STTI, Case SA0002, Care of the Patient With an Unstable Cerebral Aneurysm

Meet the Author

Title	Care of the Patient With an Unstable Cerebral Aneurysm Case Study SA0002
Author	Marie Lasater, RN, MSN, CCRN
Contact Hours	1.0
Target Audience:	Public health nurses, neurosurgical nurses, emergency room nurses, intensive care nurses, and case managers
Purpose/Goal:	To educate the nurse in signs and symptoms of cerebral aneurysm in order to promote prompt treatment, and to educate the nurse in a normal therapeutic course for successful outcome of afflicted patients.

Objectives	Triple-H Therapy
Instructions	Course of Care
Introduction	Discussion
Medical/Nursing History	References
Physical Exam Findings	TEST QUESTIONS
Laboratory/Test Data

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Marie Lasater Marie Lasater, RN, MSN, CCRN
Ms. Lasater is an advanced clinician in the surgical intensive care unit at Grossmont Hospital, La Mesa, California. She attended undergraduate school at Vanderbilt University in Nashville, Tennessee, and obtained her master's degree from the Medical University of South Carolina in Charleston, South Carolina. She has been a registered nurse for twenty-two years, specializing in critical care, in both the civilian and military setting. She served overseas as a civilian nurse in Panama during the Noriega regime, caring for critically ill soldiers. Her research interests include epidemiology, congestive heart failure, and noninvasive monitoring utilizing new biomedical advances. She has published in dozens of peer-reviewed medical and nursing journals, and enjoys mentoring new writers and researchers. Her research has been presented at local, regional, and national conferences. She is a member of the American Association of Critical Care nurses and Sigma Theta Tau.

Instructions

Medical/Nursing History:
DE was a healthy 52-year-old female who was preparing to be married in the upcoming month. She was experiencing headaches and neck pain one week prior to admission. She attributed these symptoms to stress and did not seek medical attention until the headaches became severe and intermittently blinding. She suffered no nausea, vomiting, or alterations in level of consciousness. Her fiancé drove her to the emergency department.

Physical Examination Findings:
Initial emergency neurological examination revealed normal Glascow coma score of 15, no decrease in level of consciousness, equal strength bilaterally, and cranial nerves 2 through 12 intact. DE offered complaints of a headache of 10 (on a scale of 1 to 10, with 10 being the worst) with nuchal rigidity and mild photophobia. Her blood pressure was 180/95mmHg, and she had a heart rate of 82, normal sinus rhythm, and a temperature of 98.9(F).

Laboratory/Test Data:
The computerized tomography (CT) scan of the head (without contrast) revealed a small, left subarachnoid hemorrhage with bleeding into the suprasellar cistern that indicated a Grade I SAH. This patient was allergic to iodine and, therefore, could not undergo cerebral angiography. DE was taken for magnetic resonance angiography (MRA) to determine aneurysmal size and placement. The MRA showed a 3mm, berry-shaped, left middle cerebral aneurysm (MCA) located at a bifurcation. (Another MCA view)

Complications of Subarachnoid Hemorrhage

The principle medical complications of aneurysmal SAH include rebleeding, cerebral vasospasm, and volume and osmolar disturbances, such as hypernatremia.

Risks for rebleeding from an unsecured aneurysm vary with time, approximately 4 percent on the first postbleed day and 1.5 percent/day up to day 286 (Cruz, 1998). The incidence of rebleeding is 20-30 percent in the first month if the aneurysm is left unrepaired. Mortality with aneurysmal rebleeding following the diagnosis of SAH exceeds 75 percent (Cruz, 1998). To prevent this occurrence, patients will receive blood pressure control and aneurysm precautions.

The presence of cerebral vasospasm significantly affects the outcome of the aneurysm patient. Cerebral vasospasm is a narrowing of the lumen of the cerebral arteries believed to be caused by subarachnoid blood coating the outer surface of the blood vessels creating a focal vasoconstriction.

This vasoconstriction can lead to decreased perfusion, ischemia, injury, and infarction of brain tissue. These injuries are manifested by the appearance of neurological deficits such as a decreased level of consciousness, pupillary changes, and weakness. The extent of these deficits is directly related to the degree of brain injury. It is estimated that 50 percent of all SAH patients develop vasospasm. Thirty-two percent of these patients are symptomatic with some degree of neurological impairment. Of the 32 percent, 15-20 percent will experience permanent neurological damage or death from the vasospasm.

Vasospasm can develop 4-14 days following initial SAH, often peaking at day 7, and can last 3-4 weeks. One non-surgical method to detect vasospasm is the use of the transcranial Doppler, which measures the flow velocity in the major cerebral vessels (American Association of Neuroscience Nurses, 1996).

Triple-H Therapy

Common treatments for vasospasm include "Triple-H" therapy and pharmacological therapy with a calcium antagonist. The prevention and/or treatment of vasospasm changes depending whether the patient has undergone surgical repair of the aneurysm, because "Triple-H" therapy and a calcium antagonist can aggravate an unruptured aneurysm in the preoperative patient.

"Triple-H" therapy refers to the three treatment modalities--hypervolemic, hemodilution, and hypertensive therapy--that can be used to prevent vasospasm in the postoperative cerebral aneurysm patient.

Hypervolemic therapy involves administering volume expanders to elevate the patient's volume status. Hypervolemia can be obtained by infusion of colloids (i.e., 5 percent albumin) or crystalloids (i.e., normal saline) to achieve a central venous pressure of 10-12 mmHg, or a pulmonary artery wedge pressure (PAWP) of 15-18 mmHg, and cardiac index greater than 2.2 l/m (American Association of Neuroscience Nurses, 1996; Brisman & Bederson, 1997; Campbell & Edwards, 1997; Hickey, 1997; McKhann & LeRoux, 1998; Rudy, 1996).

