Bleeding Disorders

Semifinals Notes

Hemostasis phospholipid (formerly

known as factor IV)
an intricate balance between clot formation and clot V (proaccelerin, labile Co-factor of X with
dissolution factor) which it forms the
prothrombinase complex
Primary hemostatic mechanisms: VI Unassigned - old name
1. vascular changes of Factor Va
2. platelet plug formation VII (stable factor) Pro Convertin - Activates
IX, X
Secondary hemostatic mechanism VIII (Anti Hemophilic Co-factor of IX with
factor A) which it forms the
3. coagulation / clot formation tenase complex
IX (Anti Hemophilic Factor Activates X: forms
I. Vascular abnormalities B or Christmas factor) tenase complex with
= local bleeding factor VIII
X (Stuart-Prower factor) Activates Il: forms
II. Platelet or coagulation factor prothrombinase complex
abnormalities with factor V
= bleeding anywhere XI (plasma thromboplastin Activates IX
antecedent)
a. platelet defects: petechiae on skin and mucous XII (Hageman factor) Activates factor XI, VII
membranes and prekallikrein
b. coagulation factor defects: bleeding occurs XIII (fibrin-stabilizing Activate Wit Go to PC
deeper (hematomas, hemarthroses) factor) settingCrosslinks fibrin
von Willebrand factor Binds to VIII, mediates
platelet adhesion
Clotting Factors

Factor I Fibrinogen Immune (Idiopathic) Thrombocytopenic

Factor II Prothrombin Purpura
Factor III Tissue Thromboplastin
Factor IV Calcium lons An autoimmune bleeding disorder characterized by the
Factor V Labile Factor development of autoantibodies to one’s own platelets
Factor VII Stable Factor leading to the destruction of platelets
Factor VIII Antihemophilic Factor
TYPES:
Factor IX Christmas Factor, or
Plasma Thromboplastin A. Acute ITP – common in children after a viral
Component (PTC) illness; remission in 6 mos
Factor X Stuart-Prower Factor B. Chronic ITP – adults
Factor XI Plasma Thromboplastin
CAUSES:
Factor XII Antecedent (PTA)
o Precise cause unknown
o Preceded by viral infections
Coagulation factors and related substances
o Sulfa drugs o SLE
o pregnancy
I (fibrinogen) Forms clot (fibrin)
II (prothrombin) Its active form (lla) What happens in ITP?
activates I, V, VII, VIII, Antiplatelet antibodies bind to pt’s platelets’s membrane
XI, XIII, protein C,
platelets
Tissue factor Co-factor of Vlla
(formerly known as Macrophages ingest the platelets
factor II)
Calcium Required for coagulation
factors to bind to Decreased no. of platelets
Bleeding Disorders
Semifinals Notes

CLINICAL MANIFESTATION 3. Vincristine (Oncovin) – block receptors on

➢Easy bruising macrophages; stimulates thrombopoiesis
➢Heavy menses
4. Anti-D (WinRho)
➢Petechiae
-For Rh D (+) patients; unknown mechanism
➢Dry purpura:
- theory: Anti-D binds to RBCs ➔ destroyed by
•Simple bruising or petechiae
macrophages ➔ receptors in RES becomes saturated w/
•Fewer complications
sensitized RBCs ➔ ↓ removal of antibody-coated plt
➢Wet purpura:
•Bleeding from mucosal surfaces (GIT,
5. For chronic ITP: Romiplostin (N plate) – a
pulmonary)
thrombopoeisisstimulating protein
•Greater risk for intracranial bleeding
6. Aminocaproic Acid (fibrinolytic enzyme inhibitor) -Slows
the dissolution of clots -- for patients w/ mucosal bleeding
refractory to other treatments

Note: Transfusion is avoided.

ASSESSMENT & DIAGNOSTIC FINDINGS
➢Decreased platelet count (<20,000/mm3)
➢Increased megakaryocytes upon
➢Correlation of ITP and Helicobacter pylori
NURSING MANAGEMENT
1. Assess pt’s lifestyle to determine the risk of bleeding
2. use of OTC medications, herbs, and nutritional
supplements
3. Be alert of sulfa-containing medications and other
meds that alter platelet function (aspirin based, NSAIDs)
4. Assess for history of:
- recent viral illness
- Headache & visual disturbances (s/s of
intracranial bleeding)
5. neurologic assessment
BMA 6. Avoid injections or rectal meds; rectal temperature
measurements

MEDICAL MANAGEMENT PATIENT TEACHING

•primary goal of treatment: a “safe” platelet 1. Signs of exacerbation
count (  30,000/mm3) 2. How to contact health personnel
•platelet count <10,000/mm3 = risk for bleeding 3. ITP inducing meds
•30,000 – 50,000/mm3 = observed closely 4. Current medical treatment (meds, tapering, S/E)
•Stop quinine, sulfa-containing medications 5. Frequency of Plt monitoring
•Immunosuppressive agents: block the binding 6. should avoid:
receptors on macrophages - constipation
-Prednisone - Valsalva maneuver
-Dexamethasone (Decadron) - vigorous flossing
–Azathioprine(Immuran) 7. Electric razors should be used for shaving
8. Use of soft-bristled toothbrushes
1. IV immune globulin G - binds the receptors  in the - dental caries
macrophages; requires high dosage; expensive; effect is 9. Avoid vigorous sexual intercourse when the platelet
transient count is <10,000/mm3
10. Complications of long term corticosteroid therapy:
2. Splenectomy - osteoporosis
•Result: sustained normal plt count only 50% of the time - proximal muscle
- many can maintain safe plt count of >30,000/mm3 Wasting
- risk: sepsis ➔ 2-3wks before: pneumococcal - cataract formation
(Pneumovax)- 5-10 yrs, H. influenza B and meningococcal - dental caries
vaccines
Bleeding Disorders
Semifinals Notes

HEMOPHILIA MEDICAL MANAGEMENT

✓transfusions of factor VIII or factor IX concentrates
A group of hereditary bleeding disorders characterized
✓Recombinant forms:
by a deficiency of one of the factors necessary for
coagulation of the blood 1. Aminocarproic acid (EACA, Amicar)
– inhibits fibrinolysis, stabilizing the clot
= used to treat mucosal bleeding
➢inherited as X-linked traits:
- almost all affected people are males
2. Desmospressin (DDAVP)
- females can become carriers but are almost
= transient rise in Factor VIII; unknown
always asymptomatic
mechanism
- not effective in patients with severe factor
TYPES
deficiency

HEMOPHILIA A HEMOPHILIA B
NURSING MANAGEMENT
•Def. in Factor VIII •def. in Factor IX
•More common than B •Aka CHRISTMAS DISEASE •Coping
•Teaching on activity restrictions; safety at home and in
workplace
•Instruct to avoid any agents that interfere with platelet
CLINICAL MANIFESTATIONS aggregation:
MILD: (6% to 50% of normal levels): -aspirin
hemorrhage tends to occur secondary to trauma -NSAIDS
-Herbs
SEVERE: (<1% of normal levels): -nutritional supplements
•spontaneous hemorrhage -Alcohol
(Hemarthroses and hematomas) -OTC meds (cold remedies)
•requires frequent factor replacement •Dental hygiene
therapy •Apply pressure to minor wounds
•Splints/orthopedic devices
HEMARTHROSES - extravasation of blood into a joint •Avoid Nasal packing, injections, invasive procedures
- can result to chronic pain, ANKYLOSIS •Carry or wear medical ID
•Recent surgery: assess surgical site for bleeding.
HEMATOMAS - Extravasation of blood into tissues of the •Analgesics
skin or organ •During bleeding episodes:
-Peripheral nerves can be compressed -Assess extent of bleeding
- decreased sensation -Avoid heat
-weakness -Provide cold application
-atrophy
VON WILLEBRAND’S DISEASE
OTHERS: -hematuria GI bleeding
-mucous membranes •A common bleeding disorder affecting males and
-Most dangerous: head females equally, is usually inherited as a dominant trait
-Poor wound healing
•The disease is caused by a deficiency of vWF, which is
necessary for factor VIII activity. vWF is also necessary
for platelet adhesion at the site of vascular injury

Three Types of Von

Willebrand’s Disease
Type 1: most common; characterized by decreases in
structurally normal vWF

Type 2, shows variable qualitative defects based on the

specific vWF subtype involved

Type 3, is very rare and is characterized by a severe vWF

Bleeding Disorders
Semifinals Notes

deficiency as well as significant deficiency of factor VIII MEDICAL MANAGEMENT

CLINICAL MANIFESTATIONS Focus: Treat the underlying cause

1. Nosebleeds; easy bruising 1. Cryoprecipitate – to replace fibrinogen & factors V &
2. heavy menses VII
3. prolonged bleeding from cuts 2. FFP – to replace coagulation factors
4. postoperative bleeding 3. Fibrinolytic inhibitors: Aminocaproic acid (EACA,
5. do not have massive soft tissue or joint hemorrhages Amicar) may be used w/ heparin
(unless w/ severe type 3 vWD) 4. Recombinant activated protein C – anti-inflammatory &
anticoagulant properties
5. Antithrombin infusions
ASSESSMENT & DAIGNOSTIC FINDINGS:
▪Normal Plt NURSING INTERVENTIONS
▪Prolonged bleeding time 1. Avoid procedures/activities that can increase
▪Slightly prolonged aPTT intracranial pressure.
▪Ristocetin cofactor (vWF collagen binding assay) – 2. Monitor vital signs closely, including neurologic
measures vWF activity checks.
3. Avoid medications that interfere with platelet function
if possible.
MEDICAL MANAGEMENT GOAL: 4. Avoid rectal probes, rectal medications.
REPLACE THE DEFICIENT PROTEIN 5. Avoid IM injections.
1. Desmopressin 6. Monitor amount of external bleeding carefully.
2. Replacement products: Humate-P & Alphanate 7. Use low pressure with any suctioning needed.
(commercial concentrates of vWF & Factor VIII) 8. Administer oral hygiene carefully.
= 7-10 days after major surgery 9. Reposition carefully; use pressure-reducing matress
= 3-4 days postpartum 10. Skin care every 2 hrs
3. Aminocaproic acid – mucosal bleeding 11. Apply prolonged pressure after injection
4. Estrogen-Progesterone compounds – diminish extent
of menses
5. Platelet transfusion – significant bleeding
6. Avoid meds that interfere w/ platelet function

DISSEMINATED INTRAVASCULAR
COAGULATION (DIC)

➢a complex systemic thrombohemorrhagic disorder

involving the generation of intravascular fibrin and the
consumption of procoagulants and platelets. The
resultant clinical condition is characterized by
intravascular coagulation and hemorrhage.

➢ is not a disease but a sign of an underlying condition

➢may be triggered by:

- sepsis
- trauma
- cancer
- shock
- abruptio placentae
- toxins
- allergic reactions

The severity of DIC is variable but it is potentially life

threatening.
ACID BASE BALANCE AND IMBALANCES
Semifinal Notes
ACIDS
- “H+” ion donors
2 Forms:
1. Volatile - excreted as gas
CO2 + H2O ➔ H2CO3 (carbonic acid)
LUNGS partial pressure of Carbon dioxide
e.g. PC02= 35-45 mmHg
- indicates CO2 levels in blood &
reflects ventilation
2. Nonvolatile - excreted as body fluids (urine)
e.g.sulfuric acid, lactic acid, phosphoric acid
BASES
- “H+” ion acceptors
Substances that bind with H+ when dissolved in H2O
E.g
Strong bases
•Na OH (sodium hydroxide)
•NH3 (ammonia)
Weak bases
•Al OH (aluminum hydroxide)
•HCO3 (bicarbonate)
KIDNEYS
*Normal: HCO3= 22-26 mEq/L
pH
- the negative logarithm of the H+ ion concentration
Increased pH: Decreased H+ ions
Decreased pH: Increased H+ ions
- expresses the acidity or alkalinity of a solution
Normal but slightly acid 7.35 – 7.39
Normal but slightly alka 7.41 – 7.45
Normal 7.40
Acidosis Alkalosis
Normal = 7.35 – 7.45
Decreased : Acidic
Increased : Alkaline
Plasma pH
- an indicator of Hydrogen ion (H+) concentration
maintained normal due to the body’s homeostatic
mechanisms consist of: buffer systems, the kidneys, and
lungs.
• The greater the concentration, the more acidic the
solution, and the lower the pH
Buffer systems
• systems comprised of substances/ organs capable of
binding (removing) H+ ion from body fluids or releasing
H+ quickly to prevent major changes in pH
• Important regulator of pH
1. Chemical Buffers
a. Bicarbonate-carbonic acid buffer
• major extracellular buffer system
HCO3 (bicarbonate) and H2CO3 (carbonic acid)
combine w/ HCl
= decrease the strength of potentially
damaging acids & bases
b. Phosphate buffer system
• Increased amount of NaHCO3 (sodium
bicarbonate) in the ECF making it more alkaline
c. Protein buffer
• Hgb – a major protein buffer w/c maintains
pH in the blood
2. Respiratory Buffers
• The lungs regulate blood levels of CO2
• CO2 = H2O = H2CO3 (carbonic acid)
• Increased H2CO3 ➔ decreased pH (more H+)
• 2nd line of defense; twice as effective but
only temporary
Hyperventilation – more CO2 is excreted = less CO2 left
in the body = alkalosis
Hypoventilation – less CO2 is excreted = more CO@ left
in the body = acidosis
3. Renal Buffer
• Kidneys conserve circulating stores of HCO3
and to excrete H+
• Effective yet relatively slow (hours to days)
• Increase urinary excretion of H+ & conserving
plasma HCO3 ➔ if blood is too acidic
• Decrease urinary excretion of H+ & urinary
excretion of HCO3 ➔ if blood is too alkaline
ACID BASE BALANCE AND IMBALANCES
Semifinal Notes

ABG ANALYSIS AND INTERPRETATION PH PCO2 CHO3 Interpretation

7.14 49 40 Partially
1. Classify pH whether normal, acidosis, alkalosis acidosis acidosis alkalosis Compensated
• 7.35-7.45 (normal) respiratory
 7.35–7.39 (Normal but slightly acidosis) acidosis
 7.40 (neutral)
 7.41–7.45 (Normal but slightly alkalosis) I. COMPENSATED
•(less than) < 7.35 (acidosis) a. Partially Compensated if:
• (greater than) >7.45 (alkalosis) pH abnormal abnormal
PH PCO2 CHO3 Interpretation PCO2 acidosis OR alkalosis
7.14 HCO3 alkalosis acidosis } Opposite
acidosis interpretation

2. Assess PCO2, whether normal, acidosis, alkalosis b. Fully Compensated if:

• 35-45 (normal) pH normal normal
PCO2 acidosis OR alkalosis
• less than <35 mmHg (alkalosis)
• Greater than >45 mmHg (acidosis) HCO3 alkalosis acidosis } Opposite
interpretation
PH PCO2 CHO3 Interpretation
7.14 49
II. NON-COMPENSATED/UNCOMPENSATED if:
acidosis acidosis
pH acidosis alkalosis
PCO2 acidosis OR alkalosis OR
3. Assess HCO3, whether normal, acidosis, alkalosis
• 22-26 (normal) HCO3 acidosis alkalosis
• less than <22 mEq/L (acidosis)
• greater than >26 mEq/L (alkalosis) pH acidosis alkalosis
PH PCO2 CHO3 Interpretation PCO2 acidosis OR alkalosis OR
7.14 49 40 HCO3 normal normal
acidosis acidosis alkalosis
pH acidosis alkalosis
4. Determine the primary problem. PCO2 normal OR normal OR
• If PCO2 has the same interpretation as the pH, then it's a
HCO3 acidosis alkalosis
respiratory disorder
• If HCO3 has the same interpretation as the pH, then it's a
EXAMPLES:
metabolic disorder
pH PCO2 HCO3 Interpretation
PH PCO2 CHO3 Interpretation
1.) 7.37 48 28 Fully compensated
7.14 49 40 Respiratory
N. acidosis alkalosis Respiratory acidosis
acidosis acidosis alkalosis acidosis
acidosis
2.) 7.49 33 17 Partially
Mixed Imbalance: Always uncompensated
Alkalosis alkalosis acidosis compensated
 alka-alka-alka – Mixed alkalosis / Metabolic &
Respiratory
respiratory alkalosis
alkalosis
 acid-acid-acid – Mixed acidosis
3.)7.47 30 29 Mixed alkalosis
alkalosis alkalosis alkalosis
5. Determine the presence of compensation by checking
4.)7.33 37 16 Uncompensated
the value not the same as the pH
acidosis Normal acidosis metabolic acidosis
• Partially compensated- If either PCO2, or HCO3, has the
5.) 7.44 36 24 Normal / Normal
opposite interpretation with pH and pH is abnormal
N. Normal Normal ABG / Acid – base
• Fully compensated- If either PCO2, or HCO3, has the opposite
alkalosis balanced
interpretation with pH and the pH is normal
6.) 7.37 40 24 Normal / Normal
• Uncompensated- if either PCO2 or HCO3 is normal and
N.acidosis Normal Normal ABG
pH is not normal
7.) 7.33 48 17 Mixed acidosis
acidosis acidosis Acidosis
ACID BASE BALANCE AND IMBALANCES
Semifinal Notes

8.) 7.43 15 17 Fully compensated - Kidney disorders – renal

N. alkalosis acidosis Respiratory insufficiency decreased urinary excretion of
alkalosis alkalosis acids thru the urine

9.) 7.49 40 32 Uncompensated - Diabetic acidosis – ketone

alkalosis Normal alkalosis metabolic alkalosis overproduction
10.) 7.63 17 18 Partially - Lactic acidosis increased accumulation of
fixed acids in the body
alkalosis alkalosis acidosis compensated Clinical - Headache, confusion, drowsiness
respiratory alkalosis Manifestation - Weakness
- Increase respiratory rate and depth
Kussmaul`s breathing deep, labored
Matabolic Alkalosis pH Plasma HCO3 breathing (hyperventilation)
Main Problem A condition characterized by acid loss or - Nausea and vomiting
base gain due to: - Peripheral vasodilation
- Vomiting or gastric (ph 1-3) suction (hypotension) & decrease CO  pH
loss of H+ and CI ions <7.0
- Loop / Thiazide diuretic use – K Laboratory Data ABG reveals: pH below 7.35; HCO3 below 22
(potassium) loss = hypokalemia (hypersecretion of mEq/L pH (acidosis) = H+
cortisol)
- Hyperkalemia (initial) followed by
- Cushing dse. – adrenocorticoid
hypokalemia as acidosis is corrected
excess
- Dysrhythmias due to hyperkalemia
- Hypokalemia
Nursing Risk for acid – base imbalance
- Excessive alkali ingestion from
Diagnosis
antacid
Interventions  Correct the cause
- Use of sodium carbonate
 Hemodialysis / Peritoneal dialysis
Clinical - Lethargy
Manifestation - Tetany (hypocalemia) Respiratory Alkalosis
Due to ionized calcium as more CA combine with Main Problem A condition characterized by loss of Carbon
proteins dioxide due to:
- ECG Changes – PVCs / U-wave - Hyperventilation
- Hypoventilation – adaptive - Extreme anxiety (hyperventilation)
Leads to retention of CO2 (acid) to neutralize the
alkalosis Can stimulate the respiratory drive
Laboratory Data ABG reveals: pH above 7.45; HCO3 – above  hypocapnia

26 - Hypoxemia from respiratory

- Hypoxemia due to hypoventilation disorders
(semi – concious, unconcious, debilitated) - Fever
- Hypokalemia - Inappropriate ventilator settings
Nursing Risk for acid – base imbalance - Chronic hypocapnia (decreased PCO2)
Diagnosis Clinical - Lightheadedness due to vasoconstriction
Interventions  Restore fluid balance – administer Manifestation & less cerebral blood flow
IV volume depletion can worsen alkalosis - Restlessness
 0.9% saline as prescribed NSS-Normal - Paresthesiasis, confusion
Saline Solution - Numbness and tingling
 Chloride administration (to replace CI - Dyspnea, tachycardia
losses; allows excretion of HCO3 (kidneys absorb
NA with CI)
- Dysrhythmias due to hypokalemia
 Carbonic Anhydrase Inhibitors – Laboratory ABG reveals: pH above 7.45 (alkalosis); pCO2
Acetazolamide - promotes Data below 35 mmHg (alkalosis)
excretion of HCO3 as prescribed - hypokalemia and hypocalemia
Nursing Ineffective Breathing Pattern
Matabolic Acidosis pH plasma HCO3 Diagnosis
Main Problem A condition characterized by excessive Interventions  Breathe into a paper bag
blood acidity due to:  Sedative for very anxious clients
- Gastrointestinal disturbance  Treat underlying cause
(diarrhea) loss of HCO3
ACID BASE BALANCE AND IMBALANCES
Semifinal Notes

Respiratory Acidosis
Main Problem A condition characterized by retention of
Carbon dioxide with inadequate ventilation
due to:
- Lung Disorders - E.g severe
pneumonia, ARDS (Acute Respiratory
Distress Syndrome) COPD, Acute
pulmonary edema, Pulmonary
embolism (blood clot), pneumothorax,
atelectasis causing hypoventilation  acid
accumulation in the body
- Airway obstruction
- Drug (sedative)
- Neuromuscular disorders – E.g.
myasthenia (descending paralysis )
- Gravis, Guillain – Barre syndrome
(ascending paralysis )
Clinical - Dyspnea, tachypnea
Manifestation - Tachycardia
- Restlessness, mental cloudiness,
confussion
- Dull headache, feeling of fulness to
the head
- Severe acidosis – increase ICP
(intracranial pressure) , papilloedema
(swelling of the optic disc)
Laboratory Data ABG reveals: pH below 7.35 (acidosis); pCO2
greater than 45 mmHg (acidosis)
- Hyperkalemia
- Dysrhythmias
Nursing Ineffective Breathing Pattern
Diagnosis
Interventions  Correct the cause
 Deep breathe (to excrete more CO2) &
cough; adequate hydration (2-3L /
day)
 Supplemental O2
 Mechanical ventilation
 Pharmacologic: bronchodilators ( to
decrease bronchial spasm), antibiotics (for
respi, infection), thrombolytics (to manage
pulmonary embolism) and
anticouagulants
BURNS
Semifinal Notes

Burn Injuries 3rd degree – involves subcutaneous layer, pearly

 Approximately 1.1 million people require medical white, no pain
attention for burns every year, and about 4,500 persons 4th degree – involves the muscles and bones, blackish
die of burns and associated inhalation injuries every year. or charred, no pain

 Incidence: any person, any time, any place, across

socioeconomic groups

 Most burns occur in the home, can occur in workplace

(<4y.o; >65 y.0)

 Young children and the elderly are at high risk for burn Zones of Burn Injury
injuries.

 Nurses must play an active role in the prevention of burn

injuries by teaching prevention concepts and promoting
safety legislation.

