UBP 2.5 (Long Form): Neuro – Cerebral Aneurysm Flashcards

Secondary Subject -- Elevated ICP/Known Difficult Airway/Hunt & Hess Classification/Deliberate Hypotension/ Brain Protection/ST-Depression/Ruptured Aneurysm/Extubation Criteria/Ventilator Management/Cerebral Vasospasm/ Neurogenic Pulmonary Edema/SIADH & Cerebral Salt Wasting Syndrome

1
Q

Intra-operative Management:

How would you induce anesthesia in this patient?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

Pair down your answer… e.g. “I would be concerned about… Therefore, I would….”

Given this patient’s cerebral aneurysm, CAD, chronic hypertension, and known difficult airway, my goals for induction would be – to safely secure the airway while, at the same time, maintaining cerebral and cardiac perfusion, and avoiding increases in transmural pressure (mean arterial pressure minus intracranial pressure) that might result in rupture of the aneurysm.

Therefore, I would get difficult airway equipment in the room, optimize the patient’s volume status, ensure adequate beta blocker, provide minimal sedation, anesthetize the airway with blocks and topical anesthetic, administer intravenous lidocaine (being aware of toxicity limits) – provide adequate analgesia to prevent sympathetic response – , and perform an awake fiberoptic intubation.

Following placement of an endotracheal tube, I would perform a slow controlled induction with fentanyl and propofol (similar to thiopental in it’s effects on cerebral blood flow and cerebral metabolic rate), administer a non-depolarizing muscle relaxant, and ensure a deep plane of anesthesia prior to insertion of the head pins to avoid a hypertensive response.

Pair down your answer… e.g. “I would be concerned about… Therefore, I would….”

**Place pre-induction arterial line.**

Extra Q: What is transmural pressure? – see above. If you have rapid lowering of ICP or increase in MAP from strong sympathetic response, you risk rupture of aneurysm.

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2
Q

Intra-operative Management:

The surgeon asks you to lower the blood pressure prior to clipping.

Do you agree with this management decision?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

Deliberate hypotension may help to reduce transmural pressure and reduce the risk of aneurysm rupture during placement of the clip.

However, it also results in global decreases in cerebral perfusion pressure, which may further contribute to ischemia in areas where brain retraction leads to local vasospasm.

This concern is supported by evidence suggesting that even limited periods of controlled hypotension results in worsened outcomes (poorer degree of recovery) and increased incidence and severity of vasospasm.

Moreover, given this patient’s chronic hypertension and coronary artery disease, deliberate hypotension may place the patient at unacceptable risk of cardiac ischemia.

Therefore, I would discuss the possibility of temporary clipping of supplying arteries to reduce transmural pressure in lieu of deliberate hypotension.

If the surgeon insisted that deliberate hypotension was necessary, I would only agree to minimal decreases in blood pressure with careful monitoring for signs of end-organ ischemia.

Extra Question – The surgeon says he NEEDS deliberate hypotension… temporary clipping of supplying/feeding arteries is not adequate to proceed with surgery. What would you say? – See last sentence above.

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3
Q

Intra-operative Management:

How low will you allow the blood pressure to go?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

Due to his coronary artery disease, I would only allow the MAP to decrease about 10-20 mmHg,

while carefully monitoring for signs of cerebral and/or cardiac ischemia as indicated by – jugular bulb oximetry, regional cerebral oximetry, EEG, transcranial Doppler, EKG, or TEE.

Additionally, I would avoid conditions that may contribute to cerebral and/or cardiac ischemia, such as – hyperthermia, hyperglycemia, anemia, and hypoxemia.

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4
Q

Intra-operative Management:

The surgeon decides to go ahead and place a temporary clip on the anterior cerebral artery.

Does this alter your management?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

Yes,

placing a temporary clip on a feeding vessel results in decreased focal blood flow through the aneurysm, obviating the need for deliberate hypotension.

During temporary occlusion, the mean arterial pressure should be maintained at higher than normal pressures to support collateral flow of blood.

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5
Q

Intra-operative Management:

Is there anything you could do to provide protection while the temporary clip was in place?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

The administration of thiopental, etomidate, or propofol, can be neuroprotective in the setting of focal ischemia secondary to reductions in CMRO2.

