Vocht- en electrolytenhuishouding

Post-operative management
Fluid balance & Electrolyte abnormalities
P. Van der Niepen
Dept. Nephrology & Hypertension
Universitair Ziekenhuis Brussel (VUB)
Brussel, 21 maart 2014
Outline
 Introduction
 Fluid management (volume disturbances)
 Hypo- and hypernatraemia (concentration d)
 Hypo- and hyperkalaemia (composition d)
 Hypo- and hypercalcaemia (idem)
 Mg/Phosphate
(idem)
 Acidosis and alkalosis
 Conclusions - THM
2
Introduction
Fluid and electrolyte management are paramount
to the care of the surgical patient.
Changes in both fluid volume and electrolyte
composition occur
 preoperatively,
 intraoperatively, and
 postoperatively,
as well as in response to trauma and sepsis.
3
Introduction
Three principles of management of fluid &
electrolyte balance
4
1.
Correct any abnormalities before surgery
2.
Provide the daily requirements
3.
Replace any abnormal and ongoing losses
(peri-operative)
How to calculate a patient's fluid
requirements?
There is a distinction to be made between
1. the volume required to maintain the body's
normal functions and
2. the volume required to replace any
abnormal losses
The normal maintenance fluid requirements will
vary depending on



5
patient's age,
gender,
weight and body surface area.
Total Body Water

45 - 60% of total body weight

Muscle and solid organs have higher water
content than fat and bone
Higher proportion of water in:
 Young
 Lean
 Males

Obese individuals
10 – 20% less TBW (estimates)
Malnourished individuals
10% more TBW
6
Total Body Water: three fluid compartments
extracellular compartment
Plasma 5%
1/3
20%
Interstitial fluid 15%
1/4
3/4
2/3
40%


intracellular compartment
Male (70 kg)
42 l
ECF: 70 x 20/100 = 14 l
 PV: 70 x 5/100 =
 IF : 70 x 15/100 =

7
3,5 l
10,5 l
ICF : 70 x 40/100 = 28 l
Basic requirements - Fluid

The normal daily fluid requirement to maintain a
healthy 70-kg adult is between 2 and 3 L.
 The individual will lose about 1500 mL (800 – 1200)
in the urine and
 about 600 mL from the skin, lungs (insensible loss)
and 250 mL stool (loss from the skin will vary with
the ambient temperature)
8
The electrolyte composition of intracellular (ICF)
and extracellular fluid (ECF) varies:
Sodium is the predominant cation in the ECF
Potassium predominates in the ICF
Electrolyte
Extracellular fluid
Intracellular fluid
(mmol/L)
(mmol/L)
135
4
2.5
1.5
100
27
1.5
10
150
2.5
10
10
10
45
Sodium
Potassium
Calcium
Magnesium
Chloride
Bicarbonate
Phosphate
Only small
9
between PV & IF
Composition of Gastrointestinal Secretions
The normal daily requirements of sodium and of
potassium will balance the daily loss of these two
cations in the urine.
Stomach: H+ 70 mmol/l
10
Replacement if deprived of normal daily
intake of fluid & electrolytes

Volume depletion
 without electrolyte disturbances (fever, intake)
 accompanied by electrolyte deficit (e.g. vomiting,
ileus, fistula, diarrhea)

The source of fluid loss will determine the type of
electrolyte lost < considerable variation in electrolyte
content of different gastrointestinal secretions:
 Loss from the upper digestive tract tends to be rich in acid,
 while loss from the lower tract is high in sodium and
bicarbonate
patients with severe and prolonged vomiting from gastric outlet
obstruction may develop metabolic alkalosis.
11
Management of fluid requirements


can be done on a daily basis, but
fluid and electrolyte replacements of an acutely ill
surgical patient necessitates close monitoring and
adjustment.
 Clinical assessment and appreciation of the types of fluid loss
will give an approximate guide to the scale of the problem, but
 regular biochemical electrolyte estimations will be required
to determine the precise needs of what needs to be replaced.

12
in most instances, measurement of plasma electrolyte
concentrations will provide sufficient information, but
occasionally it may be necessary to estimate the
electrolyte contents of the various fluids being lost.
Disturbances in Fluid Balance

Most common in surgical patients
Extracellular volume deficit:
 Acute
 Cardiovascular signs (TC, OH)
 Central nervous system signs
 Chronic
 Decrease skin turgor
 Sunken eyes
 CVS and CNS


13
OsmU > OsmPl
[Na+]u < 20 mEq/l and [Na+]pl N – ( ) – ( )
Water depletion / dehydration

Clinical features








Thirst
Dryness of mouth
Dry loose skin
Oliguria
Sunken eyes
Hypotension
Delirium
Hemoconcentration
(↑ PCV )
 Oliguria, RF
14

