806

November 1976 TheJournalofPEDIATRICS

Myocardial infarction associated with umbilical cord hematoma Mary A n n

F l e t c h e r , M . D . , * Chicago, Ill.,

Margaret Meyer, M . D . ,

Stanley E.

Kirkpatriek, M.D., Stanley Papelbaum,

M.D., Louis Gluck, M.D.,

a n d K u r t B e n i r s c h k e , M . D . , S a n Diego, Calif.

M Y O C A R D I A L INFARCTION in the n e o n a t e usually occurs in association with congenital h e a r t disease?..2 T h e r e have been isolated case reports o f myocardial infarction occurring d u r i n g the perinatal period in the absence o f recognized predisposing factors. A case is reported here which suggests that e m b o l i s m of systemic vessels via fetal circulatory pathways m a y occur in complicated deliveries, which predispose the n e o n a t e to hypoxia and hemostasis, with resultant t h r o m b u s formation. CASE HISTORY Patient A.P. was the 4,622 gm product of a 42 weeks' gestation in a 31-year-old, gravida 3, para 2, VDRL-negative woman. Two previous pregnancies had been unremarkable. This pregnancy was complicated by transient abdominal cramping and' vaginal bleeding seven weeks prior to delivery. The remainder of gestation was unremarkable. Labor was 2-1/2 hours in duration; artificial rupture of the membranes occurred five minutes before delivery. The baby was born as an assisted double-footling breech with a tigh~ nuchal cord. The one minute Apgar score was 8. Within a few minutes the baby appeared ashen and had tachypnea and tachycardia. There was a Grade 2/6 systolic murmur; pulses were nonpalpable. The liver edge was 4 cm below the costal margin. The baby cried weakly and had poor muscle tone. After infusion of albumin, the central hematocrit was 31%; blood pressure in the lower extremities was 68 mm/Hg. Extensive

From the Departments of Pediatrics and ObstetricsGynecology, Northwestern University Medical School, and the Departments of Pathology, Cardiology, Pediatrics, and Biology, University of California, San Diego. *Reprint address: Prentice Women's Hospital and Maternity Center, 333 East Superior St., Chicago, Ill. 60611.

VoL 89, No. 5, pp. 806-807

petechiae and oozing developed. The platelet count was 32,000/ mm :~. Partial thromboplastin and prothrombin times both were greater than 90 seconds. Following an exchange transfusion, the hematocrit was 45%, platelets were 122,000/m :~, PTT 40.5 seconds, and PT 17 seconds. The murmur increased in intensity and became regurgitant in character. There was a thrill at the left sternal border in the third and fourth intercostal spaces. Chest radiograph indicated cardiomegaly with no parenchymal or vascular abnormalities. An electrocardiogram at 12 hours of age suggested an anterior myocardial infarction (Fig. 1). An echocardiogram demonstrated normal left-sided structures with tricuspid value excursion patterns consistent with insufficiency.

Abbreviations used PTT: partial thromboplastin time PT: prothrombin time ECG: electrocardiogram EEG: electroencephalogram The serum glutamic oxaloacelic transaminase and creatinine phosphokinase values were significantly elevated but the glutamic pyruvic transaminase, electrolytes and glucose values were normal. Arterial blood gases indicated a mild arterialalveolar gradient at FIo._, of 0.35. The cerebrospinal fluid was xanthochromic and had a glucose concentration of 78 mg/dl, protein 140 mg/dl, RBCs 1,310, WBCs 3. Serum concentration of IgM was normal. Hospital course. At eight hours of age the infant developed seizures that were multifocal on electroencephalogram. These were clinically intermittent but frequent and were poorly controlled with anticonvulsant therapy. At 54 hours the infant became pale and lethargic, with gasping respirations. ECG showed atrial fibrillation reverting to first-degree heart block with right bundle-branch block. Despite aggressive therapy, progressive cardiac decompensation continued.

