Appendix 1: The Glasgow Coma Scale

Glasgow coma scale Points

Eye opening

Spontaneous 4

To speech 3

To pain 2

Nil 1

Best motor response

Obeys commands 6

Localizes to pain 5

Withdraws to pain 4

Abnormal flexion to pain 3

Extends to pain 2

Nil 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

Nil 1

Appendices

145

Appendices

Appendix 2: Causes of Altered Consciousness

Cause of altered conscious level History and examination Investigations

Traumatic Extradural hematoma History of traumaClassic lucid intervalExternal signs of head injury e.g., skull fractureFocal neurological signsSigns of raised ICP

Abnormal CT

Subdural hematoma Acute type as above without lucid intervalChronic type may follow innocuous trauma and have a more insidious onset

Abnormal CT

Intracerebral hematoma/ contusions/ traumatic subarachnoid hemorrhage

As for extradural hematoma without lucid interval

Abnormal CT

Diffuse axonal injury As for extradural hematoma without lucid intervalMay be few external signs of injury

Abnormal CT-may only become evident >24 h

Vascular Subarachnoid hemorrhage Sudden onsetHistory of headachesSigns of meningismConsider polycystic kidney disease

Abnormal CT (10% are normal) Increased red blood cells/ xanthochromia in CSF

Intracerebral hemorrhage History of hypertension, coagulopathy or anticoagulants

Abnormal CT

Thrombo-embolic Sudden onsetVascular disease, atrial fibrillation

Abnormal CT-may only become evident >48–72 hEchocardiography

Vascular bruitsSigns of endocarditis

Carotid Doppler angiography

Hypertensive crisis Blood pressureFundoscopy

Hypotension/ low cardiac output state

Low blood pressureEvidence of reduced perfusion to other tissues (skin, kidneys)

Cardiac output monitoringEchocardiography

Infective Brain abscess Slow onsetMay be systemically unwellConsider ENT or dental source of infection

Abnormal CT (contrast)Blood cultures

Meningitis Hours to days onsetSigns of meningismPurpuric meningococcal rash

Abnormal CSFBlood culturesCT may be abnormal

Encephalitis Hours to days onsetViral-like illness

CT/ MRI may be abnormalEEG

Generalized sepsis May be obvious infective sourceSigns of SIRS

Raised white cell count/ C-reactive protein

Metabolic Hypo/ hypernatremiaHypo/ hyperglycemiaHypoxiaHypercapniaHypo/ hyperthermiaHepatic failureRenal failure

History may be usefulConsider medications

Abnormal venous/ arterial blood results

Specific features on examination e.g., features ECG changes

of chronic liver disease,

breath odor, fistulae

Endocrine Myxedema Usually apparent from history Abnormal blood results e.g., thyroid function tests,

Adrenal insufficiency Features of a specific condition e.g., myxoedemic facies, hypothermia, abnormal pigmentation

short synacthen test, more complex endocrine tests

Hypopituitarism Neurological signs of pituitary tumor

(continued)

147

Appendices

Cause of altered conscious level History and examination Investigations

Pharmacological Sedatives May be apparent from history Drug/ substance levels in blood/ urineNeedle marks

Breath odor Improvement after antidote administered

Narcotics Pupil signs

Alcohols Depressed respiration

Psychotropic drugs Cardiac arrhythmias

Seizures

Poisons (e.g., carbon monoxide)

Changes in skin color

Substance withdrawal Agitation rather than coma with acute withdrawal

Neoplastic Brain tumor Usually slow onsetConsider metastasisFocal signsRaised intracranial pressure

Abnormal CT

Paraneoplastic syndromes Can present as “asceptic meningitis”

Neurological Seizures Usually typical history Abnormal EEG

Nonconvulsive are rare Need CT to exclude underlying lesion

Consider underlying cause Anticonvulsant levels

Demyelination Disseminated in time and place Abnormal MRI

Psychological/behavioral

ICU psychosisSleep deprivationPseudocomaCatatonia

No specific features Diagnoses of exclusion

148

Appendices

Appendix 3: Initial Stabilization of the Brain Injured Patient on ICU

/kg

149

Appendices

Appendix 4: Acute Brain Herniation

Warning signs:

Reduction in conscious levelUnilateral third Nerve palsyLateralizing motor signs e.g., hemiparesis, extensor posturingHypertension, bradycardia or respiratory irreg-ularity (Cushing’s Triad)

Management

• Rapidintubation and ventilation (great care needed to avoid exaggerated pressor response to laryngos-copy and intubation – experienced anesthetist essential. Invasive blood pressure monitoring ideal, but do not delay establishing ventilation)

• Hyperventilate to PaCO2 3.5–4.0 kPa as a tempo-rary measure

• Mannitol 20% 0.5 g/kg over 10 min• Sedation to reduce cerebral metabolic rate (e.g.,

propofol, thiopentone) supplemented with opioid analgesic (e.g., fentanyl, alfentanil)

• Head up position and good neck position to encourage venous drainage

• MaintainadequateMAP (ideally 90–100 mmHg) with pressor. Do not treat hypertension (may reduce cerebral perfusion)

• 100%O2 (hyperoxia) may reduce cerebral blood volume and ICP (especially in younger patients) and can be utilized whilst more definitive treat-ment is sought

• A CT scan will be required as soon as thepatient is stable enough to be moved to exclude surgical lesions such as hydrocephalus or a hematoma

• ContactRNC for further advice

151

Appendices

Appendix 5: Drug Doses

DrugSuggested dose range

Infusion concentration

Dose range (mL/h) for 70 kg patient Notes Route

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)

Use for refractory hypotension in low cardiac output states where other agents e.g., dobutamine have been ineffective. Severe tachycardia may be seen

CVC

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)

Predominantly a agonist with some b1 agonism. More potent than phenylephrine. May mask hypovolemia. Reflex bradycardia may occur

CVC

Phenylephrine(Neosynephrine)

1.0–10 mcg/kg/min

50 mg in 50 mL 0.9% NaCl

4.2–42 mL/h (1.0–10 mcg/kg/min)

Useful agent that can be given peripherally whilst central venous access is being established

Large vein

Dobutamine 2.5–20 mcg/kg/min

250 mg in 50 mL 0.9% NaCl

2.1–16.8 mL/h (2.5–20 mcg/kg/min)

b1 agonist used to augment cardiac output. Can be given peripherally whilst central venous access is being established. Tachycardia frequently seen

Large vein

Dopamine 2–15 mcg/kg/min

400 mg in 50 mL 0.9% NaCl

1.0–7.5 mL/h (2–15 mcg/kg/min)

Predominant effect depends on dosage. At lower doses acts as b1 agonist. More a effects at higher doses (>10 mcg/kg/min)

CVC

Vasopressin 0.01–0.04 units/min

50 units in 50 mL 0.9% NaCl

0.6–2.4 mL/h (0.01–0.04 units/min)

Side effects include reduced CO and hepatosplanchnic blood flow. Doses >0.04 units/min may lead to cardiac arrest

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.

153

Appendices

Appendix 6: Neuro-Surgical Referral of Traumatic Brain Injuries

NEURO-SURGICAL REFERRAL OF TRAUMATIC BRAIN INJURIES

Patient identified in A&E for referral to NSU at LGI or Hull

Anaesthetic/A&E doctor to make telephone call to nearest on-call registrar for Neurosurgery

LGI: 0113 243 2799Mobile: xxxxxxxx

Patient DeclinedReason

Patient Accepted NSU is responsible for finding a bed even if

none available

Admit locally Time:

_ _ : _ hrs

Send scan via image linkTime: _ _ : _ _ hrs

NSU will call referring hospital back as soon as possible

Time _ _:_ _ hrs

Time of CT Request Time of CT Scan Time of CT Results

General Comments:

Call WYMAS/TENYAS

Critical Care Transfers Dedicated Call Line for WYMAS-01924 834515

TENYAS – Phone 999

Leave for NSU_ _ : _ _ hrs

Call NSU with ETA

REFERRING HOSPITAL SHOULD ONLY NEED TO MAKE ONE PHONE CALL TO NSU

Fill in patient check list (PTO)

Enter Dialogue – Time: _ _ : _ _ hrs

Patient Details

Date:

Take patient to ___________________________at LGI

Time of arrival:_ _ : _ _ hrs

Name of Person Completing Form _______________________________________

Signature __________________________________ Date _____________________

PLEASE FILE IN PATIENT’S RECORDS

Indications for Manitol

� 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

Monitoring during ventilated transfers

a. ECG b. Direct arterial and NIBP c. SaO2

d. EtCO2 (calibrated against PaCO2) e. Temperature f. Urinary catheter g. Pupillary size and reaction

Avoid secondary cerebral insult � Maintaining cerebral oxygen delivery � Controlling cerebral oxygen consumption � Avoid increases in intracranial pressure

See Neuro Care Bundle

Mass lesion requiring urgent surgery

Urgent surgery not required

Call 999, transfer without delay

Optimise for transfer

Refer after 24 hrs if

concerned, deteriorates

or fails to improve

155

Appendices

Appendix 7: Referral Checklist – for Traumatic Brain Injured Patients to Neuro Centre

Distributed by WYCCN – Tel: 01924 210049

REFERRAL CHECKLIST – FOR TRAUMATIC BRAIN INJURED PATIENTS TO NEURO CENTRE

Referring Doctor:Referring Consultant:

1

:latipsoHgnirrefeR2 Time of Call:

egA

3 Patients Details: Name

DOB

Sex

4 Injury mechanism e.g. RTA / Assault etc:

5 Time of Injury:

Time Pupils Eye Opening Motor Response

6 GCS, pupils and time of arrival on scene:

Verbal Response Time Pupils Eye Opening Motor Response

7 GCS, pupils and time of arrival at A&E:

Verbal Response Time Pupils Eye Opening Motor Response

8 GCS, pupils at time of call:

Verbal Response

9 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? Yes No Don’t Know

13 Referral Clinician Tel No & Ext No:14 Name of Neuro SpR spoken to:15 Time of first contact with Neuro SpR:

PATIENT ACCEPTED

PATIENT DECLINED

16 Outcome of call - comments:

PLEASE TICK APPROPRIATELY

USEFUL TELEPHONE NUMBERS: LGI Switchboard: 0113 243 2799 (Ask to page Neuro-Sciences Registrar)

LGI Neuro ITU Tel: LGI Neuro ITU Fax:

0113 392 7106 0113 392 7306

Glasgow Coma ScoreMotor6 Obeys Commands 5 Localises Pain 4 Flexes To Pain 3 Abnormal Flexion 2 Extension To Pain 1 No Movements Verbal5 Orientated 4 Confused 3 Words Not Sentences 2 Noises Not Words 1 No Sounds Eyes4 Open Spontaneously 3 Open To Voice 2 Open To Pain 1 Closed

PRIORTOTRANSFERFAXBOTHSIDESOFFORMTOLGINEUROICUON01133927306EVENIFPATIENTISDECLINED

157

Appendices

Appendix 8a

Apatientincardiogenicorsepticshockisresusci-tated and subsequentlymanaged on an IntensiveCare Unit to attain a blood pressure at the lower threshold of autoregulation for that individual’s organs.Asystolicbloodpressureof80–90mmHgis often accepted, provided the cerebral, renal, and myocardial perfusions are adequate, as demon-strated by the patient remaining lucid (if conscious), havinganadequateurineoutputandnoevidenceof myocardial ischemia. The notion of striving to attain supra-physiological values for cardiac output andoxygendeliveryhaslongbeendiscarded.Simi-larly,forapatientwithARDS,we“permit”adegreeof hypercapnia and hypoxia with a strategy of lung-protective ventilation rather than striving to nor-malize physiological parameters.

This is where Neurocritical Care differs from GeneralIntensiveCare.Itisimplicit,whenemploy-ing an ICP directed protocol for the management of intracranial hypertension, that mean arterial pressure is maintained at values which exceed whatwouldnormallybeconsideredadequateinageneral ICU patient because cerebral perfusion mustbemaintained.TouseananalogyfromATLS,dysfunction is given primacy over breathing and circulation. Therefore, patients are often over-dosed on sedatives in order to achieve burst sup-pression, 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 autoregu-lation. 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; measuringadequacyofcerebraloxygenationmayallow lower threshold cerebral perfusion pres-sures and more rationally set PaCO2 levels to be targeted, thereby avoiding iatrogenic morbidity. Eventually, treatment protocols may becomesophisticated enough to distinguish between subsets of patients who will benefit from a CPP directed approach (i.e., those who are autoregulat-ing) verses a Lund approach (i.e., failure of auto-regulation where primacy must be given to minimizing vasogenic edema).

