UBP 3.2 (Short Form): Neuro – Acute Cervical Spinal Cord Injury Flashcards
Secondary Subject -- Autonomic Hyperreflexia / Neurologic Monitoring / Elevated ICP / Methemoglobinemia / Premature Ventricular Contractions / Spinal Shock / Succinylcholine-induced Hyperkalemia / Recent Coronary Stent Guidelines / Chronic Spinal Cord Injury / Vaporizer Spill / Interrupted Central Oxygen Supply
During the initial examination, it is determined that the patient is unable to move his extremities and he complains of difficulty breathing. What do you think may be going on?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
Considering his recent motor vehicle accident and facial injuries, I would be very concerned that his extremity weakness and dyspnea were related to cervical spine injury above the level of C6.
Injuries at the level of C3-5 affect diaphragmatic function;
injuries at C6-7 affect chest wall innervation, which can lead to paradoxical respiratory motion and an inability to cough effectively or clear secretions (these effects ultimately result in atelectasis and infection).
However, I would also consider other factors that could be causing or contributing to his dyspnea such as:
- pneumothorax, possibly secondary to his rib fractures;
- pulmonary edema, secondary to –
- cardiac tamponade,
- myocardial ischemia (CAD, recent coronary stent placement, chronic hypertension),
- pulmonary embolism, and/or
- neurogenic pulmonary edema (brainstem regulation of vasomotor tone could be lost secondary to his head injury or cervical spine injury);
- pulmonary embolism, secondary to his long bone fracture (fat embolism) or venous thrombosis (loss of lower extremity vasomotor tone can lead to arterial and venous pooling, with subsequent thrombosis); and/or his
- asthma.
Assuming this was acute cervical spinal cord injury, what are your concerns in relation to this type of injury?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
I have several concerns, including:
- respiratory dysfunction, secondary to –
- loss of diaphragmatic function (C3-C5)
- (which would make mechanical ventilation necessary) and/or
- intercostal and abdominal muscle function (C5-T7)
- (which may also make ventilatory support necessary, depending on the extent of compromise);
- loss of diaphragmatic function (C3-C5)
- hypotension, secondary to the loss of sympathetic vascular tone below the level of injury and the loss of cardioaccelerator fibers (T1-T4);
- pulmonary aspiration, since –
- GERD,
- paralytic ileus (secondary to trauma and/or cervical spinal cord injury),
- impaired airway reflexes (secondary to cervical spinal cord injury), and
- possible recent food ingestion – increase his risk for aspiration pneumonitis;
- worsening spinal cord injury, which can result secondary to inadequate spinal stabilization, hypotension, acidosis, hypoxia, and/or anemia;
- difficult airway management, secondary to –
- respiratory dysfunction (i.e. decreased functional residual capacity),
- the need for in-line stabilization, and
- increased risk of aspiration;
- thermal regulation, since the loss of vasoconstriction and temperature sensation below the level of the injury causes these patients to become poikilothermic;
- arrhythmias, which are more likely secondary to the autonomic dysfunction often associated with spinal cord injury;
- end-organ ischemia (i.e. cerebral or myocardial), which may result secondary to elevated intracranial pressure, coronary artery disease, hypotension, acidosis, hypoxia, and/or anemia; and
- patient positioning injury, which is more likely due to his unstable cervical spine and a lack of sensation below the level of injury.
As time progressed, I would be concerned about –
- autonomic hyperreflexia (a condition that develops in 85% of patients following the resolution of spinal shock);
- a susceptibility to hyperkalemia following the administration of succinylcholine;
- an increased risk for developing pneumonia, secondary to an impaired ability to cough and clear secretions; and
- an increased risk for DVT and pulmonary embolism.
(Assuming this was acute cervical spinal cord injury)..
Would you administer steroids?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
I would not administer high dose steroids (i.e. methylprednisolone) for acute spinal cord injury, recognizing that this practice is no longer recommended due to the lack of evidence demonstrating any clinical benefit.
