2014 Quick Shot Presentations
SCIENTIFIC SESSION VIII:QUICKSHOTS
UNLEASH THE CLOT: HYPERCOAGULABILITY AFTER ENERGY DRINK
CONSUMPTION
Pommerening MJ, Cardenas JC, Radwan ZA, Wade CE, Holcomb JB, Cotton BA,
University of Texas Medical School at Houston
Background
Energy drink consumption in the United States has more than doubled over the last
decade and has been implicated in cardiac arrhythmias, myocardial infarction, and even
sudden cardiac death. We hypothesized that energy drink consumption may increase
the risk of cardiovascular events by increasing platelet aggregation thereby resulting in
a relatively hypercoagulable state and increased risk of thrombosis.
Methods
Thirty-two healthy volunteers ages 18-45 were asked to consume 16 oz. of bottled
water or a standardized, sugar-free energy drink on two separate occasions, one week
apart. Subjects were asked to refrain from consuming alcohol or caffeine for at least 24
hours prior to their blood draws. Both study beverages were consumed on an empty
stomach over a 30 minute time period. Coagulation parameters and platelet function
were measured 90 minutes after consumption using both kaolin and rapid
thrombelastography (TEG) as well as Multiplate impedance aggregometry. Data was
analyzed using the Wilcoxon signed-rank test for paired data.
Results
No statistically significant differences in coagulation were detected using kaolin or rapid
TEG. In addition, no differences in platelet aggregation were detected using ristocetin,
collagen, TRAP, or ADP-induced Multiplate impedance aggregometry. However,
compared to water controls, energy drink consumption resulted in a significant increase
in platelet aggregation via arachidonic acid-induced activation (AUC 72.4 vs. 66.3;
p=0.018).
Conclusion
Consumption of energy drinks increases platelet aggregation via the arachidonic acid
pathway. Because this is the same pathway inhibited by aspirin therapy, our findings
support a potential mechanism by which energy drink consumption may lead to an
increased risk for cardiovascular events. In addition, these findings have numerous
implications for trauma patients, including potential explanations for early cardiovascular
deaths in young individuals, hypercoagulable defects not previously addressed with
thromboembolism prophylaxis and, on the opposite end of the spectrum, a potential
resource for reversal of trauma-induced platelet dysfunction and hemorrhage.
MELATONIN INHIBITS THERMAL INJURY INDUCED HYPERPERMEABILITY IN
MICROVASCULAR ENDOTHELIAL CELLS
Han MS, Wiggins-Dohlvik K, Stagg HW, Davis ML, Tharakan B, Department of Surgery,
Texas A&M Health Science Center College of Medicine and Scott and White Memorial
Hospital, Temple, TX
Background
Burns are known to induce hyperpermeability. It is known that the breakdown of
endothelial cell adherens junctions is integral in inducing hyperpermeability, and that
reactive oxygen species play a large role in initiating this process. We hypothesized
that burn induced junctional damage and hyperpermeability could be attenuated with
the use of the antioxidant Melatonin.
Methods
After IACUC approval, Sprague Dawley rats were assigned to either sham or burn
groups. FITC-albumin was administered intravenously. Mesenteric post capillary
venules were examined with intravital microscopy to analyze and determine the flux of
albumin from intravascular space to the interstitium. Fluorescence intensities were
measured and serum was collected. Rat lung microvascular endothelial cells were then
grown as monolayers on Transwell inserts. Wells were divided into four groups (n=six)
and sham, burn, Melatonin plus sham and Melatonin plus burn serum were applied.
FITC-albumin flux across the monolayer was obtained as an indicator of permeability.
Immunofluorescence staining for adherens junction proteins β-catenin, VE Cadherin,
and rhodamine phalloidin staining for F-actin were performed. Stastical analysis was
conducted with a student’s t-test (p< 0.05).
Results
Data from intravital microscopy revealed a significant increase in vascular
hyperpermeabiltiy following burn trauma. Monolayer permeability was increased with
burn serum when compared with sham. However, this increase in permeability was
attenuated with Melatonin (p< 0.05). Immunofluorescence showed that damage of
microvascular endothelial cell adherens junctions occurred with exposure to burn
serum. Melatonin restored integrity. Rhodamine phalloidin staining showed an increase
in F-actin stress fiber formation following exposure to burn serum and Melatonin
decreased this.
Conclusion
Burns induce microvascular hyperpermeability and damage endothelial adherens
junctions: Melatonin attenuates this process. This insight into the mechanisms of burn
induced fluid leak confirms the role of reactive oxygen species but more importantly
hints at the possibility of exciting new treatments to combat vascular hyperpermeability
in burn.
