Hemorrhagic Stroke
Introduction
The National Stroke Association (2009) defines stroke as an ‘attack’ to the brain cells and tissues that often cuts off perfusion. Hemorrhagic strokes results when a blood vessel that supplies a certain area of the brain breaks or ruptures causing blood leakage into the brain tissue (Magistris, Bazak, and Martin, 2013).
Prevalence of stroke in the United States (US) is estimated at 800,000 per year and mortality rate is about 160,000 people per year (National Stroke Association, 2009). In Canada, stroke accounts for more than 14,000 deaths per year (Magistris, Bazak, and Martin, 2013). However, hemorrhagic stroke account for 15% of all the forms of stroke but contributes to about 30% of deaths that result from stroke globally (National Stroke Association, 2009; National Institute for Health and Care Excellence, 2009).
This submission examines the etiology, pathophysiology, diagnosis, and treatment options in a patient with hemorrhagic stroke. This submission also presents a case on the same and care plans developed based on the presentation of the patient.
Disease process
Etiology and Risk factors
Ballooning of blood vessels (aneurysm) has been associated with rupture of brain vessels leading to hemorrhage. High blood pressure can also lead to rupture of small brain vessels. Uncontrolled high blood pressure accounts for more than 60% of cases of hemorrhagic stroke.
The risk factors for hemorrhagic stroke include frequent bouts of high blood pressure; too much alcohol intake; tobacco use and prolonged use of medication with anti-clotting properties. These drugs thin the blood and increase the risks of hemorrhage in case of irritation or rupture of a blood vessel. Moreover, blood disorders like hemophilia and sickle cell anemia also predisposes the individual to intracerebral bleeds (Huether & McCance, 2012). According to Magistris, Bazak, and Martin (2013) a significant proportion of stroke patients have reported either history of hypertension (60%) or use of thrombolytic drugs (7-10%).
Previous episode of transient ischemic attack or cerebral vascular accident and history of drug abuse (especially cocaine) also predisposes a person to hemorrhagic stroke (Masotti et al. 2011). Having aneurysms especially in the brain has been identified in about 6% of patients who died from stroke related illness. Aneurysms are at high risk for rupture due to irritation or increase blood pressure, and they may lead to subarachnoid bleeding (National Stroke Association, 2009). However, American Heart Association (2012) indicates most aneurysms remain undiagnosed. Other risk factors include old age, vasculitis, intracranial malignancies, coagulopathy, and cerebral amyloidosis. Vascular malformations contribute to a majority of stroke episodes in children (National Institute for Health and Care Excellence, 2009).
Pathophysiology
When an individual is exposed to the risk factors or suffers actual cause (as discussed above), rupture of the affected vessel occurs resulting in hemorrhage. Intracerebral hemorrhage often leads to the formation of a hematoma that may extend to the adjacent brain tissue. Hematoma formation and expansion occurs within hours following the blood vessel injury. Continuous bleeding and hematoma formation results in cerebral edema and consequently increased intracranial pressure and destruction of the integrity of the blood brain barrier.
Intracerebral hemorrhage may spread to the ventricles leading to a sudden occurrence of obstructive hydrocephalus that compresses the brain cells and tissue leading to inflammation, irritation, and reduced cerebral tissue perfusion. What ensues is the occurrence of neurological deficits as sudden numbness, weakness, severe headache, nausea, and sudden loss of consciousness. Other manifestations may also ensue depending on the part of the brain affected.
Signs and symptoms
According to National Stroke Association (2009), manifestations of hemorrhagic stroke are of sudden onset. However, the presentation may not be the same across the population since it depends on which part of the brain is affected.
The common manifestations include semi-consciousness or total loss of consciousness, nausea and vomiting, and sudden onset of paresthesis of the arm, face, and or leg. The body weakness or numbness usually occurs on one side of the body. Some individuals may also complain of an acute severe headache, sudden sensitivity to light,
Diagnosis
The attending doctor may request either a computed tomography scan or magnetic resonance imaging scan of the head. From the scans, it can be observed which part of the brain is experiencing a hemorrhage (National Stroke Association, 2009). Computed tomography (CT) and magnetic resonance imaging (MRI) are thought to be 100% effective in detecting acute hemorrhages, hematoma, herniation, and vascular malformations. However, magnetic resonance imaging is contraindicated in patients with metallic devices in the eyes, or any part of the central nervous system. Another test that may be requested is an X-ray and angiogram. These are requested to analyze the suspect blood vessel for abnormalities or injuries (Ackley & Ladwig, 2013).
