Location: A block (mostly A4) and outliers throughout the medical wards (uncommon)

Other places: neurophysiology (A block 3rd floor next to SHO office)- for telemetry/EEG and electrophysiology tests Neuroradiology seminar room (ask SpRs for location as it is difficult to describe) for meetings on Friday at 1:30.

Team members: The team is organised by firm (in turn organised by subspecialty) with one registrar per ferm. The SHO covers all the firms. They are as follows: Firm 1 Cognitive/Movement disorders/General neurology. NHS: Worth, Brown, Buttery, Graham; Academic: Barker, Rowe, Chan. Firm 2 (Neuroinflammation, General) NHS: Thorpe, Molyneux, Cox; Academic: Compston, Sawcer, Coles, Jones, Pluchino, Zandi. Firm 3 Epilepsy, Headache, General. NHS: Manford, Mitchell, Crawley, Phillips, Anderson; Academic: Reddy. Firm 4 (Stroke, Neuromuscular, NCCU) NHS: Martin, Brierley, Hensiek, Damian, Graves, Alawneh; Academic: Markus, Roberts.

The registrars rotate between firms every few months but the consultants remain the same.

Specialist nurses: Libbi and Harri, who help with liaising with family, procedures (LP), arranging scans and cognitive assessments amongst other things

Consultant ward rounds twice/week: -Monday 10am and Thursday 2pm for neuroinflammatory team -Tuesday afternoon and Friday afternoon for all teams

Other activities: Teaching clinic on Wednesdays from 1:30 (or 2pm) in R3. You are permitted to attend and although it is not bleep-free, the registrars are discouraged from bleeping you then, according to consultants (none of them have clinics at the same time so the ward should be covered)

Handover 8am in SHO office. Check bloods and prepare ward lists Neurology team handover at 9am on ward A4 During the day: Urgent discharges and jobs from the handover. Possibly a ward round or two (there are 4 teams). Do jobs generated from the ward rounds (the registrars will typically find you / bleep you to tell you about these. Make sure you get to go to the scheduled Wednesday afternoon clinic! End of day: check all the neurology patients have been seen and see any patients who have been missed.

THE FOLLOWING NEUROLOGICAL EMERGENCIES ARE DISCUSSED

1. ACUTE/SUBACUTE NEUROMUSCULAR FAILURE (INCLUDING GUILLAIN BARRE AND MYASTHENIA) 2. STATUS EPILEPTICUS 3. COMA 4. ENCEPHALITIS 5. ACUTE RELAPSE OF MS 6. ADULT BACTERIAL MENINGITIS 7. STROKE 8. SUBARACHNOID HAEMORRHAGE 9. ACUTE COMPRESSION OF THE SPINAL CORD OR CAUDA EQUINA

1. ACUTE/SUBACUTE NEUROMUSCULAR FAILURE (INCLUDING MYASTHENIA AND GUILLAIN BARRE)

What are the key features?

Progressive facial, limb and truncal weakness Dysphagia and dysarthria Breathlessness and orthopnea

These symptoms may fluctuate

What are the causes?

The commonest cause is Guillain Barre. Other “common causes” include myasthenia gravis and motor neuron disease. Rarer causes include myotonic dystrophy, polymyositis, muscular dystrophy, acute brainstem or upper cervical cord disease and botulism. Wound botulism occurs in intramuscular drug abusers.

How should I assess the patient initially?

You need to do basic resuscitation assessing the airway, breathing and circulation. The next crucial assessments are of respiratory function and swallowing.

How do I assess respiratory function?

Patients with neuromuscular causes of respiratory compromise often have NO respiratory symptoms. They can look well and then arrest. Clinical assessment is crucial and the following features indicate a high likelihood of respiratory problems: Breathlessness Speaking in short phrases Orthopnea Poor Cough Weak face and neck

The most important investigation is Vital Capacity (measured with a spirometer). The vital capacity should be measured 2 hourly until the pattern is clear. A face mask is needed to measure vital capacity in patients with facial weakness.

All other common methods of assessing respiratory function are very insensitive to neuromuscular failure. Hypoxia or hypercapnia in the blood gases or low peak flow are signs of impending respiratory arrest in a patient with neuromusular respiratory failure. Patients with these features ought to be on ITU.

