Intracardiac Injection Of Potassium Chloride Research Articles

Fetal intracardiac potassium chloride injection to avoid the hopeless resuscitation of an abnormal abortus: I. Clinical issues

Following the diagnosis of a genetic anomaly, some couples choose to have a legal abortion. However, following later abortions at greater than 20 weeks, the rare but catastrophic occurrence of live births can lead to fractious controversy over neonatal management. To avoid this situation, we have added fetal intracardiac potassium chloride injection to cause fetal cardiac arrest before induction of labor. The ethical issues surrounding such a practice are complex. We support this practice for three reasons: 1) The women's decision for abortion is protected because this practice assures her right for non-interference; 2) potential psychological harm to the patient and other family members is avoided; and 3) the potential for coercive intervention by other health care personnel is eliminated. At least three objections can be raised: 1) All abortions are unjust; 2) newborns and second-trimester fetuses at similar weights with identical defects should be managed in like fashion; and 3) the patient is not entitled to death of the fetus, only to evacuation of the uterine contents. On balance, we believe that our approach is justifiable ethically as it reduces the burden of conflict between the wishes of the patient and those of the neonatal care givers. It should be introduced only in situations in which the likelihood of civil or criminal liability or unwarranted medical intervention is high.

Fetal exsanguination following intrauterine angiographic assessment and selective termination of a hydrocephalic, monozygotic co‐twin

Selective termination by intracardiac potassium chloride injection was performed in twins discordant for hydrocephaly at 20 weeks' gestation. Because of the potential for vascular anastomoses to exist between the twins, fetal angiography was performed prior to the selective termination procedure. Determination of vascular connections between the fetuses was hindered by fetal bradycardia following intracardiac administration of contrast material. Selective termination was performed without difficulty using intracardiac potassium chloride (KCl) to produce asystole in the twin with hydrocephaly. The unaffected fetus appeared active and had a normal heart rate during and immediately after the procedure. However, both twins were found to have died the following day. Pathologic examination documented several vascular anastomoses between the monochorionic, diamniotic fetuses. A likely cause of death was exsanguination of the normal twin into the abnormal one. This case illustrates the difficulties encountered in selective termination of monozygotic twins and, to our knowledge, represents the first reported use of intrauterine fetal angiography.

Early Third Trimester Selective Feticide of a Compromising Twin

We report successful selective feticide of an anomalous, comprising twin by using intracardiac potassium chloride injection at 26 weeks gestation. This was associated with later delivery and survival of a very low birth weight infant with normal neurodevelopmental follow-up at 2 years. We suggest that selective feticide in such cases may have an important role to play in management.

Selective termination of multiple gestations.

Twenty-two selective terminations in multiple gestations were performed by a number of different methods. In 17 dichorionic pregnancies there was a successful delivery in surviving singletons or twins. In five monochorionic pregnancies undergoing selective termination there was a successful delivery in only one and a pregnancy loss in the other four. Six of the 18 delivered pregnancies were complicated by premature labor and delivery. Among the several methods used for selective termination, intracardiac potassium chloride injection appears to be the procedure of choice in dichorionic pregnancies.

Ischemic brain damage in rats following cardiac arrest using a long-term recovery model.

A model is described in which transient complete cerebral ischemia is induced in rats by intracardiac injection of potassium chloride. The animals were intubated and mechanically ventilated with a nitrous oxide/oxygen (70:30) mixture. Cardiac arrest was achieved following a brief period of ventricular fibrillation. After 5-6 min, the circulation was restored by cardiopulmonary resuscitation and partial exchange transfusion. Local CBF (LCBF) during ischemia and cardiac resuscitation was studied by injection of [14C]iodoantipyrine into the right auricle at various periods during cardiac arrest, and was subsequently analyzed by autoradiography. No radioactive tracer could be visualized in any brain structure, demonstrating the absence of CBF during the cardiac standstill. LCBF was also studied at 5 min and 6.5 h after cardiac resuscitation. Five minutes of recirculation showed an increase in blood flow in all brain structures studied, ranging between 130 and 400% of control values. After 6.5 h of recirculation, the CBF was decreased in 13 of 24 brain structures by 20-50%, concomitantly with the depressed rate of glucose utilization found in 15 brain structures. The neocortical, hippocampal, and striatal concentrations of labile phosphates, lactate, pyruvate, phosphocreatine, glucose, and glycogen were measured 5 min after cardiac arrest. Extensive energy failure and elevation of lactate levels were observed and were similar to earlier reported values. One week following recovery from the ischemic insult, the animals were perfusion-fixed with formaldehyde. The brains were embedded in paraffin, subserially sectioned, and stained with cresyl violet/acid fuchsin. Histopathological changes were assessed by light microscopy as the number of acidophilic or pyknotic neurons. Morphological changes were observed in the hilus of the dentate gyrus, the hippocampal CA1 and subicular regions, the dorsal and lateral septum, the olfactory tubercle, the primary olfactory cortex, the entorhinal cortex, the amygdaloid nuclei, and the reticular nucleus of the thalamus. The distribution of the morphological changes suggests a transsynaptic mechanism, causing neuronal necrosis primarily in the limbic brain areas.