Rosen & Barkin's 5-Minute Emergency Medicine Consult (579 page)

• Headache:
  
  • Typically described as constant, bilateral
    
  • Pressure like
    
  • Worse in the morning
    
  • Worse with Valsalva maneuver
    
• Nausea and vomiting
  
• Tinnitus or pulsatile intracranial noise
  
• Diplopia
  
• Dizziness
  
• Scotoma
  
• Transient visual obscurations lasting seconds
  
• Blind spots
  
• Constriction of vision
  

• Visual field defects (in up to 90%):
  
  • Typically inferior nasal visual field loss
    
• Papilledema
  
• Lumbar puncture improves symptoms
  
• 6th cranial nerve palsy
  
• Loss of visual acuity
  
• Otherwise normal neurologic exam except:
  
  • Visual changes
    
  • Abducens palsy
    
  • Rarely 7th cranial nerve palsy
    

• Usually presents with strabismus as opposed to headache and visual field loss
  
• Also associated with obesity and medications (tetracycline antibiotics, steroids)
  

• Thorough history and physical exam
  
• Detailed neurologic assessment and fundoscopic exam
  

• Lumbar puncture: CSF normal or low protein with a normal cell count
  
• Opening pressure >25 cm H
  ₂
  O or >20 cm H
  ₂
  O in nonobese, relaxed patient
  
• Consider CBC, coagulation studies prior to lumbar puncture
  
• Improvement of symptoms with lumbar puncture
  

• Head CT/MRI to rule out mass lesions (prior to lumbar puncture)
  
• Classically, the head CT will demonstrate slitlike frontal horns of the lateral ventricles
  
• MRI recommended in the full workup:
  
  • Can be done as an outpatient
    
  • Cerebral venous thrombosis can mimic pseudotumor cerebri in all regards including normal head CT
    

• Modified Dandy criteria for diagnosis:
  
  • Symptoms of raised intracranial pressure
    
  • No localizing symptoms with exception of 6th nerve palsy
    
  • Patient is awake and alert
    
  • Normal CT/MRI findings without evidence of thrombosis
    
  • Lumbar puncture opening pressure >25 cm H
    ₂
    O (some suggest >20 cm H
    ₂
    O in nonobese, relaxed patients)
    
• Lumbar puncture
  
  • Opening pressure should be performed in lateral decubitus position with neck and legs straight
    
  • Observing respiratory variation ensures good transmission of pressure
    
  • Improvement of symptoms may occur with lumbar puncture
    

• Migraine headache
  
• Hypertensive headache
  
• Anoxic headache
  
• Tension headache
  
• Cluster headache
  
• Subarachnoid hemorrhage
  
• Aneurysm/arteriovenous malformation
  
• Meningitis/encephalitis
  
• Subdural hematoma
  
• Epidural hematoma
  
• Tumor
  
• Abscess
  
• Trigeminal neuralgia
  
• Giant cell/temporal arteritis
  
• Sinusitis
  
• Glaucoma
  
• Central retinal vein/artery occlusion
  
• Congenital optic nerve head elevation
  
• Optic nerve drusen
  
• Labyrinthitis
  
• Optic neuritis
  
• Cerebral venous thrombosis
  
• Chronic carbon dioxide retention
  

TREATMENT

Pain control as appropriate

• Airway and circulation management as indicated
  
• IV fluid hydration
  

• Large-volume lumbar puncture of 20–30 mL of CSF:
  
  • Only if confident of correct diagnosis and head CT demonstrates open basilar cisterns and 4th ventricle
    
• Acetazolamide
  
• Pain control
  
• Neurology consult
  
• Ophthalmology consult
  
• Neurosurgery consult for acute or impending visual loss unresponsive to diuretics (for lumboperitoneal shunt)
  
• Optic nerve fenestration is another surgical option
  
• Venous sinus stenting if stenosis is present
  
• Weight loss
  
• Discontinue any drugs that could be causative
  
• Typically resolves spontaneously
  

• Acetaminophen: 500 mg PO (peds: 10–15 mg/kg; do not exceed 5 doses/24 h) PO q6h; do not exceed 4 g/24 h
  
• Acetazolamide: 500 mg slow-release PO BID (peds: 25 mg/kg/d div. TID/QID) PO/IV
  
• Ibuprofen: 600–800 mg (peds: 10 mg/kg) PO q8h
  
• Lasix: 0.5–1 mg/kg IV/PO
  
• Morphine: 0.1 mg/kg IV/IM
  
• Prednisone: Helpful when severe visual symptoms present, 5-day course recommended (longer treatment not recommended)
  

• Acetazolamide
  
• NSAIDs
  

Topiramate has been suggested as a 2nd-line agent but is not FDA approved for this use

FOLLOW-UP

Acute or impending visual loss

• Consultation obtained from neurology and ophthalmology
  
• Appropriate follow-up arranged
  
• Tolerating oral diuretics
  
• Pain under control
  

Timely referral and return precautions:

• Visual loss
  
• Focal neurologic deficit
  
• Worsening headache
  

Follow-up is recommended with neurology and ophthalmology

• Consider this diagnosis in younger patients with chronic headache
  
• Consider measuring opening pressure when performing lumbar puncture for headache
  
• Measure opening pressure with neck and legs straight in lateral decubitus position
  
• Visual changes can portend visual loss
  

• Bradley WG, Daroff R, Fenichel G, et al., eds.
  Neurology in Clinical Practice
  . 5th ed. Philadelphia, PA: Butterworth-Heinemann, 2008.
  
• Galgano MA, Deshaies EM. An update on the management of pseudotumor cerebri.
  Clin Neurol Neurosurg
  . 2013;115:252--259.
  
• Lee AG, Wall M. Idiopathic Intracranial hypertension. In: UpToDate, Basow DS, eds.
  UpToDate
  : Waltham, MA, 2013.
  
• Randhawa S, Van Stavern GP. Idiopathic intracranial hypertension (pseudotumor cerebri).
  Curr Opin Ophthalmol
  . 2008;19:445–453.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Giant Cell Arteritis
  
• Headache
  
• Headache, Migraine
  
• Labyrinthitis
  
• Trigeminal Neuralgia
  

CODES

348.2 Benign intracranial hypertension

BASICS

• Chronic, noncontagious, inflammatory skin condition
  
• Disease of hyperproliferation
  
• Recently classified as an autoimmune disease
  
• Presents with erythematous plaques with silver scaling
  
• Most commonly affects the elbows, knees, lumbar area, gluteal cleft, and glans penis
  
• Up to 1/3 of patients develop associated arthritis and 10% have ocular manifestations
  
• Course is unpredictable; marked variability in severity over time and remissions may be seen
  
• Exact cause unclear: triggers may be infectious, stressors, medications, or trauma
  
• Tends to show improvement in summer months, possibly related to UV exposure
  
• Associated with metabolic syndrome
  
• Caucasians and atopics most affected
  
• 2 peaks of onset: between ages 20–30 and 50–60
  
• Affects 2.2% of US population, slightly higher incidence in females
  
• Rare cause of mortality, but at least 100 deaths annually in US related to severe disease and/or treatment adverse effects
  
• Several clinical presentations:
  
  • Plaque-type psoriasis (psoriasis vulgaris):
    
    • Most common form (75–80%) with erythematous, raised plaques with well-demarcated borders distributed over the scalp, back, and extensor side of the knees and elbows
      
  • Guttate psoriasis:
    
    • Abrupt appearance of multiple, discrete, salmon-colored, “drop-like” papules with a fine scale in a patient with no prior history of psoriasis
      
    • Most commonly seen on the trunk and proximal extremities
      
    • Often preceded by a streptococcal infection and resolves spontaneously
      
  • Pustular psoriasis:
    
    • Occasionally isolated to the palms and soles, but can present as widespread erythema, scaling, and sheets of superficial pustules with erosions
      
    • Patient may appear toxic and have other systemic symptoms, like malaise, fever, and diarrhea
      
    • Potentially severe and life threatening and treated as an inpatient if generalized
      
  • Erythrodermic psoriasis:
    
    • Generalized erythema and pruritis with a fine scale
      
    • Increased risk for infection, dehydration
      
    • Often treated as inpatients
      
  • Nail psoriasis
    
    • Pitting over the nail plate or change in nail bed
      
    • Nail changes in up to 50% of patients
      
  • Inverse flexural psoriasis:
    
    • A variant that causes lesions in flexural areas and in skin folds that do not exhibit scaling due to moisture in these areas
      
  • HIV-induced psoriasis:
    
    • May be the first manifestation of AIDS, more frequent and severe in HIV population
      
• Genetics:
  
  • There is a genetic predisposition and gene loci have been identified
    
  • 40% of patients with psoriasis have a family history in a 1st degree relative