fluids & electrolyte, Fluid and electrolytes

FLUID AND ELECTROLYTE
(PRINCIPLES OF SURGERY)
DR.SHITU.

CONTENT
 Introduction to Body Fluids
 Body Fluid Changes
 Fluid and Electrolyte Therapy
 Electrolyte Abnormalities in Specific Surgical Patients

CONTENT
Introduction to Body Fluids
• Total Body Water (TBW)
• Fluid Compartments
• Composition of Fluid Compartments
• Osmotic Pressure
Body Fluid Changes
• Normal Exchange of Fluid and
Electrolytes
• Classification of Body Fluid Changes
• Disturbances in Fluid Balance
• Volume Control
• Concentration Changes
• Composition Changes: Etiology and
Diagnosis
• Acid-Base Balance

CONTENT
Fluid and Electrolyte Therapy
• Parenteral Solutions
• Alternative Resuscitative Fluids
• Correction of Life-Threatening
Electrolyte Abnormalities
• Fluid Therapies
 Preoperative
 Intraoperative
 Postoperative
• Special Considerations for the Postoperative Patient

INTRODUCTION
• Fluid and electrolyte in surgery:
(1) Needs change preop, intraop & postoperatively.
(2) Needs vary in response to trauma and sepsis.

BODY WEIGHT
Fluids ----------60%
Solids-----------40%

TOTAL BODY WATER (TBW)
• TBW = 50% & 60% in female and male respectively.
• Body fat determines; lean tissue e.g. muscle and solid organs have
↑water than fat and bone.
• Young lean males ↑water than elderly & obese.
• ↓TBW % in females –plenty adipose, low muscle
• TBW % ↑10% in malnourished, & ↓10 -20% in obese individuals.
• New born with High %TBW = 80%; by 1year = 65%.

FLUID COMPARTMENTS OF TBW
3 functional compartments:
 Plasma (intravascular compartment)
 Extravascular interstitial( between and around cells)
Intracellular fluid (ICF)
ECF is measured by indicator dilution method; using NaBr and radioactive
Sulphate distribution.
ICF determined by indirect method.
ICF = TBW - ECF
Extracellular fluid
(ECF)

FUNCTIONAL BODY FLUID COMPARTMENTS
TBW = total body water

Regulation of fluid balance
• Water in the body is in a constant state of motion.
Shifting between the three major fluid compartments of the body
• In a normal, healthy human being :
WATER INPUT = WATER OUTPUT.
• Maintaining this ratio : is of prime importance in maintaining health.
• Approximately 90% of the body's water intake comes via the gastro-intestinal
tract.
• The remaining 10% is called metabolic water and is produced as the result of
various chemical reactions in the cells of the body's tissues.

Regulation of fluid balance
The mechanisms for the regulation of body fluids:
1- Thirst center in the hypothalamus.
• receives input from the digestive tract
• helps in the control of thirst.
2- Hypothalamic-pituitary axis
3- Anti Diuretic Hormone (ADH)
Main regulator of fluid volume and extracellular osmolarity

COMPOSITION OF FLUID COMPARTMENTS
• ECF:
principle cations is Na
principle anions is Cl
• ICF:
Principle cation is K, then Mg
Principle anion is phosphate, then Sulfate, proteins.
• Cell membrane ATP-Driven Na-K Pumps maintain conc gradient
between compartments.
• Interstitial fluid differs slightly from plasma(↑protein).

Chemical composition of body fluid compartments

OSMOTIC PRESSURE
• Physiologic activity of electrolytes in solution depend on the number
of:
particles(mmol/L)
electric charges (mEq/L)
osmotically active ions (mOsm/L)
• Equivalent = Atomic Weight/Valence
• Univalent ions e.g. Na; 1mEq = 1mmol
• Divalent ions e.g. Mg; 2mEq = 1mmol
• mEq of cations must balance with mEq of anion.

