Midterm Topics:
• Concepts of Fluids and Electrolytes
• Acid Base Imbalances
• Fluids, Electrolytes & Acid Base Imbalances
• Burn Injuries
• Renal disorders
• Communicable disease concepts
• Immunization
• Measles, German Measles, Chicken Pox, Influenza,
COVID 19
• PTB, Pneumonia, Diphtheria, Pertusis, Mumps
CONCEPT OF FLUIDS & ELECTROLYTES
Fluids
 50-60% of body weight is water
 The volume of fluid in each location varies with age
and sex
 Location:
 Within the cells = Intracellular fluids
 Outside the cells = Extracellular fluids
Fluid Intake
 Average oral fluid intake in a healthy adult :
2,500ml/day (1500-3000 ml/ day)
 Daily fluid intake standard formula (Kayser-Jones et
al., 1999; Mentes, 2000)
 100ml/kg for the 1st 10 kg of wt, plus
 50ml/kg for the next 10 kg of wt, plus
 15ml/kg per remaining kg of wt
Sources of Body Fluids
 Liquids
 Food
 Other sources: IVF, TPN, Blood products
Fluid Output
 Average fluid loss amounts to 2500ml/day
counterbalancing the input to maintain equilibrium
 Routes:
 Urination (1500ml/day: 30-50ml/hr: 0.5-1ml/kg/hr),
bowel elimination (200ml), perspiration & breathing
 Sensible loss
 Insensible loss = unnoticeable/ unmeasurable
Functions of the Body Fluids
 Transporter of nutrients, etc…
 Medium or milieu for metabolic processes
 Body temperature regulation
 Lubricant of musculoskeletal joints
 Insulator and shock absorber
Composition of Body Fluids
 Composed of solute, solvents, electrolytes, proteins,
 Plasma and interstitial fluids contain essentially the
same electrolytes and solutes, but plasma has a
higher protein content
 The major ICF é are K+ , PO-4 & Mg++
 The major ECF é are Na+ , HCO-3 & Cl
Translocation
 The delicate balance of fluid, electrolytes, acids, and
bases is ensured by an:
 Adequate intake of water and nutrients
 Physiologic mechanisms that regulate fluid volume
 Chemical processes that buffer the blood to keep its
pH nearly neutral
Tonicity of Body Fluids
 concentration of particles in a solution
 Body fluids are ISOTONIC comparable with 0.9%
NaCl
 The of body fluids is 275-300 mOsm/L normal
tonicity or osmolarity
 Hypotonic fluids have a lesser or lower solute conc.
than plasma; ex. is 0.45%, 0.33%NaCl soln
 Hypertonic fluids have a higher or greater conc. of
solutes (usually sodium) compared with plasma; ex.
is 3%NaCl
Fluid and Electrolyte Regulation
 Under normal conditions, the following mechanisms
regulates normal fluid volume and electrolyte
concentrations
 Osmoreceptors
 RAAS
 ANP
 Primarily, fluid volume is regulated by intake (thirst)
and output (urine) Osmoreceptors
 Specialized neurons in the hypothalamus
 Highly sensitive to serum osmolality
 Increased osmolality – osmoreceptors stimulates
hypothalamus to synthesize ADH
 Decreased osmolality – ADH is inhibited
 Triggers thirst promoting increased fluid intake
 Thirsty when ECF volume decreases by approx
700ml (2% of body weight)
 Also sensitive to changes in BV & BP through the
info relayed by baroreceptors (stretch)
Osmoreceptors
 A decrease in BV by 10%
 Systolic BP falls below 90 mm Hg
 RA is underfilled
 ADH is suppressed when BV, BP increases, and RA
is overfilled
Renin-Angiotensin-Aldosterone System (RAAS)
Natriuretic Peptides
 Overstretching (atrial & ventricular walls)  ANP &
BNP are released
 ANP & BNP inhibit the release of RENIN,
ALDOSTERONE and ADH =  Blood volume
 “POTENT diuretic”
 “Na-wasting”
 (-) thirst
Gastro-intestinal regulation
 The GIT digests food and absorbs water
 Passive & active transport of é, H2O, & solutions,
maintain the fluid balance in the body.
 Fluids & electrolytes move among cells,
compartments, tissue spaces, and plasma by the
processes of
 Osmosis
 Filtration
 Diffusion and
 Active transport
Osmosis
 Movement of water/liquid/solvent across a
semipermeable membrane from a lesser
concentration to a higher concentration
 Osmotic pressure - the power of a solution to draw
water toward an area of greater concentration
 Colloidal osmotic pressure - the osmotic pull
exerted by plasma proteins (e.g., albumin, globulin,
fibrinogen)
Filtration
 Movement of both solute and solvent across a
semipermeable membrane from an area of higher
pressure to lower pressure
 180 L of fluid from the blood is filtered by the
kidney each day
 Hydrostatic pressure – the pressure exerted by the
fluids within the closed system; pushes water
 If HP > OP = Filtration
Diffusion
 Movement of particles, solutes, molecules from an
area of higher concentration to an area of a lower
concentration through a semipermeable membrane
 Factors affecting rate of diffusion:
 Size of the molecules- larger size moves slower than
smaller size
 Concentration of solution- wide difference in conc.
has a faster rate of diffusion
 Temperature -  in To =  rate of diffusion
Facilitated Diffusion
 Require assistance from a carrier molecule to pass
through a semipermeable membrane
 E.g., insulin-glucose
Active Transport
 Movement of solute from lower concentration to
higher concentration using energy (ATP)
 e.g., Na-K
Fluid balance
- Water and its electrolytes are distributed in two major
compartments:
- 63% of the total body water is found within cells across
the age groups.
- 37% of the total body water is found outside the cells,
mainly in tissue spaces, plasma of blood, and lymph.
- The intracellular and extracellular fluid compartments
are maintained in a steady state to ensure proper
physiologic functioning.
Intracellular Fluid Compartment
- Includes all the water and electrolytes inside the cells
of the body.
- Approximately 25% of the 40 liters of body fluid in an
average-sized individual, or 63% of the total body water,
is contained within cell membranes.
- Contains high concentrations of potassium, phosphate,
magnesium and sulfate ions, along with most of the
proteins in the body.
- EXAMPLE: How much water is in the intracellular
fluid compartment of a 25-year old male patient who
weighs 60 kg?
• Step #1: Compute the total body water (TBW) based
on age and sex.
TBW = (60 kg) (0.6)
= 36 kg → weight of water
= 36 liters → volume of water
• Step #2: Compute for the intracellular fluid volume
(usually 63% of the total body water is intracellular
fluid)ICF = (36 liters) (0.63)
= 22.7 liters
Extracellular Fluid Compartment
- Includes all the fluid outside the cells: interstitial fluid,
plasma, lymph, secretions of glands, fluid within
subcompartments separated by epithelial membranes.
- Constitutes approximately 37% of the total body water.
- Contains high concentrations of sodium, chloride and
bicarbonate.
- One-third of the ECF is in plasma.
- EXAMPLE: How much water is in the circulatory
system of a 32-year old female patient who weighs 52
kg?
• Step #1: Compute for the total body water based on
age and sex.
TBW = (52 kg) (0.5)
= 26 kg → weight of water
= 26 liters → volume of water
• Step #2: Compute for the extracellular fluid volume
(usually 37% of the total body water).
ECF = (26 liters) (0.37) = 9.6 liters
• Step #3: Compute for the plasma volume.
Plasma = (9.6 liters)/3 = 3.2 liters
Serum Osmolality
- Reflects the amount of solute particles in a solution and
is a measure of the concentration of a given solution.
- Can be calculated using the formula:
• Osmserum = 2 (Na) + BUN + glucose
• Normal value = 285 – 295 mosm/kg
- Sodium is the most active determinant of serum
osmolality and is therefore actively moved across
membranes to ensure normal osmolality.
Regulation of Extracellular Fluid Composition
- Homeostasis requires that the intake of substances such
as water and electrolytes equal their elimination.
- Over a long period, the total amount of water and
electrolytes in the body does not change unless the
individual is growing, gaining weight, or losing weight.
- The regulation of water and electrolytes involves the
coordinated participation of several organ systems,
especially the uroexcretory system.
Thirst
- The hypothalamus contains the thirst center which
controls water intake.
- When the osmolality of blood increases, the thirst
center responds by initiating the sensation of thirst.
- This is one of the important means of regulating the
extracellular fluid volume and concentration.
- The mechanism is controlled by serum osmolality and
blood pressure:
• When water or some other dilute solution is
consumed, the osmolality of blood decreases, and
the sensation of thirst also decreases.
• When blood pressure decreases, the thirst center is
activated and the sensation of thirst is triggered.
- Ions also influence the concentration of water inside
and
outside the cells and contribute to the thirst mechanism.
Ions
- Factors which influence the concentration of water and
solutes inside the cells:
• Transport mechanisms
• Permeability of the cell membrane
• Concentration of water and solutes in the
extracellular fluid
Fluid Imbalances
Hypovolemia (Fluid Volume Deficit)
 Hypovolemia = Low volume of ECF
 Dehydration =  body fluid volume in both ECF &
ICF
 Occurs when loss of ECF volume exceeds the intake
of fluid.
 Different from dehydration
 FVD (hypovolemia) should not be confused with
DEHYDRATION, which refers to loss of water
alone, with increased serum sodium levels.
 VD may occur alone or in combination with other
imbalances.
 ECF loss is greater than the fluid intake – It occurs
when water and electrolytes are lost in the same
proportion as they exist in normal body fluids, so
that the ratio of serum electrolytes to water remains
the same.
 Etiology:
 Inadequate fluid intake
 Hemorrhage
 Prolonged vomiting and diarrhea
 Wound loss (burn injury)
 Profuse urination or perspiration
 Translocation of fluids (abdominal cavity)
 Pathophysiology:
 HR to maintain adequate CO
 BP falls with postural changes, or it may become
severely lowered when blood is rapidly lost
 Hemoconcentration occurs = potential for blood
clots, urinary stones (compromises kidney’s function
to excrete nitrogen wastes)
 Eventually it depletes ICF which can affect cellular
functions = change in mentation
 Abnormal fluid losses
 Vomiting, diarrhea, GI suctioning, Sweating,
nausea, lack of access to fluids,
 Third – space fluid shifts – edema, ascites
 Diabetes insipidus
 decreased ability to concentrate urine
 Interferes with water reabsorption
 Adrenal insufficiency – impaired production of
aldosterone
 Osmotic diuresis – increase in urine output
 Hemorrhage
 Coma
 Low fluid volume
 Urination
 Reabsorption
 ECF loss
 Assessment findings
 Thirst = one of the earliest symptoms
 Weight loss ≥2lb/24 hr
 BP, T°, rapid & weak thready pulse, rapid &
shallow respiration, scant & dark yellow urine, dry
& small volume stool, warm & flushed dry skin,
poor skin turgor “tents”, sunken eyes, clear lungs,
effortless breathing, weakness, flat jugular veins,
reduced cognition, sleepy
 Medical Management
 Treating its etiology
 Increasing the volume of oral intake
 Administering IVF replacement
 Controlling fluid losses
 Correction of Fluid Loss: oral route, IV route,
isotonic electrolyte solutions
 Strict Monitoring: I & O, weight, vital signs, CVP,
LOC, breath sounds, skin color, treatment is based
on the severity of fluid loss
 Renal Function: determine the cause of depressed
renal function, prerenal azotemia, acute tubular
necrosis, fluid challenge test
 Shock: 25% intravascular volume loss or rapid fluid
volume loss
 Nursing Management
 Gathers assessment data
 Plans measures to restore fluid balance  Etiology:
 Evaluates the outcomes of interventions  Excessive oral intake, rapid IV infusion
 Provide health teaching  Heart failure
 Intake and Output  Kidney disease
 q8 or q1  Excessive salt intake
 May impact the mortality of patients  Adrenal gland dysfunction
 Expect a concentrated urine  Administration of corticosteroids (prednisolone)
 Daily body weight: 0.5 kg weight loss is  Pathophysiology
approximately 500 ml fluid loss  Circulatory overload; compromises cardiopulmonary
 Closely monitored: tachycardia, severe hypotension, function
tachypnea, ↓ peripheral pulses, ↓ temperature, ↓  The heart compensates: BP,  force of contraction
CVP  Pitting edema develops (if there is 3L excess in IV
 Skin and tongue turgor volume)
 pinch skin o dependent on interstitial fluid  Assessment Findings:
volume  Early signs: weight gain, elevated BP, increased
 skin flattens more slowly breathing effort
 remain elevated for many seconds  Dependent edema (feet, ankles, sacrum, buttocks)
 over the sternum o inner aspects of the thighs  Rings, shoes & stockings leave marks in the skin
 forehead o tongue turgor is not affected by age  Prominent jugular vein when sitting
 smaller tongue o longitudinal furrows  Moist breath sounds (fluid congestion in the lungs)
 Dry mouth  Diagnostic Findings
 Urine Specific Gravity > 1.020 healthy renal  Hemodilution ( blood cell count,  hematocrit)
conservation of fluid  Low Urine SG
 Mental Function: ↓ cerebral perfusion - mild anxiety,  CVP (>10 cm H2O) ( 145 meq/L
confusion and agitation, comatose  Medical Management
 Hemodynamic: acute cardiopulmonary  Treat the underlying cause
decompensation  Restriction of oral & parenteral fluid intake
 Preventing Hypovolemia: identify patients at risk  Nursing Management
and take measures to minimize fluid losses  Implements prescribed interventions (limiting Na+
 Correcting Hypovolemia: oral fluids – oral & water intake)
rehydration solutions, antiemetics, Parenteral –  Administering ordered medications
Isotonic, Enteral  Elevates client head, legs, change position q2°,
 Gerontologic Considerations apply elastic stockings
 I & O from all sources Third Spacing
 Daily weight  Translocation of fluid from the IV or intercellular
 SE of medications space to tissue compartments & becomes trapped &
 documentation and prompt reporting useless
 skin turgor  Associated with
 Functional assessment: nurse provides if the patient  loss of colloids (hypoalbuminemia)
is unable to carry out self-care activities  Burns
 Incontinence - wear diapers, urinal, pace fluid intake  severe allergic reaction that alter capillary & cellular
 remind to drink adequate fluids membrane permeability
 Health Teaching  It can lead to hypotension, shock & circulatory
 Respond to THIRST because it is an early indication failure
of reduced fluid volume  Assessment Findings
 Consume at least 8-10 (8 ounce) glasses of fluid  S/sx of hypovolemia except weight loss
each day, and more during hot, humid weather  Enlargement of organ cavities (ascites)
 Drink water as an inexpensive means to meet fluid  Anasarca “brawny edema”
requirements  Management
 Avoid beverages with alcohol & caffeine  Restoration of colloidal osmotic pressure (albumin),
 Include a moderate amount of table salt or foods then diuretics
containing sodium each day  Nursing care combines the assessment techniques
 Rise slowly from a sitting or lying position to avoid for detecting both hypovolemia & hypervolemia
dizziness and potential injury Electrolyte Imbalances
Hypervolemia (Overhydration) Electrolytes “ions”
 High volume of water in the IV compartment
 Substances present in ICF & ECF that carry sodium ions are excreted.
electrical charge  Aldosterone
 Cations  help the reabsorption of sodium ions in the loop of
 Anions Henle is very efficient.
Sources of Electrolytes  When it is absent, the reabsorption of sodium in the
 Food intake/ ingested fluids nephron is greatly reduced and the amount of
 Medications sodium lost in the urine increases.
 IVF, TPN solutions  Sweat Mechanism- excretion from the body
Dynamics of Electrolyte Balance  Primary mechanisms that regulate the sodium ion
 Distribution concentration in the extracellular fluid:
 Na, Ca, Cl concentration are higher in ECF  Changes in the blood pressure
 K, Mg, PO4 concentrations are higher in ICF  Changes in the osmolality of the extracellular fluid
 Excretion Hyponatremia
 Urine, feces, surgical/wound drainage, pathological  less than 135 meq/L.
conditions  Most common electrolyte abnormality
 Regulation  Initial approach is the determination of serum
 Kidneys, GIT, hormones (aldosterone, ANF, PTH, osmolality
calcitonin)  Causes:
NORMAL VALUES AND MASS CONVERSION  Profuse diaphoresis & diuresis
FACTORS  Excessive ingestion of plain water
Normal Plasma Mass  Administration of electrolyte –free solution
Values Convertion  Prolonged vomiting, GI suctioning, draining fistulas
Sodium (Na+) 135 – 145 meq/L 23 mg = 1 meq  Addison’s disease
Potassium (K+) 3.5 – 5.0 meq/L 39 mg = 1 meq  Manifestations:
Chloride (Cl-) 98 – 107 meq/L 35 mg = 1 meq  Mental confusion, personality changes
- Bicarbonate 22 – 26 meq/L 61 mg = 1 meq  Muscular weakness
(HCO3 )  Anorexia, restlessness
Calcium (Ca2+) 8.5 – 10.5 mg/dL 40 mg = 1  Elevated BT, tachycardia, N&V
mmol  Severe: convulsions & coma
Phosphorus 2.5 – 4.5 mg/dL 31 mg = 1  Management:
mmol • Underlying cause is corrected
Magnesium (Mg2+) 1.8 – 3.0 mg/dL • Mild deficits: oral administration of Na+
24 mg = 1 • Severe deficits: IV solutions
mmol  Treatment:
Osmolality 285 – 295  Hypertonic (3%) saline with furosemide
mosm/kg  Water Restriction, Isotonic Saline Infusion And
Administration Of Demeclocycline- For
Sodium (Na+ ) 135-145mEq/L (mmol/L) asymptomatic patients, approach includes
 Major cation in ECF; major contributor of plasma Hypernatremia
osmolality  > 145 meq/L
 About 90 to 95% of the osmotic pressure  Develops from excess water loss, frequently
 ECF Na+ level determines whether water is retained,  accompanied by an impaired thirst mechanism.
excreted or translocated  Hypokalemia, hypercalcemia or sickle cell anemia
 Regulated by kidney (aldosterone, ADH, NP) can cause nephrogenic diabetes insipidus.
  serum Na = (-) aldosterone, (+) ADH & NP  Clinical Findings:
  serum Na = (+) aldosterone, (-) ADH & NP  Intact thirst mechanisms usually prevent
 Functions: hypernatremia.
 Skeletal/ heart muscle contraction, nerve impulse  Its presence is commonly associated with
transmission, Normal ECF osmolality, Normal ECF encephalopathy of any cause, or cerebrovascular
volume disease.
 Average dietary intake of sodium is about 6-14  Orthostatic hypotension and oliguria are typical.
g/day  Hyperthermia, delirium and coma may be seen with
 1 tsp of table salt = 2000 mg severe hyperosmolality.
 1 tsp soy sauce = 1029 mg  Causes:
 1 medium banana = 451 mg  Profuse watery diarrhea
1 medium avocado 1097 mg  Excessive salt intake without sufficient water intake
- Kidneys provide the major route by which the excess
 Decreased water intake (elderly, debilitated,  lead to an increase in serum or plasma osmolality.
unconscious clients)  Symptoms:
 Excessive administration of solutions containing  Anorexia
Na+  Nausea
 Excessive water loss without accompanying loss of  Vomiting
sodium  Apathy
 Results in:  Weakness
 Thirst  Orthostatic lightheadedness
 Dry, sticky mucous membranes  Syncope
 Decreased UO  Weight loss is an important sign and provides an
 Fever  estimate of the magnitude of the volume deficit.
 Rough, dry tongue  Other physical findings:
 Lethargy  Orthostatic hypotension
 Coma if severe  Poor skin turgor
 Treatment:  Sunken eyes
 Depends on the cause  Absence of axillary sweat
 Oral administration of plain water  Oliguria
 IV administration of hypotonic solutions  Tachycardia
 Nursing Management:  Shock and coma (severe volume depletion)
 Early detection  Causes of ECF depletion:volume
 Maintain accurate I&O measurements  Gastrointestinal losses
 Assess VS q1-4 hr  Diuretics
 Closely monitor IV fluid infusion  Renal or adrenal disease
 Implements prescribed dietary restrictions or  Blood loss
supplements  Sequestration of fluid
 Gathers data that indicate increased or decreased  Treatment
symptoms & notify the physician  restoration of the ECF volume with solutions
Fluid and Electrolyte Management General containing the lost water and electrolytes.
Management of Fluids  Daily assessment of weight, ongoing fluid losses and
Maintenance Therapy: Minimum Water serum electrolyte concentrations.
Requirements  Orally- Mild degrees of volume
- Can be estimated from the sum of the urine output  Intravenous Isotonic Fluid - severe deficit
necessary to excrete the daily solute load (500 mL per accompanied by circulatory compromise
day if the urine concentrating ability is normal) plus the until hemodynamic stability has been restored. One to
insensible water losses from the skin and respiratory two liters of fluid should be given over the first hour..
system (500 to 1000 mL per day), minus the amount of ECF Volume Excess
water produced from endogenous metabolism (300 mL  Manifestations:
per day)  Weight gain is the most sensitive and consistent sign
- Two to three liters of water are needed to produce a  of ECF volume excess.
urine volume of 1 to 1.5 liters daily.  Edema is usually not apparent until 2 to 4 kg of
- Weighing the patient daily is the best means of fluid have been retained.
assessing net gain or loss of fluid, since the  Dyspnea
gastrointestinal, renal and insensible fluid losses of the  Tachycardia
hospitalized patient are unpredictable.  Jugular venous distention
Fluid / Electrolyte Replacement: Insensible Water  Hepatojugular reflux
Losses  Rales on pulmonary auscultation
 Usually average 500-1000 mL daily, and depend on  Causes:
 respiratory rate, ambient temperature, humidity and  Heart, liver or renal failure
body temperature.  Excessive renal sodium and water retention
 increase by 100-150 ml daily for each degree over  Unnecessary salt administration
37°C.  Treatment
 Fluid losses from sweating  Treatment of the nephrotic syndrome and the
 Mechanical ventilation accentuate losses from the  cardiovascular volume overload associated with
respiratory tract. renal failure.
ECF Volume Depletion  Treatment of heart failure and cirrhosis
 Occurs with losses of both sodium and water.
 Potassium (ECF: 3.5-5.0mEq/L or mmol/L) (ICF:
140)
 Major ICF cation
 Functions: Regulates CHON synthesis, glucose use
& storage, maintains action potentials in excitable
membranes
 Any change in blood K+ seriously affects
physiologic activities (a decrease of 1 meq/L = 25%
difference in total ECF K+ concentration)
Hypokalemia
 A total body deficit of about 350 meq occurs for
each 1 meq/L decrement in serum potassium
concentration.
 Changes in blood pH and hormones (insulin,
aldosterone, and β-adrenergic agonists)
independently affect serum potassium levels.
 Causes:
 K+-wasting diuretics (furosemide [Lasix],
ethacrynicacid [Edecrin], hydrochlorothiazide
[HydroDIURIL]
 Severe vomiting & diarrhea, draining intestinal
fistula, prolonged suctioning
 Large doses of corticosteroids
 IV administration of insulin & glucose
 Prolonged administration of non electrolyte
parenteral fluids
 Signs & symptoms:
 Fatigue
 Weakness
 Anorexia
 N&V
 Cardiac dysrhythmias
 Leg cramps
 Muscle weakness, paresthesias
 Severe: hypotension, flaccid paralysis, DEATH from
cardiac arrest/ respiratory arrest
 ECG changes:
 ST-segment depression
 Flat or inverted T wave
 Increased U wave
 Treatment:
 Elimination of the cause
 Substitute K-wasting with K-sparing diuretics
 (Spirinolactone [Aldactone]
 Increase oral intake of K-rich foods/ K
supplements - mild cases
 Safest way is with oral potassium.
 Severe Cases
 KCL
 Intravenous replacement
 a peripheral intravenous line at rate up to 40
meq/L/hr.
 > 2.5 meq/L, and there are no ECG abnormalities, it
can be given at a rate of 10 meq/L/hr in
concentration that should never exceed 40 meq/L.
Hyperkalemia
 Many are spurious or associated with acidosis
 Common practice of repeatedly clenching and
 unclenching the fist during venipuncture may raise
the potassium concentration by 1-2 meq/L by
causing local release of muscles from forearm
muscles.
 Causes:
 Renal failure
 Severe burns
 Administration of K-sparing diuretics
 Overuse of K supplements, salt substitutes
 potassium rich foods
 Crushing injuries
 Addison’s disease
 Rapid administration of parenteral K salts
 Signs/ Symptoms:
 Diarrhea
 Nausea
 Muscle weakness
 Paresthesias
 Cardiac dysrhythmias
 Peak T waves
 Prolonged PR intervals
 Flat or absent P wave
 Wide QRS complex
 Treatment: depends on the cause and severity
 Decrease K-rich food intake, d/c oral potassium
replacement until laboratory values are normal (mild
cases)
 Administration of cation-exchange resin like sodium
polystyrene sulfonate (kayexalate) or combination of
 IV regular insulin & glucose (severe cases)
 Peritoneal dialysis/ hemodialysis for removing toxic
substances from the blood
 Nursing Management
 Assess clients for conditions with the potential
tocause potassium imbalances
 Identifies signs & symptoms
 Monitors laboratory findings
 Administer medications: KCL – diluted in an IV
solution & administered at a rate below 10mEq/hr
Calcium++ 9-10.5 mg/dl (2.25-2.75 mmol/L)
 2 forms: bound & unbound (ionized)
 Bound – attached to CHON (albumin)
 Ionized – “free” calcium; active form; ECF –
 Functions: Bone strength & density, activation of
enzymes or reactions, skeletal/ cardiac muscle
contraction, nerve impulse transmission, blood
clotting
 Regulated by: Vitamin D, PTH, thyrocalcitonin
Hypocalcemia
 Seen commonly in critically ill patients due to
acquired defects in parathyroid- vitamin D axis.
 Results occasionally in hypotension which responds
to calcium replacement therapy
 Causes:
 Vit D deficiency malignant diseases that do not respond to other
 Hypoparathyroidism forms of therapy
 Acute pancreatitis  Nursing Management:
 Corticosteroids  Encourage increased fluid intake
 Rapid administration of multiple units of blood that  Collaborates with dietitian to limit food sources of
contain an ant calcium additive Ca++
 Intestinal malabsorption  Ambulation as tolerated!!!
• Accidental removal of parathyroid glands  Provide assistance; avoid falls
 Signs & symptoms: Phosphorus (P) 3-4.5 mg/dl (0.97-1.45 mmol/L)
 Tingling sensations (extremities, around the mouth)  Major anion ICF (80% is in bones)
 Muscle & abdominal cramps  Functions: Activating B-complex vitamins, ATP,
 Carpopedal spasms (+ Trousseau’s sign) assisting in cell division, cooperating in CHO,
 Mental changes CHON & FAT metabolism, acid-base buffering,
 + Chvostek’s sign (spasm of facial muscle) calcium homeostasis; balanced & reciprocal
 Laryngeal spasms relationship w/ Ca++
 Tetany (muscle twisting)  Regulated by PTH:
 Seizures  PTH = P
 Bleeding  PTH = P
 Cardiac dysrhythmias - Phosphate and sulfate are reabsorbed by active
 Treatment: transport in the kidneys.
 Administration of oral Ca++ & Vitamin D (mild - Rate of reabsorption is slow
cases) Phosphorus Imbalance
 IV administration of Ca++ salts (Calcium gluconate) - Phosphorus imbalance refers to conditions in which the
–severe cases element phosphorus is present in the body at too high a
 Nursing Management: level (hyperphosphatemia) or too low a level
 Closely monitor for neurologic manifestations (hypophosphatemia).
(tetany, seizures, spasms) - Almost all of the phosphorus in the body occurs as
 Seizure precautions phosphate (phosphorus combined with four oxygen
 Provide bed rest for comfort, avoid falls atoms), and most of the body's phosphate (85%) is
 Cardiac dysrhythmias & airway obstruction located in the skeletal system, where it combines with
 Check for signs of bruising or bleeding calcium to give bones their hardness.
Hypercalcemia - PHOSPHATE (HPO4)
 Associated with • Phosphorus primary anion in ICF
 Parathyroid gland tumors • Most deposited with calcium in bones
 Multiple fractures • Maintenance requires adequate renal functioning
 Hyperparathyroidism • Sources: meats, fish, dairy products, nuts
 Excessive doses of vitamin D Hypophosphatemia
 Prolonged immobilization • Hypophosphatemia (low blood phosphate) has
 Certain malignant diseases (multiple myeloma, acute various
 leukemia, lymphomas)  Causes.
