Fluid and

Electrolytes
Disturbances
Daniela Filipescu
Prof. of Anaesthesia & Intensive Care
Medicine

Fluid and Electrolytes

60% of body consists of fluid
Intracellular space [2/3]
Extracellular space [1/3]
Electrolytes are active ions:
positively and negatively charged

Extracellular Fluid (ECF)

20% of total body
weight
Intravascular
Blood plasma

Interstitial fluid
Between cells
Cerebrospinal fluid
Intraocular fluid

Copyright 2007, 2006, 2001, 1994 by Mosby, Inc., an affiliate of Elsevier Inc.

Aging and Distribution of Body

Fluids
Water is the main component of
body mass
Adults
50% to 60% of total body weight

Newborn
About 80% of total body weight

Childhood
60% to 65% of total body weight

Further declines with age

Copyright 2007, 2006, 2001, 1994 by Mosby, Inc., an affiliate of Elsevier Inc.

Necesar lichidian zilnic

inlocuirea pierderilor (adult)

Ci fiziologice de eliminare a apei din organism

Total

25-35 ml/kg/24 ore

2000 ml/24 ore

Rinichi

15-20 ml/kg/24 ore

1000 ml/24 ore

Cutanat

8 ml/kg/24 ore

500 ml/24 ore

Plmn

7 ml/ kg/24 ore

400 ml/24 ore

Scaun

1-2 ml/kg/24 ore

100 ml/24 ore

Necesar minim lichidian recomandat

greutate (kg)

ml/kg/ora

ml/kg/zi

1-10

120-150

11-20

50-100

> 20

25-40

> 40

25-40

Necesar perioperator de lichide

solutii saline
lichid de mentinere + inlocuire volum pierdut +
4 ml/kg - trauma minima
6 ml/kg - trauma moderata
8 ml/kg - trauma mare

Distributia lichidelor perfuzate

cresterea de volum (V) estimata =
V infuzat x V plasmatic normal/ V de distributie
Vi = V estimata x Vd/Vp
Exemplu:
necesar de sol glucoza 5% sau ser fiziologic
pentru a creste volemia cu 2 L
G 5% => 2 L x 42 L / 3 L = 28 L
NaCl 0,9% => 2 L x 14 L / 3 L = 9,3 L

Compoziia soluiilor volemice n comparaie cu plasma (mmol/l)

Na+

Cl-

Plasma
(albumina)

140

NaCl 0,9 %

K+

Mg++

Ca++

Tampon

pH

102 3.7

0.8.

1.2

HCO324

7,4

154

154 -

5,7

Sterofundin
iso

145

127 4.5

2.5

Acetat
24

5.15.9

Ringer lactat

131

109 5

Lactat
28

6,4

Solutie
gelatina
Gelofusin

154

120 -

7,17,7

Solutie
gelatina
Gelaspan

151

103 4

Acetat
24

Soluii de
amidon

154

154

4-7

Membrane Permeability
Most cell membranes are relatively
highly permeable to water
Membranes are semi-permeable to
certain anions and cations
Difference in permeability between
water and dissolved solutes

Compoziia ionic a spaiilor hidrice

Plasma Lichid
interstiial

Lichid
intracelular

Sodiu (mmol/l)

140

145

10

Potasiu (mmol/l)

3,7

3,8

155

Calciu ionizat (mmol/l)

1,2

1,2

<0,01

Magneziu (mmol/l)

0,8

0,8

10

Fosfat (mmol/l)

1,1

1,0

105

Clor (mmol/l)

102

115

Bicarbonat (mmol/l)

28

30

10

Cationi

Anioni

Diffusion
Due to constant motion of atoms,
molecules, ions in solution
Passive process
Moves particles from area of higher
concentration to area of lower
concentration

Concentration gradient
Copyright 2007, 2006, 2001, 1994 by Mosby, Inc., an affiliate of Elsevier Inc.

Filtration across Capillary

Wall

Starling equation

Copyright 2007, 2006, 2001, 1994 by Mosby, Inc., an affiliate of Elsevier Inc.

