Printable list of all neurology and neurosurgery SAQs

College Answer

Hiccoughs may be due to

-     Irritation of diaphragm (subphrenic abscess, cholecystitis, pneumonia, pericarditis)

-     Irritation of stomach wall (distension, ulcer, ileus)

-     Phrenic nerve stimulation /irritation (neoplasm, goitre)

-     Brainstem lesion (neoplasm, ischaemia, surgery)

-     Metabolic (uraemia)

Management is often unsatisfactory:

-      diagnosis and treatment of underlying cause (NG tube, drain subphrenic )

-     many medications have been used, indicative of their poor efficacy (eg chlorpromazine, metaclopramide, haloperidol,  phenytoin, carbamazapine)

-     physical stimulation of posterior pharynx by NG tube may interrupt the reflex arc

In the event of persistent, fatiguing hiccoughs phrenic nerve block has been tried.

Discussion

Never since this question have "hiccoughs" been asked about in the ICU fellowship paper. However, one must answer these things.

A hiccup, or singultus, or synchronous diaphragmatic flutter, is a myoclonic spasm of the diaphragm, which is stimulated by the prehinc nerve. The signal to hiccup is sent from the nucleus tractus solitarius. This signal can be stimulated by a number of pathological conditions. A brief review lays these bare:

• Foeign body in the external auditory canal
• Medullary lesions (especially PICA artery)
• Medullary demyelination
• Spinal syrinx
• Encephalitis
• Meningitis
• Gastro-esophageal reflux
• Gastric distension
• Pancreatitis
• Thoracic aortic aneurysm
• Mediastinal tumours
• Pleural and pericardial effusion
• Uremia
• Hypocalcemia
• Hyponatremia
• Methyldopa

The review article remarks that "The more than 100 forms of physical or pharmacological treatment for intractable hiccups include prayers to St Jude, the patron saint of lost causes". As reliable remedies, the author recommends to raise the PaCO₂ and to vigorously stimulate the posterior pharynx. Apparently, chlorpromazine remains the most consistently effective agent. Other lesser known solutions are discussed elsewhere.

Kolodzik, Paul W., and Mark A. Filers. "Hiccups (singultus): review and approach to management." Annals of emergency medicine 20.5 (1991): 565-573.

Howard, Robin S. "Persistent hiccups." BMJ: British Medical Journal 305.6864 (1992): 1237.

College Answer

This is not an uncommon question in long-stay ICU patients. Is eating possible? The two parts to be covered are:

(a)        How does a tracheostomy interfere with swallowing?

Normal swallowing requires timing and coordination of many muscles and several cranial nerves, which are under voluntary and involuntary nervous control. The phases are; (1) oral preparatory –mastication and creation of a bolus, (2) oral transit –delivering the bolus to the back of the tongue, soft palate is elevated to allow passage, (3) pharyngeal – is most complex with pharyngeal constriction to create a dynamic pressure gradient, breath-holding, elevation of  arytenoids,  cord  adduction  and  epiglottic  inversion,  (4)  oesophageal  stage  –with coordinated  contraction  and  relaxation  of  oesophageal  sphincters  and  peristaltic  waves carrying the bolus.

A list of therefore could have included: Placement of a tracheostomy -

-           impedes laryngeal elevation

-           impairs hypopharyngeal and laryngeal sensation by desensitisation

-           leads to disuse atrophy of laryngeal and pharyngeal muscles

-           impairs glottic reflex closure

-           reduces subglottic pressure

 (b)      How will you assess her ability to swallow safely?

A tracheostomy cuff does not guarantee prevention of aspiration. Assessment is best achieved by:

- assessment of (1) general condition and (2) specific ability to handle a test swallow.

A breathless and weak patient, who is unwell with sepsis etc., is unable to coordinate swallowing.

- motor movements of the lips face tongue jaw and palate are evaluated for strength, symmetry, speed, accuracy and range of motion for specific nerve deficits. Elevation of the larynx with attempted swallowing should be observed. Strength of cough and timing and fullness of laryngeal excursion give clues to general laryngeal protection.

-test of swallowing and airway protection: this is commonly performed with blue dye mixed with a variety of food consistencies. A bolus of thick liquid is more easily maintained in a bolus and more safely swallowed. After swallowing the tracheostomy is suctioned at intervals to detect leak of dye into the airway. Unfortunately, false negative tests are common (confirmed by video fluoroscopic imaging) so vigilance should be maintained even if the test is passed.

Discussion

A good paper from 1971 discusses this question in some detail.

In summary, the swallowing defects due to tracheostomy are as follows:

• It prevents the larynx from elevating normally
  • thus, hypopharyngeal sphincter fails to open
  • thus, food spills into the larynx
• It desensitises the sensation of the larynx, preventing normal cough in response to aspiration. The effect is likened to stroke-related bulbar dysfunction
• Long periods of being NG-fed result in the deconditioning of muscles involved in swallowing

Assessment of swallowing is a fine art. See this detailed proforma to help speech pathologists. Others are even more extensive.

To summarise,

• Physical assessment:
  • intact cough reflex
  • intact gag reflex
  • adequate laryngeal elevation
  • absence of obvious cranial nerve signs
• Investigations
  • videolaryngoscopy
• Test swallow
  • blue food dye in the swallow
  • sequential tracheal aspirates to demonstrate that no blue dye is in the lung
  • alternatively, barium swallow
• The gold standard is a videofluoroscopic swallowing study, AKA the modified barium swallow.

LITFL have a good page on this (they have a good page on everything).

Bonanno, P. C. "Swallowing dysfunction after tracheostomy." Annals of surgery174.1 (1971): 29.

Mann, Giselle. MASA, the mann assessment of swallowing ability. Vol. 1. Cengage Learning, 2002.

Goldsmith, Tessa. "Evaluation and treatment of swallowing disorders following endotracheal intubation and tracheostomy." International anesthesiology clinics38.3 (2000): 219-242.

Prigent, Hélène, et al. "Effect of a tracheostomy speaking valve on breathing–swallowing interaction." Intensive care medicine 38.1 (2012): 85-90.

Macht, Madison, et al. "ICU-Acquired Swallowing Disorders." Critical care medicine 41.10 (2013): 2396-2405.

College Answer

Hypertonic Saline has theoretical advantages in the initial resuscitation of head injured patients because smaller volumes of fluid are required and blood pressure restoration is more effective. Brain oedema may be decreased to lower ICP and CPP may be increased. Post resuscitation use is less clear. In this setting, reduction in intracranial hypertension is due to improved systemic and cerebral haemodynamics and modulation of vasospasm. Adverse effects include renal impairment, rebound ICP rise and osmotic myelinolysis. Trials are continuing and a well defined role is not apparent as yet.

Mannitol has a long history of use in the management of head injuries. It lowers ICP initially by increasing CBF and producing a compensatory vasoconstriction. An osmotic effect and diuresis produce delayed fall in ICP. Efficacy would be dependent initially on the presence of adequate brain with intact autoregulation. Prolonged use may lead to leak into damaged brain with concomitant increase in ICP and swelling. The accepted role is in the urgent lowering of ICP before definitive therapy (eg. evacuate haematoma or perform decompression craniectomy). Chronic use is not supported by evidence.

Discussion

Another question is very similar- Question 4 from the first paper of 2007. It asks one to discuss hypertonic saline, which of course is impossible without discussing mannitol.

In brief:

aised intracranial pressure falls within the realm of osmotherapy, which enjoys a thorough discussion elsewhere:

• Intracranial pressure as a therapeutic target
• Management of raised intracranial pressure
• Osmotherapy for management of raised intracranial pressure

From those summary, a table of comparison can be compiled, which is presented below.

Oh's Intensive Care manual:

Chapter 43 (pp. 563) Cerebral protection by Victoria Heaviside and Michelle Hayes, and

Chapter 67 (pp. 765) Severe head injury by John A Myburgh.

Francony, Gilles, et al. "Equimolar doses of mannitol and hypertonic saline in the treatment of increased intracranial pressure*." Critical care medicine 36.3 (2008): 795-800.

Kamel, Hooman, et al. "Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: A meta-analysis of randomized clinical trials*."Critical care medicine 39.3 (2011): 554-559.

Nau, Roland. "Osmotherapy for elevated intracranial pressure." Clinical pharmacokinetics 38.1 (2000): 23-40.

Rickard, A. C., et al. "Salt or sugar for your injured brain? A meta-analysis of randomised controlled trials of mannitol versus hypertonic sodium solutions to manage raised intracranial pressure in traumatic brain injury." Emergency Medicine Journal (2013).

Lazaridis, Christos, et al. "High-Osmolarity Saline in Neurocritical Care: Systematic Review and Meta-Analysis*." Critical care medicine 41.5 (2013): 1353-1360.

Bhardwaj, Anish, and John A. Ulatowski. "Hypertonic saline solutions in brain injury." Current opinion in critical care 10.2 (2004): 126-131.

Arbabi, Saman, et al. "Hypertonic saline induces prostacyclin production via extracellular signal-regulated kinase (ERK) activation." Journal of Surgical Research 83.2 (1999): 141-146.

R LAWRENCE REED, I. I., et al. "Hypertonic saline alters plasma clotting times and platelet aggregation." Journal of Trauma-Injury, Infection, and Critical Care 31.1 (1991): 8-14.

College Answer

Management priorities will be determined by the exact clinical scenario, though the general principles are consistent. Consider recommendations (eg. Brain Trauma Foundation).
•    Ensure simple reversible causes are not present (elevate head, maintain head in central position with no venous occluding tapes, adequate sedation, treatment of seizures, adequate volume status, adequate oxygenation, arterial carbon dioxide not elevated).
•    Consider exclusion of reversible mass lesion (CT or repeat CT).
•    Drain CSF from ventricle (if drain in situ).

Further techniques that could be considered at this point include: further decrease in arterial carbon dioxide (to 30-35 mmHg), mannitol (keeping euvolaemic and osmolarity < 320 mOsm/L), additional sedation (including barbiturates) ± paralysis (decrease straining against ETT/ventilation), hypertonic saline, induced hypothermia, decompressive craniectomy, (? hypertensive therapy, further hyperventilation).

Discussion

This question closely resembles Question 12 from the first paper of 2004.

Stereotypical steps in ICP management:

• Position the head (45 °head up, facing straight)
• Loosen the ETT ties
• Remove the C-spine collar
• Decrease PEEP as much as possible
• Increase sedation
  • Propofol sedation to decrease distress and thus decrease ICP
  • Benzodiazepines may be of use (but they do not decrease the CMRO₂ as much as propofol)
• Drain some CSF from the EVD
• Paralysis with neuromuscular junction blocker
• Osmotherapy
  • Mannitol 20%
  • Hypertonic saline
• Super-refractory ICP
  • Hypothermia
  • THAM
  • Dihydroergotamine
• Controversial measures
  • Barbiturate coma if other methods of lowering ICP have failed
  • Decompressive craniectomy

College

•    Potential causes include: prolonged effects of sedative drugs, metabolic encephalopathy (especially renal or hepatic failure), endocrine problems (especially hypothyroidism), systemic sepsis, and a myriad of specific neurological problems (eg. status epilepticus, raised intracranial pressure, intracranial haemorrhages, severe Guillain Barre, critical illness polyneuropathy). Residual muscular paralysis must be excluded.
•    Sedative drugs may have a prolonged effect because of altered kinetics (including context sensitive half-time, or decreased biotransformation or excretion eg. renal or hepatic failure) or altered dynamics (potentiation of effect by other drugs or organ failure, sensitivity to effect of usual dosage).
Assessment of contributory factors may be a complex process. Important steps include:
•    Detailed history of neurological state, drugs administered, previous neurological problems
•    Careful examination (in particular neurological, but also for signs of other chronic diseases).
Detailed neurological exam should include global CNS assessment (including ability to move eyes or poke out tongue if no other apparent motor responses: locked in syndrome, severe myoneuropathy), and search for focal signs (pupils, tone, movement, reflexes). Nerve stimulator should be used to assess residual paralysis.
•    Biochemical investigations for severity of electrolyte imbalance, creatine kinase, renal and hepatic dysfunction (including ammonia), and to exclude treatable endocrine disorders (including T4/TSH).
•    Consider use of specific reversal agents (eg. naloxone and flumazenil [may need multiple ampoules]).
•    May require other specific investigations (but put into context, and not done as a routine).
Such investigations include CT scan of head, MRI, EEG, EMG and lumbar puncture.

Discussion

List the potential  causes of delayed awakening? There could be thousands.

A tabulated answer is called for.

Thus, investigations should consist of:

• Biochemistry:
  • BSL, EUC, CMP, LFT, TFT and random cortisol
• Samples:
  • Blood cultures
  • CSF analysis
• Imaging:
  • CT brain pre and post-contrast
  • CTA
  • MRI / MRA
• Functional studies:
  • EEG
  • Routine monitoring obs of BP and SaO₂

Management would obviously be directed at the possible causes.

College Answer

Horner’s Syndrome is due to damage to the cervical sympathetic pathway, and exhibits a smaller pupil , a variable degree of ptosis and anhydrosis [impaired sweating over variable area] ± bloodshot eye [loss of vasoconstrictor].   The presence of enophthalmos is controversial.   Likely causes include common lesions along the path of the sympathetic pathway: including from brainstem (CVA) and cervical cord lesions (including trauma and local anaesthetic eg. epidural), through T1 root lesions (malignant disease eg. Pancoast syndrome; traction injuries to arm or aneurysms of aortic arch or subclavian artery), along the chain in the neck (malignancy, neck surgery, carotid artery dissection).   Transient Horner’s can occur with cluster headaches and with migraine. Many cases have no demonstrable cause.

Discussion

Features of Horner's Syndrome:

• Ptosis
• Miosis
• Anhidrosis of the forehead
• Enophthalmos

College Answer

Profound weakness in the critically ill can be as a result of a number of different pathophysiologic mechanisms.     Residual  paralysis  should  be  considered  and  excluded  by  nerve  stimulator examination   (minimal   response   to   train   of   four;   post-tetanic  facilitation,   possibly  some improvement with reversal of blockade).  Residual sedation should also be considered, but once aroused, patient should be able to demonstrate more appropriate strength (and/or response to antidotes: e.g. naloxone, flumazenil).  Critical illness polyneuropathy presents after a week or so of critical illness, typically with limb weakness and atrophy, reduced deep tendon reflexes, loss of peripheral sensation to touch and pin prick, but relative preservation of cranial nerve function. Electrophysiological studies reveal motor and  sensory axonal neuropathy, and  biopsies reveal axonal degeneration and denervation atrophy of muscles.   An acute myopathy (especially in association with neuromuscular blockade and corticosteroids) may present with similar motor findings  but  with  no  sensory  abnormalities.  Creatine  kinase  should  be  elevated. Electrophysiological testing is consistent with a myopathy, and muscle biopsy reveals loss of thick filaments. Spinal cord lesions should be associated with a sensory level and hyperreflexia.  Cranial nerve abnormalities suggest brain-stem problems or Guillain-Barre syndrome.

Discussion

The topic of weakness comes up frequently in these exams.

A generic approach to the patient with generalised weakness in the ICU is discussed elsewhere.

In short:

• Exclude sedation and paralysis
• Gather a history to exclude an existing illness which might be contributing
• Perform a physical examination looking for characteristic signs

The following tests and imaging studies could be useful:

• Electrolyte levels
• CK level
• B12 level
• Acetylcholine receptor antibodies (for myasthenia gravis)
• CXR looking for malignancy (as support for a diagnosis of Eaton-Lambert syndrome)
• Inflammatory markers
• Lumbar puncture
• Nerve conduction studies
• Electromyography
• MRI of the brainstem and spine
• Muscle biopsy if no satisfactory explanation is found.

Oh's Intensive Care manual:

Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer

Chapter   57   (pp. 617)  Neuromuscular  diseases  in  intensive  care by George  Skowronski  and  Manoj  K  Saxena

Yuki, Nobuhiro, and Hans-Peter Hartung. "Guillain–Barré syndrome." New England Journal of Medicine 366.24 (2012): 2294-2304.

Jani, Charu. "Critical Illness Neuropathy." Medicine (2011): 237.

Young, G. Bryan, and Robert R. Hammond. "A stronger approach to weakness in the intensive care unit." Critical care 8.6 (2004): 416.

Mareska, Michael, and Laurie Gutmann. "Lambert-Eaton myasthenic syndrome." Seminars in neurology. Vol. 24. No. 2. [New York]: Thieme-Stratton Inc.,[c1981-, 2004.

Reeves and Swenson have an excellent online textbook chapter (12) entitled "Evaluation of the Patient with Weakness"

College Answer

Raised intracranial pressure (usually considered > 20 to 25 mmHg) in the setting of severe closed head injury is a relatively frequent phenomenon. The causes usually dictate the specific therapy. specific causes to be considered included artefact, transient elevations associated with coughing/valsalva manoeuvres, , increased brain parenchymal volume (ie. cerebral oedema), increased cerebral blood volume (especially haematomata), increased CSF volume (especially decreased drainage). The likelihood of each is related to the individual circumstances, and relative timing with respect to the injury itself.

Principles of management depend upon what techniques/interventions have already been instituted, but include: provision of adequate oxygenation, ventilation (usually mechanical, aiming for normocapnia if normal bicarbonate [situation less clear if abnormal bicarbonate]) and circulation (adequate CPP [usually considered > 70 mmHg] with euvolaemia and/or use of vasopressors); elevation of head and neck, and ensuring that there is no obstruction to venous drainage; if not already done, establishment of invasive monitoring (to confirm diagnosis and allow titration of therapy); exclusion of artefactual error (zeroing, levelling and calibration as able); minimisation of coughing/valsalva and reduction of metabolic demand with sedation and/or paralysis; drainage of CSF via ventricular drain (if available); detection and drainage of intracerebral haematomata; correction of hyponatraemia (administration of hypertonic saline may provide some short term control); techniques to decrease metabolic demand include anti-seizure treatment/prophylaxis, and temperature control at least to normothermic levels (induced hypothermia is controversial, but seems to decrease ICP in refractory cases); osmotherapy using mannitol may be useful in refractory cases or when buying time before definitive surgery (keeping osmolality < 320 mOsm/kg); other techniques for refractory cases include barbiturate coma, decompressive craniectomy, and possibly hyperventilation (for short term use only).

Discussion

This was a broad question, about a familiar topic, and could be answered with gusto. A detailed examination of  management of raised intracranial pressure  is available elsewhere.

Causes:

• Increase in the volume of CSF (eg. hydrocephalus)
• Increase in the volume of the brain parenchyma (eg. cerebral oedema)
• Increase in the volume of intracranial blood (eg. haemorrhage or decreased venous drainage)
• Foreign material inside the skull (eg. tumour or abscess).

Methods of management: I will not digress extensively about these;

In summary:

• Draining the EVD
• Positioning the head
• Removing the C-spine collar
• Sedation
  • Propofol sedation to decrease distress and thus decrease ICP
  • Barbiturate coma if other methods of lowering ICP have failed
• Paralysis
• Osmotherapy
• Controversial measures
  • Decompressive craniectomy
  • Hypothermia
  • Dexamethasone

Oh's Intensive Care manual:

Chapter 43 (pp. 563) Cerebral protection by Victoria Heaviside and Michelle Hayes, and

Chapter 67 (pp. 765) Severe head injury by John A Myburgh.

Brain Trauma Organisation Guidelines for Management Traumatic Brain Injury.

College Answer

Swallowing is a complex reflex and requires an oral preparatory phase, and oral voluntary phase, a pharyngeal phase and as oesophageal phase. A myriad of potential causes exist. Possible causes of altered swallowing include: drug induced (eg. anti-cholinergic, neuroleptics), mechanical (eg. trauma from Trans-Oesopgageal Echocardiography or endotracheal intubation; presence of tracheostomy; rarely pre-existing structural problems eg. diverticula/pouches), infectious (eg mucositis), metabolic (eg. thyrotoxicosis), myopathic (eg. specific or non-specific neurological syndromes effecting bulbar function) and neurological (eg. stroke, severe head injury, Guillain-Barre syndrome etc.). Assessment is via history (previous problems, recent procedures and medications) and examination (local mechanical and bulbar neurological problems, systemic diseases and
systemic neurology). Specific procedures may involve watching attempts at swallowing (eg. speech therapist ± dye or different consistencies of food, looking for signs of aspiration
etc.), or more sophisticated techniques including naso-endoscopy (mainly anatomic assessment), and video-fluoroscopy or barium swallow (both providing a functional assessment).

Discussion

This question closely resembles Question 14 from the second paper of 2008.

