UBP 3.6 (Long Form): Cardiovascular – Thoracic Aortic Disection Flashcards

Secondary Subject -- DeBakey Classification / Aortic Regurgitation / Perioperative b-blockade / Lumbar Drain / Evoked Potential Monitoring / Invasive Monitoring / COPD / Neuraxial Anesthesia in the Coagulopathic Patient / Hypothermia / Blood Conservation Strategies / Post-operative Ventilator Management / Post-operative Coagulopathy / Thromboelastography

1
Q

Intra-operative Management:

What monitors would you place for this case?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV*<em>1</em> / FVC = 65%
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

In addition to the standard ASA monitors, I would require:

  1. a 5-lead EKG with ST-segment analysis to monitor for cardiac ischemia (aortic repair is associated with a high incidence of intraoperative myocardial ischemia and arrhythmias);
  2. both upper and lower extremity arterial lines to facilitate arterial blood gas sampling and rapid treatment of hemodynamic instability (secondary to hypertension, blood loss, and aortic cross-clamping);
  3. a large bore central line to provide access for the safe central administration of vasoactive drugs, the rapid transfusion of fluid and blood products, and the insertion of a pulmonary artery catheter and/or a transvenous pacemaker;
  4. a pulmonary artery catheter to assess fluid status and cardiac function;
  5. TEE to help confirm the extent and severity of his aortic disease, monitor real-time cardiac function, and identify ischemia (TEE is the most sensitive modality for detecting myocardial ischemia – ischemia-induced wall motion abnormalities on TEE appear earlier than either ST-segment or PAC waveform changes);
  6. core and peripheral temperature monitors;
  7. somatosensory and motor evoked potential monitoring to detect spinal cord ischemia, and
  8. a Foley catheter to assess urine output and, indirectly, fluid status and renal perfusion.

Clinical Notes:

  • Central Venous Pressure Monitoring:
    • In the setting of normal right ventricular function, the central venous pressure may give an indirect estimation of right ventricular end-diastolic volume and right ventricular preload. This information may then be used to guide fluid replacement and, where ventricular compliance is normal, to allow estimation of left heart pressures.
    • Isolated CVP measurements are difficult to interpret and should be assessed rather as a trend analysis, keeping in mind the patient’s hemodynamic variables and overall condition.
    • The CVP is informative only when the pressure is very low or very high because of the relatively increased compliance of the right side of the heart as compared to the left.
  • Temperature Monitoring:
    • Core Temperature – can be monitored via the bladder, nasopharynx, tympanic membrane, pulmonary artery, or distal esophagus.
    • Peripheral Temperature – can be monitored via the axilla or the rectum.
  • MEPs / SSEPs:
    • Neurologic injury is associated with a loss of signal lasting 15-30 minutes.
    • MEPs may be used to identify critical intercostal arteries supplying the cord, and then confirm successful reimplantation of those same arteries (SSEPs are not adequate for this purpose because the response to ischemia is too slow).
    • SSEPs are ablated with conduction blockade (i.e. epidural or spinal anesthesia).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Intra-operative Management:

Does it matter where you place the arterial line?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

Given the potential for hypertension above the aortic clamp and inadequate perfusion below the aortic clamp, I would place proximal and distal arterial lines to allow for rapid identification and treatment of any hemodynamic instability.

Since clamping of the left subclavian artery may become necessary during the procedure (the clamp is often placed proximal to the left subclavian artery for surgery involving the proximal descending aorta), I would place the upper extremity arterial line in the right arm to avoid surgical interference.

During aortic cross-clamping, the proximal arterial line would provide more accurate information concerning cerebral and cardiac perfusion pressures as well as cardiac afterload, while the lower extremity arterial line would allow close monitoring of distal perfusion pressure to the kidneys, spinal cord, and mesenteric circulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Intra-operative Management:

Is a pulmonary artery catheter (PAC) necessary?

How would it change your management?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

I would place a PAC in this patient.

It would help in fluid management, assessment of the cardiac function, and timely identification of cardiac ischemia during the case and throughout the postoperative period.

Intra-operatively, I would use the PAC in conjunction with TEE to better identify and manage cardiac ischemia, fluid status, and valvular disease.

However, TEE is not usually continued in the postoperative period, and the PAC could be left in place to guide management during this period of considerable cardiac risk (i.e. myocardial ischemia and cardiac failure).

