Fluid and Electrolyte Management Flashcards
What percentage of a child’s body weight is water, compared to an adult?
WATER
PERCENTAGE BODY WEIGHT
At birth = 80%
Falls gradually with age
In adulthood = 60%
What comparments is body water distributed over? What forces affect this?
WATER
COMPARTMENTS OF THE BODY
- Intravascular
- Interstitial
- Intracellular
Affected by pressure and osmotic gradients.
How do you work out the fluid requirement for well normal children?
FLUID REQUIREMENT
NORMAL, WELL CHILDREN
First 10 kg 100 ml/kg/ day
Second 10 kg 50 ml/ kg/ day
Subsequent kg 20 ml/kg day
What is a normal urine output?
URINE OUTPUT
~ 3 ml/ kg/ hour
What are the sources of fluid loss from the body?
FLUID LOSSES
- Urine ~ 30 ml/ kg/ day or 1-2 ml/ kg/ hr
- Stool ~ 0 - 10 ml/ kg/ day
- Insensible losses (sweat, respiration) ~ 10 - 30 ml/ kg/ day - affected by:
- ambient temp/ humidity
- fever
- caloric content of feeds
- skin quality
How much fluid much be lost (ml/kg) to cause shock Vs. clinical dehydration and what is the importance of this?
SHOCK = 20 ml/kg lost from intravascular space
CLINICAL DEHYDRATION = at least 25 ml/kg lost before evident (2.5 - 5% dehydration)
i. e. 2.5 ml fluid lost per 100 g body weight
i. e. 25 ml lost for every 1000 g
i. e. 25 ml/ kg
=> SHOCK MAY OCCUR BEFORE CLINICAL SIGNS OF DEHYDRATION!!!
Dehydration may also occur in the absence of shock.
Or both may occur together.
Depends on the rate of fluid loss and rate of fluid shifts.
What % dehydration do (a) a child without shock and (b) a child with shock have?
% DEHYDRATION
NO SHOCK: 5% dehydration
SHOCK: = / > 10% dehydration
What parameters is pathology from electrolyte changes related to?
ELECTROLYTE DERANGEMENT
Extreme levels
Rapid rates of change
What are the clinical signs of dehydration vs. shock?
CLINICAL SIGNS
DEHYDRATION VS. SHOCK
- Clinical appearance:
- unwell Vs. Pale/ lethargic/ mottled
- Dehydration only
- skin turgor: reduced
- eyes: sunken
- fontanelle: depressed
- mucous membranes: dry (except mouth breathers)
- A + B
- RR: normal / tachypnoea Vs. tachypnoea
- C
- HR: normal/ tachycardia Vs. tachycardia
- Peripheral pulses: Normal Vs. weak
- CRT: normal/ mildly prolonged Vs. prolonged
- extremities: warm Vs. cold
- BP: normal Vs. low
- D
- GCS: altered responsiveness e.g. irritable, lethargic Vs. decreased
- E
- decreased UO (both)
What is the intravascular volume of an infant and of a child? Bearing this in mind, what does e.g. 5% dehydration mean relative to these values?
INTRAVASCULAR VOLUME
Infant = 80 ml/kg
Older child = 70 ml/kg
5% dehydration = loss of 5g fluid per 100g body weight
Extrapolate –> 50 ml in 1000 ml
i.e 50 ml in 1 kg or 50 ml/kg
What are the critical clinical questions in the management of fluid and electrolyte management?
FLUID AND ELECTROLYTE Mx
CRITICAL CLINICAL QUESTIONS
- Shock? –> correct rapidly
- Dehydration? –> correct over 24 - 48 hrs
- Acid base abnormality?
- Electrolyte abnormalities?
What is the specific management of shock?
SHOCK Mx
- ABCDEFG
- Fluid bolus
- 20 ml/kg
- 10 ml/kg in raised ICP, trauma, cardiac pt’s
- 0.9% saline
- care if using Hartmann’s esp. in renal impairment - contains K+
- hyper and hyponatraemia do not affect choice of fluid during initial resus
- Electrolyte abnormalities
- correct slowly UNLESS
- dysrhythmia
- neuro abnormality
- correct slowly UNLESS
- Treat shock 1st before turning attention to hydration status/ Mx of dehydration
What is the only clinical available objective measure of total body fluid changes? What measure is used in emergency situations and why?
