This document discusses the approach to patients presenting in a coma. It defines coma as a state of unresponsiveness where patients cannot be aroused even with vigorous stimulation. It describes various stages between alertness and coma. Coma is caused by dysfunction of the brainstem or both hemispheres of the brain. A thorough assessment is needed to determine the cause and guide management, including a neurological exam to identify any focal signs. Key aspects of the exam include vital signs, pupil response, eye movements, motor response and reflexes. Different patterns on exam can localize the lesion causing the coma. Immediate life-saving interventions are also often needed.

1. Approach to Coma
A TOPIC ALWAYS NEEDS TO BE
AROUSED

2. DEFINING COMA
"unarousable unresponsiveness"
• Defined coma as a state of unresponsiveness in
which the patient lies with his eyes closed and
cannot be aroused to respond appropriately to
stimuli even with vigorous Stimulation
• The patient may grimace in response to painful
stimuli and limbs may demonstrate stereotyped
withdrawal responses, but the patient does not
make localized responses or discrete defensive
movements

3. COMA IS PROLONGED UNCONSCIOUSNESS

4. Consciousness
• Perception -Awareness of self and
environment ( Sensory System)
• Reaction – Meaningful responsiveness (Motor
system)
• Wakefulness – (Sleep wave cycle)

5. Stages of (un)Consciousness
• The terms stupor, lethargy, and
obtundation 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. Coma Pathophysiology
• Coma implies dysfunction of:
– Ascending Reticular Activating System or
– Both hemi-cortices
• Anatomically, this means
– central brainstem structures (bilaterally) from
caudal medulla to rostral midbrain
– both hemispheres

7. Coma - Aetiology
Metabolic:-
– Ischemic hypoxic
– Hypoglycaemic
– Organ failure
– Electrolyte disturbance
– Toxic
Structural:-
– Supratentorial bilateral
– Unilateral large lesion
with transtentorial
herniation
– Infratentorial

8. ASSESSMENT OF COMA

9. Assessment of coma
• Coma is an acute, life threatening situation. Evaluation must be swift,
comprehensive, and undertaken while urgent steps are taken to
minimize further neurological damage
• Emergency management should include:
• Resuscitation with support of cardiovascular and
respiratory system
• Correction of immediate metabolic upset, notably
control of blood glucose and thiamine if indicated;
control of seizures and body temperature; any
specific treatments—for example, naloxone for
opiate overdose

10. • History—through friend, family or emergency medical personnel
• General physical examination
• Neurological assessment—to define the nature of coma
• where is the lesion responsible for coma?
• what is its nature?
• what is it doing?

11. • Neurological diagnosis is based on history,
thoughtful examination, and the appropriate
choice of investigations
• This is essential, as there is little point in
performing a cranial computed tomographic
(CT) scan in a patient in hypoglycaemic coma
where urgent correction of the metabolic
disorder is paramount and any delay—for
example, waiting for a scan—is unacceptable

12. • The approach to clinical evaluation is used to categorise coma into:
• Coma without focal signs or meningism. This is the
most common form of coma and results from
anoxic-ischaemic, metabolic, toxic, and drug
induced insults, infections, and post ictal states
• Coma without focal signs with meningism. This
results from subarachnoid haemorrhage,
meningitis, and meningoencephalitis
• Coma with focal signs. This results from
intracranial haemorrhage, infarction, tumour or
abscess

13. Keep in mind
• Multifocal structural pathology, such as venous sinus
thrombosis, bilateral subdural haematomas, vasculitis or
meningitis, can present with coma without focal signs or
meningism and so mimic toxic or metabolic pathologies
• Conversely, any toxic/metabolic cause for coma may be
associated with focal findings—for example, hypoglycaemic or
hepatic encephalopathy
• Also focal signs may be the consequence of pre-existing
structural disease; in the septicaemic patient with a previous
lacunar infarct, for example, the focal neurology may be
mistakenly accepted as signs of the current illness

