23 August 2010

Fluid and Electrolytes, Urinary Disorders  LIFESPAN CONSIDERATION

Rey Ramirez Age Total Body Factors affecting body fluid
Fluid
Newborn 85% metabolic and respiratory
 FLUID (preterm) rates are higher  ↑ sensible
 anything that flows; constantly moving Newborn 70-80% loss
 composed of: (term)
 water Child (1-2 64%
 universal solvent; medium for all chemical years)
processes (metabolism) Puberty to M: 60% (↑ - exercises/ strenuous
 serves as lubricant 39 y/o muscle) activities may lead to fluid and
 transporter of nutrients, waste products, etc F: 52% (↑ fats) electrolyte imbalances
 insulator and shock absorber - FAD diets
 regulator of body temperature
40 – 60 y/o M: 55% - ↓ adipose tissue
 electrolytes
F: 47% - nephrons die (30-40%
 charged ions (charged particles); not all ions
Older 60 M: 52% functioning)  inability to
are electrolytes but all electrolytes are ions
y/o F: 46% concentrate and conserve
 cation (+) and anions (-)
body fluids
 usually when diluted in water can conduct
- prone to diseases that leads
electricity
to imbalances
 chemical components that partially
- meds (diuretic, laxatives)
dissociates/separates into particles
- calcium levels (lifestyle)
 cells
 semi-permeable membrane
 NORMAL SERUM ELECTROLYTES
 bounded by plasma membranes
 Na (135 – 145 mEq/L)
 ex: blood
 K (3.5 – 5.0 mEq/L)
 trace minerals
 Ca ( 4.5 – 5.6 mEq/L)
 they don’t have charges
 Mg (1.5 – 1.9 mEq/L)
 ex: Zinc (for immune response); Fe > Heme >
 Cl (95 – 108 mEq/L)
Hgb (for oxygen-carrying capacity); Cu; Li
 PO4 (1.72 – 1.96 mEq/L)
 homeostasis – balance in the body needed to sustain life
 HCO3 ( 22 – 26 mEq/L)
 FLUID COMPARTMENTS
 MOVEMENT OF BODY FLUIDS
 Intracellular fluid
 Osmosis
 cytosol (fluid inside cell); 2/3 body fluids are
 for equal concentration H20
found inside cell (60%); within cells
 movement of a pure solvent from lesser to
 K, Mg, PO4, SO4
greater concentration
 Extracellular fluid
 passive movement
 35% of body fluids; 20% of body weight; outside
 osmotic pressure
cells
 water mov’t through osmosis
 Na, Cl, HCO3
 number of hydrostatic pressure needed to
 Interstitial fluid
stop the flow of water by osmosis
− surrounding the cells (lymph – excess
 drawing force of water
of fluids in interstitial which are
 ↑ solute = ↑ osmotic pressure
drained in intravascular vessels)
 affected by Na and albumin
− space in the matrix of tissue
− Na
 Intravascular
− Albumin – called as oncotic pressure;
− fluid components of the blood
protein that cannot pass through
− inside blood vessels; 8%
membrane
 Transcellular fluid
 Osmolality
 beyond the cell; found in the body cavities; 2%
 number of osmotically active particles per
 cranium > subarachnoid space > CSF
kg of water
 eyes > aquaeous humor > intraocular pressure
 Osmolarity
 oral cavity > saliva
 number of osmotically active particles per
 heart > pericardial fluid > pericardial effusion
liter of water
 pleura > pleural fluid > pleural effusion
 ESO = (Na x 2) + BUN/3 + Glucose/18
 peritoneum > peritoneal fluid
− ESO (extracellular serum osmolarity)
 GIT > gastric secretion
− ESO (280 – 295)
 joints > synovial space > synovial fluid
− BUN (10 – 20mg/dL for adult; 8 –
15mg/dL for child)
− CHO (80 – 120mg/dL)
1
//carengreyes
 − osmotic pressure of solution
− >295 = ↑ osmotic pressure = more  factors:
fluids to intravascular space − ↑ plasma osmolality
 Diffusion − angiotensin II
 movement of particles (solute and solvent) of a angiotensin II
higher concentration to lower concentration
 facilitated diffusion – use of carrier substance adrenal gland
 Filtration
 both solutes and solution move together in adrenal cortex adrenal medulla
response to fluid pressure to create an
corticosteroids catecholamines
equilibrium
 hydrostatic pressure vs colloid oncotic pressure vasoconstriction
 hydrostatic = fluid pressure mineralocorticoids androgen glucocorticoids

