Pre-op/Post-op Care Flashcards

1
Q

what are the H+ and K+ shifts in acidosis and what are the results?

A

H+ ions move from an area of high conc. (extracellular) to an area of low conc. (intracellular), causes K+ to move out of the cell → thus, acidosis

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2
Q

what are the H+ and K+ shifts in alkalosis and what are the results?

A

H+ ions move from area of high conc. (intracellular) to an area of low conc. (extracellular), causes K+ to move into the cell → thus, alkalosis is a/w hypokalemia

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3
Q

alkalosis vs acidosis pH?

A

alkalosis = >7.45

acidosis = <7.35

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4
Q

what are the plasma bicarb levels like for metabolic acidosis?

A

Plasma HCO3 < normal = metabolic acidosis

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5
Q

what are the plasma bicarb levels like for metabolic alkalosis?

A

Plasma HCO3 > normal = metabolic alkalosis

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6
Q

metabolic acid-base d/o’s are d/o’s of what?

A

d/o’s of bicarb

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7
Q

respiratory acid-based d/o’s are d/o’s of what?

A

d/o’s of CO2

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8
Q

what is respiratory acidosis a result of?

A

retention of CO2 b/c of pulm. alveolar hypoventilation

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9
Q

what are causes of respiratory acidosis?

A

Acute Resp. Failure:

  • CNS depression (d/t opioids, sedative, trauma, anesthetic)
  • Cardiopulmonary arrest
  • Pneumonia
  • Decr. resp. effort d/t pain from incisions/trauma
  • PE, hemorrhoids/pneumothorax

Chronic Resp. Failure:
-Advanced lung disease (ex. COPD) -> results in compensated hypoventilation & is well tolerated

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10
Q

respiratory acidosis is primary when what change occurs?

A

*Primary if pH and PaCO2 change in opposite directions

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11
Q

what’s the s/s of respiratory acidosis?

A

Hypercapnia and hypoxia

Restlessness and agitation

Mild HTN

As levels rise → confusion, somnolence, and ultimately coma, cardiac arrest

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12
Q

what’s the tx for respiratory acidosis?

A
  • Remove cause and ensure adequate oxygenation, or mechanical ventilation
  • Improve pain control

Do NOT correct too rapidly -> can cause severe dysrhythmias (V-tach)

***DON’T ADMIN BICARB W/OUT TREATING THE CAUSE

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13
Q

when should you NOT administer bicarb in respiratory acidosis?

A

***DON’T ADMIN BICARB W/OUT TREATING THE CAUSE

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14
Q

what are the 2 major causes of metabolic acidosis?

A
  1. Loss of bicarb from extracellular space (normal anion gap - hyperchloremic)
  2. Incr. metabolic acid load (high anion gap)
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15
Q

what’s the cause of non-anion gap metabolic acidosis?

A

Lost HCO3 is replaced by Cl- → there’s an accumulation of Cl- conc.

***Occurs acutely w/ GI d/o (diarrhea, external pancreatic fistula)

Occurs chronically w/ renal dysfunctions, ureterointestinal anastomosis, decr. mineralocorticoid activity, use of diuretic acetazolamide, burn patients

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16
Q

what’s the causes of high anion gap metabolic acidosis?

A
  • **MUDPILES
  • Methanol, Uremia, DKA, Propylene glycol, Isoniazid/Infection, Lactic Acidosis, Ethylene Glycol, Salicylates (also Rhabdo/renal failure)
  • **Lactic Acidosis = MCC
  • Occurs w/ shock
  • Type A (hypoxia)
  • Type B (not hypoxia) - d/t liver failure, renal failure, thiamine ef. ETOH intox, metformin
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17
Q

what does MUDPILES stand for and what does it cause?

A

Methanol, Uremia, DKA, Propylene glycol, Isoniazid/Infection, Lactic Acidosis, Ethylene Glycol, Salicylates (also Rhabdo/renal failure)

causes high anion gap metabolic acidosis

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18
Q

what’s the MCC of high anion gap metabolic acidosis?

A

Lactic acidosis

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19
Q

when is metabolic acidosis primary?

A

*Primary if pH and PaCO2 change in same direction

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20
Q

what’s the s/s of metabolic acidosis?

A

Resp. compensation occurs w/ both acute and chronic metabolic acidosis

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21
Q

what’s the tx of metabolic acidosis?

