Acute pancreatitis: a clinical study in some toxicity with helical computed tomography

This study was conducted on 15, 48, 23 patients exposed to scorption sting, anticholinesterase insecticide, and methanol intoxication respectively with total number of 86 patients admitted to Poison Control Centre, Ain Shams University Hospitals, Cairo Egypt. On admission, and on discharge, serum amylase, and serum lipase, in addition to pseudo-cholinesterase [butyryl cholinesterase Bu-ChE], blood pH, and blood bicarbonate were determined and compared with those of normal control subjects. Abdominal ultrasonography and helical computed tomography [CT] were performed for cases with increased serum amylase and lipase. Acute pancreatitis was diagnosed in 6, 20, and 8 patients exposed to scorpion sting, anticholinesterase insecticide, and methanol intoxication respectively. All those patients demonstrated significantly elevated serum amylase, and lipase levels when compared with control group and other patients. Helical Computed Tomography [CT] showed findings suggestive of acute pancreatitis in 31 patients [91%]. There was a significant correlation between developing acute pancreatitis and severity of toxicity. Pancreatic necrosis, estimated on early, contrast-enhanced CT and seen only in patients with severe manifestations, was a specific predictor of morbidity. The present study showed that acute pancreatic injury might be more common than was previously thought. So, it is suggested that diagnosis of acute pancreatic injury should be considered in such cases to avoid deterioration and improve prognosis

Medicolegal aspects of blunt splenic trauma with special reference to delayed rupture/presentation [a prospective study]

Deaths due to splenic rupture are still reported in hospital statistics. It is either acute or delayed rupture. Delayed splenic injury includes either true delayed rupture that represents an actually delayed development of an initially latent, insignificant, splenic injury [i.e. injury in evolution] minor enough to go undetected on initial CT scans of the abdomen, or delayed presentation which represents an initially missed injury [i.e. delay in diagnosis]. We had encountered a number of patients presented with splenic rupture days after blunt abdominal trauma. We conducted this study to review the experience with this clinical entity of blunt splenic rupture with special emphasis on delayed rupture/presentation for patients presented 48 hours or more after trauma. Ninty five emergency examinations were performed for the sole purpose of detecting splenic rupture in patients who had experienced blunt abdominal trauma during a period of 8 years. Twenty three patients out of the ninty five underwent urgent laparotomy and splenectomy within 48 hours from the occurrence of the trauma [24.2%] due to hemodynamic instability as a result of continuously bleeding splenic injury. Left rib fracture was encountered in 47.8% of the cases and bowel and mesenteric injury was found in 17.4% of the cases. Nine patients presented with delayed rupture/presentation of spleen 48 hours or more after the initial trauma [9.4%] were analyzed and formed the basis of this study. The mechanisms of injury and accompanying injuries were documented. The time lag from trauma to operation and the cause of delay were also documented. Regarding the cases of delayed rupture, abdominal computed tomography [CT] was performed in eight hemodynamically stable patients, as the 9[th] patient presented in shock with acute abdomen and emergency laparotomy was performed after positive diagnostic peritoneal lavage. CT demonstrated hemoperitoneum in 7 patients, 2 had subcapsular hematoma, 2 had grade II injury, 2 had grade III injury and one patient had grade IV injury with multiple pseudoaneurysms. Emergency laparotomy was performed for 2 patients due to hemodynamic instability. Three patients were operated upon after a brief period; the reaons for operating were hemodynamic instability or they showed manifestations of diffuse peritoneal irritations. Two patients were diagnosed to have true delayed rupture of sleen and managed initially conservatively; unfortunately, nonoperative management failed because of deterioration of clinical condition in one patient and repeated blood transfusions in the other patient. Splenectomy was performed in 8 patients. The last patient was managed nonoperatively and followed with repeat CT scans. In conclusion, Splenic rupture is frequently associated with collapse and other organ injury specially left rib fractures. This may be a useful marker for suspecting cases of delayed rupture. Also, delayed splenic rupture/presentation represents either an actually delayed development of an initially latent, minor splenic injury or an initially missed injury with late presentation. Patients may be displaced from one grade to another within few days. So, a high index of suspicion, observation, follow up of hematological parameters and liberal utilization imaging techniques are essential for the identification of delayed splenic rupture, which may be hazardous to patients life, and an actual challenge for physicians to avoid being condemned with negligence or malpractice

Importance of nucleophilic thiols in modulating cyclophosphamide toxicity on the heart, urinary bladder and bone marrow of adult albino rats

Cyclophosphamide [CPH] is a synthetic antineoplastic agent, N-acetyl cysteine [NAC] and mesna [sodium 2 mercaptoethane sulphonate] are two members of the nucleophilic thiols. One hundred adult albino rats were used in this study. They were calssified into 10 equal groups. Groups I, II and III were control groups [-ve and +ve controls]. Group IV: [Mesna alone]. The animals of this group received 4 doses of Mesna each of 25mg/kg I.P for 5 days as follows: the 1[st] dose was given followed by the 2[nd] dose after 1/3 of an hour, then the 3[rd] dose was given after 3 hours followed by the 4[th] dose after another 3 hours. Group [V] [NAC alone]: the animals of this group received NAC at a dose of 100 mg/kg orally for 5 days. Group [VI] [Mesna and NAC]: the animals of this group received 4 doses of mesna and one dose of NAC concomitantly with the 2[nd] dose of mesna for 5 days following the same regimen and dose for each. Group [VII] [CPH alone]: the animals of this group received cyclophosphamide in a dose of 50 mg/kg I.P for 5days. Group [VIII] [CPH and Mesna]: the animals received 4 doses of mesna. CPH was given concomitantly with the 2[nd] dose of mesna. Both were given at the same previously mentioned doses and routes for 5 days. Group [IX] [CPH and NAC]: the animals received CPH concomitantly with NAC at the same previously mentioned doses and routes for 5 days. Group [X] [CPH, mesna and NAC]: the animals of this group received 4 doses of mesna. CPH and NAC were given concomitantly with the 2[nd] dose of mesna. All were given at the same previously mentioned doses and routes for each for 5 days. Animals of all groups were sacrificed 24 hours after the last dose. Blood samples were collected for investigating complete blood count [CBC], serum lactic dehydrogenase [LDH] and creatine phosphokinase [CPK] enzymes. Heart, urinary bladder and bone marrow were examined both histologically and histochemically. Cyclophosphamide significantly reduced the total leukocytic count [TLC], platelet count, hemoglobin concentration and lymphocytic count and increased the blood levels of LDH and CPK enzymes. Histologically CPH caused focal areas of cardiac necrosis, intramyocardial hemorrhage and Dilated, congested blood vessels. Whereas, it caused urinary bladder mucosal ulceration, interstitial edema and congestion with mononuclear cellular infiltration. Bone marrow hypocellularity, undifferentiated leukocytic series were also noticed in CPH group. Concomitant administration of mesna recovered completely the CPH-induced urinary bladder toxicity. However, it didn't improve either the blood picture or the cardiac enzymes and didn't recover completely neither the hemopoietic nor the cardiac toxicity of CPH. Whereas, concomitant administration of NAC or NAC and mesna with CPH improved completely the CPH induced hemopoietic and cardiac toxicity as indicated biochemically and histologically and to lesser extent the urinary bladder toxicity. So, it is recommended to prescribe NAC and mesna together with alkylating agents particularly cyclophosphamide to modulate its toxicity