CSF interpretation Flashcards

1
Q

what positions can an LP be performed?

A
  • Lying in foetal: can get opening pressure
  • Sitting hunched over table  opens up spine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what landmarks do you follow to get correct LP place?

A
  • Follow iliac crest  gets to L3/4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why do you not want any higher than L2?

A
  • Any higher would get spinal cord  risk of nerve damage  paralysis
  • L2 and lower gets individual nerves  cauda equina region
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why do you insert LP needle at L3/4 region?

A

the nerves are all individual nerve roots - not the spinal cord any more
the needle is designed so that it can push nerve roots out of the way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the complications of a LP?

A

post LP headache
bleeding
infection
haemorrhage
dry tap
nerve damage
brain herniation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why does a headache occur and what can help?

A
  • Post LP headache caused by low pressure  dark room, lying down and caffeine can help. Usually occurs 24-48hrs post LP

due to the pressure change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

why might there be local pain and bleeding with a LP?

A
  • Local pain – needle. Disc herniation if needle is too far
  • Bleeding – micro trauma by needle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what may cause haemorrhaging following a LP?

A

low platelets/ coagulopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why might you get a dry path within a LP?

A

: misplaced or dehydrated patient – not enough csf

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how might nerve pain present and what is done to avoid it within a LP?

A
  • Nerve damage: extremely rare as should be low enough not to hit nerves  leg pain, electrical sensation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how can a LP cause a brain herniation?

A
  • Brain herniation: caused by the drastic change in pressure – high intercranial pressure and low pressure in spinal cord and this causes brain to move down into brain stem  potentially fatal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is normal opening pressure of CSF?

A

12-18cm H20 in foetal position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which position and why can inly get opening pressure?

A

foetal only - as sitting gives higher csf pressure compared to brain due to gravity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what can elevated opening pressure and what is the cut off before worrying?

A
  • Elevated if tense or anxious
  • Higher if obese - <25
  • Pathology: infection, idiopathic intercranial hypertension, hydrocephalus, SoL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

normal CSF is clear and colourless, what would bacteria in csf look like?

A
  • Pathology – turbid: bacterial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

normal csf is clear and colourless what would turbid csf indicate?

A

fungal/ TB presence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what WCC is deemed normal within csf?

A

<5 x10^9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what might elevate WCC?

A

traumatic LP
bacteria
viral presence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what WCC would you expect with bacterial csf presence and what cell type?

A

100s to 1000s
mainly neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

if there are viruses present in csf, what WCC and cell type would you expect?

A

100s to 500s
lymphocyte predominately

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

even with viral and bacterial presence what may have lower the WCC?

A

empirical ABx - the counts would be lower than expected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is normal protein count in csf?

A

<0.5g/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

if a csf was normal, except a very high protein what could that indicate?

A

GBS

24
Q

how would viruses effect csf protien levels?

A

slight increase

25
Q

what would indicate a bacterial presence within csf?

A

1<

26
Q

what would a low glucose in csf indicate?

A

Glucose: >2/3 of serum glucose
- Low: bacterial

27
Q

what would show a bacterial picture?

A

bacteria eats all the glucose - very low
bacteria poos out the protein - very high (>1)
mainly neutrophils

28
Q

when would xanthochromia present in csf?

A

bilirubin from heme breakdown
- Seen in LP performed 12hrs post SAH headache onset

29
Q

when would oligoclonal bands be seen?

A

MS
- Can be seen in other inflam conditions eg sarcoidosis/ SLE

30
Q

what are common bacterial causes of meningitis and which demographics are mainly affected?

A

N. menigitidis  teens, uni students
- Strep. Pnuemoniae  paeds, elderly
- Listeria: provides lymphocytic picture  neonates, elderly, immunocompromised and pregnancy
- TB: provides lymphocytic picture  immunocompromised, high prev areas

31
Q

what can cause raised intercranial pressure?

A
  • Idiopathic intercranial hypertension
  • SoL
  • Infection
  • Venous sinus thrombosis
32
Q

what can papilledema indicate?

A

raised intercranial pressure

33
Q

what can cause optic neuritis?

