Consciousness = a state of awareness of the self and the environment

Yüklə 177,5 Kb.
ölçüsü177,5 Kb.


PY Mindmaps
Consciousness = a state of awareness of the self and the environment
- depends on:
(i) wakefulness (arousal) – RAS & thalamus

(ii) awareness – cortex

Levels of Arousal:
(i) alert - normal

(ii) lethargy - a state between alertness and stupor

(iii) stupor - a state where a strong stimulus can transiently restore wakefulness

(iv) coma is characterised by an uninterrupted loss of capacity for arousal

Structural causes of coma
- supratentorial or infratentorial compartment

- coma is caused by compression of the RAS and disruption of axoplasmic flow

(i) Central Herniation
- bilateral symmetrical displacement of the supratentorial contents occurs through the tentorial notch into the posterior fossa

- clinical manifestations progress as follows with increasing herniation:

1. Impaired alertness (early)

2. Pupils become small but remain reactive

3. Bilateral upper motor neuron signs develop

4. Cheyne stoke breathing, grasp reflexes and roving eye movements develop

5. Midbrain compression leads to fixed mid position pupils

6. Spontaneous extensor posturing may occur

7. Variable breathing patterns develop

8. Autonomic cardiovascular and respiratory functions cease as medullary centres fail

(ii) Uncus Herniation
- results from laterally placed hemisphere lesions which cause side to side cerebral displacement as well as transtentorial herniation

- focal hemisphere dysfunction -> ipsilateral compression of the 3rd cranial nerve -> enlarged pupil that responses sluggishly -> a fixed dilated pupil and an oculomotor palsy (with eye turned downward and outward)

- the ipsilateral posterior cerebral artery compression as it crosses the tentorium -> occipital lobe ischaemia

- a hemiparesis may develop on the same side of the lesion due to compression of the opposite cerebral peduncle against the contralateral tentorial edge (Kernohan's notch)

- with increased mass effect herniation proceeds in the same pattern as seen with central herniation
- acute intrinsic lesions of the brainstem cause abrupt onset of coma + abnormal neuro-ophthalmological findings

- pinpoint pupils -> disruption of pontine sympathetic fibres

- dilated pupils -> destruction of the 3rd cranial nerve nuclei exiting fibres

- vertical eye movements are relatively spared

- upper motor neuron signs develop -> quadriplegic

- flaccidity in the upper limbs and flexor withdrawal responses in the lower limbs -> midbrain/pontine damage

- downward herniation of the cerebellar tonsils through foramen magnum -> medullary dysfunction -> respiratory and circulatory collapse

- less severe impaction of the tonsils -> obstructive hydrocephalus and consequent bihemispheric dysfunction with altered arousal

Non-structural causes of coma
- non structural disorders produce coma by diffusely depressing the function of the brainstem and cerebral arousal mechanisms

- metabolic encephalopathy is often characterised by fluctuations in the patient's level of arousal and consciousness; motor abnormalities are usually symmetrical if present

- hypoxia

- hypercapnoea

- hyponatraemia

- hypo/hyperglycaemia

- hyper/hypothermia

- hyper/hypo-osmolarity

- adrenal insufficiency

- hypopituitism

- hypothyroidism
- uraemia

- hepatic encephalopathy

- sedatives

- narcotics


- psychotropics

- CO

- many more….

Vegetative state
= wakefulness without awareness

- consequence of various diffuse brain insults

- they have spontaneous eye movements and stereotypical facial and limb movements; however, they have NO evidence of cognitive function or purposeful movement

- they can have a normal body temperature, cardiorespiratory and GI function but are incontinent

- it may be a transient phase as they wake due to cerebral cortex recovering more slowly than the brainstem

- persistent vegetative state - after 1 month

- permanent - after 3 months after non-traumatic injury and 12 months after traumatic injury
Locked in Syndrome
= voluntarily capable of only vertical eye movements and/or blinking

- causes: pontine infarction due to basilar artery thrombosis (most common), pontine haemorrhage, central pontine myelinolysis and brainstem masses

- transection of anterior pontine lesion bilaterally -> all descending motor pathways but spares the ascending sensory and RAS systems

- neuromuscular causes: acute inflammatory demyelinating polyradiculoneuropathies, myaesthenia gravis and botulism (differentiated by the lack of sparing of vertical eye movements)

Akinetic Mutism
- rare

- subacute or chronic state of altered behaviour in which an alert appearing patient is both silent and immobile but not paralysed

- causes: bilateral frontal lobe lesions, hydrocephalus & 3rd ventricular masses

- external evidence of cognitive activity is not obtainable

- associated with psychiatric disease

- characterised by stupor or excitement and variable mutism, posturing, rigidity and grimacing

- patients do not move spontaneously and appear unresponsive to the environment despite normal arousal.

