THIS SEMINAR GIVES THE BASIC OVERVIEW THAT HOW YOU CAN MANAGE THE PATIENT WHO COMES TO YOU A FLUID AND ELECTROLYTE IMBALANCE . AND BASIC MECHANISM OF HOMEOSTASTIS

1. Presenter : Diwakar vasudev
PG 2nd
year

2.  Why do we need to drink water…
 Where does all this water go…
 Why we drink only this much of water…

3. 1 All chemical reactions occur in liquid medium.
2 It is crucial in regulating chemical and bioelectrical
distributions within cells.
3 Transports substances such as hormones and nutrients.
4 O2
transport from lungs to body cells.
5 CO2
transport in the opposite direction.
6 Dilutes toxic substances and waste products and transports
them to the kidneys and the liver.
7 Distributes heat around the body

4. Where does all this water go…
• Water constitutes an average 50 to 70% of the total body weight
Young males - 60% of total body weight
Older males – 52%
Young females – 50% of total body weight
Older females – 47%
• Variation of ±15% in both groups is normal
• Obese have 25 to 30% less body water than lean people.
• Infants 75 to 80%
- gradual physiological loss of body water
- 65% at one year of age

5. Functional Components of the Body
Fluid
The water of the body makes up 50%-70% of total body weight.
(TBW – 60%)
Intracellular Fluid –
40% of the body weight
67% total body water
Extracellular Fluid –
20% of the body weight
33% total body water
interstitial fluid
15% of BW
25% total body
water
Intravascular
5% of BW
8% total body
water

6. Fluid Distribution variations

7. In HOMOEOSTASIS
1. output = intake
2. Dynamic fluid equilibrium
at
a) Blood & interstitial fluid
level
b) Interstitial fluid and cell
level
3. Thirst & Satiety
4. Kidney fluid control
5. Hormonal regulation

8.  Compartmental exchange is regulated by osmotic and hydrostatic
pressures.
 Net leakage of fluid from the blood is picked up by lymphatic
vessels and returned to the bloodstream.
 Exchanges between interstitial and intracellular fluids are complex
due to the selective permeability of the cellular membranes.
 Two-way water flow is substantial.

9.  Ion fluxes are restricted and move selectively by active transport.
 Nutrients, respiratory gases, and wastes move unidirectionally.
 Plasma is the only fluid that circulates throughout the body and links
external and internal environments.
 Osmolalities of all body fluids are equal; changes in solute
concentrations are quickly followed by osmotic changes.

10. Driving force for intake ...thirst
Baroreceptors and Osmo receptors - detectors
↓ of 10% plasma volume or ↑ in plasma
osmolality by 1% & Hypernatremia
↓
dry mouth
↓
impulses sent to Thirst Control Centers in the
Hypothalamus which
also controls ADH release
↓
relay information to the Cerebral Cortex where thirst becomes a conscious
sensation

11. 1. Blood Pressure: An increase causes a greater rate of
filtration.
2. Increased Concentration of Salts or Glucose in
Blood : It results in decrease in urine output.
3. Decreased Plasma Protein: It decreases urine output.
4. Vasopressor Hormone: It prevents diuresis.
5. Water Loss from Other Sources: Urine volume varies
inversely with water lost from other systems eg. perspiration or
diarrhoea.
6. Diuretics : promotes diuresis.

12. ADH regualtion of urine output

13. Composition of Body Fluids
• Water is the universal solvent
• Solutes
– Electrolytes – inorganic salts, all acids and bases, and
some proteins.
– Non-electrolytes –Most non electrolytes are organic
molecules – glucose, lipids,
creatinine and urea
• Electrolytes have greater osmotic power than non
electrolytes
• Water moves according to osmotic gradients

15. The concentration of osmotically active particles is expressed in
‘osmoles’
 Osmolarity - mOsm/L of solution
 Osmolality - mOsm/Kg of water (solvent)
 Osmolality defines concentration of solution

16.  1) changes in volume (hypovolemia and
hypervolemia)
 2) changes in concentration (hyponatremia and
hypernatremia)
 3) changes in composition (acid base imbalances and
concentration changes in calcium, magnesium, and
potassium)

17. Hypovolemia
 Poor skin turgor
 Dry mucous membrane
 Dry axilla
 Flat neck vein
 Tachycardia
 Hypotension
 Weightloss
 Sunken eyes
Hypervolemia
Shortness of breath
at rest and exertion.
Hepatojuglar reflex
Ascites
Pitting edema
Weight gain

18. Hypovolemia
 Serum electrolyte
 SUN/Cr
 Hematocrit
 Urine electrolytes
and specific gravity
serum albumin
 24-hour urine for Cr
clearence
Hypervolumia
Serum electrolytes
Urine specific gravity
24-hour urine for Cr
clearence
Total protein
Cholesterol
Liver enzyme
bilirubin

19.  Goal of fluid maintenance therapy is to replace
fluids lost normally during the course of a day.
 Standard recommendations
 Hourly maintenance
 0-10 kg = 4ml/Kg
 11-20 kg= 2ml/kg
 >20 kg = 1ml/kg

20.  Normal level : 135-145mEq/L.
 It is the single most abundant electrolyte in the ECF
 Holds a central position in fluid and electrolyte balance
 It is the only electrolyte exerting significant osmotic
pressure
 Sodium salts:
◦ Account for 90-95% of all solutes in the ECF
◦ Contribute 280 mOsm of the total 300 mOsm ECF solute
concentration
 Regulated by dietary intake, aldosterone & kidneys

23.  Signs and symptoms of hyponatremia
 Confusion
 Lethargy
 Coma
 Nausea
 Vomiting
 Headache
 seizures

25.  Acute serum sodium <110-
115mEq/Lt
 Symptomatic – Seizures, Coma
 Rapid correction
 Till serum sodium 120-125mEq/Lt
If it is asymptomatic gradual
correction over 48 hrs.
If it is asymptomatic gradual
correction over 48 hrs.

26. Hypernatremia is defined as serum sodium greater
than 145 mEq/L.
SIGN AND SYMPTOMS OF
HYPERNATREMIA
 Confusion
 Lethargy
 Coma
 Seizures
 hyperreflexia

28. Correction of
Hypernatremia
Treat the underlying cause
Asymptomatic
5% dextrose in H2O
0.45% Saline preferable in
hyperosmolar diabetic coma.
Very large volumes of 5litres a
day may be needed to be given.
Symptomatic
Serum sodium > 160mEq/Lt
Serum osmolality > 350mOsm
Treatment
1. 0.9% saline to correct volume
deficit after volume restoration
changed to a hypotonic I.V.
fluid
2. Correct over a period of 48 hrs
as rapid correction may lead to
cerebral oedema.

29.  The rate of correction of plasma osmolality should
not exceed 2 mOsm/kg/h.
 Overly aggressive correction may lead to central
pontine myelinolysis.

30.  Major cation in intracellular compartments
◦ Regulates metabolic activities, necessary for glycogen
deposits in liver and skeletal muscle, transmission and
conduction of nerve impulses, normal cardiac conduction
and skeletal and smooth muscle contraction .
◦ Regulated by dietary intake and renal excretion.
◦ Normal level – 3.5-5.1mEq/L
Body conserves potassium poorly.
Increased urine output decreases serum K+

31.  Serum K > 3.5mEq/L
Signs and symptoms of hypokalemia
Neuromuscular
Muscle weakness, Paralysis,
Rhabdomyolysis, Hyporeflexia
Gastrointestinal
Paralytic ileus
Renal
Polyuria, Polydipsia
Cardiac
EKG findings: T-wave flattening/
inversion, U-wave, ST depression
Cardiac toxicity to digitalis
Causes of hypokalemia
Decreased dietary intake
Gastrointestinal losses
Renal losses
Cellular shift

32.  Treatment for hypokalemia initially is aimed at correcting the
existing metabolic abnormalities.
 Potassium chloride is administered at 10 mEq/L/h peripherally or 20
mEq/L/h centrally if EKG changes are present.Hypokalemia alone
rarely produces cardiac arrhythmias.
 Oral supplements : Increased intake of fresh fruits and vegetables
or potassium supplements of 20 to 40mmol daily.
 Patients with high renal losses (use potassium sparings diuretics
E.g. Spironolactone.)

