Subarachnoid Hemorrhage .pptx sms mc jaipur

By Dr Akash Jani
Under the guidance of Dr Arvind Vyas Sir

Introduction
● Overall, about 20% of strokes are hemorrhagic, with SAH and Intracerebral
hemorrhage (ICH) each accounting for 10%.
● A subarachnoid hemorrhage (SAH) is defined as the accumulation of blood in the
space between the arachnoid membrane and the pia mater around the brain
referred to as the subarachnoid space

Pathophysiology
● Hemodynamic stress is the initiating factor for intracranial aneurysm (IA) formation
● Hence it occurs at arterial junctions, bifurcations, or abrupt vascular angles where excessive hemodynamic
stresses are exerted on arterial walls.
● The typical locations include the bifurcation of the basilar artery at the junction of the ipsilateral posterior inferior
cerebellar artery (PICA), vertebral artery, and the anterior communicating artery
● Large unruptured aneurysms compress the adjacent cerebral tissue causing neurological signs. However, the
rupture of these lesions creates a state of reduced blood flow and vasospasm leading to cerebral ischemia.
● Hemodynamic insult initiates the inflammatory process. It leads to matrix metalloproteinases (MMPs)–mediated
degradation of the extracellular matrix and apoptosis of smooth muscle cells (SMCs), which are the predominant
matrix-synthesizing cells of the vascular wall. These processes significantly weaken the arterial wall, resulting in
dilatation, aneurysm formation, and ultimately rupture

NATURAL HISTORY AND OUTCOME OF
aSAH
● Modifiable medical conditions should be identified
early because their outcomes are significantly more
favorable.
● Some of these conditions include seizures,
hydrocephalus, electrolyte abnormalities such as
hyponatremia, status epilepticus, and hypothermia.
● Irreversible brain injury :These patients may have
partially or completely absent brainstem reflexes,
lack of purposeful responses to noxious stimuli,
large ischemic infarct on admission computed
tomography (CT), or presence of global cerebral
edema consistent with anoxic brain injury

CLINICAL
MANIFESTATIONS AND
DIAGNOSIS OF aSAH
● The classic clinical presentation of aSAH in an
awake and alert patient is a headache that is
sudden in onset and immediately reaches
maximal intensity
● When performed within 6 hours of symptom
onset, a negative head CT was likely to miss
<1.5 in 1000 SAHs.

● Application of the rule requires that
patients who present with a severe
headache and meet any of the criteria
may need to undergo additional testing,
as directed by the treating physician
● Use of the Ottawa SAH Rule can
therefore identify a subset of patients
(albeit small) who are unlikely to have
aSAH and thereby avoid additional
imaging and workup that use resources
and expose patients to unnecessary risk

HOSPITAL
CHARACTERISTICS AND
SYSTEMS OF CARE
Lower mortality rates have been demonstrated in some
nonrandomized studies when patients with aSAH are
treated by experienced cerebrovascular surgeons and
neuroendovascular interventionalists
In hospitals with larger volumes of aSAH cases (eg, >35
aSAH cases per year, used in the 2012 aSAH guideline)
compared with smaller volumes of aSAH cases (eg, <10
aSAH cases per year, used in the 2012 aSAH guideline)
and when care is provided in dedicated neurocritical care
units.

EARLY BRAIN INJURY AND CEREBRAL EDEMA AFTER ANEURYSMAL
SUBARACHNOID HEMORRHAGE
● With aneurysmal rupture, intracranial pressure can acutely increase, leading to transient
ischemia and loss of consciousness.
● The combined effects of ischemia and extravasated blood products can lead to early brain
injury, which are processes sustained within the first 72 hours after ictus and are increasingly
the focus of investigation.
● The pathophysiology of early brain injury includes microvascular dysfunction, blood-brain
barrier disruption, inflammation, oxidative cascades, and neuronal death

Acute management
Common complications of aneurysmal SAH related to initial bleeding, rebleeding,
vasospasm and delayed cerebral ischemia, hydrocephalus, increased intracranial
pressure, seizures, and cardiac complications should be sought.