OSMOTIC PRESSURE continued
• Apart from use of mEq, osmotic pressure can be used to compare solutes in
solution.
• Water moves from the side of the cell membrane with a lower solute
concentration to one with a higher concentration to establish osmotic
equilibrium.
• Osmotic Pressure (OP) is measured in mOsm.
• 1 mOsm = number of osmotically charged particles
• E.g. NaCl = 2 mOsm; 1Na + 1 Cl
• Principle determinants of osmolarity are related in an equation:
• ICF=290mOsm, ECF=320mOsm.
Calc Serum osmolarity = 2Na +
Glucose/18 + BUN/2.8

BODY FLUID CHANGES:
Normal exchange of fluid and electrolyte
• Kidney must excrete 500-800 ml of urine/ day; to clear products of
metabolism.
• 3-5g of salt consumed daily – balanced by kidney.
• Kidney can regulate salt excretion of 1 – 5000 mEq/d. (Salt wasting
kidneys are the exception).
• Little Na is lost through sweat – hypotonic.
• GI losses are isotonic to slightly hypotonic.

Water exchange (60- to 80-kg man)

CLASSIFICATION OF BODY FLUID CHANGES
Categories of Disorders in body fluid balance:
• Volume
• Concentration
• Composition
All the three (3) can occur simultaneously.
• Gain or loss of isotonic fluid leads to extracellular volume change.
• Osmolarity equalized between the 2 compartments by loss of H+ from
ECF.

• Alteration of Na+ conc in ECF changes total number of osmotically
active particles.
• Anions do not; they only produce a compositional change.
• Doubling K+ causes profoundly alters myocardial function; without
significant volume or conc change.

DISTURBENCE IN FLUID VOLUME
Signs & symptoms of volume disturbances
• Usually occurs in ECF
• Can be acute or chronic
• Acute – CVS and CNS
• Chronic – Tissue signs (skin turgor, sunken eyes)
plus CVS and CNS.
• Labs –Elevated (BUN) in severe deficit due to
decreased GFR and hemoconcentration
• Urine osmolarity higher than that of blood.
• Na usually low; <20mEq/L

CAUSES OF VOLUME DEFICIT
• Loss of GIT fluids via NGT, vomiting and diarrhea, ECF
• Sequestration secondary to soft tissue injury; Burns, and intra-abdominal
processes like peritonitis, IO, prolonged surgery.

ECF EXCESS
• CAUSES:
Iatrogenic
Secondary to renal dysfunction
CHF
Cirrhosis
• Both plasma and interstitial fluid are increased.

CLINICAL MANIFESTATIONS
• Symptoms are primarily CVS and pulmonary.
• Hyper-dynamic circulation and edema.
• They are exaggerated in elderly and cardiac patients leading to CHD
and pulmonary edema.

Volume control
• Sensors of volume changes:
 Chemoreceptors
 Baroreceptors
• Osmoreceptors - Detect changes in fluid osmolarity and drive changes in thirst and
diuresis through kidneys
DECREASE in plasma osmolarity?
↓ ↓
supraoptic &paraventricular lateral preoptic
Nuclei area
↓ ↓
↓
Normal osmolarity

Volume control
• Baroreceptors respond to volume and pressure changes by pressure sensors in aortic arch
and carotid sinus.
• Baroreceptor responses are both neuro and hormonal
• Neuro:
 Sympathetic pathway
 Parasympathetic pathway
• Hormonal:
 Renin-angiotensin
 Aldosterone
 Atrial natriuretic peptide (ANP)
 Renal prostaglandins
Volume is restored to normal by alteration in renal sodium excretion and free water
reabsorption

CONCENTRATION CHANGES
• Changes in serum sodium concentration is proportional to 1/TBW
• Abnormal sodium concentration is a reflection of abnormality in total
body water(TBW).

HYPONATREMIA
• Due to Na depletion or dilution
–Aetiology:
Excessive oral water intake
Iatrogenic Iv fluid administration
Postop secrete ↑sed ADH which results into volume expansion and
hyponatremia
Drugs e.g antipsychotics , TCAs & ACE inhibitors.