A

Treat and correct the underlying d/o

Hypovolemia must be corrected, bleeding must be stopped, sepsis controlled, and/or cardiac fxn improved to improve tissue perfusion

*Admin of bicarb w/out correcting the underlying problem will not return the pH to normal

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22
Q

what’s the pH and CO2 like in respiratory alkalosis?

A

Incr. in pH related to a decr. in PaCO2

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23
Q

what’s the cause of respiratory alkalosis?

A

***Incr. in pH related to alveolar hyperventilation

Common in surgical pts d/t pain (MC in young, not elderly - would cause hypoventilation and respiratory acidosis in elderly)

hypoxia, fever, brain injury, sepsis, liver failure, mechanical ventilation

Compensatory mechanism = renal excretion of bicarb (only w/ acute)

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24
Q

what’s the s/s of respiratory alkalosis?

A

Paresthesias, carpopedal spasm, Chvostek’s sign

K+, Mg, Ca, Phosphate metabolism are all disturbed

Decr. cerebral blood flow (esp. In acute brain injury, atherosclerosis of cerebral blood vessels)

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25
Q

what’s the tx for respiratory alkalosis if spontaneously breathing?

A

correct the underlying cause of the hyperventilation

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26
Q

what’s the tx for respiratory alkalosis if mechanically ventilated?

A

reduce the amount of ventilation

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27
Q

what’s the pH and bicarb like in metabolic alkalosis?

A

Incr. pH related to a incr. In HCO3 (bicarb)

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28
Q

what’s the MC acid-base d/o in surgical patients?

A

metabolic alkalosis

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29
Q

what electrolyte abnormalities occur in metabolic alkalosis?

A

GI and renal losses of K+ and Cl- ions can occur & cause hypochloremic hypokalemic metabolic acidosis

caused by -> ***Vomiting/NG suction (loss of gastric HCl), chronic diarrhea, loop diuretics

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30
Q

what’s the s/s for metabolic alkalosis?

A

K+ depletion → paralytic ileus, digitalis toxicity, cardiac arrhythmias

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31
Q

what’s the tx for metabolic alkalosis?

A

Replacement of electrolytes (esp. chloride and potassium) and of fluids specific to the type of loss, and control of ongoing losses

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32
Q

what’s the worst single finding predicting high cardiac risk? how’s it treated?

A

JVD

-treated w/ ACEIs, BBs, digitalis, and diuretics before surgery

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33
Q

what cardiac pt should avoid surgery and needs further evaluation prior to an elective procedure/

A

pt with unstable angina

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34
Q

what’s Virchow’s triad?

A

stasis, hyper coagulability, endothelial injury

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35
Q

what is the MC type of hypo-osmolality w/ hypervolemia?

A

hyponatremia

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36
Q

what are causes of hyponatremia?

A

SIADH (increased ADH secretion)

Loss of isotonic fluid d/t GIT d/o (body forced to retain water)

Hyperglycemia (causes cells to release water, diluting Na)

Low blood volume/BP (incr. ADH)

Hypertonic mannitol admin

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37
Q

what are the primary sx’s of hyponatremia?

A

CNS dysfunction

-muscle cramps/seizures

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38
Q

what are sx’s of untreated severe hyponatremia?

A

seizures, coma, areflexia,d eath

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39
Q

what’s the tx for hypotonic hyponatremia? (Isovolemic, Hypervolemia, Hypovolemic)

A

Isovolemic: H20 restriction

Hypervolemia: H2O + Na restriction

Hypovolemic: NS

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40
Q

what’s the tx for hypertonic hyponatremia?

A

NS until hemodynamically stable → switch to ½ NS

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41
Q

what’s the tx for severe hyponatremia?

A

Hypertonic saline + Furosemide

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42
Q

when must you be cautious in treating hyponatremia?

A

if you do it too quickly!!!
-repleting Na too quickly may result in Central Pontine Myelinolysis (demyelination of cells from shrinkage caused by rapid shift of serum Na)

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43
Q

what’s the MCC of hypernatremia?

A

volume depletion/hypovolemia

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44
Q

what are causes of hypernatremia?

A

MCC is volume depletion/hypovolemia

diarrhea, burn, DI, hyperglycemia

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45
Q

what are the s/s of hypernatremia?

