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     TRAUMA: ICU Fluids –

    Electrolytes, Shock

    D. Kapp, M.D.

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    TraumaIt is widely accepted to follow Advanced Trauma Life

    Support (ATLS) precepts of the American College ofSurgeons.

    The Main Three Elements of ATLS protocol are

    1. Primary Survey/ resuscitation

    2. Secondary survey3. Definitive care

    5 steps of Primary survey are ABCDE’s – Airway (& C-spine stabilization), Breathing, Circulation, Disability,

    Exposure and Environment.

    CIRCULATION is VITAL for adequate perfusion/oxygenation of tissues. Therefore, it must be continuallyassessed and fluids must be quantified and accounted for.

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    Trauma Triad of Death

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    Copyright © 2012 McGraw-Hill Medical. All rights reserved.

    Tissue hypoperfusion algorithm. The most common etiology for shock in the trauma patient is hypovolemia from loss of circulatingvolume.

    Legend:

    From: Chapter 12. Management of Shock

    Trauma, 7e, 2013

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    Copyright © 2012 McGraw-Hill Medical. All rights reserved.

    Tissue hypoperfusion algorithm. Trauma patients can be categorized into three general groups with respect to their response toresuscitative maneuvers.

    Legend:

    From: Chapter 12. Management of Shock

    Trauma, 7e, 2013

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    TRAUMA-Fluids

    2 Large-Bore IVs (14- 16 gauge), IV catheters in the upper

    extremities (peripheral IV access)

    For Pediatric Trauma: use the 20-20-10 rule for fluid

    resuscitation of the unstable pediatric trauma patient:

    First give a 20-cc/kg LR bolus followed by a 2nd bolus of 20-cc/

    kg LR bolus if needed; if the pt is still unstable after the 2nd LR

     bolus, then administer a 10-cc/kg bolus of blood.

    For burn patients in adults, most practitioners use initial rate

    of 1L/hr and then adjust fluid administration based on UOP.

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    Basics of Fluids/Electrolytes

    Colloid = Fluid with large particles (Albumin & FFP)

    Crystalloids = MC NS but in Trauma setting LR, ! NS, etc)

    60% of body weight is fluid, 2/3 of which is intracellular,1/3 = extracellular which is intravascular (plasma) or

    interstitial (btw cells)!! Intracellular = 40% Total body

    weight, Extracellular = 20%... (60, 40, 20) (TIE)

    On avg. blood accounts for 7% of body weight; so 70 kg man= 5 L of Blood

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    Fluid Requirements/24 hours

    Water " 30-25 mL/kg

    K+ " 1 mEq/kg

    "  Cl- " 1.5 mEq/kg

    Na " 1-2 mEq/kg

    Insensible fluid losses: Skin/lungs: total 600-900 mL/dayso ~25-62 mL/hr

    Normal daily fluid losses =

    Urine – 1200-1500 ml (25-30ml/kg)

    Sweat – 200-400 mL

    Resp losses -500-7000 mL

    Feces- 100-200 mL

    #  Normal Daily loss

    #  Na & K+ = 100 mEq

    # Cl = 150 mEq

    Levels of Na/Cl in sweat"40mEq/L

    Major electrolyte in colonic

    feculent fluid – K+--65mEq/L

    NG tube suction (if NG output$ take that into account, ifsignificant or excessive considerreplacing amount or ! ofamount

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    IVF replacement by anatomic site:

    Gastric (NGT) D5 ! NS + 20 KCl

    Biliary LR +/- Na HCO3-

    Pancreatic LR +/- Na HCO3-

    Small bowel (ileostomy) LR

    Colonic (diarrhea) LR +/- Na HCO3-

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    More Fluids

    Prolonged vomiting: results in hypokalemia, hypochloremia,metabolic alkalosis; early urine is alkaline…BUT as Na+ isconserved$ H+/K+ are lost w/ HCO3$ resulting inparadoxical aciduria

    Note: The most important treatment for hyperkalemia is:

    Ca ++ (vs. insulin, HCO3, etc.) because it is the only agent thatactually stabilizes the myocardium.

