Ischemic Brain Injury: Hemodynamic & Oxygenation

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Questions and Answers

What is the timeline for neuronal injury progression after ischemic insult?

Neuronal injury is dynamic and continues for hours to days after the initial ischemic insult.

What percentage of the body's cardiac output does the brain account for?

The brain receives 15% of cardiac output.

What percentage of the body's oxygen consumption does the brain account for?

The brain uses 20% of the body's oxygen.

What causes cytotoxic edema after cerebral ischemia?

ATP depletion disrupts osmotic gradients, leading to water influx into cells. Signup and view all the answers

What is the Monro-Kellie doctrine?

The skull is a fixed-volume container; increases in brain, blood, or CSF volume must be offset by reductions in other components, or ICP will rise. Signup and view all the answers

How does elevated ICP exacerbate ischemic injury?

Increased ICP reduces cerebral perfusion pressure (CPP = MAP – ICP), lowering blood flow and worsening ischemia. Signup and view all the answers

What are the hemodynamic targets for mean arterial pressure (MAP) and cerebral perfusion pressure (CPP)?

Maintain MAP >65 mmHg and CPP >60 mmHg to ensure adequate cerebral blood flow. Signup and view all the answers

What PaO2 range is recommended to avoid hypoxemia and hyperoxemia?

Target PaO2 of 80–120 mmHg and oxyhemoglobin saturation in the high 90s. Signup and view all the answers

Why is hyperoxemia harmful in brain resuscitation?

Excess oxygen generates reactive oxygen species, worsening neuronal injury. Signup and view all the answers

Which of following are included in the stepwise approach to managing elevated ICP?

All of the above. (D) Signup and view all the answers

When is therapeutic hyperventilation appropriate?

Only for life-threatening cerebral herniation or severe ICP elevation as a short-term bridge to definitive therapy (e.g., surgery). Target PaCO2 35–40 mmHg. Signup and view all the answers

How should acute seizures be managed?

Treat with IV lorazepam. Avoid prophylactic antiepileptics; use continuous EEG if seizures are suspected. Signup and view all the answers

Why is fever control critical in brain injury?

Fever increases metabolic demand and inflammation, exacerbating secondary injury. Treat temperatures >38°C with acetaminophen. Signup and view all the answers

What is targeted temperature management (TTM), and how is it applied?

Maintain comatose cardiac arrest survivors at 33-36°C for 24 hours in the ICU to reduce metabolic demand and improve outcomes. Signup and view all the answers

Why is neurological prognostication unreliable before 72 hours post-normothermia?

Early exams lack accuracy; delayed neuronal injury and recovery timelines require prolonged observation. Signup and view all the answers

What is the most common cause of death in cardiac arrest survivors?

Withdrawal of life-sustaining treatment due to perceived poor neurological prognosis. Signup and view all the answers

What role do emergency physicians play in family communication?

They must set realistic expectations, emphasize uncertainty in early prognosis, and advocate against premature care withdrawal. Signup and view all the answers

What organizations provide post-cardiac arrest care guidelines?

AHA, ERC, and ESICM, based on ILCOR's CoSTR recommendations. Signup and view all the answers

What survival rates are reported for out-of-hospital vs. in-hospital cardiac arrest?

Out-of-hospital: 12% survival (75% with favorable neurology). In-hospital: 25% survival. Signup and view all the answers

How do standardized post-resuscitation protocols impact outcomes?

They improve survival and neurological recovery by addressing multisystem insults (e.g., hemodynamics, temperature, seizures). Signup and view all the answers

What are the three components of intracranial volume?

Brain (~80%), blood (~10%), and CSF (~10%). Signup and view all the answers

What is the final consequence of uncontrolled intracranial hypertension?

Cerebellar tonsillar herniation through the foramen magnum, compressing medullary cardiorespiratory centers. Signup and view all the answers

Why has no neuroprotectant therapy succeeded in clinical trials?

Despite targeting molecular pathways in ischemic injury, none have shown reproducible clinical benefit. Signup and view all the answers

How does cerebral arteriolar vasodilation worsen ICP?

Vasodilation increases cerebral blood volume, raising ICP and further reducing CPP (vicious cycle). Signup and view all the answers

What conditions share overlapping pathophysiology with hypoxic-ischemic brain injury?

Stroke and traumatic brain injury (TBI). Signup and view all the answers

What compensatory mechanisms delay ICP elevation initially?

Shifting CSF to the spinal subarachnoid space and reducing venous blood volume. Signup and view all the answers

Explain how compression of the oculomotor nerve (CN III) during uncal herniation leads to ipsilateral pupillary dilation, detailing the specific mechanism at play.

Compression of CN III disrupts parasympathetic fibers responsible for pupillary constriction, resulting in unopposed sympathetic tone and subsequent pupillary dilation on the same side as the herniation. Signup and view all the answers

Describe the pathophysiology behind contralateral hemiparesis in the context of uncal herniation, including how the cerebral peduncle and tentorium cerebelli are involved.

