Transcript How should I be thinking? (a suggested way of doing it)

Dr. Ed Martinez
(Intensivist wanna be)
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
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:
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who to admit and not admit
Resuscitate vs. Diagnose
Obtain relevant information
Recognize and respond rapidly to adverse events
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
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
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
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
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...
Common problems in ICU
2. How to tackle them when we first encounter them
1.
The Shocked Patient
The Shocked Patient
 Shock:
 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
– Obstructive
– Hypovolaemic
-Septic
-Neurogenic
-Anaphylactic
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
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?
The Shocked Patient
 Look for clues
 Hypovolaemic shock
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Fluid balance
Actively bleeding?
Check for haemothorax and distended abdomen
Any other major fluid losses (eg. Intra-abdo in pancreatitis)
The Shocked Patient
 Look for clues
 Obstructive shock
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Tension pneumothorax? ICCs blocked?
Cardiac tamponade
PE? Signs of DVTs?
The Shocked Patient
 Look for clues
 Distributive Shock
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Septic?
Febrile, warm, vasodilated?
Meningococcal rash, neck stiffness?
Neurological shock due to spinal injury?
Anaphylaxis or Addisonian crisis?
The Shocked Patient
 Look for clues
 Cardiogenic shock
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HR
Rhythm
Preload
Pump function
After load
The Shocked Patient
 Confirm your diagnosis
 CXR
 ECG
 Echo
 ABGs and lactate
 FBCs, EUCs
 Troponin
The Shocked Patient
 Make a plan
 Immediate
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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
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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 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
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Recommendations with the intention of improving outcome,
some of the conclusions are still being debated
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
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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 Patient
 Evidence
 Early revascularization in acute myocardial infarction
complicated by cardiogenic shock. N Eng J Med 1999;
341:625-634
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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 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
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Both says there’s no clear evidence of which is better or worse
The Anuric Patient
The Anuric Patient
 Acute renal failure:
 rapid decrease in the kidney’s ability to eliminate waste
products.
 Clinical classification:
 Prerenal
 Parenchymal
 Postrenal
The Anuric Patient
The Anuric Patient
 Common scenarios in ICU
 ARF related to
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Shock
MOF
Rhabdomyolysis
Hepatorenal failure
Nephrotoxic drugs or contrast agents
Ruptured AAA
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?
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
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
The Anuric Patient
The Anuric Patient
The Anuric Patient
 Make a Plan
 To treat ARF we need to:
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1) reverse its cause
2) maintain homeostasis while recovery occurs
 Immediate:
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do we need to resuscitate this patient?
Are they hyperkalaemic to the point they could die?
The Anuric Patient
 Make a plan
 Short term:
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Nutritional support
Metabolic acidosis
Anaemia
Adjust drug doses
Lasix if they still making urine to avoid fluid overload
Vascath and CRRT
The Anuric Patient
 Make a plan
 Short term:
 Indications for CRRT
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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 Patient
 Make a plan
 Short term:
 Indications for CRRT
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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 Patient
 Make a plan
 Long term
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Involve the renal or urology team
Will this patient need dialysis long term?
Will they need a fistula?
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
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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 Patient
 Evidence
 CVVHDF vs. IHD for acute renal failure in patients with
multiple organ dysfunction: a multicenter randomized
trial. Lancet 2006; 368: 379-385
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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 Injury
 Primary Brain Injury
 Severity determined by degree of neuronal damage
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Determines outcome
 Include all types of injury to brain parenchyma and
vasculature
 Adverse outcomes include:
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Traumatic SAH
Non-evacuable mass lesions
The Patient with a Head Injury
 Secondary brain injury
 Reduction in cerebral substrate utilization, mostly
oxygen
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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 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.)
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?
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
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
The Patient with Head Injury
 Make a plan
 Immediate: in ED
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Immobilize
Decide whether we need to intubate
 Severe TBI=GCS<9
 Rapidly declining LOC
 Altered LOC and “uncooperative”
The Patient with Head Injury
 Make a plan
 Immediate: in ED
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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
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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 Patient
 Make a plan
 Short term
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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 Injury
 Make a plan
 Long term
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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 Injury
 Evidence for what we do
 Brain Trauma Foundation guidelines. Management and
prognosis of severe traumatic brain injury.
www.braintrauma.org
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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 Injury
 Evidence
 Lack of effect of induction of hypothermiaafter acute
brain injury. N Eng J Med 2001; 344: 556-563.
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Cooling them doesn’t work, although ICP were lower in
hypothermia
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 placebocontrolled trial. Lancet 2004; 364: 1321-1328
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Methylpred. Vs. Placebo
Increased risk of death from all causes in those who got
steroids
Mechanism of harm is unclear
So...
 Lots to learn
 Its better to be systematic
 Come up with your own system and run with it!
Thank you!