Medical Aspects of Chemical Warfare (2008) - The Black Vault

Medical Management of Chemical Toxicity in PediatricsExhibit 21-4 continuedArterial blood gases were as follows:• pH: 7.27,• pCO 2: 14,• pO 2: 83, and• HCO 3: 6.3.Chest X-ray showed bilateral, diffuse infiltrates. Bone marrow hypoplasia developed within a few days. On day 5 ofadmission, hematocrit dropped to 23%, white blood cell count fell to 2100 mm 3 with 82% neutrophils and 18% lymphocytes,and blood cultures grew coagulase-positive staphylococci. The patient died 7 days after exposure despiteantibiotic therapy and supportive treatment.BP: blood pressurebpm: beats per minuteBUN: blood urea nitrogenHR: heart rateK+: potassium ionNa+: sodium ionPMN: polymorphonucleocytesRR: respiratory rateData source: Azizi MD, Amid MH. Clinical presentation of chemical warfare injuries in children and teenagers. Med J Islamic RepIran. 1990; 4(2):103–108.for hours, 76–78 so victims may not recognize toxicity untilwell after exposure. During this time, sulfur workssubclinically to damage the skin. Mustard exposurecan affect the CNS and bone marrow, as displayed bysymptoms of fatigue, headache, and depression. 77 Itcan also lead to pneumonia, which was the cause ofdeath for many mustard casualties during World WarI in the absence of antibiotics. 77 A leukopenic pneumoniacan develop between 6 and 10 days after mustardexposure. The manifestation of leukopenia (specificallylymphopenia) results from the myelosuppressive effectsof mustard agents. 77Laboratory FindingsAlthough there is no confirmatory diagnostic testfor mustard exposure, some laboratory tests can proveuseful. Erythrocyte sedimentation rate has been shownto be elevated in pediatric patients after mustard exposure.79 CBCs (complete blood cell counts) may showabnormalities, depending on the severity of the vaporinhalation or exposure, 76,78 and may show low hematocritand leukopenia if the exposure was severe. Whiteblood cell count may show only a transient decreaseand subsequent recovery. 76,78 In pediatric cases of mustardvapor exposure, decreases in hematocrit or whiteblood cell count were likely to occur in the first 2 weeks,with the lowest levels of hemoglobin, hematocrit, whiteblood cells, and neutrophils observed in the samplestaken 6 to 10 days after exposure. 78 These pediatric patientsalso suffered from hypoxemia and renal failure, 78but serum creatinine and renal function tests were notfound in this particular study’s charts. Arterial bloodgases may provide useful information, but they mayshow a varied picture. In one pediatric study of mustardcasualties, most cases (43%) showed a simple metabolicacidosis. 78 The other groups showed the following:• mixed metabolic acidosis and respiratoryalkalosis (29%),• simple respiratory alkalosis (14%),• mixed metabolic and respiratory acidosis(7%), and• mixed metabolic alkalosis and respiratoryacidosis (7%). 78Blood urea nitrogen can be elevated in pediatric casualtiesfrom severe mustard exposure cases; however,it does not predict mortality. Rather, it is a marker ofmustard exposure in children. Increased blood urea nitrogenwill normalize in pediatric patients that survivesevere mustard exposure. In one case report, elevatedblood urea nitrogen levels returned to normal in three,while the other three died. 78Pediatric VulnerabilitySulfur mustard exposure affects children more severelythan adults. 76 Because premature infants havethinner skin, and because their dermal-epidermal669