Short Answer Questions Anaesthesia & Intensive Care For FCAI, FRCA & EDAIC Part: - Intensive Care Medicine Modified by AYMAN EDAROUS Anaesthesia, Pain & Intensive Care Secrets Academy [APICSA] ‫بسم الله الرحمن الرحيم‬ For Original Materials and Editors, Please refer to: North Ireland School of Anaesthesia Website http://www.nischoolofanaesthesia-finalfrca.org.uk/SAQs/intensivecare/ MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 1- Ventilator Associated Pneumonia (VAP) a) What is meant by the term Ventilator Associated Pneumonia (VAP)? (3 marks) b) List the factors that increase the risk of the development of VAP (10 marks) c) What measures may reduce the risk of development of VAP? (7 marks)  Ventilator Associated Pneumonia (VAP): Pneumonia occurring 48-72 hours after ETT intubation, characterised by (Diagnostic Criteria): -Clinical Signs: Pyrexia, raised WCC, Purulent Bronchial Secretion -Microbiological Evidence: Positive Sputum Culture -Radiological Signs: New or Progressive Pulmonary Infiltrates The common pathogens associated with VAP: Mainly caused by G-ve organisms, but G+ve bacteria such as MRSA are not uncommon Typically, bacteria causing early onset VAP include:  Streptococcus pneumonia  Haemophilus influenzae  Methicillin-sensitive Staphylococcus aureus (MSSA)  Gram-negative bacilli  Escherichia coli  Klebsiella pneumonia  Enterobacter and Proteus species  Serratia marcescens Culprits of late VAP are drug-resistant organisms such as MRSA, Acinetobacter, Pseudomonas aeruginosa, and extended-spectrum beta-lactamase producing bacteria (ESBL) Pathogenesis of VAP:  It is thought to be caused by entry of infected secretions into distal bronchi  Patients are usually immunosuppressed, and their oropharynx becomes colonised with organisms, especially G-ve bacteria  Oral and nasal tubes cause trauma, leading to infections such as sinusitis  The natural protections like cough reflex, tracheobronchial secretions, mucociliary linings, saliva, and nasal mucosa are less effective in these patients  The pathogens enter the lower lung through mechanical routes such as around the endotracheal tube cuff, suction catheter, and ventilation tubings  Factors that Increase the Risk of the Development of VAP: 1- Patient factors Advanced age Low serum albumin ARDS, COPD and other lung diseases Impaired consciousness Trauma and Burns Multiple Organ Failure Large volume gastric aspirates Upper respiratory tract colonisation MODIFIED BY AYMAN EDAROUS 2- Interventional factors: Prolonged ventilation Level of sedation Use of neuromuscular blocking agents Use of Antacids,PPI and H2 blockers Nasogastric tube Supine position Frequent circuit changes Transfer outside ICU INTENSIVE CARE MEDICINE  Measures may reduce the Risk of development of VAP (VAP bundle): General measures: Use of sterile equipment, regular hand washing, using barrier nursing such as gloves and an apron, and minimal contact with patient usually reduce the incidence of any infection in ICU Specific measures: This include reducing the load of pathogens and their entry into lower respiratory tract Reducing Oral Colonisation *Good Oral Cavity Care including Regular Brushing of Teeth *Use of Antiseptic Mouthwash (e.g Chlorhexidine) *Use of Silver coated ETT (prevents build up of Biofilms on ETT lumen) *Selective decontamination of digestive tract (SDD) using non-absorbable antimicrobials such as Polymyxin E and Amphotericin B has been tried with variable success [NB: It encouraging Clostridium diffcilie, antimicrobial resistance, and the emergence of multi-drug resistant pathogens] • Reducing Aspiration *Patients nursed in 30-45o degree head-up position *Use of ETT with subglottic secretion drainage port with regular subglottic suction *Regular Monitoring /4 hr and maintainence of ETT Cuff Pressure (20-30 cmH2O) • Minimising duration of Mechanical Ventilation: *This is achieved by early tracheostomy, which has proven to lower the incidence of VAP *Periodic ‘sedative interruptions’ and daily assessment of readiness to extubate may reduce the duration of mechanical ventilation • Stress Ulcer Prophylaxis: *Reducing the acidity of stomach in stress ulcer prophylaxis is claimed to increase the incidence of VAP by increasing the proliferation of gram-negative bacteria Use of H2 blockers or Sucralfate, instead of PPIs, are suggested to reduce the risk *Enteral feeding can increase the risk of VAP by altering the gastric acidity and risk of aspiration, but benefits of enteral feeding usually outweigh this small risk •Deep Venous Thrombosis (DVT) Prophylaxis: MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE Clinical Pulmonary Infection Score (CPIS) for VAP The CPIS takes into account:  Clinical:Temperature, Presence of tracheal secretions  Physiological: Leucocytosis and worsening gas exchange  Microbiological: Positive culture of tracheal aspirate  Radiographic: evidence to assign a numerical value **Scores can range from to 12 with a score of ≥ 6: good correlation with the presence