PROBLEM BASED LEARNING

MODUL 4

“URINARY INCONTINENTIA”

Tutor : dr. Yusriani Mangerangi, M.Kes

GROUP 15

A. Nadya Aulia Budaya 11020140009

Suci Walidalhuda 11020140023
Akhmad Fadil Noor 11020140033
Dian Hariati 11020140039
Muhammad Akbar 11020140051
Muhammad Alghifari S 11020140063
Aisyah Rahmi 11020140072
Qonita Faizah Basri 11020140096
Irna Novianti Irwan 11020140109
Evi Sriwhyuni 11020140133

MEDICAL FACULTY
MUSLIM UNIVERSITY OF INDONESIA
MAKASSAR
2017
SCENARIO 1
Anamnesis: 68 years old Woman was taken to hospital by his family with
complaintshas always been incontinent. This State endured already since 8 months
ago in which the sufferer may not hold at all if you want to urinate, so sometimes his
art spilling water on the floor. There are no complaints of pain during urination.
According to his family since a week ago sufferers is heard coughing, mucus is
thickand rather a lot of shortness of breath, as well as appetite is greatly reduced,
but nofever. Sufferers have 8 children, comprising 5 men and 3 women. A history
of the disease over the past 15 years, since sufferers have regular medical
treatment and diabetes with drug Glibenklamide 5 mg, with high blood pressure drug
Captopril 25 mg and to my two knees often swollen and sore.
Physical examination: physical examination obtained blood pressure 180/70 mmHg
and when laying down 160/70 mmHg, 92x pulse/minute, aksiler temp rature 370C,
respiratory 24 x/minute. On auscultation of the lungs found the presence of
ronkhi wet rough on the medial part of the right and left lung. The heart, liver and
spleen impression in the normal range. Weight 72 kg and height 155 cm.
Examination Support: Pem. laboratory levels of Hb 12.3 GR.%, Leukocyte/mm3
13,400, GDS 279 mg/dl, ureum 63 mg/dl, creatinin 1.85 mg/dl uric acid, 9.2 mg/dl.
Analysis of urine Sediment: leukocytes: 1-3/lpb, thoracic Examination photo found
the presence of homogeneous perselubungan in the medial regions of both lungs.
Ultrasound Abdomen not found abnormalities.

KEYWORDS
1. A women, 68 years old.
2. Invariably incontinent.
3. Since 8 month
4. Sometimes her art spilling water on the floor.
5. No pain of during urination.
 6. Since a week ago sufferers coughing sounds, a lot of mucus thick and
somewhat as well as appetite is gearly reduce, no fever
7. Sufferers have 8 children
8. Medication history : Glibenklamide 5 mg, Captopril 25 mg
9. Disease history : DM, OA, Hypertension,
10. Physical examination :
Obesitas : 29,96 kg/cm
BP : sit : 180/70
Stand up : 160/70
11. Ronkhi wet routh on the medial part of the right&left lungs
12. Additional examination
Leukocytosis : 13400/mm3
GDS : 279 mg/dl
Ureum: 63 mg/dl
Kreatinin: 1,8 mg/dl
Urid acid: 9,2 mg/dl
Sedimen leukosit : 1-3/ field of view
Chest x-ray examination found: homogeny in 2 both of medial lungs.

QUESTIONS
1. Explain the normal micturition process !
2. What are the etiology of incontinence ?
3. What are the types of incontinence ?
4. Is there any relation between illness history and the incontinence ?
5. Is there any relation between the parity history and the incontinence ?
6. What are the laboratory interpretation and nutritional state based on the
scenario ?
7. Is there any relation between the medication history and the incontinence ?
8. How are the treatment based on the scenario ?
 9. What are the complication of incontinence ?
10. What are the islamic perspective based on the scenario ?

