Liver / GI Flashcards
Acute liver failure
- no cirrhosis
- liver injury
- coagulopaty
- encephalopathy
- < 26 weeks (jaundice –> HE time)
- hyper acute < 1 week
- acute 1-4 weeks
- subacute 4-12 weeks
Causes of ALF
- paracetamol toxicity
- Drug induced - abx, AED, recreational
- viral hepatitis, A B E EBV CMV
- ischaemic
- pregnancy
Budd - chiari syndrome
hepatic vein obstruction - clot / tumour
abdo pain, hepatomegaly, gross ascites
Manifestations of ALF
Failure of
- gluconeogenesis - hypoglycaemia
- ammonia clearance - hyperammonaemia
- lactate clearance - lactic acidosis
- synthetic function - coagulopathy
Other featutes
- ARDS
- hypotension / low SVR / high CO
- Raised ICP, cerebral oedema
- AKI
Hepatic encephalopathy
ammonia not cleared by liver
crosses BBB
Ammonia + glutamate –> glutamine in brain
glutamine - apoptosis, mitochondrial dysfunction
cerebral oedema, raised ICP
Acute liver screen
Assessing disease severity
- PT / INR / coagulation screen
- LFTs, conjugated/unconjugated bilirubin, CK, LDH
- Assessment of renal function
- ABG, lactate, arterial ammonia
Assessing aetiology
- Urine toxicology screen
- serum paracetamol
- Viral screen
- HBsAg, Anti-HBC IgM
- Anti-HAV IgM
- Anti- HEV IgM
- Anti-HSV IgM
- Anti-VZV IgM
- CMV PCR
- HSV PCR
- EBV PCR
- Parvovirus PCR
- VZV PCR
- Autoimmune screen
- ANA, ASMA, anti-soluble liver antigen, ANCA, globulin profile
Lipase
Amyalse
Standard care ALF
Glucose infusion 10-20%
stress ulcer prophyalxis
restrist clotting factors unless bleeding
NAC
avoid sedatives, nephrotoxic and hepatotoxic drugs
HE –. Critical care
Intubate if Gr 3 HE
antibiotics if inflammatory, haemodynamic alteration or progressive HE
Normal Na, Mg, Pho, K
Critical care management of ALF
Specialist - aetiology, transplant, TIPSS (variceal bleed, refractory ascites
Supportive care
- Resp : HFNO > NIV. low PEEP (ICP vs ARDS)
- intubate for gr 3 HE
- fluid resuscitation, Norad first line
- nutrition
- CVVH (ammonia removal > 150)
- antimicrobials
- avoid toxins
- NAC
Prevention of encephalopaty
- thiamine, lactulose, rifaximin, RRT
Referral to specialist centre
Paracetamol / hyper acute
- pH < 7.3 / bicarb < 18
- INR > 3 day 2 or > 4 after
- oliguria / elevated creatinine
- hypoglycaemia
- altered consciousness
- lactate unresponsive to fluid
Non-paracetamol
- pH < 7.3
- INR > 1.8
- oliguria, renal failure, Na < 130
- encephalopathy, hypoglycaemia, acidosis
- Bili > 300
- Shrinking liver size
Poor prognosis in ALF-
- more severe liver injury
- extra hepatic organ failures
- subacute presentations
transplant should be considered in those fulfilling Kings College criteria
Kings College criteria
Paracetamol
- pH < 7.25 after resusictation or
- latate > 3 or
- All 3 of INR > 6.5, creat > 300, gr 3 HE
Non-paracetamol
- INR > 6.5 or
- 3 out of 5
- Indeterminate or drug induced aetiology
- age < 10 or > 40
- jaundice - HE > 7 days
- Bili > 300
- INR > 3.5
transplant contraindications
substance misuse, overwhelming sepsis, refractory shock, uncontrolled intracranial hypertension
Alcohol
- alcoholic hepatitis
- > 2 episodes in 2 year of non-adherence with medical care
- > 2 episode’s in 2 years of returning to drinking
- illicit drug use
Specific complications in ALF
Coagulpathy - vit K, use TEG, avoidance f clotting factors unless bleeding
Ascites - low sodium, diuresis, drain if SBP or resp compromise
- portopulmonary hypertension - pulmonary vasodilators (hepatopulmonary syndrome = hypoxaemia and SOB sure to pulmonary dilation and shunting)
Decompensated liver disease
