Ներգանգային արյունազեղում (ICH), հայտնի է նաև ուղեղային արյունահոսություն,
ներգանգային արյունահոսության տեսակ է որը տեղի է ունենում ուղեղային հյուսվածքում կամ փորոքներում[1]; also known as cerebral bleed, is a type of
intracranial bleed that occurs within the
brain tissue or
ventricles.[1]Ախտանիշները կարող են ներառել գլխացավ, միակողմանի թուլություն, փսխում, ցնցումներ, գիտակցության մթագնում, և պարանոցի կարկամություն[2]։ Symptoms can include
headache, one-sided weakness, vomiting, seizures,
decreased level of consciousness, and
neck stiffness.[2] Հաճախ ախտանիշները ժամանակի հետ վատանում են[3];Often symptoms get worse over time.[3]Fever is also common.[3]Շատ հաճախ արյունահոսությունն առկա է լինում և ուղեղային հյուսվածքում և փորոքներում[3]; In many cases bleeding is present in both the brain tissue and the ventricles.[3]
Պատճառագիտություն և Ախտորոշում
Հիմնական պատճառներն են գլխուղեղի վնասվածք, անևրիզմաներ, զարկերակերակային մալֆորմացիաներ ևգլխուղեղի ուռուցքներ[3]; Causes include
brain trauma,
aneurysms,
arteriovenous malformations, and
brain tumors.[3]Սպոնտան արյունահոսությունների ամենամեծ ռիսկի գործոնն են հանդիսանում բարձր զարկերակային ճնշումն ու ամիլոիդոզը[2]; The largest risk factors for spontaneous bleeding are
high blood pressure and
amyloidosis.[2]Այլ ռիսկի գործոններ են հանդիսանում ալկոհոլիզմը,արյան մեջ ցածր խոլեստերինը, արյան մածուծիկությունն իջեցնող դեղերը և կոկաինի օգտագործումը[2]։Other risk factors include
alcoholism,
low cholesterol,
blood thinners, and
cocaine use.[2]Հիմնական ախտորոշիչ մեթոդը համակարգչային շերտագրումն է[3]։ Diagnosis is typically by
CT scan.[3]Իշեմիկ կաթվածը այն վիճակներից է, որը դրսևորվում է նույն նշաններով[3]։ Other conditions that may present similarly include
ischemic stroke.[3]
Կանխարգելում և բուժում
Բուժումը պետք է իրականացվի ինտենսիվ թերապիայի բաժանմունքում[3]։Treatment should typically be carried out in an
intensive care unit.[3]Գայդլայները խորհուրդ են տալիս իջեցնել արյան սիստոլիկ ճնշումը 140մմս․ս․[3][4]; Guidelines recommended decreasing the
blood pressure to a
systolic of 140 mmHg.[3][4]Հակամակարդիչների ընդունումը հնարավորության դեպքում պետք է դադարեցվի իսկ արյան մեջ գլյուկոզի մակարդակը պետք է պահպանվի նորմայի սահմաններում[3]; Blood thinners should be reversed if possible and
blood sugar kept in the normal range.[3]Հիդրոցեֆալիայի բուժման համար կարելի է իրականացնել վիրահատական միջամտություն փորոքային դրենաժի տեղադրմամբ, բայց կորտիկոստերոիդներ բուժման սխեմայում չեն օգտագործվում[3]; Surgery to place a
ventricular drain may be used to treat
hydrocephalus but
corticosteroids should not be used.[3]Որոշ դեպքերում օգտակար են վիրահատական ճանապարհով արյան հեռացումը[3]; Surgery to remov the blood is useful in certain cases.[3]
Համաճարակաբանություն
գլխուղեղային արյունահոսությամբ ամեն տարի տառապում են
Cerebral bleeding affects about 2.5 per 10,000 people each year.[2] It occurs more often in males and older people.[2] About 44% of those affected die within a month.[2] A good outcome occurs in about 20% of those affected.[2]Strokes were first divided into their two major types, bleeding and insufficient blood flow, in 1823.[5]
Signs and symptoms
People with intracerebral bleeding have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed.[6] Other symptoms include those that indicate a rise in
intracranial pressure caused by a large mass putting pressure on the brain.[6]
Intracerebral bleeds are often misdiagnosed as
subarachnoid hemorrhages due to the similarity in symptoms and signs. A severe headache followed by vomiting is one of the more common symptoms of intracerebral hemorrhage. Another common symptom is a patient can collapse. Some people may experience continuous bleeding from the ear. Some patients may also go into a coma before the bleed is noticed.
Causes
Intracerebral bleeds are the second most common cause of
stroke, accounting for 10% of hospital admissions for stroke.[8]High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times.[7] More common in adults than in children, intraparenchymal bleeds are usually due to
penetrating head trauma, but can also be due to depressed
skull fractures. Acceleration-deceleration trauma,[9][10][11] rupture of an
aneurysm or
arteriovenous malformation (AVM), and bleeding within a
tumor are additional causes.
Amyloid angiopathy is a not uncommon cause of intracerebral hemorrhage in patients over the age of 55. A very small proportion is due to
cerebral venous sinus thrombosis.
ներգանգային արյունազեղման ռիսկի գործոններն են[12]; Risk factors for ICH include:[12]
Traumautic intracerebral hematomas are divided into acute and delayed. Acute intracerebral hematomas occur at the time of the injury while delayed intracerebral hematomas have been reported from as early as 6 hours post injury to as long as several weeks.
Diagnosis
Both
computed tomography angiography (CTA) and
magnetic resonance angiography (MRA) have been proved to be effective in diagnosing intracranial vascular malformations after ICH.[13] So frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage[14] or to detect a "spot sign".
