Subarachnoid hemorrhage: Difference between revisions

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==Background==
==Background==
Defined as hemorrhage into the subarachnoid space (between the arachnoid membrane and the pia mater ). This may occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head injury.
[[File:Meninges-en.svg|thumb|Anatomy of the meninges]]
Defined as hemorrhage into the subarachnoid space (between the arachnoid membrane and the pia mater). This may occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head injury.
===Epidemiology===
===Epidemiology===
The prevalence of SAH in patients presenting with true thunderclap headache is estimated at ~10%. <ref>Dubosh NM et al. Sensitivity of Early Brain Computed Tomography to Exclude Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis. Stroke 2016. PMID: 26797666</ref>
The prevalence of SAH in patients presenting with true thunderclap headache is estimated at ~10%. <ref>Dubosh NM et al. Sensitivity of Early Brain Computed Tomography to Exclude Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis. Stroke 2016. PMID: 26797666</ref>


===Risk Factors===
===Risk Factors===
*Genetics (polycystic kidney disease, Ehler-Danlos, family hx)  
*Genetics (polycystic kidney disease, Ehler-Danlos, family history)  
*Hypertension  
*Hypertension  
*Atherosclerosis  
*Atherosclerosis  
*Cigarette smoking  
*Cigarette smoking  
*Alcohol  
*[[Alcohol]]
*Age &gt;50  
*Age >50  
*Cocaine use  
*[[Cocaine]] use  
*Estrogen deficiency
*Estrogen deficiency
===Etiology of Spontaneous SAH===
===Etiology of Spontaneous SAH===
*Ruptured aneurysm (85%)  
*Ruptured aneurysm (85%)  
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*Differentiate from aneurysmal rupture
*Differentiate from aneurysmal rupture
*Supportive care with prevention of hypertension, elevated ICP, and vasospasm with PO nimodipine
*Supportive care with prevention of hypertension, elevated ICP, and vasospasm with PO nimodipine
*Observation and repeat head CT for stable patients
*Patients with normal neurologic exam NOT on anticoagulation may not need a repeat head CT<ref>Borczuk, et al. Patients with traumatic subarachnoid hemorrhage are at low risk for deterioration or neurosurgical intervention.  J Am Coll Surg.  2014; 219.</ref><ref>Nahmias JT, et al.  Mild Traumatic Brain Injuries Can Be Safely Managed Without Neurosurgical Consultation: The End of a Neurosurgical "Nonsult"? American Association for the Surgery of Trauma.  Annual Meeting.  2016</ref>
**Recommend 6 hour observation


==Clinical Features==
==Clinical Features==
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**Sudden onset is more important finding than worst [[headache]]
**Sudden onset is more important finding than worst [[headache]]
*May be associated with [[syncope]], [[seizure]], [[nausea/vomiting]], meningismus  
*May be associated with [[syncope]], [[seizure]], [[nausea/vomiting]], meningismus  
**Meningismus may not develop until hrs after bleed (blood breakdown -&gt; aseptic meningitis)
**Meningismus may not develop until hrs after bleed (blood breakdown aseptic meningitis)
*[[Retinal hemorrhage]]
*[[Retinal hemorrhage]]
**May be the only clue in comatose patients
**May be the only clue in comatose patients
*Sentinel bleed headache 6-20 days before serious SAH in 30-50% of patients
*Sentinel bleed headache 6-20 days before serious SAH in 30-50% of patients


== Differential Diagnosis ==
==Differential Diagnosis==
{{Intracranial hemorrhage DDX}}
{{Intracranial hemorrhage DDX}}


===Other===  
===Other===
*Drug toxicity  
*Drug toxicity  
*Ischemic [[Stroke (Main)|Stroke]]  
*Ischemic [[Stroke (Main)|Stroke]]  
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*Primary headache syndromes (benign thunderclap headache, [[Migraine]], [[Cluster Headache]])
*Primary headache syndromes (benign thunderclap headache, [[Migraine]], [[Cluster Headache]])


== Diagnosis  ==
==Evaluation==
[[File:SubarachnoidP.png|thumb|Noncontrast CT showing subarachnoid hemorrhage (white area in the center stretching into the sulci).]]
[[File:SubarachnoidP.png|thumb|Noncontrast CT showing subarachnoid hemorrhage (white area in the center stretching into the sulci).]]
===Ottawa SAH Rules<ref>Ottawa SAH Rule JAMA. 2013 Sep 25;310(12):1248-55. doi: 10.1001/jama.2013.278018</ref>===
===Ottawa SAH Rules<ref>Ottawa SAH Rule JAMA. 2013 Sep 25;310(12):1248-55. doi: 10.1001/jama.2013.278018</ref>===
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**No limited neck flexion on physical exam  
**No limited neck flexion on physical exam  


