Ch 61: ICP Flashcards

Question

When measuring ICP in a patient, which location allows for the most accurate and direct reading? A. Subdural space B. Subarachnoid space C. Ventricular space D. Epidural space

Answer 1

C. Ventricular space Rationale: The ventricular system provides the most direct and accurate measurement of ICP and allows for therapeutic CSF drainage, making it the gold standard for monitoring.

Answer 2

B. Elevate the head of the bed to 30 degrees Rationale: Elevating the HOB promotes venous drainage and decreases ICP. It is a noninvasive first-line intervention. Bearing down increases intrathoracic pressure and would worsen ICP.

Answer 3

The hydrostatic force measured in the brain CSF compartment

Answer 4

C. Displacement of CSF into spinal subarachnoid space Rationale: One of the body’s first compensatory responses to increased intracranial volume is to reduce CSF volume by displacing it into the spinal subarachnoid space, or altering its production and absorption.

Answer 5

B. Compression of brain tissue Rationale: In later stages of compensation, brain tissue volume adapts through distention of the dura and compression of brain tissue to maintain normal ICP, though this is limited and eventually leads to ischemia.

Answer 6

A. Cerebral venous vasoconstriction Rationale: The second category of compensatory mechanisms involves changes in intracranial blood volume, including regional vasoconstriction or dilation and venous outflow alterations.

Answer 7

D. Decompensation is occurring, leading to ischemia Rationale: When compensatory mechanisms are exhausted, ICP rises uncontrollably, leading to tissue compression and cerebral ischemia—a dangerous, decompensated state.

Answer 8

A. Collapse of cerebral veins D. Compression of brain tissue E. Displacement of CSF to the spinal subarachnoid space Rationale: Collapse of cerebral veins, compression of brain tissue, and CSF displacement are normal compensatory mechanisms. Increased CSF production and arterial vasodilation increase ICP rather than reduce it.

Answer 9

B. Stable neurologic exam Rationale: A stable neurologic exam suggests cerebral perfusion is maintained, indicating that compensatory mechanisms (such as CSF displacement or venous outflow changes) are effectively managing the volume shift.

Answer 10

B. “Venous outflow can adapt to help manage increased volume.” Rationale: One of the second-line compensatory mechanisms includes adjusting venous outflow to reduce cerebral blood volume and help maintain ICP.

Answer 11

A. Rapid increase in ICP and signs of herniation Rationale: Once compensatory mechanisms are overwhelmed, ICP rises rapidly. This can lead to brain tissue compression and potentially fatal herniation syndromes.

Answer 12

C. The brain depends on a constant supply of oxygen and glucose due to high metabolic demand. Rationale: The brain uses 20% of the body’s oxygen and 25% of its glucose, making continuous blood flow essential to prevent hypoxia and ischemia.

Answer 13

D. Decreased CBF has led to cerebral hypoxia and altered function Rationale: The brain requires consistent blood flow to receive oxygen and glucose. A drop in cerebral perfusion compromises brain function, leading to symptoms like confusion and altered mental status.

Answer 14

A. Even brief interruptions in CBF can cause permanent brain damage. Rationale: The brain has minimal ability to store oxygen or glucose, so interruptions in CBF—even for a short time—can cause irreversible damage.

Answer 15

A. The global CBF is approximately 50 mL/min/100 g of brain tissue. C. Adequate CBF is essential for delivering glucose to the brain. E. Maintaining CBF is critical due to the brain’s high metabolic demands. Rationale: Global CBF is about 50 mL/min/100 g of tissue. The brain uses 25% of the body’s glucose and 20% of its oxygen, making options A, C, and E correct. The brain cannot survive long without blood flow.

Answer 16

B. Bradycardia with a MAP of 52 mm Hg Rationale: Cerebral perfusion is pressure-dependent. A MAP less than 60 mm Hg can critically reduce cerebral blood flow, leading to symptoms of cerebral hypoperfusion such as confusion and dizziness.

Answer 17

The automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintain a constant blood flow with changes in arterial blood pressure

Answer 18

the pressure needed to ensure blood flow to the brain

Answer 19

B. The MAP is below the lower limit of autoregulation, decreasing CBF. Rationale: A MAP <70 mm Hg is below the threshold of effective autoregulation, causing a drop in cerebral blood flow and symptoms of ischemia like blurred vision.

Answer 20

C. CPP is 65 mm Hg, which may not be sufficient in localized swelling. Rationale: CPP = MAP − ICP → 90 − 25 = 65 mm Hg. While this is technically within normal limits (60–100), in patients with localized injury or stroke, a higher CPP may be required to ensure adequate perfusion to damaged areas.

Answer 21

B. It ensures consistent cerebral blood flow by adjusting vessel diameter. Rationale: Autoregulation maintains consistent cerebral blood flow (CBF) despite changes in systemic pressure by adjusting cerebral vessel diameter.

Answer 22

A. CPP = MAP − ICP B. Normal CPP is 60–100 mm Hg C. CPP < 50 mm Hg may cause ischemia Rationale: Options A–C are correct based on standard definitions. Option D is false—CPP <30 mm Hg is incompatible with life. Option E is false because CPP may not reflect local perfusion due to swelling or compression.

Answer 23

A. Prepare for emergency CSF drainage. Rationale: CPP = 80 − 30 = 50 mm Hg, indicating risk for cerebral ischemia. Immediate interventions to lower ICP (e.g., draining CSF) are priority to prevent neuron death.

Answer 24

C. 150 mm Hg Rationale: The upper limit of autoregulation is a MAP of 150 mm Hg. Beyond this, vessels can no longer constrict to protect brain tissue, increasing risk of hyperperfusion and damage.

Answer 25

A. To enhance CPP and perfusion to affected brain tissue Rationale: In localized injury like stroke, raising MAP helps elevate CPP in areas of compromised perfusion and prevent further ischemic injury.

Answer 26

D. CPP is 50 mm Hg, which may lead to ischemia Rationale: CPP = 95 − 35 = 60 mm Hg, which is borderline low. In a patient with brain trauma, local swelling may mean even 60 mm Hg is insufficient, putting them at risk for ischemia.

Answer 27

B. MAP of 160 mm Hg with normal ICP Rationale: A MAP >150 mm Hg exceeds the upper limit of autoregulation. Beyond this, vessels are maximally constricted, losing their ability to regulate CBF.

Answer 28

A. Cerebral blood flow becomes pressure-dependent B. CPP falls to dangerous levels D. Local ischemia may occur Rationale: When autoregulation fails, CBF varies directly with MAP (A), CPP can fall dangerously (B), and local ischemia (D) can result. Options C and E are false—vessels can no longer adjust, and brain metabolic needs remain high.

