F&E FINALS NOTES 1.

Sodium – Chloride (Direct)

ELECTROLYTE IMBALANCES - They move together (e.g., in salt = NaCl).
Electrolytes - If sodium increases, chloride usually increases too.
- are active chemicals in body fluids 2. Sodium – Potassium (Inverse)
• cations – which carry positive charges - When sodium is high, potassium tends to be low, and
• anions – which carry negative charges vice versa.
- The major cations in body fluid are: - Example: Too much sodium → body may excrete
✓ Sodium potassium to balance.
✓ Potassium 3. Calcium – Phosphorus (Inverse)
✓ Calcium - High calcium levels lower phosphorus, and high
✓ Magnesium phosphorus lowers calcium.
✓ hydrogen ions - Controlled by parathyroid hormone (PTH).
- The major anions are: 4. Calcium – Vitamin D (Direct)
✓ Chloride
- Vitamin D helps the body absorb calcium from the gut.
✓ Bicarbonate
- Low vitamin D → low calcium absorption.
✓ Phosphate
5. Magnesium – Calcium (Direct)
✓ Sulfate
- Magnesium is needed for calcium regulation (e.g.,
✓ proteinate ions
muscle contraction, bone health).
- plays a role in:
o conducting nervous impulses - Low magnesium → poor calcium balance.
6. Magnesium – Potassium (Direct)
o contracting muscles
o keeping the body hydrated and regulating - Magnesium helps maintain potassium levels inside
body’s pH levels. cells.
Electrolyte Imbalances - Low magnesium often leads to low potassium.
- The level of an electrolyte in the blood can become too 7. Magnesium – Phosphorus (Inverse)
high or too low, leading to an imbalance. - As magnesium increases, phosphorus tends to
- Electrolyte levels can change in relation to water levels decrease.
in the body as well as other factors. ELECTROLYTES
Important electrolytes lost in sweat during exercise: Electrolytes Normal Value Functions
o Sodium 135 – 145 helps transmit impulses in the
I. Sodium
o Potassium mEq/L nerves and muscles fibers.
Electrolyte concentration can also be affected by: assists in skeletal and cardiac
II.
3.5 – 5 mEq/L muscle contraction and
o Rapid loss of fluids Potassium
electrical conductivity.
▪ Diarrhea promotes enzyme reactions
▪ Vomiting III. 1.6 – 2.6
within the cell during
Magnesium mEq/L
Replacement: carbohydrates metabolism.
- These electrolytes must be replaced to maintain healthy Serum level:
levels. 8.9 – 10.1
is responsible for the
mg/dL
Regulation: IV. Calcium formation and structure of
Ionized:
- The kidneys and several hormones regulate the bones and teeth.
4.5 – 5.2
concentration of each electrolyte. mEq/L
- If levels of a substance are too high → kidneys filter it from V. 2.5 – 4.5 plays an important role in cell
the body. Phosphorus mEq/L membrane integrity.
- Different hormones act to balance the levels. 96 – 106 helps maintain serum
VI. Chloride
Imbalance: mEq/L osmolality and water balance.
HYPO
- Becomes a health issue when concentration of a certain
❖ Not severe: Isotonic
electrolyte is higher than the body can regulate.
❖ Sever: Hypertonic
- Low levels of electrolytes can also affect overall health.
HYPER
Electrolyte Relationships
❖ Not severe: Isotonic
1. Sodium – Chloride Direct
❖ Sever: Hypotonic
2. Sodium – Potassium Inverse
3. Calcium – Phosphorus Inverse
4. Calcium – Vitamin D Direct
5. Magnesium – Calcium Direct
6. Magnesium – Potassium Direct
7. Magnesium – Phosphorus Inverse
I. Sodium (Na) ✓ Diarrhea
- helps transmit impulses in the nerves and muscles ✓ Excessive sweating
fibers. ✓ Fistula
- Accounts for 90% of ECF CATIONS ✓ Diuretic use
- Most abundant solute in the ECF ✓ Adrenal insufficiency
- Normal Serum Na Level – 135 to 145 mEq/L SIGNS AND SYMPTOMS
- Inside the cell – 10 mEq/L • Headache
Functions: • Nausea
✓ It helps maintain proper ECF concentration • Abdominal cramps
✓ It helps transmit impulses – nerves and muscles fibers. • Muscle twitching
✓ It helps regulate acid-base balance – by combining with • Tremors
chloride and bicarbonate. • Weakness
Dietary sources: • Changes in Level of Consciousness (LOC)
o Canned foods o shortened attention span
o Cheese o lethargy
o Ketchup o confusion
o Processed meat o stupor
o Salt o coma
o Salty snack foods o seizures
o Sea foods Hypovolemia (Depletional Hyponatremia)
Balancing Na
• Dry mucous membrane
- Hold the salt you fucking bitch
• orthostatic hypotension
• poor skin turgor
• tachycardia
Hypervolemia (Dilutional Hyponatremia)
• Hypertension
• rapid bounding pulse
• weight gain
LABORATORY FINDINGS
HYPONATREMIA ❖ Serum osmolality – decreased
- Sodium DEFICIENCY in relation to body water ❖ Serum Na level – decreased
- Serum sodium level of < 135 mEq/L ❖ Urine specific gravity – decreased
TWO CLASSIFICATIONS TREATMENT
1) Depletional hyponatremia 1) Restrict fluid intake
a) Hypovolemic hyponatremia 2) High Na diet
➢ decrease in total body water with
3) IVF – NSS (if w/ hypovolemia)
disproportionately greater decrease in total
4) ICU - < 110 mEq/L
serum sodium
- Hypertonic Solution (D5NSS)
➢ presence of clinically evident volume depletion
NURSING INTERVENTIONS
2) Dilutional hyponatremia
1) Monitor and record V/S
a) Hypervolemic hyponatremia
2) Monitor neurologic status frequently
➢ increase in total body water with a relatively
3) Accurately measure and record I & O
smaller increase in the total serum sodium
4) Weigh patient daily
➢ presence of clinically evident edema
5) Assess skin turgor
➢ heart failure
6) Watch for extreme changes in lab
b) Euvolemic/Isovolemic hyponatremia
7) Increase intake of dietary Na
➢ mild to moderate increase in total body water
8) Administer Na supplements as ordered
with normal or near normal sodium levels
9) Administer IV as ordered
➢ absence of clinically evident edema
10) Provide safe environment
➢ Syndrome of Inappropriate Antidiuretic
HYPERNATREMIA
Hormone Secretion (SIADH)
- Sodium EXCESS in relation to body water
− Excess secretion of ADH → kidneys - Serum sodium level of >145 mEq/L
retain water → dilutes sodium in the CAUSES:
blood. ✓ Excessive sodium intake
CAUSES: ✓ Medications
✓ Vomiting
 ✓ Near Drowning 3) Measure and record I & O
✓ Cushing’s Syndrome 4) Assess skin and mucous membrane
➢ a hormonal disorder caused by too much 5) Assist oral hygiene
cortisol in the body, often from steroids or II. Potassium (K)
adrenal gland problems. - assists in skeletal and cardiac muscle contraction and
✓ Hyperaldosteronism electrical conductivity.
➢ a condition where the adrenal glands make too - Major cation in the ICF (98% - is in ICF, 2% - in ECF)
much aldosterone, leading to salt and water - Serum K level - 3.5-5 mEq/L
retention and potassium loss. Functions:
✓ Insensible water losses ✓ Maintains cells’ electrical neutrality and osmolality
✓ Extensive burns ✓ Aids in neuromuscular transmission of nerve impulses
✓ Severe watery diarrhea ✓ Assists in skeletal and cardiac muscle contraction and
✓ Hyperosmolar Hyperglycemic Nonketotic Syndrome electrical conductivity
➢ a serious complication of type 2 diabetes with ✓ Affects acid- base balance
very high blood sugar, severe dehydration, but Dietary sources:
little or no ketones. - K must be ingested daily because the body can’t
✓ Diabetes Insipidus conserve it.
➢ a disorder where the body makes too little o Chocolates
antidiuretic hormone (ADH) or the kidneys o Dried – fruits, nuts and seeds
don’t respond to it, causing excessive o Fruits – oranges, bananas
urination and thirst. o Meats
SIGNS AND SYMPTOMS o Vegetables – potatoes, mushrooms,
Neurologic signs tomatoes, carrots
• Restlessness Balancing K
• Agitation - 80% of K intake is excreted in the urine, the rest is
• Weakness excreted in feces and sweat
• Lethargy ❖ Anabolism – K moves from ECF to ICF
• Confusion ❖ Sodium-Potassium pump – moves Na from the cell
• Stupor into the ECF and pumps K into the cell
• Seizure ❖ Na and K – have a reciprocal relationship
❖ pH – Hydrogen ions and K ions freely exchange
• coma
across plasma cells
Signs of neuromuscular irritability
HYPOKALEMIA
• Twitching
- Potassium DEFICIENCY in relation to body water
• Hyperreflexia
- Serum potassium level of < 3.5 mEq/L
• Ataxia
CAUSES:
• tremors
✓ Too much output
Other:
✓ Diuretics
• low-grade fever
✓ Corticosteroids
• flushed skin ✓ Insulin
• extreme thirst ✓ Alkalosis
• hypervolemia – ↑ BP, bounding pulse, dyspnes ✓ Malabsorption syndrome
• hypovolemia - dry MM, oliguria, orthostatic SIGNS AND SYMPTOMS
hypotension • Skeletal muscle
LABORATORY FINDINGS • Weakness
❖ Serum osmolality – increased • Constipation
❖ Serum Na level – increased
• Paralytic ileus
❖ Urine specific gravity – increased
➢ A condition where the intestines stop moving
TREATMENT
(no peristalsis), even though there’s no
1) Increase OFI
physical blockage.
2) Low Na diet
➢  The bowel becomes “paralyzed,” so food,
3) IVF – salt-free (D5W), followed by half-NSS
fluids, and gas can’t move forward.
4) Diuretics
LABORATORY FINDINGS
NURSING INTERVENTIONS
❖ ECG:
1) Monitor and record V/S
o Flattened T wave
2) Insert IVF as needed
o Depressed ST segment
 o Characteristic U wave 4) Hemodialysis
❖ Serum K level decreased 5) Drugs – Sodium polystyrene sulfonate
❖ ABG result elevated pH and HCO3 6) Emergency cases (>6mEq/L)
❖ Elevated serum glucose o Closely monitor cardiac status
TREATMENT o Administer 10%Calcium Gluconate
1) High K diet o Acidosis – administer sodium bicarbonate
2) Oral K supplements o Administer 10 units regular insulin IV
3) IV K replacement therapy o Kayexalate - Potassium-removing resin
NURSING INTERVENTIONS NURSING INTERVENTIONS
1) Monitor VS 1) Assess VS
o especially pulse and BP – weak, irregular; 2) Monitor I and O
orthostatic hypotension 3) Prepare patient for dialysis – acute hyperkalemia
o HR – tachyarrhythmias 4) Implement safety measures
o RR – WOF shallow and rapid respiration 5) Health Teachings
2) Monitor serum K levels o Select foods that don’t stimulate peristalsis
3) Monitor I and O o Explain S/Sx of hyperkalemia
4) Check for signs of alkalosis III. Magnesium (Mg)
o irritability - promotes enzyme reactions within the cell during
o paresthesia carbohydrates metabolism.
5) Insert and maintain an IV access as ordered - After K, magnesium is the 2nd most abundant cation in
6) Provide safe environment the ICF (ECF – 1%, ICF – holds the rest)
7) Check for signs of constipation - Bones – contain 60% of the body’s magnesium
8) Health teachings: - Normal Serum Magnesium Level – 1.6 to 2.6 mEq/L
o Importance of taking K supplements as - Inside the cells – about 40mEq
prescribed Functions:
o If client is on digoxin therapy, teach patient to ✓ Promotes enzyme reactions within the cell during
recognize and report S/Sx of digoxin toxicity carbohydrates metabolism
o Make sure the client can identify the signs and ✓ Helps the body produce and use ATP
symptoms of hypokalemia ✓ Takes part in protein synthesis
HYPERKALEMIA ✓ Influences vasodilation, helping the CV system function
- Potassium EXCESS in relation to body water normally
- Serum potassium level of >5mEq/L ✓ Helps sodium and potassium ion cross the cell
CAUSES: membranes
✓ Little output ✓ regulates muscle contraction
✓ Beta-blockers ✓ influences calcium level
✓ K-sparing diuretics Dietary sources:
✓ Chemotherapy o Chocolate
✓ Severe infection o Dry beans and peas
✓ Trauma/Crush injury o Green, leafy vegetables
✓ Acidosis o Meats
✓ Insulin deficiency o Nuts
✓ Blood transfusion o Seafoods
SIGNS AND SYMPTOMS o Whole grains
• Skeletal muscle weakness Balancing Mg
• Nausea GIT
• Diarrhea - If the serum Mg level drops – GIT absorb Mg and V.V.
