Keywords
bradycardia - negative chronotropy - lumbar spine - mechanism - spinal-cardiac reflex
Introduction
Back pain is a common reason to seek emergency care.[1] Lower back pain is a symptom and not a specific disease.[2] Lower back pain has many potential causes, the vast majority of which can and should
be managed conservatively, while many require surgical management.[1]
[2]
[3] Examples of cases which require surgical interventions include nonradicular lower
back pain with degenerative changes (disc disease), diskectomy for radiculopathy with
lumbar disc herniation, and decompressive laminectomy (with or without fusion) for
symptomatic spinal stenosis.[3] In general, such spinal surgery is safe, especially in healthy young individuals
without comorbidities, where early surgery may be important in allowing patients to
regain important day-to-day function and return to work.[4]
[5]
The interaction between the cardiovascular system and the nervous system is complex.
Acute hemodynamic disturbance due to neural mechanisms is well known in cranial neurosurgical
patients and spinal surgery in the cervical and upper dorsal segments.[6]
[7]
[8] However, adverse cardiovascular changes during lumbosacral spinal surgery are exceedingly
rare, with only six reported papers as of 2023. Of these, only four are case reports,
while two are letters/commentaries. The authors report a case of elective lumbosacral
decompression surgery where negative chronotropic changes were encountered and review
the available literature on cardiovascular changes during lumbar spine surgery.
Case Presentation
A 34-year-old male presented due to our neurosurgery department with a long-standing
history of lower back pain, which began radiating bilaterally to his lower limbs over
the last 4 months. His condition had deteriorated further over the last 10 days with
increasing pain, restricted straight left leg raising ability, and numbness at the
L5 dermatomal territory in his left foot. Power was 5/5 (Medical Research Council
scale) bilaterally, and reflexes were mildly brisk. An magnetic resonance imaging
of the lumbosacral spine revealed lumbar stenosis most pronounced at L4/L5 and disc
bulges at L3/L4 and L5/S1 ([Figs. 1] and [2]). His visual analogue pain score (VAS) was now 6. The patient was a police officer
whose symptoms now severely hindered his job, causing time off and stress, significantly
impairing his quality of life. Given his clinical condition, it was decided to opt
for surgical intervention. The patient was booked for surgery the next day. As per
our hospital's protocol for any major surgery, a comprehensive anesthetic and cardiology
evaluation was performed, including blood work, electrocardiogram, and echocardiogram.
This is our hospital's anesthesia department policy for patients undergoing their
first surgery, as there is often a lack of previous medical input/primary care information
in our country due to poor infrastructure. The patient had no prior medical history
and had an athletic build, weighing 90 kg and was 6 feet tall (body mass index 26.9).
He did not have any past medical, pharmacological, or family history, nor did he smoke
or drink alcohol.
Fig. 1 Magnetic resonance imaging lumbosacral spine T2 sequence. Sagittal view showing lumbar
stenosis most pronounced at L4/L5 and prolapsed intervertebral discs at L3-L4 and
L5-S1.
Fig. 2 Magnetic resonance imaging lumbosacral spine T2 sequence. Axial view of posterior
intervertebral discs and stenosis. Top row shows tight stenosis at L3-L4. Middle row
showing mild stenosis at L4-L5. Bottom row shows mild stenosis at L5-S1.
General anesthesia was induced in a prone position with propofol 180 mg, midazolam
2 mg, nalbuphine 10 mg, and suxamethonium 100 mg. A lumbar incision was made from
L2 to S1. The muscles were separated, and the spinous process of L4 was completely
removed, while the L3 and L5 spinous process and laminae were partially removed. Intraoperatively,
it was noted that there was very tight stenosis from a thickened ossified ligamentum
flavum at L3/L4 and L4/L5 and bilateral compression of nerve roots at both levels.