Answer 29

B. Lower head of bed to reduce ICP Rationale: Lowering the head of bed can reduce ICP, which increases CPP when MAP remains constant (CPP = MAP − ICP). Maintaining a CPP >70 mm Hg ensures adequate perfusion.

Answer 30

C. CPP is 55 mm Hg, which is below the threshold for adequate perfusion. Rationale: CPP = 65 − 10 = 55 mm Hg. This is below the normal limit (60 mm Hg), indicating cerebral hypoperfusion and ischemic symptoms.

Answer 31

A. Increased resistance impairs brain perfusion. Rationale: As cerebrovascular resistance increases (due to arteriolar constriction or swelling), blood flow is reduced even if CPP appears normal.

Answer 32

C. To support CPP and maintain oxygen delivery Rationale: Maintaining MAP ensures adequate CPP when ICP is elevated, supporting cerebral oxygenation and perfusion.

Answer 33

D. Administer vasopressors to increase MAP Rationale: CPP = 70 − 22 = 48 mm Hg. Vasopressors will raise MAP, which increases CPP and improves perfusion. Other options either reduce MAP or are not clinically appropriate for increasing CPP.

Answer 34

B. Vasodilation leading to increased CBF Rationale: An elevated PaCO₂ causes cerebral vasodilation, decreasing cerebrovascular resistance and increasing CBF.

Answer 35

A. 30 mm Hg Rationale: A PaCO₂ of 30 mm Hg is below the normal range, leading to cerebral vasoconstriction, increased resistance, and decreased CBF.

Answer 36

A. Elevated PaCO₂ B. Decreased PaO₂ below 50 mm Hg D. Acidosis Rationale: Elevated PaCO₂ and decreased PaO₂ below 50 mm Hg cause vasodilation, increasing CBF. Acidosis (increased hydrogen ion concentration) also leads to vasodilation. Alkalosis and hyperventilation (which lowers PaCO₂) cause vasoconstriction, decreasing CBF.

Answer 37

C. Vasodilation to increase CBF Rationale: A PaO₂ below 50 mm Hg triggers cerebral vasodilation to increase CBF and improve oxygen delivery.

Answer 38

A. Vasodilation to increase CBF Rationale: Acidosis leads to vasodilation in cerebral vessels, decreasing resistance and increasing CBF to meet metabolic demands.

Answer 39

B. Hyperventilation-induced hypocapnia Rationale: Hypocapnia from hyperventilation causes cerebral vasoconstriction, which can impair autoregulation and decrease CBF.

Answer 40

B. Decrease cerebral blood flow Rationale: Hyperventilation lowers PaCO₂, causing cerebral vasoconstriction, which decreases CBF and subsequently lowers intracranial pressure.

Answer 41

B. PaCO₂ 50 mm Hg, PaO₂ 60 mm Hg, pH 7.35 Rationale: Elevated PaCO₂ and lower PaO₂ levels promote cerebral vasodilation to increase CBF.

Answer 42

A. Severe hypoxia B. Traumatic brain injury C. Hypercapnia E. Systemic infections Rationale: Severe hypoxia, traumatic brain injury, hypercapnia, and systemic infections can disrupt the mechanisms of cerebral autoregulation. Hypocapnia typically causes vasoconstriction but does not directly lead to loss of autoregulation.

Answer 43

B. Increases due to vasodilation Rationale: Metabolic acidosis increases hydrogen ion concentration, leading to cerebral vasodilation and increased CBF.

Answer 44

D. Decreases due to loss of perfusion pressure Rationale: Cardiac arrest leads to a cessation of effective circulation, resulting in decreased cerebral perfusion pressure and CBF.

Answer 45

D. Causes vasodilation, increasing CBF Rationale: Hypercapnia (elevated PaCO₂) causes cerebral vasodilation, increasing CBF and potentially raising intracranial pressure.

Answer 46

A. Administer mannitol to decrease intracranial pressure Rationale: Mannitol is an osmotic diuretic used to reduce intracranial pressure by drawing fluid from the brain tissue into the vascular space. A lumbar puncture is contraindicated in increased ICP due to risk of brain herniation. Plasmapheresis is not indicated here. Cushing’s triad indicates late signs of brain herniation, so waiting for this would delay care.

Answer 47

D. Unilateral fixed and dilated pupil Rationale: A unilateral fixed and dilated pupil indicates increased ICP with possible herniation, which is a neurologic emergency. Other values are concerning but not immediately life-threatening.

Answer 48

A. Brain abscess B. Cerebral edema D. Brain tumor Rationale: Brain abscess, cerebral edema, and brain tumors are all known causes of increased ICP. Liver failure and hypokalemia are not direct causes.

Answer 49

C. Cerebral acidosis impairs autoregulation and increases cerebral edema Rationale: Cerebral acidosis leads to impaired autoregulation and worsens cerebral edema, contributing to sustained ICP elevation. Hypocapnia causes vasoconstriction, not vasodilation.

Answer 50

C. Elevate the head of the bed to 30 degrees Rationale: Elevating the HOB to 30 degrees promotes venous drainage and decreases ICP. Supine position can worsen ICP. Surgery and opioids may be appropriate later but are not the first nursing priority.

Answer 51

D. It results in compression of the medulla and cessation of respiratory function Rationale: Brain herniation compresses the medulla, which contains the respiratory center. If unrelieved, this can result in respiratory arrest and death.

Answer 52

A. Bradycardia, widened pulse pressure, and irregular respirations Rationale: This describes Cushing’s triad, a classic late sign of increased ICP and impending herniation.

Answer 53

A. Loss of gag reflex Rationale: The gag reflex is controlled by cranial nerves IX and X, which emerge from the brainstem. Loss of this reflex may indicate brainstem dysfunction or herniation.

Answer 54

C. Cerebral edema and hypercapnia cause further acidosis and vasodilation Rationale: Hypercapnia and lactic acid both contribute to acidosis, leading to vasodilation and further increasing ICP.

Answer 55

D. Hyperoxygenate and prepare for mechanical ventilation Rationale: Hyperoxygenation can reduce ICP by preventing hypoxia. Mechanical ventilation may be necessary if respiratory effort is compromised. Trendelenburg increases ICP and should be avoided.

Answer 56

D. Brainstem compression Rationale: Cheyne-Stokes respirations and pupillary changes are classic signs of brainstem involvement, suggesting worsening herniation and increased ICP.

Answer 57

A. Elevate HOB to 30 degrees B. Keep neck in a neutral position D. Cluster care to minimize disturbances Rationale: Elevating HOB and neutral neck positioning promote venous drainage. Clustering care reduces stimulation. Vigorous suctioning and rapid fluids can raise ICP.

Answer 58

A. Respiratory arrest Rationale: The respiratory center is in the medulla. Compression leads to respiratory failure and death if not reversed quickly.

