Download GI Emergencies

GI Emergencies
Core Content Part III
Tintinalli Chapters 82-84, 86-87
8 June 2005
GI Emergencies
• Hepatic Disorders and Hepatic Failure
• Acute and Chronic Pancreatitis
• The Liver Transplant Patient
Hepatic Disorders and Hepatic Failure
• Acute and Chronic Liver Disease
• Prevalence of chronic liver disease, cirrhosis and
•
•
•
•
ESLD steadily increasing
Chronic liver disease is 10th leading cause of
death among US adults
25,000 deaths yearly=1% all deaths
Majority ESLD= alcohol abuse (50%)
Increasingly chronic viral hepatitis
Epidemiology Hepatitis C
• 40% chronic liver dz related to HCV=8-10,000
•
•
•
•
•
•
•
deaths yearly
By comparison, HIV-related deaths= 14,000
yearly
Chronic infection in 85%
70% chronic cases develop chronic liver dz
Majority of HCV-infected are 30-49 years old
Infection often sub clinical
Sxs chronic liver disease/cirrhosis delayed 1020 years
Increased risk of HCC
Hepatitis C Virus
Epidemiology Hepatitis C
• Anticipate # of patients with chronic liver dz from HCV to
increase sharply over next decades
Epidemiology HBV
• Effective vaccination has lead to
•
•
•
•
•
decline in prevalence of hepatitis B
Still, approximately 140-320,000 new
cases yearly
140-320 annual deaths from acute
infection
Chronic infection occurs in 6-10%
5-6,000 deaths yearly
1-1.25 million Americans with chronic
HBV infections
Liver tumor from HBV
Epidemiology HDV
• Hepatitis D virus uncommon
• Defective virus-depends on concomitant infection with
•
•
HBV
In chronic HBV states, superinfection with HDV results in
fulminant liver dz and high mortality
Commonly associated with IVDU
Epidemiology HAV
• Fecal-oral route
• 33% Americans have acquired immunity against HAV
•
•
•
•
secondary to exposure
125-200,000 cases reported annually
100 related deaths
Fulminant liver failure is rare
Chronic infection does NOT occur
Epidemiology Liver dz
• LFT abnormalities occur commonly with
other acute illnesses
– EBV
– CMV
– HSV
– Coxsackie virus
• Unlikely to cause clinically evident
hepatitis and jaundice in otherwise
healthy individuals
Epidemiology Liver dz
• Alcoholic liver dz and viral hepatitis
most acute/chronic cases liver dz
• Other causes:
–
–
–
–
Toxins
Idiosyncratic drug reactions
Autoimmune
Hepatobiliary dzs
Causes of Acute Hepatitis
• Viral: Hepatitis A, B, C, D, E, CMV
• Toxins:
– Alcohol
– Carbon Tetrachloride
– Mushroom poisoning (Ammanita phalloides)
• Drugs:
–
–
–
–
–
Acetaminophen
Isoniazid
Halothane Anesthesia
Chlorpromazine
Erythromycin
Causes of Chronic Hepatitis
(>6 months)
• Viral: Hepatitis B, C, D
• Drugs:
– Methyldopa
– Amiodarone
– Isoniazid
• Idiopathic:
– Autoimmune features (lupoid hepatitis)
– No autoimmune features
• Metabolic Liver Disease:
– Wilson disease
– Alpha-1 antitrypsin deficiency
Causes of Chronic Liver Disease
and Cirrhosis
•
•
•
•
Alcohol
Hepatitis B and C
Drugs: Methyldopa, MTX, Amiodarone
Biliary cirrhosis: Primary and Secondary:
–
–
–
–
–
Bile duct strictures
Sclerosing cholangitis
Biliary atresia
Bile duct tumors
Cystic Fibrosis
Causes of Chronic Liver Disease
and Cirrhosis
• Chronic hepatic congestion:
– Budd-Chiari syndrome
– Chronic R sided heart failure
– Constrictive pericarditis
• Genetic metabolic diseases
–
–
–
–
Hemachromatosis
Wilson’s disease
Alpha-1 antitrypsin deficiency
Galactosemia
Pathophysiology
• Hepatobiliary diseases classified according to main
•
•
•
•
pathologic process involved
Hepatocellular
Cholestatic
Immunologic
Infiltrative