• Abdominal cramping Kidneys
LABORATORY FINDINGS - Balance Mg by altering reabsorption at the proximal
❖ ECG: tubule and loop of Henle
o Tall, Tented T wave - If serum Mg level rises – the kidneys excrete excess in the
❖ Serum K level increased urine
❖ ABG result decreased pH HYPOMAGNESEMIA
TREATMENT - Magnesium DEFICIENCY in relation to body water
1) Restrict K in the diet - Serum magnesium level of < 1.6mEq/L
2) Loop diuretics CAUSES:
3) Discontinue medications associated with high K levels ✓ Poor dietary intake of Mg
 ✓ Absorption problems 6) If patient is receiving digoxin, monitor for signs of digoxin
✓ GI Problems toxicity
✓ Urinary Problems 7) Institute seizure precautions.
SIGNS AND SYMPTOMS 8) Keep emergency equipment nearby for airway protection
A low serum Mg level irritates the CNS leading to: HYPERMAGNESEMIA
• Altered LOC - Magnesium EXCESS in relation to body water
• Hallucinations - Serum magnesium level of >2.6mEq/L
• Ataxia CAUSES:
• Insomnia ✓ Excessive Mg intake
• Confusion ✓ Renal Dysfunction
• Psychosis SIGNS AND SYMPTOMS
• Delusions • High serum Mg level depresses the neuromuscular
• Seizures system
o Decreased muscle and nerve activity – hypoactive
• Depression
DTR
• Vertigo
o Generalized weakness – starts with weak hand
Skeletal muscle weakness
grasp (progresses to flaccid paralysis)
• Tremors
o Occasional Nausea and vomiting
• Twitching
o Decreased LOC – drowsy – coma
• Tetany
• Respiration – slow, shallow, depressed
• Hyperactive Deep Tendon Reflexes (DTR)
• Weak pulse, bradycardia, arrhythmias - decreased
➢ reflex response (like knee jerk when tapped) is
cardiac output and cardiac arrest
exaggerated or stronger than normal.
• Hypotension - patient feel flushed and warm all over
Other:
LABORATORY FINDINGS
• Foot or leg cramps
❖ ECG:
• Paresthesia
o Prolonged PR interval W
• Breathing difficulties – laryngeal stridor
o idened QRS complex
• Hypocalcemia o Tall T wave
• Tachycardia, arrhythmias ❖ Increased serum Mg
• Hypertension TREATMENT
• Anorexia 1) Increase fluid intake – oral or IV
• Dysphagia 2) Loop diuretic
• Nausea and vomiting 3) Ca Gluconate
• Digoxin Toxicity 4) Hemodialysis – Mg-free dialysate
• Yellow-tinged vision NURSING INTERVENTIONS
LABORATORY FINDINGS 1) Monitor VS
❖ ECG: 2) Assess Neuromuscular system
o Prolonged PR interval 3) Restrict dietary Mg intake & avoid giving medications
o Widened QRS complex with Mg
o Prolonged QT interval 4) Provide adequate fluids – oral / IV
o Depressed ST segment IV. Calcium (Ca)
o Broad, flattened T wave - is responsible for the formation and structure of bones
o U wave and teeth.
❖ Hypocalcemia (because of the effects of Mg to PTH) - is a positively charged ion found in both the ECF and ICF
❖ Decreased serum Mg - 99% of the body’s Ca – found in the bones and teeth
TREATMENT - 1% - serum and soft tissue
1) Dietary Functions:
2) Magnesium Supplements ✓ Responsible for the formation and structure of bones
3) Magnesium Sulfate – IV or IM and teeth
NURSING INTERVENTIONS ✓ It helps maintain cell structure and function
1) Assess for mental status and report changes ✓ Plays a role in cell membrane permeability and impulse
2) Evaluate the patient’s neuromuscular status regularly transmission
3) Check for dysphagia before food is given ✓ Affects contraction of muscles (cardiac, smooth and
4) Monitor and record VS skeletal muscle)
5) Monitor respiratory status ✓ Participates in blood clotting process
Two ways in measuring Ca ✓ Anticonvulsants (Phenobarbital and Phenytoin
❖ Serum Ca Level (8.9 to 10.1 mg/dL) (Dilantin)
❖ Ionized (free) Ca (4.5 to 5.1 mg/dL) ➢ Interfere with Vitamin D metabolism → low
Dietary Sources: calcium absorption.
o Bonemeal ✓ High Phosphorous level
o Dairy products – milk, cheese, yogurt ➢ Binds calcium, lowering free calcium in the
o Green-leafy vegetables blood.
o Legumes ✓ Excessive Ca loss, Diuretics – loop (Lasix)
o Nuts ✓ Edetate Disodium (Disodium EDTA)
o Whole grains ➢ Binds calcium, lowering levels.
Balancing Ca ✓ Hypomagnesemia
Parathyroid Hormone ➢ Low magnesium reduces parathyroid hormone
• Low serum Ca level – parathyroid gland release PTH (PTH) release → low calcium.
(which draws Ca from bones and promotes transfer of Ca ✓ Drugs – cisplatin & gentamycin
into the plasma) – increase Ca level ✓ Hyperphosphatemia
• PTH also promotes kidney reabsorption of Ca and ➢ Excess phosphate binds calcium, lowering free
stimulates the intestinal absorption of Ca (Phosphorus calcium.
is excreted at the same time) ✓ Alkalosis
• Hypercalcemia – body suppresses the release of PTH ✓ Blood Transfusion (BT)
Calcitonin ➢ Citrate in stored blood binds calcium →
• a hormone produced in the thyroid gland and acts as an hypocalcemia.
antagonist to PTH SIGNS AND SYMPTOMS
• Hypercalcemia – thyroid gland releases Calcitonin • Neurologic S/Sx
(inhibits bone resorption) – causes a decrease in the o Anxiety
serum Ca level o confusion and irritability
• Calcitonin – also decreases absorption of Ca and o seizure
enhances its excretion by the kidneys • Paresthesia – toes, fingers and face (esp. around the
Vit. D. mouth – circumoral)
• is ingested with foods (dairy products) • Twitching, Muscle Cramps, Tremors – laryngeal and
abdominal muscles are prone to spasm
• skin is exposed to UV light, it synthesizes Vit. D
• Active form of Vit. D promotes Ca absorption through • Tetany – secondary to nerve excitability
intestines, Ca resorption from the bones, which raises • (+) Trousseau’s – carpopedal spasm caused by inflating
serum Ca level the blood-pressure cuff to a level above systolic pressure
Phosphorus for 3 minutes
• inhibits Ca absorption in the intestines (opposite effect • (+) Chvostek’s – twitching of facial muscles in response
of Vit D) to tapping over the facial nerve
• An inverse relationship between Ca and P exists in the • Fractues, brittle nails, dry skin and hair
body • Diarrhea
Serum pH • DTR – hyperactive
• also has an inverse relationship with ionized Ca level • Diminished response to Digoxin – digoxin toxicity
• inc pH (alkalosis) – more Calcium binds with protein LABORATORY FINDINGS
and ionized Ca level drops (hypocalcemia) ❖ ECG:
• pH drops (acidosis) – less calcium binds to CHON and o Prolonged ST segment
the ionized Ca increases o Lengthened QT interval
HYPOCALCEMIA o Arrhythmias - Torsades De Pointes
- Calcium DEFICIENCY in relation to body water ❖ Serum Ca level – decreased
- Below 8.9mg/dL (Total Ca) ❖ Ionized Ca level – decreased
- Below 4.5mg/dL (Ionized Ca) TREATMENT
CAUSES: 1) Acute Hypocalcemia
✓ Inadequate intake of Ca - IV Ca Gluconate
✓ Malabsorption 2) Chronic Hypocalcemia
✓ Severe diarrhea - Vit D supplements
✓ Laxative abuse - Oral Ca Supplements
✓ Lack of Vitamin D in the diet - Increase dietary intake or Ca
✓ Renal failure - Aluminum Hydorixde – in cases where the
patient also has a high Phosphorus level
NURSING INTERVENTIONS LABORATORY FINDINGS
1) Monitor VS ❖ ECG:
o RR (WOF dyspnea, stridor) o Shortened QT interval
2) Keep tracheostomy tray, resuscitation bag at bedside o Shortened ST segment
3) Place on cardiac monitor ❖ Serum Ca level – increased
o notify physician if develops arrhythmias ❖ Ionized Ca level – increased
4) Check for signs of Tetany TREATMENT
o Chvostek’s 1) Reduction in the intake of Ca – diet, medications
o Trousseau’s containing Ca must be stopped
5) Administer Ca replacement therapy carefully 2) Hydration – to increase excretion of Ca
6) WOF 3) NSS – Na increases renal excretion of Ca
o arrhythmias 4) Loop diuretics – promote Ca excretion
7) Ensure patency (IV) 5) Dialysis – for life-threatening hypercalcemia
o infiltration can cause tissue necrosis and 6) Corticosteroids – block bone resorption and decrease
sloughing Ca absorption from the GIT
8) Administer oral replacements as ordered 7) Pamidronate/Etidronate disodium – reduces bone
9) Give Ca supplements 1 to 1 ½ hours after meals resorption
10) If GI upset occurs 8) Mithramycin – chemotherapeutic agent
o give with full stomach (milk) 9) Calcitonin – also inhibits bone resorption
11) Seizure precautions NURSING INTERVENTIONS
o padding bedside rails 1) Monitor VS – WOF bradycardia
12) Provide calm, quiet environment 2) Assess neurologic and neuromuscular function – report
HYPERCALCEMIA any changes
- Calcium EXCESS in relation to body water 3) Insert and maintain IV access - NSS – 200 to 500 ml/ hour
- Above 10.1mg/dL (Total Ca) 4) Monitor for signs of pulmonary edema – crackles and
- Above 5.1mg/dL (Ionized Ca) dyspnea
CAUSES: 5) Encourage patient to drink 3-4 L of fluid daily unless
✓ Increase in the resorption of Ca from bone contraindicated
✓ Hyperparathyroidism 6) Strain urine for calculi – check for flank pain
✓ Cancer 7) Provide a safe environment
o bone metastases 8) Keep side rails raised
o multiple myeloma 9) Bed in lowest position, wheels locked
o lung/breast 10) Handle patient gently – prone to pathologic fractures
✓ Hypophosphatemia V. Phosphorus (P)
✓ Acidosis - plays an important role in cell membrane integrity.