Answer 59

increased accumulation of fluid in the extravascualr spaces of brain tissue

Answer 60

B. Disruption of the blood-brain barrier allowing fluid to shift into extracellular space Rationale: Vasogenic edema is caused by a breakdown in the blood-brain barrier, typically due to tumors or trauma, allowing plasma proteins and fluid to leak into the extracellular space, increasing brain volume and ICP.

Answer 61

A. Cytotoxic edema Rationale: Cytotoxic edema is common after ischemia or hypoxia. It results from failure of the sodium-potassium pump in brain cells, leading to intracellular swelling and increased brain volume.

Answer 62

C. Obstructive hydrocephalus causing CSF leakage into brain parenchyma Rationale: Interstitial edema occurs primarily with hydrocephalus, where CSF flows across the ependymal lining into surrounding brain tissue, increasing brain volume and ICP.

Answer 63

D. Vomiting without nausea Rationale: Vomiting without nausea (projectile vomiting) is a classic sign of increased ICP, commonly associated with worsening cerebral edema.

Answer 64

A. Brain tumor B. Head trauma E. Meningitis Rationale: Vasogenic edema is caused by BBB disruption, commonly seen with tumors, trauma, and infections like meningitis. Stroke and hypoxia more often result in cytotoxic edema.

Answer 65

D. Administering hypertonic saline solution Rationale: Hypertonic saline draws fluid from swollen brain cells into the intravascular space, reducing cerebral edema and ICP. Flat positioning and increased fluids can worsen ICP; deep suctioning may increase ICP due to stimulation.

Answer 66

B. Disruption of the blood-brain barrier Rationale: Vasogenic cerebral edema is caused by the disruption of the blood-brain barrier, which allows large molecules (like proteins and blood products) to enter brain tissue, leading to edema.

Answer 67

C. Blood-brain barrier disruption allows blood products and proteins to enter the brain Rationale: In vasogenic cerebral edema, the disruption of the blood-brain barrier allows large molecules, including proteins and blood products, to enter the brain, resulting in swelling and increased ICP.

Answer 68

C. A change in mental status, from confusion to coma Rationale: A rapid decline in mental status, including confusion progressing to coma, is indicative of worsening cerebral edema and increased ICP.

Answer 69

A. Systemic blood pressure and the site of the brain injury Rationale: Systemic blood pressure and the site of the brain injury influence the extent of vasogenic edema because the blood-brain barrier’s disruption can vary based on these factors.

Answer 70

B. Osmotic changes leading to fluid accumulation in brain tissue Rationale: In vasogenic cerebral edema, osmotic changes occur as large molecules enter brain tissue, creating an osmotic gradient that draws fluid into the extracellular space, leading to increased ICP.

Answer 71

C. Sudden onset of severe headache with altered mental status Rationale: A sudden onset of severe headache combined with altered mental status, such as confusion, is indicative of worsening cerebral edema and requires immediate attention.

Answer 72

D. Neurologic status, including level of consciousness Rationale: Changes in neurologic status, including level of consciousness, are critical to monitor in patients with vasogenic cerebral edema as it can rapidly progress from confusion to coma and death.

Answer 73

D. “Vasogenic edema occurs mainly in the gray matter of the brain.” Rationale: Vasogenic edema occurs primarily in the white matter, not the gray matter. This reflects a misunderstanding that needs correction.

Answer 74

A. Administering corticosteroids to reduce inflammation Rationale: Corticosteroids are commonly used to reduce cerebral edema by decreasing inflammation and stabilizing the blood-brain barrier, which helps reduce ICP.

Answer 75

B) Fluid and protein shifts into the cells Rationale: Cytotoxic cerebral edema results from the disruption of cell membranes in brain tissue, causing fluid and protein to shift from the extracellular space into the cells, leading to cellular swelling. The blood-brain barrier remains intact in this type of edema, differentiating it from vasogenic edema.

Answer 76

B) Impaired cellular function due to swelling and fluid shift into the cells Rationale: Cytotoxic cerebral edema occurs due to fluid and protein shifts into the brain cells, resulting in cellular swelling. This swelling impairs cellular function and causes tissue damage, unlike vasogenic edema, which involves the leakage of large molecules due to blood-brain barrier disruption.

Answer 77

D) Sudden onset of confusion and a change in mental status Rationale: Cytotoxic cerebral edema causes swelling of brain cells, which may lead to a gradual or sudden decline in neurological function. Symptoms often include confusion, changes in mental status, and possibly loss of consciousness as the swelling increases. Severe cases may progress to coma or death, but subtle changes in mental status are an early sign.

Answer 78

A) Monitoring the patient’s oxygenation and ensuring adequate ventilation Rationale: Oxygenation is critical in managing cytotoxic cerebral edema, as hypoxia or anoxia exacerbates brain injury. Ensuring adequate oxygenation helps prevent further cellular damage and reduces the risk of worsening edema. Hyperventilation or elevated CO2 levels could worsen edema, so managing oxygenation is crucial.

Answer 79

A) Decreased serum sodium levels Rationale: Cytotoxic cerebral edema can occur in the setting of hypoxia and anoxia. A common result is the syndrome of inappropriate antidiuretic hormone (SIADH) secretion, which leads to water retention and dilutional hyponatremia (decreased serum sodium levels). This electrolyte imbalance occurs due to the kidneys’ retention of water in response to elevated ADH levels.

Answer 80

C) Hypertonic saline to decrease intracranial pressure Rationale: Hypertonic saline is commonly used to reduce intracranial pressure in patients with cerebral edema by drawing fluid out of brain cells into the bloodstream. Corticosteroids are more effective for vasogenic edema, not cytotoxic edema. Dehydration therapy is not an appropriate method for managing cerebral edema and could lead to further complications.

Answer 81

a buildup of fluid in the brain

Answer 82

B) Ventricular enlargement Rationale: Interstitial cerebral edema occurs due to the buildup of cerebrospinal fluid (CSF) in the brain, commonly seen in hydrocephalus. This condition leads to ventricular enlargement, which is a hallmark sign of hydrocephalus. It is caused by an excess production of CSF, obstruction in its flow, or an inability to reabsorb it.

Answer 83

C) Obstruction of CSF flow, leading to fluid buildup Rationale: Interstitial cerebral edema is often caused by hydrocephalus, which results from either an overproduction of CSF, obstruction of CSF flow, or an impaired ability to reabsorb CSF. The obstruction leads to a buildup of CSF in the ventricles, causing ventricular enlargement and increased pressure on brain tissue.

Answer 84

A) Increased intracranial pressure (ICP) Rationale: As hydrocephalus leads to a buildup of cerebrospinal fluid (CSF) and enlargement of the ventricles, it causes an increase in intracranial pressure (ICP). This pressure can compress brain tissue, leading to interstitial cerebral edema and associated neurological symptoms such as decreased consciousness and possible focal deficits.