Water Movement Between ICF and

ECF
Osmosis
Flow of fluid across a semi-permeable
membrane from a lower solute
concentration to a higher solute
concentration
Osmotic pressure determined by:
Number and molecular weights
Permeability of membrane
Copyright 2007, 2006, 2001, 1994 by Mosby, Inc., an affiliate of Elsevier Inc.

Osmosis

Copyright 2007, 2006, 2001, 1994 by Mosby, Inc., an affiliate of Elsevier Inc.

Electrolyte Balance
Potassium is the chief intracellular cation
and sodium the chief extracellular cation
Because the osmotic pressure of the
interstitial space and the ICF are
generally equal, water typically does not
enter or leave the cell

Na+

K+

Electrolyte Balance

A change in the concentration of

either electrolyte will cause water to
move into or out of the cell via
osmosis
A drop in sodium will cause fluid to
enter the cell

Click to see
animation

H2O Na+

Na

H2O

Na

K+
H2O

Na+
H2O

H2O

K+

H2

K
O

H2O

K+

H2O

Plasma osmolality
(2 x Na + G/18 + U/2,8) =
290 mOsm/kg H2O
Tonicity = (2 x Na + G/18 ) =
285 mOsm/kg H2O

Solutions
Hypertonic solution
Hypotonic solution
Isotonic solution

Hyponatremia

Definition
Epidemiology
Physiology
Pathophysiology
Types
Clinical Manifestations
Diagnosis
Treatment

Hyponatremia
Definition:
serum sodium concentration <135 mmol/L
represents a relative excess of water in relation to sodium.

Hyponatremia
We define mild hyponatraemia as a biochemical
finding of a serum sodium concentration between 130
and 135 mmol/L as measured by ion specific electrode.
We define moderate hyponatraemia as a biochemical
finding of a serum sodium concentration between 125
and 129 mmol/L as measured by ion specific electrode.
We define profound hyponatraemia as a biochemical
finding of a serum sodium concentration<125 mmol/L
as measured by ion specific electrode.

Spasovski G et al. ICM 2014:320

Hyponatremia
We define acute hyponatraemia as
hyponatraemia that is documented to exist
< 48 h.
We define chronic hyponatraemia as
hyponatraemia that is documented to exist
for at least 48 h.
If the hyponatraemia cannot be classified,
we consider it being chronic, unless there
is clinical or anamnestic evidence of the
contrary
Spasovski G et al. ICM 2014:320

Hyponatremia
We define moderately symptomatic
hyponatraemia as any biochemical
degree of hyponatraemia in the presence
of moderately severe symptoms of
hyponatraemia
We define severely symptomatic
hyponatraemia as any biochemical
degree of hyponatraemia in the presence
of severe symptoms of hyponatraemia
Spasovski G et al. ICM 2014:320

Symptoms
Moderately severe
Nausea without vomiting
Confusion
Headache
Severe
Vomiting
Cardio-respiratory distress
Abnormal and deep somnolence
Seizures
Coma (Glasgow Coma Scale < 8)
Spasovski G et al. ICM 2014:320

Hyponatremia
Epidemiology:
Frequency
Hyponatremia is the most common
electrolyte disorder
incidence of approximately 1%
surgical ward, approximately 4.4%
30% of patients treated in the intensive care
unit

Drugs and conditions

associated with acute
hyponatraemia
Postoperative phase
Post-resection of the prostate, post-resection of
endoscopic uterine surgery
Polydipsia
Exercise
Recent thiazides prescription
3,4-Methyleendioxymethamfetamine (MDMA, XTC)
Colonoscopy preparation
Cyclophosphamide (intravenous)
Oxytocin
Recently started desmopressin therapy
Recently started terlipressin, vasopressin
Spasovski G et al. ICM 2014:320

Hyponatremia
Types
Hypovolemic hyponatremia
Euvolemic hyponatremia
Hypervolemic hyponatremia
Redistributive hyponatremia
Pseudohyponatremia

Redistributive
hyponatremia
Water shifts from the intracellular to the
extracellular compartment, with a
resultant dilution of sodium
The TBW and total body sodium are
unchanged
this condition occurs with hyperglycemia
administration of mannitol

 We recommend excluding hyperglycaemic

hyponatraemia by measuring the serum
glucose concentration and correcting the
measured serum sodium concentration
for the serum glucose concentration if the
latter is increased. (1D)
Hyponatraemia with a measured
osmolality <275 mOsm/kg always reflects
hypotonic hyponatraemia. (not graded)

Spasovski G et al. ICM 2014:320

Pseudohyponatremia

The aqueous phase is diluted by

excessive solutes (proteins or lipids)
The TBW and total body sodium are
unchanged.
hypertriglyceridemia
multiple myeloma

Hypovolemic
hyponatremia
develops as sodium and
free water are lost and/or
replaced by
inappropriately hypotonic
fluids
Sodium can be lost
through renal or nonrenal routes
www.grouptrails.com/.../0-Beat-Dehydration.jpg

Hypovolemic
hyponatremia
Nonrenal loss
GI losses
Vomiting, Diarrhea, fistulas, pancreatitis

Excessive sweating
Third spacing of fluids

www.jupiterimages.com

ascites, peritonitis, pancreatitis, and burns

Cerebral salt-wasting syndrome

traumatic brain injury, aneurysmal
subarachnoid hemorrhage, and intracranial
surgery
Must distinguish from SIADH

Compoziia secreiilor tubului digestiv

Lichid/
compoziie

Volum
ml/zi

Sodiu
mmol/l

Potasiu
mmol/l

Clor
mmol/l

Bicarbonat
mmol/l

Suc gastric

10002500

60-100

10-20

100-130

Suc pancreatic

300-800 135-145

5-10

70-90

40-120

Bila

300-600

140

5-10

90-130

30-70

Lichid jejunal

20004000

120-140

5-10

90-140

30-40

Lichid ileal

10002000

80-150

2-8

45-140

30

60

30

40

5002000

2-30

20-30

8-35

0-30

Lichid colonic
Saliva

Insensible fluid loss through burned wounds after 24 hours:

ml/hours= (25+% surface burned area) x body surface area

Hypovolemic
hyponatremia
Renal Loss
Diuretics

www.ct-angiogram.com/images/renalCTangiogram2.jpg

Euvolemic hyponatremia
Normal sodium stores and a total body
excess of free water
psychogenic polydipsia, often in psychiatric patients
administration of hypotonic intravenous or irrigation
fluids in the immediate postoperative period
Infants who may have been given inappropriate
amounts of free water
bowel preparation before colonoscopy or colorectal
surgery
SIADH

SIADH
Caused by various etiologies
CNS disease tumor, infection, CVA, SAH
Pulmonary disease TB, pneumonia, sarcoidosis,
PPV
Cancer Lung, pancreas, thymoma, ovary,
lymphoma
Drugs NSAIDs, SSRIs, antipsychotics, diuretics,
opiates
Surgery - Postoperative
Idiopathic most common

SIADH
essential criteria
Serum osmolality <275 mOsm/kg
Clinical euvolemia
Absence of adrenal, thyroid, pituitary or renal
insufficiency
No recent use of diuretic agents
Urine osmolality greater than 100 mOsm/kg
though generally greater than 400-500 mOsm/kg
in setting of low serum osmolality (inappropriate)
Urine sodium concentration > 30 mmol/L with
normal dietary salt and water intake

Supplemental criteria
Serum uric acid<0.24 mmol/L (<4
mg/dL)
Serum urea<3.6 mmol/L (<21.6 mg/dL)
Failure to correct hyponatraemia after
0.9 % saline infusion
Fractional sodium excretion> 0.5 %
Fractional urea excretion> 55 %
Fractional uric acid excretion> 12 %
Correction of hyponatraemia through
fluid restriction

Hypervolemic
hyponatremia
Total body sodium increases, and
TBW increases to a greater extent
Can be renal or non-renal
acute or chronic renal failure
dysfunctional kidneys are unable to excrete
the ingested sodium load

cirrhosis, congestive heart failure, or

nephrotic syndrome

Prognostic implications
of hyponatremia in HF
142 pts
72.1 11.6 years
Worsening HF NYHA III-IV

Na (mEq/l)

136

135131

130

In hospital mortality
1.8
(%)

3.4

6.4

60 day mortality (%) 4.7

7.2

13.7

60 day
27.2
29.1
39.3
rehospitalization (%) Vaitsis J et al. Crit Care 2009: abstr 456

