Sim Cliff Notes - October 2017

Every month we summarize our simulation cases. No deep dive here, just the top 5 takeaways from each case.  This month's cases included pediatric status epilepticus, Idiopathic Intracranial Hypertension and spinal epidural abscess.


5 Step approach to Pediatric Status Epilepticus


1.  Understand the stages of pediatric status epilepticus to guide your sequence of medication administration.

  • Definitions
    • “Impending status” (5-30 minutes in duration)
    • “Refractory status”  (Failure to respond to 2 or 3 meds)
    • "Status epilepticus" - continued seizure activity or recurrent seizure without full recovery in between seizures
  • Any patient brought in via EMS still seizing is probably impending status

2.   Take care of your priorities in SE - ABCD

  • Airway/Breathing:  O2, position, suction, oral/nasal airway- hypoxia is the enemy of the seizing brain!
  • Circulation: Cardiac monitor, IV/IO access, bedside glucose, blood to hold
  • Disability:  Stop the seizure!  Treat hypoglycemia, look for trauma, prevent brain injury by treating hyperthermia, (from seizure or underlying infection), preventing hypoxia

3.  The treatment of status epilepticus cycles through different receptors (GABA, sodium channel blockers, calcium channel blocker)

  • Here area few overall guiding principles regarding treatment
    • The longer the seizure lasts, the longer it will last/harder it will be to break (most self terminating seizures last 3 minutes)
    • After 15 minutes of seizure activity, there are fewer "off switches" (GABA receptors) on cell membrane, increased number of “on switches” (NMDA receptors) 
    • 20 mg/kg is a common initial drug dose for
      • Fosphenytoin
      • Levetiracetam
      • Phenobarbital
  •    First Line Medications: GABA receptor agents: Benzodiazepines
    •  IV/IO in place ? --> give  IV/IO lorazepam
    • No IV/IO ? -->  give midazolam via buccal, IM, INH, or PR routes
  •   Second Line Medications: Sodium Channel Agents
    • Begin after 2 doses of benzodiazepines
    • Fosphenytoin first choice (20 PE/kg IV)
  • Calcium Channel Blocker (Depakote) or New Kid on the block (Levetiracetam)
  • Throw the kitchen sink at 'em
    • Phenobartibal (enhances GABA effects)
    • Coma Induction (Midazolam bolus and infusion)

Maine medical Center Pediatric

Status epilepticus protocol

 Produced by Marisa Hori, MD and Nate Mick, MD;  the above guideline can be found at

Produced by Marisa Hori, MD and Nate Mick, MD;  the above guideline can be found at


4.  Consider additional workup during treatment.

  • Younger child more likely to have acute symptomatic cause (< 6 mo)
  • Lab work: 
    • Immediate testing should include:  Glucose, metabolic panel, calcium, magnesium
    • Additional tests to consider: Blood culture, anti-epileptic drug levels, toxicology screen, consider lumbar puncture if indicated
  • CT head;  Higher yield in younger infant status, unlikely to be helpful in the older status child but should likely still be obtained

5.  Consider ordering a stat EEG for non-convulsive status (e.g. subtle eye movements, lip smacking).

  •  Neonatal seizures in particular can be subtle and difficult to recognize (eg. lip smacking, repetitive eye movements).
This video demonstrates a seizure in a six day old infant. The cause of the seizure is unknown at the time of the video being uploaded. The seizure appears to be focal tonic class of neonatal seizure. We thank the parents of this infant for willingly allowing the video to be used for teaching others how to recognize neonatal seizures.

Obtained from youtube site of Larry Mellick, MD



1. Trinka E, Cock H, Hesdorffer D, et al. A definition and classification of status epilepticus-Report of the International League Against Epilepsy (ILAE) Task Force on Classification of Status Epilepticus. Epilepsia. 2015 Oct;56(10):1515-23.

2. Glauser T, Shinnar S, Gloss D, et al. Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society. Epilepsy Curr. 2016 Jan-Feb;16(1):48-61.

3. Riviello JJ Jr, Ashwal S, Hirtz D, et al. Practice parameter: diagnostic assessment of the child with status epilepticus (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. 2006 Nov 14;67(9):1542-50 full-text, reaffirmed 2016 Jan 23.

4. Smith DM, McGinnis EL, Walleigh DJ, Abend NS. Management of Status Epilepticus in Children. J Clin Med. 2016 Apr 13;5(4):pii.E47.

5. Brophy GM, Bell R, Claassen J, et al; Neurocritical Care Society Status Epilepticus Guideline Writing Committee. Guidelines for the evaluation and management of status epilepticus. Neurocrit Care. 2012 Aug;17(1):3-23 or at National Guideline Clearinghouse 2012 Sep 24:37274, editorial can be found in Neurocrit Care 2012 Aug;17(1):1



Idiopathic Intracranial Hypertension (IIH)


1. What is it and why should I care?

  • Raised intracranial pressure in absence of a space-occupying lesion
    • Often presents as a headache syndrome with signs and symptoms of increased intracranial pressure (ICP)
    • The composition of the cerebrospinal fluid is normal but opening pressure is elevated
    • No other cause of increased intracranial pressure identified (e.g. dural venous thrombosis) 
    • There is no evidence of hydrocephalus, mass, structural or vascular lesion
  • The most significant sequela of IIH is blindness or permanent visual impairment caused by prolonged papilledema, with secondary optic atrophy.

2.  Major risk factors for IIH include:

  • Obesity (doubles risk), or recent weight gain
  • Associated conditions (PCOS, Hypertension)
  • Female gender (4:1 to 15:1 female to male ratio)

3.  History and Physical

  • Top 3 symptoms
    • Constant, gradual onset, generalized, severe headache in 68%-98% of patients
      • Headache may show features of raised intracranial hypertension (e.g. headache exacerbated by coughing, straining, valsalva maneuver)
    • Transient visual obscurations (shadows, dark patches, or black spots in one or both eyes) in 57%-72%
    • Pulsatile tinnitus (including "whooshing" or "roaring") in 60%
  • Papilledema is a characteristic feature and is nearly always observed in acute presentation
    • If the pretest probability for IIH is high and you are unable to see the fundus, strongly consider using short acting mydriatic (e.g. tropicamide) to dilate and screen for this condition


4.  Perform a lumbar puncture with opening pressure (OP) to evaluate for elevated ICP.

  • Must be measured in the lateral recumbent position with legs and neck straight to be most accurate
  • The normal range for OP is reported differently in various sources, with most reporting a normal range of 7-18 cm H2O in adults, though some consider the normal range 5-25 cm H2O. 
  • A pressure >25 cm H2O or <5 cm H2O should certainly prompt you to look for a source
  • Check out these great tips on measuring opening pressure from Academic Life in EM

5. Treatment of Idiopathic Intracranial Hypertension

  • Weight reduction recommended for all patients (5%-10% of body weight)
  • Neurology follow up after ED visit
  • Acetazolamide as first line (carbonic anhydrase inhibitor that reduces CSF production)
  • Surgical treatment indicated if fulminant disease or when other treatments have failed to prevent progressive vision loss (eg. cerebrospinal fluid shunting or optic nerve sheath fenestration)


1.  Reichman E F, Polglaze K, Euerle B. Neurological and Neurosurgical Procedures: Lumbar Puncture. In: Emergency Medicine Procedures. McGraw Hill; 2013:747-761.

2.  Lee S, Lueck C. Cerebrospinal fluid pressure in adultsJ Neuroophthalmol. 2014;34(3):278-283. 

3.  Giuseffi V1, Wall M, Siegel PZ, Rojas PB. Symptoms and disease associations in idiopathic intracranial hypertension (pseudotumor cerebri): a case-control study. Neurology. 1991 Feb;41(2 ( Pt 1)):239-44.

4.  Wall, M, George D.  Idiopathic intracranail hypertension. A prospective study of 50 patients. Brain. 1991 Feb;114 ( Pt 1A):155-80.

5. Ball AK, Clarke CE. Idiopathic intracranial hypertension. Lancet Neurol. 2006 May;5(5):433-42

6. Skau M, Brennum J, Gjerris F, Jensen R. What is new about idiopathic intracranial hypertension? An updated review of mechanism and treatment. Cephalalgia. 2006 Apr;26(4):384-99  EBSCOhost Full Text

7. Thurtell MJ, Wall M. Idiopathic intracranial hypertension (pseudotumor cerebri): recognition, treatment, and ongoing management. Curr Treat Options Neurol. 2013 Feb;15(1):1-12 full-text

8. Friedman DI, Liu GT, Digre KB. Revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. Neurology. 2013 Sep 24;81(13):1159-65

