Learning Objectives Respiratory Failure Acute Respiratory Failure

Total Page:16

File Type:pdf, Size:1020Kb

Learning Objectives Respiratory Failure Acute Respiratory Failure Sepsis: 1, 2, 3, RAC Attack! Respiratory Failure: Definition and Sequencing Guidelines William Haik, MD, FACCP, CDIP, AHIMA‐Approved ICD‐10‐CM/PCS Trainer Director DRG Review, Inc. Fort Walton Beach, FL1 Learning Objectives • At the completion of this educational activity, the learner will be able to: – Identify the clinical elements that validate the reporting of acute respiratory failure – Identify the clinical criteria that support Sepsis‐1, Sepsis‐2, and Sepsis‐3 definitions 2 Respiratory Failure Severe Hypoxia ↓ Pulmonary Acute Respiratory Insufficiency Insufficiency → Respiratory ← Failure ↑ Respiratory Acidosis 3 2017 Copyright, HCPro, an H3.Group division of Simplify Compliance LLC. All rights reserved. 1 These materials may not be copied without written permission. Respiratory Failure • Respiratory failure should be specified as acute, chronic, or acute on chronic (hypoxemic/hypercapneic). Acute Respiratory Failure • Respiratory failure is a condition categorized by inadequate exchange of oxygen and/or carbon dioxide by the lungs. • The diagnosis of respiratory failure is a life‐threatening disorder requiring aggressive management and monitoring. A patient with acute respiratory failure usually exhibits evidence of increased work of breathing (rapid respiratory rate, use of accessory muscles of respiration) or possibly cyanosis and/or paradoxical breathing. • Treatment includes frequent respiratory therapy and possibly support with either invasive mechanical ventilation or noninvasive modalities such as CPAP/BiPAP and/or high flow oxygen therapy (HFT). The absence of mechanical ventilation, however, does not exclude the diagnosis of acute respiratory failure. 4 Respiratory Failure 4. Arterial blood gas determinations are helpful in determining acute respiratory failure. a) A patient with acute respiratory failure with previously normal lungs • pO2 < 60 mmHg, pCO2 > 50 mmHg, pH < 7.35 on room air (FiO2 = 21%) • Hemoglobin oxygen saturation < 90% on room air (FiO2 = 21%) • P/F ratio (pO2/FiO2) < 300 (Example: pO2 of 90 mmHg on 32% oxygen) P/F = 90/0.32 = 281 b) Acute respiratory failure in a patient with previously abnormal lungs such as chronic obstructive lung disease • pH < 7.35 with a pCO2 > 50 mmHg • Generally, in a patient with chronic lung disease, the arterial blood pH is a more useful criteria than simply efollowing th pCO2 • A change in the pO2 < 60 mmHg representing a drop of 10–15 mmHg from the previous "normal" pO2 5 Respiratory Failure c) Oxygen delivery device conversion to FiO2 (estimate based on normal tidal volume) • Nasal O2 1 L 24% 2 L 28% 3 L 32% 4 L 36% 5 L 40% 6 L 44% 6 2017 Copyright, HCPro, an H3.Group division of Simplify Compliance LLC. All rights reserved. 2 These materials may not be copied without written permission. Respiratory Failure • Simple mask 5–8 LPM FiO2 0.35 to 0.55 • Venturi mask Variable LPM FiO2 0.24 to 0.50 • Partial rebreather 10 LPM FiO2 0.50 to 0.70 • Non‐rebreather 15 LPM FiO2 0.70 to 1.0 7 7 Respiratory Failure d) Hemoglobin oxygen saturation conversion to pO2* Hemoglobin oxygen Partial pressure of saturation oxygen 50% 27 mmHg 75% 40 mmHg 88% 55 mmHg 90% 60 mmHg 98% 100 mmHg *Hemoglobin oxygen saturation conversion to pO2 is only an approximation as several factors such as pH, temperature, and DPG content may impact it. References: Murray and Nadel’s Textbook of Respiratory Medicine, Sixth Edition, pp. 1723, 1740. Guyton and Hall Textbook of Medical Physiology, 12th Edition, Chapter 39. 8 Respiratory Failure • Chronic Respiratory Failure – No significant deviation from baseline ABGs – pO2 < 60 mmHg – Without significant increase in work of breathing – Continuous oxygen use or ventilatory support – P/F ratio not useful • The cause(s) of the respiratory failure such as COPD, intestinal lung disease, bronchiectasis, etc. should be clearly stated. 