Nursing Assessment of the Special Patients - Case Study Example

CARE DELIVERY Introduction This is a case study focussing on the nursing assessment and prioritisation of the patients physical and psychological needs and will include a brief, summary of the anonymous patient's demographic and clinical history. Mrs. B is a 35 year old patient, who presented in A&E with a history of sudden onset of severe headache. She described it as " the worst headache [she] had ever experienced" with associated photobia, nausea and vomiting and neck stiffness. Upon assessment, Mrs B had a GCS of 14/15, apyrexial, and her blood pressure was 155 over 92, pulse 86. Her respiratory rate was 16, and sao2, 96%. With regards to her health history, a subarachnoid haemorrhage (SAH) was suspected, a CT scan was consequently performed. The CT showed haemorrhage in the right Sylvian fissure. Subarachnoid haemorrhage is catastrophic bleeding from a cerebral aneurysm situated on the Circle of Willis or from an arteriovenous malformation . Subarachnoid haemorrhage is associated with high morbidity and of the patients who survive the potential for rebleeding and ischeamia increase morbidity and mortality. Hence subarachnoid haemorrhage is deemed to be a life threatening condition and management and care of the patient is subsequently based on prevention of complications and achieving the optimum outcome for the patient. In order to observe and assess Mrs B appropriately and deliver proactive preventative nursing management Mrs B was admitted to the neurosurgical special care unit (NSCU). Subarachnoid Hemorrhage Incidence According to studies in the United States, approximately 25000 to 30000 persons (6-11 per 100000) experience SAH (Pfohman, 2001) each year. It was indicated that rupture of cerebral artery aneurysms accounts for 50% to 80% of these cases (Falyar, 1999). Likewise, other causes include bleeding from a cerebral tumour, cocaine abuse, hypertensive cerebral haemorrhage, anticoagulant therapy, and ruptured arteriovenous malformations (Rees, 2002). Servadei et al (2002) reported that SAH has also been noted on the initial CT scans of approximately 40% of all patients with major head injuries. Etiology Aneurysms are described as bulges or areas of outpouching that occur at a site of weakness in a vessel wall, most commonly at the junction or bifurcation of 2 vessels. Many cases are considered congenital, while others are associated with vascular disorders caused by uncontrolled hypertension, bacterial or fungal infections, and connective tissue diseases such as Marfan or Ehlers-Danlos syndromes (Pfohman, 2001). It was indicated that regardless of the cause, when an aneurysm ruptures, arterial pressure forces blood into the subarachnoid space between the arachnoid mater and the surface of the brain. Eventually, free blood travels through the fissures, into the basal cisterns, and across the surface of the brain (Rees, 2002). This blood interfere with the circulation and re-absorption of cerebrospinal fluid (CSF) upon clotting, thereby potentially causing an obstructive hydrocephalus and increased intracranial pressure. Risk Factors Studies claim that an important and non-modifiable risk factor to SAH is familial predisposition. It had been indicated that between five and twenty percent of patients with SAH have a positive family history (Schievink, 1997). Accordingly, first-degree relatives of patients with SAH have a 3- to 7-fold increased risk of being struck by the same disease while in second-degree relatives, the incidence of SAH is similar to that found in the general population (Bromberg et al, 1995). Clinical Findings Rusy (1996) proposed that blood in the subarachnoid space is a powerful meningeal irritant, and it is this irritation that causes most of the initial signs and symptoms of SAH. Nevertheless, findings vary from insignificant to serious, depending on the extent of hemorrhage (Rees, 2002). According to Corsten (2001), the characteristic initial symptom of patients with SAH is sudden headache described as the most painful ever experienced while changes in mental status are also common. Patients' initial experience may vary from awake and alert to deeply comatose. Clinical findings also indicate nuchal rigidity, photophobia, nausea and vomiting, hypertension, electrocardiographic changes, pyrexia, cranial nerve deficits, visual changes, sensory or motor deficits, fixed and dilated pupils, seizures, herniation, and and even sudden death (Corsten, 2001). Below is Hunt and Hess scheme for grading cerebral aneurysms: Source: Hunt & Hess, 1968. Outcome Rees (2002) confirms that both severity of disability and length of rehabilitation after SAH are linked to the extent of the initial injury so that SAH takes a tremendous physical and emotional toll on patients and their families. In addition, an estimated 