1/172
Looks like no tags are added yet.
What is AKI?
Acute kidney injury; rapid, but reversible loss of kidney function (hours to days)
What causes AKI?
Sepsis
Critical illness
Circulatory shock
Burns
Trauma
Cardiac surgery (especially with CPB)
Major noncardiac surgery
Nephrotoxic drugs
Radiocontrast agents
Poisonous plants and animals
Dehydration or volume depletion
Advanced age
Female gender
Black race
CKD
Chronic diseases (heart, lung, liver)
Diabetes mellitus
Cancer
Anemia
Manifestations of AKI
AMS, flank pain, fluid retention, poor fluid output
s/s of AKI
AKI levels/parameters
-Increase in SCr by ⩾0.3 mg/dl (⩾26.5 μmol/l) within 48 hours; or
- Increase in SCr to ⩾1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
- Urine volume
AKI Cause: Prerenal
Sudden or severe drop in BP (shock), or interruption of blood flow to the kidneys
Dehydration, low blood pressure, heart failure
AKI Cause: Intrarenal
Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply
Kidney damage (infection, injury, medications)
AKI Cause: Postrenal
Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor, injury
Blocked urine flow (kidney stones, tumors)
Management of AKI
Treat underlying cause, rehydrate, investigate, stop nephrotoxic drugs, escalate and observe.
Assessment of AKI
Strict Is/Os
Daily Weights
Report urinary outpit if < 0.5 mL/kg/hr x 2+ hours
Oliguria (UO < 400 mL/day)
Azotemia: Build-up of Wastes in the Blood (Increased Blood Osmolarity, Creatinine, & BUN)
Laboratory Assessments
Creatinine: Waste Material from Muscle
Breakdown Cleared in Urine = Creatinine Clearance
Increased Serum Creatinine, Decreased Creatinine Clearance
Increased BUN
Monitor Electrolytes (potassium)
Varies Depending on Progression of Disease:
Osmolarity: Urine Osmolarity Low or Normal Depending
Serum Osmolarity Elevated in Volume-Depleted States Otherwise Normal
Specific Gravity: High or Low, it Depends
GFR: Decreasing (more to diagnose CKD, not AKI)
AKI Treatment
-diuretics
-antihypertensives
-dialysis: clear out metabolic waste
-fluids and electrolytes
-nutrition
-may need low sodium, potassium, phophorous diet
- Maintain regular BP
- Maintain Normal Fluid Status
- AVOID Nephrotoxic Drugs/Agents
- If Unavoidable, Monitor Drug Levels & Adjust Dosing
- Check Kidney Function Prior to Contrast
- Is/O's, Daily Weights, Monitor Electrolytes
- FVE: Diuretics
- IVF: Hypovolemia Suspected
- Fluid Challenge: 500-1000 mL Over 1 Hour
What is a fluid challenge
How much fluid will be excreted vs how much intake
Nutrition therapy for AKI
- AKI: Causes Increased Rate of Protein Breakdown in Muscles
- Registered Dietician: Calculates Protein & Caloric Needs
- Assess Food Intake q Shift
- Oral Supplements, Enteral or Parenteral Nutrition
- Kidney-Specific Formulations
What diet should someone follow if they have AKI?
Limited sodium, potassium, and phosphorus, and may involve fluid restrictions. Protein and caloric needs will vary.
Stage 1 CKD
Normal Kidney Function
Either Abnormal Urine Findings, Structural Abnormalities, or Genetic Traits r/t Kidney Disease
GFR > 90 mL/min
Manage: HTN, DM, Anatomic or Urinary Tract Abnormalities
Screen for Genetic Kidney Disease
Reduce Exposure to Nephrotoxins
CKD Stage 2
Mild CKD
Slightly Reduced Renal Function
Lab Values Point to Kidney Disease
Albuminuria may be Present (Marker of Kidney Damage)
Increased Dilute UO
Structural Changes Present
GFR 60-89 mL/min
Focus on Reduction of Risk Factors
CKD Stage 3
Moderate CKD
GFR 30-59 mL/min
Albuminuria Present
Implement Strategies to Slow Disease Progression
Restrict Fluids, Proteins, & Electrolytes Like Potassium & Salt
CKD Stage 4
Severe CKD
GFR 15-29 mL/min
Jaundice Around the Eyes May be Present
Manage Complications
Discuss Patient Preferences & Values
Educate About Options
Prepare for Renal Replacement Therapy
CKD Stage 5
End-Stage Kidney Disease (ESKD)
GFR < 15 mL/min
Implement Renal Replacement Therapy or Kidney Transplantation
The lower the GFR the (better or worse) the kideys are
worse
AKI Prevention
Maintenance of fluid volume before and after surgery or diagnostic procedures or when nephrotoxic drugs or contrast agents are used
AKI Education
Low protein/high fluid
malnutrition
Daily weight after voiding
Daily BP
Why is protein rough on the kidneys
Stress on the kidneys; Protein is broken down into amino acids, which the kidneys must filter and remove from the blood. High protein intake increases the workload on the kidneys, as they have to process a larger amount of waste products
Meds for AKI
ACEs and ARBs
Diuretics (e.g., furosemide, hydrochlorothiazide)
Non-steroidal anti-inflammatory drugs (NSAIDs, e.g., ibuprofen, naproxen): Can worsen AKI but may be used cautiously in low doses.
Medications to Remove Toxins:
Dialysis: A procedure that removes waste products and excess fluid from the blood.
Antibiotics: If AKI is caused by an infection, antibiotics may be necessary.
Antidotes: Specific antidotes may be used for certain types of kidney injury, such as lithium or ethylene glycol poisoning.
Medications to Support Vital Functions:
Potassium-binding resins (e.g., sodium polystyrene sulfonate): Help control high potassium levels.
Calcium supplements: May be needed if calcium levels are low.
Vitamin D supplements: Helps maintain healthy calcium levels.
What do the kidneys do?
Excrete water and waste (filter blood and produce urine)
What important hormones do the kidneys excrete?
erythropoietin (stimulates red blood cell production), calcitriol (the active form of vitamin D, important for calcium absorption), and renin
What are important hormones that the kidneys regulate/respond to?
Aldosterone: A hormone from the adrenal gland that signals the kidneys to reabsorb sodium and excrete potassium, helping to regulate blood pressure and fluid balance.
Antidiuretic Hormone (ADH): From the pituitary gland, it regulates water excretion by telling the kidneys to reabsorb more water.
Parathyroid Hormone (PTH): Influences the kidneys to reabsorb calcium and excrete phosphate
What are things that are bad for the kidneys (just in general)
HTN, heart problems, nephrotoxic agents (contrast, NSAIDs, metformin, -mycins), CKD
AKI will have a (fast or slow) onset?
fast
Can you bave an AKI with CKD?
Yeppers
What is CKD
chronic kidney disease; progressive, irreversible loss of kidney function
S/s of CKD
- hyperkalemia
- HTN
- anemia
- calcium and vitamin D deficiency
- oliguria
- azotemia
- decreased GFR
- fluid retention
- uremia
CKD vs AKI
CKD = longstanding disease to the kidneys leading to renal failure
AKI = abrupt decrease in renal function; kidney function can return but not at 100%...can also lead to CKD
CKD management and treatment
Same as AKI but with NO DIURETICS
- Restricted protein, sodium, phos, mag intake
- Increase Calcium!
-
Preventing CKD
Be healthy, no NSAIDS for long periods of time, family history...
Meds for CKD
digoxin, sodium polystyrene, epoetin alfa, ferrous sulfate, calcium carbonate, furosemide or bumetanide
Hemodialysis
A technique in which an artificial kidney machine removes waste products from the blood

Good meds to give before hemodialysis
- Metformin
- Heart meds
- Maybe not BP meds (it'll be washed out and dialysis can make you hypotensive)
What is intermittent hemodialysis
Scheduled 3x a week sessions for 4-5 hrs
Weight/fluid balance important
Quality of life? not ideal, advance directives, EOL care talks...
Typically through an arteriovenous fistula or hemodialysis catheter.
4-5 L of fluid is removed so the patient is going to feel wiped out afterwards
Hemodialysis complications
- Thrombosis of AV Access
- Stenosis of AV Access
- Infection:
o Prepare Skin W/Antibacterial Agent Prior to Access
o Use Agents Approved for the Dialysis Catheter
- Aneurysms: Formed From Repeated Needle Punctures & Pressure Exerted During Dialysis
o Too Large, Surgical Removal & Resection Needed
- Ischemia: Fistula Blocks Blood Flow to Tissues Below Site
o Cold, Numb Fingers
o New Fistula Needed & Old One Deactivated
o Heart Failure
Hemodialysis management
Fistula
- Assess bruit/thrill
- Can get clotted
- If absent = medical emergency
- Patient complaint of numbness/tingling same arm as fistula: Take pulse and call provider
- No BP/IV starts/venipunctures
Medication considerations
Fistula care
No BP, blood draw, IV, injection in extremity
Monitor patency (bruit or thrill)
Note temp. and capillary refill time
Avoid restriction clothing, watches, jewlery
Protect from injury
How soon can a fistula be used once placed?
8 to 12 weeks wait time, so until then, HD is done through a port (HD catheter)
What is CRRT?
Continuous renal replacement therapy which typically done in an ICU setting and is continuous so that the client doesn't have drastic fluid shift. It's never more than 80mL of blood out of the body at 1 time being filtered and therefore does not stress the cardiovascular system as much.

Continuous Renal Replacement Therapy (CRRT)
o Differences from HD and PD.
o ICU floor
o Concept remains the same, we're 'cleaning' the blood.
o Gentler, less instability.
o Indicated for patients who would not be able to hemodynamically tolerate HD.
peritoneal dialysis
dialysis in which the lining of the peritoneal cavity acts as the filter to remove waste from the blood

Can peritoneal dialysis be done at home?
Yeppers
What should the patient have in order to do peritoneal dialysis at home?
o Clean Room
o Space for Dialysis Supplies & Dialysis Machine
o Additional Storage for 6 weeks of Supplies
o Care Partner to Help or be with During Treatments
Access & Preparation Requires Sterile Technique
Complications of peritoneal dialysis
High Risk of Peritonitis (red, pain, puffy at site, cloudy output), HERNIAS, pulmonary issues (plural effusions... so evaluate their ability to breathe...)
Is it normal to experience pain with peritoneal dialysis?
Possily.. Might occur in the first 1-2 Weeks
Warm Dialysate Using Warming Chamber (No Microwave)
Who is at risk for Dialysis Disequilibrium Syndrome?
patients who are skipping dialysis treatments
Dialysis Disequilibrium Syndrome
caused by the rapid removal of urea during hemodialysis; Caused by osmosis - Urea concentration in brain is different than in blood. Takes longer to shift levels than what is done in dialysis.
How to treat Dialysis Disquilibrium Syndome?
Slow it down or stop it altogether
s/s of dialysis disequilibrium syndrome
Headache, nausea, hypotension, restlessness, confusion, blurred vision, seizures DURING dialysis
What would dehyration labs look like
increased serum osmolality, higher levels of blood urea nitrogen (BUN) and creatinine, and concentrated urine.
Blood tests can also show elevated hematocrit and hemoglobin levels due to lower plasma volume, which can temporarily make anemia look worse.
Electrolyte levels like sodium may be higher, although they can sometimes be normal or low
After a kidney transplant, should the patient be peeing a lot?
Yes. We don't want dehydration. We want a happy, perfusing kidney.. and it has a lot to do after a transplant.
Would a patient with a newly transplanted kidney still need dialysis?
Possibly! Depends. The kidney may need extra help adjusting.
Hyper acute rejection
- Onset: Within 48 hrs of Surgery
- Increased Temperature
- Increased BP
- Pain at Transplantation Site (Iliac Fossa)
- Immediate Remove of Transplanted Kidney Required
- Return to Dialysis
Acute rejection
- A Week to Several Weeks after Surgery
- Oliguria or Anuria
- Temperature > 100
- Increased BP
- Enlarged, Tender Kidney
- Lethargy
- Elevated Creatinine, BUN, & Potassium Levels
- Fluid Retention
- Increased Dose of Immunosuppressive Drugs
Chronic rejection
- Occurs Gradually Over Months to Years
- Gradual Increase in BUN & Serum Creatinine
- Fluid Retention
- Electrolyte Imbalance (BUN and Cr will increase
- Fatigue
- Conservation Management Until Dialysis Required
What is the primary cause of kidney transplant failures?
Lack of adherence to immunosuppressive meds
What is MS
Multiple Sclerosis
Multiple sclerosis is characterized by what
Autoimmune stuff- the immune system attacks healthy nerve tissue throughout the entire body.
What disease is characterized by autoimmune problems affecting myelin and nerve fibers? It leads to disability with variable progression and affects more women than men. S/S can include fatigue, headache, numbness and tingling, dizziness, vision problems, and walking problems.
MS
How do you diagnose MS?
Review of s/s
Abnormal CSF (increased myelin and WBC)
MRI shows plaques (2 different areas of white matter demyelination)
LP shows increased lymphocytes
Management of MS
Treatment Strategies: treatment of relapses, symptom management, disease modification, rehabilitation, psychosocial support
Preventing MS
Healthy lifestyle and diet
Risk factors for MS
COLDER CLIMATES
NORTHERN EUROPEAN ANCESTRY
1ST DEGREE RELATIVE
ONSET 20-50 YEARS OLD
Effects women more than men
Education for MS
AVOID OVEREXERTION
AVOID STRESS
AVOID EXTREME TEMPERATURES
AVOID EXTREME HUMIDITY
AVOID PEOPLE WITH INFECTIONS
ALWAYS BALANCE REST WITH ACTIVITY
Medications for MS
-corticosteroids are used to decrease inflammation
-immunomodulators slow progression and reduce number of attacks
-monoclonal antibodies, natalizumab (tysabri, reduces the frequency of attacks with relapsing MS, but is given only by specifically trained MDS)
-antispasmotics such as baclofen (lioresal) can reduce muscle spasm
-CNS stimulants can control fatigue
-antidepressants can assist with depression
-PTs with urinary retention can be treated with bethanechol (ureocholine)
Multiple Sclerosis
A chronic autoimmune disease that affects the central nervous system, leading to the deterioration of the myelin sheath around nerve fibers.
Myelin
A protective sheath that surrounds nerve fibers, facilitating the rapid transmission of electrical signals in the nervous system.
Autoimmune Disorder
A condition in which the immune system mistakenly attacks the body's own tissues, leading to inflammation and damage.
Symptoms of MS
Common manifestations of multiple sclerosis include fatigue, difficulty walking, numbness, vision problems, and cognitive changes.
Relapsing-Remitting MS
The most common form of multiple sclerosis, characterized by episodes of new or increasing neurological symptoms followed by periods of recovery.
Secondary Progressive MS
A stage of multiple sclerosis that follows relapsing-remitting MS, where the disease progressively worsens over time.
Primary Progressive MS
A form of multiple sclerosis characterized by a gradual accumulation of disability from the onset, without distinct relapses.
MRI for MS
A diagnostic imaging technique often used to visualize lesions in the brain and spinal cord associated with multiple sclerosis.
Corticosteroids for MS
Anti-inflammatory medications commonly used to manage acute relapses of multiple sclerosis.
Lifestyle Management of MS
Strategies such as exercise, diet, and stress management that can help improve quality of life for individuals with multiple sclerosis.
Injury to T6 and above poses a risk for these two problems
neurogenic shock and autonomic dysreflexia
What is neurogenic shock
A type of distributive shock caused by loss of sympathetic nervous system tone, leading to vasodilation, hypotension, and bradycardia.
What causes neurogenic shock
Spinal cord injury (typically above T6), spinal anesthesia, or severe head injury that disrupts autonomic pathways.
What happens to blood vessels during neurogenic shock
blood pooling, decreased venous return, and decreased cardiac output.
s/s of neurogenic shock
Hypotension
Bradycardia
Warm, dry skin (due to vasodilation)
Poikilothermia (inability to regulate body temperature)
Neurogenic vs hypovolemic shock
Neurogenic shock presents with bradycardia and warm skin, while hypovolemic shock has tachycardia and cool, clammy skin.
Nursing interventions for neurogenic shock
Maintain airway and oxygenation
Stabilize spinal injury (immobilization)
Administer IV fluids for hypotension
Vasopressors (e.g., norepinephrine) to support BP
Atropine for bradycardia
Monitor temperature and prevent hypothermia
Patient education for neurogenic shock
t's a temporary condition caused by nerve damage
Stabilization and careful positioning are key
Long-term outcomes depend on spinal cord recovery
What is autonomic dysreflexia?
A life-threatening emergency that occurs in patients with spinal cord injury (usually at or above T6), caused by an excessive, uncontrolled sympathetic response to a noxious stimulus below the level of injury.
Triggers fo autonomic dysreflexia
Bladder distention (most common)
Bowel impaction
Tight clothing or devices
Skin irritation or pressure ulcers
Pain or temperature extremes
What happens in the body during autonomic dysreflexxia
Noxious stimuli below the injury trigger massive sympathetic discharge → vasoconstriction below injury → severe hypertension → baroreceptors trigger parasympathetic response above injury → vasodilation and bradycardia.
s/s of autonomic dysreflexia
Severe, pounding headache
Sudden hypertension (systolic ↑ 20-40 mmHg above baseline)
Bradycardia
Flushed skin, sweating above injury
Cool, pale skin below injury
Nasal congestion and blurred vision
Autonomic dysreflexxia nursing interventions
Sit the patient upright to lower BP.
Loosen tight clothing.
Check bladder: empty with catheter if distended.
Check bowel: remove impaction if safe.
Monitor BP every 2-3 min.
Administer antihypertensives (nifedipine, hydralazine) if unresolved.
Identify and remove the cause.
NITRATES
Preventing autonomic dysreflexia
Maintain regular bladder and bowel programs
Ensure catheter patency
Prevent skin irritation or pressure injuries
Educate on avoiding tight clothing
Teach early recognition of symptoms
Patient education on autonomic dysreflexia
Recognize early warning signs (headache, flushing, sweating)
Sit up immediately and call for help
Avoid triggers through bladder, bowel, and skin care routines
Carry emergency treatment instructions or card
Complications of autonomic dysreflexxia
Hypertensive stroke
Seizures
Retinal hemorrhage
Myocardial infarction
How to treat autonomic dysreflexia
treat the cause!
A patient that is LESS SENSITIVE TO TEMPERATURES means.....
higher risk for autonomic dysreflexia
Severe hypertension + headache + flushed/sweaty skin above the injury
Autonomic dysreflexia