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“How Do You Solve A Problem like VIKI?” Rommel N. Tipones, MD, FPCP, FPCCP Section of Pulmonary Medicine, NKTI.

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Presentation on theme: "“How Do You Solve A Problem like VIKI?” Rommel N. Tipones, MD, FPCP, FPCCP Section of Pulmonary Medicine, NKTI."— Presentation transcript:

1 “How Do You Solve A Problem like VIKI?” Rommel N. Tipones, MD, FPCP, FPCCP Section of Pulmonary Medicine, NKTI

2 Terms ALI – Acute Lung Injury AKI – Acute Kidney Injury VILI – Ventilator-induced Lung Injury VIKI – Ventilator-induced Kidney Injury ARDS – Adult Respiratory Distress Syndrome MV – Mechanical ventilation PEEP – Positive end-expiratory pressure

3 Objectives We will focus on the role of ventilator-induced kidney injury in the pathogenesis of AKI in patients with ALI. We will review the current understanding of lung– kidney interactions including the renal effects of ALI and mechanical ventilation. We will review the management of ventilator-induced kidney injury.

4 Knowing VIKI Is VIKI real? What causes VIKI? How do you recognize VIKI? How do you solve a problem like VIKI?

5 Pulmonary-Renal Syndrome Goodpasture's disease Wegener's granulomatosis Multiple organ dysfunction syndrome – "slippery slope of critical illness" Ventilator-induced Kidney Injury The concept of “organ crosstalk”

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7 “Both acute lung injury and acute kidney injury (AKI) are frequent and serious problems in intensive care medicine. Therefore, the avoiding of any iatrogenic insult to these organs is of great importance. While an increasing body of evidence suggests that mechanical ventilation is capable of inducing lung and distant organ injury, the complex underlying molecular mechanisms remain insufficiently understood.” Pulmonary and renal protection: targeting PARP to ventilator-induced lung and kidney injury? Martin Matejovic 1 and Peter Radermacher 2 Critical Care 2010, 14:147doi: /cc8982

8 CASE 1 “VILI vs. VIKI?” Patient Billy is a case of ARDS from severe pneumonia, is intubated and hooked to a mechanical ventilator on assist-control mode with a tidal volume of 500 ml, Fi02 of 100%, and a positive end expiratory pressure of 15cm with blood pressure of 90/60 mmHg. His creatinine has been noted to be slightly increasing from normal for the past 3 days. The ICU resident believes the patient is going into multiple organ dysfunction from the sepsis, but wants to limit kidney injury that might be ventilator-induced. What are your suggestions?

9 CASE 1 “VILI vs. VIKI?” A. Decrease tidal volume to 6ml/kgIBW. B. Decrease FiO2 to maintain O2 satn > 90%. C. Decrease PEEP. D. Shift to a pressure support mode. E. Fluid administration and use of vasoactive drugs (dopamine at 2-5 ug/kg/min).

10 Effects of Mechanical Ventilation and ALI on Renal Function Hemodynamic Effects of Positive Pressure Ventilation (PPV) Neurohormonal Effects Inflammatory Mediators Organs Crosstalk Effects of Permissive Hypercapnia during Lung Protective Strategy

11 Effects of Mechanical Ventilation and ALI on Renal Function Hemodynamic Effects of Positive Pressure Ventilation (PPV) Neurohormonal Effects Inflammatory Mediators Organs Crosstalk Effects of Permissive Hypercapnia during Lung Protective Strategy

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14 Hemodynamic consequences of mechanical ventilation Decreased venous return Impaired cardiac filling Increased pulmonary vascular resistance and right ventricular afterload Decreased cardiac output

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17 Positive End Expiratory Pressure

18 may reduce cardiac output increase in intrathoracic pressures increases right ventricular afterload left ventricular distensibility also decreases, (PEEP greater than 15 cm H 2 O) any decrease in cardiac output caused by PEEP affects RBF

19 Positive End Expiratory Pressure blood flow is redistributed from the cortical to the juxtamedullary nephrons decreased urine output decreased creatinine clearance increased fractional resorption of sodium

20 Effects of Mechanical Ventilation and ALI on Renal Function Not all studies have shown a decrease in renal blood flow with positive pressure ventilation. Those patients who are volume depleted are more susceptible to reduced cardiac output.