MEDICAL MEASURES TO PREVENT
REBLEEDING AFTER aSAH
1)Prompt obliteration of the ruptured aneurysm is the
only treatment proven to be effective to reduce the
likelihood of rebleeding. Increased BP variability has
been associated with worse outcomes in aSAH and
excessive BP reduction may compromise cerebral
perfusion and induce ischemia, especially in patients
with elevated ICP
2)Immediate anticoagulation reversal in any patient
presenting with aSAH is strongly recommended
3)RCT evaluating ultraearly, short-term antifibrinolytic
therapy in patients with aSAH, ULTRA (Ultra-Early
Tranexamic Acid After Subarachnoid Hemorrhage), did
not show a significant reduction in the rate of
rebleeding and demonstrated no improvement in
functional outcomes

Blood Pressure Control
Sudden surge in central sympathetic stimulation associated with aSAH results in hypertension
Recommendations published in 2023 by the Neurocritical Care Society (NCS) and American Heart Association/American
Stroke Association (AHA/ASA) do not make specific target blood pressure recommendations, but the AHA/ASA guidelines
emphasize a mean arterial pressure goal of 65 mm Hg or higher with the use of the neurologic examination to ensure
sufficient cerebral perfusion
In contrast, the 2012 AHA/ASA recommendations targeted a systolic blood pressure below 160 mm Hg to reduce the
hypothetical risk of rebleeding. In 2013 the European Stroke Organization recommended maintaining a presecurement
systolic blood pressure below 180 mm Hg
To avoid an excessive reduction in blood pressure,especially in patients whose low absolute blood pressure might lead to
inadequate cerebral perfusion, as older studies showed an association between greater reduction in blood pressure and
infarction.Indeed, the 2013 European Stroke Organization guidelines recommended a lower limit of mean arterial pressure of
90 mm hg
The goal should be to avoid extremes of blood pressure to reduce the risk of rebleeding while maintaining cerebral perfusion
pressure

Intermittent dosing medications
Labetalol
beta-blocker
administered over 2
minutes in doses
ranging from 5 to 20
mg IV every 15
minutes
Hydralazine
Vasodilators decrease
systemic resistance and
reduce blood pressure
Incremental IV doses of
20 to 40 mg every 30 to
60 minutes

Continuous infusions
Nicardipine
continuous IV infusion in
titrated doses from 5 to 15
mg/hr
Maintain the systolic blood
pressure of 150 to 160 mm
Hg to prevent rebleeding
Clevidipine
Calcium channel blocker
The onset of action is about 2
to 4 minutes, with a half-life
of about 15 minutes.
Dosing and titration begin at
1 to 2 mg/hr and repeated
every 90 seconds.

Intubation
● A patient with aneurysmal SAH may require tracheal intubation because of poor
oxygenation, hypoventilation, reduced level of consciousness, hemodynamic
instability, or the need for heavy sedation or paralysis.
● During intubation, short-acting induction agents and nondepolarizing agents
should be used for rapid sequence intubation.
● Once intubated, PaCO2 should be maintained between 35 mm Hg and 45 mm hg

Vasospasm Prevention and Treatment
The drug categories that prevent and treat vasospasm include calcium channel blockers,
magnesium, endothelin antagonists, and statins
Calcium Channel Blockers
Calcium channel blockers (CCBs) reduce cardiac and smooth muscle contraction without an effect
on skeletal muscle
Nimodipine is the only treatment with consistent, high-quality evidence for decreasing DCI and is
now standard of care in patients with aSAH
Administration of intraventricular nimodipine showed improvements over standard oral
administration
Oral nimodipine is given in doses of 60 mg every 4 hours or 30 mg every 2 hours for 21 days. If
hypotension is a recurring problem, the recommendation is to administer smaller, more frequent
dosing

