NEURO - SUBARACHNOID HEMORRHAGE

● GENERAL DATA
● 37 years old
● Female
● Right handed
● Call center agent
● Admission: July 20, 2020
● Source of Info:
○ Mother
○ (100% reliability)
● CHIEF COMPLAINT
○ DEPRESSED SENSORIUM
● HISTORY OF PRESENT ILLNESS
○ 6 HRS PTA
■ Severe headaches, nausea and vomiting
■ Medication taken:
● Mefenamic acid 500mg- analgesic (relieve mild to moderate pain)
● Metoclopramide- anti-emetic
○ 2 HRS PTA
■ Frothy salivation + upward rolling of eyeballs + stiffening of extremities (2
mins)
■ Could not be aroused and just moaned when stimulated with no eye
opening
○ Further Management
■ BP of 180/100 mmHg systole (above normal vs. Normal BP: < 120/80
mmHg)
■ Management applied:
● IV line
● 2 mg. bolus of Nicardepine- treat high blood pressure
● PAST MEDICAL HISTORY
○ Not a known hypertensive, diabetic, asthmatic
○ No FDA
○ Non-smoker, non-alcoholic
○ No hospitalizations, no maintenance medications
○ No illicit drug use
○ No history of seizures
○ LMP: June 4, 2020, Irregular menstrual cycles
● PHYSICAL EXAM
○ Vital signs:
■ BP: 220/116 mmHg
● HYPERTENSIVE ENCEPHALOPATHY
● Hypertension causes turbulent flow to the weak wall of the blood
vessel, contributing to development of aneurysmal rupture
● insults to the CNS triggers generalized sympathetic nervous system
activation (High NE production)
■ HR: 94bpm
■ RR: 22/min
■ Temp: 38.5 C
● Meningeal irritation may induce temperature elevations up to 39
deg C (102.2 deg F)
● Fever- cytokine-induced upward displacement of the set point of
the hypothalamic thermoregulatory center.
● CAN ALSO ADD TO DECREASE SENSORIUM
○ HEAD AND NECK
■ (-) thyroid enlargement
■ (-) neck veins engorgement
■ (-) LAD
○ CARDIOVASCULAR
■ (-) murmurs
■ Normal heart rate
■ Regular rhythm
○ RESPIRATORY
■ (+) tachypnea
■ (+) harsh breath sounds
■ Equal chest expansion
■ insults to the CNS triggers generalized sympathetic nervous system
activation (High NE production)
○ PERIPHERAL VASCULAR
■ Full and equal pulses
■ (-) cyanosis
○ FUNDOSCOPY
■ Unsuccessful due to restlessness
■ IF EVER PERFORMED, MAY SHOW ACUTE HEMORRHAGES FROM SUDDEN
INCREASED ICP OR SUBHYALOID (SUPERFICIAL RETINAL) HEMORRHAGES
● STRONGLY SUGGESTIVE OF SAH
 ● It is an intraocular collection of blood contained between the layer
of vitreous and retina
● TERSON SYNDROME - the combination of SAH and subhyaloid
hemorrhage (blood from the subarachnoid space erupt directly
into the retinal space through the optic nerve (CN II) sheath)
○ OTHER SYSTEMS: UNREMARKABLE
● NEURO EXAM
○ MSE
■ (+) stupor
■ No eye opening to pain
■ With aneurysmal rupture, bleeding occurs mainly in the subarachnoid
space rather than the brain parenchyma (intracerebral hemorrhage),
therefore prominent focal neurologic signs are uncommon.
○ CRANIAL NERVE EXAMINATION
■ CN II and III - Pupillary reactions
● Pupils 2mm
● BERTL (Brisk and equally reactive to light)
● Isolated dilation of a pupil and loss of the pupillary light reflex
may reflect brain herniation as a result of rising intracranial
pressure (pressure inside the skull).