 Signs & symptoms  Hyperparathyroidism, a condition in which the
 Deep bone pain  parathyroid gland produces too much PTH
 Constipation, anorexia, N & V  .Poor kidney function
 thirst  Overuse Of Diuretics
 Pathologic fractures  chronic diarrhea or a deficiency of vitamin D
 Mental changes (decreased memory & attention  Malnutrition due to chronic alcoholism
span)  diabetic ketoacidosis or severe burns can provoke
 Kidney stones hypophosphatemia
 Management  Respiratory alkylosis, brought on bhyperventilation,
 Determining & correcting the cause  Symptoms:
 Increase fluid intake & limit Ca++ consumption  occur only when phosphate levels have decreased
(mild cases) profoundly.
 0.45% or 0.9%NaCL (acute cases) and diuretics:  muscle weakness, tingling sensations,tremors, and
furosemide (Lasix); oral phosphates; calcitonin bone weakness.
(Cibacalcin)  may also result in confusion and memory loss,
 Corticosteroids or plicamycin (Mithracin) – used for seizures, and coma.
 Diagnosis•
assessed by measuring serum or plasma levels of
phosphate and calcium.
is diagnosed if the blood phosphate level is less than 2.5
mg/dl
 Management
 focuses on correcting the underlying cause of the
imbalance and restoring equilibrium.
 surgical removal of the parathyroid gland
 ceasing intake of drugs or
 instigating measures to restore proper kidney
function.
 drinking a prescribed solution that is rich in
phosphorus; solution can cause diarrhea
 doctor recommend that patients drink 1 qt (0.9 L) of
skim milk per day instead
 Other phosphate-rich foods include green, leafy
vegetables; peas and beans; nuts; chocolate; beef
liver; turkey
Hyperphosphatemia
 Causes
 decline in the normal excretion of phosphate in urine
as a result of kidney failure or impaired function.
 Hypoparathyroidism
 Pseudoparathyroidism,
 Overuse of laxatives or enemas that contain
phosphate.
 Hypocalcemia
 Symptoms
 Generally asymptomatic;
 Numbness and tingling in the extemities, muscle
cramps and spasms, depression, memory loss, and
convulsions.
 When calcium-phosphate crystals build up in the
 blood vessels, they can cause arteriosclerosis, which
 can lead to heart attacks or strokes.
 When the crystals build up in the skin, they can
cause severe itching.
 Diagnosis•
 assessed by measuring serum or plasma levels of
phosphate and calcium.
 is diagnosed if the blood level is above 4.5 mg/dl.
 assessments of kidney function, dietary intake, and
appropriate hormone levels.
 Management
 focuses on correcting the underlying cause of the
 initiating hormone therapy caused by
hypoparathyroidism;
 ceasing intake of drugs or imbalance
 instigating measures to restore proper
kidney function.
 Restoring phosphorus equilibrium in cases of mild
 Mild- involves restricting intake of phosphorus-rich
foods and taking a calcium-based antacid
 Severe - an intravenous infusion of calcium
gluconate may be administered.
 Dialysis may also be required in severe cases to help
remove excess phosphate from the blood
Magnesium (Mg++) 1.3-2.1 mg/dl (0.65-1.05 mmol/L)
 60% stored in bones & cartilages; much more is
stored in ICF (heart, liver, skeletal muscles)
 Functions:
 ICF – skeletal muscle contractions, CHO
metabolism, ATP formation, Vit.B-complex
activation, DNA synthesis, CHON synthesis
 ECF – regulates blood coagulation & skeletal
muscle contractility
 Regulated by the kidney & GIT (exact mechanism
are not known)
 Excretion is via the kidney.
Hypomagnesemia
 Nearly half of hospitalized patients have
unrecognized hypomagnesemia.
 In critically ill patients, arrhythmias and sudden
death may be complications.
 Causes:
 Chronic alcoholism
 Severe renal disease
 Severe malnutrition
 Intestinal malabsorption syndromes
 Excessive diuresis (drug induced)
 Prolonged gastric suction
 Signs & symptoms:
 Tachycardia & other dyshrythmias
 Neuromuscular irritability
 Paresthesias of the extremities
 Leg & foot cramps
 Mental changes
 (+) Chvostek’s & Trousseau’s sign
 Seizures
 Management:
 Oral magnesium salts/ magnesium rich foods
 IV magnesium sulfate
Hypermagnesemia
 result of renal insufficiency and the inability to
excrete what has been taken in from food or drugs,
especially antacids and laxatives.
 Potentially life-threatening as it impairs both central
nervous system and muscular function.
 Causes:
 Renal failure,
 Excessive use of antacids or laxatives
 Signs & symptoms:
 Flushing, warmth, hypotension, lethargy,
drowsiness, bradycardia, muscle weakness,
depressed respirations, coma
 Management:
• Decrease oral magnesium intake
• Discontinue parenteral replacement
• Hemodialysis (severe cases)
 Nursing Management:
 Closely observe for dysrhythmias & early signs of
 neuromuscular irritability • Heparin (1,000 units/mL)
 If giving MgSO4, always check the BP!!! • Alcohol
(vasodilation) • Cotton balls (soaked with alcohol AND dry)
 Antidote: Calcium gluconate (kept available) • Container with ice water
 Monitor vital signs 3) Aspirate 1 mL of heparin using a glass syringe
 Provide health teaching 4) Coat the inner surface of the syringe with heparin,
 Identify the electrolyte imbalance each client is taking care to pull and push the plunger to make sure
most likely manifesting: heparin evenly coats the syringe.
 Client 1 nauseated & weak. The ECG shows a 5) Expel the excess heparin from the syringe.
prominent U wave 6) Palpate for the radial pulse.
 Client 2 muscle twitching and tingling around 7) With the needle directed at a slight angle from the
mouth. When the nurse applies a BP cuff to the vertical, and pointed cephalad, gradually puncture the
client’s arm and occludes blood flow for 3 minutes, site and wait for arterial blood to rush in.
the fingers and wrist become flexed 8) After obtaining the specimen, secure the needle and
 Client 3 thirsty, lethargic and excreting only scant place the syringe with the specimen in ice water.
urine. 9) Apply direct pressure on the puncture site for at least
Chloride (Cl- ) 98-106 meq/L (mmol/L) one minute, or until bleeding stops using a dry sterile
 Major ECF anion; work w/ Na+ to maintain ECF cotton ball.
osmotic pressure 10) Send the specimen directly to the laboratory.
 Important in the formation of HCL in the stomach 11) A sample is allowed to stand for a maximum of two
 Participates in chloride shift (exchange between Cl- hours only.
& HCO3 - ) Respiratory regulation
ACID BASE IMBALANCES - Retains or eliminates carbon dioxide (potential acid)
 Body fluids contains ACIDS & BASES aside from Renal regulation
electrolytes  Eliminates or retains HCO3
 H2CO3 acid & base content influence the pH  Eliminates or retains hydrogen ion
 HCO3 of the body (amount of H+ in a solution) 1. Bicarbonate Buffer System
 Normal plasma pH is maintained by - Is a mixture of carbonic acid (H2CO3) and its salt,
 Chemical regulation (bicarbonate-carbonic acid sodium bicarbonate (NaHCO3) (potassium or
buffer system) 20:1 magnesium bicarbonates)
 Adding/ removing H+ ions - If strong acid is added:
 Respiratory & renal regulation • Hydrogen ions released combine with the bicarbonate
 Releasing & conserving CO2 ions and form carbonic acid (a weak acid)
 Retaining or excreting HCO3 • The pH of the solution decreases only slightly
Acid-Base Disturbances - If strong base is added:
- Regulation of pH is accomplished by: • It reacts with the carbonic acid to form sodium
• Kidneys bicarbonate (a weak base)
• Lungs • The pH of the solution rises only slightly
• Buffer systems - This system is the only important ECF buffer
- Information obtained from the arterial blood gas 2. Phosphate Buffer System
measurements: - Nearly identical to the bicarbonate system
• pH - Its components are:
• Partial pressure of carbon dioxide (pCO2) • Sodium salts of dihydrogen phosphate (NaH2PO4¯), a
• Partial pressure of oxygen (pO2) weak acid
• HCO3 level • Monohydrogen phosphate (Na2HPO42¯), a weak base
• Oxygen saturation (O2Sat) - This system is an effective buffer in urine and
Normal values: intracellular fluid
a. pH = 7.35 – 7.45 3. Protein Buffer System
b. pCO2 = 35 – 45 mmHg - Plasma and intracellular proteins are the body’s most
c. pO2 = 80 – 100 mmHg plentiful and powerful buffers
d. HCO3 = 22 – 26 meqs/L - Some amino acids of proteins have:
e. O2Sat > 95%-100% • Free oganic acid groups (weak acids)
Steps in obtaining an ABG specimen: • Groups that act as weak bases (e.g., amino groups)
1) Check the bleeding parameters of the patient. - Amphoteric molecules are protein molecules that can
2) Prepare the following: function as both a weak acid and a weak base
• Glass syringe
  Increased bicarbonate or decreased H+ ion
concentrations
 Excessive oral or parenteral use of bicarbonate
containing drugs or alkaline salts
 Vomiting, prolonged gastric suctioning,
hypokalemia, hyperaldosteronism (retention of
sodium bicarbonate)
 Assessment findings:
 Anorexia, N & V, circum oral paresthesias,
confusion, carpo pedal spasm, hypertonic reflexes,
tetany low RR (compensatory effort)
 ABG: high pH, high HCO3 (N to high PaCO2)
 Medical Management:
Metabolic Acidosis  Eliminating the cause
 There is increased organic acids (other than carbonic  Prescribing potassium (K+) to correct hypokalemia
acid) or decreased bicarbonate  NaCL if there is rapid ECF volume depletion
 Cause:  Causes:
 Anaerobic metabolism (form’n of byproduct lactic  Gain of bicarbonate (HCO3): Alkali intake
acid) = shock & cardiac arrest  Loss of hydrogen ion: Vomiting, Suction
 Starvation, diabetic ketoacidosis = fatty acids  Loss of potassium: Diuretics
accumulation  Manifestations:
 Kidney failure (cannot reabsorbed HCO3)  Respiratory depression
 Aspirin overdosage, profuse diarrhea, intestinal  Hypokalemia
wound drainage (HCO3 is lost)  Decreased GI motility and paralytic ileus
 Loss of bicarbonate (HCO3)  ECG: extra “U” wave
 Intestinal loss  S/Sx of hypocalcemia
 Diuretics  Tingling and spasms
 Accumulation of acids  Dx:
 Lactic acid  ABG analysis
 Ketoacids  Hypokalemia
 Uremia/Azote  ECG: Extra “U” wave
 Salycilate poisoning  Med/Nsg Mngt:
 Assessment findings:  Avoid antacids
 Kussmaul’s breathing (deep & rapid breathing)  Anti-emetics
 Anorexia, N & V, headache, confusion, flushing,  Correct underlying cause
 lethargy, malaise, drowsiness, abdominal pain or Respiratory Acidosis Acute/ Chronic
discomfort, weakness  Causes:
 Cardiac dysrhythmias can develop, force of cardiac  DISORDERS that restrict/limit the RELEASE of
contraction can be weakened Carbon dioxide in the LUNGS
 Stupor & coma (severe cases)  Pneumothorax, Hemothorax, Pulmonary edema
 ABG: decrease pH, decrease HCO3 (N to decrease  Acute bronchial asthma
PaCO2)  Atelectasis
 Medical Management:  Hyaline membrane disease, RDS in NB
 Treating the cause & replacing F&E that may have  Pneumonia
been lost  Drug overdose
 IV bicarbonate (severe cases)  Head injuries
 Hemo/peritoneal dialysis  Chronic- emphysema, bronchiectasis, bronchial
 Manifestations: asthma
 INCREASED RESPIRATORY RATE  Assessment findings:
 (Kussmaul’s respiration)  Client may breathe slowly or irregularly, or stop
 CNS depression breathing
 hyperkalemia  Decreased expiratory volumes
 Dx:  Tachycardia (dysrhythmias), Cyanosis
 ABG analysis  Behavioral changes- mental cloudiness, confusion,
 Hyperkalemia disorientation, hallucinations (accumulation of CO2)
 ECG: Tall Peaked T-wave  Tremors, muscle twitching, flushed skin, headache,
Metabolic Alkalosis
 weakness, stupor, coma pH remains ABNORMAL
 ABG: decrease pH, increase PaCO2 (N to increase c. Uncompensated: Either the CO2 or HCO3 does not
HCO3) adjust (NORMAL), pH still ABNORMAL
 Medical management Nursing Management: Acid- Base Imbalances
 Treatment is individualized depending on the cause  Document all presenting S/Sx (baseline data)
of imbalance  Monitor laboratory findings and report it to the
 Mechanical ventilation (may be necessary to support physician
 respiratory function)  Monitor fluid status: accurate I & O
 IV NaHCO3 if ventilation efforts do not adequately  Implements prescribed medical therapy
restore a balanced pH  F & E replacements
 Bronchodilators, antibiotics, airway suctioning  Suctioning the airway
 Manifestations:  Maintaining mechanical ventilation
 TACHYcardia  Monitoring cardiac rate & rhythm
 TACHYpnea  Administering CPR whenever necessary
 Mental cloudiness BURN INJURY
 Cerebrovascular dilation Burns
 Hyperkalemia  Tissue damage caused by exposure to excessive
 Increased ICP (severe) heat.
 Dx:  Traumatic injury to the skin and underlying tissues
 ABG analysis caused by heat, chemical, & electrical injuries (most
 Hyperkalemia severe!!!)degree of tissue damage is related to:
 ECG: Tall-peaked T wave  What agent caused the burn
 Med/Nsg Mngt:  Temperature of the burning agent
 Correct underlying cause  Duration of contact with the agent
 BRONCHODILATOR  Thickness of the skin
 Semi-fowler’s position  Types of burns by etiology:
Respiratory Alkalosis a. Thermal Burns
 Results from carbonic acid deficit  Dry heat – flames, hot objects
 Anxiety, high fever, thyrotoxicosis, early salicylate  Moist heat – hot liquids, steam
(aspirin) poisoning, mechanical ventilation b. Chemical Burns – Acids, alkali
 Assessment findings: c. Electrical Burns – Electric current
 high RR d. Radiation Burns – Ionizing radiation e.g., nuclear
 Lightheadedness, numbness & tingling of the fingers energy, radiation therapy
& the toes, circumoral paresthesia’s, sweating, Pathophysiology
panic, dry mouth, convulsions (severe cases) - Immediate initial cause of cell damage is HEAT
 ABG: high pH, low PaCO2 (N to low HCO3) • Coagulation of CHONs in the cells
 Causes: • Tissue liquefaction
 EXCESSIVE release of Carbon dioxide in the • Electrical burn: internal damage (cardiac
LUNGS dysrhythmias, CNS complications)
 Hyperventilation - Serious burns cause various neuro-endocrine changes
 Manifestations: within the 1st 24hr
 Lightheadedness (vasoconstriction) - ACTH & ADH (released in response to hypovolemia)
 Numbness and tingling (hypocalcemia) • Mineralocorticoid (aldosterone) = Na+ retention,
 Dx: ABG analysis peripheral edema, oliguria
 Med/Nsg Mngt: • Glucocorticoids = causes hyperglycemia
 Correct underlying cause - Client eventually enters hypermetabolic state to
 BROWN BAG compensate for the accelerated tissue catabolism
 Slow breathing (increased O2 & nutrition demand)
 Purse-lip breathing - Intravascular fluid deficit:
ABG Interpretation • After a burn, fluid from the body moves toward the
1. Interpret all burned area = edema at the burn site
2. What is the problem of the pH? • Fluid lost (water vapor & seepage)
3. Who has the same problem as the pH? - Affects fluid & electrolyte status: Fluid shifting,
Level of compensation: electrolyte deficit, loss of extracellular CHONs
a. Fully compensated: pH (NORMALIZED) - Anemia (RBC destruction)
b. Partially compensated: CO2 and HCO3 adjusts but
- Extent of burn injury
body cells & organs
- Risk for Mortality: 90%
• 60y/o
• 40% of TBSA
• presence of inhalation injury
1) Superficial-thickness wounds
 epidermis is the only part injured;
 desquamation occurs for 2-3 days after the burn &
heals in 3-5 days without a scar or complications
e.g., sunburn, short (flash) exposure to a high
intensity heat
2) Partial-thickness wound
 entire epidermis & varying depths of the dermis
 2 types:
a. Superficial partial-thickness wound
 There is involvement of the upper 3rd of the dermis
 leaving a good blood supply; wounds are red, moist
& blanch (whiten) when pressure is applied
 Blister formation (leakage of large amount of plasma
from the injured small vessels lifting off the
destroyed epidermis)
 Intense pain due to exposed nerve endings especially
when stimulated by touch & temperature changes with
standard care,
 heals in 10-21 days with no scar, but some minor
pigment changes may occur
b. Deep partial-thickness wound
 wounds that extend deeper into the skin, dermis and
fewer healthy cells remain; wounds are red & dry
with white areas in deeper parts due to ischemia,
hypoxia & even infection it can progress to full-
thickness wounds
 No Blister formation because dead tissue layer is so
thick & sticks
 Lesser degree of pain (more nerve endings have
been destroyed), moderate edema is present
 generally heals in 3-6 weeks with scar formation
5) Full-thickness wound
 destruction of the entire epidermis & dermis, leaving
 no residual epidermal cells to repopulate; wound
may be waxy, white, deep red, yellow, brown or
black, hard, dry, leathery eschar (burn crust)
 Eschar is a dead tissue; it must slough off or be
removed from the burn wound before healing can
occur avascular, no sensation,
 healing can take from weeks to months depending
on the establishment of a good blood supply to the
injured areas
6) Deep full-thickness wound
 wounds that extend beyond the skin into underlying
fascia & tissuesdamages the muscle, bone, and
tendons & leave them exposed
 wound is blackened and depressed, and sensation is
completely absent
How big an area of the body is involved % of burn
injury
 Rule of Nines
 Special charts & graph (Berkow Method)
 Palm method
Quick initial method
 Disadvantage: overestimation
 more accurate for evaluating the size of the injury
 uses a diagram of the body divided into sections,
with the representative % of TBSA for all ages
 most practical method employed in patients with
 scattered burns
 the size of the palm of the PATIENT (not the
examiner’s) is approximately 1% of the TBSA
Assessment Findings
 Skin color: light pink to black (depth)
 Edema or blistering
 Pain in all areas (except full thickness burn)
 Hypotension, tachycardia, oliguria or anuria
(hypovolemic shock)
 Breathing may be compromised (inhalation injury)
 Sore throat, singed nasal hairs, eyebrows, eyelashes,
 hoarseness, carbon in sputum, shortness of breath,
stridor
 Entrance & exit wounds (electrical burns
Medical management
 Outcome depends on the initial 1st aid provided and
the subsequent treatment in the hospital or burn
center
 Life threatening:
 inhalation injury
 hypovolemic shock
 infection
 Initial 1st Aid
 Prevent further injury (at the scene of the fire)
 Observed closely for respiratory difficulty
(inhalation injury) during transport
 O2 is administered, IV fluid
Acute Care
 Quick assessment (extent of burn injury, additional
trauma – fractures, head injuries, lacerations)
 Maintain adequate ventilation
 Bronchoscopy (assess internal airway)
 Warmed humidified O2
 ET should be available for insertion
 Eschar (a hard leathery crust of dehydrated skin) in
the neck area = tracheostomy
 Mechanical ventilation
 Hyperbaric O2 treatment (100% O2 3x greater than
atmospheric pressure in a specifically designed
chamber)
 Initiating fluid resuscitation
 Goal:
 Restore IVF, Prevention of tissue & cellular
ischemia, maintenance of vital organ function
 UO: 0.3-0.5 ml/kg/hr = SUCCESFUL!!! separated circulation if tightly
 Fluid-replacement regimen is calculated from the • Reduces pain during applied
time the burn injury occurred position changes
 Lactated Ringers: alkalinizing sol’n; Na+, Cl-, K+
 , Ca++ plus Lactate w/c is converted to HCO3 in the Antimicrobial therapy
Liver (met. acidosis)  Silver sulfadiazine (Silvadene) 1% ointment
 management of extensive burns may require  Mafenide (Sulfamylon)
placement of a large-bore central venous catheter so  Silver nitrate (AgNO3) 0.5% solution
that massive fluid loads can be given  Acticoat (contains a thin, soluble film coat of silver)
 peripheral lines are less useful because they become  Povidone-iodine (Betadine)
dislodge or fluid flow is cut off when massive  Gentamicin (Garamycin) 0.1% cream
peripheral edema compresses the IV catheter  Nitrofurazone (Furacin)
 Pain  Mupirocin (Bactroban)
 Morphine is generally the DOC  Clotrimazole (Lotrimin)
 Severe: 50 mg/hr  Ciclopirox (Loprox)
 If respiratory depression occurs: naloxone (Narcan) Surgical Management
 Tetanus immunization is also administered Debridement
Wound management  Removal of necrotic tissue
 Wear powder-free sterile gloves  four ways:
 Body hair around the perimeter of the burns is 1. Natural (tissue sloughs away)
shaved 2. Mechanical (tissue adheres to dressings or detached
 Blisters that have ruptured are removed with scissors 3. during cleansing)
 Clean the burned areas to remove debris 4. Enzymatic (application of topical enzymes)
 Open method – Wound is left uncovered 5. Surgical (use of forceps & scissors)
 Closed method – Wound is covered Skin grafting
Open method (Exposure method)  Necessary for deep partial-thickness & full-thickness
- Abandoned already (except in face & perineum) burns
Advantages Disadvantages  Purpose:
• Reduces laborintensive • Contributes to wound  Lessen the potential for infection
care desiccation (dryness)  Minimize fluid loss by evaporation
• Causes less pain • Promotes loss of water  Hasten recovery
during wound care and body heat  Reduced scarring
• Facilitates inspection • Exposes wound to  Prevent loss of function
• Decreases expense pathogens  Sources for skin graft:
• Contributes to pain a. Autograft (client’s own skin)
during repositioning b. Allograft or homograft (from a human cadaver)
• Compromises modesty  Temporarily covers large areas of tissue(sloughaway
approx 1 week)
Closed method (Exposure method)  Short supply; it could be a source of other pathogen
- Covered first with non adherent & absorbent dressings c. Heterograft or xenograft (from animals)
(gauze impregnated w/ petroleum jelly or ointment-  Temporary
based antimicrobials)  Rejected in days to weeks & must be removed &
- Occlusive or semi occlusive dressing made of replaced at that time
polyvinyl, polyethylene, polyurethane & hydrocolloid  Types of Autografts
materials as final dressing a. Split-thickness graft
Advantages Disadvantages - Epidermis & a thin layer of dermis are harvested
• Maintains moist wound • Requires more time - Cosmetic appearance is less than desirable, less
• Promotes maintenance • Adds to expense elastic, hair does not grow from their surface
of body temperature • Enhances growth of b. Full-thickness graft
• Decreases cross pathogens beneath - Epidermis, dermis & some subcutaneous tissue
contamination of dressings - Comparable appearance to normal skin
wound • Interferes with wound - Tolerate more stress once they become
• Provides wound assessment permanently attached to the burn wound
debridement during • Causes more blood loss c. Slit/ lace/ expansile graft
dressing removal with removal
• Keeps skin fold • Can interfere with
 Application of a skin substitute Location of Burns
 Biobrane  Head, Neck Face – smoke inhalation, respiratory
 (nylon silicone membrane coated with a protein obstruction, cosmetic problem.
derived from pig tissue)  Ears – decrease blood supply – increase infections.
 contains a gelatin that interacts with clotting factors  Hands and feet – abundant blood and nerve supply
in the wound. nerve supply blood volume and contractures severe
 causes the dressing to adhere better, forming a more limit.
durable protective layer.  Joints - deformities; decrease ROM
 Process of application  Genitalia – urethral stricture decrease sensitivity
a. Identify appropriate wound  Circumferential burns of chest – restriction of
b. Remove the sterile biobrane sheet from package breathing
c. Cut to fit and apply under a moderate stretch, Other Injuries Incurred With Burns
Attached product to surrounding unburned skin with  Fractures
steri-strips  Major Soft Tissue Damage
d. When healed biobrane turns whitish and dry in  Respiratory distress Critical
appearance Gently peel off then that wound with  Increase ICP – cerebral damage
moisturizer If small area still open, treat with Pre-existing Medical-Surgical Conditions
bacitracin or Neosporin (triple mix).  DM
 TranCyte  CAD
 from cultured human fibroblasts from the  COPD
dermis with a biosynthetic semipermeable  CRF
membrane attached to nylon mesh  Buerger’s (P.V.D.)
 stored and sealed in a cassette with two pieces per Classification of Severity
cassette. Product is thawed just prior to use.  Critical Burns
Application of cultured skin  Partial thickness burns > 25-30% T.S.B.A.
 Growing the client’s own skin cells in a laboratory  Full thickness burns > 10% T.S.B.A.
culture medium  Burns complicated by:
 Postage stamp-sized skin entire body (3weeks) a. Respiratory distress
 Disadvantage: pigmentation does not perfectly b. Fractures
match the original skin c. Major soft tissue damage
Nursing management  Cerebral confusions – increase ICP
 Focus: assessing the wound & how the burn injury  Spleen, kidney, liver damage
has affected the client’s status  Bleeding
 Calculates fluid-replacement requirements & infuses  All electrical burns
the prescribed volume according to agency’s  Moderate Burns
protocol  P.T.B. > 15%, < 25-30% T.S.B.A.
 Quickly recognized & efficiently treats signs of  F.T.B. > 2%, 10% T.S.B.A. provided that face, feet,
shock hands, neck and genitalia are NOT INVOLVED.
 Administer prescribed analgesics  Minor Burns
 Wound care  P.T.B. < 15% T.S.B.A.
 Helps the client & family to cope with the change in  F.T.B. < 2% T.S.B.A.
body image  Need no Hospitalization and IVF replacement
 Health teaching (pressure garments, skin care, etc…) treated on an O.P. basis
Criteria for nursing assessment: Stage I (Acute/ Emergent/ Hypovolemic/ Oliguric
Total Surface of Burned Area (T.S.B.A.) Phase)
 Determines extent of damage
 Uses assessment guides such as: Rule of Nine’s and
Lund and Browder Chart
 RULE of NINE’s:
• Head and Neck = 9%
• Upper extremities = 9% each arm (total-18%)
• Lower extremities = 18% each leg (total-36%)
• Anterior Trunk = 18%
• Posterior trunk = 18%
• Genitalia = 1%
• TOTAL = 100%
 Stage II (Recovery Phase)
Stage III (Rehabilitation/ Healing Phase
Parkland (Baxter) Formula
 Plain Crystallains: LR, plain 4 ml/kg./1% T.S.B.A.
Ó Alteration in C.O.; Deficit Potential
 Example: 50% T.S.B.A./60 kg B. weight
 60 kg x 4 ml x 50 = 1,200 cc in 1st 24 hours
Brooke Formula & Old:
 0.5 ml/kg B.W./ 1% TSBA (colloids)
 1.5 ml/kg B.w./1% TSBA (crystalloid) 2000 cc of
D5W
 Revised: (’79): 2-3 ml of crystalloids/kg B.W. / 1%
TSBA &
 Ex: 50% TSBA; 60 kg B.W.
 60 x 1.5 x 50 = 4,500 cc = plain LR
 2,000 cc = D5W
 6,500 cc = totals fluids
 60 x 0.5 x 50 = 1,500 colloids
Monafo
 Hypertonic Na+ = 250 mEq/L lactate = 150 mEq/L
CI = 100 mEq/L
 Evan’s Formula:
 1.5 ml/kg body weight/1% TSBA
 0.5 ml/kg body weight/ 1% TSBA (colloids)
Nursing Care in Burns
Nursing Diagnostic #1: Potential for Actual:
 Ineffective airway clearance related to smoke
inhalation.
 Impaired breathing pattern.
 Gas exchange impaired.
 Goal #1: Maintain adequate Airway and Ventilation
 Action #1: Assess
• SIS of airway obstruction related to smoke inhalation.
• History of BURNS of face, neck, head, burned eyelids,
lashes. < Soot in nasal passageway and sputum <
Singed nasal hair.
• History of BURNS in an enclosed space
• Hoarseness, stridor, stertorous respiratory. < History
of BURNS in an upright position
o SIS of C.O. poisoning
o History of BURNS in an enclosed space especially
in new buildings.
o Cherry pink skin with SIS of hypoxia
o SIS of pulmonary edema
1) BP, HR, RR, blood tinged sputum
2) Suction off oropharyngeally PRN.
3) Assist with insertion of tracheal intubation
4) O2 inhalation-nasal cannula 6-7 L/min/humidi
5) Assisted ventilation if which SIS of respiratory
insufficiency PO2 - ¯50; PCO2 – 50
6) Assist inserting central lines early before pulmonary
edema set in.