 2 pressures: aldosterone
− oncotic (albumin)/osmotic (Na)
Na retention
− hydrostatic
 they are 2 opposing pressures: serum osmolality − dry pharyngeal mucous membranes
− hydrostatic (pulling) + oncotic − psychological factors (stress)
osmoreceptors
(pushing) = balance angiotensin II
 factors affecting filtration: thirst
 volume – the ↑ the volume, the ↑ deactivates activates
filtration process (hydrostatic pressure) parasympathetic sympathetic
 vasoconstriction – ↑ pressure, ↑ volume
cholinergics salivation
 distance from the source of contraction –
the nearer the more contracted GI secretions
 viscosity – the more viscous the blood, the − ↓ plasma volume
↑ hydrostatic pressure needed = ↑  Food oxidation
filtration  CHO  CO2 + H20
 Starling’s Law of Capillaries  CHON  CO2 + H20 + NH3
− movement of fluid away from IVF to  fats  CO2 + H20 + NH3 + ketone bodies
ISS  Food intake
− how perfusion happens  calcium – dairy products
− with HTN, hypovolemia  sodium – processed food, bread products, dairy
(all salty foods are ↑ Na content but not all Na
capillary bed are salty foods – ex. bread)
HP = 32mmHg HP = 12mmHg
OP = 22mmHg OP = 22mmHg  potassium – bananas, melon, orange
FP = 10mmHg FP = - 10mmHg  fluid intake comes from the ff:
 oral fluid intake – 50%
Arterial End Venous End  food intake – 40%
 Active Transport  metabolism – 10%
 requires energy to facilitate movement  solid foods are ↑ in fluid: lean meat, veggies
 allows cell to admit larger molecules from  Fluid output
lesser to larger concentration against a  urine
concentration agent  sweat
 food of cell = glucose  respiration
 glucose + insulin + K = inside cell  bowel movement
 excitatory – reacts on electric signals  insensible fluid loss
 ATP will facilitate force to release Na back  “kidney” – primary regulator of body fluids
outside and followed by K back inside  22% cardiac output
 Na-K pump  filtration process
 Na binds with ATP to be released again in  Hormones
the outside cell from inside cell  Anti-diuretic hormone (ADH)
 stored the posterior pituitary gland
 REGULATION OF BODY FLUIDS ↑ osmolality
 Fluid intake
osmoreceptors in the hypothalamus are stimulated
 Thirst mechanism
 hypothalamus – thirst center release of ADH
 osmoreceptors monitor the serum osmotic
renal tubules and collecting ducts
pressure
 ↑ osmolality = stimulation of the ↑ H20 permeability
hypothalamus
H20 return to systemic circulation
 blood is the only thing you can measure
(ECF only) dilutes blood

2
//carengreyes
 ↓ osmolality
 influence kidney function and structure
 Renin-angiotensin-aldosterone (RAA) system  maintains neuromuscular excitability
↑ plasma K levels  N: 3.5 – 5.0 mEq/L
 sources: citrus fruits, spinach
stimulates aldosterone release
 always incorporate in IV (drip method), not via IV push
acts on the distal portion of the renal tubule  FACTORS INFLUENCING K MOVEMENT:
 aldosterone
↑ reabsorption of Na and secretion and excretion of K
 changes in pH
↑/maintenance of volume  changes in blood sugar level
↓ glucose
ECF volume
adrenal cortex
↓ renal perfusion
glucocorticoids
release of renin

split angiotensinogen glycogenolysis gluconeogenesis

 Atrial Natriuretic Peptide (ANP) (stored as glycogen) (catabolism of CHON, fats)
 atrium – receiving chamber of heart
glucose
 natriuretic – urinate Na protein fats
 ↑ H20 = ↑ Na (oncotic pressure) = ↑
muscle adipose
volume = ↑ pressure
↑ blood volume
ketone bodies + ketones
↑ atrial pressure  changes in blood Na level
release of ANP (atrial and ventricular myocytes) ↓ Na ↓ BP

acts on nephron
RAA system
Na excretion
aldosterone
↓ blood volume
reabsorption of Na removal of K+
 REGULATION OF ELECTROLYTES
 Sodium (Na)  HYPOKALEMIA
 Potassium (K) – maintains osmotic pressure  CAUSES:
 Calcium (Ca) – bones; aids in coagulation; Factor VIII  ↑ GIT fluid loss (ex. diarrhea)
 Magnesium (Mg)  prolonged diuretic therapy
 Chlorine (Cl)  ↓ K+ intake
 ↑ aldosterone production
Hypo Hyper  CLINICAL MANIFESTATIONS:
Na/K hypoactive s/sx hyperactive s/sx  disturbed muscle function
Ca/Mg hyperactive s/sx hypoactive s/sx  GIT, skeletal, cardiac = ↓ reflexes
 muscle irritability/weakness
 speech changes
 POTASSIUM  rapid, weak, irregular pulse
 controlling the cellular osmotic pressure because it is  drop in BP
found inside cells  abdominal distention (↓ peristalsis)
 activates several enzyme action  flatulence
 helps regulate acid-base balance  visiting and paralytic ileus
 ex: in acidosis, there are more H+ outside; tendency  EKG changes in diagnosis
of K is to go out and so hyperkalemia occurs  K, Mg, Ca concentration changes
H+ H+
inside cell  HYPERKALEMIA
+ +  CAUSES:
K+ K K
K+  ↑ K+ intake
H+
H+  Addison’s disease (hypercortisolism/
H+
hypofunction of adrenal glands)
 ex: in hypokalemia, there are less K+ inside the cell;  renal diseases
tendency of H+ is to go inside the cell and alkalosis  prolonged K-sparing diuretic therapy
occurs  CLINICAL MANIFESTATIONS:
 weakness
H+
inside cell  malaise
K+  nausea
K+
H+
H+ 3
//carengreyes
  intestinal colic  renal/extrarenal causes: GI or skin
 diarrhea problems
 muscle irritability  older adults and debilitated people
 flaccid paralysis  insufficient fluid replacement associated with
 oliguria fever, vomiting, diarrhea, polyuria, tube-
 EKG changes: Q-wave and ST-segment feeding, prolonged hyperventilation
elevation  IV admin of hypertonic saline
 retention of Na in cardiac, renal or liver dse
 SODIUM  Cushing’s syndrome (hypersecretion of
glucocorticoids = aldosterone from adrenal
 responsible for osmotic pressure in ECF cortex)
 influence kidney’s regulation of body water and  hyperaldosteronism
electrolyte status  corticosteroid therapy
 promote irritability of nerve and muscle tissue and the  uncontrolled DM (polyuria = dehydration =
conduction of nerve impulses and influence the body secondary hypernatremia)
acid-base balance  diabetes insipidus (hyposecretion of ADH which
 N: 135 – 145 mEq/L is responsible for Na and water retention)
 FUNCTION:  CLINICAL MANIFESTATIONS:
 cell metabolism  early manifestations
 activates many enzyme systems  polyuria then oliguria, anorexia, n/v,
 SOURCES: weakness, restlessness
 meat, green vegetables, whole grains, nuts  neurologic
 early: restlessness, agitation, irritability,
 HYPONATREMIA muscle weakness
 TYPES:  severe: confusion, seizures, coma,
 hypovolemic hyponatremia – Na loss > water irreversible brain damage
loss  rigid paralysis (grave sign)
 euvolemic hyponatremia – moderately ↑ total  cardio
body water (TBW) and Na levels are normal  hypovolemic: orthostatic HPN with
 hypervolemic hyponatremia – greater ↑ in compensatory tachycardia
TBW than in TBW  hypervolemic: HTN BP, jugular vein
 redistributive hyponatremia – there is no distention, prolonged peripheral vein
change in TBW or Na but instead a shifting emptying, S3 gallop, and generalized
between ICF and ECF compartments weight gain and edema
 ETIOLOGY AND RISK FACTORS:  pulmonary
 cardiac, renal, and liver diseases  crackles, dyspnea, pleural effusion (d/t ↑
 healthy individuals – athletes, outdoor laborers, hydrostatic pressure)
military personnel (at risk from excessive  renal
perspiration)  hypervolemic: excrete some of excess
 older adults with lower percentage of TBW water
 CLINICAL MANIFESTATIONS:  hypovolemic: oliguria (compensatory
 neurologic mechanism)
 confusion, hallucinations, behavioral  integumentary
changes, seizures  dry and flushed skin, dry and sticky
 cardio mucous membranes, tongue furrows
 ↓ systolic and diastolic BP, orthostatic (wrinkles)
HPN, weak and thread pulse  ↑ thirst, fever
 tachycardia (compensatory response)
 respiratory
 crackles in lungs  CALCIUM
 changes in RR and DOB: tachypnea,  a necessary ingredient of cell cement, Ca helps body cells
dyspnea, orthopnea, and feeling SOB together (body – hardness)
 GI  Ca exchanges between bone and serum – deposition and
 n/v, hyperactive bowel sounds, abdominal resorption of bone
cramping, diarrhea  Thyrocalcitonin – towards the bone
 integumentary Parathormone (↑ Ca = ↓ parathormone) – outside the
 dryness of skin, tongue and mucous bone
membrane  N: 4.4 – 5.5 mEq/L
 FACTORS INFLUENCING CA BALANCE:
 HYPERNATREMIA  deposition and resorption of bones
 ETIOLOGY AND RISK FACTORS:  cellular components of bones and osteocytes
 TBW deficit relative to the total body Na (bone cell); ↑Ca = ↑osteoclast activity
content, which results in hyperosmolality  absorption of Ca from GIT

