Perioperative Management—Ch 2
1
Surgery Midterm
Chapter 2
Advance directives = are legal documents that inform general wishes of patient regarding level of care to be
provided if the patient should not be able to speak for himself.
AMPLE history
A = Allergies
M = Medications
P = Past medical history
L = Last meal
E = Events preceding the emergency
Indications for screening EKG
Men who are older than 40 and women older than 50 years should have a baseline recording. Pt with
symptomatic cardiac disease, HTN, diabetes. Pt who undergo thoracic, intraperitoneal, aortic, or
emergency surgery are candidates.
Cardiac Evaluation
Surgery puts stress on the heart in two ways.
1) catecholamine surge in response to pain & anxiety
2) myocardial blood flow is reduced by the vasoconstrictive effect of the alpha-1-receptor stimulation
& the reduced time for blood flow through the myocardium as a reduction in diastolic time.
Most innocent murmurs are apical. New murmurs, any rubs, third hear sounds, JVD, etc.
In pt with previous MI, the risk of postoperative infarction is 5 – 10% overall with attendant mortality at
50%. Pt with no previous infarct is 0.5% risk.
Pt with unstable angina should avoid surgery except for CABG.
Diabetes increases the suspicion for occult cardiac problems.
Quantification of surgical risk: Dripps-American Surgical Association Classification
Categorizes pts into 5 groups.
Class 1 = Healthy pt, limited procedure
Class 2 = Mild to moderate systemic disturbance
Class 3 = Severe systemic disturbance
Class 4 = Life-threatening disturbance
Class 5 = Not expected to survive, with or without surgery.
Goldman scale for calc. cardiac risk (aka post-op MI)
Class
Points
Pot. Fatal Cardiac Risk Factors
1
0-5
0.7%
2
6-12
5.0%
3
13-25%
11.0%
4
>26
22.0%
Cardiac Death
0.2%
2.0%
2.0%
56.0%
Perioperative Management—Ch 2
2
PULMONARY EVALUATION
Post-op pulmonary complications are the most common cause of post-operative morbidity.
Risk Factors include type of operation (the area of incision and resultant pain and length of operation).
Anesthesia is in itself a risk, by going under you loose 11% FRC. Tracheal intubation promotes direct
colonization of the upper airway by Gram negative organisms and sets the stage for infection.
Absorption Atelectasis = high levels of inspired oxygen compound arterial hypoxemia by causing
absorption atelectasis. This is what occurs when alveoli are filled with gas mixtures that contain a high
conc of oxygen and low nitrogen. As oxygen is absorbed into the pulmonary capillaries, less gas is left in
the alveoli to maintain functional residual capacity thus atelectasis.
Risk of pulmonary complication varies widely from 10 – 70%. Thus 1/3 of all mortality post-op is directly
or indirectly attributed to pulmonary insufficiency.
Smokers risk is 2-6 times greater than non-smokers. Helps if smokers quit for 6 weeks before the
procedure.
COPD and Asthma also increases risk. Pts who cannot cough or breath deeply. Obesity is a direct
impairment of respiratory function. Occupation exposure also places a person at increased risk (asbestos,
silicone, etc).
There is no evaluation strategy that precisely defines the pulmonary risk of a given patient. Although it is
possible to indicate which patients are like to fare extremely well or poorly, the middle group is difficult to
stratify.
--Pulmonary fxn tests can uncover or quantify an abnormality (which would either help stratify or could be
optimized before surgery.)
Pulmonary eval for pulmonary operations:
Pts receiving pulmonary procedures need special attention especially if they have preexisting pulmonary
problems. Most are likely to have a significant smoking history. Pts who have “greater than eight-packs-ayear history” are at particular risk for chronic bronchitis. In general, the idea is the leave the patient with a
FEV of at least 800 mL postoperatively. One way to determine post –op FEV is multiply the pre-op FEV
by the percentage of lung tissue to be left after resection. Ex) Pre-op FEV = 1.8 L and 80% of lung is to
remain post-op. Thus post op FEV should be 1.8(.8) = 1.4 L.
If a patient is at very high risk, whose predicted post-op FEV is less than 1.0 then use split perfusion
radionucleotide lung scanning to help predict post-op lung function. If after this the residual FEV is less
than 800 mL then the pt is considered inoperable (aka a low chance the pt will even get off of the
ventilator).
Stair test = If pt can climb 5 flights of stairs they can have a pneumonectomy. If three then a lobectomy. (a
less sophisticated pulmonary fxn test).
*Note*PE is the most common cause of sudden death in hospitalized patients.
Evaluation of the Patient with renal dysfunction:
Chronic renal failure patients need careful perioperative monitoring but should not be denied a necessary
procedure or beneficial surgery based on history of renal failure alone.
Pts with renal disease need to be careful of fluid status (many are chronically hypovolemic).
Pts with renal failure have a difficult time excreting potassium (K). The risk of malignant hyperkalemia is
directly proportional to the pts K level before their last dialysis. K should be less that 5mEq/L before
surgery. Serum bicarb levels should be greater than 18 mEq/L (many CRF pts are chronically acidotic).
Pts will become acidotic due to Hydrogen released from dead cells and they should compensate by
hyperventilation. If a pt is unable to compensate then a profound acidosis can occur. Aggressive
pulmonary toilet should be used to prevent hypoventilation, atelectasis, pneumonitis, & over sedation.
CRF pts often have hypocalcaemia secondary to hyperphosphatemia. Follow ionized calcium
perioperatively and supplement as needed. Also hypermagnesium is also common thus avoid magnesium
containing antacids.
Perioperative Management—Ch 2
3
Management to detail is the key for these patients. In/Outs that are accurate and close attention to nutrition
status are impairative. Note that many drugs are nephrotoxic and thus should be used sparingly or avoided
all together if possible.
Eval of patients with hepatic dysfunction:
There is nearly a universal agreement that sodium and water restriction is the cornerstone of managing pts
with liver disease, with or without ascites.
The alcoholic patient must be protected from withdrawl by the administration of sedatives. Untreated
delirium tremens carries a post-op mortality of as high as 50%.
Pts with liver disease are more apt to bleed due to the lack of vit. K dependent coagulation factors.
Cirrhosis is frequently manifested by massive upper GI bleed from esophageal or gastric varices. Vitamin
deficiencies are common in alcoholics. Thiamine should be administered before glucose and
magnesium/phosphate deficiencies are common.
The Diabetic Patient
Goal = make the pt euglycemic
If glucose is too low then death can quickly occur due to glucose dependent tissues (aka the brain) being
deprived of energy.
1) Pts who are instructed not to eat or drink after midnight in preparation for an operation the next
morning should reduce their morning insulin dose by half the usual for intermediate and regular
acting insulin the morning of operation.
2) The patient should receive a continuous infusion of 5% dextrose to provide 10g glucose/hr.
Fingerstick glucose should be monitored intraoperatively and q6 hrs postoperative. Even patients
who take oral diabetic medications should be managed with insulin. Brittle diabetics should be
very carefully monitored. DKA can develop in patients who have Type I or Type II diabetes. A
glucose level of less than 250mg/dL does not mean that the pt is not able to have DKA. DKA
develops because of the metabolism of fuel in the absence of glucose. Hence the development of
DKA does not depend on a certain glucose, but best managed with a continuous infusion of
intravenous IV insulin usually 1 to 3 units/hr. If sliding scale is used subcutaneous is preferred
except when the subcutaneous tissue is not well perfused.
Men with diabetes may have twice the risks of cardiovascular mortality than others.
Women have approximately four times the risk.
The risk of infection is substantially greater for diabetic patients.
The Adrenally Insufficient Patient
Pts on chronic steroid therapy need to be covered with glucocoricoids to prevent the sequela if adrenal
suppression. The amount of steroids is determined by the amount of stress the patient is expected to
undergo in surgery.
The Pregnant Patient
Pregnancy is a unique state that presents different problems. The expanding uterus displaces the
abdominal viscera thus pain from the appendex for example may present superiorly. A gravid uterus
may also compress the vena cava and reduce venus return when the pt is supine. It is important for the
surgeon to realize that they are caring for two patients. If the mother is unduly stresses, the placenta
will be deprived of blood supply. The expanded blood volume of the pregnant woman can mask blood
loss and thus fetal distress. Respiratory rate and tidal volume are increased in pregnant women as well.
It is best when possible to avoid a surgical procedure during pregnancy but surgical emergencies must
be handled when present. If surgery is needed, it is best performed in the second trimester when the
risk of precipitating spontaneous abortion is low (about 5% in women under general and abdominal
surgery). Also low risk of precipitating labor and fetal demise.
Appendicitis and biliary tract disease are the most common cause of surgery in preg.
Even pts with breast cancer can have conservative surgery and begin chemotherapy (after the 1 st
trimester) but radiation must be delayed until after pregnancy. Continuation of pregnancy does not
appear to adversely affect the outcome of women.
Fetal loss occurs in 15% of all women severely injured in pregnancy. Placental abruption can occur
even after minor injury and is not consistently accompanied by vaginal bleeding. DIC is an ominous
Perioperative Management—Ch 2
4
complication that can occur within hours of placental abruption or amniotic fluid embolization (when
can be fatal).
The Geriatric Patient
The elderly have less reserve than their younger counterparts and thus may not recover or tolerate
surgical procedures as well. The rest is about knowing the patients wishes for aggressive treatment.
Basically, living wills and DNR/DNI.
The Medical Record
This area is completely useless and I think we know that this document should be accurate and concise.
The best interest of the patient, etc.
Wound Care
Surgical wounds are typically healed by first intention (sutures) or second intention (leaving the wound
open to granulate over). Wounds must be properly dressed and kept clean. The wound should be
epithelized in 48 hours.
Pain Management
Close attention to pain management is very important in surgery. That is about all they had to say.
DVT Prophylaxis
Venous thromboembolism will afflict 25% of postoperative patients if they are not given prophylaxis.
This is due to Virchow’s triad (stasis, hypercoagulability, and endothelial injury). Heparin
prophylaxis, low-molecular weight heparin, or IPC (the leg sqeezers= Intermittent pneumatic
compression devices).
POSTOPERATIVE COMPLICATIONS
Malignant Hypertension
Potentially fatal, hypermetabolic, autosomal dominant condition of skeletal muscle that is reported to
occur in one in 14,000 children and one in 50,000 adults. Several genetic mutations are associated but
all disrupt intracellular calcium metabolism. Inhalational halogenated anesthetic agents and
succinylcholine are known triggers of the syndrome which manifests itself as violent and sustained
muscle contraction, rigidity, heat production, acidosis. Muscle necrosis and rhabdomyolysis may
occur.
A family history of relatives who have had problems with anesthetic agents may be the only
preoperative clue. Susceptible individuals may be confirmed with a muscle biopsy and stimulated
contraction studies.
*An abrupt rise in end-tidal carbon dioxide is the first sign. Massester muscle rigidity is seen early in
children.
Early recognition is the key to treatment.
Today mortality is less than 5%. The first step in management is to discontinue the offending agent.
Dantrolene, a muscle relaxant that blocks Ca release from the sarcoplasmic reticulum is the only agent
available for treatement.
Atelectasis
Despite the frequent occurrence of atelectasis, up to 90% of patients with general anesthetic, there is no
consensus regarding etiology, treat, or clinical significance. The before discussed reasons for this are
repeated.
Fever
The text is extensively vague and “An elevation in core body temperature is so common that many
mistakenly consider it a normal postoperative state.” This is the only useful stuff in the entire passage.
*Short courses of antipyretics in approved doses carry a low risk of toxic side effects.
*The benefits of antipyretic use to the patient are uncertain, other than analgesia.
*The increase in metabolic demand (10% for each degree C) associated with fever may be poorly
tolerated in the elderly or debilitated, especially those with cardiac or pulmonary condition.
Perioperative Management—Ch 2
5
*Children should not be given aspirin.
*Antipyretics do not prevent febrile seizures or raise the seizure threshold.
*Cooling blankets should not be used to treat fever.
*If antipyretics are used, they should be used on a scheduled basis and not as the occasion arises.
*Indomethacin and NSAIDS should NOT be used in patients with coronary artery disease.
*Anything that increases the cerebral metabolic rate in pts with traumatic brain injuries which
increases cerebral oxygen demand and cerebral blood flow. This can increase intracranial pressure.
Fluids, Electrolytes, Acid-Base Balance—Ch 3
6
NB—~1/3 of objectives were not in chapter, worked out most of those (& looked on internet), but then got
tired of messing with it; rest provides good outline of chapter, though.
1.
Know the range of normal values of Na+, K+, HCO3-, and Cl- in serum, gastric aspirate, bile, and
ileostomy aspirate.
Na+
K+
HCO3ClSerum
135-145 3.5-5.0
24-30
95-105
Gastric aspirate
10-150
4-12
120-160
0
Bile
120-170
3-12
80-120
30-40
Ileostomy aspirate 80-150
2-8
70-130
20-40
2.
Understand the contributions that extracellular, intracellular, and intravascular volumes make to
body weight and how they vary with age and obesity.
a. TBW = 60% wt 70kg ♂, 50-55% ♀
b. ↓% wt w/ age (d/t ↓musc mass), obesity (d/t ↑fat)
c. Intracellular water: 67% of TBW, 40% wt
d. Extracellular water: 33% TBW, 20% wt
i. Interstitial: 25% TBW, 15% wt
ii. Intravascular: 8% TBW, 5% wt
3.
List four hormones or substrates that affect renal absorption and excretion of sodium and water.
a. Aldosterone
i. Renin-angiotensin-aldosterone system
ii. Action: ↑Na resorption in exchange for K and H in distal tubules
iii. Stimulants:
1. Volume rec in RA
2. ↓[Na]ECF
3. ↑[K]serum
4. ACTH
iv. Suppressants:
1. ECV expansion
2. ↑Na
3. ↓K
b. ADH
i. ↑tubular resorption of H2O in collecting ducts
ii. Regulated by intracranial osmorec, vol rec in RA & LA
iii. Vol-dep responses usu override osmorec system if conflict
c. ?ANP/BNP (not in chapter)
i. Released from atria/ventricles in response to ↑BP
ii. ↑Na excr → diuresis
4. Compare the physical findings or symptoms of dehydration in the young and the elderly.
System
Young
Elderly
Intravascular 1. Orthostatic hypotension
1. Common in healthy elderly
2. Hypotension
2. May be masked by pre-existing HTN
3. Tachycardia
3. Max HR ↓ w/ age
4. ↓pulse volume
4. Masked by rigid vessels
5. ↓CVP or PaOP
5. May not reflect heart fxn or vol status
6. Oliguria
6. May be less marked if pre-existing renal
impairment is present
7. No si or fluid overload or heart 7. Pre-existing hypoproteinemia and ankle edema
failure
may be present
Interstitial
1. Dry skin and MM
1. Common in elderly
2. Dry tongue
2. Unreliable at any age
Fluids, Electrolytes, Acid-Base Balance—Ch 3
7
Misc
3. ↓tongue vol
4. Sunken eyes
5. ↓skin turgor
1. ↓DTRs
2. Distal anesthesia
3. Drowsiness
4. Apathy
5. Anorexia
6. Stupor or coma
7. Ileus
3. May be useful
4. Late sign at any ane
5. Unreliable in elderly
1. May be age-related change
2. May be age-related change
3. May be caused by inf, meds, hypothyroid, or
depression
4. May be caused by inf, etc.
5. May be caused by inf, etc.
6. Late, nonspecific si
7. Late, nonspecific si
5.
