Delayed Ischemia Due to Cerebral Vasospasm Post Operate Subarachnoid Hemorrhage Clipping - Essay Example

? Delayed ischemia due to cerebral vasospasm post operate subarachnoid hemorrhage clipping. Subarachnoid hemorrhage is half of spontaneous a traumatic intracranial hemorrhages, which is actually the result of the arteriovenous malformation, leakage or rupture results in bleeding that occurs within the brain parenchyma. Intracranial hemorrhage comprises 20% of all strokes that is because the extravasation of the blood in the subarachnoid space between the pile and arachnoid membrane. This hemorrhage has a detrimental effect on the brain function that’s results in high morbidity rate and mortality rate. This disease mostly strike at fairly young age and proved to be fatal. Its effects are similar to the cerebral infarction or intracerebral hemorrhage. Diagnosis and acute management of the subarachnoid represents a great challenge to the neurologists, neurosurgeons, interventions radiologists and intensivists. In this case study we analyze the factors that are involved in the subarachnoid hemorrhage and their relation with the delayed ischemia that is occur because of the cerebral vasospasm. In this study we also evaluate the role of the practitioners regarding to this disease. In most of the population the incidence of subarachnoid hemorrhage is 6-7 individuals per 100, 000 persons in a year. Incidence of subarachnoid hemorrhage increases with the age. Their risk factors are smoking, constant or excessive alcohol intake and hypertension. In the patients who have positive family history for subarachnoid hemorrhage, the average age at which the disease strikes to them is younger age than in patients with the sporadic subarachnoid hemorrhage. So, genetic factors also play significant role in this disease. Factors that are involved in the rupture of the arachnoid membrane are very complex; it happens because of the sudden increase in trans mural arterial pressure, activities such as exercise, straining and intercourse are reported as 20% necessary factor in the prevalence subarachnoid hemorrhage (Zentner, et al., 1996). The main characteristic symptom of subarachnoid hemorrhage is the head ache. This head ache is different from the normal head ache that usually occurred in individuals in their daily routine life due to extensive hard work. Head ache usually last 1- 2 weeks and sometime longer and of very high intensity. Vomiting is also the characteristic of this disease but it is not distinctive one because it also occurred in the patients of non-hemorrhagic. Focal neurological deficits occur when an aneurysm compresses a cranial nerve or bleeds into the brain parenchyma or from focal ischemia due to acute vasoconstriction immediately after aneurysmal rupture. Sometimes, therefore, the clinical manifestations of a ruptured aneurysm are indistinguishable from a stroke syndrome from cerebral infarction. Complete or part third-nerve palsy is a well-recognized sign after rupture of aneurysms, mostly of the internal carotid artery at the origin of the posterior communicating artery (Wartenberg, et al., 2006). Systematic feature which are associated with the subarachnoid hemorrhage are sever hypertension, hypoxemia and electrocardiographic changes which can mimic the myocardial infarction and lead to erroneous examinations and treatments. The first investigation if the subarachnoid hemorrhage is suspected is CT scan. Their detection depends on the amount of blood that leaked into the subarachnoid space. The indication of surgery in patients of subarachnoid hemorrhage can be done if the overall medical condition of the patient is out of control, like aneurysm size and location, accessibility of the aneurysm for surgical repair, and presence or absence of thrombus, are also important (Wartenberg, et al., 2006). Cerebral vasospasm is the intensive and prolonged vasoconstriction of the large conducting arteries in the subarachnoid space that is initially surrounded by the clot. The further narrowing of the vessels develop gradually over the first few days after the aneurysmal rupture. Delayed cerebral ischemia is the result of cerebral vasospasm is one the most common cause of death and disability after subarachnoid hemorrhage. It leads to the permanent death of neurological tissues in 17-40% patients of the subarachnoid hemorrhage. The main symptom in the cerebral vasospasm is the diffuse head ache that is associated with the slight increase in discomfort from