Textbook of Neuroanaesthesia and Critical Care - part 9 ppt

Pa g e 338 I nterventional Neuroradiolo gy Endovascular methods are considered if the CBF and clinical picture remain poor despite aggressive medical treatment. Low- p ressure balloon angioplasty may be effective in reducing the severity of the vasospasm but there is a risk that the vessel may rupture and dissect with this technique. 72 When vasospasm is confined to small vessels or angioplasty is inappropriate, papaverine can be infused. Papaverine, a phosphodiesterase inhibitor, causes the accumulation of cyclic adenyl monophosphate within smooth muscle, leading to vasodilatation. The effects of papaverine may only last 12–24 h and repeat infusions may be necessary. However p apaverine can precipitate systemic hypotension and intracranial hypertension so measures to support blood pressure and control ICP must be immediately available. 73 D rugs under Evaluation As blood in the subarachnoid space precipitates cerebral vasospasm, it has been postulated that drugs which dissolve this blood clot may reduce the incidence of cerebral vasospasm and improve outcome. However, a recent trial using tissue plasminogen activator showed a reduction in angiographic vasospasm but no improvement in symptomatic cerebral vasospasm or neurological deterioration. 74 Other treatments that have been tried to prevent or treat vasospasm include tirilizad, a non-glucocorticoid 21- aminosteroid and potent free radical scavenger. 75 None has demonstrated significant efficacy in reducing vasospasm and improving outcome in SAH. In a retrospective study, patients taking aspirin 76 before their SAH had a reduced risk of delayed ischaemic deficit and therefore the use of aspirin postaneurysm clipping requires further study. Outcome The Glasgow Outcome Scale as shown in Table 23.1 can be used to assess the outcome for any brain disease. Factors relating to outcome after SAH include the level of consciousness on admission, the amount of subarachnoid blood on CT scan, age and aneurysms of the posterior circulation. In the five-year period 1993–1998, patients admitted to our centre with an anterior circulation aneurysm who received a non-urgent operation (within 21 days of the initial event) were prospectively studied. The GOS was used to assess outcome at six months. Of the 391 patients studied, 44.7% had "early" surgery (day 1–3 postevent), 46.5% had "intermediate" surgery (day 4–10) and 8.8% "late'' surgery (11–21). There were no significant differences between the groups in the demographics, site of the aneurysm and clinical condition of the patient. Early surgery did not adversely affect outcome, with a GOS at six months of 1–2 in 82.9%, 79.7% and 85.3% in the early, intermediate and late groups respectively. A favourable outcome (GOS 1–2) was achieved in 83.5% of patients less than 65 years and 73.3% in those over 65 years. There was a 6.5% rebleeding rate with a mortality of 63%. Only 0.5% occurred within three days of the initial event. Early surgery also reduced the total inpatient stay, with a mean time of 18.3, 20.4 and 31.7 days in the three groups respectively. These data have endorsed our view that, with appropriate preparation and support of the SAH patient, the timing of surgery Table 23.1 Glas g ow Outcome Score Grade Description Definition 1 Good recovery Independent life with or without minimal neurological deficit 2 Moderately disabled Neurological or intellectual impairment but is independent 3 Severely disabled Conscious but totally dependent on others for daily activities 4 Vegetative survival 5 Dead Pa g e 339 no longer influences surgical outcome. We therefore adopt an early surgery protocol to avoid the known effects of a rebleed. Rehabilitation The aim of rehabilitation is to return the patient to the maximum level of independence possible by reducing the effects of disease or injury on daily life. Rehabilitation is tailored to the individual patient's needs and should be assessed early on in the patient's admission. Indeed, some believe the prevention of secondary neuronal injury is part of the rehabilitation process. Those patients with minimal deficits require little rehabilitation. However, in patients with major deficits, initial efforts are focused