Causes







Low intake
Poor absorption
Increased loss (GI)
Diarrhea
Vomiting
Nasogastric suction
Enterocutaneous
fistula
 Sequestration (burns,
peritonitis, obstruction, …)
15
Oliguria (<30 mL/h)
Normal urine output: 0.5 - 2 ml/kg/h


Common problem in the post-operative period
Diminished output of urine may be due to:
 poor renal perfusion (pre-renal failure: hypovolaemia
a/o pump failure)
 renal failure (acute tubular necrosis < hypotension)
 renal tract obstruction (post-renal failure)

16
Treatment of oliguria depends on the cause.
Most cases of post-operative oliguria are
secondary to hypovolaemia, and should be
considered to be due to hypovolaemia until
proven otherwise.
Hourly maintenance fluid requirement
Useful tool for approximation of hourly maintenance fluid
requirement based on body weight:
The 421 RULE - Estimates maintenance fluid requirement for
an adult per hour
1st 10 kg, 4 ml/kg/h
2nd 10 kg, 2 ml/kg/h
For each remaining kg of BW, 1ml/kg/h
Example: for a 70 kg patient:
 1st 10 kg, 4 ml/kg/h: 4 x 10 = 40 ml/h
 2nd 10 kg, 2 ml/kg/h: 2 x 10 = 20 ml/h
 Remainder 1ml/kg/h: 1 x (70 - 20) = 50 ml/h
Hourly maintenance fluid requirement: 40 + 20 + 50 = 110 ml/h = 2,640 l/d
(adjusting based on increased losses,…)
17
Daily maintenance fluid requirement
Useful tool for approximation of daily maintenance fluid
requirement based on body weight:
The 100,50,20 - Estimates maintenance fluid requirement
for an adult over 24 hours
1st 10 kg, 100 ml/kg/d
2nd 10 kg, 50 ml/kg/d
For each remaining kg of BW, 20 ml/kg/d
Example: for a 70 kg patient:
 1st 10 kg, 100 ml/kg/d: 100 x 10 = 1000 ml
 2nd 10 kg, 50 ml/kg/d: 50 x 10 = 500 ml
 Remainder 20 ml/kg/d: 20 (70 - 20) = 1000 ml
24h maintenance fluid requirement: 1000 + 500 + 1000 = 2500 ml/day
or 2500 ml/24h = 104 ml/h (adjusting based on increased losses, …)
18
Basic daily electrolyte requirements

Na+: 100 - 150 mmol/day – K+: 60 - 80 mmol/d

Requirements may be considerably higher in ill,
post-op patients (e.g. severe vomiting, fluxing stoma, …)

Daily requirements of major electrolytes





19
Sodium: 1 mmol/kg/day
Potassium: 1 mmol/kg/day
Chloride: 1 mmol/kg/day
Calcium: 2 g/day
Magnesium: 20 mEq/day
Composition of common replacement fluids

Normal saline (0.9%) solution (1L): pH 5.7 – Osm 308
 Na 154 mmol
 Cl 154 mmol
 K
0 mmol

5% Dextrose solution (1L): pH 3.5 – 6.5 – Osm 278
 50 g of Dextrose (170 kcal/l)

Hartmann's (Ringer Lactate) (1L): pH 6.4 – Osm 273





20
Na 131 mmol/l
Cl 111 mmol/l
K
5 mmol/l
Lactate 29 mmol/l (metabolized to HCO3- in the liver)
Trace Calcium (2 mmol/l)
Electrolyte solutions for parenteral adm.
Electrolyte composition (mEq/l)
Solution
Na
Cl
K
HCO3
Ca
Mg
mOsm
ECF
142
103
4
27
5
3
280-310
Lactate Ringer*
130
109
4
28
3
0,9% NaCl*
154
154
308
0,45% NaCl
77
77
154
3% NaCl
513
513
1026
5% glucose(*)
278
*isotonic
21
273
Hypernatraemia
22
Sodium



23
75 - 85% of a patients Na+ is in the extracellular
space
Exogenous fluid administration follows that
same distribution
If 1 liter of Saline is given: 250 ml will remain
within the intravascular system 750 ml will go to
the IF
Casus 1:
70 j v – 7 dagen post GI ingreep – 60 kg




Comateus - koorts
[Na+] 164 mmol/l
Diurese: ? Oligurie en Osmol in urine
Serum sodium - 140
Water deficiet: TBW* x ---------------------------140
(TBW = 45% v/h LG (60 kg) = 27 L)
27 x 24/140 = 4,629 l deficiet
Eerste 24 u: 27 x (164/156)-1 = 1,385 l glucose 5%
*estimate TBW as 50% of lean body mass in men and 40% in women
24
Hypernatraemia: [Na+] > 145 mmol/l
Oorzaken

Verminderde waterinname

Waterverlies

Toename van natrium (iatrogeen, mineralocorticoid
excess)
 Hypovolemic hypernatremia
• N/V/D
 Normovolemic hypernatremia
• Diabetes insipidus (ADH )
 Hypervolemic hypernatremia
• Hypertonic fluids
25
Hypernatraemia: [Na+] > 145 mmol/l
Oorzaken
Assess volume status
High
Iatrogenic sodium adm
Mineralocorticoid excess
Aldosteronism
Cushing’s disease
Cong. Adrenal
hyperplasia
Normal
Nonrenal water loss
Low
Nonrenal water loss
skin
skin
GI
GI
Renal water loss
Renal water loss
Renal disease
Renal (tubular) disease
Diuretics
Osmotic diuretics
Diabetes insipidus
( ADH)
Diabetes insipidus
( ADH)
Adrenal failure
26
Hypernatraemia
Diagnostiek
27
Hypernatraemia
Symptomen en tekens


Enkel symptomatisch als verstoord dorstgevoel
of vochtrestrictie, want dorst
water inname
Klinische verschijnselen als [Na+] >160 mmol/l:
 Vaak opmerkelijk weinig klinische symptomen,
vooral bij ouderen
 Neurologische symptomen tgv. Hyperosmolariteit





28
Rusteloosheid, lethargie, … delirium, E, coma
Polyurie – oligurie
Dorst
Droge mucosae
Orthostatische hypotensie, TC
Hypernatraemia
Gevaren
29

Acuut: Risico op cerebrale bloedingen, bij een
hypernatriëmie die zich in korte tijd (< 48 uur)
heeft ontwikkeld met cerebrale verschijnselen

Chronisch: Risico op hersenoedeem, bij te
snelle correctie van een langer bestaande
(> 48 u) hypernatriëmie, vanwege adaptatie van
de hersenen
Hypernatraemia


Hypernatraemia in the post-operative patient is a less
common problem than hyponatraemia.
Any hypernatraemia is usually relative rather than
absolute and occurs secondary to diminished water
intake, or secondary to increased water loss (severe
burns or high fever).


An increase in the plasma [Na+] will lead to a loss of
ECF volume and relative intracellular desiccation.
The first clinical manifestation is thirst and if the
hypernatraemia is allowed to persist, neurological
problems (e.g. confusion, convulsions, coma) may ensue.
Treatment:
 administration of water by mouth or intravenous 5% dextrose
 Aim for 0.5 mEq/L/h correction; hypotonic saline works well
30
Correction of Hypernatremia


In hypovolemic patients: restore volume with
normal saline
In normovolemic patients: replace water deficit
with hypotonic fluid (5% dextrose) or oral water
supplementation
Serum sodium - 140
Water deficit (L) = ----------------------------- x TBW
140
Estimate TBW as 50% of lean body mass (M);
40% (F)
31
Correction of Hypernatremia
Serum sodium - 140
Water deficit (L) = ----------------------------- x TBW
140
Estimate TBW as 50% of lean body mass (M); 40% (F)
Rate of fluid administration:


acute hyperNa: in Na+] <1 mEq/h (<12 mEq/d)
chronic hyperNa: < 0,7 mEq/h
Cave cerebral edema and herniation (too rapid)
32
CT- scan
33
acuut hersenoedeem
Hyponatraemia
34
Casus 2: 55 j Man – bekken#

Opname:
 [Na+] 119 mmol/L
 Creat 0.47 mg/dl
 [K+] 2.8 mmol/l
35

Na 1 week bedrust:
 [Na+] 118 mmol/L
 Creat 0.54 mg/dl
 [K+] 3.3 mmol/l

? Ongerust want heeft 1L 0.9% saline en 1L 5%
glucose gedurende 5 dagen gekregen

Wat hebben we nodig?
Casus 2: 55 j Man – bekken#


Hoe is deze pt?
Anamnese

 Hoeveel drinkt hij
 Hoeveel plast hij

Wat bepalen we nog?
 Osmolaliteit


Plasma
Urine
 Urinair natrium
Goed
 “Normaal” / 5 liter
 5 liter

Wat bepalen we nog?
 Osmolaliteit


248 mOsmol/kg
101 mOsmol/kg
 95 mmol/l
Isovolemische hypotone hyponatremie
36
Casus 2: 55 j Man – bekken#

Kan de vochtrestrictie berekend worden?
Urinair natrium + Kalium
Serum natrium
 (135 + 60)/ 118 = 1.6
500 ml/dag
Isovolemische hypotone hyponatremie
37
Hyponatraemia

Hypovolemic hyponatremia (depletional)
 GI losses: N/V/D
 Burn victims
 Renal losses: RD or Diuretics

