The Intensive Care Unit at the Mid Yorkshire Hospitals NHS Trust 20th July 2010 1

Contents Contents Contents 1 Administration 1.1 Staf ng . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.1.1 Clinical Lead . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.1.2 Consultant Medical St aff . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 9 9 9 1.1.3 Nursing Staff . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 1.1.4 SHOs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 1.2 Weekly Program . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 1.2.1 ICU Problem List Formulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 1.3 Orie ntation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 1.4 Patient admission policy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 1.4.1 Patient Triage: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 1.4.2 Elective admissi ons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 1.4.3 Refusal of patient admission . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 1.4.4 Management of patients in ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 1.5 Patient discharge policy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 1.5.1 Discharge procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 1.5.2 Deaths in the ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 1. 6 Clinical duties in the Intensive Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 1.6.1 General comments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 1.6.2 Patient Admission . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 1.6.3 Doctors Documentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 1.6.4 Daily manage ment issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 1.7 C linical Duties Outside the Intensive Care Unit . . . . . . . . . . . . . . . . . . . . . . 17 1.7.1 Cardiac Arrest Calls . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 1.7.2 Trauma Call . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 1.7.3 Intra-hospital patient transport . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 1.7.4 Out of hospital transfers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 1.8 Infection Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 1.8.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 1.8.2 Hand Hygiene and Standard Precautions . . . . . . . . . . . . . . . . . . . . . 19 1.8.3 Isolation and tr ansmission-based precautions . . . . . . . . . . . . . . . . . . 20 1.8.4 Genera l Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 1.9 Information Technology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 1.10Consent in the Intensive Care Setting . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 1.10.1Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 1.10.2Consent b y relatives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 1.10.3Consent at the Mid Yorks ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 1.11Hospital Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 1.11.1Fire and building emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 2

Contents 2 Clinical Procedures 2.0.3 Restricted procedures Contents 23 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 2.0.2 ICU Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 2.1 Peripheral IV Catheter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 2.2 Arterial Cannulae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 2.3 Central Venou s Cannulae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 5 2.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 2.3.2 Types of catheter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 2.3.3 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 2.3.4 Site . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 2.3.5 Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 2.3.6 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 2.3.7 Documentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 2.3.8 Line Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 2.4 Pulmonar y artery catheterisation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 2.4.1 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 2.4.2 Insertion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 2.4.3 Monitoring PA trace . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 2.4.4 Measureme nt of pressures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 2 .4.5 Measurement of haemodynamics . . . . . . . . . . . . . . . . . . . . . . . . . . 30 2.5 Pleural Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 2.5.1 Pleurocentesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31 2.5.2 IntercostalCatheter / Und erwater Sealed Drain . . . . . . . . . . . . . . . . . . 31 2.6 Endotracheal Int ubation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 2.6.1 Intubation Guideline . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 2.7 Fibre-optic Bronchoscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 2.8 Cricothyroidotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 2.9 Tracheostomy-Percutaneous 2 .9.1 Patient selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 2.9.2 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 2.9.3 Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 2.9.4 Timing of the proced ure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 2.9.5 Proce dure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 2.9.6 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 2.9.7 Post Insertion Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44 2.9.8 Decannulation of the Trachea . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44 2.10Nasojejunal tube inserti on . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 2.11In tra-abdominal pressure manometry . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 3 Drugs and Infusions 3.1 Introduction 47 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 3.1.1 Prescription practice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 3

Contents Contents 3.2 Cardiovascular Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 3.2.1 Inotropes and Vasoactive drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 3.2.2 Assess and correct hypovolaemia . . . . . . . . . . . . . . . . . . . . . . . . . 48 3.2.3 Instituting inotropic thera py . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 3.2.4 Vasopresso rs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 0 3.2.5 Steroid use in patients requiring vasopressors . . . . . . . . . . . . . . . . . . 51 3.3 Anti-hypertensive Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 3.4 Antiarrhythmic Drugs in Critical Care . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 3.4.1 General Principles of Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 3.4.2 Drug T herapy of Bradyarrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . 54 3.4.3 Supraventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 3.4.4 Ventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 3.5 Respiratory Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 3.5.1 Nebulised bronchodilat ors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 3.5.2 Parente ral Therapy in treatment of reversible obstructive airways disease . 59 3.6 Seda tion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 3.6.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 3.6.2 Principles of Sedation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60 3.6.3 Monitoring Sedation : Sedation Scoring . . . . . . . . . . . . . . . . . . . . . . 60 3.6.4 Sedation Holds/ Sedation Assessment . . . . . . . . . . . . . . . . . . . . . . . 61 3.6 .5 Accumulation of Sedatives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62 3.6.6 Sedative Dependence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62 3.6.7 Sleep on the ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63 3.6.8 Non-Pharmacological Methods o f aiding sleep . . . . . . . . . . . . . . . . . . 63 3.6.9 Pharmacological Meth ods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63 3.6.10Managem ent of Delirium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69 3.6.11References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 3.7 Anticoagulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 3.7.1 General Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 3.7.2 Indications fo r the use of warfarin . . . . . . . . . . . . . . . . . . . . . . . . . 73 3.7.3 Indications for the use of heparin . . . . . . . . . . . . . . . . . . . . . . . . . . 74 3.7.4 Prophylactic use of heparin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 3.7.5 Systemic anticoagulation using unfractionated he parin . . . . . . . . . . . . 75 3.7.6 Heparin Induced Thrombocytopaenia . . . . . . . . . . . . . . . . . . . . . . . 75 3.8 Endocrine Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 3.8.1 Insulin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 3.8.2 DDAVP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 3.8.3 Steroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78 3.9 Renal Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 3.9.1 Genera l Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 3.9.2 Diuretics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 3.10Gastro-intestinal drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 3.10.1Prophylaxis of gastric st ress ulceration . . . . . . . . . . . . . . . . . . . . . 80 4

Contents Contents 3.10.2Active GI Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 3.10.3Use of gastro-intestinal pro-kinetic agents . . . . . . . . . . . . . . . . . . . . 84 3.11ICU Antibiotic Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84 3.11.1Prologue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84 3.11.2 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84 3.11.3Principles of prescription . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84 4 Fluids and Electrolytes 85 4.1 Principles of Fluid Management in Intensive Care . . . . . . . . . . . . . . . . . . . . 85 4.1.1 Fluid charting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85 4.1.2 Assessment of uid balance and hydration . . . . . . . . . . . . . . . . . . . . 86 4.1.3 Body Fluid and Electrolyte Phy siology . . . . . . . . . . . . . . . . . . . . . . . 87 4.2 Electrolyte Abnorma lities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 4.2.1 Approach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 4.2.2 Hyponatraemia: Na+ < 130 mmol.L-1 . . . . . . . . . . . . . . . . . . . . . . . 88 4.2.3 Hypernatraemia: Na+ > 145 mmol.L-1 . . . . . . . . . . . . . . . . . . . . . . . 89 4.2.4 Hypokalaemia: K+ < 3.5 mmol.L-1 . . . . . . . . . . . . . . . . . . . . . . . . . 90 4.2.5 Hyperkalaemia: K+ > 5.0 mm olL-1 . . . . . . . . . . . . . . . . . . . . . . . . . 91 4.2.6 Hypophosphataem ia: Serum Phosphate < 0.7 mmol.L-1 . . . . . . . . . . . . 92 4.3 Acid-Base Dist urbances in the ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93 4.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93 4.3.2 General principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94 4.3.3 Metabolic Acidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95 4.3.4 Metabolic Alkalos is . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96 4.3.5 Respiratory Acidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97 4.3.6 Respiratory Alkalosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97 4.4 Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98 4.4.1 Enteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98 4.4.2 Parenteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101 4.5 Blood and Blood Products . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 4.5.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 4.5.2 Blood transfusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 4.5.3 Platelet transfusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 4.5.4 Fresh Frozen Plasma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 4.5.5 Cryoprecipitate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104 4.5.6 DIC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104 4.5.7 Blo od transfusion reaction guidelines . . . . . . . . . . . . . . . . . . . . . . . 105 5 Clinical Management 5.1 Introduction 106 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106 . . . . . . . . . . . 106 5.2 Cardio-Pulmonary Resuscitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106 5.2.1 Key Points in the management plan for an adult collapse 5.2.2 Induced hypothermia following cardiac arrest . . . . . . . . . . . . . . . . . . 107 5

Contents 5.3 Respiratory Therapy Contents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108 5.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108 5.3.2 Respiratory Failure 5.3.3 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109 5.3.4 When Sh ould I Consider Ventilating ( intubating) Patients? . . . . . . . . . . 109 5.3.5 Humidi cation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110 5.3.6 Mechanical Ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110 5.3.7 Ventilator settings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112 5.3.8 Positive Pressure Ventilat ion and Hypotension . . . . . . . . . . . . . . . . . . 115 5.3.9 Supportive The rapies for Severe Hypoxia . . . . . . . . . . . . . . . . . . . . . 115 5.3.10We aning from Mechanical ventilation . . . . . . . . . . . . . . . . . . . . . . . 119 5.3.11Ventilation in the prone position 5.3.13Corticosteroids in ARDS . . . . . . . . . . . . . . . . . . . . . . . . . . 122 5.3.12Non-invasive ventilation (NIPPV) . . . . . . . . . . . . . . . . . . . . . . . . . . 123 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124 5.4 Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124 5.5 Aspects of Renal Failure in Intensive Care . . . . . . . . . . . . . . . . . . . . . . . . . 125 5.5.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125 5.5.2 Aetiology of renal failure in the IC U . . . . . . . . . . . . . . . . . . . . . . . . . 125 5.5.3 Assessment of rena l function in a given patient . . . . . . . . . . . . . . . . . 126 5.5.4 Renal protective strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126 5.5.5 Renal Replacement Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127 5.6 Neurosurgical Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130 5.6.1 Neurotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130 5.6.2 Status Epilepti cus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132 5. 6.3 Subarachnoid haemorrhage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133 5.7 Microbiology Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134 5.7.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134 5.7.2 Glossary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 5.7.3 Screening for sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 5.7.4 Investigation of Pneumonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136 5.7.5 Vascular Catheter Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137 5.7.6 Fungal infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138 5.8 Drug / Tox in Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139 5.8.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139 5.8.2 Admission to ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139 5.8.3 Speci c Overdoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140 5.9 Withdrawal of Treatment in the Intensive Care . . . . . . . . . . . . . . . . . . . . . . 140 5.9.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140 5.9.2 Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140 5.9.3 Deciding not to treat (or treat any further) . . . . . . . . . . . . . . . . . . . . 141 5.10Brain death and org an donation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141 5.10 .1Declaration of brain death . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141 5.10.2Clinical certi cation of brain death . . . . . . . . . . . . . . . . . . . . . . . . . 142 6

Contents 6 Appendices Contents 144 6.1 Haemodynamic Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144 6.1.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144 6.1.2 Diagnosing hypotension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144 6.1.3 Is there any evide nce of shock ? . . . . . . . . . . . . . . . . . . . . . . . . . . 144 6.1.4 Doe s this patient require more uid resuscitation? . . . . . . . . . . . . . . . 145 6.2 The Pulmonary Artery Catheter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146 6.2.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146 6.3 The PiCCO-catheter / monitor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 6.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 47 6.3.2 Estimation of cardiac output . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148 6.4 Principles of ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149 6.4.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149 6.4.2 Ventila tory strategies to provide total ventilatory support . . . . . . . . . . . 150 6 .4.3 Objectives of mechanical ventilation . . . . . . . . . . . . . . . . . . . . . . . . 151 6.4.4 Other Ventilatory strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151 6.4.5 Ventilation Mechanics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152 6.5 The Sedation - Agitation Sc ore . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153 6.6 Classi c ation of anti-arrhythmic drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . 154 6.6.1 Classi cation of Antiarrhythmic Drugs by Their Action . . . . . . . . . . . . . 154 6.7 Guidelines for the use of patient controlled anaesthesia (P CA) . . . . . . . . . . . . 155 6.7.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 6.7.2 Acute Pain Service St andard Orders . . . . . . . . . . . . . . . . . . . . . . . . 155 6.7.3 Programm able Variables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156 6.7.4 Standard Prescriptions for PCA . . . . . . . . . . . . . . . . . . . . . . . . . . . 157 7

Contents Contents Foreword Caring for patients in the intensive care setting is a challenging but potential ly rewarding experience. As we enter the intensive care environment each one of us brings a unique mix of skills and knowledge. Inevitably though we must nd a co mmon ground on which to base our management, without which optimal patient care and safety cannot be achieved. The purpose of this document is not to provide de n itive answers for each problem, nor is it meant to be prescriptive in nature, bu t rather it describes a number of standardised approaches and helpful guidelines to facilitate good patient care. I must acknowledge that this guide has been he avily based on the one produced by the Intensive Care Staff of The Waikato Hospi tal in New Zealand. In particular, my thanks to Dr John Torrance and Dr David Ga mble for their permission to use their manual as a template. All those who acces s, use or disseminate these guidelines do so at your own risk. While you are wor king in this unit, no matter what your level of experience, you will encounter s ituations where you feel uncomfortable, confused or even scared. While this manu al is intended to assist you in caring for your patients, you should not be emba rrassed to seek help from those around you, including the Consultant Intensivist /Anaesthetist and senior nursing staff. You will nd references to articles which are useful further reading. Rajiv Srinivasa 25th June 2008 8

1 ADMINISTRATION Mid Yorkshire Hospitals Intensive Care Units The Mid Yorkshire Hospitals NHS Trust is a 900 bed district general hospital and trauma centre of the West Yorkshire region and serves a population area of 800 000. It is composed of 3 Hospitals: Pinder elds, Pontefract and Dewsbury. The Inte nsive Care Units are located in Pinder elds General Hospital and Dewsbury District Hospital with a total of 14 Level 3 and 8 Level 2 beds and admits over 1200 pat ients a year. There are also 2 Level 3 beds on the Burns unit. Approximately 30% of the admissions are surgical. The remainder are a mixture of trauma, medical and surgical patients. 76% of admissions are ventilated. Our average APACHE II s core is 16 and we have a crude mortality rate of about 24%. The intensive care c onsultant staff also assist in the management of patients in the High Dependency Unit which has 8 beds and admits over 1800 cases per year. The intensive care a lso provides medical and nursing transport teams for inter-hospital transfers. T he ICUs are af liated to the West Yorkshire Critical Care Network. The Intensive C are unit senior medical staff consists of 13 consultants. The junior cover is pr ovided by senior SHOs. We have a nursing staff of about 65 full time equivalents for ICU and 25 for HDU. 1 Administration 1.1 Staf ng 1.1.1 Clinical Lead Dr Rajdeep Singh Sandhu 1.1.2 Consultant Medical Staff Dr Hugh OBeirne Dr Anthony Main Dr Jaqueline Brook Dr Paul Clarke Dr Sameer Bhandari (Burns) Dr Tendai Mbengaranwa (Burns) Dr Jami e Yarwood (Burns) Dr Christine Hildyard Dr Rajiv Srinivasa Dr Anne Thickett Dr J ames Dodman Dr Helen Buglass 9

1.2 Weekly Program 1 ADMINISTRATION 1.1.3 Nursing Staff General Manager (Pain, Anaesthesia, Critical Care, Theatres) - Julie Clark Head of Nursing PACCT Steve Fenn Nursing and Service Manager Crit ical Care Carol Wood Senior Sister/Charge Nurses Suzanne Brompton (Practice Development) Jean Garner Jan Newton (Practice Development) Mick Reynolds Lindsay Shields Jane Womersley 1.1.4 SHOs The junior medical team consists of SHOs (or ST1/2s) who have completed their ICU blocks and are deemed competent in intensive management. They form the resident medical structure. They operate a day/night shift pattern, with the ch ange over occurring at 0800 and 2000 hours (vide infra). Non-intensive Care Trai nees Rotation through the intensive care is made by the following specialty base d training programs: the Acute Care Common Stem for Emergency Medicine and Inten sive Care. There is also provision for a Foundation Year 1 placement (a 4 month rotation). 1.2 Weekly Program 08h00 morning handover (30 minutes) in the Handover Room. 08h30 Consultant led b edside ward round, followed by HDU 16h00 Afternoon ward round and HDU review. (3 0min-1hr) 20h00 Evening hand over between trainees and HDU review All times othe r than that allocated above should involve patient review, not only in response to request by nursing staff, but also in the interests of optimising patient car e and progress. 1.2.1 ICU Problem List Formulation The ICU runs a problem list sheet to help you keep up to date with each patient. It is the responsibility of the night regist rar to review the list for each patient, and to enter new data or patients where appropriate. Towards the end of the night shift a report should be generated 10

1 ADMINISTRATION 1.3 Orientation for each patient, and this is handed to the team following on. The generated doc ument is then led in a folder as evidence of the handover. The process is repeate d for the night handover. 1.3 Orientation Prior to commencing an ICU on call rota, trainees will have to demonstrate compe tence in managing patients on Intensive Care. The training block consists of 2 m onths on ICU as a supernumary. 1.4 Patient admission policy No patient may be accepted into the Intensive Care Unit without the knowledge an d consent of the ICU Consultant or the Consultant Anaesthetist on call (out of h ours). Resuscitation or admission must not be delayed where the presenting condi tion is imminently life threatening unless speci c advance directives exist. In ge neral patients should be admitted to the Intensive Care where it is perceived th ey would bene t in some way as a result. Usually this means patients with actual o r potential organ system failure, which appears reversible with the provision of intensive support measures.

1.4.1 Patient Triage: A critical care Outreach team operates at the PGH and DDH sites between the hours of 0800 and 1800. Their primary function is to assist th e ward nurses in managing and troubleshooting critically ill patients on the war d. They will activate the MEWS pathway if required. The patients at this point a re still under the care of the primary medical team. ICU admission criteria shou ld select patients who are likely to bene t from ICU care. Patients not admitted s hould fall into two categories, too well to bene t and too sick to bene t. De ning substa tial bene t is dif cult, and no pre-admission model exists to predict outcome in a g iven patient. Rather than listing arbitrary objective parameters, patients shoul d be assigned to a prioritization model to determine appropriateness of admissio n. Priority 1: Critically ill patients in need of intensive treatment and monito ring that is not available outside of the ICU. Generally these patients would ha ve no limits placed on their care. Priority 2: Patients that require intensive m onitoring, and may need immediate intervention. No therapeutic limits are genera lly stipulated for these patients. Priority 3: Unstable patients who are critica lly ill but have a reduced likelihood of recovery because of underlying disease or the nature of their acute illness. If these patients are to be treated in ICU /HDU, limits on therapeutic efforts may be set (such as not for intubation). Exa mples include patients with metastatic malignancy complicated by infection. Prio rity 4: These patients are generally not appropriate for ICU admission as their disease is terminal or irreversible with imminent death (e.g. CVA). Included in this group would be 11

1.5 Patient discharge policy 1 ADMINISTRATION those patients not expected to bene t from ICU based on the low risk of the interv ention that could not be administered in a non-ICU setting (e.g.: haemodynamical ly stable DKA, or an awake patient following an overdose). This category of patien ts also present a conundrum and often are the subjects of passionate debates bet ween the referring physician and Intensivist as to what may reasonably be achiev ed on the ICU. 1.4.2 Elective admissions Where possible, elective surgical admissions should be booked at least 48hrs in advance. A book exists into which the names of prospec tive patients must be entered, following discussion with the surgical team and a naesthetist responsible for that patient. Con rmation of bed availability is the r esponsibility of the anaesthetist and surgeon, and must be con rmed by prior to co mmencing the anaesthetic on the morning of surgery. Beds will be ring-fenced onl y in exceptional circumstances. No elective surgical patient will be admitted in to the last bed scenario. 1.4.3 Refusal of patient admission When an outside team contacts the ICU with re gard a patient, it is imperative that you clarify whether this is a referral or a courtesy call. If it is a referral, then the patient should be assessed (at th e bedside if possible), and the problem discussed with the Consultant Anaestheti st/Intensivist at the earliest opportunity. Where a patient is reviewed but not admitted to the Intensive Care Unit, the pertinent ndings and reason for refusal must be clearly communicated to the referring team and documented in the notes. Where appropriate a directive regarding future review must be noted, and the man aging team encouraged to de ne resuscitation status. This directive holds for pati ents placed in the HDU following ICU referral. 1.4.4 Management of patients in ICU Patients in Intensive Care Unit are managed primarily by the ICU staff. Visiting Teams should be discouraged from charting d rugs, uids or other treatment directly. However, the opinion of all Specialists i nvolved in the case is valued. The Consultant Intensivist must be kept fully inf ormed of their opinion. 1.5 Patient discharge policy 1.5.1 Discharge procedure All discharges must be approved by the Consultant Anae sthetist/Intensivist. The parent team must accept care of the patient, this acce ptance must be recognised at the medical level, either through the SHO/Registrar , or in some cases to the Consultant directly. 12

1 ADMINISTRATION 1.5 Patient discharge policy All other teams involved should be advised, including the pain team, dietician, special pharmacy requirements (e.g.. TPN). A careful plan for the immediate disc harge period must be discussed with the accepting team, and be clearly documente d in the notes including: Limitation of treatment where appropriate Non-return o rders Clear medical management plan, including charting of the following for the next 24hrs: Fluids Feeding Analgesia Documentation to be completed prior to dis charge: Entry in the ICU database - this also allows printing of the discharge n ote. The database is designed in MS Access, and resides on the Desktop of the 2 computer terminals in the ICU nurses station. Nurses will not send patients to t he ward without rst checking with the on call SHO. 1.5.2 Deaths in the ICU Withdrawal of therapy is a Consultant-only decision. The Consultant Intensivist must be noti ed as soon as the patient has been examined a nd certi ed dead, unless other speci c arrangements exist (eg. where death is the ex pected outcome and the issue of a death certi cate issue has been discussed). The ICU SHO must ensure: A death certi cate has been completed or arranged (please spe ak to the General Of ce regarding this) The parent team is noti ed Referring colleag ues (including GPs) are noti ed Post-mortem consent has been acquired from the fami ly (if indicated) If appropriate, an End of Life Care Pathway must be completed and the process documented in the patients notes. If relevant and appropriate, in itiate discussions with the Transplant Coordinator (via switchboard at St James U niversity Hospitals - 70020) The Coroner must be noti ed as below: Every death tha t appears to have been without known cause, as a result of suicide, or unnatural or violent death. Every death in respect of which no doctor has given (or is pr epared to give) a death certi cate. Every death that occurs while the person conce rned was undergoing a medical , surgical or dental procedure, or some similar op eration or procedure. 13

1.6 Clinical duties in the Intensive Care 1 ADMINISTRATION Death that appears to have been a result of any such operation or procedure. Dea th that occurred while the person was affected by an anaesthetic or that appears to have been a result of the administration to the person of an anaesthetic. De ath of any patient detained in an institution pursuant to an order. Death of any patient committed in a hospital under the Mental Health Act. The death of any i nmate within the meaning of the Penal Institutions Act of 1954 The death of any person in police custody, or in the custody of a security of cer. Where a death is referred to the coroner, no death certi cate may be issued by the ICU doctor. 1.6 Clinical duties in the Intensive Care 1.6.1 General comments Staff will always shoulder a major part of the burden of continuity. Continuity is central to quality patient care and this expectation i s not diminished with a decrease in working hours. The responsibility for mainta ining continuity and for effective communication both with other unit staff and with outside teams rests largely with the SHOs. Effective communication is a basi c medico-legal requirement. There are guidelines covering the medical procedures and the administration of most of the drugs used in the ICU. These guidelines a re under constant review. The resident staff are required to be familiar with th ese guidelines and to consult them when required. In addition, any inconsistenci es or discrepancies within them should be brought to the attention of the consul tant staff. When asked by a team to review a patient, SHOs are required to obtain a full history from the patient and the patient notes, to perform a comprehensi ve examination of the patient and to formulate a differential diagnosis. They sh ould then have an outline of a suggested investigation and treatment plan, to be presented to the Consultant Anaesthetist/Intensivist. The nal plan should be cle arly documented in the patient record. It is important that there is a complete transfer of information at the handover between shifts. This will be facilitated by Comprehensive admission notes. Completion of a standardised daily update not e. Daily review of all clinical laboratory tests, microbiology and radiological tests. An update of the problem list by the night on call SHO. This will contain details of the presentation, the provisional diagnosis, investigations, consult s and opinions and unresolved issues that require follow up. The on call doctor should brie y familiarise themselves with the patients before the formal ward roun ds. When leaving the unit for whatever reason, all doctors must inform their col leagues, or if out of hours, the Charge Nurse. The ICU must never be left unatte nded unless in extraordinary 14

1 ADMINISTRATION 1.6 Clinical duties in the Intensive Care circumstances and with the permission of the Consultant, and the knowledge of th e Nurse in charge. 1.6.2 Patient Admission 1.6.2.1 Primary patient survey A: Ensure patient protect ing airway / GCS / cognition (is the patient receiving supplementary oxygen?) B: Breathing pattern acceptable, Pulse Oximetry acceptable C: Patient cardiovascul arly stable, venous access acceptable Obtain hand over information from the refe rring doctor 1.6.2.2 Secondary survey Examine patient thoroughly Notify Consultant Intensivist if this has not already been done. Document essential orders: Ventilation Sedation, analgesia, drugs an d infusions Fluid therapy Discuss management with nursing staff and team: Everyo ne must be aware of the plan! Basic monitoring and procedures: ECG Invasive / no n-invasive monitoring Urinary catheter / NG tube Basic Investigations (usually a full blood count, coagulation pro le, ICU speci c electrolyte pro le) Advanced Invest igations; CT, ultrasound Case note documentation (see below) Inform and counsel relatives in general terms 1.6.3 Doctors Documentation Doctors are responsible for documenting an admission note for all patients and a daily entry into the clinical notes as well as: Disc harge summary (includes database entry) Death certi cate 15

1.6 Clinical duties in the Intensive Care 1 ADMINISTRATION Admission Note: a pro forma sheet should be used, documentation must include: Da te / time Name/bleep of admitting doctor Reason for admission: primary and secon dary Standard medical history including current medications Thorough examination ndings Results of important investigations Assessment / severity / differential diagnosis Management plan Document noti cation of parent team and duty senior. Par ent teams should be encouraged to write a short note (at least!) when they visit the Unit. 1.6.3.1 Daily entry in clinical notes Use the Daily Notes pro forma page. Ensure each page is dated and labelled with the patients name and hospital number. Dat e / time / name of Senior ICU Doctor conducting the round. A: Mental state, GCS, airway. B: Ventilation, saturation (or PaO2 ), chest ndings. C: Pulse / BP / per ipheral perfusion / Precordial exam. Abdominal examination and description of fe eding mode. Peripheries Assessment or Impression Plan Additional notation must be made in the notes when: Invasive procedures are unde rtaken: please use the stickers when inserting central/arterial lines. Important management decisions are made. Signi cant interaction is made with patient family . 1.6.4 Daily management issues The daily handover ward round at 0800 is attended by the night on-call doctor, the incoming day staff, the Consultant or senior An aesthetist, Consultant Microbiologist and the Charge Nurse (if not too busy). Th e night doctor responsible will present a concise report of every patient. It is the responsibility of the night registrar to review the list for each patient, and to enter new data or patients 16

1 ADMINISTRATION 1.7 Clinical Duties Outside the Intensive Care Unit where appropriate. Towards the end of the night shift a report should be generat ed for each patient, and this is handed to the team following on. The generated document is then led in a folder as evidence of the handover. The process is repe ated for the night handover. Important decisions regarding patient discharge and specialist investigations may be made at this meeting and it is important that junior staff have a good understanding of the patient status, including: Patient details and demographics Day of admission Diagnosis and major problems Relevant pre-morbid problems Progress and signi cant events Important results Plan for the next 24 hours 1.7 Clinical Duties Outside the Intensive Care Unit 1.7.1 Cardiac Arrest Calls 1.7.1.1 Indications Cardiac arrest calls may be calle d for the following: In-hospital cardiac arrest Collapse of unknown origin in th e hospital environs Out of hospital arrest arriving in the A&E The anaesthetic i nput for cardiac arrests is nominally the Acutes on call team. However, if the A cutes team is otherwise occupied, the ICU doctor may attend provided the patient s on ICU are stable, and only after informing the Charge Nurse. 1.7.1.2 CPR (Car dio Pulmonary Resuscitation) We encourage the use of the UK Resuscitation Counci l Guidelines for CPR http://www.resus.org.uk/pages/als.pdf. The anaesthetist is responsible for securing the airway and establishing effective ventilation, whil st the Medical team should concern themselves with cardiac and general aspects. It would be expected however that directing advanced life support be the respons ibility of the most senior doctor present. Where CPR has been successful but furth er active treatment may not be in the interests of the patient, the decision to withdraw care must only made following consultation with senior doctors involved - this will usually be the Anaesthetic and Specialty Consultants. All involveme nt in an arrest call must be documented in the patient case notes. 1.7.2 Trauma Call Again, the rst responder for trauma calls is usually a member of the Acutes on call team. However, should that team be busy, or in the event of a poly traum a, the ICU doctor may be 17

1.8 Infection Control 1 ADMINISTRATION called upon to assist. Ensure that the ICU Charge Nurse and Consultant Intensivi st are aware of where you are going, and communicate with the ICU team once the patient has been assessed and the likely admission destination known. 1.7.3 Intra-hospital patient transport No patient may be transported from the un it without the direction of the Senior Anaesthetist/Intensivist on ICU or on cal l. Medical escort is the rule if the patient is Level 2 or 3. In a minority of c ircumstances a nurse escort may be suf cient, providing it is acceptable to the Se nior Anaesthetist and the Charge Nurse. It may not be appropriate for all ICU do ctors to undertake prolonged transport, or transport to unfamiliar areas. Always ask the senior Anaesthetist if you are unsure. Prior to embarking on an escort all equipment, oxygen supply and emergency drugs must be checked. All problems e ncountered on the escort must be recorded in the notes, and an incident form com pleted if appropriate. If a test is deemed urgent the medical escort should ende avour to get an informal report written in the notes, failing which they should request formal review and noti cation to the unit as soon as possible. 1.7.4 Out of hospital transfers Should a patient require Level 3 care in the abs ence of bed availability, the transfer process must be initiated by the parent t eam with assistance from the ICU team. The rst point of contact must be the West Yorkshire Critical Care Network Bed Bureau. The doctor who accompanies the patie nt must be competent to transfer the ventilated patient, and to manage a comprom ised airway during transfer. The doctor must also have attended a Transfer Train ing course. Transfer of a Level 2 patient is fraught with danger. It may be safe r to intubate/ventilate prior to transfer, especially if there is respiratory co mpromise. Discuss with the Consultant Anaesthetist/Intensivists at both ends (i. e. Mid Yorks and the receiving ICU/HDU). 1.8 Infection Control 1.8.1 Introduction Patients requiring intensive care are highly susceptible to i nfection due to immunosuppressive effects of drugs and disease, the use of invas ive monitoring techniques and the severity of the underlying illness requiring a dmission. The use of broad-spectrum antibiotics may predispose to infection with resistant organisms. 18

1 ADMINISTRATION 1.8 Infection Control Nosocomial infection delays patient discharge from the intensive care unit (ICU) and contributes signi cantly to morbidity. The prevalence of hospital-acquired (n osocomial) infection in the ICU can be considerably higher than other clinical a reas of the hospital. Signi cant risk factors for infection include: mechanical ve ntilation prolonged length of stay trauma or burns intravascular catheterisation urinary catheterisation prior antibiotic use The four most common nosocomial in fections seen in ICU are: Pneumonia urinary tract intra-vascular catheter-relate d bacteraemia surgical wound infection All ICU staff are responsible for ensurin g good infection control policies are adhered to, in particular good hand hygien e practice. In keeping with Trust Infection Control policies, you are required t o ensure you are bare below the elbows, and to hand wash with alcohol gel before a nd after every patient contact. Skin preparation for invasive procedures (CVP ca theters, VasCath, ICD tracheostomy) must be with the pre lled 2% chlorhexidine/alc ohol swabs. Please ensure you adopt suitable barrier protection (gowns, masks, g loves). 1.8.2 Hand Hygiene and Standard Precautions Hand washing and hand disinfection r emain the most important measures in the prevention of cross infection. Hands sh ould be washed before and after contact with every patient and after manipulatio n of the patient environment, especially after contact with a patients with C. d if cile infection or if the hands are soiled. Either use a 15-second handwash with soap and water, or alternatively the waterless hand gel may be used if hands ar e not visibly soiled. A longer handwash with antibacterial soap is required prio r to any major invasive procedures such as insertion of central venous catheter. In addition to hand hygiene standard precautions are used for all patients: Wea r gloves for all contact with blood and body uids including dressings and wounds. Gloves must be changed and discarded between patients. Hands must be decontamin ated after the removal of gloves. Wear a disposable plastic apron or uid-resistan t gown to protect the skin and clothing for procedures likely to generate splash or cause soiling. Wear a mask and eye protection to protect mucous membranes of the eyes, nose and mouth during procedures likely to generate splash or cause s oiling. 19

1.8 Infection Control 1 ADMINISTRATION Ensure patient-care equipment is cleaned and disinfected appropriately between p atient use. Staff who generate a sharp product (e.g.: needle or blade) are respo nsible for its safe disposal into an approved puncture resistant sharps containe r. 1.8.3 Isolation and transmission-based precautions In addition to standard preca utions, isolation and appropriate transmission-based precautions are to be used with the following: Multi-resistant organisms (MRO) Patients infected or colonised with the following MROs require isolation and contact precautions (gloves and gown/apron for direct pati ent care): Methicillin Resistant Staph. Aureus (MRSA) Vancomycin Resistant Enter ococcus (VRE) Extended Spectrum Beta Lactamase (ESBL) producing enterobacters Mu lti-resistant gram negative organisms Meningococcal disease - proven or suspected Patients require isolation and dropl et precautions (surgical mask within 1 meter of the patient) until 24hrs of comp leted antibiotic treatment. Miscellaneous Burns patients require isolation and contact precautions Febrile n eutropaenic patients require isolation and contact precautions High risk immunos uppressed patients require isolation and contact precautions Respiratory syncyti al virus require contact precautions 1.8.4 General Measures The ICU should be kept tidy and uncluttered. Equipment no t in use should be stored in a clean area. Movement of people through the unit s hould be kept to a minimum. This applies equally to colleagues and relatives. Al l visitors are to be encouraged to wash their hands before and after visiting th e patient. Staff with communicable diseases should take sick leave. If suffering from D&V, ensure at least 48 hours have elapsed since the last symptom before r eturning to work.use 20

1 ADMINISTRATION 1.9 Information Technology 1.9 Information Technology There are numerous terminals in the intensive care unit. All computers are netwo rked to the Intranet, which also functions as a gateway to the Internet. The com puters are logged in as a generic ICU-user, with permissions to view Pathology r esults. The intranet allows access to all inpatients in the hospital. The ward a dministrator section allows you to view the pathology results of patients on the ICU and HDU. All imaging is now lm-less, and may only be viewed on the computer terminals. You should have completed a tutorial, and received a smartcard follow ing this in order to view the images. You will be given a separate login by the IT department. This allows you access to your own account. You will have an e-ma il address with access to the Outlook mail program via a link on the Intranet fr ont page. The local area network provides access to the Internet. This is contro lled and closely monitored by the IT department. Access to the Internet requires personal login, and all websites visited may be monitored. Please ensure you cl ose the browser window when you have nished. This prevents fraudulent and unautho rised access to websites in your name. 1.10 Consent in the Intensive Care Setting 1.10.1 Introduction A competent patient may give or withhold consent for any med ical treatment. Unfortunately, patients in ICU often cannot have their competenc y established with certainty. When a patient cannot give consent in an emergency , in the absence of convincing evidence to the contrary (e.g. presence of a pers on with enduring power of attorney who can categorically state that the person d oes not wish to receive the treatment in question, or applicable advance directi ve) consent to treatment is implied. 1.10.2 Consent by relatives Relatives or friends cannot give or withhold consent for the performance of a medical treatment. However, it is strongly recommended the treating doctor takes the families views into account in deciding whether t o perform a particular treatment. 1.10.3 Consent at the Mid Yorks ICU The consent form and the attendant process c an record the attempt to take the families views into account. In any case, comp letion of the appropriate form is necessary to comply with hospital policy in ce rtain procedures. A written record of informed consent is unnecessary for the va st majority of bedside procedures in ICU. 21