acute decompensation of cirrhotic liver failure with 1 or more of:
- jaundice
- worsening ascites
- overt encephalopathy
- GI haemorrhage
- bacterial infections
- coagulopathy
Acute on chronic liver failure
- pre-existing liver failure
- decompensation
- 1 or more organ failure (CLIF-SOFA) 1a –> 3
Portal hypertension
= relatively elevated pressure in hepatic portal venous system
clinically significant if > 10mmHg
Clinical effects
- ascites (serum - ascites albumin gradient > 11g/L)
- porto-systemic shunts - varices
- decompensation
Managed by
- salt restriction
- diuresis
- NSBB - carvedilol / propanolol
- TIPSS
Hepatorenal syndrome
renal failure - infrarenal vasoconstriction, splanchnic vasodilation, pro-inflammatory, abnormal tubular electrolyte handling leading to tubular damage
HRS-AKI
- cirrhosis iwith asicate
- AKI (ICA 1-3)
- Absence of shock and nephrotoxins
- no response to 2 consecutive days of diuretic withdrawal and volume epxnaion
- no signs of structural kidney disease
Treatment
- Noradrenaline / terlipressin, albumin, treat underlying infections, RRT
SBP
bacterial infection of ascitic fluid in absence of surgically testable cause
decompensation, pain, fever, worsening distension, shock, AKI
ascite neutrophils > 250
culture +ve 40% - E.Colo
Broad spectrum abx, repeat paracentesis after 48hr
drain ascites
albumin prevents AKI (Sort et al)
Scoring systems in chronic liver disease
MELD
Child - Pugh (ascites, INR, encephalopathy, bilirubin, albumin) 12mo survival
Clif-C-ACLF - 28d mortality (organ dysfunction)
Futility in ACLF
EASL suggest withdrawal of ICU
- 7 days after diagnosis and adequate treatment
- >4 organ failures (CLIF-C-ACLF > 64)
- Liver transplant contraindicated
Diarrhoea definitions
- 3+ loose / liquid stools / day
- 200g + stool / day
- 250ml + stool / day
- Bristol stool chart 5-7
Diarrhoea on critical care
- infection - cross infection / contamination
- electrolyte imbalance
- fluid imbalance
- nursing workload
- skin breakdown
- antimicrobial stewardship
Diarrhoea classification
Mechanism - secretory, osmotic, motoric, exudative
duration - acute < 2 weeks chronic > 4 weeks
Aetiology
- infectious
- bacterial c.diff, salmonella, shigella, e.coli, campylobacter
- viral - norovirus, rotavirus, adenovirus
- non-infectious
- IBD
- pancreatic insufficiency
- short bowel
- food / feeding - intolerances, osmotic
- medication related - antibiotics, pro kinetics, laxatives, chemo/radiotherapy
Mechanisms of antibiotic associated diarrhoea
- direct pro kinetic effect
- microbial modification - excess carbohydrates
- unmetabolised bile salts
- colitis from bacterial overgrowth e.g. c diff
Management of ICU patient with diarrhoea
- infection screening / prevention
- correction of underling cause ? gut perfusion ? medications
- adjust feed e.g. reduce rate, fibre, osmolality
- Fluid balance and replacement
- Electrolye monitoring and replacement
- Skin / barrier protection e.g. bowel management system
- antidiarrhoeal medications
C.difficile
- gram positive spore forming anaerobe
- severe colitis and comlications
- toxin producing - A = intestinal permeability B = colon inflammation
risk factors - Abx - co-amox, clina, cephalopsporins
- PPI
- Age > 60
- chronic care
- exposure
Diarrhoea –> stool test - GDH antigen +ve and toxin +ve = active c.diff
- both negative = no c.diff
- antigen +ve means c.diff in bowel but if toxin -ve not causing infection
C.diff severity
Mild
- WCC normal and < 3 loose stool / day
Moderate
- WCC raised but less than 15
- 3-5 stool
Severe any of
- WCC > 15
- Creatinine > 50% baseline
