Antepartum transabdominal amnioinfusion in oligohydramnios - a comparative study

Background: The purpose of this study was to evaluate the role of antepartum transabdominal amnioinfusion in oligohydramnios with the view to improving pregnancy outcome in oligohydramnios, a serious complication of pregnancy that is associated with a poor perinatal outcome and complicates 1-5% of pregnancies.Methods: The study comprised of a prospective analysis of 130 pregnant women with oligohydramnios, divided into two groups, the study and control group of 65 patients each and were similar with regard to age, gravidity, parity, gestational age. TAA was performed on all patients in the study group and the results were compared and analyzed.Results: Mean gestational age at first treatment was 29.98 weeks in study group. Mean pre-procedure amniotic fluid index was 4.01 and post-procedure was 12.49. A total of 106 infusions were done on 65 patients (mean1.63). Mean latency period in study group was 49.53 and in controls 26.49. There was significant decrease in fetal distress in patients in study group. 30 % of patients needed caesarean section in study group compared to 60% in controls. Number of preterm deliveries was 18 and 45 respectively in study and control groups. 61% of newborns in the study group weighed more than 2.5 kg compared to only 24% in control group. Neonatal ICU admissions and newborn deaths were lesser in study group.Conclusions: Transabdominal amnioinfusion is an extremely useful procedure to reduce complications arising from oligohyramnios. It significantly increases the latency period, decreases the occurrence of fetal distress preterm deliveries, need for caesarean or instrumental deliveries, improves birth weight of the newborns and significantly reduces the neonatal morbidity and mortality

Therapeutic Options in Graves’ Hyperthyroidism

The classical approach to treating Graves’ hyperthyroidism involves rapid control of the symptoms, generally with a beta adrenergic blocker, and reduction of thyroid hormone secretion by antithyroid drugs (ATDs) and/or using one of the several modalities available, including radioactive iodine therapy (RAI), and surgery; the selection of the treatment modalities often varies according to different guidelines, patient preferences and local traditions. Thionamides are invariably used as first-line medication to control hyperthyroidism and induce remission of the disease, thereby relieving the symptoms. In case of failure of the medical therapy, which is not uncommon, definitive treatment with surgery or RAI is the standard modality of management after due consideration and discussion with the patients. However, the therapeutic options available for patients with Graves’ hyperthyroidism have remained largely unchanged for the past several decades despite the current treatments having either limited efficacy or significant adverse effects. The clinical demand for new therapeutic regimens of Graves’ disease has led to the emergence of several new therapeutic ideas/options like biologic, peptide immunomodulation and small molecules, currently under investigations which may lead to the restoration of a euthyroid state without the requirement for ongoing therapy, but the potential risk of immunocompromise and cost implications needs careful consideration

Lithium toxicity and myxedema crisis in an elderly patient

While thyroid dysfunction is a frequent complication of lithium treatment, myxedema crisis is a rare occurrence with a handful of cases described. Here, we describe a patient receiving lithium for about a decade for bipolar disorder, who presented with myxedema crisis and lithium toxicity. In this patient, myxedema crisis was likely precipitated by lithium toxicity and community acquired pneumonia. The effects of lithium on thyroid are briefly reviewed. Objective: To describe an elderly male who was diagnosed with myxedema crisis and lithium toxicity. Case Report: A 70-year-old male was admitted in our hospital with history of gradual onset progressive decrease in level of consciousness and altered behavior for last 1 month. Patient also had history of respiratory tract symptoms for 1 week. Patient was a known case of diabetes and bipolar affective disorder for which he had been receiving insulin and lithium for 10 years. One year earlier, patient was admitted in our ward for glycemic control and evaluation of complications and was found to be clinically and biochemically euthyroid; he never returned for follow up until the present admission. On examination patient had incoherent speech, hypothermia, and bradycardia. Thyroid function showed thyroid-stimulating hormone >150 IU/ml, Tetraiodothyronine (T4) <1 ΅g/dl, anti-thyroid peroxidase titer of 60 IU/ml. The serum lithium level was 2.9 nmol/L (therapeutic level 0.2-1.2 nmol/L). He was managed with levothyroxine, starting with a loading oral dose of 500 ΅g through ryles tube followed by 100 ΅g daily, IV antibiotics and fluids; lithium was stopped after consultation with a psychiatrist. From day 5, patient started showing progressive improvement and by day 10, he had a Glasgow Coma Scale of 15/15, normal electrolyte, serum creatinine of 1.8 mg/dl and serum lithium level of 0.5 nmol/L. Conclusion: Lithium-induced hypothyroidism may be life-threatening, thyroid function should be monitored before and during lithium therapy and drug should be discontinued and appropriate therapy instituted if hypothyroidism develops

Conservative management of emphysematous pyelonephritis

Emphysematous pyelonephritis, though uncommon, is a severe necrotizing kidney infection common in patients with diabetes. Surgical treatment has been advocated as the treatment of choice in most of the patients. We present the clinical course of an elderly lady who presented with emphysematous pyelonephritis and was successfully managed with medical treatment despite the presence of adverse prognostic factors like acute renal failure and thrombocytopenia

Nonreversal of adrenal hypofunction after treatment of adrenal tuberculosis

Tuberculosis of the adrenal glands is a common cause for Addison′s disease in developing countries. Whether treatment of tuberculosis normalizes adrenocortical function in these patients is controversial. We are reporting two cases of Addison′s disease because of adrenal tuberculosis, in whom treatment with antitubercular drugs did not restore normal adrenal functions. We conclude that treatment of tubercular Addison′s disease does not lead to normalization of adrenocortical function