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Clinical Correlation of GIT (Short Bowel Syndrome (Patients with greatest…
Clinical Correlation of GIT
Jaundice
Build up of bilirubin
RBC has lifespan of 120 days
For a standard 70kg man
5L of blood circulating a mniute
1.5L through the liver a minute
RBC breaks down to unconjugated bilirubin (free), goes to liver to become conjugated bilirubin (water soluble)
Rate determining step is transport into bile duct, not the conjugation
Bacteria in the colon breaks it down into urobilinogen and can be reabsorbed back into circulation
Some goes into kidney and excreted as urobilin (yellow) 10%
Rest goes back to liver - 90%
Some converted to stercobilinogen, and then to sterblin due to oxidation (brown)
If no bile, (due to bile obstruction) stools will be pale
Tests for liver functions
Serum Bilirubin
Both conjugated and unconjugated in the blood serum
Unconjugated
Insoluble in water and is bound to albumin in the blood
indirect fraction
Breakdown product of RBC
If direct <15% of total, bilirubin can be considered all indirect
Points to potential hemolysis problem
Conjugated hyperbilirubinemia
always imply liver or biliary tract disease
Urine Bilirubin
Unconj. bilirubin always bind to albumin and not filtered by kidney
Thus, any bilirubin found in the urine is conj. bilirubin
can be tested with a urine dipstick test
Blood Ammonia
produced during normal protein metabolism and by intestinal bacteria (main here), primarily those in the colon
Liver plays a role in detoxification of ammonia by converting to urea, which is excreted by the kidneys
Striated muscle also plays a role in detox of ammonia
Some use blood ammonia for detecting encephalopathy or for monitoring hepatic synthetic function
Poor correlation between either presence or severity of acute encephalopathy and elevation of blood ammonia
Occasionally useful for identifying occult liver disease in patients with mental changes
Poor correlation of blood serum ammonia and hepatic function, as it can be elevated in patients with severe portal hypertension and portal blood shunting around the liver even in presence of normal hepatic function
Serum Enzymes
Enzymes that reflect damage to hepatocytes
Aspartate aminotransferase (AST)
Found in liver, cardiac muscle, skeletal muscle, kidneys, brains, pancreas, lungs, leukocytes and erythrocytes
Alanine aminotransferase (ALT)
Found primarily in the liver --> more specific indicator of liver injury
Enzymes are released when liver cells are damaged
In alcoholic liver disease, AST:ALT is >3:1
AST increased while ALT is normal
Enzymes that reflect cholestasis
Alkaline phosphatase (ALP)
Found in liver, bone, placenta and least commonly, small intestines
Normally elevated during rapid bone growth due to bone alkaline phosphatase and late in normal pregnancies
Cholestatic disease if related to liver (if bile duct is damaged)
Can use fractionation of ALP by electrophoresis to identify source of elevated ALP
Can also use GGT to check
Gamme-glutamyl transpeptidase (GGT)
associated with liver diseases such as cirrhosis and hepatitis
Very specific to liver
Serum Albumin
synthesized exclusively by hepatocytes, with long half-life
Due to slow turnover, not a good indicator of mild or acute hepatic dysfunction
Hypoalbuneminemia more common in chronic liver disease such as cirrhosis
Should not be used for screening in patients whom liver disease is not suspected
Serum Globulins
gamma globulins (immunoglobulins) increased in chronic liver disease due to increased synthesis of antibodies, some of which are directed to intestinal bacteria
Happens because cirrhotic liver fails to clear bacterial antigens that normally reach the liver through hepatic circulation
Increase in IgG are common in autoimmune hepatitis
Increase in IgM common in primary biliary cirrhosis
Increase in IgA occur in liver disease
Coagulation factors
With exception of VIII (produced by vascular endothelial cells), blood clotting factors are made exclusively in hepatocytes
due to rapid turnovers, best acute measure of hepatic synthetic function, helpful in both diagnosis and assessing the prognosis of acute parenchymal liver disease|
Measure parameter: Prothrombin time (PT time) which collectively measures factors II, V, VII and X
International Normalized Ratio (INR) used to express degree of anticoagulation on warfarin therapy
Other diagnostic tests
Ultrasonography
First diagnostic test to use in patient whose liver test suggests cholestasis
look for presence of a dilated intrahepatic or extrahepatic biliary tree or to identify gallstones
Shows space-occupying lesions within the liver, distinguish between cystic and solid masses, help direct percutaneous biopsies
Ultrasound with doppler imaging can detect patency of portal vein, hepatic artery and hepatic veins to determine direction of blood flow
