Kathleen M. Adelgais
ALTERED MENTAL STATUS
EPIDEMIOLOGY
Altered mental status (AMS) in children is defined as failure to respond to verbal or physical stimulation in a manner appropriate for the child’s developmental level.
The incidence and etiologies of AMS in children are quite varied, and depend on the type of institution and specific definition of AMS used.
Aggressive resuscitation, stabilization, diagnosis, and treatment must occur simultaneously to prevent morbidity and death in children with AMS.
PATHOPHYSIOLOGY
Alterations in mental status result from either depression of both cerebral cortices or localized abnormalities of the reticular activating system in the brain stem and midbrain, and range from confusion or delirium to lethargy, stupor, and coma.
Pathologic conditions that result in AMS can be divided into three broad categories: supratentorial mass lesions, subtentorial mass lesions, and metabolic encephalopathy.
Supratentorial mass lesions cause AMS by compressing the brain stem and/or diencephalon. Focal motor abnormalities are often present from the onset of alteration in consciousness. Neurologic dysfunction progresses from rostral to caudal, with sequential failure of midbrain, pontine, and medullary function. Supratentorial lesions cause slow nystagmus toward, and fast nystagmus away from a cold stimulus during caloric testing.
Subtentorial lesions produce rapid loss of consciousness (due to dysfunction of the reticular activating system), cranial nerve abnormalities, abnormal breathing patterns (eg, Cheyne–Stokes respirations, neurogenic hyperventilation, ataxic breathing), and asymmetric or fixed pupils.
Metabolic encephalopathy produces decreased level of consciousness before exhibiting motor signs, which are symmetrical when present. Pupillary reflexes are intact except with profound anoxia, opiates, barbiturates, and anticholinergics. Respiratory changes are common and are often due to associated acid–base disturbances.
CLINICAL FEATURES
Historical data should focus on prodromal events, such as recent illnesses, infectious exposures, toxic exposures, and the possibility of trauma or abuse. Ask about antecedent fever, headaches, head tilt, abdominal pain, vomiting, diarrhea, gait disturbance, seizures, drug ingestion, palpitations, weakness, hematuria, weight loss, and rash; review developmental milestones, past medical history, immunization history, and family history.
Focus the physical examination on signs of infection, trauma, toxidromes, or metabolic disease.
The neurologic examination includes the child’s response to sensory input, motor activity, pupillary reactivity, oculovestibular reflexes, and respiratory pattern, as well as the child’s performance on the AVPU (alert, response to verbal stimuli, response to painful stimuli, unresponsive) or pediatric Glasgow coma score.
DIAGNOSIS AND DIFFERENTIAL
The differential diagnosis for AMS in children is diverse and differs slightly from that for adults. The familiar mnemonic AEIOU TIPS remains a useful tool in organizing diagnostic possibilities (Table 79-1).
Diagnostic adjuncts are guided by the clinical presentation and may include analysis of blood, gastric fluid, urine, stool, cerebrospinal fluid (CSF), electrocardiography, or selected radiographie studies. Obtain a rapid bedside glucose in all patients with AMS.
For suspected meningitis or encephalitis, obtain a lumbar puncture for CSF analysis as rapidly as possible after initial resuscitation and stabilization.
Capnometry may be useful for rapid assessment of acid–base status.
Obtain 12-lead ECG if pathologic auscultatory findings or rhythm disturbances are noted.
Consider blood ammonia level, serum osmolality, blood alcohol level, thyroid function tests, blood lead level, and skeletal survey and head CT for concerns of trauma or abuse.
A portable electroencephalograph may diagnose non-convulsive status epilepticus.
TABLE 79-1 AEIOU TIPS Mnemonic for Diagnosing Altered Mental Status (AMS)
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Initial treatment priorities are airway, breathing, and circulation.
Immobilize cervical spine for suspected trauma.
Initiate continuous pulse oximetry and consider capnometry; administer oxygen.
Provide fluid resuscitation (20 mL/kg three times as needed) for signs of shock.
Perform bedside glucose determination and treat hypoglycemia with 4 mL/kg of D10 in infants or 2 mL/kg of D25 in children.
Treat hypothermia or hyperthermia.
Control seizures with benzodiazepines (eg, lorazepam, 0.1 milligram/kg IV/IO).
Give naloxone for suspected opiate or clonidine overdose, 0.01 to 0.1 milligram/kg IV/IO every 2 minutes as needed.
Give flumazenil for suspected pure benzodiazepine overdose, 0.01 milligram/kg IV/IO.
Avoid sodium bicarbonate except as specifically indicated for select toxic ingestions or serum pH <7.0.
Administer empiric broad-spectrum antibiotics as quickly as possible, before lumbar puncture if unstable, to all patients with suspected sepsis or meningitis.
Most infants and children with AMS require admission to an intensive care unit, although benign and transient causes of AMS may be treated and monitored in the ED with discharge after observation.
