Transcript Fluids & Electrolytes and Nutrition

Fluids & Electrolytes
and Nutrition
Srinivas H Reddy, MD
Trauma & Surgical Critical Care
Jacobi Medical Center
Fluids & Electrolytes
“The recognition and management
of fluid, electrolyte, and related
acid-base problems are common
challenges on the surgical service.”
Lawrence, P F, Essentials of General Surgery, 4th ed., 2005
Goals
Review concept of total body fluids
Review types of crystalloids and colloids
Review electrolyte disturbances & their treatment
strategies
Review acid-base disturbances
Na-K ATPase
67%
25%
8%
33%
© Merck
Manual
Na+/K+ ATPase
Actively pumps 3 Na+ out of
cell and 2K+ inside cell
Energy from ATP
Regulated by
Insulin
Aldosterone
Starling’s Forces
Cations and Anions in Body Fluids
Serum Osmolality
=
[2 x Na] + [BUN/2.8] + [Gluc/18]
Osmolality =
CONCENTRATION
Tonicity = ONCOTIC
PRESSURE FORCE ON WATER
Primary Regulatory Hormones
Antidiuretic hormone (ADH, Vasopressin)
Stimulates kidney to resorb water from collecting ducts
Causes systemic vasoconstriction
Stimulates thirst center
Aldosterone
Stimulates Na+ (& water) absorption and K+ loss along the DCT
Similar action on distal colon
Natriuretic peptides (ANP and BNP)
Reduce thirst and block the release of ADH and aldosterone
Renin-Angiotensin-Aldosterone System
Renin-Angiotensin-Aldosterone System
Na-K ATPase
67%
25%
8%
33%
© Merck
Manual
GI Fluid & Electrolyte Losses
Source
Volume
(ml)
Stomach
1000-4200
20-120
130
10-15
Duodenum
100-2000
110
115
15
10
Ileum
1000-3000
80-150
60-100
10-15
30-50
Colon
500-1700
120
90
25
45
Bile
500-1000
140
100
5
25
Pancreas
500-1000
140
30
5
115
Na (mEq/L) Cl (mEq/L)
K (mEq/L)
HCO3
(mEq/L)
H (mEq/L)
30-100
Lactated Ringers / Normal Saline
Lactated Ringers (LR)
Sydney Ringer’s frog hearts
(London 1882)
Alexis Hartman pediatric
cholera, added bicarbonate
(US 1930’s)
Lactate -> Pyruvate ->
Bicarbonate
Lactic Acidosis?
Immunosuppressive effect
on WBC’s?
Calcium precipitates with
citrate in PRBC transfusion
pH=6.5
Normal Saline (NS)
Does not contain calcium,
may be used to carry
PRBC transfusion
Hyperchloremic metabolic
acidosis after aggressive
resuscitation
pH = 5.5
Maintenance Fluids
Formula per day
Formula per hour
100mL/kg/d x first 10kg
4mL/kg/hr x first 10kg
50mL/kg/d x next 10kg
2mL/kg/hr x next 10kg
25mL/kg/d x each addl kg
1mL/kg/hr x each addl kg
“4-2-1 Rule - per hr”
Maintenance Electrolytes
Sodium
Calcium
1-2 mEq/kg/day
800 - 1200 mg/d
Chloride
Magnesium
1-2 mEq/kg/day
300 - 400 mg/d
Potassium
Phosphorus
0.5-1 mEq/kg/day
800 - 1200 mg/d
Normal Serum Electrolytes
Cations
Sodium (mEq/L)
135 - 145
Potassium (mEq/L)
3.5 - 4.5
Calcium (mg/dL)
4.0 - 5.5
Magnesium (mEq/L)
1.5 - 2.5
Anions
Chloride (mEq/L)
CO2 (mmol/L)
Phosphate (mg/dL)
95 - 105
24 - 30
2.5 - 4.5
Fluid Status
120
GI loss
SIADH
Hypothyroid
Cortisol
CHF
Cirrhosis
140
140
[Na]
160
GI loss
Renal loss
Osmotic
low
DI
Insensible
NaHCO3
3% NaCl
Seawater
normal
high
ECV
Composition of IV Fluid Solutions
