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Right. Hi, everyone. My name is Yo and I'm a junior clinical fellow in Urology here in London. And today's session is the second in a series um on neonatal cranial ultrasound scans. And today's session is going to be about geminal matrix and intraventricular hemorrhages and a new bone. I'll be following this hotline as a rough guide. I'm starting with a brief introduction and risk factors for intraventricular hemorrhages, discussing the pathophysiology, clinical features, degrading systems, um management complications and ending with the the long term outcomes. So, by way of introduction, um cranial intracranial hemorrhage or intraventricular hemorrhage precisely, um they are quite common um conditions in your bones in the, in the nicu. And um yeah, probably the most common acute complication in preterm man. It um the incidence tends to increase with decreasing gestational age and but with more common in infants, less than 32 weeks and with a bit weight, less than 1.5 kg. Um a risk factor. Again, prematurity, low blood weight, um any kind of sepsis, septic background, especially Chis, um fluctuations in BP and um hypertension, hypercapnia, hypoxemia and blood asia all contribute to um preterm developing intra ventricular hemorrhages. In terms of the pathophysiology, the commonest site of origin for um geminal matrix hemorrhage. And I VH is the geminal matrix. It's a highly vascular structure um located in the car thalamic groove, that's like a n groove between the head of the cared nucleus and the thalamus. And it's a highly vascular and fla fragile area. The blood vessels there um have certain characteristics. They are devoid of the basal lamina. There are some fest administrations, all of which make it predispose that area to um bleeding and hemorrhage. Um This site is also the common is the site of origin of neuroblasts and they tend to migrate about 10 weeks up until about 20 weeks and become the source of neurons and glial cells for the cerebral cortex and the basal ganglia and the general matrix tends to evolute at about 34 weeks and the evolution process is complete at about 36 weeks. And most new ones sudden drastic changes in BP, oxygen levels, carbon levels all predisposed to bleeding at this site. The timing of an hemorrhage tends to be in the 1st 3 to 4 days with about 80 to 90% occurring this time, 50% occurring on day one and 5% on day two and about 15% on day three. So most of the scans will probably pick up an M Rh within this during this timeframe. Um The in terms of the clinical features the babies are usually mostly asymptomatic and the MRI tend to be an incidental finding on routine um, newborn scans. And um sometimes we are, we notice a sudden drop in hemoglobin levels and there's no obvious site of bleeding. So we do a cranial ultrasound scan and we find a, a bleed in the brain um that we were not aware of before. So sometimes it's a sudden drop in HB levels that comes from the screening for, for possible bleed in the brain. And in some rare occasions, the babies tend to have um symptoms uh which ranges from apnea to hypertension to um bulging, fontanel seizures, reduce spontaneous movements and hypotonia to cerebrate posture and loss of consciousness at V levels of of consciousness. Potentially. Um There are two main grading systems used um in most ners. The first is the PPI system which was initially act based grading system and that's been modified and adapted for use with cranial ultrasound scans. The most commonly adapted form is the devo criteria devo grading system, which is ultrasound based solely. Um these systems allow for more objective assessment of the severity of I VH and allows for easy communication between healthcare professionals of the the severity of the I VH. It also allow us to monitor the progression or the regression of, of the hemorrhage and allow for long term progression, medication and assessment of possible long term neurological sequela. Um Of course, for a as well, right, So this table just shows the the grade in. So we are four grades, grades 1 to 4 would reduce an incident, as you can see from about 40% and grade one to about 15% and grade four. And the criteria is a fairly simple um, grading system in grade one, the hemorrhage is limited to the gal matrix. That's the cola improve in grade two. There's a general matrix hemorrhage with or without an intraventricular extension. And usually the ventricles are normal size with no dilatation. In grade three, there is a general matrix hemorrhage and intraventricular hemorrhage with some degree of ventricular dilatation. And in grade four, there's intraventricular hemorrhage with or without. So there is an intra and extension or intra hemorrhage with or without an I VH. So sometimes you have an I VH with intra chal extension or you have just an intra camera hemorrhage, some grading systems or some, it has been some findings that suggest this completely different pathology sometimes in, in the bal M Rh with the V criteria. Um again, in grade one geminal matrix hemorrhage with less than 10% extension into the ventricles. So you could have solely geminal mari hemorrhage or an IV H which doesn't occupy more than 10% of the, of the ventricular area. On the part that I told you in grade two, we have an intraventricular hemorrhage occupying about 10 to 50% of the ventricles with no ventricular megaly as seen in the pal criteria. And in grade three, we have intraventricular mr more than 50% forgive this. There should be a 50% extension into the ventricles and associated ventriculomegaly. And then grade four again, same as the BPI criteria I VH and intra canal extension. This is