Coma in a spinal patient
aka Neurological Mind-boggler 006
Remember the patient from Microbial Mystery 005? If not, make sure you read that post before this one!
Let’s recap:
A 20 year-old girl with a pre-existing spinal cord injury (C5 ASIA A) from an MVA at the age of 2, returns to ICU post-op following drainage of a large epidural abscess. She had presented with systemic sepsis 4 days previously and an MRI had demonstrated the epidural abscess. She has a long and complex medical history, including a sub-rectus sheath intrathecal baclofen pump inserted 2 years ago, several spinal fixation operations for spinal stability (the last 5 years ago), and chronic excoriation of both flanks from scratching.
The operation had gone smoothly, with the surgeons satisfied they had drained the collection. The anaesthetic had also been unremarkable and the patient had been awake and lucid in recovery.
After she had been in ICU for 15 minutes, you are called to see her, as her level of consciousness has suddenly decreased and her right pupil is much larger than the left….
Questions
Q1. What’s the differential for the decreased level of consciousness?
Answer and interpretation
There are many ways to break this down into a logical sieve. This is a modified version of the approach described by Bala Venkatesh in Oh’s Intensive Care Manual:
Differential Diagnosis of Coma
| Category | Specific Disorder | Clinical features | Key investigation |
|---|---|---|---|
| Focal signs | CVA: Ischemic; Haemorrhagic | Risk factors for CVA | CT |
| Trauma | Look signs of base-of-skull fracture | CT | |
| Space occupying lesion: Infective; Non-Infective | Look for ENT and dental sources of infection. Past history of cancer Immunosuppression | CT | |
| Meningism | Meningitis or menigoencephalitis | Fever; Meningococcal rash | LP; CT |
| Subarachnoid haemorrhage | ‘Worst headache ever’; Subhyaloid hemorrhages; SAH risk factors | LP; CT | |
| No focal signs or meningism(MESOT) | Metabolic causes: Hypoxia; Hypercapnoea; Hyponatraemia; Hyper/hypoglycaemia; Hypo/hyperthermia; Hypo/hyperosmolarity | History essential | SO2; ABG; ETCO2; UEC; BSL; Temp; ketones |
| Endocrine: Adrenal insufficiency; Hypopituitarism; Hypothyroidism; Diabetic coma | Time course; Steroid medications; Phenotype | TFT; Free T3/4; Temperature; BSL; UEC; Ca; PTH; Cortisol | |
| Seizures (including eclampsia) | ?witnessed ?post-ictal ?non-convulsive epilepsy | EEG; CT for SOL | |
| Organ Failure: Renal (uraemia); Liver (PSE) | Urine output; History/exam findings of liver disease; ?paracetamol OD | EUC; LFTs; NH3; INR | |
| Toxins/drugs: Sedatives; Narcotics; Alcohol; Psychotropics; Carbon monoxide; Many other poisons! | Toxicology risk assessment | ABG analysis; Specific drug levels; Osmolality; ECG | |
| Pseudocoma | history of mental illness; history of sleep disorder | Diagnosis of exclusion |
This, of course, is a very generic approach. Immediately post op, you can also think of causes as being:
- Related to the anaesthetic
- Related to the surgery
- Related to post-operative events
Q2. And differential for the asymmetrical pupils?
Answer and interpretation
As discussed in Ophthalmological Befuddler 001 there are two possible causes of anisocoria (unequal pupillary size)
- one pupil is abnormally small or constricted (miotic)
OR - one pupil is abnormally large or dilated (mydriatic)
Again, an approach modified from that of Bala Venkatesh in Oh’s Intensive Care Manual is shown:
| Pupil abnormality | Cause | Pathology |
|---|---|---|
| Miosis (<2mm) | ||
| Unilateral | Horner Syndrome; Local pathology/ trauma | Sympathetic paralysis; Damage to sympathetics |
| Bilateral | Pontine lesion; Thalamic haemorrhage; Metabolic encephalopathy; Senile miosis; Argyll Robertson pupils; Holmes-Adie pupil; Drugs (Organophosphate; Barbituate; narcpotics) | Sympathetic paralysis. Mechanisms: Cholinesterase inhibition; Central effects |
| Mydriasis (>5mm) | ||
| Unilateral | Uncal herniation; Midbrain lesion | CN3 stretched on petroclinoid ligament; CN3 nucleus damage |
| Bilateral fixed pupils | Bilat uncal herniation; Massive midbrain bleed; Hypoxic injury; Drugs (Atropine, TCA, Sympathomimetics) | Brain herniation; Bilateral CN3 damage; Mesencephalic damage. Mechanism (Parasympathetic paralysis, TCA’s pevent reuptake of catecholamines by nerve endings, Sympathetic stimulation) |
For further review read Neurological Mind-boggler 002 on the causes of coma with small pupils, and Ophthalmological Befuddler 001 for the causes of a dilated pupil.
Q3. What investigations would you do now?
Answer and interpretation
In addition to a close review of what happened in the operating theatre and recovery, the following investigations may help:
- ABG including glucose and lactate
- Blood tests (see Q2 above)
- CT brain +/- MRI brain +/- spine
- EEG
All of the investigations listed in Q2 were done — they were all unremarkable!
Q4. So what’s the explanation?
Answer and interpretation
The currently held belief is that as the epidural abscess was drained, canal compression was released and CSF flow was altered. A bolus of intrathecal baclofen (from the pump, which had always been running) then reached the brain in high concentration, and caused coma.
The anisocoria was also attributed to the baclofen overdose, although this usually causes bilateral pupillary dilation. It is difficult to explain why only one pupil was affected — perhaps there was a degree of post-operative Horner’s syndrome affecting the side of the ‘small’ pupil?
With supportive treatment complete neurological recovery occurred over the next 48 hours.
Read Wall et al (2006) for an open access case report of a baclofen overdose in a different context, with a literature review.
Over the next week, fevers and raised inflammatory markers persisted.
Q5. What could explain this and what would you do?
Answer and interpretation
Is antimicrobial chemotherapy inadequate?
- check that current antibiotic dosing is adequate for the MIC of cultured organism
- re-culture everything, empirically broaden cover and narrow when you get a new organism
Is there an ongoing source of sepsis?
- Was all the abscess drained? Re-drain & washout.
- Is the metal work infected? Remove it if suspected and its possible.
- Is the baclofen pump infected? Remove it!
- Look for ventilator associated pneumonia (VAP): CXR, blind tracheal aspirate & non-quantitative culture — see Canadian Clinical Trials Group (2006).
- Look for endocarditis (TTE +/- TOE depending on the TTE result)
- Look for collections elsewhere
What happened next?
Case Outcome
Antibiotic cover was increased to vancomycin & meropenem. An echocardiogram showed no vegetations. A further MRI showed evidence of remaining collection. In OT, the internal fixation was removed, the intrathecal baclofen pump was removed and the abscess drained. The only organism isolated was the MSSA and long term (at least 6 weeks) IV benzyl penicillin was all that was needed. The MSSA presumably came from her scratched skin and seeded to her metal rods/epidural space.
Of course, other complications occurred but I won’t bore you with them!
References
- Canadian Critical Care Trials Group. A randomized trial of diagnostic techniques for ventilator-associated pneumonia. N Engl J Med. 2006 Dec 21;355(25):2619-30. PMID: 17182987.
- Wall GC, Wasiak A, Hicklin GA. An initially unsuspected case of baclofen overdose. Am J Crit Care. 2006 Nov;15(6):611-3. PMID: 17053268. [free fulltext]
CLINICAL CASES
Neurological Mind-boggler
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of three amazing children.
On Twitter, he is @precordialthump.
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