Medical maps: Loss of responsiveness

A loss of consciousness (LOC) is the loss of awareness of the self and the surroundings. The clinical sign is a loss of responsiveness (LOR).

I make the distinction between LOC and LOR for two reasons:

  • There are some conditions, like psychogenic non-epileptic seizures, where it is unclear whether the patient has truly lost consciousness – but they have lost responsiveness.
  • LOC is the ‘symptom’ (what a patient complains of) and LOR is the ‘sign’ (what a clinician detects) – but the symptom isn’t particularly useful when the patient is totally unaware, so it makes more sense to focus on the sign.

There are shades of grey between being ‘totally aware’ and ‘totally unaware,’ and being ‘totally responsive’ and ‘totally unresponsive.’ A catch-all term is altered mental status.

The Glasgow Coma Scale is used clinically to quantify responsiveness based on eye movements (E), motor response (M) and verbal response (V). A score of 3 is ‘totally unresponsive’ (the minimum) and 15 is ‘totally responsive’ (the maximum).

A useful mnemonic – AEIOU-TIPS

Before discussing my approach to an unresponsive patient, a useful mnemonic to help remember the causes of loss of responsiveness/altered mental status is AEIOU-TIPS:

  • A lcohol, abuse of susbtances, acidosis
  • E pilepsy, environmental (temperature), electrolytes
  • I nfections including sepsis, inflammation
  • O verdose, oxygen low (hypoxia)
  • U nderdose, uraemia
  • T rauma, tumour (space occupying lesions)
  • I nsulin (hypoglycemia)
  • P sychogenic, poisons (CO, lead)
  • S hock, [stroke rarely]

This is unstructured, but useful as an aide memoire and is (according to Wikipedia) often quoted in emergency medicine textbooks.

But how should you approach patient who has lost responsiveness in a structured way?

Patterns of LOR

There are three patterns of LOR:

  • Rapid onset, transient 
  • Rapid onset, persistent (=coma)
  • Gradual decline, persistent (=coma)

Taking each of these in turn…

Rapid onset, transient loss of responsiveness

You may hear this being referred to as ‘TLOC’ – transient loss of consciousness. Rapid onset, transient loss of responsiveness can be traumatic or non-traumatic.

  • Traumatic:
    • Traumatic brain injury (TBI) – injury to the brain due to trauma. Caused by falls, car accidents, sports injuries, violence. More on this in a subsequent map on head injuries.
  • Non-traumatic: you need to distinguish between three possibilities…
    • Syncope (cardiac, or autonomic)
    • Seizure (provoked, or unprovoked)
    • Psychogenic, non-epileptic seizures
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Differentials of a rapid onset, transient loss of responsiveness. A little mnemonic for substances which, when withdrawn, can cause seizures is ABBA – alcohol, benzos, barbiturates and antiseizure drugs. Click to enlarge.

Distinguishing between the three causes of non-traumatic, transient loss of responsiveness depends on the clinical features of three periods – the prodrome, the unresponsive period and the recovery:

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Differentiating between syncope, seizures and psychogenic non-epileptic seizures. Click to enlarge.

Remember with transient loss of responsiveness, always consider hypoglycaemia (including in trauma patients). This can present in a similar way to syncopes or can present with seizures.

Rapid onset, persistent loss of responsiveness

When I say rapid, I mean sudden – there is no prodrome. And when loss of responsiveness is persistent, it is termed coma and the patient is said to be comatose.

The condition I’m thinking about here is diffuse axonal injury (DAI).

DAI manifests as a sudden onset, persistent loss of responsiveness following an accident – typically a high speed motor accident. It’s thought that rapid acceleration/deceleration motions cause shearing of the axons, disconnecting them, often at the junction between grey and white matter.

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Diffuse axonal injury – shear stress from trauma causes damage to axons, often at the junction between the cell body and the axon. Click to enlarge.

DAI can occur in isolation – there is little association with skull fractures and intracranial bleeds. The clinical signs are also out of proportion to imaging findings.

The classic exam scenario: someone is involved in a car accident, survives but never wakes up. Diagnosis = DAI.

Gradual decline into persistent loss of responsiveness

By gradual, I’m thinking of anything that isn’t as rapid DAI, syncopes or seizures. The conditions described here can still cause a quick decline into a coma over hours.

These problems can be caused by problems with brain chemistry or problems with blood flow and oxygen supply.