✓ Drugs - overdose of Ca - Primary anion found in the ICF
✓ Lithium (dec. Ca excretion) - 85% - exists in bones and teeth, 14% - soft tissue, 1% in
✓ Ingesting excessive amounts of Vitamin D ECF
✓ Vitamin A overdose - 1:2 ratio with Ca
SIGNS AND SYMPTOMS - Normal serum Phosphorus levels 2.5 to 4.5 mg/dL (1.8 to
• Hypercalcemia causes a decrease in cell membrane 2.6 mEq/L)
excitability especially in tissues of skeletal muscle, heart Functions:
and nervous system ✓ It plays an important role in cell membrane integrity
• Muscle weakness – hyporeflexia, decreased muscle ✓ Primary ingredient in 2,3 DPG (2,3 Diphosphoglycerate)
tone ✓ Also involved in buffering of acids and bases
• Fatigue or confusion – personality changes, lethargy – ✓ It promotes energy transfer to cells – through formation
coma of ATP
• Bradycardia – cardiac arrest ✓ It is important for WBC and platelet function
• Digoxin toxicity ✓ Is an essential component of bones and teeth
• Anorexia, Nausea and vomiting Dietary sources:
• Decreased bowel sound – abdominal pain, paralytic o Dairy products
ileus o Meats and poultry
o Fish
• Polyuria – DHN
o Eggs
• Kidney stones – Renal failure
o Nuts
• Pathologic fracture – bone pain
o Legumes
 o Vegetables o WOF – respiratory failure, decreased HR,
o Grains decreased LOC
Balancing P 2) Report signs of hypoxia
❖ Kidneys – 90% is excreted (GIT – excretes the rest) o increased RR
❖ Calcium – inverse relationship with P o confusion
❖ Insulin – moves P into the cell o restlessness
❖ Alkalosis – also shifts P into the cell o cyanosis (later stage)
HYPOPHOSPHATEMIA 3) Report signs of infection
- Phosphorus DEFICIENCY in relation to body water o Fever
- Serum phosphorus level of < 2.5mg/dl (1.8mEq/L) o increased WBC
CAUSES: 4) Monitor I and O 5) Employ safety precautions
✓ Alkalosis – hyperventilation HYPERPHOSPHATEMIA
✓ Sepsis - Phosphorus EXCESS in relation to body water
✓ acute salicylate poisoning - Serum phosphorus level of >4.5mg/dL (2.6mEq/L)
✓ Insulin CAUSES:
✓ Decrease in intestinal absorption of Phosphorus ✓ Increase intake of Phosphorus in the Diet
✓ Starvation ✓ Over administration of phosphorus supplement or
✓ Malabsorption syndrome laxatives or enemas that contain phosphorus (fleet
✓ Diarrhea enema)
✓ Laxative abuse SIGNS AND SYMPTOMS
✓ Diuretics (loop, thiazides, acetazolamide) • Paresthesia – fingertips, around the mouth and spread
✓ Hyperparathyroidism along the limbs and to the face
✓ Hypercalcemia • Weakness – spasms, cramps, pain
SIGNS AND SYMPTOMS • Hyperreflexia
Musculoskeletal • (+) Trousseau’s and (+) Chvostek’s sign
• muscle weakness – weakened hand grasp, slurred • Arrhythmias
speech, dysphagia, malaise, anorexia • Decreased urine output
• myalgia – muscle pain • Impaired vision, corneal haziness, conjunctivitis
• weakened respiratory muscle – poor contractility of the • Skin – papular eruptions
diaphragm (shallow respiration) LABORATORY FINDINGS
• bone pain – loss of bone density ❖ Serum Phosphorus level - increased
• Osteomalacia – softening of the bone ❖ Serum calcium level - decreased
• pathologic fracture TREATMENT
CNS cells malfunction 1) Diet – low-phosphorus diet
• Paresthesia, Irritability 2) Eliminate the use of phosphorus based laxatives and
• Confusion – seizure and coma decreased cardiac enemas
contractility – hypotension, low cardiac output 3) Phosphate-binding antacids – Aluminum, Mg, Ca gel
Chest pain 4) Insulin – DM 5) NSS
• decreased oxygen delivery to myocardium NURSING INTERVENTIONS
Other: 1) Monitor VS
• Anemia 2) WOF signs and symptoms of worsening hypocalcemia
• Increased susceptibility to infection o paresthesia, muscle cramps, hyperactive
• Bleeding tendencies – GI bleeding reflexes – notify MD
LABORATORY FINDINGS 3) Monitor I and O
❖ Serum Phosphorus level – decreased o Output – less than 30ml/hour – notify MD
❖ X-ray – bone fractures 4) Report any signs of calcification
TREATMENT VI. Chloride (Cl)
1) Diet – high in phosphorus-rich foods - helps maintain serum osmolality and water balance.
2) Oral supplements - Is the most abundant anion in ECF
3) Neutra-Phos-K - Side effects: nausea and diarrhea - Mix - Normal Serum Chloride level 96 to 106 mEq/L
with juice to improve taste Functions:
4) IV Phosphorus replacement ✓ Helps maintain serum osmolality and water balance
5) Should be administered slowly ✓ Chloride and sodium work together to form CSF
6) 6) WOF IV infiltration – sloughing and necrosis ✓ Choride is secreted in gastric mucosa as HCl
NURSING INTERVENTIONS ✓ Chloride helps maintain acid-base balance and assists
1) Monitor VS carbon dioxide transport in the RBC
Dietary sources: o Deep
o Fruits o rapid respiration (Kussmaul’s respiration)
o Vegetables o weakness
o Table salt o lethargy
o Salty foods • Arrhythmias – decreased cardiac output
o Processed meat • Signs of hypernatremia
o Canned foods o Dyspnea
Balancing Cl o Tachycardia
❖ Excretion – kidneys o Hypertension
❖ Cl and Na – closely linked o edema
❖ Cl and Bicarbonate – have an inverse relationship LABORATORY FINDINGS
HYPOCHLOREMIA ❖ Serum Chloride level - increased
- Chloride DEFICIENCY in relation to body water ❖ Serum pH less than 7.35
- Serum chloride level of < 96 mEq/L ❖ Serum bicarbonate level less than 22 mEq/L
CAUSES: TREATMENT
✓ Decreased chloride intake 1) Diet – sodium and chloride restriction
✓ Excessive chloride losses 2) IVF – PLRS
✓ Prolonged vomiting 3) IV sodium bicarbonate
✓ Diarrhea NURSING INTERVENTIONS
✓ Severe diaphoresis 1) Monitor VS
✓ Diuretics 2) Restrict sodium and chloride in the diet
✓ Alkalosis 3) Monitor I and O
SIGNS AND SYMPTOMS 4) Provide safe, quiet environment
• Slow and shallow respiration – respiratory arrest
• Tetany – hyperactive DTR
• Muscle hypertonicity – weakness, twitching, muscle
cramps
• Arrythmias
• Seizures – coma
LABORATORY FINDINGS
❖ Serum Chloride level - decreased
❖ Serum Na level - decreased
❖ Serum pH greater than 7.45
❖ Serum bicarbonate level greater than 26 mEq/L
TREATMENT ACID-BASE IMBALANCE
1) – salty broth - refers to a disruption in the normal balance between acids
2) IVF – NSS and bases in the body, which is essential for maintaining
3) Ammonium Chloride homeostasis and proper cellular function.
➢ An acidifying agent used in Oral replacement - This balance is typically measured by the pH level of the
alkalosis blood.
➢ Assess pain at the infusion site - A normal blood pH is tightly regulated between 7.35 and 7.45,
➢ Contraindicated in patients with severe hepatic with levels below 7.35 indicating acidosis (too much acid)
disease and levels above 7.45 indicating alkalosis (too much base).
NURSING INTERVENTIONS CLASSIFIED INTO FOUR PRIMARY CATEGORIES:
1) Monitor VS especially RR 1. Metabolic Acidosis
2) Offer foods high in chloride 2. Metabolic Alkalosis
3) Provide safe environment 3. Respiratory Acidosis
HYPERCHLOREMIA 4. Respiratory Alkalosis
- Chloride EXCESS in relation to body water 1. Metabolic Acidosis
- Serum chloride level of >106 mEq/L - Cause: Excess production or ingestion of acid, or
CAUSES: excessive loss of bicarbonate.
✓ Increased chloride intake - Examples:
✓ Acidosis o Diabetic ketoacidosis
✓ Drug related (Ammonium chloride, Kayexalate) o lactic acidosis
SIGNS AND SYMPTOMS o renal failure
• Signs of Acidosis o severe diarrhea
 - Symptoms: DIAGNOSIS:
o Rapid breathing (to expel CO2 and raise pH) 1. Acid-base imbalances
o Fatigue - are diagnosed using arterial blood gas (ABG) analysis,
o Confusion which measures:
o Nausea • Ph
o shock (severe cases) • Partial pressure of carbon dioxide (PaCO2)
- Compensation: Respiratory system tries to compensate (reflects respiratory contribution)
by increasing ventilation to blow off CO2 (acid), which • Bicarbonate (HCO3−) (reflects metabolic
helps raise pH. contribution)
2. Metabolic Alkalosis 2. Anion Gap
- Cause: Excess loss of acid or an increase in bicarbonate. - is also calculated in cases of metabolic acidosis to help
- Examples: determine the underlying cause (e.g., diabetic
o Vomiting (loss of gastric acid) ketoacidosis versus diarrhea).
o diuretic use ANION GAP CALCULATION:
o excessive bicarbonate intake - The anion gap is calculated using the following formula:
- Symptoms: Anion Gap=[Na⁺]−([Cl⁻]+[HCO₃⁻])
o Slower breathing Where:
o muscle cramps • [Na⁺] is the concentration of sodium in the blood (in
o twitching mEq/L).
o weakness • [Cl⁻] is the concentration of chloride in the blood (in
o confusion mEq/L).
- Compensation: The respiratory system compensates by • [HCO₃⁻] is the concentration of bicarbonate in the blood
decreasing ventilation to retain CO2 and lower pH. (in mEq/L).
3. Respiratory Acidosis Example Calculation:
- Cause: Decreased ventilation leading to CO2 retention. If the following lab values are provided:
- Examples: • [Na⁺] = 140 mEq/L
o Chronic obstructive pulmonary disease
• [Cl⁻] = 100 mEq/L
(COPD)
• [HCO₃⁻] = 24 mEq/
o Asthma
Then the anion gap would be:
o Pneumonia
• Anion Gap=140−(100+24)
o neuromuscular disorders
• 140−124=16 mEq/L
o drug overdose (respiratory depression)
Normal Values:
- Symptoms:
✓ A normal anion gap is typically 8-12 mEq/L.
o Headache
✓ An anion gap greater than 12 mEq/L indicates a high
o Confusion
anion gap metabolic acidosis.
o Drowsiness
✓ If the anion gap is normal but acidosis is present, this
o shortness of breath
may indicate a normal anion gap metabolic acidosis
o coma (severe cases)
(NAGMA).
- Compensation: The kidneys retain bicarbonate and
TREATMENT:
excrete hydrogen ions to balance the pH over time.
Treatment depends on the underlying cause of the imbalance:
4. Respiratory Alkalosis
Metabolic acidosis:
- Cause: Excessive loss of CO2 due to hyperventilation.
- Administering bicarbonate, treating underlying
- Examples:
conditions like diabetic ketoacidosis.
o Anxiety
Metabolic alkalosis:
o Pain
- Correcting the cause (e.g., stopping vomiting),
o Fever
administering chloride solutions.
o high altitude
Respiratory acidosis:
o pulmonary embolism
- Improving ventilation, possibly using mechanical
- Symptoms:
ventilation.
o Dizziness
Respiratory alkalosis:
o Lightheadedness
- Slowing breathing, addressing the cause of
o tingling in extremities
hyperventilation
o loss of consciousness (severe cases)
ARTERIAL BLOOD GAS (ABG) ANALYSIS
- Compensation: The kidneys excrete bicarbonate and
- is a critical diagnostic tool used to measure the levels of
retain hydrogen ions to lower pH over time
oxygen (O₂), carbon dioxide (CO₂), and the acidity (pH) of
arterial blood.
- It helps assess a patient’s lung function and the body’s ability Step 1: Assess pH
to maintain proper acid-base balance. • pH < 7.35: Indicates acidosis.
- ABG analysis is particularly important in diagnosing and • pH > 7.45: Indicates alkalosis.
managing respiratory and metabolic disorders, acid-base Step 2: Determine the Primary Cause (Respiratory vs.
imbalances, and conditions such as COPD, kidney failure, Metabolic)
and sepsis. • PaCO₂ abnormal: Likely a respiratory cause.
KEY COMPONENTS OF ABG ANALYSIS o High PaCO₂ (>45 mmHg) indicates respiratory
1. pH acidosis.
2. Partial Pressure of Carbon Dioxide (PaCO₂) o Low PaCO₂ (<35 mmHg) indicates respiratory
3. Bicarbonate (HCO₃⁻) alkalosis.
4. Partial Pressure of Oxygen (PaO₂) • HCO₃⁻ abnormal: Likely a metabolic cause.
5. Oxygen Saturation (SaO₂) o Low HCO₃⁻ (<22 mEq/L) indicates metabolic
6. Base Excess (BE) acidosis.
[Link] o High HCO₃⁻ (>26 mEq/L) indicates metabolic
- Measures the acidity or alkalinity of the blood. alkalosis.
- Normal range: 7.35–7.45. Step 3: Check for Compensation
- pH < 7.35 indicates acidosis (excess acid). • The body attempts to compensate for acid-base
- pH > 7.45 indicates alkalosis (excess base). imbalances, either through the respiratory system (by
2. Partial Pressure of Carbon Dioxide (PaCO₂) adjusting PaCO₂) or the kidneys (by adjusting HCO₃⁻).
- Reflects the amount of CO₂ in the blood, which is • Fully compensated: The pH is normal but the PaCO₂ and
regulated by the lungs. HCO₃⁻ are abnormal, indicating the body has corrected
- Normal range: 35–45 mmHg. the imbalance.
- Elevated PaCO₂ (>45 mmHg) suggests respiratory
• Partially compensated: The pH is still abnormal, but the
acidosis (hypoventilation).
body has started to adjust the PaCO₂ or HCO₃⁻ in the
- Decreased PaCO₂ (<35 mmHg) suggests respiratory
opposite direction of the imbalance.
alkalosis (hyperventilation).
