The place of D-dimer and L-lactate levels in the early diagnosis of acute mesenteric ischemia.
BACKGROUND
Acute mesenteric ischemia (AMI) is an abdominal-vascular emergency which is rare and has high mortality rates (60-80 %) due to late diagnosis (1-3). Although it is known that extravascular reasons like intestinal intussusception, volvulus, strangulated hernias and obstructions can cause intestinal gangrene, these are rarely the cause of AMI (1).


METHODS
In this study, we used male Wistar-Albino rats weighing 250-300 grams obtained from Pamukkale University Experimental Research Laboratory. Animals were exposed to light-dark cycles for 12 hours and had free access to food and water. They were kept in cages for 7 days to stabilise their intestinal flora. In animals of group I, nothing was made other than taking 0.5 ml blood intracardially. In other animals, abdomen was reached with midline laparotomy and superior mesenteric artery (SMA) was located. In group II (operative control group), SMA was isolated and manipulated but was not ligated. In Group III (intestinal ischemia group), SMAwas isolated and ligated with 3/0 silk tie distally to the aorta. After this process, intestinal ischemia was achieved which was confirmed by paleness and pulselessness of intestines, caecum and right colon. Later on, abdomen was closed with double 3/0 polyglactin sutures. At postoperative 1st, 4th and 6th hours 0.5 ml blood was taken intracardially from the animals in groups II and III in order to quantify D-dimer and L-lactate levels.


METHODS
D-dimer: Blood samples which were put into tubes containing sodium citrate, were seperated from plasma with centrifugation at 4000 rpm for 7 minutes.L-lactate: Blood L-lactate levels were determined from blood taken into capillary tubes with the help of immobilised enzyme electrode technology using YSI 1500 Sport portative lactate analyzer (Yellow Springs Instruments Inc., Ohio-USA).
Two cm long intestinal samples were taken from animals in which SMA was ligated in order to achieve mesenteric ischemia and these samples were fixed in 10 % formol.


CONCLUSIONS
As a result, in rats with SMA occlusion serum D-dimer levels were not increased significantly when compared either in the group or with the basal values of the control group and values in operative control group. Therefore, it is concluded that D-dimer is not a useful marker for early diagnosis of AMI. On the other hand, it is revealed that blood L-lactate levels began to increase significantly following 4th hour of mesenteric ischemia and it is shown that this increase continued at the 6th hour. In addition, considering the utmost importance of the early diagnosis in patients with the clinical suspicion of AMI, L-lactate seems to be a suitable marker to use in emergency departments because it is achieved with a portable device that gives fast and accurate results. Nevertheless, our results are need to be supported by clinical studies with larger patient series (Tab. 2, Fig. 11, Ref. 39).
B
B
Aydin
M
M
Ozban
M
M
Serinken
B
B
Kaptanoglu
N C
NC
Demirkan
C
C
Aydin
D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D042241:Early Diagnosis; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism*; D019344:Lactic Acid / Q000378:metabolism*; D008297:Male; D065666:Mesenteric Ischemia / Q000175:diagnosis* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; C036309:fibrin fragment D; D019344:Lactic Acid
D-dimer; L-lactate; acute mesenteric ischemia.