| Abstract|| |
Postoperative bleeding is a concern for all patients undergoing heart surgery, which could be due to surgical causes or coagulation disorder. The patients at risk for coagulopathy include those patients with complex or prolonged procedures, those exposed to preoperative anticoagulants and, to a lesser extent, patients with a preoperatively elevated prothrombin time and activated clotting time. However, intraabdominal bleeding after cardiac surgery is rare (0.3-2%). As the mortality rate of patients exposed to these complications is high (11-59%), timely recognition and prompt management is vital for patient's safety and for avoidance of postoperative complications. Here, we present a case of free intraabdominal hemorrhage as sequelae of pacing wire insertion in open heart surgery and its successful management.
Keywords: Abdominal complication, intraabdominal hemorrhage, open heart surgery, pacing wire induced complications
|How to cite this article:|
Chowdhry V, Mishra B, Rao K. Iatrogenic hemorrhage from left umbilical vein after cardiac surgery: An unusual complication. Ann Card Anaesth 2012;15:141-3
|How to cite this URL:|
Chowdhry V, Mishra B, Rao K. Iatrogenic hemorrhage from left umbilical vein after cardiac surgery: An unusual complication. Ann Card Anaesth [serial online] 2012 [cited 2019 Jul 15];15:141-3. Available from: http://www.annals.in/text.asp?2012/15/2/141/95079
| Introduction|| |
Our patient was a 34-year-old woman who underwent mitral valve replacement due to severe mitral stenosis (MS) and severe mitral regurgitation (MR). Free intraabdominal hemorrhage occurred on the day of surgery. During exploratory laparotomy, it was determined that the hemorrhage was from a vein in the free border of the falciform ligament of the liver. The complication was repaired surgically. To our knowledge, intraabdominal hemorrhage due to pacing wire-induced injury after open heart surgery has never been reported before. We report the case and present our experience regarding the management of this unusual complication.
| Case Report|| |
A thin-built, 35-year-old woman, known case of rheumatic heart disease with severe MS and severe MR, was admitted to our hospital with recurrent congestive heart failure in NYHA class IV, with bilateral pedal edema, raised jugular venous pressure (JVP) and enlarged liver. Transthoracic echocardiography (TTE) revealed severe MS, severe MR with moderate tricuspid regurgitation (TR) and pulmonary arterial hypertension (PAH) of 65 mmHg with ejection fraction of 50%. Abdominal ultrasound revealed moderate ascitis and congestive hepatomegaly with dilated intrahepatic veins. The patient's condition was optimized with diuretics, dobutamine, antibiotics and mitral valve replacement (MVR), and tricuspid valve repair was planned. A thorough preanesthetic check-up was performed and the patient was posted for MVR. Through a standard median sternotomy, after full heparinization and optimal activated clotting time, cardiopulmonary bypass was instituted with ascending aortic and bicaval cannulation. There were no difficulties during aorto-bicaval cannulation and cardiopulmonary bypass. Cardiac arrest was achieved with blood cardioplegic solution. Through a transseptal approach MVR was performed with a 31-mm mechanical prosthesis (St. Jude Medical Inc. Minnesota, USA) and tricuspid valve annuloplasty was carried out. The perioperative transesophageal echocardiogram (TEE) showed good prosthetic valve function with no paravalvular leak and mild tricuspid regurgitation. The patient came out of bypass uneventfully with moderate dose of milrinone and adrenaline. The heparin was neutralized by protamine. The aortic cross-clamp time was 56 min and the total bypass time was 78 min. After securing the bleeding sites, an epicardial pacing wire was taken on the anterior wall of the right ventricle at a bare muscular area and the other end was taken out from below the rectus sheath in the midline on to the abdominal skin and was secured there. Two units of fresh frozen plasma (FFP) and two units of platelet concentrate were transfused before chest closure as per the institutional protocol. Two chest tubes were placed, one in the mediastinum and the other in the pericardium. The chest was closed and the patient was transferred to the intensive care unit (ICU) and put on ventilator with stable hemodynamics. Immediately after shifting the patient to the ICU, the blood pressure was 116/68 mmHg, central venous pressure was 10 cm of water, in sinus rhythm with heart rate of 78/min with moderate inotropic support and hemoglobin of 9.2 gm%.