Common Scenarios in ABG Interpretation
3. Bicarbonate (HCO₃⁻) [Link] Acidosis
- Represents the metabolic component of the acid-base
✓ pH < 7.35, HCO₃⁻ < 22 mEq/L.
balance, regulated by the kidneys.
✓ Compensation: Decrease in PaCO₂ (through increased
- Normal range: 22–26 mEq/L.
breathing).
- Elevated HCO₃⁻ (>26 mEq/L) indicates metabolic ✓ Example: Diabetic ketoacidosis.
alkalosis. [Link] Alkalosis
- Decreased HCO₃⁻ (<22 mEq/L) indicates metabolic ✓ pH > 7.45, HCO₃⁻ > 26 mEq/L.
acidosis. ✓ Compensation: Increase in PaCO₂ (through slower
4. Partial Pressure of Oxygen (PaO₂)
breathing).
- Measures the oxygen content in the blood. ✓ Example: Prolonged vomiting or diuretic use.
- Normal range: 80–100 mmHg. 3. Respiratory Acidosis
- Low PaO₂ (<80 mmHg) suggests hypoxemia (insufficient
✓ pH < 7.35, PaCO₂ > 45 mmHg.
oxygen levels).
✓ Compensation: Increase in HCO₃⁻ (kidneys retain
5. Oxygen Saturation (SaO₂) bicarbonate).
- The percentage of hemoglobin saturated with oxygen.
✓ Example: COPD, hypoventilation.
- Normal range: 95–100%.
4. Respiratory Alkalosis
- Levels <90% suggest inadequate oxygenation.
✓ pH > 7.45, PaCO₂ < 35 mmHg.
6. Base Excess (BE)
✓ Compensation: Decrease in HCO₃⁻ (kidneys excrete
- Reflects the amount of excess or insufficient
bicarbonate).
bicarbonate in the blood.
✓ Example: Hyperventilation from anxiety.
- Normal range: -2 to +2 mEq/L.
Example of ABG Interpretation:
- A positive base excess (>+2) suggests metabolic
• pH: 7.30 (Acidosis)
alkalosis.
• PaCO₂: 50 mmHg (High – Respiratory acidosis)
- A negative base excess (<-2) suggests metabolic
• HCO₃⁻: 25 mEq/L (Normal)
acidosis.
- This suggests uncompensated respiratory acidosis, likely due
INTERPRETATION OF ABG RESULTS
to hypoventilation.
The ABG values must be interpreted systematically to determine
the type of acid-base disturbance and whether it is compensated.
Here is a basic approach to interpretation:
 SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE MANAGEMENT TREATMENT
SECRETION (SIADH) 1. Medications
- is a condition where the body secretes too much ✓ Furosemide (promotes diuresis)
Antidiuretic Hormone (ADH) even when it is not needed. ✓ Demeclocycline (inhibits ADH)
- ADH (vasopressin) is responsible for controlling the body’s NURSING MANAGEMENT
water balance by signaling the kidneys to reabsorb water. 1. Monitor vital signs and cardiac and neurological status.
- Excess ADH is released, but not in response to the body’s 2. Provide a safe environment, particularly for the client with
need for it. changes in level of consciousness or mental status.
- Causes include trauma, stroke, malignancies (often in the 3. Monitor intake and output and obtain weight daily.
lungs or pancreas), medications, and stress. 4. Monitor fluid and electrolyte balance.
- The syndrome results in water intoxication and hyponatremia
5. Monitor serum and urine osmolality.
- Vasopressin -causes sodium and fluid retention
6. Restrict fluid intake as prescribed.
In SIADH:
7. Administer diuretics and IV fluids (usually normal saline or
• Too much ADH → excess water retention → diluted
hypertonic saline) as prescribed; monitor IV fluids carefully
blood (low sodium levels, hyponatremia).
because of the risk for fluid volume overload (IV solutions
• Kidneys keep reabsorbing water → urine becomes very containing water are contraindicated because of the risk of
concentrated. water intoxication).
8. Administer medications that inhibit ADH-induced water
reabsorption and produce water diuresis as prescribed.
DIABETES INSIPIDUS (DI)
- The hyposecretion of antidiuretic hormone from the posterior
pituitary gland, caused by stroke or trauma, or may be
idiopathic, resulting in failure of tubular reabsorption of water
in the kidneys and diuresis.

RISK FACTORS
• Age TYPES:
• Certain drugs 1. Central diabetes insipidus.
• Conditions that decrease your body's water excretion - Caused an inherited genetic disorder, damage to
pituitary gland from a sugery, tumor or head injury which
• Intensive physical activities
affects the usual production, storage and release of
ASSESSMENT
ADH.
✓ Signs of fluid volume overload
2. Nephrogenic diabetes insipidus.
✓ Changes in level of consciousness and mental status
- Occurs when there's a defect in the kidney tubules — the
changes
structures in your kidneys that cause water to be
✓ Weight gain
excreted or reabsorbed.
✓ Hypertension
- This defect makes your kidneys unable to properly
✓ Tachycardia
respond to ADH.
✓ Anorexia, nausea, and vomiting
3. Gestational diabetes insipidus.
✓ Hyponatremia
- It occurs only during pregnancy when an enzyme made
by the placenta destroys ADH in the mother.
4. Primary polydipsia. - can range from mild impairment to complete kidney failure
- Also known as dipsogenic diabetes insipidus, this and can occur in patients with or without previous kidney
condition can cause production of large amounts of disease.
diluted urine. PATHOPHYSIOLOGY:
- The underlying cause is drinking an excessive amount of • The exact pathogenesis of AKI is unknown
fluids. CATEGORIES OF AKI
- Primary polydipsia can be caused by damage to the 1. Pre-renal Failure
thirst-regulating mechanism in the hypothalamus. 2. Intra-renal Failure
- The condition has also been linked to mental illness, 3. Post-renal Failure
such as schizophrenia. 1. PRE-RENAL FAILURE
ASSESSMENT - This is due to the impairment of blood flow to the
✓ Excretion of large amounts of dilute urine kidneys.
✓ Polydipsia - It accounts about 60-70% of AKI cases
✓ Dehydration (decreased skin turgor and dry mucous - Causes:
membranes) • Dehydration
✓ Inability to concentrate urine • blood loss
✓ Low urinary specific gravity, 1.006 or lower • severe hypotension
✓ Fatigue • heart failure can lead to decreased kidney
✓ Muscle pain and weakness perfusion.
✓ Headache Mechanisms:
✓ Postural hypotension that may progress to vascular ✓ Hypovolemia: Caused by hemorrhage, dehydration, or
collapse without rehydration fluid losses.
✓ Tachycardia ✓ Reduced cardiac output: Seen in heart failure or
TREATMENT: cardiogenic shock.
Treatment of the underlying cause: ✓ Systemic vasodilation: As in sepsis or anaphylaxis.
1. Medications ✓ Renal vasoconstriction: Due to medications (e.g.,
▪ Desmospressin - man made hormone that replaces NSAIDs inhibiting prostaglandins or ACE inhibitors
missing anti-diuretic hormone (for central DI and impairing efferent arteriole constriction).
Gestational DI) ➢ Reduced renal blood flow → decreased glomerular
2. Diet- low salt (nephrogenic DI) filtration rate (GFR).
NURSING INTERVENTIONS ➢ Activation of the renin-angiotensin-aldosterone system
✓ Monitor vital signs and neurological and cardiovascular (RAAS) to conserve sodium and water.
status. ➢ Prolonged hypoperfusion can lead to ischemic injury of
✓ Provide a safe environment, particularly for the client with the renal parenchyma.
postural hypotension. Renin-Angiotensin-Aldosterone System (RAAS)
✓ Monitor electrolyte values and for signs of dehydration. - is a hormonal cascade that plays a critical role in
✓ Maintain client intake of adequate fluids. regulating blood pressure, fluid balance, and electrolyte
✓ Monitor intake and output, weight, serum osmolality, and homeostasis. It is particularly active in response to low
specific gravity of urine. blood pressure, reduced blood volume, or sodium
✓ Instruct the client to avoid foods or liquids that produce depletion.
diuresis 2. INTRA-RENAL (INTRINSIC) FAILURE
✓ Instruct the client in the administration of medications as - This results from direct assault or damage to the renal
prescribed; DDAVP may be administered by injection, parenchyma (functional tissue layer) of the kidneys.
intranasally, or orally. - Causes:
✓ Instruct the client to wear a Medic-Alert bracelet. • Infections
COMPLICATIONS: • Toxins
1. Dehydration
• certain medications (e.g., NSAIDs, some
2. Electrolyte imbalance
antibiotics)
ACUTE KIDNEY INJURY (AKI)
• autoimmune diseases.
- Also known as Acute Renal Failure
• Acute tubular necrosis (ATN), which is the
- is a sudden decrease in kidney function that occurs over
damage to the filtering tubules or bodies of the
hours to days.
kidneys.
- This impairment leads to an accumulation of waste products,
Key causes and mechanisms:
fluids, and electrolytes, which the kidneys would typically
✓ Acute Tubular Necrosis (ATN): The most common cause,
filter out.
often due to ischemia or nephrotoxins (e.g.,
aminoglycosides, radiocontrast agents).
 ✓ Ischemia: Prolonged hypoperfusion leads to tubular cell 2. Oliguric phase
death and sloughing, forming casts that obstruct - The patient UO may be less than 100ml/day
tubules. - Notable increase of serum nitrogenous compounds like
✓ Toxins: Direct tubular cell injury disrupts cellular uric acid, urea, creatinine and serum potassium and
metabolism and membrane integrity. magnesium.
✓ Acute Interstitial Nephritis (AIN): Immune-mediated - Appearance of uremic symptoms such as
injury, often drug-induced, characterized by interstitial o Nausea
inflammation and edema. o Vomiting
✓ Glomerular diseases: Such as acute glomerulonephritis, o Anorexia
leading to inflammation and glomerular damage. o Pruritus
✓ Vascular causes: Microangiopathies (e.g., thrombotic o muscle cramps and weakness
thrombocytopenic purpura) or vasculitis causing o altered mental status.
endothelial damage and ischemia. - Cardiac effects of hyperkalemia may be noted. Prompt
Tubular injury leads to: detection is a must as this is life-threatening.
✓ Loss of epithelial cell polarity. - Sometimes, patients may present a non-oliguric form of
✓ Intracellular swelling and detachment of cells. renal failure but their ability to excrete wastes is still
✓ Formation of obstructive casts. impaired.
✓ Back-leak of filtrate, reducing effective GFR. 3. Diuretic phase
3. POST-RENAL FAILURE - Marked with a gradual increase of UO.
- The result of an obstruction somewhere distal to the - Laboratory values stop increasing and eventually
kidneys. decrease.
- Causes: - However, this does not mean that the renal function has
• Enlarged prostate glands (BPH) returned to normal.
• Obstructing renal calculus - In case of DHN, the patient may still experience uremic
• Tumors symptoms.
• Ureteral obstruction (e.g. urolithiasis or 4. Recovery phase
ureteral stones) - Signals the improvement of renal function
• Edematous stoma of an ileal conduit - May take about 3-12 months
- Symptoms: CLINICAL MANIFESTATIONS
✓ Oliguria or anuria Most of the clinical manifestations appear during the OLIGURIC
✓ Swelling in the legs, ankles, or feet (edema) PHASE
✓ Fatigue and weakness 1. Increase in serum urea, uric acid, creatinine, potassium and
✓ Shortness of breath magnesium
✓ Confusion or altered mental status 2. Urinalysis results:
✓ Nausea and vomiting - Specific gravity is concentrated.
✓ Fluid overload and hypertension - A phenomenon known as fixed specific gravity may be
Mechanisms: observed, wherein the specific gravity of the urine stays
✓ Ureteral obstruction: Due to stones, tumors, or fibrosis. the same throughout the period.
✓ Bladder outlet obstruction: Often caused by prostate - This is due to the failure of the kidneys to dilute urine.
enlargement, strictures, or neurogenic bladder. 3. Signs of heart failure
✓ Urethral obstruction: Due to strictures or anatomical 4. Elevated blood pressure
abnormalities. 5. Uremic symptoms:
Pathophysiology: • Anorexia
➢ Increased pressure in the nephron decreases the • Nausea
pressure gradient for filtration. • Vomiting
➢ Prolonged obstruction causes tubular atrophy and • Muscle weakness
interstitial fibrosis. • Altered mental status
PHASES OF AKI o This is due to the fact that the body cannot
1. Initiation Phase eliminate toxins
2. Oliguric phase • Uremic frost
3. Diuretic phase 6. Hyperphosphatemia and hypocalcemia
4. Recovery phase 7. Anemia
1. Initiation Phase 8. Hyperkalemia and fatal cardiac arrhythmias
- Begins with the initial insult to the kidneys and ends with 9. Metabolic acidosis
the oliguric phase
 DIAGNOSTICS ✓ Restrict dietary potassium, phosphorus, and sodium if
• Renal function tests imbalances occur.