The only clinically available objective measure of total body fluid changes = WEIGHT
In emergencies, pre-sickness weight often not available.
So have to use clinical signs of dehydration to estimate degree of dehydration.
Define 5% and 10% dehydration. What do these values actually represent?
5% DEHYDRATION
= LOSS of 5 ml of fluid per 100g of body WT
= loss of 50 ml of fluid per 1000 g of body WT
= 50 ml/ kg
10% DEHYDRATION
= LOSS of 100 ml/ kg
Describe the specific management of dehydration.
DEHYDRATION Mx
- ABDCEFG
- Daily maintenance + Replacement
- over a 24 hour period
- monitor every 3-6 hrs
- use WT as an objective measure - appropriate rate of gain
- crystalloids
- Route
- Oral
- oral rehydration solution is preferable if the gut is functioning
- use cup and spoon
- Continue normal feeds in addition to solution esp. if breast fed
- IV
- if excessive vomiting or damaged gut
- attempt gradual re-introduction of oral rehydration during IV therapy unless there is bowel damage
- if tolerated then stop IV completely
- Oral
Describe the composition of the commonly available crystalloid fluids:
- Sodium Chloride 0.9%
- Sodium Chloride 0.45% + dextrose 5%
- Hartmann’s solution
- Dextrose 5%
- Dextrose 10%
See image.
Describe the fluid management of a 6 kg child who is clinically shocked and 10% dehydrated as a result of gastroenteritis.
6 kg child
- SHOCK
- 20 ml/kg 0.9% saline
- 20 x 6 = 120 ml
- INFUSION = DEHYDRATION + MAINTENANCE
- DEHYDRATION
- 10% i.e. loss of 100 ml/kg of body weight
- 100 x 6 = 600 ml
- MAINTENANCE = 100 ml for the first 10 kg, 50 ml for the 2nd 10 kg, 20 ml/ kg thereafter
- 100 x 6 = 600 ml
- TOTAL DEHYDRATION REPLACEMENT + MAINTENANCE = 1200 ML
- over 24 hours
- 1200 / 24 = 50 ml / hr
- DEHYDRATION
- Monitoring
- weigh after 4-6 hrs
- losing weight –> increase fluid rate
- excessive weight gain –> decrease rate
- satisfactory –> continue
- tolerating oral fluids then start giving more of maintenance fluid as oral feeds
- weigh after 4-6 hrs
What can excessive fluid administration cause?
EXCESSIVE FLUID ADMINISTRATION
- Intravascular fluid overload
- Overhydration
- Both
Describe the relative risk of dehydration and fluid overload in paediatric patients with the following conditions:
- Nephrotic syndrome
- Myocardial dysfunction
- Renal impairment
- Nephrotic syndrome
- low serum albumin
- fluid leaks out of the intravascular space into the tissues
- diffuse severe oedema
- BUT intravascular space MAY be fluid DEPLETED
- => may need to replace fluid before diuresing to avoid shock
- Myocardial dysfunction
- intravascular compartment overfilled
- signs of fluid overload
- BUT on diuretics
- MAY also be dehydrated due to total body fluid depletion
- Renal impairment
- intravascular AND total body FLUID OVERLOAD
- giving more fluid –> pulmonary oedema
Treatment of fluid overload can be complex.
Always d/w an expert.
What are the normal daily requirements in well, normal children for the following:
- Water (ml/ kg/ day)
- Sodium (mmol/ kg/ day)
- Potassium (mmol/ kg/ day)
- Energy (kcal/ day)
- Protein (g/ day)
See image.
What is severe hypernatraemia associated with?
HYPERNATRAEMIA
SEVERE
- HIGH serum sodium
- brain cells becmome dehydrated
- brain tissue shrinks
- blood vessels assoc. w/ the brain tissue may tear or clot
- BRAIN DAMAGE
What does rapid correction of the following cause?
