Lecture 12

COMA

Definition
Coma is a pathological state of unconsciouness with dissapearance or decreasing of reaction to
external stimuli to elementary forms.

Positive diagnosis
It is sustained by severe alterations of consciousness, of active motility, of sensitivity and reflexes,
with vital function preservation in variable degrees.
Loss of conciousness: the patient has closed eyes, apparently in deep sleep. The absence of
language communication is almost total. To powerful stimuli (verbal or painful) the patient may answer,
but the answer is inadequate and without establishing a normal communication.
A fast method for evaluation of level of consciousness is formula A-V-P-U:
A - allert
V - response to verbal
P - response to pain
U - unconsciouss
The motility, reflexes and sensitivity are absent or modified, according to the depth and nature of
coma. The first that dissapears is the active motility, then the reflexes: abdominal-cutaneous, cremasterian
and osteo- tendinous.

Differential diagnosis
1. Physiological sleep- modification of vigil status, but the person is easily wake up and doesn’t fall
asleep again.
2. Hypersleepy status - quickly and reversible sleep accesses, associated with cataplexy attacks
(narcolepsy-cataplexy). It is a pathological alteration of consciousness, rapidly reversible to some
external stimuli. Pay attention to: yawn, sigh accesses, stretching movements. It appears in
hypothalamo-dyencephalic affections.
3. Akinetic mutism (mutenie)- the patient is imobile but vigile. Clinical findings include also:
- emotional indifference state with typical facies
- absence of spontaneous movements at orders or after stimulation;
- persistence of some “awake signs”: conjugated movements of eye balls, blinking movements of
eye lids.
This is present in: -bilateral frontal lesions
-mesencephalic reticular lesions
-posterior diencephalic lesions
-acute hydrocephalus.
4. Locked-in syndrome- is related to a basilar thrombosis, so all active movements are absent at limbs,
and in bulbo-protuberanceal areas (tetraplegia, facial diplegia, pharingo-laryngean paralysis, paralasis
of lateral movements of eyeball).The patients are counciouss, but the only possible movements are
opening the eyes and vertical movements of eye balls.
5. Phychogenic arreactivity- suspect this possibility in next situations:
- are present etiological conditions such as: psychosis (depression, conversion hysteria, diverse nevrosis,
or simple simulation);
- resistance at eyelids opening;
- to a suddenly passive mobilisation, basal tonus persists, even the patient seems non-responsive to
stimuli;

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- corneean and fotomotor reflexes are present, but eyeballs have diverse movements (especially vertical
ones). Attention- the presence of pendular movements of eyeballs exclude hysterical coma.
- osteo-tendinous reflexes, sensivity are normal;
- electroencephalograme is normal;
Attention:
-a hysterical behaviour can precede a real coma (toxic or metabolic encephalopathy) or can be a
sign for organic affections (cerebral /extracerebral). Therefore, this diagnosis is one of exclusion and it
will be sustained with maximum prudence, after a clinical and neurological complete examination and
complementary paraclinical exams(EEG).

Other pathological situations characterized by alteration of mental status:

6. Syncope - a short period of unconsciousness, with abscence or decreasing of respiration and
circulation. It suddenly appears and lasts seconds or minutes and is accompanied with vegetative
disorders.
7. Obnubilation, mental confusion – reduced capacity of thinking
8. Stupor - is defined like a transitory reaction to painful stimuli, with present motor reactivity,more or
less organized and a very poor comunication by language.
The term”superficial or vigil coma” is used in these cases, especially when is accompanied with agitation
state.