Understand the methods of determining fluid balance.
a. Adult estimates calculated to balance outputs of 12-15mL/kg/day urine, 3mL/kg stool
H2O, 0-1.5mL/kg sweat, 10mL/kg combined insensible losses from lungs/skin,
endogenous input of 3mL/kg H2O
b. Most accurate based on BSA
6.
Describe the typical 24-hour fluid and electrolyte needs in the postoperative patient who has no
complications.
a. Daily Fluid Requirements—1200mL per m2, plus:
i. Adult
1. 25-55yo: 35mL/kg
2. 55-65yo: 30mL/kg
3. >65yo: 25mL/kg
ii. Child >5kg:
1. 1st 10 kg: 100mL/kg
2. 2nd 10 kg: 50mL/kg
3. >20kg: 20mL/kg
b. Daily Electrolyte Requirements
i. Na—50-75mEq/m2
ii. K—50mEq/m2
iii. Cl—50-75mEq/m2
7.
Explain the composition of electrolytes in normal saline, lactated Ringer’s solution, and 5%
dextrose in water.
Glc (g/L) Na K
Cl
Lactate Ca
NS
154
154
LR
130 4.0 109
28
3.0
D5W
50
8.
Given a patient with the condition in the left column, list the direction of change in values and pH
for the serum electrolytes observed.
Na+ K+ HCO3 Cl pH
Excessive gastric losses
↓
↑?
↓
↑
↑
High-volume pancreatic fistula
↓
Small intestinal fistula
↓
Biliary fistula
↓
Diarrhea
↓
↓
↓
Closed head injury (?SIADH)
↓
9.
Given a patient with the condition listed, determine an appropriate replacement fluid.
Fluids, Electrolytes, Acid-Base Balance—Ch 3
8
a.
b.
c.
d.
e.
f.
g.
Pyloric outlet obstruction—NS (hydration, Cl- allows excr HCO3 to correct alkalosis)
Pancreatic fistula—LR or NS (isotonic fluid loss)
Small bowel fistula—LR or NS (isotonic fluid loss)
Biliary fistula—LR or NS (isotonic fluid loss)
Diarrhea—LR (b/c must replace K also)
Closed head injury—3%NaCl (use with caution and diuretics)
Massive blood loss—LR (begin correction of fluid shifts)
10. Indicate the direction of change in serum and urine values that might be obtained in patients with
each condition listed in the left column.
a. Serum
Na+ K+ HCO3 Cl Osmolarity
Acute vasomotor nephropathy
↓
?Hypo
↑
Dehydration
Hyper
↑
Inappropriate ADH secretion
↓
Hypo
Diabetes insipidus
?Hyper
↑
Congestive heart failure
↓
?Hypo
b.
Urine
Acute vasomotor nephropathy
Dehydration
Inappropriate ADH secretion
Diabetes insipidus
Congestive heart failure
Na+
↑
↓
↑
K+
HCO3
Cl
Osmolarity
?Hypo
Hyper
Hyper
?Hypo
?Hyper
11. List the differential diagnosis and treatment for each of the following conditions:
a. Hypernatremia
i. DDx:
1. Loss of H2O alone (hypothal abnl, unreplaced losses)
2. Loss of H2O & salt (GI losses, osmotic diuresis, excess diuretic use,
CDI, NDI, burns, excess sweating)
3. ADR (ETOH, amphotericin B, colchicine, Li, phenytoin)
4. ↑Na w/o H2O loss (Cushing’s, hyperaldosteronism, ectopic ACTH,
iatrogenic, seawater)
ii. Tx:
1. For every ↓1L H2O, Na ↑3mEq above 140
2. TBW deficit: ΔNa+ = (140 – [Na]serum) x (0.6 x kg)
3. Replace H2O slowly (≤ ½ over 1st 12-24 hr),
4. For pure H2O loss, use D5W
5. If a/w Na deficits
a. If dehydration predominate: replace w/ NS
b. If neuro sx predominate, use ½ NS
c. If Na loss is laerge, replece initially w/ NS
b. Hyponatremia
i. DDx:
1. Excess H2O:
a. Ingestion/infusion of excess H2O (mcc in surg pt)
b. Physiologic resp to surg stress, starvation, hypovolemia
c. SIADH
d. ↑ADH activity
e. Advanced cardiac, renal, or hepatic dz
2. Excess Na loss:
a. Thiazides
b. Metabolic alkalosis
Fluids, Electrolytes, Acid-Base Balance—Ch 3
9
c.
d.
e.
f.
c. Ketoacidosis
d. Adrenal insuff
e. Salt-wasting nephropathy
3. Artifactual: HL, hyperproteinemia
ii. Tx: dep on etiology
1. Excess H2O: fluid restriction
2. If d/t thiazides: d/c Rx
3. If a/w vol contraction: comboined Na/vol replection (usu NS or LR)
4. Hypertonic 3% saline only when hypoNa causes life-threatening neuro
distrurbances
Hyperkalemia
i. DDx:
1. Exogenous loading, transfusions of many units of stored banked blood,
too vigorous correction of hypoK
2. Endogenous loading (curst injuries, hemolysis, lysis & abs or large
hematomata, catabolism of fat and musc tissue b/c of stress or
starvation, rapid rewarming after severe hypothermia)
3. ↓renal excr (usu renal dz, may be d/t adrenal insuff & impaired
aldosterone activity)
4. DKA
5. Rx (diuretics, NSAIDs, BB, ACEI, etc.)
ii. Tx:
1. If K < 6.0: restrict K intake, elmiate causes like Rx, Tx vol or acid-base
d/o
2. If 6.5-7.5:
a. 10U insulin IV w/ 25g Glc IV over 5 min (shifts K from
extracell to intracell & may ↓K by ≤1mEq/L)
b. Or can injective 45mEq NaHCO3 IV over 5 min to induce
metabolic alkalosis
c. Sodium polystyrene sulfonate PO or PR removes K from body
d. Continuous monitor w/ EKG
3. If >7.5:
a. IV 10-30mL 10% Ca-gluconate given slowly over 5 min to
↓cardiac musc electrical excitability temporarily while other
methods used to rid body of K
Hypokalemia
i. DDx:
1. GI losses (diarrhea, vomiting, biliary or pancreatic fistulas, villous
adenoma, malabsorption)
2. Renal losses (hyperglycemia, hyperaldosteronism, RTA, ↑ACTH,
licorice ingestion, acute leukemia, corticoid excess), but often
iatrogenic (thiazides, loop diuretics, CAI)
ii. Tx:
1. Whenever poss, replace orally (≤40mE/4 hr if nl kidneys)
2. If IV, ≤10mEq/hr
3. If caused by hypomagnesemia, correction of Mg will correct K
Hyperchloremia
i. DDx:
1. May occur in a/w hyperNa, in RTA, or after admin excess KCl or
NH4Cl
2. May be caused by surg diversion of urine into segments of bowel
ii. Tx: correct underlying d/o
Hypochloremia
i. DDx:
1. Usu from loss of acidic gastric contents (vomit or NG suction)
Fluids, Electrolytes, Acid-Base Balance—Ch 3
10
2.
g.
h.
i.
j.
Can relut from rnal losses d/t diuretics, nonoliguric ARF & CRF,
compensatory renal tubular resorption of HCO3 in respiratory acidosis
ii. Tx: solution that contain NaCl and KCl in ratio determined by underlying
problem and by serum e-lyte conc
Hypercalcemia
i. DDx:
1. Hyperpathathroid
2. Malignancy, metastatic CA, lymphoma, leukemia
3. Granulomatous dz, sarcoidosis, TB, funal inf
4. Excessive dietary intake, milk-alkali syndrome, vitA or vitD
intoxication, thiazides
5. Immobilization
6. Endocrine abnl, thyrotoxicosis, adrenal insuff
ii. Tx:
1. Initial: ↓Ca intake, hydrate PRN, ↑urinary Ca excretion
2. If Sx or ↑↑Ca: hospitalize, large vol ½ NS or NS, diuretics to
↑excretion (may dev hypoMg)
3. Gallium-nitrate (nephrotoxic) used in Tx CA-related hyperCa
unresponsive to hydration
4. Corticosteroids sometimes as longer-term Tx to suppress Ca relase
from bone in pt w/ granulomatous dz, vitD intoxication, hematologic
malignancies
5. Plicamycin (antineoplastic) acutely ↓serum Ca (renal/hepatotox)
6. PO or IV PO4 supplements to form complexes w/ ionized Ca
Hypocalcemia
i. DDx:
1. Artifactual d/t hypoalbuminemia
2. Acute pancreatitis
3. Sur-ginduce hypoparathryoid
4. Necrotizing fasciitis
5. Inadeq intest abs (IBD, pancreatic exocrine dysfxn, mucosal malabs
syndromes)
6. Excess fluid loss from pancreatic or intestinal fistulae
7. Chronic diarrhea
8. Renal insuff w/ impaired Ca resorption
9. HypoMg
10. HypoPO4
ii. Tx:
1. If need urgent correction: Ca-gluconate or CaCl2
2. A/w chronic d/o: long-term Tx w/ Ca lactate PO, may need vitD
Hypermagnesemia
i. DDx:
1. Renal failure, injury that causes rhabdo, dehydration, severe metabolic
acidosis, adrenal insuff, remilial benign hypocalciuric hypercalemia,
o/d w/ Mg salts in cathartics
2. After Tx for eclampsia in mom or newborn
3. Pts w/ renal failure who use Mg-containing antacids
4. Metabolic alkalosis (d/t ↓renal excretion)
ii. Tx:
1. Mild: oral hydration, control Mg intake
2. Severe Sx reversed temporarily by IV Ca, Tx Mg excess w/ hydration
& diuretics, or hemodialysis
Hypomagnesemia
i. DDx:
1. Dietary def combined w/ GI losses (e.g., diarrhea, NG suction)
Fluids, Electrolytes, Acid-Base Balance—Ch 3
11
2.
3.
4.
Chroic alcoholism , malabs, acute pancreatitis, improperly constituted
hyperalimentation, endocrine d/o
Some diuretics, aminoglycosides, amphotericin, CsA, cisplatinum,
insulin, pentamidine
Athletes, preg ♀ may be mildly hypoMg
ii. Tx:
1.
2.
3.
4.
k.
Correct cause
If mild & not d/t abs defect → PO supplements
If moderate → IV MgSO4 50-100mEq/day
Sever: IV bolus 8-16mEq MgSO4 followed by IV infusion 12mEq/kg/day
Hypophosphatemia
i. DDx:
1. Inadeq uptake (d/t inadeq dietary intake, malabs, GI loss, prolonged
antacid use, improperly constituted hyperalimentation or vitD def)
2. ↑ renal excr (d/t diuretics, hypervol, corticoid Tx, hyperaldosteronism,
SIADH, hyperparathyroid)
3. Compartmental shifts (d/t hormones, nutrients that stim insulin release,
Tx DKA, recovery from hypometabolic states, rapidly growing CA or
respiratory alkalosis)
4. Occ, hypoPO4 1st clue to ETOH w/d
ii. Tx:
1. PO4 salts PO or IV
2. Tx other assoc. e-lyte abnl
3. May d/c diuretics
4. VIPomas surg removed
12. Indicate the directional change in values expected in patients with each condition listed in the left
column.
Arterial Blood
pH Pao2 Paco2 HCO3 Base Excess
Acute metabolic acidosis
↓
↓
Acute respiratory acidosis
↓
↑
↑
Chronic respiratory acidosis
↓
Compensated metabolic acidosis
Nutrition—Ch 4
12
Chapter 4: Nutrition
Assessment:
History: Risk factors for malnutrition include poverty, alcoholism, and extremes of age. Determine if wt
changes are unplanned. Determine whether skin or clothing have become loose. Wt loss of 10% =
significant, 15% = severe, and 20% (+) can increase operative mortality by 10x. Diminished intake is
associated w/ depression, psychological dz (bulimia, anorexia), dysphagia (e.g. esophageal CA), stroke,
COPD, etc. Increased loss can occur in malabsorption synds, IBD, gastrointestinal fistulas, chronically
draining wounds. Increased metabolic workload also results in malnutrition, such as COPD, CA, trauma,
burns, fever, and sepsis. Catabolic meds (glucocorticoids, immunosuppressants, and isoniazid) alter
nutritional requirements. Radiation and chemotherapies may alter appetite. H&P are the most sensitive
and specific methods to assess nutrition.
Anthropometric Measurements: measurement of body composition, usually involving Ht and Wt, which are
compared to ideal values adjusted for age, sex, and body frame. Obesity: mild = 15-30% body wt > ideal
wt, moderate = 30-50% > ideal wt, severe = 50-100% > ideal wt, and morbid = 100% (+). BMI = kg/m².
BMI ranges: nl = 20-25, overweight = 25-30, and obese = 30 (+). SubQ fat is measured using the triceps
skin fold. Somatic protein status is measured by determining skeletal muscle mass (= midarm
circumference – 0.314 (triceps skin fold)). Function is more important than size, test muscle force by
handgrip or forearm dynamometry (patients below 85% have ↑ postoperative complications). These
measurements are more useful in population studies than in individual pts.
Biochemical Measurements: Albumin (long term protein assessment), transferrin (iron status assessment),
retinol-binding protein (lipid and fat soluble vitamin assessment), and pre-albumin (short term protein
assessment) are used to assess nutritional status and response to feeding. Values of distribution can alter
values. Pre-albumin is the most reliable assessment of response to feeding (short ½ life). Creatinine-Ht
index estimates protein status, nl males = 23-28 mg/kg/day, nl females = 18-21 mg/kg/day. 60-80% =
moderate depletion, 40-50% = severe depletion of lean body mass.
Nitrogen balance = N in – N out, measure of urinary urea N (UUN) in 24hr urine, 6hr collection is adequate
in continuously fed pts. 3 or 4 g is usually added to the measurement to account for unmeasured N loss.
Sick pts lose more N than healthy pts, so total N is a better measurement. N loss is proportional to
catabolic states. Average N losses: starvation-adapted = 5, postop = 8-12, polytrauma = 15-20,
sepsis/burns = 20+.
Immunological measurements: malnutrition correlates w/ ↑ risks of TB, contagious dz, pneumonia, etc.
Absolute lymphocyte # reflects visceral protein status in the absence of nutritional variables (trauma, meds,
etc). Low counts w/ hypoalbuminemia are at risk of sepsis. Delayed hypersensitivity skin test (PPD, etc)
response correlates w/ nutrition in healthy pts.
Body composition Analysis: uses Bioelectrical impedance analysis (BIA) to measure body composition.
Uses a tetrapolar electrode array on hand and foot, the resistance is combined w/ Ht, wt, sex, and age to
determine fat-free mass.
Basic Nutritional Needs
Proteins & Amino Acids: “proteins do not exist in storage form; they all have structural, enzymatic,
immune, and transport functions”. Insufficient intake results in mobilization through skeletal muscle
proteolysis, the lungs, heart, kidneys, WBCs also contribute to protein mobilization. Self-consumption of
50% lean muscle mass may result in death. Protein requirement is related to health (burns require more
protein; hepatic failure requires less). 24 hr urine N is the most accurate measurement of protein need.
Adding glucose and non-protein energy substrates to protein spares it from oxidation, allowing non-protein
calories to supply energy to the body, while ingested protein is used for synthetic purposes. Pts w/
hypoalbuminemia will receive no benefit from albumin infusions. Branched-chain amino acids (BCAAs;
leucine, isoleucine, and valine) act as oxidative substrate in muscle, enhance protein synthesis, and inhibit
protein breakdown. Glutamine is an ammonia donor to kidneys, aiding in acid-base balance, and is fuel for
Nutrition—Ch 4
13
rapidly proliferating tissues, it is a precursor to glutathione. Arginine is essential for T-cell growth, it
promotes N retention, wound healing, immune fn, and is shown to ↓ postop sepsis.
