Body Surface Area (BSA)
In children, BSA is larger and allows for greater fluid loss through the skin.
GI tract is proportionally longer allowing greater fluid loss
Metabolic rate
higher and has greater metabolic waste and heat production
Kidney function
Kidneys are functionally immature
Unable to concentrate or dilute urine, conserve or secrete Na, can't acidify urine
Water balance in infants and children
Greater Need for Water
More vulnerable to alterations in fluid and electrolyte balance
Disturbances occur more frequently and more rapidly
Children adjust less rapidly to changes
ECF makes up more than half or the total Body Weight at birth
Greater content of extracellular Na and Cl
60% fluid is lost from the ECF
40% fluid lost from the ICF
Infants ingest and excrete greater amount of fluid per Kg than do older children
Infant has limited ability to conserve and has little fluid volume reserve.
Increased fluid requirements:
Fever
Vomiting and diarrhea
High - output renal failure
Diabetes Insipidus
Diabetic ketoacidosis
Burns
Shock
Tachypnea
Radiant warmer (preterm infants)
Phototherapy (infants)
Postoperative bowel surgery
Decreased fluid requirements:
Congestive heart failure
SIADH
Mechanical ventilation
Postoperative requirements
Oliguric renal failure
Increased intracranial pressure
Mechanisms of edema formation
Increased venous pressure
Capillary permeability
Diminished plasma proteins
Lymphatic obstruction
Tissue tension
Isotonic dehydration
Electrolyte and water deficits are balanced (H2O loss = NaCl loss)
Na is within normal limits = 130 - 150 mEq/L
Primary form of dehydration seen in children
Major losses from the ECF = decreased plasma volume and affects skin, muscles and kidneys
No osmotic force present to cause a redistribution of water between the ICF and ECF
Shock is the greatest threat to life in isotonic dehydration with symptoms of hypovolemic shock
Hypotonic dehydration
Electrolyte loss exceeds water loss
Serum Na <130 mEq/L
ICF more concentrated than ECF. Fluid shifts from ECF to ICF. Increases ECF volume loss
Results in shock
The Physical signs are more severe with smaller fluid loss than with isotonic or hypertonic dehydration
Hypertonic dehydration
Water loss greater than electrolyte loss
Serum Na > 150 mEq/L
Most dangerous type of dehydration for children
Fluid shifts from ICF to ECF
Rapid fluid replacement is contraindicated due to risk of water intoxication and cerebral edema
Seizures can occur, can result in permanent damage
Shock is not usually seen with hypertonic dehydration
Symptoms of Dehydration
Variable temperature
Irritable
Dry skin / mucous membranes
Lethargic
Poor skin turgor
Altered LOC
Poor perfusion
Wt. Loss
Fatigue
Decreased Urine output
Sunken fontanels
Cool mottled extremities
Prolonged cap refill
Degree of dehydration
Mild - <50 ml/kg (5%)
Moderate - 50 - 90 ml/kg (10%)
Severe - > 100ml/kg (15%)
Earliest sign of dehydration
Tachycardia
The presence of two or more of these factors are good predictors of > %% dehydration
Capillary refill greater than 2 seconds
Absence of tears
Dry mucous membranes
Ill general appearance
Decreased urinary output
The best three individual examination signs for assessing dehydration:
Prolonged capillary refill time (> 2 sec )
Abnormal skin turgor
Abnormal respiratory pattern
Treatment Of Dehydration
Oral rehydration
Parenteral rehydration
Electrolytes
Oral rehydration
Awake, alert, not in shock
Rapid fluid replacement over 4-6 hours
-Pedialyte
-Rehydrate
-Infalyte
-WHO solution
Parenteral rehydration
Replace ECF volume - Initial phase
Use isotonic solution (0.9% NS or lactated ringers, D51/4 NS, Do not use dextrose) closely match body's serum osmolality of 285 - 300 mOsm/kg
20 - 30 mL/kg IV bolus over 20 minutes and may be repeated as necessary.