14. EXAMINATION

15. Circulation
• Kocher-Cushing response -
– rise in BP->bradycardia due to rise in ICP ->
compression of floor of the iv ventricle fall in BP
and tachycardia usually terminal event due to
medullary failure

16. Breathing
• Forebrain
– Post hyperventilation
apnea
– Cheyne stoke respiration
• Hypothalamus midbrain
– Central neurogenic
hyperventilation
• Basis pontis
– Pseudobulbar paralysis
of voluntary center
• Lower pontine
tegmentum
– Apneustic breathing
– Cluster breathing
– Short cycle periodic
breathing
– Ataxic breathing
• Medulla
– Ataxic breathing
– Slow regular respiration
– Gasping

17. NEUROLOGIC EXAMINATION

18. Level of consciousness
• Arousability is assessed by noise (eg, shouting in
the ear) and somatosensory stimulation
• Pressing on the supraorbital nerve (medial aspect
of the supraorbital ridge) or the angle of the jaw, or
squeezing the trapezius, may have a higher yield
than the more commonly used sternal rub and
nailed pressure
• Important responses include vocalization, eye
opening, and limb movement

20. Cranial Nerve Exam
• Systematic assessment of brainstem function
via reflexes
• Cranial Nerve Exam
– Pupillary light response (CN 2-3)
– Oculocephalic/calorics (CN 3,4,6,8)
– Corneal reflex (CN 5,7)
– Gag reflex (CN 9,10)

21. Pupils: Key points
• Size dependent on sympathetic and parasympathetic
input
• Anatomically near the RAS
• Resistant to metabolic influences
• Small and reactive with metabolic causes
• Unilateral dilation indicates uncal herniation

22. Pupil
Atropine
Opiate
Organophosphorus

23. Pupil
• Diencephalic (metabolic) Small reactive
• Midbrain tectal Midsize,fixed
• Midbrain nuclear Irregular pear shaped
• 3rd nerve Fixed widely dilated
• Pontine Pinpoint reactive
• Opiate Pinpoint
• Organophosphorus Small
• Atropine Wide dilated

24. • Lesions above the thalamus and below the
pons preserve pupillary reactions

25. Eye movements: Exam
• Position at rest
– Straight ahead
– Dysconjugate
– Conjugate deviation
• Oculocephalic reflex
– Positive “Doll’s eyes”
– Negative “Doll’s eyes”
• Oculovestibular reflex
– Cold calorics
• Resting position
– Midline
• Deviation suggests
frontal/pontine damage
– Conjugate
• Dysconjugance suggests
CN abn.
– Moving
• Roving, dipping, bobbing

26. Eye movement
• Metabolic
– Roving eye movement,
– Oculocephalic,
– Vestibuloocular
• Supratentorial
– Contralateral conjugate palsy
• Thalamus
– Upper turn down

27. Eye movements in Coma
• Midbrain
– Ipsilateral 3rd
• Pontine
– Ipsilateral 6th
– Ipsilateral gaze palsy
– One and half syndrome
– Bilateral gaze palsy
– Ocular bobbing
– Mlf syndrome

28. Oculocephalic and caloric response
This reflex is usually suppressed (and
therefore not tested) in conscious
patients
If nystagmus occurs, the patient is
awake and not truly in coma; this can
be a useful confirmatory test for
psychogenic unresponsiveness

29. Corneal reflex
The reflex can be suppressed acutely contralateral to a large, acute
cerebral lesion, and also with intrinsic brainstem lesions. Loss of the
corneal reflex is also an index of the depth of metabolic or toxic coma;
bilaterally brisk corneal reflexes suggest the patient is only mildly
narcotized. Absent corneal reflexes 24 hours after cardiac arrest is
usually, but not invariably, an indication of poor prognosis (assuming
the patient has not been sedated). Corneal reflexes may also be
reduced or absent at baseline in elderly or diabetic patients

30. Motor examination
• Muscle tone, spontaneous and elicited movements
and reflexes
• Asymmetries of these often indicate a hemiplegia
of the non-moving side, implying a lesion affecting
the opposite cerebral hemisphere or upper
brainstem
• Purposeful movements include crossing the
midline, approaching the stimulus, pushing the
examiner's hand away or actively withdrawing from
the stimulus

