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Sub-Arachnoid Hemorrhage
(Stabilization and referral in case of SAH, Raised ICP focus on SAH)
Sunil Kumar Daha
Janakpur, Nepal
Intracranial Pressure
• pressure inside the skull and thus in the brain tissue and cerebrospinal fluid (CSF).
• ICP is measured in millimeters of mercury (mmHg) and, at rest, is normally 7–15 mmHg
for a supine adult
Causes of raised ICP
Epidemiology
• Womens are affected more commonly
• Usually present before the age of 65
• Immediate mortality of aneurysmal SAH is 30%
• Survivors have a recurrence rate of 40% in the 1st 4 wks and 3% annualy
thereafter
Etiology
1. 85%Berry aneurysma:
most common site : a. Anterior communicating artery (30%)
b. Posterior communicating artery (25%)
c. Middle cerebral artery (20%)
(Increased risk in case of first degree relatives of those with saccular aneurysm,
patients with PKD and congenital connective tissue defects)
2. Non-aneurysmal haemorrhage ( Peri mesencephalic haemorrhage)
3. 5% Arteriovenous malformations and vertebral artery dissection
Clinical Features
1. Sudden, severe,thunder-clap’ headache lasting for hours or even days.
2. Thunder-clap headache accompanied by
-vomiting
- Raised blood pressure
-Neck stiffness or Pain
( commonly occurs on physical exertion, straining and sexual excitement)
On examination
•Loss of consciousness
•Distressed and irritable with photophobia
•Neck stiffness due to subarachnoid blood
•Focal hemisphere signs
Investigations
Management
• Nimodipine (30-60 mg IV for 5-14 daysfollowed by 360 mg for further 7 days.
• Insertion of platinum coils into an aneurysm (via endovascular procedure)
or, Surgical clipping of the aneurysm neck reduces the risk of both early and late
recurrence.
Complications
1. Obstructive hydrocephalus
2. Delayed cerebral ischaemia due to vasospasm
3. Hyponatremia and
4. Systemic complications associated with immobility, chest infection and
venous thrombosis
ICP following Subarachnoid haemorrhage
• sudden introduction of blood into the subarachnoid space results in CSF
outflow resistance
• Increased ICP and a resultant decrease in cerebral perfusion play a principal role
in the development of cortical damage
• The continuous monitoring of ICP aids in the early detection of secondary
cerebral insults and guides therapeutic interventions by providing real-time,
physiological feedback.
• Intracranial pressure control affords the opportunity for surgical treatment and
postoperative intensive care to effect a favorable outcome in patients suffering
from aneurysmal SAH
Severity of SAH
Recent Updates…
• Aneurysmal subarachnoid hemorrhage (SAH) is often a devastating event.
Approximately 10 percent of patients with aneurysmal SAH die prior to reaching
the hospital, 25 percent die within 24 hours of SAH onset, and about 45 percent
die within 30 days; only one-third of patients will have a good outcome after
treatment
• The most important predictive factors for acute prognosis after SAH include
• Level of consciousness and neurologic grade on admission
• Patient age (inverse correlation)
• Amount of blood on initial head computed tomography (CT) scan (inverse
correlation
• early mortality is caused by the common complications of aneurysmal SAH, which
include rebleeding, vasospasm and delayed cerebral ischemia, hydrocephalus,
increased intracranial pressure, seizures, and cardiac complications
• A patient presenting with aneurysmal subarachnoid hemorrhage (SAH) is
admitted to an intensive care setting for constant hemodynamic and neurologic
monitoring . Patients with SAH are at risk for hemodynamic instability and
neurologic deterioration. In one study, neurologic worsening occurred in 35
percent of patients within the first 24 hours of admission and heralded the onset
of complications and poor outcomes . Pulmonary edema and cardiac arrhythmias
complicate 23 and 35 percent of SAH cases respectively
Acute medical care
• Indications for endotracheal intubation include a GCS ≤8 , elevated ICP,
poor oxygenation or hypoventilation, hemodynamic instability and
requirement for heavy sedation or paralysis.
• Deep venous thrombosis (DVT) prophylaxis with pneumatic compression
stockings is started prior to aneurysm treatment .
Subcutaneous unfractionated heparin 5000 units three times daily can be
added for DVT prophylaxis once the aneurysm is treated.
• Intravenous fluid administration should target euvolemia and normal
electrolyte balance. Hyponatremia, in particular, is common; sodium levels
should be checked at least daily (See 'Intravenous fluids' below
and 'Hyponatremia' below.)
• Intravenous fluid administration should target euvolemia and normal
electrolyte balance. Hyponatremia, in particular, is common; sodium levels
should be checked at least daily
• A cohort study of 413 patients identified four variables that were
independently associated with increased risk of death or disability three
months after SAH
-Hypoxemia (arterio-alveolar gradient >125 mmHg)
-Metabolic acidosis (serum bicarbonate <20 mmol/L
-Hyperglycemia (serum glucose >180 mg/dL [10 mmol/L])
-Blood pressure instability (MAP of <70 or >130 mmHg
References
• Davidson’s Princples and practice of Medicine
Sub Arachnoid Hemorrhage (SAH)

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Sub Arachnoid Hemorrhage (SAH)