The lateral ligaments were removed at the level of L3/L4 and partially at L5/S1. The
left L4 nerve root was retracted while removing the prolapsed disc at L4/L5, and suddenly,
the anesthetist cautioned the surgeon of bradycardia, 34 beats per minute (bpm), and
the surgery was immediately stopped with the heart rate (HR) improving to 60 bpm within
30 seconds. When the root was retracted again after 3 minutes, a second episode of
bradycardia occurred, with the HR declining to 48 bpm. The surgery was stopped again,
and after 4 minutes, the anesthetist administered 600 µg of atropine. The HR then
jumped to 73 bpm, after which the surgery resumed. During the operation, there was
no point where the patient experienced a drop in oxygen saturation, end-tidal CO2,
temperature, or an upset in acid-base balance. These changes and their time of occurrence
are shown on the anesthesia monitor ([Fig. 3]). An intraoperative literature search suggested this phenomenon to be attributed
to nerve root manipulation and/or dural traction; therefore, the diskectomy proceeded
with extreme caution and was uneventful. Total blood loss was estimated to be approximately
100 mL.
Fig. 3 The second bradycardia occurring at 1:26 pm (heart rate 48 beats per minute). Bradycardia was sustained for 4 minutes, and atropine
was administered at 1:30 pm, after which the heart rate rose to 73 beats per minute at 1:31 pm.
Discussing with our cardiology and anesthesia colleagues, we all felt this was not
an allergic reaction to the anesthesia medication as the episode was specific to dural
manipulation; therefore, anaphylaxis workup was not performed (e.g., mast cell tryptase).
Additionally, our cardiology colleagues advised transferring our patient to our neurointensive
care unit for continuous cardiac monitoring for 24 hours. The patient was then transferred
to the general neurosurgical ward with cardiac monitoring, which was also unremarkable.
The patient was discharged without complication on the fourth postoperative day with
a VAS score of 3. Given his preoperative cardiac workup and postoperative monitoring,
cardiology also did not feel the need for continuous cardiac monitoring such as a
Holter monitor. At the 6-month follow-up, the patient was well and resumed his occupational
activity levels to what they were before his back pain 1 month postoperatively.
Discussion
There is a scarcity of cases demonstrating hemodynamic changes during spinal surgery,[9]
[10]
[11]
[12]
[13]
[14] but their existence suggests that there may be a reflex mechanism in the spine as
there is in the autonomous cerebral system similar to the trigeminocardiac reflex
(TCR).[15] The current understanding of such a phenomenon is based on the current case in the
literature. These are summarized in [Table 1].
Table 1
The published cases on negative chronotropic changes during lumbar spine surgery
|
Author
|
Age/Sex
|
Procedure
|
Position
|
Cardiac rhythm
|
Management
|
Outcome
|
|
Deschamps and Carvalho 2004[9]
|
37/F
|
L5-S1 spine decompression
|
Prone
|
Several episodes of bradycardia
|
IV adrenaline
|
Alive without neurological deficits
|
|
Mandal 2004[10]
|
36/M
|
L4/5 Discectomy
|
Prone
|
Two episodes of bradycardia
|
IV atropine
|
Alive without neurological deficits
|
|
Dooney 2010[11]
|
43/M
|
L4-L5 microscopic discectomy
|
Prone
|
Severe bradycardia followed by asystole
|
IV adrenaline and CPR
|
Alive without neurological deficits
|
|
Chowdhury et al 2012[13]
|
58/F
|
Lumbar decompression and fusion
|
Prone
|
Several severe hypotensive and hypertensive episodes
|
Fentanyl
|
Alive without neurological deficits
|
|
Chowdhury et al 2017[12]
|
72/F
|
Lower lumbar transforaminal interbody fusion
|
Prone
|
Severe bradycardia and hypotension
|
Removal of stimulus and ephedrine
|
Alive without neurological deficits
|
|
Mahajan et al 2015[14]
|
72/F
|
L2-L5 Lumbar spine decompression and transforaminal interbody fusion
|
Prone
|
Several episodes of bradycardia and hypotension
|
Removal of stimulus
|
Alive without neurological deficits
|
Abbreviations: CPR, cardiopulmonary resuscitation; F, female; M, male; IV, intravenous.