Diagnosis of coma’s depth

There are 4 stages of depth:

Stage 1 - vigil or superficial coma, characterized by a clinical awake possibility,
- the encephalic reflexes are preserved (pupilar, cornean) and sphincterian control is present
- exist neuro-vegetative and cardiorespiratory disorders.
Stage 2 - the patient reacts only to painful stimuli, more or less adjusted.;
-loss of sphincterian controle
-fotomotor and cornean reflexes are decreased
-don’t exist neurovegetative disorders.
Stage 3 - reactions to painful stimuli are absent. Can be present reaction of decerebration.
-fotomotor reflexe is absent
-respiratory failure or other neurovegetative disorders may occur.
Stage 4 - the whole reactivity is abolished; generalized hypotonia.
-reflexes are absent
-arreactive bilateral mydriasis
-active respiration is absent
-major neurovegetative disorders are present

For a better coma’s evaluation use GLASGOW scale. It uses 3 parameters:

1. opening the eyes -E
2. verbal response -V
3. motor response-M
The examination will be performed in order E,V,M and will be noticed the poorest responce.
The maximum score is 15 points. The minimum is 3 points.
A score less than 7 means coma.
A score less than 5 means severe coma.

Eye -spontaneous opening-4 points

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 -opening to verbal stimuli-3 points
-opening to painful stimuli-2 points
-no opening the eyes-1 point.

Verbal -orientated, knows names-5 points

-confused, words without relation-4 points
-inappropriated words-3 points
-incomprehensible, only sounds-2 points
-none-1 point

Motor -obey to command-6 points

-localises the pain-5 points
-withdraw to pain-4 points
-abnormal flexion (decortication)-3 points
-abnormal extension (decerebration)-2 points
-none-1 point.

Gravity elements of coma:

 age, associated trauma or diseases;
 late medical adressability;
 Glasgow scale<5;
 neurovegetative disorders;
 acute respiratory distress;
 convulsions;
 focal neurological signs;
 signs of midbrain suffering;
 collapse, shock status;
 cardio-respiratory arrest.

Criterias for etiological orientation

These are 2 types of criterias: clinical and anamnesis.

1. Anamnesis
 Patient’s age - young -infectious coma
-intoxications
-epilepsy
- middle age -cerebral haemorrhage
-hepatic or uremic coma
- old -coma by cerebral ramolisment
-stroke
 pathological history
-hypertension -cerebral or subarahnoidian haemorrhage;
-hypertension encephalopathy;
-hepatic cirosis-hepatic coma
-nephropathies-uremic coma
-diabetes -hyperglycemic cetoacidotic coma
-hypoglycemic coma
-hyperosmolar non-acidocetosis coma
-epilepsy
-toxicomania

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 -cranio-cerebral trauma with a free interval-intracerebral haematoma
 previous phenomenas before onset:
-convulsions -hypoglycemia
-epilepsy
-poisonings
-fever -meningitis
-encephalitis
-appereances circumstances -after trauma
-after insulin administration
 onset: -slow, gradual-suggest an intracranial expansion lesion;
-an anterior confusional state suggests a metabolic encephalopathy;
-a quick, fast onset suggests a cerebral vascular lesion.
 objects found arround the patient:-seringes;
-drugs vials
-toxic substances.
2. Clinical examination can develop modifications associated with specific causes of coma.
 fever in: -meningitis
-encephalitis
-subarachnoidian haemorrhage
 skin and mucousis membranes:
-pink-purple colour in CO intoxications
-warm tegument and profound sweatening in hypoglycemia, hyperthyroidia
-dry skin and mucous membranes in:
-diabetic ceto-acidosis
-hyperosmolar coma
-atropinic coma
-tongue bites and sanguinolent sputum in epilepsy
 odor/smell of pacient:
-alcoholic: intoxication with alcohol
-acetonemic: cetoacidotic coma
-foetor hepaticus: hepatic coma
-amonium: uraemic coma
 breathing:
-Kussmaul: metabolic acidosis
-Cheyne-Stokes: -CO intoxications
-morphyne intoxications
-intracranial hypertension syndrome-ICHT
-stertorous: -profound apoplectic coma
-epilepsy
-uraemia
-Biot: -preagonic stage
-severe meningo-encephalitis
 cardio-vascular :
-valvular sounds, atrial fibrillation - embolic cerebro-vascular stroke
-hypertension: -apoplectic coma
-uraemic coma
-eclamptic coma
-hypotension : -barbituric poisoning
-morphyne poisoning
-any severe coma with shock

