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15-20
ore
ml/kg/24
Cutana
t
8 ml/kg/24 ore
Plmn
Scaun
greutate (kg)
ml/kg/ora
ml/kg/zi
1-10
120-150
11-20
50-100
> 20
25-40
> 40
25-40
Tampon
pH
Plasma (albumina)
140
102
3.7
0.8.
1.2
HCO3 24
7,4
NaCl 0,9 %
154
154
5,7
Sterofundin iso
145
127
4.5
2.5
Acetat 24
5.1-5.9
Ringer lactat
131
109
Lactat 28
6,4
Solutie gelatina
Gelofusin
154
120
7,1-7,7
151
103
Acetat 24
154
154
Volulyte
137
110
4-7
4
1.5
Acetat 34
4-7
Membrane Permeability
Most cell membranes are relatively highly permeable to water. Membranes are semipermeable to certain anions and cations. Difference in permeability between water and dissolved
solutes
Compoziia ionic a spaiilor hidrice
Plasma
Cationi
Lichid interstiial
Lichid intracelular
Sodiu (mmol/l)
140
145
10
Potasiu (mmol/l)
3,7
3,8
155
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
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
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
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
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
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:
Severe
Vomiting
Cardio-respiratory distress
Abnormal and deep somnolence
Seizures
Coma (Glasgow Coma Scale < 8)
Epidemiology:
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
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)
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 non-renal routes
o
o
o
o
Nonrenal loss
GI losses: Vomiting, Diarrhea, fistulas, pancreatitis
Excessive sweating
Third spacing of fluids: ascites, peritonitis, pancreatitis, and burns
Cerebral salt-wasting syndrome: traumatic brain injury, aneurysmal subarachnoid hemorrhage,
and intracranial surgery => Must distinguish from SIADH
Renal Loss: Diuretics
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 postop 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
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
Clinical manifestations
Hypervolemia
Hypovolemia.
peripheral and presacral edema
poor skin turgor
pulmonary edema
dry mucous membranes
jugular venous distension
flat neck veins
hypertension
hypotension
decr. hct,
incr. Hct
decr. serum prot
incr. serum prot.
decr. bun/cr
Incr bun/cr ratio >20:1
UNa no help
UNa < 20 meq/l
Treatment of hyponatremia
Treatment is based on symptoms
Symptomatic
1st step is to calculate the total body water
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)
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)
SIADH
Water restriction: 0.5-1 liter/day
Demeclocycline: Inhibits the effects of ADH- Onset of action may require up to one week
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)
CAUSES OF HYPERNATREMIA
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
2) Sodium ion overload
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
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
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
Idiogenic osmoles accumulate inside brain cellsK+, 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
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)
o
o
o
o
o
Idiopathic (?autoimmune)
Neurosurgery or trauma
CNS tumors
Infiltrative disorders (e.g., CNS sarcoidosis)
Others (e.g., hypoxic encephalopathy, bleeding, infection)
o
o
o
o
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
Clinical manifestations
o Thirst
o Dry, swollen tongue
o Sticky mucous membranes
o Flushed skin
o 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
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
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:
How much water will it take to reduce his sodium to 140 mEq/L
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
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
Hypokalemia
Causes: diarrhea, diuretics, poor K intake, stress, steroid administration, renal disease
Intracellular movement
o Beta-stimulation
o Alcalosis
o Hypotermia
o Insulin
Clinical manifestations:
o malaise, muscle weakness, fatigue,
o decreased reflexes,
o faint heart sounds,
o hypotension,
o cardiac arrhythmias,
o increased sensitivity to digitalis
o EKG changes
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
o 2. nlocuirea deficitului de potasiu
o KCl max 20-40 mmol/l/ora
o KCl max 2,5 mmol/kg /24 ore
o Administrare pe vena central
o Administrare cu pompa de infuzie
o Diluarea soluiei native
o Monitorizare frecvent a kaliemiei
o 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
Causes:
- Decreased renal potassium excretion as seen with renal failure and oliguria
- Hypoaldosteronism
- Shift of potassium out of the cell as seen in acidosis, burns, crush injuries, infections
Inhibitori ai
angiotensinei
Anti-inflamatoare
nonsteroidiene
Ciclosporina
Betablocante
Tacrolimus
Digital
Pentamidina
Diuretice antialdosteronice
Penicilina potasic
Heparina
Trimetoprim-sulfametoxazol
Succinilcolina
enzimei
de
conversie
ai
Clinical manifestations:
o Skeletal muscle weakness/paralysis
o Irritability
o Abdominal distension
o EKG changes such as peaked T waves, widened QRS complexes
o Heart block
glucoza 50 g + insulina 20 U
agonisti beta-adrenergici
4. Inlturarea din organism
diuretice de ansa
epurare extrarenal