- HYPERnatraemia
- HYPOnatraemia
RAPID CORRECTION
- HYPERnatraemia – remember HYPER C*NT
- cerebral oedema
- CONVULSIONS
- HYPOnatraemia – remember HYPO D***
- DEMYELINATION
- permanent BRAIN INJURY
Describe the degree of sodium loss in the following conditions:
- Rotavirus Gastroenteritis/ diarrhoea
- Cholera & enteropathogenic E. Coli diarrhoea
- Diabetes insipidus
- Renal tubular dysfunction
SODIUM LOSS
- Rotavirus Gastroenteritis/ diarrhoea
- 50 mmol/L
- Cholera & enteropathogenic E. Coli diarrhoea
- 80 mmol/L
- Diabetes insipidus
- minimal
- Renal tubular dysfunction
- high
Describe the causes of HYPERnatraemia in the DEHYDRATED patient.
HYPERnatraemia in the DEHYDRATED patient
CAUSES
- LOSS (excessive) – WATER e.g.
- Diabetes insipidus
- Diarrhoea
- INTAKE (excessive) – SODIUM e.g.
- Iatrogenic
- Poisoning - NAI
- COMBINATION e.g.
- gastroenteritis/ diarrhoea AND
- excessive sodium in rehydration fluid
What do consensus guidelines recommend as the starting fluid for deficit replacement and maintenance for hypernatraemic dehydration? Why?
FLUID OF CHOICE
HYPERNATRAEMIC DEHYDRATION
- 0.9% SALINE
- 0.9% SALINE + 5% DEXTROSE
0.45% Saline no longer used - hypotonic solution - led to a rapid fall in sodium
What can be used as a guide for fluid replacement therapy in children with renal tubular dysfunction, OTHER than serum sodium?
- Urine sodium
- Urine osmolality
- Stool sodium
Describe the treatment of HYPERnatraemia.
HYPERNATRAEMIA
Mx
- Treat SHOCK
- 20 ml/ kg (or 10 ml/kg in trauma, cardiac pts, raised ICP)
- 0.9% saline
- Treat Dehydration - work out:
- replacement
- maintenance
- total & rate
- clinically assess and weigh frequenty
- Lower SODIUM:
- rate NOT > 0.5 mmol/ hour
- Electrolytes
- check potassium, calcium
- monitor frequently
- expert advice if not improving
- GLUCOSE - check
What causes hyponatraemia (in principle)?
HYPONATRAEMIA
CAUSES
- LOSS of SODIUM (excessive)
- REDUCED INTAKE e.g. dehydration
- DILUTION
- excessive water intake
- water retention
- COMBINATION
Describe the management of HYPOnatraemia.
HYPONATRAEMIA
Mx
- Seizures
- 3% saline 4 ml/kg
- over 15 mins
- raises Na ~ 3 mmol & usually stops seizures
- Treat shock
- Hydration - Calculate dehydration fluid deficit & maintenance
- dehyration - start infusion 0.9% saline
- excessive water intake/ retention - restrict to 50% normal requirement
- clinically assess hydration & weigh frequenly
- RAISE SODIUM
- NOT > 0.5 mmol/ hour
- Electrolytes
- check others e.g. K+, Ca2+
- monitor frequently
- expert advice if not improving
- GLUCOSE - check
Are the following mainly intracellular or extracellular ions?
- Sodium
- Potassium
Sodium - extracellular
Potassium - intracellular
What is the role of intracellular potassium and what can happen when this mechanism fails? What must occur for this mechanism to fail?
Intracellular potassium is a buffer which maintains the serum value within a narrow range.
Outside of this range - cardiac arrhythmias.
It is a very large buffer so clinical signs of hypokalaemia will only manifest when there is sig. TOTAL BODY DEPLETION.
The reverse is true for hyperkalaemia i.e. sig. total body overload, beyond the ability of the kidney to compensate OR massive breakdown of RBC’s.
Describe the causes of hypokalaemia.
HYPOKALAEMIA
CAUSES
VITAMIN CD
- Vascular volume depletion
- Infectious: Diarrhoea
- Metabolic: aLKalosis (Low K), primary hyperaldosteronism (Na+ retention, K+ excretion)
- Drugs: diuretic abuse
Describe the causes of HYPERkalaemia.
