1. a

2. Approach to Diagnosis
and Management
of Comatosed Patient
By
Prof. Nabil Lymon
Professor of Internal Medicine
Mansoura University

3. introduction
The state of consciousness or alertness
depends on:
An intact reticular activating system (R.A.S): this is a
collection of unclei present in the brain stem,
hypothalamus & thalamus. It receives impulses from
the pathways carrying sensations from the outside
world & transmits them through ascending fibres to
the cerebral cortex. Its function is the activation of
cerebral cortex.
An intact cerebral cortex.

4. 
Interruption
of
the
state
of
consciousness may occur at one or both
these levels:
R.A.S: a small lesion is sufficient to produce
Cerebral cortex: an extensive lesion is
necessary to produce coma.

6. Definition
Coma is sleep like state in which the patient makes
no purposeful response to the environment and from which
he or she cannot be aroused. The eyes are closed and do
not open spontaneously. The patient does not speak and
there is no purposeful movement of the face or limbs.
Verbal
stimulation
produces
no
response.
Painful
stimulation may produce no response or non purposeful
reflex movements mediated through spinal cord or
brainstem pathways.

7. Classification

Old classification based on:
 Degree of disturbance of consciousness.
 Response of the patient to external stimuli.

Glasgow coma scale: in this scale the level is evaluated
according to the patient’s response to external stimuli,
using 3 criteria:
 Eye opening
 Verbal response.
 Motor response
Each response is given a score. The total score is
summed to give an overall value of the level of
consciousness from 3-14.

8. Response to external
stimuli
State
consciousness
Lethargy or
drowsiness
Impaired
Verbal response to
increased verbal stimulation
Stupor
Impaired
Verbal response only to
vigorous & continuous
stimulation
Semi-coma
Lost
No verbal response, only
reflex response to painful
stimuli
Coma
Lost
No verbal or reflex response
to painful stimuli

9. Eye Opening
Spontaneous
Response to external
stimuli
Consciousness
4 Oriented
5
Obeys orders
5
4
Localises to pain
4
Flexes to pain
3
2
Extends to pain
2
1
None
1
In response to speech 3
Confused
In response to pain
2
Words, no sentences 3
None
1 Sounds, no words
None
According to this scale: coma (score3) is defend as a state
of loss of consciousness where there is no eye opening,
no vebral or motor response to external stimuli

10. Causes of coma
Organic
Intracrania
l
Hysterical
Exteracrani
al

11. Intracranial causes

The coma is associated with signs of
lateralisation:
Unequal pupils
Deviation of the eyes to one side
Facial asymmetry
Tilting of the head to one side.
Unilateral hypo or hypertonia
Asymmetric deep reflexes.
Unilateral +ve Babinski.
Unilateral focal or jacksonian fits.

12. Hysterical Coma
No apparent organic lesion.
 All vital signs are normal:

Pulse
Temp
B.P.
No particular smell of breath
 No finding on chemical analysis.
 Coma is usually incomplete.


13. 
Traumatic: head injury with:
 Cerebral concussion.
Contusion
Laceration.

Inflammatory
Encephalitis
○ Acute onset
○ Fever
○ Headache
○ Confusion
○ Focal cerebral signs.

14. .______________________ Cont
_ Meningitis

Fever
Headache
Neck stifness
+ve Kernig’s sign
C.S.F. changes

Cerbral abscess:
Gradual onset of low fever
Signs of increased intracranial tension
Focal cerebral signs
Septic focus (e.g. otitis media)

15. Vascular

Susbarachnoid haemorrhage
Sudden onset
Severe headache
Neck stiffness
+ve Kernig’s sign
Bloody C.S.F.

Cerberal haemorrahage
Sudden onset
Vomiting
Focal signs (e.g hemiplegia or fits)
Deeping coma

16. .___________________ Cont

Cerebral thrombosis
Basilar artery occlusion
Deep coma
Decerbrate rigidity
Respiratory embarrassment

Cerebral embolism
Acute onset
Source of emboli e.g. mitral stenosis
A.F
Bacterial endocarditis
Focal signs as hemiplegia

17. ._____________________ Cont
_

Hypertensive encephalopathy:
 Hypertension
 Rentinal changes
 Convulsions

Subdural haematoma
 Usually middle aged and elderly
 Headache and fluctuation of consciousness precedes the
coma
 Papiloedema and focal signs may be present + history of
head trauma.