Hyponatremia
Clinical manifestations
- Fluid deficit or excess
- Altered mental status

Fluid Volume Deficit

Clinical manifestations
- Acute weight loss
- Decreased skin turgor

Fluid Volume Deficit

-

Oliguria
Concentrated urine
Postural hypotension
Weak, rapid, heart rate
Flattened neck veins
Increased temperature
Decreased central venous pressure

Fluid Volume Excess

Edema

Fluid Volume Excess

Other clinical manifestations
distended neck veins, crackles,
increased blood pressure, increased
weight

Hypervolemia
Hypovolemia
peripheral and
presacral edema
pulmonary edema
jugular venous
distension
hypertension
decr. hct,
decr. serum prot
decr. bun/cr
UNa no help

poor skin turgor

dry mucous
membranes
flat neck veins
hypotension
incr. Hct
incr. serum prot.
Incr bun/cr ratio >20:1
UNa < 20 meq/l

Cerebral symptoms of
hyponatremia
Nausea and vomiting
Headache
Decreased consciousness
Lethargy
Confusion
Coma
Seizures
Muscle weakness, cramps or spasms
Respiratory distress // arrest
Death (5-50%)
Overgaard-Steenson C. Acta Anesthesiol Scand 2010:1-10
Adrogue HJ & Madias NE. NEJM 2000;342:1581-1589

Clinical manifestations
Hyponatremia 126-134 mmol/L
Alterations of cognitive function
Gait stability
Falls
Osteoporosis
Fractures and inpatient mortality
Sterns RH et al. Curr Opin Nephrol Hypertens 2010:493

Workup for hyponatremia

3 mandatory lab tests
Serum Osmolality
Urine Osmolality
Urine Sodium Concentration

Additional labs depending on clinical

suspicion
TSH, cortisol (Hypothryoidism or Adrenal
insufficiency)
Albumin, BNP, triglycerides
(psuedohyponatremia, cirrhosis, MM)

 We recommend interpreting urine osmolality of a spot

urine sample as a first step. (1D)
If urine osmolality < 100 mOsm/kg, we recommend
accepting relative excess water intake as a cause of
the hypotonic hyponatraemia. (1D)
If urine osmolality>100 mOsm/kg, we recommend
interpreting the urine sodium concentration on a spot
urine sample taken simultaneously with a blood
sample. (1D)
If urine sodium concentration < 30 mmol/L, we
suggest accepting low effective arterial volume as a
cause of the hypotonic hyponatraemia. (2D)
If urine sodium concentration >30 mmol/L, we
suggest assessing extracellular fluid status and use of
diuretics to further differentiate likely causes of the
hyponatraemia.(2D)
We suggest against measuring vasopressin for
confirming the diagnosis of SIADH. (2D)
Spasovski G et al. ICM 2014:320

Treatment of
hyponatremia
Treatment is based on symptoms
Severe symptoms = Hypertonic Saline
Mild or no symptoms = Fluid restriction

Hyponatremia
Symptomatic
1st step is to calculate the total body water
total body water (TBW) = 0.6 body weight
Sodium deficit = TBW x (desired Na actual Na)
Here comes the Math!!!
estimate SNa change on the basis of the amount of
Na in the infusate
SNa = {[Na + K]inf SNa} (TBW + 1)
OH MY GOD!!!!!!!!!!!!!!!!!!

Adrogue & Madias NEJM 2000; 342 (21):1581-9

Hyponatremia

IV Fluids

One liter of Lactated Ringer's Solution

contains:

130 mEq of sodium ion = 130 mmol/L

109 mEq of chloride ion = 109 mmol/L
28 mEq of lactate = 28 mmol/L
4 mEq of potassium ion = 4 mmol/L
3 mEq of calcium ion = 1.5 mmol/L

One liter of Normal Saline contains:

154 mEq/L of Na+ and Cl

One liter of 3% saline contains:

514 mEq/L of Na+ and Cl

Hyponatraemia with severe

symptoms
First hour management, regardless of whether
hyponatraemia is acute or chronic
We recommend prompt intravenous infusion of 150 mL
3 % hypertonic saline or equivalent over 20 min. (1D)
We suggest checking the serum sodium concentration
after 20 min while repeating an infusion of 150 mL 3 %
hypertonic saline or equivalent over the next 20 min.(2D)
We suggest repeating therapeutic recommendations
twice or until a target of 5 mmol/L increase in serum
sodium
concentration is achieved. (2D)
Spasovski G et al. ICM 2014:320

1. Follow up management in case of improvement of symptoms

after a 5 mmol/L increase in serum sodium concentration in the
first hour, regardless of whether hyponatraemia is acute or
chronic
We recommend stopping the infusion of hypertonic saline.
(1D)
We recommend keeping the intravenous line open by
infusing the smallest feasible volume of 0.9 % saline until
cause-specific treatment is started. (1D)
We recommend starting a diagnosis specific treatment if
available, aiming at least to stabilize sodium concentration.
(1D)
We recommend limiting the increase in serum sodium
concentration to a total of 10 mmol/L during the first 24 h
and an additional 8 mmol/L during every 24 h thereafter until
the serum sodium concentration reaches 130 mmol/L. (1D)
We suggest checking the serum sodium concentration after 6
and 12 h, and daily afterwards until the serum sodium
concentration has stabilised under stable treatment. (2D)

Spasovski G et al. ICM 2014:320

2. Follow up management in case of no improvement of

symptoms after a 5 mmol/L increase in serum sodium
concentration in the first hour, regardless of whether
the hyponatraemia is acute or chronic
We recommend continuing an intravenous infusion of
3 % hypertonic saline or equivalent aiming for an
additional 1 mmol/L/h increase in serum sodium
concentration (1D).
We recommend stopping the infusion of 3 %
hypertonic saline or equivalent when the symptoms
improve, the serum sodium concentration increases
10 mmol/L in total or the serum sodium concentration
reaches 130 mmol/L,whichever occurs first (1D).
We recommend additional diagnostic exploration for
other causes of the symptoms than hyponatraemia
(1D).
We suggest checking the serum sodium concentration
every 4 h as long as an intravenous infusion of 3 %
hypertonic saline or equivalent is continued (2D).

Spasovski G et al. ICM 2014:320

What if the sodium increases

too fast?
The dreaded complication of increasing
sodium too fast is Central Pontine
Myelinolysis which is a form of osmotic
demyelination
Symptoms generally occur 2-6 days after
elevation of sodium and usually either
irreversible or only partially reversible
Symptoms include: dysarthria, dysphagia,
paraparesis, quadriparesis, lethargy, coma
or even seizures

Effects of hyponatremia on the brain

and adaptive responses

Adrogue HJ et al NEJM 2000; 342 (21):1581-9

Central pontine myelinolysis

Pietrini V et al. Neurol Sci (2010) 31:227230

Hyponatraemia with
moderately severe symptoms

We recommend starting prompt diagnostic assessment. (1D)

Stop, if possible, medications and other factors that can contribute to
or provoke the hyponatraemia. (not graded)
We recommend cause-specific treatment. (1D)
We suggest immediate treatment with a single intravenous infusion of
150 mL 3 % hypertonic saline or equivalent over 20 min. (2D)
We suggest aiming for a 5 mmol/L/24 h increase in serum sodium
concentration. (2D)
We suggest limiting the increase in serum sodium concentration to 10
mmol/L in the first 24 h and 8 mmol/L during every 24 h thereafter,
until a serum sodium concentration of 130 mmol/L is reached. (2D)
We suggest checking the serum sodium concentration after one, 6 and
12 h. (2D)
We suggest additional diagnostic exploration for other causes of the
symptoms if the symptoms do not improve with an increase in serum
sodium concentration. (2D)
We suggest considering to manage the patient as in severely
symptomatic hyponatraemia if the serum sodium concentration further
decreases despite treating the underlying diagnosis. (2D)