Intraparenchymal hemorrhage can be recognized on
CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain because of
edema, and therefore shows up darker on the CT scan.[14]
Location
When due to
high blood pressure, intracerebral hemorrhages typically occur in the
putamen (50%) or
thalamus (15%), cerebrum (10-20%), cerebellum (10-13%), pons (7-15%), or elsewhere in the brainstem (1-6%).[15][16]
Treatment
Treatment depends substantially on the type of ICH. Rapid
CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery.
Tracheal intubation is indicated in people with decreased level of consciousness or other risk of airway obstruction.[17]
One review found that
antihypertensive therapy to bring down the blood pressure in acute phases appears to improve outcomes.[18] Other reviews found an unclear difference between intensive and less intensive blood pressure control.[19][20] The
American Heart Association and
American Stroke Association guidelines in 2015 recommended decreasing the blood pressure to a SBP of 140 mmHg.[3] However, the evidence finds tentative usefulness as of 2015.[21]
Giving
Factor VIIa within 4 hours limits the bleeding and formation of a
hematoma. However, it also increases the risk of
thromboembolism.[17] It thus overall does not result in better outcomes in those without hemophilia.[22]
H2 antagonists or proton pump inhibitors are commonly given for to try to prevent
stress ulcers, a condition linked with ICH.[17]
Corticosteroids, were thought to reduce swelling. However, in large controlled studies, corticosteroids have been found to increase mortality rates and are no longer recommended.[24][25]
A
craniectomy may take place, where part of the skull is removed to allow a swelling brain room to expand without being squeezed.
Prognosis
The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the
brain stem.[27] Intraparenchymal bleeds within the
medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the
vagus nerve, which plays an important role in
blood circulation and breathing.[9] This kind of hemorrhage can also occur in the
cortex or subcortical areas, usually in the
frontal or
temporal lobes when due to head injury, and sometimes in the
cerebellum.[9][28]
For spontaneous ICH seen on CT scan, the death rate (
mortality) is 34–50% by 30 days after the insult,[7] and half of the deaths occur in the first 2 days.[29] Even though the majority of deaths occurs in the first days after ICH, survivors have a long term excess mortality of 27% compared to the general population.[30]
The inflammatory response triggered by stroke has been viewed as harmful in the early stage, focusing on blood-borne leukocytes, neutrophils and macrophages, and resident
microglia and
astrocytes.[32] A human postmortem study shows that inflammation occurs early and persists for several days after ICH.[33] Modulating microglial activation and polarization might mitigate intracerebral hemorrhage-induced brain injury and improve brain repair.[34] A new area of interest is the role of
mast cells in ICH.[35]
^
abYeung R, Ahmad T, Aviv RI, Noel de Tilly L, Fox AJ, Symons SP (2009). "Comparison of CTA to DSA in determining the etiology of spontaneous ICH". Canadian Journal of Neurological Sciences. 36 (2): 176–180.
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^Tsivgoulis, G; Katsanos, AH; Butcher, KS; Boviatsis, E; Triantafyllou, N; Rizos, I; Alexandrov, AV (21 October 2014). "Intensive blood pressure reduction in acute intracerebral hemorrhage: A meta-analysis". Neurology. 83 (17): 1523–9.
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^Ma, J; Li, H; Liu, Y; You, C; Huang, S; Ma, L (2015). "Effects of Intensive Blood Pressure Lowering on Intracerebral Hemorrhage Outcomes: A Meta-Analysis of Randomized Controlled Trials". Turkish Neurosurgery. 25 (4): 544–51.
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^Boulouis, Gregoire; Morotti, Andrea; Goldstein, Joshua N.; Charidimou, Andreas (1 April 2017). "Intensive blood pressure lowering in patients with acute intracerebral haemorrhage: clinical outcomes and haemorrhage expansion. Systematic review and meta-analysis of randomised trials". Journal of Neurology, Neurosurgery, and Psychiatry. 88 (4): 339–345.
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^Ma, J; Li, H; Liu, Y; You, C; Huang, S; Ma, L (2015). "Effects of Intensive Blood Pressure Lowering on Intracerebral Hemorrhage Outcomes: A Meta-Analysis of Randomized Controlled Trials". Turkish Neurosurgery. 25 (4): 544–51.
doi:
10.5137/1019-5149.JTN.9270-13.0 (inactive 2022-06-11).
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cite journal}}: CS1 maint: DOI inactive as of June 2022 (
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^Yuan, ZH; Jiang, JK; Huang, WD; Pan, J; Zhu, JY; Wang, JZ (June 2010). "A meta-analysis of the efficacy and safety of recombinant activated factor VII for patients with acute intracerebral hemorrhage without hemophilia". Journal of Clinical Neuroscience. 17 (6): 685–93.
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^Roberts, Ian; Yates, David; Sandercock, Peter; Farrell, Barbara; Wasserberg, Jonathan (9 October 2016). "Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial". Lancet. 364 (9442): 1321–1328.
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^Sanders MJ and McKenna K. 2001. Mosby's Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and Facial Trauma." Mosby.
^Graham DI and Gennareli TA. Chapter 5, "Pathology of Brain Damage After Head Injury" Cooper P and Golfinos G. 2000. Head Injury, 4th Ed. Morgan Hill, New York.
^Broderick, J.; Connolly, S.; Feldmann, E.; Hanley, D.; Kase, C.; Krieger, D.; Mayberg, M.; Morgenstern, L.; Ogilvy, C. S.; Vespa, P.; Zuccarello, M. (3 May 2007). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage in Adults: 2007 Update: A Guideline From the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists". Stroke. 38 (6): 2001–2023.
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