Post on 22-Jan-2018
transcript
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