Case 3- HPB Flashcards
Cholecystitis features
RUQ pain
Fever
Murphy’s sign
Nausea and vomiting
General malaise
Right shoulder pain
Ascending cholangitis features
Charcot’s triad- RUQ pain, fever, jaundice
Reynold’s Pentad- RUQ pain, fever, jaundice, hypotension, altered mental status
NB- cholangitis is jaundice, cholecystitis isn’t
Primary sclerosing cholangitis
Damage to the medium and large bile ducts
Associated with IBD
Causes cholestasis- itching/pain/fatigue/weight loss/jaundice
Primary biliary cholangitis
Small bile ducts are affected
Associated with women/autoimmunity/sicca syndrome
Causes cholestasis- itching/pain/fatigue/weight loss/jaundice
Stepwise progression of ALD
Alcohol related fatty liver
Alcoholic hepatitis
Cirrhosis (irreversible)
Investigations for ALD
Bed side- observations, abdominal examination
Bloods- LFT FBC (anaemia- raised MCV) UE alphafetoprotein albumin clotting screen gamma GT viral serology (drinkers may be at more risk)
Imaging and specialist- Liver ultrasound, fibroscan- elastography, Biopsy, endoscopy (varices), CT/MRI (HCC)
Wernickes encepahlopathy triad
Confusion
Oculomotor disturbance
Ataxia (co-ordinated movements)
Korsakoff’s syndrome
Memory impairment- confabulation
Behavioural changes
Causes of liver failure
Acute- paracetamol overdose, alcohol
Chronic- viral hepatitis, yellow fever, alcohol, fatty liver disease, PBS, PSC, hemochromatosis, malignancy
Cirrhosis management
Alcohol abstinence
Ultrasound and alpha alphafetoprotein every 6 months
Endoscopy every 3 years (varices)
High protein low sodium diet
UKLED score every 6 months (assess transplant need)
Management of specific complications
Investigations for suspected pancreatic cancer
LFT, FBC, UE, calcium (metastatic cancer)
Ca19-9 tumour marker
CT abdomen (double duct sign)- investigation of choice
Pre-hepatic jaundice stool and urine
Normal stools
Normal urine
Hepatic jaundice stool and urine
Dark urine
Normal (pale) stools
Post-hepatic jaundice stool and urine
Dark urine
Pale stools (acholic)
Management of alcoholic liver disease
All investigations listed previously
Encourage to stop drinking alcohol- help from a detox regime
Nutritional support (esp. thiamine (B1) and protein)
Features of liver cirrhosis
Jaundice – caused by raised bilirubin
Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
Splenomegaly – due to portal hypertension
Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
Palmar Erythema – caused by hyperdynamic cirulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising – due to abnormal clotting
Ascites
Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease
Atrophic testes
Cirrhosis investigations
Bed side- observations, abdominal examination, ascetic tap (if relevant)
Bloods- LFT FBC UE alphafetoprotein viral serology (viral hepatitis) albumin clotting screen autoantibodies
Imaging and specialist- Liver ultrasound, fibroscan- elastography, Biopsy, endoscopy (varices), CT/MRI (HCC)
NB- Thrombocytopenia (platelet count <150,000 mm^3) is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease
Pancreatitis investigations
LFT FBC Lipase (longer half life than amylase) CRP haematocrit Ca (hypercalcaemia can cause it)
CXR exclude others causes
USS abdomen (gallstones?) or CT scan (goldstandard for chornic)(can do X-RAY- pancreatic calcification)
ERCP or MRCP
NB- a diagnosis can be made based on clinical findings and a lipase/amylase 3x normal level, but early USS is important to assess aetiology
Pancreatitis differentials
PUD, perforated viscous, oesophageal spasm, intestinal obstruction, AAA, cholangitis, cholecystitis, MI
Pancreatic cancer tumour marker
CA 19-9
Cholecystitis vs cholelithiasis/ biliary colic
Cholelithiasis causes biliary colic- repeated attacks of abdominal pain (often after a heavy meal- not necessarily fatty)
Cholecystitis- more acute illness. Inflamed gallbladder (usually due to stones) causes nausea, vomiting, pain and fever
Biliary colic/cholecystitis/cholangitis investigations
Bedside- observations, abdominal examination, urine dip (exclude UTI)
Bloods- FBC (WCC), UE (loss of appetite), LFT, CRP (inflammation- cholangitis), Calcium (can cause abdo pain), Lipid profile (increases chance of stones), cultures from 2 sites (if concerned about cholangitis) , Lipase/ amylase- rule out pancreatitis