Energy Needs: Caloric requirements are 25-80 kcal/kg/day. Carbs = 3.4 kcal/g, Lipids = 9.3 kcal/g, and
Proteins = 4.0 kcal/g. Carbs are stored as glycogen (75g in liver, 300g in muscle), enough is stored to last 2
days. It is glycolysed into lactate and pyruvate in muscles, and made into glucose by the liver (cori cycle).
Pyruvate is made into alanine, a substrate for hepatic gluconeogenesis. Non-glycolitic tissues receive their
energy from fat. Resting metabolic expenditure (RME) is estimated using the Harris-Benedict equation
(HBE). Factors such as fever, ambulation, surgery, trauma, sepsis, and burns must be taken into account.
The HBE is inaccurate in approx. 40% of pts. Respiratory quotient (RQ; CO2 expired to O2 consumed)
can be used to measure an individual’s energy expenditure. RQ values can be used to determine which
fuels are being utilized. Carb utilization = 1.0, lipid utilization = 0.71, and increased fat storage = 1.0+.
Indirect Calorimetry can be used to compute measured resting energy expenditure (MREE), but is
expensive, technically rigorous, and must be extrapolated to 24 hrs. Nitrogen excretion can also be used to
determine total energy expenditure (TEE), this is estimated by multiplying ideal wt by 25 kcal/kg/day. In
obese pts, body wt cannot be used to determine energy needs. Instead, use an adjusted body wt (ideal body
wt + 50% of the difference between actual and ideal wts).
Vitamins: 4 fat soluble (ADEK) and 9 water soluble (B1, 2, 3, 5, 6, 12, biotin, folic acid, and C) vitamins.
Vit A: visual photochemical and preserves epithelial membranes. Vit D: enhances gut absorption and
resorption from bone of Ca and phosphorus. Vit E: antioxidant. Vit K: cofactor for coagulation factors II,
VII, IX, and X. Requires bile salts, so abnormal coagulation in bile duct obstruction, also altered with
antibiotics due to colonic microflora changes. Usually given w/ TPN to prevent coagulopathy. Folic acid
is the most common deficiency, usually seen w/ alcoholism.
Trace Elements: Zinc: in metalloenzymes (carbonic anhydrase, alcohol dehydrogenase, alkaline
phosphatase), required for nl wound healing, immune fn, taste, smell, and night vision. Deficiencies are
common in pts w/ loss of GI secretions, can cause diarrhea, CNS disturbances, dermatitis (nasolabial,
perineum, elbows, and digits), alopecia, and poor growth in children. Copper: found in lysoxidase,
ceruloplasmin, and tyrosinase. Deficiency causes anemia, leucopenia, and bone demineralization. Copper
is not replaced in the presence of biliary obstruction (excreted in bile). Chromium: a cofactor for insulin.
Deficiency causes wt loss, glucose intolerance, and peripheral neuropathy. Selenium: component of
glutathione peroxidase in RBCs. Deficiencies cause skeletal myopathy and cardiomyopathy, excess can
cause CNS dysfn. Overall, deficiencies are rare and respond rapidly to supplementation.
Metabolic Patterns that Affect Nutrition
Postprandial: glucose to brain, RBCs, bone marrow, renal medulla, and nerves. Lipids to all other tissues.
Postabsorptive: after an overnight fast. Glycogenolysis supplemented by gluconeogenesis from muscle.
Free fatty acids released to fuel liver and muscle.
Early Starvation: glycogen depleted in 1 to 2 days, insulin drops. Catabolic changes occur (muscle
breakdown). Lipolysis increases, oxidation of fatty acids produce ketone bodies.
Starvation-Adapted: body minimizes protein breakdown, energy expenditure decreases. Ketones replace
glucose as primary fuel. Brain uses ketones. N is retained.
Catabolic: stimulated by injury, inflammation, infection, cytokines (IL-1, TNF), lipid mediators
(prostaglandins, leukotrienes), bacteria (endotoxins), and pain. Energy expenditure increases significantly
in fractures, burns, and sepsis. Increased catecholamines are permissive; glucagon, proteolysis,
gluconeogenesis, and ureagenesis increase. N loss in urine increases. Muscles oxidize BCAAs,
ketogenesis is blocked in the liver. FFA increase, but disposal is impaired, so septic hyperlipidemia can
result.
Techniques of Nutritional Support
Both enteral and parenteral nutrition will meet a pt’s needs. Parenteral is well defined and easy to
maintain, but expensive. Enteral is cheap, but harder to maintain. During parenteral nutrition, unused gut
shows reduction in villus ht, enzyme content, absorptive ability, IgE production, permeability, and altered
bacterial populations. Bacteria may migrate into the portal system, resulting in multi-organ failure.
Nutrition—Ch 4
14
Therefore, if the gut is working, use it. Timing: POD #4 is when the decision to begin nutritional support is
usually made. Burn pts should begin feeding w/in 24 hrs. Pts w/ trauma require fluid resuscitation first,
improper fluid resuscitation can lead to bowel ischemia following feeding. Rate of Increase: Target
nutrition is usually reached in 48 hrs, increasing nutrition to quickly can result in bowel necrosis and
hyperglycemia.
Enteral Nutrition:
Polymeric: blenderized food, contains intact macronutrients. High is residue, viscosity, and osmolarity,
must be delivered thru large bore tubes.
Chemically defined (elemental): have relative chemical simplicity. This is used in pts w/ impaired
digestive ability, it requires little digestion, only absorption.
Modular: contains only single or very few macronutrients, do not provide complete nutrition. Used in pts
w/ special nutritional needs, such as hyperglycemic diabetics.
Access for Enteral Nutrition: Indication include NPO > 5days, CA (oral, gastric, etc), eating disorders,
cachexia, COPD, dietary indiscretion (alcoholics), depressed consciousness, dysphagia, mechanical
ventilation, mechanical disability (quadriplegia), major burns, multiple trauma, brain injury, and sepsis.
Gastric (prepyloric) placement: NG tube, G tube (gastrostomy), and gastrocutaneous fistula (Janeway
gastrostomy), greater latitude in diet selection and maintenance, but increased risk of reflux, vomiting, and
aspiration; gastric emptying must also be assessed. Postpyloric Placement: (duodenal vs. jejunal).
Duodenal: easily displaced back into stomach. Includes nasoduodenal and gastroduodenal tubes. Jejunal:
distal to the ligament of Trietz. Includes nasojejunal tube, jejunostomy tube (J tube), needle catheter
jejunostomy, and percutaneous endoscopic gastrojejunostomy (PEG/J). Placement of all tube by
radiography must be determined before administration of nutrients.
Implementation and Administration: bolus feeding is better because no pump is needed. Pts should be
positioned w/ their head elevated 30º. Feeding too rapidly into the jejunum can cause distention, weakness,
sweating, hyperperistalsis, cramps, and diarrhea (jejunum is less flexible). All must be administered w/
some amount of free water.
Complications: include aspiration, reflux, parotitis, bacterial contamination, otitis media, erosions, tube
obstruction, diarrhea, malabsorption, cramping, N/V, distention, prerenal azotemia, electrolyte
abnormalities, hyperglycemia, FFA deficiency, and nonketonic coma. Co-administration of sorbitol
containing meds may exacerbate diarrhea. Antidiarrheal meds may be added to the feeding (but not if C.
diff is present), promotility meds (erythromycin, metaclopramide) may also be added.
Parenteral Nutritional Support: used when the gut is unavailable, such as paralytic ileus, short bowel synd,
necrotizing entercolitis, malabsorption, esophageal stricture or malignancy. Also used in pancreatitis,
prematurity, intractable diarrhea, wound dehiscence/evisceration, catabolic states (burns, sepsis,
polytrauma), radiation induced enterocolitis, IBD, hepatitis/hepatic failure, BM transplant, and
perioperatively.
Three types: Protein sparing (3% amino acids, 5% dextrose, in peripheral vein), Peripheral parenteral (3%
amino acids, 10% dextrose, w/ lipid emulsion, hyperosmolar, given in peripheral vein), and TPN (all
energy and N needs, hypertonic, delivered into central vein).
Complications include glucose dysregulation (hyperglycemia, osmotic diuresis, dehydration, ketoacidosis,
rebound hypoglycemia, coma), respiratory failure (glucose converted into CO2), hyperchloremic acidosis,
amino acid imbalances, hyperammonemia, prerenal azotemia, hyperlipidemia, FFA deficiency,
hypophosphatemia, neuromuscular problems (weakness, tremor, hyporeflexia), hematologic problems
(hemolytic anemia, decreased leukocyte fn, decreased clot and platelet survival), impaired myocardial
contractility, cardiomyopathy, hypo/hypercalcemia, hypokalemia, hypomagnesemia. Hypokalemia and
hypophosphatemia occur following intracellular shift.
Nutrition—Ch 4
15
Access for Parenteral Nutrition: most commonly accessed thru percutaneous cannulation of the subclavian
or internal jugular vein (catheter tip must be in SVC, and be placed using sterile technique). Dry dressing
should be changed 3 times/wk, or immediately if they become wet, transparent occlusive dressing may be
changed weekly. Blood should not be drawn thru the parenteral catheter, and meds should not be
administered into it (unless a multi-lumen catheter is in place).
Parenteral nutrition w/ Lipid Emulsions: use emulsions of safflower, soybean, or canola oil, which contain
long-chain FAs, are isotonic, and approximately the size of a chylomicron. Lipid emulsions are
advantageous in pts w/ glucose intolerance, those that require volume restriction, and those on ventilation
(fat metabolism has a lower RQ, so less CO2 retention). Essential FAs include linoleic acid (C:18:2) and
linolenic acid (C:18:3). Signs of FA deficiency include anemia, thrombocytopenia, alopecia, and
eczematous dermatitis of body folds.
Complications: occur in 3-10% of pts, categorized as technical mishaps, central venous thrombosis, and
sepsis. The internal jugular approach has fewer technical mishaps, but higher risk of sepsis. Other
complications include pneumo/hemothorax, emphysema, arterial injury, hematoma, cardiac perforation,
thoracic duct injury, brachial plexus injury, horner’s synd, phrenic n injury, emboli, hydrothorax, cardiac
tamponade, endocarditis, AV fistula.
Home Parenteral Nutrition: may be provided in unstressed pts whose GI tract cannot meet their nutritional
needs. Pts require a PICC, cuffed catheter, or a completely implanted subQ port. Require a team to deliver
nutrition (doctor, pharmacist, RN, dietician, home health company, capable caregivers).
Selected Surgical Situations:
Cancer: malnutrition is common in CA. Tumors themselves can cause metabolic abnormalities (such as
inefficient metabolism, accelerated breakdown of fats, proteins, carbs, etc). Radiation and chemotherapy
cause additional nutritional compromise.
Cardiac Dz: malnourished pts receiving valve replacements are at much higher risk than healthy pts
receiving valve replacements. Perioperative control of hyperglycemia (<180 mg/dL) reduces the risk of
sternal wound inf’n.
IBD: steroid therapy greatly increases N excretion, deficiencies in Ca, Vit D, Vit B12, and zinc are
common. Nutritional support has been shown to decrease dz activity, improve remission rates, decrease the
need for drug therapy, and decrease hospitalizations in Crohn’s dz as effectively as steroid (no benefit seen
in Ulcerative Colitis).
Radiation Enteritis: symptoms dependent on dose, time, fractionation, and volume in field. Radiation alters
mucosal brush border, sometimes producing bloody diarrhea. Administration of an elemental diet has been
shown to prevent acute phase radiation injury.
Short Bowel Synd: a consequence of massive bowel removal or dysfunction. These pts are malnourished,
dehydrated, and have diarrhea. Therapy focuses on fluid and electrolyte replacement.
Miscellaneous:
Omega-3 FAs compete w/ arachodonic acid for cyclooxygenase metabolism, reducing the inflammatory
response. Nandrolone decanoate (anabolic steroid) reduces N loss and increases plasma amino acid levels.
Stanzolol improves N balance in postcolectomy pts. Oxandrolone (anabolic steroid) is effective in HIVassociated wasting and cirrhosis. Oxymetholone (anabolic steroid) improves N retention in HIV and
erythropoiesis in anemia. GH enhances N retention in pts w/ burns, COPD, CA, and other critical illnesses,
it also conserves muscle protein mass and enhances lipolysis.
Functional Foods/ biotherapeutics/ nutraceuticals: interchangeable terms used to describe foodstuffs used to
manipulate specific fns, and not for metabolism. Prebiotic: a nondigestible carb that stimulates growth of
bacteria in the colon. This stimulates colonocytes and beneficially alters glucose absorption.
Nutrition—Ch 4
16
Fructooligosaccharides are being used as mucosal reconditioners. Probiotics: live microbial food
supplements beneficial to health. These include lactobacilli, bifidobacteria, G(+) cocci, and yeasts. Uses
include prevention of antibiotic associated diarrhea and C.diff, prevention of vaginal inf’ns, enhancing
lymphoid tissue immunity, altering cholesterol levels, and improving Ca absorption. Antibiotic resistance
is increasing due to increased use of antibiotics in animal and plant agriculture.
Surgical Bleeding—Ch 5
17
Chapter 5 Surgical Bleeding
Hemostatic process
-Immediately after injury
- hemostasis w/ vasoconstriction – controls bld loss for brief time
-platelets adhere to areas of vasc. Injury
-platelets extrude contents (adenosine diphosphate)
-platelet aggregation occurs (this platelet to platelet sticks causes initial thrombus)
-“white” clot formation is independent of coag pathway (not strong enough)
-Coag pathways use coag factor to form fibrin
-Two pathways: Extrinsic & Intrinsic both feed into Common pathway
-End product of coagulation is Fibrin, Factor 13 required to create optimal strength.
-Deficiency in any factor except Factor 12, can lead to blding
Evaluation of Pt
-Detect & Correct blding ds before surgery
-Careful screening essential part of preop eval
History (All pts)
-Blding Hx – most important step in eval.
-Ask about prolonged blding following minor cuts, dental extractions, previos operations. Bruising easily,
nosebleeds ?
PE (All pts)
-Most pt w/ mild-mod. Bld ds have no physical signs
-Signs: hepatoslenomegally, hemarthroses, petechiae (platelet ds), or ecchymoses (coag ds).