  • Problems with brain chemistry:
    • Exogenous substances – ingestion of toxins, poisons, medications, alcohol
    • Endogenous substances – electrolytes (Na+, Ca++), urea, sugar (hypos and DKA)
    • Temperature – heat stroke and hypothermia
    • pH – acidosis, either metabolic or respiratory
  • Problems with blood flow and oxygen:
    • Shock – where the cardiac output doesn’t meet the body’s demand (more discussion in ‘shock’ map)
      • Obstructive – the heart is working, but something is obstructing its outflow
      • Cardiogenic – the heart isn’t working properly
      • Distributive – neurogenic, septic or anaphylactic, where there is peripheral vasodilation reducing total peripheral resistance and hence cardiac output (remember: CO = ABP/TPR)
    • Raised ICP – this can cause LOR due to (i) reduced cerebral perfusion pressure (CPP) and (ii) brain herniation.
      • Increased brain volume – space occupying lesions, cerebral oedema or inflammation (meningitis/encephalitis)
      • Increased blood volume – venous thrombosis, vascular malformations
      • Increased CSF volume – hydrocephalus

It’s important to recognise the signs of raised ICP: reduced responsiveness, headache, vomiting, papilloedema and focal signs associated with brain herniation. Cushing’s triad is a late sign and is thought to reflect brainstem compression – the triad is widened pulse pressure (systolic increases, diastolic remains stable), bradycardia and irregular breathing:

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Pathogenesis of Cushing’s triad, a late stage finding in cases of raised ICP. The triad consists of widened pulse pressure, bradycardia and irregular breathing. Click to enlarge.

Here’s the framework for looking at a gradual decline into persistent loss of responsiveness.

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Differentials for a gradual decline in responsiveness, resulting in a coma. Click to enlarge.

More on: brain herniation

Brain herniation is a potentially fatal consequence of raised ICP, where parts of the brain are squeezed across fixed structures (dural folds, bone) in the cranial vault.

There are four important ‘herniation syndromes’ you should recognise:

  • Cingulate gyrus (aka subfalcine) herniation:
    • Drags the ipsilateral anterior cerebral artery with it, causing contralateral lower limb paralysis
  • Central downwards herniation of thalamus, temporal lobes:
    • Can tear basilar artery branches leading to dot-and-blot ‘Duret’ haemorrhages, which are often fatal
    • Compression of the dorsal midbrain (colliculi, oculomotor nuclei) can cause the ‘setting sun’ eye sign
  • Uncal herniation (uncus = anterior part of parahippocampal gyrus):
    • Ipsilateral posterior cerebral artery compression, causing visual cortex ischaemia and contralateral homonymous hemianopia
    • Ipsilateral oculomotor nerve compression causing a blown pupil and down-and-out appearance of the eye (unopposed lateral rectus and superior oblique action)
    • Duret haemorrhages
    • Contralateral cerebral peduncle indentation – termed Kernohan’s notch – with compression of the contralateral corticospinal tract (CST); this is a false localising sign, because it leads to hemiparesis ipsilateral to the mass lesion
      • (remember – the CST crosses below the peduncles at the junction of the medulla and spinal cord)
  • Downward herniation of cerebellar tonsils through the foramen magnum 
    • Compression of the lower brainstem leads to headaches, neck pain, labile blood pressures, paralysis and respiratory/cardiac arrest (=death)

Here is a diagram and table summarising this info:

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Important brain herniation syndromes. The table outlines the structure herniating, structure(s) compressed or damaged by the herniation, and the clinical sequelae. Click to enlarge.

There are other types of herniation too, but these are the key ones.

More on: hydrocephalus

Hydrocephalus is defined as an accumulation of CSF in the ventricles of the brain. It is one cause of raised ICP.

The main distinction to make is between communicating or non-communicating. Besides one exception, you can think of the distinction as depending on whether the issue is before or after the foramen of Magendie/foramina of Luschka.

  • Non-communicating occurs before and is due to obstructions to flow:
    • Congenital malformations
    • Tumours
    • Fibrosis following a bleed
    • Inflammation (meningitis)
  • Communicating occurs after and is generally due to reduced CSF absorption at the arachnoid villi:
    • Fibrosis following a bleed
    • Inflammation (meningitis)
    • *exception* – choroid plexus inflammation, papilloma, carcinoma (where the problem is increased CSF production)

There are two other types of hydrocephalus – normal pressure hydrocephalus (NPH) and hydrocephalus ex-vacuo.

  • NPH is idiopathic accumulation of CSF in the ventricles
    • Normal lumbar puncture opening pressure
    • Thought to be due to dysfunctional absorption of CSF at the arachnoid villi
    • Triad of ‘wet’ (urinary incontinence), ‘wacky’ (dementia) and ‘wobbly’ (ataxia)
  • Hydrocephalus ex-vacuo – a misnomer as it isn’t true hydrocephalus
    • Loss of brain tissue leads to expansion of subarachnoid space and ventricles (there is no obstruction, reduced CSF absorption or increased CSF production)
    • Associated with cortical degenerative conditions

They don’t progress to a coma like the other forms, because the ICP is not increased and therefore cerebral perfusion pressure is maintained. There isn’t brain herniation.

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CSF circulation in black, and ‘sites’ of hydrocephalus pathology in purple. Note that choroid plexus neoplasms/inflammation cause a communicating hydrocephalus. Click to enlarge.

Medical map

This is a big one – here is the overall medical map for loss of responsiveness:

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Overall medical map for loss of responsiveness. Click to enlarge.

This post covers quite a significant chunk of neurology (and an important part of emergency medicine) – so I hope it’s useful for those of you about to go on neurology placement.

 

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