The Biomechanical Effects of Flaccid Paralysis Induced by Botulinum Toxin a After Damage Control Laparotomy
| Status: | Completed |
|---|---|
| Conditions: | Neurology |
| Therapuetic Areas: | Neurology |
| Healthy: | No |
| Age Range: | 18 - Any |
| Updated: | 11/8/2014 |
| Start Date: | November 2011 |
| End Date: | December 2014 |
| Contact: | Martin D Zielinski, M.D. |
| Email: | Zielinski.martin@mayo.edu |
| Phone: | 507-255-2923 |
The Biomechanical Effects of Flaccid Paralysis Induced by Botulinum Toxin a After Damage Control Laparotomy: A Pilot Study
Damage control laparotomy (DCL) is a life saving maneuver used with success in trauma and
acute general surgery patients. The technique involves source control of sepsis and
hemorrhage with an abbreviated laparotomy. In other words, the surgical procedure is cut
short to allow for resuscitation in the ICU after the immediately life threatening pathology
is treated. Planned re-exploration is then performed within 24-48 hours. It is at this
procedure that the injuries are reconstructed. This technique, unfortunately, has several
complications implicit with its use including wound infection, enterocutaneous fistula
formation, and intra-abdominal abscess development.[1] Additionally, in patients whom
primary fascial closure is not achieved, extensive abdominal wall reconstruction will be
required in 6-12 months. The key for preventing these complications is definitive closure
of the abdominal fascia, however, 10-50% of patients will have a planned ventral hernia with
an open abdominal wound at dismissal [1,2] Proven methods for decreasing the rate of
planned ventral hernia utilize tension in the midline to counter the effects of lateral
abdominal muscular retraction.[3,4,5] Despite these improvements, however, the planned
ventral hernia rate continues to be substantial.[2] Botulinum toxin a (BTX) is an FDA
approved neuron modulating agent which has been used extensively in cosmetic, motor and pain
disorders over the past 20 years [6,7]. The toxin blocks acetylcholine and pain modulator
release (calcitonin gene related peptide and substance P) from the pre-synaptic cholinergic
nerve terminal. The peptides are unable to bind at their motor end plate receptors through
a process that cleaves proteins involved in the transport protein cascade. This results in
flaccid paralysis and neuromodulation of the abdominal wall muscles resulting in reduced
lateral tension and pain. Theoretically, this could increase the rates of primary fascial
closure, improve pain sensation, decrease the rate of complications associated with open
abdomens all while lowering the costs and need for future abdominal wall reconstruction.
acute general surgery patients. The technique involves source control of sepsis and
hemorrhage with an abbreviated laparotomy. In other words, the surgical procedure is cut
short to allow for resuscitation in the ICU after the immediately life threatening pathology
is treated. Planned re-exploration is then performed within 24-48 hours. It is at this
procedure that the injuries are reconstructed. This technique, unfortunately, has several
complications implicit with its use including wound infection, enterocutaneous fistula
formation, and intra-abdominal abscess development.[1] Additionally, in patients whom
primary fascial closure is not achieved, extensive abdominal wall reconstruction will be
required in 6-12 months. The key for preventing these complications is definitive closure
of the abdominal fascia, however, 10-50% of patients will have a planned ventral hernia with
an open abdominal wound at dismissal [1,2] Proven methods for decreasing the rate of
planned ventral hernia utilize tension in the midline to counter the effects of lateral
abdominal muscular retraction.[3,4,5] Despite these improvements, however, the planned
ventral hernia rate continues to be substantial.[2] Botulinum toxin a (BTX) is an FDA
approved neuron modulating agent which has been used extensively in cosmetic, motor and pain
disorders over the past 20 years [6,7]. The toxin blocks acetylcholine and pain modulator
release (calcitonin gene related peptide and substance P) from the pre-synaptic cholinergic
nerve terminal. The peptides are unable to bind at their motor end plate receptors through
a process that cleaves proteins involved in the transport protein cascade. This results in
flaccid paralysis and neuromodulation of the abdominal wall muscles resulting in reduced
lateral tension and pain. Theoretically, this could increase the rates of primary fascial
closure, improve pain sensation, decrease the rate of complications associated with open
abdomens all while lowering the costs and need for future abdominal wall reconstruction.
Inclusion Criteria
- male or female, aged ≥ 18 years or older
- signed Informed Consent form by appropriate patient representative
- undergone a DCL for trauma or acute general surgery
Exclusion Criteria
- death prior to BTX injection
- failure to achieve hemodynamic stability within 24 hours (stable or decreasing
vasopressor support within 6 hours in combination with a stable or improving base
deficit or lactate level)
- Viable pregnancy
- At risk populations (<18 years of age, prisoners)
- BMI > 50
- Pre-existing pareses (Amyotrophic Lateral Sclerosis, myopathies, motor
polyneuropathies
- impaired neuromuscular transmission (Myasthenia Gravis, Lambert-Eaton Syndrome)
- concurrent aminoglycoside use
- chronic obstructive pulmonary disease
- known metastatic malignancy
- pre-existing cirrhosis
- necrotizing fasciitis of the trunk
- hypocoagulable state (INR >1.5)
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