31. • Decorticate posturing consists of upper-extremity
adduction and flexion at the elbows, wrists, and
fingers, together with lower-extremity extension,
which includes extension and adduction at the hip,
extension at the knee, and plantar flexion and
inversion at the ankle . This occurs with
dysfunction at the cerebral cortical level or below
and may reflect a "release" of other spinal
pathways
• Decerebrate posturing consists of upper-extremity
extension, adduction, and pronation together with
lower-extremity extension and traditionally implies
dysfunction below the red nucleus, allowing the
vestibulospinal tract to predominate

32. Motor response to pain.
(A) Left hemisphere lesion. The
two figures illustrate localisation of
pain with the left hand and flexion
(left hand figure) or extension (right
hand figure) on the right
(B) Subcortical: unilateral left sided
lesion exerting a variable contralateral
effect. The figures illustrate flexion to
pain with the left hand with either
extension (right hand figure) or flexion
with the right and hyperextension in
both lower limbs
(C) Midbrain upper pontine: a
bilateral upper and lower limb
extension response
(D) Lower pontine/medullary: a bilateral
extensor upper limb posture with either
flaccidity or minimal diminished flexor
response in lower limbs

36. ECG changes in coma
(SAH, ICH, INFARCT)
– Tall T, prolonged QT
– Q wave with st depression
– SVT, AF, AFL
– Sinus bradycardia,arrest, nodal rhythm
– A-V block or dissociation
– PVc's, VFL, VF

39. Case 1
• 24Yrs laborer presented to the hospital with H/O
fall down from height. Admitted the patient in
ER. On the time of admission in ER patient was
unconscious and agitated, GCS 3/15.
– BP= 120/70 mmHg
– PR=110 bpm
– RR= 20 mts
– Temp=37.4 ⁰C
– SPO²= 98%

40. CT done

41. Diagnosis
Sub Arachnoid Hemorrhage

42. Case 2
62 years old male admitted to ED of KAUH on 13
May, 2009. Confusion since today morning,
disorientation, lethargy, abdominal pain,
constipation.
Past medical history: DM ( on OHG agent),
CLD(LC, Hematemesis), HCV, HBV, Portal
hypertension, post splenectomy, esophagitis.
Family history: No family history of similar
condition.

43. Examination:
o General condition: Disorientation &
Confusion
o Skin: No jaundice, no skin rash
o CVS: S1 + S2 + 0
o CNS: Normal reflexes, flapping tremors
o Chest: Bilateral basal crepitation
o Abdomen: Distended, soft, lax,
hepatomegally, mild ascitits

44. Vital signs:
RR: 22 BP: 135/78
Pulse: 75 bpm Temp: 36.22º C
Lab:
Na: 144 mmol/L K: 4.1 mmol/L
Bilirubin: 7 umlo/L Cr: 100 umol/L
Glucose: 12.1 mmol/L CK: 2468 IU/L
Albumin: 22 g/L ALT: 69 U/L
AST: 110 U/L GGT: 92 U/L
Troponin-I 1.6 ug/l

45. MRI

46. Diagnosis
Hepatic encephalopathy

47. Case 3
• 64/F, no significant past medical history.
• Elective L/S BTL 0900. During the surgery, D5 at
125 cc/ hr.
• Pt in ICU. “Too sedated to go home.” Got IV
meperidine. No PO intake, IV D5 continued.
• 2:45 AM next day, pt. C/O headache, verbal order
for Tylenol #3.
• At 9:00 AM, nurse tells surgeon of a sodium of
127 mEq/L. No new orders, IV fluids were
continued. At 1:30 pm, pt. lethargic and pain
medications, pain meds held.

48. • At 3:30 pm, she had seizures and respiratory
failure. Neurology call given for seizures. The
patient intubated and ventilated. Repeat of
Serum sodium 122 mEq/L.

49. Diagnosis
Hyponatremia

50. SOME MORE IMAGES

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