Urinary Incontinence

UrinaryIncontinence

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UrinaryIncontinence

Whenaddressing an elderly patient with a urinary incontinence problem, itis important to use formal language in order to establish respect.One might choose to ask the patient their preferred form ofaddressing. It’s important to avoid patronizing terms such as‘dear’ instead use formal terms such as Mr., Miss or Mrs. Ifnecessary, it is important to guide the elderly patients in fillingforms and explaining to the caregiver the importance of everyprocedure taken so that the caregiver translates it to the patient.The patient should have full knowledge of every developing to fostercooperation (Barkley, 2012).

Clearintroduction, a show of empathy, clear explanation of my role as themedical caregiver or refreshing Alvita’s memory of my role are someof the ways of establishing rapport. Demonstration of empathyinvolves watching for any opportunities to respond to Alvita’semotions. Phrases like “I think we can work on it together” and“I am sorry for your problem, but I believe working together canhelp both of us” promotes patient’s understanding, satisfactionand treatment adherence (Barkley, 2012).

Keepingtime is important. Emphasis should also be put on apologies in caseof any delays. If Alvita is a new patient, establishing rapport canbe fostered by asking friendly questions about her family, her lifeor activities for stress relief. It is also important not to rush,adequate time should be spent discussing Alvita’s problem betweenher and her caretaker, allowing their concerns to be addressed. Thiswill also allow the gathering of important information that couldlead to improved adherence to treatment and cooperation.Interruptions should be avoided as they reduce the chances of thepatient’s willingness to reveal all her concerns. This will alsoavoid unnecessary follow-up visits or phone calls. Speaking moreslowly enables elderly patients like Alvita to have time to processthe questions asked. Active listening skills such as maintaining eyecontact, facing the patient and the use of frequent but briefresponses such as “I see,” enables the patient to maintain afocused discussion. It also makes the patient know that their problemis being understood and the concerns addressed. It is also importantto avoid communication barriers by addressing problems such assensory impairments often seen in older patients. Ask these patientsif they have any hearing or visual problems and their last time tohave a visual or hearing examination. Compensation for hearing lossesincludes clarity in talking, informing the patient when a subject ischanged and avoiding high-pitched voices. Visual impairment can becompensated by involving the caretaker and making sure that unwritteninstructions are very clear (Barkley, 2012).

Theconclusion of the visit should be done by ensuring that the patienthas understood everything. The patient should understand her mainhealth problem, what she needs to do and the importance of doing it.Teach-back method is an effective way of ensuring that patientsunderstand health care proceedings. This can be done by asking Alvitawhat she understands from her visit. Additionally, it is important toask the patient or the caregiver if there will be any barrier to theadherence to their treatment plan.

Question1

Urinaryincontinence that is coupled with limited mobility can beneurological or skeletal. There are four explanations for Alvita’scondition, which consider the age of the patient, her previoushistory, and her possibly neurological status. To begin with, thecondition might be caused by stress incontinence. It is usuallyprevalent in individuals who have internal sphincter dysfunction dueto urologic conditions or operations that end up damaging it. Theurethra from the urinary bladder is supported by fascia that formspart of the pelvic floor. The weakening of the pelvic floor due tothe increased pressure that is caused by pregnancy causes the supportmechanism to be insufficient. Actions that increase theintra-abdominal pressure, thus force the bladder to move downwardsallowing it to pass urine against the will of the patient. In thiscondition, most lab parameters such as cystometry and urine analysisare normal (Grossman et al., 2014). Her condition might be worsenedby menopause due to decreasing levels of estrogen. This hormone notonly ensures bone strength and architecture throughout life, but italso ensures that the bladder and urethra are healthy and functioningwell. Decreased estrogen decreases dynamic support of the bladder asthe muscles on the pelvic floor weakens, giving insufficient supportto the bladder. In additional, the urethral tissue weakens.Therefore, the urinary incontinence progressively worsens with years,as it is experienced in Alvita’s case.

Theangle between the posterior proximal urethra and the bladder is 900to 1000in women. This angle, also called the urethrovesical junction, isvital for continence. When the first phase of micturition occurs, theangle is lost, allowing the flow of urine. However, this angle canalso be lost in increased pressure on the urinary bladder, such asthe effects of pregnancy coupled with a weakening pelvic floor anddynamic support for the urethra. Patients who have a weakened pelvicfloor have a permanent obliteration of the posterior urethrovesicalangle, which is very critical in maintaining continence. Surgicalprocedures during childbirth, the effects of childbirth and aging arefactors that contribute to the loss of this angle (Barrett, Barman &ampBoitano, 2010). All these are important positives for Alvita’sclinical presentation. There is a high likelihood that this patienthas lost the muscle tone of the pelvic floor, which is associatedwith normal aging leading to funneling and descent of the bladderneck in addition to backward and inferior rotation of the bladder.Furthermore, increased age leads to decreased mobility, an increasein the number of drugs taken, comorbidities, infections and impactionof stool, all of which contribute to urinary incontinence.

Thehallmark signs and symptoms of this condition include leakage ofurine with a simultaneous increase in intra-abdominal pressure causedby actions that facilitate Valsalva maneuver such as sneezing,laughing, coughing, bending or exercise (Kumar, Abbas &amp Aster,2012). In her case, all these are important positives because hercondition is aggravated by these activities. In elderly women, thiscondition is caused by urinary bladder prolapse caused by pelvicrelaxation due to multiple pregnancies coupled with the effect ofaging. These are also important positives from the history of thepatients. The aging coupled with multiparty and prolapse of theurinary bladder cause movement limitation. In addition, some drugssuch as alpha-adrenergic antagonists such as Tamsulosin (Flomax) usedfor treating hypertension and Raynaud’s disease can also cause thiscondition (Masters &amp Trevor, 2011). These drugs causeincontinence by over-relaxing the muscles involved in regulatingmicturition. Overrelaxation of the muscles of the pelvic floorpredisposes the bladder to prolapse, further tilting the posteriorurethral vesical angle, which allows for involuntary voiding tooccur. (Grossman et al., 2014).

Over-activityof the detrusor muscles of the urinary bladder is another possiblecause of Alvita’s condition. This condition is the commonest amongcauses of urinary incontinence in elderly patients, with a prevalenceof about 40% to 70% of elderly patients who present for clinicalconsultation and treatment (Kumar, Abbas &amp Aster, 2012).Micturition is a process involving high cognitive function. Thisincludes the use of higher brain cortex, spinal cord, pons, somaticand sensory afferents of the lower urinary tract and the peripheralautonomic innervation as well as other anatomical supportingstructures for regulation. A malfunction in any of these causes anoveractive bladder. Normally, micturition occurs due to a response tosignals from the afferent nerves of the lower urinary tractcontrolled by the neural circuits of the nervous system. Their roleis coordination of the activities of the detrusor smooth muscles, thesmooth muscles of the urethra and the skeletal muscles of the pelvicfloor and urethral sphincter. Therefore, this nervous communicationinvolves parasympathetic, sympathetic and somatic innervation.Receptors that are sensitive to stretch are activated during thefilling phase, conveying impulses to the brain informing that thebladder has reached its capacity (Barrett, Barman &amp Boitano,2010). Changes in non-neural and neural acetylcholine associated withaging can contribute to an overactive bladder. Age causes increasedstretch-induced acetylcholine derived from non-neural cells that arefound in the urothelium in addition to a reduction in the release ofthe neuronal acetylcholine, which responds to stimulation of theelectrical field. The action of the non-neural acetylcholine in anautocrine or paracrine fashion may facilitate contraction of thedetrusor muscles (Mayo Clinic, 2015). Additionally, progesterone andestrogen have an influence on female innervation. These femalehormones have an influence on bladder contraction and the frequencyof voiding. A reduction in the dopamine levels that is characterizedby aging may lead to the decreased inhibitory activity of theautonomic innervation predisposing the patients to an overactivebladder (Ciccone, 2015).