Hemodilution therapy reduces the blood viscosity, which maximizes oxygen delivery to tissues that facilitate cerebral oxygenation and perfusion. This target hematocrit is 33-38 percent (Brisman & Bederson, 1997; Campbell & Edwards, 1997). Transfusions of whole blood are given to anemic patients. Phlebotomy is performed on polycythemic patients, and volume is replaced with colloids (Marshall, Marshall, Vos, & Chestnut, 1990; Rudy, 1996).

Hypertension is provided to increase cerebral perfusion to any potentially vasospastic areas. Hypertensive goals include use of prophylactic pressors to maintain a minimally hypertensive state (10 mmHg above baseline). In general, patients should be maintained normotensive with systolic blood pressure 110-160 mmHg (Bleck, 1997; Brisman & Bederson, 1997).

Cerebral perfusion pressure is largely driven by arterial pressure. A simple equation for determining cerebral perfusion pressure is: mean arterial pressure minus intracranial pressure equals cerebral perfusion pressure (MAP - ICP = CPP). The Brain Trauma Foundation guidelines promote maintaining the CPP greater than 70 mmHg (Brain Trauma Foundation, 1996). Dopamine (Intropin), dobutamine (Dobutrex), norepinephrine (Levophed), and phenylephrine (Neosynephrine) may be infused to achieve these hypertensive goals (Bleck, 1997; Brisman & Bederson, 1997; Campbell & Edwards, 1997). No one of these medications has a proven advantage over the others in a clinical setting. Dobutamine may further support cerebral perfusion by enhancing collateral cerebral blood flow.

Clinical risks of "Triple-H" therapy include increased intracranial pressure, intracranial bleeding, cerebral edema, rupture of an unclipped aneurysm, pulmonary edema, electrolyte imbalances, dilutional hyponatremia, congestive heart failure, and myocardial infarction (American Association of Neuroscience Nurses, 1996; Bleck, 1997; Brisman & Bederson, 1997; Campbell & Edwards, 1997; Hickey, 1997; Marshall et al., 1990).

Pharmacological treatment of vasospasm includes the use of calcium channel blockers that act on the smooth muscle, causing relaxation and vasodilation. Nimodipine (Nimotop) is lipid-soluble and readily crosses the blood brain barrier. It is believed to dilate cerebral vessels surrounding the areas of vasospasm, which increases the collateral circulation to the ischemic tissues. Usual treatment begins immediately after the hemorrhage and should continue for 17-21 days in the non-surgical patient. The average adult dose is 60mg every 4 hours taken either orally or via nasogastric tube (Rudy, 1996).

Course of Care:
DE was admitted to the intensive care unit and placed on aneurysm precautions. A left frontotemporal craniotomy and orbital zygomatic osteotomy for clipping of the left MCA aneurysm was performed (within 24 hours) without complications.

A right frontal intraventricular catheter was placed for intracranial pressure (ICP) monitoring. "Triple-H" therapy was employed postoperatively. The surgeon set goals using phenylephrine to maintain a systolic blood pressure of 140-160mmHg and a cardiac index greater than 3.0 L/m2 using continuous hemodynamic monitoring. Due to low volume status, blood and crystalloids were administered to the patient postoperatively. Neurological assessments were performed hourly to include Glascow Coma Scale, motor strength, ICP, cerebral perfusion pressure (CPP), and cranial nerve assessments. ICP was maintained less than 15mmHg via external ventriculostomy drainage of CSF (cerebral spinal fluid), and CPP was maintained greater than 80. Core body temperature was maintained less than 99.0(F) with acetaminophen (Tylenol) and cooling measures. The head of the bed was maintained at 300. The patient was mechanically ventilated overnight (surgeon preference due to evening surgery) and maintained normocapneic with PaCO2 of 40mmHg and oxygenation PaO2mmHg greater than 100mmHg. Pain was managed with intravenous morphine sulfate.

A postoperative CT scan was performed the following day and revealed no complications. On postoperative day (POD) one, DE was extubated and continued to receive "Triple-H" therapy, pain control, and frequent neurological assessments. She began to eat a soft diet and advance her activity. DE continued to make progress, and "Triple-H" therapy was discontinued on POD three; she was transferred to the neurological unit. On POD five, DE was discharged home with Tylenol and codeine to resolve headaches and incisional pain. She was married the subsequent month and is recovering without complication.

Discussion:
Recent advances in managing the patient with cerebral aneurysm have contributed greatly to both recovery and quality of life postoperatively. Through preservation of brain function through "Triple-H" therapy, many patients return to their previous level of function. In addition, practicing nurses are in an ideal position to get out the message: A person experiencing the "worst headache of his/her life" should treat it as a medical emergency and not delay treatment.

Please select the correct answer for each of the following questions. If you answer 80% or more correctly, you will be given the opportunity to register for continuing education credit. After receipt of the registration information and fee, a continuing education certificate will be mailed to you.

It occurs most often in men.
It is extremely rare.
It is always singular.
It often presents as "the worst headache of my life."

A patient presents with moderate headache, nuchal rigidity, and cranial nerve palsy with no other deficits. According to the Hunt and Hess Classification, this patient would be classified as:

Hypervolemic, hypertensive, and hemodilution
Hyperthermic, hypertensive, and hemodilution
Hypotensive, hemodilution, and hypervolemic

The following aneurysm precautions are maintained in both the preoperative and postoperative period: