Upgrade to remove ads
Ischemia of the brain
Terms in this set (35)
Cerebrovascular disease is divided into 2 major categories:
Vital components needed for brain tissue survival
The brain needs 15% of the cardiac output
Uses 20% of total body oxygen consumption
Very sensitive to alterations in blood flow , oxygen content of blood or inhibition of oxygen use by the tissue
Neurons are dependent on
as an essential energy source and are particularly susceptible to ischemia (undergo necrosis within 3-5 minutes)
General causes of decreased delivery of oxygen to the brain
The cerebral blood flow normally remains stable over a wide range of blood pressure and intracranial pressure because of autoregulation of vascular resistance. The brain may be deprived of oxygen by two general mechanisms:
1. Functional hypoxia: caused by a low partial pressure of oxygen (high altitude), impaired oxygen carrying capacity (severe anemia, CO poisoning), or inhibition of oxygen use by tissue (cyanide poisoning)
2. Ischemia: either transient or permanent, due to tissue hypoperfusion, which can be caused by hypotension, vascular obstruction or both.
Consequences of reduced blood flow depends on
Collateral circulation: As collateral circulation increases, severity of ischemia decreases. Most likely to see in elderly who have capacity and time to develop collateral circulation
Duration of ischemia: Other areas of body may be able to endure several minutes of oxygen deprivation without significant damage. Depriving the brain of oxygen for even a couple minutes will result in irreversible brain damage, possible death
Magnitude and rapidity of the reduction of flow
These factors will determine:
1. The anatomic site of the lesion (focal vs global)
2. The size of the lesion
3. The clinical deficit
Types of ischemia
1. Global: entire brain affected
2. Focal: region of brain affected
Moderate global ischemia
leads to infarcts in watershed areas (area lying between regions fed by the anterior and middle cerebral artery) and damage to
highly vulnerable regions
1. Pyramidal neurons of the cerebral cortex (layers 3,5,and 6) leads to laminar necrosis (lines of necrosis in the layers).
(temporal lobe): important in long term memory
: integrates sensory perception with motor control. You will have cerebellar signs.
When patients with severe global ischemia (irreversible injury) are maintained on mechanical ventilation the brain gradually undergoes autolysis resulting in the so-called "respirator brain"
marked necrosis, edema and widespread destruction of the brain due to recurrent cycles of edema and vasocompression resulting in autolysis and softening of the brain which prevents its fixation in formalin. Often seen in children on ventilator for extended period of time. With injury to the brain (mechanical, hypoxic, etc.), a major response is edema. As the brain swells, it begins to encroach on blood vessels, impeding blood flow to the brain resulting in further injury and edema. Patient on a ventilator can have waxing and waning of edema and swelling which overtime results in vasocompression, autolysis and softening of the brain
Upon autopsy, brain is falling apart
General Morphology of Global Cerebral Ischemia
In the setting of global ischemia, the brain is swollen, with wide gyri and narrowed sulci. The cut surface shows poor demarcation between gray and white matter.
Global Ischemia causes
1. Cardiac Arrest
2. Acute decrease in blood flow (cardiogenic shock)
3. Marked hypotension
4. Chronic hypoxia (anemia leads to decrease O2 delivery). Asphyxia
5. Repeated episodes of hypoglycemia (insulinoma).
Mild global ischemia results in transient confusion with prompt recovery such as in an insulinoma after being given glucose in the hospital they recover. Severe global ischemia results in diffuse necrosis, survival leads to a "vegetative state"
You will see red neurons as neurons are going through apoptosis.
Microscopic Features of of Irreversible Ischemic Injury (Infarction)
1. Eosinophilic change in the cytoplasm of neurons undergoing apoptosis are called
. Occuring 12-24 hours after insult, you initially have microvacuolization, followed by cytoplasmic eosinophilia, and later nuclear pyknosis and karyorrhexis.
2. Necrosis (24 hours)
3. Inflammation: Neutrophils (days 1-3)
4. Inflammation: microglial cells (macrophages) remove liquid debri (days 4-7)
5. Healing: gliosis (weeks 2-3) Gliosis is reactive astrocytes as neurons are permanent cells unable to regenerate, the brain's best attempt at repair is replacement with gliotic tissue. The distribution of neuronal loss and gliosis in the neocortex typically is uneven with preservation of some layers and devastation of others- a pattern termed pseudolaminar necrosis.
Result in formation of a fluid filled cystic space because it underwent liquefactive necrosis surrounded by gliosis.
Focal cerebral ischemia (stroke) causes
Localized cessation of blood flow to localized areas of the brain due to large or small blood vessel disease (atherosclerosis, thrombi, emboli). Location of blood vessel involvement will determine clinical presentation.
Focal neurological deficits lasting >24 hours. If symptoms last <24 hours, the event is termed a transient ischemic attack (TIA) not a stroke.
1. Thrombotic (most common)
Thrombotic stroke is due to rupture of an atherosclerotic plaque leading to exposure of sub-endothelial collagen and subsequent formation of thrombosis at the site of injury. This will lead to a
infarct at the
periphery of the cortex
. Because plaque rupture even if you lyse thrombosis it will quickly form again because of exposure of sub-endothelial collagen. Atherosclerosis usually develops at branch points (bifurcation of internal carotid and middle cerebral artery in the circle of Willis).
Most common sites of primary thrombosis leading to infarction are the carotid bifurcations, the origin of the middle cerebral artery and the basilar artery. Can listen for bruit in the carotids as part of physical exam. Bruit may indicate an abnormality in blood flow which may indicate atherosclerotic change which may lead to thrombi formation and focal ischemia. Occlusion can be caused by anterograde progression of the thrombus or fragmentation and subsequent embolization. Occlusion is associated with systemic diseases such as diabetes and hypertension being some of the more common.
White stroke: do not re-establish blood flow
Embolic stroke is due to thromboemboli. Most common source of emboli is the left side of the heart (atrial fibrillation) that gets lodged in vessel in the brain. Usually involves the middle cerebral artery.
Results in a
periphery of the cortex
. Cuts the blood supply long enough for cells to die but then embolism gets lysed and blood goes back in hemorrhagic infarction.
Red stroke: blood flow is re-established
Source of the emboli in stroke
1. Mural thrombi in the left ventricle after an acute MI: Seen when there was a change in blood flow through the heart chambers (such as post-MI). This may predispose thrombi formation on the chamber wall. Thrombi can fragment and embolize up through the carotid and into the brain.
2. aortic and or mitral valve vegetations
3. left atrium in atrial fibrillation: particularly notable as a progenitor of embolic strokes due to thrombus formation in the left atrium from stasis of blood.
Where are embolic strokes commonly seen?
Commonly seen in the area of distribution of the middle cerebral artery. The middle cerebral artery is a direct extension of the internal carotid artery. Emboli tend to lodge at bifurcations of these arteries resulting in problems feeding both vessels. Often the location of the embolus cannot be identified at autopsy because of lysis.
fracture of long bones results in release of bone marrow and fat into circulation, often occur following a motor vehicle accident. Embolism occurs approximately 24-48 hours after the initial injury. Can result in widespread white matter hemorrhages and generalized cerebral dysfunction
Air emboli: can result from
1. Penetrating injury to cervical vessels: stab wound to the neck resulting in communication between lungs and blood vessels
2. Intravenous injection of air: Requires approximately 50cc of air to cause death
3. Sex: Oral sex being performed on a pregnant women can result in an air emboli due to the particular permeability of placental membranes
many sarcomas and some carcinomas can embolize. Portions of tumor break off, travel to the brain. Seen more with sarcomas since they usually spread via hematogenous route. Certain carcinomas can also spread hematogenously including:
1. Hepatocellular carcinoma
2. Renal cell carcinoma
Amniotic Fluid Emboli
Usually occur during a particularly vigorous birth. Rupture of uterine veins exposes amniotic fluid to vasculature. Can result in DIC, high mortality rate
Lacunar stroke occurs secondary to hyaline arteriolosclerosis, a complication of chronic hypertension. Most commonly involves lenticulostriate vessels from the middle cerebral artery, resulting in small cystic areas of infarction that look like lakes.
Involvement of the internal capsule leads to pure motor stroke.
Involvement of the thalamus leads to a pure sensory stroke.
