DOI: 10.1148/radiol.2283011829
(Radiology 2003;228:693-696.)
© RSNA, 2003
Case 62: Lobar Hemorrhage from Thrombosis of the Vein of Labbé1
Blaise V. Jones, MD
1 From the Department of Radiology, Children’s Hospital Medical Center, 3333 Burnet Ave, Cincinnati, OH 45229. Received November 14, 2001; revision requested January 29, 2002; revision received March 13; accepted April 2. Address correspondence to the author.
Index terms: Brain, hemorrhage, 176.43 • Brain, infarction, 134.78 • Cerebral blood vessels, thrombosis, 176.769 • Diagnosis Please
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HISTORY
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A full-term female neonate required resuscitation at delivery because of complications that arose from spontaneous, massive fetal-maternal hemorrhage. (This hemorrhage is a perinatal transfusion of fetal blood to the mother, which sometimes occurs as a complication of placental abruption.) There was no inciting cause identified in this case. The neonate had marked anemia and thrombocytopenia, but she responded well to resuscitative measures. She had no signs of sepsis. On day 2 of life, she had a seizure. Transcranial ultrasonography (US) (Fig 1) was performed on day 3 of life, and magnetic resonance (MR) imaging of the brain was performed on day 4 of life (Figs 2–4).
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Figure 2a. Transverse inversion-recovery T1-weighted MR images (repetition time msec/echo time msec/inversion time msec, 2,000/20/800) through the level of the third ventricle. (a) Large hematoma (arrows) is centered in the lateral aspect of the left temporal lobe. (b) Mass effect from the lesion obliterates the temporal horn and displaces the third ventricle to the right of midline (arrows). The peripheral aspect of the lesion is hyperintense, but the central aspect is iso- to hypointense relative to the brain.
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Figure 2b. Transverse inversion-recovery T1-weighted MR images (repetition time msec/echo time msec/inversion time msec, 2,000/20/800) through the level of the third ventricle. (a) Large hematoma (arrows) is centered in the lateral aspect of the left temporal lobe. (b) Mass effect from the lesion obliterates the temporal horn and displaces the third ventricle to the right of midline (arrows). The peripheral aspect of the lesion is hyperintense, but the central aspect is iso- to hypointense relative to the brain.
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Figure 3. Transverse fast spin-echo T2-weighted MR image (repetition time msec/echo time msec, 2,500/99) shows hematoma (arrows) as heterogeneous and markedly hypointense. Peripheral aspect of hematoma is markedly hypointense. In association with the area of hyperintensity in Figure 1, this is consistent with the presence of methemoglobin. Central areas of the lesion have signal intensity characteristics more consistent with those of deoxyhemoglobin (hypointense on T2-weighted images and isointense on T1-weighted images).
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Figure 4. Coronal fast spin-echo T2-weighted MR image (5,200/120) through the level of the fourth ventricle. The acute angle made by the hematoma with adjacent cerebrum (black arrow) is consistent with an intraaxial location, although the infolding of the cortex suggests that at least some component is subpial. Scalp edema over the right convexity (white arrows) is a common result of vaginal delivery.
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IMAGING FINDINGS
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Initial US examination (Fig 1) showed a large echogenic mass in the left temporal lobe that appeared to be entirely intraparenchymal. The MR images demonstrated this mass in the lateral aspect of the left temporal lobe. On the T1-weighted image (Fig 2), the mass was characterized by central hypointense signal and a peripheral rim of hyperintense signal. The lesion was predominantly hypointense on T2-weighted images (Figs 3, 4), with distorted parenchyma and edema resulting in some mixed signal intensity. These signal intensity characteristics were consistent with those of lobar hemorrhage, with the central signal intensity representing deoxyhemoglobin and the peripheral signal intensity representing intracellular methemoglobin. The hemorrhage did not have subarachnoid, subdural, or epidural components and resulted in a moderate degree of mass effect, with medial deviation of the ipsilateral uncus. No unusual vessels were seen adjacent to the lesion, and the structure of the unaffected brain was normal. No other lesions were demonstrated. An MR image obtained 4 months after initial examination (Fig 5) showed encephalomalacia and some hemorrhagic staining in the lateral left temporal lobe but no residual mass or abnormal vasculature. An image obtained with MR venography (Fig 6) showed flow in the vein of Labbé on the right but no flow in the corresponding vein on the left.
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Figure 5. Transverse conventional spin-echo T2-weighted MR image (2,500/100) obtained 4 months after initial examination shows resolution of mass effect with volume loss in the left temporal lobe. Marked hypointense signal in the region (arrows) is consistent with hemosiderin staining.
