Subarachnoid hemorrhage

  • Blood accumulation into the space between the arachnoid and pia
  • Trauma is the most common cause of SAH. Traumatic SAH (trSAH) is the most common traumatic extraaxial hemorrhage
  • Nontraumatic SAH (ntSAH) accounts for 3-5% of all acute “strokes”
  • Aneurysmal rupture is the cause of ~80% of ntSAH. AVM accounts for ~5%. Arterial dissection, pituitary apoplexy, vasculitis, vasculopathies, coagulopathies, dural sinus thrombosis, drugs (eg cocaine), sickle cell anemia are less common causes. In 10-12% of cases, no cause is identified
  • Peak age for aneurysmal SAH (aSAH) is 55-60 years
  • 30% of aSAH occur during sleep
  • At least 75% of patients with aSAH present with thunderclap headache that peaks within seconds to minutes
  • 10-50% of patients with aSAH experience sentinel headaches 2-8 weeks before the SAH
  • 20-40% of aSAH are complicated by intracerebral hemorrhage
  • 13-28% of aSAH are complicated by intraventricular hemorrhage
  • 2-5% of aSAH are complicated by subdural hemorrhage
  • Seizures occur in ~20% of patients with aSAH, most commonly in the first 24 hours
  • 10–15% of patients with aSAH die before reaching the hospital
  • 30-day mortality in aSAH approaches 46%
  • 30% of survivors of aSAH have moderate to severe disability
  • Outcome after aSAH is worse in patients ≥70 years old
  • Perimesencephalic nonaneurysmal SAH (pnSAH) is probably caused by venous hemorrhage, is much more limited than aSAH and has good prognosis. It is often confined to the interpeduncular, ambient, and prepontine cisterns and rarely extends into the sylvian fissures.
  • Convexal SAH is localized to superficial sulci over the cerebral convexities. The most common causes are cortical vein occlusion, amyloid angiopathy, vasculitis, and reversible cerebral vasoconstriction syndrome (RCVS)

Risk factors for SAH

  • Hypertension
  • Smoking
  • Chronic alcohol abuse
  • Sympathomimetic drugs
  • Age >50 years
  • Female gender (1.24 times higher incidence than men)
  • African american or Hispanic race
  • Presence of cerebral aneurysm
  • Family history of (first-degree family member with) cerebral aneurysm
  • Polycystic kidney disease
  • Ehlers-Danlos type IV

Imaging

  • CT: trSAH usually appears as peripheral, linear hyperdensities in sulci adjacent to areas of parenchymal contusion and is more focal than the diffuse hemorrhage of aSAH. In aSAH the hyperdensity is more diffuse and extends into cisterns and sulci. Ventricular hemorrhage and parenchymal or subdural hemorrhage may be present
  • The sensitivity of modern CT scanners for detecting SAH within the first 6 hours after onset of headache approaches 100%
  • MR: FLAIR is the most sensitive sequence. Blood appears hyperintense to CSF (“dirty CSF”)
  • Severe cerebral edema may appear like SAH (“pseudo-SAH”)
  • High FiO2, meningitis, neoplasms, IV contrast and various artifacts may cause bright CSF on FLAIR and mimic SAH
  • In convexal SAH look for signs of sinus or venous thrombosis
  • CTA is 90-95% sensitive for detecting aneurysms ≥2mm
  • TOF MRA is 85-95% sensitive for detecting aneurysms ≥3mm
  • DSA is the gold standard for the detection and evaluation of cerebral aneurysms
  • DSA identifies vascular pathology in 13% of atraumatic SAH cases with negative CTA
  • ~15% of atraumatic SAH are angiogram-negative, of which 3-4% remain negative after 3D rotational angiography. Repeat angiography is advised in such cases as they carry a high rebleed risk and have poor outcome. Repeat DSA identifies an aneurysm in an additional 4% of such cases

