Fluid and Electrolytes Flashcards

1
Q

What are the insensible losses and water requirements for a neonate?

A

Insensible losses = 30-35mL/kg/day

H2O requirements = 150ml/kg/day, reduce to 4:2:1 rule when > 10kg

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2
Q

What is the type and rate of maintenance fluids in a neonate?

A
  • D10/0.25% NS
  • May add 10-20mEq/L of KCl on 2nd or 3rd day of life
  • May change to D5/0.25% NS in 2-3 weeks
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3
Q

What are the K+ and Na+ requirements for a neonate?

A

2 -3 mEq/kg/day

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4
Q

How do you estimate fluid requirements for a child?

A
  • 0 - 10 kg = 150mL/kg/day
  • 10 - 20 kg = 1000 + 50mL/kg/day over 10
  • > 20 kg = 1500 + 20mL/kg/day over 20
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5
Q

Where is the best location for trauma IV access in kids?

A
  • saphenous veins

- antecubital veins

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6
Q

How do you calculate the blood volume of a baby?

A

80cc/kg

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7
Q

How do you calculate transfusion amount for a baby?

A
  • blood = 10cc/kg

- platelets = 10cc/kg

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8
Q

How do you calculate a bolus for a child?

A

10 - 20 mL/kg of RL over 30 minutes

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9
Q

How does SV, CO and HR relate in infants?

A
  • SV is fixed

- only way to increase CO is to increase HR

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10
Q

How do you replace enteral losses in children?

A

Source = Replacement

  • Gastric = 1/2NS + 10mEq/L KCL
  • Pancreatic = RL or 1/2NS + 50mEq/L NaHCO3
  • Bilious = RL or 1/2NS + 50mEq/L NaHCO3
  • Ileostomy = RL or 1/2NS + 25mEq/L NaHCO3
  • Diarrhea = RL or 1/2NS + 25mEq/L NaHCO3
  • Pleural or peritoneal = RL + 5% albumin
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11
Q

What metabolic derangements occur in pyloric stenosis?

A
  • dehydration
  • hypoCl-
  • hypoK+
  • metabolic alkalosis
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12
Q

How do you replace the metabolic derangements caused from pyloric stenosis?

A
  • D5 + 1/2 NS until they void, then D5 + 1/2 NS + KCl
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13
Q

How are pharmacokinetics different in children?

A
  • decreased protein binding
  • decreased hepatic glucuronidation > slow clearance rate
  • decreased GFR in newborns until 2yrs > adult values
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14
Q

What is the calculation for osmolality?

A

2Na + Urea + Glucose + EtOH

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15
Q

How do you calculate TBW in adults?

A
  • 600cc/kg

- 60% of body weight

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16
Q

Hoe much whole blood is in an adult?

A

60cc/kg

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17
Q

How much plasma is in an adult?

A

40cc/kg

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18
Q

How much erythrocyte volume is in an adult?

A

26cc/kg

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19
Q

What is the ideal fluid for replacing losses?

A
  • RL

- some ionic concentration as plasma

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20
Q

What is the disadvantage of replacing losses with RL?

A

Low Na+ content > hyponatremia with long term use or in those who can’t excrete free H2O

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21
Q

What can happen with replacement of a large volume of normal saline?

A
  • total body Na+ overload and hyperCl-

- added Cl- > hyperCl- > overwhelms kidneys > metabolic acidosis

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22
Q

What are ion concentrations in common replacement fluids?

A

ECF = Na-142, K-4, Ca-5, Mg-3, Cl-103, HCO3-27, Osm-295
NS = Na-154, Cl-154, Osm-308
RL = Na-130, K-4, Ca-2.7, Cl-109, HCO3-28, Osm-273
D5/NS = Na-154, Cl-154, Osm-560
D5/0.45%NS = Na-77, Cl-77, Osm-406
2/3 & 1/3 = Na-56, Cl-56, Osm-?271
D5W = Osm-252

Albumin 5% = Na-145, Cl-145, Osm-300
Albumin 25% = Na-145, Cl-145, Osm-1500
Pentastarch 10% = Na-154, Cl-154, Osm-326

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23
Q

What salts are commonly lost in various bodily secretions?S

A
  • Salivary = Na-50, K-20, Cl-40, HCO3-30
  • Basal gastric = Na-100, K-10, Cl-140, H-30
  • Stimulated gastric = Na-30, K-10, Cl-140, H-100
  • Bile = Na-140, K-5, Cl-100, HCO3-60
  • Pancreatic = Na-140, K-5, Cl-75, HCO3-100
  • Duodenum = Na-140, K-5, Cl-80
  • Ileum = Na-140, K-5, Cl-70, HCO3-50
  • Colon = Na-60, K-70, Cl-15, HCO3-30
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24
Q

What are the best replacement fluid for various enteral losses?

