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Shrivastava, Das, and Kumar: Aorta and caval perforation during laparoscopic sleeve gastrectomy – a rare complication


Laparoscopic sleeve gastrectomy (LSG), introduced in 1990 as an alternative to distal gastrectomy, is an effective and safe procedure in the treatment of morbid obesity. However, a number of complications have been reported in the literature, such as iatrogenic oesophageal transection,1 iatrogenic nasogastric (NG) perforation with a NG tube,2 stapling and section of the NG tube during LSG, stapled NG tube misplaced into the airway,3 and inadvertent intrapleural placement or placement into the bronchi. Early complications4 that can arise include bleeding, staple-line leak, deep-vein thrombosis, pulmonary embolism and damage to the organs.5 Injuries to the major retroperitoneal vascular structures are uncommon but important complications of laparoscopic procedures.7

Case report

A 45-year-old woman with a body mass index of 39 kg/m2 was posted for elective LSG. She had a history of asthma and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Her airway was assessed and graded as Mallampati III. Anaesthesia was induced with 200 mg of propofol, 40 μg of dexmedetomidine, 25 mg of ketamine and 14 mg of the muscle relaxant cisatracurium. A video laryngoscope and stylet were used for intubation. Propofol and dexmedetomidine infusion along with desflurane was initiated for maintenance of anaesthesia. During the operation she also received a total intravenous (i.v.) dose of 50 mg of ketamine, 6 mg of midazolam, 20 mg of cisatracurium, 75 mg of diclofenac and 1 g of paracetamol.

Pneumoperitoneum was achieved after insertion of a Veress needle into the abdominal wall. Initial gas flow was 1.5 l of CO2 with pressure of 6 mmHg, indicating proper placement of the intra-abdominal needle tip. Around 3 l of CO2 was insufflated to ensure correct pneumoperitoneum, and intra-abdominal pressure was set at 15 mmHg. When the first trocar was inserted via a supraumbilical incision, the patient suddenly became bradycardic, and her blood pressure and oxygen saturation dropped. She responded to three bolus doses of atropine 0.6 mg and three doses of 10 mg ephedrine. Phenylephrine infusion was then initiated. Surgeons were asked to stop the procedure and abdominal gases deflated. Once the patient appeared to be stable, the procedure was restarted. A camera was inserted and bleeding was identified under the first trocar. A small tear in the mesentery of the small bowel close to the start of the jejunum was noted, and could not be controlled. In addition, her oxygen saturation was unrecordable. An immediate decision was made to open the abdomen, thereby allowing the bleeding site in the small mesentery to be controlled.

A large retroperitoneal haematoma on the left side of the abdomen, extending from the infrarenal area to the area before the bifurcation of the aorta, was identified; the vascular surgeon was informed. The patient was in severe hypotensive–hypovolaemic shock. The blood bank and haematologist were advised of the emerging need for a massive blood transfusion. A large-bore i.v. cannula, central line and arterial line were inserted. The patient received 4000 ml of 0.9% normal saline, 2000 ml of Ringer’s lactate, 500 ml of Gelofusine (4% gelatine; B. Braun Melsungen AG, Melsungen, Germany), 500 ml of 20% mannitol, 100 ml of 20% human albumin, 12 units (3000 ml) of packed red blood cells, 12 units (2400 ml) of fresh-frozen plasma, 12 units (486 ml) of platelets and 2 units (120 ml) of cryoprecipitate. Initially she received 4 units of O-negative blood. High doses of noradrenaline (28.57–47.61 μg/kg/h) and adrenaline (28.95 μg/kg/h) infusions were initiated, along with dobutamine (62.5 mg/h). Despite this, the patient developed ventricular fibrillation and direct current shock was applied three times. She received six doses of adrenaline (1 mg/dose), 240 mg of 2% lignocaine, a 300-mg bolus of amiodarone, 200 mg of hydrocortisone, 500 mg of methylprednisolone, 250 ml of 8.4% bicarbonate (100 ml + 100ml + 50 ml), 20 mg of furosemide and 30 ml of calcium chloride. The patient showed a gradual response to resuscitation measures and her blood pressure began to increase. Dobutamine was discontinued, adrenaline was gradually reduced to 0.4 ml/h (40 μg/h) and then was discontinued, and noradrenaline was reduced to 600 μg/h and then to a minimum dose of 0.4 ml/h (40 μg/h).

Retroperitoneal hematoma was cleared, and, as the injury to the aorta was through and through, this was sutured. Further inspection revealed a small injury in the vena cava before the bifurcation in the left side, which was also sutured. The LSG was abandoned and the abdomen closed with appropriate drains.

A series of six blood gas analyses completed intraoperatively revealed a pH from 7.152 to 7.197. Haemoglobin dropped to 4.5 g/dl, reached 9.6 g/dl and then 11.8 g/dl before the patient was transferred to the intensive care unit (ICU). Base excess was –7.1 mmol/l and bicarbonate was 14.7 mmol/l. As glucose was 441 mg/dl, an insulin infusion of 2 ml/h at 2 units/ml was initiated.

