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HeadacheBackground:HA is common presenting sxMost causes of HA are benign; however, although representing only 0.5% to 6% of presentations of acute headache to the ED, the most important and commonly encountered life-threatening cause of severe sudden head pain is subarachnoid hemorrhage (SAH)Unfortunately this is missed 25% of the timePathophysiologythe brain parenchyma is insensitive to pain. The pain-sensitive areas of the head include the meninges, the arteries and veins supplying the brain, and the various tissues lining the cavities within the skullmost pain assoc w/ HA, particularly w/ vascular headaches and migraines, is mediated through CNVDifferential DiagnosisHistory and Physical Examdetermine pattern and onsetis it similar to prior headaches > marked variation could signal new or serious problem rapid and severe onset of pain (“thunderclap” headache) assoc w/ serious causes of headache“Almost all studies dealing with subarachnoid bleeding report that patients moved from the pain-free state to severe pain within seconds to minutes. The thunderclap headache is common in acute presentations of SAH but is not highly specific. If the patient with moderate or severe headache can indicate the precise activity in which he or she was engaging at the time of the onset of the headache, the suddenness of onset warrants consideration of SAH. Careful questioning about the onset of headache may lead to the correct diagnosis of SAH, even if the pain is improving at the time of evaluation.” Rosensdetermine the pt’s activity at onset of pain HA that come on during exertion have a relationship to vascular bleedingadditionally, although the syndrome of postcoital headache is well known, coitus is also recognized as an activity associated with SAH, so a pattern of previous postcoital headache is key, as is understanding whether the current headache fits that patternhx of trauma? Ddx switches markedly toward epidural and subdural hematoma, traumatic SAH, or intraparenchymal hemorrhage, skull fracture and closed head injury (concussion, diffuse axonal injury)IntensityPain scale might help differentiate patients intitially > has more value in monitoring response to therapyCharacter of pain (ie, throbbing, pressure) may be helpful to describe and for billing but doesn’t help differentiate the underlying diagnosis Location of head pain – at onset and as the pain progresses > helps examiner look for external casues of pain. Unilateral pain is more suggestive of migraine or localized inflammatory process in skull (sinus, TMJ) or soft tissue (TA, dental infection)Muscle tension usually starts at the base of the skill and can extend over the entire head (following occipital-frontal aponeurosis)Exacerbating or alleviating factors Do headaches occur only when patient goes to a certain area? (ie. Basement workshop) > could be COSignsHigh yield physical exam findingsCN III, IV, and VI defecits > mass lesion or IIHHeadache + red eye >> acute angle glaucoma > investigate intraocular pressureAncillary testings:A CT scan performed within 6 hours of onset of headache has been shown to be sufficiently sensitive to exclude the diagnosis of SAH when using a third-generation CT scannerDiagnostic AlgorithmIndications of patients at higher risk for serious cause of headache who are candidates for more comprehensive evaluation include (1) sudden onset of headache, (2) patient description of the headache as “the worst ever,” (3) altered mental status, (4) meningismus, (5) unexplained fever, (6) focal neurological deficit on examination, (7) symptoms refractory to appropriate treatment or worsening despite treatment, (8) onset of headache during exertion, (9) history of immunosuppression, or (10) pregnancy or peripartum state.Empiric ManagementBreak HA into two categories:w/ AMSassume brain tissue is compromisedprinciples of cerebral resuscitation address the seven major causes of evolving brain injurylack of substrate (glucose, O2)cerebral edemaintracranial lesionendogenous or exogenous toxinmetabolic alteration (fever, seizure)ischemiaelevated ICP recall: ICP = MAP - CCPw/o AMSopioids are not first-line for any time of