Nature
 40%: flame related
 30%: scald injuries: occurs more often in children
particularly the toddlers
 4%: electrical
 3%: chemical

Goals Related to Burns

1. Prevention Factors to Consider in Determining Burn Depth
2. Institution of life-saving measures for the severely burned  How the injury occurred
person  Causative agent
3. Prevention of disability and disfigurement through early  Temperature of agent
specialized and individualized care  Duration of contact with the agent
4. Rehabilitation through reconstructive surgery and  Thickness of the skin
rehabilitation programs
Classification of Burns by Extent of Injury
Classification of Burns
 Superficial Partial Thickness 1. MINOR BURN INJURY
1st degree – involves epidermis, reddish, painful • Second-degree burn of <15% total body surface
area (TBSA) in adults or <10% TBSA in children

• Third-degree burn of <2% TBSA not involving special

care areas (eyes, ears, face, hands, feet, perineum,
joints) major burn injury
 Deep Partial Thickness
2nd degree – involves dermis. Moist surface, with • Excludes all patients with electrical injury,
vesicles, painful inhalation injury, or concurrent trauma and all poor-
risk patients (eg, extremes of age, intercurrent
disease)

2. MODERATE, UNCOMPLICATED BURN INJURY

• Second-degree burns of 15-25% TBSA in adults or
10-20% in children

 Full Thickness
BURNS
Semifinal Notes
• Third-degree burn of <10% TBSA not involving
special care areas
• Excludes electrical injury, inhalation injury, or
concurrent trauma and all poor-risk patients (eg,
extremes of age, intercurrent disease)
3. MAJOR BURN INJURY
• Second-degree burns >25% TBSA in adults or >20%
in children
• All third-degree burns >10% TBSA
• All burns involving eyes, ears, face, hands, feet.
Perineum, joints
• All inhalation injury, electrical injury, or concurrent
trauma, and all poor-risk patients
Methods to Estimate Total Body Surface Area (TBSA)
Burned
 Rule of nines – quick way; the system assigns
percentages in multiples of nine to a major body
surface
 Lund and Browder method – more precise method;
recognizes that the percentage of surface area of
various anatomic parts, esp. the head & legs, changes
with growth
o More precise: recognizes that the
percentage of TBSA of various anatomic
parts, especially the head and legs, and
changes with growth
o initial evaluation is made on the patient’s
arrival at the hospital and is revised within
the 1st 72 hours
 Palm method – scattered burns; 1 size of palm is
approximately 1% of the TBSA
Pathophysiology of Burns
Burns are caused by a transfer of energy from a heat source
to the body.
 Thermal – hot objects or substances; due to
fires in the home, auto acidents , playing
with matches, poorly stored gas , faulty
electrical systems, space heaters, fire
crackers, kitchen accidents, scalding
 Chemical – caused by contact, ingestion,
inhalation, injection of strong acids or alkali
 Electrical – from contact with malfunctioning
electrical appliances, wires, flash electrical
arcs from any high voltage power lines,
machine and lightning
 Radiation – excessive exposure to sunlight
Burn related Respiratory Injuries
1. Smoke Inhalation
- Carbon monoxide CO (most common)
- released when organic substances are burned
- Colorless, odorless gas that combines with Hgb 200x
more than O2 causing Tissue Hypoxia
BURNS
Semifinal Notes
- Causes headache, dizziness, confusion, syncope,
coma, respiratory failure
Treatment: 100% O2 administration; Hyperbaric O2
chamber to reduce CO level
2. Smoke Poisoning
- results from noxious chemicals formed in the
burning process and is prevalent with nonorganic
substances (plastic); decreases ciliary action in
respiratory tract and mucosal edema, bronchospasm,
carbon-flecked sputum and then sloughing of the
tracheobronchial mucosa with cough up of purulent
mucus
3. Heat Injury
- affects the upper airway with edema causing
obstruction in the first 24 to 48 hours after burn
Physiologic Changes
 Burns less than 20% TBSA produce a primarily local
response.
 Burns more than 20% may produce a local and
systemic response and are considered major burns.
 Systemic response includes release of cytokines
immunomodulating agents and other mediators into the
systemic circulation.
 Fluid shifts and shock result in tissue hypoperfusion
and organ hypofunction.
Effects of Major Burn Injury
 Fluid and electrolyte shifts
 Cardiovascular effects
 Pulmonary injury
o Upper airway
o Inhalation below the glottis
o Carbon monoxide poisoning
o Restrictive defects
 Renal and GI alterations
 Immunologic alterations
 Effect upon thermoregulation
Fluid and Electrolyte Shifts: Emergent Phase
 Generalized DHN-evaporative loss, fluid shift
dehydration
 Reduced blood volume and hemoconcentration
(Hct is high)
HCT:
Male: 41 – 50%
Female: 36 – 48%
 Trauma causes release of potassium into
extracellaur fluid: hyperkalemia.
K= 3.5 – 5.0mEq/L
 Extensive local edemamaximal 24H, begins to
resolve 12days;completely resolved 7-10days
 Decreased urine output
0.5 – 1.0 mL/kg/hr E.G 50kg patient
25 – 50 mL/hr
 Sodium traps in edema fluid and shifts into cells
as potassium is released: hyponatremia
Na = 135 – 145 mEq/L
 Metabolic acidosis
pH is low
HCO3 is low
F&E Shifts: Acute Phase
 Fluid re-enters the vascular space from the
interstitial space.
 Increased urinary outputFluid shift into IVC
increases renal blood flow and causes increased
urine formation
 Potential Hypokalemia : Potassium shifts from
extracellular fluid into cells
 Hemodilution (↓HCT)results as fluid enters the
IVC; loss of RBCs due to lysis at burn site
 Hyponatremia: Sodium is lost with diuresis and
due to dilution as fluid enters vascular space
 Metabolic acidosis
Cardiovascular Alterations:
 ↓ Cardiac Output (5 to 6 L /min) even without significant
changes in blood volume
 SNS stimulation due to Burn Shock (decrease CO, increased
vascular resistance, hypovolemia, hypoperfusion) releases Adrenal
corticoid hormones and Catecholamines leading to
vasoconstriction→ further ↓ in CO
 24-36 hrs (peak at 6-8H)= Fluid Leak

Increases Blood volume (hypervolemia)

Increased renal perfusion

BURNS
Semifinal Notes

DIURESIS( up to 2 weeks)  Gastric bleeding due to massive physiologic stress=

CURLING’s ulcer (stress ulcer) (acute ulcerative duodenal
 Anemia due to destruction of RBC (but HCT level is disease 24 H post burn)
increased)
Phases of Burn Injury
Pulmonary Alterations
 Emergent or resuscitative phase
 Bronchoconstriction- Histamine, serotonin, - Onset of injury to completion of fluid
thromboxane (for platelet coagulation, vasoconstriction & resuscitation
proliferation)
 Upper airway-above glottis edema  Acute or intermediate phase
 Inhalation below the glottis-decrease ciliary function, - From beginning of diuresis to wound closure
Hypersecretion, Severe mucosal edema,
Bronchospasm, decrease surfactant leading to  Rehabilitation phase
Atelectasis → Acute Respiratory Failure - From wound closure to return to optimal physical
Treatment: Intubation, Mechanical ventilation
and psychosocial adjustment
 Carbon monoxide poisoning (headache, dizziness,
weakness, upset stomach, vomiting, chest pain, and Emergency procedures at the Burn Scene
confusion 1. Extinguish flames
 Restrictive defects – Escharotomy > victim "drops and rolls"
> smother the flames
Renal Alterations > effects on standing and running
 Due to decreased blood volume, hemolysis (Hgb in > disconnect electrical source
the urine), and muscle damage (Myoglobin)
 2. Cool the burn
Occlusion of the renal tubules > application and soaking with cool water on burned
 areas
Acute tubular necrosis > no direct application of ice

RENAL Failure
3. Remove restrictive objects
> clothing and jewelry removed to prevent
Immunologic Alterations
constriction due to edema
 Diminished resistance to infection

4. Cover the wound
SEPSIS
> immediate covering with sterile dressings
 Abnormal inflammatory factors, altered level of
> minimize bacterial contamination
IgA(found in the linings of the respiratory tract and digestive tract, saliva,
> prevent air from contact with burned areas
tears, breastmilk), impaired neutrophil functions(for
> no medication/ material applied except sterile
viral/bacterial infections), decrease lymphocytes (for production
of antibodies)
dressings

Immunosuppression 5. Irrigate chemical burns
> rapid, sustained flushing
 Loss of skin integrity > brush off chemical agents
 Release of abnormal inflammatory factors, altered > remove clothes immediately
levels of immunoglobulin and serum complement, > rinse off the body with cool water
impaired neutrophil function, lymphocytopenia
Emergent or Resuscitative Phase: On-theScene Care
GI Alterations  Prevent - Prevent injury to rescuer
 ↓peristalsis and bowel sounds  Stop - Stop injury: extinguish flames, cool the burn,
Normal = 5 to 35 bowel sounds per minute irrigate chemical burns.
Hypoactive bowel sounds  Establish - ABCs: Establish airway, breathing, and
 Gastric distention and Nausea= vomitting circulation.
 Start - Start oxygen and large-bore IVs.
BURNS
Semifinal Notes

 Remove - Remove restrictive objects and cover the • Day 2: Half of previous day’s colloids and
wound. electrolytes
 Do - Do assessment, surveying all body systems, and
obtain a history of the incident and pertinent patient BROOKE ARMY FORMULA
history.
 Note - Note: Treat patients with falls and electrical
injuries as for potential cervical spine injury.

Emergent or Resuscitative Phase

 Patient is transported to emergency department.
 Rapid assessment; v/s q 15mins
 Maintain ABC; look for signs of inhalation injury
 Fluid resuscitation is begun.
 Foley catheter is inserted.
 Patients with burns exceeding 20-25% should have
an NG tube inserted and placed to suction.
 Patient is stabilized and condition is continually
monitored.
 Patients with electrical burns should have an ECG.
 Address pain; only IV medication should be PARKLAND/BAXTER FORMULA
administered.
 Psychosocial consideration and emotional support • Lactated Ringer’s solution: 4 mL x kg body weight x
should be given to patient and family. % TBSA burned
➢Day 1: Half to be given in first 8 h; half to be given
Management of Shock: Fluid Resuscitation over next 16 h
➢Day 2: Varies. Colloid is added.
Maintain BP above 100 mm Hg systolic and urine
output of 0.51.0mL/kg/hr. Maintain serum sodium at Nursing Management
near-normal levels.
 Monitor v/s closely, (RR,PR,BP)
Consensus formula
 Monitor I&O
Evans formula  Asses frequently urine specific gravity (1.010 –
Brooke Army formula 1.025), glucose(70 – 100 mg/dL), protein (Negative or
Parkland Baxter formula trace >30 mg/dl - Abnormal), hgb (M: 12 – 16 g/dL ; F: 11 –
Hypertonic saline formula 15 g/dL) ; Burgundy colored urine suggests
Note: Adjust formulas to reflect initiation of fluids at the time of presence of hemochromogen & myoglobin due
injury. to muscle damage
 Elevate burned extremity (to help decrease the edema)
CONSENSUS FORMULA
 Monitor IV therapy, obtain infusion pump
Lactated Ringer’s Solution (or other balanced saline solution)
Nursing Process: Care of the Patient in the Emergent

Phase of Burn Care: Diagnosis
2ml x kg body weight x % TBSA burned
2-4 mL x kg body weight x % TBSA burned
Impaired gas exchange
Half to be given in 1st 8 Remaining half to be given
hours over next 16 hours Ineffective airway clearance
Fluid volume deficit
EVANS FORMULA Hypothermia
 Colloids: 1mL x kg body weight x %TBSA Acute pain
 Electrolytes (Saline): 1mL x kg body weight x %TBSA Anxiety
 Glucose (5% in water): 2000 mL for insensible loss
• Day 1: Half to be given in the first 8 hours
and the remaining half over next 16 hours
BURNS
Semifinal Notes
Acute or Intermediate Phase
 Begins 48-72 hrs. after the burn injury
 Priorities of care: Continued assessment and maintain
respiratory and circulatory support; F&E balance,
prevention of infection, wound care, pain
management, and nutritional support
 Cautious administration of fluid because of fluid shifts
from the interstitial to the intravascular
compartment, losses of fluid from large burn wounds
 Fever: caused by bacteremia and septicemia ; treated
with acetaminophen and hypothermia blanket
Continued Assessment of Circulatory Status, F&E:
Hemodilution
Increased UO
Hyponatremia
Hypokalemia
Acidosis
Continuous and monitored fluid resuscitation
Burn Wound Care
1. Wound cleaning
 Hydrotherapy- cleaning of wounds &
exercising the extrimities.
✓The temperature of the water is
maintained at 37.8 C (100 F)
✓The temperature of the room should be
maintained between 26.6 C and 29.4 C (80
oF to 85 oF)
✓Limited to a 20-30 minute period to
prevent chilling and additional metabolic
stress.
2. Wound débridement - the removal of foreign material and
devitalized tissue until surrounding healthy tissue is exposed;
two goals:
• To remove tissue contaminated by bacteria and
foreign bodies, thereby protecting the patient from
invasion of bacteria.
• To remove devitalized tissue or burn eschar in
preparation for grafting and wound healing.
Escharotomy
 treat full thickness (third-degree)
circumferential burns
 used primarily to combat compartment
syndrome
 performed by making an incision through
the eschar to expose the fatty tissue in order
to lessen its pull on the surrounding tissue.
Topical Antibacterial Agents for Burns
 Silver Sulfadiazine 1%(Silvadene) - bactericidal agent
• Minimal penetration of the eschar
• Apply 1/16 inch layer of cream with sterile glove 1-
3x/day Nursing Implications:
• Leucopenia 2-3days
• Pseudoeschar formation
 Mafenide Acetate 5%-10% (Sulfamylon)
✓ Effective against gram – or + microorganism
✓ Diffuses rapidly through the eschar
✓ In 10% strength, it is the agent of choice for electrical
burns because of its ability to penetrate the eschar
✓ Apply thin layer with sterile glove 2x daily and leave
open as prescribed; if the wound is dressed, change q6h
as prescribed
Nursing Implications:
 Monitor ABG levels because it causes metabolic
acidosis with its effect on renal buffering
 Analgesic for pain mgt- may cause pain
 Silver Nitrate - Bacteriostatic and fungicidal
✓ Does not penetrate the eschar
✓ Apply to gauze dressing, place over wound. Keep
dressing wet but covered w/ dry gauze & blankets to
prevent vaporization. Re-moisten q2h; redress wound 2x
daily
Nursing Implications:
 Monitor Na & K serum levels because of its
hypotonicity
 Protect bed linen/clothing in contact as it causes
black staining
 Acticoat- Effective against gram – or + microorganism and
some yeasts and molds
✓ Delivers a uniform, antimicrobial concentration of
silver to the burn wound
✓ Moisten w/sterile water only; Apply directly to
wound.
✓ Cover with absorbent secondary
dressing.Remoisten w/ sterile water q3-4h .
Nursing Implications:
 No oil-based products or topical antimicrobials
 Keep moist ▪ Left in place 3-5 days
BURNS
Semifinal Notes
 Other agents:
o Aquacel, Siversorb, Silverlon, Povidoneiodine
ointment 10%; gentamicin sulfate; nitofurazone;
Dakin’s solution; acetic acid; miconazole; clotrimazole
Bacitracin is used for facial burns
Burn Wound Care
 Wound dressing, dressing changes
 light dressing for joints areas (allow motion); areas
with splint (maintain body contour); on face (absorb
exudates going into the eyes)
 circumferential dressings applied from distal to
proximal; fingers and toes wrapped individually
 burns on face left open to air
 occlusive dressings are used over areas with new skin,
graft; this thin gauze with antimicrobial agent remains
in place for 3-5 days
 changing of dressings is done 20 minutes after
analgesic agent is prescribed
 note for color, odor, size, exudates, signs of re-
epithelialization, eschar and other changes
 peripheral extremities must be checked frequently
and burned areas elevated on 2 pillows
Wound Grafting
 Purposes: to decrease risk of infection
 to prevent further loss of protein, fluids
&electrolytes
 to minimize heat loss through evaporation
 permits earlier functional ability
 reduces wound contractures
 temporary grafting is done before patient’s own skin
is possible
 main areas for grafting are the face, hands and feet,
and areas that involve joint
 granulation process to take place first before graftin
Comparison of Integra Template and Split-Thickness
Autograft
Care of the Graft Site
 Use of occlusive dressings to immobilize the graft.
 First dressing change is performed 2-5 days after
surgery.
 Sterile saline to prevent drying of the graft.
 Patient positioned and tuned carefully to avoid
disturbing the graft
 Elevate grafted extremity to minimize edema.
 Patient to exercise the grafted area 5-7 days after
grafting.
Care of the Donor Site (area from which skin is taken)
▪ Moist gauze dressing applied after surgery to
maintain pressure and stop bleeding.
▪ Thrombostatic agents applied to the site.
▪ Covering of donor sites with biosynthetic dressings.
▪ Pain relievers.
* A donor site heals within 7-14 days with
proper care.
Pain Management
 Burn pain has been described as one of the most
severe forms of acute pain.
 Pain accompanies care and treatments such as
wound cleaning and dressing changes.
 Types of burn pain
o Background or resting: exists on 24 hour
basis
o Procedural: caused by manipulation of
wound bed during dressing changes or ROM
exercises
o Breakthrough: occurs when blood levels of
analgesic agents decreased below the level
required
 Analgesics
o IV use during emergent and acute phases
o Morphine
o Fentanyl
o Other
 Role of anxiety in pain
 Effect of sleep derivation on pain
 Nonpharmacologic measures Relaxation techniques;
deep breathing exercises, distraction, guided
imagery, hypnosis, therapeutic touch, humor, and
information giving, music therapy
Nutritional Support
 Burn injuries produce profound metabolic
abnormalities. Patients with burns have great
nutritional needs related to stress response,
Increased catabolic hormones (cortisol and
catechols), hypermetabolism, and wound healing.
 Goal of nutritional support is to promote a state of
nitrogen balance and match nutrient utilization.
BURNS
Semifinal Notes
 Nutritional support is based on patient’s preburn
status and % of TBSA burned.
 Enteral route is preferred. Jejunal feedings are
frequently used to maintain nutritional status with
lower risk of aspiration in a patient with poor
appetite, weakness, or other problems.
Calories:
•High Protein (15%-25%): 2-3g/kg BW/every 24 hours
•High Carbohydrates (55%-85%)
•Low fat (3%-20%)
Vitamin supplementation:
•A: skin & mucous membrane integrity
•B: enhances metabolism
•C: ↑ resistance to stress & infection
 Oral fluids must be initiated slowly
 High protein and high vitamin food
 High calorie nutritional supplements
 Vitamins and Mineral supplements
 Enteral feeding of bolus formula if not possible by
mouth
 Parenteral nutrition if GI function is compromised
 Weigh patient daily and record
Disorders of wound healing:
1. Hypertrophic scars: form within the boundaries of the initial
wound and push outward on the perimeter of the wound.
• Areas over joints
• Hypopigmented/hyperpig mented
2. Scars: red, raised and hard
Prevention and Treatment of Scars
1. Compression: early in burn wound treatment
• Elastic Bandage wraps: desensitize the
patient’s skin, protect healing areas, apply
pressure, and promote venous return
• Elastic pressure garments: loosens
collagen bundles and encourages parallel
orientation of the collagen to the skin
surface
• Worn 23 hrs a day
 Silicone Sheets: for small troublesome
areas
 Gentle superficial scar massage w/
moisturizer: smaller areas
 Steroid injections
3. Keliod: irregularly formed scar, extends beyond the margins
of the original wound
• Large, nodular, ropelike
• Itchy, tenderness
4. Contractures: burn wound tissue shortens because of the
force exerted by the fibroblasts
• and the flexion of muscles in natural wound healing
• Tx: splints, traction, and purposeful movement and
positioning: counteract deformity in burns affecting
joint
Care of the Patient During Acute Phase:
1. Assessment:
▪ Focuses on hemodynamic alterations, wound
healing, pain and psychosocial responses, early
detection of complications.
▪ Frequent assessment on vital signs, peripheral
pulses, edema, dysrhythmias, electrolyte imbalance,
residual gastric volumes, and pH.
BURNS
Semifinal Notes

▪ Assess burn wounds as to size, color, odor, eschar, 3. Deficient knowledge about post-discharge home care and
exudates, abscess formation, epithelial buds follow-up needs
bleeding, granulation, status of grafts and donor sites, NI : Demonstrate knowledge of required self-care
and quality of surrounding skin. and follow-up care
▪ Focus on pan and psychosocial responses, daily EO: Describes surgical procedures and Tx accurately
weights, caloric intake, general hydration, serum  Verbalizes detailed plan for follow-up care
electrolytes, Hgb and Hct levels.  Demonstrate ability to perform wound care and
prescribed exercises
Nursing Process: Care of the Patient in the Acute Phase of  Returns for follow up appointments
Burn Care: Diagnosis  Identifies resource people and agencies to contact for
specific problems
▪ Excessive fluid volume
▪ Risk for infection
▪ Imbalanced nutrition
▪ Acute pain
▪ Impaired physical mobility
▪ Ineffective coping
▪ Interrupted family processes
▪ Deficient knowledge

Nursing Diagnosis
Other Major Care Issues
1. Activity intolerance r/t pain on exercise, limited joint • Pulmonary care
mobility, muscle wasting, and limited endurance • Psychological support of patient and family
NI : Promoting Activity Tolerance • Patient and family education
▪ Insomnia due to frequent nightmares (listening; • Restoration of function
prescribed hypnotic agents)
▪ Metabolic stress (relieve pain; preventing chilling or Potential Complications/Collaborative Problems
fever)  Acute respiratory failure
▪ Muscle atrophy (therapy exercises)
 Distributive shock
▪ Low endurance (play therapy)
 Acute renal failure
EO: Obtains adequate sleep daily
 Compartment syndrome
▪ Reports absence of nightmares or sleep disturbance
 Paralytic ileus
▪ Shows gradually increasing tolerance and endurance
in physical activities  Curling’s ulcer
▪ Can concentrate during conversations
Rehabilitation Phase
▪ Has energy available to sustain desired daily
activities
Rehabilitation is begun as early as possible in the emergent
2. Disturbed body image r/t altered physical appearance and phase and extends for a long period after the injury.
self-concept or Impaired coping Focus is upon wound healing, psychosocial support, self-
NI : Improving Body Image and Self-concept image, lifestyle, and restoring maximal functional abilities
 Refer patient to support group so the patient can have the best-quality life, both personally
 Meet others with same experience and learn coping and socially.
strategies The patient may need reconstructive surgery to improve
 Constantly assess the patient’s psychological function and appearance.
reactions Vocational counseling and support groups may assist the
EO: Verbalizes alterations in body image patient.
and accepts physical appearance
 Demonstrates interest in resources
 Use cosmetic; wigs; and prostheses;
 Socialize with others
 Seeks and achieve family and societal roles
BURNS
Semifinal Notes

Complications in Rehabilitation Phase of Burn Care Home Care Instructions

1. Neuropathies, nerve entrapment - Electrical injury, large Mental health

deep burns, improper positioning, edema, scar tissue Skin and wound care
Nursing Interventions: Exercise and activity
 Assess peripheral pulses and sensation. Nutrition
 Prevent edema and pressure by elevation, Pain management
positioning, prevention of constricting dressings. Thermoregulation and clothing
 Assess splints for proper fit and application. Sexual issue
 Consult OT and PT for positioning.
2. Heterotopic ossification - Prolonged immobility
▪ abnormal formation of true bone within Collaborative Problems/Potential Complications
extraskeletal soft tissues
Nursing Interventions: Heart failure and pulmonary edema
 Perform gentle range-of-motion exercises Sepsis
Acute respiratory failure
3. Hypertrophic scarring - Partial and fullthickness burns Visceral damage (electrical burns
Nursing Interventions:
 Keep skin pliable and soft.
 Apply pressure garments as prescribed.
 Massage.

4. Contractures - Partial and full-thickness burns

Nursing Interventions:
 Maintain position of joints in alignment.
 Perform gentle range-of-motion exercises.
 Consult OT and PT for exercises and positioning
recommendations.

5. Wound breakdown -sheer, pressure, inadequate nutrition

Nursing Interventions:
 Teach patient about importance of good nutrition.
 Protect wound from pressure and shearing forces.

6. Gait deviations - Pain; burn wound; donor site, scarring of

joints, electrical injury of the brain
Nursing Interventions:
 Provide adequate pain management.
 Consult OT and PT.
 Promote ambulation and mobility training.

7. Complex regional pain syndrome - Trauma and burns

Nursing Interventions:
 Provide adequate pain management.
 Consult OT and PT for exercises.
 Promote gentle motion of affected extremities.

8. Joint instability - Burn wound, burn scar, and contractures

Nursing Interventions:
 Maintain joint through appropriate application of
splints.
 Monitor joint pinning if indicated.
 Consult OT and PT.
DERMATOLOGIC INFECTIONS
Semifinals Notes

MANAGEMENT OF PATIENTS WITH DERMATOLOGIC

PROBLEMS

BACTERIAL SKIN INFECTIONS

 Impetigo – superficial infection of the skin
characterized by honey-colored crusts
 Furuncle (boil) - a deep form of folliculitis

Etiologic Agent:
1. Staphylococci, streptococci, or multiple bacteria
2. Bullous impetigo – S. Aureus
 Carbuncle - an abscess of the skin & SQ tissue
that invades several follicles

Mode of Transmission
• Direct and Indirect contact

Treatment Modalitities
1. Systemic Antibiotic Therapy
Treatment Modalities
– Non-bullous – Benzathine penicillin or oral penicillin 1. Do not rupture
– Bullous – penicillinase resistant penicillin ( cloxacillin 2. Systemic antibiotic therapy (after C&S)
[Cloxapen], dicloxacillin [Dycill]) •Oral claxacillin & dicloxacillin (1st line)
•Cephalosporin & erythromycin
2. Topical Antibacterial therapy – mupirocin (Bactroban) 3. Incision and drainage

Nursing Management/ Prevention and Control Nursing Management

1. Bathe once a day with bactericidal soap
2. Cleanliness and good hygiene
3. Use individual towel and washcloth
4. Avoid contact with infected people
FOLLICULITIS, FURUNCLES AND CARBUNCLES
Etiologic Agent: Staphylococci
 Folliculitis – arises within the hair follicles
1. Supportive treatment (fluids, fever reduction)
2. Warm, moist compress
3. Clean surrounding area with antibacterial soap and apply
antibacterial ointment
4. Proper handling of soiled dressing
5. Observe standard precaution
VIRAL SKIN INFECTIONS
 Herpes Zoster (Shingles) – acute viral infection of the
sensory nerve caused by a variety or chickenpox virus
DERMATOLOGIC INFECTIONS
Semifinals Notes
• Prevent secondary infections
• Prevent entrance of microorganism into the lesion
especially if they break
• Do not delay pain relievers (neuralgic pain)
• Diversional activities

• Herpes simplex – appearance of sores & blisters

 Etiologic Agent: Varicella zoster (V-Z virus)

 Incubation Period: Unknown (believed to be 13-17
days)
 Period of Communicability: A day before the
appearance of the first rash until 5 to 6 days after the
last crop
Manifestations:
Mode of Transmission: Mild to Moderate
– Direct contact (droplet and airborne) 1. Oral herpes – gingivostomatitis
– Indirect contact 2. Labial herpes – “cold sores” or “fever blisters” (3-
10days)
Clinical Manifestations 3. Ocular herpes – herpetic keratitis ➔ blindness
 Red rashes➔ vesicles ➔ pustule ➔ crust (unilateral; 4. Cutaneous herpes – any part of the body
+ pruritus) 5. Erythema multiforme – an allergic reaction of the
 Burning or stabbing pain (1-5days prior to rashes) – skin
worst at night, intensified by movement 6. Genital herpes – one of the most common STI
 Corneal anesthesia (CN5 trigeminal nerve): Gasserian
ganglionitis
 Paralysis of the facial nerve (CN7) & vesicles in the
external auditory canal: Ramsay Hunt Syndrome
(severe ear pain, facial nerve paralysis, vertigo,
hearing loss, mild general encephalitis)

Diagnosis:
1. Characteristic skin rash
2. Tissue culture
3. Smear of vesicle fluid
4. Microscopy

Treatment Modalities
1. Symptomatic
2. Antiviral drugs (acylovir, famicyclovir)
3. Analgesics
4. Anti-inflammatory

Nursing Management:

• Provide instructions (antiviral medications, analgesics

& anti-inflammatory drugs, lesion care, dressings, and
hand hygiene) Severe to Fatal
• Keep patient comfortable 1. Newborns – neonatal herpetic infection
• Strict isolation 2. Eczema varicelliform eruption – most common in
• Apply cool, wet dressing w/ NSS to pruritic lesions individuals with atopic dermatitis
DERMATOLOGIC INFECTIONS
Semifinals Notes
3. Encephalitis 3. Wear clean, cotton clothing next to the skin

• Tinea barbae (Barber’s itch) - colonization of the bearded

areas of the face and neck

Treatment Modalities
1. Oral antiviral – acyclovir, famicyclovir, valacyclovir
2. Personal hygiene Etiologic Agent: Trichophyton mentaggrophytes,
3. Restore F&E balance trichophyton verrocosum
4. Isolation (eczema herpeticum or neonatal herpes)
5. Universal precaution Mode of Transmission
1. Contact with cattle, dogs or other animals
2. Indirect contact – shavers used in barber shops
FUNGAL SKIN INFECTIONS
• Tinea Flava (Tinea alba/ Tinea vesicolor) Manifestations
– a common, benign, superficial, cutaneous infection 1. Mild superficial – erythema, papules and pustules
characterized by hypopigmentation or hyperpigmentation 2. Inflammatory or deep – pustular and kerion crusting
around the hair (loose and brittle); permanent
alopecia

3. Circinate variety – spreading vesiculopustular border

with central scaling
• Etiologic Agent: Malassezia furfur (normal human flora
that can be an opportunistic pathogen) Management
• Incidence: puberty age (men & women equal) • Systemic antifungal (2-3 weeks) – griseofulvin, ketoconazole,
fluconazole, itraconazole, terbinafine
Manifestations
• Abnormal pigmentation (white to reddish brown)
• Fine, dust-like scale covers the lesions • Tinea Corporis/ Trichophytosis (Ringworm)
• Mild pruritus

Treatment Modalities
Topical antifungal agents:
• Micoconazole
• Ciclopirox colamine
• Propylene terbinafine
• Benzoyl peroxide 2 Types:
1. Dry type – with rounded macular areas of
Nursing Management reddish or yellowish-brown color in varying size
1. Use clean cloth and wash towel daily to as large as a coin; sometimes elevated above
2. Dry all skin areas and folds thoroughly the skin
DERMATOLOGIC INFECTIONS
Semifinals Notes
Body Lice
2. Moist type – less common; may arise from the • Laundry (dry clean) or boil the clothing and beddings
dry lesion and rapidly becomes pustular • Good body hygiene
Prevention and Control Crab Lice
1. Avoid contact with infected animal • Kwell or Gamene (lindane) cream or lotion
2. Avoid sharing comb or razors • Rub crotaminon (Eurax, Geigy) into the affected area and
3. Observe personal hygiene repeat after a week
• Simultaneously treat the person who had sexual contact
with the patient
PARASITIC SKIN INFECTIONS • Remove remaining nits mechanically

• Pediculosis (Phthiriasis) • Scabies – age-old skin infection caused by itch mite

- Three varieties of these flattened, wingless insects
commonly attack man, although some infect the lower
forms of animals and may become temporarily deposited
upon human host

Etiologic Agent:
Pediculosis humanos (capitis) - head lice
Pediculosis humanos (corporis) - body lice
Phthirus pubis - pubic/crab lice

• Etiologic Agent: Sarcoptes scabiei

• Incubation Period: The itch mite may burrow under the
skin and lay ova within 24 hours Period of
• Communicability: Entire period that the host is infected

Mode of Transmission
1. Direct transmission of an infected individual
2. Sleeping in an infested bed or wearing infested
clothing
3. Contact with dogs, cats and small animals

Manifestations
• Itching (more pronounce at night)
• Lesions are slightly elevated, straight or twitching
burrows, thread-like that are either brown or black in
color (5 to 6 mm in length)

Common sites: spaces between fingers, warm folds of the

skin
Males: External genitalia
Females: Crotch area, around nipples, peri-umbilical area
Infants: Head and neck

• Secondary lesions: Vesicles, papules, pustules,

excoriations and crusts
• Bacterial super infection may result from constant
excoriation of burrows and papules
Treatment:
Head Lice Diagnostic Procedure
• Dusting the scalp with 1% malathion powder • A drop of mineral oil placed over the burrow, followed by a
• Massage gamma benzene hexachloride shampoo on the superficial scraping and examination of expressed material
scalp for 4 minutes then rinse under a low-power microscope, may reveal the mite, ova, or
mite feces
DERMATOLOGIC INFECTIONS
Semifinals Notes

Treatment
• Pediculicide ( 5% permethrin cream, Crotamiton or
lindane lotion)
✓ Instruct patient to take a warm, soapy bath; allow
skin to cool; apply for 5 consecutive nights to entire
body, not including the face or scalp; leave on for 12
to 24 hours
• Neosporin ointment 4-5x/day
• Eurax and Kwell may also be effective
• Wash clothing and bedding in hot water and dry in a hot
dryer
• Treat all contacts at the same time
• Pruritus may continue for several weeks and does not
mean retreatment is required
• Perform terminal disinfection
• Avoid contact with infected persons
SEXUALLY TRANSMITTED INFECTIONS
Semifinals notes

SEXUALLY TRANSMITTED INFECTIONS (STI) Manifestations:

 a.k.a Sexually Transmitted Diseases (STD); or Males: urethritis with dysuria (painful urination), urinary frequency
Venereal Diseases (VD) with clear to mucopurulent (muco = mucus; pu= pus) discharge
 Any infections that are transmitted with sexual
contact or contact with contaminated blood and Females: edematous cervix with yellow mucopurulent vaginal
fluids discharge, with spotting at menstrual midcycle or with sexual
intercourse; urethritis with dysuria and urinary frequency
COMMON FALLACIES ABOUT STIs
 Fallacy #1 Both: Proctitis (rectal sex) and pharyngitis (orogenital sex)
I need to have sexual intercourse to become
Diagnostic Tests
 Fallacy #2
1. Culture of tissue (endocervix/urethra) (best and most sensitive but
I cannot get it if I have oral or anal sex expensive and technically difficult to preform)
 Fallacy #3 2. Test for antibodies to chlamydia
I cannot have 2 STI’s at a time 3. Polymerase chain reaction (PCR) or ligasechain reaction –
 Fallacy #4 specific tests on urine and vaginal swab specimens
I don’t have any signs and symptoms of STIs, so I 4. Test for gonorrhea (chlamydia and gonorrhea often co exist with one
can’t be infected another)

Treatment:
RISK FACTORS OF STI:
 Men and non-pregnant women: single oral dose of
1. IUD and Oral contraceptive availability
Azithromycin (macrolide) (Zithromax) or Doxycycline
2. Younger age
(tetracycline) (Vibramycin) twice per day for 7 days
3. Multiple sex partners
4. IV drug use  Pregnant women: Erythromycin (macrolide) or Ofloxacin
(fluroquinolone) twice per day for 7 days
5. Inner city residence
6. Persons of color and poverty
7. Poor hygiene
Gonorrhea
CAUSATIVE AGENTS:
1. bacteria
2. viruses
3. fungi

BACTERIAL SEXUALLY TRANSMITTED INFECTIONS

Chlamydia trachomatis
 “The Great Sterilizer”it targets the urethra, cervix and
rectum  infertility

Mode of Transmission:
 Direct sexual contact
 During delivery through the birth canal

Incubation Period: 2-8 days

Categories:
1. Local Infection – affects the mucosal surfaces of
Modes of Transmission cervix, urethra and rectum; vestibular glands,
 Any form of sexual contact pharynx or conjunctiva
 Through the birth canal 2. Dessiminated Gonococcal Infection – involves
bacteremia with polyarthritis, dermatitis,
Incubation Period: 1 – 3 weeks endocarditis and meningitis
SEXUALLY TRANSMITTED INFECTIONS
Semifinals notes

Manifestations: Syphilis
Male : dysuria, serous, milky or purulent discharge; regional
lymphadenopathy

Female: dysuria, urinary frequency, abnormal menses, heavy,

yellow-green purulent vaginal discharge, cervical erythema;
red, swollen, sore vulva, dysparuenia (painful sexual intercourse)

Anal & Rectal Gonorrhea: pruritus, mucopurulent rectal

discharge, rectal bleeding and pain, constipation Treponema (a spirochete highly contagious)  Syphilis
 Almost transmitted thru sexual contact
Gonoccocal Pharyngitis: fever, sore throat, enlarged lymph  Almost always a systemic infection  spreads to
glands the blood and lymphatics

Complications: Modes of Transmission:

1. Salpingitis ➔ PID (pelvic inflammatory disease) leading to 1. Direct contact to open lesions during sexual contact
internal abscesses, chronic pain, ectopic pregnancy, 2. Transplacental cross
infertility 3. Direct contact with infected blood or saliva
2. Neonate: blindness, infection of joints, septicemia
3. Epididymitis & prostatitis : infertility Incubation Period: average 21 days
4. Spread of infection to blood and joints
5. Increased susceptibility to HIV Clinical Stages:
1. Primary Syphilis (4 weeks after initial infection)
Diagnostic Tests:  Appearance of chancre (oval ulcers w/ raised margins that does
not bleed easily; painless unless infected; women – usually unnoticed)
1. Physical examination
and regional lymph adenopathy (near the chancre)
2. Identification of gonococcus on smear
3. Culture of exudates from affected areas (test of choice for
non-genital specimens)
4. Analysis of fluid specimen
5. Urinalysis

Treatment:
For uncomplicated cases: 2. Secondary Syphilis (6 weeks – 6 months after initial chancre)
 Ceftriaxone (Rocephin) single dose IM or Single IM  Skin rashes (maculopapular rashes; non – pruritic) especially on
injection of Spectinomycin (Trobicin) palms of hands and soles of feet
 single oral dose of:
 Cefixime (Suprax)
 Ciprofloxacin (Cipro)
 Ofloxacin (Floxin)
 Levofloxacin (Levaquin)
❖ Quinolones- not for men who had sex with men

For Dessiminated infection:

 Mucous patches in mouth and sore throat (gray &
 Ceftriaxone IM or IV every 24 hours and continued superficial)
24-48hrs after improvement begins then Cefixime
or ciprofloxacin orally for 1 week

 Generalized lymphadenopathy
SEXUALLY TRANSMITTED INFECTIONS
Semifinals notes

 Condylomata lata in the genital area or mouth (broad 2. Syphilis of undetermined length
– based anf highly contagious)  3 doses of penicillin at weekly intervals
3. Doxycycline for clients allergic to penicillin

ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)

 Flu-like symptoms (nausea, headache, chronic fever,

muscle, joint & bone pain)
 Patchy hair loss on eyebrows & scalp

Characteristics :
 It is acquired.
 Involves immune deficiency.
 It is a syndrome, a combination of signs and
symptoms that form a distinct clinical picture of
disorder.
Symptoms of secondary syphilis – disappear in 2 to 6 weeks
Incubation Period = 7 to 12 years
3. Latent Syphilis (2 or more years after initial infection)
 No symptoms (seroactive) (with (+) blood test) Mode of Transmission :
 Not contagious except through blood and  Sexual intercourse
transplacental spread  Blood transfusions and sharing of infected syringes
and needles
4. Tertiary Stage Syphilis (1-35 yrs after primary infection) (not  Vertical and perinatal transmission
contagious but may be terminal)
 Infiltrating tumors (gummas) in skin, bones & liver
Several Ways of Receiving Blood :
(chronic bone and joint inflammation, CVD, visual,
auditory an d CNS problems)  Blood transfusion
 Sharing of unsterilized syringes and needles used for
intravenous injections
 Transmission during pregnancy
 Organ donation
 Accidental exposure in hospitals or clinics

8 STEPS IN REPLICATION OF HIV:

Diagnostic Tests: 1. ATTACHMENT- virus by means of gp120 molecule
1. VDRL (Venereal Disease Research Laboratory) and binds with CD4 T-cell receptors
RPR (Rapid Plasma Reagin) – detects non-specific 2. UNCOATING- unlocks receptors, enter cell, inject
antibodies protein coat and RNA
2. FTA-ABS (Fluorescent Treponemal antibody 3. REVERSE TRANSCRIPTASE - Viral RNA produces a
Absorption) test – more specific; used when VDRL (+) mirror image of the host’s DNA
but not certain 4. INTEGRATION - of viral DNA into host DNA with
3. Immunofluorescent staining (antibodies against syphilis) integrase enzyme
4. Darkfield microscopy – confirms primary and 5. TRANSCRIPTION - of the inserted viral DNA to
secondary syphilis produce viral mRNA
6. TRANSLATION - of viral mRNA to viral polyprotein
Treatment: 7. CLEAVAGE - of poloyproteins into individual viral
1. Primary and secondary syphi protein that makes up the new virus
 Benzathine penicillin G single dose IM 8. ASSEMBLY AND RELEASE - of new virus to the host’s
system
SEXUALLY TRANSMITTED INFECTIONS
Semifinals notes

HIV INFECTION  Cancers = kaposi’s sarcoma, cervical dysplasia,

3 – 8 weeks cervical carcinoma (human papilloma virus),
 nonhodgkin’s lymphoma
Acute Illness  Parasitic = toxoplasmosis, cryptosporidiosis
(Fever, rash, joint and muscle pain, sore throat)
 Laboratory Assessment:
months to years • Lymphocyte Count - N̊ = 4, 500- 11,000 cells/mm3 ct
 with AIDS are leucopenic with WBC of <3, 500 and
Chronic Illness lymphophenic ( 1,500 lymphocytes/mm3) N CD4+
 count- 500- 1600 cells/mm3
Opportunistic infections, weight loss, diarrhea,
lymphadenopathy, fatigue • CD4+/CD8+ count- Normal ratio 2:1; Low CD4+ cells
 and low CD4+/CD4+ ratio are associated with
AIDS
increased manifestations of the disease

• Antibody Tests- Usually made 3 weeks to 3 mos after
 Complications :
infection ( some would take 36 wks after initial infxn)
Kaposi’s sarcoma, pneumocystis carinii, pneumonia,
o ELISA (Enzyme- link Immunosorbet Assay)
cryptococcal meningitis (non specific antibody test)
o Western Blot (confirmatory test)
Signs and Symptoms :
Minor Signs : Treatment Modalities :
 persistent cough for 1 month • Nucleoside Reverse Transcriptase Inhibitors
 generalized pruritic dermatitis (NRTI’s)– they inhibit the enzyme called reverse
 recurrent herpes zoster transcriptase which is needed to “copy” information
 oropharyngeal candidiasis for the virus to replicate. These drugs are :
 chronic disseminated herpes simplex o RESCRIPTOR (delavirdine)
 generalized lymphadenopathy o SUSTIVA (Efavirenz)
o VIRAMUNE (nevirapine, NVP)
Major Signs :
 loss of weight – 10 % of body weight • Non Nucleoside Reverse Transcriptase Inhibitors –
 chronic d similar to NRTI’s
 prolonged fever for 1 month o Combivir (Ziduvadine/ Lamivudine)
o Epivir ( lamivudine)
TOP 10 Symptoms of HIV/AIDS : o Retrovir ( Ziduvadine)
 depression o Zerit ( stavudine)
 diarrhea o Ziagen ( Cabavir)
 thrush
Fusion Inhibitors - newest class and
 weight loss
prevents HIV from entering healthy T cells
 lipodystrophy (fat redistribution syndrome)
(injection 2x a day q 12 H)
 sinus infection
o Enfuviritide (Fuzeon)
 fatigue
 nausea and vomiting
 Protease Inhibitors – they work by inhibiting the
 lactic acidosis enzyme protease which are needed for the assembly
 burning and tingling of the feet and hands of viral particles. It prevents the virus from
maturingThese drugs are :
Common Opportunistic Infections : o Agenerase (Ampenavir)
 Bacterial = mycobacterium avium complex, o Crixivian (Indinavir)
tuberculosis, salmonillosis o Fortovase (Saquinavir)
 Viral = herpes, hepatitis, genital warts, CMV o Kaletra ( Lopanavir/ Ritonavir)
(cytomegalovirus), malluscum contagiosum o Norvir ( Ritonavir)
 Fungal = candidiasis, cryptococcal meningitis, o Viracept (Nelfinavir
histoplasmosis  Recommended Combo:
 Pneumonias = bacterial pneumonia, pneumocystis o 2 NRTI + either 1 NRTI or 1 PI/ 2 PI’s
carinii pneumonia (PCP)
SEXUALLY TRANSMITTED INFECTIONS
Semifinals notes

o 3 NRTI’s The Four C’s in the Management of HIV/AIDS :

- This is an attempt to prevent drug resistance
Nursing Management :
Health education. The healthcare worker must :
 give practical advice
 inform client about disease process and mode of
transmission
 emphasize “AIDS awareness program”
 avoid judgmental and moralistic messages
 be consistent and concise in giving instruction
especially in taking medications
 use positive statement
 encourage client to trace or identify previous
contact for proper management
Practical universal/standard precaution :
 There is a need for thorough medical handwashing
all the time.
 Use of universal barrier or personal protective
equipment.
Prevention :
 Care should be taken to avoid accidental pricks from
sharp instruments which are contaminated.
 Gloves must be worn when handling blood
specimens and other body secretions of the infected
patient.
 Blood and other specimens should be labeled with
special warning.
 Blood spills should be cleansed immediately using
“chlorox”.
 Needles must be disposed into a puncture-resistant
container.
 Patient’s personal articles should not be shared with
other members of the family.
 Patients with active AIDS should be reverse isolation.
 Clients considered at risk for HIV should not be
allowed to donate blood.
 Encourage monogamous relationship.
 HIV-infected pregnant women should go into regular
prenatal, interpartal, and postpartal care.
 Speak openly with partners about safer sex
techniques and HIV status.
 Compliance – giving of information and counseling to
the client which result to the client’s successful
treatment, prevention, and recommendation.
 Counseling/education :
o Giving instruction about the treatment
o Disseminating information about the disease
o Providing guidance on how to avoid
contracting STD again
o Sharing facts about HIV and AIDS
 Contact tracing – tracing out and providing
treatment to partners.
 Condoms – promoting the use of condom, giving
instructions about its use, and giving away available
condoms.
WAYS TO PREVENT STI’s
 Total abstinence from sexual activities
 have sexual intercourse only with a long-term,
mutually monogamous relationship with an
uninfected partner
 Limiting sexual partners
 Avoid sexual contact with a partner who has no
symptoms of or is being treated for STI
 Consistent and correct use of latex condoms
 Don’t use spermicide if it irritates the skin in your
genital area
 Having regular check-ups

Common Nursing Diagnoses :

 Knowledge deficit
 Social isolation
 Risk for infection
 Anxiety
 Self-esteem disturbance
 Altered role performance
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes

Anatomic and Physiologic Overview • Whole blood normally contains about 15 g of

 Consists of the blood and the sites where blood is
produced.
 Blood is composed of plasma and various types of
cells.
 Plasma is the fluid portion of blood; it contains
various proteins such as albumin, globulin, fibrinogen,
and other factors necessary for clotting, as well as
electrolytes, waste products, and nutrients.
 About 55% of blood volume is plasma and 45% are
blood cells (RBC, WBC, and platelets).
hemoglobin per 100 mL of blood.
• For normal erythrocyte production, the bone marrow
requires iron, vitamin B12, folic acid, pyridoxine
(vitamin B6), protein and other factors.
Hemoglobin:
M = 13 – 18 g / dL
F = 12 – 16 g / dL

BLOOD
• Blood consists of three primary cell types:
• Erythrocytes (RBCs)
• Leukocytes (WBCs)
• Thrombocytes (platelets)
• Blood makes up approximately 7% to 10% of the
normal body weight and amounts to 5 to 6 L of RBCS SIZE/SHAPE COLOR
volume.
• Blood carries oxygen absorbed from the lungs and Normal Normocytic Normochromic
nutrients absorbed from the gastrointestinal (GI)
tract to the body cells for cellular metabolism. Abnormal Microcytic/ Hypochromic
• Blood also carries hormones, antibodies, and other RBCs Macrocytic
substances to their sites of action or use.
• It also carries waste products produced by cellular
metabolism to the lungs, skin, liver, and kidneys.

BONE MARROW Normochromic, normocytic

• The bone marrow is the site of hematopoiesis (blood RBCS
cell formation)
• Marrow is one of the largest organs of the body (4%
to 5% of total body weight)
• It consists of islands of cellular components:

1. Red marrow
• More active in hematopoieses
2. Yellow marrow
• Less active in hematopoises Hypochromic, microcytic
• Mostly fat RBCs
BLOOD CELLS
Erythrocytes (Red Blood Cells)
RBC count: LEUKOCYTES (WHITE BLOOD CELLS)
M = 4.6 – 6.2 million / cumn
F = 4.2 – 5.4 million / cumn • In normal blood, the total leukocyte count is 5,000 to
• Normal erythrocyte is a biconcave disk 10,000 cells per cubic miilimeter.
• It is so flexible that it can pass easily through
capillaries • Leukocytes protect the body from invasion by
• It is very thin so that gases, such as oxygen and carbon bacteria and other foreign entities.
dioxide, can easily diffuse across it.
• Erythrocytes consist primarily of hemoglobin, which • Of these, approximately 60% to 70% are granulocytes
contains iron and makes up 95% of the cell mass. and 30% to 40% are lymphocytes
• Hemoglobin transports oxygen between the lungs
• Both of these types of leukocytes primarily protect
and tissues.
the body against infection and tissue injury.
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes

I. Granulocytes • Plasma proteins consist primarily of albumin and

 Are defined by the presence of granules in the globulins
cytoplasm of the cell.
 Are divided into three main subgroups by the staining Clotting Factors - are circulating plasma proteins.
properties of these granules:
1. Eosinophils
 Bright-red granules
 Function in hypersensitivity reaction
 Important in the phagocytosis of parasites.
2. Basophils
• Deep-blue stain
• Produce and store histamine as well as other
substances involved in hypersensitivity reactions.
3. Neutrophil
• Also called polymorphonuclear neutrophils
• The most numerous cell
• Pink to violet stain
• Major function is phagocytosis
RETICULOENDOTHELIAL SYSTEM
II. Agranulocytes  The RES is composed of special tissue, macrophages,
• Granule-free cytoplasm which are derived from monocytes
• Also called mononuclear leukocytes
 Macrophages have a variety of important functions:
• Approximately 5% of the total leukocytes
1. They defend the body against foreign invaders
via phagocytosis.
2. They remove old or damaged cells from the
circulation.
3. They stimulate the inflammatory process and
present antigens to the immune system.

HEMOSTASIS
PLATELETS (THROMBOCYTES)
 Is the process of preventing blood loss from intact
• Are not technically cells; rather, they are granular
vessels and of stopping bleeding from a severed
fragments of giant cells in the bone marrow called
vessel.
megakaryocytes.
 Requires adequate numbers of functional platelets.
• Platelets play an essential role in the control of
bleeding
• Platelets have a normal life span of 7 to 10 days.
Assessment of Hematologic Disorders
Platelet count: 150, 000 – 450, 000 / microliter
• Most hematologic diseases reflect a defect in the
1. Hematopoietic system
2. Hemostatic system
3. Reticuloendothelial system

• The defect can be:

1. Quantitative (increased or decreased
PLASMA and PLASMA PROTEINS production of cells)
• The liquid portion of blood 2. Qualitative (the cells that are produced
• More than 90% of plasma is water. are defective in their normal functional
• The remainder consists primarily of plasma proteins, capacity)
clotting factors (particularly fibrinogen), and small 3. Both
amounts of other substances such as nutrients,
enzymes, waste products, and gases.
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes

Hematologic Studies Classification of Anemia

• The most common tests used are:
1. Complete blood count (CBC)  Defect in their production (hypoproliferative
2. Peripheral blood smear anemia)
 Destruction (hemolytic anemia)
• The CBC identifies:  Loss (bleeding )
1. Total number of blood cells (RBC, WBC,
Platelets) A. Hypoproliferative Anemia
2. Hemoglobin
3. Hematocrit (percentage of blood volume  The marrow cannot produce adequate numbers of
consisting of erythrocytes) erythrocytes.
4. RBC indices  Reflected by an inappropriately normal or low
reticulocyte count.
WBC COUNT : 4,000 – 11, 000 cells / cumn  May result from marrow damage due to medications
Hct COUNT : M: 41% - 50% (e.g. chloramphenicol) or chemicals (e.g. benzene) or
F: 36 – 48 % from a lack of factors (e.g. iron, vitamin B12, folic acid,
RBC INDICES: erythropoietin) necessary for erythrocyte formation
1. MCV (80 – 100 fl)
2. MCH (27.5 – 33.2 pg) B. Hemolytic Anemia
3. MCMH (33.4 – 33.5 g/dL)
 Premature destruction of erythrocytes results in the
liberation of hemoglobin from the erythrocytes into
Peripheral Blood Smear
the plasma.
- Examination of blood cell’s morphology (shape and
 The increased erythrocyte destruction leads to tissue
appearance)
hypoxia, which in turn stimulates erythropoietin
production.
Bone Marrow Aspiration and Biopsy
Clinical Manifestations
• Done when additional information is needed to
Aside from the severity of the anemia itself, several factors
assess how a person’s blood cells are being formed
influence the development of anemia-associated symptoms:
and to assess the quantity and quality of each type of
• The rapidity with which the anemia has developed
cell produced within the marrow.
• The duration of the anemia (its chronicity)
• Also used to document infection or tumor within the
• The metabolic requirements of the patient
marrow.
• Other concurrent disorders or disabilities
(cardiopulmonary disease)
• Special complications or concomitant features of the
condition that produced the anemia
Bone
HYPOPROLIFERATIVE ANEMIAS
Marrow Aspiration
I. Iron Deficiency Anemia
• The most common type of anemia in all age groups.
• Particularly prevalent in developing countries
• Results when the intake of dietary iron is inadequate
for hemoglobin synthesis.
ANEMIA • In children, adolescents, and pregnant women, the
cause is typically inadequate iron in the diet to keep
 A condition in which the hemoglobin concentration is up with increased growth.
lower than the normal, reflects the presence of fewer • In adults with IDA, the cause is blood loss.
than normal erythrocytes within the circulation. • Other causes include iron malabsorption, as is seen
 As a result, the amount of oxygen delivered to body after gastrectomy or with celiac disease.
tissues is also diminished.
 It is not a disease per se, but a sign of an underlying Clinical Manifestation
disorder. • Patients with IDA have the symptoms of anemia.
 It is particularly prevalent among the elderly.
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes
• If the deficiency is severe or prolonged, they may also
have a smooth, sore tongue, brittle and ridged nails;
and angular cheilosis.
stomatitis
glossitis
Cheilitis
Brittle nails
Assessment and Diagnostic Findings
 Bone marrow aspiration – the definitive method of
establishing the diagnosis
 MCV (mean corpuscular volume) – measures the size
of the erythrocytes – decreased
 Hematocrit and RBC levels are low in relation to the
hemoglobin levels.
 Low ferritin level
 Low serum iron level
Medical Management
• Stool exam should be tested for occult blood
• People 50 years old and above = should have
periodic colonoscopy, endoscopy, X-ray of the GIT
• Administration of oral iron preparations (ferrous
sulfate, ferrous gluconate, ferrous fumarate) to treat
IDA for as long as 6 to 12 months
• Vitamin C facilitates the absorption of iron
• IV or IM administration of iron dextran (check for
allergy)
Nursing Management
1. Preventive education
• IDA is common in menstruating and pregnant
women
• Advise patients to take iron-rich foods with a source
of vitamin C to enhance the absorption of iron
• Nutritional counseling to patients with a history of
eating fad diets or strict vegetarian diets
• Instruct the patient to take the supplement an hour
before meals (iron is best absorbed on an empty
stomach)
• Avoid antacids and dairy products when taking iron
supplement (diminishes absorption)
• Instruct the patient to take the liquid form of iron
through a straw (to avoid staining nof the teeth)
• Inform the patient that iron salts may color the stool
dark green or black.
• For IM injection of iron, use Z-track method
ANEMIA IN RENAL DISEASE
• In general, patients do not become significantly
anemic until the serum creatinine level exceeds
3mg/100mL (normal serum creatinine is .5 –
1.2mg/mL)
• This anemia is caused by both a mild shortening of
erythrocyte life span and a deficiency of
erythropoietin (necessary for erythropoiesis)
Management
• Administration of recombinant erythropoietin:
• Epoetin alfa (epogen, Procrit)
• Darbepoetin alfa (Aranesp)
• Check the hematocrit frequently to prevent
hypertension (dose of erythropoietin should be
titrated to the hematocrit)
APLASTIC ANEMIA
• Is a rare disease caused by a decrease in or damage
to marrow stem cells, damage to the
microenvironment within the marrow, and
replacement of the marrow with fat.
• The precise etiology is unknown, but it is
hypothesized that the body’s T cells mediate an
inappropriate attack against the bone marrow,
resulting in bone marrow aplasia (markedly reduced
hematopoiesis).
• In addition to anemia, significant neutropenia and
thrombocytopenia are also seen.
Pathophysiology
• Can be congenital or acquired but most cases are
idiopathic
• Infections and pregnancy can trigger it
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes
• It may be caused by certain medications, chemicals,
or radiation damage
Clinical Manifestations
• Infection and symptoms of anemia (fatigue, pallor,
dyspnea)
• Purpura (bruising) may develop later
• Repeated throat infections with cervical
lymphadenopathy
• Splenomegaly
• Retinal hemorrhages
Assessment and Diagnostic Findings
• In many situations, aplastic anemia occurs when a
medication or chemical is ingested in toxic amounts.
• In a few people, it develops after a medication has
been taken at the recommended dosage.
• A bone marrow aspirate shows an extremely
hypoplastic or even aplastic (very few to no cells)
marrow replaced with fat.
Medical Management
• Those who are younger than 60 years, healthy, and
who have a compatible donor can be cured of the
disease by a bone marrow transplant (BMT) or
peripheral blood stem cell (PBSCT)
• Immunosuppressive therapy using a combination of
antithymocyte globulin (ATG) and cyclosporine.
Side effects may include:
• Fever and chills (common)
• Rashes and bronchospasm may herald anaphylaxis
and requires prompt management
• Patients receiving this immunosuppressive therapy
have a 55% 7-year survival rate
• Any offending agent is discontinued.
Nursing Management
• Assess carefully for signs of infection and platelet
deficiencies.
MEGALOBLASTIC ANEMIA
• Anemias caused by deficiencies of vitamin B12 or
folic acid
• Identical bone marrow and peripheral blood changes
occur because both vitamins are essential for normal
DNA synthesis.
• The erythrocytes that are produced are abnormally
large and are called megaloblastic red cells
• A bone marrow analysis reveals hyperplasia
(abnormal increase in the number of cells), and the
precursor erythroid and myeloid cells are large and
bizarre in appearance.
• In advanced stages of disease, the hemoglobin value
may be as low as 4 to 5 g/dL, the leukocyte count
2,000 to 3,000/mm3, and the platelet count less than
50,000/mm3.
RBCs in Megaloblastic Anemia
Pathophysiology
FOLIC ACID DEFICIENCY
• Folic acid is stored as compounds referred to as
folates.
• They are quickly depleted when the dietary intake of
folate is deficient (within 4 months)
• Found in green vegetables and liver
• Folate deficiency occurs in people who rarely eat
uncooked vegetables
• Alcohol increases folic acid requirements
• Folic acid requirements are also increased in patients
with chronic hemolytic anemias and in women who
are pregnant (increased erythrocyte production is
needed)
• Some patients with malabsorptive diseases of the
small bowel, such as sprue, may not absorb folic acid
normally.
VITAMIN B12 DEFICIENCY (Cobalamin or Pernicious Anemia)
• Can develop in strict vegetarians who consume no
meat or dairy products (rare)
• Faulty absorption from the GI tract is more common
( Crohn’s disease, after ileal resection, or
gastrectomy)
• Another cause is the absence of intrinsic factor, as in
pernicious anemia.
• Without intrinsic factor, orally consumed vitamin B12
cannot be absorbed, and erythrocyte production is
eventually diminished.
Clinical Manifestations
• Symptoms of folic acid and vitamin B12 deficiencies
are similar, and the two anemias may coexist.
• However, the neurologic manifestations of vitamin
B12 deficiency do not occur with folic acid deficiency,
and they persist if vitamin B12 is not replaced.
• Careful distinction between the anemias must be
made.
• Patients with pernicious anemia develop a smooth,
sore, red tongue and mild diarrhea.
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes
• They are extremely pale, particularly in the mucous
membranes.
• They may become confused; paresthesias in the
extremities.
• They may have difficulty maintaining their balance
(damage to the spinal cord)
• They also lose position sense (proprioception)
• Without treatment, patients can die after several
years, usually from heart failure secondary to anemia.
Assessment and Diagnostic Findings
• Schilling test (to determine the cause of vitamin B12
deficiency)
• Intrinsic factor antibody test (more useful and easier
test)
Medical Management
• Folate deficiency is treated by increasing the amount
of folic acid in the diet and administering 1 mg of folic
acid daily.
• Folic acid is administered IM only to people with
malabsorption problems.
• Folic acid replacement can be stopped after
hemoglobin level returns to normal.
• Vitamin B12 deficiency is treated by vitamin B12
replacement.
• Monthly IM injections of vitamin B12 (for defects in
absorption or absence of intrinsic factor)
Nursing Management
• Assessment of patients who have or are at risk of
megaloblastic anemia includes inspection of the skin
and mucous membranes.
• Mild jaundice (sclera)
• Vitiligo (patchy loss of skin pigmentation)
• Premature graying of hair
• Smooth, red, and sore tongue
Vitiligo
Careful neurologic assessment including tests of position and
vibration sense
 Pay particular attention to ambulation
 Assess the patient’s gait and stability and
the need for assistive devices and
assistance in managing daily activities
• Ensure safety
• Physical and occupational therapy
referrals may be needed
• Instruct patient to avoid excessive
heat and cold
• The nurse advises the patient to
eat small amounts of bland, soft
foods.
HEMOLYTIC ANEMIA
• In hemolytic anemias, the erythrocytes have a
shortened life span
• Fewer erythrocytes result in decreased available
oxygen, causing hypoxia, which in turn stimulates an
increase in erythropoietin release from the kidney.
• The erythropoietin stimulates the bone marrow to
compensate by producing new erythrocytes and
releasing some of them into the circulation somewhat
prematurely as reticulocytes.
SICKLE CELL ANEMIA
• Is a severe hemolytic anemia that results from
inheritance of the sickle hemoglobin gene.
• This gene causes the hemoglobin molecule to be
defective.
• The sickle hemoglobin (HbS) acquires a crystal-like
formation when exposed to low oxygen tension losing
its round, pliable, biconcave disk shape and becomes
deformed, rigid, and sickle-shaped.
• These long, rigid erythrocytes can adhere to the
endothelium of small vessels; when they adhere to
each other, blood flow to a region or an organ may be
reduced.
• If ischemia or infarction results, the patient may have
pain, swelling, and fever.
• If the erythrocyte is again exposed to adequate
amounts of oxygen before the membrane becomes
rigid, it can revert to a normal shape.
• For this reason, the “sickling crises” are intermittent.
• Cold can aggravate the sickling process, because
vasoconstriction slows the blood flow.
• The HbS gene is inherited in people of African descent
and to a lesser extent in people from the Middle East,
the Mediterranean area, and aboriginal tribes in
India.
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes

• Most children with sickle cell anemia have had a

splenic infarction by 10 years of age, and the spleen is
then no longer functional (autosplenectomy).
• In adults, the common organs involved in
sequestration are the liver and more seriously, the
lungs.

ACUTE CHEST SYNDROME

• Is manifested by a rapidly decreasing hemoglobin
level, tachycardia, fever, and bilateral infiltrates seen
on the chest x-ray.
• These signs often mimic infection, but in fact the most
common cause appears to be infarction within the
pulmonary vasculature.
• Although this syndrome is potentially lethal, prompt
intervention can result in a favorable outcome.

Pulmonary Hypertension
• Is a common sequel of sickle cell disease.
• Patients with sickle cell anemia are most likely to die
of either pulmonary hypertension or chronic lung
disease.
Clinical Manifestations
• Symptoms and complications result from chronic
Assessment and Diagnostic Findings
hemolysis or thrombosis.
• The patient with sickle cell trait usually has a normal
• The sickled erythrocytes have a shortened life span.
hemoglobin level, a normal hematocrit, and a normal
• Anemia is always present
blodd smear.
• Jaundice is characteristic and is usually onvious in the
• In contrast, the patient with sickle cell anemia has a
sclera.
low hematocrit and sickled cells on the smear.
• The bone marrow expands in childhood in a
• The diagnosis is confirmed by hemoglobin
compensatory effort to offset the anemia leading to
electrophoresis.
enlarged bones of the face and skull.
• Tachycardia, cardiac murmurs, cardiomegaly due to
Prognosis
chronic anemia
• Patients with sickle cell anemia are usually diagnosed
• Dysrhythmias and heart failure may occur in adults.
in childhood, because they become anemic in infancy
• Complications of sickle cell anemia include infection,
and begin to have sickle cell crises at 1 or 2 years of
stroke, renal failure, impotence, heart failure, and
age.
pulmonary hypertension.
• Some children die in the first years of life, typically of
infection, but antibiotic use and parent teaching
Sickle Cell Crisis
strategies have greatly improved the outcomes for
3 Types:
these children.
1. Sickle crisis
• Most common and very painful
Medical Management
• Results from tissue hypoxia and necrosis due to
• There are only four primary treatment modalities for
inadequate blood flow to a specific region of tissue or
sickle cell disease:
organ.
• Bone marrow transplant
2. Aplastic crisis
• Hydroxyurea
• Results from infection with the human parvovirus.
• Arginine
• The hemoglobin level falls rapidly and the marrow
• Long-term RBC transfusion
cannot compensate, as evidenced by an absence of
reticulocytes.
Pharmacologic Therapy
3. Sequestration crisis
1. Hydroxyurea
• Results when other organs pool the sickled cells.
• A chemotherapy agent
• The spleen is the most common organ responsible for
sequestration in children.
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes
• Increases hemoglobin F levels in patients with sickle
cell anemia thereby decreasing the permanent
formation of sickled cells.
• Side effects include chronic suppression of leukocyte
formation, teratogenesis, potential for later
development of malignancy.
2. Arginine
• Has antisickling properties
• Can enhance the availability of nitric oxide, a potent
vasodilator, resulting in decreased pulmonary artery
pressure.
• Synergistic with hydroxyurea, can be useful as
combination therapy for managing pulmonary
hypertension.
Transfusion Therapy
• Chronic RBC transfusions have been effective in
several situations:
1. In an acute exacerbation of anemia (aplastic crisis)
2. In the prevention of severe complications from
anesthesia and surgery
3. In improving the response to infection
4. In diminishing episodes of sickle cell crisis in pregnant
women (not to improve fetal survival)
Risks of complications from transfusion to consider:
1. Iron overload (necessitates chronic chelation
therapy)
2. Poor venous access (necessitates a vascular
access device)
3. Infections (hepatitis, HIV)
4. Alloimmunization from repeated
transfusions(an immune response to antigens
from donor cells)
5. Increased blood viscosity without reduction
in the concentration of hemoglobin S
 Exchange transfusion may be performed to reduce the
risk of increasing the viscosity excessively.
 Patients with sickle cell anemia require daily folic acid
replacements to maintain the supply required for
increased erythropoiesis from hemolysis.
 Infections must be treated promptly with appropriate
antibiotics
 Acute chest syndrome is managed by prompt initiation of
antibiotic therapy
 Incentive spirometry has been shown to decrease the
incidence of pulmonary complications
 Brochoscopy may be required to identify the source of
pulmonary disease.
 Fluid restriction may be more beneficial than aggressive
hydration.
 Corticosteroids may be useful.
Supportive Therapy
Pain management is a significant issue.
• Many patients have pain on a daily basis
• Pain is severe enough to interfere with the ability to
work and function within the family unit.
• Pain is self-limited, lasting hours to days.
• Adequate hydration is important during a painful
sickling episode.
• IV hydration with dextrose 5% in water (D5W) or
dextrose 5% in 0.25 normal saline solution
• Supplemental oxygen may also be needed.
• Aspirin is very useful in diminishing mild to moderate
pain; it also diminishes inflammation and potential
thrombosis (antiplatelet aggregator)
• NSAIDs are useful for moderate pain or in
combination with opioid analgesics.
• Morphine is the drug of choice (opioid analgesic)
• PCA is frequently used (restores the patient’s control
over analgesia during hospitalization)
POLYCYTHEMIA
• Literally meaning, “too many cells in the blood”
• Refers to an increased volume of erythrocytes
• It is a term used when the hematocrit is elevated (to
more than 55% in males, more than 50% in females)
• Classified as either primary or secondary
• Also known as primary polycythemia
• Is a proliferative disorder in which the myeloid stem
cells seem to have escaped normal control
mechanisms.
• The bone marrow is hypercellular, and the
erythrocyte, leukocyte, and platelet counts in the
peripheral blood are elevated.
• The erythrocyte elevation is predominant; the
hematocrit can exceed 60%
• Over time, the spleen resumes its embryonic function
of hematopoiesis and enlarges.
• Eventually, the bone marrow may become fibrotic,
with a resultant inability to produce as many cells
(“burnt out” or spent phase)
• The incidence of polycythemia has been estimated at
2.3 per 100,000 people.
• Median survival exceeds 10 years with treatment but
is only 6 to 18 months without treatment.
Clinical Manifestations
• Ruddy complexion
• Splenomegaly
• Symptoms result from increased blood volume
- Headache
- Dizziness
- Tinnitus
- Fatigue
- Paresthesias
- Blurred vision
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes

• Removing enough blood (initially 500 mL once or

twice weekly) to diminish the blood viscosity and to
deplete the patient’s iron stores
Rudy complexion

• Increased blood viscosity

- Angina Phlebotomy
- Claudication
- Dyspnea • Chemotherapeutic agents (Hydroxyurea)
- Thrombophlebitis - To suppress bone marrow function
• Hypertension (but increases the risk of leukemia)
• Elevated uric acid resulting in gout and renal stone • Anagrelide (Agrylin)
formation - Inhibits platelet aggregation
• Generalized pruritus (due to histamine release) - Also a leukomogenic
• Erythromelalgia (burning sensation in the fingers and • Allopurinol (Zyloprim)
toes) - Is used to prevent gouty attacks in
- Can be relieved by cooling patients with elevated uric acid
concentrations

Nursing Management
• Assess for risk factors for thrombotic complications
- Smoking
erythromelalgia - Obesity
- Poorly controlled hypertension
• Reduce the likelihood of DVT
- Avoidance of tight or restrictive
clothing (particularly stockings)
- Crossing of legs
Assessment and Diagnostic Findings • Patients with a history of bleeding are usually advised
• Diagnosis is based on an elevated erythrocyte mass to avoid aspirin and aspirin-containing medications
• Enlarged spleen • Minimizing alcohol intake should also be emphasized
• Elevated leukocyte and platelet counts • The patient should be instructed to avoid iron
supplements
Complications • For pruritus, the nurse may recommend bathing in
• Increased risk for thromboses resulting in a CVA tepid or cool water and avopid vigorous toweling-off
(brain attack, stroke) or MI after bathing.
• Thrombotic complications are the most common • Sodium bicarbonate dissolved in bath water may also
cause of death be effective, along with applications of cocoa butter –
• Bleeding (due to dysfunctional platelets) or oatmeal-based lotions and bath products.
• Nosebleeds
• Ulcers SECONDARY POLYCYTHEMIA
• Frank GI bleeding • Is caused by excessive production of erythropoietin
• Hematuria • This may occur in response to a reduced amount of
• Intracranial bleeding oxygen, which acts as a hypoxic stimulus, as in
cigarette smoking, COPD, or cyanotic heart disease,
Medical Management or in nonpathologic conditions such as living at a high
• The objective is to reduce the high blood cell mass. altitude.
• Phlebotomy is an important part of the therapy. • It can also occur from neoplasms (renal cell
carcinoma) that stimulate erythropoietin production
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes
Medical Management
• Management of secondary polycythemia may not be
necessary
• It involves treating the primary conditions
• Therapeutic phlebotomy may be necessary in
symptomatic patients to reduce blood viscosity and
volume.
LEUKOPENIA
• A condition in which there are fewer leukocytes than
normal
• Results from neutropenia, or lymphopenia
(diminished lymphocytes)
NEUTROPENIA
• A neutrophil count of less than 2,000/mm3
• Results from decreased production of neutrophils or
increased destruction of these cells
• Neutrophils are essential in preventing in and
limiting bacterial infection.
• A patient with neutropenia is at an increased risk for
infection from both exogenous and endogenous
sources.
• The actual number of neutrophils, known as the
absolute neutrophil count (ANC), is determined by a
simple mathematical calculation using data obtained
from the CBC and differential.
ANC = Total WBC count x (% neutrophils + % bands)
100
• Normally, the neutrophil count is greater than
2000/mm3
For example, if the total WBC count is 3000/mm3 with 72%
neutrophils and 3% bands, the ANC would be calculated as
follows:
ANC = 3000 (72 + 3)
100
= 2250
• This result is not indicative of neutropenia, because
the ANC is greater than 2000 despite the low total
WBC count
• The risk is significant when the ANC is less than
1000/mm3, is high when it is less than 500/mm3, and
is almost certain when it is less than 100/mm3.
Clinical Manifestations
• There are no definite symptoms of neutropenia until
the patient becomes infected.
• A routine CBC with differential, as obtained after
chemotherapy treatment, can reveal neutropenia
before the onset of infection
Medical Management
• If the neutropenia is medication-induced, the
offending agent is stopped immediately
• Corticosteroids may be used is the cause is an
immunologic disorder
• The use of growth factors such as G-CSF or GM-CSF
can be effective in increasing neutrophil production
when the cause of the neutropenia is decreased
production.
• Withholding or reducing the dose of chemotherapy or
radiation therapy may be required when the
neutropenia is caused by these treatments.
• If the neutropenia is accompanied by fever, the
patient is considered to have an infection and is
usually admitted to the hospital.
Nursing Management
• Patient teaching is important particularly in the
outpatient setting
• Patients at risk of neutropenia should have blood
drawn for a CBC with differential
• Nurses need to be able to calculate the ANC and to
assess the severity of neutropenia and the risk of
infection.
LEUKEMIA
• Literally “white blood” is a neoplastic proliferation of
one particular cell type (granulocytes, monocytes,
lymphocytes, or infrequently erythrocytes or
megakaryocytes)
• The defect originates in the hematopoietic stem cell,
the myeloid, or the lymphoid tissue, usually derived
from B lymphocytes.
• The common feature of the leukemias is an
unregulated proliferation of leukocytes in the bone
marrow.
• In acute forms (or late stages of chronic forms), the
proliferation of leukemic cells leaves little room for
normal cell production.
• The cause of leukemia is not fully known, but there is
some evidence that genetic influences and viral
pathogenesis may be involved.
• Bone marrow damage from radiation exposure or
from chemicals such as benzene and alkylating agents
can cause leukemia.
• Leukemias are commonly classified according to the
stem cell line involved, either lymphoid or myeloid
• They are also classified as either acute or chronic
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes
ACUTE MYELOID LEUKEMIA (AML)
• Results from a defect in the hematopoietic stem cell
that differentiates into all myeloid cells: monocytes,
granulocytes (neutrophils, basophils, eosinophils),
erythrocytes, and platelets.
• The prognosis is highly variable.
• Patient age may be a factor. Younger patients may
survive for 5 years or more after diagnosis of AML
• Patients who are older or have a more
undifferentiated form of AML tend to have a worse
prognosis.
Clinical Manifestation
• Fever and infection (from neutropenia)
• Weakness and fatigue (from anemia)
• Bleeding tendencies (from thrombocytopenia)
• Pain from an enlarged liver or spleen
• Hyperplasia of the gums
• Bone pain from expansion of marrow
Assessment and Diagnostic Findings
• CBC shows a decrease in both erythrocytes and
platelets
• A bone marrow analysis shows an excess of immature
blast cells
Complications
• Bleeding and infection (major causes of death)
• Ecchymoses (bruises)
• Petechiae (pinpoint red or purple hemorrhagic spots
on the skin)
ecchymoses
petechiae
Medical Management
• The overall objective of treatment is to achieve
complete remission, in which there is no evidence of
residual leukemia in the bone marrow.
- Aggressive administration of
chemotherapy, called induction therapy,
requires hospitalization for several weeks
- Induction therapy typically involves high
doses of:
a. Cytarabine (Cytosar, Ara-C)
b. Daunorubicin (Cerubidine)
c. Mitoxantrone (Novantrone)
d. Idarubicin (Idamycin)
• During this time, the patient is typically very ill, with
bacterial, fungal, and occasionally viral infections,
bleeding, and severe mucositis, which causes
diarrhea and a marked decline in the ability to
maintain adequate nutrition.
• When the patient has recovered from the induction
therapy, he or she typically receives consolidation
therapy (postremission therapy) to eliminate any
residual leukemia cells that are not clinically
detectable and to reduce the chance for recurrence.
• Another aggressive treatment option is BMT or PBSCT
Complications of Treatment
• Massive leukemic cell destruction from
chemotherapy results in the release of intracellular
electrolytes and fluids into the systemic circulation
• Increases in uric acid levels, potassium, and
phosphates are seen
- Makes the patient vulnerable to renal stone
formation and renal colic, which can progress to acute
renal failure.
- Hyperkalemia and hypercalcemia can lead to cardiac
dysrhythmias, hypotension, neuromuscular effects
such as muscle cramps, weakness, and
spasm/tetany; confusion; and seizures.
- Patients require a high fluid intake, alkalization of
the urine, and prophylaxis with allopurinol to prevent
crystallization of uric acid and subsequent stone
formation.
• GI problems may result from the infiltration of
abnormal leukocytes into the abdominal organs and
from the toxicity of the chemotherapeutic agents.
• Anorexia, nausea, vomiting, diarrhea, and severe
mucositis are common.
CHRONIC MYELOID LEUKEMIA
• Mutation in the myeloid stem cell
• Normal myeloid cells continue to be produced
• A wide spectrum of cell type exists, from blast forms
through mature neutrophils
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes
• Extramedullary hematopoiesis: hepatomegaly &
splenomegaly
• A section of DNA is missing from the BCR gene of
chromosome 22 (Philadelphia chromosome) and is
translocated onto the ABL gene on chromosome 9
• The BCR-ABL gene produce tyrosine kinase protein –
causes leukocytes to divide rapidly
• Uncommon in people below 20 y.o.
• Problems with infection and bleeding are rare.
• Can progress to the acute phase (blast crisis)
Clinical Manifestations
• Asymptomatic
• Leukostasis inhibits blood flow through the capillaries
of lungs and brain = SOB and slight confusion
• Splenomegaly & hepatomegaly
• Insidious symptoms: malaise, anorexia, wt. loss
• Lymphadenopathy: rare
• 3 stages in CML:
a. chronic
b. transformation: bone pain, fever, wt.
loss
c. accelerated/ blast crisis: life-threatening
infections and bleeding
Medical Management
1. Oral tyrosine kinase inhibitor, imatinib mesylate
(Gleevec)
 Blocks signals that express the BCR-ABL
protein
 Imatinib: drug-drug interactions are
common; antacids and grapefruit limit drug
absorption
2. BMT (for healthy pts, <65 y.o., chronicphase)
3. PBSCT
• Oral chemotherapeutic agents: hydroxyurea or
busulfan (Myleran)
• Extreme leukocytosis: leukapheresis (temporarily
reduces the number of leukocytes)
ACUTE LYMPHOCYTIC LEUKEMIA
• Results from uncontrolled proliferation of immature
cells (lymphoblasts) derived from the lymphoid stem
cell.
• Most common in children(boys more than girls; peak
incidence = 4 y.o.)
• Responsive to treatment
• Frequently invades the CNS
• Viral infections are common
Clinical Manifestations
• Immature lymphocytes proliferate and impede the
development of normal myeloid cells
• Decreased erythrocyte and platelet counts
• Leukocyte counts either low or high nut there is
always a high proportion of immature cells
• Leukemic cell infiltration into other organs more
common than with other forms
• Pain from spleno and hepatomegaly
• Bone pain
• CNS infiltration: headache and vomiting
Medical Management
• Preventive cranial irradiation or intrathecal
chemotherapy
• Corticosteroids and vinca alkaloids
• Anthracycline: asparaginase (Elspar)
• Allogeneic transplant
• Imatinib
• Monoclonal antibodies
• Corticosteroids
• BMT or PBSCT
CHRONIC LYMPHOCYTIC LEUKEMIA
• A common malignancy of older adults
• Derived from a malignant clone of B lymphocytes
• Most of the leukemia cells are fully mature
• Early stage:
• Leukocytosis (>100,000 mm3)
• Pulmonary and cerebral complications of
leukocytosis in myeloid leukemias are not
found in CLL
• Lymphadenopathy
• Hepatomegaly and splenomegaly
• Later stage:
• Anemia and thrombocytopenia may develop
• Autoimmune = RES destroys bodies own RBC or
platelets
• Beta2-microglobulin = protein found on the surface of
lymphocytes
Clinical Manifestations
• Asymptomatic
• Lymphocytosis is always present
• RBC and platelet ct may be normal or decreased
• Lymphadenopathy
• Splenomegaly
• “B symptoms” = fevers, drenching night sweats,
unintentional weight loss
• Anergy: absent or decreased rxn to skin sensitivity
tests
Assessment and Management of Patients With Hematologic Disorders
Semifinals Notes
Fluid and Electrolytes:
Balance and Disturbances
REGULATION OF FLUID

 Normal movement of fluids through capillary

walls into tissues depends on:
◦ Hydrostatic pressure
◦ Osmotic pressure

HYDROSTATIC PRESSURE

- pressure exerted by the fluid on the walls of

blood vessel at the arterial & venous ends when it
is at rest
OSMOTIC PRESSURE
Exerted by the protein in the plasma (oncotic
pressure); the amount of hydrostatic pressure needed to
stop the flow of water by osmosis

NOTE: Note: The direction of fluid movement depends

on the differences of hydrostatic pressure and osmotic
pressure

REGULATION OF FLUID

• Osmosis
• Diffusion
• Filtration
• Active Transport

OSMOSIS

 Movement of fluid from a region of low solute

FLUID
“Third spacing”: loss of ECF into a space that does
not contribute to equilibrium
➢ Early evidence: decreased UO despite
adequate fluid intake
➢ E.g. ascites, burns, peritonitis, bowel
obstruction, massive bleeding into a joint or
body cavity
concentration to the region of high solute
concentration until the solutions are of equal
concentration
 The magnitude of osmosis depends on the
number of particles dissolved in the solution,
which influences the movement of fluid
between compartments.
 Tonicity: ability of solutes to cause an osmotic
driving force promoting water movement
from one compartment to another
 Oncotic pressure: the osmotic pressure
exerted by proteins
 Osmotic diuresis: increase in UO caused by
the excretion of substances such as glucose,
mannitol, or contrast agents in the urine

DIFFUSION
Fluid and Electrolytes:
Balance and Disturbances
 Natural tendency of molecules and ions to move
from an area of higher concentration to an area
of lower concentration
 Ex: O2 & CO2 exchange, tendency of sodium
movement from ECF to ICF
FILTRATION
 Movement of water and solutes from an area of
higher hydrostatic pressure to an area of lower
hydrostatic pressure
 Ex.
➢ Fluid from intravascular to interstitial
space from the pumping action of the
heart
ACTIVE TRANSPORT
 Physiologic pump that moves fluid from an area
of lower concentration to one of higher
concentration
 Movement is against a concentration gradient
 Sodium-potassium pump maintains the higher
concentration of extracellular sodium and
intracellular potassium
 Requires adenosine (ATP) for energy
Lab Tests for Evaluating Fluid Status
 Osmolality- the total number of dissolved
particles per kg; controls water movement
between & within body fluid compartments
◦ Serum osmolality – 280 – 300 mOsm/kg
◦ Urine osmolality – 200 – 800 mOsm/kg;
determined by urea, creatinine, and uric
acid
 Osmolarity – the total number of dissolved
particles per liter of solution
 Urine specific gravity – 1.010 to 1.025
◦ Less reliable indicator of concentration
than urine osmolality because increased
glucose or protein can falsely elevate
values
 BUN – end product of protein metabolism(from
both muscle & dietary intake) by the liver
◦ N = 10 – 20 mg/dL
◦ increase BUN: decreased renal function,
GI bleeding, DHN, increased protein
intake, fever, and sepsis
◦ Decrease BUN: end-stage liver disease,
low protein diet, starvation
 Creatinine – end product of muscle metabolism
◦ N = 0.7 – 1.4 mg/dL
 Hematocrit – measures the volume percentage of
RBC in whole blood
◦ N= males 42% - 52% ; females 35% -
47%
Urine Sodium – assess volume status, sodium
imbalances and acute renal failure
N= 50-220 mEq/24h

HOMEOSTATIC MECHANISMS
◦ Kidneys
◦ Lungs
ROUTES OF GAINS AND LOSSES ◦ Heart
◦ Adrenal Glands
 Gains
◦ Dietary intake of fluid and food or ◦ Parathyroid glands
enteral feeding ◦ Pituitary Glands
◦ Parenteral fluids
FLUID LOSSES Kidney Functions
o Regulation of ECF volume & osmolality
by selective retention & excretion of
body fluids
o Regulation of electrolyte levels in the
ECF
o Regulation of pH of the ECF
o Excretion of metabolic wastes & toxic
substances
Fluid and Electrolytes:
Balance and Disturbances
 Heart & Blood vessel functions
◦ Pumping action of heart allows urine
formation
◦ Failure of the pumping action interferes
with renal perfusion and water &
electrolyte regulation
 Lung Functions
◦ Sensible loss through exhalation
◦ Maintain acid-base balance
 Pituitary Functions
◦ Storage of ADH
◦ Adrenal Functions
◦ Aldosterone: Na and water retention, K
loss
◦ Cortisol: produce sodium & fluid
retention & potassium deficit (less
mineralocorticoid activity)
◦ Storage of ADH
 Other Mechanisms
◦ Baroreceptors
 Detect changes in pressure
within blood vessels
 Regulate sympathetic &
parasympathetic neural activity
as well as endocrine activities
◦ Osmoreceptors
 Sense changes in sodium
concentration then causes
release of ADH
◦ Renin-Angiotensin-Aldosterone System
 Aldosterone released with:
decreased Na, increased K, and
increased ACTH
Release of Atrial Natriuretic Peptide
 Released by the atrial cells in
response to increase atrial
pressure, angio II, endothelin, &
sympa stimulation
 Action is the direct opposite of
Renin-angiotensin-Aldosterone
system & decreases blood
pressure & volume
◦ ADH & thirst
 Maintain sodium concentration
& oral intake of fluids
 Released with: increased serum
osmolality or decrease in blood
volume
GERONTOLOGIC CONSIDERATIONS
 Reduced homeostatic mechanisms: cardiac, renal,
and respiratory function
 Decreased body fluid percentage
 Medication use
 Presence of concomitant conditions
FLUID VOLUME IMBALANCES
 Fluid volume deficit (FVD): hypovolemia
 Fluid volume excess (FVE): hypervolemia
FLUID VOLUME DEFICIT (HYPOVOLEMIA)
 Loss of ECF volume exceeds intake of fluid;
Water and electrolytes are lost in the same
proportion – ratio of serum electrolytes to water
remains the same
 Dehydration - loss of water alone with increased
serum sodium level
 Causes:
 Loss of body fluids - vomiting, diarrhea,
GI suctioning, sweating
 decreased intake,- nausea, lack of access
to fluids
 Third-space fluid shifts
 Risk factors: diabetes insipidus, adrenal
insufficiency, osmotic diuresis, hemorrhage, coma
Fluid and Electrolytes:
Balance and Disturbances
FLUID VOLUME DEFICIT: ASSESSMENT AND
DIAGNOSTIC FINDINGS
 elevated BUN to creatinine ratio
 increased hematocrit,
 possible serum electrolyte changes
 Hypokalemia – GI & renal
losses
 Hyperkalemia: - adrenal
insufficiency
 Hyponatremia - increased thirst
& ADH release
 Hypernatremia - increased
insensible losses & diabetes
insipidus
 Increased urine specific gravity and urine
osmolality
CORRECT HYPOVOLEMIA
GERONTOLOGIC CONSIDERATIONS
 ⇧ sensitivity to F&E changes
 Alterations in skin elasticity
 Changes in ability to determine/meet food &
fluid needs
FLUID VOLUME DEFICIT: MEDICAL
MANAGEMENT
 provide fluids to meet body needs
◦ Oral fluids
◦ IV fluids
 Isotonic solution: e.g. Lactated
Ringer’s or 0.9% NaCl
 Hypotonic solution: e.g. 0.45%
NaCl
 once pt. is normotensive
 Provide water &
electrolytes for renal
excretion of metabolic
wastes
 Fluid challenge Test: if oliguric
◦ Volumes of fluid administered at specific
rates & intervals while the patient’s
hemodynamic response is monitored
◦ 100 to 200 mL of NSS over 15 mins ⇢ ⇧
UO, ⇧ BP and ⇧ CVP
FLUID VOLUME DEFICIT: NURSING
MANAGEMENT
 ASSESSMENT
◦ I&O
◦ weight
◦ VS
◦ skin and tongue turgor, mucous
membranes
◦ Urine concentration
◦ Mental status
◦ s/s of decreased peripheral tissue
perfusion
 PREVENT HYPOVOLEMIA
◦ Identify pts at risk
◦ Minimize fluid loss
 Diarrhea – antidiarrheal agents,
fluids at frequent intervals
Oral fluids
Frequent mouth care
Provide nonirritating fluids
Oral rehydration solutions
Nausea – antiemetics
FLUID VOLUME EXCESS (HYPERVOLEMIA
 Isotonic expansion of the ECF caused by the
abnormal retention of water and sodium
 Causes: fluid overload or diminished fxn of
homeostatic mechanisms
 Risk factors: heart failure, renal failure, and
cirrhosis of the liver
 Contributing factors: excessive dietary
sodium or sodium-containing IV solutions
Fluid and Electrolytes:
Balance and Disturbances
✓ Use salt substitutes with caution: contain
FLUID VOLUME EXCESS: CLINICAL K! ammonium chloride!
MANIFESTATIONS ✓ Use distilled water
✓ Avoid water softeners
 High protein diet
 Edema  Teach about edema:
 distended neck veins
 abnormal lung sounds ✓ Causes
 Tachycardia, increased BP, pulse pressure, and
CVP  Increased capillary fluid pressure
 increased weight  Decreased capillary oncotic
 increased UO pressure – decreased albumin
 shortness of breath and wheezing
 Increased interstitial oncotic
pressure- obstruction to
FLUID VOLUME EXCESS: ASSESSMENT AND
lymphatic flow
DIAGNOSTIC FINDINGS
 Meds: NSAIDS, corticosteroids,
 BUN & HCT are decreased
antihypertensives
 Serum osmolality and sodium levels decreased
 Xray - pulmonary congestion ✓ Localized or generalized; ascites

FLUID VOLUME EXCESS: MEDICAL

MANAGEMENT FLUID VOLUME EXCESS: NURSING
INTERVENTIONS
directed at the cause restriction of fluids and sodium, and
the administration of diuretics  Elevate edematous extremities
1. Restriction of fluids & sodium  Use semi-Fowler’s position for orthopnea
2. Diuretics  Skin care and positioning/turning
➢ Thiazide for mild to moderate
hypervolemia
*ayaw nag palabi sa tuon megs*
➢ Loop diuretics for severe hypervolemia
S/E: Hypokalemia, Hyperkalemia, PART 2
Hyponatremia, Hypomagnesemia
ELECTROLYTE BALANCE AND IMBALANCE
2. Hemodialysis / Peritoneal Dialysis
3. Nutritional Therapy  Active chemicals that carry positive (cations) and
negative (anions) electrical charges
 Major cations:
FLUID VOLUME EXCESS: NURSING
MANAGEMENT • Major anions:
 I&O and daily weights; assess for lung sounds ◦ Sodium
 Edema – check for indentation; measure ◦ Potassium
circumference ◦ Calcium
 monitor responses to medications such as ◦ Magnesium
diuretics ◦ Hydrogen ions
 sodium and fluid restrictions Electrolyte concentrations differ in the fluid
✓ Avoid foods high in Na compartments
✓ Avoid OTC meds  Expressed in milliequivalents (mEq)/L
✓ Light salting of food  Electrolyte concentrations in the ICF differ from
✓ Read food labels those in the ECF
✓ Use Seasoning substitutes: lemon juice,
onions, garlic
Fluid and Electrolytes:
Balance and Disturbances
 irrigation of NGT with water
ICF  Compulsive H2O drinking
CLINICAL MANIFESTATIONS:
Cation: potassium
 Poor skin turgor, dry mucosa, headache,
Anion: phosphates & sulfates decreased salivation, decreased BP, nausea,
abdominal cramping
ECF  Neurologic changes: altered mental status, status
epilepticus & coma; obtundation
Cation: Sodium  Anorexia, muscle cramps, feelings of exhaustion
Anion: Chloride  When serum Na level decreases to < 115 mEq/L
◦ Increased ICP; lethargy; confusion;
muscle twitching; focal weakness;
ELECTROLYTE IMBALANCES hemiparesis; pappiledema; seizures
◦
 Sodium: hyponatremia and hypernatremia
HYPONATREMIA: LABORATORY FINDINGS
 Potassium: hypokalemia and hyperkalemia
 Calcium: hypocalcemia and hypercalcemia  Serum sodium- <135 mEq/L
 Magnesium: hypomagnesemia and  SIADH
hypermagnesemia
 Phosphorus: hypophosphatemia and ➔ Se Na as low as 100 mEq/L
hyperphosphatemia ➔ ↑ specific gravity >1.012 & urine
 Chloride: hypochloremia and hyperchloremia Na >20mEq/L
 Serum osmolality- <270 mOsm/kg (diluted)
SODIUM (NA)  Low Specific gravity 1.002-1.004 (overdehydrated)

 N = 135 to 145 mEq/L

 Most abundant: ECF
 Primary determinant of ECF volume and
osmolality
 Control distribution of water throughout the
body
 Regulated by: ADH, thirst, RAAS
 Loss or gain is accompanied by a loss or gain
of water
 Establish the electromechanical state
necessary for muscle contraction and
transmission of nerve impulses
HYPONATREMIA
 Serum sodium less than 135 mEq/L
Causes:
 Imbalance of water rather than sodium
 Diuretics
 non-renal: vomiting, diarrhea, sweating
 dilutional hyponatremia: ECF volume increased
without any edema
 adrenal insufficiency
 SIADH
 Hyperglycemia increase H2O intake
 use of tap-water enemas
HYPONATREMIA: MEDICAL MANAGEMENT
1. Sodium replacement
a. Na administration (oral, NGT, parenteral) -
Should not exceed 12 mEq/L/24hrs (neurologic
damage due to osmotic demyelination)
b. Dietary intake of Na
c. Infusion of Lactated Ringer’s solution or isotonic
saline (0.9 % sodium chloride)
2. Water restriction
a. LOF: 800 mL/day
b. Administer small amount of a hypertonic sodium
solution, 3 % to 5 % NaCl if neurologic
symptoms are present
◦ administered slowly and in small
volumes
◦ monitored closely for fluid
overload
◦ patient receives a loop diuretic to
prevent ECF volume overload
and to increase water excretion
Fluid and Electrolytes:
Balance and Disturbances
HYPONATREMIA: NURSING MANAGEMENT
 Monitor I/O and daily weight.
LABORATORY FINDINGS
 Note abnormal losses of sodium or gains of
water.
 Monitor GI manifestations
 Monitor neurological changes
 Encourage foods and fluids with a high sodium
diet. MEDICAL MANAGEMENT
 Observe lithium toxicity for patients taking
lithium.
 Determine actual fluid needs – based on I&O,
urine specific gravity, and serum sodium levels
HYPERNATREMIA
Etiology: NURSING MANAGEMENT
 Caused by a gain of sodium in excess of water or
by a loss of water in excess of sodium (may occur
with normovolemia, FVD or FVE) – common:
very old, very young & impaired patients
 Ingestion of more sodium than water
 Fluid deprivation (comatose)
 Administration of hypertonic enteral feedings
without adequate water supplements
 Watery diarrhea & ↑insensible water loss
 Diabetes insipidus or ADH deficiency
 Heat stroke, near-drowning in sea water,
malfunction of hemodialysis/peritoneal
dialysis; IV administration of hypertonic
saline or excessive use of sodium bicarbonate
MANIFESTATIONS:
 primarily neurologic and ↑ plasma osmolality
 leads to a concentrated ECF
1. Primary characteristic: Thirst (may be impaired in
elderly & ill)
2. Moderate hypernatremia
◦ restlessness and weakness
moves into cells when:
3. Severe hypernatremia
◦ disorientation, delusions, and
hallucinations
◦ permanent neurologic damage can occur
◦ slightly elevated temperature; dry, moves out of the cells during:
swollen tongue; sticky mucosa;
neurologic symptoms; restlessness;
weakness; postural hypotension,
oliguria; flushed skin, peripheral &
pulmonary edema
 Serum sodium level > 145 mEq/L
 Serum osmolality >300 mOsm/Kg
 Increased urine specific gravity and urine
osmolality
1. Hypotonic electrolyte solution (0.3% NaCl) or
isotonic solution (D W)
5
2. Diuretics
3. Desmopressin acetate (DDAVP) – a synthetic
ADH for treatment of hypernatremia due to DI
 Assess use of OTC drugs (e.g. Alka-Seltzer)
 Adequate fluid intake and water with tube
feedings
 Prevention: Offer fluids at regular intervals.
Unconscious patients by alternative routes
 For Diabetes insipidus- adequate water intake
must be ensured
 To correct hypernatremia: Parenteral fluids,
monitor on serum sodium levels and monitor
neurologic changes
POTASSIUM (K+)
 N = 3.5-5.0 meq/L
 Functions:
◦ Assist in regulation of intracellular
osmolality
◦ Necessary for cellular growth and
metabolism
◦ Helps promote conduction of impulses
◦ Helps promote proper function of
skeletal & cardiac muscle activity
◦ Potassium:
◦ glucose is metabolized
◦ during beta adrenergic stimulation
◦ during alkalosis
◦ strenuous exercise
◦ cellular metabolism is impaired
◦ when cells die
◦ during acidosis
Fluid and Electrolytes:
Balance and Disturbances
◦ Regulation : Kidneys
HYPOKALEMIA
Etilogy:
1. Inadequate intake of K+ (dietary habits, nausea,
anorexia; acute alcoholism; extreme dieting; NPO
orders; parenteral fluids are low in K+ and high
in Na+)
2. Increased utilization of K+ during the healing
phase of burns
3. Excessive loss of K+ (diuretics & antibiotics;
adrenal steroid therapy; excessive infusions of
saline solutions without K+ replacement;
gastric & intestinal suction, operations
involving drainage from the surgical site like
colostomies, ileostomies, large or small bowel
resections
4. Conditions of the GIT: vomiting & diarrhea
5. Metabolic disorders like hyperaldosteronism;
Cushing’s syndrome; Insulin therapy
6. Alkalosis due to K shift into cell in exchange
for hydrogen ion
7. Renal disorders like nephropathies and
diuretic phase of acute renal failure
CLINICAL MANIFESTATIONS
1. Due to ↓ neuromuscular irritability- weakness; speech
changes; flaccid paralysis; shallow respirations; decreased
intestinal motility; abdominal distention; anorexia;
paralytic ileus
2. Weakness of cardiovascular smooth muscle and
prolongation of myocardial repolarization
◦ predisposes the patient to digitalis
toxicity
3. Polyuria & nocturia- due to inability of kidneys to
concentrate urine
NURSING DIAGNOSIS
 Alteration in urinary elimination patterns due to
inability of kidneys to concentrate urine
 Anxiety and fear due to flaccid paralysis, shallow
respirations, and cardiac disturbances
 Altered nutrition: less than body requirements
due to anorexia and paralytic ileus
 Knowledge deficit involved in the administration
of diuretics, extreme dieting, & self-induced
vomiting
MEDICAL MANAGEMENT
 Increase dietary potassium (50-100 meq/L)
 Potassium replacement: Oral (Potassium
Chloride, Potassium Citrate, Potasssium
Bicarbonate, Potassium Triplex) and IV for severe
deficit
◦ IV Potassium: administered only after
adequate urine flow has been established;
stop infusion if urine volume is 20 ml/hr
for 2 consecutive hours
◦ administered using an infusion pump
and NEVER by IV push or IM or IV
drip
◦ Dilute well with PNSS
the maximum concentration of
potassium administered is 20 mEq/100
ml and the rate no faster than 20
mEq/hour
PREVENTING HYPOKALEMIA
 Increase intake of K-rich foods
 Educate: abuse of laxatives and diuretics
 Monitor I&O (40 mEq of potassium is lost every
liter of urine output)
 Monitor ECG changes
NURSING MANAGEMENT
 Assess carefully (severe hypokalemia is life-
threatening),
 Monitor of electrocardiogram (ECG), arterial
blood gases (ABGs), and dietary potassium,
 Provide nursing care related to IV potassium
administration
HYPERKALEMIA (>5.0 MEW/L)
Three major causes:
1. Retention of K+ in the body: renal failure, post-
operative individuals with poor urine output;
with adrenocortical insufficiency
2. Excessive release of potassium from cells: burns,
traumatic injuries, infection, or acidosis especially
with reduced renal function
3. Excessive intravenous infusions: rapid infusion of
K+
 also attributed by medications such as: KCl;
heparin; ACE inhibitors; captopril; NSAIDS and
potassium sparing diuretics
Fluid and Electrolytes:
Balance and Disturbances
6. Essential for building of bones and teeth
CLINICAL MANIFESTATIONS 7. Essential for secretions of many
hormones
 Cardiac effects: > 8 mEq/L = ECG changes • Calcium requirements:
➔ dysrhythmias & cardiac arrest
 Skeletal muscle weakness & paralysis 1. adult, at least 0.8 gm daily
 Slowed ventricular conduction
 Respiratory & speech muscle paralysis 2. infants and children, 0.17 – 1.4 gm daily
 GI manifestations: nausea, diarrhea 3. pregnant and lactating women, 1.3 – 1.5
gm daily
MEDICAL MANAGEMENT
• Ca intake:
 Decrease Potassium Intake- eliminate oral and
parenteral sources of K+ 1. ¾ supplied by milk and milk products
▪ Cation-exchange resins: sodium polysterene
sulfonate (Kayexalate) 2. ¼ supplied by vegetables and fruits
▪ Severe: IV calcium gluconate (antagonizes the
• Ca absorption:
action of hyperkalemia to the heart)
▪ Monitor BP 1. depends in part on presence of Vit. D
▪ IV administration of sodium bicarbonate (to
alkalinize plasma) 2. controlled by parathyroid gland
▪ IV insulin and a hypertonic dextrose solution
• Ca excretion: in urine and feces
(temporary shift of K into cells)
• Inverse relationship between Ca and Phosphorus
NURSING MANAGEMENT
+
1. when calcium is elevated, phosphorus is
 Assess serum K levels low
 Observe for signs of muscle weakness & 2. when calcium is low, phosphorus is
dysrrhythmias, paresthesias, GI symptoms
+ elevated
 Mix well IVs containing K
• Regulation of serum Ca
 Monitor medication effects
 Initiate dietary potassium restriction and dietary 1. controlled by PTH and calcitonin
teaching for patients at risk (food sources with
minimal K+ content: butter, margarine, cranberry HYPOCALCEMIA
juice, ginger ale, hard candy, rootbeer, sugar,
 Serum level less than 8.5 mg/dL must be
honey)
considered in conjunction with serum albumin
 Use salt substitutes sparingly
level
 Teach on K-sparing diuretics
 Causes: Excessive removal of Ca from the body
due to acute pancreatitis, diarrhea,
CALCIUM (8.6- 10.2 mg/dL) hypoparathyroidism, and renal diseases;
Thyroidectomy with accidental removal of
• Distribution of Ca++: 99 % in bones ; 1 % in parathyroid glands; Pregnancy and lactation (high
plasma demand of Calcium); Inadequate intake of
(ionized, bound, complexed) vitamin D; Following correction of acidosis and
• Functions include: alkalosis
1. Promotes normal neuromuscular
irritability
2. Promotes normal muscular contractility CLINICAL MANIFESTATIONS
3. Promotes transmission of nerve impulses
 Increased neuromuscular irritability producing
4. Strengthens capillary membranes
hyperaction of motor and sensory nerves to
5. Essential for blood clotting
stimuli:
Fluid and Electrolytes:
Balance and Disturbances
◦ Tetany - refers to the entire symptom
complex induced by increased neural
excitability (same with hypomagnesemia)
◦ tingling and numbness of fingers and
circumoral regions; painful tonic spasms;
facial spasms/tetany facies; grimacing;
fatigue; laryngospasm; (+) Chvostek’s and
Trosseau’s signs; convulsions
◦ mental changes (depression, impaired
memory, confusion, delirium,
hallucinations)
◦ hyperactive bowel sounds, dry and brittle
hair and nails, abnormal clotting for
chronic hypocalcemia
Hypocalcemia
 Altered cardiac muscle function
◦ definitive ECG tracing of prolonged QT
segment ; palpitations; arrythmias;
torsades de pointes (ventricular
tachycardia)
Laboratory Tests:
◦ Serum level below normal
◦ Serum phosphorus elevated
◦ Sulcowitch urine test(24 hr urine test)
shows no precipitation
NURSING DIAGNOSIS
 Acute pain due to tonic muscle spasms
 Anxiety and fear r/t increased neuromuscular
irritability, laryngospasm, and impending tetany
 Decreased cardiac outputr/t altered cardiac
muscle function
 Risk for injury r/t increased neuromuscular
irritability
MEDICAL MANAGEMENT
• corrected by oral, IM, IV CA salts:
 Calcium lactate, Calcium
gluceptate, Calcium chloride- do
not administer IM because it
irritates tissues
 Calcium gluconate
 administered slowly to
avoid hypotension,
bradycardia, arrythmias,
cardiac arrest
 a solution of 10%
calcium gluconate with 1
liter of 5% dextrose in
water and administered
as a slow IV bolus or a
slow IV infusion using a
volumetric infusion
pump
MANAGEMENT:
◦ Give 30 minutes before meals and/or at
bedtime for best absorption
 Vitamin D given in conjunction with Calcium
and for better GI absorption
 Patient with CRF must be prescribed with
Aluminum hydroxide, calcium acetate, or
calcium carbonate antacids to decrease elevated
phosphorus levels before treating hypocalcemia
 Increase dietary intake of calcium to at least
1,000 – 1,500 mg/day
* Food sources: milk products; green, leafy
vegetables; canned salmon; sardines; fresh oysters
NURSING MANAGEMENT
 Nursing management: assessment as severe
hypocalcemia is life-threatening, weight-bearing
exercises to decrease bone calcium loss, patient
teaching related to diet and medications, and
nursing care related to IV calcium administration
 seizure precautions for severe hypocalcemia
 monitor status of airway due to laryngeal stridor
 instruct patient to have an adequate dietary
calcium and consider calcium supplements
 a once-a-month biphosphonate drugs
administered to reduce the rate of bone loss
 inform patients on the following risk factors:
 alcohol and caffeine
inhibit calcium
absorption
 cigarette smoking
increases urinary
excretion of calcium
 risk of falls
 avoid the overuse of
laxatives and antacids
that contain phosphorus
because it decreases
calcium absorption
Fluid and Electrolytes:
Balance and Disturbances
HYPERCALCEMIA
 Serum level above 10.5 mg/dL
Etilogy:
 Hyperparathyroidism and malignancies,
 Movement of Ca from bones to serum (bone
tumors; multiple myeloma)
 Decreased renal excretion of Ca due to renal
failure
 Excessive administration/ingestion of Ca
 Excessive intake of Vitamin D(↑Ca absorption)
 Administration of thiazide diuretics(↓urinary
Ca)excretion, Milk-alkali syndrome
CLINICAL MANIFESTATIONS
 Hypercalciuria- Ca deposits in renal pelvis &
parenchyma;
 Lost of kidneys’ ability to concentrate urine;
Flank pain; kidney infection; kidney stones;
polyuria; renal failure; Excessive thirst
 Gastrointestinal disorders dt an increase Ca ions
in sympathetic ganglia (impedes transmission of
stimuli) diarrhea, constipation, atony of intestinal
tract, peptic ulcer, anorexia, N/V; complicated
with abdominal distention & paralytic ileus
 Behavioral changes due to neurologic
hypofunction: lethargy; exhaustion; mental
confusion; slurred speech; loss of interest in
surroundings; coma serum Ca level at 16 mg/dL
 Decalcification of bones (calcium moves from
bones into blood):bone pain; osteoporosis;
osteomalacia; pathologic fractures
 Increased calcium in serum; increased renal Ca
excretion; altered cardiac muscle function
- calcium levels above 11 mg/dl; definitive ECG
tracing; phosphorus often decreased; Sulcowitch
test shows increased Ca precipitation
 Hypercalcemic crisis
DIAGNOSTIC FINDINGS
 serum Ca > 10.2 mg/dL
 dysrythmias; shortening of the QT interval;
prolonged PR interval
 PTH increased in hyperparathyroidism and
suppressed in malignancy
 X-ray reveals osteoporosis
 Dense precipitation due to hypercalciuria
NURSING DIAGNOSIS
 Knowledge deficit regarding excessive ingestion of
Ca and Vit. D
 Knowledge deficit regarding need for hydration
and weight bearing activity when vulnerable to
Ca excess
 Altered urinary elimination patterns r/t
hypercalciuria
 Risk for injury due to mental confusion
 Risk for injury due to fractures arising from loss
of Ca from the bone matrix
 Impaired in bowel elimination: constipation or
diarrhea
Medical management: treat underlying cause, administer
fluids, furosemide, phosphates, calcitonin, and
biphosphonates
Nursing management: assessment as hypercalcemic crisis;
fluids of 3 to 4 L/d, provide fluids containing sodium
unless contraindicated and fiber for constipation, and
ensure safety
MEDICAL MANAGEMENT
To promote Ca excretion:
 ensure adequate hydration using saline solutions(
inhibit tubular reabsorption of Ca)
 use phosphate supplements- enhance Ca deposits
in bone and soft tissue; to reduce absorption of
intestinal Ca( administered orally or in NGT-
Phospho-soda; Neutra-phos)
 employ glucocorticoids- ↓ absorption from GIT
& reabsorption of tubular Ca
 administer mithramycin, used for hypercalcemia
due to malignancy(used to treat testicular
neoplasm; causes thrombocytopenia; renal and
hepatic damage)
 Administer calcitonin - lower Ca levels due to
excessive parathyroid activity; by IM (has a
risk of anaphylaxis; keep epinephrine,
antihistamines, and O2 on hand; useful for
those with heart disease and renal failure)
To prevent Hypercalcemia
 encourage early and regular ambulation
 ensuring adequate hydration and diuresis
 inform people taking vitamins that overdose
of Calcium and vitamin D can cause Ca
excess
Fluid and Electrolytes:
Balance and Disturbances
NURSING MANAGEMENT
 Inform patient the importance of frequent
ambulation.
 Fluids containing sodium should be
administered unless contraindicated;
favors Ca excretion.
 Patients are encouraged to drink 3- 4
quarts of fluid daily.
 Adequate fiber diet.
 Inform patient and family that mental
changes are reversible with treatment.
 Assess patient s/s for digitalis toxicity.
Cardiac rate and rhythm are monitored for any
abnormalities.
MAGNESIUM (1.3- 2.3 meq/L or 1.8-3 mg/dl)
 Most abundant intracellular cation after
potassium
 Functions of Magnesium: neuromuscular
function, CV effects: Vasodilation & ↓ peripheral
resistance
 Ingestion of Mg++ requires 200-300 mg/day
 Absorption of Mg++ is only 45 %
 Excretion in the feces
 Inhibit the release of Acetylcholine
 Similar with Calcium
HYPOMAGNESEMIA
 Serum level less than 1.8 mg/dL; evaluate in
conjunction with serum albumin
 Causes: alcoholism, GI losses, enteral or
parenteral feeding deficient in Mg,
meds:(Aminoglycosides, diuretics, digitalis); rapid
administration of citrated blood;
 Manifestations: neuromuscular irritability,
muscle weakness, tremors, athetoid movements
(slow, involuntary twisting & writhing) ECG
changes and dysrhythmias, and alterations in
mood and level of consciousness
 Medical management: diet, oral magnesium, and
magnesium sulfate IV
 Nursing management: assessment, ensure safety,
patient teaching related to diet, medications,
alcohol use, and nursing care related to IV
magnesium sulfate
 Hypomagnesemia is often accompanied by
hypocalcemia
 Monitor and treat potential
hypocalcemia
 Dysphagia is common in magnesium-
depleted patients; assess ability to
swallow with water before administering
food or medications
 Serum level more than 2.7 mg/dL
 Causes: renal failure, diabetic ketoacidosis, and
excessive administration of magnesium
 Manifestations: flushing, lowered BP, nausea,
vomiting, hypoactive reflexes, drowsiness, muscle
weakness, depressed respirations, ECG changes,
and dysrhythmias
 Medical management: IV calcium gluconate, loop
diuretics, IV NS of RL, hemodialysis
 Nursing management: assessment, avoid
administering medications containing
magnesium, and provide patient teaching
regarding magnesium-containing OTC
medications
HYPOPHOSPHATEMIA
 Serum level below 2.5 mg/dL
 Causes: alcoholism, refeeding of patients after
starvation, pain, heat stroke, respiratory alkalosis,
hyperventilation, diabetic ketoacidosis, hepatic
encephalopathy, major burns,
hyperparathyroidism, low magnesium, low
potassium, diarrhea, vitamin D deficiency, and
diuretic and antacid use
 Manifestations: neurologic symptoms, confusion,
muscle weakness, tissue hypoxia, muscle and
bone pain, and increased susceptibility to
infection
 Medical management: oral or IV phosphorus
replacement
 Nursing management: assessment, encourage
foods high in phosphorus, and gradually
introduce calories for malnourished patients
receiving parenteral nutrition
 Serum level above 4.5 mg/dL
 Causes: renal failure, excess phosphorus, excess
vitamin D, acidosis, hypoparathyroidism, and
chemotherapy
Fluid and Electrolytes:
Balance and Disturbances
 Manifestations: few symptoms, soft-tissue
calcifications, symptoms occur due to associated
hypocalcemia
 Medical management: treat underlying disorder;
use vitamin D preparations, calcium-binding
antacids, phosphate-binding gels or antacids, loop
diuretics, NS IV, and dialysis
 Nursing management: assessment, avoid high-
phosphorus foods, and provide patient teaching
related to diet, phosphate-containing substances,
and signs of hypocalcemia
HYPOCHLOREMIA
 Serum level less than 96 mEq/L
 Causes: Addison’s disease, reduced chloride
intake, GI loss, diabetic ketoacidosis, excessive
sweating, fever, burns, medications, and
metabolic alkalosis
 Loss of chloride occurs with loss of other
electrolytes, potassium, and sodium
 Manifestations: agitation, irritability, weakness,
hyperexcitability of muscles, dysrhythmias,
seizures, and coma
 Medical management: replace chloride—IV, NS,
or 0.45% NS
 Nursing management: assessment, avoid free
water, encourage high-chloride foods, and
provide patient teaching related to high-chloride
foods
Serum level more than 108 mEq/L
Causes: excess sodium chloride infusions with water
loss, head injury, hypernatremia, dehydration, severe
diarrhea, respiratory alkalosis, metabolic acidosis,
hyperparathyroidism, and medications
Manifestations: tachypnea, lethargy, weakness, rapid,
deep respirations, hypertension, and cognitive changes
Medical management: restore electrolyte and fluid
balance, LR, sodium bicarbonate, and diuretics
MAINTAINING ACID-BASE BALANCE
 Normal plasma pH is 7.35 to 7.45: hydrogen ion
concentration
 Major extracellular fluid buffer system;
bicarbonate-carbonic acid buffer system
 Kidneys regulate bicarbonate in ECF
 Lungs under the control of the medulla regulate
CO and, therefore, carbonic acid in ECF
2
 Other buffer systems
◦ ECF: inorganic phosphates and plasma
proteins
◦ ICF: proteins, organic and inorganic
phosphates
◦ Hemoglobin
METABOLIC ACIDOSIS
 Low pH <7.35
 Low bicarbonate <22 mEq/L
 Most commonly due to renal failure
 Manifestations: headache, confusion, drowsiness,
increased respiratory rate and depth, decreased
blood pressure, decreased cardiac output,
dysrhythmias, shock; if decrease is slow, patient
may be asymptomatic until bicarbonate is 15
mEq/L or less
 Correct the underlying problem and correct the
imbalance; bicarbonate may be administered
 With acidosis, hyperkalemia may occur as
potassium shifts out of the cell
 As acidosis is corrected, potassium shifts back
into the cell and potassium levels decrease
 Monitor potassium levels
 Serum calcium levels may be low with chronic
metabolic acidosis and must be corrected before
treating the acidosis
METABOLIC ALKALOSIS
 High pH >7.45
 High bicarbonate >26 mEq/L
 Most commonly due to vomiting or gastric
suction; may also be caused by medications,
especially long-term diuretic use
 Hypokalemia will produce alkalosis
 Manifestations: symptoms related to decreased
calcium, respiratory depression, tachycardia, and
symptoms of hypokalemia
Fluid and Electrolytes:
Balance and Disturbances
 Correct underlying disorder, supply chloride to
allow excretion of excess bicarbonate, and restore
fluid volume with sodium chloride solutions

RESPIRATORY ACIDOSIS

 Low pH <7.35
 PaCO >42 mm Hg
2
 Always due to a respiratory problem with
inadequate excretion of CO
2
 With chronic respiratory acidosis, the body may
compensate and may be asymptomatic; symptoms
may include a suddenly increased pulse,
respiratory rate, and BP; mental changes; feeling
of fullness in the head
 Potential increased intracranial pressure
 Treatment is aimed at improving ventilation

COMPLICATIONS OF IV THERAPY
RESPIRATORY ALKALOSIS
 Fluid overload
 High pH >7.45  Air embolism
 PaCO <35 mm Hg  Septicemia and other infections
2
 Infiltration and extravasation
 Always due to hyperventilation
 Phlebitis
 Manifestations: lightheadedness, inability to
 Thrombophlebitis
concentrate, numbness and tingling, and
 Hematoma
sometimes loss of consciousness
 Clotting and obstruction
 Correct cause of hyperventilation

ARTERIAL BLOOD GASES

 pH 7.35 (7.4) to 7.45

 PaCO 35 (40) to 45 mm Hg
2
 HCO ˉ 22 (24) to 26 mEq/L (assumed average
3
values for ABG interpretation)
 PaO 80 to 100 mm Hg
2
 Oxygen saturation >94%
 Base excess/deficit ±2 mEq/L
Communicable Disease Nursing
Semifinals Notes

TERMINOLOGIES 6. Opportunistic organisms causing infection in

• INFECTION
 the implantation and successful replication of an
organism in host tissue resulting to signs and
symptoms as well as immunologic response.
• CARRIER
- an individual who harbors the organism and is
capable of transmitting it to susceptible host without
showing manifestations of the disease.
• CONTACT
- Is a person or animal who is in close association with
an infected person, animal, or freshly soiled
materials.
immuno-compromised patients
7. Most people have not received immunization
8. Increased air travel can cause spread of virulent
organisms to a heavily populated area in hours.
9. Use of biologic warfare and bioterrorism
10. The expanded use of immunosuppressive drugs and
invasive procedures increases the risk of infection.
Chain of Infection

• ISOLATION
- separation from other persons of an individual suffering
from a communicable disease.

• HABITAT
- Is a place where an organism lives or where the
organism is usually found.
-
• HOST
- Is a person, animal, or plant on which a parasite A. Infectious/ Causative Agent
depends for its survival  Any microbe capable of producing a disease
1. Bacteria
• RESERVOIR 2. Spirochete
- composed of one or more species of animal or plant 3. Viruses
in which an infectious agent lives and multiplies for 4. Rickettsiae
survival and reproduces itself in such a manner that 5. Chalmydiae
it can be transmitted to man. 6. Fungi
7. Protozoa
• SURVEILLANCE 8. Parasites
- the act of watching
B. Reservoir
• COMMUNICABLE DISEASE 1. Human reservoir
- an illness caused by an infectious agent or its toxic a) Frank Cases or the very ill
products that are transmitted directly or indirectly to a b) Sub-clinical or ambulatory
well person through an agency, a vector or an inanimate c) Carrier
object. - Incubatory carrier : a person incubating
• INFECTIOUS DISEASE the illness
- transmitted not only by ordinary contact but requires - Convalescent carrier: a person at the
direct inoculation of the organism through a break in recovery stage of illness but continues to
the skin or mucous membrane. shed the pathogenic organism
- Intermittent carrier: occasionally sheds the
WHY INFECTION OCCURS? pathogenic organism
1. Resistance developed by bacteria to some antibiotics - Chronic or sustained carrier: always has the
2. Emerging strains of some microbes that cannot be infectious organisms in his or her system.
protected by a single vaccine 2. Animals
3. Resistance of virus to some antiviral meds 3. Nonliving things
4. Occasionally arising infectious agents (e.g. HIV,
anthrax, Ebola)
5. Localization of some microbes in areas of the body
difficult to treat
Communicable Disease Nursing
Semifinals Notes

F. Susceptible Host
– not possessing immunity to a particular pathogen

C. The Portal of Exit

- path or way in which the organisms leave the reservoir

1. Respiratory system ILLNESS FOLLOWING AN ENTRANCE OF PATHOGEN INTO THE

2. Genitourinary system BODY DEPENDS ON THE HOST:
3. Gastrointestinal tract 1. Age, sex, genes, and constitution;
4. Skin and mucous membrane 2. Nutritional status, fitness, environmental factors;
5. Placenta 3. General condition, physical, emotional, and mental
state;
4. Absence of or abnormal immunoglobulins;
D. Mode of Transmission means by which the infectious 5. Co-morbid states
agent passes through the portal of exit of the reservoir to 6. Treatment with certain antimicrobials,
the susceptible host. corticosteroids, radiation, or immunosuppressive
 the easiest link to break the chain of infection. drugs.
1. Contact Transmission
a. Direct – person-to-person transfer COURSE OF INFECTIOUS DISEASE
b. Indirect – susceptible person comes in 1. INCUBATION PERIOD
contact with contaminated object - time of infection to appearance of signs and
c. Droplet spread – contact with respiratory symptoms
secretions when the infected person 2. PERIOD OF PRODROMAL SYMPTOMS/ PRODROMAL PERIOD
coughs, sneezes, or talks - early symptoms that may mark the onset of a
2. Air-borne transmission – Spread by air current and is disease
inhaled by susceptible host. 3. PERIOD OF INVASION
3. Vehicle transmission – through articles or substances that - the disease reaches its full development and
harbor the organism until it is ingested or inoculated into the maximum intensity
host. - also referred to as Fastigium or Acme
4. Vector-borne transmission – occurs when intermediate 4. COMMUNICABLE PERIOD
carriers transfer the microbes to another living organism. -period after infection when an infectious agent can
be transmitted to another host.
5. LATENT PERIOD
-period after infection when an infectious agent
cannot be transmitted to another
6. DEFERVESCENCE OR DECLINE
-The stage during which the manifestations subside.

E. Portal of Entry OCCURRENCE

- a venue where the organism gains entrance into the 1. SPORADIC DISEASE
susceptible host - occasional and irregular(e.g. Tetanus, herpes,
skin diseases, leprosy in Manila)

2. EPIDEMIC DISEASES
- disease attacks a large number of people in a
community at the same time, or during the same
season, and in which disease tends to spread
rapidly to others (e.g. cholera, dengue)
Communicable Disease Nursing
Semifinals Notes

3. ENDEMIC 6. ENVIRONMENTAL DISINFECTION

- those that are present in a population or  Clean surfaces daily with disinfectant (diluted
community at times; usually involves few people household bleach, 70 percent alcohol)
during specific periods (typhoid fever in Manila,
dysentery) PREVENTIVE ASPECT OR CARE OF PATIENTS WITH
4. PANDEMIC COMMUNICABLE DISEASE
- an epidemic that affects several countries or 1. Health education
continents (e.g. HIV/AIDS, SARS) 2. Immunization
3. Environmental Sanitation
INFECTION CONTROL & work practice control MEASURES • Water Supply Sanitation
1. Employees shall wash their hands as soon as possible • Proper Excreta and sewage disposal
after the removal of gloves or other protective • Food Sanitation
equipment and after hand contact with blood or • Waste Management
other potentially infectious materials.
2. All personal protective equipment shall be removed HEALTH EDUCATION
immediately upon leaving the work area. • Educate the family and the client with respect to:
3. Used needles and other sharps shall not be sheared, o the availability and importance of
bent, broken, recapped, or re-sheathed by hand. prophylactic immunization
4. Eating, drinking, smoking, applying cosmetics or lip o the manner in which infectious illness is
balm, or handling contact lenses are prohibited in spread and the methods of avoiding the
work areas where there is potential occupational spread
exposure. o the importance of seeking medical advice for
5. Food and drinks shall not be stored in refrigerators, any sign of health problem
freezers, or cabinets where blood or other potentially o the importance of environmental cleanliness
infectious materials are stored. and personal hygiene
6. All procedures involving blood or other potentially o the means of preventing contamination of
infectious materials shall be performed in such a food and water supply
manner as to minimize splashing, spraying, and
aerosolization. IMMUNIZATION
7. Mouth pipetting/suctioning is prohibited.
• the introduction of specific protective antibodies or
THE USE OF BARRIER APPARELS the production of cellular immunity in a susceptible
1. MASKING person or animal
 All staff should wear mask.
 Patients with respiratory problems should be asked to Immunity
wear mask • a condition of being secure against any particular
2. HANDWASHING disease
 Practice proper hand washing with the use of soap Types of Immunity
and water. 1. Natural
 Wash hands before and after patient contact and a. Passive – acquired through placental
after removing the gloves. transfer (Maternal)
3. GLOVING b. Active – acquired through recovery
 Wear gloves for all direct contact with patients. from a certain disease (Infection)
 Change gloves and wash hands after every contact 2. Artificial
with each patient. a. Passive – acquired through the
4. GOWNING administration of antitoxin, antiserum,
 Wear gown during procedures which are likely to convalescent serum, and gammaglobulins
generate splashes or sprays of blood and body fluids, (Antibody transfer)
secretions, or excretions. b. Active – acquired through the administration
5. EYE PROTECTION (goggles) of vaccine and toxoid (Immunization)
 Wear goggles for aerosol/splash-generating
procedures. Types of Antigen/vaccines
 Avoid aerosols 1. Inactivated (killed organism)
a. Not long lasting
b. Multiple doses needed
Communicable Disease Nursing
Semifinals Notes

c. Booster dose needed AIRBORNE PRECAUTIONS

2. Attenuated (live organism) • Standard precautions plus:
a. Single dose needed • Place the patient in a private room that has
b. Long lasting immunity monitored negative air pressure, a minimum six air
exchanges per hour, and appropriate filtration of air
WHAT DAMAGES VACCINES? before it is discharged from the room.
• Heat and sunlight (esp live vaccines) • Wear respiratory protection when entering the room.
• Freezing damages the killed vaccines and toxoids. • Limit movement and transport of the patient. Place a
• Use water only in cleaning the refrigerator/freezer. mask on the patient if he or she needs to be moved.
Antiseptics, disinfectants, and detergents or alcohol • Conventional diseases requiring airborne
may lessen the potency of vaccines. precautions: measles, varicella, pulmonary
tuberculosis
KEEP ALL VACCINES AT THE CORRECT COLD TEMPERATURE • Biothreat diseases requiring airborne precautions:
(0-8 degrees Celsius) smallpox

The Cold Chain System DROPLET PRECAUTIONS

Maintenance of correct temperature for vaccines starts from • Standard precautions plus:
the manufacturer • Place the patient in a private room or cohort them
↓ with someone with the same infection. If not feasible,
Airport maintain at least 3 feet between patients.
↓ • Wear a mask when working within 3 feet of the
Central Vaccine Store patient.
↓ • Limit movement and transport of the patient. Place a
Regional Store mask on the patient if they need to be moved.
↓ • Conventional diseases requiring droplet precautions:
District Hosp. invasive haemophilus influenza and meningococcal
↓ disease, drug-resistant pneumococcal disease,
Health Centers or Outreach Service → Dispensary diphtheria, pertussis, mycoplasma, GABHS,
Immunizing Staff → Client influenza, mumps, rubella, parvovirus.
• Biothreat diseases requiring droplet precautions:
ENVIRONMENTAL SANITATION pneumonic plague
• Water Supply Sanitation
• Proper Excreta and sewage disposal CONTACT PRECAUTIONS
• Food Sanitation • Standard precautions plus:
• Waste Management • Place the patient in a private room or cohort them
with someone with the same infection if possible.
PATIENT ISOLATION PRECAUTIONS (Veenema, 2007). • Wear gloves when entering the room. Change gloves
STANDARD PRECAUTIONS after contact with infective material.
• Wash hands after patient contact. • Wear a gown when entering the room if contact with
• Wear gloves when touching blood, body fluids, patient is anticipated or if the patient has diarrhea, a
secretions, excretions, and contaminated items. colostomy, or wound drainage not covered by a
• Wear a mask and eye protection, or a face shield, dressing.
during procedures likely to generate splashes or • Limit the movement or transport of the patient from
sprays of blood, body fluids, secretions, or excretions. the room.
• Handle used patient-care equipment and linen in a • Dedicate use of noncritical patient-care equipment
manner that prevents the transfer of microorganisms (such as stethoscopes) to a single patient, or cohort
to people or equipment. of patients with the same pathogen. If not feasible,
• Use care when handling sharps and use a mouthpiece adequate disinfection between patients is necessary.
or other ventilation device as an alternative to • Conventional diseases requiring contact
mouth-to-mouth resuscitation when practical. precautions: MRSA, Clostridium difficile, RSV,
parainfluenza, enteroviruses, enteric infections in
Standard precautions are employed in the care of ALL the incontinent host, skin infections (HSV, impetigo,
patients. lice, scabies), hemorrhagic conjunctivitis
• Biothreat diseases requiring contact precautions:
viral hemorrhagic fevers
Communicable Disease Nursing
Semifinals Notes
AMOEBIASIS
Semifinals Notes

AMOEBIASIS
(Amoebic Dysentery)

• A gastrointestinal infection which initially involves the

colon, but may spread to soft tissues, most commonly
the liver and lungs, by contiguity or hematogenous or
lymphatic dissemination

ETIOLOGIC AGENT: PATHOGENESIS

Entamoeba Histolytica Ingestion of bacteria
• Prevalent in unsanitary areas 
• Common in warm climates Multiplication in mucosa
• Acquired by swallowing 
• Cyst survives a few days outside the body Endotoxin production, affecting the lining of the small
• Cyst  Large intestine and hatches into a intestines, colon & capillaries
trophoizoite  mesenteric veins  portal 
vein  liver (amoebic liver abscess) Necrosis of the mucosal layer

SOURCE: Human excreta Ulceration

Gangrene

TOXEMIA Death

2 Developmental Stages of E. histolytica
1. Trophozoites/ vegetative form
 Facultative parasites that may invade the tissue
or may be found in parasitized and liquid colonic
contents
2. Cyst
 Passed out with formed or semi-formed stools
and is resistant to environmental conditions
 Considered as the infective stage
INCUBATION PERIOD
• Severe infection: 3 days
• Sub-acute & chronic form: several months
• Average cases: 3-4 weeks
PERIOD OF COMMUNICABILITY
Entire duration of the illness
MODE OF TRANSMISSION
1. Fecal-oral transmission
2. Direct contact (orogenital, oroanal & proctogenital
sexual contact/ activity)
3. Indirect contact: Ingestion of food (uncooked leafy
vegetables or foods contaminated with fecal material
w/ E. histolytica cysts)
 Food or drinks may be contaminated by cysts
thru pollution of water supply, exposure to
flies, use of night soil for fertilizing
vegetables, and thru unhygienic practices of
food handlers
AMOEBIASIS
Semifinals Notes

CLINICAL MANIFESTATIONS TREATMENT MODALITIES

1. Acute Amoebic Dysentery 1. Metronidazole (Flagyl) 800mg TID x 5 days
a) Slight attack of diarrhea, altered with periods of 2. Tetracycline 250mg every 6 hours
constipation & often accompanied by tenesmus 3. Ampicillin, quinolone, sulfadiazine
b) Diarrhea, watery and foul-smelling stools often with 4. Streptomycin SO4, chloramphenicol
blood-streaked mucus 5. Replace lost fluids and electrolytes
c) Colic and gaseous distention of the lower abdomen
d) Nausea, flatulence, abdominal distention, and COMMON NURSING DIAGNOSES
tenderness in the right ileac region over the colon • Altered nutrition: Less than body requirements
• Altered bowel elimination
2. Chronic Amoebic Dysentery • Risk for infection
- lasts for several days, usually succeeded by • Anxiety
constipation • Hyperthermia
a) Tenesmus accompanied by the desire to defecate
b) Anorexia, weight loss and weakness NURSING MANAGEMENT
c) Hepatomegaly 1. Observe isolation and enteric precaution
d) Stools at first are semi-fluid, but soon become watery, 2. Health education:
bloody and mucoid a. Boil water for drinking or use purified water
e) Vague abdominal distress, flatulence, constipation or b. Avoid washing food with water from open
irregularity of bowel movement drums or pails
f) . Mild toxemia, constant fatigue, and lassitude c. Cover leftover foods
g) g. The abdomen loses its elasticity when picked up d. Wash hands after defecation and before eating
between the fingers e. Avoid eating ground vegetables (lettuce,
h) h. On sigmoidoscopy, scattered ulceration, with carrots)
yellowish and erythematous borders 3. Proper collection of stool specimen:
i) Gangrenous type (fatal): appearance of large sloughs • Never give paraffin or any oil preparation for at
of intestinal tissues in the stools, accompanied by least 48 hours prior to the collection of
hemorrhage specimen
• Instruct patient to avoid mixing urine with stools
• If whole stools cannot be sent to the laboratory,
select as large portions containing blood and
mucous if possible
• Send the specimen immediately
• Label the specimen properly
3. Extraintestinal forms 4. Skin care
a. URQ pain w/ liver tenderness • Maintain clean and wrinkle-free bed linens
b. Jaundice 5. Mouth care
c. Intermittent fever 6. Provide optimum comfort
d. Loss of weight or anorexia • Keep patient warm
e. Abscess may break thru the lungs: “anchovy-sauce 7. Diet
sputum” • Acute stage: force fluids
• Beginning of an attack: cereals & strained meat
DIAGNOSTIC EXAM broths w/o fat
1. Stool exam (cyst; white & yellow pus w/ plenty of • Convalescence: chicken & fish may be added
amoeba) • A bland diet w/o cellulose or bulk-producing
2. Blood exam (leukocytosis) foods should be maintained for a long time
3. Proctoscopy/ Sigmoidoscopy METHODS OF PREVENTION
1. Health education
2. Sanitary disposal of feces
3. Protect, chlorinate, and purify drinking water
4. Observe scrupulous cleanliness in food preparation
and food handling
5. Detection and treatment of carriers
6. Fly control
AMOEBIASIS
Semifinals Notes
CHOLERA
Semifinals Notes