○ SENSORY
■ Withdraws extremities from painful stimuli (bilateral)
○ MOTOR
■ (-) clonus
■ Few spontaneous at times purposeful movements of extremities
○ REFLEXES
■ (+) Babinski (bilateral)
■ +3 DTRs bilaterally (very brisk, may or may not be normal)
○ CEREBELLAR
■ (-) Nystagmus
○ MENINGEALS
⬥ (+) Nuchal rigidity
⬥ (+) Brudzinski
⬥ (+) Kernig’s
⬥ Meninges—the arachnoid mater and pia mater—are inflamed. While the
dura mater may have little to no inflammation, its nerve fibers may
become activated and contribute to neck pain and nuchal rigidity.
 ● IMPRESSION
○ Category of lesion
■ Vascular, non-infectious, non-traumatic
■ Vascular - because of sudden onset
■ If infectious - it is already meningitis
■ Non traumatic - because the patient does not have any traumatic injury
○ Etiology of lesion
■ Rupture of a saccular “berry” aneurysm
○ Localization
■ 85-90% occur in anterior circulation of willis (according to
sciencedirect.com and Harrisons)
■ According to GREENBERG
● MIDDLE CEREBRAL ARTERY DISTRIBUTION = most common
location
■ According to HARRISONS
● 85% of berry aneurysm occur in the anterior circulation of willis
Etiology of SAH
● Subarachnoid hemorrhage - bleeding between the arachnoid and pia mater.
● In general, head trauma is the most common cause of subarachnoid hemorrhage
○ If there is absence of head trauma, berry aneurysm is the most common cause
● Spontaneous (primary or non-traumatic) subarachnoid hemorrhage usually results
from ruptured aneurysm
● Congenital intracranial saccular or berry aneurysm is the cause in about 85% of
patients. Bleeding may stop spontaneously.
● Aneurysmal hemorrhage may occur at any age but is most common from age 40 to 65.
● Less common causes are mycotic aneurysms, arteriovenous malformations, and
bleeding disorders.
Pathophysiology of SAH
● Blood in the subarachnoid space causes a chemical meningitis that commonly increases
intracranial pressure for days or a few weeks.
● Secondary vasospasm may cause focal brain ischemia; about 25% of patients develop
signs of a transient ischemic attack (TIA) or ischemic stroke.
● Brain edema is maximal and risk of vasospasm and subsequent infarction (called angry
brain) is highest between 72 hours and 10 days.
● Secondary acute hydrocephalus is also common.
● A 2nd rupture (rebleeding) sometimes occurs, most often within about 7 days.

Classic presentation
● sudden onset of severe headache (thunderclap headache), often described as the
"worst headache of my life."
○ Rupture of intracranial artery elevates ICP and distorts pain-sensitive structures,
producing headache
○ Intracranial pressure may reach systemic perfusion pressure and acutely decrease
cerebral blood flow; together with the concussive effect of the rupture, this is
thought to cause the loss of consciousness.
○ SUDDEN ONSET OF HEADACHE
■ Most important clinical manifestation (HARRISONS)
■ Essential feature of SAH (GREENBERG)
○ SUDDEN ONSET OF COMA
■ suggest a vascular origin, especially SAH
● Less severe hemorrhages may cause headache of moderate intensity, neck pain, and
nonspecific symptoms.
● Headache in the setting of a ruptured intracranial aneurysm is common and probably
represents amnesia for the event.
● The headache may be accompanied by nausea and/or vomiting from increased ICP and
meningeal irritation.
a. NORMAL ICP = 0 and 18 mmHg
b. INCREASED ICP = >20 mmHg lasting for 5 minutes or longer
● Symptoms of meningeal irritation, including
a. nuchal rigidity and pain
b. back pain, and
c. bilateral leg pain, (a-c, occur in as many as 80% of patients with SAH but may
take several hours to manifest)
d. Photophobia and visual changes are common.
e. Focal neurologic deficits may also occur.
 ● Sudden loss of consciousness (LOC) occurs at the ictus in as many as 45% of patients as
intracranial pressure (ICP) exceeds cerebral perfusion pressure (blood flow to the brain is
limited)
a. Elevated intracranial pressure
Cerebral Perfusion Pressure (CPP)- pressure gradient between the systemic blood
pressure and the pressure in the cranial compartment. The pressure difference is the
gradient that is necessary to "drive" blood from the aorta into the cranial compartment.
