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Case Reports

Indian Pediatrics 2004;41:267-270 

Subgaleal Hematoma and Seven Exchange Transfusions


Sourabh Dutta
Amuchou Singh
Anil Narang

From the Division of Neonatology, Department of Pediatrics, Post Graduate Institute of Medical Education and Research, Chandigarh 160 012, India.

Correspondence to: Dr. Sourabh Dutta, Assistant Professor, Department of Pediatrics, Advance Pediatric Center, PGIMER, Chandigarh 160 012, India.
 E-mail: sourabhdutta@yahoo.co.in.

Manuscript received: August 12, 2002; Initial review completed: November 5, 2002; Revision accepted: August 7, 2003.

Abstract:

A 3 kg baby was delivered by cesarean section after prolonged labor. He had massive subgaleal hematoma. He developed anemia requiring packed cell transfusions and hyperbilirubinemia requiring a total of seven exchange transfusions and highly intensive phototherapy. There were no adverse complications of the hyperbilirubinemia or the exchange tranasfusion.

Keywords: Exchange transfusion, Jaundice, Subgaleal hematoma

 

Subgaleal hematoma (SGH) is a potentially life-threatening extra-cranial bleed that occurs most commonly in neonates after difficult instrumental deliveries(1). It can present acutely as hemorrhagic shock or anemia, and later as neonatal hyperbili-rubinemia(1,2). We report a case of SGH resulting in anemia and severe hyper-bilirubinemia requiring an unusually large number of exchange transfusions.

Case Report

Baby M, a 3000 g male infant, was delivered at 38 weeks gestation by emergency cesarean section for non-progress of labor. There was no evidence of perinatal asphyxia or encephalopathy. On day 2 he was referred to our hospital for pallor and a scalp swelling. At admission, his hemodynamic and respiratory parameters were stable, his occipito-frontal circumference (OFC) was 37 cm, there was severe pallor and a SGH extending from the upper eyelids to the nape of the neck. There was no bruising or bleeding from any site.

His hemoglobin was 6.9 g/dL, platelets were adequate and there was no evidence of coagulopathy. Computed tomographic (CT) scan of the head revealed circumferential scalp swelling crossing suture boundaries suggest-ing of SGH. The intracranial structures were normal (Fig . 1).

Fig.1. NCCT scan head showing circumferential scalp swelling (patchy hypoattenuation) around skull bones (dense white).

He was treated with vitamin K injection and blood transfusions (15 ml/Kg) twice on the day of admission. On day 5 of life, he developed jaundice with total serum bilirubin (TSB) of 16 mg/dL and phototherapy was started. The blood groups of the baby and mother were both B positive. The direct Coombs test was negative and glucose-6-Phosphate dehydrogenase level was normal. The reticulocyte count was 2%. Inspite of phototherapy, the TSB progressively rose and hence he underwent a double volume exchange transfusion (DVET) on day 6. He subsequently underwent 3 more DVETís within next 36 hrs, all for TSB values above 20 mg/dL. On the 10th day the TSB (predominantly unconjugated) again rose rapidly and hence he underwent 3 more DVETís over the next 2 days. All donor blood aliquots were of B positive group, and none was more than 5 days old. There was no evidence, either clinically or hematologically, of a hemolytic reaction after any of the DVETs. It is our policy to send a sample of blood from all blood transfusion bags for G6PD assay, and we found in this case that none of the donors were G6PD deficient. The patient received highly intensive single surface phototherapy with special blue lights (Philips TL 52 with irradiance of 18 W/cm2/nm) throughout the duration of hyper-bilirubinemia. We did not drain or attempt to aspirate the SGH. No medication was used to treat the hyperbilirubinemia. At discharge he was mildly jaundiced, neurologically normal with OFC 33.5 cm. At follow up after one month the size of the swelling had decreased and brain stem evoktesponse audiometry was normal.

Discussion

This case of massive SGH is unusual for the large number of exchange transfusions required for treating the hyperbilirubinemia. The sub-aponeurotic space accommodates as much as 250 ml of blood when filled to just 1 cm in thickness(3). It is potentially life threatening because of the potential of hemorrhagic shock.

The reported incidence of SGH ranges from 1.6-3/1000 live births(2,4). The risk factors are instrumental delivery, prolonged second stage of labor; precipitate labor, coagulopathy, prematurity, large infants, fetal dystocia and severe head moulding(2,4-7). The incidence of SGH in ventouse-associated deliveries is 60 times higher than other modes of delivery(5). Male preponderance was reported(5). The index patient was a male child delivered after labour of 48 hours. There was no instrumentation or bleeding diathesis.

