Adrenal hemorrhage in asphyxiated neonates and the importance of ultrasonography

432 THE INDIAN JOURNAL O~ PEDIATRICS

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2. Nemir RH, O'Hare D. Congential tuber- culosis. Am J Dis Child 1985; 139 : 284-287.

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Adrenal Hemorrhage in Asphyxiated Neonates and the Importance of Ultrasonography

S/ikrii Kiifiik6diik, famail fslek, Hiiseyin Akan,* Murat Aydin, Cengiz Dilber and Nuran Gfittes

Departments of Pediatrics and *Radialogy, Ondolo~z Mayis University, School of Medicine; Samsun, Turkey

A d r e n a l hemorrhage is not rare in neonates. Massive adrenal hemorrhage diagnosed during life in neonates was first described in 1924.1 Adrenal gland is more prone to traumatic hemorrhage in the newborn in comparison with other groups, since it has a large volume and rich vascularity, z Sepsis, hemorrhagic abnormalities, hypoprothrombinemia, asphyxia and birth t rauma are common risk factors for adrenal hemorrhage? Incidence of perinatal asphyxia varies from 1% to 1.5%. This incidence is 9% for neonates with gestational age younger than 36 weeks, and 0.5% for neonates with gestational age older than 36 weeks. ' In asphyxia, blood flow to vital organs such as brain, myocardium and adrenal gland is preserved or increased; on the other hand, the blood flow to kidneys, intestines, muscles and skin is decreased due to selective vasoconstriction, s Because of that,

asphyxiated neonates are prone to adrenal hemorrhage.

So far, varied clinical pictures and con- troversies about the t reatment of choice have been reported for adrenal hemor- rhage in neonates. Although some authors prefer surgical approach, s; the others ad- vocate conservative management. .,9 In this article, eight neona te cases diagnosed as .adrenal hemorrhage with clinical signs and laboratory findings between 1988 and 1993 are summarized in Table 1, 2, 3 and case 4 is presented in detail.

CAsz REPorr

In our neonatal unit, 4,620 patients were treated between 1988 and 1993. Two hundred and fifty one of them were diagnosed as asphyxiated neonate and fo | lowed up. When there were signs and symptoms of probable adrenal

1994; Vol. 61, No. 4 THE INDIAN JOURNAL OF PEDIATRICS 433

hemorrhage, abdominal ul t rasonograpy (US) examination was performed in these neonates. In patients whom US showed the adrenal cystic lesions as evaluated adrenal hemorrhage,, computed tomography (CT) examination was performed to define the characteristic features and size of the lesions distinctly. Adrenal hemorrhage was diagnosed by clinical and laboratory findings in eight cases who were referred to our hospital because of apnea, cyanosis, convulsion or jaundice in the first week of life except one. Two of them were female and the others were male, and birth weights varied from 2400 g to 3800 g. All were vertex presentation at birth and had history of asphyxia. None of them had evidence of septicemia, coagulation defect and blood .group incompatibility on admitting to hospital. Clinical and laboratory findings are summarized in

Table 1, 2, 3, and case 4 is presented in detail. Case 4. One day old male patient was referred because of perinatal asphyxia and convulsion. On physical examination, tachypnea and spastic appearance were present and newborn reflexes were lost. Laboratory results were as follows : urine analysis : normal, hemoglobin (Hb) : 12.9 gr /dl , WBC : 24.900/ml, BUN : 31 mg/dl , creatinin 1.4 mg/d l , Na : 145 mEq/L, K : 6.4 mEq/L, glucose : 53 m g / d l , total bilirubin : 7.8 mg/d l , direct bilirubin 0.6 mg /d l , Ca : 9.1 mg /d l , fibrinogen : 377 mg/dl , SGOT : 76 U/L, SGPT : 45 U/L, PT and FIT : longer than one minute, plasma cortisol : 6.7 pgdl, in 24 hours urine; homovanillic acid (HVA) : 9 I~g/mg creatinin, Vanil mandelic acid (VMA) : 0.4 mg/d l . Transfontanel u l t rasonography showed brain edema and cranial

T^SLe 1. Clinical Manifestations of the Cases

Case no.