References

RobertsonCS,ValadkaAB,HannayHJ,etal. (1999) Pre-vention of secondary ischemic insults after severe headinjury.CritCareMed27:2086–2095

ContantCF,ValadkaAB,GopinathSP,etal.(2001)Adultrespiratory distress syndrome: a complication of induced hypertension after severe head injury. JNeurosurg95:560–568

159

Appendices

Appendix 8b: Flow Diagram for the Management of Raised Intracranial Pressure

161

Appendices

Appendix 8c: Flow Diagram for Hemodynamic Management in the Context of Raised ICP in Adult Patients

Adequate hemodynamicsCPP>60, ICP <20

Continue with ICP &CPP directed therapy

Accepted Lower CPP threshold

Based on adequacy ofcerebral oxygenation

PtBO2, SjvO2

Remove ICP fromequation

DecompressiveCraniectomy

Abandon ICP &CPP directed

therapy

Adequate hemodynamics cannot be achievedand/or signs of myocardial ischaemia

ICP < 20LOW MAP

CPP remains < 60Start Phenylephrine or

Noradrenaline**Daily 12 Lead ECG

Fluid Boluses250ml 6% starch aliquots

CPP < 60

ICP > 20MAP ADEQUATE

ICP PROTOCO L

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 TestAssess adequacy of CPP (PtB O2, SjvO2)

LOW CARDIAC INDEXOptimise fluid status

Dobutamine/Adrenaline**Baseline Cardiac Echo

ADEQUATE CARDIAC INDEXContinue noradrenaline/phenylephrine**

Optimise fluid statusVasopressin if above measures fail

** Noradrenaline (norepinephrine): 0.05-1.0mcg/kg/min via CVCPhenylephrine (neosynephrine): 1.0-10mcg/kg/minDobutamine: 2.5-10mcg/kg/minDopamine: 2-15mcg/kg/minAdrenaline (epinephrine): 0.05-1.0mcg/kg/min

163

Appendices

Appendix 9: Stages and Treatment of Tonic–Clonic Status Epilepticus

· Airway,Breathing,Circulation,Disability· Check blood glucose· Givethiamineorpyridoxineifappropriate

Pre-status:Aphaseofescalatingseizureslastinghours or days.

· BuccalMidazolam (5–10 mg) or oral Cloba-zam (10–20 mg/day)

Early status:Seizureor serial seizures lastingupto 30 min.UseoneofthefollowingIVbenzodiazepines.65%chanceofterminatingSE.

· Lorazepam (first choice): 2–4 mg; long duration of action, recurrent seizures less likely

· Midazolam: 0.05–0.2 mg/kg; short action, rapid metabolism, best choice for continuous benzo-diazepine infusion

NB.Dosesmayneedtobereducedintheelderly.Additionaltherapymustbestartedatthispointtoprevent further seizures.

Established status:30–60min

· Phenytoin15–20mg/kgIV@50mg/min,or· Fosphenytoin15–20mg/kgIV/IM@150mg/min

NBBothrequirecontinuousECGmonitoringIf seizures continue, additional phenytoin or fosphenytoin 5–10 mg/kg and check levels.Refractory status:Seizureslasting>1hSeveraloptions:ICUcarerequiredforventilatorysupport and invasive monitoringUsecontinuousEEGmonitoringifavailable

· 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 beadded (if phenytoin levels ok) Levetiracetam is gaining popularity as adjunctive therapy and is availableinbothoralIVpreparations.

NB:deepsedationisrecommendedforatleast12hbefore reducing and looking for evidence of seizure activity,ideallyusinganEEGforguidance.Ensureadequate levels of anticonvulsants for chronicseizure control. Hemodialysis may be helpful in cases of drug-induced status (especially antibiot-ics, theophylline).If seizures continue after a period of deep seda-tiondespiteadequateanticonvulsantdrug levels,additional agents such as Phenobarbital may be added.

165

Appendices

Appendix 10

Glasgow Outcome Score

GOS=1(GoodRecovery)

Capacity to resume normal occupational and social activities, although there may be minor physical or mental deficits or symptoms.