A

Source = Replacement

  • Gastric = 1/2NS + 10mEq/L KCL
  • Pancreatic = RL or 1/2NS + 50mEq/L NaHCO3
  • Bilious = RL or 1/2NS + 50mEq/L NaHCO3
  • Ileostomy = RL or 1/2NS + 25mEq/L NaHCO3
  • Diarrhea = RL or 1/2NS + 25mEq/L NaHCO3
  • Pleural or peritoneal = RL or 1/2 NS + 5% albumin
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25
Albumin
- main determinant of plasma oncotic pressure - half-life = 20 days - on electrophoresis, it accounts for 52 - 66% of protein
26
How do you calculate maintenance fluid in adults?
- Insensible H2O losses = 8 - 12 mL/kg/day (increases 10% for every degree > 37.2 celsius) - 4:2:1 rule - Na = 1 - 2 mEq/kg/day - K = 0.5 - 1 mEq/kg/day - 0.33% NaCl + 20 - 30 mEq/L LCl best fits daily requirements
27
What are predisposing conditions to HypoCa2+?
- hypoparathyroidism - PTH resistance - vit D deficiency - vit D resistance - acute hypocalcemic syndromes - tumor lysis syndrome
28
How does tumor lysis syndrome affect body ions?
- hypocalcemia - hyperphosphatermia (chelates Ca > hypoCa) - hyperuricemia - hyperkalemia - due to massive tumor death
29
How can hypocalcemic syndromes occur?
- when there is acute chelation or precipitation of Ca2+ - happens when lots of citrate is infused: large volumes of fluid in resuscitation, large transfusions, rapid infusion of phosphate, acute pancreatitis when Ca2+ is saponified
30
What are the manifestations of hypoCa?
Neuromuscular excitability - paresthesias - hyperreflexia & laryngospasm - seizures - tetany - chvostek's sign - trousseau's sign - paralytic ileus Cardiac Dysfunction - direct suppression of contractility - hypotension - decreased pulse pressure - delayed repolarization - heart block - long S/QT segment
31
What is the management of hypoCa?
- PO maintenance for 0.65 - 0.8 mmol/L - IV replacement only when symptomatic or < 0.65 mmol/L - correct hypoMg first
32
What are the predisposing conditions to hyperCa?
- primary hyperparathyroidism - malignancy - drugs (thiazides, lithium, tamoxifen) - immobilization - familial hypocalciuric hypercalcemia - granulomatous disease (sarcoid, TB) - thyrotoxicosis - milk alkali syndrome - malignant hyperthermia - paget's disease of the bone
33
What are the manifestations of hyperCa?
- CNS: decreased LOC - Neuromuscular: proximal muscle weakness, hyporeflexia - GI: A/N/V, constipation, paralytic ileus, PUD, pancreatitis - Renal: polyuria (nephrogenic DI), nephrocalcinosis, nephrolithiasis - CVS: HTN, short QT, exacerbates digoxin toxicity - MSK: bone pain
34
What is the management of hyperCa?
- diuretics + isotonic saline + lasix (standard tx) - bisphosphonates - calcitonin - mithramycin - IV phosphates (absolute last resort) - corticosteroids (in sarcoidosis) - chloroquine phosphate (in sarcoidosis) - gallium nitrate - surgical excision (of excess functioning tissue)
35
How do you diagnose Paget's Disease of the bone?
X-Ray - increased bone density - cortical thickening - abnormal architecture - bowing - overgrowth Labs - increased ALP - increased urinary excretion of pyridinoline crosslinks - Ca and PO4 levels usually normal Bone Scan - increased localization to affected sites
36
What causes hyperMg and what physiologic change does it cause?
- seen in RF and Mg-containing antacid abuse | - high Mg blocks entrance of Ca into myocardial cells and causes heart failure
37
What is the treatment for hypoMg2+?
IV MgSO4
38
What is the etiology of hypoMg2+?
- chronic diarrhea - prolonged aggressive diuresis - DM w/ persistent osmotic diuresis - heavy EtOH abuse - pancreatitis - hypoPO4
39
What are the clinical manifestations of hypoMg2+?
Neuromuscular Manifestations - changes in mental status - seizures - tremors - hyperreflexia Cardiac Manifestations - prolonged PR interval - prolonged QT - T-wave flattening - tachyarrhythmias - atrial fibrillation - torsades de pointes - digitalis toxicity enhanced as both inhibit the membrane pump
40
What is the division of ECF and ICF in TBW?
ECF = 1/3 - plasma 1/4 - interstitial/lymphatic 3/4 ICF = 2/3
41
How is osmolality regulated?
- 285 - 295 mOsm range - ADH > regulates [Na+] via H2O reabsorption - aldosterone > regulates total body Na+
42
What is ADH secretion stimulated by?
- osmolality > 280 mOsm - decreased intravascular volume > 10% - decreased mean arterial pressure > 10% - pain + emotional stress
43
What is aldosterone secretion stimulated by?
- hypovolemia (via RAAS) | - hyperkalemia