21 Effects of Mechanical Ventilation and ALI on Renal Function Hemodynamic Effects of Positive Pressure Ventilation (PPV) Neurohormonal Effects Inflammatory Mediators Organs Crosstalk Effects of Permissive Hypercapnia during Lung Protective Strategy

22 Neurohormonal Effects of MV Atrial natriuretic peptide (ANP) Antidiuretic hormone (ADH) Sympathetic outflow, adrenergic hormones Renin-angiotensin-aldosterone axis

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24 Effects of Mechanical Ventilation and ALI on Renal Function Hemodynamic Effects of Positive Pressure Ventilation (PPV) Neurohormonal Effects Inflammatory Mediators Organs Crosstalk Effects of Permissive Hypercapnia during Lung Protective Strategy

25 ALI / ARDS Severe respiratory distress with one or more risk factors Clinical syndrome characterized by inflammatory pulmonary edema, severe hypoxemia, reduced lung compliance, and diffuse epithelial and endothelial injury Criteria for diagnosis – PaO2 / FiO2 < 200 mmHg = ARDS < 300 mmHg= ALI – Bilateral infiltrates – PCWP < 18mm or no signs of increased LAP

26 Exudative phase of ARDS

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28 Biotrauma and the Kidney Rabbits with acid aspiration lung injury ventilated with -injurious (high TV-low PEEP) strategy -Non-injurious (low TV – high PEEP)strategy After 8h the injurious group had Higher serum creatinine 1.3 vs 1.06 More apoptotic tubular epiithelial cells Imai et al. JAMA 2003; 289:

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31 Nitric Oxide PPV with injurious high tidal volumes (20 ml/kg) induced NOS expression in both the lung and the kidney. An increase in systemic microvascular leak was also seen in both organs.(VEGF) NOS response was blunted when the animals undergoing PPV were adequately fluid resuscitated Improvement in renal function was amplified using the NOS inhibitor L-NAME (N-nitro-L-arginine methyl ester). Choi WI, et al: Systemic microvascular leak in an in vivo rat model of ventilator-induced lung injury. Am J Respir Crit Care Med 2003; 167: 1627–1632. Choi et al.

32 Effects of Mechanical Ventilation and ALI on Renal Function Hemodynamic Effects of Positive Pressure Ventilation (PPV) Neurohormonal Effects Inflammatory Mediators Organs Crosstalk Effects of Permissive Hypercapnia during Lung Protective Strategy

33 Effects of Permissive Hypercapnia Hypercapnia is inversely correlated with RBF and causes renal constriction by direct and indirect mechanisms. The direct mechanisms include activation of the sympathetic nervous system by release of norepinephrine. The increased sympathetic activity reduces RBF and GFR and contributes to a nonosmotic release of vasopressin. The indirect mechanism is a decrease in systemic vascular resistance due to systemic vasodilatation.

34 Effects of Permissive Hypercapnia decrease in systemic vascular resistance, and increased cardiac output despite a decrease in cardiac contractility raises pulmonary vascular resistance causes a rightward shift of the oxygen- hemoglobin dissociation curve and improves tissue oxygen delivery in shock.

35 Effects of Permissive Hypercapnia Kregenow et al. showed that the adjusted odds ratio for 28-d mortality rate associated with hypercapnic acidosis (defined as pH 45 mmHg) was 0.14 (95% confidence interval, 0.03–0.070; P = 0.016) for those receiving high tidal volumes (12 ml/kg; the injurious ventilation strategy) in isolated perfused animal hearts, hypercapnic acidosis has been shown to have a dose-dependent protective effect against myocardial ischemia-reperfusion injury

36 Effects of Permissive Hypercapnia inactivation of calcium channels reduction in cellular oxygen demand decrease the conversion rate of inhibitor of nuclear factor kappa B (I- B) to nuclear factor kappa B (NF- B), and accordingly decrease the release of cytokines (IL-8 and ICAM-1) decrease the release of other cytokines (TNF- and IL-1) by inhibition of toll-like receptors

37 Effects of Permissive Hypercapnia However, there is no clinical confirmation of the putative protective effects of hypercapnic acidosis in ALI patients ventilated with low tidal volumes, so the current approach to acid-base management of these complex patients continues to include buffer therapy when severe acidosis develops. We suggest that the guideline for pH management used in the ARDS Network low tidal volume trial is an appropriate approach. Mechanical Ventilation and the Kidney Jay L. Koyner a Patrick T. Murray b. Blood Purif 2010;29:52–68

38 Fraction of Inspired Oxygen Severe hypoxemia (PaO 2 <40 mm Hg) causes renal vasoconstriction and increased renal vascular resistance, which leads to renal hypoperfusion, decreased GFR, and functional renal insufficiency. A high fraction of inspired oxygen causes formation of cytotoxic oxygen free radicals.