Nursing Diagnostic #2: Alteration in Comfort; Pain
- Goal # 2: Relief of Pain Actions:
1) Assess: Pain
2) Administer narcotic analgesics as ordered morphine
SO4 – given if sedation is needed; caution for ¯ RR –
Frequently for respiratory depression
Nursing Diagnostic #3: Alteration in Fluid Volume
Deficit:
- Goal #3: Maintain Adequate Fluid Balance (1st 48o)
- Actions 1: Assess: SIS of Hypovolemia
• VIS; BP, HR, RR
• hyponatremia
• EKG monitor
• Hyperkalemia
• CVP, PCWP, C.O.
• hemodynamic change
• Urine output
• urine Sp. Gr.: HCT, weight
• I&Q, weight, HCT: adequate of fluid replacement,
L.O.C., Hematuria
• Urea, U.A., Cr: Nitrogenous Prod.
- Assist with NF replacement via a venous cutdown (if
20%
of an adult’s body surface is involved)
• LR, plain of DSLR – for fluid replacement and
electrolyte balance – NA+, CI-, & H2O volume.
• D5W – for replacement of insensible H2O less.
• Colloids or Dextran and other plasma expanders to
maintain C.O.P.
• Use of the broke formula: 1.5 ml/kg. B.W./1% TSBA;5
ml/kg B.W./1% TSBA
Nursing Diagnostic #4: Alteration in Nutrition: Body
Regular
- Goal #4: Maintain Adequate Nutrition Actions:
1) NPO 1st 48o or until GIT peristalsis returns; ü SIS of
paralytic ileus.
2) Thirst by moistened gauze; frequent oral hygiene
allow nursing of mouth.
3) Osteorized feedings with NGT until client tolerate
feedings by mouth. CHON, chloric diet supplemental
between meal high protein feedings (to cal./kg B.W.
and 2-3 gm CHON).
4) When allowed p.o., small frequency feedings, vitamin
B.C. assist with p.o. feedings – near sitting position.
5) Dressing to be done before mealtimes.
Nursing Diagnostic#5: Self-Care Deficit: Potential for
Infection (most common complication)
- Goal #5: Prevent and Control Infections Action:
1) Reverse isolation (isolation tent, (+) air pressure units,
air circulatory system). $ Pushes out used air and
keep a constant flow of flesh air into the room.
2) Cleanliness.
3) Proper handwashing.
4) Wound skin precautions for skin infections.
5) Diagnose infections early:
• > 100,000 colony count (usual in full thickness
burns)
• strep., staph., prateus aeruginosa, proteus
vulgaris
GM (-) Infections
• Gradual or sudden ¯in temperature
• Leukopenia hypothermia, rapid wound deterioration
• Petechiae, eechymosis, oozing
GM (+) Infections
• Temperature
• RR, PR
• Disorientation
• Management: Antibiotics, massive doses topical
antibacterial IVF’s, BT’s
Care of the BURN wound
- Cleanse with sterile NSS or distilled H2O. Debride
detached epithelium. - Use sterile technique.
- Methods:
• Open (exposure) method – used in burns of face, neck,
trunk, limbs, back, perineum.
o Clean eschar
o Apply antibacterials protect from drafts
o Sterile sheets
o Use bedcradles to protect from bedclothes
o Use of circolectric bed or stryker frame
• Semi-open – cleanse, debride, thin layer of dressing
used – Anti-microbials
• Closed – use of sterile gauze after application of
antimicrobials.
o Frequent change of dressing
o Cleanse/soften eschars by hydrotherapy and wet
soars (Husband and Whirlpool Batio)
Cover BURN wound: Graft
- Goal – close burn would prevent infection and fluid
loss
restore appearance and function.
- Types – temporary/permanent.
- Kinds
• Homograft (Allograft) – graft between genetically
disseminated members of same species.
o For temporary covering of the extensive burns
until patients own skin is avail for grafting.
o Performed early (2-3 days post-BURN)
o REJECTION may be expected 2-3 weeks after graft.
o Sources: cadaver amniotic membrane.
• HETEROGRAFT (Xenograft) – grafts between from
synthetic skin. – Sources – pigskin synthetic grafts
(Tefron, Nylon, Velour)
• ISOGRAFT – grafts between indentical or
histocompatible antrogens. Example: IDEN.TWIN
• AUTOGRAFT – graft from same person
o Full thickness grafts – 0.035” thickness or .
o Split thickness grafts – 0.015”- 0.30” thickness
o Types of full thickness grafts
a) Pedicle graft – blood supply from pedicle
attached to original site.
b) Free graft – blood supply from granulation
tissue.
Nursing care
• Use of heat lamps to facilitate healing 15” from donor
site.
– Use of scarlet red – bacterio static agent used for
covering donor sites; dries and trimmed daily.
• Elevate site to prevent edema (Donor site heals 7-10
days)
Ice bags for comfort and bleeding pressure bandage may
be used to prevent edema.
• Protect from: M – otion, T – rauma, I – nfection
• Bactericidal agents: Metabolic acidosis, Sulfamylon
(Matenide Acetate), Nitrofurantoin
• Hydrotherapy Silver Sulfadiazen’s
RENAL DISORDERS
Anatomy and physiology
A) Kidney
- The two bean-shaped kidneys are located
retroperitoneally (behind the Peritoneum) and lateral
to the thoracic lumbar area.
- Each kidney is surrounded by a thin, fibrous capsule
(Bowman’s capsule). Inside the capsule the kidney is
divided into three parts: the cortex, the medulla, and
the renal pelvis.
- Blood is supplied teach kidney through the renal
artery, which enters the kidney at the hilus.
- receive approximately through the renal
cardiac output. Blood leaves each kidney through the
renal vein.
- The nephrous, the functional units of the kidneys, are
the sites of urine production. Each kidney contains
more than one (1) m million nephrons. Each nephron
is composed of a glomerulus (a network of capillaries)
and a tubular system (which consist of proximal
tubule, loop of Henle, and distal tubule). Urine is
formed in the nephrons by a combination of three
processes: filtration, reabsorption, and secretion.
• Filtration: Filtration-refers to the passage of blood
through the filtering membrane of the glomerulus
as a result of pressure differential. The fluid that
passes through the membrane consist of water,
electrolytes and other small molecules and is
referred to as the ultrafiltrate. The rate of
glomerular filtration is referred to as the
glomerular filtration rate (GFR); the normal GFR
for an average-sized adult male is 125 ml. Per
minute.
• Reabsorption: Essential materials (e.g., glucose,
and description, amino acids, Sodium, water) are
reabsorbed from the tubules into the capillaries
through the processes of diffusion, osmosis, and
active transport. (See pages 15-16 for description
of these processes).
• Secretion: Certain substances (potassium, creatinine,
and hydrogen) are actively transported from the blood
into the tubules. Urine that is formed in the nephrons
consists of nonessential materials and secretions
(water, phosphates and sulfates. For every 125 ml. Of
ultrafiltrate, approximately 1 ml. is excreted as urine.
The remaining 124 ml. is reabsorbed. Fluids and
electrolyte balance in the b body is maintained by a
negative feedback system between the nephrons and
the body’s fluids and tissues. The diluting and
concentrating mechanisms of the nephrons that
regulate the body’s fluid volumes are controlled
primarily by two hormones: antidiuretic hormone
(ADH), which id produced by the pituitary gland and is
involved in water reabsorption, and aldosterone,
which is produced by the adrenal cortex and is
involved in sodium reabsorption and potassium
secretion. In addition the kidney is involved in
regulation of the body’s acid-base balance and
several metabolic and endocrine functions; e.g.,
secretion of erythropoietin (which stimulates RBC
production by the bone marrow), metabolism of
vitamin D, and secretion of renin (which as a result of
its effect on angiotensin, is involved in the regulation
of blood pressure).
B) Ureters
- The ureters are the tubes that transport urine from the
renal pelvis of The kidneys to the bladder. Transport
urine is accomplished through peristaltic action.
C) Bladder
- The bladder is made of muscular elastic tissue it act
as a temporary reservoir for urine until it is excreted
from the body. Two muscles control the opening of
the bladder into the urethra: The internal sphincter is
under automatic (involuntary) nervous system control.
The external sphincter is under central (voluntary)
nervous system control. The normal capacity of the
adult is 300-500 ml.
General assessment of the renal system
• Medical History
- Disease related to renal problems (. e.g., hypertension,
Diabetes mellitus, gout, cystitis, renal calculi, kidney
infections); medications that affect renal functioning (.
e.g., phenacetin, anticoagulants, diuretics, exposure
to nephrotoxic chemicals (carbon tetrachloride,
phenol, ethylene glycol); diet and fluid intake; general
activity level.
• Family History
- Congenital urinary tract abnormalities; polycystic
renal disease; Urinary tract infection; urinary calculi;
hypertension, diabetes mellitus, gout.
• Signs and Symptoms
- General signs and symptoms associated with renal
diseases include; fatigue, headache blurred, vision
anorexia, nausea, vomiting, Abdominal discomfort,
increased blood pressure, excessive thirst, itching,
chills edema, and weight gain.
• Urinary signs and Symptoms include:
1) Pain: dyssuria, tenesmus, pain in the costovertebral
angle, groin, flank, etc
2) Changes in the urinary output (volume oliguria,
anuria,
and polyuria
3) Changes in the urinary patterns: frequency. Urgency,
burning on urination Nocturia, incontinence, enuresis
4) Changes in urinary consistency and color hematuria
albuminuria
Physical examination
Inspection
1) Skin: pallor, yellow-brown or yellow green cast:
bruises
urate crystals, pruritus
2) Mouth: Stomatitis: urinous breath odor
3) Face: Abdomen, extremities: General edema
Palpation
- Kidney and bladder not usually palpable if normal
sized
Percussion
- Tenderness over the costovertebral angle
Diagnostic Examination: Urine Exam
• Routine Urinalysis: Screening test for urinary system
pathology. Macroscopic exam. Assess color, clarity,
odor specific gravity (normal = 1.025-1.030), pH
(normal = 4.5-8.0), and presence of protein, glucose and
ketones (normal = 0). Microscopic exam. Assesses
RBC's WBC’s casts, crystals, and bacteria. Nursing
Responsibilities: Obtain first voided a.m. specimen; have
specimen examined with in 1 hour of collection; instruct
patient not to let collection out cup touch his/her body.
• Urine Culture (Clean-catch midstream Specimen)
Detects presence of urinary tract infections. Infection
suggested by presence of>10,000-organisms/ mm.
Nursing Responsibilities: Use sterile container and
instruct patient on clean-catch procedure (cleanse glands
perineal area
begins voiding into toilet or bed pans; stop urination &
then continue voiding into container).
• Creatinine Clearance: Estimate rate of glomerular
filtration by measuring volume of blood cleared of
creartinine in 1 min. Normal =85-135 ml/min. Nursing
Responsibilities: 24 hour urine specimen (discard first
sample of 24 hour period; collect all urine voided for 24
hours; add chemical preservative or refrigerate
specimen; have patient void at end of 24 hour period &
include this specimen); draw one sample of blood during
the 24 hour period.
• Concentration Test: evaluates renal concentration
ability. Normal specific gravity =1.020-1.035. Nursing
responsibilities: NPO after evening meal on night before
test to obtain 3 urine early-morning specimens collected
at specified intervals.
• Residual Urine: Determine amount of urine left in
bladder after voiding. Normal = 50 ml. Or less. Nursing
Responsibilities: Catheterize patient immediately after
he/she voids.
• Phenolsulfophthalein Excretion Test: (PSP): PSP (a red
dye) administered IV to assess renal plasma flow and
evaluate tubular functioning. Nursing Responsibilities:
Encourage fluids 1 hour before and during test to
maintain urine flow; warm patient that urine will be red;
have patient void before injection of PSP; record time
dye is administered; collect urine in 15 min., 30 min. and
1 hour; label each specimen and include collection time.
• Blood Urea Nitrogen: (BUN) assesses concentration of
urea in the blood (blood level of urea is regulated by rate
at which kidney excrete urea). Normal = 20-30 mg/dl.
Nursing Responsibilities: Explain tests and observes
injection site for bleeding.
• Serum Creatinine: Assesses renal glomerular filtration.
Normal = 0.5-1.5 mg/dl. Nursing Responsibilities: See
BUN.
• KUB: (kidney ureters bladder): X-ray film of lower
abdomen permits assessment of size, shape and position
of these organs and presence of abnormalities. Nursing
Responsibilities: Bowel preparation as ordered.
• Intravenous Pyelogram: (IVP)/Excretory Urogram: IV
Injection of radiopaque dye (Hypaquerenografin) that
concentrates in the urine & X-ray visualization of injury
tract. Nursing Responsibilities: Explain procedure &
obtain consent; cathartic enema & laxatives evening
prior to test; NPO 8 hour prior to procedure unless
contraindicated; assesses for allergies to iodine.
Following procedure, force fluids to flush dye unless
contraindicated; observe for adverse reaction to dye &
have emergency equipment& drug a available
(epinephrine, corticosteroid, vasopressors); assess for
renal failure observe forhematomas at injection site.
• Retrograde Pyelogram: Injection of contrast medium
via catheter passed through cystoscope and Xray
visualization of drainage structures. Nursing
Responsibilities: explain test and obtain consent; NPO 7
hour prior to test if general anesthesia is to be used;
administered pre-medication as ordered, following test,
maintain catheters and monitor urinary output; observe
for gross hematura.
• Renal Asngiography/Arteriography: Catheter threaten
though femoral artery into aorta or renal artery; contrast
medium injected; X-rays permits visualization of renal
arterial supply. Nursing Responsibilities: Explain
procedure & obtain consent; assess for allergies to
iodine; NPO 8 hour before test; shave injection site;
administer sedative or analgesic; tell patient he/she will
feel heat when dye in injected. Following procedure,
keep patient flat on bed 8-12 hours; monitor vital signs
until stable; check peripheral pulse in legs to detect
occluded blood injection or hematoma; pressure dressing
over puncture site immediately after catheter removed;
apply cold compress to relieve pain & edema
• Cystourethrography: Injection of contrast medium via
urethral catheter, an X-ray visualization of size and
shape of urethra and bladder. Voiding
Cystourethrography:fluoroscopic films while patient
voids.Nursing Responsibilities: Explain procedure and
obtain consent; assess for iodine allergies; administer
sedative voiding; observe for hematuria; encourage
fluids; observe for reaction to dye.
Radioisotope Studies
- Renogram: IV injection of radioisotopes; seize and
shape of kidneys recorded via gamma scintillation
camera; lesions appear as “cold” spots. Nursing
Responsibilities: Explain procedure and obtain consent;
following procedure, observe for hypersensitivity
reaction.
Cystoscopy
- Direct visualization of urethra and bladder by names of
fiberroptic scope. Also used to obtain urine specimen,
biopsy, and to remove calculi. Nursing Responsibilities:
Explain procedure and obtain consent; NPO if general
anesthesia used; 1-2 glass of water prior to test;
administer sedative as ordered. Following procedure;
relieve pain and moist heat to lower body, sits bath and
analgesic as ordered; observe; observe for urinary
retention, hematuria signs of perforation or hemorrhage;
encourage fluids
Ultrasonography
- Ultrasound waves projected into abdomen, waves
reflected back displayed on scilloscope. Noninvasive
technique
Renal Biopsy
- Needle biopsy of kidney via percutaneous needle
biopsy through renal tissue or open biopsy through small
flank incision. Nursing Responsibilities: Explain
procedure & obtain consent assist with coagulation &
other studies; fasting regimen 6-8 hours before biopsy;
establish IV line; skin preparation; instruct patient to
hold his/her breath when needle is inserted; administer
mild sedative as ordered; have patient avoid just before
procedure. Following procedure, apply pressure dressing
to biopsy site; position patient in prone position to
minimize bleeding for 12 hours; observe for signs of
hemorrhage;monitor vital signs; encourage fliuds; advise
patient to avoid strenous activity for 2 weks following
procedure.
Pyelonephritis
- Acute or chronic bacterial infection of the kidney and
the lining of the collecting system (kidney pelvis)
- Acute pyelonephritis
• Moderate to severe symptoms that usually last 1-2
weeks
chronic pyelonephritis
- Pathophysiology:
• Bacteria ascend to the kidney and kidney pelvis by
way of the bladder and urethra
• E. coli (85%), K. pneumoniae, P. mirabilis, Strep.
Fecalis, P aeruginosa, S. aureus
• Inflammation (kidneys grossly enlarge)
- Risk factors:
• Instrumentation of the urethra & bladder
(catheterization, cystoscopy, urologic surgery)
• Inability to empty the bladder, Pregnancy
• Urinary stasis, Urinary obstruction (tumors, strictures,
calculi, prostatic hypertrophy)
• DM, other renal disease (polycystic kidney disease),
neurogenic bladder (stroke, multiple sclerosis, spinal
cord injury)
• Women with increased sexual activity, failure to void
after intercourse, history of recent UTI, infection with
HIV
- Signs & symptoms:
• Flank pain & tenderness
• Chills
• Fever
• Malaise
• Urinary frequency with burning sensation (bladder
infection)
• Some are asymptomatic (chronic)
• Polyuria & nocturia (when tubules of the nephrons fail
to reabsorb water efficiently)
- Diagnostic findings:
• Urinalysis – PYURIA
• Urine culture – identifies the causative organism
• Ultrasound, CT scan – determines obstruction in the
urinary tract
• Cystoscopy, IV pyelogram (not done in acute cases)
or retrograde pyelogram – demonstrate obstruction or
damage to structures of the urinary tract
• KUB x-ray – reveal calculi, cysts, tumors
– impaired renal function
- Medical Management:
• Relieving fever & pain
• Antimicrobial drugs
o Trimethoprim-sulfamethoxazole (TMP-SMZ,
Septra), Gentamicin w/ or w/out ampicillin,
Cephalosporin, Ciprofloxacin
• Antispasmodics & anticholinergics
o relax smooth muscles of the ureters & bladder,
promote comfort & increase bladder capacity
o Oxybutynin (Ditropan), propantheline (ProBanthine)
- Nursing Management:
• Obtain complete medical, drug & allergy histories
• Assess VS (T°, BP)
• Physical exam: determine the location of discomfort &
any signs of fluid retention (peripheral edema,
shortness of breath)
• Observe & document the characteristics of the
client’s urine
• Encourage liberal fluid intake if not contraindicated
(3-4L)
• Administer prescribed medications
- Nursing Management:
• Evaluates laboratory test results
o BUN, Creatinine, serum electrolytes, urine culture
to determine client response to therapy
• Provide health teaching:
o Provide information about the disease
o Medications
o Increase fluid intake
o Acid forming diet (meat, fish, poultry, eggs, corn,
cranberries, prunes) – to prevent Ca++ & MgPO4
stone formation
Glomerulonephritis
- Occurs most frequently in children (boys 6-7y/o) &
young adults
- Most client recover spontaneously or with minimal
therapy without sequelae
- Some develop chronic glomerulonephritis
- Pathophysiology:
• Most believe that the inflammatory response is from
Antigen-Antibody stimulation in the glomerular
capillary membrane
- Signs & symptoms:
• 50% are asymptomatic
• Sudden onset with pronounced symptoms
• Fever, nausea, malaise, headache, generalized
edema, periorbital edema, puffiness around the eyes
• Pain or tenderness over the kidney area
• Mild to moderate hypertension
• Poor appetite, irritability, shortness of breath
• Hematuria, convulsions (due to hypertension), CHF,
oliguria (UO 100-400ml/day), anuria (<100 ml/24hr)
- Medical Management: No specific treatment exist:
guided by the symptoms & the underlying abnormality.
• Bed rest
• Na+ - restricted diet (edema, HPN) Diuretics,
antihypertensive drugs
• Antimicrobials (penicillin)
• Vitamins to improve general resistance
• Oral iron supplements (anemia)
• Corticosteroids & immunosuppressive agents o Pain is tolerable if the stone is 5mm or less in
- Nursing Management: diameter and moving
• Monitor VS (BP q4°), collects daily urine specimens to o Vigorous hydration
evaluate client response to treatment o Analgesics (opioids and NSAIDs)
o Antimicrobials
• Ensure adequate fluid intake & measure I&O • Larger calculi
• Diet: Na & CHON restricted; adequate CHO intake o ESWL (extracorporeal shock wave lithotripsy)
(prevents catabolism of body CHON stores) o Laser lithotripsy
• Provide health teaching - Surgical Management:
Nephrotic Syndrome • Indicated for large or complicated by obstruction,
- A condition of increased glomerular permeability that ongoing UTI, kidney damage or constant bleeding
allows larger molecules to pass through the membrane o Percutaneous nephrolithotomy
into the urine and be removed from the blood o Ureterolithotomy
- Most common cause: Immune or inflammatory process o Pyelolithotomy
- Treatment: depends on the cause o nephrolithotomy
• Immunologic – steroids o Nursing Process
• ACE inhibitors – decreases proteinuria - Assessment:
• Cholesterol-lowering drugs • History
• Heparin – lower proteinuria & renal insufficiency • Pain intensity & location, N&V
• GFR is normal – complete CHON diet • Vital signs
• GFR is decreased – low CHON diet • Urine (strain)
• Mild diuretics & Na restriction – edema & HPN - Diagnosis, Planning, Interventions
• Assess hydration: vascular dehydration - 3 main goals
Urolithiasis • Improve urinary output
- Presence of calculus/calculi (stone) in the urinary tract • Relive pain
• Nephrolithiasis (kidney) • Prevent infection
• Ureterolithiasis (ureter) Renal Failure
- Predisposing factors: - Inability of the nephrons in the kidneys to maintain
• Calciuria, hyperparathyroidism, calcium-based F&E,
antacids, excessive vit.D intake Acid-Base balance, excrete nitrogen waste products &
• Dehydration perform regulatory function
• UTI esp. if cause by P. mirabilis (makes urine alkaline - 2 types:
& Ca++ ppt.) • ACUTE renal failure
• Obstructive d/o (enlarged prostate) - sudden, rapid decrease in renal function
• Gout (UA crystallizes) - Reversible with early, aggressive treatment
• Osteoporosis • CHRONIC renal failure
• Prolonged immobility (sluggish emptying of urine) - Progressive (months to years) & irreversible
- Signs & Symptoms: damage to the nephrons
• Sudden, sharp, severe flank PAIN that travels to the Acute Renal Failure
suprapubic region & external genitalia (Renal colic, - Causes: Prerenal, Intrarenal, Postrenal
painful spasm) - Prerenal
• Severity of pain causes nausea, vomiting, shock • Hypovolemic shock
• Chills, fever, hypotension (if infection develops) • Cardiogenic shock 2° to CHF
• Urinary retention, dysuria (obstruction) • Septic shock
- Diagnostic findings: • Anaphylaxis
• Urinalysis • Dehydration
o Gross or microscopic hematuria • Renal artery thrombosis or stenosis
o pH conducive to stone formation • Cardiac arrest
• Lethal dysrhythmias
- Intrarerenal
• Radiography (KUB) • Ischemia
• IVP • Nephrotoxicity 2° to drugs (aminoglycosides)
• Ultrasonography • Acute & Chronic glomerulonephritis
- Medical Management: • Polycystic disease
• Small calculi • Untreated pre&post renal disorders
o Passed naturally with no specific interventions - Postrerenal
• Ureteral calculi • Percutaneous renal biopsy shows destruction of
• Prostatic hypertrophy nephrons
• Ureteral stricture • Radiography & ultrasonography demonstrate
• Ureteral or bladder tumor structural defects in the KUB
- Four phases: Initiation phase, Oliguric phase, Diuretic • Renal angiography identifies obstructions in blood
phase, Recovery phase vessels
- Initiation phase - Medical Management
• Begins with the onset of the contributing event • Prevention of ARF is an important consideration
• Risk for dehydration- adequately hydrate the client
• ATN (acute tubular necrosis) Death of cells in the • Treat shock & hypotension as quickly as possible
collecting tubules (replacement of fluids & blood)
- Oliguric phase (less UO) • Treat infection promptly
• Begins within 48hr after the initial cellular insult (10- • Continuous renal function monitoring
14 days or longer) • Dopamine (Intropin), hemodialysis, peritoneal dialysis
• FVE develops (edema, HPN, cardiopulmonary • Diet; low CHON, high calories, low Na, low K
complications) • Kayexalate, IV infusion of insulin & glucose for
• AZOTEMIA (accumulation of urea & nitrogenous hyperkalemia
waste • Na bicarbonate for acid-base imbalance
- Medical management of CRF is similar to that for
death ARF, except the period of treatment is lifelong (unless a
• Low urine SG, hyperkalemia, metabolic acidosis, kidney transplantation is performed)
UREMIA develops - Chronic anemia – Epoetin alfa (Epogen) is
- Diuretic phase: administered
• Diuresis begins as the nephrons recover rather than blood transfusion
- Nursing Management: Excess fluid volume r/t
electrolytes continues to be impaired impaired renal function
• Weight
- Recovery phase • Output
• Normal glomerular filtration & tubular function is • Assess lung sounds, RR, effort, heart sounds, jugular
restored (1 or more years) vein
Chronic Renal Failure • Monitor lab studies
- Kidneys are extensively damaged • Administers prescribed diuretics & anti HPN
- 3 stages; • Prepare client for dialysis
• Reduced renal reserve – 40 to 75% loss of nephrons - Imbalanced nutrition: risk for less than body
function requirements
• Renal insufficiency - 75 to 90%; Kidney loses ability to r/t anorexia
concentrate urine (polyuria, nocturia), anemia • Monitor & record clients dietary intake
develops • Provide frequent small feedings
• ESRD - <10% of nephrons are functional; Regular • Encourage client to be involved with food choices &
course of dialysis is needed or kidney transplantation times for meals
- Assessment findings: • Explains restrictions & provide list of nutritional needs
• Elevated BP, weight gain, UO decreased & acceptable food choices
• Puffy face appearance Nausea & Vomiting
• Pale skin - Nausea – a feeling of discomfort in the epigastrium
• GIT ulceration & bleeding with a conscious desire to vomit; occurs in association
• Vague symptoms (lethargy, headache, anorexia, dry with & prior to vomiting
mouth) - Vomiting – forceful ejection of stomach contents from
• Pruritus, dry, scaly skin the upper GI tract (Emetic center in medulla is
• Urine breath odor, muscle cramps, bone pain or stimulated (e.g., by local irritation of intestine or
tenderness & spontaneous fractures can develop stomach or disturbance of equilibrium), causing the
ures, vomiting reflex)
coma) - Contributing factors:
- Diagnostic findings: • GI disease
• CNS disorders (meningitis, CNS lesions)
• Circulatory problems (CHF)
• IVP – reveals renal dysfunction • Metabolic disorders (uremia)
• Side effects of certain drugs (chemotherapy,
antibiotics)
• Pain
• Psychic trauma
• Response to motion
- Assessment findings
• Weakness, fatigue, pallor, possible lethargy
• Dry mucous membrane and poor skin turgor/ mobility
(if prolonged with dehydration)
• Serum sodium, calcium, potassium decreased
• BUN elevated (if severe vomiting and dehydration)
- Nursing interventions
• Maintain NPO until client able to tolerate oral, intake
• administer medications as ordered and monitor
effects/side effects
• Notify physician if vomiting pattern changes
• Maintain F & E balance
o Administer, IV fluids as ordered, keep accurate
record of l&O
o Record amount/frequency of vomitus
o Assess skin tone/turgor for degree of hydration
o Monitor laboratory/electrolyte values
o Test NG tube drainage or vomitus for blood, bile;
monitor pH
• Provide measures for maximum comfort
o Institute frequent mouth care with tepid
water/saline mouthwashes
o Remove encrustations around nares
o Keep head of bed elevated and avoid sudden
changes in position
o Eliminate noxious stimuli from environment
o Keep emesis basin clean
o Maintain quiet environment and avoid
unnecessary procedures
• When vomiting subsides;
o provide clear fluids (ginger ale, warm tea) in small
amounts
o gradually introduce solid foods (toast, crackers),
o and progress to bland foods (baked potato), in
small amounts
• Provide client teaching and D/C planning concerning
o Avoidance of situations, foods, or liquids that
precipitate nausea and vomiting
o Need for planned, uninterrupted rest periods
o Medication regimen, including side effects
o Signs of dehydration
o Need for daily weights with frequent
anthropometric measurement
Diarrhea
- Increase in peristaltic motility, producing watery or
loosely
formed stools
- Diarrhea is a symptom of other pathologic processes
- Causes:
• Chronic bowel disorders, Malabsorption problems
• Intestinal infections, Biliary tract disorders
• Hyperthyroidism, Saline laxatives
• Magnesium-based antacids
• Stress, Antibiotics, Neoplasms
• Highly seasoned foods
- Assessment findings
• Abdominal cramps/distension, foul-smelling watery
stools, increased peristalsis
• Anorexia, thirst, tenesmus, anxiety
• Decreased potassium and sodium if severe
∗ Diarrhea
- Nursing interventions
• Administer antidiarrheals – diphenoxylate with
atropine (Lomotil), paregoric, loperamide (Imodium),
Kaopectate as ordered; monitor effects.