Magnesium
● Vasodilation results from an inhibition of Voltage-gated calcium channel-mediated smooth
muscle contractions.
● Various spasmogenic agents such as endothelin-1, norepinephrine, angiotensin II, and serotonin
are counteracted by magnesium
● Magnesium for Aneurysmal Subarachnoid Hemorrhage (MASH-2) trial was a phase 3,
randomized, placebo-controlled trial. A total of 1,204 patients were enrolled. The study concluded
with no improvement in outcomes in the intervention group
● Cochrane metaanalysis also concluded that magnesium cannot be recommended for routine
administration in aSAH

Endothelin Antagonists
● Endothelin antagonists (ET-A) are another potential treatment under investigation
● Clazosentan is a selective ET-A receptor antagonist that demonstrated a decrease and a
reversal in vasospasm after SAH.
● One study, CONSCIOUS-1 (Clazosentan to Overcome Neurological Ischemia and Infarct
Occurring after Subarachnoid Hemorrhage), found a significant dose-dependent effect on
vasospasm when evaluated with angiography.
● Subsequent studies with clazosentan have reported no benefit with this drug

Statins
● Research with statin drugs have also demonstrated a lack of efficacy and have shown no
benefit in the treatment of vasospasm and neither does it improve short term or long term
outcomes in aSAH.
● To date, the recommendations have been to continue the statin medication if the patient had
been taking it prior to the onset of the SAH

Reversal of Anticoagulation
● It is recommended to discontinue all antithrombotic agents and reverse all
anticoagulation until the aneurysm is definitively repaired by surgery or coiling.
● Patients presenting with aSAH on anticoagulant therapy have a worse
prognosis and outcomes.
● Anticoagulants tend to increase the amount of bleeding at the time of rupture,
thereby increasing the overall amount of blood in the subarachnoid space,
basal cisterns, and the parenchyma

VTE Prophylaxis
Thrombotic complications related to venous
thromboembolism (VTE) may be equally as lethal in
patients with stroke.
An accepted clinical practice is to initiate
pharmacological prophylaxis therapy 24 to 48 hours
after surgery with unfractionated or a low-molecular-
weight heparin.
Nurse-driven protocols often support VTE prevention
measures intermittent pneumatic compression (IPC)
devices on admission to the critical care unit
Additional measures may consist of early mobilization
and prevention of dehydration

Hypovolemia (in the perioperative period) may contribute to the incidence
of DCI, whereas hypervolemia lacks benefit.Hence maintenance of
euvolemia is the target
The optimal method to assess and continuously monitor intravascular
volume status and fluid responsiveness in critically ill patients, including
patients with aSAH, remains controversial
Central venous pressure correlates poorly with circulating blood volume
and is not able to predict hemodynamic response to a fluid challenge in
critically ill patients. Therefore, central venous pressure is not an adequate
surrogate measure for intravascular volume status
Intravascular volume depletion in SAH can occur as a result of natriuresis
and may be associated with DCI and poor outcome
Optimization of hemodynamic parameters, including cardiac output,
preload, and stroke volume variability to guide fluid and hemodynamic
management in aSAH during endovascular/surgical therapy and ICU care,
can increase the detection and treatment of dehydration/intravascular
volume depletion and is associated with reduced rates of subsequent DCI,
ICU length of stay (LOS), and unfavorable outcome (mRS score 4–6).
Intravascular volume and
electrolyte management

● Hyponatremia, with or without polyuria or natriuresis, is a prominent clinical feature in
aSAH
● Fludrocortisone to be effective in reducing excess sodium excretion, urine volume,
hyponatremia, and intravenous fluid use during acute aSAH, but fludrocortisone did
not consistently reduce DCI or affect outcome
● Other agents, including high-dose hydrocortisone, have been studied in RCTs and
demonstrated similar effects on serum sodium, urinary sodium excretion, and
natriuresis but reported more medical complications such as hyperglycemia,
hypokalemia, gastrointestinal hemorrhage, and congestive heart failure

Glycemic
Control
● Hyperglycemia on admission, during
aneurysm surgery, or within 72 hours of
aSAH presentation has been associated
with vasospasm, DCI, unfavorable short-
term and long-term functional outcomes,
and risk of death in both patients with
diabetes and those without diabetes in
multiple studies
● Glucose level of 80 to 120 mg/dL had
significantly lower infection rates but had no
effect on overall outcome.
● The prevention of intraoperative
hyperglycemia and hypoglycemia during
aneurysm surgery is probably indicated.

