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The pharmacologic treatment of vasospasm after subarachnoid hemorrhage: a case study.

L.R., a 28-year-old female, was watching television with her husband when she experienced a generalized tonic/clonic seizure. She had no significant past medical history and no history of seizures. She was brought to the emergency department (ED) by ambulance.

Upon arrival to the ED, she was awake, but postictal, confused to place and time, and somewhat lethargic. She was arousable to voice, but required continuous stimulation to stay awake and would follow commands only when continuously aroused. She complained of a severe headache. Computed tomography (CT) of her head revealed a subarachnoid hemorrhage (SAH), Fisher grade III (Table 1). Cerebral angiography demonstrated the presence of a left middle cerebral artery (MCA) aneurysm. L.R. was admitted to the neurosurgical intensive care unit (NSICU). An externalized ventricular drain (EVD) was placed for intracranial pressure (ICP) monitoring and cerebrospinal fluid (CSF) drainage.

L.R. remained lethargic and somewhat confused and complained of headaches mad photophobia. A craniotomy was performed the next day for clipping of the aneurysm. The patient was then returned to the NSICU with her neurologic examination unchanged. Medication orders are summarized in Table 2.

Aneurysm rupture is a common cause of SAH. The subarachnoid space is contiguous with the ventricles of the brain and is normally filled with CSF. When an aneurysm ruptures, blood is released into the subarachnoid space causing signs and symptoms such as severe headache, nausea and vomiting, lethargy or decreased level of consciousness, photophobia, nuchal rigidity, and seizures. Patients will often complain of "the worst headache of my life."

L.R.'s case is a common presentation for SAH with subsequent vasospasm. This article focuses on the pharmacologic agents commonly prescribed for patients with SAH. Specific attention is given to drugs used to treat vasospasm and hyponatremia, both frequent complications of SAH. Monitoring parameters and nursing interventions also are discussed.


On postoperative day 5 (posthemorrhage day 6), L.R. became difficult to arouse, responded inappropriately to questions, and could not follow simple commands. These symptoms occurred intermittently and with varying intensity. An emergent head CT was performed. It demonstrated only normal operative changes. Transcranial dopplers (TCDs) revealed the presence of vasospasm. TCDs measure cerebral blood flow velocity. There is an inverse relationship between flow velocity and size of the blood vessel. Therefore, higher flow velocities reflect a greater degree of vasospasm (Falyar, 1999). L.R's mean TCD values were 150-170 cm/sec, which indicated moderate vasospasm. The diagnosis of vasospasm was confirmed by cerebral angiography.

Vasospasm refers to narrowing of the cerebral arteries, which in turn can cause cerebral ischemia. It commonly occurs after SAH, especially in patients with higher Fisher grades (Rusy, 1996). This puts the patient at risk for developing a delayed ischemic neurologic deficit (DIND), which increases morbidity and mortality.

The exact mechanism by which vasospasm occurs is still unclear. Current research suggests that spasmogenic substances such as serotonin, prostaglandins, catecholamines, and histamine are released as the hemorrhagic clot dissolves. There is also some evidence that vasospasm may be a localized reaction due to irritation caused by the presence of subarachnoid blood. Another hypothesis is that chemical substances released from subarachnoid clots interfere with the movement of calcium into and out of the cells, causing alteration in smooth muscle contraction (Rusy, 1996). These theoretical mechanisms serve as the basis for treating SAH.

The signs and symptoms of vasospasm may include worsening headache, onset of confusion or deterioration in the level of consciousness, inappropriate behavior, focal motor paresis, and aphasia. These symptoms are usually gradual in onset and may wax and wane (Rusy, 1996).

Vasospasm can occur anywhere from day 4 to 16 days after hemorrhage, with peak incidence between days 8 and 12. It almost never occurs earlier than 48 hours or later than 14 days (Armstrong, 1994). The goal of treatment of vasospasm is to maintain cerebral blood flow and minimize DIND. Commonly used approaches include nimodipine and triple H therapy among others.