1.11 Hospital Emergencies 1 ADMINISTRATION When it is necessary to obtain consent for a particular procedure to be performe d on an ICU patient, it is appropriate for ICU medical staff to play a role in t his process. That role may not necessarily mean obtaining consent directly, but may mean ensuring that the staff performing a procedure make the requisite infor mation available to the ICU doctor to enable them to get consent, or in many cas es obtain consent themselves. 1.11 Hospital Emergencies Mass casualty Communications or utility failure Cardiac Arrest Earthquake Fire ( or smoke smell) Hazardous substance spill Personal safety threat Threat from tel ephone, letter or suspicious object Bomb or arson Radiation spill Dialling 4444 and thereby contacting the switchboard will in most circumstances allow you to i nitiate an emergency response that is appropriate to the threat. 1.11.1 Fire and building emergencies Attend formal re training sessions Become fa miliar with location of re exits Assess medical condition of persons in an emerge ncy area, and the likely effects of evacuation on them. Follow instructions of t rained accredited staff. 22

2 CLINICAL PROCEDURES 2 Clinical Procedures Introduction It is inevitable that during your stay in the Intensive Care Unit y ou will be exposed to a number of procedures with which you are not familiar. Al l staff are encouraged to become pro cient with routine procedures: 2.0.2 ICU Procedures Endotracheal intubation Peripheral venous catheterisation C entral venous catheterisation Arterial cannulation / PiCCO insertion Pulmonary a rtery catheterisation Urinary catheterisation Lumbar puncture Intercostal drain insertion or pleurocentesis Naso-gastric / jejunal tube insertion Patient consen t should be obtained if appropriate as outlined elsewhere in these guidelines. N o member of staff is permitted to attempt a procedure without adequate training. Staff with previous experience must af rm this with the Senior Anaesthetist or Co nsultant Intensivist prior to attempting unsupervised procedures. All junior sta ff should be supervised for their rst 2 arterial cannulations and at least 5 cent ral venous access procedures prior to performing these procedures unsupervised. No matter how experienced you are, repeated unsuccessful vascular punctures are unacceptable and a more experienced member of staff should be asked to help. All procedures must be annotated in the case notes, including the indication / comp lications for the procedures. 2.0.3 Restricted procedures Specialised procedures should only be performed by t he Senior Anaesthetist or Consultant Intensivist. They may not be attempted prio r to discussion with the Consultant. Percutaneous tracheostomy Fibreoptic bronch oscopy 2.1 Peripheral IV Catheter 2.1.0.1 Indications 23

2.2 Arterial Cannulae 2 CLINICAL PROCEDURES Initial IVI access for resuscitation Stable or convalescent patients where more invasive access is not warranted. 2.1.0.2 Management All lines placed in situations where aseptic technique was not followed must be removed (eg. Placement by emergency staff at the roadside). Periph eral lines must be removed after 72 hours (or before, if not required), and repl aced if there is a continuing need for peripheral IV access. Acceptable aseptic technique must be followed including: Thorough hand-washing Skin preparation wit h alcohol swab Occlusive but transparent dressing All lines should be removed if not being actively used, or if > 2 days old. An exception may be made where ven ous access is challenging (eg. IV drug abusers). 2.1.0.3 Complications Infection Thrombosis Extravasation 2.2 Arterial Cannulae 2.2.0.4 Indications Invasive measurement of systemic blood pressure in ICU or du ring patient transport / retrieval. Multiple blood gas sampling and laboratory a nalysis 2.2.0.5 Site and catheter choice 1st choice: Radial artery 2nd choice: Femoral. Site of choice for PiCCO catheter monitoring (Pulsiocath 5F 16 cm catheter) is g enerally the femoral artery. The axillary artery may be considered after consult ation with the Consultant (usually 4F catheter). The Brachial artery is an end-a rtery, and catheterisation has been considered a risk for distal arterial compli cation (although this has also been disputed). It may be used if there are no al ternatives. 24

2 CLINICAL PROCEDURES 2.3 Central Venous Cannulae 2.2.0.6 Technique All catheters should be inserted with full sterile technique ( gown, sterile gloves, topical antiseptic) The arterial line must be rmly anchored (suturing is not recommended) The insertion site and all connectors must be vis ible through the applied dressing. 2.2.0.7 Complications Infection Thrombosis Di gital Ischaemia Vessel trauma and stula formation. NB: Interpretation of arterial waveforms requires familiarity with normal arterial waveforms as well as trace damping, ampli cation and arterial harmonics. If you are unsure as to the reliabil ity of a trace / reading you must seek assistance before removing the arterial c annula. 2.3 Central Venous Cannulae 2.3.1 Introduction The use of CVCs is associated with adverse effects both hazar dous to patients and expensive to treat. More than 15% of patients with CVCs hav e some complication from them: Mechanical 5-19% Infectious 5-26%use Thrombotic 2 -26% The rst 5 CVC insertions performed by the trainee should be performed under direct supervision and then (if the competency is signed off) the trainee may in sert the lines without supervision, on the understanding that when a dif cult cath eterisation is anticipated, they will ask for senior assistance. Failure to inse rt the catheter after 3 attempts, should prompt the clinician to seek help rathe r than continue to attempt the procedure, as the incidence of mechanical complic ations after three or more insertion attempts is six times the rate after one at tempt. 2.3.2 Types of catheter 2.3.2.1 Anti-microbial-Impregnated Catheters Thes e catheters have been shown to lower the rate of catheter-related bloodstream infections. Consider the use of n Anti-microbial-Impregnated CVC for adult patients who require shortterm (1-3 eeks) CVC and who are at high risk for catheter-related blood stream infection CR-BSI) It may be appropriate to use this type of CVP in selected patients, ie hose with neutropaenic sepsis. 25 a w ( t

2.3 Central Venous Cannulae 2 CLINICAL PROCEDURES 2.3.2.2 Single-lumen and Multi-lumen catheters The number of lumina does not dir ectly affect the rate of catheter-related complications, so the choice of either single- or multilumen catheter should be dictated by clinical need. 2.3.3 Indications 2.3.3.1 Monitoring haemodynamic variables Fluid administration (particularly if large volumes of uids or blood products are required) Infusions of TPN Inotropes Hypertonic solutions Irritant solutions Chemotherapy Potassium solutions For haemo ltration or haemodia ltration 2.3.4 Site Subclavian Internal Jugular Femoral Internal jugular catheterisation can be dif cult in morbidly obese patients, although with ultrasound may be made e asier. Subclavian venous catheterisation should be avoided in patients with seve re hypoxaemia, as the risks and complications of pneumothorax and haemothorax ar e greater than with internal jugular approach. Femoral catheterisation should be avoided in patients with grossly contaminated inguinal regions, as the risk of development of catheter-related infections is increased. If central venous acces s is needed rapidly in the shocked patient, the femoral approach may be the fast est technique and used for the initial resuscitation. 2.3.5 Technique Asepsis Full scrub Sterile gown Sterile gloves 26

2 CLINICAL PROCEDURES Large sterile drape Skin decontamination Alcoholic chlorhexi dine gluconate for skin Allow to dry before cannulation Use Seldinger technique to access vein 2.3 Central Venous Cannulae NICE guidance on use of ultrasound for placing CVCs 1.1 Two-dimensional (2-D) im aging ultrasound guidance is recommended as the preferred method for insertion o f central venous catheters (CVCs) into the internal jugular vein (IJV) in adults and children in elective situations. 1.2 The use of two-dimensional (2-D) imagi ng ultrasound guidance should be considered in most clinical circumstances where CVC insertion is necessary either electively or in an emergency situation. 1.3 It is recommended that all those involved in placing CVCs using two dimensional (2-D) imaging ultrasound guidance should undertake appropriate training to achie ve competence. 1.4 Audio-guided Doppler ultrasound guidance is not recommended f or CVC insertion. Flush all parts of catheter with heplock prior to insertion Trendelenburg tilt f or internal jugular or subclavian routes Use blade to ensure insertion site on s kin will allow passage of dilator and catheter Insert catheter to estimated appr opriate depth, according to insertion site and patient anatomy Aspirate from eac h port. Easy aspiration of blood should be possible from each line, and then ush each line with heplock, and the the catheter ports must then be closed with caps . Secure the catheter to the skin by suturing the holder on the catheter to the skin (not the clip for adjusting the catheter position) Apply a sterile semi-per meable polyurethane dressing to the catheter insertion site eg Tegaderm. If the insertion site is bleeding or oozing, a sterile gauze dressing may be used. Ches t X-Ray when the catheter is secure, to look for pneumothorax and assess cathete r tip position 2.3.6 Complications At Insertion 27

2.3 Central Venous Cannulae Arterial puncture Pneumothorax Neural injury Guidewire i nduced arrhythmia Air embolus 2 CLINICAL PROCEDURES During catheter presence Infection Thrombosis Embolism Pulmonary infarct or PA r upture (with PAF catheter) Arterio-venous stula 2.3.6.1 Mechanical complications the commonest Arterial puncture, haematoma and pneumothorax are Frequency of mechanical complications, according to approach : Internal Jugular Arterial Punture Haematoma Haemothorax Pneumothorax Total 6.3-9.4% <0.1-2.2% NA <0.1-0.2% 6.3-11.8% Subclavian 3.1-4.9% 1.2-2.1% 0.4-0.6% 1.5-3.1% 6.2-10.7% Fem oral 9-15% 3.8-4.4% NA NA 12.8-19.4% 2.3.6.2 Infectious complications approach. The available evidence is that subclavian catheterisation is less likely to result in catheter-related infection than use of the inte rnal jugular or femoral Data from a systematic review of complications of CVS ha s shown the rate of bloodstream infections may be as high as 8.6% with jugular a ccess, and 4.0% with subclavian access. 2.3.6.3 Thrombotic complications The risk of catheter-related thrombosis varies according to site of catheter. Approximate gures are: 21% of patients with femora l catheters 2% of patients with subclavian venous catheters 8% of patients with internal jugular The clinical importance of catheter-related thrombosis remains unde ned, although all thromboses have the potential to embolize. 28

2 CLINICAL PROCEDURES 2.4 Pulmonary artery catheterisation 2.3.7 Documentation Documentation of the procedure undertaken should appear in t he patient case notes using a procedure sticker. ALL complications or dif culties encountered, should be documented beneath the sticker. 2.3.8 Line Management Routine line replacement is not necessary The practice of changing the central line over a guidewire should be avoided unless it is the on ly option Lines should be removed as soon as a clinical indication no longer exi sts if patient shows signs of unexplained systemic infection if insertion site a ppears infected or blood cultures suggest infection with a skin organism (eg sta ph epidermidis). The catheter-tip should be sent to microbiology for culture and sensitivities If suspecting catheter-related bloodstream infection, a wound swa b should be taken from the catheter insertion site, and blood should cultured fr om the suspect line and from a sample taken from a peripheral stab. References 1. NICE Technology Appraisal Guidance No.49, ultrasound locating devi ces for placing central venous catheters - September 2002. Moved to static list of guidance November 2005 follo wing period of consultation. 2. Guidelines for the prevention of intravascular catheter-related infections. C enters for Disease Control and Prevention. MMWR 2002;51(NoRR-10):1-33 3. Preventing Complications of Central Venous Catheterization. McGee DC, Gould M K The New England Journal of Medicine. 2003 Vol 348:1123-1133 4. National Evidence-based guidelines for preventing healthcare associated infec tions in NHS hospitals in England. London. Richard Wells Research Centre, Thames Valley University, 2006 epic2. 5. Complications of central venous catheters: Internal jugular versus subclavian access A systematic review. Ruesch S, Walder B, Tramer M. Critical Care Medicine 30(2):454-460, Febr uary 2002 2.4 Pulmonary artery catheterisation The PA Catheter is not a resuscitation tool and should only be inserted in a con trolled environment after discussion with the senior Anaesthetist. Dwindling use of the PA catheter has resulted in a loss of familiarity with its use. Junior m edical staff and nursing staff not familiar with this instrument should not mani pulate / advance / in ate the PA catheter balloon. 29

2.5 Pleural Procedures 2 CLINICAL PROCEDURES 2.4.1 Indications Haemodynamic measurement: (cardiac output, stroke volume, syst emic vascular resistance) Measurement of right heart pressures (pulmonary hypert ension, pulmonary embolus) Estimation of preload to the left ventricle - controv ersial. 2.4.2 Insertion PA Catheter insertion is technically dif cult and requires a worki ng knowledge of right heart pressures and waveforms. They should only be inserte d by accredited staff. See appendix on pulmonary artery catheterisation 2.4.3 Monitoring PA trace An adequate tracing should be visible on the monitor a t all times. A damped tracing may represent a wedged catheter, clot at the cathe ter tip or inappropriate equipment set-up (wrong monitor calibration, faulty pre ssure transducer). Flush the distal lumen generously (using closed mechanism) Wi thdraw catheter until a trace is present. NB: Never withdraw the catheter with a n in ated ballon. 2.4.4 Measurement of pressures Pressure should be referenced to the mid-axillary line The true wedge pressure is measured at end-expiration PEEP may in uence wedg e pressures, however this is not a factor at PEEP < 10 mmHg, and patients should not be disconnected from the ventilator to measure PAC pressures. 2.4.5 Measurement of haemodynamics Cardiac output measurement should only be att empted by staff familiar with the use of PA Catheters. 10 ml 5% dextrose at room temperature is rapidly injected into the appropriate lumen. This is usually rep eated three times, with results varying > 10% from average discarded. 2.5 Pleural Procedures As with all invasive procedures this should not be attempted by inexperienced st aff. 30

2 CLINICAL PROCEDURES 2.5 Pleural Procedures Indications for accessing pleural space Pneumothorax ( temporising procedure if u nder tension) Haemothorax Symptomatic or infected pleural effusion Needle Thoracostomy for Tension Pneumothorax 16G cannula placed in mid clavicula r line, 2nd intercostal space Proceed to formal intercostal drain insertion. 2.5.1 Pleurocentesis 2.5.1.1 Indications Diagnostic procedure: Exudate vs Transu date, or to exclude infected collection or malignancy. Therapeutic procedure: Dr ainage of an infected collection requires an underwater sealed drain. It is not appropriate to perform one-off drainage. The practice of draining non-infected ple ural collections by pleurocentesis is controversial and should not be performed without direction by the senior Anaesthetist. 2.5.1.2 Technique Local anaesthesia and sterile technique. Unless the uid collect ion is grossly detectable on clinical examination and on plain radiology, pleuro centesis should be ultrasound directed. Investigation of pleurocentesis uid Aspirated uid should , at the very least, be s ubmitted for pH or analysed in ICU blood gas analyser (pH < 7.20 = empyema, 7.20 -7.25 = equivocal) 2.5.2 IntercostalCatheter / Underwater Sealed Drain 2.5.2.1 Insertion Local Anae sthesia is mandatory in awake patients, and should be used in sedated patients S trict aseptic technique 28F catheter inserted into 3-4th intercostal space, midaxillary line, using blunt dissection as described and recommended in the ATLS g uidelines. The Catheter must be guided through the ribs without use of sharp ins truments (preferably nger). Trochar aided insertion techniques are not acceptable . 31

2.6 Endotracheal Intubation 2 CLINICAL PROCEDURES 2.5.2.2 Maintenance possible. Drains placed in un-sterile environs should be removed as soon as Drains should remain in-situ until radiological resolution has occurred and ther e is no further bubbling or drainage of signi cance ( < 150 ml.24-hr ) In patients at risk (due previous large air leak, or multiple rib fractures) who remain on positive pressure ventilation, the drain may be clamped for 4hrs prior to remova l as a safety measure, although this is by no means universally practiced. Drain s placed electively in theatre are the responsibility of the surgeon 2.5.2.3 Complications Incorrect placement Pulmonary laceration Pneumothorax Blee ding as a result traumatic drain insertion (intercostal or, lateral thoracic art ery, lung etc) Microbial innocculation 2.6 Endotracheal Intubation 2.6.0.4 Introduction have a dif cult airway. All staff should familiarise themselv es with the intubation trolley and equipment. Whenever possible make sure that y ou have capable and trained staff to assist you. If you are alone or inexperienc ed always call for assistance. If the senior anaesthetist cannot be reached for some reason, or is detained, then assistance should be sought from an anaestheti c colleague. Rapid sequence induction is the rule in ICU patients unless previou sly discussed with senior medical staff. Endotracheal intubation in ICU patients is a high risk but vital emergency procedure in patients who often have limited reserve, are dif cult to positi on and may 2.6.0.5 Indications Institution of mechanical ventilation To maintain an airway Upper airway obstruction or threat Control of arterial carbon dioxide content (e g. in the setting of traumatic brain injury) Patient transportation To protect a n airway Patients at risk of aspiration 32

2 CLINICAL PROCEDURES Altered conscious state Tracheal toilet 2.6 Endotracheal Intubation 2.6.0.6 Techniques Orotracheal intubation is the rule. Blind nasal awake intubat ion, or breoptic awake intubation, may be indicated in selected patients with cer vical spine injury, limited mouth opening or oro-facial surgery / trauma. These techniques should only be undertaken by staff with current experience of these t echniques, and only after discussion with and the presence of the Consultant Int ensivist. 2.6.0.7 Standard endotracheal tube choice All patients in the Intensive Care Unit should be intubated with a low pressure high volume PVC tube (eg Portex blue line oral/ nasal tube) 2.6.0.8 Non-standard tubes Patients returning from theatre (or transported from another centre) may have a different ET tube (eg. armoured ETT) in situ. Where there is no good reason for this to remain it should be changed to the standard ETT if it is anticipated that the patient will require intubation > 48 hrs, and would not be exposed to signi cant risk during the ETT change. 2.6.1 Intubation Guideline 2.6.1.1 Personnel Skilled assistance is mandatory, wh ere possible a team of 4 is required. Intubator who controls and co-ordinates the procedure. Drug administration A person to apply in-line traction where the stabil ity of the cervical spine is unclear. Cricoid Pressure: Cricoid pressure is recomm ended in all emergency situations and should be applied at the commencement of i nduction. Cricoid pressure may distort the larynx so that intubation is made mor e dif cult. It should be modi ed at the discretion of the intubator, and requires an understanding of the procedure. 2.6.1.2 Preparation Secure adequate IVI access Check all equipment prior to intu bation: Adequate lighting Selection of oropharyngeal airways Working suction wit h Yankauer attachment AMBU bag assembly and appropriate mask 100% oxygen with ow capability > 15 l/min 33

2.6 Endotracheal Intubation 2 CLINICAL PROCEDURES 2 working laryngoscopes with appropriate choice of blade Magill forceps Malleabl e introducer and gum-elastic bougie 2 ETT: estimated patient size and one smalle r size. (Female = 7-8 mm, Male = 8-9 mm) A selection of laryngeal masks Emergenc y cricothyrotomy kit: (#15 scalpel and 6.0mm cuffed ETT) Ensure adequate monitor ing Pulse oximetry Reliable blood pressure monitoring (eg. invasive if necessary ) ECG telemetery Dif cult intubationKit trolley. This contains: An intubating LMA A dif cult intubation kit can be found on the side of the intubation McCoy laryngoscopes Light wands Emergency cricothyrotomy kit Jet ventilation sys tem 2.6.1.3 Drugs Induction agent eg. Thiopentone, Fentanyl, Ketamine, Midazolam Muscle relaxant Suxamethonium 1-2 mg/kg Consider Rocuronium 1-2 mg/kg if Suxemet honium contra-indicated ie: Burns patients > 48 hrs post injury Spinal injury pa tients where spasticity is present Chronic neuromuscular disease (Myasthenia Gra vis, GBS) Hyperkalaemic states Miscellaneous Atropine 0.6-1.2 mg Adrenaline 10 ml of 1:10 000 solution. Metaram inol 0.5 mg/ml (usually in 10 ml) 34

2 CLINICAL PROCEDURES 2.6 Endotracheal Intubation 2.6.1.4 Procedure: Rapid sequence induction and orotracheal intubation Pre-oxyge nate for 3-4 minutes with 100% oxygen. Patients receiving non-invasive ventilati on should continue on this form of ventilation until the point of induction, and a PEEP valve applied to the AMBU-bag mask assembly. Administer induction agent and suxamethonium Apply cricoid pressure Intubation under direct visualisation I n ate ETT cuff until there is no air leak during ventilation Con rm ETT placement wi th capnograph and chest auscultation with manual ventilation. Release cricoid pr essure Secure ETT at correct length (Female = 19-21cm at incisors, Males = 21-23 cm at incisors) Do not cut ETT at less than 26 cm (if at all). Connect patient to ventilator Ensure adequate sedation and analgesia to cover period of muscle r elaxant and continue as indicated by clinical scenario. Insert naso-/-orogastric tube or naso-jejunal tube if not already present. A follow-up CXR should be per formed as soon as convenient. 2.6.1.5 Maintenance of endotracheal tubes Tapes ETT are generally secured with white tape. Tapes are changed daily or PRN by nursing staff. In certain circumstances person alised ETT security may be required. Cuff integrity Suf cient air should be placed into the cuff to prevent an air leak, as assessed by auscultating over the trachea. ETT manometry is not routinely required, and m ay be misleading as the correlation with mucosal pressure is unreliable. Persistent cuff leakage cuff should be reviewed for: Any ETT that constantly requires additional air instilled into the Herniation above the cords Cuff damage (rare) Malfunctioning pilot tube valve (w hich can be excluded by placing distal pilot tube into container of water and ob serving for bubbling) 35

2.6 Endotracheal Intubation 2 CLINICAL PROCEDURES Airway suctioning Airway suction may be performed every 2-3 hrs prn Routine suctioning should be avoided where: it requires disconnection of PEEP (o pen suction system) may exacerbate the patients condition (asthma, reactive Intr a-cranial pressure, orid pulmonary oedema). 2.6.1.6 Endotracheal tube change Equipment and assistance sive and promote atelectasis. The procedure / setup is the same as for intubation de novo Ensure patient is adequately oxygenated (Saturation 98-100%). An FiO2 of 1.0 may be excesEnsure adequate anaesthesia and muscle relaxation Procedure Perform direct laryngoscopy: If a good view of the larynx and vocal cords is obtained then proceed to manual exchange of ETT with application of cricoid pressure, or proceed as below using gum-elastic bougie. If direct laryngoscopy reveals abnormal or swollen anatomy, or only partial view of anatomy, then proceed as follows: Place gum elastic or v entilating bougie through the ETT and insert to a length corresponding to a few cm distal to the end of the ETT. With an assistant stabilising the bougie, and a pplying cricoid pressure, remove faulty ETT under direct laryngoscopy, while mai ntaining bougie in the same position. Con rm the bougie is still in place through cords once ETT removed, and then replace new ETT over the top of the bougie appa ratus. If the ETT does not progress smoothly through the cords, rotate 90 deg an ti-clockwise and attempt again (ie. realign beveled edge of ETT along upper bord er of bougie) Check position of ETT and secure as for de novo intubation procedu re. 2.6.1.7 Extubation guideline for intubation Ensure adequate assistance, monitoring and equipment as Extubation should generally not be performed overnight, or when the responsibili ty to reintubate might fall on a less experienced staff member. Patients may be extubated if this action is part of an established care plan or algorithm (eg. c ardiothoracic), or at the direction of the duty specialist. No patient should be extubated without medical staff being aware and available to assist. 36

2 CLINICAL PROCEDURES 2.7 Fibre-optic Bronchoscopy Patient Selection For a more extensive description see section on mechanical ventilation The patient must be awake enough to maintain their own airway. Any threat to air way patency as a result of surgery or injury may require consultation with the c o-managing team (ENT/Plastic surgery/MaxFac) prior to extubation. Patient should demonstrate adequate pulmonary reserve. There are a number of ways of assessing pulmonary reserve although none is perfect: Resp rate < 30 FVC > 15 ml.kg-1 Pa0 2 / FiO2 ratio > 200 Resp rate / tidal volume 1 min after disconnection from ven tilator (use T-piece ) The last method has the best predictive value. All patien ts should receive supplemental oxygen post extubation. 2.7 Fibre-optic Bronchoscopy Policy Only to be performed by adequately trained staff, after authorisation by the Consultant Intensivist. 2.7.0.8 Indications Persistent lobar collapse that is refractory to normal bronc hial toilet Foreign body in airway Diagnostic broncho-alveolar lavage (BAL): Thi s is not routinely performed to diagnose nosocomial infection, but may be employ ed in selected circumstances. Fibre-optic intubation 2.8 Cricothyroidotomy Policy The recommended procedure for urgent surgical airway access (not percutan eous tracheostomy). When urgent surgical airway is required, call for help then proceed without delay. 2.8.0.9 Indications Failed intubation drill Inability to maintain an airway desp ite basic manoeuvres. 2.8.0.10 Equipment is described below. Purpose made kits exist in the unit using direct access and/or a seldinger technique. In the event of these not being available, the simplest technique # 15 scalpel and handle 37

2.9 Tracheostomy-Percutaneous 2 CLINICAL PROCEDURES Size 6.0 cuffed ETT Oxygen delivery circuit and ventilation device (eg. Laerdal bag) 2.8.0.11 Procedure Palpate cricothyroid membrane Perform 2cm horizontal incision through skin and cricothyroid membrane Insert blade handle into wound and turn vertically to enlarge wound (do not use blade or sharp instrument such as a pair of scissors) Insert ETT into trachea Connect oxygen circuit Con rm correct placem ent with end-tidal CO2, auscultation, and if possible CXR. Perform tracheal toil et as soon as adequate oxygenation achieved Arrange de nitive surgical airway as s oon as possible. 2.9 Tracheostomy-Percutaneous Tracheostomy is a very common procedure in critical care. Its history is quite a ncient and although the percutaneous route is a relatively new procedure, it is by far the commoner means of performing tracheostomy in the critical care settin g. 2.9.1 Patient selection Patients on whom tracheostomy is being considered should have a reasonable likelihood of survival and have a reversible condition. The b ene ts of performing the procedure and subsequent critical care management must ou tweigh the risks. It is not good practice to perform this treatment in a patient whose demise is inevitable. Policy Percutaneous tracheostomy is the preferred method for elective tracheostomy in s uitable critically ill patients. The decision to perform percutaneous tracheostomy rests with the Consultant Intensivist. Consent should be obtained if appropriate as outlined in the unit guidelines. Percutaneous tracheostomies may only be per formed by experienced specialist staff. 2.9.2 Indications as for surgical tracheostomy Airway maintenance: Prolonged int ubation ( > 10 days), or anticipation thereof Prolonged upper airway obstruction 38

2 CLINICAL PROCEDURES Laryngeal pathology Subglottic stenosis Airway protection De layed return of glottic re exes Tracheal toilet / ineffective cough mechanism 2.9 Tracheostomy-Percutaneous 2.9.2.1 Bene ts over prolonged transtracheal intubation (> 7 days) less use of sed ative drugs and inotropes better communication patients able to eat and drink re duced time on invasive ventilation reduced length of stay facilitates physiother apy 2.9.3 Contraindications General unacceptable cardiovascular instability unaccept able risk of inducing hypoxaemia during the procedure: i.e. PEEP > 10 cmH2 O, pe ak airway pressures > 25 cmH2 O, Fi O2 > 0.5 with borderline blood gases coagulo pathies: platelets < 50 109 , INR > 1.5, APTT > 1.5x local infection Elevated or unstable measured intra-cranial pressure Renal failure with uncorrected uraemic state high likelihood of dif cult intubation/ventilation (should the need arise d uring the procedure) lack of personnel or equipment Local altered anatomy in the region of the trachea fat neck bony cervical pathol ogy causing inadequate access previous tracheostomy prominent vessels overlying the trachea on ultrasound imaging short cricosternal distance Previous neck surg ery Unstable cervical spine injury 39

2.9 Tracheostomy-Percutaneous 2 CLINICAL PROCEDURES 2.9.4 Timing of the procedure Once the indications are met and all contraindicat ions are excluded, the patient must be assessed clinically. One must consider wh ether the procedure would jeopardise the patients safety, and test the likelihood of weaning. If the patient characteristics exhibit features of being able to we an, it would be reasonable to allow the patient the bene t of the procedure and at tempt to wean, with an emphasis on safety and doing no harm. Such factors may in clude Clinical examination: crackles/wheeze, sputum production Respiratory: Fi O 2 , Paw , PEEP, respiratory rate, SpO2 , ABG, CXR Cardiovascular: stability, ino tropic requirement, myocardial injury Metabolic: acid-base status, uid balance, u remia Neurological: sedation requirements, mental state when conscious, effectiv eness of cough, muscular strength Nutritional state If these parameters are sati sfactory, a further assessment is made following a short period of minimally ass isted ventilation (PSV 8 cmH2 O, PEEP 5 cmH2 O, Fi O2 < 0.4) when minimally seda tion. This may give an indication of likelihood of weaning and extubation. If th e patient fails this assessment on three consecutive days after 5 days of ventil ation (or 3 days after re-intubation), a tracheostomy may be considered. This ap proach allows for a more consistent and effective decision making process regard ing the need for tracheostomy. The TracMan study considering the bene t of early v s late tracheostomy is in progress. A further meta-analysis concluded demonstrat ed that early tracheostomy led to decreased period of ventilation, length of sta y on ICU, and overall hospital stay. 2.9.5 Procedure The patient is not consente d, unless consent was obtained before the patient was anaesthetised or intubated , or is awake and able to comprehend and understand the procedure and its implic ations. However, it is good practice to inform the relatives of the patient of t he indications, bene ts and risks of the procedure. Percutaneous tracheostomy is c ommonly performed using two experienced operators Anaesthetist / endoscopist: Re sponsible for administering a suitable anaesthetic and managing the airway. Surg eon-operator Monitoring and drugs are as for standard endotracheal intubation, w ith the recommended addition of the breoptic bronchoscope. Adequate lighting esse ntial An ultrasound imaging of the neck is performed to identify any prominent v essels, thyroid mass, or displaced trachea. The patient is ventilated on 100% ox ygen utilising a pressure controlled ventilation mode. 40

2 CLINICAL PROCEDURES 2.9 Tracheostomy-Percutaneous 2.9.5.1 Equipment A Cook Ciagliakit using a blue rhino dilatational technique or the Ohmeda UltraPerckit are standard. Tracheostomy tubes: The Portex blue line tracheos tomy tube is the standard tube used in this unit. All tubes inserted must have a n inner cannula available as part of the kit or as an add-on. The usual size ins erted is a acuffed 8.0mm ID Portex BlueLinetube. All equipment necessary for resu scitation should available and at hand - this includes ET tubes, functioning lar yngoscopes (McCoy), syringes, bougie, suction. No patient should leave the ICU w ithout the inner cannula being placed prior to discharge 2.9.5.2 Education and training SpRs and selected advanced trainees will be invited to learn how to perform percutaneous tracheostomies. This will involve hands-on tra ining with a skilled operator scrubbing alongside the trainee. 2.9.5.3 Airway management Endoscopic con rmation of surgical technique is not practiced universally, but it is a useful adjunct to correct placement. Method 1 Place the breoptic bronchoscope in the trachea beyond the distal tip of the ETT. Under direct laryngoscopy retract the ETT (with de ated cuff) so that the cuff is above the vocal cords and in ate the cuff with 10-15 ml of air. Use an as sistant to secure tube in place and apply slight downward force on the ETT to ma intain a seal to ventilate the patient. Retract bronchoscope to a point proximal to planned tracheal puncture. Method 2 Place the breoptic bronchoscope in the trachea beyond the distal tip of the ETT Withdraw the ETT 2-3 cm with the cuff de ated, then rein ate cuff. Request t he surgeon-operator apply digital pressure over intended tracheal puncture site, and con rm this is distal to ETT tip and bronchoscope. Beware ETT puncture or bro nchoscope damage. Observe correct placement of needle-guidewire by Seldinger tec hnique, and sequential dilatation. Once tracheal tube in situ, connect to ventil ator and insert bronchoscope into tracheostomy. Con rm tip of tracheostomy clear o f carina, and absence of ongoing haemorrhage. 2.9.5.4 Tracheostomy insertion technique Position patient: 30 deg head up, with neck in extension but supported. 41

2.9 Tracheostomy-Percutaneous 2 CLINICAL PROCEDURES Both the anaesthetist and the operator don adequate protection (mask, goggles) t o guard against splashes/spraying of biological uids. The anaesthetist suctions t he oral cavity and the endotracheal tube. The anaesthetist then ensures the pati ent is monitored for anaesthesia (BP, ECG, SpO2 , ETCO2 as a minimum), and all e quipment necessary for resuscitation is available and at hand. Anaesthesia is ad ministered utilising a propofol/alfentanil infusion. Adopt strict aseptic techni que In ltrate with 10 ml of 1% lignocaine / 1:100 000 adrenaline over the pre-trac heal rings Check trachy cuff, lubricate and insert dilator into trachy tube maki ng sure there is a good t. Perform a 1-2cm horizontal incision over the 2nd trach eal ring. Dissect bluntly to fascia. Insert sheathed needle catheter in to trach ea at midline. Con rm placement by aspirating air and con rming with endoscopist. Re move needle, and feed guidewire through sheath. Remove sheath and dilate with mi ni-dilator. Place white dilator -guide over sheath. Proceed to dilatation with rh ino (to appropriate size according to desired size tracheostomy) Remove dilator a nd use guidewire to insert dilator and tracheostomy into the trachea. Remove dil ator and wire, in ate cuff. Correct placement of the tube is con rmed by bronchoscop y capnography chest wall inspection and auscultation Once it is con rmed the tube is in place, the oral endotracheal tube is withdrawn. Secure with tapes. Perform a control CXR. 2.9.6 Complications The overall early and late complication rate is between 4% a nd 30%, which compares favourably with surgical tracheostomy (6-50%). Before dec annulation, the main complications are infection and bleeding. Surgical tracheos tomies have 2-3 times the rates as percutaneous. Post decannulation, airway sten osis predominates, and it is dif cult to compare between the two procedures. Death Death directly due to tracheostomy is low ( 0.4%). Overall survival to decannula tion is in the order of 50%. 42

2 CLINICAL PROCEDURES 2.9 Tracheostomy-Percutaneous Bleeding Up to 6% bleed problematically leading to technical dif culty or airway soiling. It usually arises from large super cial vessels encountered during dissection, or on needling the trachea. Tamponade by the tracheostomy tube usually controls the bleeding in the vast majority of cases. Infection Stomal infection can occur in up to 4% in the percutaneous group and 2 9% in the surgical group. It can result in sternal osteomyelitis or mediastiniti s. Granulation tissue deposits These occur anyway between the stoma and where the tube abuts the tracheal tissues. Occult granulomas may manifest themselves in bleedin g during decannulation, or causing obstruction in a fenestrated tube when phonat ion is attempted. Paratracheal misplacement This is avoided by using intraoperative tracheoscopy. Pneumothorax Rates of up to 2% have been suggested. It may be due to needle injury to the pleura, malposition followed by positive pressure ventilation, or guide wire damage to the small airways if the J-tip is not used. Subcutaneous emphysema This is usually due to tracheal injury caused by multiple attempts to needle the trachea, or laceration of the posterior wall of the trac hea. Rarely, it may be associated with a pneumothorax. Tracheal cannula displacement suspected in the presence of high airway pressures subcutaneous emphysema This is said to occur in less than 1% of cases and may be an inability to suction the trachea an audible speech with an intact in ated cuff A track between skin and tracheostomy hole takes about 7-10 days to become estab lished. Changing the tube during this period increases the likelihood of displac ement. A bougie or airway exchange catheter must be used in these circumstances. Tracheo-oesophageal stula This is a rare complication associated with pulmonary i nfection due to recurrent aspirations, a high level of tracheal secretions, high cuff in ation pressures and an ongoing air leak from the breathing system. 43

2.9 Tracheostomy-Percutaneous 2 CLINICAL PROCEDURES Tracheo-innominate stula This is another rare but immediately lethal complication associated with low placement of the tracheostomy. One option is for the trache ostomy tube to be replaced by a translaryngeal tube with the cuff below the stula . The other is to extend the tracheostomy wound down to the sternal notch and di gitally compress the artery against the mediastinum. Tracheocutaneous stula Prolonged dependence on the tracheostomy or recurrent stomal infection and granulation allows epithelialisation of the track. Airway injury Tracheal stenosis occurs in up to 26% of percutaneous tracheostomy (60% following surgical tracheostomy). However, only 2% of these are severe enough (> 75% occlusion of the lumen) to cause symptoms. Symptoms usually occur after 2-12 weeks post decannulation, and are non-speci c such as cough, dyspnoea, stridor, a nd failure to clear secretions. Transtracheal tubes are more likely to be associ ated with subglottic lesions, and tracheostomy tubes with tracheal lesions. The lesions occur at the stoma, cuff site, or the cannula tip. Obliquely placed tube s, or those just below the cricoid are associated with stenosis. Cuff related st enosis is not as prevalent now that high volume low pressure cuffs are the norm. 2.9.7 Post Insertion Management The tracheal cannula is secured by tapes to prev ent dislodgement. Cuff pressures must be monitored to help prevent tracheal muco sal damage or stenosis. The stoma must not be subject to weight loading from the breathing system. The lumen must be kept clean by regular debridement of the in ner tubes and the use of warmed humidi ed oxygen. Changing the tube is variable, a nd is dependent on clinical, patient and tube factors - but is best avoided befo re 10 days post procedure. Nasogastric feeding is commenced early and is only st opped if there is evidence of gross aspiration. Oral intake is facilitated when the patient is more alert, has a good cough re ex, and the cuff de ated to help with coordination of swallowing. 2.9.8 Decannulation of the Trachea The patient should be well into the recovery phase of their illness. They must have an effective cough capable of expectorati on into the mouth past the de ated cuff, and have intact upper airway re exes. Facto rs that indicate a sustainable work of breathing include 44