GASTRIC PNEUMATOSIS WITH SPONTANEOUS RESOLUTION IN A 12 MONTH
DOWN'S SYNDOME CHILD WITH ISOLATED DUODENAL ATRESIA
Paulette I. Abbas, Leon Chen, Douglas S. Fishman, Mary L. Brandt, Baylor College of
Medicine
Background
Gastric pneumatosis, or air within the wall of the stomach, is a relatively infrequent
radiographic finding with significant diagnostic implications. In children, gastric
pneumatosis is often described in relation to severe life-threatening ischemic bowel
disease. However, recently, this finding has become more frequently linked to
nonischemic causes such as a distal obstruction1. Although cases describing
pneumatosis intestinalis from distal obstruction have been reported, these cases are
rare and even fewer have documented as rapid a radiographic resolution of the
pneumatosis as seen in our case. Furthermore, patients typically have additional
abdominal solid organ anomalies associated with the obstruction, which was not
identified in our patient.
Methods
A 12 month old Down’s syndrome male presents to an outside hospital (OSH) with a
four day history of abdominal distension and postprandial emesis. Prior to this episode,
he was tolerating feeds at home. At the OSH, a KUB was obtained revealing gastric
pneumatosis prompting transfer to our institution. Upon arrival, the patient was clinically
stable with normal vital signs and a benign abdominal exam. A repeat KUB on
admission indicated resolution of the previously noted gastric pneumatosis despite
persistent feeding intolerance. An upper gastrointestinal contrast study revealed a
dilated proximal duodenum with distal narrowing and proximal dimpling concerning for a
duodenal web. To avoid surgical resection, the patient underwent an
esophagogastroduodenoscopy (EGD) by gastroenterology as endoscopic therapies
have been successfully reported.2, 3 Upon advancing the endoscope to the second
portion of the duodenum no distal lumen could be visualized, only a small opening with
bilious secretion was noted and presumed to be the ampulla. Given the unclear
anatomy, a surgical intervention was deemed most appropriate. The patient underwent
an exploratory laparotomy, duodenoduodenostomy, and an inversion appendectomy.
Upon entry, it was noted that the cecum was unattached to the abdominal wall but
without evidence of malrotation. The bowel was dilated proximal to the area of
duodenal stenosis. An enterotomy was performed proximal to the area of stenosis and
a catheter was placed into the presumed ampulla; however, rather than entering the
biliary tree, the catheter passed to the distal loop of bowel. Thus, a distal enterotomy
was performed and bilious fluid was noted, accounting for the bilious fluid seen on EGD.
The remainder of the duodenoduodenostomy was performed without complication and
the diagnosis of duodenal stenosis from atresia was confirmed. His post-operative
course was uncomplicated and he was discharged on POD 7 tolerating an oral diet.
Conclusion
Duodenal atresia results from incomplete luminal re-canalization during embryologic
development. 25-40% of patients with this anomaly have Down’s syndrome. It is also
commonly associated with congenital heart disease, annular pancreas, and
malrotation.5 This atresia and subsequent stenosis leads to bowel obstruction and a
constellation of obstructive gastrointestinal symptoms including nausea, vomiting, and
abdominal distension. The diagnosis of obstruction tends to be delayed in Down’s
syndrome patient as vague, milder abdominal symptoms are often attributed to their
mental incapacities rather than underlying etiology. 4, 5 In rare cases of bowel
obstruction, the radiographic findings of gastric pneumatosis can be present. This is
thought to be due to the resultant increases in intra-gastric pressure ultimately causing
tears in the gastric mucosa and subsequent entry of air into the gastric wall 5, 6, 7, 8.
A unique finding in our case is the rapid resolution of our patient’s pneumatosis.
Pneumatosis from a non-ischemic etiology often spontaneously resolves, but the typical
time to resolution is an average of nine days.9 Our patient had radiograph resolution
within two days. It is unclear why his radiographic findings resolved so quickly as he
continued to have the source of obstruction, but it may have been related to prompt
decompression and withholding oral intake. Previous studies do not associate time of
resolution to prognosis.
In conclusion, this report reinforces the idea that patients with radiographic presentation
of isolated pneumatosis without clinical or laboratorial findings concerning for ischemia
bowel disease is an indication for evaluating for intestinal abnormalities. Furthermore,
it is important for medical professionals to recognize the symptoms of obstruction in
patients with Down’s syndrome in order to prevent a prolonged delay in diagnosis and
intervention. Additional studies are warranted to evaluate if there is any correlation
between time to radiographic resolution of the pneumatosis and patient outcomes.