542609
research-article2014
CPJXXX10.1177/0009922814542609Clinical PediatricsPermar et al
Resident Rounds
Rare Etiology of Abdominal Pain in an Adolescent Female
Clinical Pediatrics 2015, Vol. 54(1) 94–97 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922814542609 cpj.sagepub.com
Stephanie Permar, MD1, Kathleen Gorman, MD1, Daniel Lercher, MD1, and Kathleen K. Bradford, MD1 Case Report A 16-year-old Hispanic female, with a medical history significant for anemia, menorrhagia, and intermittent constipation, was admitted to our hospital from the emergency department with abdominal pain and hematemesis. In the week preceding admission, she had been evaluated twice by her primary care pediatrician and once in the emergency room for shortness of breath, chest pain, abdominal pain, and several episodes of hematemesis. Outpatient evaluation revealed anemia (hemoglobin 8.6 mg/dL) and a mild transaminitis for which she was given a proton pump inhibitor for a possible gastritis and/or a Mallory Weis tear, as well as oral contraceptive pills with instructions to begin iron supplementation when her emesis and abdominal pain subsided. Despite this therapy, she developed worsening, constant, periumbilical pain, and further episodes of coffee ground emesis prompting her to return to the emergency room and admission to the hospital. Physical examination at our institution revealed an awake teenage female in moderate distress secondary to abdominal pain. Cardiovascular and respiratory exams were unremarkable. Abdominal exam revealed normoactive bowel sounds, a soft, nondistended, diffusely tender abdomen without rebound or guarding. Other than a flat affect, neurological examination, including strength, sensation, and reflexes was normal. Skin and musculoskeletal examinations were unremarkable. Initial laboratory values were as follows: sodium 135 mmol/L; chloride 93 mmol/L; bicarbonate 26 mmol/L; blood urea nitrogen 15 mg/dL; creatinine 0.49 mg/dL; glucose 84 mg/dL; calcium 9.8 mg/dL; magnesium 2.0 mg/dL; phosphorus 4.9 mg/dL; aspartate aminotransferase (AST) 70 U/dL; alanine aminotransferase (ALT) 81 U/L; alkaline phosphatase 55 U/L; total bilirubin 1.4 mg/dL; direct bilirubin 0.4 mg/dL; albumin 5.1 g/dL; total protein 6.5 g/dL; lipase 509 U/L; γ-glutamyl transpeptidase 82 U/L; uric acid 3.6 mg/dL; lactate dehydrogenase 428 U/L; white blood cells (WBC) 7.3 × 109/L (neutrophils 7.2; lymphocytes 1.9; monocytes 0.6; eosinophils 0.2; basophils 0.0); Hemoglobin 8.6 g/dL; hematocrit 26.8 mg/dL; platelets 240 × 109/L; red blood
cells (RBC) 3.11 × 1012/L; RBC distribution width 15.4%; mean cell volume 73 fL. Peripheral smear comments: WBC toxic vacuolation present, RBC basophilic stippling present. Lead level sent and pending. Peripheral smear is seen in Figure 1. Urinalysis specific gravity 1.009; pH 5.0; leukocyte esterase 1+; nitrites negative; protein negative; glucose negative; ketone negative; urine white blood cells 8 per high-power field (HPF); urine red blood cells 2 per HPF; urine squamous epithelial cells 1 per HPF. Initial imaging revealed an unremarkable single view abdominal radiograph and abdominal ultrasound revealed a grossly normal liver, gallbladder, and pancreas with no evidence of cholelithiasis or biliary ductal dilatation. On hospital day 2, repeat labs showed increasing transaminases and an elevated lipase (1333 U/L) that were suggestive of pancreatitis secondary to obstructing common bile duct stone, though there was no radiographic evidence of a stone (abdominal ultrasound and magnetic resonance cholangiopancreatography showed no ductal dilatation or stone present in the biliary system). Endoscopy was performed on hospital day 2, which demonstrated only gastritis. On hospital day 4, a serum lead level returned at 75 µg/dL, indicating severe lead toxicity. On further discussion for source identification, the patient reported drinking from a painted terra-cotta clay pot, bought on a trip to Mexico. The patient’s mother reported that the pot was intended for decorative use and as a result of frequent drinking, the inside had started to break down. In addition, the patient had also started to chew on the pot. The specific pot had since been thrown away, but the patient’s mother reported an additional collection of similar pots within the home.