Clinical Note:

  • PAC signs of myocardial ischemia include:
    • Prominent A-waves – result when the atrium contracts into a stiff left ventricle
    • Prominent V-waves – result when ischemic effects on the papillary muscles, chordae tendinae, and/or myocardium cause functional mitral regurgitation
  • Increased pulmonary artery occlusion pressure and increased pulmonary artery diastolic pressure – secondary to ischemia-induced increases in LVEDP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Intra-operative Management:

How would you induce and secure the airway of this patient?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

When inducing this patient I would:

  1. ensure appropriate intravenous access and monitoring (including invasive monitoring);
  2. make sure difficult airway equipment is available
    • (GERD, double-lumen tube placement, potential aneurysmal airway compression, potential diabetic stiff-joint syndrome);
  3. administer a bronchodilator to optimize his COPD;
  4. ensure adequate B-blockade to reduce the risk of myocardial ischemia and/or aortic rupture/propagation;
  5. provide aspiration prophylaxis (GERD and diabetes);
  6. obtain a baseline set of vital signs, PA catheter data, and evoked potential signals;
  7. preoxygenate the patient to reduce the risk of hypoxia (coronary artery disease);
  8. apply cricoid pressure; and
  9. perform a carefully titrated, high-narcotic intravenous induction with the goals of avoiding hemodynamic instability, tachycardia, and bradycardia (the latter would exacerbate his aortic valve insufficiency).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Intra-operative Management:

How would you maintain anesthesia following induction?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

Assuming the surgeon desired to employ SSEP and MEP monitoring, I would provide a total intravenous anesthetic in order to avoid anesthetic-induced signal depression.

My primary goal during maintenance of anesthesia is to maintain adequate end-organ perfusion, particularly during aortic cross-clamp placement.

To this end, I would:

  1. maintain his heart rate between 60-80 beats per minute,
  2. maintain his cardiac index between 2-2.5 L/minute/m2;
  3. provide a stable anesthetic to facilitate the accurate interpretation of evoked potential monitoring;
  4. carefully titrate a short-acting neuromuscular blocker to maintain electrical muscle amplitude at approximately 50% of baseline;
  5. maintain a systolic blood pressure between 105-115 mmHg, a mean arterial pressure around 100 mmHg above the cross-clamp, and a mean arterial pressure above 50 mmHg distal to the cross-clamp; and
  6. have various short-acting vasoactive agents available to maintain hemodynamic stability, especially during cross-clamp application and removal (i.e. nitroglycerine, nicardipine, esmolol, and nitroprusside).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Intra-operative Management:

Immediately after placement of the aortic cross clamp, the SSEP signal shows decreased amplitude and increased latency.

What would you do?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

Assuming a stable anesthetic, the institution of partial bypass, and a significant change int he SSEP signal (50% decrease in amplitude and/or 10% increase in latency), I would:

  1. optimize the patient’s hemodynamics (i.e. adequate MAP),
  2. check an ABG, and
  3. ask the perfusionist to both increase pump flows distal to the aortic clamp and correct any metabolic disturbances (i.e. hypo/hypercarbia and acidosis).
  4. If this were unsuccessful, I would – ask the surgeon to release or reposition the aortic clamp
    • (repositioning may be effective if it resulted in renewed flow through a critical intercostal artery),
  5. ensure adequate hypothermia at 30-34 ºC (Class IIa recommendation),
  6. withdraw 10-20 cc of CSF from the lumbar drain to achieve a target ICP of 8-10 mmHg (Class I recommendation for patients at significant risk for neurologic injury during thoracic aneurysm repair), and
  7. consider pharmacological intervention.

Various drugs that potentially reduce the incidence of spinal cord ischemia include – corticosteroids (i.e. methylprednisolone or dexamethasone), naloxone, dextrorphan, magnesium, intrathecal papaverine, and calcium channel blockers.

Clinical Notes:

  • A 50% decrease in amplitude of the MEP signal is considered clinically significant (some sources suggest that a “significant” decrease in MEP amplitude requires a 75-80% change).
  • Hypothermia
    • Reduces oxygen requirements by 5-7% for each ºC decrease in temperature
    • In the setting of aortic arch or ascending aorta surgery, deep hypothermic cardiac arrest is required (15ºC)
    • Both systemic and regional cooling are beneficial
      • Systemic hypothermia – achieved with full CPB or partial bypass (active cooling) or by allowing the patient to cool passively to 30-34 ºC
      • Regional cooling – achieved with the epidural infusion of 4 ºC saline
  • CSF Drainage
    • Spinal cord perfusion = distal mean aortic pressure - CSF pressure or the central venous pressure (whichever is greatest)
    • CSF drainage is important because CSF pressure may increased by 10-15 mmHg with cross-clamping of the descending aorta.
    • Low CSF pressures should be maintained postoperatively, raising the pressure back to 10-12 after 48 hours, and then to 12-15 when there is confirmation of preserved motor function.
    • Complications associated with CSF drainage include:
      • Headache
      • Spinal/epidural hematoma
      • Intracranial bleeding secondary to tearing of cerebral bridging vessels
      • Meningitis
      • Persistent CSF leak
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Intra-operative Management:

You have the perfusionist increase flows to the lower extremities and the SSEP signal improves.

Describe the blood supply to the spinal cord.

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

Two posterior spinal arteries supply the posterior 1/3rd of the spinal cord (sensory).

A single anterior spinal artery arising from the basilar and vertebral arteries supplies the anterior 2/3rd of the spinal cord (motor function), receiving contributions from 6-8 transverse radicular arteries (originating from the aorta at variable locations), the most important being the artery of Adamkiewicz.

Autoregulation of spinal cord blood flow is relatively constant between 50-125 mmHg, but may be ablated in the setting of hypoxia or hypercarbia.

The artery of Adamkiewicz serves as the major supply to the anterior, lower 2/3rd of the spinal cord.

It is usually located on the left side, originating anywhere from L5-T5 (T9-T12 60% of the time).

This variation in the origin of the Artery of Adamkiewicz may explain why paraplegia may even occur with infrarenal aortic aneurysm repair.

When the aortic cross-clamp is applied distal to this radicular artery, the risk of spinal cord ischemia is extremely low.

While distal aortic perfusion (i.e. left-heart-bypass) helps maintain spinal cord perfusion below the artery of Adamkiewicz during aortic cross-clamping, it does little to maintain perfusion above this radicular artery (above the artery, but still below the aortic clamp), because resistance to flow moving up the anterior spinal artery (proximal to the artery of Adamkiewicz) is 51 times greater than that going down the anterior spinal artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Intra-operative Management:

The surgeon asks you to start rewarming the patient prior to releasing the aortic cross-clamp.

Would you utilize forced-air warming?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

I would suggest that actively warming the patient via the left heart bypass circuit would be more effective.

However, if forced air warming were utilized in conjunction with the bypass circuit (which contains a heat exchanger), I would ensure it was only applied to the patient’s upper body.

Forced air warming of the lower body is contraindicated because warming ischemic tissue increases metabolic requirements, acidosis, and ischemic injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Intra-operative Management:

Later in the surgery, the surgeon releases the cross-clamp and the patient’s blood pressure drops to 68/44 mmHg.

Why do you think this occurred?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

The timing of his hypotension suggests that his hypotension is most likely the result of cross-clamp release.

The primary cause of hypotension following cross-clamp release is – central hypovolemia and the resulting decrease in cardiac preload.

The application of the cross-clamp to the aorta leads to distal tissue ischemia and vasoactive mediator release, with a subsequent drop in systemic vascular resistance, increased venous capacitance distal to the clamp, and increased capillary permeability (the latter develops by the end of the cross-clamp period).

The increased venous capacitance leads to a distal shift of blood volume, while the increased capillary permeability results in a loss of intravascular fluid, both of which contribute to central hypovolemia.

Moreover, central hypovolemia is further exacerbated by blood loss during the procedure.

With removal of the cross-clamp, acid metabolites and vasoactive mediators are released from tissues distal to the clamp, leading to –

  • decreased myocardial contractility
    • (which is further compromised secondary to the reduced preload associated with central hypovolemia),
  • increased pulmonary vascular resistance
    • (secondary to the released acid metabolites and vasoactive mediators), and
  • increased capillary permeability
    • (which further contributes to central hypovolemia).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Intra-operative Management:

Later in the surgery, the surgeon releases the cross-clamp and the patient’s blood pressure drops to 68/44 mmHg.

What would you do?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

I would:

  1. start a fluid bolus,
  2. place the patient in the trendelenburg position,
  3. administer a vasopressor, and
  4. attempt to identify any other potential causes or contributing factors to hypotension, such as –
    • hemorrhage (low filling pressures, surgical and/or anesthesiologist observation),
    • arrhythmia,
    • anesthetic-induced cardiovascular depression,
    • myocardial ischemia (wall-motion abnormalities, EKG changes, elevated filling pressures),
    • tension pneumothorax,
    • metabolic and electrolyte abnormalities,
    • citrate-induced hypocalcemia, and
    • hypothermia.
  5. If the hypotension persisted, I would – ask the surgeon to reapply the aortic cross-clamp,
  6. correct any abnormalities (i.e. anemia, arrhythmia, myocardial ischemia, tension pneumothorax, and metabolic abnormalities),
  7. decrease the depth of anesthesia (particularly volatile agents), and
  8. volume load the patient (vasodilators such as nitroprusside and/or nitroglycerin may facilitate volume loading, but these should be discontinued before unclamping).
  9. I would then – ask the surgeon to gradually release the cross-clamp to prevent further hypotension by allowing time for physiologic compensation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Intra-operative Management:

Would you extubate this patient in the operating room?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

I would not attempt to extubate the patient in the operating room because of –

  • his significant pulmonary disease (FEV1 = 78% predicted; FEV1 / FVC = 65%),
  • the deleterious effects of this type of surgery on pulmonary function (one-lung ventilation, surgical manipulation of the diaphragm and the lungs, and phrenic nerve and recurrent laryngeal nerve injury), and
  • the potential for airway and pulmonary edema following thoracic aortic repair (secondary to significant fluid administration and the increased capillary permeability associated with aortic cross-clamping).

Rather, I would:

  1. transport the patient to the ICU;
  2. allow sufficient time for hemodynamic stabilization;
  3. ensure complete reversal of neuromuscular blockade;
  4. confirm adequate respiratory function
    • (i.e. vital capacity >/= 10 mL/kg,
    • tidal volume > 6 mL/kg,
    • negative inspiratory force > 20 cm H20,
    • PaO2 > 60 with Fio2 < 50%,
    • PaCO2 < 50 mmHg, and
    • respiratory rate < 30 breaths/minute);
  5. verify normothermia and adequate pain control;
  6. perform a “cuff leak test” (auscultate for breath sounds with the cuff deflated and the patient breathing spontaneously); and
  7. extubate the patient when he was awake and cooperative with an intact gag reflex.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Post-operative Management:

If the patient required post-op ventilation, which mode of ventilation would you recommend?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

Assuming the patient’s lung compliance was normal, I would place the patient on synchronized intermittent mandatory ventilation.

This would provide adequate ventilatory support while allowing the patient to assist in the work of breathing and exercise respiratory muscles until weaned from the ventilator.

Given the history of aortic regurgitation, the recent administration of large amounts of fluids and blood products, the use of one-lung ventilation, and possible surgical trauma (i.e. surgical manipulation of the diaphragm and the lungs; phrenic nerve and recurrent laryngeal nerve injury, surgically-induced tracheobronchial bleeding),

he may have reduced pulmonary compliance secondary to pulmonary edema and/or atelectasis.

In this case, I would consider a pressure control mode of ventilation to maximize oxygenation and avoid ventilator associated lung injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Post-operative Management:

Postoperatively, the patient continues to have excessive bleeding and the surgeon suggests giving more protamine.

Would you agree?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

While additional protamine may be the appropriate treatment, I would first assess the patient for other potential causes of post-operative bleeding, such as –

  • hypothermia,
  • thrombocytopenia,
  • thrombocytopathia, and
  • depletion of coagulation factors.

My assessment would include – ordering a PTT, PT, INR, platelets, fibrinogen level, a thromboelastogram (TEG), and an ACT or heparin-protamine titration assay.

If either the ACT or heparin-protamine titration assay indicated residual heparin effects, I would consider administering additional protamine, recognizing that excessive protamine could lead to paradoxical bleeding.

If bleeding continued despite these interventions, surgical exploration may be required to check anastomotic sites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Post-operative Management:

How does hypothermia result in a coagulopathy?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

Mild hypothermia (33-37 ºC) can induce a coagulopathy secondary to – cold-induced defects in platelet aggregation and adhesion.

Coagulation enzyme activity, however, is only minimally affected within this range of temperatures.

Therefore, thromboelastography may prove more helpful than an aPTT in identifying the coagulation defect in a mildly hypothermic patient (an aPTT does not measure platelet function).

On the other hand, at temperatures below 33 ºC, both platelet function and coagulation enzyme activity are abnormal, which would be detected by either test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Post-operative Management:

How does thromboelastography measure coagulation?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

The thromboelastogram (TEG) measures the viscoelastic properties of blood during induced clot formation.

