diselectrolitemii 2015nov

Fluid and Electrolytes Fluid and Electrolytes DisturbancesDisturbances

Daniela FilipescuProf. 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.

IF= ECV-PV

Blood volume (5L)

IPV (3L)RBC

[ Ke+] ~ 4.0 mEq/L[ Ki

+] ~ 150 mEq/L

[ Nae+] ~ 140 mEq/L[ Nai

+] ~ 10 mEq/L

ECV (14L)ICV (28L)

IF= ECV-PV

Blood volume (5L)

IPV (3L)RBC

[ Ke+] ~ 4.0 mEq/L[ Ki

+] ~ 150 mEq/L

[ Nae+] ~ 140 mEq/L[ Nai

+] ~ 10 mEq/L

ECV (14L)ICV (28L)

TOTAL BODY WATER (42L)

TOTAL BODY WEIGHT (70 KG)

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


Necesar lichidian zilnicinlocuirea pierderilor (adult)

Căi 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

Plămân 7 ml/ kg/24 ore 400 ml/24 ore

Scaun 1-2 ml/kg/24 ore 100 ml/24 ore

Necesar minim lichidian recomandatgreutate (kg) ml/kg/ora ml/kg/zi

1-10 4 120-150

11-20 2 50-100

> 20 1 25-40

> 40 1 25-40

Necesar perioperator de lichidesolutii salinelichid de mentinere + inlocuire volum pierdut + 4 ml/kg - trauma minima6 ml/kg - trauma moderata8 ml/kg - trauma mare

Distributia lichidelor perfuzatecresterea 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 LNaCl 0,9% => 2 L x 14 L / 3 L = 9,3 L

Compoziţia soluţiilor volemice în comparaţie cu plasma (mmol/l)

Na+ Cl- K+ Mg++ Ca++ 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 1 2.5 Acetat 24 5.1-5.9

Ringer lactat 131 109 5 - 2 Lactat 28 6,4

Solutie gelatinaGelofusin

154 120 - - - - 7,1-7,7

Solutie gelatina Gelaspan

151 103 4 1 1 Acetat 24

Soluţii de amidon Voluven

154 154 4-7

Volulyte 137 110 4 1.5 - Acetat 34 4-7

Membrane PermeabilityMembrane Permeability

• Most cell membranes are relatively highly Most cell membranes are relatively highly permeable to waterpermeable to water

• Membranes are semi-permeable to certain Membranes are semi-permeable to certain anions and cationsanions and cations

• Difference in permeability between water and Difference in permeability between water and dissolved solutesdissolved solutes

Compoziţia ionică a spaţiilor hidrice

Plasma Lichid interstiţial

Lichid 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

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


Osmosis


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

KK++

NaNa++

Electrolyte Electrolyte BalanceBalance• 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

KK++

H2OH2O

H2O H2O

H2O

H2O

H2O H2O

KK++

KK++

KK++

NaNa++

NaNa++NaNa++

NaNa++

Click to seeanimation

Plasma osmolalityPlasma osmolality

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

SolutionsSolutions• Hypertonic solution• Hypotonic solution• Isotonic solution

Hyponatremia• Definition• Epidemiology• Physiology• Pathophysiology• Types• Clinical Manifestations• Diagnosis • Treatment

HyponatremiaHyponatremia

• Definition:– serum sodium concentration <135 mmol/L

– represents a relative excess of water in relation to sodium.

Hyponatremia

• We define ‘mild’ hyponatraemia as a biochemicalfinding of a serum sodium concentration between 130and 135 mmol/L as measured by ion specific electrode.• We define ‘moderate’ hyponatraemia as a biochemicalfinding of a serum sodium concentration between 125and 129 mmol/L as measured by ion specific electrode.• We define ‘profound’ hyponatraemia as a biochemicalfinding of a serum sodium concentration<125 mmol/Las 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


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


Symptoms

Moderately severe• Nausea without vomiting• Confusion• HeadacheSevere• Vomiting• Cardio-respiratory distress• Abnormal and deep somnolence• Seizures• Coma (Glasgow Coma Scale < 8)


• 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 conditionsassociated 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


• Types– Hypovolemic hyponatremia– Euvolemic hyponatremia– Hypervolemic hyponatremia– Redistributive hyponatremia– Pseudohyponatremia


Redistributive hyponatremiaRedistributive 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)


PseudohyponatremiaPseudohyponatremia

– The aqueous phase is diluted by excessive solutes (proteins or lipids)