● LOC often is transient; however, approximately 10% of patients remain comatose for
several days, depending on the location of the aneurysm and the amount of bleeding.
● Seizures during the acute phase of SAH occur in 10-25% of patients.
● Seizures result from the sudden rise in ICP or direct cortical irritation by blood.
● No correlation exists between the seizure focus and the anatomic site of aneurysm
rupture.

8. DIFFERENTIAL DIAGNOSIS
I. ACUTE BACTERIAL MENINGITIS
● classic triad of fever, headache, and neck stiffness.
● symptoms can develop over several hours or over 1-2 days. And worsens 3-5 days
after
● Other symptoms can include the following:
○ Nausea
○ Vomiting
○ Photalgia (photophobia) - Discomfort when the patient looks into bright
lights
○ Sleepiness
○ Confusion
○ Irritability
○ Delirium
○ Coma
● Photophobia and petechiae/ purpuric lesions are not seen in our patient
II. VIRAL MENINGITIS
● Classic triad consists of fever, nuchal rigidity, and headache, but not all patients
have all 3, and almost all patients have headache
● Altered sensorium
● Not elicited by the patient: Photophobia, Pain on moving the eyes, Mild
lethargy/ drowsiness, Abdominal pain/diarrhea, Myalgia, Altered sensorium
III. VIRAL ENCEPHALITIS
● Inflammation of the brain parenchyma
● Symptoms
○ Headache
○ Fever
○ (+) Nuchal rigidity
○ Altered sensorium
● Symptoms not elicited by the patient:
○ Focal/diffuse neurologic signs and symptoms
○ Hallucination
○ Agitation
○ Confusion
○ Behavioral change, personality change
○ Focal/generalized seizures
IV. BRAIN ABSCESS
● focal, suppurative infection within the brain parenchyma, typically surrounded by
a vascularized capsule
● CLASSIC CLINICAL TRIAD = headache, fever and focal neurological deficit.
○ Headache
■ Is the most common symptom of brain abscess (>75% cases)
■ often characterized as a constant, dull, aching sensation
○ Fever
■ The second most common symptom
■ present in only 50% of patients at the time of diagnosis
○ Focal neurologic deficit is not seen in the patient of our case study.
■ present in <50% of brain abscess cases
■ Include hemiparesis, aphasia, visual field defects
● Nystagmus and ataxia
○ Common signs of cerebellar abscess
○ not seen in our patient
● Elevated ICP
○ Dominant presentation of cerebellar abscess
○ nausea, vomiting - seen in our patient
○ papilledema and drowsiness or confusion - not seen in our patient
 V. HYPERTENSIVE INTRAPARENCHYMAL HEMORRHAGE
● Usually results from spontaneous rupture of a small penetrating artery deep in
the brain
● The most common sites are the basal ganglia, (especially the putamen),
thalamus, cerebellum and pons
● CLINICAL MANIFESTATIONS
○ occur while the patient is awake and when stressed
○ presents as the abrupt onset of focal neurologic deficit that worsens
steadily over 30-90 mins
○ associated with diminishing level of consciousness and signs of increased
ICP such as headache and vomiting.
○ characterized by occipital headache, repeated vomiting, and ataxia of
gait.
○ Dizziness and vertigo may be prominent.
● hyperapnea, severe hypertension and hyperhidrosis - not seen in our patient
● Seizures - seen in our patient but absent in intraparenchymal hemorrhage
● Contralateral hemiparesis - the sentinel sign.
● As the hours pass, the patient often becomes stuporous and then comatose
from brainstem compression or obstructive hydrocephalus.
VI. SUBDURAL/EPIDURAL HEMATOMA
● Are hemorrhages beneath the dura or between the dura and skull
● CLINICAL MANIFESTATION
○ Unilateral headache and slightly enlarged pupil on the side of the
hematoma
○ Stupor, coma, hemiparesis, and unilateral pupillary enlargement are signs
of larger hematomas
○ Drowsiness, confusion, or mild hemiparesis- not seen in patient
○ Chronic subdural hematoma = headache is common.
