Symptom-Based Diagnosis in Pediatrics (CHOP Morning Report) 1st Ed.

CASE 8-1

Three-Year-Old Boy

NATHAN TIMM

HISTORY OF PRESENT ILLNESS

The patient is a 3-year-old African-American boy who, according to his father, became unresponsive soon after he began “acting strange.” The father reports that over the course of the afternoon his son complained of a headache and seemed to be sleepier. The boy regained consciousness after his father took him outside into the cold fall air. He was well prior to that afternoon and did not have any other illness. There was no witnessed ingestion. There were no sick contacts at home; however, that afternoon, both the mother and father developed nausea, headaches, and dizziness as well. The family had spent the day inside cleaning the attic, starting the furnace, and organizing the kitchen. An 8-month-old sister was taking a nap at home and did not appear to have any symptoms.

MEDICAL HISTORY

The boy had a febrile seizure at 1 year of age. He had an inguinal hernia repaired at 3 months of age. His medical history was otherwise unremarkable.

PHYSICAL EXAMINATION

T 37.5°C; RR 23/min; HR 100 bpm; BP 111/51 mmHg

Weight 50-75th percentile

Physical examination revealed an alert and playful child in no apparent distress.

There were no oral lesions. There was no lymphadenopathy. The lungs were clear and the heart sounds were normal. His neurologic examination was intact, and the remainder of his examination was also normal.

DIAGNOSTIC STUDIES

During the initial evaluation, the father revealed a key piece of history prompting a simple blood test that revealed the diagnosis.

DISCUSSION CASE 8-1

DIFFERENTIAL DIAGNOSIS

The etiology of central nervous system depression in a 3-year-old is diverse. Common causes include accidental toxin exposures including opiates, carbon monoxide, iron, sedative-hypnotics, clonidine, antihistamines, and alcohol. Metabolic disorders such as hypoglycemia, hyper/hyponatremia, and hypocalcemia should also be considered. Infectious causes such as food poisoning or postviral syndromes may cause multiple family members to experience similar symptoms. Less likely infectious causes are encephalitis and meningitis. Complex partial seizures with a brief postictal period should also be considered. The features of this case that are remarkable are the central nervous system depression that rapidly resolved when the child was taken outside and the similar symptoms present in other family members.

DIAGNOSIS

The father reported that he had turned on the furnace earlier in the day for the first time that fall. The child’s carboxyhemoglobin (HbCO) value was 16.9%. The diagnosis is carbon monoxide poisoning.

INCIDENCE AND PHYSIOLOGY OF CARBON MONOXIDE POISONING

Accidental carbon monoxide poisoning accounts for nearly 500 deaths each year. House fires are responsible for the majority of these deaths; however, tobacco smoke, automobile exhaust, and faulty heating equipment causing incomplete combustion release carbon monoxide and contribute to accidental exposure. The gas is odorless and colorless and binds to hemoglobin with an affinity 200-300 times that of oxygen leading to tissue hypoxia (Figure 8-1). Increased minute ventilation and the presence of fetal hemoglobin make young children particularly susceptible to the effects of carbon monoxide.

Image

FIGURE 8-1. Oxygen/carbon monoxide dissociation curve. (Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th Edition: http:/www.accessmedicine.com. Copyright © The Mc-Graw-Hill Companies, Inc. All rights reserved.)

CLINICAL PRESENTATION

A high index of suspicion for carbon monoxide poisoning should be given to any child who is a fire victim or exposed to other devices that cause incomplete combustion. Clinical symptoms can be categorized into mild, moderate, or severe. Mild symptoms include headache, exercise-induced dyspnea, and confusion. Moderate poisoning causes nausea, vomiting, drowsiness, and incoordination. Severe intoxication leads to coma, convulsions, hypotension, and death. The classic “cherry red” skin color is rarely seen at any level of exposure.

DIAGNOSTIC APPROACH

Carboxyhemoglobin level. Carboxyhemoglobin level is the diagnostic and often prognostic test for carbon monoxide poisoning. Spectrophotometric detection methods using co-oximetry are most useful clinically because they distinguish between HbCO and oxygenated hemoglobin. HbCO levels may help stratify patients into mild, moderate, or severe intoxication; however, blood HbCO levels will fall rapidly over time and may not correlate with persistent cellular dysfunction. Mild symptoms develop with HbCO levels of 20%. HbCO levels 20%-60% present with moderate symptoms, while levels greater than 70% are often fatal.

Other studies. Anemia, myoglobinuria, and metabolic acidosis are other significant complications from carbon monoxide poisoning; therefore, complete blood count, urinalysis, electrolytes, electrocardiogram, and arterial blood gas should be obtained. Pulse oximetry is likely to be normal since it does not discriminate between the forms of hemoglobin.

TREATMENT

The antidote for carbon monoxide poisoning is oxygen. The half-life of carboxyhemoglobin is approximately 4 hours in a patient breathing room air at sea level. If that same patient is placed on 100% oxygen, the half-life of HbCO drops to 1 hour. The goal is to administer 100% oxygen until the HbCO level is less than 5%. Hyperbaric oxygen at 2-3 atmospheres further reduces the half-life of HbCO to 30 minutes; however, its routine use is still controversial. Risks from hyperbaric oxygen treatment include pneumothorax, oxygen toxicity, tympanic membrane rupture, and decompression sickness. Nevertheless, indications for hyperbaric oxygen include victims who are neonates, pregnant, or have history of coma, seizures, or arrhythmias secondary to intoxication and consultation with a hyperbaric center early on should be considered. Other management issues include correction of anemia if Hb is less than 10 g/dL to maximize oxygen-carrying capacity, decrease patient activity level with bed rest, and maintain urine output of more than 1 cc/kg/h if myoglobinuria is present, and monitoring acid-base status and treating metabolic acidosis with sodium bicarbonate if pH is less than 7.15.

Neurologic injuries such as impairment of concentration, attention, memory, and motor function occur in 25%-50% of patients with loss of consciousness or carboxyhemoglobin levels greater than 25%. These deficits may appear soon after exposure to carbon monoxide or up to 3 weeks later. These symptoms can last for 1 month or more in the most severe cases.

SUGGESTED READINGS

1. Baum CR. Environmental emergencies. In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2000:949-951.

2. Ellenhorn M, ed. Ellenhorn’s Medical Toxicology. 2nd ed. Baltimore: Williams & Wilkins; 1997:1465-1475.

3. Morgan I. Carbon Monoxide Poisoning. In: Bates N, ed. Paediatric Toxicology. New York: Stockton Press; 1997:321-325.

4. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002;347:1057-1067.