9 2017 Copyright, HCPro, an H3.Group division of Simplify Compliance LLC. All rights reserved. 3 These materials may not be copied without written permission. Respiratory Failure Sequencing Guidelines • Do not code acute respiratory failure as the principal diagnosis when there is a chapter‐specific coding guideline (sepsis, obstetrics, poisoning, HIV, newborn) or an Alphabetic Index or Tabular List directive that takes precedence over the general respiratory failure guidelines and examples listed above. Examples: – Acute respiratory failure, secondary to Pneumocystis carinii pneumonia in a patient with HIV. The human immunodeficiency virus (B20) is reported as the principal diagnosis. – Patient is admitted with acute respiratory failure secondary to Valium overdose. The poisoning (Valium overdose) is reported as the principal diagnosis. – A patient is admitted with aspiration pneumonia with associated sepsis and acute respiratory failure. Sepsis is reported as the principal diagnosis. 10 Sepsis • None of these SIRS terms code to ↓ sepsis • Blood cultures do not define sepsis • SIRS has infectious Bacteremia Urosepsis as well as non‐ → Sepsis ← infectious etiologies • “SIRS due to infection” does not ↑ equate to sepsis in Sepsis ICD‐10‐CM Syndrome 11 Sepsis A. Infection (B99.9): Invasion of normally sterile tissue, fluid, or body cavity by pathogenic microorganisms B. Bacteremia (R78.81): A laboratory finding of viable bacteria in the blood without evidence of a systemic inflammatory response. C. Systemic Inflammatory Response Syndrome (SIRS) (R65.10): A syndrome defined by the presence of two or more of the following features of systemic inflammation: 1. Fever (core temperature > 38.3°C or 100.9°F) or hypothermia (core temperature < 36°C or 96.8°F) 2. Leukocytosis (white count > 12,000) or leukopenia (white count < 4,000 or > 10% bands) 3. Tachycardia (> 90 beatsr pe minute or more than two SD above the normal value for age) 4. Tachypnea (respiratory rate > 20 breaths per minute or a pCO2 of < 32 mmHg) 12 2017 Copyright, HCPro, an H3.Group division of Simplify Compliance LLC. All rights reserved. 4 These materials may not be copied without written permission. Sepsis D. Sepsis (A41.9): An infection‐induced syndrome defined by the presence of at least two unexplained features of systemic inflammation: 1. Fever (core temperature > 38.3°C or 100.9°F) or hypothermia (core temperature < 36°C or 96.8°F) 2. Leukocytosis (white count > 12,000) or leukopenia (white count < 4,000 or > 10% bands) 3. Tachycardia (> 90 beats per minute or more than two SD above the normal value for age) 4. Tachypnea (respiratory rate > 20 breaths per minute or a pCO2 of < 32 mmHg) 5. Altered mental status 6. Significant edema or positive fluid balance (> 20 mL per kg over 24 hours) 7. Hyperglycemia, unexplained (glucose > 140 mg/dL in the absence of diabetes) 8. Evidence of hypoperfusion [hyperlactatemia (> 1 mmol/L)] or decreased capillary refill or mottling 9. Ileus (absent bowel sounds) 10. Arterial hypoxemia (PaO2/FiO2 < 300) 11. Acute oliguria (urine output < 0.5 mL/kg/hr for at least 2 hrs, despite adequate fluid resuscitation) 12. Creatinine increase > 0.5 mg/dL or 44.2 umol/L 13. Hyperbilirubinemia (> 2 mg/dL)* 14. Plasma C‐reactive protein more than two SD above the normal value 15. Plasma procalcitonin more than two SD above the normal value 13 Sepsis E. Septicemia (A41.9): An antiquated, ambiguous term that has been used nonspecifically in the past to imply either bacteremia or sepsis; therefore, should be eliminated from current medical usage. F. Severe sepsis (R65.20): Defined as sepsis‐induced tissue hypoperfusion or organ dysfunction (any one of which due to infection): 1. Sepsis‐induced hypotension [systolic blood pressure (SBP) < 90 mmHg, mean arterial pressure (MAP) < 70 mmHg, or an SBP decrease by > 40 mmHg in