Sub-Arachnoid Hemorrhage - 2 Nursing CEs
Author: Kristi Hudson RN MSN CCRN
Written: December 24, 2004
Updated: August 31, 2009
Course Objectives
Upon completion of this course, the student will be able to:
- Describe the pathophysiology involved with a sub-arachnoid hemorrhage
- List 3 signs and symptoms of sub-arachnoid hemorrhage
- Have a better understanding of how the Hunt-Hess Grading scale is used
- Discuss 3 risk factors for vasospasm
- Describe 3 signs and symptoms of vasospasm
- Explain methods used to diagnose vasospasm
- Discuss the benefits of daily Transcranial Doppler studies to rule out vasospasm
- Explain the risk vs. benefit of using Nimodipine for treatment of vasospasm
What is a Sub-Arachnoid Hemmorhage?
Subarachnoid hemorrhage occurs when there is bleeding into the space between the brain and the arachnoid membrane (the middle membrane covering the brain). This may occur either by a spontaneous or traumatic rupture of a cerebral aneurysm, an arteriovenous malformation, or from other unidentified causes. Risks include: disorders associated with aneurysm or weakened blood vessels, including a history of polycystic kidney disease, fibromuscular dysplasia (FMD), other connective tissue disorders, aneurysms in other blood vessels, high blood pressure and smoking.
Signs and Symptoms:
Hunt-Hess Grading System
The Hunt-Hess classification is used to help guide the physician in diagnosing the severity of a Sub-Arachnoid Hemorrhage secondary to aneurysmal bleeding, as well as assist in the timing surgical intervention. It can also be used to judge the risk of vasospasm. The patient is assigned to a category on admission to the hospital. Changes in the patient’s condition are then monitored according to the baseline.
Hunt Hess Grading Scale
Grade |
Clinical Appearance |
Grade O |
Asymptomatic and have unruptured aneurysms. |
Grade 1 |
Mildly symptomatic with headache. |
Grade 2 |
Severe headache associated with Nuchal rigidity and possibly a cranial nerve deficit. |
Grade 3 |
Drowsy or confused and may have a mild focal Neurologic deficit. |
Grade 4 |
Stuporous with a moderate to severe hemiparesis and possibly early decerebrate rigidity. |
Grade 5 |
Comatose with decerebrate rigidity or flaccidity. |
Note: Surgical risk increases with the clinical grade, which predicts eventual Neuro outcome.
A second scale that is gaining momentum as a clinical indicator scale is the World Federation of Neurological Surgeons (WFNS). The WFNS is based on the sum score of the Glasgow Coma Scale (a very reliable method for evaluating the level of consciousness) and the presence of focal neurologic signs. The higher the grade; the worse the prognosis.
Clinical Grading Scale of the World Federation
of Neurological Surgeons
|
Grade |
Score on Glasgow
Coma Scale |
Clinical Appearance |
|
1 |
15 |
No motor deficit |
|
2 |
13–14 |
No motor deficit |
|
3 |
13–14 |
Motor deficit |
|
4 |
7–12 |
With or without motor deficit |
|
5 |
3–6 |
With or without motor deficit |
Vasospasm
Of the estimated 21,000 persons annually who survive initial aneurysmal rupture, 4,000 either die or are seriously disabled from cerebral vasospasm. Vasospasm is most frequently reported within 4 to 14 days post aneurysm bleed. Clinically significant vasospasm rarely occurs before day 4 and vasospasm is most likely to occur between days 7 through 10. Risk factors for vasospasm include:
- Amount of Blood that was in the Subarachnoid space
- Age
- Hydrocephalus
- Antifibrinolytics (Increases risk by 50%)
- Grade upon admission
- Timing of Surgery (Early surgery has shown decreased mortality from vasospasm).
Signs and Symptoms (Depending on Location of Vasospasm)
Middle Cerebral Artery:
- Hemiparesis affecting the arm more than the leg
- Facial weakness
- Dysphagia (difficulty swallowing)
- Aphasia (difficulty speaking) if the brain's left hemisphere is involved
- Anosognosia (denial of paralysis) if the right hemisphere is affected
Anterior Cerebral Artery:
- Hemiparesis (one sided weakness affecting the leg more than the arm)
- Flat affect
Posterior Cerebral Artery:
Vertebrobasilar Arteries:
- Cranial nerve palsies
- Ataxia (difficulty walking
Diagnosis of Vasospasm
Frequent Neuro assessment because vasospasm is often seen as a gradual neurologic deterioration. 50% of patients can remain asymptomatic during vasospasm and approximately 20% to 30% will have some delayed neurological ischemia. Decreased LOC or confusion is often the first signs of vasospasm.
Transcranial Doppler Study (TCD) is a non-invasive ultrasound technology used to assess blood flow velocity in the major basal intracranial arteries on a real time, beat-to-beat basis. Blood flow velocity is calculated and used to make determinations about intracranial hemodynamics. Transcranial Doppler Studies are used in early (sub-angiographic) bedside detection of vasospasm in Subarachnoid hemorrhage patients, evaluation of stroke and transient ischemic attack, as an adjunct in the assessment of cerebral circulatory arrest, and as a monitoring tool for patients undergoing intracranial interventional procedures.
