Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine) 4th Ed.

CHAPTER

5

Altered Mental Status and Coma

Susan Fuchs

HIGH-YIELD FACTS

• For coma to occur, there must be an insult to both cerebral hemispheres or to the reticular activating system.

• Decorticate posturing signifies dysfunction of the cerebral hemispheres with an intact brain stem.

• Decerebrate posturing signifies a lesion in the midbrain.

• Intussusception can have a “neurologic” presentation ranging from lethargy to obtundation.

The term altered mental status refers to an aberration of a patient’s level of consciousness. It always implies serious pathology and mandates an aggressive search for the underlying disorder. More precise terminology describes the degree of altered mental status and has important implications for differential diagnosis and management:

• Lethargy is a state of reduced wakefulness in which the patient displays disinterest in the environment and is easily distracted but is easily arousable and can communicate.

• Delirium is characterized by agitation, disorientation, delusions, hallucinations, fearful responses, irritability, and sensory misperception.

• Obtundation is severe blunting of alertness with a decreased response to stimuli.

• Stupor exists when the patient can only be aroused by extremely vigorous and repeated stimulation.

• Coma occurs when a profound reduction in neuronal function results in unresponsiveness to sensory stimuli. It constitutes the most severe manifestation of altered mental status. Coma is further categorized depending on the area of the brain affected.13 Several scoring systems exist that permit objective and reproducible assessment of the degree of altered mental status and allow effective communication among health care providers. The most widely used is the Glasgow Coma Scale (GCS), which scores three responses with a range from 3 to 15.2,4 The GCS has been modified so that it can be applied to infants and children. The main difference is the verbal response (Table 5-1).2,5

TABLE 5-1

Glasgow and Children’s Coma Scale

image

PATHOPHYSIOLOGY

In general, patients with altered mental status have suffered a diffuse insult to the brain. For patients with no history of trauma, the most common causes are metabolic abnormalities, poisonings, and infectious etiologies, such as meningitis and encephalitis. For coma to occur, the underlying abnormality must be either damage or dysfunction to both cerebral hemispheres or to the ascending reticular activating system, which transverses the brain stem through the upper pons, midbrain, and diencephalon, and plays a fundamental role in arousal. Coma can result from structural damage to tissue, infectious processes, metabolic derangements, poisonings, or inadequate cerebral perfusion. Metabolic, infectious, and toxic etiologies tend to produce diffuse but symmetric deficits, such as confusion, that precede other abnormalities, such as motor deficits. Structural lesions result in focal deficits that progress in a predictable pattern. Supratentorial lesions produce focal findings that progress in a rostral–caudal fashion, whereas subtentorial lesions result in brain stem dysfunction followed by a sudden onset of coma, cranial nerve palsies, and respiratory disturbances. The causes of coma are listed in Tables 5-2 and 5-3.6,7

TABLE 5-2

Etiology of Altered Mental Status Based on the Mnemonic “Tips from the Vowels”

image

TABLE 5-3

Mnemonic for Coma Using Childhood Immunizations

image

HISTORY

The history of a patient with altered mental status focuses on events prior to the onset of mental status changes including headache, febrile illness, trauma, and drug ingestion. Associated symptoms such as fever, vomiting, diarrhea, or respiratory difficulties are essential clues. Important past medical history includes diabetes, seizure disorder (in the patient or a family member), or underlying heart disease. A prior history of similar episodes may imply an underlying metabolic abnormality, such as an inborn error of metabolism.

PHYSICAL EXAMINATION

The physical examination focuses on assessing the degree of neurologic impairment and localizing the lesion responsible for the patient’s altered mental status. Particular attention is paid to the vital signs, including temperature. Many systemic illnesses that result in central nervous system dysfunction are associated with abnormalities in basic physiologic parameters. Conversely, primary central nervous system pathology often affects cardiovascular and respiratory status. Airway, breathing, and circulation must be evaluated and managed before completing the examination. Important parameters of the general physical examination in patients with altered mental status are outlined in Table 5-4.2

TABLE 5-4

Important Parameters of the General Physical Examination of

Patients with Altered Mental Status

image

The general neurologic evaluation focuses on an exact description of the patient’s mental status, which provides a baseline for comparison during the course of illness. Cranial nerves and motor function are assessed for potentially localizing findings, which may indicate a mass lesion. For patients with severely depressed mental status, it is especially important to evaluate the response of the extremities to a painful stimulus. The biceps, triceps, patellar, and Achilles reflexes are tested for strength and symmetry and the patient is evaluated for the presence of a Babinski response, which indicates an upper motor neuron lesion.

