DOCSLIB.ORG

Acid–Base Status and Its Clinical Implications in Critically Ill Patients

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Acid–Base Status and Its Clinical Implications in Critically Ill Patients Drolz et al. Ann. Intensive Care (2018) 8:48 https://doi.org/10.1186/s13613-018-0391-9 RESEARCH Open Access Acid–base status and its clinical implications in critically ill patients with cirrhosis, acute‑on‑chronic liver failure and without liver disease Andreas Drolz1,2*† , Thomas Horvatits1,2†, Kevin Roedl1,2, Karoline Rutter1,2, Richard Brunner1, Christian Zauner1, Peter Schellongowski3, Gottfried Heinz4, Georg‑Christian Funk5, Michael Trauner1, Bruno Schneeweiss1 and Valentin Fuhrmann1,2 Abstract Background: Acid–base disturbances are frequently observed in critically ill patients at the intensive care unit. To our knowledge, the acid–base profle of patients with acute-on-chronic liver failure (ACLF) has not been evaluated and compared to critically ill patients without acute or chronic liver disease. Results: One hundred and seventy-eight critically ill patients with liver cirrhosis were compared to 178 matched con‑ trols in this post hoc analysis of prospectively collected data. Patients with and without liver cirrhosis showed hyper‑ chloremic acidosis and coexisting hypoalbuminemic alkalosis. Cirrhotic patients, especially those with ACLF, showed a marked net metabolic acidosis owing to increased lactate and unmeasured anions. This metabolic acidosis was partly antagonized by associated respiratory alkalosis, yet with progression to ACLF resulted in acidemia, which was present in 62% of patients with ACLF grade III compared to 19% in cirrhosis patients without ACLF. Acidemia and metabolic acidosis were associated with 28-day mortality in cirrhosis. Patients with pH values < 7.1 showed a 100% mortality rate. Acidosis attributable to lactate and unmeasured anions was independently associated with mortality in liver cirrhosis. Conclusions: Cirrhosis and especially ACLF are associated with metabolic acidosis and acidemia owing to lactate and unmeasured anions. Acidosis and acidemia, respectively, are associated with increased 28-day mortality in liver cirrhosis. Lactate and unmeasured anions are main contributors to metabolic imbalance in cirrhosis and ACLF. Keywords: Acid–base, Cirrhosis, Acute-on-chronic liver failure, Mortality Background Yet, only a few studies assessed the impact of underlying Derangements in acid–base balance are frequently chronic liver disease on acid–base equilibrium in critical observed in critically ill patients at the intensive care illness [7, 8]. While a balance of ofsetting acidifying and unit (ICU) and present in various patterns [1–4]. Severe alkalinizing metabolic acid–base disorders with a result- acid–base disorders, especially metabolic acidosis, have ing equilibrated acid–base status has been described in been associated with increased mortality [5, 6]. As a con- stable cirrhosis [9], severe derangements with result- sequence, acid–base status in critically ill patients with ing net acidosis owing to hyperchloremic, dilutional and various disease entities has been extensively studied. lactic acidosis were observed when cirrhosis was accom- panied by critical illness [7, 8]. Acute liver failure (ALF) *Correspondence: [email protected] is characterized by a diferent acid–base pattern with †Andreas Drolz and Thomas Horvatits contributed equally to the work dramatically increased lactate levels [10]. Te acidifying 2 Department of Intensive Care Medicine, University Medical Center, efect of this increase in lactate was neutralized by hypoal- Hamburg‑Eppendorf, Martinistraße 52, 20246 Hamburg, Germany Full list of author information is available at the end of the article buminemia in non-paracetamol-induced ALF [11]. © The Author(s) 2018. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Drolz et al. Ann. Intensive Care (2018) 8:48 Page 2 of 12 Despite advantages in intensive care medicine, which tomography scanning), or via histology, if available. ACLF have led to an improved outcome over the last decade was identifed and graded according to recommendations [12], mortality in cirrhotic patients admitted to ICU is of the chronic liver failure (CLIF) consortium of the Euro- still high [13–15]. Measurement and knowledge of spe- pean Association for the Study of the Liver (EASL) [20]. cifc acid–base patterns and their implications in criti- CLIF-SOFA score [20] and CLIF-C ACLF score [21] were cally ill patients with liver cirrhosis may help to improve calculated. Septic shock was defned according to the rec- patient management, especially in the ICU setting [16]. ommendations of the Surviving Sepsis Campaign [22]. However, to our knowledge, the acid–base profle of Twenty-eight-day mortality and 1-year mortality critically ill cirrhotic patients with acute-on-chronic were assessed on site or by contacting the patient or the liver disease (ACLF) has not been compared to criti- attending physician, respectively. cally ill patients without acute or chronic liver disease. Tis study is based on a post hoc analysis of prospectively Most information on the acid–base status of critically ill collected data [23]. Te Ethics Committee of the Medical patients with cirrhosis was obtained by comparing these University of Vienna waived the need for informed consent patients with healthy controls [8]. Yet, part of metabolic due to the observational character of this study. disturbances in critically ill patients with liver cirrhosis may be attributable to critical illness per se, rather than Sampling and blood analysis to the presence of chronic liver disease. On admission, arterial blood samples were collected Te aim of this study was to assess acid–base patterns from arterial or femoral artery and parameters for the of critically ill patients with liver cirrhosis and ACLF, assessment of acid–base status were instantly measured. respectively, in comparison with critically ill patients pH, partial pressure of carbon dioxide (PaCO2), ionized without acute or chronic liver disease. calcium (Ca2+) and lactate were measured with a blood gas analyzer (ABL 725; Radiometer, Copenhagen, Den- Methods mark). Samples of separated plasma were analyzed for Patients concentrations of sodium (Na+), potassium (K+), chlo- All patients admitted to 3 medical ICUs at the Medical ride (Cl−), magnesium (Mg2+), inorganic phosphate (Pi), University of Vienna between July 2012 and August 2014 albumin (Alb), plasma creatinine, blood urea nitrogen were screened for inclusion in the study. For the pre- (BUN), aspartate aminotransferase (AST) and alanine sent study, only patients who had arterial blood samples aminotransferase (ALT) by a fully automated analyzer drawn within 4 h after ICU admission were eligible for (Hitachi 917; Roche Diagnostics GmbH, Mannheim, inclusion. Patients with acute liver injury in the absence Germany). Na+ and Cl− were measured using ion-selec- of chronic liver disease were excluded. One hundred and tive electrodes. Lactate was measured with an ampero- seventy-eight patients with liver cirrhosis were identifed metric electrode. as eligible for inclusion. Te control group of 178 criti- cally ill patients without acute or chronic liver disease Acid–base analysis was selected by propensity score matching (PSM). Arterial concentration of bicarbonate (HCO3−) was cal- On admission, Simplifed Acute Physiology Score II culated from measured pH and PaCO2 values according (SAPS II) [17], SOFA [18], infections and organ dysfunc- to the Henderson–Hasselbalch equation [24, 25]. Base tions were documented. excess (BE) was calculated according to the formulae by All patients were screened for the presence of acute Siggaard-Andersen [24–26]. kidney injury (AKI) defned by urine output and serum Quantitative physical–chemical analysis was per- creatinine according to the Kidney Disease: Improving formed using Stewart’s biophysical methods [27], modi- Global Outcomes (KDIGO) Clinical Practice Guidelines fed by Figge and colleagues [28]. for Acute Kidney Injury [19]. Apparent strong ion diference (SIDa) was calculated: Te presence of liver cirrhosis was defned by a combi- SIDa = Na+ + K+ + 2 × Mg2+ + 2 × Ca2+ − Cl− − lactate nation of characteristic clinical (ascites, caput medusae, (SIDa in mEq/l; all concentrations in mmol/l) spider angiomata, etc.), laboratory and radiological fnd- ings (typical morphological changes of the liver, sings of Efective strong ion diference (SIDe) was calculated in portal hypertension, etc., in ultrasonography or computed order to account for the role of weak acids [29]: PaCO SIDe = 1000 × 2.46 × 10−11 × 2 + Alb × (0.123 × pH − 0.631) + Pi × (0.309 × pH − 0.469) 10−pH SIDe