Treatment by ultrasound-guided local infiltration in adhesion-related abdominal pain and intractable hiccups: A case report.

RATIONALE: Abdominal pain and hiccups secondary to intra-abdominal adhesion are surgical complications that are often treated by painkillers and secondary surgeries with an unsatisfactory therapeutic effect. This study presents a new treatment method that uses ultrasound-guided local infiltration in peritoneal and abdominal wall adhesions in patients with hiccups and abdominal pain. PATIENT CONCERNS: A 62-year-old patient presented to our hospital with a history of intractable hiccups and abdominal pain for 30 years. DIAGNOSES: Her abdominal examination revealed a scar with an approximate length of 10 cm on the abdominal umbilical plane; pressing the right scar area could simultaneously induce abdominal pain and hiccups. Intraperitoneal computed tomography examination clearly demonstrated that the bowel had no obvious expansion. Ultrasonographic examination found that peritoneal motility below the normal peritoneal adhesion regions was significantly slower than in the normal regions. The diagnosis of chronic postoperative pain syndrome was clear. INTERVENTIONS: The symptoms were significantly alleviated by a successful treatment with ultrasound-guided local infiltration in the peritoneal and abdominal wall scar adhesions. OUTCOMES: After 3 stages of hospitalization and 1 year of follow-up, the patient's abdominal wall pain was relieved by approximately 80% and hiccups were relieved by approximately 70%. LESSONS: The above treatment is a useful option for managing abdominal adhesion and accompanying pain or hiccups resulting from abdominal surgery. This method could ease the psychological and economic burden of patients and improve their quality of life.

Ulinastatin attenuates neuropathic pain via the ATP/P2Y2 receptor pathway in rat models.

Ulinastatin, a serine protease inhibitor, which has anti-inflammatory properties and neuroprotective effects, is used to treat acute inflammatory disorders. Recent evidence indicates that administration of ulinastatin alleviates pain in rat model of neuropathic pain (NPP). However, its effect on NPP and the underlying mechanism requires further study. In this study, we evaluated the role of intrathecal administration of ulinastatin in rats with sciatic nerve ligation and observed the effect of ulinastatin on the ATP/P2Y2 receptor pathway. We performed mechanical and thermal sensitivity measurements, immunohistochemistry and double-label immunofluoresence studies to evaluate P2Y2 receptor and adenosine 5'-monophosphate-activated protein kinase (AMPK) expression in the dorsal horn of the lumbar enlargement region of the spinal cord, and a luciferase assay for the detection of ATP levels in the cerebrospinal fluid. The results showed that ulinastatin prevented the development of mechanical allodynia and thermal hypersensitivity in the rat sciatic nerve ligation model. Ulinastatin reduced the level of extracellular ATP, down-regulated P2Y2 receptor and AMPK expression in the spinal dorsal horn of the chronic constrictive injury model. We found that increased expression of P2Y2 receptor in microglia was likely involved in the activation of microglia after nerve injury, and ulinastatin inhibited the abnormal microglia activation in the dorsal horn after nerve injury. These findings demonstrated that ulinastatin might be a potential and effective drug for the treatment of NPP via the suppression of the ATP/P2Y2 receptor pathway.

A preliminary study on the role of the complement regulatory protein, cluster of differentiation 55, in mice with diabetic neuropathic pain.

The aim of this study was to investigate the role of the complement regulatory protein cluster of differentiation 55 (CD55) in the pathogenesis of diabetic neuropathic pain (DNP). Healthy adult male C57BL/6J mice were intraperitoneally injected with streptozotocin (STZ) in order to induce DNP. Peripheral blood glucose and protein, and the mRNA expression levels of C3 and CD55 in the spinal cord were determined. In addition, the behaviors of these mice were observed. The results showed that STZ­treated mice displayed the clinical manifestations of diabetes mellitus, and that their peripheral blood glucose was markedly increased. On the 21st and 28th days following the STZ injection, the mechanical pain threshold and thermal pain threshold of the mice were dramatically reduced (P<0.05). |Additionally, 14 days post­STZ injection, the mRNA expression of C3 in the spinal cord was significantly increased, which continued for 28 days. On the 21st and 28th days, the number of C3 positive cells in the spinal cord was markedly increased. Seven days after the STZ injection, the number of cells positive for CD55 was markedly reduced in the spinal dorsal horn and subsequently remained at a low level. The mRNA expression of CD55 also was significantly reduced (P<0.05) and remained so for 28 days. The reduction in the expression levels of CD55 occurred earlier than the changes in the expression of C3, suggesting that the downregulation of CD55 expression precedes, and has an important role regarding, the activation of C3 in the occurrence and development of DNP.