Answer 85

B) Shunt placement to drain excess cerebrospinal fluid (CSF) Rationale: In hydrocephalus, the most appropriate intervention to manage interstitial cerebral edema is to address the buildup of cerebrospinal fluid (CSF) by placing a shunt. The shunt diverts excess CSF away from the ventricles and into other areas of the body, helping to reduce ventricular enlargement and intracranial pressure.

Answer 86

A) Perform a neurological assessment, including cranial nerve reflexes Rationale: Any patient who becomes acutely unconscious should be suspected of having increased ICP. The first priority is to perform a thorough neurological assessment, including checking cranial nerve reflexes, as this will help determine the severity of brain involvement and guide further actions, including the need for imaging studies like CT scans.

Answer 87

B) Decreased level of consciousness Rationale: Decreased level of consciousness (LOC) is one of the most important clinical manifestations of increased ICP. As ICP increases, it can compress the brainstem, leading to a decreased LOC. Early recognition of this change can lead to prompt intervention and prevent further brain injury.

Answer 88

C) Pupillary changes and abnormal eye movements Rationale: Pupillary changes and abnormal eye movements are significant clinical manifestations of increased ICP. These changes may indicate brainstem involvement or pressure on the cranial nerves, which can rapidly worsen if not addressed. Immediate intervention is necessary to assess the degree of brain dysfunction.

Answer 89

D) Pressure on brain tissue from a mass effect, edema, or hemorrhage Rationale: Increased ICP is most commonly caused by pressure on brain tissue due to factors such as a mass (e.g., tumor, hematoma), edema, or hemorrhage. These conditions cause brain tissue compression, which increases ICP and can lead to acute unconsciousness, a key clinical manifestation of increased ICP.

Answer 90

an abnormal state of complete or partial awareness of self or environment

Answer 91

A. Change in level of consciousness Rationale: The most sensitive and earliest indicator of neurologic deterioration or increased ICP is a change in LOC. This occurs due to decreased cerebral perfusion and impaired function of the cerebral cortex or RAS. Pupillary changes, bradycardia, and vomiting are later signs of increased ICP.

Answer 92

B. Notify the provider immediately and prepare for potential intubation Rationale: A declining LOC with reduced response to painful stimuli indicates potential progression toward coma. Airway protection becomes a priority as the patient may lose gag and swallow reflexes. While monitoring urine and administering mannitol may be appropriate later, airway is the immediate concern.

Answer 93

C. Reticular activating system Rationale: The RAS, located in the brainstem, is crucial for maintaining arousal and wakefulness. Impairment of the RAS leads to varying degrees of unconsciousness, depending on the extent of damage.

Answer 94

C. Loss of pupillary reflex Rationale: Loss of pupillary reflexes may indicate brainstem involvement and impending herniation, which is a neurological emergency. Other symptoms indicate progression of increased ICP but are not as immediately life-threatening as brainstem dysfunction.

Answer 95

A. Decreased level of attention B. Flattened affect D. Disorientation to time Rationale: Subtle signs of declining LOC include changes in affect, orientation, and attention. Sudden hemiplegia and inability to cough are more advanced neurologic signs seen in late or severe brain injury.

Answer 96

A. Absent corneal reflex Rationale: In deep coma, the patient loses reflexes such as the corneal and pupillary reflexes. The absence of the corneal reflex is a grave sign indicating severe dysfunction of the brainstem.

Answer 97

D. Elevate the head of the bed to 30 degrees Rationale: A change in LOC following a head injury suggests rising ICP. Elevating the head promotes venous drainage and reduces ICP. A lumbar puncture is contraindicated if ICP is suspected to be elevated due to risk of herniation.

Answer 98

C. Suppressed or absent neuronal activity Rationale: In coma, EEG typically shows suppressed or absent activity, indicating minimal or absent cortical brain function. This confirms severe neurological impairment.

Answer 99

C. These may be early indicators of increased ICP Rationale: Flat affect and decreased orientation are subtle yet important signs of increasing ICP. Prompt recognition and intervention are essential to prevent further neurologic deterioration.

Answer 100

A. Unresponsive to verbal and painful stimuli C. Absent corneal and pupillary reflexes E. Suppressed EEG activity Rationale: In coma, the patient does not respond to pain, has absent brainstem reflexes (corneal, pupillary), and shows severely reduced neuronal activity on EEG. They are typically incontinent and have no protective reflexes like swallowing or gagging.

Answer 101

systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, irregular respirations

Answer 102

C. The client is showing signs of Cushing triad Rationale: Cushing triad is a classic, late sign of increased ICP and indicates brainstem compression and impending death. It is characterized by systolic hypertension with widening pulse pressure, bradycardia with a full bounding pulse, and irregular respirations. These are compensatory responses triggered by the brainstem in response to increased ICP. Shock would typically present with hypotension and tachycardia. This is a medical emergency requiring immediate intervention.

Answer 103

B. Direct hypothalamic dysfunction due to pressure Rationale: The hypothalamus regulates temperature. When ICP increases and compresses the hypothalamus, it can disrupt temperature regulation, causing hyperthermia. While infection could also cause fever, a sudden high temperature in the absence of infection in a neurologic client suggests central (neurogenic) fever due to hypothalamic involvement.

Answer 104

A. BP 200/100 with pulse pressure of 100 mm Hg B. HR 48 bpm and bounding C. Irregular respiratory pattern E. Apnea followed by deep, rapid breathing Rationale: * A: Wide pulse pressure is part of Cushing triad. * B: Bradycardia with a bounding pulse is classic. * C: Irregular respirations occur due to brainstem involvement. * E: Cheyne-Stokes respirations or other irregular patterns often appear. * D: A low temperature is not commonly associated unless hypothalamus is involved in a different way. * F: Tachycardia and thready pulse are more typical of shock, not increased ICP.

Answer 105

D. Medulla oblongata Rationale: The medulla is the primary respiratory control center. As ICP increases and pressure is exerted on the brainstem, particularly the medulla, respiratory rate and rhythm become irregular, signaling a dangerous progression of ICP.

Answer 106

C. Notify the HCP immediately Rationale: These signs indicate Cushing triad, a medical emergency signaling brainstem compression and the possibility of herniation. While preparing for intubation may be needed soon, the first priority is rapid notification of the provider so life-saving interventions to reduce ICP can be implemented.

Answer 107

D. Compensation to maintain cerebral perfusion pressure Rationale: As ICP increases, the body attempts to maintain cerebral perfusion by increasing systolic blood pressure, while the diastolic may remain the same or drop slightly, resulting in a widening pulse pressure. This is part of Cushing’s triad and is a compensatory mechanism to maintain adequate CPP (MAP - ICP).