Thesepatients usually have an early and abrupt action of the detrusormuscles way before the bladder is full. Therefore, they end upreleasing small volumes of urine from time to time. This is the basisfor the hallmark presentation of the disease, which is described asabrupt and the imminent release of urine, regardless of streaming ornot, coupled with increased frequency. However, these patients have atypically normal Post-void residual Urine Test (PVR) urine volume ofless than 51 mL (Hall, 2010). This condition can be caused by defectsin the central nervous system that alter inhibition or sensoryafferents to the urinary bladder. Some of the conditions associatedwith this include space-occupying lesions such as aneurysms, tumorsand hemorrhage, diseases that cause demyelination, for example,Alzheimer`s disease, multiple sclerosis and Parkinson`s disease.Other conditions that are less likely to have caused her conditionare atrophic urethritis, uterine prolapse due to multiparity, lowerurinary tract infections such as cystitis or fecal impaction (Kumar,Abbas &amp Aster, 2012). A history of spinal cord injury, diabeticneuropathy or spinal stenosis would have helped to rule out impairedcontractility of the detrusor muscle, which is relatively uncommon.However, this condition is usually co-diagnosed with detrusorover-activity in about 33% of elderly patients in a nursing home(Hall, 2010).

Overflowincontinence is another possible cause of the patient’s condition.This condition is observed in 7% to 11% elderly patients withincontinence (Barrett, Barman &amp Boitano, 2010). It ischaracterized by a reduced caliber and force of the urinary stream,the feeling of incomplete bladder emptying and incompletemicturition. The main causes of this condition include obstruction ofthe outlet and dysfunction in the contractility function of thebladder. Both conditions increase the volume of the bladder. Inoutlet obstruction, blockage by a physical condition causes urinaryflow obstruction. It is commonly associated with severe genitourinaryprolapses, fecalomas or urogenital cancers, which are likely atAlvita’s age. Lesions of the sacral spinal cord or use ofanticholinergic drugs like narcotics, neuroleptics, muscle relaxantsand some tricyclic antidepressants can cause dysfunction of bladdercontractility (The Netherlands: European Association of Urology,2013). Diuretics such as Thiazides (hydrocholorthiazide) and Loopdiuretics (furosemide and torsemide) are known to increase the volumeof urine into the bladder, increasing pressure due to high urinaryvolume hence causing overflow incontinence. Long-term treatment withoral hormone replacement therapy may also increase the risk ofdeveloping incontinence (Masters &amp Trevor, 2011). Older patientsmay be undergoing this treatment in order to strengthen theirskeletal structure and support system to the bladder (Kumar, Abbas &ampAster, 2012).

Thelast possible cause of the condition is functional incontinence. Thiscondition is characterized by a chronic deterioration of thepatient’s cognitive function, which then affects her toilet skills.It is common in old age and in patients developing demyelinatingdiseases such as multiple sclerosis, whose cognitive functions worsenwith a prolonged disease condition. It also affects the mobility of apatient. Demyelinating localized areas called plaques cause thedestruction of the oligodendroglia and perivascular inflammation,which cause protein and lipid changes in myelin. This leads to damageof the axonal processes with preservation of cell bodies. There isthe development of fibrous gliosis, which is then spread throughoutthe nervous system in the posterior, lateral and periventricularareas. It affects tracts found in the pons, midbrain and cerebellum.In addition to urinary incontinence, the patients develop weaknessand clumsiness of their limbs, easy fatigability of the limbs andgait changes, all of which are seen in Alvita. Spastic paresthesialeads to gait changes and limited mobility. Spinal cord involvementis closely related to dysfunction of the urinary bladder.Chronicimpairment of the cognitive function should be an exclusion diagnosis(Grossman et al., 2014).

