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Allison TayloeClinical Case Study: Subarachnoid Hemorrhage NUR 7202WSU, CONHClinical Case Study: Subarachnoid HemorrhageSource: 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, HypothyroidismSurgical History: Appendectomy 1981, dilation and curettage 1984Social 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 dailyAllergies: PenicillinReview of Systems:ROS is positive for headache, dizziness, nausea, vomiting, diplopia, and blurry vision General: Denies weight loss or gain, fatigue/malaise, or fever/chillsHEENT: 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 ?FGeneral: Appropriate appearance for age, restless in bed holding head, eyes closedHEENT: 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 ResultsResultDiagnostic Lab ResultsResultNa (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/LRBC: (4.2-5.7 m/mm3)4.6m/mm3Glucose (70-100 mg/dL)102 mg/dLHgb (12.0-14.8 g/dL)14.6 g/dLCl (96–107 mEq/L)100 mEq/LHct (37.8-43.9%)39.8 %Creat (< 1.3 mg/dL)1.0 mg/dLPlt (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/dLT3, 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: 7.35-7.457.38PTT (30-50)33.3CO2 (35-45 mm Hg)38 mm HgUrinalysis: 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)87glucose, protein, nitrates, ketonesnegO2 sat (>93%)97%WBC (0)0-5RBC (0)0Table 2: Additional Diagnostic TestingCT head without contrast on arrivalEKG on arrival to emergency roomChest x-ray on arrival3 mm subarachnoid hemorrhage at the area of the superior internal carotid artery at the origin of the posterior communicating artery. Fischer scale: grade IIRhythm: ST, normal axis, no ST elevation or depression, T wave inversion, Rate: 106 bpmPR interval : 0.16QRS interval: 0.10QTc: 380 msecNo infiltrates, effusions, or areas of consolidation. Borderline cardiomegaly, clear lung fields. Differential DiagnosisDifferential 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 TestingThe 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 PlanPrioritized 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-upCare 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. ReferencesAlexander, S., Gallek, M., Presciutti, M. & Zrelak, P. (2009). Care of the patient with aneurysmal subarachnoid hemorrhage. AANN Clinical Practice Guideline Series, 1-30. Committee of Prescriptive Governance (2014). Formulary with index for CTP holders. Ohio Board of Nursing, Nursing Practice. Retrieved from , E.S., Rabinstein, A.A., Carhuapoma, J.R., Derdeyn, C.P., Dion, J. (…) Vespa, P. (2012). Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke: Journal of the American Heart Association, 43: 171-1737. doi: 10.1161/STR.0b013e3182587839Cook, N. (2008). Emergency care of the patient with subarachnoid haemorrhage. British Journal of Nursing, 17(10), 624-629.DeAngelis, L.M. & Wen, P.Y. (2012). Chapter 379. Primary and metastatic tumors of the nervous system. In Longo, D.L., Fauci, A.S., Kasper, D.L., Hauser, S.L., Jameson, J., Loscalzo, J. (Eds), Harrison's Principles of Internal Medicine, (18th ed.). Retrieved from , M.N., Bleck, T.P., Hemphill, J.C., Menon, D., Shutter, L., (…) Zipfel, G. (2011). Critical care management of patients following aneurysmal subarachnoid hemorrhage: Recommendations from the neurocritical care society’s multidisciplinary consensus conference. Neurocritical Care, 15:211–240. doi: 10.1007/s12028-011-9605-9Etminan, N., Mervyn, D.I., Vergouwen, D.I. & Macdonald, R.L. (2011). Effect of pharmaceutical treatment on vasospasm, delayed cerebral ischemia, and clinical outcome in patients with aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. Journal of Cerebral Blood Flow & Metabolism, 31, 1443–1451. doi:10.1038/jcbfm.2011.7Hackman, J.L., Johnson, M.D., & Ma, O. (2011). Chapter 160. Spontaneous subarachnoid and intracerebral hemorrhage. In Tintinalli, J.E., Stapczynski, J., Ma, O., Cline, D.M., Cydulka, R.K., & Meckler, G.D. (Eds), Tintinalli's Emergency Medicine: A Comprehensive Study Guide, (7th ed.). Retrieved from , J., III, Smith, W.S., & Gress, D.R. (2012). Chapter 275. Neurologic critical care, including hypoxic-ischemic encephalopathy, and subarachnoid hemorrhage. In Longo D.L., Fauci, A.S., Kasper, D.L., Hauser, S.L., Jameson, J, Loscalzo, J. (Eds), Harrison's Principles of Internal Medicine, (18th ed). Retrieved from , A. & Black, P. (2012). Chapter 63. Common neurosurgical conditions. In McKean, S.C., Ross, J.J., Dressler, D.D., Brotman, D.J., & Ginsberg, J.S. (Eds), Principles and Practice of Hospital Medicine. Retrieved from et al., (Ed). 2012. Principles of Internal Medicine. (18th ed.). New York: McGraw Hill.Koopman, K., Teune, L. K., ter Laan, M., Uyttenboogaart, M., Vroomen, P. C., De Keyser, J., & Luijckx, G. J. (2008). An often unrecognized cause of thunderclap headache: reversible cerebral vasoconstriction syndrome. The Journal of Headache and Pain, 9(6), 389-391. doi:10.1007/s10194-008-0068-0Marino, P. (2014). The ICU Book. (4th ed.). Philadelphia: Williams & Wilkins.Olkowski, B. F., Devine, M. A., Slotnick, L. E., Veznedaroglu, E., Liebman, K. M., Arcaro, M. L., & Binning, M. J. (2013). Safety and feasibility of an early mobilization program for Patients with aneurysmal subarachnoid hemorrhage. Physical Therapy, 93(2), 208-215. doi:10.2522/ptj.20110334Roos, K.L. & Tyler, K.L. (2012). Chapter 381. Meningitis, encephalitis, brain abscess, and empyema. In Longo, D.L., Fauci, A.S., Kasper, D.L., Hauser, S.L., Jameson, J., (Eds), Harrison's Principles of Internal Medicine, (18th ed.). Retrieved from , M., Chang, D., Odell, M., & Sperber, K. (2006). Rehabilitation implications of non-traumatic subarachnoid haemorrhage. Brain Injury, 20(7), 679-685.Tierney, L., McPhee & Papadakis, M. (2014). Current medical diagnosis and treatment. (53rd ed.). CT: Appleton & Lange.Usatine, R.P., Smith, M.A., Chumley, H.S., & Mayeaux. E.J., Jr. (2013). Chapter 230. Cerebral vascular accident. In Usatine, R.P., Smith, M.A., Chumley, H.S., Mayeaux. E.J., Jr. (Eds), The Color Atlas of Family Medicine, (2nd ed.). Retrieved from , C. J., Vandenberg, B., Hasan, D., & Kumar, A. B. (2013). Stress cardiomyopathy with an 'inverse' takotsubo pattern in a patient with acute aneurysmal subarachnoid hemorrhage. Echocardiography, 30 (8), E224-6. doi:10.1111/echo.12266Wermer, M.J.H., Van der Schaaf, I.C., Velthuis, B.K., Algra, A., Buskens, E., & Rinkel, G.J.E. (2005). Follow-up screening after subarachnoid haemorrhage: frequency and determinants of new aneurysms and enlargement of existing aneurysms.Brain: A Journal of Neurology, 128(10), 2421-2429. doi: 2421-2429 ................
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