ANSWERS
1. Micturition Process
The normal urination process requires coordination of sequential
physiological processes that are divided into 2 phases, namely the storage
phase and the emptying phase. This process involves the voluntary and
involuntary mechanisms because the anatomically lower urinary tract system
gets innervation of afferent nerve fibers derived from urinary vesica and
urethra and efferent nerve fibers in the form of parasympathetic, sympathetic,
and somatic systems. The external urethral sphincter and the pelvic floor of
the pelvis are under the control of the voluntary mediated by N. pudendus,
whereas m. Detrusor vesicae and spinchter internal urethra are under control
of the autonomic nervous system, which may be modulated by the cerebral
cortex.
In the filling (storage) phase, the first urinary voiding sensation
usually arises when the volume of urine vesica fills between 150-350 ml of
normal capacity of about 300-600 ml. In this state, afferent fibers from the
walls of the urinary vesica receive stretch receptor carried by N. pelvicus to
the spinal cord S2-4 (Nucleus intermediolateralis cornu lateralis medulla
spinalis / NILCLMS S2-4) and pass to the cortical nerve center and
Subcortical (basal ganglia and cerebellum) through the tractus
spinothalamicus. This signal will provide information to the brain about the
volume of urine in vesica urinaria. The subcortical center causes m. Detrusor
vesica urinaria relax and m. The internal urethral spinchter contracts as a
result of an increase in sympathetic nerve activity derived from NILCLMS
Th10-L2 carried by N. hypogastricus so that it can fill without causing a
 person to urge to urinate. When urinary vesica filling continues, the flavor of
vesica urinary development is recognized, and the cortical center (in the
frontal lobes) works to inhibit urinary expenditure.
When the urinary vesica is fully charged and the urge to urinate
begins, the emptying phase begins, stimulating the parasympathetic system
derived from NILCLMS S2-4 and brought by N. eregentes, causing muscle
contraction. Detrusor vesicae. In addition, inhibition of sympathetic system
that causes relaxation spinchter internal urethra. Miction then occurs when
there is a relaxation of spinchter urethra externa due to decreased activity of
somatic nerve fibers brought by N. pudendus and intra vesical pressure
overrides intraurethral pressure.
Reference
1. Sudoyo , Aru W. dkk. 2006. Ilmu Penyakit Dalam Jilid III Edisi IV.
Jakarta : Pusat Penerbitan Fakultas Ilmu Penyakit Dalam FKUI
2. Purnomo, Basuki. 2008. Dasar-dasar Urologi. Jakarta : Sagung Seto.

2. Etiology Of Incontinence
Bladder Dysfunction
a) Urge incontinence
1. detrusor over activity
2. detrusor overactivity of nonneurogenic origin
3. detrusor overactivity of neurogenic origin
4. poor compliance
b) Overflow incontinence
1. Urethral Dysfunction
c) Stress incontinence
1. anatomic ( due to mobility of the bladder neck)
2. intrinsic sphincter deficiency (due to bladder neck dysfunction)
3. Transient Causes Of Incontinence (Diappers)
CAUSE COMMENT
Delirium Incontinence may be secondary to
delirium and will often stop when acute
delirium resolves.

Infection Symptomatic infection may prevent a

patient from reaching the toilet in time.

Atrophic vaginitis Vaginitis may cause the same symptoms

of an infection.

Pharmacologic
• Sedatives Alcohol and long-acting benzodiazepines
may cause confusion and secondary
incontinence.
• Diuretics
A brisk diuresis may overwhelm the
bladder's capacity and cause uninhibited
detrusor contractions, resulting in urge
• Anticholinergics incontinence.

Many nonprescription and prescription

medications have anticholinergic
properties.
Side effects of anticholinergics include
• alpha-adrenergics urinary retention with associated
frequency and overflow incontinence.
 Tone in the bladder neck and proximal
sphincter is increased by alpha adrenergic
• alpha-Antagonists agonists and can cause urinary retention,
particularly in men with prostatism.

Tone in the smooth muscles of the

bladder neck and proximal sphincter is de
creased with alpha adrenergic
antagonists. Women treated with these
drugs for hypertension may develop or
Psychological have an exacerbation of stress
incontinence.

Excessive urine production Depression may be occasionally

associated with incontinence.

Excessive intake, diabetes,

hypercalcemia, congestive heart failure
Restricted mobility and peripheral edema can all lead to
polyuria, which can lead to incontinence.

Incontinence may be precipitated or

Stool impaction ggravated if the Patient cannot get to a
toilet quickly enough.

