1. 1. Please discuss your rationale for specific information obtained and how that informs your differential diagnosis, identification of ‘precautions/contraindications to physical examination and management’ and your patient-specific ‘management’.

Sarah is a young, elite athlete in whom UI may at first seem surprising, but she has had two vaginal deliveries, which is a known risk factor for the development of UI (MacLennan et al., 2000). A high prevalence of UI has been reported among elite athletes performing high-intensity physical activities, including hockey (Bø, 2004; Bø and Borgen, 2001). Questions about her history of incontinence served to probe the function of her bladder and pelvic floor prior to pregnancy and childbirth, as childhood problems may persist into adulthood, suggesting more complex pathology (Feldman and Bauer, 2006). Her mother had a vaginal prolapse as a younger woman, suggesting a possible genetic link via a collagen deficiency (Chiaffarino et al., 1999).

Pregnancy is a time of great hormonal and musculoskeletal changes, which are commonly associated with pelvic floor dysfunction (Landon et al., 1990). These factors could explain the onset of more bothersome symptoms even before her second delivery, especially with a possibly compromised pelvic floor after the birth of baby Tom (DeLancey et al., 2008). Furthermore, her pregnancies were close together, which could contribute to incomplete resolution of any impairments after the first delivery.

Sarah’s birth history provides a rationale for the development of pelvic floor dysfunction. Childbirth is a risk factor for the development of urinary incontinence (Persson et al., 2000) and POP (Hendrix et al., 2002). Vaginal childbirth and an instrumental delivery are each associated with an increased risk of anterior pelvic floor damage and POP development associated with avulsion of the pubovisceral muscle from the pubic symphysis and ramus, either unilaterally or bilaterally (Dietz and Simpson, 2008) (Fig. 21.1A and B).

A forceps delivery also predisposes the mother to anal sphincter damage (Sultan, 1999), but Sarah had no symptoms of anal incontinence or urgency suggestive of this. Sarah initially reported typical symptoms of SUI (i.e. leakage with sneezing and exertion), but the second delivery precipitated the overt symptoms of exercise-induced SUI. In addition to her symptoms of SUI, her symptoms of UU and UUI are typical of overactive bladder syndrome (wet) (i.e. urgency that results in incontinence). This symptom may be associated with a urinary tract infection, which was excluded on the negative results of urinalysis, or with polydipsia (i.e. excessive fluid intake), a common female phenomenon in the 21st century due to erroneous beliefs about hydration (Valtin, 2002). Other differential diagnoses in a young woman include multiple sclerosis causing bladder-sphincter dyssynergia and a voiding dysfunction due to a hypotonic detrusor (bladder muscle), both leading to incomplete bladder emptying, which in Sarah’s case had been excluded because she had no post-void residual on TAUS assessment. Multiple sclerosis was considered unlikely in a young woman performing sport at a high level without any neurological symptoms. A hypotonic detrusor may result from an episode of acute retention post-delivery, but this was not reported in Sarah’s birth history, and absence of a residual following voiding also made this unlikely. Thus, no red flags were identified which would trigger a specialist referral.

The 3-day bladder diary provided objective evidence of fluid consumption and bladder function, which confirmed excessive total fluid intake over 24 hours and high bladder volumes. The reasons for Sarah’s high fluid intake appeared to be benign, but polydipsia may be due to diabetes insipidus or diabetes mellitus. Persistent thirst, after normalizing fluid intake, should be investigated by a medical practitioner.

The PF Bother Questionnaire supported the subjective findings in that no other pelvic organ symptoms were present and that constipation with possible habitual straining was not contributing to the pressures on her pelvic floor. Question 9 confirmed that she was sexually active and that sexual pain was not present, as the presence of pain would have been a red flag for other possible pathology, such as an infectious or inflammatory condition or a sexually transmitted infection, triggering referral to her general practitioner for further investigation. Pain would not have been an absolute contraindication to internal examination but would have suggested a more cautious assessment. It is important for the clinician to exclude a history of sexual abuse, even in the absence of reports of pain, as it may make a vaginal examination traumatic and cause the patient to dissociate (i.e. relive the trauma during the examination) if it has not previously been identified. Sarah did report pain with intercourse postnatally, but this was consistent with the time taken for the episiotomy to heal and from the influence of postnatal hypooestrogenization causing vaginal dryness.

Sarah had previously been advised to stop her urine flow as a PFM exercise. This, however, is a test of urethral sphincter function, and although it should be possible, it is not advised as an exercise for the pelvic floor muscles because it may disturb the voiding reflexes responsible for the complex neurological interactions between bladder and urethra (Bø and Mørkved, 2015). The urethral sphincter has a separate nerve supply from the levator ani (pudendal nerve compared with direct branches from the S2–S4 nerve roots) so that action of one structure does not predict the activity of the other.

Sarah was also advised to ‘hang on’ to improve her bladder’s ability to hold urine. This advice is appropriate in someone with urgency related to reduced bladder volumes because the practice may improve the bladder capacity. However, without a bladder diary, the physiotherapist could not know that the advice was inappropriate, and potentially harmful, because Sarah’s bladder volumes were already at the upper end of the normal range (up to 700 ml), with the potential for damage to the detrusor muscle caused by overstretching.

A TAUS had been performed to assess her pelvic floor function (i.e. by visualizing movement of the bladder base), and this indicated no activity. Sarah was told that she had weak pelvic floor muscles, which motivated her to try harder to strengthen them. However, when using TAUS, the amount of movement of the bladder base does not reflect the force of the pelvic floor muscle contraction because other factors may be involved. It is therefore important to consider whether the pelvic floor muscles are able to completely relax (Dietz and Shek, 2008a; Messelink et al., 2005) and whether activity of the other muscles around the abdominal-pelvic cavity is increasing intra-abdominal pressure (Junginger et al., 2010; Neumann and Gill, 2002; Thompson et al., 2006a; Thompson et al., 2006b), mandating a digital vaginal assessment to confirm the hypothesis of a weak PFM.

Sarah had also been advised to do Pilates to improve her ‘core’ muscles and pelvic floor, but she had no awareness of her pelvic floor and was apparently unable to activate it functionally. Repetitive core abdominal work resulting in increased intra-abdominal pressure in the absence of a functional pelvic floor could exacerbate its dysfunction (Bø et al., 2009). Addressing the PFM dysfunction first would have been advisable in order to train the normal pattern of recruitment and neuromuscular control around the abdominopelvic cavity (Sapsford et al., 2001; Thompson et al., 2006b) (Fig. 21.2).

At this stage, the diagnosis of SUI was likely given her history of leakage during high levels of exertion and occasionally with extreme coughing and sneezing. This subjective finding could be supported by an objective stress test such as the Expanded Paper Towel Test (EPTT) (Neumann et al., 2004) performed with standardized bladder filling to demonstrate objective UI with a sudden rise in intra-abdominal pressure, for example, as occurs with coughing and jumping.

The urinary urgency and frequency symptoms can be explained by the excessive fluid output of 4.0 L. The bladder chart confirms a normal bladder capacity and frequency appropriate for the volume of fluid intake.

The systematic and thorough subjective assessment of Sarah has been used to ensure her complete symptom presentation is revealed and understood and so that potential causes and contributing factors are explored. This, combined with the necessary knowledge of clinical patterns potentially associated with Sarah’s presentation, enables differential diagnoses to be considered and tested further. Revealing the complete symptom presentation is essential to thorough clinical reasoning because patients will often omit relevant information for a variety of reasons, including not appreciating its relevance, embarrassment or simply not remembering. ‘Screening questions’ to optimize thoroughness and minimize clinical assumptions (as presented in Chapter 1) include the following:

• • Screening for additional symptoms or problems not spontaneously volunteered (e.g. as with the PF Bother Questionnaire for Sarah)
  
• • Screening for additional activity and participation restrictions and capabilities not volunteered (e.g. screening Sarah for symptoms associated with sexual intercourse)
  
• • Screening for ‘patient perspectives’ (i.e. psychosocial factors) and their relationship to the clinical presentation (e.g. screening Sarah’s understanding, beliefs about fluids and her pelvic floor and her coping strategies regarding her problem)
  
• • Screening for general health comorbidities and red flags