in mEq/l; PaCO2 in mmHg, Alb in g/l and Pi in mmol/l Drolz et al. Ann. Intensive Care (2018) 8:48 Page 3 of 12 Te efect of unmeasured charges was quantifed by the operating curve (ROC) analysis was performed, and the strong ion gap (SIG) [30]: area under the ROC curve (AUROC) was calculated to SIG = SIDa − SIDe evaluate the prognostic value of diferent metric vari- (all parameters in mEq/l) ables. Impact of acid–base disorders on mortality was assessed using Cox regression. A p value < 0.05 is consid- Based on the concept that BE can be altered by plasma ered statistically signifcant. Statistical analysis was con- dilution/concentration refected by sodium concentra- ducted using IBM SPSS
Load more

Recommended publications
  • Clinical Versus Laboratory for Estimating of Dehydration Severity
    Clinical versus laboratory for estimating of dehydration severity Majid Malaki Pediatric Health Research Center, Tabriz Medical University, Tabriz, Iran ABSTRACT Background: Acute gastroenteritis is a common cause of dehydration and precise estimation of dehydration Materials and Methods: D is a vital matter for clinical decisions. We try to find how much clinically diagnosed scales are compatible with ORIGINAL ARTICLE laboratory tests measures. uring 2 years 95 infants and children aged between 2 and 108 months entered to emergency room with acute gastroenteritis. They were categorized as mild, moderate and severe dehydration, their recorded laboratory tests include blood urea nitrogen (BUN), creatinine, venous blood gases values were expressedP by means ±95% of confidence intervalResult and compared by mann-whitney test in each groups with SPSS 16, sensitivity, specificity and likelihood ratio measured for defined cut off values in severe dehydration group, value less than 0.05 was significant. : Severe dehydration includes 3% Conclusionof all hospitalization: R due to dehydration. Laboratory tests cannot differentiate mild to moderate dehydration definietly but this difference is significant between severe to mild and severe to moderate dehydration. outine laboratory test are not generally helpful for dehydration severity estimation but they can be discriminate severe from mild or moderate dehydration exclusively. Creatinine higher than 0.9 mg/dl and BaseKey words deficit: beyond-16A are specific (90%) for severe dehydration estimation
    [Show full text]
  • Severe Metabolic Acidosis in a Patient with an Extreme Hyperglycaemic Hyperosmolar State: How to Manage? Marloes B
    Clinical Case Reports and Reviews Case Study ISSN: 2059-0393 Severe metabolic acidosis in a patient with an extreme hyperglycaemic hyperosmolar state: how to manage? Marloes B. Haak, Susanne van Santen and Johannes G. van der Hoeven* Department of Intensive Care Medicine, Radboud University Medical Center, Nijmegen, the Netherlands Abstract Hyperglycaemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are often accompanied by severe metabolic and electrolyte disorders. Analysis and treatment of these disorders can be challenging for clinicians. In this paper, we aimed to discuss the most important steps and pitfalls in analyzing and treating a case with extreme metabolic disarrangements as a consequence of an HHS. Electrolyte disturbances due to fluid shifts and water deficits may result in potentially dangerous hypernatriema and hyperosmolality. In addition, acid-base disorders often co-occur and several approaches have been advocated to assess the acid-base disorder by integration of the principles of mass balance and electroneutrality. Based on the case vignette, four explanatory methods are discussed: the traditional bicarbonate-centered method of Henderson-Hasselbalch, the strong ion model of Stewart, and its modifications ‘Stewart at the bedside’ by Magder and the simplified Fencl-Stewart approach. The four methods were compared and tested for their bedside usefulness. All approaches gave good insight in the metabolic disarrangements of the presented case. However, we found the traditional method of Henderson-Hasselbalch and ‘Stewart at the bedside’ by Magder most explanatory and practical to guide treatment of the electrolyte disturbances and in exploring the acid-base disorder of the presented case. Introduction This is accompanied by changes in pCO2 and bicarbonate (HCO₃ ) levels, depending on the cause of the acid-base disorder.
