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COLLEGE OF NURSING
Our Lady of Fatima UniversityNCM 107 B
Our Lady of Fatima University
Valenzuela City, College of Nursing
Case Study: Subarachnoid Hemorrhage
Student: Estanislao, Carmela Marie J.
NCM 107 (RLE) 4Y2-2A, 2nd Semester
Clinical Instructor: Vanessa Umali, RN MAN
Jannuary 30, 2015
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Our Lady of Fatima UniversityNCM 107 B
Introduction
Subarachnoid hemorrhage is sudden bleeding into the subarachnoid
space. The most common cause of spontaneous bleeding is a ruptured aneurysm.
Symptoms include sudden, severe headache, usually with loss or impairment of
consciousness. Secondary vasospasm (causing focal brain ischemia),
meningismus, and hydrocephalus (causing persistent headache and obtundation)
are common. Diagnosis is by CT or MRI; if neuroimaging is normal, diagnosis
is by CSF analysis. Treatment is with supportive measures and neurosurgery
or endovascular measures, preferably in a comprehensive stroke center.
Subarachnoid hemorrhage is bleeding between the arachnoid and pia mater. In
general, head trauma is the most common cause, but traumatic subarachnoid
hemorrhage is usually considered a separate disorder (see Traumatic Brain
Injury (TBI)). Spontaneous (primary) subarachnoid hemorrhage usually results
from ruptured aneurysms. A 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.
Headache is usually severe, peaking within seconds. Loss of
consciousness may follow, usually immediately but sometimes not for several
hours. Severe neurologic deficits may develop and become irreversible within
minutes or a few hours. Sensorium may be impaired, and patients may become
restless. Seizures are possible. Usually, the neck is not stiff initially
unless the cerebellar tonsils herniate. However, within 24 h, chemical
meningitis causes moderate to marked meningismus, vomiting, and sometimes
bilateral extensor plantar responses. Heart or respiratory rate is often
abnormal. Fever, continued headaches, and confusion are common during the
first 5 to 10 days. Secondary hydrocephalus may cause headache, obtundation,
and motor deficits that persist for weeks. Rebleeding may cause recurrent or
new symptoms.
Usually non-contrast CT and, negative, lumbar puncture. Diagnosis is suggested by characteristic symptoms. Testing should proceed as
rapidly as possible, before damage becomes irreversible. Noncontrast CT
is > 90% sensitive and is particularly sensitive if it is done within 6 h of
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symptom onset. MRI is comparably sensitive but less likely to be immediately
available. False-negative results occur if volume of blood is small or if
the patient is so anemic that blood is isodense with brain tissue. If
subarachnoid hemorrhage is suspected clinically but not identified by
neuroimaging or if neuroimaging is not immediately available, lumbar
puncture is done (see Lumbar puncture (spinal tap)). Lumbar puncture is
contraindicated if increased intracranial pressure is suspected because the
sudden decrease in CSF pressure may lessen the tamponade of a clot on the
ruptured aneurysm, causing further bleeding.
CSF findings suggesting subarachnoid hemorrhage include numerous RBCs,
xanthochromia, and increased pressure. RBCs in CSF may also be caused by
traumatic lumbar puncture. Traumatic lumbar puncture is suspected if the RBC
count decreases in tubes of CSF drawn sequentially during the same lumbar
puncture. About 6 h or more after a subarachnoid hemorrhage, RBCs become
crenated and lyse, resulting in a xanthochromic CSF supernatant and visible
crenated RBCs (noted during microscopic CSF examination); these findings
usually indicate that subarachnoid hemorrhage preceded the lumbar puncture.
If there is still doubt, hemorrhage should be assumed, or the lumbar
puncture should be repeated in 8 to 12 h.
In patients with subarachnoid hemorrhage, conventional cerebral
angiography is done as soon as possible after the initial bleeding episode;
alternatives include magnetic resonance angiography and CT angiography. All
4 arteries (2 carotid and 2 vertebral arteries) should be injected because
up to 20% of patients (mostly women) have multiple aneurysms.
On ECG, subarachnoid hemorrhage may cause ST-segment elevation or
depression. It can cause syncope, mimicking MI. Other possible ECG
abnormalities include prolongation of the QRS or QT intervals and peaking or
deep, symmetric inversion of T waves.
About 35% of patients die after the first aneurysmal subarachnoid
hemorrhage; another 15% die within a few weeks because of a subsequent
rupture. After 6 mo, a 2nd rupture occurs at a rate of about 3%/yr. In
general, prognosis is grave with an aneurysm, better with an arteriovenous
malformation, and best when 4-vessel angiography does not detect a lesion,
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presumably because the bleeding source is small and has sealed itself. Among
survivors, neurologic damage is common, even when treatment is optimal.
Treatment in a comprehensive stroke center Nicardipin if mean arterial
pressure is > 130 mm Hg. Nimodipine to prevent vasospasm. Occlusion of
causative aneurysms Patients with subarachnoid hemorrhage should be treated
in a comprehensive stroke center whenever possible.