Normovolemic hyponatremia
 SIADH

Hypervolemic hyponatremia (dilutional)
 Congestive Heart Failure
 Hepatic failure
 Chronic Renal Failure
38
39
Water Excess (water toxicity)

Clinical features









40
Headache
Nausea / vomiting
Cramps
Raised BP
Polyuria
Cardiac overload
Haemodilution
Peripheral edema
Weight gain

Causes
 Excessive intake
(spontaneous/iatrogenic)
 Renal retention /
dysfunctional
nephrosis
 Nephrotic syndrome
 Liver damage hypoproteinemia
 ADH (SIADH)
 Drugs e.g. narcotics
 Hypothyroidism
Hyponatraemia
Fluids Commonly Lost
Urine
41
Sodium Concentration
(mEq/L)
variable
Diarrhea
40
Gastric secretions
55
Furosemide diuresis
75
Sweat
80
Small bowel secretions
145
Hyponatraemia



Na+ < 136 mmol/l
Na+ < 125 mmol/l: serious symptoms,
onmiddellijk behandelen met hypertoon saline
Symptoms: CNS – MS – GI – CV - R








42
Weakness
Confusion
Fatigue
Muscle cramps
Headache
Seizures
Coma
Cerebral edema
Hyponatraemia: [Na+] < 136 mmol/l
Oorzaken
Assess volume status
High
intake
Hyperglycemia*
Post-op ADH secretion
Drugs ( )
Normal
Plasma lipids/proteins
SIADH
Water intoxication
Diuretics
* For every 100 mg/dl plasma glucose
43
Low
intake
GI losses
Renal losses
Diuretics
Renal disease
plasma sodium 1.6 mEq/l
Management of Hyponatremia
44

Exclude hyperosmolar causes (mannitol, glycemia)


Depletion versus dilution
Dehydration or over hydrated

Normal volume

Na losses
 Urine Na <20 mEq/L = extrarenal sodium loss
 Urine Na >20 mEq/L = Renal sodium loss
evaluate ADH
45
Hyponatraemia
Treatment ~ etiology

Hyponatraemia due to losses
 Correction can be done with saline infusion
 Hypertonic saline (3% NS) can be used, too rapid
correction can lead to central pontine myelinolysis
Aim for 0.5 mEq/L/h (<1 mEq/L/h)
46
MRI
osmotische demyelinisatie syndroom
Osmotic stress caused by rapid
correction of hyponatremia
results in focal loss of
oligodendrocytes and myelin,
with sparing of neurons and
axons, and can cause transient
BBB disruption.
Weakness, paresis, E, akinetic
movements, unresponsiveness,
ev. permanent brain damage &
death
47
Hyponatraemia due to losses

How much sodium needs to be given?
 [Na+] needed = (target [Na+] - actual [Na+] ) × 0.6 BW
(patients weight in kg)
 Rate of infusion (ml/h) = ([Na+] needed (mmol) x 1000)/
infusate [Na+] (mmol/l) x time (hours)
Example: 90 kg women with a coma & [Na+] of 120 mEq/L
(140 - 120) × 0.6 (90) = 1080 mEq Na needed or 7
liters of saline (1 L – 0.9% = 154 mmol: 1080/154 = 7.01 l)
(1080 x 1000)/ (154 x 40) = 175 ml/h
48
Behandeling:

Acute hyponatriëmie: onmiddellijk met
hypertoon zout behandelen ongeacht de
oorzaak. Bereken hoeveelheid hypertoon zout
(3% NaCl) met Adrogué-Madias formule:
(514 – 120)/ (0.6 x 90) +1 = 7.16 mmol
(5)/ (7.16) = 0.698 l of 700 ml

49
Chronische hyponatriëmie: vermijd te snelle
correctie en richt behandeling op onderliggende
oorzaak.
Treatment
50
Correctie hyponatriëmie

Correctiesnelheid:
 Hypotone hyponatriëmie: maximale correctiesnelheid < 10 mmol/l
in de eerste 24 uur en < 18 mmol/l in de eerste 48 uur.
 Acute hyponatriëmie mag initieel gecorrigeerd worden met 1 - 2
mmol/l/u.
 Bij chronische hyponatriëmie of bij risicofactoren voor osmotische
demyelinisatie syndroom: maximaal < 8 mmol/l/dag.
 Snelle correctie tot 120 mmol/l en daarna langzamer is niet
bewezen effectief en niet veilig.

