AIR AND PRECIPITATION

AIR AND PRECIPITATION - keywords
air and precipitation CUS r e f e r e n c e s scheme air microbubble ----> ischaemia and endothelial compression ----> neuronal injury after Muth and Shank 2000 manipulation n a v i g a t o r > pneumatosis < In principle brain precipitations will be suspected during cranial ultrasound when unexpected (according to anatomy) very bright dots or short linear structures, often grouped, are recognised. The initial reflex is to think of calcifications, but there is a differential diagnosis to be made. When the finding of hyperechoic bright ultrasound objects (UBOs) is transient and (often) related to manipulation of a vessel or indwelling line, air embolism can be suspected. The air reflections disappear in minutes to hours. When initially absent but in the second week present, grouped fine speckle clouds can be due to precipitation of P (with calcium ?). These precipitations remain visible for weeks and even up to term equivalent age. Following asphyxia, about 2 weeks after the insult, a graveyard of thalamic neurons may become hyperechoic due to deposition of calcium and iron. This image can be mimicked (in the late neonatal period) by precipitation of oxalate crystals in primary hyperoxaluria. Petechial haemorrhage might in priciple also be a mimick, but location and behaviour in serial scans will learn that this is the case. In the seond week the echoic aspects of a haemorrhage are clearly changing. Multiple angiomas could also be listed in the differential diagnosis, but these are exceedingly rare and should be bigger dan air, calcium or P precipitates. The nodules appearing during gram-negative of yeast encephalitis, often preceding abscedation, are not as bright as calcified spots and are often of similar size and rounded (not linear). calcification oxalate multiple angiomata (neonatal MRI, courtesy dr Pryds, Arhus) air brain precipitation preterm infant with klebsiella septicaemia phosphate Abuelo DN, Barsel-Bowers G, Tutschka BG, Ambler M, Singer DB (1981) Symmetrical infantile thalamic degeneration in two sibs. J Med Genet 18:448-450. Ambler M, O’Neill W (1975) Symmetrical infantile thalamic degeneration and focal cytoplasmic calcification. Acta Neuropathologica 33:1-8. Anderson C, Eggert L, Fitzgerald K, Jackson D, Farr F. Calcium and Phosphate Solubility Curve Equation for Determining Precipitation Limits in Compounding Parenteral Nutrition. Hosp Pharm. 2022 Dec;57(6):779-785. Ansari MQ, Chincancham CA, Armstrong DL (1990) Brain calcification in hypoxic-ischemic lesions: an autopsy review. Pediatr Neurol 6:94-101. 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N Engl J Med. 2000 Feb 17;342(7):476-82. Nellhaus G, Haberland C, Hill BJ. Sturge-Weber disease with bilateral intracranial calcifications at birth and unusual pathologic findings. Acta Neurol Scand. 1967;43(3):314-47. Newton DW, Driscoll DF. Calcium and phosphate compatibility: revisited again. Am J Health Syst Pharm. 2008 Jan 1;65(1):73-80. Patel PJ (1987) Some rare causes of intracranial calcification in childhood : computed tomographic findings. Eur J Pediatr 146:177-180. Perez-Fontan JJ, Herrera M, Fina A, Peguero G (1982) Periventricular calcifications in a newborn associated with aneurysm of the great vein of Galen. Pediatr Radiol 12:249-251. Ramonet D, Pugliese M, Rodríguez MJ, de Yebra L, Andrade C, Adroer R, Ribalta T, Mascort J, Mahy N. Calcium precipitation in acute and chronic brain diseases. J Physiol Paris. 2002 Apr-Jun;96(3-4):307-12. Rickert CH, Rieder H, Rehder H, Hülskamp G, Hörnig-Franz I, Louwen F, Paulus W. Neuropathology of Raine syndrome. Acta Neuropathol. 2002 Mar;103(3):281-7. Rosales RK, Riggs HE (1962) Symmetrical thalamic degeneration in infants. J Neuropath Exp Neurol 21:372-376. Sabatino G, Domizio S, Verrotti A, Ramenghi LA, Pelliccia P, Morgese G (1994) Fetal encephalopathy with cerebral calcifications: a case report. Child’s Nervous System 10:195-197. Samson JF, Barth PG, de Vries JIP, Menko FH, Ruitenbeek W, van Oost BA, Jakobs C (1994) Familial mitochondrial encephalopathy with fetal ultrasonographic ventriculomegaly and intracerebral calcifications. Eur J Pediatr 153:510-516. Schell-Feith EA, Kist-van Holthe JE, van der Heijden AJ. Nephrocalcinosis in preterm neonates. Pediatr Nephrol. 2010 Feb;25(2):221-30. Schiffmann JH, Wessel A, Bruck W, Speer CP (1992) Idiopathic infantile arterial calcinosis. A rare cardiovascular disease of uncertain etiology. Case report and a review of the literature. Monatsschr Kinderheilk 140:27-33. Shefer-Kaufman N, Mimouni FB, Stavorovsky Z, Meyer JJ, Dollberg S (1999) Incidence and clinical significance of echogenic vasculature in the basal ganglia of newborns. Am J Perinatol 16(6):315-9. Shaw WW, Cohen WA (1993) Viral infections of the CNS in children : imaging features. Am J Roentgenol 160:125-133. Stippel, G. (2004). Speckle Suppression, Segmentation and Registration of Medical Ultrasound Images. PhD thesis, Ghent University, Belgium. Takashima S, Becker LE (1985) Basal ganglia calcification in Down’s syndrome. J Neurol Neurosurg Psychiatr 48:61-64. Thijssen J Oosterveld B (1990). Texture in tissue echograms: Speckle or information. Journal of Ultrasound Med, 9:215–229. Thomas-Sohl KA, Vaslow DF, Maria BL. Sturge-Weber syndrome: a review. Pediatr Neurol. 