ABSTRACT
BACKGROUND: Management of pain is the most frustrating problem associated with chronic pancreatitis. Pain is progressive and difficult to quantify. Uncontrolled, it eventually destroys the patient's quality of life, leading to drug addiction. STUDY DESIGN: This study reports the results of 258 operations on 239 consecutive patients treated for pain related to chronic pancreatitis between 1969 and 1999. The operations performed were 42 pancreaticoduodenectomies, 48 side-to-side pancreaticojejunostomies, 68 distal pancreatectomies, 21 85% to 95% distal pancreatectomies, 70 cystenterostomies and 9 sphincteroplasties. Efforts were made to choose the operation most appropriate for the pathological conditions encountered in each patient. Results of treatment were satisfactory if patients were entirely relieved of pain and unsatisfactory if there was any residual pain. Presence or absence of pain was based on patient's own evaluation at the time of their last followup examination. RESULTS: Results were overall satisfactory in 71% of patients after pancreaticoduodenectomy, 68% after side-to-side pancreaticojejunostomy, 69% after distal pancreatectomy; 69% after 85% to 95% distal pancreatectomy, 51% after cystenterostomy, and 44% after sphincteroplasty. The mean followup of patients was 4 y (range 0 to 23 y). CONCLUSIONS: The cause of chronic pancreatitis is obscure. As a consequence, there have been few advances in the treatment of this condition. There are new techniques to resect the pancreas, but the results are little better than those obtained with older methods. Advances in the treatment of chronic pancreatic pain will come from knowledge concerning its cause. Discovery of mechanisms stimulating the pathways that lead to the perception of pain and methods for interruption of these mechanisms may provide new treatments.
Subject(s)
Enterostomy , Pain/etiology , Pain/prevention & control , Pancreatectomy , Pancreaticoduodenectomy , Pancreaticojejunostomy , Pancreatitis/complications , Pancreatitis/surgery , Sphincterotomy, Transduodenal , Adult , Aged , Chronic Disease , Enterostomy/adverse effects , Enterostomy/methods , Follow-Up Studies , Humans , Middle Aged , Pain/diagnosis , Pain/psychology , Pain Measurement , Pancreatectomy/adverse effects , Pancreatectomy/methods , Pancreaticoduodenectomy/adverse effects , Pancreaticoduodenectomy/methods , Pancreaticojejunostomy/adverse effects , Pancreaticojejunostomy/methods , Patient Selection , Quality of Life , Sphincterotomy, Transduodenal/adverse effects , Sphincterotomy, Transduodenal/methods , Time Factors , Treatment OutcomeABSTRACT
PURPOSE: To determine the degree of neutrophil activation caused by hemorrhagic shock and resuscitation. METHODS: Awake swine underwent 15-minute 40% blood volume hemorrhage, and a 1-hour shock period, followed by resuscitation with: group I, lactated Ringer's solution (LR); group II, shed blood; and group III, 7.5% hypertonic saline (HTS). Group IV underwent sham hemorrhage and LR infusion. Neutrophil activation was measured in whole blood using flow cytometry to detect intracellular superoxide burst activity. RESULTS: Neutrophil activation increased significantly immediately after hemorrhage, but it was greatest after resuscitation with LR (group I, 273 vs. 102%; p < 0.05). Animals that received shed blood (group II) and HTS (group III) had neutrophil activity return to baseline state after resuscitation. Group IV animals had an increase in neutrophil activation (259 vs. 129%; p < 0.05). CONCLUSION: Neutrophil activation occurring after LR resuscitation and LR infusion without hemorrhage, but not after resuscitation with shed blood or HTS, suggests that the neutrophil activation may be caused by LR and not by reperfusion.
Subject(s)
Isotonic Solutions/pharmacology , Isotonic Solutions/therapeutic use , Neutrophil Activation/drug effects , Shock, Hemorrhagic/immunology , Animals , Blood Transfusion, Autologous , Resuscitation/methods , Ringer's Lactate , Saline Solution, Hypertonic/pharmacology , Saline Solution, Hypertonic/therapeutic use , Shock, Hemorrhagic/physiopathology , Shock, Hemorrhagic/therapy , SwineABSTRACT
OBJECTIVE: The aim was to define the following: (1) if reperfusion of ischaemic limbs could cause myocardial damage; (2) if reactive oxygen metabolites are involved in such possible damage. METHODS: Ten rats underwent ischaemia-reperfusion of the lower limbs (group A) and 10 underwent the same procedure following treatment with ascorbic acid (group B). Ten rats were used as a control group (group C). RESULTS: The incidence of severe myocardial mitochondrial damage and serum malondialdehyde concentrations 30 min after reperfusion were both higher in group A than in groups B and C [8/10, 2/10, and 0/10, p < 0.05 and 7.25 (SEM 0.33), 5.30(0.26), and 4.89(0.23) mumol.litre-1, p < 0.05, respectively]. CONCLUSIONS: Ischaemia-reperfusion of the lower limbs may cause mitochondrial damage in the myocardium and reactive oxygen metabolites could mediate this damage.
