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Antibiotics can prove invaluable in the treatment of mastitis, but before you prescribe them, it's important to distinguish breast engorgement from infectious mastitis.
|Jump to:||Choose article section... Just how common is mastitis? Reviewing the pathophysiology Recognizing the risk factors Identifying the bacterial causes Diagnosing mastitis Managing the infection In conclusion Key points Coding for puerperal mastitis|
Antibiotics can prove invaluable in the treatment of mastitis, but before you prescribe them, it's important to distinguish breast engorgement from infectious mastitis.
If you've cared for many women with red, swollen, tender breasts, you're only too aware of how painful this problem can become. And if your practice includes many lactating patients, you also know how common it is: By some estimates, these signs and symptoms affect almost one in four women. Reports range from 2.9% to 24% of all lactating women, with the lower figures being based on studies involving clinical examination, and the higher rates derived from patients' self-reports.1-4
This wide range of statistics draws attention to the fact that some clinicians and researchers arrive at the diagnosis of mastitis based solely on the presence of erythema, edema, and breast tenderness and on patients reporting they had "breast infection."5 It's more accurate, however, to include fever in the diagnostic workup. Breast engorgement alone, which results from retention of milk in the ducts of the breast, can also cause edema, tenderness, and occasionally erythema but isn't accompanied by high fever.
Most cases of mastitis, whether related to lactation or not, occur sporadically. In general, we no longer see the epidemics that once occurred in crowded, multi-patient wards and with longer maternal and neonatal hospital stays. And although it's not uncommon for mastitis to recur in a lactating woman, a persistent or recurrent infection in a nonlactating woman should immediately prompt a clinician to consider inflammatory carcinoma of the breast as a diagnosis.
Our purpose here is to review the risk factors for mastitis, as well as its microbiology, and to summarize the best approach to diagnosis and treatment.
Arriving at accurate statistics is difficult for several reasons: Some researchers have based the diagnosis on prospective data while others have used a retrospective analysis of medical charts. As previously mentioned, some estimates have also been based on a clinical diagnosis of febrile disease while others include self-reported symptoms and no examination. It appears that up to one quarter of lactating mothers will develop symptoms of engorgement with swelling, tenderness, and even some erythema, but with a temperature at or below 99.8°F. Only 3% to 5% of nursing women will develop febrile mastitis.
Although it may be possible to distinguish engorgement from mastitis by self-reporting, I believe that a patient should be examined to determine the source of the fever, to obtain expressed milk for culture when infection recurs, and to advise the mother about the best approach to treatment.
Puerperal mastitis is an acute cellulitis with extension of the infection to the periglandular connective tissue (Figure 1). The infection extends into the connective tissue in a V-shaped area between lobes along the lactiferous apparatus of the breast (Figure 2). The cellulitis and stromal extension results in erythema of the skin, edema, and tenderness of the involved area of the breast, and with persistence of bacterial infection, eventually fever (Figure 3). Chills and myalgia often accompany fever.
How do bacteria infect a seemingly intact organ like the breast? While experts have yet to agree on the mechanism of action, failure to empty the breast during lactation and the resulting breast engorgement may contribute to the condition by plugging the milk ducts and causing stasis. That in turn may establish a nidus for infection if bacteria gain access to these ducts.
Nipple cracking and fissuring may also allow the mother's normal skin floraincluding staphylococci and streptococcito invade the nipple and ascend along the ducts. Similarly, the nursing infant's oropharynx can act as a source of potentially pathogenic bacteria, which in turn can ascend through cracked nipples and infect the breast.
Actually, mastitis probably results from a combination of these events. Not all mastitis patients have engorged breasts, although infection often causes a woman to feed less frequently and for shorter periods of time, resulting in milk retention. Not all mastitis patients have cracked nipples, but there is usually some site of irritation or break in the integument that allows the organisms to invade.
Thomsen and co-workers have subdivided mastitis into three categoriesmilk stasis, noninfectious inflammation, and acute mastitisbased on how the disease progresses (Table 1).6 They described milk stasis as an area of the breast where swelling and knots occur as the result of engorgement from the slowing of milk flow. The patient may feel warmth in the breast, the leukocyte count of the milk is less than 106/mL, the bacterial count is less than 103/CFU/mL and the symptoms usually last only a few days.
|Milk stasis||Noninfectious inflammation||Acute mastitis|
|Fever||Low grade (< 99.8°F)||Low grade ( <99.8°F)||High grade (>9.8°F)|
|Breast||Engorged, nodular||Tender, swollen, red, hot||Tender, swollen red, hot|
|Milk Leukocytes Bacteria||<10||>10||>10|
When milk stasis is persistent and marked, noninfectious inflammation may result. This process is characterized by edema, erythema, heat, pain, tenderness, and low-grade fever. Leukocytes in the milk number more than 106/mL but the bacterial count is usually less than 103 CFU/mL. When self-limited, the condition usually lasts for 5 to 6 days.