4
//carengreyes
  depend on dietary intake  neurologic depression
 Vit D promotes Ca absorption via intestines  weakness, fatigue, depression and
 excretion of Ca difficulty concentrating
 PO4, Vit D, PTH regulates Ca excretion in the  osmotic diuresis
urine and feces together to both ↑ and ↓  with Ca gallstones
serum Ca levels  severe colicky pain d/t urinary blockage
 impairs glomerular blood flow which can
 HYPOCALCEMIA lead to renal failure
 ETIOLOGY AND RISK FACTORS:  bone pain which can be d/t bone cancer
 older adults d/t inadequate intake  progressive neuro depression
 inadequate intake of Vit D  extreme lethargy, depressed sensorium,
 lactose intolerance, GI dse, liver dse, confsion, coma
alcoholism, anorexia, bulimia  severe hypercalcemia
 ↑ CHON, weight-reduction diets  ↑ conduction transmission, shortened
 prolonged institutionalization repolarization (shortened QT interval,
 pancreatitis (binding of FFA to Ca) widened T-wave), severe cardiac
 open wounds depression (cardiac dysrhythmias, ECG
 Cushing’s syndrome (promotes excretion of Ca) changes, cardiac arrest), hypokalemia
 overcorrection of acidosis (alkalosis causes ↓
Ca ionization)
 receiving multiple transfusions of stored blood
 MAGNESIUM
 Mg = increased acetylcholine (neurotransmitter)
 medications
 most of the Mg in the body is found in our bones,
 Mg SO4, aspirin, PO4 prep, biphosphates,
providing structural and storage functions
steroids, loop diuretics, antacids, laxatives
 assists hundreds of enzymes throughout body; regulates
 CLINICAL MANIFESTATIONS:
nerve and muscle functions, including actions of the
 neuromuscular hyperexcitability
heart, has a role in blood clotting process and immune
 numbness and tingling of hands, toes, lips
system
and emotional lability (irritability)
 N: 1.5 – 1.9 mEq/L
 hypoparathyroidism
 cardiac palpitations and restlessness
 severe hypocalcemia  HYPOMAGNESEMIA
 cardiac insufficiency, HPN, dysrhythmias,  ETIOLOGY AND RISK FACTORS:
prolonged QT interval, Trosseau’s and  Ca, PO4, Na and K imbalances
Chvostek’s sign, prolonged bleeding time  common cause of refractory (not responding to
 which progresses to seizures, laryngeal treatment) hypokalemia and hypocalcemia
stridor, tetany, hemorrhage, cardiac  critically ill paients, pregnancy and pregnancy-
collapse, eventually death related conditions, DM clients, infectious dse,
 prolonged hypocalcemia ischemic heart dse
 cataracts  alcoholic clients
 trophic changes  ↓ intestinal enzymes = ↓ absorption
 dry, sparse hair and rough skin,  Mg wasting
spontaneous fractures  severe/chronic malnutrition, malabsorption
syndromes (Crohn’s dse, celiac dse,
pancreatitis, GI losses from vomiting, GI
 HYPERCALCEMIA
suction, diarrhea, high volume ileostomies,
 ETIOLOGY AND RISK FACTORS:
fistulae, laxative abuse, radiation pancreatitis)
 metastatic malignancy
 acute renal failure and hyperphosphatemia
 breast, lungs, ovary, head and neck, lymph
 prolonged IV or TPN therapy without Mg
tissues, prostate, bladder, bone (multiple
 hyperparathyroidism, Cushing’s syndrome,
myeloma), kidney
hyperaldosteronism
 hyperparathyroidism
 inhibit Mg reabsorption
 bone decalcification and development of
 diabetic acidosis = osmotic diuresis = loss of Mg
renal calculi (kidney stone) containing Ca
 alkalosis
 thiazide diuretic therapy
 excessive phosphorus in intestine
 inhibits Ca excretion
 medications
 hypophosphatemia
 diuretics (loop, osmotic, thiazide),
 inhibits ability of kidney to excrete excess
antibiotics, corticosteroids, digitalis,
Ca
cocaine abuse
 CLINICAL MANIFESTATIONS:
 CLINICAL MANIFESTATIONS:
 moderate
 myocardial irritability
 anorexia, n/v, polyuria, muscle weakness,
 GI changes = ↓ contractility
fatigue, lethargy, dehydration, and
 anorexia, nausea, abdominal distention
constipation
 psychological
5
//carengreyes
  depression, psychosis, confusion

