Running head: TAYLOE CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
Allison Tayloe
Clinical Case Study: Subarachnoid Hemorrhage
NUR 7202
WSU, CONH
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CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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Clinical Case Study: Subarachnoid Hemorrhage
Source: patient (reliable source) and patient’s daughter (reliable source)
Chief Complaint: “severe headache with nausea and vomiting x two hours”
History of Present Illness:
D.A. is a 57 year old African American female who was brought to the emergency room
via medic with the chief complaint of a severe headache with associated nausea, vomiting, and
blurry vision that began two hours ago. She reports she developed a headache five days ago that
was similar to her previous headaches and was improved with ibuprofen, but never really went
away. However, this morning, she woke from sleep with a headache that began within seconds
and was like nothing she had ever previously experienced, described as severe, unilateral, and
located near the back of her head, but she states: “at times it hurts all over.” The patient also
admits to onset of nausea and vomiting immediately following the onset of the headache. She
denies any alleviating factors and reports that she was unable to try and take any medication due
to her continued nausea and vomiting. She states: “I have had headaches many times before, but
I have never had a headache this intense, I know there is something wrong; this is the worst
headache in my life.” She denies any fevers, chills, syncope, recent traumatic events, upper
extremity or lower extremity weakness, or aphasia. She is unsure if she lost consciousness. She
admits to worsening of symptoms with activity or even opening her eyes. The patient’s
daughter, who is present at the bedside, reports that this morning the patient was disoriented to
place and time, which prompted her to call 911.
Medical History: Hypertension, Hypothyroidism
Surgical History: Appendectomy 1981, dilation and curettage 1984
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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Social History: D.A. currently works as an administrative assistant for a large accounting firm in
Cincinnati, Ohio. She is divorced and is not in a sexual relationship at this time. She admits to
consuming one-two glasses of wine once a week and currently smokes one pack per day x
twenty years. She states she has not seen her family physician in about a year for a routine
physical, but she has been receiving her yearly flu shots and is up to date on all of her childhood
vaccines. She tries to walk at least a mile with her dog one to two times per week.
Family History: Her paternal grandfather died at age 82 from colorectal cancer, her paternal
grandmother died at age 34 during childbirth. Her maternal grandmother died at age 78 from a
myocardial infarction and her maternal grandfather died at age 80 from complications of
diabetes. Her mother is living at age 72 with a history of hypertension. Her father died at age 68
from a ruptured cerebral aneurysm. She has one living sister age 62 who has hypertension.
Current Medications: Levothyroxine (Synthroid®) 137 mcg daily, Hydrochlorothiazide 25 mg
daily, Amlodipine (Norvasc®) 5 mg daily
Allergies: Penicillin
Review of Systems:
ROS is positive for headache, dizziness, nausea, vomiting, diplopia, and blurry vision
General: Denies weight loss or gain, fatigue/malaise, or fever/chills
HEENT: Denies changes in hearing, sore throat, nasal drainage, ear drainage or pain.
Neuro: Denies weakness, syncope, or near syncope, seizures, or loss of consciousness.
Cardiovascular: Denies chest pain, palpitations, orthopnea, leg swelling, or paroxysmal
nocturnal dyspnea.
Respiratory: Denies shortness of breath, cough, sputum production, hemoptysis, or wheezing.
Gastrointestinal: Denies diarrhea, constipation, abdominal pain, and melena.
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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Genitourinary: Denies dysuria, changes in voiding habits, vaginal discharge, or abnormal
vaginal bleeding.
Skin: Denies any lesions, scars, or rashes.
Musculoskeletal: Denies joint or bone tenderness or pain. Denies frequent or recent falls.
Psychosocial: Denies anxiety or depression.
Environmental: Denies any seasonal allergies or recent chemical exposures.
Physical Exam:
Vitals: B/P 182/96, HR 104 bpm, O2 sat: 97% on room air, RR 28 bpm, temperature: 99.2 ᵒF
General: Appropriate appearance for age, restless in bed holding head, eyes closed
HEENT: Head normocephalic. External ears symmetrical bilaterally with no visible drainage.
Nose, mouth and throat no significant lesions, mucous membranes moist, pink. No palpable
tenderness over sinuses or lymph nodes. No thyromegaly, no goiter, trachea midline on
palpation. See eye examination below in neurological findings.
Neck: No lymphadenopathy, nuchal rigidity is present.
Skin: Warm, dry, intact. No appreciable rashes or lesions. Hair with appropriate texture and
thickness.