Tests (Pt w/ evidence of bld ds or nature of surg.-excessive bld)
Platelet Count – automated methods, less accurate at counts < 40,000
-also less accurate in pseudothrombocytopenia (RBC frags)
-at low #s need manual counts
PT – evals extrinsic factors: VII, also common factors: X,V,II, fibrinogen
-used to monitor Warfarin levels
-reported as INR (standardized)- adequate anticoag 2.5-3.0 INR
aPTT – evals intrinsic factors: XII, XI, IX, VIII and common factors
-used to monitor heparin
Blding time – prolonged blding time can be seen in aging or long-term corticosteroid therapy
(assoc w/ senile ecchymoses)
-prolonged bld time associated w/ sigif. Blding at surgery
-newly found > bld time caused by: thrombocytopenia, abn platelets(meds, granular ds), v. Will’s
dz
Thrombin time – evals fibrinogen to fibrin conversion
-Causes: hypofibrinogenemia, dysfibrinogenemia, fibrin & fibrinogen split products, & heparin
-used to eval DIC and chronic liver dz
Causes of excessive blding
-Bld loss prior to surg (trauma)
-Some operations assoc. w/ lg bld loss: Cardiopul. Bypass, liver transplant, prostate surg, construction of
portocaval shunts
-these pt at risk to develop DIC
Preexisting Defects
-suspected by hx or abn blding w/in first 30 min operative
Congenital Disorders- uncommon, often asymptomatic
-Type A hemophilia - deficiency factor VIII, males, normal platelet function, treated w/
purified factor VIII
- v. Will’s dz – deficiency factor VIII, ,both sexes, abd platelet fcn, treated w/
cryprecipitate or desmopressin (DDAVP) therapy
Acquired Disorders – more common
-Liver dz –coag abn, decreased levels of prothrombin, factors V, VII, X,
Surgical Bleeding—Ch 5
18
Causes prolonged PT, PTT
-Hypersplenism – depress platelet count
-Anticoag therapy
-Coumadin – depresses factors II, VII, IX, X
Causes prolonged PT, PTT
-Heparin – increases activity of antithrombin III
Causes prolonged PTT & thrombin time
-Acquired thrombocytopenia
-decreased plat. production (aplastic anemia)
-increased plat. destruction (ITP, DIC)
-splenic pooling in enlarged spleen (cirrhosis)
-combination if above (alcoholic liver failure)
-Platelet fuction ds
-aspirin, NSAIDS – ASA irreversible defect
-Plavix- irreversible defect
-Both should be stopped 7-10 days prior to surg
-uremia – dialysis required to correct plat. dysfuction
Intraoperative Complications
-Shock, hypothermia cause consumptive coagulopathy
-Massive transfusion (>=10 units stored PRBCs) – dilute clotting factors, causing blding
-Acute bld transfusion rxn – cause DIC
-Blding from dissection, needle holes, etc should be controlled locally w/ hemostatic agents
Postoperative Blding
-50% postop blding caused by inadequate hemostasis during surgery
-Other causes:
-Circulating heparin s/p bypass surg
-Shock
-Altered liver fnc s/p partial hepatectomy
-Vit K dependent clotting factors deficiency s/p poor nutrition
-Factor XIII def.
-DIC & Fibrinolysis
Common Blding Disorders
DIC (Disseminated Intravascular Coagulation)
-characterized by diffuse intravascular coag and thrombosis
-systemic deposition of platelet-fibrin microthrombi  diffuse tissue injury
-clotting factors become consumed  diffuse blding
Etiology
-release of tissue debris into bld stream following trauma, obstetric problem
-aggregation of platelets by activation w/ adenosine diohospate & thrombin (septicemia &
immune complex dz)
-extensive endothelial damage (burns & vasculitis)
-hypotension leading to stasis  coag inhibitors can not reach miscrothrombi
-blockage of reticuloendothelial system
-some prostate, lung, malignant tumor ops
-severe liver ds
Diagnostic studies
-prolonged PT, aPTT
-hypofibrinogenemia
-thrombocytopenia
-presence of fibrin & fibrinogen split products (D-dimer)
Treatment
-Most important – remove the precioitating factor (eg: treat septicemia)
-replacement of coagulation factors (Cryo, FFP, platelets)
Surgical Bleeding—Ch 5
19
-Use of heparin if controversial as antithrombin III is also consumed
Increased Fibrinolysis
Primary Fibrinolysis
-occurs most commonly following fibrinolytic therapy (TPA, urokinase, etc)
-Prostate gland (high in urokinase) procedures as well as liver failure, & α2-antiplasmin deficiency
are also causes
-treat by removing precipitating cause
-if severe, ε-amino caprioc acid is used cautiously (predisposed to thrombosis)
Sec. Fibrinolysis
-most often a response to DIC
-treat by correcting DIC
Hypercoagulable States
-Both congenital & acquired ds put surg pt @ risk for thromboembolism
Etiology
-Congenital Ds
-most common -> activacted protein C reistance (APCR)
-most common cause APCR  factor V Leiden- lacks protein C
binding
site, can not be turned off
-also deficiencies of antithrombin III, proteins C & S
-hyperhomocystinemia
-prothrombin 20210
 events occurring in the 40s or younger suggest inherited hypercoagulable
state
-Acquired Hypercoag States
-Decreased prod. Anticoagulants (liver failure)
-Reduced or defective plasminogen
-Very high levels clotting factors (stress, trauma)
-Platelet counts > 1,000,000
-antiphospholipid syndromes (Lupus)
-Chronic DIC
-hyperhomocystinemia (Renal failure)
Diagnostic Lab Studies
-activated protein C resistance
-antithrombin III activity
-proteins C & S activity
-assay for antiphospholipid antibody
-prothrombin activity
-serum homocystine level
Management
-interfer w/ coag pathway (Heparin, coumadin, both)
-interfer w/ platelet fnc (ASA, other platelet inhibiting drugs)
-treat hyperhomocystinemia (folic acid, B12)
 therapy should be individualized to pt & site, duration should be carefully considered
 perioperatively: SubQ Heparin used for pt w/ hx thromboemboli
Bld Replacement Therapy
Collection & Storage of BLD
-Whole bld separated into 4 major components: plasma, platelets, WBCs, RBCs.
-Preferred therapy administering only deficient component.
-Packed RBC’s may be stored @ 4 degrees for 5 weeks, however there is gradual reduction in
RBC viability to approx 70% by week 5.
-Platelet rich plasma is obtained thru centrifuge of whole bld. Stored 3-5 days @ 22 degrees.
-Platelet poor plasma may be frozen (FFP) or fractioned into Cryo. FFP stored up to 12 months @
-30 degrees.
Surgical Bleeding—Ch 5
20
Bld Component therapy
-Major indication for use of fresh whole bld is massive bld loss. Otherwise specific bld components should
be used.
-Major bld groups  A,B, O.
-Major bld types  Rh+, Rh-Universal donor red cells  O-negative (not universal plasma donor)
-type & crossmatch pts preoperatively if transfusion anticipated
-type & screen for low blding risk
-Minor transfusion rxn are common.
-Most common adverse transfusion rxn (minor) febrile rxn, controlled w/ antipyretics & antihistamines.
-Major transfusion rxns  stop transfusion immediately, bld return for repeat crossmatch
-Safest bld transfusion practice  pt banking own bld prior to procedure
-Hemolytics rxns require: bld pressure support, maintenance of renal perfusion, & management of
DIC
Transfusion of RBCs (Decreased red cell mass)
-Important considerations: pt age, presence of hemodynamic instability, underlying med
conditions, and etiology, degree & time course of anemia
-Acute hemorrhage(loss 30% bld vol) vol support poss. RBC transfusion
-Chronic anemia only transfused when systemic effects present.
Estimating RBC transfusion needs
-Total bld vol = weight (kg) X 0.07
-1 unit RBCs raises Hct 4%
-Normal Hct = 40%
Plasma component therapy
-Plasma does not require crossmatch but should be A,B,O compatible
-FFP can be used to correct all clotting factor deficiencies
Est. Factor 8 transfusion requirements
-plasma vol = 4% of total body weight (kg)
-need to raise clotting factors to 50% (controls most blding)
- # units needed to transfuse = (0.50 - % clotting factor) X plasma vol
Management of hemophilia
-Type A  cryoprecipitate or monoclonal factor VIII is transfused
-Minor trauma, minor surgery  15-20% activity factor VIII
-Major trauma, major surgery  50-60% activity
Mgt. of von Willebrand’s dz
-Factor VIII hard to predict, must be individualized
-DDVAP therapy given 1 hr preop as 30 min infusion, repeat dose given 12 hrs later if needed,
interval doses of 2-3 days permits good correct of aPTT and blding time.
Other indications
-Factor IX to treat factor IX deficient hemophilia, risk of hepatitis & HIV
-Albumin is primarily an oncotic agent
Transfusion safety
-To ensure safety avoid the following:
Immunologic rxns
-Include: hemolytic & febrile transfusion rxns, post-transfusion thrombocytopenia, anaphylactic
shock, urticaria, and graft-v-host dz.
-Hemolytic transfusion rxn:
-Symptoms: fever, chest tightening, lumbar back pain.
-Signs: fever, hypotension, hemoglobinuria, blding due to DIC, renal failure.
-Treatment: volume expanders and vasoactive drugs (hypotension), diuretics (renal fnc),
bicarb (alkalinize urine), and coag factor, platelet replacement. Dialysis indicated for
acute renal failure.
Infection
-Uncommon
-Viral bugs: Hep A,B,C, HIV, CMV, and HTLV-1,2. Bld screened for HIV and Hep. (1/100,000
Hep C; 1/500,000 HIV)
Surgical Bleeding—Ch 5
21
-Bact. Transmission rare
-Parasitic bugs: malaria, T. cruzi.
Volume overload
-Usually from plasma (cont. proteins, draw fluid into intravascular space)
-Signs: dyspnea, orthopnea, hypoxia)
-Treatment: diuretics
Risks mass transfusion
-“transfusion of bld products greater in volume than pt’s normal bld volume in less than 24 hrs”
-Complications:
-coagulopathy (platelet, coag factor depletion)
-hypothermia (chilled bld products)
-citrate toxicity (pt w/ hepatic dysfnc)
-electrolyte abns (acidosis, hyperkalemia)
Bld Substitutes
-Ex: O2 carries (perfluorocarbons, hemoglobin-based carriers), plasma derivatives (immune globulins,
protease inhibitors and coag products)
-At present no single bld substitute can duplicate the real thing
Conclusion
-Surgeons should perform screening preop and be prepared to handle hemostatic emergenies.
-If a possible blding ds is likely, the pt should be evaluated by a hematologist preoperatievely to optimize pt
safety.
Surgical Bleeding—Ch 5
22
Chapter 6 – SHOCK
I.
Introduction
a. Traditional definition uses systolic hypotension as the defining variable and implies that evidence of
“altered circulation” is sufficient for diagnosis. This description isn’t great because some etiologies of
hypotension don’t cause significant end-organ damage (i.e. neurogenic vasodilation after SCI) and shocklike injury can occur without significant hypotension.
b. A better definition is that shock is a condition in which total body cellular metabolism malfunctions.
When treated aggressively, this metabolic dysfunction is reversible. When allowed to continue, shock
results in cellular death, organ damage, and eventual death.
c. Hypoperfusion begets inflammation, and inflammation begets hypoperfusion
i. Two mechanisms of cellular injury and death:
1. Inadequate oxygen delivery (hypoperfusion)
2. Toxic cellular insult by endogenous molecules (inflammatory response) that can progress even
when sufficient oxygen is delivered
ii. The two mechanisms are additive
iii. When a patient is in shock, must assess both the circulation for oxygen delivery and the state of
inflammation for cell toxicity.
d. Primary goals of managing shock: Restore excellent circulation and Treat severe inflammation
II.
Normal Physiology of the Circulation and of Inflammation
Hemodynamic and Oxygen Delivery Variables
CVP (Central venous P)
CVP = Right atrial pressure
CVP = Right ventricular end-diastolic pressure
LAP (Left atrial P)
LAP = Left ventricular end-diastolic pressure
PCWP
PCWP = LAP
MAP (Mean arterial P)
MAP = DP + 1/3 (SP-DP)
CI (Cardiac Index)
CI = CO/m2 body surface area
SI (Stroke Index)
SI = SV/ m2 body surface area
SVR (Systemic vascular resistance)
SVR = (MAP-CVP) x 80/CO
PVR (Pulmonary vascular
PVR = (MAP-PAOP) x 80/CO
resistance)
CaO2 (arterial O2 content)
CvO2 (mixed venous O2 content)
C(a-v)O2 (arterial-venous O2
C(a-v)O2 = CaO2 – CvO2
content difference)
*O2D (O2 delivery)
O2D = CO x CaO2 x 10
O2C (O2 consumption)
O2C = C(a-v)O2 x CO x 10
5-15 mmHg
5-15 mmHg
5-15 mmHg
80-90 mmHg
2.5 -3.5 L/min/ m2
35-40 mL/beat/ m2
1000-1500 dyne-sec/cm5
100-400 dyne-sec/cm5
20 vol %
15 vol %
3.5-4.5 vol %
900-1200 mL/min
250 mL/min
* Main function of circulation is to deliver O2 to capillaries. As the formula for O2 delivery shows, the pulmonary
component of this effort is limited to providing good arterial O2 saturation—a goal readily achieved with modern
respiratory therapy. Hemoglobin can be increased with transfusion. Usually, the most difficult component to treat
is cardiac output. CO is determined by ventricular function and venous return. Thus, sometimes it is more useful to
alter ventricular function and sometimes to alter venous return.
a. Ventricular Physiology
i. Preload: magnitude of myocardial stretch (aka the stimulus to muscle contraction as described by
Frank-Starling mechanism, where increased stretch  increased contraction) Preload should be
measured by EDV, but volume is not easily measured, so end-diastolic pressure is used to estimate
volume.
1. CVP for right heart
2. PCWP for left heart
ii. Afterload: resistance to ventricular ejection. With constant preload, increased afterload diminished
ventricular ejection, and decreased afterload augments ejection.
iii. Contractility: force of contraction under conditions of a predetermined preload or afterload
Surgical Bleeding—Ch 5
23
1. Factors that increase contractility: Catecholamines, Inotropic drugs, Increased preload,
Decreased afterload
2. Factors that decrease contractility: Depleted catecholamines or receptor malfunction, Alpha
and beta blockers, Calcium channel blockers, Decreased preload, Overstretched myocardium,
Severe inflammation and ischemia
iv. Heart Rate: directly proportional to cardiac output until rapid rates diminish ventricular filling during
diastole.
b. Venous Return
i. VR = (MSP – CVP) / (RV + RA/19) where MSP = mean systemic pressure, CVP = central venous
pressure, RV = venous resistance, RA = arterial resistance.
ii. Alterations in arterial resistance have much LESS effect on venous return than alterations in venous
resistance.
iii. MSP is the pressure in small veins and venules. This pressure must be higher than CVP so blood can
flow from periphery to the thorax.
iv. Venous resistance occurs primarily in the large veins of abdomen and thorax in contrast to arterial
resistance that occurs mostly in arterioles.
v. Surgical patients frequently have diseases or therapeutic interventions that may inhibit venous return.
Increased Venous Return
Increased MSP
Increased vascular tone
Increased vascular volume
External compression
Trendelenburg position
Decreased CVP
Negative pressure respiration
Decreased venous resistance
Decreased venous constriction
Diminished Venous Return
Decreased MSP
Hypovolemia
Vasodilation
Increased CVP
Intracardiac: CHF, Cardiogenic shock, Tricuspid
regurgitation, Right heart failure
Positive pressure respiration
Cardiac tamponade
Increased abdominal pressure: ascites, bowel distension,
intraabdominal hemorrhage, tension pneumoperitoneum,
retroperitoneal hemorrhage
Increased venous resistance
Increased thoracic pressure: Positive pressure
respiration, tension pneumothorax
c. Physiology of Inflammation
i. Initial response to tissue damage by trauma is bleeding and coagulation. (This response is less likely,
but not impossible, with damage from ischemia or infection.)
1. Platelet activation releases PDGF, TGF-β
2. Initial vasoconstriction (short-lived)
3. Vasodilation and increased capillary permeability  Exudate (protein-rich edema fluid)
4. PMNs migrate to inflammatory site (w/in minutes if good circulation) with help of
chemoattractants, adhesion molecules, and chemokine gradient.
5. PMNs phagocytize dead tissue and foreign objects. They release IL-1 to mediate temperature
elevation via thermoregularoy centers and to stimulate other inflammatory activity. Last for
hours.
6. Hours later, macrophages migrate to area and stay for days to weeks. Release IL-1, TNF,
PDGF, TGF-β, TGF-α and fibroblast growth factor.
7. Fibroblast migration and angiogenesis begin next. Combined activity produces granulation
tissue.