2004 May;30(5):303-10. Vansteenkiste E (2007) Quantitative Analysis of Ultrasound Images of the Preterm Brain. PhD thesis at Gent University, dept. Telecommunication and Information Processing, Faculty of Engineering. Venkatesh S, Coulter DL, Kemper TD (1994) Neuroaxonal dystrophy at birth with hypertonia and basal ganglia mineralization. J Child Neurol 9:74-76. Voit T, Lemburg P, Neven E, Lumenta C, Stork W (1987) Damage of thalamus and basal ganglia in asphyxiated full-term neonates. Neuropediatrics 18:176-181. AIRSivan Y, Nelson MD, Lee S, Wood BP (1990) Radiological case of the month: cerebral air embolism. Am J Dis Child 144:1351–1352. Muth CM, Shank ES. Gas embolism. N Engl J Med. 2000 Feb 17;342(7):476-82. Bubble Obstructing End-Arterial Flow in a Cerebral Vessel with a Diameter of 30 to 60 μm, Causing Distal Ischemia. The obstruction causes the metabolic processes of neurons to fail. Sodium and water enter the vessel, and cytotoxic edema develops. The surface of the bubble generates a foreign-body response through cellular and humoral immune mechanisms. The bubble also mechanically irritates the arterial endothelium. Both processes result in vasogenic edema and greater impairment of perfusion. The neuronal injury extends beyond the area of obstruction. Al-Hathlol K, Al-Mane K, Al-Hathal M, Al-Tawil K, Abulaimoun B. Air emboli in the intracranial venous sinuses of neonates. Am J Perinatol. 2002 Jan;19(1):55-8. Air bubbles in the intracranial venous sinuses are known as a consequence to different causes including trauma, infection, and administration of intravenous contrast. Most of the previous reports demonstrated such cases in adults, with subsequent complications. We are presenting two premature babies who developed asymptomatic air bubbles in the right cavernous and left transverse sinuses, introduced accidentally upon cannulation of scalp veins. In both babies the air embolism disappeared in a few days without complications. Our cases suggest that these accidents could happen more frequently in neonates following scalp vein cannulation, which is a common procedure in sick babies, but they were overlooked as the outcome was uneventful. However, the precise nature and clinical significance of this lesion is not well understood in neonates. Fortrat JO, Saumet M, Savagner C, Leblanc M, Bouderlique C. Bubbles in the brain veins as a complication of daily management of a scalp vein catheter. Am J Perinatol. 2005 Oct;22(7):361-3. Recently, it has been suspected that venous dural sinus air embolisms could occur as a result of scalp vein infusion. The possible mechanism for this complication has not been documented to date, and procedures to avoid venous dural sinus air embolism have not been presented. We report a preterm neonate who demonstrated venous dural sinus air embolism following daily management of a scalp vein catheter. The air embolism disappeared in a few days without complications. Clinicians should avoid injecting air into a scalp vein catheter and leaving it open to air. Following careful examination and review of the infant's case, we were able to conclude that positioning the infant in either supine or Trendelenburg position during daily management of scalp venous infusions and using an air-occlusive dressing once the catheter is removed could limit the risk of venous dural sinus air embolisms caused by scalp vein infusions. Taylor SP, Hoffman GM. Gas embolus and cardiac arrest during laparoscopic pyloromyotomy in an infant. Can J Anaesth. 2010 Aug;57(8):774-8. High volume tubing is used to deliver carbon dioxide during laparoscopic procedures. Failure to prime the tubing with carbon dioxide prior to abdominal insufflation may result in the delivery of nitrogen-containing air to the abdominal cavity. We report a case in which initial insufflation of laparoscopic gas resulted in immediate cardiovascular collapse requiring prolonged resuscitation. Persistent intracranial emboli following the arrest may have resulted from nitrogen contamination of the delivered gas. A 12-day-old female underwent laparoscopy for pyloric stenosis. During initial insufflation of the abdomen, the patient had an abrupt decrease in end-tidal carbon dioxide (CO(2ET)) associated with bradycardia and pulseless electrical activity. Three hours after successful resuscitation and open pyloromyotomy, computerized tomography documented intra-arterial gas within the cerebral and hepatic circulations that resolved following hyperbaric oxygen therapy. Magnetic resonance imaging five days later revealed watershed infarcts