Solution
Na+
Cl-
K+
Ca+2
HCO3- Gluc
Plasma
141
103
4-5
5
26
0
NS
154
154
0
0
0
0
LR
130
109
4
3
28
0
D5W
0
0
0
0
0
50g
D5 1/2NS+20KCl
77
77
20
0
0
50g
Serum Osmolality = [2 x Na] + [BUN/2.8] + [glucose/18]
Replacement Fluid Strategies
Sweat: D5¼NS + 5mEq KCl
Gastric: D5½NS + 20mEq KCl
Biliary/Pancreatic: LR
Small Bowel: LR
Colon: LR
3rd space losses: LR
Resuscitation
Crystalloids first, initial bolus 20mL/kg (1-2L),
may be repeated, usually NS or LR
If they have transient response, give additional
fluids
Once 3-4 liters of crystalloid has been given
consider blood
Current recommendations in hemorrhagic shock
from trauma, transfuse 1:1 PRBC:FFP
(previously, and for other bleeds 3:1 ratio)
Fluid Pearls
Resuscitation – isotonic fluid (LR or NS), no dextrose,
if ongoing losses consider using colloid
Post-op – LR or NS until pt euvolemic, then switch to
maintenance
Bolus – isotonic fluid, no dextrose
Mobilization – movement of fluid from 3rd space into
intravascular space
Indicators of Successful Resuscitation
PULSE <100 - 120 bpm
URINE OUTPUT
Child >1.0 ml/kg/hr
Adult >0.5 ml/kg/hr
Clearance of LACTATE
Resolution of BASE DEFICIT
BLOOD PRESSURE is a POOR INDICATOR!
Hypovolemia
Acute volume loss
Tachycardia
Hypotension
Decreased UO
Changes in mental status
Gradual volume loss
Loss of skin turgor, dry mucus membranes
Thirst
Low CVP
Hemoconcentration (Hct rise)
BUN:Cr ( >20:1)
Metabolic acidosis due to hypoperfusion
Hypervolemia
Large UO
Pitting edema
JVD
Crackles on lung auscultation
Hypoxia
CXR – cephalization of vessels, pulmonary edema
Hyponatremia
Serum Na+ < 130mEq/L
Sx- nausea, emesis, weakness, altered MS, seizure
May be hypovolemic, euvolemic, or hypervolemic
Tx
Fluid restriction
Replete with Normal Saline
For severe hyponatremia <120-125mEq/L
and/or mental status changes, use
Hypertonic Saline
Remember: do NOT correct faster than 0.5
mEq/L/hr to avoid central pontine
myelinolysis
Causes of Hyponatremia
Hypovolemic
Causes – Na+ and water are lost and replaced with hypotonic
solutions
Renal – salt wasting nephropathy
GI – diarrhea, vomiting, fistulas
Skin – excessive sweating
3rd spacing – ascites, peritonitis, pancreatitis, burns
Hypoaldosteronism
Euvolemic
Causes – SIADH, psychogenic polydipsia
Hypervolemic
Causes - renal failure, nephrotic synd, CHF, cirrhosis
Hypernatremia
Serum Na+ > 145
Sx – altered level of consciousness, seizure, coma,
signs of dehydration
Causes – DI, hyperosmolar diuresis, EtOH (suppresses
ADH)
Tx calculate Free Water Deficit
FWD = 0.6 x wt (kg) x (measured Na+ - 140) / 140
Replace first ½ in 24hrs, then 2nd ½ in next 24 hrs
No faster than 10mEq/day to avoid cerebral edema
Use D5W, ½ NS, or ¼ NS
Hypokalemia
K+ < 3.5
Sx – fatigue, weakness, ileus, N/V, arrhythmia,
rhabdomylosis, flaccid paralysis, resp compromise
 EKG changes - long QT, depressed ST, low T waves,
U waves
Causes – vomiting, NGT drainage, diarrhea, high
output enteric/pancreatic fistula,
hyperaldosteronism, loop diuretics