2 CLINICAL PROCEDURES normal respiratory rate Fi O2 0.4 yielding acceptable SpO2 o r blood gases 2.10 Nasojejunal tube insertion clinically acceptable breathing pattern The patient should have minimal CPAP ( 5 cmH2 O) requirements with the cuff in ated or be on a high ow circuit with the cuf f de ated and maintained at this level without resort to positive pressure ventila tion or increasing CPAP for at least 48-72 hours. Following decannulation, the p atient must be observed for an appropriate period of time on the HDU before tran sfer to the wards. Supplemental oxygen may be required during this period. Some patients may be discharged to the ward with the tracheostomy tube in-situ. This requires a careful consideration of the ability of the receiving ward to adequat ely and appropriately care for the patient with a tracheostomy tube. The parent Consultant and the Nurse in charge on the ward must be made aware and agree to t he transfer (as with all patients). 2.10 Nasojejunal tube insertion 2.10.0.1 Indications Instillation of feed into the jejunum is an effective way o f feeding patients with: Prolonged gastric stasis ( > 3 days) Gastric stasis res istant to treatment with pro-kinetic agents (erythromycin, metoclopramide) Pancr eatitis or other scenario?s where feeding distal to the duodenum is desired. 2.10.0.2 Procedure Position the patient Rt side down to at least 45o , Remove an y gastric tube. Use a Bengmark 10 Fr tube 140 cm long with stylet. Close tube si deport and attach 3 way tap to ow through stylet hub. Measure out Xiphisternum to ear plus ear to nose distance from the tip of the tube. Insert tube to this dis tance, con rm intragastric placement by auscultation during air injection. Adminis ter 200 mg of erythromycin or 10-20 mg of metoclopramide as slow IVI bolus. In ate the stomach with 500 ml of air while the prokinetic is being administered. Gent ly advance the tube. You should feel a steady resistance. If there is increasing then sudden loss of resistance this means you have thrown the tube into a loop in the stomach. Withdraw the tube until resistance is felt and start slowly adva ncing the tube again. Insert the tube to the 120-125 cm mark if possible. Try to aspirate uid from the tube. If uid can be aspirated check the pH with a urine dip stick. An alkaline pH suggests duodenal or further insertion (may be a false pos itive if the patient is on PPIs). Position the patient at again and order an upper abdomen-lower chest x-ray. Just before x-ray exposure inject 10 mls of contrast (Gastroview) down the tube. 45

2.11 Intra-abdominal pressure manometry 2 CLINICAL PROCEDURES Check tube position on x-ray. If the tube is in a satisfactory position a gastri c tube can now be inserted to decompress the stomach if this is desired. Remembe r to leave the stylet in any ne bore tube during manipulation of the nasogastric tube. Keep the stylet in a plastic bag at the head of the bed so it can be reins erted into the oesophageal and gastric segment of the ne bore tube during procedu res such as NG tube or ET tube removal to stiffen the ne tube and prevent its acc idental partial removal. 2.10.0.3 Complications Endobronchial placement Other ectopic placement Migration ., Kinking or Knotting 2.11 Intra-abdominal pressure manometry Policy Renal perfusion pressure may be compromised by raised intra-abdominal pre ssure following: Surgery Trauma Intra-abdominal pathology (eg: pancreatitis) The occur rence of acute renal failure in an intensive care patient signi cantly increases t he risk of adverse outcome. The measurement of intra-abdominal pressures in pati ents that are at risk of developing abdominal compartment syndrome may allow ren al salvage in patients where there is a remedial cause. A measured pressure of > 20 mmHg (referenced to the symphysis pubis) may precipitate acute abdominal com partment syndrome and renal failure. 2.11.0.4 Procedure Connect a 100ml bag of saline to a ?metriset? which is then c onnected to a manometer. A 20G needle is then attached to the manometer tubing. Place patient supine Empty bladder Clamp indwelling catheter distal to the cultu re aspiration point. Clean aspiration point with an alcohol swab and insert 20G needle (prepared as above). Inject 100 ml warmed sterile saline into patients bla dder. Open stopcock to transducer and allow 30 seconds to equilibrate. Once pres sure measurement completed, remove 20G needle from aspiration point, unclamp uri nary catheter and allow free drainage of the bladder. 46

3 DRUGS AND INFUSIONS 2.11.0.5 Complications Instillation of bacteria into the bladder Triggering auto nomic dysfunction (NB vagal) on injecting into the bladder, particularly if the bladder is incompletely drained. Patient discomfort (if awake) Arti cially elevate d readings due to bladder spasm or local pelvic haemorrhage may precipitate inte rventions that are associated with signi cant morbidity. 3 Drugs and Infusions 3.1 Introduction Most patients admitted to the ICU will have had medications prescribed for concu rrent or premorbid conditions. A new ICU drug chart must be started on each pati ents arrival in ICU. Re-charting of all drugs implies an active review of the app ropriateness of drug administration and dosage, in changing clinical conditions. It is important that drug charts are accurate, legal and legible. Use of drug t rade names is not acceptable practice. Similarly only drugs which are approved b y the ICU medical staff may be given to ICU patients. For this reason only ICU m edical staff may write (prescribe) in the patients drug chart while the patient i s in the ICU. Charting of drugs by outside teams must be discouraged. On dischar ge to the ward it is the responsibility of the discharging medical person to rev iew patient drug and uid orders. 3.1.1 Prescription practice In general the following principles should be consid ered when prescribing any drugs for ICU patients. A drug should only be institut ed where the potential bene t is well described, or the risk for adverse effects l ow when bene t is unproven. Unit protocols and guidelines should be used where the se exist for a given drug. ICU patients often have vastly altered drug pharmacok inetics (what the body does to the drug) and pharmacodynamics (what the drug doe s to the body). Where therapeutic drug monitoring is available this should be un dertaken with the assistance of the Pharmacist. Good drug prescribing practice i s mandatory, including: Legible hand writing, use of generic (not trade) names f or drugs, clear delineation of dose, frequency and duration of treatment. Extens ive guidelines for drugs commonly used in critically ill patients are available within the ICU and in the BNF. 47

3.2 Cardiovascular Drugs 3 DRUGS AND INFUSIONS 3.2 Cardiovascular Drugs 3.2.1 Inotropes and Vasoactive drugs Inotropes & Vasopressors are commonly presc ribed drugs on Critical Care areas. These drugs include Norepinephrine, Dobutami ne, Dopexamine & Vasopressin. Epinephrine is a drug of resuscitation & should on ly be instituted by infusion in exceptional circumstances. Epinephrine is known to cause lactic acidosis, and may increase oxygen demand to a greater extent tha n dobutamine for a given increase in cardiac output. All patients should be adeq uately uid resuscitated before starting vasoactive drugs. Hypotension should be e stablished : Absolute: Systolic Blood Pressure < 90 mmHg Relative: Systolic 30% < normal for that patient. Consideration should be taken into end organ hypo-per fusion: Renal: urine output < 0.5ml/Kg/hr Cerebral: cognitive state Peripheries: unreliable in septic patients Several methods of cardiac output monitoring are available (pulmonary artery otation catheter - PAFC, oesophageal Doppler, LidCo), and should be used if there is any doubt as to the pathophysiology. However, PA FCs have not been shown to improve patient outcome and are associated with signi ca nt morbidity. They should therefore only be inserted on the advice of a senior A naesthetist, preferably an Intensivist. 3.2.2 Assess and correct hypovolaemia This simple concept is in practice very di f cult to perform accurately. In the ICU there are a number of ways to assess intr avascular volume status although each has shortcomings. Clinical assessment of ui d status including JVP Variation of arterial waveform characteristics with venti latory cycle. Measurement of CVP. Right heart catheterisation. Calculation of in trathoracic blood volume and extrapolation to extravascular lung water using the PiCCO meter. Echocardiographic techniques. Except in very clear-cut cases (ie g ross uid overload or cardiac failure), in a situation where there is doubt as to the patients uid status a trial of uid administration should be considered. 3.2.3 Instituting inotropic therapy Only once the above steps have been consider ed should inotrope therapy be considered. 48

3 DRUGS AND INFUSIONS 3.2 Cardiovascular Drugs No single inotrope (or mixture of inotropes) has been shown to be superior to an other. Please consult appendix on haemodynamic principles. 3.2.3.1 Short notes on using common agents Dopamine / adrenaline / noradrenaline : For ease of application many claim these three agents have a -adrenergic action in low dose and a progressive -effect in increasing doses. Each however has a ch aracteristic feature worth noting: Dopamine in low doses (2.5 g.kg-1 .min-1 ) has a direct diuretic effect which may result in increased urine volume, there is n o evidence of a renal sparing or protective effect. In fact, there is evidence t hat it may be harmful to patients. Adrenaline is a useful /-gonist, however it do es have signi cant 2 -effect which may result in unwanted metabolic effects (hyper glycaemia, excess lactate production unrelated to organ perfusion). Noradrenalin e is generally held to have a predominant -effect and is therefore useful as a in otrope-vasopressor, particularly in septic shock. Dobutamine a synthetic inotrop e, does not have signi cant -effects (may have some myocardial -effect) and is there fore useful in increasing heart rate and stroke volume, but may cause a paradoxi cal fall in blood pressure due to peripheral -drenergic activity. Dopexamine act s via DA1 receptors, and is used at a low dose to promote splanchnic perfusion. Adrenaline and noradrenaline infusions should be started at 0.1 g.kg-1 .min-1 and titrated to response. Infusions of these agents require 3-5 minutes to achieve steady state. Changes in rate more frequently than every 3-5 minutes (unless in an emergency) should be discouraged as it may lead to a roller-coaster effect. 3.2.3.2 Inotropes Inotropes increase myocardial contractility, and mediate their effect through cardiac 1 -receptors. This leads to both an enhanced force of contraction, toget her with a variable increase in heart rate. As a consequence, they have variable effects on myocardial oxygen demand. They alter peripheral vascular tone & regi onal blood ow to a varying degree ( 2 -mediated). This should be taken into accoun t when considering which drug to use. There is marked inter-individual variation in response to a chosen inotrope, due to: Qualitative & quantitative changes in adrenergic receptor kinetics in both acute illness (sepsis) & chronic condition s (heart failure) Underlying variability in disease state (cardiogenic shock, se psis, hypovolaemia) 3.2.3.3 Dobutamine This is a synthetic derivative of Dopamine. It is a very pote nt 1 - & 2 -agonist, providing direct inotropic action, together with systemic v asodilatation & afterload reduction. 49

3.2 Cardiovascular Drugs 3 DRUGS AND INFUSIONS 3.2.3.4 Dopexamine This is also a synthetic derivative of Dopamine. It is a very potent 2 -agonist, and a rather weak 1 -agonist. It improves splanchnic perfusion and a lso promotes a diuresis. It is not thought to alter outcome in renal failure, bu t the diuresis may be bene cial. 3.2.3.5 Phosphodiesterase inhibitors (Milrinone and Amrinone) Phosphodiesterase inhibitors increase cAMP by non-adrenergic mechanisms. They are not therefore af fected by down-regulation of adrenoreceptors as occurs in sepsis or heart failur e. For this reason milrinone is the drug of choice for refractory (ie following adequate volume resuscitation) low cardiac output states. They result in: Increa sed myocardial contractility Systemic and pulmonary vasodilatation (often requir es co-administration of a vasopressor / noradrenaline) Improved diastolic relaxa tion (useful in patients with diastolic heart failure) Notes on pharmacology of milrinone These drugs usually require a loading dose on commencement which may predispose to additional hypotension by virtue of vasodi latation. The relatively long half-life of these agents requires forethought bef ore administration, as their action is not easily reversed, and titration of inf usions to effect cannot be effected rapidly. Phosphodiesterase inhibitors use is extremely infrequent in this Unit, which re ects the unconvincing evidence for it s use in sepsis. 3.2.4 Vasopressors 3.2.4.1 General Principles These agents are used primarily to induce vasoconstriction & thus elevate blood pressure They may increase cardiac afterload and thus cardiac wall stress These agents should not be used to treat hypotension due to hypovolaemia Vasopressors should be used with extreme cautio n in patients with a suspected low cardiac output state, as they may have a detr imental effect. In cases of doubt, senior advice should be sought or adjuncts to monitoring should be used. 3.2.4.2 Norepinephrine is the vasopressor of choice in critical care. Indirectly acting agents (phenylephrine, metaraminol) should generally be restricted to peri-opera tive practice where temporary vasodilatation results from speci c intervention (ge neral or regional anaesthesia). It exerts its vasopressor action by the 1 -recept or, and also exhibits 1 -agonist activity. Its peripheral action is to induce int ense vasoconstriction in the splanchnic & pulmonary visceral beds. This may oppo se its inotropic effect in a dose dependent fashion. 50

3 DRUGS AND INFUSIONS 3.2 Cardiovascular Drugs Consideration should be taken as to the effects on the splanchnic, renal & perip heral circulations at higher doses. 3.2.4.3 Vasopressin (Argipressin) may be indicated (after discussion with an Intensivist) where hypotension is refractory to norepinephrine. In early septic shock, endoge nous levels of vasopressin are (appropriately) high. In established septic shock levels fall, the reasons for which are unclear. Replacement therapy may therefo re reduce, or even abolish the need for inotrope & vasopressors. Vasopressin enh ances the sensitivity of vessels to catecholamines. High doses may induce angina , hypertension and water intoxication. It has variable effects on renal vessels and urine output. 3.2.5 Steroid use in patients requiring vasopressors In patients with severe sep sis, & hypotension refractory to high doses of vasopressors, the coadministratio n of physiological doses of intravenous steroid is potentially bene cial. However, the Sepsis Guidelines published in March 2008 now recommend that steroids be in stituted only if the patient is unresponsive to inotropes (taken to mean increas ing requirement for inotropes and/or noradrenaline rate 0.5g.kg-1 .min-1 ). Hydroc ortisone is prescribed at 50mg four times daily. It is not necessary to taper th e dose prior to discontinuation. Agent Dobutamine Dopexamine Norepinephrine Vasopressin Standard Infusion 250 mg / 50 ml 5% Dextrose 50 mg / 50 ml 5% Dextrose 8 mg / 100 ml 5% Dextrose 2 0 Units /50 ml 5% Dextrose Dose 5-20 g.kg-1 .min-1 2-3 g.kg-1 .min-1 0.02-1.0 g.kg-1 .min-1 1-6 ml.hr-1 Norepinephrine should be infused through a central line. Dobutamine, Dopexamine & Argipressin may be infused peripherally in some circumstances, although a CVP should be in situ to allow assessment of lling. References 1. Sladen RN. Inotropic agents. Chapter 17.1.19 In: Oxford Textbook o f Critical Care. 2. Delinger RP, Carlet JM, Masur h, Gerlach H et al. Surviving Sepsis Guidelines, Crit Care Med 2004; 32: 858-873 3. Holmes CL, Patel BM, Russe ll JA, et al. Chest 2001; 120 (3) 989-1001. Physiology of Vasopressin relevant t o septic shock 4. Tsuneyoni I, Yamada H et al. Critical Care Medicine 2001; 29 ( 3) 487-93. Haemodynamic and Metabolic effects of low dose vasopressin infusions in vasodilatory septic shock 51

3.3 Anti-hypertensive Agents 3 DRUGS AND INFUSIONS Table 1: Inotropic agents commonly used in ICU Agent Standard Infusion Indications CPR Cardiogenic Shock Adrenaline 10 mg in 100mls 5% Dex Acute severe asthma Anaphylaxis (correct hypovolemia!) Medical pacing Septic Shock (1st line inotrope) 4mg in 100mls 5% Dex (single Noradrenaline strength) Conditions where mixed / effect required with predominant effect 50mg in 50 mls 0. 9% NaCl, run Dopexamine at 2.4 mls.hr-1 Promote splanchnic perfusion Pure adrenergic agent used in low CO/high SVR state s Dobutamine 250mg in 100mls 5% Dex Effect diminished in sepsis and CCF (down regulation of receptors Loading dose: 12.5-50g.kg-1 over 20 min Infusion: 10mg in 50 mls 5% Cardiogenic s hock due to diastolic failure Pulm hypertension Rescue following catecholamine i nduced downregulation of receptors The drugs may accumulate in renal failure Milrinone Dex, infuse @ 0.375-0.75 g.kg-1 .min-1 (8-15 mls.hr-1 in 70kg patient) 3.3 Anti-hypertensive Agents 3.3.0.1 General Principles Elevated blood pressure should be viewed in the conte xt of each patient, and should include an appraisal of pre-morbid blood pressure. Acut e hypertension in the intensive care should not elicit direct treatment, but rat her a review of the cause of blood pressure elevation. Elevated blood pressure i s commonly seen in patients who are agitated, delirious, or who have some other

cause for overt sympathetic drive. This should be addressed with analgesia and s edation where appropriate. A dual purpose drug such as an 2 -agonist (clonidine) may be useful. Neurogenic Hypertension in the setting of intra-cranial pathology m ay be self limiting. No attempt should be made to actively lower elevated blood pressure with anti-hypertensive agents unless the intra-cranial pressure is bein g monitored, and cerebral perfusion pressure is not threatened. Vasodilators par ticularly may increase intra-cranial pressures further while dropping cerebral p erfusion pressure to dangerous levels. 52

3 DRUGS AND INFUSIONS 3.4 Antiarrhythmic Drugs in Critical Care 3.3.0.2 Indications Acute Peri-operative control of hypertension post-cardiac, c arotid or other vascular surgery, or for patients with critical myocardial ischa emia. In this instance target blood pressures should be discussed with the surge on involved, and con rmed with the Consultant Intensivist Accelerated hypertension : Malignant Hypertension Hypertensive Proteinuric Pregnancy states (Eclampsia) Act ive Phaeochromocytoma (NB: always preceed -lockde with alpha blocker. Non-hyper tensive indications Reduction of afterload in cardiac ischaemia and failure Decr ease P / t in patients with aortic dissection 3.3.0.3 Complications Hypotension Tachyphylaxis (GTN - consider rescue therapy wit h N-acetylcysteine if necessary to continue GTN, although ef cacy unproven) Cyanid e Toxicity-Sodium Nitroprusside Pulmonary vasodilatation causing increased pulmo nary shunting and hypoxia 3.4 Antiarrhythmic Drugs in Critical Care 3.4.1 General Principles of Treatment In therapy of arrhythmias, prior considera tion should be given to causal or aggravating factors: Hypoxmia High, occasionall y low, pH Hypokalmia, hypomagnesmia Pre-existing drug effects or toxicity (includi ng bronchodilators and inotropes) Presence of right heart lines (including pacem akers) Myocardial or coronary compromise, especially pulmonary oedema The need f or therapy should be carefully evaluated. For instance atrial tachyarrhythmias w ith a ventricular response similar to that of the preceding sinus rhythm need no t be slowed down or abolished at the cost of additional hypotension. Reperfusion VT associated with myocardial infarction (fascicular or otherwise) or non-parox ysmal junctional tachycardia (NPJT) at 130 min-1 may be as acceptable as sinus o r junctional bradycardia at 40 min-1 and equally self-limiting. Non-pharmacologi cal therapy should also be always considered - even if only to be dismissed, as in the case of precordial thump for VT. In patients with permanent pacemakers, a magnet may abolish both VT or SVT by xed overdrive pacing. DC cardioversion is a lways available. 53

3.4 Antiarrhythmic Drugs in Critical Care 3 DRUGS AND INFUSIONS The value of precise diagnosis is increasingly deconstructed by the likes of sot alol or amiodarone. Still, as a general rule, if antiarrhythmics are to be used, a 12-lead ECG should be obtained. Arrhythmias can only be de ned electrocardiogra phically. On the other hand, a full ECG obtained on a pulseless patient is medic o-legally indefensible. In many ICU patients the need for continued therapy ceas es as they improve and the drug often the ubiquitous amiodarone - can be stopped . 3.4.2 Drug Therapy of Bradyarrhythmias The cognoscenti prefer pacing when this i s mentioned, but there are clinical situations when pacing is either impracticab le or fails. A number of drugs have some utility in the setting of bradycardia-b radyarrhythmia. 3.4.2.1 Adrenaline A mixed - / - agonist, adrenaline has declined in popularity mainly due to its metabolic side effects mediated by -receptor stimulus (increased lacti c acid production, hyperglycaemia). In emergency situations where bradycardia is asscciated with hypotension and patient compromise adrenaline remains the rst li ne agent, at least in the short term. 3.4.2.2 Atropine Alkaloid from Atropa belladonna, competitive acetylcholine antagonist at post-ganglionic parasympathetic endings. It comes in 0.6 mg ampoules. Small dose s (or early stages of administration) may cause central vagal stimulation. Its v agolytic action is useful in the very early stages of (usually inferior) myocard ial infarction complicated by signi cant bradycardia or block; later stages of AV block are more likely to respond to aminophylline. Intraventricular, Mbitz II blo ck is made worse. Escape-capture bigeminy may be replaced by slower 2:1 block. I t may also be used in re ex bradycardia associated with upper airway manoeuvres, s uch as suctioning. In brady-asystolic cardiac arrest, it is next to useless; its administration here is con ned to junior hospital staff and protocol-driven ambul ance of cers. The main hazard of atropine is tachycardia in the presence of critic al coronary ischmia. Actual poisoning is now rare; the victim is memorably hot as a hare, blind as a bat, dry as a bone, red as a beet and mad as a hen. 3.4.2.3 Isoprenaline Isoproterenol is a pure agonist producing marked vasodilatation and cardiac stimulation; these actions have long ago necessitated its replacemen t by selective 2 bronchodilators in asthma. It is sometimes used for: 3o or adva nced 2o AV block as a bridge to pacing 54

3 DRUGS AND INFUSIONS 3.4 Antiarrhythmic Drugs in Critical Care to promote tachycardia and shorten the QT interval, against potential or manifes t torsade de pointes. Here, too, pacing offers greater exibility and stability. I t is less useful than even atropine in bradyarrhythmic arrest due to the vasodil ation and very high oxygen cost; it usually precludes successful resuscitation. 3.4.2.4 Aminophylline It may be indicated for symptomatic 2o or 3o AV block in later stages of inferior myocardial infarction, as mentioned above. 3.4.3 Supraventricular Arrhythmias Some agents control the ventricular response through AV blocking action, some interrupt the reentry circuit and abolish the p aroxysm; many do both. 3.4.3.1 Adenosine Endogenous adenosine production is enhanced by ischmia and it may well be the mediator of sustained AV block following inferior infarction. Its ha lf-life is only 0.61.5 sec, requiring larger dose with peripheral access, e.g. 6 mg where 3 mg given centrally would do. In SVT, both AV nodal and non-nodal reentrant tachycardias (AVNRT and AVRT), the slow pathway is blocked and cycle len gth alternans may occur. With incremental doses, over 90% effectiveness is seen. The response can also be used to differentiate broad complex tachycardia due to aberrancy from its ventricular look-alike, even though adenosine-sensitive VT n eeds consideration. Chest pain induced by adenosine, like that of dipyridamole, can be severe; other side effects include ushing, headache, dyspn?a and cough. Si nus bradycardia or arrest and ventricular arrhythmias are frequent, but almost n ever actionable. AF or utter may follow cardioversion of SVT; they are less durab le than with verapamil. SVT recurs early in 10-30% of cases. Indications for adenosine Narrow complex tachycardia: Adenosine may be the drug of choice in investigating and or treating such arrhythmia. It may terminate AVnodal and AV re-entry tachycardia, or reveal underlying atrial utter or brillation . Broad complex tachycardia: Adenosine may terminate SVT with intra-ventricular conduction block. It will not cardiovert true VT. It may be useful therefore in treatment of regular broad complex tachycardia not thought to be of ventricular origin. Dose: Adults: Incremental 3 mg, 6 mg, 12 mg, 18 mg. Given via large peripheral o r central vein followed by saline ush. Some practitioners use 6mg as rst dose. Ple ase be aware that administration of adenosine may cause the patient to feel very unwell (hot, ushed, nauseous) and you should warn the person beforehand if possi ble 55

3.4 Antiarrhythmic Drugs in Critical Care 3 DRUGS AND INFUSIONS 3.4.3.2 Verapamil Verapamil inhibits the slow inward Calcium channel and blocks the slow antegrade pathway in AVNRT; it stops AVRT by AV block. Its effect on SVT should be apparent within three minutes. If a 1-5 mg bolus (tailored to age and co-morb idity) is ineffective, a bigger (5-10 mg) dose 10 minutes later is recommended. Before adenosine, verapamil was the drug of choice in treatment of SVT. It can b e used to slow the ventricular response in AF, but this is rarely done now. It r emains quite useful for the same purpose in multifocal atrial tachycardias (wher e atrial rate may also be slowed), usually as an infusion. Hypotension may be a problem. It is obviated by preceding the bolus by 5 mmol of Calcium; there is no loss of anti-arrhythmic activity. Verapamil should be given slowly in patients with known myocardial disease. Other side effects are similar to those of adenos ine-sinus pauses, bradycardia and occasionally AF. Unlike adenosine, it should n ever be given to diagnose a broad-complex tachycardia: cardiogenic shock or card iac arrest may result. 3.4.3.3 Amiodarone This is currently the drug of choice for AF with rapid response in the ICU, given as a 5-10 mg.kg-1 loading dose over 20-60 minutes (occasionally bolus ) and followed by 1200 mg.day-1 infusion. Its advantage over digoxin is the rapi d (within one hour) control of the ventricular rate; unlike digoxin, it also pro pitiates the return of sinus rhythm. It is also quite successful for cardioversi on of SVT although it is rarely used for this purpose Acutely, amiodarone blocks the AV node (prolonging the PR interval in sinus rhythm); there is no immediate effect on the sinus rate, QRS duration or QT interval. It prolongs action poten tial and lengthens the effective refractory period throughout the heart; hence s lowing of the sinus rate and prolongation of the QT interval follow. Amiodarone has to be given via a central vein as it causes severe thrombophlebitis. Other s ide effects are ushing, nausea and transient hypotension. In patients with LV dys function, overt failure and shock may occur. In these patients it is wise to omi t the bolus and start with an infusion. Long-term side effects are serious and w ell known; they are rarely of great moment in the ICU. 3.4.3.4 Flecainide It slows the phase zero of the action potential, interfering with the fast inward Sodium current; it depresses the diastolic repolarisation. The action pot ential is not prolonged-hence its 1C classi cation. PR, QRS and QT are prolonged. It is a potent PVC killer but has suffered greatly in the CAST trial: its pro-arrh ythmic propensity precludes its long-term use in post-MI patients. The bad reput ation has spread. This has little to do with its bene ts in the ICU, where it rema ins the drug of choice for both SVT and AF & utter in patients with WPW syndrome. It slows conduction in the atrium. It is also a good drug for pharmacological c ardioversion of AF and utter in patients with normal conduction. Its pro-arrhythm ic effects are of less moment in continuously monitored ICU patients. 56

3 DRUGS AND INFUSIONS 3.4 Antiarrhythmic Drugs in Critical Care Preferred dose in the ICU = 150 mg in 5% dextrose IVI over 30 minutes. One impor tant side effect is the elevation of the pacing threshold; the patient may becom e un-paceable. This limits its use in the pacemaker-dependent post-CABG patients . 3.4.4 Ventricular Arrhythmias The pharmacological therapy is mostly concerned wi th treatment of VT and prevention of VF. Isolated VEBs, accelerated idiofocal rh ythms, escape beats or parasystole are usually treated by mistake. 3.4.4.1 Lignocaine Lignocaine has for a long time been the drug of choice for th e emergency treatment of ventricular arrhythmias. At one stage it was de rigueur in the early management of acute infarction, as a prophylactic; it was also use d to suppress the warning arrhythmias in this setting. Its great advantage is its relative lack of toxicity; its equally great disadvantage is the frequent (80-90 %) ineffectiveness in VT. The toxicity is mostly on the CNS, with slurred speech , twitching and seizures; a rare change in intraventricular conduction is usuall y trivial, but interesting. The standard dose is 75 mg, followed by 2-4 mg / min infusion in 5% D. 3.4.4.2 Amiodarone The drug is effective for sustained monomorphic VT and has some activity, like the now withdrawn bretylium, even in VF. It is the drug of choice for VT in ICU. 3.4.4.3 Sotalol Sotalol, in addition to its amiodarone or bretylium-like class a ctivity, is also a non-selective -locker (in its l-isomer). It prolongs QT and P R intervals and appears to produce more episodes of torsade de pointes than amio darone (but probably less than ecainide). It is excreted unchanged in the urine. A loading dose is 0.5-1.5 mg.kg-1 over 10 minutes, followed by infusion of 0.2-0 .4 mg.kg-1 .hour-1 in 5% Dextrose or by oral tablets. It is a signi cant negative inotrope; some VT patients in the emergency department setting had to be shocked at the end of the needle. A lower initial dose is prudent. Other side effects, li ke asthma, are shared with -lockers. On the other hand, the -lockde is a reason for its being the drug of choice for VT in patients with IHD. Its use in the tr eatment of supraventricular tachycardias is not recommended. 3.4.4.4 Magnesium A major indication is true torsade de pointes VT, where 2-4 g bolus is followed by 3-20 mg.min-1 infusion. Polymorphous VT with normal precedi ng QT is usually seen in the setting of acute ischmia and responds to Magnesium w ith the same frequency as sustained monomorphic VT: very rarely. Amiodarone, -lo ckers and urgent revascularisation are the best strategy here. 57

3.5 Respiratory Drugs 3 DRUGS AND INFUSIONS 3.4.4.5 Procainamide Its effects are very similar to those of quinidine; it is a Class 1A Sodium channel blocker, prolonging the QRS complex (25% effect, 50% toxicity) and th e QT interval. It is less vagolytic than quinidine and has little, if any, gangl ion-blocking properties. Dose: loading dose: 1 g in 50 cc 5% D (20 mg.ml-1 ) at 10-20 mg.min-1 . Alternat ively, 100 mg boluses over 1 minute can be repeated at 5 min intervals, watching the BP. It is quite effective drug for VT and probably most effective of all dr ugs to slow down the conduction by an anomalous pathway in WPW, AF or utter. It i s rarely used; part of the problem is the relatively long time (20 min) to load an effective dose. 3.4.4.6 Phenytoin Beside KCl, diphenylhydantoin is the drug of choice for VT caused by digoxin toxicity; it is also effective for digitalis-induced paroxysmal atrial t achycardia with block, but less so for non-paroxysmal junctional tachycardia. It is best given, like procainamide, as 100 mg boluses every 5 min; the usual anti arrhythmic dose is approximately 700 mg (beyond 1000 mg it is unlikely to succee d). 3.5 Respiratory Drugs 3.5.1 Nebulised bronchodilators 3.5.1.1 General principles These agents are used in the treatment of bronchospasm in Intensive Care (including acute severe asth ma). These agents do not necessarily need to be delivered by nebuliser, but can be administered as a metered dose inhaler into the appropriate port on the inspi ratory limb of the ventilator circuit. This is particularly important in patient s that cannot afford to lose applied PEEP while inserting the nebuliser into the circuit , and resultant lung de-recruitment. Once these agents have been commen ced they should be reviewed daily, as is the case with all prescribed drugs. Thi s is usually assessed by improvements in audible wheeze, lung compliance, respir atory rate and blood gases. 3.5.1.2 Indications Pre-existing obstructive airways disease where reversibility is suspected Acute severe asthma Acute exacerbation of obstructive airways dise ase Problematic sputum plugging or poor sputum clearance. 58

3 DRUGS AND INFUSIONS 3.6 Sedation 3.5.2 Parenteral Therapy in treatment of reversible obstructive airways disease 3.5.2.1 Indications Adjunctive therapy for acute severe asthma in patients not r esponding to nebulised agents 3.5.2.2 Complications Hypokalaemia, metabolic alkalosis Arrhythmias (theophyllin e) Intercurrent infection Polyneuropathy Lactic acidosis ( 2 -stimulants) 3.6 Sedation This section is authored by Dr Simon Enright and Dr Jacquiline Brook, and covers the delivery and monitoring of sedative agents used on the Intensive Care Units at Pinder elds General Hospital and Dewsbury District Hospital (Mid Yorkshire NHS Trust). It has been agreed by Consultant Intensivists and senior nursing staff who work on both units. It is intended as a guide and will outline the reasons f or sedation, sedation monitoring and the commonly used drugs on the units 3.6.1 Introduction Sedation is an extremely important part of the management of the critically ill. It allows the depression of awareness of the environment and reduction in the response to external stimulation. The intensive care is a frig htening place for patients for a number of reasons, and adequate sedation can re duce this. With the development of post-ICU follow-up clinics, the need for adeq uate sedation on ICU has been shown to be even more important and can reduce the incidence of longer term psychological complications. There is not a simple pre scription for all, and sedation requirements will depend on many factors includi ng age, general medical condition, presence or absence of painful stimuli (such as recent surgery), previous alcohol/drug habits and so on. There is no perfect sedative regimen but below commonly used agents are considered. Generally, patie nts should be given the sedation necessary to tolerate the presence of an endotr acheal tube, other catheters (N/G tube, urinary catheter), practical procedures (such as central line changes, physiotherapy), painful stimuli and arti cial venti lation. Sedatives should be regularly reviewed and changed if appropriate (for e xample much less sedation is required to tolerate IPPV after tracheostomy is per formed). Always consider the pharmacological actions of all drugs used. Particul ar attention must be given to patients who are given neuromuscular blocking agen ts. 59

3.6 Sedation 3 DRUGS AND INFUSIONS The guidelines given below will cover most patients. There will be occasions whe n patients will have different requirements, these must be discussed with senior medical staff. 3.6.2 Principles of Sedation Patients should be made as comfortable as possible and general measures taken when considering sedation (eg pain relief especially post-operatively, urinary catheterization, quiet environment). Any avoidable sou rce of physical discomfort should be excluded . The need for any uncomfortable o r disturbing therapies should be reviewed (eg line insertion) A perceived need t o increase sedation may be due to clinical deterioration. Drug, alcohol and nico tine withdrawal need to be considered and treated appropriately before increasin g sedation. Presence of parents/relatives may have an effect on sedative require ments (positively or negatively) especially with paediatric patients. Sedation s hould be tailored to a patients needs eg may require increased sedation for proce dures such as physiotherapy. Patients should be comfortable but rousable, co-ope rative and able to tolerate uncomfortable procedures 3.6.3 Monitoring Sedation : Sedation Scoring Both oversedation and undersedation can have adverse effects on patients and may lead to an increased stay in inten sive care. Therefore, there is a clear need to assess levels of patient sedation and titrate sedative drugs accordingly ( Saggs, P 1998). 3.6.3.1 Complications of Under-sedation Agitation Pain and discomfort Displaceme nt of monitoring Inadequate ventilation/disco-ordination with ventilator potenti al hypoxi Hypertension Tachycardia Patient awareness (especially when using neur o-muscular blockers) Complications of raised intra cranial pressure (if patient is at risk) Sudden changes in level of conciousness : displacement of invasive l ines, haemodynamic instability 60

3 DRUGS AND INFUSIONS 3.6 Sedation 3.6.3.2 Complications of Over Sedation Withdrawal syndromes Respiratory depressi on Hypotension Bradycardia Intra abdominal complications Immunosuppression, incr eased risk of infection Nosocomial infections Renal dysfunction Deep vein thromb osis Hepatotoxicity Reduced mobilisation and muscle wasting Psychological distur bances Metabolic abnormalities Cost 3.6.3.3 Sedation Scores modi ed Ramsay, Riker. There are a number of sedation scoring systems available eg On the ICUs at Mid Yorkshire Trust, the scoring system used is the Richmond Agita tion Sedation Score (RASS), which combines a commonly used scoring system (incre asing negative for deepening sedation, increasing positive for increasing agitat ion). This scoring system can be used in conjunction with the inattention scorin g to detect delirium. Score +4 +3 +2 +1 0 -1 -2 -3 -4 -5 Table 2: RASS Scoring system Term Description Combative Very Agitated Agitated Restless Alert and Calm Drowsy Light sedation M oderate sedation Deep sedation Unrousable Opens eyes to voice in <10secs, eye co ntact Opens eyes to voice in >10secs, eye contact Movement or eye open to voice, no eye contact Movement or eye opening to physical stimulation No response to v oice or physical stimulation combative, violent, immediate danger to staff Pulls tubes, aggressive Frequent non-purposeful movements Anxious, but movements not aggressive 3.6.4 Sedation Holds/ Sedation Assessment A sedation hold (also known as sedation holiday) involves stopping a patients sedation to allow assessment, usually on a daily basis. After sedation is stopped, the patient is assessed 61

