Managing Subarachnoid Haemorrhage
The following paper will examine the pathophysiology, diagnosis of, and management of, a subarachnoid haemorrhage (SAH), from both an acute and holistic perspective. A SAH will be defined. Cerebral anatomy and physiology will then be reviewed in order to determine the pathophysiology of a SAH. Clinical manifestations of a developing SAH will then be discussed, followed by the development of its diagnosis examined. Current nursing and medical management of this condition will then be examined by assessing a wide range of journal articles and research papers. Lastly, complications with management will then be discussed.
A subarachnoid haemorrhage defined
So what is a subarachnoid haemorrhage? According to Mosby’s Medical, Nursing and Allied Health Dictionary a subarachnoid haemorrhage is ‘an intracranial haemorrhage into the cerebrospinal fluid (CSF) filled space between the arachnoid and pial membranes on the surface of the brain’ (Anderson, Anderson, and Glanze 1998 p. 1554). It is further identified by Oh as refereeing to a bleed ‘primarily within the subarachnoid space, rather than into the brain parenchyma’ (Oh 1997, p.389).
Cerebral anatomy and physiology
In order to further understand the concept of a SAH a health care professional must understand both the cerebral anatomy and physiology so that the underlining pathophysiology may be understood. The brain is divided into four main sections: the brain stem, cerebellum, diencephalon, and cerebrum (see appendix A). The brain is protected by cranial bones, which make up the cranial vault and cranial meninges, which surround and encapsulate the brain (Tortora and Grabowski 1996, p.392). The cranial meninges, which surround the brain and spinal cord, include the dura mater (outer layer), arachnoid mater (middle layer) and the pia mater (inner layer) (see appendix B). The brain and spinal cord are nourished and further protected against physical and chemical injury by cerebrospinal fluid (CSF)(Tortora and Grabowski 1996, p. 393). This fluid circulates within the subarachnoid space, which is located between the arachnoid and pia mater. Blood and nutrients are then supplied to the CSF via two main arteries: ‘the internal carotid arteries (anterior circulation) and the vertebral arteries (posterior circulation)’ (Brown and Edwards 2005, p. 1529). The ‘anterior and posterior cerebral circulation is then connected at the circle of Willis and the anterior and posterior communicating arteries’ (Brown and Edwards 2005, p. 1529)
With a SAH, blood escapes from a defective or injured vasculature into the subarachnoid space. When the cerebral vasculature tears, most commonly through a berry aneurysm (Bendok, Getch, Malisch, and Batjer, 1998, p. 521) or arteriovenous malformation (AVM), blood under pressure is pumped into the subarachnoid space. This blood irritates the meningeal and other neural tissues and so produces an inflammatory response (Brown and Edwards 2005, p. 1529) Furthermore, this blood covers the nerve roots, and blocks arachnoid granulations, which impairs CSF reabsorption and clogs the foramina within the ventricular system, thus impairing CSF circulation. This results in an increase in intracranial pressure (ICP), while cerebral blood flow (CBF) and cerebral perfusion pressure (CPP) decrease. According to McCance and Huether, ‘the expanding haematoma acts like a space-occupying lesion, compressing and displacing brain tissue’ (2002, p. 512). As granulation tissue forms, scarring of the meninges occurs, resulting in a further decrease in CSF reabsorption and therefore secondary hydrocephalus may occur (Al-Shahi, White, Philip. Davenport, and Lindsay, 2006, p14). If this continues, the reduction in CPP will lead to insufficient cerebral perfusion, hypoxia and subsequent cerebral infarction, due to the anaerobic production of adenosine triphosphate (ATP).
Furthermore, if left untreated, ‘the pressure within the subarachnoid space may become so great that it will actually force the brain parenchyma through the foramen magnum, causing a brain stem herniation’ (McCance and Huether 2002, p. 513).