HYPONATREMIA
Na depletion :
• ↓Na in take
• Enteral feeds with low Na
• GI losses through V/D & NG-tube
• Pressure changes – Renal loss →Diuretic use, renal disease.
• Hyponatremia can occur in an excess of salt relative to free water →untreated
hyperglycemia, mannitol administration.
• Glucose increases osmotic force →water moves from intra to extracellular space.
• Corrected Na concentration should be calculated:
• For every 100mg/dL increment in plasma glucose above normal, plasma Na should
decreased by 1.6mEq/L **(2.4meq/l)
• Pseudohyponatremia →from ↑plasma lipids and proteins.

clinical manifestations of hyponatremia
• Hyperosmolar causes include:
• Hyperglycemia
• Mannitol use
• Pseudohyponatremia
• Depletion Vs. dilutional causes be evaluated.
• In depletion, ↓urine Na <20mEq/L; but in renal sodium wasting, it is
>20 mEq/L.
• Hypervolemic circulation → Dilutional causes.
• SIADH →hyponatremia in a normal volume status
Should be excluded by
systemic review

TABLE: clinical manifestations of hyponatremia

HYPERNATREMIA
• AETIOLOGY:
• Loss of free water
• Gain of Na in excess
• Like Hyponatremia, Hypernatremia can be associated with ↑ IC
volume, normal IC volume, or ↓ IC volume.
• Hypervolemic causes:
• Iatrogenic administration of Na containing fluids [NaHCO3]
• Mineral corticoid excess e.g. in hyper-aldosteronism, Cushing’s
syndrome, congenital adrenal hyperplasia.

HYPERNATREMIA ctn
• Normovolemic Hypernatremia
• Aetiology:
• Renal causes- Diabetic Inspidus, diuretic use, Renal disease.
• Non Renal water loss from GIT or skin.
Typically--- thirst is the first symptom.
• weakness and sluggishness.
• A very high sodium level can cause confusion,
• paralysis, coma, and seizures.

CLINICAL MANIFESTATIONS OF HYPERNATREMIA
• Manifests at serum concentrations of >160mEq/L
• Have significant morbidity and mortality.
• CNS predominate due to hyperosmolarity
• Water shifts from intracellular to extracellular space
• Cellular dehydration → traction on cerebral vessels
→subarachinoid hemorrhage
• CNS symptoms range from Restlessness & Irritability to seizures,
coma, & death.

Clinical manifestations of hypernatremia

• POTASSIUM ABNORMALITIES
• Normal dietary intake = 50-100mEq/d
• Excreted primarily in urine
• Renal excretion of K is maintained between 10-700mEq/d
so that EC K is maintained.
• Only 2% of TB K (4.5 mEq/L x 14L = 64mEq) is in
extracellular fluid.

• K is critical for cardiac and neuromuscular function.
• A small alteration can cause a major effect on cardiac activity.
• Factors affecting intra & extracellular K distribution
Surgical stress
Injury
Acidosis
Tissue catabolism

HYPERKALEMIA
• Serum potassium conc’n is > NR (3.5→5.0 mEq/L)
Causes: ↑K intake
• ↑Release of K from cells i.e. RBC lysis (↑transfusion)
• Impaired K excretion from kidneys
• Release of intracellular K into ECF due to hemolysis, crush injuries.
• A shift of K from intra to EC compartment due to acidosis, ↑EC
osmolality by hyperglycemia, IV mannitol
• 98% of K is IC, a small shift EC causes severe change

HYPERKALEMIA
• Meds: K-sparing diuretics, ACE inhibitors, NSAIDs, Spironolactone
• ACE-I interfere with Aldosterone activity; impairing normal renal
mechanisms of K excretion.
• Acute renal insufficiency & chronic R.I impair K excretion

Symptoms of hyperkalemia
• GIT: N,V,D, Intestinal colic
• Neuromuscular: Weakness, Ascending paralysis to respiratory failure
• Cardiovascular: Ranges from ECG changes to hemodynamic
symptoms of arrhythmia & cardiac arrest

• ECG changes include;
• Early:- High peaked T- waves
• Widened QRS complex
• Flattened P-wave
• Prolonged PR interval (1st
degree Block)
• Sine wave formation
• Ventricular fibrillation

fluids & electrolyte, Fluid and electrolytes

HYPOKALEMIA
• More common than hyperkalemia in surgical patients
• Etiology:
• Inadequate K intake
• Excessive renal potassium excretion
• K loss in ↑GI secretions;- Diarrhea, fistula, ↑NG output
• Intracellular shift from metabolic alkalosis or insulin therapy.

