AKI & Male Reproductive Disorders (copy)

CKD vs AKI

• Chronic Kidney Disease (CKD):

  • Progressive, irreversible loss of kidney function

• Acute Kidney Injury (AKI):

  • A potentially reversible, abrupt decline in kidney function leading to increased creatinine, decreased urine output, or both.

  • Usually associated with other life-threatening conditions

  • MOST COMMONLY: AKI follows severe, prolonged hypotension, hypovolemia, or exposure to a nephrotoxic agent

  • Develops over hours – days

  • High mortality rate

RIFLE Criteria

Classification of degree of injury based on GFR and urine output

• R – RISK

• I – Injury

• F – Failure

• L – Loss

• E – ESRD

AKI - Etiology & Pathophysiology

• Clinical manifestations range:

  • Mildly elevated serum creatinine → anuric renal failure

Causes leading to AKI:

• Prerenal 

  • External to the kidneys (ie hypovolemia or meds)

  • Usually, reversible

• Infrarenal

  • Conditions that cause direct damage to renal tissue (parenchyma) → impaired nephron function (ie ATN due to ischemia, nephrotoxins, or sepsis)

  • Due to prolonged ischemia OR the presence of nephrotoxins (ie gentamycin, ACE inhibitors/ARBs or CT contrast dye), Hgb from hemolyzed RBC’s (ie sickle cell disease) or myoglobin released from necrotic muscle cells

• Postrenal

  • Mechanical obstruction of urine outflow (ie BPH, Prostate Ca, renal calculi, tumors).

  • Usually reversible if identified before permanent kidney damage occurs 

Contrast-Induced Nephropathy

• Contrast dye can affect the kidneys by directly harming tubular cells, causing blood vessel constriction that reduces blood flow, and creating an osmotic effect that further damages them

  • Renal vasoconstriction: Contrast causes decreased renal blood flow, especially in the outer medulla, leading to ischemia (oxygen deprivation of kidney tissue).

  • Direct tubular toxicity: The contrast agent is toxic to renal tubular epithelial cells, leading to cell injury and necrosis.

• Tx: IV hydration to promote diuresis and flush out contrast (verify kidney function before administering contrast to ensure the kidneys are capable of effectively eliminating the contrast both before and after the procedure)

  • Monitor kidney function labs

AKI - Clinical Manifestations

• Prerenal and postrenal AKI correctible – ADDRESS THE CAUSE

• Untreated prerenal and postrenal causes +/ or intrarenal causes → Acute Tubular Necrosis (ATN)

• ATN has three phases:

  • Initiation

  • Maintenance

  • Recovery

• NOTE: In some situations, the patient does not recover from AKI and CKD develops

AKI - 1: Initiation Phase

• Characterized by:

  •  ↑ serum creatinine + BUN

  • ↓ urine output

AKI - 2: Maintenance Phase

• Days to weeks

• May be anuric, oliguric, or nonoliguric 

  • Nonoliguric – dilute urine but uremic toxins present (low specific gravity)

  • Oliguric

    • Lasts 10-14 days usually. The longer it is prolonged, the poorer the outcome

  • Oliguric manifestations include:

    • Urinary Changes: U/O ↓ to <400mL/24h

    • Fluid volume excess: JVD, edema, hypertension → pulmonary edema, pericardial and/ or pleural effusions

    • Metabolic acidosis: Kussmaul’s resps (deep rapid) to increase blowing off CO2 → lethargy/ stupor (if prolonged)

    •  Sodium Balance: Hyponatremia

    • Potassium Excess: Hyperkalemia→ tall, peaked T waves (ECG)

    • Hematological Disorders: Anemia, ↑ bleeding,, ↓ WBCs. 

    • Calcium and Phosphate: Hypocalemia + hyperphosphatemia

    • Waste Product Accumulation: ↑ creatinine, ↑ BUN, ↓ eGFR

    • Neurological Disorders: Fatigue/ difficulty concentrating → seizures, stupor, coma

AKI - 3: Recovery Phase

• Marked by return of BUN, Creatinine and GFR towards normal states

• Diuresis → fluid & electrolyte abnormalities

  • Begins 1-3 L/ 24h → 3-5 L/ 24h

  • Pts must be monitored for hyponatremia, hypokalemia and dehydration

  • May last 1-3 weeks 

• Patient’s acid-base, electrolyte and waste product values begin to normalize

• Renal function may take up to 12 mos to stabilize. 

AKI - Diagnostic Studies

• Urinalysis

  • Sediment WITH casts, cells or proteins → intrarenal disorders

• Urine specific gravity, sodium content, osmolality → helps differentiate different types of AKI

• Renal ultrasound: anatomy and function

• Renal CT: can identify causes of obstruction, but exposure to radiation and nephrotoxic contrast is greater risk

• MRI is not recommended

AKI - Collaborative Care

• GOALS of CARE:

  • Eliminate the cause(s)

  • Manage signs and symptoms

  • Prevent complications

• IMPORTANT - Is there sufficient INTRAVASCULAR VOLUME and CARDIAC OUTPUT to perfuse the kidneys? 

• Diuretic Therapy

  • Loop diuretics (ie Lasix)

  • Osmotic diuretic (ie mannitol)

• Fluid Restriction: 600mL (insensible losses) + previous 24h losses

• Treatment of Electrolyte imbalances

• Renal Replacement Therapy (RRT) – Usually, hemodialysis (HD)

• If AKI is already established, fluids and diuretics will not be effective and may be harmful. Generally, begin early RRT to minimize symptoms and prevent complications. 

Nutritional Therapy

• Main challenge → Balancing adequate calories to prevent catabolism despite restrictions required to prevent electrolyte and fluid disorders

• Energy from fat and carb sources prioritized to prevent ketosis 

• 25-35kCal/kg

• Electrolyte replacement in accordance with serum levels

  • Sodium is restricted

  • Hyperphosphatemia, hypermagnesemia and hypocalcemia 

• Enteral or parenteral feeding may be required (though parenteral would be done ++ cautiously if pt on RRT)

AKI - Nursing Management

• ***Health Promotion:

  • ID high-risk populations for AKI - sepsis!

  • Control nephrotoxic drugs (ie IV contrast, gentamicin)

  • Prevent prolonged episodes of hypovolemia or hypotension

• STOPPED acronym - for general mngmt of AKI

• Manage fluid and electrolyte balance

• Monitor AND record accurate intake and output

• Daily weights (at the same time, same scale)

  • 1 kg = 1L of fluid  

• Reduce risk of infection

  • Blunted febrile response

• Give corrected dose of antibiotics for renal impairment

• Skin care and mouth care

STOPPED acronym

for general mngmt of AKI

• S - sepsis (cause for hypovolemia (pre-renal); causative factor for AKI = must be ruled out as a cause

• T -  toxins - nephrotoxic drugs that can cause intrarenal dmg (are they on meds that dmg? NSAIDS? gents?)

• O - output and intake (AKI: often fluid challenge pt, IV rehydrate unless can take in PO, flush kidneys out (very diff from CKD)

• P - potassium - critical to trend and track d/t irritability it causes in myocardium = worsens kidney function 

• P - potassium+++

  • CBIGKDrop - Calcium gluconate (stabilize myocardium), Beta2 agonists (salbutamol), Insulin (shift potassium into cells), Glucose (b/c not diabetic), Kayexalate (PO; binds K+ in the gut - slower acting), Diuretics/Dialysis (dialysis only if GFR low - generally below 10)

• E - electrolytes

• D - dialysis 

Rhabdomyolysis

• Definition: “..characterized by skeletal muscle injury and release of intracellular contents into the systemic circulation – namely, potassium, phosphate, myoglobin, creatinine kinase (CK) and lactate dehydrogenase (LDH).”

• Can cause intrarenal AKI secondary to myoglobin obstruction of the renal tubules due to muscle breakdown

Rhabdomyolysis - Etiology: DOTS

• Drugs (amphetamines salicylates)

• Over-exertion (NMS, seizures, long-distance running)

• Trauma (falls, long periods of immobility, crush injuries)

• Statins (cholesterol drugs) 

  • if newly on a statin, may come into hospital with AKI

Rhabdomyolysis - Diagnosis

• History – crush injury, fall followed by prolonged immobility, concomitant drug use, status epilepticus 

• Physical exam

• Elevated serum Creatine Kinase (CK) >1000

  • most sensitive indicator - CK (breakdown product of muscle) 

  • if over 5x the amount, anything over 700 (usually under 140) - dont tend to be aggressive unless CK > 4000

• Urinalysis +’ve for blood (but microscopy NOT), suggesting myoglobin as cause for urinalysis result.

