Gastrointestinal Disorders Flashcards
what diagnostic test can be done to check if a patient is on apixaban/edoxaban/rivaroxaban, if the AC is therapeutic or supratherapeutic?
direct measurement of factor Xa levels
since factor Xa level measurement is not readily available what other lab test might be helpful?
PT and INR might be elevated; but they might still be normal in a therapeutic or supratherapeutic patient
what diagnostic test can be done to check if a patient is anticoagulated w/ dabigatran?
thrombin time
what test is highly sensitive in excluding clinically therapeutic dabigatran therapy and eliminates it as a contributor to clinically relevant bleeding?
a normal thrombin time
if a thrombin time is elevated does that point to one specific DOAC as the culprit?
no, it can be any of the DOACs; a normal thrombin time only eliminates dabigatran as the culprit
in a patient who p/w bleeding while taking a DOAC, evaluation should be made as to whether or not it is a major bleed; what are the 2 main determining factors?
- site of bleed
- volume of bleed
what site of bleeding are considered critical?
- intracranial
- intraocular
- intra or extra-axial spinal hemorrhage
- pericardial tamponade
- posterior epistaxis
- intrathoracic
- intraabdominal
- retroperitoneal
- intramuscular
- intraarticular
intraluminal GI bleeding is not considered a critical bleeding site; what might make a GIB considered to be major?
the volume of bleed leading to hemodynamic instability
what is the reversal antidote for factor X (abiXABAN, edoXABAN, rivoroXABAN) agents?
andeXanet alpha
what are the 2 major concerns regarding administration of andexanet alpha?
- cost of medication (stupid expensive)
- rebound thrombophilia w/ subsequent high rates of thrombotic events
what can be used to reverse anti-Xa DOACs if andexanet alpha is not available?
4-factor prothrombin complex concentrate (4F-PCC)
4-factor prothrombin complex concentrate (4F-PCC) contains what?
factors II, IX, X, and VII
what must be given in conjunction w/ 4F-PCC and why?
- vitamin K 10 mg ivp
- factors II, IX, X, and VII are vitamin K-dependent coagulation factors
what is the reversal antidote for dabigatran?
idarucizumab
what treatment measures are NOT helpful in reversing factor-Xa DOACs?
- FFP; contains very little factor X
- cryoprecipitate; does contain any factor X
what is the mechanism of hepatotoxicity from acetaminophen overdose?
depletion of glutathione which overwhelms glucuronidation pathway, leading to a shift in metabolism toward NAPQI production which is a hepatotoxic metabolite
how does N-acetylcysteine (NAC) help in acetaminophen overdose?
replenishes glutathione activity and restores glucuronidation pathway
treatment decisions for acetaminophen overdose are based on what?
serum acetaminophen concentration measured at least 4 hours after a single overdose when absorption is complete
the Rumack-Matthew nomogram for acetaminophen toxicity should NOT be used under what scenario?
- if the h/o overdose time is NOT reliable
- patient has been taking acetaminophen chronically
- chronic alcohol use
- preexisting liver disease
what are a couple of reasons why the Rumack-Matthew nomogram cannot be used for acetaminophen toxicity in a patient w/ chronic alcohol use?
- chronic alcohol ingestion also depletes glutathione and upregulates CYP2E1, leading to decreased glucuronidation and increased NAPQI production
- alcoholism may lead to inordinate delays in seeking medical attention
in patients whom the Rumack-Matthew nomogram cannot be used to assess hepatotoxicity risk, what is the best next step?
treat w/ NAC
treatment for presumed esophageal variceal bleed
octreotide
treatment for variceal bleed
EGD w/ banding followed by emergent transjugular intrahepatic portosystemic shunting (TIPS)
EGD w/ banding followed by TIPS has what benefits?
