Textbook of Neuroanaesthesia and Critical Care - part 10 ppt

Pa g e 386 Table 27.4 T yp ical cardiovascular and ECG chan g es associated with BSD Event Result Clinical change ECG changes Cerebral ischaemia Vagal activation Increased heart rate, cardiac output and blood pressure Sinus bradycardia and bradyarrhythmias Ischaemia in the pons sympathetic stimulation Vagal activation and output and increased blood Decreased heart rate, cardiac no ischaemia pressure → MAP (Cushing's reflex) Sinus bradycardia, Medullary ischaemia Ischaemic vagal cardiomotor nucleus Unopposed sympathetic stimulation – 'storm' Increased heart rate, cardiac output, blood pressure, vascular resistance and left atrial pressure (pulmonary oedema) Sinus tachycardia, multifocal ventricular ectopics, marked ischaemia Spinal cord ischaemia Ischaemic sympathetic nuclei Decreased heart rate, cardiac output, blood pressure and vascular resistance (spinal shock) Sinus rhythm, reduced R- wave size, persistent ischaemic changes The classic rostrocaudal progression of events may not develop in the clinical setting. Following BSD, catecholamine levels fall. Together with relative hypovolaemia, hypothermia, autonomic dysfunction and the myocardial changes described above, this leads to a fall in cardiac output, systemic vascular resistance and mean arterial pressure. Asystole usually occurs within 48 h without cardiovascular support but there is evidence that infusions of epinephrine and vasopressin can delay this for several weeks, 24 information that may be of relevance if organ donation is being considered. P ulmonar y Chan g es During the sympathetic storm, the rapid rise in left atrial pressure (LAP) which may even exceed pulmonary artery pressure, in combination with an expanded lung blood volume (from an enhanced venous return and subsequent increased right ventricular output), may result in capillary disruption, protein-rich pulmonary oedema and interstitial haemorrhage. 20 This may lead to a deterioration in gas exchange and hypoxaemia. E ndocrine Chan g es H yp othalamic-Pituitar y Axis The discovery that BSD in animals is often followed by a decrease in plasma levels of T3, insulin and cortisol 20 has stimulated research on the hypothalamicpituitary axis (HPA) during and after BSD, with mixed results. 12,13,17,25–28 Ill-defined hormone reference ranges in acutely ill patients, the use of free-standing hormone levels rather than their dynamic axis function and poor understanding of the interactions between various hormones probably accounts for the inconsistency of the results. Posterior Pituitar y Function N eurogenic diabetes insipidus (DI) occurs in up to 84% of patients with BSD. 14 Polyuria >200 ml/h should alert the clinician to the possibility of DI. The serum osmolality is usually >310 mosmol/l with a urine osmolality of <200 mosmol/l. Electrolyte disturbances such as hypernatraemia, hypokalaemia, hypocalcaemia, hypophosphataemia and hypomagnesaemia occur rapidly without treatment. Antidiuretic hormone (ADH) has intrinsic vasoconstrictive properties. Therefore, decreased levels of ADH may contribute to the cardiovascular instability associated with BSD. Replacement therapy has been shown to attenuate some of this instability in BSD patients. 32 Prolactin levels may be normal or low. The use of dopamine infusions in BSD patients may account for some of the low values that have been reported. 29 Anterior Pituitar y Function There are conflicting reports regarding changes in anterior pituitary hormones following BSD. 14,29,30 Follicule stimulating hormone (FSH) and luteinizing hormone (LH) remain relatively unchanged. Circadian release of growth hormone (GH) and its Pa g e 387 Figure 27.1 Cardiovascular effects of brainstem death role in the stress response complicate interpretation of the changes seen in its levels after BSD. 12,14,29 Levels of adrenocorticotrophic hormone (ACTH) remain within the normal laboratory range after BSD. 12,14,30 Cortisol levels may also be 'normal' for non-stressed patients but this may indicate a relative deficiency, which might be uncovered with stress testing (short synacthen test). No relationship between cortisol levels and severe hypotension has been demonstrated. 14 Th y roid Hormones Changes in thyroid hormone levels after BSD are similar to those found in patients with sick euthyroid syndrome (Table 27.5). 