HYPOKALEMIA
• Calculation of change in K associated with alkalosis
• K decreases by 0.3 mEq/L for every 0.1↑pH above normal.
• Drugs that cause Mg depletion cause renal K wastage; they include
Amphotericin B, Aminoglycosides, Cisplastin, & Fosfamide.
• In this case, you first correct hypomagnesaemia before K repletion.

Symptoms of hypokalemia
• Related to failure of normal contractility of GI smooth
muscle, skeletal muscle & cardiac muscle.
• Ileus, constipation, weakness, fatigue, ↓tendon reflexes,
paralysis, cardiac arrest
• Symptoms may be initially masked, and worsened by further
dilution.
• ECG: U-wave, T-wave flattening, ST-segment changes,
arrhythmias (with digitalis therapy)

CALCIUM ABNORMALITIES
Ca distribution=99% bone
• <1% ECF
• Serum Ca:
Protein 40%
Complexed to phosphate 10%
Ionised 50%
Ionised Ca is responsible for neuromuscular stability & can be
measured directly

• Total serum Ca level measured:
• Adjusted total serum Ca ↓by 0.8mg/dl for every 1g/dl ↓Albumin
• Change in pH affects ionised Ca
• Acidosis ↓protein binding; increasing the ionised fraction of Ca
• Daily Ca intake = 1→3g/day
• Most is excreted via bowel; some in urine.

HYPERCALCEMIA
• Ca level above NR (8.5 → 10.5 mEq/L)
OR
• Increase in ionised Ca >4.2→4.8mg/dl
• Causes of ↑Ca:
• Primary hyperthyroidism- Out-patient
• Malignancy- Bone mets-In-patient

Symptoms of hypercalcemia
• Vary with degree of severity
• Neurological impairment
• Musculoskeletal weakness & pain
• Renal dysfunction
• GI symptoms: N, V, abdominal pain.
• Cardiac symptoms:
Short QT-Interval
Prolonged PR & QRS intervals
↑QRS voltage
T wave flattening & widening
AV- block; which can progress to heart block & cardiac arrest.

HYPOCALCEMIA
• Serum Ca <8.5 mEq/L or ↓Ionized Ca <4.2mg/dL
• Causes:
• Pancreatitis
• Massive soft Tissue Injury e.g. in Necrotizing fasciitis
• Renal failure
• Pancreatic & small bowel fistulas
• Hypothyroidism
• Tumor Lysis Syndrome
• Removal of parathyroid adenoma (→Transient hypocalcemia due to atrophy of the
remaining gland & ↑bone remineralization)
• Malignancies associated with ↑osteoblastic activity; i.e.
• Breast ca & prostatic ca. Which lead to ↑ bone formation.

CLINICAL FEATURES
• Neuromuscular symptoms occur for Ca below 2.5 mg/dL
• Parathesias of face & extremeties
• Muscle cramps
• Carpopedal spasms
• Stridor
• Tetany & seizures
• Hyper-reflexia
• Positive Chvostek’s sign (spasm resulting from tapping over facial nerve)
• Positive Trousseau,s sign.
• Decreased cardiac contractility & heart failure

ECG:
• prolonged QT interval
• T-wave inversion
• Heart block
• Ventricular fibrillation

PHOSPHORUS ABNORMALITIES
• The primary intracellular divalent anion.
• Abundant in metabolically active cells
• Energy production e.g glycolysis –ATP
• Levels controlled by renal excretion

HYPERPHOSPHATEMIA
• AET: ↓urine excretion
• ↑P intake
• Endogenous metabolism of P in clinical condn→ ↑cell destruction
e.g. rhabdomyosarcoma, hemolysis, sepsis, TLS, severe hypothermia,
malignant hyperthermia
• Hypoparathyroiditis
• Hyperthyroidism
C/F= Usually asymptomatic
↓renal excretion

HYPOPHOSPHATEMIA
• AET: ↓P dietary intake
• Intracellular shift of P
• ↑P excretion
• ↓GIT uptake in malabsorption, admin of P binders
• Reduced intracellular shift in association with respiratory alkalosis,
insulin therapy, re-feeding syndrome.
• Hungry bone syndrome

