Selected publications from PubMed
Introduction Anticoagulation in patients undergoing surgical procedures is challenging. Interrupting anticoagulation for a procedure increases the risk of thromboembolism. Surgery has associated bleeding risks that are increased by the anticoagulants administered for thromboembolism prevention. First of all, we are going to explain the coagulation cascade in a simple way. [Image] Damaged blood vessel: Injury to vessel lining triggers the release of clotting factors. This step changes the prothrombin into thrombin. Formation of platelet plug: Vasoconstriction limits blood flow and platelets form a sticky plug. With the presence of thrombin, the fibrinogen changes into fibrin. Development of clot: Fibrin strands adhere to the plug to the form an insoluble clot. Exists a lot of blood thinners that works in this cascade of coagulation. Like Warfarin, Direct thrombin inhibitor, Factor Xa inhibitors, etc. In the case of the Warfarin: Inhibits the vitamin K-dependent clotting factors II, VII, IX and X, as well as the t iregulatory factors protein C, protein S, and protein Z It takes several days until the anticoagulant effect is reduced and then reestablished perioperatively. It is used in these pathologies. [Image] This is how the warfarin affects blood clotting. Warfarin reduces the body’s ability to make vitamin K, which interferes with protein creation. Lower levels of clotting protein makes blood cells less likely to clot. [Image] The newer direct oral anticoagulants: Direct thrombin inhibitor Dabigatran. Factor Xa inhibitors Rivaroxaban, Apixaban, Edoxaban. Have shorter half-lives, easier to discontinue and resume rapidly. But the direct factor Xa inhibitors lack an approved drug-specific antidote. This raises concerns about treatment of bleeding and management of patients who require an urgent surgery. This figure shows the Factors Xa inhibitors: Apixaban and Rivaroxaban and the direct thrombin inhibitors in the factor II : Dabigatran. [Image] Comparison of Warfarin vs Heparin [Image] ESTIMATING THROMBOEMBOLIC AND HEMORRHAGIC RISK? Annual risk thromboembolic and hemorrhagic. [Image] Very high thrombotic risk: Patients with a risk of more than 10 %, with a mitral valve prosthesis, recent stroke , atrial fibrillation, and recent VTE. High bleeding risk procedure: [Image] BleedMAP This is the stratification of perioperative hemorrhagic risk, based on four predictive factors: History of bleeding from patient Be a carrier of mechanical mitral valve Have an active neoplasm Low platelet count BleedMAP => Hemorrhage HAS – Bleeding score Score ≥3 was the most predictive variable for bleeding [Image] DOACs suspension prior to surgery: INR less than 1.5 at the time of surgery. Time that has been estimated depends on the drug, standing in 5 days in the case of warfarin and being enough 2-3 days in the case of acenocoumarol. Interval may be shortened in those associated cases at lower hemorrhagic risk, in which it can be allowed an INR 1.5-1.8. If the INR is >1.5, administer a low dose oral vitamin K (1 to 2 mg) to hasten normalization of the PT/INR. Restarting the drug after surgery: After 24 hours after surgery if it has been possible to start oral tolerance, the same dose that the patient was receiving preoperatively. If warfarin is withheld for 5 days before surgery and is restarted soon, patients would have a subtherapeutic INR for approx 8 days (4 days before and 4 days after surgery). For patients at very high or high thromboembolic risk, or cases where it is not possible to start oral tolerance, bridging may be appropriate. Use of bridging PREoperatively: Reserve bridging for individuals considered at very high or high risk of thromboembolism. Recent stroke, mechanical heart valve, CHA2DS2-VASc score of 7 or 8. In these cases, the bridging agent (therapeutic subcutaneous dose of LMW heparin) is started three days before surgery. Therapeutic dosing For individuals with a potential arterial thromboembolic source (atrial fibrillation, mechanical heart valve) or VTE within the preceding month. Typical regimens include enoxaparin, 1 mg/kg subcutaneously twice daily. Intermediate dosing Individuals with atrial fibrillation or VTE within the preceding month when bridging is needed but concerns about bleeding are greater. Typical regimens include enoxaparin, 40 mg twice daily. Prophylactic dosing Is not used for bridging in patients with AF, there is no evidence that prophylactic dose heparin prevents stroke in this setting. This dose level may be reasonable in patients who have had a VTE event between within the preceding 3 to 12 months. Typical prophylactic regimens include enoxaparin, 40 mg once daily. Timing We discontinue LMW heparin 24 hours before the planned surgery or procedure. If a twice-daily LMW heparin regimen is given, the evening dose the night before surgery is omitted. If a once-daily regimen is given, one-half of the total daily dose is given on the morning of the day before surgery. Use