  • 1. Sub-Arachnoid Hemorrhage (Stabilization and referral in case of SAH, Raised ICP focus on SAH) Sunil Kumar Daha Janakpur, Nepal
  • 2. Intracranial Pressure • pressure inside the skull and thus in the brain tissue and cerebrospinal fluid (CSF). • ICP is measured in millimeters of mercury (mmHg) and, at rest, is normally 7–15 mmHg for a supine adult
  • 4.
  • 5. Epidemiology • Womens are affected more commonly • Usually present before the age of 65 • Immediate mortality of aneurysmal SAH is 30% • Survivors have a recurrence rate of 40% in the 1st 4 wks and 3% annualy thereafter
  • 6. Etiology 1. 85%Berry aneurysma: most common site : a. Anterior communicating artery (30%) b. Posterior communicating artery (25%) c. Middle cerebral artery (20%) (Increased risk in case of first degree relatives of those with saccular aneurysm, patients with PKD and congenital connective tissue defects) 2. Non-aneurysmal haemorrhage ( Peri mesencephalic haemorrhage) 3. 5% Arteriovenous malformations and vertebral artery dissection
  • 7. Clinical Features 1. Sudden, severe,thunder-clap’ headache lasting for hours or even days. 2. Thunder-clap headache accompanied by -vomiting - Raised blood pressure -Neck stiffness or Pain ( commonly occurs on physical exertion, straining and sexual excitement)
  • 8. On examination •Loss of consciousness •Distressed and irritable with photophobia •Neck stiffness due to subarachnoid blood •Focal hemisphere signs
  • 10. Management • Nimodipine (30-60 mg IV for 5-14 daysfollowed by 360 mg for further 7 days. • Insertion of platinum coils into an aneurysm (via endovascular procedure) or, Surgical clipping of the aneurysm neck reduces the risk of both early and late recurrence.
  • 11. Complications 1. Obstructive hydrocephalus 2. Delayed cerebral ischaemia due to vasospasm 3. Hyponatremia and 4. Systemic complications associated with immobility, chest infection and venous thrombosis
  • 12. ICP following Subarachnoid haemorrhage • sudden introduction of blood into the subarachnoid space results in CSF outflow resistance • Increased ICP and a resultant decrease in cerebral perfusion play a principal role in the development of cortical damage • The continuous monitoring of ICP aids in the early detection of secondary cerebral insults and guides therapeutic interventions by providing real-time, physiological feedback. • Intracranial pressure control affords the opportunity for surgical treatment and postoperative intensive care to effect a favorable outcome in patients suffering from aneurysmal SAH
  • 14.
  • 15.
  • 16. Recent Updates… • Aneurysmal subarachnoid hemorrhage (SAH) is often a devastating event. Approximately 10 percent of patients with aneurysmal SAH die prior to reaching the hospital, 25 percent die within 24 hours of SAH onset, and about 45 percent die within 30 days; only one-third of patients will have a good outcome after treatment • The most important predictive factors for acute prognosis after SAH include • Level of consciousness and neurologic grade on admission • Patient age (inverse correlation) • Amount of blood on initial head computed tomography (CT) scan (inverse correlation
  • 17. • early mortality is caused by the common complications of aneurysmal SAH, which include rebleeding, vasospasm and delayed cerebral ischemia, hydrocephalus, increased intracranial pressure, seizures, and cardiac complications • A patient presenting with aneurysmal subarachnoid hemorrhage (SAH) is admitted to an intensive care setting for constant hemodynamic and neurologic monitoring . Patients with SAH are at risk for hemodynamic instability and neurologic deterioration. In one study, neurologic worsening occurred in 35 percent of patients within the first 24 hours of admission and heralded the onset of complications and poor outcomes . Pulmonary edema and cardiac arrhythmias complicate 23 and 35 percent of SAH cases respectively
  • 18. Acute medical care • Indications for endotracheal intubation include a GCS ≤8 , elevated ICP, poor oxygenation or hypoventilation, hemodynamic instability and requirement for heavy sedation or paralysis. • Deep venous thrombosis (DVT) prophylaxis with pneumatic compression stockings is started prior to aneurysm treatment . Subcutaneous unfractionated heparin 5000 units three times daily can be added for DVT prophylaxis once the aneurysm is treated. • Intravenous fluid administration should target euvolemia and normal electrolyte balance. Hyponatremia, in particular, is common; sodium levels should be checked at least daily (See 'Intravenous fluids' below and 'Hyponatremia' below.)
  • 19. • Intravenous fluid administration should target euvolemia and normal electrolyte balance. Hyponatremia, in particular, is common; sodium levels should be checked at least daily • A cohort study of 413 patients identified four variables that were independently associated with increased risk of death or disability three months after SAH -Hypoxemia (arterio-alveolar gradient >125 mmHg) -Metabolic acidosis (serum bicarbonate <20 mmol/L -Hyperglycemia (serum glucose >180 mg/dL [10 mmol/L]) -Blood pressure instability (MAP of <70 or >130 mmHg
  • 20. References • Davidson’s Princples and practice of Medicine

Editor's Notes

  1. Tetracycline, vit. A intoxication, Attitude sickness
  2. Ehlers-Danlos syndrome
  3. Focal hemisphere signshemiparesis or aphasia may be present if associated with intracerebral haemotoma A third nerve palsy may be present due to local pressure from an aneurysm of the posterior communicating artery, but this is rare
  4. -360 mg given to prevent delayed ischemia in acute phase.
  5. It was first described in 1968 by two neurosurgeons from Ohio, USA: William Edward Hunt (1921-1999), neurologist and neurosurgeon; also of Tolosa-Hunt syndrome Robert M Hess, neurosurgeon