Vasopressin therapy in cardiac surgery.

BACKGROUND: Arginine vasopressin (AVP) is a naturally occurring peptide with diverse effects mediated through selective V1 and V2 receptors. About 10% of patients undergoing cardiopulmonary bypass develop postoperative vasodilatory shock requiring high-dose catecholamines. We sought to examine the role of AVP therapy in cardiac surgery. METHODS: A search of Medline was conducted through September 2018 using key words and medical subject headings (MeSH) relating to AVP, copeptin, and cardiac surgery. A systematic review was performed on articles as they pertained to AVP for use as a vasopressor after cardiovascular surgery complicated by vasodilatory shock. RESULTS: A relative or absolute deficiency of Arginine vasopressin is associated with vasodilatory shock after cardiopulmonary bypass. Physiologic replacement with exogenous Arginine vasopressin results in significant increases in systemic vascular resistance and mean arterial pressure with decreased requirements of catecholamines. At doses of <0.1 U/min Arginine vasopressin is safe with very few adverse effects. CONCLUSION: Post-cardiopulmonary bypass vasodilatory shock is largely due to a relative deficiency of Arginine vasopressin. Exogenous administration of low-dose Arginine vasopressin alone or in combination with traditional catecholamines is a safe and effective way to manage this type of vasodilatory shock.

Early High-Volume Hemofiltration versus Standard Care for Post-Cardiac Surgery Shock. The HEROICS Study.

RATIONALE: Post-cardiac surgery shock is associated with high morbidity and mortality. By removing toxins and proinflammatory mediators and correcting metabolic acidosis, high-volume hemofiltration (HVHF) might halt the vicious circle leading to death by improving myocardial performance and reducing vasopressor dependence. OBJECTIVES: To determine whether early HVHF decreases all-cause mortality 30 days after randomization. METHODS: This prospective, multicenter randomized controlled trial included patients with severe shock requiring high-dose catecholamines 3-24 hours post-cardiac surgery who were randomized to early HVHF (80 ml/kg/h for 48 h), followed by standard-volume continuous venovenous hemodiafiltration (CVVHDF) until resolution of shock and recovery of renal function, or conservative standard care, with delayed CVVHDF only for persistent, severe acute kidney injury. MEASUREMENTS AND MAIN RESULTS: On Day 30, 40 of 112 (36%) HVHF and 40 of 112 (36%) control subjects (odds ratio, 1.00; 95% confidence interval, 0.64-1.56; P = 1.00) had died; only 57% of the control subjects had received renal-replacement therapy. Between-group survivors' Day-60, Day-90, intensive care unit, and in-hospital mortality rates, Day-30 ventilator-free days, and renal function recovery were comparable. HVHF patients experienced faster correction of metabolic acidosis and tended to be more rapidly weaned off catecholamines but had more frequent hypophosphatemia, metabolic alkalosis, and thrombocytopenia. CONCLUSIONS: For patients with post-cardiac surgery shock requiring high-dose catecholamines, the early HVHF onset for 48 hours, followed by standard volume until resolution of shock and recovery of renal function, did not lower Day-30 mortality and did not impact other important patient-centered outcomes compared with a conservative strategy with delayed CVVHDF initiation only for patients with persistent, severe acute kidney injury. Clinical trial registered with www.clinicaltrials.gov (NCT 01077349).

Trauma, transfusions, and use of recombinant factor VIIa: A multicenter case registry report of 380 patients from the Western Trauma Association.

BACKGROUND: This study describes the current use of recombinant activated factor VII (rFVIIa) for hemorrhage after trauma in the United States. We hypothesized that we could describe the setting in which rFVIIa would be most successful in arresting hemorrhage after injury. STUDY DESIGN: This case registry study of patients with traumatic injuries at risk for death from hemorrhage at Level I and II trauma centers in the United States analyzed the administration of rFVIIa from admission to death from hemorrhage. Secondary outcomes measures of interest were the use of blood products, days in the ICU, organ failure, and thrombotic complications. RESULTS: Three hundred and eighty injured patients who received rFVIIa as an adjunct for hemorrhage control were included in this analysis. The mean time from admission to administration of rFVIIa was 4.6 hours, with an average transfusion of 18 U blood before administration (range 0 to 99 U). Death from hemorrhage rate was 30%. Predictors of a poor response to rFVIIa were a pH <7.2 (p < 0.0001), a platelet count <100,000 (p = 0.046), and blood pressure ≤90 mmHg (p < 0.0001) at the time of administration. CONCLUSIONS: Based on this case registry review, the precise role of rFVIIa in traumatic hemorrhage is unclear. Surgeons choosing to use this drug as an adjunctive measure to reverse coagulopathy are advised to first correct shock, acidosis, and thrombocytopenia.

Vasopressin, when added to norepinephrine, was not associated with increased predicted mortality after cardiac surgery.

