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Intensive Care Medicine
TopicsfortheFinalFRCA
Dr. Andrew Ferguson
Why ICU matters for the FRCA…
 20 specific questions in MCQ
 Helps with medicine/surgery MCQs
 SAQs - 1 or 2 questions for sure…maybe more
 SOE 1 - potential topic/part of topic
 SOE 2 - 10 minutes of pure fun!
Be calm…
 The examiners are human (honestly!!!)
 The questions are (mostly) mainstream
 You will have seen many of the cases
 Guillain-Barre / Myasthenic crisis / weakness
 Brainstem death
 Status epilepticus and asthmaticus
 Trauma
 Septic shock
 ARDS
 Acute pancreatitis
 Burns
 Some questions just won’t lie down and die e.g. PAC
But don’t be complacent…
 People still fail the exam! 10/17 passed in 2008
 Don’t assume you know enough…make sure you do
 Structure…structure…structure!
 Don’t waffle - answer the actual question, not the one you
wanted to be asked!!
Other potentials…
• Acute hepatic failure
• Sedation
• Fluid balance and outcome
• Nutritional therapy
• Tissue oxygenation and oxygen delivery
• Abdominal compartment syndrome
• Cardiogenic shock
• Clostridium difficile
• Scoring systems
Examples…
In the question on the brain-stem dead patient, too many candidates
included detail of brain stem testing in their answers, which was not
required. Candidates are reminded to answer the question as written; no
credit will be given for irrelevant information
It cannot be emphasised enough that the answer provided to the examiners
is less than a page and is focused completely to the question.
Case scenario 1
 49 year old female, history of depression & anxiety found
unconscious in apartment having failed to turn up for work
 On arrival A&E GCS 5-6, BM = 0.4
 After 50ml 50% glucose BM = 14.5 and GCS 12-14
 Bruising left buttock and thigh
 Tender abdomen, jaundiced, BP 75/45, HR 104, Temp 34.1
 CT brain NAD, CT abdo - mild hepatomegaly, ? fatty
 Labs: Lactate 10.2, Bili 27, AST 4465, ALT 1945, INR 4,
Paracetamol 25, tox negative, K 1.9, Ca 0.8, PO4 0.4, Hb 10.4, WBC
15.9, Plts 102, CK 595
Questions for discussion
What are the main differential diagnoses?
What other information/tests would you like?
Why is the GCS abnormal?
How do you assess fluid status and responsiveness?
What does the lactate level tell you?
Why is the B low and how will you tackle it?
How do you assess the adequacy of oxygen delivery?
Does this patient need antibiotics?
What problems are likely in the next 24-48 hours?
Acute hepatic failure
 Early death despite support
 Survival with supportive therapy (liver regeneration)
 Unlikely to survive with supportive therapy alone
 candidate for emergency transplant
 NOT candidate for emergency transplant
INFO
“Life-threatening multi-system illness resulting from massive liver
injury. The defining clinical symptoms are coagulopathy and
encephalopathy occurring within days or weeks of the primary
insult in patients without pre-existing liver injury”
Auzinger G, Wendon J. Curr Opin Crit Care 2008; 14: 179-188
Aetiology based therapy
INFO
Aetiology Therapy Comments
Paracetamol N-Acetylcysteine (NAC)
Early non-paracetamol
ALF
N-Acetylcysteine (NAC) Lee WM, Rossaro L, Fontana
RJ et al. Hepatology 2007;
46(Suppl 1); 268A.