Neurological: Restless, somewhat drowsy, awakens to name. Oriented to self, place, disoriented
to time. Cranial nerve I not tested. Cranial nerve II unable to be tested due to patient’s inability
to keep eyes open. Fundoscopic examination does not reveal subhyaloid hemorrhage. Cranial
nerve III left eye dilated to 3 mm, sluggish pupillary response to light. Right eye round, reactive
to light and accommodation. EOMI intact, facial movements appropriate and symmetric, no
facial drooping. Cranial nerves, IV-XII grossly intact. GCS 13, Hunt-Hess 2. NIHSS 1 for LOC
questions (unable to state month). Sensory function intact to light touch/pain in BUE and BLE.
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CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
Cardiac: Regular rhythm and rate. S1, S2 normal. No S3 or S4. Point maximal impulse is not
displaced. No carotid bruits. No tenderness on palpation of chest wall. No appreciable
murmurs or rubs.
Pulmonary: Thoracic expansion is equal bilaterally. Clear to auscultation bilaterally with no
wheezing, crackles, or rhonchi.
Gastrointestinal: Normoactive bowel sounds in all four quadrants. Abdomen is soft and
nontender on palpation. No palpable masses, hepatospenomegaly, liver border 8 cm on
palpation. Tympany to percussion in all four quadrants.
Genitourinary: Urinary meatus normal in appearance, no edema or erythema.
Musculoskeletal: 5/5 strength to BUE/BLE with normal ROJM to BUE/BLE. +Kernig sign.
Deep tendon reflex 2+ BUE/BLE with no clonus in plantar region. No cervical, thoracic, or
lumbar tenderness on palpation.
Table 1: Diagnostic Lab results
Diagnostic Lab Results
Result
Na (135-145 mEq/L)
135 mEq/L
K (3.5-5.0 mEq/L)
4.1 mEq/L
Glucose (70-100 mg/dL)
102 mg/dL
Cl (96–107 mEq/L)
100 mEq/L
Creat (< 1.3 mg/dL)
1.0 mg/dL
BUN (5–18 mg/dL)
12 mg/dL
CO2 (22-28 mmol/L)
24mmol/L
Ca (8.5–10.5 mg/dL)
9.2 mg/dL
GFR ( >70 mL/min)
86 mL/min
ABG: pH: 7.35-7.45
7.38
CO2 (35-45 mm Hg)
38 mm Hg
HCO3 (22-26 mm Hg)
22
BE (0±2)
-1
PaO2 (80-100)
87
O2 sat (>93%)
97%
Diagnostic Lab Results
WBC (5-10 k/mm3)
RBC: (4.2-5.7 m/mm3)
Hgb (12.0-14.8 g/dL)
Hct (37.8-43.9%)
Plt (150 -450 k/mm3)
TSH (0.3 - 5.0 U/mL)
T4, free (0.8 -2.8 ng/dL)
T3, total (0.8 - 2.0 ng/ml)
INR (0.5-1.1)
PTT (30-50)
Urinalysis: Color/clarity
pH (5.0-9.0)
Specific gravity (1.005-1.030)
glucose, protein, nitrates, ketones
WBC (0)
RBC (0)
Table 2: Additional Diagnostic Testing
CT head without contrast on arrival EKG on arrival to emergency room
Result
10.9 k/mm3
4.6m/mm3
14.6 g/dL
39.8 %
217 k/mm3
0.98 U/mL
1.12 ng/dL
0.9 ng/ml
0.9
33.3
Yellow, clear
6.0
1.025
neg
0-5
0
Chest x-ray on arrival
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CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
3 mm subarachnoid hemorrhage at
the area of the superior internal
carotid artery at the origin of the
posterior communicating artery.
Fischer scale: grade II
Rhythm: ST, normal axis, no ST
elevation or depression, T wave
inversion,
Rate: 106 bpm
PR interval : 0.16
QRS interval: 0.10
QTc: 380 msec
No infiltrates, effusions, or areas of
consolidation. Borderline
cardiomegaly, clear lung fields.
