An unexpected temporary suppression of lactation after a local corticosteroid injection for tenosynovitis

Abstract

Introduction: Intra-lesional glucocorticosteroid (GCS) injections are used widely for painful musculoskeletal conditions in general practice.

Case: A 26 year old female, was given an intra-lesional injection of 24 mg methyl prednisolone acetate (MPA) with 15 mg lidocaine for treatment of DeQuervain's tenosynovitis. She was six weeks postpartum and predominantly breast feeding. Lactation was suppressed at approximately 30 h post injection and this persisted for a period of approximately 36 h before spontaneous resumption of milk production. Lactation returned to normal 90 h after the injection.

Discussion: Studies done in lactating animals have shown that injected GCS have led to a reduction of milk production, but there is limited data on these injections in lactating humans. The dose of GCS administered and the site of the GCS injection appear to contribute to this phenomenon. Very large doses of GCS have caused suppression of lactation in humans as opposed to low doses of GCS. Injections of GCS into areas of the body subjected to high activity level like the knee or wrist could lead to greater systemic absorption of GCS than GSC administered to body sites with lower physical activity like the shoulder.

Conclusion: Local injection of MPA reversibly suppressed lactation in a young woman for a period of 24–48 h. Doctors using injectable GCS in lactating women should apprise patients of this possibility. Mothers can take precautions like expressing and storing enough breast milk to cover this period prior to receiving these injections.

Keywords::

• adverse effects
• methyl prednisolone acetate
• breast feeding

KEY MESSAGE:

• A rare side effect of using low dose, intra-lesional injections of methyl prednisolone acetate in women during the post partum period is the temporary suppression of lactation.

• If it happens then spontaneous resumption of lactation should be expected within 24-48 hours.

INTRODUCTION

Intra-lesional glucocorticosteroid (GCS) injections are commonly administered by primary care doctors, in clinic settings, as a means to reduce pain in a variety of musculoskeletal conditions (1). There are systemic effects of these GCS on endocrine function involving the hypothalamus-pituitary-adrenal axis, which affects endocrine function, hematologic indices and inflammatory markers in persons receiving these injections (2). The product insert of methyl prednisolone acetate (MPA) gives little information on its effect on lactation except advising caution in its use due to the possibility of secretion in the milk and the possible effects of the steroid on the baby (3). The case report below attempts to add evidence to the research question: ‘does an intra-lesional injection of low dose MPA suppress lactation in a woman with established lactation, and if so what is the outcome?’ The patient gave written consent to use her information for the purpose of this report.

CASE

Our patient was a right-handed, 26 year old female, final year dental student, who presented with right wrist pain of eight weeks duration. She was six weeks postpartum and predominately breastfeeding her new-born baby. The pain affected her ability to use the dental equipment in her care of patients and caused her difficulty in caring for her baby. She was concerned as her final exams were three months away.

Examination revealed that she had a right DeQuervain's tenosynovitis. She was offered either a referral to physiotherapy or an intra-lesional injection of methyl prednisolone. She requested the injections as she would have been able to resume her normal duties faster after the injection. She received 24 mg of methyl prednisolone mixed with lidocaine 15 mg intra-lesionally.

She called two days later to say that her lactation had ceased about 30 h post injection and she was worried as her baby was distressed at not receiving breast milk. Her breasts were soft and not engorged. She was advised to observe the situation for a further 24 h and if no lactation resumed then a trial of domperidone would be started (4). She called the next day to state that lactation had resumed spontaneously a total of 36 h after it had ceased. It started slowly at first and by 24 h later, lactation was normal again. she was lactating again, her baby was feeding and her wrist pain had resolved. Two months after the injection she had no pain, was caring well for her baby and preparations for her examinations were going as planned.

DISCUSSION

This case reports on the temporary cessation of lactation in a woman who was six weeks postpartum after receiving a low dose of an intra-lesional depot corticosteroid injection of 24 mg of methyl prednisolone acetonide (MPA). This suppression of lactation was short-lived and the resumption of lactation occurred spontaneously. This case report is the first to document a temporary suppression of lactation in a woman receiving a low dose of intra-lesional glucocorticosteroids (GCS).

