Hypothermia attenuates the severity of oxidative stress development in asphyxiated newborns

Purpose

This retrospective case-control study aimed to examine the development of oxidative stress in asphyxiated infants delivered at more than 37 weeks of gestation.

Material and Methods

Thirty-seven neonates were stratified into 3 groups: the first group experienced hypothermia (n = 6); the second received hypothermia cooling cup treatment for 3 days, normothermia (n = 16); and the third was the control group (n = 15).Serum total hydroperoxide (TH), biological antioxidant potential, and oxidative stress index (OSI) (calculated as TH/biological antioxidant potential) were measured within 3 hours after birth.

Results

Serum TH and OSI levels gradually increased after birth in hypothermia and normothermia cases. At all time points, serum TH and OSI levels were higher in hypothermia and normothermia cases than in control cases. Serum TH and OSI levels were higher in normothermia cases than in hypothermia cases at days 3, 5, and 7.

Conclusion

This study demonstrated that hypothermia attenuated the development of systemic oxidative stress in asphyxiated newborns.     

Hemodynamics and vasopressor support in therapeutic hypothermia after cardiac arrest: Prognostic implications

Aim

Inducing therapeutic hypothermia (TH) in Out-of-Hospital Cardiac Arrest (OHCA) can be challenging due to its impact on central hemodynamics and vasopressors are frequently used to maintain adequate organ perfusion. The aim of this study was to assess the association between level of vasopressor support and mortality.

Methods

In a 6-year period, 310 comatose OHCA patients treated with TH were included. Temperature, hemodynamic parameters and level of vasopressors were registered from admission to 24 h after rewarming. Level of vasopressor support was assessed by the cardiovascular sub-score of Sequential Organ Failure Assessment (SOFA). The population was stratified by use of dopamine as first line intervention (D-group) or use of dopamine + norepinephrine/epinephrine (DA-group). Primary endpoint was 30-day mortality and secondary endpoint was in-hospital cause of death.

Results

Patients in the DA-group carried a 49% all-cause 30-day mortality rate compared to 23% in the D-group, p_log-rank < 0.0001, corresponding to an adjusted hazard ratio (HR) of 2.0 (95% CI: 1.3–3.0), p = 0.001). The DA-group had an increased 30-day mortality due to neurological injury (HR = 1.7 (95% CI: 1.1–2.7), p = 0.02). Cause of death was anoxic brain injury in 78%, cardiovascular failure in 18% and multi-organ failure in 4%. The hemodynamic changes of TH reversed at normothermia, although the requirement for vasopressor support (cardiovascular SOFA ≥ 3) persisted in 80% of patients.

Conclusions

In survivors after OHCA treated with TH the induced hemodynamic changes reversed after normothermia, while the need for vasopressor support persisted. Patients requiring addition of norepinephrine/epinephrine on top of dopamine had an increased 30-day all-cause mortality, as well as death from neurological injury.     

Cerebral tissue oxygen saturation during therapeutic hypothermia in post-cardiac arrest patients

Aim of the study

This observational study was performed to assess the cerebral tissue oxygen saturation during and after therapeutic hypothermia in comatose patients after out-of-hospital cardiac arrest.

Methods

We performed a prospective observational study on the cerebral tissue oxygen saturation (SctO₂) in post-cardiac arrest patients treated with therapeutic hypothermia (TH) between March 2011 and April 2012. SctO₂ (measured by near-infrared spectroscopy) was non-invasively and continuously measured in 28 post-cardiac arrest patients during hypothermia and active rewarming.

Results

At the start of mechanically induced TH, SctO₂ was 68% (65–72) and PaCO₂ was 47.2 mmHg (36.9 – 51.4). SctO₂ and PaCO₂ significantly decreased to 59% (57–64; p = 0.006) and 36.6 mmHg (33.9–44.7; p = 0.002), respectively, within the first 3 h of mechanically induced TH. Cerebral tissue oxygen saturation was significantly lower in non-survivors (n = 10) compared with survivors (n = 18) at 3 h after induction of hypothermia (p = 0.02) while the decrease in PaCO₂ was similar in both groups. During TH maintenance, SctO₂ gradually returned to baseline values (69% (63–72)) at 24 h, with no differences between survivors and non-survivors (p = 0.65). Carbon dioxide remained within the range of mild hypocapnia (32–38 mmHg) throughout the hypothermic period. During rewarming, SctO₂ further increased to 71% (67–78).