Clinical Features
• Presentation of acute liver disease is variable
• Symptoms of hepatocellular necrosis accompanying viral
•
•
hepatitis: anorexia, N/V, low grade fever
Cholestatic dz: varying degrees of jaundice, pruritis, clay
-colored stools, dark urine
Chronic liver dz presents with cirrhosis sxs, portal
hypertension: abdominal pain, ascites, GI bleeding,
fever, AMS or simply fatigue
Historical Features
•
•
•
•
•
•
•
•
•
•
Sexual behaviors
Travel
Volume and duration of alcohol use
Illicit drug use
Consumption of nutritional substances (Vit A)
Hx of blood transfusions
Needle-stick exposures
Herbal remedies
Mushroom ingestion
Raw oyster consumption
Historical Features
•
•
•
•
Family History:
Gilbert’s syndrome
Dubin-Johnson/Rotor syndrome
Wilson’s dz, hemachromatosis, alpha-1 antitrypsin
deficiency
Physical Findings
• Acute hepatitis findings often limitedmoderate hepatomegaly with TTP
• Chronic liver disease:
–
–
–
–
–
–
Sallow complexion
Appendicular wasting
Palmar erythema
Distinctive cutaneous spider nevi
Parotid gland enlargement
Testicular atrophy/gynecomastia
• Liver may be enlarged and firm or
• Shrunken and nodular in advanced cirrhosis
• Splenomegaly, ascites with portal HTN
Liver Function Tests
• Bilirubin:
• Breakdown product of hemoglobin, heme-containing
•
•
•
proteins and cytochromes
Unconjugated bili poorly soluble anion, bound to
albumin
Taken in to liver, conjugated, secreted into bile, stool
Total serum bili usually < 1.1 and 70% unconjugated
Differential Dx of
Hyperbilirubinemia
• Unconjugated Hyperbilirubinemia >80% indirect:
• Overproduction: Hemolysis
– Spherocytosis
– Autoimmune disorders
• Decreased hepatic uptake:
– Gilbert’s Sx
– Neonatal jaundice
– Drug related (Rifampin, contrast agents)
• Decreased conjugation:
–
–
–
–
–
Gilbert’s sx
Crigler-Najjar sx
Neonatal jaundice
Hepatocellular dz
Drug inhibition-chloramphenecol
Differential Dx of
Hyperbilirubinemia
• Conjugated hyperbilirubinemia > 50% direct
• Intrahepatic cholestasis (impaired hepatic secretion)
– Familial disorders –Rotor sx, Dubin -Johnson sx, benign
recurrent cholestasis
– Cholestasis of pregnancy
– Drug induced cholestasis (Phenothiazines, OCPs)
– Primary biliary cirrhosis
– Gram negative sepsis
– Post operative
• Extrahepatic cholestasis (mechanical obstruction to bile
flow)
–
–
–
–
Common duct gallstones
Bacterial cholangitis
Tumors
Strictures
Transaminases
• AST derives primarily from liver, also released from
heart, smooth muscle, kidney and brain= relatively
nonspecific
• Meds causing increased AST:
–
–
–
–
Acetaminophen
NSAIDS
ACEs
Griseofulvin, fluconazole
• ALT more specific marker hepatocellular dz
• Mild elevations in hundreds/units/liter=ongoing
inflammatory hepatocellular damage
– Viral hepatitis or subclinical hepatotoxic drugs
Transaminases
• Values in one thousands suggests acute hepatocellular
•
•
•
•
•
necrosis signifying extensive liver damage=shock liver
Value in measuring both enzymes? AST:ALT ratios
Ratios>2 common in alcoholic hepatitis
AST stimulated by Etoh
In acute and chronic viral hepatitis, ratio generally<1
In absence of ongoing Etoh use, mild elevation in
AST/ALT with ratio>1 suggests underlying cirrhosis
Alkaline Phosphatase
• Increased level associated with biliary obstruction and
•
•
•
•
•
cholestasis
However mild to moderate elevations accompany
virtually all hepatobiliary dz
In general, alk phos elevations>4x normal indicate
cholestasis rather than hepatocellular process (i.e.
hepatitis)
Elevations may be nonspecific b/c alk phos derived from
bone, placenta, kidneys and leukocytes
Specificity increased with GGT (gamma glutamyl
transpeptidase)
When elevated supports dx of cholestasis
Alkaline Phosphatase
• GGT, like AST also stimulated by Etoh and drugs=
phenobarbital and warfarin
• GGT elevated in:
–
–
–
–
–
acute and chronic pancreatitis
MI
Uremia
COPD
RA
• Isolated elevations in alk phos in absence of
hyperbilirubinemia (AP:bilirubin of 1000:1) characteristic
of infiltrative or granulomatous dz
–
–
–
–
Lymphoma
Fungal infections
Sarcoid
TB
• Elevated 2-3x adult levels in children
Clinical Syndromes
• Jaundice = yellow pigmentation to skin, sclera, mucous
membranes by elevated bilirubin
• Develops w/ overproduction of bili and/or defect in
hepatic bili uptake, conjugation or biliary excretion
• In absence of underlying or concomitant liver dz
hemolysis does NOT result in jaundice
Jaundice
• In acutely ill or febrile patient, jaundice may be viral
hepatitis or bacterial cholangitis
• Bacterial cholangitis associated with elevations in alk
phos
• Subacute jaundice w/o prior liver dz likely infiltrative dz
or slowly obstructing extrahepatic tumor (ie head of
pancreas)
Cirrhosis
• Fibrous scarring mixed with hepatocellular regeneration
in response to sustained insult
–
–
–
–
Inflammatory
Congestive
Metabolic
Toxic
• Functional anatomy replaced w/ scar tissue
• Portal HTN develops…
• Complications from ESLD emerge
Gastroesophogeal Varices and
Hemorrhage
• Cirrhosis results in progressive increase in resistance to
•
•
•
•
•
portal blood flow through liver
Shunting of blood through venous collaterals into
systemic circulation
Increased blood flow/pressure in these collateral veins
promote formation of submucosal varices in gastric
fundus and esophagus
Varices prone to ulceration/ hemorrhage
25-70% of cirrhotics will have bleeds
Acute hemorrhage carries 30-60% mortality rate
Esophageal Varices
• Hematemesis, hematochezia, and/or melena
• Varying HD instability
• Complicated by preexisting thrombocytopenia, anemia,
•
•
•
coagulopathy
DDX less important than aggressive management
Priorities
– Airway protection
– IV access for meds, fluids, blood
Caution w/ central lines-coagulopathies
Esophageal Varices
• Gastric lavage indicated w/ active bleeding to evacuate
•
•
•
•
stomach and relieve vomiting
Vomiting may exacerbate bleeding
May provide gross assessment of ongoing blood loss
Known GE varices not a contraindication to careful NG
placement
GI consult for endoscopy=diagnostic and therapeutic
Esophageal Varices
• Replace blood, fluids
• Vasopressin or somatostatin (special order form and GI
•
•
•
•
•
like this)
Decrease portal venous blood pressure, by different
mechanisms
Vasopressin causes splanchnic arteriolar
vasoconstriction, reducing portal venous inflow and
pressure
Somatostatin decreases splanchnic blood flow by causing
direct and selective relaxation of mesenteric vascular
smooth muscle
Vasopressin action is nonspecific
Potential cardiac and HD side effects
Esophageal Varices
• Vasopressin especially hazardous in older folks
• May provoke coronary vasospasm leading to
•
ischemia, MI, arrhythmias
CVA, mesenteric, limb ischemia
Esophageal Varices
• Somatostatin is effective without significant side effects
• Limited by short half life 1-2 min
• Octreotide (Sandostatin), an analogue of somatostatin also very
effective
• Minimal HD side effects
• Very useful in HD unstable patients who cannot tolerate emergent
endoscopy
Esophageal Varices
• Sengstaken-Blakemore tube
•
•
•
•
•
for balloon tamponade used
infrequently
