RESUMO
The use of antibiotics has increased drastically over the last few decades. Many antibiotics can target the commensal microbiota and promote gut dysbiosis. These alterations contribute to disease onset and exacerbation. Although the etiology of inflammatory bowel disease (IBD) is mostly unknown, it involves a complex interaction among host genetics, microbiota, environmental factors, and aberrant immune responses. Studies have shown a relationship between very-early-onset inflammatory bowel disease (VEO-IBD) and microbiota alterations. The case discussed in this report endorses the current clinical evidence for this interaction. This is an anonymous record review with no identifiers involving a 23-month-old female patient who was brought to the emergency department by her parents due to persistent bloody diarrhea. Eight days before the presentation, she had experienced watery diarrhea that progressed to bloody stools. The patient had a history of acute otitis media, acute enteritis, and right-arm cutaneous abscess, for which she had received multiple antibiotic therapies. Strategies to manipulate the microbiome through diet, probiotics, antibiotics, or fecal microbiota transplantation (FMT) may be used therapeutically to modulate disease activity. A high index of clinical suspicion for VEO-IBD should be maintained for patients with a history of multiple, recurrent antibiotic use. We believe this case report will raise awareness about the issue of early anaerobic antibiotic exposure and help prevent its unnecessary use and, consequently, prevent gut microbiota dysbiosis that can lead to VEO-IBD. Also, our literature review will hopefully prompt clinicians to consider alternative therapeutic options for this patient population, such as rebuilding intestinal microbiota composition to improve VEO-IBD activity.
RESUMO
INTRODUCTION AND IMPORTANCE: We are reporting a case of a delayed hepatothorax due to a right-sided diaphragmatic rupture 13 years after a blunt trauma due to a motor vehicle accident, who presented as isolated gastritis without any type of respiratory symptomatology. CASE PRESENTATION: Patient refers that his symptoms remained refractory to medical treatment and had gotten worse over time. Chest wall inspection showed asymmetric thoracic expansion and a decreased movement of right hemithorax when compared to the left. Cardiorespiratory auscultation was significant for growling sounds on the right second intercostal space and reduction of breath sounds on the right lower lobe region of the lung when compared to the left side. CLINICAL DISCUSSION: Thoracotomy was indicated since patient presented late. Meanwhile, laparotomy would have been appropriate if the patient had presented immediately after trauma. After the procedure, the patient presented in great condition and all the gastrointestinal symptoms associated with the traumatic diaphragmatic hernia had resolved. We propose that the absence of respiratory symptoms in our patient could be due to the progressive adaptation of small, cumulative changes in decreasing breathing capacity through time. CONCLUSION: A case like ours has not been reported in the literature and clinicians should take this case report into consideration when suspecting a possible diagnosis of a delayed traumatic diaphragmatic hernia that may be complicated by a hepatothorax. We recommend maintaining a high index of clinical suspicion for hepatothorax due to delayed traumatic diaphragmatic hernia for all patients with a history of trauma.