44
What can cause hypertonic hyponatremia?
- hyperglycemia - decreased Na by 2.5 for every increased glucose by 10 - mannitol - other effective osmole
45
What can cause isotonic hyponatremia?
- lab artifact from increased lipids or increased proteins | - absorption of glycine or sorbitol
46
What are the various types of hypotonic hyponatremia?
- hypovolemic hypotonic hyponatremia - hypervolemic hypotonic hyponatremia - euvolemic hypotonic hyponatremia
47
What can cause hypovolemic hypotonic hyponatremia?
- depletion of Na volume - loop diuretics - thiazides - Addison's disease - osmotic diuresis - vomiting - diarrhea - fistualas - third spacing - weeping wounds
48
What can cause hypervolemic hypotonic hyponatremia?
- CHF - nephrotic syndrome - cirrhosis - psychogenic polydipsia - SIADH
49
What can cause euvolemic hypotonic hyponatremia?
- SIADH - adrenal insufficiency - hypothyroidism - psychogenic polydipsia - low solute intake ("tea and toaster")
50
How do you delineate extrarenal losses from renal losses in hypovolemic hypotonic hyponatremia?
- UNa < 10 = kidney holding onto Na+ > extrarenal | - UNa > 20 = kidney not holding onto Na+ > renal
51
How do you delineate extrarenal from renal in hypervolemic hypotonic hyponatremia?
- UNa < 10 = kidney holding onto Na+ > extrarenal or nephrotic syndrome - UNa > 20 = kidney not holding onto Na+ > renal failure
52
How do you delineate the various causes for euvolemic hypotonic hyponatremia?
- UOsm > 110 = SIADH, adrenal insufficiency, hypothyroidism - UOsm < 100 = psychogenic polydipsia, low solute intake - UOsm variable = screwed up "osmostat"
53
How do you treat hypovolemic hypotonic hyponatremia?
- Na+ > 120 = NS | - Na+ < 120 = 3% hypertonic NS
54
How do you treat hypervolemic hypotonic hyponatremia?
- Na+ > 120 = volume restriction to as little as 10mL H20/kg/day - Na+ < 120 = small volume 3% NS +/- dialysis
55
How does SIADH present?
euvolemia or hypervolemia + low plasma osmolality + high urine osmolality renal & adrenal function normal K+ normal
56
What is the DDX for SIADH?
- malignancy: SCLC, pancreatic, H&N epithelial carcinomas, hematological (hodgkin's) - pulmonary disorders: bacterial, fungal, tuberculosis infections - CNS: infection, injury - medications: carbamazepine, clofibrate, clorpropramide, thiazides, cyclophosphamides, cisplatin, vinblastine, vincristine, NSAIDs, SSRIs - medical conditions: hypothyroid, renal impaiment with salt losing nephritis, mineralocorticoid deficiency, psychogenic polydipsia, EtOH withdrawal - other: pain, nausea, post-op state
57
How is SIADH diagnosed?
urine Na+ > 20 mEq/L + urine osmolality > plasma osmolality
58
How is SIADH managed?
- Na < 120 = H2O restrict 7 - 10 mL/kg/day - malignancy: demeclocycline (antagonizes renal action of ADH), lithium - when H2O restriction inadequate: osmotic diuresis + furosemide
59
What is the advised correction rate for sodium?
Chronic - 0.5 mEq/L.hr - don't exceed 10 - 15 mEq over 24hrs Acure - don't exceed 1 mEq/L/hr until Na+ of 120 reached
60
What is the most common cause of hypertonicity?
Hypernatremia
61
What are aetiologies of hypertonicity?
- DI - burns - exfoliative dermatitis - vomiting - diarrhea - sweating - fever - resp losses - inadequate AVP secondary to EtOG - fistulas - endoluminal tubes - DKA - hyperglycemic induced diuresis
62
What happens when hypertonic patients become hypotensive?
Kidneys can no longer produce hypertonic urine and thus they can't achieve a net H2O balance
63
What is the treatment for hypernatremia?
- IV isotonic solution - DDAVP can be used for central DI patients. Desmopression is the preparation of choice given intranasally. Chlorpropramide can be used to enhance renal effects of DDAVP. - Thiazides can be used paradoxically - Carbamazepine and clofibrate can be used with caution - Indomethacin may be modestly effective
64
What are the 2 types of diabetes insipidus?
Central - endocrine disorder resulting from blunted or existent synthesis or release of AVP/ADH Nephrogenic - kidney doesn't respond to AVP/ADH
65
What is the etiology of central DI?
- brain injury - brain surgery - brain tumor - SAH - Reset DI > osmoreceptors that trigger AVP release are reset to go off at an osmolality > 280 - Idiopathic > autoimmune
66
What is the etiology of nephrogenic DI?
