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Reprinted from Caprini JA. Thrombosis risk assessment as a guide to quality
patient care. Dis Mon. 2005;51 (2-3):70-78. PMID: 15900257, with
permission from Elsevier.
Outpatient surgery is generally considered to be low risk for
VTE.
Recent risk stratification models have shown that a distinct,
high-risk subgroup exists within the generally low-risk
outpatient surgery population.
The risk stratification model shown below can predict 30day VTE risk and identify both low- and high-risk patients.
No data are available for VTE prevention among
outpatients.
The role of chemoprophylaxis remains unknown.
Unless a contraindication is present, all patients having
surgery under general anesthesia or IV sedation
should have SCDs placed.
ANESTHETIC CONSIDERATIONS
PECTORAL BLOCKS
Pectoralis nerve (PECS) block is a fascial plane block that
provides analgesia to the upper anterior chest wall, most
indicated for analgesia for breast surgery post-op. They are an
alternative to and more efficacious than paravertebral blocks for
breast surgery, as well as better pain scores and less opioid use
overall in post-op periods.
*PECS I block lateral pectoral nerve from C5 to C7 that
runs between pec major and minor and medial pectoral
nerve from C8 to T1 that runs deep to pec minor. Useful
for breast expanders, subpectoral prosthesis.
*PECS II block anterior and lateral divisions of the
thoracic intercostal nerves T2-T6, which run between
intercostal muscles and provides analgesia along long
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thoracic nerve (C5-C7) to the serratus anterior muscle
and thoracodorsal (C6-C8) to latissimus dorsi muscle.
Useful for extensive breast surgery/mastectomy
involving pec major and minor, serratus anterior
muscle, and the axilla.
LOCAL ANESTHETIC SYSTEMIC
TOXICITY
Signs/symptoms: prodromal symptoms of perioral
numbness/paresthesia’s/tinnitus, dizziness/confusion, tremors
followed by central nervous system seizures/loss of
consciousness followed by respiratory
depression/cardiovascular collapse
*Treatment for adult over 70 kg: lipid emulsion 20% 100 mL
over 2 minutes followed by 250 mL over 20 minutes (repeat
bolus/infusion if unstable).
LAST ACLS use less epi (<1 mcg/kg) and avoid local
anesthesia, calcium channel blockers/β-blockers, and
vasopressin.
Bupivacaine (Marcaine) toxic dose limit is 2.5 mg/kg.
Bupivacaine 0.25% allows for mL used to match the weight
(kg) of patient
A patient that weighs 70 kg may receive up to 70 mL of
bupivacaine
Bupivacaine 0.50% allow for ½ mL used to be half the
weight of patient
A patient that weighs 70 kg may receive up to 35 mL of
bupivacaine
Always confirm toxic doses with anesthesiologist before
injecting large amounts
Other local anesthetic toxic doses
Lidocaine: 4.5 mg/kg
Lidocaine with epinephrine: 7 mg/kg
Ropivacaine/tetracaine: 3 mg/kg
Chlorprocaine: 12 mg/kg
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MALIGNANT HYPERTHERMIA
Malignant Hyperthermia
Life-threatening reaction to certain anesthetic agents,
including volatile anesthetics and succinylcholine.
Uncontrolled increase in skeletal muscle metabolism due to
mutation in ryanodine receptor inherited in an autosomaldominant fashion.
The disorder exhausts oxygen and leads to rapid increase
in carbon dioxide overcoming the body’s ability to excrete.
*Initial signs can be an increase in end-tidal carbon
dioxide, masseter muscle rigidity, and
tachycardia/arrhythmia with temperature increase as a
late sign.
Left unchecked, circulatory collapse and death will occur.
*Appropriate treatment includes discontinuation of
offending agent, IV dantrolene 2.5 mg/kg, and cooling
treatment (ice-filled sponges, gastric lavage, cold
wound irrigation) in addition to cardiovascular support.
Monitor ABG/electrolytes, I/O balance, core temp, CVP, and
CK in ICU for 24 hours.
Patients with a personal or family history of malignant
hyperthermia should be referred to anesthesia
preoperatively.
PEARLS
1. “First do no harm.” Assess each surgical candidate for their
perioperative risk and treat/prophylaxis accordingly. Anesthetic,
endocarditis, cardiac, and VTE risks should be specifically
considered.
2. The most overlooked risk factor for VTE is a positive family
history.
3. Consider a PECS II block for extensive breast
surgery/mastectomies to improve patient’s postoperative
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1.
2.
3.
4.
recovery.
4. Lipid emulsion 20% is used emergently for patients with local
anesthetic systemic toxicity.
5. IV dantrolene 2.5 mg/kg is used emergently for patients with
malignant hyperthermia.
QUESTIONS YOU WILL BE ASKED
1. Which patient characteristics increase the risk for VTE?
Many factors are known to increase risk for perioperative VTE.
Major factors include cancer, central venous catheters, and a
personal or family history of VTE.
2. What options exist for prophylaxis against perioperative VTE?
The most important decision-making tool for prophylaxis is
appropriate risk stratification. Once risk has been quantified,
appropriate prophylaxis may include SCDs, early ambulation,
and/or chemoprophylaxis. Risk factor modification is also
important in the preoperative setting.