1
University of North Carolina School of Medicine, Chapel Hill, NC, USA Corresponding Author: Stephanie Permar, MD, University of North Carolina School of Medicine, 101 Manning Drive, Chapel Hill, NC 27514, USA. Email: [email protected]
Downloaded from cpj.sagepub.com at Selcuk Universitesi on January 10, 2015
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Figure 2. Examples of pottery found within the patient’s home. None of the items had manufacturer’s stamps, but all were reportedly purchased in Mexico.
Figure 1. Peripheral blood smear. The peripheral blood smear shows anemia and nonspecific erythroid anisopoikilocytosis. Coarse basophilic stippling is present in scattered red cells (arrow and insets); original objective magnification: 100×.
In discussion with the Carolina Poison Control Center, the patient was initiated on a 5-day inpatient chelation therapy regimen consisting of dimercaprol/ BAL (British anti-Lewisite) 75 mg/m2 intramuscular every 4 hours and calcium disodium EDTA (ethylenediamine tetraacetic acid) 1000 to 1500 mg/m2/d intravenous divided every 6 hours. She was then started on a 19-day oral chelation therapy regimen of Chemet succimer 350 mg/m2 thrice a day for 5 days, then 350 mg/ m2 twice a day for 14 days. The appropriate county health department was notified and an environmental health lead specialist was sent to the home for inspection of lead sources to ensure a safe environment. For the past 9 years, the patient lived with her family in a home built in the 1980s. There was no source of lead found in the soil, dust, or plumbing structures within the home. Similar clay pots were found to have 223 parts per million lead content by X-ray fluorescence with the legal limit being
research-article2014
CPJXXX10.1177/0009922814542609Clinical PediatricsPermar et al
Resident Rounds
Rare Etiology of Abdominal Pain in an Adolescent Female
Clinical Pediatrics 2015, Vol. 54(1) 94–97 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922814542609 cpj.sagepub.com
Stephanie Permar, MD1, Kathleen Gorman, MD1, Daniel Lercher, MD1, and Kathleen K. Bradford, MD1 Case Report A 16-year-old Hispanic female, with a medical history significant for anemia, menorrhagia, and intermittent constipation, was admitted to our hospital from the emergency department with abdominal pain and hematemesis. In the week preceding admission, she had been evaluated twice by her primary care pediatrician and once in the emergency room for shortness of breath, chest pain, abdominal pain, and several episodes of hematemesis. Outpatient evaluation revealed anemia (hemoglobin 8.6 mg/dL) and a mild transaminitis for which she was given a proton pump inhibitor for a possible gastritis and/or a Mallory Weis tear, as well as oral contraceptive pills with instructions to begin iron supplementation when her emesis and abdominal pain subsided. Despite this therapy, she developed worsening, constant, periumbilical pain, and further episodes of coffee ground emesis prompting her to return to the emergency room and admission to the hospital. Physical examination at our institution revealed an awake teenage female in moderate distress secondary to abdominal pain. Cardiovascular and respiratory exams were unremarkable. Abdominal exam revealed normoactive bowel sounds, a soft, nondistended, diffusely tender abdomen without rebound or guarding. Other than a flat affect, neurological examination, including strength, sensation, and reflexes was normal. Skin and musculoskeletal examinations were unremarkable. Initial laboratory values were as follows: sodium 135 mmol/L; chloride 93 mmol/L; bicarbonate 26 mmol/L; blood urea nitrogen 15 mg/dL; creatinine 0.49 mg/dL; glucose 84 mg/dL; calcium 9.8 mg/dL; magnesium 2.0 mg/dL; phosphorus 4.9 mg/dL; aspartate aminotransferase (AST) 70 U/dL; alanine aminotransferase (ALT) 81 U/L; alkaline phosphatase 55 U/L; total bilirubin 1.4 mg/dL; direct bilirubin 0.4 mg/dL; albumin 5.1 g/dL; total protein 6.5 g/dL; lipase 509 U/L; γ-glutamyl transpeptidase 82 U/L; uric acid 3.6 mg/dL; lactate dehydrogenase 428 U/L; white blood cells (WBC) 7.3 × 109/L (neutrophils 7.2; lymphocytes 1.9; monocytes 0.6; eosinophils 0.2; basophils 0.0); Hemoglobin 8.6 g/dL; hematocrit 26.8 mg/dL; platelets 240 × 109/L; red blood