Clinical manifestations and Diagnosis
According to Van Gijn and Rinkel a ‘definitive diagnosis of a SAH is done through clinical presentation, lumbar puncture, and a non-contrast computer tomography (CT) scan (2001, p. 249). Although, there may be other diagnostic measures.
Through a thorough examination of clinical manifestations, medical staff may identify specific clinical signs and symptoms of a SAH, because these signs and symptoms often result from the pathophysiology of a SAH. Although these may not determine a definitive diagnosis of SAH, they may be used as warning bells to the clinician to perform a lumbar puncture and non-contrast CT to confirm a diagnosis of a SAH. According to Linn, Wijdicks, Van der Graaf, Weerdesteynvan, Bartelds, and Van Gijn, ‘a sudden severe headache, which maximizes in intensity immediately or within minutes, and lasting an hour or more (usually days) is a classic first sign of a SAH’ (1994, p. 590).
According to McCance and Huether, common clinical manifestation of a SAH include ‘episodic headache, transient changes in mental status or level of consciousness, nausea and vomiting, focal neurological defects, including both visual and speech defects, facial palsy and a stiff neck’ (2002, p. 512). Many of these signs and symptoms may be directly related to the rise in ICP and meningeal irritation. For example, an episodic headache may result from an increased ICP irritating the meninges, altered conscious state may directly be related to altered ICP, while visual, speech and facial nerve palsy, are the direct result of a raised ICP placing pressure on the optic nerve (2nd cranial nerve), oculomotor nerve (3rd cranial nerve) and the facial nerve (7th cranial nerve) (Brown and Edwards 2005, p. 1482-3).
By performing a lumbar puncture, medical staff can measure CSF pressure, and perform a chemical analysis, which may suggest the presence of a SAH (Whitfield and Kirkpatrick 2002, p. 17). Unless there is any suspicion of an alternative diagnosis such as meningitis, it is agreed that a ‘delayed lumbar puncture for at least six hours, preferably 12 hours, after headache onset, will give the most accurate diagnostic reading for SAH’ (Van Gijn and Rinkel 2001, p. 249). This allows sufficient time for haemoglobin to degrade into oxyhaemoglobin and bilirubin. According to Williams, ‘Bilirubin signifies a subarachnoid haemorrhage because it is only synthesised in vivo, unlike oxyhaemoglobin, which may result from a traumatic tap or prolonged storage or agitation of bloodstained cerebrospinal fluid in vitro’ (2004, p. 174).
According to the UK National External Quality Assessment Scheme for Immunochemistry Working Group, ‘the opening pressure of cerebrospinal fluid must be recorded as an early indicator for likely changes in ICP’ (2003, p.481).
Definitive diagnosis of a SAH can only be determined by performing a non-contrast CT scan. According to McCance and Huether an ‘arteriographic examination is the definitive diagnostic measure used for identifying an aneurysm or AVM’ (2002, p. 513) (See Appendix C). Multi-slice computed tomography angiography (CTA) is able to determine accurate diagnosis’ of a spontaneous SAH because of its ‘speed, tolerability, convenience, and the ability to provide three dimensional reconstructions’ (White, Wardlaw, and Easton 2000, p. 361). The ‘accuracy of this procedure for identifying aneurysms greater than 3 mm diameter is about 96%,’ (White et al 2000, p.368) but poorer for smaller aneurysms (Van Gelder 2003, p. 598). Further studies may include four vessel catheter angiography if aneurysmal SAH is strongly suspected but the CTA is normal (White et al 2000, p. 368). Repeated cerebral catheter angiography, spinal catheter angiography, or magnetic resonance imaging may be necessary to identify alternative causes in some cases. For people with a purely perimesencephalic distribution, a normal, good quality computed tomography angiogram allows a diagnosis of idiopathic perimesencephalic subarachnoid haemorrhage without the need for further investigation (Van Gijn and Rinkel 2001, p. 249).
