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Intensive Care Medicine Topics for the Final FRCA Dr. Andrew Ferguson

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Page 1: ICU topics for Final FRCA

Intensive Care MedicineTopics for the Final FRCA

Dr. Andrew Ferguson

Page 2: ICU topics for Final FRCA

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!

Page 3: ICU topics for Final FRCA

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

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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!!

Page 5: ICU topics for Final FRCA

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

Page 6: ICU topics for Final FRCA

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.

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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

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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?

Page 11: ICU topics for Final FRCA

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

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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

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Paracetamol toxicity

INFO

Enhanced risk

1.Excess alcohol2.Enzyme-inducing

drugs carbamazepine phenytoin, phenobarbitone St John's Wort rifampicin3. Glutathione depletion malnutrition eating disorders malabsorption HIV

NAPQI

Major paths

Minor path

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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

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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

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Referral criteria - Kings College Hospital

INFO

Paracetamol Non-paracetamol

Arterial pH < 7.3 after resuscitationOR

Grade III/IV encephalopathy

PT > 100s (INR > 6.5)OR

any 3 of the following

Creatinine > 300Aetiology = 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

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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

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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

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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.

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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

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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?

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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

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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

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Echo indicators of mortality

INFO

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Pathophysiology

INFO

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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 orCardiac tamponade

1.7%

Myocardial contusion

LVOT obstruction (AS/HOCM)

End-stage cardiomyopathy

Obstructed LV filling (MS)

Myocarditis

INFO

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Pathophysiology

Target for therapy?

At least 20% of CS patients have SIRS and low SVR

INFO

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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

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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

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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

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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)

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Abdominal CompartmentSyndrome

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)

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INFO

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INFO

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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

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Q: Comments on Xray appearance?

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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

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Sepsis: Know what you mean… SIRS - 2 or more of the following

Temperature > 38 or < 36 oC 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

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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

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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

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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?

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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!

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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

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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)

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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

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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)

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INFO

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www.criticalcarenutrition.com

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Fluid Balance & Outcome

It’s not IF they should be dry... it’s WHEN

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