(BQ) Part 2 book Neurocritical care A guide to practical management presentation of content: Seizures on the adult intensive care unit, acute weakness in intensive care, coma, confusion, and agitation in intensive care, imaging the brain injured patient, ethical dilemmas within intensive care,...
8 Seizures on the Adult Intensive Care Unit Morgan Feely and Nicola Cooper Key Points Seizures are commonly encountered in the ICU They can be provoked by acute illness, medicines, or alcohol The causes of seizures tend to differ in different age groups Tonic-clonic status epilepticus carries a significant mortality Early and effective treatment is essential EEG can distinguish between tonic-clonic status and non-epileptic attack disorder (NEAD) and diagnose nonconvulsive status Long-term treatment of epilepsy depends on the type of seizures and the characteristics of the patient – involve an expert Introduction Seizures are commonly encountered in the critical care setting, either as a primary event in epilepsy or as a symptom of acute illness, for example, brain injury This chapter discusses the recognition and management of the different types of seizure disorders encountered in the intensive care unit (ICU), which are: · Status epilepticus · Seizures occurring as part of an acute illness or following neurosurgery · Incidental seizures in a patient with epilepsy · Non-epileptic attack disorder (NEAD) (“pseudostatus”) A brief overview of seizures is essential before discussing specific disorders Viewed as a single condition, epilepsy is the most common serious neurological condition, affecting 1:130 people in the United Kingdom Epilepsy refers to a tendency to have recurring, unprovoked seizures Types of Seizure Seizures (as opposed to epilepsy) are far more common in the general population and can be provoked by prescribed medication, benzodiazepine or alcohol withdrawal, metabolic disturbances, and brain injury Figure 8.1 outlines the different types of common seizures that occur When a physician sees a patient who has had a seizure, three questions must be considered: Was this episode a seizure? As many as 25% of patients diagnosed as having epilepsy in the United Kingdom not have the condition at all Seizures are diagnosed almost entirely using a detailed eye-witness account, and inexperienced doctors generally not ask the right questions, nor recognize important clues Were there any obvious provoking factors? Medicines and alcohol are the most common factors that provoke seizures 69 www.ebook3000.com 70 M Feely and N Cooper SEIZURES Provoked (tonic clonic) Due to acute illness (tonic-clonic or partial seizures) Part of epilepsy (recognised or unrecognised) GENERALISED EPILEPSY (Mostly idiopathic; young people with structurally normal brains ) • LOCATION-RELATED EPILEPSY (Mostly symptomatic; people with a focal brain abnormalit y) • Absences (brief episodes of detachment, easily missed) Partial seizures +/- secondary generalization (tonic-clonic seizures) • Myoclonic jerks • Tonic-clonic seizures Simple partial seizures Complex partial seizures - Conscious - Impaired consciousness - Focal rigidity/jerking - Unresponsive/glazed - Abnormal sensations - Automatisms - Speech disturbance - Focal rigidity or jerking All seizure types can occur as status epilepticus Figure 8.1. Types of seizures Does this patient have previously unrecognized epilepsy? A tonic-clonic seizure can be the presenting symptom in people with previously unrecognized epilepsy A detailed history should be taken to uncover previous myoclonic, absence or partial seizures In one study, 74% of patients presenting with a first tonicclonic seizure had experienced seizures before Types of Seizures The main causes of seizures differ with age In the teens to early twenties, alcohol use commonly triggers seizures in patients who have a common form of idiopathic generalized epilepsy called “juvenile myoclonic epilepsy.” The patient often experiences myoclonic jerks, usually first thing in the morning, and may think these are normal The condition is especially sensitive to triggers such as sleep deprivation, alcohol, and stress Between the late twenties and the fifties, excessive alcohol is the commonest cause of first tonicclonic seizures in men These patients not have epilepsy but are experiencing provoked seizures Although in many cases this occurs during withdrawal or after a binge, it is distinct from overt alcohol-withdrawal syndrome Other conditions 8. Seizures on the Adult Intensive Care Unit such as primary brain tumors and metabolic disorders should be excluded Over the age of fifty, cerebrovascular disease is the commonest cause of epilepsy and the incidence of epilepsy is now highest in the over-eighties A previous stroke or transient ischemic attack (TIA) may cause “location-related” epilepsy and partial seizures Epilepsy is frequently unrecognized in the elderly Dementias, secondary brain tumors and metabolic disorders are other causes of seizures in this age group Location-related epilepsy is the commonest form of epilepsy across all ages, which is why it is important to ask about other seizure types when a patient presents with tonic-clonic seizures Causes include mesial temporal sclerosis (following childhood febrile convulsions), subarachnoid hemorrhage, stroke, and traumatic brain injury Imaging and EEG Imaging (CT or MRI) is carried out to find any underlying cause for seizures A focal lesion points toward location-related epilepsy, even if there is no clinical history to suggest focal seizures Patients suffering from refractory epilepsy, with a focal abnormality on imaging and an anatomically corresponding abnormality on EEG during an attack, may benefit from epilepsy surgery An MRI is superior to CT in detecting small tumors, arteriovenous malformations, areas of sclerosis, and post-traumatic changes Although young people with idiopathic generalized epilepsy or obviously provoked seizures may not require imaging, patients with location-related epilepsy, refractory epilepsy, or status epilepticus should always be scanned Patients with location-related epilepsy should go on to have an MRI scan if their CT scan is normal The electroencephalogram (EEG) is used to help classify an epilepsy syndrome, establish a suspected clinical diagnosis, and distinguish between epilepsy and NEAD It is also of use in the diagnosis of herpes simplex encephalitis The EEG is affected by the patient’s state of arousal, medication, and other diseases Normal background EEG activity consists of alpha and occasional beta waves, theta waves in light sleep and delta waves in deep sleep Generalized slow waves are seen in drowsy or sedated patients and can be caused by drugs, metabolic disturbances, stroke, 71 encephalitis, or a post-ictal state Focal slow waves can be a non-specific indicator of a focal brain abnormality such as stroke Spikes (narrow upward deflections) are caused by the simultaneous depolarization of a large number of neurons and occur in seizures Half of patients with clinical epilepsy will have a normal EEG between