Lumbar puncture

  • Use small gauge spinal needle and remove only a small amount of CSF as lowering the CSF pressure may cause re-bleeding
  • CSF appearance in SAH: bloody fluid that does not clear in subsequent tubes
  • RBC count (usually >100,000RBCs/mm3) does not decrease in subsequent tubes
  • Protein may be elevated
  • Glucose is normal or slightly reduced as RBCs may metabolize some glucose over time
  • Xanthochromia detection by spectrophotometry:
    • Xanthochromia is the result of heme metabolism to bilirubin by macrophages, arachnoid membrane and choroid plexus cells. Oxyhemoglobin from lysed red blood cells after a traumatic tap isnot converted to bilirubin
    • Oxyhemoglobin peaks at 36 hours after onset
    • Bilirubin becomes apparent at 2–4 hours, peaks at 48 hours and may be detectable up to 10 days after onset
  • LP might be negative earlier than 2-4 hours after onset. Sensitivity is highest at 12 hours, approaching 100%

Complications

  • Hydrocephalus: may be acute, obstructive from large volume of intraventricular blood or the patient may develop communicating hydrocephalus later in the course
  • Delayed Cerebral Ischemia (DCI)
    1. Occurence of new focal neurologic deficit with or without drop in consciousness, when other causes of neurological decline (hydrocephalus, re-bleeding, hyponatremia, etc) have been ruled out
    2. Affects ~20% of patients after aneurysmal SAH
    3. Usually starts 3-5 days after onset of SAH, risk peaks between day 5 and 14
    4. Only about 30-70% of patients with DCI have angiographic signs of vasospasm
    5. DCI is a clinical diagnosis but imaging should be used to rule out other causes of neurologic deterioration
    6. Nimodipine improves outcome but does not have any effect on the angiographic presence of vasospasm
    7. Cerebral blood flow (CBF) ≤ 25 mL/100g/min is associated with the development of irreversible damage
    8. Missmatch with normal CBF is associated with reversible damage
    9. Mean transit time (MTT) thresholds range from 5-6.5 sec
  • Seizures
  • DVT and pulmonary embolism

Management

  • Secure Airway, Breathing, Circulation
  • Admit in ICU unit or specialized stroke unit with adequate monitoring capabilities
  • Maintain 30o head elevation
  • Indications for intraventricular catheter placement include:
    1. Acute hydrocephalus
    2. Large volume of intraventricular hematoma
    3. Hunt&Hess grade ≥3
  • Monitor ICP and consider mannitol if persistently elevated. Maintain optimal cerebral perfusion pressure
  • Be watchful for cerebral vasospasm. Use transcranial doppler if available to monitor intracranial arteries’ velocities and Lindegaard ratio
  • Administer oral nimodipine to all patients with aSAH
  • Maintain euvolemia and avoid prophylactic hypervolemia
  • Maintain a systolic blood pressure of 120-160 mmHg in all patients with aSAH
  • Maintain euglycemia
  • Measure weight daily and be watchful for SIADH or cerebral salt wasting syndrome
  • Monitor urine output and plasma osmolality
  • Monitor for cardiac arrythmias
  • Consider prophylactic AEDs
  • Administer prophylactic H2 or proton pump inhibitors
  • Provide thromboemboembolic prophylaxis
  • Administer laxatives, prevent constipation



References

  • Spontaneous subarachnoid haemorrhage Lancet. 2022 Sep 10;400(10355):846-862. doi: 10.1016/S0140-6736(22)00938-2
  • Spontaneous subarachnoid haemorrhage Lancet. 2017 Feb 11;389(10069):655-666. doi: 10.1016/S0140-6736(16)30668-7.
  • Greenberg M Handbook of Neurosurgery 8th edition, Thieme
  • Osborn A Osborn’s Brain 2th edition, Lippincott Williams & Wilkins 2018
  • Nonaneurysmal perimesencephalic subarachnoid hemorrhage: CT and MR patterns that differ from aneurysmal rupture AJNR Am J Neuroradiol. Sep-Oct 1991;12(5):829-34