The pathogenesis of gastroduodenal ulcer perforation in association with crack cocaine use remains unclear. Cocaine acts by blocking reuptake of dopa-mine, epinephrine, and norepinephrine, leading to sympathetic nervous system stimulation and subsequent vasoconstriction.1,16 Several other pathophysiologic mechanisms have also been proposed, including focal ischemia,3,17 microthrombi, embolism,12 delayed gastric emptying,1,14 and an increase in intra-abdominal pressure due to chronic aerophagia.9,18 A possible association with Helicobacter pylori infection has also recently been described. One retrospective chart review of 50 cases of acute gastroduodenal perforation associated with crack cocaine use reported an 80% incidence of H. pylori infection in antral biopsies1; however, this finding has not been subsequently confirmed. Currently, the leading theory is that cocaine-associated perforation is caused by focal ischemia secondary to profound vasoconstriction and does not follow a traditional ulcer-related developmental pathway.2,3,7
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Figure 1. Scheme of the load-time curve of the Vickers indentation. Automated image acquisition was triggered at the start of the unloading ramp. Radial cracks at the corner of the indent were observed to grow after a delay time δ.
Table 1. Total number of cracks initiated after 60 s (N60s) and 65 s (N65s), number of indents (z) and the probability of crack initiation F60s and F65s.
Figure 2. Cumulative frequency distribution F(δ) of the number of initiated cracks tested in dry (A) and humid (B) environments. Lines connecting data points are intended as visual guides.
Figure 4. Cumulative frequency F of the crack length c50s in dry and humid environments (A). Part (B) shows corresponding Weibull plots of cumulative frequencies. Solid lines are the best fit (MMR and MLE) through the data with parameters compiled in Table 2, while dotted lines are 95% confidence intervals. Yellow stars indicate the mean crack length cav.
Figure 7. Mean crack propagation rate vav vs. uncalibrated stress intensity KI/χB. Lines of slope n (as indicated) are best linear fits through data. Error bars show standard deviation of the crack length distributions of Table 2.
Table 3. Crack growth exponent n of the equation vav = A(KI/χB)n and v = AKIn of Vickers induced and DCB cracks in soda-lime silicate glasses, respectively.
Figure 8. Mean crack propagation rate vav (N = 259 and 370) and crack propagation rates v of single cracks (stress calibrated DCB specimens) of the hydrous glass 6W-MSG500. Stress intensities KI of the Vickers induced vav data of this study are shown for χB = 0.008 (red dots), 0.009 (green dots) and 0.010 (blue dots). Partial pressure of H2O as indicated. DCB data from Waurischk et al. (2020). Error bars show standard deviation of the crack length distributions of Table 2.
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