INTRAVENTRICULAR HEMORRHAGE-CASE BASED DR.MICHAEL DAVID HOZZA (SHO RADIOLOGY) 12 TH SEPTEMBER 2025
DEMOGRAPHYC: Name: GY 17 Yo , Female, Sec school student. Informant(Mother) CC: Sudden-onset severe headache 1/7 Associated with Generalized Seizures(tonic- clonic ), Both upper and lower limbs. No urine/fecal incontinence. PMSHx : No Hx of Chronic illness or admission, No BT, No Hx of Surgical intervention OE: Clinically Unstable in O2. Vitals: BP 121/78mmHg, PR 114BPM, RR: 19 C/m Temp: Not taken. GCS: 9 E3 V2 M4 This case shows the importance of timely neuroimaging in young adults presenting with acute neurologic symptoms and highlights the radiologic features and potential etiologies of IVH in adolescents.
Findings: Hyperdense(39 HU) fluid collection seen within the lateral and third ventricles consistent with acute intraventricular hemorrhage. Evans Index 0.23 No parenchymal hematoma, mass lesion, or signs of herniation Basal cisterns preserved, no hydrocephalus at time of imaging The rest of brain parenchymal, orbits, PNS and bones appears normal Conclusion: NECT shows Acute isolated intraventricular hemorrhage with no apparent source (without associated parenchymal hemorrhage or mass effect) Recommendation: Further vascular imaging (CTA or MRA) to rule out AVM or aneurysm Management: Patient condition were still deteriorating and was referred to Mbarara RRH within 3 hours of stabilization.
Management and Outcome Pt to ICU for close neurological monitoring. Seizure control with intravenous antiepileptics Airway protection (O2) due to low GCS Planned CT angiography (CTA) and/or MRI to identify underlying vascular cause Under Neurological team External ventricular drainage (EVD) was planned Within 6-hour following trying to stabilization the patient, neurological status remained un-stable, referred to Mbarara Regional Referral Hospital for MRI and further Neurological management.
1.INTRODUCTION (ANATOMY) COMPONENTS OF CEREBRAL VENTRICULAR SYSTEM LATERAL VENTRICLES (I,II) Paired structures located in each cerebral hemisphere Each lateral ventricles consists of a body and three horns(Anterior, Posterior and Interior) It is connected to the third ventricle via the Intraventricular foramina (of Monro) THIRD VENTRICLE (III) A narrow, slit-like cavity located in the diencephalon, between the thalamus and hypothalamus Communicating with the fourth ventricle via the Cerebral aqueduct(of Sylvius).
FOURTH VENTRICLE(IV) A diamond shaped cavity located between the rainstem (pons and medulla) and the cerebellum Connects to the Central canal of the spinal cord inferiorly and the subarachnoid space via the median apertures (of Magendie) and lateral apertures (of Luschkas )
CHOROID PLEXUS AND CSF PRODUCTION Choroid plexus: highly vascularized structure located in the ventricles, responsible for Cerebrospinal fluid (CSF) production. CSF: rate of 500ml/day although total vol of CSF in the ventricles is only about 150 mls at any given time ( ie continuous production and re-absorption) Plexus: composed of specialized epithelial cells that actively transport ions and water from the CSF.