L.R. received nimodipine (Nimotop) to decrease the risk of vasospasm. Nimodipine is a lipid soluble calcium channel blocker that easily crosses the blood-brain barrier. At the cellular level it inhibits calcium ion transfer and reduces smooth muscle contraction, thereby reducing or preventing cerebral vasospasm (Feigin, 1998). Nimodipine therapy begins immediately after hemorrhage and continues for 21 days in order to protect the patient during the period of highest risk for vasospasm (American Heart Association, 1994). The dose is 60 mg orally every 4 hours. This dose is cut in half for patients with liver failure. The main side effect is hypotension. If the patient cannot swallow the capsule, the liquid inside may be aspirated and given via nasogastric tube, although this method is not FDA approved.

Patients on nimodipine must be observed closely for hypotension. Onset of hypotension may occur 30 minutes after dosing. If the patient is hypotensive at the time the next dose is due to be given, the dose may need to be held or decreased.

Nimodipine may also relax the bowel muscles, commonly producing constipation. Some patients may develop an ileus, and rarely, nimodipine has contributed to obstruction and bowel perforation. Thus, bowel function must be closely assessed in patients receiving nimodipine.

Triple H Therapy

Triple H therapy--hypervolemia, hypertension, and hemodilution--may be used to increase cerebral blood flow (Manno, 1998). Elements of triple H therapy may be prescribed prophylactically or as a therapeutic intervention (Armstrong, 1994; Rusy, 1996).

Hypervolemia is accomplished by infusion of crystalloids, such as normal saline or lactated ringers, or colloids, such as albumin or fresh frozen plasma (FFP). The patient may receive 125-200 ml of IV fluid per hour, along with 12.5 grams of albumin or 1-2 units of FFP every 4 hours. Target goals include central venous pressure (CVP) 10-12 mm Hg, pulmonary artery wedge pressure (PAWP) 14-20 mm Hg, and cardiac index (CI) 5-6 L/min/[m.sup.2] (Campbell & Edwards, 1997). The net effect of hypervolemia is to keep the cerebral blood vessels dilated by forcing large volumes through them.

Hemodilution decreases blood viscosity, which indirectly augments blood flow. Hypervolemia usually produces some degree of hemodilution. Colloids produce a greater degree of hemodilution than crystalloids. The hematocrit must be maintained at or above 33% so as not to diminish the oxygen carrying capacity of the blood (Armstrong, 1994; Rusy, 1996).

Hypertension is accomplished via hypervolemia or by use of vasopressors such as dopamine, dobutamine, or neosynephrine. Systolic blood pressure (SBP) is maintained at about 60 mm Hg above baseline, but not in excess of 240 mm Hg. In the presence of an unclipped aneurysm, the SBP is not allowed to exceed 160 mm Hg (Campbell & Edwards, 1997).

Other Options

If the patient does not respond to triple H therapy intracerebral papaverine is another treatment option. Papaverine is a nonspecific smooth muscle relaxant. It can be delivered during angiography directly into the arteries that are in spasm. The usual dose is approximately 300 mg per vessel infused over 20-60 minutes while the patient is carefully monitored (Elliott et al., 1998). Side effects include increased ICP, decreased cerebral blood flow, and respiratory arrest. The side effects usually resolve quickly after the infusion is discontinued; however, so do the beneficial effects. Therefore, patients may require more than one papaverine infusion.

Nursing Considerations

Potential complications of triple H therapy include rupture of an unclipped aneurysm, pulmonary edema, congestive heart failure, cerebral edema, myocardial infarction, hypertensive cerebral hemorrhage, and dilutional hyponatremia (Armstrong, 1994).

Patients receiving triple H therapy must be closely monitored for signs and symptoms of fluid overload. Heart sounds and breath sounds should be auscultated every 2 hours (Rusy, 1999). In elderly patients or those with a history of cardiac disease, a transthoracic echocardiogram may be performed prior to initiation of triple H therapy in order to assess baseline cardiac function. These patients require more frequent monitoring, such as auscultation of heart and lung sounds every hour and hemodynamic profiles every 1-2 hours.

L.R. was started on an infusion of normal saline with 20 milliequivalents of potassium chloride per liter at 125 cc/hr. She was also started on dopamine at 5 mcg/kg/min, with an order to titrate the medication to keep the SBP greater than 160 mm Hg.

L.R. responded well to therapy and tolerated it without complications. Her mental status improved; she remained awake and able to participate in bedside physical therapy. On day 5 of triple H therapy, the nurse noted that her serum sodium had dropped to 131 mEq/L.