ABe (day)

Sex Birth Perinatal weight asphyxia

Symptoms Clincal findings

1 F 3770 +

1 M 3850 +

2 M 2400 +

1 M 3450 +

6 M 3150 +

7 M 3800 +

27 F 3900 +

7 M 3900 +

Cyanosis, convulsion

Cyanosis, apnea, convulsion

Convulsion

Convulsion

Jaundice

Convulsion, oliguria, hematuria

Vomiting,

Jaunmce, poor

Left upper abdominal mass

Dispnea, cyanosis, areflexia

Hypoactivity, areflexa

Tachypnea, areflexia

Hypoactivity, icterus, left flank mass

Left upper abdominal mass

Cyanosis, tachypnea, left flank mass

Icterus, bilateral upper abdominal masses

434 THE INDIAN JOURNAL OF PEDIATRICS 1994; Vol. 61. No. 4

, ~ 1 7 6

jj!

1994; voi. 61. No. 4 THE INDIA_h/JOURNAL OF PEDIA'/'R/CS

TABLe 3. Ultrasonography and Computed Tomosraphy Findings, and Clinical Results of the Cases

435

Case US Findings CT Findings Clinical Results

I. Hypoechoic cys~c masses Hypodense cystic masses in Conservative in right adrenal (13 x 11 ram), both adrenal region management, died on and left adrenal (23 x 19 mm) the 5th day

2. Anechoic cystic masses in Cystic masses in both adrenal both adrenal glands region (44x 19 mm, 48x 20ram)

3.

4.

.

.

.

8.

Hypoechoic cystic mass in right adenai gland

Hypoechoic cystic mass in both adrenal glands (Figure 1)

Anechoic cystic masses in both adrenal glands (26 x 11, 25 x 29 ram), hyperechosen enlarseci kidney

Hypoechioc cystic masses in both adrenal 81ands �9 ~d h y ~ o g ~ erdarg~t kidneys

Cystic masses in both adrenal ~ and hyper~hoic, ~xlarg~l life kidney

Anechoic cystic masses in both adrenal gland (20 x 30, 30 x 35 ram)

Cystic mass in right adrenal r ~ o n

Hypodeme cyslic masses in both adrenal region (Figure 2)

Bilateral adrenal hemorrhagic cystic masses ( F ~ m 4) and, left rm~al vein and vm~a cava inferior thrombosis

Bilateral adrenal hemorrhagic cystic mases, enlarsed kidneys, contrast enhancement neither in renal veins and vena cava inferior.

Cystic mass in left adenal region, no excr~on of con~ast medium on left m i a r ~ ~ctr~y

Conservative management, died on

22rid day

C o n s e r v a t i v e mana~ment, recovmq~d and d~.harg~ on bhe 17th day

Consevafive management, recovered and discharged on the 13th day

Conservative management, recovered and discharsed on the 28th day

Conservative mama~ment, p~toneal d~alysis, r~covemd and dischar~d on the 31st day

Conservative management, peritoneal dialysis, died on the 27th day

~ t i v e manasmnmt, mcov~r~! and ~ L ~ I on ~ 1 ~ clay

o6 T ~ n~DL~ JOURNAL OF P~h~TmCS 1994; VoL 61. Nix 4

computed tomography demonstrated hemorrhage at.right tentorium (Figure 1). Abdominal US showed cystic lesions in adrenal glands. Abdominal CT demonstrated hypodense cystic lesions in both adrenal glands, but larger in left than right (Figure 2). He was supported with appropriate fluid and electroyte therapy and given phenobarbital 5 m g / k g / d a y and dexamethasone 0.8 mg/kg /day , and only once vitamin K 1 mg IM. He recovered and was discharged on the 12th day of hospitalization. In the follow-up examination, resolution of adrenal hemorrhage was shown at US. After~nlne months, abdominal US demonstrated adrenal calcification with acoustic shadowing (Figure 3).

DISCVSSlON

Adrenal hemorrhage is a less common cause of intraabdominai masses for which hydronephrosis and multicystic displastic kidney are most conunon, x~ It is reported that hemorrhage affects right adrenal gland three to four times more frequently than left, and bilateral hemorrhage is presented in 8-10% of cases. The fragility of right adrenal gland is due to its compresion between the liver and spines, and to that it is more sensitive to change in venous pressure for the right adrenal vein usually drains directly into the inferior vena cava. ~ The rate of bilateral adrenal hemorrhage was higher in our cases than the literature. This may be explained by severity of birth trauma and asphyxia.

Although evident adrenal hemorrhage is rare, it is a life threatening event. Adrenal insufficiency is rare. For development of adrenal, insufficiency,

hemorrhage should be bilateral and adrenocortical tissue damage should be at least 90%. Signs may be silent or late. Even if bilateral hemorrhage, functioning islands of zona giomerulosa cells are usually well preserved. Hypoglycemia are more frequent than salt loss. u In our cases, although hemorrhage is bilteral in all except one, there were no signs of adrenal insufficency as clincal and laboratory findings.