• Control fluid/food intake – Avoid milk and milk
products, Provide liquids with gradual introduction of
bland, high-protein, high-calorie, low-fat, low-bulk
foods
• Monitor and maintain fluid and electrolyte status;
record number, characteristics, and amount of each
stool.
• Prevent anal excoriation – Cleanse rectal area after
each bowel movement with soap and water and pat
dry; Apply ointment or Desitin to promote healing; Use
a local anesthetic as needed
• Provide client teaching and discharge planning
concerning
o Medication regimen
o Adherence to prescribed diet and avoidance of
foods that are known to produce diarrhea
o Importance of perineal hygiene and care and daily
assessment of skin changes
• Provide client teaching and discharge planning
concerning
o Importance of good handwashing techniques
after each stool
o Need to report worsening of symptoms
stool)
o Need to assess daily weights with frequent
anthropometric measurements
Client with a Urinary Tract Infection (UTI)
- Bacterial infections of urinary tract are a very common
reason to seek health services
- Common in young females and uncommon in males
under age 50
- Common causative organisms
• Escherichia coli (gram-negative enteral bacteria)
causes most community acquired infections
• Staphylococcus saprophyticus, gram-positive
organism causes 10 – 15%
• Catheter-associated UTI’s caused by gram-negative
bacteria: Proteus, Klebsiella, Seratia, Pseudomonas
- Normal mechanisms that maintain sterility of urine
• Adequate urine volume
• Free-flow from kidneys through urinary meatus
• Complete bladder emptying - Longer a catheter is in place, greater risk for infection
• Normal acidity of urine - Bacteria may enter catheter system at connection
• Peristaltic activity of ureters and competent between catheter and drainage system or through
ureterovesical junction emptying tube of drainage bag
• Increased intravesicular pressure preventing reflux - UTI’s may be asymptomatic
• In males, antibacterial effect of zinc in prostatic fluid - Most infections resolve with removal of catheter and
Pathophysiology short
- Pathogens which have colonized urethra, vagina, or course of antibiotic
perineal area enter urinary tract by ascending mucous - Most significant complication is gram-negative
membranes of perineal area into lower urinary tract bacteremia
- Bacteria can ascend from bladder to infect the kidneys 3. Pyelonephritis
- Classifications of infections - Inflammation of renal pelvis and parenchyma
• Lower urinary tract infections: urethritis, prostatitis, (functional
cystitis kidney tissue)
• Upper urinary tract infection: pyelonephritis - Acute pyelonephritis
(inflammation of kidney and renal pelvis) • Results from an infection that ascends to kidney from
Risk Factors lower urinary tract
• Aging • Risk factors
- Increased incidence of diabetes mellitus o Pregnancy
- Increased risk of urinary stasis o Urinary tract obstruction and congenital
- Impaired immune response malformation
• Females: short urethra, having sexual intercourse, use o Urinary tract trauma, scarring
of contraceptives that alter normal bacteria flora of o Renal calculi
vagina and perineal tissues; with age increased incidence o Polycystic or hypertensive renal disease
ofcystocele, rectocele (incomplete emptying) o Chronic diseases, i.e. diabetes mellitus
• Males: prostatic hypertrophy, bacterial prostatitis, anal o Vesicourethral reflux
intercourse - Pathophysiology
• Urinary tract obstruction: tumor or calculi, strictures • Infection spreads from renal pelvis to renal cortex
• Impaired bladder innervation • Kidney grossly edematous; localized abscesses in
• Bowel incontinence cortex surface
• Diabetes mellitus • E. Coli responsible organism for 85% of acute
• Instrumentation of urinary tract pyelonephritis; also Proteus, Klebisella
1. Cystitis - Manifestations
- Most common UTI • Rapid onset with chills and fever
- Remains superficial, involving bladder mucosa, which • Malaise
becomes hyperemic and may hemorrhage • Vomiting
- General manifestations of cystitis • Flank pain
• Dysuria • Costovertebral tenderness
• Frequency and urgency • Urinary frequency, dysuria
• Nocturia - Manifestations in older adults
• Urine has foul odor, cloudy (pyuria), bloody • Change in behavior
(hematuria) • Acute confusion
• Suprapubic pain and tenderness • Incontinence
- Older clients may present with different manifestations • General deterioration in condition
• Nocturia, incontinence - Chronic pyelonephritis
• Confusion • Involves chronic inflammation and scarring of tubules
• Behavioral changes and interstitial tissues of kidney
• Lethargy • Common cause of chronic renal failure
• Anorexia • May develop from chronic hypertension, vascular
• Fever or hypothermia conditions, severe vesicourteteral reflux, obstruction
- Readily responds to treatment of urinary tract
- Untreated, may involve kidneys • Behaviors: Asymptomatic, Mild behaviors: urinary
- Severe or prolonged may cause sloughing of bladder frequency, dysuria, flank pain
mucosa with ulcer formation - Collaborative Care
- Chronic cystitis may lead to bladder stone formation • Eliminate causative agent
2. Catheter-Associated UTI • Prevent relapse
• Correct contributing factors
- Diagnostic Tests
• Urinalysis: assess pyuria, bacteria, blood cells in
urine; Bacterial count >100,000 /ml indicative of
infection
• Rapid tests for bacteria in urine
o Nitrite dipstick (turning pink = presence of
bacteria)
o Leukocyte esterase test (identifies WBC in urine)
• Gram stain of urine: identify by shape and
characteristic (gram positive or negative); obtain by
clean catch urine or catheterization
• Urine culture and sensitivity: identify infecting
organism and most effective antibiotic; culture
requires 24 – 72 hours for results; obtain by clean
catch urine or catheterization
• WBC with differential: leukocytosis and increased
number of neutraphils
- Diagnostic Tests for adults who have recurrent
infections
or persistent bacteriuria
• Intravenous pyelography (IVP) or excretory urography
o Evaluates structure and excretory function of
kidneys, ureters, bladder
o Kidneys clear an intravenously injected contrast
medium that outlines kidneys, ureters, bladder,
and vesicoureteral reflux
o Check for allergy to iodine, seafood, radiologic
contrast medium, hold testing and notify
physician or radiologist
• Voiding cystourethrography: instill contrast medium
into bladder and use xray to assess bladder and
urethra when filled and during voiding
• Cystoscopy
o Direct visualization of urethra and bladder
through cystoscope
o Used for diagnostic, tissue biopsy, interventions
o Client receives local or general anesthesia
• Manual pelvic or prostate examinations to assess
structural changes of genitourinary tract, such as
prostatic enlargement, cystocele, rectocele
- Medications
• Short-course therapy: 3 day course of antibiotics for
uncomplicated lower urinary tract infection; (single
dose associated with recurrent infection)
• 7 – 10 days course of treatment: for pyelonephritis,
urinary tract abnormalities or stones, or history of
previous infection with antibioticresistant infections;
clients with severe illness may need hospitalization
and intravenous antibiotics
• Antibiotics commonly used for short and longer
course therapy include trimethoprimsulfamethoxazole
(TMP-SMZ), or quinolone antibiotic
such as ciprofloxacin (Cipro)
• Intravenous antibiotics used include ciprofloxacin,
gentamycin, ceftriaxone (Rocephin), ampicillin
• Possible outcomes of treatment for UTI, determined
by follow-up urinalysis and culture
o Cure: no pathogens in urine
o Unresolved bacteriuria: pathogens remain
o Persistent bacteriuria or relapse: persistent
source of infection causes repeated infection
after initial cure
o Reinfection: development of new infection with
different pathogen
• Prophylactic antibiotic therapy with TMP-SMZ, TMP
alone or nitrofurantoin (Furadantin, Nitrofan) may be
used with clients who experience frequent
symptomatic UTIs
• Catheter-associated UTI: removal of indwelling
catheter followed by 10 – 14 day course of antibiotic
therapy
- Surgery
• Surgical removal of large calculus from renal pelvis or
cystoscopic removal of bladder calculi which serve as
irritant and source of bacterial colonization; may also
use percutaneous ultrasonic pyelolithotomy or
extracorporeal shock wave lithotripsy (ESWL)
• Ureteroplasty: surgical repair of ureter for stricture or
structural abnormality; reimplantation if
vesicoureteral reflux; clients usually return from
surgery with catheter and ureteral stent in place for 3
–5 days
- Nursing Care: Health promotion to prevent UTI
• Fluid intake 2 – 2.5 L daily, more if hot weather or
strenuous activity is involved
• Empty bladder every 3 – 4 hours
• Females
o Cleanse perineal area from front to back
o Void before and after sexual intercourse
o Maintain integrity of perineal tissues
o Avoid use of commercial feminine hygiene
products or douches
o Wear cotton underwear
• Maintain acidity of urine (use of cranberry juice, take
Vitamin C, avoid excess milk and milk products,
sodium bicarbonate)
- Nursing Diagnoses
• Pain: Additional interventions include warmth,
analgesics, urinary analgesics, antispasmodic
medications
• Impaired Urinary Elimination
• Ineffective Health Maintenance: Clients must
complete full course of antibiotic therapy
- Home Care: Teaching: prevention of infection and use
alternatives to indwelling catheter whenever possible
Client with Urinary Calculi
- Urinary calculi are stones in urinary tract
• Nephrolithiasis: stones form in kidneys
• Urolithiasis: stones form in urinary tract outside
kidneys
- Highest incidence in southern and Midwestern states
- Males more often affected than females (4:1)
- Most common in young and middle adults
Risk factors
- Majority of stones are idiopathic (no demonstrable
cause)
- Prior personal or family history of urinary calculi
- Dehydration: increased urine concentration
- Immobility
- Excess dietary intake of calcium, oxalate, protein
- Gout, hyperparathyroidism, urinary stasis, repeated
UTI infection
Pathophysiology
- Factors leading to lithiasis include supersaturation
(high
concentration of insoluble salt in urine), pH of urine
- Types of calculi
a) Calcium stones (calcium oxalate, calcium phosphate)
- Associated with high concentrations of calcium in
blood or urine\
- Genetic link
b) Uric acid stones
- Associated with high concentration of uric acid in
urine
- Genetic link
- More common in males
- Associated with gout
c) Struvite stones
- Associated with UTI caused by bacteria Proteus
- Stones are very large
- Staghorn stones in renal pelvis and calyces
d) Cystine stones
- Associated with genetic defect
- Manifestations: depends upon size and location of
stones
• Calculi affecting kidney calices, pelvis
a) Few symptoms unless obstructed flow
b) Dull, aching flank pain
• Calculi affecting bladder
a) Few symptoms
b) Dull suprapubic pain with exercise or post voiding
c) Possibly gross hematuria
• Calculi affecting ureter, causing ureteral spasm
a) Renal colic: acute, severe flank pain of affected
side, radiates to suprapubic region, groin, and
external genitals
b) Nausea, vomiting, pallor, cool, clammy skin
• Manifestations of UTI may occur with urinary calculi
- Complications
• Obstruction: manifestations depend upon speed of
obstruction development; can ultimately lead to renal
failure
• Hydronephrosis: distention of renal pelvis and
calyces; unrelieved pressure can damage kidney
(collecting tubules, proximal tubules, glomeruli)
leading to gradual loss of renal function
a) Acute: colicky pain on affected side
b) Chronic: few manifestations: dull ache in back or
flank
c) Other manifestations: hematuria, signs of UTI, GI
symptoms
- Collaborative Care
• Relief of acute symptoms
• Remove or destroy stone
• Prevent future stone formation
- Diagnostic Tests
• Urinalysis: hematuria, possible WBCs and crystal
fragments, urine pH helpful to diagnose stone type
• Chemical analysis of stone: All urine must be strained
and saved; stones or sediment sent for analysis
• 24-urine collection for calcium, uric acid, oxalate to
identifiy possible cause of lithiasis
• Serum calcium, phosphorus, uric acid: identify
factors in calculi formation
• KUB xray (kidney, ureters, bladder): flat plate to
identify presence and location of opacities
• Renal ultrasonography: sound waves to detect stones
and detect hydronephrosis
• CT scan of kidney: identify calculi, obstruction,
disorders
• IVP
• Cystoscopy: visualize and possibly remove calculi
from urinary bladder and distal ureters
- Medications
• Treatment of acute renal colic: analgesia and
hydration
• Narcotic such as intravenous morphine sulfate,
NSAID, large amounts of fluid by oral or intravenous
routes
• Medications to inhibit further lithiasis according to
analysis of stone:
a) Thiazide diuretics: promotes reduction of urinary
calcium excretion
b) Potassium citrate: used to alkalinize urine for
stones formed in acidic urine (uric acid, cystine,
and some calcium stones)
- Dietary Management: Prescribed to change character of
urine and prevent further lithiasis
• Increased fluid intake to 2 – 2.5 liters daily, spaced
throughout day
• Limited intake of calcium and Vitamin D sources if
calcium stones
• Phosphorus and/or oxalate may be limited with
calcium stones
• Low purine (rich meats) diet for clients with uric acid
stones
• Control of pH to maintain pH that inhibits lithiasis
a) Promote alkaline urine for clients with uric acid or
cystine stones
b) Promote acid urine for clients with calcium
stones or urinary tract infections
- Lithotripsy: Use of sound or shock waves to crush
stones
• Extracorporeal shock-wave lithotripsy: acoustic shock
waves aimed under fluoroscopic guidance to
pulverize stone into fragments small enough to be
eliminated in urine; sedation or TENS used to
maintain comfort during procedure
• Percutaneous ultrasonic lithotripsy: nephroscope
inserted into kidney pelvis through small flank
incision; stone fragmented using small ultrasonic
transducer and fragments removed through
nephroscope
• Laser lithotripsy: stone is disintegrated by use of laser
beams; nephroscope or ureteroscope used to guide
laser probe
• Stent may be inserted into affected ureter after
procedure to maintain patency after lithotripsy
procedures
- Surgery
• May be indicated as treatment depending on stone
location, severe obstruction, infection, serious bleeding
• Types:
a) Ureterolithotomy: incision into affected ureter to
remove calculus
b) Pyelolithotomy: incision into and removal of stone
from kidney pelvis
c) Nephrolithotomy: surgery to remove staghorn
calculus in calices and renal parenchyma
d) Cystoscopy: crushing and removal of bladder
stones through cystocope; stone fragments
irrigated out of bladder with acid solution
- Nursing Care
• Focus on comfort during renal colic, diagnostic
procedures, ensure adequate urine output, prevent
future stone formation
• Health promotion: adequate fluid intake for all clients,
adequate weight-bearing activity to prevent bone
resorption, hypercalcuria, prevention of UTI
- Nursing Diagnoses
• Acute Pain
o Adequate pain management
o Intensity of pain can cause vaso-vagal response;
client may experience hypotension, syncope;
client safety must be maintained
• Impaired Urinary Elimination
o Teaching client and strain all urine; send
recovered stones for analysis
o Complete obstruction causes hydronephrosis on
involved side; other kidney continues forming
urine; monitor BUN, Creatinine
o Maintain patency and integrity of all catheters; all
catheters need to be labeled, secured, and
sterility maintained
• Deficient Knowledge: Client participation in
treatment and prevention
- Home Care
• Education regarding management current
treatment
and prevention
• Clients may be discharged with catheters, tubes,
dressings; home care referral
Client with a Urinary Tract Tumor
- Malignancies in urinary tract: 90% bladder; 8% renal
pelvis; 2% ureter, urethral; 5 year survival rate for
bladder cancer is 94%
- Bladder cancer: 4 times higher in males than females; 2
times higher in whites than blacks; occurs over age 60
- Risk factors
• Carcinogens in urine
• Cigarette smoking
• Occupaional exposure to chemicals and dyes
• Chronic inflammation or infection of bladder mucosa
- Pathophysiology
• Tumors arise from epithelial tissue which composes
the lining
• Tumors arise as flat or papillary lesions
• Poorly differentiated flat tumor invades directly and
has poorer prognosis
• Metastasis commonly involves pelvic lymph nodes,
lungs, bones, liver
- Manifestations
• Painless hematuria is presenting sign in 75% cases;
• Inflammation may cause manifestations of UTI
• May have few outward signs until obstructed urine
flow or renal failure occurs
- Collaborative Care
• Removal or destruction of cancerous tissue
• Prevent invasion or metastasis
• Maintain renal and urinary function
- Diagnostic Tests
• Urinalysis: diagnosis of hematuria
• Urine cytology: microscopic examination of cells for
tumor or pre-tumor cells in urine
• Ultrasound of bladder: detection of bladder tumor
• IVP: evaluation of structure and function of kidneys,
ureters, bladder
• Cystoscopy, ureteroscopy: direct visualization,
assessment, and biopsy of lesion(s)
• CT scan or MRI: determine tumor invasion, metastasis
- Medications
• Immunologic or chemotherapeutic agent
administered by intravesical instillation used as
primary treatment of bladder cancer or to prevent
recurrence following endoscopic removal of tumor
• Agents include Bacillus Calmette-Guerin (BCGLive,
TheraCys), doxorubicin, mitomycin C
• Adverse reactions include bladder irritation,
frequency, dysuria, contact dermatitis
- Radiation Therapy
• Adjunctive therapy used treatment of urinary tumors
• Used to reduce tumor size prior to surgery, palliative
treatment
- Surgery
• Cystoscopic tumor resection by
a) Excision
b) Fulguration: destruction of tissue using high
frequency electric current
c) Laser photocoagulation: light energy to destroy
tumor
• Radical cystectomy: standard treatment to treat
invasive cancers; removal of bladder and adjacent
muscles and tissues
a) Males: includes prostate and seminal vessels
b) Females: hysterectomy, salpingo-oophorectomy
• Client needs to have urinary diversion done to provide
for urine collection and drainage through ileal conduit
or continent urinary diversion (ureters are implanted
in portion of ileum which is surgically made into a
reservoir for urine and stoma brought to surface of
abdomen)
- Nursing Care
• Treatment with recovery from initial treatment
• Continual care for recurrence
• Management for elimination
• Coping with cancer diagnosis
- Health Promotion
• Encouragement of clients not to smoke
• Smoking cessation programs
• Periodic examination of urinalysis and possibly urine
cytology
- Nursing Diagnoses
• Impaired Urinary Elimination
• Risk for Impaired Skin Integrity
a) Urine is irritating to skin around stoma
b) Care includes using appliance with adhesives and
sealants
c) Urine will have shreds of mucus in it from bowel
d) Collection bag emptied frequently (every 2 hours)
during day
e) Connected to bedside drainage bag while asleep
• Disturbed Body Image
a. Abdominal stoma requiring drainage appliance or
regular catheterization of stoma to drain urine
b. Removal of reproductive organs has made client
sterile
c. Side effects from chemotherapy or radiation
d. Risk for infection
 Home Care
 Involves continual surveillance for cancer recurrence
 If client has had urinary diversion surgery requires
teaching regarding stoma and skin care
 Home care referral
 Smoking cessation
Client with Urinary Retention
 Incomplete emptying of bladder leading to
overdistention of bladder
 Poor bladder contractility
 Inability to urinate
 May develop hydronephrosis
 Pathophysiology
• Mechanical obstruction of bladder outlet or functional
problem leads to urinary retention including
a) Benign prostatic hypertrophy (BPH)
b) Acute inflammation associated with infection or
trauma of bladder
c) Status post abdominal or pelvic surgery
disrupting detrusor muscle function
d) Anticholinergic medications
e) Failure to void regularly, resulting in bladder
overfill and loss of detrusor muscle tone
• Client may experience overflow voiding or
incontinence 25 – 50 ml at frequent intervals
- Collaborative Care: Treatment focuses on removing
or repairing obstruction, e.g. prostrate gland resection
- Treatment may include
• Catheterization indwelling or intermittent
• Cholinergic medications such as bethanechol
chloride (Urecholine) promoting detrusor muscle
contraction and bladder emptying
• Elimination of medications with anti-cholinergic
effects
- Nursing Care
• Focus on monitoring urine output of at risk clients
including those receiving medications that interfere
with detrusor muscle function
• With acute urinary retention, catheterization may be
necessary; if bladder is overdistended, drain only 500
ml at 5 – 10 minute intervals to prevent vaso-vagal
response and hematuria
- Home Care: Specific teaching depends on prescribed
treatment which may include
• Intermittent self-catheterization
• Care with over-the-counter medications that may
have anticholinergic effects
• Double voiding; scheduled voiding
• Indwelling catheter
Client with Neurogenic Bladder
- Disruption of central or peripheral nervous system that
interferes with normal mechanisms involved with
bladder filling, perception of fullness, need to void,
bladder emptyingSpastic Bladder Dysfunction
- Normal physiology: simple reflex between bladder
and
spinal cord (S2 – S4): stimulus of >400 ml of urine in
bladder causes reflex contraction of detrusor muscle and
bladder emptying unless voluntary control suppresses it
- Pathophysiology includes disruption of CNS
transmission above sacral spinal cord segment; bladder
filling causes frequent spontaneous detrusor muscle
contraction and involuntary bladder emptying
- Causes include: spinal cord injury, multiple sclerosis,
Stroke Flaccid Bladder Dysfunction
- Client cannot perceive bladder fullness; loss of detrusor
muscle tone and bladder over distends: occurs in clients
with myelomeningocele and during spinal shock stage
post spinal cord injury above sacral region
- Peripheral neuropathies lead to incomplete bladder
emptying with large residual volumes after voiding;
occurs
in clients with diabetes mellitus, multiple sclerosis,
prolonged overdistension of bladder
- Collaborative Care
• Maintenance of continence
• Voiding complications
• Client self-care
- Diagnostic Tests
• Urine Culture: determine UTI
• Urinalysis (presence of albumin, RBC’s), BUN,
Creatinine to determine renal function
• Post-void catheterization for residual urine: should be
< 50 ml.
• Cystometrography: testing to evaluate bladder filling
and detrusor muscle done and function
- Medications
• To improve detrusor muscle contraction with flaccid
bladder, such as post-operatively or after childbirth,
with bladder training:
a) Cholinergic drug (e.g. Bethanechol)
b) Anticholinesterase drugs (e.g. neostigmine
(Prostigmin)
• To relax detrusor muscle and contract internal
sphincter, increasing bladder capacity in clients with
spastic bladder:
a) Anticholinergic medications
o Oxybutynin (Ditropan)
o Tolterodine (Detrol)
o Propantheline (Pro-Banthine)
o Flavoxate (Urispas)
b) Adverse effects include dry mouth, blurred vision,
constipation
- Dietary management
• Moderate to high fluid intake, timing to promote
continence
• Acidify urine to prevent UTI with cranberry juice
- Bladder Retraining
• Scheduled toileting with stimulated reflex voiding by
using trigger points, e.g. stroke or pinch abdomen,
inner thighs for clients with spastic bladder
• Crede method: applying pressure to suprapubic
region, manual pressure on abdomen, Valsalva
maneuver to promote bladder emptying with either
type or neurogenic bladder (Do not use with spinal
cord injury clients at risk for autonomic dysreflexia)
• Intermittent catheterization
- Surgery
• May be used with clients unresponsive to other
therapies
• Includes rhizotomy (destruction of nerves supplying
detrusor muscle) with spasticity
• Urinary diversion
- Nursing Diagnoses
• Impaired Urinary Elimination
• Self-care Deficit
• Risk for Infection
- Home care: Involves teaching client, family about
methods to control voiding, promote bladder emptying,
medications, manifestations of UTI, reducing
complications
Client with Urinary Incontinence
- Urinary incontinence is involuntary urination; leads to
• Physical problems including skin breakdown and
infection
• Psychosocial aspects: embarrassment, isolation,
depression
- Up to 30% older women in community have
incontinence;
50% of long term care and home bound populations
- Pathophysiology:
• Pressure within the urinary bladder exceeds urethral
resistance
• Conditions leading to incontinence include
a) Relaxation of pelvic musculature
b) Disruption of cerebral and nervous system
control
c) Disturbances in bladder and its musculature
• Acquired, irreversible causes include chronic
neurological conditions
• Acute, reversible causes include confusion, effects of
medications, prostatic enlargement, vaginal and
urethral atrophy, UTI, fecal impaction
• Categories include
a) Stress incontinence
b) Urge incontinence (overactive bladder)
c) Overflow incontinence
d) Functional incontinence
e) Mixed incontinence (stress and urge)
• Incontinency associated with increased risk for falls,
pressure ulcers, UTI, depression, caregiver stress,
and cause for institutionalizing client
- Collaborative Care
• Focus is identification and correction of cause if
possible; otherwise management of urinary output
• Evaluation includes history including duration,
frequency, volume and circumstancesassociated with
incontinence (e.g. prostatic enlargement, cystocele,
rectocele); voiding diary
- Diagnostic Tests
• Urinalysis and urine culture: assess for UTI
• Postvoiding residual: < 50 ml is expected; >100 ml
indicates need for further testing
• Cystometrography: evaluation of neuromuscular
function of bladder; urge to void occurs at 150 – 450
ml; bladder feels full at 300 – 500 ml.
• Uroflowmetry: noninvasive test to evaluate voiding
pattern
• IVP: evaluates structure and function of urinary tract
• Cystoscopy or ultrasound: identify structural
disorders
- Medications
• Mild stress incontinence may be improved by using
medications that contract smooth muscles of bladder
neck such as phenylpropanolamine which is often
used in over-the-counter decongestants and diet aids
• Incontinence with postmenopausal atrophic vaginitis
responds to topical estrogen therapy
• Urge incontinence treated with medications that
increase bladder capacity: oxybutynin (Ditropan),
tolterodine (Detrol)
• Clients may have other medical conditions adversely
affected by medications used to treat incontinence
- Surgery: Treatments for stress incontinence
• Suspension of bladder neck by laparoscopic, vaginal,
or abdominal approach treats stress incontinence
associated with cystocele
• Prostatectomy may be used to treat enlarged prostate
gland and urethral obstruction
- Complementary Therapies: Biofeedback and relaxation
techniques
- Nursing Care
• Health promotion includes education that
incontinence is not normal with aging
• Educate females about pelvic floor exercises
• Educate males about treatment for prostatic
enlargement
• Availability of therapies and health practitioners
- Nursing Diagnoses
• Urinary Incontinence: stress and/or urge
a) Clients with difficulty emptying bladder should
not stop flow while voiding
b) Limit fluids that are irritating to bladder: caffeine,
alcohol, citrus juices, artificial sweeteners
• Self-care Deficit: Toileting
a) Assist client in independence
b) Planned toileting schedule
• Social Isolation
- Home Care
• Assisting clients to deal effectively with incontinence
lessens risk for institutionalization; address causes,
availability of treatment, management interventions
• Assess toileting environment for safety and assist to
obtain mobility aids such as safety bar, raised toilet
seat
• Clients who have had bladder neck suspension
surgery often are discharged with catheter in place;
client and family teaching, home health referral
Nursing Care of Clients with Kidney Disorders
Age-Related Changes in Kidney Function
a) Decline in glomerular filtration rate (GFR) to half or
less related to
• Arteriosclerosis
• Decreased renal vascularity
• Decreased cardiac output
b) Reduced clearance of drugs excreted through kidneys:
prolonged half-life of such medications as
• Cardiac drugs: digoxin, procainamide
• Antibiotics: aminoglycosides, tetracyclines,
cephalosporins
• Histamine H2 antagonists: cimetidine
• Antidiabetic agents: chlorpropamide
c) Increased risk for fluid and electrolyte imbalance
• Decreased ability to concentrate urine and
compensate for altered salt intake
• Decreased effectiveness of antidiuretic hormone
(ADH) and reduced thirst response
• Decreased potassium excretion due to lower
aldosterone levels
Client with a Congenital Kidney Malformation
- Affect form and function of kidney
• Agenesis: absence of kidney; renal function normal as
long as other kidney is functioning
• Hypoplasia: underdevelopment of kidney; renal
function normal as long as other kidney is functioning
• Horseshoe kidney: embryonic kidney fails to ascend
normally and result in single horseshoe-shaped
organ; increased risk for hydronephrosis and
recurrent UTI, renal calculi
- Education is important to maintain and prevent renal
complications from developing
Client with Polycystic Kidney Disease
- Hereditary disease characterized by cyst formation and
massive kidney enlargement
- Adult form of disorder is autosomal dominant
polycystic
kidney disease and accounts for 10% of persons in End
Stage Renal Disease (ESRD)
- Pathophysiology
• Renal cysts are fluid-filled sacs affecting nephrons;
cysts fill, enlarge, multiply thus compressing and
obstructing kidney tissue; renal parenchyma
atrophies, becomes fibrotic
• Cysts occur elsewhere in body including liver, spleen
- Manifestations
• Disease is slowly progressive; symptoms develop in
age 30 – 40’s
• Common manifestations include
a) Flank pain
b) Microscopic or gross hematuria
c) Proteinuria
d) Polyuria and nocturia (impaired ability to
concentrate urine)
e) UTI and renal calculi are common
f) Hypertension from disrupted renal vessels
g) Kidneys become palpable, enlarged, knobby
h) Symptoms of renal insufficiency and chronic
renal failure by age of 50 – 60 D. Collaborative
Care: Determine extent of polycystic kidney
disease
- Diagnostic tests
• Renal ultrasonography: primary choice for diagnostic;
assesses kidney size, identifies and locates renal
masses: cysts, tumors, calculi
• Intravenous pyelography (IVP): evaluate structure and
excretory function of kidneys, ureters, bladder
• CT scan of kidneys: detects and differentiates renal
masses
- Management
• Mainly supportive: prevent further renal damage from
UTI, nephrotoxic substances, obstruction,
hypertension
• Fluid intake of 2000 – 2500 mL to prevent UTI, calculi
• Control of hypertension with ACE inhibitors and other
antihypertensive agents
• Eventually require dialysis or transplantation (typically
good candidates)
- Nursing Care and Nursing Diagnoses
• Risk for Ineffective Coping: address genetic
counseling and screening for family members
• Excess Fluid Volume
• Anticipatory Grieving
• Knowledge Deficit: of measures to preserve kidney
function
Client with a Glomerular Disorder
- Leading cause of chronic renal failure in U. S.
