After completion of a voiding cystometry, the study interpretation leading to a urodynamic diagnosis is mainly based on pressure recordings and the value of detrusor pressure at maximum flow (pdet.Qmax). Detrusor pressure is calculated by subtracting the abdominal pressure pabd from the vesical pressure (pves). Hence, there is a critical role for abdominal pressure in this process. 
During voiding, the changes in abdominal pressure can be threefold, decreased, unchanged, or increased. Two of these three processes, increase or decrease pabd, can have an effect on the final urodynamic diagnosis, especially for the diagnoses of detrusor underactivity (DU) or bladder outlet obstruction (BOO) which rely primarily on pdet.Qmax. 
The goal of this study was to analyze the changes in abdominal pressure during voiding in women, to search for incidence on detrusor pressure at maximum flow and possible misdiagnosis urodynamics.

Urodynamic tracings of 271 non-neurologic women age range [20-88 years old] who were referred for investigation of various LUTS to our specialized unit were retrospectively analyzed. Exclusion criteria were advanced cognitive impairment (MMSE ≤ 20), diabetes mellitus, grade ≥ 2 pelvic organ prolapse, complete urinary retention and/or severe mobility impairment. Each patient file comprised demographic data, medical history, 3-day bladder diary, and current medications. Main complaint was categorized as stress urinary incontinence (SUI), urge urinary incontinence (UUI) mixed urinary incontinence (MUI), and “OTHER” (dysuria-frequency complaint, meaning LUTS but no urinary incontinence). Each analyzed file included a filling cystometry followed by an intubated flow (IF), then UPP with bladder filled at 250 mL. Abdominal pressure was recorded using a punctured intrarectal balloon catheter filled with 2 mL of saline according to the report of Good Urodynamic Practice guidelines. 
After the urodynamic session a urodynamic diagnosis (UD) was posed according to the ICS/IUGA recommendations: bladder outlet obstruction (BOO), detrusor hyperactivity with impaired contractility (DHIC), detrusor overactivity (DO), detrusor underactivity (DU). Some investigations were found “normal” (N) and other related to urethral dysfunction (intrinsic sphincter deficiency (ISD)) or voiding triggered by urethral relaxation (URA)). Diagnoses of BOO and DU are based on the following criteria:
1- pdet.Qmax ≥ 25 cm H2O and Qmax ≤ 12 mL.s-1 for BOO [1]
2- for DU,due to the lack of consensus for terminology and definition, two cutoff criteria were used: the first pdet.Qmax< 20 cm H2O, Qmax< 15 mL.s-1 and BVE < 90% usable for all women [2], the second PIP1 (pdet.Qmax + Qmax) < 30 mainly proposed for elderly females suffering of urge incontinence. Evaluation of the VBN detrusor contractility parameter k was added as it had been demonstrated that PIP1 and k gave consistent evaluations of detrusor contractility for females [3]. 
After evaluation of pabd at maximum flow, a correction of pdet.Qmax erasing the artificially increase or decrease of pdet.Qmax was made. 
Then, with this evaluation of pdet.Qmax independent of change of pabd from baseline, we investigated possible changes in UD.

1- Decreasing abdominal pressure during voiding (Table 1)
Among the whole population, 73 women (26.9%) had a significant decrease (≥5 cmH2O) in pabd from baseline at the time of Qmax resulting in artificially increase in pdetQmax.
After correction of pdetQmax: all BOO remained BOO, among 51 N, 3 gained DU and had significant  decrease of PIP1 and k. 

2- No change of abdominal pressure during voiding (Table 1)
Forty five (16.6%) patients had no change of detrusor pressure during voiding and thus no new evaluation of urodynamic diagnosis.

3- Increasing abdominal pressure during voiding (Table 1)
Among the whole population, 52 women (19.2%) had a significant increase (≥5 cmH2O) in pabd from baseline at the time of Qmax resulting in artificially decrease in pdet.Qmax. Among these patients, and after exclusion of tracings without spikes of pabd during voiding, UD were 5 N and 3 DU.
After correction of pdet.Qmax, among the 5 patients with N diagnosis, 1 gained BOO diagnosis and among the 3 patients with DU diagnosis, 1 gained BOO diagnosis. All had significant increase of PIP1 and k.

In total, change of UD was 5/271 (1.84%) for the whole population, 3/145 (2.07%) for the patients with decrease of abdominal pressure during voiding and 2/81 (0.6%) for the patients with increase of abdominal pressure during voiding.
significant decrease of PIP1 and k.

Changes of abdominal pressure during voiding are very frequent in women whether it be decrease or increase. Small fluctuations are frequently due to live signals and are rubbed out with acute examination of the traces. This study is interested in the permanent and regular variations during voiding. Muscular relaxation causes decrease of abdominal pressure with consequence a rise of detrusor pressure while rectal contraction causes increase in abdominal pressure without change in vesical pressure but decrease in detrusor pressure. In our non neurologic female population, 145 (53.5%) have a decrease and 81 (29.9%) an increase of abdominal pressure without significant association with one complaint.
Some decreases and increases between the beginning of voiding and the time of Qmax are of low amplitude (+5 to -5 cm H2O) so are without consequence, mainly due to accuracy of static pressure measurement in urodynamic system and don’t need detrusor pressure correction. More care should be taken in the population with increase of pabd because there are possible straining episodes.
BOO and DU depend of evaluation of pdet.Qmax and could be revised with a correction of pdet.Qmax. All changes in UD lead to values of parameters PIP1 and k in the order of magnitude expected for age and modified urodynamic diagnosis

Despite a high percentage in the non-neurologic female population who had changes of abdominal pressure during voiding, that condition has low incidence on urodynamic diagnosis.

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