The differential diagnoses include syncope, seizure, and sepsis. Thus, care should be taken not to miss out on the stroke. For this reason, the Recognition of Stroke in Emergency Room (ROSIER) scale (Magistris, Bazak, and Martin, 2013) can be used as a tool for rapid assessment of the presence of stroke. This tool has scores that range from -2 to +5 and checks on parameters as visual disturbance, speech difficulties, and body/limb weakness. Thus, a patient who scores more than 0 has a 90% more likely to be suffering from stroke (National Institute for Health and Care Excellence, 2009).
Complications
The possible complications of hemorrhagic stroke include disability, hemiplegia, and aspiration pneumonia, neurological deficits like speech disturbance, increased intracranial pressure, and eventually death in severe cases.
Treatment options
The management protocol depends on the cause, site, and the extent of brain damage secondary to the intracerebral hemorrhage. However, the goal of treatment would entail establishing and removing the cause as well as preventing neurological complications. Thus, treatment may entail a combination of several techniques including medical, behavioral, surgical, and endovascular interventions.
The initial part of the management may focus on finding out the cause (Ackley & Ladwig, 2013) after which it is eliminated or treated as appropriate. For example, if the cause is high blood pressure, the antihypertensive medications are administered. Some rupture of blood vessels are caused by aneurysms (Masotti et al. 2011). Such causes are managed surgically to reduce the ballooning of vessels. Magistris, Bazak, and Martin (2013) indicate that endovascular coiling and clipping can be used to prevent the occurrence of aneurysms in the brain in individuals at risk.
The surgical intervention may involve performing craniotomy to fix alloy clips around aneurysms. This reduces blood flow and hence risk of aneurysm rupture. Endovascular interventions like angiography and fluoroscopy may be performed by accessing the aneurysm through major arteries (aorta, femoral and carotid) and inserting coils that reduce the amount of blood reaching the aneurysm.
Huether and McCance (2012) also adds that vasospasms that are common causes of morbidity and mortality after an episode of intracerebral hemorrhage may be treated with medication, blood pressure monitoring and monitoring of cerebral perfusion. Thus, regular check up of blood pressure is an important prevention initiative. This is because the rise in blood pressure can promptly be detected, and treatment measures initiated. However, untreated high blood pressure may lead to injury and consequently rupture of vessels especially in the brain (American Heart Association, 2012).
Stroke scoring scales as the Intracerebral Hemorrhage (ICH) Score, Functional Outcome Risk Stratification (FUNC) score, and Glasgow Coma Scales can be used in monitoring the progression of stroke and outcome of treatment interventions (National Institute for Health and Care Excellence, (2009). Monitoring of neurological and physiological parameters is done during surgery and postoperative period. Thus, the patients with Glasgow coma scale less than eight may require rapid endotracheal intubation to optimize airway clearance and enhance gaseous exchange.
Evidence based practice
According to National Institute for Health and Care Excellence (2009), patient assessment should be accurately and adequately done using assessment tools like ROSIER score, FUNC, ICH scores, and Glasgow Coma Scale to establish the extent of risk and potential complications. Moreover, comprehensive history taking should be done to identify the risk factors and the actual cause. American Heart Association (2012) indicates that patients with ROSIER score of more than zero with Glasgow coma scale less than eight may be suffering from stroke and CT scan or MRI should be done to confirm the presence of intracerebral hemorrhage. However, endotracheal intubation should be done soonest to promote ventilation (Magistris, Bazak, and Martin, 2013). The cause should be adequately dealt with to prevent deterioration in state of the patient.
Other symptomatic management protocols should also be continued as the patient is prepared for endovascular or surgical interventions. Huether and McCance (2012) recommend nursing the patient in a quiet room with reduced number of visitors as this reduces irritability, exertion, and even stress. According to Magistris, Bazak, and Martin (2013), the head should be adequately elevated up to 30o to ensure venous return and monitoring of cardiovascular and neurological functions. This helps to promptly intervene and/or refer the patient in case of severe deterioration of vital signs and neurological functions. National Institute for Health and Care Excellence (2009) also recommend the initiation of medications like aspirin 300mg daily for two weeks (if patient does not have coagulopathies), mannitol to reduce cerebral edema and increased intracranial pressure, Oxygen if the saturation levels are less than 95% (Ackley & Ladwig, 2013), and continuous monitoring of the blood pressure, pulse rate, and level of consciousness.