GOS=2(ModerateDisability)

Independent and can resume almost all activi-ties of daily living. Disabled to the extent that they cannot participate in a variety of social and work activities.

GOS=3(SevereDisability)

No longer capable of engaging in most previ-ous 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(PersistentVegetativeState)

Not aware of surroundings or purposely respon-sive to stimuli.

GOS=5(Dead)

Rankin Disability Score

Rankin=0Nosymptomsatall.

Rankin=1Nosignificantdisabilitydespitesymp-toms; able to carry out all usual duties and activities.

Rankin=2Slightdisability.Unabletocarryoutallnormal activities but able to look after own affairs without assistance.

Rankin=3 Moderate disability requiring somehelp but able to walk without assistance.

Rankin=4Moderatelyseveredisability.Unabletowalk without assistance, and unable to attend to own bodily needs without assis-tance.

Rankin=5 Severe disability. Bedridden, inconti-nent and requiring constant nursing care andattention.

167

Appendices

Appendix 11: Management of a Fall in GCS after Subarachnoid Haemorrhage

Withdraw SupportSee Editorial Note,

Chapter 4

Fall in GCS more than 2 points or 1 point in the motor score

1. Airway, Breathing, Circulation - safety first

2. Intubate and ventilate if GCS < 8

- Optimise oxygenation with PEEP

- Normalise PaCO2 (4.5-5.0kPa) unless “coning” where PaCO2 can be

reduced to 3.5-4.0kPa as a temporary measure only

3. Always check blood sugar

4. 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

5. Investigations: ECG, CXR, FBC, U&Es, Clotting, Mg2+

6. Once stable, CT brain scan

CT SCAN UNCHANGED -LIKELY CEREBRAL VASOSPASM

CT SCAN CHANGEDRe-bleed, Infarction, worsening

oedema, hydrocephalus

Contact Regional NeurosurgicalCentre

Transfer toRNC

Re-assess off sedation

Transfer toRNC

See Figure 4.5

Clinical Improvement

Ongoing DGH Management

Poor Clinical Condition

Definitive treatment of aneurysm at RNC after 14days if good neurological condition

169

Appendices

Appendix 12: Management of Vasospasm (NB Diagnosis of Exclusion)

171

AAcidosis, 107, 111Acinetobacter, 78Acute idiopathic axonal degeneration, 96Acute inflammatory demyelinating polyradiculopathy

(AIDP), 92Acute lung injury (ALI), 79, 80Acute motor axonal neuropathy (AMAN), 92Acute motor sensory axonal neuropathy (AMSAN), 92Adams, J.P., 19–30, 51–60, 77–85Adhesion molecules, 80Adrenal insufficiency, 83Alveolar–arterial (A–a) oxygen difference, 79Anemia, 85Angiography, cerebral, 105, 108, 109Anterior horn cell disease, 90Antibody, anti-ganglioside, 93Anti-epileptic drugs (AEDs)

barbiturates, 73carbamazepine, 72clobazam, 73, 74clonazepam, 73diazepam, 72fosphenytoin, 73lamotrigine, 71levetiracetam, 72, 73lorazepam, 72–74midazolam, 72, 73phenytoin, 72–75sodium valproate, 73

Apnea test, 110–111Arginine vasopressin, 84Autonomic disturbance, 91, 94, 95Autoregulation, 10, 12–14

BBarnes, L., 89–96Barotrauma, 78

Barré, 92Bell, D., 19–30Bell, M.D.D., 1–7, 137–144Biopsy, muscle, 91Bispectral analysis, 14–15Blood pressure, 80–82Botulism, 94–95Brain injury

hypoxic, 11management principles, 5

Brain natruiretic peptide (BNP), 84Brain edema, mechanisms, 4Brainstem death, 105–111

clinical testing, 109diagnosis, 106, 107

Brainstem death, pathophysiology, 113–115Brain tissue oxygenation, 10, 13, 16Burst suppression, 16