Treatment of Hyponatremia

Hyponatremia is defined as a serum sodium level <135 mEq/L (Kee, 1998). Hyponatremia may develop secondary to vomiting, diarrhea, gastric suctioning, water intoxication, syndrome of inappropriate antidiuretic hormone (SIADH), severe tissue injury with shifting of fluids, or cerebral salt wasting (CSW). It may also occur as a side effect of triple H therapy (Harrigan, 1996).

Sodium is the major cation in the extracellular fluid, and it has a water-retaining effect. Signs and symptoms of hyponatremia are confusion, lethargy, coma, seizures, hypotension, anxiety, muscle twitching or weakness, headaches, tachycardia, and cold, clammy skin (Harrigan, 1996).

Nursing interventions for the hyponatremic patient are strict intake and output measurement, use of norreal saline to irrigate gastric tubes or wounds, and fluid restriction. Oral fluids with solutes should be offered, such as broths or juices instead of plain water. Concentrated tube-feeding formulas are available for patients on fluid restriction. Likewise, parenteral nutrition formulas can be prepared in a concentrated form. Urine specific gravity should be checked every 4 hours, as it will usually fall below 1.010. Infusion of 3% saline may be considered when the serum sodium level falls to 129 mEq/L or lower.

Prior to administration of hypertonic saline, the nurse should assess the patient for signs and symptoms of hyponatremia. It is also important to recheck documented serum sodium levels, which should reflect a downward trend. If the serum sodium has dropped precipitously, the level should be rechecked prior to starting the infusion.

Hypertonic saline should be infused via a pump to prevent accidental over-administration. It is preferable to infuse it into a central venous line, because it can be irritating to peripheral veins. The order must specify rate, volume to be infused, and duration of infusion. Hypertonic saline is usually infused over 4 hours, and then the infusion is stopped and a serum sodium level is drawn. Depending on how much the level has increased, the patient may be given more hypertonic saline, or the infusion may be discontinued. Care should be taken to avoid overcorrection or too rapid correction of serum sodium because it may cause further brain damage (Harrigan, 1996).

Other Medications

Phenytoin (Dilantin) is the drug most commonly used for seizure prophylaxis. It acts on the motor cortex to inhibit spread of seizure activity. The therapeutic blood level range is 12-20 gms/dl (Kee, 1998) achieved by dosing 300-400 mg daily, orally or intravenously. The most common adverse reaction to phenytoin is a skin rash. It usually appears as a red, raised rash on the trunk or back and then spreads to the extremities. If the patient develops this rash, phenytoin should be immediately discontinued and a different antiepileptic drug should be prescribed. The rash is self-limiting but may take several days to fully resolve. Other potential side effects of phenytoin are lethargy, nausea, vomiting, impaired coordination, and gingival hyperplasia.

Fosphenytoin (Cerebyx) is a prodrug that is rapidly converted to phenytoin in the body, so the nurse might see this variation of the drug ordered for L.R. (Meek et al., 1999). It can be administered intravenously or intramuscularly. Fosphenytoin can be administered at a much faster rate than phenytoin, and it has less cardiotoxic side effects (Jamerson et al., 1994). It is also stable in all intravenous solutions, including those containing dextrose. The patient must be monitored for hypotension during administration. In this patient population, use of antiepileptic drugs is controversial and should be based on the patient's presentation and seizure risk. If used, antiepileptic drugs can usually be weaned off after 3 to 6 months, as long-term use is not routinely recommended (American Heart Association, 1994).

The intraventricular method is considered the "gold standard" for ICP monitoring because it allows for drainage of CSF as well as monitoring of ICP (Littlejohns & Bader, 2001). Cefazolin was prescribed for L.R. to prevent infection from the ventricular catheter. It is a fairly broad-spectrum antibiotic and is well tolerated, but contraindicated in patients with allergies to cephalosporins. The usual dose is I gram intravenously every 8 hours until the EVD is discontinued. The most common side effect is an allergic reaction.

Stress ulcer is a common occurrence in critically ill patients. Many drugs can be used for gastrointestinal prophylaxis, including cimetidine, sucralfate, or even aluminum hydroxide. Famotidine (Pepcid) was prescribed for L.R., and she received it throughout her hospital stay.

It is important to administer analgesics to keep the patient as comfortable as possible. Intravenous morphine was prescribed for L.R. The patient's pain score should be documented as often as her other vital signs, along with response to medication. Side effects of opioid administration may include respiratory depression and confusion, but these side effects are not common with low dose therapy.