8. 5 days out, fibroblasts produce collagen
ii. The molecules that are necessary for effective local inflammatory activity can cause distant or systemic
tissue injury by the endocrine effect of these proinflammatory substances. This is particularly
important in regards to PMN and endothelial cell activation.
iii. Effective inflammation controls infection, heals wounds, and THEN STOPS. Anti-inflammatory
molecules include IL-6, IL-10, IL-13 and Cortisol.
Surgical Bleeding—Ch 5
24
III.
Hypoperfusion States
Hypoperfusion is a decrease in total body or regional blood flow sufficient to result in cellular malfunction
or death. The immediate effects of hypoperfusion on cell viability are secondary to the interruption of
oxidative metabolism.
a. The Neurohumoral Response to Hypoperfusion
i. Total body hypoperfusion usually manifests as reduction in cardiac output. Reduction in CO from loss
of volume or loss of cardiac function may result in the responses shown in table below.
Increased
Epinephrine
Norepinephrine
Dopamine
Glucagon
Renin
Angiontension
Arginine vasopressin
ACTH
Cortisol
Aldosterone
Growth hormone
Decreased
Insulin
Thyroxine
Triiodothyronine
LH
Testosterone
Estrogen
FSH
ii. Clinically, the effects of the neurohumoral response to hypoperfusion are:
1. Tachycardia
2. Vasoconstriction
3. Diaphoresis
4. Oliguria with Na and water conservation
5. Hyperglycemia
iii. Goal is to preserve blood flow to vital organs (heart, lungs, brain) while diminishing flow to less
vital organs (kidneys, GI tract). This maintains or increases intravascular volume by limiting urine
output.
iv. This response is most homeostatic in hypovolemic hypoperfusion. In cardiogenic hypoperfusion,
tachycardia, vasoconstriction and water retention may aggravate hypoperfusion by decreasing
ventricular filling time, increasing afterload and increasing myocardial stretch.
b. The Effects of Hypoperfusion on Inflammation
i. The most clearly documented association of hypoperfusion with inflammation is the effect of ischemia
followed by reperfusion (reperfusion injury). Clinically, this effect is most obvious in pts with
isolated limb ischemia (compartment syndrome) and in some pts with localized intestinal ischemia.
Recent evidence indicates it may be the hypoperfusion itself that stimulates inflammatory mediators,
even before reperfusion.
ii. Mechanism of reperfusion injury requires local and systemic factors. Complex interaction of oxygen
free radicals, thromboxane, leukotrienes, phospholipase A2, and leukocytes affect capillary
permeability and organ function. PMNs produce free radicals and are thus central to this process.
iii. Damage may occur to intestine, limb, kidney, liver and lung even if a specific organ (i.e. lung) was not
initially hypoperfused. These organs are susceptible anyway.
iv. Clinically, it is difficult to separate tissue injury secondary only to hypoperfusion from damage from
other mechanisms (i.e. direct trauma). Whatever the cause, hypoperfusion and inflammation
commonly occur together.
c. The Effects of Hypoperfusion on Cellular Metabolism
i. Classic effect of hypoperfusion on cellular metabolism is anaerobic metabolism caused by an oxygen
deficit: decreased mitochondrial function  decreased ATP  inability to meet cellular needs  cell
death.
Surgical Bleeding—Ch 5
25
ii. Elevated levels of lactic acid characterize anaerobic glycolysis as primary means of ATP production in
anaerobic states.
iii. Decreased ATP can also impair cell membrane function and allow increased Na and Ca entry followed
by increased water entry. Intracellular water sequestration leads to a deficit in extracellular fluid
which may accentuate the fluid requirements during resuscitation.
IV.
Etiologies, Diagnosis, and Management of Hypoperfusion States
Decreased Venous Return
Hypovolemia
Pericardial Tamponade
Tension Pneumothorax
Increased abdominal pressure
Bowel obstruction
Tension pneumoperitoneum
Massive bleeding
Diagnostic laparoscopy
Pneumatic antishock garment
Ascites
Decreased Myocardial Function
Congestive heart failure
Cardiogenic shock
a. Decreased Venous Return: Hypovolemia
i. Hypovolemia is the most common etiology of decreased venous return secondary to decreased MSP. It
is the most common cause of hypotension.
ii. Common causes of hypovolemia:
1. Hemorrhage (most frequently studied etiology)
2. Severe inflammation or infection
3. Trauma
4. Pancreatitis or other causes of peritonitis
5. Burns
6. Vomiting or other intestinal losses
7. Excess diuresis
8. Inadequate oral intake
iii. Hemorrhagic shock obviously decreases venous return, but can also cause cardiovascular alterations –
increased systemic vascular resistance, decreased ventricular contractility, decreased ventricular
compliance, and increased atrial contractility.
iv. Cellular effects other than lactic acidosis include diminished transmembrane potential difference,
increased intracellular sodium, and decreased intracellular ATP.
v. Movement of interstitial fluid into cells and increased capillary permeability are the mechanisms that
account for plasma volume loss above that which is due to the direct insult (i.e. hemorrhage) itself.
This “extra” loss exacerbates the obvious loss.
vi. Physical exam – vital sign changes and other findings occur in proportion to degree of hypovolemia.
1. 10% loss produces little, if any, disturbance (i.e. blood donation)
2. 20% loss  tachycardia, orthostatic hypotension
3. 30% loss  hypotension while pt is supine
4. Remember, hypotension is unreliable sign; pt may be normotensive even with great loss.
5. Agitation, tachypnea, and peripheral vasoconstriction are common with any etiology of
hypoperfusion. Hypotension is most common secondary to hypovolemia, and much less likely
due to cardiogenic shock.
6. Venous distension in the neck is not common unless hypovolemia is accompanied by
extracardia increase in CVP (i.e. tension pneumothorax, tamponade, etc)
7. S3 gallop not usually present
vii. Lab studies
1. If severe, metabolic acidosis recognized via serum electrolytes or ABG.
2. Elevated BUN and creatinine are indicative of renal malfunction.
3. CVP and PCWP are low
Surgical Bleeding—Ch 5
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4. Other tests – hemoglobin, serum chemistries, x-rays – are helpful to determine etiology rather
than severity of hypoperfusion.
viii. Treatment
1. Diagnosis and intervention of underlying cause (i.e. stop the bleeding)
2. Simultaneously, restore circulation (i.e. rapid fluid resuscitation)
3. In general, crystalloid or colloid are used for volume replacement.
Crystalloid
Isotonic
Ringer’s Lactate
0.9% Saline
Hypertonic saline
Colloid
Red blood cells
Fresh frozen plasma
Albumin
Processed human protein
Low-molecular-weight dextran
Hydroxyethyl starch
4. Administering RBCs causes increased CO, increased oxygen-carrying capacity, and little
leakage of red cells into the interstitium. The primary disadvantage is the increasing evidence
that these exogenous cells increase the risk of nosocomial infection.
5. Chapter contains a debate about crystalloid vs. colloid, the advantages and disadvantages of
FFP administration, use of dopamine, and other topics like this. If you think it is important for
the test, read it yourself – pg. 109-110. It is too involved for this outline. One interesting
sentence reads, “Curiously, recent evidence has suggested that lactated Ringer’s solution may
actually augment the inflammatory response, especially when ischemia/reperfusion is the
mechanism.”
b. Decreased Venous Return: Pericardial Tamponade
i. Primary mechanism for decreased venous return during pericardial tamponade is an extracavitary
increase in CVP.
ii. Most common etiologies are chest trauma and bleeding after cardiac surgery.
iii. PE: evidence of hypoperfusion, distended neck veins, muffled heart sounds, increased paradoxical
pulse (>15 mmHg).
iv. Labs: low voltage on ECG, elevated CVP, enlarging heart on CXR. With severe hypovolemia, the
CVP may be normal until after fluid resuscitation.
v. Importance of determining this etiology of hypoperfusion vs. CHF is emphasized because reducing
fluid intake or administering diuretics would further reduce venous return in tamponade. One way to
differentiate is blood pressure. CHF usually results in normal or increased BP while tamponade results
in hypotension.
vi. Pericardiocentesis/Repair of the cardiac wound is the most effective therapy and can result in dramatic
improvement in CO. It should be accompanied by vigorous fluid administration.
c. Decreased Venous Return: Tension Pneumothorax
i. Reduces venous return by producing an extracavitary increase in CVP and by increasing venous
resistance in the chest.
ii. Etiologies: spontaneous rupture of a bleb, penetrating or blunt trauma
iii. PE: evidence of hypoperfusion, decreased breath sounds and tympany over affected thorax, tracheal
deviation away from affected thorax, and distended neck veins.
iv. Treatment is emergent release of the tension (i.e. needle to chest, covering a penetrating wound)
followed by closed thoracostomy. Administration of IV fluids is also beneficial.
d. Decreased Venous Return: Increased Abdominal Pressure
i. Increased abdominal pressure (>25 mmHg) diminishes venous return by increasing intrathoracic
pressure, producing an extracavitary increase in CVP, and increasing venous resistance in abdominal
veins.
ii. This may be particularly bad for renal blood flow.
Surgical Bleeding—Ch 5
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iii. Etiologies: ascites, bowel distension, massive edema in abdominal cavity, intraabdominal hemorrhage,
retroperitoneal hemorrhage, tension pneumoperitoneum.
iv. Most easily measured with a bladder catheter.
v. PE: evidence of hypoperfusion, tensely distended abdomen, possibly distended neck veins.
vi. Treatment is pressure release. Sometimes, aggressive fluid management is the only available option if
abdominal exploration is considered too risky.
vii. Actually, any increase in intraabdominal pressure above 0 is potential detrimental to venous return,
especially in patients who have a compromised circulation for whatever reason. Thus, some patients
with pressure less than 25 mmHg will benefit from interventions to reduce impairment to venous return.
e. Cardiogenic Hypoperfusion and Cardiogenic Shock
i. To cause cardiogenic hypoperfusion, cardiac function must be severely disrupted (Cardiac index < 2.2
L/min/m2 ). See table below for etiologies.
Etiologies if cardiogenic shock
Acute ischemia – ventricular wall infarct, papillary muscle
infarct, ventricular septal defect
Acute valvular disease – mitral, tricuspid, or aortic
regurgitation
Arrhythmias – rapid supraventricular, bradycardia,
ventricular tachycardia
Miscellaneous
End-stage cardiomyopathy – severe myocardial contusion,
severe myocarditis, left ventricular outflow obstruction, left
ventricular inflow obstruction
Treatment of cardiogenic shock
Reverse underlying disease – CABG, valve replacement,
Rx myopathy, repair VSD
Reduce preload – decrease water intake, diuretics, venous
dilation, nitroglycerin, Ca channel blockers, narcotics
Reduce afterload – nitroprusside, antihypertensives,
diuretics, narcotics
Increase contractility – IV inotropes
Increase arterial oxygen – supplemental O2, mechanical
ventilation
ii. Hypoperfusion of this magnitude, especially due to MI, is associated with a high mortality rate.
iii. Hypotension is more often a disease of hypovolemia than of severe impairment of cardiac function.
iv. Cardiogenic shock is the only major circulatory deficit that can be worsened by administration of
fluid. Therefore, when a clinician decides not to administer fluid to a hypotensive person, they are
actually making a diagnosis of cardiogenic shock.
v. These etiologies are not subtle. Cardiogenic shock is secondary to severe, usually obvious, cardiac
disease, and you should be able to document the occurrence of a marked insult to cardiac function.
Without this documentation, you should consider the hypotensive patient to be hypovolemic and not in
cardiogenic shock.
vi. PE: hypotension, tachycardia, tachypnea, peripheral vasoconstriction, distended neck veins, agitation,
confusion, possible S3 gallop, associated murmurs in valvular dysfunction.
vii. Labs: CXR evidence of pulmonary edema, metabolic acidosis, increased CVP and PCWP, increased
BUN and creatinine. ECG shows evidence of acute ischemia, infarct or arrhythmias. Echocardiogram
can give info about wall motion and valve function.
viii. Treatment is based on etiology. Arrhythmias are most readily treated. For other etiologies, a
combination of inotropic drug support and vasodilation is frequently used.
ix. An Intraaortic balloon pump (IABP) can increase CO while reducing preload and afterload. Can be
adequate support until cardiac function improves or surgical intervention occurs. Complications include
injury to femoral vessels, ischemic extremity, hemolysis or thrombocytopenia, and infection.
f.
Endpoints for Resuscitation of the Circulation
i. Depend on variables such as primary etiology of deficit, underlying state of patient’s circulation, and
the magnitude of cellular and organ malfunction. Normal circulation can usually be assessed at the
bedside by recognizing normal or increasing blood pressure, pulse rate of less than 80, normal or
improved mental status, urine output greater than 0.5 mL/kg/hr, warm extremities, and resolution of
metabolic acidosis.
ii. Obviously, some patients may require more complex hemodynamic monitoring such as pulmonary
artery catheterization, echocardiogram, and cardiac catheterization. In these cases, increasing cardiac
Surgical Bleeding—Ch 5
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index, along with normal oxygen delivery and consumption may allow cellular and organ function
recovery.
iii. One determination of oxygen delivery to tissues is the mixed venous oxygen saturation (Sv02)
measured by the pulmonary artery catheter. Healthy people deliver Hb close to 100% saturated with
oxygen and consume about 25%. Thus the normal Sv02 is 75%. When the Sv02 is in the 50s, it is
apparent that cells are demanding more oxygen than the circulation is delivering. Values in the 60s are
somewhat ambiguous. This measurement is subject to inaccuracies and any value should be taken in
context of the patient.
iv. Basically, clinical evaluation is usually sufficient to recognize the end points of resuscitation – normal
BP, slow pulse, good urine output, normal mental status, resolution of metabolic acidosis. For those
patients who do not improve despite aggressive efforts, more complicated evaluations may be helpful
(catheters, echo).
V.
Severe Inflammation States
a. Localized inflammation in response to an insult is usually beneficial. However, severe tissue injury from a
variety of causes can result in inflammation distant from the original disease: systemic inflammation. This
inflammation can cause cellular malfunction and death in remote organs.
i. Etiologies:
1. Infection (meets definition of sepsis)
2. Trauma
3. Burns
4. Ischemia or reperfusion: regional or total body
5. Pancreatitis
6. Drug reactions
7. Hemolytic transfusion reactions
ii. Definition of systemic inflammatory response syndrome (SIRS) – two or more of the following:
1. temperature > 38.5 C or < 36 C
2. heart rate > 90
3. respiratory rate > 20
4. total leukocyte count > 12,000, < 4,000 or > 10% immature forms
iii. Many patients with systemic inflammation but without evidence of shock may meet the definition of
SIRS.
iv. Patients with hypothermia and leucopenia tend to have more severe disease.
v. Patients with SIRS who are in shock also have elevated BUN and creatinine, oliguria, altered mental
status, decreased arterial oxygenation, increased bilirubin, and decreased platelets. When infection is
proven to be cause of shock, it is called septic shock.
b. Effects of Severe Inflammation on the Circulation
i. Mechanisms that reduce CO during systemic inflammation include
1. Hypovolemia: peripheral vasodilation, increased capillary permeability, intracellular migration
of fluid, sequestration of GI tract lumen
2. Myocardial depression
3. Increased pulmonary vascular resistance: hypoxia, platelet emboli, thromboxane release,
serotonin release, white blood cell aggregation
4. Deficits in microcirculation: GI tract, Renal
ii. The most common cause of inadequate CO during inflammation is decreased venous return due to loss
of intravascular fluid and vasodilation. Intravascular fluid is lost to the interstitium as exudate.