• This includes serum BUN, creatinine and uric acid ✓ Aim for protein intake of 0.8–1 g/kg/day to prevent
• 24-hour creatinine clearance catabolism without worsening uremia.
• Serum electrolytes 2. Specific Management Based on AKI Type
• ABGs A. Prerenal AKI
• CBC ✓ Restore effective blood flow: Volume resuscitation with
• Ultrasonography of the kidneys crystalloids for dehydration or hypovolemia
✓ Treat underlying conditions like heart failure or sepsis.
• ECG
✓ Avoid prolonged hypotension by optimizing cardiac
MANAGEMENT of AKI
output and perfusion pressure.
A. Identify and Treat the Underlying Cause
B. Intrinsic AKI
✓ Perform a thorough history, physical examination, and
❖ Acute Tubular Necrosis (ATN):
diagnostic workup to identify the etiology (e.g.,
✓ Supportive care is the mainstay; no specific
hypovolemia, nephrotoxins, obstruction).
therapies reverse ATN.
✓ Address the primary cause (e.g., treat sepsis, remove
✓ Minimize further injury by avoiding nephrotoxins.
nephrotoxic agents, relieve obstruction).
❖ Acute Interstitial Nephritis (AIN):
B. Optimize Hemodynamic Status
✓ Identify and discontinue offending drugs (e.g., beta-
❖ Fluid Resuscitation:
lactam antibiotics, NSAIDs).
✓ Administer isotonic fluids (e.g., normal saline) for
✓ Consider corticosteroids (e.g., prednisone) if severe
volume depletion.
inflammation is present and infection is excluded.
✓ Use caution in patients at risk of fluid overload (e.g.,
❖ Glomerulonephritis:
heart failure, cirrhosis).
✓ Use immunosuppressive therapy (e.g.,
✓ Avoid colloids like hydroxyethyl starch, which may
corticosteroids, cyclophosphamide) for immune-
worsen outcomes.
mediated causes.
✓ Vasoactive Agents: Use vasopressors (e.g.,
✓ Manage complications such as hypertension and
norepinephrine) in patients with septic or
edema.
cardiogenic shock to maintain adequate perfusion
example of a beta-lactam antibiotic:
pressure.
❖ Penicillins are part of a broader group of beta-lactam
✓ Ensure mean arterial pressure (MAP) is ≥65 mmHg
antibiotics, which also include: Cephalosporins (e.g.,
to optimize renal perfusion.
ceftriaxone, cefuroxime) Carbapenems (e.g., imipenem,
C. Avoid Nephrotoxins
meropenem) Monobactams (e.g., aztreonam)
✓ Discontinue nephrotoxic drugs such as NSAIDs,
C. Postrenal AKI
aminoglycosides, radiocontrast agents, and certain
✓ Relieve obstruction:
antibiotics.
✓ Catheterize for bladder outlet obstruction.
✓ Consider alternative agents or adjust doses based on
✓ Perform nephrostomy or ureteral stenting for upper
renal function.
urinary tract obstruction.
D. Monitor and Correct Electrolyte Imbalances
✓ Treat underlying conditions (e.g., stones, tumors).
✓ Hyperkalemia: Use measures to lower potassium levels
3. Renal Replacement Therapy (RRT)
✓ Stabilize cardiac membranes with calcium gluconate.
Indicated in severe or refractory cases:
✓ Shift potassium intracellularly with insulin and glucose
✓ Acid-base imbalance (severe metabolic acidosis, pH
or beta-agonists.
<7.1).
✓ Remove potassium using diuretics, sodium
✓ Electrolyte disturbances (severe hyperkalemia,
polystyrene sulfonate, or dialysis.
refractory hyperphosphatemia).
✓ Acidosis: Administer sodium bicarbonate if severe
✓ Intoxications (e.g., lithium, ethylene glycol).
metabolic acidosis (pH <7.2).
✓ Overload (fluid overload refractory to diuretics).
✓ Hyponatremia: Correct slowly to avoid osmotic
✓ Uremia (symptomatic, e.g., encephalopathy,
demyelination.
pericarditis).
E. Manage Fluid Overload
✓ RRT options include intermittent hemodialysis (IHD),
✓ Use loop diuretics (e.g., furosemide) for volume
continuous renal replacement therapy (CRRT), or
overload; however, this does not improve kidney
peritoneal dialysis
recovery but helps with symptoms.
4. Follow-Up and Monitoring
✓ Initiate renal replacement therapy (RRT) if refractory fluid
❖ Regularly monitor:
overload threatens life.
✓ Serum creatinine, electrolytes, and acid-base
F. Nutritional Support
status.
✓ Provide adequate caloric intake to meet metabolic
✓ Urine output and fluid balance.
demands.
 ❖ Evaluate for signs of recovery: ✓ Prepare for emergency dialysis if hyperkalemia is life-
✓ Gradual decline in creatinine and restoration of threatening.
urine output. B. Fluid Overload
❖ Prevent recurrence: ✓ Restrict fluids as per orders.
✓ Avoid future exposure to nephrotoxins. ✓ Elevate the head of the bed to improve breathing.
✓ Manage comorbid conditions (e.g., hypertension, ✓ Administer prescribed diuretics or RRT if indicated.
diabetes). C. Acidosis
NURSING MANAGEMENT ✓ Administer sodium bicarbonate cautiously for severe
1. Assessment and Monitoring metabolic acidosis (pH <7.2).
Vital Signs D. Anemia
✓ Monitor blood pressure for hypotension or hypertension. ✓ Monitor hemoglobin and hematocrit.
✓ Assess heart rate and respiratory rate for signs of fluid ✓ Administer erythropoietin-stimulating agents or
overload or compensation. transfusions as prescribed.
✓ Check temperature for fever indicating infection. 4. Supporting Recovery
Fluid Balance A. Nutritional Support
✓ Measure and record intake and output (I&O) accurately. ✓ Collaborate with dietitians for individualized plans.
✓ Monitor for signs of fluid overload: Edema, crackles in ✓ Implement a low-protein diet to minimize uremic
lungs, weight gain, jugular venous distention (JVD). symptoms while preventing malnutrition.
✓ Daily weight measurement to track fluid retention or ✓ Restrict potassium, phosphorus, and sodium intake as
loss. needed.
Renal Function B. Psychosocial Support
✓ Monitor serum creatinine, blood urea nitrogen (BUN), ✓ Address anxiety and fear about the condition.
and glomerular filtration rate (GFR). ✓ Educate patients and families about AKI, its causes, and
✓ Check urine output and characteristics: recovery expectations.
✓ Color, presence of blood or sediment, and specific 5. Patient Education
gravity. ✓ Teach patients to recognize signs of fluid overload (e.g.,
Electrolytes and Acid-Base Status weight gain, swelling) or worsening kidney function.
Monitor for: ✓ Stress the importance of medication adherence and
✓ Hyperkalemia: Assess for ECG changes (peaked T follow-ups.
waves, widened QRS). ✓ Advise avoiding nephrotoxic agents (e.g., over-the-
✓ Hyponatremia: Watch for confusion, seizures. counter NSAIDs).
✓ Acidosis: Observe for respiratory compensation ✓ Promote adequate hydration, especially in high-risk
(Kussmaul breathing). scenarios (e.g., strenuous exercise, illness).
2. Preventing Further Kidney Damage 6. Collaboration with the Healthcare Team
A. Maintain Adequate Perfusion ✓ Work closely with physicians, dietitians, and
✓ Ensure hydration with appropriate fluids (e.g., isotonic pharmacists to adjust treatment plans.
saline) in hypovolemic patients. ✓ Assist in the preparation and care of patients undergoing
✓ Use diuretics cautiously if indicated for fluid overload. RRT (e.g., hemodialysis or CRRT).
✓ Administer vasopressors as ordered for patients in 7. Evaluation of Outcomes
shock. ✓ Improvement in urine output and laboratory values
B. Avoid Nephrotoxins (creatinine, BUN).
✓ Ensure medication doses are adjusted for renal ✓ Resolution of electrolyte imbalances and fluid overload.
impairment. ✓ Prevention of complications such as infection or
✓ Avoid nephrotoxic drugs such as NSAIDs, contrast progression to chronic kidney disease (CKD).
agents, and aminoglycosides. CHRONIC RENAL FAILURE OR END-STAGE RENAL DISEASE
C. Infection Control - It is the progressive, irreversible deterioration of renal
✓ Practice strict aseptic technique during invasive function in which the body’s ability to maintain metabolic,
procedures (e.g., urinary catheter insertion). and fluid and electrolyte balance fails resulting in azotemia
✓ Administer prescribed antibiotics promptly in cases of or uremia.
sepsis. - is a long-term condition characterized by the progressive loss
3. Managing Complications of kidney function over time.
A. Hyperkalemia - The GFR is less than 20% of normal.
✓ Administer medications as prescribed: COMMON CAUSES:
✓ Calcium gluconate to stabilize cardiac membranes. • DM (leading cause)
✓ Insulin with glucose to shift potassium intracellularly. • HTN
✓ Diuretics (e.g., furosemide) if appropriate. • Chronic glomerulonephritis
 • Pyelonephritis 3. Glomerulosclerosis and Tubulointerstitial Fibrosis
• Obstruction of the urinary tract ✓ Glomerulosclerosis: Scarring of glomeruli due to
• Hereditary lesions (polycystic kidney disease) ongoing stress and inflammation.
• Vascular disorders ▪ Caused by deposition of extracellular matrix
• Infections proteins, mesangial expansion, and podocyte
• Medications or toxic agents injury.
• lupus ✓ Tubulointerstitial Fibrosis: Fibrosis in the spaces
STAGES OF CKD/ESRD BASED ON GFR surrounding tubules and capillaries.
Stage 1: ▪ Driven by chronic inflammation, oxidative stress,
- Kidney damage with normal or increased GFR (≥90 and activation of fibrogenic pathways (e.g.,
mL/min/1.73m²). transforming growth factor-beta [TGF-β] signaling).
Stage 2: 4. Disruption of Filtration Barrier
- Mild reduction in GFR (60-89 mL/min/1.73m²). ➢ Damage to the glomerular filtration barrier
Stage 3: (endothelium, basement membrane, and podocytes)
- Moderate reduction in GFR (30-59 mL/min/1.73m²), often results in:
divided into: ▪ Proteinuria: Leakage of proteins into the urine,
✓ 3a (GFR 45-59) which itself exacerbates kidney damage by
✓ 3b (GFR 30-44). triggering inflammation and tubular injury.
Stage 4: ▪ Loss of selective filtration increases the workload
- Severe reduction in GFR (15-29 mL/min/1.73m²). on surviving nephrons.
Stage 5: 5. Inflammation and Immune Activation
- Kidney failure or end-stage renal disease (ESRD) (GFR <15 ➢ Persistent injury activates immune responses, leading
mL/min/1.73m² or dialysis). to:
The normal GFR is 125mL/min/1.73m2 ✓ Recruitment of inflammatory cells (macrophages, T
cells).
✓ Release of pro-inflammatory cytokines (e.g., TNF-α,
IL-6) and reactive oxygen species (ROS).
✓ Chronic inflammation contributes to progressive
fibrosis.
SIGNS ANND SYMPTOMS 6. Dysregulation of Renin-Angiotensin-Aldosterone System
Early stages of CKD are often asymptomatic, but as the disease (RAAS)
progresses, symptoms may include: ➢ Activation of RAAS in CKD serves to preserve kidney
✓ Fatigue perfusion but contributes to:
✓ Swelling in legs, ankles, and feet (edema) ✓ Vasoconstriction, which worsens glomerular
✓ Nausea or vomiting hypertension.
✓ Loss of appetite ✓ Sodium and water retention, leading to
✓ Muscle cramps hypertension and edema.
✓ Changes in urination (frequency or appearance) ✓ Fibrosis and oxidative stress, exacerbating nephron
✓ High blood pressure loss.