3.6 Sedation 3 DRUGS AND INFUSIONS and sedation is then gradually recommenced, hopefully at a lower level. Sedation holds have been shown to reduce the overall length of stay on the ICU. After st opping the sedation, drugs may be recommenced when the patient is considered to be awake, i.e. to be able to respond to at least 3 out of 4 of the following comma nds: Opens eyes in response to voice Uses the eyes to follow the assessor on req uest Sticks out the tongue to command Squeezes the hand to command Ideally sedat ion should be stopped on a daily basis at around 08.00hrs to evaluate neurologic al status and prevent accumulation of sedative agents, unless: Patients achievin g target score i.e. 0 on sedation scoring tool Patient is receiving neuromuscula r blocking agents Patient is ventilated in prone position Patient dif cult to vent ilate in previous few hours Patient is suffering from status asthmaticus or seve re bronchospasm Patient is cardiovascularly unstable As prolonged use of sedativ e infusions may lead to numerous complications as previously mentioned, daily in terruptions of these infusions can be an easy and effective way of addressing th is. (Gehlbach B.K. Kress J.P. 2002) 3.6.5 Accumulation of Sedatives This occurs commonly especially if there is hepa tic or renal dysfunction. This can lead to over-sedation, haemodynamic instabili ty and prolonged duration of intubation. The action of IV anaesthetic agents (eg propofol) is generally terminated by redistribution not clearance ; therefore d rugs with a low clearance given as infusion may accumulate. Accumulation and ove r-sedation may be reduced or avoided by the use of sedation scoring and sedation holds. 3.6.6 Sedative Dependence Patients exposed to more than 1 week of high dose opio id or sedative may develop tolerance and/or dependence. The symptoms of opioid w ithdrawal are: pupillary dilatation, sweating, lacrimation, rhinorrhea, yawning, tachycardia, irritability, anxiety. Symptoms of BDZ withdrawal : dysphoria, tre mor, headache, nausea, sweating, agitation, anxiety, sleep disturbance, myoclonu s, delirium, seizures. Propofol withdrawal is not well described but is reported to resemble BDZ withdrawal. 62

3 DRUGS AND INFUSIONS 3.6 Sedation 3.6.7 Sleep on the ICU Sleep is a natural periodic state of rest for the mind an d body, in which the eyes are usually closed and conciousness is completely or p artially lost, so that there is a decrease in bodily movement and responsiveness to external stimuli. It is an important component in recovery from critical ill ness and sleep deprivation may impair tissue repair and overall cellular immune function. Sleep is dif cult to assess and achieve on the ICU. 3.6.8 Non-Pharmacological Methods of aiding sleep Modi cation of environment and r eduction in excess noise. Sleep occurs best below 35dB (80dB will cause arousal from sleep). Lighting to give diurnal rhythm (day-night) is helpful. Music thera py can decrease HR, myocardial oxygen demand, anxiety and aid sleep. 3.6.9 Pharmacological Methods Benzodiazepines such as zopiclone can be used, alt hough they may also precipitate delirium. They decrease sleep latency while incr easing total sleep time, without affecting sleep architecture in stages 3 and 4 and decrease REM sleep. Concerns included addiction, morning hangover, rebound i nsomnia. A newer melatonin receptor agonist, ramelteon, is being used experiment ally for sleep deprivation on the ICU, with promising early results. 3.6.9.1 Commonly Used IV Anaesthetic/Sedative Agents which are generally used on the units : Propofol Alfentanil Remifentanil Benzodiazepines : Diazepam, Midazo lam, Lorazepam Clonidine Morphine (less commonly) Below is a list of the agents (On the ICUs in the Mid Yorkshire Trust, the usual combination of sedative agents for the vast majority of patients is Propofol + Alfentanil). PROPOFOL General: Rapid onset IV anaesthetic agent with excellent sedative prope rties. Vasodilator properties similar to GTN (this property may be useful eg red uction of preload/afterload, warming patient post-operatively). Milk of amnesia : similar degree of amnesia as BDZs. No analgesic properties. Onset: Rapid < 1min Offset: Rapid < 10 mins (longer in elderly) 63

3.6 Sedation 3 DRUGS AND INFUSIONS Table 3: Sedative Drugs in ICU Dose: 0.5-4 mg.kg1 .hr1 by infusion (occasionally may need to higher) Problems: BP (potent vasodilator), lipid overload (triglycerides should be checked if used > 3 days), pancreatitis. Requires dedicated line. Admin: 1% or 2% form is availab le. The 2% formulation has the advantage of less volume and less lipid load, but it must be remembered that only half the volume should be given. Nb :The dose m ust be prescribed in mg.hr1 not ml.hr1 . The standard formulation in Mid Yorks is 1% propofol ALFENTANIL General: Short acting opioid analgesic with sedative properties Onset : Rapid 1-2 min Offset: Rapid (depends on duration of infusion) Dose: Adult 0.5 - 5mg.hr1 (half dose in elderly) Problems: Respiratory depression, chest rigidity , prolonged duration of action in renal/hepatic disease Admin: IV infusion 0.5mg .ml1 REMIFENTANIL 64

3 DRUGS AND INFUSIONS 3.6 Sedation General: Ultra-short acting opioid, potent agonist, usually given as a single ag ent. Not generally rst-line agent, should be discussed with consultant before use. Onset: Very rapid, highly predictable Offet: Very rapid, predictable, not depend ent on normal hepatic/renal function, stable contextsensitive half-time (3-10 mi ns) Dose: only given by infusion, rate 0.1-0.15 cg.kg1 .min1 to start, adjusted at 5 min intervals by increments of 0.025 cg.kg1 .min1 according to response. If adequ ate sedation is not achieved at 0.2 cg.kg1 .min1 , then additional agent may be req uired Problems: haemodynamic (reduction in MAP, HR) esp if greater dose than 0.1 cg.kg1 .min1 . Acute-onset withdrawal symptoms and tolerance have occurred. The co st of remifentanil is signi cantly higher than alfentanil. Admin: IV infusion (var iable concentration depending on weight) BENZODIAZEPINES (BDZs) In general they offer greater cardiovascular stability th an IV anaesthetic agents and should be considered as the major sedative in patie nts with severe haemodynamic instability (such as septic shock with inotropic su pport). They produce sedation by modulating the effects of GABA, the main inhibi tory neurotransmitter in the CNS. They bind to the GABAA ligand gated Cl- ion ch annel. They may be given by bolus or continous infusion. However, we suggest tha t they are generally given by by intermittent bolus and generally not by infusio n on the ICU due to high lipid solubility, long elimination half-life and prolon ged duration of action. Diazepam (preferred) and midazolam are most commonly use d. The bolus should be titrated slowly to the response and it must be remembered that these drugs can cause respiratory depression and hypotension. Concerns wit h their use include dependence, withdrawal agitation and acute delirium. MIDAZOLAM General: Highest clearance of benzodiazepines (most suitable BDZ for i nfusion), metabolised to active compounds in the liver Dose: Bolus : 1-4 mg prn, or infusion : 0.04 0.2 mg.kg1 .hr1 Onset: around 1 min Duration: 1-2 hours, the m ost suitable BDZ to be given by infusion DIAZEPAM (diazemuls) General: Effective sedative/anxiolytic with amnesic action Dose: Adult : up to 10mg (given 2mg at a time) by slow IV bolus. This may be pre scribed as frequently as hourly. If frequent boluses are required, the sedative regime should be reassessed. Remember to reduce dose in elderly. May be given or ally. Onset: 1-2 mins 65

3.6 Sedation 3 DRUGS AND INFUSIONS Duration: 1-8 hours (longer in elderly, renal failure, hepatic failure). Metabol ized in the liver to active compounds, should not be given as infusion Problems: prolonged effect, active metabolites Infrequently used IV Sedative/Anaesthetic agents : SODIUM THIOPENTONE The only use of sodium thiopentone is by continuous infusion in the management of refractory status epilepticus. It has a low clearance and t ends to accumulate. When given as an infusion its metabolism becomes linear (zer o order) due to saturation of hepatic enzymes. Accumulation can give toxicity in cluding immunosuppression and cardiac depression. ETOMIDATE Etomidate has a good haemodynamic pro le but is not administered by infu sion due to its suppressive effect on adrenocortical function . Etomidate is not recommended for use on the ICU. KETAMINE Ketamine is a phencyclidine derivative which acts as an antagonist to glutamate (excitatory) at NMDA receptors. It is an excellent analgesic and produces a diss ociative anaesthesia/sedation. Ketamine is a sympathomimetic agent, causing stim ulation of heart rate and increased cardiac work. Common side-effects include ha llucinations, nausea, delirium and nausea/vomiting. It is a potent bronchodilato r : its only role on ICU is in the management of refractory bronchospasm (status asthmaticus). It may also be used for control of pain in awake patient. 3.6.9.2 NEUROMUSCULAR BLOCKADE Neuromuscular blockade (paralysis, muscle relaxat ion) on ICU has speci c indications and should not be used routinely. Special atte ntion to detail is necessary to avoid paralysis without adequate sedation. If th e decision is made on clinical grounds to instigate neuromuscular blockade, then blockade should be complete (there is no indication for partial N-M blockade). The adequacy of N-M blockade should be checked with a peripheral nerve stimulato r. These drugs should be stopped when there is no clinical indication. Indicatio ns for neuromuscular blockers include : poor oxygenation with high FiO2 (such as ARDS), reduction in oxygen consumption poor compliance with ventilator ( ghting th e ventilator) despite adequate sedation complex ventilation modes (inverse ratios , high pressures) management of raised intracranial pressure special circumstanc es eg prone ventilation 66

3 DRUGS AND INFUSIONS 3.6 Sedation 3.6.9.3 Problems inadequate sedation leading to awareness (while paralysed) prol onged paralysis or muscle weakness (major factor in critical illness polyneuropa thy/myopathy) hypostatic pneumonia venous thromboembolism (all reasonable measur es should be taken to reduce this) peripheral oedema ATRACURIUM General: useful on ICU due to non-enzymic elimination and predictable duration of action Dose: bolus 0.5mg/kg then infusion 0.5-1mg/kg/hr (remember t achyphylaxis develops and increased dose needed if patient pyrexial) Onset: 2-3m ins (initial bolus) Duration: 10-30 mins after stopping infusion Problems: BP (h istamine release), tachyphylaxis (less with cis-atracurium) If complete neuromus cular blockade is dif cult to achieve with high doses of atracurium but necessary clinically, it is worth adding in another drug such as pancuronium (0.1mg.kg1 ) o r vecuronium (0.1mg.kg1 ) by bolus every 1-2 hourly. Both of these drugs have a s ynergistic action with atracurium. 3.6.9.4 Centrally acting gonists Unlike other sedatives, 2 -agonists do not caus e major problems with respiratory depression or haemodynamic instability. They m ay therefore be given as a sedative to both mechanically ventilated and spontane ously breathing patients. They are often given as an adjunct to other sedatives, especially when there are concerns over withdrawal from other drugs, alcohol or nicotine. CLONIDINE 2 > 1 -agonist Clonidine is an 2 -agonist. Initial pressor effect due to 1 stimulation of arterio les, then central 2 stimulation in CNS inhibits sympathetic activity, reduces pla sma epinephrine and norepinephrine levels It is useful in the management of agit ation and withdrawal of benzodiazepines, opioids or alcohol. It can be given as a bolus (50-150 mcg TDS) or infusion (0.5-1.5 mg/24hrs). DEXMEDETOMIDINE More selective 2 -agonist than clonidine and therefore more potent. Stronger sedative and analgesic properties. It has a shorter elimination half-li fe than clonidine. Not widely used in UK at present. 67

3.6 Sedation 3 DRUGS AND INFUSIONS 3.6.9.5 Dif cult sedation patients This may be a problem in alcoholic or opioid ab users and in long-term ICU patients who develop what has previously been named a n ICU psychosis. This term covers a host of psychological disturbances on the ICU. Butyrophenones (haloperidol) and phenothiazines (chlorpromazine) are occasional ly used in small doses. Haloperidol 1-5mg (oral or IM), chlorpromazine (5-25mg I V). These drugs should be used with caution as they may cause drop in blood pres sure and over-sedation. Delirium is discussed in detail in the last part of the guidelines. Alcohol/Drug Withdrawal Alcohol or opioid withdrawal in adults is best treated with CLONIDINE (50-200mcg IV OD) and not traditional therapies such as Heminevrin (this ac cumulates and leads to severe sedation, respiratory depression and possibly pulm onary aspiration). Examples of Sedative Regimes : 1. 50yr old (70kg) man admitte d to ICU for IPPV after laparotomy for perforated duodenal ulcer. Sedation probl ems : sedation required to tolerate presence of endotracheal tube and facilitate IPPV analgesia required (post-laparotomy) Regimen : a) Propofol infusion (up to 200mg/hr, 20ml 1% propofol) b) Alfentanil infusion (up to 5 mg/hr) c) Diazemuls (5-10mg) by intermittent bolus, given by nursing staff (can be given in anticip ation of stimulating procedures (eg line insertion, physiotherapy) d) Remember a djuncts to analgesia such as thoracic epidural, morphine PCAS 2. 80yr old lady ( 50kg) with acute exacerbation of COAD. Sedation problems : sedation reqd to tole rate endotracheal tube and IPPV no painful stimuli may be dif cult to comply with ventilator so may require neuromuscular blockers possibly hypovolaemic due to de hydration Regimen a) Propofol infusion 120mg per hour (12 ml/hour of 1% propofol ) b) Alfentanil infusion (up to 1.5mg/hr) c) Diazemuls up to 5mg by intermittent bolus (given very slowly to titrate response) d) Remember, sedation requirement s will fall to around 30% if tracheostomy performed 68

3 DRUGS AND INFUSIONS 3.6 Sedation 3.6.10 Management of Delirium De nition: an acute, reversible, organic mental synd rome with: (a) disorders of attention and cognitive function, (b) increased/decr eased psychomotor activity (c) disordered sleep-wake cycle Typical onset: after 2 days, typical duration 4 days Cognitive impairment : Memory: especially registration and recall of recent even ts Orientation: in time>place>person Attention: increased distractibility Percep tion: increased misinterpretations, illusions, hallucinations Logical thought: m uddled thinking and speech 3.6.10.1 Types of delirium Hyperactive: Agitated/paranoid (1%) Hypoactive: withd rawn, quiet, paranoid (35%) Mixed: combination of 2 types (64%) Hypoactive lethargic, drowsy, quiet, disorientated, easily missed as patient is quiet, often treated as depression (nb disorientation is rare in depression) Hyperactive Continual movement, disorientated, may use violence, may not follow commands, inappropriate, pain exaggerated, abnormal vital signs Mixed most common, combination of above Delirium is under-recognised in the crit ically ill (70% missed and symptoms wrongly attributed to dementia or confusion) Delirium is a medical emergency Delirium should not be ignored : it results in : increased 6 month mortality, longer stay in ventilated patients, longer hospit al stay, neuropsychological disturbances after ICU stay, increased cost, Common : 15-80% in critically ill 69

3.6 Sedation 3 DRUGS AND INFUSIONS Prevention Non-pharmacological: provide support and orientation, provide an unam biguous environment, maintain competence, remove potential organic drivers Pharm acological: stop medication no longer required 3.6.10.2 Risk Factors Age over 70 Transfer from nursing home History of depressi on, dementia, epilepsy, alcohol abuse Psychoactive drugs Hypo/hyper-natraemia/gl ycaemia/thyroidism/thermia Renal dysfunction Liver disease CCF HIV CVP/bladder c atheters Malnutrition Visual/hearing impairment 3.6.10.3 Associated Drugs : Analgesics Antidepressants Anticonvulsants Antihista mines Antiemetics Antipsychotics Antimuscarinics Cardiovascular agents Corticost eroids Hypnotic agents Miscellaneous agents (ranitidine, furosemide) 3.6.10.4 Assessment /Screening for Delirium Assess patient with RASS scale and u se CAM-ICU tool Exclude or minimise organic drivers of delirium (hypoxia, hyperc arbia, acidosis, pain, unnecessary medications) 70

3 DRUGS AND INFUSIONS 3.6 Sedation Consider whether alcohol withdrawal or alcohol withdrawal syndrome is likely Con tinue to assess patient with RASS scale and use CAM-ICU tool, at least daily, ev en when on treatment 3.6.10.5 TREATMENT SUGGESTIONS Alcohol withdrawal LORAZEPAM 1-4mg (IV or IM) Consider PROPOFOL Consider CLONIDI NE Alcohol withdrawal delirium LORAZEPAM 1-4mg (IV or IM) Consider HALOPERIDOL if s till agitated / altered perception / disturbed thinking Consider PROPOFOL CLONID INE is unlikely to help Delirium detected by screening HALOPERIDOL low dose regular enterally / IV route , or OLANZAPINE 5mg enterally Overtly delirious with IV access HALOPERIDOL IV use titration method or OLANZAPI NE 2.5 10 mg IM, repeat if necessary MIDAZOLAM 5 10 mg IV (for dangerous motor a ctivity), repeat as needed Night sedation 50mg TRAZADONE enterally at night for seven days or 2-5mg HALOPER IDOL intravenously at night How to manage patient with hypoactive delirium Ensure the diagnosis is not depre ssion or dementia Management is as for hyperactive / mixed delirium, although me thylphenidate may be useful if this treatment fails or cannot be used METHYLPHEN IDATE - Consider 10-30mg methylphenidate daily in divided doses in addition to n ormal therapy if not responding. 71

3.6 Sedation 3 DRUGS AND INFUSIONS Titrate to maximum 50mg daily in divided doses if required. This is a stimulant, and a controlled drug) OLANZAPINE 5-10mg enterally or IV (This is an antipsycho tic) Notes on Haloperidol use Do not use in patients with Parkinsons disease Start wi th low dose if any concern over cardiovascular status or if elderly (ie 1-2mg) I f extra-pyramidal side effects occur, treat with Procyclidine 5-10mg iv If using IV titration, (doubling dose every 20-30 minutes until effect achieved) do not exceed 80mg per 24 hours without consultant approval For any patient on regular haloperidol, perform daily 12-lead ECG to ascertain QTc value, reduce dose if QT c exceeds 480 ms Perform daily measurement of serum magnesium and potassium If t reatment is effective in controlling delirium, plan to reduce haloperidol (or ot her drug for delirium) dosing regime gradually over a few days Notes on Lorazepam use for alcohol withdrawal and alcohol withdrawal delirium LO RAZEPAM (Parenteral) Lorazepam 1-4mg intravenously every 5 to 15 minutes until c alm (or 1-4mg intramuscularly every 30to 60 minutes until calm), then every hour to maintain light somnolence. LORAZEPAM (Enteral) Lorazepam 2mg every six hours for 4 doses, then 1mg every 6 hours for 8 doses. Additional doses can be given when required if needed for poorly controlled symptoms Problems with commonly used drugs traditionally used for sedation / agitated beh aviour Benzodiazepines diazepam is deliriogenic and REM Chlordiazepoxide delirio genic and REM Clonidine NOT deliriogenic, but REM Opioids Codeine, Fentanyl, Mor phine, Pethidine are all deliriogenic and all REM Propofol NOT believed to be de liriogenic or to result in REM-rebound when stopped Antipsychotics Chlorpromazin e is deliriogenic SSRI eg citalopram, paroxetine night sedation REM Zolpidem or Zopiclone are not recommended substitutes for short acting benzodiaz epines for 72

3 DRUGS AND INFUSIONS 3.7 Anticoagulation Other Drugs commonly used in critical care that have been shown to be deliriogen ic Amitriptyline Phenytoin, Phenobarbital, Thiopental, Chlorphenamine, Promethaz ine Prochlorperazine Atropine, Hyoscine Atenolol, Digoxin, Dopamine Lidocaine De xamethasone, Hydrocortisone, Prednisolone Furosemide, Ranitidine 3.6.11 Referenc es www.icudelirium.org UKCPA: Detection, prevention and treatment of delirium in critically ill patients. June 2006 3.7 Anticoagulation 3.7.1 General Principles Anticoagulation in critically ill patients is a challen ging issue, with patients at risk of bleeding diatheses as well as hypercoagulab le states. Often a single patient will move through a state with a high risk of bleeding (including surgical sites) to one of high risk of developing venous sta sis and thrombosis. The decision to administer anticoagulation is often based on a relative risk-bene t assessment. Where anticoagulants are contra-indicated, alt ernative methods should be employed to prevent venous stasis in the lower limbs (graded compression stockings and sequential calf compressors), although it is u nclear as to whether these confer adequate protection against thrombosis and emb olisation. As a general rule heparin infusions should be used to effect anticoag ulation, titrated intravenously to a therapeutic APTT where this is required, or administered subcutaneously for DVT prophylaxis. Low molecular weight heparins require measurement of anti-factor Xa to quantify effect, and are more dif cult to reverse than unfractionated heparin. Where any doubt exists with regard the use of an anticoagulant in a given surgical or trauma patient, this should be con rme d with the Surgeon involved. 3.7.2 Indications for the use of warfarin Post oper ative prosthetic valve (According to cardiothoracic guidelines) Previous thrombo -embolism: Selected cases only Maintenance of thromboprophylaxis in selected hig h risk patients only 73

3.7 Anticoagulation 3 DRUGS AND INFUSIONS 3.7.3 Indications for the use of heparin DVT prophylaxis (LMWH) Proven venous or arterial thrombo-embolism Myocardial ischaemia syndromes Prosthetic heart valve s Prior to commencing oral anticoagulants During an acute illness where oral ant icoagulation is unsuitable Atrial Fibrillation-sustained Continuous Renal Replac ement Therapy (CRRT - See below) 3.7.4 Prophylactic use of heparin DVT prophylaxis should be commenced within 2436 hrs of admission to the ICU. Low molecular weight heparin is generally consi dered as safe, and in some instances marginally superior (eg. orthopaedic patien t populations) to unfractionated heparin. Enoxaparin (Clexane) is the chosen LMW H in the ICU (20mg s/c daily). Non-pharmacological methods of DVT prophylaxis :e lasticated compression stockings (ECS) or sequential compression devices (SCD) m ay confer some protection against DVT formation. 3.7.4.1 Exclusions to heparin DVT prohylaxis Clinical coagulopathy or thrombocyt opaenia Therapeutic anticoagulation (eg Warfarin, heparin) Signi cant intra-cerebr al haemorrhage Heparin Induced Thrombocytopaenia. 3.7.4.2 DVT prophylaxis by category Medical ICU patients: Enoxaparin when bleedi ng risk felt to be minimal. When bleeding risk high, use ECS and SCD. Surgical p atients: ECS plus Enoxaparin when possible. Add SCD if enoxaparin contraindicate d. Head injury with CT evidence of frank haemorrhage or haemorrhagic stroke: ECS and SCD for 72 hrs. Substitute enoxaparin for SCD at 72 hours if appropriate. S pinal Cord injury with intra-spinal haemorrhage on MRI: As for intra-cerebral ha emorrhage above. Pelvic fractures and patients with signi cant trauma: Thrombotic and initial bleeding risk high. If enoxaparin felt inappropriate at 24-36hrs the n consider placement of temporary caval lter. 74

3 DRUGS AND INFUSIONS 3.7 Anticoagulation 3.7.5 Systemic anticoagulation using unfractionated heparin Weight based nomogra ms are more effective in achieving therapeutic anti-coagulation in a shorter per iod of time. Proceed with loading dose if safe: 70 units / kg. Continue with 20 units.hr-1 .kg-1 as continuous infusion (10 000 units heparin in 100 ml Normal S aline = 100 iu.ml-1 Check APTT 4-6 hrly and adjust infusion rate according to ch art. N.B. For APTTs within 12 hours of starting thrombolytic therapy do not disco ntinue or decrease the infusion unless: signi cant bleeding occurs APPT is > 150 s ecs Adjust the infusion as per nomogram if APPT < 50 secs. Heparin toxicity (pro longed APTT) in a patient that is actively bleeding should be reversed with Prot amine Sulphate 50 mg aliquots IVI (usually diluted). Administration of Protamine may aggravate peripheral vasodilatation and hypotension in susceptible patients . 3.7.6 Heparin Induced Thrombocytopaenia 3.7.6.1 Introduction HIT occurs in two f orms. Dose related: Platelet clumping as an effect of the larger glycosaminoglycans co ntaining the active pentasaccharide of heparin. Immediately obvious, dose relate d and usually mild. Auto-immune: IgG antibody mediated. Therefore usually occurs 7-10 days after exposure in non-sensitised patients. Idiosyncratic, often sever e. HIT may appear more common in the setting of continuous renal replacement the rapy. This might re ect patient condition and platelet adsorption to dialysis lter. 3.7.6.2 Diagnosis Decrease in platelet count: Usually < 50 000109 .L-1 . Rarely < 20 000109 .L-1 Skin lesions at heparin injection sites Dominant nding of thrombosi s (not bleeding) Formation of Heparin antibodies (heparin ? PF4 ELISA = Sensitiv e but not speci c). 3.7.6.3 Treatment Measures Stop all Heparin immediately and reconsider indicatio n for anti-coagulation. Warfarin, if commenced, should not be used alone as it e xacerbates thrombotic risk. Use of Low Molecular Weight Heparin in these patient s is not considered safe (cross-reactivity rates in excess of 90% reported). 75

3.8 Endocrine Drugs 3 DRUGS AND INFUSIONS 3.8 Endocrine Drugs 3.8.1 Insulin 3.8.1.1 Introduction Glycaemic control in the critically ill has b ecome one of the most debated aspects of care. There is some evidence that tight control of blood suga r (4.4-6.0 mmol.L-1 ) is associated with improved outcome. This effect may be pr eserved at levels less than 8 mmol.L-1 . This area of ICU practice is evolving a nd requires regular review. Target blood sugar levels between 4.4-6.0 mmol.L-1 , levels above 8.0 mmol.L-1 must be aggressively treated. 3.8.1.2 Indications for insulin in the ICU Diabetic emergencies: NB Rapid glycae mic control is not a priority in patients with either hyperosmolar or ketotic di abetic states. In fact rapid correction of severe hyperglycaemic states may aggr avate cerebral oedema. Patients admitted to the ICU with these conditions should be actively co-managed with the endocrine service. Perioperative diabetic patie nts Glucose intolerant or overtly diabetic patients with acute coronary syndrome s Hyperglycaemia (single blood glucose >15 mmol.L-1 or 2 readings 4 hours apart > 10 mmol.L-1 ) or glycosuria associated with acute illness orsteroid administra tion. Hyperglycaemia associated with catecholamine infusions. Treatment of hyper kalaemia: ie 50 ml 50% dextrose administered with 10 units actrapid insulin. 3.8.1.3 Administration of insulin saline to a concentration 1 IU.ml . -1 Mix regular short acting insulin (actrapid) with normal Administer in a 50 ml syringe via syringe driver. Maximum infusion rate never to exceed 25 IU.hr-1 . Discard at 24 hrs of use. 3.8.1.4 Monitoring of blood glucose admission, and 4 hrly thereafter. Blood sugar levels should be monitored hourly until stable within desirable range. Once stable, monitor at least 2 hrly in the hrs of ICU rst 48

Ongoing requirement for insulin beyond acute phase: Patients requiring insulin f or established or known diabetes should be converted to subcutaneous insulin as a medium or long acting form with/without a short acting insulin constructed acc ording to subcutaneous sliding scale. As these patients may need long term follo w-up, they should be referred to the endocrine service for assistance. 76

3 DRUGS AND INFUSIONS 3.8 Endocrine Drugs 3.8.2 DDAVP 3.8.2.1 For Diabetes Insipidus General DI may occur in the following settings: Evolving brain death or severe b rain injury Post ablative pituitary surgery, or injury to pituitary stalk (anter ior cranial fractures) Nephrogenic causes are typically mild and do not require treatment. Fluid mobilisation during convalescent phase of injury should not be mistaken for DI. Indications for DDAVP in diabetes insipidus Persistent polyuria >300 ml.hr-1 for more than 3-4 hours with incremental hypernatraemia. Low urine osmolality in th e presence of high plasma osmolality (or hypernatraemia) Pre-existing hyperosmol ar state or intravascularly deplete patient. Dose of DDAVP in diabetes insipidus 1-2 g IVI bd as required. Fluid orders: Isotonic uid replacement in under-resuscitated patients. 5% Dextros e or 0.45% Saline in patients where hypernatraemia exists (maximum decrease in s erum Sodium should not exceed 2 mmol.L-1 .hour-1 ) 3.8.2.2 For Platelet dysfunction Indications of Uraemia Cirrhosis Adjunctive treatment in bleeding patients with platelet dysfunction as a result Von-Willebrands Disease Drug (NSAIDs or aspirin) or cardiac surgery related plate let dysfunction Contraindications Use in patients with severe oronary or cerebrovascular atherosclerosis may cause arterial thrombosis. Dose 0.3 g.kg-1 IVI over 30 minutes or 300 g intra-nasally. In some instances a se cond dose may be administered, although a rapid fall-off in effect per dose (tachy phylaxis) is the norm. 77

3.8 Endocrine Drugs 3 DRUGS AND INFUSIONS 3.8.3 Steroids 3.8.3.1 General The use of steroids in the critically ill has bee n the subject of much debate and some research. At present their use in ICU is dependant upon the personal ex perience and practice of the consultant staff involved with the case. Steroids s hould not be prescribed by junior staff, except for those indications listed bel ow as proven, unless this has rst been discussed with the Consultant. Proven Indications Hypoadrenalism (Addisons disease or crisis) Acute severe asthm a Panhypopituitarism Haemophilus meningitis in children (discuss with paediatric team rst) Pneumocystis Carinii pneumonia (PaO2 < 6.0 kPa) Collagen Vascular dise ases Active Immunosuppression (GVHD, solid organ transplant) Myasthenia Gravis Unproven ICU indications Non-infected ( broproliferative) ARDS: Meduri protocol = Methylprednisolone 2 mg.kg-1 for 14 days, tapered 1.0-0.5 mg.kg-1 for next 14 da ys. Shock associated with vasodilated states which are refractory to high dose, or prolonged administration of, inotropes. Myocarditis Exacerbation of chronic a irway obstruction Bronchiolitis obliterans Reduction of cerebral oedema around n on-traumatic CNS lesions. Anaphylaxis 3.8.3.2 Conditions where steroids are not indicated or actively contra-indicated Active infection (except in the inotrope dependent septic shock scenario) Acute Head or spinal cord injury Guillain-Barre Syndrome Fat embolism syndromes 78

3 DRUGS AND INFUSIONS 3.9 Renal Drugs 3.9 Renal Drugs 3.9.1 General Principles Acutely ill patients are at risk for developing, or exa cerbating, renal dysfunction. Good intensive care practice, and renal care, enco mpasses: Avoiding renal hypoperfusion: ICU patients generally do not have the ab ility to autoregulate renal blood ow and GFR, as these become increasingly depend ant on systemic perfusion pressures. For this reason urinary output is a good ma rker of total body perfusion, and resuscitation status. Ensure adequate volume r esuscitation Avoid renal toxins if possible: aminoglycoside antibiotics, contras t mediums etc Consider local complicating conditions: eg. abdominal compartment syndromes. Administration of agents such as dopamine in low dose, or frusemide, are not however renoprotective, and their use strongly deprecated. 3.9.2 Diuretics 3.9.2.1 Indications Symptomatic uid overload without intravascula r depletion Pulmonary oedema Congestive Cardiac Failure / Cor Pulmonale Ascitic states where abdominal volume is thought to be a compromising factor Hypertensio n Conjunctive therapy in Cardiac failure (not primarily diuretic): ACEI and thia zide, Low dose (25 mg.day-1 ) spironolactone. Metabolic alkalosis: e..g recoveri ng ventilated patients allowed permissive hypercapnoea, prolonged renal replacem ent therapy with bicarbonate overshoot. (ie. acetazolamide). 3.9.2.2 Contraindications Hypovolaemia Anuria: Frusemide in particular acts on t he luminal side of the renal tubule. States where there is no, or low, GFR will not respond to drug administration, and may complicate hypotension by direct aft erload reduction. Failure to respond to trial dose Drug hypersensitivity: NB Sul phonamides 79

3.10 Gastro-intestinal drugs 3 DRUGS AND INFUSIONS 3.9.2.3 Complications Hypovolaemia (often hyperosmolar) Hyponatraemia or hyperna traemia Electrolyte disturbance of K+ , Mg2+ and PO4 3- . 3.10 Gastro-intestinal drugs 3.10.1 Prophylaxis of gastric stress ulceration Evidence base Critically ill patie nts commonly develop gastrointestinal tract problems as a result of severe physi ological stress. These include stress related mucosal disease, gastrointestinal motility problems and mucosal oedema. Gastric acidity has been identi ed as a sign i cant risk factor for stress ulcer bleeding and stress ulcer prophylaxis has beco me standard practice in critically ill patients. Initial studies looked at ef cacy of available agents for stress ulcer prophylaxis [1]. These included antacids, sucralfate and H2 receptors antagonists. Studies reported an increased risk of v entilator associated/ nosocomial pneumonia with the use of H2 receptor antagonis ts compared to sucralfate [2, 3, 4, 5, 6]. Other studies however were unable to support this [7, 8]. These conclusions were then resolved in a meta analysis whi ch suggested that there was strong evidence of reduced clinically important gast rointestinal bleeding with H2 receptor antagonists and sucralfate may be as effe ctive in reducing bleeding as gastric pH altering drugs and is associated with l ower rates of pneumonia and mortality. There is insuf cient data to determine the net effect of sucralfate compared with no prophylaxis [9]. A further study obser ved a lower incidence of clinically important stress ulcers with ranitidine and a lower incidence of nosocomial pneumonia with sucralfate. Mortality and length of ICU stay were similar in both groups [10]. Administration of sucralfate throu gh a nasogastric tube probably limits its use and has possibly contributed to th e success of intravenous H2 antagonists such as ranitidine as the rst choice agen t for stress ulcer prophylaxis. The use of intravenous proton pump inhibitors is now becoming widespread. They decrease the rate of peptic ulcer re-bleeding aft er endoscopic haemostasis [11, 12], and are effective in gastro-oesophageal re ux disease. This data is likely to be extrapolated to suggest that proton pump inhi bitors are superior in stress ulcer prophylaxis. There is preliminary work to su ggest that PPIs are safe and effective for stress ulcer prophylaxis [13, 14] but further studies are required to fully de ne the role of PPIs in this role [15, 16]. The comparison between drugs used for rst line prophylaxis and second line or hi gh-risk patient groups is consistent with the understanding that PPIs are more ef c acious than H2 receptor antagonists. Ranitidine is effective for stress ulcer pr ophylaxis in rst line therapy but the evidence is less clear for high-risk groups . 80

