Urinary Incontinence and UTI

Urinary Incontinence

• Functional incontinence occurs in geriatric patients needing assistance to the bathroom.
• Neurogenic incontinence results from spinal cord injuries, causing a lack of bladder control.
• Urgency incontinence is seen in patients taking loop diuretics or with infections.
• Overflow incontinence occurs when the bladder doesn't empty properly, potentially due to urethral blockage from BPH.
• Signs and symptoms include involuntary leakage of urine.
• Risk factors include being geriatric - increased frequency, decreased bladder capacity, nocturia, and a history of pregnancy with vaginal delivery.
• Teaching includes decreasing coffee intake, stopping smoking, preventing constipation/stress, and using the bathroom and voiding every 4-6 hours for functional issues.

Lower UTI: Cystitis & Urethritis

• The pathophysiology involves infection from bacteria, fungus, parasite, chemical irritant, foreign body, or trauma.
• Cystitis is a bladder infection associated with urine stasis.
• Urethritis can be caused by STIs, immunosuppression, poor hygiene, or impaired protective mechanisms.
• Protective mechanisms include one-way urine flow, the epithelial lining of the urinary tract, and the acidity of the environment which prevents bacterial growth.
• Signs and symptoms include frequency, urgency, dysuria, pain, pink/cloudy urine, pelvic pain, and delirium in geriatric patients.
• Labs to pull include CBC and CMP.
• Medications to administer include Trimethoprim/Sulfamethoxazole (antibiotic) – 2 tabs every 12 hours for 2 weeks. Also, administer Phenazopyridine (urinary analgesic) – 200mg 3 times per day.
• Patient teaching for Phenazopyridine involves drinking 8 glasses of water daily, using sunscreen, and being aware that urine will turn orange.

Acute Pyelonephritis

• The pathophysiology includes obstruction or urethral reflux where contaminated urine backflows into the kidney.
• It can be caused by renal calculi.
• Symptoms include costovertebral angle tenderness, fever, chills, nausea/vomiting, and dehydration.
• Diagnosis involves IV pyelogram and monitoring BUN/Creatinine with contrast.
• Treatment involves intravenous fluids with NS (0.9% NaCl) for patients at risk for dehydration.
• Labs to monitor include creatinine, which is increased more than 2 times the normal amount (0.9mg/dL).

Chronic Pyelonephritis

• Pathophysiology involves chronic reflux of contaminated urine and the kidney becomes smaller or inflamed.
• Obstruction from renal calculi causes urinary stasis/bacteria growth.
• The kidney is scarred and atrophied.
• Signs and symptoms are vague and inconsistent.
• Diagnosis/treatment involves monitoring BUN/Creatinine.
• Administer urinary analgesics, antipyretics, and antibiotics.
• Input/output should be similar if not restricted; then 1500mL per day minimum - Intake: 3-4L per day.

Renal Calculi (Nephrolithiasis/Urolithiasis)

• Pathophysiology includes an increased concentration of particles in urine causing stone formation, which leads to obstruction.
• Signs and symptoms include renal colic, dull/localized flank pain, nausea/vomiting, and hematuria.
• Treatment involves opioids for pain and drinking 2 glasses of water at bedtime.
• Prevention teaching involves avoiding activities with excessive sweating/dehydration and decreasing protein intake which includes avoiding spinach, strawberries, and wheat bran (oxalate).

Acute Glomerulonephritis

• Pathophysiology: There is an infection (virus/bacteria) where the immune system attacks glomeruli walls.
• Glomerular membranes are more permeable which increases GFR.
• Signs and symptoms include coffee-colored urine, headache, hypertension, periorbital edema, and shortness of breath.
• Treatment involves vital signs every 4 hours, daily CBC/CMP, fluid restriction to prevent overload, and eating carbs for energy to reduce protein breakdown.

Chronic Glomerulonephritis

• Kidneys are hard and small due to chronic proteinuria and hypertension, causing renal damage (scarring/atrophy) that leads to CKD.
• Signs and symptoms include weight loss, decreased strength, nocturia, hyperkalemia, metabolic acidosis, headache, anemia, and pericardial rub.
• Treatment/diagnosis involves a high-protein diet, diuretics, antihypertensives, dialysis, and strict I/O monitoring.