The uncus shifts and compresses the contralateral cerebral peduncle against the tentorium cerebelli. This compression affects the motor fibers descending from the cerebral cortex, leading to weakness or paralysis on the side of the body opposite the herniation. Signup and view all the answers

Explain the rationale behind using hypertonic saline to treat uncal herniation and detail the specific mechanism that contributes to the reduction of intracranial pressure (ICP).

Hypertonic saline increases serum osmolality, creating an osmotic gradient that draws water from the brain tissue into the vasculature. This reduces cerebral edema and intracranial pressure (ICP) by decreasing the volume of fluid in the brain. Signup and view all the answers

Describe the potential consequences of anterior cerebral artery compression during uncal herniation, specifically detailing the areas of the brain affected and the resulting neurological deficits.

Compression of the anterior cerebral artery can lead to infarction of the medial cerebral hemisphere, particularly affecting the frontal and parietal lobes. This can result in motor and sensory deficits in the contralateral lower extremity, as well as behavioral and cognitive changes. Signup and view all the answers

Explain the significance of Duret hemorrhages in the context of uncal herniation, detailing their location, mechanism of formation, and clinical implications.

Duret hemorrhages are small, linear hemorrhages in the midbrain and pons caused by the shearing and stretching of penetrating arteries during severe downward displacement of the brainstem. Their presence indicates a grave prognosis, often leading to coma and death. Signup and view all the answers

Discuss the role of an external ventricular drain (EVD) in managing uncal herniation, explaining how it works to reduce intracranial pressure (ICP) and the potential risks associated with its use.

An EVD involves placing a catheter into one of the brain's ventricles to drain cerebrospinal fluid (CSF), thus acutely reducing ICP. Risks include infection (ventriculitis), bleeding, catheter malfunction or obstruction, and over-drainage leading to ventricular collapse. Signup and view all the answers

Describe the long-term neurological complications that can arise from uncal herniation, even after successful initial treatment, and explain the underlying mechanisms contributing to these deficits.

Long-term complications include motor deficits, cognitive impairment, and seizures due to permanent damage to brain tissue from compression, ischemia, and neuronal death. Gliosis and altered neural circuitry contribute to ongoing functional deficits. Signup and view all the answers

Explain how the anatomy of the tentorium cerebelli contributes to the pathophysiology of uncal herniation, detailing its location and how it influences the direction and impact of the herniation.

The tentorium cerebelli is a dural structure that separates the cerebrum from the cerebellum. The free edge of the tentorium creates a fixed opening (the tentorial notch), and the uncus herniates through this opening, compressing adjacent structures like the brainstem and cranial nerves. The rigid nature of the tentorium exacerbates the compressive effects. Signup and view all the answers

How does the anatomical location of uncal herniation differ from that of cerebellar herniation, and why is this distinction critical in predicting the structures affected?

Uncal herniation occurs supratentorially, affecting CN III and the posterior cerebral artery. Cerebellar herniation is infratentorial, compressing the medulla oblongata through the foramen magnum, which is critical for respiratory and cardiovascular function. Signup and view all the answers

In uncal herniation, compression of the contralateral cerebral peduncle against the tentorium cerebelli can result in hemiparesis. Explain why the resulting motor deficit occurs on the same side of the body as the herniation, contrary to what might be expected from typical corticospinal tract anatomy.

Compression of the contralateral cerebral peduncle results in ipsilateral hemiparesis because the fibers have already crossed at the pyramidal decussation in the medulla. Therefore, damage to the peduncle above this decussation affects the same side of the body. Signup and view all the answers

Differentiate between the primary mechanisms by which uncal and cerebellar herniations lead to respiratory compromise, detailing the specific anatomical structures involved in each case.

Uncal herniation may indirectly affect respiration through global brainstem compression due to increased ICP. Cerebellar herniation directly compresses the medulla oblongata, disrupting the respiratory centers located there. Signup and view all the answers

Why is prompt surgical decompression more critical in cerebellar herniations compared to uncal herniations, considering the pathophysiological consequences of each?

Cerebellar herniation directly threatens vital respiratory and cardiovascular centers in the medulla, requiring immediate decompression to prevent rapid deterioration and death. Uncal herniation, while serious, may progress slightly less rapidly, allowing for a more measured approach. Signup and view all the answers

Explain how compression of the posterior cerebral artery (PCA) in uncal herniation leads to visual field deficits, and specify the type of visual field cut that is most likely to occur.

Compression of the PCA can cause ischemia in the occipital lobe, leading to contralateral homonymous hemianopia due to infarction of the visual cortex. Signup and view all the answers

Compare and contrast the roles of osmotic therapy (e.g., mannitol) in the acute management of both uncal and cerebellar herniation, noting any differences in the expected time course of therapeutic effect and potential risks.

