Definitions, Tables, Facts - Gastro Flashcards
Causes of acute liver failure
Paracetamol Mushroom poisoning Drug induced - esctasty, metamphet, valproate, isnoniazind Viral Hep - A, B, E EBV, CMV, Ischaeamic hep Budd Chiari Wilsons Post resection
Causes of chronic liver failure
Viral B, C Alcoholic liver disease Non alcoholic steatohep Haemachromatosis Veno-occlusive disease Right side failure??
Autoimmune - hepatitis, PSC, PBS
Defining trial of ALF
Coagulopathy
Jaundice (hyperbili)
Enceph (with raised ICP)
Defining features of chronic failure/cirrhosis
Jaundice Ascites and SBP Variceal disease Encephalopathy WITHOUT raised ICP Hepatorenal synd Risk of HCC
Define ALF
Rare
Life threatning disease
With risk of MOF and Death
Triad of
Encephalopathy
Coag
Jaundice
Timing of ALF
Onset from jaundice to enceph
Hyperacute - <7 days
Acute 7-28 days
Sub acute 5-12 weeks
Manifestations of ALF
Haemodynamic instability - high output vasodilation
AKI
Coagulapathy
Encephalopathy and coma (higher ammonia, higher risk of ICP)
Infection - sepsis
Grade encephalopathy
West Haven system
Grades 1 -4
1 - Lack of awareness, euphoria, anxiety, impaired addition
2 - Lethargy, apathy, suble persona change, impaired subtraction, inapprpriate
3 - Somnolence —> semi stupour, confusion, disorientation, responds to voice
4 - Coma
Management feaures
Specialist input —> transfer to liver centre Specific therapies —> NAC Supportive - ABC and RRT Manage enceph and ICP Manage coag Transplant
Features of treating enceph and ICP
1) remove ammonia
Lactulose, LOLA, rifaxmine
RRT
2) manage oedema Temperature Sedation 30 degree head up nursing Loose ties Optimise CPP
Features of coagulapthy management in ALF
Routine correction - afffects PT and therefore transplant decisions
Only if needing cover for procedures
Contra indictations to liver transplant in ALF
Severe cerebral oedema
Rising vasopressor needs
Uncontrolled sepsis
Major psych co-morbidity
Kings Criteria - Paracetamol
Ph< 7.3 (24 hours post admission AND following fluid resus)
OR
Grade 3 to 4 enceph
PT >100s
Cr>300
OR
Arterial lactate >3,5 at 4 hours
OR
>3 at 12 hours
Kings Criteria for non paracetamol
PT>100
OR
3 of
PT>50 Non hep A/B aetiology Age <10 or >40 Bili > 300 Duration of jaudice prior to enceph > 7 days
Why would chronic liver failure get into ITU
Variceal haemorrhage
Management of encephalopathy
Renal/metabolic dysfunction
Ascites and hepato renal syndrome
Extra hepatic —> sepsis, resp failure
CVS changes in cirrhosis
Hyperdynamic circ —> low PVR, inc CO, decreased BP
Cirrhotic cardiomypoathy —> diastolic dysfunction
Alterations in hepatic/splanchnic flow —> hepatic resistance—> portal congestion, varices
Vascular changes to other organs - pulmonary vasodilation, VQ mismatch
Renal vasoconstriction —-> hepato renal
Mortality scoring systems in CLD
Child-Pugh Score
MELD
UKELD
General systems - SOFA better than APACHE II in cirrhosis
CLIF - SOFA
Features of Child Pugh score
Graded 1-3 per category
Bilirubin Albumin INR Ascites Enceph
A - 5-6
B - 7-9
C - >9
Feautres of MELD
Creatinine, INR and Bilirubin
Placed in eqn.
UKELD , adds in sodium
Why is renal dysfunction common in cirrhotivcd
Hypovolaemia —-> laxatives, blood loss from GI, sepsis, loop/spiro often used
Sepsis
Nephrotoxic agents - diuretics
HRS
Types of HRS
Type 1 - Higher mortality —> two fold increase in Cr in 2 weeks
Type 2 - Ascites refractory to dieurtetic therapy
Diagnosis of HRS
Cirrhosis with ascites
No improvement in creatinine after 2 days of diuretic withdrawel AND volume explansion
Albumin 1g/kg per day to a max of 100g
No shock
No current or recent nephrotoxics
Absence of parenchymasl kidney disease
(Proteinurial 4500mg/day, microhaematuria +/- abnormal renal US
Management of renal dysfunction in HRS
Volume replacement HAS is colloid of choice 1g/kg load then 20-40g/day May bind cytokines Where sepsis predominates over HRS —> crystalloid
Vasoconstriction Terlipressin Splanchnic vasoconstriction —> renal perfusion increases and effective volume Avoid with high dose norad Can be given outside of ITU 1mg 4-6 hours
Non-responders - 50%
RRT as bridge to trasnsplant
Livefr support devices not in use
Causes of ascites
Portal hypertension —> cirrhosis, Budd Chiari, Heart Failure
Hypoalbuminaemia —> nephrotic, malnutirion
Peritonal disesae —> infection, ovarian Ca, mesothelioma
Consequences of ascites
Pressure —> ACS
Resp comprimise
SBP
Hepatic hydrothorax
HRS
PAIN
Treatment of ascites
Sodium restriction
Furosemide and spiro
Paracentesis
Total abdominal paracent —> remove ALL fluid in a time frame
Limited paracent —> remove to an end point (e.g. IAP <20mmHg)
Benefits and risk of paracentesis
Benefits
Reduce intra abdominal pressure
Improved organ blood flow
Improved lung compliance
Patient comfort
Risk Cutaenous or abdominal infection Haemodyamic collapse Renal dysfunction from low BP Viscous perf
How long should an ascitic drain be left in
6 hours - infection risk
How much HAS after draining ascites
100mls of 20% for every 1-2 litres
Classification of hepatic encephalopathy (in terms of causes)
Not the ALF criteria
A - related to ALF
B - related to porto-systemic bypass
C - relates to cirrhosis
Difference from ALF is it happens for different reasons, and there is no rise in ICP
Causes of hep enceph in cirrhosis
Sepsis, Constipation Electroylte disturbance GI bleed Meds - benzos, propanolol (portal hypertension)
Management of hepatic enceph
Lactulose
Phosphate enemas
LOLA
RRT - indicated in hyperammonia
Gut -
Rifaximin
TIPPS —> reduce calibre
Indications for Liver trasnplanbt
ALF HCC Decompensated CLD ACquired or chronic biliary disease Metabolic disease
Peri-transplant issues
3 phases
Resection
Anhepatic phase
Reperfusion
Monitoring
Plasma lactate, normalises in first 6 hours
Monitor coag and gluconeogeneis (rising plasma glucose)
Immunosuppresion
iv Abx and antifungal
Peri op hydrocort/m-pred
Enteral early - tacrolimus, cyclosporin, azathioprine If renal dysfunction - low dose tacrolimus and alternatives given basiluxamab
Post transplant complications
Primary Non Function
Failure to start enzymatic procceses
Transaminases dont normalise or rebound hyperbili, coag
Hep artery thrombosis
Doppler at 24 huors
If weak, triple phase CT
Revascularise, or regraft
Venous thrombosis
Biliary Issues Bile leak/obstruction Rising bili and ALP ERCP?? Beware biliary peritonitis, drain/repair biliary
Sepsis
Define upper GI haemorrhage
Any bleed from the pharynx to the ligament of Treitz
Causes of non-variceal bleeds
H.pylori
Peptic ulcer disease
NSAIDs
NG tube trauma Erosive tumour Vascular ectasia Mallery Weiss Angiodysplasia Dieulafoy lesions
Transfusion target in non variceal bleed
70g/dL reduced mort compared to 90
Features of non variceal bleed management
ABCDE Early aggressive resus Correct coag Transfuse to 70 Risk stratify PPI - Hong Kong
Name the risk stratifying scores in non variceal bleeds
Glascow Blatchford Score
Rockall (but needs endoscopy to be done to complete the score)
Feautres of Glascow Blatchford Score
On admission Blood Urea Hb (different scores for men and women) Systolic BP Other (pulse>100) Melanea Syncope Liver disese Heart failrue
Features of Rockall Score
Score 0-3
Age Shock Co-morbidities Diagnosis (mallery, other, GI cancer) Evidence of bleeding
Endotherapy options in non-variceal bleeds
Submucosal adrenlaine 1:10000