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 -extreme bradycardia in:-meningeal coma
-coma associated with ICHT
-morphyne poisoning
 pupils: -mydriasis: -atropine intoxication
-cocaine intoxication
-myosis: -pontine haemorrhage
-organophosphorate substances intoxication
-morphyne intoxication
-anisocoria: -cerebral tumors
-cerebral abscess
 meningeal syndrome in: -meningitis
-meningo-encephalitis
-subarachnoidian haemorrhage
 hemiplegia/monoplegia in:-cerebral haemorrhage
-ischaemic stroke
 paresis/cranial nerve paralysis or oculomotor nerve : -cerebral haemorrhage
-cerebral tumors
 Babinski sign is inverted in: -cerebral haemorrhage
-tricyclic antidepressive substances poisoning
-CO intoxications
-hypoglycemia

Clasification of coma
1. Traumatic coma
- cranian trauma
- medullary trauma
- politrauma
2. Metabolic coma (metabolic encephalopathies)
- hypoxic coma
- hypercapnic encephalopathy
- hypoglycemic coma
- cetoacidotic coma
- hepatic coma
- uremic coma
- endocrinological causes: addisonian, tireotoxic, mixedematos)
- hypothermia, hyperthermia
- electrolitical disorders ( dihydration, diskaliemia)
- vitamins deficiency B1, B6.
3. Neurological coma
- intracranian tumors
- epilepsy
4. Neurovascular coma
- stroke
- subarahnoidian haemorrhage
- meningo-cerebral haemorrhage

5. Toxic coma
- drugs poisoning
- chemical subsatnces poisoning
6. Infectious coma

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 - encephalitis
- meningoencephalitis.

Laboratory findings
Paraclinical tests will be chosen function the etiologic suspicion.
To all coma patients must to be performed: hemograme, sanguine group, glycemia, urea, creatinine,
ionograme, blood gases, urine exam, pulmonary x-ray, ECG.
Function etiological suspicion, can be done :
-colinesterase
-toxicological tests
-EEG
-fundoscopique exam
-lumbar punction and cerabrovascular fluid exam
-cranian x-ray is indicated in cranio-cerebral trauma suspicion
-CT scan is essential in trauma or cerebral haemorrhage
-RMN is superior to CT scan in ischaemic or infections comas
Lumbar punction must be preceded by fundoscopique exam and is indicated in all cerebral comas
without ICHT signs.The presence of this syndrome contraindicates the performing of lumbar punction.

General treatment in coma

In all cases, coma represents a medical emergency. It’s extreme gravity is determined by
etiopathogeny and association with vital distress.
In absence of etiopathogenic diagnosis,exist some therapeutical methods used in all cases. These
must be applied by a medical team, as quick as possible, together with medical exams that will establish
the ethiology, for the specific treatment.
1.Confirm the unconscioussness status- A-V-P-U

2.Secure airway and establish adequate ventilation:

a. open airway
- open airway with manual manouvres: head tilt, chin lift, jaw thrust
- relieve airway obstruction: extract foreign bodies, aspirate the secretions
- Guedel pipe is indicated due to the risk of airway obstruction by falling posterior of the tongue at
patient in coma II, III, IV- th degree, in absence of possibilities for immediately endotracheal intubation
(ETI)
- ETI and traheal aspiration are indicated in next situations:
- II-nd degree coma with a lot of secretions in airway
- III-rd and IV –th degree coma when exist risk of aspiration of gastric fluid in airway
- coma associated with vital distress
- toxic coma ( ETI preceds gastric lavage).
The aims of ETI are:
- protection of airways
- assure artificial breathing.
In the present, any patient with coma Glasgow scale <7 has indication of ETI.
ETI must be preceded by: ventilation on facial mask with oxygen administration.
- suspicion of cervical spine injury is a contraindication for head tilt during ETI.
-eventually Atropine 0,5-1 mg i.v.(it prevents the vagal hyperexcitation).
b. Administration of oxygen by facial mask or endonasal tube to all the patients
c. Artificial ventilation: ventilation of an unconsciouss patient is insufficient and artificial ventilation is
required.
Indications:

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 -clinically: -respiratory arrest
-cardiac arrest
-coma of III-IV-th degree with respiratory disorders
- respiratory sounds at bases of lungs are absent, and respiratory rate is<8 resp./min.
-blood gases dosage is the only certainty criteria for ventilation insufficiency to a coma patient.
PaP CO2 >50-55 mm Hg and PaP O2<60 mmHg is indication of asisted ventilation.
The methods for artificial ventilation are:
-ventilation with Ruben or Ambu bag.
-mechanical ventilation

3. Maintaining circulation:
The patient will be clinically monitorized (BP, pulse, cardiac rate) and ECG.
Colect blood for CBC, glycemia, hepatic and renal function tests, calcium, magnesium, electrolytes, blood
gases, toxicological tests.
Measures:
-CPR with external chest compression indicated in cardio-respiratory arrest
-i.v. line and start correction the hypovolemia, when exists hypotension tendency with cristaloids
substances (saline, Ringer solution) or coloids (Dextran, human albumin, hexaethylamidon)
-if this measure is not sufficient for B.P. balance, give vasoconstrictors drug:
Dopamine-p.e.v. with 5-15 microg/b.w/min. 1v=50 mg.
Dobutamine-p.e.v. with 5-20 microg/b.w/min. 1v=250 mg.
- Treat any malignant arrythmias.

4.For a coma with unknown etiology, you must administrate:

-hypertone glucose 50%, 50 ml. i.v.in 3 min., or 3-5 vials of glucose 33%.
-naloxone (antidote of morphyne) 0,4mg bolus i.v. repeated if needs
-thiamine (vit. B1) 100 mg. i.v., for preventing a Wernicke encephalopathy.

OTHER TREATMENT DEPENDING THE ETIOLOGY

1.Decreasing ICHT
- hyperosmolar substances
- Manitol 20% i. v. 1,5-2 g/b.w.. It has fast and long effect.
p.e.v.-500-1000 ml/24 h
- Glycerol with similar effects, but is less accesible.
- Ureea 1-5 g/kg.b.w. i.v.
Nausea and vomiting are frequently appear.
- glucocorticoids
 HHC i. v. 200 mg.i.v.
 Methilprednisolon 60 mg. i.v.
 Dexametazone 10 mg. i.v.
- hyperventilation represents a fast method for decreasing ICHT, but it has transitory effect.

2.Anticonvulsant treatment
Seizures crises, especially repeated crises, worsen coma’s evolution and may cause death.
Give Diazepam i.v. 10 mg. once (1v=10mg.), repeated if needs after 15 min.(another 10 mg.), and
if the crises doesn’t stop, 10 mg. at every 30 min., untill a total dose of 40-60 mg.
This big doses are given only if is available a mechanic ventilation device, because the respiratory
distress is frequent.

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 After 1v of Diazepam i.v., you can associate immediately 1v of Fenobarbital i.m.(1f=100 mg.), to
increase anticonvulsant effect.
After crises stopped, can give Phenitoine 500mg-1g. p.e.v. slowly, to controle further crises. If
seizures reappear repeate Diazepam.
In case of failure of anterior treatment, use barbituric anesthesia with Tiopenthal under ETI and
assisted ventilation (0,5g Tiopenthal in 500 ml. glucose 5%, in p.e.v., 10 drops/min.)
The permanent partial crises from metabolic encephalopaties are less harmful for brain and they
don’t need anticonvulsant drugs in big doses.

