FLUID BALANCE AND REPLACEMENT THERAPY

FLUID BALANCE, REPLACEMENT THERAPY AND PATHOPHYSIOLOGYPRESENTERS : DR. ANNE IRUNGU DR . NGATIA EUNICEDR. IFRAH HERSI FACILITATOR : DR. E.S OTIENO

OBJECTIVESTo learn and understand the physiology of TBW and its compartmentsTo understand the homeostasis of water and electrolytesTo know the factors that determine fluid replacementTo know the composition of various commonly used replacement fluids.

NORMAL PHYSIOLOGYIn an average adult of weight 60 kgs, water makes 70% which is 42 litres.In the lean = 70%, in obese = 50%, in babies up to 78%Intracellular - 50% - 30litresExtracellular 20%- Interstitial -12% - 7.2L - Intravascular -8%-4.8LTranscellular 1-3%(RTS,GIT,RS, Syst,Glands,eye)

4Intracellular Fluid CompartmentConstitute approximately 28 of the 42 liters (about 40 % of the total body weight)

The main electrolytes are potassium and magnesium5Extracellular Fluid CompartmentConstitute approximately 14 of the 42 liters (about 20 % of the TBW)Interstitial Fluid = of extracellular fluid (15% of TBW)Plasma= of the extracellular fluid = 3 liters (5% of TBW)The main electrolytes are sodium and chloride.6Blood volumeContains both: Extracellular fluid (the fluid in plasma)Intracellular fluid (the fluid in the red blood cells).The average blood volume of adults = 5.4 liters (8 % of body weight)60 % - plasma40 %- red blood cells7Transcellular FluidConstitute approximately 1 2L of body fluidIncludes fluids in the:SynovialPericardialPeritonealIntraocularCSFPleural

8FLUID BALANCE

DEFINITIONSDiffusion movement of particles down a concentration gradient Osmosis diffusion of water across a selectively permeable membraneOsmotic pressure- The precise amount of pressure required to prevent the osmosis. OSMOTIC PRESSUREIn an ideal solution, osmotic pressure (P) P=nRT/Vn is the number of particles, R is the gas constantT is the absolute temperatureV is the volume.For this reason, the concentration of osmotically active particles is usually expressed in osmoles.

ContThe osmolarity is the number of osmoles per liter of solution (e.g., plasma), whereas the osmolality is the number of osmoles per kilogram of solvent Tonicity to describe the osmolality of a solution relative to plasma.Solutions that have the same osmolality as plasma are said to be isotonic; those with greater osmolality are hypertonic; and those with lesser osmolality are hypotonic.13The cell membrane is highly permeable to water but not to most of the electrolytes in the body. The capillary membrane is highly permeable to both water and electrolytes.

13Fluid Movement Among CompartmentsCompartmental exchange is regulated by osmotic and hydrostatic pressuresNet leakage of fluid from the blood is picked up by lymphatic vessels and returned to the bloodstreamExchanges between interstitial and intracellular fluids are complex due to the selective permeability of the cellular membranesTwo-way water flow is substantialExtracellular and Intracellular FluidsIon fluxes are restricted and move selectively by active transportNutrients, respiratory gases, and wastes move unidirectionallyPlasma is the only fluid that circulates throughout the body and links external and internal environmentsOsmolalities of all body fluids are equal; changes in solute concentrations are quickly followed by osmotic changes

Continuous Mixing of Body Fluids

Fluid balance regulationHormones involved; ADH, RAAS/aldosterone, ANP/BNP, cortisolOrgans involved: Hypothalamus, kidneys, skin, adrenals, liver, heartPolyuria : Urine >2.5 litersOliguria : 295 m-osmol/L).

Note: the above is variable.