Conclusions

Induction of TH in comatose post-CA patients changes the balance between oxygen delivery and supply. The decrease in SctO₂ was less pronounced in patients surviving to hospital discharge.     

Association of serum lactate and survival outcomes in patients undergoing therapeutic hypothermia after cardiac arrest

Introduction

Recent studies have suggested that serum lactate may serve as a marker to predict mortality after resuscitation from cardiac arrest (CA). The relationship between serum lactate and CA outcomes requires further characterization, especially among patients treated with therapeutic hypothermia (TH) and aggressive post-arrest care.

Methods

A retrospective analysis of patients resuscitated from non-traumatic CA at three urban U.S. hospitals was performed using an established internet-based post-arrest registry. Adult (≥18 years) patients resuscitated from CA and receiving TH treatment were included. Logistic regression analysis was used to adjust for potential confounders to survival outcomes. Survival to discharge served as the primary endpoint.

Results

A total of 199 post-CA patients treated with TH between 5/2005 and 11/2011 were included in this analysis. The mean age was 56.9 ± 16.5 years, 85/199 (42.7%) patients were female, and survival to discharge was attained in 84/199 (42.2%). While lower initial post-CA serum lactate levels were not associated with increased survival to discharge, subsequent lactate measurements were significantly associated with outcomes (24-h serum lactate levels in survivors vs. non-survivors, 2.7 ± 0.5 vs. 4.2 ± 0.4 mmol/L, p < 0.01). Multivariable logistic regression confirmed this relationship with survival to discharge (p < 0.01).

Conclusion

Lower serum lactate levels at 12 h and 24 h, but not initially following cardiac arrest, are associated with survival to hospital discharge after resuscitation from CA and TH treatment. Prospective investigation of serum lactate as a potential prognostic tool in CA is needed.     

Blood pH is a Useful Indicator for Initiation of Therapeutic Hypothermia in the Early Phase of Resuscitation after Comatose Cardiac Arrest: A Retrospective Study

Background

Therapeutic hypothermia (TH) is one of the key treatments after cardiac arrest (CA). Selection of post-CA patients for TH remains problematic, as there are no clinically validated tools to determine who might benefit from the therapy.

Objective

The aim of this study was to investigate retrospectively whether laboratory findings or other patient data obtained during the early phase of hospital admission could be correlated with neurological outcome after TH in comatose survivors of CA.

Methods

Medical charts of witnessed CA patients admitted between June 2003 and July 2009 who were treated with TH were reviewed retrospectively. The subjects were grouped based on their cerebral performance category (CPC) 6 months after CA, as either good recovery (GR) for CPC 1–2 or non-good recovery (non-GR) for CPC 3–5. The following well-known determinants of outcome obtained during the early phase of hospital admission were evaluated: age, gender, body mass index, cardiac origin, presence of ventricular fibrillation (VF), time from collapse to cardiopulmonary resuscitation, time from collapse to return of spontaneous circulation, body temperature, arterial blood gases, and blood test results.

Results

We analyzed a total of 50 (25 GR and 25 non-GR) patients. Multivariate logistic analysis showed that initial heart rhythm and pH levels were significantly higher in the GR group than in the non-GR group (ventricular tachycardia/VF rate: p = 0.055, 95% confidence interval [CI] 0.768–84.272, odds ratio [OR] 8.047; pH: 7.155 ± 0.139 vs. 6.895 ± 0.100, respectively, p < 0.001, 95% CI 1.838–25.827; OR 6.89).

Conclusion

These results imply that in addition to initial heart rhythm, pH level may be a good candidate for neurological outcome predictor even though previous research has found no correlation between initial pH value and neurological outcome.     

Effect of cardiac compressions and hypothermia treatment on cardiac troponin I in newborns with perinatal asphyxia

Background

The American Heart Association, the European Resuscitation and the International Liaison Committee issued new neonatal resuscitation guidelines (2010) where therapeutic hypothermia is introduced after hypoxic-ischaemic encephalopathy (HIE) in term infants to prevent brain injury. Our study aimed to investigate whether hypothermia can reduce the release of a cardiac cellular marker, cardiac troponin I (cTnI), in HIE infants compared to normothermia care, if cTnI can be used as a prognostic marker for long term neuro-developmental outcome and if cardiac compression at birth affects the level of cTnI.

