Dr Gerrard Marmor
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Dr Gerrard Marmor
Coma – Topics to Discuss
DefinitionPathophysiologyAn approach to the comatose ED patient
Special testsOutcomes
Definition of “Coma”From the Greek word “Koma” meaning “Deep sleep”1
What constitutes “Coma”?Four Features:1. Absence of alertness & awareness (unconsciousness)
2. Absence of voluntary response to external stimuli3. Absence of normal sleep-wake cycle. (ie. The patient isn’t just sleeping)
4. The condition is due to a pathological process.• A syndrome caused by many underlying pathologies. • The underlying diagnosis will dictate the patient’s
prognosis.
Patho-Physiology of Coma
Alertness is dependent on the Reticular Activating Centre (R.A.S) in the Midbrain and dorsal Pons2.
Awareness is generated by neuronal pathways between the R.A.S, the thalamus and multiple higher cortical centres bilaterally
Coma results from dysfunction along this pathway –Brainstem (R.A.S) – thalamus – Bilateral cerebral cortex
Isolated unilateral cortical lesions do not cause coma
Differential Diagnosis in ComaBrain mass
Anoxic-hypoxic brain disease with return of spontaneous circulation after cardiac arrestRaised intracranial pressure
Subdural or epidural haematomaIntracerebral haemorrhageAcute ischaemic stroke
HydrocephalusCerebral oedema resulting from stroke, Cerebellar oedema resulting from stroke
Cerebral venous sinus thrombosisSepsis
CNS infectionsNon-convulsive or minimally convulsive status epilepticus
HypoglycaemiaHyperglycaemia, diabetic or alcoholic ketoacidosis
HyponatraemiaHypercalcaemiaHyperammonaemiaRenal failure
Hepatic encephalopathyThyroid storm
Myxoedema comaAdrenal crisis
Pituitary apoplexyWernicke’s encephalopathySedative hypnotic agents
OpioidsMDMAInhalants
Toxic alcoholsHistotoxic agents causing hypoxia
Carbon monoxideMethaemoglobinaemiaPsychiatric medicationsAntiepileptic drugs
ClonidineHerbicidesIsoniazidSalicylates
Simple asphyxiantsNeuroleptic malignant syndrome
Serotonin syndromeTaken from: Table 1 - Reversible causes of Coma
(Reference 1 )
Approaches to Diagnosis in Coma
Importance of a structured approach to Coma.Four Categories & questions to ask:1. Traumatic or Non - Traumatic Coma (N.T.C)?2. Are there focal or lateralising signs?– Implies structural CNS disease
3. Is there meningism? (without focal/lateralising signs)4. Coma without focal / lateralising signs or meningism?– Implies diffuse neuronal dysfunction
Adapted from Life in the fast Lane by Dr Chris Nickson 3
1. Trauma versus Non - Traumatic Coma (N.T.C)
Traumatic cause of coma narrows the possible causes:
Airway & Breathing: Hypoxia
Circulation: Haemorrhagic shock / hypovolaemia
Direct CNS injury: Cortical or Brainstem injury
Exposure – Hypothermia, Hyperthermia
v Consider the possibility of both traumatic and non-traumatic causes occurring concurrently- ie. Overdose and fall, - Blast injury & C.O inhalation
2. Are there focal or lateralising signs? Implies structural CNS disease: Cerebro-vascular disease – ischaemic, haemorrhagic Space occupying lesion - infective, non-infective
3. Is there Meningism without focal/lateralising signs? Meningo-encephalitis Subarachnoid haemorrhage
4. Coma Without focal/lateralising signs or meningism
Implies diffuse neuronal dysfunction:S – Seizures – Non-convulsive status epilepticusT – Toxins – Drugs, exposures, envenomationsO – Organ failure – Uraemia, Hepatic, Shock (sepsis)P – Pseudocoma – Locked-in syndrome, Psychiatric (ie.
catatonia)
M – Metabolic – Thermal, pH, electrolytes (incl. glucose), osmolality, nutritional
E – Endocrine – thyroid, adrenal, pituitary apoplexy
Importance of Clinical Assessment
A good collateral History will give key clues Focused examination:
In trauma identify non-traumatic factors Identify stigmata of disease (mixoedema coma) Identify toxidromes Clues to unusual diagnoses – envenomations, methaemoglobinaemia
Bedside tests Blood gas – pH, Anion gap, Co-oximetry
Quiz
Question 1.In an intracranial haemorrhage, how often is a dilated pupil contra-lateral to the lesion? (ie. a ‘falsely localising sign’)
Answer: At most 10% of cases4.
Question 2.Can unequal pupils in an awake person be a sign of raised intracranial pressure?
Answer:If the patient is alert, GCS 15 then no. However, In the patient without a completely normal level of alertness, early abnormalities in pupil size may herald impending deterioration*
* Personal Discussion with a senior neurosurgical colleague
“Routine” Investigations in Coma
Reveals the cause in a majority of cases.