Biploar diathermy
Aluminium clipping
Haemostatic sprays
Differences between stress ulcers and peptic
Stress more likely to appear in gastric fundus
Bleeding is a diffuse ooze
Often related to reduced splanchnic flow
Risks or features associated with stress ulcer
Mechanical vent for more than 48 hours Coagulopathy MOF History of GI bleeds Trauma or burns Steroids Renal failure
Stress ulcer prophylaxis
Enteral feed early —> improves splanchnic flow
Drugs: PPI H2 antag Sucrafate - protect mucosa Antacids
PPI superior to H2, but mortality same
Sucrafate not as effective as either - second line
Sucrafate - inhibit digoxin and warfain, phenytoin
PPI - interact with anti-platelets
Risk of nosocomial pneumonia through acid suppresion (poor evidence)
Association between c.diff and acid suppresion
Compare non variceal to variceal treatments
Pre-endo, endoscopic, and resuce
Pre - Non variceal - iv PPI, variceal —> terlipressin and Abx
Endo - Adrenaline, diathermy, clips. VERSUS endoscopic band ligation and sclerotherapy
Rescue - Repeat, mesentertic angio and embolise, surgery
VERSUS repeat, Sangstaken Blackmore, Stent, TIPPS, transplant
Normal portal pressure in a non-cirrhosis
Less than 5mmHg
Portal hypertension value
Value at which haemorrhage occurs
Greater than 5mmHg
Greater than 10mmHg
Places where varices can form
Oesophagus —> retrograde splenic/long gastric vein flow Gastric fungus Rectum Retroperitoneal Abdominal wall Liver bare area
Grade of varices
3 grades
1 - Small, disappear on insufflation of oesophagus
2 - between 2 and 3
3 - Large varices, occluding lumen
Management options of a variceal bleed
Antibiotics
Secondary infections
Prophylaxis reduces mortality
Cipro/ceftriaxone
Vasoactive
Terlipressin - constricts mesenteric arterioles
Sengstaken
Endoscopy
1 - no tx
2 and 3 beta blockade and band ligation
TIPPS
Features of risk of rebleeding in varices
High Child-Pugh score
Increasing portal pressure
High risk endoscopic features
Indications for TIPSS
Refractory variceal haemorrhage
Recurrent/refractory ascites
Hepatopulmonary syndrome
Hepatic hydrothorax
Things to do before TIPSS
Doppler of portal / biliary system
Relieve biliary obstruction before TIPSS
Echo - RH —> TIPPS causes increased RV preload
EEG - TIPPS can cause HE (not really in practise)
Describe a TIPPS
Venous access - RIJ
Catheter down SVC to hepatic vein
Portal vein identified —> needle directed from hep vein to portal vein
Guidewire and stent deployed
Contra-indications to TIPSS
Severe tricuspid regurgitation
Severe pulmonary hypertension
CCF
Complications of TIPPS
Access —> liver capsule rupture, biliary rupture and fistula, hepatic infarct
Stent —> thrombsis, migration
Shunt —> encephalopathy
Define diarrhoea
WHO —> 3 or more loose or watery stools a day
BGS —> 200g a day
Bristol - types 6 or 7
Types of diarrhoea
Osmotic Can’t absorb osmotically active substances Mg, Bile salt, lactulose Malapbsorptiopn —> coeliac STOP WITH STARVATION
Secretory
Increased secretion from mucosa
Decreased absorption
Infective diarrhoea and example —Cholera…secretes chloride
Inflammatory
Loss of muscles integrity
?bloody
IBD or infection — E. coli, shigella, salmonella
Dysmotile
After ileus for example
What is c.diff
Gram negative anaerobe, spore forming
Risk factors for c.diff
Use of Abx —> penicillins cephalosporins, clinicamycin
Long standing IBD
Intestinal surgery
PPI
Long hospital stay
Cancer, immunosuppresion, DM
Diagnosis of C.diff
PCR —> colonisation/carrier
CDT (toxin B) —> active infection
Colonoscopy —> pseudomembranes
Complications of c.diff
Bowel Perf
Toxic mega colon —> colonic dilation >7cm
Fulminant colitis severe abdo pain, lactic acidosis hypovolaemia fever raised WCC
Tx of c.diff
Metronidazole —> oral or iv
Vancomycin —-> oral only
Fidaxomicin —> non inferior to vanc but less SE
Faecal transplant
Surgery
colectomy
Other infective agents in diarrhoea
Inflammatory E.coli Shigella (cipro/ceftriaxone) Campylobacter (cipro) Salmonella (cipro)
Cholera (cipro/doxy)
Viral - Noro, rota, adeno ,CMV (ganciclovir)
Parasite - giardia, entamoeba (metronidiazole)
Causes of acute pancreatitis
Alcohol abuse ERCP Gallstones Trauma Metabolic - hyperlipids, hyper algae Mia Drugs - Azathioprine, steroids Infection -CMV, mumps