Methods

We retrospectively collected resuscitation data at birth and cTnI levels for the first 3 days in HIE infants who fulfilled cooling entry criteria. These infants received either normothermia care or induced hypothermia treatment in the neonatal period and were then followed up and tested by standard cognitive and motor assessments. The outcome is defined as death, disability or good.

Results

We confirmed an increase in cTnI after cardiac compressions (p = 0.003, Mann–Whitney test). We found that hypothermia significantly reduced the release of cTnI (peak level and area under the curve within 24 h of age), p = 0.002, linear regression. Receiver operating characteristic curves showed a level of cTnI at 24 h of age <0.22 ng/ml for normothermic and <0.15 ng/ml for hypothermic infants predicts a good outcome.

Conclusions

Our results suggest that hypothermia is cardio protective after HIE. The level of cTnI at 24 h of age is a good prognostic marker for neuro-developmental outcome at 18–22 months in both normothermia and hypothermia infants.     

Hypothermia and associated outcomes in seriously injured trauma patients in a predominantly sub-tropical climate

Aim

This study aimed to determine factors linked to hypothermia (<35 °C) in Queensland trauma patients. The relationship of hypothermia with mortality, admission to intensive care and hospital length of stay was also explored.

Methods

A retrospective analysis of data from the Queensland Trauma Registry was undertaken, and included all patients admitted to hospital for ≥24 h during 2003 and 2004 with an injury severity score (ISS) > 15. Demographic, injury, environmental, care and clinical status factors were considered.

Results

A total of 2182 patients were included; 124 (5.7%) had hypothermia on admission to the definitive care hospital, while a further 156 (7.1%) developed hypothermia during hospitalisation. Factors associated with hypothermia on admission included winter, direct admission to a definitive care hospital, an ISS ≥ 40, a Glasgow Coma Scale of 3 or ventilated and sedated, and hypotension on admission. Hypothermia on admission to the definitive care hospital was an independent predictor of mortality (odds ratio [OR] = 4.05; 95% confidence interval [CI] 2.26–7.24) and hospital length of stay (incidence rate ratio [IRR] = 1.22; 95% CI 1.03–1.43). Hypothermia during definitive care hospitalisation was independently associated with mortality (OR = 2.52; 95% CI 1.52–4.17), intensive care admission (OR = 1.73; 95% CI 1.20–2.93) and hospital length of stay (IRR = 1.18; 95% CI 1.02–1.36).

Conclusions

Trauma patients in a predominantly sub-tropical climate are at risk of accidental and endogenous hypothermia, with associated higher mortality and care requirements. Prevention of hypothermia is important for all severely injured patients.     

The prognostic value of continuous amplitude-integrated electroencephalogram applied immediately after return of spontaneous circulation in therapeutic hypothermia-treated cardiac arrest patients

Introduction

The purpose of this study was to examine the prognostic value of continuous amplitude-integrated electroencephalogram (aEEG) applied immediately after return of spontaneous circulation (ROSC) in therapeutic hypothermia (TH)-treated cardiac arrest patients.

Methods

From September 2010 to August 2011, we prospectively studied comatose patients treated with TH after cardiac arrest who were monitored with aEEG. Monitoring at the forehead was applied as soon as possible after ROSC in the emergency department and continued until recovery of consciousness, death, or 72 h after ROSC. Neurological outcome was assessed with the Cerebral Performance Category (CPC) scale at hospital discharge, and good neurological outcome was defined as a CPC score of 1 or 2.

Results

A total of 55 TH-treated patients were included. Monitoring started at a median of 96 min after ROSC (interquartile range, 49–174). At discharge, 28 patients had a CPC of 1–2, and 27 patients had a CPC of 3–5. Seventeen patients had a continuous normal voltage (CNV) trace at the start of monitoring, and this voltage was strongly associated with a good outcome (16/17 [94.1%]; sensitivity and specificity of 57.1 and 96.3%, respectively). No development of a CNV trace within the recorded period accurately predicted a poor outcome (21/21 [100%]; sensitivity and specificity of 77.8 and 100%, respectively).

