Spontaneous or idiopathic splenic rupture is a rare cause of acute abdominal pain and hemoperitoneum and its incidence is 1% of all cases of splenic rupture. The etiology of spontaneous splenic rupture can be idiopathic or it may occur as a complication of an infectious, neoplastic or hematologic disease. Splenic rupture presents with pain in the left upper quadrant with shock and features of peritoneal irritation, like Kehr’s sign (left shoulder pain due to diaphragmatic irritation) and Balance sign (palpable tender mass in left upper abdomen). The diagnosis of spontaneous splenic rupture presents a diagnostic challenge due to the absence of a history of trauma. Focused Abdominal Sonography for Trauma FAST may be suggestive but due to its limitations, Computerized Tomography Scan CT scan of abdomen is the best imaging modality both for detection and grading of splenic injury. Management can be non-operative or surgical depending on grade and hemodynamic status of the patient. We report a rare case of spontaneous rupture of the spleen, which was idiopathic and fulfills the criteria of Orloff and Peskin, due to absence of any history of trauma, absence of perisplenic adhesions or scarring, and it without any evidence of disease affecting the spleen with macro and microscopically normal spleen. This case also adheres to fifth criteria described by Crate and Payne, as there was no immunological evidence suggestive of any viral infections affecting the spleen.

BACKGROUND: Short-term interruption of feeding is ordinary in modern life but negatively impacts appetite control and body weight. Estradiol (E) imposes long-term inhibitory tonus on food consumption; however, E influence on energy repletion secondary to food deprivation (FD) is unclear. This study investigated the hypothesis that E signal strength regulates hyperphagic responses to FD of varying duration. METHODS: Ovariectomized female rats were implanted with E-containing silastic capsules (30 [E-30] or 300 µg [E-300]/mL) to replicate plasma concentrations at cycle nadir versus peak levels. RESULTS: Data show that food intake was increased equally in E-30 and E-300 rats after 12 hours of food deprivation (FD-12); yet, FD of 18 hours (FD-18) amplified refeeding by E-300 versus E-30. Caudal fourth ventricular administration of the 5′-monophosphate-activated protein kinase (AMPK) inhibitor compound C (Cc) did not modify FD-induced hyperphagia in E-30 (regardless of FD interval) or E-300 animals exposed to FD-12, but diminished refeeding after FD-18 in E-300 rats. Cc-reversible hyperglycemia occurred in refed FD-18 groups. Serum insulin was resistant to FD-12 plus refeeding, but was elevated by AMPK-dependent mechanisms in refed E-300 FD-18 rats; equivalent Cc-insensitive decrements in circulating leptin occurred in all FD groups. CONCLUSION: Current results show that estrous cycle peak, but not baseline, E levels engage hindbrain AMPK signaling to intensify hyperphagia in response to prolongation of FD. Observations of hindbrain AMPK-dependent hyperglycemia, alongside elevated insulin secretion, in refed rats exposed to FD-18 implicate this sensor in insulin resistance mechanisms of glucose partitioning in response to this metabolic imbalance.
AMP-Activated Protein Kinases ; Animals ; Appetite ; Body Weight ; Capsules ; Eating* ; Estradiol* ; Estrous Cycle* ; Female ; Food Deprivation ; Glucose ; Humans ; Hyperglycemia ; Hyperphagia ; Insulin ; Insulin Resistance ; Leptin ; Plasma ; Protein Kinases ; Rats ; Rhombencephalon