Differential Diagnosis
Differential diagnoses for a patient presenting with these symptoms should include those
pertaining to acute intracranial processes such as subarachnoid hemorrhage, ischemic or
hemorrhagic stroke, meningitis, drug toxicity, migraine or cluster headache, encephalitis, or
intracranial tumor (Hackman, Johnson, & Ma, 2011). Although many acute intracranial
processes present may have similar presentations requiring further diagnostic tests in the form of
various imaging, the onset and severity of this patient’s presentation help to decrease the
likelihood of some diagnoses while increasing the likelihood of several others. In addition, due
to the increased mortality of missed diagnoses associated with acute intracranial processes such
as meningitis, ischemic or hemorrhagic stroke, or subarachnoid hemorrhage, accurate and timely
assessment findings as well as diagnostic testing to confirm a diagnosis is needed to increase the
patient’s chance of survival (Tierney, McPhee & Papadakis, 2014 ).
The most likely diagnosis for this patient is a subarachnoid hemorrhage (SAH) (Connolly
et al., 2012). This patient presented to the emergency department with the classic signs of a
SAH, including sudden onset of a severe headache, often called a “thunderclap headache,” that is
typically different and much more severe than any previous headache (Hackman, Johnson, &
Ma, 2012). In addition, due to increased morbidity and mortality associated with misdiagnosis,
American Heart Association (AHA) and American Stroke Association recommend a high level
of suspicion for SAH in patients who present with a sudden, severe headache (Class 1, Level of
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Evidence [LOE] B) (Connolly et al., 2012). Nausea, vomiting, and photophobia, all of which are
described by this patient, are often associated symptoms of patients who present with an acute
SAH, usually do to meningeal irritation (Kasper et al., 2012). Subarachnoid hemorrhages can be
acute or chronic in nature. Acute SAH can further be classified into traumatic or nontraumatic
causes, and the most likely cause for nontraumatic SAH is caused by a ruptured cerebral saccular
aneurysm (Hackman, Johnson, & Ma, 2012). An acute SAH due to aneurysm is likely in this
patient’s case because this patient does not have any recent trauma and this patient also has
several risk factors for aneurysmal SAH, such as current tobacco use, hypertension, “nonwhite”
ethnicity, and family history of subarachnoid hemorrhage (Diringer et al., 2011).
Although a SAH seems likely, other acute intracranial processes must be ruled out due to
the high mortality associated with misdiagnosis in this situation. Ischemic stroke should be
considered in the differential diagnosis of this patient. This patient has a history of
hyperlipidemia and is a current smoker, which both increase the chance of cerebrovascular
disease leading to an ischemic or hemorrhagic cerebrovascular accident (CVA) (Usatine, 2013).
Although this patient’s presentation was acute and she describes photophobia with a severe
headache, she is not described as having a focal neurological deficit such as left or right sided
hemiplegia, aphasia, or heminopia which is often present due to cerebral infarct in the middle
cerebral artery (Usatine, 2013). The absence of these focal neurologic deficits make an acute
cerebral vascular accident less likely, but not impossible. Therefore, if the patient did display a
focal neurological deficit that mimicked a CVA, a noncontrast computed tomography (CT) of the
head would again be performed to assess for hemorrhagic CVA before treatment would be
pursued, much in the same way a SAH would be evaluated. In this patient’s case, a CT was
performed which noted a subarachnoid hemorrhage, but no ischemic CVA. If a CT was
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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nondiagnostic for any acute findings, magnetic resonance imaging may be warranted (Kasper et
al., 2012).
Meningitis, an acute neurologic emergency, can often mimic the signs and symptoms of
SAH because headache, photophobia, and nuchal rigidity are considered hallmark signs of
meningeal irritation (Roos &Tyler, 2012). Yet, this patient is afebrile and denies recently feeling
“ill,” making the diagnosis of meningitis less likely. Often, a patient presenting with
neurological complaints such as the ones stated above will undergo a noncontrast CT of the head,
however, if this is inconclusive for a SAH or hemorrhagic CVA, a lumbar puncture should be
performed next to rule out meningitis or SAH not visible on CT scan (Roos & Tyler, 2012).
Although a lumbar puncture was not needed with this patient’s presentation due to positive CT
finding, a lumbar puncture would help to differentiate SAH from meningitis when considering
cerebrospinal fluid analysis. A cerebrospinal fluid analysis revealing decreased glucose,
elevated protein and white blood cell count would lean towards the diagnosis of meningitis,
whereas xanthrochromia and elevated red blood cell count with normal white blood cell, glucose,
and protein levels would be indicative of SAH, not meningitis (Kasper et al., 2012). This patient
has a minimal temperature elevation, which would likely be more pronounced in a patient with
meningitis.