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40 CASE 1 “VILI vs. VIKI?” Patient Billy is a case of ARDS from severe pneumonia, is intubated and hooked to a mechanical ventilator on assist-control mode with a tidal volume of 500 ml, Fi02 of 100%, and a positive end expiratory pressure of 15cm with blood pressure of 90/60 mmHg. His creatinine has been noted to be slightly increasing from normal for the past 3 days. The ICU resident believes the patient is going into multiple organ dysfunction from the sepsis, but wants to limit kidney injury that might be ventilator-induced. What are your suggestions?

41 CASE 1 “VILI vs. VIKI?” A. Decrease tidal volume to 6ml/kgIBW. B. Decrease FiO2 to maintain O2 satn > 90%. C. Decrease PEEP. D. Shift to a pressure support mode. E. Fluid administration and use of vasoactive drugs (dopamine at 2-5 ug/kg/min).

42 “Hello, VIKI, Is That You?” The patient is usually afflicted with a condition that can cause AKI regardless of the mechanical ventilation. Pure VIKI very difficult to recognize or isolate. Important to recognize risk factors for VIKI. Prevention is the key!

43 “Hello, VIKI, Is That You?” The patient is usually afflicted with a condition that can cause AKI regardless of the mechanical ventilation. Pure VIKI very difficult to recognize or isolate. Important to recognize risk factors for VIKI. Prevention is the key!

44 Meet VIKI’s Friends Injurious tidal volumes PEEP (?) Permissive hypercapnia (?) Biotrauma Oxidative stress (?)

45 Tidal Volume Injurious ventilation in ALI – 12 to 20 ml/kg IBW What is the best TV? ARDSNet – 6 ml/kg IBW (for ARDS only) – IBW [height in inches – 60] for males, [height in inches-60] for females

46 ARDSNet: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome: the Acute Respiratory Distress Syndrome Network. N Engl J Med342 :1301 –1308,2000 This study was stopped early after 861 patients were enrolled because of a mortality benefit seen in the lower tidal volume group. The mortality rate was 39.8% in the group treated with traditional tidal volumes and 31.0% in the group treated with lower tidal volumes (p=0.007) Use of tidal volumes in the range of 4 to 6 ml/kg ideal body weight with a plateau pressure <30 cm H 2 O. Maintaining acceptable oxygenation by modulating PEEP and fraction of inspired oxygen.

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48 Lung Protective Strategy In the ARDS Network trial, patients who were ventilated with the low tidal volume strategy were slightly less likely to develop AKI. number of "renal failure–free days" – 20 ± 11 versus 18 ± 11 in control subjects; (P = 0.005). Induced a lesser systemic and intrapulmonary inflammatory response (as measured by serum and bronchoalveolar lavage fluid levels of TNF-, IL-6, and IL- 8). Ranieri et al.

49 Lack of Evidence There are no definitive therapeutic trials for the treatment of PPV- and positive end expiratory pressure (PEEP)-induced renal hypoperfusion and AKI. Several small trials have shown that fluid administration and the use of vasoactive drugs (dopamine at 5 µg/kg per min or fenoldopam) may improve renal function (but results are not consistently positive (for example, no benefit of dopamine at 2 µg/kg per min) It is unlikely that approaches focused solely on the hemodynamic and neurohormonal mechanisms of ALI- induced AKI will be clinically effective in preventing or treating this multifactorial problem.

50 CASE 2 “How much acidosis is too much acidosis?” Patient Billy was placed on a protective lung strategy by the intensivist based on the ARDS Network Protocol, with a tidal volume of 300ml or 6 ml/kg IBW. His creatinine was still noted to be steadily increasing for the past 3 days. An ABG done showed the pCO2 to be 60 mmHg with a pH of “It’s permissive hypercapnia”, the intensivist tells you. A few hours later, the ICU resident refers an ABG result which showed a pH of 7.18, HCO3 of 30 meq/L and pCO2 of 70 mm Hg, and tells you he wants to start a bicarbonate infusion. What are your suggestions?

51 CASE 2 “How much acidosis is too much acidosis?” A. Give a bicarbonate infusion. B. Increase ventilator rate up to a maximum of 35 or until pH >7.3 or PaCO2 < 25 mmHg. C. Increase the tidal volume by 1mg/kg until pH > 7.3 to blow off more CO2. D. Give a buffer infusion of Tris-hydroxymethyl aminomethane (THAM) E. Initiate renal replacement therapy.