– The TBW and total body sodium are unchanged. • hypertriglyceridemia• multiple myeloma

Hypovolemic hyponatremiaHypovolemic 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


• 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

www.jupiterimages.com

Compoziţia secreţiilor tubului digestiv

Lichid/ compoziţie

Volumml/zi

Sodiummol/l

Potasiummol/l

Clormmol/l

Bicarbonatmmol/l

Suc gastric 1000-2500

60-100 10-20 100-130 0

Suc pancreatic 300-800 135-145 5-10 70-90 40-120

Bila 300-600 140 5-10 90-130 30-70

Lichid jejunal 2000-4000

120-140 5-10 90-140 30-40

Lichid ileal 1000-2000

80-150 2-8 45-140 30

Lichid colonic - 60 30 40 -

Saliva 500-2000

2-30 20-30 8-35 0-30

Insensible fluid loss through burned wounds after 24 hours: ml/hours= (25+% surface burned area) x body surface area


• Renal Loss– Diuretics

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

Euvolemic hyponatremiaEuvolemic 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

SIADHSIADHCaused 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

SIADHSIADH

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 hyponatremiaHypervolemic 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

Vaitsis J et al. Crit Care 2009: abstr 456

Na (mEq/l) ≥136 135-131 130In hospital mortality (%) 1.8 3.4 6.460 day mortality (%) 4.7 7.2 13.760 day rehospitalization (%) 27.2 29.1 39.3

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 Cerebral symptoms of hyponatremiahyponatremia

• 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 2010:1-10Adrogue HJ & Madias NE. NEJM 2000;342:1581-1589

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

Clinical manifestationsClinical manifestations

Workup for hyponatremiaWorkup 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)


Treatment of hyponatremiaTreatment of hyponatremia

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

• 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


• 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 mL3 % hypertonic saline or equivalent over 20 min. (1D)• We suggest checking the serum sodium concentrationafter 20 min while repeating an infusion of 150 mL 3 %hypertonic saline or equivalent over the next 20 min.(2D)• We suggest repeating therapeutic recommendationstwice or until a target of 5 mmol/L increase in serum sodiumconcentration is achieved. (2D)


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)


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).


What if the sodium increases too fast?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 Effects of hyponatremia on the brain and adaptive responsesand adaptive responses

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

Central pontine myelinolysisCentral 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)


Acute hyponatraemia without severeor 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)


Chronic hyponatraemia without severeor 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


Vasopressin receptor antagonistsVasopressin receptor antagonistsAQUARETICSAQUARETICS

• 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 Practical therapeutic approach to hyponatremia in HFto 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


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

Practical therapeutic approach to Practical therapeutic approach to symptomatic hyponatremia in HFsymptomatic hyponatremia in HF

• Saline solution - Hypertonic?No worsening of pulmonary congestionIncrease in urine outputReduction in serum blood urea nitrogenNo change in HF functional classLower readmission rateLower hospital mortality


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

HypernatremiaHypernatremia

• Normal range for blood levels of sodium is 135 - 145 mmol/liter

• HypernatremiaHypernatremia refers to an elevated serum sodium level (145 -150 mmol/liter)

Na+

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

Most cases are due to water deficit due to loss or inadequate intake

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 hypernatremiaCNS 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 focal intracerebral & subarachnoid

hemorrhageshemorrhages, blood clots, and neurological dysfunction

H2

O

Symptoms of hypernatremiaSymptoms 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 mechanismsCNS 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 hypernatremiaPathogenesis of hypernatremiaNormal-Volume HypernatremiaNormal-Volume Hypernatremia• Conditions associated with a loss of “electrolyte free” fluids (loss of pure water)Conditions associated with a loss of “electrolyte free” fluids (loss of pure water)

High-Volume HypernatremiaHigh-Volume Hypernatremia• Conditions associated with ingestion or administration of sodium containing Conditions associated with ingestion or administration of sodium containing

hypertonic solutionshypertonic solutions

Low-Volume HypernatremiaLow-Volume Hypernatremia• Conditions associated with the loss of hypotonic fluids (fluids containing more Conditions associated with the loss of hypotonic fluids (fluids containing more

water than sodium)water than sodium)

Normal-volume hypernatremiaNormal-volume hypernatremiaPure Water LossPure Water Loss

• Renal LossRenal Loss– Central diabetes insipidusCentral diabetes insipidus– Nephrogenic diabetes insipidusNephrogenic diabetes insipidus