College Answer

Potential causes of delayed awakening early after surgical clipping of a SAH include specific neurological causes (rebleeding, cerebral infarction/ischaemia [including intra- operative technical problems, hypotension]; too early for vasospasm), metabolic causes (including hypothermia, hypo- or hyper-natraemia and hypo- or hyper-glycaemia, hyper- or hyper-capnia) and pharmacological causes (including prolonged effects of sedatives [relative or absolute] and muscle relaxants [not reversed or prolonged/excessive effects: including suxamethonium apnoea].

Management strategy requires exclusion of treatable causes prioritised according to their urgency. Early consultation with the treating neuro-surgical team is critical. Clinical history and examination reveal details of drugs used (including amounts and timing of doses), temperature, ventilation, haemodynamics, and identifies specific surgical issues/problems. Specific investigations that should be considered range from bedside (eg. nerve stimulator to assess residual neuromuscular blockade, or BIS monitor to assess EEG) and simple blood tests (eg. blood gases [oxygenation and exclude significant abnormalities in ventilation], electrolytes [especially Na] and glucose), to more complex and invasive (eg. repeat head CT [to exclude re-bleed, ischaemia] or angiography). These latter investigations would be organised in concert with the treating neuro-surgical team.

Discussion

The approach to this unconscious patient is going to be vary similar to the generic Approach to the unconscious patient in the ICU except you will have some strong suspicions.

Let us recall the broad list of differentials for unconsciousness, and select from it only those which can be sensibly applied in this instance:

The remaining causes:

• Use of long-acting sedatives (eg. thiopentone) in theatre
• Delayed drug metabolism post-operatively
• Hypothermia and delayed rewarming postoperatively
• Metabolic abnormalities (glucose, CO₂)
• Cerebral infarction
• Contusions due to retraction
• Re-bleeding from the aneurysm
• Non-convulsive status epilepticus

Approach to management

• Ensure the ABCs are stable:
  • normoxia
  • normocapnea
  • normotension
• Collect routine bloods and correct the correctable metabolic abnormalities
• Inform the neurosurgeon
• Ask the anaesthetist regarding the specifics of the operation
• Get a CT brain
• Consider an EEG
• Avoid sedatives and muscle relaxants

College Answer

The Electro-EncephaloGram is the recording of brain electrical activity from standard sites on the scalp.  It is commonly used in ICU to evaluate patients with abnormal movements or neurological impairment.  Studies have not been directed at the use or not of EEGs and their effect on outcome except for prognostication (eg. after cardiac arrests).  The EEG is useful to distinguish between potential causes of encephalopathy (eg. metabolic or drug induced) and to establish the presence of and guide therapy for potential epileptiform activity (eg. generalised or focal).   More recent applications include prognostication (eg. after cardiac arrests) where it still has significant limitations regarding sensitivity and specificity.  The more widespread and successful use of BiSpectral monitoring in anaesthesia to limit the incidence of awareness in high risk patients (“B-Aware” Myles Lancet 2004), may have relevance for some components of ICU practice.

Somato-Sensory Evoked Potentials (SSEP) are the averaged electrical responses in the CNS to somatic stimulation (usually from median nerve at the wrist, or nerves in the leg).  The predominant use in Intensive Care has been to evaluate patients after cerebral hypoxic insult (eg cardiac arrest).  In this setting median nerve SSEPs (eg. Bilateral absence of the N20 component) have been used in normothermic patients, comatose for at least 72 hours after cardiac arrest, to predict poor outcome with 100% specificity (see metanalysis: Zandbergen Lancet 1998).

Discussion

A 2012 article by Eric S Rosenthal -"The utility of EEG, SSEP, and other neurophysiologic tools to guide neurocritical care"- seems tailor-made to answer this question, even though it was published almost seven years after the paper.

I have used it to compile the tabulated answer below. It is a merger of two tables, available in the respective sections:

• The utility of the EEG in the ICU
• The utility of SSEPs in the ICU

EEG:

• Advantages
  • Characteristic findings can distingusih between different causes of encephalopathy
  • Can detect non-convulsive status epilepticus
  • Can monitor response to antiepileptic treatment
  • Can localise epileptiform activity to a focus
  • Can detect organised activity in patients with locked-in syndrome
  • Can monitor awareness in anaesthetised patients
  • Can be used to confirm brain death
  • Non-invasive
• Disadvantages
  • This is a low-yield investigation
  • It requires specialist interpretation
  • It is confounded by sedation and hypothermia

Somatosensory Evoked Potentials (SSEP):

• Advantages:
  • Non-invasive
  • Absence of responses can be used to confirm diagnosis of severe hypoxic brain injuryafter cardiac arrest
  • Can be used to identify cortical blindness
  • May be useful in prognostication of neurological recovery after cardiac arrest
  • Less confounded by sedation or hypthermia than EEG
• Disadvantages:
  • This is a low-yield investigation
  • It requires specialist interpretation
  • In subarachnoid haemorrhage or traumatic brain injury, it is of limited value

Tjepkema-Cloostermans, Marleen Catharina, J. Horn, and M. J. A. M. Putten. "The SSEP on the ICU: Current applications and pitfalls." Netherlands journal of critical care 17.1 (2013): 5-9.

Rosenthal, Eric S. "The utility of EEG, SSEP, and other neurophysiologic tools to guide neurocritical care." Neurotherapeutics 9.1 (2012): 24-36.

Zandbergen, Eveline GJ, et al. "Systematic review of early prediction of poor outcome in anoxicischaemic coma." The Lancet 352.9143 (1998): 1808-1812.

Zandbergen, E. G. J., et al. "SSEPs and prognosis in postanoxic coma Only short or also long latency responses?." Neurology 67.4 (2006): 583-586.

Guérit, J-M., et al. "Consensus on the use of neurophysiological tests in the intensive care unit (ICU): electroencephalogram (EEG), evoked potentials (EP), and electroneuromyography (ENMG)." Neurophysiologie Clinique/Clinical Neurophysiology 39.2 (2009): 71-83.

College Answer

The benefits of monitoring ICP in closed head injury are still debated.  Standard guidelines have been published but no prospective studies have demonstrated clear outcome benefits. The main purpose of monitoring the ICP is to allow the clinician to either guide therapy (add or remove) based on the ICP or CPP, or to alert the clinician to changes which may require further investigation.  The lowest risk patients are least likely to benefit, so most criteria are based on a combination of patient characteristics and CT abnormalities.

Some risks (eg. haemorrhage) are related to insertion, and others (especially infection) are more likely with longer times in situ.  Additional risks are associated with incorrect readings (abnormally high or low leading to the risk inappropriate/un-necessary interventions or investigations.  Risks (and additional benefits) associated with ICP monitoring are largely dependent on the type of monitoring device.

Intraventricular catheters are more difficult to place, and are associated with a higher risk of haemorrhage during insertion, and subsequent infection (which increases in incidence with longer time in situ).  These catheters have the additional advantage of being able to drain CSF (potentially therapeutic) and sample CSF (monitoring for infection and bleeding). Intraparenchymal  devices  (eg.  fibreoptic  Camino  system)  are  easier  to  insert  and  are associated with a lower risk of haemorrhage and infection.  Unfortunately, the transducer cannot be recalibrated, so reliability becomes a problem.

Less commonly used devices include: subarachnoid bolts which often clog with debris, and epidural catheters which are often inaccurate.

Discussion

The methods of ICP monitoring are discussed elsewhere.

Additionally, the chapter on the indications for ICP monitoring has a section outlining the risks of this practice.

In short:

Risks of ICP monitoring:

• Risks of anaesthesia
• Risks of craniotomy
• Risks of haemorrhage
• Risk of infection
• Malposition and poor monitoring quality
• Incorrect readings may stimulate incorrect management
• EVDs may clog with debris; parenchymal monitors may "drift" from their zero calibration value
• CPP-guided therapy may not improve outcomes

Benefit of ICP monitoring:

• Prevention of secondary brain injury (however, may not improve outcomes)
• Guide for hemodynamic therapy
• Guide for timing of imaging and neurosurgical intervention
• With EVD, the option to drain CSF contributes to ICP management
• With EVD, sampling of the CSF is possible

In detail:

Rosner, M. J., and D. P. Becker. "ICP monitoring: complications and associated factors." Clinical neurosurgery 23 (1975): 494-519.

Bekar, A., et al. "Risk factors and complications of intracranial pressure monitoring with a fiberoptic device." Journal of Clinical Neuroscience 16.2 (2009): 236-240.

Smith, Martin. "Monitoring intracranial pressure in traumatic brain injury."Anesthesia & Analgesia 106.1 (2008): 240-248.

College Answer

Recent published experience demonstrates that there are some significant potential benefits associated with coiling of cerebral aneurysms.  These include decreased costs, no need for craniotomy and associated neuroanaesthetic, and increased independent survival (“ISAT” Lancet 2002; 360:1267-74).  Other potential advantages include no need for temporary clipping. Major disadvantages include the need for a skilled operator, the fact that technique is not suitable for all aneurysms, requirement for anticoagulation, and inability to deal with major complications.   A neurosurgical procedure may still be required if complications ensue.

Clipping has a long track record with clearly defined risks, with no evidence of increased mortality.  Most aneurysms are amenable to clipping, though in some regions (eg. posterior fossa), because of accessibility, coiling is considered the procedure of choice. Disadvantages of surgical clipping include need for a skilled operator, a craniotomy and neuroanaesthesia, and potentially increased costs.

Both techniques require some degree of sedation/paralysis, and subsequent neuro-Intensive care with close monitoring and re-evaluation for complications.  Either technique may be quite prolonged.

Discussion

The coiling vs clipping debate is aired briefly in the chapter on management of the unsecured aneurysm in subarachnoid haemorrhage.  In it, there is this table:

Bakker, Nicolaas A., et al. "International subarachnoid aneurysm trial 2009: endovascular coiling of ruptured intracranial aneurysms has no significant advantage over neurosurgical clipping." Neurosurgery 66.5 (2010): 961-962.

Connolly, E. Sander, et al. "Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association." Stroke 43.6 (2012): 1711-1737.

This could be answered using a table format. Suggestions include the following:

Discussion

Approach to the ICU patient with generalised weakness is discussed elsewhere.

This table is a detailed version. The features listed by the college here have been incorporated into the greater table in the abovelinked summary ("Causes of Weakness in Intensive Care Patients ")

In short:

• Only Guillain-Barre will have delayed nerve conduction, increased CSF protein and sensory features
• Only myasthenia will have characteristic fatiguability, and will respond to anticholinesterase treatment (or plasmapheresis)
• Only motor neuron disease will have increased reflexes, and will be assymetrical.

Oh's Intensive Care manual:

Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer

Chapter   57   (pp. 617)  Neuromuscular  diseases  in  intensive  care by George  Skowronski  and  Manoj  K  Saxena

Reeves and Swenson have an excellent online textbook chapter (12) entitled "Evaluation of the Patient with Weakness"

College Answer

Diagnosis: status epilepticus as > 5 minutes generalised convulsive, non-convulsive, (no return of consciousness), simple partial [Definition 2 or more convulsions with no recovery in between, or continuous convulsion > 30 min (alternative more recently accepted definition is > 5 min)]

Support: Airway, Breathing, Circulation.

Control: using hierarchy of drugs: benzodiazepine (midazolam) + phenytoin loading, propofol, barbiturate (phenobarbitone loading, thiopentone infusion), isoflurane, others. EEG to confirm, avoid paralysis.

Restore: therapeutic prophylaxis drugs if appropriate - check levels. Consider add newer generation agent in difficult cases.

Look for and treat cause:

History of epilepsy, Anti-convulsant compliance, Check and correct biochemical disturbance eg Na

(appropriate speed), hypoglycaemia, low Ca++, severe azotemia.

Look for toxins (TCA, theophylline, amphetamine and other recreational drugs, salicylate, glycols, alcohols, hydrocarbons etc).

Diagnose infective, hypoxic, vascular, metabolic or structural (trauma, neoplasm), physical(hyperthermia) cause - CT, LP, MR, porphyrins.

Treat CNS viral and bacterial infection empirically until excluded. Eclampsia specific management including LSCS, Mg, BP control.

Don't forget factitious epilepsy - look for atypical features, check lactate, EEG, reflexes etc. Consider drug withdrawal.

Treat complications - aspiration, rhabdomyolysis, hyperthermia.

Discussion

Its another one of those.

• Attention to the ABCS, with management of life-threatening problems simultanous with a rapid focused examination and a brief history.
• An attempt to reverse the status epilepticus with a bolus dose of benzodiazepine may be undertaken while the above assessment takes place.
• Airway:
  • The need for airway support shoud be assessed
  • The patient will likely need to be intubated
  • This has the added benefit of exposing the patient to barbiturate anaesthetics, benzodiazepines or propofol
• Breathing/ventilation
  • Routine pursuit of normoxia and normocapnea;
  • Minute volume may need to be titrated up in view of increased metabolic CO₂production
• Circulatory support
  • Hypotension arsiing from the use of sedating medications may require vasopressors
• Supportive management
  • Nutrition, thromboprophylaxis and pressure area care need attention, as the patient may remain immobile for a prolonged period
• Specific investigations
  • A CT brain and an EEG to confirm status epilepticus (if it is non-convulsive)are all but mandatory
  • Drug screening of serology, urine and history should be undertaken, to exclude reversible causes (eg. intoxication or withdrawal)
• Specific management
  • Correction of the aetiology (eg. intoxication)
  • First line antiepileptics should be given (phenytoin )
  • If response is not achieved, second and third line agents may be deployed (levitiracetam, valproate, benzodiazepine infusion)
  • Barbiturate coma may be required with EEG monitoring of response

Related content would consist of the following chapters:

• Management of Status Epilepticus in ICU
• Non-convulsive status epilepticus
• Relationship of seizure duration and neurological outcome
• Extracranial consequences of status epilepticus
• Causes of status epilepticus
• Features that discriminate "true" seizures from pseudoseizures

Oh's Intensive Care manual:

Chapter 49   (pp. 549) Disorders  of  consciousness  by Balasubramanian  Venkatesh

Chapter   50   (pp. 560) Status  epilepticus  by Helen  I  Opdam

Brophy, Gretchen M., et al. "Guidelines for the evaluation and management of status epilepticus." Neurocritical care 17.1 (2012): 3-23.

College Answer

This appears to be a chronic problem, and there is probably not time to discuss possible/probable
futility of more active therapy. Key features of management should include:
•    clinical assessment to help establish the diagnosis (especially sensation, pattern of weakness
[eg. lower motor neurone, long tract signs etc])
•    reasonable  to  intubate/ventilate  (hopefully  after  a  full  clinical  examination  has  been performed)
•    drugs for intubation – such as the acute risk with suxamethonium, and the potential harm associated with the use of neuromuscular blockade
•    establishment of specific diagnosis (from disorders of muscle, neuromuscular junction, peripheral nerves, anterior horn cell disease, cord lesions and central lesions)
•    collaboration with neurologists,
•    relevant investigations (eg. EMG, LP, CT, MRI etc)
•    general supportive care, including consideration of early tracheostomy.

Common problems related to lack of relevant detailed knowledge.

Discussion

This question brings about another round of differential diagnosis generation, for the question "what is causing this whole-body weakness". The assessment of the critically ill patient with weakness is well discussed elsewhere.

Thus:

• First, one would take a detailed history, and perform a focused clinical examination, with attention paid to airway and breathing.
• If these are stable (i.e. intubation is not imminent) then a complete neurological examination can be performed.
• Then, the airway control can be definitively established. The patient needs intubation before she aspirates.
• Muscle relaxant choice would rest with some sort of non-depolarising agent
• Once intubated, the ventilation can be addressed, and normoxia established.
• Now, aspiration pneumonia can be investigated with a chest Xray, which would also confirm line placement and ETT position.
• Once the ABCs have been controlled, investigation of the underlying disrder can be approached
• Potential causes and their investigations include
  • Central cerebral lesions - CT brain
  • Brainstem lesions - CT/MRI
  • Spinal cord lesions - MRI
  • Infectious and autoimmune CNS pathology - LP
  • Peripheral nerves - nerve conduction studies
  • NMJ diseases - electromyography (EMG) and acetylcholine receptor antibodies
  • Myopathy - raised CK and muscle biopsy
  • Critical illness polyneuropathy - clinical diagnosis
  • Steroid myopathy - history, and its a clinical diagnosis
  • Electrolyte derangement - electrolyte levels
• Collaboration with neurologists is essential, because you will be discharging this patient into their care
• A tracheostomy needs to be thought about if the course of ventilation is expected to be prolonged.

Oh's Intensive Care manual:

Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer

Chapter   57   (pp. 617)  Neuromuscular  diseases  in  intensive  care by George  Skowronski  and  Manoj  K  Saxena

Yuki, Nobuhiro, and Hans-Peter Hartung. "Guillain–Barré syndrome." New England Journal of Medicine 366.24 (2012): 2294-2304.

Jani, Charu. "Critical Illness Neuropathy." Medicine (2011): 237.

Young, G. Bryan, and Robert R. Hammond. "A stronger approach to weakness in the intensive care unit." Critical care 8.6 (2004): 416.

Mareska, Michael, and Laurie Gutmann. "Lambert-Eaton myasthenic syndrome." Seminars in neurology. Vol. 24. No. 2. [New York]: Thieme-Stratton Inc.,[c1981-, 2004.

College Answer

The causes of polyuria in this patient include

a)  Diabetes insipidus

b)  Mannitol or other diuretics

c)  Use of hypertonic saline

d)  Cerebral salt wasting syndrome

e)  Effects of ingested alcohol prior to the trauma

Evaluation and treatment

a)  DI : Serum and urine osmolality and Na measurements,

b)  If mannitol: check serum osmolar gap, and ensure it is < 320 mOsm/kg to prevent renal toxicity

c)  Hypertonic saline: Large urine outputs are a feature of hypertonic saline therapy and this can be confirmed by high serum and high urine Na.

d)  CSW: Low intravasc volume, low serum Na, high urine Na.

e)  Residual alcohol: based on index of suspicion, check serum osmolar gap and ethanol levels.

Discussion

LITFL do justice to this topic; theirs is a succinct and accurate answer. In addition to it, one may wish to read a relevant article by Bradshaw and Smith.

To paraphrase the already well-written college answer, the causes of polyuria following a head injury include the following:

• Diabetes insipidus
• Cerebral salt wasting
• Appropriate post-resuscitation diuresis
• Appropriate natriuresis following hypertonic saline infusion
• Mannitol-induced diuresis
• Hypothermic diuresis due to therapeutic cooling

A more detailed tabulated answer would look like this:

One should hope that the ADH-inhibiting effects of alcohol would have worn off after 18 hours, or else this gentleman had a minimum blood alcohol level of around 0.36% at the time of his injury (which is not entirely unreasonable).

The college did not ask for treatment options in their question, and so I have offered none.

Bradshaw, Kate, and Martin Smith. "Disorders of sodium balance after brain injury." Continuing Education in Anaesthesia, Critical Care & Pain 8.4 (2008): 129-133.

Robertson, Gary L. "Differential diagnosis of polyuria." Annual review of medicine 39.1 (1988): 425-442.

References

Definition : CPP = MAP-ICP Advantages: Easily monitored

Can be monitored continuously

Nursing staff familiar

BTF guidelines endorse use of CPP at 60

Limitations: Used as a surrogate for CBF

CVR is variable and therefore changes in CBF not detected by CPP

Does not allow for differential autoregulation in the normal and injured brain. Therapy to maintain CPP can result in lung injury

No Class I data to support use

Poor correlation between CPP and indices of brain oxygenation

Discussion

This question closely resembles Question 1 from the second paper of 2009.

College Answer

Key Features

Obvious attention to ABC.                                                                            

a)     Urgency is required for the best results here.                                                                    .

b)         Investigation: CTA scan of brainstem to exclude a bleed (Although not the best investigation compared to a MRI, but quickest and easiest to arrange) and to elucidate the vascular supply.   Plus exclusion of an embolic cause ie TOE should be done.

c)         Therapy: Discussion with neurologist/interventional neuroradiologist re urgent regional thrombolysis/ angioplasty / platelet antagonists.                                                       .

d)         Discussion with family re therapy and outlook.

Discussion

This brainstem stroke question is another one of these "outline your management" questions, where one ought to go through a stereotypical pathway. Yes, you would direct your attention to the A B Cs and you would maintain airway patency, ensure normoxia and normocapnea with mechanical ventilation, etc etc. Ultimately, it is not the general supportive management which is the real question here. The college - I assume - wants to know how well you understand the management of stroke. This topic is well explored elsewhere.

