Gastroenterology

GI bleed

Etiology

Pre-endoscopic clinical risk stratification

Clinical judgment always comes first.

Picture1.png

  *Major co-morbidity defined as CAD, CHF, renal failure, liver disease, sepsis, disseminated malignancy, altered  

       mental status, pneumonia, COPD, asthma.

Evaluation


Management

Evaluation and Stabilization:

IMG_4956.jpg

Common Management of Upper and Lower GI bleed

  1. metabolic alkalosis (2/2 citrate metabolism) in setting of renal impairment
  2. hypokalemia (precipitated by alkalosis)
  3. hypocalcemia (due to citrate binding)
  4. hypothermia
  5. hyperkalemia (particularly with older blood products)
  6. Avoid NSAIDs, ASA, anticoagulants
  7. Surgery consult if recent surgical procedure or rebleeding (>6u pRBC)
  8. Re-bleeding:
  9. Preferred treatment is repeat endoscopic therapy
  10. If patient has persistent bleeding after endoscopy, consider CT angiogram or IR embolization. For uncontrolled bleeding requiring >6u pRBC there is no significant difference (rates of re-bleeding, subsequent therapy, or mortality) for IR embolization vs. surgical intervention.
  11. Other diagnostic modalities (discuss with GI first)
  12. Tagged RBC scan (can detect bleed rate >0.1cc/min,  localizes bleeding to area of abdomen but variable localization to portion of intestinal tract, can re-scan several times over 24-48h after tagged RBC administration for intermittent bleeding). If positive, consider IR embolization.
  13. CT (mesenteric) angiography (requires >1 cc/min.)


Specific management for suspected variceal bleed

Endoscopy

The following are endoscopic findings that a GI consultant uses to further risk stratify patients:

IMG_4957.jpg

* Risk of (rebleeding, mortality rate)

Key points


Reference: Hospitalist Handook

Ascites

Definition

Symptoms

Signs

Most common etiologies

 Labs

Ascites fluid assorted labs

Serum

Imaging

Medication Management

    1. Spironolactone and
    2. Thiazide or Loop Diuretic (diuretic dosage should be adjusted to a daily weight loss of no more than 500 g/day in patients without peripheral edema and 1 kg/day in patients with peripheral edema)
    3. Electrolyte correction
    4. Consider Hepatic encephalopathy management
    5. Paracentesis (consider Albumin)
    6. Antibiotic (therapeutic/prophylaxis for SBP)
    7. Electrolyte replacement, restriction of daily sodium intake to 80–120 mmol 

Executive summary of recommendations

  1. Diagnostic paracentesis in new- onset ascites

    • 1.1. A diagnostic paracentesis is recommended in all patients with new-onset ascites. (Quality of evidence: moderate; Recommendation: strong)

    • 1.2. The initial ascitic fluid analysis should include total protein concentration and calculation of the serum ascites albumin gradient (SAAG). (Quality of evidence: moderate; Recommendation: strong)

    • 1.3. Ascites fluid analysis for cytology, amylase, brain natriuretic peptide (BNP), and adenosine deaminase should be considered based on the pretest probability of specific diagnosis (Quality of evidence: moderate; Recommendation: weak)

  2. Spontaneous bacterial peritonitis

    • 2.1. Diagnostic paracentesis should be carried out without delay to rule out spontaneous bacterial peritonitis SBP) in all cirrhotic patients with ascites on hospital admission. (Quality of evidence: moderate; Recommendation: strong)

    • 2.2. A diagnostic paracentesis should be performed in patients with GI bleeding, shock, fever or other signs of systemic inflammation, gastrointestinal symptoms, hepatic encephalopathy, and in patients with worsening liver or renal function. (Quality of evidence: moderate; Recommendation: strong)

    • 2.3. Ascitic neutrophil >250/mm3 count remains the gold standard for the diagnosis of SBP and this can be performed either by manual microscopy or using automated counts, based on flow cytometry for counting and differentiating cells. (Quality of evidence: moderate; Recommendation: strong)

    • 2.4. Ascitic fluid culture with bedside inoculation of blood culture bottles should be performed to guide the choice of antibiotic treatment when SBP is suspected. (Quality of evidence: moderate; Recommendation: strong)

    • 2.5. Immediate empirical antibiotic therapy should be determined with due consideration of the context of SBP (community-acquired or healthcare-associated), the severity of the infection, and the local bacterial resistance profile. Cefotaxime has been widely studied, but the choice of antibiotic should be guided by local resistance patterns and protocol. (Quality of evidence: moderate; Recommendation: strong)