    [Show full text]
  • Study on Acid-Base Balance Disorders and the Relationship
    ArchiveNephro-Urol of Mon SID. 2020 May; 12(2):e103567. doi: 10.5812/numonthly.103567. Published online 2020 May 23. Research Article Study on Acid-Base Balance Disorders and the Relationship Between Its Parameters and Creatinine Clearance in Patients with Chronic Renal Failure Tran Pham Van 1, *, Thang Le Viet 2, Minh Hoang Thi 1, Lan Dam Thi Phuong 1, Hang Ho Thi 1, Binh Pham Thai 3, Giang Nguyen Thi Quynh 3, Diep Nong Van 4, Sang Vuong Dai 5 and Hop Vu Minh 1 1Biochemistry Department, Military Hospital 103, Hanoi, Vietnam 2Nephrology and Hemodialysis Department, Military Hospital 103, Hanoi, Vietnam 3National Hospital of Endocrinology, Hanoi, Vietnam 4Biochemistry Department, Backan Hospital, Vietnam 5Biochemistry Department, Thanh Nhan Hospital, Hanoi, Vietnam *Corresponding author: Biochemistry Department, Military Hospital 103, Hanoi, Vietnam. Email: [email protected] Received 2020 May 09; Accepted 2020 May 09. Abstract Objectives: We aimed to determine the parameters of acid-base balance in patients with chronic renal failure (CRF) and the rela- tionship between the parameters evaluating acid-base balance and creatinine clearance. Methods: The current cross-sectional study was conducted on 300 patients with CRF (180 males and 120 females). Clinical examina- tion and blood tests by taking an arterial blood sample for blood gas measurement as well as venous blood for biochemical tests to select study participants were performed. Results: Patients with CRF in the metabolic acidosis group accounted for 74%, other types of disorders were less common. The average pH, PCO2, HCO3, tCO2 and BE of the patient group were 7.35 ± 0.09, 34.28 ± 6.92 mmHg, 20.18 ± 6.06 mmol/L, 21.47 ± 6.48 mmHg and -4.72 ± 6.61 mmol/L respectively.
    [Show full text]
  • A Practical Approach to Acid-Base Balance for Small Animal Practitioners
    A PRACTICAL APPROACH TO ACID-BASE BALANCE FOR SMALL ANIMAL PRACTITIONERS IVMA CE Self-Study Offering Dr Nicola Parry, DipACVP Midwest Veterinary Pathology, LLC Lafayette, IN AIM OF THIS ARTICLE Acid-base balance (ABB) is a convoluted concept that requires detailed comprehension of the metabolic pathways used to eliminate the H+ ion from the body. Not surprisingly, many practitioners find it daunting to retain the key concepts and apply them in a meaningful way clinical practice. This article aims to review some of the major points about ABB, and to provide a stepwise approach to evaluating laboratory data in order to identify key aspects of acid-base disorders. Although the chemical/biochemical basis of ABB is important, this article aims to share a practical and more factual, informal approach to the subject that will hopefully appeal to the majority of practitioners. Readers who crave extensive derivations of the Henderson-Hasselbalch equation are welcome to revisit their dusty textbooks for increased levels of excitement! LEARNING OBJECTIVES Following completion of this continuing education article, you will be able to: Indicate whether the pH level indicates acidosis or alkalosis List major sources of acids in the body Identify the major chemical buffer systems in the body Identify the cause of the pH imbalance as either respiratory or metabolic Distinguish between acidosis and alkalosis resulting from respiratory and metabolic factors Describe the importance of respiratory and renal compensations to ABB Determine if there is any compensation for the acid-base imbalance Identify the causes of high anion gap metabolic acidosis Use a systematic, step-by-step approach to diagnose acid-base disorders from laboratory data SO WHAT IS ABB & WHY DO WE CARE ABOUT IT? ABB is fundamental to physiologic homeostasis and refers to the way in which the body maintains a relatively constant pH despite continuous production of metabolic end products.