In brief:

Definitive management option:

• Intravenous thrombolysis
• Intraarterial thrombolysis
• Endovascular embolectomy
• Conservative management and subsequent antiplatelet therapy

Supportive management:

• Airway: intubation, for the protection thereof (being mindful that it may be futile)
• Ventilation: aiming for normocapnea and normoxia
• Circulatory support: to keep BP normal, and below 220 mmHg systolic (or 180 if thrombolysis is being explored as an option)
• Sedation: as needed to tolerate ICU management in comfort
  • Management of raised intracranial pressure is not going to be a major issue outside of the setting of malignant MCA.
  • If the brainstem stroke is extensive or involves a large proportion of the cerebellum, decompression may still be relevant. Hydrocephalus may eventually develop and an EVD may be useful as a route of CSF egress.
• Electrolyte and endocrine control: ensuring normoglycaemia and normothermia
• Fluid balance management to ensure protection of renal function following contrast
• Enteric nutrition may commence by the nasogastric route
• Heparin is not indicated given the risk of haemorrhagic transformation
• Family discussion so as to address the possibility of poor prognosis 

After the airway has been controlled, the ventilation managed and the circulation appropriately supported, one needs to establish whether this patient has had an embolic stroke (from his AF) or whether there has been a haemorrhage. This is best done with a non-contrast CT brain.

If a haemorrhage has developed, giving features of brainstem pathology, it must be a central one, or one which is extensive. In any case, hydrocephalus may develop, and one would get on the phone to the neurosurgeons to get an EVD in, if not to evacuate the bastard. Surely the earlier this is done the better.

If there is no haemorrhage, there is no point debating whether the stroke is embolic or ischaemic. One would give thrombolysis immediately. The evidence for this is discussed elsewhere. Suffice to say, we give people alteplase because the NINDS Study demonstrated a neurological recovery benefit without any increased bleed-related mortality. Mechanical embolectomy is an option if thrombolysis is contraindicated, but it is a poorer option, and not as well supported.

Then, the next 24 hours will be spent in anxious anticipation of a killing-blow intracranial bleed (as with thrombolysis) or recovering from neurosurgical evacuation and EVD insertion. In either case, one ought to have a word with the next of kin, so as to manage their expectations.

Though not immediately indicated, a carotid doppler and TOE should be performed to determine whether the carotid artery or the fibrillating atrium are sources of the clot.

Oh's Intensive Care manual

Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer.

The Internet Stroke Centre has an excellent summary of stroke syndromes.

Kammersgaard, Lars Peter, et al. "Short-and long-term prognosis for very old stroke patients. The Copenhagen Stroke Study." Age and Ageing 33.2 (2004): 149-154.

National Collaborating Centre for Chronic Conditions (Great Britain). "Stroke: national clinical guideline for diagnosis and initial management of acute stroke and transient ischaemic attack (TIA)." Royal College of Physicians, 2008.

Friedman, Howard S., W. J. Koroshetz, and N. Qureshi. "Tissue plasminogen activator for acute ischemic stroke." N Engl J Med. 1995;333(24):1581.

College Answer

Principal Advantages 
•    The effect is rapid, peaking at 10 minutes and waning after 1 hour. 
•    End point for therapy is serum Na between 145-155 and easily achieved in ICU through blood gas machines. 
•    Less potential for hypovolemia than with mannitol.
•    May have a better effect on CBF for a given reduction in ICP. 
•    Theoretical benefit in modulating the inflammatory response
•    HS is inexpensive

Disadvantages 
•    Need for a central venous access .
•    "Hypokalaemia and hyperchloraemic acidosis
•    Lack of outcome data, 
•    Increase in circulating volume and risk of CCF. 
•    Coagulopathy-HS may affect APTT and INR as well as platelet aggregation.
•          Rapid changes in serum sodium concentrations may result in seizures and encephalopathy
•         Some suggest that HS affects normal brain more that injured brain which theoretically may worsen herniation

Discussion

The use of hypertonic saline in the treatment of raised intracranial pressure falls within the realm of osmotherapy, which enjoys a thorough discussion elsewhere:

• Intracranial pressure as a therapeutic target
• Management of raised intracranial pressure
• Osmotherapy for management of raised intracranial pressure

From those summary, a table of comparison can be compiled, which is presented below.

Oh's Intensive Care manual:

Chapter 43 (pp. 563) Cerebral protection by Victoria Heaviside and Michelle Hayes, and

Chapter 67 (pp. 765) Severe head injury by John A Myburgh.

Francony, Gilles, et al. "Equimolar doses of mannitol and hypertonic saline in the treatment of increased intracranial pressure*." Critical care medicine 36.3 (2008): 795-800.

Kamel, Hooman, et al. "Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: A meta-analysis of randomized clinical trials*."Critical care medicine 39.3 (2011): 554-559.

Nau, Roland. "Osmotherapy for elevated intracranial pressure." Clinical pharmacokinetics 38.1 (2000): 23-40.

Rickard, A. C., et al. "Salt or sugar for your injured brain? A meta-analysis of randomised controlled trials of mannitol versus hypertonic sodium solutions to manage raised intracranial pressure in traumatic brain injury." Emergency Medicine Journal (2013).

Lazaridis, Christos, et al. "High-Osmolarity Saline in Neurocritical Care: Systematic Review and Meta-Analysis*." Critical care medicine 41.5 (2013): 1353-1360.

Bhardwaj, Anish, and John A. Ulatowski. "Hypertonic saline solutions in brain injury." Current opinion in critical care 10.2 (2004): 126-131.

Arbabi, Saman, et al. "Hypertonic saline induces prostacyclin production via extracellular signal-regulated kinase (ERK) activation." Journal of Surgical Research 83.2 (1999): 141-146.

R LAWRENCE REED, I. I., et al. "Hypertonic saline alters plasma clotting times and platelet aggregation." Journal of Trauma-Injury, Infection, and Critical Care 31.1 (1991): 8-14.

College Answer

Discussion

The college produces a nice table of explanations. Unfortunately, my copy-and-paste process has done some serious harm to its layout. In reponse to this failure, I have produced my own table, which neither better nor worse than the college table. This table can be found in the chapter on Examination of pupil reactivity and diameter (CN II, III)

Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Chapter 58 The Pupils - by Robert H. Spector.

Broadway, David C. "How to test for a relative afferent pupillary defect (RAPD)."Community Eye Health 25.79-80 (2012): 58.

Fincham, Edgar F. "The accommodation reflex and its stimulus." The British journal of ophthalmology 35.7 (1951): 381.

College Answer

Treatment 
b) Triple H therapy-HT, hypervolemia and hemodilution-controversial, not evidence based 
c) Early clipping / coiling 
d) Nimodipine -useful in prophylaxis, 
e) Endoluminal·therapies: Balloon angioplasty and intra-arterial papaverine 

Investigational therapies -proven in animal models, no hard clinical evidence, no RCT 
1) Statins-Early human data 
2) Cisternal tPa 
3) Endothelin antagonists

Discussion

This topic is well developed in the chapter on subarachnoid haemorrhage.

True to the college answer, there is only strong evidence for nimodipine and endovascular vasodilators. Of the "triple-H" therapy, the only evidence-based component is probably hypertension, and even this is being debated.

Judging by the college answer, they did not want a discussion of Class I recommendations from highly regarded advisory bodies. The model answer mentions some wacky "failed therapies" for vasospasm which have subsequently receded into historical background noise.

In summary:

Well-supported therapies

• Once vasospasm is suspected, DSA (the gold standard investigation) should be performed.
• On DSA, one can access the vessels involved and inject intra-arterial papaverine or verapimil.
• Nimodipine is the only preventative pharmacotherapy supported by evidence. The BRANT trial from England has demonstrated a 34% decrease in the risk of SAH-induced stroke.
• Of the "Triple H" circulating volume expansion strategies, only hypertension persists as a valid treatment - and it is only supported by a consensus of neurosurgeons.

Poorly supported therapies

• "Triple H therapy" in general- i.e. prophylactic hypertension, haemodilution and hypervolaemia - has little to recommend it. Myburgh was already tearing shreds out of it in 2005.

• Intrathecal thrombolysis is promising, but not well supported - a 2004 Japanese study found intrathecal urokinase decreased the incidence of vasospasm by almost 50%.
• Statins - no benefit (STASH trial)
• Endothelin 1 antagonists (eg. clazosentan) - no strong support, perhaps some subtle benefit (CONSCIOUS-1 trial)
• Magnesium – no benefit (MASH-2 trial)
• Tirilazad - a non-glucocorticoid aminosteroid that blocks lipid peroxidation - fiver RCTs; only one showed any benefit, and its efect was lost in the noise accoridng to a Cochrane meta-analysis.
• Fasudil - a Rho kinase inhibitor that prevents the effects of extracellular calcium on smooth muscle contraction - promising on the basis of 8 RCTs, but still not fully supported by the evidence according to a 2012 meta-analysis.
• Eicosapentaenoic acid - which also inhibits Rho kinase, like fasudil - promising results of one small study (the EVAS trial); thus far it still falls into the "experimental" category.

Connolly, E. Sander, et al. "Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association." Stroke 43.6 (2012): 1711-1737.

Myburgh, J. A. "Triple h” therapy for aneurysmal subarachnoid haemorrhage: real therapy or chasing numbers." Crit Care Resusc 7.3 (2005): 206-212.

Bederson, Joshua B., et al. "Guidelines for the management of aneurysmal subarachnoid hemorrhage a statement for healthcare professionals from a special Writing Group of the Stroke Council, American Heart Association."Stroke 40.3 (2009): 994-1025.

Kawamoto, Shunsuke, et al. "Effectiveness of the head-shaking method combined with cisternal irrigation with urokinase in preventing cerebral vasospasm after subarachnoid hemorrhage." Journal of neurosurgery 100.2 (2004): 236-243.

Vergouwen, Mervyn DI, et al. "Biologic effects of simvastatin in patients with aneurysmal subarachnoid hemorrhage: a double-blind, placebo-controlled randomized trial." Journal of Cerebral Blood Flow & Metabolism 29.8 (2009): 1444-1453.

Macdonald, R. Loch, et al. "Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage (CONSCIOUS-1) Randomized, Double-Blind, Placebo-Controlled Phase 2 Dose-Finding Trial."Stroke 39.11 (2008): 3015-3021.

College Answer

a) List the most significant abnormalities that are present on this CT 
scan?                           ·

a)   R. fronto parietal subdural

b)  Midline shift

c)   Obliteration of R.lateral ventricle

d)  Effacement of sulci

e)   Traumatic subarachnoid hemorrhage

f)   Contusions

b) List the major factors that may adversely affect his prognosis?

a)  Age
b)  ICP control
c)  Severity of injury -  GCS, traumatic SAH
d)  Hypoxia
e)  Hypotension

c) What is the simplest score in common usage that could be used to describe the patient's outcome?

a)  (Extended) Glasgow outcome score

b)  SF-36

Discussion

The image for the CT I have used is obviously not the (missing)image from the college paper, but one which was used in this BMJ paper to illustrate the progression of SAH. On this CT, there is an SDH, an SAH and cerebral contusions which are undergoing haemorrhagic transformation. Certainly, the ventricle and the sulci are effaced, and grey-white differentiation is lost.

As for the prognostic influences on the fate of traumatic brain injury patients - these are well covered elsewhere. I will summarise by saying that they consist of

• Age over 60
• Low presenting GCS
• The presence of pupillary abnormalities
• An abnormal CT
• Hypoxia and hypotension
• Medical comorbidities

The utility of the Glasgow Coma Scale is also discussed in another chapter; and the SF-36 is not in common use. The GCS was actually initially designed with outcome in mind, and the motor components particularly are well correlated with survival.

The college answer mentions the Extended Glasgow Coma Score (which is the eight-point version). This revision was made by Jennett et al in 1981, to better classify patients who had regained consciousness.

Chesnut, R. M., et al. "Part 2: Early indicators of prognosis in severe traumatic brain injury." Journal of Neurotrauma 17.6-7 (2000): 555-+.

Fearnside, Michael R., et al. "The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre-hospital, clinical and CT variables." British journal of neurosurgery 7.3 (1993): 267-279.

TEASDALE, GRAHAM, and BRYAN JENNETT. "Assessment of coma and severity of brain damage." Anesthesiology 49.3 (1978): 225.

Green, Steven M. "Cheerio, laddie! Bidding farewell to the Glasgow Coma Scale." Annals of emergency medicine 58.5 (2011): 427-430.

Gill, Michelle R., David G. Reiley, and Steven M. Green. "Interrater reliability of Glasgow Coma Scale scores in the emergency department." Annals of emergency medicine 43.2 (2004): 215-223.

Riechers, Ronald G., et al. "Physician knowledge of the glasgow coma scale."Journal of neurotrauma 22.11 (2005): 1327-1334.

Jennett, B., et al. "Disability after severe head injury: observations on the use of the Glasgow Outcome Scale." Journal of Neurology, Neurosurgery & Psychiatry 44.4 (1981): 285-293.

College Answer

Potential causes include: 
prolonged effects of sedative drugs, metabolic encephalopathy (especially renal or hepatic failure), endocrine problems (especially hypothyroidism), systemic sepsis, and a myriad of specific neurological problems ( eg. status epilepticus, raised intracranial pressure, intracranial haemorrhages, severe Guillain Barre, critical illness polyneuropathy). Residual muscular paralysis must be excluded.

Sedative drugs may have a prolonged effect because of altered kinetics (including context sensitive half-time, or decreased biotransformation or excretion eg. renal or hepatic failure) or altered dynamics (potentiation of effect by other drugs or organ 
failure, sensitivity to effect of usual dosage).

Assessment of contributory factors may be a complex process. Important steps include: 
1) Detailed history of neurological state, drugs administered, previous neurological problems 
2) Careful examination (in particular neurological, but also for signs of other chronic diseases). Detailed neurological exam should include global CNS assessment (including ability to move eyes or poke out tongue if no other apparent motor responses: locked in syndrome, severe myoneuropathy), and search for focal signs (pupils, tone, movement, reflexes). Nerve stimulator should be used to assess residual paralysis. 
3) Biochemical investigations for severity of electrolyte imbalance, creatine kinase, renal and hepatic dysfunction (mcluding ammonia), and to exclude treatable endocrine disorders (including T4/TSH). 
4) Consider use of specific reversal agents (eg. naloxone and flumazenil [may need multiple ampoules]). · 
5) May require other specific investigations (but put into context, and not done as a routine). Such investigations include CT scan of head, MRI, EEG, EMG and lumbar puncture.

Discussion

This is a question about the approach to the unconscious patient in the ICU, with a view to generate a nice juicy series of differentials. The key feature of the question is that the patient is failing to wake after a prolonged ICU stay.

Let us go though the differentials systematically.

How does one approach such a patient?

1. A history is mandatory
2. A physical examination is in order, looking for focal signs and characteristic findings
3. Some basic bloods, looking for hepatic and renal derangement
4. One ought to at least think about reversal agents such as naloxone.
5. A CT brain, to exclude structural cerebral disease
6. An LP or MRI may be in order depending on the history
7. An EEG may be the last investigation, to exclude non-convulsive status epilepticus

Oh's Intensive Care manual: Chapter 49   (pp. 549) Disorders  of  consciousness  by Balasubramanian  Venkatesh

College Answer

1.  Mannitol therapy

2.  There is increased measured plasma osmolality with an elevated osmolar gap. The

gap is 44 mosmol/kg, if we use a calculated osmolality of 1.86 × ([Na] + [K]) + [urea]

+ [glucose]. If we use the simple formula of 2 × [Na] + [urea] + [glucose] for calculated osmolality, the gap is 32 mosmol/kg. (There are also other formulae which are more difficult to remember). In the setting of treatment for an exacerbation of intracranial hypertension, the increased osmolar gap is likely to be due to mannitol administration. The high urinary osmolality rules out diabetes insipidus, and supports the diagnosis of mannitol induced polyuria.

3.  Mannitol should be ceased until the measured plasma osmolality is < 320 mosmol/kg.

There is no benefit and higher death rates in case controlled studies at higher induced osmolality.

4.  Acute (uncompensated) respiratory alkalosis.

5.  Minute ventilation should be reduced as soon as possible to return the PaCO2 to 35 –

40 mm Hg. Hypocapnia should be reserved for brief intermittent use to buy timeduring critical neurological events (eg pupillary dilation, new lateralising signs). Prolonged hypocapnia reduces cerebral blood flow and oxygenation, and eventually becomes ineffective as CSF pH returns towards normal.

Discussion

This question is remarkably similar to Question 3.1 from the second paper of 2010, and Question 22.1from the second paper of 2011.

Let us dissect these results systematically.

1. The A-a gradient cannot be calculated
2. There is alkalaemia
3. The PaCO2 is contributing to the alkalosis
4. The SBE is -1.5, suggesting a normal acid-base balance; it and the bicarbonate is mildly decreased suggesting a trend towards metabolic acidosis
5. The metabolic compensation is appropriate. It is expected that the bicarbonate would decrease by 2mmol/L for every 10mmHg decrease in PaCO₂, and thus we would expect to see a bicarbonate value around 22, which we do.
6. The anion gap is slightly raised:
   (147+3.2) - (110+21) = 19.2
   The delta ratio suggests that there is a combination of pure high anion gap metabolic acidosis and metabolic alkalosis here.
   (19.2 - 12) / (24 - 21) = 2.4
7. The osmolar gap is increased:
   333 - (2 × 147 + 3 + 4) = 32 (normal is under 10)

The head injury story and the polyuria together make one want to cry "DI!" but in actual DI the urinary osmolality is frightfully low, as torrents of dilute urine issue forth from the vasopressin-deficient patient. The urinary osmolality here is given, so that the candidate does not become confused. The history of a recent spike in ICP inflames the imagination, promoting the idea that someone may have given this patient some hypertonic syrup.

The physiological consequences of mannitol therapy are discussed in greater detail elsewhere.

So, "what action needs to be taken" concerning the polyuria?

Well. The mannitol should be ceased, for one. And then the tincture of time should be liberally applied. The mannitol will exit via the urine, taking with it some water, and the serum osmolality will settle into a more tolerable range.

The ventilation adjustment required to correct this hyperventilation is a decreased respiratory rate. No head-injured patient needs a PaCO₂ of 28; hyperventilation in head injury is a last-ditch effort to decrease intracranial pressure, and it may reduce cerebral blood flow in the process.

UpToDate has a nice article on the complications of mannitol therapy.

The specific features of it, being the diuresis and the resulting electrolyte derangement, are well explored in this ancient yellowed scroll from NEJM:

GIPSTEIN RM, BOYLE JD. HYPERNATREMIA COMPLICATING PROLONGED MANNITOL DIURESIS. N Engl J Med. 1965 May 27;272:1116-7.

College Answer

A moderate head injury has a presenting coma score in the range 9 to 12 or 13, and is the best score in the absence of sedation and post non-surgical resuscitation.

Prognostic determinants:

a)  Age > 60

b)  Pupillary abnormalities

c)  Presence of hypotension and hypoxia

d)  CT scan abnormalities – intracranial collections, presence of traumatic subarachnoid haemorrhage

e)  Co-morbidities

Factors warrant admission in intensive care :

i)    Presence of a skull fracture,

j)           convulsions,

k)  influence of any drug including alcohol, anticoagulation,

l) presence of other injuries

Discussion

Well, from one's feeble memory one may be able to extract the recollection that "mild" head injury is one with a GCS of 14-15, and "severe" head injury is a GCS of less than 8, which would mean that "moderate" head injury should have a GCS between 9 and 13.

The major determinants of prognosis are

• Age
• GCS on admission
• Hypotension
• Hypoxia
• Pupillary abnormalities
• CT scan abnormalities
• Medical comorbidities

Prognosis in severe brain injury is discussed elsewhere.

What  factors would warrant admission of these patients to an intensive care or a high dependency unit? Well. The semiconscious patient in general should be managed in the ICU or HDU. But more precisely, I would use the following criteria:

• Need for airway control
• Seziures and the sedating consequences of benzodiazepines
• Multiple traumatic injuries
• Multiple medical comorbidities
• Influence of illicit substances, distorting the level of consciousness and decreasing the accuracy of physical examination though incooperation.

Wu, Christopher L., et al. "Thoracic epidural analgesia versus intravenous patient-controlled analgesia for the treatment of rib fracture pain after motor vehicle crash." Journal of Trauma-Injury, Infection, and Critical Care 47.3 (1999): 564-567.

MACKERSIE, ROBERT C., et al. "Prospective evaluation of epidural and intravenous administration of fentanyl for pain control and restoration of ventilatory function following multiple rib fractures." Journal of Trauma-Injury, Infection, and Critical Care 31.4 (1991): 443-451.

Kieninger, Alicia N., et al. "Epidural versus intravenous pain control in elderly patients with rib fractures." The American journal of surgery 189.3 (2005): 327-330.

Moon, M. Ryan, et al. "Prospective, randomized comparison of epidural versus parenteral opioid analgesia in thoracic trauma." Annals of surgery 229.5 (1999): 684.

Jarvis, Amy M., et al. "Comparison of epidural versus parenteral analgesia for traumatic rib fractures: a meta-analysis." OPUS 12 (2009): 50-57.

Scherer, R., et al. "Complications related to thoracic epidural analgesia: a prospective study in 1071 surgical patients." Acta anaesthesiologica scandinavica 37.4 (1993): 370-374.

Kapral, Stephan, et al. "The effects of thoracic epidural anesthesia on intraoperative visceral perfusion and metabolism." Anesthesia & Analgesia 88.2 (1999): 402-406.

College Answer

Discussion

A description of the various vegetable-like states is available elsewhere.

It is easy to summarise:

PVS is characterised by a preserved autonomic regulation and sleep-wake cycle, but the absence of any behavioural evidence of consciouseness. The lesion is typically diffuse, eg. severe hypoxic brain injury.

Locked in syndrome is usually caused by damage to the ventral pons, and the characteristic features are total tetraplegia and facial/oral musuclar paralysis, with preserved eye opening and vertical eye movements, in the presence of a totally intact level of consciousness.

Akinetic mutism is usually caused by bilateral frontal lobe damage, and the characteristic features are immobility and silence with preserved eye tracking. These people are not paralysed, but rather lack any volition to move.

The abovelinked summary contains a table to help discriminate between states of persistent unconsciousness, which I will reproduce below to simplify revision.

This table, as the summary it is derived from, is based heavily on the diagnostic guidelines published in 2003 by the Royal College of Physicians.

Oh's Intensive Care manual: Chapter 49   (pp. 549) Disorders  of  consciousness  by Balasubramanian  Venkatesh

Working Party of the Royal College of Physicians. "The vegetative state: guidance on diagnosis and management." Clinical Medicine 3.3 (2003): 249-254.

Schnakers, C., J. Giacino, and S. Laureys. "Coma: Detecting signs of consciousness in severely brain injured patients recovering from coma."Coma Science Group, Cyclotron Research Centre University of Liege, Liège, Belgium

Monti, Martin M., Steven Laureys, and Adrian M. Owen. "The vegetative state."Bmj 341.c3765 (2010): 292-296.

Giacino, Joseph T., et al. "The minimally conscious state definition and diagnostic criteria." Neurology 58.3 (2002): 349-353.

Plum, Fred, and Jerome B. Posner. The diagnosis of stupor and coma. Vol. 19. Oxford University Press, 1982.

Smith, Eimear, and Mark Delargy. "Locked-in syndrome." BMJ: British Medical Journal 330.7488 (2005): 406.

Cairns, Hugh, et al. "Akinetic mutism with an epidermoid cyst of the 3rd ventricle." Brain 64.4 (1941): 273-290.

College Answer

Techniques that have proven or demonstrated potential in the diagnosis and monitoring of vasospasm include:
Clinical; in the conscious patient, may be detected clinically by new focal neurology or a drop in GCS.
Major disadvantage is lack of specificity often necessitating CT/angiography. EEG; May provide prognostic information, focal areas of slowing correlate with
angiographic vasospasm and a decrease in alpha to delta ratio strongly correlates with ischaemia. Sensitivity and specificity for detecting vasospasm is high.
Disadvantage: Not readily available however and their may be issues with interpretation.Conventional 4 vessel DSA angiography-
-                 remains the gold standard for diagnosis of DIND
-                  may allow therapeutic intervention (angioplasty) at the time.

Disadvantages -invasive, risks of bleeding, embolism, radiation/contrast exposure and transport. Requires skilled interventional radiology and therefore resource heavy.

Transcranial Doppler (TCD):

-                 It is low risk, performed at the bedside, non invasive and able to be repeated daily enabling trend analysis.

Disadvantages:
-                 The technique is however operator dependent and there is a high inter observer variability.
-                 Debate exists regarding correlation of flow velocity and vasospasm and although high velocities (> 200cm/sec) are predictive, lower velocity may not be as good.
-                 The technique may be more accurate when MCA velocity is indexed to the ipsilateral extracranial carotid artery (Lindegaard index, >3 strongly predictive).
-                 Colour coded TCD may offer greater accuracy than plain TCD alone.

CTA/MRI: may be combined with perfusion allowing characterisation of both vascular anatomy and associated perfusion abnormalities.
Image clarity will be affected by clip/coil and contrast related issues need consideration. The overall diagnostic capability of this modality however remains unclear until further prospective studies are performed. MR diffusion weighted imaging accurately identifies brain tissue at high risk of infarction; perfusion weighted imaging reveals asymmetries in regional perfusion. Both methods show correlation with DIND

SPECT/PET:
-can be used to obtain a picture of brain perfusion and metabolism and have shown variable correlation with vasospasm as assessed by more conventional methods.

Disadvantages: They are resource heavy not easily available, radiation exposure, patient transport are issues.

The use of measures of tissue oxygenation using parenchymal sensors and microdialysis for monitoring biochemical indices of ischaemia are largely research tools.

Discussion

This question closely resembles Question 2 from the second paper of 2013.

College Answer

a) List the indications for the use of this device in traumatic brain injury.

1.  Intracranial pressure monitoring in patients with traumatic brain injury associated with an initial non-sedated Glasgow Coma Score > 8 prior to non-surgical resuscitation
a.   AND an abnormal CT scan associated with trauma:
i.  Diffuse axonal injury grade II – IV or ii.   Mass lesions with midline shift > 5mm
b.  AND in the following patients with a normal CT Scan

i.  Age >40
ii.  Lateralising signs

iii.  Hypotension
iv.  Significant extra-cranial trauma

b) List 3 important principles of measurement/management of this device

1.  Attached flushed transducer to fluid-filled catheter – do not inject
2.  Set transducer to reference level (EAM or aortic root)
3.  Attach drainage manometer and set at 10-20 cm H2O at level of EAM.
4.  Monitor ICP continuously with intermittent drainage (hourly) unless clinically
indicated, for which drainage may be increased in frequency or continuously.
5.  Septic surveillance of CSF daily.

Discussion

Methods of intracranial pressure monitoring and indications for intracranial pressure monitoring are discussed elsewhere.

The modern indications for ICP monitoring come from the Brain Trauma Foundation  (4th edition), which are simply  "anyone with an abnormal CT and GCS 3-8 gets ICP monitoring".

The setup of the EVD, its waveforms, and various other tidbits all have their own chapter.

In short, the normal principles of ICP measurement are:

• Inserted into the lateral ventricle, about 2.5 centimetres left or right from the midline, 11cm posterior to the junction between the frontal bone and the nasal bones.
• The drain connects to the transducer via a three-way tap
• The connecting tubing is incompressible, and primed with saline
• The transducer is zeroed to atmospheric pressure at the level of the tragus.
• The height of the drain is set to a certain specified height (in cm) above the patients tragus; lets say, 15cm
• The ICP is measured continuously; drainage occurs hourly, or sporadically.
• Daily CSF samples are sent for protein, glucose, cell count, Gram stain and culture.

Chawla, Lakhmir S., et al. "Lack of equivalence between central and mixed venous oxygen saturation." CHEST Journal 126.6 (2004): 1891-1896.

College Answer

a) What does the visual field testing indicate?
Rt. homonymous hemianopia 

b) List 3 likely anatomical sites of lesion which may result in this visual defect.

Left optic tract
Left optic radiation
Left occipital lobe

Discussion

The localisation of visual field defects lends itself especially well to a massive insane-looking eyeball diagram, which I have put together many years ago in med school.

For detailed references, one can be directed to Chapter 116 by R.H Spector from Clinical Methods(1990), or "Topical diagnosis of chiasmal and retrochiasmal disorders" by Levin, from Walsh and Hoyt clinical neuro-ophthalmology, 6th ed.

Alternatively, one can explore this table cut-and-pasted from the Required Reading section (Visual fields and lesions of the visual pathways). As you can plainly see, one can put "tumour" down as a cause for pretty much any of these 

Levin, Leonard A. "Topical diagnosis of chiasmal and retrochiasmal disorders."Walsh and Hoyt clinical neuro-ophthalmology, 6th ed. Baltimore: Williams & Wilkins (2005): 503-573.

Robert H. Spector. "Visual Fields." (1990). Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition.

College Answer

a). What is your assessment  of the CSF result and provide a reason ?
Ventriculitis : due to raised WCC:RCC ratio and a positive gram stain

b). List two likely organisms commonly reported on the Gram stain in this setting.
Staphylococcus epidermidis
Staphylococcus aureus

c). List 2 therapies you may consider based on this report .
Removal of EVD / replacement
Vancomycin

Discussion

This patient has ventriculitis. The ratio of WCCs to RBCs is around 1:10, rather than 1:500-1500. Therefore, there is "CSF pleocytosis". The presence of monocytes is also much higher than would be expected purely from the presence of the EVD.

The gram positive cocci found in this CSF sample are likely tourist organisms from the skin, which took a ride into the brain on the back of the EVD. Likely, these are going to be either Staphylococcus aureus, Staphylococcus epidermidis or Streptococcus pyogenes.

The two things one should immediately consider is

1) Get the infected EVD out

2) Start some antibiotics, which in the context of unknown sensitivities should consist of cephalosomething and vancomycin.

The normal properties and contents of the CSF are discussed in detail elsewhere.

Meningitis is favoured with a chapter in Oh's Manual, and is also discussed elsewhere.

Beer, R., P. Lackner, and B. Pfausler. "Nosocomial ventriculitis and meningitis in neurocritical care patients." Journal of neurology 255.11 (2008): 1617-1624.

College Answer

a). What is the most important diagnostic  investigation indicated in this clinical scenario?
MRI of the spine

b). What is the most likely diagnosis?
Epidural abscess

Discussion

This elderly diabetic woman has a bilateral motor and sensory loss in her legs. The CSF looks infected; perhaps the glucose is raised, but this could be because the serum glucose is also raised, so I would not be deterred from a suspicion of epidural abscess by the presence of these findings.

The most important investigation in this context would be an MRI of the whole spine.

Reihsaus, E., H. Waldbaur, and W. Seeling. "Spinal epidural abscess: a meta-analysis of 915 patients." Neurosurgical review 23.4 (2000): 175-204.

College Answer

Causes:

•    Iatrogenic - Medications – chemotherapy, antihistaminics, neuroleptics. Trauma - TOE, intubation , tracheostomy
•    Infectious - candidial mucositis. Metabolic – thyrotoxicosis, Cushing’s
•    Myopathic – myasthenia gravis, connective tissue disorders, myotonic dystrophy
•    Neurological – severe head injury, stroke, Guillain-Barre syndrome. Structural - Zenker's diverticulum, Oropharyngeal and oesophageal tumours.

Assessment:

•    History – hoarseness, weak cough – vocal cord palsy, slurred speech, nasal regurgitation – neuromuscular. Odynophagia – infections , malignancy
•    Clinical assessment – oral cavity –poor dentition, dry mouth. Neurological –
cranial nerves – V. VII, IX, X, XI, XII.
•    Bedside assessment by speech therapist – coordination of swallowing, aspiration of dye (methylene blue).
•    Nasopharyngeal laryngoscopy – visual inspection oropharynx, vocal cords for anatomical abnormality.
•    Video fluoroscopy – accurately analyses aspiration, pooling of secretions and movements of muscles during swallowing.
•    Barium swallow – identifies anatomical abnormalities – diverticuli, tumours, Upper GI endoscopy.

Discussion

Altered swallowing in an ICU patient could be the result of a number of aetiological processes. Not all of the belowmentioned processes are causing an "altered reflex" per se.

Investigation of abnormal swallowing in ICU follows a familiar pattern:

• History (suggestive of stroke or malignancy)
• Examination (of whole body neurology, but focusing on the cranial nerves)
• Speech therapist assessment
• Nasendoscopy to observe the vocal cords directly
• Barium swallow
• CT of the neck
• A VFSS (videofluoroscopic swallowing study) is the gold standard.

de Larminat, Valentine, et al. "Alteration in swallowing reflex after extubation in intensive care unit patients." Critical care medicine 23.3 (1995): 486-490.

Macht, Madison, et al. "ICU-Acquired Swallowing Disorders." Critical care medicine 41.10 (2013): 2396-2405.

College Answer

Recognised indications

• Malignant MCA infarction

Indications for which there is anecdotal  evidence:

• Refractory intracranial hypertension following TBI
• Cerebral swelling from vasospasm and SAH
• Hypertensive bleeds
• Encephalitis
• Cerebral venous thrombosis

Complications:

• Infection
• Collections –subgaleal and subdural collections usually on the ipsilateral side.
• Bleeding
• Brain herniation through the craniotomy
• Venous thrombosis secondary to herniation through the defect and occlusion of venous circulation.
• Sinking flap syndrome
• Paradoxical subtentorial herniation with LP or CSF drainage – due to atmospheric pressure – intracranial pressure gradient
• Hydrocephalus
• Bone flap resorption
• Worsening of brain injury

Outcome:

 Long term data are lacking. Although hospital survival is improved in patients with refractory ICP in head injury and malignant infarction, quality of survival needs further evaluation. Age is important in patient selection and current recommendation for DCI in malignant MCA infarcts is <50 and considered on a case by case basis over 50. Paediatric data suggest better outcome in paediatric head injuries.

Discussion

Decompressive craniectomy in general, and within the specific context of a malignant MCA infarction, is discussed in great detail elsewhere:

• Decompressive craniectomy for traumatic brain injury
• Decompressive craniectomy for malignant MCA infarction

Additionally, LITFL have a nice summary page on this topic.

To simplify revision, a summary table is lazily pasted here.

In a nontabulated form, one might answer thus:

Indications for a decompressive craniectomy:

• Raised intracranial pressure due to
  • Traumatic brain injury
  • Severe intracranial haemorrhage with midline shift
  • Malignant MCA infarction syndrome
  • Subarachnoid haemorrhage
  • Intraparenchymal intracranial haemorrhage
  • Dural sinus thrombosis
  • Encephalitis
  • Subdural haematoma

Why is malignant MCA infarction a "recognised indication"? Well. Three European trials confirmed that mortality from massive MCA infarction is halved with craniectomy, and that is hard to argue with.

Complications of decompressive craniectomy:

• Brain hernation though the opening
• Delayed paradoxical herneation
• Subdural hygroma

• Infection
• Bleeding
• Post-traumatic hydrocephalus
• Syndrome of the Trephined, or "Sinking Flap Syndrome"
• Bone resorption

Outcome of decompressive craniectomy:

• MCA infarct patients: mortality improved by 50%
• Traumatic brain injury patients: mortality unchanged, but neurological outcome was worse in the craniectomized patients.

Cooper, D. James, et al. "Decompressive craniectomy in diffuse traumatic brain injury." New England Journal of Medicine 364.16 (2011): 1493-1502.

Vahedi, Katayoun, et al. "Sequential-design, multicenter, randomized, controlled trial of early decompressive craniectomy in malignant middle cerebral artery infarction (DECIMAL Trial)." Stroke 38.9 (2007): 2506-2517.

Hofmeijer, Jeannette, et al. "Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial." The Lancet Neurology 8.4 (2009): 326-333.

Jüttler, Eric, et al. "Decompressive surgery for the treatment of malignant infarction of the middle cerebral artery (DESTINY) a randomized, controlled trial." Stroke 38.9 (2007): 2518-2525.

Lee, Kyeong Woo, et al. "Functional Outcomes of Patients with Severe MCA Infarction after Decompressive Craniectomy." Brain & Neurorehabilitation 7.1 (2014): 48-53.

Tuzgen, Saffet, et al. "Decompressive craniectomy in patients with cerebral infarction due to malignant vasospasm after aneurysmal subarachnoid hemorrhage." Journal of neurosciences in rural practice 3.3 (2012): 251.

Murthy, J. M. K., et al. "Decompressive craniectomy with clot evacuation in large hemispheric hypertensive intracerebral hemorrhage." Neurocritical care 2.3 (2005): 258-262.

Güresir, Erdem, et al. "Decompressive craniectomy in subarachnoid hemorrhage." Neurosurgical focus 26.6 (2009): E4.

Keller, E., et al. "Decompressive craniectomy in severe cerebral venous and dural sinus thrombosis." New Trends of Surgery for Stroke and its Perioperative Management. Springer Vienna, 2005. 177-183.

Schirmer, Clemens M., Daniel A. Hoit, and Adel M. Malek. "Decompressive hemicraniectomy for the treatment of intractable intracranial hypertension after aneurysmal subarachnoid hemorrhage." Stroke 38.3 (2007): 987-992.

Adamo, Matthew A., and Eric M. Deshaies. "Emergency decompressive craniectomy for fulminating infectious encephalitis." (2008). Journal of Neurosurgery January 2008 / Vol. 108 / No. 1 / Pages 174-176

Hutchinson, Peter, Ivan Timofeev, and Peter Kirkpatrick. "Surgery for brain edema." Neurosurgical focus 22.5 (2007): 1-9.

Margules, Andrew, and Jack Jallo. "Complications of decompressive craniectomy." JHN Journal 5.1 (2010): 4.

College Answer

All patients with severe head injury and moderate head injury whose progress can not be followed by serial neurological evaluation should be considered for ICP monitoring.

The Brain Trauma Foundation guidelines suggest ICP-monitoring should be considered in the following settings:
•    Severe head injury (GCS 3-8) + abnormal CT scan
•    Severe head injury (GCS 3-8) + normal CT scan if 2 of the following are presen):
o Age > 40
o BP < 90 mmHg
o Abnormal motor posturing

Individual intracranial pressure monitors have different limitations:
•    Intraparenchymal monitors/subdural bolts: can not be calibrated, subject to “drift”, do not allow CSF drainage for control of ICP
•    Require expertise and resource availability for placement
•    Infection

No RCTs have demonstrated that ICP-guided therapy improves patient-centred outcomes.

Some observational studies have noted an association between ICP guided management and prolonged length of stay (Cramer, 2005) and worse outcome (Shafi, 2008).

Discussion

The indications listed in the college answer (including age, posturing etc) are from the old 3rd edition of the BTF guidelines. The enlightened 4th edition had reduced these recommendations to simply "anyone with an abnormal CT and GCS 3-8".

Limitations of intracranial pressure monitoring:

• No evidence that it impoves outcomes
• Monitors can become infected, inaccurate due to drift, or they can cause more intracranial bleeding.
• Neurosurgical expertise is required to insert these monitors

The college answer references papers by Cramer (2005) and Shafi (2008).

Presumably, they meant Olaf L. Cremer, who in 2005 was the first author of a retrospective cohort study which associated ICP-guided therapy with increased intensity of therapy and more prolonged mechanical ventilation, without a benefit to either survival or functional outcome. The examiners also mention Shahid Shafi's 2008 analysis of The National Trauma Data Bank (1994–2001) which found that ICP monitoring was associated with a 45% reduction in survival.

Greated detail is afforded by the summary of indications for intracranial pressure monitoring andmethods of intracranial pressure monitoring in the Required Reading section; to simplify revision the relevant grey boxes have been reproduced below.

Oh's Intensive Care manual

Chapter 43 (pp. 563) Cerebral protection by Victoria Heaviside and Michelle Hayes, and

Chapter 67 (pp. 765) Severe head injury by John A Myburgh.

Brain Trauma Organisation Guidelines for Management Traumatic Brain Injury.

Narayan, Raj K., et al. "Intracranial pressure: to monitor or not to monitor? A review of our experience with severe head injury." Journal of neurosurgery 56.5 (1982): 650-659.

Forsyth, Rob J., Susanne Wolny, and Beryl Rodrigues. "Routine intracranial pressure monitoring in acute coma." Cochrane Database Syst Rev 2 (2010).

Meythaler, Jay M., et al. "Current concepts: Diffuse axonal injury - associated traumatic brain injury." Archives of physical medicine and rehabilitation 82.10 (2001): 1461-1471.

Tasker, R. C., et al. "Monitoring in non-traumatic coma. Part I: Invasive intracranial measurements." Archives of disease in childhood 63.8 (1988): 888-894.

Cremer, Olaf L., et al. "Effect of intracranial pressure monitoring and targeted intensive care on functional outcome after severe head injury*." Critical care medicine 33.10 (2005): 2207-2213.

