DOCSLIB.ORG

Clinical Versus Laboratory for Estimating of Dehydration Severity

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

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

is a vital matter for clinical decisions. We try to find how much clinically diagnosed scales are compatible with laboratory tests measures. Materials and Methods: During 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 expressed by means ±95% of confidence interval 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, P value less than 0.05 was significant. Result: Severe dehydration includes 3% of all hospitalization 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. Conclusion: Routine 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 Base deficit beyond-16 are specific (90%) for severe dehydration estimation in infant and children.

Key words: Acute gastroenteritis, children, dehydration, laboratory tests

more yield for prediction of dehydration severity[4-5,8,11]

Introduction

Yilmaz et al.[12] find serum Urea and bicarbonate can be predictive for dehydration severity in small children and infants as high risk groups to dehydration and We try to findthatwhatlaboratorytestscanbemorecompatiblefor dehydration estimation compared to clinical estimation that can be helpful for physicians in perplexing cases.

  • Acute gastroenteritis is
  • a
  • common reason of

hospitalization.[1] It seems that precise diagnosis of dehydration severity may be dependent on laboratory tests,[2] many tried to define dehydration severity with clinically guideline.[3-6] Capillary refill time, abnormal skin turgor, and respiratory pattern were suggested as the best signs.[7] All these valuable signs may be neither sensitive nor specific for dehydration severity.[8-9] Clinical dehydration scale (CDS) considers general appearance, eyes changes, mucous membrane moisture and tears existence[10] hospital staying duration can be related to CDS not to laboratory tests (PH and serum bicarbonate) disturbances. With respect to this truth that clinical findings are not sensitive for estimating of dehydration severity solely and importance of laboratory tests results besides to clinical estimation of dehydration grades give

Methods and Materials

95 children aged between 2 and 108 months diagnosed during 48 month from April 2009 to April 2011 as acute gastroenteritis categorized as mild, moderate and severe with standard criteria[13] by a pediatrician at emergency room. After preparation of laboratory results (blood urea nitrogen, creatinine, venous blood gas, electrolytes include sodium, potassium) these documents evaluated and matched with clinical definition for dehydration severity. Information about age, sex, duration of disease and complaints were asked by a pediatrician residence children height and weight recorded beside to vital signs (blood pressure, pulse rate, respiratory rate and temperature), no one of cases received hypnotic and cholinergic drugs. None of patients had previous diseases like as metabolic disease, renal dysfunction, malnutrition or surgical operation, they affected to dehydration due to acute gastroenteritis in recent days.

Access this article online
Website:

www.atmph.org

Quick Response Code:
DOI:

10.4103/1755-6783.109262

Correspondence:

Dr. Majid Malaki, Pediatric Health Research Center, Tabriz Medical University, Tabriz, Iran. E-mail: [email protected]

Annals of Tropical Medicine and Public Health | Nov-Dec 2012 | Vol 5 | Issue 6

559

Malaki: Laboratory tests in dehydration

  • Their tests include urea creatinine electrolytes (sodium
  • (3) The mean ± SD (Minimum, Maximum) of BUN

to creatinine ratio in mild dehydration was 47±16 (28,100) albeit it was not differed significantly related to moderate dehydration 49 ±19, (30,130) (p 0.56). BUN/Cr was higher significantly in severe dehydration 64±36, (34,170) compare to both moderate and mild dehydration (p 0.04) and potassium) venous blood gas (base excess, base, Co2 pressure) weight, height, sex and age of children were also recorded. Serum sodium 135-145 mEq/dl and potassium 3/5-5/5 mEq/dl considered as normal. All results expressed as percent, ratio, means, 95% of confidence interval, minimum and maximum and relation of mentioned laboratory tests in each dehydration severity groups compared by one way ANOVA test and followed by Post-Hoc test of Tukeys test in parametric distribution data for non-parametric ones the mann-whitney test used to compare every two groups individually (mild -moderate), (mild -severe) and (moderate-severe). Four laboratory tests include blood urea nitrogen above 40 mg/dl, creatinine more than 0.9 mg/dl, venous HCO3 below 17 and base deficit beyond to-16 considered as cut off points for severe dehydration and we try to find sensitivity, specificity and positive likelihood ratio(+LR) of these defined values for estimating severe form of dehydration particularly. p was significant if less than 0.05.
(4) The mean ± SD of venous HCO3 level (mEq/L) in mild dehydration was 16±3 it was not significantly differed to moderate dehydration 14.5±4 (P>0.05) but the mean ± SD of HCO3 was different in severe dehydration 10±3 compare to both mild or moderate dehydration forms (P<0.001) [Table 1]. Venous HCO3 measures below 17 mEq/L were observed in 15 out of 29 with mild, 30 out of 43 with moderate and 22 out of 23 patients with severe group (+ LR 1.5 sensitivity 98% specify 38% for severe dehydration form at cut off point of 17 meq/l) [Table 2].