CCardiac enzymes, 81, 82Cardiac output, 80Catecholamines, 78, 82, 83Cerebral abscess, 43, 46–49Cerebral angiography, 79Cerebral blood flow (CBF), 10, 11, 13, 14, 37Cerebral blood volume, 5Cerebral function analyzing monitor (CFAM), 14Cerebral function monitor (CFM), 14Cerebral oxygen, 16

consumption, 3, 4, 7delivery, 3, 4, 6extraction, 12, 13

Cerebral perfusion pressure (CPP), 10–12, 14, 16Cerebral salt wasting syndrome (CSWS), 84Cerebral spinal fluid (CSF), 91, 93, 94, 96Cerebral vascular reactivity, 12, 14Cerebrospinal fluid, 5

Index

173

Index

Cervical spine injuryairway management, 52autonomic hyper-reflexia, 55–56awake fibre optic intubation, 52, 53Brown-Séquard syndrome, 55causes, 51central cord syndrome, 55clearing the cervical spine, 58diaphragm function, 53–54fluid balance, 58fractures, types, 56–58incomplete injury, 55infection, 59initial stabilisation, 52–58lung function, effect of level of injury on, 53lung volumes, 53, 54manual in line stabilisation (MILS), 52, 53neurogenic pulmonary edema, 53, 55neurogenic shock, 51, 55pressure sores, 54, 58, 59primary injury, 51, 52, 55radiology, 56respiratory care, 54sacral sparing, 55secondary injury, 51, 52, 55spinal shock, 55, 58stability, 56–59steroids, 58–59succinylcholine (suxamethonium), 52surgical management, 59temperature regulation, 59thromboprophylaxis, 59weaning, 54, 59

CK-MB, 82Clark, M., 97–103Clinical and logistical process, 5Clonidine, 81Clostridium botulinum, 94Clostridium tetani, 95CMRO2, 37Coagulation disorders, 85Compound action potential, 93, 94Compressed spectral array, 15Coning, 107Continuous aspiration of subglottic secretions

(CASS), 81Controlled donation after cardiac death

(DCD), 115Cooper, N., 69–75Cough assist device, 92Crisis

cholinergic, 95myasthenic, 92, 95

Critical illnessmyopathy, 96neuropathy, 96

CSF filtration, 94CT brain scan after head injury, indications, 6Cytokines, 78, 80

DDavies, S., 9–16Death, diagnosis, 117–118Demeclocycline, 84Denton, M., 43–49Diabetes insipidus (DI), 84, 107, 115Disseminated intravascular coagulopathy (DIC), 85Distal latency, 93Dobutamine, 83Donnan, G., 63Dopamine, 80Doppler shift, 13Doppler, transcranial, 109Dysrhythmias, 81, 82

EEchocardiography, 82, 83Edrophonium, 95Electroencephalography (EEG), 14–16, 71–75, 106Electrolyte disturbance, 116Electromyography (EMG), 90Encephalitis, 43, 46, 107Enterobacteriaceae, 78Epidural abscess, intracranial, 49Epilepsy surgery, 71Epinephrine, 80, 83Erythromycin, 91Esmolol, 37Esophageal doppler, 83Ethical issues, intensive care

capacity, 137–139elective ventilation, 141HIV testing, 141, 142hospital clinical ethics committees, 138Human Fertilization and Embryology Authority

(HFEA), 140Human Tissue Act, 141, 143independent mental capacity advocate (IMCA), 139life-sustaining medical treatment (LSMT), 138Mental Capacity Act, 137–139, 143needle-stick injuries, 143non-heart beating organ donation, 140, 143Organ Donor Register, 140, 142

Extra vascular lung water (EVLW), 79, 80, 83

FFeely, M., 69–75Fieschi, C., 63Fludrocortisone, 84Fourier analysis, 15

GGlasgow coma scale (GCS), 9, 11, 15Goddard, T., 121–135Guillain, 92Guillain Barré syndrome (GBS), 92, 93

174

Index

HHacke, W., 63Haemophilus influenzae, 78Hassan, A., 61–66Herpes simplex encephalitis, 71Holbrook, S.P., 33–41Horner’s syndrome, 9Hui, A., 73Hydralazine, 83Hydrocephalus, 11, 107Hyperemia, 10, 12, 13Hypernatraemia, 84, 116Hypertension, intracranial, 107, 108, 114Hypertonic saline, 84Hypoglycemia, 107Hypokalemia, 85Hypomagnesemia, 36Hyponatremia, 38, 83, 84, 107Hypothalamic stress, 82Hypothermia, 106, 107, 116Hypoxic brain injury, 72, 73, 107Hypoxic pulmonary vasoconstriction, 90