Shafi, Shahid, et al. "Intracranial pressure monitoring in brain-injured patients is associated with worsening of survival." Journal of Trauma and Acute Care Surgery 64.2 (2008): 335-340.

Lane, Peter L., et al. "Intracranial pressure monitoring and outcomes after traumatic brain injury." Canadian Journal of Surgery 43.6 (2000): 442.

College Answer

°     Irritative lesion of the left frontal lobe

°     Paralytic lesion of the right frontal lobe

°     Rt. Pontine lesion

Discussion

The college sure do love the disorders of conjugate gaze.

A right-sided lesion in Brodmann's Area 8 (right prefrontal cortex) tends to produce a tonic deviation towards the lesion. I suppose a stroke can be described as a "paralytic" lesion, although decribing stroke as "paralytic" or "apoplectic" has gone out of fashion since definitions of stroke underwent some revisions in the mid-1950s.

Alternatively, epilepsy can cause a tonic deviation of the eyes (and head), in which case the eyes will deviate away from the clearly lateralised seziure focus. I suppose, by this odd nomenclature, one could describe a clearly lateralised focus of epilepsy as an "irritative lesion".

A pontine lesion causes an interruption of ipsilateral gaze motor control, resulting in a deviation of the eyes away from the lesion, towards the intact pons and towards the hemiparetic side of the patient. Thus, a right gaze deviation could never be caused by a right pontine infarct. In this, the college answer is probably wrong.

The non-tonic version of this finding is called Prévost's sign, and is associated with hemineglect (the eyes merely "trend" towards one side).

In general, the chapter on Examination of eye movements contains some relevant persistent eye deviation syndromes and their associated observation findings  whereas the chapter on  Disorders of conjugate gaze deals more with findings on active oculomotor examination.

Berger, M. Fruhmann, et al. "Deviation of eyes and head in acute cerebral stroke."  BMC neurology 6.1 (2006): 23.

Kernan, J. C., et al. "Lateralizing significance of head and eye deviation in secondary generalized tonic‐clonic seizures." Neurology 43.7 (1993): 1308-1308.

Bassetti, Claudio, et al. "Isolated infarcts of the pons." Neurology 46.1 (1996): 165-175.

College Answer

°     Meningitis/encephalitis

°     Subarachnoid hemorrhage

°     Post fossa syndrome

°     Tetanus

°     Cervical spondylitis

°     Neck abscess

°     Wry neck / Torticollis

Discussion

To this predictable list, I could also add

• dural sinus thrombosis
• epidural abscess
• cervical facet joint arthritis
• "whiplash" - musculoskeletal hyperextension injury

And many others. One can go right to town on this. Consider a cause for neck stiffness from any of the major pathological categories, and I guarantee you will find one.

Observe:

Vascular:

• Dural sinus thrombosis
• Subarachnoid hemorrhage

Infectious:

• Epidural abscess
• Neck abscess
• Meningitis/encephalitis
• Tetanus

Neoplastic:

• C-spine vertebral metastasis or primary

Drug-related:

• Dystonic reaction
• Withdrawal

Idiopathic/inflammatory:

• Osteoarthritis
• Cervical spondylitis
• Torticollis

Autoimmune:

• Rheumatoid arthritis
• Ankylosing spondylitis

Traumatic

• Whiplash
• C-spine dislocation, subluxation or fracture
• Prolonged neck hyperextension during surgery (eg. tracheostomy)

Endocrine:

• Hypocalcemia

College Answer

Definiton : CPP = MAP-ICP

• Advantages:
• Easily monitored
• Can be monitored continuously
• Nursing staff familiar
• BTF guidelines endorse use of CPP at 60

Limitations:

• Used as a surrogate for CBF.CVR is variable and therefore changes in CBF not detected by CPP
• Does not allow for differential autoregulation in the normal and injured brain.
• Therapy to maintain CPP can result in lung injury
• No Class I data to support use
• Poor correlation between CPP and indices of brain oxygenation

Discussion

The general topic of cerebral bloodflow autoregulation is discussed elsewhere.

More specific information regarding using CPP as a therapeutic target in traumatic brain injury is explored in the Required Reading section.

In brief:

Cerebral perfusion pressure is the driving pressure gradient which produces flow in the cerebral circulation against the resistance of cerebral vessels. Thus, it is the difference in mean cereberal arterial pressure and the mean cereral venous pressure. Because we can hardly measure the latter and we only guess at the former, a useful approximation is to subtract intracranial pressure (ICP) from the mean systemic arterial pressure (MAP). Thus, CPP = (MAP - ICP).

There are some advantages of using CPP as a treatment target in traumatic brain injury. The brain-injured patient is unable to autoregulate their cerebral blood flow, and thus they rely on you to make sure that their cerebral arterial pressure remains reasonably high. Its easy enough to monitor it continuously if you have both an arterial line and an ICP monitor.

However, it is not a measure of cerebral blood flow. Flow is a very different property; cerebral blood flow is a function of both the pressure gradient and the resistance. Cerebral vascular resistance might change randomly and regionally, all without any change in systemic MAP. Not only that, but "flow" alone does not determine cereberal oxygenation - there are even more factors involved in this, such as the oxygen carrying capacity of red cells, the viscosity of the blood, etc etc...

In short, as has been demonstrated experimentally, CPP does not correlate well with brain tissue oxygenation.

Furthermore, targeting a CPP tends to ignore the fact that no brain is uniformly injured, and that there are regions which are still able to autoregulate their bloodflow. In one's desperate bid to protect the brain, one may inadvertantly flood the patient with fluid and cause pulmonary oedema, or exacerbate existing neurogenic pulmonary oedema.

Lastly, the college makes a statement regarding there being no Class I evidence to suport the use of CPP-guided blood pressure management in traumatic brain injury. True, but the entire set of BTF guidelines only has one single piece of Class I evidence, which is "don't you ever use steroids". Thus, one cannot single out the CPP guidelines as somehow "baseless" on the grounds that no investigator has thus far dared to randomise a group of brain-injured patients to an experimental group in whom the CPP is totally unmanaged.

Oh's Intensive Care manual

Chapter 52   (pp. 580)  Cerebral  protection by Victoria  Heaviside  and  Michelle  Hayes

Harper, A. MURRAY. "Autoregulation of cerebral blood flow: influence of the arterial blood pressure on the blood flow through the cerebral cortex." Journal of neurology, neurosurgery, and psychiatry 29.5 (1966): 398.

Phillips, Stephen J., and Jack P. Whisnant. "Hypertension and the brain."Archives of internal medicine 152.5 (1992): 938-945.

Paulson, O. B., S. Strandgaard, and L. Edvinsson. "Cerebral autoregulation." Cerebrovascular and brain metabolism reviews 2.2 (1989): 161-192.

Busija, David W., and Donald D. Heistad. Factors involved in the physiological regulation of the cerebral circulation. Springer Berlin Heidelberg, 1984.

Eriksson, Evert A., et al. "Cerebral perfusion pressure and intracranial pressure are not surrogates for brain tissue oxygenation in traumatic brain injury."Clinical Neurophysiology 123.6 (2012): 1255-1260.

College Answer

11.1     What are your differential diagnoses for his weakness?

• Gullian-Barre syndrome
• Myasthenia gravis
• Motor neurone disease
• Paraneoplastic syndrome – Eaton Lambert
• (Myotonic dystrophy)
• Periodic paralysis
• Botulism
• (Endocrine & metabolic myopathies)
• (Drug induced myopathies)

11.2     The  above  patient  is admitted to  ICU  post-op.  A perforated DU was  oversewn  in theatre.

a)          What are the essential pieces of information you would expect from the anaesthetist at handover upon the patient’s  admission to ICU?

Specific:
GA drugs used – esp muscle relaxants; muscle relaxation in response to sux (if used)

Findings on nerve stimulator NMJ monitoring
Reasons extubation could not be attempted

General:
Operative findings

Haemodynamic stability

Antibiotics used

11.3     What investigations could help you establish the diagnosis for his weakness?

• Edrophonium or neostigmine test (with atropine cover)
• ACh receptor Abs
• EMG NCS – Muscle biopsy
• LP – CSF protein
• Neurological review

Discussion

The fist part of the question is a straightforward differential-generating exercise. What are the causes of subacute-onset weakness in a smoker? Guillain-Barre, myasthenia gravis and motor neuron disease are reasonable guesses which apply everywhere. Particularly, diplopia would make one think of myasthenia gravis. The Lambert-Eaton (or Eaton-Lambert) Myasthenic Syndrome is a special one, which relates partiocularly to people with neoplasms (it is a paraneoplastic syndrome of autoantibody secretion, resulting in the destruction of voltage-gated calcium channels). Botulism is thrown in for some reason. Periodic paralysis is also mentioned, even though it is an insanely rate genetic disorder. Drug-induced myopathies are more common, but are mentioned last.

What would you want to know from the anaesthetist?

Well; for one, you would like to know whether they used any muscle relaxant, and if yes- then how much, what kind, and when. One would also be interested in the nerve stimulator test. The administration of gentamicin may potentiate NMJ disturbances and it would be good to know whether one should expect something like this.

As for investigations... A panel of standard tests would include the following:

• Electrolyte levels
• CK level
• B12 level
• Acetylcholine receptor antibodies (for myasthenia gravis)
• CXR looking for malignancy (as support for a diagnosis of Eaton-Lambert syndrome)
• Inflammatory markers
• Lumbar puncture
• Nerve conduction studies
• Electromyography
• MRI of the brainstem and spine
• Muscle biopsy if no satisfactory explanation is found.

It is worth noting that the college is not too proud to seek a neurology consult when confronted by this sort of problem.

Approach to the ICU patient with generalised weakness is discussed elsewhere.

Oh's Intensive Care manual: Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer

Chapter   57   (pp. 617)  Neuromuscular  diseases  in  intensive  care by George  Skowronski  and  Manoj  K  Saxena

Yuki, Nobuhiro, and Hans-Peter Hartung. "Guillain–Barré syndrome." New England Journal of Medicine 366.24 (2012): 2294-2304.

Jani, Charu. "Critical Illness Neuropathy." Medicine (2011): 237.

Young, G. Bryan, and Robert R. Hammond. "A stronger approach to weakness in the intensive care unit." Critical care 8.6 (2004): 416.

Mareska, Michael, and Laurie Gutmann. "Lambert-Eaton myasthenic syndrome." Seminars in neurology. Vol. 24. No. 2. [New York]: Thieme-Stratton Inc.,[c1981-, 2004.

Engel, Andrew G., ed. Myasthenia gravis and myasthenic disorders. Oxford University Press, 2012.

College Answer

1. Nystagmus
2. Titubation (head bobbing)
3. Truncal ataxia
4. Staccato speech
5. Dysarthria
6. Hypotonia
7. Kinetic tremor

Discussion

This is cheating, because kinetic tremor and hypotonia are difficult to test without involving the limbs.

Walker, in the below-linked book chapter, identifies the following signs:

• Titubation
• Resting tremor of the trunk
• Trunkal ataxia
• Nystagmus
• Ocular dysmetria (the eyes overshooting the target of their gaze)
• Impaired smooth tracking of gaze
• Stacatto speech
• Dysarthria (ataxia of speech)

Walker, Henry Kenneth, Wilbur Dallas Hall, and John Willis Hurst. Clinical Methods: The History, Physical, and Laboratory Examinations. Chapter 69, by Kenneth Walker. Butterworths, 1990.

College Answer

1. New onset seizures
2. Immunocompromised state
3. Moderate to severe impaired level of consciousness
4. Focal neurological signs (signs suspicious of a space occupying lesion)

Discussion

The question is really asking, "what are the features of increased intracranial pressure in the presence of a space-occupying lesion?"

• Hypertension and bradycardia
• Focal neurological signs
• Decreased level of consciousness
• No previous history of epilepsy
• Predisposition to infection (eg. immunocompromised state)
• Papilloedema
• History of stroke or intracranial space-occupying lesion

Clinical features of increased intracranial pressure, specifically referring to patients with meningitis, are discussed elsewehere. The References section below contains a single article on this topic, well worth reading. The most important feature of it - Tabel 2 - is reproduced below to simplify revision.

Tunkel, Allan R., et al. "Practice guidelines for the management of bacterial meningitis." Clinical infectious diseases 39.9 (2004): 1267-1284.

College Answer

29.1     Define delirium.

A disturbance of consciousness with inattention accompanied by a change in cognition or perceptual disturbance that develops over a short period of time and fluctuates over time. DSM4. Inattention is one of the hallmarks and pivotal features of delirium.

29.2     What is the prevalence of delirium in the critically ill?

Reported as being greater that 8 out of 10 (An answer suggesting that it is highly prevalent should get some credit.

29.3     What is its prognostic significance?

The presence of delirium has been assoc with increased mortality, prolonged ICU and hospital stay, greater dependency on community services and care on discharge and higher nursing home placement rates.

29.4     Briefly outline how you will manage delirium in the critically ill patient.

Treatment of Delirium (marks) – Early recognition
Identify etiology (metabolic, infective, drugs, drug withdrawal,alcohol etc) and treat this

Non Pharmacologic treatment i.e. recurrent orientation of patients, early mobilization, early removal of catheters etc
Pharmacologic- 
Benzodiazepines Thiamine Haloperidol
decrease analgesics sedatives and anticholinergic drugs. NOTE there are NO FDA drugs approved for the treatment of delirium.

Discussion

Delirium is discussed in greater detail elsewhere ("Delirium in the ICU").

It is also covered in some depth in the answer to Question 6 from the second paper of 2013, "Define delirium and describe your management approach to this problem in the ICU. "

However, prevalence and prognostic significance are not discussed in the 2013 paper.

Thus:

Prevalence of delirium in the ICU

"An answer suggesting that it is highly prevalent should get some credit." Indeed, recent publicationsquote a figure of 32-77%.

Prognostic significance of delirium in the ICU

The 2004 Ely prospective cohort study gets brought out whenever anybody talks about the prognostic significance of delirium in the ICU. There are many others. In summary, their findings were as follows:

• Mortality at 6 months: increases × 3.2
• Length of hospital stay doubles
• Every additional day of delirium increases the hazard of deatha t 1 year by about 10%.
• Increased risk of cognitive impairment in the long term (in ~ 70%)

Cavallazzi, Rodrigo, Mohamed Saad, and Paul E. Marik. "Delirium in the ICU: an overview." Ann Intensive Care 2.1 (2012): 49.

Ely, E. Wesley, et al. "Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit." Jama 291.14 (2004): 1753-1762.

College Answer

Discussion

This question closely resembles Question 14.1 from the first paper of 2013.

This college answer is slightly different, and better organised.

Chapter   57   (pp. 617)  Neuromuscular  diseases  in  intensive  care by George  Skowronski  and  Manoj  K  Saxena

UpToDate: An approach to the patient with muscle weakness

Young, G. Bryan, and Robert R. Hammond. "A stronger approach to weakness in the intensive care unit." Critical care 8.6 (2004): 416.

College Answer

Discussion

The college table is fairly comprehensive. One cannot add very much to this list of advantages and disadvantages.

A discussion of EVDs and the indications/contraindications of ICP monitoring can be found here:

• Methods of intracranial pressure monitoring
• Indications for intracranial pressure monitoring
• Interpretation of intracranial pressure waveforms
• Correlation of ICP waveforms with intracranial pathology

Specifically, methods of ICP monitoring are discussed, and a table similar to the above is constructed on the basis of published data. This table is reproduced below:

Brean, A., P. K. Eide, and Audun Stubhaug. "Comparison of intracranial pressure measured simultaneously within the brain parenchyma and cerebral ventricles." Journal of clinical monitoring and computing 20.6 (2006): 411-414.

Raboel, P. H., et al. "Intracranial pressure monitoring: invasive versus non-invasive methods—a review." Critical care research and practice 2012 (2012).

Lozier, Alan P., et al. "Ventriculostomy-related infections: a critical review of the literature." Neurosurgery 51.1 (2002): 170-182.

Saladino, Andrea, et al. "Malplacement of ventricular catheters by neurosurgeons: a single institution experience." Neurocritical care 10.2 (2009): 248-252.

Bekar, A., et al. "Risk factors and complications of intracranial pressure monitoring with a fiberoptic device." Journal of Clinical Neuroscience 16.2 (2009): 236-240.

Khan, S. H., et al. "Comparison of percutaneous ventriculostomies and intraparenchymal monitor: a retrospective evaluation of 156 patients."Intracranial Pressure and Neuromonitoring in Brain Injury. Springer Vienna, 1998. 50-52.

College Answer

27.1.   List the differential diagnoses for her confusion and temperature.

Pregnancy related: Eclampsia / preeclampsia / HELLP, Retained products with sepsis, Sheehan’s syndrome / pituitary apoplexy, Posterior reversible encephalopathy syndrome (PRES), Hypertensive encephalopathy

Primary  neurological:  Infection  (meningitis  /  encephalitis),  cerebral  venous  thrombosis, seizure disorder, other cerebro-vascular

Metabolic: Sodium (hypo/hyper), Glucose (hypo/hyper), Renal failure, Liver failure (HCV / Paracetamol / Antidepressants),

Drugs: Accidental / intentional overdose, drug reactions (serotonin syndrome) Infection: Uterine, intracranial, other (renal, chest etc)

27.2.   Outline your approach to establishing the diagnosis.

History:  Collateral,  Pregnancy  issues,  Ongoing  blood  loss,  bleeding  /  bruising,  drug ingestions, mood / affect, headaches

Examination:  BP,  uterine  size  /  discharge,  oedema,  meningism,  neurological  (tone, reflexes, symmetry), chronic liver disease

Investigations: 
FBC: Bleeding, platelets, WCC
UEC: urea / creatinine, Na, Ca, glucose
Coagulation: DIC, INR for CLD
LFT / Ammonia: hepatic encephalopathy, drug reactions
ABG: hypoxia / hypercarbia
Urinary drug screen / paracetamol level
Sepsis Screen, CT head +/- LP

Discussion

The college have presented a high quality systematic answer.

One can generate no better differentials for this decreased level of consciousness. They even included cerebral venous thrombosis.

The history is rich in possibilities.

Vascular causes:

• cerebral venous thrombosis
• PRES
• Hypertensive encephalopathy

Infectious causes

• Sepsis due to retained products
• Meningitis / encephalitis

Neurological causes

• Seizures (potentiated by tramadol)
• Serotonin syndrome

Drug related

• Intoxication

Autoimmune

• Cerebral vasculitis

Traumatic

• Head injury

Endocrine/metabolic/electrolyte related

• Hyponatremia
• Hypoglycaemia
• Hepatic encephalopathy (HELLP)
• Uremia

A genric approach to the unconscious patient in the ICU  is available locally.

College Answer

a)  What  is the most likely explanation  for the polyuria?  Give the reasoning behind your answer.

Mannitol therapy

There is increased measured plasma osmolality with an elevated osmolar gap. The gap is 44 mosmol/kg, if we use a calculated osmolality of 1.86 × ([Na] + [K]) + [urea]
+ [glucose]. If we use the simple formula of 2 × [Na] + [urea] + [glucose] for
calculated osmolality, the gap is 32 mosmol/kg. (There are also other formulae which are more difficult to remember). In the setting of treatment for an exacerbation of intracranial hypertension, the increased osmolar gap is likely to be due to mannitol administration. The high urinary osmolality rules out diabetes insipidus, and supports the diagnosis of mannitol induced polyuria

Discussion

This question is identical to Question 22.1 from the second paper of 2011, and Question 3 from the second paper of 2007 (which contains an answer with a more complete interpretation of this issue).

College Answer

b)  List the major determinants of prognosis in traumatic brain injury.

Prognostic determinants:

•    Age > 60
•    Pupillary abnormalities
•    Presence of hypotension and hypoxia
•    Low GCS on presentation
•    CT scan abnormalities – intracranial collections, presence of traumatic subarachnoid haemorrhage
•     Co-morbidities

Discussion

Part a) of this question (Question 3.1) was a more electrolyte-based question: "What  is the most likely explanation  for the polyuria?  Give the reasoning behind your answer."

The answer to the question about prognosis of traumatic brain injury can be found in the Brain Trauma Foundation's document on the Early Indicators of Prognosis in Severe Traumatic Brain Injury .

• Age > 60 (poor outcome risk increases by 20-30%)
• Pupillary abnormalities (70-90% mortality with bilaterally absent light reflex)
• Presence of hypotension (doubles mortality)
• Presence of hypoxia (doubles the likelihood of a poor neurological outcome)
• Low GCS on presentation (65% mortality if the GCS is 3)
• CT scan abnormalities (absence of abnormalities equates to a better prognosis)
• Co-morbidities

This is discussed in greater detail in "Prognosis in severe brain injury" from the Required Reading section.

