Kees H Polderman

University of Pittsburgh, Pittsburgh, Pennsylvania, United States

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Publications (100)778.5 Total impact

  • Kees H Polderman
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    ABSTRACT: This article discusses the potential of levosimendan to treat calcium-induced myocardial dysfunction associated with deep hypothermia. Moderate hypothermia (30 to 34°C) usually improves myocardial contractility and stabilizes heart rhythm, but deep hypothermia can cause severe myocardial dysfunction, which is mediated by intracellular calcium overload. In experimental studies, levosimendan appears effective in reversing this. Clinical studies are needed to confirm these findings and to determine whether levosimendan could also be used for accidental hypothermia and perhaps to mitigate diastolic dysfunction under moderate hypothermia.
    Critical care (London, England) 12/2013; 17(6):1018. · 4.72 Impact Factor
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    ABSTRACT: INTRODUCTION: Mild therapeutic hypothermia (MTH) is a worldwide used therapy to improve neurological outcome in patients successfully resuscitated after cardiac arrest (CA). Preclinical data suggest that timing and speed of induction are related to reduction of secondary brain damage and improved outcome. METHODS: Aiming at a rapid induction and stable maintenance phase, MTH induced via continuous peritoneal lavage (PL) using Velomedix(R) Inc. automated PL system was evaluated and compared to historical controls in which hypothermia was achieved using cooled saline intravenous infusions and cooled blankets. RESULTS: In sixteen PL patients time to reach core target temperature of 32.5oC was 30 minutes (interquartile range [IQR]: 19-60), which was significantly faster compare to 150 minutes (IQR: 112-240) in controls. The median rate of cooling during the induction phase in the PL group of 4.1oC/hr (IQR: 2.2-8.2) was significantly faster compared to 0.9oC/hr (IQR: 0.5-1.3) in controls. During the 24 hours maintenance phase mean core temperature in the PL patients was 32.38+/-0.18oC (range: 32.03-32.69oC) and in control patients 32.46+/-0.48oC (range: 31.20-33.63oC), indicating more steady temperature control in the PL group compared to controls. Furthermore, the coefficient of variation (VC) for temperature during the maintenance phase was lower in the PL group (VC: 0.5%) compared to the control group (VC: 1.5%). In contrast to 23% of the control patients, none of the PL patients showed overshoot of hypothermia below 31oC during the maintenance phase. Survival and neurological outcome was not different between the two groups. Neither shivering nor complications related to insertion or use of the PL method were observed. CONCLUSIONS: Using PL in post CA patients results in rapidly reached target temperature and a very precise maintenance, unprecedented in clinical studies evaluating MTH techniques. This opens the way to investigate the effects on neurological outcome and survival of ultra-rapid cooling compared to standard cooling in controlled trials in various patient groups. Trial registration: ClinicalTrials.Gov NCT01016236.
    Critical care (London, England) 02/2013; 17(1):R31. · 4.72 Impact Factor
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    ABSTRACT: Cardiac arrest is the most common cause of death in North America. Neurocritical care interventions, including therapeutic hypothermia (TH), have significantly improved neurological outcomes in patients successfully resuscitated from cardiac arrest. Therefore, resuscitation following cardiac arrest was chosen as an Emergency Neurological Life Support protocol. Patients remaining comatose following resuscitation from cardiac arrest and who are not bleeding are potential candidates for TH. This protocol will review induction, maintenance, and re-warming phases of TH, along with management of TH side effects. Aggressive shivering suppression is necessary with this treatment to ensure the maintenance of a target temperature. Ancillary testing, including electrocardiography, computed tomography imaging of the brain, continuous electroencephalography, monitoring, and correction of electrolyte, blood gas, and hematocrit changes are also necessary to optimize outcomes.