References References Nosocomial or ventilator associated pneumonia has been associated with the use o f drugs which alter gastric pH and leads to increased bacterial growth coupled w ith aspiration into the trachea leading to pneumonia. This lead to the support f or sucralfate as it does not alter gastric pH. Several studies have been complet ed and the results are inconclusive [6, 20]. Comparisons between H2 receptor ant agonists and proton pump inhibitors are inconclusive [21]. Stress ulcer prophyla xis is once again a topical issue in the United Kingdom with the development of Ventilator Care Bundles that have a stress ulcer prophylaxis component. References [1] Priebe HJ, Skillman JJ, Bushnell LS et al. Antacid versus cimetidine in prev enting acute gastrointestinal bleeding. A randomised trial in 75 critically ill patients. New England Journal of Medicine 1980; 302: 426-30. 80 [2] Driks MR, Cr aven DE, Celli BR et al. Nosocomial pneumonia in intubated patients given sucral fate as compared with antacids or histamine type 2 blockers. The role of gastric colonisation. New England Journal of Medicine 1987; 317:1376-82. 80 [3] Tryba M . Risk of acute stress bleeding and nosocomial pneumonia in ventilated intensive care unit patients: Sucralfate versus antacids. American Journal of Medicine 19 87; 83(3B): 117-24. 80 [4] Apte NM, Karnad DR Medhekar TP, et al. Gastric coloni sation and pneumonia in intubated critically ill patients receiving stress ulcer prophylaxis: A randomised controlled trial. Critical Care Medicine 1992; 20: 59 0-93. 80 [5] Eddleston JM, Vohra A, Scott P, et al. A comparison of the frequenc y of stress ulceration and secondary pneumonia in sucralfate or ranitidine treat ed intensive care unit patients. Critical Care Medicine 1991; 19: 1491-96. 80 [6 ] Prodhom G, Leuenberger P, Koerfer J, et al. Nosocomial pneumonia in mechanical ly ventilated patients receiving antacid, ranitidine, or sucralfate as prophylax is for stress ulcer. A randomised controlled trial. Annals of Internal Medicine 1994; 120: 653-62. 80, 81 [7] Simms HH, DeMaria E, McDonald L, et al. Role of ga stric colonisation in the development of pneumonia in critically ill trauma pati ents: Results of a prospective randomised trial. Journal of Trauma 1991; 31: 531 -36. 80 [8] Pickworth KK, Falcone RE, Hoogeboom JE, et al. Occurrence of nosocom ial pneumonia in mechanically ventilated trauma patients: A comparison of sucral fate and ranitidine. Critical Care Medicine 1993; 21: 1856-62. 80 [9] Cook DJ, R eeve BK, Guyatt GH, et al. Stress Ulcer Prophylaxis in Critically Ill Patients: Resolving discordant Meta-analyses. Journal of the American Medical Association; 1996: 275: 308-14. 80 [10] Cook DJ, Guyatt GH, Marshall J, et al. A comparison of sucralfate and ranitidine for the 81

References References prevention of upper gastrointestinal bleeding in patients requiring mechanical v entilation. New England Journal of Medicine 1998; 338: 791-97. 80 [11] Lin HJ, L o WC, Lee FY, et al. A prospective randomised comparative trial showing that ome prazole prevents rebleeding in patients with bleeding peptic ulcer after success ful endoscopic therapy. Archives of Internal Medicine 1998; 158: 54-8. 80 [12] L au JYW, Sung JJY, Lee KKC, et al. Effect of intravenous omeprazole on recurrent bleeding after endoscopic treatment of bleeding peptic ulcers. New England Journ al of Medicine 200; 343: 310-16. 80 [13] Phillips JO, Metzler MH, Huckfeldt RE, et al. A multicenter, prospective, randomised clinical trial of continuous infus ion IV ranitidine vs. omeprazole suspension in the prophylaxis of stress ulcers. Abstract. Critical Care Medicine 1998; 26(Supplement): A101. 80 [14] Jung R, Ma claren R. Proton pump inhibitors for stress ulcer prophylaxis in critically ill patients. Annals of Pharmacotherapy 2002; 36: 1929-37. 80 [15] Steinberg KP. Str ess related mucosal disease in the critically ill patient: Risk factors and stra tegies to prevent stress-related bleeding in the intensive care unit. Critical C are Medicine 2002; 30 (Supplement): S362-64. 80 [16] Cash BD. Evidence based med icine as it applies to acid suppression in the hospitalised patient. Critical Ca re Medicine 2002; 30(Supplement): S373-78. 80 [17] Maclaren R, Jarvis CL, Fish D N. Use of enteral nutrition for stress ulcer prophylaxis. Annals of Pharmacother apy 2001; 35: 1614-23. [18] Fennerty MB, Pathophysiology of the upper gastrointe stinal tract in the critically ill patient: Rationale for the therapeutic bene ts of acid suppression. Critical Care Medicine 2002; 30 (Supplement) S531-55. [19] Raff T, Germann G, Hartmann B. The value of early enteral nutrition in the proph ylaxis of stress ulceration in the severely burned patient. Burns; 1997: 23:31318. [20] Tryba M. Sucralfate versus antacids or H2 antagonists for stress ulcer prophylaxis: A meta-analysis on ef cacy and pneumonia rate. Critical Care Medicine 1991; 19: 942-48. 81 [21] Mallow S, Rebuck JA, Osler T, et al. Do proton pump i nhibitors increase the incidence of nosocomial pneumonia and related infectious complications in critically ill trauma patients? Current surgery 2004; 61: 452-5 8. 81 GIT Stress Ulcer Prophylaxis Guideline for Critical Care Start Enteral feeding A SAP Ranitidine 50mg tds i.v. First line antacid prophylaxis Prescribe if enterna l feeding not established Omeprazole 40mg once daily i.v. For high risk groups: 82

References Burns victims Major trauma Acute brain injury Patients with history o f PUD / GORD Patients already on PPI pre Critical care admission. References Patients admitted post endoscopy with proven ulcer will need Omeprazole infusion as per Trust protocol On a daily basis check: Is possible to start enteral feed ing? If not why not? Need for prokinetic? Need for N/J tube? Review prescription chart Take advice from Critical Care Dietician Involve the Nutritional Support team Not indicated in enterally fed patients, even at low volumes, unless the pa tient is known to have pre-existing or subsequently (in-hospital) proven peptic ulceration. Consider use of a prophylactic agent (ranitidine 50 mg IVI 8 hrly) i f patient is not enterally fed and: Pre-existing or intercurrent coagulopathy Me chanical ventilation > 48hrs 3.10.2 Active GI Bleeding 3.10.2.1 Diagnosis Revealed blood: Nasogastric blood, haematemesis, malaena A fall in systolic blood pressure > 20 mmHg Drop in Hb > 2 0 g.L-1 in 24 hours, or requiring transfusion of blood 3.10.2.2 Management ABC / resuscitate Correct coagulopathy/cease heparin Omepraz ole40-80 mg IVI 12-8 hrly, consider oral/nasogastric once stable. Endoscopy scle rotherapy/colonoscopy/angiography and attempted vessel embolism if clinically ap propriate. 83

3.11 ICU Antibiotic Guidelines References 3.10.3 Use of gastro-intestinal pro-kinetic agents 3.10.3.1 General Gastric stas is, colonic and small intestinal ileus are common management problems in the intensive care unit. It may be necessary to explore jejunal feeding tube placement and or the use of prokinetic agents to facilitate entera l feeding (see algorithm on enteral feeding). 3.10.3.2 Contra-indications Erythromycin interacts signi cantly with other drugs metabolised by the Cytochrome P450 enzyme system, with potentially lethal side effects (eg. arrhythmia). Potential drug interactions must be reviewed prior to commencing th ese medications. 3.11 ICU Antibiotic Guidelines 3.11.1 Prologue Emerging bacterial resistance is one of the major challenges fac ing modern intensive care. It is the duty of all members of staff to actively pa rticipate in the appropriate use of anti-microbials, while adopting proven infec tion control behaviour. 3.11.2 Introduction This section cannot be a comprehensive guide, but should aid staff as to the unit preferences in antibiotic prescribing practice. Junior sta ff may not prescribe or change antibiotics without prior discussion with the Int ensivist or the Consultant Microbiologist. All antibiotic charting must be revie wed daily. The unit microbiological results must be reviewed daily and recorded in the patient notes. All suggested drug dosages (magnitude and frequency) given in this section are intended for the general population, with normal renal func tion. When prescribing drugs in the elderly, and any patients with signi cant rena l or hepatic insuf ciency, you must allow for modi ed drug handling. 3.11.3 Principles of prescription 3.11.3.1 Prophylaxis General Prophylactic antimicrobial therapy should be restricted to situations in which it has been shown to be effective, or where the consequences of infection are disastrous. Antimicrobials should be directed against likely causative orga nisms, however it is not rational to attempt to cover all possible microbes. 84

4 FLUIDS AND ELECTROLYTES Timing Antibiotics for the purpose of prophylaxis should be administered at the time of anaesthetic induction, and to cover the period of surgery and / or micro be implantation. A second dose of antibiotic may be warranted if the operation c ontinues beyond one half of the normal dosing interval for the agent being used. There may be some evidence in speci c types of surgery (eg. vascular surgery) for extending prophylactic cover beyond the immediate operative period, however in general there is little evidence to support such a practice. Preferred antibiotics Please con rm antibiotic choice and duration with each individual surgeon at the time of admission of the patient to the Intensive Care Unit. The antibiotic choices given below would constitute a rational approach, however it is generally not the role of the ICU staff to direct surgical choice of agent or duration of prophylaxis. 3.11.3.2 Complications of antibiotic use Drug hypersensitivity: Dermal eruptions , anaphylactoid/anaphylactic reactions Drug toxicity: Idiosyncratic (non-dose re lated) or dose related. Flucloxacillin-hepatotoxicity Aminoglycoside-renal toxic ity Emergence of bacterial resistance Selection of nosocomial colonising organis ms (and potential pathogens) Pseudomembranous colitis 4 Fluids and Electrolytes 4.1 Principles of Fluid Management in Intensive Care 4.1.1 Fluid charting 4.1.1.1 Prologue All uid prescriptions must be reviewed dail y. Non-standard / bolus uid orders must be charted individually Fluid orders shou ld be considered in two components 4.1.1.2 Maintenance or replacement uids Daily total uid administration including e nteral feeding = 30-40 ml.kg-1 day-1 or 80-100 ml.hr-1 , selected according to p atient serum Sodium and/or glucose tolerance + additional uid tailored to excessi ve losses where appropriate. 4% dextrose and one 5th normal saline 85

4.1 Principles of Fluid Management in Intensive Care 4 FLUIDS AND ELECTROLYTES 5% dextrose Patients who are anuric or ive maintenance uids. 4.1.1.3 Resuscitation uids The intensive care community is divided on the relative suitability of each uid in the resuscitation of a critically ill patient. In general if crystalloid (0.9% saline or Hartmanns solution) is chosen in the rst instance, no more than 2000 ml should be administered, followed by colloid. Fluid boluses should optimally be titrated against a measurable end-point, although most in c urrent use are at best imperfect. 4.1.2 Assessment of uid balance and hydration 4.1.2.1 Clinical markers Skin turgo r, mucous membrane hydration (poor indicator) Heart rate and blood pressure Peri pheral perfusion, capillary re ll Biochemical markers Serum Na+ , Cl- , osmolality Urea/creatinine Bicarbonate Haematocrit Charted uid balance - at best a rough gu ide Charted intake (Charted losses of all types + Insensible losses) 4.1.2.2 Predictors of increased cardiac output in response to administration of u id JVP / CVP: Useful in patients with normal lungs and right heart function. In other patients a trend in pressures may be useful. Pulmonary artery pressures (p articularly diastolic), and pulmonary capillary pressure. At best these are poor ly related to a response to further uid (pre-load), and are not widely employed i n Mid Yorks ICUs. PiCCO derived estimates of intra-thoracic blood volume and ext ra vascular lung water. Variation in arterial wave form peak with positive press ure ventilatory cycle. This is a notoriously dif cult aspect of critical care prac tice. Often the decision to administer uid is governed by a conglomeration of eac h of the following. If you are in any doubt consult the senio Anaesthetist, but do not delay the administration of uid in the acute resuscitation phase. 86 uid overloaded should not necessarily rece

4 FLUIDS AND ELECTROLYTES 4.2 Electrolyte Abnormalities 4.1.3 Body Fluid and Electrolyte Physiology A working knowledge of the distribut ion of uid and electrolytes throughout the body is required before any rational p rescribing process can begin. What follows are salient notes on uid and electroly te distribution, and some of the more common disorders encountered in the intens ive care setting. 4.1.3.1 Determinants of solute movement and concentration Passive transport mechanisms Diffusion: movement of a solute from an area of hig her concentration to one of lower Non-ionic diffusion Gibbs-Donnan effect: The u nequal distribution of diffusible ions on either side of a membrane can be expla ined if one side contains a poorly diffusible ion (eg. albumin-anion), since at equilibrium: The product of the diffusible ions in one compartment will equal th e product of the same ions in the other compartment. Within each compartment the total cationic charges equal the total anionic chargeselectrical neutrality mus t be maintained in passive systems. Active transport mechanisms Energy requiring mechanisms which distribute a subst ance across a membrane, in a manner not achievable by physical forces alone. The se are essential for establishing electrical and ionic differences across membra nes, the basis for tissue excitability and other fundamental functions of the bo dy. 4.2 Electrolyte Abnormalities 4.2.1 Approach Electrolyte derangement should be viewed as resulting from one of the following. Erroneous results: Lab error Haemolysed specimen Factitious resu lts: eg hyperglycaemia and hyponatraemia; lipaemic serum. Blood taken in proximi ty to an intravenous infusion Decreased or increased intake Decreased or increas ed loss (renal versus extra-renal) Shifts between compartments: eg potassium dri ven intra-cellularly by insulin. 87

4.2 Electrolyte Abnormalities 4 FLUIDS AND ELECTROLYTES Treatment of electrolyte disturbance should be aimed at not only the apparent pr oblem but also the underlying cause. Consideration should be given to the conseq uences of rapid correction of measured plasma electrolyte imbalances, particular ly the longstanding and chronic forms, where there may have been some intracellu lar accommodation. 4.2.2 Hyponatraemia: Na+ < 130 mmol.L-1 4.2.2.1 Aetiology Factitious Measured plasma osmolarity > 290 mmol.L-1 : Hyponatraemia in hypergly caemia: For every 10 mmol.L-1 increase in glucose, serum sodium falls 3 mmol.L-1 . It is in a sense a real hyponatraemia, however treatment aimed at correcting the blood glucose will resolve the hyponatraemia. Mannitol: not usually a clinic al issue, however later diuresis and hypernatraemia may be. Alcohol (including m ethanol) Measured plasma osmolarity 270-290 mmol.L-1 Hyperlipidaemia Hyperprotei naemia Neither of the above should be a problem with current ion-speci c electrode s. Measured plasma osmolarity < 270 mmol.L-1 Renal diuretics Addisons Polyuric r enal failure or diuretic recovery phase of renal dysfunction Extra-renal GIT los s Burns Hypervolaemia (water excess) Renal failure: acute or chronic Extra-renal Excessive intake (IVI 5% dextrose) Oedematous states: CCF, cirrhosis, nephrotic syndrome, hypoalbuminaemia. Normovolaemia Hypovolaemia with Sodium depletion 88

4 FLUIDS AND ELECTROLYTES Psychogenic polydipsia SIADH Hypothyroidism Acute adrena l insuf ciency 4.2 Electrolyte Abnormalities 4.2.2.2 Management of Severe Hyponatraemia with tting or decreased LOC Resuscitat ive measures and ABC principles should not be delayed. Hypertonic saline (3, 20, 29% ) may be indicated but should not be used without prior discussion with the Consultant Intensivist, unless the patient is actively tting. Hypertonic saline is very irritant and is best administered via central venous access where time a llows. An infusion of 50-70 mmol.hr-1 of sodium should increase the serum sodium by approximately 2 mmol.L-1 hour-1 . The serum sodium should not be allowed to increase more than 20 mmol.L-1 in the rst 24 hours, and certainly should not be o vercorrected (serum sodium > 130 mmol.L-1 ). In very rare circumstances where tti ng or encephalopathy are life threatening, 500 ml of 20% mannitol has been used. Hypovolaemic states Restore volume with normal saline or colloid according to clinical estimate ( uid balance, weight, JVP, CVP). Urine Sodium may be misleading in the c ontext of diuretic administration or use of catecholamines. Hypervolaemic states-most common scenario clinically Fluid restriction if safe t o do so ( < 15 ml.kg-1 day-1 ) Excess should correct as ADH levels re-set (often ADH post surgery) Address underlying cause (cardiac failure etc) SIADH-often misdiagnosed Low serum osmolarity Diagnosis: Urine osmolarity > plasma osmolarity Urine Sodium > 40 mmol.L-1 with normal rena l, hepatic and cardiac function, and no diuretic use. Management: Fluid restrict ion ( < 1000 ml / day) 4.2.3 Hypernatraemia: Na+ > 145 mmol.L-1 Aetiology 89

4.2 Electrolyte Abnormalities 4 FLUIDS AND ELECTROLYTES Water depletion Virtually all body uids have a Sodium concentration less than tha t of plasma Renal loss Diuretics or osmotic diuresis ARF / CRF Diabetes insipidu s: * Neurogenic (including Guillain-Barre) * Nephrogenic: Hypercalcaemia, hypoka laemia, drug related (lithium), congenital GIT losses: diarrhoea, vomiting stulae , small bowel obstruction Skin losses: fever, vasodilated states, burns, thyroto xicosis Inappropriate uid restriction or under administration (elderly, post oper ative nil by mouth) Salt gain Iatrogenic administration of Sodium containing feed or IVI uids. Minera locorticoid excess Management Water depletion / hypovolaemia Resuscitate if necessary Restore volume over 24-28 hrs using a relatively hyponatraemic uid (half normal s aline or 5% dextrose), if necessary a rough estimate of uid de cit can be calculate d: Water de cit = (measured serum Na+ )140 body weight0.6 140 e.g. a 70kg male with a serum sodium of 160 mmol.L-1 might be expected to have a uid de cit of 6 litres. Do not correct Sodium by more than 2 mmol.hr-1 . Consider DDAVP if central diabetes insipidus has been con rmed. Excess salt intake Address cause 4.2.4 Hypokalaemia: K+ < 3.5 mmol.L-1 4.2.4.1 Aetiology/classi cation Increased lo ss Renal 90

4 FLUIDS AND ELECTROLYTES Diuretics serum Magnesium, serum Calcium Steroids and min eralocorticoid excess Renal tubular acidoses 4.2 Electrolyte Abnormalities GIT: diarrhoea, hypersecretory states (villous adenoma, small bowel stulae) Inade quate dietary intake or daily administration Transcellular shifts: stimulnts (c atecholamines, salbutamol) Insulin (endogenous or exogenous) Familial periodic p aralysis and related syndromes (consider thyrotoxic states). pH 4.2.4.2 Management Potassium replacement intravenously or orally. Intravenous replacement should not exceed 40 mmol.hr-1 , concentrated solutions should be administered centrally and the patient carefully monitored. Concentrat ed solutions should not be administered peripherally. Address cause of K+ loss. A low threshold should be adopted for co-administration of magnesium as an essen tial cofactor in Na+ -K+ pumps. Patients who are magnesium de cient will remain hy pokalaemic despite generous administration of potassium. 4.2.5 Hyperkalaemia: K+ > 5.0 mmolL-1 4.2.5.1 Aetiology/classi cation Factitious S ampling in proximity to venous infusion Haemolysis: i.e. collection using vacuum tube systems (venous sampling via vacutainer with narrow gauge needle) Extremes of thrombocytosis and leukocytosis. Release from intra-cellular compartments: A cidosis: pH by 0.1 serum K+ by 0.5 mmol.L-1 . = Tissue disruption: tumour lysis s yndromes, rhabdomyolysis, intravascular haemolysis, burns Suxamethonium (note: s ee section on drugs for intubation 2.6.1.3) Insulin de ciency: the hyperkalaemia ass ociated with diabetic ketoacidotic states is related to lack of insulin and a ch ange in serum pH but is usually associated with a total body potassium de cit. 91

4.2 Electrolyte Abnormalities 4 FLUIDS AND ELECTROLYTES Increased intake: Not usually a problem unless patient has impaired renal functi on. Reduced potassium clearance: Acute renal failure Renal tubular acidosis: typ e 4 Potassium sparing diuretics: spironolactone, amiloride 4.2.5.2 Management Patients with a slow rise in serum potassium usually tolerate elevated levels better than following an acute rise. Where elevated serum potassium (generally > 6.0 mmol.L-1 ) is associated with acute ECG changes or haemodynami c compromise this should be considered a medical emergency and treated as follow s: Calcium Chloride 10 ml IVI stat, repeated in 20 minutes if appropriate. Membr ane stabilisation. First line action. Has no effect on serum potassium concentra tion. Insulin Bolus: 10 units actrapid equivalent insulin with 50 ml 50% dextros e infusion OR 20 units of actrapid insulin in 500 ml 10% dextrose over 30-60 min . Intracellular transfer of potassium. Temporising measure. Probable decrease in serum potassium concentration of 1 mmol/L for 30-60 minutes with some effect up to 3 hours (either method) Calcium and a dextrose-insulin preparation are appro priate measures to institute in the short term, pending use of de nitive treatment (eg. resuscitation, exchange resin, or haemodialysis). Bicarbonate bolus equiva lent to 50-100 mmol. Promotes cellular uptake of potassium by reducing hydrogenpotassium exchange. Temporising measure only. Do not administer with Calcium sal ts. Not appropriate in hypovolaemic acidotic patients. Exchange resins: resonium sodium (or Calcium) resonium 30-60g orally or rectally 8 hourly. Sometimes give n with lactulose 20ml. Exchanges K+ for alternative cation in gut, therefore act ion delayed for > 120 minutes. De nitive but delayed treatment. May be dif cult to a dminister in ICU patients with abnormal gut motility. 2 stimulants: Nebuliser: 1 0-20 mg by nebuliser over 10 minutes. IVI: 0.5 mg IVI over 10-15 minutes. Intracellular transfer of potassium. Temporising agent although concern exists over t he use of an arrhythmogenic agent in the critically ill. 4.2.6 Hypophosphataemia: Serum Phosphate < 0.7 mmol.L-1 Low serum phosphate is a ssociated with serious clinical consequences, and is probably underappreciated i n critically ill patients. Some studies suggest an incidence of up to a third of all ICU patients may be phosphate de cient. 4.2.6.1 Aetiology 92

4 FLUIDS AND ELECTROLYTES Inadequate input 4.3 Acid-Base Disturbances in the ICU GIT phosphate binders (eg. laxatives, antacids) Starvation Vomiting or nasogastr ic suctioning Relative or absolute Vit D de ciency Transcellular shifts Carbohydra te loading, re-feeding phenomenon. Drugs: Insulin, catecholamines, steroids, ?2agonists Excessive losses Massive diuresis Dialysis, including continuous replac ement modalities. 4.2.6.2 Clinical effects All energy requiring processes may be involved. Cardiac: Decreased contractility. Respiratory: Failure to wean. Muscle / bone: M yopathy, Rhabdomyolysis, Osteomalacia. Haematological: Dysfunction of all formed elements of blood. Renal: Acute tubular necrosis. 4.2.6.3 Phosphate replacement >0.7mmol.L-1 0.16 mmol.kg-1 over 4-6 hrs 0.5-0.7mm ol.L-1 0.32 mmol-1 kg over 4-6hrs <0.5mmol.L-1 0.64 mmol.kg-1 over 8-12hrs. 4.3 Acid-Base Disturbances in the ICU 4.3.1 Introduction Critically ill patients commonly have a deranged acid base st atus. Despite this, explanations of the physiology behind the process are not un iversally accepted. It is necessary to have an approach to the clinical importan ce of each of the common major abnormalities, even given the complex and often m ixed scenarios you might encounter. You are encouraged to read widely on the sub ject of acid-base disorders and the opposing ideologies put forward to explain t hem. Correction of acid-base disturbance should be aimed at the underlying cause , and not at correction of the super cial abnormality. 93

4.3 Acid-Base Disturbances in the ICU 4 FLUIDS AND ELECTROLYTES 4.3.2 General principles The concept of pH: pH = negative log of the hydrogen io n concentration. Normal range = 7.36 -7.40 4.3.2.1 Regulation of pH Without regulation of acid-base, the daily production o f nonvolatile H+ in a normal person (about 70 mmol) would reduce the pH in a vol ume of water similar to that of a 70kg man (42 L) from 7.4 to a pH of 2.78. The human body is an open system in which other organ systems and tissues contribute to the maintenance of the free [H+ ] within a narrow, biologically tolerable ra nge. Henderson Equation: [H+] = K CO2 [HCO3 ] Henderson/Hasselbach Equation: pH = 6.1 + log [HCO3 ] Pa CO2 0.03 From both the above it is clear that any mechanism responsible for regulating or affecting pH does so by changing the relative concentrations of HCO- , PaCO2 or H+ directly. 3 The response of the body to an enforced change in one of these parameters take s place in three broad groups: Adjusting minute ventilation (increasing respirat ory rate or tidal volume) to manipulate PaCO2 Buffering systems: Bicarbonate ion Haemoglobin Protein substrates Phosphate Renal compensation: delayed > 6-12hrs Primary and secondary acid-base derangements End point: constant PCO2 : HCO3 ratio Respiratory acidosis Primary change: PCO2 Compensatory change: HCO3 Respiratory alkalosis Primary change: PCO2 Compensatory change: HCO3 Metabolic acidosis Pri mary change: HCO3 94

4 FLUIDS AND ELECTROLYTES Compensatory change: PCO2 Metabolic alkalosis Primary ch ange: HCO3 Compensatory change: PCO2 4.3 Acid-Base Disturbances in the ICU Compensatory changes are never complete, and certainly overcompensation does not occur. Adequacy of compensation The expected magnitude of compensation for a pr imary abnormality is given below. In critically ill or ventilated patients this compensation may not be possible, presenting as a mixed or complex problem. 4.3.3 Metabolic Acidosis 4.3.3.1 The anion gap Classically metabolic acidoses ar e classi ed according to the concept of anion gap. Whilst the body must maintain overall electrical neutrality t here are a number of unmeasured ions which result in a difference when the major cations are compared to the major anions. ie. Anion Gap = [Na+ + K+ ]-[Cl- + HC O- ] = 12-17 mmol.L-1 = unmeasured anions 3 Unmeasured anions Proteins (albumin) 15 mmol.L-1 Organic acids (lactate, ketones) 5 mmol.L-1 Phosphates 2 mmol.L-1 S ulphates 1 mmol.L-1 Unmeasured cations Calcium 2.5 mmol.L-1 Magnesium 1.2 mmol.L-1 IgG Other An incr ease in anion gap usually means an increase in an organic acid. In some patients with low serum albumin this may be masked unless you adjust accordingly. 4.3.3.2 Aetiology Raised anion gap metabolic acidosis Lactic acidosis Ketoacidosis 95

4.3 Acid-Base Disturbances in the ICU 4 FLUIDS AND ELECTROLYTES Rhabdomyolysis Drugs or toxins: Aspirin (may result in elevated salicylate, lact ate, ketones Ethanol Methanol Ethylene glycol Paraldehyde Renal failure: usually only mildly elevated anion gap ( < 23) Low or normal anion gap acidosis Hyperchloraemic metabolic acidosis: Infusion IV I of NaCl Resolving renal failure Renal tubular acidosis / carbonic anhydrase in hibitors GIT losses including stulae Hypoalbuminaemia Myeloma 4.3.3.3 Management High anion gap Address cause. Bicarbonate administration is not indicated Normal anion gap bicarbonate directly. Address underlying cause. In some situations (eg. renal tubular acidosis) it may be appropriate to replace / administer Approx de cit = (24-[HCO- ]) (body weight 0.6) in mmol. 3 Generally one third to one half of the estimated de cit should be replaced and then acid-bas e status reviewed. 4.3.4 Metabolic Alkalosis 4.3.4.1 Aetiology Common causes Diuretics Vomiting 96

4 FLUIDS AND ELECTROLYTES Post hypercapnoea > 48 hrs 4.3 Acid-Base Disturbances in the ICU Any uid loss replaced with insuf cient Na+ , associated with H+ loss (contraction a lkalosis). Association with hypovolaemia and / or hypokalaemia H+ /Proton loss R enal Na+ reabsorption Cushings syndrome including exogenous steroid administrati on Proximal tubulopathies: Bartters syndrome, Liddles syndrome Hypercalcaemia / hypomagnesaemia associated with diabetes insipidus Diuretics GIT NG suctioning o r protracted vomiting Diarrhoea (acidosis more likely) Increased administration of bases CVVHDF-lactate buffered solution 4.3.4.2 Management Correct hypovolaemia and electrolyte abnormalities. Review drugs, and administration of exogenous bases (lactate buffered dialysate, citrate). Ace tazolamide has been used to increase renal losses of bicarbonate, however this s hould not be considered routine practice. 4.3.5 Respiratory Acidosis 4.3.5.1 Aetiology Any cause of hypoventilation, wheth er respiratory failure or planned (permissive hypercapnoea ventilation). 4.3.5.2 Treatment Address underlying respiratory pathology 4.3.6 Respiratory Alkalosis 4.3.6.1 Aetiology Any cause of hyperventilation in I CU eg. early sepsis Early hypoxic situations Anxiety Hysteria (NB this is a diag nosis by exclusion, and presumes normal oxygenation) Neurogenic hyperventilation : usually a marker of severity of head injury. 97

4.4 Nutrition Treat underlying problem. 4 FLUIDS AND ELECTROLYTES 4.3.6.2 Treatment 4.4 Nutrition 4.4.1 Enteral Nutrition The prevalence of malnutrition is increasing in hospital ised patients due to the aging process of the general population and the develop ment of aggressive medical and surgical treatments for chronic debilitating dise ases. The positive consequences of enteral feeding however may go beyond nutriti on and extend to immune modulation, and possibly bacterial translocation through the gut. Enteric feeding is the preferred mode of nutritional support and shoul d be considered in all patients admitted to the ICU. 4.4.1.1 Advantages In some patient subgroups (trauma) early enteral feeding impr oves patient outcome. Enteral feeding helps retain gut integrity and reduce atro phic changes. May reduce the incidence of gastric erosions and stress ulceration Cost effective: Cheaper than TPN (2p.day-1 vs 80.day-1 )! Complications of centr al access for TPN are reduced (invasive procedures, infective risk) 4.4.1.2 Disadvantages Regurgitation / aspiration (no difference gastric versus d istal feeding) Diarrhoea: diarrhoea may be a result of osmotic load to the gut, however it is not the most likely reason for diarrhoea in critically ill patient s, and other causes should be sought and excluded. 4.4.1.3 Indications enteral feeding. All ICU patients with a secure airway and functioning gut may receive Patients admitted post surgical intervention should have the intention to feed c leared with the surgeon in charge. Patients with operatively placed jejunostomy may commence feeding within 6 hours of placement (again, confer with the surgeon ). Where gastric feeding has not been established by day 5 of ICU admission (or earlier if undernourished), a post-pyloric (duodenal / jejunal) tube should be c onsidered for distal feeding. Use of hypercaloric feeds may be considered to ens ure reasonable intake. Consider placing a ne bore feeding tube, to reduce irritat ion and ulceration, once feeding has been established for a reasonable length of time (5-7 days). 98

4 FLUIDS AND ELECTROLYTES 4.4 Nutrition 4.4.1.4 Contra-indications Absolute Non-functional gut: anatomical disruption, o bstruction, gut ischaemia Generalised peritonitis Severe shock states Relative E xpected short period of fasting (except trauma patients) Abdominal distension wh ile feeding enterically Localised peritonitis, intra-abdominal abscess, severe p ancreatitis Comatose patients at risk of aspiration Extremely short bowel ( < 30 cm) 4.4.1.5 Feeding Guideline Place a 12F or larger nasogastric tube to allow r eliable aspiration (orogastric tube should be considered in patients with anteri or and middle cranial fossa trauma). Check position of feeding tube with abdo Xray prior to feeding. It may not be obvious from standard CXR or AXR that the tu be is adequately placed, requiring a modi ed lm or both views. Nurse the patient at 30-45 degrees head up. Commence feeds at 30 ml/hr and feed continuously accordi ng to the attached protocol. Aspirate the tube 4 hrly (do not attempt routine as piration of jejunostomies, naso-duodenal or naso-jejunal tubes. Flush jejunostom y or gastrostomy tubes with 10-20 ml of saline 6 hourly if not being used. 4.4.1 .6 Prokinetics: If feeding is persistently not tolerated > 48hrs then consider Reduction in narcotic dosage Use of a prokinetic agent: metoclopramide 10 mg IVI 6 hrly, then if necessary erythromycin 70 mg mg IVI od. Post-pyloric feeding 4. 4.1.7 Choice of enteral feed (see appendix for enteral feed content) Most patients should be commenced on a standard isocaloric feed such as Osmolyte (standard) Nutritional supplementation should be adjusted to provide approximat ely 20-35 kCal.kg-1 .day-1 of non protein energy, and 1.5 g.kg-1 body weight of protein per day. Immuno-forti ed feed (with glutamine, arginine, nucleotides, omeg a-3-fatty acids) have shown some bene t in small studies to date. Their use is acc epted to be of bene t in polytrauma patients. Despite this there is as yet no de ned place for these feed types in the ICU setting 99

4.4 Nutrition 4 FLUIDS AND ELECTROLYTES Figure 1: Enteral Feeding Agorithm 100

4 FLUIDS AND ELECTROLYTES 4.4 Nutrition 4.4.2 Parenteral Nutrition 4.4.2.1 General Historical attempts at hyper-alimenta tion may have resulted in the role of TPN in the ICU diminishing over the last 10 20 years. Concerns still exist ov er potential immuno-suppression, hyperglycaemia and the infection risk coupled w ith central venous access. TPN should not be ordered unless requested by the Con sultant Intensivist. 4.4.2.2 Indications Total parenteral nutrition should only be considered in pati ents who are not suitable for enteric feeding. Short term: No oral intake likely > 2 weeks Weight loss > 10 % starting body weight Long term: Structural or func tional short bowel syndrome 4.4.2.3 Vascular access peripheral IV nutrition. TPN is generally administered by central venous access. Where duration of TPN is envisaged to be less than 2 weeks it may be acceptable to consider 4.4.2.4 Complications Depression of immune function Gut villous atrophy Metaboli c imbalance: Electrolyte disturbance Glucose intolerance Hyperosmolar dehydratio n syndrome Rebound hypoglycaemia on ceasing TPN Hyperbilirubinaemia Fluid imbala nce Trace element and vitamin de ciency Complications of central venous access. 4.4.2.5 Charting TPN Choice of formula 101

4.5 Blood and Blood Products 4 FLUIDS AND ELECTROLYTES 4.5 Blood and Blood Products 4.5.1 Introduction The decision to transfuse a patient, or administer other bloo d products, is the prerogative of the Consultant Intensivist. Whenever reasonabl e, the patients informed consent to proceed with transfusion should be obtained. 4.5.2 Blood transfusion 4.5.2.1 Acute resuscitation Excessive ongoing haemorrhag e is usually surgical in origin. In these circumstances transfusing blood products should be viewed as a bridging procedure until de nitive treatment is undertaken. Platelet count and coagulation s studies should be performed, and if abnormal addressed as required. Blood repl acement in an otherwise t patient should be considered once blood loss is anticip ated to exceed 25% of total blood volume (or 1000-1500ml). A full cross match ma y take up to 20 minutes, if blood is required faster than this consider one of t he following: Group speci c (ABO, Rh+) blood without full compatibility testing ma y be available faster (5-10 minutes). O negative blood can be issued immediately in a true emergency, while similarly O positive blood can be used for men, or w omen past child bearing age. 4.5.2.2 Elective transfusion of 10 g.dL g.dL-1 . -1 Traditionally a haematocrit of 30% or absolute haemoglobin have been used as a trigger to transfuse a patient. In stable patients with adequate oxygenation there is no need to transfuse until Hb < 7.0 Critically ill patients with poor oxygenation, myocardial ischaemia, a cute head injury or ongoing risk of blood loss may require earlier transfusion. 4.5.3 Platelet transfusion 4.5.3.1 Indications being issued. Spontaneous haemorr hage is rare at platelet counts of > 10 109 .L-1 (or > 20 109 .L-1 in febrile patie nts) Prophylactic transfusion before surgery or invasive procedure: Platelet cou nt < 50 109 .L-1 Permission may have to be sought from a Haematologist prior to p latelets 102

4 FLUIDS AND ELECTROLYTES 4.5 Blood and Blood Products Platelet count > 50 109 .L-1 where there is evidence of abnormal platelet functio n (eg. uraemia, aspirin therapy) Uncontrolled haemorrhage: Transfuse platelets a t platelet count < 100 109 .L-1 Consider transfusing platelets at any threshold i f there is reason to suspect platelet dysfunction. Bone Marrow failure, TTP ,ITP , or H.I.T.S. Seek advice from haematology team. Seek input from haematology tea m. 4.5.3.2 Dosing of platelets One dose of platelets usually means pooled donor pla telets from 4 or more donors. One dose approximates 3-3.5 1011 platelets, or eno ugh to increase the platelet count by 20-25 109 .L-1 at 24 hours, in the absence of further problems. 4.5.3.3 Risk of transfusion In general the risk is similar to that for blood tra nsfusion with the following addition: There is a higher risk of bacterial contam ination than whole blood (0.6 / 1000 cases per dose) HLA allo-immunisation may o ccur in 45-62% of long term recipients, resulting in transfusion resistant throm bocytopaenia. Platelet speci c antibodies may develop (4% of patients) 4.5.3.4 Adjunctive treatment Administration of DDAVP 0.3-0.4 g.kg-1 over 30 minutes may increase levels of factor VIII:C and VIII:vWF with increased platelet adhesi on. Indication Haemophilia A, type I von Willebrands Disease. Bleeding post cardio-p ulmonary bypass Uraemia Platelet dysfunction secondary to aspirin Other scenario s where platelet dysfunction is suspected and platelet transfusion might be dela yed, or stock exhausted. 4.5.4 Fresh Frozen Plasma 4.5.4.1 Indications Prophylactic transfusion prior to surgery or other invasive procedure 103