3.Hydro-electrolitical and acido-basic treatment

For a very strict treatment, lab tests are obligatoryt. Both, severe methabolic acidosis and alcalosis can
produce arrythmias, but the risk of death is present especially in methabolic acidosis.
In case of acidosis (pH,7,1) give Sodium bicarbonate i.v. 1mEq/b.w. (1ml/kg.b.w from 84%0
molar solution), untill pH is more than 7,2.
Insert a urinary catheter and monitor the diuresis to all coma patients.

4.Antiboitic treatment
The infection is an aggravating factor for any type of coma. Before starting the treatment, take blood for
hemocultures, and cerebrospinal fluid exam.

5.Protection of eye-balls
If the patient’s eyes remain partial or complete opened, after 4-6 hours may appear cornean errosive
lesions, which will be infected later.
Prophylactic, use an ophtalmologic pomade and assure the passive closing of eyelids; repeat local cares
every 12 hours.

6.Stomach lavage
In toxic coma must to be performed gastric lavage. Usually to a coma patient is recomanded to evacuate
the gastric content after ETI.

7.Treatment of complications and associated lesions- ex. fractures.

8. Specific treatment- function of the ethiology.

Transporting of coma patient:

 the decision of transporting a comatose patient is taken only after stabilisation of ventilatory and
hemodinamic status;
 during transport, the patient will be put in safety position, layed on a flat surface:
-simple safety position-with head turned lateral -if don’t exist cervical lesions;
-elevated inferior limbs than head;
-lateral safety position
 during the transport, the patient will be observed by a doctor;
 the rescue persons will phone to the hospital to give the informations about the patient.

Specific types of coma:

1. HYPOGLYCEMIC COMA

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Unlike other organs, the brain relies mainly on glucose to supplyits energy requirements. Abrupt
hypoglycemiarapidly interferes with brain metabolism and quickly produces symptoms.
Important for possitive diagnosis are:
-hystory- treatment with insulin (administration of insulin without eating after that;
increased doses of insulin);
-oral hypoglycemic drugs overdose;
-beware of rebound hypoglycemia from a long-acting insulin and oral hypoglycemic
agents;
-sudden onset-can be:
1. with a short adrenergic prodromal syndrom: signs of sympatetic nervous system
activity: tachycardia, sweating, anxiety;
Be carrefull : these signs can be masked by propanolol and other beta-blockers and may be
absent in caser of diabetic autonom neuropathy.
2. without prodromal signs.

Clinical findings:
- generalized seizures
- sweating
- hypotension
- tachycardia
- decreased level of conciouss (stupor to unconciousness)
- can exist focal signs
- Babinski can be possitive
- reactive dilated pupils.
- in final phases appear the decerebrate rigidity, small pupils, bradycardia, flacid
tone and depressed reflexes.

Be carreful at a patient with epylepsy, alcoholism, stroke- they can associate a hypoglycemia,so
you must identifie immediately this situation.
Hypoglycemic coma may be tolerated for 60-90 min.but once the stage of flacidity with
hyporeflexia has been reached, glucose administration within 15min. is mandatory to avoid irreversible
damages.
! Before treatment, collect blood for measure the glucose blood level and collect urine for glicozuria.

Treatment
-glucose 50.% 50ml i.v.Once the diagnosisof hypoglycemia is confirmed, give aditional glucose 50ml. as
needed or begin an infusion with dextrose 5%.
-patients will be observed for 1-2 hours to ensure that hypoglycemia does not reccur before he is
discharged from hospital.
-hospitalisation can be necessary in the next cases:
- long acting hypoglycemia
- hypoglycemia with reccurency in spite of correct treatement
- insulin overdose.

2. CETOACIDOTIC COMA

In cetoacidotic coma history is very important: the patient can have an infectious disease, or fever,
or can eat more than normal without treatment.
Clinical findings:

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-the onset of coma is slowly, progressivly, with poliuria, polidipsia, dehydration ( persistence of skin fold,
dry tongue, hypotonia of eyeballs), hypotension, Kussmaul breathing, acetonemic smell, vomiting,
abdominal pain.
! Attention-make a correct differential diagnosis with the acute abdomen.
Collect blood for glycemia, ASTRUP parametres, blood ionograme, ureea. Also collect urine for dosage
of cetonemic bodies and glycozuria.
Put an i.v. line with saline.
Hospitalize the patient for correcting the hyperglicemia, metabolic acidosis.