adults or less than two SD below normal for age] 2. Lactate above upper limits of laboratory normal 3. Acute oliguria (urine output < 0.5 mL/kg/hrr fo more than 2 hrs, despite adequate fluid resuscitation) 4. Creatinine increase > 2.0 mg/dL 5. Platelet count < 100,000/uL 6. Coagulopathy (international normalized ratio > 1.5) 7. Acute lung injury with PaO2/FiO2 < 250 in the absence of pneumonia as an infection source 8. Acute lung injury with PaO2/FiO2 < 200 in the presence of pneumonia as an infection source 9. Hyperbilirubinemia (plasma total bilirubin > 4 mg/dL*) 14 Sepsis G. Septic shock (R65.21): Severe sepsis with hypotension (systolic blood pressure < 90 mmHg or a 40 mmHg drop from the previous normal blood pressure) unresponsive to fluid resuscitation, requiring vasopressor intervention. *Personal email communication with Mitchell M. Levy, MD, on May 14, 2013. Bilirubin levels for sepsis and severe sepsis were reversed with additional modifications to the clinical elements also ebased on th communication. References: Dillinger, Levy, et al., “Surviving Sepsis Campaign, 2012,” Critical Care Medicine, 2013;41(2). Levy, M.D., M.M., “International Sepsis Definition Conference, 2001,” Critical Care Medicine, 2003;31:1250–1256. Bone, M.D., R.C., “ACCP/SCCM Consensus Conference,” Chest, 1992;101:1044–1055. 15 2017 Copyright, HCPro, an H3.Group division of Simplify Compliance LLC. All rights reserved. 5 These materials may not be copied without written permission. The Third International Consensus Definition for Sepsis and Septic Shock (Sepsis‐3) • Since the previous consensus definitions of sepsis1, 2 and its related terminology (sepsis syndrome, septicemia, severe sepsis, and septic shock), there have been considerable advances in pathobiology • Therefore, a third international consensus definition representing experts from the
Recommended publications
  • Central Nervous System Dysfunction As the First Manifestation of Multiple
    Bone Marrow Transplantation (2000) 25, 79–83 2000 Macmillan Publishers Ltd All rights reserved 0268–3369/00 $15.00 www.nature.com/bmt Central nervous system dysfunction as the first manifestation of multiple organ dysfunction syndrome in stem cell transplant patients B Gordon1, E Lyden2, J Lynch2, S Tarantolo3, ZS Pavletic3, M Bishop3, E Reed3, A Kessinger3 and W Haire3 Departments of 1Pediatrics, 2Preventive and Societal Medicine, and 3Internal Medicine, University of Nebraska Medical Center, Omaha, NE, USA Summary: Organ system dysfunction is a frequent complication of hematopoietic stem cell transplantation. Single and multior- Development of CNS dysfunction in the setting of hema- gan dysfunction may be due to the culmination of an uncon- topoietic stem cell transplant (HSCT) has been pre- trolled inflammatory response to some initial event, viously shown to predict for subsequent second organ mediated by an as yet incompletely understood interplay of dysfunction and death. In this paper, we describe the cytokines, complement, and the coagulation system. In the characteristics of this isolated CNS dysfunction, and its setting of acutely ill non-transplant patients, this has been relationship to multiple organ dysfunction syndrome termed the systemic inflammatory response syndrome.1 (MODS) after HSCT. Twenty-one of 186 patients This syndrome has been well described in patients with undergoing HSCT developed CNS dysfunction as their trauma or severe infection,1–3 but has only recently been first organ dysfunction a mean of 22.8 ± 0.9 days after recognized in patients undergoing HSCT. the start of the preparative regimen. Compared with The occurrence of single organ system dysfunction in 137 patients who developed no organ dysfunction, the post-transplant period has been shown to predict for patients presenting with CNS dysfunction were more subsequent development of multiple organ dysfunction and likely to have undergone allogeneic HSCT (P = 0.001) death.