35% of patients who experience SAH will not survive the initial haemorrhage (Chiappetta, 1998). Another finding also indicate that patients who outlive the original haemorrhage face a multitude of potential complications in the acute phase as well as functional limitations requiring extensive rehabilitation and may result in permanent deficits. Causes of SAH Cause Frequency (%) Site of blood on CT Characteristic features Ruptured aneurysm 85 Basal cisterns or none Non-aneurysmal perimesencephalic haemorrhage 10 Basal cisterns Pattern of haemorrhage on CT Rare conditions 5 Arterial dissection (transmural) Basal cisterns Preceding neck trauma or pain; lower cranial nerve palsy Cerebral arteriovenous malformation Superficial Vascular lesion often visible on CT Dural arteriovenous fistula Basal cisterns History of skull fracture Vascular lesions around the spinal cord Basal cisterns Pain in lower part of neck or in back. Radicular pain or cord deficit Septic aneurysm Usually superficial History; preceding fever or malaise Pituitary apoplexy Usually none Visual or oculomotor deficits; adenoma on CT Cocaine abuse Basal cisterns or superficial History Trauma (without contusion) Basal cisterns or superficial History Source: Brain, 2001. Vasospasm Symptomatic vasospasm also called delayed ischemic deficits (Aiyagari, 2001), delayed ischemic neurological defects (Warnell, 1996), and cerebrovascular spasm, has been reported as the most common serious complication after aneurysmal rupture and is the leading cause of death for patients who survive the rupture (Smith, 2000). Vasospasm-induced narrowing of cerebral vessels has been estimated to occur in 70% to 90% of patients hospitalized for SAH and vasospasm is symptomatic in 30 percent of these patients (Smith, 2000). Definition Vasospasm was defined as a sustained arterial contraction unresponsive to vasodilator drugs (Levati, 1998) commonly classified as either angiographic or clinical. While angiographic vasospasm refers to visible narrowing of the dye column in an artery, as shown on cerebral angiograms, clinical vasospasm is defined as the functional manifestation of cerebral ischemia produced by this arterial narrowing (Falyar, 1999). Smith (2000) described episodes of vasospasm as benign or devastating. 70 percent of patients with SAH were indicated to have angiographic evidence of vasospasm but no clinical evidence of vasospasm while the remainder or those with clinical vasospasm have changes in findings on neurological examination. The onset of new or worsening neurological signs or symptoms is the most reliable indicator of vasospasm as indicated in clinical findings (Falyar, 1999). Symptoms and assessment may be subtle and include headache, lethargy, and intermittent disorientation, which can progress to focal neurological deficits such as hemiparesis and speech dysfunction (Pfohman, 2001). Accordingly, deficits vary to the degree of vessel constriction and the cerebral artery affected (Falyar, 1999). The untreated reduction in cerebral blood flow may lead to permanent disability and even death (Smith, 2000). Clinical Course A common predictive factor of vasospasm is the initial size of the SAH evident on CT scans characterised by the presence of diffuse, thick, subarachnoid blood, particularly around the base of the brain. This has been correlated with a high incidence and severity of vasospasm while CT findings of focal, thin blood are associated with a lower vasospasm rate (Chiappetta, 1998). The systems most commonly used to grade acuity of SAHs are the Fisher Scale and the Hunt and Hess grading scheme (please refer to above). For both of these instruments, studies have shown a direct correlation between the severity of the clinical grade of cerebral aneurysm and the incidence of vasospasm after SAH (Rusy, 1996). In addition, vasospasm is more prevalent if haemorrhage occurs in one of the vessels of the circle of Willis (Falyar, 1999). In some cases, spasm spreads across the entire distribution area of a cerebral artery, but it is usually localized to the vessels closest to the site of leakage (Rees, 2002). The incidence of vasospasm peaks at 5 to 12 days after rupture of the aneurysm, but the actual time of onset can be anywhere from 3 to 21 days after haemorrhage (Falyar, 1999). The condition generally persists for 12 to 16 days (Corsten, 2001). Pathophysiology Although the etiology and pathophysiology of cerebral vasospasm after SAH are complex and are only partially understood, precise molecular mechanisms of vasospasm remain to be elucidated as they include a combination of both increased constrictor mechanisms and decreased dilator functions (Chiappetta, 1998). Several theories offered to explain the multifaceted processes known to be involved include the hypothesis that oxyhemoglobin plays a primary role in the development of