Veno-venous extracorporeal membrane oxygenation support in the resuscitation from extreme metabolic acidosis (pH < 6.5) after drowning cardiac arrest: a case report.

BACKGROUND: Resuscitation in drowning victim with cardiac arrest is difficult because of severe metabolic acidosis and multiple organ dysfunction. There is insufficient evidence to support that veno-venous extracorporeal membrane oxygenation (VV-ECMO) is beneficial for patient. CASE PRESENTATION: A 44-year-old female was trapped under river when she attempted to rescue her drowning father. Furthermore, she underwent a loss of consciousness, with extreme metabolic acidosis, hypothermia and hypotension. Hence, the VV-ECMO, continuous renal replacement therapy (CRRT) and other resuscitative infusion were required. In this case, the patient did not experience any complication or neurologic deficit and reaching a complete recovery after 21 days of hospitalization. CONCLUSIONS: Our case adds further concerns in supporting a patient with extreme metabolic acidosis (pH < 6.5) and hypothermia after severe drowning cardiac arrest, including extracorporeal life support, renal support, targeted temperature management, cerebral resuscitation, etc., due to the reversible nature of this condition.

Nursing Management of Temperature in a Patient with Stroke.

Fever is common in patients with stroke and is associated with worse outcomes. Studies in brain injury informed interventions commonly termed therapeutic temperature management (TTM) to improve the monitoring and management of fever. While the role and benefit of TTM in stroke patients has not been well studied, the nurse and healthcare team must extrapolate existing data to determine how to best monitor and apply TTM after stroke. Nurses should be knowledgeable about interventions to monitor and manage complications of TTM (eg, shivering), the studies underway to quantify the impact of fever treatment and emerging technology expected to improve TTM.

Survival to hospital discharge and neurological outcomes with targeted temperature management after in-hospital cardiac arrest: a systematic review and meta-analysis.

BACKGROUND: Multiple randomized controlled trials have shown that targeted temperature management (TTM) has favorable effects in out-of-hospital cardiac arrest. However, the benefit of TTM in patients with in-hospital cardiac arrest (IHCA) remains to be verified. METHODS: The PubMed, Cochrane Library, and EMBASE databases were searched for clinical studies with the primary outcomes of survival to hospital discharge and neurological outcomes. Neurological outcomes were evaluated by the categorical scale of cerebral function (CPC); a score of 1-2 points was considered neurologically good, and a score of 3-5 points was considered a poor outcome. Revman 5.3 and Stata 14 software with the random effects model were used for analysis. P<0.05 was considered statistically significant. RESULTS: Six retrospective controlled studies with a total of 14,607 patients (TTM group: 1,845, control group: 12,762) were included and analyzed. There were no statistically significant differences between the two groups in survival to hospital discharge [odds ratio (OR) =1.02, 95% CI: 0.77-1.35, P=0.89, I2=47%] or favorable neurological outcomes (OR =1.06, 95% CI: 0.56-2.02, P=0.85, I2=79%). After excluding patients with non-shockable initial rhythms, TTM did not show any significant improvement in survival to hospital discharge. Subgroup analysis was performed according to the sample size. No significant improvement was observed between the two groups in terms of survival to hospital discharge or neurological outcome. DISCUSSION: In this meta-analysis, the effects of TTM on discharge survival and neurological prognosis were evaluated by studying the results of IHCA in 14,607 patients. We found that the TTM did not improve survival and neurological function in discharged patients. Our results showed that the sample size discrepancy had a large effect on the heterogeneity; to address this, subgroup analyses were performed according to the different sample sizes. However, TTM treatment in different sample size subgroups showed no significant effect on survival to hospital discharge. Moreover, in the large sample size subgroup, therapeutic hypothermia was associated with increased unfavorable neurological outcome compared with no hypothermia.

A case of cardiopulmonary arrest due to left ventricular free wall rupture successfully treated with sutureless repair supported by venoarterial extracorporeal membrane oxygenation.

Extracorporeal membrane oxygenation for cardiopulmonary arrest due to left ventricular free wall rupture is considered effective, because it enables rapid cardiopulmonary support and introduction of targeted temperature management.

Parameters Influencing Brain Oxygen Measurement by Regional Oxygen Saturation in Postcardiac Arrest Patients with Targeted Temperature Management.