12–14,29 The syndrome, often associated with acute illness, results in impaired peripheral conversion of thyroxine (T 4 ) to triiodothyronine (T 3 ) and a rise in reverse T 3 (rT 3 ). Table 27.5 Thyroid hormones levels in the sick euth y roid s y ndrome Hormone Level Total T 3 Increased Free T 3 Decreased rT 3 Normal or increased Total T 4 Normal or decreased TSH normal T 4 = thyroxine; T 3 = triiodothyronine; TSH = thyroid-stimulating hormone Although the exact significance of a reduced T 3 level is unknown, experimental work suggests an association with reduced myocardial function and an alteration in cellular mitochondrial metabolism from aerobic to anaerobic producing a lactic acidosis. 20 Furthermore, hypothyroidism reduces myosin Ca 2+ activated ATPase activity and T 3 is probably an important regulator of Na + /K + ATPase in the heart. 30 Although haemodynamics or metabolic acidosis is not improved by the sole administration of T 3 in BSD, 11,12,26,27 when used in combination with other hormones T 3 has been shown to result in cardiovascular and metabolic improvements which lead to an increase in the number of suitable organs for transplantation in potential donors. 20,25,29 Insulin A degree of peripheral resistance to insulin is common in BSD patients. 32 This may be aggravated by the increased level of catecholamines (endogenous and exogenous), the use of steroids and the concomitant acidosis often present. R enal Changes The cardiovascular changes associated with BSD, vasoconstriction with subsequent reduced cardiac output, hypotension and hypovolaemia may result in renal damage. 32 Experimental evidence suggests that in BSD renal parenchymal cell integrity, as measured by cellular Na + :K + ratio, is impaired. 33 Damage to renal cell parenchyma may be prevented (in animals at least) by the administration of T 3 , cortisol and insulin independent of improvement in systemic haemodynamics. 33 Pa g e 388 H e p atic and Coa g ulation Chan g es In an animal model of BSD, hepatic function remained unaffected by profound hypotension. 34 The arterial ketone body ratio did not change significantly, suggesting an adequate oxygen supply. Fibrinolytic agents and plasminogen activators are released from damaged brain tissue into the circulation in patients with BSD and can cause coagulation defects, including disseminated intravascular coagulopathy. These defects may be aggravated by hypothermia. M etabolic Changes Changes in oxidative processes have been demonstrated after BSD. 20 Reductions in plasma glucose, pyruvate and palmitate with parallel rises in lactate and fatty acids may indicate a shift from aerobic to anaerobic mitochondrial metabolism. This change could lead to reductions in cellular high-energy phosphates and thus cellular and organ function. Delivery-dependent oxygen consumption and high plasma lactate levels have been reported in BSD patients. It is not clear whether this is due to a reduction in tissue oxygen extraction or mitochondrial impairment. 21,35 The possible complications of BSD are highlighted in Tables 27.6 and 27.7 and Figure 27.1 and 27.2. Dia g nosis of Brain Death The criteria for the diagnosis of brain death published by the Honorary Secretary of the Royal Colleges and their faculties in the United Kingdom, 7 and the Harvard Report in the United States, became the basis for the confirmation of brain death in many other countries. 7 However, the exact criteria upon which brain death is diagnosed vary between countries, with Table 27.6 Com p lications associated with BSD Complication Frequency Contributing factors Haemodynamic instability Very common Autonomic dysfunction Myocardial damage β-receptor dysfunction Hypovolaemia Hypothermia Hypoxia Common Pulmonary oedema, retained secretions, atelectasis Hypovolaemia Common Diabetes insipidus Endothelial damage Diuretics Hyperglycaemia Fluid restriction Haemorrhage Hyperosmolality Common Diabetes insipidus Hyperglycaemia Common Insulin resistance Acidosis Intravenous dextrose Endogenous and exogenous steroids Endogenous and exogenous catecholamines Hypothermia Common Hypothalamic ischaemia Vasodilatation Reduced basal metabolic rate Coagulation defects Uncommon Fibrinolytic agents Cytokines Plasminogen activators Hypothermia Transfused blood products Pa g e 389 Table 27.7 Electrol y te disturbances associated with BSD Electrolyte disturbances Contributing factors Hypernatraemia Diabetes insipidus Hypokalaemia Diabetes insipidus Insulin Diuretics Catecholamines Hyperventilation Endogenous and exogenous steroids Hypomagnesaemia Diabetes insipidus Diuretics Hypocalcaemia Diabetes insipidus Diuretics Hypophosphataemia Diabetes insipidus Diuretics Insulin some but not all countries requiring confirmatory tests of absent brain function, such as EEG or cerebral angiography. The diagnosis of BSD in the United Kingdom will be described in detail. A revision of the Code of Practice for the Diagnosis of Brainstem Death was published in 1998. 