First test ordered if suspected of having Budd-Chiari syndrome (occlusion of hepatic veins draining liver)
Noninvasive tests
Fibrotest
Multiparameter blood test
Haptoglobin, bilirubin, GGT, apolipoprotein A-I and alpha 2 macroglobulin
Advanced fibrosis in patients with chronic hep B, hep C, alcoholic liver disease
Transient elastography (TE)
Ultrasound waves to measure hepatic stiffness non-invasively
Accurate to identify advanced fibrosis in patients with chronic hep C, primary biliary cirrhosis, hemochromatosis, nonalcoholic fatty liver disease and recurrent chronic hepatitis after liver transplant
Magnetic Resonance Elastography (MRE)
Superior to TE for staging liver fibrosis in patients with a variety of chronic liver diseases
Need access to MRI scanner
Other parameters to look at
Hemoglobin levels
To test if hemolysis is present (will be low)
Platelets
Low platelet count is due to splenic sequestration
Portal hypertension cause pooling and sequestration of all corpuscular elements of blood, predominantly thrombocytes, in enlarged spleens (ie. platelets)
In liver function test
Hepatocellular and obstructive tend to have a mixed picture and imaging to exclude biliary dilation required
Ultrasound
CT
If found to have obstructive jaundice
Find out what is blocking
Use ERCP to image from the inside (compare size of channels to scope)
If have gallstones, ERCP can fish it out
If there are more in gallbladder, need to remove the gallbladder
Chronic Pancreatitis
incurable, chronic inflammatory condition
Due to genetic mutations, alcohol exposure, duct obstruction due to trauma, gallstones and tumors, metabolic diseases and autoimmune disease
Tropical pancreatitis: results from ingestion of certain starches
For alcohol, metabolites such as acetaldehyde, combined with oxidant injury, results in local parenchymal injury
Metabolic diseaseL hyperparathyroidism and hyperlipidemia
Acute Liver Failure (ALF)
Occurs when rate and extent of hepatocyte death extends the regenerative capabilities
Defined by development of hepatic encephalopathy within 26 weeks of sever liver injury without history of liver disease or portal hypertension
Cerebral edema, hemodynamic instability, increased susceptibility to bacterial and fungal infection, renal failure, coagulopathy, metabolic disturbances
Even with current care, can progress rapidly to hepatic coma and death
Diagnosis and clinical management
possibility of viral infections, medications and other toxins, previous liver disease, mental status
If acetaminophen overdoes (panadol), administration of N-acetylcysteine right away
should also be given to patients with ALF of unknown etiology as replenishing glutathione may be beneficial
Lookout for infections, fluid management, ulcer prophylaxis, hemodynamic monitoring, electrolyte management
Monitor intracranial pressure
Administration of blood products for thrombocytopenia and prolonged PT only in setting of hemorrhage or before invasive procedures
Protect renal function as acute renal failure is a frequent complication
Liver transplantation
Only definitive therapy for patients who CANNOT regenerate sufficient hepatocyte in a timely manner, but there is a shortage
Emerging technologies looking to tackle this
Cirrhosis and portal hypertension
Cirrhosis: presence of fibrous septa throughout liver subdividing parenchyma into hepatocellular nodules
Consequence of sustained wound healing in response to chronic liver injury
Progress to end stage liver disease (ESLD)
Complications include progressive hyperbilirubinemia, malnutrition, decreased synthetic function of liver, coagulopathy, portal hypertension, hepatic encephalopathy and life-limiting fatigue
Micronodular cirrhosis
Thick regular septa, small uniform regenerative nodules and involvement of virtually every hepatic lobule
Macronodular cirrhosis
septa and regenerative nodules of varying sizes
Regenerative nodules irregularly sized hepatocytes with large nuclei and cell plates of varying thickness
Demonstrates right hepatic lobe atrophy, caudate and left lateral segment hypertrophy and portal hypertension
Can be due to viral, autoimmune, drug-induced, cholestatic and metabolic diseases
Clinical manifestations
Spider angiomata and palmar erythema - alterations in estrogen metabolism
Finger clubbing - hypoalbuminemia
feminization of males (gynecomastia, loss of chest and axillary hair and testicular atrophy
Portal hypertension
Caput medusae
Ascites
Asterixis - hepatic encephalopathy
Child-Turcotte-Pugh Score (CTP)
Originally developed to evaluate risk of portocaval shunt procedures performed for portal hypertension, subsequently useful in predicting surgical risks of other intra-abdominal operations in cirrhotic patients
Class A: 10% mortality
Class B: 30%
Class C: 75-80
At class C, little justification to bring in to operation theatre due to poor liver function and thus, resection is not feasible
Imaging of portal venous system