In several studies, regional cerebral oxygen saturation (rSO2) has been measured in patients with postcardiac arrest syndrome (PCAS) to analyze the brain's metabolic status. However, the significance of rSO2 in PCAS patients remains unclear. In the present study, we investigated the relationship between rSO2 and physiological parameters. Comatose survivors of out-of-hospital PCAS with targeted temperature management (TTM) at 34°C for 24 hours were included. All patients were monitored for their rSO2 and additional parameters (arterial oxygen saturation [SaO2], hemoglobin [Hb], mean arterial pressure [MAP], arterial carbon dioxide pressure [PaCO2], and body temperature]) measured at the start of monitoring and 24 and 48 hours after return of spontaneous circulation (ROSC). Patients were divided into favorable and unfavorable groups, and the correlation between rSO2 and these physiological parameters was evaluated by multiple regression analysis. Forty-nine patients were included in the study, with 15 in the favorable group and 34 in the unfavorable group. There was no significant difference in the rSO2 value between the two groups at any time point. The multiple regression analysis of the favorable group revealed a moderate correlation between rSO2 and SaO2, Hb, and PaCO2 only at 24 hours (coefficients: 0.482, 0.422, and 0.531, respectively), whereas that of the unfavorable group revealed moderate correlations between rSO2 and Hb values at all time points, PaCO2 at 24 hours and MAP at 24 and 48 hours. rSO2 was moderately correlated to MAP in unfavorable patients. To optimize brain oxygen metabolic balance for PCAS patients with TTM measuring rSO2, we suggest total evaluation of each parameters of SaO2, Hb, MAP, and PaCO2.

Hypothermia Inhibits Cerebral Necroptosis and NOD-Like Receptor Pyrin Domain Containing 3 Pathway in a Swine Model of Cardiac Arrest.

BACKGROUND: Targeted temperature management (TTM) is commonly used in hypothermia after cardiopulmonary resuscitation (CPR), and its mechanism to improve cerebral function is complex. This study aimed to investigate the effects of TTM on necroptosis and the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome in the brain tissue of pigs after CPR. MATERIALS AND METHODS: Ventricular fibrillation was induced, and CPR was performed 10 min later in nine pigs in the normothermia group and nine pigs in the TTM group. The body temperature in the TTM group was dropped to 33°C after CPR and maintained for 24 h, whereas in the normothermia group, it was maintained at 38°C. Before CPR and at 30 h after CPR, serum neuron-specific enolase and S-100ß were measured. At 30 h after CPR, pigs were euthanized, and brain tissues were collected for measurement of receptor-interacting protein kinase (RIPIK) 1, RIPK3, mixed lineage kinase domain-like (MLKL), NLRP3, cysteinyl aspartate-specific proteinase (caspase)-1, interleukin (IL)-1ß, and IL-18. RESULTS: Serum neuron-specific enolase and S-100ß were increased significantly (P < 0.05) in the two CPR-treated groups compared with the sham group and more obviously in the normothermia group. In addition, the expression of RIPK3, phosphorylated MLKL, and NLRP3 in brain tissues was increased. The expression of RIPK3, phosphorylated MLKL, NLRP3, and caspase-1 as well as the levels of IL-1ß and IL-18 were lower (P < 0.05) in the TTM group compared with the normothermia group. CONCLUSIONS: Necroptosis and the NLRP3 pathway were activated after CPR. TTM may attenuate postresuscitation brain injury through the regulation of necroptosis and the NLRP3 pathway.

Thermoregulation in brain injury.

Different mechanisms explain thermoregulatory dysfunction following ischemic stroke, hemorrhagic stroke, and traumatic brain injury. Temperature instability following brain injury likely involves hypothalamic injury, pathologic changes in cerebral blood flow, metabolic derangement, and a neurogenic inflammatory response. Although targeted temperature management (TTM) exerts pleiotropic effects, the heterogeneity of brain injury has hindered identification of patient subsets most likely to benefit from TTM. Early optimism about TTM's role in brain injury has been tempered by the failure of successive clinical trials to show improved patient outcomes. However, given the deleterious effects of fever, aggressive fever management is still warranted in the critically ill neurologic patient.

Pre-existing medical comorbidity is not associated with neurological outcomes in patients undergoing targeted temperature management following cardiac arrest.

