Intracranial hemorrhage
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| Intracranial hemorrhage Classification and external resources | |
 | |
|---|---|
| ICD-10 | I60.0-I62., S06. |
| ICD-9 | 430-432, 850-854 |
| DiseasesDB | 6870 |
| MedlinePlus | 000796 |
| eMedicine | neuro/177 |
| MeSH | D020300 |
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Overview
An intracranial hemorrhage is a hemorrhage, or bleeding, within the skull. Intracerebral bleeds are the second most common cause of stroke, accounting for 30–60% of hospital admissions for stroke.[1]
High blood pressure raises the risk of spontaneous intracerebral hemorrhage by two to six times.[1] More common in adults than in children, intraparenchymal bleeds due to trauma are usually due to penetrating head trauma, but can also be due to depressed skull fractures, acceleration-deceleration trauma,[2][3][4] rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor. A very small proportion is due to cerebral venous sinus thrombosis.
Differential diagnosis of causes of intracranial hemorrhage
Intracranial bleeding occurs when a blood vessel in the head is ruptured or leaks. It can result from physical trauma (as occurs in head injury) or nontraumatic causes (as occurs in hemorrhagic stroke) such as a ruptured aneurysm (ballooning blood vessel).
Extradural Hemorrhage
- Rarely hemorrhage from a fracture gap, injured venous sinus or arachnoid villi
- Skull fracture
Intracerebral Hemorrhage
- After cerebral infarction
- Aneurysm
- Angioma
- Anticoagulant medication
- Hypertension
- Perinatal hemorrhage
- Trauma
- Tumor
- Risk Factors
- Anticoagulation medication
- Decreased platelet count
- Disseminated Intravascular Coagulation (DIC)
- Embolic strokes
- Hemophilia
- Hypertension
- Sickle Cell Anemia
Subarachnoid Hemorrhage
- Alcoholism
- Arteriovenous malformation
- Bacterial Endocarditis
- Brain tumor
- Fibromuscular Dysplasia (FMD)
- Hemorrhagic diathesis
- Hypertension
- Infections
- Leukemia
- Mycotic aneurysm
- Other aneurysms
- Other connective tissue diseases
- Polycystic kidney disease
- Ruptured intracerebral aneurysm
- Smoking
Subdural Hemorrhage
- Acute subdural hematoma
- Subacute subdural hematoma
- Usually due to head injury
- Risk Factors
- Alcoholism
- Anticoagulant medication
- Any disorder that results in falling
- Chronic use of aspirin
- Head injury
- Very young or advanced age
Classification
Types of intracranial hemorrhage are roughly grouped into intra-axial and extra-axial.
Intra-axial hemorrhage
Intra-axial hemorrhage is bleeding within the brain itself. This category includes:
- Intraparenchymal hemorrhage, or bleeding within the brain tissue.
- Intraventricular hemorrhage, bleeding within the brain's ventricles (particularly of premature infants).
Extra-axial hemorrhage
Extra-axial hemorrhage, bleeding that occurs within the skull but outside of the brain tissue, falls into three subtypes:
- Epidural hemorrhage is caused by trauma, and results from laceration of an artery, most commonly the middle meningeal artery. This is a very dangerous type of injury because the bleed is from a high-pressure system and deadly increases in intracranial pressure can result rapidly.
- Patients have a loss of consciousness (LOC), then a lucid interval, then sudden deterioration (vomiting, restlessness, LOC)
- Head CT shows lenticular (convex) deformity.
- Subdural hemorrhage results from tearing of the bridging veins in the subdural space between the dura and arachnoid mater.
- Head CT shows crescent-shaped deformity
- Subarachnoid hemorrhage, like intraparenchymal hemorrhage, can result either from trauma or from ruptures of aneurysms or arteriovenous malformations. Blood is seen layering into the brain along sulci and fissures, or filling cisterns (most often the suprasellar cistern because of the presence of the vessels of the circle of Willis and their branchpoints within that space). The classic presentation of subarachnoid hemorrhage is the sudden onset of a severe headache. This can be a very dangerous entity, and requires emergent neurosurgical evaluation, and sometimes urgent intervention.
Diagnosis
CAT scan (computed axial tomography) is the definitive tool for accurate diagnosis of an intracranial hemorrhage.
Cerebral Amyloid Angiopathy [5]
- Cerebral amyloid angiopathy manifests radiologically as part or all of a constellation of findings including:
- Acute or chronic ICHs in a distinctive cortical-subcortical distribution
- Leukoencephalopathy
- Atrophy
- CT allows rapid establishment of the presence or absence of an ICH and exclusion of an acute cerebral infarction.
- Non-enhanced head CT is the preferred imaging modality for initial work-up as it provides crucial information regarding the characteristics of the ICH, including size, location, shape, and extension to the extraaxial spaces
- If an ICH is present in a cortical-subcortical location suspicious for Cerebral amyloid angiopathy, the patient should undergo additional evaluation with MR imaging.
- GRE is currently the most sensitive MR imaging sequence for detection of the chronic cortical-subcortical microhemorrhage.
Epidural Hematoma
- Typical appearance is a biconvex, elliptical, extra-axial fluid collections.
- Acute EDH may contain both a hyperattenuating clot and a swirling lucency (believed to represent a mixture of active bleeding and the serum remaining after previous clot formation).
- Subacute EDH becomes homogeneously hyperattenuating.
- Chronic EDH is at least partly hypoattenuating as the clot undergoes breakdown and resorption.
