1. The document discusses the approach to patients presenting in a comatose state, including definitions of different levels of consciousness, pathophysiology, common causes, management, and prognosis. 2. Management involves stabilization of airway, breathing, circulation, disability, and exposure, then detection of the underlying cause through history, exam, and investigations like imaging and labs. 3. Definitive therapy focuses on treating the specific cause, monitoring intracranial pressure, controlling seizures, and providing supportive care measures. Prognosis is generally poor when the GCS is very low or signs of herniation are present.

1. Approach to coma
by :Nancy Mohammed Alaa
Assistant lecturer of Pediatrics
Assiut university

2. • 1-definitions different conscious level
• 2-pathophysiogy of consciousness
• 3-causes of coma
• 4-management of comatosed patient
• A-stabilization
• B-detection of the cause
• C-definite therapy
• 5-prognosis

3. 1- DEFINITION
Consciousness :
• it is a state of awareness including
responsiveness to stimulation and ability to
recall past events and to respond
spontaneously and appropriately to external
and internal stimuli.

4. 1-Alertness: The patient is awake and fully aware of
normal external and internal stimuli.
2-Lethargy: The patient is not fully alert, tends to drift to
sleep when not stimulated, When aroused has appropriate
response.
3-Stupor: Respond only to persistent vigorous stimulation
When aroused, is able only to groan or mumble.
4- coma :A state of unconsciousness from which the child
cannot be aroused by ordinary verbal, sensory, or physical
stimuli.

5. • The terms stupor and lethargy refer to states
between alertness and coma
• An alteration in arousal represents an acute, life
threatening emergency, requiring prompt
intervention for preservation of life and brain
function

6. 2-PATHOPHYSIOLOGY
 The ascending reticular activating system (ARAS) is a
network of neurons originating in the tegmentum of the
upper pons and midbrain, believed to be integral to induce
and maintain alertness
 These neurons project to structures in the diencephalon,
including the thalamus and hypothalamus, and from there to
the cerebral cortex
 Alterations in alertness can be produced by focal lesions
within the upper brainstem by directly damaging the ARAS
 Injury to the cerebral hemispheres can also produce coma,
but in this case, the involvement is necessarily bilateral and
diffuse, or if unilateral, large enough to exert remote effects
on the contralateral hemisphere or brainstem

7.  The medial longitudinal fasciculi, which connect the
abducens & oculomotor nuclei, and the oculomotor &
trochlear nuclei are situated amid the neurons of the
pontine & midbrain portions of the ARAS.
- Therefore, when unresponsiveness is caused by
brainstem damage, the lesion affects the mechanisms
of ocular motility as well, and its location can often be
determined by abnormal patterns of ocular motility.

8. 3-Causes of coma
• A-with focal signs (intracranial)
• B-without focal signs but with meningeal signs
• C- without focal nor meningeal signs
(extracranial)

9. Signs of lateralization
• Unequal pupils
• Deviation of the eyes to one side
• Facial asymmetry
• Turning of the head to one side
• Unilateral hypo-hypertonia
• Asymmetric deep reflexes
• Unilateral extensor plantar response (Babinski)
• Unilateral focal fits

10. Meningeal signs
• 1-neck rigidity
• 2-opisthotonus position
• 3-Kering sign
• 4-Brudzinski (knee , neck ) signs

13. Coma with focal signs
1) Intracranial haemorrhage
2) Stroke: arterial ischemic or sinovenous thrombosis
3) Tumours
4) Focal infections :brain abscess
5) Acute disseminated encephalomyelitis
Coma without focal signs and with
meningeal irritation
1) Meningitis
2) Encephalitis
3) Subarachnoid haemorrhage

14. Coma without focal signs and without
meningeal irritation
1) Hypoxia-Ischemia: Cardiac or pulmonary failure, Shock,
Near drowning
2) Metabolic disorders: Hypoglycaemia , Hyperammonemia
(e.g. Hepatic encephalopathy, urea cycle disorders ),
Uremia.
3) Systemic Infections: Bacterial: gram-negative sepsis ,
toxic shock syndrome
3) Drugs ,toxins and post DPT.
4) Hypertensive encephalopathy
5) Non-convulsive status epilepticus

15. 4-MANAGEMENT
• A- Stabilization
• B-detection of the cause
• C-definite therapy
15

16. A- STABILIZATION:
Airway
Breathing
Circulation
Disability
Exposure

17. 1-AIRWAY
 Clear
 Maintainable
 Not Maintainable
Maintainable
• Methods to open airway
• A- head tilt chin lift
• B- jaw thrust
• C-oral or nasopharyngeal airway .
17

18. 2-Breathing
 Respiratory rate and pattern
 Respiratory effort
 Chest expansion and air movement
 Abnormal lung and airway sounds
 Oxygen saturation by pulse oximetry
 If respiratory distress , low oxygen saturation :
 Start oxygen therapy

20. 3-circulation
 Heart rate and rhythm
 Central and peripheral pulses
 Capillary refill time
 Skin color and temperature
 Blood pressure

21. 4-Disability
• 1-conscious level by
• GCS
• AVPU
• FOUR score
• 2-pupillary reaction
• 3-blood glucose level

24.  Rapid neurogical assesment
 A score of 'P' corresponds to a Glasgow Coma
Scale (GCS) of 8, and suggests the airway
should be protected by intubation to prevent
aspiration

25. FOUR score

26. • Clinical management decisions should not be based
solely on the FOUR Score in the acute setting and
should be used in conjunction with other clinical
information.
• Very low FOUR scores (≤4) are more predictive of in-
hospital mortality as compared to the lowest GCS (3T).
• Improvement in score of >2 is predictive of survival in
cardiac arrest (Fugate 2010).
• Each point increase in the FOUR Score is associated
with decreased mortality and morbidity.

28. Pupils Lesion/Dysfunction
Pinpoint Pons, opiates, cholinergic intoxication ,
Mid position –
fixed or irregular
Midbrain lesion
Unilateral , dilated
and fixed
Uncal herniation as 3 rd nerve compression
Bilateral , dilated
and fixed
Diffuse damage, central herniation, global
hypoxia ischemia, barbiturates, atropine

30. 5-Exposure
 Temperature
 Skin: rash or trauma

31. B-Detection of the cause
• 1-history
• 2-examination
• 3-investigation

32. 1-History
1. Onset :
a) Sudden onset: vascular injury or a convulsion
b) Acute onset in normal child: ingestion of drug, toxin,
poison.
c) Gradual onset : infectious process, metabolic
derangement.

33. 2. Associated symptoms of CNS causes:
a) Fever : Infections
b) Headache, Vomiting and Diplopia : Increase intracranial
pressure
c) Neck stiffness : Meningitis, subarachnoid haemorrhage
d) Rash : Meningococcemia
e) History of excess cry, irritability, enlarging head in infants :
Meningitis, Hydrocephalus
f) History of Trauma
g) Seizures : intracranial space-occupying lesions , Epilepsy,
Post-ictal

34. 3. Recurrent episodes: Epilepsy, Inborn errors of
metabolism
4. History of recent infectious diseases : Mumps
(Parotid swelling), measles (rash)
5. Failure to thrive, vomiting, peculiar skin odour :
Metabolic cause
6. Jaundice, abdominal distension, hematemesis,
melena, bleeding : Hepatic encephalopathy
7. ↓ Urine output, swelling, periorbital puffiness,
Nausea, vomiting, loss of appetite : Uremic
encephalopathy

35. 8. History of loose stools :hemolytic uremic syndrome
(bloody diarrhea), Hypovolemia ,Ingestion of
toxins/poisons, medications
9. Family History of TB, migraine, epilepsy
10.Birth History of Birth asphyxia and History of
recurrent hypoglycemia
11.Developmental delay or regression
12.History of envenomation ,drug intake, heat stroke
or hypothermia

36. 2-Examination
• 1-vital signs:
A-Pulse
• Bradycardia: brain tumors, opiates, myedema.
• Tachycardia: hyperthyroidism, uremia
B-Blood Pressure
• High: hypertensive encephalopathy
• Low: Addisonian crisis, barbiturate

37. C-Temperature
Hypothermia
Hypopituitarism, Hypothyroidism
Barbiturate ,opioid
Exposure to low temperature environments, cold-water
immersion

38. Hyperthermia (febrile Coma)
Infective: encephalitis, meningitis
Vascular: pontine, subarachnoid hge
Metabolic: thyrotoxic, Addisonian crisis
Toxic: belladonna, salicylate poisoning
Sun stroke, heat stroke
Coma with 2ry infection: UTI, pneumonia, bed sores.