cells (RBC) 3.11 × 1012/L; RBC distribution width 15.4%; mean cell volume 73 fL. Peripheral smear comments: WBC toxic vacuolation present, RBC basophilic stippling present. Lead level sent and pending. Peripheral smear is seen in Figure 1. Urinalysis specific gravity 1.009; pH 5.0; leukocyte esterase 1+; nitrites negative; protein negative; glucose negative; ketone negative; urine white blood cells 8 per high-power field (HPF); urine red blood cells 2 per HPF; urine squamous epithelial cells 1 per HPF. Initial imaging revealed an unremarkable single view abdominal radiograph and abdominal ultrasound revealed a grossly normal liver, gallbladder, and pancreas with no evidence of cholelithiasis or biliary ductal dilatation. On hospital day 2, repeat labs showed increasing transaminases and an elevated lipase (1333 U/L) that were suggestive of pancreatitis secondary to obstructing common bile duct stone, though there was no radiographic evidence of a stone (abdominal ultrasound and magnetic resonance cholangiopancreatography showed no ductal dilatation or stone present in the biliary system). Endoscopy was performed on hospital day 2, which demonstrated only gastritis. On hospital day 4, a serum lead level returned at 75 µg/dL, indicating severe lead toxicity. On further discussion for source identification, the patient reported drinking from a painted terra-cotta clay pot, bought on a trip to Mexico. The patient’s mother reported that the pot was intended for decorative use and as a result of frequent drinking, the inside had started to break down. In addition, the patient had also started to chew on the pot. The specific pot had since been thrown away, but the patient’s mother reported an additional collection of similar pots within the home.
1
University of North Carolina School of Medicine, Chapel Hill, NC, USA Corresponding Author: Stephanie Permar, MD, University of North Carolina School of Medicine, 101 Manning Drive, Chapel Hill, NC 27514, USA. Email: [email protected]
Downloaded from cpj.sagepub.com at Selcuk Universitesi on January 10, 2015
95
Permar et al
Figure 2. Examples of pottery found within the patient’s home. None of the items had manufacturer’s stamps, but all were reportedly purchased in Mexico.
Figure 1. Peripheral blood smear. The peripheral blood smear shows anemia and nonspecific erythroid anisopoikilocytosis. Coarse basophilic stippling is present in scattered red cells (arrow and insets); original objective magnification: 100×.
In discussion with the Carolina Poison Control Center, the patient was initiated on a 5-day inpatient chelation therapy regimen consisting of dimercaprol/ BAL (British anti-Lewisite) 75 mg/m2 intramuscular every 4 hours and calcium disodium EDTA (ethylenediamine tetraacetic acid) 1000 to 1500 mg/m2/d intravenous divided every 6 hours. She was then started on a 19-day oral chelation therapy regimen of Chemet succimer 350 mg/m2 thrice a day for 5 days, then 350 mg/ m2 twice a day for 14 days. The appropriate county health department was notified and an environmental health lead specialist was sent to the home for inspection of lead sources to ensure a safe environment. For the past 9 years, the patient lived with her family in a home built in the 1980s. There was no source of lead found in the soil, dust, or plumbing structures within the home. Similar clay pots were found to have 223 parts per million lead content by X-ray fluorescence with the legal limit being