Only the vital capacity gives an adequate warning that the patient is in need of respiratory support.

What vital capacity do I worry about?

Any vital capacity under 1.5 litres warrants an immediate anesthetic opinion with a view to ITU transfer. A patient with a steadily deteriorating vital capacity should be assessed by an anesthetist once their vital capacity drops to 2.0 litres. Any patient with a rapidly falling vital capacity should see an anesthetist.

How do I assess swallowing?

Choking, coughing or cyanosis on swallowing are all important features of aspiration. Aspiration can also occur silently. Examine the swallow, gag reflex and look for pooling of saliva. An ability to give a good cough is reassuring. If there is doubt over swallowing the patient should be nil by mouth and if appropriate a NG tube inserted and a speech therapy assessment arranged. Any patient with acute dysarthria is likely to have swallowing problems.

What tests should I consider?

Creatinine kinase, autoantibody screen, ANCA,anti-acetyl choline receptor antibodies, thyroid function, electrolytes, glucose, magnesium and calcium. Chest Xray Screen for infection Blood Gases

Others tests such as lumbar puncture, Craniocervical MRI, Neurophysiology, tensilon test may well be appropriate after appropriate discussion.

How do I manage Neuromuscular failure?

Once the patient has been assessed and respiratory and swallowing are monitored then it is sensible to seek advice from a senior colleague who may well want to discuss matters with the neurology team. Conditions such as myasthenia and Guillain Barre respond well to immunotherapy but the top priority is supportive care.

2. STATUS EPILEPTICUS

What is status epilepticus?

A seizure or series of seizures lasting at least 30 minutes without recovery

How do I assess the patient?

You need to secure the airway and give oxygen. Check the breathing and circulation. If the jaw is clenched then do not intubate. Check blood glucose, calcium, U&Es. Take blood for toxicology and baseline anticonvulsant drug levels.

What treatment do I start immediately?

Give 50 mls of 20% intravenous glucose solution if the blood sugar level is low/unknown

Then give 4mg of lorazepam intravenously.

There is a risk of respiratory depression with lorazepam

Give parenteral thiamine (eg pabrinex) if you suspect alcohol abuse

There is a risk of anaphylaxis with parenteral thiamine

What if the seizures continue?

If the patient is still fitting 10 minutes later then give a further 4mg intravenous lorazepam.

There is a risk of respiratory depression with lorazepam

What if the seizures continue?

If the patient is still fitting 10 minutes after the second dose of lorazepam load with phenytoin by slow intravenous infusion at a dose of 15mg/kg at a rate of 100mg/min. Use BNF guidelines including cardiac monitoring.

There is a risk of arrhythmia with phenytoin

What if the seizures continue?

Arrange transfer of the patient to ITU and administer phenobarbitone 15mg/kg iv or anesthetise with propofol or with thiopentone. Liaise with Neurology team locally or at Addenbrooke's.

What should I do once the patient is on ITU?

Continue the medication started - e.g. phenytoin 100mg tds. Monitor drug levels and aim to stabilize them in the upper therapeutic range Seek a cause of the status. Regularly assess patient’s neurological and medical condition preferably including EEG or other cerebral function monitoring. Contact relatives or the GP for further details of the history Paralyzed patients may continue to have seizures with no physical signs.

Liaise with neurology team .

What investigations should I arrange?

It is of crucial importance to establish the cause of status. If the patient has no history of seizures then it is highly likely that there is an underlying treatable cause. These would include encephalitis, meningitis and other intracranial infections, trauma, venous thrombosis, haemorrhage, tumour, alcohol/drug use or abuse, metabolic disturbances. These causes need to be actively sought with appropriate investigations – urgent cranial imaging, bloods, followed by lumbar puncture if appropriate and advice sought.

Patients with established epilepsy may have any of the above causes for status. Status is very unusual in patients with well controlled epilepsy. Other causes in patients with known epilepsy will include drug withdrawal and poor compliance.

Can I use phenobarbital as an alternative to phenytoin?

Yes, phenobarbital is a useful alternative, particularly for patients already on phenytoin or who are allergic to phenytoin. Phenobarbital is given slowly (100mg/min) intravenously at a dose of 15 mg/kg.