- Primary disorders involve mainly kidney
• Immunologic
• Idiopathic
- Secondary disorders relate to inherited or multisystem
disease
• Diabetes mellitus
• Systemic lupus erythematosus (SLE)
• Goodpasture’s syndrome
- Pathophysiology
• Glomerular disease affects structure and function of
glomerulus affecting filtration and increasing
permeability in glomerulus
• Results in manifestations
a) Hematuria
b) Proteinuria (most important indicator; increases
progressively with glomerular damage)
c) Edema (results from hypoalbuminemia)
• GFR falls resulting in azotemia (increased blood level
of nitrogenous waste products) and hypertension
• Involvement may be diffuse (all glomeruli) or focal
(some glomeruli)
• Oliguria (urine output < 400 ml in 24 ml)
Primary glomerular disorders
• Acute glomerulonephritis
- Inflammation of glomerular capillary membrane
- Most common form is poststreptococcal
glomerulonephritis
- Circulating antigen-antibody immune complexes
formed in primary infection are trapped in glomerular
membrane; complement system activiated; glomeruli
inflamed and increasingly permeable
- Manifestations:
o Abrupt onset of hematuria, proteinuria, salt and
water retention, azotemia 10 – 14 days post initial
infection
o Urine is cocoa or coffee-colored
o Edema noted in face, particularly periorbital,
dependent edema in hands and upper extremities
o Fatigue, anorexia, nausea, vomiting
o Older adults have less apparent symptoms:
nausea, malaise, arthralgias, proteinuria,
pulmonary infiltrates
- Adults: 60% recover fully; remainder have persistent
symptoms and permanent kidney damage
• Rapidly progressive glomerulonephritis (RPGN)
- Severe glomerular damage without specific
identifiable cause
- Primary or secondary to SLE or Goodpasture’s
syndrome
- Diffuse glomerular damage with rapid progressive
disease with irreversible renal failure over weeks to
months
- May have flulike illness preceding onset resulting in
oliguria, abdominal or flank pain, moderate
hypertension, hematuria, proteinuria
• Chronic glomerulonephritis
- Typically end stage of other glomerular disorders
(RPGN, lupus nephritis, diabetic nephropathy)
- Symptoms develop insidiously, may be unrecognized
until signs of renal failure develop
- Course of disease varies with time between diagnosis
and development of end-stage renal failure
• Nephrotic syndrome
- Group of clinical findings, not specific disorder
- Characterized by
o Massive proteinuria
o Hypoalbuminemia
o Hyperlipidemia
o Edema (often facial and periorbital)
- Several disorders affect glomerular capillary
membrane
- Clients have increased risk for atherosclerosis
- Complication is thromboemboli leading to renal vein
and deep vein thrombosis, pulmonary embolism
- Adults: < 50% recover; remainder develop persistent
proteinuria and progress to ESRD
Common secondary forms of glomerular disease
• Diabetic nephropathy
- Leading cause of ESRD in U. S.
- 30% of clients with diabetes type 1; 20% of clients
with diabetes type 2
- Initial evidence is microproteinuria typically seen 10 –
15 years after onset of diabetes; nephropathy
develops within 15 – 20 years after initial diagnosis
- Characteristic lesion is glomerulosclerosis and
thickening of glomerular basement membrane
- Arteriosclerosis and hypertension contribute to
disease
• Lupus nephritis
- 40 – 85% of clients develop manifestations of
nephritis
- Immune complexes trigger glomerular injury
- Manifestations range from microscopic hematuria to
massive proteinuria; progression varies form slow and
chronic to fulminant
- Improved management and dialysis and
transplantation improved prognosis
- Collaborative Care
• Identification of underlying disease process
• Preservation of renal function
- Diagnostic Tests
• Throat or skin cultures: detect group A beta-hemolytic
streptococci; used with identification of
poststreptococcal glomerulonephritis
• Antistreptolysin O (ASO) titer: detect streptococcal
exoenzymes; used with identification of
poststreptococcal glomerulonephritis
• Erythrocyte sedimentation rate (ESR): indicator of
inflammatory response as with poststreptococcal
glomerulonephritis or lupus nephritis
• KUB (kidney, ureters, bladder) abdominal xray:
evaluate kidney size; enlarged with acute
glomerulonephritis; small with chronic
glomerulonephritis
• Kidney scan: nuclear medicine procedure reveals
delayed uptake with glomerular disease
• Biopsy: microscopic examination of kidney tissue
most reliable diagnostic procedure for glomerular
disorders; determines type, prognosis, and
appropriate treatment of glomerulonephritis
• Serum BUN, Creatinine: evaluate kidney function;
creatinine is good indicator of kidney function since
entirely excreted by kidneys
• Urine creatinine: levels decrease with impaired renal
function
• Creatinine clearance: very specific indicator of renal
function and GFR
• Serum electrolytes: evaluate values affected by
impaired kidney function, especially serum potassium
• Urinalysis: shows red blood cells, abnormal protein
• 24-hour urine for protein: determine amount of
protein in urine
- Medications
• Not curative but treatment for underlying disorders,
decrease inflammation, symptom management
• Antibiotics: treatment for poststreptococcal
glomerulonephritis if any remaining bacteria (avoid
nephrotoxic antibiotics)
• Immunosuppressive therapy: aggressively treat acute
inflammatory processes (RPGN), Goodpasture’s
syndrome, SLE
a) Prednisone, glucocorticoid in large doses
b) Cyclophosphamide (Cytoxan) or azathioprine
(Imuran)
c) ACE inhibitors to reduce protein loss associated
with nephrotic syndrome, diabetic nephropathy
d) Antihypertensive medications
- Treatment
• Bedrest: treatment of acute phase of
poststreptococcal glomerulonephritis
• Sodium restriction to 1 – 2 gm/day with nephrotic
syndrome
• Protein intake may be restricted and should be of high
biologic value (complete proteins: have all essential
amino acids)
• Plasmapheresis: procedure to remove damaging
antibodies
• Dialysis procedures
- Nursing Care: Health Promotion
• Effective treatment of streptococcal infections with
completion of full course of antibiotics
• Effective management of chronic conditions such as
diabetes mellitus and SLE and hypertension
• Avoiding potentially nephrotoxic medications
- Nursing Diagnoses
• Excess Fluid Volume: monitor effects on cardiac
workload, blood pressure, respiratory status
• Fatigue: manifestation of anemia, hypoproteinemia,
anorexia, nausea
• Ineffective Protection: increased risk for infection
• Ineffective Role Performance
- Home Care
• Teach clients that glomerular disorders are selflimiting
or progressive
• Course is lengthy
• Self-management is essential
Client with a Vascular Kidney Disorder
• Hypertension
- Sustained elevation of systemic blood pressure
results from or causes kidney disease
- Damages walls of arterioles and accelerates process
of atherosclerosis, including afferent and efferent
arterioles and glomerular capillaries in kidney
- Untreated malignant hypertension can lead to rapid
decline in renal function
• Renal Artery Occlusion
- Pathophysiology
a) Primary process affecting renal vessels
b) Result from emboli, clots, other foreign materials
- Risk Factors for acute renal artery thrombosis
a) Severe abdominal trauma
b) Vessel trauma from surgery or angiography
c) Aortic or renal artery aneurysms
d) Severe aortic or renal artery atherosclerosis
e) Emboli from atrial fibrillation, post myocardial
infarction, vegetative growth on heart valves from
bacterial endocarditis, fatty plaque in aorta
- Manifestations
a) Slow onset may be asymptomatic
b) Acute occlusion: severe localized flank pain,
nausea, vomiting, fever, hypertension, hematuria,
oliguria • Hematuria, gross or microscopic
c) In older client, new onset or worsening of • Flank or abdominal pain
hypertension • Localized swelling, tenderness, ecchymoses in flank
- Diagnostic Tests region
a) WBC: leukocytosis • Turner’s sign: bluish discoloration of flank
b) Elevated renal enzymes: aspartate transaminase • Acute blood loss: signs of shock: hypotension,
(AST), lactic tachycardia, tachypnea, cool and pale skin, alterered
c) dehydrogenase (LDH) level of consciousness
d) Tests showing acute renal failure if bilateral - Diagnostic Tests
arterial occlusion and infarction • Falling hemoglobin and hematocrit levels
- Treatment • Urinalysis: hematuria
a) Surgery to restore blood flow to affected kidney • AST levels rise
with acute occlusion • Renal ultrasound: reveal renal bleeding and damage
b) Management includes anticoagulant therapy, • CT scan
hypertension control, supportive treatment • IVP
• Renal Vein Occlusion • Renal arteriography
- In adults, usually occurs with nephrotic syndrome - Treatment
- Gradual or acute deterioration of renal function is only • Minor kidney injuries
manifestation a) Conservative treatment: bedrest and observation
- If thrombus breaks loose, results in pulmonary b) Minimal bleeding and self-limiting
embolism • Major kidney injuries
- Diagnosis: visualization of thrombus on renal a) Immediate treatment to control hemorrhage,
venography prevent and treat shock
- Treatment: thrombolytic drugs to dissolve clot; b) Surgery including surgical repair, partial or total
anticoagulant therapy nephrectomy
• Renal Artery Stenosis c) Percutaneous arterial embolization during
- Causes 2 – 5% of cases of hypertension affecting one angiography
or both kidneys; in males: atherosclerosis with - Nursing Care
gradual occlusion of renal artery; in females, • Accurate assessment
fibromuscular dysplasia • Interventions
- Manifestations • Prevention of complications
a) Hypertension before age 30 or after 50 without Client with a Renal Tumor
prior history - Pathophysiology
b) Epigastric bruit • Primary renal tumors are renal cell carcinomas
- Diagnostic Tests a) Account for 2% adult cancers
a) Renal ultrasound shows small and atrophied b) Often metastasized when diagnosed
kidney c) Metastasis tends to occur in lungs, bone, lymph
b) Captopril test for renin activity shows higher nodes, liver, and brain
levels of renin • Tumor may produce hormones resulting in
c) Renal angiography visualizes renal stenosis hypercalcemia, hypertension, hyperglycemia
- Treatment • Increased incidence in males, over age 55
a) Dilation of stenotic vessel by percutaneous - Risk Factors
transluminal angioplasty • Smoking
b) Surgery: bypass graft of renal artery beyond • Obesity
stenosis • Renal calculi
Client with Kidney Trauma • Genetic factors
- Pathophysiology: - Manifestations
• Kidneys damaged by blunt force or penetrating injury • Often few manifestations
• Minor injuries: contusion, small hematoma, capsule • Gross hematuria
or cortex laceration • Flank pain
• Major injuries • Palpable abdominal mass
a) Kidney fragment or “shatter”: significant blood • Systemic: fever without infection, fatigue, weight loss
loss, urine extravasation - Diagnostic Tests
b) Tearing of renal artery or vein • Renal ultrasonography: detect renal masses
c) Renal artery, vein, or pelvis laceration • CT scan: determine tumor size, extension, regional
- Manifestations lymph node or vascular involvement
• IVP and MRI: evaluate renal structure and function
• Renal angiography to evaluate extent of vascular
involvement
• Chest xray, bone scan, liver function tests to identify
metastases
- Treatment
• Radical nephrectomy is treatment of choice with
regional lymph node resection
• No effective treatment for metastases, attempt
biologic therapies or chemotherapy
- Nursing Care: Focus on needs related to diagnosis and
surgical intervention
- Nursing Diagnoses (surgery and cancer diagnosis)
• Pain
• Ineffective Breathing Pattern
• Risk for Impaired Urinary Elimination
• Anticipatory Grieving
- Home Care: Focus on protecting remaining kidney,
monitor for recurrence
Clients with Renal Failure
- Condition in which kidneys are unable to remove
accumulated metabolites from blood; leads to altered
fluid, electrolyte and acid-base balance
- May be due to kidney (primary disorder) or resulting
from
another disease in another organ or systemic (secondary
disorder)
- Classified as acute (abrupt onset and may be reversible)
or chronic (develops slowly and insidiously with few
symptoms until kidneys are severely damaged and
unable
to meet body’s excretory needs)
- Common and costly disease with people with End
Stage
Renal Disease requiring dialysis or transplant to live
- 5 year survival rate for clients on dialysis is 31.3%
Acute Renal Failure (ARF)
- Rapid decline in renal function with azotemia fluid and
electrolyte imbalances
- High mortality rate but is related to clients being
seriously
ill and aged
- Risk Factors
• Major surgery or trauma
• Infection
• Hemorrhage
• Severe heart failure, liver disease
• Lower urinary tract obstruction
• Use of nephrotoxic contrast media and medications
- Pathophysiology involved with cause categories
• Prerenal
a) 55 – 60% cases of ARF
b) Cause: Conditions that affect renal blood flow
and perfusion
o Decrease vascular volume
o Decrease cardiac output
o Decrease vascular resistance
• Intrarenal
a) 35-40% cases of ARF
b) Cause: Acute damage to renal parenchyma and
nephron
o Acute glomerulonephritis
o Vascular disorders including vasculitis,
malignant
o hypertension, arterial or venous occlusion
o Acute Tubular Necrosis (ATN): Destruction of
tubular epithelial cell with abrupt decline in
renal function from:
1) Prolonged ischemia (>2 hours) as with
surgery, severe hypovolemia, sepsis,
trauma, burns
2) Nephrotoxins – Aminoglycoside
antibiotics, Radiologic contrast media,
Other potential drugs: NSAIDs, heavy
metals, ethylene glycol (antifreeze)
3) Nephrotoxins have increased risk with
clients with preexisting renal
insufficiency or state of dehydration
4) Rhabdomyolysis: excess myoglobin from
skeletal muscle injury clogs renal tubules
(muscle trauma, drug overdose,
infection)
5) Hemolysis: red blood cell destruction
• Postrenal
a) <5% cases of ARF
b) Cause: Obstructive; prevents urine excretion
o Benign prostatic hypertrophy
o Renal or urinary tract calculi or tumors
- Course and Manifestations of ARF in 3 phases
• Initiation Phase
a) Lasts hours to day
b) Begins with initiating event ends when
maintenance phase begins
c) Good prognosis if treated at this phase
d) Few manifestations; identified when maintenance
phase begins
• Maintenance Phase
a) Characterized by significant fall in GFR and
tubular necrosis
b) Oliguric or non-oliguric but kidneys not
eliminating wastes, water, electrolytes, acids:
azotemia, fluid retention, electrolyte imbalances
(hyperkalemia, hypocalcemia,
hyperphosphatemia), acidosis (impaired
hydrogen ion elimination)
c) Anemia after several days due to suppressed
erythropoietin secretion; impaired immune
function
d) Salt and water retention leading to hypertension
and risk for heart failure and pulmonary edema
e) Hyperkalemia: cardiac dysrhythmias and EKG
changes, muscle weakness, nausea, diarrhea
f) Confusion, disorientation, agitation or lethargy,
hyperreflexia, possible seizures, coma
g) Vomiting, decreased or absent bowel sounds
• Recovery Phase
a) Progressive tubule cell repair and regeneration;
return of GFR to preARF levels
b) Diuresis occurs as kidney recover but BUN,
Creatinine, potassium and phosphate remain
high
c) Renal function improves rapidly first 5 – 25 days
but improvement may continue for up to a year
- Collaborative Care
• Prevention of ARF is goal for all clients, especially
those at high-risk
a) Preserve kidney perfusion by adequate vascular
volume, cardiac output and blood pressure
b) Limiting use of nephrotoxic medications or using
minimal effective dose, maintaining hydration,
monitoring renal function tests
• Treatment goals
a) Identify and correct underlying cause
b) Prevent additional renal damage
c) Restore urine output and kidney function
d) Compensate for impaired renal function:
maintain fluid and electrolyte balance
- Diagnostic tests to identify ARF
• Urinalysis
a) Fixed specific gravity 1.010 (low)
b) Proteinuria, if glomerular damage
c) Presence of red blood cells (glomerular
dysfunction), white blood cells (inflammation),
renal tubule epithelial cells (ATN)
d) Cell casts (protein and cellular debris molded in
shape of tubular lumen); brown color may
indicate hemoglobinuria or myoglobinuria
• Serum BUN and creatinine
a) Creatinine rises rapidly (24 – 48 hours) and peaks
in 5 – 10 days; rise is slower if output maintained
b) Halt in rise of BUN and Creatinine signals onset of
recovery• Serum Electrolytes
a) Monitored to determine whether to initiate
dialysis
b) Moderate rise in potassium
c) Hyponatremia related to water excess
• CBC showed moderate anemia and low hematocrit
(Iron and folate may be low and add to anemia)
• Renal ultrasound: used to identify any obstruction,
identify acute from chronic renal failure
• CT scan: identify obstruction and kidney size
• IVP, retrograde pyelography, or antegrade pyelography
a) Assess renal structure and function
b) Retrograde and antegrade testing less toxicity
from contrast media
• Renal biopsy: determine cause, differentiate acute
from chronic
- Medications
• Intravenous fluids and blood volume expanders to
restore renal perfusion
• Low dose Dopamine (Intropin) intravenous infusion to
increase renal blood flow and improve cardiac output
• Diuretic: Furosemide (Lasix) or osmotic diuretic such
as mannitol along with intravenous fluids; “washes
out” nephrons; prevents oliguria reducing azotemia
and electrolyte imbalance
• Antihypertensive medications including ACE
inhibitors
to limit renal injury
• Medications to prevent possible complications
a) Prevention of gastrointestinal bleeding (at risk due
to stress, impaired platelet function)
o Antacids
o H2 receptor antagonists
o Proton-pump inhibitors
b) Hyperkalemia: serum K > 6.5 mEq/L puts client at
risk for cardiac arrest
o Calcium chlorides
o Bicarbonate
o Insulin and glucose
o Sodium polystyrene sulfonate (Kayexalete)
1) Removes potassium from body primarily
in large intestine
2) If given orally, is combined with sorbitol
3) May be given as retention enema with tap
water enema to follow after 30 – 60
minutes
c) Hyperphosphatemia
o Aluminum hydroxide (AlternaGEL, Amphojel,
Nephrox)
o Binds with phosphates in GI tract and is
eliminated from
o bowel
- Fluid Management
• Once vascular volume and renal perfusion restored,
fluids are restricted
• Often intake is calculated by adding output from
previous 24 hours and 500 ml for insensible losses
• Fluid balance monitored by daily weights and serum
Na level
- Dietary Management
• Renal insufficiency and underlying disease creates
increased rate of catabolism (breakdown of body
proteins) and decreased rate of anabolism (tissue
repair)
• Client needs adequate nutrition and calories to
prevent catabolism but protein intake needs to be
limited to minimize azotemia
• Protein limited to 0.6g/kg body weight per day; protein
should be of high biologic value (contains essential
amino acids)
• Carbohydrate intake is increased for adequate
calories and protein-sparing effect
- Dialysis
• Dialysis is the diffusion of solute molecules across
semipermeable membrane from area of higher solute
concentration to lower concentration
• Dialysis used to remove excess fluid, waste products
from client with renal failure; can rapidly remove
nephrotoxins from blood
- Hemodialysis: Dialysis process
• In this type of dialysis, blood is taken from client via
vascular access and pumped into a dialyzer; blood is
separated from the dialysate (dialysis solution) by
semipermeable membrane
• Processes of diffusion and ultrafiltration remove
waste products, electrolytes, excess water
• Glucose, electrolytes, water can pass through, but
larger molecules (protein, red blood cells) are blocked
• Substances can be added to dialysate to diffuse into
the blood of the client
• Client with ARF may undergo hemodialysis daily
initially, then 3 – 4 times/week according to client
condition; 3 – 4 hours at a time
- Complications associated with hemodialysis
• Hypotension, most common, related to changes in
osmolality, rapid removal from vascular department,
vasodilation
• Bleeding related to platelet function and use of
heparin during dialysis
• Infection, local or systemic; Staphylococcus aureus
septicemia associated with infected vascular access
site; higher rates of hepatitis B and C,
cytomegalovirus, HIV in hemodialysis clients
- Continuous Renal Replacement Therapy (CRRT)
• Technique used, which allows more gradual fluid and
solute removal than hemodialysis; used for clients
with ARF unable to tolerate hemodialysis
• Done over period of 12 hours or more
- Vascular Access for Hemodialysis
• Acute or temporary access is gained inserting double
lumen catheter into subclavian, jugular, or femerol
vein
• Blood is drawn from proximal portion of catheter and
returned to circulation through distal end of catheter
• Arteriovenous (AV) fistula created for longer term
access for dialysis
a) Surgical anastomosis of artery and vein in
nondominant arm, usually radial artery and cephalic
vein
b) Usually cannot use fistula for hemodialysis
access for a month while it matures
c) Nurse or client can assess functional fistula for
complications
1) Thrombosis (clotted off): check for palpable
thrill, audible bruit
2) Infection: check for redness, drainage
d) Venipunctures and blood pressures should not be
done in arm with the AV fistula
e) AV fistulas are commonly used for vascular
access for dialysis clients with chronic renal
failure
- Peritoneal dialysis process involves:
• Peritoneal membrane of client is used as dialyzing
surface
• Warmed sterile dialysate instilled into peritoneal
cavity through a catheter that has been inserted into
peritoneal cavity
• Metabolic waster products and excessive electrolytes
diffuse into dialysate while it remains in abdomen
• Water diffusion is controlled by glucose in the
dialysate which acts as an osmotic agent
• Fluid is drained off by gravity into sterile bag at set
intervals, thus removing waste products and excess
fluid
- Disadvantages of peritoneal dialysis
• Dialysis is more gradual and may be slow for ARF
• Risk of peritonitis
• Contraindicated for clients with abdominal surgery,
peritonitis, significant lung disease
- Health Promotion: Prevention of ARF
• Maintenance of fluid volume and cardiac output
• Reduce risk of exposure to nephrotoxins
• Report output < 30 ml per hour in clients at risk
• Report dehydration, monitor renal function tests in
clients receiving nephrotoxic medications
• Observe clients for signs of transfusion reactions
- Nursing Diagnoses for clients in ARF
• Excess Fluid Volume
• Imbalanced Nutrition: Less than body requirements
• Deficient Knowledge
- Home care: Client who is recovering from ARF will
need
teaching for prescribed diet and fluid intake, avoidance
of
nephrotoxins, prevention of infection, continue under
medical supervision
Client with Chronic Renal Failure (CRF)
- Progressive renal tissue destruction and loss of function
- May progress over many years without being
recognized
until kidneys are unable to excrete metabolic wastes and
regulate fluid and electrolytes: Endstage Renal Disease
(ESRD)
- Incidence is increasing especially in older adults;
higher in
African Americans, Native Americans
- Conditions causing chronic renal failure diffuse
bilateral
disease of kidneys with progressive destruction and
scarring; diabetes is leading cause of ESRD; then
hypertension
- Pathophysiology and Manifestations of Stages
• Decreased Renal Reserve: Early Stage
a) Unaffected nephrons compensate for lost
nephrons
b) GFR is about 50% of normal
c) Client is asymptomatic
d) BUN and serum creatinine are normal
• Renal Insufficiency
a) GRF falls to 20 – 50% of normal
b) Azotemia and some manifestations
c) Insult to kidneys could precipitate onset renal
failure (infection, dehydration, exposure to
nephrotoxins, urinary tract obstructions)
• Renal failure
a) GRF < 20% of normal
b) BUN and serum creatinine rise sharply
c) Oliguria, manifestations of uremia
• End-stage renal disease (ESRD)
a) GRF < 5 % of normal
b) Renal replacement therapy necessary to sustain
life
c) ESRD: Uremia (“urine in blood”)
• Early manifestations
a) Nausea, apathy, weakness, fatigue
b) Progresses to frequent vomiting, increasing
weakness, lethargy, confusion
• Fluid and electrolyte effects
a) Urine less concentrated with proteinuria and
hematuria
b) Sodium and water retention
c) Hyperkalemia (Muscle weakness, paresthesia,
EKG changes)
d) Hyperphosphatemia, hypocalcemia,
hypermagesemia
e) Metabolic acidosis
• Cardiovascular effects
a) Systemic hypertension
b) Edema and heart failure; pulmonary edema
c) Pericarditis: metabolic toxins irritate pericardial
sac; less often now with dialysis
d) Cardiac tamponade: fluid in pericardial sac
• Hematologic effects
a) Anemia contributing to fatigue, weakness,
depression, impaired cognition, impaired cardiac
function
b) Impaired platelet function
• Immune system effects
a) WBC declines
b) Humoral and cell-mediated immunity impaired
c) Fever suppressed
• Gastrointestinal effects
a) Anorexia, nausea, vomiting, hiccups
b) GI ulcerations, increased risk for GI bleeding
c) Uremic fetor: urinelike breath odor
• Neurologic effects
a) Changes in mentation, poor concentration
b) Fatigue, insomnia
c) Psychotic symptoms, seizures, coma
d) Peripheral neuropathy: “restless leg syndrome”,
sensations of crawling, prickling
e) Muscle weakness, decreased deep tendon
reflexes, gait disturbances
• Musculoskeletal effects
a) Renal osteodystrophy (renal rickets)
characterized by osteomalacia (bone softening)
and osteoporosis
b) Bone tenderness and pain
• Endocrine and metabolic effects
a) Elevated uric acid levels; risk for gout
b) Resistance to insulin, glucose intolerance
c) High triglyceride and < HDL levels resulting in
accelerated
d) atherosclerotic process
e) Menstrual irregularities; reduced testosterone
levels
• Dermatologic effects
a) Yellowish hue to skin
b) Dry skin with poor turgor
c) Pruritis due to metabolic wastes deposited in skin
d) Uremic frost crystallized deposits of urea on skin
- Collaborative Care
• Eliminate factors that further decrease renal function
• Maintenance of nutritional status with minimal toxic
waste products
• Identify and treat complications of CRF
• Preparation for dialysis or renal transplantation
- Diagnostic Tests: Identify CRF and monitor renal
function
by following levels of metabolic wastes and electrolytes
• Urinalysis: fixed specific gravity at 1.010; excess
protein, blood cells, cellular casts
• Urine culture: identify infection
• BUN and serum creatinine: evaluate kidney function
1) BUN levels
o Mild azotemia: 20 – 50 mg/dL
o Severe renal impairment: > 100 mg/dL
o Uremic symptoms: > 200mg/dL
2) Creatinine levels >4 mg/dL indicate serious renal
impairment
• Creatinine Clearance: evaluates GFR and renal
function
a) Decreased renal reserve: 32.5 – 130 mL/min
b) Renal insufficiency: 10 – 30 mL/min
c) ESRD: 5 – 10 mL/min
• Serum electrolytes: monitored throughout course of
CRF
• CBC: moderately severe anemia with hematocrit 20 –
30%; low hemoglobin; reduced RBCs and platelets
• Renal ultrasonography: CRF: decreased kidney size
• Kidney biopsy: diagnose underlying disease process;
differentiate acute from chronic
- Medications
• General effects of CRF on medication effects
a) Increased half-life and plasma levels of meds
excreted by kidneys
b) Decreased drug absorption if phosphate-binding
agents administered concurrently
c) Low plasma protein levels can lead to toxicity
when protein-bound drugs are given
d) Avoid nephrotoxic meds or give with extreme
caution
• Diuretics (furosemide, other loop diuretics)
a) Reduce edema
b) Reduce blood pressure
c) Lower potassium
• Antihypertensive medications: ACE inhibitors
preferred
• Sodium bicarbonate or calcium carbonate correct
mild acidosis
• Oral phosphorus binding agents (calcium carbonate,
calcium acetate) to lower phosphate levels and
normalize calcium levels
• Aluminum hydroxide for acute treatment of
hyperphosphatemia
• Vitamin D supplements to improve calcium
absorption
• To treat dangerously high potassium levels
a) Intravenous bicarbonate, insulin, glucose
b) Sodium polystyrene sulfonate (Kayexalate)
• Folic acid, iron supplements to combat anemia
• Multiple vitamin supplement
- Dietary and Fluid Management
• Early in course of CRF: diet modifications to slow
kidney failure, uremic symptoms, and complications
• Restrict proteins (40 gm/day) of high biologic value
• Increase carbohydrate intake (35kcal/kg/day)
• Limit fluid to 1 – 2 L per day; limit sodium to 2 g/day
• Restrict potassium (60 -70 mEq/day); no salt
substitutes
• Restrict phosphorus foods (meat, eggs, dairy
products)
- Renal Replacement Therapies: considered when
medications and dietary modifications are no longer
effective
• Hemodialysis: establish vascular access (create AV
fistula) months ahead
• Peritoneal dialysis: can be initiated when indicated;
training client and/or family involved
• Transplantation: tissue typing and identification of
living related potential donors including health
assessment of donor
- Dialysis
• Considerations
a) Dialysis manages ESRD, but does not cure it
b) Hemodialysis or peritoneal dialysis is constant
factor of life Depending on individual client
situation and total health, client may prefer death
to dialysis
• Hemodialysis for ESRD
a) Treatments are 3 times per week for 9 – 12 hours
b) Specific dialysis orders according to body size,
residual renal function (based on that day’s current lab
test results), dietary intake,
concurrent illnesses
c) Complications during treatment are hypotension
and muscle cramps; dialysis disequilibrium
syndrome
d) Long term complications are infection and
vascular access problems
e) Cardiovascular disease is leading cause of death
for hemodialysis clients; higher death rate than
clients on peritoneal dialysis or transplanted
• Peritoneal Dialysis for ESRD
a) Continuous ambulatory peritoneal dialysis
(CAPD) most common
b) 2 liters of dialysate instilled into peritoneal cavity
and catheter sealed; empty and replace every 4 –
6 hours
c) Continuous cyclic peritoneal dialysis (CCPD)
uses delivery device during nighttime hours and
continuous dwell during day
d) Advantages over hemodialysis
o Eliminates vascular access and
heparinization
o Avoids rapid fluctuation in extracellular fluid
o Diet intake is more liberal with fluids and
nutrients
o Regular insulin can be added to dialysate to
manage hyperglycemia for diabetics
o Client more able to self-manage
e) Disadvantages of peritoneal dialysis
o Less effective metabolite elimination
o Risk for infection (peritonitis: dialysate returns
cloudy; should be straw colored)
o Serum triglyceride levels increase
o Altered body image with peritoneal catheter
- Kidney Transplant
• Treatment of choice for ESRD
• Primarily limited by availability of kidneys
• Many persons on waiting list for kidney
• Improves survival and quality of life for ESRD client
• Organ Donors
a) Majority are from cadavers
b) Transplants from living donors increasing
c) Close match between blood and tissue type
desired; HLA are compared; 6 in common is
perfect match
d) Living donors must be in good physical health;
nephrectomy is major surgery and remaining
kidney must be healthy
• Cadaver donors
a) Cadaver kidney from persons who
o Meets criteria for brain death
o Are aged < 65 years old
o Are free of systemic disease, malignancy, or
infection including HIV, hepatitis B, C
b) Kidney removed and preserved by hypothermia
o Transplant in 24 – 48 hours disease, cataract formation
o Use technique: continuous hypothermic - Health Promotion
pulsatile perfusion, and transplant up to 3 a) Ensure all clients with impaired renal function are
days well
o Donor kidney placed in lower abdominal hydrated, especially while receiving nephrotoxic drugs
cavity, renal artery, vein, and ureter are b) Encourage clients with ESRD to explore transplant
anastomosed options
• Immunosuppressive therapy - Nursing Diagnoses
a) Necessary to block immune response that would • Impaired Tissue Perfusion: renal
reject transplanted organ • Imbalanced Nutrition: Less than body requirements
b) Medications include • Risk for Infection
o Glucocorticoids: prednisone and • Disturbed Body Image
methylprednisolone used for maintenance - Home Care
and treatment of acute rejection episodes • CRF and ESRD are long-term processes requiring
o Azathioprine: inhibits cellular and humoral client management
immunity; metabolized by liver • Extensive teaching required
o Mycophenolate mofetil: more potent and a) Monitoring health status
minimal bone marrow suppression b) Compliance with fluid and dietary restriction and
o Cyclosporine: affects cellular immunity; is medications
hepatotoxic and nephrotoxic c) Care involved with hemodialysis, peritoneal
o Rejection dialysis, or living with transplant
1) Can occur at any time BASIC CONCEPTS IN COMMUNICABLE AND
2) Acute rejection OF INFECTION DISEASE
Communicable Disease Concepts
- An illness due to a specific infectious agent or its toxic
cells products that arises through transmission of that agent
directly or indirectly to well person or its products from
- Rise in serum creatinine an infected person, animal (vector) or inanimate
- Possibly oliguria reservoir to a susceptible host.