A prospective study of X-ray imaging combined with skin stimulation potential-guided percutaneous radiofrequency thermocoagulation of the Gasserian ganglion for treatment of trigeminal neuralgia.

OBJECTIVE: To investigate the clinical efficacy of X-ray imaging combined with skin stimulation potential-guided percutaneous radiofrequency thermocoagulation of the Gasserian ganglion for treatment of primary trigeminal neuralgia. DESIGN: This is a prospective, randomized study. Sixty patients with primary trigeminal neuralgia were randomly assigned to a study group or control group. In the study group, the patients underwent X-ray imaging combined with skin stimulation potential-guided percutaneous radiofrequency thermocoagulation of the Gasserian ganglion. The patients in the control group underwent C-arm X-ray-guided puncture through the foramen ovale, and then the puncture needle was microscopically adjusted according to the intensity of the masticatory muscle response and the patients' reactions. Puncture success, postoperative adverse reactions, and short- and middle-term analgesic efficacies were statistically compared between the two surgical approaches. RESULTS: The incidence of postoperative side effects was significantly reduced, and immediate and mid-term analgesic efficacy was better in patients in the study group comparing with those in the control group (P < 0.01). CONCLUSION: Using skin stimulation potential-guided puncture may enable more accurate microscopic adjustment of the targets localization damaged by radiofrequency and significantly enhanced clinical efficacy in this study.

Early high volume lung lavage for acute severe smoke inhalation injury in dogs.

The aim of the present study was to investigate the safety and short­term results of early high volume lung lavage in the treatment of acute severe smoke inhalation injuries in dogs. A high­volume normal saline complex solution lavage in the left lung was performed 1 h subsequent to bilateral pulmonary acute severe sawdust smoke inhalation injury in dogs. Lavage of the right lung was conducted following an interval of 30 min or 4 h. The perfluorodecalin lavage was performed in dogs with unilateral pulmonary acute severe sawdust smoke inhalation injury. The present study identified that lavage with an interval of 4 h between two lungs was safer compared with a 30­min interval. Following lavage, the increase in the levels of free radical metabolites and inflammatory mediators in the lung homogenate was reduced. Acute severe smoke inhalation injury in one lung evidently caused a secondary injury to the other lung in the dogs. Perfluorodecalin lavage did not achieve the same effect in cleansing the lungs as the normal saline, but a greater comprehensive short­term outcome was obtained. These observations demonstrated that early high­volume lung lavage following severe smoke inhalation injury could relieve primary injuries and secondary local and general inflammatory reactions in dogs. An improved comprehensive short­term outcome was obtained in the perfluorodecalin­lavaged dogs.

Abnormal activation of complement C3 in the spinal dorsal horn is closely associated with progression of neuropathic pain.

The aim of the present study was to investigate the role of complement activation in the pathogenesis of neuropathic pain (NPP) induced by peripheral nerve injury. We modified a classical chronic constriction injury (CCI) model (mCCI), and verified its reliability in rats. Furthermore, reverse transcription-PCR and immunohistochemistry were conducted to investigate complement activation in the spinal dorsal horn and the effect of a complement inhibitor, cobra venom factor (CVF), on the behavior of the mCCI model rats. We found that rats in the mCCI group presented a better general condition, without signs of autophagy of the toes. Moreover, mCCI induced a significant increase (+40%) in the expression of component 3 (C3) mRNA in the spinal dorsal horn, which was associated with hyperalgesia. Correlation analysis showed a negative correlation between the mechanical pain threshold and the expression of C3 in the spinal cord. Administration of CVF reduced the occurrence of hyperalgesia in mCCI rats and nearly reversed the hyperalgesia. In addition, the mCCI rats exhibited significantly less spinal superoxide dismutase activity and significantly greater levels of maleic dialdehyde compared to the sham-operated rats. Transmission electron micrographs revealed mitochondrial swelling, cell membrane damage, and cristae fragmentation in the neurons of the spinal dorsal horn 14 days after mCCI. Mitochondrial swelling was attenuated in mCCI rats receiving CVF. The findings demonstrated that abnormal complement activation occurred in the dorsal horn of the spinal cord in rats with NPP, and C3 in the spinal dorsal horn could play an important role in the cascade reaction of complements that are involved in the development of hyperalgesia.

