icu topics for final frca
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
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 alcohol2.Enzyme-inducing
drugs carbamazepine phenytoin, phenobarbitone St John's Wort rifampicin3. 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 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
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 orCardiac 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 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)
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 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
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
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www.criticalcarenutrition.com
Fluid Balance & Outcome
It’s not IF they should be dry... it’s WHEN