    • 2.6. A second diagnostic paracentesis at 48 hours from the start of treatment to check the efficacy of antibiotic therapy should be considered in those who have an apparently inadequate response or where secondary bacterial peritonitis is suspected. (Quality of evidence: low; Recommendation: weak)

    • 2.7. Patients presenting with gastrointestinal bleeding and underlying ascites due to cirrhosis should receive prophylactic antibiotic treatment (cefotaxime has been widely studied but the antibiotic should be chosen based on local data) to prevent the development of SBP. (Quality of evidence: strong; Recommendation: strong)

    • 2.8. Patients who have recovered from an episode of SBP should be considered for treatment with norfloxacin (400 mg once daily), ciprofloxacin (500 mg once daily, orally), or co-trimoxazole (800 mg sulfamethoxazole and 160 mg trimethoprim daily, orally) to prevent a further episode of SBP. (Quality of evidence: low; Recommendation: weak)

    • 2.9. Primary prophylaxis should be offered to patients considered at high risk, as defined by an ascitic protein count <1.5 g/dL. However, it is important that the potential risks and benefits and existing uncertainties are communicated to patients. (Quality of evidence: low; Recommendation: weak)

  3. Dietary salt restriction

    • 3.1. Patients with cirrhosis and ascites should have a moderately salt-restricted diet with a daily salt intake of no more than 5–6.5 g (87–113 mmol sodium). This translates to a no added salt diet with avoidance of precooked meals. (Quality of evidence: moderate; Recommendation: strong)

    • 3.2. Patients with cirrhosis and ascites should receive nutritional counseling on the sodium content in the diet. (Quality of evidence: weak; Recommendation: strong)

  4. Diuretics

    • 4.1. In patients with the first presentation of moderate ascites, spironolactone monotherapy (starting dose 100 mg, increased to 400 mg) is reasonable. In those with recurrent severe ascites, and if faster diuresis is needed (for example, if the patient is hospitalized), combination therapy with spironolactone (starting dose 100 mg, increased to 400 mg) and furosemide (starting dose 40 mg, increased to 160 mg) is recommended. (Quality of evidence: moderate; Recommendation: strong)

    • 4.2. All patients initiating diuretics should be monitored for adverse events. Almost half of those with adverse events require diuretic discontinuation or dose reduction. (Quality of evidence: low; Recommendation: weak)

    • 4.3. Hypovolaemic hyponatremia during diuretic therapy should be managed by discontinuation of diuretics and expansion of plasma volume with normal saline. (Quality of evidence: low; Recommendation: weak)

    • 4.4. Fluid restriction to 1–1.5 L/day should be reserved for those who are clinically hypervolaemic with severe hyponatremia (serum sodium <125 mmol/L). (Quality of evidence: low; Recommendation: weak)

    • 4.5. Hypertonic sodium chloride (3%) administration should be reserved for those who are severely symptomatic with acute hyponatremia. Serum sodium should be slowly corrected. (Quality of evidence: low; Recommendation: weak)

    • 4.6. It may be appropriate to consider the use of midodrine in refractory ascites on a case-by-case basis. (Quality of evidence: low; Recommendation: weak)

  5. Large volume paracentesis (LVP)

    • 5.1. Patients should give informed consent for a therapeutic or diagnostic paracentesis. (Quality of evidence: low; Recommendation: strong)

    • 5.2. Ultrasound guidance should be considered when available during LVP to reduce the risk of adverse events (Quality of evidence: low; Recommendation: weak)

    • 5.3. Routine measurement of the prothrombin time and platelet count before therapeutic or diagnostic paracentesis and infusion of blood products are not recommended. (Quality of evidence: moderate; Recommendation: strong)

  6. Use of human albumin solution (HAS)

    • 6.1. Albumin (as 20% or 25% solution) should be infused after paracentesis of >5 L is completed at a dose of 8 g albumin/L of ascites removed. (Quality of evidence: high; Recommendation: strong)

    • 6.2. Albumin (as 20% or 25% solution) can be considered after paracentesis of <5 L at a dose of 8 g albumin/L of ascites removed in patients with ACLF or high risk of post-paracentesis acute kidney injury. (Quality of evidence: low; Recommendation: weak)

    • 6.3. In patients with SBP and increased serum creatinine or rising serum creatinine, infusion of 1.5 g albumin/kg within 6 hours of diagnosis, followed by 1 g/kg on day 3, is recommended. (Quality of evidence: low; Recommendation: weak)

  7. Transjugular intrahepatic portosystemic shunt (TIPSS)

    • 7.1. TIPSS should be considered in patients with refractory ascites. (Quality of evidence: high; Recommendation: strong)