2. Colloids (Plasma expanders).

Colloids are suspension intravenous fluids containing particles with large molecular weight. Molecules with large molecular weight cannot pass through a normal capillary wall. Therefore, when infused, they cannot leave the intravascular space. Colloids are indicated in treatment hypovolaemia and other types of shock. They can be classified into 3 main groups:Carbohydrate polymers. E.g. dextran and glucomerProtein polymers. E.g. hemacel, gelatinSynthetic plastic polymers. E.g. methyl cellulose

ADVANTAGESCRYSTALLOIDSInexpensiveNon allergicReplace depleted ECFLong shelf life

COLLOIDSLarge molecules hence retained longer in intravascular spaceIf membrane permeability is intact, expand plasma volume hence lower fluid requirementDISADVANTAGESCRYSTALLOIDSShort lived hemodynamic effectsLarger fluid volumes risk of peripheral and pulmonary edemaCOLLOIDSExpensiveAnaphylactoid reaction Infections (HES)CoagulopathyImpaired x-matching In diseased states with inc capillary permeability, can leak, cerebral edema, raised ICP343. Blood and blood productsWhole blood Packed cellsPlateletsPlasma

4. Parenteral nutrition fluids.Parenteral nutrition fluids can grouped into : Carbohydrate solutions e.g. Sorbitol, xylitol, 25% dextrose.Lipid (fatty acids) solutions e.g. intralipid, lipovenousProtein (amino acids) solutions e.g. Aminosol.

DONT FORGETWARM FLUIDS In hypothermia the oxyhaemoglobin dissociation curve is shifted to the left which impairs peripheral oxygen unloading.Shivering will compound the lactic acidosis that accompanies hypovolaemia.increases bleeding.increases the risk of infection & cardiac morbid eventsClose patient monitoring vitalsORDER LABS electrolytes, creatinineInput output chartDaily weights (especially infants and geriatrics)Disorders of water balance: DehydrationWater loss exceeds water intake and the body is in negative fluid balanceCauses include: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, and diuretic abuseSigns and symptoms: cottonmouth, thirst, dry flushed skin, and oliguriaProlonged dehydration may lead to weight loss, fever, and mental confusionOther consequences include hypovolemic shock and loss of electrolytes

Disorders of water balance- dehydration

Excessive loss of H2O from ECFECF osmotic pressure risesCells lose H2O to ECF by osmosis; cells shrink(a) Mechanism of dehydrationDisorders of Water Balance: Hypotonic HydrationRenal insufficiency or an extraordinary amount of water ingested quickly can lead to cellular over hydration, or water intoxicationECF is diluted sodium content is normal but excess water is presentThe resulting hyponatremia promotes net osmosis into tissue cells, causing swellingThese events must be quickly reversed to prevent severe metabolic disturbances, particularly in neurons

Disorders of Water Balance: Hypotonic Hydration

Excessive H2O enters the ECFECF osmotic pressure fallsH2O moves into cells by osmosis; cells swell(b) Mechanism of hypotonic hydrationDisorders of Water Balance: EdemaAtypical accumulation of fluid in the interstitial space, leading to tissue swellingCaused by anything that increases flow of fluids out of the bloodstream or hinders their returnFactors that accelerate fluid loss include: Increased blood pressure, capillary permeability Incompetent venous valves, localized blood vessel blockage Congestive heart failure, hypertension, high blood volumeEdemaHindered fluid return usually reflects an imbalance in colloid osmotic pressures Hypoproteinemia low levels of plasma proteinsForces fluids out of capillary beds at the arterial endsFluids fail to return at the venous endsResults from protein malnutrition, liver disease, or glomerulonephritis

EdemaBlocked (or surgically removed) lymph vessels:Cause leaked proteins to accumulate in interstitial fluidExert increasing colloid osmotic pressure, which draws fluid from the bloodInterstitial fluid accumulation results in low blood pressure and severely impaired circulation

Electrolyte BalanceElectrolytes are salts, acids, and bases, but electrolyte balance usually refers only to salt balanceSalts are important for:Neuromuscular excitabilitySecretory activityMembrane permeabilityControlling fluid movementsSalts enter the body by ingestion and are lost via perspiration, feces, and urine