? increased infection risk due to
reduced neutrophil burst
? antiplatelet action
Fatty liver of pregnancy or
HELLP
Delivery! Usually reverses before
need for transplant
Acute hepatitis B Lamivudine
Amanita Phalloides Penicillin G
Paracetamol toxicity
INFO
Enhanced risk
1.Excess alcohol
2.Enzyme-inducing drugs
carbamazepine
phenytoin,
phenobarbitone
St John's Wort
rifampicin
3. Glutathione depletion
malnutrition
eating disorders
malabsorption
HIV
NAPQI
Major paths
Minor path
N-acetylcysteine
INFO
(1) Initially 150mg/kg in 200mL glucose 5% given over 15 minutes, then
(2) 50mg/kg in 500mL glucose 5% given over 4 hours, then
(3) 100mg/kg in 1000mL glucose 5% given over 16 hours
Referral criteria
INFO
Day 2 Day 3 Day 4
Arterial pH < 7.3 Arterial pH < 7.3 INR > 4.4 or PT > 75s
INR > 3 or PT > 50s INR > 4.4 or PT > 75s Progressive rise in PT
Oliguria Oliguria Oliguria
Creatinine > 200 Creatinine > 200 Creatinine > 300
Hypoglycaemia Encephalopathy Encephalopathy
Severe thrombocytopaenia Severe thrombocytopaenia
Hyperacute Acute Subacute
Encephalopathy Encephalopathy Encephalopathy
INR > 2 or PT > 30s INR > 2 or PT > 30s INR > 1.5 or PT > 20s
Renal failure Renal failure Renal failure
Hypoglycaemia Hypoglycaemia Hypoglycaemia (rare)
Hyperpyrexia Hyponatraemia
Shrinking liver on CT
Non-paracetamol
Paracetamol
Referral criteria - Kings College Hospital
INFO
Paracetamol Non-paracetamol
Arterial pH < 7.3 after resuscitation
OR
Grade III/IV encephalopathy
PT > 100s (INR > 6.5)
OR
any 3 of the following
Creatinine > 300
Aetiology = seronegative hepatitis or
drug-induced liver failure
PT > 100s (INR > 6.5) Age < 10 or > 40
Lactate > 3.5 @ 4hrs or > 3 @ 12 hrs Jaundice to encephalopathy > 7 d
Hypoglycaemia Bilirubin > 300
PT > 50s (INR > 3.5)
Paracetamol Non-paracetamol
Clinical Issues in ALF
 CNS
 Encephalopathy - ammonia => glutamate
 Intracranial hypertension - oedema
 Cardiovascular
 Intravascular volume depletion
 Vasodilatation
 Subclinical myocardial damage (Tn > 0.1 in 66%)
 Respiratory
 Hypoxia - effusions, atelectasis, shunting, splinting, ALI
INFO
Clinical Issues in ALF
 Renal
 Oliguria
 Acute renal impairment - drugs, hepatorenal, pre-
renal, ATN, intra-abdominal hypertension
 Haematological
 Thrombocytopaenia and coagulopathy
 Procedural bleeding possible
 Spontaneous bleeding rare
 Infection
 Monocyte (HLA-DR), complement, Kupffer cell failure
Responsible for most deaths!
INFO
Useful references
INFO
Kramer DJ, Canabal JM, Arasi LC. Application of Intensive Care
Medicine Principles in the Management of the Acute Liver Failure
Patient. Liver Transplantation 2008; 14: S85-89.
Auzinger G, Wendon J. Intensive Care Management of Acute Liver
Failure. Current Opinion in Critical Care 2008; 14: 179-188.
Stravitz T. Critical Management Decisions in Patients with Acute Liver
Failure. Chest 2008; 134: 1092-1102.
Case scenario 2
 56 year old male, history of IHD/PVD/smoker/MI/EF 35%
 Admitted to ICU following emergent leaking AAA repair…complicated by
intraoperative ST depression and hypotension
 On arrival ICU BP = 90/45, HR 121 SR, NA @ 0.5 mg/kg/min, lactate 5
 CVP 14, pO2 11 on 70% O2 with PEEP 5, creps bilaterally
 ECG: infero-lateral ST depression
 In theatre 4 L crystalloid, 2 L tetraspan, 6 packed cells, 2 FFP
 Abdomen distended and tense, skin clammy
 Over next 4 hours: NA increasing, lactate 8, U/O poor
 Labs: Hb 9.5, Plts 85, WBC 7.9, Na 141, K 5.3, U 10.5 Creat 168, APTT 47,
PT 18, fibrinogen 0.95
Questions for discussion
 List the main clinical issues in this case
 How would you approach the respiratory failure?
 What factors contribute to the hypotension/malperfusion?
 What is your strategy to improve haemodynamics?
 What is your target for fluid balance in the next 24 hours?
 How does PPV assist the left ventricle?
 What other monitors/investigations might assist you?
 When would you involve the surgeons?
Cardiogenic Shock
• Definition
• Incidence
• Aetiology
• Pathophysiology
• Therapy
Clinical:
• Hypotension i.e. SBP below 90 mmHg
• Impaired tissue perfusion
• After correction of non-cardiac factors
Haemodynamic:
• Cardiac index < 2.2 litres/min/m2
• Systolic blood pressure < 90 mm Hg
• LAP/RAP > 18 mm Hg or PCWP > 16
• Urine output < 20 ml/hr
• SVR > 2100 dynes-sec·cm–5
INFO
Incidence & Mortality
Study Incidence Mortality Patient group Country
CREATE-ECLA [1] 6.5% 68% STEMI China, India, Pakistan
NRMI [2] 8.6% 47.9% STEMI USA
COMMIT [3] 4.4% 68% AMI (93% STEMI) China
5.0% 68% Metoprolol
3.9% 72% Plcaebo
SHOCK [4] 20% 75% CS on admission USA/Belgium
80% 56% Delayed CS
[1] The CREATE-ECLA Trial Group. Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST-
segment elevation myocardial infarction: the CREATE-ECLA Randomized Controlled Trial. JAMA 2005; 293: 437–446.