in the right frontal and parietal regions. Nitrogen, an insoluble gas not easily eliminated from the body, was likely the gas present within the patient's circulation several hours after the event. It was unlikely carbon dioxide, which is a highly soluble gas that binds to hemoglobin and is rapidly buffered by the carbonic anhydrase system and excreted by the lung. Room air contamination of high volume insufflation tubing allows nitrogen to enter body cavities during endoscopic procedures. Persistence of emboli following endoscopic procedures suggests that the entrained gas is insoluble. Room air contamination increases the potential for catastrophic events during laparoscopy and other endoscopic procedures. Muneuchi J, Kuraoka A, Ochiai Y, Nishibatake M, Sese A, Joo K. Fatal systemic air embolism in a neonate with absent aortic valve. Pediatr Cardiol. 2011 Aug;32(6):839-41. A 32-year-old pregnant woman was referred at 33 weeks' gestation for prenatal ultrasound demonstrating fetal hydrops due to absent aortic valve with free aortic valve insufficiency. Elective caesarian section at 34 week's gestation was performed. Surgical intervention was planned immediately after labor at which time mitral valve closure and atrial septostomy using cardiopulmonary bypass would be performed. However, before insertion of the cannula for cardiopulmonary bypass, a gush of air from the right atrium was noted. The surgical procedure was abandoned because systemic air embolism was suspected. The child died 2 h after birth. Autopsy showed absent aortic valve with closed foramen ovale and left-ventricular hypertrophy. Microscopic findings showed pulmonary and systemic lymphangiectasis, which caused the introduction of air into systemic venous system by way of lymphatic duct just after birth. air and precipitation references Injury to thalamus in the newborn is diverse. Focal injury to thalamus (often symmetrical) can occur in some inborn errors of metabolism like mitochondrial disorders (typically the Leigh phenotype) and primary hyperoxaluria type I (Ardemani et al. 2017). The oxalate crystal deposition in thalamus may be similar to the cases reported on apathite crystals by Ambler and O’Neil 1975. a 2-month-old infant was admitted, and was diagnosed with renal failure; abdominal ultrasound images revealed enlarged and hyperechoic kidneys; additionally, on CUS hyperechoic changes of thalami were noted, reminiscent of perinatal hypoxic-ischaemic brain damage; however, MRI of the brain did not show any abnormal signal intensities compatible with asphyxia the hyperechoic appearance of deep grey matter, was therefore not due to asphyxiated brain damage but seemed related to the deposition of oxalate salts; macular crystals were detected at ophthalmoscopy primary hyperoxaluria Unilateral rare lesions may also present in thalamus. Thalamus can be affected as part of extensive brain destruction by postinfectious haemophagocytosis. Vascular anomalies may present in thalamus: bleeding from a choroidal AVM can extend into thalamus, and on rare occasion a DVA is observed in thalamus. The quality of cranial ultrasound differs per neonatal unit, because machines differ in resolution and doppler quality, and because interpretation is by variably experienced raters. Entities often described in VLBW infants are germinal matrix and intraventricular haemorrhage, white matter injury, arterial infarction, sinovenous thrombosis, germinolysis and fetal infection. This describes a new entity, cloudy precipitation of phosphate and calcium (P/Ca) specifically affecting VLBW infants and only diagnosed by targeted serial CUS, for now a pure sonographic entity. The relevance of the situation may have an impact on care in units where parenteral nutrition is provided according to guidelines, because experience suggests it is a recent abnormal finding and there seem to be no alternative explanations than fine granular precipitation of Ca with something else. Precipitation of Ca and P to particles of size similar to the brain speckles, was simulated in vitro. It is most likely that extra P injections near the tip of the line with parenteral nutrition led to precipitation and microembolism. The peculiar regional specificity (frontal white matter and thalamus) of the speckle clouds is unexplained. Either microemboli follow specific routes according to their nature and characteristics of regional brain perfusion, or the precipitation is triggered by some local brain factor encouraging P to precipitate. To turn this hypothesis into a genuine finding, postmortem confirmation is necessary. Alternatively the hypothesis can be tested in experimental settings. The potential of permanent injury to the brain (and other organs) by this event has to be considered. simulation of P precipitation CaP precipitation in the lung of an adult, associated with chronic parenteral nutrition (Knowles et al. 1989) item page phosphate precipitation Exceptional