Answer 108

A. The patient is experiencing increased ICP with possible brainstem compression Rationale: These vital sign changes are hallmarks of Cushing triad, which suggests a severe increase in ICP. This scenario is an urgent, life-threatening neurologic event that requires immediate intervention to prevent herniation and death. This is not consistent with stroke alone or hypovolemia.

Answer 109

B. Fixed and dilated pupil on the right side Rationale: A fixed, unilateral, dilated pupil is a neurologic emergency indicating uncal herniation with CN III compression. It signifies brain herniation, requiring immediate intervention. Options A, C, and D may suggest increased ICP but are not as immediately life-threatening as a unilateral fixed and dilated pupil.

Answer 110

B. Cranial Nerve III Rationale: Compression of CN III (oculomotor nerve) causes ipsilateral pupil dilation, ptosis (drooping eyelid), and an inability to move the eye upward. CN II is responsible for vision, CN IV controls downward movement, and CN VI affects lateral movement.

Answer 111

D. Compression of the oculomotor nerve Rationale: Unilateral ptosis and unequal pupil size (anisocoria) are hallmark signs of CN III compression, often due to shifting brain tissue from a mass effect like a tumor. This is a serious finding that indicates increased ICP and possible herniation.

Answer 112

A. Unilateral dilated pupil Rationale: Uncal herniation compresses CN III on one side, leading to a unilateral dilated, nonreactive pupil. Central herniation typically results in bilateral sluggish pupils, and pinpoint pupils are more consistent with pontine damage.

Answer 113

A. Notify the provider immediately Rationale: A fixed, dilated pupil is a neurological emergency indicating potential brain herniation. Immediate action is required to prevent irreversible brain damage or death. This finding is not one to simply monitor or assess further before notifying the provider.

Answer 114

A. Blurred vision B. Ptosis D. Diplopia Rationale: Blurred vision, ptosis, and diplopia are all associated with compression of CNs II, III, IV, or VI. Pinpoint pupils are not characteristic of CN compression from increased ICP, and nystagmus is not mentioned as a typical manifestation in this context.

Answer 115

D. It is a nonspecific sign of sustained increased ICP Rationale: Papilledema, or optic disc swelling, is a nonspecific indicator of persistent elevated ICP. It doesn’t necessarily indicate acute herniation or damage but supports the need for further investigation of ICP status.

Answer 116

A. Central herniation Rationale: Central herniation may present with bilateral sluggish pupil responses due to symmetric pressure on the brainstem. In contrast, uncal herniation typically presents with unilateral dilation.

Answer 117

D. Report to the healthcare provider immediately Rationale: Sudden visual changes such as blurred vision and diplopia suggest worsening ICP with possible cranial nerve involvement. These are early neurologic changes that could progress to herniation, and they require prompt medical evaluation.

Answer 118

an edematous optic disc seen on retinal examination

Answer 119

opposite side

Answer 120

C. It indicates disruption of motor fibers in the midbrain and brainstem Rationale: Decerebrate posturing is a sign of more serious brain injury and results from disruption of motor pathways in the midbrain and brainstem. It is a worse sign than decorticate posturing, which originates from cortical damage.

Answer 121

B. Flexion of arms with internal rotation, legs extended Rationale: Decorticate posturing is characterized by arm flexion, internal rotation, and leg extension. It suggests damage to the corticospinal tract above the brainstem, specifically within the cerebral cortex.

Answer 122

A. Progression of brain injury indicating brainstem involvement Rationale: The described posture is decerebrate, which is associated with more severe injury and involvement of the brainstem. It is not normal and indicates worsening neurologic status.

Answer 123

A. Hyperextension of the legs C. Arms stiffly extended E. Plantar flexion of the feet F. Hyperpronation of the arms Rationale: Decerebrate posture involves rigid extension of the arms (C), hyperextension of the legs (A), plantar flexion of the feet (E), and hyperpronation of the arms (F). Internal rotation and flexion of the arms (B and D) describe decorticate posturing, not decerebrate.

Answer 124

B. Left cerebral hemisphere Rationale: Motor deficits are typically contralateral to the lesion. So, right-sided hemiplegia indicates a lesion in the left cerebral hemisphere. The cerebellum primarily controls coordination, and brainstem involvement would likely cause more global or bilateral deficits.

Answer 125

A. Withdrawal from the stimulus Rationale: Withdrawal to pain suggests higher-level motor control and some degree of cortical integrity. Decorticate and decerebrate posturing indicate progressively worse neurologic function, with decerebrate being more severe. No response is the most concerning.

Answer 126

B. Withdraws to pain Rationale: Pulling away from painful stimulus is a withdrawal response, indicating that the spinal cord and some cortical pathways are intact. Localization would involve purposeful movement toward the source of pain, not just pulling away.

Answer 127

D. Notify the provider immediately Rationale: Transition from decorticate to decerebrate posturing indicates neurological deterioration and brainstem involvement, which is life-threatening. Immediate notification is necessary to initiate urgent interventions.

Answer 128

D. Arm flexion in decorticate, arm extension in decerebrate Rationale: The key difference is in arm positioning: decorticate posture involves arm flexion, while decerebrate posture involves arm extension and pronation. Decerebrate posturing is a sign of more severe brain injury.

Answer 129

C. It may be a sign of increased intracranial pressure Rationale: Morning or nocturnal headaches that worsen with activities like coughing or straining are classic signs of increased ICP, potentially from a mass or obstructed CSF flow. The brain tissue doesn’t feel pain, but compression of surrounding structures (e.g., blood vessels or cranial nerves) can lead to this type of headache.

Answer 130

D. Notify the provider; findings suggest a possible increase in ICP Rationale: This headache presentation—worse in the morning, aggravated by Valsalva-like maneuvers (e.g., sneezing, bending)—is concerning for increased ICP, possibly from a mass or lesion. Early identification and neuroimaging are crucial to prevent further complications.

Answer 131

A. “My headache wakes me up at night and is worst when I first get out of bed.” Rationale: A headache that occurs at night or early morning is a red flag for increased ICP, especially when it disrupts sleep and worsens with postural changes. This may indicate a space-occupying lesion or other ICP-related pathology.

Answer 132

A. Coughing B. Straining during bowel movement C. Morning time D. Agitation or movement Rationale: Headaches associated with increased ICP are worsened by activities that raise intrathoracic pressure, like coughing (A) and straining (B). These increase cerebral venous pressure and ICP. Morning time (C) is often when ICP is highest due to recumbent positioning overnight. Agitation or movement (D) may also exacerbate symptoms. Quiet rest (E) may relieve, not worsen, the headache.

Answer 133

vomiting, not preceded by nausea

Answer 134

C. Projectile vomiting not preceded by nausea Rationale: Projectile vomiting without preceding nausea is a classic and nonspecific indicator of increased ICP. It occurs due to direct stimulation of the vomiting center in the brainstem from elevated pressure. This is a neurologic emergency, especially when paired with other signs like headache or altered LOC.

Answer 135

D. Notify the provider of possible increased ICP Rationale: Projectile vomiting without nausea, particularly in the setting of head trauma and headache, raises a strong concern for elevated intracranial pressure. This symptom must be reported immediately to allow for urgent evaluation (e.g., neuroimaging, ICP monitoring). Anti-nausea meds won’t treat the underlying cause.

Answer 136

A. Vomiting without warning or nausea B. Projectile vomiting Rationale: Unexpected (A) and projectile vomiting (B) are both hallmark, nonspecific indicators of increased ICP. These symptoms result from pressure on the vomiting center in the medulla and are not related to GI illness or food intake. Options C, D, and E are more suggestive of gastrointestinal or situational causes.

Answer 137

C. Increased ICP is likely stimulating the vomiting center Rationale: In patients with space-occupying lesions, such as tumors, the development of sudden vomiting without nausea is strongly linked to increased ICP, which affects the brainstem vomiting center directly. This symptom must not be dismissed or attributed solely to chemotherapy or GI causes.

Answer 138

A. “I woke up and threw up suddenly—no nausea at all before it.” Rationale: Vomiting without prior nausea—especially if sudden or projectile—is a neurologic red flag suggestive of increased intracranial pressure. This finding is especially important when evaluating for conditions like tumors, hydrocephalus, or hemorrhages.

Answer 139

D) Elevated serum ammonia Rationale: Elevated serum ammonia is a hallmark of hepatic encephalopathy and contributes to cerebral edema by increasing astrocyte swelling due to ammonia’s neurotoxic effects.

Answer 140

A) Vasogenic edema Rationale: Vasogenic edema, resulting from the breakdown of the blood-brain barrier, is commonly associated with TBI, leading to fluid accumulation in the extracellular space.

Answer 141

A) Cytotoxic edema Rationale: Lead poisoning can cause cytotoxic edema due to direct neuronal injury and disruption of cellular metabolism, leading to intracellular fluid accumulation.

Answer 142

B) Vasogenic edema Rationale: Infections like brain abscesses often lead to vasogenic edema due to increased permeability of the blood-brain barrier, allowing fluid to leak into the extracellular space.

Answer 143

C) Vasogenic edema from increased capillary permeability Rationale: HACE is primarily caused by vasogenic edema resulting from increased capillary permeability at high altitudes, leading to fluid leakage into the brain’s extracellular space.

Answer 144

A) Accumulation of neurotoxins like ammonia Rationale: In acute liver failure, the accumulation of neurotoxins, particularly ammonia, leads to astrocyte swelling and cerebral edema.

Answer 145

B) Vasogenic edema Rationale: Meningitis can disrupt the blood-brain barrier, leading to vasogenic edema characterized by fluid leakage into the extracellular space.

Answer 146

B) Cytotoxic edema Rationale: In the early stages of ischemic stroke, cytotoxic edema occurs due to energy failure and subsequent intracellular fluid accumulation.

Answer 147

D) Disruption of the blood-brain barrier Rationale: Subdural hematomas can disrupt the blood-brain barrier, leading to vasogenic edema from fluid leakage into the extracellular space.

Answer 148

A) Cytotoxic edema due to toxin accumulation Rationale: Uremia leads to the accumulation of toxins that can cause direct neuronal injury, resulting in cytotoxic edema.

Answer 149

B) Vasogenic edema Rationale: Cerebral venous sinus thrombosis can lead to increased venous pressure and disruption of the blood-brain barrier, resulting in vasogenic edema.

Answer 150

D. Cerebral herniation Rationale: Cerebral herniation is a life-threatening complication of uncontrolled ICP and represents a shift of brain tissue from its normal location. This can cause compression of vital structures, especially the brainstem, and often results in irreversible damage or death.

Answer 151

a tent-like cover over the cerebellum

Answer 152

C. Tentorium cerebelli Rationale: The tentorium cerebelli is a fold of dura mater that forms a tent-like separation between the cerebrum and cerebellum. It’s clinically important because it creates compartments within the skull, and herniation through this structure (e.g., uncal or central herniation) can compress the brainstem and be fatal.

Answer 153

D. Cerebral tissue is displaced downward through the foramen magnum Rationale: Central (tentorial) herniation involves downward movement of cerebral structures through the tentorial notch, compressing the brainstem. This is a critical emergency because the brainstem houses vital autonomic centers, including respiratory and cardiovascular regulation.

Answer 154

A. Cingulate herniation occurs under the falx cerebri C. Uncal herniation involves downward movement of the temporal lobe D. Central herniation is associated with compression of the brainstem E. Cerebral herniation can impair cerebral perfusion Rationale: * A: Cingulate herniation involves tissue shifting under the falx cerebri. * C: Uncal herniation occurs laterally and downward, pushing the medial temporal lobe. * D: Central herniation is also known as tentorial herniation and compresses the brainstem. * E: All forms of herniation compromise cerebral blood flow and lead to hypoxia or ischemia. B is incorrect—tentorial herniation compresses brainstem structures, not the cerebellum directly.

Answer 155

B. Lateral shift of cerebral tissue seen on imaging Rationale: Cingulate herniation occurs when brain tissue is pushed laterally under the falx cerebri. This can often be seen as a midline shift on CT or MRI and may initially present without profound clinical signs. As it progresses, neurological deterioration can occur.

Answer 156

A. Fixed and dilated pupil on the ipsilateral side Rationale: In uncal herniation, the medial temporal lobe compresses CN III, leading to ipsilateral pupil dilation that becomes fixed. This is a classic early sign and a neurologic emergency indicating brainstem involvement.

Answer 157

A. Respiratory arrest B. Bradycardia C. Brainstem compression E. Irreversible coma Rationale: Cerebral herniation can cause brainstem compression, leading to loss of autonomic function (A, B), and often progresses to irreversible coma or death (E). D is incorrect—spinal reflexes may diminish or be lost depending on the location of compression.

Answer 158

C. Falx cerebri Rationale: The falx cerebri is a vertical fold of dura mater between the right and left cerebral hemispheres. In cingulate herniation, brain tissue is pushed beneath this midline structure, which may disrupt perfusion and worsen ICP.

Answer 159

B. CN III (Oculomotor) Rationale: The oculomotor nerve (CN III) is often compressed during uncal herniation, leading to a fixed, dilated pupil on the same side of the lesion. This occurs as the medial temporal lobe presses downward on the brainstem, impinging CN III fibers.

Answer 160

D. The patient is restless, agitated, and confused Rationale: Early signs of impaired cerebral perfusion include subtle changes in behavior, restlessness, or altered mental status, as the brain becomes hypoxic. This is an early clue to decreased perfusion due to rising ICP and precedes more severe signs like herniation or coma.

Answer 161

C. Lumbar puncture Rationale: A lumbar puncture is contraindicated in patients with suspected increased ICP because it can cause a sudden release of pressure below the skull, increasing the risk of brain herniation through the foramen magnum—a fatal complication.

Answer 162

A. CT scan B. EEG C. Infrascanner E. Positron emission tomography (PET) Rationale: * CT scan (A): Standard imaging to evaluate structural causes of increased ICP. * EEG (B): Useful for evaluating cerebral function or detecting seizure activity. * Infrascanner (C): Handheld device to identify life-threatening intracranial bleeding. * PET scan (E): Detects metabolic changes in the brain and blood flow. D (serum sodium) is not a direct diagnostic tool for ICP, though important in management.

Answer 163

B. Infrascanner Rationale: The Infrascanner uses near-infrared light to detect intracranial bleeding by identifying areas where light absorption is altered by pooled blood from a hematoma.

Answer 164

A. Transcranial Doppler Rationale: Transcranial Doppler ultrasonography is used to monitor cerebral blood flow velocity and resistance, which is particularly useful in patients with traumatic brain injury or stroke.

Answer 165

D. LICOX catheter Rationale: The LICOX catheter directly measures brain tissue oxygenation (PbtO2) and temperature. It’s an invasive monitoring tool used in ICU settings for patients at risk for brain hypoxia due to increased ICP.

Answer 166

B. Infrascanner detection of abnormal light absorption C. MRI revealing mass effect and midline shift D. LICOX catheter revealing PbtO2 of 12 mm Hg E. Transcranial Doppler revealing reduced cerebral blood flow velocity Rationale: * B: Infrascanner detects light absorption changes from bleeding. * C: MRI can show midline shift and mass lesions, which are ICP indicators. * D: Low PbtO2 (<20 mm Hg) suggests inadequate brain oxygenation. * E: Decreased CBF velocity on Doppler = elevated ICP or poor perfusion. A (PET scan hypermetabolism in brainstem) is nonspecific and less useful here.

Answer 167

B. EEG Rationale: An electroencephalogram (EEG) records brain electrical activity and is useful for detecting seizure activity, especially in patients with altered consciousness or unexplained changes in neurologic status.

Answer 168

A. PET scan Rationale: A PET scan provides functional imaging, including glucose metabolism and blood flow, helping clinicians assess areas of hypometabolism or ischemia in patients with neurologic concerns.

Answer 169

C. Cerebral angiography Rationale: Cerebral angiography is the gold standard to visualize intracranial vessels, detect aneurysms, AV malformations, or assess vascular occlusion in stroke or trauma.

Answer 170

B. Transcranial Doppler is non-invasive C. Infrascanner is useful in pre-hospital or field triage E. LICOX catheter monitors oxygen and temperature in brain tissue Rationale: * B: Transcranial Doppler is non-invasive and monitors blood flow velocity. * C: The Infrascanner is portable and useful in field trauma settings. * E: LICOX catheter gives continuous oxygenation (PbtO2) and temperature readings. A is incorrect—LP is contraindicated with increased ICP. D is incorrect—PET shows function, not just anatomy.

Answer 171

B. Decreased cerebral blood flow velocity Rationale: Decreased velocity suggests increased cerebrovascular resistance, a hallmark of elevated ICP and impending perfusion impairment, requiring urgent intervention.

Answer 172

D. “A lumbar puncture is safe to perform to confirm elevated ICP.” Rationale: This is incorrect and dangerous. A lumbar puncture is contraindicated in patients with increased ICP due to the risk of cerebral herniation following a sudden drop in pressure below the skull.

Answer 173

D. Initiate intracranial pressure monitoring Rationale: ICP monitoring is indicated for patients with a GCS score ≤8 and abnormal CT/MRI findings (e.g., bleeding or edema). This combination suggests a high risk for increased ICP and the need for direct pressure monitoring to guide treatment.

Answer 174

A. A patient with a GCS score of 7 and an MRI showing a contusion C. A patient with bacterial meningitis and a fluctuating LOC E. A patient with a brain tumor and signs of increased ICP Rationale: * A: GCS ≤8 and contusion = classic indication. * C: Meningitis with LOC changes = risk for increased ICP; monitoring helps guide care. * E: Brain tumors can cause mass effect and increased ICP. B is stable and does not meet ICP monitoring criteria. D might be monitored depending on risk factors, but normal CT reduces the urgency.

Answer 175

C. To guide therapy and reduce risk of secondary brain injury Rationale: The main goal of ICP monitoring is to track pressure trends and guide treatment decisions, such as adjusting fluids, osmotic therapy, or sedation, to optimize cerebral perfusion and prevent secondary injury.

Answer 176

A. Prepare for intracranial pressure monitoring Rationale: This patient has both a low GCS and significant cerebral edema, meeting criteria for ICP monitoring. It helps detect and manage dangerous pressure elevations before irreversible brain damage occurs.

Answer 177

B. A patient with a mild concussion and GCS 15 Rationale: ICP monitoring is not indicated in patients with mild neurologic injuries (GCS >13) and no structural brain abnormalities. This patient is stable and does not show signs of increased ICP or deterioration.

Answer 178

B. “Patients with traumatic brain injury and cerebral contusions are high-risk.” C. “ICP monitoring is often needed if CT imaging shows cerebral edema.” E. “A sudden change in LOC can indicate the need for ICP monitoring.” Rationale: * B: TBI with contusion = high risk. * C: Cerebral edema on imaging is a red flag for ICP. * E: Sudden LOC changes suggest brain swelling or bleeding—triggers for monitoring. A is incorrect—a GCS ≤8, not 9+, is the usual cutoff. D is false—stroke patients, especially those with hemorrhagic stroke, often require monitoring.

Answer 179

a specialized catheter is inserted into the lateral ventricle and coupled to an external transducer

Answer 180

an air-filled pouch to measure ICP

Answer 181

C. Ventriculostomy Rationale: The ventriculostomy is the gold standard for ICP monitoring. It provides direct measurement of pressure and allows for CSF sampling and drug administration.

Answer 182

A. Leveling the transducer with the tragus of the ear Rationale: The transducer must be level with the foramen of Monro, which is referenced using the tragus of the ear. This ensures that the ICP measurement is accurate and consistent, regardless of the patient’s positioning.

Answer 183

A. Infection at the insertion site Rationale: Infection is a serious complication associated with ICP monitoring, especially with ventriculostomy, which can result in meningitis or other systemic infections. It is critical to monitor the insertion site and use aseptic technique.

Answer 184

A. CSF leaks around the monitoring device B. Kinks in the ICP tubing C. Incorrect height of the drainage system relative to the reference point Rationale: * A: CSF leaks compromise the pressure readings and the system’s integrity. * B: Kinks in the tubing block or distort the pressure waveforms. * C: The height of the drainage system must be correctly positioned to the reference point (foramen of Monro). D and E are not direct causes of inaccurate readings, though prone positioning may affect the positioning of the catheter or transducer. Fiberoptic catheters have their own characteristics but do not cause inaccurate readings due to positioning.

Answer 185

B. Report the abnormal waveform and monitor the patient for signs of deterioration Rationale: A P2 elevation above P1 indicates poor ventricular compliance, which suggests increased ICP. This requires immediate attention, and the nurse should report the abnormal waveform to the healthcare provider and carefully monitor the patient for signs of deterioration.

Answer 186

B. Closing the CSF drain for at least 6 minutes before taking a reading Rationale: To obtain accurate ICP readings, the CSF drain should be closed for at least 6 minutes to ensure that there is no influence from draining before taking the pressure reading.

Answer 187

B. It provides direct measurement of brain pressure without needing a transducer Rationale: The fiberoptic catheter uses a sensor transducer located at the catheter tip to directly measure brain pressure. Unlike the ventriculostomy, it does not require a separate external transducer.

Answer 188

A. Air bubbles in the tubing Rationale: Air bubbles in the ICP monitoring system can dampen the waveform, leading to false readings. It is crucial to check the system for air bubbles and remove them to ensure accurate readings.

Answer 189

A. 5-10 mm Hg Rationale: Normal ICP typically ranges between 5-10 mm Hg. Values above this range indicate increased ICP, which can lead to poor cerebral perfusion and other complications.

Answer 190

D. Report the findings to the healthcare provider and prepare for intervention Rationale: A sudden increase in ICP with an abnormal waveform requires immediate notification to the healthcare provider, as this indicates deteriorating neurological status and may require urgent intervention.

Answer 191

A. Meningitis B. CSF leak E. Catheter obstruction Rationale: * A: Infection (e.g., meningitis) is a common complication of ICP monitoring. * B: CSF leaks can lead to inaccurate readings or infections. * E: Catheter obstruction from clots or tissue can distort readings. C and D are not typical complications directly associated with ICP monitoring.

Answer 192

B. Use aseptic technique when handling the insertion site Rationale: The nurse should use aseptic technique to avoid introducing infection. Regular dressing changes and careful handling reduce the risk of meningitis or other complications. Flushing and antibiotics are not routine practices unless infection is suspected.

Answer 193

A. The CSF drainage device must be closed for at least 6 minutes before taking a reading Rationale: Closing the drainage device for at least 6 minutes ensures that the measurement reflects true ICP without the influence of draining CSF.

Answer 194

A. Fiberoptic catheter B. Ventriculostomy D. Pneumatic air pouch system

Answer 195

C. Use aseptic technique during the insertion and maintenance of the device Rationale: Using aseptic technique during both insertion and maintenance of the ICP device significantly reduces the risk of infection. Proper hand hygiene, sterile dressings, and avoiding unnecessary manipulation of the device are essential.

Answer 196

C. Notify the healthcare provider for further assessment and management Rationale: A CSF leak could result in inaccurate ICP readings and increased infection risk. It’s essential to notify the healthcare provider to evaluate the situation and determine whether the device needs to be adjusted or replaced.

Answer 197

C. Report the abnormal reading to the healthcare provider immediately Rationale: Abnormal ICP waveforms with P2 rising above P1 indicate that the patient is experiencing increased ICP and may be at risk for neurological deterioration. This requires immediate reporting to the healthcare provider for possible intervention.

Answer 198

D. Keep the insertion site covered with a sterile dressing and monitor for redness or drainage Rationale: To prevent infection, the insertion site should be covered with a sterile dressing. The nurse should monitor for signs of infection such as redness, drainage, or increased warmth around the site. Changing the dressing should occur every 24 hours, not every 72 hours, to ensure proper hygiene.

Answer 199

A. Open the drainage system and allow CSF to drain for 2 to 3 minutes, then close it Rationale: Intermittent drainage requires the nurse to open the system for 2 to 3 minutes to allow CSF to drain, then close the system to maintain the integrity of ICP monitoring. Continuous drainage would require monitoring the volume of CSF drained.

Answer 200

B. Monitor the volume of CSF drainage to avoid excessive removal Rationale: When using continuous CSF drainage, it is essential to monitor the volume of CSF removed to prevent over-drainage, which could lead to complications like ventricular collapse or herniation. Normal CSF production is around 20 to 30 mL/hr, so it is important to keep this in mind.

Answer 201

A. Cerebral herniation or subdural hematoma formation Rationale: Rapid decompression of ICP can cause cerebral herniation or subdural hematoma formation, both of which are serious complications. Proper monitoring and controlled drainage are critical to avoid these risks.

Answer 202

C. Ensure that the system is intact and leveled at the foramen of Monro Rationale: For accurate ICP readings, it is essential to level the system at the foramen of Monro (the reference point) and ensure the system remains intact to prevent errors in ICP measurements.

Answer 203

A. Close the stopcock immediately and monitor for any changes in ICP Rationale: The stopcock should be closed after intermittent drainage to maintain the integrity of the ICP monitoring system. The nurse should monitor the ICP for any changes to ensure proper pressure management.

Answer 204

B. Report the issue to the healthcare provider for assessment and possible intervention Rationale: CSF leakage around the insertion site should be reported immediately to the healthcare provider. This could indicate a problem with the catheter or the insertion site that may need adjustment or further intervention to prevent complications.

Answer 205

A. Ventricular collapse Rationale: Removing too much CSF can cause ventricular collapse, as the brain can lose the cushioning effect provided by the CSF. This can lead to further neurological complications and increased ICP if not corrected.

Answer 206

A. Ensure the drainage system is level with the tragus of the ear Rationale: The system must be leveled at the tragus of the ear (the reference point) to ensure accurate ICP readings when repositioning the patient. Proper positioning is essential to prevent changes in ICP measurements.

Answer 207

B. Use aseptic technique to prevent infection Rationale: Using aseptic technique during dressing changes is critical to prevent infection. Infection is a significant complication with ICP monitoring and should always be carefully avoided through proper technique.

Answer 208

B. Notify the healthcare provider for further instructions and assessment Rationale: The nurse should notify the healthcare provider immediately when there is excessive CSF drainage. This could indicate a problem with the system or a need for a change in treatment, such as stopping or adjusting drainage.

Answer 209

C. Maintain a controlled and safe amount of CSF drainage Rationale: To avoid ventricular collapse, it is crucial to maintain controlled and safe amounts of CSF drainage. The nurse should monitor and adjust the drainage system as needed to prevent excessive CSF loss, which can lead to complications.

Answer 210

B. Perform routine sterile dressing changes to prevent infection Rationale: Routine sterile dressing changes are essential to prevent infection at the insertion site of the ventriculostomy. Keeping the system intact and sterile is critical