A

***Incr. BUN:Cr >20:1 (b/c dehydrated), dry mucous membranes, hypotension

CNS dysfxn: hypertonicity shifts water out of cells → shrinkage of brain cells
-Confusion, lethargy, coma, muscle weakness, seizures

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46
Q

when does severe hypernatremia occur?

A

Severe hyperNa occurs when person can’t obtain water

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47
Q

what’s the tx for hypernatremia?

A

D5W IV → monitored every 2 hrs until Na < 145
-Then infusion decr. to 1 mL/kg/hr until Na is 140

Goal is to lower serum Na by 1-2 mEq/L per hr in < 24 hrs (don’t want to lower too quickly)

Caution hyperglycemia

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48
Q

what should you be cautious about when treating hypernatremia?

A

about causing hyperglycemia b/c giving pt D5W

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49
Q

what’s the tx of Diabetes Insipidus?

A

Desmopressin (ADH analog)

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50
Q

what are the MC causes of hypokalemia?

A

Increased urinary/GI losses like:

  • ***diuretic therapy
  • vomiting, diarrhea
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51
Q

what are other causes oh hypokalemia?

A

metabolic alkalosis, insulin, hypomagnesemia, hyperaldosteronism (increases K+ excretion from kidneys)

Meds (that cause large shifts of K+ from extracellular to intracellular)

  • diuretics (loops & thiazides)
  • insulin
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52
Q

when to the s/s of hypokalemia manifest?

A

when K+ < 3.0 mEq/L

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53
Q

what are the s/s of hypokalemia?

A

muscle cramps, constipation, T wave flattening, U wave

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54
Q

what’s the tx of hypokalemia?

A
  • **K+ replacement with KCL PO (if possible)
  • IV KCl given for rapid tx/severe sx

K sparing diuretics (spironolactone, amiloride)

if hypomagnesemia present, need to give Mg (to correct hypoK)

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55
Q

what can too rapid of IV K+ replacement cause?

A

hyperkalemia and fatal cardiac arrhythmias

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56
Q

what fluids make hypokalemia worse?

A

dextrose fluids b/c increases insulin causing more K to go into the cells

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57
Q

what are causes of hyperkalemia?

A

Decreased renal excretion

Decr. aldosterone (hyperaldosteronism, adrenal insufficiency)

Meds: K supplements, K-sparing diuretics, ACEI/ARBs, digoxin, BBs, NSAIDs

Metabolic acidosis (DKA)*

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58
Q

what are the s/s of hyperkalemia?

A

cardiac sx’s

  • pearked T waves
  • prolonged QRS -> sin wave -> arrhythmias (v-fib)
  • muscle fatigue
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59
Q

what arrhythmia can develop in hyperkalemia?

A

v-fib

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60
Q

what’s the tx for hyperkalemia?

A

IV Calcium gluconate*** (stabilizes cardiac membrane)

Insulin w/ glucose (shifts K+ intracellularly) + bicarb

Kayexalate (enhances GI K+ excretion)

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61
Q

when you have hypomagnesemia, what do you also have?

A

hypokalemia and hypophosphorus

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62
Q

what are causes of hypomagnesemia?

A

Malabsorption:
-**ETOHics, Celiac disease, small bowel bypass, diarrhea, vomiting, laxatives

Renal losses (diuretics, PPIs)

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63
Q

what are the 2 MC causes of hypermagnesemia?

A

Renal insufficiency (decr. Mg excretion)

Increased Mg intake (ex. Overcorrection of hypoMg)

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64
Q

what are the s/s of hypermagnesemia?

A

muscle weakness, decreased DTRs

prolonged QT/PR and wide QRS

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65
Q

what’s the tx for hypermagnesemia?

A

IV saline and control MG intake

Calcium Gluconate

diuretics (furosemide) or dialysis

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66
Q

what is the classic cause of hypochloremia?

A

Classically results from loss of acidic gastric contents → vomiting or NG suction

67
Q

what are the s/s of hypochloremia?

A

s/s are those of the accompanying d/o

68
Q

what’s the tx for hypochloremia?

A

solutions containing sodium chloride and potassium chloride

69
Q

what are causes of hypocalcemia?

