Intensive Care MedicineTopics for the Final FRCA :Intensive Care MedicineTopics for the Final FRCA Dr. Andrew Ferguson


Why ICU matters for the 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!


Be calm… :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… :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… :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… :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 :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 :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 :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 :Aetiology based therapy INFO


Paracetamol toxicity :Paracetamol toxicity INFO Enhanced risk Excess alcohol 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 :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 :Referral criteria INFO Non-paracetamol Paracetamol


Referral criteria - Kings College Hospital :Referral criteria - Kings College Hospital INFO Paracetamol Non-paracetamol


Clinical Issues in ALF :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 :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 :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 :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 :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 :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 18 mm Hg or PCWP > 16 Urine output 2100 dynes-sec·cm–5 INFO


Incidence & Mortality :Incidence & Mortality [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 :Echo indicators of mortality INFO


Pathophysiology :Pathophysiology INFO


Cardiogenic Shock :Cardiogenic Shock Definition Incidence Aetiology Pathophysiology Therapy INFO


Pathophysiology :Pathophysiology Target for therapy? At least 20% of CS patients have SIRS and low SVR INFO


Therapy - Reducing iNOS :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 :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 :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 :Intra-abdominal pressure INFO Abdominal perfusion pressure = MAP - IAP (aim > 60 mmHg)


Abdominal CompartmentSyndrome :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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Case scenario 3 :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? :Q: Comments on Xray appearance?


Slide 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


Sepsis: Know what you mean… :Sepsis: Know what you mean… SIRS - 2 or more of the following Temperature > 38 or 90 bpm Respiratory rate > 20/min or pCO2 12000/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 40 mmHg PLUS hypoperfusion despite adequate fluid resuscitation i.e. sepsis-induced hypotension requiring vasopressors INFO


Principles of septic shock management :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… :When septic shock isn’t just septic… TOXIC SHOCK SYNDROME Toxins act as “superantigens” Activate up to 30% of neutrophils (normal 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? :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 :Nutrition Support/Therapy INFO When to feed = EARLY ( 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 :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 :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 :Nutrition Support/Therapy INFO 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? :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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www.criticalcarenutrition.com :www.criticalcarenutrition.com


Fluid Balance & OutcomeIt’s not IF they should be dry... it’s WHEN :Fluid Balance & OutcomeIt’s not IF they should be dry... it’s WHEN