If the stasis and inflammation do not resolve, acute infectious mastitis may occur. Thomsen divides this state into two classes6:
Cellulitis is infection of the interlobular connective tissues that results from the introduction of bacteria through cracked or fissured nipples. The symptoms and signs include edema, erythema, pain, myalgias, chills, fever, and tenderness.
Adenitis occurs when one or more breast ducts are plugged and then infected. The clinical signs and symptoms are usually less severe, but suppuration is more common. Abscesses usually do not occur if nursing is continued. Pathogens may ascend through the lactiferous sinuses from a nipple fissure, with spread to the periductal lymphatics. Hematogenous spread may also occur.
While this classification is helpful, in practice the clinician must differentiate between stasiswith or without inflammationthat will respond to conservative therapeutic measures and infection that requires these same measures plus antibiotics. Once again, evaluation of the individual patient is key so it is not advisable to make the diagnosis over the phone based on a patient's self-report.
Women who have had mastitis during a previous pregnancy have a three- to fourfold increased risk with the current pregnancy.7,8,9 This may be related to the persistence of other risk factors, including poor hygiene, an altered immune system, or the propensity to develop cracked nipples. The latter is the most frequently reported risk factor in most studies (Table 2).3,8,9
Although not easily detected, blocking of the milk ducts has also been reported as a risk factor.9 Engorgement and milk stasis may result from incomplete emptying or decreased frequency of feeding, which allows the ducts to become plugged and presents bacteria with an ideal culture medium.
Fatigue and stress have also been linked to mastitis. When a mother is tired, she may not position her baby properly, which in turn can cause pulling on the nipple and subsequent cracking. In fact, improper positioning has been reported to be a major risk factor.10 Stress and fatigue can also affect a mother's nutrition and potentially her immune system, decreasing her resistance to infection.
HIV type I-infected women appear to have an increased risk for developing mastitis and those with a high viral load (median of 700 copies/mL) and mastitis have a significantly greater chance of transmitting HIV to their nursing infant.11
Other ancillary factors linked to the development of mastitis include manual breast pumps and breast creams, particularly papaya cream.8,9
Mothers should be instructed about proper "latching on" techniques and careful feeding when the infant begins teething. They should avoid suddenly changing the number and duration of feedings, breast trauma, and inadequate emptying of blocked ducts. Also warn patients to avoid tight-fitting bras. Breast shells used for flat or inverted nipples, although helpful, can increase the risk of milk stasis if worn while sleeping or for prolonged periods.
Many different bacteria have been isolated from the infected milk of women with acute puerperal mastitis including Staphylococcus aureus, staphylococcal species (coagulase negative), group B streptococci, Escherichia coli, Klebsiella pneumoniae, Streptococcus pneumoniae, and various anaerobes including Bacteroides fragilis and Prevotella bivius.
Mycobacterium tuberculosis and atypical mycobacteria have been recovered from patients with nonpuerperal mastitis but not from women with puerperal disease. Granulomatous mastitis often presents with an ill-defined mass effect and a biopsy must be performed to rule out a malignant process.12
In 1978, researchers alerted us to the fact that S aureus was the most frequent isolate from women with puerperal mastitis.13 Although others have recovered S aureus less frequently, it still remains the leading isolate in most reports.14 We isolated coagulase-positive and -negative staphylococci from 60% of our patients with puerperal mastitis.3
A separate study that evaluated 41 women with mastitis grouped by the outcome of bacterial cultivation of breast milk found that one group of 25 women tested positive for bacterial skin contaminants.15 The remaining 16 women had positive cultures for potentially pathogenic bacteria. There were no complications in the first group and all patients responded to conservative measures, including emptying of the breasts. Staphylococcus aureus was the most frequent isolate in the second group of women, who had a more severe and protracted illness that required antibiotics.
When quantitative cultures of human milk from women with clinically diagnosed mastitis have been performed, 106109 CFU of bacteria/mL of milk have been isolated. In spite of the presence of pathogenic bacteria, one study found that infants do not become clinically ill while continuing to nurse.16 This observation has led most experts to conclude that it is all right to allow infants to continue breastfeeding during infection, as long as an abscess is not present. Some infants, however, may reject the infected breast which leads to engorgement and worsening of the process. Therefore, the mother must ensure that the infected breast is emptied regularly.