For patients in coma, the area of the brain involved can be localized by considering physical examination findings (Table 5-5).2,3,6,8

TABLE 5-5

Localization of the Area of Brain Dysfunction Using Physical Findings

image

DIAGNOSTIC TESTING

All patients with altered mental status should have a bedside glucose determination and the serum glucose should be checked. Other helpful studies include complete blood count with differential and platelets, electrolytes, calcium, renal functions, and urinalysis. In some cases, arterial blood gas and serum ammonia are indicated. For patients who may have ingested a toxin, consider a urine drug screen, as well as blood levels for suspected toxins such as alcohol. Other lab tests should be individualized, but may include liver function tests, thyroid functions, or carboxyhemoglobin concentration. Infants suspected of suffering from inborn errors of metabolism are usually identified by abnormalities of blood gas, blood sugar, lactate, or ammonia. If infection is suspected, cultures are obtained from the blood, urine, and cerebrospinal fluid. Lumbar puncture is withheld until increased intracranial pressure (ICP) is excluded.2,3,6,8,9

Radiographic examination of the cervical spine is performed if there is any suspicion of trauma. If physical examination findings suggest a structural lesion, herniation, or increased ICP, a computed tomography (CT) scan should be performed. Although magnetic resonance imaging (MRI) may provide more information for certain etiologies of coma, a CT scan quickly identifies life-threatening conditions requiring emergent interventions. An electroencephalogram (EEG) is useful to diagnose seizures and some metabolic and infectious disorders but is not an emergency department procedure unless needed to diagnose nonconvulsive status epilepticus.2,3,6,810

THERAPY

The first priority in the emergency department management of a patient with altered mental status is stabilization of the airway, breathing, and circulation. Intubation is required for patients with altered mental status who have lost protective airway reflexes and who are at risk for aspiration. Intubation is also indicated for patients with evidence of critically increased ICP.

All patients should receive oxygen and, if hypoglycemia is suspected, 0.5 to 1.0 g/kg of glucose. If ingestion is suspected, a trial of naloxone (0.1 mg/kg up to 2 mg) may prove useful. If there is concern for infection, antibiotics (ceftriaxone 100 mg/kg, vancomycin 15 mg/kg, and acyclovir 20 mg/kg) should be given.8 Patients who are hypotensive are resuscitated with crystalloids. Fluids are titrated carefully for patients who may have increased ICP, in whom overaggressive hydration can precipitate herniation. But hypotension must be corrected, since it can result in cerebral hypoperfusion and ischemia.2,810

Hypertension can be secondary to increased ICP, but can also be due to hypertensive encephalopathy. If the etiology is the latter, the blood pressure should be lowered slowly. The goal is to lower the diastolic blood pressure to 100 to 110 mm Hg or a maximum of 25% over 2 to 6 hours.9,11

Hyperventilation produces vasoconstriction of the cerebral arteries and has been used as the treatment for impending herniation due to elevated ICP. If there are no signs of impending herniation, it is best not to reduce the PCO2below 35 Torr because severe vasoconstriction and cerebral ischemia can result. Elevating the head of the bed to 30 degrees may also be beneficial.5,12 In cases where ICP monitoring is desired, a neurosurgeon should be consulted. Mannitol or furosemide may be useful adjuncts for patients with severely increased ICP, but hypotension must be avoided. Hypertonic saline (3%) has been found to be beneficial in reducing increased ICP in pediatric traumatic brain injury and in diabetic ketoacidosis, but exact dosing is unclear.13,14 Additional therapy is directed at maintaining normal body temperature, controlling seizures, and correcting acid–base or electrolyte abnormalities. Further management in the emergency department may include the administration of antibiotics or antidote therapy for poisons.2

DISPOSITION

Patients with significant alteration in mental status are best managed in an intensive care unit. For patients with milder disease, the decision to admit to the hospital or discharge from the emergency department largely depends on the etiology of the problem.