of VAP MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 2- Surviving Sepsis Campaign 2018 You are asked to assess a 45 year old woman in A&E resus who has a provisional diagnosis of Gallbladder Sepsis a) Define (i) Sepsis (ii) Septic Shock (25%) b) What diagnostic criteria for sepsis as suggested by the 2012 Surviving Sepsis Campaign would you apply to this patient? (25%) c) Outline the targets for management and categorise into accepted timeframes (25%) d) What are the major changes in the 2012 recommendations compared to the original? (25%)  Sepsis: Life-threatening Organ Dysfunction caused by Dysregulated Host Response to Infection - Septic Shock: Subset of sepsis with circulatory and cellular/metabolic dysfunction associated with higher risk of mortality MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE  Diagnostic criteria for sepsis as suggested by the 2016 Surviving Sepsis Campaign: MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE  The Targets for Management: Hour-1 Surviving Sepsis Campaign Bundle of Care (2018) Te most important change in the revision of the SSC bundles is that the 3-h and 6-h bundles have been combined into a single “hour-1 bundle” with the explicit intention of beginning resuscitation and management immediately We believe this reflects the clinical reality at the bedside of these seriously ill patients with sepsis and septic shock-that clinicians begin treatment immediately, especially in patients with hypotension, rather than waiting or extending resuscitation measures over a longer period More than h may be required for resuscitation to be completed, but initiation of resuscitation and treatment, such as obtaining blood for measuring lactate and blood cultures, administration of fluids and antibiotics, and in the case of life-threatening hypotension, initiation of vasopressor therapy, are all begun immediately  Measure Lactate Level If initial lactate is elevated (> mmol/L), it should be re-measured within 2–4 h to guide resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion  Obtain Blood Cultures (prior to Antibiotics) Sterilization of cultures can occur within minutes of the first dose of an appropriate antimicrobial, so cultures must be obtained before antibiotic administration to optimize the identification of pathogens and improve outcomes Appropriate blood cultures include at least two sets (aerobic and anaerobic) Administration of appropriate antibiotic therapy should not be delayed in order to obtain blood cultures  Administer Broad-Spectrum Antibiotics Empiric broad-spectrum therapy with one or more intravenous antimicrobials to cover all likely pathogens should be started immediately for patients presenting with sepsis or septic shock Empiric antimicrobial therapy should be narrowed once pathogen identification and sensitivities are established, or discontinued if a decision is made that the patient does not have infection The link between early administration of antibiotics for suspected infection and antibiotic stewardship remains an essential aspect of high-quality sepsis management If infection is subsequently proven not to exist, then antimicrobials should be discontinued MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE  Administer Intravenous Fluid Initial fluid resuscitation should begin immediately upon recognizing a patient with sepsis and/or hypotension and elevated lactate, and completed within h of recognition The guidelines recommend this should comprise a minimum of 30 ml/kg of intravenous crystalloid fluid Because some evidence indicates that a sustained positive fluid balance during ICU stay is harmful, fluid administration beyond initial resuscitation requires careful assessment of the likelihood that the patient remains fluid responsive  Apply Vasopressors If blood pressure is not restored after initial fluid resuscitation, then vasopressors should be commenced within the first hour to achieve mean arterial pressure (MAP) of ≥ 65 mmHg MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 10  ‘Stand Down Time’ for Various Organ Retrieval Each organ is susceptible to warm ischaemia by various amounts, which has implications for graft function and complications following transplantation Stand down time = allowed period of functional warm ischaemia (FWI), or from time of withdrawal of life sustaining treatment (WLST) until asystole; this is specific for each organ Stand down times are also specific for each centre Examples of typical stand down times: Kidney: 120 mins of FWI or from WLST Liver: 30 mins FWI, 60 mins from WLST Pancreas: 30 mins FWI or from WLST  Contraindications to donation after circulatory death Untreated systemic infection HIV disease (but HIV positive status not an absolute CI) Active invasive cancer in the last three years (excl primary brain and nonmelanomatous skin cancer) Haematological malignancy nvCJD (age > 90 years occasionally mentioned)  Outline the donation process, including the staff groups involved For controlled DCD: Decision WLST (independent of any consideration for transplant) MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 12 Medical staff Assessment for donation potential Medical staff SN-OD Organ donor register Family (assent) Lab staff (tissue typing etc) Consent and authorisation Involvement of recipient centres Medical staff SN-OD Maintenance of donation potential / donor optimisation Mobilisation of retrieval teams Notification of donor recipients & their respective teams Medical staff – optimisation of donor SN-OD and paramedical staff WLST, diagnosis of death, transfer to theatre for retrieval (within constraints of stand down times) Critical care and theatre staff Retrieval team(s) with transport staff Cold perfusion, packaging, departure of retrieval teams Last offices / clerical input Mortuary staff Portering staff Post donation debrief Contact with family Medical, nursing, paramedical staff MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 12 MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 12 35- Post Cardiac Arrest Care and Cooling You have been asked to admit a 75 year old man to ICU who has had an OOH VF arrest for ventilation and therapeutic hypothermia (a) What were the major changes in the ILCOR 2010 resuscitation guidelines for adult cardiac arrest? (b) What is induced hypothermia and what is the proposed mechanism by which it exerts its effects? (c) What are the adverse systemic consequences of hypothermia? (15%) (d) Outline the principles of management of therapeutic hypothermia (30%) (e) Describe a scoring system by which neurological outcome may be predicted post critical care admission (15%)  The Major Changes in the ILCOR 2010 Resus Guidelines for Cardiac Arrest in Adults removal of rescue breaths early CPR minimally interrupted CPR; less than seconds CPR during charging of defibrillator use of cpr feedback devices role of praecordial thump de emphasised drugs no longer recommended via trachael route drugs recommended via IO route if IV cannot be established less focus on early intubation unless expert assistance available capnography recommended for intubated patient atropine removed from PEA algorithm amiodarone and adrenaline recommended at 3rd shock/cycle in shockable algorithm recognition of potential of USS in cardiac arrest e.g FEEL algorithm focus on post arrest syndrome care unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32-34°C for 12 to 24 hours when the initial arrest rhythm was ventricular fibrillation (VF) therapeutic hypothermia may also be useful in cases where the initial rhythm was nonshockable or after in-hospital arrest  What is induced hypothermia and what is the proposed mechanism by which it exerts its effects?(20%) induced hypothermia - intentional reduction of patient's core temperature to below 36 degrees therapeutic hypothermia - induced hypothermia between 32-34 degrees mechanism not fully known MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 12 reduces ICP reduces CMRO2; 7% for every degree of cooling reduces reperfusion injury; free radical release, excitatory amino acid production, calcium shifts What are the adverse systemic consequences of hypothermia? (15%) cardiac - pro arrythmic, reduced contractility, diastolic dysfunction, hypertension renal - diuresis, electrolyte disturbances, hypokalaemia, phosphataemia, magnesaemia endocrine - hyperglycaemia respiratory - alteration in solubility of gases in blood haematology - coagulopathy, platelet dysfunction biochemical - use alpha stat analysis for blood gases, caution with drug administration (reduced metabolism) skin - burns, pressure sores shivering immunosuppression  Outline the principles of management of therapeutic hypothermia (30%) decision to cool - meets criteria for cooling, feasible in centre, intubated and ventilated aim to cool within 2-4 hours for 12-24 hours induction - cool core temperature to 32-34 degrees as rapidly as possible maintenance - maintain with 0.2-0.5 degree fluctuations re warming - aim to passively reward 0.2-.3 degrees per hour, max 0.5 paralyse to avoid shivering (40-100% increase in o2 consumption) above 34 degrees avoid long term paralysis sedate adequately adjust ventilator settings appropriately acknowledge normal physiology of hypothermia e.g deranged lfts monitor for sepsis reduce feeding rate consider platelets before invasive procedure  Describe a scoring system by which neurological outcome may be predicted post critical care admission (15%) Prognosis after resuscitation score (PAR) validated against inpatient cardiac arrest population point based system with score >5 predicting non survival (this has since been shown not MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 12 to be the case) metastatic malignancy 10 non metastatic malignancy sepsis dependent functional status pneumonia creatinine >130 age > 70 acute MI -2 other predictors include; Day myoclonus status Day absent pupil reflexes, absent or extensor reflexes Day GCS persistently