attacks Serial EEGs or one recorded in a condition of sleep deprivation increase the chance of yielding abnormalities Twenty-four hour EEGs and video-EEG telemetry are used in difficult cases In the critical care setting, the principle uses of the EEG are: To distinguish between tonic-clonic status epilepticus and NEAD To confirm or exclude a diagnosis of nonconvulsive status epilepticus An EEG during an attack is the gold standard in the differentiation between tonic-clonic status and NEAD The absence of post-ictal slowing after a prolonged attack adds weight to the diagnosis of NEAD Post-ictal slowing, however, can be caused by benzodiazepines, and therefore does not necessarily indicate a seizure Nonconvulsive status epilepticus should be considered in patients with unexplained states of semiconsciousness or coma Anti-Epileptic Drugs The choice of anti-epileptic drug (AED) depends on the type of epilepsy and the characteristics of the patient Figure 8.2 shows the commonly used first-line AEDs AEDs have several different mechanisms of action, and some have more than one Some AEDs worsen one seizure type while benefiting another For example, lamotrigine is effective for tonicclonic seizures but can be ineffective or even exacerbate myoclonic jerks Checking drug levels may be of value in the context of overdose or to assess a patient’s compliance with medication, but is rarely helpful when adjusting dosages The one exception is phenytoin, which has a narrow therapeutic index; levels should be monitored in status epilepticus Status Epilepticus The three commonest seizure types presenting as status epilepticus are tonic-clonic status, focal 72 M Feely and N Cooper Primary generalised epilepsy Location-related epilepsy Sodium valproate (Epilim) – IV/PO Carbemazepine (Tegretol) PO/PR Lamotrigine (Lamictal) – PO Sodium valproate –IV/PO Levetiracetam (Keppra)* – IV/PO Lamotrigine Levetiracetam (Keppra) – IV/PO Phenytoin (Epanutin)** - IV/PO *Although levetiracetam was not included as 1st line therapy in the 2004 NICE guidelines (it did not have a monotherapy license at the time), many neurologists are now using it as first choice **Different preparations of the same drug are not always equivalent and a change may affect epilepsy control, particularly in the case of phenytoin Figure 8.2. Commonly used first line AEDs and routes of dosing motor status (epilepsia partialis continua), and non-convulsive status Status epilepticus is defined as a continuous seizure, or serial seizures without recovery in between, lasting for 30 or more Care givers of patients with epilepsy are advised to give “rescue” medication, for example, buccal midazolam, if a tonic-clonic seizure lasts for 5 minutes or more · Status epilepticus is the first presentation of epilepsy in 12% of patients · The overall mortality of status epilepticus in studies is around 23%, lower in younger patients, and higher in the over sixties · The underlying cause and duration of status epilepticus are the main determinants of outcome Tonic-clonic status epilepticus occurs in stages (Fig. 8.3) During early status, the systemic and cerebral metabolic consequences of status are still contained by homeostatic mechanisms In established status, the homeostatic mechanisms start to fail, the patient decompensates in terms of vital signs, and brain oxygenation and metabolism starts to fall In refractory status, there is a high risk of hypoxic brain injury The condition becomes progressively harder to treat and motor activity declines so that only subtle twitches around the eyes and mouth may be visible Subtle tonic-clonic status epilepticus, commonly encountered in the elderly, carries a very high mortality In established or refractory status, the task of ICU staff is to: · Provide supportive care · Ensure appropriate treatment for seizures is given · Ask if there is something more than status epilepticus going on Tonic-clonic status epilepticus causes significant physiological compromise and supportive care starts with the basic assessment and management of Airway, Breathing, Circulation and Disability, whilst treatment is initiated Further supportive care on ICU consists of ventilation, cardiovascular support, and correction of metabolic abnormalities Systemic complications of status epilepticus include dehydration, pyrexia, arrhythmias, hyperkalemia, and rhabdomyolysis (see Fig. 8.4) and will require appropriate intervention IV thiamine should be given if alcohol withdrawal is suspected Muscle relaxants are usually avoided so that seizures can be monitored However, if they are required to facilitate gas exchange or control the lactic acidosis caused by recurrent seizures, then continuous EEG monitoring (e.g., CSA, CFAM) should be used wherever possible Possible reasons for failure to terminate seizure activity in status epilepticus include: · If diazepam was used rather than lorazepam (shorter duration of action) · Failure to initiate additional therapy in early status · Using inadequate doses of phenytoin or anesthetic drugs in refractory status Aim for phenytoin levels at the high end of the normal range, before adding another drug 8. Seizures on the Adult Intensive Care Unit • • • 73 Airway, Breathing, Circulation, Disability Check blood glucose Give thiamine or pyridoxine if appropriate Pre-status: A phase of escalating seizures lasting hours or days • Buccal Midazolam (5-10mg) or oral Clobazam (10-20mg/day) Early status: Seizure or serial seizures lasting up to 30 minutes Use one of the following IV benzodiazepines 65% chance of terminating SE • Lorazepam (1st choice): 2-4mg; long duration of action, recurrent seizures less likely • Midazolam: 0.05-0.2mg / kg; short action, rapid metabolism, best choice for continuous benzodiazepine infusion NB Doses may need to be reduced in the elderly Additional therapy must be started at this point to prevent further seizures Established status: 30-60 minutes • Phenytoin 15-20mg / kg IV @ 50mg / min, or • Fosphenytoin 15-20mg / kg IV / IM @ 150mg / NB Both require continuous ECG monitoring If seizures continue, administer additional phenytoin or fosphenytoin 5-10mg/kg and check levels Refractory status: Seizures lasting > hour Several options: ICU care required for ventilatory support and invasive monitoring Use continuous EEG monitoring if available • • • • Propofol: 2mg / kg bolus, 150-200mcg / kg / infusion, or Thiopental: 5-10mg / kg bolus, 1-10mg / kg / hr infusion, or Midazolam: 0.2mg / kg bolus, 0.1-0.2mg / kg / hr infusion Valproate: 400-800mg / kg IV bolus may be added (if phenytoin levels ok)1 NB: deep sedation is recommended for at least 12 hours before reducing and looking for evidence of seizure activity, ideally using an EEG for guidance Ensure adequate levels of anticonvulsants for chronic seizure control Haemodialysis may be helpful in cases of drug-induced status (especially antibiotics, theophylline) If seizures continue after a period of deep sedation despite adequate anticonvulsant drug levels, additional agents such as Phenobarbital or levetiracetam may be considered Figure 