The prognostic significance of chronic medical illness in comatose survivors of cardiac arrest who undergo targeted temperature management (TTM) remains largely unknown. We sought to assess the association between overall burden of pre-existing medical comorbidity and neurological outcomes in survivors of cardiac arrest undergoing TTM. We analyzed a prospectively collected cohort of 314 patients treated with TTM following cardiac arrest at a tertiary care hospital between 2007 and 2014. Overall burden of medical comorbidity was approximated with the use of the Charlson Comorbidity Index (CCI). Poor neurological outcome at hospital discharge, defined as a cerebral performance category (CPC) score >2, was the primary outcome. Secondary outcomes included death prior to hospital discharge and at 1 year following cardiac arrest. Multivariable logistic regression was used to assess the association between CCI scores and outcomes. A poor neurological outcome at hospital discharge was observed in 193 (61%) patients. One hundred and seventy-nine (57%) patients died prior to hospital discharge and a total of 195 (62%) patients had died at 1-year post-arrest. In multivariable logistic regression, elevated CCI scores were not associated with increased odds of poor neurological outcomes (OR 1.04, 95% CI 0.90-1.19, p = 0.608) or death (OR 0.99, 95% CI 0.86-1.13, p = 0.816) at hospital discharge. No association was seen between CCI scores and death at 1-year post-arrest (OR 1.09, 95% CI 0.95-1.26, p = 0.220). Increasing burden of medical comorbidity, as defined by CCI scores, is not associated with neurological outcomes or survival in patients treated with TTM.

Temperature variability during targeted temperature management is not associated with neurological outcomes following cardiac arrest.

INTRODUCTION: Recent studies on comatose survivors of cardiac arrest undergoing targeted temperature management (TTM) have shown similar outcomes at multiple target temperatures. However, details regarding core temperature variability during TTM and its prognostic implications remain largely unknown. We sought to assess the association between core temperature variability and neurological outcomes in patients undergoing TTM following cardiac arrest. METHODS: We analyzed a prospectively collected cohort of 242 patients treated with TTM following cardiac arrest at a tertiary care hospital between 2007 and 2014. Core temperature variability was defined as the statistical variance (i.e. standard deviation squared) amongst all core temperature recordings during the maintenance phase of TTM. Poor neurological outcome at hospital discharge, defined as a Cerebral Performance Category (CPC) score>2, was the primary outcome. Death prior to hospital discharge was assessed as the secondary outcome. Multivariable logistic regression was used to examine the association between temperature variability and neurological outcome or death at hospital discharge. RESULTS: A poor neurological outcome was observed in 147 (61%) patients and 136 (56%) patients died prior to hospital discharge. In multivariable logistic regression, increased core temperature variability was not associated with increased odds of poor neurological outcomes (OR 0.38, 95% CI 0.11-1.38, p=0.142) or death (OR 0.43, 95% CI 0.12-1.53, p=0.193) at hospital discharge. CONCLUSION: In this study, individual core temperature variability during TTM was not associated with poor neurological outcomes or death at hospital discharge.

Therapeutic hypothermia impacts leukocyte kinetics after cardiac arrest.

BACKGROUND: Patients admitted to the hospital after primarily successful cardiopulmonary resuscitation (CPR) are at a very high risk for neurologic deficits and death. Targeted temperature management (TTM) for mild therapeutic hypothermia has been shown to improve survival compared to standard treatment. Acute cardiovascular events, such as myocardial infarction (MI), are a major cause for cardiac arrest (CA) in patients who undergo CPR. Recent findings have demonstrated the importance and impact of the leukocyte response following acute MI. METHODS: In this retrospective, single center study we enrolled 169 patients with CA due to non-traumatic causes and primarily successful CPR. A total of 111 subjects (66%) underwent TTM aiming for a target temperature of 32-34 °C. RESULTS: Analysis of 30 day follow up showed a significantly improved survival of all patients who received TTM compared to patients without hypothermia (P=0.0001). Furthermore TTM was an independent variable of good neurological outcome after 6 months (P=0.0030). Therapeutic hypothermia was found to be beneficial independent of differences in age and sex between both groups. While a higher rate of pneumonia was observed with TTM, this diagnosis had no additional impact on survival or neurological outcome. The beneficial effect on mortality remained significant in patients with the diagnosis of an acute cardiac event (P=0.0145). Next, we evaluated the kinetics of leukocytes in this group over the course of 7 days after CA. At presentation, patients showed a mean level of 16.5±6.7 of leukocytes per microliter. While this level stayed stable in the group of patients without hypothermia, patients who received TTM showed a significant decline of leukocyte levels resulting in significantly lower numbers of leukocytes on days 3 and 5 after CPR. Interestingly, these differences in leukocyte counts remained beyond the time period of TTM while C-reactive protein (CRP) levels were suppressed only during ongoing cooling, but differences between the groups were diminished after TTM was terminated (from day 3 on, P>0.2). Finally, patients who received TTM and showed a leukocyte count of less than 12.7/µL on day 3 had an improved survival (P=0.0214) and neurological outcome (P=0.0049) compared to patients above that level. CONCLUSIONS: Our data underline the beneficial effects of TTM and demonstrate an impact of hypothermia on leukocyte counts after CA.