- passive movement demonstrates waxy flexibility

- choreoform jerks of the extremities and facial grimaces are common

General management

Immediate management
(i) protect the airway

(ii) ensure adequate oxygenation and ventilation

(iii) ensure circulation adequate to maintain cerebral perfusion
NB: throughout the initial resuscitation it is important to gather as much information about the neurological state as possible as neurological examination is limited by intubation & sedation
- repeated generalised seizures damage the brain

- benzodiazepines +/- phenytoin (the latter is ineffective in toxicological seizures) immediate specific therapies:

(i) glucose should be administered to hypoglycaemic patients

(ii) thiamine should be given prior to or with glucose to prevent Wernicke's encephalopathy in malnourished thiamine depleted patients

(iii) naloxone 0.4-2mg iv provides effective reversal or opioid induced coma

(iv) flumazenil 1-5mg reverses benzodiazepines (but may produce refractory seizures in benzodiazepine dependent patients)

(v) physostigmine 1-2mg iv reverses the anticholinergic sedative effects of tricyclics
- witnessed events - head injury, seizure, details of accident, circumstances under which patient was found

- evolution of coma - abrupt or gradual, headache, progressive or recurrent weakness, vertigo, nausea and vomiting,

- recent medical history - surgical procedures, infections, medications

- past medical history - epilepsy, head injury, drug or alcohol abuse, stroke, hypertension, diabetes, heart disease, cancer, uraemia

- previous psychiatric history - depression, suicide attempts, social stressors

- access to drugs - sedatives, narcotics, illicit drug

- see notes on ‘Examination of the Comatosed patient’

- currently the most expedient imaging technique in a comatose patient and gives the most rapid information about possible structural lesions with the least risk

- demonstrates: mass lesions, haemorrhage and hydrocephalus

- not good at demonstrating: early infarction (less than 12 hours), encephalitis, isodense subdural haemorrhage and posterior fossa pathology (obscured by bone artefact)
- use in the urgent setting is limited c/o length of time required for the procedure and inaccessibility of the patient during imaging

- particularly useful: early stroke, encephalitis, central pontine myelinolysis and traumatic shear

- metabolic and toxic disorders -> reflects the degree and severity of altered arousal or delirium (decreased frequency of the background rhythm and the appearance of diffuse slow activity in the theta (4-7Hz) &/or delta (1-3Hz) range)

- sedatives -> rapid beta activity (greater than 13Hz) i

- acute focally destructive lesions -> focal slow activity

- HSV encephalitis -> lateralised epileptiform discharges appear in one or both temporal lobes

- poor prognosis -> a non reactive, diffuse alpha pattern (seen in anoxic brain damage)

- psychiatric disease, locked in syndrome and akinetic mutism -> a normally reactive EEG

- not currently helpful in post-resuscitation prognostication

- non-convulsive generalised status epilepticus and repeated complex partial seizures may produce altered levels of awareness or arousal

- status epilepticus -> continuous EEG monitoring optimises management and shows a high incidence of unsuspected seizure activity
Jugular Venous Oximetry
- measures the relationship between cerebral metabolic rate and cerebral blood flow

- no data to show it improves outcome

Transcranial doppler
- allows non invasive measurement of blood flow in the basal cerebral arteries and allows early detection of vasospasm in subarachnoid haemorrhage
Evoked potentials
- used to follow the level of CNS function in comatose patients

- clinical use of brainstem auditory evoked potential and short latency somatosensory evoked potential

responses stem from the correlation between EP waveform and presumed generators within the CNS

- EPs are less affected than EEG readings by sedative medications and septic or metabolic encephalopathy

- absent bilateral SEPs in patients with hypoxic coma are associated with very poor outcome

- in traumatic coma they may be a less definitive prognostic indicator.

ICP Monitoring
- a review of published randomised controlled studies of ICP monitoring in acute coma vs no ICP monitoring looking a mortality and severe disability concluded that there are insufficient data to clarify the role of routine ICP monitoring in all severe cases of acute coma

- ICP monitoring is of value in traumatic brain injury

Non-traumatic acute coma
- numerous descriptive scoring systems -> prognostication

- only 15% will make a good recovery

- 61% will die

- almost all patients who reach hospital after a sedative overdose will recover

- absent pupillary responses at any time and absent vestibulocaloric reflexes after 1 day indicate very poor prognosis (except in barbiturate or phenytoin poisoning)

- no patient with absent pupillary light reflexes, corneal reflexes, oculocephalic or caloric responses, or a lack of motor response to noxious stimulation at 3 days after onset is likely to ever regain independent function (except for sedative drug poisoning)

- post anoxic convulsive status epilepticus or myoclonic jerks reflect a poor prognosis -> occasional patients will regain consciousness but remain handicapped but most patients die or become vegetative
Traumatic coma
- generally better than medical coma

- the most reliable predictors of outcome at 6 months are:

(i) patient age (worse outcome especially after 60 years)

(ii) depth and duration of coma

(iii) pupil reaction and eye movements (absence at 24 hours predicts death or a vegetative state in 90%)

(iv) motor response in the 1st week of injury

- sustained elevated ICP >20mmHg is an independent predictor of poor prognosis

- subdural haematomas that result in coma have a less than 10% chance of recovery

Jeremy Fernando (2011)

Yüklə 177,5 Kb.

Dostları ilə paylaş:

Verilənlər bazası müəlliflik hüququ ilə müdafiə olunur © 2020
rəhbərliyinə müraciət

    Ana səhifə