[2] Babaev A, Frederick PD, Pasta DJ, et al. Trends in management and outcomes of patients with acute myocardial
infarction complicated by cardiogenic shock. JAMA 2005; 294:448–454.
[3] Jeger RV, Harkness SM, Ramanathan K, et al. Emergency revascularization in patients with cardiogenic shock on
admission: a report from the SHOCK trial and registry. Eur Heart J 2006; 27:664–670.
[4] Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial
infarction: randomized placebo controlled trial. Lancet 2005; 366:1622–1632.
INFO
Echo indicators of mortality
INFO
Pathophysiology
INFO
Cardiogenic Shock
• Definition
• Incidence
• Aetiology
• Pathophysiology
• Therapy
Cause of CS Proportion
LV failure post-MI (8.5% of
STEMI, 2.5% of NSTEMI)
70-75%
Acute severe mitral regurgitation 8.3%
Ventricular septal rupture 4.6%
Isolated RV failure 3.4%
Ventricular free-wall rupture or
Cardiac tamponade
1.7%
Myocardial contusion
LVOT obstruction (AS/HOCM)
End-stage cardiomyopathy
Obstructed LV filling (MS)
Myocarditis
INFO
Pathophysiology
Target for
therapy?
At least 20% of CS patients have SIRS and low SVR
INFO
Therapy - Reducing iNOS
“Excessive NOS results in high levels of nitric oxide that, in turn, lead to inappropriate
systemic vasodilatation, progressive systemic and coronary hypoperfusion, and
myocardial depression”
Effect of Tilarginine Acetate in Patients With Acute Myocardial Infarction and
Cardiogenic Shock - The TRIUMPH Randomized Controlled Trial. JAMA 2007; 297: 1657-1666
INFO
Cardiogenic Shock: Therapy
• Optimise volume / oxygenation / rhythm
• Inotropic agents & vasopressors
 b agonists
 a agonists
 PDE III inhibitors
 LEVOSIMENDAN
• sensitizes myocardial contractile proteins to calcium
• independent of sympathetic NS and so NO increase in MVO2
• Prolonged action beyond infusion duration
• IABP
• PCI
INFO
Abdominal compartment syndrome
 Increasingly recognised problem
 LOOK for it! - don’t forget “medical” ICU patients
 Thinks about screening if
 Large volume resuscitation > 3.5 L in 24 hours
 Abdominal Surgery/Primary Fascial Closure
 Coagulopathy or polytransfusion
 Pulmonary, renal or hepatic dysfunction
 Acidosis
 Hypothermia
 Ileus
 Physical exam is NOT accurate
INFO
Intra-abdominal pressure
INFO
Patient Intra-abdominal pressure
Normal adult 0-5 mmHg
Typical ICU patient 5-7 mmHg
Post-laparotomy patient 10-15 mmHg
Septic shock patient 15-25 mmHg
Acute abdomen 25-40 mmHg
Grade of IAH Pressure
Grade I 12-15 mmHg
Grade II 16-20 mmHg
Grade III 21-25 mmHg
Grade IV > 25 mmHg
Abdominal perfusion pressure = MAP - IAP (aim > 60 mmHg)
Abdominal Compartment
Syndrome
INFO
ACS = sustained IAP > 20 mmHg (with or without APP < 60
mmHg) that is associated with new organ dysfunction/failure
World Society of the Abdominal Compartment Syndrome (www.wsacs.org)
INFO
INFO
Case scenario 3
 25 year old female, “fit and well”
 Admitted to ICU after 6 day prodromal illness (fever, aches) followed by
confusion, shortness of breath and now fluid-resistant hypotension
 Intubated in A&E as hypoxic and combative, received 3 L saline
 On arrival ICU BP = 75/40, HR 135 SR, NA @ 0.7 mg/kg/min, lactate 7,
CVP 9, pO2 9 on 100% O2 with PEEP 7, creps bilaterally
 Temperature 39.7, flushed
 Over next 2 hours: NA increasing, lactate 9, U/O poor
 Labs: Hb 10.5, Plts 65, WBC 27.9, Na 137, K 3.3, U 12.5 Creat 138,
APTT 47, PT 19, fibrinogen 1.0, CK 290
Q: Comments on Xray appearance?
 What is the differential diagnosis?
 What are the possible sources?
 What are the principles of management?
 Describe your haemodynamic targets and approach
 How do you make the diagnosis of ARDS?
 What ventilator settings will you choose?
 What principles guide your ventilation strategy?
 What are your ventilator targets?
Questions for discussion
Sepsis: Know what you mean…
 SIRS - 2 or more of the following
 Temperature > 38 or < 36 o
C
 Heart rate > 90 bpm
 Respiratory rate > 20/min or pCO2 < 4.2 kPa
 WBC > 12000/mm3 or < 4000/mm3 or > 10% bands
 Sepsis
 Systemic response to infection
 SIRS + infection
 Severe sepsis
 Sepsis + organ dysfunction, hypotension or hypoperfusion
 May be oliguria, encephalopathy or lactate rise
 Septic shock
 Sepsis induced SBP < 90 mmHg or SBP fall > 40 mmHg
 PLUS hypoperfusion despite adequate fluid resuscitation
 i.e. sepsis-induced hypotension requiring vasopressors
INFO
Principles of septic shock management
 Initial resuscitation
 Fluid resuscitation - ? EGDT (Rivers)
 Diagnosis
 Antibiotic therapy
 Source identification and control
 Haemodynamic and adjunctive therapy
 Vasopressors and/or inotropes (know characteristics & pros and cons)
 Steroids (know relative adrenal insufficiency principles)
 rhAPC (know trials and controversies)
 Other support
 Blood products
 Safe ventilation in ALI/ARDS (know ARDSNet etc.)
 Sedation (know sedation breaks)
 Glucose control (know controversies medical v surgical pts)
 RRT
 DVT prophylaxis
 Stress ulcer prophylaxis (relationship to Cdiff?)
 Limitation of therapy?
INFO
When septic shock isn’t just septic…
 TOXIC SHOCK SYNDROME
 Toxins act as “superantigens”
 Activate up to 30% of neutrophils (normal <0.1%)
 Cytokine storm => MSOF
 Differences in treatment from “simple” septic shock
 Prodromal illness…source can be subtle => LOOK HARD
 Remember vaginal infections
 Predominant organisms
 S. aureus (often blood culture negative)
 Menstrual and non-menstrual forms
 May not have protective antibodies
 Group A strep (majority blood culture positive)
 Therapeutic principles
 As for septic shock BUT
 Toxin suppressing antimicrobial: clindamycin or linezolid
 Immunoglobulin 1g/kg then 0.5 g/kg for 4-5 days
INFO
Q: Nutrition - how and why?
 Your patient stabilises over the next 18-24 hours
 She weighs 60 kg at baseline
 She hasn’t eaten at home for 5 days
 How are you going to support her nutrition?
 What are her requirements?
 How much do you give her today?
 How do you manage “intolerance”
 Why is nutrition important?
Nutrition Support/Therapy
INFO
 When to feed = EARLY (< 36 hours) if possible
 Support EN with TPN but EN preferred
 Early nutrition decreases infection, hospital LOS and may
decrease mortality
 CUMULATIVE ENERGY DEFICIT KILLS!!!!
 > 10000 kcal deficit correlates with poor outcome
 = 5 days off food in sepsis!!
 every day in ICU without feeding is a day closer to death!
Nutrition Support/Therapy
INFO
 Nutrition modulates stress response
 Nutrition modulates systemic immunity
 Gut surface area = tennis court!!
 Exposure to and in harmony with trillions of organisms
 GALT = gut associated lymphoid tissue - appropriate
exposure enhances systemic immunity
Nutrition Support/Therapy
INFO
 No feeding + systemic illness = leaky gut (BAD)
 Antibiotics = higher pH and less anaerobic flora (BAD)
 Anaerobes produce substances which enhance immune
response (GOOD)
 Fewer anaerobes = poor WBC function and more systemic
infection (BAD)
 Leaky gut = bugs and cytokines (BAD)
 GUT-LUNG conduit: bugs/cytokines via thoracic duct and
heart to pulmonary capillary bed => lung inflammation (BAD)
Nutrition Support/Therapy
INFO
Anaerobe levels Mortality Bacteraemia
Maintained 16% 6%
Low then recover 25% 50%
Persistently low 81% 75%
 Short-chain fatty acids related to anaerobe levels
 Short-chain fatty acids are colonocyte fuel
 WBCs have receptors for SCFA = imprived function!
 Attention to nutrition/antibiotics and pre/probiotics
What and how much?
INFO
 Energy (kcal)
 generally 25 kcal, up to 35 kcal/kg
 start at 25-35% of requirement if refeeding syndrome risk
 Protein
 generally 1.25 g/kg
 no need for < 1g/kg in acute liver disease
 Lipids
 ? omega-3 FA’s in ARDS (favour anti-inflammatory eicosanoids)
 Trace elements
 selenium in sepsis?
 Amino acids
 arginine (vasodilatory)
 glutamine (enterocyte fuel and ? better WBC function in trauma)
INFO
INFO
INFO
INFO
INFO
INFO
INFO
www.criticalcarenutrition.com
Fluid Balance & Outcome
It’s not IF they should be dry...
it’s WHEN
ICU Topics for the Final FRCA
ICU Topics for the Final FRCA
ICU Topics for the Final FRCA
ICU Topics for the Final FRCA
ICU Topics for the Final FRCA
ICU Topics for the Final FRCA
ICU Topics for the Final FRCA
ICU Topics for the Final FRCA

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ICU Topics for the Final FRCA

  • 2. Why ICU matters for the FRCA…  20 specific questions in MCQ  Helps with medicine/surgery MCQs  SAQs - 1 or 2 questions for sure…maybe more  SOE 1 - potential topic/part of topic  SOE 2 - 10 minutes of pure fun!
  • 3. Be calm…  The examiners are human (honestly!!!)  The questions are (mostly) mainstream  You will have seen many of the cases  Guillain-Barre / Myasthenic crisis / weakness  Brainstem death  Status epilepticus and asthmaticus  Trauma  Septic shock  ARDS  Acute pancreatitis  Burns  Some questions just won’t lie down and die e.g. PAC
  • 4. But don’t be complacent…  People still fail the exam! 10/17 passed in 2008  Don’t assume you know enough…make sure you do  Structure…structure…structure!  Don’t waffle - answer the actual question, not the one you wanted to be asked!!
  • 5. Other potentials… • Acute hepatic failure • Sedation • Fluid balance and outcome • Nutritional therapy • Tissue oxygenation and oxygen delivery • Abdominal compartment syndrome • Cardiogenic shock • Clostridium difficile • Scoring systems
  • 6. Examples… In the question on the brain-stem dead patient, too many candidates included detail of brain stem testing in their answers, which was not required. Candidates are reminded to answer the question as written; no credit will be given for irrelevant information It cannot be emphasised enough that the answer provided to the examiners is less than a page and is focused completely to the question.
  • 7.
  • 8.
  • 9. Case scenario 1  49 year old female, history of depression & anxiety found unconscious in apartment having failed to turn up for work  On arrival A&E GCS 5-6, BM = 0.4  After 50ml 50% glucose BM = 14.5 and GCS 12-14  Bruising left buttock and thigh  Tender abdomen, jaundiced, BP 75/45, HR 104, Temp 34.1  CT brain NAD, CT abdo - mild hepatomegaly, ? fatty  Labs: Lactate 10.2, Bili 27, AST 4465, ALT 1945, INR 4, Paracetamol 25, tox negative, K 1.9, Ca 0.8, PO4 0.4, Hb 10.4, WBC 15.9, Plts 102, CK 595
  • 10. Questions for discussion What are the main differential diagnoses? What other information/tests would you like? Why is the GCS abnormal? How do you assess fluid status and responsiveness? What does the lactate level tell you? Why is the B low and how will you tackle it? How do you assess the adequacy of oxygen delivery? Does this patient need antibiotics? What problems are likely in the next 24-48 hours?
  • 11. Acute hepatic failure  Early death despite support  Survival with supportive therapy (liver regeneration)  Unlikely to survive with supportive therapy alone  candidate for emergency transplant  NOT candidate for emergency transplant INFO “Life-threatening multi-system illness resulting from massive liver injury. The defining clinical symptoms are coagulopathy and encephalopathy occurring within days or weeks of the primary insult in patients without pre-existing liver injury” Auzinger G, Wendon J. Curr Opin Crit Care 2008; 14: 179-188
  • 12. Aetiology based therapy INFO Aetiology Therapy Comments Paracetamol N-Acetylcysteine (NAC) Early non-paracetamol ALF N-Acetylcysteine (NAC) Lee WM, Rossaro L, Fontana RJ et al. Hepatology 2007; 46(Suppl 1); 268A. ? increased infection risk due to reduced neutrophil burst ? antiplatelet action Fatty liver of pregnancy or HELLP Delivery! Usually reverses before need for transplant Acute hepatitis B Lamivudine Amanita Phalloides Penicillin G
  • 13. Paracetamol toxicity INFO Enhanced risk 1.Excess alcohol 2.Enzyme-inducing drugs carbamazepine phenytoin, phenobarbitone St John's Wort rifampicin 3. Glutathione depletion malnutrition eating disorders malabsorption HIV NAPQI Major paths Minor path
  • 14. N-acetylcysteine INFO (1) Initially 150mg/kg in 200mL glucose 5% given over 15 minutes, then (2) 50mg/kg in 500mL glucose 5% given over 4 hours, then (3) 100mg/kg in 1000mL glucose 5% given over 16 hours
  • 15. Referral criteria INFO Day 2 Day 3 Day 4 Arterial pH < 7.3 Arterial pH < 7.3 INR > 4.4 or PT > 75s INR > 3 or PT > 50s INR > 4.4 or PT > 75s Progressive rise in PT Oliguria Oliguria Oliguria Creatinine > 200 Creatinine > 200 Creatinine > 300 Hypoglycaemia Encephalopathy Encephalopathy Severe thrombocytopaenia Severe thrombocytopaenia Hyperacute Acute Subacute Encephalopathy Encephalopathy Encephalopathy INR > 2 or PT > 30s INR > 2 or PT > 30s INR > 1.5 or PT > 20s Renal failure Renal failure Renal failure Hypoglycaemia Hypoglycaemia Hypoglycaemia (rare) Hyperpyrexia Hyponatraemia Shrinking liver on CT Non-paracetamol Paracetamol
  • 16. Referral criteria - Kings College Hospital INFO Paracetamol Non-paracetamol Arterial pH < 7.3 after resuscitation OR Grade III/IV encephalopathy PT > 100s (INR > 6.5) OR any 3 of the following Creatinine > 300 Aetiology = seronegative hepatitis or drug-induced liver failure PT > 100s (INR > 6.5) Age < 10 or > 40 Lactate > 3.5 @ 4hrs or > 3 @ 12 hrs Jaundice to encephalopathy > 7 d Hypoglycaemia Bilirubin > 300 PT > 50s (INR > 3.5) Paracetamol Non-paracetamol
  • 17. Clinical Issues in ALF  CNS  Encephalopathy - ammonia => glutamate  Intracranial hypertension - oedema  Cardiovascular  Intravascular volume depletion  Vasodilatation  Subclinical myocardial damage (Tn > 0.1 in 66%)  Respiratory  Hypoxia - effusions, atelectasis, shunting, splinting, ALI INFO
  • 18. Clinical Issues in ALF  Renal  Oliguria  Acute renal impairment - drugs, hepatorenal, pre- renal, ATN, intra-abdominal hypertension  Haematological  Thrombocytopaenia and coagulopathy  Procedural bleeding possible  Spontaneous bleeding rare  Infection  Monocyte (HLA-DR), complement, Kupffer cell failure Responsible for most deaths! INFO
  • 19. Useful references INFO Kramer DJ, Canabal JM, Arasi LC. Application of Intensive Care Medicine Principles in the Management of the Acute Liver Failure Patient. Liver Transplantation 2008; 14: S85-89. Auzinger G, Wendon J. Intensive Care Management of Acute Liver Failure. Current Opinion in Critical Care 2008; 14: 179-188. Stravitz T. Critical Management Decisions in Patients with Acute Liver Failure. Chest 2008; 134: 1092-1102.
  • 20. Case scenario 2  56 year old male, history of IHD/PVD/smoker/MI/EF 35%  Admitted to ICU following emergent leaking AAA repair…complicated by intraoperative ST depression and hypotension  On arrival ICU BP = 90/45, HR 121 SR, NA @ 0.5 mg/kg/min, lactate 5  CVP 14, pO2 11 on 70% O2 with PEEP 5, creps bilaterally  ECG: infero-lateral ST depression  In theatre 4 L crystalloid, 2 L tetraspan, 6 packed cells, 2 FFP  Abdomen distended and tense, skin clammy  Over next 4 hours: NA increasing, lactate 8, U/O poor  Labs: Hb 9.5, Plts 85, WBC 7.9, Na 141, K 5.3, U 10.5 Creat 168, APTT 47, PT 18, fibrinogen 0.95
  • 21. Questions for discussion  List the main clinical issues in this case  How would you approach the respiratory failure?  What factors contribute to the hypotension/malperfusion?  What is your strategy to improve haemodynamics?  What is your target for fluid balance in the next 24 hours?  How does PPV assist the left ventricle?  What other monitors/investigations might assist you?  When would you involve the surgeons?
  • 22. Cardiogenic Shock • Definition • Incidence • Aetiology • Pathophysiology • Therapy Clinical: • Hypotension i.e. SBP below 90 mmHg • Impaired tissue perfusion • After correction of non-cardiac factors Haemodynamic: • Cardiac index < 2.2 litres/min/m2 • Systolic blood pressure < 90 mm Hg • LAP/RAP > 18 mm Hg or PCWP > 16 • Urine output < 20 ml/hr • SVR > 2100 dynes-sec·cm–5 INFO
  • 23. Incidence & Mortality Study Incidence Mortality Patient group Country CREATE-ECLA [1] 6.5% 68% STEMI China, India, Pakistan NRMI [2] 8.6% 47.9% STEMI USA COMMIT [3] 4.4% 68% AMI (93% STEMI) China 5.0% 68% Metoprolol 3.9% 72% Plcaebo SHOCK [4] 20% 75% CS on admission USA/Belgium 80% 56% Delayed CS [1] The CREATE-ECLA Trial Group. Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST- segment elevation myocardial infarction: the CREATE-ECLA Randomized Controlled Trial. JAMA 2005; 293: 437–446. [2] Babaev A, Frederick PD, Pasta DJ, et al. Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA 2005; 294:448–454. [3] Jeger RV, Harkness SM, Ramanathan K, et al. Emergency revascularization in patients with cardiogenic shock on admission: a report from the SHOCK trial and registry. Eur Heart J 2006; 27:664–670. [4] Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomized placebo controlled trial. Lancet 2005; 366:1622–1632. INFO
  • 24. Echo indicators of mortality INFO
  • 26. Cardiogenic Shock • Definition • Incidence • Aetiology • Pathophysiology • Therapy Cause of CS Proportion LV failure post-MI (8.5% of STEMI, 2.5% of NSTEMI) 70-75% Acute severe mitral regurgitation 8.3% Ventricular septal rupture 4.6% Isolated RV failure 3.4% Ventricular free-wall rupture or Cardiac tamponade 1.7% Myocardial contusion LVOT obstruction (AS/HOCM) End-stage cardiomyopathy Obstructed LV filling (MS) Myocarditis INFO
  • 27. Pathophysiology Target for therapy? At least 20% of CS patients have SIRS and low SVR INFO
  • 28. Therapy - Reducing iNOS “Excessive NOS results in high levels of nitric oxide that, in turn, lead to inappropriate systemic vasodilatation, progressive systemic and coronary hypoperfusion, and myocardial depression” Effect of Tilarginine Acetate in Patients With Acute Myocardial Infarction and Cardiogenic Shock - The TRIUMPH Randomized Controlled Trial. JAMA 2007; 297: 1657-1666 INFO
  • 29. Cardiogenic Shock: Therapy • Optimise volume / oxygenation / rhythm • Inotropic agents & vasopressors  b agonists  a agonists  PDE III inhibitors  LEVOSIMENDAN • sensitizes myocardial contractile proteins to calcium • independent of sympathetic NS and so NO increase in MVO2 • Prolonged action beyond infusion duration • IABP • PCI INFO
  • 30. Abdominal compartment syndrome  Increasingly recognised problem  LOOK for it! - don’t forget “medical” ICU patients  Thinks about screening if  Large volume resuscitation > 3.5 L in 24 hours  Abdominal Surgery/Primary Fascial Closure  Coagulopathy or polytransfusion  Pulmonary, renal or hepatic dysfunction  Acidosis  Hypothermia  Ileus  Physical exam is NOT accurate INFO
  • 31. Intra-abdominal pressure INFO Patient Intra-abdominal pressure Normal adult 0-5 mmHg Typical ICU patient 5-7 mmHg Post-laparotomy patient 10-15 mmHg Septic shock patient 15-25 mmHg Acute abdomen 25-40 mmHg Grade of IAH Pressure Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV > 25 mmHg Abdominal perfusion pressure = MAP - IAP (aim > 60 mmHg)
  • 32. Abdominal Compartment Syndrome INFO ACS = sustained IAP > 20 mmHg (with or without APP < 60 mmHg) that is associated with new organ dysfunction/failure World Society of the Abdominal Compartment Syndrome (www.wsacs.org)
  • 33. INFO
  • 34. INFO
  • 35. Case scenario 3  25 year old female, “fit and well”  Admitted to ICU after 6 day prodromal illness (fever, aches) followed by confusion, shortness of breath and now fluid-resistant hypotension  Intubated in A&E as hypoxic and combative, received 3 L saline  On arrival ICU BP = 75/40, HR 135 SR, NA @ 0.7 mg/kg/min, lactate 7, CVP 9, pO2 9 on 100% O2 with PEEP 7, creps bilaterally  Temperature 39.7, flushed  Over next 2 hours: NA increasing, lactate 9, U/O poor  Labs: Hb 10.5, Plts 65, WBC 27.9, Na 137, K 3.3, U 12.5 Creat 138, APTT 47, PT 19, fibrinogen 1.0, CK 290
  • 36. Q: Comments on Xray appearance?