Doppler Ultrasound
CT and Magnetic Resonance Angiography
Portal hypertension
Abnormal increase in portal venous pressure
Normal: 5-7mm Hg
if >12 mm Hg = Portal hypertension
Vasoactive agents (postglandins, NO etc) not filtered through liver, go to collateral flow with long half life, cardiac output increases, collaterals open up and bypass blockage
3 causes
Pre
Rare (portal vein thrombosis)
Post
Rare (Hepatic vein thrombosis)
intra
Cirrhosis of liver
Development of varices when portal pressure exceed 20 mm Hg, collateral veins dilate as they form porto systemic shunts and are known as varices
Most common places:
Lower esophagus
portal: oesophageal branches of left gastric veins
Sys: Azygous Veins
Upper anal canal
Portal: superior rectal vein
sys: Middle/inferior rectal veins
Umbilical (Caput Medusae)
portal: veins of ligamentum teres
sys: superior/inferior epigastric veins
Bleeding is the most impt outcome to avoid
Use of scope down throat to see esophageal varices (which can tear from food)
treatment
Endoscopic banding
Most important treatment
Ligate the varices, cause it to thrombose
Sengstaken Blackmore tube
Gastric balloon goes into stomach, esophageal balloon inflated
Compress on veins to stop bleeding
Cant over inflate as could rupture esophagus
Gastric aspiration tube to prevent patient from choking
Temporary (cant use for >24 hrs due to necrosis of esophagus
Somatostatin
Drop blood pressure in splanchnic circulation
Trans-jugular Intra-hepatic Porto-systemic Shunt (TIPS)
Puncture hepatic vein and portal vein, put metal stent between and link the two veins
Could get encephalopathy due to build up of ammonia
Preferred over post caval shunts
Post caval shunts
Non-selective shunts
Shunt to IVC, no filter, can get encephalopathy
Can do partial shunt
selective shunts
Avoid certain shunts
Hardly done anymore
Antibiotics
Kill bacteria and prevent build up of bacteria due to the environment
Decrease ammonia produced by bacteria due to processing of blood
Also give lactulose to increase passing out of stools, decreasing build up of blood
Ascites
Short Bowel Syndrome
Normal human small intestine range between 3 and 8m in length
Short bowel defined in adults as <200 cm of small intestine
Could be due to one or more enterectomies or congenital
Nutrient, electrolyte and fluid absorption is proportional to amount of residual intestine
Patients with greatest risk of developing dehydration, generalized protein-calorie malnutrition, and multiple nutrient deficiencies are those with a
duodenostomy or jejunoileal anastomosis and <35cm of residual small intestine
Jejunocolic or ileocolic anastomosis and <60cm of residual small intestine
End jejunostomy and <115cm of small intestine
Those with residual colon in continuity will have enhanced energy and fluid absorption
Surgical resection of bowel
usually related to multiple resections for recurrent Crohn's disease (inflammatory bowel disease) or massive enterectomy due to catastrophic vascular events such as mesenteric arterial embolism, venous thrombosis, volvulus, trauma or tumor resection in adults
Possible to have functional short bowel syndrome, where bowel length is still intact
Following resection, intestine adapts to ensure more efficient absorption per unit length
hypertrophies and nutrient absorption becomes more efficient
diameter and villus height increase -> increase in absorptive surface
evolve over 1 or 2 years
TPN dependence (total paenteral nutrition)
If < 100cm in absence of intact and functional colon
If <60 cm in presence of completely functional colon
Residual ileum able to adapt and assume role of macronutrient absorption when jejunum resected, but specialized cells of terminal ileum (for B12/intrinsic factor receptor) cannot be replaced by jejunal hypertrophy
Goal of medical therapy is to resume work and normal lifestyle, thus need to decrease gradually requirement for TPN and at best, eliminate its need (by slowly weaning patients of TPN)
Most important management
Adequate nutrition (macro and micronutrients), provide sufficient fluids and to correct and prevent acid-base disturbances
Most macro, including carbs, nitrogen and fat, are absorbed within first 100cm and up to 150 cm of jejunum
Typically, patient who went through massive enterectomy require TPN for first 7-10 days (first day depends on hemodynamic stability of patient)
Reduction of gatric fluid secretion: H2 antagonist and proton pump inhibitors
Ensure isotonic drink to help facilitate more uptake of water, and cautioned against drinking plain water
increase salt in diet
Trace metals: Mg, Ca, Fe (if bleeding)
Bulk of sugar provided is dextrose
Need to monitor blood glucose levels, and cater insulin if needed (>160mg/dL) to prevent energy loss, dehydration and infection risks
replace with lipids (more calorie dense)
Protein supplied in form of amino acid, 1-1.5g/kg/day, then supplement rest with carbs and lipids