Electrolyte BalanceElectrolytes are salts, acids, and bases, but electrolyte balance usually refers only to salt balanceSalts are important for:Neuromuscular excitabilitySecretory activityMembrane permeabilityControlling fluid movementsSalts enter the body by ingestion and are lost via perspiration, feces, and urine

Sodium in Fluid and Electrolyte BalanceSodium holds a central position in fluid and electrolyte balanceSodium salts:Account for 90-95% of all solutes in the ECFContribute 280 mOsm of the total 300 mOsm ECF solute concentrationSodium is the single most abundant cation in the ECFSodium is the only cation exerting significant osmotic pressureSodium in Fluid and Electrolyte BalanceThe role of sodium in controlling ECF volume and water distribution in the body is a result of:Sodium being the only cation to exert significant osmotic pressureSodium ions leaking into cells and being pumped out against their electrochemical gradientSodium concentration in the ECF normally remains stable

Sodium in Fluid and Electrolyte BalanceChanges in plasma sodium levels affect:Plasma volume, blood pressureICF and interstitial fluid volumesRenal acid-base control mechanisms are coupled to sodium ion transport

HypernatremiaDefined as serum sodium >/= 145mEq/L

Causes:Excess sodium intakeConcentrated formula, salt ingestion (seawater, accidental, Munchausen-by-proxy), hypertonic IV fluids, sodium bicarbonate, blood productsIncreased free water lossesRenal: diabetes insipidus, diuretics, tubular disorderGI: diarrhea, vomiting, colostomy/ileostomy output, malabsorptionInsensible: fever, tachypnea, burnsDecreased free water intakeIneffective breastfeeding, poor access to water, blunted thirst mechanisms, fluid restriction

Clinical Manifestations and Evaluation of HypernatremiaEarly neurologic signs include agitation and irritabilitycan progress to seizure and coma

Neurologic exam can reveal increased tone, brisk reflexes and nuchal rigidity

Lab evaluation can include:Serum osmolaritySerum glucoseUrine osmolarity and specific gravityNeurologic SequelaeIn acute phase: Intracellular fluid moves to extracellular space-volume loss in brain separation from meninges

If hypernatremia has existed for >2-3 days:Neurons protect themselves by making osmolytes to maintain gradientWith rapid correction, neurons can swell leading to cerebral edema

Mortality estimated at 10-16% despite correct rate of rehydration

Discussion: The facilitator can ask learners what pathologic sequelae may occur from the meningeal separation (hemorrhage, demyelination, venous sinus thrombosis)

51HyponatremiaDefined as serum sodium 7 mEq/L and/or symptomatic- severeHypokalemia3-3.4 mEq/L mild to moderate< 2.5-3 mEq/L and/or symptomatic-severe

PseudohyperkalemiaLab findings of falsely elevated serum K due to K movement out of the cells during or after a blood draw. Suspect in an asymptomatic patient with no apparent cause for K elevationLysis of red blood cellsSpecimen deterioration (cooling, prolonged storage)white blood cells, plateletsDrawing blood downstream from a vein into which K is infusing Trauma: forcible expression of blood (milking a heel stick)Exercise: fist clenching with blood draws

Hypokalemia CausesI. Shifting of K into intracellular spaceA) AlkalosisB) Insulin C) Beta-adrenergic activity

II. K losses ( total body K)A) GI trackB) UrineC) Sweat

III. K intake ( total body K): rarely the only cause

I. Shifting of K into intracellular spaceA) AlkalosisB) Insulin C) Beta-adrenergic activity II. K losses ( total body K)A) GI track: K concentration in lower GI track higher than in upper GI track B) Urine1) Meds: diuretics, amphotericin B, aminoglycosides 2) Renal dz (salt wasting nephropathies, renal tubular acidosis)3) Polyuria 4) Hypomagnesemia C) Sweat (think marathon running in the desert or CF)III. K intake ( total body K): rarely the only cause