A

HypoCa w/ decreased PTH (hypoparathyroidism = MC overall cause)

HypoCa w/ increased PTH (chronic renal disease MC cause, vit d def., hypomagnesemia, hypoalbuminemia)

70
Q

what are the s/s of hypocalcemia?

A

prolonged QT interval

Chvostek’s sign, Trousseau’s sign, tetany

71
Q

how do you dx hypocalcemia?

A

decreased ionized Ca+ & total serum Ca (<8.5 mg/dL)

72
Q

what’s the treatment for symptomatic hypocalcemia?

A

IV Calcium gluconate

73
Q

what’s the tx for mild hypocalcemia?

A

PO Ca + vit. D (ergocalciferol, calcitriol)

K+ & Mg repletion may be needed

NEED CORRECTED CA IN PTS W/LOW SERUM ALBUMIN

74
Q

what’s the MC overall cause of hypocalcemia?

A

hypoparathyroidism

75
Q

what’s the MC cause of increased PTH?

A

chronic renal disease

76
Q

what’s the MC cause of hypercalcemia?

A

PRIMARY HYPERPARATHYROIDISM OR MALIGNANCY!

77
Q

what’s the triad of Primary hyperparathyroidism?

A

increase Ca, increase PTH, decrease phosphate

78
Q

what drugs cause hypercalcemia)?

A

thiazides, lithium

79
Q

what’s the s/s of hypercalcemia?

A

Stones (kidney stones)

Bones (painful bones, fx’s)

Abd groan (ileus, constipation*)

Psychiatric moans (weakness, fatigue, AMS, decr. DTRs, depression/psychosis)

EKG: shortened QT, prolonged PR, wide QRS

80
Q

how do you dx hypercalcemia?

A

increased ionized Ca & total serum Ca >10 mg/dL

81
Q

what’s the 1st LINE tx for symptomatic hypercalcemia? others?

A

IV saline & Furosemide = 1st line tx

Others tx = Calcitonin, Bisphosphonates in severe cases (IV Pamidronate)

82
Q

what diuretics should be avoided in hypercalcemia?

A

thiazide durietcs (ex. HCTZ)

83
Q

what’s the MC cause of hyperphosphatemia?

A

renal failure (decr. Ca+, incr. Phosphate, incr. PTH)

84
Q

what’s the s/s of hyperphosphatemia?

A

soft tissue calcifications

most asx, heart block

85
Q

what’s the tx for hyperphosphatemia?

A

Phosphate binders:

-Calcium acetate, Calcium carbonate, Sevelamer

86
Q

what’s the s/s of hypophosphatemia?

A

Diffuse muscle weakness, flaccid paralysis (d/t decr. ATP)

87
Q

what’s the tx for hypophosphatemia?

A

Treat the underlying cause

Phosphate repletion -> potassium phosphate, sodium phosphate

88
Q

what’s the MCC of hypotension and low urine output?

A

loss of intravascular volume (volume depletion)

89
Q

what’s the most valuable value to dx hypo/hypervolemia?

A

urine output

90
Q

what’s the labs for hypovolemia?

A

increased HR, decreased BP, decreased urine output, increased HCT, increased BUN/Cr

91
Q

what’s the tx for hypovolemia?

A

LR or NS

92
Q

what’s the fluid of choice for blood loss?

A

LR’s

93
Q

what type of fluid do you start resuscitation with?

A

crystalloids

94
Q

what are crystalloids vs colloids?

A

crystalloids = LR or NS (isotonic fluids)

colloids = blood (pRBC, FFP), albumin
-have osmotic pull

95
Q

what are causes of hypovolemia?

A

bleeding, inflammation (“itits)

96
Q

what’s the labs like for hypervolemia?

A

decreased urine output, decreased Hct

97
Q

what are s/s of hypervolemia?

A

pulmonary/peripheral edema, ascites, JVD

98
Q

what are causes of hypervolemia?

A

CHF, hepatic failure, renal failure

99
Q

what’s the treatment of hypervolemia?

A

Less severe → fluid or sodium restriction

More severe → diuresis w/ loop diuretics and replacement of associated K+ losses

100
Q

what’s the best way to achieve euglycemia?

A

best by continuous infusion of insulin

101
Q

what’s the management for pt with DM and on rapid-acting or short-acting insulin and getting surgery?

