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Progression of ganglionic germinal matrix bleed to intraparenchymal hemorrhages

Intraparenchymal bleed in a premature neonate with germinal matrix bleed is due to extension of the periventricular hemorrhagic infarction beyond the periventricular area.

Prognosis of neonates with ganglionic germinal matrix hemorrhages

The prognosis of neonates with germinal matrix hemorrhage depends on its evolution. Germinal matrix hemorrhage without any progression has a good prognosis. The prognosis of germinal matrix hemorrhages that progress to intraventricular hemorrhages depends on its subsequent evolution. Neonates whose intraventricular hemorrhages resolve have a better prognosis that those neonates with intraventricular hemorrhages that produce hydrocephalus.
A grading system to prognosticate the likely outcome of neonates with germinal matrix hemorrhages based ultrasonographic findings is sometimes used. This system classifies germinal matrix bleeding as grades I to IV. Grade I intraventricular hemorrhages are restricted to the germinal matrix; grade II intraventricular hemorrhages consist of blood in the germinal matrix and in the ventricles; grade III intraventricular hemorrhages con
sist of blood in the germinal matrix and ventricles, and ventricular dilatation; and grade IV hemorrhages consist of blood in the germinal matrix hemorrhage extending to the parenchyma. The incidence of neurological sequela is about 10% for grade I and II intraventricular hemorrhages, about 50% for grade III intraventricular hemorrhages, and about 90% for grade IV intraventricular hemorrhages. Premature neonates with germinal matrix hemorrhages do not require any specific laboratory investigations to look for an etiology for the bleed.


The site of an intra-axial hematoma in the fullterm neonate differs from that of the premature neonate. Intra-axial hematomas in the fullterm neonate may occur in the periventricular area, centrum semiovale, thalamus, or ventricles.
Periventricular hemorrhagic infarctions are rare in fullterm neonates because they result from germinal matrix hemmorrhages and germinal matrix hemorrhages are rare in fullterm neonates. The cause of periventricular hemorrhagic infarction is usually not found. Coagulation studies are usually not done in these patients.
Centrum semiovale and thalamic hemorrhages usually occur in neonates with clotting disorders. The most common cause of clotting disorders in neonates is thrombocytopenia. Neonates with platelet count below 20,000 per cubic millimeter are at high risk for bleeding. Sepsis is probably the most common cause of thrombocytopenia in the neonatal period. Maternal immune thrombocytopenic purpura, systemic lupus erythematous, and exposure to thiazide or digoxin are also associated with low platelets. Bleeding diathesis may occur with factors VII, VIII, or IX, or vitamin K deficiencies. Centrum semiovale hemorrhages may occur with vascular malformations, aneurysms, cerebral tumors, and meningitis.

Figure 256.1. CT of the brain demonstrating centrum semiovale hematoma. Cerebral edema and displacement of the lateral ventricles.

Patients on extracorporeal membrane oxygenation are at risk for intraparenchymal bleeding because of the use of heparin. Coarctation of the aorta may contribute to the production of intraparenchymal bleeding. The cause of intraperenchymal hemorrhage is often not found.
Intraventricular hemorrhages in fullterm neonates usually arise from the choroid plexus. Coagulation defects are usually not found in these patients, hence coagulation studies are not often done.
Treatment of intra-axial bleeding is usually supportive. Correction of the bleeding diathesis is necessary. Neurosurgical treatment is seldom possible in patients with parenchymal bleeding.


Cerebellar, brainstem, and spinal cord hemorrhages are very rare in the neonatal period. Cerebellar hemorrhages may occur as a result of arteriovenous malformation rupture, venous infarction, cerebellar contusion, or due to extension of an intraventricular or subarachnoid hemorrhage. Cerebellar hemorrhages are more common in premature infants than in fullterm infants. The possibility of a bleeding diathesis, a posterior fossa skull fracture, or von Hippel-Lindau disease should be considered in a neonate with cerebellar hematomas. von Hippel-Lindau disease is characterized by retinal angiomas; cerebellar and spinal cord spinal cord hemangioblastomas; renal cell carcinomas; pheochromocytomas; angiomas of the liver and kidney; and cysts of the pancreas, kidney, liver and epididymis. von Hippel-Lindau is a an autosomal dominant disorder due to a defective tumor supressor gene at chromosome 3p25-26.Most neonates with cerebellar hematomas require observation only (Figure 256.2). Surgical treatment is restricted to large surface cerebellar hematomas with mass effect.


Figure 256.2. Cerebellar hematoma. [A] T1-coronal view demonstrates a large circular lesion with peripherally increased signal in the right cerebellar hemisphere. [B] T2-coronal view demonstrates a large circular lesion devoid of signal.

Spinal cord hemorrhages are usually due to trauma. Bleeding diathesis and arteriovenous malformations are infrequent causes of intraparenchymal spinal cord bleeding (Figure 256.4).


Figure 256.4. [A] Intraparenchymal spinal cord hematoma and extradural arachnoid cyst compressing the spinal cord; [B] extradural arachnoid cyst compressing the spinal cord.



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