Subarachnoid Hemorrhage: A Case Study 1

Subarachnoid hemorrhage is also known as or subsumes Meningeal hemorrhage. Drs. Hornik

and Brorson of the University of Chicago review the epidemiology, pathophysiology, diagnostic
evaluation, and treatment of spontaneous subarachnoid hemorrhage and its secondary
complications, including aneurysm rebleed, hydrocephalus, hyponatremia, seizures, delayed
cerebral ischemia, and cardiopulmonary problems. Newer hypotheses on the mechanism of
delayed cerebral ischemia following subarachnoid hemorrhage are explained. Updated
recommendations from the 2011 Neurocritical Care Society Guidelines and the 2012 American
Heart Association/American Stroke Association guidelines for the management of aneurysmal
subarachnoid hemorrhage are included.
Key points
Subarachnoid hemorrhage constitutes a life-threatening neurologic emergency and
typically presents with a sudden severe headache, most often occurring from ruptured
intracranial aneurysm.
The most common diagnostic error accounting for missed diagnosis of subarachnoid
hemorrhage is failure to obtain a noncontrast head CT.
The most important predictive factors for acute prognosis after subarachnoid
hemorrhage include level of consciousness, neurologic grade on admission, patient age,
and amount of blood on initial scan.
Delayed cerebral ischemia following subarachnoid hemorrhage has been considered to
be a direct consequence of vasospasm; however, an emerging body of literature
suggests a multifactorial etiology beyond pure cerebral arterial constriction.

Subarachnoid Hemorrhage: A Case Study 2
Pathophysiology
Aneurysms are acquired lesions related to hemodynamic stress on the arterial walls at
bifurcation points and bends. Saccular or berry aneurysms are specific to the intracranial
arteries because their walls lack an external elastic lamina and contain a very thin adventitia
factors that may predispose to the formation of aneurysms. An additional feature is that they lie
unsupported in the subarachnoid space.
Aneurysms usually occur in the terminal portion of the internal carotid artery and the branching
sites on the large cerebral arteries in the anterior portion of the circle of Willis. The early
precursors of aneurysms are small outpouchings through defects in the media of the arteries.
These defects are thought to expand as a result of hydrostatic pressure from pulsatile blood
flow and blood turbulence, which is greatest at the arterial bifurcations. A mature aneurysm has
a paucity of media, replaced by connective tissue, and has diminished or absent elastic lamina.
The probability of rupture is related to the tension on the aneurysm wall. The law of La Place
states that tension is determined by the radius of the aneurysm and the pressure gradient
across the wall of the aneurysm. Thus, the rate of rupture is directly related to the size of the
aneurysm. Aneurysms with a diameter of 5 mm or less have a 2% risk of rupture, whereas 40%
of those with a diameter of 6-10 mm have already ruptured upon diagnosis.
Although hypertension has been identified as a risk factor for aneurysm formation, the data
with respect to rupture are conflicting. However, certain hypertensive states, such as those
induced by use of cocaine and other stimulants, clearly promote aneurysm growth and rupture
earlier than would be predicted by the available data.
Subarachnoid Hemorrhage: A Case Study 3
When an aneurysm ruptures, blood extravasates under arterial pressure into the subarachnoid
space and quickly spreads through the cerebrospinal fluid around the brain and spinal cord.
Blood released under high pressure may directly cause damage to local tissues. Blood
extravasation causes a global increase in intracranial pressure (ICP). Meningeal irritation occurs.
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 h and 10 days. Secondary acute hydrocephalus is also common. A
2nd rupture (rebleeding) sometimes occurs, most often within about 7 days.

Subarachnoid Hemorrhage: A Case Study 4
Biographic Data
Name: RD
Age: 47 y/o
Gender: Male
DOB: Jan 15, 1947
Address: 51 Milagros Street Villa Sabina Subdivision, Talipapa Q.C
Religion: Roman Catholic
Nationality: Filipino

Chief Complaint:
Behavioral changes with a duration of a few hours

Present History of Illness
Five days prior to admission, patient was in good shape until he experienced bifronto-parietal
headache radiating up to the neck with a pain scale of 10/10. Pain felt by the patient was
accompanied by vomiting. Patient consulted a local hospital first; complete blood count and
urinalysis were done revealing an elevated WBC with neutrophile predominance and WBC in the
patients urine. It was then treated to be a case of urinary tract ifection wherein patient was
given the following medications; Oxacilin, tramadol, Vitamin B Complex and Benadryl which was
able to provide temporary relief for the patient.
A few hours prior to admission, the symptoms stated above persisted. Patient became
unconscious for a period of 5-10 minutes. Patient was noted to have behavioural changes and
disorientation to time and place when awakened. Patient was then brought at Pacific Medical
Center and was diagnosed as a case of viral encephalitis versus alcohol withdrawal versus
Subarachnoid Hemorrhage: A Case Study 5
bacterial meningitis. Patients family was advised that a cranial CT scan must be done but due to
financial constraints, they decided to transfer the client thus the admission to our institution.