Candidal species, principally albicans, frequently infect the skin on a woman's breast, the areolae, and nipples. These mothers present with severe erythema and irritation, but are usually afebrile. Be sure to rule out diabetes mellitus and HIV infection in these women. Not infrequently, the nursing infant will have oral candidiasis (thrush) and both mother and baby will require treatment.
To accurately diagnose postpartum fever requires a careful history and a comprehensive physical examination that includes the breasts. Most patients with puerperal mastitis present after discharge from the hospital. We have found that typically about 55 days go by from delivery until the onset of symptoms and the median duration of symptoms before a diagnosis is made is about 47 hours.3
The most frequent presenting symptoms are malaise, myalgia, fever, chills, and pain in the breast and axilla. The breast is swollen, indurated, erythematous, and so tender to palpation that patients frequently refuse examination. The skin is often taut and shiny. The erythema is in a V-shaped pattern, which corresponds to the lactiferous apparatus of the breast. Although bilateral disease has been reported in about 8% to 10% of patients, the condition is usually unilateral. Cracking or fissuring of the nipples has been found in 65% to 70% of patients.3,5 The mean white blood cell count at diagnosis will be 11,000 to 12,000.3
If the infection has progressed to abscess formation, there will be a tender, fluctuant mass present. Most of these women will have a higher temperature and white blood count and will appear more ill.
The diagnosis of puerperal mastitis can be made on clinical grounds. If your patient is suffering from persistent or recurrent disease, or has an abscess, obtain expressed breast milk for culture, as well as blood cultures, complete blood count, and other appropriate labs. To obtain milk for culture, the mother should be placed on her side, the nipple and areola cleaned with povidone-iodine, three to five drops of milk expressed and discarded, and then 1 to 2 mL expressed into a sterile, flushed tube for collection and transport to the laboratory. Cultures are reported in colony forming units per milliliter (CFU/mL). Milk may also be sent for analysis of sodium content; elevation (>60 meq/mL) is consistent with inflammation of the breast.
Encourage women with engorged breasts to empty them. If the infant cannot consume enough milk, recommend an atraumatic, hospital-grade, piston-type breast pump. Before nursing, the lactating mother should wash her hands carefully and gently clean the nipple and areola with a soft cloth and mild soap.
Examine the breasts to look for swelling, erythema, and heat. Examination is also key to determining if an abscess is present. When an abscess does occur, the mother will usually experience high fever (100°F103°F), chills, sweats, and a deep penetrating pain at the site. There may be discoloration of the overlying skin. Ultrasound may help to differentiate a galactocoele from a breast abscess if the diagnosis is uncertain.
When mastitis is diagnosed, several conservative measures should be introduced: the patient should continue nursing; empty the breasts; use warm, moist compresses on the involved area; increase rest and fluid intake, decrease salt intake; and use acetaminophen or a nonsteroidal anti-inflammatory agent for control of inflammation, pain, and fever (see Patient Information).
Antibiotics may speed recovery and should be used in the febrile patient. No single antibiotic is ideal for all patients, although an agent that will cover S aureus is usually prescribed. Studies have evaluated beta-lactamase-susceptible penicillins, penicillinase-resistant penicillins, cephalosporins, erythromycin, trimethoprim-sulfamethoxazole, and metronidazole.3,6,18 Several investigators have reported success using an antibiotic with less-than-ideal effectiveness versus S aureus.13,19 In a comparison of amoxicillin and cephalexin, however, both treatment failures (15.6%) and the only abscess (1 of 25) occurred in the amoxicillin group.3
In our most recent susceptibility testing from 779 isolates of S aureus, 57% were susceptible to a first- generation cephalosporin, 50% to dicloxacillin, 58% to amoxicillin/ clavulanate potassium, 69% to clindamycin, and 99% to trimethoprim/ sulfamethoxazole. Although the sensitivities to the most frequently used antibiotics are similar, it is sometimes difficult to find dicloxacillin in community pharmacies. Most pediatricians prefer that nursing mothers not use trimethoprim/sulfamethoxazole because it may aggravate physiologic jaundice. One of the agents listed in Table 3 would be my choice for antibiotic therapy. Cephalexin, dicloxacillin, and azithromycin are the least expensive of these antibiotics. Dosing should be adequate for obtaining satisfactory minimal inhibitory concentrations against the most frequent isolates. Anaerobic coverage is not essential unless an abscess is present.