Intracranial tumor could also be considered in this patient, as headache is a common
presenting symptom in these patients (Tierney, McPhee & Papadakis, 2014). However,
headaches in patients with brain tumors often have vague descriptions such as a dull,
intermittent, deep ache that is not acute in onset and begins in the morning and improved
throughout the day (DeAngelis & Wen, 2012). That description is contrasting to this patient’s
description of a severe headache that began acutely as described above. Also, patients with brain
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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tumors often have gait disturbances or personality changes that are not described in the case
above. Regardless, a head CT would often be performed first in an acute setting of a headache
and neurologic changes due to morbidity and mortality associated with neurologic emergencies,
however if inconclusive and CSF results are unyielding, MRI is the test of choice for diagnosis
of intracranial tumor ( Kasper et al., 2012).
Drug toxicity, infection, migraine, or cluster headaches remain least even less likely
diagnoses based on this patient’s presentation. As stated above, this patient denies recent sick
contacts and is not noted to have a fever, marked leukocytosis, or significant mental status
changes, making an infectious process such as encephalitis, less likely (Tierney, McPhee &
Papadakis, 2014). This patient does have a history of hypothyroidism on synthroid, however,
thyroid hormone levels were checked and were appropriate levels, ruling out the diagnosis of
thyroid storm. Physical exam findings also noted no goiter or thyroid bruit, which may be
common findings in thyroid storm (Kasper et al., 2012). As mentioned above, the patient denied
any illicit drug use and is not on other medications that would likely cause the above stated
symptoms, making drug toxicity again an unlikely diagnosis. Lastly, the patient could very well
be experiencing a migraine headache, however, more severe and timely diagnosis is needed for
neurological emergencies such as SAH, meningitis, and CVA, therefore, migraine headache
would be a diagnosis of exclusion rather than inclusion. In addition, migraine headache are
typically not acute in onset, although are often associated with photophobia and nausea and
vomiting (Goadsby & Raskin, 2012). Cluster headaches typically occur in middle aged males
and are often in a cluster pattern with associated ipsilateral rhinorrhea and conjunctival
lacrimation, which is atypical for the presentation of the above stated patient (Kasper et al.,
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2012). Even though this could be a cluster headache, CT imaging should be the first step in
diagnosis of this patient to rule out other intracranial abnormalities that may be life threatening.
Diagnostic Testing
The initial diagnostic test of choice when any acute intracranial process is suspected, such
as subarachnoid hemorrhage, is a noncontrast computed tomography (CT) of the head (Diringer
et al., 2011). The noncontrast CT of the head is extremely sensitive in diagnosis of subarachnoid
hemorrhage (up to 98%) within twelve hours following the onset of symptoms, but sensitivity
declines following this time period (Hackman, Johnson, & Ma, 2011). In this patient’s case, her
onset of symptoms would allow for low chance of false negative results and as such her head CT
did confirm the presence of blood read by the radiologist as an acute subarachnoid hemorrhage.
However, in the chance that the noncontrast head CT for a patient with a suspected subarachnoid
hemorrhage is negative, generally a cerebrospinal fluid (CSF) analysis from a lumbar puncture is
supported as the next best test by the American Heart Association, American Stroke Association,
and the Neurocritical Care Society (Connolly et al., 2012). The CSF in a patient with a
suspected SAH needs to be examined for the presence of blood or xanthochromia (Hackman,
Johnson, & Ma, 2011). Xanthrochromia is present due to the breakdown of blood, causing the
release of bilirubin, however this often takes up to twelve hours after the onset of SAH to
develop (Hackman, Johnson, & Ma, 2011). Due to the unreliability of xanthochromia in
diagnosis of SAH, the number of red blood cells present in CSF fluid is frequently used to
support the diagnosis of SAH (Connolly et al., 2012). Nevertheless, there is no definitive
number of red blood cells in cerebral spinal fluid analysis that confirm the diagnosis of SAH,
mostly due to the fact that lumbar punctures can be traumatic and SAH can be varying sizes
producing wide differences in red blood cell counts. Rather, absence of xanthochromia and
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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minimal red blood cell count (<5 x 10^6 cells/L) on cerebral spinal fluid analysis, as well as
negative head CT results can dependably exclude diagnosis of SAH (Hackman, Johnson, & Ma,
2011). An MRI is often not pursued if CT of the head is negative due to the increased cost,
length of test, and decreased sensitivity when compared to CT (Kasper et al., 2012).
