Echoencephalogram is an obsolete examination nowadays (▶Fig. 12.1). It was the initial and basic test of severe head injuries in the pre-CT scan era.
12.1 The Unconscious Patient
The state of arousal is determined by the function of the central reticular formation that extends from the brain stem to the thalamus. Coma occurs when this center is damaged by a metabolic abnormality or by an invasive lesion which compresses this center. Coma is also caused by damage to the cerebral cortex.
The various levels of consciousness vary from consciousness, which means awareness of oneself and the surroundings in a state of wakefulness, to coma, which is a state of unarousable unresponsiveness. Rather than using these broad terms in clinical practice it is preferable to describe the actual state of the patient in a sentence. For more details please refer to the following table.
Reduced awareness and wakefulness | ||
Responds only to painful stimuli (sternal rubbing with knuckles) without arousing | ||
Kumar PJ, Clark ML. Clinical Medicine. 5th ed. London: Bailliere Tindall; 2003
12.2 Hysterical “Unconscious” Patient
One of the most puzzling problems in emergency medicine is how to diagnose the unconscious patient caused by the conversion reaction (hysteria). These patients really experience their symptoms (as opposed to the pretending patient) and resist most normal stimuli, including painful stimuli.
12.3 Blackouts: Episodic Loss of Consciousness
Episodic or transient loss of consciousness is a common problem. The history is important to determine whether the patient is describing a true blackout or episodes of dizziness, weakness or some other sensation. Various causes of blackouts are discussed below.
It is the most common cause of blackouts. There are various types, the most dramatic being the tonic–clonic seizure where patients have sudden loss of consciousness without warning. Associated features are:
Cyanosis, then heavy “snoring” breathing
Tongue biting may or may not be there
Incontinence of urine or feces may or may not be there
With partial complex seizures there is aura (sensory or psychological feelings) and automatisms (e.g., fidgeting, lip smacking).
In syncope, there is a transient loss of consciousness, but with warning symptoms and rapid return of alertness following a brief period of unconsciousness (seconds to 3 minutes). There are several forms of syncope:
Vasovagal “attack” or common faint
The patient invariably remembers the onset of fainting. Most common syncope of the benign vasomotor type and tends to occur in young people, especially when standing still (e.g., choir boys). It is the main cause of repeated fainting attacks. The differential diagnosis includes all the other causes of transient loss of consciousness and, in particular, a seizure disorder. Its associated features are:
i. Occurs while standing, or rarely sitting
ii. Warning feelings of dizziness, faintness, or true vertigo
iii. Nausea, hot and cold skin sensations
iv. Fading hearing or blurred vision
v. Sliding to ground (rather than heavy full-length fall)
vi. Rapid return of consciousness
vii. Pallor and sweating and bradycardia
This uncommon event may occur after micturition in older men, especially during the night when they leave a warm bed and stand void. The cause appears to be peripheral vasodilatation associated with reduction of venous return from standing.
Severe coughing can result in obstruction of venous return with subsequent blackout. This is also the mechanism of blackouts with breath-holding attacks.
Caused by pressure on a hypersensitive carotid sinus (e.g., in some elderly patients who lose consciousness when their neck is touched).
Exertion or effort syncope is due to obstructive cardiac disorders, such as aortic stenosis and hypertrophic obstructive cardiomyopathy.
Hyperventilation is a common cause of dizziness and faintness but rarely causes syncope. It is a benign disorder which is caused by overbreathing in response to anxiety. It occurs most commonly but not exclusively in teenage or young women.
Sudden collapse can follow choking. Also known as “café coronary” or
“barbecue coronary” when patient suddenly becomes cyanosed, is speechless, and grasps the throat while eating. This is caused by inhaling a large bolus of meat which obstructs the larynx.
These are episodes of “blackouts” in which the patient falls to the ground and then immediately gets up again. They involve sudden attacks of weakness in the legs. Drop attacks occur in middle-aged women and are considered to be brainstem disturbances producing sudden changes in tone in the lower limbs. Other causes of drop attacks include vertebrobasilar insufficiency, Parkinson’s disease, and epilepsy.
Stokes–Adams attacks and cardiac syncope are manifestations of recurrent episodes of loss of consciousness, especially in the elderly, caused by cardiac arrhythmias. The blackout is sudden with the patient falling to the ground without warning and without convulsive movements, and then by an equally rapid recovery of consciousness, the entire episode usually lasting a matter of seconds. The diagnosis can be confirmed by 24-hour ambulatory monitoring.
Loss of consciousness can occur with vertebrobasilar insufficiency (VBI) transient ischemic attack. Typical preceding symptoms of VBI include dyspnea, vertigo, vomiting, hemisensory loss, ataxia, and transient global amnesia.
