The document discusses the importance of water in the human body, detailing its role in various chemical and physiological processes, and the distribution of body fluids. It outlines the consequences of variations in fluid balance, including symptoms of hypovolemia and hypervolemia, as well as the regulation of electrolytes such as sodium, potassium, and calcium. Additionally, it emphasizes principles of fluid therapy and considerations for fluid resuscitation during medical treatment.
Introduces the presenter and poses questions about water consumption and its significance.
Details the importance of water in chemical reactions, nutrient transport, body weight, and variations across demographics.
Describes body fluid distribution, intracellular and extracellular fluid compartments, and the dynamics of fluid exchange. Explains homeostasis, kidney fluid control, osmotic pressures, and movement of fluids and ions across compartments.
Discusses the physiological detection of thirst, influence on ADH release, and factors affecting urine output.
Covers ADH regulation, normal fluid composition, body fluid abnormalities, and considerations for fluid maintenance.
Details sodium management, normal range, hyponatremia and hypernatremia signs, and correction strategies.
Discusses potassium and magnesium imbalances, their physiological impacts, and treatment options.
Explains hypophosphatemia and hyperphosphatemia, related symptoms, and treatment methods.
Explores the osmolarity of body fluids, causes of fluid deficits, and the significance of hydration levels.
Outlines key questions for fluid therapy, crystalloid vs. colloid considerations, and fluid resuscitation strategies.
Discusses assessment for loss, crystalloid use, formulas for burn resuscitation, and fluid strategies. Addresses fluid management in burn injuries, the importance of early diagnosis in shock, and treatment protocols.
Presents the references used in the presentation and concludes with a thank you.
Why dowe need to drink water…
Where does all this water go…
Why we drink only this much of water…
3.
1 All chemicalreactions 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 allthis 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 ofthe 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
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 exchangeis 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 fluxesare 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 forintake ...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.
Composition of BodyFluids
• 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 ofosmotically active particles is expressed in
‘osmoles’
Osmolarity - mOsm/L of solution
Osmolality - mOsm/Kg of water (solvent)
Osmolality defines concentration of solution
16.
1) changesin 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 skinturgor
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 offluid 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 andsymptoms of hyponatremia
Confusion
Lethargy
Coma
Nausea
Vomiting
Headache
seizures
25.
Acute serumsodium <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 definedas serum sodium greater
than 145 mEq/L.
SIGN AND SYMPTOMS OF
HYPERNATREMIA
Confusion
Lethargy
Coma
Seizures
hyperreflexia
28.
Correction of
Hypernatremia
Treat theunderlying 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 rateof correction of plasma osmolality should
not exceed 2 mOsm/kg/h.
Overly aggressive correction may lead to central
pontine myelinolysis.
30.
Major cationin 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 forhypokalemia 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 emergencysituation 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
Helen
Giannakopoulos, DDS,
MDa, LeeCarrasco,
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 andtreat 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 andsymptoms
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 symptomof 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
Hypomagnesemiais 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
Hypermagnesemiais 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 isserum
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 isdefined 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 compositionvery 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. Lossof 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 inbody 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 FluidTherapy
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 persistancePoor 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 lossis 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 largemolecules that do not diffuse across membranes readily.
Colloids are efficient plasma expanders.
53.
Disadvantages of Colloidaladministration
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 determiningresuscitation
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.
Intraoperative blood salvageinvolves 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 donot 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 innormal 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 goalof 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 injuriesof 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 mostcommonly used formulas are the
Parkland,
Brooke,
Evans and
Monafo’s formulas.
67.
Initial 24hours: 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 24hours: 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
Monaforecommends 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 idealburn 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 caseof 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 textof 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