Although CT scan and lumbar puncture are often diagnostic for an acute SAH, cerebral
arteriography is often used to confirm aneurysm as the cause for SAH, diagnose the anatomic
location of the aneurysm, and to evaluate if other unruptured aneurysms exist (Hemphill, Smith,
& Gress, 2012). Cerebral angiography can help to guide potential treatment options such as coli
embolization and clipping in patients with SAH to prevent rebleeding when an aneurysm is
identified (Huang & Black, 2012). Cerebral angiography is not without complications such as
hematoma, bleeding, emboli, acute renal failure, and pseudoaneurysm, but this test is still
supported by the AHA and ASA in patients with SAH to document the presence of aneurysm
(Class I, LOE B) (Connolly et al., 2012). If cerebral angiography is unable to be performed,
magnetic resonance angiogram and computed tomography angiogram may be utilized (Connolly
et al., 2012).
There are also several different neurologic exam scales that are often used to grade
clinical condition after an acute head injury, including SAH, however the literature remains
sparse on which of these scales, if any, has an accurate prediction of associated morbidity and
mortality following SAH due to lack of uniformity (Connolly et al., 2012). The Glasgow coma
score (GCS) is an assessment tool used on the majority of patients who present to the emergency
department with an acute head injury and is supported by the AHA as an appropriate system to
assess clinical outcomes of patients with an acute SAH, although this scale doesn’t take into
account the subtle neurological deficits and cognitive deficiencies patients with SAH may have
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when returning to an outpatient setting (Connolly et al., 2012). GCS is scaled from 3-15 based
on best motor, verbal, and eye score, with a score of 15 being indicative of minimal neurological
deficit and better outcome, and a score of 3 with indications for severe brain injury (Hemphill,
Smith, & Gress, 2012). GCS would be an appropriate test, not necessarily in the diagnosis of
SAH, but rather to gauge the severity of the injury of any patient with a diagnosis of SAH on
arrival as well as during the hospital stay in regards to long term decisions and prognosis. In the
World Federation of Neurological Surgeons Subarachnoid Hemorrhage grading scale, the GCS is
combined with presence or absence of motor deficits to give a grade of I-V with I having
excellent prognosis and V with grim prognosis (Kasper et al., 2012). In addition to these scales,
the Hunt-Hess is a scale specifically for subarachnoid hemorrhage that is used in combination
with the GCS to grade presenting manifestations of patients with SAH (Kasper et al., 2012). The
grades range from I-V with grade I including a minimal headache, normal mental status, and no
focal neurologic deficits and grade V including coma with reflex posturing (Hemphill, Smith, &
Gress, 2012). Based on the exam findings above, this patient has a GCS of 13 and Hunt-Hess
grade of II, which would be used to evaluate appropriate treatment options. Additionally,
Fischer grading scale is used by radiologist when evaluating CT scan results of patient in regards
to hemorrhage, with scales ranging from 0-IV, with 0 being an unruptured aneurysm and IV
revealing intracerebral or intraventricular clot with diffuse or no subarachnoid blood (Kasper et
al., 2012). This scale is again used as reference point when repeat imaging is performed and as a
gauge of clinical condition after an SAH.
Prioritized Plan
Prioritized plan for a patient with acute SAH includes appropriate blood pressure
management, measures to prevent further hemorrhage, treatment of hydrocephalus and
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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hyponatremia, and prevention of vasospasm (Tierney, McPhee & Papadakis, 2014). The first
step of this process would be admittance to a neuro critical care unit with continuous pulse
oximetry, cardiac monitoring, and blood pressure management as well as every one hour neuro
assessments with GCS scales and appropriate national institute of health stroke scales.
Admittance to a neuro intensive care unit would allow for rapid sequence intubation if this
patient declines from a neurologic standpoint with a decreased level of consciousness, or if she
begins to show signs of elevated intracranial pressure or brain herniation (Hemphill, Smith, &
Gress, 2012). Following intubation, ventilator rate settings should be adjusted to achieve a
carbon dioxide (CO2) level of 30-35 mm Hg, as hyperventilation and hypocapnia allow for
vasodilation and increased cerebral perfusion pressure, but too much hyperventilation may cause
vasospasm (Kasper et al., 2012). Appropriate analgesics will also be needed in addition to
appropriate sedation as the headache of SAH continues far past the presenting symptoms.
Aspirin should be avoided at all cost due to the recent hemorrhagic injury this patient endured.
