Publications by authors named "Eduardo C Ayuste"

7 Publications

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Mandatory Laparotomy in Penetrating Abdominal Injuries with Omental Evisceration: Experience in a Major Trauma Center in the Philippines.

Cureus 2019 Sep 18;11(9):e5688. Epub 2019 Sep 18.

Surgery, Philippine General Hospital, Manila, PHL.

Background: Omental evisceration due to abdominal stab injuries connotes peritoneal penetration and translates to around 70% risk of intra-abdominal injury. Such cases are being managed with mandatory laparotomy at the Philippine General Hospital. This study aims to review the patient profile and laparotomy outcomes in such cases.

Methods: This is a retrospective review of 98 consecutive laparotomies performed for patients with omental evisceration secondary to abdominal stab wounds between January 2004 to April 2018.

Results: Almost all patients were male (99%) with a mean age of 32.1 years (range 14-70). The majority (81%) had a therapeutic laparotomy, and only 19 patients (19%) had a non-therapeutic laparotomy. The most commonly injured organs include the small bowel, stomach, colon, diaphragm, and liver. There was no significant difference in age, sex, duration of injury, systolic blood pressure and heart rate at presentation between the two groups. There were significantly more patients who presented with peritonism in the therapeutic laparotomy group compared to the non-therapeutic laparotomy group (82% vs 53%, p=0.005). Patients who presented with peritonism were six times more likely to have a therapeutic laparotomy. There was no significant difference between morbidity and mortality rates in the two groups. The length of hospital stay for the non-therapeutic laparotomy group was significantly shorter compared to the therapeutic laparotomy group (3.6 vs 5.7 days, p=0.006).

Conclusion: The rate of therapeutic laparotomy remains to be significantly higher among patients with omental evisceration. Hence, omental evisceration, particularly those associated with peritonism, should continue to prompt operative management.
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http://dx.doi.org/10.7759/cureus.5688DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6823020PMC
September 2019

Exporting simulation technology to the Philippines: a comparative study of traditional versus simulation methods for teaching intravenous cannulation.

Stud Health Technol Inform 2009 ;142:346-51

Department of Surgery, Philippine General Hospital, University of the Philippines, Manila, Philippines.

This study examines effectiveness of a donated Laerdal Virtual I.V. simulator when compared with traditional methods of teaching intravenous (IV) cannulation to third year medical students in the Philippines. Forty novice Filipino medical students viewed an instructional video on how to start intravenous lines and were then randomly divided into two groups of twenty. The "Traditional" group observed an IV insertion on an actual patient performed by an experienced practitioner, and then subsequently performed an IV on an actual patient which was videotaped. The "Simulation" group practiced the Virtual I.V. simulator until they successfully completed level three using the "doctor" setting. These students then performed an IV on an actual patient which was videotaped. The videotapes for both groups were reviewed by two pre-trained (Inter-rater reliability of > or =0.84) observers who were blinded to the group using a previously validated checklist for IV insertion. Students trained on the Virtual I.V. showed significantly greater success in successfully starting an IV on an actual patient (40% VS. 15%, p<0.05), decreased constrictive band time (p<.05), increased raw score on the check list (p<.03), and decreased overall time to start an IV (p<.05). The technology was well received but wider application in the non western world is limited by lack of in country company support and the relative expense.
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June 2009

Impact of resuscitation strategies on the acetylation status of cardiac histones in a swine model of hemorrhage.

Resuscitation 2008 Feb 5;76(2):299-310. Epub 2007 Sep 5.

Trauma Research and Readiness Institute for Surgery, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.

Background: Chromatin remodeling through histone acetylation is a key control mechanism in gene transcription. We have shown previously that fluid resuscitation in rodents is coupled with highly structured post-translational modifications of cardiac histones. The current experiment was performed to validate this concept in a clinically relevant large animal model of hemorrhage and resuscitation, and to correlate the changes in histone acetylation with altered expression of immediate-early response genes.