Spasovski G et al. ICM 2014:320

Acute hyponatraemia without

severe
or moderately severe
Make sure that the
serum sodium concentration has
symptoms
been measured using the same technique as used for

the previous measurement and that no administrative

errors in sample handling have occurred. (not graded)
If possible, stop fluids, medications and other factors
that can contribute to or provoke the hyponatraemia.
(not graded)
We recommend starting prompt diagnostic
assessment. (1D)
We recommend cause-specific treatment. (1D)
If the acute decrease in serum sodium concentration
exceeds 10 mmol/L, we suggest a single intravenous
infusion of 150 mL 3 % hypertonic saline or equivalent
over 20 min. (2D)
We suggest checking the serum sodium concentration
after 4 h, using the same technique
as used for the
Spasovski G et al. ICM 2014:320
previous measurement. (2D)

Chronic hyponatraemia without

severe
or moderately severe symptoms

Stop non-essential fluids, medications and other factors

that can contribute to or provoke the hyponatraemia. (not
graded)
We recommend cause-specific treatment. (1D)
In mild hyponatraemia, we suggest against treatment with the
sole aim of increasing the serum sodium concentration. (2C)
In moderate or profound hyponatraemia, we recommend
avoiding an increase in serum sodium concentration of >10
mmol/L during the first 24 h and> 8 mmol/L during every 24 h
thereafter. (1D)
In moderate or profound hyponatraemia, we suggest checking
the serum sodium concentration every 6 h until the serum
sodium concentration has stabilised under stable treatment.
(2D)
In case of unresolved hyponatraemia, reconsider the
diagnostic algorithm and ask for expert advice. (not graded)
Spasovski G et al. ICM 2014:320

Hyponatremia
SIADH
Water restriction
0.5-1 liter/day

Demeclocycline
Inhibits the effects of ADH
Onset of action may require up to one week

Vasopressin receptor
antagonists
AQUARETICS
Excretion of electrolyte-free water
Beneficial impact on serum Na
Lack of evidence on long term beneficial
effects
Absence of disease-modifying properties
Risk of overcorrection
Cost
Kazory A. Clin Cardiol 2010:322-329

Practical therapeutic
approach
to hyponatremia in HF
Establish the diagnosis
Limit Na-free fluid intake
Prescribe iv.loop diuretics saline solution
Prescribe vasopressin receptor antagonist
Institute UF/renal replacement therapy

Kazory A. Clin Cardiol 2010:322-329

Paterns P et al. Am J Cardiol 2009;103:93-102

Practical therapeutic
approach to symptomatic
hyponatremia in HF
Saline solution - Hypertonic?
No worsening of pulmonary congestion
Increase in urine output
Reduction in serum blood urea nitrogen
No change in HF functional class
Lower readmission rate
Lower hospital mortality
Kazory A. Clin Cardiol 2010:322-329

ULTRAFILTRATION

Summary of Hyponatremia
Hyponatremia has variety of causes
Treatment is based on symptoms
Severe symptoms = Hypertonic Saline
Mild or no symptoms = Fluid restriction

Overcorrection, more than 10 mmol increase

in 24 hours must be avoided with monitoring
Serum Osmolality, Urine Osmolality and
Urine sodium concentration are initial tests
to order

Hypernatremia
Normal range for blood levels of sodium
is
135 - 145 mmol/liter
Hypernatremia refers to an elevated
serum sodium level (145 -150
mmol/liter)

Na+

CAUSES OF
HYPERNATREMIA
Most
cases are due to water deficit
due to loss or inadequate intake

1) Water loss
Insensible and sweat losses
GI losses
Diabetes Insipidus (both central and nephrogenic)
Osmotic diuresis
Hypothalamic lesions which affect thirst function
tumors, granulomatous diseases or vascular
disease

CAUSES OF
HYPERNATREMIA
2) Sodium ion overload

Hypernatremia
Pathophysiology
- Fluid deprivation in patients who cannot
perceive, respond to, or communicate
their thirst
- Most often affects very old, very young,
and cognitively impaired patients
- Infants without access to water or
increased insensible water loss can be
very susceptible to hypernatremia

CNS reaction to
hypernatremia
As the result of an osmotic gradient,
water shifts from the interstitium and
cells of the brain and enters the
capillaries
The brain tends to shrink and the
capillaries dilate and possibly
rupture
Result is focal intracerebral &
subarachnoid hemorrhages,
hemorrhages blood
clots, and neurological dysfunction