Fever
● Fever is common in acute aSAH, often
refractory to conventional antipyretics, and
associated with worse outcomes in multiple
studies
● Fever in SAH can be due to infectious and
noninfectious causes such as central fever;
systemic inflammatory syndrome and the
etiology should be treated.
● Available fever control/TTM modalities
include pharmacological treatment, surface
cooling devices with or without a feedback
loop, and endovascular cooling devices

Pain Control
● With complaints of the “worst headache of my life health care team needs to provide interventions
to make the patient as comfortable as possible
● Nonopioid medications such as acetaminophen (650 mg PO or 1,000 mg IV) are first line
medications and be administered every 4 to 6 hours; however, consideration must be given to
contraindications, that is, liver diseaase
● Opioid medications such as fentanyl (12.5 to 25 mg IV every hour as needed), Dilaudid (0.2 to 4 mg
IV every 3 to 4 hours as needed), and morphine sulfate (2 to 4 mg IV every 1 to 2 hours as required)
may provide pain relief as well as a degree of sedation and serve to decrease anxiety
● NSAIDs like aspirin should be avoided until the aneurysm is secured

Securing the Aneurysm
● Acute rebleeding occurs in 8% to 23% of patients with aneurysmal SAH, generally
within the first 24 hours of initial rupture
● Studies also suggest better outcomes if aneurysm securement occurs less than 24
hours versus more than 24 hours after ictus
● The most effective action to prevent rebleeding is early and complete aneurysm
securement.

● The treatment goal for aneurysm securement is the complete obliteration of the
ruptured aneurysm. When this is not feasible, partial obliteration is achieved until a
later date when a more complete treatment can be pursued.
● In patients with posterior circulation aneurysms, coiling is preferred if feasible based
on the physical characteristics of the aneurysm.
● For anterior circulation aneurysms (with good-grade SAH) that are deemed equally
amenable to coiling and clipping, there may be better 1-year functional outcomes
with coiling, but equal effects in the long term
● Data does not seem to support any benefit to coiling over clipping for patients older
than 70 years
● For patients younger than 40 years, there may be long-term benefit to clipping

ENDOVASCULAR
METHODS FOR TREATMENT
OF RUPTURED CEREBRAL
ANEURYSMS
Early treatment of ruptured aneurysms reduces the risk
of rebleeding and facilitates treatment of DCI
Retreatment, typically within 1 to 3 months,as allowed
by the patient’s functional status and recovery is
advisable to prevent future rebleeding

● Within the cohort of patients >65 years of
age in ISAT, outcome was dependent on
aneurysm location, with coiling superior in
those with internal carotid and posterior
communicating artery aneurysms but
clipping superior for those with ruptured
middle cerebral artery (MCA) aneurysms
● Longer life expectancy and better long-term
protection from rerupture related to clipping
favor consideration of clipping in young
patients

Although stent-assisted coiling and flow diverters are
associated with higher reported risks of
complications and rebleeding than primary coiling
(including balloon-assisted techniques) or clipping,
their use can be effective in achieving aneurysm
occlusion or reducing rebleeding when other options
for aneurysm treatment are not feasible

Anesthetic Management in Surgical
and Endovascular Treatment of aSAH
Goals include hemodynamic stability, favorable ventilatory
strategies, and absolute lack of movement during
exposure, clipping, or deployment of coils. Anesthetic
medications should be titrated in a manner to facilitate
acquisition of a neurological examination as soon as the
procedure is complete
Both mannitol and hypertonic saline have been used to
decrease ICP and increase cerebral blood flow (CBF) and
brain relaxation.Mannitol is a potent diuretic and can
cause hypovolemia and hypotension, whereas hypertonic
saline increases blood sodium
Multimodal regimen of medication targeting different
chemoreceptors is recommended.Although serotonin 5-
HT3 receptor antagonists (eg, ondansetron), steroids (eg,
dexamethasone), and their combination are the most
frequently used antiemetics, the addition of propofol,
reduction of narcotics, and euvolemia are generally
advocated