(5) The mean ± SD of Base excess (BE) decreases significantly (P<0.0001) in severe dehydration compared to mild (-17±5 mEq/L vs-8±4) and moderate dehydration (-17±5 vs-10±5). BE average was not differed between mild and moderate (-8±4 vs.-10±5)(p 0.19) [Table 1]. Base excess beyond to -16 mEq/L has not observed with mild dehydration, it happened in 7 out of 43 with moderate and 15 out of 23 patients with severe group. (+ LR 6.5, sensitivity 65%, specificity 90% in severe dehydration form) [Table 2].

Results

95 children means age (Minimum, Maximum), 19 months (2, 108) include 29 children with mild dehydration means age (month) ± SD equal to 27±1.5 months, 43 children with moderate dehydration means age ± SD equal to 15±1 and 23 children with severe form aged 14±5 months.

(1) Average blood urea level ± SD (mg/dl) in mild and moderate were 27±12 and 29±13 these measures were not differed between these two groups (mild and moderate), BUN level in severe form was 49±27 it was higher significantly in severe dehydration compared to mild or moderate dehydration. (P<0.001) [Table 1]. two out of 29 patients with mild, 8 out of 43 with moderate and 11 out of 23 patients with severe dehydration have BUN more than 40 mg/dl (positive LR 3.4, sensitivity %48 specificity 86% for severe form occurrence) [Table 2].

Discussion

Attempts to estimate dehydration severity has been done for a long time but using laboratory tests for accurate dehydration severity was noticed recently.[8,11] Some signs considered as the best tools for dehydration severity.[7] For example losing weight[14] although baseline weights may not be inaccessible and signs like as skin turgor, deep breathing and capillary filling time have some limitations to use for dehydration severity assessment.[7] Urea and bicarbonate level were valuable to predict dehydration severity, serum bicarbonate above 15 can be valuable for mild and moderate dehydration while it occurs infrequently in severe dehydration they consider urea above 100 mg/ dl suggestive for severe dehydration although serum bicarbonate below 18 mEq/L is another index that can be used for severe or moderate dehydration estimation.[15] Another study showed that bicarbonate above 15 mEq/L can occur in 7% of severe dehydration episodes. They suggested urea and bicarbonate level can be helpful beside to clinical findings to estimate
(2) Mean ± SD of creatinine (mg/dl) in mild dehydration was 0.6±0.4 while in moderate grade it was 0.6± 0.1 there is not difference between mild and moderate dehydration for creatinine levels but in severe dehydration creatinine level was 0.9±0.6 it was significantly higher in relation to mild and moderate dehydration (p 0.01) [Table 1]. Creaetinine levels above 0.9 mg /dl observed 1 out of 29 with mild, 5 out of 43 with moderate and 8 out of 23 with severe dehydration group (+ LR 4.3, sensitivity 34%, specificity 92% for severe form) [Table 2].

Annals of Tropical Medicine and Public Health | Nov-Dec 2012 | Vol 5 | Issue 6

560 560

Malaki: Laboratory tests in dehydration

Table 1: Comparison of laboratory tests among three groups of dehydration there is not difference between mild and moderate dehydration but it was significant between severe and moderate /mild forms. (p significant if less than 0.05)

  • Variables Severe
  • Dehydration severity

  • Mild
  • P value

0.59

Moderate

29 13

P value

0.0001*
0.01*

Severe

  • 49 27
  • BUN (mg/dl)
  • 27 12

  • 0.6 0.4
  • Creatinie (mg/dl)

Base deficit (mEq/l) Venous Hco3 (mEq/l) BUN/Cr

  • 0.51
  • 0.6 0.1
  • 0.9 0.6

  • -8
  • 4
  • 0.19
  • -10

16

  • 5
  • 0.0001*

0.0001* 0.047*
-17 10
5

  • 14.5
  • 4
  • 0.06
  • 3
  • 3

  • 47 16
  • 0.56
  • 49 19
  • 64 36

beyond-16 has an acceptable specificity (90%) and the highest likelihood values (+ LR=6.5) compare to other tests. BUN/Cr ratio higher than 20 occur in all patients and it is not a specific test. As our study clinical estimation of dehydration beside to laboratory tests have more informative for management policies and correct diagnosis in difficult situation if we consider the mentioned cut off points for each tests