    [Show full text]
  • BLOOD GAS ANALYSIS Deorari , AIIMS 2008
    Deorari , AIIMS 2008 BLOOD GAS ANALYSIS Deorari , AIIMS 2008 Contents 1. Introduction, indications and sources of errors 2. Terminology and normal arterial blood gases 3. Understanding the print outs 4. Details about (i) pH (ii) Oxygenation, oxygen saturation, oxygen content, alveolar gas equation, indices of oxygenation (iii) Carbon dioxide transport, Pco2 total CO2 content, and bicarbonate levels (iv) Base excess and buffer base 5. Simple and mixed disorders 6. Compensation mechanisms 7. Anion Gap 8. Approach to arterial blood gases and exercises 9. Arterial blood gases decision tree 10. Practical tips for sampling for ABG. 2 Deorari , AIIMS 2008 Abbreviations ABE Actual base excess ABG Arterial blood gas AaDO2 Alveolar to arterial oxygen gradient Baro/PB Barometric pressure BB Buffer base BE Base excess BEecf Base excess in extracellular fluid BPD Bronchopulmonary dysplasia CH+ Concentration of hydrogen ion CO2 Carbon dioxide ECMO Extra corporeal membrane oxygenation FiO2 Fraction of inspired oxygen HCO3 Bicarbonate H2CO3 Carbonic acid MAP Mean airway pressure O2CT Oxygen content of blood PaCO2 Partial pressure of carbon dioxide in arterial blood PaO2 Partial pressure of oxygen in arterial blood pAO2 Partial pressure of oxygen in alveoli pH2O Water vapour pressure PPHN Persistent pulmonary hypertension in newborn RBC Red blood corpuscles 3 Deorari , AIIMS 2008 RQ Respiratory quotient Sat Saturation SBE Standard base excess - St HCO 3/SBC Standard bicarbonate TCO2 Total carbon dioxide content of blood THbA Total haemoglobin concentration UAC Umbilical artery catheter 4 Deorari , AIIMS 2008 The terminology of arterial blood gas (ABG) is complex and confusing. It is made worse by the printouts generated by recent microprocessors.
    [Show full text]
  • Lab Dept: Chemistry Test Name: VENOUS BLOOD GAS (VBG)
    Lab Dept: Chemistry Test Name: VENOUS BLOOD GAS (VBG) General Information Lab Order Codes: VBG Synonyms: Venous blood gas CPT Codes: 82803 - Gases, blood, any combination of pH, pCO2, pO2, CO2, HCO3 (including calculated O2 saturation) Test Includes: VpH (no units), VpCO2 and VpO2 measured in mmHg, VsO2 and VO2AD measured in %, HCO3 and BE measured in mmol/L, Temperature (degrees C) and ST (specimen type) Logistics Test Indications: Useful for evaluating oxygen and carbon dioxide gas exchange; respiratory function, including hypoxia; and acid/base balance. It is also useful in assessment of asthma; chronic obstructive pulmonary disease and other types of lung disease; embolism, including fat embolism; and coronary artery disease. Lab Testing Sections: Chemistry Phone Numbers: MIN Lab: 612-813-6280 STP Lab: 651-220-6550 Test Availability: Daily, 24 hours Turnaround Time: 30 minutes Special Instructions: See Collection and Patient Preparation Specimen Specimen Type: Whole blood Container: Preferred: Sims Portex® syringe (PB151) or Smooth-E syringe (956- 463) Draw Volume: 0.4 mL (Minimum: 0.2 mL) blood Note: Submission of 0.2 mL of blood does not allow for repeat analysis. Processed Volume: 0.2 mL blood per analysis Collection: Avoid using a tourniquet. Anaerobically collect blood into a heparinized blood gas syringe (See Container. Once the puncture has been performed or the line specimen drawn, immediately remove all air from the syringe. Remove the needle, cap tightly and gently mix. Do not expose the specimen to air. Forward the specimen immediately at ambient temperature. Specimens cannot be stored. Note: When drawing from an indwelling catheter, the line must be thoroughly flushed with blood before drawing the sample.