Nursing Interventions and
Activities

● After the securement of the aneurysm, attention is directed to the prediction, prevention,
detection, and treatment of delayed cerebral ischemia
● Delayed cerebral ischemia occurs in 20% to 30% of patients with SAH, most commonly with onset
on day 4 to day 10 after ictus, and has a negative impact on outcome
● Clinical deterioration caused by delayed cerebral ischemia is indicated by neurologic signs not
attributable to alternative mechanisms such as seizure, metabolic derangement, or infection
● The definition includes focal neurologic impairment or a decrease of 2 points or greater on the
Glasgow Coma Scale (GCS) for at least 1 hour that is not present immediately after aneurysm
securement
● The definition is operationalized to also include infarction on CT or MRI seen within 6 weeks of SAH
or on autopsy, but not present within 48 hours of aneurysm securement or related to aneurysm
treatment, ventricular catheter, or hematoma

● Vasospasm is likely the most common cause of delayed cerebral ischemia
● Vasospasm is more likely with a higher volume of subarachnoid blood and location
close to the major vessels of the circle of Willis
● Treatment with augmented blood pressure or intraarterial vasodilation is indicated
when patients develop neurologic symptoms

DCI Risk stratification - The VASOGRADE SCALE
The Vasograde scale is a grading system used to predict
the risk of delayed cerebral ischemia (DCI) after an
aneurysmal subarachnoid hemorrhage (aSAH):
● VASOGRADE-Green
(modified Fisher scale 1 or 2 and World Federation
of Neurosurgical Societies scale [WFNS] 1 or 2);
● VASOGRADE-Yellow
(modified Fisher 3 or 4 and WFNS 1–3);
● VASOGRADE-Red
(WFNS 4 or 5, irrespective of modified Fisher
grade).

● The relation between the VASOGRADE and DCI was assessed by logistic regression
models
● VASOGRADE-Yellow had a tendency for increased risk for DCI (odds ratio [OR], 1.31; 95%
CI, 0.77–2.23) when compared with VASOGRADE-Green;
● those with VASOGRADE-Red had a 3-fold higher risk of DCI (OR, 3.19; 95% CI, 2.07–4.50)

Prevention of Delayed Cerebral Ischemia
● Aggressive maintenance of euvolemia
● Individualized monitoring may enable more quantitative goals to ensure adequate perfusion states
● Prophylactic nimodipine, is a mainstay of aneurysmal SAH treatment as it has been shown to improve
outcomes by reducing the incidence and severity of ischemic deficits
● At first, this was thought to be mediated through treatment of vasospasm, but this effect has been difficult to
consistently demonstrate.Rather, nimodipine has pleiotropic effects that in sum prove to be neuroprotective,
and therefore it is administered for 21 days postbleed. The hypotensive threshold at which to hold nimodipine
is a gray area.
● Systemic hypotension may lower cerebral perfusion pressure and worsen ischemia, so if nimodipine results in
hypotension, then dosing intervals should be changed to more frequent lower doses (30 mg every 2 hours
rather than 60 mg every 4 hours). If significant hypotension continues, nimodipine may be discontinued.

The 2023 EARLYDRAIN trial
revealed that early lumbar drainage of 5 mL of CSF hourly, started within 72 hours postbleed
in addition to EVD when clinically indicated, reduced the risk of unfavorable neurologic
outcome (mRS score of 3 to 6) at 6 months (32.6% versus 44.8%) and the risk of secondary
infarctions at discharge (28.5 versus 39.9%).