BACKGROUND AND AIMS: Arginin vasopressin (AVP) is a potent vasoconstrictor which has been used in vasodilatory shock when therapy with catecholamines and fluids has failed. In this study we evaluated the association of AVP with organ failure and mortality in cardiac surgical patients suffering from vasodilatory shock refractory to norepinephrine (NE) treatment. MATERIAL AND METHODS: Cardiac surgical patients who received AVP in addition to NE (N=33, AVP-group) and 33 control patients (NE group) who were treated with an equal dose of NE compared with AVP patients when AVP infusion started. Data on preoperative risk factors according to EuroSCORE and predicted mortality calculated by logistic EuroSCORE were collected preoperatively. Data on hemodynamics, organ dysfunctions, length of intensive care unit stay and mortality were collected. RESULTS: EuroSCORE did not differ between the groups, AVP:10.4 +/- 3.9 vs. NE 8.9 +/- 4.0. Observed 30 day mortality was lower than predicted in both groups, AVP: 7 (21.7%) vs. predicted mortality 25.9% and NE: 2 (6.1%) vs. 16.0%, respectively. There were more renal complications (36.4% vs. 9.1%, p = 0.008) and infections (30.3% vs. 3.0%, p = 0.003) in patients receiving AVP. Cardiovascular complications did not differ between the groups. CONCLUSIONS: In this prospectively observed cohort of cardiac surgical patients, AVP did not increase mortality predicted by Euroscore. Anyhow renal and infection complications were common.

Vasopressors and intestinal mucosal perfusion after cardiac surgery: Norepinephrine vs. phenylephrine.

OBJECTIVES: To evaluate the potential differential effects of norepinephrine, an alpha1-, beta1-, and beta2-receptor agonist, to the alpha1-agonist phenylephrine on jejunal mucosal perfusion, gastric-arterial PCO2 gradient, and the global splanchnic oxygen demand-supply relationship after cardiac surgery. DESIGN: A randomized, prospective, interventional crossover study. SETTING: A university cardiothoracic intensive care unit. PATIENTS: Ten patients were studied during propofol sedation and mechanical ventilation after uncomplicated coronary artery bypass surgery. INTERVENTIONS: Each patient received randomly and sequentially norepinephrine (0.052+/-0.009 microg/kg/min) and phenylephrine (0.50+/-0.22 microg/kg/min) to increase mean arterial blood pressure by 30%. MEASUREMENTS AND MAIN RESULTS: Data on jejunal mucosal perfusion, jejunal mucosal hematocrit, and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial Pco2 gradient (tonometry) and splanchnic oxygen extraction were obtained before (control) and during a 30-min drug infusion period after the target mean arterial blood pressure was reached. The procedure was sequentially repeated for the second vasopressor. Both drugs induced a 40-46% increase in systemic vascular resistance with no change in cardiac index. Neither jejunal mucosal perfusion, jejunal mucosal hematocrit, red blood cell velocity, nor gastric-arterial Pco2 gradient was affected by any of the vasopressors. Splanchnic oxygen extraction increased from 38.2% to 43.1% (p<.001) with norepinephrine and from 39.3% to 47.5% (p<.001) with phenylephrine. This increase was significantly more pronounced with phenylephrine compared with norepinephrine (p<.05). Mixed venous-hepatic vein oxygen saturation gradient increased with both drugs (p<.01), and the increase was more pronounced with phenylephrine (p<.05). Splanchnic lactate extraction was not significantly affected by any of the vasopressors. CONCLUSIONS: Phenylephrine induced a more pronounced global alpha1-mediated splanchnic vasoconstriction compared with norepinephrine. Neither of the vasoconstrictors impaired perfusion of the gastrointestinal mucosa in postcardiac surgery patients. The lack of norepinephrine-induced, alpha1-mediated impairment of gastrointestinal perfusion is not explained by a beta2-mediated counteractive vasodilation but instead by possible mucosal autoregulatory escape.

Steroid cover in dentistry: recommendations following a review of current policy in UK dental teaching hospitals.

This article reports a project that was undertaken to determine current UK dental hospital policy with regard to the management of patients taking therapeutic doses of corticosteroids receiving dental treatment under local anaesthesia. There is variation in the medical management of this patient group, and whether practice should be standardized by means of a national policy document warrants consideration.

Antidiuretic hormone replacement therapy to prevent or ameliorate vasodilatory shock.

Vasodilatory shock is a syndrome with high mortality. It is becoming evident that depletion of antidiuretic hormone (ADH) after cardiac surgery or during sepsis plays an important role in the pathogenesis of this condition. Established vasodilatory shock responds well to exogenous ADH infusion. It is possible that preventing ADH depletion at an earlier stage may abrogate the onset of vasodilatory shock, or at least reduce its severity. This paper examines the evidence supporting this concept, and the potential areas of concern in considering this particular type of hormone replacement therapy.

[Anesthesia in domestic animals (small mammals, psittacines and reptiles)]. / Zur Anästhesie bei Heimtieren (Kleinsäuger, Psittaciden und Reptilien).