    Sweat: normally hypotonic but can approach isotonicityduring periods of high secretion; Na+ secretion parallels Cl-(both < plasma); K+ approaches plasma levels; urea andNH3 >> plasma concentrations

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    Electrolytes

    BMP/CMP Magnesium and Phosphate

    Major electrolyte abnormalities that are seen are hypo- and

    hypernatremia and hypo- and hyperkalemia. Hyperkalemia

    will be seen frequently in crush injuries due to myoglobin.

    Correct hypo and hypernatremia slowly.

    In head injuries– SIADH or Diabetes Insipidus

    IV PBs using NS or D5W

    Always do corrected calcium with albumin

    Always check glucose levels with hypernatremia

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    HyperkalemiaSurgical Causes:

    Iatrogenic overdose, Blood transfusion, renalfailure, diuretics, acidosis, tissue destruction(injury hemolysis)

    Always rule out pseudohyperkalemia-laberror, hemolysis, tight or prolongedtourniquet

    EKG changes – peaked T waves, QRSwidening, PR interval prolongation, loss ofP waves and a sine wave pattern, PEA/VF(EKG low sensitivity, cardiac arrest can befirst electrical manifestation

    If severe hyperkalemia and/or if EKGchanges present, first and foremost give IVcalcium, bc cardioprotective stabilitzesresting membrane of myocardium (decreasesmembrane excitability)

    Other tx options- Sodium bicarb, Glucoseand insulin, Kayexalate, hemodialysis

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    Hypokalemia

    Loss of GI fluids (NG/OG tube suction) &vomiting-volume

    depletion and metabolic alkalosis also ntestinal fistulae,

    loop diuretics, certain antibiotics,

    Epinepherine (beta 2 agonists) –Hypokalemia occurs in

    50-60% of trauma patients, perhaps due to increased

    epinepherine levels and/or metabolic acidosis

    EKG changes- U waves, +/- QT interval, ventricular ectopy(PVCs, VT, VF) ST segment depression

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    Third Spacing

    Fluid accumulation in the interstitial tissues, as in edema,

    e.g., loss of fluid into the interstitium and lumen of a paralytic bowel following surgery (think of the intravascular and intracellular

    spaces as first two spaces )

    “Third spacing” is confusing term because it describes mobilizationof third-spaced fluid back into the intravascular space around POD#3 (Note: Beware of fluid overload once the fluid begins to returnto the intravascular space); switch to hypotonic fluid and decrease

    IV rate

    Classic signs of third spacing are Tachycardia and decreased UOP

    Treatment is IV hydration w/ isotonic fluids

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    Shock

    What is the definition of shock?

    Inadequate Tissue Perfusion (or inadequate delivery of O2 to

    tissues leading to cellular dysfunction and injury.)

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    What are the 5-7 types of

    Shock?

    Hypovolemic* MAJORITY OF TIME IN TRAUMASETTING shock is hypovolemic/hemorrhagic

    Cardiogenic

    Neurogenic- also seen with SC injury

    Septic/Inflammatory

    Obstructive

    Traumatic

    Anaphylactic

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    What is a “burn shock”?

    Burn shock describes the loss of fluid from intravascular

    space as a result of burn injury, which causes “leaking

    capillaries” that require crystalloid infusion.

    What is the Parkland formula?

    V= TBSA (Total Body Surface Area) [%] x Weight (kg) x 4

    Formula widely used to estimate the volume (V) of crystalloid

    necessary for initial resuscitation of the burn patient; half of the

    calculated volume is given in the first 8 hours, the rest in the next16 hours.

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    What are 5-10 signs of shock???Pale

    Diaphoretic

    Cool skin** (usually)

     Hypotension

    Tachycardia

    Tachypnea

     Altered mental status

    Decreased Pulse Pressure

    Poor capillary refill

     Poor urine output/Oliguria

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    Hemodynamic changes in Shock

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    SHOCK-Hemodynamic changes

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    What are the best indicators  of

    tissue perfusion?