✓ Difficulty concentrating 7. Electrolyte Imbalances
PATHOPHYSIOLOGY OF CHRONIC KIDNEY DISEASE (CKD) ✓ Hyperphosphatemia: Reduced phosphate excretion due
1. Initial Kidney Injury to declining GFR.
✓ CKD often begins with damage to the glomeruli, tubules, ✓ Hypocalcemia: Secondary to phosphate retention and
or interstitial tissues due to conditions like diabetes, decreased activation of vitamin D.
hypertension, or glomerulonephritis. ✓ Hyperkalemia: Reduced potassium excretion in
✓ This injury triggers inflammation and fibrosis, disrupting advanced CKD stages.
normal nephron function ✓ Metabolic Acidosis: Accumulation of acid due to
2. Loss of Nephrons impaired hydrogen ion excretion.
✓ Nephrons are the functional units of the kidney. As 8. Progression to Systemic Complications
individual nephrons are damaged or destroyed: ➢ As kidney function declines:
▪ Compensatory hyperfiltration occurs in the ✓ Cardiovascular Disease: Accelerated by
remaining nephrons to maintain overall kidney hypertension, anemia, and uremic toxins.
function. ✓ Bone and Mineral Disorders (CKD-MBD):Parathyroid
▪ This hyperfiltration leads to glomerular hormone (PTH) levels increase (secondary
hypertension and further structural damage, hyperparathyroidism) in response to low calcium
creating a vicious cycle. and high phosphate, leading to bone resorption.
 ✓ Anemia: Reduced erythropoietin production leads Additional Diagnostics
to decreased red blood cell formation. ✓ Kidney Biopsy:
✓ Uremia: Accumulation of nitrogenous waste ▪ Performed if glomerular diseases or other specific
products causes systemic toxicity. causes are suspected.
End-Stage Kidney Disease (ESKD) ▪ Helps confirm diagnosis and guide treatment.
✓ In the final stages, the kidneys are no longer able to ✓ Autoimmune and Infectious Disease Testing:
maintain homeostasis. ▪ ANCA, ANA, complement levels, and tests for
✓ Patients require renal replacement therapy (dialysis or infections like hepatitis B/C or HIV if autoimmune or
transplantation) to survive. infectious causes are suspected.
DIAGNOSTICS ✓ Genetic Testing:
Kidney Function Assessment ▪ For hereditary kidney diseases like polycystic kidney
✓ Estimated Glomerular Filtration Rate (eGFR): disease.
▪ Calculated using serum creatinine and factors like Criteria for CKD Diagnosis
age, sex, and race. - CKD is diagnosed if one or more markers of kidney damage or
▪ Persistent eGFR <60 mL/min/1.73 m² for ≥3 months reduced kidney function (eGFR <60 mL/min/1.73 m²) persist
indicates CKD. for ≥3 months, including:
✓ Cystatin C (optional): ✓ Albuminuria (UACR ≥30 mg/g).
▪ May be used to confirm eGFR in certain cases, ✓ Abnormal urine sediment (e.g., casts).
especially when creatinine is influenced by muscle ✓ Structural abnormalities (e.g., small kidneys, cysts).
mass. ✓ History of kidney transplantation.
Markers of Kidney Damage NURSING RESPONSIBILITIES:
▪ Urine Albumin-to-Creatinine Ratio (UACR): 1. Monitoring and Assessment
✓ Measures albuminuria, a sign of kidney damage. ❑ Vital Signs:
✓ Normal: <30 mg/g; Microalbuminuria: 30–300 mg/g; ✓ Monitor blood pressure to detect hypertension,
Macroalbuminuria: >300 mg/g. which accelerates CKD progression.
▪ Protein-to-Creatinine Ratio (PCR): ✓ Observe for signs of fluid overload (e.g., increased
✓ Alternative to UACR for detecting proteinuria. heart rate, elevated blood pressure).
▪ Urine Dipstick Test: ❑ Renal Function:
✓ A quick screen for albumin or blood in the urine. ✓ Regularly check laboratory results (e.g., serum
▪ Urine Sediment Analysis: creatinine, eGFR, UACR, electrolytes).
✓ Identifies red blood cell casts, white blood cell ✓ Monitor urine output and characteristics.
casts, or other abnormalities. ❑ Fluid Balance:
Imaging Studies ✓ Track daily weights and input/output for signs of
▪ Renal Ultrasound: fluid retention or dehydration.
✓ Detects structural abnormalities (e.g., small ✓ Look for edema, particularly in the legs, feet, and
kidneys, cysts, hydronephrosis). around the eyes.
✓ Assesses kidney size, symmetry, and cortical ❑ Signs of Complications:
thickness. ✓ Monitor for anemia (fatigue, pallor), hyperkalemia
▪ CT or MRI: (muscle weakness, arrhythmias), and uremic
✓ For further evaluation of masses, obstructions, or symptoms (nausea, confusion, pruritus).
vascular abnormalities if ultrasound findings are 2. Medication Management
inconclusive. ❑ Administer Medications:
Blood Tests ✓ Antihypertensives (e.g., ACE inhibitors, ARBs).
✓ Serum Creatinine: Used to calculate eGFR. ✓ Diuretics for fluid overload.
✓ Blood Urea Nitrogen (BUN): Indicates kidney function ✓ Phosphate binders, vitamin D analogs, and
but less specific than eGFR. erythropoiesis-stimulating agents as prescribed.
✓ Electrolytes and Acid-Base Balance: Check for ❑ Monitor for Adverse Effects:
hyperkalemia, metabolic acidosis, and other ✓ Be vigilant for medication toxicity, as CKD patients
imbalances. are at higher risk due to impaired drug clearance.
✓ Complete Blood Count (CBC): Detects anemia, which ❑ Educate on Medication Compliance:
is common in CKD. ✓ Ensure patients understand the purpose, timing,
✓ Calcium, Phosphorus, and Parathyroid Hormone and potential side effects of their medications.
(PTH): Assess mineral and bone disorders associated 3. Patient Education
with CKD. ❑ Dietary Modifications:
✓ Low-sodium, low-potassium, and low-phosphorus
diets as per dietitian recommendations.
 ✓ Adequate but controlled protein intake to reduce • Neurologic effects (cerebral edema) due to
kidney workload. hypernatremia
❑ Fluid Restriction: • Anemia
✓ Educate on limiting fluids if prescribed to avoid fluid • Bone diseases
overload. MODALITIES OF RENAL REPLACEMENT THERAPY (RRT)
❑ Lifestyle Changes: - are treatment modalities that take over or replace the
✓ Encourage smoking cessation, physical activity, and function of the damaged kidney
weight management. When should RRTs be considered:
❑ Symptoms to Report: ✓ When the serum BUN and creatinine levels can’t be
decreased
✓ Educate patients on recognizing signs of worsening
✓ FVE is compromising the heart and the lungs
CKD (e.g., reduced urine output, swelling, severe ✓ Hyperkalemia and metabolic acidosis can’t be treated
fatigue). successfully
4. Emotional and Psychological Support TYPES OF RRTs
❑ Counseling: A. HEMODIALYSIS
✓ Provide emotional support for dealing with a chronic B. CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT)
illness. C. PERITONEAL DIALYSIS
✓ Refer to social workers or counselors for assistance A. HEMODIALYSIS
with coping mechanisms and financial challenges. - The machine acts like the kidney (also known as the
❑ Support Groups: dialyzer)
✓ Encourage participation in CKD support groups to - It does not cure renal disease nor does not compensate
connect with others facing similar challenges. with the loss of endocrine or metabolic functions of the
Prevention of Complications kidneys.
❑ Infection Control: - It is done 3-4 times per week.
✓ Emphasize hygiene and vaccination (e.g., influenza, ✓ Remind the patient to watch what he eats or
hepatitis B) to prevent infections. drinks in-between treatments.
❑ Fall Risk Reduction: - As the blood is cycled through the machine, he will
✓ CKD-associated bone disorders can increase receive heparin to prevent blood clots from forming.
fracture risk; take precautions to prevent falls. - Prior to starting each hemodialysis session, assess the
❑ Skin Care: patient’s fluid status
✓ Address uremic pruritus by using emollients and - During hemodialysis, the blood pressure, vital signs and
advising against scratching. electrolytes are watched carefully.
6. Collaboration and Referrals - Can all patients tolerate hemodialysis?
❑ Work with a Multidisciplinary Team: ✓ NO! Patients with unstable CV status cannot
✓ Coordinate care with nephrologists, dietitians, and tolerate hemodialysis and may be
social workers. contraindicated for them.
❑ Refer to Dialysis or Transplant Services: - Around 300 to 800ml of blood is drawn and reintroduce
✓ Prepare patients for renal replacement therapy (cycle) per minute.
when CKD progresses to end-stage renal disease Vascular access
(ESRD). - A method or device used to remove blood and to
7. End-of-Life Care (If Needed) reintroduce filtered blood to the patient’s body.
✓ For patients with advanced CKD opting for - A site where access to a large blood vessel because rapid
conservative management, provide palliative care blood flow is essential for hemodialysis.
focusing on symptom control and quality of life. Types of vascular access:
Key Priorities: 1. Arteriovenous fistula (AVF)
✓ Prevent progression and manage complications. - A fistula or anastomosis
✓ Empower patients with knowledge for self-management. (communication) is
✓ Provide holistic care addressing physical, emotional, created between a large
and social needs. vein and artery, usually in
✓ Nurses play a vital role in CKD management by the forearm is created.
combining clinical skills, patient education, and - The arterial end is where
compassionate care. the blood is drawn from the body to the hemodialysis
COMPLICATIONS machine and the venous end is where the filtered blood
• Hyperkalemia which may lead to life-threatening cardiac is reintroduced to the body.
arrhythmias if not corrected
• Pericarditis, pericardial effusion and cardiac tamponade
• Hypertension
2. Arteriovenous graft (AVG) - No more than 800ml of blood is drawn out of the body at
- A biologic, semi- one time and is filtered, thereby, there is no significant
synthetic or synthetic stress to the cardiovascular system.
graft is used to join an - CRRT is the method of choice for those clients with
artery and the vein. fragile cardiovascular status and with those with AKI.
- This is usually done for patient’s whose vessels are not Types:
suitable for AVF, like for those with diabetes. ✓ Continuous Venovenous Hemofiltration (CVVH)
3. Central vascular access device ✓ Continuous Venovenous Hemodialysis (CVVHD)
- Are centrally-inserted ✓ Continuous Venovenous Hemodiafiltration (CVVHDF)
vascular access device, Advantages:
made up of double-lumen ✓ Gentle on unstable patients.
catheter. ✓ Allows for precise fluid balance management.
- Usually inserted into the Disadvantages:
subclavian, internal jugular or femoral veins. ✓ Requires specialized equipment and expertise.
- These devices are usually used for long-term use. ✓ Resource-intensive.
CARING FOR THE VASCULAR ACCESS (AVF and AVG) C. PERITONEAL DIALYSIS
1. Do not use for any access, such as for drawing blood or - The peritoneum is utilized as the filtering membrane
administering medications - A dialysate usually made up of fluid with high dextrose
2. Do not use the arm for taking blood pressure, needle sticks. (or sorbitol) solutions
3. Ensure that no pressure or constriction is applied to the arm - The dialysate is infused to the peritoneal cavity through
with the access. an access device (e.g Tenckhoff catheter)
ASSESSING THE PATENCY OF THE VASCULAR ACCESS - Usual dialysate volume is from 1000ml to 3000ml.
1. Palpate for thrill (cat-purring sensation - It take about 10 minutes for the dialysate to infuse into
2. Auscultate for the bruit (a sound produced from turbulent the peritoneal cavity and remains there for a prescribed
blood flow) amount of time known as the dwell time.
You feel the THRILL and hear the BRUIT - The dialysate bag is then lowered and allowed to drain.
COMPLICATIONS OF HEMODIALYSIS The drainage is now called as the effluent.
1. Elevated triglycerides - Exchange is the entire process of infusing and draining
2. CV complications like CHF, angina, peripheral vascular the dialysate.
insufficiency - The effluent should be clear or straw-colored. Any signs
3. Curling’s ulcer of cloudiness may mean an infection. Bloody streaks
4. Sleep disturbances may mean trauma or any other bleeding in the peritoneal
5. Hypotension cavity. This should alert the patient to call his physician.
6. Muscle cramps due to rapid shifts of electrolytes and fluids - The dialysate should be infused in body temperature.
7. Dysrhythmias Cold dialysate causes vasoconstriction and may restrict
8. Air embolism the blood flow in the peritoneal cavity affecting the
9. Dialysis disequilibrium effectiveness of the dialysis.
a. Shifting of fluids in the brain - Peritoneal dialysis may be used for people who cannot
b. Signs and symptoms: tolerate hemodialysis or someone who chooses this
i. Headache method.
ii. Nausea & Vomiting APPROACHES OF PERITONEAL DIALYSIS
iii. Restlessness 1. Continuous Ambulatory PD (CAPD)
iv. Altered LOC - The patient must have the energy and the desire to be
v. Seizures active in their treatment and also has the ability to learn
Advantages: and follow instruction.