Imaging- Abdominal ultrasound (look for stones), MRCP
Liver failure
Development of coagulopathy and encephalopathy (better to monitor PT time as it has a shorter half life than albumin)
In previously healthy person- acute
On background of cirrhosis- chronic
Fulminant- resulting from massive necrosis of liver cells
Liver failure symptoms
Jaundice, hepatic encephalopathy, fetor hepaticus, asterixis and apraxia
NB- cirrhosis would have all tell tale signs of liver disease (hepatomegaly, ascites, but difference with liver failure is that you get encephalopathy and deranged clotting)
Liver failure investigations
Mini mental state examination (test mental impairment/ encephalopathy)
FBC UE (hepatorenal syndrome) LFT Clotting screen ammonia Viral serology alpha fetoprotein
Abdominal ultrasound
CT scan
OGD- assess for varices
Management of alcoholic hepatitis
Glucocorticoids
NB- Maddrey’s discriminant function (DF) is often used during acute episodes to determine who would benefit from glucocorticoid therapy
it is calculated by a formula using prothrombin time and bilirubin concentration
(Pentoxyphylline is sometimes used)
Management of ascites
Reduce dietary sodium- most important
Fluid restriction (sodium below 125)
Aldosterone antagonist eg. Spironolactone
Tense ascites- paracentesis (requires albumin cover eg. IV human albumin solution)
Prophylactic ABX if cirrhosis present and protein below 15 (ciprofloxacin)
Surgery- TIPS
Autoimmune hepatitis features
Signs of chronic liver disease or acute hepatitis (fever, jaundice etc.)
Amenorrhea
Investigations- ANA, SMA, LKM1, anti-LC1 antibodies, raised IgG, LFT- raised AST/ALT (hepatic picture), diagnosis can be confirmed via biopsy if in doubt
Management of autoimmune hepatitis
Steroids/other immunosuppressants eg. Azathioprine
Liver transplantation
Bile acid malabsorption
Causes of chronic diarrhoea
Causes
Primary- excessive bilateral acid production
Secondary- Crohn’s disease, cholecystectomy, coeliac disease
Investigation- SeHCAT scan
Management- bile acid sequestrant eg. Cholestyramine
Causes of budd chiari syndrome (hepatic vein thrombosis)
Polycythaemia rubra Vera
Thrombophilia eg. Antitnrombin III deficiency
Pregnancy
Combined OCP
Features of budd chiari syndrome
Sudden onset abdominal pain
Ascites
Tender hepatomegaly
USS with Doppler flow studies- gold standard (not venogram initially)
Drugs that cause hepatocellular liver disease
Paracetamol
Sodium valproate
MAOI
Anti TB drugs
Statin
Alcohol
Amiodarone
Drugs that cause cholestasis (+/- hepatic) liver disease
Combined OCP
Flucloxacillin, co amoxiclav, erythromycin
Anabolic Steroids
Chlorpromazine, prochlorperazine
Sulfonylureas
Drugs that can cause cirrhosis
Methotrexate
Methyldopa
Amiodarone
Gilbert’s syndrome
Autosomal recessive
Unconjugated hyperbilirubinaemia (not in urine)- jaundice may only be seen during an inter current illness, exercise, or fasting
Investigation- rise in bilirubin following fasting (do other tests to exclude other pathology)
No treatment
Features of haemachromatosis
Autosomal recessive
Lethargy and arthralgia (hands)- Pseudogout
Erectile dysfunction
Bronze skin pigmentation
Diabetes Mellitus
Stigmata of liver disease
Cardiac failure (dilated cardiomyopathy)
Hypogonadism (secondary to cirrhosis and pituitary dysfunction)
Cranial diabetes insipidus
Investigations for haemochromatosis
Iron studies
High transferrin saturation (men 55, women 50)
Raised ferritin and iron
Low TBIC
Imaging- liver biopsy (Perls stain), joint x ray (chondrocalcinosis (calcium deposits in joint space aka. pseudogout)), MRI whole body (iron deposits)
NB- obviously other tests to rule out other causes including bloods and exam, and HFE genetic testing for family members
NB- ferritin and transferrin % are used in monitoring
Management of haemochromatosis
Genetic counselling, avoid alcohol
Regular venesection (keep transferrin and serum ferritin below 50)
Desferrioxamine second line
Management of hepatic encephalopathy
Treat underlying cause
As with any delirium- reassure, calm, same staff, re orientate etc.