    • 7.2. Caution is required if considering TIPSS in patients with age >70 years, serum bilirubin >50 µmol/L, platelet count <75×109/L, a model for end-stage liver disease (MELD) score ≥18, current hepatic encephalopathy, active infection or hepatorenal syndrome. (Quality of evidence: moderate; Recommendation: strong)

  8. Umbilical hernia

    • 8.1. Suitability and timing of surgical repair of umbilical hernia should be considered in discussion with the patient and multidisciplinary team involving physicians, surgeons, and anesthetists. (Quality of evidence: low; Recommendation: strong)

  9. Hepatic hydrothorax (HH)

    • 9.1. TIPSS should be considered in patients with HH after discussion with the multidisciplinary team. (Quality of evidence: low; Recommendation: strong)

    • 9.2. In patients with HH who are not undergoing a TIPSS and/or a liver transplant evaluation, alternative palliative interventions should be considered. (Quality of evidence: low; Recommendation: strong)

  10. Non-selective beta-blockers (NSBB) and ascites

    • 10.1. Refractory ascites should not be viewed as a contraindication to NSBB. (Quality of evidence: moderate; Recommendation: strong)

    • 10.2. Patients with refractory ascites who are taking NSBB should be monitored closely, and dose reduction or discontinuation may be appropriate in those who develop hypotension or acute/progressive renal dysfunction. (Quality of evidence: moderate; Recommendation: strong)

Reference

  1. Pedersen JS, Bendtsen F, Møller S. Management of cirrhotic ascites. Ther Adv Chronic Dis. 2015;6(3):124-137. doi:10.1177/2040622315580069
  2. Aithal GP, Palaniyappan N, China L, et al Guidelines on the management of ascites in cirrhosis Gut 2021;70:9-29.

SBP

Definition

SBP is a bacterial infection of the ascitic fluid.

Diagnosis:

PMN count >= 250 cells/mm3 OR ascitic fluid WBC >= 500 cells/mm3 with a positive fluid culture.

Diagnostic clinical signs: New onset fever, confusion or abdominal pain, hepatic encephalopathy, vomiting, diarrhea.

Diagnosis of Culture-negative neutrocytic ascites: PMN count >= 250 cells/mm3 with a negative fluid culture (subtract 1 PMH for every 250 RBCs).

Pathogens causing SBP: Common organisms are E. coli, Klebsiella pneumoniae, Enterobacteriaceae, Streptococcus pneumoniae, and Enterococcus.

Patients with Cirrhosis: Cirrhotic patients can also get secondary bacterial peritonitis, which usually requires surgical intervention. One should suspect secondary peritonitis with perforation if the ascitic fluid meets 2 or more of the following: Total WBC >10,000, Total protein > 1 g/dl, Glucose < 50 mg/dl OR LDH > 225 milliunits/ml (or higher than upper normal for serum). One should also be suspicious if multiple organisms are cultured or if there is a failure to improve after 48 hours of standard therapy.

Risk Factors for SPB: Severe liver disease, GI hemorrhage, Prior SBP, Ascitic fluid protein <= 1 g/dl.

Diagnosis of SBP: Abdominal paracentesis, send fluid for cell count and differential and send fluid directly in the culture bottles.

Treatment for SBP:

Start antibiotic therapy as soon as the diagnosis of SBP is made based on fluid PMN count OR earlier if clinically indicated.

Use a third-generation cephalosporin (cefotaxime or a similar third generation cephalosporin) HIGH dose 2gm every 8 hours for 5 days.

Any person with cirrhosis and ascites who has signs or symptoms concerning for SBP should be treated with antibiotic therapy regardless of ascites fluid PMN count.

Antibiotic Prophylaxis for SBP: Prophylaxis should be given to persons with cirrhosis with a prior history of SBP or acute GI bleeding and should be considered in those who have renal or hepatic dysfunction if total ascitic fluid protein is less than 1.5g/dL.

Primary and Secondary SBP Prophylaxis: Ciprofloxacin 500 mg daily or trimethoprim-sulfamethoxazole one double strength tablet daily.  If patient has cirrhosis and acute GI hemorrhage, IV ceftriaxone 1 gram daily is recommended for a total duration of 7 days. 

Acute Pancreatitis

Definition

indicates inflammation of the pancreas.

Acute pancreatitis: results from the leakage of pancreatic enzymes into pancreatic tissue, leading to autodigestion.

Chronic pancreatitis: causes are varied and lead to destruction of the pancreatic tissue.  Patients may present with pain and/or weight loss due to fat and protein malabsorption.