CSF CIRCULATION Lateral ventricles/3 rd ventricle/cerebral aqueduct/4 th ventricle/ Subarachnoid space(via median and lateral apertures)/central canal of the spinal cord In the subarachnoid space, CSF circulate around the brain and spinal cord providing buoyancy & protection. Subarachnoid cisterns : enlarged spaces within the subarachnoid spaces where CSF accumulate , it also provide additional protection from mechanical shock and trauma. CSF : reabsorbed back into the venous system through arachnoid granulation i n the dural venous sinuses (primarily in the superior sagittal sinus)
CEREBRAL VENTRICULAR SYSTEM FUNCTIONS Plays a crucial role in maintaining brain function through CSF production/circulation Mechanical and immunological protection (shock & transport of immune cells btn blood and lymphatic system) Homeostasis Maintain intracranial pressure (adjusting CSF production/absorption) Facilitate clearance of toxins and waste products from neural tissue via the lymphatic system. Regulate pH, electrolytes and neurotransmitter level for proper neuronal function
COMMON PATHOLOGIES OF THE CEREBRAL VENTRICULAR SYSTEM i /Ex-vacuo ventriculomegaly: (due to atrophy) ii/Hydrocephalus Obstructive (non-communicating) due to blockage of CSF flow Aqueduct stenosis of occlusion(Eg due to blood clots) Colloid cyst(often localized at the foramen of Monro) CSF pathway compression by tumor, expansive cerebellar infections Communicating With Impaired CSF absorption(Post Meningitis scarring, subarachnoid hemorrhage) With overproduction of CSF( Coroid plexus papilloma/carcinoma) Normal pressure hydrocephalus(NPH)-triad of gait disturbance, urinary incontinence, cognitive impairment iii/ Ventriculitis (infections within the ventricles Eg Meningitis) iv/ Intraventricular hemorrhage (IVH)
2.DFN, CLASSIFICATION & ETIOLOGY (PRIMARY AND SECONDARY IVH) Intraventricular hemorrhage (IVH) aka Hemocephalus is characterised by presence of blood in the brain's ventricles . IVH prevalence: Preterm infants is approximately 36% 3.1% of nontraumatic central nervous system hemorrhages. TYPES PRIMARY IVH (isolated) SECONDARY IVH (More common 25-40%, extension from ICH)
CLASSIFICATION AND ETIOLOGY PRIMARY IVH Blood in the ventricles with little or no blood in parenchymal Possible causes Vascular malformation (subependymal AVMs and Cavenous malformations) Coagulopathy ( Eg. Walfarin ) Intraventricular tumor(Ependymoma, choroid plexus mets , etc ) Hypertensive bleeding due to rupture of the periventricular vessels
SECONDARY IVH More common than Primary IVH, with significant extraventricular component(either parenchymal or subarachnoid) Propagation of intracerebral hematoma (up to 45% of ICH pts) SAH (Possible reflux from the spinal SAH) Trauma
3.RISK STRATIFICATION Prognostic tool eg. Graeb score, Modified Graeb score, or the LeRoux IVH score assess IVH severity and predict outcomes.
GRAEB SCORE
CLINICAL PRESENTATION Primary IVH presents similarly to Aneurysmal SAH, with headache, neck stifness , photophobia, nausea Neurological deficits in secondary IVH depen on the Primary hemorrhagic klesion ( Eg. Basal ganglia ICH, thalamic hemorrhage ) Massive IVH increases intracranial pressure, leading to hydrocephalus, brainstem compression, coma and Respiratory failure.
NECT 1 st line imaging modality (IVH: hyperdense (50-90 HU) material within the Ventricular system always located in occipital horns due to gravity F/up CT necessary to monitor hematoma progression and ventricular enlargement
MRI Sensitive to small amount of blood, especially in the posterior fossa(where CT may be inconclusive) FLAIR: Signal intensity of blood in time- dependent and complex based on Hb degradation products GRE/SWI: Detect very small amounts of blood in the occipital horns(shows hypointense rim/blooming artifact)
VASCULAR IMAGING(CTA,MRA,DSA) When Vascular cause suspected ( Eg.AVM , Aneurysm, Moyamoya) commonly in young patients without traditional risk factors. CTA: Rapid, Widely available and detects major vascular abnormalities MR+MRA: Time of Flight, uses the Time of Flight(TOF)MRA DSA: Gold standard for Subtle vascular lesion.
Case: AVM
Case: IVH due to Cavernous angioma
CT images showing intraventricular blood, and CTA revealing an unusually small right MCA that was substantially smaller than the left. DSA same pt revealing an abnormal cluster of collateral vessels near the distal carotid that was the result of longstanding stenosis of the proximal middle cerebral artery due to Moyamoya disease.
Differential Diagnosis Ruptured AVM – common cause in this age group (Gross & Du, 2013) Periventricular aneurysm Vascular neoplasm (e.g., choroid plexus papilloma) Idiopathic IVH Bleeding diathesis – less likely in absence of clinical history