Question2

Shortlyafter the birth of her second child, Alvita started experiencing mildincontinence that was aggravated by action such as laughing orcoughing. This condition is most likely stress incontinence, acondition that is caused by relaxation of the pelvic bones and thepelvic flow, leading to prolapse of the urinary bladder. One of thehallmark presentations of this condition is incontinence that isassociated with actions that cause a Valsalva maneuver, such ascoughing, laughing, sneezing, bending or squatting. These actionsincrease the internal abdominal pressure, which then causes anexertion of force on the urinary bladder leading to relaxation of thedetrusor and sphincter muscles, causing the release of urine. Thiscondition is associated with the release of small volumes of urine(Kumar, Abbas &amp Aster, 2012).

Thesphincters of the urinary bladder are muscular valves lying at thebottom of the bladder. Their work is to control urinary flow, byupholding inhibition and release of urine according to nervouscommunication. During pregnancy, there is an expansion of the uterinebody, which then exerts additional pressure on the urinary bladder. The muscles of the bladder, such as the detrusor muscles, thesphincter muscles and those of the pelvic floor become overwhelmedwith the forced of the overlying uterus, leading to increasedfrequency therefore, promoting over-activity of the urinary muscles(Grossman et al., 2014). Thus, detrusor over-activity could be one ofthe causes of the condition experienced by Alvita after the pregnancybecause the withdrawal of the pregnancy does not automatically meanthe end of the symptoms. Some cases may be severe enough to persistlong after the pregnancy. A combination of overactivity of thedetrusor muscles, relaxation of the pelvic flow, weakening of thesphincters and prolapse of the urinary bladder can cause urinaryincontinence long after the pregnancy (Hall, 2010).

Otherconditions that could be closely related to Alvita’s incontinenceafter the pregnancy include nerve injury, an episiotomy ordisplacement of urinary structures (Wehrberger et al., 2012). Damageto the nerves that supply the urinary bladder causes an alteredregulation of the genitourinary system. In addition, the fact thatpregnancy causes the displacement of the bladder and the urethra isenough to cause incontinence after pregnancy. If the obstetrician isnot keen enough during childbirth when performing an episiotomy, theycan cause damage to the regulating structures on the pelvic floor ordamage some nerves that supply the bladder, also causing chronicincontinence (Hall, 2010).

References

Barkley,P., S. (2012). Building Rapport with your Patient: Positive CaseManagement Outcomes. National Association for Homecare and Hospice.

Barrett,K. E., Barman, S. M., &amp Boitano, S. (2010). Ganong`sreview of medical physiology. New Delhi: McGraw Hill, 2010.

Ciccone,C. D. (2015). Pharmacology in rehabilitation. FA Davis.

Grossman,S., Porth, C. M., Conelius, J., Gerard, S. O., Moriber, N., O`Shea,E. R., &amp Wheeler, K. (2014). Porth`s Pathophysiology: Concepts ofaltered health states.

Hall,J. E. (2010). Guyton and Hall textbook of medical physiology.Elsevier Health Sciences.

Kumar,V., Abbas, A. K., &amp Aster, J. C. (2012). Robbins basic pathology.Elsevier Health Sciences.

Masters,S., &amp Trevor, A. (2011). Basic and clinical pharmacology.McGraw-Hill Medical.

MayoClinic. (2015). Urinary Incontinecne fromhttp://www.mayoclinic.org/diseases-conditions/urinary-incontinence/basics/definition/con-20037883

TheNetherlands: European Association of Urology. (2013). Guidelines on. Arnhem.

Wehrberger,C., Madersbacher, S., Jungwirth, S., Fischer, P., &amp Tragl, K. H.(2012). Lower urinary tract symptoms and urinary incontinence in ageriatric cohort–a population‐basedanalysis. BJU International, 110(10), 1516-1521.