IImmunoglobulin therapy, 94Insulin, 116International subarachnoid aneurysm trial (ISAT), 41Intoxication, drug, 108–109Intracranial pressure, 3–5

measurement, 11monitoring, 10waveforms, 11–12

Ischemia, brainstem, 106–108, 115

JJugular venous oximetry (SjvO2), 10, 12, 13, 16

LLabetalol, 37, 82Lactate oxygen index, 13Left ventricular stroke work index (LVSWI), 80, 83Lindley, A., 9–16Lorazepam, 101Lundberg waves, 11

MMagnesium, 80Magnesium sulfate, 95Major tranquilisers, 101–103Malignant middle cerebral artery infarction

decompressive craniectomy, 65, 66Mankad, K., 121–135Mannitol, indications, 6Marmarou, A., 10McKinlay, J., 51–60, 97–103

Medical complications, 77, 78Medulla oblongata, 105, 107, 109Meningitis, 107Meningitis, bacterial

activated protein C, 45causes, 44clinical feature, 44complication, 45–46CSF analysis, 45–46definition, 43early goal directed therapy, 45epidemiology, 43investigations, 44meningitis with sepsis, 44outcome, 46pathology, 44steroids, 45treatment, 44

Methylprednisolone, 116Metoclopramide, 91Midazolam, 99, 101Midbrain, 109, 110Miller Fisher syndrome, 92Milrinone, 80, 83Miosis, 9Multimodal monitoring, 16Murphy, P.G., 105–111, 113–118Myasthenia gravis, 95Myocardial ischemia, 113Myocardial stunning, 77, 83Myoclonic jerks, 70, 71, 73Myopathy, 96

NNear infrared spectroscopy (NIRS), 16Neurogenic pulmonary edema (NPE), 36, 38, 41,

77–79, 115Neuroleptic agents, 101Neuromuscular paralytic syndrome, 92Nicotine, 101, 103Nitroprusside, 83Non-epileptic attack disorder (NEAD), 69, 71, 73, 75Non-neurological organ failure, 77Noradrenaline (norepinephrine), 116Norepinephrine, 80Nucleotide ventriculography, 83Nutrition, 91Nystagmus, 109

OOlanzapine, 101Organ donation, consent, 116–117Organ donor

management, 116, 117optimisation, 117

Organophosphate poisoning, 96Oxygen delivery, 10, 12, 13, 16

175

Index

PPatient transfer, indications, 3Persistent vegetative state, 98Phenoxybenzamine, 80Phentolamine, 80Phenytoin, 84Plasma exchange (plasmapheresis), 93–95Post-ictal slowing, 71Pralidoxime, 96Pressure reactivity index, 12Pressure sore, 92Prokinetics, 91Prone position, 81Propofol, 99, 102Propranolol, 80Pseudomonas aeruginosa, 78Ptosis, partial, 89Pulmonary artery catheter, 116Pulmonary aspiration, 78Pulmonary capillary wedge pressure (PCWP), 80Pulmonary edema, 79–80Pulmonary micro embolism, 78Pulmonary vascular resistance, 80Pulsatility index (PI), 14Pulse contour analysis, 80, 83Pyridostigmine, 95

QQuinn, A.C., 33–42

RReflex

brainstem, 109–110cold caloric vesibulo-ocular, 110cough, 110deep central pain, 110gag, 110pupillary light, 110

Regional Neurosurgical Centre, role, 2, 5Remifentanil, 99, 102Respiratory dysfunction, 77, 78, 80, 81Respiratory failure, 78, 113Reticular activating system, 97Reticular formation, 109Risperidone, 101Risus sardonicus, 95Rogers, F.B., 79

SSecondary cerebral insults

intracranial causes, 3systemic causes, 3

Seizurescauses

alcohol withdrawal, 69, 70, 72arteriovenous malformations, 71

drugs, 71–73, 75hyperosmolar non-ketotic hyperglycemia, 74mesial temporal sclerosis, 71neurosurgery, 69, 74–75traumatic brain injury, 71

prolactin levels, 75provoked, 70, 71, 75provoking factors, 69, 75types

complex partial, 70idiopathic generalized, 70juvenile myoclonic epilepsy, 70location-related epilepsy, 70, 71provoked seizures, 70refractory epilepsy, 71simple partial, 70

