Fluid & Electrolytes

*Review electrolytes, assessment of imbalances, normal values for Na+, K+, BUN,
Creatinine

Electrolytes: substance that, on dissolving in solution, ionizes, that is, some

of its molecules split or dissociate into electrically charged atoms or ions.
Homeostasis:
o Body fluids and electrolytes plan an important role in maintaining
homeostasis, the stable internal environment of the body.
o Body fluids are in constant motion transporting nutrients, electrolytes
and oxygen to cells and carrying waste products away from cells.
o The body uses a number of adaptive responses associated with these
activities to keep the composition and volume of body fluids and
electrolytes within the narrow limits of normal to maintain homeostasis
and promote health.
Body Fluid Compartments
o The two fluid compartments in the body are the intracellular space
(inside the cell) and the extracellular space (outside the cell). These
compartments are separated by semipermeable membrane.
o Intravascular Space
Refers to fluid inside a blood vessel
o Intracellular Space
The intracellular space refers to all fluid inside the cells
(intracellular fluid- ICF)
Most bodily fluids are inside the cells
o Extracellular Space
Refers to fluid outside the cells. This fluid is known as the
extracellular fluid (ECF).
The extracellular compartment includes the interstitial fluid,
which is fluid between cells (third-space), blood lymph, bone,
connective tissue, water and transcellular fluid.
The ECF also contains transcellular fluid, which is fluid within
specialized cavities of the body, such as cerebrospinal fluid, fluid
in the gastrointestinal tract, pleural, synovial, peritoneal,
intraocular, and pericardial fluid.
Fluid Shifts
o Third Spacing
An accumulation and sequestration of trapped extracellular fluid
in an actual of potential body space as a result of a disease or
injury.
Fluid may be trapped in body spaces such as the pericardial,
pleural, peritoneal, or joint cavities the bowel; or the abdomen,
or within soft tissues after traumas or burns.
 oEdema
Edema is an excess accumulation of fluid in the interstitial
space; it occurs as a result of alterations in oncotic pressure,
hydrostatic pressure, capillary permeability, and lymphatic
obstruction.
Localized edema occurs as a result of traumatic injury from
accidents or surgery, local inflammatory processes, or burns.
Generalized edema, is an excessive accumulation of fluid in the
interstitial space throughout the body and occurs as a result of
conditions such as cardiac, renal, or liver failure.
Normal Values
o Na+: 135-145 mEq/L
o K+: 3.5-5.0 mEq/L
o BUN: 6-20 mg/dL
BUN is used to detect renal problems.
o Creatinine: 0.6-1.3 mg/dL
More reliable than BUN as a determinant of renal function.
Creatinine is end product of muscle and protein metabolism.

SODIUM Hypernatremia Hyponatremia

135-145 mEq/L Na > 155 Na < 135

When does this Water loss OR sodium gain
happen
*primary protection is thirst from
hypothalamus
o Clinical states (Diabetes
insipidus)
o Hyperosmolality as a result of:
o Hyperosmolar tube feedings
o Osmotic diuretics (mannitol)
o Sensible losses (fever)
o Excessive sweating
o Sodium gain
Water excess OR sodium loss
*can lead to hypoosmolality
leading to cellular swelling and
explosion
Sodium depletion from:
o Diuretics
o Diarrhea
o Fistula drainage
o NG suction
o Abnormal losses via diaphoresis
o Hyperglycemia (glucose-
induced diuresis)
o Adrenal insufficency
Water intoxication:

