1. Altered Level of Consciousness, Coma & Limitations of Management
EMET Townsville

2. Definitions
Consciousness defined as being awake and aware of both one’s self and one’s surroundings, OR it is the human awareness of both internal and external stimuli
Level of consciousness : is a measurement of a person’s arousability and responsiveness to stimuli from the environment.
Altered Consciousness covers a spectrum of states:
Consciousness
Lethargy
Stupor or Obtunded
Coma

3. Definitions
Lethargy: mild depression in level of consciousness and can be aroused with little difficulty.
Obtunded: More depressed level of consciousness and can not be fully aroused ( slow response and sleepness)
Stuporous: Can not be aroused from a sleep like state.( only respond by grimacing or drawing away from painful stimuli)
= E1 V1-2 M ?weak 5  Max 8 = Intubation LEVEL
Coma: More depressed level of consciousness and unable to make any purposeful response.

4. GCS 5
Decorticate posturing, with elbows, wrists and fingers flexed, and legs extended and rotated inward
Lesion in cortex or subcortical white matter

5. GCS 4 Decerebrate posturing – rigid extension of arms and legs
Lesion at brainstem, usually pons

6. The Glasgow Coma Scale
The Glasgow Coma Scale or GCS is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment.
Works well for trauma – that is what is was made for – not so good for other ALOC!
BEST RESPONSE!!!!

7. The Glasgow Coma Scale

8. GCS Severe, with GCS ≤ 8  ETT territory
Moderate, GCS 9 – 12  likely I&V
Minor, GCS ≥ 13.  could be safe for now

9. Causes

10. Etiologies Altered Level of Consciousness (ALOC):
One of the most difficult diagnostic and management problems.
Requires quick action to avoid irreversible damage
Wide array of possible diagnoses
ALOC is a symptom of another problem, not a diagnosis itself

11. Causes A – Alcohol, Abuse (physical or substance)
E – Encephalopathy, Electrolytes
I – Insulin( hypoglycemia)
O – Overdose, Oxygen deficiency
U - Uremia
T – Trauma, Temperature abnormality, Tumor
I - Infection
P – Poisoning, Psychiatric, Psychogenic
S – Shock, Stroke, Seizures, Shunt
Helpful mnemonic is AEIOU TIPS

12. Electrolytes ALOC may be caused by: Hypoglycemia – most common
Abnormality in any cation (Na, Ca, Mg, Phosphorus)
Metabolic acidosis or alkalosis
Hypoglycemia – most common
Hyperglycemia – especially new onset diabetes have ALOC due to hyperosmolarity
DKA can lead to cerebral edema
 All ALOC get a BSL and ISTAT!!! IO will do!!!

13. Seizure
All seizures except petit mal are followed by a post-ictal state
Drug levels for patients on anticonvulsants – N/A.
Keep in mind when treating !!!!
Comatose patients may have non-convulsive seizures – consider and treat if likely / RSQ will be able to help!
PROBLEM HERE IS COMA = I&V + M&M + RSQ

14. Trauma TENDS TO BE OBVIOUS! BEWARE ALCOHOLICS & Anticoagulants
Epidural Hematoma – classic lucid window!
SDH – often slow/delayed onset

15. Can lead to increased ICP
Cerebral Contusion
Can lead to increased ICP
PARAMOUNT: PROTECT BRAIN, CALL RSQ – HYPOXIA AND HYPOTENSION
ARE PROVEN KILLERS!!!!!
WATCH CO2 and WHOLE BED 30DEGREE UP

16. Meningitis
Bacterial
Most common infection severe enough to cause profound ALOC
Non-bacterial
Slower onset of symptoms

17. Infection Brain Abscess
Chronic sinusitis, chronic otitis, dental infection, endocarditis or uncorrected cyanotic congenital heart disease can increase risk

18. Encephalitis
Encephalitis – inflammation of the brain parenchyma usually due to viral infection
HSV – most common devastating cause
Death or permanent neurologic damage in 70% of cases
Affects temporal lobes causing seizures, parenchymal swelling and uncal herniation

19. INFECTIOUS CAUSES
TREAT AS PER CLINICAL NEED = LEVEL OF GCS/SEIZURES ETC
ANTIBIOTICS/ANTIVIRALS ON SPEC!!!
DO NOT DELAY and call RSQ

20. Stroke
Haemorrhagic – can have more of headache, clinically NOT reliably different
Thrombosis or Embolic Stroke
Occlusion of anterior, middle or posterior cerebral artery will NOT cause coma
SYNCOPE IS VERY UNUSUAL FOR CVA/STROKE
Infarcts eventually lead to increased ICP
Cerebellar infarcts rarely have coma
Basilar Artery infarcts cause rapid coma due to brainstem damage

