What is the approach to diagnosing and managing alteration of consciousness?

Approach to Altered Consciousness: Diagnostic Algorithm

Immediate Life-Threatening Assessment (First 10 Seconds)

Any unconscious patient with absent or abnormal breathing must be assumed to be in cardiac arrest until proven otherwise, and CPR should be initiated immediately if no definite pulse is detected within 10 seconds. 1

• Check for pulse for no more than 10 seconds; if absent or uncertain, assume cardiac arrest and begin CPR 1
• Recognize that agonal breathing (present in 40-60% of cardiac arrest victims) is commonly misinterpreted as adequate breathing, causing dangerous delays in resuscitation 1
• Administer supplemental oxygen at 10 L/min for all patients with altered consciousness and hypoxemia (saturation <94%) 1

Primary Survey: ABCDE Approach

Once cardiac arrest is ruled out, systematically assess in order of life-threatening priority:

Airway

• Ensure patent airway; altered consciousness commonly leads to airway compromise 2, 3
• Position patient appropriately and consider airway adjuncts if needed 3

Breathing

• Assess respiratory rate, pattern, depth, and oxygen saturation 3, 4
• Monitor for respiratory depression, particularly in suspected overdose 5

Circulation

• Measure blood pressure and heart rate 3, 4
• Assess for signs of shock; in children with coma and shock, consider 20-40 mL/kg of 0.9% saline or 4.5% human albumin, with human albumin preferred 1
• For pediatric patients with persistent shock despite 40 mL/kg fluid, proceed to elective intubation and central venous catheter placement 1

Disability (Neurological Assessment)

• Use Glasgow Coma Scale (GCS) as the primary tool for initial assessment 1, 6
• GCS evaluates: eye opening (1-4 points), verbal response (1-5 points), motor response (1-6 points), total 3-15 1
• For severely affected, intubated, or suspected brainstem injury patients, prioritize the FOUR Score over GCS 1, 6, 7
• FOUR Score evaluates: eye response, motor response, brainstem reflexes, and respiratory pattern (0-4 points each) 1
• For rapid triage, use AVPU/ACDU scale (Alert, Verbal, Pain, Unresponsive) 6

Exposure

• Check for signs of trauma, needle marks, rashes, or other physical findings 3, 4

Differential Diagnosis Framework

Distinguish TLOC (Transient Loss of Consciousness) from Other Conditions

Syncope characteristics (most common cause of transient LOC, affecting 1 in 4 people):

• Sudden, transient loss of consciousness with inability to maintain postural tone 8
• Spontaneous return to baseline with no therapeutic intervention 8
• No prolonged confusion 8
• Typical triggers: pain, emotion, seeing blood, blood draws, prolonged standing 1
• Duration: brief (5-10 seconds of complete cerebral perfusion disruption) 8

Red flags distinguishing from syncope:

• Oral automatisms (chewing, smacking, blinking) suggest epilepsy 8
• Cyanotic face suggests epilepsy or cardiac syncope 8
• Eyes open during unconsciousness suggests epilepsy or syncope (eyes closed only in shallow syncope) 8
• Eyes closed during unconsciousness suggests psychogenic pseudosyncope, psychogenic non-epileptic seizures, or concussion 8
• Lateral tongue biting (uni- or bilateral) strongly suggests epilepsy over syncope 8
• Prolonged head turning (>30 seconds) suggests epileptic seizure 8
• Stertorous (snoring) breathing lasting >10 seconds suggests epileptic seizure 8
• Apparent LOC lasting 10-30 minutes indicates NOT true TLOC—consider psychogenic causes or metabolic/traumatic LOC 8
• Eye fluttering suggests psychogenic non-epileptic seizures over epilepsy 8

Three Mechanisms of Syncope

1. Vasomotor instability: decreased vascular resistance or venous return 8
2. Reduced cardiac output: pump failure, mechanical obstruction, or arrhythmias (most lethal) 8
3. Neurologically reduced cerebral perfusion: cerebrovascular disease or vasospasm 8

Historical Clues for Diagnosis

High-Risk Features (Cardiac Syncope)

