1. Dr. Ed Martinez (Intensivist wanna be)

2. Our patients In ICU almost all of our patients are very sick Very old Multiple co morbidities Multiple injuries Susceptible to multiple complications Haven’t looked after themselves

4. The CICM says that: “Intensive care specialists require an extensive knowledge of medical and surgical conditions and mastery of practical skills. The intensive care specialist anticipates clinical problems, is able to assess and define clinical problems in the critically ill in the broader context and can develop and facilitate a diagnostic and management plan, which has the highest probability of a satisfactory outcome.” Objectives of advanced training and competencies. College of intensive care medicine of Australia and New Zealand.

5. The Approach to Acute Illness Immediate assessment and therapy (resuscitation) – Prioritize: who to admit and not admit Resuscitate vs. Diagnose Obtain relevant information Recognize and respond rapidly to adverse events

6. The Approach to Acute Illness Assessment Obtain and record relevant info from patient, relatives, others Recognise and diagnose system failure or diseases Order appropriate investigations

7. Approach to Acute Illness Problem Definition Create a list of DDx. You might need to confirm or refute some of these before your data gathering is complete Deal with ambiguity Make contingency plans

8. Approach to Acute Illness Make a Plan Choose the best course of action considering risk vs. Benefit ICU requires multidisciplinary input and decide who else needs to be involved Plan counter measures Define the circumstances where supportive therapy should be limited or discontinued

9. Approach to Acute Illness Progress Use clinical and physiological markers to assess severity and likely outcome Know that sudden gross changes in certain parameters are life threatening Develop criteria for discharge

13. A Structured Approach Make a List of DDx Look for clues Confirm your suspicions Make a plan – Immediate: resuscitate – Short term: therapy, who else needs to be involved – Long term: where is this patient going to go after ICU

14. So now... 1. Common problems in ICU 2. How to tackle them when we first encounter them

15. The Shocked Patient

16. Shock: Clinical state that occurs when an imbalance of oxygen supply and demand results in the development of tissue hypoxia

17. The Shocked Patient Physiologically – Hypoxic – Anaemic – Stagnant – histotoxic Clinically – Cardiogenic-Septic – Obstructive-Neurogenic – Hypovolaemic-Anaphylactic

18. The Shocked Patient Common scenarios in ICU Sepsis: as a primary cause of admission or as a consequence of nosocomial infections Trauma with ongoing blood loss Cardiogenic shock in association with APO

19. The Shocked Patient Look for clues Are they bleeding? What is their MAP and pulse pressure? HR and rhythm: SR vs. AF? CVP: high or low? Sats: is there an adequate trace? What is their U/O?

20. The Shocked Patient Look for clues Hypovolaemic shock Fluid balance Actively bleeding? Check for haemothorax and distended abdomen Any other major fluid losses (eg. Intra-abdo in pancreatitis)

21. The Shocked Patient Look for clues Obstructive shock Tension pneumothorax? ICCs blocked? Cardiac tamponade PE? Signs of DVTs?

22. The Shocked Patient Look for clues Distributive Shock Septic? Febrile, warm, vasodilated? Meningococcal rash, neck stiffness? Neurological shock due to spinal injury? Anaphylaxis or Addisonian crisis?

23. The Shocked Patient Look for clues Cardiogenic shock HR Rhythm Preload Pump function After load

24. The Shocked Patient Confirm your diagnosis CXR ECG Echo ABGs and lactate FBCs, EUCs Troponin

29. The Shocked Patient Make a plan Immediate Resuscitate with IVF. How much? Which type? Inotropes, vasopressors or both? Transfuse. RPC, FFP, Platelets? Steroids? Do we need to plumb this patient? When is a good time to that?

30. The Shocked Patient Make a plan – Short term OT to control bleeding, source control? – Involve Anes. and Sx. ATBs? Which ones? – Involve ID Ongoing transfusion due to coagulopathy? – Involve Haematology Do they need to go to angio suite? – Involve the cardiologist.

