This is all about generating a broad range of differentials.
One's assessment of the unconscious patient searches for focal neurological signs and meningism. If these are absent, one is left looking for subtle clues in the examination which may explain the decreased level of consciousness. Apart from our very own Oh's Manual, one may also examine an excellent article by David E Bateman from 2001, which details the neurological assessment of coma. A suggested pattern of examination for the unconscious patient in the CICM exam is available elsewhere.
SAQs requiring the candidates to generate a list of differentials for unconsciousness have included the following:
With focal signs
Intrinsic neurological causes
Without focal signs
Intrinsic neurological cause
Endocrine and metabolic causes:
This is typically easy. Something is structurally wrong with the brain.
There is either a stroke, bleeding, pus or tumour.
Again, this is easy. Not many things can irritate the meninges.
One must consider either meningitis or a subarachnoid haemorrhage.
This is much more difficult. One has to cast one's net widely.
Vascular causes: brainstem infarct or haemorrhage; alternatively, a stroke which has wiped out a large portion of the brain mass (eg. a hemispheric infarct)
Infectious causes: encephalitis due to an infectious agent
Neoplasm: more likely, multiple metastases
Drugs: of these, there is more than a handful.
Autoimmune: Lupus cerebral vasculitis springs to mind, but here are several others
Trauma: concussion, cerebral contusions or a diffuse axonal injury can give rise to a loss of consciousness without any focal features.
Endocrine and metabolic causes: these are numerous:
Many scales are available, but most people rely on the old and trusted Glasgow Coma Scale.
The GCS has a few important problems, and a good editorial on this topic is available, which summarises the problems pretty well.
In spite of its shortcomings, the GCS should form the first steps of a neurological assessment, particularly where it comes to an undifferentiated unconscious patient.
Testing the pupils gives one some reassurance regarding the entire optic pathway. The retina, the optic nerve, the chiasm, the midbrain and third nerve - all play a role in the light response. In general, the presence of full conjugate movement on oculovestibular stimulus suggests that much of the brainstem is intact.
The possible causes of abnormal pupils are discussed in the following table:
|Unilateral miosis||Bilateral miosis||Unilateral mydriasis||
Hypoxic brain injury
Bilateral midbrain lesion
From this table, one should carry away the awareness that midbrain lesions cause a dilated pupil, whereas pontine lesions cause a constricted one (as the sympathetic outflow is interrupted by pontine lesions, but only the third nerve is affected by midbrain lesions).
This whole eye examination thing can really get out of hand. If one is interested in an extensive discussion of eye signs, one can pursue their demented lust for cranial nerve physiology in the chapter on examination of the cranial nerves in the critically ill patient.
Uncal herniation causes a third nerve palsy by stretching the oculomotor nerve over the petroclinoid ligament, a delicate band of dura stretching between the clinoid process and petrous portion of the temporal bone (purists may remark that it is an extension of the tentorium cerebelli). As the brainstem is pushed down through the foramen magnum, so the oculomotor nerve is dragged down with it, and the ligament becomes the fulcrum point where it is compressed. The parasympathetic fibres in the nerve no longer supply the iris in such circumstances, and there is unopposed sympathetic input into the pupil's diameter.
This pattern occurs early in uncal herniation because the third nerve is stretched before any major structures are being crushed. In contrast, when the herniation is central, the pupils are usually small - their parasympathetic supply remains undisturbed while the sympathetic fibers in the brainstem are being squashed. Late in the game, Cheyne-Stokes respiration and fixed mid-dilated pupils develop.
As far as the eye movements go, there are several pearls one should recall:
Any spontaneous movement is good. Even abnormal movements are good -abnormal movements are a focal sign and may give one some clue as to where the lesion is:
This is a part of the motor score in the GCS, and if not present spontaneously, it can be elicited by a painful stimulus.
The red nucleus of the rostral midbrain is responsible for this physical sign. The rubrospinal tract, when unopposed by cortical activity, will cause a flexion of the upper limbs, resulting in the characteristic posture of the decorticate patient. Lesions below the red nucleus prevent this flexor response, and in response to pain the patient will tense and extend the limbs- this is called reactive extensor postural synergy. Spinal reflex arcs are still present, and this extension will produce a reflexive flexion of the opposing muscle groups, which results in the observed whole-body rigidity.
Each seems as bad as the other, but there is a reason why they are given different ratings in the Glasgow Coma Scale. There is an empirically observed survival difference between the two findings. The creators of the scale (in 1974) found that head-injured Scottish drunks with decorticate posturing recovered in 37% of cases, whereas the decerebrate drunks only recovered in 10% of cases.
Confusingly, metabolic states can result in this sort of finding. One article from the 1960s reports on both being present (and being reversible) in a patient with hepatic encephalopathy.
A decreased respiratory rate makes one think of opiates first. However, hypothyroidism can also be to blame. Additionally, the decreased respiratory rate can be the cause of coma, as it can cause hypercapnia due to an otherwise trivial non-anaesthetic opiate dose.
An increased respiratory rate is sometimes seen in midbrain lesions and in various sorts of metabolic encephalopathy. Certainly, these various metabolic problems are rarely without an acid-base component, and the disturbance is almost always an acidosis.
Cheyne-Stokes respiration is an "oscillatory" pattern of breathing, with rate alternating between fast and slow- and occasionally with apnoea. An ancient paper on the subject (from 1909, co-authored by J.S. Haldane!) describes this pattern very well for those who have never seen it. It is seen mainly in patients with metabolic encephalopathy and (nocturnally) in heart failure; however, the mechanism can extend to patients with increased intracranial pressure due to some sort of diffuse insult. The issue seems to be still debated. In general, the mechanism is thought to be some sort of dysregulation of the central control of breathing, with periodic hyperventilatory overcompensation for hypoxia and hypercapnia leading to periods of apnoea, and thus more hypoxia and hypercapnia.
Oh's Manual also mentions "apneustic breathing" where one pauses in inspiration (apparently a pontine problem) and "ataxic breathing" which is totally disorganised and apparently a feature of pre-terminal medullary dysfunction.
Prognostication in coma is a delicate thing, particularly if one is not sure what has caused it.
At least where it comes to hypoxic brain injury, we have some clinical predictors to fall back on. More of this is explored in the chapter on the prognostication of neurological recovery after cardiac arrest. In short, the following is a list of poor prognostic features:
Of course, these findings are all from studies which were done before the era of therapeutic hypothermia. As we are reminded by Venkatesh, who the hell knows what the outcomes are for cooled patients. It is possible that excessive negativity and pessimism on our part is leading to a number of unfair decisions to withdraw care.
Though the list of differentials is broad, a stereotypical response should be reproduced for any case of unexplained coma.