8.3. Stages and treatment of tonic-clonic status epilepticus · Not using deep barbiturate or propofol sedation for a minimum of 12 h (ideally with EEG monitoring) · Incorrect diagnosis (e.g., NEAD) Continued seizures and myoclonic jerking occurring early after a hypoxic brain injury are frequently associated with a very poor prognosis Hui et al reported a series of 18 patients who developed postanoxic myoclonic status following a cardiac arrest The myoclonus developed a mean of 11.7 h after the arrest and lasted a mean of 60.5 h Sixteen patients died and the remainder were left vegetative or highly dependant As well as being distressing for the patient’s family, myoclonic status can be very difficult to control Agents such clonazepam or sodium Levetiracetam is gaining popularity as adjunctive therapy and is available in both oral and IV preparations 74 M Feely and N Cooper Metabolic • Respiratory and metabolic acidosis • Hypoglycemia • Hyperkalemia • Rhabdomyolysis after neurosurgery) Treatment is essentially the same, except that oral clobazam is the preferred benzodiazepine as it is less likely to reduce the conscious level or cause respiratory depression Non-convulsive status epilepticus is underrecognized • Dehydration • Increased ADH secretion Autonomic • Fever • Hypertension or hypotension • Cardiac arrhythmias • Urinary retention Others • Leucocytosis • Aspiration pneumonia • Venous thromboembolism • Trauma Figure 8.4. Systemic complications of tonic-clonic status epilepticus valproate have been traditionally used, although newer agents such as as levetiracetam have been tried with some success Continued epileptic seizures following a hypoxic injury can also be difficult to treat and are often associated with a bad outcome The seizures should be treated according to the status epilepitcus algorithm, and serial EEG examiWhenever seizure control is difficult, it is sensible to seek expert help from a neurologist at an early stage nations may be required Wherever possible, it is sensible to render the patient seizure free for a period of 24–48 h before making prognostic decisions In addition, status epilepticus can be a symptom of another illness, and a thorough evaluation to look for an underlying cause (e.g infection) is always required Focal motor status epilepticus (epilepsia partialis continua) is manifested by a continuous jerking of one side of the body This patient is usually conscious and signs may be subtle, for example, twitching of the corner of the mouth Focal seizures can spread, leading to a reduced conscious level or a tonic-clonic seizure Causes include structural brain lesions, hyperosmolar non-ketotic hyperglycemia, and penicillin therapy in the presence of a local breakdown in the blood–brain barrier (e.g., Case Histories A 30-year-old lady who was 32 weeks pregnant was admitted to the delivery suite following a tonic-clonic seizure She was known to have primary generalized epilepsy and was usually fit and well, apart from a recent urinary tract infection Following her tonic-clonic seizure she had an altered conscious level for 24 h Her eyes were open and she spontaneously moved all four limbs, but she did not speak and appeared “glazed.” An EEG confirmed absence status; she was given intravenous lorazepam and she then woke up, asking what had happened An 80-year-old man, known to have epilepsy following a small stroke, was admitted with severe sepsis He was successfully resuscitated, but 24 h later was still unconscious His relatives had noticed jaw twitching and occasional jerking of his right arm throughout the day An EEG confirmed nonconvulsive status In a case of coma without an obvious cause, an EEG will exclude nonconvulsive status e pilepticus, which was treated with intravenous lorazepam and phenytoin Seizures Occurring as Part of an Acute Illness or Following Neurosurgery Seizures occur as part of many acute illnesses, especially metabolic disorders (e.g., hypoglycemia, hyponatremia) and brain diseases (e.g., meningo-encephalitis, subarachnoid hemorrhage) Acutely ill patients presenting with seizures require careful evaluation, and consideration should be given to performing a lumbar puncture Seizures can also be difficult to control in patients with epilepsy if there is a concurrent illness that reduces the seizure threshold, for example, hypocalcemia or hypothyroidism Tonicclonic seizures affect ventilation and some 8. Seizures on the Adult Intensive Care Unit patients with severe chronic lung disease may develop acute respiratory failure and may require mechanical ventilation The prevention and early treatment of seizures is important following neurosurgery, because seizures can precipitate serious complications, including secondary intracranial bleeding, hypoxia, aspiration and raised intracranial pressure Seizures can be provoked by hyponatremia, acidosis, alcohol withdrawal, hypoxemia, sepsis, steroid therapy, or a postoperative hematoma In the United Kingdom, it is not common practice to give prophylactic AEDs to patients after neurosurgery or following traumatic brain injury or subarachnoid hemorrhage Early postoperative seizures (within 24 h) may be considered provoked seizures rather than a manifestation of epilepsy, and not necessarily require ongoing treatment Seizures occurring later than this indicate a structural brain lesion and may need treatment.Although phenytoin is used acutely, patients should normally be discharged on an alternative drug Its narrow therapeutic index and unpleasant long-term side effects (e.g., gum hypertrophy and hirsutism) make it an unsuitable first-line drug for most people Case History A 60-year-old man on the neurosurgical HDU had had a very stormy postoperative course and was making a slow recovery He had a low albumin and was receiving phenytoin via a nasogastric tube Despite several low levels and subsequent dose adjustments, he continued to have seizures Low albumin makes it difficult to interpret the levels of highly protein-bound drugs such as phenytoin The patient was switched to valproate and his seizures stopped Incidental Seizures in a Patient with Epilepsy Since epilepsy is a common neurological condition, many patients with epilepsy present for surgery or to critical care Almost any acute illness can precipitate seizures Patients should be maintained on their usual AED, by an alternative route if necessary, at all times If a seizure occurs because treatment was omitted, the patient will not be allowed to drive for one year The other important consideration is 75 to avoid provoking factors, including commonly prescribed medications, that lower the seizure threshold, for example, ciprofloxacin, tramadol, antipsychotics, antihistamines, antimalarials, baclofen, bupropion (zyban), and theo-phyllines Non-epileptic Attack Disorder (“pseudostatus”) NEAD accounts for a significant number of admissions to ICU for “status epilepticus.” Distinguishing true tonic-clonic status from NEAD can be difficult Features of NEAD include fluctuating thrashing activity, back arching, eyes screwed shut, hyperventilation