Box 1. Family Medicine in Trinidad & Tobago.

Trinidad and Tobago is a twin island state in the Caribbean. Family Medicine, a growing discipline, is offered by The University of the West Indies as a two-to-four year training programme which leads to a Diploma or Doctor of Medicine (DM) in Family Medicine. Primary care services are provided by Family physicians, who practice in government-run primary health care centres which are free of charge; and privately, mainly in solo practices on a fee for service basis.

Physiology of lactation

The process of lactation involves milk production and milk ejection. Corticosteroids and prolactin are important for lactation to occur. Oxytocin is important for milk ejection (5). This patient had depressed milk production rather than decreased milk ejection as her breasts were not engorged. This suggests that the corticosteroid injection had some effect on prolactin levels but not oxytocin levels. This effect could be reversed by domperidone (4). In this case report domperidone was not used because lactation restarted spontaneously 36 h after it ceased.

The effect of GCS on milk production in animals and humans

Corticosteroid injections have been found to decrease the volume of milk produced in animals (6). Similarly, Henderson and colleagues have looked at the effect of intramuscular betamethasone on lactation in women who had preterm delivery. Intramuscular betamethasone was found to affect the timing of lactation and volume of milk produced in these women, with the volume of milk produced being less in those who received antenatal GCS for longer periods (7).

Possible influence of dosage and sites of GCS injection on lactation

The site of injection as well as the dosage of GCS appears to be important in determining the effect of GCS on lactation. A case report by McGuire described a lactating mother 14 months postpartum, who experienced no effect on lactation after receiving an intra-bursal injection of betamethasone 5.7 mg (equivalent to 40 mg methyl prednisolone) into her shoulder. This reduced the shoulder pain for about four weeks. When, however, the patient later received a high dose of triamcinolone of 80–120 mg of triamcinolone (equivalent to 80–120 mg of methyl prednisolone) via epidural injection, milk production was suppressed. This suppression of lactation started three days after receiving the injection and its effects were reversed with the use of domperidone (8). It should be noted that the dose of triamcinolone used in this cited case report was much higher than the doses used in primary care clinics where the equivalent of 10–40 mg of MPA is commonly used for most injections (9). Since the time-frame between injections was not stated in this case report, it is not known if the two GCS injections had some cumulative effects on the duration of lactation suppression.

Many authors have studied the effect of intra- articular GCS injections on glycaemic control. Knee injections (10) but not shoulder injections (11) have been found to worsen glycaemic control in diabetic patients who received such injections indicating that after shoulder injections, the systemic effects of the GCS was negligible. This may, in part, reflect the activity level of the knee versus the shoulder joint. Although McGuire did not explain her findings, lack of suppression of lactation after an intrabursal injection in the shoulder may be due to the less activity of the shoulder and lower uptake of GCS from this area of the body.

Implications

In our case the patient had an injection into her wrist area—an area heavily used by this patient. The suppression of lactation in our patient may have been partially explained by the location that she received the injection. It would have been interesting to know the effect on lactation had the wrist which received the injection been immobilized for 72 h. Further studies are needed to determine the effect of anatomic location of injection and the dose of GCS injected on lactation in postpartum women.

From the authors’ perspective, we would give a GCS injection in a lactating mother but only after weighing the pros and cons of the injection. If the pain is not very severe and home support is available then in the early phases of lactation, a trial of physiotherapy is indicated. If the severity of pain is affecting her care-giving duties and work, there is little assistance at home and she is willing to accept that she may have temporary suppression of lactation, we would then use the lowest recommended dose of GCS. Patients should be advised that the suppression of lactation is reversible and if it does occur then a wait and see approach should be adopted for a period of 24–36 h. Expressing and storing milk for this period could be an option for mothers prior to the injection.

CONCLUSION

Reasonable advice from GPs administering intra-lesional corticosteroids to lactating mothers should be that GCS has the potential to interfere with lactation and, therefore, should only be used if absolutely necessary. The lowest dose possible to get a therapeutic response should be used.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.