There is a risk of respiratory depression with phenobarbital.

Phenobarbital is essentially the same drug as thiopentone and therefore propofol should generally be used as the anesthetic agent if required.

Are there alternatives to Lorazepam?

Intavenous lorazepam 4mg is the best choice for status in hospital but if there is a delay in obtaining lorazepam then iv 10mg diazemuls (or buccal midazolam 10mg) can be used. Rectal diazepam (stesolid) 10mg is very useful out of hospital to prevent further seizures

What about non epileptic status?

A proportion of patients with apparent status will be having non-epileptic (pseudo-)seizures. These patients need to be assessed and discussed on an individual basis. Important information to gather includes: vital signs and physical examination, blood gases and oximetry (acidosis and hypoxia indicate organic disease), urgent EEG. If you strongly suspect pseudoseizures then you should involve the neurology team early.

If in doubt treat as genuine status epilepticus.

3. COMA (DEFINED AS GLASGOW COMA SCALE ≤ 8)

What are the common causes of coma?

Drugs (prescribed, illegal and overdoses), intracranial haemorrhage, trauma, brainstem and major hemispheric strokes, meningitis, encephalitis, metabolic diseases (respiratory, liver or renal failure, hypoglycaemia), epileptic seizures, venous sinus thrombosis.

How do I assess the patient initially?

The first priorities are airway, breathing and circulation. A bmstix and blood glucose should be done. A history obtained from ambulance crew or relatives. The patient needs a medical and neurological assessment. There are very often clues to the diagnosis: stiff neck, papilloedema, needlestick scars, pinpoint pupils, ketotic or alcoholic breath, purpuric rash etc.

What treatment do I start immediately?

Give intravenous thiamine if you suspect alcohol abuse Give 50 mls of 20% intravenous glucose solution into a large vein if there is hypoglycaemia (or blood glucose unknown). Give naloxone for opiate overdose, give flumazenil for benzodiazepine overdose Start treatment if appropriate for other drug overdoses such as paracetamol according to local protocols

If you suspect CNS infection then take blood cultures and give intravenous ceftriaxone 2gm plus aciclovir 10mg/kg.

If in doubt then start treatment.

What investigations should I order?

Investigations should generally include:

Blood sugar, electrolytes, liver function, calcium, FBC, ESR, paracetamol/salicyate levels, toxicology screen, arterial blood gases, blood cultures CXR

If there are neurological signs or the diagnosis is unclear then the patient needs an urgent CT brain scan. If the scan is normal, the diagnosis remains unclear and the patient is not recovering, then adult patients should normally have a lumbar puncture (see sheet 4 encephalitis for CSF tests). It is important to record the CSF pressure and take 5-10 mls of CSF.

Children under the age of 18 should be assessed by a paediatrician who should advise on lumbar puncture.

What if the diagnosis remains unclear?

Discuss with senior colleague, then neurology team. Foreign travel, immunodeficiency and medical history will alter the differential diagnosis.

4. ENCEPHALITIS

What are the key features of encephalitis?

Altered state of awareness – from mild disorientation to coma Fever Seizures

If any of these are present then encephalitis should be considered; it can present with acute/subacute disorientation without other features.

There are many other causes of these symptoms to be considered as well.

What are the causes of encephalitis?

Herpes simplex is the classical cause but only accounts for a minority of cases. Many other viruses can also cause encephalitis. If there has been travel abroad there are a large number of other viral encephalitides and always remember malaria. An immunosuppressed patient can have other viral, bacterial or fungal causes.

Encephalitis also occurs with bacterial infections, TB, listeria and atypical infections such as Legionnaire’s disease. It can be mimicked by neurosurgical emergencies such as cerebral abscess or subdural empyaema and other neurological diseases such as venous stroke, meningitis and subclinical seizures.

Encephalitis is rare and help needs to be sought promptly from the neurology and infectious diseases teams.

The differential diagnosis of fever, seizures and altered awareness is very wide and includes metabolic and autoimmune diseases.

Added by Claire McCarthy Dec14- consider autoimmune encephalitis if patient has features of encephalitis plus a movement disorder e.g. posturing, rhythmical facial movements etc. In anti-NMDAR Ab cases urgent administration of steroids and identification and removal of ovarian teratoma is crucial, discuss with neurology SpR/consultant.