 severe
 ACID-BASE IMBALANCE
 Chvostek’s and Trosseau’s signs, tetany,  pH
convulsions, vasopasm leading to stroke  measure of acidity and alkalinity of a solution
 cardio  H represent H concentration in ion
 PVCs, atrial or ventricular fibrillation, and  ACID
ECG changes (prolonged QT intervals,  release H+
widened QRS complexes, and broadening  proton donors
of T-waves)  strong vs weak acids (HCl vs H2CO3)
 ex. ketone bodies, H3PO4 (phosphoric acid),
H2CO3 (carbonic acid), lactic acid
 HYPERMAGNESEMIA
 BASE
 ETIOLOGY AND RISK FACTORS:
 H+ acceptors
 renal insufficiency
 proton acceptors
 excessive use of Mg-containing antacids
 strong vs weak base (NaOH vs HCO3)
 administration of K-sparing diuretics (which
 BUFFER SYSTEM
conserves Mg)
 help prevents large changes in pH by absorbing/
 severe dehydration from ketoacidosis
releasing H+ ions
 ↓ synthesis of aldosterone (Addison’s dse)
 allows acid and base to be transported from where
 overuse of IV Mg SO4 for controlling premature
they are produced to where they are excreted
labor or pre-eclampsia
 CLINICAL MANIFESTATIONS: Precursor
 blocked release of acetylcholine from Chemistry Anatomy Organ
myoneural junction = ↓ muscle cell activity Acid H+ CO2 Lungs
 mild Base OH- HCO3 Kidneys
 vasodilation = HPN  Organ systems involved:
 ECG changes: prolonged PR and QT  Lungs
intervals  respiration affects the acid-base balance
 extreme by influencing the amount of CO2 in the
 severe muscle weakness, lethargy, bloodstream
drowsiness, loss of deep tendone reflexes,  CO2 + H2O = H2CO3 (weak), which breaks
respiratory paralysis and loss of down into H + HCO3
consciousness  any pulmonary dse concerning CO2
 cardio ↑ CO2
 delayed myocardial conduction = ECG with
wide QRS complexes, elevated T-wave, H20 (60%) + ↑ CO2 acidosis
heart block, and PVCs ↑ H2CO3

 FLUID LOSS AND OVERLOAD ↑ H + HCO3

stimulates medulla (respiratory center)

 Hyperosmolar
↑ solute ↓ water intake ↑ water loss ↑ ventilation

 Kidneys
s/sx of dehydration  all metabolic disorders: GIT, renal,
endocrine, accessory
 Hyposmolar
↑ HCO3
↓ solute ↑ water intake ↓ water loss
alkalosis

s/sx of fluid overload kidneys excrete HCO3

 Isotonic Volume Deficit ↓ HCO3

↓ solute and solvent acidosis

dehydration kidneys reabsorb HCO3

polyuria, “bleeding”, GIT fluid losses  CHEMICAL BUFFER SYSTEM

 PO4 buffer system
 Isotonic Volume Excess
 renal tubules and ICF
↑ solute and solvent  PO4 + H = H3PO4; excreted in the urine
fluid overload
 CHON buffer system
 most active; handling three-quarters of the
edema buffering of body fluids

