Alteration in Fluid & Electrolyte Balance: Acute Kidney Injury & Chronic Kidney Disease

Acute Kidney Injury (AKI) =

rapid loss of kidney function with progressive nitrogenous waste collection in the blood

Acute Kidney Injury (AKI) labs

rise in serum BUN and creatinine and/or reduction in urine output

AKI mortality rate

high, 70-80%

Is AKI reversible?

potentially

Most common cause of death in AKI?

infection

AKI: 3 pathologic states

prerenal, intrarenal, postrenal

AKI: prerenal

external to kidneys, reduction of systemic circulation impacting renal blood flow

AKI: prerenal symptoms

heart failure, MI, cardiogenic shock, thrombosis, hypovolemia, burns, dehydration, diarrhea, hemorrhage

Is prerenal reversible?

yes

AKI: Intrarenal

direct injury to kidney, acute tubular necrosis

ATN occurs from

prolonged ischemia and nephrotoxisis, disruption of BM

Is ATN reversible?

potentially reversible if basement membrane is not destroyed and epithelium can grow back

AKI: postrenal

mechanical obstruction of outflow, hydronephrosis

AKI: postrenal sequella

bilateral renal obstruction can lead to swelling of the kidney

AKI: postrenal prolonged obstruction

can lead to tubular atrophy and can be irreversible

hydronephrosis =

swelling of the kidney

Stages of AKI: RIFLE

serum creatine increase, GFR decreases during disease progression

Clinical manifestations of AKI: phases

oliguric, diuretic, recovery

Oliguric: occurs

1-7 days after injury, can last 10-14

Oliguric: oliguria

Oliguric: fluid and electrolyte abnormalities

hyperkalemia, hyponatremia, hypocalcemia, creatinine found

Oliguric: clinical manifestations

uremia, anemia, platelet abnormalities, metabolic acidosis, neuro changes

Oliguric: FLuid overload

decreased urine output, urine retention, bounding pulses, edema, heart failure

Oliguric: metabolic acidosis

excess H ions are excreted to maintain pH balance

Diuretic: occurs

1-3 weeks

Diuretic: begins with

gradual increase in daily urine output

Diuretic: nephrons are not

fully functional

Diuretic: is the urine filtered?

no

Diuretic: uremia may be severe

low creatinine clearance, elevated serum creatinine and BUN levels, persistent s/sx

Diuretic: complications from

diuresis, excess urine

Recovery: GFR

increases

Recovery: labs

BUN and creatinine plateau then decrease

Recovery: stabilization of kidneys

up to 12 months

Recovery: outcome

some people never recover

Diagnosis of AKI

pmh, psh, med hx, allergies, labs, urinalysis, ultrasound, ct scan, biopsy, treat underlying cause

Diagnosis of AKI: pmh/psh

hx of blood loss, severe heart disease, dehydration, contrast medium

Diagnosis of AKI: labs

may not be detected until loss of 50% kidney function

Diagnosis of AKI: urinalysis

urine osmolality, sodium content, gravity

Diagnosis of AKI: kidney ultrasound

imaging w/o exposing them to nephrotoxic dyes

Diagnosis of AKI: Biopsy

best for intrarenal cause

Contraindicated diagnostic studies

MRI, CIN, hydration to reduce damage risk

AKI: Nursing assessment

vs, LOC, lung, I&Os, examine urine, fluid volume status, EKG, labs

Primary Goals of a Patient with AKI

eliminate the cause, manage symptoms, prevent complications

Management of AKI

prevention, comorbs, excess fluid volume, potential complications, imbalanced nutrition, infection, fatigue, anxiety, psychosocial

AKI Management: Excess Fluid volume

determine adequate intravascular vol and cardiac output, diuretic therapy, monitor fluid intake, daily weights

AKI Management Excess Fluid volume: Diuretic therapy

low doses of loop diuretics

AKI Management Excess Fluid volume: Monitor fluid intake

possible fluid restriction, 1 kg gained is a L retained

AKI Management: Electrolyte imbalance

hyperkalemia, hyperphosphatemia

Electrolyte imbalance: Hyperkalemia

IV insulin concurrently w/ glucose, sodium bicarb IV, calcium gluconate, Kayexalate, RRT, diet

IV insulin pushes

potassium back into cells, glucose then given for rebound hypoglycemic effects

Sodium bicarbonate

corrects acidosis, shifts potassium back into the cell

Calcium gluconate

raises excitation threshold to which dysrhythmias occur

only 2 measures to actually remove potassium from the body

kayexalate, renal replacement therapy

Kayexalate

given by mouth or enema, osmotic diarrhea, exchanges potassium for sodium in bowel, potassium excreted via stool

Renal replacement therapy (RRT)

most effective way to remove K, requires central venous access

Diet

not used for acute elevation

Hyperphosphemia

RRT, diet

AKI Management: Alternative or Adjunctive Therapy

¨Continuous renal replacement therapy (CRRT)

¨Continuous renal replacement therapy (CRRT)

Helps with volume overload, excess potassium, cleans blood when its in metabolic acidosis, used in hemodynamically unstable pts

AKI Management: Nutrition - Goal

prevent catabolism

AKI Management: Nutrition - Adequate caloric intake

carbs, fat to prevent ketosis

AKI Management: Nutrition - limited

sodium, phosphate, potassium intake

AKI Management: Nutrition - poor oral intake

enteral feeding

AKI Management: Nutrition - if gut can’t tolerate feeding

parenteral nutrition

AKI Management: Infection

leading cause of death, site assessment or systemic, antibiotics

Nursing Implementation

health promotion, acute intervention, home care patient education

Health promotion

identify and monitor high risk pops, prevention of hypertension and hypovolemia, nephrotoxic drugs and chemicals

Chronic Kidney Disease (CKD):

Progressive irreversible loss of kidney function

Chronic Kidney Disease (CKD): clinically defined as

presence of kidney damage or GFR < 60, longer than 3 months

Chronic Kidney Disease (CKD): End Stage Renal Disease (ESRD)

GFR

Facts about CKD

more common than AKI

Causes of CKD

DM, HTN, Glomerulonephritis, Systemic lupus erythematosus, Polycystic kidney disease

Risk Factors: CKD

DM, HTN, age, CV disease, fx, exposure to nephrotoxic drugs

CKD: DM - risk factor and cause

kidneys w/ tiny filters, protein & RBC too big, DM damages thru glucose, useful proteins wasted, sclerosis and harden

CKD: HTN - risk factor and cause

increased force on blood vessels, blood vessels stretch, stretching and scarring weakens blood vessels, extra fluid in bv increases bp

CKD: Additional factors

access to health care, socioeconomic status, health literacy

Stages of CKD: stage 1

kidney damage

Stages of CKD: stage 2 & 3

moderate to severe

Stages of CKD: stage 4

preparing for kidney dialysis

Stages of CKD: stage 5

renal replacement therapy or dialysis necessary

Clinical Manifestations of CKD: urinary system

early stages of CKD, polyuria, anuria

Clinical Manifestations of CKD: metabolic disturbances

waste product accumulation, altered carb metabolism, elevated triglycerides

Clinical Manifestations of CKD: LDLs and HDLs

increase LDLs, decrease HDLs

Clinical Manifestations of CKD: Electrolyte and Acid-Base Disturbances

potassium, sodium, calcium, phosphate, magnesium, metabolic acidosis

Clinical Manifestations of CKD: Potassium

can cause fatal dysrhythmias

Metabolic Alkalosis

doesn’t really happen, loss of acid thru vomiting or gastric suctioning

Clinical Manifestations of CKD: Hematologic

anemia, infection, bleeding tendencies

Clinical Manifestations of CKD: CV

most common cause of death, risk factors, fluid overload

Clinical Manifestations of CKD: Respiratory

kussmaul’s resps, fluid overload

Clinical Manifestations of CKD: integumentary

pruritus, dry skin

Clinical Manifestations of CKD: Reproductive

infertility, decreased libido, amenorrhea

Clinical Manifestations of CKD: Psychological

depression, personality or behavior changes, anxiety, fatigue

Clinical Manifestations of CKD: GI

stomatitis, metallic taste, ulcerations, uremic factor, constipation risk

Clinical Manifestations of CKD: Neuro

expected as kidney failure progresses

Clinical Manifestations of CKD: muscoskeletal

CKD mineral bone disorder

CKD Mineral Bone Disorder

mineral and bone metabolism

CKD Mineral Bone Disorder: How?

kidneys activate Vit D, body unable to excrete phos, Ca drops, PTH stims Ca to be pulled from bone

CKD Mineral Bone Disorder: results

osteomalacia - softening of bone, osteitis fibrosa - replacing bone w/ fibrous tissue

CKD: diagnostic studies

urine dipstick, urinalysis, ultrasound, renal biopsy, GFR, BUN, creatinine, creatinine clearance

Best diagnostic study for CKD

GFR