60Hypokalemia Signs and SymptomsResolve with hypokalemia correctionI. MuscleA. Ascending WeaknessB. Ischemia: cramping, rhabdomyolysis, myoglobinuria. II. Cardiac A. Conduction abnormalities and arrhythmiasB. EKG Changes:ST segment depression and prominent U wave

Resolve with hypokalemia correctionI. MuscleA. Ascending Weakness : Can include respiratory muscles. GI musclesileusB. Ischemia: cramping, rhabdomyolysis, myoglobinuria. Normal exercise causes K release from muscle cells vasodilation muscle blood flow. In profound hypokalemia there is no K to be released and no vasodialationII. Cardiac A. Conduction abnormalities and arrhythmias: premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular block, and ventricular tachycardia or fibrillation C. EKG Changes (not seen in all pts): ST segment depression and prominent U wave

61Hyperkalemia CausesShifting of K into extracellular spaceA. Tissue (lots of cells) damage: burns, crush injury, rhabdomyolysis, tumor lysis B. AcidosisC. Hyperosmolar statesD. Insulin deficiencyII. Impaired Renal Excretion ( total body K)A. Renal insufficiency/failureB. Endocrine: adrenal insufficiency, renin, aldosterone, pseudohypoaldosteronism

III. IatrogenicA. K in IVF or TPNB. Medications: NSAIDS, ACE inhibitors, beta blockers, K sparing diuretics, trimethoprim, and many, many others

I. Shifting of K into extracellular spaceA. Tissue (lots of cells) damage: burns, crush injury, rhabdo, tumor lysis. Pt is dependent on others for positioning and movement. Could he have rhabdomyolysis due to being left in the same position for too long. Very unlikely with nl CKB. Acidosiss. H+ enter cell while Na+ and K+leave. Could be contributing (bicarb 13)C. Hyperosmolar states: An elevation in plasma osmolality results in osmotic water movement from the cells into the extracellular fluid. Also could be contributing since pt has elevated Na and elevated BUND. Insulin deficiency. Unlikely with nl glucoseII. Impaired Renal ExcretionExcretion depends on aldosterone and sufficient delivery of salt water to the nephronA. Renal insufficiency/failure: very likely given the oliguriaB. Encocrine: renin, aldosterone, Adrenal insufficiency, Pseudohypoaldosteronism: all less likely given pts age and presentationIII. IatrogenicHow much K are we giving in IVF or TPN. Unlikely to be a big contributor but the trainee should remember take K out of pts fluids! Lots of meds (NSAIDS, ACE inhibitors, beta blockers, K sparing diuretics, trimethoprim) NSAIDS decrease GFR and impair renin secretion. Definitely could be contributing. Stop ketoralac now and review medication list for nephrotoxicity and possible side effects of hyperkalemia

62HYPERKALEMIA SIGNS & SYMPTOMS. MuscleA. Ascending muscle weakness and paralysis B. Respiratory muscle weakness rare

II. CardiacA. Conduction abnormalities and arrhythmiasB. EKG Changes1. Peaked T waves

2. Loss of P wave

3. Widened QRS 4. Sine wave pattern

Signs and symptoms resolve with correction of the hyperkalemia.I. Severe muscle weakness or paralysis: ascending muscle weakness and paralysis (mimicks Guillain-Barr) Sphincter tone and cranial nerve function are typically intact, and respiratory muscle weakness is rare.