In a recent report, 102 mastitis patients were treated with antibiotics with no treatment failures noted. There were recurrences of mastitis in 10.2% of the women. Twenty-six patients had abscesses and were successfully treated with antibiotics and aspiration (10) or incision and drainage (16). Abscesses were thought to result primarily from delays in diagnosis and therapy.20 Adequate drainage is key to the successful treatment of a breast abscess, which may occur in 4% to 12% of mastitis patients.3,16,19
If candidal cellulitis occurs, antifungal creams (azoles) are not as effective as oral fluconazole in a dose of 150 mg every other day for three doses. The infant should be treated for thrush by the pediatrician.
Although breastfeeding often causes breast engorgement and discomfort, acute, febrile mastitis occurs in only 3% to 5% of nursing mothers and 4% to 12% of those go on to develop an abscess.
Be certain to give all lactating mothers specific instructions about latching on and how to position a baby during lactation, breast hygiene, keeping breastfeeding sessions relatively short, emptying of the breast, and use of lanolin-only creams for nipple preparation. If symptoms of engorgement and early mastitis occur, encourage patients to report them immediately. This is best accomplished by a team effort that includes a lactation nurse, postpartum nurse, and physician.
The key to avoiding prolonged illness and abscess is early diagnosis by careful clinical examination and the use of moist compresses, anti-inflammatory agents, and appropriate antibiotic therapy, along with attention to breast emptying.
1. Kaufmann J, Foxman B. Mastitis among lactating women: occurrence and risk factors. Soc Sci Med. 1991;33:701-705.
2. Jonsson S, Pulkkinen MO. Mastitis today: incidence, prevention and treatment. Ann Chir Gynaecol Suppl. 1994;208:84-87.
3. Hager WD, Barton JR. The treatment of sporadic acute puerperal mastitis. Infect Dis Obstet Gynecol. 1996;4:97-101.
4. Fetherston C. Characteristics of lactation mastitis in a Western Australian cohort. Breastfeed Rev. 1997;5:5-11.
5. Vogel A, Hutchison BL, Mitchell EA. Mastitis in the first year postpartum. Birth. 1999;26:218-225.
6. Thomsen AC, Espersen T, Maigaard S. Course and treatment of milk stasis, noninfectious inflammation of the breast and infectious mastitis in nursing women. Am J Obstet Gynecol. 1984;149:492-495.
7. Riordan JM, Nichols FH. A descriptive study of lactation mastitis in long-term breastfeeding women. J Hum Lact. 1990;6:53-58.
8. Foxman B, D'Arcy H, Gillespie B, et al. Lactation mastitis: occurrence and medical management among 946 breastfeeding women in the United States. Am J Epidemiol. 2002;155:103-114.
9. Kinlay JR, O'Connell DL, Kinlay S. Risk factors for mastitis in breastfeeding women: results of a prospective cohort study. Aust N Z J Public Health. 2001;25:115-120.
10. Fetherston C. Risk factors for lactation mastitis. J Hum Lact. 1998;14:101-109.
11. Semba RD, Kumwenda N, Hoover DR, et al. Human immunodeficiency virus load in breast milk, mastitis, and mother-to-child transmission of human immunodeficiency virus type 1. J Infect Dis. 1999;180:93-98.
12. Memis A, Bilgen I, Ustun EE, et al. Granulomatous mastitis: imaging findings with histopathologic correlation. Clin Radiol. 2002;57:1001-1006.
13. Niebyl JR, Spence MR, Parmley TH. Sporadic (nonepidemic) puerperal mastitis. J Reprod Med. 1978;20:97-100.
14. Carroll L, Osman M, Davies DP, et al. Bacteriological criteria for feeding raw breastmilk to babies on neonatal units. Lancet. 1979;2:732-733.
15. Osterman KL, Rahm VA. Lactation mastitis bacterial cultivation of breastmilk, symptoms, treatment, and outcome. J Hum Lact. 2000;16:297-302.
16. Marshall BR, Hepper JK, Zirbel CC. Sporadic puerperal mastitis. An infection that need not interrupt lactation. JAMA. 1975;233:1377-1379.
17. Semba RD, Kumwenda N, Taha TE, et al. Mastitis and immunological factors in breast milk of lactating women in Malawi. Clin Diagn Lab Immunol. 1999; 6:671-674.
18. McGregor JA, Weifert MR. Maternal problems in lactation. In: Neville MC, Neifert MR, eds. Lactation Physiology, Nutrition and Breastfeeding. New York, NY: Plenum Press; 1983:333-348.
