Fluid Advance Therapy
nFLUID Therapy
nFluid and electrolyte balance is an extremely complicated thing.
nImportance
nNeed to make a decision regarding fluids in pretty much every hospitalized patient.
nCan be life-saving in certain conditions
nloss of body water, whether acute or chronic, can cause a range of problems from mild lightheadedness to convulsions, coma, and in some cases, death.
nThough fluid therapy can be a lifesaver, it's never innocuous, and can be very harmful.
nKinds of IV Fluid solutions
nHypotonic - 1/2NS
nIsotonic - NS, LR, albumen
nHypertonic – Hypertonic saline.
n
nCrystalloid
nColloid
nCrystalloid vs Colloid
Type of particles (large or small)
nFluids with small “crystalizable” particles like NaCl are called crystalloids
nFluids with large particles like albumin are called colloids, these don’t (quickly) fit through vascular pores, so they stay in the circulation and much smaller amounts can be used for same volume expansion. (250ml Albumin = 4 L NS)
–Edema resulting from these also tends to stick around longer for same reason.
–Albumin can also trigger anaphylaxis.
n
There are two components to fluid therapy:
nMaintenance therapy replaces normal ongoing losses, and
nReplacement therapy corrects any existing water and electrolyte deficits.
nMaintenance therapy
nMaintenance therapy is usually undertaken when the individual is not expected to eat or drink normally for a longer time (eg, perioperatively or on a ventilator).
nBig picture: Most people are “NPO” for 12 hours each day.
n
nPatients who won’t eat for one to two weeks should be considered for parenteral or enteral
nutrition.
n
Maintenance Requirements can be broken
into water and electrolyte requirements:
nWater —
nTwo liters of water per day are generally sufficient for adults;
nMost of this minimum intake is usually derived from the water content
of food and the water of oxidation, therefore
nit has been estimated that only 500ml of water needs be imbibed given normal diet and no increased losses.
nThese sources of water are markedly reduced in patients who are not eating and so must be replaced by maintenance fluids.
n
nwater requirements increase with:
fever, sweating, burns, tachypnea, surgical drains, polyuria, or ongoing significant gastrointestinal losses.
nFor example, water requirements increase by 100 to 150 mL/day for each C degree of body temperature elevation.
nSeveral formulas can be used to calculate maintenance fluid rates.
n
nA comparison of formulas produces a wide
variety of fluid recommendations:
n2000 cc to 3378 cc for an obese woman who is
65 inches tall and weighs 248 pounds (112.6 kg)
nThis is a reminder that fluid needs, no matter what formula is used, are at best an estimation.
n4/2/1 rule a.k.a Weight+40
nI prefer the 4/2/1 rule (with a 120 mL/h limit) because it is the same as for pediatrics.
n
n4/2/1 rule
4 ml/kg/hr for first 10 kg (=40ml/hr)
then 2 ml/kg/hr for next 10 kg (=20ml/hr)
then 1 ml/kg/hr for any kgs over that
This always gives 60ml/hr for first 20 kg
then you add 1 ml/kg/hr for each kg over 20 kg
This boils down to: Weight in kg + 40 = Maintenance IV rate/hour.
For any person weighing more than 20kg
nMaintenance IV rate:
4/2/1 rule -> Weight in kg + 40
nWhat to put in the fluids
n
nStart: D5 1/2NS+20 meq K @ Wt+40/hr
na reasonable approach is to start 1/2 normal saline to which 20 meq of potassium chloride is added per liter.
(1/2NS+20 K @ Wt+40/hr)
nGlucose in the form of dextrose (D5) can be added to provide some calories while the patient is NPO.
nThe normal kidney can maintain sodium and potassium balance over a wide range of intakes.
nSo,start:
D5 1/2NS+20 meq K
at a rate equal to their weight + 40ml/hr, but no greater than 120ml/hr.
nthen adjust as needed, see next page.
nStart D5 1/2NS+20 meq K, then adjust:
nIf sodium falls, increase the concentration (eg, to NS)
nIf sodium rises, decrease the concentration (eg, 1/4NS)
nIf the plasma potassium starts to fall, add more potassium.
nIf things are good, leave things alone.
nUsually kidneys regulate well, but:
Altered homeostasis in the hospital
nIn the hospital, stress, pain, surgery can alter the normal mechanisms.
nIncreased aldosterone, Increased ADH
nThey generally make patients retain more water and salt, increase tendency for edema, and become hypokalemic.
n
n
n
n
n
Now onto Part 2 of the presentation:
nHypovolemia
nHypovolemia or FVD is result of water & electrolyte loss
nCompensatory mechanisms include: Increased sympathetic nervous system stimulation with an increase in heart rate & cardiac contraction; thirst; plus release of ADH & aldosterone
nSevere case may result in hypovolemic shock or prolonged case may cause renal failure
nCauses of FVD=hypovolemia:
n
nGastrointestinal losses: N/V/D
nRenal losses: diuretics
nSkin or respiratory losses: burns
nThird-spacing: intestinal obstruction, pancreatitis
nReplacement therapy.
