Bitches and queens should deliver in a familiar area where they will not be disturbed. Unfamiliar surroundings or strangers may impede delivery, interfere with milk letdown, or adversely affect maternal instincts. This is especially true in young or primiparous animals. The dam's apprehension or nervousness may subside in a few hours, but in the meantime the neonates must receive colostrum and be kept warm.

A nervous dam may ignore the neonates or give them excess attention. She may lick and bite at the umbilical stump, causing hemorrhage or damage to the abdominal wall that may lead to evisceration. Excess grooming of the neonate may prevent it from nursing. If the dam's maternal instincts fail, she may assume sternal recumbency and not allow nursing, or leave the neonates unattended. It is not unusual for the dam to pick up the pups and to rearrange them in the box, especially after delivery of each pup; however, she should then assume the normal nursing position.

The principal metabolic disease associated with pregnancy is puerperal hypocalcemia (see Disorders of Calcium Metabolism: Puerperal Hypocalcemia in Small Animals). It is rare in cats and most common in dogs weighing <20 kg, exacerbated by improper perinatal nutrition (excessive calcium/phosphorus supplementation or an imbalanced prenatal diet).

Common inflammatory diseases in the postpartum period include metritis and mastitis. Retention of a placenta or its remnants usually leads to metritis. Signs include continued straining as if in labor, the presence of a fusiform mass associated with the uterus best identified by ultrasonographic evaluation, abnormal vulvar discharge, fever, and lethargy as the infection develops. If given within 24 hr of labor, oxytocin may cause passage of the placenta; if oxytocin is ineffective, prostaglandin F_2α (0.1 mg/kg, SC, every 12–24 hr) or cloprostenol (1–3 μg/kg, SC, every 12–24 hr to effect) can usually induce passage of the placenta.

Mastitis (see Reproductive Diseases of the Female Small Animal: Mastitis in Small Animals) is more common in bitches than in queens. The bacteria associated with mastitis tend to be coliforms or Staphylococcus spp. Galactostasis can predispose bitches to mastitis, as can excessive human manipulation of the mammary glands.

Significant postpartum uterine hemorrhage is rare. Treatment with ergonovine (15 mg/kg, IV) may be tried; if it fails to stop the hemorrhage, ovariohysterectomy must be performed. An underlying coagulopathy should be suspected.

Uterine subinvolution results in hemorrhagic spotting for >12–16 wk (the normal period of involution in the bitch). Treatment is unnecessary unless blood loss is significant because the condition resolves spontaneously. Future fertility is unaffected.

Agalactia (other than that caused by severe illness) is uncommon in dogs and cats. Determination that lactation is adequate should be performed before elective cesarean section. If an emergency cesarean section is required, regardless of the status of lactation, intervention is indicated (see below). Bitches and queens with inadequate lactation at term should be thoroughly evaluated for metabolic or inflammatory disorders (metritis, eclampsia, mastitis), as well as for nutritional and hydration status, and treated appropriately. Evaluation of a hemogram, serum chemistries, vaginal discharge, and ultrasonographic evaluation of the uterus may be required. The normal presence of colostrum (typically not copious) should not be confused with agalactia. The level of neonatal contentment and daily weight gain (after the first 24 hr) indicates adequate lactation. Milk letdown is promoted by oxytocin release, a reflex triggered by nursing, therefore neonates must spend adequate time suckling. Disruption of the pituitary-ovarian-mammary gland axis can result in idiopathic agalactia. Agalactia can be associated with premature delivery of neonates.

Because estrogen promotes lactogenesis, the adequacy of mammary development should be assessed before removal of the ovaries at cesarean section. Ovariohysterectomy should not have a negative effect on bitches and queens with adequate lactogenesis at term. If this is seen, a genetic component may be involved.

Lactation can be stimulated if treatment is prompt. Mini-dose oxytocin (0.5–2.0 U/dose, SC, every 2 hr) should be administered. The neonates should be removed from the dam before each injection and returned 10 min later. The neonates should be supplemented adequately to ensure survival, but not excessively, so that they will suckle vigorously. Gentle hand stripping of the mammary glands should take place if suckling is not vigorous. Concurrent administration of metoclopramide (0.1–0.2 mg/kg, SC, tid-qid) promotes prolactin release. Acepromazine at mild tranquilization dosages may also facilitate milk letdown. Therapy should continue until lactation is adequate, usually 12–24 hr later.

Last full review/revision July 2011 by Autumn P. Davidson, DVM, MS, DACVIM