Docusate is a stool softener. It is used to prevent straining at stool, which increases ICE The usual dose is 100 mg orally three times a day.

Patient Outcome

L.R.'s intravenous fluids were decreased from 125 to 75 cc/hour. She continued to receive intravenous dopamine at 5 mcg/kg/min. She was placed on oral fluid restriction as well. Thirty-six hours later, her serum sodium had increased to 134 mEq/L. She remained in the NSICU under close observation, with frequent neurologic examinations and monitoring of daily laboratory values.

On posthemorrhage day 14, L.R. was weaned off triple H therapy and the EVD was discontinued. On day 15 she was moved out of the NSICU. Her laboratory values remained within normal limits, and she had no further signs or symptoms of vasospasm. She was discharged home from the hospital on post-hemorrhage day 16.


The patient with a diagnosis of SAH and subsequent vasospasm presents many nursing challenges and requires complex pharmacologic management. By paying careful attention to the therapeutic and potential side effects of the medications prescribed, the nurse can be instrumental in the patient's recovery.
Table 1. Fisher Grading System

Grade Blood on CT

1 No subarachnoid blood visualized
2 Diffuse or vertical layers of blood <1 mm thick
3 Localized clot and/or vertical layer >1 mm thick
4 Intracerebral/intraventricular clot with diffuse or no SAH

Table 2. Medication Orders

Medication Order Nursing Considerations

Phenytoin 100 mg p.o. t.i.d. Monitor serum drug levels, assess for

Nimodipine 60 mg p.o. every Monitor blood pressure and assess patient
4 hours for signs and
 symptoms of vasospasm.

Cefazolin 1 gram IV every Monitor for allergic reaction.
8 hours

Famotidine 20 mg p.o. b.i.d. Assess patient for GI complications.

Docusate 100 mg p.o. t.i.d. Assess bowel sounds and check for
 abdominal distention.
 Document frequency of bowel movements.

Morphine 2 mg IV every 3 Document patient's pain scale score and
hours p.r.n. response to medication.
 Observe for over-sedation/respiratory


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Campbell, P.J., & Edwards, S.M. (1997). Hyperdynamic therapy: The nurse's role in treatment of cerebral vasospasm. Journal of Neuroscience Nursing, 29(5), 318-324.

Elliott, J.P.. Newell, D.W,, Lain. DO., Eskridge, J,M., Douville, C.M. LeRoux, P.D., et al. (1998). Comparison of balloon angioplasW and papaverine infusion for the treatment of vasospasm following aneurysmal subarachnoid hemorrhage. Journal of Neurosurgery, 88, 277-283.

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Feigin, V.L, (1998). Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage: A systematic review. Neurology, 50(4), 876-883.

Harrigan, M.R. (1996). Cerebral salt wasting syndrome: A review. Neurosurgery, 38(1), 152-160.

Jamerson. B.D., Dukes, G.E., Brouwer, K.L., Donn. K.H., Messenheimer, J.A., & Powell, J.R. (1994). Venous irritation related to intravenous administration of phenytoin versus fosphenytoin. Pharmacotheratherapy, 14(1), 47-52.

Kee. J.L. (1998). Handbook of laboratory and diagnostic tests with nursing implications (3rd ed.). Stamford, CT: Appleton & Lange, (Original work published 1990).

Littlejohns, L.R., & Bader, M.K. (2001). Guidelines for the management of severe head injury: Clinical application and changes in practice. Critical Care Nurse. 21(6) 48-65.

Manno, E.M. (1998). Effects of induced hypertension on transcranial doppler ultrasound velocities in patients after subarachnoid hemorrhage. Stroke,, 29(2), 422-428.

Meek, P.D., Davis, S.N., Collins, D.M., Gidal, B.E., Rutecki. P.A., Burstein. A.H., et al. (1999). Guidelines for the nonemergency use of parenteral phenytoin products: Proceedings of an expert panel consensus process. Archives of Internal Medicine, 159, 2639-2644.

Rusy, K,L. (1996). Rebleeding and vasospasm after subarachnoid hemorrahage: A critical care challenge. Critical Care Nurse. 16(1). 41-48.
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Title Annotation:Pharmacology update
Author:LeStrange, Danielle G.
Publication:Journal of Neuroscience Nursing
Date:Dec 1, 2003
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