What are the signs I should look for in encephalitis?

The commonest is fever. Patients may be mildly disorientated with no other signs or may have a hemianopia, hemiplegia or other focal signs.

What tests should I order?

Tests should include: FBC, ESR, Electrolytes, glucose, liver function tests, autoantibody screen, viral titres, CXR, blood cultures. Added by Claire McCarthy Dec14- consider anti-NMDAR Ab, VGKChAb and anti-TPO antibodies. If anti-NMDAR Ab suspected urgent transvaginal USS to detect ovarian teratoma.

Patients with suspected encephalitis must have an urgent brain scan preferably a MRI. If this shows no contraindication to lumbar puncture and the patient is over 18 this should be followed by a lumbar puncture. Children under the age of 18 should be assessed by a paediatrician who should advise concerning lumbar puncture.

What tests should I ask for from the Lumbar puncture?

First measure the pressure. Second take an adequate sample 5-10 mls in total in 3 bottles plus glucose and blood glucose. Ask for microscopy, staining, culture and sensitivies, glucose, protein, PCR for Herpes Simple, Zoster, and Enterovirus. Many other tests may be approproiate – looking for AAFBs, cryptococcal Ag etc. Added by Claire McCarthy Dec14- consider CSF anti-NMDAR Ab testing.

What treatment should I start if I suspect encephalitis?

The normal starting regime is intravenous Aciclovir 10mg/kg tds and Ceftriaxone 2 gm bd and amoxycillin 2g 4 hourly. If in doubt start treatment.

The differential diagnosis is very wide and if there are unusual features such as: immunodeficiency, HIV infection, or foreign travel it is imperative to seek advice from microbiology and/or the infectious disease team.

Which investigations help?

Many investigations may be needed, extensive serological tests are often justified and it is important to consider vasculitis, autoimmune (limbic and Hashimoto’s) and paraneoplastic causes.

A large majority of patients with acute encephalitis have:

Abnormalities on MRI scan – swelling and high signal in the temporal lobes A mild increase in white cells in the CSF- 10-300 lymphocytes would be typical. The protein is usually raised the glucose may be mildly reduced. Typical changes on an EEG.

If these tests are negative the diagnosis of encephalitis is not excluded and treatment should be continued but alternative diagnoses need to be sought.

5. ACUTE RELAPSE OF MULTIPLE SCLEROSIS

Which patients with MS relapses need steroids?

Patients with acute relapses which are causing significant disability. These include:

Acute brainstem relapse particularly those involving speech, swallowing or respiration (the 3 tend to go together). Acute motor relapse causing disability Optic neuritis leading to bilateral visual impairment (eg patients with 1 good eye which becomes affected) Optic neuritis with prominent retro orbital pain or with visual acuity less than 6/24. Marked proprioceptive loss in an upper limb

The more acute the relapse, the more likely the patient is to respond to steroids. Mild symptoms do not need steroid treatment.

What tests should I order?

Screen for infection by history, examination and urinalysis.

Urgent neuroimaging is indicated if there is doubt over the diagnosis of MS or the episode.

If infection is suspected then it is usual to start treatment for this first and re-assess the need for steroids according to the urgency of the clinical problem and the response to antibiotics.

How do I give the steroids?

In hospital give 1 gram of methyl prednisolone in 100mls of normal saline over 1 hour for 3 successive days. Outpatients can have oral methyl prednisolone 500mg daily for 5 days.

How do I recognize a patient with a brainstem relapse?

MS patients with acute onset of speech disturbance, swallowing problems, breathing problems, diplopia or vertigo are likely to have a brainstem relapse.

How do I assess a patient with a brainstem relapse?

The assessment of speech, breathing and swallowing is crucial. Please refer to sheet 1 on neuromuscular failure.

Occasionally patients with acute brainstem relapses need to be treated in intensive care because of respiratory problems. Alternative causes of neuromuscular failure or brainstem diseases must be considered in patients with MS.

6. ADULT BACTERIAL MENINGITIS

Please refer to local protocols if these are available.

What are the typical features of bacterial meningitis?

Photophobia, fever, headache, reduced conscious level, stiff neck, purpuric rash. It can be difficult to distinguish viral and bacterial meningitis. Investigations are necessary but must not delay empirical treatment.

