A 1-year-old sexually intact female domestic shorthair cat weighing 3.6 kg (7.92 lb) was evaluated because of a 5-day history of grossly enlarged mammary glands, difficulty nursing, anorexia, and signs of progressive discomfort. The cat had delivered 3 kittens 7 days earlier. During the first 1 or 2 weeks of the cat's pregnancy, the owner had noticed the mammary glands were much larger than usual and were firm and cool to the touch. Ulceration of the skin covering the glands was noticed in late pregnancy. After parturition, the mammary glands changed in shape and increased in size, and the area of skin ulceration also grew. The kittens reportedly nursed at the 2 most cranial (ie, the thoracic) mammary glands only.
When admitted to the hospital, the cat appeared thin (body condition score, 3/9) and was judged as 5% to 7% dehydrated on the basis of tacky oral mucus membranes and mildly delayed skin-tent response. Two of the kittens appeared bright, alert, and responsive, but the third was weak with obtunded mentation. Physical examination of the cat revealed mild tachypnea (60 breaths/min; reference limits, 16 to 40 breaths/min) and hyperthermia (rectal temperature, 41.3°C [106.3°F]; reference limits, 38.2° to 38.8°C [100.8° to 101.8°F]). Systemic arterial blood pressure was 118 mm Hg as determined by use of Doppler ultrasonography.
All other findings were unremarkable except for the mammary glands. All 8 mammary glands were enlarged: both inguinal, all 4 abdominal (caudal and cranial), and both thoracic glands. The inguinal mammary glands were the most severely affected and measured 10 to 12 cm in diameter. The cranial and caudal abdominal glands were asymmetric and measured 8 to 10 cm in diameter. The thoracic mammary glands were also asymmetric, with the diameters of the left and right glands measuring 3 to 4 cm and 2 to 3 cm, respectively. The inguinal and cranial and caudal abdominal glands had prominent dilated veins and were firm, fluctuant, and hot to the touch. The skin of the mammary glands was markedly stretched and had a thin, fragile appearance. Multiple pockets of fluid could be seen and palpated through the skin, and skin ulceration was evident around the nipples. An oval area of skin approximately 5 cm long and overlying the right caudal abdominal mammary gland was black with purple edges and was hard and cool to the touch. A 2-cm area of skin with a similar appearance was evident over the right inguinal mammary gland. The right thoracic mammary gland was normal in appearance, whereas the left thoracic mammary gland was mildly enlarged in comparison. Signs of discomfort were evident during ambulation and during palpation of the mammary glands.
Examination of a lateral survey radiograph disclosed a homogeneous fluid opacity in the 3 caudal pairs of mammary glands. The body wall appeared intact, and no radiographic abnormalities were detected in the thorax and abdomen. A blood sample was collected and submitted to a private laboratory for a CBC and serum biochemical analysis. Results of the CBC included leukocytosis (18.0 × 109 WBCs/L; reference limits, 4.0 × 109 WBCs/L to 16.0 × 109 WBCs/L) and neutrophilia (13.86 × 109 cells/L; reference limits, 2.70 × 109 cells/L to 10.56 × 109 cells/L), with an increase in the number of band cells (2.16 × 109 cells/L; reference limits, 0.00 × 109 cells/L to 0.10 × 109 cells/L) with moderate toxic change as well as lymphopenia (1.08 × 109 cells/L; reference limits, 1.77 × 109 cells/L to 6.56 × 109 cells/L). The cat was anemic (4.6 × 1012 RBCs/L; reference limits, 6.3 × 1012 RBCs/L to 10.8 × 1012 RBCs/L), with a low Hct value (23%; reference limits, 32% to 49%), low hemoglobin concentration (70 g/L; reference limits, 104 to 160 g/L), and low mean RBC hemoglobin concentration (303 g/L; reference limits, 306 to 352 g/L). A few Döhle bodies were detected, and moderate echinocytosis was evident, with a reticulocyte count < 1%. Platelets were clumped but adequate. Results of serum biochemical analysis revealed a low serum creatinine concentration (55 μmol/L; reference limits, 71 to 203 μmol/L) and low alanine aminotransferase activity (26 U/L; reference limits, 28 to 76 U/L).
On the basis of the cat's history, clinical findings, and laboratory results, a presumptive diagnosis of mastitis with abscessation of mammary glands and early sepsis was made. Because of the history of mammary gland enlargement beginning in early pregnancy, an underlying disease process was suspected; mammary neoplasia and FAH were considered possibilities. Given the cat's age and disease progression, neoplasia was deemed less likely. Surgical drainage and drain placement in the abscessed mammary glands, debridement of necrotic tissues, and antimicrobial treatment were pursued.
