INTRODUCTION:

The outcomes associated with therapeutic hypothermia (TH) after cardiac arrest, while overwhelmingly positive, may be associated with adverse events. The incidence of post-rewarming rebound hyperthermia (RH) has been relatively unstudied and may worsen survival and neurologic outcome. The purpose of this study was to determine the incidence and risk factors associated with RH as well as its relationship to mortality, neurologic morbidity, and hospital length of stay (LOS).

METHODS:

A retrospective, observational study was performed of adult patients who underwent therapeutic hypothermia after an out-of-hospital cardiac arrest. Data describing 17 potential risk factors for RH were collected. The primary outcome was the incidence of RH while the secondary outcomes were mortality, discharge neurologic status, and LOS.

RESULTS:

141 patients were included. All 17 risk factors for RH were analyzed and no potential risk factors were found to be significant at a univariate level. 40.4% of patients without RH experienced any cause of death during the initial hospitalization compared to 64.3% patients who experienced RH (OR: 2.66; 95% CI: 1.26-5.61; p=0.011). The presence of RH is not associated with an increase in LOS (10.67 days vs. 9.45 days; absolute risk increase=-1.21 days, 95% CI: -1.84 to 4.27; p=0.434). RH is associated with increased neurologic morbidity (p=0.011).

CONCLUSIONS:

While no potential risk factors for RH were identified, RH is a marker for increased mortality and worsened neurologic morbidity in cardiac arrest patients who have underwent TH.

Post-operative course after complex pediatric cardiac surgery is unpredictable. Although, change in arterial lactate levels has been used as a surrogate marker for many years, scientific evidence correlating the early perioperative lactate levels with outcome is still lacking.To evaluate the trends in lactate levels from intraoperative period to an extended post-operative period in pediatric intensive care unit (PICU) and to assess its usefulness as a prognostic marker.Prospective observational study.Tertiary pediatric cardiac surgical unit.Thirty-five non-consecutive children aged 1-140 months who underwent surgery for congenital heart diseases (CHD) on cardiopulmonary bypass (CPB).None.ARTERIAL BLOOD LACTATE LEVELS WERE OBTAINED AT THE FOLLOWING TIME POINTS: After induction of anesthesia, 15 and 45 min after institution of CPB, at the start of rewarming, after sternotomy closure, then at 1, 6, 24, and 48 h in PICU. Other hemodynamic and clinical variables, CPB variables, blood gas values, and laboratory variables were also recorded.Four patients died out of 35 patients (11.4%). Non-survivors showed significant persistent elevation in lactates (>4.0 mmol/l). Peak lactates correlate significantly with longer aortic cross clamp time, CPB duration, ventilation hours and PICU stay.Early point of care lactate can be a useful prognostic marker in post-cardiac surgery patients in adjunct with other parameters measured in PICU. This reiterates the importance of measuring lactates and timely recognition of at-risk patients, which on early intervention can help in reducing post-operative morbidity and mortality.

Frostbite is a local freezing injury that can cause tissue loss. Historically, it has been a disease of wars, but it is a hazard for anyone who ventures outdoors in cold weather. Frozen tissue is damaged both during freezing and rewarming. Frozen tissue is numb. Rewarming causes hyperemia and is often painful. Blisters and edema develop after rewarming. Hard eschar may form with healthy tissue deep to the eschar. Frostbite can be classified as superficial, without permanent tissue loss, or deep, with varying degrees of permanent tissue loss, often less than appearances suggest. It can be difficult to predict the amount of tissue loss at the time of presentation and early in the subsequent course. Prevention is better than treatment. It may be advisable not to rewarm frozen extremities in the field, but spontaneous thawing is often unavoidable. Extremities that have thawed should be protected from refreezing at all costs. Once in a protected environment, extremities that are still frozen should be rapidly thawed in warm water. Therapy with aspirin or ibuprofen may be helpful, but evidence is limited. Thrombolytic treatment within the first 24 hours after rewarming seems to be beneficial in some cases of severe frostbite. Prostacyclin therapy is very promising.