31. The Shocked Patient Evidence for what we do Surviving Sepsis campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004: 32: 858-873 Recommendations with the intention of improving outcome, some of the conclusions are still being debated

32. The Shocked Patient Evidence for what we do A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Eng J Med 2004; 350: 2247-2256 Multicenter RCT w/ 6997 pts. No difference in 28-day mortality, no difference in how they did overall. Subgroup analysis did show a trend to reduced mortality w/albumin in septic shock and increased mortality in trauma patients, especially those w/ TBI. So, lets try and use crystalloids because it’s cheaper.

33. The Shocked Patient Evidence Early revascularization in acute myocardial infarction complicated by cardiogenic shock. N Eng J Med 1999; 341:625-634 Cardiogenic shock complicates 10% of AMI and is associated with 80% mortality. RCT w/302 pts. Who underwent revascularization (PCI or CABG) or medical management; 80% in both groups got IABPs No difference in 30 day mortality but at 6mo. Pts. Who got revasc. Had a survival advantage

34. The Shocked Patient Evidence Vasopressor use in septic shock: an update. Current Opinion in Anaesthesiology. 2008; 21: 141-7 Catecholamines for shock: the quest for high-quality evidence. Crit Care Resusc. 2007 Dec; 9(4): 352-6 Both says there’s no clear evidence of which is better or worse

35. The Anuric Patient

36. Acute renal failure: rapid decrease in the kidney’s ability to eliminate waste products. Clinical classification: Prerenal Parenchymal Postrenal

37. The Anuric Patient

38. Common scenarios in ICU ARF related to Shock MOF Rhabdomyolysis Hepatorenal failure Nephrotoxic drugs or contrast agents Ruptured AAA

39. The Anuric Patient Look for clues from the history Is this acute, acute on chronic or chronic ? Is there a pre-renal cause? Is there raised intra-abdo pressure? Is there a renal cause? Have nephrotoxins or contrasts been given? Is there a vasculitis? Is there a post-renal cause? Is the IDC blocked? Has the patient had pelvic Sx?

40. The Anuric Patient Look for clues from the examination Compartment syndromes: tense limbs, buttocks, abdo Abdo scar from major vascular or abdo surgery Signs of chronic liver disease Signs suggesting diabetes: scarred fingertips, abdo fat atrophy or hypertrophy from insulin injections

41. The Anuric Patient Confirm your suspicions EUC, CMP, LFTs Urine dipstick and microscopy: leukocytes and nitrites as indices of infection, blood reflecting urinary tract trauma, haemoglobin or myoglobinuria Check serum and urinary electrolytes: help differentiate pre-renal from renal causes ABGs: look for metabolic and electrolyte derrangements

42. The Anuric Patient

44. Make a Plan To treat ARF we need to: 1) reverse its cause 2) maintain homeostasis while recovery occurs Immediate: do we need to resuscitate this patient? Are they hyperkalaemic to the point they could die?

45. The Anuric Patient Make a plan Short term: Nutritional support Metabolic acidosis Anaemia Adjust drug doses Lasix if they still making urine to avoid fluid overload Vascath and CRRT

46. The Anuric Patient Make a plan Short term: Indications for CRRT Oliguria: U/O<200ml/12hrs Anuria: U/O 0-50ml/12hrs Ur.>35mmol/L Cr.>400mmol/L K+>6.5mmol/L or rapidly rising APO unresponsive to diuretics

47. The Anuric Patient Make a plan Short term: Indications for CRRT Uncompensated met. Acidosis pH<7.1 Na+ 160mmol/L Temp. >40 Uraemic complications: encephalopathy, myopathy, neuropathy, pericarditis Overdose w/dialysable toxin: eg. Lithium

48. The Anuric Patient Make a plan Long term Involve the renal or urology team Will this patient need dialysis long term? Will they need a fistula?