II. CardiacA. Conduction abnormalities and arrhythmias: sinus bradycardia, sinus arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and asystoleC. EKG changes: Peaked T wavesLoss of P waveWidened QRS sine wave patternRough (NOT perfect) correlation b/w EKG changes and K Hyperkalemia can be life-threatening even if EKG nlK 6-6.8: EKG changes in 43% >6.8: EKG changes in 55%Any EKG changes should be treated as an emergency

63Hyperkalemia Treatment. Do no harm A. Remove any K containing fluids B. Remove any medications that could be contributingII. Stabilize cell membranes: IV calcium III. Drive K back into cells A. Insulin and glucose B. AlbuterolIV. Remove excess K from the body A. Loop diuretics B. Cation exchange resin: Sodium polystyrene sulfonate (Kayexalate) C. Hemodialysis

I. Do no harm: remove any exacerbating factors. Stop any K containing IVF or TPN. Stop any medications that could be causing hyperkalemia either primarily or secondarilyII. Stabilize cell membranes: calcium Stabilizes myocardium. Effective even for normocalcemic pts. Movement of K into the cells via Na-K ATP pump is responsible for the resting membrane potential. If extracellular K , concentration gradient across myocytes eventually leading to slowing of myocardial functioning. -Give if there are any ekg changes and/or K is rapidly increasing K (if peaked T waves alone and rapidly acting methods being initiated could consider holding Ca) Onset: immediate. Should see EKG improvement in 1-5min. Duration: 30min-1hr10-20mg/kg Repeat q5-10min if the ECG changes persist or recur Calcium chloride: venous irritation and extravasation Calcium gluconate: requires liver metabolism (so might not work in pts with shock and poor liver perfusion)

III. Drive K back into cellsactivates the Na-K-ATPase pump Insulin and glucose: Onset: 15-30 minDuration: Peak 30 60min Lasts 4-6hrs-Q1hr BGK by 0.5-1 mEq/LAlbuterolWatch for tremor, tachycardia, anxiety, flushing. K by 0.5-1.5 mEq/L15-30min. The peak at 90 minutes with nebulization

IV. Remove excess K from the bodyLoop diuretics: 1mg/kg/dose. total body K by renal K excretion . Consider adding NS bolus to maximize distal sodium delivery and flowOnset: 15 min to 1hrKayexelate:

64Calcium (Ca2+)

There are 1300 g (33,000 mmol) in the body, 99% being in bone and only 1% being freely exchangeable. The normal serum concentration is 2.2-2.5 mmol/lCa2+ disorders:Osteomalacia (Rickets in children)OsteoporosisHypercalcaemiahypocalcermia

MagnesiumThis is distributed mainly in bone (500-600mmol) and the ICF (500-850 mmol). GI losses are the most common cause of hypomagnesaemiaHypomagnesaemia causes blood PTH levels to fall, with secondary hypocalcaemia. Patients present with neuromuscular irritability convulsions and arrthymiasReplace magnesium intravenously over 48 hours

Phosphate

This is an important constituent of food, the normal intake being 800-1400 mg/day. Most is in the ICF, and the normal serum concen- tration lies between 0.89 and 1.44 mmol/l. Symptoms of hypophosphatemia include myopathy, dysphagia, ileus, respiratory failure, impaired cardiac contractility and encephalopathy. Severe cases may necessitate cautious intravenous administration phosphate and saline over 6-12 hours with frequent monitoring of serum PO4 and other electrolytes. Excessive or too rapid intravenous administration risks precipitating acute hypocalcaemia and deposition of Ca2+ in soft tissues.

References Guyton AC, Hall JE. The microcirculation and the lymphatic system: capillary fluid exchange, interstitial fluid, and lymph flowReview of Medical Physiology, by GanongFluid choice for resuscitation of the trauma patient: a review of the physiological, pharmacological, and clinical evidence. Can J Anaesthesia. 2004 May;51(5):500-13. British Medical Bulletin 1999, 55 (No 4) 821-843; Fluid replacementCrystalloids and colloids in trauma resuscitation: a brief overview of the current debate; J Trauma. 2003 May;54(5 Suppl):S82-8 Phillips DP, et al.: Crystalloids vs. colloids: KO at the twelfth round? Critical Care 2013, 17:319.Perioperative fluid balance. English WA, English RE, Wilson IHPlasma substitutes. Minerva Anesthesiol. 2005 Dec;71(12):741-58