33.  In emergency situation 20-40mEq / hr of potassium can be given
with frequent monitoring of cardiac status and serum potassium
levels.
 In non-emergency situations 10mEq of potassium / hr
 Use glucose free solutions as glucose drives potassium
intracellularly.
 In the absence of specific indications potassium should not be
given
1. To oliguric patients
2. During the first 24 hours following severe surgical stress
or trauma.
Remember

34. Hyperkalemia (K+
> 5.1mEq/L)
Signs and symptoms of
hyperkalemia
Neuromuscular
Weakness
Paresthesia
Flaccid paralysis
Cardiac
EKG findings: peaked T waves,
flattened P waves, prolonged PR,
widened QRS
Ventricular fibrillation
Cardiac arrest
Causes of hyperkalemia
Pseudohyperkalemia
Transcellular shift
Impaired renal excretion
Excessive intake
Blood transfusions

35. Helen
Giannakopoulos, DDS,
MDa, Lee Carrasco,
DMD, MDa,
Jason Alabakoff,
DDSa, Peter D. Quinn,
DMD, MDa,b,T
Table taken
from Oral
Maxillofacial
Surg Clin N Am
18 (2006) 7 – 17

36.  Identify and treat cause
 Specially check renal function
 10 – 20 mL intravenous 10% Calcium Chloride/ Calcium Gluconate
over 10 min in patients with ECG abnormalities
 50 mL 50% dextrose plus 10 units short acting insulin over 2-3min
 Monitor plasma glucose and K+ over next (30-60 min)
 Regular Salbutomol nebulizers
 Consider oral or rectal Ca+2
 Resonium (ion exchange resin)
 Haemodialysis for persistent hyperkalemia.

37. Stored in bone, plasma and body cells
◦ 90% in bones
◦ 1% in ECF
 In plasma, binds with albumin
◦ Necessary for bone and teeth formation, blood clotting,
hormone secretion, cell membrane integrity, cardiac
conduction, transmission of nerve impulses, and muscle
contraction
◦ Normal level – 4.5-5.5mEq/L or 8 – 11 mg%
◦ Regulated by
 Calitonin
 Paratharmone
 Calcitriol

38.  Signs and symptoms
 hypotension, larngeal spasm,
paresthesias, Pathological
fractures ,tetany
 (Chvostek’s and Trousseau’s
signs), anxiety, depression,
 and psychosis
 Etiology
 hypoalbuminemia,
hypoparathyroidism
 Vitamin D deficiency,
Pancreatitis, Alkalosis
 Massive blood transfusion with
citrate.
IIn adults who have normal renal function, calcium replacement is 1 g
(gluconate or chloride) in 50 mL dextrose 5% in water or normal
saline. Intravenous solutions should be infused for 30 minutes.

39.  Frequently symptom of underlying disease with excess bone
resorption and release of calcium
Hyperparathyroidism, malignant neoplastic disease, Paget’s
disease, Osteoporosis, prolonged immobization, acidosis
 S&S: anorexia, nausea and vomiting, weakness, kidney stones
 Diagnosis
 Radiographs show bone resorbtion
 Cardiac irregularities
 Treatments include hydration with normal saline, bisphosphonates,
calcitonin, glucocorticoids, and phosphate.

40.  Normal conc. 1.5 – 2.4 mg%
 Essential for proper functioning of enzyme systems
 Depletion characterised by neuromuscular & CNS
hyperactivity.

41.  HYPOMAGNESMIA
 Hypomagnesemia is greater than 1.8 mg/dL.
Signs and symptoms include arrhythmias,
prolonged PR and QT intervals on EKG,
hyperreflexia, fasciculations, and Chvostek’s and
Trousseau’s Trousseau’s signs.

42.  HYPERMAGNESMIA
 Hypermagnesemia is serum mangensium
greaterthan 2.3 mg/dL. Signs and symptoms
includerespiratory depression, hypotension,
cardiac arrest,nausea and vomiting, hyporeflexia,
and somnolence.
 Treatment for hypermagnesemia may include
calcium infusion, saline infusion with a loop
diuretic,or dialysis.

43.  Hypophosphatemia is serum
phosphate less than
 2.5 mg/dL; however,
symptomatic hypophosphatemia
 usually is less than 1 mg/dL.
Signs and
 symptoms of hypophosphatemia
include lethargy,
 hypotension, irritability, cardiac
arrhythmias, and
 skeletal demineralization.
Treatment

44.  Hyperphosphatemia is defined as serum phosphate greater than 5
mg/dL.
 Pruritus is the only remarkable symptom of hyperphosphatemia.
 Treatment includes dietary phosphate restriction, phosphate binders
(calcium acetate or carbonate), hydration (to promote excretion), or
D50 and insulin to shift phophate into cells.