    [Show full text]
  • Postconditioning in Major Vascular Surgery: Prevention of Renal Failure
    Aranyi et al. Journal of Translational Medicine (2015) 13:21 DOI 10.1186/s12967-014-0379-7 RESEARCH Open Access Postconditioning in major vascular surgery: prevention of renal failure Peter Aranyi1, Zsolt Turoczi1, David Garbaisz1, Gabor Lotz2, Janos Geleji3, Viktor Hegedus1, Zoltan Rakonczay4, Zsolt Balla4, Laszlo Harsanyi1 and Attila Szijarto1* Abstract Background: Postconditioning is a novel reperfusion technique to reduce ischemia-reperfusion injuries. The aim of the study was to investigate this method in an animal model of lower limb revascularization for purpose of preventing postoperative renal failure. Methods: Bilateral lower limb ischemia was induced in male Wistar rats for 3 hours by infrarenal aorta clamping under narcosis. Revascularization was allowed by declamping the aorta. Postconditioning (additional 10 sec reocclusion, 10 sec reperfusion in 6 cycles) was induced at the onset of revascularization. Myocyte injury and renal function changes were assessed 4, 24 and 72 hours postoperatively. Hemodynamic monitoring was performed by invasive arterial blood pressure registering and a kidney surface laser Doppler flowmeter. Results: Muscle viability studies showed no significant improvement with the use of postconditioning in terms of ischemic rhabdomyolysis (4 h: ischemia-reperfusion (IR) group: 42.93 ± 19.20% vs. postconditioned (PostC) group: 43.27 ± 27.13%). At the same time, renal functional laboratory tests and kidney myoglobin immunohistochemistry demonstrated significantly less expressed kidney injury in postconditioned animals (renal failure index: 4 h: IR: 2.37 ± 1.43 mM vs. PostC: 0.92 ± 0.32 mM; 24 h: IR: 1.53 ± 0.45 mM vs. PostC: 0.77 ± 0.34 mM; 72 h: IR: 1.51 ± 0.36 mM vs.
    [Show full text]
  • Life-Threatening Metabolic Alkalosis in Pendred Syndrome
    European Journal of Endocrinology (2011) 165 167–170 ISSN 0804-4643 CASE REPORT Life-threatening metabolic alkalosis in Pendred syndrome Narayanan Kandasamy, Laura Fugazzola1, Mark Evans, Krishna Chatterjee and Fiona Karet2 Institute of Metabolic Science, University of Cambridge, Cambridge, UK, 1Endocrine Unit, Fondazione IRCCS Ca’ Granda, Milan, Italy and 2Department of Medical Genetics and Division of Renal Medicine, University of Cambridge, Cambridge, UK (Correspondence should be addressed to F Karet at Cambridge Institute for Medical Research, Addenbrooke’s Hospital Box 139, Hills Road, Cambridge CB2 0XY, UK; Email: [email protected]) Abstract Introduction: Pendred syndrome, a combination of sensorineural deafness, impaired organification of iodide in the thyroid and goitre, results from biallelic defects in pendrin (encoded by SLC26A4), which transports chloride and iodide in the inner ear and thyroid respectively. Recently, pendrin has also been identified in the kidneys, where it is found in the apical plasma membrane of non-a-type intercalated cells of the cortical collecting duct. Here, it functions as a chloride–bicarbonate exchanger, capable of secreting bicarbonate into the urine. Despite this function, patients with Pendred syndrome have not been reported to develop any significant acid–base disturbances, except a single previous reported case of metabolic alkalosis in the context of Pendred syndrome in a child started on a diuretic. Case report: We describe a 46-year-old female with sensorineural deafness and hypothyroidism, who presented with severe hypokalaemic metabolic alkalosis during inter-current illnesses on two occasions, and who was found to be homozygous for a loss-of-function mutation (V138F) in SLC26A4. Her acid–base status and electrolytes were unremarkable when she was well.
