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Interventional Case Record
Interventional Case Record
Emergency TIPSS in a case of acute variceal bleeding
Emergency TIPSS in a case of acute variceal bleeding
Contributed by : Salman Mapara
Contributed by : Salman Mapara
Introduction:
Introduction:
The transjugular intrahepatic portosystemic shunt (TIPSS) procedure involves angiographically guided creation of a connection between the hepatic vein and the intrahepatic portal vein that allows blood to flow from the portal vein to the inferior vena cava and back to systemic circulation with little resistance. Emergent TIPSS creation is a lifesaving procedure most often employed in the setting of acute variceal hemorrhage. Acute haemorrhage due to ruptured varices is a clinical emergency and if not adequately controlled, uncontrollable haematemesis can cause a patient’s death in 80% of cases. [1,2] TIPSS is recommended as “rescue TIPSS” treatment that is performed soon after the initial pharmacological and endoscopic treatment, within 72 hours - better, within the first 24 hours—of the start of the bleeding, a so-called “early TIPSS”. [3] Early non salvage TIPSS creation is an emerging indication in variceal hemorrhage and has shown promising results [4].
The transjugular intrahepatic portosystemic shunt (TIPSS) procedure involves angiographically guided creation of a connection between the hepatic vein and the intrahepatic portal vein that allows blood to flow from the portal vein to the inferior vena cava and back to systemic circulation with little resistance. Emergent TIPSS creation is a lifesaving procedure most often employed in the setting of acute variceal hemorrhage. Acute haemorrhage due to ruptured varices is a clinical emergency and if not adequately controlled, uncontrollable haematemesis can cause a patient’s death in 80% of cases. [1,2] TIPSS is recommended as “rescue TIPSS” treatment that is performed soon after the initial pharmacological and endoscopic treatment, within 72 hours - better, within the first 24 hours—of the start of the bleeding, a so-called “early TIPSS”. [3] Early non salvage TIPSS creation is an emerging indication in variceal hemorrhage and has shown promising results [4].
Case presentation:
Case presentation:
A 30 year old woman presented with complaints of hematemesis and melena with pain in the abdomen for three days. She is a known case of decompensated chronic liver disease with prior episodes of hematemesis that had been managed with three settings of oesophageal variceal ligation. The patient also had repeated episodes of yellowish discoloration of skin and sclera associated with malaise. Laboratory investigations showed Hb 6.5 gm%, fibroscan 43 kPa. She had a CTP-5A score, and a MELD score of 12.
A 30 year old woman presented with complaints of hematemesis and melena with pain in the abdomen for three days. She is a known case of decompensated chronic liver disease with prior episodes of hematemesis that had been managed with three settings of oesophageal variceal ligation. The patient also had repeated episodes of yellowish discoloration of skin and sclera associated with malaise. Laboratory investigations showed Hb 6.5 gm%, fibroscan 43 kPa. She had a CTP-5A score, and a MELD score of 12.
The patient was transfused three pints of blood. An upper gastrointestinal endoscopy showed grade II gastroesophageal varices GOV2/IGV1 with refractory post oesophageal variceal ligation - ulcer bleed. Subsequently, a Dannis Ella stent was placed in the distal oesophagus and GE junction region to control the bleeding. The patient had persistent symptoms despite endoscopic management and was then referred to us for further intervention.
The patient was transfused three pints of blood. An upper gastrointestinal endoscopy showed grade II gastroesophageal varices GOV2/IGV1 with refractory post oesophageal variceal ligation - ulcer bleed. Subsequently, a Dannis Ella stent was placed in the distal oesophagus and GE junction region to control the bleeding. The patient had persistent symptoms despite endoscopic management and was then referred to us for further intervention.
Porto hepatic Doppler was suggestive of chronic parenchymal disease of the liver with features of portal hypertension. Her triple phase CECT of the abdomen and pelvis showed nodular liver surface with caudate lobe hypertrophy consistent with liver cirrhosis. There were multiple periesophageal venous collaterals. (Figure 1a and 1b) , This was associated with mild splenomegaly and narrowed MHV and LHV confluence with intrahepatic collaterals. The Dannis Ella stent was seen in the distal third of oesophagus. (Figure 1c)
Porto hepatic Doppler was suggestive of chronic parenchymal disease of the liver with features of portal hypertension. Her triple phase CECT of the abdomen and pelvis showed nodular liver surface with caudate lobe hypertrophy consistent with liver cirrhosis. There were multiple periesophageal venous collaterals. (Figure 1a and 1b) , This was associated with mild splenomegaly and narrowed MHV and LHV confluence with intrahepatic collaterals. The Dannis Ella stent was seen in the distal third of oesophagus. (Figure 1c)
Figure 1a- Coronal CECT venous phase image showing Dannis Ella stent in the oesophagus and stomach ; the nodular liver with parenchymal changes and ascites .