Nephrotic Syndrome

• Pathophysiology involves increased glomerular permeability and massive proteinuria which damages the glomerular membrane.
• Systemic diseases such as lupus, infection, cancer, DM, vasculitis can cause nephrotic syndrome.
• Edema occurs due to loss of albumin causing a decrease in oncotic pressure and fluid escapes.
• Hepatocytes increase lipid synthesis causing hyperlipidemia.
• Signs and symptoms include increased risk for thrombus and generalized edema.
• Treatment/diagnosis involves monitoring skin integrity (sacral area), monitoring for thrombus/PE, and urine analysis for protein and WBCs.
• Medications used include ACE inhibitors, diuretics, and lipid-lowering medications.

Polycystic Kidney Disease

• Pathophysiology is either recessive or dominant.
• If dominant, it spreads to other structures and organs.
• The distinction between recessive and dominant involves a liver biopsy.
• Recessive signs/symptoms include respiratory distress, enlarged kidneys, and systemic hypertension.
• Dominant signs/symptoms include onset at 40-50 years, decreased urine concentration, hypertension, proteinuria, hematuria, and pain.
• Treatment includes supportive care, applying heat to the abdomen to decrease discomfort, preventing dehydration with fluid intake, and avoiding NSAIDs.

Acute Kidney Injury (AKI)

• Acute loss of renal function due to decreased perfusion - MI, DM, HTN, BPH, nephrotoxic drugs
• Types of AKI:
  • Pre-renal: Peripheral vascular disease decreases blood flow TO the kidney.
  • Intra-renal: Nephrons constricted/blocked which disrupts INSIDE the kidneys.
  • Post-renal: Obstruction.
• Cardiac infarction can cause pre-renal injury due to decreased kidney perfusion.
• If pre-renal issues aren’t treated/corrected it can progress to intra-renal injury.
• Signs and symptoms include electrolyte/ABG imbalances.
  • Oliguric phase: no urine.
  • Diuretic phase: hypovolemia; urine not concentrated.
  • Recovery phase: electrolytes are normalizing (like potassium).
• Acute tubular necrosis involves damage to tubules seen in intra-renal injuries and vasoconstriction.
• Risks include hemorrhage - volume is decreased causing less perfusion to the kidneys, resulting in injury.
• Treatment involves limiting NSAIDs, contrast, and nephrotoxic medications.
  • Strict I&O
  • Diet: high in carbs with no potassium or phosphorus.

Chronic Kidney Disease (CKD)

• Damage to the nephrons causes them not to work.
• Other nephrons try to compensate but ultimately fail.
• Can be seen with uncontrolled HTN, DM, smoking, long-term impaired circulation.
• Patients are at risk for anemia due to decreased production of erythropoietin.
• Stage 5 patients have bone disorders due to a deficiency of Vitamin D, increased phosphorus, and decreased calcium.
• Signs and symptoms include edema, pulmonary congestion, and pericardial friction rub.
• Types of dialysis include hemodialysis, peritoneal dialysis, and continuous renal replacement therapy.
• Nursing interventions include monitoring weight gain and notifying the provider of decreased urinary output.
• Hold BP/cardiac meds for dialysis because dialysis will remove them.
• Teaching points include no potassium/phosphorus and a high-carb diet.
• Medications include diuretics, calcium binders, and antihypertensives.
• Ketorolac is nephrotoxic.

Kidney Labs

• Abnormal lab values:
  • BUN (10-20): Increased.
  • Creatinine (0.6-1.2 & 0.5-1.1): Increased.
  • GFR (90-120): Decreased.
  • Hgb (14-18; 12-16): Low (anemia).
  • RBC (4.7-6.1; 4.2-5.4): Low.
  • Triglycerides (40-60; 35-135): High.
  • Potassium (3.5-5): Increased.
  • Calcium (9-10.5): Low.
  • Phosphorus (2 – 4.5): Increased.

Geriatric Considerations for GU

• Medications may not be metabolized properly due to decreased filtration.
• Implement pelvic muscle exercises (Kegels) and set bathroom breaks.

