The effect of mild therapeutic hypothermia on renal function after cardiopulmonary resuscitation in men

Zeiner, Andrea; Sunder‐Plassmann, Gere; Sterz, Fritz; Hölzer, Michael; Losert, Heidrun; Laggner, Anton N.; Müllner, Marcus

doi:10.1016/j.resuscitation.2003.11.006

Cited by 84 publications

(55 citation statements)

References 22 publications

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“…not stated whether median ⁄ mean, IQR ⁄ range etc), p = 0.51). Creatine kinase is excreted renally and glomerular filtration rate (GFR) is reduced in mild hypothermia hypothermic [48], thus the CK-MB levels may not have been an accurate measure of infarct size.…”

Section: Resultsmentioning

confidence: 99%

The effects of mild induced hypothermia on the myocardium: a systematic review

Kelly

Nolan

2010

Anaesthesia

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SummaryMild induced hypothermia improves neurological outcome and reduces mortality among initially comatose survivors of out-of-hospital cardiac arrest. Similar pathological processes occur in the heart and the brain, namely ischaemia followed by reperfusion injury. Animal data indicate that mild induced hypothermia results in improved myocardial salvage, reduced infarct size, reduced left ventricular remodelling and better long-term left ventricular function. Several small human studies suggest that infarct size may be reduced by mild induced hypothermia, although this has not reached significance in any human study to date. There are variable reports of harm to the myocardium caused by mild induced hypothermia, including reduced myocardial contractility and cardiac output, electrocardiographic changes and arrhythmias, especially bradycardia. These harmful effects are reversible with rewarming. Most patients who have a cardiac arrest do not survive, and full neurological recovery occurs in only 6-23% [1]. In order to improve survival and reduce such neurological injury, guidelines have recently been published describing the post-cardiac arrest bundle of care: this includes early coronary reperfusion if appropriate (primary angioplasty or thrombolysis), haemodynamic optimisation, and control of ventilation, blood glucose, temperature and seizures [2,3].Therapeutic hypothermia has become established as a recognised intervention following cardiac arrest [2]. Two randomised controlled trials have shown improved neurological outcome and reduced mortality in adults who were therapeutically cooled following out-ofhospital ventricular fibrillation (VF) cardiac arrest, where the patient was comatose following initial resuscitation, and where cooling was initiated within minutes to hours [4,5]. The International Liaison Committee on Resuscitation has recommended that all unconscious adult patients with spontaneous circulation after out-of-hospital VF cardiac arrest should be cooled to 32-34°C for 12-24 h [6]. Such cooling may also be beneficial for other rhythms or in-hospital cardiac arrest [6].Cardiac arrest is thought to cause neurological injury by several mechanisms, including perfusion failure leading to cerebral ischaemia, and reperfusion leading to re-oxygenation injury [7][8][9][10]. Therapeutic hypothermia is thought to attenuate both these processes. Firstly, hypothermia is thought to protect against many of the processes associated with reperfusion and re-oxygenation [14][15][16][17][18]. Secondly, hypothermia reduces the cerebral metabolic rate for oxygen (CMRO 2 ) [11], and may therefore provide protection from ongoing cerebral ischaemia [12,13].Similar pathological processes occur in the heart following cardiac arrest and ⁄ or acute myocardial infarction (AMI), including perfusion failure followed by reperfusion and re-oxygenation injury [19][20][21][22]. It has been suggested that mild induced hypothermia may also be beneficial to the myocardium in a similar way that it is neuroprotective to the brain [2...

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Section: Resultsmentioning

confidence: 99%

The effects of mild induced hypothermia on the myocardium: a systematic review

Kelly

Nolan

2010

Anaesthesia

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“…14 In another study, renal function was impaired transiently in out-of-hospital post-cardiac arrest patients treated with therapeutic hypothermia, required no interventions, and returned to normal by 28 days. 239 The indications for starting renal replacement therapy in comatose cardiac arrest survivors are the same as those used for critically ill patients in general. 240 …”

Section: Renal Failurementioning

confidence: 99%

Post–Cardiac Arrest Syndrome

Neumar¹,

Nolan²,

Adrie³

et al. 2008

Circulation

1,233

398

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“…However, the reduced Cc under hypothermia suggested the opposite view. According to previous research, a possible explanation may be that the increase in renal vascular resistance during hypothermia reduced renal blood flow, and the spurious improvement in sCr level may be derived from a consecutive reduction in creatinine release from muscles 7,17 . In addition, considering the Effect of mild hypothermia on renal ischemia/reperfusion injury after cardiopulmonary resuscitation in a swine model Yuan W et al effects on hemodynamics by hypothermia, the decline in CO may reduce renal blood flow, but the lower lactate level in the TH group reflected the reduction of systemic oxygen consumption concurrently 18,19 .…”

Section: ■ Discussionmentioning

confidence: 99%

“…Therapeutic hypothermia (TH) can reduce a patient's core temperature in an attempt to protect an organ at risk of injury [4][5][6] . Some previous studies suggest a potential benefit of hypothermia for kidney injury, but both animal and clinical evidence is inconclusive [7][8][9] . Moreover, even though the RIFLE criteria (risk, injury, failure, loss, end stage) is extensively used in diagnosis and classification of AKI.…”

Section: ■ Introductionmentioning

confidence: 99%

Effect of mild hypothermia on renal ischemia/reperfusion injury after cardiopulmonary resuscitation in a swine model

Yuan

Zhao

et al. 2017

Acta Cir. Bras.

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Purpose: To investigate the effect of intravascular cooling on renal function after resuscitation. Methods: Twenty four pigs were randomized into three groups (n=8 in each group): therapeutic hypothermia group (TH group), normothermia group (NH group) and sham operation group (SHAM group). After 6 minutes of untreated VF, CPR was performed. Upon ROSC, the TH group received the intravascular cooling. The NH and SHAM group did not undergo therapeutic hypothermia. Haemodynamic parameters were recorded. The bloods were analyzed for serum creatinine (sCr), CysC and NGAL. The kidney was surgically removed observe pathologic changes under a light microscope. Results: The sCr increased in both TH and NH groups after ROSC, compared to baseline. Between two groups, the sCr and creatinine clearance (Cc) showed lower level in the TH group. The urine volume per hour in the TH group were higher during cooling. After resuscitation, NGAL and CysC in the NH group were higher than in the TH group. Under the light microscope, compared with the TH group, the renal injury was prominent in the NH group. Conclusion: Mild hypothermia had a protection to renal ischemia reperfusion injury after resuscitation.

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The effect of mild therapeutic hypothermia on renal function after cardiopulmonary resuscitation in men

Cited by 84 publications

References 22 publications

The effects of mild induced hypothermia on the myocardium: a systematic review

The effects of mild induced hypothermia on the myocardium: a systematic review

Post–Cardiac Arrest Syndrome

Effect of mild hypothermia on renal ischemia/reperfusion injury after cardiopulmonary resuscitation in a swine model

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