Conclusions

An initial CNV trace in aEEG applied to forehead immediately after ROSC is a good early predictor of a good outcome in TH-treated cardiac arrest patients. Conversely, no development of a CNV trace within 72 h is an accurate and reliable predictor of a poor outcome with a false-positive rate of 0%.     

Is enteral feeding tolerated during therapeutic hypothermia?

Objective

To determine whether patients undergoing therapeutic hypothermia following cardiac arrest tolerate early enteral nutrition.

Methods

We undertook a single-centre longitudinal cohort analysis of the tolerance of enteral feeding by 55 patients treated with therapeutic hypothermia following resuscitation from cardiac arrest. The observation period was divided into three phases: (1) 24 h at target temperature (32–34 °C); (2) 24 h rewarming to 36.5 °C; and (3) 24 h maintained at a core temperature below 37.5 °C.

Results

During period 1, patients tolerated a median of 72% (interquartile range (IQR) 68.7%; range 31.3–100%) of administered feed. During period 2 (rewarming phase), a median of 95% (IQR 66.2%; range 33.77–100%) of administered feed was tolerated. During period 3 (normothermia) a median of 100% (IQR 4.75%; range 95.25–100%) of administered feed was tolerated. The highest incidence of vomiting or regurgitation of feed (19% of patients) occurred between 24 and 48 h of therapy.

Conclusions

Patients undergoing therapeutic hypothermia following cardiac arrest may be able to tolerate a substantial proportion of their daily nutritional requirements. It is possible that routine use of prokinetic drugs during this period may increase the success of feed delivery enterally and this could usefully be explored.     

Therapeutic hypothermia and vasopressor dependency after cardiac arrest

Objective

Clinical trials of therapeutic hypothermia (TH) after cardiac arrest excluded patients with persistent hemodynamic instability after return of spontaneous circulation (ROSC), and thus equipoise may exist regarding use of TH in these patients. Our objective was to determine if TH is associated with worsening hemodynamic instability among patients who are vasopressor-dependent after ROSC.

Methods

We performed a prospective observational study in vasopressor-dependent post-cardiac arrest patients. Inclusion criteria were age >17, non-trauma cardiac arrest, comatose after ROSC, and persistent vasopressor dependence. The decision to initiate TH (33–34 °C) was made by the treating physician. We measured cumulative vasopressor index (CVI) and mean arterial pressure (MAP) every 15 min during the first 6 h after ROSC. The outcome measures were change in CVI (primary outcome) and MAP (secondary outcome) over time. We graphed median CVI and MAP over time for the treated and not treated cohorts, and used propensity adjusted repeated measures mixed models to test for an association between TH induction and change in CVI or MAP over time.

Results

Seventy-five post-cardiac arrest patients were included (35 treated; 40 not treated). We observed no major differences in CVI or MAP over time between the treated and not treated cohorts. In the mixed models we found no statistically significant association between TH induction and changes in CVI or MAP.

Conclusion

In patients with vasopressor-dependency after cardiac arrest, the induction of hypothermia was not associated with a decrease in mean arterial pressure or increase in vasopressor requirement.     

Assessment of risk factors for post-rewarming “rebound hyperthermia” in cardiac arrest patients undergoing therapeutic hypothermia

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.     

Cerebellar Purkinje cell neurodegeneration after cardiac arrest: Effect of therapeutic hypothermia

Aims

The cerebellum is among the brain regions most vulnerable to damage caused by cardiac arrest, and cerebellar Purkinje cell loss may contribute to neurologic dysfunction, including post-hypoxic myoclonus. However, it remains unknown whether cerebellar Purkinje cells are protected by post-cardiac arrest therapeutic hypothermia (TH). Therefore, we examined the effect of post-cardiac arrest TH onset and duration on cerebellar Purkinje cell loss.

Methods

Samples from a previously published study of post-cardiac arrest TH were utilized for the present analysis. Adult male rats subjected to asphyxial cardiac arrest and cardiopulmonary resuscitation were block randomized to normothermia (37.0 °C) or TH (33.0 °C) initiated 0, 1, 4, or 8 h after return of spontaneous circulation (ROSC) and maintained for 24 or 48 h. Cerebella from rats surviving 7 days after ROSC were processed for histology and immunohistochemistry. Purkinje cell density was quantified in Nissl-stained sections of the primary fissure of the cerebellar vermis.