Detection of Delayed Cerebral Ischemia
● A protocolized clinical nursing examination documenting neurologic change via GCS score is
most often used to detect delayed cerebral ischemia.
● Prospective detection of neurologic deterioration indicative of delayed cerebral ischemia
requires frequent assessments over many days.
● Even with frequent assessments, the attribution of neurologic deterioration to delayed cerebral
ischemia is sometimes delayed or missed in the context of clinical mimics (eg, nonconvulsive
seizure, delirium) or disordered consciousness from structural brain injury or sedating
medications
● Thus, delayed cerebral ischemia is often a retrospectively adjudicated diagnosis.

Transcranial Doppler
● Useful in identifying vasospasm of the large arteries of the circle of Willis and has the best sensitivity for
vasospasm detection in the large arteries where the angle of insonation relative to the angle of the vessel is more
consistent (ie, the middle cerebral artery [MCA] and basilar arteries; 67% for the MCA, 62% for the basilar artery,
33% for the anterior cerebral artery
● Thresholds for concern for vasospasm are a mean flow velocity greater than 120 cm/s (mild), 150 cm/s (moderate),
or 200 cm/s (severe)
● Elevated mean flow velocities could be due to hyperemia, and thus a normalizing ratio can be applied; it is called
the Lindegaard ratio and is the mean flow velocity of the MCA divided by the mean flow velocity of the terminal
internal carotid artery.
● A Lindegaard ratio less than 3 implies hyperemia, while greater than 3 is indicative of vasospasm (greater than 3 is
mild, greater than 4 is moderate, and greater than 5 is severe)
● Elevated velocities on TCD can be used to identify patients who need confirmatory testing or treatment of
vasospasm with cerebral angiography

CT perfusion
● CT perfusion to evaluate for delayed cerebral ischemia and make management decisions as it
improves the accuracy of CT angiography alone for the detection of vasospasm and is more
sensitive than CT angiography
● Time-dependent perfusion parameters (ie, mean transit time, time to peak, and time to drain)
are the most commonly used quantitative features of CT perfusion to detect vasospasm
● There is a strong association between angiographic vasospasm on CT perfusion and infarction.
● CT perfusion seems to have both quantitative and qualitative value in its association with
delayed cerebral ischemia

continuous EEG (cEEG)
● An alpha-to-delta ratio decrease of 10% below baseline lasting 6 consecutive hours or an alpha-to-
delta ratio decrease of at least 50% below baseline lasting 2 or more hours predicts delayed
cerebral ischemia.
● Decreasing relative alpha power variability,
● Rhythmic and periodic ictal-interictal continuum patterns,
● Isolated alpha suppression
● Appearance of epileptiform abnormalities including lateralized rhythmic delta activity, generalized
periodic discharges, and lateralized periodic discharges is a harbinger of delayed cerebral ischemia.

Partial pressure of brain tissue oxygen (Pbto2)
● Pbto2 provides a surrogate measure of regional CBF and represents the balance among oxygen supply,
diffusion, and consumption.
● Pbto2 has been found to help in the early detection of DCI and brain hypoxia
Lactate pyruvate ratio
● Metabolic measure of cerebral oxygen supply and may serve as a biochemical marker of impending
hypoxia/ischemia.
● Lactate/pyruvate ratio and glutamate concentrations have been correlated with DCI in patients with high-
grade aSAH.
Major disadvantage is that they provide information of the regional brain milieu; thus, placement in the highest-
risk area for DCI may be important

Treatment of Delayed Cerebral
Ischemia and Vasospasm

MANAGEMENT OF MEDICAL
COMPLICATIONS ASSOCIATED WITH aSAH
A significant number of patients with aSAH develop multisystem medical complications
● Fever resulting from infectious and noninfectious causes such as central fever;
● Systemic inflammatory syndrome;
● Hyponatremia attributable to cerebral salt wasting or syndrome of inappropriate antidiuretic hormone;
● Infectious complications such as pneumonia and sepsis;
● VTE complications;
● Seizures
● Hydrocephalus
● Cardiac complications, including neurogenic stunned myocardium;
● Respiratory failure requiring mechanical ventilatory support, including ARDS

Management of Hydrocephalus
● The risk of acute hydrocephalus after aSAH
ranges from 15% to 87% in the acute stage.
● aSAH with associated acute symptomatic
hydrocephalus should be managed urgently
by CSF diversion (EVD or lumbar drainage)
to improve neurological condition
● Aseptic technique and the use of antibiotic
impregnated catheters are widely accepted
as best practices to decrease CSF positive
cultures and reduce rates of
ventriculostomy-associated infection.