Patients with impacted stool can have

urge or overflow urinary incontinence
and may also have fecal incontinence.
 Reference:
https://www.urology.wisc.edu/system/assets/935/module9_urinary_incontinen
ce.pdf?1347982562

3. Classification of Inkontenensia urine

Urinary incontinence can be classificated into two i.e. incontinence that
occurs in acute and chronic incontinence living. Urine ncontinence occursin
acute (Transient incontinence) which is usually reversible.
Incontinence that occurs in this acute, sudden happens, usually related to the
condition of the pain that is being inflicted on or problem drug use
(iatrogenic). Incontinence willbe improved, when acute illness suffered cured or r
emedy the cause is stopped.
Transient urinary incontinence is often abbreviated DIAPPERS, namely:
a) D Delirium or confusion: awareness of declining influence on micturition
stimulation, as well as knowing the place of micturition. Delirium is the
main cause of urinaryfor those admitted to hospital, when the delirium,
incontinence improving recovered well.
b) I Infection – infection of the urinary tract such as urethritis can cause
irritation of the bladder and the arising of frequency, dysuria and urgency
which led to someone not being able to reach a toilet for urination.
c) A Atrophic Urethritis or Vaginitis with – a network of irritated skin can
cause the onset of urgency which is very berespon towards the granting
of estrogen therapy.
d) P Pharmaceuticals: Medicines is one of the main causes of incontinence
types while, for example, diuretic, antikolinergik, psikotropik, analgesic
opoid, alfa blockers in women, Alpha agonis in men, and an inhibitor
of calcium
 e) P Psychological Disorder:D epresi retradasi weight with psychomotor can
decrease the ability or motivation to reach micturition.
f) E Excessive Urine Output: excessive urine Expenditure can outstrip the
ability of elderly people reach a nifty little rooms. In addition to drugs,
another cause of diuretika often occurs for example the treatment of heart
failure, metabolic disorders such as Hyperglycemia or drinking too much.
g) R Restricted Mobility – can decrease other physical condition that
interferes with the mobility to reach a toilet.
h) S Stool Impaction: stool impaction is the cause of incontinence that often
they treated or immobile. When the obstipation is resolved, will restore
the kontinens again

Inkontinesia living/chronic/persistent,
a) type stress urinary incontinence: urinary incontinence happens when urine
by uncontrollably out due to increased pressure within the abdomen,
weakening of the pelvic floor muscles, operation and penuru nan-estrogen.
On the symptoms include coughing, straining while urinating, laughing,
sneezing, running, or anything else thatmening katkan pressure in the
abdominal cavity. The treatment can be done without surgery-gan den
(e.g. with Kegel exercises, and some types of drugs), or by surgery.
b) type urge urinary incontinence: incidence on the State of the detrusor
muscle of the bladder are not stable, where these muscles react in excess
urinary incontinence can be marked with puan delay urination after the
sensation of urinary manifest can appear is feeling like to pee suddenly
(urge), urinary (frequency) and urinating at night (noktu-ria).
c) Urinary incontinence type overflow: in this situation the urine flows out of
its contents with the result that already too much in the bladder, generally
due to detrusor muscle of the bladder are weak. Typically this is found
in nervous disorders resulting from diabetes, injury to the spinal cord,
 urinary tract and the tersumbut. Symptoms can be either tastes satisfied
after urinating (feel the urine remaining in the urinary dung), urine comes
out little bit and was weak.
d) Functional type: urinary incontinence can occur due to a decrease in the
weight ofphysical and cognitive function so that the patient could not
reach ketoilet at the right time. This happens on demen-neurologic
disorders is heavy, vain, impaired mobility and psikologik.

References:
Boedhi Darmojo,,h. Hadi Martono. Geriatric (Elderly Health Science) issue: 4.
FK UI: Jakarta. 2009. Case: 231-233

