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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
15-20 ml/kg/24 hrs

8 ml/kg/24 hrs

7 ml/ kg/24 hrs

1-2 ml/kg/24 hrs

25-35 ml/kg/24 hrs

Smorenberg et al. Perioperative Medicine 2013;2-17


Daily fluids need
Weight (kg) ml/kg/hrs ml/kg/day
1-10 4 120-150
11-20 2 50-100
> 20 1 25-40
> 40 1 25-40

Perioperatively: Saline solutions


Maintenance + Loss +
4 ml/kg – minimal trauma
6 ml/kg - moderate
8 ml/kg – severe trauma

Insensible fluid loss through burned wounds after 24 hours:


ml/hour = (25+% surface burned area) x body surface area
Distributia lichidelor perfuzate
cresterea de volum (V) estimata =
V infuzat x V plasmatic normal/ V de distributie

Vi = ΔV 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
Composition of fluids compared to plasma (mmol/l)

Na+ Cl- K+ Mg++ Ca++ Tampon pH


Plasma (albumina) 140 102 3.7 0.8. 1.2 HCO3- 7,4
NaCl 0,9 % 154 154 - - - - 5,7
Sterofundin iso 145 127 4.5 1 2.5 Acetat 5.1-5.9
Ringer lactat 131 109 5 - 2 Lactat 6,4
Solutie gelatina 154 120 - - - - 7,1-7,7
Gelofusin
Solutie gelatina 151 103 4 1 1 Acetat
Gelaspan
Soluţii de amidon 154 154 4-7
Voluven
Volulyte 137 110 4 1.5 - Acetat 4-7
Smorenberg et al. Perioperative Medicine 2013;2-17
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
Compoziţia ionică a spaţiilor hidrice

Plasma Lichid Lichid


interstiţial intracelular

Cationi
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
Anioni
Clor (mmol/l) 102 115 3
Bicarbonat (mmol/l) 28 30 10
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
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+ K+ K+ H2O


H2O
Na +
H2O

Na +
K
+ K+
Na+ H2 O H2O
H2O 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
• 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-Methylendioxymethamfetamine (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
Redistributive hyponatremia
• 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)
Add 2.4 mmol/l to the measured serum sodium for every 100 mg/dl incremental rise

• Hyponatraemia with a measured osmolality <275


mOsm/kg always reflects hypotonic hyponatraemia.
(not graded)

Spasovski G et al. ICM 2014:320


Pseudohyponatremia

– 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 non-renal routes

www.grouptrails.com/.../0-Beat-Dehydration.jpg
Hypovolemic hyponatremia
• Non-renal 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
Compoziţia secreţiilor tubului digestiv
Lichid/ Volum Sodiu Potasiu Clor Bicarbonat
compoziţie ml/zi mmol/l mmol/l mmol/l mmol/l
Suc gastric 1000- 60-100 10-20 100-130 0
2500
Suc pancreatic 300-800 135-145 5-10 70-90 40-120
Bila 300-600 140 5-10 90-130 30-70
Lichid jejunal 2000- 120-140 5-10 90-140 30-40
4000
Lichid ileal 1000- 80-150 2-8 45-140 30
2000
Lichid colonic - 60 30 40 -
Saliva 500- 2-30 20-30 8-35 0-30
2000
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
• 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 Excretion of Sodium (FENa) = (PCr * UNa ) / (PNa x UCr) %

• 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) ≥136 135-131 130


In hospital mortality (%) 1.8 3.4 6.4
60 day mortality (%) 4.7 7.2 13.7
60 day rehospitalization (%) 27.2 29.1 39.3

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 • poor skin turgor


edema • dry mucous membranes
• pulmonary edema • flat neck veins
• jugular venous distension • hypotension
• hypertension • incr. Hct
• decr. hct • incr. serum prot.
• decr. serum prot • Incr bun/cr ratio >20:1
• decr. bun/cr • UNa < 20 meq/l
• UNa no help
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
• ΔSNa = {[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) 31:227–230


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 symptoms
• Make sure that the serum sodium concentration has 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 previous
measurement. (2D)
Spasovski G et al. ICM 2014:320
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


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 H2
capillaries dilate and possibly rupture
O
– Result is focal intracerebral & subarachnoid
hemorrhages,
hemorrhages blood clots, and neurological
dysfunction
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 H2
from protein catabolism O
– 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
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
Impairment in urinary concentration due to partial or 
complete loss of ADH secretion 2° to CNS pathology

• Idiopathic (?autoimmune)
• Neurosurgery or trauma
• CNS tumors
• Infiltrative disorders (e.g., CNS sarcoidosis)
• Others (e.g., hypoxic encephalopathy, bleeding, infection)
Nephrogenic Diabetes Insipidus
Impairment in urinary concentration due to inability of 
collecting duct to respond to ADH

• 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

P________
Na 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 let’s 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 5 L
• 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 body’s 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
Distribuţia potasiului în organism

Capital de potasiu 48-50 mmol/kg


Intracelular 120-160 mmol/l
Extracelular 55-70 mmol
Interstiţial/intravascular 3,1–4,2 mmol/l.
Salivă 15-20 mmol/l
Transpiraţie 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 intracelulară de
potasiu
2. Înlocuirea deficitului de potasiu
• KCl max 20-40 mmol/l/ora
• KCl max 2,5 mmol/kg /24 ore
• Administrare pe vena centrală
• Administrare cu pompa de infuzie
• Diluarea soluţiei native
• Monitorizare frecventă 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
Blocanţi ai receptorilor pentru Ciclosporina
angiotensina
Betablocante Tacrolimus
Digitală Pentamidina
Diuretice antialdosteronice Penicilina potasică
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 oricărui 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. Inlăturarea din organism
• diuretice de ansa
• răşini schimbatoare de ioni administrate în clisma sau oral
• epurare extrarenală

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