Bij overcorrectie:
 Staken van huidige behandeling (bv. stop isotoon of hypertoon infuus)
 Starten van hypotoon infuus (bv. 0,45% NaCl of 5% glucose)
 Toedienen van desmopressine.
51
Water restriction
52

SIADH, hartfalen, nierfalen, leverfalen, primaire
polydipsie

(100 + 60)/ 120 = 1.3
Potassium



2% of total body K+ is located in EC
compartment
Normal [K+]pl: 3,5 – 5,0 mEq/l

Critical to cardial & neuromuscular functions

53
Average daily intake: 50 – 100 mEq/l
Renal excretion: 10 – 700 mEq/day
Hyperkalaemia
54
Hyperkalaemia

Hyperkaliëmie: [K+] > 5,0 mmol/l

Risicogroepen:
 Patiënten met nierinsufficiëntie
 Hyperglycemie
 Onoordeelkundig gebruik van kaliumsupplementen
of medicatie die de kaliumhuishouding beïnvloedt
 Ouderen
55
Hyperkalaemia
Oorzaken


Pseudohyperkaliëmie, bv. onzorgvuldige bloedafname
intake:
 Supplements
 Blood transfusion

Release from cells (Redistribution)
 Rhabdomyolysis, tumor necrosis
 Acidosis; hyperglycemia (Osm

56
shift)
Impaired potassium excretion
 Renal failure
 Potassium sparing diuretics (spironolacton) or RAAS blockers
 Hypoaldosteronism or aldosteron resistance, Adrenal insufficiency,
salt wasting
Hyperkalaemia
Klinische verschijnselen en Gevaren


Meestal geen symptomen
GI symptomen:
 nausea, vomiting, intestinal colic, diarrhea

Neuromusculaire symptomen:
 Slecht reagerende patiënt/ lethargie, slap - zwak
dyspneu - respiratory failure

paralyse
CV symptomen:
 Hypotensie (< 90 mm Hg)
 ECG-afwijkingen: Peaked T waves, widened QRS complex,
prolonged PR interval
VF or asystole

57
Ernstige hyperkaliëmie is potentieel levensbedreigend
door het optreden van hartritmestoornissen, een acute
hartstilstand of spierverlammingen.
Hyperkalaemia

With normal renal function, severe and life-threatening
hyperkalaemia is rare (may occur in severe trauma, sepsis
and acidosis)

58
High [K+] in the ECF can be associated with cardiac
rhythm disturbances and asystole
Hyperkalaemia
Behandeling


Exogene bron STOPPEN
Acuut:
 Shift van kalium van ECF



IC
NaHCO3- (100 ml 8.4%): werkt na 5 à 10 min, gedurende 2
u en kan na 2 u herhaald worden
Insuline en Glucose: 50 à 100 ml glucose 50% met 10 E
AR, gevolgd door drip en Glucose-infuus: werkt na 15 min,
ged. 4 u
Nebulized albuterol 10 - 20 mg (ventolin)
 Potassium removal



59
Lasix 1 mg/kg IV (cave: polyurie)
Kayexalaat peroraal of lavement: 15 à 30 g in 50 à 100 ml
sorbitol 20% (max effect na 6 u)
Hemodialyse
Hyperkalaemia
Behandeling

Acuut:
 Bij ECG veranderingen: Ca2+: vermindert de verhoogde
membraan-excitabiliteit; werkt slechts 5 min, kan herhaald
worden (1 g Ca2+): 5 – 10 ml 10% calciumgluconaat

Subacuut:
 Insuline (drip aan 4 E/h) en Glucose 20% aan 100 ml/h
 Zo nodig dialyse
60
Hypokalaemia
61
Hypokalaemia
62

Low levels of potassium in postoperative patients are
common but hypokalaemia is rarely so severe as to
produce muscle weakness, ileus or arrhythmias.

At risk are
 Patients with large and continuous fluid loss from the
gastrointestinal tract are prone to develop
hypokalaemia.
 Patients treated with diuretics
 Elderly patients
Hypokalemie
Risicogroepen
63

Gebruik van diuretica

Patiënten met braken en diarree

Ouderen
Hypokalaemia
Oorzaken:
 Vals: tgv verhoogde leucocytose (>100.000/µl)
 Excessieve kalium excretie (renaal): diuretica,
hypomagnesiëmie, overmaat mineralocorticoïden,
hyperaldosteronisme, genetische renale tubulaire defecten,
polyurie
 GI losses: braken/ maagdrainage, diarrhee,
malabsorptie, laxativa
 Huid: zweten, brandwonden
 Transcellulaire shift: alkalose (hyperventilatie), verhoogde
insuline-beschikbaarheid, ß-adrenerge activiteit, hypothermie
 Verminderde intake door alcoholisme, anorexie;
kaliumvrije infusen
64
Hypokalaemia
Symptomen:
 Neurologisch/neuromusculair: spierzwakte, paralyse,
kramp, myalgie, paresthesieën, rhabdomyolyse,
verminderde peesreflexen
 Gastrointestinaal: ileus, obstipatie, nausea/vomitus
 Cardiaal: ECG-afwijkingen (U-golven) met of zonder
ritmestoornis (ES, sinusBC, AVB, VF) (cave combinatie
hypokaliëmie en digoxine)
 Renaal: concentratiestoornis (nefrogene DI): polyurie/
polydipsie
 Endocrien: Hyperglycemie
65
Hypokaliëmie
Gevaren



