Coma causes, pathophysiology, approach and treatment

1. Ahmed Sarteel Al-Shammary
Stager
Alteration In Consciousness

2. Cerebral Cortex
Reticular
Activating
System
Consciousness

3. Consciousness: is state of awareness of self and
environment, responsiveness to external stimulation and inner
need and wakefulness (eyes are open).
Coma: state of unconsciousness from which pts cannot be
aroused even by powerful stimuli .
Stupor: can be awakened only by vigorous stimuli.
Drowsy: simulate light sleep can easy aroused & persist of
alertness for brief period.

4. Causes of Coma :
1-Lesion in RAS (unilateral)
2-Both cerebral hemisphere.
3-Metabolic.

7. Proximity of RAS to structure that control
pupillary function & eye movement (brain
stem)permit clinical localization. (pupillary
abnormality suggest brainstem
While normal pupillary function either lesion or
metabolic suppression of cerebral hemispheres.

8. Brain Displacement and Herniations
Supratentorial
(should be extensive)
Infratentorial (even small)

11. Clinical Approach To The Patient

13. History
Examination
Investigations
Management
All Together
Try to go to the Patient and see him ASAP

14. Approach in ED
Primary Survey
• Airway
• Breathing
• Circulation
• Disability (GCS, Pupils)
• Exposure
Vitals
Blood glucose
Brief History of events (SAMPLE)
Secondary Survey (Head to toe)

15. Immediate Interventions
Intravenous Access
Oxygen supplement
Cardioscope monitoring
Blood glucose
ECG
Emergent Head CT

16. Ancillary Testing
Blood Glucose
Arterial / Venous Blood gas
Electrolytes
Serum creatinine, BUN
CBC
Coagulation – PT, aPTT
Thyroid profile
Urine routine and Toxicology screening

18. From an initial survey, many of the common
causes of coma, such as severe head injury,
alcoholic or other forms of drug intoxication,
and hypertensive brain hemorrhage, are readily
recognized.

20. History
• Trauma
• Cardiac arrest
• Drug overdose/ ingestion
• Neurological-
– Circumstances & rapidity
– Antecedent symptoms – Confusion, weakness, headache, fever, seizures,
double vision, vomiting
– Use of Meds, Drugs and Alcohol
– Chronic liver, kidney, heart, other medical disease
• Direct interrogation with Family members, bystanders, Ambulance
staff/ paramedics

22.  Alterations in vital signs (temperature, heart rate,
respiratory rate, and blood pressure) are important aids in
diagnosis.
 Fever is most often the result of a systemic infection such as
pneumonia or bacterial meningitis or viral encephalitis. An
excessively high body temperature (42°C [107.6°F] or 43°C
[109.4°F]) associated with dry skin should arouse suspicion
of heat stroke or intoxication by a drug with anticholinergic
activity.
 Hypothermia is observed in patients with alcohol or
barbiturate intoxication, drowning, exposure to cold,
peripheral circulatory failure, advanced tuberculous
meningitis, and myxedema.

23.  Shallow, slow, but regular breathing suggests
metabolic or drug depression.
 Rapid, deep (Kussmaul) breathing usually implies
metabolic acidosis but may also occur with
pontomesencephalic lesions.
 Cheyne-Stokes respiration in its classic cyclic form,
ending with a brief apneic period, signifies
bihemispheral damage/bilateral thalamic lesions or
metabolic suppression and commonly accompanies
light coma.

 Patients with lesions of the midbrain and pons often
have prolonged and rapid hyperpnea (neurogenic
hyperventilation)

24.  Apneustic breathing is characterized by a long inspiratory pause, after which the
air is retained for several seconds and then released. This abnormality appears
with lesions of the lateral tegmentum of the lower half of the pons.
 Cluster Breathing-Breathing with a cluster of breaths following each other in an
irregular sequence may result from low pontine or high medullary lesions.