45.  Ionic composition very different
 Total ionic concentration very similar
 Total osmotic concentrations virtually identical
Osmolarity is identical in all body fluid compartments

46.  Renal insufficiency, Chronic heart faliure
 Iatrogenic
 Cirrhosis
 Drugs – NSAIDS, Mineralocorticiods
 ECF is diluted – sodium content is normal but excess water is
present called as Hypotonic Hydration
 The resulting hyponatremia promotes net osmosis into tissue cells,
causing swelling.
 These events must be quickly reversed to prevent severe metabolic
disturbances, particularly in neurons.

47. ECF Deficit
CAUSES
1. Loss of GI fluids due to:
a. Vomiting
b. Diarrhea
c. Nasogastric suction
d. Fistular drainage
2. Soft tissue injuries and infections
3. Intraabdominal and Intraperitoneal inflammatory
processes
4. Burns
5. Insensible losses
6. Sweat

48. Clinical Evaluation
Changes in body weight should be recorded accurately
and repeatedly on a day to day basis….
Weight loss > 300 to 500gms per day indicate
dehydration secondary to decreased fluid intake and
/ or increased water losses.
Water loss Degree of Dehydration
4% of body wt Mild
6% “ “ Moderate
8% “ “ Severe

49. Principles of Fluid Therapy
Whenever fluid therapy is contemplated in a patient, the
following basic questions must be considered….
1. Does the patient need fluid..?
2. Which fluid would be most suitable..?
3. How much fluid is needed..?
4. At what rate..?
5. Which route is to be used..?
6. What are the likely complications..?

50. Crystalliod Colloid
Intravascular persistance Poor Good
Haemodynamic stabilisation
Transient
t1/2 ~ 30 mins
Prolonged
t1/2 ~ 90 mins
Required infusion volume
Large
Ratio 3:1 to loss
Moderate
Ratio 1:1 to loss
Risk of tissue oedema Obvious Insignificant
Enhancement of capillary perfusion Poor Good
Risk of anaphylaxis Nil Low to moderate
Plasma colloid osmotic pressure Reduced Maintained
Inexpensive Expensive

51. When blood loss is mild (less than 15% of blood volume), no volume
resuscitation is necessary.
With moderate to severe blood loss, the vascular space must be filled
to support cardiac output.
The only effective management of hypovolumia is volume resuscitation.
CRYSTALLOIDS
COLLOIDS

52. Colloids are large molecules that do not diffuse across membranes readily.
Colloids are efficient plasma expanders.

53. Disadvantages of Colloidal administration
It may result in hypotension secondary to decreased
systemic vascular resistance.
The administration of hetastarch and dextran in large
volumes can result in dilutional coagulopathies.
Hetastarch, when administered in greater than 1000 mL (in
a 70-kg patient), can precipitate a decrease in factor VIII.
Dextran can decrease platelet adhesiveness and may
cause an anaphylactoid or anaphylactic reaction.
In addition, dextran also facilitates the agglutination of red
blood cells

56. Method for determining resuscitation
volume sequence
1. Estimate normal blood volume
2. Estimate percent loss of blood volume
3. Calculate volume deficit
4. Determine resuscitation volume
The allowable blood loss should be calculated preoperatively for patients in
whom severe bleeding may be expected.
ABL= estimated blood volume X (Hi – Hf)
Hi,
Where estimated blood volume =weight (kg) X average blood volume,
Hi = initial hematocrit,
Hf = the final acceptable hematocrit.

58. AMERICAN RED CROSS GUIDELINES FOR BLOOD COMPONENTS
ADMINSTRATION

59. TRANSFUSION REACTIONS
Febrile
Allergic
Hemolytic
COAGULATION DISORDERS
Dilutional thrombocytopenia
Factors V and VIII deficency
DIC
METABOLIC ABNORMALITY
Hyperkalemia
Hypocalcemia
Metabolic Alkalosis
Hypothermia
Acute lung injuery
Microaggregates

61. Intraoperative blood salvage involves the collection, washing, and
storage of red blood cells by a semiautomated system.
The hematocrit of salvaged blood is between 50% and 60%, and
the pH is alkaline.
Contraindications to intraoperative blood salvage include blood-
borne diseases, malignancy, and contamination.
Hemodilution involves the removal of arterial or venous blood
preoperatively, followed by plasma volume restoration with
crystalloid or colloid fluids.
The blood then is stored in the operating room and transfused to the
patient after cessation of bleeding.
This procedure may be used for surgeries in which intraoperative
blood loss of 2 or more units is anticipated.

