Az anion gap (rés) szerepe a szepszis diagnózisában
Cikk címe: Az anion gap (rés) szerepe a szepszis diagnózisában
Szerzők: Dr. Kovács Ákos
Intézmények: DRC Balatonfüred Szent István és Szent László Kórház
Évfolyam: XVI. évfolyam
Lapszám: 2017. / 09. lapszám
Oldal: 15-20
Rovat: INFEKCIÓKONTROLL
Alrovat: INFEKCIÓKONTROLL
Absztrakt:
A laktát acidózis a szepszisben jelentkező metabolikus acidózis meghatározó tényezője. A szérum anion rés =[Na + +K + ]–[Cl – +HCO 3 – ] számos vizsgálat tanúsága szerint jól korrelál az emelkedett laktát szinttel szepszisben, és a szepszis korai szakaszában is fölhívhatja a figyel- met fertőző folyamatok jelenlétére, tehát nagyon hasz- nos infektológiai paraméter is, melyet világszerte rutin- szerűen alkalmaznak. Az anion rés emelkedése a szepszisen kívül más, meghatározott kórfolyamatokban is előfordul, ezek elkülönítése a klinikai és laboratóriumi adatok ismeretében lehetséges. A szepszis diagnózisának nincsen egyetlen klinikai vagy laboratóriumi paramétere sem, mely önmagában azt specifikusan és egyértelműen bizonyítja, ezért számos laboratóriumi és klinikai komponens együttléte szükséges a diagnózishoz. A szérum bikarbonát meghatározása vénás vérből ugyanazzal a kémiai panellal együtt történik, amelyben a Na, K és Cl is szerepel, így az anion rés meghatározása kiterjedten, gyorsan és olcsón hozzáférhető. Jelenleg Magyar országon a bikarbonát rutinszerű meghatározása a klinikai gyakorlatban nem történik meg, így az anion rés sem áll rendelkezésre a potenciális szeptikus folyamatok minél korábbi felismerése érdekében. Az anion rés tehát a szeptikus folyamatok gyorsabb felismerését, más paraméterek együttes figyelembe vételével a diagnózis nagyobb biztonságát segíti elő. A szepszis sikeres terápiájának pedig a legfontosabb előfeltétele a mielőbbi diagnózis, ehhez járul hozzá az anion rés általános és kiterjedt használata.
Abstract:
The role of anion gap in the diagnosis of sepsis. Lactic acidosis is a decisive factor of metabolic acidosis in sepsis. The serum anion gap =[Na + +K + ]–[Cl – +HCO 3 – ] correlates well with elevated lactate level in sepsis and it has the potential of drawing attention to infectious pro- cesses present in the early stage of sepsis. It has proven to be a useful parameter for infectious diseases and it is generally used worldwide. Elevated anion gap occurs in various pathologic situations besides sepsis. The sepa- ration of these from each other is possible based on the knowledge of various clinical and laboratory data. There is no one particular clinical or laboratory parameter that proves sepsis specifically by itself therefore one has to combine numerous clinical and lab components in order to make the diagnosis. The determination of serum bicar- bonate from venous blood is provided as part of the same „basic metabolic panel” that includes serum Na, K, Cl so anion gap can be determined routinely quickly and at low cost. At this time no determination of serum bicarbonate from venous blood is generally done in cli- nical practice in Hungary therefore the anion gap is usu- ally not available for early recognition of infectious pro- cesses. The anion gap therefore is a tool also for quicker diagnosis of sepsis and with the consideration of other relevant parameters a higher level of diagnostic certainty can be achieved. The prerequisite of successful treat- ment of sepsis is the earliest possible diagnosis and extensive use of anion gap enhances this goal.
XVI. évfolyam
2017. / 09. lapszám / Október
| Szerző | Intézmény |
|---|---|
| Dr. Kovács Ákos | DRC Balatonfüred Szent István és Szent László Kórház |
[1] Gabow PA: Disorders associated with an altered anion gap, Kidney Int, 1985, 27(2):472.
[2] Rose BD, Post TW: Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York ,2001, p.583.
