Selective hepatic arterial embolization of grade IV and V blunt hepatic injuries: an extension of resuscitation in the nonoperative management of traumatic hepatic injuries.

BACKGROUND: Recognizing the significant mortality and complications inherent in the operative management of blunt hepatic injuries, hepatic arterial embolization was evaluated as a bridge between operative and nonoperative interventions in patients defined as hemodynamically stable only with continuous resuscitation. METHODS: Seven of 11 patients with grade IV or V hepatic injuries identified by computed tomography underwent hepatic arterial embolization. A prospective evaluation of hepatic embolization based on subsequent hemodynamic parameters was assessed by matched-pair analysis. A summary of this study population's demographic data and outcomes is presented, including age, Glasgow Coma Scale score, Injury Severity Score, Revised Trauma Score, computed tomography grade, intensive care unit and hospital length of stay, transfusion requirements, complications, and mortality. RESULTS: No statistical difference was demonstrated between pre-embolization and postembolization hemodynamics and volume requirements. After embolization, however, continuous resuscitation was successfully reduced to maintenance fluids. Hepatic embolization was the definitive therapy for all seven patients who underwent embolization. CONCLUSION: Results of this preliminary investigation suggest that hepatic arterial embolization is a viable alternative bridging the therapeutic options of operative and nonoperative intervention for a subpopulation of patients with hepatic injury.

Clinical analysis of the utility of repeat computed tomographic scan before discharge in blunt hepatic injury.

OBJECTIVES: Nonoperative management of hemodynamically stable blunt hepatic injury has emerged as an acceptable and safe treatment. Surveillance of this population's injuries is costly. As a prelude to establishing practice guidelines, the utility of repeat computed tomographic (CT) scans was investigated. METHODS: A retrospective study was conducted on 243 hepatic injuries. The CT scans of 95 patients managed nonoperatively who did not have ongoing transfusion requirements were reviewed and graded according to the American Association for the Surgery of Trauma (AAST) hepatic injury scale. Patients were grouped according to injury grade, assigned to two subgroups (patients with one CT scan versus more than one CT scan) and compared with respect to several physiologic and clinical variables. RESULTS: Statistical analysis revealed no significant difference between subgroups with the same grade of injury. No significant difference was demonstrated between subgroups' length of stay. CONCLUSIONS: No patients failed nonoperative treatment or succumbed to their injuries. Findings on repeat CT scan have not altered the decision to discharge the clinically stable patient having suffered a grade III or lower liver injury.

A clinical experience with ADSOL preserved erythrocytes.

This study was undertaken to determine how ADSOL (adenine, glucose, mannitol and sodium chloride) preservative affects the 24 hour post-transfusion survival values of human erythrocytes during storage at 4 degrees C. for 35, 42 and 49 days. The results show that acceptable 24 hour post-transfusion survival values were observed only after storage at 4 degrees C. for 35 days.

Endorphins in primate hemorrhagic shock: beneficial action of opiate antagonists.

The endogenous opiate beta-endorphin is released concomitantly with adrenocorticotropin from the pituitary during stress. In the present study we investigated the possible involvement of opiate receptors in the cardiovascular depression associated with hypovolemic shock in the nonhuman primate. Changes in circulating levels in beta-endorphin were monitored during hemorrhagic shock in 18 female baboons. Plasma levels of beta-endorphin increased significantly during hemorrhagic shock and were significantly correlated with a decrease in cardiac output (P less than 0.05). Single bolus administration of the opiate receptor antagonist naloxone (2 or 5 mg/kg) produced a transient but significant improvement in cardiac output (P less than 0.05) and mean arterial pressure (P less than 0.05). Hemodynamic improvement was maintained with a constant infusion of naloxone. Opiate receptor blockade with the longer acting antagonist naltrexone (2 or 5 mg/kg) significantly increased mean arterial pressure (MAP; P less than 0.05), and CO (P less than 0.05), and decreased heart rate. Our results suggest that the baboon is an excellent model for the study of hemorrhagic shock and provide further evidence for endogenous opiate involvement in the cardiovascular pathophysiology of hemorrhagic shock.