headache, except when ICH (including SAH) is thought to be presentempiric tx does not precede diagnostic studies except when suspect meningitis Dispositionpts who are not thought to have a serious cause for their head pain requiring hospitalization but who are w/o a specific diagnosis are provided with appropriate return precautions and recommendations for follow-up carecan suggest pts start headache journal to bring to outpatient follow upIdiopathic Intracranial HypertensionPrinciplesAlso called “Pseudotumor cerebri” or benign intracranial HTN (but don’t be fooled, this is not benign > can causes permanent vision loss)Other risk factors: antibiotics (tetracyclines mc), vitamin A, retinoids, and human growth hormoneEpidemiologyIncidence: 1-2/100,000 people Higher incidence in obese women btw 15-44: 4-21/100,000Highest incidence ws reported in Ireland (28/100,000)Risk Factors: Mc seen in young obese women of childbearing ageIn a prospective study of 50 consecutively diagnosed IIH patients, 92 percent were women with a mean age of 31 years (range 11 to 58 years), and 94 percent were obese [10]. Wall, M George D. Brain. “Idiopathic intracranial hypertension. A prospective study of 50 patients.” 1991. Dept of Neuro, TulaneOther case series in different geographic areas and ethnic groups report consistent findings (see UTD)However, IIH can also occur in males, elderly, kids as young as 4mths, and normal weight patients However, work up for secondary causes is even more important in these ptsOne study showed that in orlder pts (44-88) w/ IIH were more often male and less often obese Recent wt gain is a risk factor > one case-control series showed there was an average 1.8kg wt gain over 2mth preceding sx onset. Another showed an average wt gain of 10lbs in preceding yearIdiopathic Intracranial Hypertension Treatment Trial (IIHTT), 5 percent of patients reported a family history of IIH > suggesting genetic componentMedicationsGrowth hormone 2007 study estimated incidenc of IIH in kids tx w/ growth hormone to be 27.7 per 100,000 treatment yearsusually presents w/I one year of tx initiationstopping or resuming a lower dose often stops IIHTetracyclines (including minocycline and doxycycline)Onset usually w/I few weeks to months after onset of txUsually goes away with drug withdrawalHypervitaminosis A from excessive dietary intakeDerm retinoids (all-trans retinoic acid, isotretinoin, retinol, and tretinoin)Other anecdotal evidenceThyroid replacementCorticodsteroid withdrawalLithiumNalidixic acidNitrofurantoinOther systemic illness assoc w/ IIH besides obesityAddison disease Hypoparathyroidism Anemia, usually severe Sleep apneaSystemic lupus erythematosus (SLE)Beh?et syndromePolycystic ovary syndrome Coagulation disorders Uremia Pathogenesis not well well understood. Theories: imbalance of CSF production and reabsorption [Rosen’s]cerebral venous outflow abnormalities (ie. Venous stenosis or venous HTN)increased CSF outflow resistance at level of arachnoid granulations or CSF lymphatic drainage sites obesity-related increased abdominal and intracranial venous pressurealtered sodium and water retention mechanismsabnormalities of vitamin A metabolism intracranial venous hypertensionElevated intracranial venous pressure is postulated both as a primary mechanism and as a "final common pathway" for IIH. This theory is supported by the similar clinical appearances of IIH and secondary intracranial hypertension due to cerebral venous thrombosis and other causes of obstructed venous outflow. Some patients thought to have IIH have been later discovered to have one of these conditionsClinical features sx: HA is usually gradual in onset and moderate in intensity (occurs in 84-92% of pts per UTD)sometimes headache is worsened by eye movementcan be constant of come in wavesmay awaken pt from sleepincreases when pt bends forward or Valsalva maneuver (both impede cerebral venous return)kids are less likely to present with HA (one study showed 29% of kids did not have HA)visual complaints are commonpts may complain of transient visual obscurations (TVOs) (68-72% of pts per UTD or 2/3 of pts with papilledema)> momentary blackouts of vision most likely due to temporary