The diagnosis should be suspected if there are feelings of hunger, sweating, nervousness and palpitations coupled with episodes of confusion, abnormal speech, or unusual behavior in a patient not at risk for seizures or syncope, and most frequently in diabetics taking oral hypoglycemic agents or insulin. A blood glucose level < 2.5 mmols/l is considered to be hypoglycemia.
Head injuries and unconsciousness
Some non-life-threatening head injuries are serious enough to cause significant loss of consciousness and retrograde amnesia.
Hysterical blackouts or fits are not uncommon and have to be differentiated from hyperventilation. It is unusual for hyperventilation to cause unconsciousness but it is possible that consciousness gets clouded, especially if the patient is administered oxygen.
Other features that suggest psychogenic rather than organic factors are:
12.4 Glasgow Coma Scale (GCS)
12.4.1 Advantages
The advantages of the GCS are that it has face validity, wide acceptance, and established statistical associations with adverse neurological outcomes, including brain injury, neurological intervention, and mortality. However, these are off-set by several important limitations.
12.4.2 Limitations
The GCS predicts mortality well at its extremes and poorly in its midrange, and thus most of its predictive capacity is anchored by the endpoints. The GCS is not reliable. A clinical scale must be reproducible to be accurate and useful. Unfortunately, the GCS contains multiple subjective elements and has repeatedly demonstrated surprisingly low interrater reliability in a variety of settings. The GCS was accurately used by experienced users, while inexperienced ones made consistent errors (up to 4- or 5-point scales) mainly in the intermediate levels of consciousness. The GCS is criticized for failure to incorporate brainstem reflexes which are considered good indicators of brainstem arousal systems’ activity. In addition, the GCS does not incorporate the size and reactivity of patient’s pupils to light. The reliability of the GCS is further compromised in patients with tracheal intubation because verbal response can no longer be evaluated. The GCS is only grossly predictive. The prognostic value of the GCS is weak enough that it cannot accurately predict outcomes for individual patients. Data from the German Rescue System showed that GCS scores of 3–6 during the first two posttraumatic days did not correspond to the outcome after 1 year. Several clinical conditions have great impact on GCS rating, such as sedation, high blood alcohol concentrations (> 240 mg/100 ml) are associated with a 2–3 point reduction in GCS. Similarly, the GCS use in the assessment of the acutely poisoned patient should not be recommended. Mechanism of injury (penetrating versus blunt) and age (> 55 years) were also found to have a major effect in the predictive value of GCS. The stimulation techniques are of utmost importance. The pressure of the finger nail bed with a pencil as was proposed in the GCS falsely lowers the level of responsiveness. The GCS is an ordinal scale. The difference between unit values is not consistent and compares only better with worse. Yet, minimal differences of GCS scores are important in terms of prognosis.
12.5 The Full Outline of Unresponsiveness (FOUR) Score Coma Scale
The FOUR score provides greater neurological detail than the GCS, recognizes a locked-in syndrome, and is superior to the GCS due to the availability of brainstem reflexes, breathing patterns, and the ability to recognize different stages of herniation. The probability of in-hospital mortality was higher for the lowest total FOUR score, when compared with the lowest total GCS score. However, it is even more complicated than the GCS (4 component scales), requires more time to calculate, and has similarly limited interrater reliability.
Wijdicks EF, Bamlet WR, Maramattom BV, Manno EM, McClelland RL. Validation of a new coma scale: The FOUR score. Ann Neurol 2005;58(4):585–593
12.6 Neurotrauma Paediatric Scales
Cranial traumas have different particularities in infants, toddlers, preschool children, school children, and teenagers. The assessment of these cases must be individualized according to age. It is completely different in children than in adults. Trauma scales are very useful in grading the severity and predicting outcome in traumatic brain injury (TBI), but trauma scales used in adults must be adapted for the use in children. Children have age-related specificity and anatomic particularities for each of the period of development.
12.6.2 Paediatric coma scale/children’s coma scale
Simpson D, Reilly P. Pediatric coma scale. Lancet 1982;2(8295):450
12.6.3 Children’s coma score (CCS)
This scale also evaluates eye-opening response and motor response to stimuli, but it is limited only for infants and toddlers. Maximum CCS assignable is 11, and minimal 3. CCS is very useful for all paediatric TBIs in infants and toddlers.
Abbreviation: EOM, extraocular muscles. Source: Raimondi AJ, Hirschauer J. Head injury in the infant and toddler. Coma scoring and outcome scale. Childs Brain 1984;11:12–35 |