Results

With post-cardiac arrest normothermia, Purkinje cell density in the primary fissure was severely reduced compared to sham-injured controls (3.8 ± 1.8 cells mm⁻¹ vs. 35.9 ± 2.4 cells mm⁻¹, p < 0.001). TH moderately improved Purkinje cell survival in all groups combined (14.0 ± 5.6 cells mm⁻¹, p < 0.001 compared to normothermia). There was no statistical difference in Purkinje cell protection based on TH onset time or duration.

Conclusion

These results indicate that post-cardiac arrest TH protects selectively vulnerable cerebellar Purkinje cells within a broad therapeutic window. The potential clinical implications for improving Purkinje cell survival require further investigation.     

Post-hypothermia fever is associated with increased mortality after out-of-hospital cardiac arrest

Objective

Post-cardiac arrest fever has been associated with adverse outcome before implementation of therapeutic hypothermia (TH), however the prognostic implications of post-hypothermia fever (PHF) in the era of modern post-resuscitation care including TH has not been thoroughly investigated.The aim of the study was to assess the prognostic implication of PHF in a large consecutive cohort of comatose survivors after out-of-hospital cardiac arrest (OHCA) treated with TH.

Methods

In the period 2004–2010, a total of 270 patients resuscitated after OHCA and surviving a 24-h protocol of TH with a target temperature of 32–34 °C were included. The population was stratified in two groups by median peak temperature (≥38.5 °C) within 36 h after rewarming: PHF and no-PHF. Primary endpoint was 30-days mortality and secondary endpoint was neurological outcome assessed by Cerebral Performance Category (CPC) at hospital discharge.

Results

PHF (≥38.5 °C) was associated with a 36% 30-days mortality rate compared to 22% in patients without PHF, p_log-rank = 0.02, corresponding to an adjusted hazard rate (HR) of 1.8 (95% CI: 1.1–2.7), p = 0.02). The maximum temperature (HR = 2.0 per °C above 36.5 °C (95% CI: 1.4–3.0), p = 0.0005) and the duration of PHF (HR = 1.6 per 8 h (95% CI: 1.3–2.0), p < 0.0001) were also independent predictors of 30-days mortality in multivariable models. Good neurological outcome (CPC1-2) versus unfavourable outcome (CPC3-5) at hospital discharge was found in 61% vs. 39% in the PHF group compared to 75% vs. 25% in the No PHF group, p = 0.02.

Conclusions

Post-hypothermia fever ≥38.5 °C is associated with increased 30-days mortality, even after controlling for potential confounding factors. Avoidance of PHF as a therapeutic target should be evaluated in prospective randomized trials.     

Early antibiotics improve survival following out-of hospital cardiac arrest

Introduction

Therapeutic hypothermia (TH) has become standard management following out of hospital cardiac arrest (OHCA). Recent evidence suggests TH increases the incidence of pneumonia. We retrospectively assessed infective indicators after OHCA and evaluated the effect of antibiotics on survival.

Method

We identified all patients admitted to the ICU of a regional primary angioplasty hospital following OHCA from May 2007 to December 2010. We collected demographic and outcome data, evidence of infection and the use of antimicrobial therapy.

Results

138 patients were admitted to ICU following OHCA. The mortality rate was 68.1% with mean ICNARC predicted mortality of 77.5%. Of 138 patients, 135 (97.8%) had at least one positive marker of infection within 72 h.53 of 138 patients (38.4%) received antibiotics during the first 7 days of their ICU stay. The hospital mortality rate for these patients was significantly less than those not receiving antibiotics (56.6% vs. 75.3%; p = 0.025) with NNT of 5. Multivariate analysis demonstrated that antibiotic use was an independent predictor of survival.

Conclusion

The post-arrest management of OHCA is commonly complicated by infections, the accurate diagnosis of which is impaired by the associated increase in inflammatory markers, body temperature control, delay in the processing of samples and poor quality chest radiography.We have shown a significant reduction in mortality in patients who received antibiotics compared with patients who did not. This suggests that a formal clinical trial is warranted.     

Methylphenidate and amantadine to stimulate reawakening in comatose patients resuscitated from cardiac arrest

Background

Despite critical-care packages including therapeutic hypothermia (TH), neurologic injury is common after cardiac arrest (CA) resuscitation. Methylphenidate and amantadine have treated coma in traumatically-brain-injured patients with mixed success, but have not been explored in post-arrest patients.