Paralyse ademhalingsspieren, respiratoire insufficiëntie
Hartritmestoornissen
Rhabdomyolyse
U-golf
66
Vlakke T-golf
ST-segment veranderingen
Hypokaliëmie
Diagnostiek

Onderscheid renaal en extrarenaal verlies.
 Als kalium in de urine < 20 mmol/24u: extrarenaal verlies, zuurbase-evenwicht meten en verder onderscheid maken:
67
Hypokaliëmie
Diagnostiek

Onderscheid renaal en extrarenaal verlies.
 Als kalium in de urine > 30 mmol/24u: renaal verlies, eerste
stap is de beoordeling v/d bloeddruk. Bij normotensieve patiënt
verder onderscheid maken met behulp van zuur-baseevenwicht en diagnostische lijn:
68
Hypokaliëmie
Diagnostiek

69
Bij hypertensie serum renine en aldosteron meten en
vervolgens beoordeling zoals onderstaand:
Hypokaliëmie
Behandeling ~ (a)symptomatisch

Orale supplementen
40 mEq KCl

Parenterale supplementen
 1 g KCl = 13 mEq K
 Maximaal 2 x 10 à 20 mEq over 1 à 2 uur (uitz. tot 4x)
 Gemiddeld extra over 12 uur: 20 – 40 – 60 mEq volstaan.
*Faster rates may precipitate arrhythmias and should only be undertaken on a unit
where the patient can be monitored for any ECG changes.
70
Treatment - Potassium replacement

Rule of thumb:
10 mEq IV replaces 0.1 mmol/L in serum

e.g. K+ 2.6 mmol/l
3.8 mmol/l
 1.2 mmol/l correction
 0.1 mmol/l = 10 mEq
 1.2 x 10/0.1 mmol = 120 mEq
71
Hypokaliëmie
Behandeling ~ (a)symptomatisch

Opmerkingen:
 Chronische hypokaliëmie bij asymptomatische patiënten moet
niet onmiddellijk genormaliseerd worden
 Overcorrectie kan meer schade aanrichten dan de hypokaliëmie
zelf. Doses van 10 - 20 mEq/u kunnen snel leiden tot
hyperkaliëmie, vnl. bij begeleidende acidose, diabetes mellitus,
renale tubulaire acidose en in aanwezigheid van NSAID, RAAS
blokkers en -blokkers.
 Kalium via een perifeer infuus is caustisch en doet pijn.
 Het kaliumdeficit bedraagt ongeveer
 300 mEq bij K < 3 mEq/L
 700 mEq bij waarden < 2 mEq/L.
72
Hypocalcaemia
73
Calcium


<1% of total body calcium is located in the EC
compartment
Three forms:
1. 40% protein bound
2. 10% complexed to phosphate and other anions
3. 50% ionized: responsible for neuromuscular stability




74
For every 1 g/dl decrease in albumin adjust
total serum calcium by 0.8 mg/dl
Daily intake: 1 – 3 g/day
Excretion: bowel & (renal)
[Ca2+]: 8.5 – 10.5 mg/dl or 2.15 – 2.60 mmol/l
Hypocalcaemia: [Ca2+ ] < 8.8 mg/dl
Symptoms & Causes










75
Paresthesia, cramps, Neuromuscular spasms
Hyperreflexia - Tetany – Chvostek’s/ Trousseau’s sign - E
Increased QT interval
VF
Cardiac depression – heart failure
Pancreatitis, pancreatic and small bowel fistulas
Chronic Renal Failure
Decreased Vitamin D
Hypoparathyroidism or post thyroid surgery
Massive soft tissue infections (necrotizing fasciitis), Sepsis
Polytransfusion (citrate)
Hypocalcaemia: [Ca2+ ] < 8.8 mg/dl
Treatment


Calcium and Vitamin D replacement
Asymptomatic
 Calcium carbonate PO
 Calcium gluconate IV (2 g)

Acute symptoms
 Calcium gluconate IV (10%)

76
Refractory hypocalcemia if coexisting hypomagnesemia
Hypercalcaemia
77
Hypercalcaemia: Total [Ca2+] > 10 mg/dl
Causes


Hyperparathyroidism (primary or 2nd)
Cancer-bony metastases
These 2 reasons account for 90% of
hypercalcaemia
78
Hypercalcaemia: Total [Ca2+] > 10.5 mg/dl
Symptoms
 N/V common, ileus, constipation, abdominal pain,
anorexia & thirst (polydipsia)
 Hypovolemia, hypotension
 Arrythmia’s: shortened QT interval, prolonged PR &
QRS
AVB … arrest
 Polyuria and nephrolithiasis
 Confusion, coma
Symptoms usual occur [Ca2+] > 12 mg/dl
Critical level: [Ca2+] > 15 mg/dl
79
Hypercalcaemia: Total [Ca2+] > 10 mg/dl
Treatment