Figure 1b- Axial CECT venous phase image showing Dannis Ella stent in the oesophagus with adjacent periesophageal venous collaterals and ascites . There are nodular changes in the liver parenchyma suggesting changes of chronic liver parenchymal disease with portal hypertension.
Figure 1c- Coronal CECT - venous phase image showing Dannis Ella stent in the oesophagus with adjacent periesophageal venous collaterals and splenomegaly suggesting changes of portal hypertension.
She underwent a rescue TIPSS procedure when measures by endoscopy and Dannis Ella stenting failed. Through a right common femoral artery access an arterio-porto gram was obtained. It showed the portal vein with intrahepatic bifurcation and its branching pattern.(figure 2)
She underwent a rescue TIPSS procedure when measures by endoscopy and Dannis Ella stenting failed. Through a right common femoral artery access an arterio-porto gram was obtained. It showed the portal vein with intrahepatic bifurcation and its branching pattern.(figure 2)
Figure 2 DSA image showing arterioportogram showing the main, right and left portal veins.
Interventional Technique:
Interventional Technique:
A right internal jugular venous access was obtained and through this access the right hepatic venous cannulation was done over terumo glidewire using a 4F H1 catheter. (figure 3a). Following this an AUS stiff wire access was obtained and the short sheath was exchanged for a10F long sheath. Using this sheath and AUS wire the Colapinto needle and a long Chiba needle were inserted and a tract from right hepatic vein to right portal vein was created. (Figure 3b)
A right internal jugular venous access was obtained and through this access the right hepatic venous cannulation was done over terumo glidewire using a 4F H1 catheter. (figure 3a). Following this an AUS stiff wire access was obtained and the short sheath was exchanged for a10F long sheath. Using this sheath and AUS wire the Colapinto needle and a long Chiba needle were inserted and a tract from right hepatic vein to right portal vein was created. (Figure 3b)
Figure 3a DSA image of right hepatic venogram done with 4FH1 catheter. Also seen is the Dannis Ella stent and NG tube
Figure 3b- DSA image of portal venous venogram done with 4F pigtail catheter (dotted line). Showing portal vein main, right and left branches
The tract was subsequently balloon dilatated. After this pigtail catheter angiogram was obtained (figure 4a and 4b) . This shows formation of an adequate track and dilated gastric varices near the portal venous end. Subsequently, a TIPSS nitinol hybrid stent wasplaced. Post stenting balloon plasty was done. Post plasty angiogram shows successful TIPSS placement with resolution of blood flow across the varices.(figure 4c)
The tract was subsequently balloon dilatated. After this pigtail catheter angiogram was obtained (figure 4a and 4b) . This shows formation of an adequate track and dilated gastric varices near the portal venous end. Subsequently, a TIPSS nitinol hybrid stent wasplaced. Post stenting balloon plasty was done. Post plasty angiogram shows successful TIPSS placement with resolution of blood flow across the varices.(figure 4c)
Figure 4a DSA image showing balloon plasty of hepatic tract between RHV and right portal vein.
Figure 4b- DSA image showing deployment of stent graft Nitinol over the AUS stiff wire.
Figure 4c Figure 4c- DSA image showing final post balloon plasty stent graft Nitinol connecting right hepatic vein and right portal vein.
Figure 5a- DSA image showing angiogram obtained from pigtail catheter before stent and plasty showing dilated left gastric vein and collaterals.
Figure 5b- DSA image showing angiogram taken post tips stenting (red arrow) showing the adequate opacification of tract and non visualisation of left gastric vein and collaterals.