Prolonged disruption of plasma beta-endorphin dynamics following surgery.

The purpose of the present study was to examine the effects of surgery on plasma beta-endorphin dynamics. Plasma beta-endorphin levels were measured by liquid chromatography/radioimmunoassay in seven patients undergoing elective surgery. Blood samples were obtained every 4 hr for two 24-hr periods: one beginning 48 hr before surgery and the other beginning 48 hr after surgery. Computer analysis of beta-endorphin levels as a function of clock time demonstrated a true circadian rhythm preoperatively with a mean of 28.0 +/- 5.9 pg/ml. In the postoperative period mean beta-endorphin levels were significantly elevated (85.6 +/- 20.7 pg/ml, P less than 0.005). Surgical procedures caused significant phase shifting in the grouped mean circadian rhythm of plasma beta-endorphin (mean = 2.4 hr). When the data was analyzed individually, plasma circadian rhythms were found to be totally abolished in the three patients with the longest operative times (mean = 3.8 hr) and significantly displaced in time in the remaining four patients. These prolonged alterations in plasma endogenous opioid peptide levels following surgery have not been previously reported, and should be considered in the management of the postsurgical patient.

Beta-endorphin, cortisol and postoperative delirium: a preliminary report.

A transient delirium, including hallucinations and disorientation, occurred at some time during a 48 to 72 hr postoperative period in patients recovering from elective surgery in an intensive care unit. The occurrence of delirium in these patients was associated with a significant and unusually prolonged postoperative increase in circulating levels of beta-endorphin (B-endorphin) and cortisol, and a total disruption of normal plasma circadian rhythms of B-endorphin and cortisol. Postoperative mean 24-hr plasma levels of B-endorphin and cortisol were not significantly different from preoperative baseline levels in those patients who did not exhibit post-surgical delirium. Circadian rhythms of B-endorphin and cortisol in the non-delirious patients also remained normal following surgery, although peak plasma concentrations were significantly phase-shifted to later in the day. A disruption in circadian rhythms of the endogenous opiate/hypothalamic-pituitary-adrenal axis may represent an important component of post-operative psychological changes that are frequently observed in the intensive care unit setting.

Effect of an opiate antagonist (naloxone) and an agonist/antagonist (nalbuphine) in primate hemorrhagic shock: relationship to catecholamine release.

Recent evidence has suggested a relationship between the endogenous opioid peptides and the pathophysiology of various shock states. In the present study, we investigated the relationship between the effectiveness of naloxone (an opiate antagonist) and nalbuphine (an opiate agonist/antagonist), and the changes in circulating levels of catecholamines in the nonhuman primate subjected to hemorrhagic shock. Plasma levels of catecholamines were measured using high-performance liquid chromatography (HPLC) during hemorrhagic shock in 15 female baboons. Plasma levels of both epinephrine and norepinephrine increased significantly during hemorrhagic shock (p less than 0.05), which correlated with an increase in heart rate. Bolus administration of naloxone (5 mg/kg) significantly increased both plasma epinephrine (p less than 0.01) and norepinephrine (p less than 0.05) over shock levels along with a transient but significant increase in cardiac output (p less than 0.05) and mean arterial pressure (p less than 0.05), and a significant decrease in heart rate (p less than 0.05). Improvements in hemodynamics were maintained with a constant infusion of naloxone (5 mg/kg/hr), which also caused a further significant increase in plasma epinephrine (p less than 0.01). Administration of a single bolus of the opiate agonist/antagonist nalbuphine (5 mg/kg) dramatically decreased cardiac output and mean arterial pressure and had no effect on circulating catecholamines. Our results suggest that (1) the beneficial action of high-dose naloxone in primate hemorrhagic shock may be attributable in part to a drug-induced increase in circulating endogenous catecholamines; and (2) the failure of high-dose nalbuphine to improve cardiovascular function may be related to its partial agonist (cardiodepressant) properties at higher doses.