    Neurocritical Care 08/2012; 17 Suppl 1:21-8. · 3.04 Impact Factor
  • Kees H Polderman
    Critical Care 06/2012; 16(2). · 4.93 Impact Factor
  • Kees H Polderman
    Critical Care 06/2012; 16(2). · 4.93 Impact Factor
  • Kees H Polderman, Peter J D Andrews
    The Lancet Neurology 05/2011; 10(5):404-5; author reply 406-7. · 23.92 Impact Factor
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    Kees H Polderman
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    ABSTRACT: In vitro studies and clinical observations suggest that both accidental and controlled/therapeutic hypothermia have a strong immunosuppressive effect, and that hypothermia increases the risk of infections, especially wound infections and pneumonia. In the previous issue of Critical Care, Kamps and colleagues report that when hypothermia was used for prolonged periods in patients with severe traumatic brain injury in conjunction with selective decontamination of the digestive tract, the risks of infection were the same or lower in patients treated with therapeutic cooling. The risk of infection is widely regarded as the most important danger of therapeutic cooling. The findings of Kamps and colleagues need to be verified in prospective trials and in higher-resistance environments, but raise the possibility of cooling for prolonged periods with greatly reduced risk. We may be able to have our cake and eat it.
    Critical care (London, England) 03/2011; 15(2):144. · 4.72 Impact Factor
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    ABSTRACT: Traumatic brain injury is a major cause of death and severe disability worldwide with 1,000,000 hospital admissions per annum throughout the European Union.Therapeutic hypothermia to reduce intracranial hypertension may improve patient outcome but key issues are length of hypothermia treatment and speed of re-warming. A recent meta-analysis showed improved outcome when hypothermia was continued for between 48 hours and 5 days and patients were re-warmed slowly (1 °C/4 hours). Previous experience with cooling also appears to be important if complications, which may outweigh the benefits of hypothermia, are to be avoided. This is a pragmatic, multi-centre randomised controlled trial examining the effects of hypothermia 32-35 °C, titrated to reduce intracranial pressure <20 mmHg, on morbidity and mortality 6 months after traumatic brain injury. The study aims to recruit 1800 patients over 41 months. Enrolment started in April 2010.Participants are randomised to either standard care or standard care with titrated therapeutic hypothermia. Hypothermia is initiated with 20-30 ml/kg of intravenous, refrigerated 0.9% saline and maintained using each centre's usual cooling technique. There is a guideline for detection and treatment of shivering in the intervention group. Hypothermia is maintained for at least 48 hours in the treatment group and continued for as long as is necessary to maintain intracranial pressure <20 mmHg. Intracranial hypertension is defined as an intracranial pressure >20 mmHg in accordance with the Brain Trauma Foundation Guidelines, 2007. The Eurotherm3235Trial is the most important clinical trial in critical care ever conceived by European intensive care medicine, because it was launched and funded by the European Society of Intensive Care Medicine and will be the largest non-commercial randomised controlled trial due to the substantial number of centres required to deliver the target number of patients. It represents a new and fundamental step for intensive care medicine in Europe. Recruitment will continue until January 2013 and interested clinicians from intensive care units worldwide can still join this important collaboration by contacting the Trial Coordinating Team via the trial website http://www.eurotherm3235trial.eu. Current Controlled Trials ISRCTN34555414.
    Trials 01/2011; 12:8. · 2.21 Impact Factor
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    ABSTRACT: OBJECTIVES: To address the issues of Prevention and Management of Acute Renal Failure in the ICU Patient, using the format of an International Consensus Conference. METHODS AND QUESTIONS: Five main questions formulated by scientific advisors were addressed by experts during a 2-day symposium and a Jury summarized the available evidence: (1) Identification and definition of acute kidney insufficiency (AKI), this terminology being selected by the Jury; (2) Prevention of AKI during routine ICU Care; (3) Prevention in specific diseases, including liver failure, lung Injury, cardiac surgery, tumor lysis syndrome, rhabdomyolysis and elevated intraabdominal pressure; (4) Management of AKI, including nutrition, anticoagulation, and dialysate composition; (5) Impact of renal replacement therapy on mortality and recovery. RESULTS AND CONCLUSIONS: The Jury recommended the use of newly described definitions. AKI significantly contributes to the morbidity and mortality of critically ill patients, and adequate volume repletion is of major importance for its prevention, though correction of fluid deficit will not always prevent renal failure. Fluid resuscitation with crystalloids is effective and safe, and hyperoncotic solutions are not recommended because of their renal risk. Renal replacement therapy is a life-sustaining intervention that can provide a bridge to renal recovery; no method has proven to be superior, but careful management is essential for improving outcome.