    URINE OUTPUT

    MENTAL STATUS

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    Which lab tests help assess

    tissue perfusion?

    Lactic acid

    Why?

    Elevated with inadequate tissue perfusion d/t anaerobic respiration

    Base Deficit (look at Base excess on ABG and it will be the negative

    of this number$ BE = -6.0 than BD = 6.0)

    pH from ABG

    (Acidosis associated with inadequate tissue perfusion)

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    Hypovolemic Shock

    Decreased circulating Blood volume$ dec Preload and CO

    Rate of volume loss is v. important. Slower loss = greatereffectiveness of compensatory mechanisms. Acute loss = higherM&M

    Patients w/ significant medical comorbidities (esp. cardiac) may beunable to compensate in early stages of hypovolemic shock.

    4 classes based on severity

    Causes divided into Hemorrhagic v. Nonhemorrhagic

    Hemorrhagic = Trauma, GIB, Retroperitoneal

    Nonhemorrhagic = Voluminous vomiting, Severe diarrhea, Severedehydration d/t any cause, Burns, 3rd space losses in bowelobstruction

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    Severity of Hypovolemic Shock

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    Hypovolemic Shock

    Dx: If diagnosis is unclear from patinets VS and clinical picture, a

    central venous line or a pulm artery catheter can give invaluable

    information for hemodynamic monitoring: Decreased CVP/PCWP,

    Decreased CO, INCREASED SVR

    Treatment: Airway and breathing- in Severe shock and circulatory

    collapse generally require intubation and mech ventilation

    Circulation- hemorrhage apply direct pressure

    IV hydration- class I –no IVF, II benefit from fluids, class III and IV

    require IVF, Bolus followed by continuous infusion and reassess

    For nonhemorrhagic shock blood is not necessary. Crystalloid soltn

    with appropriate electrolyte replacement = adequate.

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    Neurogenic Shock

    Failure of Sympathetic NS to obtain adeq vascular tone(sympathetic denervation)

    Causes d/t SC injury, severe TBI, spinal anesthesia,pharmacological symp. Blockade

    Characterized by peripheral vasodilation with decreased SVR

    Warm, well perfused skin, low –nl UOP, Bradycardia & hoTN(tachycardia can occur) CO is decreased

    Treatment:

    Judicious use of IV fluids = mainstay of treatment. Vasoconstrictors torestore venous tone but w/ caution

    Supine or Trendelenburg position

    Maintain body temperature

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    Septic ShockSIRS is characterized by two or more of the following:• Fever  (>38°C) or hypothermia  (20 bpm) or PaCO2 < 32 mm Hg

    • Tachycardia (>90 bpm)

    • Increased WBC count (>12,000 cell/hpf, 10% band

    forms)

    Sepsis• When blood cultures are positive and SIRS is present• Blood cultures: Obtain two sets from two different sites (each set shouldhave aerobic and anaerobic bottles). Draw blood before antibioticadministration.

    Septic Shock – Severe decrease in SVR Secondary to PeripheralVasodilation• Hypotension induced by sepsis persisting despite adequate fluidresuscitation

    Multiple Organ Dysfunction Syndrome (MODS)• Altered organ function in an acutely ill patient, usually leading to death

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    Cardiogenic ShockOccurs when heart is unable to generate a CO sufficient for tissueperfusion

    Can be defined as SBP 2.2, PCWP

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    Difference in Fluid resuscitation in

    Albumin vs. Saline has NOT been shown to be

    statistically significant in Trauma & Severe

    Sepsis & Overall

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    Maintenance Fluid Therapy

    The goal of Maintenance fluid therapy is preservation of

    water and electrolyte balance and to provide nutrition if

    patients are unable to eat or drink

    Hospitalized patients who are afebrile, not eating and

    physically inactive require less than 1L of electrolyte free

    H20 as maintenance fluid. Requirements are increased if thereare increased fluid losses .

