A 70-year-old man is brought to the emergency department due to left-sided weakness and slurred speech upon awakening 30 minutes ago. The patient was asymptomatic when he went to bed last night. Medical history includes type 2 diabetes mellitus, hypertension, and hyperlipidemia. The patient is a former smoker with a 30-pack-year history. Physical examination shows a right gaze preference, left lower facial droop, and hemiplegia and hemisensory loss on the left. CT scan of the brain reveals early infarction in the right middle cerebral artery territory with no acute hemorrhage. The patient is hospitalized for further management. Several hours later, he becomes progressively obtunded with elevated intracranial pressure. A repeat CT scan reveals edema in the region of acute infarction causing mass effect. Which of the following is the primary contributor to the pathogenesis of this patient's raised intracranial pressure?

Question

A 70-year-old man is brought to the emergency department due to left-sided weakness and slurred speech upon awakening 30 minutes ago.  The patient was asymptomatic when he went to bed last night.  Medical history includes type 2 diabetes mellitus, hypertension, and hyperlipidemia.  The patient is a former smoker with a 30-pack-year history.  Physical examination shows a right gaze preference, left lower facial droop, and hemiplegia and hemisensory loss on the left.  CT scan of the brain reveals early infarction in the right middle cerebral artery territory with no acute hemorrhage.  The patient is hospitalized for further management.  Several hours later, he becomes progressively obtunded with elevated intracranial pressure.  A repeat CT scan reveals edema in the region of acute infarction causing mass effect.  Which of the following is the primary contributor to the pathogenesis of this patient's raised intracranial pressure?

Quizplus · Accepted Answer

This patient had a right hemispheric ischemic stroke and developed altered mental status and increased intracranial pressure (ICP) secondary to cerebral edema. The fixed volume of the skull necessitates that a significant increase in volume of any component of the CNS (eg, brain tissue, blood, cerebrospinal fluid) will raise ICP. This increased ICP can cause progressive neurologic impairment through direct pressure-induced cell injury or mechanical damage due to brain herniation. Irreversible ischemic neural and glial cell injury initiates a sequence of chemical changes that promote edema: Cytotoxic (ionic) edema begins hours after the ischemic injury due to decreased ATP. The failure of ATP-dependent ion pumps, combined with the release of excitatory amino acids (eg, glutamate), leads to the accumulation of intracellular Na⁺ and water in neural and glial cells despite an intact blood-brain barrier. Vasogenic edema follows 24-48 hours later, when the release of inflammatory mediators disrupts the tight junctions of the blood-brain barrier, allowing proteins (eg, albumin) and water to enter the interstitial space. This vasogenic phase can cause persistent cerebral edema for weeks after the initial injury. (Choice A) Although a decrease in oncotic pressure can cause peripheral edema (eg, nephrotic syndrome), it is not a significant factor in the development of cerebral edema. Mannitol is used in the treatment of cerebral edema because it increases plasma oncotic pressure and temporarily disrupts the blood-brain barrier, allowing movement of fluid out of the CNS to decrease ICP. (Choice C) Inadequate absorption of cerebrospinal fluid at the arachnoid granulations can cause communicating hydrocephalus. Although this process raises ICP, ventriculomegaly would likely be prominent on CT scan. (Choice D) Increased hydrostatic pressure secondary to central venous thrombosis or hypertensive encephalopathy can cause cerebral edema and increased ICP. However, patients typically have gradually worsening headache before development of neurologic abnormalities. (Choice E) Gliosis is the process of repairing damaged tissue in the CNS by proliferating astrocytes and microglia. This process occurs slowly in the months to years after CNS injury and would not be expected to cause acute changes in ICP. Educational objective: The primary mechanism underlying cytotoxic (early) edema following cerebral ischemia is the accumulation of intracellular Na⁺ and water due to the failure of ATP-dependent ion transporters in hypoxic cells. Cerebral edema causes progressive neurologic decline by raising intracranial pressure, which can directly damage neural tissue or result in mechanical damage due to brain herniation. __________ References: Brain edema after ischaemic stroke. (http://www.ncbi.nlm.nih.gov/pubmed/27994292)

A 70-Year-Old Man Is Brought to the Emergency Department Due