There is, on the other hand, substantial evidence (Class I, II, and III) indicating that high dose methylprednisolone administration in this population of patients is associated with a number of adverse side effects including – infection, gastrointestinal bleeding, respiratory compromise, and even death.
Other complications associated with steroid administration in general include – fluid retention, hypertension, electrolyte imbalances, hyperglycemia, impaired wound healing, and immunosuppression (i.e. increased rates of sepsis and pneumonia).
What monitoring would you employ if this patient requires cervical spine surgery?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
Given this patient’s increased risk for myocardial (CAD, HTN), cerebral (possibly elevated ICP), and spinal cord (neck motion in the setting of an unstable cervical spine can lead to narrowing of longitudinal blood vessels supplying the cord) ischemia, combined with the potential for hemodynamic instability (HTN, loss of sympathetic vascular tone and cardioaccelerator fibers below the level of spinal cord injury),
I would require the standard ASA monitors along with:
- a 5-lead EKG, to monitor for signs of cardiac ischemia;
- an arterial line, to provide continuous hemodynamic monitoring and facilitate intermittent arterial blood gas and hematocrit analysis;
- a central venous pressure catheter, to provide for volume resuscitation and the measurement of right atrial filling pressures;
- an esophageal temperature probe, to ensure normothermia in this poikilothermic patient; and a
- Foley catheter, to facilitate bladder emptying and facilitate fluid management.
- Moreover, I would have a discussion with the surgeon and electrophysiologist about – neuromonitoring (SSEPs and/or MEPs) and
- pulmonary artery catheter placement.
Given the patient’s apparent head injury, would you initiate hyperventilation prior to intubation?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
While hyperventilation would likely reduce his intracranial pressure by inducing cerebral vasoconstriction, I would prefer NOT to initiate it due to the risk of inducing cerebral and/or spinal cord ischemia (hypocarbia decreases spinal cord blood flow as well as cerebral blood flow; patients with head trauma often experience a reduction in cerebral blood flow during the first 24 hours following the injury).
However, if his intracranial pressure became life-threatening (i.e. brainstem herniation) and other methods of intracranial pressure reduction were unsuccessful, I would hyperventilate him to a CO2 of 25-30 mmHg.
The patient’s dyspnea is significant and you decide to intubate him. On airway exam you note a Mallampati score of II.
How will you proceed with intubation?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
Given the importance of avoiding aspiration and additional injury to the spinal cord, and recognizing that fiberoptic assisted intubation requires the least distraction of the cervical spine, I would:
- provide aspiraton prophylaxis (proton pump inhibitors should be avoided in this patient since they may inhibit the antiplatelet effects of clopidogrel and aspirin, placing this patient with a stent at increased risk for stent thrombosis);
- administer a B2-agonist to optimize his asthma (this may be causing or contributing to his dyspnea);
- establish inline stabilization to minimize cervical neck motion during topicalization of the airway (coughing can result in cervical spine movement) and intubation;
- verify the presence of difficult airway equipment and a surgeon capable of obtaining a surgical airway;
- ensure adequate airway analgesia so as to prevent a sympathetic response (undesirable in a patient with hypertension, CAD, and potentially elevated ICP) and/or coughing during intubation;
- place the patient in 30° reverse-trendelenburg to improve respiratory mechanics (make sure that this positioning is hemodynamically tolerated in this trauma patient who may develop spinal shock);
- pre-oxygenate with 100% oxygen; and
- perform a careful awake fiberoptic assisted intubation.
Clinical Note:
- This patient could certainly be induced prior to fiberoptic intubation.
- However, the risk for difficult airway management, aspiration, and hemodynamic instability should be considered.
You utilize airway blocks to provide analgesia for the airway, but are unable to successfully intubate the patient with fiberoptic assistance due to the impairment of adequate visualization by blood in the oropharynx.
You are considering a different plan when you notice premature ventricular contractions (PVCs) on the EKG.
What is the “R-on-T phenomenon”?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
When premature ventricular contractions (which originate from foci below the atrial ventricular node) occur during the relative refractory period of the cardiac action potential (the middle of the T-wave), it is referred to as the “R-on-T phenomenon”.
The development of this phenomenon is concerning because it can lead to ventricular tachycardia or ventricular fibrillation.
Google image “R on T pvc”
There does not appear to be any R-on-T phenomenon, but the PVCs persist.
What will you do?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
PVCs are relatively common during anesthesia, especially in the setting of preexisting cardiac disease, and don’t always require treatment.
However, I would initiate treatment if his PVCs were –
- frequent (more than 3 PVC’s per minute),
- polymorphic,
- occurred in runs of three or more, or
- demonstrated an R-on-T phenomenon,
recognizing that these conditions are associated with an increased incidence of ventricular tachycardia and/or ventricular fibrillation.
If treatment were necessary, I would begin with identifying and eliminating any causative factors such as –
arterial hypoxemia, myocardial ischemia, hypokalemia, hypomagnesemia, sympathetic activation, and/or mechanical irritation (such as may occur from a central venous line or a pulmonary artery catheter).
I would also discontinue any drugs that are pro-dysrhythmic or prolong the QT interval.
Additionally, I would ensure the presence of a defibrillator, in case a life-threatening dysrhythmia should develop.
If the patient became symptomatic or hemodynamically unstable, I would consider –
- overdrive pacing and/or
- an antidysrhythmic, such as amiodarone, procainamide, a beta-blocker, or sotalol (the latter should not be used if the QT is prolonged because it can induce Torsades).
If the patient developed ventricular tachycardia, I would immediately cardiovert (unstable) or administer amiodarone (stable).
- Clinical Note:*
- More than 5-6 PVCs per minute preoperatively is associated with increased perioperative morbidity.
You pull back the central line and the PVCs resolve.
A few minutes later, you notice his blood pressure has dropped to 84/36 mmHg.
What is your differential for his hypotension?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
Given this patient’s recent car accident, cervical spine injury, coronary artery disease, long bone fracture, and ACE inhibitor therapy, there could be a number of factors contributing to his hypotension, such as:
- the loss of sympathetic vasomotor tone and the cardioaccelerator fibers (T1-T4) below the level of injury;
- cardiac tamponade;
- tension pneumothorax (a higher risk considering his likely rib fractures and recent central line placement);
- myocardial ischemia or infarction (secondary to CAD, anemia, hypoxia, hypotension, increased myocardial oxygen demand, coronary stent thrombosis);
- occult bleeding (i.e. abdomen and/or long bone fracture);
- pulmonary embolism, secondary to his long bone fracture (fat embolism) or venous thrombosis (loss of lower extremity vasomotor tone can lead to arterial and venous pooling, with subsequent thrombosis); and
- blunting of his renin-angiotensin-aldosterone system by lisinopril (the sympathetic system of these patients may be compromised, making them even more dependent on the renin-angiotensin-aldosterone system for maintenance of blood pressure).
What is spinal shock?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
Spinal shock is a condition that may occur following acute spinal cord injury, and is characterized by –
flaccid paralysis, paralytic ileus, and the loss of sensation, spinal reflexes, sympathetic vasomotor tone, and temperature regulation below the level of injury.
With higher lesions, the patient may experience the loss of diaphragmatic function (may require mechanical ventilation), intercostal abdominal muscle function (contributing to respiratory dysfunction, an inability to effectively clear pulmonary secretions, and the risk for pulmonary infection), and the cardioaccelerator fibers (loss of the T1-T4 sympathetic innervation of the heart limits the ability to compensate for hypovolemia and decreased systemic vascular resistance).
–
(How long can this condition last?)
