Case Presentation by Dr. Aditee Jodhani
CC: I’m vomiting blood
55 year old female with past medical history of HTN, DM, cirrhosis, IVDA and alcohol abuse presents to the ED for hypotension associated with several episodes of hematemesis. The patient states that 3-4 days ago she began having bloody stools and generalized weakness. She approximates two liquid BMs per day that are mixed blood. She also describes being nauseated and had 2 episodes of hematemesis over the last 3 days. Pt denies any symptoms of fever or abdominal pain.
PMH: alcoholism, IVDA, hep C, cirrhosis, anemia, PUD, internal hemorrhoids
PSH: Last colonoscopy and EGD was 10/23/12 which showed internal hemorrhoids and a large duodenal bulbar ulcer respectively. IVC filter placed during same admission
Medications: acetaminophen/hydrocodone, docusate, iron, folic acid, bactrim and thiamine but patient has been noncompliant
Family History: denies DM and HTN
Social History: Denies smoking, positive for alcohol and heroin use
Vitals: P105, BP94/66 T36.2 (oral) R14
Gen: slightly lethargic
Head: Normocephalic, atraumatic
Eyes: Pupils equal, round and reactive to light. No sclera icterus
ENT: Mucous membranes slightly dry. Dry blood seen around her mouth.
Neck: is supple. Trachea midline. No JVD.
Respiratory: Normal respiratory effort. Good breath sounds heard bilaterally.
Cardiovascular: Regular rate and rhythm, S1 and S2 are auscultated, no murmurs, rubs or gallops. Pulses palpable in the lower extremities
Abdomen: Soft, nontender, nondistended. +BS. No rebounding or guarding. Was unable to palpate liver edge, no ascites present.
Musculoskeletal: Full range of movement in all extremities. Cap refill ❤ sec in all four extremities.
Skin: Warm and dry. No rashes or lesions.
Neurologic: Alert and orient to person, and time. Cranial nerves II-VII intact. Patient is lethargic, does answer questions, but is slow to respond. Per sister at bedside, patient is not at baseline.
Electrolytes: 142/4.7/110/22/12/1.6 anion gap 10, glucose 89
Coag: INR 1.29 PT 13.4 PTT 33
LFTs: AST: 75 ALT: 45 alk P: 141 lipase 269, ammonia 122, albumin 2.0, bilirubin total 1.5, bilirubin direct 1.1
EKG: ventricular rate of 100 beats per minute. Axis is normal. PR interval is 122 milliseconds. QRS duration is 72 milliseconds. QTC is 410 milliseconds. No acute ST or T-wave abnormalities seen. There is good R wave progression. Twelve-lead ECG is interpreted as sinus rhythm with no evidence of acute ST-segment elevation MI.
While in the ED the patient had three more bloody bowel movements and one episode of hematemesis. The patient refused NGT placement. She was given antiemetics, and started on a pantoprazole drip. She received 1 unit of PRBCs and was given 2 L of fluids. The surgery service was consulted. Due to patient’s PMH of chronic alcohol abuse there was concern that the hematemesis was caused by esophageal varices.
1.) What prophylactic medication is recommended for cirrhotic patients with confirmed varices to prevent bleeding?
2.) In addition to a pantoprazole drip, what other medication is important to start in patients with a history of cirrhosis and have an active GI bleed?
3.) In the above clinical scenario, what is the patient’s Child’s score and class at admission?
a.)2; class A
b.)8; class B
c.)10; class B
d.)15; class C
Discussion & Answers:
1.)A; Cirrhotic patients with diagnosed esophageal varices should be started on beta blockers, specifically propranolol. Beta blockers reduce the likelihood of acute bleeding as well as ascites, SBP, hepatic encephalopathy and hepatorenal syndrome. Nonselective beta-blockers prevent bleeding in more than half of patients with medium or large varices. Along with propranolol patients can also be started on isosorbide mononitrate. However not all patients respond to pharmacological treatment and other interventions should be considered (discussed below).
Resources: Abraldes, Tarantino, Turnes, Bosch. Hemodynamic response to pharmacological treatment of portal hypertension and long-term prognosis of cirrhosis. Hepatology. 30 DEC 2003 DOI: 10.1053/jhep.2003.50133
2.)C; In addition to protonix, an octreotide drip should also be started. The mechanism of action of octreotide is not completely clear. It is believed to reduce portal pressure and splanchnic blood flow. Another alternative medication is vasopressin, but is used less frequently due its effect of worsening coronary ischemia. A new drug similar to vasopressin but with less side effect is terlipressin it is a somatostatin analogue that also acts to reduce portal hypertension through splanchnic vasoconstriction. A study done out of Japan from 2009 showed equal efficacy of terlipressin to octreotide and reduced hospital stay, but there was no clinical improvement.
Resource: Terlipressin vs. Octreotide in Bleeding Esophageal Varices as an Adjuvant Therapy with EBL: A randomized double-blind Placebo-controlled Trial. The American Journal of Gastroenterology 2009. 104:617-623.
3.)B; 8; class B. Bilrubin 1.5, albumin 2.0, INR <1.29, physical exam no ascites, mild hepatic encephalopathy -pt not at her baseline per family but can still respond to questioning, ammonia 122.
||One year survival
||Two year survival
Pathophysiology of varices: Figure 1
Hepatic cirrhosis causes increased resistance and thus increased pressure (portal hypertension) in the portal vein that leads to backup of blood in the tributaries, (eg inferior mesenteric vein, periumbilical veins, gastroesophageal veins, and superior mesenteric vein). The gastroesophageal vessels are located in an area with little supporting tissue and easily become distended and more likely to bleed. In the setting of worsening liver failure and associated coagulopathy, bleeding is significant risk in these patients.