'''If concerned for SAH and CT normal strongly consider LP'''
'''If concerned for SAH and CT normal strongly consider LP, especially if CT obtained >6 hrs after symptom onset'''


===Non-Contrast Head CT ===
===Non-Contrast Head CT===
{| class="wikitable"
{| class="wikitable"
| align="center" style="background:#f0f0f0;"|'''Time from onset of symptoms'''
| align="center" style="background:#f0f0f0;"|'''Time from onset of symptoms'''
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*SAH due to trauma - look at convexities of frontal and temporal cortices
*SAH due to trauma - look at convexities of frontal and temporal cortices


===Lumbar Puncture===  
===Lumbar Puncture===
*Elevated RBC count that doesn't decrease from tube one to four  
*Elevated RBC count that does not decrease from tube one to four  
**Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl
**Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl
*Opening pressure &gt;20 (60% of patients)  
*Opening pressure >20 (60% of patients)  
**Can help differentiate from a traumatic tap (opening pressure expected to be normal)  
**Can help differentiate from a traumatic tap (opening pressure expected to be normal)  
**Elevated opening pressure also seen in cerebral venous thrombosis, IIH
**Elevated opening pressure also seen in cerebral venous thrombosis, IIH
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**Tube 4 RBC count <500 has negative predictive value of 100% for SAH. Tube 4 RBC decrease of 70% compared to tube 1 excludes a radiographically detectable SAH.<ref>Gorchynski J, Oman J, and Newton T. Interpretation of traumatic lumbar punctures in the setting of possible subarachnoid hemorrhage: who can be safely discharged? Cal J Emerg Med. 2007; 8(1): 3–7.</ref>
**Tube 4 RBC count <500 has negative predictive value of 100% for SAH. Tube 4 RBC decrease of 70% compared to tube 1 excludes a radiographically detectable SAH.<ref>Gorchynski J, Oman J, and Newton T. Interpretation of traumatic lumbar punctures in the setting of possible subarachnoid hemorrhage: who can be safely discharged? Cal J Emerg Med. 2007; 8(1): 3–7.</ref>
**One study found that >2000 RBCs had a sensitivity of 93% and specificity of 93% for SAH, sensitivity increased to 100% when xanthochromia added.<ref>Perry JJ, Alyahya B, Sivilotti MLA, et al. Differentiation between traumatic tap and aneurysmal subarachnoid hemorrhage: prospective cohort study. BMJ : British Medical Journal. 2015;350:h568.</ref>
**One study found that >2000 RBCs had a sensitivity of 93% and specificity of 93% for SAH, sensitivity increased to 100% when xanthochromia added.<ref>Perry JJ, Alyahya B, Sivilotti MLA, et al. Differentiation between traumatic tap and aneurysmal subarachnoid hemorrhage: prospective cohort study. BMJ : British Medical Journal. 2015;350:h568.</ref>
===CT Angiogram===
*A CT followed by CTA is an acceptable alternative to CT and LP<ref>Walsh B, Vilke GM, Coyne CJ. Clinical Guidelines for the Emergency Department Evaluation of Subarachnoid Hemorrhage. Meurer WJ, JEM. 2016; 50(4) 696-701.</ref>
*CTA has a 98% sensitivity for aneurysms >3mm


