Myron M. Nichols

Complete Heart Block and Fatal Right Ventricular Failure in an Infant

### Drs David W. Sapire and Suzanne M. Lopez #### Maternal History The mother of this child was a 22-year-old primigravida in apparent good health. There was no clinical or biochemical evidence indicating use of ethanol, addictive drugs, or other possibly teratogenic substances. Fetal heart rate on ultrasonograms done early in her pregnancy was about 150 beats per minute. Near the end of her fifth month of pregnancy, she was referred to the John Sealy Hospital at the University of Texas Medical Branch (UTMB) because the fetal heart rate had decreased to 86 beats per minute. Although the atrial rate on subsequent examinations remained about 150 beats per minute, the ventricular rate ranged from 40 to 50 beats per minute. Two weeks before delivery, atrial and ventricular rates were 144 and 47 beats per minute, respectively. When the ventricular rate began to slow even further, it was decided that risk of intrauterine death was imminent, and a Caesarean section delivery was performed at approximately the 28th week of gestation. There was no significant family history relevant to the case. The mother’s serological studies for lupus erythematosus and antiphospholipid syndrome were negative. #### Infant’s Hospital Course The baby was in no major distress just after delivery, but her heart rate increased very little in response to increasing doses of isoproterenol. Within hours after birth, it was decided that an electronic pacemaker was advisable. During epicardial placement of electrodes near the left ventricular apex, the surgeon noted that the “infiltrated” right ventricular myocardium was thin and that it did not respond to electronic pacing. Over the following weeks, there were no conducted atrial beats, although there were regular P waves. Occasional single and multiple ventricular premature beats were recorded, but the heart was driven primarily by the electronic pacemaker. The main clinical problem was increasing right ventricular failure that did not respond to intensive care in the high-risk …

Primary pulmonary hypoplasia in the neonate

Infants with primary pulmonary hypoplasia with respiratory distress immediately after birth, but usually elude early diagnosis. They have no other abnormalities, but frequently develop signs and symptoms of the PFC syndrome. Roentgenographically, they show small, clear lungs and are prone to develop complicating pneumothoraces. The clinical, roentgenographic, and pathologic features of eight infants with primary pulmonary hypoplasia are presented.

Retinal Hemorrhage in an Infant After Cardiopulmonary Resuscitation

Unexplained retinal hemorrhages in infants are usually indicative of child abuse. We present the case of an infant with retinal hemorrhages following cardiopulmonary resuscitation, who had not been abused. Cardiopulmonary resuscitation should be added to the list of causes of retinal hemorrhages in infants and children.

Effects of magnesium sulfate on uterine contractility, intrauterine fetus, and infant

Abstract 1. Magnesium sulfate injected in a dose of 4 Gm. intravenously reduces uterine intensity, frequency, and tonus. The degree and duration of this action varied with the individual patient. Subsequent enhancement of uterine contractility was observed. 2. No evidence of potentiation of synthetic oxytocin was obtained. Valyl oxytocin action on the other hand was potentiated by magnesium in all 4 cases studied. 3. The effect of magnesium on the human uterus appears to be twofold: (a) that on the myometrial cell at its cellular level, and (b) that resulting from generalized relaxation of striated muscle and concomitant changes of arterial blood pressure. 4. Fetal heart rate changes during labor in patients treated by magnesium were consistent with those related to specific types of uterine contractility produced by magnesium. 5. No evidence was obtained of depressant effects of magnesium therapy on the infant during the neonatal period due to maternal sedation or analgesic action.

Effects of Hemodialysis and Dimercaprol in Acute Dichromate Poisoning

A 22-month-old infant died after ingesting sodium dichromate his father had brought from work. Treatment included folic acid and dimercaprol administration, hemodialysis, and exchange transfusion. To evaluate this treatment, four dogs were hemodialyzed after receiving intravenous sodium dichromate: their dialyzer chromate clearance was similar to their renal chromate clearance and their dialyzer chromate clearance was not significantly different before or after dimercaprol administration. This and other cases in the literature indicate that although chromate poisoning is often fatal, supportive care, forced diuresis, and chelating agents may be helpful. Hemodialysis may be required if renal failure occurs. Awareness of toxicity and prevention remain the most important approaches.

Bronchiolar wall changes in sudden infant death syndrome: morphometric study of a new observation.

Sudden infant death syndrome (SIDS) infants have significantly thicker and more cellular bronchiolar walls than control infants of similar age. A morphometric study of 25 SIDS and 18 control infants was undertaken to measure the bronchiolar wall thickness using a Cue-2 image analysis system. A mathematical formula (relative index) was used to compare the thickness of bronchioles of varying diameter. Data analysis using a nested design two-way analysis of variance and covariance of the measured bronchioles showed a significant difference between the SIDS and control infants with a P value less than .001. Manual counting of the cells in the bronchiolar walls and data analysis using an unpaired two-tailed t test showed that the SIDS infants had a significantly greater number of cells than control infants (P less than .01). Our preliminary results indicate that the cells in the bronchiolar wall are either peripheral nerve-derived (Schwann cells) or Langerhans cells. We postulate that these cells are increased in number in response to chronic hypoxia in SIDS infants.

Twin transfusion syndrome associated with placental venous calcification

An unbalanced arteriovenous shunt in monozygous twins may result in the twin transfusion syndrome which, if mild. presents as a slight discrepancy of hematocrits in the twins or, if severe, may result in the death of the anemic donor in ufem or of the recipient with polyhydramnios, hyperviscosity. and cardiac failure( 1). Several hypotheses have been proposed as to the triggering factor which causes the massive shift of fetal blood in these twins. The present report describes a case of twin transfusion syndrome associated with the chorionic venous calcification in donor twin. To the best of our knowledge, this is the first report of the twin transfusion syndrome from such an entity.

Insulin allergy; case report, with response to boiled insulin.

Summary A case of generalized insulin allergy in an 11-year-old white girl, consisting of generalized edema, urticaria, and a weight gain of 5 pounds, responded well to the emergency treatment of boiled, regular insulin. The patient ultimately was desensitized to insulin, enabling her to take commercial NPH insulin.