allisontayloe.weebly.com file · Web viewD.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

Running head: TAYLOE CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE 1

Allison Tayloe

Clinical Case Study: Subarachnoid Hemorrhage

NUR 7202

WSU, CONH

CLINICAL CASE STUDY: SUBARACHNOID HEMORRHAGE 2

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


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.


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.


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 resultsDiagnostic Lab Results Result Diagnostic Lab Results Result

Na (135-145 mEq/L) 135 mEq/L WBC (5-10 k/mm3) 10.9 k/mm3K (3.5-5.0 mEq/L) 4.1 mEq/L RBC: (4.2-5.7 m/mm3) 4.6m/mm3Glucose (70-100 mg/dL) 102 mg/dL Hgb (12.0-14.8 g/dL) 14.6 g/dLCl (96–107 mEq/L) 100 mEq/L Hct (37.8-43.9%) 39.8 %Creat (< 1.3 mg/dL) 1.0 mg/dL Plt (150 -450 k/mm3) 217 k/mm3BUN (5–18 mg/dL) 12 mg/dL TSH (0.3 - 5.0 U/mL) 0.98 U/mLCO2 (22-28 mmol/L) 24mmol/L T4, free (0.8 -2.8 ng/dL) 1.12 ng/dLCa (8.5–10.5 mg/dL) 9.2 mg/dL T3, total (0.8 - 2.0 ng/ml) 0.9 ng/mlGFR ( >70 mL/min) 86 mL/min INR (0.5-1.1) 0.9ABG: pH: 7.35-7.45 7.38 PTT (30-50) 33.3CO2 (35-45 mm Hg) 38 mm Hg Urinalysis: Color/clarity Yellow, clearHCO3 (22-26 mm Hg) 22 pH (5.0-9.0) 6.0BE (0±2) -1 Specific gravity (1.005-1.030) 1.025PaO2 (80-100) 87 glucose, protein, nitrates, ketones negO2 sat (>93%) 97% WBC (0) 0-5

RBC (0) 0

Table 2: Additional Diagnostic TestingCT head without contrast on arrival EKG on arrival to emergency room Chest x-ray on arrival


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 bpmPR interval : 0.16QRS interval: 0.10QTc: 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


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


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


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.,


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


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


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


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


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).


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


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)


(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 (2-

3%) 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


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).


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,


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.


References

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allisontayloe.weebly.com file · Web viewD.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