Pulmonary thromboendarterectomy (PTE) has evolved as a treatment of choice for chronic thromboembolic pulmonary hypertension (CTEPH). This study aimed to characterize if pulmonary oligemia maneuver (POM) can alleviate pulmonary artery injury during PTE procedure.A total of 112 cases of CTEPH admitted to Beijing Anzhen Hospital from March 2002 to August 2011 received PTE procedure. They were retrospectively classified as non-POM group (group A, n = 55) or POM group (group B, n = 57). Members from group B received POM during rewarming period, whereas members from group A did not.There were three (5.45%) early deaths in group A, no death in group B (0) (Fisher's exact test, P = 0.118). Six patients in group A needed extracorporeal membrane oxygenation (ECMO) as life support after the PTE procedure, no patients in group B needed ECMO (Fisher's exact test, P = 0.013). The patients in group B had a shorter intubation and ICU stay, lower mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR), higher partial pressure of oxygen in artery (PaO2) and arterial oxygen saturation (SaO2) and less medical expenditure than patients in group A. With a mean follow-up time of (58.3 ± 30.6) months, two patients in group A and one patient in group B died. The difference of the actuarial survival after the procedure between the two groups did not reach statistical significance. Three months post the PTE procedure, the difference of residual occluded pulmonary segment between the two groups did not reach statistical significance (P = 0.393).POM can alleviate pulmonary artery injury, shorten ICU stay and intubation time, and lower down the rate of ECMO after PTE procedure.

 

INTRODUCTION:

Optimal cryoballoon ablation parameters for pulmonary vein (PV) isolation remain to be defined. We conducted a randomized preclinical trial to compare 2- versus 4-minute ablation lesions and assess the safety of active (forced) cryoballoon deflation.

METHODS AND RESULTS:

Thirty-two dogs underwent PV isolation with a second-generation 23 mm cryoballoon catheter. The left superior (LSPV) and inferior (LIPV) PVs were randomized in a factorial design to (1) a single 2- versus 4-minute cryoapplication, and (2) passive versus active cryoballoon deflation. Animals were survived for 30 days, after which histopathologic analysis was performed. Acute PV isolation was attained in 89.8% of PVs after a single application (93.8% LSPV, 85.2% LIPV; P = 0.2823). Mean time to PV isolation was 29.5 ± 18.5 seconds. Although 4-minute lesions were associated with a thicker neointima than 2-minute lesions (223.8 μm versus 135.6 μm; P = 0.007), no differences were observed in procedural characteristics (freezing temperature, rewarming time), rates of acute PV isolation, or the achievement of complete circumferentially transmural lesions at 30 days (78.7% overall; 86.2% for 2 minutes vs 70.0% for 4 minutes; P = 0.285). Active deflation was associated with faster balloon rewarming but not with significant differences in mean or maximum neointimal thickness.

CONCLUSION:

A single application with the second-generation cryoballoon catheter results in a high rate of PV isolation. The degree of vascular injury was not increased by active balloon deflation and no differences in acute efficacy or mature transmural circumferential lesions were observed with 2- versus 4-minute applications.

OBJECTIVE::

Cardiac surgery, especially when employing cardiopulmonary bypass and deep hypothermic circulatory arrest, is associated with systemic inflammatory responses that significantly affect morbidity and mortality. Intestinal perfusion abnormalities have been implicated in such responses, but the mechanisms linking local injury and systemic inflammation remain unclear. Intestinal mast cells are specialized immune cells that secrete various preformed effectors in response to cellular stress. We hypothesized that mast cells are activated in a microenvironment shaped by intestinal ischemia/reperfusion, and investigated local and systemic consequences.

DESIGN:

: Rat model of deep hypothermic circulatory arrest.

SETTING:

: University research laboratory.

SUBJECTS:

: Twelve- to 14-week-old male Sprague-Dawley rats.

INTERVENTIONS:

: Rats were anesthetized and cooled to 16°C-18°C on cardiopulmonary bypass before instituting deep hypothermic circulatory arrest for 45 minutes. Specimens were harvested following rewarming and 2 hours of recovery.

MEASUREMENTS AND MAIN RESULTS:

: Significant intestinal barrier disruption was found, together with macro- and microscopic evidence of ischemia/reperfusion injury in ileum and colon, but not in lungs or kidneys. Immunofluorescence and toluidine blue staining revealed increased numbers of mast cells and their activation in the gut. In animals pretreated with the mast cell stabilizer, cromolyn sodium, mast cell degranulation was blocked, and intestinal morphology and barrier function were preserved following deep hypothermic circulatory arrest. Furthermore, cromolyn sodium treatment was associated with reduced intestinal neutrophil influx and blunted systemic release of proinflammatory cytokines.

