timely repair of ruptured aneurysms reduces the risk of rebleeding and allows for more targeted and safer management of DCI

Early aneurysm securement, i.e. w/i 24–72 h from onset of aSAH, yields better outcomes than delayed treatment after 7–10 days

Complete obliteration of the aneurysm during initial treatment is vital to minimize rebleeding risk and risks associated with the need for retreatment.

if complete obliteration is not immediately feasible, securing the rupture site during the acute phase reduces the risk of early rebleeding. Retreatment within 1–3 months is then recommended to prevent future rebleeding

Good-grade aSAH patients from ruptured aneurysms of the anterior circulation are often equally suitable for both primary coiling & clipping;

primary coiling generally preferred to clipping ∵ improved 1-year functional outcomes

older patients → coiling
better long-term protection from re-rupture → clipping

most posterior circulation aneurysms → coiling

wide neck aneurysm → clipping

placing high-density stents (such as pipeline) over the necks of aneurysms unsuitable for clipping or coiling can be considered

Post-op Mx

ICU management

• close monitoring
• optimization of systemic function
• preventing & treating cranial + systemic complications

Sedation:

• Benefit of minimizing sedation
  • ↓ duration of MV & LOS
  • clinical neuromonitoring
    • for early detection of neurodeterioration
• sedation may be required for
  • manage intracranial hypertension
  • pain / agitation
  • status epilepticus
  • severe respiratory failure.

Intracranial complication

Delayed cerebral ischaemia

• occurs in about 30% of patients w/ aSAH
  • mostly between days 4–14 after ictus
• the leading cause of functional disability in survivors

often a/w angiographic vasospasm

• but documentation of vasospasm is not sine-qua-non for Dx of DCI

half of patients w/ angiographic vasospasm develop ischaemic symptoms
but DCI may develop w/o angiographic vasospasm

Recent work has suggested that other factors may contribute to DCI

• cortical spreading depolarization
• impaired autoregulation w/ ↓ regional blood flow
• intravascular volume contraction
• microthrombosis

Vasospasm can affect small vessels escaping angiographic detection

Poor initial clinical (i.e. Hunt Hess or WFNS score) and radiographic (i.e. modified Fisher, Hijdra) grades are established predictors of DCI. Other risk factors, variably associated, include female sex, smoking, hydrocephalus, hyperglycaemia, and diabetes

Guideline-recommended strategies to reduce DCI risk include

• enteral administration of nimodipine
• prevention of hypovolaemia and hypotension

Nimodipine reduces infarction rates and improves functional outcomes despite not significantly preventing angiographic vasospasm

Intravenous nimodipine more often leads to hypotension cf oral, with significant drops in blood pressure in one-third of patients after the start of IV nimodipine as opposed to after every tenth oral intake

Hypotension may require dose adjustment, discontinuation, or vasopressor support increase

Nimodipine can also be used as a potential intraarterial vasodilator, although robust data on eventual burden of DCI are lacking for such use

Guideline recommendations: AHA, Neurocritical Care Society, European Stroke Organization

Clinical monitoring through serial neurologic assessments is fundamental
but misses DCI-related neurologic changes in one-fifth of patients

The gold standard for diagnosis of large-vessel vasospasm, digital subtraction angiography, enables endovascular treatment if indicated

Computed tomography-angiography (CTA) reaches 82% and 97% sensitivity and specificity for angiographic vasospasm detection. CT perfusion may allow recognition of impaired perfusion, which may occur independently of vasospasm

Transcranial Doppler ultrasonography (TCD)
low sensitivity for vasospasm detection, reaching only 38% in a recent review
agreement between CTA and TCD is limited

Treating DCI aims to improve perfusion and minimize or prevent infarction. Haemodynamic augmentation through induced hypertension is often used as a primary intervention in patients with DCI in the absence of cardiac failure and severe baseline hypertension. Induced hypertension may reduce the risk of DCI-related cerebral infarction and lead to better outcomes, but optimal target blood pressures remain unclear, and the only randomized controlled trial on this topic failed to support induced hypertension in this setting but likely was underpowered

Haemodynamic augmentation appears safe in the presence of other small, unruptured and untreated aneurysms

While cardiac output changes generally do not affect cerebral blood flow, they may do so in SAH patients

Endovascular rescue therapy with either intraarterial infusion of vasodilators (i.e. verapamil, nicardipine or milrinone) and/or balloon angioplasty may be considered when haemodynamic augmentation fails or is contraindicated
no robust data yet

Seizures

Electrographic seizures & high-frequency periodic discharges (> 2.5 Hz) → ↑metabolic demand that may be insufficiently compensated for by local increases in cerebral blood flow.
a/w worse outcomes
associations do not imply causal effects and possibly relate to other secondary complications, such as late diagnosis of delayed cerebral ischaemia