on preventing the development of medical, musculoskeletal, bowel and bladder problems. After this, rehabilitation tries to provide the optimum medical, social and environmental conditions that will maximize the recovery process. Coping techniques and compensatory strategies will be taught to allow the patient to become as independent as possible. Patients who survive a SAH will have a wide spectrum of cognitive and neurological deficits. Whilst many survivors function independently with few or no significant motor or sensory deficits one year after the event, many suffer from unrecognized subtle cognitive and emotional effects. These include confusion, amnesia, impaired judgement and emotional liability. Medical and nursing staff, family members, physiotherapists, occupational and speech therapists, psychologists and social services are all involved in the rehabilitation process. Some patients who have significant deficits but are well motivated with good social circumstances may benefit from transfer to a rehabilitation unit where they can continue to improve. Future Develo p ments Whilst there has been an improvement in mortality rates for patients with an intracerebral haemorrhage, little has been effective in altering the high initial mortality in SAH patients. In those patients who survive the initial insult, early surgery has improved outcome by preventing rebleeding. However, future developments are focused on improving our understanding of the pathophysiological mechanisms behind secondary neuronal injury. Once these are better understood, a specific mechanism-targeted approach may improve outcome. References 1. Kajita Y, Suzuki Y, Oyama H et al. 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Mannitol causes compensatory cerebral vasoconstriction and vasodilatation in response to b lood viscosity changes. J Neurosurg 1983; 59: 822. 43. Ravussin P, Archer DP, Tyler JL et al. Effects of rapid mannitol infusion on cerebral blood volume. A positron emission study in dogs and man. J Neurosurg 1986; 64(1): 104 – 113. 44. Schar A, Tsipstein E. Effect of mannitol and furosemide on the rate of formation of cerebrospinal fluid. Exp Neurol 1978; 69: 584. 45. Illievich UM, Spiss CK. Hypothermic therapy for the injured brain. Curr Opin Anaesth 1994; 7: 394 – 400. 46. Lee MW, Deppe SA, Sipperly ME et al. The efficacy of barbiturate coma in the management of uncontrolled intracranial hypertension following neurosurgical trauma. J Neurotrauma 1994; 11: 325 – 331. 47. Schalen W, Masseter K, Nordstrom CH. Cerebrovascular reactivity and the prediction of outcome in severe traumatic brain lesions. Acta Anaesthesiol Scand 1991; 35: 113. 48. McGrath BJ, Guy J, Borel CO et al. Perioperative management of aneurysmal subarachnoid hemorrhage: Part 2. Postoperative management. Anesth Analg 1995; 81: 1295 – 1302. Pa g e 341 49. Kassell NF, Torner JC, Jane JA et al. The international cooperative study on the timing of aneurysm surgery. Part 1: overall management results: J Neurosurg 1990; 73: 18. 50. Weber M, Grolimund P, Seiler RW. Evaluation of posttraumatic cerebral blood flow velocities by transcranial Doppler ultrasonography. Neurosurgery 1990; 27: 106 – 112. 51. Weir B, Grace M, Hansen J et al. Time course of vasospasm in man. J Neurosurg 1978; 48: 173. 52. Mayberg M. Pathophysiology, monitoring and treatment of cerebral vasospasm after subarachnoid hemorrhage. J Stroke Cerebrovasc Dis 1997; 6(4): 258 – 260. 53. Fischer CM, Kistler JP, Davis JM. Relationship of cerebral vasospasm to subarachnoid hemorrhage visualized by computed tomography screening. Neurosurgery 1988; 19: 268 – 270. 54. Mayberg MR, Okada T, Bark TH. 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J N eurosurg 1996; 84: 221 – 228. 