n
nA variety of disorders lead to fluid losses that deplete the extracellular fluid .
nThis can lead to a potentially fatal decrease in tissue perfusion.
nFortunately, early diagnosis and treatment can restore normovolemia in almost all cases.
n
nThere is no easy formula for assessing the degree of hypovolemia.
nHypovolemic Shock, the most severe form of hypolemia, is characterized by tachycardia, cold, clammy extremities, cyanosis, a low urine output (usually less than 15 mL/h), and agitation and confusion due to reduced cerebral blood flow.
nThis needs rapid treatment with isotonic fluid boluses (1-2L NS), and assessment and treatment of the underlying cause.
nBut hypovolemia that is less severe and therefore well compensated is more difficult to accurately assess.
nHistory for assessing hypovolemia
nThe history can help to determine the presence and etiology of volume depletion.
nWeight loss!
nEarly complaints include lassitude, easy fatiguability, thirst, muscle cramps, and postural dizziness.
nMore severe fluid loss can lead to abdominal pain, chest pain, or lethargy and confusion due to ischemia of the mesenteric, coronary, or cerebral vascular beds, respectively.
nNausea and malaise are the earliest findings of hyponatremia, and may be seen when the plasma sodium concentration falls below 125 to 130 meq/L. This may be followed by headache, lethargy, and obtundation
nMuscle weakness due to hypokalemia or hyperkalemia
nPolyuria and polydipsia due to hyperglycemia or severe hypokalemia
nLethargy, confusion, seizures, and coma due to hyponatremia, hypernatremia, or hyperglycemia
nBasic signs of hypovolemia
nUrine output, less than 30ml/hr
nDecreased BP, Increase pulse
n
nPhysical exam for assessing volume
nphysical exam in general is not sensitive or specific
nacute weight loss; however, obtaining an accurate weight over time may be difficult
ndecreased skin turgor - if you pinch it it stays put
ndry skin, particularly axilla
ndry mucus membranes
nlow arterial blood pressure (or relative to patient's usual BP)
northostatic hypotension can occur with significant hypovolemia; but it is also common in euvolemic elderly subjects.
ndecreased intensity of both the Korotkoff sounds (when the blood pressure is being measured with a sphygmomanometer) and the radial pulse ("thready") due to peripheral vasoconstriction.
ndecreased Jugular Venous Pressure
nThe normal venous pressure is 1 to 8 cmH2O, thus, a low value alone may be normal and does not establish the diagnosis of hypovolemia.
nSIGNS & SYMPTOMS OF Fluid Volume Excess
nSOB & orthopnea
nEdema & weight gain
nDistended neck veins & tachycardia
nIncreased blood pressure
nCrackles & wheezes
npleural effusion
nFor the EBM aficionados out there.
nA JAMA 1999 systematic review of physical diagnosis of hypovolemia in adults
nCONCLUSIONS: A large postural pulse change (> or =30 beats/min) or severe postural dizziness is required to clinically diagnose hypovolemia due to blood loss, although these findings are often absent after moderate amounts of blood loss. In patients with vomiting, diarrhea, or decreased oral intake, few findings have proven utility, and clinicians should measure serum electrolytes, serum blood urea nitrogen, and creatinine levels when diagnostic certainty is required.
nWhich brings us to:
Labnormalities seen with hypovolemia
na variety of changes in urine and blood often accompany extracellular volume depletion.
nIn addition to confirming the presence of volume depletion, these changes may provide important clues to the etiology.
nBUN/Cr
nBUN/Cr ratio normally around 10
nIncrease above 20 suggestive of “prerenal state”
n(rise in BUN without rise in Cr called “prerenal azotemia.”)
nThis happens because with a low pressure head proximal to kidney, because urea (BUN) is resorbed somewhat, and creatinine is secreted somewhat as well
nHgb/Hct
nAcute loss of EC fluid volume causes hemoconcentration (if not due to blood loss)
nAcute gain of fluid will cause hemodilution of about 1g of hemoglobin (this happens very often.)
nPlasma Na
nDecrease in Intravascular volume leads to greater avidity for Na (through aldosterone) AND water (through ADH),
nSo overall, Plasma Na concentration tends to decrease from 140 when hypovolemia present.
nUrine Na
nUrine Na – goes down in prerenal states as body tries to hold onto water.
nGetting a FENa helps correct for urine concentration.
nScrewed up by lasix.
nCalculator on PDA or medcalc.com
nIV Modes of administration
nPeripheral IV
nPICC
nCentral Line
nIntraosseous
nIV Problem:
Extravasation / “Infiltrated”
nThe most sensitive indicator of extravasated fluid or "infiltration" is to transilluminate the skin with a small penlight and look for the enhanced halo of light diffusion in the fluid filled area.
nChecking flow of infusion does not tell you where the fluid is going