Objective

Compare the outcome of comatose post-arrest patients treated with neurostimulants to a matched cohort.

Methods

Retrospective cohort study from 6/2008 to 12/2011 in a tertiary university hospital. We included adult patients treated with methylphenidate or amantadine after resuscitation from in-hospital or out-of-hospital CA (OHCA) of any rhythm, excluding patients with traumatic/surgical etiology of arrest, terminal re-arrest within 6 h, or withdrawal of care by family within 6 h. Primary outcome was following commands; secondary outcomes included survival to hospital discharge, cerebral performance category (CPC), and modified Rankin scale (mRS). We compared characteristics and outcomes to a control cohort matched on TH and 72 h FOUR score ± 1.

Results

Of 588 patients, 8 received methylphenidate, 6 received amantadine, and 2 both. Most were female suffering OHCA with median age 61 years. All received TH and a multi-modal neurological evaluation. Initial exam revealed median GCS 6 and FOUR 7, which was unchanged at 72 h. Six patients (38%) followed commands prior to discharge at median 2.5 days (range: 1–18 days) after treatment. Patients receiving neurostimulants trended toward improved rate of following commands, survival to hospital discharge, and distribution of CPC and mRS scores.

Conclusions

Neurostimulants may be considered to stimulate wakefulness in selected post-cardiac arrest patients, but a prospective trial is needed to evaluate this therapy.     

Early cardiac catheterization is associated with improved survival in comatose survivors of cardiac arrest without STEMI

Aim

To determine if early cardiac catheterization (CC) is associated with improved survival in comatose patients who are resuscitated after cardiac arrest when electrocardiographic evidence of ST-elevation myocardial infarction (STEMI) is absent.

Methods

We conducted a retrospective observational study of a prospective cohort of 754 consecutive comatose patients treated with therapeutic hypothermia (TH) following cardiac arrest.

Results

A total of 269 (35.7%) patients had cardiac arrest due to a ventricular arrhythmia without STEMI and were treated with TH. Of these, 122 (45.4%) received CC while comatose (early CC). Acute coronary occlusion was discovered in 26.6% of patients treated with early CC compared to 29.3% of patients treated with late CC (p = 0.381). Patients treated with early CC were more likely to survive to hospital discharge compared to those not treated with CC (65.6% vs. 48.6%; p = 0.017). In a multivariate regression model that included study site, age, bystander CPR, shock on admission, comorbid medical conditions, witnessed arrest, and time to return of spontaneous circulation, early CC was independently associated with a significant reduction in the risk of death (OR 0.35, 95% CI 0.18–0.70, p = 0.003).

Conclusions

In comatose survivors of cardiac arrest without STEMI who are treated with TH, early CC is associated with significantly decreased mortality. The incidence of acute coronary occlusion is high, even when STEMI is not present on the postresuscitation electrocardiogram.     

Warming with an underbody warming system reduces intraoperative hypothermia in patients undergoing laparoscopic gastrointestinal surgery: A randomized controlled study

Background

Intraoperative hypothermia is a common event during laparoscopic abdominal surgery. On one hand, intraoperative hypothermia can delay the metabolism and prevent tissue damage. One the other hand, long-term and severe intraoperative hypothermia may also lead to perioperative complications, such as increasing of peripheral resistance, coagulation dysfunction, intraoperative hemorrhage and postoperative shivering. Maintenance of normothermia during surgical procedures may improve the quality of patient care.

Objectives

This study investigated the feasibility and efficacy of intraoperative cutaneous warming with an underbody warming system during laparoscopic gastrointestinal surgery.

Methods

110 patients undergoing laparoscopic surgery for gastrointestinal cancer between January and December 2011 were randomized into the laparoscopic control (Control) group and laparoscopic intervention (Intervention) group. Nasopharyngeal temperature, prothrombin time, activated partial thromboplastin time, and thrombin time were measured before and during surgery, intraoperative and postoperative complications, as well as shivering after anesthesia and visual analog scale score for pain evaluation after surgery were also recorded. Clinical risk factors that may cause intraoperative hypothermia during laparoscopic surgery were also analyzed by correlation analysis.

