Glue Injection of gastric varices

how to inject the Glue

GIST

Gastrointestinal stromal tumours (GISTs)

GISTs are rare connective tissue tumours that show similar differentiation patterns to the interstitial cells of Cajal and approximately 60e70% arise in the stomach.
Activating mutations of the KIT or PDGFRA protooncogenes are thought to be the causal molecular events.
Approximately 95% of tumours are therefore positive for CD117 (c-KIT) by immunohistochemistry.
The degree of local and metastatic spread of gastric GISTs should be evaluated by CT scan and endoscopic ultrasound.
If the tumour is localised to the stomach it should be surgically resected.
If the tumour is unresectable or if metastases are present at diagnosis or during follow-up, treatment with the tyrosine kinase inhibitor, imatinib, should be considered and treatment should usually be continued until progression, intolerance or patient refusal occurs.


‘Consensus meeting for the management of gastrointestinal stromal tumors’.

Histopathologic image of gastrointestinal stromal tumour of the stomach. Hematoxylin-eosin stain

Liver diseases in pregnancy

1- Hyperemesis Gravidarum:
1-20/1000 in the 1st trimester, 50% hospitalized
25% have abnormal liver biochemistry
raised conjugated bilirubin, ALP x2 normal, ALT up to 200iu/l
aetiology unknown
? rapidly rising steroid level
complications related to repeated vomiting
outcome of pregnancy normal

2-per-eclampsia:
hypertension, protienurea, odema
5-7% of pregnancies
2nd and 3rd trimester
can lead to seizures, renal failure, coma and death
hepatic infarction and rupture occur rarely

3-HELLP syndrome:
complication of severe pre-eclampsia
4-20% eclamptic pregnancies
3rd trimester 2/3, postpartum 1/3
Haemolysis (elevated LDH)
ELevated liver enzymes (ALT x 2-10)
Low Platelets (<100 p="">presentation: N/V, malaise, headache, RUQ pain, hepatomegaly.
mortality: 1% maternal, 35% fetal
severe morbidity: DIC, placental rupture, renal failure, pul odema.
lab tests: uric acid >7.8, LDH >600, ALT>100, smear: haemolysis

4-AFLP acute fatty liver of pregnancy:
rare, 1:7000-13000, potentially fatal
3rd trimester, 1st and multiple pregnanies
Mild features of pre eclampsia
Jaundice after 1-2 weeks
hypoglycaemia, clotting abnormality
Untreated leads to fulminant hepatic failure
lab tests: elevated ALT and bilirubin, DIC, coagulopathy, elevated amonia, renal failure
maternal mortality up to 10-20%, fetal mortality 20-50%

5-obstetric cholestasis:
2nd and 3rd trimester (>26 weeks)
prurius (plams and soles)
juandice uncommon 25%
raised ALT 60%, gamma GT 30%
raised serum bile acids
imaging of the lliver normal
close monitoring, delivary by 37-38 weeks
treat with UDCA and/or dexamethsone, vit K prevent post-partum bleed

The serum-ascites albumin gradient

SAAG is a calculation used in medicine to help determine the cause of ascites.

SAAG = (albumin concentration of serum) - (albumin concentration of ascitic fluid).

High gradient

A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension with 97% accuracy.

Important causes of high SAAG ascites (> 1.1 g/dL) include:

high protein (> 2.5): heart failure, Budd Chiari syndrome

low protein (< 2.5): cirrhosis of the liver, nephrotic syndrome

Low gradient
A low gradient (< 1.1 g/dL ) indicates causes of ascites not associated with increased portal pressure such as tuberculosis, pancreatitis, nephrotic syndrome and various types of peritoneal cancer.

King's college criteria

The most widely accepted prognostic tool for patients who present with ALF. Although fulfilment of these criteria has a high specificity for mortality, the sensitivity and negative predictive value remain low. Therefore, not fulfilling the criteria does not ensure survival.