cerebral vasospasm associated with aneurysmal SAH (Warnell, 1996). The initial hemorrhage is followed by erythrocytes trapped in the subarachnoid cisterns that slowly hemolyze, releasing oxyhemoglobin and other by-products of red cell lysis or bilirubin and methe-moglobin, to circulate within the subarachnoid space (Bell, 1996). It had been found that the spasminogens increase the influx of calcium into the vascular smooth muscle, altering myocyte function and causing prolonged contraction and vessel constriction (Bell, 1996). In addition, oxyhemoglobin had been found to contribute to the release of free radicals and peroxidation of lipids (Bell, 1996) promoting the synthesis of vasoactive eicosanoids and endothelin and inhibit endothelium-dependent relaxation of the arterial wall (Warnell, 1996). Likewise, it is also suspected that the failure of nitric oxide-dependent relaxation mechanisms within cerebral arteries to be involved in vasospasm (Chiappetta, 1998). Some studies of CSF after SAH indicated elevations in levels of free fatty acids, implicating these agents in the development of vasospasm as well (Pilitsis, 2002). The presence of prostaglandins, thromboxane A2, leukotrienes, and histamine in the CSF after hemorrhage, supports the theory that vasospasm is associated with an inflammatory response in the subarachnoid space (Warnell, 1996). Another hypothesis is that sloughing of endothelial cells resulting in structural changes in the inner layer of the arterial wall allows vaso-constrictive substances, including serotonin, catecholamines, and oxy-hemoglobin, to reach the medial layer producing vasospasm (Falyar, 1999). SAH causes spasm of local vessels and disturbance of cerebral autoregulation and impaired autoregulation reduces the ability of the brain to maintain adequate cerebral perfusion pressures and also enhance the propensity of cerebral arteries to constrict in response to vasoactive substances (Pilitsis, 2002). Reduced size of the vessel lumen restricts blood flow to the brain tissue and causes temporary irreversible vasoconstric-tion (Falyar, 1999). In addition, prolonged increases in cerebral vascular resistance and decreased regional blood flow are followed by ischemia and potential infarction of the cerebral parenchyma (Rusy, 1996). It was indicated that the blood-flooded subarachnoid space is clearly a "pathological factory" stimulating vasospasm through a variety of mechanisms. Nevertheless, this multiplicity of biochemical reactions offers many potential targets for antispastic drugs (Chiappetta, 1998). Diagnosis Signs and Symptoms Vasospasm can be recognized by means of frequent, thorough neurological examinations. Patient's baseline assessment must be clearly documented and it should be noted that signs and symptoms may be subtle, generally have a gradual onset, and tend to wax and wane (Falyar, 1999). Clinical findings can include changes in level of consciousness, headache, periods of disorientation, inappropriate behaviour, language impairment, hemi-paresis, and seizures (Rusy, 1996). Attending nurses must detect and report immediately any changes in a patient's neurological status. But if unrecognized, the deficits associated with vasospasm can become permanent disabilities (Bell, 1996). TCD Imaging According to Falyar (1999), TCD imaging is a noninvasive technique often used to diagnose vasospasm performed at the bedside, usually on a daily basis, after SAH. This imaging technique is used to measure the velocity of blood flow through segments of arterial vessels as trends in flow velocity allows early identification of patients at risk for vasospasm. However, many factors can affect the validity of TCD findings (Rusy, 1996). Carefully documented and regular TCD correlated with the results of a patient's neurological examination, facilitate the rapid diagnosis and treatment of cerebral vasospasm (Falyar, 1999). Angiography Use of both CT angiography and magnetic resonance angiography have been investigated, but standard angiography remains the definitive study for the diagnosis of cerebral vasospasm (Smith, 2000). It was reported that spasm is indicated by evidence of narrowing of arterial vessels, and that these changes may be apparent on angiograms before the advent of clinical signs and symptoms (Smith, 2000). Interventions for Vasospasm For the past 50 years, researchers and clinicians have sought to discover optimal ways to prevent and manage cerebral vasospasm but failed to identify a single therapy (Bell, 1996). Nevertheless, most authors agree that clipping the aneurysm or using an endovascular intervention such as coiling, stenting, or angioplasty within 48 hours of the initial haemorrhage is imperative to minimize the occurrence of both vasospasm and rebleeding (Bell, 1996). Early surgical clot removal also limits the amount of oxyhemoglobin