C/F
• Occur only when level falls significantly
• Symptoms are related to adverse effects on:
• Oxygen for tissues
• ↓ATP
• Leading to cardiac dysfunction or muscle weakness

MAGMESIUM ABNORMALITIES
• 4TH
most common mineral in body
• Mostly intracellular, like P
• >1/2 TB Mg in bone (2000mEq) it is slowly exchangeable
• 1/3 of ECF Mg is bound to protein (serum albumin)
• Dietary in take is about 20mEq/d
• Excreted in both urine & feces
• Renal excretion can be up to 1mEq- conservative

HYPERMAGNISEMIA
• Rare
• Seen in sever renal insufficiency
• There is a parallel change in K excretion
• Mg containing anti-acids & laxatives →toxicity in renal patients
• ↑intake as in TPN
• Massive trauma
• Thermal injury
• Severe acidosis

C/F
• N & V
• Neuromuscular dysfunction with weakness, lethargy, hyporeflexia,
impaired cardiac co-ordination →cardiac arrest
• ECG-↑PR interval
• ↑T-waves
• Widened QRS complex (as in ↑K)

HYPOMAGNISEMIA
• Common in hospitalized patients especially in critically ill.
• There are Ca/Mg receptors in renal tubules →Mg homeostasis
• AET: ↓intake in starvation, alcoholism,
• ↑renal excretion- alcohol abuse, diuretic use, Amphotericin B,
primary aldosteronism
• Pathologic losses; GIT losses as in diarrhea, malabsorption,
pancreatitis

hypomagnesemia
• Mg is for proper function of enzymes
C/F;
• CNS hyperactivity
• Symptoms similar to those of Ca deficiency
• Hyperactive reflexes
• Muscle tremors, tetany
• Chvostek’s sign +
• Trousseau's sign +

Severe deficiency:
• Delirium, seizures
• ECG changes;
Prolonged QT interval
prolonged PR interval
ST- segment depletion
Flattening or inversion of P-wave
Torsade's de pointes ()
Arrhythmias

• Direct effect on nervous system
• Can produce hypocalcemia
• First treat co-existing ↓Mg; this helps restore K & Ca

ACID BASE BALANCE
• Kidney produces large amounts of bicarbonate &
large acid loads are produced as by-products of
metabolism.
• The PH of the body fluids must be maintained with
in a narrow range.
• Important buffers include:
Intracellular proteins
Phosphates
Intracellular bicarbonates- carbonic acid system

• Acid-Base derangements can be compensated for by respiratory
mechanisms
• Respiratory derangements are catered for by metabolic mechanisms
• Metabolic abnormalities → H sensitive chemoreceptors in carotid
body & brain stem →change in ventilation
• Acidosis →stimulates chemoreceptors →↑ventilation
• alkalosis → ↓activity of chemoreceptors → ↓ventilation

• Renals ↑bicarbonate absorption in respiratory acidosis & ↓ it in
respiratory alkalosis
• Respiratory response is prompt
• Renal response is slow (in 6 hours)
• ACUTE: Resp acid-Base derangements occurring before renal
compensation
• CHRONIC: those persisting after renal compensation
• In excess of predicted pH change → mixed Acid-Base abnormality

METABOLIC DERANGEMENTS
• METABOLIC ACIDOSIS
Aet:
• ↑intake of acids
• ↑ generation of acids
• ↑ loss of bicarbonate
MECHANISM of body response: Producing buffers
Extracellular bicarbonates
Intracellular buffers from bone & muscle
Increased ventilation (Kussmaul’s respiration)
↑ renal absorption & generation of bicarbonate
Kidneys increase secretion of Hydrogen & thus ↑urine excretion of NH4+
H+ + NH3+ = NH4+

• Evaluation of a patient with ↓serum bicarbonate & metabolic
acidosis includes determination of the Anionic Gap (AG).
• Normal AG is < 12 nmol
• It is mainly due to albumin effect
• So, Estimated AG must be adjusted for Albumin (Hypo-
albuminemia reduces AG)
AG = (Na+) – (Cl- + HCO3-)

