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BLOOD LACTATE AND BODY TEMPERATURE AS INDICATORS OF MULTI ORGAN FAILURE
ASN KISHAN*, BG PONNAPPA**, M PAUL KORATH***, K JAGADEESAN****
*Surgical Registrar (General Surgery); **Surgical Registrar; ***Chief Physician; ****Professor of Surgery, Director; KJ Hospital, 927, PH Road, Chennai - 600 084.
INTRODUCTION
Multiple organ failure (MOF) is a common cause of death in surgical critical care units. MOF means the presence of altered organ function in an ill patient such that homoeostasis cannot be maintained without intervention. Initially it was believed that progressive organ failure was related to uncontrolled infection. Recently it is clear that the noninfectious insults such as trauma, pancreatitis, burns and massive transfusion may produce a syndrome of multiple organ dysfunction clinically indistinguishable from infectious cause. An awareness of the setting of the various problems contributing to the syndrome allows us to predict the possibilities of organ failure and to maintain support to these organs before they fail. Furunaga A et al found that IL-6 and 8 were raised in systemic inflammatory response syndrome (SIRS). [2] Simons RK et al suggested elevated selection levels as markers of MOF. [3] Increase in gastric mucosal hydrogen ion concentration was presumed to be the harbinger of MOF by Nilsen VG et al. [4] One such factor which we have noticed is the rise in blood lactate levels and fall in body temperature, which we propose as indicators to predict forth coming catastrophe of multiple organ failure.
MATERIAL AND METHOD
Thirty six critically injured patients were subjects of this study. They included road traffic accident (RTA) (27), assault (6), and domestic accident (3). Table 1 shows lactate and temperature in patients not proceeding to MOF. The patients were rendered all the necessary emergency care and a baseline data of laboratory values were recorded which included blood lactate level. Body temperature measurements were a routine ICU protocol. All patients were put on parenteral antibiotics at admission itself. Nine patients were intubated and ventilated. Haemodynamic changes were monitored with intra-arterial pressure monitors, CVP and hourly urine output were charted. Peripheral O2 saturation was continuously monitored and where necessary were under taken when essential. Blood lactate was measured once a day. Any patient showing a tendency of drop in temperature was provided thermal blankets.
RESULTS
Twenty four patients were successfully supported and were discharged, and none of them had any features of SIRS or MOF. All these patients had their lactate levels well within normal range (4.5 - 19.8 mg) and over time showed a tendency of staying within the normal range. None of these patients were recorded to have hypothermia at any time. Five patients, all due to RTA and four having endotracheal intubation (ET) and one without ET showed a gradual raise in their blood lactate level compared to the baseline value and were considered to be in SIRS. When this was noticed a review of all the organ systems were done, organ support instituted immediately which included fresh plasma transfusion, and all these patients were successfully resuscitated. Seven patients who progressed from SIRS in spite of organ support ended up with MOF and succumbed to their injury. This was found to be statistically significant according to the student "t" test (p < 0.001) when compared to the other cases. The lactate levels of this group did not show any signs of decline in spite of using the same treatment regimen being used as for SIRS patients. On the other hand temperature showed a trend towards hypothermia. Large differences between rectal and great toe temperatures suggest reduced peripheral blood flow. This temperature gradient is a non-specific monitor.5
Showing lactate and temperature in patients not proceeding to MOFSl. No. Lactate levels at admission (in mg) Maximum lactate levels recorded (in mg) Temperature recorded at peak lactate level 1. 5 8.4 97.8 2. 6.5 6.6 98 3. 6.2 8.3 102 4. 7.8 15.4 104 5. 8.1 17.4 100 6. 6.6 7.3 98.4 7. 5.7 8 97.4 8. 5.5 7.5 97.2 9. 10 19.1 97.6 10. 12.8 29.5 96 11. 4.9 7.1 103.2 12. 6.7 9.2 98.2 13. 15.2 18.2 101.8 14. 8.1 13 100 15. 6.5 12.2 100.6 16. 7.8 10 99 17. 9.3 14 101.1 18. 8.4 9.3 99.2 19. 13 16.7 102.4 20. 10.4 25 96 21. 9.8 15.4 99.2 22. 12.2 26.2 97 23. 5.9 18 99.8 24. 4.6 5.9 97 25. 14.2 26.8 96.6 26. 9.2 20.8 96.6 27. 4.7 15.2 97.2 28. 6 12 97.9 29. 4.7 18.6 100.6
Showing lactate and temperature in MOF patientsSl. No Lactate levels at admission (in mg) Maximum lactate levels recorded (in mg) Temperature recorded at peak lactate level 1. 7.6 20 95.7 2. 18.2 27.3 95.2 3. 18.8 20.4 95.4 4. 16.7 21.8 95 5. 11.1 28.2 95.4 6. 17.7 29 95.2 7. 19.5 31.6 95
CONCLUSION
MOF may be either primary or secondary [6] . Primary arises as a direct result of an insult to the host, which leads to dysfunction because of ischaemic injury and reperfusion injury. Once host inflammatory response has been primed the process gets amplified and is self perpetuating, auto-destructive inflammatory response. Organ dysfunction scoring [7] based on commonly measured laboratory or physiologic parameters are not sensitive enough to detect organ hypoperfusion. Hence we found that lactate levels which rise in tissue hypoxia as a result of hypoperfusion as a good guide to predict MOF early. The body temperature which drops in spite of overwhelming infection because of the inability of the body to mount a counter assault and its inability to meet its normal metabolic requirements in a situation of increased demand also is a useful parameter as per our study.
REFERENCES
1.Bone RC, Ficher CJ Jr, Clemmen TP, et al. Sepsis syndrome. A valid clinical entity. Crit Care Med 1989; 17 : 389.
2.Furunaga AT, Suboi H, et al. Nippon - Kyobu - Geka - Zassni. June, 1996; 44 (6) : 790 (4).
3.Simons RK, Hoyt DB. J Trauma Oct., 1996; 41 (4) : 653-62.
4.Nielsen VG, Tal S, et al. Crit Care Med Aug., 1996; 24 (8) : 1339-44.
5.Cusheiri A, Giles GR, Moosa AR. Essential surgical practice 3rd Ed. Pg. 293.
6.ACCP/SCCM : American college of chest physicians / Society of critical care medicine consensus conference definition for sepsis and organ failure and guideline for the use of innovative therapy in sepsis. Crit Care Med 1992; 20 : 864.
7.Moore FA, Moore EE. Evlving : Concepts in the pathogenesis of post injury multiple organ failure surg. Clin North Am 1995; 75 : 257.
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