3. HYPOXEMIC COMA

Hypoxemia produces brain damages only as a result of concomitent cerebral ischaemia. Cerebral
blood flow decreases and brain ischaemia occurs when the arterial pO2 falls to 20-45 mmHg.
In cerebral anoxia due to cardiac arrest, where the duration can be timed precisely, 4-6 minutes of
asystole begins a permanent damage of central nervous system. Following asystole, the pupils dilate
rapidly and become fixed and tonic posturing is observed.
At these pacients:
-measure the blood gasis
-support the cardiac output
-give suplemental oxygen or practice asisted breathing (ETI and
mechanical ventilation) to mantain arterial PO2 above 60 mmHg.
The definitive treatment of hypoxemia depends of the cause. So, hospitalise all patients for diagnosis and
specific treatment.

4. HEPATIC ENCEPHALOPATHY

It can occur to the patients with severe acute or chronic liver disease. Jaundice need not be present.
To the patients with preexisting liver disease, the gastrointestinal haemorrhage can be a trigger factor for
rapidly developping the encephalopathy.
Clinical signs:
 alterated mental status: from somnolence, delirium to coma
 increased muscle tone
 hyperreflexia is present
 foetor hepaticus
 asterixis
 seizures-generalized or focal- occur infrequently
 hyperventilation with respiratory alkalosis- measure the arterial blood pH, arterial
blood gasis, ASTRUP parametres.
In emergency: -provide initial supportive measures only
-hospitaisation is indicated to all patients.

5. UREMIC COMA

Important:
-hystory of renal failure
-clinical: uremic foetor (amonium smell)
-Kussmaul respiration

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 -vomitting, diarheea, headache
-asthenic syndrome
-signs of dehydration to poliuric patients and signs of hyperhydration to
oliguric patients
Treatment in emergency-same like for hepatic encephalopathy.

6. METABOLIC ENCEPHALOPATIES

Metabolic encephalopaties are characterized by a period of progressive somnolence, intoxication,

toxic delirium or agitation, after which the patient gradually sinks into a stuporous and finally comatose
state.
Headache is not an initial symptom of methabolic encephalopathies, except in the cases of
meningitis, subarahnoid hemorrhage or poisoning with carbon monoxide or organophosphorated
compounds.
Neurologic exam reveal focal hemispheric lesions (hemiparesis, hemisensory loss, aphasia) before
loss of consciousness. Neurologic findings are symmetric, except in hepatic encephalopathy and
hypoglycemic coma, which may be accompanied by focal signs (ex. hemiparesis) that may alternate sides.
The hall mark of methabolic encephalopathies is reactive pupils (a mid brain function) in the
presence of impaired function of lower brain stem.
Treatment depends entirely on the cause of coma. All the patients require hospitalisation for
supportive care and specific therapy.

7. NEUROLOGICAL COMA

a.Supratentorial mass lesions:

Symptoms and signs of unilateral hemispheric dysfunction are usually present before onset of coma.
Neurologic deficits follow a characteristic progression fromrostral to caudal (cerbral to medulla).
Can appear:
- hemiparesis, hemihypesthesia, aphasia, agnosia
-somnolence or coma because of bilateral cortical involvement; asymmetric motor and sensory
abnormalities
-modification of pupils: dilatation, pinpoints pupils
Treatment: -hyperventilation to an arterial PCO2 of 25-30 mmHg
-give mannitol 1,5-2g/b.w over 30 min.-1 hour
-give glucocorticoids i.v.-the most rapidly acting to reduce cerabral edema- Dexametasone
10 mg. then 4mg./4 times a day

b.Hypertensive intracerebral hemorrhage:

Obtundation is unremittingand worsens steadly over minutes or hours, to stupor and coma. All the
patients are hypertensive
- headache, vomiting, nuchal rigidity
- conjugated deviation of the eyes with gaze directed to toward the side of lesion
- the ocular fundi may show hemorrhage secondary to intracranial pressure
- hemiplegia contralateral to the hemorrhageis s common early sign
- seizures are rare
- the cerebrovascular fluid is bloody in 90% of cases and the pressure is above 200 mmHg water.
Even the hemorrhage stopped, the patient’s condition is worsening because of cerebral edema.

