Successful resuscitation during fetal surgery

Successful Resuscitation During Fetal Surgery By Joy L. Graf, Bettina W. Paek, Craig T. Albanese, Jody A. Farrell, Joseph A. Kitterman, Russell W. Jennings, and Michael R. Harrison San Francisco, California

After in utero resection of a sacrococcygeal teratoma coupled with a transfusion of packed red blood cells, a 23-weekgestation fetus had bradycardia. Chest compressions were begun and epinephrine, atropine, and sodium bicarbonate were given, while the fetus remained bathed in warm saline. After 3 rounds of drugs, and just before withdrawing support, the fetal heart resumed beating and normal cardiac

function. Based on to this case, the authors developed a resuscitation protocol for fetal surgery. J Pediatr Surg 35:1388-1389. Copyright © 2000 by W.B. Saunders Company.

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Compressions alone did not restore cardiac function so epinephrine, sodium bicarbonate, and atropine were given via the umbilical vein. Compressions were begun again, and after several minutes the fetal cardiac function was evaluated by sonogram and remained very poor. The drugs were repeated, 5 mL of PRBC were given, and compressions restarted, without obvious effect. As a last effort, a third round of drugs were given while simultaneously performing chest compressions. Throughout the arrest, the fetus was bathed with warm normal saline, and, at this point, warmer saline was used. Subsequently, the heart was evaluated with ultrasound scan and had a steadily increasing rate to 180 beats per minute with good ventricular function. The fetus was returned to the uterus, the hysterotomy closed, and the mother awakened from anesthesia. Postoperatively, the fetal heart rate returned to normal within several hours and displayed normal postoperative variability. Serial fetal sonograms showed normal cardiac function, and careful serial examinations of the fetal brain showed no evidence of swelling or hemorrhage. The infant was delivered 5 weeks postoperatively because of preterm labor and did well. She was discharged home at 3 months of age and is now an active, healthy, 3-year-old. In view of her intraoperative cardiac arrest and resuscitation, she has undergone extensive neurologic testing including cerebral ultrasound scan, physical and developmental examinations, and magnetic resonance imaging, the results of which have been normal. Subsequent analysis of stored blood suitable for transfusion in a premature neonate (ie, cytomegalovirus negative, irradiated, and less than 3 days old) from our blood bank showed marked acidosis and hyperkalemia in several samples (Table 1).

HE SURVIVAL RATE of premature infants in intensive care nurseries who require cardiopulmonary resuscitation (CPR) is quite low.1 Factors found to decrease survival after CPR include increasing prematurity and very low birth weight.2,3 Fetuses who undergo fetal surgical intervention exemplify these negative risk factors: they are “premature,” very small, and, additionally, have a congenital anomaly that either is threatening fetal viability or perinatal survival. During a recent in utero resection of a fetal sacrococcygeal teratoma (SCT), a fetus suffered a cardiac arrest and required full resuscitation before cardiac function returned to normal. This successful fetal resuscitation and a fetal surgery resuscitation protocol developed subsequent to this case are the basis of this report. CASE REPORT A 23-weeks-gestation fetus with a large SCT had hydrops, and an in utero tumor resection was undertaken. Before tumor resection, an umbilical vein blood sample was obtained and showed a fetal hematocrit of 22% (approximately 39% is normal in a 23-week fetus),4 a pH of 7.28, a pO2 of 31, and a pCO2 of 52. The SCT resection was performed without complication, and the fetal heart rate, which was monitored by ultrasound scan, remained between 120 and 140 beats per minute. After the SCT resection was complete and the fetus was returned to the uterus, we transfused the fetus with 15 mL of warmed packed red blood cells (PRBC) via the umbilical vein. Immediately after the transfusion, ultrasound scan showed the fetal heart rate to be quickly declining with poor ventricular function. There was no improvement over the next several seconds; therefore, external cardiac compressions were begun using thumb and forefinger at a rate of over 100 compressions per minute.

From the Division of Pediatric Surgery, Department of Surgery, Fetal Treatment Center, University of California, San Francisco, CA. Address reprint requests to Craig T. Albanese, MD, The Fetal Treatment Center, University of California, San Francisco, 513 Parnassus Ave, Room 1601 HSW, San Francisco, CA 94143-0570. Copyright © 2000 by W.B. Saunders Company 0022-3468/00/3509-0032$03.00/0 doi:10.1053/jpsu.2000.9348 1388

INDEX WORDS: Fetal Surgery, resuscitation, cardiac arrest, sacrococcygeal teratoma, hydrops.