Opiates should only be used as a last resort in nonintubated patients and short acting when used
for analgesia in intubated patients as not to hinder accurate neurologic assessment (Huang &
Black, 2012). Nutrition therapy should be pursued via oral route if cough and gag reflexes are
intact, or enterally through an nasogastric tube if the patient remains intubated and should be
started 48 hours following initial insult (Alexander, Gallek, Presciutti, & Zrelak, 2009). A foley
catheter will need to be inserted as the patient will be on strict bed rest and accurate intake and
output is necessary to ensure adequate volume resuscitation and vital organ perfusion. This
patient does not have a history of diabetes, but glucose should be monitored on daily metabolic
panels to ensure control of glucose < 180 mg/dL (Connolly et al., 2012). Continuous cardiac
monitoring is important due to the ST-T wave changes that can result on an electrocardiogram of
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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a patient who has recently suffered a SAH (Hemphill, Smith, & Gress, 2012). These changes are
thought to be due to increased catecholamine surges after intracranial hemorrhage producing
inverted T waves and prolonged QT intervals which may lead to a reversible cardiomyopathy,
ventricular arrhythmias, or acute exacerbation of congestive heart failure (Waller, Vandenberg,
Hasan, & Kumar, 2013). A baseline EKG should be obtained and careful monitoring for signs
and symptoms of heart failure should be observed during this patient’s hospitalization. An
echocardiogram may be warranted if EKG changes are noted or signs and symptoms of heart
failure develop (Alexander et al., 2009).
Prevention of further hemorrhage would include invasive treatment options for a
bleeding aneurysm such as clipping or coil embolization. Clipping would involve a craniotomy
and clip to be placed across the aneurysm, which would immediately stop the bleeding but may
be associated with higher mortality due to surgical risk as well as increased risk of vasospasm
earlier in the course following SAH (Kasper et al., 2012). Coil embolization can be performed
endovascularly, which may decrease surgical risk, but is not necessarily associated with lower
mortality, as supported in the literature (Hemphill, Smith, & Gress, 2012). Furthermore, some
aneurysms may not be appropriate for endovascular repair and therefore surgical options should
also be considered. Current guidelines recommend surgical clipping or endovascular coiling
based on the individual patient’s presentation, anatomic location of the bleed, and ability to
obliterate the entire vessel as the more vessel that is obliterated the less chance there is for
rebleeding (Class I, LOE B) (Connolly et al., 2012). Regardless of intervention performed,
careful attention should be paid to avoiding intraoperative hypotension in order to avoid
vasospasm or further ischemia (Connolly et al., 2012).
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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Adequate cerebral blood flow and appropriate management of blood pressure in a patient
with SAH has often been achieved through the use of triple H therapy: hypervolemia,
hypertension, and hemodilution (Kasper et al., 2012). However, current research and guidelines
proposed by the American Heart Association (AHA) and American Stroke Association have
pushed focus to include euvolemia and permissive hypertension with hemodilution in the
treatment of patients with acute SAH (Connolly et al., 2012). Adequate fluid resuscitation and
euvolemia should be pursued in an effort to decrease the chance of delayed cerebral ischemia
caused by vasospasm (Class 1, Level of Evidence [LOE] B) (Connolly et al., 2012). Adequate
fluid resuscitation in this patient would include isotonic 0.9% normal saline, as hypotonic
solutions would induce cerebral edema and promote hyponatremia (Hackman, Johnson, & Ma,
2012). There is no exact amount of fluid needed to appropriately resuscitate a patient, although
history of cardiac dysfunction and heart failure should be taken into account as not to overload
the patient. Because there is no history of systolic or diastolic heart failure in this patient, fluids
will infuse at a rate of 100 mL/hr with total fluid intake not to exceed two to three liters per day
to maintain an SBP > 130 mm Hg, mean arterial pressure (MAP) > 70 mm Hg and < 130 mm
Hg, and a central venous pressure of approximately five to eight (Alexander et al., 2009).
