PEDIATRIC PUZZLER

May 1, 1999

An obtunded 2-year-old: A volatie situation.

PEDIATRIC PUZZLER

Jump to:Choose article section...An obtunded 2-year-old: A volatile situationAiring out the possibilitiesPolishing up the diagnosis

An obtunded 2-year-old: A volatile situation

Travis Ganunis, MD, Fred J. Heldrich, MD, and Walter T. Tunnessen, Jr.,MD

The call from the emergency department announces the arrival of an obtunded2-year-old who has just arrived by ambulance. Fortunately, the youngsteris breathing spontaneously and has a palpable pulse. The paramedics respondedto a call from his 16-year-old babysitter, a neighbor, who could not arousehim from a nap. The history given to the paramedics was that the youngsterwas put down for his nap after a peanut butter and jelly sandwich and asmall glass of milk. About two hours later the sitter heard a loud cry.When she entered the bedroom she saw the youngster make three or four bodyheaves "like he was going to vomit" and then fall asleep again.He was unarousable and floppy after this episode.

The initial physical examination shows a temperature of 35.8° C,pulse 82 beats per minute, respiratory rate 26 breaths per minute, bloodpressure 92/60 mm Hg, and pulse oximetry 100% in an FiO2 of 40%.He is breathing spontaneously with good air entry and no abnormal adventitialsounds. The pulses are easily palpated. His skin is cool, and the capillaryrefill time is 2 seconds. A rapid neurologic assessment shows that his pupilsare 3 mm bilaterally and sluggishly reactive to light. The gag reflex isstrong. He is diffusely hypotonic; the DTRs are symmetric at 1+ response.There is no clonus and the toes are down-going. His testes are retracted,obscuring the cremasteric reflexes, but there is no superficial abdominalreflex. He withdraws in response to painful stimuli, but his eyes stay closedand he remains nonvocal. You estimate that the Glasgow coma score is 6.While you are palpating the abdomen, his pulse falls to the 60s, but itquickly rises to 100 beats per minute on sternal stimulation. No murmursare heard on cardiac examination. The prepuce of the penis is swollen anderythematous, and you find several darkly discolored areas on the part ofthe buttocks covered by the diaper. Their size is approximately 3 cm by6 cm; the overlying skin is wrinkled but not denuded.

Thoughts of child abuse run through your mind. As you complete your examinationyou detect a fruity odor, suggestive of ketones, emanating from the child'sbody, particularly the diaper area. Strange, there is no similar odor onthe breath.

Blood has already been sent for an arterial blood gas (ABG), CBC, SMA-20,and toxicology screen. A fingerstick glucose was 88 mg/dL. A dose of naloxoneis given without effect. You catheterize the bladder and obtain urine forroutine and toxicologic analysis. You also obtain an EKG to check the complexes,after the episode of bradycardia. The rate is 110 per minute, with sinusrhythm, normal axis, and normal PR, QRS, and QT intervals.

Airing out the possibilities

The youngster is breathing spontaneously and has strong peripheral pulses.While awaiting laboratory results, you consider possible explanations forthis picture and how best to proceed with further evaluation. Certainlytrauma, possibly abuse, needs to be considered. The sudden change in this2-year-old could also be the result of an ingestion of some sort. Is thisa post-ictal state, or an encephalitis or encephalopathy? What about aninborn error of metabolism?

The father's entrance into the cubicle interrupts your train of thought.He has just returned home from work and discovered that his son was takento the emergency department. The child's mother is still at work and cannotbe reached. The father informs you that his son was well the day beforewhen he was dropped off at the babysitter's to spend the night, not an uncommonevent. The babysitter and her family are neighbors and close family friends.The father relates that the sitter informed him that his son had been actingnormally before the nap.

You proceed to ask further history of the father. His son has been ingood health, with no significant infections and only one episode of otitismedia. All immunizations have been received. Reluctantly, he reports thathis son was seen in the ED six months ago with a fractured humerus. Youask the staff to quickly obtain the record of that visit. The youngsterlives at home with both parents and a 14-year-old sister. Except for hypertensionin a maternal grandmother, there is no family history of significant illness.

You step out of the cubicle to check on the laboratory results. A policeofficer who accompanied the child to the ED reports that upon respondingto the 911 call and finding an unconscious child, he searched the home andfound no evidence of drugs, medications, or a neglectful environment. Theofficer relates that he also interrogated the sitter and found no suggestionof suspicious behavior or activity.

Some of the laboratory studies are available, and you are both reassuredand perplexed since they offer little help. The electrolytes, chemistrypanel, and urinalysis are normal, except for a slightly elevated blood glucoseof 174 mg/dL and trace ketones in the urine. The ABG, with an FiO2of 40%, shows a pH of 7.43, pCO2 38 mm Hg, pO2 479mm Hg. The carboxy-hemoglobin is 2.6% (normal, 0 to 10%), and the methemoglobin0.1 g/dL (normal, 0 to 0.5 g/dL).