with normal SpO2, and rapid recovery despite a prolonged seizure Prolactin level is an unreliable test to distinguish tonic-clonic seizures from NEAD In about one third of cases of NEAD, the patient also has epilepsy NEAD commonly occurs in young adults with a history of psychological trauma or social problems, and is rare in the elderly A normal EEG during the attack almost always confirms the diagnosis If in doubt, treat for tonic-clonic status and get expert help Many patients with NEAD genuinely believe the attacks are real In our experience, explaining that these attacks are a genuine illness, but not due to epilepsy, and thus require different treatment, is the best way to explain the diagnosis Further Reading Guberman A, Bruni J (1999) Essentials of clinical epilepsy Butterworth Heinemann, Boston, MA Hui A, Cheng C, Lam A et al (2005) Prognosis following postanoxic myoclonus status epilepticus Eur Neurol 54:10–13 Manford M (2003) Practical guide to epilepsy Butterworth Heinemann, Boston, MA NICE 2004 guidelines: The diagnosis and management of the epilepsies in adults and children in primary and secondary care www.nice.nhs.uk/nicemedia/ pdf/CG020fullguideline.pdf Panayiotopoulos C (2002) A clinical guide to epileptic syndromes and their treatment Bladon Medical Publishing, Oxfordshire, UK Shorvon S (1994) Status epilepticus – its clinical features and treatment in children and adults Cambridge University Press, UK Walker M (2005) Clinical review Status epilepticus: an evidence based guide BMJ 331:673–77 Non-Neurological Complications of Brain Injury John P Adams Key Points Medical complications are now recognized as significant contributors to patient outcome after severe neurological injury Respiratory complications may account for up to 50% of deaths following brain injury Neurogenic pulmonary edema (NPE) requires aggressive management with positive pressure ventilation and careful restoration of the systemic circulating volume Patients with NPE and myocardial stunning often appear moribund, but have a good chance of rapid recovery if appropriately managed Patients with severe cardiac dysfunction after brain injury require invasive cardiovascular monitoring (e.g., pulmonary artery catheter) to accurately guide therapy Cerebral salt wasting is common after subarachnoid hemorrhage (SAH), and must be distinguished from SIADH Medical complications are now recognized as significant contributors to patient outcome after severe neurological injury They may arise as a direct effect of the injury or as a consequence of its treatment Early studies in patients with subarachnoid hemorrhage (SAH) focused on two main complications: neurogenic pulmonary edema (NPE) and “myocardial stunning.” It is now clear that, individuals suffering from other types of neurological insult, including traumatic brain injury, are also susceptible to these life-threatening medical complications and indeed, many other organ systems can be involved The etiology of these complications is still poorly understood and the management of such conditions is often poorly described in the literature This chapter aims to examine the current evidence base and suggests some practical solutions for the management of these problems One study of over 450 patients with SAH found that nearly all the patients had one or more medical complication, and classified this as severe in 40%(Solenski et al 1995) Twenty-three percent of all deaths were attributed to medical complications, 19% to the primary bleed, 22% to re-bleeding, and 23% to vasospasm Eighty-three percent of those who died had a life-threatening complication compared to 30% of the survivors Half of the “medical” deaths were from pulmonary complications and a poor GCS at presentation, not surprisingly, seemed to correlate with a higher degree of respiratory dysfunction Table 9.1 outlines the relative frequencies of the medical complications in the study In another series of 242 patients with SAH (Gruber et al 1999), medical complications were again commonplace with 81% of patients developing dysfunction of at least one non-neurological organ system, and 26% developing organ system failure Non-neurological organ dysfunction correlated with severity of the SAH Mortality was 31% for SAH and single non-neurological organ 77 J.P Adams 78 Table 9.1. Relative frequencies of medical complications in patients with SAH (Solenski et al 1995) Complication Frequency (%) Anemia Hypertension Arrhythmia Pulmonary oedema Pneumonia Hepatic dysfunction Coagulopathy Renal dysfunction Thrombocytopenia Electrolyte disturbance 37 36 35 23 22 24 4 7 4 16 failure, 91% with two organ failure, and 100% when three or more organs were involved Non-neurological organ system dysfunction is also prevalent in traumatic brain injury (TBI) Zygun et al studied 209 patients with severe TBI and found that 89% developed non-neurological organ system dysfunction, with 35% having overt organ failure (Zygun et al 2005) Respiratory dysfunction was commonly implicated, occurring in 23% of patients Non-neurological organ dysfunction was independently associated with mortality and Glasgow Outcome Score, with mortality rising sharply with each sequential organ failure Respiratory System Respiratory dysfunction is the commonest medical complication in the brain-injured patient, and may account for up to 50% of deaths after brain injury The type of respiratory problem and its treatment may be different between different categories of brain injury Respiratory failure is significantly associated with an increase in ICU stay and a higher risk of vasospasm after SAH (Friedman et al 2003) There are three main causes of respiratory dysfunction in the brain-injured patient (Pelosi et al 2005): Structural parenchymal abnormalities These are the commonest reason for respiratory insufficiency in the brain-injured patient Hypoventilation and hyperventilation are common after brain injury and when associated with poor cough and retention of secretions can lead to atelectasis and consolidation Pneumothorax or rib fractures following direct trauma may also lead to respiratory embarrassment Release of both brain and systemic inflammatory mediators after brain injury can lead to peripheral organ dysfunction Pulmonary aspiration can also cause a systemic inflammatory response Additionally, treatment of impaired gas exchange with invasive ventilation can cause barotrauma and volutrauma, which in turn may trigger the release of pulmonary cytokines (Pelosi et al 2005) Brain injury is usually followed by intense sympathetic hyperactivity with high levels of circulating catecholamines Besides producing hypertension and tachycardia, they may also have effects on the pulmonary circulation with increases in alveolar capillary barrier permeability and pulmonary lymph flow (Pelosi et al 2005) Brain-injured patients are at particular risk for the development of Ventilator-Associated Pneumonia (VAP) (Sirvent et al 2000; Ewig et al 1999) It is classified as “early” if it occurs within the first four days of ICU admission and the usual responsible