1. IL COMA.

luigi.vetrugno@asuiud.sanita.fvg.it
Clinica di Anestesia e Rianimazione
Azienda Ospedaliero-Universitaria
Università degli Studi di Udine
Anesthesia
COMA IN TERAPIA INTENSIVA
knowledge of the most frequent causes of coma.
May improve the management
 Coma is best defined as a completely unaware
patient unresponsive to external stimuli with only
eye opening to pain with no eye tracking or fixation,
and limb withdrawal to a noxious stimulus
at best (often with reflex motor movements).

COMA (A&E 2012)

One can be awake and aware, awake but not aware and
not awake and not aware.

These two components are interrelated but

sometimes dissociated.
 An important
first discrimination should be made between structural
causes and non-structural causes of NTC by means of a
computer tomography (CT) scan.
 Usually, as a first diagnostic step a differentiation is made
between traumatic and non-traumatic coma (NTC).

26 y/o patient with traumatic brain injury. A. CT scan only shows

impression fracture and mild swelling. B. MRI shows severe contusion of
right temporal lobe and bilateral mesencephalic lesions causing coma.
 Structural coma can
be due to cerebral infarction, intracranial hemorrhage,
intracranial malignancy and central nervous system
infection(e.g. encephalitis or abscess).
The cause of NTC is a challenge
for the physician.
In patients with a normal CT scan and no explanation for coma, a
lumbar puncture must be done to rule out infection.
Na 145 – Cl 100 – HCO 15 = 15
 EEG has lost some of its diagnostic value in the
evaluation of coma but is able to document nonconvulsivestatus
epilepticus in otherwise unexplainedcases.
Non-structural coma include coma as a result of:
- poisoning,
- epilepsy,
- extracranial
- infections,
- circulatory shock,
- post-anoxic,
- cardiac arrest,
- respiratory failure,
- metabolic problems
(such as hypoglycemia,ionic and acid– base disorders, hypothermia),
- hepatic encephalopathy
- uremic encephalopathy
The most common causes for NTC were:

160

140

120

100

80

60

40

20

stroke
post-anoxic
poisoning
epilepsy
 The average mortality rate in NTC patients
reported was 25-87% and varied markedly between studies.

100

80

60

40

20 Serie2
Serie1
0
stroke post-anoxic poisoning epilepsy *Africa
studies
poisoning
Stroke can be divided into ischemic stroke and intracranial
hemorrhage. Ischemic stroke has a lower mortality rate than
intracerebral hemorrhage at 30 day mortality.

40

35

30

25

20

15

10 Ischemic stroke
5
Intracerebral hemorrhage
0
Post-anoxic coma was identified as a second important cause of
NTC. Generally, post-anoxic coma is the result of an out-of-hospital
cardiac arrest.

The mortality associated with post-anoxic coma ranged from 54% to

89%.
The group of metabolic NTC is a very diverse group but diabetic
derangements and hepatic failure are the most prominent causes
of metabolic NTC.
 Once treated, comatose patients can recover
suddenly (eg, after quick correction of hypoglycaemia)
 Diabetic ketoacidosis with associated coma is associated with
mortality rates <1% while hyperglycemic hyperosmolar state is
associated with mortality rates of 5-20%

25

20

15

10

Diabetes Res Clin Pract. 2011;94(3):340–51.

Hepatic encephalopathy has an even worse prognosis!

hepatic encephalopathy admitted to the ICU of which 76% of patients were admitted with
coma (the mean GCS at admission to the ICU was 7.7 ± 4). During the ICU stay, 35% of
patients died and the 1 year-mortality was 54%.
Sorting out the cause of coma is what neurologists
do best—compared with other specialists.
Comatose patients have several outcomes:

- lose all brain function (brain death);

- remain unconscious (persistent vegetative state);
- regain consciousness (minimally conscious, fully conscious but disabled, or good
recovery)
Persistent vegetaOve state (PVS) is defined as:
▶ No awareness of self or environment.
▶ No sustained reproducible, purposeful or voluntary behavioural response to
visual, auditory, tacOle or noxious sOmuli.
▶ No language comprehension or expression.
▶ Mostly intact cranial nerve reflexes.
▶ Roving nystagmoid eye movements.
▶ Presence of sleep and wake cycles, oWen eyes
open during the day.
▶ Stable unsupported blood pressure and intact
respiratory drive.
▶ Bowel and bladder inconOnence.
Minimally conscious state (MCS) is defined as:
▶ PaOents make eye contact or turn head when being talked to.
▶ An abulic emoOonless state but with eye tracking movements.
▶ May mouth words, may fend off pain.
▶ Eyes following moving person.
▶ Some intelligible verbalisaOon.
▶ May hold object or use object when asked.
 ▶ Brain death is recognised by absent eye opening to pain, no
motor response to pain, and absent pupil and corneal responses.
Ocular vestibular reflexes are absent and there is noevidence of
spontaneous breathing.
▶ MCS is far more common than PVS within
6 months from brain injury.