    American Journal of Respiratory and Critical Care Medicine 05/2010; 181(10):1128-55. · 11.04 Impact Factor
  • Arthur R H van Zanten, Kees H Polderman
    Critical care medicine 07/2009; 37(6):2106-8. · 6.37 Impact Factor
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    Kees H Polderman
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    ABSTRACT: Mild to moderate hypothermia (32-35 degrees C) is the first treatment with proven efficacy for postischemic neurological injury. In recent years important insights have been gained into the mechanisms underlying hypothermia's protective effects; in addition, physiological and pathophysiological changes associated with cooling have become better understood. To discuss hypothermia's mechanisms of action, to review (patho)physiological changes associated with cooling, and to discuss potential side effects. Review article. None. A myriad of destructive processes unfold in injured tissue following ischemia-reperfusion. These include excitotoxicty, neuroinflammation, apoptosis, free radical production, seizure activity, blood-brain barrier disruption, blood vessel leakage, cerebral thermopooling, and numerous others. The severity of this destructive cascade determines whether injured cells will survive or die. Hypothermia can inhibit or mitigate all of these mechanisms, while stimulating protective systems such as early gene activation. Hypothermia is also effective in mitigating intracranial hypertension and reducing brain edema. Side effects include immunosuppression with increased infection risk, cold diuresis and hypovolemia, electrolyte disorders, insulin resistance, impaired drug clearance, and mild coagulopathy. Targeted interventions are required to effectively manage these side effects. Hypothermia does not decrease myocardial contractility or induce hypotension if hypovolemia is corrected, and preliminary evidence suggests that it can be safely used in patients with cardiac shock. Cardiac output will decrease due to hypothermia-induced bradycardia, but given that metabolic rate also decreases the balance between supply and demand, is usually maintained or improved. In contrast to deep hypothermia (<or=30 degrees C), moderate hypothermia does not induce arrhythmias; indeed, the evidence suggests that arrhythmias can be prevented and/or more easily treated under hypothermic conditions. Therapeutic hypothermia is a highly promising treatment, but the potential side effects need to be properly managed particularly if prolonged treatment periods are required. Understanding the underlying mechanisms, awareness of physiological changes associated with cooling, and prevention of potential side effects are all key factors for its effective clinical usage.
    Critical care medicine 07/2009; 37(7 Suppl):S186-202. · 6.37 Impact Factor
  • Kees H Polderman, Ingeborg Herold
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    ABSTRACT: Hypothermia is being used with increasing frequency to prevent or mitigate various types of neurologic injury. In addition, symptomatic fever control is becoming an increasingly accepted goal of therapy in patients with neurocritical illness. However, effectively controlling fever and inducing hypothermia poses special challenges to the intensive care unit team and others involved in the care of critically ill patients. To discuss practical aspects and pitfalls of therapeutic temperature management in critically ill patients, and to review the currently available cooling methods. Review article. None. Cooling can be divided into three distinct phases: induction, maintenance, and rewarming. Each has its own risks and management problems. A number of cooling devices that have reached the market in recent years enable reliable maintenance and slow and controlled rewarming. In the induction phase, rapid cooling rates can be achieved by combining cold fluid infusion (1500-3000 mL 4 degrees C saline or Ringer's lactate) with an invasive or surface cooling device. Rapid induction decreases the risks and consequences of short-term side effects, such as shivering and metabolic disorders. Cardiovascular effects include bradycardia and a rise in blood pressure. Hypothermia's effect on myocardial contractility is variable (depending on heart rate and filling pressure); in most patients myocardial contractility will increase, although mild diastolic dysfunction can develop in some patients. A risk of clinically significant arrhythmias occurs only if core temperature decreases below 30 degrees C. The most important long-term side effects of hypothermia are infections (usually of the respiratory tract or wounds) and bedsores. Temperature management and hypothermia induction are gaining importance in critical care medicine. Intensive care unit physicians, critical care nurses, and others (emergency physicians, neurologists, and cardiologists) should be familiar with the physiologic effects, current indications, techniques, complications and practical issues of temperature management, and induced hypothermia. In experienced hands the technique is safe and highly effective.
