Volumen
8 Número 4 Julio - Agosto 1996
Reporte Breve
| Dr. Orlando Tamariz-Cruz Dr. Luis A. Jáuregui F Dr. Raúl González Correspondencia: Vasco De Quiróga 15. Delegación Tlalpan, C.P. 14000. Tel. 573-12-00 Ext. 5021 Fax: 538-94-75 E-Mail: Periop @ Planet. Com.Mx Recibido: Febrero 12, 1996. Aceptado para publicación: Abril 8, 1996. |
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Introducción: La descripción de estos casos clínicos, atendidos en una Unidad de Cuidados Intensivos de un centro de tercer nivel, intenta analizar las diferencias entre la saturación de oxígeno hepática obtenida de manera continua y las variables globales de oxigenación en etapas tempranas de falla orgánica múltiple de pacientes sépticos. Material y métodos: Fueron incluidos un total de dos pacientes sépticos que requirieron corrección quirúrgica. Estudiamos la cinética global y hepática utilizando catéteres de flotación pulmonar, uno colocado en la vena suprahepática derecha y otro en arteria pulmonar. La saturación de oxígeno hepática (ShO2) fue determinada en forma continua utilizando un catéter de flotación de tres lúmenes, recubierto de heparina, que fue introducido por vía yugular interna derecha y bajo control fluoroscópico. Resultados: Un paciente, portador de un absceso de cuello, sobrevivió; el otro paciente, portador de sepsis abdominal, murió. Los valores promedio de ShO2 fueron de 72.7 ± 4% para el paciente sobreviviente y de 59.3 ±13% para el paciente que falleció. El análisis de oxigenación global mostró fenómeno de dependencia patológica de aporte que no modificaba con maniobras terapéuticas en ambos casos. Discusión: Las observaciones aquí presentadas apoyan la necesidad de realizar estudios clínicos controlados, dirigidos a establecer si la alteración de ShO2 determinada en forma continua, puede ser de utilidad como predictor temprano de falla orgánica múltiple.
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Introduction: This clinical cases description done at a medical and surgical intensive care unit in a third level Institute, intends to analyze differences between hepatic oxygen saturation continuous determination and global oxygen derived variables, in early stages of multiple organ failure of septic patients. Material and methods: Two septic patients requiring surgical correction were included. Global and hepatic oxygen kinetics were studied using both flow directed pulmonary artery and right hepatic vein catheters. The hepatic vein oxygen saturation (ShO2) was determined continuously using triple lumen heparin bonded fiber optic catheter, inserted via right internal jugular vein, under fluoroscopic guidance. Results: One patient survived (neck and pharyngeal abscess) and one patient died (abdominal sepsis). The mean Sh02 values were 72.7 ± 4% for the surviving patient and 59.3 ±13 % for the patient who died. Global oxygenation analysis showed transport-dependent oxygen consumption, not modified by the therapeutic maneuvers in both cases. Discussion: The presented observations support the need of a controlled clinical trial, conducted to determine if the affection of ShO2 as detected by continuous determination, may be used as an early MOF predictor.
Palabras clave: Oxigenación esplácnica, enfermedades hepáticas, sepsis, hemodinamia
Key words: Splanchnic oxigenation, hepatic diseases, sepsis, hemodynamics.
For the last two decades, research concerning oxygen kinetics has been intense, and most of the basic and clinical investigations may be synthesized in two main points:
a) identification of the transport-limited oxygen consumption (VO2), and
b) description of the clinical significance of splanchnic oxygen metabolism..
Not disregarding the evidence collected describing and defending the existence of transport (DO) limited VO2, recent studies consider that initial results are explained by "mathematical coupling". observing lack of concordance between DO2 maintenance above critical level (or correction of transport limited VO2), and clinical outcome.
With reference to splachnic oxygen metabolism, the most important finding may be the identification of gastrointestinal tract and liver perfusion compromise (analyzed both by direct or indirect measurements) as the earliest events in the multiple organ failure (MOF) sequence.
Descriptions of the present cases intend to analyze differences between global and liver oxygenation behavior, emphasizing the clinical correlation, in two septic patients.
CASE 1
A previously healthy 40 year-old male was admitted for a 7 day history of dental pain, sore throat, hyperthermia and dysphagia. Oral cavity examination showed purulent gingival exudates and important edema, which almost occluded the pharynx.
Vital signs obtained at admission showed: temperature 39 °C, heart rate 115 bpm, blood pressure 80/40 mmHg.
The following relevant laboratory values were obtained: hemoglobin 12.7 mg/dl, hematocrit 39.1%, leukocytes 25 000, neutrophiles 70% and bands 15%. Liver and renal function tests were normal. Arterial blood gases (BG) determination revealed a bicarbonate concentration (HCO3) of 7.3 mmol/L, base excess (BE) -12.1 mmol/L, PaO2 90 mmHg and pH 7.2.