Produce small infarcts which undergo liquefactive necrosis leaving small cavities or lacunae (lake-like) most commonly seen in the basal ganglia. Usually a couple millimeters in dimension. May be asymptomatic but as they progress over time problems can develop. Consist of tissue loss and lipid-laden macrophages surrounding by gliosis. Brain is high in myelin and lipids
and as the tissue breaks down, macrophages will engulf that material.
Focal ischemia due to vascular inflammation
Arteritis: small and large vessel inflammation was once commonly seen in syphilis and TB but now seen mostly in the immunosuppressed
1. PAN (polyartitis nodosa) and collagen vascular diseases can involve cerebral vessels causing single or multiple infarcts
2. Primary angiitis of the CNS: involves small to medium sized parenchymal and subarachnoid vessels with infiltration by chronic inflammatory cells and giant cells (relatively distinct feature). Limited to the CNS. Involves giant cells, a relatively distinct feature. Not to be confused with giant cell arteritis which is a different entity
Most due to localized arteriolar disease but some are associated with systemic disorders
: PCV (Polycythemia vera), sickle cell, malignancies
of extracranial arteries especially those in the neck
: particularly stimulants such as methamphetamine and cocaine, but heroin has been implicated as well. Sympathomimetics (drugs stimulating sympathetic nervous system) can lead to focal ischemia. Cocaine is also a vasoconstrictor, contributing to injury. Even non-stimulates such as heroine has been implicated in focal ischemia.
Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy. Associated with mutations in the
. Characterized by recurrent strokes and dementia. Ischemic damage results as strokes accumulate over time. Abnormalities of white matter and concentric narrowing of the adventitia and media of leptomeningeal arteries. Rare hereditary form of stroke
Several different types but all involve a lack of oxygenated blood reaching the brain
3. Chemical asphyxiation
inhibiting air from getting into the lungs via:
4. Mechanical asphyxia
5. Suffocating gases
Entrapment and Environmental Suffocation
Inadequate oxygen in environment. May be seen with certain occupations such as a sewer worker. Autopsy alone will not give cause of death (COD. "Lack of oxygen" cannot be measured in a dead body. Need to know the circumstances surrounding the death. May go into the area of question and use sensors to determine oxygen levels
Mechanical obstruction or occlusion of the external airway (nose, mouth). Usually homicidal, suicidal or accidental
1.Homicidal: Easier to do on a child. Many cases previously attributed to SIDS (Sudden Infant Death Syndrome) were actually homicidal smothering. Performed by covering nose and mouth of young baby, who is usually unable to struggle or fight. If an adult is smothered, will usually see signs of a struggle
2. Suicidal: Individual may wrap something around nose and mouth such as duct tape
3. Accidental: Adult co-sleeping with young child and rolls over the child, covering their external airway. Often minimal autopsy findings are present.
Obstruction of the internal air passages (larynx, most common trachea)
1. Natural: epiglottitis. Infection of Haemophilus influenzae, epiglottis swells, occluding internal airway
2. Homicidal: movement of a gag. Case where an elderly women was tied to chair and a gag placed in her mouth. Her assailants thought she could still breath through nose. Gag worked its way back into the throat, completely occluding air passage and resulting in asphyxiation. Also seen in newborns due to someone putting rags down the child's throat
3. Accident: inhalation of food or foreign objects
Usually accidental. Usually associated with drugs or alcohol. Person falls and becomes trapped in positions which impairs breathing
Congestion, cyanosis and petechiae of head/face. Compression of right side of heart or neck vessels and blood is unable to drain from the head. Engorgement of the head results in rupturing of small blood vessels, most often seen on conjunctiva of the eyes and eye lids.
Heavy weight compresses the chest or upper abdomen. Congestion and petechiae often present due to compression of the right side of the heart. Blood is unable to drain from inferior vena cava. Head and face become engorged with blood resulting in purple appearance and petechiae
Accidental: something large and heavy falls on chest
Overlaying: adult co-sleeping with child. Adult overlays or rolls over child. Can result in smothering or traumatic asphyxia
Burking: person (or persons) sitting on someone's chest. Named after William Burke, a Scottish man from the early 1800's. During this time, medical schools had a very difficult time obtaining cadavers. Burke, along with his accomplice Hare, had the idea to travel around to pubs and ply individuals with alcohol. Once the person was intoxicated, they would get them to a remote location and sit on their chest until they died. Would turn around and sell the bodies to medical school. Occurred for years before being discovered. Burke was hanged and his body donated to medical school. Burking still occurs today and should be considered, especially if someone dies in police custody.