- reduces recurrent esophageal bleeding
- reduces 3-month mortality
what additional treatment has been shown to reduce mortality in variceal bleeding?
abx, especially ceftriaxone or fluoroquinolones
hb transfusion thresholds are well studied in critically ill patients, and in general, a hb threshold of 7 g/dL has been found to be similar or better in outcomes compared w/ higher transfusion thresholds; what patient subset was excluded from these studies?
active GI bleeding, but a later study directly addressed this question
one RCT specifically compared outcomes of patients p/w UGIB w/ both shock and variceal bleeding, and were randomized to receive transfusion of prbc if their hb was < 7 g/dL vs < 9 g/dL; what were the results?
the patients in the lower hb transfusion threshold had improved survival
why might there be a survival benefit in UGIB patients w/ variceal bleeding and shock when they receive prbc transfusions at a lower threshold of < 7 g/dL?
patients w/ esophageal varices developed higher portal pressure and more bleeding when they were transfused to a higher hb threshold
what is the Child-Pugh score?
estimates cirrhosis severity
how is the Child-Pugh score determined?
- total bilirubin
- albumin
- INR
- ascites
- encephalopathy
what are the Child-Pugh scores and their associated 1-year survival rates?
- 5-6 points; class A; 100% survival
- 7-9 points; class B; 80% survival
- 10-15 points; class C; 45% survival
hepatic encephalopathy grading
- grade 0 = normal
- grade 1 = restless, sleep disturbance, agitated, tremor
- grade 2 = lethargic, disoriented, inappropriate, asterixis, ataxia
- grade 3 = somnolent, stuporous, hyperactive reflexes, rigidity
- grade 4 = unrousable coma, decerebrate
emergency orthotopic liver transplantation (OLT) has been shown to improve outcomes in which patients?
acute or decompensated hepatic failure from alcoholic hepatitis
numerous large randomized studies have shown what clinical outcomes when comparing transfusing the freshest units of prbcs and the oldest units?
no difference
clinical syndrome of acute liver decompensation and portal hypertension in individuals w/ chronic and active alcohol abuse
alcoholic hepatitis (AH)
alcoholic hepatitis is more common in what patient populations?
- younger patients
- females
- binge drinkers
patients w/ alcoholic hepatitis typically p/w subacute and nonspecific c/o
- fatigue
- jaundice
- other common symptoms attributable to liver failure
physical exam of alcoholic hepatitis
- fever
- tachycardia
- tachypnea
common laboratory abnormalities seen in alcoholic hepatitis
- leukocytosis w/ left shift
- elevated AST and ALT w/ AST/ALT ratio > 1.5
- elevated total bilirubin
- coagulopathy
alcoholic hepatitis can both contribute to and be confused w/ what conditions?
- nonalcoholic steatohepatitis (NASH)
- viral hepatitis
- drug toxicity including acetaminophen
in obese patients w/ an unreliable alcohol history, what can be helpful in differentiating AH from NASH?
alcohol-nonalcohol index
what is a common and significant cause of morbidity and mortality in patients w/ alcoholic hepatitis and should be excluded?
- infection
- septic w/u including paracentesis
what is the alcohol-nonalcohol index, aka alcoholic liver disease/nonalcoholic fatty liver disease index (ANI)?
scoring system that is highly accurate in distinguishing ALD from NAFLD
what is the alcohol-nonalcohol index, aka alcoholic liver disease/nonalcoholic fatty liver disease index (ANI) score based on?
- AST
- ALT
- MCV
- weight
- height
- gender
what is the best next step in patients w/ severe, refractory alcoholic hepatitis who are being treated w/ corticosteroids?
d/c corticosteroids d/t risk of infection
what percentage of patients w/ alcoholic hepatitis do not respond to corticosteroids?
50-60%
score that predicts mortality in patients w/ alcoholic hepatitis not responding to corticosteroids after 1 week of therapy
Lille score > 0.45
Model for End-Stage Liver Disease (MELD-UNOS) score of what defines severe AH w/ an estimated 20% mortality?
≥ 20
although controversial, current guidelines recommend what therapy in the setting of severe AH w/ a Maddrey discriminant function ≥ 32 or MELD-UNOS score ≥ 20?
- prednisone 40 mg po daily
- methylprednisolone 32 mg iv daily (if unable to take po)
a recent high-quality systematic review showed what regarding the use of corticosteroids in patients w/ severe AH?
no benefit in all-cause mortality, health-related quality of life, or serious adverse events in either mild or severe AH
the use of what medication had generated interest, but randomized studies have failed to demonstrate efficacy in severe AH or as salvage therapy for steroid nonresponders?
pentoxifylline (phosphodiesterase inhibitor)
a recent RCT showed what regarding the combination of prednisolone and NAC regarding survival benefit in patients w/ severe AH?