Chesnut, R. M., et al. "Part 2: Early indicators of prognosis in severe traumatic brain injury." Journal of Neurotrauma 17.6-7 (2000): 555-+.

Fearnside, Michael R., et al. "The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre-hospital, clinical and CT variables." British journal of neurosurgery 7.3 (1993): 267-279.

Oddo, Mauro, et al. "Brain hypoxia is associated with short-term outcome after severe traumatic brain injury independently of intracranial hypertension and low cerebral perfusion pressure." Neurosurgery 69.5 (2011): 1037-1045.

McHugh, Gillian S., et al. "Prognostic value of secondary insults in traumatic brain injury: results from the IMPACT study." Journal of neurotrauma 24.2 (2007): 287-293.

Collaborators, MRC CRASH Trial, et al. "Predicting outcome after traumatic brain injury: practical prognostic models based on large cohort of international patients." bmj 336.7641 (2008): 425-9.

Stevens, Robert D., and Raoul Sutter. "Prognosis in severe brain injury." Critical care medicine 41.4 (2013): 1104-1123.

Steyerberg, Ewout W., et al. "Predicting outcome after traumatic brain injury: development and international validation of prognostic scores based on admission characteristics." PLoS medicine 5.8 (2008): e165.

Lingsma, Hester F., et al. "Early prognosis in traumatic brain injury: from prophecies to predictions." The Lancet Neurology 9.5 (2010): 543-554.

Utomo, Wesley K., et al. "Predictors of in-hospital mortality and 6-month functional outcomes in older adults after moderate to severe traumatic brain injury." Injury 40.9 (2009): 973-977.

Holcomb, Erin M., Scott R. Millis, and Robin A. Hanks. "Comorbid Disease in Persons With Traumatic Brain Injury: Descriptive Findings Using the Modified Cumulative Illness Rating Scale." Archives of physical medicine and rehabilitation 93.8 (2012): 1338-1342.

College Answer

List 4 clinical signs of intracranial hypertension.

•    Unilateral or bilateral papilledema
•    Unilateral or bilateral papillary dilatation
•    Impaired conscious state
•     Bradycardia

Discussion

Little can be added to this answer.

In the section on the methods of monitoring intracranial pressure, one can find this table:

There, one can also find extensive digressions on the advantages and disadvantages of using these clinical signs instead of waveform-generating piezoelectric devices.

However, the college did not ask for that.

College Answer

With regard to the EEG:

a) List three indications for the use of the EEG in a critically ill patient

•    Detection of non convulsive seizures and characterization  of spells in patients with altered mental status with: (A history of epilepsy, Fluctuating level of consciousness, Acute brain injury, Recent convulsive  status epilepticus,  Stereotyped  activity such as  paroxysmal   movements,   nystagmus,   twitching,   jerking,   hippus,   autonomic variability)
•    Monitoring  of ongoing therapy: Induced coma for elevated intracranial  pressure or refractory status epilepticus, Assessing level of sedation
•    Prognosis: Following cardiac arrest, acute brain injury

b) What are the clinical implications  of non-convulsive  status epilepticus (NCSE) in the critically ill patient?

An underdiagnosed entity.

In several studies, the presence of NCSE and delay to diagnosis and treatment were each associated with significantly more frequent mortality. Periodic epileptiform discharges (PED) have  also  been  associated  with  a  significant  increase  in  death  or  severe  disability  at hospital discharge in particular in neurologic disease/injury. NCSE may also occur in those without  primary  brain  injury  e.g.  sepsis  and  conveys  the  same  prognosis.  Aggressive treatment as for convulsive status epilepticus is recommended.

c) List two EEG patterns that may be seen after hypoxic brain injury thought to be associated with a poor prognosis.

Note: none of these patterns are specific for death or poor outcome and must be regarded along with clinical assessment.
•    Generalised suppression/isoeletric
•    Generalised burst suppression especially if accompanied by epileptiform activity
•    Epileptiform and generalised periodic discharges, especially myoclonus
•    Alpha pattern coma

Discussion

a) This answer comes from Box 49.2 in Oh's Manual (page 556).

• Confirmation of non-convulsive status epilepticus
• Continuous monitoring of general anaesthetic infusion for status epilepticus
• Confirmation of brain death or prognosis of hypoxic/ischaemic brain injury

b)

• Brain injury (excitotoxicity) could occur due to unrecognised seizures
• Cerebral metabolic rate may be higher, and cerebral metabolic demand may not be met if the NCSE is not recognised and treated, giving rise to ischaemia
• NCSE patients have a poorer prognosis than patients with a disorder of consciousness from other causes
• The underlying cause of NSCE is the most important prognostic factor

c) Again, the same box in Ohs Manual has the answers. Severe hypoxic encephalopathy is associated with the following EEG features:

• Presence of theta activity
• Diffuse slowing
• Burst suppression
• Alpha coma

Oh's Intensive Care manual: Chapter 49   (pp. 549) Disorders  of  consciousness  by Balasubramanian  Venkatesh

College Answer

a) List three likely anatomical sites of lesions that can result in these eye signs

Any three anatomical sites of the lesion:
•    Hemispheric lesion (hemispherectomy, massive hemispheric CVA, thalamic CVA)
•    Brainstem   lesion   (brainstem   infarct,   multiple   sclerosis,   brainstem   tumour   or encephalitis)
•    Central cord lesion (syringomyelia, glioma, ependymoma, traumatic)
•    T1 root  lesion  (Pancoast  tumour,  cervical  rib, brachial  plexus  avulsion,  aortic  or subclavian aneurysm
•    Sympathetic  chain  (laryngeal,  pharyngeal,  thyroid  or  parathyroid  surgery,  carotid artery lesion, malignancy at base of skull)

b) Give two associated  clinical  features  that would  help determine  the site of the lesion?

Any two of:
•    distribution of loss of sweating
•    distribution of loss of pain and temperature sensation
•    motor deficit
•    signs of central cord syndrome

•    wasting of small muscles of hand and clubbing
•    cervical LNs
•    Signs of head / neck surgery/trauma
•    Subclavian artery bruit

Discussion

This question is well revised from Table 10-12 of the most recent edition of Talley and O'Connor, which I have fancifully reinterpreted below:

In brief, one could answer the question in the following manner:

a) three likely anatomical sites of lesions:

• Cortical hemisphere (eg. stroke or tumour)
• Brainstem (eg. stroke or tumour)
• Brachial plexus (eg. pancoast tumour)

b) two associated  clinical  features  that would  help determine the site:

• Contralateral hemiparesis (cortical hemisphere or brainstem infarct)
• Brainstem nuclei signs (diplopia, vertigo, ataxia)
• Brachial plexus signs (eg. arm pain or weakness, small muscle wasting)

This could be really over-done. For example, in the cranial nerves section, there is a much longer list:

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where.

College Answer

a) Name the neurological structures involved in the reflex being tested

•    VIII nerve and vestibular nucleus
•    III and VI nerves and nuclei
•    Median longitudinal fasciculus

b)  What  does  the  result  shown  in  the  illustrations  suggest  about  the  cause  of unconsciousness?

The cause is unlikely to be due to an anatomical  lesion affecting  the reticular  activating system (Brain stem function is still present)

Discussion

The reflex arc for this physical sign can be found in Fetter's 2007 review article.

a) The vestibulocochlear nerve, the brainstem nuclei of the vestibulocochlear nerve, the fibers to the cerebellum, the fibers from the cerebellum, the medial longitudinal fasciculus (MLF) and the 3rd and 6th cranial nerves.

b) The cause of the unconsciousness in a patient with a negative  oculocephalic reflex is some sort of destructive brainstem pathology or brain death.

A positive oculocephalic reflex is a good sign. In an intubated patient with comically huge eyeballs, it should look like this:

The pathways which command this reflex involve vestibular nuclei, lower pontine tegmentum, the upper pontine tegmentum, the midbrain paramedian tegmentum, and the medial longitudinal fasciculus. These are large, central brainstem regions, which overlap with the ascending arousal system. Thus, it would be highly unlikely that a structural lesion of some sort (like a stroke) has taken out the rest of the brainstem, leaving these regions intact.

In other words, if the oculocephalic reflex is intact, the coma is unlikely due to a structural brainstem lesion.

A more detailed overview of this reflex can be found at LITFL's page on the examination of the unconscious patient. Plum and Posner, on page 66 of their famous textbook (4th edition), include a well known diagram of lesions at different levels and their associated findings on oculocephalic and caloric testing, and the image from the college question has been ..borrowed ... from there.

Nathanson, Morton, Philip S. Bergman, and Paul J. Anderson. "Significance of oculocephalic and caloric responses in the unconscious patient." Neurology7.12 (1957): 829-829.

Fetter, Michael. "Vestibulo-ocular reflex." (2007): in: Developments in Ophthalmology, Vol.40 (ed: A.Straube and U.Buttner), Karger 35-51.

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where.

College Answer

Activate the stroke team if available in this hospital as urgent intervention is needed for the best
potential outcome – involves neurologist and interventional neuroradiologist.

Attention to ABC (confirm tube position, adequacy of ventilation, control hypertension and treat
hypotension to ensure adequate CPP)

Investigations / Interventions
• CT scan to exclude bleed and confirm diagnosis – can miss post fossa and brainstem lesions
in the early stages so MRA may be indicated
• Interventional cerebral angiography and thrombectomy if within time window and facilities and
resources available.
• Thrombolysis with tPA within 4.5 hours of event if intervention unavailable or unsuccessful
• Heparin infusion
• Aspirin

Physiological monitoring and maintenance of normal parameters (BP, Na, BSL etc)

Role of EVD if hydrocephalus is present

Ongoing neurological assessment – at risk of progressing to locked in syndrome

Supportive care of the intubated ventilated critically ill patient

Discussion with family re therapy and outlook plus risk factors for poor outcome

Discussion

This question does not seem to stem from any specific guidelines.The college is asking what one might do with a brainstem stroke; in order to pass the candidate needs to

• demonstrate that they understand the importance of early thrombolysis
• know about the role of interventional neuroradiology in stroke
• appreciate the need to exclude intracranial haemorrhage, and the limitations of CT in posterior fossa lesions
• know how to manage stroke if neither thrombolysis nor clot retrieval is possible
• appreciate the possibility of hydrocephalus developing with posterior fossa strokes
• appreciate the prognosis of such a stroke, and the need to manage family expectations.

A detailed discussion of the definitive management options in acute stroke is available elsewhere.

Supportive management of acute stroke is also covered in a summary article.

If one were to summarise in brief the approach to management here, it would resemble this:

Definitive management option:

• Intravenous thrombolysis
• Intraarterial thrombolysis
• Endovascular embolectomy
• Conservative management and subsequent antiplatelet therapy

Supportive management:

• Airway: intubation, for the protection thereof (being mindful that it may be futile)
• Ventilation: aiming for normocapnea
• Circulatory support: to keep BP normal, and below 220 mmHg systolic
• Sedation: as needed to tolerate ICU management in comfort
• Electrolyte and endocrine control: ensuring normoglycaemia and normothermia
• Fluid balance management to ensure protection of renal function following contrast
• Enteric nutrition may commence by the nasogastric route
• Heparin is not indicated given the risk of haemorrhagic transformation*
• Antibiotic therapy if contaminated aspiration is suspected

* It should be pointed out that though the college (writing in 2011) suggest the use of a heparin infusion, this strategy has already fallen out of favour by this stage, given that it seems to kill people. Certainly, the 2007 AHA guidelines were not in favour of its use.

Regarding early thrombolysis:

Wardlaw JM, Zoppo G, Yamaguchi T, Berge E. Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev. 2003;(3):CD000213.

The Stroke Foundation guidelines for management of acute stroke

Regarding early cerebral angiography and thrombectomy:

The Stroke Foundation guidelines dont actually recommend mechanical clot retrieval ("insufficient evidence", they say) but they do recommend intra-arterial thrombolysis, and the reference they give is the 2009 update of the Wardlaw meta-analysis mentioned above.

Regarding the need to exclude intracranial haemorrhage:

The need itself does not require references - it is common sense. CT or MRI? Here is a Cochrane review; diffusion-weighted imaging seems to be more sensitive in detecting ischaemic stroke.

Brazzelli M, Sandercock PA, Chappell FM, Celani MG, Righetti E, Arestis N, Wardlaw JM, Deeks JJ. Magnetic resonance imaging versus computed tomography for detection of acute vascular lesions in patients presenting with stroke symptoms. Cochrane Database Syst Rev. 2009 Oct 7;(4):CD007424. doi: 10.1002/14651858.CD007424.pub2.

Regarding antiplatelet agents and anticoagulation:

Again, the Stroke Foundation guidelines for management of acute stroke recommend aspirin and hemaprin in patients who definitely have no haemorrhage.

Regarding the possibility of hydrocephalus

I have not found any literature about the actual risk of this happening with undifferentiated posterior fossa lesions, but cerebellar infarction stands out as the leading culprit:

Hornig CR, Rust DS, Busse O, Jauss M, Laun A. Space-occupying cerebellar infarction. Clinical course and prognosis. Stroke. 1994 Feb;25(2):372-4.

Regarding the prognosis of brainstem stroke:

There is a good (though dated) article regarding the prognosis of stoke in the ICU. Sensibly, it seems older patients and those in a coma on admission have the poorest prognosis.

Steiner T, Mendoza G, De Georgia M, Schellinger P, Holle R, Hacke W.Prognosis of stroke patients requiring mechanical ventilation in a neurological critical care unit. Stroke. 1997 Apr;28(4):711-5.

Regarding the danger of heparin infusion:

Adams, Harold P., et al. "Guidelines for the Early Management of Adults With Ischemic Stroke " Circulation 115.20 (2007): e478-e534.

College Answer

a)  What is the most likely explanation for the polyuria?

Mannitol therapy

b)  Give your reasoning.

Increased measured plasma osmolality with an elevated osmolar gap - 32 mOsm/kg with formula (2xNa + glucose + urea) or 44 mOsm/kg with 1.86 x (Na+K) + urea + glucose. High urinary osmolality rules out diabetes insipidus. History supports osmotherapy to treat episode of raised ICP

Discussion

This question is identical to Question 3.1 from the second paper of 2010, and Question 3 from the second paper of 2007 (which contains an answer with a more complete interpretation of this issue).

College Answer

• Nystagmus
• Titubation
• Staccato speech
• Skew deviation of the eyes
• Impairment of finger-nose test

Discussion

This question interrogates one's knowledge of the highly regarded Talley and O'Connor manual of physical examination.

Talley and O'Connor visits the cerebellum twice, once in the chapter on the neurological examination of the head, and once in the discussion of "Correlation of physical signs and neurological disease". Neither time is there discussion of what specifically to look for in the patient's head. Its just not that specific.

Similarly, L.I.G Wortheley in the 3rd edition of CECIP (Clinical Examination of the Critically Ill Patient) makes mention of the cerebellum, but does not actually go through it in quite such a fashion.

So, where does one go for a thorough summary of what one can expect from a cerebellum-damaged head?

It seems, nowhere.*

Thankfully, from our medical school days, it seems about 84% of us can remember at least a few of the cerebellar signs. But, in searching for the specific signs mentioned by the college, I came across something. A website by the Coopers. ** These seem to be a couple who have moved from Australia to Ohio. This, in a deliciously unexplained twist, is completely irrelevant to the extravagant and all-encompassing mass of neurological examination material which abounds on their site. I have taken the liberty of linking to some of the documents they host.

Bob and Christina Cooper, I salute you.

* Several years after writing this rant, I have discovered a venerable document from 1990, available for free for all to read, which conveniently divides the cerebellar examination into body regions. This resource has subsequently given rise to a locally available summary of cerebellar physical signs and examination technique. The obsolete rant still remains in situ for structural reasons. - AY.(2015)

** That Coopers website is now down. http://www.hy-q.com/ now sends you to something completely unlike the cranial nerves. I believe it now belong to the manufacturer of industrial sensors. At this  stage, the whereabouts of the Coopers are unknown. Their site can still be seen by accessing the archived copy on the Wayback Machine Internet Archive, where some of the PDF documents are still preserved. - AY.(2018)

Schmahmann JD (2004). "Disorders of the cerebellum: ataxia, dysmetria of thought, and the cerebellar cognitive affective syndrome". J Neuropsychiatry Clin Neurosci 16 (3): 367–78

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where.

My own gibberish notes from medical school.

Walker, H. Kenneth, W. Dallas Hall, and J. Willis Hurst. "The Neurologic System." (1990). Specifically: Chapter 69, "The Cerebellum"

College Answer

Right side of the midbrain. It is a crossed hemiplegia suggesting a brainstem stroke and the 3rd nerve nucleus is located in the midbrain.

Discussion

This question interrogates one's knowledge of the highly regarded Talley and O'Connor manual of physical examination.

Let us reason through this. A left hemiparesis suggests right sided cerebral pathology.

A right sided unreactive pupil suggests that the third nerve is somehow involved, and the nucleus for it is in the midbrain. Ergo, the right midbrain has infarcted. The hemiparesis reflects damage to the right-sided motor tracts above the level of the decussation (which is at the medulla).

The Internet Stroke Centre has an excellent summary of stroke syndromes.

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired wherever good books are sold or stolen.

College Answer

a) If the ICP is refractory to your initial management of sedation, paralysis and correct
positioning, what further measures will you consider and why?

• Ensure EVD patent and CSF draining (reduce CSF component of ICP)
• Measures to maintain CPP > 60 mmHg
  • Fluids (avoid albumin – SAFE TBI)
  • Vasopressors
• Repeat CT scan to exclude a new mass lesion
• Osmotherapy (hypertonic saline or mannitol)
  • Goal Na+ 150, Osm 300-320
• Consider barbiturates or propofol (decrease CMRO2)
• Consider continuous paralysis (decrease CMRO2)
• Consider moderate hypothermia (decrease CMRO2 and potentially neuroprotective)
  • Adverse outcome in paediatric TBI RCT from CCCTG
  • McIntyre MA suggesting titrated to ICP and prolonged duration may be beneficial
  • Ongoing trials including POLAR in ANZ
• Decompressive craniotomy is contentious
  • DECRA showed decreased ICP and reduced ICU length of stay but no mortality benefit and a greater number of patients with an unfavourable neurological outcome in those who received decompressive craniectomy.
  • Patients with mass lesions (unless too small to require surgery) were excluded so this patient may not have been included in the study.
  • Only a single surgical intervention was used.

b) What are the risk factors for post-traumatic seizures in patients with traumatic brain injury?

• GCS < 10
• Cortical contusion
• Depressed skull fracture
• Subdural, epidural or intracerebral haematoma
• Penetrating head wound
• Seizure within 24 hours of injury

Discussion

This question interrogates the candidate's familiarity with the more outré methods of decreasing a person's intracranial pressure.

Lets face it, anybody can sedate, paralyse and position the patient. Those measures are basic.

a)What further measures will you consider and why?

The Brain Trauma Organisation Guidelines for Management Traumatic Brain Injury contain a set of guidelines, which I have mindlessly parroted here.

Ultimately, there is an escalating series of management strategies which are standard for this scenario.

b) The risk factors for post-traumatic seizures

This answer was taken directly from the Brain Trauma Organisation Guidelines for Management Traumatic Brain Injury. Word for word, in fact; copy and paste. See it here.

I will reproduce them here for ease of reference;

• Glasgow Coma Scale (GCS) Score < 10
• Cortical contusion
• Depressed skull fracture
• Subdural hematoma
• Epidural hematoma
• Intracerebral hematoma
• Penetrating head wound
• Seizure within 24 h of injury

I should probably also digress for a moment to discuss the duration of seizure prophylaxis (the Brain Trauma Foundation recommends no more than 1 week). Post-traumatic seizure management is well covered elsewhere.

Oh's Intensive Care manual:

Chapter 43 (pp. 563) Cerebral protection by Victoria Heaviside and Michelle Hayes, and

Chapter 67 (pp. 765) Severe head injury by John A Myburgh.

Brain Trauma Organisation Guidelines for Management Traumatic Brain Injury is the definitive source.

College Answer

General introduction

The GCS is a neurological scoring system used to assess conscious level after head injury. It is now usually scored out of 15 and is comprised of 3 categories, best eye response, best vocal response and best motor response. It has recently been used to categorise traumatic brain injury into mild, moderate and severe.