A

withheld when pt stops PO intake (midnight before day of surgery)

102
Q

what’s the management for pt with DM and on Intermediate-acting & long-acting insulin and getting surgery?

A

administered ⅔ the normal evening dose before surgery & 1/2 the normal morning dose the morning of surgery

103
Q

what’s the management for pt with DM and on long-acting PO agents and getting surgery?

A

stopped 48-72 hrs before surgery

104
Q

what’s the management for pt with DM and on short-acting PO agents and getting surgery?

A

held night before or day of surgery

105
Q

what’s the MC cause of increased pulmonary risk for surgery?

A

smoking

106
Q

when should pts stop smoking before surgery?

A

at least 6 weeks

107
Q

what are the 6 “W’s” of post-op fever?

A
  1. Wind (atelectasis, pneumonia)
  2. Water (UTI)
  3. Wound (wound infection/surgical site infection)
  4. Walking (DVT)
  5. “W” abscess
  6. “W”onder drugs (anytime other etiologies are ruled out)

and then ***surgical complication

108
Q

what’s the MC source of post-op fever on POD 1?

A

Atelectasis

109
Q

what’s the definition of atelectasis?

A

alveolar collapse

110
Q

what are s/s of atelectasis?

A
  • Pain
  • Somnolence from analgesic use
  • Suppressed cough
  • Lack of mobility
  • Nasopharyngeal instrumentation
111
Q

what day of post-op are patients at highest risk of atelectasis and why?

A

POD 1 (b/c that’s when pain is the highest) and d/t pain & not being able to expand lungs

112
Q

what surgeries put pts at risk for atelectasis?

A

abdominal surgery and thoracic surgery

113
Q

does atelectasis cause fever?

A

NO! but can lead to pneumonia, which causes fever

114
Q

how do you prevent atelectasis?

A

OOB, IS, deep coughing/breathing

115
Q

what are you worried about atelectasis turning into?

A

pneumonia

116
Q

when does pneumonia develop post-op?

A

POD 3 if atelectasis is not resolved

117
Q

when does UTI develop post-op? what is it d/t?

A

POD 2-3

UTI post-op is d/t Foley

118
Q

when does DVT develop post-op?

A

POD 5-7

119
Q

when does wound infection/surgical site infection develop post-op?

A

if caused by C. perfringes then occurs w/in 24 hrs

or POD 5-7 days

120
Q

what is the location of a wound infection post-op?

A

above fascia, below the skin (superficial infection)

121
Q

when does C. perfringes wound infection develop post-op?

A

w/in 24 hrs of post-op

122
Q

what is C. perfringes post-op infection hallmarked by?

A

foul-grey odor

123
Q

how many days does it take wound to become air tight?

A

2 days

124
Q

how is a post-op wound infection with abscess treated?

A

I&D to drain all pus out

pack it and change dressings or pack with wick and remove in 48-72 hrs

125
Q

how is an abscess treated vs cellulitis?

A

abscess -> I&D

cellulitis -> abx

126
Q

what is primary intention healing of wounds?

A

Wounds edges have been apposed (by sutures, wound clips, tapes, or dermal adhesives)

127
Q

what is secondary intention of healing wounds?

A

Wounds edges have been left unapposed

Dressing is used to collect wound fluids and help keep the wound from closing prematurely

-Common in the management of an abscess

128
Q

what are the first cells to enter to begin clotting process?

A

platelets

129
Q

what are the 3 phases wound healing?

A
  1. Substrate phase (inflammatory)
  2. Proliferative phase
  3. Maturation phase (remodeling)
130
Q

what are the main cells in phase 1 of wound healing (inflammatory phase)?

A
Polymorphonuclear leukocytes (PMNs)
-appear shortly after injury and hang around for 48 hrs

Platelets

Macrophages (main cells involved in wound debridement)

131
Q

what are the MAIN CELLS involved in wound debridement

A

Macrophages

132
Q

how long does phase 1 of wound healing (inflammatory phase) last? what does wound look like during this phase?

A

4 days

wound is edematous and erythematous and is sometimes hard to distinguish from infection

133
Q

when does phase 2 (proliferative phase) of wound healing being and how long does it last?

A

Relatively constant phase and begins when wound is covered by epithelium

Occurs indefinitely until the wound surface is closed by ectodermal elements (epithelium for skin, mucosa in gut)

134
Q

what is phase 2 (proliferative phase) of wound healing characterized by?