• Corrected AG = Actual AG – [2.5(4.5-Albumin)]
Metabolic acidosis with ↑AG occurs from:
• Ingestion of exogenous acid e.g. Ethylene glycol, salicylates, or
Methanol.
↑Endogenous acid production as in:
ᵦ Hydroxybutyric acid & Acetoacetate
Lactate in Lactic acidosis
• Lactic acidosis →common cause of metabolic acidosis in surgery
• Circulatory shock → inadequate tissue perfusion →Hypoxia →Lactate

• Management is to restore perfusion with Volume resuscitation;
not with exogenous bicarbonate.
• The liver rapidly metabolizes Lactate, restoring normal pH.
• Over zealous administration of Bicarbonate can lead to metabolic
alkalosis.
• This shifts the Oxgyen dissociation curve to the Left →interfering
with Oxygen unloading at tissue level → Arrhythmias.

METABOLIC ALKALOSIS
Causes:
– loss of fixed acids or the gain of bicarbonate.
• Aet:
• ↑HCO3- generation
• Impaired renal excretion of HCO3-
• Loss of fixed acids
• Gain of Bicarbonate
• It is worsened by K depletion because EC K+ is exchanged with intracellular H+ &
allow them to buffer excess HCO3-
• Loss of gastric contents→Hypochloremia & hypokalemia

• BODY RESPONSE:
• Initially, ↑Bicarbonate in urine to compensate for alkalosis.
• H+ reabsorption + K+ excretion
• K excretion then ↑ due to aldosterone mediated Na
reabsorption.
• Resultant hypokalemia leads to excretion of H+ in alkalosis; a
paradoxical aciduria.

• TREATMENT
• Replacement of volume deficit with isotonic saline &
• K+ replacement once adequate urine output is achieved.

RESPIRATORY DERANGEMENTS
• Respiratory center in Pons & Medulla oblongata control alveolar ventilation to
maintain blood PCO2
RESPIRATORY ACIDOSIS
• Aet:
• ↓alveolar ventilation→retention of CO2
Causes
• Acute respiratory acidosis, treat underlying cause &
• Institute measures for adequate ventilation;
• Patient initiated volume expansion using none invasive bilevel positive air
way pressure
• Or Endotracheal intubation to ↑ minute ventilation.

RESPIRATORY ALKALOSIS
• In surgical patients, causes are acute,
secondary to alveolar hyperventilation
• Pain
• Anxiety CNS injury – assisted ventilation
• Drugs eg salicylates
• Fever
• Hypoxemia
• Acute hypocapnea →uptake of K & P into cells→↑binding of Ca to
albumin→hypokalemia,hypophosphatemia, hypocalcemia →arrhythmias,
parasthesias, muscle cramps, seizures

Respiratory and metabolic components of acid-base
disorders
• N = normal; Pco2 = partial pressure of carbon dioxide.

Etiology of metabolic acidosis

Etiology of metabolic alkalosis

Etiology of respiratory acidosis: hypoventilation

FLUID & ELECTROLYTE THERAPY
• Type of fluid to administer depends on:
Patient’s volume status
Concentration/ composition abnormality
• Both NS & RL are considered isotonic
• Commonly used solutions in table below.

Electrolyte solutions for parenteral administration

• NaCl ideal for correction of metabolic acidosis associated with
Hypochloremia, Hyponatremia, metabolic alkalosis.
• 0.45% saline is ideal for replacement of ongoing Cl- losses,
maintenance of Fluid therapy in post-ops.
• It provides sufficient free H2O for insensible losses & Na for
kidneys function.

• Addition of 5% Dextrose (50g/L) to soln of 0.45% NaCl supplies
200kcal/L.
• This maintains osmolarity & prevents lysis of RBCs which occurs in
rapid transfusion of hypotonic fluids
• Before addition of K, renal out-put has to be ascertained.