Tx – replete 10 mEq KCl for every 0.1 below 4.0, oral
or IV not more than 10-20mEq/hr, if persistent
hypokalemia, may also need Mg 2+ replacement, also
available K phos or K acetate
Hyperkalemia
K+ > 5.0
Sx – weakness, N/V, abdominal cramping, diarrhea,
arrhythmias
 EKG – peaked T waves, prolonged PR, widened QRS,
V-fib, diastolic cardiac arrest
Causes – iatrogenic, renal failure, acidosis, hemolysis,
crush injury, reperfusion injury
Tx
Treatment of Hyperkalemia
Cardiac monitoring, EKG
If EKG changes, give Calcium gluconate or chloride (stabilizes
cardiac membrane) CaCl : CaGluc = 3 : 1 elemental calcium
Dextrose and Insulin
Bicarbonate
Albuterol
Kayexalate
Renal Replacement Therapy (Dialysis)
Hypocalcemia
Ca2+ < 8.5
Sx – parasthesias, muscle spasms, tetany, seizures,
Chvostek, Trousseau
EKG – prolonged QT, can progress to complete
heart block or V-fib
Causes – pancreatitis, tumor lysis syndrome, blood
transfusion, renal failure, thyroid or parathyroid
surgery, diet deficient in Vit D or Ca, inability to
absorb fat-soluble vitamins
Tx – chronic hypocalcemia give supplemental oral
calcium & vitamin D, and for symptomatic
hypocalcemia, give IV calcium ± PO calcium/vit D
Hypercalcemia
Ca2+ > 10.5
Sx – stones, moans, groans, psychologic overtones
Causes – ‘CHIMPANZEES’
Tx –
Identify and treat cause
Severe/symptomatic hypercalcemia, treat with IVF,
diuretics (saline diuresis)
Bisphosphonates, if due to release of Ca2+ from bone
Acid / Base
Respiratory
Acidosis
Metabolic
Alkalosis
BE = 0
HCO3 = 24
Respiratory
Alkalosis
Metabolic
Acidosis
7.4
Acid-Base Disturbances
Mechanisms Regulating
Acid-Base Balance
Chemical buffers in cells and ECF
Instanteous action
Combine acids or bases added to the system to prevent
marked changes in pH
Respiratory System
Minutes to hours in action
Controls CO2 concentration in ECF by changes in rate
and depth of respiration
Kidneys
Hours to days in action
Increases or decreases amount of NaHCO3 in ECF
Buffer Mechanisms of pH Control
Buffer system consists of a weak acid and its anion
Three major buffering systems:
1. Protein buffer system
Amino acid
H+ are buffered by hemoglobin buffer system
2. Carbonic acid-bicarbonate
Buffer changes caused by organic and fixed
acids
3. Phosphate
Buffer pH in the ICF
Relationship between PCO2 and Plasma pH
Central Role of Carbonic Acid-Bicarbonate Buffer
System in Regulation of Plasma pH
Central Role of Carbonic Acid-Bicarbonate Buffer
System in Regulation of Plasma pH
ABG Rules
Rule #1: increase or decrease in PaCO2 of 10 mm
Hg, is associated with a reciprocal decrease or
increase of 0.08 pH
Rule #2: increase or decrease in HCO3- of 10
mEq/L is associated with a directly-related
increase or decrease of 0.15 pH
Severe Acidosis
pH < 7.2
 decreased responsiveness to
catecholamines
 cardiac dysfunction
 arrhythmias
 increased potassium serum levels
Nutrition
Goals

Why important?

What nutrients are needed?

How much nutrition is necessary?