Subsequently, in severe inflammatory states, interstitial fluid is then depleted as it migrates across
compromised cellular membranes.
iii. Ileus is common during severe inflammation, regardless of the location of the primary focus. Ileus
can cause fluid to accumulate in the lumen of the GI tract and can be as voluminous as that sequestered
during bowel obstruction.
iv. Together, the exudation of plasma volume into inflammatory foci, accumulation of fluid in GI tract, and
migration of fluid into cells is known as the third space. The magnitude of the third space is roughly
Surgical Bleeding—Ch 5
29
proportional to the magnitude of tissue injury or infection present. Obviously, third space fluid
accumulation depletes intravascular volume and impairs venous return.
v. Severe inflammation may directly depress the function of normal myocardial cells. Less severe
inflammation may augment malfunction of previously abnormal cardiac tissue. Thus, CO may be
impaired and a cardiogenic picture may present itself.
vi. Severe inflammation is also associated with increased pulmonary vascular resistance leading to dilation
of right ventricle, decreased right ventricular ejection, and impaired filling of the left ventricle.
vii. Finally, severe inflammation may cause deficits in the microcirculation resulting in regional ischemia to
organs and within organs. This accentuates cell and organ injury. GI tract and kidney are especially
susceptible.
c. Effects of Severe Inflammation on Cellular Function
i. “Cytopathic hypoxia” – cells behave as if there is too little oxygen because of an inflammationinduced alteration in cellular function, not because there is too little oxygen for cellular function. For
example, the lactic acidosis that occurs is not due to cellular anaerobic metabolism. It is secondary to
alterations in glucose metabolism associated with increased pyruvate production or decreased pyruvate
metabolism.
ii. Cell membrane depolarization also occurs in severe inflammation as it does in hypoperfusion. This
results in sodium and water accumulation in cells.
iii. Basically, cytopathic hypoxia in inflammatory states can mimic true cellular hypoxia.
VI.
Diagnosis and Management of Severe Inflammation
a. The Patient at Risk
i. Patient who recently acquired a disease (pancreatitis) or had an injury (pelvic fx with spleen rupture)
characterized by severe inflammation
ii. Patient who has an underlying condition (immunosuppression) or who recently underwent a procedure
(colon resection) that makes systemic inflammation, particularly from an infection, more likely
iii. Any patient who has had a significant episode of hypoperfusion is also at risk for systemic
inflammation, either at the time or days later
b. Physical Examination
i. Restlessness, altered mental status (ranging from delirium to coma) may precede obvious hemodynamic
or respiratory findings.
ii. If intravascular volume is decreased, skin is cool and possible mottled. Capillary refill time is also
decreased.
iii. Vitals: decreased BP, increased HR, increased RR, elevated temperature. Hypothermia may be present
in the most severe cases.
iv. Lungs may be clear, even in ARDS is present. Rales, rhonchi and bronchospasm may be found.
Findings of consolidation may assist in locating inflammatory process, but they aren’t specific to
systemic inflammation.
v. Cardiovascular exam: hypotension and tachycardia are usually present. Hypotension with warm hands
and feet most often represents the response to inflammation, although anaphylaxis and a high SCI can
produce similar findings. Jugular venous pressure is low.
vi. Edema and weight gain may appear due to fluid sequestration. Fluid administration is directed at
restoring and maintaining plasma and blood volume threatened by this sequestration.
c. Lab Studies
i. Increased white cell count, especially young PMNs (bands), is most common
ii. Leukopenia denotes more severe disease
iii. Thrombocytopenia and evidence of DIC denotes more severe disease
iv. Hemoglobin may increase as plasma exudes into insterstium (hemoconcentration)
v. Decreased arterial PO2 and PCO2
vi. Lung si/sx and lab findings during severe inflammation may mimic those of CHF, the importance of
distinguishing the true cause is emphasized
Surgical Bleeding—Ch 5
30
vii. Oliguria and lab results consistent with a prerenal state: elevated urine specific gravity, low urine
sodium, increased urine osmolality, elevated BUN:creatinine ratio
viii. Elevated blood glucose is common
ix. Decreased ionized calcium, the magnitude of which correlates with severity of disease. This is not
specific for inflammation, but it is pretty sensitive. Thus, a normal ionized calcium is unusual during
severe inflammation or hypoperfusion.
x. Metabolic acidosis and elevated lactic acid level is often seen
d. Treatment
i. Treat the underlying cause (i.e. infection, drug or transfusion reaction, tissue injury)
1. In some patients, inflammation appears to become self-sustaining and may continue despite
adequate resolution of the initiating insult.
ii. Supporting organ function: Cardiovascular and Pulmonary
1. Rapid restoration of the circulation during severe inflammation has been shown to reduce
mortality. This improves CO, extremity temperature, mental status, and urine output.
Unfortunately, pulmonary function does not characteristically improve dramatically with
treatment of hypovolemia alone. Ionized calcium deficits and metabolic acidosis may or may
not improve with fluid resuscitation.
2. RBC transfusion is reserved for patients with ongoing hemorrhage or hemoglobin levels < 9 g /
100 mL or are symptomatic for inadequate oxygen delivery.
3. Dopamine is commonly administered during severe inflammation because it tends to increase
left ventricular end-diastolic pressure as CO increases.
4. In cardiogenic states, more complicated monitoring may be necessary (i.e. inserting pulmonary
artery catheter) to acquire hemodynamic data and assist in diagnostic and therapeutic decision
making. PACs have significant associated risks, and should only be used when the potential
advantage is considered worth the risk.
5. Myocardial depression may be due to decreased function of the myocardial catecholamine
receptors. Phosphodiesterase inhibitor drugs (e.g. amrinone) do not require this receptor
function and may be particularly useful inotropic agents to use.
6. In patients that are hyperdynamic, have elevated CO and low systemic resistance states, the use
of vasoconstrictors may be indicated.
7. Endpoints for resuscitation during severe inflammation are as controversial as those described
for hypoperfusion states. One indicator may be a decrease in the cardiac index toward normal.
8. Mechanical ventilation may be necessary to support pulmonary function.
iii. Antagonize inflammatory and metabolic mediators (table on pg. 118)
1. Area of much experimental and clinical research. Important to find the balance between the
beneficial and detrimental effects of inflammation. Aggressive suppression of inflammation
may have short-term benefits but the loss of the beneficial effects may result in death secondary
to recurrent infection or wound breakdown.
2. Therapies that allow local inflammation to continue while the systemic inflammation is
suppressed may allow the proper inflammatory balance.
3. Recent therapies showing limited benefit:
a. Recombinant human activated protein C (Zygris)
b. Physiologic (vs. pharmacologic) doses of hydrocortisone
VII.
A Practical Guide to the Patient in Shock
a. Recognize the Patient in Shock
Characteristics of those at risk for
shock
Trauma or burn
Vascular catastrophe
Acute cardiac disease
Acute abdominal disease
Severe extraabdominal infection
Drug exposure
Bedside exam indicators of shock
Common lab abnormalities
Hypotension, tachycardia, tachypnea
Hyperthermia or hypothermia
Peripheral vasoconstriction
Hypotension with warm extremities
Agitation, altered mental status
Oliguria
Metabolic acidosis
Elevated BUN, creatinine
Leukocytosis or leucopenia
Elevated blood glucose
Thrombocytopenia
Decreased ionized calcium
Surgical Bleeding—Ch 5
31
b. Provide an Excellent Circulation
i. Replacement with isotonic crystalloid solution requires a 3:1 ratio as the crystalloid distributes
throughout the extracellular space. Therefore, 4500 mL crystalloid solution is required to begin plasma
volume restitution in the patient who has lost 30% of their intravascular volume (approx. 1500 mL in a
70-kg person).
ii. Replace fluid rapidly (within minutes, if possible)
c. Treat Severe Inflammation
i. Recognize inflammatory state is present
ii. Localize and treat the focus
VIII.
Conclusion – Total body cellular malfunction (i.e. shock) can result from various insults that may be broadly
categorized as severe hypoperfusion or severe inflammatory disturbances. Almost invariably, hypoperfusion and
inflammation coexist in patients who have shock. Restoring an excellent circulation and treating severe
inflammation are the keys to preserving cellular and organ function and preventing death from shock.
Wounds—Ch 8
32
Ch. 8 Wounds and Wound Healing
Physiology of Wound Healing
--Inflammation common to all woundsredness (rubor), heat (calor), pain (dolor), and loss of function
Biochemical aspects
--Trauma activates chemoattractants such as PDGF, and complement peptide (C5A)
--Initial event of clotting and recruitment of cells occurs in the first 1-2 hours after injury
--The first cells to enter wound are platelets which release PDGF and TGF-B
--Macrophages release TGF-B, MDGF, TGF-a, and basic fibroblast growth factor (bFGF)
--Keratinocytes release TGF-B, TGF-a, and keratinocyte-derived autocrine factor (KAF)
--These cytokines are involved in synthesis of extracellular matrix and new capillary formation, and some act as
attractants for fibroblasts and neutrophils
--Degradation of arachidonic acid into prostanoid derivatives of prostaglandins and thromboxanes induces the
inflammatory response including vasodilation, swelling, pain
Physiologic aspects
--Along with biochem. events, leukocytes marginate and migrate through vessel walls, venules dilate, and lymphatics
are blocked
Phases of Wound Healing
1. Substrate phase (Inflammatory)
--Main cellsPMNs (predominant for first 48 hours), platelets, macrophages
--Monocytes reach max. numbers 24 hours later, and develop into macrophages
--Tissue matrix metalloproteinases (TMMP) are activated and begin to degrade surrounding matrix proteins (collagen
and necrotic cellular macromolecules), TMMP inhibitor activity falls
--IL-1 induces fever, enhances fibroblast proliferation, and activation of T cells
--In primary healing, substrate phase occurs over about 4 days
2. Proliferative phase
--Begins when the wound is covered by epithelium
--Characterized by production of collagen in the wound
--Primary cell is the fibroblast
--Collagen production cofactorsferrous ion, a-ketoglutarate, ascorbic acid
--About 1 month
3. Maturation phase (Remodeling)
--Maturation of collagen by intermolecular cross-linking
--Adults9-12 months
Classification of Healing Wounds
--Classified as acute, chronic, clean, or contaminated
--Chronic become arrested in inflammation phase and fail to advance
--Clean wounds have minimal bacterial or particulate loads and are open less than 12 hours
--Contaminated wounds have high bacterial counts (>105 organisms/gm tissue) or large amount of particulate matter
--Partial thickness don’t completely penetrate the top epithelial layer of skin, and basal stem cells remain active and
proliferate sufficiently to replenish the damaged superficial layer
--Full thickness entail damage to the entire layer of keratinocyte epithelium including sweat glands and hair follicles
that contain stem cells
Primary healing
--Closed by direct approximation of the epithelial wound edges
--Can be performed in clean and contaminated wounds
--Large defect may require pedicle flaps or skin grafts
--Epithelialization occurs in 12-24 hours
Secondary healing
--Wound is left open and allowed to heal spontaneously from the edges
--Closes by contraction and epithelialization (1 mm/day under optimal circumstances)
Wounds—Ch 8
33
--If the wound fails to epithelialize the granulation tissue will continue and result in an unclosed wound with friable
tissue outgrowing the epithelial edges
Tertiary healing
--Closed by active means after a delay of days to weeks
--Closure only in wounds that have a bacterial count <105 organisms/gm tissue
Factors that Affect Wound Healing
Local factors
--Wound must be cleaned, debrided, and closed appropriately
--Bleeding must be controlled
--Wounds at risk for virulent streptococci species should not be closed
--Proper prophylaxis for Clostridium tetani
Systemic factors
--Nutrition is an extremely important factor
--Folic acid critical to proper formation of collagen
--Vitamin K essential for carboxylation in the synthesis of clotting factors (II, VII, IX, X)
--Vitamin A increases the inflammatory response, increases collagen synthesis, and increases influx of macrophages
--Magnesium required for protein synthesis
--Zinc is a cofactor for RNA and DNA polymerase
--Uncontrolled diabetes inhibits fibroblast and endothelial cell proliferation within the wound
--Steroids blunt the inflammatory response
--Chronic illness predisposes to infection, protein deficiency, and malnutrition
--Smoking has a systemic effect by decreasing the O2 carrying capacity of hemoglobin
General Management of Wounds
Local anesthetics
--Amide group most commonly used includes xylocaine, bupivacaine, mepivacaine, and prilocaine
--Esters include procaine, chlorprocaine, tetracaine, and cocaine
--Don’t use esters in patients sensitive to p-aminobenzoic acid (PABA)
--Solubility, protein binding, and the pH and vascularity of tissues determine duration of action
--If dose needed will exceed max dose use general anesthesia
--Major side effectsCNS (tinnitus, blurred vision, tremors, and depression) and CV (myocardial depression, AV
block, and decreased CO)
--Don’t use with vasoconstrictors in end organs (nose, digits, penis, ears) due to risk of ischemia
Classification of wounds
--Clean woundrelatively new (<12 hours) and minimal contamination
--Avulsion injuryshearing forces undermine and elevate tissue creating a flap or total loss of skin
--AbrasionSuperficial loss of epithelial elements (requires only cleansing and protection from desiccation)
--Puncture wounds generally don’t require closure
--Crush injurydebride nonviable tissue and close with skin graft or myocutaneous flap
Suture material
--More zeros = smaller suture
--3-0 or 4-0 on torso and extremities, 5-0 or 6-0 on face and neck
Wound closure
--No tension on wound edges
--Sutures of torso/extremities left for 7-10 days, face/neck for 4 days
--Secure but not tight knots (risk of tissue strangulation)
--Monofilament on skinless reactive
--Absorbable deep suture placed in tissues with greatest strength (fascia for muscle, dermis for skin)
Management of the Contaminated, Infected, and Chronic Wound
Contaminated wound
Wounds—Ch 8
34
--Exceptions to primary closurehigh bacterial count, long time since injury, virulent bacterial species, severe crush
injury
--Excessive use of buried suture provides foreign body for bacterial contaminationuse monofil.