5 step approach to diagnosing a spinal epidural abscess

1.  Generate a differential and consistent method to evaluate for high risk etiologies of lower back pain.

  • Spinal epidural abscess (SEA) is a relatively uncommon yet highly morbid and potentially lethal pyogenic infection of the central nervous system (CNS)
  • Spinal epidural abscess can rapidly and unpredictably evolve to irreversible neurologic injury via pathophysiologic mechanisms that culminate in ischemic necrosis of the spinal cord
  • In isolation, most elements of history and physical exam are insufficient to rule in or rule out this disease

2.  Assess the patient's risk factors for spinal epidural abscess.

  • Compromised immunity is found in 50% of SEA (diabetes mellitus, alcohol abuse, end stage renal disease, malignancy, AIDS)
  • Recent instrumentation (spinal surgery, epidural)
  • Local or hematogenous spread of bacteria (IV drug abusers, indwelling catheters, recent remote infection - especially skin and soft tissue infections)
  • Recent fever
  • Bounceback” patient
    • SEA patients more likely to have been given recent antibiotics or had recent visit to other health care provider
    • Be careful not to have bias against these "bounceback" patients - they are giving you a second chance to catch what was missed on the first visit

3. The presentation for SEA can be vague, variable, indolent and inconsistent.

  • Back pain in 85%
  • Paresthesias in 35%
  • Fever 66%
  • Neurologic deficits (if you wait for these to diagnose SEA, you are missing the boat!)
    • Radicular pain
    • Sensory or motor deficits
    • Meningismus
    • Loss of bowel or bladder function
  • Only 33% of patients present with the "classic triad" of fever, back and and neurologic deficit
  • Looks for signs of meningitis
    • Kernig sign - patient does not extend the leg at the knee when the thigh is flexed
    • Brudzinski sign - severe neck stiffness causes a patient's hips and knees to flex when neck flexed forward
    • Spine shows tenderness to percussion
  • Noncontiguous coinfections were documented in 53.7% of cases (pneumonia, distant osteomyelitis, infective endocarditis, and soft tissue or foreign body site) - BE WARY OF EARLY DIAGNOSIS CLOSURE WHEN LOOKING FOR A CAUSE OF THE PATIENT'S FEVER!
 Clinical Manifestations and Lab results of spinal epidural abscess patients compared to controls&nbsp;&nbsp; Open Forum Infect Dis 2016 Sep 14;3(4):ofw19

Clinical Manifestations and Lab results of spinal epidural abscess patients compared to controls  Open Forum Infect Dis 2016 Sep 14;3(4):ofw19


4.    Have a low threshold to order an ESR, CBC, CRP for the appropriate patient context (risk factors, signs/symptoms) or go straight to MRI with gadolinium.

  • Comparing laboratory abnormalities in 162 patients with epidural lesion vs. 88 patients without epidural lesion:
    • White blood cell count (WBC) > 11,000 cells/L in 66.7% vs. 40.2%% (p < 0.001)
    • Erythrocyte sedimentation rate (ESR) > 50 mm/hr in 78.8% vs. 25.9% (p < 0.001)
    • C-reactive protein (CRP) > 3 mg/L in 81.2% vs. 35% (p < 0.001)
  • Imaging of the entire spine is preferred as SEA can be variable in location, involve more than once column, or have skip lesions.
  • Magnetic resonance imaging (MRI) with gadolinium is the modality of choice for detecting SEA

5.  SEA is almost always a surgical disease in addition to antibiotics.  Consult neurosurgery for source control/surgical decompression if you suspect SEA and neurologic symptoms are present (complete paralysis cited 30 min – 24 hours after).


1. Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006 Nov 9;355(19):2012-20.

2. Pradilla G, Ardila GP, Hsu W, Rigamonti D. Epidural abscesses of the CNS. Lancet Neurol. 2009 Mar;8(3):292-300.

3. Shah NH, Roos KL. Spinal epidural abscess and paralytic mechanisms. Curr Opin Neurol. 2013 Jun;26(3):314-7.

4. Grewal S, Hocking G, Wildsmith JA. Epidural abscesses. Br J Anaesth. 2006 Mar;96(3):292-302 full-text.

5. Tompkins M, Panuncialman I, Lucas P, Palumbo M. Spinal epidural abscess. J Emerg Med. 2010 Sep;39(3):384-90

6.  Artenstein AW et al.  Spinal Epidural Abscess in Adults: A 10-Year Clinical Experience at a Tertiary Care Academic Medical Center, Open Forum Infect Dis 2016 Sep 14;3(4):ofw19.


Helfpul Guidelines

Written and posted by Jeffrey A Holmes, MD