- renal disease: post-obstructive diuresis, sickle cell nephropathy, medullary cystic disease, ESRD - medications: lithium, glyburide, amphotericin B, foscarnet, demeclocycline, methoxyflurane - electrolyte disturbances: hyperCa, hypoK
67
How does DI present clinically?
Sustained urine output > 100cc/hr + hyperNa
68
How is DI diagnosed?
Urine osmolality < 300 + serum Na+ > 150 Increased AVP = nephrogenic Decreased urine output in response to DDAVP = central
69
What is the water deprivation test?
Patients with DI cannot concentrate their urine, event in the context of complete water deprivation
70
What is the treatment for central DI?
- rehydration with isotonic solution - DDAVP - chlorpropramide
71
What is the treatment for nephrogenic DI?
- rehydration with isotonic solution | - correct underlying renal disease
72
What is the management of post-obstructive diuresis?
- low risk = PO replacement - moderate risk = D5 1/2 NS + 20 KCl at 1/2 previous hours urine output rate when they have > 200cc/hr - increased Cr/CHF/metal obtundation/peripheral edema = replace urine output mL for mL with NS
73
What are the mechanisms of post-obstructive diuresis?
- volume overload - renal insensitivity to ADH - urea osmotic diuresis - elevated ANP
74
How do beta-2 adrenergic agents affect extracellular K+?
Increased Na-K-ATPase activity = decreased extracellular K+
75
Where is the majority of K+ absorbed and excreted?
- reabsorbed in proximal tubules | - excretion carried out by cortical collecting ducts under the influence of aldosterone
76
What are the signs and symptoms of hypokalemia?
- arrhythmias: u-waves, flattened t-waves, inverted t-waves, prolonged QT - weakness - acute respiratory failure: if marginal respiratory function to begin with - worsening hepatic encephalopathy - nephrogenic DI
77
What is the relationship between potassium and digoxin?
- hypokalemia exacerbates digoxin toxicity | - use cholestyramine to decrease digoxin toxicity
78
What is the etiology of hypokalemia?
Excessive renal loss - loop diuretics (lasix) - increased exchange of Na for K in distal convoluted tubule - barter's syndrome and gitelman's syndrome - primary hyperaldosteronism (adrenal cortex tumor) - excess renin production (renal a. stenosis) Uncompensated GI losses - villous adenoma Medications - salbutamol, insulin, cortisol, vit B12
79
What is the distribution of potassium in the body?
- ECF = 1 mmol/kg - ICF - 30 - 40 mmol/kg small decrease in serum K+ = big decrease in total body K+
80
What does refractory hypoK+ suggest?
HypoMg2+
81
What are the various K+ salts and when should you use them?
KCl - enables absorption of Na+ in proximal tubule therefore aids with volume expansion KHCO3 - if diarrhea is cause therefore bicarb loss is present KPO4 - nutritional support of catabolic patients - recovery of DKA
82
What is hypokalemic hypochloremic alkalosis?
- litres of gastric juices lost (decreased HCl) > hypoCl + alkalemic > nephron decreases Cl- dependent reabsorption of Na+ in the proximal tubule > increased delivery of Na+ to distal tubule > aldosterone driven excretion of K+ - urine K+ > 20 mEq/L & paradoxically acidic - treat wth KCl fluids
83
What is the etiology of hyperkalemia?
PseudohyperK - hemolyzed sample, leukocytosis, thrombocytosis, prolonged tourniquet, upstream IV with KCl Redistributional - acidosis, hypoinsulinism, tissue necrosis, reperfusion syndrome, digoxin poisoning, succinylcholine Elevated total body K - renal failure, excessive intake, aldosterone deficiency, DM, spironolactone use Drugs - trimethoprim, pentamidine, amlodipine, ACEi, succinylcholine
84
What EKG changes can you see from hyperK?
- prolonged PR interval - peaked T waves - loss of P waves - slurring of QRS - terminal, broad V tach
85
What are the treatment options for hyperK?
- Tx needed in mins: 10mL calcium gluconate over 3 - 5 mins then another 10mL over 10 min + 50 - 100 mEq NaHCO3 IV over 10 - 20 mins - Tx needed within in 1 hr: D50W 50 mL IV + 10 U insulin + hemodialysis - Tx needed within hours: rectal kayexalate + lasix
86
What are the sign and symptoms of hypophosphatemia?
- lassitude - fatigue - weakness - convulsions - death - RBC hemolysis - impaired O2 delivery - impaired WBC phagocytosis
87
How do you treat hyperphosphotemia?
Diuresis + phosphate-binding antacids
88
What are common diuretics?
- CAI: acetazolamide - Loop: lasix - Thiazides: HCTZ, chlorthaladone, metolazone - K-sparing, blk-aldo: spironolactone - K-sparking, blk-Na: amiloride