Modification of oxytocin use through a coaching-based intervention based on the WHO Safe Childbirth Checklist in Uttar Pradesh, India: a secondary analysis of a cluster randomised controlled trial.

OBJECTIVE: To understand the prevalence of intrapartum oxytocin use, assess associated perinatal and maternal outcomes, and evaluate the impact of a WHO Safe Childbirth Checklist intervention on oxytocin use at primary-level facilities in Uttar Pradesh, India. DESIGN: Secondary analysis of a cluster-randomised controlled trial. SETTING: Thirty Primary and Community public health facilities in Uttar Pradesh, India from 2014 to 2017. POPULATION: Women admitted to a study facility for childbirth at baseline, 2, 6 or 12 months after intervention initiation. METHODS: The BetterBirth intervention aimed to increase adherence to the WHO Safe Childbirth Checklist. We used Rao-Scott Chi-square tests to compare (1) timing of oxytocin use between study arms and (2) perinatal mortality and resuscitation of infants whose mothers received intrapartum oxytocin versus who did not. MAIN OUTCOME MEASURES: Intrapartum and postpartum oxytocin administration, perinatal mortality, use of neonatal bag and mask. RESULTS: We observed 5484 deliveries. At baseline, intrapartum oxytocin was administered to 78.2% of women. Two months after intervention initiation, intrapartum oxytocin (I) was administered to 32.1% of women compared with 70.6% in the control (C) (P < 0.01); this difference diminished after the end of the intervention (I = 48.2%, C = 74.7%, P = 0.03). Partograph use remained at <1% at all facilities. Resuscitation was performed on 7.5% of infants whose mother received intrapartum oxytocin versus 2.0% who did not (P < 0.0001). CONCLUSIONS: In this setting, intrapartum oxytocin use was high despite limited maternal/fetal monitoring or caesarean capability, and was associated with increased neonatal resuscitation. The BetterBirth intervention was successful at decreasing intrapartum oxytocin use. Ongoing support is needed to sustain these practices. TWEETABLE ABSTRACT: Coaching + WHO Safe Childbirth Checklist reduces intrapartum oxytocin use and need for newborn resuscitation.

Effect of cyclical therapy with phosphorus and etidronate on axial bone mineral density in postmenopausal osteoporotic women.

Forty seven women with postmenopausal osteoporosis and at least one but no more than four vertebral compression fractures received sequential and cyclical therapy with phosphorus and etidronate (p/etid). During the same 2-year period of observation, three other groups of patients received either sodium fluoride (n = 12), estrogen replacement therapy (n = 12), or vitamin D and calcium (Ca++) alone (n = 15). Axial bone mineral density (BMD) was measured by means of dual-photon absorptiometry. Lateral thoracic and lumbar spine radiographs were taken to assess fractures. Bone mineral density increased from baseline during p/etid therapy: Mean 15.7 +/- 1.6% (SD) (P less than 0.001). During the same time, the patients in the sodium fluoride group showed a comparable increase in their BMD from baseline: mean 15.7 +/- 1.1% (P less than 0.001). During the first year of therapy, patients in the estrogen replacement group had an increase in their BMD from baseline: mean: 4.6% +/- 1.1% (P less than 0.05). No change in BMD was seen in the control group that received vitamin D and Ca++ alone. No patient who received p/etid, sodium fluoride, or estrogen replacement therapy had any new vertebral compression fractures or height loss, whereas in the control group that received vitamin D and Ca++ alone 6 out of 15 had height loss and at least one new vertebral fracture (P less than 0.01). p/etid therapy increases BMD in women with postmenopausal osteoporosis comparable to sodium fluoride but without side effects or toxicity and stabilizes vertebral compression fractures.

Hypodipsia in geriatric patients.

Hypernatremia in elderly patients is most often due to the patients mental incapacity or physical inability to obtain water despite intact thirst sensation. Hypodipsia leading to hypernatremia is not often considered in alert, elderly subjects since hypodipsia is not a recognized consequence of nonaphasia-producing cerebrovascular accidents. Described herein are six elderly patients who had such cerebrovascular accidents and who had recurrent hospitalizations for dehydration and hypernatremia. Hypernatremia in this group was due to hypodipsia and could only be prevented by prescribing daily fluid intake as a medication order. Hypodipsia should be considered as a cause of hypernatremia in elderly subjects even when they seem fully capable of requesting and obtaining water.

Mastitis and mammary duct disease.

A review of the cases of major inflammatory disease of the breast seen during an 11-year period found that 49 (77%) of the 64 cases that required hospitalization were not associated with pregnancy or lactation. In such cases, an aggressive surgical approach including excision of central nipple ducts revealed a variant of mammary duct ectasia in 13 of the 14 patients operated on. We believe that when surgery is required for treatment of mastitis, it should include nipple duct excision.

The risk of sepsis in the asplenic adult.

The risk of postsplenectomy sepsis in children is well established. The risk of sepsis following splenectomy in the adult remains unknown. This study provides data on this important subject. All adults (ages 16--91) who underwent splenectomies in three hospitals of the Louisiana State University Medical Center between 1965 and 1975 were identified. There were 298 patients included in the study. Postsplenectomy information was collected on 256 patients. The mean period of observation was 45 months (960 patient years). There were seven deaths from fulminant sepsis (incidence rate: 2.7%). Data were collected on 250 patients who had either a gastrectomy or cholecystectomy without splenectomy. The mean period of observation was 61 months (1270 patient years). There were no deaths due to fulminant sepsis (p less than 0.05). When postsplenectomy sepsis was compared with the risk of sepsis in the population at large (0.001%), the difference is significant (p less than 0.001). In the subgroup of 69 patients with hematologic or malignant disease, there were three deaths from sepsis (4.3%). In 187 patients with no underlying diseases, four patients developed sepsis, which is an incidence of 2.2% (p less than 0.05 when compared with the population at large and control group). The risk of sepsis appears to be greater in patients with chronic disease, but has no relationship to age. These data speak for the conservation of splenic tissue when possible.

Polyuric prerenal failure.

Prerenal failure is traditionally accompanied by oliguria and represents the normal renal adaptation to retain salt and water and correct the prerenal state. Nonoliguria occurring in the setting of acute renal failure usually represents acute tubular necrosis (ATN) since the kidney has lost its ability to extract salt and water. We report nine cases of patients with acute renal failure occurring in the setting of impaired systemic hemodynamic states and yet who were nonoliguric without strong evidence for ATN. The common defect in these subjects with "polyuric prerenal failure" was a blunted urinary concentrating ability. Polyuria and renal failure occurring despite evidence for impaired systemic hemodynamics may not necessarily be ATN, may still be prerenal, and should be recognizable and promptly reversible if treated appropriately.

Hypomagnesemia. Suppression of secondary hyperparathyroidism in chronic renal failure.

Chronic renal failure is accompanied by secondary hyperparathyroidism. Inhibition of parathyroid hormone secretion has been reported to be induced by hypomagnesemia in conditions other than chronic renal failure, since severe hypomagnesemia is rare in chronic renal failure. In the case reported here, the patient had chronic renal failure and malabsorption-induced hypomagnesemia; she exhibited hypoparathyroidism while hypomagnesemic, and hyperparathyroidism after magnesium was replaced. Hypomagnesemia induced parathyroid hormone suppression in this patient with chronic renal failure, despite the presence of chronic hyperfunctioning parathyroid cells.