36 There are three sequential steps in making the diagnosis of BSD. To avoid unnecessary testing and to eliminate the chance of making an incorrect diagnosis, it is essential that steps 1 and 2 are completed before beginning step 3. S tep 1— P reconditions The patient is deeply comatose and is being maintained on a ventilator because spontaneous ventilation had previously been inadequate or had ceased altogether. There should be no doubt that the patient's condition is due to irremediable brain damage of known aetiology. 7 An accurate history of events before and after the onset of the coma is essential. S tep 2— E xclusions If the preconditions have been fulfilled, the necessary exclusions must be considered. These are to ensure that neither the state of apnoea nor the coma is contributed to or caused by a reversible condition. The major groups of conditions that may produce this clinical picture are: Figure 27.2 En d -or g an effects of brainstem death • hypothermia, < 35°C; • depressant drugs, both therapeutic and non-therapeutic; • metabolic disorders, e.g. hyponatraemia; • endocrine abnormalities, e.g. myxoedema. Altered drug metabolism due to concurrent pathology or, less commonly, enzyme variants should be borne in mind at this stage. In the absence of toxicological screening, it has been suggested that three days is a reasonable time to allow potential drug effects to disappear. 37,38 Metabolic and endocrine abnormalities may be suspected from the history, examination and routine blood tests, i.e. full blood count, arterial blood gas, electrolytes and blood glucose measurements, Pa g e 390 although more sophisticated tests may be necessary. Certain abnormalities accompanying BSD (e.g. hypernatraemia) do not preclude the diagnosis of BSD. 38 Specific conditions, such as the 'locked-in' syndrome and brainstem encephalitis (Bickerstatt's encephalitis or the Miller Fisher syndrome), may produce a clinical picture similar to that seen in BSD. When such conditions are suspected, BSD tests should not be undertaken as the patient does not comply with the precondition 'there should be no doubt that the patient's condition is due to irremediable brain damage of known aetiology. 37 The 'locked-in' syndrome is produced by a lesion in the pons which paralyses the limbs, respiratory muscles and lower cranial nerves. Patients are conscious and able to blink and produce vertical eye movements. Brainstem encephalitis may produce a comatose, areflexic, apnoeic patient, with motor and central nerve paralysis including internal and external ophthalmoplegia. Full recovery from brain encephalitis is possible. 39 Therefore, the importance of obtaining an adequate history consistent with the clinical picture together with strict adherence to the preconditions and exclusions before BSD testing cannot be overemphasized. If any doubt exists as to the cause of the patient's condition, BSD tests should not be performed. S tep 3— The Tests The tests should not be performed unless steps 1 and 2 have been fulfilled. Who and When? BSD tests should be performed by two medical practitioners who have been registered for more than five years and are competent in this field. At least one of the practitioners should be a consultant and neither practitioner should be a member of the transplant team. Two sets of tests should be performed; the two practitioners may perform the tests separately or together. The tests should be repeated to ensure no observer error has occurred. The timing of this second set of tests is a matter for the doctors involved but should be adequate for the reassurance of all those directly concerned. 40 The interval between the two sets of tests can be used to discuss the possibility of organ donation with the relatives if they have not already raised the subject. How? For confirmation of BSD, five tests of the brainstem reflexes and testing for apnoea are required (Table 27.8). The tests are easily performed at the bedside and have unambiguous endpoints. In the United Kingdom there is no requirement to perform cerebral angiography or electroencephalography for the confirmation of BSD. Testin g for A p noea This test is considered positive if the patient does not exhibit any respiratory movements whilst disconnected from the ventilator despite a PaCO 2 of at least 6.65 kPa Table 27.8 The five tests of reflexes Test BSD criteria Cranial nerves tested 1. A bright light is shone into both pupils No reaction in either pupil II and III 2. A strong stimulus is applied to the corneas No blinking V and VII 3. 