Clinical Symptoms of Acute Pancreatitis:

sudden onset of epigastric pain that lasts for hours to days and radiates to the back, nausea and vomiting, sweating, weakness, and anxiety. The patient often feels better when sitting up and leaning forward.

Physical examination findings of Acute Pancreatitis:

The patient may be febrile, tachycardic, tachypneic, and hypotensive. The skin of the periumbilical area may be discolored (Cullen’s sign). Flank ecchymoses (Grey Turner’s sign) may be present. The abdomen may have mild distention (because of ileus). Upper abdominal and epigastric tenderness (usually without rebound or rigidity) is often present.

Laboratory findings of Acute Pancreatitis:

Elevated serum amylase and lipase. Blood amylase or lipase levels are typically elevated three times the normal level during acute pancreatitis.

Other findings may include leukocytosis (12,000–15,000/μ‎L), hypoalbuminemia, hyperglycemia, and elevated aspartate aminotransferase (AST, SGOT), alkaline phosphatase, and bilirubin.

 Imaging for Suspected Acute Pancreatitis [but not necessary]:

CT ABDOMEN- PELVIS.

Causes of Acute Pancreatitis:

Biliary stones, Alcohol abuse, Drugs, Hyperlipidemia or Hypercalcemia, Idiopathic or Infectious, Trauma, Surgery (after endoscopic retrograde cholangiopancreatography [ERCP], intra-abdominal surgery) or Scorpion sting.

Ranson’s criteria are used to assess severity and prognosis.

Ranson’s criteria are assessed at admission and during the initial 48 hours.

Ranson’s Criteria During the Initial 48 Hours.  Ranson’s greater than 3 is SEVERE.

Base deficit >4 mEq/L

Calcium <8 mg/dL

Hematocrit decrease >10%

Sequestration of fluid >6 L

Oxygen <60 mm Hg

Blood urea nitrogen (BUN) increase of >5 mg/dL 

As the number of criteria met increases, so does the mortality rate.

 Treatment of Acute Pancreatitis:

Complications of Acute Pancreatitis: 

Alcoholic Hepatitis

 3 Histological Stages

MELD SCORE [calculate with mdcalc]

Model for End-Stage Liver Disease (MELD) score is a prognostic scoring system used to predict 3-month mortality due to liver disease

MELD scores range from 6 to 40; the higher the score, the higher the 3-month mortality related to liver disease

MDF SCORE  [calculate with mdcalc]

Maddrey Discriminant Function (MDF) score is a measure of disease prognosis in alcoholic hepatitis (AH) used to identify patients at highest risk of mortality and determine the need for initiation of pharmacologic treatment.

An acute inflammatory syndrome that develops in the setting of chronic liver inflammation w/ alcohol use.

Risk Factors

Amount of alcohol, duration of alcohol use (>5-10 yrs for cirrhosis), gender (F>M), ethnicity (↑risk in AA & Hispanics), HCV (>30x ↑risk for cirrhosis), genetic mutations (PNLPA3) and obesity

Clinical Presentation

Hepatomegaly, jaundice, ascites, encephalopathy and fever. 

Of note: alcohol related hepatitis can lead to portal HTN and varices and ascites in the absence of cirrhosis due to hepatic swelling and portal venous obstruction.

Diagnosis

Treatment for Alcohol Related Hepatitis

Nausea

Nausea

Nausea is the unpleasant sensation of about to vomit.  This can occur alone or with vomiting.  Many differentials are associated with nausea depending on patient's symptoms.  

Always check patients electrolytes if they have been having severe vomiting and replete electrolytes if required. Suggestive labs could include BMP (checking electrolytes), UA (checking for ketones and specific gravity).  

Treatment of nausea includes:

Things to prevent nausea include:

Neuroleptic Malignant Syndrome can be caused by excessive use of Compazine or Droperidol (stop antiemetic and start Lorazepam 1-2mg IV 4-6hrs or Dantrolene 1-2.5 mg/kg IV with max dose of 10mg/kg/day).  

Advise all patients that Antiemetics can cause drowsiness

Combination of anti-emetics will resolve patient's nausea if patient is unresponsive to a single medication. 

Constipation

Check if patient has Bowel Obstruction before giving anything PO

Stool Softeners - Colace 100-250mg po qd or bid 

Osmotic Laxatives  

Suppository - Dulcolax 10mg qd, mineral oil enema, fleet enema

Patients started on narcotics should be advised about constipation.  Also patient's on chronic narcotics should be on bowel regimen to prevent constipation.