The pattern of changing shear-elasticity enables the evaluation of clot formation kinetics and growth, as well as the strength and stability of the formed clot.

Clinically, the TEG allows the identification of platelet dysfunction, primary fibrinolysis, stage I and II DIC, as well as residual anticoagulants.

The most common parameters derived from the study include:

  1. R – the time to initial clot formation, representing intrinsic pathway factor function;
  2. K & the alpha angle – the speed of clot formation, representing deficient thrombin and fibrin formation; and
  3. MA – the strength of the clot, a reflection of platelet number and function.

http://uktraumaprotocol.blogspot.com/2013/03/teg.html

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Post-operative Management:

Following emergence the patient is unable to move his legs.

What do you think is going on?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

This leg weakness is very concerning, since it could represent either –

  • an epidural/spinal hematoma with cord compression (secondary to lumbar drain and/or epidural catheter placement),
  • neurologic injury secondary to intra-operative spinal cord ischemia, or
  • the infusion of local anesthetics through an epidural catheter inadvertently placed in the intrathecal space.

Any of these complications should be considered extremely serious, requiring immediate intervention to prevent further harm.

Therefore, I would:

  1. perform a neurologic examination,
  2. increase the mean arterial pressure to > 80 mmHg to optimize spinal cord perfusion,
  3. discontinue the epidural infusion (the motor weakness associated with neuraxial local anesthetics may confuse the clinical picture),
  4. aspirate the epidural catheter for CSF to identify intrathecal placement,
  5. decrease the CSF pressure to 5-10 mmHg to maximize spinal cord perfusion; and
  6. give consideration to a CT/MRI and neurological consult.
17
Q

Post-operative Management:

How does surgical dissection and placement of an aortic cross-clamp increase the risk of spinal cord ischemia?

  • (A 62-year-old, 87 kg male presents for open repair of a dissecting aneurysm in the descending thoracic aorta.*
  • PMHx: Tobacco use for 45 years, Hypertension, Diabetes, Severe GERD, Aortic regurgitation, CAD with placement of a drug-eluting stent 3 months ago*
  • Meds: atenolol, hydrochlorothiazide, simvastatin, sublingual nitroglycerine, aspirin*
  • Allergies: NKDA*
  • PE: Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 °C*
  • CV: 3/6 diastolic murmur, high-pitched murmur - over left sternal border*
  • Airway: Mallampati II*
  • CXR: no acute pulmonary process*
  • CT: Descending thoracic aneurysm at 6.5 cm diameter*
  • Echo: moderate aortic valve insufficiency; Ejection Fraction = 65%; no wall motion abnormalities*
  • PFTs: FEV1 = 78% predicted; FEV1 / FVC = 65%*
  • Lab: H/H = 13/38; Blood sugar = 148)*
A

The risk of spinal cord ischemia is increased because surgical ligation of significant radicular arteries and the application of the aortic cross-clamp can lead to hypoperfusion of the spinal cord.

The anterior spinal cord is particularly vulnerable due to its reliance on a single anterior spinal artery for blood supply, the largest and most important of these being the artery of Adamkiewicz.

Moreover, spinal cord perfusion may be further compromised by the increase in CSF pressure associated with aortic cross-clamp application (application of the cross-clamp leads to cerebral hyperemia with subsequent shifting of CSF into the spinal compartment).

This increase in CSF pressure in combination with decreased distal aortic pressures can lead to decreased spinal cord perfusion and ischemia.

The risk of spinal cord ischemia can be reduced by:

  1. avoiding hypotension (the maintenance of proximal hypertension should be considered – especially when planning a “clamp and sew” technique without distal bypass),
  2. minimizing aortic cross-clamp time,
  3. reattaching critical segmental arteries,
  4. achieving an appropriate level of hypothermia,
  5. lowering CSF pressure via passive drainage and maintaining lower pressures postoperatively,
  6. monitoring spinal cord function using SSEPs and MEPs,
  7. utilizing a shunt or bypass to increase distal perfusion,
  8. ensuring a normal hematocrit and PaO2, and
  9. considering the administration of one or more of the various pharmacologic agents utilized for spinal cord protections, such as –
    • corticosteroids (i.e. dexamethasone or methylprednisolone), magnesium, barbiturates, calcium channel blockers, dextrorphan, papaverine, mannitol, and naloxone.