20 ml of iced water is injected into both external auditory meatae No eye movement III, VI and VIII 4. painful stimulus is applied – supraorbital pressure** No motor response in the cranial nerve distribution III, IV, V, VI, VII, IX, X, XI and XII 5. suction catheter is passed into the trachea No coughing or gagging IX and X *The tympanic membranes should first be visualized and seen to be intact. **Spinal reflexes may be present. Pa g e 391 (50 mmHg). The lungs are normally hypoventilated with 100% O 2 for 10 min prior to disconnection to achieve a PaCO 2 >6.6 kPa and to prevent hypoxaemia. Insufflation of oxygen at 6 l/min via a catheter passed into the trachea during disconnection will further reduce the risk of hypoxaemia during disconnection. Common Difficulties Encountered When Performin g Tests for BSD The difficulties commonly encountered during BSD testing are summarized in Table 27.9. Death is pronounced after the second set of tests but the legal time of death is recorded when the patient fulfils the first set of BSD criteria. When BSD has been diagnosed the relatives should be informed and the clinician should ensure that the relatives fully understand that death has occurred. If there is no absolute contraindication to organ donation, management of the patient should now b e directed to preservation of organ function (Tables 27.10, 27.11). The completion of the first set of BSD tests is a suitable time to discuss organ donation with the patient's relatives. In the United Kingdom, refusal by relatives accounts for the failure to donate organs in about 30% of potential organ donors. The local transplant coordinator should be contacted as soon as possible after the first set of BSD criteria have been fulfilled as they are experienced in dealing with bereaved relatives who are considering organ donation. Mana g ement of Patients with Brainstem Death After permission for organ donation has been obtained from the patient's relatives, the intensivist in charge of the patient's care should contact the local transplant coordinator to discuss specific treatments which may be requested by the transplant team, e.g. hormone therapy. A continued high standard of nursing care, the use of invasive monitoring and prompt treatment to preserve organ function will increase the chances of successful organ donation. The patient management goals are similar to those before the diagnosis of BSD with the exception of specific measures to maintain cerebral perfusion pressure and oxygen delivery. Optimize Cardiac Output and Tissue Oxygen Delivery Cardiac output is optimized by volume loading guided by central venous and/or pulmonary artery wedge pressures. Blood, colloid and crystalloid solutions are used as appropriate to maintain the circulating volume. A combination of inotropes and peripheral vasoconstrictors is usually required to improve cardiac Table 27.9 Common difficulties encountered when p erformin g the tests for BSD Difficulty Advice Patients with cataract(s)/false eye(s) and or disrupted tympanic membrane(s) The published criteria are 'guidelines rather than rigid rules'. 'It is for the doctors at the bedside to decide when the patient is dead'. 40 The patient is now hypothermic and/or has a metabolic disturbance, e.g. hypernatraemia Abnormalities accompanying BSD do not preclude the diagnosis of BSD. 37 Although the exact temperature below which hypothermia is likely to be the cause of coma is uncertain, we do not perform BSD tests in patients whose core temperature is <35° C. The patient has chronic obstructive pulmonary disease A 'normal' set of arterial blood for that patient is obtained during disconnection and then the PaO 2 is allowed to fall by a further 1–2 kPa whilst observing for respiratory effort. 40 Does the patient have other conditions that can account for the symptoms? (differential diagnosis) Ensure the preconditions and exclusions have been strictly adhered to. [...]