    [Show full text]
  • Multiple Organ Dysfunction Syndrome Timothy G. Buchman, Ph.D., MD
    Physiologic Failure: Multiple Organ Dysfunction Syndrome Timothy G. Buchman, Ph.D., M.D. Edison Professor of Surgery Professor of Anesthesiology and of Medicine Washington University School of Medicine St. Louis, Missouri 63110 [email protected] Acknowledgement: This work was supported, in part, by award GM48095 from the National Institutes of Health 2 Buchman Humans, like other life forms, can be viewed as thermodynamically open systems that continuously consume energy to maintain stability in the internal milieu in the face of ongoing environmental stress. In contrast to simple unicellular life forms such as bacteria, higher life forms must maintain stability not only in individual cells but also for the organism as a whole. To this end, a collection of physiologic systems evolved to process foodstuffs; to acquire oxygen and dispose of gaseous waste; to eliminate excess fluid and soluble toxins; and to perform other tasks. These systems—labeled respiratory, circulatory, digestive, neurological, and so on—share several features. • Physiological systems are spatially distributed. Food has to get from mouth to anus. Urine is made in the kidneys but has to exit the urethra. Blood may be pumped by the heart but has to reach the great toe. • Physiologic systems are generally spacefilling and structurally fractal. Each cell has demand for nutrients; each cell excretes waste. Information has to travel from the brain throughout the body. While not every physiologic system is self-similar at all levels of granularity, there is typically a nested architecture that facilitates function: microvillus to villus to intestinal mucosa; alveolus to alveolar unit to bronchial segment; capillary to arteriole to artery.
    [Show full text]
  • Sepsis-3 Definitions. What Are They, and How Should We Use Them?
    Sepsis-3 definitions. What are they, and how should we use them? William T. Browne, MD, FCCM October 28, 2016 ACCP/SCCM Consensus Definitions • SIRS (Systemic Inflammatory Response Syndrome) – Temperature > 38° C or < 36° C – Heart rate > 90 – Respiratory rate > 20 or pCO2 < 32 mm Hg – WBC > 12,000 or < 4,000 or > 10% bands • Any two of the criteria needed for SIRS diagnosis ACCP/SCCM Consensus Definitions • Sepsis – Must have diagnosis of SIRS – Clinical evidence of infection • bacteremia • infiltrate on CXR • abscess on imaging study ACCP/SCCM Consensus Definitions • Severe sepsis – must have diagnosis of sepsis – evidence of organ dysfunction • Organ dysfunction – increase in BUN/creatinine – elevated LFTs – hypoxia – elevated serum lactate ACCP/SCCM Consensus Definitions • Septic shock – must have findings of severe sepsis – hypotension after adequate fluid resuscitation – systolic BP 40 mm Hg below baseline – may not have hypotension if receiving pressor agents Was this a useful bedside tool? Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection Under these new definitions Sepsis(new) = Severe Sepsis(old) Key concepts of sepsis (1) • Sepsis is the primary cause of death from infection, especially if not recognized and treated promptly. Its recognition mandates urgent attention • Sepsis is a syndrome shaped by pathogen factors and host factors (eg, sex, race and other genetic determinants, age, comorbidities, environment) with characteristics that evolve over time. What differentiates sepsis from infection is an aberrant or dysregulated host response and the presence of organ dysfunction. Key concepts of sepsis (2) • Sepsis-induced organ dysfunction may be occult; therefore, its presence should be considered in any patient presenting with infection.