What is the initial management in an adult?

1. Assess airways, breathing and circulation and resuscitate. 2. Full neurological and general examination and otoscopy 3. Insert intravenous cannula take blood cultures, FBC, CRP, clotting, U&Es, glucose. 4. 10mg dexamethasone should be given with the first dose of 2gms of intravenous ceftriaxone. 5. local microbiological advice should be sought. The usual regime is dexamethasone 10mg every 6 hours for the next 4 days. Plus ceftriaxone 2g bd. 6. Patients who are or may be immunocompromised or have traveled abroad have a wide differential diagnosis and treatment should be discussed with the relevant infectious disease/microbiology team. Listeria needs to be considered in pregnancy and older patients. If there is doubt whether the patient could have encephalitis then treat for this as well. 6. Organize urgent CT of brain.

Should I perform a lumbar puncture in an adult?

Lumbar puncture carries a small risk in meningitis but provides valuable information (even in a patient on treatment). A lumbar puncture should generally be performed on all adults once it is considered safe (clotting problems are relative contraindications).

How do I assess the safety of lumbar puncture?

Some physicians are happy to order an LP in a fully alert, orientated and immunocompetent patient with no focal signs or papilloedema without imaging and this is reasonable practice.

In a patient with a depressed level of consciousness, papilloedema or focal signs a CT scan must be performed first, this must not delay treatment. If the CT scan is normal and the patient is over 18 years of age then the benefits of LP generally outweigh the small risks.

Children under the age of 18 should be assessed by a paediatrician who should advise concerning lumbar puncture.

If the CT is abnormal then neurological or neurosurgical advice should be sought prior to LP.

What tests should I ask for from the Lumbar puncture?

First measure the opening pressure. Second take an adequate sample 10 mls in total in 3 bottles plus glucose and blood glucose. Ask for microscopy, staining, bacterial culture and sensitivies, glucose, protein, PCR for Herpes Simplex and Zoster and Enterovirus, TB and Bacterial pathogens, viral titres. Many other tests may be appropriate – looking for AAFBs, cryptococcal Ag etc if results are hard to interpret (eg if pretreated with antibiotics) please discuss with infectious diseases team at Addenbrooke’s

Should the patient be isolated?

A patient who has suspected meningitis should be regarded as potentially infectious and nursed in a single room. If the patient has a purpuric rash, or the working diagnosis is meningoccal meningitis all staff who enter the room should wear a face mask.

7. STROKE

The Addenbrooke’s stroke guidelines have now been withdrawn following the publication of comprehensive guidelines from NICE available at www.nice.org.uk

8. SUBARACHNOID HAEMORRHAGE

What are the typical clinical features of subarachnoid haemorrhage?

Typically patients have a sudden onset of a severe generalized headache. The headache is usually maximal at or near onset and is usually associated with vomiting, collapse and neck stiffness. Subarachnoid haemorrhage can also present with acute confusion,coma or a focal deficit without a clear history of headache, particularly in the elderly.

What is the initial management of subarachnoid haemorrhage?

The patient should have their airway, circulation and breathing assessed and be resuscitated if necessary. The patient needs a neurological examination and careful documentation of conscious level (with the Glasgow Coma Scale) or orientation. Neurological observations should be started. The patient needs an urgent CT scan. If this confirms the diagnosis then they need neurosurgical referral. Equivocal scans should also be discussed with the Neurosurgeons. Patients with a subarachnoid haemorrhage diagnosed on CT do not need a LP. If the CT scan is normal the patient should have a lumbar puncture which should include measurement of the pressure, taking adequate samples (>2mls) in at least 3 bottles and sending the samples for micorobiological analysis, cell counts and xanthochromia. It is crucial that the samples are analyzed without delay and sphectrometry for xanthochromia requested. Xanthochromia appears 6 hours after the ictus and lasts for up to 3 weeks. The lumbar puncture may need to be delayed for at least 6 hours after the ictus. If the sample is blood stained cell counts should be performed on all 3 bottles and one sample spun down immediately for xanthochromia. Even if you suspect a bloody tap the patient should be discussed with the neurosurgeons.

What treatment should I start?

