Crtical Care Management

of liver diseases
Dr.Anish Joshi
Narayana Multispeciality Hospital
Ahmedabad
Classification
 Hyper acute- within 1wk
 Acute – 1-4 wk
 Subacute – 4-26 wk

 Fulminant (<2wks)
 Subfulminant (2-26wks)
Etiology
 Viruses- HAV, HBV, HEV, HCV, HDV, EBV, CMV,
HSV.

 DRUGS-Paracetamol (acetaminophen)
overdose, idiosyncratic reaction eg
tetracycline, troglitazone, INH ,Rifampicin
halothane,dilantin,valproic acid,herbal
remedies
 Poisoning –Phosphorus, Rat poision

 Alcohol
Continued…
Metabolic-
Reye syndrome-child with a viral infection
Wilson's disease
Acute fatty liver of pregnancy
Vascular –Budd chairi syndrome, massive
infiltration with tumor ,
lymphoma, shock
Autoimmune

IDIOPATHIC
Evaluation
 History taking & clinical examination

• Drugs
• Toxins
• Viral infection
• Underlying chronic etiology
Initial lab analysis
 Prothrombin time/INR
 Complete blood count
 Liver function test: AST, ALT,
alkaline phosphatase, GGT, total bilirubin,
albumin
 Creatinine, urea/blood urea nitrogen,
sodium, potassium, chloride, bicarbonate,
calcium, magnesium, phosphate
 Glucose
 Amylase and lipase
 Arterial blood gas, lactate
 Blood type and screen
Continued…
 Paracetamol (Acetaminophen) level, Toxicology
screen
 Viral hepatitis serologies: anti-HAV IgM, HBSAg,
anti-HBc IgM, anti-HEV
 Autoimmune markers: ANA, ASMA, ,
Immunoglobulin levels
 Ceruloplasmin Level
 Pregnancy test
 Ammonia level
 HIV status
MANAGMENT
 Keep in ICU with close monitoring
 Main stay of treatment
• Nutrition
• Fluid & electrolyte balance
• Encephalopathy, coagulopathy
• Decrease intracranial pressure
• Mech ventilation,dialysis
• LIVER TRANSPLANTATION
Specific therapies
 Acetaminophen induced : NAC ( N-
acetylcysteine)
 Acyclovir - Herpetic, CMV- gancylovir
 Fatty liver of pregnancy/ HELLP-emergency
delivery
 Fulminent hepatitis B – Lamivudine (?)
 Amanita mushroom poisoning- Penicillin
 Autoimmune hepatitis-Immunosuppression
 Wilsons disease- Anticopper therapy,
Transplant
Nutrition

 Enteral nutrition via a gastric or

post-pyloric tube
 Cal- 30-50 kcal/d, protein 1gm/d
 Ulcer prophylaxis
 Pro-kinetic agents in patients with
large gastric aspirates
 TPN in case enteral not possible.
Fluid & electrolyte balance
 Hypoglycemia
 Hyponatremia
 Hypokalemia
 Acidosis
 Hypovolemia
Cerebral oedema
 Brain stem herniation is the dreaded
complication
 Accumulation of NH3 & loss of cerebral
autoregulation resulting in hyperaemia due to
abnormal accumulation of vasoactive mediators
 Accumulation of false neurotransmitters, CNS
depressants, & inflammatory mediators which
may reduce consciousness
 Features of severe cerebral edema with resultant
intracranial hypertension are diffificult to detect
in critically ill patients with MOF and regular
clinical evaluation is necessary
Management of raised ICP
 Head elevation
 Hyperventilation
 IV mannitol
 Barbiturate
 Sedative – propofol
 Hypothermia 32-34 c
 Vasopressor to maintain CPP>60mmhg
 ICP monitoring
Vasodilatory shock
 Relative or absolute hypovolemia due to
 Poor fluid intake
 Abnormal external fluid losses
 Loss of intravascular volume into the
interstitium
 Vasodilatation
 Requires inotropic support
Coagulopathy
 Hepatic synthesis of clotting factors fails
& thrombocytopenia
 Bleeding at insertion sites or
spontaneously
 Hypercoagulable state
 Digital ischemia, portal vein thrombosis
or lower limb DVT
 Normalization of INR suggests hepatic
regeneration
 Coagulation
 Correct when bleeding
 Plasma, Platelets, Fibrinogen,

NovoSeven
 Specific treatment

 In desperate situations
 Plasmapheresis
Renal failure
 Incidence 40-85%
 Cause & mech-
• Prerenal d/t hypovolemia
• Renal ischemia
• ATN as in paracetamol toxicity
• Hepatorenal syndrome
M/m
• Fluid resuscitation
• Maintain hemodynamic stability
• Dialysis-CRRT

Terlipressin should not used –

raises ICP
Sepsis
 Gram negative & Fungal
 Pathogens may emerge from a patient’s
own microbiological flora or may be
acquired from the hospital environment
 Sites
 LRT
 Urinary tract
 Intravascular access devices
Infection