21. Hypoxia TENDS TO BE OBVIOUS!! IF YOU CHECK!!!
Permanent CNS dysfunction can occur within 4-5 minutes of total anoxia at body temperature
Hypercarbia can also cause neurologic depression and coma – this is more common than thought and can happen quickly
ISTAT !!!!!!!! Venous/IO CO2 normal = no hypercarbia

22. Temperature Hypothermia Hyperthermia
Each drop by 1 degree celcius causes a 6% drop in cerebral blood flow
Hyperthermia
Headache, vomiting, seizure, obtundation, or coma result especially above 41 degrees C

23. Investigations ABG vs VBG ???? Serum Glucose Electrolytes
LFTs – clinically very unusual to just pop up!
Urea(Crea)
COAG – unusual
Calcium
= ALL ISTAT!!!
Serum
Ammonia – unreliable & n/a but easy miss in chronic liver patient with ALOC
Ketones (fingerprick!!!!!)
Alcohol n/a (hx – smell)
Drug concentrations n/a
ABG vs VBG ????

24. Investigation TREATMENT OFTEN MORE IMPORTANT!
Anybody with significant ALOC – gets transferred (within LIMITS)
Obviously will get CTB, maybe angio/maybe MRI (not common)
Levels and other blood tests are most likely irrelevant
ALWAYS CHECK BSL OR GIVE GLUCOSE!!!

25. Deal with abnormalities as you find them

26. Treatment
Basic
A. Establish an airway, maintain as indicated, suction as needed; assist ventilations as indicated.
B. Administer high concentration oxygen or DON’T … BIPAP/CPAP … funny thing dogmas, isn’t it?
C. Transport the patient in the coma/recovery position (if trauma is suspected, transport supine with cervical collar and backboard).

27. Airway When not to intubate?... If I can reverse the issue. ARP???
Sugar
Naloxone
… scary Flumazenil????? (EXTREMELY RARE!!!)
?? Hypotension … remember in the extreme ALS starts with CPR, not with intubation!!!!
ARP???
- Intubate if GCS <8 comes mostly from trauma literature
- Poisoned patients are unlikely to suffer from secondary brain injury, but decreased consciousness and loss of protective airway reflexes predispose to respiratory failure and aspiration
injury. However, the risk of aspiration is not confined to patients with a GCS of 8 or less, and the loss of airway reflexes cannot be reliably predicted using the GCS alone
- GCS is not a good predictor of pharyngeal control, however, risk of aspiration does increase as GCS decreases.
Donald, C. et al. Predictors of the need for rapid sequence intubation in the poisoned patient with reduced Glasgow coma score.
Emerg Med J Jul;26(7):510-2.
- Single centre prospective observational study of all poisoned pts over one year (73 pts). None of the 12 pts with a GCS <8 had a poor outcome. However, all were in a monitored setting (ED) and some required OPA, NPAs.

28. Treatment IF RESP ARREST – BVM and/or I&V
IF BREATHING … is it patent? Is it safe??
COPD – reduced GCS is probably a relative CI
Ask: WHAT IS MY ALTERNATIVE??

29. Treatment
▲ Administer thiamine 100 mg IV if dextrose is to be administered. – technically this is very important in alcoholics … Wernicke!!!
▲ If IV access cannot be secured and the patient's blood glucose level is <4mmol/L, get IO !!! or/and administer 1 mg glucagon IM.
Then treat underlying cause.

30. Circulation Hypotension: Hypertension:
Multiple causes – BUT remember Addison’s!!!
Usually intubation will worsen this!!!! TREAT IN PARALLEL
Hypertension:
hypertensive encephalopathy – rarely full COMA!!
COMA plus HTN = intracranial pathology until proven otherwise

31. Hot and Altered GCS Meningitis/Encephalitis/Abscess Thyroid storm
Hyperthermia – environment or DRUGS!!!!!
CVA/CNS bleeds
Tox
Sympathomimetics/Anticholinergics
Withdrawal
Cholinergics
Most MH drugs!!!

32. Cold and Altered Environmental (maybe south of Townsville )
Should be rare as pure cause
Infection!!!
Thyroid?? VERY RARE
Wernicke’s (hypothalamic dysfunction) – again initially unlikely as pure cause – massive sepsis risk

33. Glucose Consider it the 5th vital sign
If hypoglycemic, treat with 1-2 amps of D50

34. Coma cocktail - DONT BE CAUTIOUS NOT TO MAKE THINGS WORSE!!!!!
DO YOU REALLY WANT SOMEONE TO WAKE UP AND TO WHAT EXTEND!!!!
Naloxone – dosing (0.1 mg/kg peds or 2-4mg adults)   start with low dose and titrate in those that are on chronic or long acting or long acting (methadone)opioid users.  May need larger doses for some narcotics (ie fentanyl) - half-life of Naloxone 30-60mins, it is a common mistake to reverse an opiate overdose, then move on the the next pt. and find out the LOC starts to decline again. The general principal is always to start a Naloxone infusion if a bolus had clinical effect.
Oxygen - maintain O2 sat >90%
Thiamine 100mg IV - Ataxia, vertical and horizontal nystagmus, confusion, hypotension, and ophthalmoplegia   conditions where you might see thiamine deficiency: Alcoholic, hyperthyoid state, neoplasia, anorexia nervosa, hyperemesis gravidarum, AIDS, - little downside to giving it
Flumazanil? - could trigger seizure if multi-drug overdose