Current medical and nursing management is influenced by the SAH grading of the client, and its relationship with the client’s pre-existing medical history. Management often utilises various SAH grading classification systems and actual grade. According to Bendok, Batjer and Hunt, ‘there is still much debate amongst neurologist as to the best SAH grading systems, and therefore universal diagnosis and treatment varies considerably around the world’ (2006, p. 2).
The most popular systems include the: Hunt and Hess SAH classification scale (see appendix D) the World Federation of Neurological Surgeons (WFNS) grading scale (see appendix E), the Fischer Scale (see appendix F) and the Glasgow Coma Scale (see appendix G). In Australia the Hunt and Hess SAH scale is currently the most common classification scale used, primarily because ‘it is what neurologists know and are used to, not necessarily because it is the best practice’ (Sepelt 2005, p. 2).
Medical and Nursing management of the patient with a SAH can be divided into pre-operative, surgical and post-operative care (Oh 1997, p. 391).
Pre-operative nursing care involves bed rest with oxygen, sedation and analgesia as required (Oh 1997, p.391). Basic care of the unconscious patient if his/her condition has reached this stage, including appropriate attention to the client’s: Airway, Breathing, Circulation, Disability and Exposure’ (Sepelt 2005, p. 1). Further pre-operative nursing care involves maintaining regular and thorough neurological, cardiovascular and respiratory assessments, and developing interventions to maintain homeostasis.
A neurological assessment of: GCS, conscious state, pupillary responses and extremity movement and strength should be regularly completed because, ‘a change in any of these may indicate an increased ICP and the need for an immediate intervention of both nursing and medical for the benefit of the client’ (Brown and Edwards 2005, p. 1542).
A cardiovascular assessment of: heart rate, heart rhythym, BP, MAP, CVP, fluid intake and output is paramount to good outcome and should be ‘aimed at maintaining cardiovascular homeostasis’ (Brown and Edwards 2005, p. 1542). According to Sepelt, ‘all SAH patients should have an arterial and central venous line inserted as soon as practically possible’ (2005, p1) in order to maintain accurate BP and CPP monitoring. Inatropes such as nor-adrenaline or vasopressin should be used to maintain a MAP of 80 mmHg (Sepelt 2005, p. 1).
A respiratory assessment of: respiratory rate, tidal volume, minute volume, oxygen saturation (SaO2) and end tidal carbon-monoxide (ETCO2) should be continuously conducted. According to the Brain Trauma Foundation, ‘patients with a suspected SAH should be kept normocarbic at a Partial Pressure of Carbon Monoxide (PaCO2) of 36-40 mmHg or an End Tidal Carbon Monoxide (ETCO2) of 31-35 mmHg’ (2000, p. 451).
Medical administration of antifibrinolytics, which inhibit clot lysis, ‘have been shown to reduce the rate of recurrent haemorrhage, but because of their disadvantages in overall health care of the client, their usefulness has been questioned’ (Roos, Y. 2002, p. 2).
Surgical clipping of the aneurysm is currently the preferred definitive treatment, with trapping, proximal ligation, bypass graft and reinforcement of the sac (Oh 1997, p. 391). However, according to Van der Schaaf, Algra, Wermer, Molyneux, Clarke and Van Gijn, ‘Although neurosurgical ‘clipping’ has become the standard treatment of aneurysms in the 20th century, endovascular occlusion of ruptured aneurysms using detachable coils is now superseding clipping in survivability’ (2005, p. 85) For aneurysms suitable for either treatment, coiling confers an absolute risk reduction over clipping of about 7% (25% relative risk reduction) for dependency or death at one year, with benefit sustained to seven years (Molyneux, Kerr, Yu, Clarke, Sneade, and Yarnold, 2005, p. 809) the number needed to coil to prevent one poor outcome is 14 (95% confidence interval 10 to 25) (Van der Schaaf, et al 2005, p. 85).
