Stridor: a rare complication of magnesium sulfate therapy in a pregnant patient

Magnesium sulfate is frequently used in severe preeclampsia and eclampsia for the prevention and reoccurrence of seizure activity. Their adverse effects of magnesium sulfate are minor but it cause respiratory depression and tetany. We report a case of stridor due to laryngospasm as result of hypocalcemia in a pregnant patient on magnesium sulfate therapy.A 30 year old gravida5 para 4 had severe preeclampsia started on magnesium sulfate therapy and to control her hypertension she was on labetalol and nifidipine. One hour after the lower segment cesarean section, she developed severe laryngospasm and stridor, no upper airway secretion but found to have hypocalcemia. She responded to immediate intravenous calcium chloride with dramatic clinical improvement. Patients on magnesium sulfate can have life threatening hypocalcemia and stridor. The calcium channel blockers may augment the hypocalcaemic effect of magnesium sulfate

Peripartum Pulmonary Embolism

Pregnancy and peripartum increase the risk of venous thromboembolism (VTE) by many folds. Interestingly, the VTE is more common during the pregnancy, whereas the pulmonary embolism is more frequent in postpartum period. There are various risk factors for the VTE and pulmonary embolism in these patients. The important risks are improper thromboprophylaxis, obesity, and multigravida. The clinical parameters and the d-dimer are not used for diagnosis of thromboembolism during pregnancy and in the postpartum period. The compression ultrasonography (CUSG) is commonly used for VTE diagnosis; for the pulmonary embolism diagnosis, one has to consider the radiation hazard to the fetus as well as to the mothers. Ventilation/perfusion scan is the imaging of choice for patient who has respiratory signs with normal chest radiograph. If chest X-ray is abnormal with suspicion of peripartum pulmonary embolism (PPE), the choice should be computed tomographic angiography. Heparin and its derivatives remained the anticoagulation of choice for the treatment of VTE as well as the PPE, as it is a shorter acting, easy to reverse with protamine sulfate. Proper thromboprophylaxis is the key for prevention of VTE and peripartum pulmonary embolism

Posteclampsia Sudden Cardiac Arrest (SCA): A Rare Etiology

Eclampsia is associated with high maternal and fetal morbidity and mortality. The mortality in eclampsia is reported to be secondary to cerebrovascular accidents, neurogenic pulmonary edema, or acute kidney injury leading to cardiac arrest. A rarely reported etiology is sudden cardiac arrest (SCA) immediately after the seizure activity. We report a case of morbidly obese multigravida, complicated into postnatal eclampsia developing postseizure SCA due to apnea. Case. A 35-year-old woman in 38 weeks of gestation presented to the women’s hospital emergency with hypertension and proteinuria and had lower section caesarean section under epidural anesthesia and required labetalol infusion. She developed convulsions in the 1st postoperative day, and she was started on magnesium sulphate therapy. After a few minutes, the patient had a 2nd episode of convulsions, apnea, cyanosis, and cardiac asystole requiring cardiopulmonary resuscitation and spontaneous circulation returned in 3 minutes. Her endotracheal intubation was difficult, but we succeeded in the 2nd attempt. She was sedated, ventilated, and required noradrenaline to maintain hemodynamics. Her ECG, echocardiogram, cardiac biomarkers, CT chest/brain, and serum magnesium levels were within normal range. The patient was weaned from vasopressor and ventilator by day 2 and extubated. She became awake; labetalol and magnesium sulphate infusions were stopped by day 3. The patient was transferred to the ward on day 5; from there she was discharged home on day 8 on oral labetalol. She was followed up in an outpatient clinic after 4 weeks and remained comfortable, and blood pressure was controlled with tablet labetalol and repeat echocardiogram was normal. Conclusion. Eclampsia patients can have apnea after seizures, progressing to SCA

Preeclampsia: From Etiopathology to Organ Dysfunction

Preeclampsia is a hypertensive disorder of pregnancy affecting 6–12% of the population. There are various risk factors for the development of preeclampsia, ranging from advanced maternal age to genetics. The proposed etiologies for preeclampsia are abnormal placentation, immunological intolerance, endothelial damage, and genetic inheritance. The pathogenesis includes endothelial activation and dysfunction leading to vasospasm. Preeclampsia is divided into two stages: asymptomatic and symptomatic stages. Preeclampsia causes multiple organ involvement, namely central nervous system, respiratory, cardiovascular, hematological dysfunction, HELLP (hemolysis elevated liver enzymes, low platelets) syndrome, endocrine, renal, hepatic, and uteroplacental dysfunction. These organ dysfunctions increase morbidity and mortality in preeclamptic pregnant patients