Management needs to be guided by the Addenbrooke’s neurosurgical team who should be contacted immediately

1. Nimodipine should be started orally 60mg every 4 hours 2. If the blood pressure is raised, discuss with neurosurgeons. 3. Start normal saline 2-3 litres over 24 hours. 4. Use adequate codeine phosphate to control pain.

What should I do if the patient deteriorates?

There are a number of common complications of SAH re-bleeding, hydrocephalus and arterial spasm. Generally an urgent CT head scan is needed to distinguish these possibilities and neurosurgical advice sought.

9. ACUTE COMPRESSION OF THE SPINAL CORD OR CAUDA EQUINA

What are the key features?

Weakness of the limbs Sensory loss in the limbs Urinary urgency, painless urinary retention Constipation Back or neck pain

Not all patients with acute cord compression will have all the above features eg it may be painless

Bladder involvement necessitates immediate imaging

In cauda equina compression, the legs and sphincters will be affected with features that can include footdrop, sacral numbness and lower motor neurone features In spinal cord compression the arms as well as legs may be affected with upper motor neurone features. In the acute stage there may be hypotonia and absent reflexes. In cervical cord disease there may be upper or lower motor neuron features.

What are the common causes?

Spondylosis Disc herniation Bony metastases Primary tumours Epidural haematoma or abscesses Trauma A fall may precipitate cord compression particularly in the elderly with cervical spondylosis Guillain Barre syndrome can be hard to distinguish from acute cord compression

How should I assess the patient initially?

A full neurological history and examination is essential. There will usually be clinical features to help localize the lesion: Eg severe lumbar pain, sciatica and absent ankle jerks suggests cauda equina compression Thoracic pain, spared arms and a sensory level at T6 suggests thoracic cord disease

What investigations should I order?

Spinal cord imaging is the essential step. MRI is the best and the patient needs to be discussed immediately with the on call radiologist. If cord compression is suspected and imaging is not available locally (or the patient is unsuitable for MRI eg has a pacemaker) then the patient needs to be discussed immediately with the on call neurosurgeon or neurologist at Addenbrooke’s.

It is essential that all relevant parts of the spine are imaged, if in any doubt the whole spine should be imaged. If the patient is quadriplegic then any single spinal lesion must be in the cervical cord. But a spastic paraparesis can be caused by a spinal lesion anywhere from the foramen magnum to the bottom of the conus (or bilateral cranial lesions) and it is a mistake to ask for imaging only of the lumbar spine.

Other investigations may be very helpful including CXR, clotting (urgent if the patient is on anticoagulants), plain spinal films, ESR, Calcium and B12 but none of these takes the place of MRI..

How do I treat cord compression?

If a compressive lesion is found surgical intervention or radiotherapy is the essential step. Dexamethasone 4mg qds should usually be given in the meantime.

In certain circumstances where the suspicion of malignant compression is high then steroids may be given pre-imaging with senior advice. If there is any suspicion of B12 deficiency then parenteral B12 should be given.

CSF collection Epic orders: • CSF culture (includes microscopy and routine bacterial culture; TB culture needs to be specified) – single white universal container • CSF protein, CSF oligoclonal bands – single white universal container • Serum oligoclonal bands – brown serum tube, label using the ‘CSF oligoclonal bands’ sticker (lab automatically process CSF oligoclonal bands from the CSF protein tube) • CSF glucose/CSF lactate – yellow fluoride tube. Lactate should be sent on ice • Plasma glucose/plasma lactate – yellow fluoride tube (note there is also an Epic order for serum glucose, collected in a brown serum tube). Lactate should be sent on ice • CSF spectophotometry – single white universal container (protect from light) • CSF cytology – request in Epic under ‘Diagnostic cytology’, ideally obtain 20ml CSF in white universal container. • CSF flow cytometry – request under ‘CSF (haematology)’, specify that the sample is for flow cytometry, mark for the attention of the HODS lab

Out-of-hours CSF sample processing: Leave CSF culture sample in the incubator (which is switched off) on 6th floor of pathology department. Cytology sample in the fridge on 6th floor of pathology department. Biochemistry samples to 4th floor pathology reception. Flow cytometry sample to haematology/transfusion reception on 3rd floor.

