Urinary Incontinence and Cystitis

Urinary Incontinence

• Functional incontinence affects geriatric patients needing assistance to ambulate to the bathroom
• Neurogenic incontinence is associated with spinal cord injuries, resulting in a lack of bladder control
• Urgency incontinence is seen with patients taking loop diuretics or those with an infection
• Overflow incontinence occurs when the bladder is not emptying properly, often due to urethral blockage seen with BPH
• Clinical manifestation of urinary incontinence is involuntary leakage of urine
• Geriatric considerations include the need to use the bathroom more frequently, decreased bladder capacity, and nocturia
• Pregnancy with vaginal delivery is a risk factor for urinary incontinence
• Interventions include decreasing coffee intake, stopping smoking, preventing constipation, and voiding every 2-4 hours for functional incontinence

Lower UTI: Cystitis / Urethritis

• UTIs pathology can be infection from bacteria, fungus, parasite, chemical irritant, foreign bodies, or trauma
• Cystitis is a bladder infection characterized by stasis of urine
• Urethritis can result from STIs, immunosuppression, or poor hygiene and impaired protective mechanisms
• Protective mechanisms include one-way urine flow, epithelial cells lining the urinary tract, and acidity
• If protections are ineffective, a UTI can occur
• Clinical manifestations include urinary frequency, urgency, dysuria, pain, and pink/cloudy urine
• Delirium may be present in geriatric patients
• Pelvic pain can be an indication
• Labs: CBC, CMP
• Medications include trimethoprim/sulfamethoxazole (antibiotic) 2 tabs every 12 hours x 14 days
• Phenazopyridine (urinary analgesic) 200mg 3x day, drinking 8 glasses of water, using sunscreen, knowing urine will be orange

Acute Pyelonephritis

• Obstruction or ureteral reflux causes contaminated urine to backflow into the kidney
• Renal calculi can cause this
• Clinical manifestations include costovertebral angle tenderness, fever, chills, nausea/vomiting, and dehydration
• IV Pyelogram monitors labs like BUN/Creatinine with contrast.
• Patient at risk for dehydration needs IVF with normal saline (0.9% sodium chloride)
• Monitor for creatinine increased greater than 2x the normal amount of 0.9 mg/dL

Chronic Pyelonephritis

• Chronic reflux of contaminated urine causes the kidney to be smaller and inflamed
• Obstruction from renal caliculi causes urinary stasis and bacteria growth
• Backflow of infected urine into the kidneys results in scarring and atrophy
• Vague and inconsistent Symptoms
• Monitor BUN/Creatinine for Tx/Dx
• Administer urinary analgesics, antipyretics, and antibiotics
• Target an input and output of 1500 ml minimum a day if not restricted
• Maintain an intake between 3-4L day

Renal Calculi (Nephrolithiasis/Urolithiasis)

• Increased concentration of particles in urine causes stone formation and obstructions
• Clinical manifestations include renal colic, dull/localized flank pain, nausea/vomiting, and hematuria.
• Opioid medication for pain.
• Drink 2 glasses of water at bedtime
• To prevent excessive sweating and dehydration, decrease protein, and remove spinach, strawberries, and wheat bran from the diet

Acute Glomerulonephritis

• An infection somewhere else in the body causes the immune system to attack glomeruli walls, increasing GFR
• Clinical manifestations: coffee-colored urine, headache, hypertension, periorbital edema, edema, shortness of breath
• Monitor VS Q4H
• Perform CBC and CMP daily
• Limit to control fluid overload
• Increase carbs to fuel up and reduce protein breakdown

Chronic Glomerulonephritis

• Kidneys become hard and small due to chronic Proteinuria and hypertension, causing renal damage (scarring, atrophy), leading to CKD
• Clinical manifestations include weight loss, decreased strength, nocturia, hyperkalemia, metabolic acidosis, headache, anemia, and pericardial rub
• High protein diet required
• Use diuretics and antihypertensives
• Dialysis and strict I/O management