disruption of microcirculation to optic nerve headusually occur with postural changes > do not predict vision loss diplopia 18-38% - usually caused by unilateral or bilateral 6th CN palsey or divergence insufficiency from increased ICPretrobulbar pain 44%photopsia (brief sparkles or flashes of light) 48-54%Intracranial noises (pulsatile tinnitus or rushing of wind/water) occurs in 52-60% n/v, dizziness and pulsatile tinnitusPhysical Exam50% of pts will have papilledema and visual field deficitson occasion, 6th n palsey is noted (false lateralizing sign)papilledemafundoscope > graded by Frisen scale > the more severe the higher risk of permanent vision lossvision lossvisual field loss occurs before changes in visual acuityvisual field loss usually peripheralDDxCVT, mass lesions, obstructive hydrocephalus, and leptomeningeal infiltration by neoplastic or infectious processUTD : Intracranial mass lesions (tumors, abscess)Obstruction of venous outflow, ie (venous sinus thrombosis, jugular vein compression, neck surgery)Obstructive hydrocephalusDecreased CSF absorption (ie. Arachnoid granulation adhesions after bacterial or other infectious meningitis, subarachnoid hemorrhage)Increased CSF production (ie. Choroid plexus papilloma)Malignant systemic HTNDiagnostic TestingMRI w/ MRV is preferred modality for diagnosis b/c is detects mass lesions and hydrocephalus, as well as cerebral venous thrombosis or meningeal processesIf neuroimaging is normal, doctor should get LP in lateral decubitus position to measure CSF opening pressure and get CSF studies (cell count, protein, glucose, cultures, and cytology)Opening pressure of >/= 250mmH2O (normal is 70-180) is needed to make diagnosis [Rosens]Traditionally, the ULN is 200mmHg but obese pts may have a higher ULN, with opening pressures that may normally approach 250mmHg (UTD)In young children <8yrs), they seem to have an a higher ULN. Dx based on 90th percentile to be > 250-280mmHg in kids not sedated or obeseAlso order ophtho consult for detailed visual field testingManagement Patients that present w/o vision loss, sx therapy is all that is necessaryWeight loss Low-Na+ weight reduction program > some might need surgical intervention for morbid obesityHowever, medications are generally given at the same time as weight loss since it takes awhile to lose weight Removal of a large amount of CSF (>20mL) to decrease CSF pressure to relieve that patient’s HAis recommended in all tx guidelines for IHHAvoid serial lumbar punctures CSF re-accumulates w/I 6hrs so has short effectLPs are uncomfortable and painful to many There are complications with LPs (low pressure HA, CSF leak, CSF infxn, intraspinal epidermoid tumors)In obese pts, LPs are difficultHowever, can use serial LPs as a temporizing measure before surgery or in pregnany patietns who wish to avoid therapyIf has sx vision loss, tx with meds to lower ICPAcetazolamide –> usually started at 500mg BID > advance as tolerated up to 2-4g per dayIn kids, starting dose is 25mg/kg/day (max dose of 100mg/kg or 2g per day)MOA: carbonic anhydrase inhibitor > decreased rate of CSF productionAverage tx duration was 14 months per 1 long term follow up studySE: digital and oral paresthesias, anorexia, malaise, metallic taste, fatigue, nausea, vomiting, electrolyte changes, mild metabolic acidosis, and kidney stones (usually dose related)The IIHTT study found monitoring electrolytes during acetazolamide tx was not necessary if it is the only diuretic usedDiamoxi sustained release could be used by patients who can’t tolerate generic version but is much more moneyMethazolamide (Neptazane) is another CAinhibitor that can be tried Contraindications: sulfa allergy (releative…little clinical or pharm basis for this rec) A true cross-reaction between sulfonamide antimicrobials and the sulfa moiety in acetazolamide and furosemide is unlikely. Therefore, if no severe reaction, have a risk and benefits discussion with patient.Pregnancy (relative contraindication > Class C pregnancy risk)Particularly first 20 weeksTeratogenic effects have been reports in high doses in animals, and a single case of teratoma was seen in humansHave risk and benefit discussion with patient and Ob/Gyn