Discussion:
Discussion:
Portosystemic shunts act as “release valves” to reduce the portal pressure; in the bargain, act as bypasses to normal liver flow. They thus represent an insufficient compensatory mechanism, not allowing for adequate reduction of portal pressure, but decrease hepatic portal-venous perfusion. [1,2] The hyperdynamic circulation and portal venous congestion attendant to longstanding liver cirrhosis contribute to the formation of oesophageal and gastric varices, particularly in the presence of a hepatic venous pressure gradient exceeding 10 mm Hg. [3] Oesophageal varices are historically located within the lower 5 cm of the distal oesophagus, gastric varices exist at locations which are demarcated by the Sarin classification system. Given the high prevalence of varices in liver cirrhosis, patients with this condition undergo screening endoscopy at the time of liver disease diagnosis [4,5].
Portosystemic shunts act as “release valves” to reduce the portal pressure; in the bargain, act as bypasses to normal liver flow. They thus represent an insufficient compensatory mechanism, not allowing for adequate reduction of portal pressure, but decrease hepatic portal-venous perfusion. [1,2] The hyperdynamic circulation and portal venous congestion attendant to longstanding liver cirrhosis contribute to the formation of oesophageal and gastric varices, particularly in the presence of a hepatic venous pressure gradient exceeding 10 mm Hg. [3] Oesophageal varices are historically located within the lower 5 cm of the distal oesophagus, gastric varices exist at locations which are demarcated by the Sarin classification system. Given the high prevalence of varices in liver cirrhosis, patients with this condition undergo screening endoscopy at the time of liver disease diagnosis [4,5].
Primary prophylaxis is initiated in patients with large varices, those with small varices and advanced liver disease, and those with varices demonstrating signs of bleeding on endoscopy (such as no pulsatile spurting, oozing, adherent clot, or a red wale sign).[4,6 and 7] . Non selective β-blockers have been shown to slow progression of variceal size, reduce the risk of hemorrhage, and improve mortality the use of carvedilol—a nonselective β-blocker with anti-α adrenergic properties. Endoscopic treatment, such as band ligation, is an effective option for patients with medium to large varices in whom pharmacologic therapy is contraindicated or poorly tolerated.[9]
Primary prophylaxis is initiated in patients with large varices, those with small varices and advanced liver disease, and those with varices demonstrating signs of bleeding on endoscopy (such as no pulsatile spurting, oozing, adherent clot, or a red wale sign).[4,6 and 7] . Non selective β-blockers have been shown to slow progression of variceal size, reduce the risk of hemorrhage, and improve mortality the use of carvedilol—a nonselective β-blocker with anti-α adrenergic properties. Endoscopic treatment, such as band ligation, is an effective option for patients with medium to large varices in whom pharmacologic therapy is contraindicated or poorly tolerated.[9]
The SX-Ella Danis stent is easy to deploy, safe and effective in achieving haemostasis in all patients and used the stent in patients who were poor risk candidates for TIPSS insertion or had contraindications for balloon tamponade. [8,10] The SX-Ella Danis stent has atraumatic edges and radiopaque markers at both ends and at the midpoint to assess its position by a plain chest X-ray. [11]. Retrieval loops with gold markers at both stent ends allow the endoscopic extraction of the stent with a specifically designed system. [7,8,9] The stent can be positioned for 7-14 days, thereby giving adequate time for the patient to fully recover from the bleeding, unlike the Sengstaken-Blakemore tube, which needs decompression and removal within 24 hours. Advantages of the SX-Ella Danis stent includes the presence of a security pressure valve that minimizes the risk of oesophageal perforation. Early institution of an oral diet is possible with lowered risk of aspiration during subsequent endoscopy.[9]
The SX-Ella Danis stent is easy to deploy, safe and effective in achieving haemostasis in all patients and used the stent in patients who were poor risk candidates for TIPSS insertion or had contraindications for balloon tamponade. [8,10] The SX-Ella Danis stent has atraumatic edges and radiopaque markers at both ends and at the midpoint to assess its position by a plain chest X-ray. [11]. Retrieval loops with gold markers at both stent ends allow the endoscopic extraction of the stent with a specifically designed system. [7,8,9] The stent can be positioned for 7-14 days, thereby giving adequate time for the patient to fully recover from the bleeding, unlike the Sengstaken-Blakemore tube, which needs decompression and removal within 24 hours. Advantages of the SX-Ella Danis stent includes the presence of a security pressure valve that minimizes the risk of oesophageal perforation. Early institution of an oral diet is possible with lowered risk of aspiration during subsequent endoscopy.[9]