Past Medical History
Patient was tested having none of the following: Hypertension, Diabetes Mellitus, neither
Cancer nor asthma. The patients immediate family also had neither of the following diseases
stated above.
The patient was a smoker for years and also used to drink heavily for almost every day.
Nursing Physical Assessment
Patient R.D was conscious, coherent and flat on bed. The patient was disoriented of the date
time and place. The patient was not in cardio-respiratory distress. The patients temperature
was 36.5C, his blood pressure was 150/90mmHg, his pulse rate was 86 and his respiratory rate
was 18cpm. The patient had intravenous fluid of PNSS 1L at 30gtts/min. R.Ds skin was brown in
color, moist with good skin turgor, no active lesions and no active dermatoses. His Head and
neck was normocephalic and anicteric sclera. His eyes were pink palpable conjunctiva. There
was no aural discharge and tenderness with his ears. The nose was clear, and there was no
naso-aural discharge. The throat had no tonsil pharyngeal congestion. The chest and lungs was
symmetrically expanding with no tractions, no lagging, and clear breath sounds. The heart had a
dynamic precordium, tachycardia but no murmurs noted. The abdomen was soft, flat, no
tenderness and no masses. Lastly, the extremities had full equal pulses, no edema, no cyanosis,
no fractures and deformities and it has glossy normal extremities. The patient was on high
protein, high calorie diet and restricted to fat intake. The patient was attentive and
accommodating. The patient was also oriented in his condition and was able to perform
independent activities of daily living.

Subarachnoid Hemorrhage: A Case Study 6
Related Treatment
According to the history of (Patients name) there is no known allergy with medications. His
current treatment beside intravenous fluids, he was prescribed nimodipine, amlodipine,
keterolac, lactulose, mannitol, simvastatin, paracetamol. Nimodipine and Amlodipine are
calcium channel blockers, calciums entry critical for the conduction of the electrical signal that
passes from muscle cell to muscle cell of the heart, and signals the cells to contract. It also is
necessary in order for the muscle cells to contract and thereby pump blood. It is for
Hypertensive patients. Another medication prescribed was Simvastatin, The primary uses of
simvastatin are for the treatment of dyslipidemia and the prevention of cardiovascular disease.
It is recommended to be used only after other measures such as diet, exercise, and weight
reduction have not improved cholesterol levels sufficiently. Moreover, Lactulose was part of
(Patients name) treatment, as stated in 2003, (copyrighted in 2014) It is for the prevention and
treatment of portal-systemic encephalopathy, including the stages of hepatic pre-coma and
coma. In addition, Mannitol promotes diuresis in the prevention or treatment of the oliguric
phase of acute renal failure before irreversible renal failure becomes established. Reduction of
intracranial pressure and brain mass, Reduction of high intraocular pressure when the pressure
cannot be lowered by other means, and Promotion of urinary excretion of toxic materials.
Subarachnoid Hemorrhage: A Case Study 7
Nursing Care Plan
Cerebral aneurysm is an outpouching of the wall of a cerebral artery that results from
weakening of the wall of the vessel. It is difficult to determine the frequency of cerebral
aneurysm because of differences in the definitions of the size of aneurysm and the ways that
aneurysms are detected. The prevalence is estimated to range from 5% to 10%; unruptured
aneurysms account for approximately 50% of all aneurysms.
Cerebral aneurysm have a variety of sizes, shapes, and causes. Most cerebral aneurysm are
sacular or berry-like with a stem and a neck. The incidence of cerebral aneurysm has been
estimated at 10 per 100,000 per population, with approximately 15% to 25% of patients having
multiple aneurysms, often bilateral in the same location on both sides of the head. Clinical
concern arises if an aneurysm ruptures or becomes large enough to exert pressure on
surrounding structures. When the vessel wall becomes so thin that it can no longer withstand
the surrounding arterial pressure, the cerebral aneurysm ruptures, causing direct hemorrhaging
of arterial blood into the subarachnoid space (subarachnoid hemorrhage).
Complications of a ruptured cerebral aneurysm can be fatal if bleeding is excessive.
Subarachnoid hemorrhage can lead to cerebral vasospasm, cerebral infarction, and death.
Rebleeding often occurs in the first 48 hours after the initial bleed but can occur any time within
the first 6 months. Other complications include meningeal irritation and hydrocephalus.
Possible causes are congenital structural defects in the inner muscular or elastic layer of the
vessel wall; incomplete involution of embryonic vessels; and secondary factors such as arterial
hypertension, atherosclerotic changes, hemodynamic disturbances, and polycystic disease.
Cerebral aneurysm also may be caused by shearing forces during traumatic head injuries.
Prior to rupture, cerebral aneurysm are usually asymptomatic. The patient is usually seen
initially after subarachnoid hemorrhage (SAH). Ask about one or more incidences of sudden
Subarachnoid Hemorrhage: A Case Study 8
headache with vomiting in the weeks preceding major SAH. Other relevant symptoms are a stiff
neck, back or leg pain, or photophobia, as well as hearing noises or throbbing (bruits) in the
head. Warning leaks of the aneurysm in which small amounts of blood ooze from the
aneurysm into the subarachnoid space can cause such symptoms. These small warning leaks
are rarely detected because the condition is not severe enough for the patient to seek medical
attention.