Surgical aneurysm clipping should be attempted as soon as practicable (within 3–4 days) after onset of SAH to prevent re-bleeding. It is believed that ‘morbidity seems to occur more often after clipping in the second week after haemorrhage when the risk of delayed cerebral ischaemia is greatest (Whitfield and Kirkpatrick 2002, p.3). Immediate evacuation of some intracerebral haematomas caused by aneurysm rupture, with concomitant aneurysm clipping, is supported by one small randomised trial (Dorsch, N. 2002, p. 128).
Postoperative medical and nursing management of SAH includes analgesic and general supportive care. Nursing care should be focused on continuous assessment of respiratory, neurological and cardiovascular systems as well as ICP and CPP monitoring, and implementing interventions that act to maintain these at homeostatic balances (Brown and Edwards 2005, p. 1542).
All patients with a ‘SAH should be positioned and nursed at 30 degrees head up, unless haemo-dynamically unstable to maximise venous drainage and minimise ventilator associated pneumonia’ (Sepelt 2005, p. 1)
Maintaining electrolyte homeostasis is important. The important electrolytes to monitor in SAH primarily include: sodium, potassium, calcium and magnesium (Huether and McCance 2002, p.513), with magnesium being important in neuroprotection. The optimal plasma magnesium concentration for neuroprotection remains uncertain at this moment in time. A study in 2005 suggested that a higher than normal level of magnesium is required for neuroprotection. According to Westermaier, Zausinger, Baethmann , and Schmid-Elsaesser ‘a continuous infusion of magnesium sulphate (MgSO4) to maintain a plasma magnesium concentration between 2 and 3 mmol/L appeared to produce maximal protection against transient cerebral ischemia (2005, p. 55).
Early mobilisation post SAH may increase positive outcome. In a randomised study between early mobilisation out of bed (3 days) compared to late mobilation (>6 days) post cerebral vascular accident (CVA), Diserens, Michel, and Bogousslavsky found that ‘early mobilisation as part of routine stroke unit care does seem to contribute to good long-term outcome’ (2006, p.190).
According to Rebuck, ‘ increased ICP is related to higher mortality rates and poorer functional outcomes’ (2000, p.38). Therefore, nursing management of the patient with a SAH should always include ICP monitoring and, if available, ‘ventriculostomy ICP monitoring should be used as this allows the therapeutic option of CSF drainage if required’ (Brain Trauma Foundation 2003, p. 4).
Once an ICP monitor has been implanted fluid and inatropes should be used to maintain a CPP (which may be calculated by MAP minus ICP) of greater than 60 mmHg. Although severe hypertension is not beneficial, hypotension dramatically affects the likelihood of a good health outcome. According to the Brain Trauma Foundation, ‘a single episode of hypotension dramatically worsens prognosis’ (2003, p. 2).
Complications with management
There are multiple complications associated with SAH both preoperatively and postoperatively. Complications can be both neurological and non-neurological in aetiology.
According to Harrod, et al, ‘cerebral vasospasm is a devastating medical complication of aneurysmal SAH that is associated with high morbidity and mortality rates, even after the aneurysm has been treated’ (2005, p. 1) A Transcranial Doppler (TCD) sonography is a well-established technique for investigating changes in cerebral hemodynamics (Compton, Redmond and Simon 1987, p.1499). The TCD technique can detect increased velocities in the proximal segments of the internal carotid, middle cerebral, anterior cerebral, posterior cerebral, vertebral, and basilar arteries, which are presumably caused by vessel lumen reduction. A rise in TCD velocity in the basal cerebral vessels occurs in nearly all patients after SAH, and a rapid rise to high levels is frequently associated with clinical deterioration caused by vasospasm and subsequent delayed ischemia (Harrod et al 2005, p. 3).