organisms are Staphylococcal aureus, Hemophilus influenzae and Streptococcus pneumoniae After days it is termed “late” and is usually caused by Pseudomonas aeruginosa, Enterobacteriaceae and Acinetobacter species (Pelosi et al 2005) Risk factors are outlined in Table 9.2 Ventilation–Perfusion mismatch Many brain-injured patients have moderate to severe hypoxemia without radiographic evidence of interstitial or alveolar edema It may be caused by ventilation–perfusion mismatch with suggested mechanisms including redistribution of pulmonary blood flow mediated by the hypothalamus, pulmonary microembolisms leading to an increase in dead space, and depletion of surfactant (Pelosi et al 2005; Schumacker et al 1979) Table 9.2. Risk factors for Ventilator-Associated pneumonia Risk factors for VAP in brain-injured patients Altered GCS Aspiration Emergency intubation IPPV >3 days Re-intubation Age >60 years Supine position Co-existing disease Prior antibiotic use 9. Non-Neurological Complications of Brain Injury 79 Figure 9.1. Chest x-ray of a patient with acute aneurysmal SAH showing diffuse bilateral infiltrates consistent with neurogenic pulmonary edema (NPE) Neurogenic Pulmonary Edema Etiology: In the 1960s, Simmons reported that 85% of combat soldiers dying of isolated severe head injury demonstrated alveolar edema, hemorrhage, and congestion which were not seen in those with chest trauma (Simmons et al 1969) Rogers subsequently showed that 32% of patients dying at the scene of an accident with head injury had NPE (Rogers et al 1995) Onset is commonly within 4 h of the initial cerebral insult and 90% will have diffuse bilateral infiltrates on the CXR (see Fig. 9.1) Mortality is high (up to 10%) but survivors usually recover very quickly with appropriate intervention In SAH, NPE is associated with increasing age and poor WFNS grade (Solenski et al 1995) It is commonly seen at presentation or at the time of intervention but can be seen up to 14 days after the initial insult It is not significantly associated with triple H therapy (aggressive fluid loading), cerebral angiography, ECG changes or pre-existing cardiorespiratory disease (Solenski et al 1995; Macmillan et al 2002) Neurogenic pulmonary edema has a different etiology to acute lung injury (ALI) following an inflammatory insult, although brain injury (especially SAH) can trigger a systemic response, which in turn leads to ALI (Macmillan et al 2002) Neurogenic pulmonary edema requires a normal circulating volume to occur, as blood is shunted from the systemic circulation to increase the pulmonary vascular volume It seems that a massive catecholamine surge leads to a and b adrenoceptor activation and cardiac injury resulting in increased transpulmonary pressures and pulmonary edema (Macmillan et al 2002; Davidson and Charuzi 1973) A massive, but not necessarily prolonged surge in pulmonary artery pressure (PAP) leads to an increase in extra vascular lung water (EVLW), which causes a reduction in compliance and an increase in the alveolar–arterial (A–a) oxygen difference (Davidson and Charuzi 1973; Touho et al 1989) Although hydrostatic mechanisms appear to be the common pathophysiological Appendices 153 Appendix 5: Drug Doses Drug Suggested dose range Infusion concentration Dose range (mL/h) for 70 kg patient Adrenaline (epinephrine) 0.05–1.0 mcg/ kg/min 5 mg in 50 mL 0.9% NaCl 2.1–42.0 mL/h (0.05–1.0 mcg/kg/min) Noradrenaline (norepinephrine) 0.05–1.0 mcg/ kg/min 4 mg in 50 mL 5% glucose 2.6–52 mL/h (0.05–1.0 mcg/kg/min) Phenylephrine (Neosynephrine) 1.0–10 mcg/kg/ 4.2–42 mL/h (1.0–10 mcg/kg/min) Dobutamine 2.5–20 mcg/kg/ 50 mg in 50 mL 0.9% NaCl 250 mg in 50 mL 0.9% NaCl Dopamine 2–15 mcg/kg/ 1.0–7.5 mL/h (2–15 mcg/kg/min) Vasopressin 0.01–0.04 units/ 400 mg in 50 mL 0.9% NaCl 50 units in 50 mL 0.9% NaCl 2.1–16.8 mL/h (2.5–20 mcg/kg/min) 0.6–2.4 mL/h (0.01–0.04 units/min) Notes Route Use for refractory hypotension in low cardiac output states where other agents e.g., dobutamine have been ineffective Severe tachycardia may be seen Predominantly a agonist with some b1 agonism More potent than phenylephrine May mask hypovolemia Reflex bradycardia may occur Useful agent that can be given peripherally whilst central venous access is being established b1 agonist used to augment cardiac output Can be given peripherally whilst central venous access is being established Tachycardia frequently seen Predominant effect depends on dosage At lower doses acts as b1 agonist More a effects at higher doses (>10 mcg/kg/min) Side effects include reduced CO and hepatosplanchnic blood flow Doses >0.04 units/min may lead to cardiac arrest CVC CVC Large vein Large vein CVC CVC NB These drug infusion regimes are for illustrative purposes All drug concentrations and infusion rates should be independently verified and, where possible, locally policy established In all circumstances the circulating volume should be optimized; invasive cardiovascular monitoring may be required Appendices 155 Appendix 6: Neuro-Surgical Referral of Traumatic Brain Injuries NEURO-SURGICAL REFERRAL OF TRAUMATIC BRAIN INJURIES Patient Details Patient identified in A&E for referral to NSU at LGI or Hull Fill in patient check list (PTO) Date: Anaesthetic/A&E doctor to make telephone call to nearest on-call registrar for Neurosurgery Time of CT Request Time of CT Scan Time of CT Results LGI: 0113 243 2799 Mobile: xxxxxxxx General Comments: Enter Dialogue – Time: _ _ : _ _ hrs Send scan via image link Time: _ _ : _ _ hrs Avoid secondary cerebral insult � Maintaining cerebral oxygen delivery � Controlling cerebral oxygen consumption � Avoid increases in intracranial pressure See Neuro Care Bundle NSU will call referring hospital back as soon as possible Time _ _:_ _ hrs Indications for Manitol Patient Declined Reason Patient Accepted NSU is responsible for finding a bed even if none available � � � Admit locally Time: _ _ : _ hrs Refer after 24 hrs if concerned, deteriorates or fails to improve Leave for NSU _ _ : _ _ hrs Time of arrival: _ _ : _ _ hrs � Mass lesion requiring urgent surgery Urgent surgery not required Call WYMAS/TENYAS Call 999, transfer without delay Optimise for transfer Unilateral pupillary dilatation Unilateral progressing to bilateral dilatation (primary bilateral dilatation may represent fitting, drug intoxication or overdose, or overwhelming brain injury) Dose: 0.5 gm/kg (approximately 200 mls of 20% solution in adults) over five minutes Must be catheterised Critical Care Transfers Dedicated Call Line for WYMAS-01924 834515 TENYAS – Phone 999 a b c d e f g Monitoring during ventilated transfers ECG Direct arterial and NIBP SaO2 EtCO2 (calibrated against PaCO2) Temperature Urinary catheter Pupillary size and reaction Call NSU with ETA Take patient to _at LGI Name of Person Completing Form _ Signature Date _ PLEASE FILE IN PATIENT’S RECORDS REFERRING HOSPITAL SHOULD ONLY NEED TO MAKE ONE PHONE CALL TO NSU Appendices 157 Appendix 7: Referral Checklist – for Traumatic Brain Injured Patients to Neuro Centre REFERRAL CHECKLIST – FOR TRAUMATIC BRAIN INJURED PATIENTS TO NEURO CENTRE Referring Doctor: Referring Consultant: Referring Hospital: Time of Call: Patients Details: Name Age DOB Sex Injury mechanism e.g RTA / Assault etc: Time of Injury: GCS, pupils and time of arrival on scene: GCS, pupils and time of arrival at A&E: GCS, pupils at time of call: Any treatment given? e.g intubated/ ventilated 10 Current vital signs: P, BP, Sa02: 11 Other significant injuries and past medical history: 12 Is patient on Warfarin, Asprin or Clopidogrel? 