- temperature > 38.5
- severe colitis on imaging
Life thretaing
- megacolon
- hypotension
- ileus
C.diff management
enteral abx
- Vancomycin PO 125mg ads
- fidaxomicin 2nd line
- severe - Vanc 500mg qds + metronidazole
10 day treatment
faecal transplant, ivies
Ulcerative Colitis
Inflammatory bowel disease characterised by inflammation starting vitally, continuous extension proximally
complications - perforation, adenocarcinoma, haemorrhage, megacolon
Acute severe = truelove witts
- > 6 bloody stool / day
- 1 of fever, HR > 90 Hb < 105, CRP > 30
treatment = steroid, 2nd line, bloods, stool mc/s, sigmoidoscopy
response = < 4 stool, no rectal bleeding
surgical review if continued systemic toxicity, toxic megacolon > 8 stool / day
Crohns disease
chronic complex GI inflammatory condition
variable onset and location
skip lesions, ill involvement, granulomatous inflammation
complications - perforation, fistulas, strictures
IBD immunosuppression
- 5-ASA - mesalazine (nephrotoxicity)
- Thiopurines - azathioprine (myelotoxicity, hepatotoxicity)
- steroids
- Anti-TNF - infliximab, adalibumab
- Anti-metabolite - methotrexate (GI, hepatoxicitity, pneumonitis)
- calcineurin inhibitors - ciclosporin (nephrotoxicity)
HALT-IT trial
TXA bolus and infusion in acute UGI bleed
No difference in mortality, rebleeding, transfusions
Significantly higher VTE
Re-feeding syndrome
acute metabolic derangement with electrolyte and fluid abnormalities occurring upon reintroduction of nutrition after period of starvation
metabolic abnormalities include
- hypophosphataemia (phosphorylation of glucose)
- hypomagnaesaemia (cell uptake)
- hypokalamiea (rapid cell uptake (insulin))
- glucose imbalance
- thiamine deficiency (cofactor in glycolysis)
Pathophysiology of refeeding syndrome
Starvation
- catabolic state - gylogenolysis gluconeogenesis, protein catabolism
- overal depletion of protein, carbohydrate, fat, minerals, electrolytes
refeeding
- fluid, salt, carbohydrate intake
- FFA / ketone –> carbohydrate metabolism
- insuline secretion
- protein, fat, glycogen synthesis
- intracellular uptake of glucose, K, Mg, Pho
- thiamine utilisation
- intracellular compartment depletion - wide concentration gradient - rapid depletion of extracellular ions
risk factors
One of
- BMI < 16
- 15% weight loss
- 10 days of starvation
- prexisting low K / Phos / Mg
Two of
- BMI < 18
- 10% weight loss
- 5 days starvation
- alcoholism
PATEINT GROUPS AT RISK OF MALNUTRITION
Reduced intake
- anorexia nervos
- social deprivation / homelssness
- alcoholism / substance addition
- malignancy
- post-operative
Excess loss / decreased absorption
- vomiting. diarrhoea/ obstruction
- pancreatitis
- GI inflammation
- bariatric surgery
Prevention / treatment refeeding syndrome
- screening
- correct underlying risk e.g. hypo K etc
- commencement of lower feed rates (10kcal / kg/ day, 5 if extreme)
- correction of electrolytes
- vitamin supplements - thiamine
- monitoring electrolytes > daily, glucose hourly
- cautious fluid balance
Endogenous toxins accumulating in liver failure
- bilirubin
- bile salts
- lactate
- ammonia
extracorporeal liver support
extracorporeal circuit used to prevent toxin build up and injury in liver failure
- bioartifical liver support - hepatocytes incorporated into plasmaphoresis
- MARS - molecular adsorbent recirculation system - extracorporeal albumin dialysis. ultra filtrate exposed to albumin rich solution across a membrane - albumin bound substances move down concentration gradient/ ultra filtrate then then conventional dialysied.