Stomatitis

• Pathophysiology involves idiopathic ulcerations of the oral mucosa and bacterial or viral infections (HSV).
• Commonly seen in chemo patients, those undergoing radiation therapy, and those with autoimmune disorders.
• Signs and symptoms include pain and ulcers in the mouth.
• Monitor concerns with swallowing and the ability to chew.
• If a patient cannot eat, an NG tube or PICC is needed for TPN.
• Treatment involves magic mouthwash.

GERD

• Pathophysiology: The lower esophageal sphincter is not closing efficiently.
• Causes include restrictive clothes, weight gain, smoking, pregnancy, caffeine/alcohol, and fatty food.
• Signs and symptoms include heartburn, chest pain, dysphagia, and Barrett's esophagus.
• Treatment involves Omeprazole (Proton pump inhibitor) and Ranitidine (H2 blocker).
• Teaching points include:
  • Omeprazole: Long-term use has concerns for fractures and may cause diarrhea/HA; DO NOT CRUSH.
  • Stop smoking/drinking, eat a low-fat diet, no milk, peppermint, or soda, and pursue weight loss.

Hiatal Hernia

• Pathophysiology involves idiopathic loosening of the muscular band around esophagus/diaphragmatic junction. Part of the fundus is above the diaphragm.
• Signs and symptoms include dysphagia and GERD symptoms.
• Life-threatening is strangulation: belching/regurgitation.
• Diagnosis involves a barium swallow study or EGD.

Esophageal Varices

• Pathophysiology: Enlarged veins of the esophagus due to portal hypertension.
• Signs and symptoms include variceal bleeding: hematemesis, melina, anemia, hemorrhage (shock).
• Treatment: IV Octreotide (anti-diarrheal; splanchnic vasoconstriction)

Gastritis

• Pathophysiology: inflammation of stomach lining from aspirin, alcohol, H. Pylori, irritation.
• Signs and symptoms: Asymptomatic OR nausea/vomiting, postprandial discomfort during/after meals.
• Avoid NSAIDs/ASA for pain.
• Educate patients to avoid high-stress activities and alcohol/caffeine.
• Notify PCP if stool is dark, indicating a possible GI bleed.

Gastroenteritis

• Pathophysiology: acute inflammation of the stomach and small intestine.
• Signs and symptoms: diarrhea, pain, N/V, fever, malaise, abdominal discomfort.
• Diagnose and treat like a stomach bug - IVF and bowel rest.

Peptic Ulcer Disease

• Pathophysiology: stomach acid in the upper GI damages the lining of the digestive tract.
• Breakdown of epithelial mucosal barrier (duodenal/gastric area)
• Signs and symptoms: pain, burning, nausea, hematemesis which is concerning (GI bleed).
• Dyspepsia when stomach is empty.
• Notify the provider when there is coffee-ground emesis or NG tube drainage.
• Also notify if the patient has heart flutters 30 mins after eating (dysrhythmia).

Ulcerative Colitis

• Inflammatory bowel disease that only affects the colon.
• Starts at the base of Lieberkuhn and leads to abscess formation in the epithelia of crypts.
• Causes exudative diarrhea.
• Patients at risk for colon cancer.
• Serious complication: toxic megacolon, which is swelling/inflammation of the colon that stops working/ruptures. Symptoms: abdominal pain, bloody diarrhea, rectal bleeding.
• Treatment: low fiber, high protein, high calorie diet.
• Corticosteroids, immunomodulators, antibiotics. 
• Labs to monitor: CBC (for bleeding), stool (occult blood), albumin decreased.

Crohn's Disease

• Inflammatory bowel disease that affects the entire GI tract.
• Cobblestone-like appearance through GI tract.
• Can also see ulcers, fissures, fistulas, abscesses.
• Symptoms include: malnutrition (anemia/malaise), and toxic megacolon
• Symptoms also include abdominal pain, arthritis, and fever.
• Diarrhea (bloody but not as bad as UC)
• Treatment: corticosteroids, antibiotics, TPN.
• Labs to monitor: WBC elevated and ESR elevated.
• Complications are normally seen when potassium is decreased and there are abnormal electrolytes.

Enterocolitis

• Pathophysiology: C. Diff
• Large intestine exposed to bacterial toxins causing inflammation/mucosal necrosis
• Symptoms: elevated WBC; fever; abdominal pain; sepsis.
• Perfume watery foul-smelling diarrhea
• Treatment: contact precaution and antibiotics.