Advantages

It is the most widely recognised of all conscious level scoring systems in the world. It is quick and reproducible. It is skewed towards motor score, which is good since this is the most reliable measure of short-term prognosis in TBI. The distinction between a motor score of 2, 3 and 4 is a very useful clinical indicator of the severity of TBI, and the area of brain function that has been affected.

Disadvantages

• It fails to incorporate brain-stem reflexes
• It is unreliable in patients in the middle range of 9-12
• There is poor inter-observer reliability
• It is difficult for untrained staff to apply properly, especially distinguishing between M= 3,4,5
• Variation in scoring V in intubated patients
• M score does not factor in unilateral pathology

Controversy in the literature

• There is little evidence demonstrating validity and reliability of the GCS
• There are numerous other neurological scoring systems that have demonstrated greater validity and reliability e.g. the FOUR score
• Debates within the literature as to when GCS can be first applied after TBI, i.e when is the first post-resuscitation GCS applicable

How I use GCS in my practice.

• A statement of when and how GCS is used in TBI
• An appreciation of the need for all staff on the intensive Care Unit to be aware of the same criteria for its use and application
• An appreciation that on-going education is needed to make sure that it is used correctly

Discussion

The college answer is fairly comprehensive.

A thorough discussion of the advantages and disadvantages of the GCS can be found elsewhere.

It forms a part of the greater topic, the Assessment of the Unconscious Patient.

In brief, the major disadvantages are:

• It was never meant as an assessment tool for trauma.
• It is unreliable in patients in the middle range of 9-12
• People dont know how to use it correctly.
• It has high inter-observer variability
• It is inadequate to assess higher cortical functions.
• It is inadequate to assess brainstem reflexes.
  • Therefore, it cannot be used as a trigger for intubation (GCS of 8)
• The eye score is unreliable if the eyes are damaged.
• The eye score may be meaningless (it is possible to score an E4 even if one is braindead)
• The total score is meaningless:
  • The components are more important individually
  • Depending on the individual component score, the prognosis may be very different for patients with the same total score.
• It is affected by drugs and alcohol.
  • However, it is still used in assessing drug overdose patients.
• It is affected by language barriers
• Intubation makes a mockery of its verbal conponent
• It needs to be modified for use in young children.

The article by Green (2011) is the definitive resource on this topic, as it is a comprehensive review, in spite of being one person's opinion. 

Green, Steven M. "Cheerio, laddie! Bidding farewell to the Glasgow Coma Scale." Annals of emergency medicine 58.5 (2011): 427-430.

Gill, Michelle R., David G. Reiley, and Steven M. Green. "Interrater reliability of Glasgow Coma Scale scores in the emergency department." Annals of emergency medicine 43.2 (2004): 215-223.

Riechers, Ronald G., et al. "Physician knowledge of the glasgow coma scale."Journal of neurotrauma 22.11 (2005): 1327-1334.

College Answer

a) List of differential diagnoses for his weakness

• • Critical illness myopathy / Acute quadriplegic myopathy* (high dose steroids, with or without nondepolarising paralyzing agent use, Beta agonists)

• Critical Illness polyneuropathy/myopathy* (SIRS, sepsis, MODS)
• *Residual sedation and other drug influences (Renal [&/or liver] impairment contributing, aminoglycoside with NMJ effect)

• *Electrolyte abnormalities (PO4, Ca++, K+)
• Deconditioning with weakness exacerbated by subclinical sepsis
• Underlying polyneuropathy/myopathy exacerbated by critical illness Alcohol, B12 deficiency, paraneoplastic, consider diabetic
• GBS
• Rhabdomyolysis (drugs (e.g. statins), infections) should be thought of given renal failure
• acute myelitis or watershed infarction (acute upper motor neuron lesions may not yet have developed hypertonia and hyper-reflexia)
• Autoimmune neuropathy or myopathy (rare)

b) Diagnosis

Any relevant history.

Clinical examination:

• • Normal higher functions and cranial nerves favour a critical illness neuromyopathy (CINM) or a purely peripheral nervous system. Spinal lesion possible although less likely + normal sensory examination
  • Symmetrical features on peripheral neurological exam also favours CINM. Cerebral watershed infarction is possible but less likely given distal power is usually relatively spared.
  • Critical illness myopathy often affects the diaphragm
  • Tendon reflexes are absent or profoundly decreased in neuropathies and decreased in myopathies. They should be essentially normal in de-conditioning or with residual sedative effect.
  • Plantars are unhelpful as they are equivocal
  • Lack of focal neurology or relative sparing of distal motor power (watershed infarction) tends to exclude central causes (eg CVA) or mononeuropathies.]
  • Distribution of weakness is symmetrical in all other causes and tends to be more profound proximally in myopathies, facial involvement tends to occur more in myopathies than in neuropathies (rare exception Miller-Fisher GBS variant).
  • Muscle wasting may be present with myopathies and when there exists a pre-existing myopathy or neuropathy. Muscle fasciculation is uncommon but if present supports a lower motor neuron lesion, severe neuropathy or myopathy.

Investigations:

• • Check biochem and ABGs (U&E’s, LFT’s – espy K, PO4, Ca, Mg, pH, PaCO2), FBE and inflammatory markers, Vit D and Gentamicin level
  • Review cultures and sensitivities and abx used to determine the possibility of ongoing or resistant infection.
  • CK – timing of test to be considered (Best done in first 7 days of illness – if not performed add test to previous blood samples - Elevated in myopathies
  • Nerve conduction studies and Electromyographic studies help support diagnoses of neuropathy and myopathy (vs severe deconditioning or central causes)
  • CSF analysis (GBS), may be required .
  • Muscle Biopsy may be required.
  • MRI if central cause suspected or NCS and EMG don’t support CINM

Discussion

The college answer is extensive and covers the territory well.

For revision purposes, several chapters exist locally:

• Ch.5.5.1 - Approach to the ICU patient with generalised weakness
• Ch.5.5.2 - Features that distinguish myopathy from neuropathy
• Ch.5.5.3 - Intensive Care for Guillain-Barre Syndrome
• Ch.5.5.4 - Critical illness polyneuromyopathy
• Ch.5.5.5 - Features that distinguish Guillain-Barre syndrome from critical illness polyneuromyopathy

From the above resources (specifically, from the table in chapter 5.5.1) I will pick some relevant conditions and put them in a sensible pattern to assist their recollection:

Differential diagnosis for weakness:

• Central:
  • Spinal or brainstem ischaemia (unlikely)
• Peripheral nerve:
  • Autoimmune polyneuropathy, eg. Guillain-Barre syndrome
  • Criticial illness neuromyopathy
  • Nutritional polyneuropathy, eg. B12 deficiency
• Neuromuscular junction
  • Myasthenia gravis (unlikely)
  • Aminoglycoside-induced weakness (in association with neuromuscular junction blockers)
• Muscle
  • Atophy due to prolonged ICU stay, hypercatabolic state and malnutrition
  • Criticial illness neuromyopathy
  • Steroid myopathy
  • Electrolyte derangement, eg. hypophosphataemia, hypocalcemia, hypermagnesemia or hypokalemia

Clinical examination

• GCS (brainstem-damaged or "locked in" syndrome)
• Gross bilateral power (looking for symmetry, distal sparing, lateralising motor feature)
• Cranial nerve examination (Normal cranial nerves suggest a purely peripheral problem)
• Tendon reflexes (absent in neuropathies, decreased in myopathies)
• Fatiguability (Myasthenia gravis vs. "reverse" fatiguability with Lambert-Eaton syndrome)

A panel of investigations:

• Electrolyte levels
• CK level
• B12 level
• Inflammatory markers
• Lumbar puncture
• Nerve conduction studies
• Electromyography
• MRI of the brainstem and spine
• Muscle biopsy if no satisfactory explanation is found.

Oh's Intensive Care manual:

Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer

Chapter   57   (pp. 617)  Neuromuscular  diseases  in  intensive  care by George  Skowronski  and  Manoj  K  Saxena

Yuki, Nobuhiro, and Hans-Peter Hartung. "Guillain–Barré syndrome." New England Journal of Medicine 366.24 (2012): 2294-2304.

Jani, Charu. "Critical Illness Neuropathy." Medicine (2011): 237.

Young, G. Bryan, and Robert R. Hammond. "A stronger approach to weakness in the intensive care unit." Critical care 8.6 (2004): 416.

College Answer

• a) Retinal Haemorrhage (Coagulopathy, thrombocytopenia)
• b) Papilloedema (Raised intracranial pressure)
• c) Optic disc swelling, retinal haemorrhages and infarcts or cotton wool spots. (Malignant Hypertension)

Discussion

This is a bog-standard pattern recognition question.

I need to point out that the image in a) is one of branch retinal vein occlusion - it just so happens that it also features retinal haemorrhage.

Common fundoscopy findings are discussed with (slightly) more detail in the relevant Required Reading section.

The Stanford School of Medicine has an excellent resource on fundoscopy.

So does Walker's Clinical Methods (3rd ed, 1990) - the chapter on fundoscopy is particularly good for pathophysiological correlations.

College Answer

Definition:

Change in behaviour and or mental processes from baseline associated with continuous epileptiform EEG changes but without major motor signs. NCSE comprises a group of syndromes with a wide range of response to anti-convulsants from virtually self-limiting forms to refractory forms. No universally accepted definition yet exists

Difficulties in Diagnosis:

Little agreement on diagnostic criteria, clinical forms, consequences and treatment Difficulty telling when coma is due to ictal symptomatology and differentiating it from non ictal symptoms associated with underlying pathology such as posthypoxic, metabolic or septic encephalopathies and effects of sedative drugs.

On EEG there are cross over features between epilepsy and encephalopathies which are being still standardized and the diagnosis of NCSE should not be on EEG changes alone.

Early recognition and treatment are essential to optimize response to treatment and to prevent neurological and systemic sequelae. However overdiagnosis and aggressive use of anticonvulsants may also contribute to morbidity and mortality.

Risk factors:

• Systemic infection in patient with pre-existing epilepsy
• Stroke including intracerebral & subarachnoid haemorrhages
• Dementia 
• Neoplasia
• Previous neurosurgery
• Patients with pre-existing epilepsy have a lower mortality (3%) than where NCSE is due to acute medical disorders (27%).

Management: 

• Difficulties in diagnosis as outlined above
• Index of suspicion in patients with risk factors and suggestive clinical features

Investigations

• Blood tests to exclude electrolyte abnormalities (low Ca, low Mg), liver and renal dysfunction, haematological causes (e.g TTP) 
• Lumbar puncture: looking for CNS infection
• EEG and response on EEG and clinically to Benzodiazepines
• MRI to exclude structural cause not evident on CT

Treatment

• Treatment of underlying cause Benzodiazepines: Diazepam or Lorazepam
• Valproate: if failure to respond to benzodiazepines
• Keppra increasingly used
• Reversal of factors that lower seizure threshold eg drugs such as cefepime, fever, hypoxia, hypoglycaemia, hyponatraemia

Discussion

Non-convulsive status epilepticus comes up often enough to merit its own little summary page.

a)

The diagnosis of non-convulsive status epilepticus requires the following:

• A change in behaviour or responsiveness
• A duration of change for longer than 30 minutes
• No obvious seizure activity
• Epileptiform discharges on EEG

b)

The difficulty in making the diagnosis is the protean nature of its manifestations, which range from confusion and delirium to unconsciousness. As there are numerous pathologies which are more common and which can present in this way, the diagnosis (by EEG confirmation) is frequently delayed.

c)

Risk factors for non-convulsive status epilepticus are similar to the risk factors for epilepsy in general, and include:

• Structural brain disease:
  • Stroke
  • Space occupying lesion (blood, pus or tumour)
  • Gliosis due to previous stroke, brain injury or neurosurgery
  • Dementia
• Metabolic
  • Sepsis in a patient with known epilepsy

d) Approach to management:

• Attention to the ABCS, with management of life-threatening problems simultanous with a rapid focused examination and a brief history
• Supportive management
  • Assessment of the airway, and airway control if appropriate
  • Ventilation support, or supplemental O₂ in the spontaneously breathing patient
  • Circulatory support to ensure normotension
  • Endocrine and metabolic support to ensure correction of electrolyte derangement and control of blood glucose
• Specific management
  • Benzodiazepines: midazolam or lorazepam
  • Anticonvulsants: phenytoin, valproate or levitiracetam

Oh's Intensive Care manual:

Chapter 49   (pp. 549) Disorders  of  consciousness  by Balasubramanian  Venkatesh

Chapter   50   (pp. 560) Status  epilepticus  by Helen  I  Opdam

Fountain, Nathan B. "Status epilepticus: risk factors and complications."Epilepsia 41.s2 (2000): S23-S30.

Meierkord, Hartmut, and Martin Holtkamp. "Non-convulsive status epilepticus in adults: clinical forms and treatment." The Lancet Neurology 6.4 (2007): 329-339.

College Answer

TWO of the following:

Intravenous thrombolysis

The patient is within the suggested time window for thrombolysis and by current guidelines should receive intravenous rtPA. Overall this treatment reduces deaths and dependency but is associated with a risk of potentially fatal intracranial haemorrhage.

Indications include patients with acute ischaemic stroke presenting within the appropriate time window (note to examiners – while initial guidelines suggested a time window of three hours there is data suggesting use up to 4.5 hours may be beneficial)

Contraindications include:

• Stroke or head trauma in previous 3 months
• Intracranial haemorrhage: past or present
• Major surgery in previous 14 days
• GI or urinary tract bleeding in previous 21 days
• MI in previous 3 months
• Non-compressible arterial puncture in previous 7 days
• Persistent severe hypertension
• Active bleeding or acute trauma
• Thrombocytopaenia

Intra-arterial thrombolysis

Although intra-arterial thrombolysis results in higher rates of re-cannulation there is no evidence that it reduces mortality or morbidity. However in patients who have undergone recent surgery (and therefore have a contra-indication to intravenous thrombolysis) or exceed the 6 hour time window for intravenous thrombolysis intra-arterial thrombolysis may be useful

Endovascular Thrombectomy

This technique may be used in large vessel thrombus,especially if recanalisation has not occurred with intravenous thrombolysis, or the patient is outside the time window . It requires specialist expertise that may not be generally available, and carries the risk of vascular damage or dissection with potential worsening of symptoms.

Indications would include ischaemic stroke in a large vessel in patients who have either failed thrombolysis or have a contraindication to it.

Contraindications include:

• Tortuous vessels precluding angiographic access
• Pre exisiting coagulopathy
• Established infarct on imaging
• Contrast allergy

Discussion

In essence, a stroke patient presents well within the timeframe for reperfusion therapy.

Let us tabulate this answer.

The window for thrombolysis seems to be three hours according to the college answer, though  "there is data suggesting use up to 4.5 hours may be beneficial". That probably refers to  Hacke et al (ECLASS III, 2008) who went as late as 4.5 hours post stroke. Modern Australian Stroke Foundation guidelines recommend 4.5 hours as the cut-off on the basis of the meta-analysis articles by Wardlaw et al (2014) and Emerson et al (2014). The MERCI trial investigators managed to get good outcomes even 8 hours post infarct, which is encouraging. However, these outcomes were still poorer than historical controls. 

The issue of acute stroke management is discussed in brief summary elsewhere.

Oh's Intensive Care manual: Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer.

Smith, Wade S., et al. "Safety and efficacy of mechanical embolectomy in acute ischemic stroke results of the MERCI trial." Stroke 36.7 (2005): 1432-1438.

Nogueira, R. G., et al. "Endovascular approaches to acute stroke, part 2: a comprehensive review of studies and trials." American Journal of Neuroradiology30.5 (2009): 859-875.

Brinjikji, Waleed, et al. "Patient outcomes with endovascular embolectomy therapy for acute ischemic stroke a study of the national inpatient sample: 2006 to 2008." Stroke 42.6 (2011): 1648-1652.

Kidwell, Chelsea S., et al. "Design and rationale of the mechanical retrieval and recanalization of stroke clots using embolectomy (mr rescue) trial."International Journal of Stroke 9.1 (2014): 110-116.

Jansen, Olav, et al. "Neurothrombectomy for the treatment of acute ischemic stroke: results from the TREVO study." Cerebrovascular Diseases 36.3 (2013): 218-225.

Furlan, Anthony, et al. "Intra-arterial prourokinase for acute ischemic stroke: the PROACT II study: a randomized controlled trial." Jama 282.21 (1999): 2003-2011.

Sacks, David, et al. "Multisociety consensus quality improvement guidelines for intraarterial catheter‐directed treatment of acute ischemic stroke, from the American Society of Neuroradiology, Canadian Interventional Radiology Association, Cardiovascular and Interventional Radiological Society of Europe, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of NeuroInterventional Surgery, European Society of Minimally Invasive Neurological Therapy, and Society of Vascular and ...." Catheterization and Cardiovascular Interventions 82.2 (2013): E52-E68.

Ogawa, Akira, et al. "Randomized trial of intraarterial infusion of urokinase within 6 hours of middle cerebral artery stroke The Middle Cerebral Artery Embolism Local Fibrinolytic Intervention Trial (MELT) Japan." Stroke 38.10 (2007): 2633-2639.

Hacke, Werner, et al. "Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke." New England Journal of Medicine 359.13 (2008): 1317-1329.

Wardlaw, Joanna M., et al. "Thrombolysis for acute ischaemic stroke." The Cochrane database of systematic reviews 7 (2014): CD000213.

Emberson, Jonathan, et al. "Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials." The Lancet384.9958 (2014): 1929-1935.

College Answer

DCI is a common (occurring in about 30%) and serious complication following SAH. Defined as any neurological deterioration presumed related to ischaemia that persists for more than an hour and cannot be explained by any other physiological abnormalities. It is mostly caused by vasospasm.

May be reversible but may develop into cerebral infarction. Its highest risk of occurrence is from day 3 to 14 after presentation.

Aetiology still poorly understood

Assessment of DCI

Whilst up to 20% of patients can have a cerebral infarct despite being entirely asymptomatic, the mainstay of clinical monitoring is repeated clinical neurological examination.

DSA is the gold standard for vasospasm but as a screening test, multimodal CT imaging with CT perfusion is accurate and less invasive.

Transcranial Doppler has a high specificity but only moderate sensitivity. The other physiological modalities including EEG, brain tissue oxygen monitoring, cerebral microdialysis are less well established as monitoring modalities

Management of DCI

Aim is to prevent or minimise secondary injuries by haemodynamic management, drugs and endovascular procedures.

Haemodynamic strategies

Avoid hypotension. 
Triple H therapy:

1. Induced hypertension improves CBF independent of blood volume. The most common agents used being Norad and phenylepherine. Secure aneurysm first.
2. Hypervolaemia does not offer any benefit over euvolaemia, however it is important to avoid hypovolaemia.

1. There is no place for haemodilution except for people with polycythaemia. Milrinone infusion has been used as alternative to Triple H.

Pharmacological management · Calcium-channel blockers 
The main intervention shown to be beneficial is the use of Nimodipine.

Other CCBs have been shown to reduce vasospasm with beneficial effects on DCI but RCTs still needed.

·  Intra-cisternal thrombolytics

Used in some centres on selected patients · Statins

Evidence is conflicting. Awaiting results of STASH · Magnesium sulphate

MASH-II did not show a benefit compared with placebo · Endothelin-1 antagonists

Recent published studies evaluating clazosentan have shown no clinical benefit

Other agents

E.g. NO donors, EPO, enoxaparin, rho-kinase inhibitor either shown not to be beneficial or still being studied

Endovascular procedures

Angioplasty and/or Intra-arterial vasodilators may be used in addition to nimodipine and haemodynamic management if indicated and expertise available.

Overall optimal triggers for escalating and de-escalating therapy not well defined

Discussion

The discussion of DCI in the college answer is a complete and satisfying summary of the topic.

To make it easier to remember, one can trim some fat.

DCI description:

• Any new neurological deficit
• Occurs on days 3-14
• Can progress to stroke

DCI diagnosis

• Repeat examination is a screening tool with poor sensitivity but little cost.
• DSA is gold standard
• CTA is next best option
• Transcranial Doppler is another option with poor sensitivity

DCI management

• Nimodipine infusion
• Triple H therapy - remains debated;
  • hypertension may not be helpful; at least maintain normotension
  • hypervolemia may not be helpful; at least maintain normovolemia
  • hemodilution is not helpful. Fullstop.
• Intra-arterial vasodilators such as papaverine and verapamil are a good option.

A LITFL review of vasospasm and DCI is a treatment with satisfying levels of detail.