Some common signs on physical exam consistent with portal hypertension are gynecomastia, caput medusae, ascities, and bilateral lower extremity swelling.
Unfortunately esophageal varices cannot be identified on physical exam; they are diagnosed by endoscopy. Over 70% of cirrhotic patients with UGI bleeding is thought to be due to esophageal varices. Therefore, all cirrhotic patients with an UGI bleed should be considered variceal bleeders until proven otherwise. These patients have a mortality of 16% at presentation. Classically, patients with varices present with melana or hematochezia as well as hematemesis. Initial vital signs are prognostic. Mortality approaches 30% in patients with signs of shock or their SBP is <100mmHg or HR is >100bpm at presentation.
Workup: Addressing the ABCs is critical. Early intubation is recommended in order to decrease aspiration and facilitate optimal endoscopy, especially in patients with decreased mental status caused by hepatic encephalopathy. These patients need good intravenous access, 2- large bore IVs or cordis catheter.
In addition to routine labs, coagulation studies are helpful in determining whether or not the patient has liver disease-induced coagulopathy. It is also recommended to obtain, blood cultures, troponin and lactic acid. A hemoglobin less than 10g/dl is associated with a poorer prognosis in patients. It is important to obtain an ECG. One study indicated that over 50% of patients admitted to the ICU for GI hemorrhage had evidence of cardiac injury. A nasogastric tube should be placed. There is unfounded concern that placing an NG tube will lead to increased bleeding in patients with varices. NGT placement is important to prevent the risk of aspiration and also can be used to perform a NGT lavage to help determine if the bleed is proximal to the duodenum and if it is still active.
Although lavage is helpful for identifying the location of the bleed, a negative lavage cannot rule out a GI bleed. Do not use guaiac cards, to test aspirate for blood, they are inaccurate.
Patient should be transfused with PRBCs to keep hemoglobin above 8g/dL. In coagulopathic patients, fresh frozen plasma and platelets can be transfused. Over-transfusion can lead to worsening portal hypertension and does not reliably correct coagulopathy. FFP should be transfused when there is an elevated PT and platelets should only be transfused at levels are below <50,000. Clinicians should monitor for the development of DIC in patients undergoing massive transfusion.
Patients with variceal hemorrhage should be started on several pharmacologic therapies early in the ED course. Pantoprazole should be bolused at 80mg and then infused at 8mg/h. Octreotide drip should be bolused at 50 micrograms then infused at 25-50micrograms/hr for 2-5 days.
Patients can also be started on erythromycin 200mg IV to prepare for endoscopy. Erythromycin accelerates gastric emptying and reduces need for repeat endoscopy. Antibiotics norfloxacin 400mg bid or ceftriaxone 1g/d for 5-7 days should also be started in the ED. Release of bacterial endotoxins cause vasodilation and worsens liver function. Early treatments help to reduce early rebleeding.
These patients need early consult to a Gastroenterologist and interventional radiologist for potential TIPS procedure. TIPS is also commonly used as a prophylactic procedure for esophageal varices. It is associated with reduced risk of rebleed and reduced mortality. However, TIPS as a salvage procedure increases the risk of hepatic encephalopathy.
Endoscopic band ligation (EBL)and sclerotherapy are the most frequently used treatments for acute hemorrhage, however EBL is thought to be superior.
Balloon tamponade is used for actively exsanguinating patients using a Sengstaken-Blakemore tube (figure 3). There is a high complication rate associated with the procedure, including aspiration pneumonia, airway obstruction, and esophageal perforation. Recombinant factor VIIa can be used as an adjunct therapy. Some studies show no improved control of bleeding or prevention of rebleeding, but there is an improvement in 6-week mortality.
Patient’s Course: The patient was admitted to the MICU. In the MICU, a cordis catheter and triple lumen central line were placed. Blood and vasopressors (norepinephrine) were administered. Her hemoglobin was monitored Q6. She had 2 more episodes of hematemesis, which led to endotracheally intubation and insertion of a NG tube. The following morning she developed worsening hematochezia and a rectal tube was placed that collected continuous bright red blood. The massive transfusion protocol was initiated and repeat endoscopy showed varices. A TIPS procedure was performed. Despite the TIPS procedure she continued to have rectal bleeding. Lactulose was administered. A tagged RBC study was preformed that also revealed a LGI bleed. The location could not be isolated by angiography. The patient developed DIC and multiple electrolyte abnormalities. Family was informed of the poor prognosis and subsequently agreed to place the patient in palliative care. The patient was transferred to the floor and eventually received a trach and PEG. She was then moved to hospice in early January. She returned back to the hospital for malnutrition was treated and discharged back to the hospice.
1.)Hartman, Aldeen. Focus On: Variceal Hemorrhage www.acep.org/Content.aspx?id=80193, ACEP news Feb 2011.
2.)Bosch, Abraldes, Berzigotti, Garcia-Pagen. Portal Hypertension and Gastrointestinal Bleeding. Seminars in Liver Disease. Vol 28, No 1 2008.
3.)Portal Hypertension. http://hopkins-gi.org/GDL_Disease.aspx?CurrentUDV=31&GDL_Disease_ID=E19DBE4A-EE02-4BDE-9FF9-A8371834DE4A&GDL_DC_ID=9AA60584-3607-4D15-A459-BD3F67A3A4A7. Accessed Feb 20, 2013.
4.)Tintinalli, Judith. Upper GI Bleeding. Tintinalli’s Emergency Medicine A Comprehensive Study Guide 7th Edition. P543-545, 2011.
Filed under: Intern Report | Tagged: cirrhosis, esophageal varices, GI Bleed, portal hypertension | 1 Comment »