Prospective data from the US Acute Liver Failure Study Group revealed the King's College Criteria had an overall specificity of 85.7% but lower sensitivity of 48.3% in prediction of mortality in 838 patients with ALF. The specificity was increased to 92.4% in the 374 patients who presented with ALF secondary to paracetamol (acetaminophen) overdose.

ALF secondary to paracetamol overdose:
-pH <7>
-INR >6.5 (PT >100 seconds) and 
-serum creatinine >300 micromol/L (>3.4 mg/dL) in patients with grade 3 or 4 hepatic encephalopathy.

Non-paracetamol associated ALF:

INR > 6.5 (PT > 100 sec) or

any 3 of the following:

-age between 10-40 yrs,

-aetiology non-A, non-B hepatitis or idiosyncratic drug reaction,

-duration of juandice before hepatic enchephalopathy > 7days,

-INR >3.5 (PT >50), 

-Serum bilirubin > 300 mmole/l

Forrest classification

Used for  stratifying patients with upper gastrointestinal hemorrhage into high and low risk categories formortality. It is also a significant method of prediction of the risk of rebleeding and very often is used for evaluation of the endoscopic intervention modalities.

Rockall score

Identify patients at risk of adverse outcome following acute upper gastrointestinal bleeding. 
The scoring system uses clinical criteria (increasing age, co-morbidity, shock) as well as endoscopic finding (diagnosis, stigmata of acute bleeding). 
A convenient memnoic is ABCDE - i.e. Age, Blood pressure fall (shock), Co-morbidity, Diagnosis and Evidence of bleeding.

The utility of a modified Rockall score (that is, a score lacking endoscopic findings) has not been established. 
The definition of mild, moderate, or severe risk remains a matter of clinical judgement.
According to SIGN guidleines, only patients with Rokall score of 0 can be savely managed as outpatient.
The predicted mortality:
Score 0     0.2%
Score 1    2.4%
Score 2    5.6%
Score 7    50%

MELD score

Scoring system for assessing the severity of chronic liver disease. 

It was initially developed to predict death within three months of surgery in patients who had undergone TIPS and was subsequently found to be useful in determining prognosis and prioritizing for receipt of a liver transplant. 

This score is now used by the United Network for Organ Sharing (UNOS) and Eurotransplant for prioritizing allocation of liver transplants instead of the older Child-Pugh score.

The MELD range from 6 to 40 points. This range predict 3 months survival without liver transplantation in patients with liver cirrhosis.

MELD = 3.78[Ln serum bilirubin (mg/dL)] + 11.2[Ln INR] + 9.57[Ln serum creatinine (mg/dL)] + 6.43

• 40 or more — 71.3% mortality

• 30–39 — 52.6% mortality

• 20–29 — 19.6% mortality

• 10–19 — 6.0% mortality

• < 9 — 1.9% mortality

The United Kingdom MELD (UKELD) score is derived from the patient's serum sodium, creatinine and bilirubin, and INR.
Minimal listing criteria require that the patient should have a projected 1-year liver disease mortality without transplantation of more than 9%. This is predicted by a UKELD score of 49 or greater. 
A UKELD score of 60 is predictive of a 50% 1-year survival.

at MELD score of 15 or greater, survival is enhanced 1 year after liver transplantation versus remaining in the waiting list. Therfore, most transplant centres designate a MELS score of 15 as the minimal listing score for liver transplantion.

Child-Pugh score

Used in patients with liver cirrhosis to assess the severity of the clinical condition. 

Five variables are considered (severity of ascites and of encephalopathy, abnormality in the serum bilirubin, serum albumin and clotting times), and a score (of between 1 and 3) is accordingly assigned to each of these factors. 
This grade is used as a general means to verify the prognosis of the patient. 
Child A 1 yr survival: 100%,  2 yr survival:85%
Child B 1 yr survival: 81%,    2 yr survival:57%
Child C 1 yr survival:45%,     2 yr survival:35%

Child-Turcotte-Pugh classification, My Gastro Room blog

Crohn's disease Vs ulcerative colitis

CD:

Mucosal architecture:

Mucosal surface, normal, irregular, villous

Crypt atrophy (shortened, widely spaced crypts)

Distorted, dilated, branching crypts

Inflammatory changes:

Basal plasmacytosis, increase in cells in basal third of lamina

propria

Increased lamina propria cellularity (round cells and

neutrophils)

Basal lymphoid aggregates

Specific features:

Epithelioid granuloma

Basal giant cells

Excess histiocytes in lamina propria

Features related with activity (separating IBD from normal):

Neutrophils in surface epithelium

Neutrophils in crypt epithelium

Ulceration

UC:

Architecture:

Severe crypt architectural distortion

Severe widespread decreased crypt density

Frankly villous surface

Inflammatory:

Heavy diffuse transmucosal lamina propria cell increase

Diffuse basal plasmacytosis

Miscellaneous:

Increased intensity of the alterations towards the distal colon

Severe mucin depletion

Paneth-cell metaplasia distal to the hepatic flexure

CT:Non-Cancerous cystic Liver Lesions

Hemangiomas are the most common of all benign lever masses. 

Focal nodular hyperplasia is the second most common liver mass.

Appears as lobulated intrahepati lesions with central lucency (scar)

a large, round, low attenuated lesion with enhancing ring.

Rt lobe abscess + Rt hemidiaphragm elevation + recent travel =Amebic liver abscess

aspiration is not mandatory.

Typical echinococcal liver cyst in the right lobe of the liver.

sheepherder + cough + liver cyst with septations, eggshell calcification and hydated sand =Echincoccosis

Haptic adenoma

Well demarcated mass with early enhancement in the arterial phase before iso-attenuation in the delayed phase. strongly associated with OCP. MRI spoked wheel appearance. Can rupture: resect/ embolise.

Liver imaging atlas

Crohn's Disease

granulomas with giant cells in submucosa and serosa. This is an important diagnostic feature of Crohn's disease. Note lymphocyte inflammation in adjacent tissue

Wilson disease

Rhodanine stain of the liver in Wilson disease. Red granules of copper are seen in the hepatocytes.

Noalcoholic fatty liver disease

histology of nonalcoholic steatohepatitis. 
Mallory's hyaline bodies (pink filamentous structures,black arrowhead) are cytoplasmic inclusions in hepatocytes consisting of abnormal keratin, hyaline, and other proteins. They are usually found in hepatocytes that are ballooned (black arrow) and are morphologic hallmarks of alcoholic and nonalcoholic steatohepatitis. Mallory's bodies are not cause but rather consequence of cellular injury. Usually hepatocytes with Mallory's bodies do not contain large fat vacuoles, although microvesicular fat may be seen. In this frame, other hepatocytes are present, containing macrovesicular fat globules (white arrow), which occupy almost all cytoplasm, displacing nucleus (white arrowhead) to periphery

Primar sclerosing cholangitis

PSC with "onion skin" oblitrative fibrosis on trichrome staining.

alpha-1-antitrypsin deficiency

This image shows part of liver biopsy taken from a patient with alpha-1-antitrypsin deficiency. 
It has been stained with period-acid Schiff, which strongly stains intrahepatic globules pink [long black arrow]. The hepatocytes containing the globules are concentrated adjacent to a band of fibrous tissue [long black and white arrow]. A mild inflammatory infiltrate and myofibroblastic cells are seen associated with the fibrous tissue [short black and white arrow]. It is likely that this patient has early fibrosis wild mild active hepatitis. If this continues the patient is at risk of developing overt cirrhosis.

Cystic Pancreatic tumours

1- Serous Cystadenoma:

10% of all cystic lesions of the pancreas

Large, palpable asymptomatic upper abdominal mass.

occur equaly in males and females

CT scan: shows a lobulated cystic mass with a central scar, microcytic cluster of small cysts. 20-30% have stellate scar "sunburst".

EUS: shows multiple anechoic cystic cavities 

Histologically consist of multiple tiny cysts that contain watery fluid.

While SCAs rarely have malignant potential, surgical resection for symptomatic lesions or lesions greater than 4 cm is recommended in good operative candidates.

2- Mucinous Cystadenoma:
Almost exclusively in women 40-60 years old
Usually have thick fibrotic walls and can be multiple
Cysts do not communicate with the main pancreatic duct
1-2% of pancreatic endocrine tumours
Histologically consist of multiple cysts containing sticky mucous
The stroma is refered to as 'ovarian like'
Treatment is surgical resection in approperiate patients.

3-Intraductal Papillary Mucinous Tumour IPMT:
Consist of intraductal papillary growth of mucin-producing columnar epithelium.
obstructive pancreatits frequently occurs
CT: dilated main or side ducts
Main duct IPMN: Because of the high risk of invasive cancer in the main duct, surgical resection is recommended ( Whipple's )
Side chain IPMN: still high risk of malignancy. advice resection or survay
At ERCP, half of the patients have the diagnostic finding of a patulous papilla extruding mucous.

coeliac disease

typical duodenal scalloping that is seen in patient with celiac sprue

Marsh classification:

• Marsh stage 0: normal mucosa
• Marsh stage 1: increased number of intra-epithelial lymphocytes, usually exceeding 20 per 100 enterocytes
• Marsh stage 2: proliferation of the crypts of Lieberkuhn
• Marsh stage 3: partial or complete villous atrophy
• Marsh stage 4: hypoplasia of the small bowel architecture

esophageal candidiasis

esophageal candidiasis can be confirmed with esophageal brushings. 

The best treatment option for candida esophagitis is a systemic antifungal agent such as fluconazole. 

Topical antifungal agents such as nystatin may not  sufficient. 

eosinophilic esophagitis (EoE)

eosinophilic esophagitis (EoE) :

Esinophilic oesophagitis ( Dr E Said)

The esophageal rings in this patient with eosinophilic esophagitis (EoE) represent more esophageal fibrosis with remodeling than inflammation.

Remember that endoscopy in EoE is unreliable and often confusing. A history of dysphagia is a clear indication for biopsy sampling even in the absence of evident abnormalities.

Defention od EoE:

Represent a chronic, immune mediated eosophageal disease characterised clinically by symptoms related to oesophageal dysfunction and histologically by an eosinophilic predominent inflammation.

EoE is food related disease that persumed to result from eosionphilic activation to deitary antigen which is limited to the oesophagus.

? abnormalities in chromosome 7

Symptoms:

Adults:

1-Dysphagia for solids 100%

2-Long lasting food impaction 35%

3-Non swallowing related retro sternal pain 50%

Children:

1-Food refusal

2-Failure to thrive

3-Vomiting, regurgitation

4-Chest pain/ abdominal pain

5-Diarrhea

Histology:

> 15 eso/ hpf

eosinophils micro abscesses

surface laying of eosinophils

Its a patchy disease, so several Bx should be taken from proximal and distal oesophagus.

Treatment:

1-Diet:

elemental/ elemination diet

6 food diet elimination ( caw milk, wheat, eggs, soy, nuts,seafood, shellfish )

2-Drugs:

topical corticosteroids

3-Dilatation:

post procedure pain, risk of deep ulceration/ perforation

2nd line treatment.

Check this article: Eosinophilic oesophagitis in adults

pseudomembranous colitis

Pseudomembranous colitis is due to C. difficile infection, gram-positive bacillus that colonize the gut following transmission via the feco-oral route and disruption of the gut flora following course of antibiotic.
The organism produces 2 exotoxins: toxin A (enterotoxin) and toxin B (cytotoxin).
C. difficile May be detected in 1-3% of healthy adults and up to 50% of infants and children carry it. 
Treatment of asymptomatic carriers is not recommended. 
Pseudomembranous colitis occurs in only 10% of cases of antibiotic-associated diarrhea. 
In 5-19%, it may be localized to the proximal colon. 
Studies suggest that C. difficile and inflammatory bowel disease are being seen together more frequently. Rates have increased 2-fold for Crohn’s disease and 3-fold for ulcerative colitis. 
When severe disease is encountered as manifested by pseudomembranes, colon wall thickening, WBC>15,000, creatinine rise by 50%, decreased albumin, and/or increased lactate treatment with vancomycin 125 mg qid for 7-14 days is recommended. 
Recurrent C. difficile infection is thought to occur in 10-25% of patients. After one recurrence, additional recurrences are 40-60% more likely.

Autoimmune pancreatitis

AIP is type of chronic pancreatitis characterized by an autoimmune inflammatory process in which prominent lymphocye infiltration with associated fibrosis of the pancreas cuases organ dysfunction.
AIP is one component of multisystem IgG4 associated fibro-inflammatory disease.
The diagnosis is based on combination of clinical, radiological and pathological criteria.

Clinical features include:
-painless jaundice
-upper abdominal discomfort
-Wt loss
-DM i in 75%
-other associaed autoimmune disorders

Radiological features:
-CT: sausage-shaped pancreas
-ERCP: low CBD stricture, diffuse pancreatic stricturing.

histologicaly, there are 2 types:
1-Lymphoplasmacytic LPSP
   IgG4 positive,
  fibrosis > inflammation
  older age, M > F
2-Idiopathic duct centric IDCP
   IgG4 negative ( i.e no serum marker)
   inflammation > fibrosis
   younger age, M=F

Treatment:
corticosteroids
The failure to differentiate AIP from malignancy may lead to unnecessary pancreatic resection.

sausage-shaped pancreas
The CT image displays the characteristic pattern of autoimmune pancreatitis. The pancreas is "sausage" shaped and has a characteristic inflammatory "halo." The initial mode of therapy is oral prednisone which is effective in over 60-70% of cases.

Acute Pancreatitis

In the western world gallstones and alcohol account for the vast majority of cases. Other causes include hyperlipidaemia, hypercalcaemia, medications, trauma, viral infection and ERCP. The severity of the pancreatitis may range from mild and self-limiting to extremely severe with extensive pancreatic and peripancreatic necrosis as well as haemorrhage. In its most severe form the mortality rises to between 40-50%. Pathogenesis Mechanisms by which pancreatic necrosis occurs remain speculative. Any theory must take into account how a very diverse group of aetiological factors can produce the same end point. There is some suggestion that the final common pathway is a marked elevation of intracellular calcium which in turn leads to activation of intracellular proteases. It is these activated enzymes which are responsible for cellular necrosis. In the case of gallstone-related pancreatitis it is believed stones occlude the pancreatic drainage at the level of the ampulla leading to pancreatic ductular hypertension. Such ductular hypertension has been shown in animal models to increase cytosolic free ionized calcium. There is also evidence that alcohol interferes with calcium homeostasis in pancreatic acinar cells.

Clinical features Acute pancreatitis is a differential diagnosis in any patient with upper abdominal pain. The pain usually begins in the epigastrium accompanied by nausea and vomiting. As inflammation spreads throughout the peritoneal cavity the pain becomes more intense. Involvement of the retroperitoneum frequently leads to back pain. The patient may give a history of previous similar episodes or be known to have gallstones. An attack may follow an alcoholic binge. However, in many cases there are no obvious aetiological factors. severity Initial assessment: clinical + amylase/ lipase + organ failure + APACH II 24-48 hours: Glasgow score and CRP 72 hours: CT or MRI. Complete extent of pancreatic and peripancreatic necrosis may only be clear after 72 hr after the onset.

Treatment The initial management of acute pancreatitis is similar, whatever the cause. A multiple factor scoring system (ideally APACHE II with a modification for obesity) should be carried out at the end of the first 24 hours after presentation to allow identification of the 25% of patients with a predicted severe attack. This should be repeated at 48 hours to identify a further subgroup who appear to be moving into the severe category. These patients should then be managed on a high-dependency or intensive care unit. Even patients outside of the severe category may require considerable supportive care. Early fluid losses in acute pancreatitis may be large, requiring well-maintained intravenous access as well as a central line and urinary catheter to monitor circulating volume and renal function. Nasogastric suction prevents abdominal distension and vomitus and hence the risk of aspiration pneumonia. Baseline arterial blood gases determine the need for continuous oxygen administration. Prophylactic antibiotics. Broad-spectrum antibiotics, e.g. cefuroxime or aztreonam, reduce the risk of infective complications and are given from the outset. 20 % develop extra-pancreatic infection. Use of routine prophylactic antibiotic is not recommended. Analgesia requirements. Pethidine and tramadol are the drugs of choice, usually administered by a patient control system. The morphine derivatives should be avoided because they can cause sphincter of Oddi contraction. Feeding. In patients with a severe episode there is little likelihood of oral nutrition for a number of weeks. Total parenteral nutrition has been associated with a high risk of infection and has been replaced by enteral nutrition. This is administered via a nasojejunal tube, which is well tolerated and can maintain adequate nutritional input. The nasojejunal position of the feeding tube placed endoscopically overcomes the frequent problem of gastric paresis and there is less likelihood of pancreatic stimulation. In a small proportion of patients, multiorgan failure will develop in the first few days after presentation reflecting the extent of pancreatic necrosis. Such patients will require positive-pressure ventilation and often renal support. The mortality in this group is extremely high (in excess of 80%). Gallstone-related pancreatitis In patients with gallstone-related pancreatitis and associated cholangitis, endoscopic intervention with sphincterotomy and stone extraction is of proven benefit and is the treatment of choice. In the absence of cholangitis, sphincterotomy and stone extraction is only of proven benefit when the episode of pancreatitis is predicted as severe. In less severe cases of gallstone-related pancreatitis intervention can be deferred until full recovery is obtained (an approximate 6-week period).

Intestinal resection and short bowel syndrome

Intestinal resection is usually well tolerated, but massive resection is followed by the short-bowel syndrome. 
The effects of resection depend on the extent and the areas involved. 
Because the gut is long, a 30-50% resection can usually be tolerated without undue problems. 
Shortened bowel depends on several factors:
-the length of the bowel resected
-the location of the bowel resected
-the integrity of the bowel remaining
-the presence of the colon

Residual jejunum shows less capacity for structural and functional adaptation than residual ileum.

The ileum has specific receptors for the absorption of bile salts and vitamin B12, so that relatively small resections will lead to malabsorption of these substances. Removal of the ileocaecal valve increases the incidence of diarrhoea. The following occur in ileal resection: Bile salts and fatty acids enter the colon and cause malabsorption of water and electrolytes leading to diarrhoea. Increased bile salt synthesis can compensate for loss of approximately one-third of the bile salts in the faeces. Greater loss than this results in decreased micellar formation and steatorrhoea, and lithogenic bile and gallstone formation. Increased oxalate absorption is caused by the presence of bile salts in the colon. This gives rise to renal oxalate stones. There is a low serum B12 and macrocytosis. Glucagon-like peptide 2 (GLP-2) is low following ileal resection. GLP-2 is a specific growth hormone for the enterocyte and this deficiency may explain the lack of adaptation with an ileal resection. Investigations include: small bowel follow-through, measurement of B12, bile salts and occasionally fat absorption. hydrogen breath test will show rapid transit. Many patients require B12 replacement and some need a low-fat diet if there is steatorrhoea. If diarrhoea is a problem, colestyramine, which binds bile salts, often helps.

Jejunal resection:

The ileum can take over the jejunal absorptive function. Jejunal resection may lead to gastric hypersecretion with high gastrin levels; the exact mechanism of this is unclear. Structural and functional intestinal adaptation take place over the course of a year, with an increase in the absorption per unit length of bowel.

Massive intestinal resection (short-bowel syndrome):

This most often occurs following resection for Crohn's disease, mesenteric vessel occlusion, radiation enteritis or trauma. There are two types of short-bowel syndrome:

1-Shortened small intestine ending at a terminal stoma:

The major problem is of sodium and fluid depletion and the majority of patients with 100 cm or less of jejunum remaining will require parenteral supplements of fluid and electrolytes, often with nutrients. Sodium losses can be minimized by increasing salt intake, restricting clear fluids between meals and administering oral glucose-electrolyte mixture with a sodium concentration > 90 mmol/L. Jejunal transit time can be increased and stomal effluent loss of fluids and electrolytes reduced by treatment with the somatostatin analogue octreotide, and to a much lesser extent, with loperamide, codeine phosphate or co-phenotrope. There is no benefit of a low-fat diet, but fat assimilation can be increased on treatment with colestyramine and synthetic bile acids.

2-Shortened small intestine in continuity with colon

Only a small proportion of these patients require parenteral supplementation of fluid, electrolytes and nutrients because of the absorptive capacity of the colon for fluid and electrolytes. Unabsorbed fat results in impairment of colonic fluid and electrolyte absorption so patients should be on a low-fat diet. A high carbohydrate intake is advised as unabsorbed carbohydrate is metabolized anaerobically to short-chain fatty acids (SCFAs). SCFAs are absorbed and act as an energy source (1.6 kcal/g) and stimulate fluid and electrolyte absorption in the colon. Patients are often treated with colestyramine, which binds dihydroxy bile acids which otherwise have a deleterious effect on colonic fluid and electrolyte absorption and increase colonic oxalate absorption to form renal stones.

Note:
if less than 100 cm if the ileum is resected, the liver can compansate for the loss of absorptive capacity by producing an increased amount of bile salts, which enter the colon and cause bile irritant diarrhea. this type of diarrhea is treated with cholestyramine, which bind the excess bile salts and improves diarrhea.note:

if more than 100 cm is resected, the liver can no longer compansate. the resulting bile salt deficiency leads to steatrrhea.this can be managed by prescribing diet that consist of medium chain triglycerides.

Bacterial overgrowth

The gut contains many resident bacteria with anaerobic bacteria, e.g. Bacteroides, bifidobacteria, being 100-1000 times more abundant than aerobic (facultative anaerobes), e.g. Escherichia, Enterobacter, Enterococcus. This gut microflora has major functions: -metabolic, e.g. fermentation of non-digestible dietary residues into short chain fatty acids as an energy source in the colon. -initiate vitamin K production. -control epithelial cell proliferation -involved in the development and maintenance of the immune system. -protect the gut mucosa from colonization by pathogenic bacteria.

The upper part of the small intestine is almost sterile, containing only a few organisms derived fromthe mouth. Gastric acid kills most organisms and intestinal motility keeps the jejunum empty. The normal terminal ileum contains faecal-type organisms, mainly Escherichia coli and anaerobes and the colon has abundant bacteria

Bacterial overgrowth is normally only found associated with a structural abnormality of the small intestine, although it can occur occasionally in the elderly without such abnormality. E. coli and/or Bacteroides, both in concentrations greater than 106/mL are found as part of a mixed flora. These bacteria are capable of deconjugating and dehydroxylating bile salts, so that unconjugated and dehydroxylated bile salts can be detected in aspirates by chromatography. The clinical features are chiefly diarrhoea and steatorrhoea. Steatorrhoea occurs as a result of conjugated bile salt deficiency.

The bacteria are able to metabolize vitamin B12 and interfere with its binding to intrinsic factor, thereby leading to B12 deficiency. Conversely some bacteria produce folic acid giving a high serum folate.

Bacterial overgrowth has only minimal effects on other substances absorbed from the small intestine. The vitamin B12 deficiency is not so severe as to produce a neurological deficit. Confirmation of bacterial overgrowth is with the hydrogen breath test; aspiration studies are not routinely performed.

Although bacterial overgrowth may be responsible for the presenting symptoms, it must be remembered that many of the symptoms may be due to the underlying small bowel pathology.

Treatment

If possible, the underlying lesion should be corrected (e.g. a stricture should be resected). With multiple diverticula, grossly dilated bowel, or in Crohn's disease, this may not be possible and rotating courses of antibiotics are necessary, such as metronidazole, a tetracycline, or ciprofloxacin.