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Treatment- elevated intracranial pressure respond usually to mannitol 1,5-2g/b.w.over 30min. and
sometimes to glucocorticoides. In some cases ( lobar hemorrhage) surgery may be lifesaving.
Immediate hospitalisation is required, primarily for supportive care

c. Cerebral massive infarction produces contralateral hemispheric compression by brain swelling of

cerebral edema or transtentorial herniation that will result in coma. This is maximal 48-72 hours after
the infarct.
Clinical findings: hemiparesis or hemisensory loss (and aphasia if the dominant hemisphere is involved).
The blood is absent in cerebrovascular fluid. CT rules out cerebral hemorrhage.
Treatment - glucocorticoids and dehydrating agents can be tried
-antihypertensive drugs should be used with caution during the acute stages, because of the
dangers of hypoperfusion of the ischemic hemisphere.
-hospitalisation is indicated to all patients.

8. HYPERTERMIA/HYPOTERMIA

These are associated with symmetric neurologic dysfunction that may progress to coma.
All the comatose patients, must have rectal temperature taken.
Hositalisation is mandatory.
a. Hypertermia - internal body temperature above 41-42 degrees is associated with coma and may
rapidly cause brain damage. Seizures are common. Skin is hot, flushed, dry (sweating may be
present). Hyperventilation produces initial alkalosis then methabolic acidosis.
Treatment: -place the patient in a cold place
-undress him, sponge him with cold water, put ice on the axilla, posterior neck,
inguinal area
-maintain airway and ventilation
-give oxigen, monitor BP, blood gasis
-maintain adequate urinary output-30-50ml/h
-if he is not responsive begin peritoneal lavage with potassium free dialysate
2l/15min.
-infusion of cristalloid solution and inotropic agents is necessary
-treat the possible complications.
b.Hypotermia- internal body temperature below 26 degrees cause coma. Core temperature above 32
degrees does not cause coma. Between 26-32 degres exist varying degrees of obtundation.
Pupilary reactivity will be sluggish below 32 and lost below 26 degrees. Exist also bradycardia and
hypotension. On ECG is specific J wave - QRS complexes are narrow and deformed at their terminal
portions by a slurred wave
Treatment -hospitalisation and monitoring in intensive care unit;
-if cardiorespiratory arrest occurs-CPR
-maintain airway, ETI if is necessary
-give warm, humidified oxygen; avoid hyperventilation
-rapid rewarming may be hazardous because the risk of lethal cardiac arrhytmias.
Rate of rewarming is 1-2 degrees/hour.
Active rewarming is necessary to patients with cardiovascular instability.Thera are external and internal
methods.
External methods: heated blankets.
Internal methods: peritoneal dyalisis with warm potassium free dyalisate 2l/min. until rectal temp. reaches
35 degrees.
-treat the possible arrythmias , and other complications

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 9. HYSTERICAL COMA

The diagnosis of hysterical coma is one of exclusion, that should be made only after careful
examination.
The general physical examination should elicite no abnormalties. Neurological exam can reveal
flaccid, symmetrically decreased muscle tone, normal and symmetric reflexes and normal downward
response to Babinski stimulation.The pupils are normal size and reactive to light. Can exist visual fixation
Exist voluntary muscle tone of the eyelids during passive opening .
EEG is normal.
Treatment- obtain psyhiatric consultation . Hospitalisation may be required.

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