You are
requested to your local short-term rehabilitation center for a 67 year old male
with respiratory distress. You arrive to
find a patient in significant respiratory distress and altered mental
status. Per staff, the patient sustained
an ischemic stroke ten days ago, which resulted in left-sided hemiparesis and
some swallowing difficulties. He has a
past medical history of coronary artery disease and hypertension. This morning, the patient developed acute
respiratory distress and 911 was called.
You are concerned about pneumonia or pulmonary embolism in this
bed-bound patient, and at this time it does not appear that he is protecting
his airway. Vitals are notable for BP
98/58, HR 128, sinus tachycardia on the monitor, respirations 40, and pulse
oximetry 84% on RA. You call medical
control for delayed sequence intubation orders.
What regimen would you like to request?
After multiple clinical pearls on the topic
summarizing the latest evidence, there should be little debate on the induction
agent for this hypotensive patient.
Etomidate should be avoided in the hypotensive patient in extremis. You request ketamine for induction sedation
for this patient.
How many of you would choose succinylcholine for
this patient? Probably most of the
readers would choose succinylcholine. As
you know, succinylcholine exerts its effects by depolarizing the neuromuscular
junction by activating acetylcholine receptors.
The succinylcholine continues to activate the receptors, preventing
repolarization, or a resetting, of the neuromuscular junction. The effect continues until pseudocholinesterase,
an enzyme in the body, metabolizes the succinylcholine. The action of the depolarization does cause a
potassium ion flux into the blood, typically no more than 1 mEq/L, even in
instances of acute renal failure (e.g., dehydration, diabetic ketoacidosis).1
Most clinicians can rattle off the typical
contraindications to succinylcholine administration, such as renal
failure/hemodialysis, crush victims, burn victims, and prolonged
immobilization/"found down." Hopefully, if there is
enough time to obtain a history, the question of, “Have you or anyone in your
family had any problems with anesthesia in the past?” is being asked to
ascertain the possibility of the very dangerous malignant hyperthermia. If you’re really good, you may know that
patients with myopathies, such as muscular dystrophy, may result in an acute
rhabdomyolysis syndrome from the sudden muscle contractions of the
depolarization process. This may result
in a sudden increase in serum potassium.
In fact, there is a black box warning on succinylcholine for this
phenomenon, particularly in the pediatric population in which the myopathy may
not yet be diagnosed in the patient.2
Much less known, though, is the critical illness
polyneuropathy (CIP). This clinical
entity is seen primarily in ICU patients and patients with acute denervating
injuries, such as a spinal cord injury or cerebrovascular accident. In response to the sudden lack of nerve
impulses coming from the upper motor neurons (i.e., the brain or spinal cord),
the body starts to upregulate, or increase, the number of acetylcholine
receptors at the neuromuscular junction in an attempt to make them more
sensitive to any nerve signals coming their way. While the body is unable to activate these
neuromuscular junctions due to a functional blockade (e.g., severed spinal
cord, ischemic area of brain), succinylcholine can still activate these
junctions. Since there are many more
receptors, the activation of them will result in a greater flux of potassium
out of the cells. Potassium increases of
5-15 mEq/L have been seen in these instances, which can certainly cause
cardiac arrest. Because there is a delay
in the production of additional receptors, the first 24 hours after an acute
neurologic injury is typically safe for succinylcholine, so this should not
change your practice with acute strokes.
The risk peaks 5 to 15 days after the denervating injury, and it
is believed to last for 2-6 months afterwards.
However, some clinicians believe any patient with a history of
denervating injury to be at risk for life-threatening hyperkalemia after
succinylcholine.1,3–5
If you didn’t know this, you’re not alone. After some clinicians in the UK had two
hyperkalemic cardiac arrests in patients like this in their ICU after using
succinylcholine, they surveyed other physicians who would be familiar with
emergent intubations. They found that
68.7% of survey respondents chose succinylcholine for intubation.6
To summarize, true contraindications to succinylcholine remain renal failure
(particularly on hemodialysis), burns (cardiac arrests have occurred with as
little as 8% body surface area involved), crush injuries, prolonged
immobilization (e.g., found down at home and concern for rhabdomyolysis),
myopathies, history of malignant hyperthermia, and, now, recent history of
acute denervating injury, such as CVA or spinal cord injury.1
Case
resolution: You intubate the patient
using ketamine and rocuronium, and you administer fentanyl and ketamine for
post-intubation sedation. The patient’s
vital signs improve mildly. At the
emergency department, he is found to have a large saddle pulmonary embolus on
CT angiography. He goes to
interventional radiology for thrombectomy (removal of the clot), as he cannot
receive tissue plasminogen activator (tPA) due to the recent ischemic stroke. His cardiodynamics improve significantly and
he is extubated on hospital day #3. He
returns to rehab, albeit on a different regimen of anticoagulation.
References
1.
Stollings JL, Diedrich DA, Oyen LJ, Brown DR. Rapid-sequence intubation: a
review of the process and considerations when choosing medications. Ann.
Pharmacother. 2014;48(1):62-76. doi:10.1177/1060028013510488.
2. Sandoz Inc. ANECTINE- succinylcholine
chloride injection, solution (package insert). 2012. Available at:
http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=579ff759-3099-45f5-befe-c4b79106c87e.
Accessed September 21, 2014.
3. Biccard BM, Grant IS, Wright DJ, Nimmo SR,
Hughes M. Suxamethonium and critical illness polyneuropathy. Anaesth.
Intensive Care 1998;26(5):590-591.
4. Mallon WK, Keim SM, Shoenberger JM, Walls RM.
Rocuronium vs. succinylcholine in the emergency department: a critical
appraisal. J. Emerg. Med. 2009;37(2):183-8.
doi:10.1016/j.jemermed.2008.07.021.
5. Booij LH. Is succinylcholine appropriate or
obsolete in the intensive care unit? Crit. Care 2001;5(5):245-6.
6. Hughes M, Grant IS, Biccard B, Nimmo G.
Suxamethonium and critical illness polyneuropathy. Anaesth. Intensive Care
1999;27(6):636-638.