HYPERkalaemia
CAUSES
- EXCESSIVE INTAKE +
- Vascular: cell lysis (released from RBC), inadequate CO (in the critically ill neonate)
- Metabolic: renal failure (MOST COMMON), acidosis, adrenal insuffiency, hypoaldosteronism
Describe the management of hypokalaemia.
HYPOKALAEMIA
Mx
- rarely an emergency
- usually the result of losses from diarrhoea ie. total body depletion
- Mx
- Oral (if possible)
- IV
- do NOT exceed 40 mmol/L (i.e. 20 mmol in 500 ml)
- unless given centrally w/ cardiac monitoring (pptates arrythmia)
- Hypokalaemia due to:
- alkalosis
- salbutamol
- insulin
- high intracellular K+ stores
- redistribution of K+ into cells
- not a true K+ deficiency
- => treat the underlying cause
Describe the emergency management of hyperkalaemia.
HYPERKALAEMIA
Mx
- dangerous
- arrythmias at 7.5 mmol/ L (rarely below)
- ensure not spurious result from squeezed sample (lyses blood cells)
- MONITOR
- ECG, BP
- UO
- WT
- U+Es incl. Ca2+ - often low if hyperkalaemia esp. in sepsis/ renal failure
-
STOP
-
K+ in
- diet
- fluids
-
drugs that cause HyperK
- ACE inhibitor
- angiotensin II blockers
- b-blockers
-
K+ in
- Rpt urgently ? haemolysis or lab result from a long time ago
-
ARRHYTHMIA?
- e.g. heart block, ventricular arrythmia
- apply continuous ECG monitoring
- YES –> CALCIUM 0.1 mmol/ kg IV
- has no effect on K+
- Stabilise myocardium IF:
- ECG changes
- K+ sig. > ULN or rising
- 10% calcium gluconate 0.5 - 1 ml/kg
- max 20 ml
- over 5 mins
- undiluted
- effect w/i mins, lasts ~1 hr
- rpt w/i 5-10 mins if necessary
- NO –>
-
SALBUTAMOL (2.5 - 10 mg NEB)
- shifts K+ into cells
- < 2 yo = 2.5 mg
- =/> 2 yo = 5 mg
- rpt 2 hrly
- effect w/i 30 mins but max effect at 60-90 mins
-
Repeat K+
-
Falling –> CALCIUM RESIONUM 1g/kg PO/PR (F*C*)
- or ? 250 mg/ kg, max 15 g
- 6 hourly
- PR - rpt if expelled w/i 30 mins
- removes K+ from the body
- PO unpalatable - limited use
- consider specific arrhythmia protocol
- –> Dialysis if necessary (needs specialist centre)
-
High (Glucose makes you high!)
- pH > 7.35
-
Glucose 10% 5 ml/kg/ hr (20% at 2.5 - 5 ml/ kg/ hr if central access)
- BEWARE large volumes of fluid in renal failure
- AIM blood GLU 10-15 mmol/L
- physiological homeostasis will increase insulin production
- if blood sugar > 15 after 1 HOUR –>
-
+/- Insulin 0.05 units/ kg/ hr IV
- 50 units of insulin
- in 50 ml 0.9% saline
- = 1 unit/ ml
- maintain blood glucose 10-15
- adjust infusion rate in steps of 0.05 ml/ kg/ hr
- monitor GLU
- 15 min after starting/ changing dose
- –> every 30 mins until stable
- –> Calcium resonium
- –> Dialysis if necessary
-
Glucose 10% 5 ml/kg/ hr (20% at 2.5 - 5 ml/ kg/ hr if central access)
- pH < 7.34
- Sodium bicarbonate 1-2 mmol/kg IV
- 1 mmol = 1 ml of 8.4% NaHCO3
- dilute 1:5 in 5% dextrose
- over 30 mins
- –> Repeat K+
- –> Back to the top of STEP 3
- pH > 7.35
-
Falling –> CALCIUM RESIONUM 1g/kg PO/PR (F*C*)
How does salbutamol work in the management of hyperkalaemia?