3. What is the appropriate treatment for patients suspected of
having malignant hyperthermia?
Appropriate treatment for malignant hyperthermia includes
removing the offending agent, administration of dantrolene, and
cardiovascular support as necessary.
Recommended Readings
Caprini JA. Thrombosis risk assessment as a guide to quality patient care. Dis
Mon. 2005; 51(2-3):70-78.
Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis.
Recommendations by the American Heart Association. Circulation.
1997;96(1):358-366.
Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on
perioperative cardiovascular evaluation and management of patients
undergoing noncardiac surgery: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation. 2014;130(24):e278-e333.
Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC focused update of
the 2014 AHA/ACC Guideline for the management of patients with valvular
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5.
6.
heart disease: a report of the American College of Cardiology/American Heart
Association Task Force on Clinical Practice Guidelines. Circulation.
2017;135(25):e1159-e1195.
Pannucci CJ, Dreszer G, Wachtman CF, et al. Postoperative enoxaparin
prevents symptomatic venous thromboembolism in high-risk plastic surgery
patients. Plast Reconstr Surg. 2011;128(5):1093-1103.
Pannucci CJ, Fleming KI, Bertolaccini C, et al. Optimal dosing of prophylactic
enoxaparin after surgical procedures: results of the double-blind, randomized,
controlled, fixed or variable enoxaparin (FIVE) trial. Plast Reconstr Surg.
2021;147(4):947-958.
*
Denotes common in-service examination topics.
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13
Cleft Lip
Gina N. Sacks
OVERVIEW
Cleft lip (CL) and cleft lip/palate (CLP) are the same entity along
a morphologic continuum (Fig. 13-1).
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Figure 13-1 The spectrum of cleft lip. A.
Microform unilateral cleft lip. B. Incomplete
unilateral cleft lip. C. Complete unilateral
cleft lip. D. Incomplete bilateral cleft lip. E.
Complete bilateral cleft lip with “flyaway”
premaxilla. F. Right complete cleft and left
incomplete cleft lip. (From Chung KC.
Grabb and Smith’s Plastic Surgery. 8th ed.
Wolters Kluwer; 2020. Figure 25.5.)
Variable extent of clefting of the primary palate occurs
(Fig. 13-1) in CL, including: upper lip, nasal floor (or nostril
sill), alveolus, and hard palate (anterior to incisive foramen).
May involve the secondary palate (posterior to incisive
foramen), and this combination is termed “cleft lip and
palate.”
EPIDEMIOLOGY
Incidence of CL with or without cleft palate
Caucasian ancestry: 1:1000 live births
Asian ancestry: 1:500 live births
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African ancestry: 1:2000 live births
Demographics
Male:female = 2:1
Left:right:bilateral = 6:3:1
*Risk of clefting in subsequent children
*If one child or one parent has CLP, there is a 4%
chance of subsequent clefting in successive
pregnancies
*If two children have CLP: 9%
*If one child and one parent both have CLP: 17%
ETIOLOGY
Most cases are sporadic, multifactorial, and no genetic cause is
identified
Risk factors
Fetal exposure to substances including phenytoin, EtOH,
steroids, phenobarbital, diazepam, and isotretinoin
Maternal smoking
Maternal diabetes
Parental age, especially advanced paternal age
Family history of clefting (see above)
CLP is syndromic in <15% of cases
Van der Woude syndrome
Most common syndrome associated with CL
Autosomal dominant, with variable penetrance. Due
to mutations in IRF6 gene
Associated with lip pits (accessory salivary glands)
May also have hypodontia (absent second molar),
syndactyly, abnormal genitalia, and popliteal pterygia
Waardenburg syndrome (sensorineural hearing loss, iris
pigment abnormality, hair hypopigmentation, and lateral
displacement of medial canthi)
Trisomy 21 (Down syndrome)
Trisomy 13 (Patau syndrome)
Trisomy 18 (Edward syndrome)
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EMBRYOLOGY/PATHOPHYSIOLOGY
*Cleft lip is caused by interrupted mesenchymal migration
and failure of fusion between the medial nasal process and
maxillary prominence
Neural crest cells are responsible for fusion of facial
prominences.
Critical developmental period: 4-6 weeks
Medial nasal processes fuse with maxillary prominences to
form philtrum and primary palate (failure causes CL).
Maxillary prominences become the lateral upper lip and
maxilla and secondary palate.
The two lateral palatine shelves that initially lie in a vertical
plane adjacent to the tongue move into horizontal plane and
fuse at midline along with the primary palate (failure causes
CP).
Nasal septum forms from fusion of medial nasal
prominences and grow downward to join the fused palatal
shelf.
CLASSIFICATIONS
Unilateral vs bilateral
Unilateral CL (Fig. 13-1A-C): divided into greater segment
and lesser segment
Lesser segment collapse, with medial and posterior
displacement
Bilateral CL (Fig. 13-1D-F)
Central prolabium and premaxilla
May have “flyaway” premaxilla (Fig. 13-1E) and
collapsed bilateral lesser segments
Variable severity per side (Fig. 13-1F)
More likely to be complete, wide clefts
Severity/extent (Fig. 13-1)
Microform CL (“forme fruste” or “minor cleft lip”; Fig. 13-
1A)
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