✓ Efficient removal of waste products and toxins. - Usually done 4 times a day, every day.
✓ Regular monitoring by healthcare professionals (in- - Patients with vertebral disc disease or arthritis cannot
center). tolerate this approach as this causes pressure in the
Disadvantages: back.
✓ Requires vascular access (e.g., arteriovenous fistula, - Also, patients with colostomy is a contraindication of
graft, or catheter). this approach as this increases the risk for infection.
✓ Time-intensive (3–5 hours per session, 2–3 times a 2. Automated PD or Continuous Cyclic PD
week). - The PD catheter is usually connected to a cycler
B. CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT) machine usually at night and the exchanges is done
- Typically done in ICU setting and the dialysis is automatically while the patient is asleep.
continuous thus no drastic fluid shifts may occur.
 - The patient usually receives 3 to 5 exchanges during the o Assess for thrill and bruit at least every 8 hours.
night. Absence may mean that the
- A fresh dialysate is infused to the abdomen in the ✓ access is blocked.
morning and the catheter is disconnected from the ✓ Do not use the arm with the access for any procedure
cycler. The dialysate remains in the abdomen until the ✓ Observe for any signs of infection.
catheter is reattached to the cycler at night. Precaution on IV therapy
- The patient has more freedom. ✓ Regulate fluids STRICTLY. Infuse IV fluids using
Advantages: volumetric infusion pumps.
✓ Can be done at home, offering greater flexibility. ✓ Accurate I ad O.
✓ Avoids vascular access. ✓ Watch out for signs and symptoms of FVE.
Disadvantages: Monitoring symptoms of uremia
✓ Risk of peritonitis (infection). Assess cardiac and pulmonary functions
✓ May not be suitable for patients with abdominal issues ✓ Assess CV status by checking apical and peripheral
COMPLICATIONS OF PD pulses.
1. Exit site infection ✓ Look for pulsus paradoxus (a decrease in the blood
- Infection of the catheter site insertion pressure more than 10mmHg during inspiration.
2. Peritonitis ✓ Listen for murmurs, pleuritic friction rub or
- Major complication of PD muffled/distant heart sounds
3. Impaired body image ✓ Look for any ECG changes
- Infusion of fluids in the abdomen ✓ Assess lung sounds and oxygen saturation as well as
- Devices like the catheter and bags attached. respiratory effort.
4. Depression Controlling electrolyte levels and diet
- This may be due to: Managing pain and discomfort
• Unpredictability of the disease ✓ Uremic pruritus may be managed through:
• The overwhelming responsibility of self-care o Meticulous skin care
• Financial difficulties ▪ Application of emollients or
• Psychosocial and sexual impact of the disease moisturizers to reduce itching
and treatment ▪ Avoid applying anything near or at the
5. Sexual problems vascular access site.
CARING FOR THE PERSON WITH PD o Antihistamines (usually given in low doses)
ADDRESSING PSYCHOSOCIAL NEEDS Monitor blood pressure
✓ Arrange meeting with persons with PD who were able to Prevent infection
adapt well. ✓ Strict aseptic technique in caring and cleaning the
✓ Open opportunity for patient to raise concerns regarding vascular access
body image and sexuality. Cautious administration of medications
✓ Referral to counselor and/or sex therapist ✓ Check if the medication contains any potassium or
ADDRESSING SELF-CARE NEEDS magnesium
✓ Assess the ability of the patient and his family to learn ✓ Check if the drug dosage is adjusted to compensate with
and perform PD care. the renal condition.
✓ Teaching the patient and training him as well as his family ✓ Teach patient to avoid taking OTC drugs or herbal
members on peritoneal dialysis procedure and caring for supplements without consulting the physician.
the patient and the device in a comfortable and non- Providing emotional support
overwhelming approach. ✓ Referral of the patient and the family to support groups
✓ Teach and encourage the patient to increase fiber and ✓ Referral to counselor or spiritual adviser
protein in the diet, avoid high-carbohydrate containing ✓ Referral to mental health personnel
foods. ✓ Referral to social services
✓ No sodium, potassium and fluid restrictions. KIDNEY TRANSPLANTATION
CONTINUING CARE - It involves the transplanting a healthy kidney from a living
✓ Provide hotline of the hospital’s outpatient and donor or a deceased donor to a recipient with ESRD.
community health department. - A permanent type of RRT.
✓ Referral to home health nurse. Successful kidney transplant:
✓ For elderly clients with ESRD, suggest for transfer to a ✓ Comes from a living donor related to the recipient, with
long-term, skilled nursing facility may help. compatible ABO typing and HLA.
CARING FOR THE HOSPITALIZED PATIENT ON DIALYSIS Pre-operative management:
Protecting the vascular access ✓ Complete physical examination
✓ Assess the vascular access for patency.
 o Detect and treat any conditions that may cause • Post-operative nursing care
complications ✓ Perform baseline assessment for all post-operative
✓ Tissue typing, blood typing and antibody screening clients (VS, LOC, status of dressing)
o Check the compatibility of the donor and ✓ Encourage frequent position changes, coughing and
recipient’s tissue. deep breathing, early ambulation if appropriate.
✓ Urinary exams ✓ Use special infection control measures:
o Assess bladder neck function and detect o Strict aseptic technique when changing
ureteral reflux dressing or performing catheter care.
✓ Check for any presence of infection o Limit contact with staff and visitors.
✓ Administration of immunosuppressant drugs. o Wear surgical mask when entering the client’s
✓ Psychosocial evaluation room.
Pre-operative nursing care o Monitor WBC count and notify MD of significant
✓ Help reduce anxiety by teaching about the procedure drop or increase.
and post-operative course and care. ✓ Observe signs of tissue or organ rejection
✓ Encourage the patient to express feelings and ask o Fever
questions. o Tenderness
✓ Assess support systems and ability to care for self after o Swelling of the surgical site
surgery and follow medical regime. o Increase in WBC
✓ Instruct client that rejection of donated organ is the o Decreased UO with increasing proteinuria
major obstacle in transplantation o Sudden weight gain.
✓ Reassure the patient that rejection usually isn’t life- o HTN
threatening and the client can resume dialysis if needed. o Elevation of BUN and creatinine
✓ Begin administering immunosuppressant drugs. Discuss ✓ Provide analgesic medications as needed, pain should
the purpose and possible adverse effects with client. decrease after 24 hours
Monitor for increased BP and signs of anaphylaxis. ✓ Monitor UO closely.
✓ Plan for client to undergo dialysis the day before surgery o Report UO of less than 100ml/h
(may not be needed, if warranted), cleansing enema and o A decrease in urine may indicate thrombus
many laboratory tests. formation at the renal artery anastomosis site.
• Post-operative medical management o Expect blood-tinged urine for several days; may
✓ Administration of a combination of immunosuppressing irrigate the catheter as ordered using strict
drugs. aseptic technique.
• Examples: o For living donor transplant, urine flow should
▪ Steroids begin immediately after revascularization and
▪ Cyclophosphamide reperfusion of the donated kidney.
▪ Cyclosporine o For cadaver donor transplant: expect anuria for
▪ Azathioprine 2 days to 2 weeks. The client may need dialysis
▪ Tacrolimus during this time.
▪ Sirolimus ✓ Monitor daily renal function tests:
▪ Mycophenolate o Serum creatinine
▪ methotrexate o 24-hour creatinine clearance
✓ Assess for any signs of adverse effects of these drugs o BUN
such as nephrotoxicity, cardiotoxicity, hepatotoxicity. o Urine creatinine
myelotoxicity or neurotoxicity; infections and cancers. o Urine pH, protein and specific gravity
✓ Assess the adequacy of immunosuppression, watch-out o Serum electrolytes
for any signs and symptoms of organ rejection. ✓ Monitor cardiac function
✓ Assess the function of the newly-transplanted kidney. ✓ Weigh patient daily
• Diminishing signs and symptoms of ESRD will o Home care for the post-kidney transplant client
be observed. ✓ Carefully measure I and O. notify MD if UO falls below
✓ Doses of immunosuppressive drugs are gradually 600ml for any 24-hour period.
tapered off over a period of several weeks depending on ✓ Instruct patient how to collect 24-urine samples.
the immunologic response. However, the patient is ✓ Advise patient to weigh self at least twice a week.
required to take some form of immunosuppressive ✓ Drink at least 1 to 2 liters of fluid daily unless advised
therapy the entire time that he or she has the otherwise.
transplanted kidney. ✓ Report signs of rejection:
o Redness
o Warmth
 o tenderness or swelling over the kidney Factors Influencing Modality Selection
o fever ✓ Patient's Clinical Status: Hemodynamic stability,
o decreased UO and elevated BP (obtain and use underlying conditions.
home BP measuring device) ✓ Lifestyle: Preference for home-based vs. in-center
✓ Avoid crowds and persons with known infections for 3 therapy.
months after surgery. ✓ Availability: Access to resources, trained professionals,
✓ Practice regular, moderate exercise but avoid heavy and facilities.
lifting or contact sports for at least 3 months. ✓ Urgency: Need for immediate versus planned therapy
✓ Use shoulder but not lap-style seatbelts. MANAGING THE PATIENT WITH BURN INJURY
✓ Wait at least 6 weeks before engaging in sexual activity. BURN INJURY
✓ Advised patient not to abruptly stop immunosuppressive - occur when the skin or underlying tissues are damaged
therapy. by heat, chemicals, electricity, radiation, or friction.
✓ Advised patient to avoid OTC drugs or herbal TYPES OF BURNS
supplements without consulting the physician first. 1. First-degree burns (Superficial burns)
➢ Affect only the outer layer of skin (epidermis).
➢ Symptoms: Redness, mild swelling, and pain (e.g.,
sunburn).
➢ Treatment: Cool water, aloe vera, over-the-counter pain
relief.
2. Second-degree burns (Partial-thickness burns)
➢ Affect the epidermis and part of the dermis (the second
layer of skin).
➢ Symptoms: Red or blotchy skin, blisters, severe pain,
and swelling.
➢ Treatment: Cool the area, apply a sterile bandage, and
avoid breaking blisters. Seek medical attention if the
burn is large or infected.
RENAL TRANSPLANT REJECTION 3. Third-degree burns (Full-thickness burns)
➢ Affect all skin layers and may reach underlying tissues
like fat, muscle, or bone.
➢ Symptoms: White, charred, or leathery skin; little pain
initially due to nerve damage.
➢ Treatment: Requires immediate medical attention. May
involve surgery, skin grafts, and long-term care.
4. Fourth-degree burns
➢ Extend through all skin layers, affecting muscles,
tendons, and bones.
➢ Symptoms: Severe damage, often life-threatening.
➢ Treatment: Emergency medical intervention.
TYPES OF BURNS BY CAUSE:
❖ Thermal burns: Caused by heat sources (flames, hot liquids, or
Advantages:
steam).
✓ Restores full kidney function.
❖ Chemical burns: Result from contact with acids, alkalis, or
✓ Freedom from dialysis for many years.
corrosive substances
Disadvantages:
❖ Electrical burns: Due to electric current passing through the
✓ Requires immunosuppressive medications for life.
body.
✓ Risk of rejection or infection.
❖ Radiation burns: From exposure to radiation (e.g., sunburn,
▪ Indications: Advanced CKD or end-stage renal disease
radiation therapy).
(ESRD).
❖ Friction burns: From skin rubbing against rough surfaces.
5. Other Modalities
BURN INJURIES ACCORDING TO BODY SURFACE AREA
✓ Intermittent Hemodialysis (IHD): Traditional dialysis
➢ The following methods are used in estimating the total
used in stable patients but also applicable to some AKI
body surface area (TSBA)
cases.
1. RULE OF NINES (FOR ADULTS)
✓ Sustained Low-Efficiency Dialysis (SLED): A hybrid
➢ a simple method for quickly estimating TBSA affected by
between IHD and CRRT, useful in critically ill patients
burns.
who cannot tolerate rapid fluid shifts.
 ➢ The body is divided into regions, each accounting for How It Works
approximately 9% (or multiples of 9%) of the total ✓ Assess the burn areas by visual inspection or using
surface area: a burn assessment chart.
