Inferolateral ST-segment elevation with use of Sengstaken-Blakemore tube for variceal bleeding during orthotopic liver transplantation

Abstract

Oesophageal balloon tamponade tubes are a rare cause of ST-segment elevation (STE), thought to result from extrinsic compression of coronary arteries. This case describes STE following the use of a Sengstaken-Blakemore tube (SBT) under traction for management of bleeding oesophageal varices during orthotopic liver transplantation. This case is the first to report a significant troponin rise with STE indicative of myocardial injury following the use of SBT. Interestingly, we found that releasing traction from the SBT resulted in resolution of STE within minutes, suggesting that SBT traction may reversibly impede coronary perfusion. We recommend vigilant monitoring of patients following SBT insertion and for clinicians to consider that SBT traction may impair coronary perfusion and result in myocardial injury in patients without pre-existing coronary artery disease.

Background

Acute haemorrhage from oesophageal varices is commonly treated first with pharmacotherapy such as terlipressin or octreotide, followed by endoscopy.¹ Oesophageal balloon tamponade tubes such as Sengstaken-Blakemore tube (SBT) may be used as a rescue therapy following unsuccessful endoscopic and pharmacological treatment. SBT are a flexible plastic tube containing a gastric aspiration port and oesophageal and gastric balloons that can be inflated after insertion into the stomach via the oral or nasal cavity. Gastric balloon inflation and traction of SBT provides compression at the gastro-oesophageal junction (GOJ) to tamponade haemorrhaging varices. SBT are associated with major adverse events in up to 60% of patients including aspiration pneumonia and oesophageal rupture,² yet they remain highly effective in controlling variceal haemorrhage.³ Oesophageal balloon tamponade tubes are thought to be a rare cause of ST-segment elevation (STE).⁴ A recent alternative to SBT includes self-expandable, oesophageal metal stents which have shown efficacy in controlling bleeding from oesophageal varices.^{2 5}

This case exhibits a rare complication of the use of SBT resulting in an outcome that has not been previously described in medical literature.

Case presentation

A 61-year-old man underwent orthotopic liver transplantation for decompensated idiopathic liver cirrhosis. His liver disease had been complicated by ascites, portal hypertension and episodes of encephalopathy. Pretransplant, he had developed decompensated cirrhosis with bilirubin >800 μmol/L and a model for end-stage liver disease score of 35. Other complications included hepatorenal syndrome requiring treatment with terlipressin, and coagulopathy with an International Normalised Ratio (INR) of 2.8 and platelets of 75×10⁹/L. Endoscopy performed 6 months prior to liver transplantation had revealed grade 3 varices at the GOJ which had been treated with variceal banding. As part of preoperative assessment, a dobutamine stress echocardiogram showed no evidence of inducible ischaemia, ECG showed normal sinus rhythm and the patient had no significant cardiac risk factors or history of coronary artery disease.

During liver transplantation surgery, the patient had a marked hyperdynamic circulation with low systemic vascular resistance (SVR) and high cardiac output. This required treatment with norepinephrine and vasopressin infusions to maintain normal values for systolic and mean arterial blood pressures. Despite this, diastolic blood pressure remained low, in the range of 30–40 mm Hg.

During the anhepatic phase of liver transplantation, a large volume of dark red blood briskly drained from the nasogastric tube which had been routinely placed without trauma following induction of anaesthesia. Intraoperative oesophagogastroscopy was performed by the attending gastroenterologist, revealing a large quantity of fresh blood and clot in the oesophagus and the stomach with active bleeding evident at the GOJ. Bleeding persisted despite vasopressin infusion and treatment of coagulopathy using fresh frozen plasma, pooled platelets and cryoprecipitate. Limited endoscopic views due to haemorrhage precluded the use of targeted endoscopic intervention such as banding or sclerotherapy; therefore, a SBT was inserted to tamponade the haemorrhage. Following inflation of the gastric balloon with 250 mL of air, the SBT was placed on traction in order to maintain compression at the GOJ. A 1 L bag of saline suspended by an intravenous pole was used as a weight for traction. Drainage of blood from the SBT gastric aspiration port slowed substantially following this intervention. As ~3 L of blood had been drained from the stomach, it was necessary to restore the circulating blood volume using packed red blood cells. Haemoglobin was maintained >70 g/L and mean arterial blood pressure was maintained >60 mm Hg.

