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.
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Introduction Three principles of management of fluid & electrolyte balance
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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 =
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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)
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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.
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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.
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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
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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, …)
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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)
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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,…)
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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, …)
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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
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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
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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
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273
Hypernatraemia
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Sodium
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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
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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
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Hypernatraemia Diagnostiek
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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
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Rusteloosheid, lethargie, … delirium, E, coma
Polyurie – oligurie Dorst Droge mucosae Orthostatische hypotensie, TC
Hypernatraemia Gevaren
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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
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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
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acuut hersenoedeem
Hyponatraemia
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Casus 2: 55 j Man – bekken#
Opname: [Na+] 119 mmol/L Creat 0.47 mg/dl [K+] 2.8 mmol/l
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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
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Water Excess (water toxicity)
Clinical features
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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
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Sodium Concentration (mEq/L) variable
Diarrhea
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Gastric secretions
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Furosemide diuresis
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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
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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
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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
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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)
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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
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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
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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
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Chronische hyponatriëmie: vermijd te snelle correctie en richt behandeling op onderliggende oorzaak.
Treatment
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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.
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Water restriction
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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
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Average daily intake: 50 – 100 mEq/l Renal excretion: 10 – 700 mEq/day
Hyperkalaemia
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Hyperkalaemia
Hyperkaliëmie: [K+] > 5,0 mmol/l
Risicogroepen: Patiënten met nierinsufficiëntie Hyperglycemie Onoordeelkundig gebruik van kaliumsupplementen of medicatie die de kaliumhuishouding beïnvloedt Ouderen
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Hyperkalaemia Oorzaken
Pseudohyperkaliëmie, bv. onzorgvuldige bloedafname intake: Supplements Blood transfusion
Release from cells (Redistribution) Rhabdomyolysis, tumor necrosis Acidosis; hyperglycemia (Osm
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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
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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)
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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
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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
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Hypokalaemia
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Hypokalaemia
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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
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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
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Hypokaliëmie Gevaren
Paralyse ademhalingsspieren, respiratoire insufficiëntie Hartritmestoornissen Rhabdomyolyse
U-golf
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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:
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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:
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Hypokaliëmie Diagnostiek
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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.
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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
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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
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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
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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
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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%)
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Refractory hypocalcemia if coexisting hypomagnesemia
Hypercalcaemia
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Hypercalcaemia: Total [Ca2+] > 10 mg/dl Causes
Hyperparathyroidism (primary or 2nd) Cancer-bony metastases
These 2 reasons account for 90% of hypercalcaemia
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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
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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
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Hemodialysis
Hypophosphataemia
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Phosphate
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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
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Hypophosphataemia: PO4- < 2.6 mg/dl Symptoms
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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 )
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Hyperphosphataemia
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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, …
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Treatment Phosphate binders: Sucralfate, calcium & non-Ca Hemodialysis if RF
Hypomagnesaemia
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Magnesium
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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, …
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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
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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
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Hypermagnesaemia
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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