Underlying mechanisms may include

• gliosis
• neuroinflammation
• cerebral hyperaemia

No adequately powered clinical trial has been conducted to guide seizure prophylaxis or treatment in aSAH patients

Recent guidelines do NOT recommend the routine use of prophylactic antiseizure medication (ASM), although ASM may be reasonable in patients at high risk for seizures

Phenytoin as ASM should be avoided since it may induce harm

the benefit from prolonged levetiracetam prophylaxis was greatest for those with imaging evidence of early brain injury and others have suggested a possible benefit against DCI with newer ASMs (levetiracetam and perampanel)

All clinical or electrographic seizures that are diagnosed should be treated for at least 7 days and for those with delayed seizures or those with risk factors for seizures, more prolonged treatment should be considered.

Management of periodic discharges or other ictal-interictal patterns is highly controversial

ICP Mx

The practice of intracranial pressure (ICP) monitoring in patients with aSAH remains a matter of debate due to the absence of high-level evidence tailored to this condition

Neurocritical Care Society suggests ICP monitoring for acute brain injuries at risk of elevated ICP based on clinical and imaging features, there are no distinct indications for aSAH patients

ICP monitoring should be considered if

• GCS ≤ 8
• neurological deterioration
• acute #Hydrocephalus
• cerebral oedema
• intracranial mass lesions
• need for perioperative or drainage of CSF

The gold standard method for ICP measurement is via a ventricular catheter connected to a pressure transducer

Timing, triggers of weaning and how to discontinue ventricular drainage are subject to debate

A lumbar drain is considered a less invasive alternative to EVD but may be precluded in case or obstructive hydrocephalus and contraindicated based on head CT findings

Ventriculoperitoneal shunting is necessary in patients with persistent hydrocephalus. Risk factors for requiring ventriculoperitoneal shunting include

• intraventricular haemorrhage
• higher radiological grade (such as modified Fisher),
• older age,
• higher clinical grade (Hunt and Hess or WFNS),
• more significant acute ventricular dilatation,
• rebleeding,
• posterior location of the ruptured aneurysm,
• multiple clamp failures

threshold for treating elevated ICP

• poorly understood
• classic threshold ~20–22 mmHg
  • but poor outcomes also linked to lower values
    • → potential need to lower ICP targets?
• a “dose” concept may better quantify ICP burden + predict outcomes
  • considering both magnitude + duration of exposure to high ICP

Elevated ICP in aSAH may arise primarily from

• #Hydrocephalus (30%),
• intracerebral haemorrhage (ICH),
• early or delayed global cerebral oedema (GCO) (8–12%)

Hyperventilation, head elevation, and osmotherapy are commonly used to manage high ICP. The transient effect of hyperventilation makes it suitable for short-term ICP control but carries the risk of cerebral ischemia and should be avoided in patients at risk for DCI, while the choice of osmotherapy between mannitol and hypertonic saline remains debatable

Hypothermia and high-dose barbiturates are reserved for refractory cases due to their risks and limited supporting evidence

Decompressive craniectomy (DC) has shown efficacy in reducing ICP, but its impact on functional outcomes is questionable. While evidence for the routine use of DC for managing elevated ICP in SAH is lacking, it remains a last resort option when medical management fails.

Systemic complications

Cardiac

aSAH can disrupt the electrical sinus pacing or cause conduction abnormalities, leading to arrhythmias. Encountered rhythm abnormalities include sinus arrhythmia, atrial fibrillation, ventricular tachycardia, or ventricular fibrillation

Stress cardiomyopathy
Takotsubo cardiomyopathy

The risk of myocardial infarction is highest within the first few days after aSAH

Pulmonary

ARDS
neurogenic pulmonary oedema

Metabolic

Electrolyte imbalances, including hypokalaemia, hypomagnesemia and hypophosphatemia, are common in aSAH patients, primarily due to excess renal losses

Hyponatremia has been attributed to the syndrome of inappropriate antidiuretic hormone (SIADH), excessive salt wasting, hypovolemia

Hyperglycaemia is associated with worse outcomes

Fever

• extremely common in SAH
• early, i.e. w/i first 3 days, fever frequently neurogenic
• occurrence a/w worse outcomes
  • regardless of cause
    • neurogenic
    • infective
    • drug-related
      Recent recommendations suggest active fever treatment, continuous core temperature monitoring, and avoiding temperatures > 37.5°

DVT prophylaxis

References

Contemporary Management of Aneurysmal Subarachnoid Haemorrhage. An Update for the Intensivist