18. Neoplastic

Primary e.g. meningioma or glioma

Metastatic

Bilaterak papilloedema is usually present.
Epilepsy
History of pervious fits:

Absence of focal signs of cerbral lesion

Dilated puplis

Bilateral externsor plantar response.

19. EXTRACRANIAL CAUSES
1. Toxic:







Barbiturates: respiratory depression, circulatory failure &
subnormal temperature.
Opiates: pin–point pupil, respiratory depression, slow weak pulse
& cold skin.
Belladonna (atropine): hot flushed dry skin, fever, dilated pupil,
delirium.
Salicylates: hyperventilation, fever, bleeding tendency & dilated
pupils.
Alcohol: characteristic odour, cold skin, increased level in the
blood.
Co poisoning: cherry red skin, no respiratory distress in spite of
07 lack.
Tranquilizers & hypnotics.

20. 2. Hypoxic
Pulmonary disease.
CO2 narcosis.
3. Ischaemic
Cardiac arrest.
Cardiac arrhythmias
Myocardial infarction.
Hypotensive drugs

21. 4. Metabolic
 Hypo & hyperglycemia (D.M.).
 Hypo & hyperthermia (heat stroke).
 Uraemia.
 Cholaemia.
5. Endocrinal
 Hypopituitarism.
 Hypothyroidism.
 Hypo & hyperparathyroidism.
 Addissoes crisis.
6. Fevers
 Meningitis, encephalitis.
 Malaria specially cerebral type.
 Septicaemia.
 Status typhosus.

22. CAUSES OF FEBRILE COMA

Infective: encephalitis, meningitis & other hyperpyrexias.

Vascular: pontine haemorrhage, subarachnoid
haemorrhage.

Metabolic: diabetic ketoacidosis, hepatic cirrhosis.

Endocrinal: thyrotoxic & Addissonian crisis.

Toxic: Belladonna & salicylate poisoning.

Sun stroke & heat stroke.

Coma with 2ry infection due to hypostatis pneumonia,
U.T. infection or bed sores.

23. CLINICAL APPROACH TO A CASE OF
COMA
History taken from the patient's relatives.

Onset: may be:
Sudden e.g. cerebral haemorrhage or
embolism.
Subacute e.g. cerbral thrombosis.
Gradual e.g. brain tumour.

24. .________________________ Cont
_

Head initiry: cerebral concussion, laceration or
haemorrhage.

Convulsions: post-ictal coma, brain tumour or
overdose of antiepileptics. 4. Drug intake:
insulin overdose, drug intoxication (e.g.
barbiturates . ..).

Exposure to the sun as during the Pilgrimage in
Mecca (sun stroke).

25. GENERAL EXAMINATION

Hyperthemia: causes of febrile
poisons e.g.
coma
Afropine
TCAs
Salicylats

Hypothermia:
 Hypopituitarism, Hypothyroidism.
Barbiturate, opiate or alcohol poisoning.
Peripheral circulatory failure: cardiac causes.

26. Pulse

Bradycardia: brain tumour, opiate
poisoning, myoexedma

Tachycardia: hyperthyroidism, uraemia
atropine

Blood pressure:

High B.P.: hypertensive encephalopathy.

Low B.P.: Addissionian crisis, Alchol &
barbiturate poisoning.

27. Respiration

Slow, deep, stertorous: in morphine &
barbiturate poisoning.

Rapid, deep (Kussmaul) respiration: in
diabetic or uraemic acidosis.

Hyperpnoea regularly alternating with
apnoea (Chyne-Stokes respiration): lesions
affecting both cerebral hemispheres.

28. .____________________ Cont

Central neurogenic hyperventilation: similar
to Kussmaul's respiration but the cause is a
lesion at the junction between midbrain &
pons.

Apneustic breathing: prolonged pause at full
inspiration due to pontine lesion.

Ataxic breathing: phases of deep & shallow
breathing
alternate
medullary lesion.
irregularly:
due
to

29. Odour of breath

Acetone odour: in diabetic ketosis coma.

Fetor hepaticus: in hepatic coma.

Uriniferous odour: in uraemic coma.

Alcohol odour: in alcohol intoxication.

Others:
Phenol
Cyanide
Kerosene
Opium poisoning.

30. Inspection of skin

Injuries or bruises: in traumatic causes

Dry skin in ketosis, atropine poisoning

Moist skin: in hypoglycaemic coma.