and have patient sign informed consentFurosemideCan be used as an adjunct therapy to acetazolamide in IIHone report of eight children treated with combined therapy of acetazolamide and furosemide, all had a rapid clinical response with resolution of papilledema, reduction in the mean CSF pressure after the first week of treatment, and normalization of CSF pressure within six weeks of starting therapyDose: Adults: 20 to 40mg per dayKids: 1-2mg/kg/dayRelative Contraindication = hx of sulfa-allergySame principle applies as with acetazolamideTopiramateMOA: anti-seizure drug that inhibits carbonic anhydrase activityIts efficacy in the treatment of migraine headaches and its association with weight loss are features that make it an attractive potential therapeutic option in IIH.But more studies have to be done before it is considered first-line txSteroids – should be avoided:Can cause weight gainWithdrawal can cause severe rebound intracranial HTN assoc w/ marked vision lossSignificant systemic side effects*** can be considered in the settting of acute vision loss as a temporizing measure prior to surgical intervention One case series describes successful use of methylprednisolone (250 mg four times a day for five days followed by an oral taper) in conjunction with acetazolamide in four patients with IIH and severe, acute visual lossAvoid using too many ibuprofen or Tylenol to prevent analgesic overuse/rebound headachesIf vision loss and sx do not improve with meds, refer to ophtho for optic nerve sheath decompression or neurosurgery for CSF diversion (lumboperitoneal or ventriculperitoneal shunt)Prognosis No large studies have described the natural history of IIH >> protracted course lasting months to years appears commonPermanent vision loss is major concernEarly, hospital study showed 24% of pts developed (n=57, followed for 5-41yrs) developed blindnessCommunity and clinic-based studies have found a lower rateRecurrence: recurrence of symptoms may occur in 8 to 38 percent of patients after recovery from an episode of IIH or after a prolonged period of stabilityWeight gain will increase recurrence DispositionOptho and neurology should be involved in patient’s evaluation, tx and dispo from ER since vision loss can occur early or late in the course of IIHIIH and USPrior studies have illustrated that optic disc elevation, with a minimum disc height of 0.6 mm, obtained via ultrasound can be 82% sensitive and 76% specific for papilledema [Teismann]Using invasive intracranial monitoring as a reference standard, previous studies have revealed that an optic nerve sheath diameter of greater than five mm, measured three mm posterior to the orbit, can be a sensitive (88%) and specific (93%) marker for elevated intracranial pressure of greater than 20 cm H2O [Stone, Kimberly]REFERENCESChristopher S. Russi and Laura Walker “Headache.” Ch17. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th edition Thomas Kwiatkowski and Benjamin W. Friedman. “Headache Disorders.” Ch 93. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th editionBoyd JS, Rupp JD, Ferre RM.?EMERGENCY ULTRASOUND.?In:?Knoop KJ, Stack LB, Storrow AB, Thurman R.?eds.?The Atlas of Emergency Medicine, 4e?New York, NY: McGraw-Hill; .? April 13, 2020.John F. Salmon MD. “Neuro-ophthalmology.” Kanski's Clinical Ophthalmology, Chapter 19, 745-825 intracranial hypertension (pseudotumor cerebri): Epidemiology and pathogenesis intracranial hypertension (pseudotumor cerebri): Clinical features and diagnosis intracranial hypertension (pseudotumor cerebri): Prognosis and treatment. “Ultrasound diagnosis of papilledema and increased intracranial pressure in pseudotumor cerebri.” Am J Emerg Med. 2009 March HH, Shah S, Marill K, et al. Correlation of optic nerve sheath diameter with direct measurement of intracranial pressure.?Acad Emerg Med.?2008;15(2):201–4.Teismann N, Lenaghan P, Nolan R, et al. Point-of-care ocular ultrasound to detect optic disc swelling.?Acad Emerg Med.?2013;20(9):920–5.? Sinnott. “Papilledema: Point-of-Care Ultrasound Diagnosis in the Emergency Department” Clin Pract Cases Emerg Med. 2018 May; 2(2): 125–127. ................
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