4. The relation between illness history and the incontinence :

Cought and Many Sputum
Continence is dependent on a complex interaction of the muscles, fascia
and ligaments of the abdomino-pelvic cavity, a competent urethral sphincter
and adequate neurological control. In the resting state, the tonic activity of the
pelvic floor and urethral sphincter counteract the pressure within the bladder
and the resting intra-abdominal pressure to maintain urethral closure and
maintain continence. This transmission of pressure by the pelvic floor and
urethral sphincter to the proximal urethra is essential to preserve continence.
The urethra is supported in an intra-abdominal position by the fascia and
contraction of the pelvic floor muscles. Any increase in intra-abdominal
pressure during exertional activities is transmitted to the bladder neck and
proximal urethra, the sphincter exerts additional force and together with pelvic
floor contraction continence is maintained. Inefficient contraction of the PFM
will lead to reduced pressure transmission to the urethra, causing leakage. If the
pelvic floor fails to provide adequate support to the bladder neck, the urethra is
effectively shortened. The increases in abdominal pressure are not transmitted
to the bladder neck further compromising continence.
Leakage may occur when the detrusor muscle of the bladder wall is
unstable or ‘irritable’ causing poor control of the bladder muscle and an
inability to coordinate detrusor contraction with pelvic floor control of urethral
closure. Strong contractions of detrusor can occur inappropriately during
bladder filling either spontaneously or apparently provoked by activities such as
coughing.
Neurological control of the pelvic floor and micturation is an essential
component of the continence mechanism. The nerve supply of the pelvic floor
is via the pudendal nerve, as part of the somatic nervous system. Bladder filling
and storage of urine involves autonomic control via the sympathetic system and
bladder voiding is under parasympathetic control.
During activities which increase intra-abdominal pressure, e.g. coughing, PFM
contract in synergy (as part of a pre-programmed sequence of events) with
other muscles of the abdomino-pelvic cavity (Figure 3). These include the
diaphragm, the abdominal muscles and multifidus which together contribute to
continence, intra-abdominal pressure and spinal stability. Dysfunction of any
of the individual muscles within the abdomino-pelvic cavity is therefore likely
to disturb this synergy and interfere with the continence mechanism. The
multiple complications of CF place patients at risk for this disturbance.
The action of the muscles of the abdomino-pelvic cavity during coughing
Continence during a cough depends on a complex interaction of the
PFM, all the abdominal muscles; transversus abdominis, obliquus internus,
obliquus externus and rectus abdominis, the diaphragm and deep fibres of
lumbar multifidus. Figure 3 illustrates this interaction during a normal cough
action. At the end of expiration during tidal volume breathing, the diaphragm
has a domed shape and the tonic activity of the abdominals, PFM and spinal
stabilizers provide postural stability and maintain continence. The timely co-
 activation of these muscles maintain continence and postural stability whilst
effectively clearing the airways during a coughing manoeuvre. Prior to a cough
the inspiratory effort requires rapid descent of the diaphragm causing slight
forward movement of the abdominals which provides a pretensioning effect
which is thought to augment the contraction force during the cough. Prior to the
strong abdominal wall contraction, which generates the rapid expiratory airflow
of the cough, the PFM contract. Not only does this allow the PFM to contribute
to the increase in intra-abdominal pressure necessary for an effective cough it
also works to maintain urethral closure during the cough. The PFM contraction
prior to voluntary abdominal muscle activity suggests a pre-programmed
response to intra-abdominal pressure. However, in the presence of increased
stress to the PFM, e.g. with chronic cough, this continence threshold may be
exceeded and it is well recognized that chronic cough is a poor prognostic
indicator for successful treatment of urinary incontinence.

References :
Mary E Dodd, Hannah Langman. 2005. Urinary incontinence in Cystic
Fibrosis. United Kingdom : Journal of the Royal Society of Medicine. Volume
98. Number 45. Page 31-34.