Continuous core temperature, arterial pressure and capnography monitoring was undertaken, and body temperature was maintained by warm air blankets and temperature-controlled blood warmers. The patient’s total estimated blood loss was 5500 ml and urine output was 1400 ml. Rapid thromboelastography (TEG) performed during recovery was normal and arterial blood gas parameters excellent, with a pH of 7.366, haemoglobin of 11.8 g/dl and lactate going down to 4.3 mmol/l from 14.5 mmol/l. The patient was extubated and transferred to the ICU and then to a ward on the sixth post-operative day.

Computerized tomography of the abdomen and angiography showed a left renal vein thrombus and query faint left common iliac vein thrombus formation. The vascular surgeon advised no active intervention. The patient was started on subcutaneous clexane and warfarin, and discharged after 30 days on warfarin.


Any keyhole procedure may lead to unintentional injury to the organs near the operation site. Early intraoperative and postoperative6 complications, such as bleeding or staple line leak, need to be identified and treated immediately. The literature reports the incidence of major blood vessel injury to be 0.1%.8 Intraoperative injury to the portal vein and inferior vena cava is rare, but can lead to rapid exsanguination.8

The incidence of post-operative haemorrhage after LSG is reported to be between 1% and 6%.7 Injuries to the left and right common iliac arteries, right common iliac vein, inferior vena cava and aorta have been reported between 1994 and 2002.7 In obese patients, access to the abdominal cavity with needle insertion is technically difficult9 as accurate location of the needle tip is difficult. In obese women, the umbilicus is 2.9 cm inferior to the bifurcation of the aorta and 13 cm (±4 cm) anterior to the aorta.10

Insertion of large-bore i.v. lines, fluid resuscitation, packed cell transfusion, accurate measurement of urine output, identification of the source of the bleeding and control of bleeding by removing the haematoma and placement of a closed suction unit are vital. Each litre of crystalloid expands the blood volume by 20–30%.11 Colloids replace volume in a 1 : 1 ratio. In an acute situation, O-negative non-cross-matched blood must be administered and a blood sample taken for typing and cross-matching, preferably before blood transfusions have begun. Type-matched blood should be transfused when available.11

In patients with abdominal lesions, early initiation of vasopressor infusion maintains adequate perfusion to other organs. Vasopressors were administered in our patient as soon as blood pressure dropped. In haemorrhagic shock, initial activation of the sympathetic system results in compensatory venous and arterial vasoconstriction, which is lost gradually, and noradrenaline administration is needed to maintain mean arterial pressure. Anaesthetic agents also exert a significant effect on vasoconstrictor response to haemorrhage, even before extreme exsanguination.12 Noradrenaline reduces the need for continuous fluid infusion, which can result in tissue oedema and acute respiratory distress syndrome, reducing the water sodium load, which is beneficial during the secondary systemic inflammatory phase. A volume-sparing strategy based on vasopressor use with optimized blood pressure may help limit cerebral oedema and maintain high infusion pressure.13

Early administration of phenylephrine with crystalloid is associated with a higher survival rate, as shown by Al Spurgh et al.,14 although cardiac output is decreased. In our case, vasopressor infusion (adrenaline and noradrenaline) was primarily aimed at managing the cardiac arrest rather than treating haemorrhagic shock. Dobutamine infusion enhanced the cardiac output. The type of vasopressor and the precise timing of administration still need to be defined.1520 The first step to be considered in the management of haemorrhagic shock is fluid loading. The latest European guidelines21 for the management of haemorrhagic shock suggest the use of vasopressors (noradrenaline) to restore an adequate mean arterial pressure when fluid resuscitation therapy fails to restore blood pressure.

Coagulation was monitored by rapid intraoperative TEG to evaluate the global haemostatic process,2224 including thrombin activation, initial platelet activation, fibrin formation and fibrinolysis. The results were normal. Volume replacement with crystalloid, colloid or transfusion of red cell components leads to dilution coagulopathy.25 Fibrinogen is the first to reach a critical level of 1.0 g/l after a blood loss of 150%. Blood loss of 200% results in a 25% fall in other labile coagulation factors. It is essential that laboratory tests of coagulation are frequently monitored. We had initiated rapid TEG in the operating room.

Massive transfusion protocols specify a predefined ratio of red blood cells, fresh-frozen plasma/cryoprecipitate and platelet units (random donor platelets) in each pack to be transfused of 1 : 1 : 1.1720 This reduces the need for repeated communication with the blood bank and dependence on laboratory results, ensuring rapid and timely delivery of all blood components to facilitate resuscitation. We followed these guidelines. Bleeding was successfully controlled, and the patient stabilized, extubated and transferred to the ICU for post-cardiac arrest care.


Every hospital should have its own algorithms and guidelines to maintain adequate tissue perfusion and oxygenation with appropriate restoration of blood volume and haemoglobin levels. The judicious use of blood and blood components, preventing duplication and saving time, along with effective communication with laboratories and other supportive staff, is the key to success.

Thromboelastography measures the viscoelastic17 properties of blood throughout the entire haemostatic system, including platelet function and the fibrinolytic system. Rapid availability of results enables timely intervention.



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