Identify risk factors such as familial predisposition, hypertension, cigarette smoking, or use of
over-the-counter medications (e.g., nasal sprays or antihistamines) that have vasoconstrictive
properties. Ask about the patients occupation, because if the patients job involves strenuous
activity, there may be a significant delay in going back to work or the need to change
occupations entirely.

In most patients, the neurological examination does not point to the exact site of the aneurysm,
but in many instances, it can provide clues to the localization. Signs and symptoms can be
divided into two phases: those presenting before rupture or bleeding and those presenting after
rupture or bleeding. In the phase before rupture or bleeding, observe for oculomotor nerve
(cranial nerve III) palsydilated pupil (loss of light reflex), possible drooping eyelids (ptosis),
extraocular movement deficits with possible double visionas well as pain above and behind
the eye, localized headache, or extraocular movement deficits of the trochlear (IV) or abducens
(VI) cranial nerves. Small, intermittent, aneurysmal leakage of blood may result in generalized
headache, neck pain, upper back pain, nausea, and vomiting. Note if the patient appears
confused or drowsy.

Subarachnoid Hemorrhage: A Case Study 9
The patient has to cope not only with an unexpected, sudden illness but also with the fear that
the aneurysm may rupture at any time. Assess the patients ability to cope with a sudden illness
and the change in roles that a sudden illness demands. In addition, assess the patients degree
of anxiety about the illness and potential complications.

Primary nursing diagnosis: Alteration in tissue perfusion (cerebral) related to interruption in
cerebral blood flow or increased ICP.
Intervention and treatment:
The first priority is to evaluate and support airway, breathing, and circulation. For patients
unable to maintain these functions independently, assist with endotracheal intubation,
ventilation, and oxygenation, as prescribed. Monitor neurological status carefully every hour,
and immediately notify the physician of any changes in the patients condition.

Surgery is indicated to prevent rupture or rebleeding of the cerebral artery. The decision to
operate depends on the clinical status of the patient, including the level of consciousness and
severity of neurological dysfunction, the accessibility of the aneurysm to surgical intervention,
and the presence of vasospasm. Surgical procedures used to treat cerebral aneurysm include
direct clipping or ligation of the neck of the aneurysm to enable circulation to bypass the
pathology. An inoperable cerebral aneurysm may be reinforced by applying to the aneurysmal
sac such materials as acrylic resins or other plastics. Postoperatively, monitor the patient closely
for signs and symptoms of increasing ICP or bleeding, such as headache, unequal pupils or pupil
enlargement, onset or worsening of sensory or motor deficits, or speech alterations.
The environment should be as quiet as possible, with minimal physiological and psychological
stress. Maintain the patient on bedrest. Limit visitors to immediate family and significant others.
Subarachnoid Hemorrhage: A Case Study 10
Apply thigh-high elastic stockings and intermittent external compression boots. Discourage and
control any measure that initiates Valsalvas maneuver, such as coughing, straining at stool,
pushing up in bed with the elbows, turning with the mouth closed. Assist with hygienic care as
necessary. If the patient has a facial weakness, assist her or him during meals.

Preoperatively, provide teaching and emotional support for the patient and family. Position the
patient to maintain a patent airway by elevating the head of the bed 30 to 45 degrees to
promote pulmonary drainage and limit upper airway obstruction. Suction the patients mouth
and, if needed, the nasopharynx and trachea. Before suctioning, oxygenate the patient well, and
to minimize ICP increases, limit suctioning to 20 to 30 seconds at a time. If the patient has facial
nerve palsy, apply artificial tears to both eyes. Take appropriate measures to prevent skin
breakdown from immobility. Postoperatively, promote venous drainage by elevating the head of
the bed 20 to 30 degrees. Emotional support of the patient and family is also important. The
patient may be dealing with a neurological deficit, such as paralysis on one side of the body or
loss of speech. If the patient cannot speak, establish a simple means of communication such as
using a slate to write messages or using cards. Encourage the patient to verbalize fears of
dependency and of becoming a burden.
Discharge and home health care guidelines:
Prepare the patient and family for the possible need for rehabilitation after the acute care phase
of hospitalization. Instruct the patient to report any deterioration in neurological status to the
physician. Stress the importance of follow-up visits with the physicians. Be sure the patient
understands all medications, including dosage, route, action and adverse effects, and the need
for routine lab monitoring if anticonvulsants have been prescribed.

Subarachnoid Hemorrhage: A Case Study 11
References
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