6
//carengreyes
  AA  NH3  NH3 + H  NH4  CO2 – 33 = abN (↓) = alkalosis
 HCO3 – 20 = abN (↓) = acidosis
 O2 – 85 = N = without hypoxemia
 NORMAL ACID-BASE BALANCE  example: Fully compensated metabolic acidosis with
excessive/deficiency states moderate hypoxemia
respiratory disturbances  pH – 7.36 = N = leaning on acidosis
metabolic disturbances  CO2 – 30 = abN (↓) = alkalosis
altered acid-base balance  HCO3 – 18 = abN (↓) = acidosis
 O2 – 55 = abN (↓) = moderate hypoxemia
compensatory:
buffer, respiratory, renal
 NURSING PROCESS
(-) compensation partial complete  SUBJECTIVE DATA
 history
persistence of altered acid-balance state  illness (cardio, renal, GIT, neuro)
 surgery, burns, chronic illness
 diet
 ARTERIAL BLOOD GAS (ABG)  environment (humid)
 Normal values  lifestyle
 pH: 7.35 – 7.45  medications (diuretics)
 CO2: 35 – 45 mmHg  OBJECTIVE DATA
 HCO3: 22 – 26 mEq/L  vital signs
 O2  postural pulse rate, BP and HR, rhythm
 PaO2: 80 – 100 mmHg  sitting to standing; lying to sitting
 mild hypoxemia: 75 – 80 mmHg  if BP ↓ 10mmHg, ↑ PR = orthostatic HPN
 moderate: 65 – 75 mmHg  RR depths
 severe: < 65 mmHg  HR rhythm
 SaO2: 92 – 100% Excess Deficit
 mild hypoxemia: < 92% T N/A ↑
 STEPS IN READING ABG RESULTS: P ↑ ↑
 Step 1: determine if the levels are normal/abnormal
R ↑ ↑
 Step 2: is it compensated/uncompensated
BP ↑ early: ↑, late: ↓
 Compensated
 pH: abnormal  body weight
 systems: one system is abnormal (either  post void, pre breakfast
HCO3 or CO2)  same hour, same scale, same amt of clothing
 Uncompensated  integumentary status
 Partial  integrity (edema)
− pH: abnormal  types of edema:
− systems: both systems are abnormal − dependent
 Full  grade 1: tip of foot to ankle
− pH: normal  grade 2: above ankle to knee cap
− systems: both systems are abnormal  grade 3: knee cap to inguinal area
 Step 3: determine if alkalosis/acidosis, metabolic/  grade 4: inguinal to face
respiratory − pitting
 pH: acidosis/alkalosis  depth
 CO2: respiratory acidosis/alkalosis − weeping
 HCO3: metabolic acidosis/alkalosis  the edema goes out of the pores
 Step 4: respiratory/metabolic acidosis/alkalosis?  turgor (elasticity, no tenting)
Look for the abnormality (acid/alka) that is the same  lung auscultation (crackles)
as the abnormality of pH  neuromuscular status
 Step 5: determine if with or without hypoxemia  LOC
 ROM
 example: Uncompensated respiratory acidosis with  0/5 – no muscular contraction detected
mild hypoxemia  1/5 – barely detectable trace of
 pH – 7.33 = abN (↓) = acidosis contraction
 CO2 – 48 = abN (↑)= acidosis  2/5 – active mov’t with gravity eliminated
 HCO3 – 24 = N  3/5 – active mov’t against gravity
 O2 – 79 = abN (↓) = mild hypoxemia  4/5 – active mov’t against gravity and
some resistance
 example: Partially compensated respiratory alkalosis  5/5 – active mov’t against full resistance
without hypoxemia  reflexes
 pH – 7.48 = abN (↑) = alkalosis  (+++) – hyperreflexia