Alternative resuscitative fluids

Alternative resuscitative fluids
• Hypertonic saline (3.5%→5%) solution are useful in correction
of severe Na deficits.
• 7.5% NS – for treatment of closed head injury.
• It ↑cerebral perfusion & ↓ICP→↓brain oedema.
• Concern is ↑hemorrhage since hypertonic saline is a
vasodilator

Alternative resuscitative fluids - COLLOIDS
• Plasma expanders
• In severe hemorrhagic shock, capillary permeability ↑→colloids enter
intravascular space, worsening oedema, & ↓tissue O2
• 4 major types of colloids:
• Albumin
• Dextran
• Hetastarch
• Gelatin

Correction of life threatening electrolyte abnormalities
• HYPERNATREMIA:
• Less common than hypoNa, but has a worse prognosis
• Treat associated H2O deficit
• formula for correction of hyperNa
• Water deficit(L) = serum Na – 140 x TBW
140

Correction of life threatening electrolyte abnormalities
• Aim at Rate of IV infusion 1mEq/Hr
-12mEq /Hr in acute hyperNa.
For Chronic, 0.7 mEq/Hr.
S/E: rapid correction→cerebral oedema & herniation
Depending on severity, you can correct oraly or IV
N/S ½ or D5.
Frequent monitoring –Neurological Evaluation & Na serum levels.

Correction of life threatening- HYPONATREMIA
• TREATMENT
• Free water restriction
• Symptomatic = occur at serum level of </= 120mEq/L
• Give 3% N/S = rate of 1mEq/LHr until serum level is 130mEq/L or
neurological symptoms improve
• Asymptomatic = 0.5mEq/L/Hr to a max of 12mEq/L/day.
• Rapid correction can lead to pontine myelinolysis; presenting with
seizures, paresis, akinetic movements, permanent damage and
death.

Correction of life threatening-
POTASSIUM ABNORMALITIES
• HYPERKALEMIA
• Symptomatic;
• Aim at ↓TBK
• Shift K from extracellular to IC space, Protect cells from effects of ↑K
• Remove all sources of exogenous K; K supplements, IV, enteral, parenteral
• Use a cation exchange resin e.g. Kayexalate
• It binds K in exchange for Na orally or rectally.
• Glucose & bicarbonate infusion- it shifts K intracellularly, Albuterol (10→20mg) does
the same)
• Avoid stimulating insulin release. So give Glu & insulin together
• Caution: hyperNa & circulatory overload in kayexalate admin.

Treatment of symptomatic hyperkalemia

HYPOKALEMIA
• K repletion
• Rate; detect using symptoms
• Oral for mild asymptomatic
• With Iv KCl repletion, aim at 10mEq/Hr & 40mEq/Hr if with ECG
monitoring,
• If imminent cardiac arrest & malignant arrhythmias associated
with ↓K, more K can be administered.
• Caution in oliguria or impaired renal function.

Correction of life threatening- CALCIUM ABNORMALITIES
• HYPERCALCEMIA
• If Serum level >12mg/dL, treat
• Critical Ca level is 15mg/dL; rapid progress to death
• In treatment, aim at repleating the volume deficit
• Then induce diuresis with NS.

HYPOCALCEMIA
• Asymtomatic –
• Oral/ IV Ca
• Acute – 10% Ca Glucanate
• Aim at serum conc of 7-9mg/dL
• Correct associated deficits in Mg, K, pH; otherwise, refractory
hypocalcemia occurs.
• NB: Routine Ca supplements are not recommended in massive
transfusion.

Correction of life threatening- PHOSPHORUS
• HYPERPHOSPHATEMIA
• Aim at low serum phosphate level
• Phosphorus binders e.g. sucralfate or Aluminum containing
anti-acids
• Ca acetate if concurrent hypocalcemia exists.
• Dialysis if renal failure

Correction of life threatening- MAGNESIUM
• HYPERMAGNESEMIA
• Eliminate exogenous sources
• Correct concurrent volume deficit
• Correct acidosis if present
• Acute symptoms; Give CaCl2 (5→10ml) immediately to antagonize
cardiovascular effects.
• If elevated level or symptoms persist, do hemodialysis.

HYPOMAGNESEMIA
• Asymptomatic-
• oral –
• IV repletion, according to severity
• Severe deficit (<1.0mEq/l) or symptomatic ,
• 1→2g MgSO4 IV for 15 min.
• If ECG available, it can be given in 2min to correct torsades de pointes
(irregular ventricular rhythm).
• Caution: Large amounts of Mg lead to Mg toxicity.
• NB: concurrent Ca Gluconate counters S/E of rapid ↑Mg as well as
correcting Hypocalcemia.