In preparation for surgery, a catheter was inserted in a cephalic vein and hydromorphonea (0.05 mg/kg [0.023 mg/lb]), midazolama (0.15 mg/kg [0.068 mg/lb]), and cefazolina (22 mg/kg [10 mg/lb]) were administered IV. Intravenous administration of replacement fluidsb was initiated preoperatively at twice the maintenance rate (4.4 mL/kg/h [2 mL/lb/h]). The cat appeared considerably more comfortable after hydromorphone administration. Anesthesia was induced with propofolc and maintained with isoflurane (1.25% in oxygen), and the cat was positioned in dorsal recumbency for the procedure.
Stab incisions were made in the most dependent portion of affected mammary glands, taking care to avoid any blood vessels, the nipples, and areas of ulcerated skin. A closed suction system was used to drain a large amount of milky-white, flocculent, malodorous, seropurulent fluid from the inguinal, caudal abdominal, and cranial abdominal mammary gland pairs. All affected mammary glands contained multiple, asymmetric fluid-filled compartments separated by thin fibrous septae. The number of pockets ranged from 3 to 6/gland, and there was marked variation in size. The septae between compartments were perforated by blunt dissection through the original incision, and fluid was drained. The previously described area of necrotic skin over the right caudal mammary gland was deemed nonviable. The skin and underlying cutaneous musculature were resected en bloc. No grossly normal mammary glandular tissue was evident in the 3 caudal mammary gland pairs.
After drainage, the abscess sites were copiously lavaged with sterile saline (0.9% NaCl)b solution. A 0.64-cm Penrose draind was placed to exit through a new incision in each of the affected mammary glands. The left thoracic mammary gland was incised with a stab incision, but no fluid was observed. All skin incisions were closed with a cruciate interrupted pattern by use of 3-0 polypropylene suture.e The right thoracic mammary gland was not surgically explored.
The abdominal wall was inspected at all incision sites and appeared intact and healthy. An enlarged (3-cm) axillary lymph node was encountered during drainage of the left cranial abdominal mammary gland. The gland had a speckled appearance with miliary, cream-colored foci that had the macroscopic appearance of microabscesses. Because of owner financial limitation, no sample of the lymph node was obtained for histologic evaluation.
The cat's body weight after the mammary abscesses were drained was 2.9 kg (6.38 lb), which represented a reduction of 0.7 kg (1.54 lb) from the weight recorded at admission. No clinically important loss of blood was observed during the surgery. Taking into account the volume of fluids received during the 2-hour surgery (10 mL/kg [4.5 mL/lb]), the estimated volume of fluid removed from the abscessed mammary glands was 832 mL.
Recovery from anesthesia was without incident. After surgery, the cat received meloxicam (0.1 mg/kg [0.045 mg/lb], SC) and a second dose of cefazolin and was subsequently managed with amoxicillin–clavulanic acidf (62.5 mg, PO, q 12 h for 7 days) and buprenorphinea (0.02 mg/kg [0.009 mg/lb], PO, q 8 h for 2 days). Hot packs were applied to the mammary glands every 8 hours for 12 days. A small amount of discharge collected in the drains. Rectal temperature decreased to 39.5°C (103.1°F) within 12 hours after surgery. After anesthetic recovery, the cat was bright, alert, and responsive. It was discharged 36 hours after admission. The kittens were fed milk replacement formula, and 2 of 3 survived.
Follow-up care was provided at another hospital. Drains were removed 5 days after placement, at which time a small amount of milky discharge was observed. Enrofloxacing (5 mg/kg [2.23 mg/lb], PO, q 24 h for 7 days) was added to the treatment regimen by the attending veterinarian. Eighteen days after the initial evaluation, the mammary glands were reportedly normal in gross appearance and no abnormal findings were detected during palpation. The owner was contacted 3 weeks after the cat was discharged from the hospital and reported a high degree of satisfaction with the health of the cat and the surviving kittens.
Discussion
Fibroadenomatous hyperplasia, also described as fibroepithelial hyperplasia, is a progesterone-induced proliferation of the epithelium of mammary gland ducts and benign stromal proliferation that is manifested as marked, generalized enlargement of 1 or more mammary glands.1,2 The condition reportedly develops in young queens during early pregnancy, pseudopregnancy, or after receipt of progestogen injections. It can also develop in male cats treated with progesterone, particularly megestrol acetate.1–4 Results of studies5,6 in dogs suggest that progesterone stimulates a local release of growth hormone and insulin-like growth factors in mammary glands, which can cause tissue hyperplasia. The age of the cat reported here, its reproductive status, and its history of developing a marked degree of mammary hyperplasia in the first 2 weeks of pregnancy are all consistent with a diagnosis of FAH.