This condition typically persists for a 1-3 weeks (may last up to 3 months), during which time the patient is at risk for respiratory dysfunction, hemodynamic instability, pulmonary aspiration, deep venous thrombosis / pulmonary embolism, and hypothermia.
The patient remains dyspneic and is yet to be intubated.
Assuming the airway exam is reassuring despite the facial trauma and blood in the oropharynx, would you perform a rapid sequence induction with succinylcholine?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
While this patient is at increased risk for aspiration due to his GERD, a potentially full stomach (i.e. possible recent food ingestion; decreased gastric emptying secondary to pain and/or obesity), paralytic ileus, and impaired airway reflexes,
I would NOT perform a rapid sequence induction in this situation due to the risk for significant hypotension in this patient with chronic hypertension who is hemodynamically unstable and taking an ACE inhibitor (ACE inhibitors are associated with an increased risk of intraoperative hypotension).
The administration of a large bolus of induction drug, as occurs when performing a rapid sequence induction, would increase the risk of end-organ ischemia in this hemodynamically unstable patient, who has coronary artery disease, spinal cord trauma, and potentially elevated intracranial pressure.
Instead, I would:
- continue to administer fluids and vasoactive agents as necessary;
- ensure the presence of difficult airway equipment and a surgeon capable of obtaining a surgical airway;
- provide aspiration prophylaxis;
- pre-oxygenate the patient with 100% oxygen (patients with high spinal injury are more susceptible to significant bradycardia during tracheal suctioning, and hypoxemia accentuates this response);
- direct two people to correctly initiate manual in-line stabilization;
- remove the front of the c-collar to facilitate mouth opening (given the patient’s cervical spine injury, I would not apply cricoid pressure, despite the risk of aspiration);
- carefully titrate intravenous narcotics and etomidate to achieve an adequate plane of anesthesia to prevent bronchospasm or a sympathetic surge while, at the same time, avoiding worsening hemodynamic instability;
- administer succinylcholine to facilitate intubation and prevent patient movement; and
- perform careful laryngoscopy for ETT placement.
Is the administration of succinylcholine acceptable with acute spinal cord injury?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
The administration of succinylcholine would be acceptable for the first 24-48 hours following acute spinal cord injury.
However, the proliferation of cholinergic receptors that subsequently occurs places the patient at risk for a potentially lethal succinylcholine-induced hyperkalemic response.
This exaggerated hyperkalemic response to succinylcholine does not occur until 24-48 hours after the spinal cord injury,
is most pronounced 4 weeks to 5 months following the injury,
may persist for an extended period of time (while the risk decreases significantly 6 months following the injury, it is best to avoid succinylcholine administration in these patients, if possible), and can lead to ventricular tachycardia, fibrillation, and cardiac arrest.
You attempt to intubate the patient and are unable to visualize the cords under direct laryngoscopy.
Would you remove the c-collar in order to improve the view?
(A 51-year-old, 81 kg, man presents to the trauma suite following a motor vehicle accident, during which he was hit from behind and pushed into another car in front of him, causing significant damage to the front and rear of his car. A quick examination reveals an alert patient with a broken nose, possible left femur fracture, and likely several rib fractures. His medical history includes HTN, moderate asthma, GERD, and CAD. Although he has never had a heart attack, he did have a coronary stent placed 6 months ago. His medications include lisinopril, Plavix, Lipitor, Advair, and albuterol. Vital Signs: P = 66, BP = 117/64 mmHg, RR = 24, T = 37.1 °C)
Given this patient’s apparent cervical spine injury and the potential for further damage with mobilization of his neck,
I would NOT remove the c-collar to facilitate intubation.
Rather, I would attempt to optimize visualization by changing laryngoscopy blades and/or patient positioning (i.e. reverse-trendelenburg, if tolerated).
If these measures were unsuccessful, I would maintain in-line stabilization, provide gentle positive pressure ventilation with 100% oxygen (< 20 mmHg to prevent gastric distention), and ask the surgeon to perform a tracheostomy.