just um a victor representation of the grades. And here we have the, the, the coronal view of the, of the, of the forebrain showing the lateral ventricles with the gin matrix. In grade one, we can see this the red, the red bits that shows the grade one hemorrhage within the matrix just confined to the geminal matrix. Grade two shows some extension into the ventricles, but the ventricles remain essentially the same size with no dilatation. In grade three, we have here, we have bilateral genin matrix hemorrhage. But on the left, we can see intraventricular extension and the ventricles are dilated most on the the right of the here. And in grade four, we have came he here as you can see, but they think it's it's a venous infection showing that sometimes the different pathologies essentially now to the cranial ultrasound scan findings. Um Here is a grade one sub geminal matrix hemorrhage. It's bilateral in this case, but we can see that it doesn't extend into the ventricles. The ventricles are normal size and it's just confined to the geminal matrix. Here. In grade two, we can see again, it's on the left here. Um and red with some extension into the, again, the ventricles are normal size here. We can see clearly on the ial you, we have the tri M Rh extending into the VLES, but then the ventricles are remain normal sized. We grade three, we have a gin matrix hemorrhage bilaterally here, more so on the left extending to the ventricles and we can see the ventricles are slightly ballooned up. Um There's definitely mark var dilatation associated suggesting a grade three, all right. And in grade four, the definitive marker for grade four mor is the intra came extension, which is quite obvious across all all four or five panels here from A to D. And we can see mark to dilatation as as as well. This is just to illustrate um how we determine ventricular dilatation using the cranial ultrasound scan. We use what is called a 11 index. Um Essentially we measure the distance in from the midline from the folk to the lateral wall of the ventricle. And then we put that on the 11 chart. So we measure on the coronal plane and on the view that shows the third ventricle from the midline to the lateral wall of the ventricle. And plot on the 11 chart, we have two centers and the more concerning one is if the the dimension measured processes the 97 plus four heal. So if it's above this line, we are concerned and we need to monitor closely and or seek neurosurgical consult at some point um for posthemorrhagic ventricle dilatation, just to mention that there are different, there are other ways of assessing and ventricular dilatation which is not um covered in this session. So down to the management, which of course starts with prevention of intraventricular hemorrhage. And it's divided here into prenatal prevention and postnatal prevention and me measures. The first thing of course is preventing prematurity. Of course, as much as we can, as much as we're able to, we need to delay delivery as much as we can um and reduce the rate of premature deliveries where possible. Um Other ways we can do prevent um intraven hemorrhage is um transferring babies in particularly when women are in preterm labor, transferring the baby in utero as much as possible. Um and antenatal Glucocorticoid antisteroid have been shown to reduce the incidence of IV as well as optimal obstetric management. Fortunately, it's important to minimally handle the babies um to prevent movement, excessive movement. Um optimal resuscitation and birth to prevent hypoxia and arda that can cause the bleed. Um optimal ventilation and using synchronized synchronized method of ventilation. This prevents babies from fighting against the ventilator essentially, which can predispose to bleeds, optimal um circulatory and control support to prevent fluctuation in BP and cerebral blood flow and correcting coagulation abnormalities and as necessary. And the management um is generally supportive. Um early diagnosis is important but there's really no treatment per se for um intraventricular hemorrhage. Um other than treating anemia, correcting the coagulopathies that might be responsible, optimizing circulation or respiratory support, treating any possible seizures that might occur. And um management for possible complications like the ventricular dilatation and things like that. If there is a ventricular dilatation as a complication of the hemorrhage, then it's again important to recognize that early and when that is picked up, then we need to monitor at a conference serial. We need to do serial ultrasound scans and sometimes has to do it weekly or biweekly or it depends. And we might need to do serial lumbar punctures to drain some of the um CSF and to monitor the opening pressure. And in some cases, we might need to give diuretics like that acetaZOLAMIDE just to decrease CSF production. And of course, we might need to seek neurosurgical consult for a patient. Sometimes in terms of the long term outcomes, it can, as we might expect the, the severity we increase in severity, the outcomes tend to be poorer. Um in terms of mortality, we can see that there's an increase from about 5% from grade one to about 50% in grade four and an increase in in your clim dilatation from about 5% in grade one to about 80% in grade four and an increase in long term neuro disability from about 5% in grade one to about 90% in grade four. So in, in general, grades one and two tend to have the best outcomes and almost similar to babies without an IV. Whilst grade three and four carry um, poorer long term prognosis. These are my references if you'd like to do some more reading. Um, and I'll see you in the next session. Thank you.