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Figure 6. Coronal image obtained with two-dimensional time-of-flight MR venography (46/6.9; flip angle, 45°) shows flow signal intensity in the vein of Labbé on the right (long arrow), but no corresponding flow signal intensity in the vein on the left (short arrows).
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DISCUSSION
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Lobar hemorrhage in full-term neonates is uncommon. The most common cause of this condition is thought to be bleeding into parenchyma in which infarction occurred (1–4). Such infarctions may be due to arterial or venous compromise. Smaller unilateral hemorrhagic lesions are sometimes encountered in full-term neonates and are thought to represent hemorrhagic infarction from venous occlusion. These are frequently associated with hypercoagulability brought on by sepsis, dehydration, and hypotension. Patients with small unilateral lesions have a good prognosis, but the presence of a large intraventricular component or bilateral involvement is associated with substantial morbidity (1). In premature infants, large parenchymal hemorrhagic lesions are sometimes seen in association with germinal matrix and intraventricular hemorrhage on cranial US images and are termed grade IV hemorrhages. These are thought to result from periventricular venous congestion, with associated hemorrhagic venous infarction (1,2,5).
In arterial infarctions, recognition of characteristic vascular territories allows identification of the involved vessel. In the full-term neonate, arterial vascular beds are similar to those in the adult, and regions affected by occlusion of specific major intracranial arteries are well documented. The localization of specific territories of venous drainage is less precise. When an atypical vascular territory is involved in an infarction, less common causes of ischemic injury must be considered, including mitochondrial encephalopathy, vasculitis, and venous occlusion.
Many intracranial venous structures are unnamed, and there is considerable variability in patterns of venous drainage, especially among the superficial cortical veins; however, two of the larger cortical veins are named. The first of these veins is the vein of Labbé, which runs in an anterior-to-posterior direction along the lateral surface of the left temporal lobe and drains into the transverse sinus near its junction with the sigmoid sinus. The second is the vein of Trolard, the dominant parietal lobe cortical vein that drains superiorly into the sagittal sinus near the central sulcus. Because of their size, physiologic importance, and location, these vessels are of great interest to neurosurgeons who approach lesions in the underlying temporal, frontal, and parietal lobes.
The vein of Labbé is identifiable at autopsy in 75% of cadavers (6). It can be recognized on unenhanced MR images as a prominent flow void apposed to the lateral aspect of the temporal lobe. It is readily demonstrated on MR and computed tomographic (CT) venographic images and on cerebral arteriograms obtained during the venous phase of enhancement. Although a vein of Labbé can usually be identified over each temporal lobe, they are often asymmetric. Thrombosis of this vein results in a characteristic pattern of hemorrhagic infarction in the lateral aspect of the underlying temporal lobe (4,6). This territory of venous drainage overlaps considerably with the vascular bed of temporal branches of the middle cerebral artery. Although occlusion of these branches could cause infarction in the same territory, there is invariable involvement of the adjacent insular cortex in an arterial infarction. Venous occlusions are recognized as having a propensity to cause hemorrhagic infarction (5). When the territory of the vein of Labbé is recognized as the region of hemorrhage, it should increase confidence in the diagnosis of hemorrhagic venous infarction (7).
Hemorrhagic lesions can occur as a result of birth trauma, and these lesions usually have both intraparenchymal and extraaxial components (epidural, subdural, or subarachnoid blood). The same can be said for trauma outside of the delivery process. It is distinctly unusual for primary vascular lesions such as arteriovenous malformations and aneurysms to occur with intracranial hemorrhage in the neonate, although superimposed coagulopathy or birth trauma can induce bleeding from these lesions. Vein of Galen aneurysmal malformation is the most common intracranial vascular malformation to occur in the neonate and typically causes cardiac failure in the first few days of life. Thrombosis may also spontaneously occur after delivery in neonates with vascular malformations, appearing as a large avascular mass in association with anomalous intracranial arteries and veins. Intracranial tumors that are present at birth can spontaneously hemorrhage; the most common tumors that occur in neonates are high-grade germ cell tumors (teratoma), primitive neuroepithelial tumors, astrocytomas, and choroid plexus papillomas (8). Neonatal encephalitis can cause lobar hemorrhagic lesions, most notably herpes encephalitis. These infections are typically acquired at or shortly after delivery and manifest toward the end of the 1st week of life (1).