DISCUSSION

A fetal intraoperative cardiac arrest is likely caused by 1 of 3 etiologies: (1) inability of a severely compromised fetus to survive the stress of the surgical intervention, coupled, for instance, with severe hydrops; (2) intraoperative blood loss; or (3) metabolic or electrolyte abnormalities. Only the latter 2 etiologies are amenable to resuscitative efforts. We believe that acidemia and hyperkalemia secondary to the PRBC transfusion precipitated the arrest described in the current case.5,6 We rapidly administered PRBC via the umbilical vein that essentially delivered the transfused blood directly to the fetal heart and coronary arteries. The fetal heart in this

Journal of Pediatric Surgery, Vol 35, No 9 (September), 2000: pp 1388-1389

FETAL RESUSCITATION

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Table 1. Analysis of Stored Blood Suitable for Transfusion in a Premature Neonate Sample

Age of Blood (d)

pH

[H⫹] (nM/L)

PCO2 (mmHg)

BE (mEq/L)

K⫹ (mEq/L)

Ca⫹⫹ (mEq/L)

1 2 3 4 Mean SD

1 1 7 8 4.3 3.8

6.69 6.75 6.75 6.75 6.73 0.01

204.2 177.8 177.8 177.8 184.4 11.4

138 147 134 147 141.5 5.7

⫺16 ⫺12 ⫺14 ⫺12 ⫺13.5 1.7

⬎20 ⬎20 ⬎20 ⬎20

⬍0.25 ⬍0.25 ⬍0.25 ⬍0.25

case already was stressed by the high output state caused by massive arteriovenous shunting to the SCT, and we hypothesize that the transfusion of blood, which was probably acidotic and hyperkalemic, led to cardiac decompensation. In addition, citrate used to preserve blood binds calcium and may have caused acute hypocalcemia, further depressing the heart. In this instance recovery was most likely secondary to placental attenuation of the metabolic abnormalities with placental circulation provided by the external cardiac compression, buffering of the acidemia by sodium bicarbonate, and, after cardiac function began to recover, the epinephrine acted as an inotrope and chronotrope. Cardiac compressions alone did not lead to improvement of cardiac function. Based on this case a fetal resuscitation protocol was developed. Correction of acidosis with tromethamine (THAM) in stored blood to a pH of greater than 7.2 will reduce potassium levels to acceptable levels. Packed blood cells are diluted with normal saline to a hematocrit level of 40% to 50% to minimize rouleaux formation, which can cause thrombosis in small vessels. Calcium gluconate is given after the transfusion to treat citrateinduced hypocalcemia. Resuscitation drug dosages are based on fetal weight as estimated by gestational age or ultrasound scan and are prepared for each case preoperatively (Table 2). In emergency situations medications will be given via an umbilical vein. Less urgent situa-

tions will allow administration via an umbilical artery, thus, avoiding the potentially catastrophic complication of umbilical vein thrombosis or embolus. Fetal exposure is minimized, and the fetus is bathed with saline warmed to 37°C (normal mean amniotic fluid temperature is 36.6°C).7 External cardiac compressions are performed at a rate of 100 to 150 compressions per minute. Fetal response to resuscitative measures is evaluated by intermittent sonographic evaluation of heart rate and ventricular function. This case shows that successful cardiac resuscitation is possible in the fragile fetus. In this case, we hypothesize that compressions and medications allowed for correction of acute metabolic abnormalities caused by a fetal blood transfusion. We have developed a fetal surgery resuscitation protocol, which allows us to prepare preoperatively. Table 2. Fetal Surgery Emergency Sheet Name Estimated Fetal Weight Code Medications

Comes As

Dose

Patients Dose

Atropine

0.1 mg/mL

0.01 mg/kg

⫽ ⫽

mg mL

Tromethamine (THAM)

0.3 M/L

Calcium gluconate

100 mg/mL

3 mM/kg (⫽10 mL/kg) 100 mg/kg

Epinephrine 1:10,000

0.1 mg/mL

0.02 mg/kg

⫽ ⫽ ⫽ ⫽ ⫽ ⫽

mmol/L mL mg mL mg mL

Compressions—100-150/minute Packed red blood cell (PRBC) Transfusion , pH ⫽ Following THAM and dilution, Hematocrit ⫽ Warm to 37°C. kg ⫽ ml. Give blood SLOWLY over PRBC 15 ml ⫻ several minutes. Monitor heart rate during and after transfusion. kg After transfusion, Calcium Gluconate 100 mg ⫻ mg ⫽ mL ⫽

.

REFERENCES 1. Lantos JD, Miles SH, Silverstein MD, et al: Survival after cardiopulmonary resuscitation in babies of very low birth weight: Is CPR futile therapy? N Engl J Med 318:91-95, 1988 2. Willett LD, Nelson RM: Outcome of cardiopulmonary resuscitation in the neonatal intensive care unit. Crit Care Med 14:773-776, 1086 3. Sood S, Giacioa G: Cardiopulmonary resuscitation in very low birthweight infants. Am J Perinatol 9:130-133, 1992 4. Berkowitz RL, Lynch L: Fetal blood sampling, in Creasy RK, Resnik R (eds): Maternal-Fetal Medicine, Philadelphia, PA WB Saunders, 1994

5. Nicolini U, Santolays J, Fisk NM, et al: Changes in fetal acid base status during intravascular transfusion. Arch Dis Child 63:710-714, 1988 6. Hall TL, Barnes A, Miller Jr, et al: Neonatal mortality following transfusion of red cells with high plasma potassium levels. Transfusion 33:606-609, 1993 7. Soothill PW, Nicolaides KH, Rodek CH, et al: Amniotic fluid and fetal tissues are not heated by obstetric ultrasound scanning. Br J Obst Gynaecol 94:675-677, 1987