Faculty Bibliography

PURPOSE: A case of barium sulfate injection into the superior vena cava during an upper gastrointestinal series (UGIS) in which the patient's central venous line (CVL) was mistaken for her gastrostomy tube is reported. SUMMARY: A 17-month-old girl was brought to the fluoroscopy suite to undergo a UGIS with barium sulfate contrast. Her medical history included premature birth and short-gut syndrome after a bowel resection for necrotizing enterocolitis and gastroschisis. She had been treated for multiple bouts of sepsis and was currently receiving antibiotic therapy at home via a CVL. She was admitted to the hospital for replacement of her CVL. In the hospital, the patient developed a diarrheal illness with projectile vomiting, prompting the UGIS. In the fluoroscopy suite, approximately 3 mL of barium sulfate was injected into the patient's CVL, which was misidentified as her gastrostomy tube. The error was recognized when the first video fluoroscopic image revealed barium in the patient's right atrium, and 10 mL of blood containing a thick, chalky, whitish-pink suspension was immediately aspirated from the CVL. Peripheral venous access was established, and the CVL was removed. The patient vomited three times and developed rigors 30 minutes later. That evening, she developed a fever, which was treated with acetaminophen and a course of broad-spectrum antibiotics. Subsequent radiographs of the patient's chest failed to show any residual barium, and no respiratory distress developed. The patient was discharged in stable condition four days later. CONCLUSION: A 17-month-old girl inadvertently received barium sulfate by i.v. injection through a CVL that was mistaken for the patient's gastrostomy tube

Ethylene glycol classically produces an elevated anion gap metabolic acidosis. We report a series of patients with ethylene glycol toxicity with a component of non-anion gap metabolic acidosis without known associated confounding factors. A retrospective review of Poison Control Center records were searched more than 8 years (2000-2007) for ethylene glycol and antifreeze. Cases were reviewed and excluded for miscoding, information calls, animal exposures, or non-ingestion exposures. The bicarbonate gap, or delta ratio (DR), was calculated using the formula: DR = (

The emergence of prothrombotic agents (e.g. activated factor VII) to treat traumatic brain injury (TBI) requires a better understanding of the association of coagulopathy with isolated head injury (IHI). OBJECTIVE: To investigate the association of IHI and coagulopathy. METHODS: Prospective, observational study in an urban level I trauma center. Inclusion criteria: Adult (> or = 13 years of age) patients with IHI. Exclusion criteria: patients with known coagulopathies or on anticoagulant therapy. Predictor Variables: TBI (head abbreviated injury severity score > 2, or brain hematoma on CT scan), age, gender, mechanism of injury, Glasgow Coma Score (GCS), and loss of consciousness (LOC). Outcome variables: coagulopathy defined as elevated International Normalized Ratio (INR > 1.3) or activated partial thromboplastin time (PTT) greater than 34 s. We divided IHI subjects into two groups of patients with and without TBI. Statistical Analysis: Fisher's exact test and Mann-Whitney U were used to compare data where appropriate (alpha: 0.05, two-tailed). RESULTS: From July 2005 to December 2006, 276 patients with IHI were studied. The median age was 35 years (interquartile range: 25-52) with a 79% male predominance and 88% blunt trauma. Eight percent (95% CI, 5-12%) of patients had coagulopathy. The rate of coagulopathy in TBI patients (17%) was significantly higher than non-TBI patients (6%) (11% difference, 95% CI, 3-20%]. The relative risk of coagulopathy in TBI patients was 2.9 (95% CI, 1.3-6.6). CONCLUSION: Coagulopathy as defined by elevated INR and/or PTT is associated with TBI after isolated head injury.

INTRODUCTION: Base deficit (BD) is a validated surrogate for lactate in injured patients and correlates with trauma severity. Stewart proposed a more comprehensive measure of acidosis based on the strong ion difference (SID) (SID = Na + K + Mg + Ca -

BACKGROUND: Increase in lactate (LAC) within the central nervous system after head trauma is an established marker of traumatic brain injury (TBI). OBJECTIVE: To investigate the utility of arterial base deficit (BD) and LAC in identifying TBI in patients with isolated head injury (IHI). Materials and METHODS: TBI was defined as Glasgow Coma Scale < or =8, head Abbreviated Injury Severity Score >2 or brain haematoma on CT scan. Patients were divided into two groups: IHI with and without TBI. Data were reported as means (SDs). 131 patients with IHI were studied (mean (SD) age 39 (19) years, 78% male). RESULTS: 17% of the patients sustained TBI. The mean differences for arterial BD (0.65 mmol/l, 95% CI -0.8 to 2.1) and LAC (0.34 mmol/l, 95% CI -0.7 to 1.4) in patients with and without TBI were not significant. Analysis of receiver operating characteristic curves confirmed that arterial BD and LAC were unable to detect TBI in patients with IHI. CONCLUSION: Arterial BD and LAC are poor predictors of TBI in isolated head trauma.