The presentation of small animals and exotic pets (birds, reptiles) in veterinary practice is increasing. Physiological and ethological variations demand specific precautions in restraining/ anesthetizing these patients. In Psittacines hypoglycemia, hypoxia and hypothermia are typical side-effects. Long-acting recovery control in birds and reptiles is necessary.

Xanthine oxidase inactivation attenuates postocclusion shock after descending thoracic aorta occlusion and reperfusion in rabbits.

"Declamping shock" is observed after aortic crossclamping, with hypovolemia, hypotension, and metabolic acidemia invariably present. We hypothesized that oxidants derived from xanthine oxidase influence the resuscitative interventions required to maintain baseline hemodynamic and acid-base status after aortic occlusion and reperfusion in rabbits. We also hypothesized that inactivation of xanthine oxidase with sodium tungstate could reduce systemic injury as assessed by the release of lactate dehydrogenase and alkaline phosphatase. To test these hypotheses, we established aortic occlusion in rabbits (n = 10, standard diet; n = 8, tungstate diet) for 40 minutes by inflation of a 4F Fogarty catheter in the descending thoracic aorta followed by 2 hours of reperfusion. Sham-operated rabbits (n = 10, standard diet; n = 9, tungstate diet) served as controls. Tungstate-pretreated rabbits required significantly less Ringer's solution (28%), phenylephrine (68%), and sodium bicarbonate (30%) during reperfusion (p < 0.005). Lactate dehydrogenase and alkaline phosphatase release during reperfusion was significantly attenuated by tungstate pretreatment (p < 0.05). Tungstate pretreatment resulted in plasma xanthine oxidase activities significantly lower than those in the sham group administered a standard diet (p = 0.007). Resuscitation requirements and systemic injury were reduced by inactivation of xanthine oxidase in a rabbit model that simulates the situation of human thoracic aorta operations.

Avoiding coagulopathy in vascular surgery.

The possibility of coagulopathy can be minimized by attending to certain general perioperative details to avoid hypothermia, hypotension-shock, and multiple transfusions. In this paper, we present our protocol for avoiding coagulopathy in vascular surgery. In the past 1 1/2 years, we have used perioperative plasmapheresis in 204 patients undergoing cardiac or aortic peripheral vascular surgery. Autologous platelet-rich plasma is transfused at the completion of the operation after heparin reversal. Our data show an approximate 50% reduction in homologous blood product requirement. Seventy-five percent of patients having aortic surgery received no homologous blood products during their hospital stay. For those undergoing cardiac surgery, there has been about a 45% reduction in the use of homologous blood products. In our experience, autologous platelet-rich plasma not only decreases the risk of transmittable disease, but promotes hemostasis.

[In vivo protective action of urinastatin during extracorporeal circulation].

A patient undergoing extracorporeal circulation is in the state of controlled shock. The object of the present study is to investigate the prophylactic effect of ulinastatin (6000 U.kg-1 or 12000 U.kg-1 during extracorporeal circulation by a randomized study. Although the ratio of lactic acid/pyruvic acid did not show significant changes, the increase was inhibited in 12000 U.kg-1 treated group. In 12000 U.kg-1 treated group, beta-glucuronidase reflecting the function of lysosomal membrane, as well fibronectin reflecting the endothelial function, were suppressed. The results of the present study indicate that administration of ulinastatin 12000 U.kg-1 is effective and useful for the organism.

Might the aphorism "there is no indication in medicine for a pint of blood" lie behind some of the residual morbidity and mortality of surgery?

Reconsideration of, and some uncertainty about, the risks of whole blood transfusion are stimulating renewed debate around and about transfusion policy. This essay -- 1) considers probable risks of retreating in fright from the approach which has significantly reduced the morbidity and mortality of surgical operations over the last 100 years, so that we may balance them against the known and putative risks of transfusion. 2) questions the universality of the aphorism "There is no indication in medicine for a pint of blood" -- because it presumes and implies that everyone can "tolerate"/not be harmed by/minor blood loss, or minor hypovolaemia from any other cause, and leads surgeons and anaesthetists to aim at "minimising" the degree and duration of hypovolaemia during surgery rather than to prevent it entirely. 3) proposes that circulating volume deficiencies, including small ones, are intrinsically intolerable pathological events to be prevented by a "positive" policy aiming at normovolaemia throughout operative procedures by "priming" patients about to undergo major operations with volume expanders before surgery, minimising their intraoperative blood loss, giving non-blood plasma expanders until dilution threatens significant anaemia, and whole-blood transfusion as a last resort when it does. 4) proposes that averting "minor" short-lived circulating volume depletion might avert the residual "minor" morbidity and mortality caused by venous thrombosis, pulmonary embolism, bronchopneumonia, intestinal ileus, postoperative abdominal distension, wound and anastomotic dehiscence, fat embolism, (alone or in various combinations) and give us a greater (insight into and) control over fluid and electrolyte balance.