H2
O

Symptoms of
hypernatremia
Initial symptoms include lethargy, weakness and
irritability
Can progress to twitching, seizures, obtundation
or coma
Resulting decrease in brain volume can lead to
rupture of cerebral veins leading to hemorrhage
Severe symptoms usually occur with rapid
increase to sodium concentration of 158 mmol/l
or more

CNS protective
mechanisms

Idiogenic osmoles accumulate inside brain

cells
K+, Mg+ from cellular binding sites and
amino acids from protein catabolism
These idiogenic osmoles create an osmotic
force that draws water back into the brain and
protects cells from dehydration
If this adaptation has occurred and treatment
involves a rapid infusion of dextrose, there is
danger of cerebral edema with fluid being
drawn into brain tissues

H2
O

Pathogenesis of
hypernatremia
Normal-Volume Hypernatremia
Conditions associated with a loss of electrolyte free fluids
(loss of pure water)

High-Volume Hypernatremia
Conditions associated with ingestion or administration of
sodium containing hypertonic solutions

Low-Volume Hypernatremia
Conditions associated with the loss of hypotonic fluids
(fluids containing more water than sodium)

Normal-volume
hypernatremia
Pure Water Loss

Renal Loss
Central diabetes insipidus
Nephrogenic diabetes
insipidus

Central Diabetes Insipidus

Impairmentinurinaryconcentrationduetopartialor
completelossofADHsecretion2toCNSpathology

Idiopathic (?autoimmune)
Neurosurgery or trauma
CNS tumors
Infiltrative disorders (e.g., CNS sarcoidosis)
Others (e.g., hypoxic encephalopathy, bleeding,
infection)

Nephrogenic Diabetes
Insipidus

Impairmentinurinaryconcentrationduetoinabilityof
collectingducttorespondtoADH

Chronic lithium treatment (up to 50%)

Hypocalcaemia
Persistent severe hypokalemia
Hereditary nephrogenic DI (children)
X-linked: defects in V2 receptor gene
Autosomal recessive: defects in AQP-2 water
channel
Other (e.g., sickle cell Dz, amyloidosis, myeloma)

Diagnosis of
hypernatremia
Same labs as workup for hyponatremia:
Serum osmolality, urine osmolality and urine
sodium
Urine sodium should be lower than 25 mmol/L
if water and volume loss are cause. It can be
greater than 100 mmol/L when hypertonic
solutions are infused or ingested
If urine osmolality is lower than serum
osmolality then DI is present
Administration of DDAVP will differentiate

Urine osmolality will increase in central DI, no

response in nephrogenic DI

Low-volume
hypernatremia

Loss of Hypotonic Fluid

Clinical manifestations
Thirst
Dry, swollen tongue
Sticky mucous membranes
Flushed skin
Postural hypotension

Low-volume
hypernatremia
Treatment
Re-hydration is the primary objective in most
cases
Treatment is best handled by giving
slow infusions of glucose solutions

This dilutes high plasma

sodium ion concentrations

Low-volume
hypernatremia
Treatment
If hypotensive: then 5% of total body weight
(kg) is needed as isotonic fluids initially
Give free H2O (D5W or p.o. water to correct
hypernatremia - only after plasma (and ECF)
volume is re-expanded

Calculation of Free Water

Deficit
Free water deficit = TBWnormal - TBWpresent

And, TBWpresent x PNa present = TBWnormal x PNa normal

PNa normal
Or, TBWpresent = TBWnormal x P
Na present
PNa normal
________
)
So, free water deficit = TBWnormal (1 PNa present

Treatment of Hypernatremia
First, calculate water deficit
TBW present = current body water
assumed to be 50% of body weight in
men and 40% in women
So lets do a sample calculation:
60 kg man with 168 mEq/L
How much water will it take to reduce
his sodium to 140 mEq/L

Calculation continued
Water deficit = 0.5 x 60 (1-[140/168]) approx
5L
But how fast should I correct it?
Same as hyponatremia, sodium should not be
lowered by more than 10-12 mmol/L in 24
hours
Overcorrection can lead to cerebral edema which
can lead to encephalopathy, seizures or death

So what does that mean for our patient?