==Management==
==Management==
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#Hypertension
#Hypertension
#*AHA/ASA has no formal recommendations but states that decreasing to SBP <160 is reasonable<ref>Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012; 43(6):1711-1737.</ref>
#*AHA/ASA has no formal recommendations but states that decreasing to SBP <160 is reasonable<ref>Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012; 43(6):1711-1737.</ref>
#*A goal of SBP <140 has been shown have improved neurologic outcomes<ref>Anderson CS, Heeley E, Huang Y, Wang J, Stapf C, Delcourt C, et al; INTERACT2 Investigators. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013;368:2355–2365.</ref>
#*Rapid SBP lowering <140 has been advocated with early research showing improved functional outcome<ref>Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013; 368:2355-2365.</ref>, but more recent work has found no difference between SBP <140 and <180<ref>Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016; 1-11. [Epub ahead of print].</ref>
#*Ensure appropriate pain control and sedation before adding antihypertensives
#*Ensure appropriate pain control and sedation before adding antihypertensives
#Discontinue/reverse all anticoagulation  
#Discontinue/reverse all anticoagulation  
#*[[Coumadin]] --> (Prothrombin complex conc or [[FFP]]) + vitamin K  
#*[[Coumadin]] (Prothrombin complex conc or [[FFP]]) + vitamin K  
#*[[Aspirin]] --> [[DDAVP]]  
#*[[Aspirin]] [[DDAVP]]  
#*[[Plavix]] --> [[Platelets]]
#*[[Plavix]] [[Platelets]]
#*Dabigitran ([[Pradaxa]]) --> [[Idarucizumab]] (Praxbind): 5 grams IV
#*Dabigitran ([[Pradaxa]]) [[Idarucizumab]] (Praxbind): 5 grams IV
#[[Nimodipine]]  
#[[Nimodipine]]  
#*Only CCB studied that has been shown to prevent vasospasm (associated with improved neuro outcomes and decreased cerebral infarction)  
#*Only CCB studied that has been shown to prevent vasospasm (associated with improved neuro outcomes and decreased cerebral infarction)  
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#*Keep an eye on BP for fluctuations
#*Keep an eye on BP for fluctuations
#[[Magneisum sulfate]]
#[[Magneisum sulfate]]
#*Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain b/w 2-2.5 mmol/L
#*Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain between 2-2.5 mmol/L
#Seizure prophylaxis  
#Seizure prophylaxis  
#*Controversial; 3 day course may be preferable  
#*Controversial; 3 day course may be preferable  
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#*Controversial; evidence suggests is neither beneficial nor harmful
#*Controversial; evidence suggests is neither beneficial nor harmful
#Glycemic control  
#Glycemic control  
#*Controversial; consider sliding scale if long pt stay in ED while awaiting ICU bed
#*Controversial; consider sliding scale if long patient stay in ED while awaiting ICU bed
#Keep head of bed elevated  
#Keep head of bed elevated  
#Aneurysm treatment
#Aneurysm treatment
#*Surgical clipping and endovascular coiling are definitive tx
#*Surgical clipping and endovascular coiling are definitive treatment
#*Antifibrinolytic - Controversial; if delayed aneurysmal tx, consider short term therapy (<72 hrs) with TXA or aminocaproic acid
#*Antifibrinolytic - Controversial; if delayed aneurysmal treatment, consider short term therapy (<72 hrs) with TXA or aminocaproic acid


===Intubation===
{{Intubation with ICH}}
*Consider neuroprotective intubation
**3 minutes before intubation
***Lidocaine 1-2 mg/kg to blunt sharp MAP increase
***Fentanyl 1-2 mcg/kg as sympatholytic
**Sedation
***Etomidate if blood pressure normal
***Propofol if blood pressure high
**Succinylcholine without defasciculating dose
*Ensure pt is pain-free for post-intubation sedation
**Propofol with fentanyl
**Try to prioritize pain control with fentanyl


{{AHA SAH BP Guidelines}}
{{AHA SAH BP Guidelines}}
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*Admit
*Admit


== Complications ==
==Complications==
===Rebleeding===
===Rebleeding===
*Risk is highest within first 24 hours (2.5-4%), particularly within first 6 hours  
*Risk is highest within first 24 hours (2.5-4%), particularly within first 6 hours  
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*Characterized by decline in neuro status  
*Characterized by decline in neuro status  
*Aggressive treatment can only be started after aneurysm has been treated
*Aggressive treatment can only be started after aneurysm has been treated
**Tx for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), balloon angioplasty, or intra-arterial vasodilators{{Citation needed|reason=Reliable source needed|date=February 2016}}
**treatment for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), balloon angioplasty, or intra-arterial vasodilators{{Citation needed|reason=Reliable source needed|date=February 2016}}
**Studies have not provided strong evidence of benefit Triple-H therapy{{Citation needed|reason=Reliable source needed|date=February 2016}}
**Studies have not provided strong evidence of benefit Triple-H therapy{{Citation needed|reason=Reliable source needed|date=February 2016}}


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Most likely related to the release of catecholamines due to hypoperfusion of hypothalamus
Most likely related to the release of catecholamines due to hypoperfusion of hypothalamus
*Ischemia  
*Ischemia  
**Elevated troponin (20-40% of cases)  
**Elevated [[troponin]] (20-40% of cases)  
**ST segment depression
**ST segment depression
*Rhythm disturbances  
*Rhythm disturbances  
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*Prominent U waves
*Prominent U waves
===Hydrocephalus===
===Hydrocephalus===
*Consider ventricular drain placement for deteriorating LOC + no improvement w/in 24hr
*Consider ventricular drain placement for deteriorating LOC + no improvement within 24hr
===[[Hyponatremia]] ===
 