  • can get false positive for Hgb on urine dipstick (can falsely pick up myoglobin - both are globins)

• Hyperkalemia, hyperphosphatemia and hypocalcemia often present

• No diagnostic imaging unless trauma-related

Rhabdomyolysis - Clinical Manifestations

• Aching muscles (myalgias)

• Tea-coloured urine

• Reduced urine output

• Tachycardia secondary to pain, dehydration, or fluid shifts

• ? Muscle swelling (usu post- fluid resuscitation)

• ?Bruising/ pressure sores → compression injury

Rhabdomyolysis - Collaborative Care

STOPPED Pneumonic for mgmt. of AKI

• Sepsis – look for sepsis as a possible cause first

• Toxins – stop any drugs that will make the AKI worse

• Output and intake – Aggressive IV fluid resuscitation is the HALLMARK treatment for rhabdo

  • Want to flush myoglobin out (increase CO)

• Potassium

• Potassium

• Electrolytes

• Dialysis (if necessary)

Benign Prostatic Hyperplasia (BPH)

• Non-inflammatory enlargement of prostate gland resulting from increase in # of epithelial cells and amount of stromal tissue

• Most common urological problem in male adults

• ½ men will experience BPH in their lifetimes and ½ of these men (25% total) will have lower UTI symptoms

• Occurs in nearly all men with functioning testes

• Research is unclear whether BPH predisposes men to the development of prostate cancer

BPH - Etiology & Pathophysiology

• Hormonal changes with aging

• Develops in inner part of prostate

  • Cancer more likely to develop in outer part

• Enlargement compresses urethra → eventual partial or complete obstruction

  • Leads to development of clinical symptoms

BPH - Risk & Protective Factors

• Risk Factors

  • Aging

  • Physical inactivity

  • Diabetes

  • Obesity (large waist circumference)

  • Familial history in first-degree relative

• Protective Factors

  • Diet of fruit & veggies; lycopene

  • Physical activity

BPH - Clinical Manifestations

• Bothersome “LUTS” – lower urinary tract symptoms

• Gradual onset

• Obstructive symptoms

  • Decrease in calibre & force of urinary stream, hesitancy, intermittency, dribbling

• Irritative symptoms (associated with inflammation or infection)

  • Urinary frequency, urgency, dysuria, bladder pain, nocturia, incontinence

• Complications

  • Urinary retention, UTI & possible sepsis, calculi, renal failure

BPH - Diagnostics

• History and physical

• DRE – digital rectal exam

• PSA levels 

• Urinalysis with culture

• Postvoid residual

• Ultrasound

• Cysto -Urethroscopy

BPH - Collaborative Care

• Active Surveillance: “Watchful waiting”

• Drug Therapy

  • 5α-Reductase inhibitors

  • α-Adrenergic receptor blockers

• Invasive therapy

  • Transurethral resection of the prostate (TURP): GOLD STANDARD

  • Transurethral incision of the prostate (TUIP): local anesthetic; as effective as TURP

  • Prostatectomy: surgery of choice for larger prostates

• Minimally invasive therapy

  • TUMT, TUNA, Laser prostatectomy

Transurethral Resection of the Prostate (TURP)

• GOLD STANDARD

• Done under spinal or general anesthetic

• Associated with good outcomes in 90% of patients

• HOLD ASA or anticoagulants preop

• Pain and UTI most common preop problems necessitating TURP

TURP: Preop Care

• Urinary drainage must be restored before surgery

• Use of lidocaine jelly ++ helpful

• May require coude (curved tip) catheter

• Antibiotics usually given before invasive procedures

• Patient education on common alterations in sexual function is important – retrograde ejaculation not harmful but orgasms might be less pleasurable

• HOLD blood thinners (incl. ASA) several days before the procedure

TURP: Postop Care

• Main complications: 

  • Hemorrhage

  • Bladder spasms

  • Urinary incontinence

  • Infection

• Manage CBI – rate determined by colour of drainage. Goal is light pink with no clots. Small clots are expected for 24-36h, but bright red blood can indicate hemorrhage.