Bedside Tests Blood Glucose Level Blood Gas including co-oximetry ECG Urine Analysis +/- BHCG – may be useful
28 y.o. Female - unconsciousNo focal signs, no meningism, Temperature 37.9˚c pH: 7.43 pCO2: 20 mmHg pO2: 105 mmHg Na2+: 137 mmol/L K+: 4.7 mmol/L Cl-: 107 HCO3: 13 mmol/L Gluc: 4.5 mmol/L calc Hb: 13 g/L Normal renal function Normal LFT’s
What are likely diagnosis?
32 y.o. Male - unconscious
What are some likely diagnoses?ECG source: http://cdn.lifeinthefastlane.com/wp-content/uploads/2011/08/quetiapine-od1.jpg
Question 3.A victim from a fire at a local gold mine is brought in to department.Examination reveals:HR 130 bpm, BP 90/50 mmHg, SaO2 92%, RR 26Unresponsive, PEARL, No focal signs, no meningismNo external burns or trauma is identifiedBlood Gas: Lactate of 15 mmol/L, COHb of 8%. What is a likely cause of their altered consciousness?
Answer:Cyanide toxicity
Laboratory Investigations Provides a baseline Identify metabolic, infective and endocrine causes of coma.
Facilitate further investigations & treatment ie. Coagulation: pre - L.P or pre - operative
Avoid a ‘shot-gun’ approach. Random investigation will be low yield
Routine ImagingNon – Contrast CT Head Indications:1. Traumatic Coma2. Non-traumatic Coma with focal / lateralising signs
3. Coma with meningism4. Coma with diffuse neurological dysfunction where a cause is not found in the initial assessment (ie. opioid O.D, hypoglycaemia)
Six Pathologies to Identify on Non-contrast CT Brain in Coma
1. Intra-cerebral haemorrhage - Acute +/- chronic
2. Space – occupying lesion- Infective or non - infective
3. Thalamic hypodensities - can be subtle
4. Hydrocephalus (acute)
5. Loss of Basal Cisterns
6. Basilar Artery Thrombus
Special Investigations
“Special” investigations should be considered in the cause is not identified following initial work-up.
Further investigations should be focused by the historical and physical findings.
Questions to ask after a negative initial assessment
1. Is vascular imaging or MRI indicated?
2. Is an L.P, antibiotics and antivirals indicated?
3. Could the cause be due to a toxin which has an antidote?
4. Is an EEG indicated?
5. Could this be an endocrinopathy requiring hormonal treatment?
Vascular Imaging and MRIDifferential Diagnoses being considered: Posterior Circulation Stroke – Basilar artery
Sub-acute headache, disconjugate gaze, hallucinations Ischaemic Stroke – Thalamic, Brainstem Venous Sinus Thrombosis
Headache, visual disturbance, hormones Posterior Reversible Encephalopathy Syndrome (PRES) Headache, hypertension, seizure, visual disturbance, immunosupression
Pituitary Apoplexy Peri-partum, visual disturbance
Lumbar Puncture & Anti-infectives To L.P or not? Blood cultures prior to Antibiotics (50 – 70% positive5) and antivirals.
CT scan prior to exclude S.O.L, Severe cerebral oedema or hydrocephalus
Platelets & Coagulation if septic - exclude D.I.C
Send CSF for viral PCR – HSV most common.5
Don’t forget to measure opening pressure. Immunosupressed at risk for infective cause.
Toxins: Drugs, Exposures, Envenomations6
Often there is a clinical clue Revisit the history and re-examine
Toxicities that cause coma and have specific treatments include: Opiates Carbamazepine, Valproate & Barbituates Salicylates, Toxic Alcohols, Isoniazid
Always consider paracetamol ingestion. Commence N.A.C if levels come back positive. Massive ingestion can cause coma
Consider envenomation in appropriate settings ‘Coma’ secondary to unresponsiveness. May be aware
Quiz
What biochemical findings are associated with Sodium Valproate toxicity?6
HAGMA (lactic acidosis) Hypernatraemia Hypoglycaemia Hypocalcaemia Hyperammonaemia Multi-organ failure
Which Australian creatures can cause presentations with coma/ pseudocoma?
Tick (Ixodes sp.) Blue – Ringed Octopus (Don’t forget P.I.B) Taipan (V.I.C.C, rapid onset paralysis) Tiger Snake (V.I.C.C, slower onset of paralysis) Death Adder (isolated paralysis) Sea Snake (scuba divers) Funnel – Web Spider (autonomic storm)
Indications for an E.E.G5
Low yield without features suggestive of status epilepticus:
Presentation with prolonged seizure Examination findings of nystagmus - like eye movements, myoclonic jerks, staring into space, lip smacking, chewing and blinking.
Pre-existing seizure disorder Failure to waken after initial pathology treated. (ie. hypoxic arrest, meningo-encephalitis, etc.)