A

production of collagen in the wound

135
Q

what are the main cells in phase 2 (proliferative phase) of wound healing?

A

Fibroblasts

136
Q

what do the fibroblasts do in phase 2 (proliferative phase) of wound healing?

A

produce collagen

-Collagen = the principal structural protein of the body

137
Q

what is phase 3 (remodeling) of wound healing characterized by?

A

maturation of collagen by intermolecular cross-linking

138
Q

what occurs in phase 3 (remodeling) of wound healing? how long does this phase take?

A

Wound scar flattens takes 9-12 months in adults)

139
Q

in which phase of wound healing is collagen deposited in the wound?

A

phase 3 - maturation phase (remodeling)

140
Q

what are the 3 classifications of wound healing?

A

primary intention, secondary intention, tertiary intention

141
Q

how does the wound close in secondary intention?

A

Wound closes by contraction and epithelialization

wound is left open and allowed to heal spontaneously from the edges of the wound

142
Q

what is tertiary intention of wound healing?

A

Wound is closed by active means after a delay of days to weeks

143
Q

when should delayed closures of wounds (tertiary intention) be performed?

A

if quantitative bacterial count of wound is less than 10^5 organisms/gram of tissue

144
Q

what is required prior to delayed closure of wounds?

A

Repeated irrigation, debridement and dressing changes are required prior to closure

145
Q

what are the 5 classifications of wounds?

A

clean wound

avulsion injury

abrasion

puncture wounds

crush injury

146
Q

what is a clean wound?

A

Relatively new (<12 hrs) with minimal contamination

Clean and debride if necessary then close

147
Q

what is an avulsion injury?

A

Skin has been violated by shearing forces and underlying tissue has been undermined and elevated, creating a flap or total loss of skin

148
Q

what’s the tx for an avulsion injury?

A

cleaning, debridement of necrotic tissue and closure if appropriate

Suture flap down with absorbable sutures then close wound edges

149
Q

what’s an abrasion wound?

A

Superficial loss of epithelial elements with portions of dermis and deeper structures remaining intact

150
Q

what’s the tx for an abrasion wound?

A

Only cleansing is required

-Apply a layer of petroleum jelly or antibiotic ointment to prevent dessication (excess dryness)

151
Q

what’s the tx of puncture wounds?

A

Generally do not require closure

Examine for foreign bodies

152
Q

what type of wound SHOULD NOT be closed?

A

A wound that contains highly virulent Streptococci species should NOT be closed

153
Q

what nutrition should be considered in the pt in wound healing?

A

Folic acid

Vitamin K

Vitamin A

154
Q

what is folic acid critical for in wound healing?

A

critical in the proper formation of collagen

155
Q

what is vitamin K essential for in wound healing?

A

essential for the synthesis of clotting factors (need to prevent hematoma)

156
Q

what is vitamin A’s role in wound healing?

A

increases the inflammatory response, increases collagen synthesis and increases the influx of macrophages into the wound

157
Q

when do you stop anticoags for surgery?

A

2-4 days prior (if a-fib)

158
Q

when do you stop anti-platelet (ASA, NSAIDs) drugs for surgery?

A

7 days prior (b/c platelet half-life is 7 days)

159
Q

what is functional capacity?

A

indicator of post-op cardiac complication risk (done pre-op)

expressed in METS (metabolic equivalents)

160
Q

what does < 4 METS mean?

A

poor functional capacity

ex. self-care, ability to complete ADLs, vacuuming, walking 2mph, and writing

161
Q

what does 4-10 METS mean?

A

moderate functional capacity

ex. ability to walk up flight of stairs, walk 4mph, walk gold f course, doing yard work, cycling

162
Q

what does 10 METS mean?

A

excellent functional capacity

ex. jogging, tennis, swimming, skiing

163
Q

what meds are used to help pts quit smoking before surgery?

A
  1. **Bupropion -> block reuptake of DA & NE to reduce reward aspects of cig smoking
  2. Varenciline (MC adr is nausea)
164
Q

when is Red blood cell transfusion given to a pt? available as what?

A

given to raise Hgb in pts with anemia or to replace losses after acute bleeding episodes

available as packed RBCs (preferred) or whole blood