Other strategies to prevent cerebral ischemia include –

  • maintaining a higher than normal mean arterial pressure,
  • minimizing occlusion time,
  • utilizing neurophysiologic monitoring (i.e. EEG and SSEPs),
  • ensuring brain relaxation
    • (i.e. CSF drainage,
    • mannitol administration,
    • induced hypocapnia) to facilitate surgery and reduce required retractor pressure,
  • allowing mild hypothermia (32-34 °C), and
  • administering a barbiturate.
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6
Q

Intra-operative Management:

What about hypothermia? Why/why not?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

While the benefits are unproven, mild hypothermia (32-34 °C) may provide some brain protection from ischemia due to a reduction of oxygen consumption by 5-7% for every one °C decrease in body temperature.

While CMRO2 reduction may be as much as 50% with lower temperatures (about 27 °C), deep hypothermia is not practical for most neurosurgical interventions due to its association with delayed emergence.

Delayed emergence occurs, because anesthesia must be maintained until the patient is adequately warmed to prevent the potentially dangerous hypertensive response that often occurs when a patient is awakened while still hypothermic.

Additionally, post-operative hypothermia can result in –

slow metabolism of anesthetics and muscle relaxants, an increased rate of infection, increased oxygen consumption with shivering, myocardial ischemia, arrhythmias, and coagulation defects.

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7
Q

Intra-operative Management:

You notice ST changes on the EKG.

What do you think?

What would you do?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

EKG changes, including ST-segment depression, often occur in the presence of subarachnoid hemorrhage and have not been shown to increase morbidity or mortality.

These changes are concerning, however, because they suggest that a previously unruptured aneurysm is now bleeding or, given this patient’s cardiac history, the patient is experiencing myocardial ischemia.

In response, I would look at the surgical field and ask the surgeon about potential rupture; continue to observe the EKG, arterial line, pulse-oximeter, and CVP monitor; ensure adequate ventilation with 100% oxygen; assess hemodynamic status; and order a troponin-I level.

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8
Q

Intra-operative Management:

The surgeon confirms that the aneurysm has ruptured. What would you do? Would you raise or lower the BP?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

If possible, the surgeon should apply permanent or temporary clips to control bleeding.

If the bleeding were NOT excessive, I would:

  1. correct any conditions that may contribute to cerebral ischemia, such as hyperthermia, hyperglycemia, and hypoxemia;
  2. induce mild hypotension with sodium nitroprusside, to facilitate surgical repair; and
  3. consider administering cerebroprotective agents (i.e. volatile agents and/or a barbiturate), understanding that these actions may increase risk of end-organ ischemia (some practitioners would avoid deliberate hypotension even in these circumstances).

If massive hemorrhage were occurring, I would:

  1. compress the carotid arteries;
  2. suggest temporary clipping of the vessels proximal and distal to the aneurysm; and
  3. prepare for aggressive resuscitation with fluids and blood products.

I would avoid deliberate hypotension and cerebroprotective agents that would not likely be tolerated.

  • (per UBP online course, Some authors say that deliberate hypotension is not appropriate independent of CAD.)

And, if the surgeon were unable to control bleeding despite these measures, I would talk to the surgeon about the benefits of cardiopulmonary bypass or cardiac circulatory arrest.

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9
Q

Intra-operative Management:

The surgeon places a clip on the anterior cerebral artery to get control of the bleeding and the posterior tibial-to-vertex SSEPs disappear.

Is this concerning?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

Yes,

the loss of SSEPs may be indicative of focal ischemia secondary to placement of the clip.

As long as the bleeding was controlled, I would correct any hypoxemia, hypotension, hypovolemia, anemia, and hypo/hypercarbia in order to optimize oxygen delivery;

make sure that the depth of anesthesia had remained stable and was not interfering with the evoked potential readings; and

consider increasing the patient’s MAP in order to improve collateral circulation to the surrounding brain.

If these measures proved ineffective, I would provide a volatile agent, propofol, or a barbiturate to provide some ischemic brain protection.

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10
Q

Post-operative Management:

Are you going to extubate this patient at the end of this case? What are your extubation criteria?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

While this patient’s initial Hunt and Hess classification was low, his cerebral aneurysm ruptured intraoperatively, making it probable that he will remain obtunded with increased ICP and cerebral edema.

Additionally, mechanical ventilation may be required to manage elevated ICP, postoperatively.