NS diuresis with or without furosemide (lasix®)

Calcitonin
 Given as 4 U/kg q 12
 Mild effect (decreases Ca2+ by 0.5 mmol/L)

Biphosphonates
 Etidronate 7.5 mg/kg in 250 ml NS over 2 hours for 3 days
 Zometa 4 mg IV infusion over 15 minutes, repeat in 7 days

80
Hemodialysis
Hypophosphataemia
81
Phosphate
82

Intracellular anion

Renal excretion

Is involved in energy produced during
glycolysis

Daily intake: 0.8 - 1 gram phosphate
Hypophosphataemia: PO4- < 2.6 mg/dl
Causes

intake
 Decreased GI absorption (malabsorption, phosphate
binders, malnutrition)

excretion
 Diuretics (carbonic anhydrase inhibitors)
 Hyperparathyroidism
 Metabolic acidosis (diabetic ketoacidosis), …

Intracellular shift
 Refeeding syndrome, hungry bone syndrome
 Glucose loading + insulin
 Respiratory Alkalosis
83
Hypophosphataemia: PO4- < 2.6 mg/dl
Symptoms






84
Often silent; however
Exacerbate Chronic Heart Failure
Anemia
Decreases 2,3-diphosphoglycerate (shifts the
oxyhemoglobin dissociation curve to the left)
Muscle weakness
Cardiac dysfunctions
Hypophosphataemia: PO4- < 2.6 mg/dl
Treatment

Oral replacement for values < 2 mg/dl
 Recommendation: 1200 – 1500 mg/day (kaliumfosfaatdrank)

IV replacement for values < 1 mg/dl
 0.08-0.16 mmol/kg IV over 6 hours (kaliumnatriumfosfaat )
85
Hyperphosphataemia
86
Hyperphosphataemia: PO4- > 4.8 mg/dl


Symptoms
?
 Itching
 Chronic: metastatic calcifications
Causes
 Renal excretion: CKD, hypoparathyroidism
 Excessive administration: IV hyperalimentation,
Phosphate containing laxatives
 Cell destruction: rhabdomyolysis, Tumor necrosis,
hemolysis, sepsis, …

87
Treatment
 Phosphate binders: Sucralfate, calcium & non-Ca
 Hemodialysis if RF
Hypomagnesaemia
88
Magnesium





89
Primarily IC cation
½ of the total body Mg content = bone
In EC compartment: 1/3 is bound to serum
albumin
Daily intake: 20 mEq/day
Excretion: Feces & urine
Hypomagnesaemia: Mg2+ < 1.5 mg/dl
Causes
Common in hospitalised patients

intake: alcoholism, starvation, prolonged IV fluids

renal excretion: alcohol, diuretics (furosemide),
aminoglycosides, cisplatin, Diabetes mellitus ( aldo)

pathologic losses: diarrhea, malabsorption, acute
pancreatitis, …
90
Hypomagnesaemia: Mg2+ < 1.5 mg/dl
Symptoms

Neuromuscular & CNS hyperactivity
(~ hypocalcemia): hyperreflexia, muscle tremor, tetany,
Chvostek’s & Trousseau’s signs, seizures

Arrhythmias (prolonged QT & PR, ST … torsades de
pointes)

Can also cause




91
Decreased K+ (40%)
Decreased PO4- (30%)
Decreased Na+ (27%)
Decreased Ca2+ (22%)
Hypomagnesaemia: Mg2+ < 1.5 mg/dl
Treatment

Oral replacement
 Magnesium oxide 400 mg (Magnetop, Promagnor)
 Magnesium gluconate 500 mg (Ultra Mg)

IV replacement


1 - 2 g over 1 h infusion (MgSO4)
If Mg <1 mEq/l (<1.2 mg/dl or <0.5 mmol/l)
 1 mEq/kg in 250 ml saline over 24h during 1 day, then
 0.5 mEq/kg …..
during 2 days
92
Hypermagnesaemia
93
Hypermagnesaemia: [Mg2+] > 2.5 mg/dl
Causes & Symptoms



Is rare
Hemolysis
Renal insufficiency (cave Mg containing anti-acids &
laxatives)




94
Nausea, vomiting, weakness
Hyporeflexia – (4 mg/dl or 1.74 mmol/l)
Complete heart block – (10 mg/dl or 4.35 mmol/l)
Cardiac arrest – (13 mg/dl or 5.65 mmol/l)
Hypermagnesaemia: [Mg2+]> 2.5 mg/dl
Treatment