CONCLUSION:

: Our data provide primary evidence that intestinal ischemia/reperfusion is a leading pathophysiologic process in a rat model of deep hypothermic circulatory arrest, and that intestinal injury, and local and systemic inflammatory responses are critically dependent on mast cell activation. This identifies intestinal mast cells as central players in deep hypothermic circulatory arrest-associated responses, and opens novel therapeutic possibilities for patients undergoing this procedure.

This article reviews recent medical literature to provide an overview of the recognition and treatment of the two broad categories of cold injuries, freezing and nonfreezing. Frostbite, a freezing cold injury, is treated traditionally with rapid rewarming followed by tissue care and surgical debridement of necrotic tissue. Recently, newer therapies aimed at prevention of tissue necrosis have shown improved outcomes compared with more traditional therapies. These newer treatment regimens for frostbite include the use of various drugs such as ibuprofen, aspirin, warfarin, tissue plasminogen activator, and prostacyclin. The use of Tc bone scans, magnetic resonance imaging arthrogram, or angiography may have prognostic value for early determination of the extent of tissue loss. The more common nonfreezing cold injuries, though less severe than frostbite, may lead to short- and long-term complications requiring treatment and are discussed also.

BACKGROUND:

/st>It is unclear what factors affect the uptake of sevoflurane administered through the membrane oxygenator during cardiopulmonary bypass (CPB) and whether this can be monitored via the oxygenator exhaust gas.

METHODS:

/st>Stable delivery of sevoflurane was administered to 30 elective cardiac surgery patients at 1.8 vol% (inspiratory) via the anaesthetic circuit and ventilator. During CPB, sevoflurane was administered in the oxygenator fresh gas supply (Compactflo Evolution™; Sorin Group, Milano, Italy). Sevoflurane plasma concentration (SPC) was measured using gas chromatography. Changes were correlated with bispectral index (BIS), patient temperature, haematocrit, plasma albumin concentration, oxygenator fresh gas flow, and the sevoflurane concentration in the oxygenator exhaust at predefined time points.

RESULTS:

/st>The mean SPC pre-bypass was 54.9 µg ml(-1) [95% confidence interval (CI): 50.6-59.1]. SPC decreased to 43.2 µg ml(-1) (95% CI: 40.3-46.1; P<0.001) after initiation of CPB, and was lower still during rewarming and weaning from bypass, 39.4 µg ml(-1) (95% CI: 36.6-42.3; P<0.001). BIS did not exceed a value of 55. SPCs were higher during hypothermia (P<0.001) and with an increase in oxygenator fresh gas flow (P=0.015), and lower with haemodilution (P=0.027). No correlation was found between SPC and the concentration of sevoflurane in the oxygenator exhaust gas (r=-0.04; 95% CI: -0.18 to 0.09; P=0.53).

CONCLUSIONS:

/st>The uptake of sevoflurane delivered via the membrane oxygenator during CPB seems to be affected by hypothermia, haemodilution, and changes in the oxygenator fresh gas supply flow. Measuring the concentration of sevoflurane in the exhaust from the oxygenator is not useful for monitoring sevoflurane administration during bypass.

It is well known that saintpaulia leaf is damaged by the rapid temperature decrease when cold water is irrigated onto the leaf surface. We investigated this temperature sensitivity and the mechanisms of leaf damage in saintpaulia (Saintpaulia sp. cv. 'Iceberg') and other Gesneriaceae plants. Saintpaulia leaves were damaged and discolored when subjected to a rapid decrease in temperature, but not when the temperature was decreased gradually. Sensitivity to rapid temperature decrease increased within 10 to 20 min during pre-incubation at higher temperature. Injury was restricted to the palisade mesophyll cells, where there was an obvious change in the color of the chloroplasts. During a rapid temperature decrease, chlorophyll fluorescence monitored by a pulse amplitude modulated fluorometer diminished and did not recover even after rewarming to the initial temperature. Isolated chloroplasts were not directly affected by the rapid temperature decrease. Intracellular pH was monitored with a pH-dependent fluorescent dye. In palisade mesophyll cells damaged by rapid temperature decrease, the cytosolic pH decreased and the vacuolar membrane collapsed soon after a temperature decrease. In isolated chloroplasts, chlorophyll fluorescence declined when the pH of the medium was lowered. These results suggest that a rapid temperature decrease directly or indirectly affects the vacuolar membrane, resulting in a pH change in the cytosol that subsequently affects the chloroplasts in palisade mesophyll cells. We further confirmed that the same physiological damage occurs in other Gesneriaceae plants. These results strongly suggested that the vacuoles of palisade mesophyll cells collapsed during the initial phase of leaf injury.