of bridging POSToperatively: After warfarin is restarted in the postoperative setting, it takes 5 to 10 days to attain a full anticoagulant effect as measured by an INR above 2.0. Individuals with high or very high risk of thromboembolism needs a heparin bridging agent during this period. Until there is adequate hemostasis clinical assessment of the wound site, drainage fluid amount, expected postoperative bleeding and correct hemoglobin levels. This assessment will vary depending on the surgery type and individual patient considerations. [Image] Low bleeding risk Minor procedures associated with a low bleeding risk in which bridging is used, therapeutic-dose of LMW heparin can usually be resumed 24 hours after the procedure. Major bleeding risk Major surgery or those with a high bleeding risk procedure, the therapeutic dose of LMW heparin should be delayed for 48 to 72 hours after hemostasis has been secured. Resumed Warfarin is generally resumed on the same postoperative day as the heparin. Heparin can be discontinued when the INR reaches the therapeutic range (2,0) for individuals at moderate thromboembolism risk. Perioperative management of the oral direct thrombin inhibitors and factor Xa inhibitors [Image] Rapid offset and onset of Dabigatran/Ribaroxaban activity obviates the need for bridging anticoagulation Dabigatran, Ribaroxaban and Apixaban: High risk Resumen 48 to 72 hours after surgery. Low risk Resumen 24 hours after surgery. Urgent invasive procedure with Warfarin? [Image] Time to reversal: Discontinuing warfarin: 5-14 days. Vitamin K: 6 to 24 hours to correct the INR. Fresh frozen plasma: 12 to 36 hours for complete reversal. Prothombin complex:15 min after 10 min to 1 hour infusion. Recombinant factor VIIa: 15 min after bolus infusion. Urgent invasive procedure with Dabigatran/Ribaroxaban? [Image] Take-home messages: If the patient bleeds from the procedure, their anticoagulant may need to be discontinued for a longer period, resulting in a longer period of increased thromboembolic risk. A balance between reducing the risk of thromboembolism and preventing excessive bleeding must be reached for each patient. Resumption of bridging anticoagulation too early, especially the use of therapeutic dose heparin within 24 hours after surgery, is associated with a two- to fourfold increased risk for major bleeding compared with no bridging or prophylactic dose heparin.
Published
Oct 2019
In 1600 BC, in the Edwin Smith Surgical Papyrus, written in ancient Egypt probably by Imhotep, the builder of the Step Pyramid in Saqqara, thoracic traumas were documented. Later in 400 BC, Hippocrates described hemoptysis after rib fracture, defining hemoptysis as a significant injury to the underlying lung, much more serious than a simple rib fracture. Later, in 300 BC, Aristotle said: “The heart alone of all the viscera cannot withstand serious injury. When the heart is destroyed there is no aid that can be brought to the other organs which depend on it.” And in 100 BC, Galen noted that when heart wounds were seen in gladiators, they were uniformly fatal. So, what if we stop rewinding the tape and ask where are we now? First of all, we must take a look at the epidemiology of chest trauma. Traumatic death rate is 56 per 100,000 people, or 6% of all deaths. This death rate has slowly risen in recent years, with the lowest point occurring in 2000, at 52 per 100,000. Motor vehicle–related injuries, firearms, stabbings, assaults and falls account for more than half of these deaths (58%). The male/female ratio for firearm-related deaths is 6.5:1 There are some important facts about chest trauma that we should not forget. It is a cause of death worldwide. ⅔ of patients have a chest trauma with another injury. Blunt chest trauma is the most common with a 90% incidence. 10% of patients require surgical intervention. It represents 25 % of all trauma fatalities. Chest trauma mortality is the second highest at about 25.2 % after head injury. Trauma is the leading cause of death in people under 45 worldwide. Deaths can be prevented by prompt diagnosis and treatment. Thoracic injuries account for 60% of all trauma presentations. Looking at the pathophysiology, there are clearly mechanisms for early loss of life: Airway obstruction Loss of oxygenation and ventilation Exsanguination Cardiac failure Cardiac tamponade Management of chest trauma must be initial resuscitation based on ATLS protocols following the ABCDE algorithm. In the primary survey, the following should be discarded: Airway obstruction Tension pneumothorax Open pneumothorax Massive hemothorax Flail chest Cardiac tamponade Certain pathologies should be ruled out in the secondary survey, as they are severe pathologies that threaten patients’ lives and should be treated as soon as possible. These are: Pulmonary contusion Myocardial contusion Aortic disruption Traumatic diaphragmatic rupture Tracheobronchial disruption Esophageal disruption In the Emergency room, when performing trauma life support, the clinical examination in the primary and secondary survey with anamnestic information on the mechanism of thoracic trauma will provide information on the potential severity of thoracic injury. These tools are also used: Blood test X-Ray Chest tube FAST CT scan Thoracic injuries (85%) are managed conservatively with analgesia, respiratory support and physiotherapy. Given this information, the question arises: WHAT ABOUT THE OTHER 15%? 