SPECIAL CONSIDERATIONS

Several causes of altered mental status and coma are characteristic of the pediatric population and deserve special mention. None are common, but all represent serious problems that confront the emergency physician.

image LEAD ENCEPHALOPATHY

Although lead toxicity severe enough to cause encephalopathy is now rare, it is a consideration in the differential diagnosis of any child with profoundly altered mental status or coma. Lead encephalopathy can be associated with increased ICP and seizures. Patients with lead encephalopathy often have a history of pica and parents may have noted abdominal pain, constipation, or vomiting prior to the development of encephalopathy.6 The evaluation and management of lead encephalopathy requires the consultation with a toxicologist.

image INTUSSUSCEPTION

Intussusception is a fairly common gastrointestinal emergency in children younger than 3 years. Although this entity commonly presents with episodes of intermittent abdominal pain and vomiting, there is a “neurologic presentation” in which the child manifests a depressed level of consciousness that can range from lethargy to obtundation. The overall appearance of the patient can mimic shock, with fulminant sepsis a consideration. In some cases, the abdominal examination may reveal a mass and rectal examination shows heme-positive or “currant jelly” stools.6,10 Intussusception is discussed in detail in Chapter 48.

image REYE’S SYNDROME

Reye’s syndrome is a disorder characterized by the presence of encephalopathy, elevated liver enzymes, and the presence of microvesicular fatty changes in the liver. It is now rarely diagnosed. This is attributed to advances in diagnosis of inborn errors of metabolism (especially medium-chain acyl-CoA dehydrogenase [MCAD] deficiency).15

image INBORN ERRORS OF METABOLISM

Numerous inborn errors of metabolism can present early in life with vomiting, seizures, and altered mental status. These disorders are discussed in Chapter 79.

image HYPOGLYCEMIA

In any patient with altered mental status, hypoglycemia is a consideration. See Chapter 76 for further discussion.

image CONGENITAL ADRENAL HYPERPLASIA

In a child with congenital adrenal hyperplasia, hypoglycemia may result from the absence of cortisol. A constellation of symptoms such as lethargy, vomiting, dehydration, and altered mental status should suggest this disorder. See Chapter 77 for further discussion.

REFERENCES

1. Plum F, Posner JB. The Diagnosis of Stupor and Coma. 3rd ed. Philadelphia, PA: FA Davis; 1980.

2. Taylor DA, Ashwal S. Impairment of consciousness and coma. In: Swaiman KF, Ashwal S, Ferriero DM, eds. Pediatric Neurology: Principles and Practice. 4th ed. Philadelphia, PA: Mosby/Elsevier; 2006:1377–1400.

3. Fenichel GM. Altered states of consciousness. In: Fenichel GM, ed. Clinical Pediatric Neurology: A Signs and Symptoms Approach. 6th ed. Philadelphia, PA: Saunders/Elsevier; 2009:49–78.

4. Jennet B, Teasdale G. Aspects of coma after severe head injury. Lancet. 1977;1:878.

5. Karl SR. Trauma. In: Fuchs S, Yamamoto L, eds. APLS, The Pediatric Emergency Medicine Resource. 5th ed. Sudbury, MA: Jones and Bartlett Publishers; 2012:204–261.

6. Trainor JL, Fuchs S, Isaacman DJ. Central nervous system. In: Fuchs S, Yamamoto L, eds. APLS, The Pediatric Emergency Medicine Resource. 5th ed. Sudbury, MA: Jones and Bartlett Publishers; 2012:168–203.

7. Schunk JE. The pediatric patient with altered level of consciousness; remember your “immunizations”. J Emerg Nurs. 1992;18:419–421.

8. Michelson D, Thompson L, Williams E. Evaluation of stupor and coma. In: Basow DS, ed. UpToDate. Waltham, MA:UpToDate; 2012.

9. Thompson L, Williams E. Treatment and prognosis of coma in children. In: Basow DS, ed. UpToDate. Waltham, MA: UpToDate; 2012.

10. Nelson DS. Coma and altered level of consciousness. In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 6th ed. Philadelphia, PA: Wolters Kluwer/Lippincott, Williams & Wilkins; 2010:176–186.

11. Williams O, Brust JC. Hypertensive encephalopathy. Curr Treat Options Cardiovasc Med. 2004;6:209.

12. Kleinman ME, Chameides L, Schexnayder SM, et al. Part 14: Pediatric advanced life support, 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;112:S876–S908.

13. Kochanek PM, Carney N, Adelson PD, et al. Hyperosmolar therapy. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents, 2nd ed. Pediatr Crit Care Med. 2012;13(suppl 1):S36–S41.

14. Kamat P, vats A, Gross M, et al. Use of hypertonic saline for the treatment of altered mental status associated with diabetic ketoacidosis. Pediatr Crit Care Med. 2003;4:239–242.

15. Orlowski JP. Whatever happened to Reye’s syndrome? Did it ever really exist? Crit Care Med. 1999;27:1582–1587.