HYPERKALAEMIA
SALBUTAMOL
- stimulates cell wall pumping mechanism
- increases cellular uptake of K+
- works within 30 mins
- administered via neb
- K+ falls by 1 mmol/L with doses of 2.5 - 10 mg
How do you monitor a patient with hyperkalaemia?
HYPERKALAEMIA
MONITORING
- ECG
- continuous
- Tented T waves, absent P waves (first signs)
- BP
- Sats
- UO
- WT
- U+E - recheck urgently ? haemolysed sample ? sample repeated a long time ago
How does sodium bicarbonate work in the treatment of hyperkalaemia? What other electrolyte must be measured frequently when using sodium bicarbonate as treatment for hyperkalaemia and why?
SODIUM BICARBONATE
HYPERKALAEMIA
- Promotes intracellular K+ uptake
- effect is greater in acidotic pts
- in these pt’s hyperK+ is the result of K+ moving out of the cells
- ALWAYS CHECK CA2+
- Hyperkalaemia often accompanied by HYPOcalcaemia esp. in sepsis/ renal failure
- using bicarbonate can cause a crisis by quickly lowering the ionised calcium fraction –> TACH:
- Tetany
- Arrythmias
- Convulsions
- Hypotension
What are the only treatments that remove K+ from the body in the management of hyperkalaemia? What is the significance of this?
The ONLY treatments that REMOVE K+ from the body are
- CALCIUM RESIONIUM (ion exhange resin)
- DIALYSIS
All other Rx’s REDISTRIBUTE K+ into cells.
This DELAYS rather than TREATS the problem.
Discuss some of the causes of hypocalcaemia.
HYPOCALCAEMIA
CAUSES
VITAMIN CDE
- Inflammatory: pancreatitis
- Infectious: sepsis
- Trauma: rhabdomyolysis
- Iatrogenic: citrate infusion e.g. massive blood transfusion
- Endocrine: severe rickets, hypoPTH, acute and chronic renal failure
Name some of the symptoms of hypocalcaemia.
HYPOCALCAEMIA
SYMPTOMS
- Neuro: weakness, tetany, convulsions
- CVS: hypotension, arrhythmias
Discuss the management of hypocalcaemia.
HYPOCALCAEMIA
Mx
- treat the underlying condition
- IV Calcium in emergency followed by central line infusion
- Calcium IV is irritant
- acute doses often only transient effect as most causes of hypocalcaemia will cause sig. total body depletion
- Oral phosphate binders or DIALYSIS
- in renal failure
- because low ca2+ often accompanied by high phosphate
- this prevents the calcium level from rising
How does hypercalcaemia usually present?
HYPERCALCAEMIA
PRESENTATION
LONG-STANDING:
- Anorexia
- Vomiting
- WT loss
- Failure to thrive
- Malaise
What are some of the causes of hypercalcaemia?
HYPERCALCAEMIA
CAUSES
VITAMIN CDE
- Iatrogenic/ Drugs: Thiazide diuretic abuse
- Neoplastic: Malignancy
- Congenital: skeletal disorders, idiopathic hypercalcaemia of infancy
- Endocrine: hyperPTH, hypervitaminosis D or A
Describe the management of hypercalcaemia.
HYPERCALCAEMIA
Mx
- 0.9% Saline (volume expansion)
- FUROSEMIDE
- specific Rx for condition
Describe the pathophysiology of DKA.
DKA
PATHOPHYSIOLOGY
Relative or Absolute LACK of INSULIN
- Inability to metabolise GLUCOSE
- HYPERGLYCAEMIA
- OSMOTIC DIURESIS
- UO exceeds the ability of pt to drink
- DEHYDRATION
- FAT is used as a source of energy
- KETONES produced
- Metabolic ACIDOSIS
- Hyperventilation to compensate (resp alkalosis) = Kussmaul breathing i.e. deep, sighing respirations
- COMA - due to a combination of HAD:
- HYPEROSMOLARITY
- ACIDOSIS
- DEHYDRATION
Who experiences DKA?
