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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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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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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