Study Design: Yorkshire swine (n=49, 7/group, weight=40-58kg) were subjected to combined uncontrolled and controlled hemorrhage (40% of estimated blood volume) and randomly assigned to the following resuscitation groups: (1) 0.9% saline (NS), (2) racemic lactated Ringer's (dl-LR), (3) l-isomer lactated Ringer's (l-LR), (4) Ketone Ringer's (KR), (5) 6% hetastarch in saline (Hespan). KR contained an equimolar substitution of lactate with beta-hydroxybutyrate. No hemorrhage (NH) and no resuscitation (NR) groups were included as controls. Cardiac protein was used in Western blotting to analyze total protein acetylation and histone acetylation specifically. Lysine residue-specific acetylation of histone subunits H3 and H4 was further evaluated. In addition, Chromatin Immunoprecipitation (ChIP) technique was used to separate the DNA bound to acetylated histones (H3 and H4 subunits), followed by measurement of genes that are altered by hemorrhage/resuscitation, including immediate-early response genes (c-fos and c-myc), and heat shock protein (HSP) 70.

Results: The type of fluid used for resuscitation influenced the patterns of cardiac histone acetylation. Resuscitation with dl-LR and KR induced hyperacetylation on H3K9. KR resuscitation was also associated with increased acetylation on H3K14 and H4K5, and hypoacetylation on H3K18. The expression of genes was also fluid specific, with the largest number of changes following KR resuscitation (increased c-fos and c-myc, HSP 70 linked with H3; and increased c-myc linked with H4). Among the histone subunits studied, altered H3 acetylations were associated with the majority of changes in immediate-early gene expression.

Conclusions: Acetylation status of cardiac histones, affected by hemorrhage, is further modulated by resuscitation producing a fluid-specific code that is preserved in different species. Resuscitation with KR causes histone acetylation at the largest number of lysine sites (predominately H3 subunit), and has the most pronounced impact on the transcriptional regulation of selected (immediate-early response) genes.
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http://dx.doi.org/10.1016/j.resuscitation.2007.07.030DOI Listing
February 2008

Does the rate of rewarming from profound hypothermic arrest influence the outcome in a swine model of lethal hemorrhage?

J Trauma 2006 Jan;60(1):134-46

Trauma Research and Readiness Institute for Surgery, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.

Background: Rapid induction of profound hypothermic arrest (suspended animation) can provide valuable time for the repair of complex injuries and improve survival. The optimal rate for re-warming from a state of profound hypothermia is unknown. This experiment was designed to test the impact of different warming rates on outcome in a swine model of lethal hemorrhage from complex vascular injuries.

Methods: Uncontrolled lethal hemorrhage was induced in 40 swine (80-120 lbs) by creating an iliac artery and vein injury, followed 30 minutes later (simulating transport time) by laceration of the descending thoracic aorta. Through a thoracotomy approach, a catheter was placed in the aorta and hyperkalemic organ preservation solution was infused on cardiopulmonary bypass to rapidly (2 degrees C/min) induce profound (10 degrees C) hypothermia. Vascular injuries were repaired during 60 minutes of hypothermic arrest. The 4 groups (n = 10/group) included normothermic controls (NC) where core temperature was maintained between 36 to 37 degrees C, and re-warming from profound hypothermia at rates of: 0.25 degrees C/min (slow), 0.5 degrees C/min (medium), or 1 degrees C/min (fast). Hyperkalemia was reversed during the hypothermic arrest period, and blood was infused for resuscitation during re-warming. After discontinuation of cardiopulmonary bypass, the animals were recovered and monitored for 6 weeks for neurologic deficits, cognitive function (learning new skills), and organ dysfunction. Detailed examination of brains was performed at 6 weeks.

Results: All the normothermic animals died, whereas survival rates for slow, medium and fast re-warming from hypothermic arrest were 50, 90, and 30%, respectively (p < 0.05 slow and medium warming versus normothermic control, p < 0.05 medium versus fast re-warming). All the surviving animals were neurologically intact, displayed normal learning capacity, and had no long-term organ dysfunction.