Chest X-ray revealed no abnormalities, and neck X-ray analysis showed gas and volume enlargement of soft tissues.
The latter clinical and laboratory findings were consistent with neck and pharyngeal abscesses.
Considering the previous description, initial management was instituted, positioning a flow directed pulmonary artery catheter (PAC) and using colloids and crystaIloids.
The PAC derived measurements and their final modification according therapeutic maneuvers are shown in Table 1.
TABLE 1 |
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|
CI |
PCW |
DO2 |
VO2 |
EO2 |
SvO2 |
ShO2 |
BE |
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1 |
2 |
1 |
2 |
1 |
2 |
1 |
2 |
1 |
2 |
1 |
2 |
1 |
2 |
1 |
2 |
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Basal |
3,57 |
3.2 |
3 |
1 |
618 |
512 |
113 |
71 |
32 |
37 |
70 |
62 |
70.8 |
46.1 |
12.1 |
15.4 |
VR |
3.9 |
3.59 |
14 |
16 |
622 |
580 |
129 |
112 |
28 |
35 |
71 |
65 |
71.0 |
65.0 |
11.8 |
12.2 |
Dob |
5.6 ± 1.4 |
3.9 ± 2.1 |
114 ± 2.6 |
155 ± 2.7 |
179 9 ± 181 |
639 ± 150 |
177 ± 55.8 |
135 ± 44.1 |
19.7 ± 10.7 |
26.8 ± 11 |
172.7 ± 4.0 |
77.4 ± 3.5 |
172.7 ± 4 |
59.3 ± 12.9 |
4.7 |
13.1 |
Dobutamine corresponding data are a mean (± SD) of 6 days measurements for patient I and of 3 days for Patient 2. |
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After fluid repletion, only a slight modification of BG, hemodynamic parameters and oxygenation determinants was observed, deciding dobutamine infusion at an initial rate of 5 µg/kg/min, obtaining the results enlisted in Table 1.
Along with the previously described management, antibiotic scheme was instituted with concomitant surgical drainage, observing progressive correction of all hemodynamic and laboratory abnormalities. The patient was transferred to a hospital ward after 7 days permanence in the ICU.
CASE 2
A 42 year-old previously healthy male was admitted for a 4 day history of abdominal tenderness and distention, hyperthermia, nausea and vomiting. The physical examination showed important abdominal distention, absence of intestinal sounds and peritoneal irritation signs.
Laboratory evaluation showed hemoglobin 11.7 mg/dl, hematocrit 38.1%, leukocytes 32 000, 72 neutrophiles and 13 bands. BG analysis showed PaO2 73 mmHg, BE -15.4 mmol/L, pH 7.25 and HCO3 12.4 mmol/L, concordant with metabolic acidosis.
Vital signs evaluation showed heart rate 120 bpm, temperature 38.7 *C, blood pressure 60/40 mmHg and central venous pressure 2 cc H2O.
With this clinical picture, hemodynamic monitoring using PAC was decided obtaining the basal measurements described in Table 1.
Fluid reposition using crystaIloids and colloids was determined and later, dobutamine infusion (10 µg/kg/min) was initiated.
Radiographic evaluation demonstrated free intraabdominal air, and surgical exploration was indicated.
Surgical findings were consistent with perforated appendix, periapendicular abscess and peritonitis.
Even when the patient had surgical correction, specific antibiotic scheme and inotropic support, progressive deterioration was observed, developing multiple organ failure, and finally died.
Hemodinamic Pattern and Global Oxigenation Kinetics
Initial hemodynamic measurements in both patients denoted hyperdynamic state, with a mean basal cardiac index of 3.57 L/min/m2 and 3.2 L/min/m2 for patients 1 and 2 respectively. Basal pulmonary capillary wedge pressure (PCW) was 3 and 1 mmHg for patients 1 and 2, and volume repletion was initiated using crystaIloids and colloids.
Correction of PCW pressures was obtained, but only a slight hemodynamic improvement was achieved, with no clear clinical impact (Table 1).
Compared to basal values, DO2 was increased after fluid repletion, observing a concomitant VO2 increment in both patients. The latter finding suggested transport limited VO2, and a plateau was expected if further DO2 optimization, deciding dobutamine infusion. Nevertheless, even when DO2 was increased, no VO2 independence was observed (Table 1).
Concerning mixed venous oxygen saturation (SVO2), a clear improvement was observed in patient 2 and no changes were observed in patient 1, after therapeutic maneuvers.