May be indicated ALF - alcoholic hpatitis, PGD, progressive jaundice
P-Possum
Age
comorbidities - heart failure, dyspnoea
vitals - hr, bp, gcs
bloods - hb, wcc, na, k, urea
ecg
surgical finding - complex major, blood los, contamination, cancer
Splenic laceration
laceration / haematoma
1 - < 1cm / subscapular < 10%
2 - 1-3cm / 10-50%
3 - > 3cm / > 50%
4 - 25% devascularisation, any vessel injury
5 - any vascular injury, bleeding into peritoneum
overwhelming post splenectomy infection
encapsulated bacteria
< 1 week to 20 + years post splenectomy
rapidly fatal, prophylactic abx / vaccines reduced incidence
acute pancreatitis scoring systems
Apache II and BISAP best at predicting severity
Glasgow
Ranson
Revised Atlanta criteria
- mild - no organ fialure, no local or systemic complications
- moderate - transient organ failure, local or systemic complications
- severe - persistent organ failure
Peripancreatic collections - acute necrotic collection / wall off necrosis
Balthazar CT sevreity
Ileus
slowing of gi motiliety without mechanical obstruction
Gi causes - post-op, peritonitis, pancreatitis, ischaemia
metabolic - hypokalamiae, hyponatraemia, uraemia
medications - opioids, smootjh muscle relaxants
ileus on critical care
detection - gastric aspirates
avoid aspiration - avoid lying flat
GI decompression - ryes tube, trophic feed, IV hydration
treat underlying cause - review opioids, rule out obstruction
supporitve care - PN if prolonged
prokinetics
reduce feed rate
necrotising fasciitis
severe infection of subcutaenous tissue - superficial and deep fascia and subdermal fat.
1- polymicroial - mixed anaerobes and aerobes
2 - monomicrobial Group A strep, staph aureus
3- gram negative
4 - trauma associated
infection spread through fascial planes. local ischaemia, necrosis, thrombosis and toxin release
Boerhaave syndrome
spontaneous rupture of oesophagus
sudden increase in oesophageal pressure (vomiting, straining) combined with negative intrathoracic pressure leads to tear and passage of GI secretions and air into mediastinum
similar picture with iatrogenic leak (endoscopy), trauma, perforation from caustic substances
Macklers triad - subcutaneous emphysema, chest pain, vomiting
Boerhaave investigations
CXR - PTX, widened mediastinum, left pleural effusion
CT chest - leak site, extent, inflammation, abscess
OGD
pleural tap pH < 6, frank undigested food
Boerhaave complications
respiratory failure - pleural effusion, empyema, ards
mediastinitis
subcutaneous emphysema
tamponade
death
Boerhaave management
early intervention - primary repair, controlled fistula, resection, stent placement
fluid management
analgesia antibiotics
feeding - avoiding blind NG insertion
likely to require prolonged organ support, may need cervical oesophagostmy and feed jej
oesphagectomy
excising portion of oesophagus with anastomosis in mediastinum - gastric conduit
tricky access - thoracic and abdominal
Ivor lewis - right thoracotomy, midline laparotomy (or rooftop)
minimally invasive - thoracoscopic , laparoscopic
trandiaphrgamatic, transmittal
morbidity and mortality - comorbid, late presentation, advanced age
anastamosis vulnerable as formed at extrene end of foregut blood supply
critical care management post-oesophagectomy
- anastomotic protection - avoid NIV, enteral feed via tube placed in theatre
- optimise perfusion - normovolaemia, appropriate BP
- PPI
- vigilant monitoring
- analgesia - thoracic epidural
- ERAS
complications post-oesophagectomy
- respiratory - recurrent LN palsy, air leak, pneumonia, ARDS
- CVS - AF common
- GI - ileus, leak (first 5 days typically)
Leak
- conservative - NBM, alternative nutrition, antibiotics, chest phusio
- radiological drainage of collections
- surgical exploration
AAA
dilation of abdominal aorta > 3cm
asymptomatic / screened
pulsatility / mass
abdo–>back pain
rupture - pain, shock, cardiac arrest
- CT angio
- Ddx ACS, ureteric colic
ruptured AAA management
- haemodynamic stabilisation - 1:1 transfusion ,permise hypotension
- management of coagulopathy
- MDT discussion - operative or not
- operative - EVAR vs open
increased mortality
- severe haemodynamic instability, cardiac arrest, LOC, renal impairment
- intraoperative - intraperitoneal rupture, total operating time
- postoperative - MOF, bleeding, CVA
Repair prognosis
rupture
- open - 50% in hospital mortality. nearly 100% if CPR pre-op
- EVAR - 20% in hospital mortality - likely more stable if able to have CT A, patient selection
elective
- 7% mortality in comorbid
- 2% in fit
EVAR vs Open in rupture - 30 day mortality no difference but LA for EVAR best mortality
EVAR vs Open AAA
- EVAR - shorter LOS, lower immediate risk, avoid complications of open but risk of endoleak
- Open - not all suitable for EVAR
complications of AAA repair / rupture
hypoperfusion
- ACS
- AKI
- CVA
- spinal cord
- bowel ischaemia
- lower limb ischaemia
recovery
- pain
- respiratory failure
- massive transfusion
surgical
- endoleak
- distal embolisation
- infection
- occlusion
critical care management
- supportive care
- optimise haemodynamics and normothermia
- analgesia..
- monitoring for complications - renal, spinal cord, compartment syndromes
- treatment of complications - RRT, spinal drain, PN
Compartment syndrome
process in which pressure within a body compartment rises enough to restrict perfusion and viability of contents of that compartment
- limb
- abdominal
(orbital, cranial, cardiac)
Pathophysiology of compartment syndromes
Perfusion pressure = MAP - compartment pressure
- inadequate MAP - shock, elevation
- increased compartment pressure
- increased content - bleeding, swelling, inadequate drainage
- decreased compliance - scarring, tight dressing, surgical closure
tissue oedema, necrosis worsens compartment perfusion
Intra-abdominal compartment syndrome
intra abdominal hypertension is IAP > 12
1 - 12-15
2- 16 - 20
3 - 21-25
4 - 26 +
ACS = IAH 20mmHg + organ dysfunction
causes - severe acute pancreatitis, post-op AAA rupture
Complications of abdominal compartment syndrome
AB - reduced FRC, ventilatory compromise, aspiration risk
C - increased afterload, reduced preload, reduced CO
D - increased ICp
G - ischaema, ileus, translocation of bacteria
F - obstructive uropahty, ptrtrnlAKI, RAS activation
management of abdominal compartment syndrome
> 30mmHG strong consideration info laparotomy
stepwise
- increase MAP fluid, basoactives
- improve compliance - deep sedation analgesia, NMB
- reduce contents - NG, rectal tube, reduce enteral feed, stop enteral feed
- laparotomy
intestinal failure
reduced function of gut leading to impaired absorption of micro,macronutrients and water
can be classified by nutritional support - mild = oral supplement mod = enteral severe = PN
Causes
- acute - bowel obstruction, fistula, ileus, ischaemia
- chronic - IBD, enteritis, short bowel syndrome
short bowel syndrome
post surgical syndrome where length of bowel < 2m meaning nutritional supplementation is likely to required
- jej-colon
- jej-ileum
- jejuonsotomy
surgery resulting in short bowel
-crohns
- SMA thrombosis
- irradiation damage
weight loss, prerenal failure, confusion, renal stones, diarrhoea
aim of treatment to maintain nutritional requirements, reduce complications, use oral and enteral nutrition where possible
intestinal resection
- dsmotility
- adhesions
- water and salt loss
- malaborption (fat and fat soluble vitamins)
- hypomagnaesaemia, hypocalcaemia
Flap surgery
provide reconstruction and cosmesis for wound coverage. commonly breast and orofacial
free flap - completely disconnected and anastomosed at new site. DIEP for breast, TRAM, radial forearm
pedicle - own arterial and venous supply. pec major myocutaneous
concerns in free flap patients
- viability , microvascular anastomoses.
