The Biomechanical Effects of Flaccid Paralysis Induced by Botulinum Toxin a After Damage Control Laparotomy
This study has been completed.
First Posted: December 20, 2011
Last Update Posted: April 27, 2016
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government.
Read our disclaimer for details.
Information provided by (Responsible Party):
Martin D. Zielinski, Mayo Clinic
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. 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. 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.
Wound; Abdomen, Abdominal Wall
Drug: Botulinum Toxin Type A
Intervention Model: Single Group Assignment
Masking: Double (Participant, Investigator)
Primary Purpose: Treatment
||The Biomechanical Effects of Flaccid Paralysis Induced by Botulinum Toxin a After Damage Control Laparotomy: A Pilot Study
Primary Outcome Measures:
Secondary Outcome Measures:
- Non-invasive biomechanical testing results (surface wave elastography, traction index and durometry) [ Time Frame: 2 years ]
- Mortality [ Time Frame: 2 years ]
- Duration of mechanical ventilation [ Time Frame: 2 years ]
- Complications (wound infection, fascial dehiscence, enterocutaneous fistula formation, acute renal failure, pneumonia) [ Time Frame: 2 years ]
- Overall hospital cost [ Time Frame: 2 years ]
- Total narcotic use (morphine equivalents) [ Time Frame: 2 years ]
- ABPS score [ Time Frame: 2 years ]
| Study Start Date:
| Study Completion Date:
| Primary Completion Date:
||August 2014 (Final data collection date for primary outcome measure)
Active Comparator: Botulinum Toxin A injection
Drug: Botulinum Toxin Type A
Six 25 cc injection of Botulinum Toxin A
Placebo Comparator: Placebo (Normal Saline) injection
Placebo (Normal Saline)