*Hyponatremia is seen in 10%-40% of the patients with subarachnoid hemorrhage who are admitted to the ICU.<ref>Woo, M.H, Kale-Pradhan, P.B. Fludrocortisone in the treatment
===[[Hyponatremia]]===
*[[Hyponatremia]] is seen in 10%-40% of the patients with subarachnoid hemorrhage who are admitted to the ICU.<ref>Woo, M.H, Kale-Pradhan, P.B. Fludrocortisone in the treatment
of subarachnoid hemorrhage-induced hyponatremia. Annals of Pharmacotherapy. 1997.  31, 637–639.</ref>
of subarachnoid hemorrhage-induced hyponatremia. Annals of Pharmacotherapy. 1997.  31, 637–639.</ref>
*Cerebral Salt Wasting and [[SIADH]] are the two most common causes<ref>Albanese, A. et al. . Management of hyponatremia in patients with acute cerebral insults. Archives of Disease in Childhood, 85. (2001). 246–251.</ref>
*Cerebral Salt Wasting and [[SIADH]] are the two most common causes<ref>Albanese, A. et al. . Management of hyponatremia in patients with acute cerebral insults. Archives of Disease in Childhood, 85. (2001). 246–251.</ref>


== Prognosis ==
==Prognosis==
=== Hunt and Hess ===
===Hunt and Hess===
Subjective terminology, but good interobserver variability
Subjective terminology, but good interobserver variability
{| class="wikitable"
{| class="wikitable"
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:Grade 1 or 2 have curable disease  
:Grade 1 or 2 have curable disease  


:Add one grade for serious systemic disease (HTN, DM, severe atherosclerosis, COPD)
:Add one grade for serious systemic disease (hypertension, DM, severe atherosclerosis, COPD)


=== World Federation of Neurosurgical Societies (WFNS) ===
===World Federation of Neurosurgical Societies (WFNS)===
Objective terminology, and fair interobserver variability
Objective terminology, and fair interobserver variability
{| class="wikitable"
{| class="wikitable"
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Note: First-degree relatives are at 2-5 fold increase in SAH, so screening is considered on individual basis.
Note: First-degree relatives are at 2-5 fold increase in SAH, so screening is considered on individual basis.


== See Also ==
==See Also==
*[[Intracranial Hemorrhage (Main)]]
*[[Intracranial Hemorrhage (Main)]]
*[[Head Trauma]]
*[[Head Trauma]]

Revision as of 04:30, 16 September 2018

Background

Anatomy of the meninges

Defined as hemorrhage into the subarachnoid space (between the arachnoid membrane and the pia mater). This may occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head injury.

Epidemiology

The prevalence of SAH in patients presenting with true thunderclap headache is estimated at ~10%. [1]

Risk Factors

  • Genetics (polycystic kidney disease, Ehler-Danlos, family history)
  • Hypertension
  • Atherosclerosis
  • Cigarette smoking
  • Alcohol
  • Age >50
  • Cocaine use
  • Estrogen deficiency

Etiology of Spontaneous SAH

  • Ruptured aneurysm (85%)
  • Nonaneurysmal (15%)
    • Perimesencephalic hemorrhage (10%) - lower risk of complications
    • Other: tumor, coagulopathy, dissection, vasculitis, SCD, venous sinus thrombosis

Traumatic Subarachnoid Hemorrhage

  • Differentiate from aneurysmal rupture
  • Supportive care with prevention of hypertension, elevated ICP, and vasospasm with PO nimodipine
  • Patients with normal neurologic exam NOT on anticoagulation may not need a repeat head CT[2][3]
    • Recommend 6 hour observation

Clinical Features

  • Sudden, severe headache that reaches maximal intensity within minutes (97% of cases)
    • Sudden onset is more important finding than worst headache
  • May be associated with syncope, seizure, nausea/vomiting, meningismus
    • Meningismus may not develop until hrs after bleed (blood breakdown → aseptic meningitis)
  • Retinal hemorrhage
    • May be the only clue in comatose patients
  • Sentinel bleed headache 6-20 days before serious SAH in 30-50% of patients

Differential Diagnosis

Intracranial Hemorrhage Types

Other

Evaluation

Noncontrast CT showing subarachnoid hemorrhage (white area in the center stretching into the sulci).