Nephrotic Syndrome

• Increased glomerular permeability and massive proteinuria damage the glomerular membrane
• Can result from lupus, infection, cancer, vasculitis, DM
• Edema due to albumin loss decreases oncotic pressure and allows fluid to escape, triggering hepatocytes to increase lipid synthesis causing hyperlipidemia
• Hypoalbuminemia due to poor kidney function and albumin loss
• Increased Thrombus risk and generalized Edema Clinical Manifestations
• Monitor skin integrity in the sacral area to check for breakdown
• Monitor for thrombus/PE
• Perform UA for protein and WBC
• Use of Ace inhibitors, Diuretics, and lipid-lowering medications

Polycystic Kidney Disease

• Genetic disease either recessive or dominant
• Dominant spreads to other structures and organs. A liver biopsy can determine if recessive or dominant disorder
• Recessive form: respiratory distress, enlarged kidneys, systemic HTN
• Dominant form: 40-50 y/o, concentration of urine is decreased, HTN, proteinuria, hematuria, pain
• Supportive care
• Apply heat to the abdomen to decrease discomfort
• Prevent dehydration with adequate fluid intake
• Avoid NSAIDs

Acute Kidney Injury

• Is caused by acute loss of renal function, due to perfusion stemming from MI, DM, HTN, CA, BPH, Nephrotoxic drugs)
• Prerenal from peripheral vascular disease causes flow reduction to the kidney
• Intrarenal affects the kidney with constricted or blocked nephrons which disrupts kidney flow
• Postrenal means there is an obstruction
• Ex of pre-renal progressing kidney injury: Cardiac Infarction causes pre-renal injury due to decreased kidney perfusion, the RAAS attempts to compensate with fluid and dilation, but if unmanaged the kidneys will be injured
• Electrolyte and ABG imbalance
• Oliguric phase (no urine)
• Diuretic phase (hypovolemia/ urine not concentrated)
• Recovery phase (electrolytes are normalizing like potassium)
• Acute Tubular Necrosis causes damage to the tubules seen in intra-renal injuries, vasoconstriction
• Risks include hemorrhage (volume is decreased = less perfusion to the kidney)
• Avoid NSAIDs, contrast, and nephrotoxic medications
• Strict I/O
• High carb diet, no potassium or phosphorus

Chronic Kidney Disease

• Kidney damage to the nephrons causes not working
• Other nephrons attempt to compensate but eventually fail
• Seen in patients with uncontrolled HTN, DM, smoking, and long-term circulation
• Will require regular dialysis
• Erythropoietin production is decreased causing anemia (hormone released from the kidney that tells the bone marrow to produce RBCs)
• At risk for bone disorders (bone breakdowns and fractures) due to a deficiency in vitamin D, increased Phos, and decreased calcium in End Stage Renal Disease (when CKD is in Stage 5)
• Edema, pulmonary congestion, and pericardial friction rub
• Types of Dialysis: Hemodialysis, Peritoneal Dialysis, Continuous Renal Replacement Therapy (CRRT)
• Monitor weight gain 2lbs in a nursing shift, notify provider of decreased or minimal UOP, restrict fluids
• Hold BP and Cardiac medications during dialysis, which will be removed due to the process
• NO Ketorolac
• High carb diet, no potassium/ phosphorous
• Use Diuretics, calcium binders, and antihypertensives

Kidney Labs

• BUN (Increased): 10- 20mg/dL
• Serum Creatinine (Increased): 0.6-1.2 mg/dL
• GFR (decreased): 90-120 ml/min.
• Male Hgb (Low/Anemia): 14-18 g/dL, Female 12-16 g/dL
• Male RBC (Low): 4.7- 6.1, Female 4.2- 5.4
• Male Triglycerides (high): 40- 60mg / dL, female 35- 135 mg/dL
• Potassium (increased): 3.5-5 mEq/L
• ABG / pH: Acidosis (pH