[3] Emmett M, Narins RG: Clinical use of the anion gap, Medicine (Baltimore), 1977, 56(1):38.
[4] Narins RG, Emmett M: Simple and mixed acid-base disorders: a practical approach, Medicine (Baltimore), 1980, 59(3):161.
[5] Kraut JA, Madias NE: Serum anion gap: its uses and limitations in clinical medicine, Clin J Am Soc Nephrol, 2007, 2(1):162.
[6] Feldman M, Soni N, Dickson B: Influence of hypoalbu- minemia or hyperalbuminemia on the serum anion gap, J Lab Clin Med, 2005, 146(6):317.
[7] Adeva-Andany M, López-Ojén M, Funcasta-Calderón R, Ameneiros-Rodríguez E, Donapetry-García C, Vila- Altesor M, Rodríguez-Seijas : Comprehensive review on lactate metabolism in human health, J. Mitochondrion, 2014, 17:76.
[8] Kreisberg RA: Lactate homeostasis and lactic acidosis, Ann Intern Med, 1980, 92(2 Pt 1):227.
[9] Madias NE: Lactic acidosis. Kidney Int. 1986;29(3):752.
[10] Arieff AI, Park R, Leach WJ, Lazarowitz VC: Patho – physiology of experimental lactic acidosis in dogs, Am J Physiol, 1980, 239(2):F135.
[11] Arieff AI, Graf H: Pathophysiology of type A hypoxic lactic acidosis in dogs, Am J Physiol, 1987, 253(3 Pt 1):E271.
[12] Luchette FA, Jenkins WA, Friend LA, Su C, Fischer JE, James JH: Hypoxia is not the sole cause of lactate pro- duction during shock, J Trauma, 2002, Mar;52(3):415-9
[13] Levy B: Lactate and shock state: the metabolic view. Curr Opin Crit Care. 2006 Aug;12(4):315-21.
[14] Weil MH, Afifi AA: Experimental and clinical studies on lactate and pyruvate as indicators of the severity of acute circulatory failure (shock), Circulation, 1970, 41(6):989.[15] Kam PC, Cardone D: Propofol infusion syndrome, Anaesthesia, 2007, 62(7):690.
[16] Velez JC, Janech MG: A case of lactic acidosis induced by linezolid, Nat Rev Nephrol, 2010, Apr;6(4):236-42.
[17] Cope TE, McFarland R, Schaefer A: Rapid-onset, line- zolid-induced lactic acidosis in MELAS, Mitochond – rion,2011, Nov;11(6):992-3. Epub, 2011, Sep 1.
[18] Wallia R, Greenberg A, Piraino B, Mitro R, Puschett JB: Serum electrolyte patterns in end-stage renal disease, Am J Kidney Dis, 1986, 8(2):98.
[19] Widmer B, Gerhardt RE, Harrington JT, Cohen JJ: Serum electrolyte and acid base composition. The influ- ence of graded degrees of chronic renal failure, Arch Intern Med, 1979, 139(10):1099.
[20] Fernandez PC, Cohen RM, Feldman GM: The concept of bicarbonate distribution space: the crucial role of body buffers, Kidney Int, 1989, 36(5):747. 21.
[21] Gabow PA: Disorders associated with an altered anion gap, Kidney Int, 1985, 27(2):472.
[22] Murray T, Long W, Narins RG: Multiple myeloma and the anion gap, N Engl J Med, 1975, 292(11):574.
[23] Salem MM, Mujais SK: Gaps in the anion gap, Arch Intern Med, 1992, 152(8):1625.
[24] Oh MS, Carroll HJ, Goldstein DA, Fein IA: Hyperchlo – remic acidosis during the recovery phase of diabetic ketosis, Ann Intern Med, 1978, 89(6):925.
[25] Orringer CE, Eustace JC, Wunsch CD, Gardner LB: Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not asso- ciated with hyperkalemia, N Engl J Med, 1977, 297 (15): 796.
[26] Madias NE, Homer SM, Johns CA, Cohen JJ: Hypo – chloremia as a consequence of anion gap metabolic aci- dosis, J Lab Clin Med, 1984, 104(1):15.