    Critical care medicine 04/2009; 37(3):1101-20. · 6.37 Impact Factor
  • K H Polderman
    Annales francaises d'anesthesie et de reanimation 02/2009; · 0.77 Impact Factor
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    ABSTRACT: Optimal dosing of antibiotics is important for efficacy and avoidance of resistance. Fluoroquinolones are frequently used to treat severe infections in critically ill patients. We studied ciprofloxacin pharmacokinetics after administration of 400 mg twice a day (bid) intravenously (IV). Serum concentrations were measured in 32 intensive care unit patients (age, 68.7 +/- 17.4 years; Sepsis-related Organ Failure Assessment (SOFA) scores, 7.3 +/- 3.4). Blood samples were drawn at 7 time points after ciprofloxacin infusion. We evaluated whether areas under the curve (AUCs) exceeded minimal inhibitory concentration (MIC) values of 0.125, 0.25, 0.5, 1.0, and 2.0 mg/L by 125 times and peak concentrations (C(max)) 10 x MIC (C(max)/MIC >10). The AUC/MIC more than 125 was achieved in 100% for MIC 0.125. For MIC values 0.25, 0.5, 1.0, and 2.0, results were 84%, 31%, 3%, and 0%, respectively (P < .01). The C(max)/MIC more than 10 for MIC values of 0.125, 0.25, 0.5, 1.0, and 2.0 was realized in 100%, 97%, 69%, 25%, and 0%, respectively (P < .01). Female sex, SOFA(pulmonary) points, and SOFA(renal) points predicted higher AUC. Cumulative SOFA scores were most predictive of high AUCs. Ciprofloxacin 400 mg bid IV leads to inadequate AUC/MIC and C(max)/MIC ratios in many cases. Effective killing concentrations were only achieved in pathogens with MIC less than 0.25. As bacteria in intensive care unit patients often exceed this threshold, we recommend to use higher doses of ciprofloxacin (1200 mg daily) to ensure optimal bacterial killing and avoid antibiotic resistance.
    Journal of critical care 10/2008; 23(3):422-30. · 2.13 Impact Factor
  • Kees H Polderman, Stephan A Mayer, David Menon
    New England Journal of Medicine 10/2008; 359(11):1178; author reply 1180. · 51.66 Impact Factor
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    ABSTRACT: Acute Physiology and Chronic Health Evaluation (APACHE) II scoring is widely used as an index of illness severity, for outcome prediction, in research protocols and to assess intensive care unit performance and quality of care. Despite its widespread use, little is known about the reliability and validity of APACHE II scores generated in everyday clinical practice. We retrospectively re-assessed APACHE II scores from the charts of 186 randomly selected patients admitted to our medical and surgical intensive care units. These ‘new’ scores were compared with the original scores calculated by the attending physician. We found that most scores calculated retrospectively were lower than the original scores; 51% of our patients would have received a lower score, 26% a higher score and only 23% would have remained unchanged. Overall, the original scores changed by an average of 6.4 points. We identified various sources of error and concluded that wide variability exists in APACHE II scoring in everyday clinical practice, with the score being generally overestimated. Accurate use of the APACHE II scoring system requires adherence to strict guidelines and regular training of medical staff using the system.
    Anaesthesia 08/2008; 56(1):47 - 50. · 3.49 Impact Factor
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    Kees H Polderman
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    ABSTRACT: Increasing evidence suggests that induction of mild hypothermia (32-35 degrees C) in the first hours after an ischaemic event can prevent or mitigate permanent injuries. This effect has been shown most clearly for postanoxic brain injury, but could also apply to other organs such as the heart and kidneys. Hypothermia has also been used as a treatment for traumatic brain injury, stroke, hepatic encephalopathy, myocardial infarction, and other indications. Hypothermia is a highly promising treatment in neurocritical care; thus, physicians caring for patients with neurological injuries, both in and outside the intensive care unit, are likely to be confronted with questions about temperature management more frequently. This Review discusses the available evidence for use of controlled hypothermia, and also deals with fever control. Besides discussing the evidence, the aim is to provide information to help guide treatments more effectively with regard to timing, depth, duration, and effective management of side-effects. In particular, the rate of rewarming seems to be an important factor in establishing successful use of hypothermia in the treatment of neurological injuries.
