A parameter with ability to establish the diagnosis of acute appendicitis has always been a center of attention for physicians. Many different parameters have been examined or are under active investigation for that purpose. The pathophysiology of acute appendicitis is characterized by the mucosal ischemia of the appendix that results from ongoing mucus secretion from the appendiceal mucosa distal to an obstruction of the lumen, elevating intraluminal and, in turn, venous pressures. Once luminal pressure exceeds 85 mmHg, venules that drain the appendix become thrombosed and, in the setting of continued arteriolar in flow, vascular congestion and engorgement of the appendix become manifest . Infection is added to the inflammation of appendicitis.
WBC count is most frequently used to diagnose AA. Several reports have suggested that an elevated WBC count is usually the earliest laboratory measure to indicate inflammation of the appendix, and most patients with AA present with leukocytosis [14, 15]. We found that WBC count was significantly higher in AA. In various studies, the range of sensitivity and specificity of WBC in the diagnosis of AA have been reported 67%- 97.8% and 31.9%-80%, respectively . Similar to the literature, the present study found that the sensitivity and specificity of leukocyte level were 91% and 74%, respectively.
CRP is a sensitive acute phase protein that lacks specificity due to increased levels in all acute inflammatory processes. Its concentration increases with the duration and extent of the inflammation. In a meta-analysis examining the accuracy of CRP level in the diagnosis of AA, Hallan and Asberg found a wide range of sensitivity (40%-99%) and specificity (27%-90%) . Similar to the literature, this study found a sensitivity of 97% and a specificity of 41% for CRP in the diagnosis of acute appendicitis. Among the assessed parameters, CRP had the highest sensitivity and the lowest specificity.
RDW is commonly used to discriminate between microcytic anemia’s due to iron deficiency and those due to thalassemia or hemoglobinopathies . Increased RDW levels are related to impaired erythropoiesis or erythrocyte degradation . The typical reference range spans between 11.6 and 15.5%. Recent studies have demonstrated that higher RDW levels, even within the normal reference range, were associated with unfavorable clinical outcomes in patients with heart failure, coronary artery disease, pulmonary hypertension, diabetes mellitus, and stroke independent of hemoglobin values [8–10, 18, 19]. Furthermore RDW has been studied as a surrogate marker in many pathological conditions such as rheumatoid arthritis, inflammatory bowel disease, colon cancer, and celiac disease [6, 20, 21]. Although the exact pathophysiological basis of this relationship is unclear, chronic inflammation, aging, malnutrition, and anemia are proposed underlying factors in this topic [10, 22].
In a patient with acute pancreatitis, RDW level at the presentation has been reported to be an independent risk factor for mortality . Similarly, RDW level has also been found to be a predictor for mortality in bacteremia and septic shock [11, 13]. An increased RDW level has been reported in these inflammatory and infectious pathologies. Elevated RDW can result from any disease process that causes the premature release of reticulocytes into the circulation. Elevations in RDW have been shown to be associated with elevated inflammatory markers, such as CRP, erythrocyte sedimentation rate, and interleukin 6 [13, 23, 24]. Proinflammatory cytokines of sepsis (tumor necrosis factor A, interleukin 6, and interleukin 1b) have been shown to directly and negatively affect the survival of red blood cells in the circulation, promote deformability of the red blood cell membrane, and suppress erythrocyte maturation. These inflammatory mediators of sepsis can thus lead to newer, larger reticulocytes to enter the peripheral circulation, and thus increase RDW . Unlike the above-mentioned studies, we found a significantly lower, albeit within normal limits, RDW level in patients with acute appendicitis compared with subjects in the control group. This finding may be the result of greater RDW level in chronic inflammatory diseases compared to that in acute conditions. A strong correlation of RDW with inflammatory markers, CRP and sedimentation rate has also been observed [13, 23, 24]. In our study, on the other hand, RDW was not correlated with CRP and leukocyte count.
In conclusion, RDW level was lower in patients with acute appendicitis. No studies in literature have examined RDW level in acute appendicitis before. The magnitude of difference in RDW seen between AA and controls was so slight as to be of no utility in diagnostic testing. We think that further prospective, multicenter studies with a large sample size are needed in this field.