13 14 15 16 Referral Clinician Tel No & Ext No: Name of Neuro SpR spoken to: Time of first contact with Neuro SpR: Outcome of call - comments: Glasgow Coma Score Motor Obeys Commands Localises Pain Flexes To Pain Abnormal Flexion Extension To Pain No Movements Verbal Orientated Confused Words Not Sentences Noises Not Words No Sounds Eyes Open Spontaneously Open To Voice Open To Pain Closed Time Pupils Eye Opening Motor Response Verbal Response Time Pupils Eye Opening Motor Response Verbal Response Time Pupils Eye Opening Motor Response Verbal Response Yes No PATIENT ACCEPTED Don’t Know PATIENT DECLINED PLEASE TICK APPROPRIATELY USEFUL TELEPHONE NUMBERS: LGI Switchboard: 0113 243 2799 LGI Neuro ITU Tel: (Ask to page Neuro-Sciences Registrar) LGI Neuro ITU Fax: 0113 392 7106 0113 392 7306 Distributed by WYCCN – Tel: 01924 210049 PRIOR TO TRANSFER FAX BOTH SIDES OF FORM TO LGI NEURO ICU ON 0113 392 7306 EVEN IF PATIENT IS DECLINED 159 Appendices Appendix 8a A patient in cardiogenic or septic shock is resuscitated and subsequently managed on an Intensive Care Unit to attain a blood pressure at the lower threshold of autoregulation for that individual’s organs A systolic blood pressure of 80–90 mmHg is often accepted, provided the cerebral, renal, and myocardial perfusions are adequate, as demonstrated by the patient remaining lucid (if conscious), having an adequate urine output and no evidence of myocardial ischemia The notion of striving to attain supra-physiological values for cardiac output and oxygen delivery has long been discarded Similarly, for a patient with ARDS, we “permit” a degree of hypercapnia and hypoxia with a strategy of lungprotective ventilation rather than striving to normalize physiological parameters This is where Neurocritical Care differs from General Intensive Care It is implicit, when employing an ICP directed protocol for the management of intracranial hypertension, that mean arterial pressure is maintained at values which exceed what would normally be considered adequate in a general ICU patient because cerebral perfusion must be maintained To use an analogy from ATLS, dysfunction is given primacy over breathing and circulation Therefore, patients are often overdosed on sedatives in order to achieve burst suppression, whilst being aggressively ventilated to achieve ‘normal’ arterial tensions of CO2, and driven (often in the face of a relatively depleted intravascular compartment secondary to loop and osmotic diuretic use) to achieve a blood pressure that exceeds normal renal and cerebral autoregulation CPP goal directed protocols have been shown to have higher incidences of lung related complications (Robertson 1999; Contant 2001) in their treatment arms We have witnessed young patients suffer myocardial ischemia, cardiac arrests and myocardial deaths with aggressive ICP targeted therapies Therefore, although we present schematics for the management of raised intracranial pressure and inadequate cerebral perfusion pressure, caution must be exercised in slavishly following such protocols Increasingly, management is becoming more tailored to the individual patient; measuring adequacy of cerebral oxygenation may allow lower threshold cerebral perfusion pressures and more rationally set PaCO2 levels to be targeted, thereby avoiding iatrogenic morbidity Eventually, treatment protocols may become sophisticated enough to distinguish between subsets of patients who will benefit from a CPP directed approach (i.e., those who are autoregulating) verses a Lund approach (i.e., failure of autoregulation where primacy must be given to minimizing vasogenic edema) References Robertson CS, Valadka AB, Hannay HJ, et al (1999) Prevention of secondary ischemic insults after severe head injury Crit Care Med 27: 2086–2095 Contant CF, Valadka AB, Gopinath SP, et al (2001) Adult respiratory distress syndrome: a complication of induced hypertension after severe head injury J Neurosurg 95: 560–568 Appendices Appendix 8b: Flow Diagram for the Management of Raised Intracranial Pressure 161 163 Appendices Appendix 8c: Flow Diagram for Hemodynamic Management in the Context of Raised ICP in Adult Patients CPP < 60 ICP > 20 MAP ADEQUATE ICP < 20 LOW MAP Fluid Boluses 250ml 6% starch aliquots ICP PROTOCO L CPP remains < 60 Start Phenylephrine or Noradrenaline** Daily 12 Lead ECG Persistent hypotension (SBP < 100) Adequate CPP not maintained Evidence of myocardial dysfunction or ALI Unsure about Volume Status Advanced Cardiovascular Monitoring (e.g PA Catheter, Doppler) Short Snynacthen Test Assess adequacy of CPP (PtB O 2, S jvO 2) ADEQUATE CARDIAC INDEX Continue noradrenaline/phenylephrine** Optimise fluid status Vasopressin if above measures fail Optimise fluid status Dobutamine/Adrenaline** Baseline Cardiac Echo Adequate hemodynamics cannot be achieved and/or signs of myocardial ischaemia Adequate hemodynamics CPP>60, ICP 1 h Several options: ICU care required for ventilatory support and invasive monitoring Use continuous EEG monitoring if available · Propofol: 2 mg/kg bolus, 150–200 mcg/kg/min infusion, or · Thiopental: 5–10 mg/kg bolus, 1–10 mg/kg/h infusion, or · Midazolam: 0.2 mg/kg bolus, 0.1–0.2 mg/kg/h infusion · Valproate: 400–800 mg/kg IV bolus may be added (if phenytoin levels ok) Levetiracetam is gaining popularity as adjunctive therapy and is available in both oral IV preparations NB: deep sedation is recommended for at least 12 h before reducing and looking for evidence of seizure activity, ideally using an EEG for guidance Ensure adequate levels of anticonvulsants for chronic seizure control Hemodialysis may be helpful in cases of drug-induced status (especially antibiotics, theophylline) If seizures continue after a period of deep sedation despite adequate anticonvulsant drug levels, additional agents such as Phenobarbital may be added Appendices 167 Appendix 10 Glasgow Outcome Score GOS=1 (Good Recovery) Capacity to resume normal occupational and social activities, although there may be minor physical or mental deficits or symptoms GOS=2 (Moderate Disability) Independent and can resume almost all activities of daily living Disabled to the extent that they cannot participate in a variety of social and work activities GOS=3 (Severe Disability) No longer capable of engaging in most previous personal, social or work activities Limited communication skills and have abnormal behavioral or emotional responses Typically are partially or totally dependent on assistance from others in daily living GOS=4 (Persistent Vegetative State) Not aware of surroundings or purposely responsive to stimuli GOS=5 (Dead) Rankin