After 4 h of shifting to ICU, the total drainage through the chest tubes was 100 ml and the hemoglobin was 8.4 gm%. The blood pressure was 100/50-90/44 mmHg. The supports were marginally increased. After two more hours, the systolic blood pressure was around 80-90 mmHg, central venous pressure of 4 mmHg and hemoglobin dropped down to 7.5 gm% with insignificant drainage through the chest tubes. TEE was performed urgently for suspected cardiac tamponade and aortic dissection, but there were no signs of hemorrhage or dissection and the heart was normally contracting with no regional wall motion abnormality. Then, we performed an abdominal ultrasound, which revealed some peritoneal collection, but we ignored that thinking it to be ascitic fluid. Hence, more aggressive fluid infusion and inotropic supports were started. After all these interventions, the arterial systolic blood pressure was only 65-75 mmHg and the hemoglobin dropped down to 6.8 gm% one more hour later. At that time, we noticed abdominal distension and, therefore, a repeat abdominal ultrasonography was performed that revealed perihepatic and peritoneal free fluid and needle aspiration revealed blood in the peritoneal cavity, on which basis an urgent laparotomy was planned. During exploratory laparotomy, the systolic blood pressure was maintained around 90 mmHg with the help of colloidal solutions, crystalloids and inotropes and vasopressors without any blood transfusion. About 1.5 L of blood and clots were removed from the abdomen. The blood was coming from a hole in the vein present in the free edge of the falciform ligament, and there was no peritoneal defect other than this. Both the drains and the pacing wire seemed to be preperitoneal. We repaired the defect with a poly-propylene suture. Immediately after securing the bleeding point, one unit of packed red cells and two units of FFP were transfused. A drainage tube was inserted, the abdomen was closed and the patient was transferred to the ICU with a blood pressure of 92/46 mmHg, hemoglobin of 6.8 gm% with high inotropic and vasopressor supports. Over the next 12 h, there was no further bleeding, systolic blood pressure remained stable (around 100-110 mmHg) and urine output was marginally low, at 0.5-0.8 ml/h, with furosemide infusion at a rate of 5 mg/h. As the hemodynamics were stable, the vasopressor and inotropic supports were tapered to moderate doses. Over the next 36 h, two more units of packed red cells were transfused and the patient was extubated on the second postoperative day, with hemoglobin of 8.2 gm% and good urine output and creatinine of 1.3 mg%. The patient was hemodynamically stable; rest of the postoperative course was uneventful and she was discharged on the ninth postoperative day.
| Discussion|| |
Bleeding is a known complication of cardiac surgery. The usual site of bleeding is the operating site or the chest. Hence, when bleeding occurs, a cardiac unit first thinks about the operative zone.
In our case, there were no bleeding from the chest, as evident by TEE, but decreasing blood pressure and serial drop in hemoglobin forced us to find out the site of bleeding. Therefore, we performed an abdominal ultrasound, which revealed some collection of the peritoneal fluid, but we could not arrive at any diagnosis as this patient had ascitis in the preoperative period, adding to a diagnostic dilemma. Further, there was no obvious reason for the patient to bleed intraabdominally. After a few hours, when we noticed the abdominal distension, we went for peritoneal tapping and confirmed the diagnosis, which lead to exploratory laparotomy.
After opening the abdomen, venous bleeding was found from a hole in a patent vein present in the free margin of the falciform ligament. This was a rare case of patent or recanalyzed umbilical vein, which was punctured by the pacing wire needle. During embryologic development, there are two umbilical veins, left and right, which drain blood from the placenta to the heart.  The right umbilical vein regresses and, under normal circumstances, is completely obliterated during the second month of development.  The left umbilical vein persists and delivers blood from the placenta to the developing fetus. Within 1 week of birth, the infant's umbilical vein is completely obliterated, and forms the ligamentum teres in the adult. However, with the development of portal hypertension, the umbilical vein may recanalize and serve as a collateral route.  The remnant of the umbilical vein, the ligamentum teres, is seen on a high percentage of normal ultrasonograms. In patients with portal hypertension, the umbilical vein often reopens as a collateral vessel and can be visualized sonographically. Recognition of a patent umbilical vein is important, as it currently is the only ultrasonographic finding specific for portal hypertension.  In this case, our ultrasonographer had missed this finding in the preoperative testing.
In conclusion, intraabdominal hemorrhage, although rare,  is a possible complication of open heart surgery, which carries a high mortality. , In lean and thin patients, our suggestion is not to pass the pacing wires below the rectus sheath, particularly in the midline. Because of the deranged coagulation profile in a patient of cardiac surgery, a simple unprotected needle hole may give rise to catastrophic intraabdominal hemorrhage.
Following cardiac surgery, if a patient requires an excess of volume to maintain the hemodynamics in a setting of modest mediastinal bleeding, one should suspect third-space blood loss. The importance of intraabdominal bleeding following cardiac surgery may be missed or underestimated because, as a routine practice, the chest is frequently evaluated for evidence of any blood loss and give less importance to abdominal bleeding. However, to avoid this diagnostic dilemma, we suggest that in patients having ascitis preoperatively, a baseline abdominal girth should be measured after surgery so that one may not miss increasing ascitis or intraabdominal bleeding.
| References|| |
|1.||Yen Ho S, Nicholson AG. Development of Thorax. In: Susan S, editor. Grey's Anatomy, The Anatomical Basis of Clinical Practice. 40 th ed. Spain: Elsevier; 2008. p. 1026. |
|2.||Young TH, Lee HS. Images in clinical medicine. Recanalized umbilical vein. N Engl J Med 2007;357:e17 |
|3.||Glazer GM, Laing FC, Brown TW, Gooding GA. Sonographic demonstration of portal hypertension: The patent umbilical vein. Radiology 1980;136:161-3. |
|4.||D'Ancona G, Baillot R, Poirier B, Dagenais F, de Ibarra JI, Bauset R, et al. Determinants of gastrointestinal complications in cardiac surgery. Tex Heart Inst J 2003;30:280-5. |
|5.||Zacharias A, Schwann TA, Parenteau GL, Riordan CJ, Durham SJ, Engoren M, et al. Predictors of gastrointestinal complications in cardiac surgery. Tex Heart Inst J 2000;27:93-9. |
|6.||Ohri SK, Desai JB, Gaer JA, Roussak JB, Hashemi M, Smith PL, et al. Intra-abdominal complications after cardiopulmonary bypass. Ann Thorac Surg 1991;52:826-31. |
Department of Cardiac Anesthesiology and Critical Care, Aditya Care Hospital, Bhubaneswar 751 014, Orissa
Source of Support: None, Conflict of Interest: None