Conclusions: Rapid induction of hypothermic arrest maintains viability of brain during repair of lethal vascular injuries. Long-term survival is influenced by the rate of reversal of hypothermia.
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http://dx.doi.org/10.1097/01.ta.0000198469.95292.ecDOI Listing
January 2006

Hepatic and pulmonary apoptosis after hemorrhagic shock in swine can be reduced through modifications of conventional Ringer's solution.

J Trauma 2006 Jan;60(1):52-63

Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA.

Background: Cytotoxic properties of racemic (D-,L-isomers) lactated Ringer's solution detected in vitro and in small animal experiments, have not been confirmed in large animal models. Our hypothesis was that in a clinically relevant large animal model of hemorrhage, resuscitation with racemic lactated Ringer's solution would induce cellular apoptosis, which can be attenuated by elimination of d-lactate.

Methods: Yorkshire swine (n = 49, weight 40-58 kg) were subjected to uncontrolled (iliac arterial and venous injuries) and controlled hemorrhage, totaling 40% of estimated blood volume. They were randomized (n = 7/group) to control groups, which consisted of (1) no hemorrhage (NH), (2) no resuscitation (NR), or resuscitation groups, which consisted of (3) 0.9% saline (NS), (4) racemic lactated Ringer's (DL-LR), (5) L-isomer lactated Ringer's (L-LR), (6) Ketone Ringer's (KR), (7) 6% hetastarch in 0.9% saline (Hespan). KR was identical to LR except for equimolar substitution of lactate with beta-hydroxybutyrate. Resuscitation was performed in three phases, simulating (1) prehospital, (2) operative, (3) postoperative/recovery periods. Arterial blood gasses, circulating cytokines (TNF-alpha, IL-1, -6, -10), and markers of organ injury were serially measured. Metabolic activity of brain, and liver, was measured with microdialysis. Four hours postinjury, organs were harvested for Western blotting, ELISA, TUNEL assay, and immunohistochemistry.

Results: All resuscitation strategies restored blood pressure, but clearance of lactic acidosis was impeded following DL-LR resuscitation. Metabolic activity decreased during shock and improved with resuscitation, without any significant inter-group differences. Levels of cytokines in circulation were similar, but tissue levels of TNF in liver and lung increased six- and threefolds (p < 0.05) in NR group. In liver, all resuscitation strategies significantly decreased TNF levels compared with the NR group, but in the lung resuscitation with lactated Ringer (DL and L isomers) failed to decrease tissue TNF levels. DL-LR resuscitation also increased apoptosis (p < 0.05) in liver and lung, which was not seen after resuscitation with other solutions.

Conclusions: In this large animal model of hemorrhagic shock, resuscitation with conventional (racemic) LR solution increased apoptotic cell death in liver and lung. This effect can be prevented by simple elimination of D-lactate from the Ringer's solution.
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http://dx.doi.org/10.1097/01.ta.0000200156.05397.0bDOI Listing
January 2006

Induction of profound hypothermia modulates the immune/inflammatory response in a swine model of lethal hemorrhage.

Resuscitation 2005 Aug 19;66(2):209-16. Epub 2005 Apr 19.

Trauma Research and Readiness Institute for Surgery, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.

Unlabelled: Profound hypothermic arrest ("suspended animation") is a new strategy to improve outcome following uncontrolled lethal hemorrhage (ULH). However, the impact of this approach on the immune/inflammatory response is unknown. This experiment was conducted to test the influence of profound hypothermia on markers of immune/inflammatory system.