Cherry-red colour: in CO poisoning and
cyanide poisoning

Needle markers on limbs: in drug addiction

31. .___________________ Cont
_

Rashes: in waterhouse freidreichson’s
meningitis, in endocarditis & other exanthemata.

Bullae may be seen in babiturates, TCAs and
Copoisoning.

Cyanozed in opium and barbiturate poisoning

Pale cold clammy skin in cocaine toxicity.

Cold flushed in alcohol toxicity

32. C.N.S. Examination

Signs of lateralization: denoting an
intracranial cause for the coma.

Pupillary signs:
Dilated, irreactive to light.
○ Unilateral 3rd nerve compression, as in uncal
herniation.
○ Bilateral: .eg. atropine poisoning.

33. .___________________ Cont
_
Constricted:
○ Unilateral: Horner's syndrome however,
alone, this syndrome does not cause coma.
○ Bilateral:
Reactive to light: metabolic coma.
Irreactive to light: pontine haemorrhage,
morphine poisoning (pin–point pupil).

34. .___________________ Cont

Fundus examination: for papilloedema in
cases of increased I.C.T.

Signs
of
stiffness,
meningeal
opisthotonus.
irritation:
+ve
Neck
Kernig's
&
Lassegue's signs in cases of meningitis &
subarachnoid haemorrhage.

35. Laboratory Investigation

Blood examination:
Blood picture: leucocytosis in bacterial infections.
Blood film for malaria parasites.
Blood levels of sugar, creatinine,
Blood gases: pH, HCO-3.
Toxicological studies in cases of poisoning.

36. 
Analysis of gastric contents for possibility of
poisoning.

Urine analysis for sugar, acetone & albumin.

C.S.F. examination: e.g. bloody in S.A.H.,
purulent in bacterial meningitis

Plain x–ray skull: e.g. sellar changes in T
I.C.T., fractures in trauma.

C.T.-Scan & M.R.I show the site, size and
nature of intracranial lesions.

37. Emergency management

Immediately
Ensure adequancy of airway, ventilation and
circulation
Draw blood for serum glucose, electrolytes, liver
and renal function tests, PT, PTT and CBC.
Start IV and adminster 25 g of dextrose, 100 mg
of thiamine and 0.4 – 1.2 mg of naloxone IV.
Draw blood for arterial blood gas determinations.
Treat seizures.

38. Next

If signs of meningeal irritation are present
perform LP to rule out meningitis

Obtain a history if possible.

Perfom detailed general physcial and
neurologic examination.

Order CT scan if history or findings suggest
structural lesion or subarachnoid hemorrhage.

39. Later





ECG
Correct hyper or hypothermia.
Correct severe acid base and elctrolyte
abnormalities.
Chest X-ray.
Blood and urine toxicology studies, EEG.

40. Significance of endotracheal
tube

Maintain the airway patient

Suction of secretions

Oxygenation & mechanical retaliation

Some emergency drugs can be given
through it tube e.g.
Naloxone
Atropine
Epinephrine

41. conclusion

Coma is produced by disorders that affect
both cerbral hemispheres or the brainstem
reticular activiting system.

The possible causes of coma re limited:
mass lesion, metabolic encephalopathy,
infection of the brain (encephalitis) or its
coverings (meningitis) and sub arachnoid
hemorrhage.

42. .___________________ Cont

The examination of a comatose patient should be
focused and brief: assess whether the pupils
constrict in response to light, whether eye
movements can be elicited by rotating the head
(doll’s head maneuver) or by irrigating the
tympanic membrane with cold water (caloric
stimulation),
the
nature
(especially
bilateral
symmetry or asymmetry) of the motor response
to a painful stimulus and the presence or
absence of signs of meningeal irritation.

43. .___________________ Cont
_
 Immediately exclude hypoglycemia.

Patients who can open their eyes are not in
coma.

A sudden onset of coma suggest a vascular
origin,
especially
a
brainstem
stroke
or
subarachnoid hemorrhage.

Rapid progression from hemispheric signs such
as hemiparesis, hemisensory deficit or aphasia
to coma within minutes to hours is characteristic
of intracerbral hemorrhage.

44. .___________________ Cont
_ A more protracted course leading to coma

(days to a week or more) is seen with
tumor
abscess
or
chronic
subdural
hematoma.