The lesions on the back and buttocks, the swollen prepuce, and the reportedsudden onset of symptoms, coupled with the history of a fractured humerusat 18 months of age, raise your suspicion of trauma and abuse. You ordera CT scan of the head.

Polishing up the diagnosis

While the youngster is in Radiology for the CT scan, the nurse bringsin the child's diaper sealed in a plastic bag, which had been found in thebabysitter's home. When you open the plastic bag, the unmistakable odorof acetone assails your nostrils. Curiously, the diaper is discolored--blue!Suddenly, lights go on in your head. You remember the admonition not tosponge-bathe febrile infants with isopropyl alcohol in a confined spacefor fear of toxicity from inhalation of the vapors. CNS depression, withor without seizures, could result. Perhaps the same is true of acetone.

The CT scan is completed and is negative. A lumbar puncture is performed.The opening pressure is normal and the fluid clear; no cells and normalglucose and protein are reported later. You bet on your hunch about acetoneand opt for supportive care and further inquiry into the possible source.Within six hours the youngster begins to awaken and turn toward his father'svoice. In 12 hours he is alert and back to his baseline mental status. Furtherconfirmatory news is received when the toxicology screens of the blood andurine are reported to be negative except for a blood acetone level of 18mg% (endogenous <1 mg%; toxic estimated >20 mg%; lethal estimated>55 mg%).1

Acetone is a widely used solvent found in common household products suchas adhesives, lacquers, varnishes, and nail polish removers. Since acetoneis volatile, absorption can readily occur via inhalation. It is also absorbedby ingestion and through the skin.2 The typical signs of acetonetoxicity are CNS depression, ranging from lethargy, slurred speech, andataxia to stupor and coma, and respiratory depression.3 Excretionis primarily through the lungs, which may be why the breath sometimes hasa fruity or sweet odor.

Testifying to the intoxication potential of acetone is its abuse as aninhalant by adolescents.4 At equivalent blood levels, acetonehas a greater anesthetic potency than ethanol.2 Exposure to highvapor concentrations can also irritate the eyes and nasal and pharyngealmucosa. Topical contact has been linked to allergic dermatitis, patchy skindehydration, nailbed peeling, and splitting of the nails.5 Fortunately,permanent toxic sequelae have not been reported.

Treatment of acetone intoxication is purely supportive. After ingestion,gastric lavage may be indicated. For intoxication as a result of inhalation,the individual must be removed from the exposure. When respiratory depressionis present, oxygen and ventilatory support may be necessary.

In the case of this youngster, who recovered with no ill effects, therewere still a few nagging questions about the mode of acetone intoxication.A similar case of respiratory depression, a small amount of ketones in theurine, and a fruity odor to the breath was reported after the ingestionof fingernail polish remover by a 30-month-old.2 Nail polishremover is readily available in many households, and sure enough, the babysitter'sfavorite brand is blue, apparently explaining the bluish discoloration ofthe child's diaper.

But how did the nail polish remover get into the diaper? The mother arrivedat the hospital later that evening and reported that her son calls his diaperhis "pocket" and often puts all sorts of things, from food totoys, into it. Could he have poured polish remover into his "pocket,"or put an open bottle of the polish remover there? If he did, two methodsof intoxication are possible: skin absorption, enhanced by the occlusivediaper, and inhalation of the vapors. The unusual skin marks on the buttocks,which raised the specter of abuse, could have been from the prolonged contactwith acetone.

There were enough concerns, along with the history of the fractured humerus,to ask Child Protective Services to see the family. After an initial forensicevaluation, he was discharged home as an active CPS case.

Toxic ingestions must always be considered in the differential diagnosisof presentations that are difficult to explain. We should not forget thata toxin does not need to be ingested; toxins can be inhaled and absorbedfrom the skin. Don't remove acetone from the list when you're nailing downa diagnosis.

DR. GANUNIS is an attending pediatrician at Mount Washington PediatricHospital in Baltimore.

DR. HELDRICH is Associate Professor of Pediatrics at Johns Hopkins UniversitySchool of Medicine.

DR. TUNNESSEN. who serves as Section Editor for Pediatric Puzzler, isSenior Vice President, American Board of Pediatrics, Chapel Hill, NC, anda member of the Contemporary Pediatrics Editorial Board.

REFERENCES

1.Gamis AS, Wasserman GS: Acute acetone intoxication in a pediatric patient.Pediatr Emerg Care 1988;4:24

2. Haggard HW, Greenberg LA, Turner JM: The physiological principlesgoverning the action of acetone together with determination of toxicity.J Indust Hyg Tox 1994; 26:133

3. Ramu A, Rosenbaum J, Blaschke TF: Disposition of acetone followingacute acetone intoxication. West J Med 1978;128:429

4. Oliver JS, Watson JM: Abuse of solvents for kicks: A review of 50cases. Lancet 1977;1:84

5. Kechijian P: Nail polish removers: Are they harmful? Semin Dermatol1991;10:26