Dr. Ed Martinez (Intensivist wanna be). Our patients In ICU almost all of our patients are very sick...

Dr. Ed Martinez(Intensivist wanna be)

Our patientsIn ICU almost all of our patients are very sick

Very old Multiple co morbiditiesMultiple injuriesSusceptible to multiple complicationsHaven’t looked after themselves

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.

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

The Approach to Acute IllnessAssessment

Obtain and record relevant info from patient, relatives, others

Recognise and diagnose system failure or diseases

Order appropriate investigations

Approach to Acute IllnessProblem Definition

Create a list of DDx.You might need to confirm or refute some of

these before your data gathering is completeDeal with ambiguityMake contingency plans

Approach to Acute IllnessMake 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 measuresDefine the circumstances where supportive

therapy should be limited or discontinued

Approach to Acute IllnessProgress

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

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

So now...1. Common problems in ICU2. How to tackle them when we first encounter

them

The Shocked Patient

The Shocked PatientShock:

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

The Shocked Patient• Physiologically

– Hypoxic– Anaemic– Stagnant– histotoxic

• Clinically– Cardiogenic -Septic – Obstructive -Neurogenic– Hypovolaemic -Anaphylactic

The Shocked PatientCommon scenarios in ICU

Sepsis: as a primary cause of admission or as a consequence of nosocomial infections

Trauma with ongoing blood lossCardiogenic shock in association with APO

The Shocked PatientLook 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?

The Shocked PatientLook for clues

Hypovolaemic shock Fluid balance Actively bleeding? Check for haemothorax and distended abdomen Any other major fluid losses (eg. Intra-abdo in

pancreatitis)

The Shocked PatientLook for clues

Obstructive shock Tension pneumothorax? ICCs blocked? Cardiac tamponade PE? Signs of DVTs?

The Shocked PatientLook for clues

Distributive Shock Septic? Febrile, warm, vasodilated? Meningococcal rash, neck stiffness? Neurological shock due to spinal injury? Anaphylaxis or Addisonian crisis?

The Shocked PatientLook for clues

Cardiogenic shock HR Rhythm Preload Pump function After load

The Shocked PatientConfirm your diagnosis

CXRECGEchoABGs and lactateFBCs, EUCsTroponin

The Shocked PatientMake 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?

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.

The Shocked PatientEvidence 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

The Shocked PatientEvidence 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.

The Shocked PatientEvidence

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

The Shocked PatientEvidence

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

The Anuric Patient

The Anuric PatientAcute renal failure:

rapid decrease in the kidney’s ability to eliminate waste products.

Clinical classification:PrerenalParenchymalPostrenal

The Anuric Patient

The Anuric PatientCommon scenarios in ICU

ARF related to Shock MOF Rhabdomyolysis Hepatorenal failure Nephrotoxic drugs or contrast agents Ruptured AAA

The Anuric PatientLook 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?

The Anuric PatientLook for clues from the examination

Compartment syndromes: tense limbs, buttocks, abdo

Abdo scar from major vascular or abdo surgerySigns of chronic liver diseaseSigns suggesting diabetes: scarred fingertips,

abdo fat atrophy or hypertrophy from insulin injections

The Anuric PatientConfirm your suspicions

EUC, CMP, LFTsUrine 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

The Anuric Patient

The Anuric Patient

The Anuric PatientMake 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?

The Anuric PatientMake 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

The Anuric PatientMake 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

The Anuric PatientMake a plan

Short term:Indications for CRRT

Uncompensated met. Acidosis pH<7.1 Na+ <110mmol/L or >160mmol/L Temp. >40 Uraemic complications: encephalopathy, myopathy,

neuropathy, pericarditis Overdose w/dialysable toxin: eg. Lithium

The Anuric PatientMake a plan

Long term Involve the renal or urology team Will this patient need dialysis long term? Will they need a fistula?

The Anuric PatientEvidence 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

The Anuric PatientEvidence

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

The Patient with a Head Injury

The Patient with a Head InjuryPrimary 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

The Patient with a Head InjurySecondary 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

The Patient with a Head InjuryDDX

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.)

The Patient with Head InjuryLook 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?

The Patient with Head InjuryLook for clues

Head woundsStigmata 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

The Patient with Head InjuryConfirm your suspicions

X-rays: chest, pelvis, C-spineCT head: if there was LOC, combative with

EtOH, drugs, extracranial injuriesCerebral angiography: when vascular injury is

suspectedMRI: better used as prognostic tool

The Patient with Head InjuryMake a plan

Immediate: in ED Immobilize Decide whether we need to intubate

Severe TBI=GCS<9 Rapidly declining LOC Altered LOC and “uncooperative”

The Patient with Head InjuryMake a plan

Immediate: in ED After intubated

PO2>100mmHg PCO2 36-40mmHg Hb =100g/L MAP>90 Mannitol if: dilated pupil, deteriorating LOC

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

The Head injury PatientMake 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

The Patient with Head InjuryMake 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

The Patient with Head InjuryEvidence 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

The Patient with Head InjuryEvidence

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

The Patient with Head InjuryEvidence

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

So...Lots to learnIts better to be systematicCome up with your own system and run with

it!

Thank you!