Infected wound
-- >105 organisms/gm tissue
--Debridement most important technique to decrease the bacterial count
--Dressing changes should be limited to twice per day to prevent adversely affecting the progression of healing within
an open wound
--Systemic antibiotics don’t penetrate the granulating wound bed, but topicals are effective
Chronic wounds
--Include diabetic foot ulcers, venous stasis ulcers, and open wounds that have failed to close
--They are stalled in the inflammatory phase of healing
--They have elevated levels of TMMP
--Debridement, careful cleaning, and dressing changes most effective
--Four types common in clinical practicepressure ulcers, venous stasis ulcers, arterial insufficiency ulcers, and
diabetic neruopathic ulcers (all common in elderly)
Pressure ulcers
--Spinal cord injury patients at high risk
--Common sitesheel, sacrum, ischial tuberosities
--Pelvic pressure ulcers often have small skin defects overlying large cavities and become severely infected from fecal
soiling
--Most common care is saline-moistened gauze with twice daily changing
--New methodnegative pressure wound vacuum device (wound VAC) which is a porous sponge packed into the
wound connected to negative pressure
Venous stasis ulcers
--Most common chronic wound in adults
--Generally superficial wounds in the anteromedial aspect of the leg (“gaiter zone”), not involving the foot
--Incompetent valves in veins result in venous hypertension transmitted to microcirculation
--Exacerbated when leg is dependent and relieved when leg is elevated
--Increased filtration leads to RBC deposition and breakdown leading to increased hemosiderin
pigmenthyperpigmentation and edema (dermatofibrosis)
--Management starts with compression, and most will heal in several months with compression (refractory wounds may
require surgery to ablate the abnormal veins)
Arterial insufficiency ulcers
--Result from atherosclerotic obstruction, although may also result from thromboembolism
--May extend into deeper structures to expose bone or tendon
--Typically involve the toes which can be mummified and black or have suppuration with oozing
--Pedal pulses usually absent but vascular ultrasound is very reliable
--Management usually involves mechanical arterial interventionangioplasty, stenting, bypass surgery (25% can be
healed with local care alone)
Diabetic neuropathic ulcers
--Motor neuropathy leads to atrophy of the intrinsic muscles of the foot, leading to derangements in bony architecture
that depends on intrinsic muscle tone for proper alignment
--Sensory neuropathy and lack of proper protective reflexes also contribute
--40% have an element of arterial ischemia
--Typically have a fibrotic granulated bed surrounded by hypertrophic skin (callus), which identifies the exposure to
excess pressure
--Each year wound remains open = 25% risk of limb loss
--Management starts with control of infection
--If bone or joint penetrated, surgical debridement usually required followed by secondary healing
Wounds—Ch 8
35
Advanced care for chronic wounds
--Newer treatment modalities include negative pressure devices, topical foams, topical application of growth factors and
collagen preparations, topical broad-spectrum antibiotics, topical enzymes, engineered skin substitutes,
hyperbaric oxygen
--PDGF useful in diabetic ulcers (proven by clinical trials)
--Topical 1% silver nitrate solution, or cadexomeric iodine for antimicrobial activity
--Fetal fibroblasts growing over collagen layers mimic dermal layer of skin
--Pure oxygen at 3 ATM of pressure with daily exposure for 8 weeks
Surgical Infection—Ch 9
36
Chapter 9:
Surgical Infections
PATHOGENESIS OF INFECTION
-Bacteria soliage initiates well-defined processes of host defense
-Inflammatory Response: Kinins and histamine release alter capillary permeability complement/fibrinogen/specific or nonspecific
opsonins delivered to site Neutrophils marginationNeutrophil diapedesisNeutrophil contact may be assisted by
opsonizationPhagosome formationIntracellular killing and digestion
-Pus consists of dead phagocytic cells, fibrin, opsonic proteins, dead and viable microorganism and bacterial products; the
inflammatory environment that develops is acidic and hypoxic and thus cellular and enzyme function is inhibited.
-The primary determinant of establishing a local infection for a given level of contamination is
the density of bacteria present vs. efficiency/effectiveness of the host defenses
-Local/Systemic Factors that alter bacterial virulence and cellular host response
Local
High bacterial concentrations
Wound hematoma
Necrotic Tissue
Foreign Body
Obesity
Systemic
Advanced Age
Shock (hypoxia, acidosis)
Diabetes Mellitus
Protein Calorie Malnutrition
Acute/Chronic Alcoholism
Corticosteroid drug therapy
Transplant Immunosuppression
-Hemoglobin potentiates bacterial virulence b/c ferric iron enhances bacteria growth and hemoglobin diminishes the efficiency of the
neutrophil
-Dead tissue and foreign bodies enable bacterial growth as host defense mechanisms cannot penetrate
-Hyperglycemia results in impaired neutrophil mobility
-Obesity because blood supply to adipose tissue is poor
-Malnutrition increases vulnerability to infection
-Acute/Chronic Alcoholisms impairs host defense response as does drug therapy
-Systemic factors (shock, hypovolemia, hypoxia) acidosis and infection
PREVENTION OF SURGICAL INFECTION
Classification of Surgical Wounds
Wound
Bacteria
Infection
Frequency
3%
Polymicrobial
Source of
Contamination
OR, environment,
surgical team,
patient’s skin
Endogenous
colonization of the
patient
Gross contamination
Clean
Gram +
CleanContaminated
Polymicrobial
Contaminated
Dirty
Polymicrobial
Established Infection
40%
5-15%
15-40%
Examples
Masectomy, aortic graft, inguinal
hernia, thyroidectomy
Common duct exploration,
elective colon resection,
gastrectomy
“spill” during elective GI surgery,
perforated gastric ulcer
Drainage of abscess, resection of
infracted intestine
-Universal Precautions and isolation are applied to selected bacterial and viral infections. This is designed to prevent hospital
personnel from serving as vectors in transmission to others. Gowns and gloves should be worn and traffic into the patient room
should be limited.
-Reverse isolation is to prevent pathogens from being introduced into contact with severely immunosuppressed patients and hospital
personnel should wear masks.
-Surgical Asepsis
The frequency of clean wound infection is the most sensitive indicator of quality surgical care and is a surveillance tool that is used to
judge overall sterile technique in the OR.
Surgical Infection—Ch 9
37
(1) Limit preoperative hospitalization (2) preoperative showers (3) hair removal immediately before the procedure (4) preoperative
search for infection and if found treated (5) Shorter operative times the less risk for infection (operations  2 hrs have 40% greater
infection rate than those  1 hour)
Intraoperatively, excessive suture material or indiscriminate use of electrocautery may lead to large areas of devitalized tissue. Drains
should be closed-suction that have a separate stab wound to exit the subcutaneous space and should be promptly removed when they
become inactive. Personnel should scrub, donning gowns and gloves and when infections occur after clean operative procedures, a
break in this routine should be suspected.
-Perioperative Antibiotics
Prophylactic antibiotics must be present in the tissue at the time of bacterial contamination to be effective. Select the drug
preoperatively and ensure it is active against the anticipated pathogens.
Long-half life antibiotics are preferred and should be given within 60 minutes of the time of incision and again 4-6 hours later.
Antibiotics used in the perioperative period should not be continued past two postoperative doses to avoid the emergence of resistant
bacteria.
Prophylactic systemic antibiotics are of little value when the period of bacterial contamination is longer than a short defined period of
exposure.
Clinical studies show the effectiveness of the preoperative systemic antibiotics in reducing the incidence of tissue infections,
especially in clean-contaminated and contaminated wounds.
Few studies support prophylaxis in clean operative procedures and, in fact, the risk of an antibiotic complication is greater.
Prophylaxis is used when a foreign body is implanted because a septic complication is a fatal event.
Elective colon surgery association with high rates of infection give orally administered, poorly absorbed AB such as oral neomycinerythromycin base AB, which can reduce the wound infection rate to 10%.
For grossly contaminated wound, with a high infection rate close the fascial layers and manage the open wound with wet-dry
dressings.
***See pg. 167 Table 9-3 for Antibiotic Selections for Common Infections
MANAGEMENT OF ESTABLISHED INFECTION
Determine antibiotic sensitivity for serious invasive infections, but beware that invitro sensitivity does not always indicate clinical
responsiveness. Consider bacterial counts, tissue environment, AB concentration, metabolism/excretion of the drug, and toxicity of
the agent. Antibiotic resistance is a concern in surgical infections and ABS should only be initiated when there is sufficient evidence
of infection and should not be used over an extended period.
Community-Acquired Infections
Skin/Soft Tissue Infections ***See pg. 168 for Common Soft Tissue Infections and TX
Result from break of puncture in skin and present as cellulitis.
Group A Strep causes blanching erythema and responds to PCN therapy
Consider Staph if pus is present TX surgical drainage/debridement/naficillin/oxacillin; MRSA with vanco/linezolid
Necrotizing strep gangrene-non-blanching erythema (subdermal thrombosis of underlying blood supply), blisters, necrosis of skin.
TX: surgical debridement of the affected area with high dose PCN & Clindamycin
Breast Abscess
Common Staph soft tissue infection, postpartum women with galactoceles are at a particular risk
Localized severe tenderness, selling, redness, mass may be fluctuant, aspiration of purlent material
TX: I&D (a delay may result in necrosis of breast tissue) + Antibiotics for Staph
Perirectal Abscess
Abscesses form within the crypts of anorectal canal, can extend into pelvis in the diabetic & immunocompromised patients and can be
fatal. TX: Drainage + broad spectrum AB for anaerobes and aerobes to protect the patient from bactremia that is associated with
drainage
Gas Gangrene (C. perfingens)
Clostridial soft tissue infection –cellulitis and myonecrosis
Contamined objects enter the skin, brown watery drainage, tenderness, palpable crepitance
Tetanus toxoid immunization and debridement without primary closure if an individual is at risk for clostridial myonecrosis or
cellulitis. Tetanus antitoxin is administered to patients with high-risk wounds who have uncertain immunization record.
Age
Tetanus Prone
 6 yrs
Nontetanus Prone
 6 yrs
Surgical Infection—Ch 9
38
Type
Crush, Avulsion, Extensive Abrasion,
Sharp/clean
Burns, Frostbite
Contaminants (Soil/Saliva/etc)
Present
Absent
When gas gangrene is diagnosed the TX is immediate radical surgical debridement, high dose PCN, or metronidazole and clindamycin
when PCN cannot be used.
Tetanus (C. tetani)
Prodromal symptoms: restlessness, headache, stiffness of jaw muscles, muscular contraction in area of wound. Violent generalized
tonic muscle spasms follow within 24 hrs and respiratory arrest occurs. Debridement and Cleansing of all wounds with devitalized
tissue to prevent exotoxin production. Give immunization, add immune globulin if no immunization within past 10 yrs. Only
contraindication is neurologic or hypersensitivity reaction to a previous dose. Use of systemic AB should be considered for tetanus
prone wounds.
Hand Infections
Morbidity with loss of function
Paronychia infection at sulcus of nail border, usually Staph, simple drainage and hot soaks
Felons are deep infections in pulp space of the terminal phalanx, can occur after penetrating injuries, tx by drainage.
Subungual abscess is the extension of a deep paronychia causing fluctuance beneath the nail; remove nail for drainage.
Tenosynovitis is infection of the tendon sheath from neglected infections of fingers, drain by opening sheath along its length to
prevent necrosis and functional compromise
Deep space compartments (ex. thenar, hypothenar) can become infected. Tx with Urgent I&D + AB
Human Bites are polymicrobial; tx with copious irrigation, debridement, hand elevation, systemic AB. Do NOT employ primary
closure. Animal bites are debrided and irrigated; pathogens are likely aerobic Pasteurella species.
Foot Infections
Trauma, mechanical/metabolic derangement in diabetic patients due to neuropathy, the resultant bone deformities or vascular
compromise that results in ischemic ulceration
Osteomyelitis is a frequent component. Cultures/debridement/AB/mechanical external supports to relieve pressure points/ focus on
limb salvage
Biliary Tract Infections
Obstruction of cystic or common bile duct may result in infections with E. coli, Klebsiella, Enterococci.
Acute cholecystitis-obstruction/entrapped bacteria/empyema/possible severe systemic sepsis/loss of blood supply results in
gangrene/perforation. Prevent by early surgery.
Ascending cholangitis with fever, leukocytosis, and jaundice. Prompt surgical intervention.
Acute Peritonitis
Bacterial in the peritoneal cavity after mechanical perforation of hollow viscus
Primary peritonitis-may occur w/o perforation; uncommon, but seen in alcoholics w/ ascites or immunocompromised patients.
Secondary peritonitis-cathetic contamination from peritoneal dialysis in patients with CRF
Acute abdominal pain, fever, leukocytosis, rebound tenderness, board-like rigidity; free air beneath diaphragm
Variable in severity and dependent upon bacterial/chemical composition of segment perforated thus peritonitis is not a single disease
entity
Perforated gastroduodenal ulcers-precipitous events w/ acute abdominal pain, +/- previous symptoms of ulcer disease, 80% of
patients with free air on upright chest film. May be entirely chemical for the first 12 hrs, longer bacterial infection become severe.
TX: Operative repair w/ ulcer operation (vagotomy & pyloroplasty), AB for Gram negatives are used but may provide minimal
benefit, except in patients with delayed operation
Perforated appendix-starts as acute appendicitis, perforation may occur after 24 hrs of symptoms
Diffuse tenderness with generalized rebound tenderness. AB for aerobic (E.coli) and anaerobic (B. fragilis)
TX: appendectomy and drainage of any RLQ abscesses. Localized abscess can be drained externally.
Colonic perforation from carcinoma or diverticular disease is the most virulent cause of peritonitis. Systemic toxicity, peritoneal
signs TX: volume resuscitation and broad spectrum systemic AB for anaerobic and aerobic species; Operation is mandatory with
drainage and debridement. Left colon perforations require diversion of fecal stream as part of management.
If physical symptoms are present, a celiotomy (laparotomy) is justified. Diagnose and DO NOT delay in operative intervention while
radiology is being performed.
Viral Infections
Hep B is greatest concern due to blood and body fluids as primary route of transmission
5-10% are chronic carriers that may progress to cirrhosis, ESLD, hepatocellular carcinoma; acute infection can result in hepatic failure
and death; vaccine for health care workers with follow up titers are necessary
Hep C blood and body fluid route of transmission as well; 60% are chronic carriers, acute infection is rather mild, chronic hepatitis
and cirrhosis eventually develop with increased risk of hepatocellular carcinoma; Exercise universal precautions
HIV progresses to AIDS, exercise universal precautions
Surgical Infection—Ch 9
39
Hospital-Acquired
Post-op fever; macrophages stimulate synthesis of IL-1hypothalamus which acts to increase body temperature; temperature increase
is accompanied by neutrophilia, hypoferremia, hypozincemia, hypercupremia, and synthesis of acute phase reactants by the liver (Creactive protein) to bolster defense.
Identify source of FEVER: 5 W’s
Wind-atelectasis, pneumonia, PE
Wound-incision, devitalized tissue, abscess
Water-UT, IV fluids
Walk-DVT, IV site phlebitis
Wonder Drugs-blood product transfusion, drug infusions
Usually do not begin empiric AB without first identifying the source unless the patient is severely septic, hypotensive, hypermetabolic
or hypoxic, when meningitis is a possible cause or in an immunocompromised patient
Pulmonary Infections
1. Non-respiratory associated pneumonia results from atelectasis. Poor post-op tidal volumes from anesthesia, analgesia, and
painful abdominal or thoracic incisions can cause small airways to collapse. Usually within the first 48 hrs. Prevent by early
ambulation, coughing, deep breathing, nasotracheal suctioning, incentive spirometery. When w/in the first 48hrs laboratory
and radiographic data are unnecessary, but if fever continues despite aggressive chest physiotherapy, invasive infection has
occurred and employ systemic AB with culture and sensitivity data.
2. Post-op pneumonitis may be respirator-associated. Endotracheal tube is a foreign body that prevents bacterial and secretion
clearance, injures tracheal mucosa, and permits bacterial proliferation. Ventilator showers lungs with microorganisms so
weaning patient promptly is important. Opportunistic Gram negative (Pseudomonas, Serratia), but gram positive staph is
increasing (including MRSA)
Endotracheal or Bronchoscopy with bronchoalveolar lavage/aspiration for culture.
3. Aspiration consider in patients with gastric distension and altered mental status, the elderly, those with head injuries; gastric
decompression reduces risk, bronchoscopy is diagnostic, but should be approached cautiously in hypoxic patients to avoid
cardiopulmonary arrest. Management is systemic oxygenation, AB only after clinical and culture evidence, systemic
corticosteroid therapy has NO role in aspiration
Urinary Tract Infection
Usually from Foley, remove after serving purpose
Greater than 100,000 organisms/mL urine, but does not indicate urinary tract sepsis, not association with fever
UTIs after catheterization are NOT caused by usual pathogens (E.coli), but instead are caused by Pseudomonas, Serratia, resistant
Gram Negatives. Tx with culture and sensitivity data. Candida and Enterococci infections are increasing.
Wound Infections
Consider in differential of post-op fever, tenderness, redness, heat or mass effect, pus discharge, absence of a healing ridge. Open
wound, evacuate pus, debride fibrin, remove subQ sutures, AB if severe/progressive cellulitis or necrotizing infection.