The 5 L which will lower the sodium level by 28
should be given over 56-60 hours, or at a rate of
75-80 mL/hr
Typical fluids given in form of D5 water

High-volume
hypernatremia Treatment
Diuretics
remove Na+ and water
Replacement of water losses from
diuretic
Dialysis if concurrent renal failure

Summary of Hypernatremia
Loss of thirst usually has to occur to
produce hypernatremia
Rate of correction same as hyponatremia
D5 water infusion is typically used to
lower sodium level
Same diagnostic labs used: Serum
osmolality, Urine osmolality and Urine
sodium
Beware of overcorrection as cerebral
edema may develop

All About Potassium

Major Intracellular electrolyte
98% of the bodys potassium is inside the
cells
Influences both skeletal and cardiac
muscle activity
Normal serum potassium concentration
3.5 to 5.5 mmol/L.

Hypokalemia
Serum Potassium below 3.5 mmol/L
Causes:
diarrhea, diuretics, poor K intake,
stress, steroid administration, renal
disease

Intracellular movement
Beta-stimulation
Alcalosis
Hypotermia
Insulin

Distribuia potasiului n organism

Capital de potasiu

48-50 mmol/kg

Intracelular

120-160 mmol/l

Extracelular

55-70 mmol

Interstiial/intravascular

3,14,2 mmol/l.

Saliv

15-20 mmol/l

Transpiraie

5-20 mmol/l

Lichid gastric

10-15 mmol/l

Scaun normal

5-10 mmol/l

Bila

5-10 mmol/l

Suc pancreatic

5-10 mmol/l

Urina

30-150 mmol/l

Lichid de cecostomie

8 - 10 mmol/l

Lichid de transversostomie

70 mmol/l

Lichid de sigmoidostomie

130 mmol/l

Diaree

75 mmol/l

Hypokalemia
Clinical manifestations:
malaise, muscle weakness, fatigue,
decreased reflexes,
faint heart sounds,
hypotension,
cardiac arrhythmias,
increased sensitivity to digitalis
EKG changes

Hypokalemia
Administering IV Potassium
- Should be administered only after
adequate urine flow has been established
- Decrease in urine volume to less than 20
mL/h for 2 hours is an indication to stop
the potassium infusion

Principii de tratament in
hKaliemie
1. Corectarea cauzelor care produc translocare
intracelular de potasiu
2. nlocuirea deficitului de potasiu

KCl max 20-40 mmol/l/ora

KCl max 2,5 mmol/kg /24 ore

Administrare pe vena central

Administrare cu pompa de infuzie

Diluarea soluiei native

Monitorizare frecvent a kaliemiei

Corectarea hipomagneziemiei asociate

Hyperkalemia
Serum Potassium greater than 5.5 mEq/L
- More dangerous than hypokalemia because
cardiac arrest is frequently associated with
high serum K+ levels

Hyperkalemia
Causes:
- Decreased renal potassium excretion as
seen with renal failure and oliguria
- High potassium intake
- Hypoaldosteronism
- Shift of potassium out
of the cell as seen in
acidosis, burns, crush injuries,
infections

Medicamente care produc hiperpotasemie

Inhibitori ai enzimei de Anti-inflamatoare
conversie ai angiotensinei
nonsteroidiene
Blocani ai receptorilor pentru Ciclosporina
angiotensina
Betablocante

Tacrolimus

Digital

Pentamidina

Diuretice antialdosteronice

Penicilina potasic

Heparina

Trimetoprim-sulfametoxazol

Succinilcolina

Hyperkalemia
Clinical manifestations:
- Skeletal muscle weakness/paralysis
- Irritability
- Abdominal distension
- EKG changes such as peaked T waves,
widened QRS complexes
- Heart block

Principii de tratament in
HKaliemie
1. Oprirea oricrui aport de potasiu
2. Reversarea efectelor membranare

clorura de calciu 10 % 5-10 ml (3,4-6,8 mmol)

3. Transfer intracelular

glucoza 50 g + insulina 20 U

bicarbonat de sodiu 50-100 mmol

agonisti beta-adrenergici
4. Inlturarea din organism

diuretice de ansa

rini schimbatoare de ioni administrate n clisma sau

oral

epurare extrarenal