Volume 89 Number 5

The infant required assisted ventilation throughout the remainder of his course. Sequential ECGs suggested P-mitrale with broadened T waves and increased rightward forces. Seizure activity increased and became continuous on EEG. The infant died at 77 hours of age. Postmortem. At autopsy the heart weighed 40 gm (expected 36 gm). On its anterior surface was a 2.5 x 2.5 cm, dark red, mottled and slightly dimpled zone. The myocardium in this region was softer than surrounding tissues. The anterior walls of both ventricles, both anterior papillary muscles, and the anterior portion of the interventricular septum were hemorrhagic. The origins and anatomic courses of the coronary arteries were normal9 A thromboembolus occluded the origin of the septal branch of the left anterior descending coronary artery. The septal branch appeared to supply the abnormal myocardium. Heart valves were normal. The foramen ovale and ductus arteriosus were patent. No other abnormalities were found in the heart or great vessels9 The congested lungs showed multiple subpleurai hemorrhages and were focally atelectatic. The falx cerebri was lacerated and contained a small amotmt of hemorrhage. The brain weighed 550 gm (expected 406 gm). The meningeal vessels were congested9A 1.5 cm wedge-shaped hemorrhagic infarct was present in the left parieto-occipital (watershed) region. A smaller, nonhemorrhagic infarct was located symmetrically on the right. Microscopic examination of the heart revealed massive hemorrhagic and ischemic necrosis in the anterior myocardium. The muscle fibers lacked cross-striations and showed loss of nuclei with increased eosinophilic staining. At the periphery of the necrosis there was an active polymorphonuclear infiltrate, These findings were consistent with an infarct of three to four days' duration. Additionally, there were more recent welldemarcated, focal infarcts in other regions. An organizing, nonadherent meshwork of fibrin was seen among the trabeculae of the right ventricle. The thrombus in the septal branch of the left anterior descending artery was composed of old fibrin 9intertwined with degenerating leukocytes, red cells, and platelets. The vessel wall surrounding the thrombus was normal in serial sections. The thrombus did not adhere to the vessel at any point, making it most consistent with an embolus. The liver, spleen, kidneys, and adrenals were congested but without infarcts. The areas of infarction in the brain were consistent with a duration of two to three days. There were no visible emboli in the cerebral vessels. The umbilical cord had three vessels. There was a 10 cm long sausage-shaped hematoma in the cord 20 cm from the placental insertion. The placenta weighed 700 gm, was very congested, and had an old marginal hematoma. Microscopic examination of the cord revealed several very recent thrombi in the umbilical vein. DISCUSSION Evidence o f interruption o f coronary perfusion by occlusion appears to be the most f r e q u e n t cause for myocardial ischemia in the absence o f congenital heart disease in the neonate?- ~ In contrast to the situation in adults, primary coronary thrombosis in neonates is ex-

Myocardial infarction with umbilical cord hematoma

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Fig. 1. Electrocardiogram at 12 hours of age showing Q waves present in lead I, AVL, and V:9 with nonspecific ST-T wave changes. There is marked lack of anterior forces with overwhelming posterior forces while there is normal progression across the precordiat leads. This is typical of an anterior myocardial infarction. The ECG also shows evidence for a right bundle branch block, explaining the large R' in leads V, and V=,. tremely rare. The majority o f cases involve t h r o m b o e m boli. Systemic arterial embolization from stasis thrombi requires the presence o f shunt communications, e.g., by fetal circulation pathways. In the present case there was sufficient compression o f the umbilical cord to cause a h e m a t o m a , allowing blood loss from the infant and serving as a site for stasis t h r o m b u s formation in the umbilical vein, with s u b s e q u e n t embolization. Systemic embolization then occurred via the umbilical vein, ductus venosus, inferior vena cava, and patent f o r a m e n ovale. The brain and coronary arteries would be the most likely sites for embolization because the fetal shunting o f ductus venosus blood toward the brain and heart would be accentuated by the normal protective m a i n t e n a n c e o f blood flow to these organs during birth trauma and shocks REFERENCES

1. Esterly JR, and Oppenheimer EH: Some aspects of cardiac pathology in infancy and childhood I. Neonatal myocardial necrosis, John Hopkins Bull 119:191, 1966. 2. Bor I: Myocardial infarction and ischaemic heart disease in infants and children, Arch Dis Child 44:268, 1969. 3. Behrman R, Lees M, Peterson EN, De Lannoy CW, and Seeds AE: Distribution of the circulation in the normal and asphyxiated fetal primate, Am J Obstet Gynecol 108:956, 1970.

Myocardial infarction associated with umbilical cord hematoma.

806 November 1976 TheJournalofPEDIATRICS Myocardial infarction associated with umbilical cord hematoma Mary A n n F l e t c h e r , M . D . , * Chi...
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