- survival benefit at 28 days, but not 3 and 6 months
- higher than expected mortality in the prednisolone arm
- NAC is still not recommended for routine use
- chronic nausea and vomiting
- s/s of hypovolemia
- relief of symptoms w/ hot shower
cannabinoid hyperemesis syndrome
complete resolution of cannabinoid hyperemesis syndrome requires what?
months of abstinence, and relapses are common
what diagnosis can resemble cannabinoid hyperemesis syndrome?
cyclic vomiting syndrome (CVS)
cyclic vomiting syndrome (CVS) clinical features
- severe recurrent vomiting that lasts for hours or days followed by symptom-free periods
- episodes tend to recur at FIXED intervals
- most often begins in childhood
- usually a/w mitochondrial DNA mutations
- females > males
- bloating
- abdominal pain
- occasionally nausea/vomiting
- primarily a diarrheal illness a/w greasy stools and flatulence
giardiasis
how is giardiasis contracted?
when Giardia duodenalis cysts w/i feces of infected cats, rodents, or other mammals contaminate food/water that then eaten/drunk
who is at highest risk of contracting giardiasis?
people who drink untreated surface water from ponds, lakes, and streams
how else can giardiasis be contracted?
eating undercooked pork
in patients w/ newly diagnosed spontaneous bacterial peritonitis (SBP), it’s recommended that they be given what?
- albumin 20% or 25% 1.5 g/kg be given w/i 6 hours of diagnosis
- then albumin 20% or 25% 1 g/kg repeated on day 3
why should patients w/ newly diagnosed SBP be given albumin w/i 6 hours of diagnosis and again on day 3?
- decreased incidence of renal failure
- improved survival
patients w/ newly diagnosed SBP who have shown benefit from receiving albumin are the highest risk patients which are defined as what?
- Cr > 1 mg/dL
- BUN > 30 mg/dL, or
- bilirubin > 4 mg/dL
what is not recommended for cirrhotic patients undergoing paracentesis in the absence of evidence of peritonitis when a volume of < 5 liters is removed?
colloid replacement
what are the guidelines regarding colloid replacement in the setting of large volume paracentesis?
6-8 g of albumin 25% for each liter removed after the 5th liter
recent evidence-based guidelines suggest that ppx for stress ulcer ppx (SUP) should be limited to patients at high risk of clinically important bleeding; which patients are considered high-risk?
- MV > 48 hours
- coagulopathy (platelets < 50,000/µL, INR > 1.5, or PTT > 2x normal
- TBI
- h/o GIB or ulceration in the preceding year
what conditions w/ weaker evidence for increased bleeding may benefit from SUP?
- patients w/ sepsis
- high-dose glucocorticoid therapy
- sustained occult bleeding > 1 week
is there a difference in effectiveness between PPI and H2 receptor antagonists in reducing risk of clinically important bleeding?
no
is there a difference in effectiveness between iv and enteral PPI in reducing risk of clinically important bleeding?
hasn’t been studied in direct comparison, but both reduce bleeding risk
risk of thrombocytopenia in patients receiving PPI vs H2 receptor antagonist for SUP?
- both can cause
- exceedingly rare adverse event
- critically ill patients so have many other possible causes
is there benefit of SUP in patients receiving enteral nutrition?
no, most studies have failed to show benefit
risk of CDI in patients receiving PPI for SUP
- evidence is mixed if PPI use is a/w w/ CDI
- very high heterogeneity among studies
- abx use has been a confounder in most studies (obviously…)
risk of CDI in patients receiving H2 receptor antagonists for SUP
has not been a/w CDI
bleeding is considered clinically significant based on what criteria?
- if it causes orthostatic hypotension (> 20 mm Hg reduction in SBP, or > 20/min increase in pulse), or
- 2 g/dL drop in hb w/o an appropriate response to prbc transfusion
SUP in appropriately selected patients reduces clinically important bleeding, but what about overall mortality?
has not been shown to reduce overall mortality
what are the potential etiologies for isolated gastric varices, aka gastric varices w/o esophageal varices?
- liver dysfunction and subsequent portal hypertension
- splenic vein thrombosis w/ left-sided portal hypertension
splenic vein thrombosis w/ left-sided portal hypertension often occurs d/t what?
- pancreatitis
- pancreatic masses (pseudocysts, malignancies, cystic adenomas, etc)
- left gastric artery pseudoaneurysm compressing the splenic vein
when the splenic vein is thrombosed, venous blood from both the splenic and short gastric veins must drain back to the portal vein via collaterals, causing increased pressure in the short gastric vein, creating left-sided or sinistral portal hypertension, w/o right-sided portal hypertension; what is the treatment for this condition?
splenectomy, which can be curative
in a patient w/ isolated gastric varices and suspected splenic vein thrombosis, what is the next best diagnostic step?
CT a/p w/ and w/o iv contrast
what artery supplies blood flow to the gastric pylorus and proximal part of the duodenum, and is often embolized to stop bleeding from duodenal ulcers on the posterior wall which can erode into that same artery?
gastroduodenal artery
what procedure can be lifesaving for patients w/ refractory variceal bleeds from classic portal hypertension?
transjugular intrahepatic portosystemic shunt (TIPS)
transjugular intrahepatic portosystemic shunt (TIPS) is unlikely to help in which situation?
patient w/ sinistral portal hypertension w/ normal portal vein pressures d/t elevated pressures in the short gastric veins from splenic vein thrombosis
treatment for decreasing mesenteric and portal pressures that prevents or delays rebleeding in patients w/ varices from portal hypertension 2/2 cirrhosis
nonselective β-blocking agent such as propranolol
- protracted vomiting
- cxr showing pneumomediastinum
esophageal rupture (Boerhaave’s syndrome)
next best step for assessment of possible esophageal leak
fluoroscopic esophageal swallow study
treatment for esophageal rupture (Boerhaave’s syndrome)
emergent surgical repair
what is Mackler’s triad in the setting of spontaneous esophageal rupture?
- vomiting
- chest pain
- spontaneous emphysema
spontaneous esophageal rupture can occur under what circumstances?
- forceful retching
- barotrauma in the chest
in the majority of cases of esophageal rupture (Boerhaave’s syndrome), the rupture is described as what, and where is the tear?
- linear
- located in the distal esophagus just above the gastroesophageal junction
- in a posterolateral position
given the location of esophageal rupture (Boerhaave’s syndrome) is typically located in the distal esophagus just above the gastroesophageal junction and in a posterolateral position, what complications may occur?
- left pneumothorax
- contaminated mediastinal and pleural spaces w/ infection
- left pleural effusion is common
if thoracentesis is performed in the setting of esophageal rupture (Boerhaave’s syndrome), what are the expected results?
- exudative pleural fluid
- low pH
- extremely high amylase level (related to saliva spillage)
early diagnosis and repair for esophageal rupture (Boerhaave’s syndrome) is imperative; in most cases, definitive repair is done by thoracotomy, but another option is
stenting via endoscopy
the MELD score was initially developed to predict outcome after TIPS, then was adopted to predict outcome in outcome in patients w/ chronic liver disease and acute hepatic failure, then by UNOS to determine eligibility for liver transplantation; what is the score based on?
- serum bilirubin
- serum Cr
- PT/INR
- serum Na+
critically ill patients have delayed gastric emptying; 2 trials showed what regarding stopping feedings if nursing staff observed gastric residuals above a threshold level?
no benefit and it resulted in diminished nutrition
the Gastric Residual Volume during Enteral Nutrition in ICU patients (REGANE) trial (great name…) showed that gastric residuals up to what volume could be tolerated w/o measurable adverse effects?
500 mL
the Effect of Not Monitoring Residual Gastric VOlume on the Risk of Ventilator-Associated Pneumonia in Adults Receiving Mechanical Ventilation and Early Enteral Feeding (NUTRIREA 1) trial (seriously???) demonstrated what?
equivalent rates of aspiration and PNA, whether residual volumes were measured or not
the Scottish Intensive Care Glutamine or Selenium Evaluative Trial (SIGNET) showed what?
no benefit to glutamine supplementation
the Reducing Deaths Due to Oxidative Stress (REDOXS) trial showed what?
showed a 6.5% increase in mortality at 6 months in patients who received early high-dose parenteral feeding and enteral glutamine supplementation
in the Impact of Early Parenteral Nutrition Completing Enteral Nutrition in Adult Critically Ill Patients (EPaNIC) trial, patients were randomized to enteral nutrition alone vs the addition of parenteral nutrition to achieve caloric needs; what did the study show?
- enteral nutrition only supplied ~ 20% of estimated caloric need in the first week, BUT
- patients receiving hypocaloric nutrition (no parenteral nutrition) had an earlier d/c from the ICU and hospital, less infections, and less ICU-acquired weakness
in the Trophic vs Full-Energy Enteral Nutrition in Mechanically Ventilated Patients w/ Acute Lung Injury trial (EDEN), relatively young and well-nourished patients w/ acute respiratory failure were randomized to received small volumes of trophic feeding vs full enteral feeding in the first week of critical illness; what did the study show?
although patients randomized to more aggressive feeding received more calories and other nutrients, there was no difference in either acute or chronic outcomes
in the Early Parenteral Nutrition, patients w/ a relative contraindication to enteral feeding were randomized to enteral or early parenteral nutrition; what did the study show?
no significant difference between the groups in 60-day mortality, but the duration of MV was shorter in the parenteral nutrition group (overall, studies do not support the use of early supplemental parenteral nutrition)
what have numerous studies demonstrated regarding feeding patients w/ severe pancreatitis?
they can be fed enterally w/o increasing complications or worsening outcomes
in patients w/ alcohol use d/o, when starting feedings what should be taken into consideration?
refeeding syndrome
in patients at risk of refeeding syndrome, what management strategies should be taken into consideration?
- start enteral nutrition at a lower rate
- close monitoring of serum electrolytes (K+, PO4, Mg++)
initiating enteral nutrition in patients w/ pancreatitis w/i what timeline may improve outcomes?
w/i 48 hours
in a patient w/ advanced cirrhosis and portal hypertension c/b massive variceal hemorrhage, what might be an initial intervention to stabilize the patient?
orogastric tamponade device
what is one of the most serious complications of using a orogastric tamponade device?
esophageal necrosis and rupture
what is one part of the strategy to minimize the complication of esophageal necrosis and rupture when using a orogastric tamponade device?
deflating the balloon q12h, and if bleeding has stopped, leave the balloon deflate but in place
typically, when indicated, esophageal tamponade has been achieved w/ placement of a orogastric tamponade device; what else can be used?
expandable metal stents placed endoscopically
what might be needed when using a orogastric tamponade device to avoid dislodgement?
generous sedation +/- paralysis
what are the 3 types of orogastric tamponade devices?
- Linton-Nachlas tube
- Sengstaken-Blakemore tube
- Minnesota tube
the Linton-Nachlas tube has how many ports?
- 2 ports
- 1 port for inflating the gastric balloon
- 1 port for a gastric suction channel to monitor for bleeding below the balloon
since the Linton-Nachlas tube only has a gastric suction channel, what else needs to be placed and why?
- an additional nasogastric tube above the balloon
- to avoid pooling of secretions and aspiration
the Sengstaken-Blakemore tube has how many ports?
- 3 ports
- 1 port for inflating the gastric balloon
- 1 port for a gastric suction channel to monitor for bleeding below the balloon
- 1 port for inflating the esophageal balloon
since the Sengstaken-Blakemore tube only has a gastric suction channel, what else needs to be placed and why?
- an additional nasogastric tube
- to avoid pooling of secretions and aspiration
the Minnesota tube has how many ports?
- 4 ports
- 1 port for inflating the gastric balloon
- 1 port for a gastric suction channel to monitor for bleeding below the balloon
- 1 port for inflating the esophageal balloon
- 1 port for an esophageal suction channel
meticulous attention to the steps of inflation of a orogastric tamponade device will help avoid what disastrous outcome?
inflation of a gastric balloon in the esophagus
esophageal tamponade is a
temporizing measure
a orogastric tamponade device should be left in place for how long?
only 24-48 hours while other treatment options are arranged/implemented
management of a orogastric tamponade device involves what steps to avoid esophageal necrosis and rupture?