49. The Anuric Patient Evidence for what we do Meta-analysis of frusemide to prevent or treat acute renal failure. BMJ. 2006 Aug 26: 333 (7565): 420 Meta-analysis of 9 RCT totalling 849 pts. to investigate the potential beneficial and adverse effects of frusemide to prevent and treat acute renal failure in adults Found that frusemide is not associated with any significant clinical benefits in the prevention or treatment of adults, but, high doses can cause ototoxicity

50. The Anuric Patient Evidence CVVHDF vs. IHD for acute renal failure in patients with multiple organ dysfunction: a multicenter randomized trial. Lancet 2006; 368: 379-385 Prospective randomized study w/360 pts. w/ARF due to MODS. No difference in 60 day mortality with same efficacy, no difference in duration of renal support No more hypotension with IHD, CVVHDF caused more hypothermia

51. The Patient with a Head Injury

52. Primary Brain Injury Severity determined by degree of neuronal damage Determines outcome Include all types of injury to brain parenchyma and vasculature Adverse outcomes include: Traumatic SAH Non-evacuable mass lesions

53. The Patient with a Head Injury Secondary brain injury Reduction in cerebral substrate utilization, mostly oxygen Systemic: Hypoxia, hypotension, hypocapnia, hyperthermia, hypoglycaemia are the worst Also: hyperglycaemia, hyper and hyponatraemia, hyperosmolality, infections Intracranial: Seizures, delayed haematoma, SAH, vasospasm, hydrocephalus, neuroinfection

54. The Patient with a Head Injury DDX Is this an isolated injury or not? Was this patient intoxicated? Is this patient not waking up after trauma to another part of the body? (eg. Fat embolus) What other factors will influence management? (eg. Ortho Sx.)

55. The Patient with Head Injury Look for clues What type of sedation are they on? When was it stopped? Any neuromuscular blockers given? When was the last dose? Do they have an ICP monitor, will they need one? What are their HR, BP, Sats, Temp?

56. The Patient with Head Injury Look for clues Head wounds Stigmata of base of skull fracture: haemotympanum, CSF from ears or nose, Battle’s sign, racoon eys Assess GCS: use bilat. Central and peripheral painful stimuli Check pupils: size, shape, symmetry, light response, think of traumatic midriasis

57. The Patient with Head Injury Confirm your suspicions X-rays: chest, pelvis, C-spine CT head: if there was LOC, combative with EtOH, drugs, extracranial injuries Cerebral angiography: when vascular injury is suspected MRI: better used as prognostic tool

63. The Patient with Head Injury Make a plan Immediate: in ED Immobilize Decide whether we need to intubate Severe TBI=GCS<9 Rapidly declining LOC Altered LOC and “uncooperative”

64. The Patient with Head Injury Make a plan Immediate: in ED After intubated PO2>100mmHg PCO2 36-40mmHg Hb =100g/L MAP>90 Mannitol if: dilated pupil, deteriorating LOC

65. The Patient with Head Injury Make a plan Immediate: in ED Indications for ICP monitoring GCS<9 and abnormal CT GCS<9 and normal CT and 2 of: Age >40 Significant hypotension Motor posturing GCS>8 and Severe extracranial injuries and neuro assessment will be difficult due to prolonged anaesthesia and sedation

66. The Head injury Patient Make a plan Short term Will they need to go to OT? Involve NeuroSx, anaes Follow BTF guidelines to prevent secondary injury Homeostasis is the name of the game Control intracranial hypertension

67. The Patient with Head Injury Make a plan Long term When will we wake them up? Will they need a trachie? How are we going to prevent complications Is rehab going to be needed? Involve rehab physicians

68. The Patient with Head Injury Evidence for what we do Brain Trauma Foundation guidelines. Management and prognosis of severe traumatic brain injury. www.braintrauma.org Consensus guidelines from experts, based on evidence, provide protocols that may improve outcomes. Initially published in 1995 and revised in 2005: key change was loweriing of CPP from 70 to 60mmHg due to probable assoc. With ARDS

69. The Patient with Head Injury Evidence Lack of effect of induction of hypothermiaafter acute brain injury. N Eng J Med 2001; 344: 556-563. Cooling them doesn’t work, although ICP were lower in hypothermia

70. The Patient with Head Injury Evidence Effect of intravenous corticosteroids on death within 14 days in10,008 adults with clinically significant head injury. (MRC CRASH trial): randomised placebo- controlled trial. Lancet 2004; 364: 1321-1328 Methylpred. Vs. Placebo Increased risk of death from all causes in those who got steroids Mechanism of harm is unclear

71. So... Lots to learn Its better to be systematic Come up with your own system and run with it!

72. Thank you!