Trends of C-Reactive Protein Laboratory Values with White Blood Cell Count Levels in Maxillofacial Infections

Background

C-Reactive Protein (CRP) is an acute phase inflammatory protein secreted by the liver, involved in the attachment of dead or dying cells and bacterial surface proteins, enhancing phagocytosis by neighboring macrophages through activation of the complement system. In healthy patients, serum CRP is nearly absent. Upon tissue injury or infection, Interleukin-6 and tumor necrosis factor-alpha, induce CRP production in hepatocytes. The CRP blood test is a quantitative marker to monitor inflammation in the body.  Although CRP has high sensitivity to inflammation, it does not have high specificity and thus should be used in conjunction with current standard monitoring protocols, including white blood cell count (WBC), temperature, culture and susceptibility testing, as well as microbiological tissue biopsy. The median concentration of CRP is 0.8 mg/l, but following an acute-phase stimulus, the values may increase from less than 50ug/l to more than 500 mg/l, or 10,000-fold. CRP rises within 4-6 hours and peaks in 24-48 hours, then falls rapidly once the inflammation resolves. This rapid rise and fall of CRP makes it a more sensitive marker to follow than WBC.  Several studies have used CRP testing to indicate the severity of odontogenic infections and the presence of postoperative complications following oral surgery procedures. CRP has not been a commonly used marker when trending the infected maxillofacial surgery patient, but it has been shown to be a good indicator of severe infection and sepsis. 

Purpose

The aim of this study was to trend CRP levels in acute maxillofacial infections admitted to Temple University Hospital from July 2012 to February 2013. Findings were compared to standard markers of inflammation, particularly white blood cell count (WBC) and maximum body temperature within a 24-hour period (Tmax) as well as clinical presentation to determine resolution of infection.

Methods and Analysis:

Over a 9-month period, 18 patients (10 males and 8 females) were followed. Of those, 6 were eliminated based on exclusion criteria. Patients with inflammatory diseases, autoimmune disorders, malignancies, liver failure, hypertension, diabetes, cardiovascular disease, and coronary artery disease were eliminated from the analysis as these conditions can contribute to increased baseline CRP levels. All patients on admission were treated surgically with appropriate incision and drainage with or without usage of drains to facilitate the egress of purulent drainage, and were monitored postoperatively for resolution. All patients received a prophylactic antibiotic regimen most appropriate for each case, as well as appropriate pain control.

Results

Of the 12 patients that met the inclusion criteria, 6 of the of the 12 patients (50%) had maxillofacial infections of odontogenic origin, 5 had secondarily infected mandibular fractures (41.6%) and 1 had sialodentitis (8.3%). Two patients (16.6%) were female and 10 were male (83.3%). Based on data analysis, the CRP value was a more acute predictor of oral and maxillofacial infections and post-operative complications. In comparison, the WBC counts had a delayed response to inflammatory events, which is consistent with previously reported data. Tmax was shown to be inconsistent with the rise and fall of CRP, WBC count and clinical presentation.

Conclusion

The CRP test is an effective, rapidly attainable blood test that more accurately depicts patient course and response to treatment than more commonly used markers used in oral and maxillofacial surgery.

References

1. Pepys M, Hirschfield G. C-reactive protein: a critical update. J.Clin. Invest. 111:1805-1812(2003)

2. Sharma A, et al. Efficacy of Serum Prealbumin and CRP Levels as Monitoring Tools for Patients with Fascial Space Infections of Odontogenic Origin: A Clinicobiochemical Study. J Maxillofac. Oral Surg. 2012; 10.1007/s12663-012-0376-4.

3. Bakathir, AA et al. Factors Contributing to the Spread of Odontogenic Infections. Sultan Qaboos Univ Med J. 2009; 9(3)296-304.