PRE-OPERATIVE FLUID THERAPY
• Health on Nil P/O, →maintenance.
• Calculate daily losses & replenish them (urine, stool, insensible
loss)
• Initial therapy & maintenance →D5% +0.45% saline at
100ml/hr.

• Most surgical patients have both volume & electrolyte deficiency.
• Do pre-op evaluation of their statuses
AET of Volume deficits:
• GIT losses e.g. Diarrhea & Vomiting.
• Poor oral intake due to disease
• Functional & 3rd
space losses e.g. GI obstruction, peritoneal &
bowel inflammation, ascites, crush injuries, burns, severe Soft
tissue infections (Necrotizing fasciitis)

• DOSE:
• Give 1→2L of isotonic fluid followed by continuous IV infusion.
• Monitor closely; for reversal of S & S of vol deficit (vitals, urine OP ½-
1ml/kg/hr & correction of base deficit)
• If Persistant →ICU early invasive monitoring of CVP or Cardiac
Output.

• Severe hypernatremia associated with volume deficit is
corrected using 0.45% NS & not D5%. This corrects both
hypoNa & vol deficit without causing a rapid fall in extracellular
osmolarity.

INTRA-OPERATIVE FLUID THERAPY
Why correct volume deficit pre-op?
• Anesthetic induction causes ↓compensatory mechanisms
• Hemodynamic instability can be avoided during anesthesia by:
• Correcting known fluid losses
• Replacing on going losses
• Adequate pre op maintenance fluids

Causes of fluid losses
• During open abdominal surgeries:
• Measured blood loss
• Bowel wall oedema
• Peritoneal fluid
• Wound oedema

3rd
space losses(parasitic losses)
• Aka sequestration or 3rd
space edema.
• NB: distributional shifts with functional vol of ECF ↓; no fluid
lost from body
• Large soft tissue wounds
• Complex fracture with STI
• Burns

Evaluation of adequacy of resuscitation
• Vitals
• Urine o/p
• Correction of base deficit or lactate
• After 1st
24→48hr, change to D5% in 0.45% saline in patients un
able to tolerate enteral nutrition.
• Check renal function; if normal, add K to IVF

FORMULA FOR CALCULATING VOLUME OF
MAINTENANCE FLUIDS:
• It applies in absence of pre-
existing abnormalities.
• E.g. 60kg female receives
2300 mL of fluid daily:
 1000 mL for first 10kg BW
(10 kg × 100 mL/kg/day),
 500 mL for next 20kg BW
(10 kg × 50 mL/kg/day),
 800 mL for the last 40 kg
(40 kg × 20 mL/kg per day).
PATIENT WEIGHT I.V. FLUID
Give - ml/kg/day
first 0–10 kg 100
next 10–20 kg An additional 50
weight >20 kg An additional 20

• REFEEDING SYNDROME
• TUMOR LYSIS SYNDROME (TLS)
• Refeeding syndrome

Summary Points
1) Proper management of fluid and electrolytes facilitates crucial homeostasis.
This enables cardiovascular perfusion, organ system function, & cellular
mechanisms to respond to surgical illness.
2) Knowledge of compartmentalization of body fluids forms the basis for pathologic
shifts in fluid spaces in disease states.
A deficiency in functional EC fluid compartment requires resuscitation with isotonic
fluids in surgical & trauma patients.
3) Alterations in serum Na affects cellular function due to water shifts between IC
& EC spaces.
4) Different rates of compensation between respiratory and metabolic components
of acid-base homeostasis require frequent laboratory reassessment during therapy.

Summary Points
5) Alternative resuscitation fluids have limited clinical utility, except in specific
electrolyte abnormalities.
6) Most acute surgical illnesses are accompanied by some degree of volume
loss or redistribution.
7) Surgical patients with neurologic illness, cancer malnutrition or acute renal
failure require special attention to disease-specific abnormalities in fluid and
electrolyte status.

fluids & electrolyte, Fluid and electrolytes

More Related Content

Similar to fluids & electrolyte, Fluid and electrolytes (20)

More from HauwashituB1 (13)

Recently uploaded (20)

fluids & electrolyte, Fluid and electrolytes

Editor's Notes