Intensive Care MedicineTopics for the Final FRCA

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

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“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

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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

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Enhanced risk

1.Excess alcohol2.Enzyme-inducing drugs

carbamazepine

phenytoin,

phenobarbitone

St John's Wort

rifampicin

3. Glutathione depletionmalnutrition

eating disorders

malabsorption

HIV

NAPQI

Major paths

Minor path

N-acetylcysteine

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(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

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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

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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 > 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

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

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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!

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Useful references

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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

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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.

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Echo indicators of mortality

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Pathophysiology

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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 or

Cardiac tamponade

1.7%

Myocardial contusion

LVOT obstruction (AS/HOCM)

End-stage cardiomyopathy

Obstructed LV filling (MS)

Myocarditis

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Pathophysiology

Target for

therapy?

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

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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

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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

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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

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Intra-abdominal pressure

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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

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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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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

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

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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?

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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

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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?

Nutrition Support/Therapy

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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

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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

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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

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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?

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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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www.criticalcarenutrition.com

Fluid Balance & Outcome

It’s not IF they should be dry...

it’s WHEN