released, reducing the incidence of vasospasm (Bell, 1996) Recommendations include administration of calcium channel blockers and use of triple H therapy as these are both widely accepted interventions after clipping or coiling (Chiappetta, 1998). These measures were found to be most effective when used prophy-lactically (Rusy, 1996). But once vasospasm is established, even potent vasodilators do not effectively reverse the spasm (Levati, 1998) but treatment of refractory vasospasm may include balloon angioplasty and direct arterial instillation of papaverine. Calcium Channel Blockers Nimodipine (Nimotop) is the calcium channel blocker commonly used for cerebral vasospasm (Levati, 1998). The drug is lipid soluble and it easily crosses the blood-brain barrier (Rusy , 1996). It was indicated that nimodipine decreases spasm in the cerebral vascular bed and lead to improvement in long-term outcomes after SAH (Corsten, 2001). Patients are prophylactically given oral nimodipine at a dosage of 60 mg, every 4 hours, for 21 days (Corsten, 2001) after haemorrhage. Triple H Therapy The use of triple H therapy also referred to as HHH, THT, prophylactic hyperdynamic postoperative fluid therapy, and hemodynamic augmentation, has become common practice in patients with SAH (Aiyagari, 2001). The components of triple H therapy are hypertension, hypervolemia, and hemodilution. These interventions affect the symptoms of vasospasm rather than the underlying cause (Choudhari, 2002). In addition, hypertensive state is maintained through the use of vasopressors. Hypervolemia is obtained by using volume expansion that produces hemodilution. These routines are all designed to increase cerebral perfusion pressure, improve blood flow to the brain, and decrease the risk of ischemia (Corsten, 2001). Triple H therapy is usually started as soon as the aneurysm has been secured or clipped. Sometimes, a modified version of triple H therapy is used before securing the aneurysm in order to prevent rebleeding or rupture. Therapy is conducted for at least 14 days after the initial haemorrhage as this is the most common period for vasospasm (Rusy, 1996). Patients lose autoregulatory function in ischemic brain tissue after SAH. Sometimes, induced hypertension is designed to increase cerebral blood flow and enhance perfusion pressure (Levati, 1998Target systolic blood pressures may be as high as 200 mm Hg. Asopressor and inotropic agents such as dopamine, phenylephrine, and dobutamine are generally required to maintain systolic blood pressure at this elevated level (Aiyagari, 2001) as addition to fluid. Also, therapeutic hypertension is initiated once the aneurysm has been surgically clipped or coiled. Likewise, in cases where aneurysm has not yet been repaired surgically or is considered inoperable, systolic blood pressure is kept between 120 and 150 mm Hg to minimize the risk of rupture and rebleeding (Rusy, 1996). Use of triple H therapy in many institutions did not prevent controversy. In some studies of patients with vasospasm indicate that not every patient responds to this therapy (Egge, 2001). Despite apparent reversal of neurological deficits, no evidence indicates that morbidity or mortality is reduced after triple H therapy (Egge, 2001) and triple H therapy is also associated with a substantial number of complications (Rusy, 1996). Complications after triple H include pulmonary edema, myocardial ischemia, congestive heart failure, electrolyte imbalances, coagulopathies, and rupture of unsecured aneurysms (Egge, 2001). Following is the nursing considerations for patients given triple H therapy to treat subarachnoid haemorrhage: Source: Corsten, 2000. Angioplasty Balloon angioplasty directly treats narrowed cerebral vessels by widening the stenotic segment resulting to dramatic improvement of a patient's neurological status (Corsten, 2001).Vessels rarely restenose after angioplasty and with opening the vessel, the balloon causes functional impairment of smooth muscle in the vessel wall, reducing or eliminating further vasospasm (Smith, 2000). Limitation of balloon angioplasty is that it can be used to widen only larger vessels, such as the distal internal carotid, proximal middle cerebral, proximal anterior cerebral, distal vertebrobasilar, and proximal posterior cerebral arteries. A devastating complication associated with angioplasty is vessel rupture (Corsten, 2001). Papaverine Papaverine, a synthetic alkaloid of opium, has an antispasmodic effect on smooth muscle for patients with vasospasm refractory to triple H therapy. Selective intra-arterial injection of papaverine directly into spastic vessels can reverse spasm (Smith, 2000). The main advantage of papaverine is that it can be used to treat distal vessels, those beyond the reach of an angioplasty balloon (Smith, 2000) but the use of this agent is controversial as