    The Lancet 07/2008; 371(9628):1955-69. · 39.06 Impact Factor
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    Kees H Polderman, David K Menon, Armand R J Girbes
    Intensive Care Medicine 06/2008; 34(9):1738-9; author reply 1737. · 5.26 Impact Factor
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    ABSTRACT: This manuscript summarises the consensus on neuromonitoring in neuro-intensive care promoted and organised by the Neuro-Intensive Care and Emergency Medicine (NICEM) Section of the European Society of Intensive Care Medicine (ESICM). It is expected that continuous monitoring using multi-modal techniques will help to overcome the limitations of each individual method and will provide a better diagnosis. More specific treatment can then be applied; however, it remains to be determined which combination of parameters is optimal. The questions discussed and addressed in this manuscript are: (1) Who should have ICP monitoring and for how long? (2) What ICP technologies are available and what are their relative advantages/disadvantages? (3) Should CPP monitoring and autoregulation testing be used? (4) When should brain tissue oxygen tension (PbrO(2)) be monitored? (5) Should structurally normal or abnormal tissue be monitored with PbrO(2)? (6) Should microdialysis be considered in complex cases? It is hoped that this document will prove useful to clinicians working in NICU and also to those developing specialist NICU services within their hospital practice.
    Intensive Care Medicine 05/2008; 34(8):1362-70. · 5.26 Impact Factor
  • K H Polderman
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    ABSTRACT: Multi-centred studies in patients who remain comatose after cardiac arrest and also in newborn babies with perinatal asphyxia have clearly demonstrated that mild hypothermia (32-34 degrees C) can improve neurological outcome after post-anoxic injury. This represents a highly promising development in the field of neurocritical care. This review discusses the place of mild therapeutic hypothermia in the overall therapeutic strategy for cardiac arrest patients. Cooling should not be viewed in isolation but in the context of a 'treatment bundle,' which together can significantly improve outcome after cardiac arrest. Favourable outcomes of 50-60% are now routinely achieved in many centres in patients with witnessed arrest and an initial rhythm of ventricular fibrillation or ventricular tachycardia. These results have been achieved by combining a number of therapeutic strategies, including early and effective resuscitation with greater emphasis on continuing chest compressions throughout various procedures (including resumption of compressions immediately after defibrillation even if rhythm has been restored) as well as prevention of hypoxia and hypotension in all stages following restoration of spontaneous circulation. Regarding the use of hypothermia, early induction and proper management of side-effects are the key elements of successful implementation. Treatment should include the rapid infusion of 1500-3000 mL of cold fluids to induce hypothermia and prevent hypovolaemia and hypotension. Educational activities to increase awareness and acceptance of new therapeutic options and European Resuscitation Council guidelines are urgently required.
    European Journal of Anaesthesiology - Supplement 02/2008; 42:23-30.

Publication Stats

3k Citations
778.50 Total Impact Points

Institutions

  • 2009–2013
    • University of Pittsburgh
      • Department of Critical Care Medicine
      Pittsburgh, Pennsylvania, United States
  • 2006–2009
    • University Medical Center Utrecht
      • Intensive Care Center
      Utrecht, Provincie Utrecht, Netherlands
  • 2004–2008
    • Gelderse Vallei Hospital
      Ede, Gelderland, Netherlands
  • 2002–2008
    • VU University Medical Center
      • Department of Surgery
      Amsterdamo, North Holland, Netherlands
  • 1990–2005
    • VU University Amsterdam
      • Department of Adult Intensive Care
      Amsterdam, North Holland, Netherlands
  • 2003
    • Academisch Medisch Centrum Universiteit van Amsterdam
      Amsterdamo, North Holland, Netherlands
  • 1993–1996
    • University of Amsterdam
      • Department of Internal Medicine
      Amsterdam, North Holland, Netherlands