Mammary hypertrophy in early pregnancy with no corresponding clinical signs is not characteristic of mastitis. Mastitis is an uncommon condition in cats, usually developing in the periparturient period and often developing in association with trauma to the mammary glands.7 Common clinical signs include swollen, firm mammary gland tissue; ulceration; anorexia; cachexia; pyrexia; abnormal glandular discharge; and hungry or weak kittens. In cats with severe mammary hypertrophy, abscessed mammary glands can develop.7,8 Skin ulceration secondary to FAH has been described3,4 and is likely to have contributed to the development of mastitis in the cat reported here. The fact that the kittens were only able to nurse at the thoracic mammary glands suggested that release of milk was also affected. Skin trauma and altered lactation create an ideal environment for an ascending infection.8
Exogenous progesterone administration in cats has been implicated in the development of mammary neoplasia as well as FAH.9 Therefore, it is important to recognize that FAH is a clinical syndrome caused by an exaggerated tissue response to circulating hormones rather than the loss of regulation of cell growth that characterizes neoplasia.2,10,11
Two approaches to managing FAH have been described: control of underlying hormonal stimulation and ablation of the target tissues. Medical treatment with the progesterone-receptor antagonist aglepristone has been used successfully to resolve the clinical signs of FAH. In 2 studies, 7 of 7 cats12 and 21 of 22 cats13 with FAH had improvement after 1 to 4 weeks of SC administration of aglepristone. The incidence of reported adverse effects was low and included transient pruritus at the injection site, abortion in pregnant queens, and sudden death attributed to acute heart failure and pulmonary arterial thrombus (1 cat). Two cats were pregnant at the time of treatment and aborted their litters 2 to 5 days after the first injection. Both cats subsequently developed endometritis secondary to incomplete emptying of the uterus but were successfully treated with ovariohysterectomy.13 Fibroadenomatous hyperplasia can redevelop when aglepristone treatment is discontinued but progestin treatment is continued,13 suggesting a multimodal approach may be needed to achieve permanent resolution of this condition. Because of the role of progestins in the development of FAH and the progestin-sensitizing effect of estrogen on mammary tissues,2 ovariohysterectomy has been recommended as a stand-alone treatment or as an adjunct to other approaches. However, data regarding the effectiveness of ovariohysterectomy as a stand-alone treatment are conflicting. Resolution of clinical signs after ovariohysterectomy has been reported,2–4 but results of other studies4,13 suggest ovariohysterectomy is not effective on its own.
Removal of the affected mammary glands by mastectomy has been recommended as the surgical treatment of choice for FAH,3,13,14 but redevelopment of FAH in untreated glands has been reported.12,14 The condition can also spontaneously regress in some situations,2 although the reason for spontaneous regression has not been identified. These findings suggest that the removal of the underlying source of progesterone is important in achieving long-term resolution of FAH.
In the cat reported here, a marked improvement in clinical status was achieved within 12 hours after admission by following the basic principles of abscess management (ie, drainage, debridement, and appropriate antimicrobial treatment). Ideally, choice of antimicrobials should be based on the results of bacterial culture and antimicrobial susceptibility testing, but in cats with impending sepsis, empirical selection of an antimicrobial is warranted until laboratory results are received.8 The cat's owner had financial concerns that precluded performance of bacterial culture and susceptibility testing, so a broad-spectrum antimicrobialf with a label claim for abscess treatment was used.
Resolution of the clinical signs of FAH after discharge from the hospital may have been attributable to a combination of 2 factors: disruption of mammary tissue by severe abscessation and change in the cat's hormonal status after parturition. Given the limited understanding of this disease, it is impossible to predict the degree to which either of these factors contributed to resolution of FAH or the probability of redevelopment. Ovariohysterectomy and subsequent cessation of progesterone administration were recommended to minimize the risk of recurrence.13 In the author's opinion, it is inadvisable to use a queen that has had FAH for breeding purposes because of the possibility of disease recurrence and because there may be a heritable component to the condition. To the best of the author's knowledge, no studies have been conducted to examine the heritability of FAH, which would be an interesting topic for investigation.
The method of managing abscessation and mastitis secondary to FAH reported here led to a rapid improvement of the clinical status in the affected cat and prevented further progression to sepsis. Treatment by surgical drainage may be used as a less invasive alternative to mastectomy in managing queens with mastitis and abscessation secondary to FAH.
ABBREVIATION
| FAH | Fibroadenomatous hyperplasia |
Sandoz Canada, Boucherville, QC, Canada.
Normosol-R, Baxter, Mississauga, ON, Canada.
Abbott Laboratories, Vancouver, BC, Canada.
Covidien, Saint-Laurent, QC, Canada.
Prolene, Johnson & Johnson, Calgary, AB, Canada.
Clavamox, Pfizer Animal Health, Pointe Claire, QC, Canada.
Baytril, Bayer, Toronto, ON, Canada.
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