39. • D-RESPIRATORY RATE

42. 2-Head and neck
• The head
1. Evidence of injury
2. Skull should be palpated for depressed fractures.
• The ears and nose: haemorrhage and leakage of
CSF
• The fundi: papilloedema

43. 3-Skin
• Injuries, Bruises: traumatic causes
• Dry Skin: DKA, Atropine
• Moist skin: Hypoglycemic coma
• Cherry-red: CO poisoning
• Needle marks: drug addiction
• Rashes: meningitis, endocarditis

44. 4-Odour of breath
 Acetone: DKA
 Fetor Hepaticus: in hepatic coma
 Urineferous odour: in uremic coma
 Alcohol odour: in alcohol intoxication

45. • 5-CARDIOVASCULAR :
• EMBOLIC MANIFESTATION IN TOF
• 6-ABDOMINAL
• organomegally in metabolic ,liver cell failure
• 7-neurological :
• A-cranial nerves
• B-motor (tone ,superficial and deep reflex)

46. 3-investigations
• A-lab:
• 1-blood glucose ,electrolyte
• 2-renal function test
• 3-liver function test
• 4-toxicology screen
• 5-blood gas ,ammonia ,lactate
• 6-septic screen;CBC,CRP,CULTURE,URINALYSIS

47. • 7-METABOLIC;amino acid level in urine ,blood
• 8-CSF ;
• Suspect CNS infection

48. B-Imaging Studies
When patient is medically stable
CT offers faster results Although most patients with
coma will require CT scanning, or indeed all with
persisting coma,
(1)With contrast for space-occupying lesion
(2)Without contrast for vascular lesions
(3)With bone window for head injuries.
[MRI] can provide better soft tissue resolution.

51. C-Definite therapy
• 1-Treatment of underlying cause
• A- antibiotics in CNS infection
• B-surgery in subdural or extradural hematoma
• C-antidote in drug toxicity

52. • 2-monitor intracranial pressure (ICP):
• Management of increased intracranial tension ;
• A-head elevation in midline 30 degree
• B-hyperventilation (keep P CO2 30 mmHg ) for 48 hrs
• C-mannitol 0.5-1 gm/kg /6-12 hrs or hypertonic
saline 3% (4-6 ml/kg)
• D-avoid using hypotonic fluids
• E-diuretic
• F-sedation and analgesic
• G-therapeutic CSF drainage

53. • H-EEG monitor to detect non convulsive status
epilpticus
• i-if refractory increased ICP;
• Monitor ABG ;hypercarbia
• Repeat imaging to exclude new lesions
• Decompressive craniectomy

54. • 3-convulsions control
• 4-correction of hypoglycaemia
• dextrose 10% 2-4 ml/kg
• 5-feeding by NG tube or start TPN
• 6-FLUID restriction to 75% of maintainance

55. • 7-CARE OF;
• A-Respiratory :Physiotherapy, suction
• B-eye; drops , ointment ,pad
• C - skin; frequent change position ,clean skin
• D-urinary: catheter , monitor urine output
• E-Oral and dental hygiene

56. 5-prognosis
• Poor prognosis in ;
• A-GCS <8
• B-SIGNS OF HERNIATION ;
• 1-Irregular breathing pattern,apnea
• 2-cushing triad
• 3-unequal pupils
• C-associated with diabetes inspidus

57. • D-EEG
• Burst suppression, electrocerebral silence

59. • F- absent brain stem reflex
• A-PUPILLARY
• B-CORNEAL
• C-GAG,COUGH REFLEX
• D-OCULOCEPHALIC
• E-OCULOVESTIBULAR

63. COWS: Cold Opposite, Warm Same.
Cold water = FAST phase of nystagmus to
the side Opposite from the cold water filled ear
Warm water = FAST phase of nystagmus to
the Same side as the warm water filled ear
In other words: Contralateral when cold is
applied and ipsilateral when warm is applied.