Requirements are recalculated at 8 hour intervals
Electrolytes treatment for dehydration
Sodium Bicarbonate may be used to combat acidosis associated with dehydration
Do not administer K+ until kidney function is assessed (child voids)
K+ loss is replaced. There is a lag time for Na to reach normal levels. Water diffuses almost immediately and may cause cerebral edema
Nursing Interventions for Dehydration
Replace fluid losses (= to volume depletion)
Provide maintenance fluids / electrolytes
Determine cause of depletion
Measure I&O
Monitor VS
Monitor Urine Specific Gravity
Urine Specific Gravity
1.016-1.022
Urine Specific Gravity Newborns
1.001-1.020
Diarrhea
Abnormal intestinal / electrolyte transport. This leads to increased stool frequency with increased water content.
May lead to dehydration, electrolyte imbalance, metabolic acidosis
Acute Diarrhea
Rotavirus, E. Coli, C. difficile
Watery explosive stools, sugar intolerance
Greasy, bulky stools: fat malabsorption
Neutrophils or RBCs: bacterial infection or Irritable bowl disease
Eosinophils: protein intolerance or parasitic infection
Stool electrolytes for secretory diarrhea
Diagnostic Evaluation for Diarrhea
History
Lab evaluations
Stool specimen for diarrhea lasting longer than 3-4 days
Stool cultures with bloody stool or mucous
Stool pH < 6 = carbohydrate malabosorption or lactose deficiency
Check urine specific gravity for dehydration
Check stool electrolytes for secretory
diarrhea
Stool biopsy
Shock
Also known as circulatory failure
Characterized by inadequate tissue perfusion to meet metabolic demands of the body.
Four main types of Shock
Hypovolemic
Cardiogenic
Distributive shock
Obstructive shock
Hypovolemic shock
Reduction in circulating blood volume
Ex: trauma, bleeding, burns, diarrhea
Cardiogenic shock
from impaired cardiac muscle function that leads to decreased cardiac output
Ex: following cardiac surgery
Distributive shock
From a vascular abnormality
Ex: neurogenic shock, anaphylactic shock, septic shock
Obstructive shock
caused by cardiac tamponade, tension pneumothorax, etc.
May resemble hypovolemic shoc
Clinical Signs of hypovolemic shock
Normal-increased RR
Normal breath sounds
Compensated-normal BP
Narrow pulse pressure
Tachycardia
Weak peripheral pulses
Skin pale, cool
Cap refill >2 sec
Urine ouput Decreased
LOC: irritable early.
Clinical Signs of Cardiogenic shock
Labored RR
Crackles, grunting
hypotensive-low BP
Narrow pulse pressure
Tachycardia
Weak peripheral pulses
Skin pale, cool
Cap refill >2 sec
Clinical Signs of Distributive shock
Normal-increased RR
Normal breath sounds (Maybe crackles)
Compensated-normal BP
Variable pulse pressure
Tachycardia
Bounding or weak peripheral pulses
Skin warm or cool
Cap refill variable
LOC: Lethargic, Late.
Clinical Signs of Obstructive shock
Labored breathing
Breath sounds: crackles, grunting
Hypotensive-low BP
Narrow pulse pressure
Classifications of Shock
Compensated
Hypotensive (decompensated)
Irreversible (terminal) shock
Compensated shock
Apprehension
Irritability
Normal BP
Narrowing pulse pressure
Tachycardia
Thirst
Pallor
Diminished urinary output
Hypotensive (decompensated) shock
Tachypnea
Moderate metabolic acidosis
Oliguria
Cool pale extremities
Decreased capillary refill > 3 seconds
Pale extremities
Weakened peripheral pulses
Hypotensive (LATE sign)
Irreversible (terminal) shock
end point of shock. Nothing will reverse damage.