5. The relation between the parity history and the incontinence :

A 1989 consensus conference of the National Institutes of Health identified
parity as an established risk factor for urinary incontinence. Mode of delivery
may have a significant impact on the persistence of incontinence. The
multivariate analysis identified the length of labor pushing, fetal head
circumference, episiotomy, and birth weight as risk factors for postpartum stress
urinary incontinence, whereas cesarean birth was protective against incontinence.
Pelvic floor neuropathy is a common repercussion of childbirth—less often
recognized than vaginal and perineal injury, but arguably more significant as a
risk factor for subsequent pelvic floor dysfunction. The pudendal nerve, arising
from the S2-S4 nerve roots, supplies most of the anatomic structures maintaining
pelvic support and continence—including the perineum and vagina, levator
muscle complex, and anus. Compression and stretching of the pudendal nerve
during childbirth appears to be a major risk factor associated with subsequent
diminished levator muscle function. As a result of neuropathic changes, the sling-
like components of the levator complex, such as the pubococcygeus muscle, may
fail to reflexively contract and elevate sphincter pressure during a cough or
sneeze. Likewise, the resting tone of the shelf-like levator plate and perineal
body may diminish.
In the etiology of post-childbearing pelvic floor disorders, endopelvic
connective tissue injuries have an established role. Recent efforts have been
focused on identifying “site specific” breaks and detachments of the endopelvic
connective tissue from their anatomical insertion sites, as the origins for pelvic
organ prolapsed. For many women, pelvic neuropathy will have no clinical
consequences; for others, these nerve injuries initiate a pathophysiologic
sequence eventually leading to incontinence, prolapse and pelvic floor
dysfunction. Pudendal conduction abnormalities and denervation of the pelvic
floor after childbirth have been associated with both genital prolapse and urinary
incontinence.
Anatomically speaking, urethral hypermobility is an important change
associated with SUI and is significantly increased after vaginal delivery when
compared to cesarean delivery in both primiparous and multiparous women (p <
0.001).

Reference :
Goldberg, R. P. (2007). Effects of pregnancy and childbirth on the pelvic floor.
In Urogynecology in primary care (pp. 21-33). Springer London.
6. Interpretation based on scenario :

Vital Sign :
 Blood Pressure : 180/70 mmHg (stand)  (Hypertension grade II)
160/70 mmHg (sit)  (Hypertension grade II)
 Pulse : 92 x/minute  (Normal)
 Respiration : 24 x/minute  (Normal)
 Temperature : 370C  (Normal)
Physical examination :
 Auscultation : There was a wet ronchi roaring all over the second lung
field  (pneumonia)
 Nutritional status :
BB : 72 Kg  BB / TB = 72/1,552 = 29.96 kg/m2
TB : 155 cm (OBES I)
Supporting examination :
Laboratorium
 Hb : 12,3 gr%  (Normal) Normal : 12-16 gr %
 Leukosit : 13.400/mm3  (increase) Normal : 4500-13.000/mm3
 GDS : 279 mg/dl  (DM) Normal : 90-200 mg/dl
 Ureum : 63 mg/dl  (Increase) Normal : 10-50 mg/dl
 Creatinin : 1,85 mg/dl  (Increase) Normal : <1,1 mg/dl
 Uric acid : 9.2 gr/dl  (Increase) Normal : (female (2,7-5,4 gr/dl)
 Analize urin (leucocyte sedimen) : 1-3/lpb  (Normal) : 1-3/lpb
Thorax X-Ray : Homogeneous interactions in the medial second lungs 
(pneumonia).

Reference :
Penuntun Biokimia, FK UNHAS
7. Relation the history of treatment with main complaints?
a) Glibenklamide
Hypoglycemia is the most important side effect of SU especially if the
patient's intake is inadequate. To reduce the likelihood of hypoglycemia,
especially in the elderly selected drugs whose lifetime is the shortest. SU
drugs with long service life should not be used in old age. Hypoglycemia is
often unrecognized by the absence of a sympathetic reflex that tends to
cause muscle relaxation including detrusor muscle causing urinary
incontinence.
b) Captopril
Pharmacokinetics of ACE-inhibitor drugs are the same. The
mechanism of ACE-inhibitor lowering TD is through, among others:
1. Inhibits the formation of Ang-II in circulation or in tissues.
2. Inhibits sympathetic nerve activity by decreasing noradrenaline
release.
3. Increases the production of vasodilating substances such as NO,
bradykinin, prostaglagin and Ang- (1-7).
Side effects include:
Coughing: dry cough occurs in 5-20% of patients. These side effects
are unrelated to the dose and duration of use. More common in women. This
is due to the accumulation of bradykinin, P and / or prostaglandin.
It can lead to incontinence.