76. Juvela S. Aspirin and delayed cerebral ischaemia after aneurysmal subarachnoid hemorrhage. J Neurosurg 1995; 82: 945 – 952. Pa g e 343 24— Posto p erative Care in the Neurointensive Care Unit Helen L. Smith Introduction 345 Patient Assessment and Managemen t 345 Monitoring 345 ICU Managemen t 346 Analgesia, Sedation and Muscle Relaxation 347 Postoperative Complications and Their Managemen t 348 Intrahospital Transfe r 351 References 351 Pa g e 345 Introduction While the postoperative period is important in many areas of surgery, it can be a particularly critical phase for patients undergoing major neurosurgery. Many such patients may present preoperatively with specific risk factors including raised intracranial pressure, an altered sensorium and/or depressed airway reflexes. The further deterioration in physiological homoeostasis that occurs as a consequence of anaesthesia or surgery may additionally expose patients to the risk of respiratory compromise or cerebral ischaemia. Further, the brain is an unforgiving organ and there is an imperative to rapidly detect and correct alterations in systemic and cerebral physiology that could result in irretrievable neurological damage if left untreated. The major categories of patients who require intensive or high-dependency care following neurosurgical interventions are listed in Box 24.1. Patient Assessment and Mana g ement On arrival in the ICU area, each patient requires full assessment with history, examination and relevant investigations. Good communication between theatre and ICU staff regarding any pertinent perioperative event is essential. The history should include admission diagnosis, surgery, problems with the surgery/anaesthetic and expected problems. Preoperative cardiorespiratory illness Long surgery, large blood loss, coagulopathy, incidental hypothermia, unstable haemodynamics Patients at risk of or documented to have intracranial hypertension Patients requiring ventilation to provide stability for venous haemostasis Patients requiring or recovering from a period of hypothermia induced for cerebral protection Patients requiring postoperative intracranial pressure monitoring Requirement for blood pressure manipulation as a part of: induced hypertension for CPP maintenance or as a part of triple H therapy induced hypotension for treatment of hyperaemia following carotid or AVM surgery Box 24.1 Neurosur g ical p atients re q uirin g p osto p erative intensive/ hi g h-de p endenc y care Monitorin g Clinical assessment and reassessment is the primary form of monitoring. Regular consultation is required between neurosurgeons and intensivists. Basic physiological monitoring required for all patients in the neurointensive care unit includes blood pressure, ECG monitoring, pulse oximetery and careful recording of fluid balance. Monitoring of hourly urine output is of particular importance since neurosurgical patients are at risk of large fluid shifts from urinary losses because of their illness (e.g. due to associated diabetes insipidus) or as a consequence of therapy with osmotic diuretics such as mannitol. A rterial Blood Gases and Invasive Blood Pressure An arterial line is required in all ventilated patients for the measurement of arterial blood gases. Direct arterial pressure measurement is indicated in patients who have undergone neurovascular procedures (clipping of ruptured aneurysms, resection of arteriovenous malformations and the early postoperative period following carotid endarterectomy), patients with haemodynamic instability or intracranial hypertension (in whom there is a risk of compromise of cerebral perfusion pressure) and patients requiring vasoactive agents for blood pressure control. Central Venous Pressure (CVP) CVP monitoring is needed for patients with large volume losses, cardiac disease, vasoactive infusions and hypotension or oliguria not readily responsive to fluid challenge. CVP monitoring may also be essential in the patient with pathological polyuria due to diabetes insipidus or the condition of cerebral salt wasting that occurs following subarachnoid haemorrhage. It must be remembered, however, that the CVP is an indirect measure of the intravascular volume status and is influenced not only by venous return but also b y right heart compliance, pulmonary or right heart disease, intrathoracic pressure and posture. P ulmonar y Arter y Catheterization Pulmonary arterial (PA) catheterization offers several advantages over CVP monitoring in selected patients. Measurement of PA wedge pressure provides a more Pa g e 346 reliable index of left ventricular preload and intravascular volume status in the critically ill patient and the use of thermodilution catheters allows the measurement of cardiac output and calculation of systemic vascular resistance. These data are of particular b enefit in patients with concurrent severe cardiorespiratory disease or severe sepsis. PA catheters are also valuable to guide the use o f complex vasoactive interventions as part of cerebral perfusion pressure augmentation in intracranial hypertension or triple H therapy for vasospasm following subarachnoid haemorrhage. 