Management of Seizures
● Seizure-like episodes have been reported in up to
26% patients with aSAH
● High seizure risk features :
Presence of MCA aneurysm, high
clinical/radiological grade (HH grade >3 or Fisher
grade III/IV), cortical infarction, or hydrocephalus
has been associated with an elevated seizure risk.
● Seizure prophylaxis may be reasonable when
associated with aSAH and any of these findings
● Levetiracetam (15-20mg/kg over 30 minutes) is
generally the preferred agent for seizure
prophylaxis

● EEG parameters (quantitative or otherwise) to define
seizures
Epileptiform discharges averaging >2.5 Hz for 10
≥
seconds (>25 discharges in 10 seconds) or any pattern
with definite evolution and lasting 10 seconds.
≥
● In patients with aSAH who present with seizures, the
use of antiseizure medications for <7 days is reasonable
to reduce delayed seizure or hemorrhage risk
● Onset seizures occur at the time of the hemorrhage;
early seizures occur during the first week; and late
seizures are either postoperative or occur after 1 week
● providing antiseizure medications to patients with
aSAH and onset seizures for a period of 7 days serves
≤
to minimize early complications related to the onset
seizure in the perioperative period and decrease long-
term medication side effects

Cardiac complications
● Neurogenic stunned myocardium is common in patients with aneurysmal SAH.
● NSM is a triad of transient left ventricular dysfunction, electrocardiogram changes, and elevation in
cardiac enzymes, often mimicking a myocardial infarction
● The pathophysiology involves excessive catecholamine release during a neurologic injury that
produces increased cardiac demand, stress, and myocytolysis. Most studies showed that the insular
cortex is mostly involved in causing this autonomic dysregulation, especially in stroke patients.
● It is associated with higher rates of delayed cerebral ischemia and poor outcome.
● In the acute management of aneurysmal SAH, clinicians must consider the presence of NSM in the
context of choosing vasopressors, inotropes, or both in the treatment of delayed cerebral ischemia.

Respiratory complications
● Patients with aneurysmal SAH may develop hypoxic
or hypercarbic respiratory failure due to pneumonia,
pulmonary emboli, or neurogenic pulmonary
edema, which is the result of increased capillary
hydrostatic pressure and permeability
● The increase in interstitial and alveolar fluid occurs
very shortly after the ictus.
● While it is wise to include neurogenic pulmonary
edema in the differential of respiratory failure, there
is no targeted treatment beyond supplemental
oxygen for patients who are hypoxemic and it is self-
limited, resolving within a few days.
● The urge to diurese in the setting of pulmonary
edema should be tempered by the primary
importance of maintaining euvolemia

aSAH Long-Term Recovery
● Long-term recovery extends beyond the first
3 months in individuals with aSAH
● Screening tools to evaluate patterns of
depression, anxiety, mobility, and activities
of daily living detailed in the literature
include the State Trait Anxiety Inventory,
Hospital Anxiety and Depression Scale,
Telephone Interview for Cognitive Status,
and Barthel Index at 6 months, 1 year, and
2 years.
● Use of the International Index of Erectile
Function and the Female Sexual Function
Index within the first 4 years
● The median age at dementia diagnosis was
74 years for aSAH compared with 79 years
for ICH and 81 years for ischemic stroke

Delayed imaging is therefore
recommended to identify residual
or regrowth of the treated ruptured
aneurysm and other known,
unknown, or de novo aneurysm(s)
that may require further treatment
to reduce the risk of recurrent
aSAH

Subarachnoid Hemorrhage .pptx sms mc jaipur

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