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Assessing Coma and Management

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If the cause of coma is uncertain (e.g., CT scan is negative), consider giving Cefotaxime, Aciclovir, Pabrinex (Thiamine B1), and Naloxone until further information is available.

Coma Management
Initial assessment: ABC, administer O₂, place in the recovery position, and seek anaesthetic review if GCS < 9. Perform early CT head and exclude neck fractures. Address surgical causes: If subdural haematoma (SDH), epidural haematoma (EDH), intracerebral haemorrhage (ICH), or a tumour is suspected, refer to neurosurgery. Consider medical causes, especially if the CT scan is normal: Opiate toxicity: Small pupils, low GCS. Administer IV Naloxone 400 mcg (0.4 mg), repeatable up to 2 mg if needed. Hypoglycaemia: Administer IM Glucagon 1 mg and/or 200 ml 20% or 50 ml 50% Dextrose IV or equivalent. Suspected Meningitis: Administer Cefotaxime IV. Suspected HSV Encephalitis: Aciclovir 10 mg/kg IV every 8 hours. Artery of Percheron stroke: Consider Aspirin if low GCS. Endocrine causes: If adrenal insufficiency is suspected, administer Hydrocortisone 100 mg IV stat. Sepsis: Administer Tazocin and Gentamicin. Thyroid crisis: IV T3/T4 for suspected myxoedema coma (low temperature and bradycardia). Seizure: Consider postictal state. If non-convulsive status is suspected, assess eye movements. Consider Lorazepam/Keppra IV and consult neurologist. Large MCA stroke: Consider mechanical thrombectomy if indicated. Malignant MCA stroke: Consider decompressive hemicraniectomy. Cerebellar stroke: Consider decompressive surgery or shunting for hydrocephalus. Cerebral malaria: Administer IV Quinine and send blood films if there is a relevant travel history. Raised Intracranial Pressure (ICP): Intubate and ventilate to lower pCO₂ to 28-32 mmHg. Administer Mannitol IV boluses if appropriate. Refer for definitive surgical intervention (e.g., evacuation of haematoma, decompressive hemicraniectomy, or external ventricular drain for hydrocephalus).

Coma Management

Initial assessment: ABC, administer O₂, place in the recovery position, and seek anaesthetic review if GCS < 9. Perform early CT head and exclude neck fractures.
Address surgical causes: If subdural haematoma (SDH), epidural haematoma (EDH), intracerebral haemorrhage (ICH), or a tumour is suspected, refer to neurosurgery.
Consider medical causes, especially if the CT scan is normal:

Opiate toxicity: Small pupils, low GCS. Administer IV Naloxone 400 mcg (0.4 mg), repeatable up to 2 mg if needed.
Hypoglycaemia: Administer IM Glucagon 1 mg and/or 200 ml 20% or 50 ml 50% Dextrose IV or equivalent.
Suspected Meningitis: Administer Cefotaxime IV.
Suspected HSV Encephalitis: Aciclovir 10 mg/kg IV every 8 hours.
Artery of Percheron stroke: Consider Aspirin if low GCS.
Endocrine causes: If adrenal insufficiency is suspected, administer Hydrocortisone 100 mg IV stat.
Sepsis: Administer Tazocin and Gentamicin.
Thyroid crisis: IV T3/T4 for suspected myxoedema coma (low temperature and bradycardia).
Seizure: Consider postictal state. If non-convulsive status is suspected, assess eye movements. Consider Lorazepam/Keppra IV and consult neurologist.
Large MCA stroke: Consider mechanical thrombectomy if indicated.
Malignant MCA stroke: Consider decompressive hemicraniectomy.
Cerebellar stroke: Consider decompressive surgery or shunting for hydrocephalus.
Cerebral malaria: Administer IV Quinine and send blood films if there is a relevant travel history.

Raised Intracranial Pressure (ICP):

Intubate and ventilate to lower pCO₂ to 28-32 mmHg.
Administer Mannitol IV boluses if appropriate.
Refer for definitive surgical intervention (e.g., evacuation of haematoma, decompressive hemicraniectomy, or external ventricular drain for hydrocephalus).

Recovery Position

Assessment of Coma: Use Glasgow Coma Scale (GCS) and Examine Pupils

Download GCS Chart

Pathophysiology of Coma: Ascending Reticular Activating System (ARAS)

Consciousness is the awareness of the environment and self, maintained by the ARAS.
The ARAS connects brainstem nuclei with the cerebral cortex, involving structures like the locus coeruleus, dorsal raphe, hypothalamus, and basal forebrain.
Impairment occurs due to elevated intracranial pressure (ICP) or bilateral cortical or thalamic damage, leading to a loss of consciousness.
Brainstem compression can cause pupillary changes: bilateral mydriasis with unresponsive pupils suggests brainstem damage, while pontine damage can cause pinpoint pupils.

Anatomic basis of coma. Consciousness is maintained by the normal functioning of the brainstem reticular activating system above the mid pons and its bilateral projections to the thalamus and cerebral hemispheres. Coma results from lesions that affect either the reticular activating system or both hemispheres.

Differential Diagnosis: CT Head and Capillary Blood Glucose (CBG) Are Key

Cause	Management
Hypoglycaemia	Check CBG and give IV Glucose.
Opiate toxicity	Small pupils. Administer Naloxone. Remove opiate patches.
Stroke	CT head to confirm, protect airway, and initiate appropriate stroke care.
Post Seizure	ABC, recovery position, treat further seizures as status epilepticus if indicated.
Encephalitis/Meningitis	Administer Aciclovir and Cefotaxime. Obtain imaging and consider lumbar puncture if safe.
Carbon Monoxide	Measure COHb, provide 100% O₂, consider hyperbaric therapy.
Head Injury	Stabilize neck, obtain CT head and cervical spine.
Hyponatraemia	Consider hypertonic saline if Na < 115 mmol/L and seizures.
Sepsis	Administer IV broad-spectrum antibiotics.
Non-convulsive Status	Consider EEG and IV Lorazepam if non-convulsive status is suspected.
Subdural/Epidural Hematoma	Administer IV Mannitol, consult neurosurgery for decompression.
Cerebral Malaria	Consider in recent travel history; administer IV Quinine.