    [Show full text]
  • Cardiorenal Syndromes Presentation
    Outline Cardiorenal Syndromes: New ° Definitions Insights into Combined Heart and Kidney Failure ° Complex, bidirectional pathogenesis ° Novel diagnostic targets Peter A. McCullough, MD, MPH ° Therapy FACC, FACP, FAHA, FCCP, FNKF ° Putting it all together History Outline •1913: Sir Thomas Lewis gave a clinical lecture on paroxysmal dyspnoea in cardiocardio--renalrenal patients with special reference to “cardiac” and “uremic” asthma •1951: the term cardiorenal syndromes (CRS) was coined by Ledoux [i] •1997 to present: Schrier in multiple papers summarized the impact of salt and ° Definitions water retention combined with neurohormonal activation in the pathogenesis of CRS. [ii] [iii] [iv] ° Complex, bidirectional pathogenesis •2003: Brammah and colleagues pointed out that treatment of bilateral renal arterial disease could result in improvement of both heart and kidney function. [v] •2005: Braam demonstrated in animals that organ dysfunction in one system ° Novel diagnostic targets influences that in the other. [vi] •2008: Ronco and colleagues proposed five distinct CRS according to the temporal sequence of organ injury and failure as well as the clinical context. [vii] ° Therapy •2008: Acute Dialysis Quality Initiative (ADQI) involving nephrology, critical care, cardiac surgery, and cardiology was convened. [viii] ° Putting it all together •2011: Karger launches “Cardiorenal Medicine” James Sowers, MD, Editor •2012: ADQI conducted a second consensus conference to review the spectrum of pathophysiologic mechanisms involved in CRS [i] University College Hospital, London, November 12th, 1913. BMJ 2: 1417–1420. Ledoux P. [Cardiorenal syndrome]. Avenir Med. 1951 Oct;48(8):149-53. [ii] Blair JE, Manuchehry A, Chana A, Rossi J, Schrier RW, Burnett JC, Gheorghiade M. Prognostic markers in heart failure-congestion, neurohormones, and the cardiorenal syndrome.
    [Show full text]
  • COVID-19 Recommendations for Health Care Workers (PDF)
    MINNESOTA DEPARTMENT OF HEALTH COVID-19 Recommendations for Health Care Workers 8 / 6 /2021 This guidance was updated on August 6, 2021, to include: . All health care workers, regardless of vaccination status, should be tested for SARS-CoV-2 when symptomatic, after a higher-risk exposure, and when working in a facility experiencing an outbreak. Post-exposure testing should occur immediately and at day 3–5 after exposure. Testing of HCW for COVID-19 Health care workers (HCW) should not work while sick, even if presenting with mild signs or symptoms. HCW with fever and/or respiratory symptoms that are concerning for COVID-19 should be tested for SARS-CoV-2 as soon as possible. HCW who have had unprotected exposure to a person with confirmed COVID-19 but remain asymptomatic should be tested immediately and 3–5 days following the date of exposure at a minimum. Specific routine staff testing is required or recommended by federal and/or state guidelines in skilled nursing or assisted living facilities. Please refer to the following guidance for detailed testing recommendations, which have been updated to discuss recommendations for vaccinated HCWs: . COVID-19 Testing Recommendations for Long-term Care Facilities (www.health.state.mn.us/diseases/coronavirus/hcp/ltctestrec.pdf) HCW with exposure to COVID-19 MDH and health care organizations cooperate to identify, manage, and monitor HCW who have experienced a high-risk (unprotected) exposure to a patient, resident, co-worker, or household/social contact with confirmed COVID-19. Most HCW who have had a high-risk exposure are identified through occupational tracking of personal protective equipment (PPE) breaches and/or contact tracing and assessment of PPE worn while in contact with a COVID-19 positive patient, resident, or co-worker.