Intrabdominal Infection
Complication of elective gastrointestinal or biliary surgerypostop peritonitis or abscess
Major dehiscence of anastomosesflorid sepsis
Reoperation is based on clinical signs (abdominal tenderness/pain, fever, leukocytosis and the toxic septic state)
Most are abscesses rather than diffuse inflammation or peritonitis, but are difficult to diagnose due to incision tenderness. Signs
include localized tenderness, palpable mass, rectal exam is useful in pelvic abscess
Abdominal series may be ordered but is useful in fewer than 20% of patients; Studies with gastografin may show filling defect or
intestinal leaks in pts. with recent construction anastomoses
US is inexpensive, used at bedside, must have direct contact with skin of abdomen (may not be useful in pts, with dressings, open
wounds, stomas), poor anatomic detail and intestinal gas limits further limits the detail
CT is the most accurate (90%) and fastest for suspected intrabdominal abscesses, displays retroperitoneal collection, water soluable
contrast can be added, but contrast is contraindicated in suspected ileus
Ascites make CT difficult; radionuclide scanning with indium-111-labled autologous leukocytes the total body scan 1 day after
injection will show sites of infection
Drainage is primary treatment; infection is polymicrobial with lipolysaccharide-laden organisms and obligate anaerobes with a
synergistic relation so cover both entities---destined to fail without surgical drainage, intestinal diversion or exteriorization when
enteral perforation and debridement of soft tissue around the focus
Pleural Empyema
Complication of thoractomy or chest tube placement; may occur in pneumonic process or TB
Surgical Infection—Ch 9
40
Inadequate drainage of blood and tissue following blunt/penetrating trauma
Roentgenograms (Radiology images) show effusion/lateral chest/US/CT helpful in diagnosis especially CT when fluid is loculated;
Diagnosis is confirmed by pus by needle thoracentesis
TX is drainage of infections; Gram positive staph usually associated with chest tube placement; failure of AB indicate inadequate
drainage, rib resection to marsupialize the empyema cavity may be necessary
Foreign Body Associated Infection
Indwelling lines permit organisms to migrate from the skin to intravascular compartment, intimal injury with localized clot formation
provides an additional growth media.
All percutaneous peripheral IV cannulae, central venous catheters, and monitor devices (arterial line, Swan-Ganz) should be placed
with sterile technique and replaced within 72 hrs.
Silver impregnated catheters may be a newer method that will reduce catheter-associated infection
Suspected in pts. with positive blood cultures, especially Staph/Strep
Culture tip to confirm diagnosis
TX: Removal and AB
Persistent fever, leukocytosis, bacteremia—suggest suppurative thrombophlebitis, so examine previous IV sites
Local I&D with pus dictates excision of the entire length of vein affected; AB for organism identified with S. aureus to prevent
bacterial endocarditis complications
Infection of vascular grafts, orthopedic joints, or other permanent devices are rare and usually initiated during the operative procedure,
but consider when purulent drainage or fever workup; fluid collection around prosthesis is strong evidence of infection; Tx is removal
and requires alternate implants; may dictate prolonged use of culture specific systemic AB (mostly for S.aureus & S. epidermidis)
In anecdotal cases, impregnated beads adjacent to infected sites permits higher doses of AB
Post splenectomy Sepsis
Clearance of transient encapsulated bacteria-Pneumococcus, Meningococcus, H. Flu is impaired
Tx with systemic AB for febrile illness and draw blood cultures
C. Difficle Enterocolitis
Suspect in patient with diarrhea while receiving AB
Confirm with toxin in stool
Tx. with oral metronidazole and vancomycin enteral feeding also is helpful in reestablishing normal flora
Fungal Infections
Immunosuppressed individuals susceptible to normal environmental fungi
Candida is the most common
Tx. is debridement of infected tissue if applicable and systemic tx. with Amphotericin B (toxic effects) or Fluconazole
Sepsis/Septic Shock/Multiple Organ Failure
Sepsis is systemic activation of inflammation secondary to infection
*Clinical diagnosis is made when patients have tachycardia, tachypnea, fever, leukocytosis (does not require cultures for diagnosis)
Septic response: Increased cardiac output, decreased systemic vascular resistance, altered systemic use of oxygen leading to
metabolic acidosis
Septic Shock: vasoactive component is loss of vascular resistance leading to vasodilation, which CO cannot compensate for;
cardiogenic component is when CO is inadequate due to systemic toxicity
TX is intravascular volume support, inotropic support to maintain CO, systemic oxygenation, and control of the primary source
Sustained systemic activation of inflammation results in Multiple Organs Dysfunction Syndrome-failure of lungs, liver, kidneys, heart
due to microcirculation consequences
TX is oxygenation, cardiac support and AB; recent use of recombinant protein C may have beneficial effects
THE FUTURE OF SURGICAL INFECTION
New pathogens may emerge. New AB to combat resistance are needed. Strategies to rotate AB use in the CCU have been advocated.
Control of blood sugar, supplemental oxygen delivery, intraoperative temperature control may increase host responsiveness to
infection. Need a better understanding of the human septic response to create better therapies.
Trauma—Ch 10
41
Trauma
Algorithm
1) Primary Survey – diagnosis and treatment of all immediate life threatening injuries.
2) Resuscitation – simultaneous with above.
Airway is secured, ventilation is assured and oxygen is administered.
External blood loss controlled by direct pressure.
IVs established and balanced electrolyte solution is administered.
High flow fluid warmers to combat hypothermia +/- warm blankets.
Gastric tube placed to reduce aspiration and gastric distention.
Monitor pulse ox, BP, ECG, and urine output.
3) Secondary Survey – detailed head to toe evaluation with AMPLE history
and Events surrounding the injury.)
4) Definitive care – Surgery or something else if you’re a pansy.
(Allergies, Meds, Past illnesses, Last meal,
Airway and Breathing
- The talking patient informs the physician that the airway is patent, the brain is perfused, and ventilation is adequate.
Signs and symptoms of airway obstruction
- Stridor, snoring, or gurgling suggest a supraglottic problem.
- Dysphonia, hoarseness, or pain on speaking suggest laryngeal problem.
- Tachypnea, agitation (hypoxia), cyanosis, obtundation (hypercarbia) and use of accessory muscles.
- It is imperative to stabilize the C-spine while opening the airway.
o Jaw thrust or chin lift
- Airways – oropharyngeal (unconscious), nasopharyngeal (conscious)
- If the above fail you must provide a definitive airway.
o Orotracheal intubation
o Nasotracheal intubation
o Surgical Cricothyroidotomy (for massive facial trauma and surgery studs)
o Needle Cricothyroidotomy (kids < 12)
o Tracheostomy (not acute)
- Complications if you suck:
o Right main stem bronchus intubation – decreased breath sounds on the left.
o Pneumo or hemothorax – absent or decreased breath sounds on either side.
Circulation
- Initial management: control obvious hemorrhage with direct pressure, assess tissue perfusion, and administer IVF.
- Tourniquet = bad idea
- Assess perfusion: pulse, skin color, level of consciousness
o Systolic pressure 80, 70, 60 – carotid, femoral, radial
- Shock – inadequate organ perfusion.
- This is the trauma packet so its hemorrhagic
o Tx – stop bleeding and restore intravascular volume (Do not give vasoconstrictors, this will promote ongoing
ischemia to kidneys and splanchnic viscera.)
- Hemorrhage classification
o Class I - < 15% blood loss, urine output normal,. normal BP, HR
tx: Pepsi and a Little Debbie, +/- free T-shirt
Class II – 15%-30% blood loss, normal BP, UO 20-30ml/hr, Pulse pressure decreased, systolic normal, diastolic
elevated, Tachycardia > 100
tx: administration of crystalloid
Class III – 30%-40% blood loss, Tachycardia > 120, BP decreased, pulse pressure decreased, UO low at 5-15ml/hr,
tachypnea with RR of 30-40/min.
tx: LR and blood transfusions
Class IV - > 40% blood loss, Tachycardia >140, BP markedly decreased, pulse pressure very narrow often
unobtainable, UO often nonexistent
tx: LR and blood transfusions
- Tx: Initial management involves rapid diagnosis, replacement of intravascular volume and control of obvious hemorrhage.
o Two large bore peripheral IVs (16 guage)
o LR is resuscitation fluid of choice.
o The 3:1 rule. 3ml of crystalloid to replace 1ml of blood lost due to loss into interstitium.
o Give 20ml/kg IVF initially.
Nonhemorrhagic shock
- Cardiogenic shock – results from cardiac contusion, tamponade, air embolus, rarely MI
Trauma—Ch 10
42
- Tension pneumo – produces shock by impeding venous return
- Possible question: Differentiate tension pneumo vs. tamponade. Key – tamponade has normal breath sounds.
Thoracic Trauma
- Read the book on this section. This is not a cop out. It’s about four pages of dense material that is full of potential test
questions. Read it.
Abdominal Trauma
- Nipples to the pubic bone
- Patients often have no significant physical findings to indicate intraabdominal injury.
- Classic signs of pain, tenderness, and rebound tenderness are often camouflaged by other extraabdominal injuries or masked
by an altered level of conciousness as a result of head trauma, drugs, or alcohol.
- In patients with hypotensive trauma, normal breath sounds, and no external signs of blood loss the abdomen is a likely source
of occult hemorrhage.
- Evaluation to determine IF significant intraabdominal injury exists, not what organ is injured. IF significant injury,
exploratory laporotomy.
- Abdomen divisions: 1)Upper – liver, spleen, stomach, transverse colon, diaphragm. 2) Lower – small bowel, residual
portions of intrapertioneal colon. 3)Pelvic – Bladder, rectum, iliac vessels, uterus, ovaries. 4) Retropertioneum – kidneys,
ureters, duodenum, pancreas, aorta, vena cava, parts of the colon.
- Signs and symptoms
o No bowel sounds – suggestive of ileus
o Loud supraumbilical contiuous bruit – aortocaval fistula
o Tympany in RUQ – suggests free air from ruptured viscous
o Voluntary muscle guarding – fear of pain
o Involuntary muscle guarding – significant peritoneal inflammation
o Rebound tenderness – unequivocal sign of peritonitis.
- Evaluation of abdomen continued
o Palpation of iliac crests and symphysis pubis – manual compression of the iliac wings, inward and outward, may
show abnormal movement that indicates pelvic fracture.
o Perineal and rectal exams are part of abdominal exam
 Lower GU injury – blood at urethral meatus or scrotal hematoma
 DRE mandatory in all patients – abnormal tone implies neurologic injury
 Floating or high prostate – may indicate urethral transaction
 Blood in rectum indicates rectal injury until proven otherwise.
 In females, bimanual pelvic exam should be performed.
- Gastric and Bladder catheters
o NG tube - Decompress GI and decrease risk of vomiting and aspiration.
o Foley cath – 1) decompress bladder, 2) monitor UO both in color and volume.
o Suprapubic bladder catheter is used if urethra is injured.
-
Diagnostic Evaluation of the abdomen
o DPL – diagnostic peritoneal lavage – positive DPL is indication for exploratory laporotomy. 98% sensitive
o Abdominal Ultrasound – detect free fluid in abdomen.
o CT scan for stable patients
Pelvic Fractures
- Force great enough to cause pelvic fx can also cause tears of the sacral venous plexus, lacerations of internal iliac artery and
its branches, and injury to the viscera.
- DPL can be used as a diagnostic tool in patients with pelvic fx, but the incision should be made supraumbilical rather than
infraumbilical to avoid entering a pelvic hematoma.
Head Injury and Other Trauma
- These sections can be read on your own.
- Pay close attention to Glasgow Coma Scale
Extremitiy Trauma
- There are other topics in this section, but none that require much thought
o If its bleeding, make it stop.
o If its unattached, try to reattach it.
o If its broken, splint it.
o If its dislocated, reduce it.
o If its dirty, wash it with saline.
o If its dead, cut it off.
o Real tough stuff
Trauma—Ch 10
43
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I will highlight compartment syndrome, because we see that a lot on trauma.
Compartment Syndrome – associated with conditions that increase fascial compartmental pressure. This increase, in turn,
causes interstitial tissue pressure to become higher than capillary perfusion pressure.
o Typically occurs in the calf and forearm, but can occur in thigh, arm, hand and foot.
o Initiating events include arterial injuries, crush injuries, fractures, prolonged compression, and restoration of blood
flow to previously ischemic extremity.
o Remember P’s of Compartment Syndrome
 Paresthesias
 Pain exacerbated on Passive stretch of the involved muscles
 Pulses – decreased (usually too late at this point)
o Treatment – fasciotomy
 When you reestablish blood flow, can get myoglobin induced ARF, so make sure patient has adequate fluid
to produce high urine output 100ml/hr.
Burns—Ch 11
44
Pathophysiology of burns:
 Epidermal burns (1st degree)
- red, moderate pain, blanch with pressure, no blisters
- require supportive care and rarely cause problems
 Partial-thickness (2nd degree)
- red, blisters with proteinaceous fluid, painful
- eschar forms within 24-48 hrs (eschar is dead tissue, coagulated serum, debris)
- more superficial burns of dermis will be moist and blanches
- deeper burns of dermis will cause more necrosis and will be dry and leathery
- deeper burns will require debridement and graft due to a rigid scar that would
otherwise form
 Fullthickness (3rd degree)
- involves the full thinkness of the dermis including cutaneous nerves so no pain
- very important to watch for dermal contracture that will constrict extremities and
lead to lead ischemia
Initial Care:
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Definitive Care:
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Stopping the process
- must cool clothing and any hot substances with cool water to prevent further damage
- material should be removed carefully
Special attention to assess inhalation injury
- edema of burned airways will cause narrowing so early intubation may be needed
Look for underlying injury
Beware of “burn shock”
- systemic capillary leakage causing edema and can decrease circulating volume by
15-20%
IV fluids
- Parkland formula commonly used to determine amount
[4 x (weight in kg) x (%body surface area burned (BSA)] = ml of fluid in 1st 24 hrs
the 1st half being given in the 1st 8 hrs
- ultimately, give enough to maintain 30cc of urine output/hr
maintain circulation
- escharotomy may be needed to prevent limb ischemia
Excision
- common to perform early but may need to wait until pt stable
- partial burns may be followed for 10-14 days to see what might regenerate before
excision
- 2 types:
fascial = done with scalpel and tissue excised down to fascia; easy with little
bleeding, and good graft adherence; disfiguring and may cause deceased
mobility
tangential = thin layers are removed until good tissue seen; better, allows more
salvage of partial burns but requires more skill
grafts
- full-thickness autograft excised from other part of body
Burns—Ch 11
45
- partial-thickness autograft with various depths of dermis; can be meshed to allowed
for more coverage
- allograft from cadaver can be used as a substitute but it is only temporary
Infection control:
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burns sterile for 1st 24-48 hrs
eschar is ideal media for bacterial/fungal growth and can lead to wound sepsis
immunosuppression following severe burn contributes to infection
silver nitrate-effective against staph/strep; mafenide acetate and silver sulfadiazine for
GN; increasing resistance of pseudomonas has been a problem
Nutrition:
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metabolism will increase to >2x normal after a burn with an increase in nitrogen excretion
enteral feeding superior to IV
protein goal of 1.5 – 2 g/kg body weight
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don’t wait until healed because scar causes contracture of tissue and can lead to
immobility
remodeling of tissue can occur for up to 1 year
tight-fitting anti-scar garments can help retard hypertrophy of scar tissue
Rehab
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I was also responsible for Chap 26. Looking over that chapter I did not see anything that
needed to be summarized. It just talks about things like how to scrub-in. The other procedures
section is mostly pictures, so if you wanted to flip through and just get a sense of what they
are I think that’s all you’d need.