Self Study:Book Chapter Review Notes.

Surgery of The Breast Principles and Art Ed. Scott Spear
Chapter 33. Prosthetic Reconstruction in the Radiated Breast.

Prosthetic breast reconstruction in the radiated breast is a complex issue.

-Radiated reconstructions tend to be of poorer quality than non-radiated reconstructions.
-Radiation increases the complication rates associated with reconstructive options
-Not all radiation is the same.


The dose, location, type, and purpose of radiation substantially affects the local tissue response and thus indirectly the hospitality of those tissues to reconstructive surgery.

Radiation may be delivered to the breast under a variety of circumstances:

-As part of breast conservation treatment, along with lumpectomy and axillary sampling.
-Postmastectomy, according to the American Society of Clinical Oncology Guidelines
-Postmastectomy for a local recurrence.
-After immediate reconstruction for unfavorable tumor
-After immediate or delayed reconstruction for recurrence

If radiation prior to reconstruction:

Indications
Dose of radiation
Quality of tissues after radiation

Lumpectomy and radiation often 5,000 cGY
Patients radiated after mastectomy more likely high-dose radiation because radiation recommended on basis of extensive or aggressive disease.

Lower dose radiation: tissues look and feel reasonably normal
Higher dose radiation: tissues look tight, inelastic, thickened.

All radiation increases risk of complications.
Obvious radiation damage advised to undergo autologous or autologous assisted types of reconstruction.

Indications for radiation by American Society of Clinical Oncology:

Tumor greater than 4 cm.
4 or more positive lymph nodes
Tumor near resection margins (skin or chest wall)

Radiation dose for these indications is usually substantial 9,500 to 10,000 cGy.

Breast Reconstruction Post-Op Protein Requirements.

Proper nutrition should be an important part of everyone's daily life. Both aesthetic and reconstructive surgery place an increased metabolic demand on the body. It is important both pre-operatively and post-operatively to ensure adequate protein intake before and after surgery. Frequently nutrition comes up in consultations, so I have included below a standard post-operative diet protocol as well as an easy method for patients to understand the amount of protein they will need post operatively.

The post-operative diet below is for tissue expander/implant reconstruction. It is modified for TRAM, DIEP, and SIEA reconstructions.

Post-Operative Breast Reconstruction Diet Protocol Pathway

Post-Op Day 0

Clear Liquid Diet as Tolerated.

Post-Op Day 1

Regular Diet. Ensure 1 can three times per day between meals.

Post-Op Day 2

Regular Diet. Ensure 1 can three times per day between meals.

Discharge Diet:

Breast reconstruction surgery is very energy consuming to the body. There is also protein loss from drain output. It is important to maintain a high protein diet for two to three weeks post-operatively to maximize healing.

Regular Diet high in protein + Ensure three times/day between meals.

Goal is to eat 1 gram of protein per kg of bodyweight:

For example, if your body weight is 140 lbs, then your weight in kg is 140/2.2 or 63 kg. Therefore, patient with normal renal and liver function should eat at least 63 grams of protein per day.

Ensure 1 can: 9 grams of protein
Glucerna 1 can : 10 grams of protein

Therefore, three cans give you 30 grams of protein.

1 can of tunafish contains approximately 25 grams of protein.

or

1 chicken breast contains approximately 30 grams of protein.

Breast Reconstruction Post-Op Pain Protocol

Post-operative patient comfort is of paramount importance in breast reconstruction following mastectomy. Controlling pain can be challenging for both the patient and surgeon. The patient's goal is to have a pain score of close to zero. While this is also the surgeon's goal, many of medications used to treat pain may contain their own inherent undesirable sequelae such as nausea, vomiting, insomnia, hives, disorientation, etc.

I have found that using several different medications that work on slightly different pain receptors or that have slightly different pain targets to be the most effective. I have posted the following pain protocol pathway that I am currently using so that patients can know what to expect during their hospital stay. If significant side effects occur from the pathway or the pathway is not effective, adjustments can be made accordingly based on age, allergies, weight, and renal function.