Current management of vasospasm includes the use of cerebroselective calcium channel blockers or hypervolaemic, hypertensive, haemodilution (HHH) therapy (Brain Trauma Foundation 2003, p. 4). Management with the cerebroselective calcium channel blocker ‘nimodipine’ acts to produce mild volume expansion while minimizing the effects on systemic arterial pressure; this is designed to prevent signs and symptoms of vasospasm. If, however, these signs and symptoms develop despite this regimen, patients are then often treated with aggressive HHH therapy. According to Rebuck ‘HHH therapy is used to elevate the cerebral perfusion pressure and thus provide blood to regions of the brain with marginal perfusion because of arterial spasm’ (2000, p. 39). By clipping the aneurysm early, one can be more aggressive with this therapy without concern of aneurysm re-rupture and subsequent rebleeding. Some neurosurgeons advocate prophylactic HHH therapy in patients at high risk for spasm (for example, thick subarachnoid blood clots). Thus, prophylactically one raises the blood pressure (in the range of 160-200mm Hg systolic with inatropes or vasopressors and volume expansion while monitoring the central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) (Fujii, Takeuchi, Sasaki, Minakawa, Koike, Tanaka 1996, p. 84).
Acute hydrocephalus with large amounts of intraventricular blood is often associated with a poor clinical condition from the outset. If such patients are left untreated, >90% have a poor outcome. An indirect comparison of observational studies suggests that insertion of an external ventricular catheter is not very helpful in these patients, but that a strategy where such drainage is combined with fibrinolysis through the drain results in a good outcome in half the patients (Nieuwkamp, Gans, Rinkel, Algra 2000, p. 247).
Seizures may result in up to 6% of patients post development of a SAH (Al-Shahi, White, Philip, Davenport, and Lindsay, 2006, p. 14). Prolonged seizures may result in hypoxemia and cerebral infarction due to cerebral hypoxia. Therefore, patients who have started to have seizures should routinely be treated with phenytoin at a dose of 15mg/kg IV (Sepelt 2005, p. 2).
Non neurological include: ECG changes and arrhythmias, as a secondary result of hyponatremia and hypomagnemia commonly associated with SAH (Oh 1997, p. 389).
Deep Vein Thrombosis’ (DVTs) as a result of prolonged bed rest may occurs, so nursing interventions should include DVT prophylaxis, such as: TED stockings, sequential calf compressors, and early mobilisation (Sepelt 2005, p. 2). Furthermore, after a discussion with the neurosurgeon, heparin 5000 units subcutaneously (S/C) twice daily (bd) may be considered if no intracerebral bleeding has occurred for 48 hours after surgical haemostasis has been achieved.
The following paper has examined the pathophysiology, diagnosis of, and management of, a subarachnoid haemorrhage (SAH), from both an acute and holistic perspective. A SAH has been defined. Cerebral anatomy and physiology has then been reviewed in order to determine the pathophysiology of a SAH. Clinical manifestations of a developing SAH have then been discussed, followed by the development of its diagnosis examined. Current nursing and medical management of this condition have been examined by assessing a wide range of journal articles and research papers. Complications with management has then be discussed.
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Appendix A – Totora, G. and Grabowski, R. 1996, Principles of Anatomy and Physiology, 8th Ed Harper Collins Biological Publishers Inc, New York, USA, p. 392
Appendix B – Totora, G. and Grabowski, R. 1996, Principles of Anatomy and Physiology, 8th Ed Harper Collins Biological Publishers Inc, New York, USA, p. 393
Appendix C – Huether, S. and McCance, K. 2002, Pathophysiology the Biologic Basis for Disease in Adults & Children 4th Ed, Mosby Inc, St. Louis, Missouri, USA, p.511
Appendix D – Harrod, C. 2005, Hunt and Hess Grading Scale for Subarachnoid Haemorrhage, Neurosurgery, Volume 56(4).April .p.633
Appendix E – Harrod, C. 2005, World Federation of Neurological Surgeons grading, Neurosurgery, Volume 56(4).April .p.633
Appendix F – Harrod, C. 2005, Fischer Scale, Neurosurgery, Volume 56(4).April .p.634
Appendix G – Harrod, C. 2005, Glasgow Coma Scale, Neurosurgery, Volume 56(4).April .p.634