    [Show full text]
  • Acute-On-Chronic Liver Failure: an Update Gut: First Published As 10.1136/Gutjnl-2016-312670 on 4 January 2017
    Gut Online First, published on January 4, 2017 as 10.1136/gutjnl-2016-312670 Recent advances in clinical practice Acute-on-chronic liver failure: an update Gut: first published as 10.1136/gutjnl-2016-312670 on 4 January 2017. Downloaded from Ruben Hernaez,1 Elsa Solà,2,3,4 Richard Moreau,5,6,7,8,9 Pere Ginès2,3,4 1Section of Gastroenterology ABSTRACT extrahepatic organ failure (OF) associated with and Hepatology, Department Acute-on-chronic liver failure (ACLF) is a syndrome short-term mortality. The current narrative review of Medicine, Baylor College of Medicine and Michael characterised by acute decompensation of chronic liver will provide insights on the current understanding E. DeBakey Veterans Affairs disease associated with organ failures and high short- of ACLF with emphasis on established definitions, Medical Center, Houston, term mortality. Alcohol and chronic viral hepatitis are the epidemiology, pathophysiology and treatment/man- Texas, USA – 2 most common underlying liver diseases. Up to 40% agement options. Liver Unit, Hospital Clinic de 50% of the cases of ACLF have no identifiable trigger; Barcelona, Universitat de Barcelona, Barcelona, Spain in the remaining patients, sepsis, active alcoholism and Heterogeneity of definitions 3 ’ Institut d Investigacions relapse of chronic viral hepatitis are the most common ACLF is a syndrome characterised by acute and Biomediques August Pi i reported precipitating factors. An excessive systemic severe hepatic abnormalities resulting from differ- Sunyer (IDIBAPS), Barcelona, inflammatory response seems to play a crucial role in the Spain ent types of insults, in patients with underlying 4Centro d’Investigaciones development of ACLF. Using a liver-adapted sequential chronic liver disease or cirrhosis but, in contrast to Biomedicas en Red, organ assessment failure score, it is possible to triage decompensated cirrhosis, has a high short-term enfermedades Hepaticas y and prognosticate the outcome of patients with ACLF.
    [Show full text]
  • Role of Kidney Injury in Sepsis Kent Doi
    Doi Journal of Intensive Care (2016) 4:17 DOI 10.1186/s40560-016-0146-3 REVIEW Open Access Role of kidney injury in sepsis Kent Doi Abstract Kidney injury, including acute kidney injury (AKI) and chronic kidney disease (CKD), has become very common in critically ill patients treated in ICUs. Many epidemiological studies have revealed significant associations of AKI and CKD with poor outcomes of high mortality and medical costs. Although many basic studies have clarified the possible mechanisms of sepsis and septic AKI, translation of the obtained findings to clinical settings has not been successful to date. No specific drug against human sepsis or AKI is currently available. Remarkable progress of dialysis techniques such as continuous renal replacement therapy (CRRT) has enabled control of “uremia” in hemodynamically unstable patients; however, dialysis-requiring septic AKI patients are still showing unacceptably high mortality of 60–80 %. Therefore, further investigations must be conducted to improve the outcome of sepsis and septic AKI. A possible target will be remote organ injury caused by AKI. Recent basic studies have identified interleukin-6 and high mobility group box 1 (HMGB1) as important mediators for acute lung injury induced by AKI. Another target is the disease pathway that is amplified by pre-existing CKD. Vascular endothelial growth factor and HMGB1 elevations in sepsis were demonstrated to be amplified by CKD in CKD-sepsis animal models. Understanding the role of kidney injury as an amplifier in sepsis and multiple organ failure might support the identification of new drug targets for sepsis and septic AKI. Keywords: Sepsis, Acute kidney injury, Chronic kidney disease, Lung injury, High mobility group box 1 Introduction ICUs is also increasing.
    [Show full text]
  • Multiple Organ Dysfunction in Children Mechanically Ventilated
    Saritha Pediatric Critical Care Medicine Multiple Organ Dysfunction in Children Mechanically 10.1097/PCC.0000000000001091 Ventilated for Acute Respiratory Failure* 1529-7535 Scott L. Weiss, MD, MSCE1; Lisa A. Asaro, MS2; Heidi R. Flori, MD3; Geoffrey L. Allen, MD4; Pediatr Crit Care Med David Wypij, PhD2,5,6; Martha A. Q. Curley, PhD, RN7,8; for the Randomized Evaluation of Sedation Titration for Respiratory Failure (RESTORE) Study Investigators Weiss et al *See also p. 383. Objectives: The impact of extrapulmonary organ dysfunction, inde- 1Department of Anesthesiology and Critical Care, The Children’s Hospital pendent from sepsis and lung injury severity, on outcomes in pedi- of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. atric acute respiratory failure is unclear. We sought to determine the 2Department of Cardiology, Boston Children’s Hospital, Boston, MA. frequency, timing, and risk factors for extrapulmonary organ dysfunc- 3Division of Pediatric Critical Care, C.S. Mott Children’s Hospital, Univer- tion and the independent association of multiple organ dysfunction sity of Michigan, Ann Arbor, MI. syndrome with outcomes in pediatric acute respiratory failure. 4Division of Critical Care, Department of Pediatrics, Children’s Mercy Hos- Design: Secondary observational analysis of the Randomized Evalu- pitals and Clinics, Kansas City, MO. ation of Sedation Titration for Respiratory Failure cluster-random- 5Department of Biostatistics, Harvard T.H. Chan School of Public Health, ized prospective clinical trial conducted between 2009 and 2013. Boston, MA. Setting: Thirty-one academic PICUs in the United States. 6Department of Pediatrics, Harvard Medical School, Boston, MA. Patients: Two thousand four hundred forty-nine children mechani- 7School of Nursing, University of Pennsylvania, Philadelphia, PA.