Reference :
1. Prof. Dr. Peter Kabo PhD, MD. 2014. How to Use Cardiovascular Drugs
Rationally. Jakarta: Balai Penerbit Fakultas Kedokteran Universitas
Indonesia. Pg.45, 92.
2. Soegondo, Sidartawan. 2015. Pharmacotherapy in Control of Type 2
Diabetes Mellitus Glycemia in IPD. Jakarta: Interna Publishing. P. 2333.
8. The treatment based on the scenario:
The usual approach to the treatment of urinary incontinence is a
stepped-care plan starting with noninvasive behavioral modifications,
followed by devices and pharmacologic interventions, and finally surgery in
those whose symptoms do not respond to initial treatment. Treatment options
are shown in Table below. Lifestyle changes, including avoiding excessive
fluid intake and limiting caffeinated or carbonated beverages, are also
reasonable recommendations for all types of incontinence.13 When patients
have mixed incontinence, treatment should be directed toward the
predominant symptom.
 References :
LAUREN HERSH, MD, and BROOKE SALZMAN, MD. Clinical
Management of Urinary Incontinence in Women. Volume 87, Number 9.
2013. American Family Physician. 634-637

9. Complications Of Urinary Incontinence:

a. Urinary tract infection. Incontinence increases the risk of UTI because
the urine coming out are suddenly so that it increases the risk of infections
caused by bacteria.
b. Skin problems. Urinary incontinence can cause infection in the skin until
the ulcerdekubitus because damp caused by urine on skin area.
c. Limitations in activity. Patients who experience inkontinesia certainly will
experience limitations in activity due to a sense of wanting to waste
water which cannot be put on hold.
 d. Social disorders. Patients who experience inkontinesia will definitely
experienced social disorders such as depression, irritability, and isolated
from the environment.
e. The incidence of the disease. Patients in urinary incontinence sufferers often
encountered many cases of fracture due to often fall in suddenly.

Reference:
-http://dokumen.tips/documents/inkontinensia-urin-55ab59036f2e9.html

10. Perspektif islam

Surah Al-Hajj ayat 5:
‫ث ِمنَ َريب فِي كنتم إِن النَّاس أَيُّ َها يَا‬ ِ ‫ِمن ث َّم َع َلقَة ِمن ث َّم نطفَة ِمن ث َّم ت َراب ِمن َخ َلقنَاكم فَإِنَّا البَع‬
‫س ًّمى أ َ َجل ِإلَى َنشَاء َما ال َر َح ِام فِي َون ِق ُّر ۚ َلكم ِلنبَ ِينَ مخَلَّ َقة َوغَي ِر مخَلَّ َقة مضغَة‬
َ ‫ِطف ًل نخ ِرجكم ث َّم م‬
‫ۚ شَيئًا ِعلم بَع ِد ِمن يَعلَ َم ِلكَي َل العم ِر أَرذَ ِل إِلَى ي َردُّ َمن َو ِمنكم يت ََوفَّى َمن َو ِمنكم ۖ أَشدَّكم ِلتَبلغوا ث َّم‬
‫ض َوت ََرى‬َ ‫َامدَة ً الَر‬ ِ ‫َب ِهيج زَ وج ك ِل ِمن َوأَن َبت َت َو َر َبت اهت ََّزت ال َما َء َعلَي َها أَنزَ لنَا فَإِذَا ه‬

Artinya:
“Hai manusia, jika kamu dalam keraguan tentang kebangkitan (dari kubur), maka
(ketahuilah) sesungguhnya Kami telah menjadikan kamu dari tanah, kemudian
dari setetes mani, kemudian dari segumpal darah, kemudian dari segumpal
daging yang sempurna kejadiannya dan yang tidak sempurna, agar Kami jelaskan
kepada kamu dan Kami tetapkan dalam rahim, apa yang Kami kehendaki sampai
waktu yang sudah ditentukan, kemudian Kami keluarkan kamu sebagai bayi,
kemudian (dengan berangsur-angsur) kamu sampailah kepada kedewasaan, dan
di antara kamu ada yang diwafatkan dan (adapula) di antara kamu yang
dipanjangkan umurnya sampai pikun, supaya dia tidak mengetahui lagi
sesuatupun yang dahulunya telah diketahuinya. Dan kamu lihat bumi ini kering,
kemudian apabila telah Kami turunkan air di atasnya, hiduplah bumi itu dan
suburlah dan menumbuhkan berbagai macam tumbuh-tumbuhan yang indah.”