15% of patients with thoracic trauma require surgical intervention due to hemorrhage or to disruption of an intrathoracic organ requiring repair or reconstruction. The indications for thoracic surgical intervention are: Blood loss ≥1,500 mL initially/>200 mL/hour over 2–4 hours. Endobronchial blood loss; massive contusion with significant impairment of mechanical ventilation. Tracheobronchial tree injury (air-leakage/ hemothorax). Injury of the heart or large vessels (blood loss/ pericardial tamponade). So is there a place for minimally invasive surgery in the management of severely injured patients? Reviewing the literature, in 1922 Jacobeaus performed the first clinical application of Thoracoscopy in the management of pleural adhesions, biopsy, drainage of empyemas, and treatment of pleural effusions. Later, in 1946, Branco described its value in patients with hemothorax secondary to penetrating injuries. In 1981, Jones published a series of 36 trauma patients with hemothoraces who underwent emergency thoracoscopy under local anesthesia. Currently, thanks to the development of surgical techniques and the use of minimally invasive surgery, the indications for VATS in severely injured patients are: Penetrating injury with little blood loss in a stable patient. Persistent hemothorax. Empyema. Persistent air-leakage. Suspicion of diaphragmatic rupture. On this basis, we have conducted a retrospective review of the literature on published articles on this subject. In one article from 1997 in Annals of thoracic surgery, Dan. M. Meyer et al. described that early VATS for retained hemothoraces decreases the duration of tube drainage, the length of hospital stay and hospital cost. Early intervention with VATS may be a more efficient and economical strategy for managing retained hemothoraces after trauma. In 2005, the American Journal of Surgery published an article about thoracoscopy in acutely injured patients. This group carried out a strong research and documented the benefits of using VATS in the care of trauma patients in the Trauma Program at the University of Louisville Hospital. This area of research on VATS was performed in the Center for Advanced Surgical Technology, in a combined program of Norton Hospital and the Department of Surgery of the University of Louisville. The purpose of this review was to describe the current role of VATS in the diagnosis and treatment of some specific conditions associated with thoracic injuries. In this article they made the following recommendations: VATS has no role in the management of patients in unstable condition or in whom there are clear indications for open thoracotomy. This procedure is for retained collections and persistent post traumatic pneumothorax. VATS is used to document the integrity of the diaphragm in penetrating thoracoabdominal trauma. Later, in 2007 in a paper in Annals of thoracic surgery a group at the Rambam medical center in Israel described: For stable patients with chest trauma, video assisted thoracic surgery is feasible and safe. The incidence of wound and pulmonary complication were higher in the thoracotomy group. Patients in the thoracotomy group needed significantly higher doses of narcotic analgesia. Average time to resume normal activity was shorter in the VATS group. Later, a systematic review and meta-analysis of a comparison of video assisted thoracoscopic surgery with open thoracotomy for the management of chest trauma was published in the World Journal of Surgery in 2015. This group highlights that in addition to smaller incision and less pain, perioperative outcomes such as effectiveness, postoperative complications, perioperative mortality, and duration of hospitalization for VATS seem to be superior to open thoracotomy in treating chest trauma. However, caution should also be exercised in certain clinical scenarios. With all this information based on an extensive review of the literature, we can deduce that VATS would be an effective diagnostic and therapeutic modality in chest trauma patients. It can be applied to retained hemothorax, persistent pneumothorax, suspicious diaphragm injury and even coagulation of bleeder. A review published last year in the Journal of Thoracic Diseases by the Charité Hospital group in Berlin showed: The standard approach for an emergency thoracotomy is anterolateral but VATS can be used for diagnostic and therapeutic indications in hemodynamically stable patients. VATS has a favorable postoperative course, a greater patient satisfaction rate and a superior