Complete imaging evaluation of lobar hemorrhage in neonates is often compromised by the size and associated mass effect of the hemorrhage itself. Confident exclusion of an underlying neoplastic or primary vascular lesion is difficult in the acute setting. Conventional angiography is often unrewarding; the tamponade effect of the lesion will limit flow to the affected territory and associated vascular opacification. Because it is also dependent on flow, MR angiography has limited value in the evaluation of lobar hemorrhage in the neonate. Theoretically, CT angiography may be more helpful in the early evaluation of these lesions because all patent arteries and veins are simultaneously opacified, but this has yet to be proved. CT angiography should be less susceptible to the effects of diminished flow and can demonstrate the relationship of the parenchymal lesion and the adjacent vessels to good advantage. It is relatively unusual to confidently identify thrombus within a cortical vein as a source of venous infarction, even when specifically sought; however, absence of this finding cannot lead one to exclude this diagnosis (6).
As a result of these limitations, the diagnosis of venous thrombosis as the cause of lobar hemorrhage in the neonate is typically one of exclusion. Initial imaging is used to outline the extent of the abnormality and to try to identify any underlying primary lesion such as a tumor or vascular malformation. A full clinical evaluation is performed to assess primary or secondary coagulopathy, sepsis, and encephalitis. In the absence of a tumor or vascular malformation, clinical management is centered on treatment of any underlying coagulopathy or infection and management of any associated neurologic symptoms, the most common of which is seizure. Neurologic deficits may be surprisingly mild and well tolerated. Cranial US can be used to monitor the status of the hemorrhage itself. In the absence of new signs and symptoms or unusual evolution at US, follow-up MR imaging or CT should be performed after resolution of the hematoma, typically 6–12 weeks after ictus. At this time, a more confident evaluation for abnormal vessels can be made. Conventional angiography may be necessary to assess more fully any suspected vascular lesions and will likely be more fruitful and less risky at this time than in the neonatal period.
To summarize, this is a case of lobar hemorrhage in a neonate. No underlying neoplasm or vascular malformation is evident, which leaves hemorrhage into infarcted parenchyma as the most likely diagnosis. The hemorrhagic nature of the infarction, lack of involvement of the insular cortex, characteristic distribution of involvement, and appropriate clinical characteristics all support the diagnosis of occlusion of the vein of Labbé. The benign clinical course and appearance at follow-up imaging also support this diagnosis.
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FOOTNOTES
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Part 1 of this case appeared 4 months previously and may contain larger images.
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REFERENCES
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- Volpe JJ. Neurology of the newborn 4th ed. Philadelphia, Pa: Saunders, 2001; 397-434.
- Roland EH, Flodmark O, Hill A. Thalamic hemorrhage with intraventricular hemorrhage in the full-term newborn. Pediatrics 1990; 85:737-742.[Abstract/Free Full Text]
- Hanigan WC, Powel FC, Palagallo G, Miller TC. Lobar hemorrhages in full-term neonates. Childs Nerv Syst 1995; 11:276-280.[CrossRef][Medline]
- Ball WS, Franz DN. Neonatal brain injury. In: Ball WS, eds. Pediatric neuroradiology. Philadelphia, Pa: Lippincott-Raven, 1997; 267-270.
- Ball WS. Cerebrovascular occlusive disease in childhood. Neuroimaging Clin N Am 1994; 4:393-421.[Medline]
- Osborne AG. Diagnostic cerebral angiography 2nd ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 1999; 217-227.
- Barkovich AJ. Pediatric neuroimaging 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 2000; 202-205.
- Buetow PC, Smirniotopoulos JG, Done S. Congenital brain tumors: a review of 45 cases. AJNR Am J Neuroradiol 1990; 11:793-799.[Abstract]
Congratulations to the 8 individuals who submitted the most likely diagnosis (lobar hemorrhage from thrombosis of the vein of Labbé) for Diagnosis Please, Case 62. Credit was given only if the venous nature of the process was stipulated. The names and locations of the individuals, as submitted, are as follows:
- J. F. K. de Villiers, Gisborne, New Zealand
- Mustafa Kemal Demir, MD, Ataköy, Istanbul, Turkey
- John T. Lim, MD Newport Coast, Calif
- Harish Panicker, MD, Washington, DC
- N. Saravanan, Chandigarh, India
- Eugene Tong, MD, Austin, Tex
- Zhen Jane Wang, MD, San Francisco, Calif
- Benjamin M. Yeh, MD, San Francisco, Calif
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TOP
HISTORY
IMAGING FINDINGS