DKA
- First presentation of T1DM
- Known diabetes - decompensation due to:
- Illness including Infection
- Non-compliance w/ treatment
What are the typical symptoms of DKA?
DKA
SYMPTOMS/ HISTORY
- abdominal pain (central)
- polyuria + polydipsia / nocturnal enuresis
- weight loss
- vomiting
NB symptoms less specific in < 5 yo
They are also more prone to ketoacidosis.
Describe the examination findings in DKA. What additional signs should alert you to the possibility of sepsis causing decompensated diabetes?
DKA
Signs
- General: smell of ketones
- Neuro: drowsy/ reduced consciousness
- CVS: signs of dehydration
- Resp: Kussmaul respirations (deep, sighing, rapid)
- Sepsis:
- fever/ hypothermia
- hypotension
- acidosis: refractory or lactic
What differential diagnoses should be considered in DKA?
DKA
DIFFERENTIAL DIAGNOSES
- Salicylate poisoning
- Uraemia
Describe the management of DKA.
DKA
MANAGEMENT
- A
- assess patency
- airway opening manoeuvres
- adjuncts
- consider intubation
- B
- 100% O2
- C
- cardiac monitor ? peaked T-waves, absent p-waves (hyperkalaemia in DKA)
- IV access
- Bloods:
- Baseline incl. U+E, creat, FBC
- leucocytosis common in DKA, not necessarily due to infection
- gas
- GLU
- KETONES
- +/- BCx
- Baseline incl. U+E, creat, FBC
- FLUIDS
- Fluid bolus 10 ml/kg
- SHOCK ONLY
- SLOWLY
- not routine
- seek specialist advice if 2nd bolus needed
- Fluid REPLACEMENT for DEHYDRATION (over 48 hrs)
- do NOT subtract the first 20 ml/kg of boluses
- DO subtract any subsequent boluses from replacement volume
- BEWARE risk of cerebral oedema with rapid fluid replacement
- Calculation
-
pH < 7.1 = SEVERE DKA
- 10% fluid deficit
-
pH > 7.1 = MILD - MOD DKA
- 5% fluid deficit
-
pH < 7.1 = SEVERE DKA
- MAINTENANCE
- ‘REDUCED VOLUME’ RULES
- risk of cerebral oedema
- < 10 kg = 2 ml/ kg/ hr
- 10 - 40 kg = 1 ml/ kg/ hr
- > 40 kg = 40 ml/ hr (fixed volume)
- TOTAL
- Hourly rate = (deficit/ 48 hrs) + maintenance per hour
- avoid hypoK
- avoid rapid changes in serum osmolarity
- Fluid bolus 10 ml/kg
- Inotropes
- for hypotensive shock
- d/w CATS/ PICU
- E
- NGT
- URINE: dip - sugar, ketones +/- M/C/S
- Fever
- BCx
- CSF
- throat swab
- CXR
- urine M/C/S
- G
- gas and lab glucose
- dip urine for glucose
- Insulin
- 1-2 hrs AFTER fluids started
- soluble insulin infusion
- 0.05 - 0.1 units/ kg/ hour
- aim glucose near normal levels
- avoid hypoglycaemia
Describe the major complications of DKA, for which intensive monitoring is required on ICU.
DKA
MAJOR COMPLICATIONS
- NEURO = CEREBRAL OEDEMA
- most important cause of death & poor neuro outcome
- Avoid by:
- slow normalisation of osmolarity
- pay attention to Na+ and glucose level
- rehydrate SLOWLY over 48 hrs
- Sx - monitor for:
- neuro: headache, irritability, altered GCS
- CVS: bradycardia and HTN/ rising BP
- Resp: hyperventilation - assoc. w/ worse outcome
- Gastro: recurrence of vomiting
- Mx
- 3% hypertonic saline 3 ml/ kg
- 20% mannitol 250-500 mg/ kg 20 mins
- CVS = CARDIAC DYSRHYTHMIAS
- usually 2ndary to electrolyte disturbances
- especially K+
- RESP = PULMONARY OEDEMA
- replace fluid carefully
- avoid overloading
- RENAL = ACUTE RENAL FAILURE
- uncommon - because of high osmotic urine flow
