Category Archives: Neurology


A number of injuries can produce a GCS 3 and interventions are multiple with varying evidence of efficacy

Pragmatic, multicentre multinational RCT

Open-label with blinded follow-up

Could be randomised up to 10/7 post injury and must have had first-level interventions to treat it (head up, CSF drainage, etc)

If could not be controlled with hypothermia had barbiturates or hypertonic

Screen 2498 patients, 387 randomised

  • 188 randomised and analysed in hypothermia
  • 187 randomised and analysed in controls

No significant differences in baseline characteristics including age, severity of injury, APACHE, etc AND neurosurgical intervention prior to randomisation

Hypothermia did control ICP more than standard interventions in control group

Stopped early as greater incidence of unfavourable outcome (poor GOSE score) in hypothermia compared with controls

Unadjusted hazard ratio for mortality 1.45 (1.01,2.10) at 6/12

No difference in pneumonia rate between two groups


Conclusion: Titrated hypothermia to reduce raised ICP in addition to standard care did not improve outcomes but and increased mortality

Hypothermia for Intracranial Hypertension after Traumatic Brain Injury


EPO has a long history: EPO-2 EPO-3 may reduce mortality in trauma but concerns about thromboembolic events and efficacy have limited application.

EPO is a pleiotropic cytokine and receptors exist in the blood-brain barrier. In response to hypoxia EPO is produced within the brain. Hence worthy of investigation:

Double-blind, placebo-controlled multi-centre trial

  • GCS < 13
  • Non-penetrating TBI
  • Hb < = normal
  • < 24 h since traumatic injury
  • Valid consent


  • EPO 40 000 IU or placebo SC
    • First dose was administered within 24 h of the estimated time of traumatic brain injury
    • Then weekly for a maximum of three dose
  • Baseline screening USS < = 7 of lower limbs for DVT

Main outcome GOS-E at 6 months

  • GOS-E of 1–4 (death, vegetative state, and severe disability)
  • GOS-E of 5–8 (moderate disability and good recovery)

606 randomised after inclusion / exclusion

Populations well matched

  • Mean age 35
  • Majority male
  • Mainly RTC
  • Most had severe TBI (GCS 3-8)

No effect on proportion with severe disability at 6/12

No increase in thrombotic events (including VTE and MI)

May reduce mortality – 5% ARR at 6/12 but does not achieve statistical significance


Becomes significant after sensitivity testing but this is exploratory

Rates of proximal DVT in TBI 17%

Conclusion: Following moderate or severe traumatic brain injury, erythropoietin did not reduce the number of patients with severe neurological dysfunction (GOS-E level 1–4) or increase the incidence of deep venous thrombosis of the lower limbs. The effect of erythropoietin on mortality remains uncertain.

Erythropoietin in traumatic brain injury (EPO-TBI): a double-blind randomised controlled trial

Controversies in the Management of Neuro-ICU Patients

‘Permissive’ hypernatraemia in refractory intracranial hypertension

Continuous infusions rather than bolus osmolar therapy may make physiological sense but concerns have been raised about the hypernatraemia. Continuous hypertonic saline has been used effectively in a number of settings but what about generation of osmotic gradients at the risk of ALI/AKI.

Concerns raised in discussion about inappropriately high targets and picking appropriate patients

Continuous controlled-infusion of hypertonic saline solution in traumatic brain-injured patients: a 9-year retrospective study

New Trends in Hyperosmolar therapy?


Is there a better fluid?

Different dogma’s exist about the suitability of Hartmanns or balanced solution in neuroICU. We know chloride worsens renal function but concerns about using hypotonic or isotonic solutions have meant a preponderance of saline.

Increasing evidence suggests that the chloride can be harmful to the brain as well – we give lots of chloride in hypertonic saline as well. Meta-analyses have suggested hypertonic saline better at reducing ICP but doses were not equimolar, it might not be best for survival and mannitol has additional effects beyond ICP.

What about feeding the brain? Some evidence for lactate containing solutions in treatment of intracranial hypertension. Lactate is a vasodilator and may improve CBF.

Combination therapy might be best – saline + ringers lactate +/- sugar depending on cerebral micro dialysis with control of sugar.

The cellular mechanisms of neuronal swelling underlying cytotoxic edema.

Hypernatremia in patients with severe traumatic brain injury: a systematic review

Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials

Half-molar sodium lactate infusion to prevent intracranial hypertensive episodes in severe traumatic brain injured patients: a randomized controlled trial.

Equimolar doses of mannitol and hypertonic saline in the treatment of increased intracranial pressure


Fixed versus auto regulatory driven CPP targets

Where does ICP threshold 20mmHg comes from old data and BTF guidelines are based on poor quality evidence. Ditto CPP.

BEST-TRIP suggested ICP of 20 but it may be the burden of ICP is the main problem – some people won’t tolerate ICP of 15mmHg. Children almost never do

CPP and ICP targets need to be individualised and hence reactivity with respect to auto regulation is important and might change during treatment. THat’s why you measure it! However, we lack prospective trials and need more data. Delta CPP may correlate with outcome.

Visualizing the pressure and time burden of intracranial hypertension in adult and paediatric traumatic brain injury

Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury.


Refractory Status Epilepticus

Status epilepticus definition has changed! Now anything other than a single self-limiting status (i.e. > 5 minutes) is now in status.

Refractory status is fits after benzodiazepines and second line AED (about two hours)

Super-refractory status fitting despite anaesthesia (about 24 hours)

Quicker you treat, more likely you are to terminate seizure

Once convulsive status exists, if becomes refractory will always progress to non-convulsive status equivalent to EMD. 48% of patients who don’t wake continue to fit in non-convulsive way.

Give Loraz > Phenytoin

Then equipoise – valproate? keppra? propofol?

Midazolam infusion may be better in refractory status – loading dose of 0.2mg/kg. Propofol infusion rates may be limited by PRIS issues. What about ketamine + midazlolam rather than barbiturate?!

Oral ketamine in paediatric non-convulsive status epilepticus.

Let’s talk about Post Intensive Care Unit Syndrome – Hannah Wunsch (presented 4th October)

In this presentation, Dr Wuncsh highlights some important key points:-

There are some significant negative consequences for our patients after discharge from the ICU.  Not only is QOL decreased for at least two years after hospital discharge, but patients can also suffer psychological and physical consequences such as anxiety and mood disorders, extreme fatigue, sleep disturbance, weakness, foot drip and more.

Some general tips for improving the patient experience and decreasing the impact of PICS include:-

  • Minimising sedation
  • Tailoring the environment to reduce noise and night disturbance
  • Early physical and cognitive therapy
  • Screening for psychiatric disease
  • ICU diaries


Dr Melissa Bloomer