A

MS, diabetes
anything causing peripheral neuropathy

34
Q

how can hypercapnia affect the eyes?

A

can cause papilledema

35
Q

what are RF for idiopathic intercranial hypertension?

A

females of childbearing age
RF: obesity, Venous sinus thrombosis (common after anti-coag therapy from bleeds)
- Drugs: tetracycline, minocycline, nitrofurantoin, vitA and isotretinoin, COCP

36
Q

what investigations are needed with idiopathic intercranial pressure?

A

Investigations: need MRI
- LP: raised opening pressure and therapeutic drainage

37
Q

how do manage idiopathic intercranial hypertension?

A
  • Lifestyle: weight loss, remove causative medication
  • Therapeutic LP: bring pressure below 20mmHg
  • Drugs: acetazolamide, topiramate, loop diuretics, pred
  • Surgery: lumbar-peritoneal shunt, optic nerve sheath fenestration
38
Q

what are complications of intercranial hypertension?

A

visual loss

39
Q

how does acetazolamide work?

A

carbonic anhydrase inhibitor  helps reduce CSF production

40
Q

what is viral encephalitis?

A

viral infection of brain parenchyma (cortex, white matter, basal ganglia, brainstem)

41
Q

what are the most common causes of viral encephalitis?

A

HSV 1 most common in Europe – mostly affects temporal lobes
- HSV2: in immunosuppressed/ neonates
- CMV, EBV, VZV, HIV, Measles, mumps, rabies, tick borne, arbovirus
- Japanese B encephalitis – east asia and Australia

42
Q

what is HSV1 and HSV2?

A

herpes simplex virus 1 - very common causes cold sores
HSV2 - genital herpes

43
Q

how does viral encephalitis present?

A
  • Headache, fever
  • Focal neuro signs: hemiplegia and aphasia
  • Seizures
  • Reduced consciousness and confusion - acting very stupidly?
  • Meningism
44
Q

what is meningism?

A

meningitis symptoms without meninge inflammation – triad (headache, neckstiffness and photophobia)

45
Q

what comes first investigations or treatment?

A

treat before investigations start  base on clinical presentation then alter accordingly to results

46
Q

what would an mri show indicating viral encephalitis?

A
  • Brain imaging (MRI) : temporal lobe petechiae – small haemorrhages
47
Q

what would a LP show to indicate viral encephalitis?

A
  • LP: raised WCC – mainly lymphocytes, elevated protein, normal glucose
48
Q

what would an EEG show to indicate viral encephalitis?

A

slow periodic waves

49
Q

how do you manage viral encephalitis?

A
  • IV acyclovir – HSV 2
  • Steroids (dexamethasone) if raised ICP
  • Supportive: anti-convulsants, resp support
50
Q

what does gram positive diplococci indicate?

A

strep pnuemoniae

51
Q

how common in guillan barre syndrome?

A

not very
1 to 2 in every 100,000

52
Q

what is GBS linked to?

A

previous recent infection - last 2 weeks or so
coryzal, acute diarrhoeal, acute infection
: linked infections include – campylobacter, CMV, mycoplasma, HZV, HIV, EBV

53
Q

what are the symptoms of GBS?

A
  • Ascending symmetrical paralysis starting in lower legs
  • Pain can occur but sensory less common
  • Autonomic dysfunction: sweating, tachycardia, arrythmias, BP changes
  • Lower motor neurone signs: hypotonia, facilitations, no reflexes
54
Q

what is the miller fisher variant of GBS?

A

: opthalmoplegia (paralysis of eye muscles), ataxia and areflexia

55
Q

what is the pathophysiology of GBS?

A

rare but serious post-infectious immune-mediated neuropathy. It results from the autoimmune destruction of nerves in the peripheral nervous system

56
Q

what investigations are done for GBS?

A

MRI - rule out other pathology
CSF analysis: raised protein count
- Nerve conduction studies: reduced velocity – demyelination
- Resp function: FVC/ABG breath count – concerns due to paralysis of resp system
- Anti-ganglioside auto-antibodies – may be positive
- Investigate cause of infection – non priority

57
Q
A