How to administer nutrition to patient?
Why Nutrition?
•
Growth
•
Immunity
•
Wound healing
What Nutrition?
•
Water
•
Carbohydrate (Glucose) – 60-70% of total kcal
•
Protein – 1.0-2.0 gm/kg/day
•
Fat/Lipids – 15-40% of total kcal
•
Vitamins/Minerals/Elements
How Much Nutrition?
•
Water - You already know this part!
•
Glucose @ 2-6 mg/kg/min
•
Protein @ 1-2 g/kg/day
•
Fat/Lipids @ 1-2 g/kg/day
Vitamins/Minerals/Elements - A, D, E, K, B, C,
Zinc, Chromium, Selenium, Phosphate, etc.
•
How Much Nutrition?
•
•
•
Harris-Benedict Equation for Basal Energy
Expenditure (BEE) in kilocalories =
✓ Male: 66+(13.8xW)+(5xH)-(6.8xA)
✓ Female: 655+(9.6xW)+(1.85xH)-(4.7xA)
✓ Range: 20-40 kcal/kg/day
Multiply by stress factor (1.2-2.0)
i.e. burn, trauma, sepsis, increased activity
Indirect Calorimetry – estimate Resting
Energy Expenditure and efficiency of fuel
burning
How Much Nutrition?
Caloric Goal = 25-30 kcal/kg/day
Higher for burn patients (hypercatabolic)
• Glucose (2-6 mg/kg/min) @ 4 kcal/gm
• Protein
(1-2 g/kg/day) @ 4 kcal/gm
• Fat/Lipids (1-2 g/kg/day)
@ 9 kcal/gm
Nutritional Status Parameters
• N2 Balance = N2 in – N2 out
• N2 in = Protein intake (gm/day) / 6.25
• N2 out = UUN + 4
• Albumin / Transferrin / PreAlbumin / RBP
• Anthropometrics (TSF, MAC)
Metabolic Stress
Sepsis (infection)
Trauma (including burns)
Surgery
Once the systemic response is activated,
the physiologic and metabolic changes
that follow are similar and may lead to
septic shock
Overfeeding
Enough but not too much
Excess calories:
Hyperglycemia
Diuresis – complicates fluid/electrolyte
balance
Hepatic steatosis (fatty liver)
Excess CO2 production
Exacerbate respiratory insufficiency
Prolong weaning from mechanical
ventilation
How to Give Nutrition?
•
Enteral - via the gut
• Preferred method
• Prevent intestinal atrophy
• Protect from bacterial translocation across
basement membrane
• Gastric stress ulcer prevention
•
Parenteral - via the vein
• Only for severely protein-malnourished
patients who cannot be fed enterally in the
long-term
• Higher risk of complications and infections,
related to catheters and lipids (?)
Tube Feeding
Used when oral feeding cannot be tolerated (altered
mental status, endotracheal intubation, facial
trauma, dysphagia, etc)
Nasogastric or orogastric tube is most common route
Nasoduodenal or nasojejunal tube more appropriate
for patients at risk for aspiration, reflux, or
continuous vomiting
Enteral Tube Feeding
Alternate Routes for Enteral Tube Feeding
Percutaneous Endoscopic Gastrostomy (PEG)
Percutaneous Endoscopic Jejunostomy (PEJ)
Open (surgical) Gastrostomy
Feeding Jejunostomy
Esophagostomy
Tube-Feeding Formula
Generally prescribed by the physician
Important to regulate amount and rate of
administration
Diarrhea is most common complication
Wide variety of commercial formulas available
Parenteral Feeding Routes
Peripheral Parenteral Nutrition (PPN) : uses less
concentrated solutions through small peripheral
veins when feeding is necessary for a brief period
(<10 days)
Total Parenteral Nutrition (TPN) : used when energy
and nutrient requirement is large or to supply full
nutritional support for long periods of time through
large central vein
Questions?
Thank You!