Subgaleal hematoma is associated with hypoxic ischemic encephalopathy, head trauma such as intracranial hemorrhage, skull fracture and cerebral edema in various studies(8). In a study by Govaret et al.(9), 14 of 27 babies with SGH revealed various abnormalities of parietal bones on CT scan. Three mechanisms of bleeding were suggested: linear skull fracture, suture diastases and fragmentation of the superior margin of parietal bone. In our patient there was no skull fracture, sutural diastases or intracranial bleed on cranial CT scan.

The clinical presentation varies from insidious onset of anemia to hypovolemic shock(1,2). In a study of 101 subjects over a period of 30 months, the clinical presentation of SGH was hyperbilirubinemia in 57 patients (56.4%), anemia requiring blood transfusion in 32.7% and shock in 3 babies. Four patients developed severe unconjugated hyperbili- rubinemia, which required exchange trans-fusions(2). Our patient presented with anemia requiring blood transfusions at admission and later developed severe hyperbilirubinemia requiring seven DVETís. To the best of our knowledge this is the maximum number of DVETís a patient with SGH has undergone so far in published medical literature.

Phototherapy appears to have been ineffective in our patient, despite adequate light intensity and wavelength. This is somewhat contrary to the experience of Tan et al.(10) who found phototherapy to be equally effective in the cephalhematoma. The patient was started on prophylactic antibiotics after the third exchange, and did not develop sepsis during the hospital stay.

An important issue is whether we should have aspirated the blood at the outset to prevent repeated DVETs. The literature is ambiguous about this. There is a sizeable risk of introducing infection during aspiration of an otherwise sterile hematoma, and hence aspiration has generally been recommended only when one wishes to exclude the presence of an infected cephalhematoma(11).

The literature is also silent about the possible use of glucoronyl transferase inducers such as phenobarbitone, or the use of heme oxygenase inhibitors, such as metalloporphyrins, in the presence of large hematomas to prevent the occurrence of hyperbilirubinemia. One animal study has shown that single dose tin protoporphyrin does not reduce bilirubin formation following artificially created hematomas(12).

The mortality rate following SGH is 14-17%(4,5). The most important risk factors associated with death following SGH include severe anemia requiring urgent blood transfusion within first 12 hours of birth and significant birth asphyxia(5). After the acute phase, SGH resolves over 2 to 3 weeks. Newborns with isolated SGH who survive the acute episode show no evidence of subsequent long-term major neurological deficit or developmental delay(4,8).

Contributors: SD managed the patient and co-drafted the manuscript, AS drafted the manuscript, AN supervised the management of the patient and the drafting of the manuscript.

Funding: None.

Competing interests: None stated.

 

 References

 

1. Benaron DA. Subgaleal hematoma causing hypovolumic shock during delivery after failed vaccum extraction: case report. J Perinatol 1993: 13: 228-231.

2. Boo NY. Subaponeurotic hemorrhage in Malaysian neonates. Singapore Med J 1990; 31: 207-210.

3. Eliachar E, Breat AJ, Baradiaux M, Tassy R, Pheulpin J, Schneider M. Hematome souscutane cranien du nouneed. Arch Fr pediatr 1963; 20: 1105-1111.

4. Gebremariam A. Subgaleal hemorrhage: risk factors and neurological and developmental outcome in survivors. Ann Trop Paediatr 1999; 19: 45-50.

5. Ng PC, Siu YK, Lewindon PJ. Subaponeurotic hemorrhage in the 1990s: A 3-year surveillance. Acta Paediatr 1995; 84: 1065-1069.

6. Plauche WC. Subgaleal hematoma: A complication of instrumental delivery. JAMA 1980: 244: 1597-1598.

7. Royhans JA, Miser AW, Miser JS, Subgaleal hemorrhage in infants with hemophilia: Report of two cases and review of literature. Pediatr 1992; 70: 306-307.

8. Chadwick LM, Pemberton PJ, Kurinczuk JJ. Neonatal subgaleal hematoma: Associated risk factors, complication and outcome. J Pediatr Child Health 1996; 32: 228-232.

9. Govaret P, Vanhaesebrouck P, Depraeter C, Moens K, Leroy J. Vacuum extraction, bone injury and neonatal subgaleal bleeding. Eur J Pediatr 992; 151: 532-537.

10. Tan KL, Lim GC. Phototherapy for neonatal jaundice in infants with cephalhematomas. Clin Pediatr (Phila) 1995; 34: 7-11.

11. Leblanc CM, Allen UD, Ventureyra E. Cephalhematomas revisited. When should a diagnostic tap be performed? Clin Pediatr (Phila) 1995; 34: 86-89.

12. Posselt AM, Cowan BE, Kwong LK, Vreman HJ, Stevenson OK. Effect of tin protoporphyrin on the excretion rate of carbon monoxide in newborn rats after hematoma formation. J Pediatr Gastroenterol Nutr 1985; 4: 650-654.

 

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