Results

The two groups were comparable at the baseline. Intraoperative hypothermia was observed in 29 patients (52.7%) in Control group and 3 (5.5%) in Intervention group. Nasopharyngeal temperature in Control group was significantly decreased since 30 min after the start of operation until the end of surgery comparing to that at the start of anesthesia, but there was no difference in the Intervention group. In Intervention group, the nasopharyngeal temperature was remaining at ∼36.5 °C, indicating the feasibility and efficiency of the underbody warming system in preventing intraoperative hypothermia during laparoscopic gastrointestinal surgery. Moreover, with anesthesia and operation time increased, there was no significant change of coagulation function, hemoglobin level as well as less intraoperative hemorrhage, less postoperative shivering and lower visual analog scale score in Intervention group comparing to Control group. Multivariate logistic regression analysis revealed that anesthesia time and volume of CO₂ were independent risk factors for perioperative hypothermia.

Conclusions

Cutaneous warming with an underbody warming system is a feasible and effective method to prevent intraoperative hypothermia during laparoscopic gastrointestinal surgery.     

Value analysis of continuous EEG in patients during therapeutic hypothermia after cardiac arrest

Introduction

Therapeutic hypothermia (TH) is standard of care after ventricular fibrillation cardiac arrest (CA). Continuous EEG monitoring (cEEG) is increasingly used during TH. Analysis regarding value of cEEG utilization in this population in the context of cost and outcome has not been performed. We compared outcome and EEG charges in CA patients with selective versus routine cEEG.

Methods

A protocol for TH after CA without routine cEEG was implemented in December 2005, comprising our TH-pre-cEEG cohort. In November 2009, this protocol was changed to include cEEG in all CA–TH patients, comprising our TH-cEEG cohort. Clinical outcome using the Cerebral Performance Category (CPC) at discharge and estimated EEG charges were calculated retrospectively for both cohorts, based on National Charge Data 50th percentile charges expressed in USD per the CMS 2010 Standard Analytical File as reported in Code Correct by MedAssets, Inc.

Results

Our TH-pre-cEEG cohort comprised 91 patients, our TH-cEEG cohort 62. In the TH-pre-cEEG cohort, 19 patients (21%) had rEEGs, 4 (4%) underwent cEEG. The mean estimated EEG charges for the TH-pre-cEEG cohort was $1571.59/patient, and TH-cEEG cohort was $4214.93/patient (p < 0.0001). Two patients (2.1%) in the TH-pre-cEEG cohort had seizures, compared to five (8.1%) in the TH-cEEG cohort (p = 0.088). There was no difference in mortality or clinical outcome in these cohorts.

Conclusions

Routine use of cEEG during TH after CA improved seizure detection, but not outcomes. There was a three-fold increase in EEG estimated charges with routine use of cEEG.     

Post-cardiac arrest serum levels of glial fibrillary acidic protein for predicting neurological outcome

Aim of the study

To investigate serum levels of glial fibrillary acidic protein (GFAP) for evaluation of neurological outcome in cardiac arrest (CA) patients and compare GFAP sensitivity and specificity to that of more studied biomarkers neuron-specific enolas (NSE) and S100B.

Method

A prospective observational study was performed in three hospitals in Sweden during 2008-2012. The participants were 125 CA patients treated with therapeutic hypothermia (TH) to 32-34 °C for 24 hours. Samples were collected from peripheral blood (n = 125) and the jugular bulb (n = 47) up to 108 hours post-CA. GFAP serum levels were quantified using a novel, fully automated immunochemical method. Other biomarkers investigated were NSE and S100B. Neurological outcome was assessed using the Cerebral Performance Categories scale (CPC) and dichotomized into good and poor outcome.

Results

GFAP predicted poor neurological outcome with 100% specificity and 14-23% sensitivity at 24, 48 and 72 hours post-CA. The corresponding values for NSE were 27-50% sensitivity and for S100B 21-30% sensitivity when specificity was set to 100%. A logistic regression with stepwise combination of the investigated biomarkers, GFAP, did not increase the ability to predict neurological outcome. No differences were found in GFAP, NSE and S100B levels when peripheral and jugular bulb blood samples were compared.

Conclusion

Serum GFAP increase in patients with poor outcome but did not show sufficient sensitivity to predict neurological outcome after CA. Both NSE and S100B were shown to be better predictors. The ability to predict neurological outcome did not increased when combining the three biomarkers.