[27] Adrogué HJ, Eknoyan G, Suki WK: Diabetic ketoacido- sis: role of the kidney in the acid-base homeostasis re- evaluated, Kidney Int, 1984, 25(4):591.
[28] Adrogué HJ, Wilson H, Boyd AE, Suki WN, Eknoyan G: Plasma acid-base patterns in diabetic ketoacidosis, N Engl J Med, 1982, 307(26):1603.
[29] Rose BD, Post TW: Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York 2001, p.583.
[30] Wallia R, Greenberg A, Piraino B, Mitro R, Puschett JB: Serum electrolyte patterns in end-stage renal disease, Am J Kidney Dis, 1986, 8(2):98.
[31] Narins RG, Emmett M: Simple and mixed acid-base disorders: a practical approach, Medicine (Baltimore), 1980, 59(3):161.
[32] Widmer B, Gerhardt RE, Harrington JT, Cohen JJ: Serum electrolyte and acid base composition. The influ- ence of graded degrees of chronic renal failure, Arch Intern Med, 1979, 139(10):1099.
[33] Hakim RM, Lazarus JM: Biochemical parameters in chro- nic renal failure, Am J Kidney Dis, 1988, 11(3):238.
[34] Gabow PA: Disorders associated with an altered anion gap, Kidney Int, 1985, 27(2):472.
[35] Rose BD, Post TW: Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York 2001, p.583.
[36] Murray T, Long W, Narins RG: Multiple myeloma and the anion gap, N Engl J Med, 1975, 292(11):574.
[37] Thatte L, Oster JR, Singer I, Bourgoignie JJ, Fishman LM, Roos BA: Review of the literature: severe hyperp- hosphatemia, Am J Med Sci, 1995, 310(4):167.
[38] Kirschbaum B: The acidosis of exogenous phosphate intoxication, Arch Intern Med, 1998, 158(4):405.
[39] van Hoeven KH, Joseph RE, Gaughan WJ, McBride L, Bilotti E, McNeill A, Schmidt L, Schillen D, Siegel DS: The anion gap and routine serum protein measurements in monoclonal gammopathies, Clin J Am Soc Nephrol, 2011, 6(12):2814.
[40] Paulson WD, Roberts WL, Lurie AA, Koch DD, Butch AW, Aguanno JJ: Wide variation in serum anion gap measurements by chemistry analyzers, Am J Clin Pathol, 1998, Dec;110(6):735-42.
[41] Jurado RL, del Rio C, Nassar G, Navarette J, Pimentel JL: Low anion gap, Jr South Med J, 1998, 91(7):624.
[42] Figge J, Jabor A, Kazda A, Fencl V: Anion gap and hypoalbuminemia, Crit Care Med, 1998, 26(11):1807.
[43] Kelleher SP, Raciti A, Arbeit LA: Reduced or absent serum anion gap as a marker of severe lithium carbonate intoxication, Arch Intern Med, 1986, 146(9):1839.
[44] Kumar A. Crit.Care Med, 2006, 34:1589-1596
[45] Talan,D: Infect.Dis.Clin.N.Am. 22;2008:1-31
[46] Low presenting PCT levels should be outweighed by hig- her absolute risk for adverse outcomes, Swiss Med Wkly, 2009, Jun 13; 139 (23-24): 318-26)
[47] Gattas DJ., Cook DJ: Procalcitonin as a diagnostic test for sepsis: Health technology assessment in the ICU, Journal of Critical Care Volume 18, Issue 1, March 2003, Pages 52-58
[48] Tang BMP, Eslick GD, Craig JC, McLean AS: Accuracy of procalcitonin for sepsis diagnosis in critically ill pati- ents: systematic review and meta-analysis, The Lancet Infectious Diseases Volume 7, Issue3, March 2007, Pages 210-217
[49] Berkman M, Ufberg J, Nathanson L, Shapiro N: Anion gap as a screening tool for elevated lactate in patients with increased risk of developing sepsis in the room, J of Emerg Med, 2009, 36: 391-94.