Lactulose first line, with rifaximin (ABX) for secondary prophylaxis of hepatic encephalopathy
Nutritional support. They may need nasogastric feeding.
Risk factors for HCC
Hepatitis B (world), hepatitis C (UK)
Alcohol
Haemachromatosis
NAFLD
Any chronic liver disease
PSC
Features of HCC
Late presentation of liver cirrhosis or failure stigmata
Raised AFP for HCC, Ca19-9 for cholangiocarcinoma
Management of HCC
Early disease- surgical resection
Liver transplant
Sorafenib
Ischaemic hepatitis
Acute hypoperfusion diagnosed in presence of an inciting event eg. Cardiac arrest and marked increase in aminotransferases
Often in conjunction with AKI
NAFLD associations
Obesity
T2DM
Hyperlipidaemia
Sudden weight loss or starvation
NB- insulin resistance is thought to be involved
Investigations for NAFLD
Bedside- observations, abdominal exam
Bloods- LFT, FBC, UE, Enhanced Liver Fibrosis (ELF) blood test (HA, PIIINP and TIMP-1)
Imaging and specialist- USS, NAFLD fibrosis score, fibroscan
Pancreatic cancer associations
Increasing age
Smoking
Diabetes
Chronic pancreatitis
HNPCC
MEN
BRAC2
Features of pancreatic cancer
Painless jaundice (pale stools, dark urine, pruritus)
Anorexia, weight loss, epigastric pain
Steatorrhoea (loss of exocrine function)
DM (loss of endocrine function)
Atypical back pain
Migratory thrombophlebitis
Cholestatic liver function tests
Histology of pancreatic cancer
80% are adenocarcinoma of the head of the pancreas
Management of a phonemic liver abscess
Caused by staph in children and E. coli in adults
Drain with ABX
Amoxicillin, ciprofloxacin, metronidazole
What is Wilson’s disease
Excess copper deposition in bodily tissues
Features of Wilson’s disease
Hepatitis, cirrhosis
Basal ganglia degeneration- Parkinsonism, asterixis, chorea
Speech, behavioural, dementia, psychiatric problems
Kayser-fleischer rings (green brown rings in periphery of iris)
Renal tubular acidosis
Haemolysis
Blue nails
Investigations for Wilson’s disease
Slit lamp evaluation (Kayser-fleischer rings)
Reduced serum caeruloplasmin
Reduced total serum copper
Increased 24 hour urinary copper excretion
Liver biopsy
Management of Wilson’s disease
Copper chelation using penicillamine (or trientene)
Management of cholecystitis
Analgesia antiemetics fluids
IV antibiotics
Early laparoscopic cholecystectomy within 1 week of diagnosis
Factors suggesting severe pancreatitis
55+
Hypocalcaemia
Hyperglycaemia
Hypoxia
Neutrophilia
Elevated LDH and AST
NB- amylase level isn’t of prognostic value
Causes of pancreatitis
GallStones and alcohol are most common in UK
GET SMASHED
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyper triglyceridaemia/hypercalcaemia/hypothermia
ERCP
Drugs- azathioprine, mesalazine, furosemide, valproate
Complications of acute pancreatitis
Peripancreatic fluid collection- no wall of granulation tissue. No treatment
Pseudocysts- wall of fibrosis granulation tissue. 4 weeks after attack. Persistent mild elevation of amylase. Observe for 12 weeks, then radiological drainage