If, however, his aneurysm had not ruptured, cerebral injury from surgical dissection had been minimal, and he met extubation criteria, it would have been reasonable to attempt extubation.

My extubation criteria would have included:

  • an awake patient with intact airway reflexes,
  • adequate muscle relaxant reversal to demonstrate appropriate tidal volumes,
  • adequate oxygenation,
  • normocarbia, and
  • stable hemodynamics.
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11
Q

Post-operative Management:

The patient does not meet your extubation criteria and requires post-op ventilation in the ICU.

What mode of ventilation would you use?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

(Note – this was answered well in post-op discussion in UBP online course.)

Assuming pulmonary compliance were normal, I would start with synchronized intermittent mandatory ventilation (SIMV).

Like intermittent mandatory ventilation (IMV), SIMV allows spontaneous respirations while requiring a preset number of mandatory breaths per minute.

SIMV, however, is designed to time delivery of a mechanical breath with the beginning of a spontaneous effort.

This synchronization prevents “stacking”, in which a mechanical breath is delivered in the middle of a spontaneous breath, which can result in the delivery of larger than desired tidal volumes.

This mode of ventilation is more comfortable for the patient and provides a guaranteed baseline of ventilation during the weaning process, when the patient’s ability to ventilate adequately is in question.

If pulmonary compliance is impaired due to pulmonary edema or intrinsic disease, a pressure-controlled mode of ventilation may be more appropriate.

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12
Q

Post-operative Management:

On post-op day #2, the patient has become minimally responsive to painful stimuli.

The nurse says that he was responsive to verbal stimuli just a few hours ago.

Are you concerned?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

I am concerned,

because a sudden change in mental status could indicate a rapidly progressing problem such as –

vasospasm, hematoma formation, hydrocephalus, seizure, or increasing cerebral edema.

Therefore, I would evaluate the patient, ensure a secure airway and adequate ventilation, optimize the patient’s hemodynamics, ensure adquate pain control, obtain an urgent neurology consult, and consider imaging to aid in diagnosis.

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13
Q

Post-operative Management:

On POD #2, the patient has become minimally responsive to painful stimuli. The nurse says that he was responsive to verbal stimuli just a few hours ago.

What do you think is going on?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

My primary concern is postoperative vasospasm,

which is the number one cause of morbidity and mortality associated with cerebral aneurysms.

Increased ICP, hematoma formation, pneumocephalus, hydrocephalus, seizure, or metabolic derangements are also possible causes of his changing mental status.

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14
Q

Post-operative Management:

On POD #2, pt becomes minimally responsive to painful stimuli when he was responsive to verbal stimuli just a few hours ago.

How can you determine if this is cerebral vasospasm? Is transcranial Doppler indicated? Angiography? Which would you order?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

Given my concern that this may be cerebral vasospasm, I would utilize angiography or a transcranial Doppler to determine if cerebral vasospasm were occurring.

Angiography would have the advantage of being more specific and showing the extent and severity of vasospasm.

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15
Q

Post-operative Management:

Cerebral angiogram reveals diffuse vasospasm.

How will you treat this patient?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

First, I would secure the airway.

Next, I would begin “triple H” therapy – hypervolemia, hypertension, and hemodilution.

The goal is to improve delivery of blood to ischemic areas with impaired autoregulation by increasing perfusion pressure and decreasing viscosity.

Unfortunately, this treatment may result in worsening cerebral edema, increasing ICP, pulmonary edema, and hemorrhage.

(Extra Question – What if the vasospasm persevered and was refractory to “triple H” therapy?)

If the patient proved refractory to “triple-H” therapy, I would discuss with the surgeon the efficacy of using transluminal angioplasty to dilate major constricted cerebral vessels.

Additionally, I would consider the use of intra-arterial infusion of verapamil to dilate distal vessels too small for angioplasty.

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16
Q

Post-operative Management:

During triple H therapy, the patient develops progressive and significant hypoxia.

What do you think is the cause?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

Given the volume loading that occurs with “triple-H” therapy, this progressive hypoxia is most likely due to pulmonary edema following overzealous fluid administration.

However, I would also consider –

neurogenic pulmonary edema, myocardial infarction, arrhythmia, congestive heart failure, right mainstem intubation, pneumothorax, atelectasis, pulmonary embolism, pneumonia, ventilator associated barotrauma, or acute respiratory distress syndrome (ARDS).

17
Q

Post-operative Management:

What is neurogenic pulmonary edema?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

Neurogenic pulmonary edema may occur after any form of injury to the central nervous system, usually developing within minutes to hours following CNS injury.

The mechanism is NOT well understood, but both hemodynamic (cardiogenic) and nonhemodynamic (noncardiogenic) components contribute to edema formation.

A massive sympathetic surge generated by the injured CNS results in generalized vasoconstriction and a redistribution of blood volume to the pulmonary circulation.

It remains uncertain whether the subsequent capillary leak is produced by pressure-induced mechanical injury from elevated capillary hydrostatic pressure, or because of some direct nervous system control of pulmonary capillary permeability.

18
Q

Post-operative Management:

Assuming this were neurogenic pulmonary edema, what would you do to treat this condition?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

Treatment is primarily aimed at addressing the underlying neurological condition.

For mild cases, in which gas exchange is minimally impaired, I may just increase the patient’s Fio2.

However, in a case such as this one, where the patient is developing significant hypoxemia, I would:

  1. treat the underlying cause of CNS injury;
  2. attempt to reduce intracranial pressure;
  3. mechanically ventilate with tidal volumes between 5-6 mL/kg (lower volumes would be utilized to prevent iatrogenic injury);
  4. provide PEEP to prevent atelectasis and improve gas exchange, being careful to avoid excessively high intrathoracic pressures that could lead to decreased cerebral venous return, increased ICP, and decreased cerebral perfusion;
  5. consider administering diuretics to reduce capillary hydrostatic pressure and increase colloid osmotic pressure (it is likely that hypervolemia is contributing to his condition, given the recent treatment of vasospasm);
  6. provide optimal oxygen delivery by ensuring adequate hemoglobin ( > 10 g/dL) and cardiac output, and carefully monitoring intravascular volume; and
  7. consider pharmacologic intervention with alpha-adrenergic antagonists (i.e. phentolamine), beta-adrenergic agonists (i.e. dobutamine), or dopamine, being very cautious to avoid significant hypotension that may compromise cerebral perfusion.
19
Q

Post-operative Management:

On post-op day #3, the serum sodium is 125 mEq/L.

What is your differential?

  • (A 54-year-old, 73 kg man presents to the operating room for clipping of an anterior communicating artery aneurysm.*
  • PMHx: The patient has been complaining of severe headaches for the last 2 days and family members report an episode of impaired cognition. There are no apparent neurological deficits at this time. His history is also significant for chronic hypertension for 15 years and coronary artery disease with a myocardial infarction 2 years ago.*
  • PSHx: The patient was told he was difficult to intubate during a laparoscopic procedure 5 years ago.*
  • Meds: Nimodipine, enalapril, and furosemide*
  • Allergies: PCN*
  • PE: Vital Signs: P = 92, BP = 140/90 mmHg, RR = 16, T = 36°C*
  • General: Awake, alert, oriented, but apprehensive*
  • Airway: Mallampati Class II, micrognathia, poor dentition, limited mouth opening, full range of motion*
  • Neurologic: exam unremarkable*
  • EKG: LVH, non-specific ST changes*
  • Labs: Hgb 12.2 gm/dL, Na 145 mEq/L, K 3.1 mEq/L, creatinine 1.1 mg/dL*
  • MRA: large anterior communicating artery aneurysm, no evidence of intracranial blood)*
A

With the volume loading that occurs during “triple-H” therapy, this is most likely – dilutional hyponatremia.

However, hyponatremia would also be consistent with – cerebral salt wasting syndrome (CSWS) and the syndrome of inappropriate antidiuretic hormone (SIADH), both of which are often associated with brain injury, including cerebral aneurysm.

The two disorders may be differentiated by the volume status of the patient, since CSWS is usually associated with hypovolemia, while patients with SIADH are usually euvolemic.

In addition, patients with SIADH exhibit elevated ADH levels and rarely develop urine sodium levels > 100 mEq/L, while patients with CSWS usually have normal ADH levels and often develop urine sodium levels > 100 mEq/L.

The distinction is important because the water restriction and diuresis often employed to treat SIADH would serve to exacerbate the hypovolemia associated with CSWS and, in this patient, contribute to vasospasm.

The treatment for CSWS, on the other hand, would entail fluid and sodium replacement.

Extra Q: How can you tell the difference between CSW and SIADH?