4.5 Blood and Blood Products 4 FLUIDS AND ELECTROLYTES Patients on warfarin ro vit K de ciency: consider partial reversal with 1 mg Vit K or full reversal with 10 mg Vit K if time allows (24-36hrs). Prolonged INR or A PTT in patients with liver disease Inherited coagulation factor de ciency when fac tor concentrates not available. Uncontrolled haemorrhage Warfarin or Vit K de cien cy Prolonged INR or APTT in patients with liver disease Inherited coagulation fa ctor de ciency when factor concentrates not available DIC Massive transfusion: Con sider administering Calcium as citrated stored blood is Calcium de cient, retardin g the clotting cascade. Whole stored blood does not contain clotting factors in any appreciable number Consider transfusion when INR > 1.5 or APTT > 40 seconds. Plasma exchange in TTP and related syndromes. 10-15 ml.kg-1 (average 2-4 units) according to clotting pro le. 4.5.4.2 Dosing of FFP 4.5.4.3 FFP in the setting of heparin overdose Protamine is the drug of choice f or reversing excessive unfractionated heparin effect. Protamine is not effective in the setting of Low Molecular Weight Heparin, and it may be tempting to admin ister FFP. Theoretically this carries the risk of potentiating bleeding by furth er increasing ATIII availability. 4.5.5 Cryoprecipitate 4.5.5.1 Indications Diffuse microvascular bleeding and ogen < 1.0 g.L-1 DIC Massive transfusion Hereditary hypo brinogenaemia 4.5.5.2 Dose by 1.0 g.L -1 Ten units of cryoprecipitate would be expected to increase plasma brinogen brin

4.5.6 DIC De nition: A process representing disordered balance of the haemostatic and brinolytic systems, usually in response to severe pathophysiological stimuli as part of multisystem organ dysfunction. 104

4 FLUIDS AND ELECTROLYTES 4.5 Blood and Blood Products Characterised by: Microthrombi formation causing microvascular obstruction Consu mption of platelets and clotting factors Thrombocytopaenia 4.5.6.1 Diagnosis-DIC screen Blood smear examination for evidence of red cell fr agmentation, haemolysis, thrombocytopaenia. Extended coagulation screen: Prolong ation of thrombin clotting time, APTT, Prothrombin time. Hypo brinoginaemia Low fa ctor VIII Elevated brin breakdown products (FDPs). Liver function tests and renal function review. 4.5.6.2 Treatment bleeding. Treat the underlying cause! Replace blood components as assessed by above DIC screen if patient bleeding or at risk of 4.5.6.3 Controversial therapies Heparin, brinolytics, anti brinolytics (aminocaproic acid) and other agents have been described in the literature. They do not form part of standard therapy and should not be attempted without ICU consultant approval, a nd not before exhausting other therapies at the advice of the haematology specia lty service. 4.5.7 Blood transfusion reaction guidelines 4.5.7.1 Introduction products. The r esponse to a suspected reaction depends on the urgency of the transfusion and th e magnitude of the adverse reaction. A wide range of reactions can be manifest u pon infusion of blood 4.5.7.2 Suspected transfusion reaction Stop the infusion and check the patient d etails against that of the blood product. If there is any discrepancy then disco ntinue the transfusion. If patient and product details are correct then proceed as follows. Mild reactions Temperature rise < 1.5o C without hives, rash, bronch ospasm or cardiovascular compromise: restart transfusion at slower rate. Moderat e reactions 105

5 CLINICAL MANAGEMENT If temperature rise > 1.5o C with other manifestations, administer antipyretic ( paracetamol 1g) and restart transfusion of the same unit after 20 minutes. Sever e reactions If any signs or symptoms in addition to temperature rise, discontinu e the transfusion and return the blood product to blood bank for re-crossmatch a nd culture. Treat as for anaphylaxis: Volume resuscitation Adrenaline or vasopre ssor as necessary. Bronchodilators if signi cant airway out ow obstruction. Adjuncts : anti-histamine, theophylline, corticosteroids may not be appropriate in ICU po pulation and should be discussed with the Consultant. 5 Clinical Management 5.1 Introduction The purpose of this chapter is not to dictate rigid policies on the most appropr iate way to manage every patient. Rather it is to provide guidelines on reasonab le clinical practice based on the available evidence and where that is lacking, based on consensus practice. As you will come to realise during your stay in the ICU very few patients read the appropriate textbooks prior to becoming ill. Pat ients therefore may not behave in a classical or expected manner. It is in these patients that these guidelines may help you to adopt a reasonable and standardi sed approach. 5.2 Cardio-Pulmonary Resuscitation 5.2.0.3 Introduction It is clearly beyond the scope of this document to outline the skills, knowledge and algorithms required to implement advanced cardiac life support. Wh ilst we have little control at present over community cardiac arrests, and to a lesser extent hospital cardiac arrest, it must be stressed that vigilance and pr o-active management of critically ill patients may abort a process precipitating a cardiac arrest within the ICU. For ease of referral the combined basic life s upport and Advanced Cardiac Life Support Algorithm appear below. Please refer to the appendix ACLS Algorithms for a more comprehensive list. 5.2.1 Key Points in the management plan for an adult collapse In adult cardiac a rrest, VF / VT is the most likely rhythm, and a de brillator the only effective tr eatment. 106

5 CLINICAL MANAGEMENT 5.2 Cardio-Pulmonary Resuscitation Start effective CPR as soon after the circulatory arrest as possible. Effective arti cial circulation requires controlled, uninterrupted chest compression. The ra tio of compressions to ventilation is 15:2 in all instances except when an ETT i s in place, when it is 5:1 with no compression pause. The rate of compression is 100 / min. As soon as possible (especially in unmonitored patient) switch the d e brillator on and check or con rm the rhythm via the paddles. De brillate as soon as possible. De brillation should take precedence over all other interventions. Asses s for, and shock, VF / pulseless VT, up to 3 times (200J, 200J to 300J, 360J or equivalent biphasic) if necessary. Endotracheal intubation, IV insertion and ECG electrode placement / replacement should occur between de brillation attempts. Th e order of priority for these adjuncts is secure airway ventilate with 100% oxyg en IV administration. Augmentation of aortic diastolic pressure should be an adj unctive goal of therapy since coronary perfusion is low during conventional CPR. Adrenaline and other alpha agonists will signi cantly increase aortic diastolic p ressure. Administer adrenaline to maintain coronary blood ow if the rst three de bri llations fail. 1 mg of adrenaline every 3 minutes is an acceptable minimum. Vaso pressin 40.i.u IV is a suitable alternative in VF/VT arrests. Consider and corre ct if possible any reversible causes of circulatory arrest. (see 5Hs and 5Ts on algorithm below) During CPR, adequate ventilation is the mainstay of therapy for acid-base abnormalities. The indications for Sodium Bicarbonate are: Hyperkalae mia Tricyclic antidepressant overdose where metabolic acidosis existed prior to arrest. Late in cardiac arrest situation (at least > 10 minutes) in intubated hy perventilated patients. If VT / VF persists after 9 de brillating shocks, give ami odarone 150 mg IVI. Give earlier if a de brillating shock seems transiently succes sful. 5.2.2 Induced hypothermia following cardiac arrest 5.2.2.1 Introduction Patients subjected to therapeutic hypothermia as soon as possible following resuscitation from cardiac arrest may have a better outcome (15-25% absol ute survival advantage). Following consultation with the Consultant Intensivist, short term hypothermia should be induced as below. 107

5.3 Respiratory Therapy Apply to patients with 5 CLINICAL MANAGEMENT 5.2.2.2 Patient selection Suspected hypoxic encephalopathy. Motor score of GCS 4 or less (ie or worse) exion to pain

5.2.2.3 Cooling guideline Cool as soon as possible following return of circulati on. Sedate with propofol and alfentanil, with intermittent muscle relaxant to ab late shivering if prominent Actively cool, using water cooled blanket to tempera ture target of 33 (32.5-33.5) o C for 12 hours, as measured with rectal temp pro be. After 12 hours actively re-warm to 37 degrees. Conduct sedative free neurolo gical assessment. Progress to somato-sensory evoked potentials if awakening slow or absent. 5.2.2.4 Rapid Cooling Rapid onset cooling can be achieved by administering 30ml.kg-1 of Ringers lactate or other crystalloid, cooled to 4 o C, over a 30 minute period. Do not attempt this method unless discussed with the Consultant. 5.3 Respiratory Therapy 5.3.1 Introduction Traditionally the major reason for referral to intensive care , respiratory failure and our understanding of how best to manage it is constant ly evolving. Recent advances in ventilatory strategy, and their impact on not on ly lung injury but also on other organ dysfunction, necessitates that all staff within the ICU acquire some understanding of the pathophysiology involved. While Registrars and residents are encouraged to understand the principles of ventila tion, and indeed participate in the management of ventilated patients; decisions regarding ventilation, weaning, extubation and other extra-ordinary actions (su ch as patient proning) remain the domain of the Consultant Intensivist. 5.3.2 Respiratory Failure De nition Failure of ef cient gas exchange. Either failure to oxygenate adequately, or failure to ventilate. 5.3.2.1 Failure to oyxygenate adequately FiO2 21% (ie. room air) PaO2 < 8 kPa under the following conditions: 108

5 CLINICAL MANAGEMENT Barometric Pressure 101 kPa (sea level) No intracardiac shun t 5.3 Respiratory Therapy NB: This does not mean taking a patient off oxygen to perform an arterial blood gas, but rather inferring the need for assistance as stated below. 5.3.2.2 Failure to ventilate adequately PaCO2 > 7 kPa, unless in the presence of a primary metabolic alkalosis (pH normal or elevated) 5.3.3 Aetiology Lung insult Pulmonary oedema (hydrostatic-cardiogenic, or leaky capillary-ARDS) Pneumonia Contusion Haemorrhage Airway pathology Proximal Distal : COAD, asthma, bronchiectasis, sputum retention Neuromuscular Depressant drugs Intra-cranial pathology Guillan Barr Myasthenia Gravis Skeletal Loss of chest wal l integrity: ail chest Loss of chest wall elasticity: severe kyphosis or scoliosi s Intra-thoracic space occupying lesion: Pneumo-/ Haemothorax, pleural effusions . 5.3.4 When Should I Consider Ventilating ( intubating) Patients? 5.3.4.1 Indicato rs Clinical assessment outweighs any result such as an ABG / CXR or other object ive measurement (see below) Consider institution of ventilation in the presence of: Threatened airway Fatigue or imminent exhaustion Inability to effectively co ugh or clear secretions Respiratory failure 109

5.3 Respiratory Therapy 5 CLINICAL MANAGEMENT 5.3.4.2 Objective measurements In the appropriate clinical setting, and where time allows a combination of the following may assist your decision. Resp rate > 35 bre aths per minute Tidal volume < 5 ml.kg-1 Vital capacity < 15 ml.kg-1 Abnormal ox ygenation as indicated by: PaO2 < 10 kPa on an FiO2 > 0.4 (40% O2 ) PaO2 to FiO2 ratio < 150 Abnormal ventilation as indicated by: PaCO2 > 8 kPa 5.3.5 Humidi cation 5.3.5.1 General an ICU stay. All patients that are intubated/t racheostomised must have adequate humidi cation of inspired gases using one of two mechanisms Poor conditioning of the temperature and humidity of inspired gases leads to airway damage, sputum plugging and may even increase morbidity and mortality of during 5.3.5.2 Heat and Moisture Exchangers (HMEs) Effective rst line humidi er: Conserves patients exhaled water vapour and temperature (gas re-inspired at about 2 0 o C). Still requires patient to be able to warm and humidify inspired gas to s ome degree. Not effective at minute volume in excess of 10 l.min-1 . Must be cha nged daily Cannot be used with an in-line nebuliser. Incorporates a bacterial lte r. 5.3.5.3 Heated water humidi ers (Fisher and Paykel evaporative humidi er) Where any doubt exists about adequate humidi cation, a heated water humidi er should be the de fault humidi er, particularly those patients in whom there is bronchorrhoea, sputu m inspissation or haemoptysis. Generally these devices supply gas to the upper p roximal airways at 29-32o C and 95-100% relative humidity, requiring minimal mod i cation within the lungs. 5.3.6 Mechanical Ventilation 5.3.6.1 Introduction Mechanical ventilation is one of the mainstays Intensive Care Medicine and you should attempt during your stay to develop an understanding of the basic principles and practice of ventilation. 110

5 CLINICAL MANAGEMENT 5.3 Respiratory Therapy ST1/2s are not expected to manage patient ventilation alone. While most patients can be ventilated using a default setting (see below), ventilation of complex p atients remains the domain of the Consultant Intensivist. Senior Critical Care N ursing Staff may be useful resource people to aid in troubleshooting, and assist ing with instituting ventilation using a default setting. No change may be made to a ventilator without clear written order on the appropriate chart and communi cation with bedside staff. 5.3.6.2 Indications for mechanical ventilation Respiratory failure Maintenance o f cardiopulmonary homeostasis in an unstable or high risk environment: Following cardiac arrest Post-operative support in high risk surgical patients Control of intracranial pressure Patient Transport / assessment Relaxant anaesthesia To fa cilitate treatment in confused state 5.3.6.3 When to consider Intubating and ventilating Patients Clinical assessment Threatened airway Fatigue or imminent exhaustion Inability to effectively cough or clear secretions Respiratory failure Objective measurements Respiratory rate > 35 breaths per minute Tachycardia Hypertension 5.3.6.4 Objectives of mechanical ventilation Improve patient oxygenation and imp rove ventilation perfusion mismatch. To improve alveolar ventilation and reduce PaCO2 To increase end expiratory lung volume, preventing or treating lobar or pu lmonary collapse and atelectasis. To increase functional residual capacity: PEEP may help improve oxygenation through lung recruitment, and reduce lung injury w ith the prevention of repeated opening and closing of alveoli. 111

5.3 Respiratory Therapy 5 CLINICAL MANAGEMENT To unload the respiratory muscles when there is respiratory muscle insuf ciency or ventilatory failure. To allow adequate sedation and paralysis of the patient to aid control to enable the underlying disease state to be adequately treated. In some conditions such as trauma where there is loss of chest wall integrity such as in a ail chest, ventilation may be needed to stabilise the chest wall and to initiate other treatment such as analgesia with safety. 5.3.6.5 Complications of mechanical ventilation Haemodynamic Increased intrathoracic pressure-unmasking of hypovolaemia (although there is signi cant bene t to LV performance with application of PEEP). Respiratory Nosocomial pneumonia Volutrauma Barotrauma Ventilator dependancy Metabolic Post-hypercapnoeic metabolic alklosis SIADH Local Pressure effects from ETT, tracheostomy or face masks. 5.3.7 Ventilator settings 5.3.7.1 Default ventilator settings, and principles in optimizing ventilation in ICU patients Where there is no reason to expect mecha nical ventilation will be complex the following settings should be chosen: Mode BI-LEVEL Resembles Pressure controlled Ventilation (PCV) but differs in its ability to allow spontaneous breathing at both upper and lower pressure levels. Pressure an d inspiratory time are set by operator. Volume and ow are variable according to p atient need. Patients can breathe spontaneously during inspiratory and expirator y phase. Active value allows free breathing during any phase of breath delivery. 112

5 CLINICAL MANAGEMENT 5.3 Respiratory Therapy Initial set up PEEPL : 3cmH2 0 above lower in ection point (Best PEEP value) PEEPH : adjust to achieve 6ml.kg1 tidal volume(TV) (maximum 30cmH2 0 unless set b y Consultant Intensivist) TH : 1.5 sec Rate: 10 bpm PS: adjust to achieve 6mls.k g1 TV(maintain at less than PEEPH value) Fi O2 : adjust for SpO2 >92% or Pa O2 > 10kPa (unless otherwise directed by intensivist) FAP (Flow acceleration Percent) / Rise time: 50% Ventilator Maintenance Oxygen Increase Fi O2 and TimeH to improve oxygenation. PEEPL Adjust PEEPL to just abov e the lower in ection points on PV curves. This combined with low volume tidal vol ume has shown to improve outcome in severe ARDS. Tidal Volume The ARDS-net trial suggested 6-8 ml per kilogram ideal body weight per breath (450-550 ml per deli vered breath in a 60 kg woman, 500-650 ml in a 70 kg male). Generally 6-8mls per kilogram ideal body weight per breath. Inspiratory pressure should be adjusted after initial set up of ventilation and thereafter to achieve this. Peak and Pla teau pressure should not exceed 30 cmH2 O to achieve this unless set by Consulta nt Intensivist. Respiratory Rate 10-25 breathes per minute adjusted to an arteri al blood gas Pa CO2 in the normal range or approximating pre-morbid level. It is essential that in patients with ARDS and critical oxygenation that normal Pa CO 2 is not chased at the detriment of the patient exposing the patient to the risk of barotrauma and or volu-trauma. In these patients it is acceptable to allow P a CO2 to rise to 12kPa if the patient is able to tolerate affect of associated r espiratory acidosis on cardiovascular system. Reverse I:E Ratio Conventional ins piratory to expiratory ratio(I:E) is 1:2 to 1:4 Reverse ratios can used in criti cal oxygenation. The alveolus is held at its inspiratory volume longer. This all ows more mixing time and an improvement in ventilation perfusion mismatching. Th ere is incomplete lung emptying and auto PEEP develops. Ensure patient is adequa tely sedated and paralysis is sometimes required for patient to fully synchroniz e with the ventilator. There may be negative effects on cardiac output (increase d intrathoracic pressure impeding venous return) 113

5.3 Respiratory Therapy 5 CLINICAL MANAGEMENT FiO2 PEEP Table 4: PEEP-O2 nomogram 0.3 0.4 0.5 0.6 0.7 0.8 5 7.5 10 10 12 12 0.9 14 1.0 15 Rise time (FAP) Following Analysis of pressure time curve, and observing patient for signs of increased patient comfort and synchrony this can be increased or d ecreased. Expiratory Sensitivity (ESEN S ) De nes the percentage of the projected peak inspiratory ow (Vmax) at which the ventilator terminates ow, and thus cycles from inspiration to expiration during spontaneous breathing. If inspiratory ow te rminates too early, it can lead to a decreased tidal volume, or increased inspir atory muscle work load if the patient effort persists after the ventilator has c ycled off. Conversely, if the inspiratory ow persists beyond patient effort, whic h may happen when leaks are present, it can result in unnecessary expiratory wor k and patient/ ventilator dysfunction. PEEP As a guideline, PEEP may be applied using the nomogram below, titrated to arteri al oxygen content: 5.3.7.2 Spontaneous mode of ventilation Indications Consider if Fi O2 <0.4 and PEEP <12cmH2 O and PEEP and Fi O2 values are trending downwards T he patient has spontaneous breathing efforts Haemodynamically stable Proportional Assist Ventilation (PAV) PAV harmoniously augments the patients resp iratory effort it ampli es the effort no effort, no support. PAV harmoniously unlo ads the patients inspiratory muscles. PAV samples the patients inspiratory effort every several milliseconds and unloads the patient effort. Amplication is set as function % support, which ranges between zero and just under 100% support. Zero support is the equivalent of classic CPAP. Maximal support is 95% when PA is ac tive throughout the entire respiration. Set up: Turn on PAV on spont mode The ve ntilator analyses the work of breathing of the patient(WOBP T )over a series of breaths This is then displayed 114

5 CLINICAL MANAGEMENT The aim is to keep the WOBP T within the green zone 5.3 Respiratory Therapy If towards the left decrease the support, and increase if towards the right Once support about 30% patients can be switched to wall CPAP. Pressure Support (PS) PS is an all or none event, triggered by patient effort. Once triggered, the ven tilator drives the pressure to a clinical preset value regardless of patient eff ort. Lung thorx compliance(CL ) and insuf ation pressure lung pressure(PL ) combin e to determine the lung volume (VL =CL PL ). The goal of PS is to balance an appr opriate insuf ation pressure that, combined with patient effort, will yield the de sire VL and that will not tax the patients inspiratory reserve. Both insuf cient an d excessive PS can increase patient inspiratory work load and cause the patient to tire and become tachypnoeic and tachycardic. Support level: titrate level of PS from 10- 20 cmH2 O to achieve satisfactory tidal volumes and respiratory rate below 30 breaths.min1 (preferably less than 25 breaths.min1 . This should be slow ly reduced. PEEP set at 5-12 cmH2 O according to oxygenation. Rise time should b e adjusted for optimal ease of ventilation by optimizing the ow delivery. FAP sho uld be set at 50% initially then adjusted as required. Tube Compensation (TC) Sp ontaneous ventilation mode that overcomes the WOB(work of breathing) for the art i cial airway (ET or tracheostomy tube). TC accomplishes this support by assisting the patients spontaneous breaths with positive pressure proportional to the insp ired ow and the diameter of the arti cial airway. It then allows a constant PEEP to apply. The patient does not experience the resistive work due to inspiring thro ugh an arti cial airway. Percentage of support set at 100-70% Decreasing the level of the support can be used to train respiratory muscles 5.3.8 Positive Pressure Ventilation and Hypotension Positive pressure ventilatio n may exacerbate or induce hypotension by increasing relative intrathoracic pres sure and therefore decreasing venous return to the heart. ie Mild moderate: Loss of negative phase of inspiration and initiation of PEEP Extreme: Excessive incr ease in intrathoracic pressure (auto-PEEP or tension pneumothorax) 5.3.9 Supportive Therapies for Severe Hypoxia 5.3.9.1 Rotational Beds Is the pat ient on the correct bed? Consider rotational beds for patients with High Oxygen requirements. 115

5.3 Respiratory Therapy 5 CLINICAL MANAGEMENT 5.3.9.2 Fluid Management In patients with ALI/ARDS, there is an increase in lung water due to changes in vascular permeability. After early haemodynamic stabilization, studies have shown that uid restriction and diuresis have shown to improve lung function and shorten the duration of mechanical ventilation and intensive care s tay, improved neurological function and decrease the sedation use, without incre asing non pulmonary organ failure though no difference in 60 day mortalityi. Aim for neutral uid balance, consider use of diuretics or increase uid removal in pat ients on renal support with ALI/ARDS. 5.3.9.3 High frequency oscillatory ventilation(HFOV) Consider in patients with p neumonia, ARDS/ALI with severe hypoxia and patients with bronchopleural stula. It is better to consider early. Paw > 30, Fi O2 > 0.6 with Pa O2 <8, PEEP >12-15 P rior to use, Complete all circuit connections including the Aerogen Solo nebulis er if available. Prime the humidi er with 350 mls of sterile water prior to switch ing it on Once familiar with the controls Power up and calibrate the O2 analyser if present then with a test lung check functions Review settings and alarms, ma ke appropriate changes before use. 3 Key Controls for HFOV Frequency = CO2 clear ance - adjust 1Hz according to Pa CO2 Mean = Recruitment and Oxygenation - adjus t by 5cmH2 O according to Pa O2 Cycle Volume = CO2 clearance - adjust by 10ml ac cording to Pa CO2 Initial settings for HFOV Base Flow 15 Lpm (the continuous gas ow through the circuit) SI Setting 5cmH2 O > mean airway pressure FiO2 100 % Fre quency 8 Hz (rate of oscillations per second) MAP 5cmH2 O > than conventional ve ntilation MAP (20cmH2 O if unknown) Cycle volume 175ml (the size of each circula ting volume) Actions 1. Optimise Pa O2 (Lung Recruitment) a) start oscillation using initial settings wait 20 mins con rm baseline blood gasses b) MAP by 5cmH2 O wait 20 minut es check bloods for improved Pa O2 repeat cycle until Pa O2 no longer improves ( fully recruited) or deteriorates (over distended) 116

5 CLINICAL MANAGEMENT 5.3 Respiratory Therapy c) Consider correcting over distension by MAP again by 5cmH2 O to optimise Pa O2 2. Optimise Pa CO2 a) cycle volume by 10 ml wait 20 minutes check bloods for re duced Pa CO2 repeat until Pa CO2 reduces to within acceptable limits (or no furt her adjustment is possible) b) If CO2 clearance remains insuf cient frequency in 1 Hz steps wait 20 minutes check bloods for reduced Pa CO2 repeat until Pa CO2 va lue is acceptable c) If CO2 clearance is still insuf cient check for ETT patency, pneumothorax, consider introducing an ET cuff leak or the prone position. *If Pa CO2 remains unacceptable consider extra-corporeal CO2 extraction (i.e. using a Novalung ILA) 3. Optimise Fi O2 a) When Pa O2 and Pa CO2 are optimised and stabl e, Fi O2 in 10% steps whilst Pa O2 remains acceptable Weaning from HFOV FiO2 in 10% steps aiming for maintenance < 40% MAP in 2cmH2 O steps aiming for maintenance < 25cmH2 O If stable at above for 24 hours consider changing mode Insuf cient spontaneous effort? set to VENT mode (PCV+SIMV or CMV+S IMV) Effective spontaneous effort? consider setting to SPONT mode (CPAP+PS), Charting Mode, Base Flow, FiO2, Frequency, Mean Airway Pressure, Cycle Volume an d Amplitude Amplitude is the difference between the high and low airway pressure s during oscillation and is expressed in cmH2 O. It may be visualised between th e peaks and troughs of the displayed waveform. Closed Suction and Bronchoscopy minutes after the procedure. MAP by 5cmH2 O 5 minutes before, during and for 5 base ow to 40 L.min-1 only during the procedure

Green Paw Tube This airway pressure (Paw ) tube allows volume and pressure to be monitored inside the machine. VIP run the green Paw tube over the circuit suppo rt arm to prevent moisture ingress at the Y-piece. Volume and Pressure sensing a utomatically calibrates hourly. 117

5.3 S.I. Respiratory Therapy 5 CLINICAL MANAGEMENT Suspend Intervention stops oscillation but maintains the airway pressure at the se t value whilst the operator presses the button showing lungs. This may be used for lung recruitment, ECG, x-ray or listening to heart sounds. Check the set value before use! Accidental Disconnection System alarms HFOV stops on reconnection it gently rerecruits and alarm cancels automatically. Spontaneous Breathing Effort Is indicated by wandering MAP LEDs at the top of the display panel and measured values in the display. Consider resetting MAP high / MAP low alarms Base ow may be incrementally to support spontaneous breathing efforts . Cardiovascular Effect cardiac output. Observe for cardiovascular insuf ciency as MAP in HFOV may Conventional Mode ETS = Expiratory Trigger Sensitivity terminates inspiratory su pport during assisted breaths. Set as a % of the inspiratory trigger setting. RS B = Rate of Spontaneous Breaths. Inspiratory pressure setting in PCV is in addit ion to PEEP. Only use closed suction in PCV with a high ow rate, if using VCV swi tch to PCV during closed suction. The humidi er Prime with 350mls H2 0 before switching on, is fully automatic, schematic display shows alarm locations. After 30 days an alarm for replacement sounds but allows a further 72 hours allows for replacement. P23 alarm = over lling of the r eservoir - close the water inlet line, power off the humidi er for 3 minutes, turn power back on, leave the giving set closed for 1 hour to allow excess water to clear the reservoir before reopening the giving set. Further Points The vent circuit is PVC and latex free. Circuit breakers are provided on the rear of the machine for easy user access. * Vision has no integral battery, connect to a UPS protected mains supply if conc erned. After use Switch off at front of machine then press and hold the alarm mute butt on for three seconds to cancel the alarm. The impedance valve (at the front of t he diaphragm), oxygen analyser and humidi er heater cables are not disposable and

should be retained. The circuit, diaphragm and humidi er chamber can be discarded. 118

5 CLINICAL MANAGEMENT 5.3 Respiratory Therapy 5.3.9.4 Prone positioning Prone position has been demonstrated to improve oxygen ation, and decrease the incidence of VAP in patients with ARDS, but does not imp rove mortality. Majority of patients oxygenation respond quickly to prone positio n and should then be left in prone position for at least 12 hours. Rationale for prone ventilation volume. Improvement in ventilation perfusion matching, recruitment of atelectatic areas following a gravitational gradient and an increase in end-expiratory Indications Severe ARDS Pa O2 :Fi O2 ratio <20 Non responsive to standard suppor tive / ventilatory care Relative Contraindications Inadequate staff to perform procedure safely CRRT Ant erior chest drain Complications Dif cult airway management and access Accidental removal of invasive catheters Pressure necrosis, pressure neuropraxia and blindness 5.3.10 Weaning from Mechanical ventilation 5.3.10.1 Introduction In many patient s, especially those requiring short-term support, mechanical ventialtion can be removed quickly and easily. In more complex cases ho wever considerable dif culty may be encountered The actuarial risk of nosocomial p neumonia increases by about 1% per each day of MV, being 6.5% at 10 days and 19% at 20 days. It is crucial to discontinue ventilatory support and extubate at th e earliest time that a patient can sustain spontaneous ventilation safely. Plann ing for weaningshould start as soon as the patient is intubated, using the follo wing parameters: How long can we expect this patient to require mechanical venti lation (MV)? Is a tracheostomy likely to be needed? What is the underlying disea se process and how may this impact on weaning? Premature attempts at weaning can result in respiratory muscle fatigue and atelectasis. Premature extubation with resultant reintubation carries an appreciable risk to the patient. 119

5.3 Respiratory Therapy 5 CLINICAL MANAGEMENT 5.3.10.2 Minimum requirements for extubation Improving clinical condition. Patie nt stable on FiO2 < 0.4 with a PaO2 > 8 kPa PEEP < 5-8 cmH2 O Acceptable neurolo gical state: ie the expectation exists that the patient will be awake enough to protect their airway, and have the local ability (intact cranial nerve function or tracheostomy) to do so. Haemodynamically stable No prospect of major interven tion planned in the ensuing 24 hours 5.3.10.3 Predicting successful weaning from mechanical ventilation In a small pe rcentage of patients, there may be some doubt as to whether the patient will cop e with removal of respiratory support despite meeting the above criteria. A numb er of parameters have been studied, however at present a spontaneous breathing t rial is considered the most useful, with a positive predictive value of about 80 %. Spontaneous breathing trial The patient should receive no more than a PEEP of 5 cmH2O through a T-piece system. Generally if an SBT is conducted while on the ve ntilator, no more pressure support than is suf cient to overcome system resistance to ow should be allowed (see ETT compensation mode on newer generation Puritan-B ennett). Allow 120 minute trial (some suggestion 30 minutes may predict adequate ly) If trial successful extubate Markers of successful Spontaneous Breathing Trial 1.5 kPa) Objective Gas exchange acceptable ( Oxygen sat > 90% , PaO2 > 8 kPa , Increase in PaCO2 < 10 Stable ventilatory pattern (RR < 30 35 min-1 , RR not changed > 50%) Haemodyn amically stable Subjective No onset or worsening of discomfort Diaphoresis Clini cal evidence increased work of breathing 5.3.10.4 Chosen mode of weaning to extubate There is no evidence that a trial of unsupported breathing using a T-piece apparatus is any better or worse than dec remental levels of pressure support ventilation. 120

5 CLINICAL MANAGEMENT 5.3 Respiratory Therapy The duration of the trials is not de ned but those that fail usually do so early o n. Probably 30 minutes to two hours is all that is needed. Clinical signs of fai lure include tachypnoea, tachycardia, hypertension, obtundation, and desaturatio n. 5.3.10.5 Factors that in uence success of weaning Increase in work of breathing Increase metabolism (increasing CO2 production) Fe ver, sepsis, carbohydrate excess Reduction in pulmonary or chest wall compliance Pulmonary oedema, acute respiratory distress syndrome, atelectasis, pneumonia B ronchospasm, retention of secretions Obesity, abdominal distension Unfavourable respiratory circuit characteristics Delayed response and high negative pressure to trigger high resistance circuitry Inspiratory ow rate unable to match peak ins piratory ow Reduction in respiratory muscle power Electrolyte abnormalities Hypok alaemia, hypomagnesaemia, hypophosphataemia, metabolic alkalosis Cardiovascular failure Left ventricular failure, shock, anaemia Polyneuropathy of the criticall y ill Myopathy (eg endocrine or carcinomatous) Depression in respiratory centre Excess respiratory depressant drugs Hypothyroid ism Pain Brain Injury 121

5.3 Respiratory Therapy 5 CLINICAL MANAGEMENT 5.3.11 Ventilation in the prone position 5.3.11.1 Introduction Ventilating a pat ient in the prone position has not been shown to improve mortality, however in up to 60% of selected patients there is a signi cant i mprovement in oxygenation, often persisting beyond the period spent prone. It is unclear how long a patient should be ventilated in the prone position. The majo rity of patients that do respond do so quickly, however up to 30%may exhibit del ayed improvement. Available evidence suggests > 12hrs is recommended. The decisi on to prone a patient should not be made lightly, and is the domain of the ICU C onsultant. Once the decision has been made to prone a patient, this should be do ne under the direction of an experienced nursing team. 5.3.11.2 Rationale for pr one ventilation Increased uniformity of regional pleural pressure gradient. Impr ovement in dorsal ventilation with a reduction in shunt fraction Improved ventil ation-perfusion heterogeneity. Uniform distribution of lung water and exudate Im provement in FRC with further alveolar recruitment Reduction in diaphragmatic sp linting and improved movement of the posterior diaphragm Non-restriction of abdo minal contents 5.3.11.3 Indications Severe ARDS as given by: PaO2 : FiO2 ratio < 100 Non response to standard supportive / ventilatory care Local or anatomical factors (eg. posterior burns) 5.3.11.4 Relative Contraindications Inadequate sta ff to perform procedure safely Anterior intercostal catheter Continuous renal re placement therapy Morbid obesity 5.3.11.5 Hazards Dif cult airway management and a ccess (including ETT kinking and dislodgement) Accidental removal of invasive ca theters (and possible occult haemorrhage) Obstruction or disconnection of abdomi nal / thoracic drains. Pressure necrosis, pressure neuropraxia and blindness Lab our intensive procedure-distraction from other patients 122

5 CLINICAL MANAGEMENT 5.3 Respiratory Therapy 5.3.12 Non-invasive ventilation (NIPPV) 5.3.12.1 Introduction Mechanical ventila tion not requiring endotracheal intubation may avoid many of the complications of invasive ventilation (ie. generally associate d with less ICU acquired infection, results in shorter ICU and hospital length o f stay, and may be more acceptable to patients. Appropriate patient selection is important (restrict to indications below), as is appropriate monitoring and a c ontrolled environment with the capacity to initiate invasive ventilation without delay where necessary. Modes Continuous positive airway pressure (CPAP) Single continuous positive airw ay pressure No augmentation of tidal volume Generally seen to be useful in hypox ic states Biphasic positive airway pressure (BiPAP) Usually PEEP plus augmentati on of tidal volume Useful in the treatment of hypercarbic states 5.3.12.2 Indications This section does not attempt to address the role of NIPPV outside of acute conditions. The groups outlined below are those that have been studied, often in a limited way. Accepted indications Acute exacerbations COAD: Good evidence, albeit with some c on icting data, that NIPPV useful in hypercapnoeic patients. Pulmonary oedema. Pat ients with underlying neuromuscular, parenchymal or restrictive lung disease: NI PPV useful only if decompensation is a result of reversible infection and not di sease progression. Less accepted indications NIPPV should only be applied in the following situations on a trial basis, with well de ned end points, and in a well controlled environment (IC U generally). Weaning or early discontinuation of invasive ventilation. Stable a irway obstruction (eg: post operative patient with obstructive sleep apnoea). Pn eumonia or ARDS Asthma 123