• Avoid activities that increase abdominal pressure (ie straining)

• Remove CBI 2-4 days postop; trial of void 6h after cath removal

• Urinary dribbling/ incontinence common initially; can usually improve with Kegel exercises over first 2 months postop

• Dietary interventions / bowel protocol to avoid straining; adequate fluid intake

Prostate Cancer

• Malignant tumour of prostate gland 

• Androgen-dependent adenocarcinoma (overgrowth of cells in a gland) 

• Majority of tumours in outer aspect of prostate

• Usually slow growing but progressive if left untreated

• Can metastasize through direct extension, lymph system, or bloodstream

Prostate Cancer - Causes

• Approximate 1 in 7 men will be diagnosed with prostate cancer during their life time

• Age

• Ethnicity

• Family history

• Diet

Prostate Cancer - Risk Factors

• > 50 years of age

• Ethnicity: Black > White > Asian

• Family history

• High levels of testosterone

• Diet high in fats & low in vegetables & fruits

• Occupational exposure to cadmium

• Genetic link -mutations in luminal and basal cells of the prostate. Also links to BRCA1 and BRCA2 (genetic mutations causing breast cancer)

Prostate Cancer - Prevention

• Eat a wide variety of fruits & vegetables each day

  • Consumption of tomatoes, tomato-based products, & garlic may protect against prostate cancer

• Be physically active

• Maintain a healthy weight

Prostate Cancer - Clinical Manifestations

• Generally asymptomatic during early stages 

• Urinary symptoms may occur (similar to BPH):

  • Difficulty starting or stopping urination

  • Slow stream

  • Painful urination or ejaculation

  • Dribbling

  • Frequent urination

  • Loss of urinary control

  • Blood in urine or ejaculate

  • Night-time voiding

• Advanced prostate cancer:

  • Weight loss

  • Fatigue

  • Backache or sciatica-like pain, or swelling of legs that doesn’t go away

Prostate Cancer - Diagnosis

• Often diagnosed before symptoms occur

  • DRE:GOLD STANDARD

  • PSA screening: NOT RECOMMENDED

    • Not specific to prostate cancer!

    • Prostate biopsy required for diagnosis

• Transrectal ultrasound (TRUS) if DRE abnormal

• Biopsy to confirm (based on cell type)

• Prostate Cancer Associated 3 (PCA3) – gene in urine specific to prostate ca. 

• AFTER DIAGNOSIS:

  • Bone scan

  • CT

  • MRI

PSA Screening

• No provincial screening program in BC

  • If screening is going to be done, men between the ages of 55 and 69 most benefit from it. Routine screening not recommended over the age of 70. (CDC) 

• PSA (prostate specific antigen) used for:

  • Monitoring established prostate cancer & metastatic disease or detection of early recurrence, where prostate cancer is already known

  • Diagnostic adjunct in combination with other tests in symptomatic men

  • Screening tool

• PSA Routine Screening NO LONGER RECOMMENDED

Prostate Cancer - Diagnosis: Staging and Grading

• Whitmore-Jewett (see Table 57-5)

• TNM Classification System

  • Tumor

    • Characteristics of the primary tumor (grading)

  • Nodes

    • Involvement of lymph nodes

  • Metastasis

    • Evidence of spread

• Gleason scale (2-10)

  • Grading of tumour based on histology

  • Provides an indication of the risk for spread

Prostate Cancer - Collaborative Care

• Watchful waiting 

• Chemotherapy

  • Chemotherapy and radiation therapy side effect

    • Depends on type of therapy. 

    • Common side-effects may include: Nausea, vomiting, fatigue, hair loss …  

• Hormone therapy 

  • Hormonal side effects: Hot flashes, muscle atrophy, loss of libido

• Radical prostatectomy 

  • Specific surgical side effects:

    • Risk for incontinence or “dribbling”

    • Risk for impotence

• Cryotherapy