Background
A 58 year old male patient was brought to the accident and emergency department in an ambulance accompanied by the wife and a relative. Presenting complaint was sudden semi-consciousness, severe headache, vomiting, and numbness of the left arm.
On the assessment, it was established that the patient is a known hypertensive patient. The blood pressure on admission was 146/98mmHg, Glasgow coma scale rating was 10/15, pulse rate was 87beats/minute, temperature was 37.3oC and oxygen saturation (SpO2) was 92%.
The assessment generated an impression of an elderly male patient in a semiconscious state with mild hypertension and mild hypoxic state. He was able to obey a couple of commands. However, the left arm did not respond to pain stimuli and the reflex was sluggish.
Investigations
CT scan of the head was recommended to rule out possible transient ischemic attack and intracerebral bleeding. A random blood sugar (RBS) test was done to rule out hypoglycemia. Thus, the plasma glucose level was 5.2mmol/L. However, the CT scan indicated hemorrhage in the right middle cerebral cortex.
Treatment
The patient was admitted to an acute stroke unit for specialized care. Vitamin K combined with the prothrombin concentrate was then administered intravenously to achieve anticoagulation. The physician also prescribed administration of alteplase, which was carefully administered and the patient closely monitored for complications of thrombolytic.
Oxygen by nasal prongs was administered to relieve hypoxia since the SpO2 (peripheral oxygen saturation) levels were less than 95%. Blood pressure was constantly monitored and controlled to prevent hypertension. Regular monitoring of plasma glucose levels was also done to ensure normoglycemia of between 4-11mmol/L.
Daily assessment of ICH, FUNC score (face, arm, speech test), ROSIER and Glasgow coma scale for improvement. Monitoring of physiological parameters like blood pressure, oxygen saturation, central venous pressure, pulse rate and respiration rate were done every 2-4 hour.
Patient and family centered care was continued where the family and relatives were involved in the caring process (American Psychological Association, 2009). Homeostatasis was also ensured via intravenous (IV) fluids that ensured hydration, electrolytes and nutrient supply within the first 24 hours of admission.
Prognosis and referral
After performing a CT scan, the patient was then referred for MRI and carotid imaging but this was after stabilization of the neurological functions. The patient continued on management and the Glasgow coma scale improved to 15/15 by the end of 48 hours of admission. Oxygen saturation improved to above 97%. Mobilization was started on third day of admission and patient complied well as he could sit up stand and reach items on the bed table. However, the patient was referred to a neurosurgical centre for specialized care and follow up.
Care plans
Based on the above case study, the following care plans were developed and implemented during the care of the patient.
Hemorrhagic stroke occurs when a blood vessel ruptures causing bleeding in the brain tissue. This then results in hematoma formation, inflammation, cerebral edema and increased intracranial pressure. In the end, neurological deficits, disability and even death may ensue. A myriad of factors including hypertension, aneurysms, vascular abnormalities, and cerebral neoplasm among others have been associated with hemorrhagic stroke. Thus, the health care professional should focus on first identifying the cause before initiating therapeutic interventions. However, nurses are charged with the responsibility of initiating supportive management to relieve symptoms and prevent negative progression of the condition.
References
Ackley, B. & Ladwig, G. (2013). Nursing diagnosis handbook: An evidence-based guide to planning care (10th Ed.). St. Louis: Mosby
American Heart Association (2012). Let’s talk about hemorrhagic stroke, Washington D.C: AHA
American Psychological Association. (2009). Publication manual of the American Psychological Association (6th Ed.) Washington DC: American Psychological Association.
Huether, S.E., and McCance, K.L. (Eds.) (2012), Understanding pathophysiology. St. Louis: Elsevier Mosby.
Magistris, F., Bazak, S., and Martin, J. (2013). Intracerebral Hemorrhage: Pathophysiology, diagnosis and management, MUMJ. Vol. 10, No. 1, 15-19
Masotti, L., Napoli, M., Godoy, D., Rafanelli, D., et al. (2011). The practical management of intracerebral hemorrhage associated with oral anticoagulant therapy, International Journal of Stroke. Vol. 6, 228-240
National Institute for Health and Care Excellence (2009), Diagnosis and initial management of acute stroke and transient ischemic attack (TIA). Manchester: NICE.
National Stroke Association (2009). Hemmorrhagic stroke fact sheet. CO: NSA