- deflating the balloon q12h
- monitor the tamponading balloon pressure q1h
- maintain tamponading pressure at 30-45 mm Hg (just enough to tamponade venous bleeding w/o eliminating critical perfusion to maintain viability of esophageal mucosa)
what factors contribute to enteral feeding intolerance in patients who are critically ill?
- gastric dysmotility
- ileus
- medications
holding enteral feeding because of gastric intolerance and planned procedures is common in the ICU and can lead to
a potentially detrimental calorie deficit
the current (2016) ASPEN guidelines make what recommendation regarding routine gastric residual volume (GRV) monitoring?
recommend against checking GRV
what other signs of GI intolerance should be checked before deciding to withhold enteral feeding instead of checking GRV?
- abdominal distention
- vomiting
- regurgitation
- diarrhea
- reduced passage of flatus or stool
- abnormal abdominal radiographic findings
does GRV correlate w/ the incidence of PNA, regurgitation, or aspiration?
no
should GRV be measured in patients who are critically ill and have undergone abdominal surgery or have other intraabdominal abnormalities?
unclear
what should be considered for patients receiving enteral nutrition meeting < 60% of their protein and energy needs by day 7-10?
supplemental parenteral nutrition
instead of an hourly rate target, what has been shown to increase the proportion of prescribed protein and energy delivered by enteral nutrition?
volume-based feeding protocols that have a daily volume target
hepatic venous outflow obstruction not d/t passive causes such as cardiac disease
Budd-Chiari syndrome
primary Budd-Chiari syndrome (BCS) is defined as
venous obstruction d/t occlusion of any of the 3 major hepatic veins or IVC, usually d/t thrombosis
secondary Budd-Chiari syndrome is d/t
extrinsic mechanical or invasive causes such as compression or invasion from an extrinsic lesion
what is the best test to confirm the diagnosis of BCS by visualizing a thrombus or obstruction?
US w/ duplex flow analysis of the hepatic vasculature
BCS can manifest under what circumstances?
- acute w/ acute hepatic failure (5% of patients)
- acute w/ rapidly worsening liver disease but not yet hepatic failure (20%)
- subacute (developing over 2-3 months)
- chronic (manifesting w/ cirrhosis)
acute BCS typically p/w
- RUQ pain
- abdominal distention
- jaundice
- ascites
- hepatomegaly
- GIB if varices have formed
other findings that may be present w/ acute BCS
- edema
- fever
- rarely hepatic encephalopathy
what are the pathophysiological characteristics of BCS?
hepatic vein thrombosis leading to acute liver congestion and painful hepatomegaly d/t trapped blood in the liver –> liver congestion then leads to acute hepatic necrosis and liver enzyme elevation and can progress to acute hepatic failure, acutely, or cirrhosis, chronically
what are the most common causes of BCS?
= hormonal causes of hypercoagulability (20%)
- OCP use
- current or recent (w/i 2 months) pregnancy
= hypercoagulability from diseases (25-50%)
- myeloproliferative d/o’s
* PCV
* essential thrombocytosis
- SLE
- APS
- IBD
- Bechet
- inherited hypercoagulable d/o’s
* factor V leiden disease
* thalassemia
* protein C deficiency
* protein S deficiency
= space occupying lesions (10%)
- malignancies
* HCC
- benign space-occupying liver lesions
- infections
* liver abscesses
treatment goals for BCS
- preventing clot propagation
- opening the closed vessel if possible
- relieving the hepatic congestion
- managing liver failure-related complications
first-line therapy in BCS
usually AC w/ LMWH or UFH followed by an oral AC
in cases of acute BCS, if there is a defined clot, what can be considered?
thrombolysis
what are other treatment options for BCS?
angioplasty and stent placement in the hepatic vein
in refractory cases of BCS, what other treatment options can be considered?
- TIPS
- OLT
as part of the risk-benefit evaluation, what is recommended to assess bleeding risk before thrombolysis or AC?
EGD
what are a couple of the most common causes of drug-induced liver disease?
- acetaminophen
- amoxicillin/clavulanate