Pancreatic necrosis- necrosectomy has a high mortality rate
Pancreatic abscess
Haemorrhage- may see grey turners sign
ARDS- high mortality rate
Management of acute pancreatitis
IV fluids
Analgesia (IV opioids)
Not NBM unless vomiting- offer enteral nutrition eg. NG
Don’t offer prophylactic ABX
Treat underlying cause eg. Cholecystectomy for gall stones, ERCP to remove stones in biliary system
Management of ascending cholangitis
Conservative- pain relief, anti emetics, IV fluids, admit to hospital, bleep seniors/ general surgeons, oxygen, NBM
Medical- IV ABX (local policy)
Surgical- ERCP (remove blockage), cholecystectomy may be necessary
Features of chronic pancreatitis
Epigastric pain radiating to the back
Pain worse 15-30 minutes after eating a meal
Steatorrhoea (5-25 years later)
DM (20 years later)
Investigations for chronic pancreatitis
AXR
CT abdomen (investigation of choice- calcification)
Faecal elastase as a functional test (exocrine function)
Management of chronic pancreatitis
Conservative- Analgesia, Abstinence from alcohol and smoking
Medical- Pancreatic enzyme supplements
Surgery- to treat complications such as cysts
Key complications of chronic pancreatitis include;
Loss of exocrine function, resulting in a lack of pancreatic enzymes (particularly lipase) secreted into the GI tract
Loss of endocrine function, resulting in a lack of insulin, leading to diabetes
Management of choledocholithiasis
Analgesia antiemetics antispasmodics
Surgical-ERCP to remove the stone
Investigations for cholecystitis or cholangitis
Bedside- observations, A-E, full abdominal examination, pregnancy test (if appropriate)
Bloods- FBC UE LFT CRP 2x blood cultures ABG amylase and lipase
Imaging- RUQ USS
When does delirium tremens occur
48-72 hours after termination of drinking
Management of delirium tremens
Librium (chlordiazepoxide)
IV pabrinex (thiamine (B1) and vitamin C)
no lorazepam
Management of liver failure
Supportive- NG tube, catheter, Haemodialysis, vitamin deficiencies etc,
Medical- laxatives
Surgical- transplant
Features of hepatitis
Abdominal pain, fatigue, pruritus, myalgia, nausea and vomiting, jaundice, fever (viral hepatitis)
Investigations for hepatitis of unknown cause
Observations, full abdominal examination
Bloods- FBC, UE, LFT gamma GT (alcohol), CRP, haemanitics, coagulation screen, viral serology, antibodies (autoimmune hepatitis)
Imaging- abdominal USS
Features of acute pancreatitis
Constant severe epigastric pain, radiates to back, worse after meals and when supine, improves on leaning forward
Nausea and vomiting
Signs of shock and possible jaundice
Abdominal tenderness
Skin changes eg. Cullens or grey turners
Alcoholic ketoacidosis
A non-diabetic euglycaemic form of ketoacidosis. It occurs in people who regularly drink large amounts of alcohol.
Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration
The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis.
NB- Metabolic ketoacidosis with normal or low glucose: think alcohol
NB- this is different to alcoholic hepatitis where steroids are required
Features of gallstones ie. biliary colic
Severe, colicky epigastric or right upper quadrant pain
Often triggered by meals (particularly high fat meals)
Lasting between 30 minutes and 8 hours
May be associated with nausea and vomiting
Complications of biliary colic
Acute cholecystitis
Acute cholangitis
Obstructive jaundice (if the stone blocks the ducts)
Pancreatitis
LFT in biliary colic/gallstones
Normal
If in bile duct- may show cholestatic picture eg. raised bilirubin, raised ALP (more so than ALT/AST)
Management of gallstones
Asymptomatic- conservative ie. dietary and weight advice
Symptomatic- laparoscopic cholecystectomy
Management of cholecystitis
Conservative- admission to hospital, NBM, NG tube, IV fluids
Medical- IV ABX
Surgical- ERCP (remove stones), cholecystectomy in 1 week
Organisms that cause ascending cholangitis
Escherichia coli
Klebsiella species
Enterococcus species
Common causes of cirrhosis
Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C
Rare causes of cirrhosis
Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons Disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs (e.g. amiodarone, methotrexate, sodium valproate)
Scoring systems for cirrhosis
Child-Pugh- severity (bilirubin, PT time, ascites, encephalopathy, albumin)
UKMELD- 3 month mortality/ requirement for liver transplant ( bilirubin, creatinine, INR and sodium and whether they are requiring dialysis)
Complications of cirrhosis
Malnutrition
Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma
Common locations of varices
Gastro oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via the umbilical vein (caput medusae)
Predisposing factors for hepatic encephalopathy
Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications (particularly sedative medications)
General Management of ALD
Conservative- stop drinking alcohol, detox programme
Medical- nutritional support (thiamine (B1)), high protein diet, steroids (severe alcoholic hepatitis)
Further- Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy), Referral for liver transplant in severe disease (abstain from alcohol for 3 months prior to referral)
Alcohol withdrawal timeline
6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”
Features of delirium tremens
Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia (difficulties with coordinated movements)
Arrhythmias
Non invasive liver screen (when cause of abnormal LFT’s is unknown)
Ultrasound Liver
Hepatitis B and C serology
Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis)
Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis)
Caeruloplasmin (Wilsons disease)
Alpha 1 Anti-trypsin levels (alpha 1 anti-trypsin deficiency)
Ferritin and Transferrin Saturation (hereditary haemochromatosis)
Management of NAFLD
Conservative- Weight loss, Exercise, Stop smoking
Control of diabetes, blood pressure and cholesterol, Avoid alcohol
Causes of hepatitis
Alcoholic hepatitis
Non alcoholic fatty liver disease
Viral hepatitis
Autoimmune hepatitis
Drug induced hepatitis (e.g. paracetamol overdose)
Hepatitis A
RNA virus
Faeco-oral route
Most common worldwide
Cholestasis
Resolves without treatment
No complications
Vaccine- chronic LD/MSM/haemophilia/ high incidence/ IVDU/ occupational risks
Hepatitis B
DNA virus
Blood born, sexual, and vertical transmission
Chronic infection, cirrhosis, HCC, polyarteritis nodosa, cryoglobulinemia
10% untreatable
Vaccine available
NB- The appearance of ground-glass hepatocytes on light microscopy can point towards a diagnosis of chronic hepatitis B infection
Hepatitis C
RNA Virus
Blood borne, sexual, and vertical transmission
Chronic infection (majority), Cirrhosis , Hepatocellular cancer
Treatable with antivirals (ribavirin: no pregnancy for 6 months after)
Hepatitis C
RNA Virus
Blood borne, sexual, and vertical transmission
Yes (80%)
Chronic infection, Cirrhosis , Hepatocellular cancer
Treatable with antivirals
Management of hepatitis C
Conservative- screen for other blood borne diseases, refer to hepatology/ID, notify PHE, stop smoking and alcohol, education about transmission (contact tracing)
Medical- test for complications eg. fibro scan, Antiviral treatment with direct acting antivirals (DAAs)
Surgical- Liver transplantation for end-stage liver disease
Hepatitis D
RNA virus
Can only survive with hepatitis B
Hepatitis E
RNA virus
Transmitted via faeco-oral route
Disease is worse during pregnancy
Resolves without treatment- no long term complications or chronic infection
What is primary biliary cholangitis
Immune system attacks small bile ducts in liver