    Ex: fever, surgical drains or ongoing significant GI losses.

    Water requirements are decreased by oliguric renal failure, use

    of humidified air, edematous states, hypothyroidism and the

    presence of nonosmotic stimuli for the release of ADH (ex

    SIADH)

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    Maintenance Fluids rules100/50/20 rule MT IV fluids for a 24 hr period

      100  mL/kg for first 10 kg50  mL/kg for next 10kg

       20  mL/kg for every kg over 20

    (divided by 24 for hourly rate)

    4/2/1 rule MT fluids for hourly rate:  4  mL/kg for first 10 kg

     2  mL/kg for next 10 kg

      1 mL/kg for every kg over 20

    What is mt for a 70 kg man? Using 100/50/20:100x10 kg = 1000

    50 x 10 kg = 500

    20 x 50 kg = 1000

    Total = 2500

    Divided by 24 hours = 104 mL/hr maintenance rate

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    Maintenance Fluids cont’d

    For patients who require maintenance fluid and have normalor near-normal renal function and are otherwise stable, it ispossible to begin with 2L/day of ! NS D5 w/ 20 mEq ofKCl/L

    The original maintenance regimen can be continued unlessone of the following happens:

    Na starts to dec$

     give more concentrated solt’n ex NSIf Na starts to inc$ give a more dilute solt’n ex. # NS

    IF K starts to dec$ more K should be added, and, if it risesabove normal, K should be eliminated

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    Replacement Fluid Therapy

    The goal of replacement tx is to correct existing abnormalities in

    volume status and/or serum electrolytes

    Total fluid deficit and be estimated pre- & post- deficit body weight.

    If the degree of weight loss is unknown, the fluid deficit cannot beestimated. Clinical and lab parameters can be used to assess

    possible presence of volume depletion including bp and Urine Na.

    Rate of correction of Volume depletion depends on severity. For

    patients w/ severe volume depletion or hypovolemic shock,

    recommend 1-2 L of isotonic saline ASAP. Fluid repletion is

    continued to a rapid rate until clinical signs of hypovolemia

    improve (low bp, low UOP, &/or impaired mental status)

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    Replacement Fluids cont’d 1/2

    A less rapid rate of correction can be used if mild to moderatehypovolemia. In such cases, the rate of fluid administration must be greater than the rate of continued fluid losses, which is equal tothe urine output plus estimated insensible losses (usually 30-50mL/hour) plus any other fluid losses(GI losses)

    The choice of replacement fluid is dependent on type of fluid lostand any concurrent electrolyte disorder/imbalance. Most patientsare initially treated with isotonic or ! isotonic saline.

    Hypernatremia and hyponatremia should usually be correctedslowly since overly rapid correction is potentially harmful.

    Potassium replacement is indicated in hypokalemic patients or inthe setting of normal or even increased serum K+ patients withDKA or nonketotic hyperglycemia.

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    Replacement Fluids cont’d 2/2

    The addition of sodium bicarbonate may be required in

    patients with metabolic acidosis if the acidemia is severe

    (arterial pH < 7.2) or bicarbonate losses persist (as with

    severe diarrhea).

    In general, there is little evidence that adding or omitting

    dextrose from saline has any benefit or harms. However,

    there are setting in which dextrose should or should not be

    used.

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    THANK YOU!

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    References

    Alarcon LH, Puyana J, Peitzman AB. Alarcon L.H., Puyana

    J, Peitzman A.B. Chapter 12. Management of Shock. In:

    Mattox KL, Moore EE, Feliciano DV. Mattox K.L., Moore

    E.E., Feliciano D.V. eds. Trauma , 7e. New York, NY:

    McGraw-Hill; 2013. http://accesssurgery.mhmedical.com/

    content.aspx?bookid=529&Sectionid=41077251. Accessed

    June 23, 2014