High rate of complications
Endoscopy/sclerotherapy more
readily available
Complications: aspiration,
esophageal necrosis or rupture
Beta blockers, portosystemic
shunts or TIPS (transjugular
intrahepatic portosystemic
shunts) are effective
preventative measures for GE
varices
No role in acute management
Ascites & Spontaneous Bacterial
Peritonitis
• Ascites occurs in hepatic cirrhosis as a result of portal
•
•
•
•
HTN, impaired renal sodium and water excretion,
hypoalbuminemia
Most common complication=SBP
Yearly risk= 29%
SBP may present w/ fever, abdominal pain and
tenderness
May be relatively silent w/ subacute functional decline
and/or worsening baseline encephalopathy
SBP
• Diagnosed w/ peritoneal fluid by
•
•
•
•
•
•
paracentesis
Localize fluid collections by U/S
Or percussion of dullness in
lateral aspects of lower
quadrants w/ pt. semirecumbant
Avoid areas near surgical scars
Lidocaine, 18-20g angiocath
Withdraw 10cc
Culture results may be improved
by processing fluid like a blood
cx
SBP
• Fever, abdominal pain, tenderness
•
•
•
•
+/- worsening encephalopathy in
pt. w/ cirrhosis and ascites
Ascitic fluid:
– WBC>1000 mm3
– PMNs>250 mm3
Tx: Cefotaxime 2g IV
OR Unasyn, Zosyn, ceftriaxone
Ofloxacin 400mg po bid
– Enterobacteriacae=63%
– Streptococcus
pneumoniae=15%
– Enterococci= 6-10%
Hepatic Encephalopathy
• In fulminant liver dz
• Occurs in response to metabolic insults and cerebral
•
•
edema
May be caused by incompletely metabolized prescription
drugs, NSAIDs, tylenol, or Etoh
Determining baseline mental status often challenging but
central to dx
Hepatic Encephalopathy
• Serum ammonia often elevated
• Nonspecific finding
• Ammonia may serve as a marker but NOT as an
•
•
•
index of encephalopathy
Causes of encephalopathy:
– GI bleeding
– Increased dietary protein
– Infection
– Sepsis
– Drugs (BZDs, opiates or “muscle relaxers”)
Remember the pt. may have fallen
Admit, give lactulose or neomycin
Hepatic Encephalopathy
• Staging of Hepatic Encephalopathy
• I: General apathy
• II: Lethargy, drowsiness, variable
•
•
orientation, asterixis
III: Stupor w/ hyperreflexia, extensor
plantar reflexes
IV: coma
Acute and Chronic Pancreatitis
• Acute pancreatitis is secondary to cholelithiasis or
alcohol abuse in 90% of cases in US
• Biliary pancreatitis most female, over age 50, present to
community hospitals
• Alcoholic pancreatitis most often male b/w 35-45,
present to urban EDs
• Other causes pancreatitis:
– Drugs
– Infection
– Trauma
• Drugs account for >50% of remaining cases after biliary
and Etoh excluded
Drugs Associated w/ Acute
Pancreatitis
•
•
•
•
•
•
OCPs
Thiazides
Lasix
Salicylates
Calcium
Warfarin
•
•
•
•
•
•
Acetaminophen
Azathioprine
Glucocorticoids
Rifampin
Tetracyclines
Isoniazid
Pathophysiology
• Intracellular activation of digestive
enzymes w/ subsequent autodigestion
• Activated proteolytic enzymes
(trypsins) cause edema, insterstitial
hemorrhage, vascular damage and
cellular necrosis
• May cause remote systemic effects
unlike other intrabdominal processes
• May cause shock, ARDS
Clinical Features
• Major symptom is mid-epigastric or LUQ pain
• Usually described as boring, radiating to back and flanks,
•
•
•
•
•
chest or lower abdomen
Intensity is variable and does not correlate w/ severity of
dz
Pain exacerbated by supine position
Relieved with sitting, knees flexed
Colicky pain suggest other etiology
N/V, bloating common
PE
• Low grade fevers, tachycardia, hypotension
• 10 percent have respiratory symptoms secondary to
•
•
•
atelectasis, pleural effusion-(usually L sided)
Abdominal exam-epigastric TTP
Peritonitis is late finding- b/c pancreas RP?
Maybe decreased BS from ileus
PE
• Cullen sign-bluish discoloration around
•
•
•
•
•
umbilicus
Grey-Turner Sx-bluish discoloration of
flanks
Signs of hemmorhagic pancreatitis
Rare to find these
May present in shock
Hypotension from third spacing,
hemorrhage, cardiac depression,
vomiting
Diagnosis
•
•
•
•
•
•
•
•
•
No pathognomnic syndrome
Diagnostic gold standard is pathologic exam of pancreas
Lab and radiographic studies helpful but limited diagnostic accuracy
Amylase =digestive enzyme to cleave starch into smaller
carbohydrates
Found in pancreas, salivary glands and numerous other tissues
Poor specificity
May be normal in actual cases pancreatitis
Levels may return to normal after 3 days b/c of short half life even
w/ ongoing inflammation
Less sensitive after first 36 hours
Diagnosis
• Lipase=catalyzes breakdown of triglycerides into free
•
•
•
•
•
•
fatty acids
Predominantly in pancreas
Also in gastric/ intestinal mucosa liver
Heparin can cause release of endothelial-membrane
bound lipase into serum
W/in minutes lipase may increase
Lipase cleared renally and may be elevated 3x normal in
renal failure
½ life=7h –will remain elevated after amylase returns to
baseline
Diagnosis
• Lipase is a better test
• Amylase adds little information
• Lipase/Amylase ratios, Amylase/Cr ratio not
•
helpful
It is not cost-effective to order amylase or
lipase in every patient w/ undifferentiated
abdominal pain
Radiology
• CXR, AXR may be useful in
excluding other causes of abd
pain
• Pancreatic calcification
suggestive of dz
• Sentinel loop secondary to small
bowel ileus, may be present, but
not diagnostic
• CXR may show elevated
hemidiaphragm or pleural
effusion
Pancreatic Calcifications
Radiology
• U/S useful for biliary obstruction, GB dz but insensitive
for acute pancreatitis-especially nonbiliary causes
• CT cannot r/o dz-insensitive in mild/early cases
• ERCP not useful in ED but used later if dx is in doubt
Necrotizing pancreatitis
Ranson Criteria
•
•
•
•
•
•
On Admission:
Age over 55
Glucose>200
WBCs> 16,000
AST> 200
LDH>350
•
•
•
•
•
•
48 hours later:
Falling hct> 10%
Rise in BUN over 5 mg/dl
Decreased Ca below 8
Arterial PO2 below
60mmhg
Base deficit over 4meq/L
Ranson Criteria
•
•
•
•
•
•
On Admission:
Age over 55
Glucose>200
WBCs> 16,000
SGOT>200
LDH>350
Lipase is not part of Ranson
Criteria
•
•
•
•
•
•
48 hours later:
Falling hct> 10%
Rise in BUN over 5 mg/dl
Decreased Ca below 8
Arterial PO2 below
60mmhg
Base deficit over 4meq/L
Complications
•
•
•
•
•
•
•
Pancreatic Abscess
Pseudocysts
Develop 2-3 weeks after onset
Pulmonary: pleural effusions, ARDS
CV: Myocardial depression
Metabolic: Hypocalcemia,
hyperglycemia, hyperlipidemia,
Coagulopathy, DIC
Treatment
•
•
•
•
•
•
GI rest
Clear fluids may be ok in mild-mod cases
IVFs
Narcotics, antiemetics
No abx-only if secondary infection suspected
Admit all but very mild dz
Chronic Pancreatitis
• Chronic inflammation causes irreversible pancreatic
•
•
•
•
•
•
•
damage
80% caused by chronic Etoh abuse
Remainder are idiopathic
Mean ages of onset of dz=42
Death=52
More common in men (like Etoh abuse)
Gallstones are not cause of chronic pancreatitis
Acute pancreatitis does not progress to chronic dz unless
complications like pseudocysts or ductal strictures
present
Causes of Chronic Pancreatitis
•
•
•
•
•
•
•
•
Alcohol Abuse
Hyperparathyroidism
Pancreas divisum
Ampullary stenosis
CF
Hereditary
Trauma
Idiopathic
Clinical Features
• Abdominal pain
• May be absent in 10% cases
• In contrast to acute pancreatitis, may be chronically ill
•
appearing
Pancreatic insufficiency
–
–
–
–
Weight loss
Steatorrhea
Clubbing
Polyuria
• Stigmata of chronic liver dz
Diagnosis
• Acutely, difficult to discern b/c dx based on dz
•
•
•
•
•
•
•
reversibility
Labs may be nonspecific
Amylase/lipase may be elevated, but have no prognostic
significance
May be normal if fibrosis is advanced
Glucose tolerance impaired
Increased bili and alk phos
Pancreatic calcification on AXR present 30% cases-esp
w/ alcoholics
No gold standard to differentiate acute v. chronic dz
Treatment
• Supportive care
• r/o other dxs or
•
•
complications
Long-term goals=pain
control, relief of
mechanical obstruction,
correction of
malabsorption
Pancreatic extracts
improve absorption and
relieve pain
Treatment
• Etoh cessation is essential
• 5 year mortality rate 50% in continued alcohol abusers
• Imaging for intractable pain to r/o obstruction or
•
•
pseudocyst
Other complications=ascites, pleural effusions, splenic
vein thrombosis
Celiac plexus nerve block performed for long-term pain
control
Liver Transplant Patient
• 7000 liver transplants worldwide
•
•
•
•
•
•
each year
4000 performed in US
Number or transplants limited by
# of donors
Before 1980s, 1 year survival
rates < 30%
Better immunosuppression,
surgical techniques and patient
selection
1 year survival=87%
Post transplant problems high
Postoperative Complications
•
•
•
•
•
•
•
•
Bleeding-most occur in first week, so not seen in ED
GI bleeding-manage in usual way
May signal graft dysfunction
May be accompanied by hypoglycemia, profound
coagulapathy
Portal HTN should have been reversed by transplant
Variceal bleeding may indicate portal vein thrombosis
High dose steroids predisposed to GI bleeding
CMV, HSV, Candidal infections can cause GI bleeding
Biliary Complications
• Incidence close to 30%
• Leaks, strictures (ductal narrowing), obstruction (ductal
•
•
•
•
•
blockage)=80% of biliary complications
Leaks occur early=38% in first 30 days
80% w/in first 6 months
Early leaks tend to be more severe
Present w/ peritonitis, fever, abdominal pain, distention
May be masked from immunosuppression
Biliary Complications
• Labs = leukocytosis,
•
•
•
•
•
hyperbilirubinemia, increased alk
phos
Doppler U/S
Associated with HAT (hepatic
artery thrombosis)
Tx for biliary leak includes
drainage
Abx directed against GNs and
anaerobes
Biliary leak associated w/ high
mortality
Vascular Complications
•
•
•
•
•
Less common
Associated w/ high morbidity, mortality, graft failure
HAT most common-occurs w/in 3 weeks post-transplant
Incidence b/w 5-40%
Incidence higher in children (26%)-treated w/
anitplatelet agents
Vascular Complications
•
•
•
•
•
•
Presents w/ increased PT, LFTS
Children have more varied presentation
May be fever or sepsis
Doppler U/S 92% sensitive
If U/S not diagnostic but suspicion still highangiography
If diagnosed early, immediate thrombectomy and
anastomosis revision may preclude need for
retransplantation
Vascular Complications
• Portal vein thrombosis less
common= 2-3% of patients
• Dx suggested by variceal
hemorrhage, massive ascites, other
sxs portal HTN
• Tx directed towards reducing
portosystemic pressure gradient
• May need retransplantation
Acute Rejection
•
•
•
•
•
Acute rejection usually seen at 7-14 days
Incidence =40-80% w/in first posttransplant year
After 3 months, incidence declines steadily
May be triggered by tapering immunosuppressive agents (have you
changed doses of any of your medications lately?)
Acute rejection may be subtle presentation
–
–
–
–
–
Fever
Liver tenderness
Lymphocytosis
Eosinophelia
Increased LFTs
Acute Rejection
• Dx only by excluding other causes of graft
•
•
•
•
dysfunction and bx
Perioperative period consider infection, acute
biliary obstruction, vascular insufficiency
Acute rejection treated w/ high dose
glucocorticosteroids w/ rapid taper over 5-7 days
Effective in 65-80%
Secondary therapy w/ antilymphocyte globulin
(OKT3)
Chronic Rejection
• Occurs in 5-10% of recipients
• Major cause of late graft failure
• Primary manifestation=persistently
•
•
•
cholestatic liver injury pattern (biopsy)
Elevated alk phos, bilirubin
Associated w/ pruritis
Significant loss of hepatic fxn often not
evident until late in course of chronic
rejection
Infection
• Account for most death
• Most patients have at least one episode
• Immunosuppression-induced blunting of inflammatory
•
response may mask presentation
Three major infection periods
– <1 month
– 1-6 months
– >6 months
• In first 30 postop days=bacteria and fungi
• Immunosuppression at greatest levels, anastamoses at
most vulnerable
Infection
• Most infections <30 days normal
•
•
•
•
nosocomial agents in post-op patients
Opportunistic organisms absent in first
month
From 1-6 months most
infections=viruses
EBV from reactivation or donor
transmission
Or opportunisitic infections
Infection
• After 6 months, incidence of serious
infection declines
• Cholangitis most common
• High index of suspicion
• “Close monitoring is essential, as rapid
deterioration can take place while the
patient is still in the ED”
CMV
•
•
•
•
•
•
•
Often seen w/ bacterial infections
Most common virus affecting patients
Occurs b/w 23-85% of all liver transplant patients
Despite high incidence and morbidity, rarely fatal
unless disseminated
Rarely has significant effect on graft survival
Generally occurs within first 3 months
Peak incidence in first 3-4 weeks
CMV
• Later CMV occurrence related to increase in
•
•
immunosuppression for tx of prolonged rejection
May be primary infection or reactivation
Mononucleosis-like syndrome
–
–
–
–
–
Fever
Atypical lymphocytosis
Thrombocytopenia
Neutropenia
Mild increase in LFTs
• May present w/ pneumonitis
• B interstitial infiltrates
CMV
• CMV pneumonitis may be seen in conjunction w/ PCP
•
•
•
•
•
•
pneumonia
CMV hepatitis presents similarly to rejection-fever,
abdominal pain, hepatomegaly, liver dysfunction
Diagnosed by liver bx, but still difficult to distinguish from
chronic rejection
CMV retinitis-decreased vision, photophobia, floaters, eye
pain
Signals profound immunosuppression
Carries poor prognosis
TX: Ganciclovir for 2-4 weeks
Question
• Which types of hepatitis produce neither an
•
infection nor a carrier state?
Hepatitis A and Hepatitis E
Question
• What abnormal electrolyte finding is seen in
•
patients with pancreatitis?
Hypocalcemia
Question
• What is the most common cause of portal HTN
worldwide?
• Schistomsomiasis
Question
• What is the most common bloodborne infection
•
in the US
Hepatitis C