Hypertension should be treated only if mean arterial pressure is > 130 mm
Hg; euvolemia is maintained, and IV nicardipin is titrated as for
intracerebral hemorrhage (see Intracerebral Hemorrhage). Bed rest is
mandatory. Restlessness and headache are treated symptomatically. Stool
softeners are given to prevent constipation, which can lead to straining.
Anticoagulants and antiplatelet drugs are contraindicated.
Vasospasm is prevented by giving nimodipine 60mg po q 4 h for 21 days to
prevent vasospasm, but BP needs to be maintained in the desirable range
(usually considered to be a mean arterial pressure of 70 to 130 mm Hg and a
systolic pressure of 120 to 185 mm Hg). If clinical signs of acute
hydrocephalus occur, ventricular drainage should be considered.
Learning Objectives
Upon completion of our affiliation here Armed Forces of the Philippines Medical Center
To gain new information about the patient’s disease and its etiology,
pathophysiology, clinical manifestations as well as the standard medical
and nursing management so that we may apply this newly-acquired knowledge to
our patient as well as similar situations in the future
Patient’s Profile
Name: G.B
Age: 66 y/o
Civil Status: Married
Date Admitted: 03-01-2015
Time Admitted: 6:20 PM
Sex: Male
Religion: Catholic
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Diagnosis: CVD probably infarct R, hypertensive cardio vascular disease
Present Health HistoryCase of B.G 66y/o, male, patient was brought to the hospital due to
vehicular accident with multiple physical injuries. Patient was diagnosed
with Traumatic subarachnoid
Family History(+))Hypertension
(-) DM
(-) Allergy
Anatomy and Physiology
MeningesThe meninges (they are serous membranes) are three layers of protective
tissue called the dura mater, arachnoid mater, and pia mater — meninges of the brain and spinal cord are continuous, being linked through the magnum
foramen. Below is a simplified illustration of the meninges around the
brain.
Dura MaterMost superior of the layers —it is tough and inflexible and forms several
structures that separate the cranial cavity into compartments and protect
the brain from displacement.
Arachnoid MaterMiddle layer of the meninges — makes arachnoid villi, small protrusions
through the dura mater into the venous sinuses of the brain, which allow CSF
to exit the sub-arachnoid space and enter the bloodstream.
Cerebrospinalfluid(CSF) flows under the arachnoid in the subarachnoid space.
Pia MaterThe delicate innermost layer of the meninges a thin fibrous tissue that is
impermeable to fluid which allows it to enclose CSF (cerebrospinal fluid).
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By containing CSF, pia works with the other meningeal layers to protect and
cushion the brain. Allows blood vessels to pass through and nourish the brai
The perivascular space created between blood vessels and pia mater functions
as a lymphatic system for the brain. Lines the brain down into
its sulci (folds).Sulcus isa depression on the cerebral cortex while. Gyrus ridge on the cerebral cortex.
The Spaces Between the Layers:Epidural Space Between the dura mater and the skull. Common location for hemorrhaging in the brain.
Subdural SpaceBetween the dura mater and the middle layer of the meninges, the arachnoid
mater. When bleeding occurs, blood may collect here and push down on the
lower layers of the meninges, possible causing brain damage.
Subarachanoid SpaceFrom the fourth ventricle, the cerebrospinal fluid passes into the
subarachnoid space where it circulates around the outside of the brain and
spinal cord and eventually makes its way to the superior sagittal sinus via
the arachnoid granulations also called arachnoid villi. In the superior
sagittal sinus, the cerebrospinal fluid is reabsorbed into the blood stream.
Cerebrospinal fluid (CSF) — clear, saline bodily fluid that occupies the subarachnoid space and the ventricular system around and inside the brain.
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It is produced continuously at a steady rate and is essential for the normal
functioning of the CNS. It acts as a cushion for the neuraxis, also bringing
nutrients to the brain and spinal cord and removing waste from the system.
Pathophysiology
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COLLEGE OF NURSING
Our Lady of Fatima UniversityNCM 107 B
Exam Name Result Reference Range
Hemoglobin 159 g/ L 130 – 170
Hematocrit 46.70 % 40 – 54
RBC 5.94 10^6/ uL 4 – 6
MCV 78.60 fL 86 – 110 Low
MCH 28.80 pg 26 – 38
MCHC 34.00 g/ dL 31 – 37
WBC 24.25 10^3/ uL 4.5 – 10.5 High
Diff Count
Nuet% 86.8 % 40.0 – 80.0 High
Lymph% 8.9 % 20 – 40 Low
Baso% 0.2 % 0 - 5
Mono% 7.1 % 0 – 12
Eo% 0.1 % 0 – 6
PLT 375.00 10^3/ uL 150 – 450
RDW-SD 41.40 fL 37 - 54
Diagnostic Exams
Hematology
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CT Scan
Impression:
Acute Hemorrhage, Right Basal Ganglia with Subarachnoid Extension
Cerebral Edema
Physical Assessment
SKIN: (-) lesionHEENTS:CHEST: symmetricalHEART: (-) murmurLUNGS: (-) retractionABDOMEN: (-)murmurGENITALIA: N/A
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RECTUM: N/AEXTREMITIES: peripheral pulses are equalNEUROLOGICAL: GCS 10 L sided weakness