significant increases in intracerebral pressure can occur after instillation, and some investigators think that this intervention has no proven long-term benefit (Corsten, 2001). General management of patients with aneurysmal SAH Nursing - Continuous observation of Glasgow Coma Scale, temperature, ECG monitoring, pupils, any focal deficits. Nutrition - Oral route preferred, but only with intact cough and swallowing reflexes. Use nasogastric tube if necessary: Deflate endotracheal cuff if present on insertion Confirm proper placement by X-ray Begin with small test feeds of 5% dextrose Prevent aspiration by feeding in sitting position and by checking gastric residue every hour Tablets should be crushed and flushed down (phenytoin levels will not be adequate in conventional doses) Total parenteral nutrition should be used only as a last resort Keep stools soft by adequate fluid intake and by restriction of milk content; if necessary add laxatives Blood pressure Do not treat hypertension unless there is evidence of progressive organ damage Fluids and electrolytes Intravenous line mandatory Give at least 3 l/day (normal saline) Insert an indwelling bladder catheter if voiding is involuntary Compensate for a negative fluid balance and for fever Monitoring of electrolytes (and leucocyte count), at least every other day Pain Start with paracetamol and/or dextropropoxyphene; avoid aspirin Midazolam can be used if pain is accompanied by anxiety (5 mg intramuscularly or infusion pump) For severe pain, use codeine or, as a last resort, opiates Prevention of deep vein thrombosis and pulmonary embolism Before occlusion of aneurysm: apply compression stockings After treatment of the aneurysm: fractionated heparin Medical treatment to prevent secondary ischaemia Nimodipine 60 mg orally every 4 h; to be continued for 3 weeks Reference: Brain (2001). Vol. 124, No. 2, 249-278, February 2001. Oxford University Press Pfohman M, Criddle L. Epidemiology of intracranial aneurysm and sub-arachnoid hemorrhage. J Neurosci Nurs. 2001;33:39-41 Falyar CR. Using transcranial Doppler sonography to augment the neurological examination after aneurysmal subarachnoid hemorrhage. J Neurosci Nurs. 1999;31:285-293 Rees G, Shah S, Hanley C, Brunker C. Subarachnoid haemorrhage: a clinical overview. Nurs Stand. July 3-9, 2002;16:47-54 Servadei F, Murray GD, Teasdale GM, et al. Traumatic subarachnoid hemorrhage: demographic and clinical study of 750 patients from the European Brain Injury Consortium survey of head injuries. Neurosurgery. 2002;50:261-267 Rusy KL. Rebleeding and vasospasm after subarachnoid hemorrhage: a critical care challenge. Crit Care Nurse. February 1996; 16:41-48 Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg. 1968;28:14-20. Schievink WI. Genetics of intracranial aneurysms. [Review]. Neurosurgery 1997; 40: 651-62 Corsten L, Raja A, Guppy K, et al. Contemporary management of sub-arachnoid hemorrhage and vasospasm: the UIC experience. Surg Neurol. 2001;56:140-148 Chiappetta F, Brunori A, Bruni P. Management of intracranial aneurysms: "state of the art." J Neurosurg Sci. 1998; 42(1 suppl 1):5-13 Aiyagari V, Cross DT III, Deibert E, Dacey RG Jr, Diringer MN. Safety of hemodynamic augmentation in patients treated with Guglielmi detachable coils after acute aneurysmal subarachnoid hemorrhage. Stroke. 2001;32:1994-1997 Warnell P. Advanced concepts in the management of cerebral vasospasm associated with aneurysmal subarachnoid hemorrhage. Axone. 1996;17:86-92 Smith TP, Enterline DS. Endovascular treatment of cerebral vasospasm. J Vasc Interv Radiol. 2000;11:547-559 Levati A, Solaini C, Boselli L. Prevention and treatment of vasospasm. J Neurosurg Sci. 1998;42(1 suppl 1):27-31 Bromberg JEC, Rinkel GJE, Algra A, Greebe P, van Duyn CM, Hasan D, et al. Subarachnoid haemorrhage in first and second degree relatives of patients with subarachnoid haemorrhage. BMJ 1995; 311: 288-9 Bell TE, Kongable GL. Innovations in aneurysmal subarachnoid hemorrhage: intracisternal t-PA for the prevention of vasospasm. J Neurosci Nurs. 1996;28:107-113 Pilitsis JG, Coplin WM, O'Regan MH, et al. Free fatty acids in human cerebrospinal fluid following subarachnoid hemorrhage and their potential role in vasospasm: a preliminary observation. J Neurosurg. 2002;97:272-279 Levati A, Solaini C, Boselli L. Prevention and treatment of vasospasm. J Neurosurg Sci. 1998;42(1 suppl 1):27-31 Choudhari K. Prophylactic hyperdynamic postoperative fluid therapy after aneurysmal subarachnoid hemorrhage: a clinical, prospective, randomized, controlled study [letter; comment]. Neurosurgery. 2002;50:1170-1172. Egge A, Waterloo K, Sjoholm H, Solberg T, Ingebrigtsen T, Romner B. Prophylactic hyperdynamic postoperative fluid therapy after aneurysmal subarachnoid hemorrhage: a clinical, prospective, randomized, controlled study. Neurosurgery. 2001;49:593-605 Read More