Hemodilution should include goal of hematocrit of 28-32% which will be monitored on this
patient with daily complete blood counts (Connolly et sl., 2012). In addition, cerebral perfusion
pressure should be maintained between 60-70 mm Hg with the use of fluids, vasopressors, and
infrequently vasodilators (Hackman, Johnson, & Ma, 2012). An elevated blood pressure can
theoretically increase the risk of rebleeding, however there is little research to support this
finding, and current guidelines support treatment to maintain a MAP > 70 and systolic > 130 mm
Hg to prevent hypovolemia and subsequent vasospasm (Connolly et al., 2012). Mean arterial
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
16
pressures can be monitored through central venous access or pulmonary artery catheters and
intracranial pressures can be measured through the use of an extraventricular drain, however
these devices also increase a patient’s risk for infection over time (Kasper et al., 2012). In order
to control cerebral perfusion pressures, adequate mean arterial pressures with a goal of 70-130
mm Hg should be utilized, as a MAP < 70 or > 130 has been associated with poorer outcomes in
SAH patients (Cook, 2008). Control of blood pressure should include intravenous medications
such as betablockers like labetalol or calcium channel blocker like nicardipine to keep MAP <
130 mm Hg or vasopressors such as phenylephrine in addition to adequate fluid resuscitation to
maintain MAP > 70 mm Hg (Kasper et al., 2012). Nitroprusside sodium, and nitroglycerin
should be avoided if possible due to their ability to increase intracranial pressure (Cook, 2008).
An Acute Care Nurse Practitioner (ACNP) is legally allowed to prescribe these intravenous
vasodilators, vasopressors, and maintenance IV fluids needed during this critical time period
(Committee of Prescriptive Governance, 2014).
Euvolemia and adequate cerebral perfusion pressure with blood pressure control is also
an important factor in preventing cerebral artery vasospasm, which typically occurs seven to ten
days following the initial bleed and can last up to twenty-one days post SAH (Hemphill, Smith,
& Gress, 2012). Unfortunately, there are no known preventative treatments despite amplitude of
research due to the fact that arterial and arteriolar vasospasm can occur in both large artery and
small arteriolar circulation (Connolly et al., 2012). When severe, cerebral artery vasospasm can
cause acute focal neurologic deficits due to ischemia, and thus must be treated to prevent
progression to infarction (Alexander et al., 2009). Continued cerebral artery vasospasm can lead
to delayed cerebral ischemia (Etminan et al., 2011). Treatment of cerebral vasospasm with oral
nimodipine should be pursued in all patients with a spontaneous acute SAH (Class 1, LOE A)
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
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(Connolly et al., 2012). Nimodipine is the only calcium channel blocker that has been shown
with varying degrees of evidence to improve neurologic outcomes following spontaneous SAH,
however it hasn’t been shown to reduce cerebral vasospasm (Connolly et al., 2012). Therefore,
this patient will be placed on nimodipine 60 mg every four hours and continued for twenty one
days (Lexi-Comp, 2014). Transcutaneous Doppler (TCD) is frequently used to diagnose
vasospasm in a patient after SAH with flow velocities > 120 cm/sec and is still supported by the
AHA, although TCD has poorer overall sensitivity depending on the area involved with the
vasospasm (Class IIa, LOE B) (Connolly et al., 2009).
Hydrocephalus can also occur in the first 24 hours following an SAH due to CSF
obstruction by clotted blood (Stern, Chang, Odell, & Sperber, 2006). This is usually noted by
increased obtundation of the patient with poor pupillary response and downward gaze of the
patient’s eyes (Kasper et al., 2012). An extraventricular drain (EVD) is often used to help drain
CSF and clotted blood to maintain adequate ICP (15 mm Hg) to minimize increases in ICP.
Nursing management of the patient would also include adequate sedation and avoidance of
coughing or vomiting as all of these measures are known to increase ICP (Alexander et al.,
2009). However, it should be noted that CSF should not be drained too much, as rebleeding can
occur if CSF levels drop too quickly (Cook, 2008). Therefore, this patient should have an EVD
placed in the initial 48 hours if hydrocephalus remains a concern. Frequent monitoring of
electrolytes is also important, since hyponatremia is a common finding up to two weeks
following an SAH due to cerebral salt wasting or SIADH(Stern et al., 2006). Cerebral edema is
also a common finding during this time. After adequate fluid resuscitation, hypertonic saline (23%) at a rate of 75 mL/hr may be needed in this patient to maintain a sodium concentration
between 145-155 mEq/L and serum osmolarity of 300-320 mOsm/L to help decrease cerebral
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
18
edema (Alexander et al., 2009). During this treatment the patient will have every six hour
metabolic panels to assess sodium levels, and hypotonic fluids will be avoided as not to make the
hyponatremia or hydrocephalus worse (Class I, LOE B) (Connolly et al., 2012). Fluid restriction
is also not an appropriate therapy for hyponatremia in this patient because of it is associated with
a higher chance of vasospasm and worsening cerebral edema (Alexander et al., 2009).