Pre-operatively:

Emend 40 mg by mouth with a sip of water the morning of surgery to prevent nausea.

In Hospital Pain Regimen:

Post-Op Day 0:

Toradol: Loading Dose 30 mg IV x 1 then:
Toradol: 15 mg IV 4 times per day x 48 hours.
Dilaudid PCA pump. PCA. Patient controlled analgesia. 0.2 mg IV every 6 minute lockout for max of 2 mg/hr.
Diazepam 5 mg by mouth every 6 hours as needed for muscle spasms (tissue expander reconstruction)

Post-Op Day 1:

Continue Toradol 15 mg IV 4 times per day
Dilaudid PCA pump. PCA Patient controlled analgesia for ½ day with transition to:
Percocet 5mg/325mg i-ii tabs by mouth every 4 to 6 hours as needed.
Diazepam 5 mg by mouth every 6 hours as needed. (tissue expander reconstruction)
Colace 100 mg by mouth twice a day.

Post-Op Day 2:

Discontinue Toradol IV and transitio to Toradol Oral 10 mg po qid
Percocet 5mg/235 mg i-ii tabs by mouth every 4 to 6 hours as needed.
Diazepam 5 mg by mouth every 6 hours as needed. (tissue expander reconstruction)
Colace 100 mg by mouth twice a day.

Discharge Medications Home:

Percocet 5/325 mg i-ii tabs by mouth every 4 to 6 hours as needed.
Diazepam 5 mg by mouth every 8 hours as needed. (tissue expander reconstruction)
Ambien 10 mg by mouth at night as needed for sleep.
Colace 100 mg by mouth twice a day.

Brian P. Dickinson, M.D.

www.drbriandickinson.com

Microsurgery Notes

Recipient Vessels Veins:

1. Internal Mammary-3rd rib.
2. Internal Mammary – 2nd rib
3. External Jugular
4. Brachiocephalic
5. Thoracodorsal*

Diameters of Deep Inferior Epigastric Vessels- 2.5 mm
Pedicle Length- 5 cm

Coupler: Mobile to non-mobile (or)
Coupler: Diameter to be shortened 1st to match size discrepancy.

Perforator Flap (Venous Flow). Perforator Decision Tree

Palpable Pulse, No Venous Signal: +++
Arterial Signal, Venous Signal: +
No Arterial Signal, Venous Signal: ---

Harvest of DIEP Flap:

Vein
Artery
Vein

Anastamosis Clamps Off:

Venous Anastamosis
Arterial Anastamosis

Fill Test, Reflow Test

Doppler-Venous Augmentation Test

Self Study:Book Chapter Review & Reading Notes

Chapter 4: Pathology of Breast Disorders

Functional unit of the breast is the terminal ductal lobular unit.

The entire lobular and ductal structure of the breast is lined by two layers of cells:the inner epithelial layer and the outer myopepithelial layer.

“Breast cancer” typically refers to breast carcinoma that arises by preferential growth of the inner epithelial layer.

Benign Disorders:

Fibrocystic change-pathologic condition that correlates with ‘lumpy’ breasts.

This term is applied to a plethora of benign changes in the breast, which are best categorized based on the subsequent risk of development of breast carcinoma.

Three categories:

Non-proliferative lesions:
Proliferative lesions without atypia
Atypical hyperplasia

Nonproliferative Lesions

This is the most common category of breast disorders and includes cysts, papillary apocrine change, mild hyperplasia of the usual type, and epithelial-related calcifications.

Women with these lesions do not incur a higher risk of development of breast carcinoma than that of women who had no breast biopsy (relative risk, 0.89)

Proliferative Lesions without Atypia

Women with these lesions have a slight risk of developing breast carcinoma, 1.5 to 2 times greater than the general population. This category includes moderate or florid hyperplasia of the usual type, sclerosing adenosis, small duct papillomas, and fibroadenomas.

Sclerosis adenosis is the most common lesion and refers to expanded lobular units with a proliferation of both acini and intervening stroma. Microcalcifications are frequently seen and correspond to “benign calcifications” seen on mammography.