95
Calcium gluconate 1 g IV over 2 - 3 minutes
Volume replacement and furosemide
Hemodialysis
Acid-base homeostasis
96
Acid-base homeostasis

pH of body fluids is maintained within a narrow range
despite
 Large endogenous acid load (by-product of metabolism)
neutralized by buffer systems (intracellular proteins and
phosphates and extracellular bicarbonate-carbonic acid system)
and
excreted by lungs and kidneys
97
Acid-base homeostasis
In response to metabolic abnormalities
Changes (fast) in ventilation are mediated by hydrogensensitive chemoreceptors (carotid body and brain stem)
 acidosis stimulates CHR
ventilation
 alkalosis decreases CHR activity
ventilation
In response to respiratory abnormalities
Kidneys increase or decrease bicarbonate reabsorption
(begins after 6h)
 respiratory acidosis stimulates bicarbonate reabsorption
 respiratory alkalosis decreases bicarbonate reabsorption
98
Metabolic acidosis
Acute
(uncompensated)
Chronic
(partially
compensated)
pH
PCO2
N
Plasma HCO3-
Anion gap = (Na) – (Cl + HCO3): index of unmeasured anions
Normal AG < 12 mmol/l
Hypoalbuminemia decreases AG
AGcorrected = AGactual - 2.5 (4.5 – albumin)]
High AG
99
exogenous acid ingestion or endogenous acid production
Metabolic acidosis
Etiology
Increased AG


100
Normal AG
Exogenous acid ingestion

 Ethylene glycol
 Salicylate
 Methanol


Endogenous acid
production

 Ketoacidosis
 Lactic acidosis
 Renal insufficiency


Acid administration (HCl)
Loss of bicarbonate
GI losses (diarrhea,
fistulas)
Ureterosigmoidoscopy
Renal tubular acidosis
Carbonic anhydrase
inhibitor
Metabolic acidosis
Acute
(uncompensated)
Chronic
(partially
compensated)
pH
PCO2
N
Plasma HCO3-
Increased intake or increased generation of acids or increased loss of
bicarbonate
Body
produces buffers (extracellular bicarbonate, intracellular buffers
from bone and muscle),
increases ventilation (Kussmaul),
increases renal reabsorption and generation of bicarbonate
Increases renal excretion of H+ (NH4+)
101
Metabolic alkalosis
Acute
(uncompensated)
Chronic
(partially
compensated)
N
( )
pH
PCO2
Plasma HCO3-
Increased bicarbonate generation
Decreased renal bicarbonate excretion
Loss of acids
Worsened by K+ depletion (K+ exchange with intracellular H+)
102
Metabolic alkalosis
Etiology
Increased bicarbonate
generation


Chloride losing (>20 mEq/l)

 Mineralocorticoid excess
 Profound K+ depletion

Chloride sparing (<20 mEq/l)
 Loss from gastric secretions
(emesis or NG suction)
 diuretics

Excess administration of alkali





103
Impaired bicarbonate
excretion
Acetate in parenteral nutrition
Citrate in blood transfusion
Antacids
Bicarbonate
Milk-alkali syndrome
GFR
Increased bicarbonate
reabsorption
Respiratory acidosis
Acute
(uncompensated)
Chronic
(partially
compensated)
pH
PCO2
Plasma HCO3-
N
Retention of CO2 secondary to alveolar hypoventilation
104
Respiratory acidosis
Etiology





105
Narcotics
CNS injury
Pulmonary, significant
 Secretions, mucus plug, atelectasis
 Pneumonia, pleural effusions
Pain from abdominal or thoracic injuries or incisions
Limited diaphragmatic excursion from intra-abdominal
pathology
 Abdominal distention
 Abdominal compartment syndrome
 Ascites
Respiratory alkalosis
Acute
(uncompensated)
Chronic
(partially
compensated)
pH
PCO2
Plasma HCO3-
N
Secondary to hyperventilation due to
•
•
•
•
Pain, Anxiety
Pulmonary embolism
Neurologic disorders (CNS injury, assisted ventilation)
(salicylates, fever, gram-negative bacteremia, thyrotoxicosis,
hypoxemia)
Acute hypocapnia
hypokalemia, hypophosphatemia, hypocalcemia
arrhythmias, paresthesias, muscle cramps and seizures
106
Take Home Messages


Corrigeer vocht- en elektrolytenstoornissen
preoperatief
Meestal gecombineerde vochtelektrolytenstoornissen
 Hypovolemische hyponatremie (depletie zout en water)
 Hypovolemische hypernatremie (rel. water > zout;
zweten, diarree, brandwonden)

Bereken dagelijkse behoefte
 Hou rekening met ev. verliezen
 Vochtbilan/ G/ BD – HR/ T°
107

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