 CT: Epidural hematoma |
 CT: Epidural hematoma |
 CT: Epidural hematoma |
 CT: Epidural hematoma |
Intracerebral Parenchymal Hemorrhage
 CT: Intracerebral parenchymal hemorrhage |
 CT: Intracerebral parenchymal hemorrhage |
 CT: Intracerebral parenchymal hemorrhage |
 CT: Intracerebral parenchymal hemorrhage |
Intraventricular Hemorrhage
 CT: Intraventricular hemorrhage |
 CT: Intraventricular hemorrhage |
Subarachnoid Hemorrhage
Computed Tomography
- Subarachnoid hemorrhage appears as a high-attenuating, amorphous substance that fills the normally dark CSF-filled subarachnoid spaces.
- These findings are most evident in the largest subarachnoid spaces, such as the suprasellar cistern and Sylvian fissures.
- Acute Subarachnoid hemorrhage is typically 50-60 HU.
- When CT scanning is performed several days to weeks after the initial bleed, the findings are more subtle.
- The initial high-attenuation of blood and clot tend to decrease, and these appear as intermediate gray.
- These findings can be isointense relative to normal brain parenchyma.
- In addition to detecting Subarachnoid hemorrhage, CT is useful in localizing the source of bleeding.
 CT: Diffuse subarachnoid hemorrhage |
 CT: Diffuse subarachnoid hemorrhage |
 CT: Diffuse subarachnoid hemorrhage |
 CT: Diffuse subarachnoid hemorrhage |
MRI
- Fluid-attenuated inversion recovery (FLAIR) is the most sensitive MRI pulse sequence for the detection of SAH. SAH appears as high-intensity signal in normally low signal CSF spaces.
- T2- and T2*-weighted images can potentially demonstrate SAH as low signal intensity in normally high-signal subarachnoid spaces.
- On T1-weighted images, acute SAH may appear as intermediate- or high-intensity signal in the subarachnoid space.
- MR angiography may be useful in the evaluation of aneurysms and other vascular lesions that cause SAH.
Subdural Hemorrhage
Computed Tomography
- Unlike epidural hematomas, subdural hematomas are not restricted by dural tethering at the cranial sutures.
- They can cross suture lines and continue along the falx and tentorium.
- They do not cross the midline because of the meningeal reflections.
- In the acute phase, subdural hematomas appear as a crescent-shaped extra-axial collection with increased attenuation that, when large enough, causes effacement of the adjacent sulci and midline shift.
- The attenuation changes as the hematoma ages.
- Subacute subdural hematomas may be difficult to detect because they may have isoattenuation compared with adjacent gray matter
- Chronic subdural hematomas have isoattenuation relative to the cerebrospinal fluid.
- Rebleeding into subdural hematomas also may occur and is depicted as a layer of high-attenuation hemorrhage within a lower attenuation hematoma.
 CT: Subdural hemorrhage |
 CT: Subdural hemorrhage |
 CT: Subdural hemorrhage |
 CT: Subdural hemorrhage |
 CT: Subdural hemorrhage |
MRI
- MRI is more sensitive than CT scanning in the detection of subdural hematomas because the multiplanar and superior tissue differentiation of MRI makes detection easier.
- The shape of the subdural hematoma on axial images is the same crescent-shaped pattern seen on CT scan images.
- The signal depends on the age of the hemorrhage and follows the signal pattern of intraparenchymal hematomas in acute and subacute cases.
- Chronic subdural hematomas, which appear as isoattenuation relative to CSF on CT scans, often demonstrate increased signal intensity on T1-weighted images because of the presence of free methemoglobin, though the intensity decreases over time.
Perimesencephalic Hemorrhage [6]
 CT: Perimesencephalic hemorrhage |
 CT: Perimesencephalic hemorrhage |
 CT: Perimesencephalic hemorrhage |
Prognosis
Intracranial hemorrhage is a serious medical emergency because the buildup of blood within the skull can lead to increases in intracranial pressure, which can crush delicate brain tissue or limit its blood supply. Intracranial bleeds with a lot of bleeding are more dangerous than those with not as much blood.
The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem.[7] Intraparenchymal bleeds within the medulla 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.[2] 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.[2][8] [9]
For spontaneous ICH seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the insult.[1]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Yadav YR, Mukerji G, Shenoy R, Basoor A, Jain G, Nelson A (2007). "Endoscopic management of hypertensive intraventricular haemorrhage with obstructive hydrocephalus". BMC Neurol 7: 1. doi:10.1186/1471-2377-7-1. PMID 17204141.
- ↑ 2.0 2.1 2.2 McCaffrey P. 2001. "The Neuroscience on the Web Series: CMSD 336 Neuropathologies of Language and Cognition." California State University, Chico. Retrieved on June 19, 2007.
- ↑ Orlando Regional Healthcare, Education and Development. 2004. "Overview of Adult Traumatic Brain Injuries." Retrieved on 2008-01-16.
- ↑ Shepherd S. 2004. "Head Trauma." Emedicine.com. Retrieved on June 19, 2007.
- ↑ Christine P. Chao, Amy L. Kotsenas, and Daniel F. Broderick. Cerebral Amyloid Angiopathy: CT and MR Imaging Findings. RadioGraphics 2006 26: 1517-1531.
- ↑ Schievink, Wouter I., Wijdicks, Eelco F.M., Spetzler, Robert F. Diffuse Vasospasm after Pretruncal Nonaneurysmal Subarachnoid Hemorrhage. AJNR Am J Neuroradiol 2000 21: 521-523
- ↑ 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.
- ↑ Vinas FC and Pilitsis J. 2004. "Penetrating Head Trauma." Emedicine.com.
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