HEADACHE
EPIDEMIOLOGY
Headaches comprise up to 1% of pediatric ED visits.
The vast majority of headaches in children have a benign etiology. Occipital location of the headache and the inability of the child to describe the quality of the head pain are associated with potentially serious underlying causes.
Emergent neurosurgical conditions presenting with headache are usually associated with neurologic signs.
PATHOPHYSIOLOGY
The pathogenesis of headache is complex and varies by cause. The brain, the cranium, and most of the overlying meninges lack pain receptors. Pain is perceived from structures between the epidermis of the scalp and periosteum of the skull.
Extracranial pain can arise from cervical nerve roots, cranial nerves, or extracranial arteries traversing muscles, leading to pain within specific areas of the head and neck region.
Intracranial pain can arise from venous sinuses, dural veins or arteries, and arteries around the base of the brain. Posterior fossa pain can be referred to the occiput, ear, or throat, secondary to nociceptors from the vagus and glossopharyngeal nerves.
CLINICAL FEATURES
Headaches can be classified as either primary or secondary: primary headaches are physiologic (migraine, tension), while secondary headaches have an anatomic basis (vascular malformation, tumor, or infectious). Table 79-2outlines elements of the history and physical examination that aid in the differentiation between primary and secondary headaches.
Secondary headache is suggested by acute onset; morning vomiting; behavioral changes; AMS; worst headache ever; awakening from sleep; association with fever, trauma, or toxic exposure; or aggravation by coughing, valsalva, or position.
Benign headaches are more likely to occur in school-aged children and are often described as pulsating. They tend to be unilateral/bilateral, frontal or temporal in location, and vary from mild to intense without associated neurologic symptoms or signs.
Life-threatening headaches are more likely in preschool-aged children. The pain may be occipital and constrictive in nature if described. Pain is usually intense, and the headache is often associated with neurologic changes such as focal deficits, papilledema, ataxia, and AMS.
Physical findings suggestive of a secondary headache include blood pressure abnormalities, nuchal rigidity, head tilt, ptosis, retinal hemorrhage or optic nerve distortion, visual field defects, gait disturbances, or focal motor or sensory deficits (Table 79-3).
TABLE 79-2 Features Suggesting Secondary Headache
TABLE 79-3 Physical Examination Findings Associated with Potential Secondary Causes of Headache
DIAGNOSIS AND DIFFERENTIAL
There are no evidence-based studies to guide the diagnostic work-up of headache in children. The selection of studies should be guided by the history and physical examination.
Practice guidelines state that routine imaging is not indicated in children with recurrent headaches and a normal neurologic examination. Neuroimaging (computed tomography or magnetic resonance imaging) may be indicated in trauma or when history or physical examination suggests a secondary type of headaches.
Perform a lumbar puncture if infection or subarachnoid hemorrhage is suspected.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Obtain a throughout history and physical examination to distinguish primary from secondary headache.
For secondary headaches, treat the underlying cause and manage pain. Narcotics can be used for pain related to secondary headaches but have no role in the management of primary headaches. For secondary headaches, consider morphine 0.1 milligram/kg IV, or hydrocodone with acetaminophen (0.1 milligram/kg of hydrocodone component, PO).
For primary headaches, treat based on type of headache diagnosed by historical features. Most primary headaches can be treated with first-line oral therapy, typically ibuprofen 10 milligrams/kg PO or acetaminophen 15 milligrams/kg PO/PR.
For migraines, consider prochlorperazine 0.15 milligram/kg IV with diphenhydramine 1 milligram/kg IV to prevent dystonic reactions or use of a triptan (see cluster headache below). Dihydroergotamine 0.1 milligram/kg (ages 6–9 years), 0.15 milligram/kg (ages 9–12 years), or 0.2 milligram/kg (ages 12–16 years) is an alternative, but is contraindicated in patients with complex migraine.
Cluster and tension headaches are managed much the same way as migraines. Sumatriptan 10 milligrams (20–39 kg) or 20 milligrams (>40 kg) intranasal or 0.06 milligram/kg subcutaneously and high-flow oxygen (7 L/minute via non-rebreather mask) may be effective for cluster headaches. Tension headaches usually respond to first-line oral therapy such as ibuprofen 10 milligrams/kg.
Address potential precipitating factors to avoid reoccurrence of the headache. Consider prophylactic regimens such as β-blockers for migraines, usually in consultation with neurology.
In general, most patients with primary headache can be discharged after relief of symptoms. Those with intractable pain may require inpatient management.
Patients with secondary headache of emergent origin (eg, meningitis, tumor, severe hypertension, or hemorrhage) require inpatient treatment for definitive care.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 130, “Headaches in Children,” by Brian R. E. Schultz and Charles G. Macias and Chapter 131, “Altered Mental Status in Children,” by Jonathan I. Singer.