BY OLISAELOKA EBEOGU(MBBS)

Emergency Management of the Unconscious Patient

Introduction

PreambleAlternative States of altered consciousnessMechanisms of ComaCauses of ComaEvaluation of the Unconscious patientInvestigationsManagementConclusion

Preamble

Consciousness means wakefulness with awareness of self and surrounding.

The unconscious patient is one who does not mount an appropriate response to a stimulus with a predictable outcome.

There is a continuum of altered consciousness ranging from drowsiness to coma.

There are also alternative states that mimic coma which in fact are distinguishable from coma.

Drowsiness stimulates light sleep and is characterized by easy arousal and the persistence of alertness for brief periods.

Stupor is an abnormal sleepy state from which the subject can be aroused by vigorous or repeated stimuli accompanied by motor behaviour that leads to avoidance of uncomfortable or aggravating stimuli.

Coma means unrousable unresponsiveness.

Alternative States of Altered Consciousness

Persistent vegetative state is usually a sequel of widespread cortical damage after brain injury. Brainstem function is normal but there is loss of sentient behaviour. The patient perceives little or nothing but lies apparently awake breathing spontaneously.

The minimal conscious state describes patient with some sentient behaviour e.g apparent, vague pain perception. A patient may emerge from VS into the MCS.

Cardiac arrest with cerebral hypoperfusion and head injuries are the most common causes of VS and MCS.

The locked in syndrome is a state of unresponsiveness due to massive brainstem damage below the level of the 3rd cranial nerve nuclei. The cerebral cortex is intact and patient is fully awake as opposed to VS/MCS. The patient however cannot communicate except by vertical eye obulbar movement. It is usually caused by infaction of the ventral pons that transects all corticobulbar and corticospinal pathways. A similar de-efferented state is seen in total paralysis in severe cases of GBS, critical illness myopathy and pharmacologic neuromuscular blockade.

Mechanisms of Coma

These mechanisms affect the brain stem, reticular formation and cortex and include:

Diffuse brain dysfunction: Seen in generalized severe metabolic or toxic disorders that depress overall brain function.

Direct effect within the brain stem: A lesion that inhibits the RAS.

Pressure effect on the brain stem: A mass lesion compresses the brain stem and inhibits RAS.

Evaluation of the Unconscious Patient

An immediate assessment of respiratory and cardiac malfunction is made. This follows the traditional ABC of resuscitation.

A very brief and concise history is then obtained focusing on circumstances, witnesses, paramedics and police where available.

The airway is assessed by the ‘head tilt – chin lift’ technique. The modified jaw thrust is used in cases of suspected spinal injury. Breathing is assessed by listening closely to the patient’s mouth or placing one’s hand over it.

The absence of the first 2 steps determines the next step in evaluating an unconscious patient. CPR is advocated in when the first 2 are absent (The CAB of American Heart Association).

If the first 2 steps are present, an attempt is made to establish the presence of circulation with appropriate intervention if absent.

In the unconscious but breathing patient, the fourth component becomes to establish the cause of unconsciousness (Diagnosis).

The History

In the absence of clues to the cause of coma( e.g head trauma or self-poisonoing) the history focuses on:-the circumstance and rapidity with which neurologic symptoms developed.-the antecedent symptoms( confusion, headache, weakness, fever, seizures, dizziness, double vision and vomiting.-the use of medications, illicit drugs , or alcohol-the presence of chronic liver, kidney, lung, heart or other medical disease.

The Examination

The general examination: Temperature: Infection? Hyperpyrexia?

Subnormal?Skin: Cyanosis? Jaundice? Purpura? Rashes?

Pigmentation?Breath: Ketone? Alcohol? Hepatic or Uraemic

fetor?

Distinct patterns of respiration are occasional evident in the unconscious patient:

Cheyne-Stokes respiration may be noted. It denotes bilateral cerebral or upper brain stem dysfunction and may signify incipient coning.

Acidotic – seen in DKA and uraemia. It is also seen in pontomescencephalic lesions.

Central neurogenic hyperventilation(sustained and rapid ): Seen in pontine lesions and may switch on and off abruptly.

Ataxic: Shallow, halting and irregular respiration that preceeeds death. Indicates failing medullary centers.

Vomiting , hiccups and excessive yawning in stupor indicates a lower brainstem lesion.

Tachypnoea may seen in lymphomas of the CNS.

In the neurologic assessment, the level of consciousness is ascertained using the GCS. Any posturing of the patient is noted, decorticate or decerabrate.