Apocryphal notes on the diagnosis and management of SAH are also available:

• Risk factors for subarachnoid haemorrhage
• Grading of subarachnoid haemorrhage severity
• Monitoring for vasospasm following SAH
• Prevention and management of vasospasm following SAH
• Non-vasospasm complications of SAH
• Management of the unsecured aneurysm in subarachnoid haemorrhage

Oh's Intensive Care manual

Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer

College Answer

b)

• Plasma exchange and IVIG are both better than no therapy in hastening recovery from an episode and are equally effective. No value in both being given routinely.

c)

• - 5% mortality from medical complications in hospital.

• • • Up to 20% of patients are still significantly disabled at 6 months and 15% still have significant functional disability at 1 year.

• • Recurrence rate is 7% with the mean interval between recurrences being 7 years.

• Poor prognosis associated with:

• • Older age

• • Rapid onset (<7days) prior to presentation

• • Severe muscle weakness at presentation

• • Need for mechanical ventilation

• • EMG showing average distal motor response amplitude <20% normal

• • Preceding diarrhoeal illness (proven Campylobacter)

Discussion

The distinctions between GBS and CIPN:

• CIPN is associated with a severe illness, whereas GBS is associated with a mild one.
• CIPN does not have autonomic dysfunction, whereas GBS does.
• CIPN will not have any specific CSF findings, whereas GBS will have raised CSF protein and perhaps even a monocytosis
• CIPN nerve conduction studies will not show any decrease in conduction velocity, whereas in GBS the cardinal feature is decreased conduction velocity.

As for management, Oh's Manual recommends either plasma exchanges or IV immunoglobulin, but there is no benefit in giving both together.

A discussion of the approach to the ICU patient with generalised weakness is available elsewhere.

A generic exam-oriented approach to Guillain Barre syndrome is presented in the "Required Reading" section.

An even better table than the CICM college answer is available in this 2006 article fom Respiratory Care; it is reproduced below.

Oh's Intensive Care manual

Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer

Chapter   57   (pp. 617)  Neuromuscular  diseases  in  intensive  care by George  Skowronski  and  Manoj  K  Saxena

Yuki, Nobuhiro, and Hans-Peter Hartung. "Guillain–Barré syndrome." New England Journal of Medicine 366.24 (2012): 2294-2304.

Jani, Charu. "Critical Illness Neuropathy." Medicine (2011): 237.

Dhand, Upinder K. "Clinical approach to the weak patient in the intensive care unit." Respiratory care 51.9 (2006): 1024-1041.

College Answer

Myopathy

• Wasting is late sign
• Usually proximal weakness
• Reflexes preserved until late
• Normal sensory exam
• May be muscle tenderness

Neuropathy

• Wasting earlier
• May be fasciculations
• Often peripheral distribution
• Loss of reflexes
• May be abnormal sensory exam

Discussion

This comes down to basic common sense.

If the nerves are healthy, and the muscles are to blame,

• The sensory supply should be preserved
• The reflexes should be preserved
• Weakness should be proximal - that is where the bigger muscles are, and the weakness there will be more obvious.
• There should be no fasciculations

Also...

• There may be myocardial involvement (skeletal myopathies tend to be associated with cadiomyopathy)
• The muscles involved may be painful and tender(as in myositis)

This question has been repeated. Its doppelganger, Question 3.1 from the first paper of 2010, has a much better-organised college answer.

Chapter   57   (pp. 617)  Neuromuscular  diseases  in  intensive  care by George  Skowronski  and  Manoj  K  Saxena

UpToDate: An approach to the patient with muscle weakness

Young, G. Bryan, and Robert R. Hammond. "A stronger approach to weakness in the intensive care unit." Critical care 8.6 (2004): 416.

Dhand, Upinder K. "Clinical approach to the weak patient in the intensive care unit." Respiratory care 51.9 (2006): 1024-1041.

College Answer

Ulnar nerve injury

• Look for evidence of local trauma
• Weak finger abduction and adduction, and thumb adduction
• Sensory loss over little finger and medial half of ring finger

Lower brachial plexus

• All intrinsic muscles of hand weak (incl. LOAF muscles)
• Sensory loss over little and ring finger, extending above the wrist, and up medial aspect of arm
• Horner’s syndrome

Discussion

This forces the recall of medical school level neuroanatomy.

Particularly, the supply distribution of the brachial plexus

Thus:

Ulnar nerve palsy would be associated with weakness of only the small muscles of the hand, and of sensory loss over the area supplied by its palmar sensory branch (essentially one-and-a-half fingers worth, over the palm).

A brachial plexus C8-T1 injury - also known as Klumpke's paralysis - would result in a "claw hand", with a supinated foream and flexed fingers. The sensory loss would include the whole ulnar nerve distribution - but also the medial cutaneous nerve of the foream.

Lastly, damage to the nerve roots at C8-T1 will also result in a Horners Syndrome, as the ascending sympathetic supply will be interrupted.

For a reference, I direct the time-rich reader to Sir Sydney Sunderland's "Nerves and Nerve Injuries", from 1968. (Not available as full text in Google, unfortunately.)

For brachial plexus injuries, I recommend Alain Gilbert's book.

For peripheral nerves, there is Haymaker, Webb, and Barnes Woodhall. Peripheral nerve injuries: principles of diagnosis. Thieme, 1998.

College Answer

• Head up – bed currently flat. Elevation to 15-30 degrees may be beneficial for ICP control.
• Remove cervical collar – jugular venous compression may elevate ICP
• Assess ETT ties and if tight replace with alternative fixation method –same rationale
• External ventricular drain is too high – should be lowered
• Drainage of CSF given ICP of 35
• CPP is currently 45. Increase CPP (either by reducing ICP or increasing MAP)
• Consider paralysis; paralysis indicated if patient coughing or posturing and to prevent shivering with temperature control techniques.
• Increase respiratory rate; CO2 is 45 – aim for 35-40mmHg
• Control glucose – hyperglycaemia associated with worse outcome in head injury.
• Temperature is 38.1 – fever associated with elevated ICP; Cool to normothermia initially.
• Consider osmotherapy with hypertonic saline targeting Na+ to 155

Discussion

This question really asks, "how well do you know the Brain Trauma Organisation Guidelines for Management of Traumatic Brain Injury?" This is discussed in detail elsewhere.

It is difficult to make up a specific answer for this without the monitor photograph. From the college answer, one can predict what the picture would have contained.

In any case, whatever the stimulus photograph, the principles are are all the same:

Maintaining cerebral oxygen supply:

• Normoxia: keep the PaO₂ above 60 mmHg
• Normotension: measure the MAP, and keep the systolic above 90mmHg
• Intracranial Pressure monitoring: keep it under 20mmHg
• Cerebral perfusion pressure: keep it 50-70mmHg
• Cerebral oxygenation monitoring:keep the SjO₂ >50%, and PbrO₂ >55mmHg
• Managing increased intracranial pressure for which there is a variety of strategies:
  • Draining the EVD ( about 20ml/hr, max)
  • Positioning the head straight
  • Removing the C-spine collar
  • Sedation :
    • Propofol sedation to decrease distress and thus decrease ICP
    • Barbiturate coma if other methods of lowering ICP have failed
    • Analgesia to prevent increased ICP in response to suctioning and routine care
  • Paralysis
  • Osmotherapy
  • Controversial measures
    • Decompressive craniectomy
    • Hypothermia
    • Dexamethasone

Decreasing cerebral oxygen demand:

• Sedation
  • Propofol sedation to decrease distress and thus decrease ICP
  • Barbiturate coma if medical and surgical methods of lowering ICP have failed
• Analgesia - opioid selection is irrelevant, but opiate boluses increase ICP
• Seizure prophylaxis is infrequently indicated, and the course is 7 days only

Controversial measures:

• Decompressive Craniectomy
• Hypothermia

Our beloved Oh's Intensive Care manual has two excellent chapters to dedicate to this topic:

Chapter 43 (pp. 563) Cerebral protection by Victoria Heaviside and Michelle Hayes, and

Chapter 67 (pp. 765) Severe head injury by John A Myburgh.

There are also the Brain Trauma Organisation Guidelines for Management Traumatic Brain Injury, which one might describe as a definitive reference.

It is debatable as to which of these sources is more out of date. At the time of writing, the BTF guidelines have not been updated since 2007. Oh's Manual has undergone a more recent revision, but is not exactly a well-accepted source of guidelines.

College Answer

Techniques that have proven or demonstrated potential in the diagnosis and monitoring of 
vasospasm include: 

Clinical: 

In the conscious patient, may be detected clinically by new focal neurology or a drop in GCS. Advantages: No additional costs and readily available, can be repeated easily, non-invasive (usually), has to be performed at the bedside. Major disadvantage is lack of specificity often necessitating CT/angiography. Also lacks sensitivity, vasospasm can occur without a clinical correlate, early in the disease. Operator dependent.

Conventional 4 vessel DSA angiography: 

 Remains the gold standard for diagnosis of vasospasm. 
 May allow therapeutic intervention (angioplasty) at the time. 

Disadvantages: invasive, risks of bleeding, embolism, radiation/contrast exposure and transport. Requires skilled interventional radiology, and therefore resource heavy. Risk of stroke (quoted about 1%, but probably a little lower) just from the angio, plus the dissections etc. that occur as well. 

Detects vessel narrowing, not necessarily poor flow to distal tissue in all cases (either increased flow rate through narrow vessel or collateral supply. May lead to over treatment. 

Transcranial Doppler (TCD): 

 It is low risk, performed at the bedside, non-invasive and able to be repeated daily enabling trend analysis. 
 Disadvantages:

• The technique is however operator dependent and there is high inter- observer variability. 
• Debate exists regarding correlation of flow velocity and vasospasm and although high velocities (> 200cm/sec) are predictive, lower velocity may not be as good.
• The technique may be more accurate when MCA velocity is indexed to the ipsilateral extracranial carotid artery (Lindegaard index, >3 strongly predictive). 
• Colour coded TCD may offer greater accuracy than plain TCD alone. 
   

CTA/MRI:

• May be combined with perfusion allowing characterisation of both vascular anatomy and associated perfusion abnormalities. 
   
• MR diffusion weighted imaging accurately identifies brain tissue at high risk of infarction; perfusion weighted imaging reveals asymmetries in regional perfusion. 
   
• Both methods show correlation with delayed ischaemic neurological deficit (DIND). 
   
• Disadvantages:
  • Image clarity will be affected by clip/coil and contrast related issues need consideration. The overall diagnostic capability of this modality however remains unclear until further prospective studies are performed. Similar disadvantages as per angiography with respect to transport, radiation (for CT), contrast exposure, interpretation by experts. 
     

SPECT/PET

• Can be used to obtain a picture of brain perfusion and metabolism and have 
  shown variable correlation with vasospasm as assessed by more conventional 
  methods.
• Disadvantages: They are resource heavy not easily available, radiation exposure, patient 
  transport are issues.

EEG:

• May provide prognostic information, focal areas of slowing correlate with angiographic vasospasm and a decrease in alpha to delta ratio strongly correlates with ischaemia. Sensitivity and specificity for detecting vasospasm is high. 
  
  Disadvantage: Not readily available however and their may be issues with interpretation. 

Tissue sensors:

• The use of measures of tissue oxygenation using parenchymal sensors and microdialysis for 
  monitoring biochemical indices of ischaemia are largely research tools.

Salient points

• Clinical examination
• DSA
• CTA
• EEG
• Transcranial doppler
• Parenchymal sensors
• SPECT

Discussion

This answer lends itself well to a table format.

Apocryphal notes on the diagnosis and management of SAH are also available.

Oh's Intensive Care manual

Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer

Marshall, Scott A., Paul Nyquist, and Wendy C. Ziai. "The role of transcranial Doppler ultrasonography in the diagnosis and management of vasospasm after aneurysmal subarachnoid hemorrhage." Neurosurgery Clinics of North America21.2 (2010): 291-303.

Greenberg, E. D., et al. "Diagnostic accuracy of CT angiography and CT perfusion for cerebral vasospasm: a meta-analysis." American Journal of Neuroradiology 31.10 (2010): 1853-1860.

Sloan, M. A., et al. "Sensitivity and specificity of transcranial Doppler ultrasonography in the diagnosis of vasospasm following subarachnoid hemorrhage." Neurology 39.11 (1989): 1514-1514.

Rivierez, M., et al. "Value of electroencephalogram in prediction and diagnosis of vasospasm after intracranial aneurysm rupture." Acta neurochirurgica 110.1-2 (1991): 17-23.

College Answer

The WCC is elevated but the WCC:RCC ratio is normal (1:500) and represents normal findings after sub-arachnoid haemorrhage but does not exclude infection.

Discussion

This is a faily straightforward data interpretation question. 10,000 / 20 = 500; which is the perfect ratio. This CSF is not infected, it just has blood in it.

Of course, in order to make a more accurate analysis, it would be good to also know the serum WCC, so that one may calculate the proper ratio.

A more detailed discussion of CSF analysis is available elsewhere.

College Answer

Definition:

The acute onset of a disturbance of consciousness with inattention, changes in cognition and/orperception, that fluctuates over time, occurs as a consequence of a general medical condition and isnot better accounted for by a pre-existing, established or evolving dementia.

Management:

1. Early recognition of delirium.

2. Stabilise and ensure safety of the patient:

• • Attend to airway, breathing and circulation issues as required.

3. Consider and rule out any potentially life-threatening causes of delirium (comprehensive history and physical examination will provide clues):

• • Hypoxia
  • Hypoglycaemia
  • Intra-cerebral haemorrhage
  • Meningitis/Encephalitis
  • Poisoning
  • Wernicke’s Encephalopathy
  • Infection: local (wound, anastomotic leaks etc.), UTI, lung etc.
  • Withdrawal from drugs
  • Hypertensive encephalopathy
  • Metabolic derangements – sodium, renal, liver.

4. Consider non-pharmacological strategies to control symptoms:

• • Application of hearing aids, spectacles and dentures if worn.
  • Continuous re-orientation of patient - verbal, visual with photographs etc.
  • Enlist help of family members and/or interpreters.

• • Ensure as close to normal as possible sleep/wake cycles in a quiet and calm environment.
  • Treat pain, constipation, urinary retention if present.

• • Check drug chart and beware/attend to poly-pharmacy and cessation of drugs associated with delirium.
  • Mobilise early.
  • Avoid physical restraints if safe to do so.

5. Obtain pharmacological control of symptoms if necessary:

• • Anti-psychotics are first line agents e.g. haloperidol, olanzepine, quetiapine.

• • Haloperidol 1-5mg iv q30 PRN. Dose can be doubled and repeated. Beware long QTc.

• • Benzodiazepines as first line agents for alcohol withdrawal only. Often used in combination with anti-psychotics in difficult to control symptoms in non-alcohol withdrawal delirium.

6. Treat cause if found:
7. O2, antibiotics, thiamine, glucose, electrolyte replacement, intra-venous fluids if dehydrated.

13

Investigations:

Directed by history, physical examination and differential diagnosis but include/consider;

Basic:

FBC, EUC, Glucose, LFT, ABG, CXR, ECG, Urinalysis + Dipstick, Septic screen, Urinary Drug Screen.

Advanced:

CT Brain, LP, TTE.

Discussion

Delirium is a favourite of the examiners. It is discussed in greater depth elsewhere ("Delirium in the ICU")

In order to simplify revision, I reproduce the salient points here:

A systematic approach to this question would resemble the following:

Urgently exclude and manage any lifethreatening aetiologies of delirium:

A) - Look for airway compromise due to decreased level of consciousness

B) - Assess for hypoxia and hypercapnea

C) - Assess for hypotension (thus cortial hypoperfusion) or hypertension (thus, hypertensive encephalopathy)

D) - Exclude hypoglycaemia and intoxication or poisoning; investigate for focal intracranial causes of delirium, such as intracranial haemorrhage or space-occupying lesion. Think about non-convulsive status epilepticus as the cause of delirium. Also consider withdrawal from alcohol and other drugs.

E) - Evaluate electrolytess, looking for hyponatremia

F) - Assess renal function, looking for uremia and dehydration

G) - Assess hepatic function, suspecting hepatic encephalopathy. Don't forget Wernicke's.

H) - Assess bone marrow function - cytopenia may be a clue to a space-occupying metastatic lesion, whereas blood film findings such as macrocytosis may suggest a chronic nutritional deficiency associated with alcoholism or IV drug abuse.

I) - Assess temperature, inflammatory markers and features of sepsis, ranging from UTI to septic shock (thinking about septic encephalopathy). Consider neurosyphilis and think about meningitis or encephalitis.

Investigation of delirium:

Stemming from the abovementioned differentials,

• ABG
• Urinalysis
• EUC
• CMP
• FBC
• Blood film
• Inflammatory markers
• CT brain
• EEG
• Lumbar puncture

Management of delirium

Non-pharmacological:

• • Good analgesia
  • Clear and firm communication with the patient
  • Frequent re-orientation
  • Family presence
  • Low-noise environment
  • Restoration of hearing aids and spectacles
  • Avoidance of sleep disturbance, promotion of normal sleep–wake cycle.
  • Avoidance of physical restraints
  • Early removal of IV lines and IDCs

Pharmacological:

• • Dexmedetomidine
  • Atypical antipsychotics
  • Classical antipsychotics
  • Benzodiazepines (if withdrawing from alcohol or benzodiazepines)

Oh's Intensive Care manual: Chapter 49   (pp. 549) Disorders  of  consciousness  by Balasubramanian  Venkatesh

Girard, Timothy D., Pratik P. Pandharipande, and E. Wesley Ely. "Delirium in the intensive care unit." Critical Care 12.Suppl 3 (2008): S3.

Ely, E. Wesley, et al. "Evaluation of delirium in critically ill patients: validation of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU)."Critical care medicine 29.7 (2001): 1370-1379.

O'Keeffe, SHAUN T., and JOHN N. Lavan. "Clinical significance of delirium subtypes in older people." Age and ageing 28.2 (1999): 115-119.

Barr, Juliana, et al. "Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit." Critical care medicine 41.1 (2013): 263-306.

Ouimet, Sébastien, et al. "Incidence, risk factors and consequences of ICU delirium." Intensive care medicine 33.1 (2007): 66-73.

Girard, Timothy D., et al. "Delirium as a predictor of long-term cognitive impairment in survivors of critical illness." Critical care medicine 38.7 (2010): 1513.

Hopkins, Ramona O., and James C. Jackson. "Long-term neurocognitive function after critical illness." CHEST Journal 130.3 (2006): 869-878.

van den Boogaard, Mark, et al. "Incidence and short-term consequences of delirium in critically ill patients: a prospective observational cohort study."International journal of nursing studies 49.7 (2012): 775-783.

Stevens, Robert D., Karin J. Neufeld, and Tarek Sharshar. "Delirium in the ICU: time to probe the hard questions." Crit Care 15.1 (2011): 118.

van Boogaard, M., et al. "Development and validation of PRE-DELIRIC (PREdiction of DELIRium in ICu patients) delirium prediction model for intensive care patients: observational multicentre study." BMJ: British Medical Journal344 (2012).

Van Rompaey, Bart, et al. "Risk factors for intensive care delirium: a systematic review." Intensive and Critical Care Nursing 24.2 (2008): 98-107.

Schweickert, William D., et al. "Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomised controlled trial."Lancet (London, England) 373.9678 (2009): 1874-1882.

Skrobik, YoannaK, et al. "Olanzapine vs haloperidol: treating delirium in a critical care setting." Intensive care medicine 30.3 (2004): 444-449.

Milbrandt, Eric B., et al. "Haloperidol use is associated with lower hospital mortality in mechanically ventilated patients*." Critical care medicine 33.1 (2005): 226-229.

Moots, R. J., et al. "Old drug, new tricks: haloperidol inhibits secretion of proinflammatory cytokines." Annals of the rheumatic diseases 58.9 (1999): 585-587.

Page, Valerie J., et al. "Effect of intravenous haloperidol on the duration of delirium and coma in critically ill patients (Hope-ICU): a randomised, double-blind, placebo-controlled trial." The Lancet Respiratory Medicine 1.7 (2013): 515-523.

Gilchrist, Neil A., Ifeoma Asoh, and Bruce Greenberg. "Atypical antipsychotics for the treatment of ICU delirium." Journal of intensive care medicine 27.6 (2012): 354-361.

Jasiak, Karalea D., et al. "Evaluation of discontinuation of atypical antipsychotics prescribed for ICU delirium." Journal of pharmacy practice 26.3 (2013): 253-256.

Inouye, Sharon K., et al. "A multicomponent intervention to prevent delirium in hospitalized older patients." New England journal of medicine 340.9 (1999): 669-676.