○ Slowed thinking, vague change in personality, seizure or a mild
hemiparesis - not seen in our patient
○ Drowsiness, inattentiveness and incoherence of thought are more
generally prominent - not seen in patient
○ brief episodes of hemiparesis or aphasia that are indistinguishable from
transient ischemic attacks. - not seen in patient
○ Epidural hematoma on the other hand evolve more rapidly and are more
treacherous.
○ Most patients are unconscious when first seen.
 ○ A “lucid interval” of several minutes to hours before coma supervenes is
most characteristic of epidural hemorrhage, but is still uncommon.

9. DIAGNOSTICS
● CT SCAN
○ Patients presenting with SAH are investigated first by CT scan w/c confirms the
hemorrhage in more than 90% of patients with aneurysmal rupture
○ Generally indicates presence of blood in the SA space
○ May identify the source of bleeding
○ Most sensitive in first 6 hrs after bleeding, when sensitivity approaches 100%
○ If results are normal despite clinical findings suggestive of subarachnoid
hemorrhage, CSF should be examined.
● LUMBAR PUNCTURE
○ The hallmark of aneurysmal rupture is blood in the CSF
○ SAH CSF PROFILE
■ Appearance: pink or red (supernatant yellow)
● CSF contains 100k to >1million rbcs/uL
● As heme from rbc is degraded, first to biliverdin and then to
bilirubin, the supernatant of centrifuged CSF becomes
yellow-tinged (xanthochromic) within 12hrs after hemorrhage
■ OP: inc
■ RBC: inc
■ WBC: normal or inc
■ Glucose: normal or dec
■ Protein: normal or inc
■ Culture (-)
○ Lumbar puncture yields bloody CSF which does not clear as increasing amounts
of CSF are removed
○ Contraindication = space occupying lesion
● FOUR-VESSEL CONVENTIONAL X-RAY ANGIOGRAPHY
○ Gold standard for assessment of ruptured aneurysm
○ Both the carotid and vertebral arteries should be studied to visualize the entire
cerebral vascular anomaly (cerebrovascular arteries have absent external
lamina)
○ Helps localize and define the anatomic details of the aneurysm
○ Should be performed at the earliest convenient time
● CT ANGIOGRAPHY
○ Alternative method for locating aneurysm/unruptured aneurysm
 ○ May demonstrate an underlying vascular malformation or aneurysm
○ May be sufficient to plan definitive therapy
● OTHER TESTS NOT INCLUDED IN PPT
○ CEREBRAL ARTERIOGRAPHY
■ Detection of the underlying lesion in patients with subarachnoid
hemorrhage who are considered good operative candidates
○ TRANSCRANIAL ULTRASOUND DOPPLER
■ Detect intracranial lesions or vasospasms
10. MEDICAL MANAGEMENT
● Surgical repair: “Clipping” or “coiling” of the aneurysm
○ Clipping the neck of the aneurysm to induce clotting/to eliminate risk of
rebleeding
○ The goal of surgery is to prevent re-rupture and secure it. It will not improve
the GCS score of a patient since the damage is already there.
○ Hunt and hess grade 1 and 2 (or 3) shows improvement
○ Hunt and hess grade 4 and 5 do not benefit
● Endovascular technique: placement of platinum coils or other embolic material within
the aneurysm via a catheter
● Protect the airway
● Manage blood pressure before and during aneurysm treatment
● Prevent rebleeding prior to treatment
● Manage vasospasm
● Treat hydrocephalus- urgent placement of a ventricular catheter for external CSF
drainage; some pts will require permanent shunt placement.