Table 2: Positive likelihood ratio (+LR), sensitivity and specificity of four laboratory tests blood urea nitrogen (BUN), creatinine, venous HCO3, base deficit for predicting of severe dehydration at defined cut off points

+LR

3.4

  • Sensitivity %
  • Specificity %

  • BUN>40 mg/dl
  • 48

34
86

  • 92
  • Creatinine>0.9

mg/dl
4.3
Venous HCO3<17 Base deficit<-16
1.5 6.5
98 65
38 90

Conclusion

As our study traditionally clinical dehydration severity estimation is simple and cost effective it seems that routine laboratory tests cannot discriminate mild from moderate dehydration. These tests change significantly in severe dehydration the most sensitive test for severe dehydration diagnosis is the venous HCO3 below 17 mEq/L and the most specific test is creatinine higher than 0.9 mg/dl in the situation with base deficit less than-16 the likelihood ratio for severe dehydration is the highest compare to other identified cut off point laboratory tests. dehydration severity they suggest that urea level above 100 mg/dl and bicarbonate below 15 suggestive for severe dehydration and urea below 40 and base above 15 are compatible with mild dehydration.[12] Bonedio et al.[2] and Poole (3) suggest serum urea was not predictive for hydration status of dehydrated children while serum bicarbonate was useful for moderate to severe dehydration estimation. In another study on 97 children with acute dehydration Vega and Avner showed that addition of acidosis (bicarbonate <17 mmol/L) to clinical parameters increased the sensitivity for detecting of serious dehydration.[11]

References

As our study which evaluated serum urea, creatinine, venous base level as HCO3, base deficit and BUN to creatinine ratio in three groups of mild, moderate and severe dehydration, there is not difference in laboratory tests values between mild and moderate dehydration while it was significantly differed among severe dehydration to mild or moderate dehydration in all mentioned parameters (p less than 0.05). To find a cut off point to estimate dehydration severity correctly we found blood urea nitrogen higher than 40 mg/dl is not a sensitive test for diagnosis of severe dehydration condition but its Specificity for severe dehydration is 86%, serum creatinine higher than 0.9 mg/dl was an uncommon finding in mild dehydration but in severe dehydration it was the most specific (92%) finding test. venous base (HCO3) below 17 mEq/L happens in severe dehydration commonly as the most sensitive and the least likelihood ratio test among other tests (sensitivity 98%, +LR=1.5) Table 2. Base deficit

  • 1.
  • Pickering LK, Snyder JD. Gastroenteritis. In: Behrman RE, Kliegman

RM, Arvin AM, editors. Textbook of Pediatric. 16th ed. Philadelphia: WB. Saunders; 2000. p. 765. Bonadio WA, Hennes HH, Machi J, Madagame E. Efficacy of measuring BUN in assessing children with dehydration due to gastroenteritis. Ann Emerg Med 1989;18:755-7. Poole SR. Criteria for measurement of dehydration. Ann Emerg Med 1990;19:730-1. Mackenzie A, Barnes G, Shann F. Clinical signs of dehydration in children. Lancet 1989;2:605-7.

Teach SJ, Yates EW, Feld LG. Laboratory predictors of fluid deficit

in acutely dehydrated children. Clin Pediatr (Phila) 1997;36:395-400. Plata Rueda E, Díaz Cruz G. [Clinical and biochemical evaluation of the degree of dehydration in children with acute diarrhea]. Bol Med Hosp Infant Mex 1974;31:561-76. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated? JAMA 2004;291:2746-54. Gorelick MH, Shaw KN, Baker MD. Effect of ambient temperature on

capillary refill in healthy children. Pediatrics 1993;92:699-702

Baraff LJ. Capillary refill: Is it a useful clinical sign? Pediatrics 1993;92:723-4.
2. 3. 4. 5. 6.

