How to approach a patient in coma

1. By Hauwa Muhammad Kabir
Facilitator’s Name - Dr Ssebuliba Moses

2. DEFINITION
 Coma is a state of unarousable unconsciousness
 Consciousness: state of awareness of self and the
environment enabling responsiveness to external
stimulus and inner need
 Two major components of consciousness
 Arousal ; ascending recticular activating system
 Awareness; cortex and the thalamus
Disruption of the signaling pathways of the mentioned
structures results into coma

3. Cont… definitions
 The disruptions could be structural or diffuse systemic
nature
 For structural disruptions: bilateral cortical damage or
brainstem compression must occur to lead to coma

9. Differentials (without Focal
Neurological Signs)
 Intoxications : Alcohol, Sedative drugs, Opiates etc.
 Metabolic disturbances such as hypoglycemia ,
hyponatraemia, hypernatraemia, hypercalcemia,diabetic
ketoacidosis, uremia, addisonian crisis etc.
 Severe Systemic Infections such as Septicemia, Typhoid
Fever, Malaria etc.
 Shock from any cause.
 Post Seizure states, Status epilepticus and Non convulsive
status epilepticus.
 Hypertensive Encephalopathy, Eclampsia.
 Severe Hyperthermia, Hypothemia.

10. Differentials (with Focal
Neurological Signs)
 CNS Hemorrhage or Infarction( subarachinoid , epidural,
subdural or intraparenchyma )
 Brain Abcess or Subdural Empyema.
 Brain tumor with surrounding Edema.
 Vascular occlusion (thrombotic or embolic)
 Space occupying lesion (tumor, abscess)
 Hydrocephalus
 Traumatic brain injury, Brain Contusion.
 Metabolic Coma with preexisting Focal Damage.
 Miscellaneous : Cortical Vein Thrombosis, Septic Emboli,
Theombocytopenic Purpura, Cerebral Vasculitis etc.

11. Meningitis Syndromes
 Subarachnoid Hemorrhage from Ruptured aneurysm,
arteriovenous malformation,Trauma.
 Acute Bacterial Meningitis.
 Viral Encephalitis
 Miscellaneous : Fat Embolism, Cholesterol Embolism,
Carcinomatous and Lymphomatous Meningitis.

12. Initial Assessment and
Management
 Rapid assessment
 to facilitate resuscitation
 Stabilization
 Identification of life threatening reversible causes.
Continuous hemodynamic and neurological monitoring
strongly advised.
Senior medical personel’s help is called for.
Management is tailored to initial examination and
investigation findings.
And measures to prevent secondary cerebral damage.
ABCDE approach is utilised.

18.  Cardiac arrest : cardiopulmonary resuscitation is done
and advanced life support alogarithms followed.
 h/o of trauma: cervical spine immobilisation should be
ensured
 Adequate oxygenation through adjuncts such as
prongs, masks or endotrachial intubation.
 Indications for intubation
 Gcs <8, inadequate ventilation, loss of ability to protect
airway or loss of reflexes, respiratory seizures (relative)

19.  Adequacy of ventilation can be aided by arterial blood gas
analysis
 Initial targets should be PaCO2 4.5-5.5kpa and Pa O2 > 13kpa
until information regarding the cause of coma can be
established.
Cerebral perfussion and oxygenation
intravenous fluids with or without vasopressors can be used
to target mean arterial blood pressure of 90mmhg to achieve
an adquate cerebral perfusion pressure.
This is guided by patient circumstances and comorbidities.

20. Sodium and glucose levels.
 Hypoglycaemia glucose< 4mmol. Immediate
intravenous administration of 25ml of 50% glucose is
required
 Incase of suspected vitamin B deficiency eg in alcohol
dependence, thiamine 100mg must be co-
administered with glucose to prevent potentially fatal
precipitation of wernicke’s encephalopathy

21. Hyponatraemia and
hypernatraemia
 Carefully corrected in high dependence care setting as
too rapid correction can precipitate cerebral oedema or
cerebral pontine myelinolysis
 Maximum rate of correction is 8mmol/l within 24hrs

22. Opiate toxicity
 Naloxone 400mcg.. If response is seen.. Dose can be
repeated or an infusion is setup.
 Mgt of benzodiazepine overdose needs full
consideration, as use of flumazenil for resversal can
precipitate seizures in those with chronic dependence.
 In seizures or non conclusive status epilepticus load
with iv phenytoin or levetracetam.

23. sepsis
 Blood cultures
 Start antibiotics within one hour.

24. Further history and examination
 Once stabilised
 Detailed collateral h/o should be taken if available.
 Further clinical examination and investigations
instituted to facilitate diagnosis.
 The h/o should focus on;
 Time course of deterioration
 Potential precipiating factors
 Associated prodromal symptoms

25.  Patient’s medical and surgical h/o including
metabolic, endocrine, neurological and psychiatric
illnesses.

26. examination
 A focused medical and neurological exam done.
 Signs of meningism, lateralising signs and brain stem
reflexes.
 Meningism is a feature of subarachinoid hemorrhage
and meningoencephalitis
 Lateralising signs suggest structural lesion and prompt
early imaging.

27.  Most common form of coma is that without localizing
signs or meningism and this usually results from a
diffuse systemic cause.. Such as anoxic –ischaemic
injury or metabolic , toxic or post-ictal states.

28. Examination of the eyes
 Fundoscopy
 Pupillary responses
 Occulomotor function and corneal reflexes

29. Examination finding Potential significance
Meningism Subarachinoid hemorrhage
meningoencephalitis
Localising signs Structural lesion
Fundoscopy; papilloedema
Vitreous hemorrhages
Raised icp / asphyxia
Subarrachinoid hemorrhages
Pupillary responses
Fiixed constricted pupils
Unilateral dilated pupil
Brainstem insult or opioid overdose
Horners syndrome
Brain stem reflexes:
corneal reflex absent
Absent cough
Pontine lesion
Medullary injury

30. Motor function
Decerebrate
Posturing (pronation , extension of
the upper limbs
Lesion below the midbrain
Decorticate
Posturing (upper limb flexion ,
lower limb extension)
Brain stem lesion above midbrain
Myoclonic jerking Hypoxic ischaemic encephalopathy

31. INVESTIGATIONS
 CBC
 Electrolytes
 Liver function
 Clotting profile
 Thyroid function
 Urine sent for toxicology
Where reversible coma has not been identified by the above a
Head CT Scan is done and CT angiogram are indicated for;

32.  Critical intervention such as
 Thrombolysis or thrombectomy for acute ischaemic
stroke
 Hydrocephalus requiring CSF DIversion
 Decompressive craniectomy for raised ICP

33.  Blood cultures for febrile patients with a temperature of
above 38 degrees celicious
 Lumbar puncture following CT scan for patients with
suspected CNS infection or inflammation
 Electro encephalogram for non conclusive status
epilepticus
 Magnetic resonance imaging (MRI) with diffuse weighted
imaging (DWI) or fluid attenuatedinversion recovery
(FLAIR)

34.  DWI abnormalities result from an acute stroke
 FLAIR abnormalities suggestive of underlying
inflammatory or demyelinating condition
 Where CT Angiogram has identified a likely
underlying vascular cause digital subtraction
angiography may be performed to investigate this and
guide further management

35. Time critical situations
 Evidences of increased ICP on CT scan . Neurosurgical team
should be engaged.
 TBI patients with raised ICP from structural lesion. Interim
measures to control high ICP and prevent secondary
neurological damage include deepening of sedation ( propofol
and barbituates)
 Hyperventilation to achieve PaCO2 between 4.0 to 4.5 kpa but
shouldn’t be prolonged
 Cerebral venous drainage by raising the head to 20 degrees.
 ICP monitoring where possible for patients with abnormal CT
scan of gcs below 8