the neck stiffness and fever. Actually delayed cerebral ischemia is the development of the focal neurological signs and deterioration in the level of consciousness lasting for more time. This definition is considered to be the more meaningful in the patients of subarachnoid hemorrhage whose neurological deterioration was unrecognized. Arterial narrowing can be explained angiographically in 50-70% patients and this leads to the delayed ischemia in 19-47% patients after subarachnoid hemorrhage (Teasdale, 2005). Delayed ischemia is occurred on the third day after subarachnoid hemorrhage. Delayed ischemia becomes maximal at 5-14 days and resolved after 21 days. The presence of thick subarachnoid blood seen in CT scan and severe intraventricular hemorrhage are strongly associated with higher risk for vasospasm. In the first few hours after the initial hemorrhage, up to15% of patients have a sudden deterioration of consciousness that suggests re-bleeding. In patients who survive the first day, the risk of re-bleeding is more-or-less evenly distributed during the next 4 weeks, 35% with accumulative risk of 40% without intervention. After re-bleeding the prognosis is poor: 80% of patients die or remain disabled. Few, if any, prognostic factors predict an increased risk of re-bleeding. During the past decade, endovascular occlusion by means of detachable coils (coiling) of aneurysms has largely replaced surgical occlusion as the intervention of choice for the prevention of re-bleeding, at least in specialized centers. The technique consists of packing the aneurysm with platinum coils, with a system for controlled detachment, and is generally done under general anesthesia. Randomized trials in which coiling was compared with neurosurgical clipping have included in the patients. Most patients were in good clinical condition and had a small aneurysm on the anterior circulation. After a year of follow-up, the relative risk reduction for poor outcome for coiling versus clipping was 24%. Patients older than 70 years were underrepresented in this comparison—in view of the perceived advantage of coiling in elderly people—as were patients with aneurysms of the middle cerebral artery, because the anatomical configuration is often unfavorable for coiling, with branches arising near the neck of the aneurysm. Ideally, after coiling, the remaining lumen becomes occluded by a process of reactive thrombosis, but early or late re-bleeding can occur after technically correct procedures. Uncertainty exists about the length of time that patients need to be followed up after coiling, about the most suitable radiological technique, and about the need for a second procedure for aneurysm necks that have reanalyzed by impaction of the coils, through re-coiling or surgical occlusion. Surgical clipping for occlusion of the aneurysm has now become second choice for most patients. Modern surgical techniques are estimated to provide an absolute risk of poor outcome (Rabinstein, 2004). Hop, et al (1997) explained the different ways of nursing diagnosis for delay ischemia these are: (1) Impaired physical mobility that is associated with loss of balance, coordination, spasticity and brain injury. (2) Acute pain in which shoulders are more affected part of the body. (3) Self-care deficits (bathing, hygiene, toileting, dressing, grooming and feeding). (4) Impaired verbal communication due to neurological dysfunction. (5) Disturb thought process and patient seems to be confused or unable to follow the instructions. (6) Decreased level of mobility. (7) Disturb sensory perception due to changed sensory reception, transmission and integration. (8) Interrupted family processes related to catastrophic illness and caregiving burdens. (9) Ineffective tissue perfusion that is related to the vasospasms. (10) Anxiety related to medically imposed precautions and to illness. In health care units Nurses should do Continuous observation (Glasgow Coma Scale, temperature, ECG monitoring, pupils, any focal deficits), give nutrition through Oral route only with intact cough and swallowing reflexes and keep stools soft by adequate fluid intake and by restriction of milk content; if necessary add laxatives (Zentner, 1996). For nasogastric tube usage nurses should use the deflate endotracheal cuff (if present) on insertion, confirm proper placement on radiograph, begin with small test feeds of 5% dextrose, prevent aspiration by feeding in sitting position and by checking gastric residue every hour and tablets should be