Hepatic Monitoring
In both cases, continuous hepatic vein oxygen saturation monitoring was established, according a technique described elsewhere; briefly: via right internal jugular vein and under fluoroscopic guidance, a radiopaque, triple lumen, heparin bonded fiberoptic catheter (Opticath, Abbott Labs., Chicago, IM. , USA ) was inserted. When right hepatic vein was reached, a blood sample was taken in order to corroborate the optic fiber calibration. The catheter was connected to an oxymeter (Oxymetrix 3, Abbott Labs., Chicago , Ill. , USA ) and the right hepatic vein blood oxygen saturation (ShO2) trend was stored in the memory bank of the computer. In addition to the hepatic vein catheter, pulmonary artery and radial artery catheters were placed.
For patient 1, the ShO2 value was a result of 6 days accumulate continuous measurements showing a mean of 72.7 ± 4 %, a value clearly higher than the one obtained for patient two (59.3 ± 13%; mean of 3 days accumulates continuous measurements).
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Mortality associated to MOF in septic patients remains high and most research focusing global oxygen derived variables optimization has been done in order to modify such tendency.
Some reports consider that optimization of critical DO2 level, with the associated correction of transport dependent VO2, might reduce MOF associated mortality. Nevertheless, the latter findings are not consistent when conventional therapeutic manipulations are used (e.g. fluid administration or blood transfusion).
On the other hand, dobutamine infusion has been described as a mechanism to reach VO2 independence in the septic population, but in our two cases, even after inotropic infusion, no VO2 independence was observed. Furthermore, for the second patient, pharmacological manipulation was not capable to improve the perfusion compromise, evidenced by persistent high BE levels.
In this two cases, a DO2 level much higher than the one previously reported by us and other authors as critical for high risk surgical patients and for septic population was reached. This situation is coincident with previous descriptions concerning the nonexistence of transport-limited VO2, suggesting also that persistence of a suboptimal global DO2 during sepsis, might not be relevant as early MOF predictor.
Concerning SVO2, much information has been generated describing it as a perfusion adequacy monitor, but recent evidence obtained from postoperative cardiac patients, suggests low reliability of SVO2 P specially for regional (cerebral) perfusion compromise detection.
Similar evidence, suggesting low SVO2 reliability as global or regional flow compromise monitor, has been recently obtained in septic population and in the two patients here described, SVO2 behavior is coincident with the latter descriptions, observing that even in presence of optimal SVO2 values, adverse outcome developed for patient two.
On the other hand, promising results concerning splanchnic perfusion compromise detection and correction, not only in septic, but in other groups of patients (e.g. postoperative cardiac and trauma patients), have been reached.
Work done by Steffes et al. in septic population suggests that even before gastrointestinal compromise, hepatic perfusion mismatch may exist, and this differences support the possible efficacy of continuous ShO2 determination as early MOF predictor.
Similar evidence has been obtained in other clinical conditions which share systemic inflammatory response as common initial pattern with the septic phenomenon (e.g. hepatic surgery). In Kainuma's report, persistence of a low ShO2 value appears as a liver failure predictor. Since liver might be more susceptible to ischemia during sepsis, and considering hepatic failure has been postulated as one of the initial precursors (if not the absolute initial precursor) of MOF, the ShO2 continuous determination during sepsis might be a monitoring alternative, adequate for an early MOF detection.
The important role of hepatic regulatory mechanisms of splachnic: hemodynamics has recently been described. This experimental report shows how changes in portal venous distensibility and closing pressure, generate splanchnic blood pooling in a liver isolated model. Similar studies done during endotoxemia also find the latter hemodynamic alterations, describing associated histologic changes (focal necrosis and hemorrhage). Portal distensibility changes might also be the explanation of altered fluidity of liver plasma membrane observed during experimental endotoxemia.
Liver hemodynamics and cellular changes during endotoxemia, may explain the differences between ShO2 determination and global oxygenation variables, observed in this report. Furthermore, we consider low ShO2 mean value during sepsis, might be the first detectable alteration observed in the MOF sequence.
The latter consideration is supported on previous studies which report differences in liver perfusion and tonometric measurements (since tonometry has been described as a reliable early MOF predictor).
A point of criticism to this description might be the absence of lactate determination, in order to analyze it with the rest of the measurements. We accept this deficiency might questions our observations, but several data suggest that even when a majority of septic patients course with a high lactate level, such an elevation not necessarily reflects flow compromise and not always correlates with a specific oxygen kinetics pattern, neither global nor regional.
Finally, we found no evidence of bacterial contamination of hepatic vein catheters. Also we did not find evidence suggesting functional compromise conditioned by hepatic vein catheter permanence; nevertheless, controlled clinical trials are required to define the situation concerning these potential complications.
In summary, we consider controlled studies focusing ShO2 continuous determination are required, in order to validate the potential effectiveness as monitoring aid in septic patients. |