7
//carengreyes
  (++) – normal reflex  by-product of metabolism
 (+) – hyporeflexia  closely indicates renal function
 (-) – areflexia  N: 0.5 – 1.1 mg/dL
 muscle weakness, cramping, twitching,  NURSING DIAGNOSES
paresthesia  deficient fluid volume
 Trosseau’s sign (BP cuff)  excess fluid volume
 Chvostek’s sign (twitching of face)  risk for deficient fluid volume
 neck vein  risk for excess fluid volume
 central venous pressure (CVP)  risk for imbalanced temperature
 N: 4 – 11 cm2H2O (insertion via brachial/
femoral)  PLANNING AND IMPLEMENTATION
 pulmonary artery pressure (PAP)  replacement and maintenance of water and
 intake and output electrolytes
 type, amt, time of fluid intake  oral intake
 solid food are necessary to those pedia  administration of water and electrolytes
 foods that are semi-solids (ice cream, gelatin)  ill px: difficult to eat and drink; serve food that
are included in fluids the px likes
 ice chips are recorded by the amt of ice chips by  vomiting/diarrhea
2  Na and K loss: drainage and fistula – Na, K, Ca
 oral intake loss
 parenteral/venoclysis (IV)  salty broth, tea, soda, crackers – Na
 output  banana, citrus fruits, orange juice – Vit K
 time and amt  force fluids
 N: 30cc/hr or 0.5 – 1cc/kg/hr  ↑ fluid intake
 1 – 2 cc/kg/hr (pedia clients)  weakness: #1 s/sx of fluid deficit
 use of indwelling catheter  relief of sx
 specific gravity  thirst
 N: 1.010 (diluted) – 1.025 (concentrated)  initial sign of dehydration
 stool  relief by taking fluids
 drainage  oral care
 wound − do not give glycerin
− ileostomy, T-tube − water + saline, Bactidol (most
− weigh the dressing if bleeding is preferred)
profuse  n/v
 diaphoresis  IV replacements (usually D5LR d/t
 GI output electrolytes)
 vomitus, GIT drainage, liquid stools  anti-emetic (Metochlopromide)
 GI secretions  px on NPO
 N: pale, yellow, green, sour smell  fluid restriction
 plan with px
 LABORATORY TESTS  ice chips, gum, sugar-free candy
 Fluids and Electrolytes  remove any water at bedside
 Se osmolality  avoid salty/sweets
 ↑ fluid volume = ↓ Se osmolality  avoid alcohol-contained mouthwash (it can dry
 ↓ fluid volume = ↑ Se osmolality up mucosa)
 urine osmolality  NPO
 N: 50 - 100  nothing by mouth
 hematocrit  gavage
 concentrations of blood; blood/serum  when px have functional GUT but unable/have
 M: 39 – 49% difficulty swallowing
 F: 35 – 45%  NGT, OGT, PEG, jejunostomy
 results  H2O and physiologic solution of NaCl
 ↑ Hct = dehydrated/concentrated  H2O content can be ↑ with px if complains of
 ↓ Hct = diluted thirst
 ABG  parenteral fluids
 Allen’s test – assess patency of the ulnar artery  composition of fluids
 O2 saturation  types of solution
 BUN  isotonic
 by-product of CHON metabolism  hypertonic
 used to assess renal function  hypotonic
 N: 10 – 20 mg/dL  fluid challenge
 N: 5 – 18 mg/dL (infants) ↓ fluid volume
 creatinine D5W, PNSS
↓ renal perfusion
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 for fluid challenge forces urine from bladder into the urethra
↓ GFR (to assess client’s
kidney)
↓ urine output
 management of IV
 run IV slow  UROPATHOGENIC:
− WOF: s/sx of F&E excess  Bacteria
− especially IVF with K admin  female: bacteria exceeding 105 colonies/mL of
 ↑ K = cardiac arrest clean catch urine
− monitor urine output  male: bacteria at exceeding 104 colonies/mL of
− monitor: 1 kg = 1L loss clean catch urine
 KVO (keep vein open)  pathogens
 infuse for 24 hours  E. coli
 ex. 1L x KVO  staphylococcus sarpro
 hyperkalemia – emergency situation  enterococci
 D50/50 + insulin  enterobacter
 glucose + insulin  pseudomonas
 K will go along insulin  group B strept
 ROUTES OF INFECTION:
 ascending infection
URINARY AND RENAL DISORDERS  infection coming from the genitourinary orifices
 hematogenous spread
 URINARY TRACT INFECTION (UTI)  transurethral common route
 infectious/inflammatory renal disorder caused by  often from fecal contamination
pathogenic microorganisms  sexual intercourse/massage of the urethra
 CLASSIFICATIONS (according to anatomical involv’t):  HOST FACTORS IN THE PATHOGENESIS OF UTI:
 lower  obstruction
 cystitis  flushing mechanism of bladder protects the
 prostatitis host against infection
 urethritis  obstruction of urinary flow is one of the most
 upper important predisposing factors of UTI
 acute/chronic pyelonephritis  ex. post-renal obstruction – prostate
 renal abscess hyperplasia
 interstitial nephritis  signs: significant volume of urine retained
 MECHANISMS OF MAINTAINING STERILITY: in the bladder potentiates infection
 physical barrier of the urethra (urinary stasis), urethra strictures,
 urine flow defective bladder contraction
 uretherovesical junction  intra-renal obstruction
 secrete alkalinic substances  renal calculi, polycystic kidney dse, sickle-
 antibacterial enzymes (lysozomes) and antibodies cell dse
 IgA – mucosa (luhA, conjunctivA, salivA,  defective bladder-urethral length
bitukA)  urethral length
 IgG – gravid (mother to child)  women have short urethra which ↑ risk of
 IgM – macro (largest) – pentamere bacteria; ↑ risk of women than men
 IgE – (e)llergy  trauma to the urethra by sexual intercourse
 IgD – defense aid and the use of diaphragm ↑ UTI
 anti-adherent effects of mucosal cells of the bladder  proximity of the vaginal area and the urethra
 mucous membranes traps bacteria followed by colonization of pathogens is an
 PHYSIOLOGY OF URINARY DEFENSE AGAINST important risk factor
INFECTION:  urethra bypass, catheterization
 normal slow shedding of bladder epithelial cells and  bacteria is not being flooded
formation of glysoaminoglycan (GAG) attracts water  bladder catheter bypasses the urethra
molecules  occurs within 3-4days
 PATHOPHYSIOLOGY: overtime, bacteria migrates up the
uretherovesical reflux uretherovesical/ ureters and reach the kidneys
(more common) vesiouretal reflux
↑ concentrations of ammonia inactivate
backward flow from the backward flow from complement and inhibit migration of PMNS
urethra to the bladder bladder to urethra
bacteria can enter bloodstream
usually caused by usually caused by and cause septic shock
coughing, sneezing, straining defective bladder
 CLINICAL MANIFESTATIONS:
caused by dysfunctional bladder/urethra  Cystitis
 burning sensation on urination
↑ bladder pressure
 frequency
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 urgency  urinate after intercourse
supbrapubic pain  use white toilet paper for wiping perineum
dysuria  nursing diagnosis
incontinence  pain
nocturia  knowledge deficit
occasional discharge of pus in the urine or from  goals:
the urethra  relieve pain
 Pyelonephritis  encourage frequent voiding
 all cystitis symptoms plus fever, chills,  administer medications
costovertebral angle pain/tenderness, n/v,  application of heat
headache, malaise, HPN  encourage ↑ fluid
 DIAGNOSTIC EVALUATION:  prevent complication
 urinalysis  notify physician: n/v, fatigue
 > 10 WBC indicates pyuria (WBC in urine)  frequent kidney function test (KFT)
 showing many epithelial cells likely  avoid indwelling catheter
contaminated by vaginal secretions in women;  for recurrent UTI
inaccurate in indicating infection − acidification of urine: Vit C, cranberry
 urine gram staining for suspected phyelonephritis juice
 ↑ bacteria indicates 105 organisms − void every 2-3hrs
 urine culture  ↑ knowledge
 differentiation of contamination from true
infection
 not required with sexually active women
 ACUTE GLUMERULONEPHRITIS (AGN)
 follow-up culture is unwarranted  broad term
whenever relapse of symptoms  several disease processes that result in glomerular injury
 ultrasound  result of antigen-antibody deposits within the glomeruli
 imaging study of choice  frequently in school-age children
 upper UTI  PATHOPHYSIOLOGY:
 for persistent fever – despite antibiotics infection, impetigo, acute viral infection,
antigen (group A-B hemolytic)
 intravenous pyelography – excretory urogram (EUG)
 slightly dehydrate client deposition of antigen-antibody
 contraindicated to clients who cannot be complex in glumerulus
dehydrated
 ex. DM clients, myeoloma ↓ GFR RAA system
 CT scan – those not responding in antibiotics s/sx ↑ BP
 STD testing
 UTI and STD have same manifestations,  CLINICAL MANIFESTATIONS:
including genital-anal structures  typical
 MEDICAL MANAGEMENT:  hematuria
 Cystitis  d/t permeability  tolerable to large
 treatment course: 7 days substances like blood
 with exceptions for boys and new diabetic  tea-colored urine, oliguria
px, women with sx for more than 7 days,  proteinuria
and elderly people, drugs of choice are:  d/t permeability  protein is allowed to
− TMP – SMZ (trimethoprine- pass through
sulfamethoxazole)  anemia
− Coamoxiclav  d/t ↓ kidney function; kidney cannot
 Pyelonephritis produce erythropoietin for RBC production
 treatment course: 2 weeks  edema
 Co-amoxiclav  ↓ oncotic pressure
 suspected bacteremia  severe
 criteria: chills,  HA, malaise, fatigue
 3rd gen cephalosporins: ciprofloxacin  elderly
 NURSING PROCESS:  dyspnea
 assessment  distended neck vein
 s/sx of UTI  cardiomegaly
 association of s/sx UTI with sexual intercourse  pulmonary edema
 px knowledge on preventive health  atypical
 how to prevent cystitis  confusion
 drink 8-10 glasses (encourage frequent  somnolence (drowsy/near-sleep state)
urination) to flush out bacteria  seizures
 women should wipe front to back  CLINICAL COURSE OF AGN:
 avoid vaginal irritants, perfumes, bubble baths  90% of px will regain function within 60 days