62. Blood Products do not increase blood flow adequately and in some
cases impede flow as a result of incresed viscosity.
Therefore crystalloid and colloids fluids should be the initial management
strategy for volume resuscitation in acute hemorrhage.
Favorable clinical response include the following points
CPV =15 mm Hg
PCWP =10-12mm Hg
Adequate HR
Cardiac index = 3L/min/m2
Urine output greater than = 1ml/kg/h

63.  As in normal health - 0ral Route.
-However when rapid correction of hypovolaemia
and other electrolyte abnormalities indicated i.v.
route provides a quick access to circulation.
-Other routes of parenteral therapy include
Subcutaneous
Per Rectal

64.  The goal of fluid management in major burn
injuries is to maintain the tissue perfusion in the
early phase of burn shock,
 in which hypovolemia finally occurs due to steady
fluid extravasation from the intravascular
compartment.

65.  Burn injuries of less than 20% are associated with
minimal fluid shifts and can generally be
resuscitated with oral hydration, except in cases of
facial, hand and genital burns, as well as burns in
children and the elderly.
 Current recommendations are to initiate formal
intravascular fluid resuscitation when the surface
area burned is greater than 20%.

66.  The most commonly used formulas are the
 Parkland,
 Brooke,
 Evans and
 Monafo’s formulas.

67.  Initial 24 hours: Ringer’s lactated (RL) solution 4 ml/kg/% burn for
adults and 3 ml/kg/% burn for children.
◦ 4 ml/kg/hour for children weighing 0–10 kg
◦ 40 ml/hour +2 ml/hour for children weighing 10–20 kg
◦ 60 ml/hour + 1 ml/kg/hour for children weighing 20 kg or higher
 This formula recommends no colloid in the initial 24 hours.
 Next 24 hours: Colloids given as 20–60% of calculated plasma
volume. No crystalloids. Glucose in water is added in amounts
required to maintain a urinary output of 0.5–1 ml/hour in adults and
1 ml/hour in children.

68.  Initial 24 hours: RL solution 1.5 ml/kg/% burn plus colloids 0.5 ml/kg/
% burn plus 2000 ml glucose in water
 Next 24 hours:
 RL 0.5 ml/kg/% burn, colloids 0.25 ml/kg/% burn and the same
amount of glucose in water as in the first 24 hours
Evans formula (1952)
First 24 hours: Crystalloids 1 ml/kg/% burn plus colloids at 1 ml/kg/%
burn plus 2000 ml glucose in water
Next 24 hours: Crystalloids at 0.5 ml/kg/% burn, colloids at 0.5 ml/kg/%
burn and the same amount of glucose in water as in the first 24 hours

69. Monafo formula
 Monafo recommends using a solution containing
250 mEq Na, 150 mEq lactate and 100 mEq Cl.
The amount is adjusted according to the urine
output. In the following 24 hours, the solution is
titrated with 1/3 normal saline according to urinary
output.

70.  The ideal burn resuscitation is the one that
effectively restores plasma volume, with no adverse
effects.
Isotonic crystalloids,
 hypertonic solutions
 Colloids
 have been used for this purpose, but every solution
has its advantages and disadvantages.
 None of them is ideal, and none is superior to any of
the others.

76.  In case of Shock early diagnosis and aggressive
treatment of all physiological derangements
should be achieved to prevent irrevesible state.
 Surgical management and medical management
of oral and maxillofacial surgery patients are both
intertwined intimately .
 Oral and maxillofacial surgeons should have
thorough understanding of the surgical and
medical issues that face patients.

77. 1. Foncea text of maxillofacial trauma chapter Shock
management.
2. Human Physiology – A. K. Jain
3. Human physiology – guyton and hall
4. Oral & MaxilloFacial Sugery Clinics of North America –
HarryDym.
5. Fluid and electrolyte management and blood product usage.
Helen G Clinics of north amercia 2006.
6. Fluid and electrolyte management in burns patient.
Indian J Plast Surg. 2010 Sep

78.  THANKYOU………..