Two types of communicable diseases
- Methylprednisolone 1. Contagious disease is spread by direct contact w/
- OKT3 monoclonal antibody infectious agents causing the disease and easily
- Chronic rejection transmitted from 1 person to another through direct
or indirect means
post transplant 2. Infectious disease is a disease not only by ordinary
contact but requires direct inoculation of organism
through a break on the skin or mucous membrane.
cellular immune response Classification of disease based on occurrence
1 Sporadic disease that is intermittent occurrence of
renal failure) few isolated unrelated cases in given locality disease
• Progressive azotemia occurs occasionally irregularly, no specific pattern and
• Proteinuria Examples
• Hypertension • Cancers, Degenerative diseases.
• Complications of kidney transplant 2 Endemic disease that continuous occur throughout a
a) Hypertension period of time, of usual number of cases in a given
b) Glomerular lesions with manifestations of locality, constantly present in population, community or
nephrosis country.
c) Increased risk for myocardial infarction and Examples:
stroke • STD’s, diarrheal diseases, PTB, Influenza, different
• Complications associated with long-term types of pneumonia, Schistosomiasis, Malaria, Filariasis
immunosuppression 3 Epidemic disease which the occurrence is of
a) Infection: bacterial, viral, fungal in blood, lung, unusually large number of cases in a relatively short
CNS period of time
b) Tumors: carcinoma in situ in cervix, lymphomas, • dengue fever
skin cancers • leptospirosis
c) Steroid use leads to bone problems, peptic ulcer • mumps
• chicken pox
• measles
4 Pandemic disease is an epidemic disease that occur
worldwide, simultaneous occurrence of epidemic of
same disease in several countries and
• HIV-AIDS
• MERS-COV
• SARS
• COVID 19
Classification of disease based on severity or duration
of disease
1) Acute disease - develops rapidly (rapid onset) but
lasts only a short time
• Measles
• Mumps
• Influenza
2) Chronic disease - develops more slowly but lasts for
a long period
• TB
• leprosy
3) Sub-acute disease - is the intermediate between
acute and chronic, develops rapidly and has long
duration with the examples of bacterial endocarditis
4) Latent disease - with causative agent remains
inactive for a time but then becomes active to produce
symptoms of the disease
Types of infection
1. Recurrent infection - is the reappearance of
symptoms after infectious disease has been treated
or subsided
2. Re-infection - after an initial infectious agent has
been eliminated, a new infection occurs caused by
the same organism
3. Super-infection - additional infection occurs by
another infectious agent.
4. Autoinfection - in which the infected person is his
own direct source of reexposure
Course of infectious process
1. Incubation period - entry of microorganism to body
to onset of nonspecific signs and symptoms.
2. Prodromal period - onset of nonspecific signs and
symptoms to the appearance of specific signs and
symptoms which the pathognomonic signs.
3. Illness period - host experiences maximum
impact of infectious process and specific signs and
symptoms develop and become evident.
4. Convalescent period is a recovery period as
manifestations subside and signs and symptoms start
to abate until the client returns to normal state of
health.
The Republic Act No. 11332, repealing the act 3573,
otherwise known as the "Law on Reporting of
Communicable Diseases"
- The law hereby declared the policy of the State to
protect and promote the right to health of the people and
instill
health consciousness among them. It shall endeavor to
protect the people from public health threats through the
efficient and effective disease surveillance of notifiable
diseases including emerging and re-emerging infectious
diseases, diseases for elimination and eradication,
epidemics, and health events including chemical,
radionuclear and environmental agents of public health
concern and provide an effective response system in
compliance with the 2005 International Health
Regulations (IHR) of the World Health Organization
(WHO).
- The law have the following objectives:
a. To continuously develop and upgrade the list of
nationally notifiable diseases and health events of
public health concern
b. To ensure the establishment and maintenance of
relevant, efficient and effective disease surveillance
and response system
c. To expand collaborations beyond traditional public
health partners to include others who may be
involved in the disease surveillance and response,
d. To provide accurate and timely health information
about modifiable diseases, and health-related events
and conditions to citizens and health providers
e. To establish effective mechanisms for strong
collaboration with national and local government
health agencies
f. To ensure that public health authorities have the
statutory and regulatory authority to ensure the
following:
Mandatory reporting of reportable diseases and
health events of public health concern;
 Epidemic/outbreaks and/or epidemiologic
investigation, case investigations, (3) Quarantine and
isolation; and
 Rapid containment and implementation of measures
for disease prevention and control;
g. To provide sufficient funding to support operations
needed to establish and maintain epidemiology and
surveillance
h. To require public and private physicians, allied
medical personnel, professional societies, hospitals,
clinics, to actively participate in disease surveillance
and response; and
i. To respect to the fullest extent preserving public
health and security. possible, the rights of people to
liberty, bodily integrity, and privacy while maintaining
Chain of Infection
Infectious agent
 Which can take the form of viruses, bacteria, fungus,
parasite and protozoa
 Three factors
1. pathogenicity - its ability to produce disease
2. degree of virulence - its severity or harmfulness
3. its invasiveness - its tendency to spread.
 Reservoir
 is the principal habitat in which a pathogen lives,
flourishes and is able to multiply.
 infectious agents include humans, animals or insects
and the environment.
 2 forms in humans
1. Acute clinical cases - is infected and is displaying
signs and symptoms of the disease more likely to be
diagnosed and treated
2. Carriers - where someone has been colonized with
an infectious agent but is not unwell. can present
more of a risk to those around them because they do
not display any signs or symptoms of illness
- Four main types
a. Incubatory carriers - people who are infectious
even before their own symptoms start
b. Inapparent carriers - in which an individual is able
to transmit an infection to others, without ever
developing the infection themselves
c. Convalescent carriers - people who are in the
recovery phase of their illness but who continue to
be infectious
d. Chronic carriers - anyone who has recovered but
who continues to be a carrier for infection.
Portal of exit
- which enables a pathogen to leave the reservoir or host
- Key portals of exit
• Alimentary - via vomiting,
• Diarrhea or biting
• Genitourinary - via sexual transmission
• Respiratory - through coughing,
• Sneezing and talking
• Skin - via skin lesions; trans-placental - where
transmission is from mother to fetus
Mode of transmission
• Can be contact
• Airborne
• Droplet
• Vehicle-borne
• Vector-borne
• Trans-placental
- Two main ways
1) direct transmission
- tends to be instantaneous and occurs when there
is direct contact with the infectious agent.
Examples include tetanus, glandular fever,
respiratory diseases and sexually transmitted
diseases.
2) Indirect transmission
- can occur through animate mechanisms such as
fleas, ticks, flies or mosquitoes or via inanimate
mechanisms such as food, water, biological
products or surgical instruments
- can also be airborne, in which tiny particles of an
infectious agent are carried by dust or droplets in
the air and inhaled into the lungs.
Portal of entry
- usually this path is as the same as port of exit
- infection is able to enter a susceptible
host inhalation (via the respiratory tract) absorption (via
mucous membranes such as the eyes) ingestion (via the
gastrointestinal tract)
- inoculation (as the result of an inoculation injury)
- introduction (via the insertion of medical devices)
Susceptible host
- the final and the most important link in the chain of
infection
- their age - and in particular if they are very young or
very old
1) whether there is any presence of malnutrition or
dehydration
2) whether there is any underlying chronic disease if the
host suffers from immobility
3) if they are taking any medication which could disrupt
or suppress their immune response
4) if they received immunization
Universal / standard precaution
1) Avoid contact with the patient’s bodily fluids by
wearing
gloves, goggles, face mask, gown and shoe cover
2) Medical instruments should be handled carefully and
disposed properly in a sharp’s container.
3) Proper hand washing.
4) Considering all patients are infectious.
5) Standard precaution goes beyond universal precaution
regardless of diagnosis
6) All personnel protective equipment shall be removed
immediately upon leaving the work area. Used needles
and other sharps shall not be sheared, bent, broken,
recapped by hand.
7) Eating, drinking, smoking, applying cosmetics and
handling contact lenses are prohibited where there is
potential occupational exposure. Food and drinks shall
not be stored in refrigerators or cabinets where blood and
other potentially infectious materials are stored.
8) All procedures involving blood shall be performed in
such
a manner as to minimize splashing.
Terminologies
• Communicable Disease Nursing – is the study of an
illness due to a specific toxic substance, occupational
exposure or infectious agent, which affects a susceptible
individual
• Communicable Disease – is an illness due to a
specific infectious agent or its toxic products that arises
through transmission of that agent
• Disease control – refers to the reduction of disease
incidence, prevalence, morbidity or mortality to a locally
acceptable level
• Disease surveillance – refers to the ongoing systematic
collection, analysis, interpretation, and dissemination of
outcome-specific data for use in the planning,
implementation, and evaluation of public health practice.
• Infection – invasion of the body tissue by
microorganisms and their proliferation
• Carrier – a person who without apparent symptoms of
a disease, harbors and spread the specific with
microorganisms
• Chain of Infection – is made up of six different links:
pathogen (infectious agent), reservoir, portal of exit,
means of transmission, portal of entry, and the new host.
• Contact – any person or animal known to have been in
such association an infected person or animal exposed to
infection
• Communicable period – the period which etiologic
agent may be transferred directly or indirectly from the
body of the infected person to the body of another
person
• Contamination – invasion of surface (wound) or
article (handkerchief) or matter (water and milk) implies
the presence of undesirable substance which may contain
pathogenic microorganisms
• Sterilization – describes a process that destroys or
eliminates all forms of microbial life and is carried out in
health-care facilities by physical or chemical methods
• Disinfection – describes a process that eliminates
many or all pathogenic microorganisms, except bacterial
spores, on inanimate objects
• Concurrent disinfection – ongoing practices that are
observed in the care of the client, his supplies,
environment and control of microorganisms
• Terminal disinfection – practices to remove
pathogens from the client’s belongings and environment
after his illness is no longer communicable
• Disinfectant – substance for inanimate objects that
destroys pathogens and the spores
• Antiseptic – substance intended for persons that inhibit
the growth of pathogens but not necessarily destroy them
• Bactericidal – chemical that kills microorganisms
• Bacteriostatic – chemical that prevents the
multiplication but does not kill all forms of microbes
• Asepsis – absence of disease-producing
microorganisms; free from infection
• Sepsis – presence of infection
• Medical asepsis – practices to reduced the number and
transfer of microorganisms; clean technique.
• Surgical asepsis – practices that render and
keepobjects & areas free from pathogens; sterile
technique
• Etiology – the study of causes
• Virulence – the vigor with which the organism can
grow and multiply; refers to the degree or intensity of
disease produced
• Nosocomial Infection – infections associated with the
delivery of health care services in a health care facility
• Opportunistic pathogen – causes disease in a
susceptible person
• Resident flora – microorganisms that are always
present in specific areas of the body;
• Transient flora – microorganisms picked up by the
skin as a normal activities that can be removed easily
• Pathogens – a disease producing-microorganism
• Pathogenecity – the ability to produce a disease; the
ability of microbes to overcome the defensive powers of
the host to induce disease
• Quarantine – limitation of freedom of movement of
such susceptible persons or animals as have been
exposed to communicable diseases
• Colonization –strains of microorganisms become
resident flora, but their presence does not cause disease
• Fumigation –destruction of insects, fleas, bugs, etc.
and is accomplished by the employment of gaseous
agents
• Isolation – the separation for the period of
communicability of infected persons
• Mandatory reporting – refers to the obligatory
reporting of a condition to local or state health
authorities,
• Notifiable disease –disease that, by legal
requirements, must be reported to the public health
authorities
• Public health authority – refers to the DOH the local
health office (provincial, city or municipality), or any
person directly authorized to act on behalf of the DOH
or local health office;
IMMUNIZATION
- Is the process by which vaccines are introduced into
the body before the infection sets in.
- It promotes health and protects children from
diseasecausing agents.
Vaccines
- The causative agent of a disease so modified as to be
incapable of producing the disease yet at the same time
so little changed that it is able, when introduced into the
body, to elicit production of specific antibodies against
the disease.
- These are always antigens, therefore they always
induce
active immunity when administered thereby causing the
recipient’s immune system to react to the vaccine that
produces antibodies to fight infection, and are most
useful in the prevention of disease.
Expanded Program on Immunization (EPI)
- Launched in July 1976 by DOH in cooperation with the
World Health Organization (WHO) and UNICEF to
ensure that infants/children and mothers have access to
routinely recommended infant/childhood vaccines.
- Vaccination among infants and newborns (0-12
months) against seven vaccine-preventable diseases:
tuberculosis, poliomyelitis, diphtheria, tetanus, pertussis,
hepatitis and measles.
- Presidential decree No. 996 (September 16, 1976).
“Providing for compulsory basic immunization for
infants and children below eight years of age.”
Mandates:
- Republic Act No. 10152 “Mandatory Infants and
Children Health Immunization Act of 2011” Signed by
President Benigno Aquino III in July 26, 2010. The
mandatory includes basic immunization for children
under 5 including other types that will be determined by
the Secretary of Health.
EPI Routine Schedule of Immunization:
 Wednesday – designated immunization day in all
parts of the country.
 Monthly – in a Barangay Health Station (BHS)
 Quarterly – in far flung areas
Updates
- 2012 - Rotavirus and Pneumococcal vaccines were
introduced in the EPI. Immunization will be prioritized
among the infants of families listed in the National
Housing and Targeting System (NHTS) for Poverty
Reduction nationwide.
- 2014 - Pneumococcal Conjugate Vaccine 13 was
included in the routine immunization of EPI.
- 2016 - the Expanded Program on Immunization had a
transition to become the National Immunization Program Tetanus Toxoid Immunization Schedule for Women
(NIP). It includes immunizations of other populations
such as senior citizen immunization, school-age
immunization, and adolescent immunizations.
- 2018 - there are a total of 13 recommended
vaccinations on the updated childhood immunization
schedule for Filipino children, ages 0 to 18 years old. It's
one less vaccine compared to last year's — the dengue
vaccine was removed.
Vaccines in the Philippine National Immunization Administration of Vaccines
Program (NIP)
The following vaccines are in the 2018 NIP:
- BCG, monovalent Hep B, Pentavalent vaccine (DTwP-
HibHepB), bivalent OPV, IPV, PCV, MMR, MR, Td
and HPV.
Recommended Vaccines
- These are vaccines not included in the NIP which are
recommended by the Philippines Pediatric Society
(PPS), Pediatric Infectious Disease Society of the
Philippines (PIDSP) and the Philippine Foundation for
Vaccination (PFV)
The EPI vaccines and its Characteristics
EPI COLD CHAIN and LOGISTICS:
 Cold Chain Manager = Public Health Nurse
 Temperature monitoring of vaccines is done in all
levels of health facilities to monitor vaccine
temperature.
 Temperature checking is done twice a day early in
the morning and in the afternoon before going home.
 Temperature is plotted every day in monitoring chart
to monitor break in cold chain.
Vaccine can be stored in Refrigerator:
 Regional – 6 months
 Municipal / City – 3 months
 Main Health Center – 1 month
 Transport Box : 5 days
 FEFO ( first expiry and first out ) vaccine is
practiced to ensure that all vaccines are utilized
before its expiry date.
 Proper arrangement of vaccines and labelling of
vaccines expiry date are done to identify those near
to expire vaccines
 Vaccine Wastage – Wastage is defined as loss by
use, decay, erosion or leakage or through
wastefulness
General Principles in Vaccination
 It is safe and immunologically effective to
administer all EPI vaccines on the same day at
different sites of the body.
 The vaccination schedule should not be restarted
from the beginning even if the interval between
doses exceeded the recommended interval by
months or year.
 Giving doses of a vaccine at less than the
recommended 4 weeks interval may lessen the
antibody response. Lengthening the interval between
doses of vaccines leads to higher antibody levels.
 No extra doses must be given to children who
missed a
 dose of DPT/HB/OPV. The vaccination must be
continued as if no time had elapsed between doses.
 Do not give more than one dose of the same vaccine
to a child in one session. Give doses of the same
vaccine at
 the correct intervals.
 Strictly follow the principle of never, ever
reconstituting the freeze dried vaccine in anything
other than the diluent supplied with them.
 If you are giving more than one vaccine, do not use
the
 same syringe/needle and do not use the same arm or
leg
 for more than one injection.
 Repeat BCG vaccination if the child does not
develop a
 scar after the first injection.
 It is safe and effective with mild side effects after
 vaccination. Local reaction, fever, and systematic
 symptoms can result as part of the normal immune
 response.
 Anaphylaxis or severe hypersensitivity reaction to a
 previous dose of vaccine is an absolute
contraindication
 to subsequent doses of vaccine
 Person with a known allergy to a vaccine component
 should not be vaccinated.
 DPT2 or DPT3 is not given to a child who has
convulsions
 or shock within 3 days after DPT1. Vaccines
containing the whole cell pertussis component
should not be given to a children with an evolving
neurological disease
 (uncontrolled epilepsy or progressive
encephalopathy).
 Do not give live vaccines like BCG to a individuals
who are immunosuppressed due to malignant
disease ( child with AIDS) , going therapy with
immunosuppressive agents or radiation.
 A child with a sign and symptoms of severe
dehydration
 Fever of 38.5 C and above
 The following are NOT contraindication. Infants
with these conditions SHOULD be immunized:
 Allergy or asthma ( except if there is a known
allergy to a specific component of vaccine
mentioned above )
 Minor respiratory tract infection
 Diarrhea / vomiting
 Temp. below 38.5 C / low grade fever
 Family history of adverse reaction following
immunization
 Family history of convulsions/seizures
 Known or suspected HIV infection with no signs
and symptoms of AIDS
 Child being breastfed
 Chronic illness such as diseases of heart, lung,
kidney or live
 Stable neurological condition such as cerebral palsy
or Down’s Syndrome
 Premature or low birthweight (vaccination should
not be postponed )
 Recent or imminent surgery
 Malnutrition
 History of jaundice at birth
 Generally, one should be immunized unless the child
is so sick that he needs to be hospitalized.
 Note: If parent strongly objects to an immunization
for a sick infant, do not give it. Ask the mother to
comeback when child is well.
Immunology
 a division of biology concerned with the study of
living organisms’ exemption from harmful agents.
 Immunity refers to the body’s specific protective
response to an invading foreign agent or organism.
 Susceptibility is the reverse of immunity and the
result of the suppression of factors that produces
immunity.
 There are two types of Immunity:
1. Natural immunity which is innate and non-specific
2. Acquired immunity which adaptive and specific.
 Antigens refer to the foreign substances which elicit
an immune response.
 The three functions of immune response are-
homeostasis, defense and surveillance.
 The body has its anatomic and physiologic
defenses:
1. Intact skin and mucous membranes which the
body’s first line of defense against microorganism. It
has normal secretions (sweat) that make skin slightly
acidic: Acidity inhibits bacterial growth.
2. Resident bacteria which prevent other bacteria
from multiplying and use up available nourishment.
3. Nasal Passages that moist mucous membrane and
cilia traps microorganism, dusts, foreign materials.
4. Lungs that have alveolar macrophages (large
phagocytes) which are cells that are responsible to
ingest microorganisms and foreign particles.
5. Oral Cavity sheds mucosal epithelium to rid the
mouth of colonizers. The flow of saliva and it’s
partially buffering action help prevent infection.
6. The eyes that being protected from infection by tears
which continually wash microorganisms away.
7. Gastrointestinal Tract with the high acidity of the
stomach that normally prevents bacterial growth.
The resident flora of the large intestines prevents the
establishment of disease producing microorganism.
8. The vagina when girl reaches puberty, lactobacilli
ferment sugars in the vaginal secretions creating a
vaginal pH of 3.5-4.5. This low pH inhibits the
growth of many disease-producing microorganisms.
9. The urethra with the urine use for flushing and
bacteriostatic action keeps bacteria from ascending.
The WBC (Leukocytes) participates both on the
natural and acquired immune response.
 There are two types of WBC:
1. Granulocytes (Granular leukocytes) as classified to:
a. Neutrophils with polymorphonuclear cells
(PMN), are the first cells to arrive at the site of
inflammation and increased in acute
bacterialinfection;
b. Eosinophils which increases during allergic and
parasitic infections.
c. Basophils which are not usually affected by
infection.
2. The other type is Agranulocytes meaning without
granules and classified to:
a. Monocytes (Macrophages) which are
phagocytic
cells engulfing, ingesting, and destroying greater
numbers and quantities of foreign bodies or
toxins;
b. Lymphocytes consisting of Bcells and T-cells
that play major role in Humoral and Cell-
Mediated immune response and increases in
chronic bacterial and viral infections.
 The inflammatory responses are the inflammation
that is local and nonspecific defensive response of
tissues to an injurious or infectious agent. It is an
adaptive mechanism that destroys or dilutes the
injurious agent, prevents further spread of injury and
promotes the repair of damaged tissue.
 There are five characteristic signs of inflammation:
1. Pain (Dolor)
2. Swelling (Tumor);
3. Redness (Rubor);
4. Heat (Calor)
5. Impaired function of the part.
 The Acquired Immunity is a specific immunity
develops after birth; acquired during life but not
present at birth and occurs after exposure to an
antigen like infectious agent.
 The natural immunity comes in two forms:
1. Active immunity - host produces its own
antibodies in response to natural antigen and these
antibodies produced by himself with long term
effectivity;
 An active natural is an immunity from a recovery
of a disease (mumps, measles, chicken pox), has
lifetime protection and antibodies are formed in the
presence of active infection (disease) in the body.
 An active artificial - antigens like toxoids or
vaccines that can be live attenuated or inactivated
vaccines are usually administered to the person to
stimulate antibody production, all kinds of
immunization and has many years of protection but
not lifelong.
2. Passive immunity are antibodies that are produced
by another source, animal or human given to the
individual with long term effectivity and has
immediate protection.
 A passive natural immunity coming from a
transplacental transfer of antibodies like breastfeeding
with colostrums as a yellowish antibodies that boost the
immune system of the baby, transfer of IgA and with 6
months to 1 year protection.
 A passive artificial immunity coming from
Immune serum (antibody) from an animal or another
human is injected like tetanus Ig, gamma globulin,
antitoxin, antiserum administration with 2-3 weeks
protection.
 The lymphoid organs that house phagocytic cells
and lymphocytes: Spleen filters blood of bacteria,
viruses and other debris; destroys worn out RBC’s;
and stores lymphocytes.
 Thymus produces thymosin; programs certain
lymphocytes to carry out their protective role. Bone
marrow produces WBC’s.
 Tonsils is a small msses of lymphatic tissue that ring
the pharynx; it traps and remove bacteria or other
foreign pathogens that will enter the throat.
 Peyer’s patches is found on the wall of the small
intestine; this also traps and remove foreign
materials in the intestine.
The components of Immune Response
 Antibody-Mediated Defenses (B-Cells) also known
as Humoral (Circulating Immunity) because the
defenses reside ultimately in the B lymphocytes and
 are mediated by antibodies produced by B cells.
Defend primarily against the extracellular phases of
bacterial and viral infections.
 Cell-Mediated Defenses (T-cells) also known as
Cellular Immunity, occurs through the T-cell
system.
 The Tcells are lymphocytes that mature in the
thymus.
 Types
 T helper cells (Th cells), also known as CD4 cells,
play an important role in the immune system,
particularly in the adaptive immune system. They
help the activity of other immune cells by releasing
T cell cytokines. These cells help suppress or
regulate immune responses.
 Helper Tcells detects the infection and initiates T-
cell and B-cell responses.
 A cytotoxic T cell (also known as TC, cytotoxic T
lymphocyte, killer T cell) kills cancer cells, cells that
are infected particularly with viruses.
 A suppressor T cell is a type of immune cell that
blocks the actions of some other types of
lymphocytes, to keep the immune system from
becoming overactive.
 The B-cells mature in the bone marrow; precursor of
plasma cell specialized to recognize some specific
antigens.
 Plasma cells produce antibodies which are directed
against specific antigens.
 Memory cells have been trained to recognize
specific antigens, they will trigger a faster and
stronger immune response after encountering the
same antigen and respond immediately.