disorders. - Brainstem calcification typical of Möbius syndrome. - Aicardi-Goutières syndrome and other pseudo-TORCH syndromes (Baraitser-Reardon). - Brain disruption sequence. - An hereditary disorder has been described by Illum et al. in 1988 and is accompanied by limb flexion-deformities, an immobile face with pouting mouth (‘whistling face’), early onset of convulsions together with fine diffuse intracranial calcifications (in the leptomeninges, penetrating from there along blood vessels into parenchyma, marking the ventricular borders by a fine line and highlighting the veins in deep gray matter). - Generalised arterial calcinosis of infancy is accompanied by hypertension and hypertrophic cardiomyopathy, causing calcification in the walls of all major arteries but not always in brain arteries (Schiffmann et al. 1992). - Mitochondrial disorders with congenital lactic acidosis (Samsom 1994, van Straaten et al. 2005). - Mineralization in the basal ganglia may draw attention in cases of neonatal neuroaxonal dystrophy (Venkatesh 1994). - BLC-PMG Band-like calcification with simplified gyration and polymicrogyria. - Neu-Laxova syndrome. - Raine syndrome (lethal osteosclerotic bone dysplasia, facial dysmorphia, Binder phenotype: midface hypoplasia and small nose and brain calcification). - Norrie disease, Coats disease and other cerebroretinal angiopathies. - There are no neonatal presentations yet of Fahr disease (primary familial brain calcification)(Ramonet et al. 2002, Chen et al. 2023). - Leukodystrophy (Boltshauser et al. 1991). The only neuro-ectodermal disorders that may present with neonatal intracranial calcification, are Sturge-Weber syndrome (SWS) and tuberous sclerosis. Subependymal nodule calcification in the fetus has not been reported. Although SWS is associated with extensive calcification ater on, calcifications are absent or minimal in neonates and infants (Thomas-Sohl et al. 2004). The earliest report of calcification in SWS was in a 4-day-old neonate (Nellhaus et al. 1967) Established antenatal brain ischaemia with calcification in thalamic neurons (Ambler and O’Neill 1975, Voit et al. 1987, Ansari et al. 1990). ∆∆ [Symmetrical infantile thalamic degeneration (Ambler and O’Neil 1975). The varix wall and periventricular white matter may be calcified in vascular anomalies such as aneurysm of the vein of Galen (Perez-Fontan et al. 1982). During the organization of venous thrombosis, calcium deposit can be found in the affected vein. brain calcification in the newborn Cerebral or cerebellar calcification often follows necrosis. Histopathology of samples from 28 autopsied brains aged from 22 weeks’ gestation to 14 years were selected because they showed calcification associated with a range of different diseases (McCartney and Squier 2014). Calcification develops via two main pathways: dystrophic and vascular. - Dystrophic calcification results from membrane disruption and uncontrolled calcium entry into necrotic cells in ischaemia and infections. - Vascular calcification appears to be initiated in protein globules, sometimes intracellular, but outside the endothelium of small vessels (mutation of the occludin gene, implicating impaired endothelial integrity, showed this pattern (identical vascular calcification in Sturge–Weber syndrome)). Another form of vascular calcification involves the adventitia of arteries, the endothelium being spared. Reduced vascular compliance and altered permeability would explain associated atrophy, gliosis, and (in the developing brain) malformations of the cortex. Pericytes may also be involved in non-dystrophic brain calcification. Precipitation with P is one of the mechanisms in Fahr disease (Chen et al. 2023, Cheng et al. 2024). Non-bacterial fetal infection (Shaw and Cohen 1993). Deposition of calcium salts around the ependyma, in places where periventricular inflammation may lead to arteritis and phlebitis accompanied by necrosis. Typical of CMV, but periventricular localisation may be noted with toxoplasmosis, rubella, herpes simplex, LCM, parvovirus, zika and varicella. Meningitis and leptomeningeal thrombophlebitis and micro-arteritis are at the basis of superficial perisulcal calcification and calcium deposits in the hypothalamic region. Peripheral (not periventricular) calcification tends to suggest toxoplasmosis, but cytomegalovirus generates fine subcortical calcifications as well. Finally, many fetal brain infections are accompanied by hyperechoic striatal vasculopathy, also with mineralisation. Calcification in basal grey matter and in frontal and temporal lobes may follow neonatal HSV infection. Neonatal bacterial ventriculitis-meningitis may induce calcified lesions. Tumours may contain calcified foci: teratoma, lipoma, astrocytoma. Mac OS X 2Û ATTR Ü1Ücom.apple.TextEncodingëcom.apple.provenanceöcom.apple.quarantineutf-8;134217984Â.Im0ÖWq/0082;6a6e2557;Hype4;

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