    [Show full text]
  • A Case-Based Approach to Acid-Base Disorders
    A Case-Based Approach to Acid-Base Disorders Justin Muir, PharmD Clinical Pharmacy Manager, Medical ICU NewYork-Presbyterian Hospital Columbia University Irving Medical Center [email protected] Disclosures None Objectives At the completion of this activity, pharmacists will be able to: 1. Describe acid-base physiology and disease states that lead to acid-base disorders. 2. Demonstrate a step-wise approach to interpretation of acid-base disorders and compensatory states. 3. Analyze contemporary literature regarding the use of sodium bicarbonate in metabolic acidosis. At the completion of this activity, pharmacy technicians will be able to: 1. Explain the importance of acid-base balance. 2. List the acid-base disorders seen in clinical practice. 3. Identify potential therapies used to treat acid-base disorders. Case A 51 year old man with history of erosive esophagitis, diabetes mellitus, chronic pancreatitis, and bipolar disorder is admitted with several days of severe nausea, vomiting, and abdominal pain. 135 87 31 pH 7.46 / pCO 29 / pO 81 861 2 2 BE -3.8 / HCO - 18 / SaO 96 5.6 20 0.9 3 2 • What additional data should be obtained? • What acid base disturbance(s) is/are present? Introduction • Acid base status is tightly regulated to maintain normal biochemical reactions and organ function • Body uses multiple mechanisms to maintain homeostasis • Abnormalities are extremely common in hospitalized patients with a higher incidence in critically ill with more complex pictures • A standard approach to analysis can help guide diagnosis and treatment Important acid-base determinants Blood gas generally includes at least: Normal range Measurement Description (arterial blood) pH -log [H+] 7.35-7.45 pCO2 partial pressure of dissolved CO2 35-45 mmHg pO2 partial pressure of dissolved O2 80-100 mmHg Base excess calculated measure of metabolic acid/base deviation from normal -3 to +3 SO2 calculated measure of Hgb O2 saturation based on pO2 95-100% - HCO3 calculated measure based on relationship of pH and pCO2 22-26 mEq/L Haber RJ.
    [Show full text]
  • ACS/ASE Medical Student Core Curriculum Acid-Base Balance
    ACS/ASE Medical Student Core Curriculum Acid-Base Balance ACID-BASE BALANCE Epidemiology/Pathophysiology Understanding the physiology of acid-base homeostasis is important to the surgeon. The two acid-base buffer systems in the human body are the metabolic system (kidneys) and the respiratory system (lungs). The simultaneous equilibrium reactions that take place to maintain normal acid-base balance are: H" HCO* ↔ H CO ↔ H O l CO g To classify the type of disturbance, a blood gas (preferably arterial) and basic metabolic panel must be obtained. A basic understanding of normal acid-base buffer physiology is required to understand alterations in these labs. The normal pH of human blood is 7.40 (7.35-7.45). This number is tightly regulated by the two buffer systems mentioned above. The lungs contain carbonic anhydrase which is capable of converting carbonic acid to water and CO2. The respiratory response results in an alteration to ventilation which allows acid to be retained or expelled as CO2. Therefore, bradypnea will result in respiratory acidosis while tachypnea will result in respiratory alkalosis. The respiratory buffer system is fast acting, resulting in respiratory compensation within 30 minutes and taking approximately 12 to 24 hours to reach equilibrium. The renal metabolic response results in alterations in bicarbonate excretion. This system is more time consuming and can typically takes at least three to five days to reach equilibrium. Five primary classifications of acid-base imbalance: • Metabolic acidosis • Metabolic alkalosis • Respiratory acidosis • Respiratory alkalosis • Mixed acid-base disturbance It is important to remember that more than one of the above processes can be present in a patient at any given time.