 Memory T cells are a subset of infection- and
cancerfighting T that have previously encountered
and responded to their cognate antigen;
Some of the diagnostic procedures to evaluate the
patient’s immune competence:
 Series of blood tests;
 skin tests;
 bone marrow biopsy;
 electrophoresis.
 The nursing considerations when the patient is
undergoing such procedures: the nurse counsel,
educate, and support the patient and safety
precaution should be implemented.
Immunoglobulin
 are antibodies defend against foreign invaders and
the type of defense they will be using depends on the
structure and composition of the antigen and
immunoglobulin.
 FIVE TYPES. GAMED.
1. Immunoglobulin G (IgG)
 the most abundant immunoglobulin in serum, 80%
of the total serum immunoglobulin and relatively
abundant
 crosses placenta during gestation
 responsible for natural passive immunity of newborn
because it crosses placental barrier;
 assumes major roles in bloodborne and tissue
infections andenhances phagocytosis.
2. Immunoglobulin A (IgA)
 is the chief Ig in external secretions like breastmilk,
saliva, tears, and mucus of the bronchial,
genitourinary and digestive tracts;
 plays a major role in secretory immune response;
 has a protective function on mucosal surfaces
exposed to environment transported across mucous
membrane with secretions.
3. Immunologlobulin M (IgM)
 second most abundant antibody; the most important
Ig;
 the largest of the immunoglobulin and appears
mostly in the intravascular serum;
 provides a rapid protection because it is the first
antibody noted after antigen injection in an adult;
 first Ig class produced in primary response to
bacterial and viral infections;
 first Ig to be synthesized by the neonate; and the first
antibody to go on the site.
4. Immunoglobulin E (IgE)
 triggers the release of histamine;
 mediates the immediate hypersensitivity reactions
that are responsible for the symptoms ofhay fever,
asthma and anaphylactic shock; and
 takes part in allergic and combats parasitic
infections.
5. Immunoglobulin D (IgD)
 is a regulatory antibody;
 an antigen receptor of B cells;
 appears in small amount in serum with it biologic
function is unknown; and
 it is located on the surface of B lymphocytes that
serves as surface receptors-reaction with antigen
influences lymphocyte activity.
MEASLES, GERMAN MEASLES, CHICKEN POX,
INFLUENZA, COVID 19
Measles
 Francis Home (1757) a Scottish physician, who
first discovered measles.
 Murice Hilleman who first discovered measles
vaccine and first available in 1963 and then
improved the vaccine in 1968.
21 strains
 Rubeola
 7 day Measles
 Morbilli disease
 Heard measles
 Little Red Disease
 the disease still kills more than 100,000 people a
year, most under the age of 5.
 highly contagious illness caused by a virus that
replicates in the nose and throat of an infected child
or adult.
 when someone with measles coughs, sneezes or
talks, infected droplets spray into the air, where
other people can inhale them.
 causative agent of measles is Morbilli Virus
(paramyxovirus).
 The virus is sensitive to heat, light, and extreme
acidity and alkalinity.
 transmitted via airbornem, direct contact with
respiratory secretions coming from infected patients
and indirect contact with objects contaminated with
secretions.
 incubation period is 10-12 days but it can be
ranged from 8 to 20 days after the exposure to the
virus. period of communicability is 4 days before
and 5 days after the appearance of rashes.
Clinical Manifestation
1) Pre-Eruptive Stage
- highly contagious stage
- s/s
- high grade fever
- coryza
- cough
- conjunctivitis
- photophobia (3C1P)
- the enanthema signs (mucous membrane) presence
of tiny white spots with bluish-white centers on a red
background found inside the mouth on the inner lining
of the cheek opposite to the second molar is called
Koplik's spots which is the pathognomonic sign.
- Pathognomonic sign is a cardinal or distinctive sign of
a measles
- Stimson’s line is a line of inflammation along the
margin of lower eyelid and sore throat
2) Eruptive Stage
- rashes (exanthema)
- skin rash made up of large, flat blotches that often
flow into one another.
- It is a maculopapular rash (combination of elevated
and non-elevated skin rashes), reddish in color; spots
and bumps in tight clusters give the skin a splotchy
red appearance, warm to touch; the face breaks out
first that is why distributed as cephalocaudal in
distribution
- Pruritus
- Irritability
- Lethargy
- Anorexia
- 2 to 3 wks
- Diagnostic
• Nose and throat swab
• Urinalysis
• Blood examination and viral serology with
complement fixation
• Hemagglutinin inhibition test and neutralization
test
3) Convalescent Stage.
- Leukopenia is a characteristic sign of many viral
infections and the blood picture in measles is typical
of this effect.
- Wright's stain is a hematologic stain that facilitates
the differentiation of blood cell types.
- It is classically a mixture of eosin (red) and methylene
blue dyes. It is used primarily to stain peripheral blood
smears, urine samples, and bone marrow aspirates,
which are examined under a light microscope. In
cytogenetics, it is used to stain chromosomes to
facilitate diagnosis of syndromes and diseases.
- James Homer Wright, who devised the stain, it
distinguishes easily between blood cells, it became
widely used for performing differential white blood
cell counts, which are routinely ordered when
conditions such as infection are suspected.
- The complications of measles are bronchopneumonia
which is the most common and dreaded complication.
- People with compromised immune systems can
develop an especially dangerous variety of
pneumonia that is sometimes fatal.
- Otitis media is another common complication of
measles is a bacterial ear infection. About 1 in 1,000
people with measles develops a complication called
encephalitis.
- Encephalitis may occur right after measles, or it might
not occur until months later. Nephritis is the
inflammation of the kidney. Blindness of a having a
Vitamin A deficiency, don’t have enough vitamin A in
the diet more likely to have more severe symptoms
and complication.
- If the mother is pregnant need to take special care to
avoid measles because the disease can cause
preterm labor, low birth weight and maternal death.
The following nursing interventions are supportive and
symptomatic such as isolation because measles is
highly contagious from about four days before to four
days after the rash breaks out, people with measles
shouldn't return to activities in which they interact
with other people during this period. It may also be
necessary to keep non-immunized people, siblings,
for example away from the infected person.
- May give antipyretic and provide tepid sponge bath,
encourage to increases oral fluid intake, promote bed
rest, and provide nasal, oral, eye and skin care.
- The medical management are Pen G – to prevent
secondary bacterial complication; Antiviral of
ISOPRENOSINE.
- Vitamin A for 6 to 12 months of 100,000 IU and more
than 1 year old to 5 years old with 200,00 IU.
- Being unvaccinated is much more likely to develop
measles. The Centers for Disease Control and
Prevention recommends that children and adults
receive the measles vaccine to prevent measles. Live
Attenuated Measles Vaccine for 9 months; MMR for
1st dose: 12- 15 months and booster dose for 11-12
years; exposed: Measles Immune Serum Globulin
with 1 week after exposure. Be sure that anyone who's
at risk of getting the measles who hasn't been fully
vaccinated receives the measles vaccine as soon as
possible.
- If you've already had measles, the body has built up
its immune system to fight the infection. For everyone
else, there's the measles vaccine, which is important
for promoting and preserving widespread immunity
and preventing a resurgence of measles.
German Measles
 George de Malon (1814) was first discovered
German measles.
 German measles has 27 strains. German measles,
also known as rubella or 3 days measles, is a
contagious viral infection that causes a red rash on
the body.
 it can cause serious problems for unborn babies
whose mothers become infected during pregnancy.
 Rubella is caused by a different virus than measles,
and rubella isn't as infectious or as severe as
measles.
 Rubella is caused by a Rubivirus (Rubella Virus)
that's passed from person to person.
 Rubella virus is the only member of togavirus (with
an envelope) family that causes significant disease in
human—German measles.
 The virus can be transmitted through droplet. It can
spread when an infected person coughs or sneezes. It
can also spread by direct contact with an infected
person's respiratory secretions, such as mucus.
Indirect contact with objects contaminated with
secretions.
 Trans-placental transmission - it can also be passed
on from pregnant women to their unborn children
via the bloodstream.
 The incubation period is 2 to 3 weeks and the period
of communicability is 7 days before and 5 days after
the appearance of rashes.
The clinical manifestations of measles
1) Pre-Eruptive Stage
- Low grade fever
- Headache
- Malaise
- Anorexia
- Sore throat
- Coryza
- Conjunctivitis
- With presence of lymphadenopathy such enlargement
of the lymph nodes in the oost cervical
- Postauricular and suboccipital.
2) Eruptive stage
- The eruptive stage of measles is the stage of skin
rashes (exanthema). A skin rash made up of large, flat
blotches that often flow into one another. It is a
maculopapular rash (combination of elevated and
non-elevated skin rashes), reddish in color; spots and
bumps in tight clusters give the skin a splotchy red
appearance, warm to touch; the face breaks out first
that is why distributed as cephalocaudal in
distribution.
- There are also signs and symptoms like testicular pain
especially in younger adults, polyarthralgia and
polyarthritis.
- That is why the nurse can easily distinguish measles
from German measles from its pathognomonic and
lymphadenopathy.
- The enanthema signs (mucous membrane) presence
of a red, petechial macule on the surface of the soft
palate is called Froschauer spot which is the
pathognomonic sign. Pathognomonic sign is a
cardinal or distinctive sign of a German measles.
3) Convalescent stage.
- The convalescent stage rashes disappear in the same
manner as they appear in the body and does not
leaves a branny desquamation (shedding of
epidermis). Aside from the physical assessment, the
diagnostic tests are viral isolation from
nasopharyngeal secretions and viral serology with
complement fixation, hemagglutinin inhibition test
and neutralization test. Rubella is a mild infection.
- Once you've had the disease, the body usually
permanently immune. But, still the complications of
German Measles are encephalitis which is the most
common, Otitis media and Rubella syndrome.
- However, if the mother is pregnant and contract with
rubella, the consequences for the unborn child may
be severe, and in some cases, fatal. Up to 80% of
infants born to mothers who had rubella during the
first 12 weeks of pregnancy develop congenital
rubella syndrome.
This syndrome can cause one or more problems,
including:
• Intrauterine
• Growth Retardation
• Mental retardation
• Cardiac defects
• Eye defects with glaucoma and cataract
• Ear defects with hearing loss.
- The highest risk to the fetus is during the first trimester,
but exposure later in pregnancy also is dangerous. The
following nursing interventions are supportive and
symptomatic such as isolation because measles is highly
contagious from about four days before to four days
after the rash breaks out, people with measles shouldn't
return to activities in which they interact with other
people during this period.
- It may also be necessary to keep non-immunized
people, siblings, for example away from the infected
person. May give antipyretic and provide tepid sponge
bath, encourage to increases oral fluid intake, promote
bed rest, and provide nasal, oral, eye and skin care. The
medical management are symptomatic and supportive
with antipyretic and analgesic.
- Being unvaccinated is much more likely to develop
German measles.
- The Centers for Disease Control and Prevention
recommends that children and adults receive the German
measles vaccine to prevent German measles.
- Live Attenuated Rubella Vaccine, Mumps, Measles,
Rubella vaccine (MMR) and if exposed be given with
Immune Serum Globulin, IM within 1 week after
exposure (especially for pregnant women). The rubella
vaccine is usually given as a combined measles-mumps-
rubella (MMR) vaccine.
- It's particularly important that girls receive the vaccine
to prevent rubella during future pregnancies. Babies born
to women who have received the vaccine or who are
already immune are usually protected from rubella for
six to eight months after birth. But children who are
vaccinated early still need to be vaccinated at the
recommended ages later.
Widespread concerns have been raised about a possible
link between the MMR vaccine and autism.
- However, extensive reports from the American
Academy of Pediatrics, the National Academy of
Medicine and the Centers for Disease Control and
Prevention conclude that there is no scientifically proven
link between the MMR vaccine and autism. There is also
no scientific benefit to separating the vaccines.
Chicken Pox
- Giovanni Filippo (1500) was first discovered chicken
pox. Chickenpox is also known as varicella, a highly
contagious disease caused by the varicella-zoster virus
(VZV), a herpes virus varicillae that only pathogenic to
humans. The virus can be transmitted through airborne.
It can spread when an infected person coughs or sneezes.
It can also spread by direct contact with an infected
person's respiratory secretions, such as mucus. Indirect
contact with objects contaminated with secretions.
- Trans-placental transmission – It can also be passed on
from pregnant women to their unborn children via the
bloodstream. The incubation period is 10 to 21 days and
the period of communicability is 2 days before the
rashes appear until all vesicles have encrusted.
The clinical manifestations of measles
1) Pre-Eruptive Stage
• Fever
• Headache
• Sore throat
• Malaise
2) Eruptive Stage
- stage is exanthema (skin rashes) with vesiculopapular
rashes, centrifugal in distribution (outer to inner –
uncovered to covered) while centripetal in distribution
(inner to outer – covered to uncovered).
- The centrifugal in distribution of chicken pox
predominantly concentrated on face and extremities
with usual involvement of the palms and soles of the
feet going to the chest and abdomen. The chicken pox
is extremely pruritic because of the fluid inside the
vesicular form of rashes.
- It can cause an itchy, blister like rash. The rash
appears first on the chest, back, and face, and then
spreads over the entire body, causing between 250
and 500 itchy blisters.
- The five stages of rashes:
1) Macule - “flat”
2) Papule - “elevated”
3) Vesicle - “fluid-filled”
4) Pustule - “pus-filled”
5) Crust Scab - dry
- The celestial Map is a condition wherein all the stages
of chicken pox rash are simultaneously present.
3) Convalescent Stage
- Rashes disappear in the same manner as they appear
in the body. Aside from physical assessment, the
diagnostic tests are determination of V-Z virus
through: viral Isolation, microscopic examination of
vesicular fluid and viral serology. The complications
are skin infections such as erysipelas, cellulitis and
impetigo.
- Other complication such as pneumonia, encephalitis
and secondary bacterial infection can also occur with
chicken pox. The nursing interventions are
symptomatic and supportive.
- There are several things that the client can do at home
to help relieve chickenpox symptoms and prevent skin
infections. Calamine lotion and a cool bath with
added baking soda, uncooked oatmeal, or colloidal
oatmeal may help relieve some of the itching. Try to
minimize scratching to prevent the virus from
spreading to others and potential bacterial infection
from occurring. Keeping fingernails trimmed short
may help prevent skin infections caused by scratching
blisters. The medical management are antiviral as to
slow down vesicle formation and speed up skin
healing like Acyclovir or Zoverax, meaning acyclovir is
not a cure but only to hasten the acute stage. The
physician will also order for antipyretic: No NSAID or
do not use aspirin or aspirin-containing products to
relieve fever from chickenpox.
- The use of aspirin in children with chickenpox has
been associated with Reye’s syndrome, a severe
disease that affects the liver and brain and can cause
death. Instead, use non-aspirin medications, such as
acetaminophen, to relieve fever from chickenpox.
- The American Academy of Pediatrics recommends
avoiding treatment with ibuprofen if possible because
it has been associated with life-threatening bacterial
skin infections. Antihistamine, Calamine lotion and
Soda bath for pruritus.
- Being unvaccinated is much more likely to develop
Chicken Pox. The Centers for Disease Control and
Prevention recommends that children and adults
receive the Chicken Pox to prevent Chicken Pox. Live
Attenuated Varicella Vaccine for 2 doses at 1 month
apart (MMRV) Chickenpox can be serious, especially
in babies, adolescents, adults, pregnant women, and
people with a weakened immune system. The best
way to prevent chickenpox is to get the chickenpox
vaccine.
- Vaccinated people who get chickenpox may develop
lesions that do not crust. These people are
considered contagious until no new lesions have
appeared for 24 hours.
- The best way to prevent chickenpox is to get the
chickenpox vaccine. Everyone – including children,
adolescents, and adults – should get two doses of
chickenpox vaccine if they have never had chickenpox
or were never vaccinated. Chickenpox vaccine is very
safe and effective at preventing the disease.
- Most people who get the vaccine will not get
chickenpox. If a vaccinated person does get
chickenpox, the symptoms are usually milder with
fewer or no blisters (they may have just red spots) and
mild or no fever. The chickenpox vaccine prevents
almost all cases of severe illness.
Influenza/the flu/ La Grippe
 most common infectious diseases, is a highly
contagious droplet disease that occurs in seasonal
epidemics and manifests as an acute febrile illness
with variable degrees of systemic symptoms,
ranging from mild fatigue to respiratory failure and
death.
 causes significant loss of workdays, human
suffering, and mortality.
 In 1892, Dr. Richard Pfeiffer isolated an unknown
bacterium from the sputum of his sickest flu
patients, and he concluded that the bacteria caused
influenza. He called it Pfeiffer's bacillus, or
Haemophilus influenzae.
 caused by RNA viruses (Orthomyxoviridae family)
 Flu spreads directly and indirectly; directly from
person to person by droplets produced during
sneezing or coughing, for example, and indirectly
when contaminated droplets land on surfaces that are
subsequently touched by uninfected individuals. .
 The period of contagiousness is 3 to 5 days of illness
up to 7 days for the adult and children: up to 10 days
from the onset of symptoms.
 People with flu are most contagious in the first 3-4
days after their illness begins.
 Some otherwise healthy adults may be able to infect
others beginning 1 daybefore symptoms develop and
up to 5 to 7 days after becoming sick.
 The etiologic agent of influenza virus are A, B, C
and D.
 Human influenza A and B viruses cause seasonal
epidemics of disease (known as the flu season)
 Influenza A viruses are the only influenza viruses
known to cause flu pandemics, i.e., global epidemics
of flu disease.
 Influenza type C infections generally cause mild
illness and are not thought to cause human flu
epidemics.
 Influenza D viruses primarily affect cattle and are
not known to infect or cause illness in people.
 Influenza A is epidemic and pandemic cases.
 Influenza B is epidemic case and
 Influenza C is sporadic case.
- Influenza A viruses are divided into subtypes based on
two proteins on the surface of the virus: hemagglutinin
(H) andneuraminidase (N).
 The clinical manifestations of Influenza are
hyperpyrexia, chills, malaise, coryza, headache,
myalgia, sore throat and GI manifestations: nausea
and vomiting. Most people who get the conventional
or seasonal flu recover completely in 1-2 weeks, but
some people develop serious and potentially life-
threatening medical complications, such as
pneumonia, the most common and most dangerous.
 The diagnostic tests for influenza are nose and
throat
swab, viral culture, viral serology, WBC – decrease, and
RTPCR (Real Time Polymerase Chain Reaction) –
which the confirmatory test.
 The medical treatment for Influenza A:
 Amantadine HCl (Symmetrel)- prevention and
treatment of RTI caused by the virus,
 antibiotics for secondary infection or if with
pulmonary bacterial complication.
 AH1N1 can be given Oseltamivir (Tamiflu) and
Zanamivir (Relenza). Vaporizerreduce irritation
to respiratory mucosa. .
 The Nursing Mnagement are symptomatic and
supportive:
 Respiratory Isolations(droplet)
 Bed Rest: Limit strenuous activity
 Keep patient warm and free from drafts in bed
 Watch out for complication
 TSB
 Instruct patient to avoid crowded areas and close
contact with infected persons
COVID 19
- The coronavirus disease (COVID-19) is an infectious
disease caused by a newly discovered and a new strain
of coronavirus. This new virus and disease were
unknown before the outbreak began in Wuhan, China, in
December 2019. On 30 January 2020, the Philippine
Department of Health reported the first case of COVID-
19 in the country with a 38-year-old female Chinese
national. On 7 March, the first local transmission of
COVID-19 was confirmed.
- WHO is working closely with the Department of
Health in responding to the COVID-19 outbreak.
COVID-19 is caused by the SARS-CoV-2 virus. This
virus, which can cause mild to severe respiratory illness,
has spread globally, including the Philippines. There is
limited information available to fully describe the
different types of clinical illness associated with
COVID-19.
- This illness likely spreads to others when a person
shows signs or symptoms of being sick (e.g., fever,
coughing, difficulty breathing, etc.) or in the few days
leading up to symptoms.
- Most common symptoms: fever, dry cough, and
tiredness. Less common symptoms: aches and pains,
sore throat, diarrhea, conjunctivitis, headache, loss of
taste or smell, rash on skin, or discoloration of fingers or
toes. Serious symptoms: difficulty breathing or shortness
of breath, chest pain, and loss of speech or movement.
- Seek immediate medical attention if someone have
serious symptoms. Always call before visiting the doctor
or health facility. Most people infected with the COVID-
19 virus will experience mild to moderate respiratory
illness and recover without requiring special treatment.
Older people, and those with underlying medical
problems like cardiovascular disease, diabetes, chronic
respiratory disease, and cancer are more likely to
develop serious illness.
- The best way to prevent and slow down transmission is
be well informed about the COVID-19 virus, the disease
it causes and how it spreads. Protect yourself and others
from infection by washing the hands or using an alcohol
based rub frequently and not touching the face, primarily
the mouth, eyes and nose.
- The COVID-19 virus spreads primarily through
droplets of saliva or discharge from the nose when an
infected person coughs or sneezes, so it’s important that
you also practice respiratory etiquette (for example, by
coughing into a flexed elbow). Do not touch your mouth,
eyes and nose.
- COVID-19 affects different people in different ways.
Most infected people will develop mild to moderate
illness and recover without hospitalization. People with
mild symptoms who are otherwise healthy should
manage their symptoms at home. On average it takes 5–
6 days from when someone is infected with the virus for
symptoms to show, however it can take up to 14 days.
Different tests
1) COVID-19 (Coronavirus) Molecular (Swab) Test
(PCR) Polymerase Chain Reaction Test
- this test uses a long swab to collect material,
including physical pieces of coronavirus, from the
back of the nose where it meets the throat.
- A positive result indicates that viral genetic material is
present, but it does not indicate that bacterial or other
infections also are present.
- A negative result indicates that the SARS-CoV2 virus
that causes the COVID-19 disease was not found. It is
possible to have a very low level of the virus in the
body with a negative test result.
- This test is needed to identify the presence of the
SARS-CoV-2 virus that causes the COVID-19 disease.
2) COVID-19 (Coronavirus) Antibody (Serology) Test
(RDT) Rapid Diagnostic Test
- this is a blood test. It is designed to detect antibodies
(immunoglobulins, IgG and IgM) against the
coronavirus that causes the disease called COVID-19.
- Antibodies are proteins produced by the immune
system in response to an infection and are specific to
that particular infection.
- They are found in the liquid part of blood specimens,
which is called serum or plasma, depending on the
presence of clotting factors. IgM and IgG may either
be ordered together or separately.
- The difference between RDT and PCR, RDT just
detects the antibodies while PCR detects for the virus
itself that is why PCR is the confirmatory test.
- Having an antibody test is helpful if:
• health care provider believes that the patient may
have been exposed to the coronavirus which
causes COVID19 based on the current or previous
signs and symptoms (e.g., fever, cough, difficulty
breathing)
• live in or have recently traveled to a place where
transmission of COVID-19 is known to occur; (3)
have been in close contact with an individual
suspected of or confirmed to have COVID-19; and
(4) have recovered from COVID- 19.
- The Antibody Test for IgG (red line in graph)- this test
detects IgG antibodies that develop in most patients
within seven to 10 days after symptoms of COVID-19
begin. IgG antibodies remain in the blood after an
infection has passed.
- These antibodies indicate that the patient may have
had COVID-19 in the recent past and have developed
antibodies that may protect him from future infection.
- It is unknown at this point how much protection
antibodies might provide against re-infection. The
Antibody Test for IgM (green line in graph) - this test
detects IgM antibodies.
- IgM is usually the first antibody produced by the
immune system when a virus attacks. A positive IgM
test indicates that you may have been infected and
that the immune system has started responding to the
virus. When IgM is detected in the body may still be
infected, or may have recently recovered from a
COVID-19 infection.
- Meaning if IgM positive and IgG positive – the body is
making a long term antibodies but the virus still in the
body and infected. Need hospitalization.
- IgG positive and IgM negative – the body has
antibodies against SARS COV 2, there is already
immunity and not any more infectious.
- No need a confirmatory test and no need for
quarantine. IgM positive and IgG negative – if the
patient is positive in IgM, the patient is infected and
infectious, carrier of SARS Cov 2 and need isolation
for 2 weeks because of the chance of transmitting the
virus.
- Confirmatory test is advised. Contact tracing for those
people whom they meet along the way and be tested
and informed the LGU for the results.
- Igm negative and IgG negative – no virus in the body
and its too early for the body to produce antibodies
that RDT detects. Still even if negative result, practice
hand washing, put face mask, physical distancing and
boost the immune system and repeat the RDT after 7-
14 days.
- Antibody tests check your blood by looking for
antibodies, which may tell you if you had a past
infection with the virus that causes COVID-19.
Antibodies are proteins that help fight off infections
and can provide protection against getting that
disease again (immunity).
- Antibodies are disease specific. For example,
measles antibodies will protect you from getting
measles if you are exposed to it again, but they won’t
protect you from getting mumps if you are exposed to
mumps.
- Except in instances in which viral testing is delayed,
antibody tests should not be used to diagnose a
current COVID-19 infection. An antibody test may not
show if you have a current COVID-19 infection
because it can take 1–3 weeks after infection for your
body to make antibodies.
- At this time, there are no specific vaccines or
treatments for COVID-19. However, there are many
ongoing clinical trials evaluating potential treatments.
WHO will continue to provide updated information as
soon as clinical findings become available. There are
no drugs or other therapeutics presently approved by
the U.S. Food and Drug Administration (FDA) to
prevent or treat COVID-19.
- Current clinical management includes infection
prevention and control measures and supportive care,
including supplemental oxygen and mechanical
ventilatory support when indicated.
To prevent infection and to slow transmission of
COVID-19
• Wash your hands regularly with soap and water, or
clean them with alcohol-based hand rub.
• Maintain at least 1 meter distance between any
individual and people coughing or sneezing.
• Avoid touching the face.
• Cover the mouth and nose when coughing or sneezing.
• Stay home if feel unwell.
• (6). Refrain from smoking and other activities that
weaken the lungs.
• Practice physical distancing by avoiding unnecessary
travel and staying away from large groups of people.
• Boost the immune system by taking Vitamin C,
Vitamin D and Zinc and eat nutritious foods.
After the onslaught of COVID 19, the paradigm of the
“hew normal” in the public health sector has emerged.
At the core of it, the “New Normal” is a new way of
thinking about deciding on, and doing our usual affairs
with an invigorated sense to remain healthy by:
1) reducing the vulnerability by keeping a healthy
lifestyle
2) reducing virus transmission by observing infection
control measures
3) reducing contact with a potential disease carrier
4) reducing the duration of infection by establishing
effective disease management mechanism
5) ensuring governance and accountability by putting in
place strong health regulations and policies.
Ten Clinical Tips on COVID-19 for Healthcare
Providers
Involved in Patient Care.
Treatment and Prophylaxis:
• The National Institutes of Health has developed
guidance on treatment which will be regularly
updated as new evidence on the safety and efficacy of
drugs and therapeutics emerges from clinical trials
and research publications.
• There is currently no FDA-approved post-exposure
prophylaxis for people who may have been exposed to
SARSCoV- 2.
Symptoms and Diagnosis
• Non-respiratory symptoms of COVID-19 – such as
gastrointestinal symptoms (e.g., nausea, vomiting,
diarrhea), or neurologic symptoms (e.g., anosmia,
ageusia, headache), or fatigue or body and muscle
aches – may appear before fever and lower respiratory
tract symptoms (e.g., cough and shortness of breath).
• Children with COVID-19 may have fewer symptoms
than adults. Although most children with COVID-19
have not had severe illness, clinicians should
maintain a high index of suspicion for SARSCoV-2
infection in children, particularly infants and children
with underlying medical conditions. CDC is
investigating multisystem inflammatory syndrome in
children, a rare but serious complication associated
with COVID-19. CDC recommends monitoring
children for worsening of COVID-19 illness.
• CT scan should not be used to screen for COVID-19 or
as a first-line test to diagnose COVID-19. CT scans
should be used sparingly and reserved for
hospitalized, symptomatic patients with specific
clinical indications for CT scans.
Co-Infections:
• Patients can be infected with more than one virus at
the same time. Co-infections with other respiratory
viruses in people with COVID-19 have been reported.
Therefore, identifying infection with one respiratory
virus does not exclude SARS-CoV-2 virus infection.
• Several patients with COVID- 19 have been reported
presenting with concurrent community-acquired
bacterial pneumonia. Decisions to administer
antibiotics to COVID-19 patients should be based on
the likelihood of bacterial infection
(communityassociated or healthcare-associated), illness
severity,
and current clinical practice guidelines.
Severe Illness:
• Clinicians should be aware of the potential for some
patients to rapidly deteriorate 1 week after illness
onset.
• The median time to acute respiratory distress
syndrome (ARDS) ranges from 8 to 12 days.
• Lymphopenia, neutrophilia, elevated serum alanine
aminotransferase and aspartate aminotransferase
levels, elevated lactate dehydrogenase, high CRP, and
high ferritin levels may be associated with greater
illness severity.