Central Diabetes InsipidusCentral Diabetes Insipidus

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

Impairment in urinary concentration due to partial or Impairment in urinary concentration due to partial or complete loss of ADH secretion 2° to CNS pathologycomplete loss of ADH secretion 2° to CNS pathology

Nephrogenic Diabetes InsipidusNephrogenic Diabetes Insipidus

• Chronic lithium treatment (up to 50%) Chronic lithium treatment (up to 50%) • HypocalcaemiaHypocalcaemia• Persistent severe hypokalemiaPersistent severe hypokalemia• Hereditary nephrogenic DI (children)Hereditary nephrogenic DI (children)

– X-linked: defects in VX-linked: defects in V22 receptor gene receptor gene

– Autosomal recessive: defects in AQP-2 water channelAutosomal recessive: defects in AQP-2 water channel• Other (e.g., sickle cell Dz, amyloidosis, myeloma)Other (e.g., sickle cell Dz, amyloidosis, myeloma)

Impairment in urinary concentration due to inability of Impairment in urinary concentration due to inability of collecting duct to respond to ADHcollecting duct to respond to ADH

Diagnosis of hypernatremiaDiagnosis 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- Thirst- Dry, swollen tongue- Sticky mucous membranes- Flushed skin- Postural hypotension

Low-volume hypernatremiaLow-volume hypernatremia Loss of Hypotonic FluidLoss of Hypotonic Fluid

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

Low-volume hypernatremiaLow-volume hypernatremia TreatmentTreatment

• This dilutes high plasmasodium ion concentrations

• If hypotensive: then 5% of total body weight (kg) is If hypotensive: then 5% of total body weight (kg) is needed as isotonic fluids initiallyneeded as isotonic fluids initially

• Give free HGive free H22O (D5W or p.o. water to correct O (D5W or p.o. water to correct hypernatremia - only after plasma (and ECF) hypernatremia - only after plasma (and ECF) volume is re-expandedvolume is re-expanded

Low-volume hypernatremiaLow-volume hypernatremia TreatmentTreatment

Calculation of Free Water DeficitCalculation of Free Water Deficit

And, TBWAnd, TBWpresentpresent x P x PNa presentNa present = TBW = TBWnormalnormal x P x PNa normalNa normal

Free water deficit = TBWFree water deficit = TBWnormalnormal - TBW - TBWpresentpresent

Or, TBWOr, TBWpresentpresent = TBW = TBWnormalnormal x x PPNa presentNa present

PPNa normalNa normal

So, So, free water deficitfree water deficit = TBW = TBWnormal normal (1 - (1 - PPNa normalNa normal

PPNa presentNa 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

• DiureticsDiuretics– remove Naremove Na++ and water and water

• Replacement of water losses from diureticReplacement of water losses from diuretic

• Dialysis if concurrent renal failureDialysis if concurrent renal failure

High-volume hypernatremiaHigh-volume hypernatremia TreatmentTreatment

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 PotassiumAll 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.

HypokalemiaHypokalemia

• Serum Potassium below 3.5 mmol/LCauses:diarrhea, diuretics, poor K intake, stress, steroid

administration, renal disease

Intracellular movementBeta-stimulationAlcalosisHypotermiaInsulin

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

* Estimated deficit for a 70 kg adult

with a total body potassium content of 50 mEq/kg

258751.0

207001.5

154702.0

103502.6

51753.0

% Total Body KmEq

Serum Potassium

(mEq/L)

Potassium Deficit

POTASSIUM DEFICITS IN HYPOKALEMIA*

* Estimated deficit for a 70 kg adult

with a total body potassium content of 50 mEq/kg

258751.0

207001.5

154702.0

103502.6

51753.0

% Total Body KmEq

Serum Potassium

(mEq/L)

Potassium Deficit

POTASSIUM DEFICITS IN HYPOKALEMIA*

• Clinical manifestations:malaise, muscle weakness, fatigue, decreased reflexes, faint heart sounds, hypotension, cardiac arrhythmias,increased sensitivity to digitalisEKG 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 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 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 - 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 conversie ai angiotensinei

Anti-inflamatoare nonsteroidiene

Blocanţi ai receptorilor pentru angiotensina

Ciclosporina

Betablocante Tacrolimus

Digitală Pentamidina

Diuretice antialdosteronice Penicilina potasică

Heparina Trimetoprim-sulfametoxazol

Succinilcolina

• 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-adrenergici4. Inlăturarea din organism• diuretice de ansa• răşini schimbatoare de ioni administrate în clisma sau oral • epurare extrarenală

Documents

diselectrolitemii 2015nov