CHOLERA  intact epithelium on the vasculature of the bowel

• An acute bacterial enteric disease of the GIT
characterized by profuse diarrhea, vomiting, massive 
loss of fluid & electrolytes, which could result in
hypovolemic shock, acidosis and death outpouring of intestinal fluids (5-10%)  DHN & M. Acidosis
 The mucosal cell is stimulated to increase secretion of
ETIOLOGIC AGENT: Vibrio cholerae/ Vibrio coma/El Tor chloride, associated with water and bicarbonate loss
1. Slightly curved rod (comma-shaped) gram (-) & motile
with a polar flagellum CLINICAL MANIFESTATIONS
2. Survives well at ordinary temperatures & multiplies 1. Acute, profuse, watery diarrhea with no tenesmus or
well in temperatures ranging from 22-40°C intestinal cramping
3. Can survive longer in a. Diarrhea causes fluid loss amounting to 1 to
a. refrigerated foods 30 liters per day owing to subsequent
4. An enterotoxin, choleragen, dehydration and electrolyte loss
a. is elaborated by the organism 2. Initially, stool is brown and contains fecal materials,
b. as it grows in the intestinal but soon becomes pale gray, “rice-water” in
c. tract appearance with an inoffensive, slightly fishy odor
3. Vomiting often occurs after diarrhea has been
established.
4. 4.Tissue turgor is poor and eyes are sunken into the
orbit.
5. Cold skin and wrinkled fingers and toes (“washer-
woman’s hand”)
6. Imperceptible radial pulse and unobtainable BP
7. Cyanosis
PATHOGNOMONIC SIGN: 8. Hoarse voice and then lost (patient speaks in whisper:
Rice-water stools aphonia)
9. Rapid and deep breathing
10. Consciousness is present despite marked diminished
peripheral circulation
11. Oliguria or anuria
12. Temperature: normal at the onset of the disease but
becomes subnormal in later stage especially if the
patient is in shock
INCUBATION PERIOD: 13. Deep shock: passage of diarrhea stops
A few hours to 5 days (1-3 days) 14. Death may occur as short as four hours after onset,
but usually occurs on the first or second day if not
PERIOD OF COMMUNICABILITY: properly treated.
During the stool-positive stage, usually a days after recovery;
occasionally, the carrier may have the organism for several DIAGNOSTIC EXAMS:
months 1. Rectal Swab
2. Darkfield or phase microcopy
MODES OF TRANSMISSION 3. Stool Exam
1. Fecal-oral transmission
2. Ingestion of contaminated food or water PRINCIPAL DEFICITS
3. Thru flies, soiled hands and utensils 1. Extracellular Volume  DHN, Circulatory collapse or
Shock
PATHOGENESIS AND PATHOLOGY 2. Metabolic acidosis  Kussmaul’s respiration
enterotoxin  adenylate cyclase  conversion of the 3. Hypokalemia  abdominal distention (paralytic
adenosine triphosphate (ATP) to cyclic ileus)
adenosine monophosphate 4. Renal failure – from prolonged, untreated shock or
 unrelieved hypokalemia
5. Convulsions & tetany – loss of magnesium
(CAMP)
CHOLERA
Semifinals Notes

6. Hypoglycemia (untreated children who have been in • Knowledge deficit

stupor for several days) • Risk for fluid volume deficit
7. Corneal scarring – (stuporous patients who have lost • Diarrhea
the “wink reflex”) • Impaired skin integrity
8. Acute pulmonary edema – may follow hydration in
cases of uncorrected metabolic acidosis

TREATMENT MODALITIES
• Treatment of cholera consist of correcting the basic
abnormalities without delay – restoring the
circulating blood volume and blood electrolytes to
normal levels.

1. Rapid intravenous infusion of alkaline saline solution

containing Na, K, Cl and bicarbonate ions in proportions
comparable to that in water-stool.
2. Oral therapy rehydration (Oresol, Hydrites) unless
contraindicated or, if the patient is not vomiting.
3. Maintenance of the volume of F&E to ensure rehydration
(monitor I/O carefully)
4. Antibiotics
a. Tetracycline 500mg every 6 hours (adults), and 125
mg/kg body weight for children every 6 hours to 72
hours
b. Furazolidone 100 mg (adults) and 125mg/kg for
children every 6 hours for 72 hours
c. Chlorampenicol 500 mg (adults) and 18 mg/kg for
children every 6 hours for 72 hours
d. Cotrimoxazole 8mg/kg for 72 hours.

NURSING MANAGEMENT
1. Medical aseptic protective care & handwashing
2. Enteric isolation
3. Accurate V/S and I/O
4. Personal hygiene
5. Proper excreta disposal
6. Concurrent disinfection
7. Proper food preparation
8. Environmental sanitation
9. Weigh patient daily
10. Give appropriate diet

PREVENTION
1. Food and water supply must be protected from fecal
contamination.
2. Water should be boiled or chlorinated.
3. Milk should be pasteurized.
4. Sanitary disposal of human excreta is a must.
5. Sanitary supervision is important.

COMMON NURSING DISGNOSES

• Altered nutrition: Less than body requirements
• Altered tissue perfusion
• Activity intolerance
TYPHOID FEVER
Semifinals Notes

TYPHOID FEVER PATHOGENESIS

 A bacterial infection transmitted by contaminated Bowels  infected Payer’s patches
water, milk, shellfish, or other food 
 An infection of the GIT affecting the lymphoid tissue (1st week) swollen lymph nodes  necrosis  ulcer
(Peyer’s patches) of the small intestines 
(2nd week) slough formation (bile-colored)

(3rd week) slough separates w/ ulcerated surface 
hemorrhage & perforation

CLINICAL MANIFESTATIONS

1. PRODROMAL STAGE – bloodstream

Etiologic Agent: Salmonella typhosa/typhi
 Fever, dull headache
 Gram-negative, motile and non-spore forming
 Abdominal pain
 Pathogenic to man only
 N&V
 A hardy organism and easily survives in natural
 Diarrhea/constipation
habitat like water or organic materials
2. Fastigial /Pyrexial stage: microorg, in peyer’s patches
 3 clinical features of typhoid fever:
1. Ladder-like fever
2. Rose spots – small erythematous macules on
abdomen (presence of bacterial emboli in
capillaries); the 7th to the 9th day

INCUBATION PERIOD: 3. Splenomegaly

5 to 40 days with a mean of 10 to 20 days 3. Typhoid state/Psychosis
 Coma vigil look – staring blankly without seeing
PERIOD OF COMMUNICABILITY  Protruding tongue
variable; as long as the patient is still excreting the  Carphologia –picks up linens in a continuous fashion
microorganism, he is still capable of infecting others  Subsultus tendinum – twitching of tendons
 Sordes – accumulation of dirty brown collection of
SOURCES OF INFECTION dried mucus and bacteria in the teeth and lips
 A person who recovered from the disease or one who 4. Defervescence
took care of a patient with typhoid and was infected  Intestinal HMG
can be considered a potential carrier.  melena/hematochezia
 Ingestion of shellfish (oysters) taken from waters  Peritonitis
contaminated by sewage disposal can be a source of 5. Lysis/Convalescence
infection  Pt still observed closely
 Stool and vomitus of infected individual are sources
of infection COMPLICATIONS
 Hemorrhage or perforation – the two most dreaded
MODE OF TRANSMISSION complications
 Fecal-oral transmission  Peritonitis
 Ingestion of contaminated food, water, and milk  Bronchitis and pneumonia
 Thrombosis and embolism
 Septicemia
TYPHOID FEVER
Semifinals Notes

 Reiter’s syndrome/ Reactive Arthritis – joint pain, eye
irritation and painful urination; can lead to chronic
arthritis
 Isolation with medical aseptic technique
 Maintain or restore fluid and electrolyte balance by
giving nourishing fluids in small quantities at frequent
intervals
 Monitor the patient’s vital signs
 Prevent further injury (such as falls) of the patient
with typhoid psychosis
 Maintain good personal hygiene and mouth care
 Cooling measures are necessary during the febrile
state
 Watch out for signs of intestinal bleeding
 Terminal and concurrent disinfection

PREVENTION AND CONTROL

DIAGNOSTIC PROCEDURE
 Typhidot (confirmatory) detects IgM & IgG against S.
Typhi; (+) w/in 2-3 days of infection
 Sanitary and proper disposal of excreta
 Proper supervision of food handlers
 Enteric isolation
 Provision of adequate amounts of safe drinking water
supply
 Reporting of cases to health authorities
 Detection and monitoring of typhoid carriers
 Education of the general public on the mode of
transmission

 Widal test – involves agglutination of typhoid bacilli

when they are mixed w/ serum containing typhoid
antibodies from an individual with T. Fever
 Rectal swab

NURSING DIAGNOSES
 Self-care deficit
 Fluid volume deficit
 Constipation
 Knowledge deficit
 Risk for injury
 Anxiety
 hyperthermia

TREATMENT MODALITIES
 Chloramphenicol (drug of choice)
 Ampicillin
 Cotrimoxazole
 Ciprofloxacin or ceftriaxone
 If the patient does not respond to chloramphenicol,
3rd and 4th generation drugs are administered.

NURSING MANAGEMENT
DENGUE FEVER
Semifinal Notes

DENGUE a.k.a. - Petechial rash: endothelial swelling, perivascular

 Break-bone fever edema, extravasation of blood
 Dandy fever - Increased vascular permeability, hypotension,
 Hemorrhagic fever hemoconcentration, thrombocytopenia
 Infectious thrombocytopenic purpura
 acute, benign, febrile form of disease with systemic CLINICAL MANIFESTATIONS
symptoms – fever and often with rash, pain behind A. Dengue Fever
the eyes, joints and bones 1. Prodromal symptoms: malaise and anorexia up to 12
 Complication: Dengue Hemorrhagic Fever (fatal) hours, fever and chills with severe frontal/retroorbital
headache, ocular pain, myalgia, with severe
INCIDENCE: common 4-9 y.o., high in urban areas, higher backache, and arthralgia
during rainy season (July-Nov) and lowest Feb-April 2. Nausea and vomiting; changes in taste, sore throat,
OCURRENCE: Epidemic diarrhea, depression
3. Fever (non-remitting & persists for 3-7days)
ETIOLOGIC AGENTS: 4. Rashes (extremities & trunk)
1. Dengue Virus or Flavivirus 5. Petechiae (common: lower extremities)
2. Arbovirus Group B
3. Chikunguya virus B. Dengue Hemorrhagic Fever
- fever, hemorrhagic diathesis, hepatomegaly,
MODE OF TRANSMISSION hypovolemic shock; epistaxis
Bite by infected Aedes Egypti (vector)
 With fine white dots at base of wings, white PHASES OF ILLNESS
bands on legs 1. Febrile/ Invasion Stage (initial febrile 2-3days, some
 Day-biting with limited, low-flying lasting for 4 days)
movement a. Fever (39-40°C) with headache
 Breeds on stagnant water b. Abdominal pain
c. Febrile convulsion may occur
INCUBATION PERIOD: 3-14 days, commonly 7-10days d. Flushed palms and sole
e. (+) Tourniquet test (Rumpel-Leads Capillary-
Fragility Test)

(+) Tourniquet Test

Aedes Egypti
(+) > 10 petechiae/ in2 =
DF
(+) > 20 petechiae/ in2 =
DHF
PERIOD OF COMMUNICABILITY
1. Infective to mosquito from 1 day before to the end
of febrile period f. Anorexia, vomiting, myalgia
2. Mosquito is infective from day 8-12 after blood meal g.Macula-papular or petechial rash – starts at distal
until rest of life portion of extremities (sparing the axilla and chest),
the skin appears with blanched varied sizes –
SOURCES OF INFECTION HERMAN’S SIGN –
1. Blood of infected persons (reservoir)
2. Stagnant water (breeding places)

Vector  virus  skin  replication (site of infection &

lymphatic tissues) macrophages  viremia (lasts until 4th to 5th
day)  S/S

hypovolemic shock h. Generalized or abdominal pain
i. Hemorrhagic manifestations
DENGUE FEVER
Semifinal Notes

2. Circulatory Phase 2. Rapid fluid replacement : IV infusion, vol/vol oral

a. Drop in temperature associated with profound replacement (most important)
circulatory changes – 3rd to 5th day -for moderate to reduced intravascular volume 
b. Restlessness, irritability, cool clammy skin half to full strength normal saline in D5W or Ringer’s
c. Cyanosis Lactate
d. Profound thrombocytopenia accompanies the onset -for shock  10-20mL/kg bolus of normal saline or
of shock Ringer’s Lactate rapidly (over <20 min)
e. GIT bleeding -for circulatory failure  plasma, plasma substitutes
f. Shock – rapid and thready pulse, narrowed pulse or 5% albumin
pressure, hypotension
g. Complications: coma, metabolic acidosis, death 3. Blood transfusion (for severe bleeding)
within 2 days 4. O2 therapy (for all patients w/ decreased O2 sat or in shock,
h. With effective therapy, recovery may follow in 2- w/ cyanosis or resp. distress)
3days 5. Sedatives
i. Tourniquet test may become negative 6. Diet: low fat, low-fiber, non-irritating, non-carbonated;
noodle soup may be given; NCCF for clients w/ active bleeding
3. Convalescence or Recovery Stage (7th-10th day) 7. Minimize invasive procedures & instrumentation; bleeding
a. Generalized flushing with interventing areas of precautions
blanching
b. Appetite is regained NURSING MANAGEMENT
c. BP and V/S stable 1. Oresol for moderate DHN
2. Maintain a mosquito-free environment
CLASSIFICATIONS ACCORDING TO SEVERITY: 3. Maintain rest during bleeding episodes
 Grade I: (+) fever with non-specific constitutional 4. Monitor V/S
symptoms; (+) tourniquet test 5. Intensive close monitoring & observation of signs of
 Grade II: all signs of grade I plus spontaneous shock
bleeding from nose, gums, GIT 6. Modified trendelenburg
 Grade III: presence of circulatory failure; onset of 7. Isolation – not required
symptoms of shock
 Grade IV: Profound shock, undetectable BP and  Prevent nosebleeding
pulse  Prevent gum bleeding
 Hematemesis
COMPLICATIONS  Melena
1. Bleeding leading to hypovolemic shock
2. DHF: Metabolic acidosis, hyperkalemia, HMG into PREVENTION AND CONTROL
CNS or adrenal glands, uterine bleeding, myocarditis 1. Health education
3. Dengue encephalopathy – increasing restlessness, 2. Early detection and treatment
apprehension and anxiety, disturbed sensorium, 3. Treat mosquito nets with insecticides
convulsions, spasticity, hyporeflexia 4. House spraying / fumigation
5. Elimination of vector
DIAGNOSTIC TESTS 6. Avoid too many hanging clothes inside the house
1. Tourniquet test (Rumpel Leads Test) 7. Case finding
2. Decreased PLT count (confirmatory)
- <10,000/µL on the 8th day
1. Hemoconcentration (increased HCT)
2. Occult blood
3. Hgb determination

TREATMENT: Purely symptomatic

1. Analgesic or antipyretic. DON’T GIVE ASPIRIN!
LEPTOSPIROSIS
Semifinal Notes

LEPTOSPIROSIS PATHOGENESIS
(Weil’s Disease/Canicola Fever/ Hemorrhagic Jaundice/ Mud
fever/Swine Herd Disease)

 A zoonotic infectious bacterial disease carried by

animals, both domestic and wild

ETIOLOGIC AGENT: leptospira (Leptospira interrogans)- a

spirochete
 Chiefly saprophytic aquatic organisms which are
found in river and lake waters, sewage, and in the
sea
 Some species are pathogenic to man and animals
 Weil’s Disease- specifically caused by the serovar
icterohemorrhagiae

 Leptospira  Body
  Multiplies in the bloodstream
  Liver (Jaundice)
  Kidneys (inflammation of the
nephrons & tubular necrosis)
  Renal failure
  Muscles  Pain & edema
  Eyes (conjunctivitis, icteric –
INCUBATION PERIOD: 6-15 days orange-colored sclera)

PERIOD OF COMMUNICABILITY CLINICAL MANIFESTATIONS

 Leptospira is found in the urine between 10 to 20
days after disease onset
SOURCES OF INFECTION
 Contaminated food and water and infected wildlife
and domestic animals, especially rodents
 Rats (L. icterohaemorrhagiae)- frequently observed
among mine, sewer and abattoir workers
 Dogs (L. canicola)- veterinarians, breeders and
owners of dogs
 Mice (L. grippotyphosa)- farmers and flax workers
MODE OF TRANSMISSION
 Ingestion or contact with the skin or mucous
membranes of infected urine or carcasses of either
wild or domestic animals
 Through the mucous membranes of the eyes, nose
and mouth, and through breaks in the skin (damaging
the kidneys, liver, meninges & conjuntivae)
 Through semen of infected animals
 Common among watersport enthusiasts in certain
areas as prolonged immersion in water is known to
promote the entry of bacteria
 Occupation at risk include veterinarians, slaughter
house workers, farmers and sewer workers
 Asymptomatic to fatal
 Clinical course is generally biphasic and the majority
of the cases are anicteric
3 septic stages can be recognized:
1. Septic stage
 Marked by febrile episodes lasting from 4 to 7
days
 There is an abrupt onset of remittent fever,
chills, headache, anorexia, abdominal pain and
severe prostration
 Respiratory distress
 Fever subsides with lysis
2. Immune or toxic stage
 With or without jaundice, and lasts for 4 to 30 days
 Iritis, headache, meningeal manifestations like
disorientation, and convulsions, with CSF findings of
aseptic meningitis.
 Oliguria and anuria with progressive renal failure
 Shock, coma, and congestive heart failure are also
seen in severe cases. Death may occur between the
9th and the 16th days.
3. Convalescence - At this stage, relapse may occur during the
4th to 5th weeks
LEPTOSPIROSIS
Semifinal Notes

LABORATORY DIAGNOSIS  Infected humans and pets should be treated

 Blood urea nitrogen and creatinine  Information dissemination campaign must be
 Enzyme- linked immunosorbent assay (ELISA) conducted effectively.
 Liver function tests usually are slightly to moderately
elevated
 Leptospira antigen-antibody test (LAAT)
 Leptospira antibody test (LAT)

COMPLICATIONS
 Meningitis
 Respiratory Distress
 Renal interstitial tubular necrosis that results in renal
failure (Weil’s disease)
 Cardiovascular problem

MANAGEMENT
MEDICAL
Treatment is geared toward:
 Suppressing the causative agent
 Fighting possible complications
 Aetiotropic drugs – penicillin, doxycycline,
ampicillin, amoxicillin
 For prophylaxis = doxycycline 100mg PO
q12H x 1 week
 Peritoneal dialysis
 Administration of fluids and electrolytes
and blood as indicated
NURSING
 Isolate the patient; urine must be properly disposed
 Darken the patient’s room
 Observe meticulous skin care
 Keep clients under close surveillance
 Keep homes clean. Regularly replace water in pools,
vases, aquaria, etc., to prevent stagnation
 Eradicate rats and rodents
 Provide health education on the modes of
transmission of the disease
 Encourage oral fluid intake

COMMON NURSING DIAGNOSES

 Disturbed body image
 High risk for injury
 Anxiety
 Altered nutrition: Less than body requirements
 Impaired physical mobility
 Impaired skin integrity
 Knowledge deficit

PREVENTION AND CONTROL

 Sanitation in homes, workplaces and farms is a must
 There is a need for proper drainage system and
control of rodents (40-60% infected)
 Animals (cattle, dogs, cats and pigs) must be
vaccinated
Malaria
Semifinal Notes

PERIOD OF COMMUNICABILITY
MALARIA  more than 3 years in P. malariae
 an acute and chronic parasitic disease transmitted by  1 to 2 years in P. vivax
the bite of infected mosquitoes and confirmed mainly  not more than 1 year on P. Falciparum
to tropical and subtropical areas
 causes more disability and heavier economic burden MODE OF TRANSMISSION
than any other parasitic disease  mechanically through the bite of an infected female
Anopheles mosquito
ETIOLOGIC AGENT: Protozoa of genus plasmodia  parenterally through blood transfusion
 shared contaminated needles (rare)
Caused by 4 species of protozoa:  transplacental transmission (rare)
1. Plasmodium falciparum (malignant tertian)
 most serious malarial infection because of the PATHOGENESIS
development of high parasitic densities in the blood
(RBC)
 tends to cause agglutination, resulting in
microembolus formation
 most common in the Philippines
2. Plasmodium vivax (benign tertian)
 non-life-threatening, except for the very young and
the very old
 S/S: chills every 48 hours on the 3rd day onward,
especially if untreated
3. Plasmodium malariae (quartan)
 less frequently seen than the first two types
 non-life threatening
 Fever and chills usually occur every 72 hours, usually
on the 4th day after onset
4. Plasmodium ovale
 rare type of protozoan species
 rarely seen in the Philippines

PRIMARY VECTOR: female Anopheles mosquito

 breeds in clear, flowing and shaded streams usually in
the mountains
 bigger in size than ordinary mosquitoes
 brown in color
 a night-biting mosquito
 usually does not bite a person in motion
 assumes a 36 degree position when it alights on walls,
trees, curtains and the like

Female Anopheles Mosquito

INCUBATION PERIOD:
 12 days for P. Falciparum
 14 days for P. vivax and ovale
 30 days for P. malariae
Malaria
Semifinal Notes

CLINICAL MANIFESTATIONS  consider severe malaria as medical emergency that

 Paroxysms with shaking chills requires close monitoring of vital signs
 Rapidly rising fever with severe headache
 Profuse sweating COMMON NURSING DIAGNOSES
 Myalgia with feelings of well-being in between  Hyperthermia
 Splenomegaly, hepatomegaly  Activity intolerance
 Orthostatic hypotension  Knowledge deficit
 Paroxysms may last for 12 hours and may attack daily  Altered nutrition: Less than body requirement
or every two days
PREVENTION AND CONTROL
In children:  Report all cases
 Fever may be continuous  Thorough screening of all infected persons from
 Convulsions and gastrointestinal symptoms are mosquitoes
prominent  Destroy breeding places of mosquitoes
 Splenomegaly  Spray homes with effective insecticides that have
In cerebral malaria: residual actions on the walls
 severe headache, vomiting and changes in sensorium  Mosquito nets should be used, especially in infected
 Jacksonian or grand mal seizure areas
 Use insect repellents
DIAGNOSTIC PROCEDURE  People living in malaria-infested areas should not
 Malarial smear – a film of blood is placed on a slide, donate blood for at least three years
stained and examined microscopically  Blood donors should be properly screened
 Rapid diagnostic test (RDT) – blood test to detect
malaria parasite antigen (can be conducted outside
the laboratory and in the field); result in 10-15min

MANAGEMENT
1. Medical Management
 Anti – malarial drugs
 Chloroquine (all species, except for P. malariae)
 Quinine
 Sulfadoxine for the resistant P. falciparum
 Primaquine for relapses of P. vivax and ovale
 Erythrocyte exchange transfusion for rapid
production of high levels of parasites in the blood
2. Nursing Management
 Close monitoring
 Monitor I/O
 Daily monitoring of serum bilirubin, BUN creatinine
and parasitic count
 If with respiratory and renal symptoms, determine
the ABG and plasma electrolyte
 tepid sponges, alcohol rubs and ice cap on the head
 external heat and hot drinks for chills
 provide comfort and psychological support
 encourage plenty of fluids
 as the temperature falls and sweating begins, warm
sponge baths may be given
 keep bed and clothing dry
 monitor neurologic toxicity (from quinine infusion)
like muscular twitching, delirium, confusion,
convulsion and coma
 evaluate the degree of anemia
 watch for any signs, especially abnormal bleeding
SCHISTOSOMIASIS
Semifinal Notes

PATHOLOGY:
SCHISTOSOMIASIS Larvae (cercaria)  skin or mucus membrane
(Bilharziasis/ Snail Fever) 
 A slowly progressive disease caused by blood flukes of portal circulation (1-3 months)  some parts of the body
class trematoda. A chronic wasting disease common 
among farmers and their families blood vessels surrounding the large intestine
 High Prevalence in: Region 5 (Bicol) Region 8 (Samar & or bladder
Leyte) and Region 11 (Davao) 
Ulceration in the mucosa  eggs escape
Etiologic Agent- Schistosoma Japonicum-parasitic worm into the lumen of the intestines  feces