long-term outcome compared to open surgery in hemodynamically stable patients with blunt and penetrating chest trauma. In this literature review we found a 2018 article about patients with thoracic impalement injury and management in the emergency room. They applied an algorithm which they highly recommend, in hemodynamically unstable patients and in the presence of great vessel injury, when performing an urgent open thoracotomy. Finally, a 2019 review in the Journal of Thoracic Diseases on the pros and cons of the use of VATS in trauma patients concluded: VATS can provide greater visualisation of the intra-thoracic structures. It is therefore becoming increasingly used as a diagnostic tool to identify the extent of the injuries whilst also allowing for therapeutic intervention. These benefits translate into decreased rate of post-operative complications and a shorter length of inpatient stay. Take home messages: After this extensive review, we highlighted some important facts. In cases of previous thoracic surgery, and pleurodesis or radiological signs of dense adhesions we prefer to avoid the minimal invasive surgery. Depending on the extent of difficulty ventilating, VATS should be considered a relative contraindication Tracheobronchial injury is a challenging emergency. In this condition, VATS should not be considered. VATS can be applied to retained hemothorax, persistent pneumothorax, suspicious diaphragm injury and even coagulation of bleeder. In addition to smaller incision and less pain, perioperative outcomes such as effectiveness, postoperative complications, perioperative mortality, and duration of hospitalization for VATS seem to be superior to open thoracotomy in treating chest trauma in hemodynamically stable patients. Haemodynamically unstable patients should be resuscitated aggressively, and an open approach will allow rapid control of haemorrhage.
Published
Sep 2019
A 69-year-old male patient with a history of hypertension, morbid obesity and ischemic heart disease. He presented with a giant inguinoscrotal hernia. Surgical repair was proposed. A CT-Scan was performed in which the left inguinoscrotal hernia was found, containing the urinary bladder and the left ureteral meatus, causing an ipsilateral ureterohydronephrosis due to compression of the meatus at the level of the inguinal canal. A total of 3 trocars were used. A 12mm trocar was placed in a supraumbilical position for a 30° scope, and the other two served as working channels for the leading surgeon, the 12 mm trocar in an infraumbilical position and the 5 mm one in the hypogastrium. A 30º optical laparoscope was introduced through the umbilical incision for visualization and preperitoneal dissection, identifying the epigastric vessels. Insufflation pressure must stay below 12 mmHg. It is important not to grasp the peritoneal fold itself, to prevent tearing, and not to dissect with diathermy too closely onto the psoas muscle laterally, as this may cause nerve damage. Therefore, blunt dissection is performed mainly in the preperitoneal space until the hernial orifice is identified. Once the hernial orifice is identified, its content is reduced. The reduction of the hernial content must be very carefully performed to avoid inadvertent injuries. We can see how with blunt dissection the bladder is gradually reduced, releasing the lax adhesions without difficulty. Traction and contraction movements are important to maintain tension in the hernial content and to reduce it by means of careful maneuvers. When dissecting out a hernia sac, adequate hemostasis while retracting must be ensured to avoid small bleeders. This might also prevent seromas and hematomas. Finally the hernia dissection and reduction of spermatic cord structures are completed, in addition to the reduction of the hernia sac and its reflections. Attention must be paid to the “triangle of doom” delimited by the vas deferens (medially), the spermatic vessels (laterally), the internal inguinal ring (apex) and the peritoneum (base). During peritoneal retraction, it is important to avoid grasping the ductus deferens as this may cause fertility problems, as well as overzealous dissection of the cord structures and genital branch of the genitofemoral nerve, as this probably contributes to postoperative neuralgia. Finally, a ProGrip ™ Self-Fixating Mesh is introduced to cover the hernia sites: inguinal, femoral and obturator. The mesh is Self-Fixating in order to avoid nerve injury. The mesh is screwed in and extended by means of two forceps covering the entire hernia defect. The hernia sac is placed behind the mesh. Then, an inspection for hemostasis in the extraperitoneal space, deflation and closure of skin incisions is performed. It is also important to remember that drainage is not necessary. Outcomes The surgery took 70 minutes. The patient started oral intake 5 hours after the surgery and left hospital on the 1st postoperative day. The patient remains asymptomatic 6 months after the revision.
