General Effects Of Crack Use Include Burning Of The .
What are symptoms and signs of cocaine abuse and addiction? How do health care professionals diagnose cocaine addiction? What is the treatment for cocaine.
Cocaine is one of the alkaloids found in the leaves of the Erythroxylon coca plant. It acts at the syn-aptic terminals, where it reduces the neurotrans-mitter uptake of dopamine and norepinephrine, and it can have many systemic effects. Cocaine is an increasingly used recreational drug in the United Kingdom, with nearly 344,000 individuals estimated to have used this drug. It can be taken orally, nasally, or parenterally. Crack is a base-free form of cocaine that can be smoked, as heating does not destroy it. In this case report, a patient who developed a gastric perforation associated with smoking cocaine is presented.
Case Report
A 19-year-old female student presented to the emergency department with a 36-hour history of vague abdominal discomfort. The pain was mainly around the epigastrium but radiated to the left shoulder. The patient had presented earlier to a nearby hospital but was subsequently discharged without any investigation. When she returned home, the pain worsened significantly over the next 6 hours. There was no nausea or vomiting, and her bowels had opened normally the previous day. She had had an open appendectomy 2 years earlier but was otherwise in good health.
On examination, the patient's heart rate, respiratory rate, air saturation, blood pressure, and temperature were stable, but there was marked tenderness in the epigastrium with localized guarding and rebound tenderness. Blood tests, including leukocyte count and measurement of C-reactive protein, were normal (Table 1); however, an erect chest radiograph showed a large pneumoperitoneum (Figure 1).
Pneumoperitoneum seen on an erect radiograph.
Table 1
Test | Result |
---|---|
Hemoglobin | 13.2 g/dL |
White cell count | 10.3 × 109/L |
Platelet count | 329 × 109/L |
Sodium | 140 mmol/L |
Potassium | 4.3 mmol/L |
Urea | 3.1 mmol/L |
Creatinine | 78 μmol/L |
Aspartate transaminase | 24 IU/L |
Alkaline phosphatase | 64 IU/L |
Bilirubin | 9 μmol/L |
Total protein | 78 g/L |
Albumin | 49 g/L |
Amylase | 33 U/L |
C reactive protein | 3 mg/L |
An urgent laparotomy was performed which revealed free pus in the peritoneal cavity, left paracolic gutter, pelvis, and both subphrenic spaces. After great difficulty, a posterior perforated ulcer was found in the gastric body near the upper part of the greater curve. The defect was closed and then repaired with an omental patch. The abdomen was thoroughly lavaged with 23 liters of warmed normal saline. Waves v9r26 mac patch keygen.
The patient's subsequent recovery, which included 2 days in the intensive care unit, was unremarkable, and she was discharged on day 12. During her recovery, she confessed to regular inhalation of crack cocaine in the week preceding her presentation to the hospital. Toxicology tests were positive for cocaine abuse but negative for other substances. The patient had no significant risk factors for peptic ulcer disease: she drank only a few units of alcohol per week, drank very little coffee, was not feeling stressed, and was not anemic. She had never suffered from a chronic pain syndrome and denied using medicines such as nonsteroidal anti-inflammatory drugs or steroids. An esophagogastroduodenoscopy performed 2 months after the operation revealed no underlying pathology for the perforation. Helicobacter pylori and histopathology tests were also normal.
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Discussion
Cocaine is a widely used recreational drug that can affect almost any organ in the body. Neurologic, pulmonary, and cardiovascular effects are well established. Gastrointestinal effects are also becoming recognized.
Following intake of cocaine, patients can develop abdominal pain, nausea, vomiting, and bloody diarrhea. The onset of symptoms can occur between 1 and 60 hours after ingesting the drug. More serious acute complications include gastroduodenal or bowel perforations. Cases of ischemic colitis and large hemoperitoneum have also been reported in the literature.– These complications are more likely to occur in ruptured body packers and invariably warrant surgical intervention.