Disability Score Rankin=0 No symptoms at all Rankin=1 No significant disability despite symptoms; able to carry out all usual duties and activities Rankin=2 Slight disability Unable to carry out all normal activities but able to look after own affairs without assistance Rankin=3 Moderate disability requiring some help but able to walk without assistance Rankin=4 Moderately severe disability Unable to walk without assistance, and unable to attend to own bodily needs without assis-tance Rankin=5 Severe disability Bedridden, incontinent and requiring constant nursing care and attention Appendices 169 Appendix 11: Management of a Fall in GCS after Subarachnoid Haemorrhage Fall in GCS more than points or point in the motor score Airway, Breathing, Circulation- safety first Intubate and ventilate if GCS < - Optimise oxygenation with PEEP Normalise PaCO (4.5-5.0kPa) unless “coning” where PaCO reduced to 3.5-4.0kPa as a can be temporary measure only Always check blood sugar Full clinical examination - consider the possible causes: - Neurological, e.g seizures, re-bleeding, hydrocephalus, vasospasm , cerebral oedema - Non-neurological, e.g hypoxia, MI, PE, pyrexia, ↓[Na + ], acute abdomen Investigations: ECG, CXR, FBC, U&Es, Clotting, Mg 2+ Once stable, CT brain scan CT SCAN CHANGED Re-bleed, Infarction, worsening oedema, hydrocephalus CT SCAN UNCHANGED LIKELY CEREBRAL VASOSPASM Contact Regional Neurosurgical Centre See Figure 4.5 Transfer to RNC Re-assess off sedation Clinical Improvement Transfer to RNC Poor Clinical Condition Ongoing DGH Management Definitive treatment of aneurysm at RNC after 14 days if good neurological condition Withdraw Support See Editorial Note, Chapter Appendices Appendix 12: Management of Vasospasm (NB Diagnosis of Exclusion) 171 Index A Acidosis, 107, 111 Acinetobacter, 78 Acute idiopathic axonal degeneration, 96 Acute inflammatory demyelinating polyradiculopathy (AIDP), 92 Acute lung injury (ALI), 79, 80 Acute motor axonal neuropathy (AMAN), 92 Acute motor sensory axonal neuropathy (AMSAN), 92 Adams, J.P., 19–30, 51–60, 77–85 Adhesion molecules, 80 Adrenal insufficiency, 83 Alveolar–arterial (A–a) oxygen difference, 79 Anemia, 85 Angiography, cerebral, 105, 108, 109 Anterior horn cell disease, 90 Antibody, anti-ganglioside, 93 Anti-epileptic drugs (AEDs) barbiturates, 73 carbamazepine, 72 clobazam, 73, 74 clonazepam, 73 diazepam, 72 fosphenytoin, 73 lamotrigine, 71 levetiracetam, 72, 73 lorazepam, 72–74 midazolam, 72, 73 phenytoin, 72–75 sodium valproate, 73 Apnea test, 110–111 Arginine vasopressin, 84 Autonomic disturbance, 91, 94, 95 Autoregulation, 10, 12–14 B Barnes, L., 89–96 Barotrauma, 78 Barré, 92 Bell, D., 19–30 Bell, M.D.D., 1–7, 137–144 Biopsy, muscle, 91 Bispectral analysis, 14–15 Blood pressure, 80–82 Botulism, 94–95 Brain injury hypoxic, 11 management principles, Brain natruiretic peptide (BNP), 84 Brain edema, mechanisms, Brainstem death, 105–111 clinical testing, 109 diagnosis, 106, 107 Brainstem death, pathophysiology, 113–115 Brain tissue oxygenation, 10, 13, 16 Burst suppression, 16 C Cardiac enzymes, 81, 82 Cardiac output, 80 Catecholamines, 78, 82, 83 Cerebral abscess, 43, 46–49 Cerebral angiography, 79 Cerebral blood flow (CBF), 10, 11, 13, 14, 37 Cerebral blood volume, Cerebral function analyzing monitor (CFAM), 14 Cerebral function monitor (CFM), 14 Cerebral oxygen, 16 consumption, 3, 4, delivery, 3, 4, extraction, 12, 13 Cerebral perfusion pressure (CPP), 10–12, 14, 16 Cerebral salt wasting syndrome (CSWS), 84 Cerebral spinal fluid (CSF), 91, 93, 94, 96 Cerebral vascular reactivity, 12, 14 Cerebrospinal fluid, 173 174 Cervical spine injury airway management, 52 autonomic hyper-reflexia, 55–56 awake fibre optic intubation, 52, 53 Brown-Séquard syndrome, 55 causes, 51 central cord syndrome, 55 clearing the cervical spine, 58 diaphragm function, 53–54 fluid balance, 58 fractures, types, 56–58 incomplete injury, 55 infection, 59 initial stabilisation, 52–58 lung function, effect of level of injury on, 53 lung volumes, 53, 54 manual in line stabilisation (MILS), 52, 53 neurogenic pulmonary edema, 53, 55 neurogenic shock, 51, 55 pressure sores, 54, 58, 59 primary injury, 51, 52, 55 radiology, 56 respiratory care, 54 sacral sparing, 55 secondary injury, 51, 52, 55 spinal shock, 55, 58 stability, 56–59 steroids, 58–59 succinylcholine (suxamethonium), 52 surgical management, 59 temperature regulation, 59 thromboprophylaxis, 59 weaning, 54, 59 CK-MB, 82 Clark, M., 97–103 Clinical and logistical process, Clonidine, 81 Clostridium botulinum, 94 Clostridium tetani, 95 CMRO2, 37 Coagulation disorders, 85 Compound action potential, 93, 94 Compressed spectral array, 15 Coning, 107 Continuous aspiration of subglottic secretions (CASS), 81 Controlled donation after cardiac death (DCD), 115 Cooper, N., 69–75 Cough assist device, 92 Crisis cholinergic, 95 myasthenic, 92, 95 Critical illness myopathy, 96 neuropathy, 96 CSF filtration, 94 CT brain scan after head injury, indications, Cytokines, 78, 80 Index D Davies, S., 9–16 Death, diagnosis, 117–118 Demeclocycline, 84 Denton, M., 43–49 Diabetes insipidus (DI), 84, 107, 115 Disseminated intravascular coagulopathy (DIC), 85 Distal latency, 93 Dobutamine, 83 Donnan, G., 63 Dopamine, 80 Doppler shift, 13 Doppler, transcranial, 109 Dysrhythmias, 81, 82 E Echocardiography, 82, 83 Edrophonium, 95 Electroencephalography (EEG), 14–16, 71–75, 106 Electrolyte disturbance, 116 Electromyography (EMG), 90 Encephalitis, 43, 46, 107 Enterobacteriaceae, 78 Epidural abscess, intracranial, 49 Epilepsy surgery, 71 Epinephrine, 80, 83 Erythromycin, 91 Esmolol, 37 Esophageal doppler, 83 Ethical issues, intensive care capacity, 137–139 elective ventilation, 141 HIV testing, 141, 142 hospital clinical ethics committees, 138 Human Fertilization and Embryology Authority (HFEA), 140 Human Tissue Act, 141, 143 independent mental capacity advocate (IMCA), 139 life-sustaining medical treatment (LSMT), 138 Mental Capacity Act, 137–139, 143 needle-stick injuries, 143 non-heart beating organ donation, 140, 143 Organ Donor Register, 140, 142 Extra vascular lung water (EVLW), 79, 80, 83 F Feely, M., 69–75 Fieschi, C., 63 Fludrocortisone, 84 Fourier analysis, 15 G Glasgow coma scale (GCS), 9, 11, 15 Goddard, T., 121–135 Guillain, 92 Guillain Barré syndrome (GBS), 92, 93 Index H Hacke, W., 63 Haemophilus influenzae, 78 Hassan, A., 61–66 Herpes simplex encephalitis, 71 Holbrook, S.P., 33–41 Horner’s syndrome, Hui, A., 73 Hydralazine, 83 Hydrocephalus, 11, 107 Hyperemia, 10, 12, 13 Hypernatraemia, 84, 116 Hypertension, intracranial, 107, 108, 114 Hypertonic saline, 84 Hypoglycemia, 107 Hypokalemia, 85 Hypomagnesemia, 36 Hyponatremia, 38, 83, 84, 107 Hypothalamic stress, 82 Hypothermia, 106, 107, 116 Hypoxic brain injury, 72, 73, 107 Hypoxic pulmonary vasoconstriction, 90 I Immunoglobulin therapy, 94 Insulin, 116 International subarachnoid aneurysm trial (ISAT), 41 Intoxication, drug, 108–109 Intracranial pressure, 3–5 measurement, 11 monitoring, 10 waveforms, 11–12 Ischemia, brainstem, 106–108, 115 J Jugular venous oximetry (SjvO2), 10, 12, 