Published
Jun 2019
A 69-year-old woman with no known drug allergies, with a prior medical history of hypertension, type 2 diabetes mellitus and chronic kidney disease. Secondarily to a rectum neoplasia the patient underwent an abdominoperineal resection (Miles intervention) with a terminal colostomy. Subsequently she presented with a parastomal hernia at this level that was repaired using the Sugarbaker technique. During the follow-up the patient presented with a recurrence of the parastomal hernia so it was decided to perform a repair using Sandwich technique, which combines the keyhole and Sugarbaker techniques. Three ports were placed as follows: a 12-mm trocar on the right side of the umbilicus for a flexible laparoscope; a 12-mm trocar in the right subcostal region; and a 5-mm trocar in the right lower quadrant. Careful adhesiolysis of the abdominal wall around the stoma was performed. A parastomal fascial gap was completely freed from the greater omentum and bowel loops, which protruded into the hernia sac. After identifying the parastomal hernia orifice, the stoma loop was completely dissected free from the peritoneal adhesion to become a straight line. The size of the mesh was selected, large enough to exceed the hernia orifice by at least 5 cm in all directions. We used two titanium meshes: a (hole type) mesh incised to the center and a central band type. The first mesh is inserted rolled in the abdominal cavity with two stitches to facilitate its placement. The hole type mesh was placed around the stoma to cover the parastomal hernia orifice using the keyhole technique. The mesh was fixed using absorbable tacks, with the incised parts of the mesh medially closed. Absorbable tacks were placed around the periphery of the mesh, approximately 1 cm apart. Then we cut the stitches that keep the mesh screwed to finish unfolding and complete its fixation using more absorbable tacks Afterwards, a further mesh (central band type) was overlaid to cover the first mesh and the whole abdominal wall by the Sugarbaker technique. After fixing the second mesh using absorbable tacks, the stoma loop was placed between both meshes to facilitate the desired lateralization. Some space must be left around the stoma loop to avoid stricture by the mesh. Finally we finished the surgery. The recurrent parastomal hernia was repaired using the Sandwich technique with two meshes implanted in an intraperitoneal onlay position.
Published
May 2019
Fecal incontinence is defined as the lack of control of defecation. It is a multifactor condition, involving such factors as mechanical disruption as well as neuromuscular or idiopathic dysfunction. Most of the time it is caused by a loss of anatomic continuity, for example after childbirth, surgery, or other traumatic injury. It frequently requires surgical intervention in an attempt to successfully restore normal physical structure. The causes are multiple, although its prevalence increases with age. After 50, prevalence rises to 11 % in men and 26% in women. The standard management for symptomatic fecal incontinence includes nonoperative management: - Pelvic floor exercises - Dietary changes - Surgery for repair sphincter defect We also know that 30% of fecal incontinence is linked to urinary incontinence. Sacral nerve stimulation has been approved for use in treating urinary incontinence in Europe since 1994, so it could also be a good option for these patients. Different studies have had good results showing that sacral nerve stimulation is a good option in patients with fecal incontinence, and is more effective than medical treatment alone. For all these reasons, the use of this therapy was proposed in patients who underwent rectal surgery and presented with Low Anterior Resection Syndrome (LARS). LARS is the major problem for rectal cancer patients after a low anterior resection. They have daily episodes of incontinence, obstructed defecation and constipation, causing a huge impact on the patients’ quality of life. 25% and 80 % of LARS patients develop symptoms following a sphincter-sparing rectal surgery. Mobilization of the rectum within the pelvis can lead to intramural nerve plexus injury, with long lasting sacral nerve terminal motor impairment. For individual patients, symptoms vary in type, severity, and duration. The risk factors for developing LARS are several, in particular: neoadjuvant radiotherapy, low anastomosis and anastomotic complications. There is evidence that denervation of the remnant sigmoid colon or left colon by means of operative maneuvers (e.g. ligation of a vascular pedicle) can result in a significant increase in motility. As a result, patients with LARS have a shorter colonic transit time and a greater increase in neorectal pressure after a meal compared to patients who do not have LARS. Removal of the rectum and in particular of the rectosigmoid junction eliminates the physiological distal control center for the regulation of bowel transit, leaving the bowel activities with no "brakes." This lack of distal negative feedback signals to oppose increased proximal colonic motility further exacerbates LARS symptoms. The sum of all these factors predisposes patients to develop LARS, which has a significant impact on their quality of life. The most frequently reported symptoms are: fecal incontinence, stool frequency, flatus incontinence, urgency, pad wearing, lifestyle modification, clustering and nocturnal incontinence. By means of the Wexner Score and the LARS Score we can classify this syndrome into minor and major according to the test score. Treatment in minor LARS ranges from dietary advice to loperamide, bulking agents and