-SIADH

-Overhydration with dextrose

-Tap water enema


S/S If from salt gain:
o Edema
o Wt gain
o Bounding pulse
o Distended neck veins
o Crackles
o Dyspnea, orthopnea
o Possible HCT decrease
o Tachycardia
o Hypertension
o Restless, lethargic, agitated,
seizure, possible coma
o NEURO!
If from water loss:
o Dry skin and mucous mem.
o Decrease skin turgor
o Warm, flush dry skin
o Initial elevated temp
o Orthostatic hypotension
o Tachycardia
o Thirst
o Oliguria
o FALSELY elevated HCT
o NEURO!
Nursing Care o Restrict sodium in diet
o Avoid over infusion of saline
o Diuretics
o Assess neuro, renal, cardiac,
respiratory
o Give water in excess of sodium
if pt needs volume (ex use
NS (hypotonic) or 5% dextrose
o Try for enteral water
o Treat underlying cause
o Watch for risk related to AMS,
LOC, falls
-Hypotonic irrigating solutions
-CHF/Cirrhosis/nephrotic syndrome
CNS deterioration
Water intoxication:
o Wt gain
o Taught skin turgor
o Elevated JVD/CVP
o Risk pulm edema
o Hypertension
o LOC, HA, delirium seizures
Sodium depletion:
o HA
o Malaise
o Confusion or coma
o Muscle weakness
o Hypotension
o Decrease JVD/CVP
o Poor skin turgor
o Decrease urine output
Water intoxication:
o Restrict fluids
o Diuretics
o Monitor serum sodium, serum
osmolality and neuro status
o Initiate seizure precautions
o Infuse 3% saline very SLOWLY
(hypertonic)
o Assess respiratory, renal and
cardiac
o Treat underlying cause
Sodium depletion:
o High sodium diet with adequate
fluid intake
o NS
o Monitor sodium, serum
osmolality, neuro
 o Initiate seizure precautions
o Assess cardiac and renal
o Treat underlying cause
Other o Serum Na will be 145-147
o Serum osmolality > 300
o Normal to high HCT
o Urine specific gravity> 1.030

Potassium Hyperkalemia Hypokalemia

3.5-5.0 mEq/L K>5 K < 3.5

When does this o Acute/chronic renal failure o K+ loss exceed intake

happen o Cellular destruction
o Excessive
ingestion/administration
o K+ sparing diuretics
o Adrenal cortex insufficiency
o Decreased cardiac output
o Sodium depletion
o Acidosis
S/S CARDIAC:
o Elevated aldosterone
o Loop diuretics
o GI loss (including urine and
vomit)
o K+ move into cells
Cardiac:

o ECG changes: Tall T wave / o Vent arrhythmias

wide QRS o Impair repolarization
o Vent fibrillation o Impaired regulation of arterial
o Systoles blood flow
o Decreased contractility and o Bradycardia
conduction o ECG changes: prolonged PR, ST
Others depression, shallow T
Other:
o CNS changes
o Cramps o CNS changes
o Diarrhea o Increase risk dig toxicity
o Muscle weakness o Muscle weakness/paralysis
o Lethargy o Muscle cell breakdown (can see
o Decreased renal function myoglobin in plasma)
(check for oliguria/anuria o Decreased GI motility
o Altered airway responsiveness
o Diuresis
o hyperglycemia
Nursing Care o CARDIAC MONITORING o CARDIAC MONITORING
o As K+ increases can give or o Check serum K+
1 amp of 50% glucose IVP then o Give supplements as indicated
 10 units regular insulin IVP (NEVER IVP)
o PO or rectal Kayexalate o Watch for painful phlebitis!
(exchanges K+ for Na in the o Add K+ in diet
gut and causes diarrhea)
o Diuretic
o NaHCO3- if acidosis
o May need dialysis
o Calcium chloride or gluconate
IV to decrease cardiac
irritability
o Monitor serum K+
o Assess cardiac, GI, renal
o Avoid K+ in diet and K+ sparing
diuretics
o Treat underlying cause
Other o Will see acidosis from increased o Will see alkalosis from
H+ ions pushed in cell and K+ decreased H+ ions and K+
pushed out being drawn into the cell
o K+ is needed for transmission/conduction of nerve impulses,
maintaining cardiac rhythms, skeletal muscle contraction and acid
base balance
o Kidneys are major route for K+ loss

Calcium Hypercalcemia Hypocalcemia

9-11 mg/dl Total Ca > 11 Total Ca < 9

(total)

4.5-5.5 (ionized)

When does this o Hyperparathyroidism o Decreased PTH

happen o Malignancy o Acute pancreatitis
o Immobilization o Multiple blood transfusions
o Hypophosphatemia o Alkalosis
o Excess Vit D o Decreased intake
o Acidosis (increases Ca+ ion)
S/S o CNS deterioration o Trousseaus sign
o Decreased memory, confusion, o Chvosteks sign
disorientation o Muscle twitching
o Fatigue o Laryngeal stridor
 o Fractures o Dysphagia
o Irritability of cardiac muscle o Numbness/tingling around
impaired mouth
o Renal calculi o Numbness/tingle of extremities
o Thirst *this is on the little table o Tetany
at the end of the slides but it o CNS changes
doesnt make sense to me o ECG changes
o Increased interstitial fluid
Nursing Care o Loop diuretic o Oral or IV calcium
o Phosphate o Treatment of pain and anxiety
o Isotonic saline (NS) to prevent hyperventilation
o Synthetic calcitonin/etidronate (which would induce respiratory
o Mobilization (weight bearing alkalosis)
exercise if possible) o Initiate seizure precautions
o Acid-ash diet that will acidify
urine to prevent renal stones
(prune/cranberry/orange juice)
o Avoid high calcium foods
Other o Inverse relationship with phosphorus (more than 99% of calcium is
combined with phosphorus and concentrated in skeletal system)
o Bones readily available store calcium
o Ca blocks sodium transport and stabilizes cell membrane
o ONLY the ionized form of Ca is biologically active
o Ca Fx: transmission of nerve impulses, muscle contraction, clotting,
form teeth and bone
Controlled by PTH, Calcitonin and Vitamin D

Phosphate Hyperphosphatemia Hypophosphatemia

2.8-4.5 mg/dl Serum PO4 > 4.5 SerumPO4 < 2.8

When does this o Acute/chronic renal failure o Malnourishment

happen o Hypoparathyroidism
o Over administration (PO or IV)
S/S o Hypocalcemia
o Tetany
o Muscle fatigue
o Calcium-phosphate percipitates
in skin, soft tissue, cornea,
viscera and blood vessels
Nursing Care o Restrict foods and fluids with
o Malabsorption
o Alcohol withdrawal
o Use of phosphate-binding
antacids
o Use of parenteral nutrition with
inadequate replacement
o Anorexia
o Malaise
o Muscle wasting/weakness
o Tachycardia
o Manifestations of
hypercalcemia
o Oral supplementation
 phosphorus
o Adequate hydration
o Administer phosphate binder
(Renagel)
o Treat likely hypocalcemic
condition
o Treat underlying cause
Other o Phos Fx: muscle, RBC, nervous system
o Deposited with Ca for bone and tooth structure
o Acid-base buffering
o ATP production
o Cell use of glucose
o Metabolism of carbs, proteins, fats
o Reciprocal relationship with Ca
o Mostly excreted by kidney
o Required for release of O2 by Hgb
Magnesium Hypomagnesemia
1.5-2.5 mEq/L
When does this o Increased intake when pt has
happen renal insufficiency or failure
o KIDNEY ISSUE + Mg = BAD
S/S o Depressed CNS
o Lethargy to coma
o Depressed respirations
o Bradycardia with peaked T
wave
o Hypotension due to depressed
contractility
o Depressed neuromuscular Fx
o Muscle weakness
o Loss of deep tendon reflexes
o seizures
Nursing Care o May need dialysis
o Avoid meds that have Mg (like
o Ingestion of foods high in
phosphorus
o May need IV admin of sodium
or potassium phosphate
o Monitor serum levels of Ca and
PO4
o Discontinue phosphate binding
meds
o Assess for weakness and
thacycardia
Hypomagnesemia
o Fasting or starvation
o Chronic alcoholism
o Fluid loss
o Parenteral nutrition without
supplementation
o Diuretics (osmotics from high
glucose levels)
o Tremors
o Hyperactive deep tendon reflex
o Muscle weakness
o CNS changes
o Confusion
o Coma
o Hyperirritability
o Facial twitching
o Seizure
o Cardiac irritability
o Increase risk of Dig toxicity
o s/s similar to hypocalcemia
o Oral suppliments
o Increased dietary intake
 mylanta, milk of magnesia) o If severe, parenteral IV or IM
o Avoid foods with Mg administration
o Assess respiratory, neuro,
muscular, renal and cardiac
o IF normal renal give diuretics
or saline
o May need Ca gluconate to
minimize Sx of increased Mg
Other o 50-60% in bone
o it is a coenzyme in metabolism of protein and carbs
o Fx in normal cardiac function
o Factors that regulate Ca balance also appear to influence Mg balance

Foods high in

o Potassium-
o fruits and vegetables
Banana
Oranges
Avocado
Sweet potato
o salt substitutes
o Calcium
o cheese
o yogurt
o fortified juices
o milk
o spinach
o salmon
o Phosphates
o Processed meats and dairy
o Soda
o In many additives and fortified grains
o Pumpkin seeds, almonds, peanuts in plant form are known as phytate
o Magnesium
o Beans and nuts
o Whole grains
o Green leafy vegetables
o Dark chocolate

*Clinical manifestations and nursing actions for FVE and FVD

Fluid and movement between extracellular and intracellular fluid will cause deficits
and excess.

Water deficit = increased ECF osmolality

 o CNS changes most common as brain cells shrink
Water excess = decreased ECF osmolality
o CNS changes as brain cells swell (and can burst)

Water Regulation
***Water regulation is managed by pituitary, adrenal cortex, kidney, hypothalamus,
cardiac and GI tract.
o Pituitary:
Under control of hypothalamus, posterior pituitary releases ADH, which
regulates water retention by the kidneys.
o Adrenal Cortex:
Adrenal cortex releases hormones to regulate both water and
electrolytes
1. Glucocorticoids
2. Mineralocorticoids
a. Aldosterone is a mineralocorticoid with potent sodium-
retaining and potassium excreting capability.
o Kidneys:
Kidneys are primary organs for regulating fluid and electrolyte balance.
Selective reabsorption and excretion of eater and electrolytes
Renal tubules are sites of action of ADH and aldosterone
Impaired renal function =
- Edema
- K+ and PO4- retention
- Acidosis
- Electrolyte imbalances
o Cardiac:
Atrial natriuretic factor (ANF) is released by the cardiac atria in
response to increased atrial pressure.
B-type natriuretic peptide (BNP) is released by the cardiac ventricles in
response to decompensated heart failure.
ANF & BNP causes vasodilation and increased urinary excretion of
sodium and water.
o GI:
Gastrointestinal tract accounts for most of water intake.
Small amounts of water are eliminated by GI tract in feces.
 Fluid Volume Excess Fluid Volume Deficit
(hypervolemia) (hypovolemia)

When does this o Excess intake of fluids o Diarrhea

happen o Abnormal retention of fluids o Fistula drainage
(CHF) o Hemorrhage
o Interstitial- to- plasma fluid o Decreased intake
shift o Plasma- to- interstitial fluid
shift
S/S o NEURO o Thirst
Change in LOC (due to o Poor skin turgor
cerebral edema) o Dry mucous membranes
o Respiratory o Sunken eyeballs
Constant, irritating cough o Elevated temp
Dyspnea o Tachycardia
Crackles in lungs o Narrowed pulse pressure
Cyanosis o Flat neck veins when supine
o Cardiovascular o Weight loss
JVD o Restlessness (coma possible)
Hand vein engorgement o Orthostatic hypotension
Bounding pulse
High BP
S3
Pitting edema
Sacral edema
Weight gain (2+lbs per day
is concerning)
Medical orders o Diuretics o Isotonic (balanced) IV solutions
(including types o Fluid restriction LR, NS
of IV fluids) o Sodium restriction
o Isotonic chloride
o Blood (if it is due to blood loss)
Nursing Care o Correct underlying cause o Correct underlying cause
o Remove fluid without creating o Replace water and electrolytes
electrolyte or osmolality issues
For BOTH o Measure I/O
o Monitor for cardiovascular changes
o Assess respiratory status and monitor changes
o Neuro changes
o Daily weights (same time, same clothing, same bedding)
 o Skin assessment regularly

Hematology: 7

*Basic pathophysiology behind RBC and WBC formation (levels of maturity)

Hematology is the study of blood and blood-forming tissues. This includes

bone marrow, blood, spleen, and lymph system.
Structures and Functions of Hematologic System
o Bone Marrow
Blood cell production (hematopoiesis) occurs within the bone
marrow.
Bone marrow is the soft material that fills the central core of
bones
Although there are two types of bone marrow (yellow[adipose]
and red [hematopoietic]), it is the red marrow that actively
produces red blood cells.
All three types of blood cells (red, white and platelets) develop
from a common hematopoietic stem cell within the bone
marrow.
The hematopoietic stem cell is best described as an immature
blood cells that is able to self-renew and to differentiate into
hematopoietic progenitor cells.
As the cells mature and differentiate, several different types of
blood cells are formed.
The marrow responds to increased demands for various types of
blood cells by increasing production via a negative feedback
system.
hThe bone marrow is stimulated by various factors or cytokines
(erythropoietin,
 granulocyte colony-stimulating factor, stem cell factor, and
thrombopoietin)

The picture above shows the maturation process of blood cells. We always
start with the stem cell. Remember that blasts are indicative of the cell
being immature and cyte is the mature cell.

o Blood Cells
4-6million
About 45% of the blood is composed of formed elements, or
blood cells. The three types of blood cells are erythrocytes
(RBCs), leukocytes (WBCs), and thrombocytes (platelets).
o Erythrocytes (RBCs)
Primary function of erythrocytes is oxygen and carbon dioxide
transportation and assistance in maintaining acid-base balance.
Erythrocytes are primarily composed of a large molecule called
hemoglobin. Hemoglobin is a complex protein-iron compound
composed of heme (iron compound) and globin (simple protein),
binds with oxygen and carbon dioxide.
RBCs carry oxygen linked to hemoglobin from the lungs to the
tissue capillaries
Erythropoiesis (the process of RBC production) is regulated by
cellular oxygen requirements and general metabolic activity.
 Erythropoiesis is stimulated by hypoxia and controlled by
erythropoietin, a glycoprotein growth factor synthesized and
released primarily by the kidney!
Erythropoietin stimulates the bone marrow to increase
erythrocyte production.
Several distinct cell types evolve during erythrocyte maturation.
Three alterations in erythropoiesis that decrease RBC production
Decreased hemoglobin synthesis
Defective DNA synthesis in RBCs
Diminished availability of erythrocyte precursors
The reticulocyte is an immature erythrocyte. The reticulocyte
count measures the rate at which new RBCs appear in the
circulation.
o Leukocytes (WBCs)
Normal Range 5,000-10,000
Leukocytes originate from stem cells within the bone marrow
There are different types of leukocytes, each with a different
function.
Granulocytes- include three types
- Neutrophils: Bands (immature neutrophil) & Segs
(mature neutrophil)
- Eosinophils
- Basophils
The primary function of granulocytes is
phagocytosis, a process in which WBCs ingest or
engulf any unwanted organism and then digest and
kill it.
Agranulocytes- Leukocytes that do not have granules
within the cytoplasm.
Lymphocytes cellular & humoral immune response
Monocytes - Also strong phagocytic activity. Monocytes
are only present in the blood for a short time before
they migrate into the tissue and become
macrophages.
Kupffer cells liver, osteoclasts bone, alveolar
macrophages lungs.
o Thrombocytes (platelets)
Normal: 200,000-400,000/l

The primary function of thrombocytes, or platelets, is to initiate

the clotting process by producing an initial platelet plug in the
early phases of the process.
Platelets must be available in sufficient numbers and must be
structurally and metabolically sound for blood clotting to occur.
Platelets like other blood cells, originate from stem cells within
the bone marrow.
The stem cell undergoes differentiation by transforming
into a megakaryocyte, which fragments into platelets.
 Platelet production is partly regulated by thrombopoietin, a
growth factor that acts on bone marrow to stimulate platelet
production.

*Normal values for RBC, Hgb, Hct, WBC

RBCs: 4-6 million

Hgb: 12-14 g/dl *from ppt*
o *book* Female 11.7-16.0 g/dL
o *book* Male 13.2-17.3 g/dL
Hct:
o Male 40%-50%
o Female 35%-47%
WBC: 5,000-10,000 l

*Know your terms and nursing care for anemia(s), thrombocytopenia, neutropenia,
leukocytosis, polycythemia

Thrombocytopenia: Low platelet count (counts below 100,000l)

o Nursing Care:
Nursing care of thrombocytopenia differs based on the etiology (
immune thrombocytopenic purpura, thrombolytic
thrombocytopenic purpura, heparin-induced, and acquired)
Platelet transfusions
Corticosteroids
Patient Education
Possible chemotherapy
Discourage excessive use of OTC medications
Assess pt for s/s of unusual bleeding
Monitor platelet count, coagulation studies, hemoglobin and
hematocrit.
Provide actions to reduce falls
Neutropenia: a condition in which the absolute neutrophil count (ANC) is
less than 1000 cells/l. Neutropenia results from a number of disease
processes such as, leukemia. Or from bone marrow depression, and is
associated with a high risk of infection and death from sepsis.
o Nursing Care
Determine and treat cause of neutropenia
Protective isolation
Private room
Reverse isolation to protect patient from you
Limit visitors; usually no kids or people who are sick
Positive-pressure or HEPA filtered room
No fresh fruits/vegetables (unless they can be peeled) or
unpasteurized dairy products
No flowers
 Monitor for s/s of infection (best indicator is fever >/= 100.4 oF)
and septic shock (increased HR, hypotension even w/ fluid
resuscitation)
Cultures: blood, urine, sputum, feces
IV antibiotic therapy within one hour of temperature spike
Draw cultures first!
IV or subcut G-CSF (filgrastim [Neupogen], pegfilgrastim
[Neulasta]) or GM-CSF (sargramostim [Leukine])
May teach pts to give subcut injection

Leukocytosis: an increase in number of white blood cells (>11,000 l)

generally in response to either an infection or another inflammatory process
in the body.
o Nursing Care:
Treat underlying cause if able
Private room
Practice excellent hand hygiene
Provide thorough skin care in order to prevent infection
Monitor CBCs
Limit invasive procedures
Closely monitor temperature

Polycythemia: Production and presence of # RBCs; blood circulation is

impaired because blood viscosity (hyper viscosity) and volume
(hypervolemia)
o Nursing Care:
Therapeutic phlebotomies
-Use 18 gauge or bigger needle, vacuum bottle, be cautious
about removing more than one unit (500cc). Monitor carefully
for hypovolemia
Give Allopurinol for gout
Watch I&O dehydration will increase viscosity
Keep patient active to discourage thrombus formation

Renal: 7

*Assessment, treatment and post-procedural assessment of interventions for renal

calculi, renal disease, pyelonephritis, AV fistula

o Prerenal Etiology
Hypovolemia, hemorrhage, burns, severe hyponatremia & H20
loss, hypotension or hypoperfeusion, sepsis, CV failure, PE, renal
artery stenosis, severe dehydration
o Intrarenal Etiology
 Acute tubular necrosis (ATN), post ischemic or nephrotoxic
glomerulopathies, malignant HTN, SLE, thrombotic disorders,
aminoglycosides, radiocontrast media, sepsis, hypotension
o Post Renal Etiology
Obstructive uropathies (bilateral), ureteral destruction, bladder
neck obstruction (prostate disease).

ACUTE KIDNEY INJURY

Kidney failure is the partial or complete impairment of kidney function. It
results in an inability to excrete metabolic waste products and water and
causes functional disturbances of all body systems.
Acute kidney injury (AKI) usually develops over hours or days with
progressive elevations of blood urea nitrogen (BUN), creatinine, and
potassium with or without oliguria. It is a clinical syndrome characterized by a
rapid loss of kidney function with progressive azotemia.
The causes of AKI are multiple and complex. They are categorized into
prerenal (most common), intrarenal, and postrenal causes.
Prerenal causes are factors (e.g., hypovolemia) that reduce blood flow
to the kidney and lead to decreased glomerular perfusion and filtration.
Intrarenal causes include conditions that cause direct damage to the
renal tissue, resulting in impaired nephron function. Acute tubular
necrosis accounts for most cases of intrarenal failure.
Postrenal causes involve mechanical obstruction of urinary outflow.
Common causes are benign prostatic hyperplasia, prostate cancer,
calculi, trauma, and extrarenal tumors.
The RIFLE classification (risk, injury, failure, loss, and end-stage disease) is
used to describe and standardize the stages of AKI.
Clinically, AKI may progress through three phases: oliguric, diuretic, and
recovery. In some situations, the patient does not recover from AKI and
chronic kidney disease (CKD) results, eventually requiring dialysis or a kidney
transplant.
The oliguric phase involves a decrease in urine production. Fluid
and electrolyte abnormalities and uremia occur. Common
electrolyte abnormalities include hyperkalemia, hyponatremia, and
hypocalcemia. Elevated BUN and creatinine levels are found. Other
findings include metabolic acidosis, anemia, and platelet
abnormalities.
The diuretic phase begins with a gradual increase in daily urine
output of 1 to 3 L/day but may reach 3 to 5 L or more. The nephrons
are still not fully functional. The uremia may still be severe, as
reflected by low creatinine clearances, elevated serum creatinine
and BUN levels, and persistent signs and symptoms.
The recovery phase begins when the glomerular filtration rate (GFR)
increases, allowing the BUN and serum creatinine levels to plateau
and then decrease. Renal function may take up to 12 months to
stabilize.
The diagnosis of AKI is based on the history and physical as well as changes
in urine output and serum creatinine.
Interprofessional Care
Because AKI is potentially reversible, the primary goals of treatment are to
eliminate the cause, manage the signs and symptoms, and prevent
complications while the kidneys recover.
Common indications for dialysis in AKI are volume overload, elevated
potassium level with ECG changes, metabolic acidosis, significant change in
mental status, and pericarditis, pericardial effusion, or cardiac tamponade.
Three types of renal replacement therapy may be used: hemodialysis,
peritoneal dialysis, and continuous renal replacement therapy (CRRT).
Recovery from AKI is highly variable and depends on the underlying illness,
general condition and age of the patient, length of the oliguric phase, and
severity of nephron damage.

NURSING MANAGEMENT: ACUTE KIDNEY INJURY

Prevention of AKI is primarily directed toward identifying and monitoring high-
risk populations, controlling exposure to nephrotoxic drugs and industrial
chemicals, and preventing prolonged episodes of hypotension and
hypovolemia.
Infection is the leading cause of death in AKI, and meticulous aseptic
technique is critical.
The patient with AKI is critically ill and comorbid diseases or conditions, such
as diabetes, may be present in addition to the renal injury.
You have an important role in managing fluid and electrolyte balance during
the oliguric and diuretic phases.
The long-term convalescence (3 to 12 months) may cause psychosocial and
financial hardships for the family, and appropriate counseling, social work,
and psychiatrist/ psychologist referrals are made as needed. If the kidneys do
not recover, the patient will eventually need dialysis or transplantation.

CHRONIC KIDNEY DISEASE

Chronic kidney disease (CKD) involves progressive, irreversible loss of kidney
function.
CKD usually develops slowly over months to years. CKD is defined either the
presence of kidney damage or a decreased GFR less than 15 mL/min.
The prognosis of CKD is variable depending on the etiology, patients
condition and age, and adequacy of follow-up.
 An elevation in serum creatinine
is demonstrated only after over
50% of functioning kidney
function (nephron mass) has
been lost.
Uremia is a syndrome that
incorporates all the signs and
symptoms seen in the various
systems throughout the body in
CKD.
Fatigue, lethargy, and
pruritus are symptoms
associated with
progression of kidney
dysfunction.
Hypertension is both a
cause and a
consequence of CKD.
Hyperglycemia,
hyperinsulinemia, and
dyslipidemia may be
seen.
Metabolic alterations, including hyperkalemia, hyponatremia, and
metabolic acidosis, tend to occur in the later stages of CKD.
Normocytic anemia is due to decreased production of endogenous
erythropoietin.
The most common cause of death in patients with CKD is cardiovascular
disease, including ischemic heart disease, heart failure, and cardiac
dysrhythmias
Etiology
o Leading cause= DIABETES & hypertension
o Less common etiologies= glomerulonephritis, cystic diseases, &
urologic diseases

Complications
o infections, neurologic changes, peripheral neuropathy, CKD-mineral
and bone disease, pruritus, infertility, personality and behavioral
changes, lethargy, and depression.
Goal of care in CKD
o reducing the risk of cardiovascular disease and premature death.
Secondary goals of CKD therapy are to deter the progression of kidney
dysfunction, recognize and treat the associated complications, and provide
for the patients comfort.
Medical management is started in an effort to postpone the need for
maintenance dialysis.
In certain situations, CKD progression can be delayed by using
drug therapy to reduce the damaging effects of proteinuria
and hypertension.
 Erythropoietin and iron replacement are used for the
treatment of anemia.
Statins (HMG-CoA reductase inhibitors) are the most effective drugs for
lowering low-density lipoprotein (LDL) cholesterol levels.
Prior to dialysis, dietary protein may be restricted to slow the
progression of kidney dysfunction. Once the patient starts dialysis,
protein intake is usually increased.
Fluid intake depends on the daily urine output

NURSING MANAGEMENT: CHRONIC KIDNEY DISEASE

 The overall goals are that a
patient with CKD will
demonstrate the knowledge
and ability to participate in
treatment decisions and good
self-care practices. A goal is to
have active participation in
determining their own
treatment plans to the highest
degree that is achievable.
Most persons with CKD are
cared for in an ambulatory care
setting. Hospital care is
required for the management of
complications.
nursing diagnoses
o excess fluid volume, risk
for injury, imbalanced nutrition, and grieving.