Blood Flow Velocity (BFV) increases as flow volume increases or the diameter of the vessel decreases. Velocity readings are as follows:
- 80cm/sec = no vasospasm
- 80 – 120 cm/sec = non-critical spasm
- 120 cm/sec = critical vasospasm
Note: Initial CT scans that show blood clots that 3x5mm or a 1mm layer of blood in the basal cisterns can be an early predictor that the patient will later vasospasm.
Nursing Assessment for Vasospasm
Clinically, vasospasm can be recognized when nurses doing frequent neuro exams report subtle changes. It is important to make sure a well-documented base line neuro exam is present so it can be used for comparison. Some of the more subtle or gradual changes that can occur and should be frequently assessed include:
- Level of consciousness
- Complaints of headache
- Periods of disorientation
- Inappropriate behavior
- Language impairment
- Hemiparesis
Note: Nurses must quickly detect and report changes as these deficits if undetected, can cause permanent disability.
Treatment of Vasospasm
The cause of vasospasm is a decreased blood flow to the clinically affected arterial territory. Therefore treatment for symptomatic vasospasm is directed at increasing Cerebral Perfusion Pressure using “Triple H” therapy, which is comprised of Hypertension, Hypervolemia and Hemodilution.
Hypertension – Therapy is aimed at keeping the heart rate greater than 70 beats per minute and maintaining a 30% increase in the patients mean arterial blood pressure for the duration of the vasospasm. This can be induced with vasopressors such as Dopamine, Neosynephrine, Levophed or Dobutamine.
Hypervolemia – Central venous pressure (CVP) should be maintained at approximately 8 to 10mmHg and Pulmonary Artery Wedge Pressure should be maintained at approximately 14 to 18 mmHg. This is done with fluid resuscitation on a regular schedule, often a colloid (5% albumin) to allow for the expansion of the intravascular space.
Hemodilution – The balance of oxygen-carrying capacity and viscosity is optimized with lower then normal Hematocrit (around 25%). In order to attain this decreased concentration of cells and solids in the blood, volume expanders again can be used, or in critical situations removing blood and replacing it with plasma can achieve a decreasing blood volume.
Note: Careful assessment for pulmonary edema, electrolyte imbalances (especially hyponatremia and hypokalemia) and cerebral edema must be done frequently when using Triple H therapy.
Other Treatment Options for Vasospasm
Fibrinolytics – The most common used drug is recombinant tissue plasminogen activator (rt-PA) or streptokinase. These and other Fibrinolytic agents act by lysing the clot in the subarachnoid space.
Angioplasty – Spastic intracerebral vessels can be dilated to improve cerebral perfusion. This is done by passing a balloon through the carotid artery, and inflating and deflating it into the vessels that are in spasm.
Medications for the Treatment of Vasospasm:
Mannitol – Which is an osmotic diuretic, has been shown to increase cerebral blood flow in the setting of vasospasm, with improvement in neurological function.
Nimodipine – Is a calcium channel blocker that that has been a standard treatment for nearly a decade and has been shown to have a beneficial effect on stroke and cerebral blood flow after Sub-Arachnoid Hemorrhage. It dilates collateral arteries around the vasospasm. This therapy seems reasonable as long as the hypertension treatment of “Triple H” therapy is not compromised. If hypotension results from the use of Nimodipine, the dose can be divided in two and given twice as often. If hypotension continues after this, the practitioner should consider discontinuing its use.
References
Finn, S., RN, BSN, (2003). Traumatic Brain Injury. Dynamic Nursing Education. Orange California
Hickey, J., V., (2002). The Clinical Practice of Neurological and Neurosurgical Nursing. (5th ed.) Lippencott. Philadelphia
Kazzi, A., A., M.D. (2006). Subarachnoid Hemorrhage. Retrieved on December 3, 2006 at:
http://www.emedicine.com/emerg/topic559.htm
Medline Plus Medical encyclopedia (2006). Intracranial pressure monitoring. Retrieved on December 3, 2006 at:
http://www.nlm.nih.gov/medlineplus/ency/article/003411.htm
Giraldo, E., A. MD. Subarachnoid Hemorrhage (SAH). (2007). Retrieved on March 10, 2009 at:
http://www.merck.com/mmpe/sec16/ch211/ch211d.html
Oyama, Katie, RN, BSN, CCRN & Criddle, Laura, RN, MS, CCRN, CCNS. (October 2004). Vasospasm after aneurysmal sub-arachnoid hemorrhage. Critical Care Nurse. Vol. 24, No. 5, October 2004.
Suarez, J., I., M.D., Tarr, R., W., M.D., & Selman, W., R., M.D. (2006). Aneurysmal Subarachnoid Hemorrhage. N Engl J Med 2006;354:387-96. Retrieved on December 3, 2006 at:
med.unc.edu/obgyn/direct/residents/documents/Aneurysmal_subarachnoid_hemorrhage.pdf
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