Ottawa SAH Rules[4]

Never has been externally and prospectively validated, authors caution implementation into routine use

  • 100% sensitive to rule out SAH (97.1%-100%)
  • Can exclude SAH if all of the following are true
    • Age < 40
    • No Neck pain or stiffness
    • No Witnessed LOC
    • No onset during exertion
    • No Thunderclap symptomatology (max intensity at onset)
    • No limited neck flexion on physical exam

If concerned for SAH and CT normal strongly consider LP, especially if CT obtained >6 hrs after symptom onset

Non-Contrast Head CT

Time from onset of symptoms Sensitivity of CT
<6 hours ~100%[5]
6-12 hours 98%
12-24 hours 93%[6]
24 hours - 5 days <60%
  • SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)
  • SAH due to trauma - look at convexities of frontal and temporal cortices

Lumbar Puncture

  • Elevated RBC count that does not decrease from tube one to four
    • Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl
  • Opening pressure >20 (60% of patients)
    • Can help differentiate from a traumatic tap (opening pressure expected to be normal)
    • Elevated opening pressure also seen in cerebral venous thrombosis, IIH
  • Xanthrochromia
    • May help differentiate between SAH and a traumatic tap
    • Takes at least 2hr after bleed to develop (beware of false negative if measure early)
    • Sn (93%) / Sp (95%) highest after 12hr
  • If unable to obtain CSF consider CTA
    • CTA also highly sensitive for predicting delayed cerebral ischemia
  • If traumatic tap is suspected
    • Tube 4 RBC count <500 has negative predictive value of 100% for SAH. Tube 4 RBC decrease of 70% compared to tube 1 excludes a radiographically detectable SAH.[7]
    • One study found that >2000 RBCs had a sensitivity of 93% and specificity of 93% for SAH, sensitivity increased to 100% when xanthochromia added.[8]

CT Angiogram

  • A CT followed by CTA is an acceptable alternative to CT and LP[9]
  • CTA has a 98% sensitivity for aneurysms >3mm

Management

Physiologic derangements, such as hypoxemia, metabolic acidosis, hyperglycemia, BP instability, and fever, can worsen brain injury and has been independently associated with increased M&M, but no studies showing benefit of corrections.

  1. Avoid hypotension
    • Maintain MAP>80 (CPP of 60 as long as ICP<20)
    • Give IVF
    • Give pressors if IVF ineffective
  2. Hypertension
    • AHA/ASA has no formal recommendations but states that decreasing to SBP <160 is reasonable[10]
    • Rapid SBP lowering <140 has been advocated with early research showing improved functional outcome[11], but more recent work has found no difference between SBP <140 and <180[12]
    • Ensure appropriate pain control and sedation before adding antihypertensives
  3. Discontinue/reverse all anticoagulation
  4. Nimodipine
    • Only CCB studied that has been shown to prevent vasospasm (associated with improved neuro outcomes and decreased cerebral infarction)
    • Give 60mg q4hr PO or NGT only (never IV) within 96hr of symptom onset. NNT 13 to prevent one poor outcome
    • Keep an eye on BP for fluctuations
  5. Magneisum sulfate
    • Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain between 2-2.5 mmol/L
  6. Seizure prophylaxis
  7. Glucocorticoid therapy
    • Controversial; evidence suggests is neither beneficial nor harmful
  8. Glycemic control
    • Controversial; consider sliding scale if long patient stay in ED while awaiting ICU bed
  9. Keep head of bed elevated
  10. Aneurysm treatment
    • Surgical clipping and endovascular coiling are definitive treatment
    • Antifibrinolytic - Controversial; if delayed aneurysmal treatment, consider short term therapy (<72 hrs) with TXA or aminocaproic acid

Intubation

  • Consider neuroprotective intubation
  • Ensure patient is pain-free for post-intubation sedation
    • Propofol with fentanyl
    • Try to prioritize pain control with fentanyl

AHA Aneurysmal SAH BP Guidelines[14]

  1. No well-controlled studies exist that answer whether BP control influences rebleeding
  2. BP should be controlled to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure (Class I, Level of Evidence B).
  3. Nicardipine, labetalol, and esmolol are appropriate choices for BP control (Sodium nitroprusside may raise intracranial pressure and cause toxicity with prolonged infusion and should be avoided)

Disposition

  • Admit

Complications

Rebleeding

  • Risk is highest within first 24 hours (2.5-4%), particularly within first 6 hours
  • Usually diagnosed by CT after acute deterioration in neuro status
  • Only aneurysm treatment is effective in preventing rebleeding