DIALYSIS
Dialysis is a therapeutic intervention in which substances move from the
blood through a semipermeable membrane and into a dialysis solution
(dialysate). Dialysis solutions have an electrolyte composition similar to that
of plasma.
The two methods of dialysis are peritoneal dialysis (PD) and hemodialysis
(HD).
PERITONEAL DIALYSIS
Two types of PD are automated peritoneal dialysis (APD) and continuous
ambulatory peritoneal dialysis (CAPD).
PD is indicated (as a patient preference) when there are vascular access
problems or when a patient is intolerant of HD.
The three phases of the PD cycle (called an exchange)
o inflow (fill), dwell (equilibration), and drain (outflow).
The patient dialyzing at home will be given a daily prescription of exchanges
that is specific for the individual patient.
complications
o infection of the peritoneal catheter exit site, peritonitis, and pain.
Additional complications include hernias, lower back pain, protein loss,
bleeding, atelectasis, pneumonia, and bronchitis.
HEMODIALYSIS
The types of vascular access include arteriovenous fistulas (AVFs),
arteriovenous grafts (AVGs), and temporary catheters.
AVFs are created most commonly in the forearm with an anastomosis
between an artery (usually radial or ulnar) and a vein (usually
cephalic). Native fistulas have the best overall patency rates and least
number of complications.
AVGs are made of synthetic materials and form a bridge between the
arterial and venous blood supplies. Grafts are placed under the skin
and are surgically anastomosed between an artery (usually brachial)
and a vein (usually antecubital).
The majority of HD patients are treated in community-based dialysis facilities
and routinely dialyze for 3 to 4 hours 3 days each week.
o nurses complete an assessment that includes evaluation of a
patients fluid status (weight, BP, peripheral edema, lung and
heart sounds), condition of vascular access, and temperature.
Complications
o hypotension, muscle cramps, and blood loss.
The primary nursing goals
o help the patient regain or maintain a positive self-image and
achieve the highest degree of independent functional capacity
possible.

AV Fistula: care and assessment associated with having an AV

access for HD
 o A subcutaneous arteriovenous fistula (AVF)
is usually created in the forearm or upper
arm with an anastomosis between an artery
and a vein (usually cephalic or basilic).
o The fistula allows the blood to flow through
the vein. The vein becomes arterialized
with a larger caliber and thicker walls
(dilated). The arterial blood flow is essential
to provide the rapid blood flow required for
hemodialysis.
o Most common access, but not
necessarily performed in an acute
situation as it is best if placed 3 months
before the initiation of HD
o AVFs are more difficult to create in patients
with severe PVD, prolonged IV drug use
and/or obese women.
o In these patients, a synthetic graft may be required.

Chronic Pyelonephritis
Pyelonephritis is an inflammation of the renal parenchyma and collecting
system, including the renal pelvis.
o The most common cause is bacterial infection that begins in the lower
urinary tract. Recurring infection can result in chronic
pyelonephritis.
Clinical manifestations
o Acute
mild fatigue to the sudden onset of chills, fever, vomiting,
malaise, flank pain, and the lower UTI characteristics.
o Chronic
HTN, inability to conserve Na, Hyperkalmia and acidosis, decrease
ability to concentrate urine
Diagnostics
o UA (pyuria: pus in urine, bacteriauria, hematuria)
o CBC
o Blood Cultures
o Ultrasound
o IVP (intravenous pyelogram), CT Scan
Collaborative Care
o Antibiotic therapy
o Adequate hydration is necessary
o Interventions include teaching about the disease process with emphasis
on the need to continue drugs as prescribed, the need for a follow-up
urine culture to ensure proper management, and identification of risk for
recurrence or relapse.
o Avoid catheterization, IVP and contrast CT Scan
Nursing Diagnosis
 o Impaired urinary elimination, readiness for enhanced self-health mgmt

Renal Calculi
Risk Factors
o Warm climates, high protein diet, dehydration, family history,
immobility
o pH
o Infection: urince becomes alkaline and stones form
Types of Calculi
o Calcium oxalate (most common)
o Uric acid
o Struvite
o Cysteine
Clinical Manifestations
o Abdominal pain or flank pain
o Hematuria
o Renal colic (pain that occurs as peristaltic action of ureters is
increased)
o Coll, moist skin
o N/V
o As stone moves through the urinary tract, may feel pain in testicles,
labia, groin, and/or rectum
Diagnostic Studies
o U/A
Assess for hematuria; ph.; pyuria crystals; casts
o Stone analysis
o BUN & Cr: assess renal function
o 24-hour urine collection: determine GFR; assess for increased uric acid,
calcium, [phosphate oxalate, cysteine
Collaborative Care
o MANAGE PAIN!
o Encourage fluids, but do not force-may increase renal colic
o Expulsion therapy-corticosteroids & nifedipine
o Relaxation
o I/O
Strain urine
o Ambulation
o Restrict sodium intake
o Control of infections (struvite stones)
o Antibiotics: if infection is present
o Evaluate cause of stone formation
o Stone removal
Lithotripsy: extracorpeal shock-wave lithotripsy
Complications: hemorrhage, retained fragments, infection,
damage to surrounding tissues.
 Endourologic procedures: endoscope inserted through
urethra: stones can be pulverized with sound waves, ultrasonic
waves, laser or can be removed with basket.