100 The Vital Signs and Resuscitation
Fig. 6.4. Management of the Comatose Patient.
Management of Altered Level of Consciousness
In contrast to the traditional approach in medicine, the comatose patient or the patient with a significant alteration in level of consciousness requires immediate management before completing the physical exam and acquiring the history.
The ABCs of resuscitation are followed (Fig. 6.4). When an immobilized patient arrives in the emergency department, the cervical collar and backboard
Vital Sign #5: Level of Consciousness 101
are left in place until a cause is found for the decrease in level of conscious-ness. Naloxone (Narcan) 2 mg and thiamine (vitamin B-1) 100 mg are administered intravenously. If a fingerstick blood sugar is low or unavail-able, glucose (50 cc of 50% dextrose) is administered after thiamine to reverse hypoglycemia.
Naloxone reverses the effects of a narcotic by competitive inhibition at the opioid receptor site. Thiamine prevents Wernicke’s Encephalopathy, a rare neurological condition caused by thiamine deficiency seen in alcoholics with poor nutrition. Signs and symptoms include nystagmus, occular nerve palsy, ataxia and confusion. Thiamine functions as a coenzyme in the break-down of glucose. Glucose given before thiamine depletes what little thia-mine is available for glucose metabolism and may precipitate the syndrome. Glucose and thiamine may be administered at the same time.
Naloxone, thiamine and glucose were referred to in the past as a “coma 6 cocktail” and were often automatically administered. If a fingerstick glucose
is normal, administering glucose is not indicated. The same applies to thia-mine in the pediatric population. If a drug overdose is suspected, activated charcoal is administered by gastric tube after endotracheal intubation (Fig. 6.4).
Increased Intracranial Pressure
Increased intracranial pressure is a life-threatening event and must be dealt with immediately. Common causes are a head injury with intracranial bleeding and a hemorrhagic stroke. Signs include papilledema, loss of spon-taneous venous pulsations, an increase in systolic pressure, bradycardia, an abnormal respiratory pattern and a fixed dilated pupil.
Carbon dioxide is a potent vasodilator in the brain and hyperventilation blows off carbon dioxide and reduces pressure. Mannitol is an osmotic diuretic that removes excess fluid from the brain. Increased intracranial pressure blocks blood flow to the brain, and the hypoxia triggers an increase in systolic pres-sure to re-establish flow.The increased blood pressure causes a baroreceptor decrease in heart rate, and pressure against the RAS of the pons and medulla decreases the heart and respiratory rates. The triad of increased blood pres-sure, decreased heart rate and irregular breathing is the Cushing reflex. In adults, often only the blood pressure rises. The triad occurs more often in pediatrics. Intracranial pressure may cause the brain to push against the third cranial nerve on that side causing a fixed dilated pupil, indicating compres-sion of the lower part of the temporal lobe (uncus) against the tentorium cerebelli with impending herniation (Fig. 6.5).
Treatment: intubation, hyperventilation, the head of the bed is raised 30˚ (except in the trauma patient with a cervical collar), furosemide 40 mg
102 The Vital Signs and Resuscitation
Fig. 6.5. Increased Intracranial Pressure (ICP).
IV and/or mannitol 1 gm/kg IV is administered in consultation with a neu-rosurgeon.
Signs of Metabolic Injury
Signs of metabolic injury, implying an intact brainstem, are roving eye movements, a pupillary reaction to light (pinpoint pupils suggest opiates or a pontine lesion. Dilated reactive pupils are seen with adrenergic or anticho-linergic drugs), a normal oculocephalic reflex (doll’s eyes) consisting of abruptly rotating the head to one side while the eyes deviate in the opposite direction (this test should not be used in the trauma patient unless the c-spine has been cleared), a normal oculovestibular reflex (instilling 50 ml of cold water into the auditory canal causes deviation of the eyes toward the water) and hyporeflexia.
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Signs of Structural Injury
Signs of structural injury from trauma or stroke are fixed pupils, either large or pinpoint (pinpoint pupils suggest a pontine hemorrhage. Fixed mid-position pupils implies brainstem damage. One fixed dilated pupil suggests impending uncal herniation), no extra-ocular movements, loss ofoculocephalic and oculovestibular reflexes, differences in movements of arms and legs, asym-metry and increased deep tendon reflexes with upgoing toes (Babinski’s
Fig. 6.6. Metabolic vs. Structural Signs of Coma.
reflex) and decorticate or decerebrate posturing (arm flexion and leg ex-tension in decorticate posturing represents injury to both cerebral hemi-spheres; extension of the arms and legs in decerebrate posturing represents injury to the brainstem). Decerebrate and decorticate posturing may occur in metabolic derangements, but more commonly are seen with structural damage. Fixed ocular deviation is toward a cortical lesion (Figs 6.7, 6.8).
Vital signsmay give a clue to the etiology. Hypothermia (including meta-bolic causes such as hypothyroidism, hypoadrenalism, hypoglycemia and sepsis) and hyperthermia may all cause a decreased level of consciousness.
104 The Vital Signs and Resuscitation
6 Fig. 6.7. Oculovestibular Reflex.
Fig. 6.8. Decerebrate vs. Decorticate Posturing.
Tachyarrhythmias and bradyarrhythmias suggests cardiac disease. Hyper-ventilation is seen in diabetic ketoacidosis, uremia and cirrhosis. Hypoventilation is common in opiate drug overdoses and in pulmonary disease. Hypotension requires searching for the etiology of shock (see Chap-ter 5). Hypertension suggests hypertensive encephalopathy or drugs such as cocaine (Chapter 5).
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