Shock Treatment
Oxygenation and ventilation
Fluid administration
Vasopressor support
Septic Shock
Caused by infection
Systemic release of inflammatory mediators (systemic inflammatory response syndrome (SIRS))
Stages of Septic Shock
Early
Normodynamic
Hypodynamic
Early stage of Septic shock
Chills
Fever
Vasodilation (warm, flushed skin).
BP and UOP are normal
Normodynamic stage of Septic shock
Cool or hyperdynamic decompensated stage
Skin is cool
Pulses and BP remain normal
UOP begins to diminish
Hypodynamic of Septic shock
Cardiovascular function progressively deteriorates
Cold extremities
Weak pulses
Hypotension
Oliguria or anuria
Lethargic or comatose
Multi-organ failure
Treatment for Septic Shock
Prompt initiation of Antibiotics
Anaphylaxis
Acute clinical syndrome resulting from interaction of an allergen in a hypersensitive patient
Prevention of reaction is primary goal
Clinical manifestations of Anaphylaxis
Tachycardia
Dysrhythmia
Hypotension
Relative hypovolemia
Rhinitis (sneezing, nasal itching, rhinorrhea)
Laryngeal edema (stridor)
Bronchospasm (cough, wheezing)
Nausea and vomiting
Abdominal pain
Diarrhea
Diffuse flushing, feeling of warmth
Urticaria (itching of skin and raised rash [hives])
Angioedema (periorbital, perioral)
Sense of impending doom*
Sometimes loss of consciousness*
Headache*
Seizures
Goal of Anaphylaxis treatment
Providing ventilation
Restoring adequate circulation
Preventing further exposure by identifying and removing the cause when possible
Burns
Accidental injury or non-accidental (scalding)
Severity of Burn Wound
Extent of Injury: % of total BSA
Depth of Injury: Expressed as first, second, third, fourth (or superficial, partial-thickness, full-thickness, and full-thickness involving other underlying structures)
Severity of Injury: Minor, Moderate, or Major
Burns Pathophysiology
Edema formation
Fluid loss (resulting in hypovolemia)
Circulatory changes
Tissue repair
Cardiovascular systemic response to Burns
Burn shock-Immediate postburn period, drop in cardiac output precedes any change in circulating blood or plasma volumes
COP usually levels off at 20% of normal resting values; returns to normal within 24-36 hours;
Edema
Renal systemic response to Burns
Increased fluid requirements
BUN and Creatinine levels are elevated
Hematuria
Release of myoglobin which occludes kidney tubules resulting in high risk of renal failure
GI systemic response to Burns
Decrease in blood flow to GI system by 1/3
Atrophy of GI tract
Potential gut barrier dysfunction leading to sepsis
Increased metabolic rate
Elevated blood glucose levels
Elevated body temperature due to increased metabolic rate
Complications of Burns
Pulmonary
Wound Sepsis
GI
CNS
Pulmonary complications of Burns
Inhalation injury
Aspiration of GI contents
Bacterial pneumonia
Pulmonary edema
Emboli
Wound Sepsis complications of Burns
Initially pathogen free; but, dead tissue and exudate provide bacterial growth; 3rd postburn day this begins; by 5th day, well underway
GI complications of Burns
Feeding intolerance
Mucosa ulceration and bleeding
Potential GI tract barrier loss
CNS complications of Burns
Burn encephalopathy (lethargy, withdrawal or coma)
Management of Minor Burns:
Clean with mild soap and tepid water
Debridement with removal of embedded debris
Antimicrobial ointment
Covering of light gauze
Silver wound dressing sometimes
Watch for healing
Management of Major Burns:
Adequate airway
Fluid replacement therapy
Nutrition
Medication
Burn Wound Management
Calculation of IV Maintenance Fluids
Calculate weight of child in kilograms
Allow 100 ml per kilogram for first 10 KG
Allow 50 ML per KG for second 10 KG
Allow 20 ML per KG for remainder of weight in KGS
Divide total amount by 24 hours to obtain rate in Ml/Hr