Coma preceded by a confusional state or
agitated delirium without lateralizing signs
or symptoms is probably due to a
metabolic derangement.

45. Treatment of D.K.A
A. Prevention the patient is given guidelines
to prevent this problem such as:
1.The daily dose of insulin is mandatory and its
negligence is dangerous.
2.When the patient can't follow his usual diet due
to severe illness e.g. pneumonia, he must eat
or drink whatever he can tolerate. The patient
must test for urine glucose and ketone bodies
every 4 hours and if the tests show the need for
extrainsulin, we can add 20% to the original
dose (e.g. if the patient's usual dose is 40 U we
can add 8 U).

46. B. Curative
1. Fluid replacement
a. Suitable regimen is as follow:- 1 litre in the In 1/2 h, followed by
1 litre in 1 h, another 1 litre in 1 h, 1 litre in 2 h, 1 litre in 3 h, and
1 litre in 4 h.
b. 2 the total amount of the fluid deficit is given in 8 hours and the
other 2 over the next 16 h.
c. Normal saline is used at the start and changed to dextrose
saline when blood glucose reaches 180 mg%.
2. Insulin regimen we can use one of these two methods:a. I V. insulin infusion by the use of infusion pump:- soluble insulin
is diluted in 0.9 saline and 0.1 U/kg/h (6U/h) is given by the
infusion. The infusion is continued until the patient is well
enough (S.C.insulin is given before eating) and the insulin
infusion is discontinued after meal.
b. IM. route (soluble insulin) :- 20 U at the start, then 6 U/h till
blood glucose reaches 200 mg%.

47. .____________________ Cont
____ correction
3. Electrolyte
a. Kcl which is given from the second hour after insulin
therapy as follow:- 20 mmol is added to every litre saline if K level is 3-4 meq/L.
- 40 mmol is added to every litre saline if K level is less than 3
meq/L.
- It is contraindicated to add K if there is oliguria or K level > 5
meq/L.
b. Na HCO3:- 65 mmol over 30-60 min and can be repeated
every hour when the PH <7.1
4. Treatment of the precipitating factors e.g infection.
5. Treatment of the complications:- see later.

48. Complications
1. Acute fatty infiltration of the liver.
2. Infection
a. Rhinocerebral infection with mucormycosis may complicate this
condition
b. Treatment with amphotricin B + necrotic tissue removal, improve
the survival to about 60%.
3. Shock due to severe dehydration.
4. Vascular thrombosis due to dehydration and increased
viscosity of the blood.
5. Pulmonary edema which may occur by the volume overload due
to excess fluid.
6. Cerebral edema "rare but fatal"

49. 
Cause: It occurs 4-16 h. after initiation of therapy due
to rapid decrease of blood glucose level which lead to
movement of water into the intracellular space leading
to brain edema.

Cl.p.:
Increased
ICT
leads
to
papilledema,
ophthalmoplegia, confusion, coma.

Prevention: Avoid the rapid decrease of blood
glucose and distribute the fluid replacement over 24
hours.

Treatment: Brain dehydrating measures e.g mannitol
1-2 gm/kg over 20 min.

50. II. Hyperglycemic hyperosmolar
( non ketotic coma (HONK
Pathogenesis
A. It occurs in middle aged and elderly patients due
to the presence of low level of insulin which is
sufficient for prevention of lipolysis and ketosis
and not enough to prevent hyperglycemia.
B.
The
predisposing
ketoacidosis.
factors:
see
diabetic

51. Clinical picture
1. Severe hyperglycemia and dehydration
which may lead to renal impairment.
2.
Neurologic
manifestations
such
as
convulsions, stupors and coma.
3. Thrombotic complications may occur due
to increased viscosity of the blood.

52. Treatment
1. The same as in diabetic ketoacidosis but
we give z tonic saline to decrease the
serum
osmolality
which
exceed
340
mosm/L (N.290 mosm/L).
2. Lower rate of insulin infusion 3U/h.
3. Lower rate of S.C. heparin to prevent
thrombosis.

53. III. Lactic acidosis
1.
Occur
with:
biguanide
therapy
especially
phenformin.
2. The patient presents with acidosis (Kausmaull
respiration), late CNS and CVS inhibition.
3. Plasma ketostix value: < ++ exclude diabetic
ketoacidosis as a cause of metabolic acidosis.
4. Treatment:- by large amounts of bicarbonates.

54. T h an
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