Symptoms and signs associated with primary reasons may be seen in neonates with adrenal hemorrhage. Hypovolemic shock, anemia and prolonged jaundice may develop secondary to the hemor- rhage? In all cases, primary reason was perinatal asphyxia and usually present car- diopulmonary failure. Four cases had con- vulsions. Only in case 5, hyper- bilirubinemia developed necessiating blood exchange transfusion.

Neonatal adrenal hemorrhage suspected clincally is detected with ultrasonographic examination. In the early stage, suprarenal mass due to adrenal hemorrhage may give ultrasonographic findings varying from echoic apearance to hypoechoic and anechoic appearance. Tl~ pattern of involvement may be unilateral or bilateral, x2,~3 US findings of our cases were similar with the literature. Although neuroblastoma is seen less often than adrenal hemorrhage in the newborn, volume of the hemorrhage does not change or increase for the first few days, and it regresses after two weeks. On the other hand, neuroblastoma tends to be more echoic and volume tends to be stable or increase. 1~ Since the left adrenal vein drains into the left renal vein, there is a relation between left adrenal hemorrhage

1994; Vol. 61. No. 4 THE INDIAN JOURNAL OF PEDIATRICS 437

Fi 8. 1. US scannin 8 shows cystic masses (*) superior to fl~ kidney bi]algrally. L : Liver, rk : fight kidney, lk : left kidney

Fig. 2. CT scan of the same patient as Figure 1, demonstra~Sng cystic masses at the adrenal gland regions

438 THE INDIAN JOURNAL OF PEDIATRICS 1994; Vol. 61. No. 4

Fig. 3. US demonstration of bilateral hyperechoic lesions with acoustic shadowing at suprarenal regions which are evaluated as adrenal calcification (arrows)

Fig. 4. CT scan showing bilateral suprarenal cystic masses and left renal vein thrombosis (arrow)

1994; Vol. 61. No. 4 THE INDIAN JOURNAL OF PEDIATRICS 439

and left renal vein thrombosis? s A thrombus originating from the left adrenal vein may extend to the left renal vein, or even into the inferior vena cava. The right renal vein and adrenal vein drain into the inferior vena cava separately? ~ The left renal vein thrombosis was associated with bilateral adrenal hemorrhage in case 5, and bilateral renal vein thrombosis was associated with bilateral adrenal hemorrhage in case 6 (Figure 4). The left adrenal hemorrhage was associated with the left renal vein thromlx~is in case/

Although adrenal calcification dur ing the course of adrenal h e m o ~ h a g e is seen after two weeks, it may develop by the seventh day. As the mass regresses and is resorted, calcification become denser and has the shape of the adrenal gland. Sometimes, calcification may not develop after months} Case 1, 2 and 7 died at fifth, twenty second and twenty seventh day of hospitalization, respectively, d u e to reasons such as birth t rauma, ,~ardiopulmonary failure and sepsis. During the follow up of the other cases, adrenal calcification was detected only in case 4 at 9th month following hemorrhage {Figure 3).

Differential diagnosis of suprarenal mass should include adrenal hemorrhage, adrenal cyst, neuroblastoma, Wilm's ,umor and renal duplication which causes dilatation at upper segment. These massses could be differentiated easily by the use of intravenous urogram, arteriography, US, renal scintigraphy and CT. u7 Abdominal CT and US of our cases demonstrated adrenal hemorrhage clearly (Figures 1,2).

If neuroblastoma can ne ruled out, h0movanillic acid (HVA) and vanyl mandelic acid (VMA) in urine should be

investigated. Simulataneously obtained high levels of these tests suggest neuroblastoma with a rate of 95%. is Urine levels of VMA and HVA in all of the cases were normal.

Although medical supportive treatment is usually preferred in neonatal adrenal hemorrhage, sometimes surgical treatment may be necessary. Surgical management is advocated in infected adrenal hemorrhage, or when malignancy cannot be ruled out} ,7,19 There were no cases with infected h e m o r r b a g e and malignancy was ruled out in our cases.

Our observation on adrenal hemorrhage in eight newborn cases w i t h perinatal asphyxia shows that, beside clinical and laboratory investigations of other organs and tissues, ultrasonographic examination may be rather useful in the early diagnosis and follow up of adrenal hemorrhage in all neonates with a history of traumatic birth.

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