ICU CASES
These obviously represent the severe end of the spectrum such as the intubated CNS infections with EICP, patients requiring external ventricular drains and those with systemic manifestations of sepsis requiring organ support.
Many cases which are less severe can be managed in a ward setting.
Interpreting the CSF
This will guide the ongoing treatment
An approach
Add opening pressure
Add gram stain (what it is) / india ink etc
Something like this but modified:
OPENING PRESSURE
6-20 cm CSF
CSF WCC
< 5 cells / microL
Mainly lymphocytes
CSF PROTEIN
<0.6 g/L
CSF GLUCOSE
> 40% serum
> 2.2 mmol/L
OPENING PRESSURE
15-50 cm CSF
CSF WCC
HIGH!
May see > 1000 cells / microL
Mainly neutrophils
CSF PROTEIN
HIGH!
0.8 – 5 g/L
CSF GLUCOSE
LOW!
<40 % serum
< 2.2 mmol/L
WHAT DOES THIS MEAN?
Could be:
> Bacterial meningitis – more likely if glucose very low, WCC very high (1.9 mmol/L, WCC > 2000, CSF neutrophils > 1180 REF)
> Early meningeal response to any infection (early TB, fungal, viral, or drug-related meningitis).
> Parameningeal focus of infection (brain abscess, subdural empyema, epidural abscess)
OPENING PRESSURE
6-30 cm CSF
CSF WCC
High but not as much as bacterial
< 1000 cells / microL
Mainly lymphocytes
CSF PROTEIN
Usually High
0.3-20 g/L
CSF GLUCOSE
NORMAL
> 40% serum
> 2.2 mmol/L
WHAT DOES THIS MEAN?
Could be:
Viral meningitis (e.g., enteroviruses, HSV, HIV)
Viral encephalitis
Partially treated bacterial meningitis
Listeria meningitis
Spirochetal infection (leptospirosis, lyme, syphilis)
Rickettsial infection (rocky mountain spotted fever, ehrlichiosis)
Drug-induced meningitis
Endocarditis
Paraneoplastic encephalomyelitis
SLE, multiple sclerosis, acute disseminated encephalomyelitis
OPENING PRESSURE
15-50 cm CSF
CSF WCC
High but not as much as bacterial
< 1000 cells / microL
Mainly lymphocytes
CSF PROTEIN
HIGH!
0.8-5 g/L
CSF GLUCOSE
LOW
<40% serum
<2 .2 mmol/L
WHAT DOES THIS MEAN?
Could be:
Malignancy (leptomeningeal carcinomatosis)
Tuberculosis, fungal meningitis
Listeria
Lyme
CNS vasculitis, neurosarcoidosis
Lymphochoriomeningitis virus (LCMV)
SPECIFICS
See earlier for definitions etc
Principles:
Avoid in the first place by minimising use and duration of drainage as much as possible
If evidence of infection:
- Commence empirical antibiotics
- E.g. ceftazidime and vancomycin
- Remove drain as soon as feasible
- Consider intraventricular/intrathecal antimicrobial for resistant organisms or non-responsiveness to IV antimicrobials
If only evidence is fever with increased white cell: red cell ration in CSF and CSF cultures don’t grow organisms
The incidence of EICP with meningitis is uncertain but is more common in certain types of infection such as cryptococcal infection, as well as the more severe bacterial, viral, fungal and parasitic infections.
WHEN DOES ICP MATTER?
If your patient has clinical signs of EICP:
- Deteriorating level of consciousness
- GCS </= 8
- Non-reactive pupil(s)
- Imaging evidence of herniation or mass effect
OR has an opening pressure on LP > 20 mmHg
Consider invasive ICP monitoring with CSF drainage.
If there is no imaging evidence of herniation or mass effect, lumbar CSF drainage with a lumbar drain or repeat lumbar punctures can be used to reduce ICP
Practice around this varies but there is some evidence to support this approach.
See the EICP module for more on what CPP is and why we target it in types of brain injury.
Cerebral perfusion pressure (CPP) = MAP – ICP
As mentioned in Emergency Management, if there is clinical evidence of EICP, but ICP is unknown, it is reasonable to target a MAP > 80 mmHg, which would give a CPP of 60 if the ICP was 20 mmHg.
If an opening pressure from LP is available, MAP target can be adjusted accordingly:
ICP in mmHg = 0.7 x opening pressure (in cm of CSF)
You can then target a CPP of 60-70 as with other brain injuries (e.g. TBI)
Noradrenaline is the initial pressor of choice.
If the patient has septic shock or a septic cardiomyopathy in the context of their CNS infection and they are needing high dose noradrenaline to achieve this target, they may require additional vasopressors such as vasopressin; if they aren’t already on steroids, a stress dose of hydrocortisone may be appropriate (e.g. 50 mg q6h).
In many forms of brain injury there is a know association between fever and worse neurological outcomes.
Fever can increase intracranial pressure.
There is no evidence to support fever control specifically in meningitis.
However it is a logical part of the neurocritical care of these patients.
As with other forms of brain injury, this includes:
- Treatment of underlying cause
- Antipyretics: paracetamol, consider NSAIDS like ibuprofen
- Cools packs
- Fans
- Cooled fluids (avoiding hypervolaemia)
- Adhesive external adaptive cooling systems (which often require deepened sedation +/- paralysis)
Meningitis patients have a ~20% risk of seizure, with higher risk in sicker patients REF
There is no evidence about seizure prophylaxis in these patients.
However, there is increased mortality associated with seizures in this context, so they are often given.
Clinical seizures may be difficult to detect in sick patients with meningitis who are intubated and ventilated, therefore have low threshold to perform EEG and use cEEG if readily available.
The sick meningitis patients who are intubated and ventilated with severely altered consciousness or focal deficits need definitive neuroimaging with MRI if possible.
WHY?
High rate of abnormalities that may change management:
> Meningitis with sinus vein thrombosis (potentially requires anticoagulation)
> Brain abscess (can be initial focus of infection, may require surgery; may be missed on initial CTB)
> Subdural empyema (can be initial focus of infection, may require surgery; may be missed on initial CTB)
> Anatomic portals of entry causing meningitis (e.g. sinusitis, otitis media, encephalocele causing CSF leak)
> Anatomic distribution of encephalitis may suggest various pathogens (e.g. temporal lobe involvement suggests HSV).
Spinal epidural abscess may cause a (non-traumatic) spinal cord injury.
The principles are largely the same as with traumatic SCI.
Treating the causing of the spinal cord injury is critical, i.e. surgical decompression and anti-microbial treatment
See the SCI MODULE for more details on managing this.
Scenario test question