5.4 Bibliography 5 CLINICAL MANAGEMENT 5.3.12.3 Contra-indications to NIPPV Patient with impaired level of consciousnes s, including those that are in-extremis Haemodynamic instability Bowel obstructi on or upper GI haemorrhage (increased risk of aspiration) Agitation such that ma sk not tolerated well Impaired cough, including low GCS and bulbar dysfunction N on-reversible disease process Untreated pneumothorax 5.3.12.4 Pre-requisites The patient must be able to protect their own airway suf c iently. The patient must be accepting of the face mask There must be a reversibl e problem requiring bridging respiratory support. There must be adequate monitor ing: Continuous pulse oximetry, telemetry and at least intermittent blood pressu re and ABG recording. Nursing ratio no worse than 1:2. 5.3.12.5 Complications Aerophagia or gastric distension - Aspiration lung injury Mask intolerance and heightened anxiety Pressure necrosis of the face 5.3.13 Corticosteroids in ARDS High dose intravenous Corticosteroids have interm ittently been used through the years to try and prevent the bro-proliferation sta ge of ARDS progressing to end stage brosis. However concerns about sample size in Meduri et al study lead to the ARDS network looking at this. The late Steroid r escue study(LaSRS) showed no difference in hospital mortality. Among the cortico steroid related complications, infection rate was no different while neuromuscul ar weakness was higher in the treatment group.ii These results do not support th e routine use of methylprednisolone in patients with persistent ARDS. 5.4 Bibliography VillarJ Kacmareck RM. A high in positve end-expiratory pressure, low tidal volum e ventilatory strategy improves outcome in persistent acute respiratory distress syndrome: a randomised, controlled trial. Crit Care Med. 2006;34:1311-1318 The National heart, lung and blood Institute Acute Respiratory distress syndrome (AR DS) Clincial Trial Network. Ventilation with lower tidal volumes as compared wit h traditional tidal volumes for acute lung injury and acute respiratory distress syndrome. NEJM 2000, May 4.342(18):1301-8 124

5 CLINICAL MANAGEMENT 5.5 Aspects of Renal Failure in Intensive Care ARDS Clinical Trial network. Comparision of two uid management strategies in acut e lung injury. N Engl J Med 2006a;354(24):2564-75 Gattinoni L, Tognoni G et al. Prone-supine Study Group. Effect of prone Positioning on the survival of patient s with acute respiratory failure. N Engl J Med 2001;345: 568-73 McAuley DF et al . What is the optimal duration of ventilation in the prone position in the ARDS. ICM 2002;28:414-418 Meduri GU, headley AS et al.Effect of prolonged methylpredn isolone therapy in unresolving ARDS. JAMA1998;273:159-65 The National heart, lun g and blood Institute Acute Respiratory distress syndrome (ARDS) Clincial Trial Network. Ef cacy and safety of corticosteriods for persistent ARDS. NEJM 2006b; 35 4(16):1671-84 5.5 Aspects of Renal Failure in Intensive Care 5.5.1 Introduction Renal failure in ICU is invariably involves at least one othe r organ dysfunction or failure, and carries a mortality of up to 70% in this set ting. The advent of continuous renal replacement therapies has revolutionised th is aspect of care. Conversely renal protective strategies, established therapy i n many units have not been proven bene cial in large multi-centre trails. Acute re nal failure that develops in isolation, due intrinsic renal disease and not part of critical illness should be referred to the Specialist Renal physicians in Le eds for further management and investigation. 5.5.2 Aetiology of renal failure in the ICU The classical compartmentalisation o f pre-renal, intra-renal and post-renal factors hold true in ICU with the follow ing considerations: A missed, but reversible, cause of renal failure has dire co nsequences-time is kidney. The commonest cause of an acute kidney injury is hypo volaemia or hypoperfusion and should be excluded and treated as a matter of urge ncy. Renal perfusion (blood ow and GFR) in critically ill patients may become dir ectly related to systemic blood pressure as local autoregulation fails. Hypotens ion, even a marginal decrease, will not be well tolerated. Nephrotoxic agents an d sepsis may act alone or in combination with hypovolaemia to complicate the pic ture. The renal interstitium is relatively hypoxic even under optimal conditions . When subjected to a multilevel endothelial insult as a result of sepsis or SIR S there is a ready predisposition to a vasomotor nephropathy and progession to o vert ATN. The pharmacokinetics of many drugs in ICU are severely deranged, expos ing the patient to a much greater risk of nephrotoxic effects. Drugs and toxins (including radio-contrast) should not be administered without consideration of t heir toxicity. Occult or overt increases in intra-abdominal pressure should alwa ys be considered in patients with abdominal distension with or without previous surgery. When considered it should be measured and if necessary addressed (see I ntra-abdominal pressure measurement, section 2.11). 125

5.5 Aspects of Renal Failure in Intensive Care 5 CLINICAL MANAGEMENT 5.5.3 Assessment of renal function in a given patient 5.5.3.1 Biochemical marker s Serum creatinine is a poor marker of renal reserve. A rise in serum creatinine > 120 mol.L-1 may not occur until more than 75% of renal functio n is lost. All patients should have their renal function calculated, and drugs t ailored according to the Cockroft and Gault equation: Creatinine Clearance (ml.s ec-1 ) = (140Ptient age) weight in kg 0.8(for females) 50000 Serum creat conc in mmol.L1 From this equation it can be appreciated that a 20 year old 100kg male w ill have 6 times the creatinine clearance of an 80 year old 50kg woman, even tho ugh they have the same serum creatinine concentration. 5.5.3.2 Urine 0.5 ml.kg-1 .hr-1 The minimum urine output required to excrete obligatory daily solute load is Urine electrolyte analysis is of little use in ICU to diagnose aetiology of rena l failure but maybe useful in speci c electrolyte abnormalities. Urine sediment: U nhelpful unless a speci c reason exists (true vasculitis, nephritis) 5.5.3.3 Renal imaging Ultrasound or nuclear imaging techniques may be useful whe re preexisting pathology is suspected, or the renal vasculature has been comprom ised by surgery or trauma. Supra-renal aortic aneurysm or dissection may extend distally and compromise renal blood ow, particularly where a signi cant false lumen exists. As soon as is practical following acute repair, investigation of aortorenal vascular anatomy should be performed to facilitate a fenestration procedur e if necessary. Post-renal pathology, whilst uncommon in ICU, is embarrassing to miss and should be excluded where there is any doubt about the cause of renal f ailure. 5.5.4 Renal protective strategies 5.5.4.1 Good practice The cornerstones of good renal protection are not the administration of various drugs, but critical care practice ie. Adequate uid resuscitation (some times a dif cult concept). Haemodynamic support to maintain both a good renal perf usion pressure and adequate blood ow. Where necessary this may involve inotrope a nd/or vasopressor support. Despite historical anxiety about the use of vasopress ors (noradrenaline), it is not harmful to the kidneys and may in fact increase r enal blood ow in animal studies. Ensure adequate preload aiming for CVP 10-12 mmH g (higher if thought to have right ventricular dysfunction e.g. COPD), aiming fo r an appropriate mean arterial pressure of at least 70 mmHg. Avoid nephrotoxic d rugs where possible 126

5 CLINICAL MANAGEMENT Treat intercurrent infection 5.5 Aspects of Renal Failure in Intensive Care Active surveillance for abdominal compartment syndrome, where this is appropriat e. 5.5.4.2 Drug therapy The following drugs have been used to promote urine outp ut, but have not been found to impact in a positive way on progression to dialysis or mo rtality. Low dose dopamine (increase in urine output secondary to direct tubular effect and minor increase in effect) - however, dopamine has no place in the ma nagement of ARF and there is evidence that it may be harmful. Frusemide (must be delivered to lumen of tubule to be effective) Dopexamine at 0.25-1 g.kg-1 .min-1 if GI perfusion thought to be at risk Mannitol Aminophylline The routine use of these drugs (except dopexamine) is not advocated. 5.5.5 Renal Replacement Thera py Indications for dialysis The threshold for dialysis in a critically ill patie nt is different from that of an ambulatory ward patient. Mortality in critically ill patients is related to time averaged urea during their stay, so that dialys is should be started earlier with the aim of maintaining a optimal state, rather than cyclical clearance of urea and metabolites. The presence of two of the fol lowing would suggest dialysis should be considered Oliguria < 200 ml over 24hrs Oliguria < 50 ml over 12hrs Severe acidaemia Hyperkalaemia (K+ > 6.0) refractory to medical management Plasma Urea > 20 mmol.L-1 or uraemic syndrome (pericardit is, pneumonitis, bone marrow suppression) Plasma Creatinine > 400 mol.L-1 Pulmona ry oedema Diuretic resistant cardiac failure Anasarca (generalised oedema) Selec ted overdose (salicylates, methanol, theophylline) Severe dysnatraemia (Na+ <115 or Na+ >160) Severe metabolic acidosis - pH <7.1 Critical oxygenation Refractor y uid overload The attempted removal of cytokines and in ammatory mediators is not yet proven to reduce mortality in humans. 127

5.5 Aspects of Renal Failure in Intensive Care 5 CLINICAL MANAGEMENT 5.5.5.1 Modes of dialytic therapy in the ICU for use in unstable patients Standard intermittent dialytic therapy: Although still used in some ICUs, it is limited by resource availability and is pr obably not suitable Continuous veno-venous renal replacement therapy: A growing e ld of therapy in the ICU, this modality has become the mainstay of renal replace ment in the critically ill. Continuous Renal Replacement Therapy (CRRT) is for t he support of patients with renal dysfunction that develops as part of their cri tical illness. It is not for providing dialysis in patients with acute renal fai lure as part single organ failure i.e. intrinsic renal disease such as glomerulo nephritis. Initiation of haemo ltration is a Consultant Intensivist decision only! ated/resumed during of ce hours. It will only be initi5.5.5.2 Continuous renal replacement:-Default Prisma settings Mode CVVHD Blood ow rate 100 ml.min-1 Dialysate ow rate

1500 ml.hr-1 (usual need: 15-25 ml.kg-1 .hr-1 ) Replacement 1500 ml.hr-1 Pre-dilution 30% Fluid removal According to need Anticoagulation If considered safe, a bolus of 2000-5000 units of heparin is administered to the patient IVI at the commencement of dialysis. There is no evidence that an ticoagulation prolong lter life and prevents clotting in the lter. Anticoagulation is however widely practiced, the aim being to anti-coagulate the lter but not th e patient. Therefore: Heparin 20 000 IU is made up to 20ml with Normal Saline, a nd starting at 10-15 units.kg-1 .hr-1 is infused via stand alone syringe pump pr e- lter. APPT should then be monitored after one hour, then two hourly x2, then 4 hourly until a stable target APTT is reached. Once achieved, APTT can be monitor ed 12 hourly. Target APTT should be in the range of 1.5-2 times normal. The maxi mum APTT of 65s should not be exceeded.

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5 CLINICAL MANAGEMENT 5.5 Aspects of Renal Failure in Intensive Care Patients with deranged coagulation due to sepsis or low / abnormal platelet func tion may not require heparin administration at all. Prostacyclin Prostacyclin sh ould be used when heparin is contraindicated, or heparin resistance has occurred . It can be used concurrently with heparin (50% reduction in heparin dose), but this does increase the risk of bleeding complications. It should not be used dur ing infusion of activated protein C. Prostacyclin is made up as 500 g in 50ml NaC l 0.9% (10 g/ml) run via the Prisma ex or systemically at a rate of 2-6 ml.hr-1 . I t can cause an increase in intrapulmonary shunting. Potassium replacement The haemodialysis counter current should mean that with an effective lter in situ, the plasma exiting the lter has the same potassium. conce ntration as the dialysate entering the lter. Potassium supplementation should the refore only occur in the dialysate uid. Standard haemo ltration uid is lactate buffe red and contains [K+] = 4 mmol.L-1 . Buffering solution Most dialysate solutions contain lactate as a buffer, as this results in a stable solution. Lactate is then metabolised to bicarbonate in the liver. Commonly therefore, patients on CVVHDF will have moderately elevated lac tate levels. In the context of a stable patient (unchanged or improvingwhole blo od pH) this should not cause alarm. Solutions using bicarbonate as a buffer need to be prepared just prior to use. They are more expensive, and more prone to co ntamination. Bicarbonate buffer uid is not indicated unless there is signi cant hep atic impairment. Fluid removal The Prisma machine will allow you to set a net uid removal volume per hour. This is calculated by the machine based on the weight of the ultra ltrate bag, and the set ow rates of replacement and dialysate uids. The volume to removed from th e patient must be discussed with the Consultant Intensivist, and form part of th e daily management plan. 5.5.5.3 Complications of continuous renal replacement therapy Haemorrhage (and o ther consequences of exposure to heparin (HIT or HITT) Hypothermia, or masking o f hyperthermia (prevention of hyperthermia may be clinically useful) Complicatio ns of (prolonged) venous access. Exposure to extracorporeal circuits and lter (ac tivation of complement, sequestering of platelets) Air embolism 129

5.6 Neurosurgical Guidelines 5 CLINICAL MANAGEMENT Increased requirement for experienced staff, and increased nursing workload. 5.6 Neurosurgical Guidelines 5.6.1 Neurotrauma The effective management of neurotrauma relies upon early noti c ation of the neurosurgical team, and close liaison at all times. For obvious rea sons we have no control over the magnitude and mechanism of the primary injury, however we can in uence patient outcome by preventing a secondary insult through h ypoxia, hypotension, or electrolyte/metabolic derangement. 5.6.1.1 Acute trauma resuscitation Safe retrieval and transport around the hospi tal, and during emergency surgery Cardio-pulmonary / renal / metabolic homeostas is Maintenance of cerebral perfusion. 5.6.1.2 Monitoring the head injured patient Real time (invasive) arterial blood pressure monitoring CVC accessed and pressure transduced. End-tidal CO2 monitori ng (calibrate and establish arterial-end tidal difference). 5.6.1.3 Ventilation of the head injured patient Maintain PaO2 > 10 kPa Maintain normocapnia: PaCO2 between 4.5-5.3 kPa. Hyperventilation to PaCO2 as lo w as 3.0 kPa may decrease ICP temporarily, however there is a short term trade o ff in cerebral blood ow, and after 6 hours tachyphylaxis occurs with a potential hyperaemia on correction to a normal PaCO2 . Hyperventialtion should not be used therefore unless it forms a short term bridge to de nitive treatment (ie. impendi ng surgery). Low level PEEP has not been proven to affect outcome of head injury adversely, and may prevent secondary pulmonary pathology. Nurse 30 degrees head up with head in neutral position. 5.6.1.4 Haemodynamic priorities Maintain perfusion pressure: Mean arterial pressure (MAP) > 90 mmHg in the absence of an ICP monitor, Cerebra l perfusion pressure (see algorhythm below) > 70 mmHg where ICP is being monitor ed (CPP = MAP-ICP) Avoid inotrope or vasopressor use until patient adequately uid resuscitated. Fluid maintenance 130

5 CLINICAL MANAGEMENT Aim for euvolaemia 5.6 Neurosurgical Guidelines Use crystalloid (usually normal saline) unless a speci c contra-indication exists 5.6.1.5 Osmotherapy Indications: Signs of trans-tentorial herniation Progressive neurological deterioration not attributable to systemic pathology. The patient should be euvolaemic prior to initiating osmotherapy. Bolus therapy may be bette r than infusions: consider Mannitol 0.25 g.kg-1 or (100 ml of 20% ) Hypertonic sa line: 10-20 ml of 20% saline to a serum Sodium concentration of 150155 mmol.L-1 Measured osmolality should not exceed 320 mmol/L. Prolonged serum hyperosmolalit y will promote intracellular generation of idiogenic osmoles leading to a reboun d in cellular uid uptake (and ICP) if osmolality is allowed to correct rapidly be yond day 3 of therapy. 5.6.1.6 Sedation First 24-48hrs: It may be appropriate to use a short acting age nt such as propofol to facilitate repeated neurological assessment, particularly where no ICP measurement exists. Labile neurogenic hypertension, sympathetic st orming or emergence agitation: Consider lockde or clonidine. Barbiturate use ( thiopentone: consider loading dose, 1-1.5 g IVI) see raised ICP algorithm. 5.6.1.7 Other management issues relating to neurotrauma Steroids not proven useful in the trauma setting. Antibiotics A single dose of antibiotic should be suf cient to cover insertion of monitoring catheters. A fracture base of skull is not an indication for antibiot ic prophylaxis in the absence of a CSF leak. CSF should be sent for MC&S daily. All sampling of CSF, or other disruption of the drainage system should be perfor med using aseptic technique, including sterile gloves and gown. 131

5.6 Neurosurgical Guidelines 5 CLINICAL MANAGEMENT Seizure prophylaxis Consider use in patients with a closed head injury and struc tural damage, or penetrating injury. Phenytoin 15 mg.kg-1 over 30 minutes follow ed by 300 mg daily for 10 days when used for prophylaxis only. Thromboprophylaxis All patients should be tted with T.E.D. stockings. Consult the neurosurgical team on prophylactic heparin use. Those patients not suitable for using T.E.D. stockings should be considered for sequential calf compressors. Stress ulcer prophlaxis consider if patient likely to be ventilated for > 48hrs, and not tolerating enteral feeding Avoid hyperthermia Hyperthermia should be avoided using simple measures such as regular paracetamol The role of active cooling is controversial, and should not be instituted without consent of the Consultant. 5.6.2 Status Epilepticus 5.6.2.1 De nition Prolonged or repetitive seizures that o ccur without a period of recovery between attacks. Refractory status epilepticus refers to ongoing seizures for more than 20-30 minutes. Serial seizures may occ ur within a brief period, but as long as the patient regains consciousness in be tween this is not an indication for ICU admission. 5.6.2.2 Principles of ICU management Basic resuscitation protocol: Secure Airway , Breathing, Circulation Acquire IVI access. Control Seizures using drugs descri bed in table below. Consider precipitating causes and treat as appropriate: Gluc ose: administer an empiric dose if in doubt, or estimation delayed. Electrolytes : Ca2+ , Mg2+ , K+ , PO34 Metabolic derangement: hypoglycaemia, thiamine de ciency , intoxication or withdrawal Known epileptic: review medication compliance and r ecent changes. 132

5 CLINICAL MANAGEMENT Intracranial pathology: CVA, tumour, infection 5.6 Neurosurgical Guidelines Prevent secondary insult: Hypoxia, hyperpyrexia, prolonged seizures-rhabdomyolys is. Further investigations: CT scan head: where cause of seizure unknown, and of new onset. EEG. May be useful where pseudoseizures are suspected, the patient h as complex partial seizures with intermittent generalisation, or where muscle re laxants have been administered to the patient. Lumbar Puncture: LPs are generall y not indicated. 5.6.2.3 Useful Drugs in the treatment of refractofy status epil epticus Ketamine : NMDA receptor antagonist, may be helpful when GABA receptor r esponse to other drugs less effective Loading dose: 1-5 mg.kg-1 Infusion: 1-5 mg .kg-1 .hr-1 Propofol : Anaesthetic agent used to control refractory status in th e intubated patient 1-2 mg.kg-1 followed by 2-10 mg.kg-1 .hr-1 . Thiopentone : R eserved for failed standard treatment, where endotracheal intubation is required Loading dose: 5 mg.kg Infusion: 1-3 mg.kg-1 .hr-1 (approx 150 mg.hr-1 ) titrate d to EEG activity at the bedside. Once emergency treatment has been implemented it is expected that the assistance of the neurology team will be sought in adjus ting treatment in known epileptics, or those with focal or complex partial seizu res. 5.6.3 Subarachnoid haemorrhage 5.6.3.1 Introduction Patients will be admitted as a result of acute aneurysmal rupture, generally with impaired level of consciousness. 5.6.3.2 Planning of surgical intervention in patients with acute rupture Early ( < 3 days): Advantages: Prevents re-bleeding, may assist with reduction in assoc iated vasospasm (blood products removed) and subsequent cerebral ischaemia. Disa dvantages: More technically dif cult, higher risk of intra-operative rupture. Late ( > 11 days): Advantages: Easier procedure. Allows a period of observation, avo iding surgery in potentially non-salvageable patients. Disadvantages: re-bleed o r rupture. Increased risk of vaso-spastic complications. 133

5.7 Microbiology Guidelines 5 CLINICAL MANAGEMENT 5.6.3.3 Principles of ICU management Monitoring Pulse oximetry Invasive arterial monitoring Central venous access (pa rticularly during administration of nimodipine). Neurological observations hourl y: A deterioration in GCS that cannot be easily explained or corrected (eg. seda tion) may be due to a re-bleed, vasospasm or hydrocephalus in which case the neu rosurgical team should be noti ed. Therapeutic interventions Maintain adequate cerebral perfusion (generally a MAP > 20 mmHg above pre-morbid state, or > 90 mmHg if unknown). Aim to minimise secondary damage due to cerebral vasospasm, using Nimodipine (Calcium channel antagonist) 10 mg.hr-1 IVI (preferably via CVC) Nimodipine administration may precipitate h ypotension, in general noradrenaline is used to maintain the desired mean arteri al pressure (MAP), although this should be discussed with the Consultant Intensi vist. Change to oral administration as soon as possible Usually continued for a total of 21 days Fluid administration: Maintain at least normovolaemia using 0.9 % saline IVI Hypervolaemia has been advocated as a means of maintaining cerebral ow, although achieving hypervolaemia may be dif cult. Measures of adequate volume status should include: Warm and well perfused patient Urine output at least 0.5 ml.kg-1 .hr-1 , preferably > 1.0 ml.kg-1 .hr-1 CVP > 12 mmHg Maintain normal ser um electrolytes and total osmolality Adjuncts to treatment Direct and chemical (papaverine) angioplasty may play a role in refractory cerebral vasospasm, however they do not form part of routine practice at this stage. 5.7 Microbiology Guidelines 5.7.1 Introduction Sepsis is the most common cause of death in critically ill pa tients. The detection of active infection, as opposed to colonisation with ICU or a, is dif cult but important. 134

5 CLINICAL MANAGEMENT 5.7 Microbiology Guidelines Regular routine microbiological examination is not cost effective in the ICU, an d infective screens should only be ordered for speci c indications, using the guid elines listed below. Simple preventative measures are extremely important in the containment of infection and the prevention of bacterial resistance. ie Compuls ory hand washing by all staff who come into contact with patients. Hands should be washed both before and after patient contact. Alternatively, alcohol gel may be used. Strict aseptic technique for all procedures Rational prescription of an tibiotics. 5.7.2 Glossary 5.7.2.1 Systemic in ammatory response syndrome: SIRS activating a s igni cant in ammatory reaction. De ned by the presence of at least 2 of the following: Temp > 38 o C or < 36 o C Heart rate > 90 bpm Respiratory rate > 20 bpm (or PaC O2 < 4.0 kPa spontaneously breathing) Plasma WCC > 12000 .mm-3 or < 4000 .mm-3 o r > 10% immature neutrophils (band cells) Describes clinical picture following any insult (trauma/major surgery, burns, pancreatitis, hypersensitivit y reactions ) 5.7.2.2 Sepsis ological pathogen The presence of SIRS as de ned above in the presence of a proven microbi5.7.2.3 Septic Shock Sepsis with hypotension, despite adequate uid resuscitation, along with the presence of perfusion abnormalities that may include but are not limited to Lactic acidosis Oliguria Acute alteration in mental status 5.7.2.4 Nosocomial infection sion) Clinically evident infection that was neither present nor incubating at the time of admission to hospital (generally held to appear > 48hrs after admis5.7.2.5 Colonisation The detectable presence of micro-organisms on / in a patient that are not pathogenic or elicit an in ammatory response. 5.7.3 Screening for sepsis 5.7.3.1 Septic screen-empiric 135

5.7 Microbiology Guidelines 5 CLINICAL MANAGEMENT Urine microscopy and culture Tracheal aspirate and BAL uid Blood cultures

5.7.3.2 Components of sepsis screen-directed Fungal cultures CSF Pleural Tap X-r ay sinuses Directed or bronchoscopic examination of chest ora. 5.7.4 Investigation of Pneumonia 5.7.4.1 Community acquired pneumonia Microbiology Common organisms: Strep pneumoniae, Haemophilus in uenzae, In uenza A O ther organisms: Bacteria: Legionella sp, Gram-bacilli, S. Aureus Viral: In uenza B , Parain uenza, Adenovirus, RSV Other: Mycoplasma, Chlamydia Psittaci (birds), TB, Chlamydia pneumoniae Investigations Full blood count and differential Biochem: ICU pro le ABG CXR Microbiology Blood cultures 2 Endotracheal aspirate or sputum for microscopy and culture (urgent gram stain) Respiratory viral antigen and culture (if not intuba ted then use nasopharyngeal swab) Serology: for atypical bacteria Direct antigen detection: Urine (pneumococcal Ag), serum (Legionella Ag) by PCR . Pleural uid: where signi cant effusion present 136

5 CLINICAL MANAGEMENT 5.7 Microbiology Guidelines In immuno-compromised host Extend spectrum of detection on sputum: fungal stain and culture, Pneumocystis Carinii stain and acid fast bacilli. Viral studies for CMV, HSV, EBV HIV serology if appropriate Consider broncho-alveolar lavage or l ung biopsy if initial cultures negative. 5.7.4.2 Nosocomial pneumonia in the ICU Introduction Incidence: Up 20% of all ICU patients, 70% of patients meeting crit eria for ARDS. Clinical diagnosis, including use of tracheal aspirates, has poor sensitivity and speci city. Diagnosis A diagnosis of nosocomial infection (including ventilator associated p neumonia) should be considered if: New and persistent CXR changes Tachycardia an d tachypnoea Fever or hypothermia Leucocytosis or leucopaenia Purulent sputum De teriorating lung function or increasing ventilatory requirement. Con rmation of di agnosis: Broncho-alveolar lavage: Only specimens with Epithelial cell count < 1 % considered > 5 % intracellular organisms considered diagnostic < 5 % intracell ular organisms, treat with antibiotics only if patient unstable and subsequent c ulture reveals > 104 CFU.ml-1 . Treatment Empiric treatment should be guided by the initial gram stain. See anti biotic guideline. 5.7.5 Vascular Catheter Sepsis 5.7.5.1 Introduction It is no longer common pract ice to remove or replace central access routinely, but only when infected or no longer required. Suspect line sepsis in the presence of: New or unexplained fever Or in WCC Deterioration in organ funct ion 137

5.7 Microbiology Guidelines 5 CLINICAL MANAGEMENT Positive blood culture with likely organism in a patient with sepsis. Evidence o f local infection (in ammation or pus at the insertion site) 5.7.5.2 Guidelines Attempt to con rm bacteraemia by taking blood cultures from a peripheral vein (cultures from the line may only indicate colonisation). Remove line o n suspicion of infection. Intra-vascular catheters are not routinely submitted f or culture. 5.7.5.3 Treatment sepsis. Removal of the infected line will usually result in resolution of clinical Antibiotics are indicated only if sepsis is severe, progressive following remova l of the line, or if the patient is high risk (eg. prosthetic implants) Refer to antibiotic guidelines for selection of antibiotics. Subsequent venous access In ICU central access may be necessary for ongoing anti biotics or inotropes, so that a new line may have to be inserted immediately. Wh ere possible wait 24 hours before re-inserting a new line at a new site. Guidewi re exchanges may only be performed where mechanical problems complicate a new ca theter site. 5.7.6 Fungal infections 5.7.6.1 Introduction The incidence of systemic fungal in fections in Intensive Care has increased in recent years as a result of Increased use of broad spectrum antibioti cs Increasing numbers of immunosuppressed patients being referred to ICU. Prolon ged use of intravascular catheters Co-existent use of immunosuppressive therapy. The Consultant Microbiologist should be consulted where any doubt exists with r egard initiation of antifungal therapy. 5.7.6.2 Indications for antifungal therapy Prophylaxis in patients following bon e marrow transplant or neutropaenic patients. Single positive blood culture in a high risk patient Isolation of candida from any sterile body site except urine, or isolation of fungi in two anatomically discrete sites in selected patients. Histological evidence of yeast or mycelial forms in tissue from high risk patien ts. 138

5 CLINICAL MANAGEMENT See antimicrobial guidelines. 5.8 Drug / Toxin Overdose 5.7.6.3 Treatment 5.8 Drug / Toxin Overdose 5.8.1 Introduction The majority of overdoses are polypharmacological and respond to general supportive measures. Overall mortality is low and usually relates to cardio-respiratory arrest and / or uncontrolled siezures prior to admission. De spite an unreliable correlation between depth of coma and preservation of glotti c re exes, over the last decade emergency departments have become more aggressive at intubating patients. While speci c reversal agents such as Naloxone (opioids) o r umazenil (benzodiazepines) have some short term use, their relatively short hal f lives restrict their ef cacy in de nitive treatment. 5.8.2 Admission to ICU Intubated patients Uncontrolled siezures Coma Persistent hypotension ECG abnormalities consistent with signi cant ingestion (may be suitabl e for HDU monitoring in the absence of other features listed above): Ventricular or supraventricular tachyarrhythmias Sinus tachycardia > 140 / min 2nd or 3rd d egree heart block QT-prolongation (preferably index QTc) QRS duration > 0.12ms 5.8.2.1 Gastric lavage The place of gastric lavage in acute poisoning is debatable, and is only of bene t in the hyperacute phase of poisoning ( < 1 hour). Patients must be awake with a preserved gag re ex, or already be intubated, failing which the risks and bene ts of intubating speci cally to perform gastric lavage patient need to be evaluated. Procedure Insert 16G nasogastric tube (not a large bore sump) Instil 1 ml.kg-1 w arm water only, then attempt recovery of the lavage. 139

5.9 Withdrawal of Treatment in the Intensive Care 5 CLINICAL MANAGEMENT Do not continue to instil water until the previous volume has been removed. Cont inue until lavage is clear. 5.8.2.2 Charcoal Charcoal aspiration has a high morb idity and mortality. As for gastric lavage above, this should not be attempted in patients without a safe or protect ed airway. Instil 50g as soon as possible and 50g 4 hrly thereafter while indica tion persists. Co-administration with sorbitol has not been shown to increase ef c acy. In general charcoal should be given in a ratio of 10:1, charcoal dose to dr ug ingested dose. Indications for administering activated charcoal Virtually all patients presenting with a drug overdose. Contra-indications Elemental metals ( lithium, iron) Pesticides Strong acids or alkalis Cyanide Late presentations > 4 -6 hrs post ingestion. 5.8.3 Speci c Overdoses The Hospital intra-net site contain s a link to Medline and other Biomedical Databases, in which directory you will n d Micromedex which contains both Poisindex and Drugdex two accessible and readab le databases relating to drug and toxin ingestion. Consult the ICU Consultant pr ior to commencing therapy not considered part of basic resuscitation measures. 5.9 Withdrawal of Treatment in the Intensive Care 5.9.1 Introduction Withdrawal of treatment, or the decision not to initiate trea tment, is a Consultant responsibility. Junior staff are not expected, nor encour aged, to enter into an end-of-life discussion with a patient or their family, un less requested by a Consultant to do so. 5.9.2 Principles Patients have a right to receive quality end of life care including appropriate palliative care and he lp making decisions regarding life-sustaining treatment. Health providers are no t however obliged to provide treatments that would be perceived to be futile, or otherwise not in the best interests of a given patient. 140

5 CLINICAL MANAGEMENT 5.10 Brain death and organ donation 5.9.3 Deciding not to treat (or treat any further) The goal of intensive care is to prevent unnecessary suffering and premature death by treating reversible ill nesses for an appropriate period of time. Patients in whom treatment is to be wi thdrawn or not initiated generally fall into one of the following categories: Im minent death: A patient with an acute illness whose reversal or cure would be un precedented, and will certainly lead to death. Lethal condition: Progressive, un relenting terminal disease incompatible with survival longer than 3-6 months. Li fe sustaining treatment should not be provided for the underlying disease. Where treatment is provided for superimposed, reversible illness, this should have cl eargoals and limitations. Severe irreversible condition: A patient has a severe and irreversible condition impairing cognition or consciousness, but where death may not occur for many months. Life sustaining treatment should not be institut ed for the underlying condition, but again may be used to achieve a speci c goal ( eg. waiting for arrival of a family member). 5.9.3.1 The decision making process consensus to withdraw therapy. The ICU Consultant or primary specialist should: As early as possible discuss with patients while capable, their prognosis and w ishes for treatment. Explore why the patient or substitute decision maker wishes treatment to be continued. Discuss with the patient or decision maker the ratio nale for withholding or withdrawing of life support systems. Describe palliative measures and emphasize patient comfort and dignity. Offer hospital resources su ch as social work, chaplaincy or bioethics to assist the patient / family with t heir psychosocial, cultural, spiritual and informational needs. Document pertine nt details of this communication in the patient notes. Where there is not consen sus between the patient/family and staff, then: Negotiate a plan of care accepta ble to all parties. Obtain a second opinion should this be appropriate Initiate a clearly de ned trial of therapy If none of these are successful then external me diation may become necessary although this would be extremely rare. Generally, t here should be inter-professional team 5.10 Brain death and organ donation 5.10.1 Declaration of brain death This procedure is an absolute requirement prio r to beating-heart organ donation. 141

5.10 Brain death and organ donation 5 CLINICAL MANAGEMENT Where clinical examination is to be used alone, this must be performed by 2 doct ors of the status prescribed by local jurisdiction. The two doctors may choose t o present at each examination, however, each must perform ALL of the brain death studies independently, and be responsible for one of the examinations. In some circumstances, a clinical examination may be replaced by investigations as given below. 5.10.2 Clinical certi cation of brain death 5.10.2.1 Pre-conditions A cause of com a must be identi ed and documented Reversible causes of coma must be excluded coma caused by drugs / poisons-Morphi ne, Midazolam, barbiturates etc unresponsive state caused by neuromuscular block ing agents-vecuronium, pancuronium etc coma caused by hypothermia-core temperatu re must be ? 35o C coma caused by metabolic or endocrine disturbance-the patient s should have: normal renal function normal hepatic function normoglycaemia norm al electrolyte pro le 5.10.2.2 Clinical assessment of brain stem function con rmed until a minimum of 6 hours after onset of coma. It is recommended that this procedure is performed separately by 2 doctors at least 2 hours apart, to ensure th at death is not A minimum of four hours observation and mechanical ventilation m ust occur, during which the patient has been comatose (Glasgow Coma Score 3), ha d non-reactive pupils, absent cough and gag re exes, and no spontaneous breathing efforts. In some cases this period may be longer (eg. in primary hypoxaemic inju ries). Testing brain stem function A response at any stage deems the patient is not brain dead and further testing does not proceed absent pupillary responses to light (direct ional and consensual) tests cranial nerve III absent corneal re exes (avoid unnece ssary repetition so as not to injure the cornea) tests cranial nerve V + VII abs ent vestibulo-ocular re ex: (the tympanic membrane must be inspected and noted to be intact before proceeding).-no nystagmus (no eye deviation to the stimulated s ide) on the injection of 50 ml of iced water into the ear 142

5 CLINICAL MANAGEMENT tests cranial nerve VII + VIII absent gag re ex tests cranial nerve IX + X absent cough re ex tests cranial nerve IX + X 5.10 Brain death and organ donation absent response to painful stimuli within the cranial nerve distribution absent respiratory function: should always be done last, and the following must be adhe red to following the disconnection of the ventilator: pre-oxygenate the patient by placing oxygen tubing into the ET tube and insuf ate with 100% oxygen at 2 l.mi n-1 look for apnoea clinically sample ABG 10-15 minutes following disconnection from the ventilator. the PaCO2 should be > 8 kPa Time of death The legal time of death is at the time of the completion of the second test of brain death studies / or whatever time the doctor performing the second set o f brain death studies documents on the appropriate form and / or in the patient notes. 5.10.2.3 Non-clinical certi cation of brain death for clinical certi cation cannot b e met. For example: Objective demonstration of the absence of cerebral blood ow is required if brain death is suspected and the precon ditions (2b) facial trauma or obstruction of the external auditory canals may no t allow assessment of all the brain stem re exes. a high cervical injury will not allow assessment of all the brain stem re exes Where the effects of sedation agent s cannot be excluded A 6 hour period of observation of absent brain function is preferred prior to radiological examination when the absence of cerebral blood ow may be established by either: radionuclide cerebral perfusion scan 4 vessel ang iography Certi cation of brain death is then undertaken after the respective scan has been veri ed by a practitioner certi ed to do so. The legal time of death is at the time of radiological testing. 5.10.2.4 Frequently asked questions: Exclusions to the diagnosis of brain death The following observations do not exclude a diagnosis of brain death: spontaneou s spinal movements of the limbs respiratory-like movements (shoulder elevation and adduction, back arching or intercostal expansion without signi cant tidal volume) 143