Methods: ULH was induced in 32 female swine (80-120 lb) by creating an iliac artery and vein injury, followed 30 min later by laceration of the descending thoracic aorta. Through a left thoracotomy approach, total body hypothermic hyperkalemic metabolic arrest was induced by infusing organ preservation fluids into the aorta using a cardiopulmonary bypass machine (CPB). Experimental groups were (1) normothermic controls (no cooling, NC), or hypothermia induced at the following rates: (2) 0.5 degrees C/min (slow, SC), (3) 1 degrees C/min (medium, MC) and (4) 2 degrees C/min (fast, FC). Vascular injuries were repaired during 60 min of profound (10 degrees C) hypothermic arrest. Hyperkalemia was reversed by hypokalemic fluid exchange, and blood was infused for resuscitation during re-warming (0.5 degrees C/min). The surviving animals were monitored for 6 weeks. Levels of IL-1, TNFalpha, IL-6, IL-10, TGF-1 beta and heat shock protein (HSP-70) were measured by ELISA in serum samples collected serially during the experiment and post-operatively.

Results: Some of the immune markers were influenced by the use of CPB, independent of hypothermia (decrease in TGF-1 beta and increase in IL-1 beta). Hypothermia caused a significant decrease in IL-6, and an increase in HSP-70 expression compared to normothermic controls, independent of the cooling rate. An increase in IL-10 levels was noted which was influenced by the rate of cooling (p<0.05, MC versus NC).

Conclusions: Profound hypothermia modulates the post-shock immune/inflammatory system by attenuating the pro-inflammatory IL-6, increasing anti-inflammatory IL-10 and augmenting the protective heat shock responses.
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http://dx.doi.org/10.1016/j.resuscitation.2005.01.021DOI Listing
August 2005

Profound hypothermia protects neurons and astrocytes, and preserves cognitive functions in a Swine model of lethal hemorrhage.

J Surg Res 2005 Jun;126(2):172-81

Trauma Research and Readiness Institute for Surgery, Bethesda, Maryland, USA.

Background: Lethal injuries can be repaired under asanguineous hypothermic arrest (suspended animation) with excellent survival. This experiment was designed to test the impact of this strategy on neuronal and astroglial damage in a swine model of lethal hemorrhage. Furthermore, our goal was to correlate the histological changes in the brain with neurological outcome, and the levels of circulating brain specific markers.

Materials And Methods: Uncontrolled hemorrhage was induced in 32 female swine (80-120 lbs) by creating an iliac artery and vein injury, followed 30 min later by laceration of the thoracic aorta. Through a thoracotomy approach, organ preservation fluid was infused into the aorta using a roller pump. Experimental groups included normothermic controls (no cooling, NC), and groups where hypothermia was induced at three different rates: 0.5 degrees C/min (slow, SC), 1 degrees C/min (medium, MC), or 2 degrees C/min (fast, FC). Profound hypothermia (core temperature of 10 degrees C) was maintained for 60 min for repair of vascular injuries, after which the animals were re-warmed (0.5 degrees C/min) and resuscitated on cardiopulmonary bypass (CPB). Circulating levels of neuron specific enolase (NSE) and S-100beta were serially measured as markers of damage to neurons and astrocytes, respectively. Light microscopy and quantitative immunohistochemical techniques were used to evaluate hippocampal CA1 area and caudate putamen for neuronal injury and astrogliosis (astrocyte hyperplasia/hypertrophy). Surviving animals were observed for 6 weeks and neurological status was documented on an objective scale, and cognitive functions were evaluated using a technique based upon the concept of operant conditioning.

Results: Normothermic arrest resulted in clinical brain death in all of the animals. None of the surviving hypothermic animals displayed any neurological deficits or cognitive impairment. On histological examination, normothermic animals were found to have ischemic changes in the neurons and astrocytes (hypertrophy). In contrast, all of the hypothermic animals had histologically normal brains. The circulating levels of brain specific proteins did not correlate with the degree of brain damage. The changes in NSE levels were not statistically significant, whereas S-100beta increased in the circulation after CPB, largely independent of the temperature modulation.

Conclusions: Profound hypothermia can preserve viability of neurons and astrocytes during prolonged periods of cerebral hypoxia. This approach is associated with excellent cognitive and neurological outcome following severe shock. Circulating markers of central nervous system injury did not correlate with the actual degree of brain damage in this model.
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http://dx.doi.org/10.1016/j.jss.2005.01.019DOI Listing
June 2005