denervation - loss of sympathetic tone
compromised lympahetics
underlying pathology
flap viability
primary icshaemia - cessation of blood flor during flap transfer. related to duration of ischaemia
repercussion - vessels unclamped - ischaemia/reperfusion injury
secondary ischaemoa - after flap transfer - arterial thrombosis, venous congestion
critical care - hagan pouseille
- avoid vasocsontrction (temperature, normbocolaemia, analgesia)
- DP - low SVR, adequate perfusion pressure, adequate drainage
- viscosity - Hct 0.3
flap failure
- anastomotic breakdown
- vasospasm
- thrombosis
- compression
- edema
monitoring - dopplers
- flaps obs - CRT, temperature, colour, bleeding on pinprick
Admission of transplant patients to critical care
- immediate post-op
- early and late complications
- complications of immunosuppression
- relapse of underlying disease
- unrelated conditions
challenges
- logistics of care and communication with transplant centre
- access to records
- complex patient with risk for organ fysfunction
- balance of immunosuppression and infection
- end stage vascular access
- polyphramcy
General post-op transplant management
- analgesia
- VTE
- graft optimisation - adequate perfusion
- immunosuppresisio - level monitoring, steroid, abx propylaxis
- vigilance for complications
- cardiac - early exutubation, offload rv, low dose inotropes
- lung - LPV, early extubation, fluid resriction
- liver coagulaopathy, acid base, calcium
- kidney - monitor UO, avoid hypovolaemia
primary graft dysfunction
immediate poort function of transplanted organ
organ specific insufficiency
may be related to ischaemia refperfusion
- heart - LVEF despite inotropes, mechanical support
- lung - impaired oxygenation, diffuse opacities
- liver - lactateaemia, hypoglycaemia, coagulopathy
- renal - hyperkalaemia, poor UO
immunosuppressants
- steroids
- calcineurin inhiitors
- ciclosporin, tacrolimus
- antimetabolites - azathioprine
- mycophenalate
- biologics
Vitamins
Organic compounds which are required in small amounts to carry out essential body processes, can’t be manufactured therefore must be ingested
Fat soluble - A D E K
Water soluble - B C
specific vitamins
A - immune, vision
B2 (riboflavin) - antioxidante, red cell production, metabolism. deficiency - stomatitis
B3 - niacin - metabolic, skin, cns function. deficiency = pellagra (diarrhoea, dermatitis, dementia)
B9 - folate - cns, red cell, Dan and ran. glossitis, diarrhoea, anaemia
B12 - cobalamin - dear, RNA, red cell. pernicious anaemia
vitamin c - wiybdm cikkageb. weakness, weight loss, scurvy
Thiamine deficiency
B1 (thiamine)
- coenzyme in carbohydrate metabolism and ATP production (carb metabolism, pyruvate dehydrogenase –> AcetylCoA
Dry Beri-beri - wasting, paralysis, ataxia
Wet beri beri - high output cardiac failure, peripheral oedema
Wernickes encephalopathy - confusion, ataxia, ophthalmoplegia
Korsakoff - severe memory impairment
more vitamins
Vitamin D - calcium absorption, bone strength
Vit K - coagulation, bone metabolism
Selenium - T4–> T3
Zinc - hormone, immune
Copper - metabolic, antioxidant