19. Devereux WP. Acute puerperal mastitis. Evaluation of its management. Am J Obstet Gynecol. 1970;108:78-81.
20. Dener C, Inan A. Breast abscesses in lactating women. World J Surg 2003;27:130-133.
Patients may present with puerperal mastitis within the typical postpartum period (6 weeks) or after they have been discharged from routine obstetrical care. The services provided are the same but the coding is slightly different.
Patients with signs and symptoms suggesting mastitis often return to see the obstetrician for evaluation. The visits are reported using established Evaluation and Management Services (E/M) codes since the patient has been seen in the practice within the last 3 years. The coding options are 99212-99215 depending on the extent of the history, physical examination, and the medical decision-making provided during the encounter. Two of these three areas, known as the key components, must meet or exceed the code requirements to qualify for a particular level of service. For example, the level of care may be determined by the extent of the history and medical decision-making without regard to the level of the examination.
The requirements for the E/M services for established patients are outlined in the table below. The level of service will depend on the severity of the condition and the difficulty in establishing the diagnosis. The evaluation of a patient with minimal symptoms and an expected history of present illness will likely result in a lower level of E/M service than that for the patient who has a more pronounced illness and requires more aggressive treatment.
|Not required||Problem- focused||Expanded Problem focused||Detailed||Comprehensive|
|Not required||Problem- focused||Expanded Problem focused||Detailed||Comprehensive|
|5 minutes||10 minutes||15 minutes||25 minutes||40 minutes|
In some instances, most of the office or hospital visit will be spent counseling the patient on conservative treatment measures and preventive nursing practices. According to CPT, "When counseling and/or coordination of care dominates (more than 50%) the physician patient and/or family encounter (face-to-face time in the office/outpatient setting or floor/unit time in the hospital...), then time may be considered the key or controlling factor to qualify for a particular level of E/M service..."
The level of service in these situations may be determined by the total amount of time spent with the patient rather than the extent of the key components. The nature and extent of the counseling must be documented in the medical record. The time requirements for each level of service are noted in the table. The time requirements do not have to be met when the level of service is determined by the key components.
All services required to evaluate and treat the patient with mastitisincluding visits and laboratory studiesshould be reported in addition to routine maternity care. If the patient is seen within the typical 6 week postpartum period, then modifier 24 (Unrelated E/M Service by the Same Physician During a Postoperative Period) should be appended to the appropriate E/M code. This signifies to the payer that the service is outside that normally provided in uncomplicated maternity care. The modifier is not necessary if the patient is seen beyond the typical 6-week antepartum period.
Infections of the breast and nipple associated with childbirth are reported using ICD-9 CM codes in the 675 series. The options are:
675.0 Infection or abscess of the nipple
675.1 Abscess of breast (purulent mastitis)
675.2 Nonpurulent mastitis
One of the following fifth-digits must be added to designate the current episode of care:
0 unspecified as to episode of care or not applicable
1 delivered, with or without mention of antepartum condition
2 delivered, with mention of postpartum complication
3 antepartum condition or complication
4 postpartum condition or complication
An ICD-9 code from the 611.7 series (signs and symptoms in the breast) should be used to report services to patients presenting with breast complaints but who are not diagnosed with mastitis. Codes for generalized signs and symptoms can be found in the 780799 series of codes in ICD-9-CM.
If you have symptoms that suggest you have mastitis, you'll need to heed the following advice:
Continue breastfeeding, starting on the affected side.
If your baby doesn't feed well or will not feed on the affected breast, empty the breast using a piston-type, hospital breast pump.
If possible, remain in bed for the first 48 hours.
Drink more fluids.
Reduce your salt intake.
Take acetaminophen or ibuprofen to reduce fever and discomfort so milk letdown will occur and the breast can be emptied.
Apply moist heat to speed up milk letdown and ease soreness; cool packs may be used initially to decrease swelling.
Apply gentle massage to move the milk forward and increase drainage from the infected area.
Avoid breast shells and tight-fitting bras.
Avoid tight clothing and underwire bras.
Wash your hands before handling the infected breast.
Lanolin creams may be used to treat nipples. Your physician may prescribe medication if you develop a fungal infection of the nipple.
Make sure your baby is in a comfortable nursing position that does not pull excessively on your nipple; if necessary, talk to a lactation consultant to evaluate your nursing technique.
If you have a fever, the doctor may prescribe antibiotics for 7 to 10 days.
Schedule a follow-up appointment in 7 days so that the doctor can check for an abscess. If your symptoms don't respond within 48 hours of antibiotic treatment, notify the physician.
W. Hager. Cover Story: Managing mastitis. Contemporary Ob/Gyn Jan. 1, 2004;49:32-47.