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  10% will lead to renal failure  adequate urine output
 DIAGNOSTIC EVALUATION:
 urinalysis
 ↑ BUN, Se creatinine
 24 hrs for protein (↑) and creatinine clearance (↓)
 NEPHROTIC SYNDROME
outline the degree of renal function  cardinal signs
 ↑ antitreptolysin titer (from reaction to strepto  proteinuria
organism)  hypoalbuminemia
 ↓ albumin  edema
 ↓ Se complement  hyperlipidemia
 kidney biopsy (obstruction of glomerular   excessive leakage of albumin into the urine
chronic/acute)  PATHOPHYSIOLOGY:
 PHARMACOLOGICAL MANAGEMENT:  mechanisms for ↑ lipid is unknown
 symptomatic any condition with serious damage to the
flomerular capillary membrane:
 anti-HTN - chronic glomerulonephritis
 diuretics - DM with intercapillary glomerulosclerosis
 phosphate-binding agents - amyloidosis of kidneys 2O malignancies
- systemic lupus erythematosus (SLE)
 ↓ PO4 = ↑ Ca - renal vein thrombosis
 antibiotic therapy
 MEDICAL MANAGEMENT: hypoalbuminemia results to ↓ oncotic pressure
 restrict fluid intake
activates RAA system
 dietary protein is restricted moderately (ammonia is
not removed by kidney)  CLINICAL MANIFESTATIONS:
 CHO are ↑ liberally (so as not to convert to protein)  HA, fatigue, irritability
 restricted Na, K intake  3 cardinal signs
 COMPLICATIONS:  periorbital edema
 HTN  marked proteinuria – depletion of body CHON
 heart failure  REGULATION OF BODY FLUIDS
 fluid and electrolyte imbalance: hyperkalemia,  urinalysis
hyperphosphatemia, hypervolemia  foamy, marked proteinuria, microscopic
 malnutrition hematuria, urinary casts
 HTN encephalopathy  24-hour urine test
 end-stage renal disease (ESRD)  ↑ CHON
 NURSING PROCESS:  ↓ creatinine clearance
 assessment  CHON electrophoresis and immunoelectrophoresis
 medical hx: common infection  to categorize proteinuria
 PE: engorged neck vein, ↑ jugular vein pulse,  needle kidney biopsy
adventitious lung sounds, cardiac arrhythmia  histologic exam of renal tissue to confirm
 evaluate cardiac status diagnosis
 nursing diagnosis  serum chemistry
 ineffective renal tissue perfusion  ↓ CHON and albumin
 monitor V/S, I&O, dietary restrictions  ↑ TGA
 encourage bed rest  normal/↑ creatinine
 management  3 test tubes
 promote renal function  violet/purple – CBC
 administer meds  blue – bleeding parameters
− anti-HTN  red/plain – serum chemistry
− H2-blockers (stress-ulcer)  MEDICAL MANAGEMENT:
 improve fluid balance  treat underlying glomerular dse
− monitor s/sx HF  diuretics (use cautiously) and ACE inhibitors to
− observe for HTN encephalopathy control proteinuria
 ↑ BP = vasoconstrict = ↓ blood  corticosteroids or immunosuppressants to ↓
flow to brain = encephalopathy proteinuria
 EMERGENCY CASE  management of edema
− evidence of seizure activity  Na and fluid restriction, liberal K
 patient education  infusion of salt-poor albumin (to avoid spillage)
− explain that px must have follow-up  dietary CHON supplements
(allow client to recover)  ↓ fat
− encourage treatment of infection  COMPLICATIONS:
promptly  hypovolemia (↓ oncotic pressure = ↓ blood
− report s/sx of ↓ renal function (↓ volume)
urine output)  thromboembolic complications – renal vein
 expected outcome thrombosis