Strangulation -compression of vasculature of the neck (carotids)
Hanging: using body weight to compress structures in the neck
Ligature Strangulation: rope/belt/tie used to compress neck
Manual Strangulation: hands/forearm used to compress neck
Pathologic findings to look for in the case of hanging
It takes roughly 10 lbs. of pressure to occlude the carotid arteries. To occlude the jugular veins requires only about 4.5 lbs. of pressure.
If completely suspended, the person's body weight results in occlusion of all blood supply immediately. Will not see petechiae
If partially suspended, petechiae may be seen. Pressure on the neck may wax and wane. Jugular veins occlude first because less pressure is required while carotid arteries remain patent, pumping blood into the head. Blood is unable to drain resulting in petechiae
Why is this important?
An individual found fully suspended should not have petechiae. If petechiae are present, it may suggest the person was first strangled (with waxing and waning pressure) and then hung up to make it look as though it were a suicide
Autopsy of suspected strangulation
Careful layer-wise dissection of neck muscles is performed, looking for pockets of hemorrhage (can be subtle)
Mucosal hemorrhage in pharynx
Petechiae of the conjunctiva. Can be seen in any area above the ligature. May also be seen in someone who survived an attempted strangulation
Strangulation hold can render a person unconscious within 10 seconds. If hold is maintained for 1-2 minutes, irreversible ischemic brain damage will start to occur. To kill someone, hold must be maintained for 3-4 minutes. Thus unlikely to occur "by accident". Holding someone for that long shows premeditation and intent to kill.
Ischemic Change of the brain
On the right is a normal brain
On the left is a "dusty" or ischemic brain. Blood vessel dilate during ischemia as the body attempts to increased blood flow to the brain. Any blood remaining in the brain is no longer oxygenated. The deoxygenated blood gives the brain a dusty or salmon-colored appearance
Can be suicidal or accidental. Running a space heater or generator without proper ventilation
Colorless, odorless, tasteless. Competes with oxygen for binding sites on the oxygen carrying proteins. Hemoglobin has a higher affinity for carbon monoxide. Have proper blood flow but oxygen is unable to attach to hemoglobin and reach the brain resulting in asphyxiation
Results in cherry red discoloration of tissues. Necrosis of globus pallidus, cerebral cortex and hippocampus. Patients often present with headache, nausea, vomiting, confusion. Easily treated with oxygen therapy if caught early enough.
Lividity seen in the hands. Lividity is the settling of blood after death. Usually has a purple appearance but here is "cherry red".
Produces cellular hypoxia by competing with the ferric iron atom of intracellular cytochrome oxidase, inhibiting electron transport chain. Resulting in lack of oxygen utilization.
Seen in suicides and gas chambers. Also comes in pellet form; "cyanide capsule". Death is not usually instantaneous
Smell of burnt almonds. Only around 20% of the population is able to detect smell.
Burns of gastric mucosa. Pink discoloration of tissues due to impaired oxygen transport
Produced by fermentation of organic matter. Found in sewers and cess pools. Low doses have rotten egg smell. High doses paralyze olfactory nerves and will be unable to smell anything. High doses cause rapid death
THIS SET IS OFTEN IN FOLDERS WITH...
3 - Sensory Receptors
6 - Physiology of OMM Part 1
YOU MIGHT ALSO LIKE...
Patho of CNS Ischemia
Brain disorders Brewer UCI Lecture 2 Glossary
Acute Disorders of Brain Function (PATHO…
Alterations in Brain Function
OTHER SETS BY THIS CREATOR
Structure of the Ear and hearing
Hypertensive and Cerebral Disease
OTHER QUIZLET SETS
Civil War 3-25-21
Adolescent/Adult Development Psychology: Middle Ad…
ADULT HEALTH FINAL