▶ Patients in PVS may be kept alive for decades

but with no prospects for improvement.
Although there is no consensus on the precise cut-off
point to define coma, in general a

GCS lower than

10 points is used.
The neurological examination proceeds with
assessment of the cranial nerves and motor
response to pain.
Small or pinhole pupils (<2 mm) are due to a
ponOne lesion or opioids
Midsize light fixed pupils (4–6 mm)
are due to a midbrain lesion
Maximally dilated pupils (>8 mm) are due to a lesion of the third
cranial nerve nuclei, mesencephalon or compression of peripheral
fibres of the third nerve.

However, drugs and toxins can also dilate the pupils (eg,
lidocaine, amphetamines, cocaine).
DecorOcate responses are defined by slow
flexion of the elbow, wrist and fingers.

Decerebrate responses are defined by adducOon

and internal rotaOon of the shoulder,
arm extension and wrist pronaOon with fist
formaOon.
 CLUES (INDIZZI) FROM THE GENERAL PHYSICAL
EXAMINATION

onion
(paraldehyde)

fruity sweat (ketoacidosis)

garlic (organophosphates)
Classic foul breaths are
dirty toilet (uraemia)

musty or fishy (acute hepaOc failure),

MANAGEMENT OF COMA IN THE FIRST HOUR

▶ Improve oxygenation (face mask 40% oxygen

aiming at a pulse oximeter saturation of
>95%).
▶ Intubate if patient cannot protect the airway
(ie, increased work of breathing, pooling secretions,
gurgling sounds).
▶ Intubate any comatose patient with irregular
ineffective respiratory drive and poor
oxygenation.
▶ Intubate any comatose patient with major facial
injury or consider emergency tracheostomy.
▶ Correct hypotension by placing patient in the
Trendelenburg position and add crystalloids
(rapid infusion of 500–1000 ml normal saline
followed by 150 ml/h) and if no response, start
vasopressors (use phenylephrine intravenous
bolus of 100 µg).
▶ Correct extreme hypertension
 ▶ Correct hypothermia with warming blankets.
However, consider induced hypothermia
(33–34ÅãC) treatment in paOents who have
been successfully resuscitated from cardiac
arrest.
▶ Correct hyperthermia with cooling blankets,
icepacks and ice water lavage.
▶ No harm is done if a paOent with a high likelihood
of hypoglycaemia is immediately given
50 ml of 50% glucose, even before the blood
sugar is known (with coadministraOon of
100 mg thiamine intravenously).
▶ No harm is done administering naloxone
(0.4–2 mg every 3 min intravenously) if opioid
intoxicaOon is suspected.
▶ No harm is done administering flumazenil
(slow intravenous administraOon of 0.2 mg/
min up to max dose of 5 mg) which effecOvely
reverses any benzodiazepine toxicity; this
however is contraindicated in paOents with a
seizure disorder and in whom concomitant tricyclic
anOdepressant intoxicaOon is suspected
(may provoke seizures).
 ▶ Treat severe hyponatraemia with 3% hypertonic
saline and furosemide aWer placing central
venous catheter.
▶ Treat hypercalcaemia with saline rehydraOon
infusion followed by parenteral bisphosphonate
pamidronate.
▶ Consider eliminaOon of any toxin by haemodialysis
or haemoperfusion.
LONG TERM MANAGEMENT OF COMA
▶ If necessary, tracheostomy, percutaneous
gastrostomy, bladder and bowel care, infecOon
surveillance and deep venous thrombosis
prophylaxis.
▶ PaOents may be weaned from the venOlator
and tracheostomy removed later if secreOons
are controlled.
▶ Methicillin resistant Staphylococcus aureus
and vancomycin resistant Enterococci can be
reduced by less overcrowding, strict isolaOon
and avoidance of mulOple anObioOcs
along with meOculous hand hygiene by
staff.
▶ Contractures can be reduced but not prevented
by physical therapy.
▶ Decubitus skin breaks and ulcers can be prevented
by special beds and monitoring of pressure
sites along with superb nursing care.
▶ NeurosOmulaOon is of no use in PVS and (as
yet) unproven in MCS.
▶ Dopaminergic agents (eg, bromocripOne),
zolpidem and lamotrigine are commonly used
but unproven sOmulant drugs in MCS.
Grazie