amitriptyline. In the case of major LARS the different options are stool training and advanced education, counselling, biofeedback, rectal irrigation and as a new option: Sacral nerve stimulation as a treatment for fecal incontinence due to LARS syndrome. Sacral nerve stimulation is a minimally invasive therapy. Different studies have shown its effectiveness in the treatment of pelvic floor dysfunctions, improving the severity of symptoms, restoring continence in patients and improving quality of life. The working mechanism is based on an effect on the autonomic nervous system, modulation of anorectal reflexes, modulation of the corticospinal pathway and changes in rectal sensitivity. It improves fecal continence by improving resting and squeeze pressures of the anal sphincter, as well as rectal sensation, together with stimulation on the external anal sphincter. Different studies show good results with this new technique in this type of patients, with improvement of symptoms in a high percentage of patients which also persists over time. We also see that quality of life improves, achieving a very significant decrease in the Wexner Score in different studies. The device system is an implantable programmable neuromodulation system that delivers electrical stimulation to the sacral nerve. It is designed to deliver therapeutic nerve stimulation through the following system components: a neurostimulator, a lead with programmable electrodes, and a lead extension. The system works by sending electrical pulses, which are produced by the neurostimulator, through the lead system. The implant goes through two phases. A first phase in which the device battery is external, checking if results are satisfactory. If they are, the final implantation is carried out in a second phase in which the battery is surgically implanted. For its placement it is necessary to select a location that meets the following conditions: - It is a minimum of 20 cm away from any other neurostimulator to minimize telemetry interference and possible inappropriate therapy. - It is on the opposite side of the body from another active implanted device (eg, pacemaker, defibrillator) to minimize possible interaction between the devices. - It is away from bony structures (e.g. 3 - 4 cm away) to minimize discomfort at the neurostimulator site. - It is away from areas of restriction or pressure to minimize the potential for skin erosion, patient discomfort, or damage to components. - It is in an area accessible to the patient for proper operation of a patient control device. - It is necessary to locate S3 for the needle implant. For this you have to identify middle line, identify sciatic notches, join the recesses and you will locate S3 is 2 cm from the midline. The needle should enter parallel to the midline and at the medial border of the foramen. If it is not placed in the correct position, electrode migration can occur causing the device to malfunction. Finally, we can say that with a good selection of patients, correct placement of the device and a good management program, sacral nerve stimulation can be successful in the treatment of these patients. In summary we know that, - LARS is related to a decreased rectal reservoir and denervation of the left colon during mobilization, which can lead to hypermotility of the neorectum and which may be a causal factor in the manifestation of multiple evacuations or urgency. - Authors have concluded that SNS is effective for all LARS symptoms. - Results of SNS implantation for fecal incontinence in LARS, showed significant decreases in fecal incontinent episodes, improvement in quality of life. - However, well-designed randomized controlled trials are needed to improve patient selection criteria for this procedure.
Published
Feb 2019
We present a case of intestinal occlusion that was found in a patient after obesity surgery. Case A 57-year-old female patient, with no known drug allergies, with a previous history of HBP and Gastric bypass in 2008 due to Morbid obesity (BMI 46 > BMI 28). The patient came to the emergency room due to a 3-day abdominal pain that had increased in intensity, with no vomiting or other symptoms. A Blood test and an abdominal X-ray were performed, finding a mild leukocytosis. Due to the persistence of pain, it was decided to request an abdominal CT-Scan, which found signs of intestinal obstruction, but was unable to identify the cause. It was decided to perform an exploratory laparoscopy. The patient was placed in the supine position with open legs. The surgeon stood between he legs. A total of 3 trocars were used. A 12mm trocar was placed in a supra umbilical position for a 30° scope. A 5 mm trocar was placed at the right flank and another 5mm trocar was placed at the left flank, serving as working channels for the leading surgeon. After examining the entire abdomen, an adhesion in the liver which caused an occlusion at the level of the jejunal-jejunal anastomosis was objectivie. We proceeded to section the adhesion using the Ligasure. We then checked that the alimentary limb and the jejuno-jejunostomy were correct and looked good. The next step was to check that the rest of the bowel looked good, with no signs of intestinal occlusion, ischemia, or other injuries. We reached the ligament of Treitz ending the review. We finally checked that the Petersen defect and the mesenteric defect of the jejuno-jejunostomy were closed. Outcome The surgery took 25 minutes. The postoperative course was correct. The patient started oral intake 24 hours after the surgery and left hospital on the 2nd postoperative day.
Published
Jun 2017
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