[Establishment of a canine model of severe smoke inhalation injury on unilateral lung].

OBJECTIVE: To establish a canine model of severe smoke inhalation injury on unilateral lung, in order to observe the pathomorphological changes in the injured lung within 24 postburn hours (PBHs). METHODS: Twenty five mongrel dogs were employed in the study and randomized into 3 groups. The left lung was injured by inhaling smoke produced by burning sawdust with sparing the right lung with a breathing tube in 10 dogs in group A. A conventional model of smoke inhalation injury to bilateral lungs was reproduced in 8 dogs in group B, and dogs in group C not subjected to smoke inhalation served as controls. Hemodynamic changes, blood gas analysis and the pathophysiologic changes in the lungs were observed within 24 PBHs. RESULTS: All of the dogs in groups A and C survived. Hemodynamic indices in the dogs in groups A and C remained stable without showing signs of systemic hypoxia. The arterial oxygen partial pressure in dogs of group A was 65 +/- 5 mm Hg, and the oxygen saturation in the mixed blood was 0.64 +/- 0.04 at 24 PBHs, and they were much lower than those in group C but higher than those in group B. The pathological changes in the injured side of the lungs in group A were similar to those in group B with high consistency, and the changes, though milder, could also be identified in the contralateral uninjured lung. Five dogs died in the group B within 24 hours after smoke inhalation and the survivors showed signs of multiple organ failure. CONCLUSION: The canine model of acute severe unilateral pulmonary smoke inhalation injury was reproduced reliably, and could be an ideal model for the study on smoke inhalation injury.

[Pathomorphologic changes in rat lungs after being perfused with the bronchoalveolar lavage fluid from the dogs inflicted by smoke inhalation injury at early post-injury stage].

OBJECTIVE: To investigate the biological activities of the bronchoalveolar lavage fluid (BALF) harvested from dogs with smoke inhalation injury at early post injury stage. METHODS: BALF was harvested from normal dogs and those inflicted by smoke inhalation injury for the employment in the study. Ninety four Wistar rats were employed in the study and were randomly divided into A (n=28), B (n=29) and C (n=37) groups. The rats were perfused intra-tracheally with normal saline, BALF from normal dog and BALF from injured dog, respectively in A, B and C groups. Every 7 rats in each group were used before the perfusion as normal control. The rats in control group and those in A, B and C groups at 4, 12 and 24 hours after BALF perfusion were sacrificed. The survival rate and the pathomorphological gross and microscopic changes in pulmonary tissue in all groups were observed. In addition, the contents of prostaglandin F1alpha/thromboxane B2 (PGF1alpha/TXB2), tumor necrosis factor (TNF-alpha) and myeloperoxidase (MPO) in pulmonary tissue homogenization and the pulmonary capillary permeability were determined simultaneously. RESULTS: All the rats in A and B groups survived, but nine in C group died before sacrificing. The BALF from dogs inflicted by smoke inhalation injury could cause rat lung exhibiting pathomorphological changes similar to those in rats inhaling smoke directly. The rat pulmonary tissue contents of PGF1alpha/TXB2 in A and B groups after the perfusion tended to increase, while that in C group decreased gradually (P <0.01). The rat pulmonary tissue contents of TNF-alpha and MPO content in A and B groups after the perfusion revealed no obvious change (P >0.05), while those in C group increased evidently at 4 hour after the perfusion and decreased thereafter (P <0.05-0.01). The pulmonary capillary permeability in C group was higher than that in A and B groups at 4 hour after the perfusion (P < 0.01). CONCLUSION: The BALF from canine lungs during the early stage of inhalation injury exhibited biological activities. The primary and secondary pulmonary injury could be prevented or ameliorated by massive pulmonary lavage during early post injury stage after smoke inhalation injury.