Appendicitis

• Pathophysiology: inflammation of the vermiform appendix due to a hard strong mass of feces causing obstruction.
• Symptoms: fever; diarrhea; nausea; migrating pain at McBurney's point (RLQ).
• Nursing considerations: maintaining hydration and educating the patient to go to the ER.
• Treatment: appendectomy
• Antipyretic for fever
• Meds: antibiotics; IVF; opioids; NO LAXATIVES.

Diverticulitis/Diverticulosis

• Pathophysiology: creates polyps in the intestinal tract, resulting in constipation.
• Strongly related to low fiber intake and high pressure in the intestine.
• Diverticulitis: something gets stuck in the polyp and causes inflammation, infection, and rupture.
• Symptoms: left LQ pain; fever; elevated WBC; constipation/diarrhea
• Complications: sepsis; obstruction; perforation.
• Meds to give: antibiotics; laxatives; fiber
• Prevention education: drink 8 glasses of water daily; increase cooked veggies.
  • Avoid nuts, popcorn, or seeds
  • Use psyllium daily to increase fiber, avoid constipation.

Irritable Bowel Syndrome

• Pathophysiology: non-inflammatory; idiopathic; no identifiable pathological process.
• Either constipation or diarrhea.
• Symptoms: constipation; diarrhea; nausea; mucus in stool.
• Abdominal pain relieved with defecation.
• Meds: antidiarrheal; fiber (psyllium); antibiotics; probiotics.
• Dicyclomine antispasmodic: food will taste different; relaxes intestine muscles
• Education: monitor diet for triggers; sleep; exercise; no fluid with meals.
• Stress control may need antidepressants.

Intestinal Obstruction

• Pathophysiology: impacted feces or blockage that can be in the small or large bowel.
  • Mechanical = obstruction from scar tissue (hernia, tumor, intussusception, etc.)
  • Functional = loss of propulsive ability (occurs after surgery)
• Symptoms: abdominal distention; abdomen pain; fever.
  • Increased bowel sounds at first and then NO bowel sounds.
• Clinical manifestation: lower abdominal cramps.
• Treatment: stop tube feeding/PO feeding with obstruction.
  • Bowel rest; IVF to push fluid to break up hard stool.
  • NG tube on low intermittent suction.
• Measure abdominal girth.
• If the patient isn't responding to treatment, prepare them for surgery.
• If a patient is complaining of constipation and has a fever with tachycardia, there is concern for obstruction that has perforated (intestinal strangulation.)

Celiac Disease

• Pathophysiology: intolerance of gluten triggered by gliadin; genetically predisposed.
• Intestinal villi startsto atrophy and causes malabsorption.
• More common in females.
• Symptoms: weight loss; malnutrition; diarrhea/constipation; joint pain; tooth enamel loss.
• Education: avoid foods with gluten or other triggering foods.

Dumping Syndrome

• Pathophysiology: Impaired/rapid gastric emptying into the small intestine causing malabsorption 30 min after eating.
• Glucose is absorbed, so the patient secretes insulin which causes hypoglycemia in 1-3 hours.
• Symptoms: Abdominal pain, diarrhea, hypovolemia (fluid shifting from blood to intestine)
• Symptoms also include hypoglycemia 1–3 hours after eating
• Treatment involves monitoring hypoglycemia/treating as indicated.
• No fluids with meals; no high carbs

Short-Bowel Syndrome

• Pathophysiology: Severe diarrhea causing malabsorption of nutrients (water, electrolytes, carbs, protein, vitamins, minerals) due to surgical removal of parts of the small intestine.
• Symptoms are dependent on the location of the intestine that was removed.
• Treatment involves monitoring nutritional deficits related to malabsorption/removal of parts of the small intestine, possibly needing parenteral nutrition.
• Meds to give and education for:
  • Senna should be avoided with milk or antacids within one hour of taking.
  • Octreotide is an antidiarrheal/splanchnic vasoconstriction.
  • Dicyclomine is an antispasmodic; food will taste different.     - Omeprazole decreases gastric acid but has risks for hip fracture, diarrhea, and HA.
• Infuse formula at prescribed rate; slowly 20 mL/hr or 50 mL/hr.
• Slow feeds if the patient starts experiencing cramping.