1,2 N eurological Examination Patients recovering from neurosurgical procedures require careful monitoring of all aspects of neurological function so that early signs of bleeding or cerebral oedema can be detected. The neurological system should be reviewed with particular regard to the operation performed and the patient's preoperative neurological status. Regular neurological observations should be undertaken including the measurement of pupillary size and reaction, limb power and recording of Glasgow Coma Score. 3 Although originally designed to quantify the severity of a head injury, the Glasgow Coma Scale and Score (Box 24.2) allow categorization of patients with neurological dysfunction from other forms of brain injury and over a period of time act as a guide to any deterioration in a p atient's neurological status. Eye opening Spontaneous To voice To pain None 4 3 2 1 M otor responses Obeys commands Localizes pain N ormal flexion (withdrawal to pain) Abnormal flexion (decorticate) Extension (decerebrate) N one (flaccid) 6 5 4 3 2 1 Verbal responses Orientated Confused conversation Inappropriate words Incomprehensible sounds N one 5 4 3 2 1 Box 24.2 The Glas g ow Coma Scale I ntracranial Pressure Monitorin g Intracranial pressure (ICP) monitoring is indicated in all patients who have intracranial hypertension or are at risk of developing it. This is particularly true in patients who remain sedated and consequently cannot be assessed by regular neurological examination. While the technique used for ICP monitoring will vary between centres, it is essential that ICP measurements are related to mean arterial pressure (MAP) to provide continuous monitoring of cerebral perfusion pressure (CPP; where CPP= MAP–ICP). Many of the therapies available to treat neurosurgical patients are based on the reduction of ICP or optimization of CPP. These include a reduction in cerebral oedema by cerebral dehydration, administration of steroids, hyperventilation, blood pressure control, reduction of cerebral venous pressure, surgical decompression, cerebrospinal fluid drainage and hypothermia. Other Monitoring Modalities Transcranial Doppler ultrasound, jugular venous saturation monitoring, EEG and evoked potential monitoring are other modalities that may be useful in individual patients. Their use is dealt with elsewhere in this book. I nvesti g ations Routine postoperative tests – full blood count, clotting screen, urea and electrolytes – should be performed at the time of admission to the intensive care unit, along with arterial blood gases if the patient is ventilated or has a low oxygen saturation. A chest X-ray is indicated if the patient is ventilated, a central line has been inserted or gas exchange is abnormal. Neurological imaging procedures should be undertaken if there is deterioration in the patient's neurological state or rise in intracranial pressure. ICU Mana g ement A irway and Ventilation [...]... Neurosurgery 199 6; 38: 466–4 69 9 Prielipp RC, Coursin DB Sedative and neuromuscular blocking drug use in critically ill patients with head injuries New Horizons 199 5; 3: 456–468 10 Ronan KP, Gallagher TJ, George B, Hamby B Comparison of propofol and midazolam for sedation in intensive care unit patients Crit Care Med 199 5; 23: 286– 293 11 Reed RL Antibiotic choices in surgical intensive care unit patients... evidence-based approach BMJ Publishers, London, 199 8 8 Langhorne P, Williams BO, Gilchrist W et al Do stroke units save lives? 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Artru AA, Shapira Y, Bowdle TA. Electroencephalogram, cerebral metabolic, and vascular responses to propofol anesthesia in dogs. J Clin Anesthesiol 199 2; 4: 9 – 1 09. 13 p ressure and cerebral perfusion pressure. Crit Care Med 199 7; 25: 10 59 – 1062. 40. Warters RD, Allen SJ. Hyperventilation: new concepts for an old tool. Curr Opin Anaesth 199 4; 7: 391 – 393 . 41.