During the anhepatic phase, after variceal bleeding had slowed considerably with SBT insertion, STE in the inferior and lateral ECG leads was noted on the patient monitor (figure 1). We considered that the SBT was potentially implicated and trialled transiently taking the SBT off traction. This action resulted in rapid and marked improvement of STE. Consequently, we downsized the traction weight on the gastric balloon to a 500 mL bag of saline with modest improvement. As STE persisted and as the blood loss from the variceal bleed had markedly reduced, the SBT was taken off traction completely. This action resulted in rapid resolution of the STE over the course of a few minutes. Variceal bleeding did not resume, and traction was left off. Furthermore, the portal venous system had been decompressed with release of the portal vein clamp and reperfusion of the new liver, making further variceal bleeding less likely. The intraoperative course was otherwise unremarkable.

Figure 1.

Intraoperative electrocardiographic monitoring shows ST-segment elevation during anhepatic stage of liver transplantation after insertion of SBT for variceal bleeding. SBT, Sengstaken-Blakemore tube.

Outcome and follow-up

On postoperative day 1, there was a rise in the patient’s troponin T peaking at 400 ng/L. This represented a 27-fold increase over the upper reference limit value of 15 ng/L. The troponin normalised over the next 48 hours. Relook oesophagastroscopy demonstrated that there was no further bleeding and that the varices had collapsed. The patient developed acute renal failure requiring 2 days of haemodiafiltration commenced on postoperative day 2. Following this, he went on to recover well and was discharged with stable liver function following a period of inpatient rehabilitation.

Discussion

Variceal bleeding was likely to have been precipitated by the acute rise in portal venous pressure that occurs with surgical cross-clamping of the portal vein. Massive bleeding from varices complicating portal vein cross-clamping has been well described during liver transplantation.^{6 7} Both SBT and intraoperative banding have been successfully used in this setting to achieve haemostasis.^{8 9}

End-stage liver disease is associated with circulatory changes typified by a hyperdynamic circulation with low SVR and high cardiac output.¹⁰ Low SVR in cirrhosis is primarily mediated by nitric oxide,¹¹ which preferentially venodilates, contributing to low diastolic blood pressure despite optimisation with vasopressors and fluid administration.

Left ventricular coronary perfusion pressure (LVCPP) is the pressure gradient that drives coronary perfusion. It is defined as the aortic root diastolic pressure minus the left ventricular end-diastolic pressure. With coronary flow preferentially occurring in diastole and depending on LVCPP, diastolic blood pressure is a key determinant of coronary perfusion.¹² The subendocardium has the greatest dependence on diastolic perfusion as flow to the subendocardium is limited during systole.¹³

We theorise that pressure exerted by the gastric balloon of the SBT under traction caused transient interruption of blood flow in branches of the coronary circulation located on the basal surface of the heart, that is, branches of the right coronary and left circumflex arteries. We surmise that this effect may have been magnified by low diastolic blood pressure, as diastolic coronary flow may be less able to overcome external compression from the gastric balloon. Furthermore, the effect of anaesthesia on diaphragmatic function may render the coronary circulation on the basal surface of the heart particularly susceptible to the external compressive force exerted by the gastric balloon under traction, as normal diaphragmatic tone and contraction may provide countertraction in the non-anaesthetised patient.

ST-segment changes associated with the use of SBT have previously been described in a case report in which STE was thought to have occurred due to external compression of the heart from a combination of gastric distension and traction applied to the SBT.⁴ In this case report, gastric distension had resulted from accumulation of gastric blood that, once aspirated, led to rapid resolution of the ST changes with only a small rise in troponin. Other case reports have shown STE associated with intra-abdominal pathology including stomach distension,¹⁴ hiatal hernia^15–19 or diaphragmatic hernia.²⁰ Of these, four cases^{14–16 18} reported normal troponin measurements, one case¹⁷ reported mild troponin elevation with no change on serial troponins and two cases^{19 20} did not report troponin.

This is the first case report that describes STE associated with a substantial troponin rise following SBT use for bleeding varices. We postulate that the external compressive force from SBT traction in addition to low diastolic blood pressure in the context of a hyperdynamic circulation resulted in significant myocardial ischaemia in a patient with no previous evidence of coronary artery disease.

Learning points.

• External coronary compression is a rare complication of the use of a Sengstaken-Blakemore tube (SBT).

• SBT traction may precipitate ST-segment elevation (STE) and myocardial injury even in a patient without existing coronary artery disease.

• Release of SBT traction may rapidly improve myocardial perfusion and resolve STE within minutes.