• History of heart disease suggests arrhythmia or structural cardiac cause 8
• Sudden death in family members <40 years suggests genetic arrhythmia/cardiomyopathy 8
• Diabetes mellitus increases risk of cardiac syncope and orthostatic hypotension 8
• No prior syncope before age 35 makes vasovagal syncope less likely 8

Medication-Related

• Recent medication changes suggest vasovagal syncope (volume depletion, antihypertensives), orthostatic hypotension, or arrhythmia (long QT) 8
• Antidepressants or antipsychotics suggest orthostatic hypotension 8

Neurological Causes

• Parkinsonism, impotence, and micturition problems suggest orthostatic hypotension from autonomic failure 8
• Paresis, ataxia, brainstem signs suggest vertebrobasilar TIA or seizure 8
• Sudden severe headache with later vomiting and nuchal rigidity suggests subarachnoid hemorrhage 8
• Structural brain damage or history of epilepsy points to seizure 8

Benign Features

• Earlier vasovagal syncope before age 35 makes vasovagal syncope much more likely 8
• Family history of vasovagal syncope makes it much more likely (background rate is one-third of population) 8

Essential Laboratory and Bedside Tests

• Check blood glucose immediately: hypoglycemia (<3 mmol/L) should be considered in cases of seizures or posturing 1
• Urinary incontinence does NOT differentiate epileptic seizures from syncope, nor epilepsy from psychogenic TLOC 8

Prolonged Disorders of Consciousness (>24 hours)

Behavioral Assessment

• Use Coma Recovery Scale-Revised (CRS-R) as the reference tool to distinguish vegetative state/unresponsive wakefulness syndrome (VS/UWS) from minimally conscious state (MCS) 7, 8
• The CRS-R significantly reduces misdiagnosis rates compared to other scales 7
• Absence of behavioral response does NOT mean absence of consciousness 7

Advanced Instrumental Techniques (Multimodal Assessment)

For non-responsive patients:

• PET with FDG should be considered integral to multimodal evaluation 1, 7
• Add resting-state fMRI during any indicated structural MRI to evaluate the default mode network 1, 7, 8
• Consider active fMRI paradigms for patients without command-following at bedside (moderate evidence) 8, 7

For prognostication in traumatic brain injury:

• MRI at 6-8 weeks post-injury evaluating corpus callosum, dorsolateral upper brainstem, or corona radiata lesions (strong recommendation, level B) 1, 7
• SPECT at 1-2 months post-trauma predicts 12-month recovery (level B) 1, 7, 8

Electrophysiology:

• Visual analysis of standard EEG detects preserved consciousness with high specificity but low sensitivity 8, 7
• Quantitative high-density EEG and TMS-EEG should be considered to differentiate VS/UWS from MCS 8, 7
• Sleep EEG helps differentiate VS/UWS from MCS 8, 7
• Cognitive evoked potentials (P300) at 2-3 months post-trauma predict 12-month recovery 7
• Somatosensory evoked potentials may predict 24-month recovery in post-anoxic VS/UWS 8, 7

Critical Pitfalls to Avoid

• Sedation, powerful analgesics, and neuromuscular blockade affect FOUR score evaluation, particularly the respiratory component in ventilated patients 6, 7
• Agonal breathing mimics adequate breathing—do not delay resuscitation 1
• High misdiagnosis rates persist without CRS-R use in prolonged disorders of consciousness 7
• Instrumental techniques are essential for detecting consciousness in behaviorally non-responsive patients but have decreased utility in patients already showing minimal behavioral response 7
• Benzodiazepine overdose manifests as CNS depression ranging from drowsiness to coma; flumazenil may be used for reversal but carries seizure risk, particularly in long-term benzodiazepine users and cyclic antidepressant overdose 5

Monitoring During Assessment

• Record baseline blood pressure before any sedation, then at 3-5 minute intervals 1
• Tachycardia and hypertension indicate inadequate sedation; bradycardia and/or hypotension indicate oversedation 1
• Monitor respiration, pulse, and blood pressure continuously in altered consciousness 5