An Evolving Uncontrolled Hemorrhage Model Using Cynomolgus Macaques.

BACKGROUND: Trauma-induced hemorrhagic shock produces hemodynamic changes that often result in a systemic inflammatory response that can lead to multiple organ failure and death. In this prospective study, the pathophysiology of a nonhuman primate uncontrolled hemorrhagic shock model is evaluated with the goal of creating an acute systemic inflammatory syndrome response and a reproducible hemorrhage. METHODS: Nonhuman primates were divided into 2 groups. A laparoscopic left hepatectomy was performed in groups A and B, 60% and 80%, respectively, resulting in uncontrolled hemorrhage. Resuscitation during the prehospital phase lasted 120 min and included a 0.9% saline bolus at 20 mL/kg. The hospital phase involved active warming, laparotomy, hepatorrhaphy for hemostasis, and transfusion of packed red blood cells (10 mL/kg). The animals were recovered and observed over a 14-day survival period with subsequent necropsy for histopathology. RESULTS: Baseline demographics and clinical parameters of the two groups were similar. Group A (n = 7) underwent a 57.7% ± 2.4% left hepatectomy with a 33.9% ± 4.0% blood loss and 57% survival. Group B (n = 4) underwent an 80.0% ± 6.0% left hepatectomy with 56.0% ± 3.2% blood loss and 75% survival. Group B had significantly lower hematocrit (P < 0.05) for all postinjury time points. Group A had significantly elevated creatinine on postoperative day 1. Nonsurvivors succumbed to an early death, averaging 36 h from the injury. Histopathologic evaluation of nonsurvivors demonstrated kidney tubular degeneration. CONCLUSIONS: Nonhuman primates displayed the expected physiologic response to hemorrhagic shock due to liver trauma as well as systemic inflammatory response syndrome with resultant multiple organ dysfunction syndrome and either early death or subsequent recovery. Our next step is to establish a clinically applicable nonhuman primate polytrauma model, which reproduces the prolonged maladaptive immunologic reactivity and end-organ dysfunction consistent with multiple organ failure found in the critically injured patient.

Unconventional management of chyloascites after laparoscopic Nissen fundoplication.

BACKGROUND & OBJECTIVES: Chyloascites is a rare complication that can result from abdominal trauma, neoplasm, inflammatory conditions, or various abdominal surgeries. Few cases have been described secondary to iatrogenic injury from laparoscopic Nissen fundoplication. We describe a case in which this surgery resulted in chyloascites that was successfully treated by lymphatic glue embolization. METHODS: A 37-year-old male presented with signs and symptoms consistent with chronic reflux disease. He underwent an uneventful laparoscopic Nissen fundoplication. Two weeks postoperatively, he was admitted for dehydration. During his admission, he began to develop a persistent cough, shortness of breath, and abdominal distention. Imaging and fluid analysis from thoracocentesis and paracentesis were consistent with chyle leakage. Despite nonoperative measures, the patient's presentation persisted. RESULTS: Thoracic duct ligation was performed without success. Bipedal lymphangiography identified an extensive leak revealing a severely lacerated thoracic duct spilling contrast freely into the abdomen and no contrast entering the thoracic duct in the chest. The site of injury was successfully sealed off with percutaneous glue embolization through lymph channels. CONCLUSION: Chyloascites is a rare complication of laparoscopic Nissen fundoplication. When not successful with conservative measures, lymphatic glue embolization can provide effective treatment.