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  altered drug metabolism - ↓ CHON  more common in men (3/4), between 20-
 progression to ESRD 40 y/o

 NURSING PROCESS:
 assessment  CLINICAL MANIFESTATIONS:
 history of symptoms  pain (renal colic) depending on site of
 perform PE obstruction
 assess VS, I&O, lab values  signs of infection (bladder stones may be
 nursing diagnosis similar)
 risk for deficient fluid volume r/t disease  obstruction
process  GI problems – renointestinal reflexes and
 risk for infection r/t treatment with shared some nerve supply (celiac ganglion)
immunosuppressant between ureters and intestine
 interventions  DIAGNOSTIC EVALUATION:
 ↑ circulating volume and ↓ edema  UTZ (kidney, ureter, bladder – KUB)
 assess renal function  intravenous urography – determine site and
 encourage bed rest and ambulation (to ↓ evaluate
risk of thromboembolic complications)  spiral CT scan – full bladder
 mild to moderate Na restriction  analysis of available stone material by
 ↑ CHON diet polarization miscroscopy, x-ray diffraction and
 prevent infection infrared spectroscopy
− monitor s/sx of infection  MEDICAL MANAGEMENT:
− monitor temperature  if stones are <4mm, adequate hydration and
− aseptic technique pain control
 teach patient s/sx of NS  hospitalization for intractable pain
 adverse effects of medications (most  ESWL
especially immunosuppressants)  percutaneous nephrostomy
 dietary and fluid restriction  open surgical procedures
− ↓ Na  NURSING PROCESS:
 importance of exercise  nursing diagnosis
 severe preparation for dialysis and  alteration in comfort: acute pain
transplantation  impaired urinary elemination
− use of aseptic techniques  interventions
 administer opiod analgesic
 KIDNEY STONES  assume position of comfort
 administer anti-emetics
 NEPHROLITHIASIS  2-3L of water/day
 KIDNEY STONES − avoid overhydration  abdominal
distention
 UROLITHIASIS
 STONES ANYWHERE IN THE SYSTEM
 CAUSE:  ACUTE RENAL FAILURE
 crystallization of substances excreted in the  syndrome of varying causation is a sudden decline in
urine renal function
 oxalate  ↑ BUN and creatinine
 Ca crystals – 75%  STAGES:
 uric acid (liver, etc)  pre-renal
 struvite, amino acid cystine (less common)  perfusion problem
 HYPERCALCEMIA AND HYPERCALCIURIA CAUSED BY:  dehydration
 hyperparathyroidism  shock
 renal tubular acidosis  heart failure
 multiple myeloma (immobility)  burns
 excessive vitamin D, milk, and alkyl intake  sepsis
 causes:  intrarenal
 dehydration, poor fluid intake, immobility  acute kidney damage
 ↑ diet in purine and abnormal purine  acute tubular necrosis
metabolism (hyperuricemia and gout)  AGN
 genetic predisposition  diabetic nephropathy
 chronic infection, chronic obstruction  interstitial nephritis
 excessive oxalate absorption  post-renal
 living in mountainous, desert, tropical  urolithiasis
places d/t no water = concentrated urine  tumor
 BPH (benign prostatic hyperplasia)
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  uretal stricture
 neurogenic bladder
 bladder outlet obstruction

 CLINICAL COURSE:
 Oliguric/anuric
 HEMODIALYSIS
 ↑ urea, creatinine, organic acids  dialyzer (artificial kidney)
 complication: congestion  contains thousands of tiny cellophane tubules that
 Diuretic act as semi-permeable membranes
 complication: dehydration  COMPONENTS:
 Recovery  dialyzer (fresh, old)
 CLINICAL MANIFESTATIONS:  saline
 pre-renal  heparin pump
 ↓ tissue turgor  VASCULAR ACCESS:
 dryness of mucosal membrane  allowed to be removed, cleansed and returned
 weight loss to the px vascular system
 HPN  tunneled-cuffed catheter (TCC)
 oliguria  prosthetic-bridge graft (PBG)
 flat neck veins  arterio-venous fistula (AVF)
 tachycardia  COMPLICATIONS:
 intrarenal  atherosclerotic CVD
 edema, depends  anemia, fatigue
 obstruction to urine flow  gastric ulcers
 DIAGNOSTIC EVALUATION:  HPN d/t anti-HTN drugs
 urinalysis – ↑ Se BUN and creatinine  painful muscle
 urine chemistry  dysrhythmia d/t electrolyte imbalance
 renal UTZ – estimate renal size  air embolism (w/c is common with catheter, air
 MANAGEMENT: enters)
 identify client with pre-existing renal dse
 initiate adequate nutrition
 avoid exposure to nephrotoxins
 ACE, aminoglycosides, NSAIDs, COX2 inhibitors,
analgesics
 monitor chronic analgesic use
 prevent and treat shock
 modified trendelenberg
 bed rest
 stop bleeding
 PNSS or D5/Plain LR; inotropes/vasoconstrictors
 9 parameters
 LOC, color, breathing (RR), temperature,
PR, capillary refill, BP, peripheral pulses,
urine output
 schedule diagnostic studies
 restore and maintain BP
 treat hyperkalemia
 ECG changes – late, tented T-waves,
depressed ST-segments, wide QRS
complex
 administer cation exchange resin, Na
Polystyrene Sulfonate (Kayexalate)
 prepare for dialysis
 monitor ABG
 prepare for ventilator therapy
 administer Na bicarbonate
 nutrition: ↓ Na, K, CHON; ↑ CHO
 glucose + insulin to shift K into the cells

 CHRONIC RENAL FAILURE

 the difference with ARF is the recovery phase which does
not happen in CRF

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