A simple coma ‘5 point scale’ may be used1-fully awake2-conscious but drowsy3-unconscious but responsive to pain with purposeful movement e.g flexion/withdrawal4-unconscious but responding to pain by extension5-unconscious and not responding to pain

The pupils: -Unilateral dilated pupils that becomes fixed to light signifies compression of the 3rd CN nerve, a neurosurgical emergency.-Horner’s syndrome: Hypothalamic damage-Bilateral , light fixed, dilated pupils is a cardinal sign of brain death. However can occur in deep coma from any cause but particularly in barbiturate toxicity and hypothermia

-Bilateral midpoint reactive pupils(normal) is seen in metabolic comas and coma due to sedative drugs.-Bilateral pinpoint, light fixed is seen in pontine lesions or opiate intoxications.-Bilateral mid position light-fixed or slightly dilated pupils( 4 -6mm) , sometimes irregular are seen in brainstem lesions.Mydriatic and anticholinergic drugs, previous pupillary surgery and occular trauma can cause diagnostic difficulties.

Ocular movements: In light comas, slow roving, side to side movements are seen. Ocular axis are slightly divergent. The eyes usually look towards a hemispheral lesion or away from a pontine lesion. Skew deviation indicates brainstem or cerebellar lesion. Ocular bobbing is seen in pontine or cerebellar lesion.The reflexes:

The vestibulo-occular reflexes disappear in deep coma, in brain stem lesions and in brain death.

The Caloric stimulation test(COWS): Its preservation indicates functional or hysterical coma.

Preservation of the corneal reflexes indicates integrity of the pons.

The corneal and pharangeal reflexes may be depressed on the side of an acute hemiplegia.

Normal pupillary size and light reactions differentiates most drug induced comas from structural brain damage.

Lateralizing signs may be difficult to appreciate in the unconscious patient. Clues to this include-Assymetry to visual threat in the stuporose patient reflects hemianopia-Assymetry of face-Assymetry of tone-Assymetry of posturing – decerebrate or decorticate.-Assymetry of response to painful stimulus-Assymetry of tendon and plantar reflexes. Plantar responses are usually extensor bilaterally in the deeply comatose patients.

Examination of the other systems may also provide additional information to the cause of coma.

Investigations

These are usually tailored to the findings elicited in the history and physical examination.

Blood and urine-Drug screens(salicylates, diazepam, narcotics, amfetamines, opioids)-Routine chemistry(urea, electrolytes, glucose, calcium, LFT)-Metabolic and endocrine studies(TSH and cortisol)-Blood cultures-Others e.g thick blood film in cerebral malaria.

-Imaging(CT or MRI) may show a mass lesion or intracranial hemorrhage. It is necessary to perform this when the cause of coma is inapparent.-CSF analysis is necessary in suspected meningoencephalitis. When the index of suspicion for a mass lesion is high, it is important to do a CT prior to this to prevent coning.-EEG is also of some value in metabolic comas and epilepsy. The amount of background slowing of voltages is a reflection of the severity of encephalopathy. Predominant high voltage slowing in the frontal regions is typical of metabolic comas and widespread fast β activity implicates sedativve drugs.

Alpha coma results from pontine or diffuse cortical damage and normal alpha activity which is suppressed by stimulating the patient alerts the clinician to the locked-in-syndrome, hysteria or catatonia. The most use of EEG in coma is to reveal clinically inapparent epileptic discharges.

Management

This includes general and specific components.Careful nursing is very necessaryMeticulous attention is given to the airways and

frequent monitoring of vital signs. There may also be need to provide an airway or endotracheal intubation.

Patient may require nursing in an ICU(see next slide).

Longer term essentials are: -skin care which involves frequent turning and removal of

jewellery

-Oral hygiene-Eye care to prevent corneal damage. Taping the lids together or irrigation may be necessary-fluids given either intragastric or intravenous-Calories – Upto 1255KJ(3000 kcal) daily in the adult patient.-Sphincters – catheterization when necessary and rectal evacuation.

Specific treatment will include:-Empirical intravenous antibiotics in suspected infection pending culture results.-Mechanical ventilation or oxygen supplementation in respiratory compromise.-Activated charcoal to decrease absorption when safe in drug intoxication. -Administration of antidote where indicated in drug overdosing.

-Correction of metabolic derangements-Correction of electrolyte disorders-Administration of diuretics if raised ICP is suspected or confirmed-Instituting measures to prevent secondary insults-Neurosurgical consultation when appropriate.

Evaluation usually comes to an end when the signs that signify brain death are manifest. They include:-absent pupillary response to light-absent corneal reflex-absent vestibulo-ocular reflex-absent response to pain-absent cough and gag reflexes-absent respiration despite adequate stimulation by CO2 in the blood.

This is usually done with the exclusion of :-any drugs which may be causing CNS depression or paralysis-any endocrine or metabolic disorders causing CNS depression.-hypothermia( temp. less than 35°C)

Conclusion

Unconsciousness is seen in a significant number of hospital admissions and prognosis depends on its cause with metabolic causes having the best and head trauma, severe intracranial bleeds or infaction having the worst. Urgent measures should be taken to address respiratory and cardiac problems present in the unconscious patient before the arduous process of a detailed neurological examination which most of the time provides information that is least amenable to immediate therapy.

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