 The Philippines started classifying coronavirus
disease 2019 (COVID-19) cases as either Patients
under Investigation (PUIs) or Persons under
Monitoring (PUMs). However, due to apparent local
or community transmission of the virus and the
surge in cases, the
 Department of Health (DoH) has decided to shift
from classifying individuals as PUIs or PUMs to
using case definitions following guidelines from the
World Health Organization (WHO).
 PUM is one who may have been exposed to the
virus but shows no symptoms — is no longer
included in the new classification, as residents are
assumed to have been
 exposed due to local transmission.
 A PUI (mild, severe or critical) who was not tested
or awaiting test results is now classified as Suspect,
while a PUI (mild, severe or critical) with
inconclusive test results is considered a Probable
case. A COVID Positive case is now referred to as
Confirmed.
Suspect Case
a) Individuals with influenza-like illness (ILI).
Symptoms include fever of at least 38°C and cough or
sore throat, and either of the following:
• a history of travel to or residence in an area that
reported local transmission of COVID-19 during the
14 days prior to symptom onset
• with contact to a confirmed or probable case of
COVID-19 during the 14 days prior to symptom onset.
b) Individuals with sudden respiratory infection and
severe symptoms such as shortness of breath, difficulty
of breathing or severe pneumonia with unknown cause,
and requires hospitalization.
c) Individuals with fever or cough or shortness of breath
or other respiratory signs or symptoms and under any of
the following conditions:
• aged 60 years and above
• with a co-morbidity
• assessed as having high-risk pregnancy, or (4) a
health worker.
Probable Case
a. Suspect case whom testing for COVID-19 is
inconclusive.
b. Suspect case who tested positive for COVID-19 but
whose test was not conducted in a national or sub-
national reference laboratory, or an officially
accredited laboratory.
Confirmed Case
a) Any individual who was laboratory-confirmed for
COVID19 through RT-PCR in a national or subnational
reference laboratory, or a DoH-certified laboratory
testing facility.
PTB, PNEUMONIA, DIPHTHERIA, PERTUSIS,
MUMPS
Pneumonia
 An Inflammation of the lung parenchyma with the
production of alveolar exudates resulting to
consolidation of the air sacs. It is an infection that
inflames the air sacs in one or both lungs.
 The air sacs may fill with fluid or pus (purulent
material), causing cough with phlegm or pus, fever,
chills, and difficulty breathing.
 Cause bacteria, viruses and fungi,
 most serious for infants and young children, people
older than
 age 65, and people with health problems or
weakened immune systems.
 Edwin Klebs was the first to observe bacteria in the
airways of persons having died of pneumonia in
1875.
 The etiologic agents of pneumonia – Streptococcus
pneumonia, Haemophilus influenza, Staphylococcus
aureus, Klebsiella pneumoniae (Friedlander’s
bacilli), Mycoplasma pneumonia.
 Mode Of Transmissions - droplet transmission –
mouth & nose of an infected person via
nasopharynx, through intimate contact w/ carriers,
indirect contact contaminated objects and Systemic
infection through inhalation of caustic or toxic
chemicals, aspiration of food, fluid, and vomitus
 The incubation period is 1 to 3 days. The period of
communicability is not specified.
The Classification according to where & how the
client is exposed to the disease:
1. Community-acquired PNM
 Acquired in the course of one’s daily life; at work, at
school or at the gym. Hospitalized patient developed
 PNM in <36 hours during his stay in hospital.
 most common type of pneumonia.
 occurs outside of hospitals or other health care
facilities.
 Streptococcus pneumonia- most common cause of
bacterial pneumonia in the U.S. and in the
Philippines
 can occur on its own or after you've had a cold or the
flu.
 It may affect one part of the lung, a condition called
lobar pneumonia.
 Bacteria-like organisms –
 Mycoplasma pneumoniae
 produces milder symptoms than do other types of
pneumonia.
 Walking pneumonia is an informal name, which
typically isn't severe enough to require bed rest.
 Fungi -
 most common in people with chronic health
problems or weakened immune systems, and in
people who have inhaled large doses of the
organisms.
 can be found in soil or bird droppings and vary
 depending upon geographic location.
 Viruses - including COVID-19
 Viruses are the most common cause of pneumonia in
 children younger than 5 years.
 is usually mild.
 Coronavirus 2019 (COVID-19) may cause
pneumonia, which can become severe.
2. Hospital acquired pneumonia
 Develops while client is in the hospital;
 reflects the kind of nursing care is given to the
patient.
 more than 36 hours of hospital stay.
 can be serious because the bacteria causing it may be
more resistant to antibiotics and because the people
who get it are already sick.
 People who are on breathing machines (ventilators),
often used in intensive care units, are at higher risk
3. Health care-acquired pneumonia
 occurs in people who live in long-term care facilities
or who receive care in outpatient clinics, including
kidney dialysis centers.
4. Aspiration pneumonia
 occurs when you inhale food, drink, vomit or saliva
into your lungs.
 if something disturbs your normal gag reflex, such
as a brain injury or swallowing problem, or
excessive use of alcohol or drugs.
The Anatomical Classifications:
 Bronchopneumonia (Lobular or Catarrhal PNM) -
most common type; infection usually start from
bronchus & bronchioles & spread to alveoli of
periphery; lobules inflamed & consolidated and
caused by: Pneumococcus, Klebsiella pneumoniae,
H. influenza.
 Lobar PNM (Croupous Pneumonia) -
consolidation of entire lobe; as disease progresses,
prune juice color of sputum replaced by thinner or
yellowish color.
 Primary Atypical Pneumonia (Virus Pneumonia) -
solidification of lung that comes in patches.
The General Classification of Pneumonia
 Primary – direct result of inhalation or aspiration of
 pathogen or noxious substances;
 Secondary – develops as complication to a disease.
Sign and symptoms
 vary from mild to severe, depending on factors such
as the type of germ causing the infection, and your
age and overall health.
 Mild signs and symptoms often are similar to those
of a cold or flu, but they last longer.
 Chills with rising fever lower than normal body
temperature (in adults older than age 65 and people
with weak immune systems),
 Chest pain (stabbing), Cough (paroxysmal and
 choking) which may produce phlegm,
 Rusty or prune juice sputum- pathognomonic sign,
 Abdominal pain, Confusion or changes in mental
awareness (in adults age 65 and older), Fatigue,
Nausea, vomiting or diarrhea, flaring of nares,
labored respirations, rapid and bounding pulse,
diaphoresis.
 Newborns and infants may not show any sign of the
infection. Or they may vomit, have a fever and
cough, appear restless or tired and without energy, or
have difficulty breathing and eating.
 The single most important symptom in the diagnosis
of pneumonia is fast breathing.
 See the doctor if the client is having difficulty
breathing, chest pain, persistent fever of 102 F (39
C) or higher, or persistent cough, especially if
coughing up with pus.
The diagnostic tests
 Chest X-ray – confirmatory diagnostic exam,
sputum analysis, sputum smear and culture and
blood serologic examinations.
 The doctor will start by asking about your
medical history and doing a physical exam,
including listening to your lungs with a stethoscope
to check for abnormal bubbling or crackling sounds
that suggest pneumonia.
If pneumonia is suspected, your doctor may
recommend the following tests:
 Blood tests are used to confirm an infection and to
try to identify the type of organism causing the
infection.
 Pulse oximetry measures the oxygen level in the
blood. Pneumonia can prevent the lungs from
moving enough oxygen into the bloodstream.
 Sputum test - a sample of secretions is taken after a
deep cough and analyzed to help pinpoint the cause
of the infection.
 CT scan.- for older than 65 If the pneumonia isn't
clearing as quickly as expected, the doctor may
recommend a chest CT scan to obtain a more
detailed image of the lungs.
 Pleural fluid culture - a fluid sample is taken by
putting a needle between the ribs from the pleural
area and analyzed to help determine the type of
infection. It's especially important that people in
these high-risk groups see a doctor: (1) Adults older
than age 65; (2) Children younger than age 2 with
signs and symptoms; (3) People with an underlying
health condition or weakened immune system; (4)
People receiving chemotherapy or taking
medication that suppresses the immune system.
The medical management
 Pen G Na: Drug of Choice with alternative of
Clotrimoxazole, Tetracycline and Erythromycin,
Bronchodilators (aminophylline, salbutamol),
 Expectorants, Analgesics for pleuritic pain,
 Absolute bed rest, Humidified 02 for hypoxia,
Mechanical ventilation – resp. failure.
 Klebsiela – Aminoglycosides and Cephalosporins;
 Streptococcus – Nfcillin or Oxacillin for 14 days;
 Pneumonitis carinii – Cotrimoxazole.
The nursing management
 isolation, increase oral fluid intake may help liquefy
 secretions in order to help expectorate easily, chest
 physiotherapy, deep breathing coughing and turning
 exercise (DBCTE), elevate head & shoulders of
patient by means of pillow to relieve labored
breathing & lessen
 coughing and suction secretion when necessary.
 Children may be hospitalized if:
 they are younger than age 2 months;
 they are lethargic or excessively sleepy;
 they have trouble breathing;
 they have low blood oxygen levels; and
 they appear dehydrated.
 may experience complications, including:
 Bacteria in the bloodstream (bacteremia).
 Fluid accumulation around the lungs (pleural
effusion). .
 Lung abscess. An abscess occurs if pus forms in a
cavity in the lung. An abscess is usually treated with
antibiotics.
To help prevent pneumonia:
 Get vaccinated.
 Doctors recommend a different pneumonia vaccine
for children younger than age 2 and for children ages
2 to 5 years who are at particular risk of
pneumococcal disease
 Doctors also recommend flu shots for children older
than 6 months.
 Practice good hygiene.
 Don't smoke. Smoking damages your lungs' natural
defenses against respiratory infections.
 Keep your immune system strong. Get enough
sleep, exercise regularly and eat a healthy diet.
Diphtheria
 serious bacterial infection that usually affects the
mucous membranes of the nose and throat.
 Endemic in many countries in Asia, the South
Pacific, the Middle East, Eastern Europe and in Haiti
and the Dominican Republic.
 extremely rare in the United States and other
developed countries,
 can be treated with medications.
 in advanced stages, it can damage the heart, kidneys
and nervous system.
 Even with treatment, diphtheria can be deadly,
especially in children.
 Emil Adolf Behring who was a German
physiologist who first discovered a diphtheria
antitoxin
 Pathognomonic sign a wound marked by a patch or
patches of grayish membrane from which diphtheria
bacillus is readily cultured.
 Diphtheria is caused by the bacterium
Corynebacterium diphtheria (Klebs-loeffler
bacillus). The bacterium usually multiplies on or
near the surface of the throat.
 spreads via droplets. Indirect contact with
contaminated personal or household items can also
be transmitted the bacteria.
 People occasionally catch diphtheria from handling
an infected person's things, touching an infected
wound.
 The incubation period is 2 – 5 days, occasionally
longer and the period of communicability is 2 weeks
and seldom more than 4 weeks.
People who are at increased risk of contracting
diphtheria
 Children and adults who don't have up-to-date
vaccinations;
 People living in crowded or unsanitary conditions,
anyone who travels to an area where diphtheria
infections are more common;
Types Of Diphtheria:
1. Respiratory
 Nasal – localized in the nares; excoriation of the
upper lip and alae nasi with serosanguinous
secretions which later becomes bloody and foul
smelling.
 Pharyngeal or faucial – pharynx (tonsilar, uvular,
palatar) low grade fever; malaise; headache and sore
throat; pseudomembrane very visible within 24 hrs.
 Pseudomembrane is a false membrane, a grayish,
white color and leathery in consistency and irregular
in shape, usually inflamed which decreases the
opening of the
 Nasopharynx; bull neck – a swollen glands
(enlarged lymph nodes) in the neck; difficulty
breathing or rapid breathing.
 Laryngotracheal - more common in infants;
presence of laryngeal stridor; hoarseness of voice
and some signs of respiratory distress. In some
people, infection with
SKin
2. Skin (cutaneous) diphtheria is a second type of
diphtheria can affect the skin, causing pain, redness and
swelling similar to other bacterial skin infections. Ulcers
covered by a gray membrane conditions..
The diagnostic examinations
 are nose and throat culture to detect the etiologic
agent.
 Schick’s test – determines susceptibility and
immunity to diphtheria while
 moloney test – determines hypersensitivity to
diphtheria toxoid.
 medical management
 are antibiotics
 Penicillin – is the drug of choice and
 Erythromycin as alternative if allergy to penicillin.
 Passive immunization diphtheria antitoxin and
tracheostomy if laryngeal for infant and children are
present.
The nursing management
 Strict isolate the patient (droplet), provide liquid and
soft diet, maintain good oral hygiene and proper
airway, complete bed rest, pasteurization of milk, ice
collar for neck spasms and monitor for respiratory
distress.
 Call the family doctor immediately or go to the
nearest hospital if the child has been exposed to
someone with diphtheria.
 If not sure whether the child has been vaccinated
against diphtheria, schedule an appointment.
 Make sure that the child own vaccinations are
current.
Left untreated, diphtheria can lead to:
 Breathing Problems such as bronchopneumonia
since diphtheria-causing bacteria may produce a
toxin. This toxin damages tissue in the immediate
area of infection usually, the nose and throat.
 Heart damage - the diphtheria toxin may spread
through the bloodstream and damage other tissues in
the body, such as the heart muscle, causing such
complications as inflammation of the heart muscle
(myocarditis).
 Nephritis
 Nerve damage that can cause peripheral neuritis -
the toxin can also cause nerve damage.
 Diphtheria is fatal 5% to 10% of the time, according
to the World Health Organization. Rates of death are
higher in children.
Vaccine
 is usually combined with vaccines for tetanus and
whooping cough (pertusis).
 The three-inone vaccine is known as the diphtheria,
tetanus and pertusis vaccine.
 DTaP –
 The latest version of this vaccine vaccine for
adolescents and adults.
 is one of the childhood immunizations that doctors
in the United States recommend during infancy.
- In the Philippines, immunization of DPT in an early
age is encouraged.
- series of five shots, typically administered in the arm or
thigh, given to children at these ages: 2 months; 4
months; 6 months; 15 to 18 months and 4 to 6 years.
 Side Effect - mild fever, fussiness, drowsiness or
tenderness at the injection site after a DTaP shot.
 Some children such as those with epilepsy or
another nervous system condition may not be
candidates for the DTaP vaccine.
 immunity to diphtheria fades with time.
 Children who received all of the recommended
immunizations before age 7 should receive their first
booster shot at around age 11 or 12.
 The next booster shot is recommended 10 years
later, then repeated at 10-year intervals.
 The diphtheria booster is combined with the tetanus
booster — the tetanusdiphtheria (Td) vaccine. This
combination vaccine is given by injection, usually
into the arm or thigh.
 Tdap is a combined tetanus, diphtheria and acellular
pertussis (whooping cough) vaccine. It's a one-time
alternative vaccine for adolescents ages 11 through
18 and adults who haven't previously had a Tdap
booster.
 It's also recommended once during pregnancy,
regardless of previous vaccinations.
Pertusis/ Whooping cough
 can cause serious illness in babies, children, teens,
and adults. Symptoms of pertusis usually develop
within 5 to 10 days after you are exposed.
Sometimes pertussis symptoms do not develop for as
long as 3 weeks.
 entrance of air in the epiglottis
 is an acute contagious disease characterized by
intermittent episodes of paroxysmal cough followed
by an explosive expiration ending in an inspiratory
“whoop” and ending in vomiting (5-10x in
succession repeated 20-40x in a day).
 was considered a childhood disease.
 Deaths associated with whooping cough are rare but
most commonly occur in infants.
 Jules Bordet (1906) – discovered pertusis and
 Octave Gengou - developed the first serology and
vaccine of pertusis.
 The causative agent are Haemophillus pertusis,
Bordet Gnegou Bacillus or Bordetella pertussis
which is a Gram (-) coccobacilli.
 Mode of Transmission easily from person to person
mainly through droplets produced by coughing or
sneezing and indirect contact with contaminated
object.
 The disease is most dangerous in infants, and is a
significant cause of disease and death in this age
group.
 The first symptoms generally appear 7 to 14 days
after infection which is the incubation period.
The clinical manifestations are:
1. Catarrhal Stage–
most communicable stage even until 3 weeks or up
to 21 days after the onset of paroxysmal stage with
frequent sneezing, watery secretions, coryza and dry
and hacking cough increasing in intensity at night.
2. Paroxysmal Stage– most fatal stage with
intermittent episodes of paroxysmal cough followed
by an explosive expiration ending in an inspiratory
“whoop” and ending in vomiting (5-10x in
succession repeated 20-40x in a day) and cough
worsen. Force of coughing may cause involuntary
micturation / defection, intracerebral hemorrhage
and abdominal hernia, popping of eyeball and
protrusion of tongue and vomiting signals end of
attack.
3. Convalescent Stage when frequency of attacks is
reduced. The incidence in infants is highly
susceptible and single attack usually produces
lifetime immunity. People with pertusis are most
contagious up to about 3 weeks after the cough
begins, and many children who contract the infection
have coughing spells that last 4 to 8 weeks.
Brochopneumonia, hernia and hemorrhages are
relatively common complications, and seizures and
brain disease occur rarely. Because infants and
toddlers are at greatest risk of complications from
whooping cough, they're more likely to need
treatment in a hospital. Complications can be life-
threatening for infants younger than 6 months old.
Teens and adults often recover from whooping
cough with no problems. When complications occur,
they tend to be side effects of the strenuous
coughing, such as: bruised or cracked ribs,
abdominal hernias broken blood vessels in the skin
or the whites of the eyes.
Healthcare providers diagnose
by considering if you have been exposed to
pertussis and by doing a:
 History of typical signs and symptoms,
 Physical examination,
 Laboratory test which involves taking a sample of
mucus (with a swab or syringe filled with saline)
from the back of the throat through the nose —
cough plate or agar plate or Bordet – Gengou test.
 Obtaining a nasopharyngeal specimen for isolation
of Bordetella pertussis.
Healthcare providers generally treat pertusis with
antibiotics
 Ampicillin, erythromycin (DOC) – given for 5 to 7
days and anti-tussives: sinecod – for extremely dry
cough and early treatment is very important.
 Treatment may make the infection less serious if the
patient start it early, before coughing fits begin.
 Treatment can also help prevent spreading the
disease to close contacts
 Treatment after three weeks of illness is unlikely to
help.
The nursing management
 Bed rest;
 NPO in attacks (paroxysmal and catarrhal stage –
aspiration;
 Positioning – prone for infants and upright for older
persons;
 Isolate the patient;
 Provide a quiet, non-stimulating environment;
 Keep patient warm and out of wind;
 Small frequent feedings;
 Encourage abdominal support when coughing;
 Clothing contaminated with discharges should be
boiled for 30 minutes before laundering; and
 Adequate ventilation.
 The best way to prevent whooping cough is with the
pertusis vaccine, which doctors often give in
combination with vaccines against two other serious
diseases — diphtheria and tetanus.
 . The vaccine consists of a series of five injections,
typically given to children at these ages: 2 months, 4
months, 6 months, 15 to 18 months and 4 to 6 years.
If the child gets treatment for pertusis at home:
 Do not give cough medications unless instructed by
the doctor. Giving cough medicine probably will not
help and is often not recommended for kids younger
than 4 years old.
 Manage pertusis and reduce the risk of spreading it
to others by:
 Following the schedule for giving antibiotics exactly
as the child’s doctor prescribed.
 Keeping the home free from irritants –
 Using a clean, cool mist vaporizer to help loosen
 mucus and soothe the cough.
 Practicing good hand washing.
 Encouraging the child to drink plenty of fluids,
 including water, juices, and soups, and eating fruits
to prevent dehydration (lack of fluids). Report any
signs of dehydration to the doctor immediately.
 Encouraging the child to eat small meals every few
 hours to help prevent vomiting (throwing up) from
occurring.
Pulmonary Tuberculosis
 active infection of the lungs (latin pulmo = lung).
 It is the most important TB infection, because an
infection of the lungs is highly contagious due to the
mode of airborne transmission.
 It can be life-threatening to the patient: if left
untreated, more than 50% of patients with
pulmonary tuberculosis die.
 Worldwide, 87% of all tuberculosis cases that were
reported in 2004 were either only pulmonary TB or
included pulmonary TB.
 spread widely as an epidemic during the 18th and
19th centuries in North America and Europe.
 Tuberculosisis considered as the world’s deadliest
disease and remains as a major public health
problem in the Philippines and is a chronic bacterial
infection characterized by granuloma formation,
necrosis and calcification of involved tissues.
 Other names Koch’s Disease, Consumption and
Phthisis.
 Robert Koch (1882) - a German physician and
scientist, discovered of Mycobacterium tuberculosis,
the bacterium that causes tuberculosis (TB).
 The bacterium Mycobacterium tuberculosis
causes tuberculosis (TB), a contagious, airborne
infection that destroys body tissue. Direct invasion
through mucous membranes or breaks in the skin
may occur, but extremely RARE.
 occurs when M. tuberculosis primarily attacks the
lungs.
 curable with an early diagnosis and antibiotic
treatment.
 Other Etiologic Agent - Mycobacterium africanum,
Mycobacterium bovis and Mycobacterium cannettii.
 Bovine tuberculosis results from exposure to
tuberculosis cattle: Ingestion of unpasteurized milk
or dairy products.
 The incubation period is 2 to 10 weeks. The period
of communicability is in the active phase of the
patient. The factors affecting the communicability
are (1) number of bacilli discharge; (2) bacilli
virulence; (3) adequate ventilation; and (4) exposure
of bacilli to sun and UV lights.
The classification of PTB as
a. Class 0 – no exposure, no infection;
b. Class 1 – (+) exposure, (-) infection;
c. Class 2 – (+) infection, (-) disease;
d. Class 3 – (+) symptoms, PTB active
e. Class 4 – disease, not clinically active; and
f. Class 5 –diagnosis pending; suspect.
The clinical manifestations of PTB
 Fever – low grade in late afternoon or early evening;
 chronic cough of more than 2 weeks,
 anorexia,
 body malaise and
 weight loss,
 nocturnal sweating,
 chest and back pains,
 dyspnea,
 hoarseness of voice,
 hemoptysis
 sputum positive for AFB.
 During the examination, the doctor will conduct a
physical exam especially the lungs, ask about the
medical history, schedule a chest X-ray, order a
medical test to confirm pulmonary TB.
The diagnostic tests
• Mantoux Test/ PPD/ Tuberculin Test – an
intradermal injection of PPD (Purified Protein
Derivatives to detedt for exposure; results are read after
48-72 hours of injection; (+) for not
immunocompromised is 10 mm or more induration; and
(+) for immunocompromised is 5 mm or more
induration.
 Direct Sputum Smear Microscopy is a primary
diagnostic tool.
 Chest X-Ray determines the lesion.
 Sputum Culture or Sputum analysis for AFB is a
confirmatory test.
 Gene Xpert diagnoses TB by detecting the presence
of TB bacteria, as well as testing for resistance to the
drug Rifampicin.
 The tine test is a multiple-puncture tuberculin skin
test used to aid in the medical diagnosis of
tuberculosis (TB
 To diagnose pulmonary TB specifically,
 doctor will ask a person to perform a strong cough
and produce sputum up to three separate times.
Treatment
 Isoniazid with common side effect of peripheral
neuritis and hepatotoxicity,
 pyrazinamide with common side effect of gouty
arthritis and hyperurecemia,
 ethambutol (Myambutol) with side effect of optic
neuritis,
 rifampin (Rifadin) with side effects of
hepatotoxicity, nephrotoxicity, purpura and orange
colored secretions and streptomycin with side effect
of vestibular ototoxicity.
 The doctor might recommend an approach called
directly observed therapy (DOT) to ensure that
complete treatment is encouraged and no failures.
 Stopping treatment or skipping doses can make
 pulmonary TB resistant to medicines, leading to
MDR-TB.
 (MDR-TB) is TB that is resistant to the typical
antibiotics used to treat the condition, which are
isoniazid and rifampin. Some of the factors that
contribute to MDR-TB include:
 Healthcare providers prescribing an incorrect drug to
treat TB;
 people stopping treatment early;
 people taking poor-quality medications;
 Improper prescribing is the leading cause of MDR-
TB, according to WHO.
 Most cases of pulmonary TB are post-primary TB
infections.
 People with pulmonary TB cough a lot, because the
destruction of tissue in the lungs and airways leads to
inflammation. The body reacts to inflammation by trying
to the particle that caused it – if this happens in
the airway, the easiest way to eliminate the cause is to
cough it up.
 Initially, people with pulmonary TB have a dry,
persistent cough.
 This cough is often worse at night. This symptom
shows in about 85% of people with pulmonary TB.
inflammation in the airway.
 The risk for getting pulmonary TB is highest for
people who are in close contact with those who have
TB.
 This includes being around family or friends with
TB or working in places such as the following that
often house people with TB:
 correctional facilities;
 nursing homes;
 hospitals;
 shelters.
 People also at risk for developing pulmonary TB
disease are:
 older adults;
 small children;
 people who smoke;
 people with an autoimmune disorder
 people with lifelong conditions, such as diabetes or
kidney disease;
 people who inject drugs;
 people who are immunocompromised
The nursing management
 Isolation precaution;
 Provide patient with adequate rest periods;
 Promote adequate nutrition;
 Advise to cover nose and mouth when sneezing and
coughing and dispose secretions properly;
 Provide frequent oral hygiene and hand washing;
 Encourage to stop smoking;
 Be alert for signs of drug reaction;
 Monitor drug compliance;
 Teach the patient all about PTB;
 encourage questions to air feelings;
 Emphasize the importance of follow-up;
 Check sputum for blood and purulent expectoration.
The common preventive measures
 Submit all babies for BCG immunization;
 Avoid overcrowding and mode of transmission;
 Nutritional and health status improvement;
 Advise those who have been exposed to receive
tuberculin test.
Mumps
 a viral infection that primarily affects
salivaproducing (salivary) glands that are located
near your ears.
 is caused by a Paramyxovirus, a virus that spreads
easily from person to person through infected saliva
as a source of infection.
 can cause swelling in one or both of these glands.
 was common in the United States until mumps
vaccination became routine.
 Claud D. Johnson&Ernest W. Goodpasture1934-
found the viral etiology of mumps was finally
 discovered and documented by
 Other names - Viral Parotitis, Epidemic Parotitis and
Infectious Parotitis.
 The incubation period is 14 to 25 days and the
period of communicability is 7 days before and 9
days after the onset of parotid swelling. When signs
and symptoms do develop, they usually appear about
two to three weeks after exposure to the virus.
 The primary sign of mumps is swollen salivary
glands that cause the cheeks to puff out due to
blocked salivary gland.
 Other signs and symptoms may include:
• Pain in the swollen salivary glands on one or both
sides of the face;
• Pain while chewing or swallowing;
• Low-grade fever;
• Headache;
• Earache;
• Muscle aches;
• Weakness and fatigue;
• Loss of appetite; and
• Dysphagia.
 The diagnostic tests are: Viral Isolation,
Blood Exam, Viral Serology and Serum Amylase
Determination Test.
- The mode of transmissions are
direct contact with respiratory secretions coming
from infected patients and indirect contact with
objects contaminated with secretions.
Complications of mumps
 Orchitis which is the most dreaded complication in
males;
 Oophoritis which is the most dreaded in females;
mastitis; pancreatitis; myocarditis and hearing loss,
are potentially serious but rare.
 Try to ease symptoms with cold compresses and
overthe-counter pain relievers such as ibuprofen
(Advil, Motrin IB, others) and acetaminophen
(Tylenol, others).
The best way to prevent mumps
• To be vaccinated against the disease.
The mumps vaccine is usually given as a combined
measlesmumps-rubella (MMR) inoculation,
 Two doses of the MMR vaccine are recommended
before a child enters school. Those vaccines
 should be given when the child is: between the ages
of 12 and 15 months; and between the ages of 4 and
6 years.
 A study of a recent mumps outbreak on a college
campus showed that students who received a third
dose of MMR vaccine had a much lower risk of
contracting the disease.
 The patient don't need the MMR a vaccination if:
 Had two doses of the MMR vaccine after 12 months
of age
 Had one dose of MMR after 12 months of age and
you're a preschool child or an adult who isn't at high
risk of measles or mumps exposure;
 Have blood tests that demonstrate the immunity to
measles, mumps and rubella;
 Were born before 1957 — most people in that age
group were likely infected by the virus naturally and
have immunity;
 Also, the vaccine isn't recommended for: people
who have had a life-threatening allergic reaction to
the antibiotic neomycin or any other component of
the MMR vaccine; pregnant women or women who
plan to get pregnant within the next four weeks;
people with severely compromised immune systems.
 Some people experience a mild fever or rash or achy
joints for a short time. Rarely, children who get the
MMR vaccine might experience a seizure caused by
fever.