Differentiation between acute variceal hemorrhage and other sources of upper gastrointestinal bleeding in the cirrhotic patient is an important consideration, as this population experiences nontrivial rates of peptic ulcer disease. Patients with acute variceal hemorrhage often present with hematemesis or melena, and variable states of hemodynamic stability will often yield a history of liver cirrhosis, portal hypertension, and/or GEV. Upon confirmation of acute variceal hemorrhage, treatment aims to achieve haemostasis, prevent early rebleeding, and minimize 6-week mortality. TIPSS usually achieves a one-time, immediate decompression of the varices. The transjugular intrahepatic portosystemic shunt (TIPSS) procedure is a minimally invasive nonsurgical method of achieving portal decompression to treat some of the major complications of portal hypertension. [3,4,6]
Differentiation between acute variceal hemorrhage and other sources of upper gastrointestinal bleeding in the cirrhotic patient is an important consideration, as this population experiences nontrivial rates of peptic ulcer disease. Patients with acute variceal hemorrhage often present with hematemesis or melena, and variable states of hemodynamic stability will often yield a history of liver cirrhosis, portal hypertension, and/or GEV. Upon confirmation of acute variceal hemorrhage, treatment aims to achieve haemostasis, prevent early rebleeding, and minimize 6-week mortality. TIPSS usually achieves a one-time, immediate decompression of the varices. The transjugular intrahepatic portosystemic shunt (TIPSS) procedure is a minimally invasive nonsurgical method of achieving portal decompression to treat some of the major complications of portal hypertension. [3,4,6]
The indications to perform a TIPSS procedure can be an elective or emergency setting. The refractory ascites to diuretic therapy and secondary prophylaxis of variceal hemorrhage are the indications for elective TIPSS. While acute uncontrolled variceal bleeding is the principal indication of an emergency TIPSS.[1,2,3] Unfortunately, TIPSS is associated with a significantly higher rate of development of hepatic encephalopathy (HE) than standard therapy in the management of oesophageal varices. Due to this drawback, many advocate that TIPS be used predominately as a backup to endoscopic therapy for secondary prophylaxis of variceal bleeding.
The indications to perform a TIPSS procedure can be an elective or emergency setting. The refractory ascites to diuretic therapy and secondary prophylaxis of variceal hemorrhage are the indications for elective TIPSS. While acute uncontrolled variceal bleeding is the principal indication of an emergency TIPSS.[1,2,3] Unfortunately, TIPSS is associated with a significantly higher rate of development of hepatic encephalopathy (HE) than standard therapy in the management of oesophageal varices. Due to this drawback, many advocate that TIPS be used predominately as a backup to endoscopic therapy for secondary prophylaxis of variceal bleeding.
Indications for TIPS related to variceal bleeding [4]--
Indications for TIPS related to variceal bleeding [4]--
Indications Role of TIPS
Indications Role of TIPS
1 Secondary prophylaxis of variceal bleeding. Rescue therapy
1 Secondary prophylaxis of variceal bleeding. Rescue therapy
2 Acute variceal bleeding. Rescue therapy
2 Acute variceal bleeding. Rescue therapy
3 Portal hypertensive gastropathy. Rescue therapy
3 Portal hypertensive gastropathy. Rescue therapy
4 Recurrent acute variceal bleeding. First-line therapy
4 Recurrent acute variceal bleeding. First-line therapy
The pre-procedural work-up must include: a clinical evaluation of the patient’s life expectancy, as well as the patient’s hemodynamic status, respiratory condition, and mental state; laboratory tests, particularly regarding the liver function, coagulation status, and kidney function; a recent and valid diagnostic imaging study (usually a triphasic contrast-enhanced CT scan or, at least, a Doppler ultrasound examination) to assess the patency of the portal vein and of the hepatic veins, and to exclude the presence of any liver lesion that might prevent the creation of the porto-systemic shunt.[6,8,10]
The pre-procedural work-up must include: a clinical evaluation of the patient’s life expectancy, as well as the patient’s hemodynamic status, respiratory condition, and mental state; laboratory tests, particularly regarding the liver function, coagulation status, and kidney function; a recent and valid diagnostic imaging study (usually a triphasic contrast-enhanced CT scan or, at least, a Doppler ultrasound examination) to assess the patency of the portal vein and of the hepatic veins, and to exclude the presence of any liver lesion that might prevent the creation of the porto-systemic shunt.[6,8,10]
TIPSS creation commonly involves the formation of a tract between the right hepatic vein and right portal vein. After stent-graft deployment, the shunt tract is dilated incrementally with an 8- to 10-mm balloon to a target porto systemic gradient 12mmHg.[1,2] The porto systemic gradient may be calculated once successful portal venous access has been achieved. Importantly, balloon tamponade devices need to be deflated after shunt creation ensure variceal decompression and to allow catheter access to varices if embolization or obliteration is to be pursued.