  • 37.  What is the differential diagnosis?  What are the possible sources?  What are the principles of management?  Describe your haemodynamic targets and approach  How do you make the diagnosis of ARDS?  What ventilator settings will you choose?  What principles guide your ventilation strategy?  What are your ventilator targets? Questions for discussion
  • 38. Sepsis: Know what you mean…  SIRS - 2 or more of the following  Temperature > 38 or < 36 o C  Heart rate > 90 bpm  Respiratory rate > 20/min or pCO2 < 4.2 kPa  WBC > 12000/mm3 or < 4000/mm3 or > 10% bands  Sepsis  Systemic response to infection  SIRS + infection  Severe sepsis  Sepsis + organ dysfunction, hypotension or hypoperfusion  May be oliguria, encephalopathy or lactate rise  Septic shock  Sepsis induced SBP < 90 mmHg or SBP fall > 40 mmHg  PLUS hypoperfusion despite adequate fluid resuscitation  i.e. sepsis-induced hypotension requiring vasopressors INFO
  • 39. Principles of septic shock management  Initial resuscitation  Fluid resuscitation - ? EGDT (Rivers)  Diagnosis  Antibiotic therapy  Source identification and control  Haemodynamic and adjunctive therapy  Vasopressors and/or inotropes (know characteristics & pros and cons)  Steroids (know relative adrenal insufficiency principles)  rhAPC (know trials and controversies)  Other support  Blood products  Safe ventilation in ALI/ARDS (know ARDSNet etc.)  Sedation (know sedation breaks)  Glucose control (know controversies medical v surgical pts)  RRT  DVT prophylaxis  Stress ulcer prophylaxis (relationship to Cdiff?)  Limitation of therapy? INFO
  • 40. When septic shock isn’t just septic…  TOXIC SHOCK SYNDROME  Toxins act as “superantigens”  Activate up to 30% of neutrophils (normal <0.1%)  Cytokine storm => MSOF  Differences in treatment from “simple” septic shock  Prodromal illness…source can be subtle => LOOK HARD  Remember vaginal infections  Predominant organisms  S. aureus (often blood culture negative)  Menstrual and non-menstrual forms  May not have protective antibodies  Group A strep (majority blood culture positive)  Therapeutic principles  As for septic shock BUT  Toxin suppressing antimicrobial: clindamycin or linezolid  Immunoglobulin 1g/kg then 0.5 g/kg for 4-5 days INFO
  • 41. Q: Nutrition - how and why?  Your patient stabilises over the next 18-24 hours  She weighs 60 kg at baseline  She hasn’t eaten at home for 5 days  How are you going to support her nutrition?  What are her requirements?  How much do you give her today?  How do you manage “intolerance”  Why is nutrition important?
  • 42. Nutrition Support/Therapy INFO  When to feed = EARLY (< 36 hours) if possible  Support EN with TPN but EN preferred  Early nutrition decreases infection, hospital LOS and may decrease mortality  CUMULATIVE ENERGY DEFICIT KILLS!!!!  > 10000 kcal deficit correlates with poor outcome  = 5 days off food in sepsis!!  every day in ICU without feeding is a day closer to death!
  • 43. Nutrition Support/Therapy INFO  Nutrition modulates stress response  Nutrition modulates systemic immunity  Gut surface area = tennis court!!  Exposure to and in harmony with trillions of organisms  GALT = gut associated lymphoid tissue - appropriate exposure enhances systemic immunity
  • 44. Nutrition Support/Therapy INFO  No feeding + systemic illness = leaky gut (BAD)  Antibiotics = higher pH and less anaerobic flora (BAD)  Anaerobes produce substances which enhance immune response (GOOD)  Fewer anaerobes = poor WBC function and more systemic infection (BAD)  Leaky gut = bugs and cytokines (BAD)  GUT-LUNG conduit: bugs/cytokines via thoracic duct and heart to pulmonary capillary bed => lung inflammation (BAD)
  • 45. Nutrition Support/Therapy INFO Anaerobe levels Mortality Bacteraemia Maintained 16% 6% Low then recover 25% 50% Persistently low 81% 75%  Short-chain fatty acids related to anaerobe levels  Short-chain fatty acids are colonocyte fuel  WBCs have receptors for SCFA = imprived function!  Attention to nutrition/antibiotics and pre/probiotics
  • 46. What and how much? INFO  Energy (kcal)  generally 25 kcal, up to 35 kcal/kg  start at 25-35% of requirement if refeeding syndrome risk  Protein  generally 1.25 g/kg  no need for < 1g/kg in acute liver disease  Lipids  ? omega-3 FA’s in ARDS (favour anti-inflammatory eicosanoids)  Trace elements  selenium in sepsis?  Amino acids  arginine (vasodilatory)  glutamine (enterocyte fuel and ? better WBC function in trauma)
  • 47. INFO
  • 48. INFO
  • 49. INFO
  • 50. INFO
  • 51. INFO
  • 52. INFO
  • 53. INFO
  • 55. Fluid Balance & Outcome It’s not IF they should be dry... it’s WHEN