    [Show full text]
  • Detrimental Cross-Talk Between Sepsis and Acute Kidney Injury
    Dellepiane et al. Critical Care (2016) 20:61 DOI 10.1186/s13054-016-1219-3 REVIEW Detrimental cross-talk between sepsis and acute kidney injury: new pathogenic mechanisms, early biomarkers and targeted therapies Sergio Dellepiane1†, Marita Marengo2† and Vincenzo Cantaluppi3*† review the recent findings on the detrimental cross‐talk Abstract between sepsis and AKI and the identification of new, This article is one of ten reviews selected from the early biomarkers and targeted therapies aimed at im- Annual Update in Intensive Care and Emergency proving the outcome of these critically ill patients. medicine 2016. Other selected articles can be found online at http://www.biomedcentral.com/collections/ New pathogenic mechanisms of sepsis‐associated annualupdate2016. Further information about the aki: the ‘liaison dangereuse’ revisited Annual Update in Intensive Care and Emergency Major advances have been made in our understanding of Medicine is available from http://www.springer.com/ the detrimental connection between the systemic inflam- series/8901. matory response to infection and the acute loss of kid- ney function with consequent improvements in clinical practice. In particular, recent findings have challenged Background the dogma that in the course of severe sepsis and septic Acute kidney injury (AKI) complicates about 3–50 % of shock, AKI is merely a consequence of ischemic damage hospital admissions [1] depending on patient comorbidi- due to tissue hypoperfusion (Fig. 1). ties and on medical procedures performed during the stay. The greatest incidence of AKI is observed in the in- tensive care unit (ICU): indeed, critically ill patients with Renal overflow rather than hypoperfusion hospital‐acquired AKI have a greater in‐hospital mortal- According to old theories, tissue hypoperfusion associ- ity (30–70 %) and a more than double risk of severe ated with sepsis causes renal ischemia and consequently adverse outcomes even 5 years after discharge, including acute tubular necrosis.
    [Show full text]
  • Neurological Sequelae of Sepsis: I) Septic Encephalopathy
    2 The Open Critical Care Medicine Journal, 2011, 4, 2-7 Open Access Neurological Sequelae of Sepsis: I) Septic Encephalopathy Thomas M. Ringer*,1, Hubertus Axer1,2, Bernd F.M. Romeike3, Jan Zinke1,2, Frank Brunkhorst2,4, Otto W. Witte1,2 and Albrecht Günther1,2 1Hans Berger Clinic for Neurology, Jena University Hospital, Friedrich-Schiller-University, Erlanger Allee 101, D- 07747 Jena, Germany 2CSCC – Center for Sepsis Control and Care, Jena University Hospital, Friedrich-Schiller-University, Erlanger Allee 101, D-07747 Jena, Germany 3Department of Neuropathology, Friedrich-Schiller-University Jena, Erlanger Allee 101, D-07747 Jena, Germany 4Paul-Martini-Clinical Sepsis Research Unit, Jena University Hospital, Friedrich-Schiller-University, Erlanger Allee 101, D-07747 Jena, Germany Abstract: Septic encephalopathy (SE) or sepsis-associated delirium is the most common encephalopathy in ICU patients. It is defined by brain dysfunction due to systemic inflammatory response syndrome and extracranial infection. Clinically, acute impairment in level of consciousness and confusion are primarily defining symptoms. Precise clinical evaluation of brain function is crucial, although the necessary diagnostic tools are limited and require further verification in clinical studies. Therefore, SE is often underestimated and not frequently diagnosed. This review gives an overview of clinical features, epidemiological data, pathophysiological processes, imaging and neuropathological findings as well as diagnostic and therapeutic approaches in SE patients
    [Show full text]
  • Acute Kidney Injury and Organ Dysfunction: What Is the Role of Uremic Toxins?