7. 8. 9. 10. Friedman JN, Goldman RD, Srivastava R, Parkin PC. Development of a clinical dehydration scale for use in children between 1 and 36 months of age. J Pediatr 2004;145:201-7

Annals of Tropical Medicine and Public Health | Nov-Dec 2012 | Vol 5 | Issue 6

561

Malaki: Laboratory tests in dehydration

  • 11. Vega RM, Avner JR. A prospective study of the usefulness of clinical
  • children with vomiting, diarrhea, and dehydration. Curr Opin Pediatr

1998;10:461-9
15. Goldman RD, Friedman JN, Parkin PC. Validation of the clinical dehydration scale for children with acute gastroenteritis. Pediatrics 2008;122:545-9 and laboratory parameters for predicting percentage of dehydration in children. Pediatr Emerg Care 1997;13:179-82
12. Yilmaz K, Karaböcüoglu M, Citak A, Uzel N. Evaluation of laboratory tests in dehydrated children with acute gastroenteritis. J Paediatr Child Health 2002;38:226-8.

13. Michael J, Somers G. Clinical assessment of dehydration fluid and

electrolyte therapy in children. In: Avner ED, Harmon WE, Niaudet P, Yoshikawa N, editors. 6th ed., vol. 1, section 2, chap. 13. Berlin, Heidelberg: Springer Verlag; 2009. p. 325-53.

Cite this article as: Malaki M. Clinical versus laboratory for estimating of dehydration severity. Ann Trop Med Public Health 2012;5:559-62.

Source of support: Nil, Conflict of interest: None declared.

14. Liebelt EL. Clinical and laboratory evaluation and management of

Annals of Tropical Medicine and Public Health | Nov-Dec 2012 | Vol 5 | Issue 6

562 562

Copyright of Annals of Tropical Medicine & Public Health is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.

Recommended publications
  • Severe Metabolic Acidosis in a Patient with an Extreme Hyperglycaemic Hyperosmolar State: How to Manage? Marloes B

    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.
  • Study on Acid-Base Balance Disorders and the Relationship

    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.
  • A Practical Approach to Acid-Base Balance for Small Animal Practitioners

    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.
  • BLOOD GAS ANALYSIS Deorari , AIIMS 2008

    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.
  • Lab Dept: Chemistry Test Name: VENOUS BLOOD GAS (VBG)

    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.
  • Postconditioning in Major Vascular Surgery: Prevention of Renal Failure

    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.
  • Life-Threatening Metabolic Alkalosis in Pendred Syndrome

    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.
  • A Case-Based Approach to Acid-Base Disorders

    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.
  • ACS/ASE Medical Student Core Curriculum Acid-Base Balance

    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.
  • Effects of Perinatal Asphyxia and Myoglobinuria on Development of Acute, Neonatal Renal Failure

    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.
  • Hyperglycaemia, Glycosuria and Ketonuria May Not Be Diabetes J Gray, a Bhatti, J M O'donohoe

    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.
  • The ABC's of Acid-Base Balance

    The ABC's of Acid-Base Balance

    JPPT REVIEW ARTICLE The ABC’s of Acid-Base Balance Gordon S. Sacks, PharmD The University of Wisconsin—Madison, Madison, Wisconsin A step-wise systematic approach can be used to determine the etiology and proper management of acid-base disorders. The objectives of this article are to: (1) discuss the physiologic processes in- volved in acid-base disturbances, (2) identify primary and secondary acid-base disturbances based upon arterial blood gas and laboratory measurements, (3) utilize the anion gap for diagnostic pur- poses, and (4) outline a stepwise approach for interpretation and treatment of acid-base disorders. Case studies are used to illustrate the application of the discussed systematic approach. KEYWORDS: acid-base J Pediatr Pharmacol Ther 2004;9:235-42 Although acid-base disorders are frequently terms of H+, but due to confusing terminology it encountered in hospital and ambulatory care set- was proposed to convert H+ terminology to pH.1 tings, they are often considered the most difficult When taking the negative logarithm of the H+ areas to understand in medicine. Misdiagnosis due to common misconceptions of acid-base ho- ABBREVIATIONS: AG, Anion gap; HCO3, Bicarbonate; CNS, meostasis often delays identification of the pri- Central nervous system; ECF, Extracellular fluid; Hgb, Hemoglobin; ICU, Intensive care unit; THAM, Tromethamine mary disorder, causing a disruption in the deliv- ery of appropriate therapy. By understanding the concentration, pH represents a measure of H+ basic principles of acid-base physiology, the inter- activity. Optimal function for tissues and organs pretation of acid-base data, and the mechanisms within the human body depends on maintaining responsible for acid-base perturbations, the clini- blood pH between 7.10 and 7.60.