In both uncal and cerebellar herniation, osmotic therapy reduces ICP. The effect is faster in uncal herniation, but in cerebellar herniation, caution is needed due to the risk of precipitating a rapid shift in the posterior fossa, potentially worsening brainstem compression. Rebound ICP is a risk in both. Signup and view all the answers

A patient presents with ipsilateral pupillary dilation and contralateral hemiparesis. While uncal herniation is suspected, what other potential diagnoses should be considered, and what additional clinical findings would help differentiate them?

Besides uncal herniation, consider brainstem lesions, stroke, or mass effect causing similar symptoms. Additional findings such as cranial nerve deficits (other than CN III), sensory loss, or rapid symptom onset would point away from simple uncal herniation. Signup and view all the answers

Describe why corticosteroids are more commonly used in the treatment of uncal herniation caused by tumors than in cerebellar herniation, and explain the mechanism by which corticosteroids alleviate symptoms in this context.

Corticosteroids reduce vasogenic edema associated with tumors, thus reducing ICP and mass effect in uncal herniation. They are less effective in cerebellar herniation, where direct compression of the brainstem is the primary issue, and edema may not be as significant. Signup and view all the answers

Name and describe the outermost layer of the meninges.

dura mater Signup and view all the answers

What is the main function of the pial layer? What is most notable about its composition?

supplies blood to the neural tissue Signup and view all the answers

Describe the composition of the dural layer.

tough, fibrous layer Signup and view all the answers

What is found within the epidural space?

fat and blood vessels Signup and view all the answers

Where is the subdural space located?

between the dura mater and the arachnoid mater Signup and view all the answers

What is the primary function of the spinal column?

Protect the spinal cord Signup and view all the answers

Name the outermost layer of the meninges.

Dura mater Signup and view all the answers

What type of information is transmitted by the spinal cord?

Sensory and motor Signup and view all the answers

What is injected into the epidural space during epidural anesthesia?

Local anesthetics Signup and view all the answers

Explain how the anatomical location of the uncus contributes to the specific neurological deficits observed in uncal herniation, particularly in relation to the oculomotor nerve and the posterior cerebral artery.

The uncus's proximity to the oculomotor nerve (CN III) and posterior cerebral artery means that herniation can compress these structures. Compression of CN III leads to ipsilateral pupillary dilation and ptosis, while compression of the posterior cerebral artery can cause occipital lobe infarction, resulting in contralateral homonymous hemianopia. Signup and view all the answers

If a patient presents with altered mental status, ipsilateral pupillary dilation, and contralateral hemiparesis, what is the most likely diagnosis, and describe the underlying mechanism causing these specific symptoms in the context of uncal herniation?

The most likely diagnosis is uncal herniation. The mechanism involves compression of the ipsilateral oculomotor nerve (causing pupillary dilation), compression of the contralateral cerebral peduncle (causing hemiparesis), and distortion of the reticular activating system (causing altered mental status). Signup and view all the answers

Describe the role of emergent neuroimaging, such as CT or MRI, in the diagnosis and management of suspected uncal herniation, and explain how imaging findings guide treatment strategies.

Emergent neuroimaging, typically CT or MRI, confirms the diagnosis by visualizing the uncal herniation and ruling out other potential causes of the patient's symptoms. Imaging guides treatment by assessing the extent of herniation, presence of hemorrhage, and any mass effect, informing decisions regarding surgical intervention, osmotic therapy, or other supportive measures. Signup and view all the answers

Explain how the pathophysiology of uncal herniation can lead to a false localizing sign, such as Kernohan's notch phenomenon, and why it is critical to recognize this potential pitfall in clinical diagnosis.

Kernohan's notch phenomenon occurs when the contralateral cerebral peduncle is compressed against the tentorium cerebelli due to the herniation, resulting in ipsilateral hemiparesis. It's critical to recognize this as a false localizing sign because it can lead to incorrect identification of the side of the lesion, potentially delaying appropriate intervention. Signup and view all the answers

Discuss the relative roles and mechanisms of action of osmotic therapies (e.g., mannitol, hypertonic saline) and surgical decompression in the acute management of uncal herniation, highlighting the specific circumstances under which each approach is preferred.

Osmotic therapies such as mannitol and hypertonic saline reduce intracranial pressure by creating an osmotic gradient that draws fluid from the brain tissue into the vasculature, helping to temporarily alleviate the herniation. Surgical decompression, such as craniotomy, is preferred when there is a mass lesion causing significant mass effect and herniation that is unresponsive to osmotic therapy. Osmotic therapies are typically a temporizing measure, while surgery addresses the underlying cause. Signup and view all the answers

Flashcards

Neuronal Injury Timeline

Neuronal injury continues for hours to days after the initial ischemic insult.

Brain's Resource Consumption

The brain receives 15% of cardiac output and uses 20% of the body's oxygen.