... system and the techniques of doing so and their applications continue to expand Anaesthetists are increasingly involved in both anaesthesia and sedation for adults and children in this 'unfriendly' and often isolated environment and it is now possible to safely monitor critically ill patients for MRI The use of high-strength gradient magnetic fields and radiofrequency waves during MRI poses particular... agents and remains a mainstay of neuroradiology Contrast studies of the ventricular system have lessened in number following the improvement of imaging techniques and the introduction of computed tomographic (CT) scans3 and magnetic resonance imaging (MRI) The demands made of anaesthetists in the X-ray department have changed considerably over the last 10 years as the techniques of imaging have changed and. .. be automatic injectors Careful planning is needed in setting up the room so that the X-ray equipment and the anaesthetic equipment do not impede each other In particular, the X-ray tube, on its gantry, must be swung out of the way for induction of anaesthesia and at the end of the anaesthetic It should be possible to move the tube assembly out of the way without delay in case of an emergency during... Oxygen consumption and delivery relationship in brain-dead organ donors Br J Anaesth 1996; 76: 783–789 36 Cadaveric organs for transplantation A code of practice including the diagnosis of brainstem death HMSO, London, 1998 37 Working Group of the Royal College of Physicians and the Conference of Medical Royal Colleges and their Faculties in the United Kingdom Criteria for the diagnosis of brainstem death... 27.12.28 The 'rule of 100 s' has been suggested as a guide to treatment (Table 27.13) Adequate Oxygenation As these patients are intubated and ventilated they are at risk of atelectasis, retained secretions and nosocomial pneumonia Physiotherapy, aseptic tracheobronchial suction and low levels of positive end-expiratory pressure (PEEP) of 5 cmH2O may be used to prevent basal atelectasis and improve gas... the intensity of X-rays It is also valuable, remembering that there is some scatter of X-rays, to keep behind the source of X-rays The X-ray room should be so arranged that the anaesthetic machine and the monitoring equipment are easily visible from behind a lead glass screen and the anaesthetic team should take refuge behind the screen wherever possible The importance of a clear line of sight from behind... Committee of the Harvard Medical School A definition of irreversible coma JAMA 1968; 281: 107 0 107 1 5 Mohandas A, Chou SN Brain death – a clinical and pathological study J Neurosurg 1971; 35: 211–218 6 Jennett B, Gleave J, Wilson P Brain deaths in three neurosurgical units BMJ 1981; 28: 2533–2539 7 Working Group of Conference of Medical Royal Colleges and their Faculties in the United Kingdom Diagnosis of. .. allows the patient's conscious state to be monitored, which is of particular value if embolization is being performed near critical areas of the cerebral circulation Any technique of sedation needs to relieve anxiety and pain and to provide such relief from discomfort that the patients lie still for prolonged periods of time Young and Pile-Spellman8 suggest that patients undergoing conscious sedation... airway and ventilation before the cause of the emergency can be actively treated Several techniques are described for sedation Young and Pile-Spellman8 document their technique of neuroleptanalgesia with subsequent infusion of propofol They begin with 2–4 μg/kg fentanyl and 2.5–5 mg droperidol intravenously, also using midazolam 3–5mg During the procedure, they infuse propofol at low rates (10 20 μg/kg/min)... μg/kg) if required and then infusion of 0.5 μg/kg/min or by a bolus of propofol 0.25–0.5 mg/kg, followed by an infusion of 25 μg/kg/min They aimed for a level of sedation, which they defined as producing a patient who was resting comfortably but easily rousable and alert to obey commands There was general satisfaction with the technique of conscious sedation from both radiologists and patients Complications . scans 3 and magnetic resonance imaging (MRI). The demands made of anaesthetists in the X-ray department have changed considerably over the last 10 years as the techniques of imaging have changed and. support 5 mg/kg/min Table 27.13 Rule of 100 s Systolic blood pressure > ;100 mmHg Urine output > ;100 ml/h PaO 2 > ;100 mmHg Haemoglobin > ;100 g/l contractility and to increase organ perfusion. Group of Conference of Medical Royal Colleges and their Faculties in the United Kingdom. Diagnosis of death. BMJ 1976; ii: 1187 – 1188. 8. Working Group of Conference of Medical Royal Colleges and