Short synacthen test, 83Simmons, R.L., 79Spectral edge frequency, 15Spinal immobilisation, complications, 58Staphylococcal aureus, 78Status epilepticus

complications, 72, 74mortality, 72treatment, 72–74types

focal motor, 71, 74non-convulsive, 72, 74tonic-clonic, 71, 73, 74

Streptococcus pneumoniae, 78Stress ulceration, 85Stress ulcer, prophylaxis, 91Strohl, 92Stroke, acute ischaemic

anticoagulation, 66basilar artery occlusion, 64, 65blood pressure management, 64complications, 62glycemic control, 62neuroprotection, 62, 65pathophysiology, 61–62scoring systems, 66secondary prevention, 65–66stabilisation, 62, 65stroke recurrence, 66stroke units, 62thrombolysis

intra-arterial, 63–65systemic, 62–63

Stroke, ischaemic, 107Stunned myocardium, 83Subarachnoid hemorrhage (SAH), 14, 15, 77–82, 84Subarachnoid hemorrhage, aneurismal

analgesia, 37blood pressure management, 37causes, 34complications, 38–41CT angiography, 34, 35delayed ischemic deficit (DID), 33, 34, 37–40

176

Index

diagnosis, 34digital subtraction angiography (DSA), 34, 35fluid management, 37–38incidence, 33induction of anesthesia, 36lumbar puncture, 34, 36management, 33–42monitoring, 36morbidity, 33–34mortality, 33–34nimodipine, 37osmotherapy, 38presentation, 34sedation, 36, 37, 41sedation holds, 38statins, 40thromboprophylaxis, 38“Triple H” therapy, 38WFNS scale, 34

Subdural empyema, 46, 48–49Subendocardial ischemia, 81Succinylcholine, 91, 95Surfactant, 78Swallowing assessment, 89Syndrome of inappropriate antidiuretic hormone

secretion (SIADH), 84, 93

TTako-tsubo cardiomyopathy, 83Tensilon test, 95Tetanospasmin, 95Tetracyclic antidepressants, 101Thallium scanning, 83Thiamine, 72, 73Thrombocytosis, 85Thromboembolism, venous, 91Timothy, J., 51–60Torsades de pointes, 101Transcranial doppler ultrasound, 13Transmural pressure, 36Traumatic brain injury, 10, 16, 108

antibiotic therapy, 26cerebral oxygen delivery, 20, 22–23, 27cerebral oxygen demand, 20–22, 27cerebral perfusion pressure (CPP), 20, 22, 23, 27cerebrospinal fluid, 23–26contusional injuries, 25decompressive craniectomy, 20, 23, 27dopamine, 23haematoma, 25hypertonic saline (HSL), 25hyperventilation, 20, 25hypothermia, 21–23

intracranial pressure (ICP), 20–29jugular venous oximetry, 21, 23, 27lactate oxygen index (LOI), 23, 26loop diuretics, 24–26lund approach, 22mannitol, 20, 25, 26Monro–Kellie doctrine, 19norepinephrine (noradrenaline), 23osmotherapy, 25pathogenesis, 19–26phenylephrine, 23recombinant Factor VIIa (rFVIIa), 23Regional Neurosurgical Centre (RNC), 20, 21,

25, 27, 30sedation, 20, 21, 25, 27, 29seizures, 20steroids, 26thiopental (thiopentone), 21, 22, 25, 26, 29thromboprophylaxis, 26vasopressin, 23

Traumatic brain injury (TBI), 77, 84, 85Trazadone, 101Triiodothyronine (T3), 116Triple H therapy, 79Troponin I, 82

UUpper motor neuron disorders, 89

VVasogenic edema, 10Vasopressin, 83, 84, 116Vasospasm, 13–15, 77, 78, 80, 82Ventilator-associated pneumonia (VAP), 78, 81, 114Ventilatory failure, 90Ventricular dysfunction, 83Ventriculitis, 43, 48, 49Volutrauma, 78Vucevic, M., 89–96

WWalker, A., 43–49Water and electrolyte disturbance, 83–85Weakness

acute, 89–96neuromuscular, 92

Withdrawal of therapy, 116–117

ZZygun, D.A., 78

177