Seizures remain a fear for any patient who has recently suffered a SAH (Kasper et al.,
2012). Although this patient doesn’t have a history of seizures, seizure precautions with close
monitoring for seizures is appropriate in this case. However, current guidelines note that there is
sparse literature on the prophylactic use of antiepileptic medications, and that when instituted,
should not be continued indefinitely as this was associated with poorer outcomes in the long term
(Connolly et al., 2012). In fact, seizure prophylaxis with medication shouldn’t be perused in this
case because current recommendations only embrace patients with prior seizures, parenchymal
hematoma, or middle cerebral artery aneurysms (Alexander et al., 2009). Ativan 2 mg IV once
with an order to repeat the dose one time would be an appropriate medication during an acute
seizure, followed by the initiation of phenytoin for antiepileptic therapy, which is also allowed to
be prescribed by an ACNP in the state of Ohio (Committee of Prescriptive Governance, 2014).
In the past, treatment of SAH patients has included strict bed rest to prevent stress or
situations that may induce rebleeding. However, there have been several studies that support
early mobilization ( < 3 days) in patients with SAH that is safe, practical, and effective in
producing better cognitive outcomes in regards to neurological recovery following SAH
(Olkowski et al., 2013). Therefore, this patient should receive physical therapy early and often
after the aneurysm has been secured if vital signs remain stable (MAP > 70 mm Hg, heart rate >
40 bpm <130 bpm, respiratory rate < 30 bpm, and ICP < 15 cm H20) (Olkowski et al., 2013).
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
19
Health Promotion/Follow-up
Care of the patient with a SAH as an outpatient focuses on reducing morbidity and
associated mortality from SAH including risk factor modification to prevent future SAH or other
cerebrovascular disease (Connolly et al., 2012). Per AHA/ASA guidelines, risk factor
modification would include adequate control of blood pressure with goal < 140/90 mm Hg with
the use of antihypertensives, a diet rich in vegetables, and smoking and alcohol cessation
(Connolly et al., 2012). It would be safe to place this patient back on her Norvasc to maintain
appropriate blood pressure control as long as she does not have a low ejection fraction < 40%
from her recent SAH (Kasper et al., 2012). If the patient is discharged prior to day 21 of
hospitalization, nimodipine should be continued for 21 days (Alexander et al., 2009). The
patient should also be instructed to continue adequate fluid intake, thus hydrochlorothiazide
should be held until the patient follows up with neurology in one to two weeks following
hospitalization. She should be instructed to see her primary care physician within two to three
days following discharge. Additionally, her synthroid should be continued throughout her
hospital stay and post discharge at her home dose with adjustments made after thyroid function
tests two months following discharge. All of these medications are legally allowed to be
prescribed by the ACNP caring for her (Committee of Prescriptive Governance, 2014).
Due to this patient’s history, smoking cessation would need to be addressed while in the
hospital and on every consecutive visit as an outpatient to assess willingness to quit and
encourage continued smoking cessation. Outpatient counseling should be offered in addition to
medical therapies to aid the patient in being successful with smoking cessation. Nicotine
replacement therapy with a patch of should be offered to the patient at a dose of 21 mg/day for
six weeks, 14 mg/day for two weeks, and ending with 7mg/day for two weeks (Lexi-Comp,
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
20
2014). Wellbutrin, although a well-known therapy for smoking cessation, would not be a good
choice in this patient if she experienced a seizure following her SAH because this medication is
contraindicated in people with a past history of seizures (Lexi-Comp, 2014). Following an SAH,
this patient will need to follow-up with neurosurgery and neurology to have a repeat CT scan
completed within one month following discharge to assess if the bleeding has completely
resolved. Current guidelines don’t recommend future screening for aneurysms, rather just
control of risk factors (Connolly et al., 2012). This reasoning is twofold: preventative treatment
with coiling of some aneurysms can increase the likelihood of long term complications and
death, and some aneurysms are so small they are not appropriate for repair, which has been
shown to lead the patient who has knowledge of such information and a previous subarachnoid
hemorrhage with a decreased quality of life (Wermer et al., 2005). Outpatient treatment should
also include physical therapy, occupation therapy, or speech therapy if the patient continues to
have deficits. The patient and family should be educated that headaches post SAH can last for
six months or longer and brain recovery to its fullest ability may take six to fifteen months
(Alexander et al., 2009). Lastly, the patient and family should be instructed on signs and
symptoms of stroke in order to quickly assess and seek treatment for a neurological emergency
should it occur.
CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE
21
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