TIPSS creation commonly involves the formation of a tract between the right hepatic vein and right portal vein. After stent-graft deployment, the shunt tract is dilated incrementally with an 8- to 10-mm balloon to a target porto systemic gradient 12mmHg.[1,2] The porto systemic gradient may be calculated once successful portal venous access has been achieved. Importantly, balloon tamponade devices need to be deflated after shunt creation ensure variceal decompression and to allow catheter access to varices if embolization or obliteration is to be pursued.
In the post-TIPSS period, the acute variceal hemorrhage patient is generally monitored in the intensive care unit to monitor for hemodynamic stability, resolution of hemorrhage, TIPS-related adverse events, and neurological signs of HE. Alongside monitoring nasogastric tube output, serial haemoglobin and haematocrit values maybe obtained to monitor cessation of hemorrhage. A follow-up liver panel and coagulation panel a real obtained the day after the procedure to assess hepatic function. [5,6,7] TIPS patency may be monitored with serial Doppler ultrasound at 1,3 and 6-months post procedure. Post-TIPSS encephalopathy occurs more commonly in cirrhotic patients with refractory ascites than in those undergoing TIPSS for variceal bleeding, suggesting that patients with severe cirrhosis are more likely to experience encephalopathy. This factor should be considered in the selection of patients for the TIPSS procedure. [9,10] The main risk factors for developing HE include age > 65 years, Child score > 12, prior history of hepatic encephalopathy, placement of a large diameter stent (> 10 mm), and low portal pressure gradient (< 5 mm Hg). The risk of HE may outweigh the potential benefit of the procedure in patients possessing these risk factors[4,8].
In the post-TIPSS period, the acute variceal hemorrhage patient is generally monitored in the intensive care unit to monitor for hemodynamic stability, resolution of hemorrhage, TIPS-related adverse events, and neurological signs of HE. Alongside monitoring nasogastric tube output, serial haemoglobin and haematocrit values maybe obtained to monitor cessation of hemorrhage. A follow-up liver panel and coagulation panel a real obtained the day after the procedure to assess hepatic function. [5,6,7] TIPS patency may be monitored with serial Doppler ultrasound at 1,3 and 6-months post procedure. Post-TIPSS encephalopathy occurs more commonly in cirrhotic patients with refractory ascites than in those undergoing TIPSS for variceal bleeding, suggesting that patients with severe cirrhosis are more likely to experience encephalopathy. This factor should be considered in the selection of patients for the TIPSS procedure. [9,10] The main risk factors for developing HE include age > 65 years, Child score > 12, prior history of hepatic encephalopathy, placement of a large diameter stent (> 10 mm), and low portal pressure gradient (< 5 mm Hg). The risk of HE may outweigh the potential benefit of the procedure in patients possessing these risk factors[4,8].
Conclusion:
Conclusion:
Patients with decompensated liver cirrhosis and acute variceal hemorrhage require multifaceted, multidisciplinary treatment. Emergent TIPS creation successfully ameliorates acute VH when standard medical and endoscopic management are unsuccessful and commonly used as a nonsurgical “bridge” procedure. Liver transplantation is the goal for many patients with advanced liver dysfunction. Even though emergency TIPS has high early mortality rate and the higher incidence of complication, it is helpful in stabilizing patients until a suitable donor organ is available.
Patients with decompensated liver cirrhosis and acute variceal hemorrhage require multifaceted, multidisciplinary treatment. Emergent TIPS creation successfully ameliorates acute VH when standard medical and endoscopic management are unsuccessful and commonly used as a nonsurgical “bridge” procedure. Liver transplantation is the goal for many patients with advanced liver dysfunction. Even though emergency TIPS has high early mortality rate and the higher incidence of complication, it is helpful in stabilizing patients until a suitable donor organ is available.
References:
References:
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