Suspected CJD: Special protocols for CSF sampling from patients with suspected CJD. Contact MRC Prion Unit in Edinburgh (they deal with surveillance/epidemiology)

Intravenous immunoglobulin (IVIg) • Need patient height and weight • Consent (paper form) – thrombotic risk, blood product risks, infusion reactions, risk of renal impairment • Ensure pharmacological VTE prophylaxis prescribed as increased DVT/PE risk • Order from pharmacy using paper form on Connect • Brand of IVIg used is Privigen. Standard dose 0.4g/kg for 5 days (total dose 2g/kg). Formula for dose-determining body weight is available on the IVIg requisition form (available on Connect) • Prescribe on Epic as a linked order (e.g. for a patient receiving 25g IVIg per day, prescribe 20g bottle ‘followed by’ 5g bottle). Note that IVIg orders can expire on Epic – keep a record of when IVIg started and how much was received each day until this is resolved. • If the plan is for recurrent treatment, you can request the IVIG as part of a therapy plan on EPIC.

IVIg authorization – need to email IVIg panel for approval ivig@addenbrookes.nhs.uk (unless red indication i.e. GBS) or pre-signed prescription for elective patients, and liaise with pharmacy. Do not forget the VTE assessment (IVIG predisposes to thrombosis)

Plasma exchange (PLEX) • Consent (paper form) – line-associated risks, clotting derangements, hypocalcaemia, blood product used (albumin), blood pressure fluctuations • Pre-PLEX bloods – include coagulation screen (APTT, PT; also monitor fibrinogen while on PLEX), G&S, FBC, U&E, relevant autoantibodies • Limbic encephalitis patients may need baseline Addenbrooke’s Cognitive Examination-III (download from internet) • Apheresis line (Niagara line) - request ‘Inpatient referral to adult vascular access’ on Epic and discuss on x6020 • Refer to plasma exchange team – request ‘Inpatient referral to plasma exchange service’ on Epic and discuss on bleep 152 428/x56272 • PLEX team will advise on need for FFP transfusion – under ‘order sets’ on Epic (Adult Blood Component Request and Adult Blood Transfusion Request) • Patients usually have 5 days of PLEX; apheresis line can be removed by nursing staff on the ward when clotting is normal (watch out as bloods often taken from the heparinized lumen). Patients often discharged over the weekend (prepare a TTO in advance and instruct nurses abolut line removal)

(Taken from SHO induction document for neurology)

As the Neurology SHO you will be timetabled to start at 8am. Neurology paper-round is not until 9am. How to make the most effective use of this 1 hour? 1) Print the patient list (make sure the consultant which the patient is under is on the list, and whether VTE is complete. Clinical details are not necessary as the Registrars all know the patients). 2) Clerk in any CAMPATH, RITUXIMAB patients who are attending for day infusions on A3. 3) Complete any urgent TTOs. If you make sure all of the above are done, the rest of the working day will become a lot more manageable, as you will be bleeped/texted to do jobs for patients ad-hoc!

Some antibody tests are processed in Oxford (John Radcliffe)- immunology department reachable via their switchboard (number can be obtained from Addies Switchboard). The common tests affected by this are: NMDAR, Gly, GABA and VGKC/ subtype antibodies.

Even if a referring hospital claims these have already been sent, send your own tests. The results can either get lost, or the lab may refuse to release them to someone who was not the original requester (though they can be persuaded).

In patients with neuroinflammatory conditions (GBS, CIDP, ADEM, autoimmune encephalitis), save a few brown bottles of serum for future tests. Treatment with IVIG or PLEX invalidates many of the immunology tests you could request afterwards so pre-treatment samples are essential. The lab has a nasty habit of misplacing them unless you hand-deliver them and specifically ask for them to be stored (this is again not fool-proof, but the lab staff are generally very willing to help)

As there are only two neurology SHOs and one is nearly always on annual leave or nights, there is effectively only one neurology SHO for a large proportion of the rotation. This makes it very difficult to get study leave or time off as the policy is for there always to be one neurology SHO on to help the registrars. You have to plan far in advance, liaise with the rota coordinator (2015-2016 Rohit Sinha) and might have to ask one of the SHOs on NCCU/neurosurgery to cover you on neurology for a day as a favour.