    [Show full text]
  • Effects of Perinatal Asphyxia and Myoglobinuria on Development of Acute, Neonatal Renal Failure
    Arch Dis Child: first published as 10.1136/adc.60.10.908 on 1 October 1985. Downloaded from Archives of Disease in Childhood, 1985, 60, 908-912 Effects of perinatal asphyxia and myoglobinuria on development of acute, neonatal renal failure T KOJIMA, T KOBAYASHI, S MATSUZAKI, S IWASE, AND Y KOBAYASHI Department of Paediatrics, Kansai Medical University, Japan SUMMARY Thirty four consecutive neonates with birth asphyxia or respiratory problems were examined in the first week of life to clarify the relation between neonatal myoglobinuria and acute renal failure. Investigations included determination of creatinine clearance, fractional sodium excretion, and N-acetyl-13-D glucosaminidase index as an indicator of tubular injury. The infants' gestational ages ranged from 29 to 41 weeks (mean 36 weeks). Fifteen infants did not have myoglobinuria on the first day of life (group A); myoglobinuria was mild in eight infants (group B) and severe in eleven (group C). Two infants in group B and seven in group C developed acute renal failure (47%). Ten infants in group C (91%) had severe asphyxia, five of whom (45%) also suffered neonatal seizures and intracranial haemorrhage. We suggest that myoglobin derived from muscle breakdown in asphyxiated infants may lead to acute renal failure secondary to a reduction in renal blood flow, or to tubular damage. copyright. Myoglobinuria has been associated with acute renal and six with transient tachypnoea of the newborn. failure.' 2 Although the exact mechanism of the None had a congenital heart disease or congenital renal damage is not well established, nephrotoxicity, renal abnormality. Gestational age, assessed accord- tubular obstruction,' and alterations in renal per- ing to Dubowitz et al,5 ranged from 29 to 41 weeks fusion and vascular resistance2 have been suggested and birthweight ranged from 1480 to 3720 g.
    [Show full text]
  • Hyperglycaemia, Glycosuria and Ketonuria May Not Be Diabetes J Gray, a Bhatti, J M O'donohoe
    The Ulster Medical Journal, Volume 72, No. 1, pp. 48-49, May 2003. Case Report Hyperglycaemia, glycosuria and ketonuria may not be diabetes J Gray, A Bhatti, J M O'Donohoe Accepted 20 November 2002 Diabetic ketoacidosis is a well recognised, tenderness, maximal in the lower abdomen now important, but rare differential diagnosis ofacute with associated guarding and rebound. abdominal pain in children. We report a case A presumptive diagnosis of acute appendicitis highlighting the need for complete assessment of was made and an exploratory laparotomy any child presenting with new-onset glycosuria, undertaken through a lower mid line incision. A ketonuria and hyperglycaemia. Causes other than perforated appendix was found along with pus in diabetes may rarely produce these findings. the peritoneal cavity. Appendicectomy and CASE REPORT A girl aged three years and ten peritoneal lavage were performed. months with a six-hour history ofabdominal pain Postoperative recovery was uneventful, and she and vomiting was referred to the surgical team by was discharged home on the third postoperative a general practitioner. Past medical history day. Subsequent random blood glucose was included a diagnosis of non-specific abdominal normal at 4.6mmol/L. Her HbAlc was normal pain at three years old. There was no significant while islet cell antibodies were negative. At review family history nor recent illness in the family she was well, with no complaints orcomplications. circle. DISCUSSION On examination she was restless and thirsty, but apyrexic. There was no foetor or rash. She had Rarely diabetic ketoacidosis may present with grunting respiration with tachypnoea, but the acute abdominal pain.' As this is an important lungs were clear on auscultation.
    [Show full text]