Atpical Hyperplasia

Atypical hyperplasia confers a risk of development of breast cancer that is 3.5-5 times that of the reference population. This category includes both atypical ductal hyperplasia (ADH) and atypical lobular hyperplasia (ALH).

Radial Scars and Complex Sclerosing Lesions

Radial scars are typically small areas of scarring (less than 1 cm) surrounded by glandular elements.

Benign Neoplasms

Fibroadenoma

Fibroadenomas typically present as painless, mobile, rubbery masses. They are usually solitary but occasionally multiple. Most often present in the upper-outer quadrant and slightly more common in the left breast.

Solitary (Large Duct) Intraductal Papilloma

These tumors typically arise in a large duct in the subareolar region and present with unilateral hemorrhagic discharge.

Phyllodes Tumor

Character may be benign to malignant. Phyllodes tumors tend to have local recurrences and should be widely excised.

Lobular Carcinoma in Situ (LCIS)

LCIS is a rare multicentric entity that can not be identified clinically or on gross examination.

The invasive carcinoma that may develop may be either ductal or lobular.

LCIS is more common in younger, premenopausal women, and the mean age of diagnosis is 44 to 46 years.

LCIS is commonly bilateral and multicentric (present in more than one quadrant).

LCIS is typically an incidental finding in a breast biopsy done for a mammographically detectable lesion, which may be calcifications in adjacent sclerosing adenosis or other proliferative lesions.

Estrogen receptor (ER) is typically over expressed in cells of LCIS, whereas Her-2/neu is not. E-cadherin is a useful marker to distinguish lobular and ductal proliferations because it is preferentially expressed in ductal proliferations.

Most women with LCIS do not develop invasive carcinoma on follow-up, but it does confer a relative risk from 6.9 to 12. The carcinomas that develop are mostly invasive ductal carcinoma.

LCIS is best considered to be a risk factor rather than a precursor of invasive carcinoma. Thus, the surgical management of LCIS does not aim for negative margins, and radiation therapy has no role in management of LCIS.

Ductal Carcinoma in Situ

Ductal carcinoma in situ (DCIS) comprises lesions in which the neoplastic growth of ductal cells is restricted within the ductal system.

DCIS is considered to be a direct precursor of invasive carcinoma.

The incidence of carcinoma in patients with DCIS varies from 11% to 53% and occurs in the ipsilateral breast.

Mammographic abnormalities, which commonly show microcalcifications, are the most common presentation of DCIS.

Comedo DCIS refers to central necrosis in the ducts that are lined by poorly differentiated cells. Comedo DCIS is invariably associated with calcifications.

Comedo necrosis was the only factor found to correlate with ipsilateral recurrence in a multivariate analysis of nine histologic features of DCIS.

The distinction between LCIS and DCIS can usually be made with E-cadherin staining. E-cadherin shows no staining in lobular proliferations.

Low Grade DCIS tends to be ER and PR positive and Her2/neu negative.
High Grade DCIS tends to be ER/PR positive and Her2/neu positive.

Tamoxifen decreases recurrence rates in patients with DCIS.

DCIS specimens should be inked for margins. In NSABPB-17, only the presence of a tumor-filled duct in contact with the inked margin was categorized as a positive margin.

Silverstein et al. showed that quantification of the distance of DCIS from the margin is useful, and greater than 1 cm is deemed to be a negative margin.

Paget’s Disease of the Nipple

Association of eczematous changes in the nipple with underlying mammary carcinoma. Paget’s disease of the nipple refers to the extension of underlying breast cancer to the skin of the nipple.

Paget’s disease presents as scaling and erythema of the nipple-areola complex.

95% of cases of Paget’s have underlying carcinoma, invariably ductal, and often associated with comedo-type DCIS.

Immunohistochemical stains are useful to distinguish Paget’s from melanoma and clear cells of the epidermis.

Her2/neu, epithelial membrane antigen, and polyclonal CEA are expressed in Paget’s CK 7 is positive in both Toker cells and Paget’s disease.