52 “How much acidosis is too much acidosis?” Management of alkalemia (pH > 7.45): decrease ventilator rate, if possible; Management of mild acidemia (7.15 pH < 7.30); – Increase ventilator rate up to a maximum of 35 or until pH > 7.30 or PaCO 2 < 25 mmHg. – If ventilator rate = 35 or PaCO 2 < 25, then bicarbonate infusion may be given. Management of severe acidemia (pH < 7.15); – Increase ventilator rate to 35. – If ventilator rate = 35 and pH < 7.15 and bicarbonate has been considered or infused, then tidal volume may be increased by 1 ml/kg until pH 7.15 (under these conditions, target plateau pressure may be exceeded). ARDSNet: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome: the Acute Respiratory Distress Syndrome Network. N Engl J Med342 :1301 –1308,2000

53 Permissive Hypercapnia 57 (14%) of 423 patients who were ventilated with low tidal volumes had a serum pH <7.30 on day 1 of the trial, compared with 22 (6%) of 386 patients in the high tidal volume therapy arm of the trial despite no difference in the incidence of AKI in the two groups. The renal capacity to compensate for respiratory acidosis is limited after AKI. The mild metabolic acidosis that often accompanies early AKI will compound the respiratory acidosis of permissive hypoventilation. Although low tidal volume may protect against AKI (a finding that will require confirmation), it is important to recognize that patients who develop AKI in the setting of acute lung injury may require dialysis earlier when low tidal volume ventilation is applied, to prevent the complications of a mixed metabolic and respiratory acidosis.

54 Acidosis from Permissive Hypercapnia The ARDS. Network trial treated acidosis more aggressively than earlier trials did. The nephrologist may have to use a higher bicarbonate bath during hemodialysis or continuous renal replacement therapy because increasing the minute volume to improve acid-base control is often not an option. Tris-hydroxymethyl aminomethane (THAM) is a buffer that accepts one proton per molecule, generating bicarbonate but not carbon dioxide.

55 Renal Replacement Therapy The correct approach to use of RRT to control fluid balance or buffer permissive hypercapnic respiratory acidosis is not guided by high-level evidence. Human trials using modern CRRT for patients with ALI and AKI have yielded mixed results. Additional prospective trials are required to determine the optimal approach to delivery of RRT in the treatment of patients with AKI and ALI Mechanical Ventilation and the Kidney Jay L. Koyner a Patrick T. Murray b. Blood Purif 2010;29:52–68

56 The choice of mechanical ventilation in kidney transplant recipients with severe respiratory failure caused by pulmonary infection:invasive or noninvasive? Objectives: To summarize the clinical value of invasive mechanical ventilation (IMV)and noninvasive positive pressure ventilation (NPPV) in11patients with severe respiratory failure caused by pulmonaryinfection 2-4months after kidney transplantation. Conclusions: For kidney transplant recipients with severe respiratory failure in- duced by pulmonary infection, the initiation of NPPV is used to avoid intubation. IMV is an effective life-saving treatment and ensures the safe use of bronchoscopy to identify the infectious pathogen. As used for facilitating earlyweaning, NPPV shortens the duration on IMV. JieLi,QingyuanZhan,HuapingDai,KewuHuang,Zuj inLuo,ChenWang. BeijingInstituteofRespiratoryMedicine,BeijingCha oyangHospital-Affiliateof CapitalMedicalUniversity,Beijing,China

57 Inflammatory Mediators/Oxidative Stress Vaschetto et al, Critical Care.March 2010 – Renal hypoperfusion and impaired endothelium- dependent vasodilation in an animal model of VILI: the role of the peroxynitrite-PARP pathway. Peroxynitrite decomposition catalyst, WW85 or a PARP inhibitor, PJ-34 – attenuated lung injury, preserved blood pressure, attenuated renal endothelial dysfunction and maintained renal blood flow.

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60 Chasing VIKI There are no definitive therapeutic trials for the treatment of PPV- and positive end expiratory pressure (PEEP)-induced renal hypoperfusion and AKI. It is unlikely that approaches focused solely on the hemodynamic and neurohormonal mechanisms of ALI-induced AKI will be clinically effective in preventing or treating this multifactorial problem. The guideline for mechanical ventilation and pH management used in the ARDS Network low tidal volume trial is an appropriate approach while waiting for further research.

61 Thank you!


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