Diagnostic criteria of pacnreatitis
2 out of 3 of
Upper abdominal pain
Amylase of lipase >3 x upper range of normal
CT findings
Types of CT finding of pancreatitis
Acute interstitial oedematous 85%
Necrotic 15%
Severity class of pancreatitis Atlanta
Mild - no organ failure, no local/systemic complications
Mod - transient (<48hours) organ failure, OR complications
Severe - persistant organ failure or complication > 48 hours
What are the local complications of pancreatitis
Necrosis of the pancreas or peri-panic tissue
CT and FNAC
Systemic determinants of acute panc
Present and persistent organ failure
Sofa score >2
Transient —> less than 48 hours
New panc definitions building on Atlanta
Mild - absence of necrosis and organ failure
Mod - sterile necrosis+/- transient failure
Severe - infected necrosis +/- persistent failure
Critical - infected AND persistent failure
Pancreatitis scoring systems
Ransom Score Glasgow Imrie Score APACHE II SOFA Balthazar CT severity Index
Describe Ransons score
Risk stratifies and predict mortality
Half on admission, half 24 hours later
Admission —> Age>55 AST>250 Glucose >11.2 WCC>16 LDH >350
24 hours —>. Fall in Hct>10% PaO2<8 Base def >4 Fluid sequest > 6 litres Urea rise >1.8
Ransons score indicates:
3 is severe
0-2: 2%
3-4 15%
5-6 40%
7-8 100%
What’s on the Glasgow Imrie Score
Age PaO2 WCC Calcium Urea LDH Albumin Glucose
3 or more —> critical care
Complications of pancreatitis
Local Necrosis Pseudocyst (>4 weeks) Peri-pancreatic collections (early) Pseudoaneurysm Mesenterinc vein thrombus
Systemic —> exacerbation of co-existing disease
Organ failure —> ARDS, effusions, atectasis
Shock
AKI
Ileus, metabolic issues, ACS
Management principles of acute pancreatitist
Admit if Ranson >3
Supportive - fluid resus, analgesia, organ support (drip and suck no more)
Nutrition - no gut rest. Attempt NG feed. If not, try NJ. PN only for people who fail altogether
Feed early
Antibiotics - no. Only in infected necrosis after FNAC.
Probiotics - harmful, increased ischaemia
ERCP - gallstone pancreatitis
In presence of cholangitis
Cholestasis
Predicted severe
Do not do if mild.
Principles of necrotic pancreatitis, diag and management
Can be sterile or infected
Infected —> positive bacterial/fungal/culture on FNAC
Gas in pancreatic bed on imaging
Tx —> iv. Broad spec (carbapenem)
Wait for necrosis to wall off (4 weeks)
Percutaneous or endoscopic drainage OR minimally invasive necrosectomy Whipples…
Normal IAP
5-7mmHg
Define and grade IAH
Greater than 12mmHg
1 - 12-15
2 - 16-20
3 - 21-25
4 >25 mmHg
How to measure IAP
Direct - laparoscopic port
Indirect - ballon tipped catheter in stomach or bladder attached to transducer
Zero vesicular transducer to pubic symph
APP eqn
APP = MAP - IAP
Define ACS
IAP >20mmHg with associated organ failure +/- an APP<60
Causes of ACS
Surgical - haemorrhage, collection, ileus, large hernia, tight abdominal closure
Medical - peritoneal dialysis, intra-abdominal infection, pancreatitis, intestinal oedema
Trauma
Burns
Obesity
Consequences of ACS
Resp - splinting, reduced compliance, Adele tasks, decreased FRC. Hypoxaemia and infection
CVS - reduced venous return, SV and CO
Renal - reduced renal perf pressure at >15, anuria at >30
GI - hepatic dysfunction
Nervous - rising ICP
Measuring energy requirements
Indirect calorimetry - gold standard.
Calories on basis of oxygen consumption. No really done
Measure CO2 productio - needs stable conditions, and over feed overestimates expenditure
Estimation - Scholfied eqn, Harris Benedict eqns.
By weight - 25kcal/kg
Daily needs
Under 65 - 25kcal/kg, over 65, 20kcal/kg
Carbs - 60% of non protein calories
3.-4g/kg
Protein 1 to 1.5 g/kg
Increase for burns, trauma
Lipid 40% of noon protein
0.7-1.5G
Water 30mls/kg
Na 1-2mmol/kg K 0.7-1 Ca 0.1 Mg 0.1 Phos 0.4
Pros and con of enteral nutrition
Cheaper
Easier to do
Lower risk of infection
Gut protective (maintains integrity)
BUT
Needs functioning GI tract
?VAP
Less reliable delivery of energy
Complications of PN
Access - needs a CVP and of that
Liver - hepatic steatosis, cholestasis, failure
Sepsis
Increased hyperglycaemia
EN versus PN evidence
CALORIES - no diff in 30 day mort. EN, more vomiting and hypo
Timing of nutrition
Early less than 48 hours, concenus is start early