While cardiovascular changes occur in cranial neurosurgical patients from several
mechanisms/reflexes such as Cushing's syndrome, neurogenic, brainstem, the TCR, hemodynamic
changes in spinal surgeries are limited to major bleeds, shock, autonomic dysreflexia,
anesthesia related, medications and interactions, venous air embolisms, acid-base
upset, prone positioning, hypothermia, and anaphylaxis.[6]
[7]
[8] In our case and the six reported cases in the literature, each of these potential
reasons could be excluded, and a cause-and-effect relationship could be established
as the bradycardia coincided with the surgical stimulus.[9]
[10]
[11]
[12]
[13]
[14] The appearance of negative chronotropic changes in all cases was noted during dural
manipulation (direct or indirect), suggesting an underlying neurogenic control. Chowdhury
and Schaller[15] postulate this results from parasympathetic nerve activation, resulting in a negative
chronotropic response similar to a vasovagal reflex.[15] This may be due to a mechanical stretch of the dura, which has both intrinsic and
extrinsic innervation.[16] There may also be a certain threshold triggering such a reflex, which may explain
why every dural manipulation won't trigger such a response.
The most recent reported case by Mahajan et al[14] observed decreases in HR (38 bpm) and blood pressure (72/34 mm Hg) three times,
each coinciding with dural manipulation during transforaminal dilation.[14] This is similar to our case where the bradycardia occurred twice, each time coinciding
with nerve root retraction, but unlike Mahajan et al's case[14] the first episode improved in 30 seconds, but the second episode of bradycardia
was sustained for over one and a half minutes, and the anesthetist deemed it appropriate
to push atropine. Mahajan et al's case[14] is the only case where cardiovascular changes reverted after withdrawal of the surgical
stimulus, but the remaining five cases used anticholinergic and sympathomimetic drugs.[9]
[10]
[11]
[12]
[13]
[14] This may be due to the former waiting slightly longer to observe natural improvement,
while the remaining cases had a low threshold to intervene.
A parallel example is the TCR that also results from a stretch response during direct
or indirect manipulation of the cranial dura leading to bradycardia and hypotension
when the sensory branches of the trigeminal nerve are stimulated.[8] This spinal-cardiac reflex observed by dural manipulation may be its own entity.
Human anatomical studies confirm the existence of extrinsic and intrinsic innervation
of the spinal dura mater.[16] Surgical manipulation from decompression/dilation provokes the stimulation of afferent
parasympathetic fibers and inhibition of sympathetic fibers, providing evidence for
a unique afferent but a similar efferent pathway to the TCR.[8]
[15]
[16] Finally, some authors who observed hypotension (in addition to bradycardia) have
suggested that this underlying spinal-cardiac reflex may be more parallel to a vasovagal
(reflex celiac) reaction or the Bezold-Jarisch reflex.[14]
[17] Or, there may be a possible link with pelvic visceral afferent pathways where fibers
around the L5-S1 nerve roots can, in rare cases, be activated via afferent parasympathetic
pathways.[14] The Breuer-Lockhart reflex produces a comparable response to this whereby there
is the activation of the afferent parasympathetic fibers in response to anal/perianal
stimulation.[14] While the specific nuance of this spinal-cardiac reflex is yet to be fully understood,
we agree with previous cases that there must be some central brain stem connection
for this apparent lumbar spine-brainstem-heart loop that results in the negative chronotropic
changes.[9]
[10]
[11]
[12]
[13]
[14]
[15]
Negative chronotropy/hypotension during spinal surgery may necessitate intervention
with fluids, anticholinergic medication, and pressors. It is important to remember
that while such rare events are reported in the literature, they may not necessarily
be transient changes, as one reported case on this spinal-cardiac reflex transitioned
to asystole.[11] Most of the patients where this spinal-cardiac reflex was reported were young, fit
individuals without any comorbidities (including cardiac), which may mean young age
is a risk factor similar to vasovagal responses.[8]
[12]
[15] As invasive hemodynamic monitoring is not always done in elective spinal surgeries
and this spinal-cardiac reflex may be transient, this may be one reason why only so
few cases have been reported. Future research should evaluate this phenomenon in both
clinical and laboratory settings.
Conclusion
Lumbar spine surgery in a prone position may lead to negative chronotropic changes
secondary to the activation of an unidentified underlying neural mechanism that triggers
a physiological reflex. The most likely trigger for this is dural manipulation. The
anesthetist must carefully monitor cardiovascular changes in seemingly simple elective
spinal surgeries, and the surgeon must be cautioned of bradycardia so a dural stimulus
can be ruled out, along with the established causes. Future studies should evaluate
the potential neuronal pathways that may lead to hemodynamic changes in lumbar spinal
surgery.