25.  Vomiting at the outset of sudden coma, particularly if combined with
pronounced hypertension, is highly characteristic of cerebral
hemorrhage within the hemispheres, brainstem, cerebellum, or
subarachnoid spaces.
 The heart rate , if exceptionally slow, suggests heart block from
medications such as tricyclic antidepressants or anticonvulsants, or if
combined with periodic breathing and hypertension, an increase in
intracranial pressure.
 Marked hypertension is observed in patients with cerebral hemorrhage
and in hypertensive encephalopathy .
 Hypotension is the usual finding in states of depressed consciousness
because of diabetes, alcohol or barbiturate intoxication, internal
hemorrhage, myocardial infarction, dissecting aortic aneurysm,
septicemia, Addison disease, or massive brain trauma.

26.  Inspection of the skin may yield valuable information.
 Cyanosis of the lips and nail beds signifies inadequate oxygenation.
 Cherry-red coloration is typical of carbon monoxide poisoning.
 Multiple bruises (particularly a bruise or boggy area in the scalp), bleeding,
CSF leakage from an ear or the nose, or periorbital hemorrhage greatly
raises the likelihood of cranial fracture and intracranial trauma.
 Telangiectases and hyperemia of the face and conjunctivae are the common
stigmata of alcoholism;
 myxedema imparts a characteristic puffiness of the face.
 Marked pallor suggests internal hemorrhage.
 A Macular-hemorrhagic rash indicates the possibility of meningococcal
infection, staphylococcal endocarditis, typhus, or Rocky Mountain spotted
fever.

27.  Excessive sweating suggests hypoglycemia or shock, and excessively
dry skin, diabetic acidosis or uremia.
 Thrombotic thrombocytopenic purpura (TTP), disseminated
intravascular coagulation, and fat embolism may cause diffuse
petechiae or purpura; the last of these are often aggregated in the
anterior axillary folds.

28.  The odor of the breath may provide a clue to the
etiology of coma.
 Alcohol is easily recognized (except for vodka, which is
odorless).
 The spoiled-fruit odor of diabetic ketoacidotic coma, the
uriniferous odor of uremia, the musky and slightly fecal
fetor of hepatic coma, and the burnt almond odor of
cyanide poisoning are distinctive enough to be identified
by physicians who possess a keen sense of smell.

32.  It is usually possible to determine whether coma is
associated with meningeal irritation.

34.  With coma caused by drug intoxications and intrinsic
metabolic disorders, pupillary reactions are usually
spared, but there are notable exceptions.
 Serum concentrations of opiates that are high enough
to cause coma have as a consistent sign pinpoint
pupils, with constriction to light that may be so slight
that it is detectable only with a magnifying glass.
High-dose barbiturates may act similarly.
 Systemic poisoning with atropine or with drugs that
have atropinic qualities, especially the tricyclic
antidepressants, is characterized by wide dilatation
and fixity of the pupils.

36. These reflexes are elicited by moving the head from side to side or vertically
& observing evoked eye movements in the direction opposite to the head
movement also called dolls eyes manoeuver.
Preservation of evoked reflex eye movement integrity of brainstem ,
Absence of reflex eye movements , usually signifies damage within
brainstem

37. Irrigating the external auditory canal with cool water ,after brief latency,
result is tonic deviation of both eyes to the side of cool water irrigation &
nystagmus in the opposite direction
COWS direction of nystagmus
Cold water opposite , warm water same
Loss of movement indicate brainstem lesion.
Absence of nystagmus despite deviation of globe indicate cerebral
hemisphere or metabolic.

38.  Clinical Signs of Increased Intracranial Pressure
A history of headache before the onset of coma,
vomiting, severe hypertension beyond the
patient’s static level, unexplained bradycardia, and
subhyaloid retinal hemorrhages (Terson
syndrome) are immediate clues to the presence of
increased intracranial pressure, usually from one
of the types of cerebral hemorrhage.

39. Papilledema develops within 12 to 24 h in cases of brain
trauma and hemorrhage, and if it is apparent when coma
supervenes, it usually signifies brain tumor or abscess, i.e., a
lesion of longer duration.

40. Treatment In The Emergency Department
• Dextrose
• Naloxone
• Thiamine
Then specific Rx according to the cause.

42. MANIFESTATIONS:
 Lids close actively
 Pupils are reactive or dilated
 Oculocephalic are unpredictable
 Oculovestibular: Physiologic nystagmus present
 Motor tone is normal or inconsistent
 Euphoria or hyperventilation is usual
 No pathological reflex is present
 EEG is normal