13, 16 L Labetalol, 37, 82 Lactate oxygen index, 13 Left ventricular stroke work index (LVSWI), 80, 83 Lindley, A., 9–16 Lorazepam, 101 Lundberg waves, 11 M Magnesium, 80 Magnesium sulfate, 95 Major tranquilisers, 101–103 Malignant middle cerebral artery infarction decompressive craniectomy, 65, 66 Mankad, K., 121–135 Mannitol, indications, Marmarou, A., 10 McKinlay, J., 51–60, 97–103 175 Medical complications, 77, 78 Medulla oblongata, 105, 107, 109 Meningitis, 107 Meningitis, bacterial activated protein C, 45 causes, 44 clinical feature, 44 complication, 45–46 CSF analysis, 45–46 definition, 43 early goal directed therapy, 45 epidemiology, 43 investigations, 44 meningitis with sepsis, 44 outcome, 46 pathology, 44 steroids, 45 treatment, 44 Methylprednisolone, 116 Metoclopramide, 91 Midazolam, 99, 101 Midbrain, 109, 110 Miller Fisher syndrome, 92 Milrinone, 80, 83 Miosis, Multimodal monitoring, 16 Murphy, P.G., 105–111, 113–118 Myasthenia gravis, 95 Myocardial ischemia, 113 Myocardial stunning, 77, 83 Myoclonic jerks, 70, 71, 73 Myopathy, 96 N Near infrared spectroscopy (NIRS), 16 Neurogenic pulmonary edema (NPE), 36, 38, 41, 77–79, 115 Neuroleptic agents, 101 Neuromuscular paralytic syndrome, 92 Nicotine, 101, 103 Nitroprusside, 83 Non-epileptic attack disorder (NEAD), 69, 71, 73, 75 Non-neurological organ failure, 77 Noradrenaline (norepinephrine), 116 Norepinephrine, 80 Nucleotide ventriculography, 83 Nutrition, 91 Nystagmus, 109 O Olanzapine, 101 Organ donation, consent, 116–117 Organ donor management, 116, 117 optimisation, 117 Organophosphate poisoning, 96 Oxygen delivery, 10, 12, 13, 16 176 P Patient transfer, indications, Persistent vegetative state, 98 Phenoxybenzamine, 80 Phentolamine, 80 Phenytoin, 84 Plasma exchange (plasmapheresis), 93–95 Post-ictal slowing, 71 Pralidoxime, 96 Pressure reactivity index, 12 Pressure sore, 92 Prokinetics, 91 Prone position, 81 Propofol, 99, 102 Propranolol, 80 Pseudomonas aeruginosa, 78 Ptosis, partial, 89 Pulmonary artery catheter, 116 Pulmonary aspiration, 78 Pulmonary capillary wedge pressure (PCWP), 80 Pulmonary edema, 79–80 Pulmonary micro embolism, 78 Pulmonary vascular resistance, 80 Pulsatility index (PI), 14 Pulse contour analysis, 80, 83 Pyridostigmine, 95 Q Quinn, A.C., 33–42 R Reflex brainstem, 109–110 cold caloric vesibulo-ocular, 110 cough, 110 deep central pain, 110 gag, 110 pupillary light, 110 Regional Neurosurgical Centre, role, 2, Remifentanil, 99, 102 Respiratory dysfunction, 77, 78, 80, 81 Respiratory failure, 78, 113 Reticular activating system, 97 Reticular formation, 109 Risperidone, 101 Risus sardonicus, 95 Rogers, F.B., 79 S Secondary cerebral insults intracranial causes, systemic causes, Seizures causes alcohol withdrawal, 69, 70, 72 arteriovenous malformations, 71 Index drugs, 71–73, 75 hyperosmolar non-ketotic hyperglycemia, 74 mesial temporal sclerosis, 71 neurosurgery, 69, 74–75 traumatic brain injury, 71 prolactin levels, 75 provoked, 70, 71, 75 provoking factors, 69, 75 types complex partial, 70 idiopathic generalized, 70 juvenile myoclonic epilepsy, 70 location-related epilepsy, 70, 71 provoked seizures, 70 refractory epilepsy, 71 simple partial, 70 Short synacthen test, 83 Simmons, R.L., 79 Spectral edge frequency, 15 Spinal immobilisation, complications, 58 Staphylococcal aureus, 78 Status epilepticus complications, 72, 74 mortality, 72 treatment, 72–74 types focal motor, 71, 74 non-convulsive, 72, 74 tonic-clonic, 71, 73, 74 Streptococcus pneumoniae, 78 Stress ulceration, 85 Stress ulcer, prophylaxis, 91 Strohl, 92 Stroke, acute ischaemic anticoagulation, 66 basilar artery occlusion, 64, 65 blood pressure management, 64 complications, 62 glycemic control, 62 neuroprotection, 62, 65 pathophysiology, 61–62 scoring systems, 66 secondary prevention, 65–66 stabilisation, 62, 65 stroke recurrence, 66 stroke units, 62 thrombolysis intra-arterial, 63–65 systemic, 62–63 Stroke, ischaemic, 107 Stunned myocardium, 83 Subarachnoid hemorrhage (SAH), 14, 15, 77–82, 84 Subarachnoid hemorrhage, aneurismal analgesia, 37 blood pressure management, 37 causes, 34 complications, 38–41 CT angiography, 34, 35 delayed ischemic deficit (DID), 33, 34, 37–40 Index diagnosis, 34 digital subtraction angiography (DSA), 34, 35 fluid management, 37–38 incidence, 33 induction of anesthesia, 36 lumbar puncture, 34, 36 management, 33–42 monitoring, 36 morbidity, 33–34 mortality, 33–34 nimodipine, 37 osmotherapy, 38 presentation, 34 sedation, 36, 37, 41 sedation holds, 38 statins, 40 thromboprophylaxis, 38 “Triple H” therapy, 38 WFNS scale, 34 Subdural empyema, 46, 48–49 Subendocardial ischemia, 81 Succinylcholine, 91, 95 Surfactant, 78 Swallowing assessment, 89 Syndrome of inappropriate antidiuretic hormone secretion (SIADH), 84, 93 T Tako-tsubo cardiomyopathy, 83 Tensilon test, 95 Tetanospasmin, 95 Tetracyclic antidepressants, 101 Thallium scanning, 83 Thiamine, 72, 73 Thrombocytosis, 85 Thromboembolism, venous, 91 Timothy, J., 51–60 Torsades de pointes, 101 Transcranial doppler ultrasound, 13 Transmural pressure, 36 Traumatic brain injury, 10, 16, 108 antibiotic therapy, 26 cerebral oxygen delivery, 20, 22–23, 27 cerebral oxygen demand, 20–22, 27 cerebral perfusion pressure (CPP), 20, 22, 23, 27 cerebrospinal fluid, 23–26 contusional injuries, 25 decompressive craniectomy, 20, 23, 27 dopamine, 23 haematoma, 25 hypertonic saline (HSL), 25 hyperventilation, 20, 25 hypothermia, 21–23 177 intracranial pressure (ICP), 20–29 jugular venous oximetry, 21, 23, 27 lactate oxygen index (LOI), 23, 26 loop diuretics, 24–26 lund approach, 22 mannitol, 20, 25, 26 Monro–Kellie doctrine, 19 norepinephrine (noradrenaline), 23 osmotherapy, 25 pathogenesis, 19–26 phenylephrine, 23 recombinant Factor VIIa (rFVIIa), 23 Regional Neurosurgical Centre (RNC), 20, 21, 25, 27, 30 sedation, 20, 21, 25, 27, 29 seizures, 20 steroids, 26 thiopental (thiopentone), 21, 22, 25, 26, 29 thromboprophylaxis, 26 vasopressin, 23 Traumatic brain injury (TBI), 77, 84, 85 Trazadone, 101 Triiodothyronine (T3), 116 Triple H therapy, 79 Troponin I, 82 U Upper motor neuron disorders, 89 V Vasogenic edema, 10 Vasopressin, 83, 84, 116 Vasospasm, 13–15, 77, 78, 80, 82 Ventilator-associated pneumonia (VAP), 78, 81, 114 Ventilatory failure, 90 Ventricular dysfunction, 83 Ventriculitis, 43, 48, 49 Volutrauma, 78 Vucevic, M., 89–96 W Walker, A., 43–49 Water and electrolyte disturbance, 83–85 Weakness acute, 89–96 neuromuscular, 92 Withdrawal of therapy, 116–117 Z Zygun, D.A., 78 ... acute subarachnoid hemorrhage in patients with an abnormal electrocardiogram Anesth Analg 76 (2) :25 3 25 8 Touho H, Karasawa J, Shishido H, Yamada K, Yamazaki Y (1989) Neurogenic pulmonary edema... diagnostic information is available · Airway Cranial nerve involvement can lead to bulbar palsy, dysarthria, dysphonia, dysphagia, and a poor cough Acute aspiration may lead to sudden respiratory... infarction associated with spontaneous intracranial hemorrhage Circulation 22 :25 –38 Das M, Gonsalves S, Saha A, Ross S, Williams G (20 09) Acute subarachnoid hemorrhage as a precipitant for takotsubo cardiomyopathy: