Coma ICU Management

“80% of the Diagnosis is in the History”

Whilst this may be a load of cobblers, the history is definitely crucial in diagnosing the cause of the coma.

The family may not have the whole story.

Contact:

> Their GP

> Other treating specialists

> Other hospitals the patients has been to recently

> Anyone they are close to who may know exactly what happened prior to presentation.

Don’t miss seizures

Non-convulsive seizures are difficult to spot clinically

Commonly follow convulsive seizures (10-40%)

May have no physical signs but suspect if twitching / blinking / other eye movement signs with fluctuating consciousness

An EEG is essential to diagnose this cause of coma

20 minute EEG’s may miss electrographic evidence of seizures

Continuous EEG (cEEG) is recommended to detect NCSE in this context

The consequences of NCSE are not currently understood; the underlying cause is much more prognistic

Exactly how it should be managed is controversial.

Risk Factors for NCSE:

• Any seizure disorders
• Systemic infection in a patient with pre-existing epilepsy
• Intracerebral and subarachnoid haemorrhages
• Post cardiac arrest
• Ischaemic stroke
• Severe traumatic brain injury
• Encephalitis
• Dementia
• Metastatic cancer, particularly with brain mets
• Previous neurosurgery
• Benzodiazepine or other ASM withdrawal
• Alcohol use
• Excessive use of psychotropic drugs
• Severe metabolic derangements

Treatment:

Treat underlying cause

Good basic intensive care

Stop any medications that may lower seizure threshold

Anti Seizure Medications as per tiered approach – see Seizure Module

Less consensus over importance of treating NCSE compared to CSE

A common approach is to treat until either 12-24 hours of burst suppression or absence of epileptic activity before gradually reducing anaesthetic agents

What does it add?

> Better contrast & resolution of grey & white matter compared to CT

> More sensitive than CT at detecting:

• Acute ischaemia
• Diffuse axonal injury
• Cerebral oedema
• Tumours
• Abscesses
• Vascular lesions (with MRA / MRV)

Why don’t you do it immediately on everyone?

> May not be necessary if diagnosis already clear

> Takes a long time (c. 1h) and usually requires intubation and GA to perform safely

> It’s less available

> Need to ensure no contraindications e.g. some pacemakers, some aneurysm clips, cochlear implant

Doing the ICU essentials well buys time for the cause to be sorted out

> Intubate if at risk of aspiration

> If not intubated but have a decrease level of consciousness and have no spinal precautions, nurse on their side

> Mechanical ventilation if hypoventilating, e.g. aim PaCO2 35-45, PaO2 > 70-100 mmHg

> MAP > 65, address any causes of haemodynamic instability

> Meticulous eye & mouth care

> Rolling, pressure area care

> Monitor for and treat nosocomial infections

> Enteral nutrition via NGT unless contraindicated

> Avoid unnecessary sedation, use short acting agents (e.g. propofol), avoid paralytic agents to allow frequent neurological assessment

> VTE prophylaxis e.g. enoxaparin 40 mg daily, screening doppler USS of legs weekly if immobile

> Stress ulcer prophylaxis if intubated / on steroids

> Maintain BGL 6-10m mmol/L

Despite best efforts to treat the underlying cause of the coma, some patients remain profoundly unconscious.

These are usually patients with significant structural causes of coma such as TBI, hypoxic brain injury or specific injuries to areas involved in wakefulness as described in the fundamentals section.

A general accepted hypothesis for regaining consciousness after severe brain injury is the “Mesocircuit Model”

REF

This describes the mechanism for downregulation of the anterior forebrain mesocircuit in severe brain injuries.

Reduction of thalamocortical and thalamostriatal outflow following deafferentation and loss of neurons from the central thalamus withdraws important afferent drive to the medium spiny neurons of the striatum, which may then fail to reach firing threshold because of their requirement for high levels of synaptic background activity.

Loss of active inhibition from the striatum allows neurons of the globus pallidus interna to tonically fire and provide active inhibition to their synaptic targets, including relay neurons of the already strongly disfacilitated central thalamus, and possibly also the projection neurons of the pedunculopontine nucleus.

Why is this relevant?

Therapeutic targets to improve consciousness target different aspects of this model.

> Zolipidem

Probably works on the globus pallidus interna and possibly frontal cortex and striatum

A proportion of patients with Minimally Conscious State seem to have a period of increased consciousness

More here

> Amantadine

Probably works on Medium Spiny Neurons in the Striatum and possibly the frontal cortex

Variable results, best target population still to be identified.

There is one prospective RCT showing amantadine accelerated the pace of functional recovery during active treatment in patients with post-traumatic (TBI) disorders of consciousness. Given in rehab 4-16 weeks post TBI, 100 mg BD increased up to 200 mg BD.

More here

> Deep Brain Stimulation

To central thalamus

Emerging area of research, very little evidence at present. Has been tried post severe TBI with Minimally Conscious State and Vegetative State patients descriptive reports of returning to consciousness in 4/14 pts in one paper, but it’s unknown whether that would have happened anyway.

DBS in coma post TBI review.

> Transcranial Deep Current Stimulation

Targets frontal cortex.

Another area of active research.

e.g. 20 minutes of 2 mA intensity by two 35-cm² sponge electrodes soaked in a saline water solution with the anode positioned over the left DLPFC (F3 according to the 10–20 international EEG system) and the reference cathode positioned on the right supraorbital region (FP2). REF

Currently mixed evidence that this transiently improves consciousness but currently no evidence that there is a sustained effect.