 Mech –
• reduced complement activation
• Impaired phagocytosis & reduced cytokine
production
• Reduced clearance of endotoxins
 Only sign of infection may be
deterioration of liver function
GUIDELINES 2020
Fluid resuscitation
 We recommend against using HES &
gelatin solutions for initial fluid
resuscitation(strong
recommendation, moderate-quality
evidence)
 May exacerabate coagulopathy
Albumin As Resuscitation
Fluid
 We suggest using albumin especially
when serum albumin is low (< 3mg/dL)
(conditional recommendation, low-quality
evidence)
 Antioxidant, immunoregulatory &
endothelial regulatory functions
 Improves haemodynamics and has
mortality benefit
Blood Pressure Targets
 MAP of 65 mm Hg with concomitant
assessment of perfusion (conditional
recommendation, moderate-quality
evidence)
 Higher or lower MAP has harm
 Arterial catheter for BP monitoring
(conditional recommendation, low-
quality evidence)
Invasive Hemodynamic
Monitoring
 Should be used to guide therapy in
clinically impaired perfusion (conditional
recommendation, low-quality evidence).
 Despite empiric adjustment of standard
therapies, uncertain fluid status,
symptomatic low BP, worsening renal
function despite therapy or in those who
require parenteral vasoactive agents,
invasive monitoring can help
Choice of First-Line
Vasopressor Agent
 Noradreanline (strong recommendation,
moderate quality evidence)
 Avoid dopamine
 Adrenaline = Noradrenaline. No difference
in mortality but adrenaline causes more
splanchnic vasoconstriction resulting in
liver & mesenteric ischaemia. Also it
increases lactate
Use of Vasopressin
 Adding low-dose vasopressin to
norepinephrine who remain
hypotensive despite fluid
resuscitation (conditional
recommendation, low-quality
evidence)
HAEMATOLOGY
Assessing Bleeding and
Thrombosis Risk
 Viscoelastic testing (TEG/rotational
thromboelastometry [ROTEM]) over measuring
INR, platelet & fibrinogen (conditional
recommendation, low-quality evidence).
 INR is based on the PT, which is dependent on
pro-coagulant factors I, II, V, VII, and X.
 INR does not account for deficiencies of the anti-
coagulation system, which may result in a
hypercoagulable state not captured by a cirrhotic
patient’s elevated INR.
 Although bleeding remains of
concern, cirrhotics are thought to be
at greater risk of thrombotic
complications
 Viscoelastic testing is real time
global and functional evaluation of
altered activity of the pro and
anticoagulant pathways, identifying
platelet function, hyper-fibrinolysis,
and premature clot dissolution
Hemoglobin Targets
 Transfusion threshold of 7 mg/dL
(conditional recommendation, low-quality
evidence)
 As compared to liberal strategy of 9
mg/dl, fewer transfusion reactions &
adverse events
 RBC transfusion has been shown to be an
independent predictor of mortality post
liver transplantation by worsening
thrombosis
Venous Thromboembolism
Treatment
 LMWH or vitamin K antagonists, should be
used over no anticoagulation in patients
with PVT or PE (conditional
recommendation, very low-quality
evidence)
 PVT is estimated at 8% per year in those
awaiting liver transplantation
 Improved outcomes have been reported
in those anti-coagulated at 1 year,
especially those with more extensive
mesenteric thrombosis
Venous Thromboembolism
Prophylaxis
 LMWH over pneumatic compression
stockings (conditional
recommendation, low-quality
evidence)
 Unfractionated heparin maybe
considered for prophylaxis
Assessing Bleeding Risk for
Invasive Procedures
 Viscoelastic testing (TEG/ROTEM),is
recommended over measuring INR,
platelet,fibrinogen (strong
recommendation, moderate-quality
evidence)
 Bleeding does not appear to correlate
with platelet count or INR
 Lesser need for transfusion with no
obvious increase in complications
Use of Novel Coagulation
Agents
 Recommend against using Eltrombopag
in thrombocytopenia prior to
surgery/invasive procedures (strong
recommendation, low-quality evidence)
 Insufficient evidence to issue a
recommendation for or against
prothrombin complex concentrates
 ELEVATE study was terminated due to
increased risk of thrombotic events
PULMONARY SECTION
Tidal Volumes for Mechanically
Ventilated Patients
 Low TV strategy over high TV
strategy with ARDS(conditional
recommendation, low-quality
evidence)
PEEP
 Against using high PEEP over low
PEEP with ARDS (conditional
recommendation, low-quality
evidence)
 High PEEP has no mortality benefit
or reduction in ventilator free days &
may increase ICP and decrease
venous return
Use of PAH Therapy in
Portopulmonary Hypertension
 We suggest treating portopulmonary HT (POPH)
with agents approved for PAH in patients with
MPAP >35mm Hg (conditional recommendation,
very low-quality evidence)
 POPH has worse survival outcomes than many
other forms of PAH
 Macitentan, Riociguat, Prostacyclin analogs
parenteral epoprostenol or treprostinil
 Sildenafil & endothelin receptor antagonists such
as bosentan or ambrisentan
Hypoxemia in Patients With
Hepatopulmonary Syndrome
 Supportive care with supplemental O2 in
the Rx of HPS pending possible liver
transplantation (BPS)
 Loss of hypoxic pulmonary
vasoconstriction in ~30% of cirrhotics
leads to loss of pulmonary vascular tone
with gravitational changes resulting in
platypnea & orthodeoxia
 Liver transplantation is the only proven
beneficial therapy
 Severe hypoxemia occurs in 6–21%
of patients with HPS early on (< 24
hr) following liver transplant and
carries a 45% mortality
 Trendelenburg positioning, followed
by inhaled epoprostenol, inhaled
nitric oxide and IV methylene blue
have been suggested
Tube Thoracostomy in
Hepatic Hydrothorax
 TT in an attempt to pleurodesis for
hepatic hydrothorax in whom TIPS is
not an option or as a palliative intent
(BPS)
 Infection rates are very less
 72 % chance of complete
pleurodesis
HFNC &/or NIV
 HFNC > NIV in hypoxic critically ill
 But in hypercarbia NIV > HFNC
 HFNC has less impact on ICP or
venous return as PEEP with HFNC
flows of 35–50L/min is between 3
and 5 cm H2O
RENAL SECTION
Intraoperative RRT during
Liver Tx Sx
 If Hyperkalemia or severe acid-base
abnormalities RRT should be
continued
 No recommendation
RRT Timing: Early