Endocrine Causes of Coma Thyroid Storm and Hypothyroidism can both present with coma. Clinical picture can be confused with sepsis or environmental illness
Sepsis may be the precipitant
Addisonian Crisis Shock, hypoglycaemia, hypothermia, decreased conscious state
History of chronic corticosteroid use or anticoagulation are important (bilateral adrenal haemorrhage)
Spot serum cortisol and trial of therapy
Wernickes Encephalopathy Chronic alcohol abuse Malnourishment Hyperemesis gravidarum Bariatric surgery Malignancy Trial of high dose intra-venous thiamine
Pituitary Apoplexy Peri-partum , pre-eclampsia are risk factors Pre-existing pituitary tumour Easily missed if not specifically looked for.
Outcomes of Coma Horsting et al. (2015)7 attempted to describe the prevalence and outcomes of different causes of non-traumatic coma internationally. 14 studies – Too heterogeneous to give useful figures
Forsberg et al. (2012)8 studied 875 Swedish patients presenting to ED’s in Stockholm 27.7% were found to have a Structural cause 72.35% were found to have a Metabolic cause
Forsberg et Al 2012 - Reference 9
Key Points Assessment of Coma requires a structured approach
Detailed History and Examination gives important clues
Four Categories:Traumatic;; Focal signs;; Meningism;; No Focal signs
• If no focal or lateralising signs use STOPME acronym Seizure Toxins Organ Failures Pseudocoma Metabolic Endocrine
Non-Contrast CT findings to look for:1. Haemorrhage
2. S.O.L
3. Thalamic hypodensities
4. Basal Cisterns
5. Hydrocephalus
6. Basilar artery thrombus
If normal initial work-up then focus further investigations.
Consider: Vascular imaging, MRI Lumbar Puncture +/- anti-infectives Toxins requiring specific treatments Don’t forget paracetamol levels
EEG monitoring Endocrine causes
References1. Search: “Coma Origin”. Online Etymology Dictionary. http://www.etymonline.com, Retrieved 14
August 2015.2. Edlow, JA et al. Diagnosis of reversible causes of coma, Lancet, Vol.384:9959, 6–12 Dec. 2014,
pgs.2064–20763. Nickson, C, Life in the Fast Lane Resources: “Coma”, http://lifeinthefastlane.com/resources/coma-ddx,
Accessed 8th October 20154. Marshman LA, Polkey CE, Penney CC. Unilateral fixed dilation of the pupil as a false-localizing sign
with intracranial haemorrhage: case report and literature review. Neurosurgery 2001;; 49: 1251–55.5. Brouwer MC, Thwaites GE, Tunkel AR, van de Beek D. Dilemmas in the diagnosis of acute
community-acquired bacterial meningitis. Lancet 2012;; 380: 1684–92.6. Murray L et al. Toxicology Handbook, 2nd Edition, Churchill Livingstone. 2011. Chapters 2, 3 & 5.7. Horsting et al. The etiology and outcome of non-traumatic coma in critical care: a systematic review,
BMC Anesthesiology. 2015, 15:65 Accessed online 13th October 20158. Forsberg S, Hojer J, Ludwigs U, Nystrom H. Metabolic vs structural coma in the ED - An observational
study. Am J Emerg Med. 2012;;30(9):1986–90.9. Forsberg S, Hojer J, Ludwigs U. Prognosis in patients presenting with nontraumatic coma. J Emerg
Med. 2012;;42(3):249–53.• Image 1 (Slide 5) sourced from: https://teddybrain.files.wordpress.com/2013/08/20130829-022503.jpg
8th October 2015• Image 2 (Slide 20) “Bilateral subdural haematomas” sourced from: Edlow, JA et al. Diagnosis of
reversible causes of coma, Lancet, Vol.384:9959, 6–12 Dec. 2014, pgs.2064–2076• Image 3 (Slide 21) “medulloblastoma” sourced from:
http://www.neuroradiologycases.com/2011_08_01_archive.html. 13th October 2015• Image 4 (Slide 22) “Bilateral thalamic infarction” sourced from: http://radiopaedia.org/cases/bilateral-
thalamic-infarcts. 13th October 2015• Image 5 (Slide 23) “ Acute hydrocephalus due to obstruction of 3rd ventricle by a meningioma” sourced
from: http://radiopaedia.org/cases/acute-hydrocephalus-secondary-to-meningioma-1 .13th October 2015
• Images 6 & 7 (Slide 24) “Normal basilar cisterns. & Cerebral oedema”. Sourced from: http://www.ferne.org/JoshuaBroder/news100106.htm. 13th October 2015
• Image 8 (Slide 25) “ Basilar artery thrombus”. Sourced from: Edlow, JA et al. Diagnosis of reversible causes of coma, Lancet, Vol.384:9959, 6–12 Dec. 2014, pgs.2064–2076
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