Vasospasm

  • Leading cause of death and disability after rupture
  • Typically begins no earlier than day three after hemorrhage
  • Characterized by decline in neuro status
  • Aggressive treatment can only be started after aneurysm has been treated
    • treatment for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), balloon angioplasty, or intra-arterial vasodilators[citation needed]
    • Studies have not provided strong evidence of benefit Triple-H therapy[citation needed]

Cardiac abnormalities

Most likely related to the release of catecholamines due to hypoperfusion of hypothalamus

Hydrocephalus

  • Consider ventricular drain placement for deteriorating LOC + no improvement within 24hr

Hyponatremia

  • Hyponatremia is seen in 10%-40% of the patients with subarachnoid hemorrhage who are admitted to the ICU.[15]
  • Cerebral Salt Wasting and SIADH are the two most common causes[16]

Prognosis

Hunt and Hess

Subjective terminology, but good interobserver variability

Grade Description Survival Rate
0 Unruptured aneurysm -
1 Asymptomatic or mild HA and slight nuchal rigidity 70%
1a No acute meningeal/brain reaction, with fixed neurological def -
2 Moderate to severe HA, stiff neck, no neurologic deficit except CN palsy 60%
3 Mild mental status change (drowsy or confused), mild focal neurologic deficit 50%
4 Stupor or moderate to severe hemiparesis 20%
5 Coma or decerebrate rigidity 10%
Grade 1 or 2 have curable disease
Add one grade for serious systemic disease (hypertension, DM, severe atherosclerosis, COPD)

World Federation of Neurosurgical Societies (WFNS)

Objective terminology, and fair interobserver variability

Grade GCS Focal neurological deficit
1 15 Absent
2 13–14 Absent
3 13–14 Present
4 7–12 Present or absent
5 <7 Present or absent

Other scales are also available, including the Ogilvy and Carter scale (comprehensive, yet complex), and the Fisher scale or Claassen grading system (vasospasm index risk).

Note: First-degree relatives are at 2-5 fold increase in SAH, so screening is considered on individual basis.

See Also

External Links

References

  1. Dubosh NM et al. Sensitivity of Early Brain Computed Tomography to Exclude Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis. Stroke 2016. PMID: 26797666
  2. Borczuk, et al. Patients with traumatic subarachnoid hemorrhage are at low risk for deterioration or neurosurgical intervention. J Am Coll Surg. 2014; 219.
  3. Nahmias JT, et al. Mild Traumatic Brain Injuries Can Be Safely Managed Without Neurosurgical Consultation: The End of a Neurosurgical "Nonsult"? American Association for the Surgery of Trauma. Annual Meeting. 2016
  4. Ottawa SAH Rule JAMA. 2013 Sep 25;310(12):1248-55. doi: 10.1001/jama.2013.278018
  5. Perry JJ, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011; 343:d4277.

  6. van Gijn J and van Dongen KJ. The time course of aneurysmal haemorrhage on computed tomograms. Neuroradiology. 1982; 23:153–156.
  7. Gorchynski J, Oman J, and Newton T. Interpretation of traumatic lumbar punctures in the setting of possible subarachnoid hemorrhage: who can be safely discharged? Cal J Emerg Med. 2007; 8(1): 3–7.
  8. Perry JJ, Alyahya B, Sivilotti MLA, et al. Differentiation between traumatic tap and aneurysmal subarachnoid hemorrhage: prospective cohort study. BMJ : British Medical Journal. 2015;350:h568.
  9. Walsh B, Vilke GM, Coyne CJ. Clinical Guidelines for the Emergency Department Evaluation of Subarachnoid Hemorrhage. Meurer WJ, JEM. 2016; 50(4) 696-701.
  10. Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012; 43(6):1711-1737.
  11. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013; 368:2355-2365.
  12. Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016; 1-11. [Epub ahead of print].
  13. Bucher J and Koyfman A. Intubation of the neurologically injured patient. J Emerg Med. 2016; 49:920-927.
  14. Bederson J. et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage: A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Heart Association. Stroke. 2009;40:994-1025 PDF
  15. Woo, M.H, Kale-Pradhan, P.B. Fludrocortisone in the treatment of subarachnoid hemorrhage-induced hyponatremia. Annals of Pharmacotherapy. 1997. 31, 637–639.
  16. Albanese, A. et al. . Management of hyponatremia in patients with acute cerebral insults. Archives of Disease in Childhood, 85. (2001). 246–251.