✓ Head and Neck: 9% ✓ Identify the affected regions.
✓ Each Arm (front and back): 9% (4.5% per side) ✓ Assign percentages for each region based on the
✓ Each Leg (front and back): 18% (9% per side) patient’s age.
✓ Front of the Torso: 18% ✓ Sum up the percentages to estimate the total TBSA
✓ Back of the Torso: 18% burned.
✓ Perineum: 1% Advantages
✓ Provides greater accuracy compared to the Rule of
Nines.
✓ Especially useful in pediatric patients where body
proportions differ significantly.
3. PALM METHOD
➢ is a framework used for assessing the severity of burns,
particularly when determining the percentage of total
body surface area (TBSA) affected
➢ It is a simplified and effective approach to classify burns
and guide treatment
PALM stands for:
P: Palmar Surface
✓ The patient's palm, including the fingers, is used as a
reference for estimating burn size.
2. LUND AND BROWDER METHOD ✓ The palm (excluding the fingers) accounts for
➢ is a more precise technique for estimating the Total Body approximately 1% of the TBSA
Surface Area (TBSA) affected by burns, especially in A: Area Calculation
children and infants. ✓ The affected area of the burn is measured using the palm
➢ It accounts for variations in body proportions based on as a unit.
age, unlike the simpler Rule of Nines. ✓ The clinician compares the burned area to the size of the
Key Features: patient's palm to estimate how much of the body is
a. Age-Specific Adjustments: involved.
✓ Infants have proportionally larger heads and smaller legs L: Localization
compared to adults. ✓ Identify and record the specific areas of the body
✓ The percentage allocation for each body part changes affected by the burns.
with age to reflect these differences. ✓ Consider anatomical regions for proper documentation
b. Detailed Mapping: and assessment.
✓ The body is divided into specific areas, and each area is M: Management
assigned a percentage. ▪ Once the TBSA is calculated, determine the appropriate
✓ Partial areas (e.g., a portion of a limb) can be calculated treatment:
to the nearest fraction. ✓ <10% TBSA (minor burns): Outpatient care, wound
PERCENTAGE DISTRIBUTION BY AGE cleaning, dressing, and pain management.
✓ 10-20% TBSA (moderate burns): Potential
Body Part Infant (%) Child (%) Adult (%) hospitalization for fluids and monitoring.
✓ >20% TBSA (severe burns): Immediate resuscitation,
Head and Neck 18 12 9 fluid management, and specialized burn care.
Advantages of the PALM Method:
Each Arm 9 9 9 ✓ Quick and easy: Useful in emergency settings to rapidly
estimate burn extent.
Front Torso 18 18 18 ✓ Accessible: No special tools are required—reliable in
low-resource settings.
Back Torso 18 18 18 ✓ Effective in triage: Helps prioritize care based on burn
severity.
✓ complements other burn assessment tools like the Rule
Each Leg 14 16.5 18
of Nines and the Lund-Browder chart but is particularly
beneficial for smaller burns or when precision tools are
Perineum 1 1 1
unavailable.
 PATHOPHYSIOLOGY Renal and Gastrointestinal Effects
1. LOCAL RESPONSE ➢ Hypoperfusion can lead to:
➢ Burns damage the skin and underlying tissues, leading to • Acute kidney injury (AKI).
the following: • Stress ulcers or ileus in the gastrointestinal
a. Zone of Injury (Jackson's Burn Model) tract.
❖ Zone of Coagulation: KEY PHASES OF BURN INJURY
• Central area with the most severe damage. 1. Emergent Phase (0-48 hours):
• Irreversible tissue necrosis due to direct heat or ✓ Hypovolemia and fluid shifts dominate.
chemical destruction. ✓ Priorities: Fluid resuscitation, airway management, and
❖ Zone of Stasis: pain control.
• Surrounding the coagulation zone. 2. Acute Phase (48-72 hours):
• Tissue is ischemic due to reduced perfusion. This ➢ Diuresis begins as fluids stabilize.
area is salvageable with proper treatment. ➢ Wound care and infection prevention are key.
❖ Zone of Hyperemia: 3. Rehabilitation Phase:
• Outermost area with increased blood flow and ➢ Focuses on healing, physical therapy, and scar
minimal damage. management.
• Usually recovers fully without intervention. ASSESSMENT and DIAGNOSTICS
2. INFLAMMATORY RESPONSE 1. PRIMARY ASSESSMENT (ABCDE APPROACH)
➢ Release of pro-inflammatory mediators (e.g., histamine, A: Airway and C-Spine Stabilization
prostaglandins, cytokines) leads to: ✓ Check for airway obstruction, inhalation injury, or facial
Vasodilation: burns.
• Increased blood flow to the area. ✓ Look for soot in the mouth or nose, singed nasal hairs, or
• Increased capillary permeability: Plasma and proteins hoarseness.
leak into interstitial spaces, causing edema. ✓ Consider intubation for signs of impending airway
C. Tissue Repair and Scar Formation compromise.
➢ Burn depth determines healing: B: Breathing
▪ Superficial burns: Heal via epithelial regeneration. ✓ Assess respiratory effort, rate, and oxygen saturation.
▪ Deeper burns: May require grafting or heal with scar ✓ Look for signs of smoke inhalation or chest wall
tissue. restriction (circumferential burns).
2. SYSTEMIC RESPONSE C: Circulation
➢ When burns exceed 20-30% of total body surface area ✓ Monitor vital signs (blood pressure, heart rate, capillary
(TBSA), systemic effects occur due to the massive refill).
release of inflammatory mediators into the circulation. ✓ Establish large-bore IV access for fluid resuscitation.
Hypovolemic Shock (Burn Shock) ✓ Evaluate for signs of hypovolemic shock (cool, clammy
➢ Loss of fluids and proteins from damaged vessels leads skin, tachycardia).
to: D: Disability
• Decreased blood volume. ✓ Assess neurological status using the Glasgow Coma
• Hypotension and reduced cardiac output. Scale (GCS).
• Organ hypoperfusion. ✓ Rule out associated traumatic injuries or hypoxia-related
Metabolic Response mental status changes.
➢ Burns cause a hypermetabolic state: E: Exposure
• Increased energy demands. ✓ Fully expose the patient to evaluate the burn.
• Protein catabolism, muscle wasting. ✓ Prevent hypothermia by covering the patient with warm
• Elevated core temperature. blankets.
Immune Dysfunction 2. SECONDARY ASSESSMENT
➢ Burn injury impairs both innate and adaptive immune ➢ A detailed evaluation follows stabilization.
responses: Burn History
• Increased susceptibility to infections. ✓ Mechanism of injury: Thermal, chemical, electrical, or
• Risk of sepsis in severe burns. radiation.
Respiratory Dysfunction ✓ Time of injury.
➢ Inhalation injury can cause: ✓ Exposure to enclosed space (suggests inhalation injury).
• Airway edema and obstruction. ✓ Pre-existing medical conditions (e.g., diabetes, heart
• Smoke or chemical inhalation damage to the disease).
lungs (acute respiratory distress syndrome,
ARDS).
 Burn Depth ✓ Cover the burn with a clean, non-stick material (e.g.,
✓ Superficial (1st degree): Red, dry, painful. sterile dressing or plastic wrap) to protect from
✓ Partial-thickness (2nd degree): Red or blistered, moist, contamination.
very painful. c. Pain Management
✓ Full-thickness (3rd degree): White, leathery, painless. ✓ Administer analgesics like paracetamol or ibuprofen.
✓ 4th degree: Extends into muscles, tendons, or bones. 2. EMERGENCY DEPARTMENT CARE (ACUTE PHASE)
Burn Size a. Resuscitation
➢ Estimate total body surface area (TBSA) using: ▪ Fluid Replacement (Parkland Formula):
✓ Rule of Nines: Divides body into regions with ✓ For burns >20% TBSA: Lactated Ringer's solution is
percentages (e.g., 9% for each arm). commonly used.
✓ Lund-Browder Chart: More accurate for children. ✓ Formula: 4 mL x body weight (kg) x %TBSA burned (half in
✓ Palmar Method: Patient’s palm equals 1% TBSA. the first 8 hours, the rest over the next 16 hours).
Associated Injuries ✓ Monitor urine output (target: 0.5-1 mL/kg/hr in adults; 1
➢ Look for fractures, head trauma, or other injuries from mL/kg/hr in children).
explosions or falls. b. Airway Management
DIAGNOSTICS ✓ Intubate early for inhalation injuries or significant facial
➢ Diagnostics help identify complications and guide burns.
management. ✓ Administer 100% oxygen in cases of suspected carbon
Blood Tests monoxide poisoning.
✓ Complete blood count (CBC): To detect anemia or c. Pain Control
infection. ✓ Administer opioids (e.g., morphine, fentanyl) for severe
✓ Electrolytes: Monitor for hyperkalemia, hypokalemia, or pain.
hyponatremia. ✓ Consider non-opioid adjuncts as needed.d.
✓ Blood urea nitrogen (BUN) and creatinine: Assess renal ✓ Prevent Hypothermia
function. ✓ Cover the patient with warm blankets.
✓ Carboxyhemoglobin levels: Detect carbon monoxide ✓ Use warmed IV fluids.
poisoning. 3. WOUND CARE
✓ Arterial blood gases (ABGs): Evaluate oxygenation and a. Cleansing
acid-base status. ✓ Clean wounds with sterile saline or mild antiseptic
Imaging solutions.
✓ Chest X-ray: Check for inhalation injury or pulmonary ✓ Debride loose, dead, or contaminated tissue.
edema. b. Dressing
✓ CT scan: Rule out associated trauma or deep tissue ✓ Apply non-adherent, antimicrobial dressings (e.g., silver
involvement. sulfadiazine or hydrocolloid).
✓ Bronchoscopy: Direct visualization of airway damage in ✓ Change dressings daily or as needed to prevent infection
suspected inhalation injury. and promote healing.
Special Tests c. Blisters
✓ Electrocardiogram (ECG): For electrical burns to detect ✓ Small, intact blisters may be left undisturbed.
arrhythmias. ✓ Large or ruptured blisters should be drained or debrided.
✓ Urinalysis: Look for myoglobinuria in electrical burns, 4. INFECTION PREVENTION
which indicates muscle damage. ✓ Administer tetanus prophylaxis.
✓ Wound cultures: Assess for infections in cases of ✓ Use systemic antibiotics only for confirmed infections
delayed healing or signs of sepsis. (not prophylactically).
1. PRE-HOSPITAL CARE 5. NUTRITION
a. Remove the Source of Injury ✓ Initiate early enteral feeding for burns >20% TBSA.
✓ Stop the burning process by removing the patient from ✓ Provide high-protein, high-calorie nutrition to meet the
the heat source. hypermetabolic demand.
✓ Cool the burn with clean, lukewarm water (not ice) for 6. SPECIAL CONSIDERATIONS
10-20 minutes to reduce thermal injury. a. Inhalation Injuries
✓ Remove tight clothing, jewelry, or debris near the burn ✓ Bronchodilators for bronchospasm.
site. ✓ Frequent airway suctioning.
b. Protect the Airway and Stabilize ✓ Possible mechanical ventilation.
✓ Prioritize airway management, especially for inhalation b. Electrical Burns
injuries. ✓ Monitor for arrhythmias and rhabdomyolysis (check
serum potassium and myoglobin levels).
✓ Ensure adequate hydration to prevent renal damage.
c. Chemical Burns
✓ Irrigate with copious amounts of water or saline for 20-
30 minutes.
✓ Neutralize if the chemical agent is known (e.g., weak
acids or bases).
d. Circumferential Burns
✓ Monitor for compartment syndrome.
✓ Perform an escharotomy if needed.
7. REHABILITATION PHASE
a. Physical Therapy
✓ Early mobilization to prevent contractures and maintain
function.
✓ Splinting and range-of-motion exercises.
b. Scar Management
✓ Use pressure garments to minimize hypertrophic
scarring.
✓ Silicone sheets or gels may help reduce scarring.
c. Psychological Support
✓ Address anxiety, depression, or PTSD.
✓ Provide counseling and support groups.
8. CRITERIA FOR BURN CENTER REFERRAL
✓ Burns >10% TBSA (partial-thickness or deeper).
✓ Burns involving critical areas (face, hands, feet, genitals,
perineum).
✓ Electrical or chemical burns. Inhalation injuries.
✓ Burns in children or patients with significant
comorbidities.
9. FOLLOW-UP CARE
✓ Monitor wound healing and graft integration if
applicable.
✓ Treat secondary complications like infections or
contractures.
✓ Regularly assess nutrition and psychological well-being.