35. Treat Fever Antipyretics Cooling Benzodiazepines
- Centrally acting antipyretics, such as acetaminophen, have no effect in poisoned patients, as the hyperthermia is not caused by resetting of the hypothalamic thermostat. Rather, the hypermetabolic state is responsible for the elevated core temperatures. - actively cooling by using cooling blankets, large fans (such as those used to dry floors in hospitals) with warm mist, and ice application to maximize evaporative cooling may be life saving. - benzodiazepines are beneficial in these patients as well. Benzodiazepine therapy reduces agitation and delirium in addition to seizure activity. In contrast, antipsychotic agents from the phenothiazine and butyrophenone classes (eg, haloperidol) may actually worsen the situation—they also have anticholinergic effects and may lower the seizure threshold.

36. Agitated delirium
Clear association exists between illicit drug use and the syndrome but not universal.
Non-drug related causes are almost always psychotic (schizophrenia, bipolar)
Treat if:
Presence of excited delirium
Continued maximal struggle despite attempts at maximal restraint

37. Agitated delirium and SCD
Mechanism of death
No definite etiology usually found at autopsy
Catecholamine excess leading to stress cardiomyopathy Vs Profound metabolic acidosis likely leading to cardiac arrest?
Hyperthermia often contributory
Convulsions often contributory
Hyperkalemia often contributory
Restraint asphyxia unlikely explanation

38. Drug therapy for agitated patients
Don’t make them worse!!!
Halo/Droperidol – tend to be very safe re RESP/CVS
BENZOS – beware ABC deterioration
If planning to I&V anyway – strongly consider Ketamine
Others:
Antipsychotics
Other Benzos
Clonidine
DON’T FORGET BSL!!!!!
halperidol can be given IV and titrated to effect - initial dose of mg IV => double the dose every minutes prn (other suggest starting with 5mg IV) haloperidol should be used cautiously in patients with a prolonged QT interval, because there is some evidence that neuroleptic agents may cause torsade des pointes (some physicians would discontinue haloperidol if the QTc interval lengthens by > 25%) BZD: lorazepam good if IV access. Midaz 2.5-5mg IM if no IV access use escalating doses if not working

39. So when not to treat or limit management?
See: End-of-life care: Decision-making for withholding and withdrawing life-sustaining measures from adult patients
On QHEPS:

40. Sensitive topic … best planned for.
NFR is no longer used
ARP is a clinical document
AHD is a more legal document

41. Important Principles
In a lot of cases there should be obvious concerns that suggest a possible limitation of our management efforts
Advanced cancer
Advanced end stage disease
Extreme age … probably the poorest factor

42. Principles for providing CPR – pro is always easier!!!

43. Principles – if the plan states don’t
The only way to provoke trouble is if you have direct knowledge of a patients lack of consent to life saving measures
Hearsay and family opinion does actually not matter if there is an AHD
Withholding Mx should always be good medical practice
Any statement by the patient towards a change of heart overrides any ARP/AHD1

44. Principles
If a health directive is documented and valid (remember there may be dates/single admission plans only) this is what should be followed – the family cannot simply change that
ARP/AHD – only ever come into play IF the patient HAS LOST CAPACITY!!!!
CAPACITY IN QLD IS THE PRESUMED DEFAULT!!!! – LACK NEEDS TO BE PROVEN

45. Principle
If there is time & lack of capacity an effort should be made to contact a substitute decision maker
In the extreme this can be the Adult Guardian Office

47. Capacity Confirmation Principles
Even though QLD law implies capacity as default – always good to document the above

48. Principles
There is a major emphasis in the QLD guidelines documents to prevent issues if possible.

49. Principles Means for point 10:
If in doubt CPR should be commenced as long as it is not obviously inappropriate
The legal frame work does not suggest that every possible/conceivable measure must
be considered i.e. ventilation … it only refers to CPR, it all boils down to good medical
practice.

50. Principles – Ignoring AHD…

51. Principles … ignoring a AHD
So there are very specific points to satisfy when you ignore the AHD – and if those are stated I guess one would be able to defend such a decision BUT remember the proof would rest with YOU!!!!!!

52. Interesting
Blood by QLD law is not a life sustaining measure for the purpose of consent!!!
That means it technically always needs consent!...but
The clue to stay out of trouble here should be the expectation of reasonable efforts to gain consent. Beware JW bracelets/cards etc!!!