The development of SBP in patients with ascites is associated with a poor prognosis. It may be complicated with acute kidney injury and hepatorenal syndrome, so prophylactic albumin infusion is useful [3]. One of the main pillars in pathogenesis is bacterial translocation, so proton pump inhibitors were accused of precipitating SBP [8] While early reports mentioned that B-blockers are protective of SBP [9], recent studies recommended strict monitoring or stopping them in patients with SBP [4].
The success of the antibiotic therapy can be suspected by improvement of the clinical condition and improving the abdominal pain (3). Being a subjective measurement for treatment judging, added to the fact that many patients are asymptomatic, so reliance on diagnostic follow-up 48-h AFPC of treatment was a good alternative to adjudicate the antibiotic therapy (3).
In 1986, Runyon and Hoefs [10] in a small number study (n=24) were the first to use AFPC to follow-up the response to antibiotics in SBP patients. In fact, they measured serial AFPC to try to differentiate primary from non-perforation secondary peritonitis. After the initiation of the antibiotics, the AFPC had decreased exponentially. The total mean AFPC half-life (t½) was 34 ±35 h (t½ was 36 ±9h for the survivors and 38 ±40 h for patients who died, p >0.05). Based on the t½, the 48-h follow-up AFPC was adopted. The SBP patients who survived had 48-h AFPC <50% of the baseline.
In 1989, Fong et al. [11] in a small number study (n=33) tried to validate 48-h follow-up AFPC. The mean percent drop of AFPC was 92% in the survivors compared to 67% in the non-survivors (p = 0.001). The endpoint of treatment was AFPC <250 cell/mm3.
In 2000, based on the above studies, the first consensus for the diagnosis and management of SBP [12] suggested that 48-h AFPC should be done and considered arbitrary a cutoff of ≥25% decrease to define response to antibiotics.
AASLD guidelines 2009 [7] suggested on-demand follow-up AFPC if suspecting non-response to therapy. In 2012, the AASLD guidelines [13] suggested follow-up AFPC with nosocomial setting, culture of atypical organism, or recent B-lactam antibiotic exposure. The British guidelines [14] did not mention the follow-up AFPC in its recommendations.
The EASL guidelines 2010 [3] suggested 48-h AFPC to guide the antibiotic therapy but did not mention the cutoff in the recommendations. The case is the same with the most recent one [4].
What is new in this study? In fact, knowledge is increasing and the advance in sciences urges revisions of definitions that were considered as a taboo. For example, the definition of cure from HCV by antivirals was defined for years by negative HCV RNA measured 24 weeks from end of antiviral treatment as seen in AASLD guidelines 2009 [15]. By the progression of knowledge, the duration was recently shortened to 12 weeks [16].
Do we really need to change the time of follow- up AFPC from 48 to 24h? In the past, SBP was diagnosed clinically and by diagnostic AFPC. Treatment was continued till improvement of the clinical symptoms only. This approach was problematic in patients with asymptomatic SBP, so follow-up AFPC approach adopted by Runyon and Hoefs [10] was very helpful. Few years ago, SBP was caused mainly by gram-negative bacteria, and some guidelines suggested on-demand follow-up 48-h AFPC [7, 13] and some recommended it [3, 4].
Nowadays, SBP may be of three types community-acquired, healthcare-associated, and nosocomial type. The latter 2 are caused by usually gram-positive bacteria and have an aggressive course especially if multi-drug resistant and may progress to sepsis. They have less response to conventional therapy and need strong antibiotic therapy from the start as carbapenem, vancomycin, or linezolid [4].
With the recent aggressive change of the SBP map, early prediction of antibiotic treatment failure is warranted to avoid progression to sepsis and ominous outcome. The second point that waiting till culture results may be not helpful in critical cases especially those with high baseline AFPC and immunosuppressed state where time saving is mandatory and a lot of cases the culture is negative. As a result, changing the time point of follow-up AFPC from 48 to 24 h may be helpful.
In the current study, 399 patients with SBP were included with a baseline AFPC that range was 250–12,000 cell/mm3. Responders to antibiotics who had ≥25% decreased 48-h AFPC compared to non-responders, who had reported increased 24h AFPC.
We tried to have a cutoff predicting non-response to antibiotic therapy. The 24-h AFPC >980 cell/mm3 was associated with AFPC 48h non-response, but the AUROC is small and statistically poor. In contrast, the 24h AFNC percent drop >8% was associated with AFPC 48h response with statistically good AUROC (0.849, p =0.001, 85.82% sensitivity, 80.49% specificity). On choosing another cutoff (>25%), the sensitivity decreased (52.73%), while the specificity increased (88.62%).