4 major Types: lesions or granulomas (liver)  fibrosis  scarring

 Schistosoma japonica- Philippines hepatomegaly ascites and portal hypertension
 Schistosoma mekongi – Southeast Asia
 Schistoma mansoni- Africa DIAGNOSTIC TESTS
 Schistosoma haematobium- Middle East  Fecalysis or direct stool exam
 Kato Katz Technique - involves staining a sieved
Incubation Period: at least 2 mos. fecal sample and examining it under a microscope.
The total number of stained eggs are counted and
SOURCES OF INFECTION used to calculate the number of eggs per gram
1. Feces of infected persons  Liver Biopsy
2. Animals serve as host  ELISA
 Cercumoval Precipitin Test (COPT)- a serological test;
MODE OF TRANSMISSION confirmatory
1. Ingestion of contaminated water
2. Transmitted through skin pores
3. Transmitted through an intermediary host, a tiny
snail-Oncomelania Quadrasi
 Thrives best along the river banks,
fresh waters, creeks, canals,
swamps
 Can be found clinging to water
hyacinths, grasses and decaying
leaves, rotting woods, bamboos, KATO KATZ TECHNIQUE
coconut husks.
 Loves to stay in sandy-loam soil CLINICAL MANIFESTATIONS: (depends on the site of infection)
 Adult snail is greenish brown in  “Swimmer’s itch” / Cercarial dermatitis
color; just as big as smallest grain of
palay

 Low grade fever, rash, myalgia, cough

 Diarrhea and abdominal discomfort due to hepato-
and splenomegaly, and lymphadenopathy
 On and off bloody mucoid stool for weeks
 Icterus and jaundice


SCHISTOSOMIASIS
Semifinal Notes

 Enlarged abdominal girth (inflamed liver)  Health education: dse process,

 Several years later: weak, pale with marked muscle MOT, prevention
wasting
 Parasite reaches the brain (cerebral schistosomiasis):
headaches, dizziness, convulsion

COMPLICATIONS
 Liver cirrhosis, portal HPN
 Cor Pulmonale, Pulmonary HPN
 Heart Failure
 Ascites
 Bleeding of Esophageal varices
 Renal Failure

TREATMENT: Effective only when given early in the course of

the disease
 Praziquantel tablet for 6 mos- 1 tab BID X 3 mos., then
1 tab a day x 3 mos. (Recommended: 40mg/kg)
 Fraudin Injection- IM of IV; ct must consume 360 mg
for the entire tx
 Retreatment (endemic areas)

COMMON NURSING DIAGNOSES

 Body Image disturbance
 Impaired skin integrity
 Altered Urinary Elimination
 Social Isolation
 Self-esteem disturbance
 Knowledge Deficit
 Risk infection

PREVENTION AND CONTROL

Interrupt the life cycle of the worm
1. Stool Exam
2. Reduce snail density:
 Clearing vegetation thus exposing snail to
sunshine
 Constructing drainage to dry the land
surface where snails thrive
 Improve farming by proper irrigation and
drainage, crop rotation, removal of weeds
3. Diminish infection rate:
 Proper waste disposal
 Control of stray animals
 Prevent bathing in infected
streams
 Build footbridges over snail
infected streams
 Provide adequate water supply
and safe water for drinking
 Use rubber boots
 Mulluscicides – to treat water
(Niclosamide)
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes

PERIPHERAL VASCULAR DISORDERS

Venous insufficiency
➢An abnormal circulatory condition characterized by
decreased return of venous blood from the legs to the trunk of
the body
➢Edema is usually the first sign of the condition; pain,
varicosities, and ulceration may follow

Collateral circulation
➢An accessory blood pathway developed through
enlargement of secondary vessels after obstruction of a main
channel

A. ARTERIAL DISORDERS
a. Arteriosclerosis
b. Atherosclerosis
c. Peripheral Arterial Occlusive Disease
d. Raynaud’s Phenomenon
e. Aneurysm

B. VENOUS DISORDERS
a. Venous Thromboembolism
b. Chronic Venous Insufficiency
c. Varicose Veins

C. Arterial and Venous

Intermittent claudication a. Buerger’s Disease
➢A muscular, cramp-like pain in the extremities consistently
reproduced with the same degree of exercise or activity and ARTERIOSCLEROSIS vs. ATHEROSCLEROSIS
relieved by rest Arteriosclerosis
➢ “hardening of the arteries”; thickening
Rest pain Atherosclerosis
➢Persistent pain in the foot or digits at rest; indicating severe ➢Inflammatory process involving the accumulation
arterial insufficiency of lipids, etc. on the intimal layer

Rubor
➢Reddish blue discoloration of the extremities, indicative of
severe peripheral arterial damage in vessels that remain
dilated and unable to constrict

Bruit PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

➢Sound produced by turbulent blood flow through an
irregular, tortuous, stenotic, or dilated vessel
Arterial insufficiency
➢Inadequate blood flow in arteries
➢May be caused by occlusive atherosclerotic plaques or
emboli, damaged or diseased weak vessels
 A systemic form of atherosclerosis producing
symptoms in the cardiac, cerebral, and renal vascular
systems
 Early symptoms include intermittent claudication
and ischemic rest pain
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes

o Atrophy
o Ulcerations
Edema

Gangrene

THROMBOPHLEBITIS VS. VARICOSE VEINS

VENOUS DISORDERS
1. Edema =C
 Deep Vein Thrombosis (DVT) – presence of a 2. Pain =C
thrombus in one of the deep veins Homan’s sign
3. =A
 Thrombophlebitis – inflammation of a vein with
formation of a clot 4. Tortuous vein =B
 Phlebothrombosis – an abnormal condition in which 5. Intermittent =D
a clot forms within a vein with the wall of the vessel claudication
not inflamed; caused by hemostasis,
hypercoagulability, or occlusion.
 Venous Thromboembolism (VTE) – DVT + pulmonary A. Thrombophlebitis
embolism B. Varicose vein
C. Both
 Varicose veins – abnormally dilated, tortuous
D. Neither
superficail veins caused by incompetent venous
valves
GERONTOLOGIC CONSIDERATIONS
o More thickened intima; stiffened wall
o Increased peripheral resistance, impaired blood
flow, increased left ventricular workload
o Symptoms more pronounced
o Gangrene may be the first sign
o Prolonged pressure easily leads to ulceration

RAYNAUD’S vs. BUERGER’S DISEASE

I. THROMBOANGITIS OBLITERANS (Buerger’s disease)
 Recurring bilateral and symmetric inflammation of
the intermediate and small arteries and veins of the
lower and upper extremities resulting to thrombus
formation and occlusion of the distal vessels

RAYNAUD’S DISEASE BUERGER’S

DISEASE
DISEASE Episodic spasm of small arteries Thrombotic and
ASSESSMENT and arterioles due to exposure inflammatory
PROCESS
Pain to cold and emotional distress; occlusions of
o Intermittent claudication vs rest pain common in women small arteries and
veins among
smokers
Skin color and temperature
o Pale and cool Initial: Intermittent arteriolar Pain, intermittent
SYMPTOMS
o Rubor vasoconstriction claudication;
o Cyanosis - Severe pallor tingling sensation,
followed by impaired
cyanosis, then peripheral pulses,
Character of peripheral pulses redness upon distal coldness,
o Presence/absence, quality exposure to warmth numbness and
(white..blue..red) cyanosis leading
- Numbness and to ulceration and
s/s of chronically reduced nutrient supply:
tingling of digits gangrene
o Loss of hair
o Brittle nails
o Dry or scaling skin
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes

FACTORS warmth Rest, permanent ASSESSMENT AND DIAGNOSTIC FINDINGS:

THAT cessation of 1. Segmental Limb blood pressures - to demonstrate the
RELIEVE smoking
distal location of the lesions or occlusions
LABORATORY Allen’s test – reveal circulatory Leg arteriography
DATA problems reveals
inflammatory
lesions
Altered Peripheral Tissue Altered Peripheral
Perfusion Tissue Perfusion

Avoid cold weather Stop smoking

Wear leather gloves when Administer 2.
getting anything from the calcium channel Duplex Ultrasonography - to document patency of the
refrigerator blockers as
Stop smoking Administer ordered
proximal vessels and to visualize the extent of distal disease.
vasodilators as ordered

BUERGER’S DISEASE
 Cause: unknown, Autoimmune vasculitis
 Predisposing Factors: Age- 20-35 y.o Men in all races
in all parts of the world 3.Contrast Angiography - identify the diseased portion of the
 Causative/ Aggravating factors: Heavy smoking, anatomy
chewing tobacco
An angiogram demonstrating lack of blood flow to vessels
CLINICAL MANIFESTATIONS:
1. Burning Pain - relieved by rest, aggravated by
emotional disturbance, nicotine, or chilling
-Foot cramps of the arch (Instep claudication) after
exercise
2. Digital rest pain
3. Cold sensitivity- confined to the hands
4. Intense Rubor of the foot Classic finding in angiogram: “corkscrew” appearance of
5. Absence of pedal pulses, with normal femoral and
popliteal pulses
6. Radial and ulnar pulses absent or diminished
7. Various paresthesias
8. Definite redness and cyanosis of the part when in
dependent position
9. Complication:
10. ulceration MEDICAL MANAGEMENT
11. gangrene Main objectives:
 Improve circulation to the extremities,
Skin ulcerations and gangrene of the digits
 prevent the progression of the disease,
 protect the extremity from trauma and infection

1. Treatment of ulceration and gangrene

2. Smoking cessation
3. Regional sympathetic block or ganglionectomy -
provide vasodilation and increase blood flow
4. Below- knee amputation - if gangrene of the toe
develops as a result of arterial occlusion

NURSING MANAGEMENT
 Assist client to stop using tobacco and to manage
pain
 PERIPHERAL VASCULAR DISORDERS
Semifinal Notes

 Make lifestyle changes to manage a chronic disease: IV. Deficient knowledge regarding self care activities
modifications of diet, activity,hygiene (skin care) Goal: Adherence to self-care program
 Encourage family to assist client in ADLs Nursing Interventions:
 Build on ability to assess for postop complications  Include family/significant others in teaching
program.
PLAN OF NURSING CARE  Provide written instructions about foot care, leg care,
I. Nursing Diagnosis: Ineffective peripheral tissue and exercise program.
perfusion related to compromised circulation  Assist to obtain properly fitting clothings,
stockings, shoes.
Goal: Increase arterial blood supply to
extremities II. RAYNAUD’S DISEASE
 intermittent arteriolar vasoconstriction resulting in
Nursing Interventions: coldness, pain, and pallor of the fingertips or toes
 Lower the extremities below the level of the  Cause: unknown; most clients have immunologic
heart. disorders
 Encourage moderate amount of walking or  Symptoms result from defect in basal heat
graded extremity exercises if no production that eventually decreases the
contraindications exist ability of the cutaneous vessels to dilate
 Predisposing Factor: Female, 16-40 y.o, cold climates
Goal: Promotion of vasodilation and prevention of vascular and winter season
compression  Triggering factors: exposure to cold and emotional
Nursing Interventions:  Prognosis: varies
 Maintain warm temperature and avoid chilling.
 Discourage use of tobacco products. 2 FORMS:
 Counsel in ways to avoid emotional upsets; stress 1. Primary/Idiopathic Raynaud’s (Raynaud’s
management. Disease)
 Goal: Promotion of vasodilation and prevention of  No underlying cause
vascular compression 2. Secondary Raynaud’s (Raynaud’s
 Nursing Interventions: sundrome)
 Maintain warm temperature and avoid chilling.  Associated with connective tissue d/o,
 Discourage use of tobacco products. trauma, or obstructive arterial lesions
 Counsel in ways to avoid emotional upsets; stress
management. CLINICAL MANIFESTATIONS
1. Classic clinical picture: White, blue and red
II. Diagnosis: Chronic Pain related to impaired ability of phenomenon
peripheral vessels to supply tissues with oxygen 2. Numbness, tingling, burning pain as color changes
Goal: Relief of pain
Nursing Interventions:
 Promote increased circulation
 Administer analgesics as prescribed

III. Risk for Impaired skin integrity related to compromised

circulation
Goal: Attainment/ maintenance of tissue integrity
Nursing Interventions:
 Avoid trauma to extremities.
 Wear protective shoes and padding for pressure
areas.
 Meticulous hygiene; bathing with neutral soaps,
applying lotions, carefully trimming nails.
 Avoid scratching or vigorous rubbing.
 Promote good nutrition; adequate intake of vitamins
A and C, protein, and zinc; control of obesity.
MEDICAL MANAGEMENT
 Avoid particular stimuli (e.g,cold, tobacco) that
provoke vasoconstriction
 Calcium Channel Blockers
(Nifidipine[Procardia,Adalat]) - to relieve symptoms
 Sympathectomy - procedure which involves
interrupting the sympathetic nerves by removing the
sympathetic ganglia or dividing their branches.
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes

NURSING MANAGEMENT
 Avoid situations that may be stressful or unsafe;
effective stress management strategies
 Minimize exposure to cold
 remain indoors in areas with cold fall and winter
months, wear layers of clothing when outdoors, wear
clothing designed for cold climate
 Avoid touching cold objects
 Avoid all forms of nicotine
 Caution to handle sharp objects carefully to avoid
injuring the digits THORACIC AORTIC ANEURYSM ANEURYSM
 Inform clients about postural hypotension that may
be result from meds.

ARTERIAL ANEURYSM
 a localized sac or dilation formed at a weak point in
the wall of the artery
 tends to enlarge gradually ABDOMINAL AORTIC ANEURYSM
 some may remain stable over many years of
observation

CLASSIFICATIONS
1. shape/form: true aneurysms
a. saccular – a bulbous protrusion of one side of the
arterial wall
CAUSES OF ANEURYSM FORMATION
b. fusiform - symmetric, spindle-shaped expansion
 atherosclerotic changes in the aorta (most common)
of entire circumference of involved vessel
 congenital (i.e., Marfan’s syndrome ; Ehlers- Danlos
false aneurysm (pseudoaneurysm)
syndrome )
C.dissecting – usually a hematoma that splits the
layers of the arterial wall
Marfan’s Syndrome

Ehlers-Danlos Syndrome
2. etiology
a. mycotic (infectious) aneurysm – very small
aneurysm due to localized infection
b. anastomotic graft aneurysm
3. location
a. thoracic aortic aneurysm
b. abdominal aortic aneurysm
 mechanical (i.e., poststenotic and AV fistula,
amputation-related)
 traumatic (i.e., penetrating/blunt arterial injuries,
pseudoaneurysm)
 inflammatory (i.e., associated with arteritis and
periarterial inflammation)
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes

 inflammatory (i.e., associated with arteritis and

periarterial inflammation)
 infectious (i.e., bacterial, fungal spirochetal
infections)
 pregnancy-related degenerative (i.e., nonspecific,
inflammatory variant)
 anastomotic and graft aneurysms (i.e., infection,
arterial wall failure, suture failure, graft failure)

RISK FACTORS
 genetic predisposition
 tobacco use
 hypertension (enhances aneurysm formation)

MANIFESTATIONS
 Depends on the size and location

COMPLICATIONS
 Rupture (due to increased tension)
 Pressure on surrounding structures
 Thrombosis (due to interrupted blood flow)
 Distal embolization

A. THORACIC AORTIC ANEURYSM

 Occur most frequently in men (40 – 70 y.o.)
 Most common site for a dissecting aneurysm
 Usually asymptomatic in the early stage
 Cause: atherosclerosis (85%)
 1/3 of pts die of rupture

B. ABDOMINAL AORTIC ANEURYSM

 Usually below the renal arteries (Infrarenal
aneurysms)
 Common in Caucasians, the elderly and men (60-90
y.o.)
 Most common type of degenerative aneurysm
 Most abdominal aneurysms are asymptomatic
 Occur more often than thoracic aneurysm

CLINICAL MANIFESTATION
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes

◾ Duplex ultrasonography
C. OTHER ANEURYSMS ◾ MRI
 In the peripheral vessels: popliteal, subclavian,
renal, femoral artery MEDICAL MANAGEMENT
 Disturbs distal peripheral circulation  Treatment is based on:
 Symptoms
D. DISSECTING AORTA  Expanding
 Splitting of the arterial wall with tearing of the  Caused by iatrogenic injury
intima or degeneration of the media  Dissection
 More common in men than women (50- 70 y.o)  Involves branch vessels
 Factors: poorly controlled HPN, blunt chest trauma,  regular ultrasonography to determine change in size
cocaine use  If stable in size: control and monitor BP (preop: 100-
120 mmHg)
 Pharmacologic: antihypertensives
 Diuretics
 Beta-blockers
TWO KINDS OF DISSECTING AORTA  ACE inhibitors
 Ascending Aortic Dissection  Angiotensin II receptor antagonists
 Descending Aortic Dissection
 Calcium channel blockers
* greater possibility of rupture with increased diastolic blood
pressure (↑100 mmHg)

SURGICAL MANAGEMENT
GOAL: To repair the aneurysm and restore vascular continuity
with a vascular graft
 TOC for AAA’s more than 5.5 cm (2 in) wide
or those that are enlarging
 Prognosis of a ruptured aneurysm is poor and
CLINICAL MANIFESTATION immediately surgery is the only intervention
Types:
A. Open surgical repair: resecting the vessel and putting a
bypass graft
- exposing the aneurysm, applying clamps just above
and below the aneurysm, opening, placing a Dacron
graft; aneurysm sac is then wrapped around graft to
protect it

DIAGNOSIS
 Chest x-ray
 Transesophageal echocardiography (TEE)
 Computed tomography angiography (CTA)

AAA:
◾ Duplex ultrasonography to determine size, length
and location
◾ CT scan b. Endovascular grafting:
the transluminal placement and attachment of a sutureless
DISSECTING AORTA aortic graft prosthesis
◾ Arteriography - minimal invasion, fewer complications, rapid
◾ CT
◾ Transesophageal echocardiography
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes
- cannot be used for ruptured aneurysm
COMPLICATIONS
a.) open surgical repair
 Bleeding,
hematoma, wound
infection at the femoral insertion site
 Arterial occlusion
 Distal ischemia or embolization
 Dissection or perforation of the aorta
 Graft thrombosis or infection
 Break of the attachment system
 Graft migration
 Graft leaks
 Delayed rupture
 Bowel ischemia – d/t embolization;
 - s/s: fever, leukocytosis, ileus, diarrhea, abdominal
pain
 Renal failure – d/t sustained ischemia from â aortic
blood flow, â cardiac output, emboli, inadequate
hydration, clamping above the renal arteries during
surgery
 Acute MI – some undergo CABG before aneurysm
repair to reduce this risk
 Spinal cord ischemia – paraplegia, rectal and urinary
incontinence, loss of pain and temp. sensation
(more common with ruptured AAA)
 Retrograde ejaculation and impotence
NURSING DIAGNOSES
1. Risk for fluid volume deficit related to increased risk for
hemorrhage at the graft site
 monitor for ↑ PR, â BP, clammy skin, anxiety,
restlessness, âLOC, pallor, cyanosis, thirst,
oliguria, á abdominal girth, á chest tube output
(> 100ml for 3 hours, back pain
retroperitoneal bleeding)
 monitor CVP, left atrial pressure, pulmonary
artery pressure and PCWP continuously
 assess for changes indicating hypovolemia
2. Impaired Gas Exchange
related to ineffective cough secondary to pain from
large incision (midline incision form the xiphoid process
to symphysis pubis)
 monitor
ventilatory
settings to ensure
adequate
oxygenation
 assess lung sounds q 1-2 hrs and report
adventitious sounds
 monitor oxygen saturation continuously
 after extubation:
o incentive spirometry (to assist with
coughing)
o encourage ambulation
o provide adequate analgesia to
promote coughing with severe pain
3. Altered Tissue Perfusion related to temporary decrease in
blood supply (may be secondary to: clamped aorta while
ongoing grafting or graft site occluded with thrombus)
 assess dorsalis pedis and posterior tibial pulses q
hour x 24 hrs
 report changes in pulse quality or absent pulses
 assess dorsiflexion, plantarflexion and sensation q
hour x 24 hrs
 inspect lower extremities for mottling, cyanosis, or
numbness q 4 hrs
4. Pain related to tissue trauma secondary to surgical incision
 analgesics as ordered
(d/t  splinting incision site esp. when coughing
 non-pharmacologic measures
OTHER NURSING INTERVENTIONS (FOR ALL TYPES):
1. ASSESSMENT – anticipate for rupture of the aneurysym
- check for CV, cerebral, pulmonary and renal
impairment from atherosclerosis
SIGNS OF IMPENDING RUPTURE:
 severe back/abdominal pain in the middle or lower
abdomen to the left of the midline
 low back pain (indicating rapid expansion and thus
may rupture)
 falling BP
 decreasing hematocrit
- rupture into peritoneal cavity is fatal
2. Postop: - flat on bed for 6 hrs.
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes

- V/S and Doppler assessment of peripheral
 Deep Vein Thrombosis – a disorder involving a thrombus
in one of the deep veins of the body, most commonly the
iliac or femoral vein
 Venous thromboembolism – characterized by DVT and
PE
 Thrombophlebitis – inflammation of a vein accompanied
by the formation of a clot
 Phlebothrombosis – an abnormal condition in which a
clot forms within a vein with the wall of the vessel not
inflamed; caused by hemostasis, hypercoagulability, or
occlusion.
 Effort Thrombosis – caused by repetitive motion that
irritates the vessel wall, causing inflammation and
subsequent thrombosis

ETIOLOGY
Pathophysiology
 venous thrombi are aggregates of platelets attached
pulses q 15 mins X 4 cycles, q 30 mins X 4, then
to the vein wall that have a tail-like
q hour X 4
appendage containing fibrin, WBC’s, and many
- Check the access site
RBC’s
- Assess for signs of embolization
 fragmentation of a thrombus may occur (either
- Monitor temperature and s/s of infection
spontaneously as it dissolves naturally, or with an
- Monitor for postimplantation syndrome
elevation of venous pressure
- Notify AP of persistent coughing, sneezing,
 Recanalization can occur
vomiting, SBP >180 mmHg
- Encourage oral fluids
MANIFESTATIONS
DISORDERS OF THE PERIPHERAL VEINS
Veins
 Superficial veins – thick-walled; muscular; lie just
Phlegmasia cerulea dolens
under the skin
 Deep veins – thin-walled; less muscular
 Perforating veins – allow blood flow from the
superficial system to the deep system
 Veins have valves that permit unidirectional flow of
blood back to the heart
a. Deep veins
 Edema of the extremity
 Warmer affected extremity
 Superficial veins appear more prominent
 Tenderness
 s/s of a pulmonary embolus

 *Homan’s sign is NOT considered a reliable indicator

of DVT since it can be elicited in any painful condition
of the calf.

b. Superficial veins
 Tenderness
 Redness
 warmth in affected area
* Risk for embolization is very low because of
 Venous Thrombosis – presence of a clot in a vein in which spontaneous dissolution of the thrombus
the wall of the vessel is not inflamed; usually occurs in the
lower extremities
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes
MEDICAL MANAGEMENT
 GOAL: prevent growth and fragmentation of the
thrombus
 prevent recurrent thromboemboli
PREVENTION
 Graduated compression stockings
 Intermittent pneumatic compression device
 Early mobilization and leg exercises
 Lifestyle changes: wt loss, smoking cessation,
regular exercise
PHARMACOLOGIC
 Agents:
1. Anticoagulants
a. unfractionated heparin - SQ /IV infusion;
oral anticoagulant (Coumadin) concurrently
administered
 Monitor aPTT, INR, and plt ct.
B. low-molecular-weight heparin (LMWH)
 Longer half-life
 fewer bleeding complications
 lower risk of heparin-induced
thrombocytopenia
 Can be used safely in pregnant
women
 Pts are more mobile
 e.g. dalteparin (Fragmin) and
enoxaparin (Lovenox)
C. Oral anticoagulants
 Warfarin – Vit. K antagonist; for extended
anticoagulant therapy; slow onset of action
D. Factor Xa Inhibitor (Stuart-Prower factor or as
thrombokinase)
 Fondaparinux – given daily, SQ, Fixed
dose, excreted unchanged; coagulation
monitoring unecessary; prophylaxis
during major orthopedic surgery; with
warfarin, treatment for VTE
CONTRAINDICATIONS TO ANTICOAGULANT THERAPY
 Lack of pt cooperation
 GI, GU, respi, reproductive bleeding
 Hemorrhagic blood dyscrasias
 Aneurysms
 Severe trauma
 Recent or impending surgery
 Severe hepatic or renal disease
 Recent cerebrovascular hemorrhage
 Open ulcerative wounds
 Increase hazard for injury
 Recent childbirth
2. Thrombolytic therapy
 dissolves thrombi
 effective if given within the first 3 days of acute
thrombosis
 Three-fold greater incidence of bleeding than
heparin
SURGICAL MANAGEMENT
 Indications:
 anticoagulant or thrombolytic therapy is
contraindicated
 danger of pulmonary embolism
 severely compromised venous drainage
a. Thrombectomy – removal of the
thrombus
b. Balloon angioplasty
c. Placement of Stent
NURSING MANAGEMENT
1. Assessing and monitoring anticoagulant therapy
 infusion device for continuous IV infusions
 Assess for bleeding tendencies and renal
insufficiency
 Obtain periodic coagulation tests
a.) aPTT – for heparin; effective when it is 1.5 times
the control
b.) PT or the INR – for warfarin; effective when PT is
1.5 to 2 times the normal or INR is 2.0-3.0
2. Monitoring and managing potential complications
 Bleeding
◾ Kidneys: microscopic exam of the urine
◾ Other early signs: bruises, nosebleeds,
gum bleeding
 Antidotes:
 Protamine sulfate – reverse the effects of
heparin
- administer slowly to reduce s/e of
bradycardia and hypotension
 Vitamin K – reverse the effects of warfarin
b. Thrombocytopenia (HIT)
◾ Defined as a sudden decrease in platelet
count by at least 30% of baseline levels;
results from an autoimmune mechanism
causing destruction of platelets
◾ Avoid use of unfractionated heparin for
long term therapy
◾ Monitor platelet count, thromboembolic
and hemorrhagic complications
PERIPHERAL VASCULAR DISORDERS
Semifinal Notes

3. Providing comfort
◾ Bed rest (to prevent emolization), elevate
affected extremity, analgesics for pain relief
◾ Apply warm,moist packs over the affected
extremity
◾ Foot exercises – e.g. repetitive dorsiflexion
of foot
4. Compression therapy - used when patients begin to
ambulate
a. stockings – contraindicated in pts with severe
pitting edema
b. wraps
c. pneumatic compression devices

5. Positioning and exercise

 Elevate lower extremities above heart level
periodically
 Perform passive and active leg exercises
 Encourage early ambulation
 DBE
 Avoid sitting for more than 2 hours

6. Promoting home and community-based care

 Discontinuation of alcohol use for pts on
anticoagulant therapy

Leg Exercises and Foot Exercises