    toxins Review Acute Kidney Injury and Organ Dysfunction: What Is the Role of Uremic Toxins? Jesús Iván Lara-Prado 1 , Fabiola Pazos-Pérez 2,* , Carlos Enrique Méndez-Landa 3, Dulce Paola Grajales-García 1, José Alfredo Feria-Ramírez 4, Juan José Salazar-González 5, Mario Cruz-Romero 2 and Alejandro Treviño-Becerra 6 1 Department of Nephrology, General Hospital No. 27, Mexican Social Security Institute, Mexico City 06900, Mexico; [email protected] (J.I.L.-P.); [email protected] (D.P.G.-G.) 2 Department of Nephrology, Specialties Hospital, National Medical Center “21st Century”, Mexican Social Security Institute, Mexico City 06720, Mexico; [email protected] 3 Department of Nephrology, General Hospital No. 48, Mexican Social Security Institute, Mexico City 02750, Mexico; [email protected] 4 Department of Nephrology, General Hospital No. 29, Mexican Social Security Institute, Mexico City 07910, Mexico; [email protected] 5 Department of Nephrology, Regional Hospital No. 1, Mexican Social Security Institute, Mexico City 03100, Mexico; [email protected] 6 National Academy of Medicine, Mexico City 06720, Mexico; [email protected] * Correspondence: [email protected]; Tel.: +52-55-2699-1941 Abstract: Acute kidney injury (AKI), defined as an abrupt increase in serum creatinine, a reduced urinary output, or both, is experiencing considerable evolution in terms of our understanding of the pathophysiological mechanisms and its impact on other organs. Oxidative stress and reactive oxygen species (ROS) are main contributors to organ dysfunction in AKI, but they are not alone. The precise mechanisms behind multi-organ dysfunction are not yet fully accounted for.
    [Show full text]
  • Decreased Fluid Volume to Reduce Organ Damage: a New Approach To
    Resuscitation (2007) 72, 371—378 CLINICAL PAPER Decreased fluid volume to reduce organ damage: A new approach to burn shock resuscitation? A preliminary studyଝ S. Arlati ∗, E. Storti, V. Pradella, L. Bucci, A. Vitolo, M. Pulici Intensive Care Unit ‘‘G. Bozza’’, Niguarda Ca-Granda` Hospital, Piazza Ospedale Maggiore 3, 20162 Milan, Italy Received 28 March 2006; received in revised form 23 June 2006; accepted 14 July 2006 KEYWORDS Summary Burn injury; Objective: To evaluate the impact of decreased fluid resuscitation on multiple- Shock; organ dysfunction after severe burns. This approach was referred to as ‘‘permissive Resuscitation; hypovolaemia’’. Fluid therapy; Methods: Two cohorts of patients with burns >20% BSA without associated injuries Haemodynamics and admitted to ICU within 6 h from the thermal injury were compared. Patients were matched for both age and burn severity. The multiple-organ dysfunction score (MODS) by Marshall was calculated for 10 days after ICU admission. Permissive hypo- volaemia was administered by a haemodynamic-oriented approach throughout the first 24-h period. Haemodynamic variables, arterial blood lactates and net fluid balance were obtained throughout the first 48 h. Results: Twenty-four patients were enrolled: twelve of them received the Parkland Formula while twelve were resuscitated according to the permissive hypo- volaemic approach. Permissive hypovolaemia allowed for less volume infusion (3.2 ± 0.7 ml/kg/% burn versus 4.6 ± 0.3 ml/kg/% burn; P < 0.001), a reduced posi- tive fluid balance (+7.5 ± 5.4 l/day versus +12 ± 4.7 l/day; P < 0.05) and significantly lesser MODS Score values (P = 0.003) than the Parkland Formula.
    [Show full text]