Intensive Care

Question 1

Describe the clinical evaluation for determination of brain death.

Answer 1

Establish irreversible and proximal causes of brain death.
Exclude CNS depressants. X5 the drugs half life.
No electrolyte or endocrine disorder.
No recent administration of neuromuscular blockers confirmed by train of 4
Achieve normal core temperature >36C

Question 2

Outline the management of a 25yo male who has been certified brain dead awaiting organ retrieval?

Answer 2

Temperature management. Hypothermia is common due to exposure, inability to shiver or vasoconstrict, cold fluids, reduced metabolic rate. Avoid by warming blankets, warming room, warming fluids,
Respiratory support. Avoid fluid overload. Ventilate to normocarbia with minimal tidal volume and FiO2 as tolerated. Bronchoscope if persistent collapse, consider physiotherapy
Haemodynamic support. Maintain MAP with fluids and vasopressors (NORAD usually). Monitor fluid balance and urine output.
Metabolic, haematological and biochemical management. Test for DI and treat with DDAVP. Insulin for bsls>12. May require thyroxine. Treat coagulopathy. Avoid electrolyte disturbance -Na,Mg,Ca,Phos.
Communication with both family/relatives and the retrieval team

Question 3

Outline the preconditions that must be met prior to certification of brain death via clinical examination?

What are the imaging tests for assessment of cerebral blood flow?

Answer 3

Identification of cause.
Exclusion of sedative drugs as a cause.
Normotensive 90 systolic, MAP 60
Normothermic >35C
Capacity to examine one eye and one ear - so that brain stem reflexes may be examined
Absence/correction of metabolic, endocrine or electrolyte disorder
Intact neuromuscular function as evidenced by peripheral nerve stimulation ie., train of 4
Ability to perform apnea testing

CT angiography absent enhancement of cranial arteries or veins at 60 secs. Less experience with this technique
4 vessel angiography - absent flow in anterior circulation above the carotid siphon, absent flow above the foramen magnum in the posterior circulation
HMPOA Tc-99 scan demonstrating absent intracranial perfusion.

Question 4

What are the distinguishing features of a neuropathy vs a myopathy?

Answer 4

Site of weakness. Distal vs proximal
Sensory change. Present vs usually absent - often pure motor
Reflexes. Lost early vs late.
Fasiculations. May be present vs atypical.
Contractures. Absent vs may be present
Cardiac involvement. Absent vs may be present in dystrophies

Question 5

Outline the prognostic value of the following for determining prognosis following out of hospital cardiac arrest.
Pre-arrest factors
Clinical examination
Neuro-imaging
EEG
biochemical markers

Answer 5

Co-morbidities and per-arrest functional status likely determine outcome. Duration of CPR, initial rhythm, time to ROSC, frequently observed but little data for predictive value
Assessment requires certain per conditions-normothermic, nil sedation/muscle relaxants, adequate CVS resuscitation, correction of electrolyte, metabolic or endocrine derangement a. Not useful in first 24 hrs, generally assessed at 72hrs. Absent corneal reflex, absent pupillary response to light or GCS

Question 6

What are common brain death mimics?

Ref: evidence based guideline AAN

Answer 6

1. Spinal- high cervical spine injury
2. Lignocaine toxicity
3. Organophosphate toxicity
4. Gillian barre - fulminant
5. Vecuronium - delayed clearance
6. Baclofen overdose

Question 7

What is the definition of non convulsive status epileptics (NCSE)?
What are the diagnostic difficulties associated with NCSE?
What are the risk factors for NCSE?
What is the management of NCSE?

Answer 7

Altered behaviour or motor function with continuous epileptiform activity on EEG, but without major motor signs

Absence of uniform diagnostic criteria, treatment. Differentiation of coma from post ictal state or other pathology such as post-hypoxia, septic or metabolic encephalopathies. Requires high index of suspicion but over diagnosis and excessive use of anticonvulsants can lead to increased morbidity and mortality.
Risks: Systemic infection in epilepsy sufferer. Dementia. Neoplasm. Previous Neurosurgery. Stroke including SAH/ICH. NCSE in epileptic -3% mortality. NCSE in non epileptic -27%.
Investigate cause: electrolytes (mg,Ca), renal and liver function. Haematology eg., TTP. LP to exclude infection. EEG and MRI to exclude causes non seen on CT. Treatment: reverse precipitating factors, benzodiazepines then phenytoin infusion, some recommend levetiracem 1st line but certainly second agent consider anaesthetic (propofol has anti-seizure activity) then phenobarbital (some use thiopental but carries higher risk of cardiovascular side effects). Currently not good evidence for Na sodium valproate

Question 8

Define Stewart’s approach to acid base.

Answer 8

Stewart’s provide a mathematical explanation for the variables that control H+.
The Henderson hasselbach equation uses pH, CO2, and bicarbonate as effects of ph.
Stewart’s is a physiochemical approach as governed by the laws of electrical neutrality and the law of conservation of mass.
It uses dependent and independent variables. Independent variables can be altered from outside the system and the dependent variables cannot and are dependent on the independent variables.
It defines pH with the independent variables:
the SID (na + k + mg + ca + Cl + other strong acid/lactate. The weak organic acid ATOT and the partial pressure of CO2.