General Measures

Check CBG immediately; if uncertain, give glucose.
Establish IV access, obtain bloods, and perform a thorough physical assessment.
Check COHb levels if carbon monoxide exposure is suspected.
Perform top-to-toe examination, including removal of opiate patches.
Obtain CT head +/- neck imaging to rule out injuries or structural abnormalities.
Assess pupils for signs of herniation or toxic/metabolic causes:

Unilateral dilation suggests ipsilateral brain compression.
Small pupils suggest opioids; large pupils may indicate stimulants or severe intracranial pressure.

If CT is normal but diagnosis remains unclear, administer Naloxone, glucose, Cefotaxime, Aciclovir, and Pabrinex.
Consider EEG for non-convulsive status epilepticus.
If GCS < 9, intubation is needed to protect the airway. Consider HDU/ICU care.

Signs of Trauma

Inspection of the head may reveal signs of basilar skull fracture
Raccoon eyes—Periorbital ecchymoses.
Battle sign—Swelling and discoloration overlying the mastoid bone behind the ear
Haemotympanum—Blood behind the tympanic membrane.
Cerebrospinal fluid (CSF) rhinorrhea or otorrhea— Leakage of CSF from the nose or ear. CSF rhinorrhea must be distinguished from other causes of rhinorrhea, such as allergic rhinitis. Glucose concentration does not reliably distinguish CSF from nasal mucus, but beta-2 transferrin is unique to CSF, and its presence documents a CSF source of rhinorrhea.
Palpation of the head may demonstrate a depressed skull fracture or swelling of soft tissues at the site of trauma.

Pupils

Pupil Type	Description	Causes
Normal Pupils	Typically 3 to 4 mm in diameter (larger in children, smaller in the elderly), equal bilaterally, and constrict briskly and symmetrically in response to light. Reactive pupils in a comatose patient suggest a metabolic cause.	Normal physiology, metabolic disorders in comatose patients.
Thalamic Pupils	Slightly smaller (~2 mm) reactive pupils in the early stages of thalamic compression from mass lesions due to interruption of descending sympathetic pathways.	Thalamic compression from mass lesions.
Fixed, Dilated Pupils	Pupils greater than 7 mm in diameter and unreactive to light, caused by compression of the oculomotor (III) cranial nerve or sympathetic nerve fibers. Most commonly associated with transtentorial herniation of the medial temporal lobe.	Transtentorial herniation, anticholinergic or sympathomimetic drug intoxication, oculomotor nerve compression.
Fixed, Midsized Pupils	Pupils fixed at ~5 mm in diameter due to brainstem damage at the midbrain level, interrupting both sympathetic (pupillodilator) and parasympathetic (pupilloconstrictor) fibers.	Brainstem damage at the midbrain level.
Pinpoint Pupils	Pupils 1-1.5 mm in diameter, often unreactive to light except with magnification. Associated with opioid overdose, focal pontine lesions, organophosphate poisoning, miotic eye drops, or neurosyphilis.	Opioid overdose, pontine lesions, organophosphate poisoning, miotic eye drops, neurosyphilis (Argyll Robertson pupils).
Asymmetric Pupils	Pupillary asymmetry (anisocoria) with a diameter difference ≤1 mm is normal in 20% of the population. Pathologic anisocoria involves impaired constriction in response to light and may suggest structural lesions in the midbrain, oculomotor nerve, or eye.	Physiologic anisocoria, structural lesions affecting the midbrain, oculomotor nerve, or eye.

Pathophysiologic assessment of the Comatose patient.

Feature	Supratentorial Structural Lesion	Subtentorial Structural Lesion	Diffuse Encephalopathy/Meningitis
Pupil Size and Light Reaction	Usually normal size (3-4 mm) and reactive; large (≥7 mm) and unreactive with transtentorial herniation.	Midsized (about 5 mm) and unreactive with midbrain lesion; pinpoint (1-1.5 mm) and unreactive with pontine lesion.	Usually normal size (3-4 mm) and reactive; pinpoint (1-1.5 mm) and sometimes unreactive with opiates; large (≥7 mm) and unreactive with anticholinergics.
Reflex Eye Movements	Normal (gaze preference toward side of lesion may occur).	Impaired adduction with midbrain lesion; impaired adduction and abduction with pontine lesion.	Usually normal; impaired by sedative drugs or Wernicke encephalopathy.
Motor Responses	Usually asymmetric; may be symmetric after transtentorial herniation.	Asymmetric (unilateral lesion) or symmetric (bilateral lesion).	Usually symmetric; may rarely be asymmetric with hypoglycemia, hyperosmolar nonketotic hyperglycemia, or hepatic encephalopathy.

References

PLEASE NOTE LEGAL ADVICE: The contents are under continuing development and improvements and may contain errors of omission or fact. Feedback vital and always welcome at drokane at gmail.com. This is not to be used for the assessment, diagnosis or management of patients. It should not be regarded as medical advice. It is only for educational purposes. Please adhere to your local protocols. If you are unwell please seek healthcare advice from your doctor. This does not replace senior or specialist advice. If you do not accept this then please do not use the website. If you need medical advice, please consult a doctor or other appropriate medical professional. If you are a medical professional and you need advice then speak to your senior or colleagues.

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