Gastroduodenal perforations secondary to cocaine abuse are more likely to affect the prepyloric and duode nal junction, and they are usually small (around 3–5 mm). Feliciano and colleagues compared the epidemiologic profiles of patients with gastroduodenal perforations and found that patients with perforations due to cocaine abuse present at a much younger age (usually 7–10 years younger), are usually male, and drink a larger quantity of alcohol. What is fascinating about this case is that it was a pure gastric perforation in a female patient. Gastric perforations are not the same as duodenal perforations; hyperacidity is rarely a factor (in fact, gastric perforations can be a complication of pernicious anemia, where there is no gastric acidity), they are more commonly found in elderly patients, and they seem to bleed more often than perforate. In contrast, this patient presented with perforation associated with cocaine use at the age of 19 years, which is the youngest age reported to date. Previously, the youngest case in the published literature was a 21-year-old male.
The most intriguing aspect of this case was the unusual location of the perforation. The perforation was found with great difficulty in the posterior part of the upper gastric body near the greater curve. Perforation in this area is usually seen after injury to the short gastric arteries, which may be damaged during splenectomy or by incarcerated hiatal hernias. This perforation site would be unusual in the alcoholic patient as well, as that population is more likely to perforate the duodenum via hyperacidity. So far, only Abramson and colleagues have published a case of perforation in this region after cocaine use, and they stated that it mimicked a stress ulcer.
Due to the unusual location of the ulcer, there is a tendency for erosion and perforation into the lesser sac, resulting in a posterior perforation. A local inflammatory response and fibrosis usually result in sealing of these perforations, which explains the indolent nature of the initial symptoms, the delayed presentation to the emergency department, and the high number of perforations that are missed on initial examination. If these posterior perforations are not contained, however, then lesser sac abscess and generalized peritonitis will ensue due to contamination of the peritoneal cavity through the epiploic foramen. Even during laparotomy, the surgeon may have difficulty finding the perforation or may even miss the perforation. This difficulty occurs because such perforations can only be truly identified by actively looking for these lesions, typically by performing Kocher maneuver to mobilize the duodenum in order to enter the lesser sac. In addition, perforated gastric secretions may sometimes track in a retrograde fashion into the retroperitoneal space and thereby form an abscess around retroperitoneal organs. This abscess may divert attention from the true source of the perforation.
The patient presented here had an open primary repair of the defect followed by an omental patch. This approach is the most common and favored one for the surgical management of gastroduodenal perforations in patients using cocaine. This procedure can be performed via either open or laparoscopic methods. Some authors have expressed the opinion that concomitant anti-ulcer treatment should always be instigated postoperatively to improve outcomes in such cases, as this treatment will cover those patients who also have problems with hyper-acidity. In any case, H. pylori infection should always be considered, and a Campylobacter-like organism test should be performed whenever possible so that such patients can be identified.
The exact pathophysiology of cocaine-induced gastroduodenal injury is unclear. Cocaine overstimulates the sympathetic nervous system, causing vasoconstriction-induced ischemia and necrosis of the mucosal wall. Cocaine can also cause direct vasospasm-induced damage to the mucosal wall by enhancing the influx of calcium across the endothelial membrane. Cocaine is also believed to reduce splanchic perfusion by promoting platelet aggregation, microthrombi, and embolism. Another theory is that cocaine use leads to gastric stasis and increased intragastric pressure, which is further exacerbated by air swallowing and breath holding. A less favored hypothesis is that cocaine affects the central nervous system, resulting in either an increase in circulating steroids via stimulation of the hypothalamic-pituitary-adrenal axis or stimulation of the medullary center involved in gastric motility and vasomotor tone., Crack cocaine is more likely to cause gastroduodenal perforations compared to other forms of cocaine. This increased risk of perforation is due to the higher peak concentration when cocaine is smoked.
In previous reports, there has been no proof of a direct causal link between cocaine use and gastric perforation. This lack of a definitive connection is typically due to the presence of potentially confounding variables that may point to a multifactorial cause for the perforation, including increased alcohol abuse in this population, poor hygiene, malnutrition, use of other drugs, and other environmental effects. As many of these patients are malnourished, the possibility of a vomiting-induced tear usually cannot be completely eliminated. These compounding factors cannot be applied to our patient. The only factor that could account for the perforation was the abuse of cocaine in the weeks leading up to her presentation.
Conclusion
We report a case of acute gastric perforation in association with concomitant cocaine use in a young female student. Gastric perforation should be included in the differential diagnosis for abdominal pain in a cocaine user, no matter the age, who presents with evidence of peritonitis. The entire stomach should be thoroughly examined during laparotomy, particularly if no cause for the perforation is found.