● Treat hyponatremia
○ There is natriuresis and volume depletion with SAH, so patients become both
hyponatremic and hypovolemic. “Salt wasting”
● Prevent pulmonary embolus
● Emergent ventriculostomy - indicated due to (+) stupor
● Mild sedation and analgesia - for headache and neck pain
● Adequate hydration - to avoid a decrease in blood volume and brain ischemia
 ● Glucocorticoids - for headache and neck pain
● Nimodipine (60 mg PO every 4h) - prevents ischemic injury (calcium channel blocker)
○ Reduces vasospasm, thus reducing the sequelae of ischemic injury
● Supplemental oral salt with normal saline/hypertonic saline - for hyponatremia
● Pneumatic compression stockinc- to prevent pulmonary embolism
● Manage Increased ICP
○ Mannitol 20% infusion
○ 0.25 to 2 gm/kg by fast drip, then 75-100 cc, Q 4-6 hrs
● DR. YUSAY COMMENTS
○ PUT PATIENT IN A DARK, QUIET, FEW STIMULATION ROOM, IF NOT POSSIBLE,
SEDATE THE PATIENT
○ GIVE STOOL SOFTENERS - to avoid pressure/exertion
○ GIVE COUGH SUPPRESSOR - to avoid pressure/exertion
11. PROGNOSIS
● After craniotomy:
○ Use of inferior vena cava filters to prevent further pulmonary emboli
● After endovascular treatment:
○ Systemic anticoagulation with heparin
● 60% survival of symptom-free patients on day 1
● 30% survival of somnolent patients on day 1
● 90% of patients recover after SAH from ruptured AVM
Of those who survive, more than half are left with major neurologic deficits as a result of the
initial hemorrhage, cerebral vasospasm with infarction or hydrocephalus.
CORRECT ANSWER IS = GCS 8
Because patient has purposeful movements
(I THINK ANG GINA MEAN NILA NGA LINDGUARD SCALE, AMO NI ANG FISHER SCALE?)

Notes taken from Dr. Garcia’s preceptorial

● Gold standard for assessment of ruptured aneurysm: 4-vessel angiography
● Basal ganglia- most common site of Intracerebral Hemorrhage. Motor systems pass
through here.
● A vascular event is acute in onset, in contrast to a brain tumor.
● A contraindication for lumbar puncture: space-occupying lesion (but nka mention si doc
nga depende gyapon sa practitioner?)
● Stunned myocardium can happen due to the ruptured aneurysm leading to ECG
changes.
● More seizures = inc ICP = inc risk of re-rupture = poor prognosis
● Inc fever/temp = inc ICP = poor prognosis
● CN III - affected at symptomatic aneurysm involving the PComm. Uncal herniation and
ruptured PComm aneurysm both cause 3rd nerve palsy.
○ (HARRISONS)
○ THIRD CRANIAL NERVE PALSY
■ Associated with pupillary dilation, loss of ipsilateral (but retained
contralateral) light reflex, focal pain above or behind the eye
■ Occur at the junction of posterior communicating artery and internal
carotid artery
○ SIXTH NERVE PALSY
■ Aneurysm in the cavernous sinus, visual field defects may occur
 ■ Occur with an expanding supraclinoid carotid or anterior cerebral artery
aneurysm
○ OCCIPITAL AND POSTERIOR CERVICAL PAIN
■ Posterior inferior cerebral artery or anterior inferior cerebellar artery
aneurysm
○ PAIN IN OR BEHIND THE EYE AND LOW TEMPLE
■ Middle cerebral artery aneurysm
● Hypertension causes turbulent blood flow to the weak wall of the blood vessel,
contributing to the development of an aneurysm, eventually a rupture.
● Cerebrovascular arteries have absent external lamina.
● If at 4-vessel angiogram shows no aneurysm but there is SAH, the aneurysm is most
likely a thrombosed aneurysm. The dye cannot pass through the blood clot. (Ma repeat
raw test after 2 weeks? Kay ma lyse ang clot by then?)
● The goal of surgery for an aneurysm is to prevent re-rupture and secure it. It will not
improve GCS of a px because the damage is already there.
● The sudden increase of ICP can cause the sudden drop in GCS.
● To check brainstem function, check the cranial nerves. CN III to XII are present at the
brainstem.
● AV Malformations cause Intracerebral Hematomas, not SAH. The location of AVMs are
at the brain parenchyma.
● Transcranial Dopplers can check for vasospasms. (Something about a Lindguard scale?
Idk sa spelling hahaha. A grade of >3 suggests vasospasm).