crushed and flushed down (blood phenytoin concentrations will not be adequate in conventional doses). The parenteral nutrition should be used only as a last resort. Nurses should do not treat hypertension unless mean arterial pressure is ?130 mm Hg or if clinical or laboratory evidence of progressive end organ damage. Fluids and electrolytes are assumed to be intravenous line mandatory and give at least 3 L per day (isotonic saline, 0·9%) solution. Insert an indwelling bladder catheter and compensate for a negative fluid balance and for fever. Monitoring of electrolytes (and leucocyte count), at least every other day should be done by nursing care. In pain nurses can start with paracetamol 500 mg every 3–4 h; avoid aspirin. Midazolam can be used if pain is accompanied by anxiety (5 mg via infusion pump). For severe pain, use codeine (30–60 mg every 4 h, as needed), tramadol (50–100 mg every 4 h, as needed) or, as a last resort, piritramide 0·2–0·3 mg/kg intramuscularly maximum 80 mg/24 h, in four doses). Prevention of deep vein thrombosis and pulmonary embolism can occur through compression stockings or intermittent compression by pneumatic devices, or both. Daily Transcranial Doppler Ultrasonography is a simple, efficient monitoring tool for the delayed ischemia. It is highly efficient method used to diagnose the vasospasm in larger cerebral arteries with variable sensitivity that depends upon the operator and the systematic conditions of the patient. If the mean velocity of the flow is greater than 120cm/s, is the indication of vasospasm in the middle cerebral artery. The delayed ischemia due to vasospasm is predictive if this mean velocity comes above 200cm/s but the dynamic changes in the velocity like twofold increase may be more sensitive for the diagnosis of vasospasm (John, et al., 1998). The iatrogenic factors that can increase the risk of cerebral vasospasm include prolongation of the subarachnoid clot by antifibrinolytic drugs, hypotension, inappropriate treatment of hyponatremia, hypovolemia, hyperthermia and increased intracranial pressure. Nimodipine has been shown to improve neurologic outcome and decrease the incidence of cerebral vasospasm. Triple H therapy is a treatment designed to augment cerebral blood flow for patient with cerebral vasospasm. Hypervolemic hypertension is induced with intravenous volume expansion with crystalloid or colloid to increase cardiac output and raise blood pressure. However, small randomized trials showed no clear benefit. Recently, balloon and chemical angioplasty with super-selective intra-arterial injection of vasodilators has emerged as the primary intervention for treating medically refractory ischemia from cerebral vasospasm and in many centers is being used as a first-line treatment or even prophylactically. In addition, promising new treatments for cerebral vasospasm or its ischemic complications include magnesium sulfate, fasudil hydrochloride, tirilazad mesylate, erythropoietin, and induced hypothermia; however, all still need further clinical trials. Newly recognized mediators of cerebral vasospasm after SAH include endothelium-derived mediators, vascular smooth-muscle-derived mediators, pro-inflammatory mediators involved in blood-brain barrier disruption, cytokines and adhesion molecules, stress-induced gene activation, and platelet-derived growth factors. Moreover, observations in the laboratory have, in many circumstances, matched those of reported small series. Larger, prospective, randomized trials are needed to verify several hypotheses of molecular pathophysiology and clinical treatment regimens (Rabinstein, et al., 2004). REFERENCES HOP, J. W., RINKEL, G. J. E., ALGRA, A. and VANGIJIN, J. (1997). Case-fatality rates and functional outcome after subarachnoid hemorrhage: a systematic review. Stroke, 28: pp 660–4. JOHNSTON, S. C., SELVIN, S. and GESS, D. R. (1998). The burden, trends and demographic of mortality from subarachnoid hemorrhage. Neurology, 50: pp 1413-18. RABINSTEIN, A. A., FRIEDMAN, J. A. and NICHOLS, D. A. (2004). Predictors of outcome after endovascular treatment of cerebral vasospasm. AJNR Am J Neuroradiol, 25: pp 1778–82. TEASDALE, G. M., WARDLAW, J. M., WHITE, P. M., MURRAY, G., TEASDALE, E. M. and EASTON, V. (2005). The familial risk of subarachnoid haemorrhage. Brain, 128: pp 1677–85. WARTENBERG, K. E., SCHMIDT, J. M. and CLAASSEN, J. (2006). Impact of medical complications on outcome after subarachnoid hemorrhage. 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