6 sweating blushing tachycardia absence of diabetes insipidus (normal osmolar co ntrol mechanism) deep tendon re exes Up-going plantar re ex. APPENDICES 6 Appendices 6.1 Haemodynamic Principles 6.1.1 Introduction When faced with a patient who may have some haemodynamic impa irment you should have a systematic approach to assessing and managing this impo rtant issue. The following is one way: Ask four questions: Is the blood pressure actually low? Is there any evidence of shock (or poor tissue perfusion)? Does t his patient require more uid? Do I need to introduce an inotrope, a chronotrope o r a vasopressor substance? 6.1.2 Diagnosing hypotension 6.1.2.1 Absolutely low blood pressure De nition Systo lic BP < 90 mmHg or Mean arterial pressure < 60 mmHg. These are implied limits a t which vital organs continue to autoregulate blood ow. 6.1.2.2 Relatively low blood pressure Individual patients may normally have elev ated or indeed low blood pressure. Hypotension would then be considered as: Syst olic BP 30% lower than known values for that patient (or an absolute drop of 20 mmHg). 6.1.3 Is there any evidence of shock ? 6.1.3.1 Bedside indicators: Cerebral perf usion: restlessness or confusion Renal blood ow: oliguria ( < 0.5 ml..kg-1 .hr-1 ) Cool peripheries (unreliable) 144

6 APPENDICES 6.1 Haemodynamic Principles 6.1.3.2 Simple investigations ECG: evidence of regional ischaemic changes pH on arterial blood gas Serum lactate Central venous oxygen saturation. 6.1.3.3 Surrogate end-points Generally unwieldy eg. gastric tonometry and measur ement of gastric mucosal pH. 6.1.4 Does this patient require more uid resuscitation? 6.1.4.1 Introduction-Asse ssment of Cardiac Preload answer. All texts and wise men will urge you to adequa tely volume resuscitate the patient, while simple to say, it is dif cult to ful l. T his is the hardest question to 6.1.4.2 De ning preload Pre-load refers to the degree of ventricular degree of stretch of myocytes during diastole. 6.1.4.3 Starling Curve The more uid returned to the heart (venous return), the greater the contractile force of the heart and the greater the volume of blood expelled. At some point the distension of the heart exceeds its ability to contract and t he ventricle will fail. Should I give more uid ? Patients on the volume responsive part of the Starling c urve should increase their cardiac output in response to further intravenous uid. How do I know where the patient is on the curve ? In a number of patients this i s not problematic as they have haemorrhagic shock, vomiting, diarrhoea or some o ther reason for absolute or relative (eg. epidural, anaphylaxis) intra-vascular volume contraction. There are a number of techniques for assessing or inferring left ventricular end-diastolic volume as the determinant of pre-load in patients where this is not clear-cut. Two of these, the pulmonary artery catheter and th e PiCCO are described separately in this appendix. Clinical estimates of hydrati on (moist mucous membranes, skin turgor.) are almost useless in ICU. Estimation of JVP, or indeed invasive measures of right heart (CVP) or left heart(pulmonary capillary wedge pressure) lling pressures have some relevance in patients with h earts that have normal structure and function. Often this is not the case in ICU . 145 lling which infers the

6.2 The Pulmonary Artery Catheter 6 APPENDICES So what should I do ? Often clinical practice relies on your impression and an a ssessment of the risk of giving more uid than not doing so. ie. It would be easie r to give uid to a hypotensive person with a clear chest who is ventilated, than one with chest crackles who is developing respiratory failure, even if this is d ue to some other pathology. The decision to implement a uid challenge is inextric ably linked with a duty to closely observe the results and act accordingly. Do I need to introduce an inotrope, a chronotrope or a vasopressor ? Once the th ree questions above have been addressed adequately it may become necessary to us e an agent to bring about an increase in blood pressure and therefore organ perf usion. ie. Organ perfusion: Q = (Pi -Po ) C , where Q = organ perfusion C = regi onal conductance (a function of vascular radius, and blood rheology) Pi-Po = pre ssure gradient across the tissue bed or organ (generally blood pressure, BP) BP = Systemic vascular resistance (SVR) cardiac output , (ie = HR Stroke volume SVR ). Manipulation of blood pressure and therefore organ perfusion relies on changi ng one of the following three parameters therefore: heart rate, stroke volume an d vascular resistance. 6.2 The Pulmonary Artery Catheter 6.2.1 Introduction The PAC was designed in an effort to quantify and therefore m anipulate haemodynamic parameters ie. 1. Estimation of cardiac pre-load by measu ring pulmonary artery occlusion pressure 2. Estimation of cardiac output by ther modilution 6.2.1.1 Pulmonary artery occlusion pressure (or PCWP Pulmonary Capillary Wedge P ressure) Under conditions described in the clinical procedures section of this g uideline the PA catheter is inserted into a central vein. The PA catheter is int roduced into a segmental pulmonary artery using a ow directed technique. The prem ise behind the use of this catheter is that PAOP is determined by left atrial pr essure which bears a relationship to left ventricular end diastolic pressure and this in turn relates to left ventricular end-diastolic volume as the nal arbiter of pre-load. This relationship does not hold true if: There is not a continuous column of uid between sensor and left atrium. There is mitral regurgitation. The compliance characteristics of the left ventricle are abnormal. 146

6 APPENDICES 6.3 The PiCCO-catheter / monitor Given the above it is not surprising that the PAOP has proven to be an unreliabl e predictor of preload in clinical practice. 6.2.1.2 Complications of Pulmonary Artery Catheterisation Time spent inserting t he catheter may distract from resuscitating the patient. Insertion and mechanica l problems, thrombosis and infection are similar to those observed with central access cannulation. Balloon induced problems: Balloon rupture Catheter knotting Pulmonary infarction Pulmonary artery rupture Pulmonary and tricuspid valve dama ge Endocarditis Arrhythmias 6.2.1.3 Place in therapy The impact of a PA catheter, and the haemodynamic variables obtained with it on management, and outcome, are not well de ned. Particularly dis appointing has been the inability of pulmonary wedge (or occlusion) pressure to re ect in any useful way the pre-load status of a given patient. Understanding of the catheters limitations and usefulness varies widely among doctors and nursing staff and requires ongoing education to reduce morbidity associated with its us e, and correct interpretation of the data it provides. Proponents of its use arg ue that failure of clinical judgement in diagnosing type of shock, or institutin g successful treatment is an indication for catheterisation of the right heart, to assess haemodynamic and metabolic variables re ecting type, severity and course of circulatory compromise. Those who do not favour use of the PA catheter argue that clinical judgement (or less invasive monitoring) is not inferior to cathet erisation of the right heart. The lack of direct evidence to support the use of this type of catheter, and the increasing body of evidence documenting its inabi lity to predict response to uid loading have resulted in declining use of the PA catheter in clinical practice. 6.3 The PiCCO-catheter / monitor 6.3.1 Introduction This method evolved as an alternative to cathterisation of th e right heart in an attempt to elucidate further the concept of cardiac pre-load , and patient uid status. 147

6.3 The PiCCO-catheter / monitor 6 APPENDICES 6.3.1.1 Aims Measurement of cardiac output by less invasive means than catheteri sation of the right heart. Estimation of pre-load, intra-thoracic blood volume a nd by inference extra-vascular lung water. 6.3.1.2 Technique: contour. Trans-pulmonary thermodilution measurement and analysis of pulse 6.3.2 Estimation of cardiac output A bolus of injectate, usually cold uid, given into a large central vessel (eg. superior vena cava) can be detected in a large artery (eg. femoral or axillary) as a temperature change, giving rise to a pulse contour. This is similar in theory to the thermodilution principle used in the PA catheter where cold uid of a known volume and temperature is injected proximal ly into the catheter and a temperature change detected more distally by a temper ature sensor as the colder uid mixes with blood. The magnitude of the temperature change detected at the thermistor can be used to estimate the volume of blood i nto which the cold uid was diluted, and hence the cardiac output. When this is do ne across the entire pulmonary circulation however, and is detected in an artery the pulse contour generated by the temperature change is atter and longer, but n evertheless still gives reliable results when extrapolated to predict cardiac ou tput. 6.3.2.1 Estimation of pre-load, intra-thoracic blood volume and extra-vascular l ung water The derivation of these parameters using this technique is not simple, nor intuitive, and requires extensive extrapolation of data. 6.3.2.2 Inferences inherent in estimation of cardiac pre-load using the PiCCO te chnique By examining the contour of the temperature pulse wave generated in the systemic arterial tree by injecting cold uid centrally, it is possible to make so me inferences relating to given blood volumes. Inference 1 An injected indicator (cold uid) always mixes with largest volume accessible.

Cold water injected into a central vein will mix into uid in the following spaces , which together comprise the intra thoracic thermal volume or ITTV. Inference 2 given above. By analysing the shape and time characteristics of the temperature wave form (or pulse) it is possible to make certain assumptions with regard to the volumes of mixing as 148

6 APPENDICES 6.4 Principles of ventilation The leap of faith is that wave form analysis produced by a transpulmonary thermo dilution technique, can be used to calculate cardiac output. Derived uid volumes may allow estimation of both preload (using global end diastolic volumes or intr a thoracic blood volumes), and the amount of extravasated uid into the lungs (giv en by extra vascular lung water). Once you accept this principle you can the use these numbers to guide both further uid therapy and administration of inotropes or vasopressors. 6.4 Principles of ventilation 6.4.1 Introduction Mechanical ventilation serves two basic functions: ventilator y support and oxygenation support. Ventilatory support is designed to provide ei ther total or partial gas transport between the environment and the alveoli. Usu ally this is done by providing positive airway pressure in a manner that mimics the normal tidal volume and breathing frequency pattern. In contrast oxygenation support is designed to supplement the Fi O2 and to optimise ventilation perfusi on matching to effect alveolar gas transport. The most common technique to accom plish this is the application of positive end expiratory pressure (or PEEP), but manipulations of the ventilatory pattern and other strategies can also be used. 6.4.1.1 Classi cation of ventilators Mechanical ventilators have been classi ed acco rding to the characteristics of the inspiratory phase. If they provide a constan t inspiratory pressure they are known as pressure generators. If they provide a constant inspiratory ow they are known as ow generators. Flow Generators These usually deliver a preset volume of gas to the lung indepen dent of the change in pulmonary or chest wall compliance or airway resistance. T he pulmonary and chest wall compliance and airway resistance determine the proxi mal airway pressure produced by these machines. Pressure Generators These deliver gas at a preset pressure. They are often simple, small, robust and cheap. The volume of gas that they deli ver can be altered by a change in the patients lung or chest wall compliance or airway resistance. Modern ventilators encompass both types of generator. They ca n ventilate the patient either by preset volume, independent of compliance, or p reset pressure which is interactive with pulmonary compliance and resistance, th us altering tidal volume. 149

6.4 Principles of ventilation 6 APPENDICES It is important to become familiar with the mechanics of both modes. 6.4.2 Ventilatory strategies to provide total ventilatory support Current approa ches to total ventilatory support generally attempt to duplicate the normal bulk ow ventilatory pattern and use tidal volumes (VT) of 5-10 ml.kg-1 . Machine brea th rates of 10-30 breaths per minute and inspiratory to expiratory ratios (I:E) of 1:4 to 1:2. These positive pressure breaths are generally delivered as either ow limited volume cycle breaths or pressure limited time cycle breaths. Positive pressure ventilatory support is usually used in conjunction with elevations in baseline (end expiratory) pressure (PEEP) and supplementary oxygen. These settin gs generally provide safe and effective total ventilatory support in most patien ts in respiratory failure. In more complex patients, conventional approaches do not provide ideal blood gas values, or airway pressures may be excessively high. Under these circumstances other strategies may be considered. 6.4.2.1 Controlled mechanical ventilation Spontaneous breaths are not available. This is the most basic form of mechanical ventilation supplying all ventilation in the apnoeic patient. During pressure control ventilation (PCV) each breath is delivered as time press ure controlled breaths and tidal volume varies, dependent on the resistance of t he airway, elastance and the total PEEP. 6.4.2.2 Assist control ventilation (ACV) In addition to a preset background rate of CMV breaths the patients inspiratory effort initiates a standard CMV breath. The abi lity to control respiratory rate means that less sedation is required, however t he respiratory muscles continue to contract during these assisted breaths with o nly a small reduction in work compared to unassisted spontaneous breaths. 6.4.2.3 Intermittent mandatory ventilation (IMV) This was introduced to allow unimpaired spontaneous breaths while still ventilated with intermittent CMV breaths to minimise sedative use and to reduce respiratory muscle discoordination, allow ing more rapid weaning. 6.4.2.4 Synchronised intermittent mandatory ventilation (SIMV) Is designed to av oid breath stacking by partitioning the inspiratory time into patient initiated or spontaneous breaths. Neither IMV nor SIMV has been clearly shown to allow eas ier weaning than T-piece trials. 150

6 APPENDICES 6.4 Principles of ventilation 6.4.2.5 Pressure support ventilation (PSV) During this type of ventilation the patient breaths are supported to a preset pressure using additional gas ow. Inspiration i s usually terminated when the inspiratory gas ow falls to about 25% of the initia l ow rate. The main disadvantage of pressure support ventilation is that the tida l volume may alter so that minute volume will alter depending on respiratory dri ve, pressure support level and respiratory system compliance. Excessively large tidal volumes resulting in overstretch of the lung may occur, possibly contribut ing towards ventilator associated lung damage. On some ventilators there is a si milar type of ventilation called volume support (VS) which is a mode of adaptive pressure support ventilation where breath to breath logic is used to assure pre set tidal volume. There are many other forms of ventilation which at the moment are still being investigated. These include airway pressure release ventilation, bilevel ventilation and proportional assist ventilation. Note: PSV and VSV are spontaneous modes. They cannot be used in paralysed patients. 6.4.3 Objectives of mechanical ventilation To improve alveolar ventilation and r educe PaCO2. To improve oxygenation and ventilation perfusion mismatch. To incre ase end expiratory lung volume to prevent or treat lobar or pulmonary collapse a nd atelectasis. To increase functional residual capacity through the use of PEEP , which may help improve oxygenation or reduce lung injury through adequate recr uitment with the prevention of repeated opening and closing of alveoli. To unloa d the respiratory muscles when there is an unbalance between load and the abilit y to cope. This results in respiratory muscle insuf ciency or ventilatory failure. To allow adequate sedation and paralysis of the patient to aid control to enabl e the underlying disease state to be adequately treated. In some conditions such as trauma where there is loss of chest wall integrity such as in a ail chest, ve ntilation may be needed to stabilise the chest wall and to initiate other treatm ent such as analgesia with safety. 6.4.4 Other Ventilatory strategies 6.4.4.1 Reverse I:E Ratio 1:2 to 1:4. This ra nge of I:E ratio tends to synchronise with the patients spontaneous ventilatory drive and permits adequate expiratory time for the lung to return to functional residual capacity (FRC) using the recoil pressure of the lung. The conventional inspiratory to expiratory (I:E) ratio is generally 151

6.4 Principles of ventilation 6 APPENDICES Lengthening the inspiratory time to I:E ratios approaching 1:1 or even exceeding it (inverse ratio ventilation) can be accomplished in either volume or pressure cycled modes. Prolonging inspiration has several physiological effects. The alv eolus is held at its inspiratory volume for a longer period. This should allow m ore mixing time between the alveolus and the conducting airway and more exposure of the capillary blood to fresh gas. Some studies have shown an improvement in ventilation perfusion (V /Q) mismatching with this technique and increases in th e PaO2 . Incomplete lung emptying. Under these conditions the lung cannot return to its normal FRC and intrinsic PEEP or auto-PEEP develops. Many of the studies on long inspiratory time and inverse ratio ventilation showing an improvement i n gas exchange have probably had this occur as a consequence of auto or intrinsi c PEEP. Long inspiratory times with air trapping may also improve V /Q mismatchi ng because it functions like applied PEEP, however there is often a trade-off to allow permissive hypercapnoea. This is largely a consequence of lower set respi ratory rates to allow adequate expiration per breath. Baseline alveolar pressure rises and thereby this raises maximum alveolar pressure for a constant tidal vo lume. The main role of inverse ratio ventilation is in alveolar recruitment in a cute lung injury and ARDS. In these conditions it is used as a ventilatory strat egy in an attempt to improve oxygenation. It is important to realise that once t he I:E ratio has been inverted the need for increased sedation and neuromuscular paralysis starts to increase. The mode is inherently uncomfortable and is poorl y tolerated in lightly sedated patients. There may be negative effects on cardia c output (increased intrathoracic pressure impeding venous return) 6.4.5 Ventila tion Mechanics 6.4.5.1 Tidal volumes Traditionally an average tidal volumes of a round 10-15 ml.kg-1 were used, and 10 ml/kg can be considered a reasonably safe tidal volume in most patients including children. In patients with poorly compli ant lungs or acute respiratory distress syndrome lower tidal volumes should be u sed ( < 8 ml.kg-1 ). 6.4.5.2 Respiratory frequency compliance. 6.4.5.3 Peak insp iratory airway pressure Generally this alarm should be set on the venThe respira tory frequency required in an adult varies between 8 and 25 in ations per minute and depends on the patients expiratory time an d lung tilator to at or below 35 - 40 cmH2 O to reduce side-effects of barotrauma. Plat eau pressure is probably a more reliable guide to risk of barotrauma than peak p ressure. Please note: The actual peak airway pressure generated in the patient s hould be 30 cmH2 O. 152

6 APPENDICES 6.5 The Sedation - Agitation Score Table 5: Sedation-Agitation Score 6.4.5.4 Positive end expiratory pressure Introduction PEEP is de ned as the pressure above atmospheric maintained at the ai rway at the end of expiration. It is a supportive technique used to increase art erial oxygen content without increasing the FiO2 and maintain alveolar / small a irways recruitment. Using PEEP PEEP may be indicated in patients with pulmonary oedema of cardiogenic or non cardiogenic origin. The usual range of applied PEEP varies anywhere from 5 t o 15 cmH2 O and rarely up to 20. Problems with using PEEP PEEP is generally contraindicated in patients who have a bronchopleural stula or severe barotrauma as it may further predispose to barot rauma including mediastinal air leak and pneumothorax. PEEP may also Increase ph ysiological dead-space Reduce the capacity to excrete carbon dioxide Reduce card iac output, which is due in part to a decrease in venous return and an increase in alveolar and therefore pulmonary blood pressure, i.e. an increase in RV after load, and alteration of left ventricular geometry (intraventricular septum shift ed towards the left). Other complications may include a decrease in renal blood o w and possibly a reduction in portal blood ow. Weaning from PEEP In general to wean from PEEP we usually reduce the fractional inspired oxygen concentration rst until it is down to approximately an Fi02 of 0. 5. The PEEP is then slowly removed in aliquots of 3-5 cmH2 O providing the PaO2 is maintained at 8 kPa or greater. 6.5 The Sedation - Agitation Score One of many sedation scores developed to assess and target depth of sedation. Th is score is not interchangeable with Glasgow Coma Score, the purpose of which is to assess depth of coma following an insult to the brain. 153

6.6 Classi cation of anti-arrhythmic drugs 6 APPENDICES 6.6 Classi cation of anti-arrhythmic drugs 6.6.1 Classi cation of Antiarrhythmic Drugs by Their Action The standard classi cati on of antiarrhythmic drugs was developed by Singh and Vaughan Williams based upo n the drugs electrophysiological mechanisms of action: Class I drugs act by block ing the Sodium channel, and are divided into 3 groups, IA, IB, and IC based on t heir effects on repolarization and potency towards blocking the Sodium channel S ubclass IA drugs are potent Sodium channel blockers (prolong QRS interval), and also usually prolong repolarization (prolong QT interval) through blockade of po tassium channels (quinidine, procainamide, disopyramide) Subclass IB drugs have the lowest potency as Sodium channel blockers, produce little if any change in a ction potential duration (no effect on QRS interval) in normal tissue, and short en repolarization (decrease QT interval) (lignocaine, mexiletine, tocainide, phe nytoin) Subclass IC drugs are the most potent Sodium channel blocking agents (pr olong QRS interval), and have little effect on repolarization (no effect on QT i nterval) (encainide, ecainide, propafenone) Class II drugs act indirectly on elec trophysiological parameters by blocking beta-adrenergic receptors (slow sinus rh ythm, prolong PR interval, no effect on QRS or QT intervals) (propranolol, esmol ol, acebutalol, l-sotalol) Class III drugs prolong repolarization (increase refr actoriness) by blocking outward potassium conductance (prolong QT interval), wit h typically little effect on the rate of depolarization (no effect on QRS interv al) (dofetilide, amiodarone ibutilide, bretylium, d/l-sotalol Class IV drugs are relatively selective AV nodal L-type Calcium-channel blockers (slow sinus rhythm , prolong PR interval, no effect on QRS interval) (Verapamil, diltiazem, bepridi l) Miscellaneous: In addition to the standard classes, IA-C, II, III, and IV, th ere is also a miscellaneous group of drugs that includes digoxin, adenosine and Magnesium with actions that dont t the standard four classes. The Vaughan Williams classi cation is relatively simple and is useful as a conversational shorthand ba sed on mechanism of action, for its ability to predict adverse effects, and for preliminary decisions regarding drug therapy, but it has a number of important d rawbacks: Drugs within a class are not necessarily clinically similar; a patient may respond well to one drug in a given class, but not another Almost all of th e currently available drugs have multiple actions; it is rarely apparent which o f these actions is responsible for suppression of an arrhythmia in a given patie nt The metabolites of many of the drugs contribute to or are primarily responsib le for their antiarrhythmic actions (e.g.-procainamide and its metabolite, N-ace tylprocainamide; 154

6 APPENDICES 6.7 Guidelines for the use of patient controlled anaesthesia (PCA) encainide and its metabolite, 3-methoxy-O-desmethylencainide) The stereoisomers of several drugs can have different actions: * The stereo isomers of disopyramid e (Class IA) have opposite effects on repolarization; the predominant effect in a given patient depends on the degree of stereospeci city exhibited in elimination of the drug by that patient * Only the l-isomer of sotalol has beta-adrenergic blocking activity Some of the most widely used drugs (procainamide, disopyramide , amiodarone, sotalol) have multiple actions which might explain their utility i n treating a broad range of arrhythmias. 6.7 Guidelines for the use of patient controlled anaesthesia (PCA) 6.7.1 Introduction Generally, PCA has been associated with better pain relief an d greater patient satisfaction compared with intermittent opioid injections. The reasons for this include: Small and frequent intravenous bolus doses of opioid can be given whenever the patient becomes uncomfortable, or when a painful stimu lus is anticipated, enabling individual titration of pain relief. This exibility helps to overcome the wide interpatient variation in opioid requirements. The in tensity of acute pain is rarely constant, and PCA means that the amount of opioi d delivered can be rapidly titrated. Patients can also titrate the amount of opi oid delivered against dose-related side effects. The inherent safety of the tech nique lies in the fact that, as long as the machine is in PCA mode only (ie. the re is no continuous infusion), further doses of opioid will not be delivered sho uld the patient become excessively sedated. 6.7.1.1 Contraindications Patient confusion Inability to understand the techniqu e. Untrained staff (medical and nursing) 6.7.2 Acute Pain Service Standard Orders Oxygen is routinely ordered for at leas t the rst 8 hours. No additional opioids or sedatives, unless ordered by the APS. Only the patient may press the demand button. The IV line must contain a non-re turn valve. Change syringe every 24 hours and line every 48 hours. 155

6.7 Guidelines for the use of patient controlled anaesthesia (PCA) 6 APPENDICES 6.7.2.1 Observations Pain score, sedation score, vomiting score, and respiratory rate hourly for 8 hours, then 2 hourly for duration of PCA. Total demands, good demands, amo unt in syringe, and cumulative dose hourly for 8 hours, then 2 hourly. SpO2 to b e recorded each nursing shift. 6.7.2.2 Opioids and equipment The PCA machines currently in use require a code t o change bolus or infusion rate. This information will be provided in the course of your training. 6.7.3 Programmable Variables 6.7.3.1 Loading Dose Patient controlled analgesia m ay not be effective for some time if moderate to severe pain is present from ons et. Generally, the same opioid to be used in the PCA should be given by the anae sthetist as intraoperative analgesia. During the recovery period, to make the pa tient comfortable before PCA is commenced, a loading dose of opioid may be requi red. There is enormous inter-patient variation in the amount of opioid needed, a nd it is better to individualise for each patient 6.7.3.2 Bolus Dose The optimum bolus dose is that which results in appreciable a nalgesia without signi cant side effects. The best predictor of dose required is p atient age, as patient weight is of relatively little importance. An estimation of the rst 24 hour Morphine requirements can be given by the formula (for patient s aged 20 years and older). Morphine requirements (mg) = 100-(age in years) From this formula it can be seen that, on average, Morphine requirements for a 70 ye ar old patient are less than half the dose of a 20 year old. The size of the bol us dose should generally be halved in patients over 70 years of age, and conside ration should be given to further reducing the size of the bolus dose in patient s aged over 80 years. 6.7.3.3 Dose Duration Dose duration is usually set at stat. However, the rate of delivery can be slowed to as much as 10 minutes. 6.7.3.4 Lock-out interval This is the time from the end of delivery of one dose until the machine will respond to another demand. This allows the patient to feel the effe ct of one dose 156

6 APPENDICES 6.7 Guidelines for the use of patient controlled anaesthesia (PCA) before receiving a subsequent dose. Most patients have an inherent maximum frequ ency of demand-the average rate is 3-5 doses per hour. 6.7.3.5 Continuous (background) infusion A continuous infusion decreases the inh erent safety of PCA, as opioid will be delivered regardless of how sedated the p atient may be. This mode should only be used on the advise of the APT or the ICU Consultant. 6.7.3.6 Drug concentration Standard prescriptions are employed (see below). Howe ver, delivery of the drug may not be accurate if the volume delivered is less th an 0.5mls. Hence, dilutions are used for children and the very elderly. 6.7.4 Standard Prescriptions for PCA 6.7.4.1 Morphine Usually the opioid of hoice. Standard orders For patients aged 15 to 70 years: Bolus 1 mg, lockout 5 minutes 70 to 80 / 85 years: Bolus 0.5 mg , lockout 5 minutes If analgesia is inadequate (in all age groups), consider doubling the size of the bolus dose, or alternati ve agent (eg: Tramadol). 6.7.4.2 Special Situations PCA and the opioid tolerant patient These patients are likely to require much la rger doses of opioids and a background infusion bene ts many. To calculate an appr opriate background infusion, base it upon 50100% of the patients usual opioid re quirements. The bolus dose which is ordered (in mg.) is normally the same as the background infusion in mg/hr. Incomplete Cross Tolerance The degree of cross tolerance that occurs between opi oids is unpredictable, and appears to be incomplete. If a change is made from on e opioid to another, especially when doses have been high, it may be best to com mence the new opioid at a dose that is about 50% of the calculated equianalgesic dose of the new opioid. The equianalgesic doses given above are based on single dose studies in opioid nave patients and should be used cautiously in patients o n long term opioids. In particular, if changing opioid therapy to oral methadone , doses that are about 10-15% of the expected equianalgesic dose may be more app ropriate. This lower than expected dose may be due to the long and variable half life of methadone and also because methadone is thought to have NMDA receptor a ntagonist properties. 157 rst c

6.7 Guidelines for the use of patient controlled anaesthesia (PCA) 6 APPENDICES Illicit Opioids Where a patient has been using illicit opioids the amount and pu rity of the drug they have been using is dif cult to ascertain. As a rough guide, one should assume purity to be no more than 50% . It is safer to be conservative . 6.7.4.3 Problem Solving and PCAs Patient Confusion Patient confusion and inabili ty to understand the use of a PCA is an absolute contraindication and other means of analgesia should be used. Inadequate Analgesia access. Assess the patient. Exclude technical issues, including pump programming and function, and reliabili ty of vascular If there is increasing pain, increasing analgesic requirements, o r pain out of proportion to that expected for the procedure or for the number of days elapsed since the procedure, then there may be another cause for the pain. A complication may have developed (eg. a leaking anastomosis following bowel su rgery), or the patient may have colicky wind pain which responds poorly to opioi ds. If these are excluded and the patient is receiving 3 bolus doses per hour on average, encourage the patient to use the demand button more frequently. If sid e effects are limiting use of the PCA, treat these. If the patient is receiving 3 bolus doses per hour, and still has inadequate analgesia, increase the size of the bolus dose (usually double). If the patient complains of waking in severe p ain frequently at night, and PCA use is high, then consider adding a background infusion. The size of the background infusion should not be greater than the bol us dose. Nausea and Vomiting should be tried. An appropriate antiemetic should be given. If the patient has low analgesic requirements, then a decrease in the size of th e bolus dose Non-opioid analgesia such as regular paracetamol and NSAID supposit ories (if no contraindications such as lower GI surgery) should be added. If the patient feels a wave of nausea soon after pressing the demand button, then slow ing the rate of administration of the bolus dose (increasing the dose duration) may be of bene t. Individual patients may be more sensitive to a particular opioid . If other measures have failed, then it is worth considering a change to a diff erent opioid. However, remember that opioids are not the sole cause of post-oper ative vomiting. Pruritus Pruritus may be caused through both histamine release and u-receptor ac tivation. It is more commonly seen with Morphine that Fentanyl. In the hospital setting, pruritus is most often caused by lying on a plastic covered mattress! ( pruritus is present on the back only). 158

6 APPENDICES 6.7 Guidelines for the use of patient controlled anaesthesia (PCA) If the distribution of the pruritus is on the face and trunk, then it is likely to be due to the opioid. Treatment options are: Change the opioid. eg. Morphine to Fentanyl. Titrate small (50-100 mcg) doses of Naloxone. Antihistamines-but th ese may lead to sedation and respiratory depression. Sedation and Respiratory Depression These are unusual with a pure PCA - i.e. with no background infusion, with an appropriate size of bolus dose and no additional se dative agents. If a patient does have a sedation score of -1 (constantly or freq uently drowsy-falls asleep during conversation but easy to rouse), then a reduct ion in bolus dose (usually by half) and ceasing any background infusion is indic ated. If the patient has a respiratory rate of 8 or less, in addition to a sedat ion score of -1, then titration of Naloxone in 100mcg doses should be considered , in addition to the above. If the patient has a sedation score of -2 or less (s omnolent, dif cult to rouse) then Naloxone should be administered regardless of th e respiratory rate. Problems not infrequently arise in the opioid dependent pati ent, who becomes sedated, yet complains of high pain scores. It should be explai ned to these patients that they cannot be safely given more opioid, and that com plete pain relief may be an unrealistic aim for them. Addition of non-opioid pai n relief may be of value. Urinary Retention Urinary retention can occur, and should be treated with catheterisation. Be wary of the possibility of sedation / respiratory depression in the patient w ho has been treating the pain of a distended bladder with their PCA, who then ha s the pain relieved by a catheter. Inhibition of Bowel Motility To some extent, inhibition of bowel function is ine vitable. Patients should be discouraged from using their PCA to treat wind pains . Hypotension Opioids will not in themselves cause hypotension, but may unmask hyp ovolaemia (through a reduction in sympathetic tone). 159

Index Acid Base Disturbances, 93 Metabolic acidosis, 94 Metabolic alkalosis, 95 Respir atory acidosis, 94 Respiratory alkalosis, 94 acidosis metabolic, 94, 95 respirat ory, 94, 97 adenosine, 55 Admission patient, 15 primary survey, 15 secondary sur vey, 15 admission elective, 12 policy, 11 refusal, 12 Adrenaline, 49 alkalosis m etabolic, 95, 96 respiratory, 94, 97 Aminophylline, 55 amiodarone, 56, 57 Amrino ne, 50 anion gap, 95 anti-arrhythmic drugs, 154 Anti-hypertensive, 52 Antiarrhyt hmic drugs, 53 antibiotic prescription, 84 antibiotics guideline, 84 anticoagula tion, 73 Arterial Cannulae, 24 Atropine, 54 bicarbonate, 96 Bradyarrhythmias, 54 brain death, 141 brain stem testing, 142 Electrolyte abnormalities, 87 cardiac arrest CPR, 17 Central venous cannulae, 25 Charcoal, 140 Clinical duties on ICU, 14 outside ICU, 17 cardiac arrest, 17 Trauma, 17 Clinical Lead, 9 clonidine, 52 Consent, 21 Consultants, 9 Coroner referral, 13 CPR, 106 induced hypothermia, 1 07 Cricothyroidotomy, 37 Cryoprecipitate, 104 DDAVP, 77 ddrenaline, 54 diabetes Insipidus, 77 DIC, 104 Dif cult intubation, 34 dipyridamole, 55 discharge policy, 12 procedure, 12 diuretics, 79 Dobutamine, 49 Documentation, 15 Dopamine, 49 Dop examine, 49 DVT, 73 DVT prophylaxis, 74 bronchodilators, 58 Bronchoscopy, 37 160

Index Hyperkalaemia, 91 Hypernatraemia, 89 Hypokalaemia, 90 Hyponatraemia, 88 Hy pophosphataemia, 92 SIADH, 89 Enteral Netrition, 98 erythromycin, 84 Feeding gui deline, 99 FFP, 104 uids management, 85 replacement, 85 resuscitation, 86 Fresh F rozen Plasma, 103 Fungal infections, 138 gastric lavage, 139 gastric stress ulce r, 80 glucose blood, 76 Guideline feeding, 99 Microbiology, 134 Guidelines PCA, 155 head injury, 130 Henderson equation, 94 Henderson/Hasselbach equation, 94 he parin, 74 heparin induced thrombocytopaenia, 75 unfractionated, 75 HFOV: see Mec hanical ventilation, 116 HMEs, 110 Hospital Emergencies, 22 Humidi cation, 110 Hyp erkalaemia, 91 Hypernatraemia, 89 Hypokalaemia, 90 Hyponatraemia, 88 Hypophospha taemia, 92 hypotension, 144 magnesium, 57 Mannitol, 131 Mechanical Ventilation, 110 HFOV, 116 Pressure Support, 115 prone position, 122 Prone positioning, 119 l ignocaine, 57 ICU Procedures, 23 Arterial Cannulae, 24 Bronchoscopy, 37 Cricothy roidotomy, 37 CVC, 25 ICD, 31 Index intraabdominal pressure manometry, 46 intubation, 32 extubation guideline, 36 in tubation guideline, 33 rapid sequence, 35 Nasojejunal, 45 Peripheral IV catheter s, 23 Pleural Procedures, 30 Pulmonary artery catheter, 29 Tracheostomy, 38 IMV, 150 induction rapid sequence, 35 Infection Control, 18 Information Technology, 21 Inotropes, 48 insulin, 76 Intercostal catheter, 31 Intra-abdominal pressure m anometry, 46 intubation dif cult, 34 Intubation, endotracheal, 32 Isoprenaline, 54 proportional assist ventilation, 114 Tube Compensation, 115 weaning, 119 Milrino ne, 50 161

Index Nasojejunal tube insertion, 45 Neurotrauma, 130 Nimodipine, 134 NIPPV, 123 Noradrenaline, 49 Nutrition Enteral, 98 parenteral, 101 Omeprazole, 83 organ do nation, 141 Orientation, 11 Osmotherapy, 131 Overdose, 139 Parenteral Nutrition, 101 paroxysmal atrial tachycardia, 58 patient admission, 15 PCWP, 146 PEEP, 114 , 153 pH, 94 phenytoin, 58 Phosphodiesterase inhibitors, 50 PiCCO, 147 platelets dose, 103 transfusion, 102 Pleurocentesis, 31 pneumonia invesitgation, 136 Noso comial, 137 policy admission, 11 discharge, 12 Preload, 145 procainamide, 58 Pro kinetics, 99 Proportional Assist Ventilation, 114 Prostacyclin, 129 PSV, 151 Pul monary Artery catheterisation, 29 quinidine, 58 Sedation, 59, 131 Sedation Agita tion Score, 153 Sepsis, 135 sepsis screening, 135 Vascular catheter, 137 Septic Shock, 135 shock, 144 SIADH, 89 SIMV, 150 SIRS, 135 sotalol, 57 spontaneous brea thing trial, 120 status epilepticus, 132 refractory, 133 steroids, 78 subarachno id haemorrhage, 133 Supraventricular arrythmia, 55 Suxamethonium, 34 torsade de pointes, 57 Tracheostomy Percutaneous, 38 complications, 42 decannulation, 44 po licy, 38 procedure, 40 timing, 40 transfusion blood, 102 FFP, 103 Massive, 104 p latelet, 102 reaction, 105 risk, 103 Triage patient, 11 Renal preotective strate gies, 126 replacement therapy, 127 Renal Failure, 125 Respiratory Failure, 108 Index 162

Index ventilation assist control, 150 CMV, 150 IMV, 150 inverse ratio, 151 PSV, 151 SIMV, 150 Ventilator settings, 112 ventilators, 149 Ventricular arrythmias, 57 Verapamil, 56 warfarin, 73 Weekly Program, 10 Withdrawal of therapy, 13 Withd rawal of treatment, 140 Index 163

Index Index Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported Licence 164