 Hyperkalemia (> 6 mmol/L with ECG

changes
 Fluid overload/pulmonary edema
resistant to diuretic administration
 Severe metabolic acidosis (pH <
7.15),
 Blood urea > 35.7 mmol/L
 Kidney Disease Improving Global
Outcomes stage 3 AKI
Vasopressors in
Hepatorenal Syndrome
 Vasopressors to be used in critically
ill patients who develop HRS(strong
recommendation, moderate-quality
evidence)
 Terlipressin, norepinephrine, or
midodrine & octreotide
 Mortality benefit
TIPS for Prevention of HRS
 No recommendation
 Decreased refractory ascites and
variceal bleeding
 Side effects: Hep. encephalopathy
ENDOCRINE AND
NUTRITION SECTION
Target Glucose Control
 110–180mg/dL (strong
recommendation, moderate-quality
evidence)
 Hypoglycemia is associated with
increased mortality
Role of Stress-Dose
Glucocorticoids
 Recommended in the treatment of
septic shock (conditional
recommendation, low-quality
evidence)
 Relative adrenal insufficiency is
common in acutely ill patients with
cirrhosis
Dietary Protein Load
 Targeting protein goals comparable
with critically ill patients without
liver failure (1.2–2.0g protein/kg dry
or IBW/d (conditional
recommendation, very low-quality
evidence).
Branched-Chain Amino
Acids
 Not to be used who are tolerating
enteral medications (conditional
recommendation, very low-quality
evidence)
Route and Timing of
Feeding
 EN over PN without contraindication
for enteral feeding (conditional
recommendation, low-quality
evidence)
 Preservation of lean body mass,
maintenance of structural &
functional gut integrity, preservation
of intestinal microbial diversity &
potentially improved gut-mediated
immunity
Screening for Drug Induced
Causes of Liver Failure
 Recommended. Drug that are
proven or highly suspected to be the
cause of ALF or ACLF should be
discontinued (BPS)
Dose Adjustment of
Medications
 Medications that undergo hepatic
metabolism based on the patient’s
residual hepatic function.
 When available, a clinical pharmacist
should be consulted (BPS).
 Additionally, HRS can lead to impaired
excretion of drugs
 Optimal approach is to use therapeutic
drug monitoring when possible
Conclusion

 Rapid , fatal disease with mortality up to 90%

 Identifiable cause only up to 60-80% , acetaminophen
common in western country, HBV/HEV predominant in
India.
 Typical symptom----- H.E / coagulapathy
 Typical index ---- rapid elevation of bilirubin / prolonged PT
 Prognostic evaluation by Predictors of Kings is useful and
available
 No specific medication but intensive supportive care .
 Only reliable treatment is liver transplantation , with
survival rate around 50-60% ( 1-year) .
 HOW I WISH TO BE TREATED IN
ALF
• NOT IN: HOME, NH, WARD, ICU (NO TRANSPLANT FACILITY)
• NOT BY A HEPATOLOGIST WHO HAS NO TIME FOR NIGHT ROUND
• ICU (SINGLE ROOM), MANAGED BY WELl TRAINED INTENSIVISTS
• 2 NURSES (24 HRS)
• VENTILATOR
• FREQUENT MONITORING: GLUCOSE, INR, CREAT, ABG, ELEC,
LACTATE, PHOSPHATE, X RAY CHEST ,NEUROLOGICAL EXAM (*ICP
↑)
• HOSPITAL BILL DIRECTLY TO INSURANCE COMPANY
THANK YOU