Features of PBC
Fatigue
Pruritus
GI disturbance and abdominal pain
Jaundice
Pale stools
Xanthoma and xanthelasma
Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)
Associations with PBC
Middle aged women
Other autoimmune diseases (e.g. thyroid, coeliac)
Rheumatoid conditions (e.g. systemic sclerosis, Sjogrens and rheumatoid arthritis)
Investigations for PBC
Bedside- abdominal examination, observations
Bloods- LFT (ALP raised), autoantibodies (AMA, ANA), IgM and ESR raised
Specialist- biopsy
Treatment for PBC
Conservative- general lifestyle interventions
Medical- Ursodeoxycholic acid reduces the intestinal absorption of cholesterol and is used to prevent disease progression (even when asymptomatic), Colestyramine (prevents bile acid absorption and gives symptomatic relief from pruritus), immunosuppression (steroids)
Surgical- liver transplant (bilirubin >100)
Complications of PBC
Advanced liver cirrhosis
Portal HTN
Symptomatic pruritus
Fatigue
Steatorrhoea (greasy stools due to lack of bile salts to digest fats)
Distal renal tubular acidosis
Hypothyroidism
Osteoporosis
Hepatocellular carcinoma
What is primary sclerosing cholangitis (PSC)
A condition where the intrahepatic or extrahepatic ducts become strictured and fibrotic
Risk factors for PSC
Male
Aged 30-40
Ulcerative Colitis
Family History
Presentation of PSC
Jaundice
Chronic right upper quadrant pain
Pruritus
Fatigue
Hepatomegaly
Investigations for PSC
Bedside- observations, abdominal examination
Bloods- LFT (cholestatic picture), UE, FBC etc. (no autoantibodies are highly sensitive or specific, but can try ANA pANCA (show if there is an immune component, may respond to immunosuppression)
Imaging- MRCP (diagnostic)
Associations and complications of PSC
Acute bacterial cholangitis
Cholangiocarcinoma develops in 10-20% of cases
Colorectal cancer
Cirrhosis and liver failure
Biliary strictures
Fat soluble vitamin deficiencies
Management of PSC
Conservative- general lifestyle measures, monitor for complications
Medical- cholestyramine (reduce bile acid absorption)
Surgical- ERCP (stent any strictures)
Complications of haemochromatosis
Type 1 Diabetes (iron affects the functioning of the pancreas)
Liver Cirrhosis
Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)
Cardiomyopathy (iron deposits in the heart)
Hepatocellular Carcinoma
Hypothyroidism (iron deposits in the thyroid)
Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
What is the only suspected cancers that GP’s can directly refer patients for a CT scan (don’t need to see specialist)
Pancreatic cancer
Named signs in pancreatic malignancy
Courvoisier’s law- a palpable gallbladder along with jaundice is unlikely to be gallstones. The cause is usually cholangiocarcinoma or pancreatic cancer.
Trousseau’s sign of malignancy- migratory thrombophlebitis as a sign of malignancy, particularly pancreatic adenocarcinoma.
Antibody associated with PBC
Anti mitochondrial (IgM)
Constituents of pabrinex
Vitamin B1 (thiamine)
Vitamin C
Difference in complications of PSC and PBC
PSC- cholangiocarcinoma and CRC
PBC- HCC, cirrhosis and subsequent variceal haemorrhage, osteoporosis
NB- cirrhosis more likely in PBC
Antibiotic prophylaxis should be given to patients with ascites under what circumstances
-patients who have had an episode of SBP
-patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
NB- oral ciprofloxacin or norfloxacin
Scoring systems for acute pancreatitis
eg. Glasgow/APACHE
Some common criteria;
age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST
Scoring systems for acute pancreatitis
eg. Glasgow/APACHE
Some common criteria;
age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST
NB- amylase level is not taken into account
Gallstone Ileus
In gallstone ileus, a plain abdominal film classically shows small bowel obstruction and air in the biliary tree (symptoms similar to obstruction)
Mirizzi’s syndrome
where a gallstone within the gallbladder compresses the bile duct to cause an obstructive jaundice
Spider naevi vs telangiectasia
Spider naevi can be differentiated from telangiectasia by pressing on them and watching them fill. Spider naevi fill from the centre, telangiectasia from the edge
NB- spiders in the centre of their webs
Stratification of Acute Pancreatitis
Mild No organ failure, no local complications
Moderately severe No or transient organ failure (<48 hours), possible local complications
Severe Persistent organ failure (>48 hours), possible local complications
Management of a variceal bleed vs peptic ulcer bleed
Same stabilisation techniques
Variceal- terlipressin/IV AVX/ endoscopic intervention eg. band ligation
Peptic ulcer- IV PPI/ endoscopic intervention (adrenaline injection)
